Emergency Diagnosis - C Kieth - Anything Prepping.com

CURRENT Emergency Diagnosis & Treatment (LANGE CURRENT Series) 

by C. Keith, Md. Stone (Editor), Roger, Md. Humphries (Editor) Publisher: McGraw Hill 

Text; 5th edition (November 21, 2003) 

By OkDoKeY

CURRENT EMERGENCY DIAGNOSIS & TREATMENT - 5th Ed. (2004) 

FRONT MATTER 

Title Page 

Copyright Page 

Contents 

Authors 

Preface 

SECTION I - SPECIAL ASPECTS OF EMERGENCY MEDICINE 

SECTION II - MANAGEMENT OF COMMON EMERGENCY PROBLEMS 

SECTION III - TRAUMA EMERGENCIES 

SECTION IV - NONTRAUMA EMERGENCIES


1. Approach to the Emergency Department Patient - Mary Nan S. Mallory, MD, 

RDMS & Robert Perry Pringle, Jr., MD 

WHAT IS EMERGENCY MEDICINE? 

BIRTH & GROWTH OF EMERGENCY MEDICINE 

SCOPE OF PRACTICE 

PRINCIPLES OF EMERGENCY MEDICINE 

CONCLUSION 

TABLES 

2. Prehospital Emergency Medical Services 1 - Eric M. Sergienko, MD, & 

Thomas N. Bottoni, MD 

INTRODUCTION 

COMPONENTS OF THE EMERGENCY MEDICAL SERVICES SYSTEM 

PREHOSPITAL SKILLS & TECHNIQUES 

TABLES 

FIGURES 

3. Nuclear, Biologic, & Chemical Agents; Weapons of Mass Destruction - 

Michael W. Stava, MD, & Joachim Franklin, MD 

INTRODUCTION 

NUCLEAR WEAPONS 

BIOLOGIC WEAPONS 

CHEMICAL WEAPONS (See Table 3-5.) 

TABLES 

4. Multicasualty Incidents & Disasters 1 - Louis James Kroot, MD, & Robert B. 

Gray, MD 

INTRODUCTION 

EPIDEMIOLOGY OF DISASTERS 

PREHOSPITAL MANAGEMENT OF MULTICASUALTY INCIDENTS & 

DISASTERS 

EMERGENCY DEPARTMENT DISASTER MANAGEMENT 

STRESS MANAGEMENT & PSYCHOLOGICAL SUPPORT 

TABLES 

FIGURES 

5. Legal Aspects of Emergency Care - Charles A. Eckerline, Jr, MD, FACEP, & 

Steven D. Rothert, MD, JD 

INTRODUCTION 

GENERAL LEGAL PRINCIPLES 

COMMON LEGAL PROBLEMS IN THE EMERGENCY DEPARTMENT 

6. Emergency Procedures 1 - William Randall Partin, MD 

GENERAL INSTRUCTIONS FOR SKIN PREPARATION & STERILE 

TECHNIQUE 

UPPER EXTREMITY VENIPUNCTURE 

EMERGENCY ANTECUBITAL FOSSA VENOUS CUTDOWN 

PERIPHERAL VENOUS CATHETERIZATION WITH A CATHETER-CLAD 

NEEDLE 

PERIPHERAL VENOUS CATHETERIZATION WITH A SCALP VEIN 

(BUTTERFLY) NEEDLE 

EXTERNAL JUGULAR VEIN CATHETERIZATION 

INTERNAL JUGULAR VEIN CATHETERIZATION

SUBCLAVIAN VEIN CATHETERIZATION 

FEMORAL VEIN PHLEBOTOMY OR CATHETERIZATION 

SAPHENOUS VEIN CUTDOWN 

INTRAOSSEOUS INFUSION 

RADIAL ARTERY PUNCTURE (For Blood Gas & pH Analysis) 

DIRECT LARYNGOSCOPY, OROTRACHEAL INTUBATION, & 

NASOTRACHEAL INTUBATION 

NASOGASTRIC INTUBATION (For Gastric Evacuation or Lavage) 

INSERTION OF SENGSTAKEN-BLAKEMORE OR MINNESOTA TUBE 

CRICOTHYROTOMY 

TRANSTRACHEAL JET VENTILATION 

THORACENTESIS 

TUBE THORACOSTOMY (Insertion of a Chest Tube) 

PERICARDIOCENTESIS 

FOCUSED ASSESSMENT WITH SONOGRAPHY FOR TRAUMA 

ABDOMINAL PARACENTESIS 

PERITONEAL CATHETER INSERTION & PERITONEAL LAVAGE 

INSERTION OF INDWELLING (FOLEY) URINARY CATHETER 

PERCUTANEOUS SUPRAPUBIC CYSTOTOMY 

LUMBAR PUNCTURE 

ANTERIOR & POSTERIOR NASAL PACKING FOR CONTROL OF 

EPISTAXIS 

ARTHROCENTESIS (Knee, Shoulder, Elbow, Ankle, Wrist, Hand, & Foot 

Joints) 

INCISION & DRAINAGE OF SUPERFICIAL ABSCESS 

TRANSCUTANEOUS CARDIAC PACING 

TABLES 

FIGURES


7. Basic & Advanced Cardiac Life Support - Eric M. Sergienko, MD, & Thomas 

N. Bottoni, MD 

OVERVIEW OF CARDIAC ARREST 

ADULT BASIC LIFE SUPPORT (See Figure 7-1.) 

ADULT ADVANCED LIFE SUPPORT 

CARDIOPULMONARY RESUSCITATION IN INFANTS & CHILDREN 

NOVEL APPROACHES IN CARDIAC ARREST MANAGEMENT 

TABLES 

FIGURES 

8. Compromised Airway 1 - Harriet L. Boozer, MD, & Melissa M. Cheeseman, 

MD 

IMMEDIATE MANAGEMENT OF THE COMPROMISED AIRWAY (See Figure 

8-1.) 

PRINCIPLES OF INTUBATION 

NONSURGICAL ALTERNATIVES FOR MANAGING THE DIFFICULT 

AIRWAY 

NEEDLE CRICOTHYROIDOTOMY 

SURGICAL AIRWAYS 

USE OF DRUGS TO ASSIST IN INTUBATION 

SPECIAL CASES 

CARE OF THE INTUBATED PATIENT 

TABLES 

FIGURES 

9. Shock 1 - Peter W. Greenwald, MD 

IMMEDIATE MANAGEMENT OF SHOCK (See Figure 9-1.) 

DETERMINATION OF THE CAUSE OF SHOCK 

EMERGENCY TREATMENT OF SPECIFIC CAUSES OF SHOCK 

TABLES 

FIGURES 

10. The Multiply Injured Patient - Julia Martin, MD, & Michael McClurg, MD 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS (See 

Figure 10-1.) 

EMERGENCY TREATMENT OF SPECIFIC DISORDERS 

TABLES 

FIGURES 

11. Dyspnea, Respiratory Distress, & Respiratory Failure 1 - Sabina A. 

Braithwaite, MD, & Debra G. Perina, MD 


Figure 11-1.) 

FURTHER DIAGNOSTIC EVALUATION 


TABLES 

FIGURES 

12. Chest Pain 1 - Sean P. Barbabella, DO & William R. Dennis, Jr., MD 2,3 


Figure 12-1.) 

FURTHER EVALUATION OF THE PATIENT WITH CHEST PAIN

MANAGEMENT OF SPECIFIC DISORDERS CAUSING CHEST PAIN 

TABLES 

FIGURES 

13. Abdominal Pain 1 - Roger Humphries, MD, & Jon Andrew Russell, MD 


Figure 13-1.) 

FURTHER EVALUATION OF THE PATIENT WITH ABDOMINAL PAIN 

ADDITIONAL MEASURES FOR THE MANAGEMENT OF ACUTE ABDOMEN 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING ABDOMINAL PAIN 

CONDITIONS CAUSING ACUTE ABDOMINAL PAIN THAT ARE NOT 

AMENABLE TO SURGERY 

TABLES 

FIGURES 

14. Gastrointestinal Bleeding 1 - Charles W. Erdman, MD, & James J. 

Mensching, DO, FACEP 

INTRODUCTION 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING BLEEDING (See 

Figure 14-1.) 

FURTHER EVALUATION OF GASTROINTESTINAL BLEEDING 

EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING UPPER 

GASTROINTESTINAL BLEEDING 

EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING LOWER 

GASTROINTESTINAL BLEEDING 

TABLES 

FIGURES 

15. Diarrhea & Vomiting - Phillip A. Clement, MD, & Jason A. Gardiner, MD 

INTRODUCTION 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS 

FURTHER EVALUATION OF THE PATIENT WITH DIARRHEA & VOMITING 

EMERGENCY EVALUATION & MANAGEMENT OF INFECTIOUS CAUSES 

OF DIARRHEA & VOMITING 

TABLES 

FIGURES 

16. Coma 1 - Steven D. Kelley, MD, & Adam Saperston, MD, MS 


Figure 16-1 AND TABLE 16-1.) 

FURTHER EVALUATION OF THE COMATOSE PATIENT 


CRITERIA FOR BRAIN DEATH 

TABLES 

FIGURES 

17. Syncope, Seizures, & Other Causes of Episodic Loss of Consciousness 1 - 

Adam Saperston, MD, MS 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS (See 

Figure 17-1.) 

II. EVALUATION OF THE CONSCIOUS PATIENT WITH A HISTORY OF 

SYNCOPE 

III. EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING

EPISODIC LOSS OF CONSCIOUSNESS 

TABLES 

FIGURES 

18. Weakness & Stroke 1 - Heidi P. Cordi, MD, MS 

INTRODUCTION 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS 

ASSOCIATED WITH WEAKNESS (See Figure 18-1.) 

II. FURTHER EVALUATION OF THE PATIENT WITH WEAKNESS 

III. EMERGENCY MANAGEMENT OF SPECIFIC WEAKNESS DISORDERS 

IV. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS 

ASSOCIATED WITH STROKE 

V. FURTHER EVALUATION OF THE PATIENT WITH STROKE 

VI. MANAGEMENT OF SPECIFIC STROKE SYNDROMES 

TABLES 

FIGURES 

19. Headache 1 - C. Keith Stone, MD, & Nancy J. Antonacci, MD 

IMMEDIATE EVALUATION & MANAGEMENT OF HEADACHE CAUSED BY 

LIFE-THREATENING CONDITIONS (See Figure 19-1.) 

APPROACH TO THE DIAGNOSIS OF HEADACHE 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING ACUTE HEADACHE 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING SUBACUTE 

HEADACHE 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING CHRONIC 

HEADACHE 

FIGURES 

20. Delirium & Acute Confusional States - Eric W. Flach, MD, Timothy A. 

Coakley, MD, & James J. Mensching, MD, DO, FACEP 1,2 


Figure 20-1.) 

EMERGENCY MANAGEMENT OF SPECIFIC DISORDERS 

TABLES 

FIGURES 

21. Arthritis & Back Pain 1 - Roger L. Humphries, MD, & David O'Keefe, MD 

I. EVALUATION OF THE PATIENT WITH ACUTE ARTHRITIS (See Figure 

21-1.) 

II. EMERGENCY TREATMENT OF SPECIFIC CONDITIONS CAUSING 

ACUTE ARTHRITIS 

III. EVALUATION OF THE PATIENT WITH ACUTE BACK PAIN (See Figure 

21-2.) 

IV. EMERGENCY TREATMENT OF SPECIFIC CONDITIONS CAUSING 

BACK PAIN 

TABLES 

FIGURES

MD 


22. Head Injuries - Stephen C. Ausband, MD, FACEP, & Ritu Sahni, MD, MPH 


MANAGEMENT OF OTHER SYMPTOMS 

EMERGENCY TREATMENT OF SPECIFIC HEAD INJURIES 

MINOR HEAD INJURIES 

SPECIAL CONSIDERATIONS FOR PEDIATRICS 

INDICATIONS FOR HOSPITALIZATION 

DISCHARGE INSTRUCTIONS 

INTOXICATED PATIENTS 

TABLES 

FIGURES 

23. Maxillofacial & Neck Trauma 1 - Fermin S. Godinez, DO, & Susan J. Letterle, 


II. FURTHER DIAGNOSIS & EVALUATION 

III. EMERGENCY MANAGEMENT OF SPECIFIC INJURIES 

FIGURES 

24. Chest Trauma - James Svenson, MD, MS, & Desiree LaCharite, MD 

INTRODUCTION 


IMMEDIATELY LIFE-THREATENING THORACIC INJURIES IDENTIFIED ON 

PRIMARY SURVEY 

POTENTIALLY LIFE-THREATENING INJURIES IDENTIFIED ON 

SECONDARY SURVEY 

OTHER INJURIES 

PENETRATING TRAUMA 

FIGURES 

25. Abdominal Trauma - Luis E. Rodriguez, MD, & John E. Gough, MD, FACEP 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES 

EMERGENCY TREATMENT OF SPECIFIC INJURIES 

FIGURES 

26. Genitourinary Trauma - Geoffrey A. Wiss, MD, Claudia Whitaker, MD, & 

Robert K. Dunne, MD, FACEP 



FIGURES 

27. Vertebral Column & Spinal Cord Trauma 1 - Robert Casey Wilson, MD, & 

Louis J. Kroot, MD 

IMMEDIATE MANAGEMENT OF THE PATIENT WITH SUSPECTED SPINAL 

INJURY 

FURTHER EVALUATION OF THE PATIENT WITH SPINAL INJURY 

EMERGENCY TREATMENT OF SPECIFIC SPINAL INJURIES 

TABLES 

FIGURES 

28. Orthopedic Emergencies - Luis E. Rodriguez, MD, & John E. Gough, MD, 

FACEP 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES 

II. IMMEDIATE MANAGEMENT OF LIMB-THREATENING INJURIES

III. GENERAL ORTHOPEDIC PRINCIPLES 

IV. MANAGEMENT OF SPECIFIC ORTHOPEDIC INJURIES 

V. COMMON PITFALLS 

TABLES 

FIGURES 

29. Hand Trauma 1 - Adam Saperston, MD, MS 

EMERGENCY EVALUATION & TREATMENT 

EXAMINATION OF THE HAND & ASSESSMENT OF FUNCTION (See 

Figures 29-3 & 29-4. ) 

EQUIPMENT & MATERIALS FOR TREATMENT 

MANAGEMENT OF SPECIFIC TYPES OF HAND INJURIES 

SPECIAL EMERGENCY DEPARTMENT PROBLEMS 

FIGURES 

30. Wound Care 1 - Louis J. Kroot, MD, & David Hurst, MD 

EMERGENCY MANAGEMENT OF LIFE-THREATENING PROBLEMS 

WOUND ASSESSMENT 

EMERGENCY TREATMENT OF SPECIFIC TYPES OF WOUNDS 

TABLES 

FIGURES

SECTION IV - NONTRAUMA EMERGENCIES 

31. Eye Emergencies 1 - William R. Dennis, Jr, MD, & Alia M. Dennis, MD 

I. EMERGENCY EVALUATION OF IMPORTANT OCULAR SYMPTOMS 

II. OCULAR CONDITIONS REQUIRING IMMEDIATE TREATMENT 

III. NONTRAUMATIC OCULAR EMERGENCIES 

IV. OCULAR BURNS & TRAUMA 

V. EQUIPMENT & SUPPLIES 

VI. COMMON TECHNIQUES FOR TREATMENT OF OCULAR DISORDERS 

VII. COMMON PITFALLS TO BE AVOIDED IN THE MANAGEMENT OF 

OCULAR DISORDERS 

TABLES 

FIGURES 

32. ENT Emergencies: Disorders of the Ear, Nose, Sinuses, Oropharynx, & 

Mouth - David C. Van, MD, MS 

I. IMMEDIATE MANAGEMENT OF POTENTIALLY HARMFUL DISORDERS 

II. MANAGEMENT OF SPECIFIC DISORDERS 

TABLES 

FIGURES 

33. Pulmonary Emergencies 1 - Christopher R. Pund, MD, & C. Keith Stone, MD 


also Chapter 11.) 

EMERGENCY MANAGEMENT OF SPECIFIC CONDITIONS 

TABLES 

34. Cardiac Emergencies 21 - Roger L. Humphries, MD, & C. Keith Stone, MD 

Immediate Management 

ACUTE CORONARY SYNDROME 

HEART FAILURE 

HYPERTENSION & HYPERTENSIVE CRISIS 

PERICARDITIS, PERICARDIAL EFFUSION, & CARDIAC TAMPONADE 

MYOCARDITIS & CARDIOMYOPATHY 

AORTIC ANEURYSMS & DISSECTIONS 

CONGENITAL HEART DISEASE 

TABLES 

35. Cardiac Arrhythmias - David A. Wald, DO 

INTRODUCTION 

TACHYARRHYTHMIAS 

BRADYARRHYTHMIAS, CONDUCTION DISTURBANCES, & ESCAPE 

RHYTHMS 

IDIOVENTRICULAR RHYTHM 

ATRIOVENTRICULAR JUNCTIONAL RHYTHM 

PERMANENT CARDIAC PACEMAKERS (See Appendix, Figures 35-32, 

35-33, 35-34, 35-35, 35-36 and 35-37.) 

IMPLANTABLE CARDIOVERTER DEFIBRILLATORS 

APPENDIX: COMMONLY ENCOUNTERED CARDIAC ARRHYTHMIAS 

TABLES 

FIGURES 

36. Obstetric & Gynecologic Emergencies & Rape 1 - Melissa Platt, MD, & Mary 

Nan Mallory, MD, RDMS


EMERGENCY MANAGEMENT OF GYNECOLOGIC DISORDERS 

EMERGENCY MANAGEMENT OF OBSTETRIC DISORDERS 

TABLES 

FIGURES 

37. Genitourinary Emergencies 1 - Susan J. Letterle, MD 

IMMEDIATE MANAGEMENT OF SERIOUS & LIFE-THREATENING 

CONDITIONS 


TABLES 

FIGURES 

38. Vascular Emergencies 1 - Scott W. Hines, MD, & James J. Mensching, MD, 

DO, FACEP 

INTRODUCTION 

I. VASCULAR EMERGENCIES DUE TO TRAUMA 

II. VASCULAR EMERGENCIES NOT DUE TO TRAUMA 

TABLES 

FIGURES 

39. Hematologic Emergencies - J. Stephan Stapczynski, MD, & Geoffrey A. 

Martin, MD 

I. HEMOSTATIC DISORDERS: GENERAL CONSIDERATIONS 

II. HEMOSTATIC DISORDERS: PLATELET DISORDERS 

III. HEMOSTATIC DISORDERS: COAGULATION FACTOR DISORDERS 

IV. ANEMIA 

V. POLYCYTHEMIA 

VI. WHITE CELL DISORDERS 

VII. TRANSFUSION THERAPY 

TABLES 

FIGURES 

40. Infectious Disease Emergencies - Brian Hawkins, MD, & Daniel F. Danzl, 

MD 


II. EMERGENCY MANAGEMENT OF SPECIFIC DISORDERS 

III. MANAGEMENT OF INFECTIONS CAUSED BY SPECIFIC ORGANISMS 

IV. AIDS & HIV INFECTION (See Table 40-14. ) 

TABLES 

41. Metabolic & Endocrine Emergencies - Micheal D. Rush, MD, & Wason W. S. 

Louie, MD 

EMERGENCY MANAGEMENT OF DISORDERS OF CARBOHYDRATE 

METABOLISM 

EMERGENCY MANAGEMENT OF OTHER METABOLIC & ENDOCRINE 

ABNORMALITIES 

TABLES 

42. Fluid, Electrolyte, & Acid-Base Emergencies - Michael E. Chansky, MD, 

FACEP, Andrew Nyce, MD, & Jason Friedman, MD 1 

I. DIAGNOSIS OF FLUID & ELECTROLYTE DISORDERS 


APPENDIX: USEFUL EQUATIONS & FORMULAS 

TABLES

FIGURES 

43. Burns & Smoke Inhalation 1 - Melissa M. Cheeseman, MD, & Harriet L. 

Boozer, MD 


Figure 43-1.) 

FURTHER EVALUATION OF THE PATIENT WITH BURNS OR INHALATION 

INJURY 

EMERGENCY TREATMENT OF SPECIFIC TYPES OF BURNS 

TABLES 

FIGURES 

44. Disorders Due to Physical & Environmental Agents 1 - D. Shannon Waters, 

MD, & Rebecca C. Bowers, MD 

EMERGENCY TREATMENT OF DISORDERS DUE TO COLD 

EMERGENCY TREATMENT OF DISORDERS DUE TO HEAT 

EMERGENCY TREATMENT OF ELECTRICAL INJURIES 

EMERGENCY TREATMENT OF RADIATION INJURIES 

EMERGENCY TREATMENT OF NEAR-DROWNING 

EMERGENCY TREATMENT OF DISORDERS DUE TO ATMOSPHERIC 

PRESSURE CHANGES 

EMERGENCY TREATMENT OF DISORDERS DUE TO VENOMOUS 

ANIMALS 

TABLES 

FIGURES 

45. Poisoning 1 - D. Shannon Waters, MD, Darren Waters, MD, & Travis 

Sewalls, MD 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING CONDITIONS 

FURTHER MANAGEMENT OF VICTIMS OF POISONING 

MANAGEMENT OF CONDITIONS ASSOCIATED WITH POISONING 

EMERGENCY TREATMENT OF SPECIFIC POISONINGS 

TABLES 

FIGURES 

46. Dermatologic Emergencies - Joseph A. Salomone III, MD, FAAEM, & 

Martha Ann Pratt, MD 

IMMEDIATE RECOGNITION & MANAGEMENT OF LIFE-THREATENING 

PROBLEMS 

RECOGNITION & MANAGEMENT OF POTENTIALLY LIFE-THREATENING 

PROBLEMS 

RECOGNITION & MANAGEMENT OF NON-LIFE-THREATENING 

PROBLEMS 

47. Psychiatric Emergencies - Gregory Hall, MD, & Denis J. Fitzgerald, MD 

I. INTRODUCTION 

II. THE S.A.F.E.S.T. APPROACH TO VIOLENT OR AGITATED PATIENTS 

III. EMERGENCY DEPARTMENT SCREENING ASSESSMENT 

IV. ORGANIC CAUSES FOR PSYCHIATRIC EMERGENCIES 

V. FUNCTIONAL CAUSES FOR PSYCHIATRIC EMERGENCIES 

VI. PSYCHOPHARMACO- THERAPY 

VII. DISPOSITION 

FIGURES 

48. Pediatric Emergencies - Roger L. Humphries, MD, Keith D. Bricking, MD, &

Thomas M. Huhn, MD 1 

General Considerations 

CARDIOVASCULAR EMERGENCIES 

RESPIRATORY DISTRESS 

NEUROLOGIC EMERGENCIES 

INFECTIOUS DISEASES 

GASTROINTESTINAL DISORDERS 

HEMATOLOGIC DISEASES 

NEWBORN EMERGENCIES 

CHILD ABUSE 

TABLES 

FIGURES

CURRENT EMERGENCY DIAGNOSIS & TREATMENT - 5th 

Ed. (2004) 

FRONT MATTER 

Title Page 

a LANGE medical book 

CURRENT EMERGENCY Diagnosis & Treatment 

fifth edition 

Edited by 

C. Keith Stone, MD 

Professor and Chairman 

Department of Emergency Medicine 

Texas A&M University Health Science Center 

Scott & White Memorial Hospital 

Temple, Texas 

Roger Humphries, MD 

Assistant Professor and Residency Director 

Department of Emergency Medicine 

University of Kentucky College of Medicine 

Lexington, Kentucky 

Lange Medical Books/McGraw-Hill 

Medical Publishing Division 

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Copyright Page 

Current Emergency Diagnosis & Treatment 2004, 5th Edition 

Copyright © 2004 by The McGraw-Hill Companies, Inc. Copyright © 1978 by the 

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Contents 

Pharmacotherapy in Advanced Cardiac Life Support (See Table 7-2.) 

Authors vii

Preface xiii 

SECTION I. SPECIAL ASPECTS OF EMERGENCY MEDICINE 1 

Chapter 1. Approach to the Emergency Department Patient 1 

Mary Nan S. Mallory, MD, RDMS & Robert Perry Pringle Jr. MD 

Chapter 2. Prehospital Emergency Medical Services 6 

Eric M. Sergienko, MD, & Thomas N. Bottoni, MD 

Chapter 3. Nuclear, Biologic, & Chemical Agents; Weapons of Mass Destruction 

20 


Chapter 4. Multicasualty Incidents & Disasters 42 

Louis J. Kroot, MD, & Robert B. Gray, MD 

Chapter 5. Legal Aspects of Emergency Care 60 

Charles A. Eckerline, Jr., MD, FACEP, & Steven D. Rothert, MD, JD 

Chapter 6. Emergency Procedures 73 

William Randall Partin, MD 

Section II. Management of Common Emergency Problems 145 

Chapter 7. Basic & Advanced Cardiac Life Support 145 

Eric M. Sergienko, MD, & Thomas N. Bottoni, MD 

Chapter 8. Compromised Airway 167 

Harriet L. Boozer, MD, & Melissa M. Cheeseman, MD 

Chapter 9. Shock 191 

Peter W. Greenwald, MD 

Chapter 10. The Multiply Injured Patient 208 

Julia Martin, MD, & Michael McClurg, MD 

Chapter 11. Dyspnea, Respiratory Distress, & Respiratory Failure 222 

Sabina A. Braithwaite, MD, & Debra G. Perina, MD 

Chapter 12. Chest Pain 240 

Sean P. Barbabella, DO & William R. Dennis, Jr., MD 

Chapter 13. Abdominal Pain 257 

Roger Humphries, MD, & Jon Andrew Russell, MD 

Chapter 14. Gastrointestinal Bleeding 283 

Charles W. Erdman, MD, & James J. Mensching, DO, FACEP

Chapter 15. Diarrhea & Vomiting 296 

Phillip A. Clement, MD, & Jason A. Gardiner, MD 

Chapter 16. Coma 311 

Steven D. Kelley, MD, & Adam Saperston, MD, MS 

Chapter 17. Syncope, Seizures, & Other Causes of Episodic Loss of 

Consciousness 332 


Chapter 18. Weakness & Stroke 348 

Heidi P. Cordi, MD, MS 

Chapter 19. Headache 379 

C. Keith Stone, MD, & Nancy J. Antonacci, MD 

Chapter 20. Delirium & Acute Confusional States 391 

Eric W. Flach, MD, Timothy A. Coakley, MD, & James J. Mensching, MD, DO, FACEP 

Chapter 21. Arthritis & Back Pain 404 

Roger L. Humphries, MD, & David O'Keefe, MD 

Section III. Trauma Emergencies 421 

Chapter 22. Head Injuries 421 

Stephen C. Ausband, MD, FACEP, & Ritu Sahni, MD, MPH 

Chapter 23. Maxillofacial & Neck Trauma 435 

Fermin S. Godinez, DO, & Susan J. Letterle, MD 

Chapter 24. Chest Trauma 454 

James Svenson, MD, MS, & Desiree La Charite, MD 

Chapter 25. Abdominal Trauma 467 

Luis E. Rodriguez, MD, & John E. Gough, MD, FACEP 

Chapter 26. Genitourinary Trauma 477 

Geoffrey A. Wiss, MD, Claudia Whitaker, MD, & Robert B. Dunne, MD, FACEP 

Chapter 27. Vertebral Column & Spinal Cord Trauma 493 

Robert Casey Wilson, MD, & Louis J. Kroot, MD 

Chapter 28. Orthopedic Emergencies 510 

Luis E. Rodriguez, MD, & John E. Gough, MD, FACEP 

Chapter 29. Hand Trauma 548 

Adam Saperston, MD, MS

Chapter 30. Wound Care 573 

Louis J. Kroot, MD, & David Hurst, MD 

Section IV. NonTrauma Emergencies 599 

Chapter 31. Eye Emergencies 599 

William R. Dennis, Jr., MD, & Alia M. Dennis, MD 

Chapter 32. ENT Emergencies: Disorders of the Ear, Nose, Sinuses, Oropharynx, 

& Mouth 626 

David C. Van, MD, MS 

Chapter 33. Pulmonary Emergencies 653 

Christopher R. Pund, MD, & C. Keith Stone, MD 

Chapter 34. Cardiac Emergencies 675 

Roger L. Humphries, MD, & C. Keith Stone, MD 

Chapter 35. Cardiac Arrhythmias 694 

David A. Wald, DO 

Chapter 36. Obstetric & Gynecologic Emergencies & Rape 725 

Melissa Platt, MD, & Mary Nan Mallory, MD, RDMS 

Chapter 37. Genitourinary Emergencies 750 

Susan J. Letterle, MD 

Chapter 38. Vascular Emergencies 766 

Scott W. Hines, MD, & James J. Mensching, MD, DO, FACEP 

Chapter 39. Hematologic Emergencies 788 

J. Stephan Stapczynski, MD, & Geoffrey A. Martin, MD 

Chapter 40. Infectious Disease Emergencies 824 

Brian Hawkins, MD, & Daniel F. Danzl, MD 

Chapter 41. Metabolic & Endocrine Emergencies 867 

Micheal D. Rush, MD, & Wason W.S. Louie, MD 

Chapter 42. Fluid, Electrolyte, & Acid-Base Emergencies 890 

Michael E. Chansky, MD, FACEP, Andrew Nyce, MD, & Jason Friedman, MD 

Chapter 43. Burns & Smoke Inhalation 917 

Melissa M. Cheeseman, MD, & Harriet L. Boozer, MD 

Chapter 44. Disorders Due to Physical & Environmental Agents 930 

D. Shannon Waters, MD, & Rebecca C. Bowers, MD

Chapter 45. Poisoning 963 

D. Shannon Waters, MD, Darren K. Waters, MD, & Travis Sewalls, MD 

Chapter 46. Dermatologic Emergencies 1012 

Joseph A. Salomone III, MD, FAAEM, & Martha Ann Pratt, MD 

Chapter 47. Psychiatric Emergencies 1026 

Gregory Hall, MD, & Denis J. Fitzgerald, MD 

Chapter 48. Pediatric Emergencies 1039 

Roger L. Humphries, MD, Keith D. Bricking, MD, & Thomas M. Huhn, MD 

Authors 

Nancy J. Antonacci, MD 

President, E=mc 2 , Lexington, Kentucky 

Headache 

Stephen C. Ausband, MD, FACEP 

Assistant Professor, Department of Emergency Medicine, The Brody School of 

Medicine, East Carolina University, Greenville, North Carolina 

ausbands@mail.ecu.edu 

Head Injuries 

Sean P. Barbabella, DO 

Chief Resident, Naval Medical Center Portsmouth, Portsmouth, Virginia 

spbarbabella@mar.med.navy.mil 

Chest Pain 

Harriet L. Boozer, MD 

Emergency Medicine Staff Physician, Carolina Care, PA, Columbia, South Carolina 

hboozer@hotmail.com 

Compromised Airway; Burns & Smoke Inhalation 


Attending Staff Emergency Physician, Sentara Careplex Hampton, Hampton, Virginia 

Prehospital Emergency Medical Services; Basic & Advanced Cardiac Life Support 

Rebecca C. Bowers, MD 

Resident Physician, Department of Emergency Medicine, University of Kentucky 

Medical Center, Lexington 

Disorders Due to Physical & Environmental Agents 

Sabina A. Braithwaite, MD 

Assistant Professor, Department of Emergency Medicine, University of Virginia School 

of Medicine, Charlottesville 

sabina@virginia.edu 

Dyspnea, Respiratory Distress, & Respiratory Failure

Keith D. Bricking, MD 

Resident Physician, Department of Emergency Medicine, Indiana University School of 

Medicine, Indianapolis, Indiana 

kbrickin@iupui.edu 

Pediatric Emergencies 

Michael E. Chansky, MD, FACEP 

Chairman and Associate Professor of Emergency Medicine and Internal Medicine, 

Robert Wood Johnson Medical School, Camden, New Jersey; Cooper University 

Hospital, Camden, New Jersey 

chansky-michael@cooperhealth.edu 

Fluid, Electrolyte, & Acid-Base Emergencies 

Melissa M. Cheeseman, MD 

Assistant Professor and Emergency Medicine Physician, Department of Emergency 

Medicine, University of Kentucky College of Medicine, Lexington 

Compromised Airway; Burns & Smoke Inhalation 

Phillip A. Clement, MD 

Assistant Clinical Professor and Director of Undergraduate Education, Department of 

Emergency Medicine, The Brody School of Medicine, East Carolina University, 

Greenville, North Carolina 

clementp@mail.ecu.edu 

Diarrhea & Vomiting 

Timothy A. Coakley, MD 

Chief Resident, Naval Medical Center Portsmouth, Portsmouth, Virginia 

Delirium & Acute Confusional States 

Heidi P. Cordi, MD, MS 

Assistant Clinical Professor of Medicine, Columbia University College of Physicians and 

Surgeons; Assistant Attending Physician, The New York Presbyterian Hospital, New 

York, New York 

hcordimd@usa.net 

Weakness & Stroke 

Daniel F. Danzl, MD 

Professor and Chair, Department of Emergency Medicine, University of Louisville 

School of Medicine, Louisville, Kentucky 

dandanzl@pol.net 

Infectious Disease Emergencies 

Alia M. Dennis, MD 

Pediatric Chief Resident, Childrens Hospital of the Kings Daughters, Norfolk, Virginia 

dennisa120@cox.net 

Eye Emergencies 

William R. Dennis, Jr., MD

Attending Staff Physician and Instructor, Department of Emergency Medicine, Naval 

Medical Center Portsmouth, Portsmouth, Virginia 

dennisw120@cox.net 

Chest Pain; Eye Emergencies 


Assistant Professor, Department of Emergency Medicine, Wayne State University 

School of Medicine, Detroit, Michigan; Attending Physician, Department of Emergency 

Medicine, Sinai-Grace Hospital, Detroit, Michigan 

rkdunne@sprintmail.com 

Genitourinary Trauma 

Charles A. Eckerline, Jr., MD, FACEP 

Associate Professor, Department of Emergency Medicine, University of Kentucky 

College of Medicine, Lexington 

caecke1@uky.edu 

Legal Aspects of Emergency Care 

Charles W. Erdman, MD 

Resident, Department of Emergency Medicine, Naval Medical Center Portsmouth, 

Portsmouth, Virginia 

cwerdman@mar.med.navy.mil 

Gastrointestinal Bleeding 

Denis J. Fitzgerald, MD 

Assistant Professor, Department of Military and Emergency Medicine, Uniformed 

Services University of the Health Sciences, Bethesda, Maryland; Adjunct Assistant 

Professor, Department of Emergency Medicine, University of Cincinnati College of 

Medicine, Cincinnati, Ohio 

Psychiatric Emergencies 

Eric W. Flach, MD 

Intern, Department of Emergency Medicine, Naval Medical Center Portsmouth, 


flache@bellsouth.net 

Delirium & Acute Confusional States 

Joachim Franklin, MD 

Resident, Department of Emergency Medicine, University of Kentucky College of 

Medicine, Lexington 

Nuclear, Biologic, & Chemical Agents; Weapons of Mass Destruction 

Jason A. Gardiner, MD 

Senior Resident, Department of Emergency Medicine, The Brody School of Medicine, 

East Carolina University, Greenville, North Carolina 

gardinerj@mail.ecu.edu 

Diarrhea & Vomiting 

Fermin S. Godinez, DO

Chief Resident, Department of Emergency Medicine, Naval Medical Center Portsmouth, 


Maxillofacial & Neck Trauma 

John E. Gough, MD, FACEP 

Associate Professor and Physician, Department of Emergency Medicine, East Carolina 

University, Greenville, North Carolina 

goughj@mail.ecu.edu 

Abdominal Pain; Orthopedic Emergencies 

Robert B. Gray, MD 

Resident, Department of Emergency Medicine, University of Kentucky Medical Center, 

Lexington 

rgraydoc@hotmail.com 

Multicasualty Incidents & Disasters 

Peter W. Greenwald, MD 

Instructor in Clinical Medicine, Columbia College of Physicians and Surgeons; Attending 

Physician, Columbia Presbyterian Hospital, New York 

pg2014@columbia.edu 

Shock 

Gregory Hall, MD 

Resident, Department of Emergency Medicine, University of Cincinnati College of 

Medicine, Cincinnati, Ohio 

Psychiatric Emergencies 

Brian Hawkins, MD 

Resident Physician, Department of Emergency Medicine, University of Louisville 

Hospital, Louisville, Kentucky 

bhaw481674@cs.com 

Infectious Disease Emergencies 

Scott W. Hines, MD 

Physician, Department of Emergency Medicine, Naval Medical Center Portsmouth, 


Vascular Emergencies 

Thomas M. Huhn, MD 



tmhuhn0@uky.edu 

Pediatric Emergencies 

Roger Humphries, MD 

Assistant Professor and Residency Director, Department of Emergency Medicine, 

University of Kentucky College of Medicine, Lexington 

rlhump0@uky.edu 

Abdominal Pain; Arthritis & Back Pain; Cardiac Emergencies; Pediatric Emergencies;

Inside Front Cover: Drugs Commonly Used Intravenously in Emergencies; Inside Back 

Cover: Quick Reference Table for Pediatric Resuscitation Equipment by Weight and 

Age 

David Hurst, MD 



davidghurst@hotmail.com 

Wound Care 

Steven D. Kelley, MD 

Resident, Department of Emergency Medicine, Naval Medical Center Portsmouth, 


sdkelley@mar.med.navy.mil 

Coma 


Associate Professor, Department of Emergeny Medicine, University of Kentucky College 

of Medicine, Lexington 

Multicasualty Incidents & Disasters; Vertebral Column & Spinal Cord Trauma; Wound 

Care 

Desiree La Charite, MD 

Assistant Professor, Section of Emergency Medicine, Department of Medicine, 

University of Wisconsin Medical School, Madison 

ddl@medicine.wisc.edu 

Chest Trauma 

Susan J. Letterle, MD 

Staff Physician, Department of Emergency Medicine, Naval Medical Center Portsmouth, 


Maxillofacial & Neck Trauma; Genitourinary Emergencies 

Wason W.S. Louie, MD 

Physician, Department of Emergency Medicine, Truman Medical Center, Kansas City, 

Missouri 

Metabolic & Endocrine Emergencies 

Mary Nan S. Mallory, MD, RDMS 

Associate Professor, Department of Emergency Medicine, University of Louisville 

School of Medicine, Louisville, Kentucky 

marynanmd@pol.net 

Approach to the Emergency Department Patient; Obstetric & Gynecologic Emergencies 

& Rape 

Geoffrey A. Martin, MD 

Professor, Department of Emergency Medicine, University of Kentucky College of 


Hematologic Emergencies

Julia Martin, MD 

Associate Professor, Department of Emergency Medicine, University of Kentucky 

College of Medicine; Medical Director, University of Kentucky Air Medical Services, 

Lexington, Kentucky 

jemart2@uky.edu 

The Multiply Injured Patient 

Michael McClurg, MD 



The Multiply Injured Patient 

James J. Mensching, MD, DO, FACEP 

Physician, Department of Emergency Medicine, Good Samaritan Medical Center, 

Brockton, Massachusetts; Physician, Department of Emergency Medicine, St. 

Elizabeth's Medical Center, Boston, Massachusetts 

j.j.mensching.do@attbi.com 

Gastrointestinal Bleeding; Delirium & Acute Confusional States; Vascular Emergencies 

Andrew Nyce, MD 

Assistant Professor, Department of Emergency Medicine, Robert Wood Johnson 

Medical School, University of Medicine and Dentistry of New Jersey, Newark, New 

Jersey; Attending Physician, Department of Emergency Medicine, Cooper University 

Medical Center, Camden, New Jersey 

nyce-drew@cooperhealth.edu 

Fluid, Electrolyte, & Acid-Base Emergencies 

David O'Keefe, MD 



dlokeefe@hotmail.com 

Arthritis & Back Pain 

William Randall Partin, MD 

Assistant Clinical Professor, University of Louisville School of Medicine, Louisville, 

Kentucky; Attending Physician, Floyd Emergency Medicine Associates, Floyd Memorial 

Hospital, New Albany, Indiana 

randypartin@insightbb.com 

Emergency Procedures 

Debra G. Perina, MD 

Associate Professor, University of Virginia School of Medicine, Charlottesville; Director, 

Prehospital Care Division, University of Virginia Health Systems, Charlottesville 

Dyspnea, Respiratory Distress, & Respiratory Failure 

Melissa Platt, MD 

Physician, Department of Emergency Medicine, University of Louisville Hospital, 

Louisville, Kentucky

maproc01@hotmail.com 

Obstetric & Gynecologic Emergencies & Rape 

Martha Ann Pratt, MD 

Resident Physician and Clinical Instructor, Department of Emergency Medicine, 

University of Missouri-Kansas City School of Medicine, Kansas City, Missouri 

Dermatologic Emergencies 

Robert Perry Pringle, Jr., MD 

Resident, Department of Emergency Medicine University of Louisville School of 

Medicine, Lousiville, Kentucky 

Approach to the Emergency Patient 

Christopher R. Pund, MD 

Resident, Department of Emergency medicine, University of Kentucky, College of 


chrispund@hotmail.com 

Pulmonary Emergencies 

Luis E. Rodriguez, MD 

Director of Emergency Medicine, Roanoke Chowan Hospital, Ahoskie, North Carolina; 

Clinical Assistant Professor, Department of Emergency Medicine, The Brody School of 

Medicine, East Carolina University, Greenville, North Carolina 

lourod2000@yahoo.com 

Abdominal Trauma; Orthopedic Emergencies 

Steven D. Rothert, MD, JD 



srothert@insightbb.com 

Legal Aspects of Emergency Care 

Micheal D. Rush, MD 

Assistant Professor, Department of Emergency Medicine, Truman Medical Center, 

University of Missouri-Kansas City School of Medicine, Kansas City, Missouri 

micheal.rush@tmcmed.org 

Metabolic & Endocrine Emergencies 

Jon Andrew Russell, MD 

Chief Resident, Department of Emergency Medicine, University of Kentucky College of 


jandrewrussell@hotmail.com 

Abdominal Pain 

Ritu Sahni, MD, MPH 

Assistant Professor, Deaprtment of Emergency Medicine, Oregon Health and Science 

University School of Medicine, Portland; Medical Director, Life Flight Network, Portland, 

Oregon 

sahnir@ohsu.edu

Head Injuries 

Joseph A. Salome III, MD, FAAEM 

Associate Professor, Department of Emergency Medicine, University of 

Missouri-Kansas City School of Medicine, Kansas City, Missouri 

joseph.salomone@tmcmed.org 

Dermatologic Emergencies 


Staff Physician, Peninsula Emergency Physicians, Inc., Hampton Careplex Hospital, 

Hampton, Virginia 

dradam@worldnet.att.net 

Coma; Syncope, Seizures, & Other Causes of Episodic Loss of Consciousness; Hand 

Trauma 

Eric M. Sergienko, MD 

Staff Physician, Naval Hospital, Guam; Medical Director, Naval EMS Guam, Agana, 

Guam 

docz@ite.net 

Prehospital Emergency Medical Services; Basic & Advanced Cardiac Life Support 

Travis Sewalls, MD 


Medical Center, Lexington 

Poisoning 

J. Stephan Stapczynski, MD 

Professor, Department of Emergency Medicine, University of Kentucky College of 


jsstap01@uky.edu 

Hematologic Emergencies 

Michael W. Stava, MD 

Assistant Professor, Department of Emergency Medicine, University of Kentucky 


Nuclear, Biologic, & Chemical Agents; Weapons of Mass Destruction 


Professor and Chairman, Department of Emergency Medicine, Texas A&M University 

Health Science Center College of Medicine, Scott & White Memorial Hospital, Temple, 

Texas 

kestone@swmail.sw.org 

Headache; Pulmonary Emergencies; Cardiac Emergencies 

James Svenson, MD, MS 

Associate Professor, Section of Emergency Medicine, Department of Medicine, 

University of Wisconsin Medical School, Madison 

jes@medicine.wisc.edu 

Chest Trauma

David C. Van, MD, MS 

Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Columbia 

University College of Physicians and Surgeons, New York 

Emergencies: Disorders of the Ear, Nose, Sinuses, Oropharynx, & Mouth 

David A. Wald, DO 

Assistant Professor, Department of Emergency Medicine, Temple University School of 

Medicine and Emergency Medicine Clerkship Director, Temple University Hospital, 

Philadelphia, Pennsylvania 

waldda@tuhs.temple.edu 

Cardiac Arrhythmias 

Darren K. Waters, MD 

Chief Resident, Department of Emergency Medicine, University of Kentucky College of 


dwa1972@hotmail.com 

Poisoning 

D. Shannon Waters, MD 

Assistant Professor and Physician, Department of Emergency Medicine, University of 

Kentucky College of Medicine, Lexington 

dswaters@comcast.net 

Disorders Due to Physical & Environmental Agents; Poisoning 

Claudia Whitaker, MD 

Physician, Wayne State University School of Medicine; Resident Physician, Sinai-Grace 

Hospital, Detroit, Michigan 

whitakermd@aol.com 


Robert Casey Wilson, MD 

Physician, Department of Emergency Medicine, University of Kentucky College of 


rcwilsonmd@msn.com 

Vertebral Column & Spinal Cord Trauma 

Geoffrey A. Wiss, MD 

Attending Physician, Department of Emergency Medicine, Sinai-Grace Hospital and 

Research Fellow, Emergency Medicine Basic Science Laboratory, Wayne State 

University School of Medicine, Detroit, Michigan 

gwiss@yahoo.com 


Preface 

Current Emergency Diagnosis & Treatment, fifth edition is designed to present concise, 

easy-to-read, practical information on the diagnosis and treatment of a wide spectrum of 

conditions that present to the emergency department. The chapters emphasize the

immediate management of life threatening problems then present the evaluation and 

treatment of specific disorders. We trust that this text will aid all practitioners of 

emergency medicine in providing care to their patients. 

OUTSTANDING FEATURES 

In keeping with the tradition of the Current series, CEDT strives to provide the reader 

with a broad-based text written in a clear and succinct manner. Our goal is to provide 

practicing emergency physicians quick access to accurate and useful information that 

will aid in their everyday practice of emergency medicine. 

Because this text focuses on the practical aspects of emergency care, there is little 

discussion of the basic science or pathophysiology of disease processes. In addition, 

discussion of management restricts the material presented to treatments routinely 

provided in the ED. 

INTENDED AUDIENCE 

CEDT will be useful to all practitioners of emergency medicine, including physicians, 

residents, medical students as well as physician extenders. It will also provide valuable 

information for emergency nurses and prehospital care providers. 

ORGANIZATION 

The fifth edition of CEDT has undergone some reorganization. A new initial section 

entitled "Special Aspects of Emergency Medicine" has been created. This section brings 

together two new chapters, on the approach to the emergency department patient and 

on nuclear, biologic and chemical agents and weapons of mass destruction, with 

chapters previously included in the section on non-trauma emergencies. 

This edition retains the priority-based and problem-oriented organization of previous 

editions. Chapters in Section II, "Management of Common Emergency Problems," are 

presented in a problem-based format. Life-threatening disorders are discussed first 

followed by a presentation of specific disorders. This chapter format is carried out in the 

remainder of the book in the sections dealing with traumatic emergencies and 

non-trauma emergencies. 

SPECIAL TO THIS EDITION 

• A new chapter on the approach to the emergency patient 

• A new chapter on nuclear, biological and chemical terrorism 

• Updates of all chapters 

• New radiographic images throughout 

• Updated and color-enhanced illustrations 

ACKNOWLEDGMENTS 

We would like to thank the editorial staff at McGraw-Hill, especially Shelley Reinhardt, 

Nicky Fernando, and Christie Naglieri for their guidance, patience, and support

throughout this project. In addition, we would like to thank our wives, Gail and Kris, and 

our children, Chase, Jack, and Maddie, for their love, understanding, and support for the 

time needed to dedicate to this endeavor. 


Roger L. Humphries, MD 

September 2003 

Location In Book: 


FRONT MATTER

SECTION I - SPECIAL ASPECTS OF EMERGENCY 

MEDICINE 

1. Approach to the Emergency Department Patient - Mary Nan S. 

Mallory, MD, RDMS & Robert Perry Pringle, Jr., MD 

WHAT IS EMERGENCY MEDICINE? 

An emergency is commonly defined as any condition perceived by the prudent 

layperson—or someone on his or her behalf—as requiring immediate medical or 

surgical evaluation and treatment. Based on that definition, the American College of 

Emergency Physicians (ACEP) states that the practice of emergency medicine has the 

primary mission of evaluating, managing, and providing treatment to these patients with 

unexpected injury and illness. 

So what does an emergency physician do? This specialist routinely provides care and 

makes medical treatment decisions based on real-time evaluation of a patient's history; 

physical findings; and many diagnostic studies, including multiple imaging modalities, 

laboratory tests, and electrocardiograms. The emergency physician needs an amalgam 

of skills to treat a wide variety of injuries and illnesses—ranging from the diagnosis of an 

upper respiratory infection or dermatologic condition to resuscitation and stabilization of 

the multiple trauma patient. Furthermore, these physicians must be able to practice 

emergency medicine on patients of all ages and not just in urban tertiary-care facilities. 

Clinical emergency medicine may be practiced in emergency departments, both rural 

and urban; urgent care clinics; and other settings such as at mass gathering incidents, 

through emergency medical services (EMS), and in hazardous material and bioterrorism 

situations. 

Emergency medicine serves as the United States's health care safety net. It provides 

valuable clinical and administrative services to the health care delivery system, including 

care for the indigent and others who lack access to health care, and has evolved as the 

most visible and vital component of a patchwork of health care providers and facilities. 

These emergency departments have become the routine, and often the only, source of 

care for many of the uninsured, thereby acting as a critical safety net for our fragmented 

health care delivery system. 

Finally, emergency departments are the only element of the health care system whose 

function has been delineated by federal law. Initially authorized in 1986, the Emergency 

Medical Treatment and Active Labor Act mandates that all emergency departments 

provide screening, stabilization, and appropriate transfer to all patients with any medical 

condition. Emergency medicine is often the last resort for many patients and frequently 

the access point for competent, comprehensive, and efficient medical care. 

BIRTH & GROWTH OF EMERGENCY MEDICINE 

By current popular opinion based on reality and dramatic television productions,

emergency medicine appears to be at the forefront of medicine, providing 

compassionate and competent care by residency-trained emergency physicians. 

Unfortunately, this has not always been the case. The profession of emergency 

medicine is still quite young and continues to grow and mature. A brief timeline of 

emergency medicine growth is shown in Table 1-1. Since the first emergency medicine 

residency program began in 1970, the number of approved residency programs has 

increased dramatically (Table 1-2). Despite the rapid growth in emergency medicine 

residencies, a significant number of practitioners of emergency medicine are not 

residency trained or board certified (Table 1-3). 

SCOPE OF PRACTICE 

Emergency medicine physicians are faced with an ever-growing patient volume, 

decreasing inpatient bed availability, decreasing reimbursement, and increased 

litigation. However, these same physicians have the unique responsibility for being 

prudent stewards of a finite amount of health care resources. Based on that 

responsibility, the ACEP in 2002 endorsed the following: 

• The best medical interest of the patient should be foremost in any clinical decision 

making process. 

Criteria for appropriate use of finite resources should include: 

1. Urgency of the patient's medical condition 

2. Likelihood, magnitude, and duration of medical benefit to the patient 

3. Burdens and cost of care to the patient 

4. Cost to society 

• Emergency physicians should not allocate health care resources on the basis of a 

patient's ability to pay, contribution to society, past use of resources, or responsibility for 

their medical condition. 

In 2001, the ACEP Core Content Task Force II published its Model of Clinical Practice 

of Emergency Medicine. In this publication, the scope of practice of an emergency 

physician is well defined and yet quite expansive, to include care from the prehospital 

environment to prevention and education. Listed below are the tasks of the emergency 

physician as agreed upon by the task force. 

Prehospital Care 

Participate actively in prehospital care and education, provide direct patient care or 

on-line or off-line medical direction or interact with prehospital medical providers, and 

assimilate information from prehospital care into patient assessment and management. 

Emergency Stabilization

Conduct primary assessment, and take appropriate steps to stabilize and provide 

treatment to patients. 

Performance of Focused History & Physical Examination 

Communicate effectively to interpret and evaluate the patient's symptoms and history; 

identify pertinent risk factors in the patient's history; provide a focused evaluation; 

interpret the patient's appearance, vital signs, and condition; recognize pertinent 

physical findings; and perform techniques required for conducting the exam. 

Modifying Factors 

Recognize age, gender, ethnicity, barriers to communication, socioeconomic status, 

underlying disease, and other factors that may affect patient management. 

Professional & Legal Issues 

Understand and apply principles of professionalism, ethics, and legal concepts pertinent 

to patient management. 

Diagnostic Studies 

Select and perform the most appropriate diagnostic studies, and interpret the results. 

Diagnosis 

Develop a differential diagnosis and establish the most likely diagnoses in light of the 

history, physical examination, interventions, and test results. 

Therapeutic Interventions 

Perform procedures and nonpharmacologic therapies, and counsel patients. 

Pharmacotherapy 

Select appropriate pharmacotherapy, recognize pharmacokinetic properties, and 

anticipate drug interactions and adverse effects. 

Observation & Reassessment 

Evaluate and reevaluate the effectiveness of a patient's treatment or therapy, including 

addressing complications and potential errors; and monitor, observe, manage, and 

maintain the stability of one or more patients who are at different stages in their 

workups. 

Consultation & Disposition 

Collaborate with physicians and other professionals to evaluate and provide treatment 

to patients; arrange appropriate placement and transfer if necessary; formulate a

follow-up plan; and communicate effectively with patients, family, and involved health 

care members. 

Prevention & Education 

Apply epidemiologic information to patients at risk; conduct patient education; and select 

appropriate disease and injury prevention techniques. 

Documentation 

Communicate patient care information in a concise manner that facilitates quality care 

and coding. 

Multitasking & Team Management 

Prioritize multiple patients in the emergency department in order to provide optimal 

patient care; interact, coordinate, educate, and supervise all members of the patient 

management team; utilize appropriate hospital resources; and have familiarity with 

disaster management procedures. 

Other "Tasks" 

Emergency medicine has evolved to include much more than the above-mentioned 

"tasks." For the profession of emergency medicine to continue to progress, physicians 

must embrace the following responsibilities: 

• Basic and clinical research 

• Multidisciplinary and continuous medical education 

• Injury prevention 

• Disaster management and mass-gathering medicine 

• Toxicology and regional Poison Control Center direction 

• Hazardous material and bioterrorism management 

• Hospital and EMS systems administration 

PRINCIPLES OF EMERGENCY MEDICINE 

It is often said that emergency department patients "don't read the textbook," meaning 

that their presentations do not fit nicely into specific textbook diagnoses or classical 

presentations of illness. However, a cornerstone of an emergency physician's practice is 

the recognition of patterns in a patient's presentation; therefore, the prudent physician 

must be a detective and scientist to muddle through the muck of vague signs and 

symptoms to find the pattern.

The principles of emergency medicine are simply questions that must be answered to 

provide effective care to patients who have entrusted emergency physicians with their 

care. The questions are not to be used as a cookbook approach to the management of 

these often complex medical and psychosocial issues but are a simple method to guide 

the prudent emergency physician through the quagmire of clinical emergency medicine. 

A. Is the Patient About to Die? 

Obviously, this is the first and most important question to answer. Every patient's 

presentation is quickly prioritized to one of the following acuities: 

1. Critical—Patient has symptoms consistent with a life-threatening illness or injury with 

a high probability of death if immediate intervention is not begun. 

2. Emergent—Patient has symptoms of illness or injury that may progress in severity if 

treatment is not begun quickly. 

3. Nonurgent—Patient has symptoms that have a low probability of progression to a 

more serious condition. 

Look for symptoms of a life-threatening emergency, not a specific disease entity. 

Anticipate impending life-threatening emergencies in the apparently stable patient. 

B. What Steps Must Be Undertaken to Stabilize the Patient? 

Act quickly to stabilize the critically ill or injured patient. Focus on the primary survey 

(airway, breathing, circulation, and neurologic deficits), and make necessary 

interventions as each issue is identified. Do not delay necessary primary interventions 

while awaiting completion of ancillary testing. 

C. What Are the Most Potentially Serious Causes of the Patient's Presentation? 

Thinking of the worst-case scenario, develop a mental list of the most deadly causes of 

the patient's presentation by asking, "What will kill my patient the fastest?" Once the list 

has been developed, the vital signs, history, physical examination, and ancillary 

assessments should identify or confirm those causes highest on the list. 

D. Could There Be Multiple Causes of the Patient's Presentation? 

In addition to constant reevaluation and reprioritization of the differential diagnosis, 

continually ask, "Is this all there is?" For example, is the new-onset seizure and 

hypoglycemia in an older diabetic patient from intentional or accidental medication 

overdose or perhaps worsening renal insufficiency? Is the near-syncope and abdominal 

pain in an apparently intoxicated college coed from a ruptured ectopic pregnancy or 

perhaps a ruptured spleen secondary to undisclosed physical abuse by her boyfriend? 

Frequent reassessment and thoughtful inquiry as to the multiple possibilities responsible 

for each patient's condition are imperative. 

E. Can a Treatment Assist in the Diagnosis in an Otherwise Undifferentiated 

Illness? 

Often in emergency medicine, treatment response foretells a diagnosis. A case in point 

is the unconscious patient with no available collateral history. The patient's response to 

empiric administration of naloxone will include or exclude narcotic overdose as a

contributor to the obtundation. Referred to as the "diagnostic-therapeutic" concept, it 

underscores the emergency medicine philosophy that an established diagnosis is not a 

prerequisite to initiating appropriate treatment. Pitfalls can exist. For example, sublingual 

nitroglycerin and so-called GI cocktails can relieve symptoms of chest pain resulting 

from the same cause. 

F. Is a Diagnosis Mandatory or Even Possible? 

After emergent issues have been addressed, the patient and emergency physician are 

often left with an undifferentiated symptom complex. This frequently elicits an 

uncomfortable response by non-emergency-medicine-trained physicians. Become 

accustomed to and comfortable with the notion of determining the disposition for a 

nonemergent patient—having treated their symptoms and excluding emergency 

conditions-without a specific diagnosis. 

G. Does This Patient Need To Be Admitted to the Hospital? 

Having appropriately answered the preceding questions, make the bottom-line 

disposition decision. Once assessments and treatments are under way, decide whether 

an emergent condition exists. Consider other subtleties. Does the patient have timely, 

accessible follow-up? How far away from a medical facility does the patient live? Are 

unresolved abuse or self-care issues involved? Are you, as the emergency physician, 

comfortable discharging the patient? 

H. If the Patient Is Not Being Admitted, Is the Disposition Safe and Adequate for 

the Patient? 

More frequently than not, patients are discharged home from the emergency 

department. However, many patients do not receive a specific diagnosis, and some 

symptoms may persist. Recommend appropriate follow-up, and provide written 

discharge instructions. Invite the patient back. Instruct the patient when to return for 

further evaluation should symptoms change or worsen. Provide the patient with 

information regarding treatment and diagnosis as well. 

CONCLUSION 

Since 1970, emergency medicine has seen a tremendous growth and increase in 

awareness of the unique aspects of the profession. It remains a challenging and fulfilling 

experience for many physicians and an appealing choice of specialties for medical 

students. As emergency medicine matures as a specialty, its importance as the United 

States's health care safety net and its integral status as front-line medicine will continue 

to expand and grow. 

American College of Emergency Physicians: Definition of emergency medicine, as 

approved by the ACEP Board of Directors, April 2001. http://www.acep.org/3,411,0.html 

American College of Emergency Physicians: Emergency medicine training, competency 

and professional practice principles position statement, as approved by the ACEP Board 

of Directors, November 2001. http://www.acep.org/3,5141,0.html 

American College of Emergency Physicians: Emergency physician stewardship of finite 

resources, as approved by the ACEP Board of Directors, January 1997.

http://www.acep.org/ 3,4245,0.html 

American College of Emergency Physicians Core Content Task Force II: The Model of 

the Clinical Practice of Emergency Medicine. American College of Emergency 

Physicians, 2001. 

Asplin BR, Sosnow PL, Yeh CS: "The Safety Net and Current Federal Health Care 

Policy." Defending America's Safety Net. American College of Emergency Physicians, 

1999. 






WHAT IS EMERGENCY MEDICINE?

Table 1-1. Timeline of emergency medicine growth. 

1974: Emergency Medical Services Act (The White Paper) authorized the 

establishment and expansion of emergency medical services system and 

research. 

1975: The American Medical Association (AMA) House of Delegates approved 

Section of Emergency Medicine and standards for emergency medicine 

residencies were established. Total number of emergency medicine residencies: 

18. 

1979: The AMA and the American Board of Medical Specialties recognizes 

emergency medicine as the 23 medical specialty. 

1980: Emergency medicine specialty certification examinations begin. Total 

number of emergency medicine residencies: 43. 

1982: Accreditation Council for Graduate Medical Education approves 

requirements for emergency medicine residency programs. 

1985: Total number of emergency medicine residencies: 63. 

1989: American Board of Medical Specialties grants emergency medicine 

primary board status. 




2001: Total number of emergency medicine residencies: 124.

Table 1-2. Emergency medicine residency statistics. 

124 

Total active emergency medicine residents and fellows 3,676 

Average number of residents and fellows per program 29.6 

Average percentage female residents 28.2% 

Average percentage international medical graduate 3.4% 

Average number of full-time physician faculty 20.6 

Average number of part-time physician faculty 3.7 

Average percentage full-time female physician faculty 24.2% 

Average full-time physician faculty-to-resident ratio 0.7 






TABLES 

Table 1-2 . Emergency medicine residency statistics.

Table 1-3. Emergency physician personnel statistics. 

32,020 

Emergency physicians certified by the 

American Board of Emergency Medicine (as of 

December 2001) 

Emergency physicians certified by the 

American Osteopathic Board of Emergency 

Medicine (as of July 2001) 

Members of the American College of 

Emergency Physicians 


17,300 

1,078 

21,000 





TABLES 

Table 1-3. Emergency physician personnel statistics.

2. Prehospital Emergency Medical Services 1 - Eric M. Sergienko, MD, 

& Thomas N. Bottoni, MD 

INTRODUCTION 

1 This chapter is a revision of the chapter by Charles E. Saunders, MD, FACEP, & 

Thomas Hearne, PhD, from the 4th edition. 

The delivery of effective, organized, prehospital emergency medical services (EMS) is a 

development that dates to the 1960s in the United States. Although there were 

ambulance providers and even some local systems, there was no national approach to 

prehospital care until publication of the 1966 White Paper entitled "Accidental Death and 

Disability—The Neglected Disease of Modern Society" (National Academy of Sciences, 

National Research Council). 

When medical emergencies are reported, trained medical personnel arrive on the scene 

to provide emergency care within 6-10 minutes. The skills of these personnel range 

from basic first aid techniques and cardiopulmonary resuscitation (CPR) to advanced 

life support (ALS) techniques, including defibrillation, endotracheal intubation, and the 

use of emergency medications. Radio communications permit ongoing discussion of 

patient status and treatment between emergency medical personnel at the scene and 

the supervising physician at the base hospital. Air ambulances (fixed-wing aircraft or 

helicopters staffed with medically trained flight crews) can rapidly evacuate and 

transport patients from a remote emergency scene to a regional medical center. 

COMPONENTS OF THE EMERGENCY MEDICAL SERVICES SYSTEM 

Modern EMS systems consist of several major components: (1) professional field 

personnel trained to provide specific levels or types of care, (2) a comprehensive 

emergency communications network, (3) hospital emergency department physicians 

and nurses who supervise the treatment provided by EMS field personnel, (4) hospitals 

categorized according to their relationship with EMS field personnel and according to 

the level of care they can provide, and (5) EMS administrative officials who manage and 

coordinate the elements of the system. 

Professional EMS Field Personnel 

The health professionals and first responders who provide prehospital care are trained 

to carry out specific levels of care, ranging from basic first aid and CPR provided by first 

responders, through basic life support (BLS) given by emergency medical technicians 

(EMTs), to the ALS provided by advanced EMTs (paramedics). These personnel 

provide care only as extensions or agents of physicians and are not independently 

licensed to provide medical care. The care they deliver is authorized by standing orders 

(written authorization to administer certain treatments without prior attempt at base 

contact by radio) or protocols from physician directors or by orders transmitted by radio 

from supervisory physicians at the base hospital to EMS personnel at the scene. A

critical element in the development of EMS since 1970 has been the recognition that 

personnel without prior medical training can be prepared through relatively short 

courses to provide effective prehospital care. The designations, levels of training, and 

skills of EMS personnel are now largely standardized according to United States 

Department of Transportation (DOT) curriculum and formal categories established in 

1983 by the National Registry of Emergency Medical Technicians. The curriculum is 

regularly reviewed and updated to reflect changes in medicine and in the prehospital 

environment. The latest iteration released by the DOT was in 1998, with some 

modifications in 2000. Types of EMS field personnel and their training are described 

below and summarized in Table 2-1. 

A. First Responders 

First responders may include law enforcement officers, rescue squad members, 

firefighters, or volunteer EMS personnel. First-responder courses usually consist of 

about 40 hours of classroom instruction and clinical training in basic first aid and CPR. 

First responders are equipped with basic emergency care equipment (eg, bandages, 

dressings, tape, blanket and pillow, upper and lower extremity splint sets). Oxygen 

equipment and a self-refilling bag-valve-mask combination (eg, Ambu bag) are optional. 

First responders also carry basic tools to help them reach and extricate trapped 

individuals. Increasingly, first responders are being trained and equipped to perform 

defibrillation using automated external defibrillators (AEDs). 

B. Emergency Medical Technicians (EMTs) 

The National Registry of Emergency Medical Technicians currently recognizes 3 formal 

grades of EMTs according to the typical number of hours of training given, the breadth 

of skills covered, and the range of procedures authorized: EMT-A (basic), EMT-I 

(intermediate), and EMT-P (advanced, paramedic). Designations and levels of training 

may vary from state to state. Emergency physicians should be familiar with regional 

variations and deviations from the National Registry guidelines. 

1. EMT-A—Basic EMTs constitute the essential workforce of EMS systems throughout 

the United States. Most state laws require at least one certified EMT on board 

ambulance vehicles that transport patients. 

The basic EMT course requires at least 81 hours of training standardized by the DOT. 

Basic classes frequently exceed this minimum by up to 140 hours. Students learn basic 

principles of patient care, how to identify signs and symptoms central to patient 

assessment and diagnosis, and how to provide treatment in specific emergencies. The 

use of AEDs is now standard curriculum for EMTs in most regions. Optional modules for 

EMTs include advanced airway management, intravenous access, and assisting 

patients with self-administration of medications. Additionally, some states allow 

administration of medications, including epinephrine in anaphylaxis and aspirin in 

suspected cardiac chest pain. 

2. EMT-I—The intermediate EMT is trained to provide a level of advanced care in areas 

that are underserved by paramedics. The scope of practice has evolved since 1990 to 

incorporate many advanced cardiac life support procedures, including cardiac 

monitoring, treatment of arrhythmias, defibrillation, and advanced airway management 

with either endotracheal intubation or an alternative airway.

3. EMT-P—Advanced EMTs (paramedics) receive over 1000 hours of training in ALS 

techniques. Their skills include the basic EMT procedures as well as intravenous 

cannulation, invasive airway management (including endotracheal intubation), 

recognition of cardiac dysrhythmias, defibrillation, and the use of specific emergency 

medications. In addition to extensive classroom training, EMT-P personnel also 

complete clinical training and a field internship with experienced paramedic teams. 

Paramedics operate under standing orders and treatment protocols developed by a 

physician medical director that are usually broader and more advanced than those 

guiding basic EMTs. These protocols determine the type and level of care administered 

at the emergency site. Physicians who provide on-line medical supervision of 

paramedics (by radio and telemetry) from base hospitals may permit paramedics to 

deviate from established protocols or to provide treatment not specifically covered in 

standing orders. 

Special Qualifications 

Additional training is available at all levels of providers for specific care settings. At the 

first responder level, a Winter Emergency Care course has been developed for the 

National Ski Patrol to address special situations that occur in ski areas. Similarly there 

are Wilderness modules at all levels of training that provide additional training for care 

provided in a remote setting with anticipated long evacuations and transportation. 

EMT-Tactical courses train EMTs and paramedics to function in a tactical law 

enforcement situation in which they may support or be part of a police special tactics 

teams. Finally, Paramedic-Critical Care training enables the advanced provider to 

provide care to critically injured or ill patients who are being transferred from one facility 

to another. 

Types of EMS Systems 

EMS systems can be delivered in various ways. There are 2 basic forms of EMS 

response: a single-response system and a layered-response (or tiered-response) 

system. In a single-response system, there is only one grade of EMS unit, and the 

closest available unit is dispatched to any nearby emergency. In a layered-response 

system, 2 or more grades of EMS personnel respond hierarchically (eg, first responder, 

then EMT-A, then EMT-P) as needed. Layered-response systems usually provide for an 

EMT-A response for all less severe reported medical emergencies, reserving an EMT-P 

response for severe or life-threatening incidents (Table 2-2). 

Communications Network 

The communications network is important in tying together the components of an EMS 

system. A dispatcher at a communications center receives a telephone request from a 

caller at the site of the emergency and dispatches mobile EMS personnel via the radio 

network. Dispatchers may use a call triaging system (eg, Priority Medical Dispatching) 

to assign resources to a call. In many areas of the United States, an easily remembered 

emergency telephone number (9-1-1) provides the public with rapid access to the 

communications center. Many systems offer an "enhanced 9-1-1" service that provides

immediate callback and location information to the dispatcher. 

Communications between the EMS unit and medical facilities varies from region to 

region. For many BLS transports, contact with the base station or receiving facility is not 

required. In the event of an ALS transport, contact must be made with a medical facility. 

In some areas, the facility is called a base station hospital, which provides on-line 

direction and supervision for an entire EMS region. Information called into the base 

station hospital is then relayed to the receiving facility. In other areas, the receiving 

facility is called directly. 

Hospital Facilities & Staffing 

EMS systems typically include hospitals with a variety of treatment capabilities, ranging 

from local community hospitals with a limited emergency department staffing to large 

teaching hospitals in urban areas with emergency physicians, surgeons, 

anesthesiologists, and surgical teams available 24 hours a day. Hospital facilities are 

frequently classified according to their relationship to EMS mobile units and their ability 

to provide definitive care. 

A. Base Station Hospitals 

Physicians or specially trained nurses with physician backup in the emergency 

department of the base station hospital provide EMS units with on-line medical 

supervision during treatment. EMS units may be housed at the base station hospital, but 

this may not be necessary or feasible because the units are usually strategically 

deployed in the hospital's service area. In many EMS systems, the base station hospital 

may also be the one most capable of providing definitive follow-up care. 

B. Receiving Hospitals 

Receiving hospitals are facilities to which patients may be transported. For each patient, 

the receiving hospital is selected according to its proximity; its capability to provide 

definitive care; and the preference of the patient, family members, or family physician, 

as long as transport to the hospital does not draw the EMS unit away from its primary 

service area. 

C. Hospitals Categorized by Capability 

Hospitals may be categorized by their ability to provide acute care as determined by the 

availability of physicians, nurse, allied health personnel, and other hospital resources 

(eg, operating rooms, laboratory, blood bank). Many categorization schemes exist. The 

Joint Commission on Accreditation of Healthcare Organizations has established 4 levels 

of emergency service: 

1. Level I—This service offers emergency care 24 hours a day with at least one 

physician experienced in emergency care on duty in the emergency care area. In 

addition, there must be in-house physician coverage by residents at the senior level or 

higher for the medical, surgical, orthopedic, obstetric-gynecologic, pediatric, and 

anesthesiologic services. 

2. Level II—This service offers emergency care 24 hours a day with at least one 

physician experienced in emergency care on duty in the emergency care area. Specialty

consultation should be available within 30 minutes. 

3. Level III—This service offers emergency care 24 hours a day with at least one 

physician on duty in the emergency care area available within 30 minutes through a 

medical staff call roster. 

4. Level IV—This service is capable of performing a triage function and can administer 

life-saving first aid until transportation to the nearest appropriate facility is available. 

D. Hospitals Categorized by Areas of Care 

Hospitals can also be categorized by special areas of care (eg, trauma, burns, neonatal 

intensive care), especially where regionalization of services in these areas is practiced. 

The American College of Surgeons, for example, has established the following 

categorization of trauma facilities: 

1. Level I—This designates a full-service trauma center that can provide optimal care of 

the trauma patient. One or more experienced emergency physicians, a general surgeon, 

anesthesiology services, laboratory, blood bank, and an operating room team must be 

available in-house 24 hours a day. All surgical subspecialty services should be 

immediately available on call. A commitment to education and research in trauma must 

also be demonstrated. 

2. Level II—This trauma center is similar to a level I center but does not necessarily 

include a commitment to education or research. Occasionally patients with the most 

severe injuries or those needing highly specialized care may be transferred from a level 

II center to a level I center. 

3. Level III—This trauma center does not have all of the resources available at a level I 

or level II center but may represent the highest level available in a given community. 

Usually, initial stabilization and life-saving procedures are performed and the patient is 

then transferred to a level I or level II center. 

EMS Administration 

EMS systems may be administered through a variety of organizations, including local 

health departments, public safety agencies such as police or fire departments, hospitals, 

or privately owned provider agencies. Often several of these agencies operate EMS 

systems in the same area, and these agencies are coordinated through an EMS 

regional council, which interacts with hospitals, public safety agencies, and physician 

medical directors; sets operational standards; and monitors performance (quality 

assurance). 

Operation of the EMS System 

One way to visualize the interplay between various components of the EMS system is to 

review the sequence of events surrounding a typical emergency medical incident. There 

are 4 major phases: (1) report of the emergency and activation of the EMS system, (2) 

dispatch of appropriate prehospital units, (3) medical evaluation and field treatment by 

EMS personnel, and (4) transport of the patient to the appropriate hospital.

A. Report of the Emergency 

In many areas of the United States, a single, easily remembered telephone number 

(9-1-1) can now be used to request emergency help from the police and fire 

departments and to activate the EMS system. 

B. Dispatch 

Dispatchers receive the emergency call, interview the caller to determine the type and 

severity of the emergency, and dispatch the appropriate type of emergency medical 

response. In systems with heavy call volumes, calls may be priority ranked and then 

dispatched in order of urgency of need and resource availability. In some systems, 

dispatchers offer advice to callers to assist patients pending the arrival of emergency 

units (prearrival instructions). Algorithms may be employed to guide the dispatcher in 

decision making (Figure 2-1). Dispatchers in layered-response emergency medical 

systems frequently follow specific protocols in determining which type of EMS unit to 

dispatch (ie, ALS, BLS, first responder; see Table 2-2). Dispatchers may also be trained 

to provide CPR instructions by telephone to callers. Dispatch centers may also monitor 

hospital availability, manage the status and geographic deployment of EMS vehicles, 

and through computer-aided dispatch perform EMS management information and 

quality assurance functions. 

C. Medical Evaluation and Treatment 

Most EMS systems in urban and suburban areas are capable of responding within a few 

minutes of receiving an emergency call. First responders can frequently arrive at the 

scene within 3-6 minutes, and paramedics within 5-10 minutes of receiving the call. 

Survival following time-sensitive medical emergencies such as cardiac arrest is closely 

correlated with unit response time, especially when basic EMTs have been trained in 

defibrillation. In layered-response systems, paramedics are held in reserve for such 

critical or life-threatening incidents, where their advanced skills may provide definitive or 

stabilizing care to patients. Many systems have advanced-level first responders, such 

as engine companies manned with paramedics. These responders can provide the 

same interventions as ambulance-based paramedics but lack the means to transport 

patients. These assets can be additional resources in the single complex patient or in 

the multiple-patient incident. 

Upon arrival at the emergency scene, EMS personnel undertake patient assessment 

and examination. EMT-paramedics in most cases are authorized by standing orders to 

proceed with patient care. Following patient evaluation and treatment, the EMS unit 

contacts the supervising emergency medical physician (or, in some states, a nurse) at 

the base station hospital by radio or telephone to describe the patient's condition and 

any treatment undertaken. The physician may give specific instructions for further 

treatment at the scene or request transport to the hospital for care. 

D. Transport 

The mode of transport (ground or air, with or without sirens or lights) depends on 

availability, stability of the patient's condition, transport time and distance, risks, and the 

like. Hospital destination decisions are often guided by local protocols, with critically ill 

patients directed to the closest, most appropriate facility. For example, a community 

hospital may be bypassed in favor of the nearest designated trauma center in the case

of a severely injured patient. Noncritical cases may be transported to the hospital of the 

patient's choice. 

1. Ground transport—Most patients are transported in surface ambulances. These 

vehicles vary slightly from state to state in their configuration and on-board equipment, 

but all follow guidelines set by the DOT. Emergency vehicle operators usually are 

allowed by local and state laws to violate certain traffic laws while responding to an 

emergency or carrying a patient in a life-threatening emergency. In the vast majority of 

cases, however, the patient's life is not in danger and posted speeds and traffic laws 

should be obeyed. The time gained in using red lights and sirens to get to the hospital is 

often outweighed by the additional risk of death and disability associated with rapid 

transport. 

In most EMS systems, the responding unit is also the transporting unit. In others, 

especially layered-response systems, the responding unit may primarily evaluate and 

stabilize the patient and may summon a lower-level unit to provide transport. 

2. Air transport—Some EMS systems and regional trauma hospitals, particularly those 

serving large outlying rural areas, use helicopters or fixed-wing aircraft with trained 

medical teams on board as additional resources for prehospital care and transportation. 

The majority of these aircraft are hospital based, but some are operated by municipal or 

state governmental agencies. Where these services are unavailable, or when 

search-and-rescue missions are required, aircraft equipped for medical evacuation may 

be sent from local military bases, operating within the Military Assistance to Safety and 

Traffic program. 

Air ambulances are usually integrated into the EMS system and are activated according 

to certain locally established criteria. The decision to transport a patient by air requires 

careful consideration of the risks and benefits of air versus ground transport (see 

below). 

Medical Supervision 

A. On-Line Medical Direction 

On-line medical direction is the direction given by radio to EMS personnel at the scene 

while care is being provided. It is usually given by emergency physicians or nurses at 

the base station hospital or receiving hospital. In most systems, the use of standing 

orders is allowed (Figure 2-2). This approach allows treatment to begin as soon as 

possible. Systems that have changed over from on-line medical control to standing 

orders have not shown a decrement in medical care but have shown an increase in 

EMS provider morale. 

Even in systems that operate nearly exclusively by standing orders, some exceptions 

may require on-line direction. These may include cessation of CPR in a nonviable 

patient or the administration of restricted medications such as narcotics or paralytics. 

Systems that employ standing orders require effective monitoring, training, and quality 

assurance mechanisms. 

B. Off-Line Medical Direction

Off-line medical direction is the overall direction of the activities of EMS personnel. It 

includes establishing protocols and standing orders, ensuring adequate training and 

skills, reviewing patient care records and voice tapes retrospectively, and reviewing 

performance and outcome data. Off-line medical direction is usually provided by a 

physician experienced in emergency services or by an agency in which physicians play 

an active role. 

Performance Evaluation 

System performance evaluation has many aspects, including the evaluation of input 

resources and operating guidelines (eg, protocol validation, personnel review, training 

assessment), evaluation of the process of delivering care in the field (eg, response 

times, service volume, treatment audits for adherence to protocols), and evaluation of 

the outcome of prehospital care (eg, complications, complaints, success in the 

performance of procedures, and patient survival). Outcome data are the most difficult to 

obtain. 

PREHOSPITAL SKILLS & TECHNIQUES 

Field Assessment 

EMTs responding to a call usually have certain dispatch information, including the 

location, the nature of the complaint, and the number of patients. Upon arrival, they 

must quickly determine the presence of hazards to themselves and the patient, 

ascertain the probable mechanism of injury, and identify other patients, if any. Support 

can be summoned for hazard suppression or additional medical assistance. Patients 

who are conscious and in minimal distress may be able to provide historical information. 

Information may also be obtained from witnesses or family members. 

Patients who are very ill may require that interventions be performed simultaneously 

with assessment. Interventions aimed at stabilizing airway, breathing, or circulation (the 

ABCs) will take precedence over secondary assessment. The receiving physician 

should expect that, if the patient is seriously ill or injured, only life-saving measures may 

be performed prior to arrival. In the more stable patient, a more thorough primary and 

secondary survey should be performed. 

Field Treatment 

A. Airway Control 

Methods of airway control depend on the EMT's level of skill and certification. Initial 

steps to provide an airway include positioning the jaw and suctioning secretions (taking 

care in the trauma victim not to hyperextend the neck). Should this fail to achieve and 

maintain airway patency, the basic EMT can insert an oral or nasal airway. Ventilation 

may be assisted by a bag-valve-mask. 

EMTs and paramedics may establish alternative airways, depending on local protocol. 

The Combitube, a dual lumen tube designed to be placed blindly, can be used to 

ventilate the patient regardless of whether the tube is placed in the esophagus or the 

trachea. The laryngeal mask airway (LMA) is designed to be placed without

laryngoscopy. It has an inflatable cuff that sits over the glottis. This allows for ventilation 

while minimizing gastric insufflation and aspiration. It is not as secure an airway as the 

endotracheal tube. An improvement on the original LMA is the LMA-Fastrach, which 

allows for an endotracheal tube to be passed through the LMA. Both the Combitube and 

the LMA have been implemented successfully in the prehospital setting. 

Endotracheal intubation is the preferred method of airway control in patients with 

inadequate ventilation. Typically the success rate for prehospital intubation is greater 

than 90%. However, two recent papers have questioned the value of intubation in the 

field. A randomized trial involving pediatric intubation found that patients did as well with 

bag-valve-mask ventilation as they did with intubation. Another study found that over 

25% of adult intubations in the prehospital setting were misplaced. When intubation is 

performed in the field it is suggested that end-tidal CO 2 detection and an esophageal 

detector device be used in addition to more conventional means of confirming location. 

After the tube is confirmed in the correct location, the risk of dislodgement should be 

minimized by using a commercial endotracheal tube holder and by securing the patient 

in a cervical collar and to a long spinal board. 

B. Emergency Cardiac Care 

1. Cardiopulmonary resuscitation—The probability of survival for victims of sudden 

cardiac arrest is inversely related to the elapsed time before an effective cardiac rhythm 

is reestablished. CPR is a temporizing measure that, when initiated within 4-6 minutes, 

increases the chances of survival. In most systems, a paramedic unit cannot routinely 

reach the scene within this period. Many systems provide first responders with AEDs. 

AEDs have been successfully deployed with police and fire first responders. In addition, 

public access defibrillators provide AEDs to the public at busy venues such as sporting 

arenas and airports. 

2. Defibrillation—Ventricular fibrillation is the initial rhythm encountered in many victims 

of sudden death. The sooner defibrillation is performed, the higher the survival rate. 

AEDs (Laerdal Heartstart 2000, others) can recognize ventricular fibrillation (or 

tachycardia) and deliver a countershock. The rescuer need not be able to recognize 

dysrhythmias but must be able to recognize cardiac arrest and operate the device. 

AEDs have enabled nonparamedic first responders to provide rapid defibrillation and 

have consequently improved survival rates. 

3. Electrocardiography—In the treatment of acute coronary syndromes, the 

prehospital 12-lead electrocardiogram (ECG) significantly shortens the time from arrival 

in the emergency department to administration of thrombolytic therapy ("door to drug 

time"). Prehospital fibrinolytic therapy has had mixed results. In European trials, where 

prehospital care is typically provided by physician-staffed ambulances, 6-month and 

1-year survival rates have increased. However, trials in the United States with 

paramedic-staffed units has not shown a significant improvement over 12-lead ECG in 

the field with hospital-administered fibrinolytics. 

C. Invasive Procedures 

1. Venous catheterization—(See Chapter 6.) The use of intravenous techniques by 

EMS field personnel is usually limited to cannulation of peripheral veins of the upper 

extremities. In most EMS systems, the procedure can be initiated under standing order

y intermediate or paramedic EMTs. Basic EMTs who have had special training in 

intravenous techniques and fluid therapy may also initiate intravenous lines. Studies 

have demonstrated that skilled paramedics in the field are able to start an intravenous 

line in approximately 3 minutes and achieve a success rate greater than 90%. However, 

when transport times are short (ie, 10 minutes or less), venous catheterization is usually 

unnecessary because the volume of fluid infused or the medications administered 

during such a short period are unlikely to be life saving. Further, in penetrating trauma to 

the thorax, fluid boluses may be detrimental by disrupting the clotting process. In 

addition, field placement of intravenous lines may increase the chances of infection. 

Needlestick injuries, which may occur during venous cannulation under adverse 

circumstances, such as in the back of a moving ambulance, are an increasing concern. 

Intraosseous needles may be placed by paramedics in the event that vascular access 

cannot be obtained in the pediatric patient. 

2. Needle thoracostomy—Chest decompression for suspected tension pneumothorax 

may occasionally be life saving and is performed by paramedics in some systems. A 14- 

or 16-gauge catheter-clad needle is inserted into the second intercostal space along the 

midclavicular line immediately above the subjacent rib using sterile technique. The 

catheter is sealed with a Heimlich valve or a latex glove with the fingertip removed. (The 

open fingertip of the glove is secured around the catheter, allowing air to escape but 

preventing its reentry.) 

3. Cricothyrotomy—(See Chapter 6.) Emergency entry to the airway may be life saving 

in cases of supraglottic airway obstruction or laryngeal trauma. Cricothyrotomy may be 

performed by paramedics in some EMS systems, usually after approval by the base 

physician via radio. Cricothyrotomy may be performed using a surgical, needle, or 

Seldinger technique. Because the procedure can be unexpectedly difficult, it should be 

performed as a last resort and only by properly trained personnel. 

D. Medications 

Medications are a contentious area in the prehospital realm. Because of the lack of 

clinical trials, it is difficult to state what interventions are of benefit. The emergency 

physician should know what medications are available to their EMS providers and under 

what indications they may be used. 

1. Advanced cardiac life support—Most drugs for advanced cardiac life support are 

stocked on most ALS ambulances. Consistently, epinephrine, atropine, lidocaine, 

sodium bicarbonate, and adenosine are stocked. In addition, nitroglycerin, aspirin, and 

morphine are available for treatment of acute coronary syndromes. Amiodarone often is 

not used because of the ongoing debate about its effectiveness and because of cost 

issues. Some systems do not stock diltiazem because patients with a tachydysrhythmia 

that requires rate control are relatively stable. Fibrinolytics are rarely used because of 

their cost, the staffing needed to administer and monitor them, and the minimal benefit 

shown in prehospital use. Other medications such as labetalol, magnesium, 

procainamide, and calcium chloride are typically stocked at the discretion of the 

agency's medical director. 

2. Pulmonary—Albuterol should be available to all ALS EMS agencies. Ipratropium has 

been shown to be beneficial to patients with moderate to severe asthma and to those

with chronic obstructive pulmonary disease. In addition to sublingual nitroglycerin, 

furosemide is typically stocked for treatment of pulmonary edema. 

3. Other drugs—Benzodiazepines are typically stocked for treatment of seizures, 

anxiolysis, and sedation. The use of prehospital benzodiazepines is beneficial to 

patients presenting with recurrent seizures. Agents stocked include diazepam, 

lorazepam, and midazolam. 

Glucose, in the form of 50% dextrose in water (D 50 W) and oral glucose solution 

(occasionally D 25 W or D 10 W for pediatric patients), is stocked for treating hypoglycemia. 

E. Extrication 

Extrication is the process of removing a patient from a condition of entrapment, usually 

from a motor vehicle. It requires considerable skill and experience. Often, special tools 

are necessary, such as heavy bolt and metal cutters or large, powered spreading 

devices (eg, Jaws of Life, Hurst Tool). In most EMS systems, when there is a report of a 

trapped victim, a fire rescue team is dispatched in addition to the EMS unit to clear fire 

hazards, wash away spilled gasoline, and provide additional heavy equipment and 

personnel. 

As soon as the patient is accessible with minimal risk to emergency workers, the 

primary survey should be initiated while further efforts to free the patient continue. Once 

the patient is immobilized in place, emergency resuscitation can begin. 

F. Immobilization and Splinting 

1. Immobilization—Victims of trauma may have injuries to the spine or extremities, 

which, if manipulated, can lead to spinal cord or limb damage. Upon reaching a trauma 

victim, the rescue team must stabilize the patient's cervical spine. Manual stabilization is 

maintained throughout extrication. A cervical collar is applied as soon as practicable. 

Spine boards are sometimes difficult to maneuver in closed spaces, but alternative 

devices are available, such as the Kendrick Extrication Device (KED). In a 

hemodynamically unstable patient, rapid extrication onto a long spine board can be 

accomplished by multiple rescuers manually supporting the spine without the aid of a 

KED. Immobilization is not considered complete until the patient is secured to the spine 

board with straps, the patient's head is secured to the spine board with tape across the 

forehead and beneath the chin, and a cervical collar and lateral neck rolls or head 

immobilization device are in place. 

If endotracheal control intubation is necessary, the cervical spine should remain 

immobilized while the procedure is performed. Should vomiting occur, the patient may 

be logrolled to face sideways while one rescuer maintains cervical spine traction. 

2. Splinting—(See Chapters 28 and 29.) In general, extremities should be placed in an 

anatomic position, especially if pulses cannot be felt below a suspected fracture. If the 

patient protests or if resistance is felt, extremities should remain in a position of comfort. 

Reduction of fracture dislocations at a joint should be attempted only if vascular 

compromise is impending, the duration of transport is long, and the rescuer is 

experienced in the technique. This usually requires the base physician's approval.

A pillow, rolled-up blanket, or other material may often serve as a simple splint. Specific 

splinting devices include cardboard splints, inflatable air splints, the MAST (military 

antishock trousers) garment, and traction splints. If inflatable devices are used, care 

must be taken to monitor distal perfusion, because a compartment syndrome may occur 

with swelling of the extremity or changes in atmospheric pressure (eg, during air 

transport). Traction splints are used primarily with fractures of the femur. 

G. Protocols and Standing Orders 

Protocols are guidelines designed to assist the EMT in performing tasks in a complete 

and orderly fashion (Figure 2-3). Because situations vary widely and protocols cannot 

anticipate every variable, they are not meant to be absolute and must be accompanied 

by training, judgment, and experience. Each EMS system tailors its protocol to the 

training and skill of its EMTs and the needs of the local medical community. 

Standing orders are express authorizations for the performance of a specific task or 

procedure. Under the standing order, an EMT may be authorized to perform a task or 

procedure without first obtaining verbal authorization by radio. Standing orders are 

useful when radio contact is impractical or would delay life-saving intervention (eg, CPR, 

defibrillation). Standing orders usually contain a clear list of circumstances under which 

the authorization applies (indications) and detailed instructions on the manner in which 

the procedure should be performed. They are signed by the physician medical director, 

who shares legal responsibility for the outcome. 

H. Communications 

1. Equipment and frequencies—EMS units communicate with receiving hospitals by 

various methods. Three main radio systems exist: the HEAR network (in the 150-MHz 

range), the COR system (400 MHz), and the 800-MHz truncated system. The HEAR 

system is the oldest and has largely been replaced in urban areas by 800-MHz systems, 

which provide multiple frequencies for providers. In addition, cellular phones and 

landline telephones are used frequently for communications. Communication is simplex. 

Signals pass in only one direction at a time, and neither party can simultaneously speak 

and be heard. In rural areas, communication may be direct, via radio, without a relay 

station or ground lines. 

2. Communication technique—Radio communication must provide information in a 

concise, precise, and easily understood manner. To facilitate speed and understanding, 

a common format is followed, with slight variations depending on the community. 

However, no one should hesitate to ask for clarification, because misunderstandings 

may prove fatal. 

a. The initial contact—The caller always names the party being called first, followed by 

the caller's own identification: 

"Central Hospital, this is medic 19, how do you copy?" 

b. The initial response—The initial response confirms the contact in the same manner: 

"Medic 19, Central Hospital, receiving you loud and clear, over."

c. The report—The caller gives a concise, orderly report containing pertinent history, 

physical findings, destination, estimated time of arrival (ETA), and any necessary 

request for instructions. It should be as brief as possible: 

"Central Hospital, medic 19 en route to your location, ETA 8 minutes, with a 20-year old 

male victim of multiple, small-caliber gunshot wounds to the left chest, right flank, and 

right thigh. Patient is lethargic; blood pressure 80, pulse 140, respirations 46. Breath 

sounds absent over the left chest, abdomen soft. We have an ET tube in place, 2 IVs 

with lactated Ringer's wide open, and MAST garment inflated. Requesting permission 

for needle decompression of the left chest." 

d. The report acknowledgment—This acknowledgment is kept brief; only essential 

queries should be made: 

"Medic 19, have you checked ET tube position?" 

"That's affirmative. Withdrawn 2 centimeters without improvement." 

"Okay, medic 19; needle thoracostomy, left chest, is approved. Will stand by for 

update." 

e. The sign-off—After receiving an order, the field personnel should repeat it to 

demonstrate that it was received accurately before signing off: 

"Central Hospital, understand needle thoracostomy, left chest, is approved. Stand by." 

3. 10-Codes—"Ten codes" are phrases represented by 2 numbers, the first being 10. In 

many areas, these are used to ensure precise communication and to add some 

measure of privacy to the conversation. Unfortunately, few EMS personnel have all of 

the possible 120 codes memorized. The result is often more confusion rather than less. 

Because mistakes may be dangerous, the codes should not be used unless thoroughly 

understood by all parties. 

4. Telemetry—Receiving hospitals and ambulances may have equipment designed for 

the transmission of electrocardiographic traces (telemetry). This equipment is seldom 

used, however, because well-trained paramedics have shown the ability to interpret 

unstable rhythms (eg, ventricular fibrillation, ventricular tachycardia, bradycardia, and 

asystole) with acceptable precision, and more complex rhythms (eg, supraventricular 

tachycardia) rarely require treatment that cannot be postponed until arrival at the 

hospital. As indicated above, the prehospital 12-lead ECG has shortened the door to 

drug time in patients with acute coronary syndromes. 

I. Air Transport 

1. Indications—As noted above, the benefits to the patient must outweigh the risks 

inherent in this mode of transport. Aeromedical transport is most advantageous when 

great distances must be covered rapidly, when ground transport is unavailable or 

impeded by geographic obstacles or dense traffic, or when specialized care (eg, trauma 

resuscitation) is needed at the scene or en route. Emergency medical helicopters 

serving rural areas often provide a higher level of care and more skilled procedures (eg,

intubation, needle thoracostomy, cricothyrotomy) than are provided by localized 

services using basic EMTs. However, air transport is hazardous, and helicopters 

operating at night and in inclement weather have crashed. 

2. Requesting service—Helicopters equipped for medical evacuation can be 

requested, through the EMS communications network, from an area hospital that offers 

such services or from a local military base that participates in the Military Assistance to 

Safety and Traffic program. 

3. Patient preparation—Before departure, stabilize the patient on a spine board and 

immobilize the patient as clinically indicated. Secure airway tubes and intravenous 

catheters. 

4. Anticipated physiologic consequences of air transport— 

a. Hypoxia—Atmospheric pressure decreases with increasing altitude, as does the 

partial pressure of oxygen. Patients with existing heart or lung disease may suffer 

adverse consequences. Supplemental oxygen is required. 

b. Expansion of trapped gas—The volume of trapped gas increases with decreasing 

barometric pressure. Thus, as altitude increases, air may expand in endotracheal tube 

cuffs, air splints, MAST garments, the bowel lumen, the stomach, pneumothorax, 

abscess cavities, and the bottles and tubing of intravenous infusion apparatus. These 

compartments must be monitored frequently and vented as necessary. Intravenous flow 

rates should be adjusted accordingly. 

c. Motion, noise, and vibration—These may cause patient discomfort. Forward 

acceleration with the patient's head forward may cause transient hypotension. This may 

be prevented by positioning the patient with feet forward. 

5. Helicopter safety— 

a. Site selection and lighting—A helicopter landing site should be level, approximately 

100 feet square, and free of obstacles (eg, trees, wires) to approach and departure. It 

should also be clear of loose debris. The site should be secure from bystanders. At 

night, the site should be well lighted (eg, with vehicle headlights), but lights should never 

be directed upward toward the approaching helicopter, because they might interfere 

with the pilot's vision. 

b. Approaching a helicopter—While the rotor blades are turning, approach the aircraft 

only from the front and only after prompting by the pilot. Avoid the tail rotor. Approach in 

a crouched position. Do not run. Never approach from uphill. 

Lower tall objects such as poles associated with intravenous infusion apparatus. Secure 

sheets, hats, and loose clothing. Extinguish all smoking material. 

Abarbanell NR, Marcotte MA: Prehospital use of intravenous diltiazem (Cardizem 

Lyo-Ject) in the treatment of rapid atrial fibrillation. Am J Emerg Med 1997;15:618. 

[PMID: 9337374]

Alspach G: Preventing prehospital delays in seeking care for acute myocardial 

infarction: a patient education program. Crit Care Nurs 1999;19:10. [PMID: 10808808] 

Bond RJ, Kortbeek JB, Preshaw RM: Field trauma triage: combining mechanism of 

injury with the prehospital index for an improved trauma triage tool. J Trauma 

1997;43:283. [PMID: 9291374] 

Caldwell MA, Froelicher ES, Drew BJ: Prehospital delay time in acute myocardial 

infarction: an exploratory study on relation to hospital outcomes and cost. Am Heart J 

2000;139:788. [PMID: 10783211] 

Cannon CP, Sayah AJ, Walls RM: ER TIMI-19: testing the reality of prehospital 

thrombolysis. J Emerg Med 2000;19:21S. [PMID: 11050380] (Review.) 

Canto JG et al: The prehospital electrocardiogram in acute myocardial infarction: is its 

full potential being realized? National Registry of Myocardial Infarction 2 Investigators. J 

Am Coll Cardiol 1997;29:498. [PMID: 9060884] 

Collins D: The prehospital 12-lead EKG: starting outside the emergency department. J 

Emerg Nurs 1997;23:48. [PMID: 9128512] 

Crocco TJ et al: A nationwide prehospital stroke survey. Prehosp Emerg Care 

1999;3:201. [PMID: 10424856] 

Deschamp C: Scene times: what is reasonable for paramedic-level prehospital care? 

Emerg Med Serv 2000;29:96. [PMID: 11143044] 

Dickinson ET, Schneider RM, Verdile VP: The impact of prehospital physicians on 

out-of-hospital nonasystolic cardiac arrest. Prehosp Emerg Care 1997;1:132. [PMID: 

9709354] 

Doering GT: Customer care. Patient satisfaction in the prehospital setting. Emerg Med 

Serv 1998;27:69. [PMID: 10185418] 

Fischberg BL et al: Development and use of a prehospital-oriented EMS computer 

bulletin board service. Prehosp Emerg Care 1999;3:243. [PMID: 10424863] 

Gausche M et al: Effect of out-of-hospital pediatric endotracheal intubation on survival 

and neurological outcome: a controlled clinical trial. JAMA 2000;283:783. [PMID: 

10683058] 

Gerich TG et al: Prehospital airway management in the acutely injured patient: the role 

of surgical cricothyrotomy revisited. J Trauma 1998;45:312. [PMID: 9715188] 

Greiff SJ: Taking it to the street: advanced monitoring and 12-lead EKGs in prehospital 

care. Emerg Med Serv 1998;27:47. [PMID: 10185417] 

Grossman DC et al: Urban-rural differences in prehospital care of major trauma. J

Trauma 1997;42:723. [PMID: 9137264] 

Howes DW et al: Justification of pulse oximeter costs for paramedic prehospital 

providers. Prehosp Emerg Care 2000;4:151. [PMID: 10782604] 

Jewkes F: Prehospital emergency care for children. Arch Dis Child 2001;84:103. [PMID: 

11159280] 

Jezierski M: Family violence screening: opportunities in prehospital settings. J Emerg 

Nurs 1999;25:201. [PMID: 10346843] 

Katz SH et al: Misplaced endotracheal tubes by paramedics in an urban emergency 

medical services system. Ann Emerg Med 2001;37:62. [PMID: 11145768] 

Loos L, Runyan L, Pelch D: Development of prehospital medical classification criteria. 

Air Med J 1998;17:13. [PMID: 10176557] 

Ma MH et al: Compliance with prehospital triage protocols for major trauma patients. J 

Trauma 1999;46:168. [PMID: 9932702] 

McConnel CE, Wilson RW: The demand for prehospital emergency services in an aging 

society. Soc Sci Med 1998;46: 1027. [PMID: 9579754] 

Moore L: Measuring quality and effectiveness of prehospital EMS. Prehosp Emerg Care 

1999;3:325. [PMID: 10534034] 

Morris DL et al: Prehospital and emergency department delays after acute stroke: the 

Genentech Stroke Presentation Survey. Stroke 2000;31:2585. [PMID: 11062279] 

Myers RB: Prehospital management of acute myocardial infarction: electrocardiogram 

acquisition and interpretation, and thrombolysis by prehospital care providers. Can J 

Cardiol 1998;14:1231. [PMID: 9852937] 

Nijs HG et al: Need for consensus development in prehospital emergency medicine: 

effect of an expert panel approach. Eur J Emerg Med 1998;5:329. [PMID: 9827837] 

Nordlander R, Svensson L: Prehospital management of patients with acute coronary 

syndromes. Acta Anaesthesiol Scand Suppl 1997;110:80. [PMID: 9248542] 

Ossmann EW, Bartkus EA, Olinger ML: Prehospital pearls, pitfalls, and updates. Emerg 

Med Clin North Am 1997;15:283. [PMID: 9183273] 

Plischke M et al: Telemedical support of prehospital emergency care in mass casualty 

incidents. Eur J Med Res 1999;4:394. [PMID: 10477508] 

Pullum JD, Sanddal ND, Obbink K: Training for rural prehospital providers: a 

retrospective analysis from Montana. Prehosp Emerg Care 1999;3:231. [PMID: 

10424861]

Roth A et al: Potential reduction of costs and hospital emergency department visits 

resulting from prehospital transtelephonic triage—the Shahal experience in Israel. Clin 

Cardiol 2000;23:271. [PMID: 10763075] 

Schou J: Duration and type of prehospital emergency therapy. Eur J Emerg Med 

1999;6(3):185. [PMID: 10622381] 

Seaman KG: Emergency medical service system evaluation and planning strategies for 

prehospital chest pain in Howard County, Maryland. MD Med J 1997;Suppl:80. [PMID: 

9470352] 

Shapiro SE: Outcomes of prehospital care: do we really make a difference? J Emerg 

Nurs 2000;26:239. [PMID: 10839853] 

Spivak M: Legislating EMS. "EMS Efficiency Act of 1998" aims to improve prehospital 

services. Emerg Med Serv 1998;27:20. [PMID: 10185405] 

Spivak M: No time to wait. An overview of recent studies and departmental programs 

designed to improve prehospital response to cardiac emergencies. Emerg Med Serv 

1998;27:33. [PMID: 10185415] 

Spivak M: Trauma care in EMS: where are we? A look at the nature, origins, 

controversies and future of prehospital trauma services. Emerg Med Serv 1999;28:29. 

[PMID: 10351460] 

Stern R, Arntz HR: Prehospital thrombolysis in acute myocardial infarction. Eur J Emerg 

Med 1998;5:471. [PMID: 9919456] 

Stiell IG et al: Improved out-of-hospital cardiac arrest survival through the inexpensive 

optimization of an existing defibrillation program: OPALS Study phase II. Ontario 

Prehospital Advanced Life Support. JAMA 1999;281:1175. [PMID: 10199426] 

Streger MR: Prehospital triage. Emerg Med Serv 1998;27:21. [PMID: 10180394] 

Suominen P et al: Prehospital care and survival of pediatric patients with blunt trauma. J 

Pediatr Surg 1998;33:1388. [PMID: 9766360] 

Vaccaro AR et al: The management of acute spinal trauma: prehospital and in-hospital 

emergency care. Instr Course Lect 1997;46:113. [PMID: 9143955] 

VanRooyen MJ, Thomas TL, Clem KJ: International emergency medical services: 

assessment of developing prehospital systems abroad. J Emerg Med 1999;17:691. 

[PMID: 10431962] 

Vermeulen B et al: Prehospital stabilization of pelvic dislocations: a new strap belt to 

provide temporary hemodynamic stabilization. Swiss Surg 1999;5:43. [PMID: 10217975] 

Warwick J: How much to do at the accident scene? Paramedic agrees with most of

comments about prehospital care. BMJ 2000;320:1005. [PMID: 10753163] 

Weaver J, Brinsfield KH, Dalphond D: Prehospital refusal-of-transport policies: adequate 

legal protection? Prehosp Emerg Care 2000;4:53. [PMID: 10634284] 






INTRODUCTION

Table 2-1. Training and procedures for emergency medical personnel. 

Hours of 

Training Skills and Procedures 

-40 Patient assessment 

Cardiopulmonary resuscitation 

Control of bleeding 

Bandaging and limited splinting 

Limited extrication 

81-140 Patient assessment 

Airway management and oxygen therapy 

Control of bleeding 

Management of shock (including Military 

Anti-shock Trousers [MAST]) 

Dressing and bandaging wounds 

Splinting (including traction splints) 

Spinal immobilization 

Extrication and triage 

110-1000 All EMT-A skills plus specialized training in one or more life 

support skills, usually including: 

Manual or automatic defibrillation 

Intravenous therapy 

Selected emergency medications 

Advanced airway management 

>1000 All EMT-A skills plus specialized training in advanced life supp 

skills, including2 

Intravenous cannulation 

Invasive airway management including endotracheal intubatio 

Cardiac dysrhythmia recognition 

Defibrillation 

Emergency medications

Table 2-2. Alternative EMS system designs. 1 

Response Emergency Emergency 

ALS ALS Single-tier ALS with 

first responder 

ALS 

First responder + ALS ALS Multitier (response and BLS 

transport) with first 

responder

Figure 2-1. Sample algorithm to guide medical dispatchers when the patient's principal 

complaint or problem is unconsciousness or syncope. 






FIGURES 

Figure 2-1

Figure 2-2. Standing orders for treatments and procedures that may be performed 

without prior attempt at base station contact by radio. ALS = EMT-P ambulance; BLS = 

EMT-A ambulance. 






FIGURES 

Figure 2-2

Figure 2-3. Sample protocol (in algorithmic form) for altered mental status. Note: The 

sequence for administering naloxone or glucose should be based on history and 

physical examination at the scene. 






FIGURES 

Figure 2-3

3. Nuclear, Biologic, & Chemical Agents; Weapons of Mass 

Destruction - Michael W. Stava, MD, & Joachim Franklin, MD 

INTRODUCTION 

In the past, injuries resulting from nuclear, biologic, and chemical attack were largely 

dealt with only in the military sector. Society as a whole, and specifically the civilian 

medical community, felt it unlikely that such weapons would be used against civilian 

populations. Recent changes in the global political environment have forced changes in 

this thinking. Many smaller nations, some of which are judged unstable, are attempting 

to develop weapons of mass destruction. Likewise, many terrorist organizations are now 

actively attempting to purchase or develop such weapons. In addition to the risk of an 

overt attack, other sources of exposure could come from accidents involving many 

nuclear, biologic, and chemical agents stored in facilities throughout the United States. 

An accident at any of these facilities could result in a large number of civilian casualties. 

As with most mass casualty situations, emergency physicians will be at the forefront of 

patient care. This chapter attempts to provide specific information regarding the 

management of nuclear, biologic, and chemical weapons injuries. 

NUCLEAR WEAPONS 

Several incidents in recent history, both military and civilian, have resulted in radiation 

injuries. The most notable, and in fact the only war-time use, involved the detonation of 

nuclear weapons over Hiroshima and Nagasaki, Japan. Unfortunately, many terrorist 

organizations have attempted to obtain nuclear weapons. A terrorist attack would most 

likely involve the detonation of a nuclear bomb or the detonation of a conventional 

explosive that also dispersed radioactive material (so-called dirty bomb). 


Radiation-induced injury occurs when various types of ionizing radiation interact with 

body tissues. Radiation exposure may be external or internal. Internal contamination 

can occur via wound contamination or via inhalation or ingestion of contaminated 

particles. Four types of radioactive particles may cause damage: 

1. Alpha particles—Alpha particles are large particles that are stopped by the 

epidermis. They cause no significant external damage. Internal contamination may 

cause local tissue injury. 

2. Beta particles—Beta particles are small particles that can penetrate the superficial 

skin and cause mild burnlike injuries. 

3. Gamma rays—Gamma rays are high-energy particles that can enter tissues easily 

and cause significant damage to multiple body systems. 

4. Neutrons—Neutrons are large particles that are typically produced only during

nuclear detonation. Like gamma rays, they cause significant tissue injury. 

The effect that radiation will have on the body depends on the type of radiation, the 

amount of exposure, and the body system involved. Tissues that display higher rates of 

cellular mitosis, such as the gastrointestinal and hematopoietic systems, are more 

severely affected. At very high radiation doses, neurovascular effects will also be seen. 

Radiation injury may cause either abnormal cell function or cell death. 

Clinical Findings 

A. Symptoms and Signs 

The symptoms and signs of radiation exposure occur in 3 phases: prodromal, latent, 

and symptomatic. 

1. Prodromal phase—Patients will develop nonspecific symptoms of nausea, vomiting, 

weakness, and fatigue. Symptoms generally last no longer than 24-48 hours. With 

higher radiation exposures, symptoms will occur more rapidly and last longer. 

2. Latent period—The length of the latent period depends on the dose of radiation and 

the body system involved (neurologic, several hours; gastrointestinal, 1-7 days; 

hematopoietic, 2-6 weeks). 

3. Symptomatic phase—Symptoms will depend largely on the body system affected, 

which will depend on the radiation dose. At doses of 0.7-4 gray (Gy), 1 the hematopoietic 

system will begin to manifest signs and symptoms of bone marrow suppression. 

Because of their long life span, erythrocytes are less severely affected than are the 

myeloid and platelet cell lines. Neutropenia and thrombocytopenia may be significant 

and lead to infectious and hemorrhagic complications. At doses of 6-8 Gy, 

gastrointestinal symptoms develop. Nausea, vomiting, diarrhea (bloody), and severe 

fluid and electrolyte imbalances will occur. The neurovascular system becomes affected 

at doses of 20-40 Gy. Symptoms include headache, mental status changes, 

hypotension, focal neurologic changes, convulsions, and coma. Exposures in this range 

are uniformly fatal. If an explosive device was used to disperse radioactive material, 

patients may also have thermal and blast injuries. 

1 The gray, a unit of measure for the dose of ionizing radiation, is equal to 1 J/kg of 

tissue. One gray is equal to 100 rad. 

B. Laboratory and X-ray Findings 

Obtain a complete blood count (CBC) with differential for all patients sustaining a 

radiation injury. Although symptomatic bone marrow suppression may not be evident for 

some weeks, a drop of the absolute lymphocyte count of 50% at 24-48 hours is 

indicative of significant exposure. Monitor electrolytes in patients with gastrointestinal 

symptoms. 

Treatment 

In the absence of aggressive medical therapy, the LD50 (the dose of radiation that will

kill 50% of those exposed) is approximately 3.5 Gy. Aggressive medical care affords 

improved survival. Treat all life-threatening injuries associated with blast or thermal 

effects according to standard advanced trauma life support protocols. Perform surgical 

procedures early to avoid the electrolyte and hematopoietic effects that will occur. Clean 

wounds extensively and close them as soon as possible to prevent infection. Treat 

nausea and vomiting with standard antiemetic medications (prochlorperazine, 

promethazine, ondansetron). Treat fluid and electrolyte abnormalities with appropriate 

replacement. Anemia and thrombocytopenia can be treated with transfusion therapy. 

Leukopenia may be treated with hematopoietic growth factors such as sargramostim 

and filgrastim. In some instances bone marrow transplantation may be utilized. Follow 

neutropenic precautions at absolute neutrophil counts below 500. Some authors 

recommend prophylactic antibiotics at counts below 100. Use broad-spectrum 

antibiotics to treat infections. Infection is the most common cause of death in radiation 

patients. Despite aggressive medical care, radiation exposures above 10 Gy are usually 

fatal. 

Decontamination 

Remove all contaminated clothing. Change contaminated dressings and splints. 

Thoroughly clean the patient's skin with soap and water or a 0.5% hypochlorite solution. 

Hair should be washed and in some instances removed. Eyes may be washed with 

large amounts of water or sterile saline. All contaminated materials should be bagged if 

possible and sent for proper disposal. 

Disposition 

Patients who have been decontaminated and have only mild transient symptoms can be 

safely discharged. Because of the variable and lengthy latent period involved with this 

disorder, early admission is not indicated. Patients should be closely monitored and 

admitted when warranted. 

Goans RE et al: Early dose assessment in criticality accidents. Health Phys 

2001;81(4):446. [PMID: 11569639] (Describes techniques for estimating the severity of 

radiation exposure.) 

Military Medical Operations Office, Armed Forces Radiobiology Research Institute: 

Medical Management of Radiological Casualties, 1st ed. Military Medical Operations 

Office, Armed Forces Radiobiology Research Institute, 1999. (Produced by the U.S. 

Army, this text provides general information regarding all aspects of radiologic injuries.) 

BIOLOGIC WEAPONS 

Many agents can be used as biologic weapons. The most likely pathogens are 

presented here. Biologic agents can be classified as bacterial agents (anthrax, plague, 

tularemia, brucellosis, Q fever, glanders), viral agents (smallpox, hemorrhagic fever, 

encephalitis), and biologic toxins (botulinum, ricin, T-2 mycotoxins, staphylococcal 

enterotoxin B). A high index of suspicion will be required in order to identify patients who 

have experienced a biologic attack. A large number of patients with severe febrile 

illnesses will be the most likely clue. Keep in mind the attack most likely occurred

several days prior to patient presentation. Aerosol release of infectious material is the 

most common form of biologic attack. 

BACTERIAL AGENTS (See Table 3-1.) 

1. Anthrax 

Bacillus anthracis is a gram-positive, sporulating rod. Anthrax infection occurs naturally 

after contact with contaminated animals or contaminated animal products. A biologic 

attack would likely involve the aerosol release of anthrax spores. The spore form of 

anthrax causes infection. Clinically the disease occurs in 3 forms: inhalational anthrax, 

gastrointestinal anthrax, and cutaneous anthrax. 



1. Inhalational anthrax—Inhalation anthrax is the form of disease most likely expected 

after a terrorist attack. After spores are inhaled, a variable incubation period occurs, 

usually lasting 1-7 days. Prolonged incubation periods of up to 60 days have been 

observed. Initially, nonspecific symptoms of fever, cough, headache, chills, vomiting, 

dyspnea, chest pain, abdominal pain, and weakness occur. This stage may last from a 

few hours to a few days. Following these nonspecific symptoms, a transient period of 

improvement may be seen. When the second stage of disease is reached, high fever, 

diaphoresis, cyanosis, hypotension, lymphadenopathy, shock, and death will occur. 

Often death will occur within hours once the second stage is reached. The average time 

from onset of symptoms to death is 3 days. Once the initial symptoms of inhalational 

anthrax develop, the overall mortality rate may be as high as 95%. Early diagnosis of 

anthrax infection and rapid initiation of therapy may improve survival. 

2. Gastrointestinal anthrax—Gastrointestinal anthrax occurs when spores are 

ingested into the digestive tract. Two forms of the disease occur: oropharyngeal and 

abdominal. Oropharyngeal disease occurs when spores are deposited in the upper 

gastrointestinal tract. An oral or esophageal ulcer develops followed by regional 

lymphadenopathy and eventual sepsis. In abdominal anthrax, the spores are deposited 

in the lower gastrointestinal tract. Symptoms include nausea, vomiting, diarrhea 

(bloody), and the development of an acute abdomen with sepsis. Mortality rates for 

gastrointestinal anthrax are in excess of 50%. 

3. Cutaneous anthrax—Cutaneous anthrax is the most common naturally occurring 

form of the disease. Cutaneous anthrax occurs when spores come in contact with open 

skin lesions. This usually occurs on the arms, hands, and face. Following exposure, a 

small, often pruritic papule will develop. Eventually this papule will turn into a small ulcer 

(over 2 days), then progress to a small vesicle, and ultimately to a painless black eschar 

with surrounding edema. Then, over a period of 1-2 weeks, the eschar will dry and fall 

off. Regional lymphadenitis or lymphadenopathy may also occur. In some case 

secondary sepsis may develop. Without treatment, cutaneous anthrax has a mortality 

rate of 20%; however, the mortality rate drops to 1% with treatment. 

4. Anthrax meningitis—Anthrax meningitis can occur as a complication of any other

form of anthrax. Symptoms include headache and meningismus. Anthrax meningitis 

carries a mortality rate of nearly 100%. 


Multiple laboratory studies can be used to identify anthrax. In fulminant cases, the 

organism may be seen on routine Gram stain. Blood cultures, wound cultures, and 

nasal cultures may be obtained. Given the lack of an infiltrate, sputum cultures are 

rarely useful. Notify laboratory personnel of a possible anthrax exposure. Often Bacillus 

spp. are thought to be the contaminant and are not pursued further. Confirmatory 

enzyme-linked immunoassay (ELISA) and polymerase chain reaction (PCR) tests are 

available at some national reference laboratories. Chest X-ray may also be useful. 

Patients with inhalational anthrax will display a wide mediastinum on chest x-ray. No 

infiltrate is typically observed. 

Treatment & Prophylaxis 

Because anthrax has a rapid and fulminant course, do not delay treatment while 

awaiting confirmatory tests. Institute empiric therapy when the diagnosis is considered. 

Delaying treatment for even hours may significantly increase mortality. 

A. Antibiotics 

Most naturally occurring strains of anthrax are sensitive to penicillin. Some strains, 

however, are penicillin resistant. Weapons-grade anthrax is likely to be penicillin 

resistant. As a result, the first-line therapy is now ciprofloxacin; doxycycline is an 

acceptable alternative (see Table 3-1). Treatment should continue for 60 days. If 

cultures were obtained, later sensitivity testing may direct antibiotic use. 

B. Supportive Care 

Patients may require intensive medical support such as airway management, 

hemodynamic support, and various measures to manage multisystem organ failure. 

C. Prophylaxis 

Individuals thought to be at high risk for anthrax exposure should receive treatment as 

though infection has occurred. Later laboratory analysis may allow discontinuation of 

therapy. An anthrax vaccination is available and requires injections at 0, 2, and 4 weeks, 

followed by injections at 6, 12, and 18 months. An annual booster is also required. If a 

combination of vaccination and antibiotics is used during treatment, the course of 

antibiotics may be shortened to 30 days. 

Infection Control 

No data indicate that anthrax is spread via person-to-person contact. Use standard 

precautions during patient care activities (Table 3-2). 

2. Plague 

Yersinia pestis is a nonmotile, gram-negative bacillus. Plague occurs naturally after the 

bite of an infected arthropod vector. Biologic attack would most likely involve the 

aerosolized release of Y pestis. Plague occurs in 3 clinical forms: bubonic plague,

septicemic plague, and pneumonic plague. 



1. Bubonic plague—Bubonic plague is the most common naturally occurring form of 

the disease. Infection begins with the bite of a contaminated flea. A latent period then 

occurs and may last up to 1 week, followed by fevers, chills, and weakness. Eventually 

the organism will migrate to the regional lymph nodes where it causes destruction and 

necrosis. A swollen and tender lymph node called a bubo will develop. Bubo size ranges 

from 1 to 10 cm. Some patients may develop secondary sepsis. Without treatment, 

bubonic plague has an estimated mortality rate of 50%; however, with antibiotic therapy 

the mortality rate falls to 10%. 

2. Septicemic plague—Septicemic plague may occur either as a complication of other 

forms of plague or as a primary entity. Symptoms include fever, dyspnea, hypotension, 

and purpuric skin lesions. Gangrene of the nose and extremities may occur, hence, the 

name "black death." Complications of disseminated intravascular coagulation may also 

be evident. Without treatment, septicemic plague has an estimated mortality rate of 

100%; however, with antibiotic therapy the mortality rate falls to 40%. 

3. Pneumonic plague—Pneumonic plague may occur either as a complication of other 

forms of plague or as a primary entity. It is the most likely form of the disease to result 

from a terrorist attack. A latent period of 1-6 days following exposure is likely. Patients 

will then develop signs and symptoms of severe pulmonary infection including fever, 

cough, dyspnea, hypoxia, and sputum production. Gastrointestinal symptoms of 

nausea, vomiting, and diarrhea may also occur. Pneumonic plague has an estimated 

mortality rate of 100% if antibiotic therapy is not begun within 24 hours. 


Y pestis can be identified by several different staining techniques. Routine Gram stain 

may reveal the organism. Y pestis also has a characteristic bipolar staining pattern with 

Wright, Giemsa, and Wayson stains. Routine blood cultures, sputum cultures, and 

cultures of lymph node aspirates may be useful. Specialized rapid confirmatory tests are 

available at some laboratories. In patients with pneumonic plague, chest x-ray will 

display a patchy or confluent infiltrate. 


Plague has a rapid disease progression, and any delay in treatment will cause 

significant increases in mortality. Institute treatment on empiric grounds, and do not 

delay treatment while awaiting confirmatory tests. 


Streptomycin is the drug of choice for the treatment of plague. Gentamicin may also be 

used and is thought to have equal efficacy (see Table 3-1). Alternative antibiotics 

include doxycycline, ciprofloxacin, and chloramphenicol. 

B. Supportive Care


hemodynamic support, and other measures to manage multisystem organ failure. 


Patients in a community experiencing a pneumonic plague epidemic should receive 

antibiotic therapy if they develop a cough or a fever above 38.5 °C (101.2 °F). Any 

person who has been in close contact with an individual with plague should receive a 

7-day course of antibiotics. Antibiotic choices are the same as for treatment. 


Pneumonic plague can be spread from person to person by aerosol droplets. Use 

droplet precautions, and either the patient or caregivers should wear masks (see Table 

3-2). Once the patient has received 48 hours of antibiotics and has improved clinically, 

standard precautions may be used. 

3. Tularemia 

Francisella tularensis is a nonmotile, aerobic, gram-negative coccobacillus. Two strains 

of tularemia are known to exist. F tularensis biovar tularensis is considered highly 

virulent, whereas F tularensis biovar palaearctica is more benign. Tularemia occurs 

naturally after the bite of an infected arthropod vector or after exposure to contaminated 

animal products. Biologic attack would most likely involve the release of aerosolized F 

tularensis. Tularemia displays multiple clinical forms including ulceroglandular, 

glandular, oculoglandular, oropharyngeal, pneumonic, and typhoidal forms. The form of 

disease depends on the site and type of inoculation. 



Patients with any form of tularemia may present with the abrupt onset of fever, chills, 

headache, malaise, and myalgias. Often a maculopapular rash is seen. 

1. Ulceroglandular tularemia—Ulceroglandular tularemia usually occurs after handling 

infected animals or after the bite of an infected arthropod vector. At the inoculation site a 

papule will form that will eventually become a pustule and then a tender ulcer. The ulcer 

may have a yellow exudate and will slowly develop a black base. Regional lymph nodes 

will become swollen and painful. 

2. Glandular tularemia—Glandular tularemia displays signs and symptoms similar to 

ulceroglandular tularemia, except that no ulcer formation is noted. 

3. Oculoglandular tularemia—After ocular inoculation, a painful conjunctivitis will 

develop with regional lymphadenopathy. Lymphadenopathy may involve the cervical, 

submandibular, or preauricular chains. In some cases, ulcerations occur on the 

palpebral conjunctiva. 

4. Oropharyngeal tularemia—After inoculation of the pharynx, an exudative 

pharyngotonsillitis will develop with cervical lymphadenopathy.

5. Pneumonic tularemia—Pneumonic tularemia occurs after inhalation of F tularensis 

or following secondary spread from other infectious foci. A terrorist attack will most likely 

cause this form of disease. The findings of pulmonary involvement are variable and 

include pharyngitis, bronchiolitis, hilar lymphadenitis, and pneumonia. Early in the 

course of disease, systemic symptoms may predominate over pulmonary symptoms. In 

some cases, however, pulmonary disease progresses rapidly to pneumonia, pulmonary 

failure, and death. 

6. Typhoidal tularemia—In this form of tularemia, systemic signs and symptoms of 

disease are present without a clear infectious site. Signs and symptoms include fever, 

chills, headache, malaise, and myalgias. 

Any form of tularemia may be complicated by hematogenous spread leading to 

pneumonia, meningitis, or sepsis. The overall mortality rates for untreated tularemia 

range from 10% to 30%; however, with antibiotic therapy, mortality rates drop to less 

than 1%. 


F tularensis requires special growth media. Notify laboratory personnel of a possible 

tularemia specimen so that proper plating can be performed. Cultures may be obtained 

from sputum, pharyngeal, or blood specimens. Specialized ELISA and PCR 

confirmatory tests are also available at some reference laboratories. In the case of 

pneumonic tularemia, chest x-ray may demonstrate peribronchial infiltrates to 

bronchopneumonia. Pleural effusions are often present. 



Streptomycin and gentamicin are considered the drugs of choice for the treatment of 

tularemia (see Table 3-1). Ciprofloxacin has also displayed efficacy against tularemia. 

Second-line agents such as tetracycline and chloramphenicol may be used, but these 

agents are associated with higher rates of treatment failure. A 10-day course of 

antibiotics should be used. For second-line agents, a 14-day course should be used. 


Rarely patients may require intensive medical support such as airway management, 



Some data suggest that a 14-day course of antibiotics begun during the incubation 

period may prevent disease. Antibiotic choices are the same as for treatment. A live 

attenuated vaccine for tularemia also exists and is often used for at-risk laboratory 

workers. Vaccination decreases the rate of inhalational tularemia but does not confer 

complete protection. Given tularemia's short incubation period, and the incomplete 

protection of the vaccine, postexposure vaccination is not recommended. 

Infection Control

Significant person-to-person transmission of tularemia does not occur. Standard 

precautions are sufficient during patient care activities (see Table 3-2). 

4. Brucellosis 

Brucellae are small aerobic, gram-negative, pleomorphic coccobacilli. Many Brucella 

spp. occur naturally; however, only 4 species are infectious to humans. Each species 

typically infects a particular host organism, and human infection follows contact with 

contaminated animal material. The Brucella spp. that are infectious to humans are B 

melitensis (found in goats), B suis (found in swine), B abortus (found in cattle), and B 

canis (found in dogs). B suis has been weaponized in the past. 



The symptoms and signs of brucellosis are similar whether infection is contracted via 

oral, inhalational, or percutaneous routes. The usual incubation period following 

infection is 1-3 weeks. Because Brucella spp. infection can involve multiple body 

systems, a wide range of clinical findings is typical. Nonspecific symptoms are common 

and include fever, chills, malaise, and myalgias. Osteoarticular involvement may 

manifest as joint infections or vertebral osteomyelitis. Respiratory symptoms include 

cough, dyspnea, and pleuritic chest pain. Cardiovascular complications are numerous 

and include endocarditis, myocarditis, pericarditis, and mycotic aneurysms. 

Gastrointestinal symptoms include nausea, vomiting, diarrhea, and hepatitis. Multiple 

types of genitourinary infections can also occur. Neurologic involvement may cause 

meningitis, encephalitis, cerebral abscesses, cranial nerve abnormalities, or 

Guillain-Barre syndrome. Patients may also develop anemia, thrombocytopenia, or 

neutropenia. Central nervous system and cardiac involvement, although infrequent, 

accounts for most fatalities. Brucella spp. are not known for their lethality, and infection 

has an estimated mortality rate of less than 2%. Its interest as a biological weapon 

stems from the prolonged disease course and significant morbidity. 


Brucella spp. will grow on standard culture media. Because of their slow growth, 

cultures may need to be maintained for at least 6 weeks. Specialized biphasic culture 

techniques may improve isolation. A more common diagnostic modality is a serum tube 

agglutination test. ELISA and PCR studies are available at some reference laboratories. 

If vertebral involvement is suspected, spinal x-rays, magnetic resonance imaging, 

computed tomography scanning, or bone scintigraphy may be helpful. 



Because of the high rate of treatment failure, single drug therapy is no longer 

recommended. A prolonged course of multiple antibiotics is now considered to be the 

standard of care. The most common regimen involves the use of rifampin and 

doxycycline given for a 6-week period (see Table 3-1). Other antibiotics that have 

displayed efficacy against Brucella spp. include gentamicin, streptomycin, 

trimethoprim-sulfamethoxazole, and ofloxacin. Regardless of the antibiotics chosen,

combination drug therapy should be used. In patients with serious infections, a 3-drug 

parenteral regimen is the norm. 





No human vaccine against Brucella spp. currently exists. Some authors recommend a 

3- to 6-week course of antibiotics following a high-risk exposure such as a biologic 

attack. 


Person-to-person spread of brucellosis is thought to be uncommon. Standard 

precautions are sufficient during patient care activities (see Table 3-2). 

5. Q Fever 

Q fever is caused by a rickettsial organism known as Coxiella burnetii. C burnetii has a 

worldwide distribution and occurs naturally in many domesticated animals (dogs, cats, 

sheep, goats, cattle). The organism is shed in feces, urine, milk, and placental material. 

Much like anthrax, C burnetii produces a sporelike form. Humans become infected by 

inhaling contaminated aerosols. 



After infection, a typical incubation period ranges from 5 to 30 days. The symptoms and 

signs of Q fever are nonspecific and may occur acutely or have an indolent course. 

Typical symptoms and signs include fever, chills, malaise, myalgias, headache, and 

anorexia. If cough occurs, it tends to occur late in the disease process and may or may 

not be associated with pneumonia. Various cardiac manifestations may occur and 

include endocarditis, myocarditis, and pericarditis. Gastrointestinal findings are common 

and include nausea, vomiting, diarrhea, and hepatitis. A nonspecific maculopapular rash 

may develop. Although not as common, various neurologic symptoms may also occur. 

In some patients, Q fever may become a chronic condition. Chronic Q fever is typically 

manifest as endocarditis and tends to affect previously diseased cardiac valves. 

Although Q fever can be debilitating, it is usually not fatal. Mortality rates are generally 

less than 2.5%. 


C burnetii is difficult to grow in culture, and sputum analysis is equally futile. Several 

serologic tests are available and include indirect fluorescent antibody staining, ELISA, 

and complement fixation. These tests often must be conducted at specialized reference 

laboratories. Elevated liver enzymes are also common in C burnetii infection. 

Treatment & Prophylaxis


Most cases of C burnetii infection will resolve without antibiotic therapy. Regardless, 

antibiotics are recommended because treatment will lower the rate of complications. A 

7-day course of either doxycycline or tetracycline is usually sufficient (see Table 3-1). 

Fluoroquinolones are an acceptable alternative. 





Prophylactic antibiotics should be started 8-12 days after initial exposure. Antibiotics are 

ineffective if started sooner. A 7-day course of either doxycycline or tetracycline is 

usually sufficient. Fluoroquinolones are an acceptable alternative. An investigational 

vaccine exists but is not yet available to the general public. 


Person-to-person spread of the disease is unlikely. Standard precautions are sufficient 

while engaging in patient care activities (see Table 3-2). 

6. Glanders & Melioidosis 

Glanders and melioidosis are similar diseases caused by related bacteria. The causal 

agent of glanders is Burkholderia mallei; the causal agent of melioidosis is Burkholderia 

pseudomallei. Both organisms are gram-negative bacilli. Glanders and melioidosis 

occur naturally. Glanders is a rare disease in humans; horses and other domesticated 

animals are often infected. Melioidosis occurs more commonly in humans and is 

endemic to Southeast Asia. Infection with either organism occurs via contact with open 

wounds or mucous membranes or by inhalation. 



Both glanders and melioidosis can cause multiple clinical syndromes. 

1. Localized disease—A localized disease may be seen and typically occurs after 

wound contamination or mucous membrane exposure. With wound contamination, 

patients develop a small ulcer with associated cellulitis. Regional lymphadenopathy or 

lymphangitis is also common. If mucous membrane exposure occurs, patients develop a 

bloody purulent discharge from the infected area (eyes, nose, or mouth). If secondary 

systemic infection occurs, a pustular rash similar to smallpox may develop. 

2. Pulmonary disease—A pulmonary form of disease may also be seen. Pulmonary 

disease may occur after inhalation of aerosols or after hematogenous spread. An 

incubation period of 1-2 weeks occurs initially. Symptoms of pulmonary disease, 

including fever, chills, cough, chest pain, and dyspnea, develop eventually.

3. Septicemic disease—The most severe form of infection is the septicemic form. 

Patients present with nonspecific symptoms and signs of fever, chills, malaise, 

myalgias, photophobia, rigors, diffuse body abscesses, pustular rash, and headache. 

This condition is usually fatal; death occurs in 7-10 days. 


Both organisms can be identified by routine Gram stain and culture. Special staining 

with methylene blue or Wright stain may facilitate diagnosis. Growth may be enhanced 

by the addition of meat nutrient agar or glucose to the growth media. Specialized 

agglutination and complement fixation tests may also be used. If pulmonary involvement 

is suspected, chest x-ray may demonstrate lung abscesses, miliary nodules, or 

pneumonia. 



Both glanders and melioidosis respond to various antibiotics. Appropriate antibiotic 

choices include amoxicillin-clavulanate, tetracycline, trimethoprim-sulfamethoxazole, 

rifampin, ciprofloxacin, and ceftazidime (see Table 3-1). Various combinations of 

antibiotics have been recommended depending on the type and severity of infection. 





According to some authorities, a course of trimethoprim-sulfamethoxazole may prevent 

the onset of disease. 


Person-to-person spread of the disease is uncommon but can occur with improper 

handling of body fluids. Standard precautions are sufficient during patient care activities 

(see Table 3-2). 

VIRAL AGENTS 

1. Smallpox 

Smallpox is a disease caused by the variola virus. The variola virus is a DNA virus of 

the genus orthopoxvirus. It occurs in 2 strains: the more severe variola major and a 

milder form, variola minor. Smallpox was essentially eradicated by an aggressive 

treatment and vaccination campaign conducted by the World Health Organization. The 

last naturally occurring case was in Somalia in 1977. Two stockpiles of the virus remain, 

one in the Centers for Disease Control and Prevention in Atlanta, and the other in the 

Institute of Virus Preparations in Moscow. Concern now exists that the Russian 

stockpile may have been compromised. 

Clinical Findings


Disease begins with inhalation of the variola virus. After an initial exposure, a 7- to 

17-day incubation period begins, during which the virus replicates in the lymph nodes, 

bone marrow, and spleen. A secondary viremia then develops leading to high fever, 

malaise, headache, backache, and in some cases delirium. After approximately 2 days 

a characteristic rash will develop. The rash begins on the extremities and moves to the 

trunk. The palms and soles are not spared. The rash follows a typical progression 

beginning as macules, then papules, and eventually becoming pustular. Eventually 

lesions will form scabs that separate, leaving small scars. Unlike chickenpox, all the 

lesions in smallpox will be in similar stages of development. In unvaccinated individuals, 

mortality rates associated with variola major are approximately 30%. Variola minor has 

a similar progression to variola major, but toxicity and rash are not as severe. In 

unvaccinated individuals, the mortality rates associated with variola minor are 

approximately 1%. In 10% of cases, a variant form of rash will develop. A hemorrhagic 

rash displaying petechiae and frank skin hemorrhage may occur. This variant of 

smallpox carries a mortality rate of nearly 100%. Likewise, a malignant form exists in 

which the pustules remain soft and velvety to the touch. 


Analysis of pustular fluid will yield virus particles. All samples should be sealed in 2 

airtight containers. Variola can easily be recognized via electron microscopy. The virus 

itself can be grown in cell cultures or on chorioallantoic egg membranes. Further 

characterization of strains can be accomplished via biologic assays. PCR analysis is 

available at some reference laboratories. 


A. Specific Therapy 

Currently there is no specific therapy for smallpox. Treatment is essentially supportive 

care. Many investigational drugs are currently under study. Strict patient isolation, 

preferably in the home, should be used. Any person having close contact with infected 

patients should be either quarantined or monitored for signs of infection. Antibiotics may 

be used if secondary bacterial infection occurs. 

B. Prophylaxis 

Data indicate that vaccination within 4 days of smallpox exposure may lessen 

subsequent illness. Because of the risk of possible terrorist attack, some authorities are 

recommending a preemptive initiation of smallpox vaccination. This would be 

problematic for several reasons. First, the current supply of smallpox vaccine is 

inadequate to protect a large populace. Second, many complications were known to 

occur with smallpox vaccination. Postvaccinial encephalitis occurred in approximately 1 

in 300,000 vaccinations and was fatal in 25% of patients. Immunocompromised patients 

may develop a condition known as progressive vaccinia. In this condition, the initial 

inoculation site failed to heal, became necrotic, and necrosis spread to adjacent tissues. 

This complication was often fatal. In some patients with eczema, a condition known as 

eczema vaccinatum could occur. Here, vaccinial lesions would occur in areas previously 

involved with eczema. Fortunately, the eruption was usually self-limited. In some 

patients, a secondary generalized vaccinia could develop. In others, inadvertent

autoinoculation of eyes, mouth, or other areas occurred. Many of these complications 

could be treated with vaccinia immune globulin. Unfortunately, vaccinia immune globulin 

is also in short supply. 

Cidofovir has also displayed some efficacy in preventing smallpox infection if given 

within 48 hours. There is no evidence to suggest that cidofovir is more effective than 

vaccine. Further, cidofovir is associated with significant renal toxicity. 

Individuals vaccinated prior to 1972 are likely no longer protected, given that immunity 

lapses over a 5- to 10-year period. 


Smallpox is highly infectious. Infection is spread by aerosol droplets. It is generally 

thought that each index case will subsequently infect 10-20 secondary individuals. The 

period of infectivity begins with the onset of rash and ends when all scabs separate. Use 

airborne precautions during patient care activities (see Table 3-2). Any material in 

contact with patients should be either autoclaved or washed in a bleach solution. 

2. Hemorrhagic Fever 

Viral hemorrhagic fever represents a clinical syndrome caused by several RNA viruses. 

These viruses exist in 4 different families: the Arenaviridae, the Filoviridae, the 

Flaviviridae, and the Bunyaviridae. Numerous viruses in each family may cause slightly 

different forms of hemorrhagic fever. The different forms of hemorrhagic fever are often 

named by their geographic origin (Table 3-3). Human infection occurs after contact with 

infected animals or infected arthropod vectors. Many of these viruses are also highly 

infectious in the aerosol form. This characteristic makes them potential biological 

weapons. 



Several clinical aspects of hemorrhagic fever are unique to the individual forms (Table 

3-3). Many symptoms and signs, however, are common to all types of hemorrhagic 

fever. Alterations in the vascular bed and increased vascular permeability lead to the 

dominant features of this disease. Early symptoms and signs include fever, conjunctival 

injection, mild hypotension, prostration, facial flushing, vomiting, diarrhea, and petechial 

hemorrhages. Eventually some patients may develop shock and mucous membrane 

hemorrhage. In some instances, evidence of hepatic, pulmonary, and neurologic 

involvement will be present. Secondary bacterial infection is also common. 


A number of nonspecific laboratory abnormalities may be seen, including leukopenia, 

thrombocytopenia, proteinuria, hematuria, and elevated liver enzymes. Definitive 

diagnosis is possible with various rapid enzyme immunoassays and with viral culture. 



Ribavirin is a nucleoside analog that has been shown to improve mortality in some 

forms of hemorrhagic fever. Dosing is as follows: 30 mg/kg intravenously as an initial 

dose, followed by 16 mg/kg intravenously every 6 hours for 4 days and then 8 mg/kg 

intravenously every 8 hours for 6 days. Ribavirin is usually most effective if begun within 

7 days. Unfortunately, ribavirin is thought to be ineffective against the filoviruses and the 

flaviviruses. Convalescent plasma containing neutralizing antibodies is also effective in 

some cases. 


Intravenous lines and other invasive procedures should be limited. Use fluid 

resuscitation with caution. Because of increases in vascular permeability, peripheral 

edema and pulmonary edema are frequent complications of volume replacement. If 

frank disseminated intravascular coagulopathy develops, consider heparin therapy. 


A vaccine against yellow fever is currently available. Many other investigational 

vaccines exist but are not currently available to the general public. Protocols also exist 

for the use of ribavirin in high-risk exposures. 


The causal agents of hemorrhagic fever are highly infectious. Use caution when using 

sharps or when coming into contact with body fluids. Some forms are spread via 

aerosol, and patients with significant cough should be placed under airborne 

precautions. All laboratory specimens should be double sealed in airtight containers. 

3. Viral Encephalitis 

Much like viral hemorrhagic fever, viral encephalitis represents a clinical syndrome 

caused by numerous viruses. Of the pathogens that cause viral encephalitis, members 

of the family Togaviridae are thought to have potential as biologic weapons. The family 

Togaviridae includes the eastern equine encephalitis (EEE) virus, western equine 

encephalitis (WEE) virus, and Venezuelan equine encephalitis (VEE) virus. VEE virus 

has been weaponized in the past. In nature, these viruses are spread by infected 

arthropod vectors, and they infect humans as well as equines. They are also infectious 

in aerosol form, hence, their utility as biologic weapons. 



Nearly all forms of infection will cause nonspecific symptoms and signs of fever, chills, 

malaise, myalgias, sore throat, vomiting, and headache. A large number of associated 

equine deaths may lead one to suspect equine encephalitis. The degree to which 

encephalitis develops depends on the pathogen involved. Although nearly all cases of 

VEE are symptomatic, encephalitis occurs in less than 5% of cases. If encephalitis does 

develop, and the patient recovers, residual neurologic sequelae usually do not occur. 

Without encephalitis, VEE has an expected mortality rate of less than 1%. Although 

uncommon, if encephalitis develops, the mortality rate increases to approximately 20%.

In contrast, EEE tends to progress to neurologic involvement. Encephalitis is usually 

severe, and residual neurologic findings are common. With EEE, mortality rates range 

from 50% to 75%. WEE displays an intermediate degree of severity, with an overall 

estimated mortality rate of approximately 10%. If encephalitis develops, confusion, 

obtundation, seizures, ataxia, cranial nerve palsies, and coma may occur. 


Although nonspecific, leukopenia and lymphopenia are common. In cases of 

encephalitis, cerebral spinal fluid analysis will display a lymphocytic pleocytosis. A 

number of serologic studies such as ELISA, complement-fixation, and hemagglutination 

inhibition may aid diagnosis. Although time consuming, the gold standard test for VEE 

involves viral isolation following inoculation of cell cultures of suckling mice. Additional 

specialized tests may be available only at regional reference laboratories. 



Unfortunately, no specific treatment for equine encephalitis exists. Supportive care is all 

that can be offered. Headache may be treated with typical analgesics. Seizures are 

treated with typical anticonvulsant medications. 





An investigational vaccine against VEE virus exists. It does not provide protection 

against all strains of VEE virus, and some patients will not display an effective antibody 

response. In 20% of patients receiving the vaccine, fever, malaise, and myalgias may 

develop. 


Infection is not spread by person-to-person contact. Standard precautions are sufficient 

during patient care activities. To limit the spread of disease, patient exposure to 

arthropod vectors should be prevented. 

BIOLOGIC TOXINS (See Table 3-4.) 

1. Botulinum Toxin 

Botulism is caused by a protein toxin produced by Clostridium botulinum. C botulinum is 

a gram-positive, spore-forming, obligate anaerobe found naturally in the soil. Many 

authorities consider botulinum toxin to be among the most potent naturally occurring 

poisons. The toxin occurs in 7 antigenic types, designated types A through G. Once 

absorbed, toxin will bind to motor neurons and prevent the release of acetylcholine, 

causing a flaccid muscle paralysis. Natural infection occurs in 3 forms: wound botulism, 

foodborne botulism, and intestinal botulism. Wound botulism occurs after C botulinum 

contaminates an open wound, subsequently producing toxin. Foodborne botulism

occurs after ingesting food already contaminated by the toxin. Intestinal botulism, 

typically seen in infants, occurs after ingesting food contaminated by C botulinum, which 

in turn produces toxin. Although not occurring naturally, botulism can also be caused by 

inhalation of the toxin. This is the form of botulism that will likely occur following biologic 

attack. Contamination of food or water supplies also represents a possible terrorist 

threat. Food contamination, however, is unlikely to induce the large numbers of affected 

persons that would be seen following aerosol exposure. Water contamination would be 

difficult because current purification techniques are effective in neutralizing botulinum 

toxin. 



After initial exposure, an incubation period ranging from 12 to 80 hours will occur. The 

duration of the incubation period depends on the type and amount of exposure. After the 

incubation period, a flaccid symmetric muscle paralysis will affect the bulbar 

musculature. Patients often display ptosis, diplopia, dysphagia, dysarthria, and 

dysphonia. Dilated, poorly reactive pupils are common. Eventually the paralysis will 

extend to the lower muscle groups, leading to paralysis. Airway compromise is common, 

and patients may lose respiratory function. 

If foodborne exposure is involved, gastrointestinal symptoms such as nausea, vomiting, 

and diarrhea may occur. Botulism does not cause altered sensorium, sensory changes, 

or fever. 


A mouse bioassay is the definitive test for botulism. Specimens for evaluation may be 

obtained from suspected food, blood, gastric contents, or possibly stool. This type of 

diagnostic testing is not widely available, and specimens may need to be sent to 

specialized laboratories. In addition to laboratory studies, electromyograms may display 

patterns consistent with botulism. 



A botulinum antitoxin can be obtained from many state health departments or from the 

Centers for Disease Control and Prevention. Antitoxin therapy is most effective when 

given early in the disease course. It acts by binding free toxin but will not restore nerve 

terminals that have already been compromised. The civilian antitoxin is effective in 

neutralizing the 3 most common types of botulinum toxin found to affect humans (types 

A, B, and E). If other forms of toxin are utilized, an investigational heptavalent antitoxin 

may be available from the military. The military antitoxin is effective against all types of 

toxin (types A through G). Because some patients may develop allergic reactions to the 

antitoxin, a test dose is recommended. 


Patients may require intensive medical support such as airway management and 

ventilator support. Parenteral or tube feedings may be required. Treat secondary 

bacterial infections with antibiotics. Avoid clindamycin and aminoglycoside antibiotics

ecause they may worsen neurologic blockade. 


Some evidence suggests that initiation of antitoxin prior to the onset of symptoms may 

prevent disease. Unfortunately, large amounts of the antitoxin are not available. A more 

prudent course of action would be to institute antitoxin therapy at the first signs of 

illness. 


Person-to-person transmission of botulism does not occur. Standard precautions are 

sufficient during patient care activities (see Table 3-2). If food is suspected of being 

contaminated, thorough cooking will neutralize the toxin. 

2. Ricin 

Ricin is a polypeptide toxin that causes cell death by inhibiting protein synthesis. Ricin 

occurs naturally as a component of the castor bean, from the castor plant, Ricinus 

communis. Accidental ricin toxicity has occurred following ingestion of castor beans. 

Although ricin is less toxic than many other potential biologic agents, it is inexpensive, 

easy to produce, and can be aerosolized. These characteristics make it a potential 

biologic weapon. Ricin may be delivered by parenteral injection, ingestion, or inhalation. 

Ingestion and inhalation are the likely modes of biologic attack. 



The signs and symptoms of ricin intoxication depend on the type and amount of 

exposure. Parenteral exposure causes necrosis of local tissues and regional lymph 

nodes. As the toxin spreads, visceral organs become involved, manifested as a 

moderate to severe gastroenteritis. Parenteral exposure is an unlikely means of biologic 

attack. If ricin is ingested, symptoms of gastrointestinal exposure will occur and may 

include nausea, vomiting, hematemesis, bloody diarrhea, melena, or visceral organ 

necrosis. If death occurs following parenteral or gastrointestinal exposure, it is usually 

secondary to circulatory collapse. 

The most likely means of biologic attack involve aerosol exposure. Inhalation of ricin is 

manifested by direct pulmonary toxicity. Between 4 and 8 hours after exposure, the 

patient may develop fever, cough, chest pain, and dyspnea. Findings consistent with an 

aerosol exposure include bronchitis, bronchiolitis, interstitial pneumonia, and acute 

respiratory distress syndrome. If death occurs, it is usually secondary to respiratory 

failure and generally will occur within 36-72 hours. 


Various laboratory tests including ELISA, PCR, and immunohistochemical staining may 

aid in the diagnosis of ricin toxicity. In the event of pulmonary involvement, chest x-ray 

may display bilateral infiltrates or noncardiogenic pulmonary edema. 


The treatment of ricin toxicity depends largely on the mode of exposure. 

A. Parenteral Exposure 

With parenteral exposure, treatment is largely supportive. 

B. Gastrointestinal Exposure 

The treatment of gastrointestinal exposure primarily involves the elimination of toxin. 

This can be accomplished by vigorous gastric lavage and by the use of cathartics such 

as magnesium citrate or whole bowel irrigation. Activated charcoal may be considered. 

Correct electrolyte abnormalities, and maintain adequate volume status. Treat 

secondary bacterial infections with appropriate antibiotics. 

C. Pulmonary Exposure 

With pulmonary exposure, treatment involves providing adequate ventilatory support. 

Patients may require oxygen, intubation, and ventilator management. Treat secondary 

bacterial infections with appropriate antibiotics. 

D. Prophylaxis 

Ricin vaccines are under development. 


Ricin intoxication is not spread by person-to-person contact. Standard precautions are 

sufficient during patient care activities (see Table 3-2). 

3. T-2 Mycotoxins 

Like penicillin, mycotoxins are a diverse group of compounds produced by fungi for 

environmental protection. These compounds are frequently toxic to many animal 

species including humans. The T-2 mycotoxins are a particular group of compounds 

produced by fungi in the genus Fusarium. Although the actions of the T-2 mycotoxins 

are not completely understood, they are known to inhibit DNA and protein synthesis. 

They are most toxic to rapidly dividing cell lines. 

Many properties of these compounds make them attractive as biologic weapons. 

Specifically, they are resistant to destruction by ultraviolet radiation and are heat stabile. 

T-2 mycotoxins confer toxicity after ingestion, inhalation, or dermal exposure. Unlike 

most other biologic agents, they can be absorbed directly though the skin. 



With T-2 mycotoxin exposure, contamination via dermal, gastrointestinal, and 

pulmonary routes may occur simultaneously. The earliest symptoms and signs may 

begin within minutes to hours. Dermal exposure may be manifest as skin pain, 

erythema, blistering, and skin necrosis. Toxin exposure to the eyes and upper airway 

may cause ocular pain, redness, tearing, sneezing, rhinorrhea, oral pain, blood-tinged 

mucus, and epistaxis. Patients with pulmonary involvement will display chest pain,

cough, and dyspnea. Signs and symptoms of gastrointestinal toxicity include abdominal 

pain, nausea, vomiting, and a bloody diarrhea. With systemic toxicity, patients may 

develop weakness, dizziness, and ataxia. Similar to radiation exposure, these toxins 

may also cause bone marrow suppression resulting in thrombocytopenia and 

neutropenia. 


Two primary forms of laboratory testing may be used to identify T-2 mycotoxins. First, 

antigen detection can be performed on urine samples. The metabolites of the T-2 

mycotoxins are eliminated primarily in the urine and feces. These metabolites are 

detectable in the urine up to 1 month after exposure. Second, mass spectrometric 

evaluation can be conducted on various body fluids. Appropriate samples include nasal 

secretions, pulmonary secretions, urine, blood, and stomach contents. 



The treatment of T-2 mycotoxin poisoning is essentially supportive care. Remove all 

contaminated clothing, and wash the patient's skin with large amounts of soap and 

water. Treat dermal burns with standard therapy. Treat secondary bacterial infections 

with appropriate antibiotics. Ocular involvement requires irrigation with water or sterile 

saline. Activated charcoal may aid in gastrointestinal decontamination. Patients with 

pulmonary involvement may require advanced respiratory techniques such as intubation 

or ventilatory support. 


Vaccines against the T-2 mycotoxins are under study. The early use of soap and water 

may prevent skin toxicity. 


The T-2 mycotoxins are dispersed as an oily liquid. Contact with this liquid may cause 

cross contamination. Therefore, remove all contaminated clothing and wash the 

patient's skin with soap and water. Standard precautions are sufficient during patient 

care activities (see Table 3-2). 

4. Staphylococcal Enterotoxin B 

Staphylococcal aureus produces a number of exotoxins that produce disease in 

humans. One such exotoxin, staphylococcal enterotoxin B (SEB), is a causal agent of 

the gastrointestinal symptoms seen in staphylococcal food poisoning. It is a heat-stabile 

toxin that belongs to a group of compounds known as super antigens. These 

compounds have the ability to activate certain cells in the immune system, causing a 

severe inflammatory response. This response causes injury to various host tissues. 

Aside from injury caused by SEB in natural infections, it can be aerosolized, making it a 

potential biologic weapon. Biologic attack could involve deliberate contamination of 

foodstuffs, although a more likely scenario would involve an aerosol release. 

Clinical Findings


After exposure to SEB, a variable incubation period occurs, ranging from 4 to 10 hours 

for gastrointestinal exposure and from 3 to 12 hours for inhalational exposure. 

Regardless of the type of exposure, nonspecific symptoms and signs will develop and 

include fever, chills, headache, malaise, and myalgias. If the exposure occurred via the 

gastrointestinal route, then patients will also develop nausea, vomiting, and diarrhea. 

Conversely, if the exposure occurred via an inhalational route, the patient will also 

develop chest pain, cough, and dyspnea. Death is rare but in severe cases may occur 

from respiratory failure. Patients generally recover from symptoms after 1-2 weeks. 


The presence of SEB can be confirmed by identifying specific antigens via ELISA 

testing. Obtain serum and urine samples. Urine samples are more productive because 

toxin tends to accumulate in the urine. In the case of aerosol exposure, respiratory and 

nasal swabs may also demonstrate toxin if samples are obtained within 1 day of 

exposure. With inhalational exposure, the chest x-ray is usually normal but in severe 

cases may demonstrate pulmonary edema. 



The treatment of SEB exposure is largely supportive. Correct electrolyte abnormalities, 

and maintain volume status. If pulmonary edema develops, patients may benefit from 

diuretic therapy and in some cases may require intubation and ventilatory support. 

Steroids may be given to lessen the inflammatory response, but this approach is 

controversial. Treat secondary bacterial infections with appropriate antibiotics. 


Vaccines against SEB are under study. 


Person-to-person transmission of toxin is not a hazard. Standard precautions are 

sufficient during patient care activities (see Table 3-2). 

Arnon SS et al: Botulinum toxin as a biological weapon: medical and public health 

management. JAMA 2001;285(8):1059. [PMID: 11209178] (Review article discussing all 

aspects of botulism use as a biologic weapon). 

Dennis DT et al: Tularemia as a biological weapon: medical and public health 

management. JAMA 2001;285(21):2763. [PMID: 11386933] (Review article discussing 

all aspects of tularemia use as a biologic weapon.) 

Franz DR et al: Clinical recognition and management of patients exposed to biological 

warfare agents. JAMA 1997;278(5):399. [PMID: 9244332] (Review article discussing 

issues related to common biologic warfare agents.) 

Henderson DA et al: Smallpox as a biological weapon: medical and public health

management. JAMA 1999;281(22):2127. [PMID: 10367824] (Review article that 

discusses all aspects of smallpox use as a biological weapon.) 

Inglesby TV et al: Anthrax as a biological weapon: medical and public health 


all aspects of anthrax use as a biological weapon.) 

Inglesby TV et al: Plague as a biological weapon: medical and public health 


all aspects of plague use as a biological weapon.) 

USAMRIID Medical Management of Biological Casualties Handbook, 4th ed. U.S. Army 

Medical Research Institute of Infectious Diseases, 2001. (Produced by the U.S. Army, 

this general text provides general information regarding the most probable biologic 

agents.) 

CHEMICAL WEAPONS (See Table 3-5.) 

Like radiation and biologic agents, many chemicals can be developed into weapons of 

mass destruction. Chemical weapons are particularly attractive to rogue governments 

and terrorist organizations because of their low cost, stability, and ease of production. In 

fact, chemical agents have already been used by terrorist organizations. The terrorist 

group Aum Shinrikyo released sarin gas in a Japan subway in 1995. Chemical agents 

can be delivered as liquids, vapors, or as components of explosive devices. Chemical 

agents are generally categorized as nerve agents, pulmonary agents, vesicants, and 

cyanide agents. 

NERVE AGENTS 

The nerve agents are a diverse group of compounds that were developed by the 

Germans prior to World War II. An agent known as GA (tabun) was the first nerve agent 

produced, followed by several others including GB (sarin), GD (soman), GF, and VX. 

Each of these agents has different physical characteristics, of which volatility is the most 

critical. The G agents are more volatile than VX; as a result, the G agents form a vapor 

more readily. 

These agents are classified as organophosphates and induce toxicity by binding to and 

inhibiting various forms of the acetylcholine esterase enzyme. This causes increased 

levels of acetylcholine, leading to hyperstimulation of both central and peripheral 

muscarinic and nicotinic receptors. The stimulation of these receptors causes the 

clinical syndromes consistent with nerve agent toxicity. Toxicity can occur either from 

skin contact or from vapor exposure. Given their increased volatility, the G agents are 

more prone to cause vapor exposure. 



1. Latent period—When nerve agent exposure occurs as a vapor, there is generally no 

significant latent period and symptoms will develop within minutes. Likewise, the clinical

effects of vapor exposure do not tend to progress over time. In contrast, liquid 

contamination may have a significant latent period depending on the amount of skin 

exposure. With small exposures, latent periods of up to 18 hours may be seen. Further, 

with liquid contact, symptoms and signs may progress over a period of time. 

2. Clinical syndromes—The findings that will develop following nerve agent poisoning 

depend on the amount and type of exposure. As the degree of exposure increases, so 

does the severity of symptoms. The general clinical syndromes of nerve agent toxicity 

are as follows: 

a. Central nervous system—The effects on the central nervous system may range 

from mild to severe depending on the degree of exposure. Mild symptoms and signs 

include mood swings, difficulty concentrating, poor judgment, and sleep disturbances. 

With more significant exposures, coma, convulsions, and apnea may occur. 

b. Peripheral nicotinic stimulation—The symptoms and signs of peripheral nicotinic 

receptor stimulation are manifest primarily as alterations in skeletal muscle functioning. 

The degree of involvement depends on the degree of exposure. Initially muscle 

fasciculations or weakness will occur and may eventually progress to paralysis. 

c. Peripheral muscarinic stimulation—The symptoms and signs of peripheral 

muscarinic receptor stimulation are manifest primarily as increased exocrine gland and 

smooth muscle activity. Typical symptoms and signs of exocrine gland stimulation 

include rhinorrhea, salivation, sweating, increased gastrointestinal secretions, and 

increased pulmonary secretions. Increased pulmonary secretions may be severe 

enough to compromise the patient's airway. Increased smooth muscle activity will cause 

vomiting, diarrhea, increased urination, and abdominal pain. 


Acetylcholine esterase exists in various tissues within the body. Two important 

subpopulations of acetylcholine esterase are the plasma cholinesterase and the 

erythrocyte cholinesterase. Decreased activity within either population may indicate 

nerve agent exposure. Of the two forms, the erythrocyte cholinesterase is the more 

sensitive indicator of exposure. 

Treatment 


The treatment of nerve agent toxicity involves the use of 3 primary medications. The 

first, atropine, is an anticholinergic medication used to counteract the hyperstimulation 

of peripheral muscarinic receptors. Atropine (1-2 mg intravenously; if no effect, double 

dose every 5 minutes until secretions dry) should generally be given until secretions 

begin to dry. Atropine will not prevent central nervous system or nicotinic toxicity. In 

contrast, pralidoxime chloride (2-PAM), 1-2 g intravenously given over 15-30 minutes, 

ameliorates nicotinic toxicity by breaking the bond formed between the nerve agent and 

the esterase enzyme. The nerve agent-esterase bond may be broken as long as the 

compound has not aged, a process by which the bond becomes irreversible. For most 

of the nerve agents, the aging process is not clinically significant. One notable exception 

is GD (soman), which ages after only 2 minutes and is refractory to 2-PAM therapy.

Finally, a common complication of severe intoxication is seizure activity. Seizures may 

be treated with benzodiazepines. 


Patients may require intensive medical support such as airway management and 

ventilatory support. Frequent suctioning of secretions may also be required. 


For more specific information on decontamination, see Chemical Decontamination, 

below. 

PULMONARY AGENTS 

Many different chemicals can be classified as pulmonary or lung agents. All have a 

similar mechanism of toxicity, producing delayed onset of pulmonary edema. Of these 

agents, carbonyl chloride (phosgene) has been the most studied. Because phosgene is 

the prototypical lung agent, most of the discussion here relates to phosgene; however, 

the principles of management can be applied to all lung agents. As a military agent, 

phosgene was first used during World War I and today can be found in numerous 

industrial applications. Because of its high volatility, phosgene forms a gas readily, often 

with the faint scent of freshly cut hay. It is not absorbed through the skin, but when 

inhaled, it causes toxicity. After inhalation, phosgene is deposited in the peripheral 

airways, where it undergoes acetylation reactions. Subsequent damage to the 

alveolar-capillary membrane will occur, resulting in pulmonary edema. Phosgene may 

also interact with mucous membranes, causing local irritation. 



As noted previously, the primary effect of phosgene involves lung toxicity, although with 

some exposures, patients may have transient irritation to the eyes, nose, and mouth. In 

some cases, rhinorrhea and oral secretions may be significant. Patients may also 

complain of mild chest discomfort and cough secondary to bronchial irritation. In 

significant exposures, early death may occur secondary to laryngeal spasm. Despite 

these early effects, most of the toxicity of phosgene exposure is delayed. After 

inhalation, a variable latent period of up to 24 hours will ensue. The length of the latent 

period depends on the dose of phosgene delivered and will be shorter with higher 

exposures. Eventually the patient may develop symptoms and signs consistent with 

pulmonary edema, including dyspnea, hypoxia, chest pain, and cough. In some cases, 

pulmonary edema may be severe enough to cause hypotension. The degree to which 

each patient is affected depends on the severity of exposure. In severe exposures, 

death may occur. 


No clinical test exists for the diagnosis of phosgene exposure. Appropriate studies such 

as arterial blood gas measurements and chest x-ray should be used to manage 

pulmonary edema. Hemoconcentration secondary to pulmonary edema may also be 

evident.

Treatment 

A. Bed Rest 

Any activity, even walking, may increase the severity of pulmonary edema. As a result, 

discourage patients from any physical activity. 

B. Upper Respiratory Symptoms 

In some cases, upper airway secretions may be significant. Nasal, oral, or bronchial 

secretions should be suctioned, if needed. If bronchospasm develops, it may be treated 

with intravenous steroids and inhaled bronchodilators. Treat secondary bacterial 

infections with appropriate antibiotics. 

C. Lower Airway Symptoms 

If pulmonary edema develops, it should be managed with standard medical 

interventions including supplemental oxygen, intubation, and ventilator management. 

Positive end-expiratory pressure is a useful ventilator adjunct. Treat secondary bacterial 

infection with antibiotics. 

D. Hypotension 

Secondary hypotension may develop in the event of severe pulmonary edema. 

Treatment of hypotension is problematic, given the increased permeability of the 

alveolar-capillary membrane. Supplemental crystalloid or colloid solutions can be used 

but may worsen pulmonary edema. Vasopressor agents such as dopamine may also be 

used. 


No specific decontamination is required except removing the patient from the phosgene 

gas. 

VESICANTS 

Vesicants are a group of related compounds known to cause skin lesions, primarily 

blisters. Despite their predilection for skin involvement, multiple systemic effects are 

also seen. Although multiple agents may be used as vesicants, sulfur mustard and 

lewisite are the most common. 

1. Sulfur Mustard 

Sulfur mustard (mustard) was first used as a chemical weapon during World War I. 

Mustard is a lipophilic compound that is readily absorbed through intact skin. It causes 

significant dermal toxicity and after systemic absorption will affect various body systems. 

Exposure can occur after contact with mustard vapor or liquid. At different ambient 

temperatures, mustard may exist in either form. It displays a characteristic odor of garlic 

or mustard, hence, its name. The exact mechanism of mustard toxicity is not known but 

appears to involve DNA alkylation. Mustard also displays mild cholinergic activity. After 

systemic absorption, cell lines undergoing active mitosis are affected the most.



The symptoms and signs of mustard toxicity depend on the dose and mechanism of 

exposure. Unfortunately, initial mustard exposure is not symptomatic, and the patient 

may be unaware of contamination. Given the initial lack of symptoms, patients may not 

decontaminate, thus increasing toxicity. Depending on the dose, the latent period after 

exposure may range from 2 to 48 hours. In mild exposures, patients may display only 

mild dermal injury; in severe exposures, death may occur within hours. The specific 

symptoms and signs of mustard toxicity depend on the body areas exposed and the 

degree of systemic absorption. As noted, the skin is typically affected and will display 

areas of erythema, burning, and blister formation. The blisters may become large and 

express a clear to straw-colored fluid. The fluid does not contain mustard agent. 

The eyes are one of the organs most sensitive to mustard exposure and may develop 

symptoms and signs first. Following ocular exposure, ocular pain, photophobia, 

conjunctivitis, and blepharospasm may occur. The superficial layers of the cornea may 

be denuded, leading to corneal clouding with visual changes. 

With injury to the respiratory tree, patients may develop oronasal burning, rhinorrhea, 

sore throat, or epistaxis. In more severe exposures, findings of cough, dyspnea, mucous 

membrane necrosis, airway muscular damage, pulmonary edema, and respiratory 

failure may be seen. Symptoms and signs of gastrointestinal exposure may result either 

from the direct toxicity of mustard exposure or from mustard's cholinergic affects. 

Nausea, vomiting, diarrhea, and constipation are common findings. 

Severe mustard exposure may also affect the central nervous system; mental status 

changes and seizure activity are the most common findings. Given mustard's 

interference with DNA activity, delayed findings of bone marrow suppression may also 

occur. 


With exposure to mustard, an early leukocytosis is typical. If bone marrow suppression 

develops, later findings of anemia, leukopenia, and thrombocytopenia may be seen. If 

wound or pulmonary secretions become more purulent, a secondary bacterial infection 

should be suspected and Gram stain and culture obtained. Gastrointestinal symptoms 

may require electrolyte monitoring. The primary metabolite of mustard agent thiodiglycol 

may be detected in the urine in contaminated patients. Such specialized testing usually 

can be conducted only at reference or military laboratories. In the event of pulmonary 

involvement, chest x-ray may demonstrate a focal or diffuse pneumonitis and 

occasionally pulmonary edema. 

Treatment 

A. Decontamination 

The most critical aspect in the treatment of mustard toxicity is removal of the chemical 

agent. This is problematic given the initial lack of symptoms. Even delayed 

decontamination, however, may lessen subsequent toxicity. Washing contaminated 

areas with either large amounts of soapy water or 0.5% hypochlorite solution is the

preferred method of decontamination. For more specific information on 

decontamination, see Chemical Decontamination, below. 

B. Specific Therapy 

With skin injuries, leave small blisters intact and unroof larger lesions. Clean unroofed 

areas frequently and cover them with antibiotic cream (Polysporin, silver sulfadiazine). 

Treat other irritated areas of skin with systemic analgesics or topical lotions. With ocular 

exposure, use topical antibiotics to prevent secondary bacterial infections. Topical 

anticholinergics may prevent the discomfort of ciliary spasm. With pulmonary 

involvement, treat associated cough with typical antitussive medications. Treat episodes 

of bronchospasm with systemic steroids and inhaled bronchodilators. Treat secondary 

bacterial infection with appropriate antibiotics. Supplemental oxygen, intubation, or 

ventilator management may be required in some patients. Typical gastrointestinal 

antispasmodics may ameliorate the symptoms of gastrointestinal exposure. Bone 

marrow transplant, growth factor utilization, or factor replacement are alternatives for the 

treatment of bone marrow suppression. 


As noted above, toxin can be removed by washing contaminated surfaces with large 

amounts of soapy water or 0.5% hypochlorite solution. For more specific information on 


2. Lewisite 

Much like sulfur mustard, exposure to lewisite causes injury to contaminated body 

surfaces and may lead to systemic symptoms. Unlike mustard, however, lewisite 

exposure causes symptoms and signs without a significant latent period. Lewisite is a 

volatile agent with the odor of geraniums. Its exact mechanism of action is unknown, but 

it is thought that the arsenic component of lewisite may inhibit various enzymes. 



As noted above, the symptoms and signs of lewisite exposure begin without a 

significant latent period. Even though findings of exposure begin early, it may take 

several hours for symptoms to fully develop. The severity of clinical findings depends on 

the degree and method of exposure. Shortly after skin exposure, an area of dead skin 

will develop that will subsequently blister. These lesions may take up to 18 hours to fully 

develop. Skin necrosis may also be evident. Symptoms and signs of ocular exposure 

are similar to those associated with mustard toxicity and include conjunctivitis, iritis, 

edema, ocular pain, and corneal injury. If pulmonary toxicity develops, findings of cough, 

dyspnea, and pulmonary edema may occur. Lewisite causes increases in vascular 

permeability that may lead to third spacing of fluid with subsequent hypotension. In 

some cases, gastrointestinal, renal, and liver involvement may be seen. 


No specific test for lewisite exposure is currently available.

Treatment 


As with mustard exposure, the cornerstone of treatment involves early decontamination. 

Compared with mustard exposure, decontamination is usually more successful with 

lewisite exposure, given the early onset of symptoms. Standard washing with soap and 

water or 0.5% hypochlorite solution is sufficient. 



hemodynamic support, and various measures to manage multisystem organ failure. 

C. Specific Therapy 

British anti-lewisite (dimercaprol), 2-3 mg/kg every 4 hours, is a compound that can be 

given intramuscularly to decrease the effects of lewisite exposure. 


As noted above, the toxin can be removed by washing contaminated surfaces with large 

amounts of soapy water or 0.5% hypochlorite solution. For more specific information on 


CYANIDE AGENTS 

Historically, cyanide was classified as a blood agent. This classification is somewhat 

inappropriate because many other chemical agents exert their effects after being 

distributed within the vascular system. Nevertheless, this classification is still used 

occasionally. Once cyanide is absorbed, it distributes rapidly throughout the body. It has 

a high affinity for trivalent iron compounds and will bond to the cytochrome a3 complex 

within the mitochondria. The cytochrome a3-cyanide bond effectively blocks aerobic 

cellular respiration, and anaerobic metabolism ensues. Cyanide exposure most often 

occurs naturally after inhalation of smoke from burning synthetic materials. In a biologic 

attack, cyanide exposure would likely follow an aerosol release. Cyanide gas is known 

to exhibit the scent of bitter almonds. 



After inhalation of cyanide gas, the cytochrome a3 enzyme is effectively blocked. 

Because cells can no longer utilize oxygen, they will convert to anaerobic metabolism, 

leading to a lactic acidosis. This inability to utilize oxygen effectively smothers the 

patient. Tachycardia, hypertension, and tachypnea will be seen initially. As symptoms 

and signs progress, anxiety, mental status changes, coma, seizures, cardiac arrest, and 

death will occur. Because cyanide does not alter oxygen-hemoglobin saturation, 

cyanosis will not develop. In fact, the inability to utilize oxygen increases the venous 

oxygen saturation, leading to a cherry red appearance to the skin. It generally takes 6-8 

minutes for death to occur following cyanide exposure. 

B. Laboratory and X-ray Findings

An elevated blood cyanide concentration confirms the diagnosis. Given the short time 

interval to death, such testing is not useful in the acute setting but may later confirm the 

diagnosis. Two rapid tests, an elevated venous blood oxygen saturation and an 

increased lactic acid level, are characteristic of cyanide poisoning. 

Treatment 


In addition to cyanide's affinity for certain iron compounds, it also has a high affinity for 

sulfhydryl groups and for the methemoglobin complex. These 2 characteristics are the 

basis of the cyanide antidote kit. The kit contains 3 components: amyl nitrite (used if no 

vascular access is available), sodium nitrite, and sodium thiosulfate. First, the patient is 

given a nitrite compound (inhalation of an amyl nitrate ampule or sodium nitrite), which 

will cause the formation of methemoglobin. The dose of sodium nitrite is based on the 

patient's weight and hemoglobin concentration although 300 mg IV is the usual dose for 

non-anemic adults. Given the high affinity of methemoglobin for cyanide, it will 

preferentially bind the compound and help to remove it from the cytochrome a3 

complex. Second, the patient is given sodium thiosulfate, (typically 12.5 g IV for an 

adult), which interacts with cyanide, forming thiocyanate. Thiocyanate is then excreted 

in the urine. 

B. Supportive Measures 

Severe lactic acidosis may be treated with bicarbonate administration. Seizures may be 

treated with benzodiazepines. In many cases, patients require intubation and ventilator 

support. 


The only effective mode of decontamination involves removing the patient from the 

cyanide gas. 

CHEMICAL DECONTAMINATION 

Because of the risk of cross contamination to health care workers, the need for patient 

decontamination should be emphasized. All patients suspected of experiencing a 

chemical weapons attack should be decontaminated as soon as possible. Optimally, 

patient decontamination should be conducted in the field. Often this is not practical, and 

a decontamination station should be established in a secure location adjacent to the 

health care facility. All persons conducting decontamination duties should be provided 

adequate protective clothing and should receive specialized training. 

Decontamination involves physical removal of toxin and chemical deactivation of toxin. 

The physical removal of toxin is usually the most effective means of decontamination in 

the acute setting. Remove all clothing, jewelry, dressings, and splints. Wash the patient 

with copious amounts of soap and water. Avoid vigorous scrubbing because this may 

facilitate toxin absorption. 

After physical removal of toxin, any remaining toxin can be chemically deactivated. This 

may take some time and thus is considered secondary to physical removal of toxin. The

most common neutralizing solution is 0.5% hypochlorite solution, which detoxifies many 

chemical agents via oxidation reactions. Hypochlorite solution should not be used to 

decontaminate open peritoneal wounds, open chest wounds, exposed neural tissue, or 

ocular tissue. Irrigate these areas with copious amounts of normal saline. All 

contaminated materials should be bagged and sent for proper disposal. 

Lee EJ: Pharmacology and toxicology of chemical warfare agents. Ann Acad Med 

Singapore 1997;26:104. [PMID: 8830755] (Overall review of the 4 major classes of 

chemical agents.) 

Sidell FR: Management of Chemical Warfare Agent Casualties: A Handbook for 

Emergency Medical Services. HB Publishing, 1995. (Provides basic information 

regarding the treatment of chemical weapons injuries; specifically catered for 

emergency medical services personnel.) 

Reutter S: Hazards of chemical weapons release during war: new perspectives. Environ 

Health Perspect 1999;107:985. [PMID: 10585902] (General review of nerve and 

vesicant agents.) 

USAMRICD Medical Management of Chemical Casualties Handbook, 3rd ed. U.S. Army 

Medical Research Institute of Chemical Defense, 2000. (Published by the U.S. Army, 

this text is an overall handbook for the care of chemical weapons injuries.) 






INTRODUCTION

Table 3-1. Clinical findings and treatment of bacterial biologic agent infection 1 . 

Gastrointestinal (upper) Oral or esophageal 

ulcer. 

Cutaneous Pruritic papule ? ulcer 

? vesicle ? painless 

eschar. 

Septicemia (can be 

primary or secondary) 

Symptoms Syndrome 

Fever, chills, dyspnea, 

hypotension, purpura. 

Ulceroglandular Papule (inoculation site) ? pustule ? tender ulcer (yellow 

exudates, black base), painful regional lymphadenopathy. 

Glandular Same as above except without ulcer. 

Occuloglandular Painful conjunctivitis, 

lymphadenopathy, 

ulcerations on 

palpebral conjunctiva. 

Oropharyngeal Exudative 

pharyngotonsillitis, 

lymphadenopathy. 

Pneumonic Pharyngitis, 

bronchiolitis, hilar 

lymphadenopathy, 

pneumonia, pulmonary 

failure, death. 

Typhoidal Sepsis. 

Fever, chills, malaise, 

myalgias. 

Rifampin, 600 mg/d PO plus 

doxycycline, 200 mg/d PO × 6 

wk. 

Plague (Yersinia 

gram-negative ba 

Doxycycline, 100 

PO bid × 14 d or 

500 mg 

PO bid × 14 d. 

Q fever (Coxiella

Localized Wound 

Local disease: 

contamination,cellulitis, amoxicillin-clavulanate, 60 

lymphadenopathy mg/kg/d divided tid × 60 d. 

lymphangitis. Severe disease: ceftazidime, 120 

mg/kg/d divided tid plus 

trimethoprim-sulfamethoxazole, 8 

mg/kg/d divided qid × 2 w 

followed by prolonged oral 

therapy. 

Septicemic Fever, chills, malaise, 

abscesses, headache, 

pustular rash. 

1 Alternatives to th 

given here may b

Table 3-2. Levels of protection required during patient care activities. 

Required Equipment 

Universal precautions; hand washing; protective gloves; gown, mask, eye 

protection, if splash risk exists. 

Same as standard precautions, except add surgical or Hepa filter mask. 

Same as standard precautions, except add negative pressure room, strict 

isolation; Hepa filter mask required. 






TABLES 

Table 3-2. Levels of protection required during patient care activities.

Table 3-3. Specific forms of hemorrhagic fever and typical findings seen with 

each form. 

Specific Features 

Progression or frank hemorrhage 

Progression or frank hemorrhage 

Progression or frankhemorrhage 

Severe peripheral edema, hearing loss in survivors 

Hepatitis, jaundice, severe hemorrhage 

Hepatitis, jaundice, retinitis 

Hepatitis, jaundice 

Pulmonary involvement 

Hepatitis, jaundice, pulmonaryinvolvement 






TABLES 

Table 3-3. Specific forms of hemorrhagic fever and typical findings seen 

with each form.

Table 3-4. Clinical findings associated with biologic toxins. 

Latent 

Period Early Symptoms 

Botulism (Clostridium 

botulinum) 

Flaccid paralysis of Ricin (extract from castor 

bulbar musculature bean) 

(ptosis, diplopic, 

dysphagia, dysarthria, 

dysphonia, 

mydriasis). 

Fever, chills, cough, 

chest pain, dyspnea. 

Abdominal pain, 

nausea and vomiting, 

diarrhea (bloody). 

4-10 hours All forms: fever, chills, 

headache, myalgia. 

T-2 mycotoxins (produced 

from fungi) 

Gastrointestinal 


Cutaneous 

Inhalational 

Inhalation

Table 3-5. Clinical findings associated with chemical agents. 

Latent Period Late Findings 

Vapor: None 

Weakness, paralysis, vomiting, diarrhea, 

increased urination, seizures, coma, 

Liquid: Up to 18 hours apnea. 

0-24 hours Pulmonary edema, hypotension, 

laryngeal spasm. 

Sulfur mustard Ocular pain, conjunctivitis, photophobia, 

blepharospasm, erythema, burning 

blister formation, mucous membrane 

damage, cough, nausea, vomiting, 

diarrhea. 

Lewisite

4. Multicasualty Incidents & Disasters 1 - Louis James Kroot, MD, & 

Robert B. Gray, MD 

INTRODUCTION 

1 This chapter is a revision of the chapter by Charles E. Saunders, MD, FACEP, FACP, 

from the 4th edition. 

Multicasualty incidents and disasters share a common characteristic. Both situations 

suddenly and unexpectedly produce victims of sufficient number and severity that local 

emergency medical resources are overwhelmed and special organization and resources 

are required. Although exact terminology varies, the term multicasualty incident usually 

refers to an isolated, geographically focused event that produces a limited number of 

casualties managed within a community. The term disaster implies a more destructive 

event that damages the social and physical environment of a community or region. 

Management of the event requires resources and assistance from outside the 

community. 

The American College of Emergency Physicians has suggested the following 

terminology to categorize such events: 

Level 1—A localized multiple casualty emergency wherein local medical resources are 

available and adequate to provide for triage, field medical treatment, and stabilization. 

The patients will be transported to the appropriate local medical facility for further 

diagnosis and treatment. 

Level 2—A multiple casualty emergency in which the large number of casualties or lack 

of local medical care facilities are such as to require multijurisdictional (regional) medical 

mutual aid. 

Level 3—A mass casualty emergency wherein local and regional medical resource 

capabilities are exceeded or overwhelmed. Deficiencies in medical supplies and 

personnel are such as to require assistance from state or federal agencies. 

EPIDEMIOLOGY OF DISASTERS 

Specific types of disasters produce different patterns and numbers of injuries and have 

different effects on the social and physical environment. By understanding them and 

anticipating their potential effects on a community, effective mitigation and 

preparedness may be possible. 

NATURAL DISASTERS 

Natural disasters are events caused by natural forces and geographical events. With the 

exception of war, these are historically the most common types of large-scale events 

(Table 4-1).

Earthquakes 

An earthquake is the most likely large-scale event in the United States. Earthquake 

intensity is commonly measured by the Richter scale, a logarithmic scale that measures 

the intensity of seismic waves. An earthquake of 2.0 magnitude is barely felt, whereas 

an 8.0 magnitude event is greatly destructive. There have been 6 major earthquakes 

greater than 8.0 on the Richter scale in U.S. history (Figure 4-1). An earthquake of a 

given magnitude may produce varying amounts of destruction, depending on a complex 

interaction of many factors, including the type of ground underlying a structure, the 

degree of ground failure (eg, landslide, soil failures), and the construction quality of 

overlying structures. 

Injuries are most often due to structural collapse (ie, crush injuries), falling debris, fire, 

and falls. Illness also occurs as a result of disruption of existing community 

infrastructure (eg, food supply, power, sanitation, ongoing support for persons with 

chronic disease). Predictably, the patterns of injury seen among casualties include 

lacerations, contusions, fractures, head and spinal cord injuries, burns, effects of 

exposure, infection, and exacerbation of chronic medical problems. The speed of rescue 

efforts has an important bearing on the outcome (Figure 4-2). 

Tropical Cyclones (Hurricanes, Typhoons, & Tropical Cyclones) 

Tropical cyclones (hurricanes in the United States and Atlantic, typhoons in the eastern 

Pacific, tropical cyclones elsewhere) are a circulating mass of clouds, rain, and wind 

around a clear central area of extreme low-barometric pressure. They occur most 

commonly in the late summer months. 

The intensity of tropical cyclones is rated on a 5-point scale. For hurricanes approaching 

the United States, this information is available from the National Weather Service, which 

can also provide information about a storm's probable path. Damage is commonly due 

to high winds, which can exceed 150 mph, as well as torrential rain and high seas, 

which may produce flooding and soil instability (eg, landslides). 

Casualties may be caused by trauma from flying debris or structural collapse; by 

drowning; by famine related to damaged agriculture and food distribution systems; by 

disease related to loss of power, water, and sanitation; and occasionally by violence 

related to loss of public safety. Casualties may be reduced by effective early warning 

systems and evacuation efforts. 

Tornadoes & Severe Storms 

On an annual basis, tornadoes and severe thunderstorms are the most common cause 

of death due to natural disasters. In the United States, approximately 100,000 severe 

storms (eg, involving thunder, high winds, and hail) occur each year, including 1000 

tornadoes. Most commonly affected are the midwestern and southern United States, 

usually during the summer months, and during late afternoons. Only about 3-4% of all 

tornadoes produce injury, and most deaths occur in a small number of highly destructive 

events.

Casualties are related to trauma from structural collapse, flying debris, or being knocked 

to the ground or thrown. Head injuries, crush injuries, fractures, contusions, and 

lacerations are common. As with all disasters, secondary illness and injury may occur, 

although tornadoes most commonly tend to produce random, isolated groups of 

casualties wherever they touch down, rather than diffuse area-wide casualties and 

destruction to community infrastructure. Casualty mitigation through early warning and 

evacuation is hard to manage because tornadoes are difficult to predict and the time 

frame for evacuation or protective cover is brief. 

Floods 

Floods are typically seasonal and result from one of several causes: (1) excessive rains 

or snow melts that lead to rivers overflowing their banks in a floodplain area, (2) 

tsunamis (tidal waves) or hurricanes in low-lying coastal areas, (3) flash floods in flat 

areas where rainfall produces surface water that exceeds the runoff or absorptive 

capacity of the soil, or (4) failure of a dike or dam, usually due to heavy rains. 

In the United States, the number of deaths each year from floods is small and sporadic. 

Property damage can be considerable, as are secondary effects on crops, sanitation, 

and vector-borne infections. When casualties occur, they are usually due to drowning. 

By contrast, developing countries with poor watershed management and rapid growth of 

agriculture and urban development on floodplains have seen large number of casualties 

in isolated events. Casualties from secondary effects, such as famine, have 

occasionally been large (eg, in Bangladesh). Mitigation (eg, through watershed 

engineering projects and limiting development on floodplains) and early warning are the 

most effective means of reducing deaths. 

Tsunamis 

Tsunamis are tidal waves due to sudden geologic events occurring at sea, such as 

earthquakes and volcanic eruptions. A giant wave of water results that may travel from 

the epicenter at hundreds of miles per hour. The onset is often heralded by a sudden 

ebb of water that exposes the sea floor and is followed in minutes by a wall of water that 

may rise to 100 feet. Massive damage occurs to the shore and structures; casualties are 

due to drowning. Mitigation by building sea walls and locating structures on high ground 

and through early warning are the only effective means of reducing casualties. 

Volcanoes 

Volcanoes are channels of molten rock (magma) from deep in the earth that vent to the 

surface in one of several forms. They may cause eruptions of molten rock (lava) or 

spew ash and debris. Volcanoes tend to be localized to the boundaries of tectonic 

plates (eg, the Pacific Rim). Injury is most commonly due to falling debris, collapse of 

structures under the weight of ash, being buried in mudslides or lava flows, or toxic 

effects of gases (eg, carbon dioxide, hydrogen sulfide). Effects on agriculture and 

property can be extensive. In many cases, early warning, although imprecise, can allow 

evacuation and mitigate casualties.

Hogan DE, Askins DC, Osburn AE: The May 3, 1999 tornado in Oklahoma City. Ann 

Emerg Med 1999;34:225. [PMID: 104244927] (Good account of emergency room 

events during this disaster, outlining many of the problems encountered.) 

Peleg K et al: Earthquake disasters—lessons to be learned. Isr Med Assoc J 

2002;4:361. [PMID: 12040826] (A review of earthquake disasters and planning.) 

NONNATURAL DISASTERS 

Fires 

Collectively, fires produce approximately 5000 deaths and 300,000 injuries each year in 

the United States, although the number has been on a steady decline since the 1950s. 

Under the right conditions, hot gases can produce winds that collect in a rotating 

cyclone (called a fire storm). Most deaths are due to asphyxiation from carbon 

monoxide and other toxic gases and to burns. 

Transportation Accidents 

Transportation accidents are the most common incidents producing multiple casualties 

in the United States. Airplane crashes produce a high ratio of fatalities to total injuries; 

highway accidents have the opposite characteristic. Railway accidents may produce 

significant injuries if passengers are involved and also have resulted in release of 

hazardous materials. 

Transportation accidents are the prototypical geographically localized multicasualty 

events practiced in most communities' disaster drills. They are realistically apt to occur, 

and they lend themselves to management within the jurisdiction and structure of local 

emergency medical services (EMS). 

The patterns of injury are well known to most emergency workers and consist of 

fractures, contusions, lacerations, and head and thoracoabdominal blunt injury. 

Industrial Accidents 

Industrial accidents that cause large-scale disasters most commonly result in the 

release of a hazardous material. The most notorious occurred in 1984 in Bhopal, India, 

where a release of methyl isocyanate killed more than 2000 and injured up to 200,000. 

Injuries vary depending on the nature of the agent. Asphyxia, respiratory distress, skin 

and eye irritations, neurologic abnormalities, or teratogenic effects may occur. 

Radiation & Nuclear Accidents 

Aside from the atomic explosions in Japan in World War II, few deaths have resulted 

from nuclear disasters, although several significant incidents have occurred. The most 

deadly was the 1986 Chernobyl reactor explosion in the former Soviet Union, in which 

27 people died and 135,000 were evacuated, many of whom were exposed to high

adiation levels. 

In nuclear accidents, injuries are due to the immediate blast effects, to exposure to toxic 

chemicals used at reactor sites (eg, sulfuric acid, chlorine, ammonia), and to radiation 

exposure. 

Structural Collapse & Explosions 

Structural failure of a building or man-made structure can be precipitated by natural 

forces (eg, earthquake) or may occur unexpectedly (eg, the Hyatt skywalk collapse in 

Kansas City, 1981; 113 dead, 200 injured). However, most such events in the United 

States have been limited in scope and have not produced many casualties. Injuries are 

predictable and consist of head injuries, fractures, lacerations, and blunt 

thoracoabdominal injuries. 

Acts of Violence 

Unfortunately, acts of violence do occur in the United States. Whereas casualties can 

be massive in armed conflicts (primarily due to explosives), in the civilian arena they are 

usually limited to a small number. Injuries are usually penetrating-type trauma. 

Acts of Terrorism 

(See Chapter 3.) Given the September 11, 2001 attack on the World Trade Center, the 

prior bombing there in the parking structure, the bombing of the Murrah Federal Building 

in Oklahoma City in 1995, the sarin gas attack in Tokyo, and the 2001 anthrax scare, it 

is obvious that acts of terrorism can strike close to home and affect a hospital's ability to 

properly care for a large influx of patients. In the World Trade Center attack and 

Oklahoma City bombing, a so-called second wave phenomenon occurred: The first 

patients arrived at the emergency department within 15 minutes of the disaster, but the 

highest flow occurred between 60 and 90 minutes. Patients transported by EMS have a 

much higher acuity and admission rate than for all other forms of transport, but in these 

cases EMS transported only about one third of the patients. The majority were 

transported by personal vehicle or other modes. 

In such disasters, some experts have prepared a two-physician emergency department 

management scenario. The first physician would be an emergency medicine physician 

who is intimately familiar with the normal daily operations of the emergency department 

and who would be responsible for the overall medical and administrative operating of 

the department. The second command physician would be responsible for the delivery 

of trauma care, including assigning priorities for surgery and supervising the trauma 

teams. This role would be best filled by a trauma surgeon. 

The 2001 anthrax scare in the United States, the confirmed use of biologic agents by 

some countries on their own citizens, and the fall of the Soviet Union and the 

subsequent disorganization of its biologic warfare programs have demonstrated that the 

threat of bioterrorism is very real. In these scenarios, the emergency department 

physician becomes a first responder. Without a high level of suspicion, a bioterrorism 

event may go unrecognized or may be dismissed as a natural epidemic until the scope

of the disaster becomes catastrophic. Establishing an effective response requires 

hospital, local, state, and federal cooperation and training. An effective response should 

include four steps: (1) detection and diagnosis, (2) declaration of need, (3) defense, and 

(4) drug therapy. 

A. Detection 

A high level of suspicion on the part of the emergency department physician can pay off. 

Emergency department physicians should consider whether they have noticed multiple 

similar patients with similar clinical syndromes; severe illness in young and otherwise 

healthy people; unusual organisms identified by the lab; unusual antibiotic resistance 

patterns; atypical presentations of diseases; reports of sick or dead animals, birds, or 

plants; and the like. 

B. Declaration of Need 

Emergency department physicians should immediately contact the house hospital 

infectious disease officer, laboratory, and local officials. They, in turn, will follow 

established protocols to notify state and federal authorities. The Federal Bureau of 

Investigations is responsible for acute crisis management, whereas the Federal 

Emergency Management Agency (FEMA) is responsible for consequence management. 

The Office of Emergency Preparedness (OEP) of the Public Health Service handles 

medical assistance. The OEP is currently training 120 Metropolitan Medical Response 

System teams. These teams would be the first to respond, along with military 

assistance, in the event of a large-scale biologic attack. 

C. Defense 

Once the biologic agent is identified, each hospital should enact appropriate precautions 

to protect its employees and patients from further contamination (eg, isolation, barrier 

protection). 

D. Drug Therapy 

The determination of the biologic agent will determine drug choice and duration of 

therapy. Uncommon antibiotics, antivirals, vaccines, and immunoglobins may be 

necessary. The Centers for Disease Control are currently coordinating a regional 

stockpile program to augment their needs. 

Brennen RJ et al: Chemical warfare agents: emergency medical and emergency public 

health issues. Ann Emerg Med 1999;34: 191. [PMID: 10424921] (Overview of the risks 

that chemical warfare agents pose to civilian populations and discussion of the 

emergency medical and public health issues related to preparedness and response.) 

Cook L: The World Trade Center attack. The paramedic response: an insider's view. Crit 

Care 2001;5:301. [PMID: 11737911] (An EMS perspective on the World Trade Center 

attack.) 

Jones J et al: Future challenges in preparing for and responding to bioterrorism events. 

Emerg Med Clin North Am 2002;20: 501. [PMID: 12120489] (A review of bioterrorism 

with an emphasis on identification and preparedness.) 

Okumura T et al: The Tokyo subway sarin attack: disaster management, Part 1:

community emergency response. Acad Emerg Med 1998;5:613. [PMID: 9660289] (A 

review of the response to the Tokyo sarin attack.) 

Richards CF et al: Emergency physicians and biological terrorism. Ann Emerg Med 

1999;34:183. [PMID: 10424920] (Overview of planning and response issues central to a 

potential bioterrorism event in light of the sarin gas attack in Tokyo, the 1993 bombing of 

the World Trade Center, and the 1995 bombing of the Murrah Federal Building in 

Oklahoma City.) 

Tamber PS, Vincent JL: The World Trade Center attack. Lessons for all aspects of 

health care. Crit Care 2001;5:299. [PMID: 11737910] (Discussion of the implications of 

the World Trade Center attack on the health care system.) 

PREHOSPITAL MANAGEMENT OF MULTICASUALTY INCIDENTS & 

DISASTERS 

Preparation for disaster is an important responsibility of any community's public safety 

agencies. A community should prepare actively for those events to which the area is 

vulnerable based on historical, geologic, demographic, transportation, and industrial 

sources. Many large cities practice an airplane crash scenario each year, despite the 

extremely low probability of such an event occurring, in part because the local airport is 

mandated by the Federal Aviation Administration to conduct such drills. On occasion 

this has paid off. However, other realistic scenarios should not be neglected. 

Organization of the Response 

A. EMS versus "Civil Defense" Management 

Most events are small level 1 events and are best managed by the local public safety or 

EMS jurisdiction as an extension of day-to-day operations under an organization or 

management system that can incorporate and coordinate outside assistance (see 

Incident Command System, below). At some point, large-scale events overwhelm local 

agencies and require the management and control to extend over a larger scale. Under 

the Civil Defense model, victims are collected and treated in supplementary casualty 

collection points or field hospitals that can stabilize them pending large-scale or distant 

evacuation. In many states (eg, California), plans exist for both such models, although 

the EMS model is most commonly employed. 

B. Incident Command System 

The response by emergency personnel to a multicasualty event can be complex when 

multiple agencies are involved, jurisdictional boundaries are crossed, or the event 

occurs in multiple geographic locations. In order to devise a system to better coordinate 

events of varying size and complexity, federal, state, and local fire services joined 

together in 1982 in the FIRESCOPE project to devise the Incident Command System 

(ICS). The ICS is a management system that allows incidents of varying size and 

complexity to be managed effectively, regardless of the diversity of agencies and 

resources involved. 

The ICS has several functional components coordinated within an organizational 

framework (Figure 4-3). At the apex is the incident commander, who directs the

Operations, Planning, Logistics, and Finance sections. Within the Operations section 

are various functional divisions, branches, and groups that carry out the emergency 

response work. Various functional components or autonomous teams of individuals can 

maintain their group autonomy and fit into the organizational tree as a unit. 

In complex incidents that have limited emergency medical needs, the EMS component 

may simply occupy a small division or group in the overall ICS structure. By contrast, a 

large, purely medical event may lead to the medical commander occupying the incident 

commander role. 

C. Medical Management 

The organization of medical resources in response to a disaster depends on the nature 

and level of the event. The easiest to illustrate is the geographically focused level 1 

event. An on-scene medical commander who designates functional responsibilities to 

individuals or teams directs the medical response: triage, treatment, transport, 

communications, logistics, staging, and so on. The medical commander may, in fact, be 

a branch of division commander within a larger ICS structure or may be the event 

incident commander if the event is purely medical. 

In typical smaller-scale day-to-day incidents, the first-in ambulance remains out of 

service for the duration of the event and one paramedic assumes the role of medical 

commander while the other begins triage or treatment responsibilities. As additional 

ambulances arrive, their crews report to the medical commander, who assigns them 

roles or duties. Each crew then treats and transports patients in order of relative severity 

of injuries (as directed by a transport or loading officer). 

If physicians or nurses are available, they are best used in treatment roles, because 

their expertise in assessing and treating patients may be considerable, whereas their 

experience in working with other agencies in a command role in a fast-moving 

prehospital environment is usually limited. 

A large-scale diffuse event, such as a major earthquake, is more difficult to manage. 

There may be no central focus of casualties. Instead, victims may be scattered or 

clustered over a large area, their existence made known by many hundreds of individual 

telephone requests (eg, via 9-1-1), provided that telephone services remain intact. This 

presents a coordinating problem if a limited number of ambulances are available or 

radio communications with ambulances are interrupted. Such loss of communications 

and central coordination capability may require decentralized management: ambulance 

resources disperse to individual neighborhoods to organize casualty collection and 

treatment at that level (eg, at each fire station). 

Scene Organization 

Geographic factors play an important role in disaster response. In remote areas, 

aeromedical services may be instrumental; at sea, rescue vessels are needed; in urban 

areas, crowd and traffic control may be important. If a hazard is present, the area must 

be isolated and emergency vehicles positioned safely upwind. Figure 4-4 shows a 

typical ground schematic for a geographically focused multicasualty event.

Patients are most efficiently extricated and categorized (see Triage, below) if they are 

channeled to a single triage location and from there assigned to one of several 

treatment areas, depending on their level of treatment priority. From that point, patients 

depart the treatment areas through a single exit point. This arrangement ensures that 

the patients with the highest relative priority go first, no one is overlooked, and the total 

number of victims and their distribution are known. 

Logistics 

Logistics is a term applied to a support activity concerned with supplying and delivering 

resources to a rescue effort. Resources may be personnel, equipment, supplies, food 

and water, crew relief facilities, and the like. In the first few minutes of the EMS 

response to a typical multicasualty event, the first-in paramedic (or the medical 

commander) provides an initial report by radio to the dispatch or communications 

center, relaying information such as type of incident, estimated number of victims and 

severity of injuries, presence of any hazard, number and type of additional resources 

needed, additional agencies requested (eg, police, fire), and recommended staging 

location of incoming vehicles. As soon as possible, and if personnel are available, a 

logistics officer or team is designated by the medical commander. 

Communications 

Experience with modern multicasualty event management has shown communications 

to be the weak link in many incidents. Multiple jurisdictions and agencies may lack 

radios equipped with a common radio frequency, centralized radio relay equipment may 

be damaged, telephone services may be disabled, or simple frequency congestion may 

occur owing to heavy use. Lately, cellular telephones have added greatly to the ability to 

communicate from the field during disasters. In large-scale events, amateur radio 

operators have provided assistance. This is a particularly useful resource in remote 

areas. 

In typical events, on-scene EMS units should designate a radio frequency for 

communications with the central dispatch center to coordinate patient distribution and 

requests for additional resources. When disparate ambulance companies are involved 

that do not usually share a common frequency, they can still communicate with a central 

coordinating center if the federally designated UHF Med Channels (10 frequencies set 

aside for communications between ambulances and receiving hospitals) are temporarily 

used for this purpose. 

Normal base hospital telemetry for on-line medical direction may need to be temporarily 

suspended owing to heavy traffic. Paramedics should then act on predesignated 

standing orders. 

Triage 

A. General Considerations 

Triage is a process of sorting patients and classifying them by categories in terms of 

relative urgency. It ensures that those who need treatment sooner receive it and that 

limited resources are not wasted on victims for whom care can be delayed with little

chance of harm. Although triage systems are used in most busy emergency 

departments and are usually familiar to emergency workers, those used in disasters 

have an important difference: patients whose injuries are so severe that their survival is 

unlikely are given a low triage priority. This situation can be difficult for many emergency 

workers to accept, but it is important because diversion of precious limited resources to 

moribund victims makes them unavailable to others who could be saved. The objective 

in disaster triage is to categorize patients in a way that will do the most good for the 

largest number and to ensure that limited resources are efficiently utilized. 

B. Triage Categories 

The most effective triage systems are simple and require no complex scoring 

methodology. A 4-level system is commonly used in the United States: 

1. Immediate (I)—Patients have life-threatening injuries that probably are survivable 

with immediate treatment. Examples are tension pneumothorax, respiratory distress, 

major internal hemorrhage, and airway injuries. 

2. Delayed (II)—Patients require definitive treatment, but no immediate threat to life 

exists. Patients can wait for treatment without jeopardy. Examples include minor 

extremity fractures, laceration with hemorrhage controlled, and burns over less than 

25% of body surface area. 

3. Minimal (III)—Patients have minimal injuries, are ambulatory, and can self-treat or 

seek alternative medical attention independently. Examples include minor lacerations, 

contusions, and abrasions. 

4. Expectant (0)—Patients have lethal injuries and will die despite treatment. Examples 

include devastating head injuries, major third-degree burns over most of the body, and 

destruction of vital organs. 

C. Assessment Methods 

The method for rapidly assessing patients and deriving triage categories is based on 

evaluations that can be made quickly, easily, and by individuals with limited medical 

training. One such system employed in California is termed START (simple triage and 

rapid treatment; see Figure 4-5). Whatever system is used, the person with the greatest 

amount of experience, medical knowledge, and good judgment should be assigned the 

role of assigning triage categories. 

D. Triage Tags 

Detailed patient assessment information cannot practically be recorded in the field 

during a disaster, yet the need to communicate medical information about the patient to 

subsequent rescue workers still exists. Therefore, triage tags that are simple and visual 

have been devised that can be attached to the patient (Figure 4-6). 

Treatment 

In a disaster or multicasualty event, personnel and equipment may be in short supply. 

Hence, initially, treatment is limited to austere medical care, that is, only essential and 

urgently necessary treatments, such as endotracheal intubation, pressure dressings,

and intravenous lines for volume or essential drug administration. Prophylactic 

intravenous lines, for example, are omitted. Simplified triage using the ability to follow 

commands, as in the Glasgow Coma Scale, has been shown to have excellent 

predictive power in identifying patients who require urgent trauma care. The military has 

adopted the concept of "minimal acceptable care," but this has never been adopted by 

civilian hospitals. Indeed, surgeons of the International Committee of the Red Cross 

have used this approach in handling civilian casualties of military conflicts wherein 70% 

of the patients survived for as long as a week without definitive medical care. 

Generally, a casualty collection point is designated in a convenient, safe, and sheltered 

location near the disaster site. The area is subdivided into sections for each triage 

category (ie, immediate, delayed, minimal, expectant), identifiable by colored tarps, 

tapes and cones, tents, or the like. The areas should have controlled access and egress 

points to prevent violation of the triage and loading priority organization. Arriving EMS 

personnel and ancillary health care workers should be assigned by the medical 

commander to each area as needed. Victims, once directed to a treatment area by the 

triage officer, should be reassessed and treated according to need and the limitations of 

austere medical care. At any point, if a victim's condition changes, the victim may be 

moved to another area. 

Victims in the expectant category are segregated and made comfortable. The dead are 

often not immediately extricated from the disaster site but are left for the medical 

examiner to remove at the conclusion of the event, unless public health reasons or 

security considerations require them to be moved to a temporary morgue. 

Transport & Distribution of Patients 

Ambulances or other transport vehicles (eg, bus or van) are directed to a specified 

loading location at a controlled egress point near the treatment areas. A transport officer 

(sometimes called loading officer) continually surveys the number of victims in each 

area and, when ambulances arrive, assigns victims for transport in order of relative 

priority based on the urgency of their condition. Generally, a typical ambulance can 

transport more than one victim (eg, one immediate plus one or two delayed victims) 

depending on the stretcher and seating capacity of the ambulance and the level of 

attention required by the victims en route. 

The distribution of victims to area hospitals differs significantly during a disaster 

compared with normal operations. Normally, destination may be determined by protocol 

factors, such as nature of problem, proximity to a given facility, or patient preference. 

Multicasualty events require victims to be distributed to area hospitals on a rotation 

protocol or according to each facility's capability to receive victims. This prevents the 

closest hospital from being inundated with large numbers of victims while more distant 

facilities remain idle. 

Distribution can be accomplished by centrally coordinating destination assignments 

through the central dispatcher (if communications remain intact) or through the transport 

officer, who maintains a log of each departing ambulance's destination. The advantage 

of central coordination is that individual hospital capacity information can be solicited by 

dispatch personnel more easily than by on-scene rescue workers. If feedback

information is unavailable, a simple rotation protocol may be used. 

Public Safety 

Public safety involves protecting the public from hazards at the scene and allowing the 

rescue effort to unfold unimpeded by interference from the crowd. Most urban 

multicasualty events managed by EMS underutilize public safety personnel (ie, police 

and firefighters). Although firefighters have a prominent role when a hazard is present 

(eg, fire, explosion, collapse), an event that is predominantly medical presents a less 

clear role for them unless they are used to providing EMS care or to participating 

actively in the medical response. 

Most commonly, non-EMS firefighters may be employed for hazard suppression, victim 

extrication and movement, and to the extent their training allows, initial triage. They 

should set up an inviolate perimeter barrier around the hazard area; position equipment 

and personnel in a safe, upwind position; and observe scene organization. 

Similarly, police should enforce secure boundaries established by firefighters and EMS 

and maintain the crowd at a safe distance. Their assistance with traffic control and 

street closure may be necessary for the efficient ingress and egress of emergency 

vehicles. 

Media Involvement 

In some states, the press may have statutory right of access to a disaster site and 

cannot be denied access unless they interfere with ongoing rescue efforts, even if they 

jeopardize their own safety in the process (eg, California Penal Code, Section 409). The 

objectives of rescue workers and members of the press may sometimes seem at odds 

and lead to conflict during a disaster. However, it is usually in the broadest public 

interest to communicate timely, accurate information to the press. 

As a general rule, the following points are worth observing: 

1. Allow the press access to the disaster site, but advise them about areas and activities 

that are dangerous to them or that may interfere with ongoing rescue efforts or victims' 

treatment. 

2. Actively provide the press with information that is as timely and as accurate as 

possible, and do so frequently. Appointing a press liaison or public relations officer is 

helpful. 

3. Important information almost always involves the nature of the incident, number of 

victims, relative seriousness of injuries (eg, number of deaths), and location where the 

victims were taken. A source of information (eg, telephone hotline) for relatives of 

victims to call is an important public service. 

4. Do not speculate about facts that are not known to you. 

Air Medical Resources

Many communities and rural areas have access to air medical resources both for 

transport and for delivery of personnel and supplies. In remote areas, this may be the 

only form of disaster assistance. EMS helicopters may be utilized by designating a 

helicopter landing zone in a safe location upwind from the event. It should be distant 

enough that rotor noise and debris do not interfere with rescue activities, and it should 

be free of obstacles to landing and departing. In general, a relatively flat field (minimum 

of 100 feet square) with an unobstructed approach and departure path (into the wind) is 

ideal. An aircraft staging officer should be appointed who can coordinate arriving 

helicopters on a mutual radio frequency. 

However, not all disasters are amenable to air medical assistance, and at times, 

helicopters can be a nuisance. During the Loma Prieta earthquake in 1989, many 

structures in the San Francisco marina area were thought to be unstable and 

susceptible to collapse from helicopter rotor vibrations. As a result, access to the 

overlying airspace was restricted. 

Local Accessory Resources 

BR>Accessory resources may be needed in certain circumstances. For example, 

structural collapse may require heavy equipment such as bulldozers provided and 

operated by the city's department of public works; utility loss or live power wires may 

require the assistance of the local power company. The ICS is a useful organizational 

structure for managing these resources. 

Mutual Aid 

Mutual aid refers to assistance provided by local EMS and public safety agencies from 

neighboring counties or towns. It is intended to provide mutual back-up resources for 

common events that temporarily overwhelm local capabilities. Ideally, prearranged 

operating agreements are helpful, as is the installation of a common radio frequency for 

mutual communications. Requests for mutual aid are usually made rapidly at the 

dispatch center, although in some cases they may require authorization from a local 

authority, especially if an obligation for reimbursement occurs. 

Special Considerations 

A. Hazardous Materials 

An incident involving a hazardous material (hazmat) requires specialty management 

because a threat to the rescue workers exists that may create additional casualties from 

among the rescuers or because contamination may spread to other areas in the 

community. 

1. Priorities—The priorities in hazmat management are as follows: 

• Identify, isolate, and contain the hazard to prevent spread of the contamination. 

• Decontaminate victims. 

• Protect rescue workers and EMS personnel, who should not approach or receive

victims unless they are properly decontaminated, or the rescuers have appropriate 

protective gear, or the contamination is "contained" in a protective wrap around the 

victim. 

• Provide advance warning to receiving hospitals so that appropriate protective 

measures may be taken. 

2. Special training and equipment—Hazmat incidents are best managed by a 

specially trained team of rescue workers who wear special protective clothing and, when 

necessary, a respirator or self-contained breathing apparatus (Table 4-2). The 

appropriate training can be obtained from a variety of sources, for example, the 

200-hour course provided by FEMA's National Fire Academy. Hazmat team individuals 

are familiar with methods of identifying hazardous substances, the nature of the 

substances and their effects, methods of hazard scene management, methods of 

hazard suppression, methods of decontamination, and operation of protective gear. 

3. Specialty scene organization—The hazmat scene differs from the typical 

multicasualty event scene in that the immediate hazard area (the hot zone) is isolated 

from entry by unprotected non-hazmat personnel (Figure 4-7). Hazmat team members 

in protective gear enter the hot zone and extricate the victims to an intermediate zone or 

area where victim decontamination occurs, performed by hazmat team members also in 

protective gear. Hazmat team members should use triage principles to identify victims 

with the most immediate medical problems and the heaviest amounts of contamination. 

Decontamination often can be accomplished by removing the victim's clothing and 

dowsing the victim with copious quantities of water or another irrigant solution, taking 

care to prevent hypothermia and contain the effluent. Once decontaminated, victims are 

then transferred to awaiting EMS personnel, who perform triage and treatment as in a 

traditional multicasualty event. 

Occasionally, victims with critical injuries require immediate lifesaving treatment before 

they can be decontaminated. As a result, it is helpful to include individuals in the hazmat 

team who have medical training (eg, paramedics), who are capable of performing triage 

of victims as they are extricated, and who can perform limited lifesaving care before or 

during decontamination efforts. If decontamination is impossible, then the contamination 

should be contained in an occlusive wrap and the patient transferred to EMS personnel 

with adequate notification of the remaining contamination hazard. 

B. Diffusely Distributed Victims 

Multicasualty events or disasters that produce victims dispersed over a large geographic 

area, rather than a localized event, pose a special challenge. The method of response 

differs in approach and method of coordination and depends on the extent to which 

central command, coordination, and communications remain functional. 

1. The dispatch center is intact and operational—If radio and telephone 

communications are functioning (eg, in a moderate earthquake or natural disaster), the 

number of incoming 9-1-1 calls may be markedly increased with patients distributed 

diffusely throughout the area. Steps in managing such an event are as follows: 

a. Obtain and deploy additional ambulance resources through reserve units, back-up

arrangement, mutual aid, and the like. 

b. Increase capacity for tracking deployed units by assigning additional dispatchers, 

reassigning radio frequencies, and the like. It may be necessary to suspend telemetry 

transmission to decongest the airwaves and free the dispatchers from nonessential 

duties. 

c. Priority-rank incoming calls and notify callers of anticipated delays. It may be 

necessary to temporarily suspend response to routine service requests. 

2. The dispatch center or other elements of command and communications have 

been rendered ineffective—In this case, there is no effective means of tracking 

resources, tracking incoming calls, or dispatching ambulances, and again, a large 

number of victims are diffusely distributed in the area. This may occur with a major 

natural disaster and is the most difficult situation to manage. Steps in managing such an 

event are as follows: 

a. With loss of communications (or by declaration), centralized dispatch ceases and 

ambulances should disperse to predesignated station assignments in each 

neighborhood or area (eg, fire stations, hospitals, schools) that are natural locations for 

victims to self-report or around which neighborhood-level rescue efforts would be 

centered. Preestablished cache supplies at these sites should be utilized. 

b. EMS ambulance crews should assist the local neighborhoods in organizing casualty 

collection, triage, and treatment areas to the extent possible. It may not be practical for 

EMS crews to transport victims if they are the sole resource in a neighborhood with 

many casualties. Instead, they should concentrate on casualty collection and triage; use 

nonmedical transport, such as vans and buses, if available; and summon additional aid. 

c. The numbers of casualties at each location and need for additional resources should 

be communicated by handheld radio or by runner to a central command post for the 

area. 

d. Efforts to reestablish radio communications should proceed immediately. 

e. Additional resources should be allocated to each area as they become available, and 

idle resources should be relocated. 

f. Outside aid should be requested, and victim evacuation from casualty collection points 

should proceed if needed. 

Disaster Organizations & Assistance 

In addition to local mutual aid from neighboring communities, several other sources of 

disaster assistance are available. 

A. Military Assistance to Safety and Traffic (MAST) 

This program provides assistance from nearby military bases having a military medical

mission in the form of aeromedical resources and medical support personnel in remote 

or rural areas. MAST can be requested directly by local public safety agencies. Usually, 

the response, which may consist of one or more aeromedical helicopter units, ranges 

from 30 to 90 minutes and consists of direct patient care and transport. 

B. National Disaster Medical System (NDMS) 

FEMA and the Department of Defense established the NDMS in 1984 as a cooperative 

program involving the Veteran's Administration hospital system and civilian hospitals. Its 

role is to provide for the distribution and care of large numbers of casualties from a 

major disaster or armed conflict in the United States. The principal component of the 

system is the network of civilian and Veteran's Administration hospitals spread 

throughout the United States that have pledged to provide a designated number of beds 

for disaster victims. The military would coordinate the collection, triage, and distribution 

of victims from the disaster site to these hospitals, using military airlift resources. 

A second important component involves the on-scene management of casualties with 

disaster medical assistance teams, which consist of volunteer health care and rescue 

workers who are willing to be deployed to a disaster area within the United States and 

serve a medical clearing and staging function or serve as part of a mobile Army surgical 

unit. 

The NDMS system can be activated by request from a governor in the event of a major 

disaster, with presidential approval, or by order of the secretary of defense during a 

military conflict. 

C. Other Military Resources 

Other agencies, such as the National Guard, and local military bases may be available 

to respond with personnel, equipment, and medical resources upon request from local, 

regional, or state officials. 

D. Disaster Relief Organizations 

Various organizations, such as the American National or International Red Cross, 

Goodwill Industries, the Salvation Army, and various religious groups, are private or 

nonprofit organizations that provide assistance in the form of shelter, food, clothing, and 

services to victims of disasters. Internationally, the World Health Organization (WHO), 

while not directly participating in on-site disaster management, provides technical advice 

and assists with resources and finance. The United Nations Disaster Relief Office acts 

as a direct coordinator for disaster relief. Other assistance may be provided by 

organizations such as the Organization of American States and the regional arm of 

WHO, the Pan American Health Organization. 

E. Volunteerism 

Volunteerism by both health care and lay individuals is common during a disaster. 

However well-intentioned, volunteerism sometimes has drawbacks. Many volunteers 

are not familiar with local policies, laws, equipment, or practices; the expertise and 

certification of volunteers is difficult for rescue workers to verify; and volunteers may 

place an additional burden on the local system by their own need for food, water, and 

medical assistance if they are injured during rescue activities. Volunteers who have 

traveled to foreign countries to lend assistance during disasters have occasionally found

themselves without many basic necessities, including food, shelter, and transportation 

home. Emergency health care workers who contemplate lending such assistance 

should consider these factors. 

Asaeda G: The day the START triage system came to a stop: observations from the 

World Trade Center disaster. Acad Emerg Med 2002;9:255. [PMID: 11874794] (A case 

report of the World Trade Center attack.) 

Auf der Heide E: Disaster planning, part 2. Disaster problems, issues, and challenges 

identified in the research literature. Emerg Med Clin North Am 1996;14:453. [PMID: 

8635419] (A review of disaster challenges and planning principles and resources.) 

Bissell RA et al: Health care personnel in disaster response. Reversible roles or 

territorial imperatives? Emerg Med Clin North Am 1996;14:267. [PMID: 8635408] (A 

review of disaster medical response and the roles of health care providers.) 

Coupland RM: Epidemiological approach to surgical management of the casualties of 

war. Br Med J 1994;308:1693. [PMID: 8025468] (Classic article in dealing with large 

numbers of wounded.) 

Dormes B et al: Ethics and triage. Prehospital Disaster Medicine 2001;16:53. [PMID: 

11367943] (A review of the ethics involved in mass casualty triage.) 

Kennedy K et al: Triage: techniques and applications in decisionmaking. Ann Emerg 

Med 1996;28:136. [PMID: 8759576] (A review of the triage process.) 

Levitin HW et al: Hazardous materials. Disaster medical planning and response. Emerg 

Med Clin North Am 1996;14:327. [PMID: 8635411] (A comprehensive review of hazmat 

procedures and planning.) 

Maningas PA et al: The EMS response to the Oklahoma City bombing. Prehospital 

Disaster Med 1997;12:80. [PMID: 10187007] (A descriptive study of the EMS response 

to the Oklahoma City bombing.) 

Moles TM: Emergency medical services systems and hazmat major incidents. 

Resuscitation 1999;42:103. [PMID: 10617329] (A review of hazmat major incidents.) 

Roth PB et al: The federal response plan and disaster medical assistance teams in 

domestic disasters. Emerg Med Clin North Am 1996;14:371. [PMID: 8635413] (A review 

of national disaster response plans and resources.) 

Yeskey KS et al: Operational medicine in disasters. Emerg Med Clin North Am 

1996;14:429. [PMID: 8635417] (A review of medical support in military operations.) 

EMERGENCY DEPARTMENT DISASTER MANAGEMENT 

The term disaster may have a slightly different meaning to a hospital than to the 

prehospital community. Although a community multicasualty incident may overwhelm 

local EMS resources and require the activation of a community disaster plan, much of

the response and resource requirement may relate to public safety needs, victim 

rescue, or hazard suppression, with relatively few casualties requiring hospitalization. In 

addition, the distribution of victims among several area hospitals may lessen the impact 

on a single institution, as will the existence of special destination criteria (eg, burns, 

trauma, pediatrics). However, internal problems at a hospital, such as utility failure, 

minor fires, and broken sewer lines, may require the evacuation of the hospital or shut 

down critical services (eg, x-ray, laboratory), causing bottlenecks or patient-flow 

problems. Even unexpected staffing problems coupled with a higher-than-normal 

emergency department census can be a minor "disaster" within a facility from time to 

time. 

As a result, hospitals should have well-tested plans, worked out in advance, to provide 

special organization and management during such times. 

Planning & Drilling 

Community disasters large enough to require activation of a hospital's disaster plan are 

rare. Therefore, it is usually only through disaster drills that health care workers can gain 

experience with in-hospital disaster management. This is usually a committee or task 

force effort, and it should prominently involve input from emergency physicians and 

nurses in the hospital as well as from representatives of administration, plant services, 

security, and the like. The Joint Commission on Accreditation of Healthcare 

Organizations mandates that member hospitals have a disaster plan and conduct 

regular drills. 

Disaster plans may be classified quantitatively in terms of the number of victims 

expected (eg, level 1, up to 20 victims; level 2, 20-50; level 3, over 50) or qualitatively in 

terms of the type of incident (eg, external trauma, radiation, fire, utility failure). 

Mobilization of Disaster Resources 

A. Personnel 

Additional personnel resources, such as doctors, nurses, orderlies, and registration 

clerks, should be quickly mobilized and sent to the emergency department where 

incoming patients may soon arrive. Special support areas, such as radiology, the blood 

bank, clinical laboratories, operating and recovery rooms, and central supply, may also 

need additional staff. 

B. Supplies 

Disaster cache medical supplies, registration packets, stretchers, blood products, and 

the like should be delivered immediately to the emergency department. 

C. Space 

The emergency department should be surveyed quickly, and patients with 

non-life-threatening complaints should be moved to another area to open up treatment 

rooms for incoming victims. The operating and recovery rooms should be placed on 

standby and elective cases postponed. The intensive care units should review existing 

patients to identify those who can be moved to the wards. Opening a separate clinic 

area for minor complaints may be helpful.

Triage for Incoming Victims 

An experienced physician or nurse should perform triage for arriving casualties at the 

door and direct them to resuscitation (or operating) areas, treatment rooms, or waiting 

areas, using principles similar to those outlined earlier (ie, immediate, delayed, minimal, 

expectant levels). Use of the triage tags applied by field paramedics is important, not 

only to learn about the victim's prehospital course but also to add information until a 

chart can be established. 

Provision of Treatment 

After emergency lifesaving treatment, such as airway control, has been provided, the 

emphasis is on providing definitive treatment rapidly for those who need it immediately 

and are likely to survive as a result. (Do the most good for the most people.) Unlike in 

the field, care need not be austere, but priority ranking is important and minor 

treatments may be delayed. Surgical resuscitation may be best handled in the operating 

room, because it tends to tie up personnel, space, and equipment in the emergency 

department. 

Command & Communications Organization 

It is important to establish early an administrative command center capable of 

communicating with each of the departments, coordinating logistics, and assessing 

resource and capacity needs. A link to the local EMS dispatch center is crucial to 

provide capacity information that will help the dispatchers equitably distribute patients to 

area hospitals. 

Security Provisions 

Enforcement of designated areas in the hospital and limitation of foot traffic by security 

personnel minimizes the stress and disorder accompanying any multicasualty event and 

makes the entire effort more effective. 

Media Relations 

A press area should be set aside and a media liaison and hospital spokesperson 

designated to keep the public informed of events. Accurate victim counts as well as 

names of victims are of intense interest to concerned relatives. 

Plant Services 

An assessment of the structural integrity of the facility is critical in a damaging natural 

disaster. Problems should be communicated to the local ambulance dispatch center so 

that additional victims may be diverted elsewhere. 

Specialty Management of Hazardous Materials & Radiation 

Variations in the basic plan are required for different types of incidents and disasters. An

important variation occurs when a hazardous or radioactive substance is involved. 

Although sizable casualties of this type are rare in the United States, they may occur, 

particularly along transportation routes. 

A. Notify Team 

Once it is known that there are incoming contaminated victims, the hospital's radiation 

safety or hazmat team should be notified immediately (if one exists). Immediate 

information about the nature of the agent (if its identity is known), its effects, and 

precautions can often be obtained from the local fire department hazmat team or from a 

regional poison center. 

B. Designate Restricted Areas 

Restricted areas in the emergency department should be designated and demarcated 

by a strictly enforced hazard boundary line (hot zone). The area should include an 

intake pathway from the ambulance loading bay up to a separate decontamination area. 

It should also include one or more treatment or resuscitation rooms in the event that 

immediate resuscitation is needed before adequate decontamination is possible. 

Equipment, air intake vents, and floors should be covered with paper or plastic 

depending on the nature of the contaminant. 

C. Apply Protective Clothing 

Emergency personnel who will be involved in the evaluation and treatment of the victims 

should wear protective gear. Usually, a special hazmat suit, respirator, and 

self-contained breathing apparatus are not necessary. A surgical gown, scrubs, face 

shield, gloves, and shoe and head covering are usually adequate (the shoe covering 

should be removed when leaving the restricted area to prevent tracking of 

contamination to other areas). 

D. Decontaminate the Victim 

The patient should receive a triage examination away from the emergency department 

treatment area. Unless already decontaminated in the field, the victim should be dowsed 

with water or other appropriate decontamination solution and, if necessary, scrubbed 

with soap and water (do not abrade the skin; pay attention to hair and nails) before entry 

into the treatment area. Rarely, if lifesaving care cannot be delayed for decontamination, 

then the victim should be contained in a plastic wrap and treated by individuals 

protected as described above until stabilized sufficiently for decontamination. Care 

should be taken to avoid washing cutaneous contamination into an open wound, where 

systemic absorption will be more rapid. All clothing, dressings, and tissue specimens 

should be collected. 

E. Monitor Contamination 

In the case of ionizing radiation, a monitoring device should be used to assess 

contamination levels of the victim and of exposed areas within the emergency 

department. 

F. Treat 

Treatment varies considerably depending on the agent involved. In some cases, specific 

treatments are required, such as atropine for organophosphate toxicity and sodium 

nitrite for cyanide toxicity. In most cases, however, treatment consists of providing

airway and circulatory support and removing the offending agent. 

G. Clean Up 

The isolated area in the emergency department should be decontaminated thoroughly 

before access is granted. Depending on the agent involved, clean-up efforts should be 

directed by the hospital hazmat expert or radiation physicist. 

Burgess JL et al: Emergency department hazardous materials protocol for contaminated 

patients. Ann Emerg Med 1999;34:205. [PMID: 10424922] (A review of hazmat 

protocols.) 

Frykberg ER: Medical management of disasters and mass casualties from terrorist 

bombings: How can we cope? J Trauma 2002;53:201. [PMID: 12169923] (A review of 

the challenge, history, patterns of injury, triage, planning, and management of 

mass-casualty bombings.) 

Hirshburg A, Holcomb JB, Mattox KL: Hospital trauma care in multiple-casualty 

incidents: a critical view. Ann Emerg Med 2001;37:647. [PMID: 11385336] (Review of 

key issues relating to trauma care during multicasualty incidents including possible 

redefinition of the standard of care during these events. Also discusses computer 

simulations and tabletop war-game-type training exercises versus mass-casualty drills 

to prepare for these disasters.) 

Lewis CP et al: Disaster planning, part 1. Overview of hospital and emergency 

department planning for internal and external disasters. Emerg Med Clin North Am 

1996;14:439. [PMID: 8635418] (A review of disaster planning.) 

STRESS MANAGEMENT & PSYCHOLOGICAL SUPPORT 

Multicasualty incidents and disasters are not only stressful and fatiguing to emergency 

workers, but they may also produce extreme psychological reactions to witnessed 

trauma. These reactions may be immediate or delayed, and may be manifested as 

anxiety, fatigue, depression, guilt, sleep disorders, and nightmares. Emergency workers 

who are used to working with life-and-death situations sometimes appear outwardly 

calm and unaffected, owing to defense mechanisms, denial, and peer effects. 

In addition to an operational debriefing or so-called post-mortem event analysis, a 

critical incident stress team consisting of a psychologist or psychiatrist and others 

outside of the organization should perform a mandatory psychological debriefing. In this 

session, individuals should be encouraged to express their feelings and emotions 

related to the event and to realize that such feelings are normal, that the individuals are 

not alone in feeling them, and that support is available if needed. 

Katz CL et al: Research on psychiatric outcomes and interventions subsequent to 

disasters: a review of the literature. Psychiatry Res 2002;110:201. [PMID: 12127471] (A 

review of the literature on postdisaster psychiatric outcomes.) 

Oster NS et al: Psychiatric emergencies. Critical incident stress and challenges for the 

emergency workplace. Emerg Med Clin North Am 2000;18:339. [PMID: 10767889] (A

eview of critical incident stress debriefing.) 





Gray, MD 

INTRODUCTION

Table 4-1. Sudden natural disasters causing 10,000 or more deaths, 

1949-1985. 1 

Approximate 

Event 

Death Toll 

Floods 57,000 

Floods 40,000 

Earthquake 12,000 


Tropical cyclone 22,000 





Earthquake/avalanche 70,000 

Tropical cyclone 250,000-500,000 

Tropical cyclone 10,000-25,000 

Earthquake 225,000-650,000 






Volcanic eruption 22,000

Table 4-2. Hazard exposure protective equipment. 1 

Description 

Work uniform, safety shoes, hard hat, gloves, eye 

protection 

Add chemical-resistant suit, respirator 

Add self-contained breathing apparatus (SCBA) 

Total encapsulation with SCBA

Figure 4-1. Epicenters of significant earthquakes in the United States, 1970. 

(Reproduced from: Centers for Disease Control: The Public Health Consequences of 

Disasters. United States Department of Health and Human Services Public Health 

Service, Centers for Disease Control, 1989.) 





Gray, MD 

FIGURES 

Figure 4-1

Figure 4-2. Survival rates versus rescue time for victims trapped in the Tangshan 

earthquake, 1976. (Adapted from Smith GS: Research issues in the epidemiology of 

injuries following earthquakes. In: International Workshop on Earthquake Injury 

Epidemiology from Mitigation and Response. Johns Hopkins University, 1989.) 





Gray, MD 

FIGURES 

Figure 4-2

Figure 4-3. The Incident Command System (ICS) organizational diagram. 





Gray, MD 

FIGURES 

Figure 4-3

Figure 4-4. Scene diagram of a localized multicasualty incident. 





Gray, MD 

FIGURES 

Figure 4-4

Figure 4-5. START triage algorithm. 





Gray, MD 

FIGURES 

Figure 4-5

Figure 4-6. Example of triage tag, front and back. (Shown, with permission, from the 

Journal of Civil Defense.) 





Gray, MD 

FIGURES 

Figure 4-6

Figure 4-7. Hazmat scene organization diagram. 





Gray, MD 

FIGURES 

Figure 4-7

5. Legal Aspects of Emergency Care - Charles A. Eckerline, Jr, MD, 

FACEP, & Steven D. Rothert, MD, JD 

INTRODUCTION 

Medical malpractice lawsuits and medicolegal issues are a major concern for physicians 

and health care institutions. Most physicians expect to become involved in some 

manner in litigation alleging physician negligence. The physician may not always be a 

target defendant. In some circumstances, physicians who have provided treatment to a 

patient suing another physician may be subpoenaed to testify in court. Physicians may 

also become involved in litigation by agreeing to present medical opinion. 

The filing of a malpractice action may generate a great deal of emotional stress for the 

defendant physician. This chapter discusses medicolegal problem areas in the 

emergency department and suggests ways in which the emergency medicine physician 

can avoid malpractice litigation. 

The true extent of the emergency department malpractice problem is unknown, partly 

because emergency departments and emergency physicians are insured by many 

different insurance companies that have not pooled their claim information, and partly 

because many claims involve events that occurred not only in the emergency 

department but also in other parts of the hospital. It is clear, however, that disputes have 

increased attention to risk management, the number of emergency department 

malpractice claims and the size of malpractice judgments are increasing, and a 

malpractice insurance crisis may be brewing. 

The net effect of malpractice suits has been to make emergency physicians, like 

physicians in general, practice so-called defensive medicine. Modern emergency 

departments provide mainly episodic care in a high-pressure environment that affords 

little time for leisurely contemplation and consultation when the diagnosis or best course 

of treatment is in doubt. In addition, prompt follow-up or consultation is often impossible 

to provide. These conditions mandate obtaining more supportive laboratory or 

radiographic studies than might be obtained otherwise. Whether physicians like it or not, 

the public demands that defensive medicine be the standard of care. 

This chapter is intended to provide the practitioner with an overview of relevant 

medicolegal aspects of emergency medicine. The outcome of a particular malpractice 

case depends on its particular facts. Furthermore, both statutory and case law may vary 

considerably in different jurisdictions. For all these reasons, this chapter is not offered 

as legal advice. 

GENERAL LEGAL PRINCIPLES 

CRIMINAL VERSUS CIVIL LAW 

There are 2 major types of law in the United States: criminal and civil. In a criminal 

lawsuit, the state or federal government sues an individual for actions considered to be

against public interest, such as theft, murder, or rape. Such suits are intended to protect 

the public by apprehending and punishing the offender in a particular case and by 

deterring others from similar harmful conduct. Punishments range from fines to 

incarceration or even death in some jurisdictions. Given the relative severity of the 

punishment, the prosecution must prove its case beyond a reasonable doubt, a heavier 

evidentiary burden than in civil cases. 

Civil cases typically involve a dispute between 2 or more persons or parties, in which 

the suing party (the plaintiff) seeks redress or compensation for an injury arising from 

the alleged wrongdoing of the defendant. Such cases may involve contract disputes, 

property disputes, or torts. A civil suit seeks to resolve the dispute and, if necessary, 

compensate the plaintiff, usually with money damages. Civil cases are concerned less 

with punishment than with compensation to the injured party. The suing party must 

prove his or her case by a preponderance of the evidence. Medical malpractice is a civil 

cause of action, a subset of tort law known as professional negligence. 

NEGLIGENCE 

Negligence, broadly defined, is the failure to do something that a reasonable person 

similarly situated would do, or doing something that a reasonable person similarly 

situated would not do. Negligence is a basic concept of tort law, and courts have long 

used it to remedy damages caused by such imprudent behavior. It is also the 

predominant (but not sole) theory of liability in medical malpractice actions. To recover 

against a negligent physician, a plaintiff-patient must prove each of these four elements: 

(1) a duty of care, (2) a breach of that duty, (3) proximate cause, and (4) damages. 

Thus, succinctly stated, negligence in the medical malpractice setting is the breach of a 

duty of care proximately causing damages. 

Duty of Care 

The duty of care is a physician's obligation to provide treatment according to an 

accepted standard of care. This obligation usually exists in the context of a 

physician-patient relationship but can extend beyond it in some circumstances. The 

physician-patient relationship clearly arises when a patient requests treatment and the 

physician agrees to provide it. However, creation of this relationship does not 

necessarily require mutual assent. An unconscious patient presenting to the emergency 

department is presumed to request care, and the physician assessing such a patient is 

bound by a duty of care. The Emergency Medical Treatment and Active Labor Act 

(EMTALA) requires emergency department physicians to assess and stabilize patients 

coming to the emergency department before transferring or discharging them. Such an 

assessment presumably creates the requisite physician-patient relationship. As 

intimated above, courts often extend this duty of care outside the immediate 

physician-patient relationship to include foreseeable third parties at risk for foreseeable 

harm. 

Breach of Duty 

When caring for a patient, a physician is obligated to provide treatment with the 

knowledge, skill, and care ordinarily used by reasonably well-qualified physicians

practicing in similar circumstances. In some jurisdictions, these similar circumstances 

include the peculiarities of the locality in which the physician practices. This locality rule 

was developed to protect the rural practitioner who was sometimes deemed to have 

less access to the amenities of urban practices or education centers. However, the 

locality rule is being replaced by a national standard of care in recognition of improved 

information exchange, ease of transportation, and the more widespread use of 

sophisticated equipment and technology. 

Establishing the standard of care in a given case requires the testimony of medical 

experts in most circumstances, unless the breach alleged is sufficiently egregious to be 

self-evident to the lay jury member—for example, amputating the wrong limb or leaving 

surgical implements in the operative field. A physician specializing in a given field will be 

held to the standard of other specialists in the same field, rather than to the standard of 

nonspecialists. 

Proximate Cause 

In order to recover in a malpractice lawsuit, the plaintiff must prove that the defendant's 

negligence more likely than not caused the injury sustained. The connection between 

the negligent act or omission and the injury must be reasonably foreseeable and 

probable in a natural course of events rather than speculative or merely possible. Courts 

have approached the concept of proximate cause in a number ways. The "but for" rule 

states that the defendant's conduct is a cause of the event if the event would not have 

occurred without it; that is, the event would not have occurred but for the defendant's 

conduct. For example, but for the physician negligently transfusing an Rh-negative 

woman with Rh-positive blood, the woman's unborn child would not have suffered 

hemolytic disease of the newborn and its complications. When it is foreseeable that 2 or 

more causes could result in the event, such as when a negligent act aggravates an 

underlying disease process, proximate cause may be found when the act in question is 

a substantial factor in bringing about the event. 

This brief discussion of proximate cause only hints at the complexity of the issue, which 

is often much easier to state than to apply. The jury is charged with the responsibility of 

determining whether proximate cause exists and, as a practical matter, will find 

proximate cause if the conduct is of such closeness and significance to the event that 

imposition of legal liability is warranted. 

Damages 

Damages are awarded as compensation for loss or injury suffered as a proximate result 

of negligent conduct. A plaintiff may recover compensatory damages for disability or 

disfigurement, pain and suffering, the expense of past and future medical treatment and 

services, lost earnings, the loss of the services of a spouse, funeral expenses, and other 

expenses. In some states, punitive damages may also be awarded if the defendant 

acted with malicious intent or with reckless disregard for the consequences of his or her 

actions, that is, with willful or wanton misconduct. The jury determines the amount of 

damages awarded. This determination is afforded great weight by reviewing courts and 

will be amended only if it is clear from the evidence that the jury was moved by 

sympathy or prejudice in reaching its decision.

STATUTE OF LIMITATIONS 

The statute of limitations is a law that specifies the time within which a lawsuit must be 

initiated. In other words, any person who feels that he or she may have a claim against 

another person must file that claim before the time period specified in the statute of 

limitations runs out. Failure to do so forever bars the claim. Despite its appearance, this 

law is not intended to shield the wrongdoer. Rather, its purpose is to promote timely 

filing of claims and thus to allow the defendant to prepare an adequate defense while 

memories are fresh, witnesses are available, and material facts are accessible. 

The length of time varies for different causes of action, but the time frame for negligence 

actions (and, hence, most medical malpractice actions) is 2 years in most states. The 

time period typically begins to run once the aggrieved person knows or reasonably 

should know that a claim exists, not simply once the offense has occurred. However, 

most limitations statutes also include a longer, maximum time measured from the 

occurrence of the offense, known as the statute of repose. Both time periods will be 

extended if the offending party fraudulently conceals the negligent conduct or 

intentionally misleads the aggrieved party. Finally, of special note, most statutes of 

limitations do not begin to run against a minor until he or she reaches the age of 

majority. The age of majority varies from 18 to 21 years of age. 

Res Ipsa Loquitur 

The plaintiff in a medical malpractice case has the burden of proving each of the 

elements of the cause of action and, in order to carry that burden, normally must 

present direct factual evidence showing that the defendant acted negligently. However, 

in those instances where the injury would not have occurred in the absence of 

negligence, such as when a patient emerges from an abdominal surgery with a shoulder 

injury, the plaintiff may invoke the doctrine of res ipsa loquitur, which translated literally 

means "the thing speaks for itself." 

Under this doctrine, which arose in response to medical professionals' notorious 

unwillingness to testify against one another, the defendant's negligence may be inferred 

from circumstantial evidence alone when direct evidence of the cause of injury is 

primarily within the knowledge or control of the defendant. To invoke this doctrine, the 

plaintiff must demonstrate that (1) the injury is of the kind that ordinarily does not occur 

in the absence of negligence, (2) the injury was caused by an agency or instrumentality 

within the exclusive control of the defendant, and (3) the patient did nothing to contribute 

to the injury. The legal effect of successfully invoking this doctrine is to create an 

inference of a breach of the standard of care, and to shift to the defendant the burden of 

proving that no breach occurred. In essence, it makes the defendant speak when he or 

she would prefer to remain silent and about things it would be extremely difficult or 

impossible for the plaintiff to discover. The burden of proof shifts to the defendant only 

with relation to the breach of the standard of care. The plaintiff still retains the burden of 

proof with relation to the other elements of the cause of action. Although this doctrine is 

typically mentioned as a way to avoid the use of expert testimony to establish 

negligence, as a practical matter expert testimony is still usually required to show that 

the injury would not have occurred in the absence of negligence.

LIABILITY FOR THE ACTS OF OTHERS (Vicarious Liability) 

Normally, a person is liable only for his or her own negligent conduct. However, 

according to the principles of vicarious liability, a physician or hospital may be liable for 

the negligent conduct of employees or agents. This doctrine was developed in the realm 

of employment, and a number of justifications for its use have been offered. The 

employer, it is deemed, has general control over the employment situation and must 

bear the responsibility for this supervisory control. The employer selects and trains his 

or her employees and should therefore pay for their negligence just as he or she profits 

from their efforts. The employer is better able to absorb losses and to distribute them to 

the public through increased prices, rates, or insurance. Essentially, these justifications 

describe a public policy to deliberately allocate risk. The losses caused by the torts of 

employees that are sure to occur in the conduct of the employer's enterprise are placed 

upon the enterprise itself, as a required cost of doing business. 

Within the employment relationship, respondeat superior (Latin for "let the master 

answer") confers legal liability on the employer for the actions of the employee. A 

hospital or a physician may therefore be found liable for the negligence of an employed 

office worker, physician's assistant, or nurse. Similarly, a medical partnership may be 

held liable for the negligent acts of one of its partners, each of whom is an agent of the 

partnership. Liability is conferred, however, only if the agent or employee committed the 

negligent act within the scope of his or her employment. An employer will not be held 

liable for the intentionally wrongful acts of employees, such as sexual assault while at 

work, because such acts are not considered to be in furtherance of the business 

enterprise. 

Traditionally, hospitals were not held liable for the negligence of physicians working in 

the hospital as independent contractors, such as physicians with admitting privileges. In 

this instance, the hospital was not deemed to have sufficient control over the actions of 

the physician to justify application of vicarious liability principles. In recent years, 

however, there has been an emerging trend to hold the hospital liable for the actions of 

independent contractor physicians who provide hospital-based services integral to the 

business enterprise of the hospital. The negligence of independent contractor 

physicians working in fields such as emergency medicine, radiology, and 

anesthesiology has been attributed to the hospitals where they work under the doctrine 

of apparent agency. Courts have reasoned that if the hospital holds itself out to the 

public as providing a given service and enters into a contractual relationship with 

physicians to provide this service, and the public looks to the hospital for this service 

without regard to the identity of the particular physician providing care, the hospital 

should be vicariously liable as an employer. 

DUTY TO PROVIDE EMERGENCY CARE 

At one time, U.S. common law did not require a physician or hospital to provide medical 

treatment to all who sought it. Thus private, and some public, hospitals could refuse 

emergency care to a patient if the treatment would result in no compensation to the 

hospital.

A series of abuses of the privilege not to provide emergency care and the transfers of 

patients to hospitals that would accept those persons unable to pay, caused mounting 

concern over the practice of so-called patient dumping. This concern resulted in 

landmark legislation that has had a huge impact on the practice of emergency medicine. 

Congress enacted EMTALA as part of the Consolidated Omnibus Reconciliation Act of 

1985 (COBRA). EMTALA applies to emergency care provided to all patients presenting 

to hospitals that have a Medicare contract and receive third-party payment from 

Medicare or Medicaid. EMTALA requires that anyone presenting to an emergency 

department requesting an examination be provided with an appropriate medical 

screening exam, sufficient to determine whether an emergency medical condition exists. 

This includes the use of appropriate ancillary services. 

If no emergency medical condition is found, the duty to patients under EMTALA ends, 

although any alleged failure to provide appropriate care could still result in a malpractice 

claim. If an emergency medical condition is discovered, EMTALA requires stabilizing 

treatment for any emergency medical condition or labor. EMTALA restricts the transfer 

of patients with emergency medical conditions or women in active labor until the 

condition has been stabilized unless the benefits of transfer outweigh the risks. 

A receiving hospital may not refuse an appropriate transfer. Hospitals that receive 

inappropriate transfers are required to report suspected EMTALA violations within 72 

hours. The law provides for civil monetary penalties and revocation of a hospital's 

Medicare certification for violations. Physicians can also be subjected to fines and 

termination from the Medicare program. These penalties also apply to physicians who 

are on call and fail to appear within a reasonable time. In addition, civil suits may be 

filed in state or federal court, bypassing any peer review or arbitration system 

established in some states as part of tort reform. 

EMTALA began as well-intentioned effort to address the problem of patient dumping. It 

has expanded far beyond its original intent to apply to inpatients, psychiatric patients, 

and even patients who have not yet arrived in the emergency department. This has 

placed an additional burden on emergency physicians as well as hospitals that transfer 

or receive transferred patients. 

Hospitals have an interest in educating their medical staffs about EMTALA. Emergency 

physicians are often most knowledgeable about these issues and are looked to for 

leadership. The responsibilities of emergency care are so important that any hospital 

that does not have a qualified emergency physician on duty might find itself unable to 

discharge its full legal duty to the public under the law. 

GOOD SAMARITAN LAWS 

Good Samaritan laws are statutes enacted in each state to protect from civil liability 

health care professionals who render aid at the scene of an emergency. These statutes 

are intended to encourage assistance in emergency situations by providing an 

affirmative defense to suits arising from the event. Statutes vary somewhat in terms of 

whom they protect, ranging from physicians to all individuals. The statutes generally 

require that the person rendering aid act reasonably, in good faith, without

compensation, and without gross negligence or harmful intent. 

Good Samaritan statutes have provided protection to physicians who were not officially 

on call but who responded to an emergency department case. Several jurisdictions have 

applied Good Samaritan statutes to staff physicians called to an emergency in a hospital 

room. Good Samaritan protection does not apply to emergency medicine physicians 

seeing patients in the emergency department or to emergency medical services 

personnel in the field in the course of their employment. Good Samaritan statutes also 

do not create an affirmative duty to render aid. 

COMMON LEGAL PROBLEMS IN THE EMERGENCY DEPARTMENT 

CONSENT 

General Principles Relating to Consent 

Consent, as a legal doctrine, arose out of cases alleging battery by a physician. In these 

cases, a surgeon performing a surgery for which consent had not been obtained was 

likened to nonconsensual touching, which is the definition of the tort of battery. Thus it 

was immaterial that the patient needed the surgery, that the surgeon had performed the 

surgery well, or even that the patient would have consented if he or she had been 

asked. Infringing on the patient's right to decide what would be done with his or her body 

was the essential wrongdoing. The right to be free from nonconsensual touching is 

fundamental in U.S. civil and criminal law, in that battery is actionable in both arenas. 

These cases established that right in medical contexts as well. 

Subsequent case law has extended this doctrine from simple consent, agreeing to a 

procedure despite no discussion of risks or alternative treatments, to the modern 

concept of informed consent, which requires physicians to give patients adequate 

information about proposed treatments. 

Doctrine of Informed Consent 

Under the modern doctrine of informed consent, a physician should discuss with the 

patient the following elements: the patient's diagnosis, the nature and purpose of the 

proposed treatment, the risks and expected outcomes of the proposed treatment, 

alternative treatments and their risks, and the consequences of no treatment. 

In order to successfully sue for lack of informed consent, a plaintiff must prove that (1) 

the physician failed to obtain full and informed consent and (2) this failure proximately 

caused the injury, that is, that the patient would not have consented to the procedure 

had the material risks been disclosed. Regarding the first element, most jurisdictions 

follow a physician-oriented standard of disclosure. Under this standard, a physician is 

required to disclose what a reasonable medical practitioner of the same school in the 

same or similar circumstances would disclose. However, a number of jurisdictions, 

including New Jersey and Pennsylvania, follow a patient-oriented standard of 

disclosure. Under this standard, a physician is required to disclose the information that a 

reasonable person in the patient's situation would consider important in choosing a 

course of treatment. Reasonable people can disagree about which standard is more

appropriate. The physician-oriented standard is sometimes derided as allowing the 

medical community to specify its own scope of disclosure, which may be out of touch 

with the needs of the individual patient. By contrast, detractors of the patient-oriented 

standard point out that it is too prone to misuse by sympathetic juries in cases where 

inevitably the undisclosed, unusual complication has occurred. 

In order to prove the causation element, most jurisdictions require that the plaintiff prove 

that a reasonable person in the patient's situation would not have consented to the 

proposed treatment had adequate information been given. 

Exceptions to Consent Requirements 

Several exceptions to informed consent disclosure requirements have been consistently 

recognized throughout the United States. In medical emergencies, when the patient is 

unconscious or unable to communicate, or when there is no time to obtain informed 

consent, the physician may provide treatment under the theory of implied consent. In 

this circumstance, the law presumes that the compelling need for treatment outweighs 

the need to obtain informed consent. When a patient receives recurrent medical care 

and thus has prior knowledge of the nature of the ongoing treatment, as well as the 

material risks and alternatives, then the physician generally need not make duplicative 

disclosures in order to obtain informed consent. However, if the patient's condition or 

other circumstances change, the physician should apprise the patient of this change 

and renew the consent previously obtained. 

A patient may expressly waive the right to informed consent by stating that he or she 

does not wish to be informed about certain information pertaining to the course of 

treatment. When this occurs, the physician should inquire why the patient does not wish 

to be informed and should document these reasons in the medical record. If the patient 

knowingly and intelligently waives this right, and has reasonable justifications for doing 

so, then nondisclosure will be defensible in court. 

The final exception to consent requirements is known as the doctrine of therapeutic 

privilege. It arises in situations in which the patient is so anxious or fragile that full 

disclosure might cause serious emotional or physical harm. Circumstances justifying 

use of this doctrine are exceptionally rare, and physicians asserting this privilege must 

carefully document their decision making in the medical record. A physician's concern 

that the patient might forego recommended treatment if adequately apprised of its risks 

is not a sufficient reason to invoke this doctrine. 

Authority to Give Consent 

Informed consent obtained after adequate disclosure by the treating physician will be 

meaningful only if the patient has the authority to give consent. Under U.S. law, all 

adults are presumed to be competent to make decisions about their treatment and thus 

to have the authority to give or withhold consent. However, a physician should question 

this presumption of competence when the patient's mental capacity is altered due to 

physical or mental illness, intoxication, or diminished consciousness due to injury or 

other causes.

Competence, broadly defined, is the ability to make decisions. A competent patient is 

able to understand his or her medical condition and the proposed treatments in a 

general way and can appreciate the consequences of accepting or refusing the 

proposed treatment. If a patient lacks the requisite mental capacity to make informed 

decisions, the physician should seek consent from a qualified surrogate decision-maker. 

If the patient has previously been determined to be incompetent, he or she will likely 

have an appointed guardian with the responsibility to make medical decisions. If the 

patient has an advance directive such as a durable power of attorney or a living will, this 

document will identify the surrogate decision-maker. If no such documentation exists, 

most states have enacted statutes that identify a hierarchy of family members who can 

give or withhold consent for a patient who becomes incompetent acutely. Given the 

circumstances in most emergency departments, a physician should always involve an 

incompetent patient's closest family members in the decision-making process. Further, 

a physician should document in the medical record evidence justifying the determination 

of incompetence and his or her attempts to obtain consent from a qualified surrogate 

decision-maker. 

Intoxicated Patients 

Intoxicated patients are frequent emergency room patients and present a special risk to 

emergency room physicians. Their altered mental status may mask serious injuries that 

are too easily attributed to their intoxication, and the treating physician must exercise a 

heightened suspicion while evaluating such patients for injuries. Their intoxication may 

render them incompetent to consent to or refuse treatment, which requires that consent 

be obtained from a qualified surrogate decision-maker, as discussed above. In general, 

the emergency physician should assume that an intoxicated patient does not have the 

capacity to consent and that the patient may have a serious injury or illness, and should 

therefore perform a complete medical screening evaluation. A liberal restraint policy 

may be necessary to allow for proper evaluation. However, once the patient 

demonstrates mental competence and there is no apparent life threat, the physician has 

no legal right to detain the patient any longer, regardless of whether the patient's blood 

alcohol level is at or below the state legal limit for intoxication. 

Police Custody 

Patients who have been arrested and are on their way to jail, or persons already in jail, 

are often brought to the emergency department for treatment. Impending or actual 

incarceration does not alter their rights concerning consent for treatment. Sufficient 

consent for examination and treatment must be obtained. 

Minors 

In general, a minor does not have legal competence, and the consent of a minor's 

parent or legal guardian must be obtained before treatment can be rendered. Of course, 

several exceptions exist. In a medical emergency, consent will be implied by law. Most 

states allow an emancipated minor to consent to his or her medical care. An 

emancipated minor is a minor who is or has been married, who lives alone and is 

financially independent, or who has children of his or her own. Most states also allow 

minors to give consent for treatment of specific conditions such as pregnancy, sexually

transmitted diseases, or chemical dependency. Consent laws vary considerably from 

state to state, and emergency physicians should become familiar with their own states' 

consent laws. 

Patient Refusal to Consent 

Any competent adult patient may refuse to consent to a proposed treatment, even if that 

treatment is necessary to save the patient's life. The guiding principle being observed is 

patient autonomy: all competent patients have the right to decide what will be done with 

their bodies. 

If a patient decides to leave the emergency department without treatment and against 

medical advice, the risks of doing so should be explained and the patient should be 

asked to sign a form releasing the hospital and emergency department staff from 

liability. If the patient refuses to sign this form, this fact and the circumstances of the 

patient's departure should be documented in the medical record. 

If a patient is incompetent, he or she does not have the right to refuse treatment 

because such a patient is not deemed to have the capacity to make an informed 

decision. In this circumstance, the physician has an obligation to protect the patient, 

restrain the patient if necessary, and render appropriate care. This delicate balancing of 

patient autonomy and physician authority requires a sort of cost-benefit analysis on the 

physician's part in each case. An intoxicated patient refusing to consent to suturing of a 

small laceration might be afforded greater autonomy than a previously healthy person 

who refuses treatment of an acute myocardial infarction. Although a physician faced 

with the second scenario cannot simply override a competent patient's wishes, the 

physician should investigate more fully the patient's understanding of his or her 

condition, the proposed treatment, and the likely consequences of the decision. 

With these principles in mind, a few special cases should be noted. A psychiatric patient 

should be evaluated to determine if he or she is a threat to self or others. If so, the 

patient should be restrained for further psychiatric evaluation and therapy. However, the 

psychotic state itself does not necessarily render the patient incompetent. A psychiatric 

patient's right to refuse psychotropic medications has generally been upheld by the 

courts. The safest alternative for the emergency physician is to consult a psychiatrist to 

conduct this evaluation. 

Narcotics users who present to the emergency department in respiratory arrest and 

receive naloxone may become intensely uncomfortable due to the effects of narcotic 

reversal and acute withdrawal. They may desire to leave the emergency department to 

seek more narcotics. However, naloxone has a shorter half-life than heroin and other 

narcotics, and the patient remains at significant risk for recurrent respiratory arrest. At a 

minimum, such patients should be held in the emergency department for at least one 

half-life of naloxone. 

Emergency department personnel should use reasonable therapeutic restraint to 

evaluate and provide treatment to violent patients, because there is a correlation 

between violence and acute organic brain syndrome. If restraining such a patient places 

the staff at risk of harm, the patient should be allowed to "escape," and the police should

e notified that the patient may be a threat to self or others. Circumstances of the 

incident should be carefully documented in the medical record. 

The right of Jehovah's Witness patients to refuse receiving blood products is a 

troublesome area for physicians. Courts have generally upheld this right for competent 

adults, but a number of exceptions exist, depending on whether the state can 

demonstrate a compelling or overriding interest for authorizing the transfusion. 

Transfusions have been authorized when the patient has dependents or is pregnant, or 

when there is a reasonable doubt about the strength of the patient's convictions. Courts 

typically do not allow a Jehovah's Witness parent to refuse treatment for a minor. The 

safest course of action for a physician facing this dilemma is to contact hospital staff or 

legal counsel for guidance. 

Finally, although parents' decisions about their child's care are typically respected, they 

should not be allowed to place the child at risk of serious harm. Courts have repeatedly 

held, under the doctrine of parens patriae (the state's paternalistic interest in children), 

that a parent does not have the right to refuse life-saving treatment for a child, even on 

religious grounds. If faced with such a situation, the physician should contact hospital 

counsel and take temporary protective custody of the child based on child neglect. The 

physician may be hesitant to take custody of the child, but it should not be for fear of 

liability; the physician is protected from civil and criminal liability under child abuse and 

neglect statutes. In the past 30 years, no case has been reported in which a parent has 

successfully sued a physician for providing nonnegligent care to a child without parental 

consent. 

Consent for Blood Alcohol Samples 

Many states have enacted statutes regarding driving under the influence; these statutes 

define intoxication on the basis of blood alcohol concentration. They typically specify 

that a person arrested under the statute is deemed to have consented to blood tests for 

the purpose of determining the blood alcohol level. If the patient does not allow medical 

personnel to obtain the sample, such refusal may result in summary suspension of the 

patient's driver's license. These statutes usually provide physicians with civil liability 

protection for use of the results of these samples in legal proceedings. In some states, 

this implied consent extends only to the testing of urine and breath samples but not to 

blood samples. The provisions of these statutes vary from state to state, and emergency 

physicians should become familiar with the laws of the states in which they practice. 

PSYCHIATRIC EMERGENCIES (See also Chapter 47.) 

Patients with psychiatric disorders or altered mental status for other reasons (ie, drugs, 

alcohol, organic dysfunction) are often unable to test and evaluate external reality and 

may experience delusions, hallucinations, and personality disintegration. Such patients 

present special legal hazards with regard to the legal principles of assault and battery as 

well as false imprisonment. The key questions in deciding when and to what degree 

physical restraint can be used on a patient with mental illness is whether the patient is 

likely to cause self-harm or harm others. The emergency department staff may use 

appropriate and reasonable efforts, including the use of restraints, to protect the patient 

from self-harm and from harming others. If the staff fails to use necessary, reasonable

estraints, it risks incurring liability to innocent third parties injured by the patient and 

may incur liability to the patient if the patient causes self-harm. By contrast, 

unnecessary or excessive force may result in liability for injuries sustained by the 

patient. What constitutes excessive force depends on the circumstances of each case. 

Hospitals are required to have specific restraint policies and forms. Emergency 

department staff must be familiar with these policies and document their compliance on 

the appropriate forms. The emergency department record should contain an objective 

and thorough documentation of the patient's behavior and mental status, the physician's 

reason for restraints, and the method and duration of restraint. 

The problem may be complicated when an alert and apparently competent patient 

protests against being held in the emergency department for further assessment and 

demands to leave before his or her evaluation is complete. The emergency department 

staff may be held liable for false imprisonment if such a patient is later determined not to 

be a danger to self or others. Actions for false imprisonment may arise when a person is 

unlawfully deprived of personal liberty by another person without giving consent and is 

aware of such deprivation, and when no defense of privilege applies. Although the 

potential for liability exists in such cases, the incidence of claims is low. 

Conversely, emergency department staff may face liability for failure to hold and further 

assess a mentally unstable person if the patient is released and then causes self-harm 

or harms others. Physicians who discharged psychiatric patients who subsequently 

committed suicide have been found liable for wrongful death of these patients in 

lawsuits brought by the patients' survivors, if the juries concluded that the decisions to 

discharge their patients were made in a negligent manner. This scenario exposes the 

emergency department staff to a greater risk of litigation than the risk of false 

imprisonment. 

Maintaining the patient in the emergency department for a reasonable period of time for 

examination and evaluation by a psychiatric health professional may be the most 

prudent course of action. If a psychiatrist or other mental health professional is not 

available, the emergency department physician must decide whether to discharge the 

patient or start procedures for involuntary commitment to a psychiatric faculty. Laws 

vary greatly with regard to emergency involuntary commitments. The emergency 

department staff should be familiar with the laws in their local jurisdiction. As a general 

principle, the decision to restrain a mentally ill patient for a thorough evaluation is more 

easily defended than the decision to allow a potentially dangerous patient to be 

discharged. The key is thorough documentation. 

ABANDONMENT 

Abandonment is the unilateral termination of the physician-patient relationship by the 

physician without the patient's consent and without giving the patient sufficient 

opportunity to secure the services of another competent physician. Although much 

emergency department care is episodic in nature and does not involve follow-up 

treatment, the emergency department physician and staff still have a responsibility to 

provide appropriate discharge instructions.

Emergency department physicians may be liable for negligent disposition of the patient 

if they do not give follow-up care instructions appropriate for the patient's condition. This 

principle also requires the translation of follow-up instructions for patients who do not 

read English, if the emergency department is in an area where it would be reasonable to 

require the presence of translating personnel in the emergency department. The area of 

follow-up instructions is also one of concern to the Joint Commission on Accreditation of 

Healthcare Organizations (JCAHO). When frequently required in an emergency care 

area, a means of communications should be available in the language of the 

predominant population groups served by the emergency department. 

Follow-up Care 

Emergency departments are designed to provide episodic care for emergency 

problems. Patients discharged from the emergency department frequently require 

referral for follow-up care. Due to a shortage of primary care physicians and certain 

specialists, and frequently a lack of financial resources by emergency department 

patients, arranging appropriate follow-up care can be difficult. Generally, the emergency 

department physician should refer the discharged patient to a physician available from 

the on-call list. When follow-up becomes unavailable for whatever reason, the patient 

should be instructed to return to the emergency department. 

Instruction Sheets 

Discharge instruction sheets should be provided to every emergency department patient 

and should be signed by the patient or guardian. The instruction sheets should be as 

specific as possible and appropriate for the discharge diagnosis. The patient's 

signatures on the instruction sheet should certify that he or she has received the form 

and has been given oral instructions as indicated on the sheet. A copy of the signed 

instruction sheet should be retained in the patient's medical record. 

Telephone Consultation 

Patients may also allege abandonment or negligence via telephone consultation. An 

example is the patient who is discharged from the emergency department, experiences 

a reoccurrence of symptoms, calls the emergency department, and is told not to worry 

about it until morning. If the patient's condition worsens, or if the patient receives any 

advice subsequently deemed to be inappropriate, the emergency department staff may 

be liable for negligence and abandonment. As a general rule, although it is reasonable 

to answer basic questions, the emergency department staff should not provide 

diagnoses or treatment to patients over the telephone. 

REPORTABLE EVENTS 

All governments have statutes and administrative regulations that require reporting of 

certain events by emergency department physicians and staff. Reportable events 

include child or elder abuse, rape, gunshot and stab wounds, assaults, or other 

suspicious injuries; certain communicable disease including most sexually transmitted 

diseases, hepatitis, tuberculosis, and HIV infection; animal bites; and the receipt of 

patients who are dead on arrival. Emergency physicians and staff should know which

events are reportable and the procedure for reporting them in the area in which they 

practice, because these rules vary by state and county. 

Child Abuse 

All U.S. jurisdictions and many other countries have regulations or statutes requiring the 

reporting of actual or suspected child abuse. Some of the statutes allow the reporter to 

exercise discretion in deciding whether to report, whereas others require reporting of all 

cases under penalty of fine or imprisonment. 

Many states' reporting statutes grant immunity from civil liability (eg, immunity from 

charges of slander) to the reporting party. These immunity provisions were intended to 

make the public (including physicians and nurses) more inclined to report suspected 

child abuse cases by eliminating the fear of being sued by the parents. In some states, 

immunity for reporting and for participating in subsequent judicial proceedings is 

provided without any express qualification. Other states provide immunity for actions 

taken "in good faith" or "without malice." Generally, no immunity provision will protect 

emergency department staff members who broadcast to third parties with no official 

status or right to know that the parents are child abusers. 

In states lacking statutes granting immunity, the emergency physician and, more 

important, the child victim will be better off if suspicion of child abuse is reported to the 

appropriate agency. Failure to report a reasonably suspected case of child abuse may 

result in criminal penalties for failure to report according to state law and may also result 

in civil liability for negligence in failing to report. 

Sexual Assault 

All states have procedures for handling sexual assault investigations. Emergency 

department staff must recognize that rape is a legal conclusion and not a medical 

diagnosis. 

Protocols for management of rape victims are given in Chapter 36. 

Gunshot & Stab Wounds 

Most jurisdictions require that injuries from acts of violence, such as gunshot and stab 

wounds, or any alleged assaults be reported to the appropriate reporting agency. 

Reports of violent wounds of any sort should generally be reported to the local police. 

Communicable Diseases 

Public health laws generally require the reporting of certain communicable diseases, 

including sexually transmittal infections, HIV infection, infectious encephalitis, food 

poisoning, hepatitis, meningococcal infections, plague, bioterrorism, anthrax, and many 

others. Both documented and suspected cases should be reported. Lists of reportable 

diseases vary by locale and should be reviewed by the emergency physician. 

In general, although all medical personnel who are aware of the patient's diagnosis

(including the attending physician, nurses, and laboratory personnel) are obligated to 

report cases of communicable disease, the hospital should develop a specific 

mechanism to ensure compliance with local laws. Reporting in the United States is 

generally accomplished by means of a short written form (the Confidential Morbidity 

Reporting card). With certain virulent diseases (eg, plague, botulism, anthrax), reporting 

by telephone or e-mail may be required for obvious reasons. In most states, failure to 

report is a misdemeanor punishable by fines or brief imprisonment. The physician who 

fails to notify the health department when he or she diagnoses a reportable event faces 

a risk of license revocation or civil suit if secondary cases or other damages result from 

the failure to report. The need of the health department to know of these conditions 

transcends the absolute confidentiality of the physician-patient relationship. The 

physician should discuss with the patient the need for reporting to preserve their 

therapeutic relationship. 

Individuals other than the health department may be notified of the patient's diagnosis 

directly by the physician if there is an immediate risk to the patient's health. This 

notification may also be made by the health department. However, individuals not at 

immediate risk of contracting infection from the patient (this usually includes employers, 

fellow employees, landlords, and casual acquaintances) should not be informed of the 

patient's diagnosis by the physician. To do so could leave the physician at risk of civil 

liability for breach of confidentiality. The patient about whom such information is 

disclosed may bring a lawsuit alleging wrongful disclosure of private information. Also, 

the physician risks liability for defamation, which is defined broadly as that which tends 

to injure the plaintiff's reputation or to diminish the esteem or respect in which the 

plaintiff is held. 

Animal Bites 

Reporting laws in the United States usually require that the emergency physician and 

staff report an animal bite to the appropriate local health official within a specified 

number of hours after the bite has occurred. Such reporting is an obvious safeguard to 

protect the public from vicious animals and from the spread of animal-borne infections, 

especially rabies. 

See Chapter 30 for management of bites. 

Epilepsy 

Epilepsy and other neurologic impairments, especially those resulting in episodic loss of 

consciousness, are reportable to the agency responsible for motor vehicle licensing in 

many states. The time period after a seizure during which a patient may not drive varies 

widely among the states. It is also important to provide appropriate discharge 

instructions to patients so that they will avoid potentially dangerous activities. 

Dead on Arrival (DOA) 

All states in the United States require that receipt of a body dead on arrival at the 

emergency department be reported to the coroner or medical examiner for possible 

investigation and for assessment of the need for postmortem examination. In such

cases, the emergency physician and staff should do nothing to the corpse that would 

interfere with the gathering of evidence by the coroner or medical examiner. For 

example, the emergency department staff should not attempt to obtain blood and tissue 

for laboratory studies; all specimens in such cases should be obtained by the coroner or 

medical examiner. Similarly, the corpse should not be used to practice cardiopulmonary 

resuscitation, endotracheal intubation, or other procedures. 

THE MEDICAL RECORD 

The importance of medical records cannot be overstated. The medical record is both a 

legal document and a means of recording the cause of a patient's illness. It is subject to 

review by hospital administration, the medical staff including consulting or subsequent 

treating physicians, third-party payers, state and national accreditation agencies, 

patients, and occasionally attorneys. 

Medical records serve many purposes, including the following: 

• Recording information important to patient care now and in the future 

• Delineating level of care for billing 

• Providing medicolegal documentation to support compliance with the standard of care 

When crucial facts such as vital signs or the results of specific examinations were not 

recorded in the patient's medical records, courts and juries may conclude that they were 

not done. Although the medical record is a summary of the patient's visit rather than a 

verbatim account of everything that transpired, it behooves the emergency physician 

and staff to document carefully with specific attention to pertinent negatives and 

positives for the particular presenting complaint. Invariably, should an unfavorable 

outcome or litigation occur, the physician would wish he or she had provided better 

documentation of care. 

JCAHO requires that a medical record be established and maintained for every 

emergency department patient. The record must contain the following elements: 

• Patient identification 

• Time and means of arrival 

• Appropriate vital signs 

• Documentation of pertinent history and physical findings 

• Emergency care given prior to patient arrival 

• Diagnostic and therapeutic orders 

• Clinical observations, including the results of treatment

• Reports of procedures, tests, and results 

• Conclusions reached on completion of examination and treatment 

• Diagnostic impression 

• Final disposition 

• Patient condition on discharge or transfer 

• Documentation of discharge instructions 

Other important items include the following: 

• List of allergies 

• Current medication 

• Possibility of pregnancy, if germane 

• Tetanus immunization history, if germane 

• Name of patient's private physician 

• Documentation of prescriptions given to the patient 

• Patient's signature acknowledging receipt and understanding of discharge instructions 

• Documentation of a medical screening examination 

• Documentation of leaving against medical advice 

The information contained in the patient's medical record is confidential and should not 

be disclosed to the police, press, or other parties without the patient's written consent. 

Exceptions arise when the patient's medical record is sought by a valid subpoena or 

court order. The emergency physician can be forced to release confidential information 

by a court order requiring such release. 

Medical records of patients seen in the emergency department because of drug or 

alcohol abuse must be handled with particular attention to confidentially to avoid 

litigation for defamation. All descriptions of the patient's clinical condition must be stated 

in an objective manner. Extraneous subjective remarks betraying the physician's or 

nurse's attitudes about the patient have no place in the medical record. 

EMERGENCY PHYSICIAN & MEDICAL STAFF INTERACTION 

The practice of hospital-based emergency medicine involves constant interaction with 

many members of the medical staff as well as the hospital administration and governing 

body. The emergency physicians practice in something of a fish bowl, where his or her

clinical skills are under constant prospective and retrospective scrutiny by the entire 

medical staff. As a result, emergency physicians and other staff must work in a highly 

charged professional environment. 

A potential problem for the emergency department is created when a patient is 

instructed by a medical staff physician to go to the emergency department for treatment, 

and the physician then either fails to meet the patient and keep the appointment or fails 

to notify the emergency department staff of the patient's imminent arrival. The 

emergency physician must decide whether to exercise clinical control over the patient 

and institute diagnosis and treatment. If the patient is a nonemergency patient and 

wishes to be seen only by the private physician, there is no difficulty for the emergency 

department staff. However, when the patient's clinical problem requires immediate 

attention, the emergency physician may be sued for negligence if necessary emergency 

care is not given despite the wishes of the private physician. As a general rule, when in 

doubt, it is better to err on the side of treatment, assuming that the patient has 

consented to treatment in the first place. An effort should be made to contact the private 

physician under these circumstances, but administrative considerations should never 

interfere with appropriate patient care. 

Another difficulty for the emergency physician is dealing with medical staff physicians' 

requests that the emergency physician write admission orders for patients admitted 

through the emergency department. The responsibility for writing admission orders 

should rest with the medical staff physician to whose service the patient has been 

admitted. Having the emergency physician write admission orders as a convenience for 

the medical staff still occurs at many hospitals, but it is a policy that should be 

discouraged. It blurs the transfer-of-care responsibility, exposes the emergency 

physician to unnecessary liability, and may delay prompt examination by the admitting 

physician. 

Once a patient has been admitted through the emergency department, hospital bylaws 

usually specify how soon the patient must be seen by the admitting physician. If the 

patient's condition is serious, the patient should be seen as soon as possible after 

admission. All admitted patients should be seen within a reasonable time depending on 

their clinical condition. To ensure that this happens, the emergency physician should 

accurately convey the patient's clinical condition to the admitting physician. If uncertainty 

exists, the admitting physician should be asked to examine the patient. 

Another area of potential conflict between the hospital staff and the emergency 

physician is the area of on-call specialty consultation. EMTALA requires hospitals to 

provide a list of on-call physicians who will respond to requests from emergency 

physicians for specialty consults and follow-up care. If emergency specialty consultation 

is requested and the on-call specialist fails to respond, the emergency physician may 

transfer the patient by certifying that the benefit of transfer outweighs the risks. Care 

must be taken to document requests for on-call consultation in a timely, accurate, and 

objective manner. 

Problems such as these involving the emergency department and medical staff are of a 

delicate political nature. The emergency department and medical staff must keep lines 

of communication open so that these difficult areas can be discussed dispassionately. If

this open communication does not exist, the inevitable result is strained personal and 

professional relations, which can cause a lowered standard of patient care and create a 

climate of confusion that engenders litigation. 

EXPERT WITNESS 

Emergency medicine physicians may be asked to provide expert witness testimony in 

medical malpractice cases. Regardless of how one feels about the current legal process 

for resolving malpractice suits, fair, accurate, and impartial opinions by emergency 

physicians familiar with the standard of care are essential. Serving as an expert witness 

can be an intimidating experience. If opposing counsel is unable to rebut the opposing 

expert's opinions, they often attempt to discredit the expert. 

The American College of Emergency Physicians has issued expert witness guidelines 

for the specialty of emergency medicine (policy stated September 1995), as stated 

below: 

Expert witnesses are called on to assess the standard of care for emergency physicians 

in matters of alleged medical malpractice and peer review. Expert witnesses in the 

specialty of emergency medicine should meet the following criteria: 

• Be certified by a recognized certifying body in emergency medicine; 

• Be in the active clinical practice of emergency medicine for three years immediately 

before the date of the incident; 

• Be currently licensed in a state, territory, or area constituting legal jurisdiction of the 

United States as a doctor of medicine or osteopathic medicine; 

• Abide by the following guidelines for an expert witness: 

— The expert witness should possess current experience and ongoing knowledge in the 

area in which he or she is asked to testify. 

— The expert witness should be willing to submit the transcripts of depositions and 

testimony to peer review. 

— Pursuant to Opinion 9.07 of the Current Opinions of the American Medical 

Association's Council on Ethical and Judicial Affairs, the expert witness should not 

testify on a contingency-fee basis or offer expert witness services on a contingency-fee 

basis through an agent, representative, or other third party. 

— The expert witness should not provide expert medical testimony that is false or 

without medical foundation. The key to this process is a thorough review of available 

and appropriate medical records and literature concerning the case being examined. 

The expert's opinion after this process is completed should reflect the state of medical 

knowledge at the time of the incident. 

— The expert witness should review the medical facts in a thorough, fair, and impartial

manner and should not exclude any relevant information to create a view favoring the 

plaintiff or the defendant. 

— Expert witnesses are chosen on the basis of their experience in the area in which 

they are providing testimony and not solely on the basis of offices or positions held in 

medical specialty societies, unless such positions are material to the witness' expertise. 

Emergency physicians should not engage in advertising or solicit employment as expert 

witness where such advertising or solicitation contains representations about the 

physician's qualifications, experience, or background that are false or deceptive. 

NATIONAL PRACTITIONER DATA BANK 

The Health Care Quality Improvement Act (HCQIA) was passed by Congress in 1986 

and called for the establishment of the National Practitioner Data Bank for Advice 

Information on Physicians and Other Health Care Providers (NPDB). Its purpose is to 

collect data on medical malpractice payments. 

All medical malpractice payments must be reported to the NPDP. What effect HCQIA 

and the NPDB will have on health care and the availability of insurance is yet to be 

determined. 

HARVESTING OF ORGANS FOR TRANSPLANTATION 

Emergency physicians can be expected to be confronted with the issue of organ or 

tissue donation. Hospitals should have specific policies in place that address the issue, 

and emergency staff should be familiar with them. Most states have statutes that require 

notification of the organ donation association in the event of any death that meets 

criteria for possible organ or tissue donation. 

American College of Emergency Physicians Policy Statement: Expert Witness 

Guidelines for the Specialty of Emergency Medicine. American College of Emergency 

Physicians, 1995. 

Bitterman RA: Medicolegal and risk management. In: Marx JA et al., eds. Rosen's 

Emergency Medicine Concepts and Clinical Practice, 5th ed. Mosby, 2002. 

Freedman DL: National Practitioner Data Bank. ED Legal Letter 1999;10(8). 

Henry GL, Sullivan DJ: Emergency Medicine Risk Management, 2nd ed. American 

College of Emergency Physicians, 1997. 

Huber JR: Foresight American College of Emergency Physicians, EMTALA—New 

Developments in the Regulatory Guidelines and an Update of Recent Court Opinions. 

Issue 48, June 2000. 

Keeton WP: Prosser and Keeton on Torts, 5th ed. West, 1999. 

LeBlang TR, Basanta WE, Kane RJ: The Law of Medical Practice in Illinois, 2nd ed. 

Lawyers Cooperative Publishing, 1997.




5. Legal Aspects of Emergency Care - Charles A. Eckerline, Jr, MD, FACEP, & 

Steven D. Rothert, MD, JD


GENERAL INSTRUCTIONS FOR SKIN PREPARATION & STERILE TECHNIQUE 

Skin Preparation 

1 This chapter is a revision of the chapter by David Knighton, MD, FACS, Richard M. 

Locksley, MD, & John Mills, MD, from the 4th edition. 

There are 2 types of skin preparation: skin cleansing and skin sterilization. 

A. Skin Cleansing 

Cleansing of the skin is sufficient for routine injections (subcutaneous, intramuscular, 

intravenous) and for simple venipuncture but not for venipuncture performed to draw 

blood for culture or to permit insertion of an indwelling device. 

Skin cleansing is generally performed by swabbing the skin for a few seconds with a 

swab saturated with alcohol (70%) or organic iodine (eg, povidone-iodine or equivalent). 

To reduce the pain of venipuncture, the disinfectant should be allowed to dry on the skin 

before the skin is punctured. Note: This procedure merely cleans the skin; it does not 

sterilize it. 

B. Skin Sterilization 

Skin sterilization should be performed before all procedures that involve puncturing or 

cutting the skin, with the exception of routine venipuncture and simple injections. This 

procedure eliminates superficial skin bacterial, leaving only a few organisms deep in 

hair follicles or sweat glands. Skin sterilization may be omitted if the delay involved 

would jeopardize the patients' life (eg, thoracostomy for tension pneumothorax). 

A variety of techniques can be used to achieve skin sterilization: 

1. Scrub the skin vigorously with copious amounts of 70% alcohol for 2 minutes. Or, 

2. Using a sterile 10- × 10-cm (4- × 4-in) gauze pad, apply 2% iodine tincture to the area 

and allow the iodine to dry. Then remove it, using 70% alcohol on a sterile pad, because 

iodine may cause skin burns. Or, 

3. Apply an organic iodine disinfectant (eg, povidone-iodine or poloxamer-iodine) twice, 

allowing each application to dry. These particular disinfectants need not be removed 

before the procedure is started. 

The following guidelines should be observed in all cases: 

• Sterilize a much larger area of skin than is required for the procedure. 

• Apply the disinfectant starting at the site of the procedure and extending outward in

concentrically larger circles. 

• Use sterile gloves to apply the disinfectant. 

Sterile Technique 

It is virtually impossible to achieve sterile technique at the bedside in the emergency 

department comparable to that obtainable in an operating room; however, following the 

guidelines outlined below decreases the risk of infection. Good lighting is helpful for 

maintaining sterile technique and is essential for performing procedures successfully. 

1. Wash hands thoroughly, preferably with antiseptic soap, before performing any 

procedure. 

2. Have all necessary equipment assembled and opened at the bedside, so that once 

sterile gloves have been donned, only sterile instruments and equipment will be 

touched. Alternatively, an assistant can open packaged sterile supplies. 

3. Don sterile gloves. 

4. Sterilize the skin, as described above. 

5. Enlarge the sterile field by surrounding the sterile skin with sterile drapes made of 

cloth or paper. These may come with a window in them that is used to isolate the area 

of sterile skin selected for the procedure. 

6. Make sure that catheters, needles, stopcocks, and the like cannot roll off the drape 

onto the floor, perhaps at a critical moment. 

7. When performing complicated procedures that require stricter sterile conditions (eg, 

insertion of a catheter for total parenteral nutrition), wear a surgical cap, mask, and 

gown in addition to the sterile gloves. 

UPPER EXTREMITY VENIPUNCTURE 

Indications 

Venipuncture is performed to obtain a sample of venous blood for laboratory testing. 

Contraindications 

Contraindications to venipuncture are as follows: 

• Cellulitis over the proposed site. 

• Phlebitis. 

• Venous obstruction.

• Lymphangitis of the extremity. 

• Administration of intravenous fluid distal to the proposed site. 

Personnel Required 

One person can perform venipuncture unaided. 

Equipment & Supplies Required 

• Materials for skin cleansing (or skin sterilization, if blood culture is to be performed). 

• Syringe of adequate size (10-50 mL) for the amount of blood needed, or Vacutainer 

tubes and appropriate Vacutainer syringe hub (Vacutainer equipment consists of a 

needle with a point at each end, evacuated glass tubes with rubber stoppers, and a 

plastic barrel. Blood is forced into the evacuated tube when the needle connects the 

tube with the vein). 

• Needle (21-gauge) for the syringe, or a Vacutainer needle with an automatic valve or 

rubber cuff to stop blood flow while tubes are being changed. If a large amount of blood 

is to be drawn, it is advisable to use an 18-gauge needle. Use smaller-gauge needles or 

scalp vein needles for infants and children. 

• Tourniquet. 

• Receptacle tubes for blood for the desired laboratory tests. 

• Gauze squares, 5 × 5 cm (2 × 2 in). 

• Adhesive dressing. 

Positioning of the Patient 

The upper extremity is the site most commonly used to draw venous blood. The patient 

should be in a comfortable position, with the upper extremity resting on a solid object. If 

the patient is in bed, the supine position is best, with the arm resting on the mattress 

close to the patient's side. The ambulatory patient should be sitting with the arm on a 

table or support at a comfortable height for the operator. 

Procedure 

1. Assemble all necessary equipment, and position as described above. 

2. Apply the tourniquet above the antecubital fossa in a manner that will allow quick 

removal with one hand. The tourniquet should be tight enough to occlude venous return 

but not so tight as to cause arterial obstruction or patient discomfort. It should be 

removed before the extremity turns purple. 

3. Locate an appropriate vein. Have the patient open and close the fist of the selected

arm to help pump blood from the muscle compartment of the arm into the superficial 

venous circulation. 

a. Antecubital veins. The superficial basilic and cephalic veins course just under the skin 

on the volar side of the forearm. They run along the medial and lateral edge of the 

antecubital fossa at the elbow crease. In slender or muscular people, these veins often 

stand out and are easy to enter. If one of these veins is accessible, use it. In obese 

people, those who have had multiple venipunctures, and intravenous drug abusers, 

finding a patent antecubital vein (or any other vein) may be difficult. 

Palpate the antecubital fossa with the tip of the index finger, and feel for the buoyant 

resilience of a distended vein. Be careful to differentiate the firm cord of a thrombosed 

vein from the resiliency of a patent vessel. When the veins are not visible, they must be 

located by feel. Even a small vein deep in the subcutaneous tissue may be detected on 

the basis of its resilient feel. 

b. Arm veins. If a patient's antecubital vein cannot be found, examine the forearm on 

both the volar and the dorsal surfaces. Look for the faint bluish color of a vein under the 

skin, or better yet, feel for a vein with the tip of the index finger. 

c. Hand veins. If no vein is found on the forearm, proceed to the dorsal surface of the 

hand, and use one of the superficial veins on the hand. These veins are small, collapse 

easily, and are usually inadequate for drawing a large amount of blood. If large amounts 

of blood are needed, it is often better to go to another anatomic site such as the femoral 

vein than to persist in trying to draw large quantities of blood from a small hand vein. By 

the time an adequate amount has been obtained, it usually clots in the syringe, and 

another venipuncture then becomes necessary. 

Do not give up after one examination of the arm. Carefully palpate the arm 2 or 3 times 

if necessary. A vein suitable for venipuncture may be obscured (eg, by hair) and may 

therefore be missed on initial examination. Occasionally, slapping repeatedly over the 

vein with the pads of the first and second fingers will help to distend a faint vein, or the 

patient can dangle the arm over the side of the bed to achieve the same result. Do not 

thrust blindly at a bluish mark on the patient's arm without first palpating the area to 

confirm that a patent vein is underneath. 

4. Prepare the skin. Skin cleansing is adequate unless blood is being obtained for 

culture, in which case the skin must be sterilized (see Skin Preparation, above). 

5. Grasp the syringe or Vacutainer in the dominant hand while palpating the vein with 

the index finger of the other hand. Exert traction on the vein by pulling distally (toward 

the operator) on the skin next to the puncture site. Align the needle with the course of 

the vein, and make sure that the bevel is facing up. With a quick but smooth motion, 

push the needle through the skin at an angle of about 10-20 degrees (Figure 6-1). Then 

carefully advance the needle into the lumen of the vein with a smooth motion. 

6. When the vein has been properly penetrated, blood will flow back into the needle 

when the plunger is pulled away from the needle or when the Vacutainer tube is pushed 

onto the needle.

7. If venous blood is not obtained on the first attempt, reassess the course of the vein. 

Try palpating the vein proximal to the needle site. Withdraw the needle to just below the 

skin, and attempt a second venipuncture. 

8. Once the needle is in the lumen of the vein, withdraw the required amount of blood 

with a steady, even pull on the plunger of the syringe. If too much force is applied and 

blood flow in the vein is less than the amount being drawn into the syringe, the vein will 

collapse, occluding the lumen of the needle. If this occurs, stop and allow the vein to fill, 

and then resume at a slower pace. If a large volume of blood is required, it may be 

necessary to select another, larger vein. 

If a Vacutainer system is being used, simply fill all of the tubes required. 

9. Draw enough blood to give accurate laboratory test results; clotted or hemolyzed 

specimens will give misleading information. 

10. When enough blood has been obtained, remove the tourniquet, and then withdraw 

the needle quickly and smoothly. Have the patient immediately apply firm direct 

pressure on a 5- × 5-cm (2- × 2-in) piece of gauze over the site for 3-5 minutes. If the 

site is antecubital, flex the arm to stop the bleeding. Elevating the arm will speed 

hemostasis. 

11. Quickly fill the blood receptacle tubes with the appropriate amount of blood, and mix 

each tube thoroughly if anticoagulation or preservative is present in the tube. Label the 

tubes with the patient's name, date of birth, and date of sample, and place any 

specimens on ice as required. 

12. It is often helpful to put an adhesive dressing on the venipuncture site to absorb any 

blood that might ooze out. 

EMERGENCY ANTECUBITAL FOSSA VENOUS CUTDOWN 

Antecubital fossa cutdown provides a secure large-bore conduit for fluid resuscitation 

and central venous pressure measurement without the risks associated with placement 

of a subclavian or internal jugular vein catheter. 

Indications 

Emergency antecubital fossa cutdown is performed to gain immediate large-bore 

access to central veins for resuscitation and venous pressure measurements. 


Contraindications to emergency antecubital fossa cutdown are as follows: 

• Previous antecubital fossa cutdown at the proposed insertion site (use the other arm 

or another site).

• Trauma to the extremity proximal to the proposed cutdown site. 

• Known or suspected major vascular injury to the axillary or subclavian arterial or 

venous system on the side of the proposed cutdown. 


The operator may require an assistant to provide exposure and assist in insertion of the 

catheter. 


A. Materials 

• Materials for skin sterilization. 

• Lidocaine, 1%, with 10-mL syringe and 25-gauge needle. 


• Topical antibacterial ointment. 

• Expanded gauze roll and tape. 

• Padded armboard that fits under the mattress of the patient's gurney and extends 

(parallel to the floor) about 15 cm (6 in) beyond the patient's outstretched arm. 

• Tape to secure the patient's arm to the armboard. 

• Intravenous fluid in a container with a Y-type blood infusion set and an in-line blood 

pump. The equipment should be flushed and fully assembled, ready for use. 

B. Prepackaged Sterile Cutdown Trays 

Prepackaged sterile cutdown trays are commercially available. The following items are 

required: 

• Drapes. 

• Gauze sponges (10 × 10 cm [4 × 4 in]). 

• Silk ligatures (size 3-0) (2). 

• Nylon or polypropylene skin suture (size 4-0) on a cutting needle. 

• Needle holder. 

• No. 15 and No. 11 scalpel blades, both mounted. 

• Curved Kelly clamps (3).

• Mosquito clamps (2) (useful for small patients). 

• Tissue dissection scissors and straight suture scissors. 

• Self-retaining retractor or 2 right-angle retractors. 

• Pediatric feeding tubes, sizes 5F and 10F (1 each). (Use the largest one that fits the 

vein.) 

• Toothed and smooth forceps. 

• Plastic-coated absorbent pad to place beneath the patient's arm. 


The patient should be supine, with the arm selected for cutdown insertion extended on 

an armboard that has been wrapped in an absorbent pad. Tape the arm in place at the 

wrist. 

Anatomy Review 

The deep basilic vein is found medial to the brachial artery beneath the superficial 

fascia. Accurate identification of the basilic vein is crucial. It is usually thin-walled when 

compared to the brachial artery, and it has a bluish tinge. The median nerve is fibrous 

and relatively avascular. However, the vein may be thick-walled in an elderly person or 

an intravenous drug abuser, or the artery may carry desaturated blood, which may also 

give it a bluish tinge. 

Procedure 

1. Apply the tourniquet proximal to the antecubital fossa. 

2. Sterilize a wide area of skin around the antecubital fossa. 

3. Drape the arm. 

4. Measure the catheter (pediatric feeding tube), and cut it to the required length as 

follows: Place the hub end of the feeding tube at the antecubital fossa of the patient's 

outstretched arm, and extend the catheter to the suprasternal notch. This length 

ensures that the catheter will be long enough to reach the central venous system 

(superior vena cava) without entering the right ventricle of the heart (which can cause 

serious ventricular arrhythmias). Cut the catheter at an angle, and trim off the sharp tip 

to avoid puncturing the vein distal to the insertion site. 

5. Using the 1% lidocaine with the 10-mL syringe and 25-gauge needle, anesthetize the 

antecubital fossa over the medial aspect of the forearm at the level of the elbow crease, 

taking care not to puncture a superficial basilic vein. Omit this step if the patient is 

comatose.

6. With the No. 15 scalpel blade, make a 2.5- to 4-cm (1- to 11/2-in) traverse incision on 

the median half of the antecubital fossa at the elbow crease. The incision should be at a 

right angle to the long axis of the arm and should extend down to the subcutaneous 

tissue. It may be helpful to palpate the brachial artery as a landmark, because the 

basilic vein lies medial to it. Be careful not to lacerate any large superficial veins that lie 

just under the skin. 

7. If the patient has a large superficial basilic vein, proceed with isolation and 

cannulation, as described in steps 8-11. If no superficial vein is present, continue to 

dissect deep to isolate the basilic vein (step 8). Be sure to differentiate the vein from the 

brachial artery and the median nerve. (See Anatomy Review, above.) 

8. Using a curved Kelly clamp with the points aimed downward, dissect the 

subcutaneous tissue parallel to the long axis of the arm to isolate the basilic vein. 

Dissect the tissue on either side and then on top of the vein. Pass the clamp under the 

vein and dissect the tissue there. This maneuver should separate the vein from the 

surrounding structures and connective tissues. Small veins may be encountered in the 

subcutaneous tissue. Do not attempt to cannulate these veins. They have many valves 

and will not allow central passage of the catheter. Use the retractors to maintain 

exposure of the vein. 

9. Leave the Kelly clamp in the open position under the vein for support. Using the 

smooth forceps as a clamp, pass the 2 silk ties under the vein, one proximal and one 

distal to the intended venotomy site. Ligate or loosely tie the distal portion of the vein 

while exerting traction on the distal silk tie. Perform a venotomy with the No. 11 scalpel 

blade (Figure 6-2): Hold the scalpel parallel to the long axis of the vein with the blade in 

a horizontal position, and pass it through the midportion of the superficial (or anterior) 

wall of the vein. Then turn the cutting edge of the blade upward, and open the top of the 

vein. Be careful not to transect the vein or puncture its outer wall. 

10. Insert a closed mosquito clamp into the venotomy, and gently spread the clamp to 

dilate the vein. 

11. With the bevel up, gently insert the catheter into the vein, and advance it until the 

hub reaches the incision. Remove the mosquito clamp. 

12. Occasionally, the catheter fails to traverse the axilla and pass into the intrathoracic 

venous system. In this situation, abduct the arm, and slowly advance the catheter. This 

maneuver straightens the course of the vein and usually facilitates passage. If the 

catheter meets an obstruction at a valve, move the catheter gently backward and 

forward while rotating it, or attempt to open the valve by infusing fluid through the 

catheter. If the catheter does not pass easily into the central venous system, stop. Do 

not push so vigorously that the vein is perforated. 

The most common problem is that the catheter has not entered the basilic vein. 

Withdraw the catheter, and tie off the proximal portion of the vein. Continue dissection, 

looking for the basilic vein. Occasionally, a basilic system vein of adequate diameter is 

not present, in which case an alternative method of central venous access must be 

found.

13. Allow blood to fill the catheter, and then remove the tourniquet. Insert the 

intravenous tubing in the catheter, and start the intravenous fluid drip. Ligate the distal 

portion of the vein with the distal silk tie, and using the same tie, secure the catheter to 

the ligated distal vein. Secure the catheter in the vein with a strong tie proximal to the 

venotomy site. Make sure that the ligatures are not so tight that they occlude the 

catheter (Figure 6-3). 

14. Close the skin with a simple running skin stitch using the nylon or polypropylene skin 

suture. 

15. Secure the catheter to the skin with a stitch, and tape all connections. 

16. Dress the incision with the antibacterial ointment and a 10- × 10-cm (4- × 4-in) 

gauze sponge, and wrap the incision site with an expanded gauze roll. 

17. Obtain a chest x-ray immediately to check the position of the catheter. 

PERIPHERAL VENOUS CATHETERIZATION WITH A CATHETER-CLAD NEEDLE 

Catheter-clad needles (eg, Angiocath) are generally preferred over needle-clad 

catheters (eg, Intracath) for peripheral intravenous access because they provide the 

largest-diameter catheter lumen possible for a given size of venipuncture. Their 

flexibility gives them an advantage over rigid needles for long-term use. 

Indications 

Peripheral venous catheterization with a catheter-clad needle is performed to gain 

peripheral venous access. 


Contraindications to peripheral venous catheterization with a catheter-clad needle are 

as follows: 

• Phlebitis of the extremity. 

• Cellulitis over the projected site of insertion. 

• Potential or existing lymphedema or venous occlusive edema of the extremity. 

• Traumatic injury proximal to insertion site (eg, fracture). 


One person can insert a catheter-clad needle unaided. 

Equipment & Supplies Required



• Precut tape to secure the catheter in place. 

• Plastic-coated absorbent pad to place under the patient's arm. 

• Catheter-clad needle (eg, Angiocath) of sufficient size for the rate and type of fluid to 

be infused, but smaller than the cannulated vein. For administration of electrolyte or 

glucose solutions at rates of less than 200 mL/h, a 20-gauge catheter is usually 

sufficient. For infusion of blood or colloid solutions or rapid infusion of electrolyte 

solutions (200-1000 mL/h), an 18-gauge catheter is mandatory and a 16-gauge is 

preferred. In patients with multiple trauma, who may require large volumes of blood and 

electrolyte solutions, a 14-gauge catheter is preferable. 

• Container of fluid for intravenous administration, with proper connecting tubing. The 

equipment should be flushed and fully assembled ready for use. 


Place peripheral intravenous catheters in the upper extremity if possible. Occasionally, a 

lower extremity intravenous catheter is necessary when all veins in the upper extremity 

are inaccessible and insertion of a central venous catheter is not practical. Intravenous 

catheters in the lower extremity are associated with a much higher incidence of infection 

and thrombosis than are those inserted in the upper extremity. 

The patient should be in a comfortable supine or sitting position, with the extremity to be 

used resting on a firm surface. 

Procedure 

1. Connect the container of fluid with the tubing, fill the connecting tubing with 

intravenous fluid, and make sure that all air is flushed from the tubing. 

2. Apply the tourniquet above the antecubital fossa, and secure it so that it can be 

quickly removed with one hand. 

3. Have the patient open and close the fist to help distend the superficial veins with 

blood. If veins are difficult to identify, having the patient hang the arm below the level of 

the heart or wrapping the arm in a warm moist towel may be helpful. 

4. Select an appropriate vein. The site at which 2 veins join is an excellent choice, 

because the vein is immobilized best in such a location. Possible sites include the radial 

aspect of the forearm most proximal to the wrist ("intern's vein"), the volar aspect of the 

forearm distal to the antecubital fossa on the ulnar side, and the dorsum of the hand. In 

slender people, these veins usually distend without difficulty; however, some individuals 

have deeply buried veins that can be found only by careful palpation. Remember that a 

vein does not have to be visualized in order to be successfully catheterized. Gently

tapping over the vein may help to distend it and make identification and catheterization 

easier. If the vein lies deep in the subcutaneous tissue, make a mental picture of its 

course and branches by means of systematic palpation up and down the vein. 

5. Inspect the catheter to make sure that it slides easily off the needle and that both the 

catheter and the needle are smooth. 

6. Place the plastic-coated drape under the arm selected for insertion. 

7. Sterilize the skin around the insertion site. 

8. Either grasp the needle directly with the dominant hand or place a syringe on the 

needle and grasp the syringe. Insert the needle through the skin at an angle of about 

10-20 degrees, either on top of or next to the vein (see Figure 6-1). 

9. Pull the skin taut distal to the venipuncture site, and insert the needle and catheter 

into the vein. When the lumen of the vein is entered, blood flows back or can be 

withdrawn into the syringe. 

10. Make sure that both the needle and the catheter are in the lumen of the vein. Blood 

may flow back when only the needle is in the vein and the catheter tip is against the wall 

of the vessel and has not actually entered the vessel lumen. In this position, the catheter 

cannot be advanced over the needle into the vein. To avoid this complication, advance 

the needle and catheter into the vein about 4-6 mm (1/8-1/4 in) after blood initially 

returns. Check to be sure that blood continues to return when the needle and catheter 

are in this position. 

11. Slide the catheter off the needle (Figure 6-4). Hold the needle steady by its hub in 

one hand at an angle of 10-20 degrees to the vein while gripping the hub of the catheter 

with the other hand, and gently push the catheter forward off the needle. Advance the 

catheter up to its hub while keeping the needle firmly in place. With practice, advancing 

the catheter and withdrawing the needle can be accomplished in one smooth motion. Be 

sure not to pull out both the catheter and needle at the same time. To avoid uncontrolled 

blood loss from the open catheter, occlude the vein proximal to the end of the catheter 

by applying direct pressure before pulling the needle out of the catheter. 

12. Note: Occasionally, the catheter will encounter a valve in the vein that prevents 

complete advancement of the catheter. If this occurs, hold the catheter hub in place, 

remove the tourniquet, and connect the intravenous tubing to the catheter. Running 

intravenous fluid into the vein often opens the valve and allows complete insertion of the 

catheter. 

13. Remove the tourniquet. 

14. Attach the intravenous tubing to the catheter, and check the flow. A properly located 

catheter should allow rapid influx of fluid. If flow is slow or there is no flow at all, 

withdraw the catheter a few millimeters, and watch for change in the rate of flow. 

Occasionally, a branch vein or valve obstructs flow, and moving the catheter will be all 

that is required to achieve good flow.

15. Occasionally, the catheter is pushed through the opposite wall of the vein, causing 

swelling and pain at the insertion site as the intravenous fluid dissects the subcutaneous 

tissues. In this case, withdraw the catheter and needle completely, and try a second 

venipuncture in another vein or in the same vein proximal to the first insertion site. 

(Allow enough time for the first venipuncture to clot, or leave the catheter in place to 

occlude the venipuncture site until the more proximal catheter is inserted, and then 

withdraw the unused catheter.) 

16. Secure the catheter in place with tape as shown in Figure 6-5. Tape all connections. 

Do not apply tape completely around the arm; it can act as a tourniquet and lead to 

distal edema. It is helpful to write the catheter gauge and date of insertion on the tape. 

PERIPHERAL VENOUS CATHETERIZATION WITH A SCALP VEIN (BUTTERFLY) 

NEEDLE 

Scalp vein needles are useful for short-term intravenous infusions in adults and for both 

long- and short-term use in children. They are also useful for phlebotomy in 

uncooperative patients, especially children, because the flexible connecting tubing 

prevents dislodgment of the needle when the patient moves. 

Indications 

Indications for peripheral venous catheterization with a scalp vein needle are as follows: 

• Need to gain peripheral venous access. 

• Need to perform phlebotomy in an uncooperative patient (the needle might otherwise 

become dislodged from the vein). 


Contraindications to the use of scalp vein needles for peripheral venous catheterization 

are the same as those for catheter-clad needles. 


One person can perform venous catheterization with a scalp vein needle unaided if the 

patient is cooperative. 




• Precut tape to secure the catheter in place. 

• Plastic-coated absorbent pad to place beneath the patient's arm.

• Scalp vein needle of appropriate size. 

• Container of intravenous fluid with connecting tubing. All equipment should be flushed 

and fully assembled ready for use. 


If venipuncture in the upper extremity is planned, have the patient supine, with the arm 

extended volar side up. In infants, the veins of the scalp and the fist are also useful for 

catheterization (Figure 6-6A). 

Procedure 

1. Connect the container of intravenous fluid with the tubing, and fill the connecting 

tubing with intravenous fluid. Make sure that all air is flushed from the tubing. 

2. The short tubing connected to the scalp vein needle should be filled with fluid before 

the infusion begins. This can be accomplished either by letting the blood flow back into 

the tubing from the vein or by filling the tubing with infusion fluid before inserting the 

needle. Letting blood fill the tubing can lead to clotting if the flow of intravenous fluid is 

not established quickly. 

3. Place the plastic-coated absorbent pad under the site chosen for catheterization. 

4. If an extremity is to be catheterized, apply the tourniquet above the site. 

5. Sterilize the skin around the insertion site. 

6. Keeping the bevel of the needle facing up, grasp the plastic wings attached to the 

needle between the thumb and index finger of the dominant hand, and insert the needle 

into the vein at a 30-degree angle (Figure 6-6B). 

7. Once the needle has entered the vein (blood appears in the tubing), decrease the 

angle between the needle and the vein to 10-20 degrees. Then carefully thread the 

needle into the lumen of the vein until the entire needle is in the vein. Failure to insert 

the needle completely makes securing it more difficult. 

8. Secure the needle to the arm with tape, as shown in Figure 6-7, and tape all 

connections. 

EXTERNAL JUGULAR VEIN CATHETERIZATION 

Indications 

External jugular vein catheterization is performed to gain peripheral or central venous 

access when sites other than the external jugular vein (eg, internal jugular or subclavian 

vein) are inaccessible or if catheterization of those sites is contraindicated (eg,

coagulopathy). 


Contraindications to external jugular vein catheterization are as follows: 

• Agitated, uncooperative patient (relative contraindication). 

• Cellulitis at the insertion site. 

• Previous neck surgery (the position of the vein may be distorted, or it may have been 

ligated or removed). 


One person can perform simple external jugular vein catheterization unaided, although 

an assistant is helpful. Insertion of a central venous catheter through the external jugular 

vein by means of a J wire requires an assistant. 


A. Peripheral Venous Access 


• Catheter-clad needle (eg, Angiocath), 16- to 18-gauge. 

• Container of intravenous solution and connecting tubing. 

• Precut tape for securing the catheter. 

• Plastic-coated absorbent pad to place under the patient's head and neck. 

• Tincture of benzoin, 5 mL. 

B. Central Venous Access 


• Materials for sterile technique (cap, mask, gloves, and gown). 


• Sterile medicine cup with normal saline for flushing intravenous catheters and tubing. 

• Most adults will need a 16- to 18-gauge catheter-clad needle. Make sure the needles 

and catheters are of the proper size and construction to accept and slip over the J wire. 

• J wire (flexible angiography wire) 35.5 cm (14 in) long, about 0.089 cm (1/32 in) in 

diameter, and with a curvature that has a radius of about 3 mm (1/8 in).

• Silk skin suture (size 3-0) on a cutting needle. 


• Straight scissors. 

• Container of intravenous fluid and connecting tubing. All equipment must be flushed 

and fully assembled ready for use. 

• Gauze squares, 10 × 10 cm (4 × 4 in). 

• Plastic-coated absorbent pad to place under the patient's head and neck. 

• Sterile drapes. 

• Antibacterial ointment. 

• Tincture of benzoin, 5 mL. 


The patient should be placed in the Trendelenburg position (20-30 degrees), with the 

head turned 90 degrees away from the side of insertion. Place the plastic-coated 

absorbent pad under the patient's head and neck. 


The external jugular vein courses from behind the angle of the jaw across to the 

sternocleidomastoid muscle and superficial to it to join the subclavian vein (Figure 6-8). 

The internal jugular vein and carotid artery lie deep to the external jugular vein and are 

separated from it by the sternocleidomastoid muscle. 

Procedure 

A. Peripheral Venous Access 

1. Assemble all necessary equipment, including the container of intravenous fluid and 

tubing, and make sure the tubing has been flushed to remove all air. 

2. Position the patient. 

3. Sterilize the skin around the area of insertion from the clavicle to the ear. 

4. Have the patient take a deep breath and forcibly exhale against a closed glottis 

(Valsalva maneuver) to increase intrathoracic pressure and distend the external jugular 

vein with blood. It is sometimes helpful to have the patient put a thumb in his or her 

mouth and blow against it. If the patient is unable to cooperate, the vein may be 

distended by obstructing its outflow with a finger placed on the neck above the clavicle. 

5. Make a mental note of the position and size of the vein.

6. Have the patient resume normal breathing as soon as the size and position of the 

vein have been determined. 

7. Insert the catheter-clad needle into the vein halfway between the angle of the jaw and 

the clavicle. While the patient performs the Valsalva maneuver, apply traction cephalad 

on the vein, and insert the catheter-clad needle into the vein lumen. Withdraw the 

needle, leaving the catheter in place. (See above for technique of catheterization using 

a catheter-clad needle.) 

8. Connect the intravenous tubing to the catheter, and start the intravenous infusion. To 

avoid air embolism, make sure either that intrathoracic pressure is elevated (eg, by the 

Valsalva maneuver) or that the hub of the needle is occluded with a thumb or finger. 

9. Tape the tubing in place. When taping an intravenous line to the neck, it is helpful to 

use tincture of benzoin on both the patient's skin and the tubing. Tape the tubing up the 

side of the patient's neck and face superior to the ear, securing the line in several 

places with tape (Figure 6-9). Tape all connections. 

10. Short catheters inserted in the external jugular vein are difficult to secure because of 

the constant motion of the patient's neck. The catheter may become dislodged from the 

vein and cause infiltration of intravenous fluid into the soft tissues of the neck. Before 

administering blood or drugs through an external jugular catheter, check to see that 

there is free flow of fluid into the line, that the neck is not swollen, and that blood can 

reflux freely into the intravenous tube when the intravenous bag or bottle is lowered 

below the level of the patient. 

B. Central Venous Access 


tubing, and make sure the tubing has been flushed to remove all air. 


3. Sterilize the skin around the area of insertion from the clavicle to the ear. 

4. Drape the area, and observe sterile technique (don cap, mask, gloves, and gown). 

5. Have the patient take a deep breath and forcibly exhale against a closed glottis 

(Valsalva maneuver). 

6. Note the course of the vein, and then have the patient resume normal breathing. 

7. Select an insertion point about 4 cm (15/8 in) above the clavicle, and infiltrate the 

area with the 1% lidocaine with the 10-mL syringe and 25-gauge needle. 

8. While keeping the vein distended (by Valsalva maneuver or occlusion of outflow with 

finger compression), insert the catheter-clad needle or the needle from a needle-clad 

catheter into the external jugular vein. If a catheter-clad needle is being used, remove

the central needle at this point, and cover the end of the catheter hub with a thumb to 

prevent aspiration of air. 

9. Make sure the needle or catheter is properly placed in the vein by observing the 

return of blood through the catheter. Inject 5 mL of sterile saline, or run intravenous fluid 

through the line to establish its patency. 

10. Insert the J wire through the needle or catheter, curved end first; guide the wire 

around the bends in the course of the external jugular vein-subclavian vein junction into 

the intrathoracic portion of the subclavian vein-superior vena cava system. 

11. Secure the wire at the skin with a clamp or a finger. Do not allow the wire to slip all 

the way into the vein. If a catheter-clad needle is being used, slide the catheter over the 

wire and into position in the intrathoracic portion of the venous system. If a needle-clad 

catheter is being used, remove the insertion needle, taking care to grasp the J wire 

firmly to keep it from slipping forward all the way into the vein. Slip the catheter over the 

J wire, and be careful not to let the J wire slip all the way into the vein as the catheter is 

being advanced. 

12. Holding the catheter in place, remove the J wire, and cover the end of the catheter 

hub with a thumb until the setup can be tested for return of blood. Then start the 

intravenous infusion. 

13. Secure the catheter in place with the silk suture run first through the skin and then 

wrapped around the catheter. 

14. Take the patient out of the Trendelenburg position. 

15. Obtain a portable chest x-ray immediately to confirm placement of the catheter. 

16. Dress the insertion site with antibacterial ointment, cover it with a folded sterile 10- × 

10-cm (4- × 4-in) gauze pad, and tape the pad in place. 

17. Remember to tape all connections to prevent air embolism. 

INTERNAL JUGULAR VEIN CATHETERIZATION 

The internal jugular vein is used for insertion of central venous catheters. Pulmonary 

complications (hemothorax, pneumothorax) occur less commonly than with subclavian 

vein catheterization, but arterial injury (eg, to the carotid artery) is more common. 

Indications 

Internal jugular vein catheterization is performed to gain access to the central venous 

system for administration of fluids and measurement of central venous pressure. 

Contraindications

Contraindications to internal jugular vein catheterization are as follows: 

• Previous neck injury that might have ligated or scarred the internal jugular vein and 

thereby altered its anatomy. 

• Superior vena cava occlusion. 

• Acquired or iatrogenic bleeding disorder. 

• Cellulitis over the proposed insertion site. 


• Patient receiving cardiopulmonary resuscitation (CPR). 


The operator performing internal jugular vein catheterization requires an assistant to 

help handle sterile materials and position the patient. 


A. Materials 



• Lidocaine, 1% with 10-mL syringe and 25- and 22-gauge needles. 


• Tincture of benzoin. 

• Tape. 

• Container of intravenous fluid with all necessary tubing. All equipment should be 

flushed and fully assembled ready for use. 



required: 

• Drapes. 

• Gauze sponges, 10 × 10 cm (4 × 4 in). 

• Nylon or silk skin suture (size 3-0 or 4-0) on a cutting needle. 

• Needle holder.


• Plastic-coated absorbent pad to place beneath the patient's arm. 

• Syringe, 3-mL, with 22-gauge, 6.5-cm (21/2-in) needle (for use as a probe). 

• Central venous catheter and insertion set. Many kinds are commercially available; 

most consist of an introducing needle and radiopaque catheter, usually 30.5 cm (12 in) 

long. 


Use a bed or gurney that can be placed in the Trendelenburg position and that has a 

removable headboard. The patient should be supine, with the head turned 90 degrees 

away from the side selected for insertion. Place the patient in as steep a Trendelenburg 

position as possible in order to fully distend the internal jugular vein and also to create 

increased pressure inside the vein, thus decreasing the chances of air embolism during 

insertion. 


The internal jugular vein leaves the base of the skull and courses laterally and 

posteriorly to the carotid artery and the carotid sheath. It joins the subclavian vein at the 

thoracic outlet. The internal jugular vein runs medial to the upper portion of the 

sternocleidomastoid muscle, deep to the triangle formed by the 2 heads at the 

midportion of this muscle, and deep to its clavicular head (see Figure 6-8). 

Procedure 

A. Middle (Triangle) Approach 

(See Figure 6-10). 

1. Assemble and arrange all necessary equipment, including the container of 

intravenous fluid and intravenous tubing, and make sure the tubing has been flushed to 

remove all air. 

2. Position the patient, as described above. 

3. Observe sterile technique (don cap, mask, gown, and gloves). Sterilize the skin 

around the area of insertion from the clavicle to the ear, and drape the patient. 

4. The sternocleidomastoid muscle will be clearly outlined when the patient lifts the head 

slightly. Make a mental picture of the triangle formed by the 2 heads of the muscle, 

which has its apex pointed cephalad and its base formed by the clavicle. 

5. Palpate the carotid artery, and make a mental note of the course of the internal 

jugular vein, which runs lateral and deep to the artery.

6. Choose a point near the apex of the triangle formed by the sternocleidomastoid, and 

anesthetize the skin with the 1% lidocaine with the 10-mL syringe and 25-gauge needle. 

Change to the 22-gauge needle, and infiltrate a path through the subcutaneous tissue 

toward the internal jugular vein, directing the needle downward at an angle of 45 

degrees toward the ipsilateral nipple. Be careful when infiltrating the area to aspirate 

before injecting, so as to avoid injecting significant amounts of lidocaine into the vein. 

Omit this step if the patient is comatose. 

7. Make a probe by placing the 22-gauge, 6.5-cm (21/2-in) needle on the 3-mL syringe. 

8. Use this small-gauge needle as a probe to locate the internal jugular vein. Pierce the 

skin near the apex of the triangle formed by the sternocleidomastoid, and direct the 

needle downward at a 30- to 45- degree angle toward the ipsilateral nipple. If the right 

hand is being used to guide the syringe and needle, palpate the carotid artery with the 

left hand to make sure that the needle is moving away from it. The needle should pierce 

the vein after advancing 2.5-4 cm (1-11/2 in). If it does not, withdraw the needle until the 

point is just under the skin, reposition the needle in the subcutaneous tissue, and probe 

more medially, always keeping the left index finger on the carotid artery for reference. 

Once the needle has entered the internal jugular vein, dark venous blood should flow 

freely into the syringe. If the vein cannot be located after a few probing maneuvers, ask 

for assistance. Caution: Do not use the larger catheter insertion needle or a 

catheter-clad needle (eg, Angiocath) if the vein cannot be located with the probing 

needle. When the vein is located, withdraw the probing needle, and remove it from the 

syringe. 

9. Place the catheter insertion needle or catheter-clad needle on the syringe, and follow 

the course of the probing needle to enter the internal jugular vein. Always recheck the 

landmarks and position of the carotid artery while inserting this large needle. 

10. Maintain a slight vacuum in the attached syringe while inserting the larger needle. 

Once the needle has entered the vein, dark venous blood will flow freely into the 

syringe. While aspirating, rotate the needle 360 degrees to make sure that the bevel of 

the needle is completely within the vein; cessation of blood flow at any point indicates 

that the needle should be slowly advanced or withdrawn, because it is near one wall of 

the vein. 

11. When it is clear that the needle is properly positioned in the lumen of the vein, 

disconnect the syringe, and immediately occlude the orifice of the needle to prevent air 

embolization during inspiration. Most central venous catheters are inserted using the 

Seldinger technique. This method involves the use of a flexible guide wire or J wire that 

is placed through the lumen of the needle. The needle is then removed while allowing 

the guide wire to remain in the lumen of the vein. A No. 11 scalpel blade is then used to 

make a small incision in the skin where the wire penetrates. Next, a semirigid dilator is 

advanced over the wire and into the lumen of the vein to create a tract for the more 

pliable catheter to follow. The dilator is removed continuing to keep the guide wire in 

place. Finally, the catheter is advanced over the wire and into the lumen of the vein and 

the guide wire is removed from the catheter leaving only the pliable catheter in place in 

the vein. An alternative is to place the dilator inside the catheter (most kits are designed 

to allow this) and then advance the dilator-catheter complex over the wire and into the

vein lumen. This method permits dilation of the tract and insertion of the catheter 

simultaneously. After the dilator-catheter complex is advanced over the wire and into the 

vein lumen, the dilator and guide wire can then be removed leaving only the catheter 

behind in the lumen of the vein. 

12. When the catheter is fully inserted, check again to be sure there is good return, 

attach the intravenous tubing, and start the fluid infusion. Anchor the catheter in place 

with the nylon or silk size 3-0 or 4-0 skin suture. Make sure that the catheter is well 

secured, and tape it in place, using tincture of benzoin to help secure the tape to the 

skin and catheter. Tape all connections. Cover the insertion site with antibacterial 

ointment and a sterile 10- × 10- cm (4- × 4-in) gauze pad folded in half. 

13. Take the patient out of the Trendelenburg position, and obtain a chest x-ray 

immediately to check placement of the catheter and to detect possible pneumothorax. 

B. Posterior Approach 

(See Figure 6-11). 

4. Steps 1-4 are the same as in the anterior approach. 

5. Note the border where the posterior edge of the anterior belly of the 

sternocleidomastoid muscle meets the external jugular vein, and anesthetize with the 

1% lidocaine. Use a 25-gauge needle for superficial infiltration and a 22-gauge needle 

for deeper anesthesia. 

6. Using a 22-gauge, 6.5-cm (21/2-in) needle attached to the 3-mL syringe as a probe, 

enter the skin just distal to the posterior edge of the sternocleidomastoid muscle about 

two thirds of the way down, where the external jugular vein crosses the 

sternocleidomastoid muscle. Enter at a 45-degree angle to the vertical axis and 20 

degrees below the coronal plane. Direct the needle under the sternocleidomastoid 

muscle and toward the suprasternal notch. Pull back on the plunger as the needle is 

inserted. When the vein has been successfully entered, dark venous blood will flow 

back into the syringe. If the vein is not entered when the probing needle has been 

inserted its full length, withdraw the needle, and try again. 

7. When the vein has been located with the probing needle, withdraw this needle, and 

insert the larger catheter insertion needle or catheter-needle combination. The needle 

should be attached to a syringe in which a slight vacuum is maintained. 

8. When the vein has been successfully entered, dark venous blood will flow freely into 

the syringe. 

9. Insert the catheter using the Seldinger technique, as described above. 

The remaining steps are the same as in the anterior approach. 

SUBCLAVIAN VEIN CATHETERIZATION 

Indications

Subclavian vein catheterization is performed to gain venous access for monitoring of 

central venous pressure, insertion of a transvenous pacemaker, or administration of 

medications or intravenous fluids. 


Contraindications to subclavian vein catheterization are as follows: 

• Edema or other manifestations of superior vena cava obstruction on the proposed side 

of insertion. 

• Previous surgery or irradiation to the subclavicular area. 

• Bleeding diathesis. 

• Infection or cellulitis over the proposed insertion site. 

• Pneumothorax on the contralateral site. 

• Uncooperative patient. 

• Patient receiving CPR. 

Relative Contraindications 

Relative contraindications to subclavian vein catheterization are as follows: 

• Assisted ventilation with high end-expiratory pressures. 

• Mastectomy on the proposed side of insertion. 

• Severe hypovolemia (eg, hemorrhagic shock). 

• Recently discontinued subclavian line in the same area. 


Two people are usually required to perform percutaneous subclavian vein 

catheterization. The operator inserts the catheter, and an assistant opens sterile 

equipment and helps to position the patient. 


A. Materials 


• Materials for sterile technique (cap, mask, gloves, and gown).

• Lidocaine, 1%, with 10-mL syringe and 22- and 25-gauge needles. 


• Container of intravenous fluid with connector tubing. 

• Central venous catheter and insertion set. Many kinds are commercially available; 

most consist of an introducing needle and a radiopaque catheter, usually 30.5 cm (12 

in) long. 

• Tincture of benzoin. BR> 

• Tape (including precut lengths). 

• Standard bath towel. 



required: 

• Drapes. 


• Nylon or silk suture (size 3-0 or 4-0) on a cutting needle. 



• Syringe, 3-mL, with 22-gauge, 6.5-cm (21/2-in) needle for use as a probe (optional). 


Proper positioning of the patient is crucial to successful subclavian vein catheterization. 

Place the patient in the Trendelenburg position at an angle of 30 degrees, with the 

patient's head at a comfortable height for the operator. This position fully distends the 

subclavian vein and creates positive pressure inside the vein when the catheter is 

inserted, thus preventing air embolism. 

Place the rolled bath towel between the patient's scapulas to allow the shoulders to fall 

backward and flatten the clavicles. Both arms should be at the patient's sides. 


The subclavian vein courses under the clavicle near the subclavian artery and the apex 

of the lung (Figure 6-12). The artery is superior and deep to the vein. With a 

percutaneous approach, the vein is entered before the artery can be accidentally 

punctured. Laterally, the artery and vein drop caudally to enter the axilla.

Procedure 

1. Make sure that all equipment is close at hand and ready for use. Assemble the 

container of intravenous fluid and tubing, and flush the tubing with fluid to remove all air. 


3. Sterilize the skin over the insertion site from the lateral aspect of the clavicle to the 

ear to the suprasternal notch. 

4. The patient's head should be rotated away from the side of insertion, with the neck 

twisted as far as possible. 

5. Observe sterile technique (don cap, mask, gloves, and gown). 

6. Assemble the introducing needle and syringe, and make sure that the catheter is 

close by and quickly available. 

7. Drape the infraclavicular area. 

8. Using the index finger, palpate inferior to the clavicle to find the costoclavicular 

ligament, which connects the clavicle and the first rib. This ligament lies where the 

clavicle bends posteriorly (about one-third the length of the clavicle from the 

suprasternal notch). Place the thumb between the clavicle and the first rib just lateral to 

this ligament, and place the index finger in the suprasternal notch. The subclavian vein 

traverses the imaginary line connecting these 2 fingers (Figure 6-13). 

9. Anesthetize the skin with the 1% lidocaine using the 10-mL syringe and the 25-gauge 

needle; then use the 22-gauge needle to anesthetize the subcutaneous tissue and the 

periosteum of the clavicle along the expected route of insertion (ie, the inferior border of 

the clavicle). When anesthetizing, make sure that the needle is not in the vein (ie, that 

blood does not flow back when the plunger of the syringe is gently pulled back) before 

injecting lidocaine. 

10. Reposition the index finger in the suprasternal notch and the thumb over the 

costoclavicular ligament. Place the catheter insertion needle or catheter-clad needle on 

the 3-mL syringe, and insert the needle under the skin 3 cm (11/16 in) caudal to the 

clavicle just medial to the thumb (see Figure 6-13). Insert the needle with the bevel 

facing up, so that its orientation can be maintained after it enters the vein. It may help to 

find the vein with a smaller needle (22-gauge, 6.5-cm [21/2-in] needle attached to a 

3-mL syringe) before using the introducing needle. 

11. Advance the needle at a 10- to 20-degree angle until it contacts the clavicle. 

Decrease the angle of the needle until the needle shaft is parallel to the patient's back 

and close to the correct alignment (pointing to the finger in the suprasternal notch). 

Push the needle slowly inferiorly along the clavicle until it reaches the inferior surface. 

Always keep the tip in contact with the clavicle, and proceed slowly. When the inferior 

surface is reached, check the alignment of the needle with the suprasternal notch, and

while pulling back on the plunger of the syringe, advance the needle toward the 

suprasternal notch, keeping the needle shaft parallel to the patient's back. When the 

needle enters the vein, venous blood will flow back into the syringe. If no blood flows 

out, slowly withdraw the needle while continuing to pull back on the plunger. 

Occasionally, blood will enter the syringe as the needle is being pulled out slowly. 

12. If the first attempt fails, withdraw the needle completely, and flush it with air to clean 

out any tissue from the needle lumen. This maneuver is important, because a second 

attempt at catheterization with an obstructed needle will also fail. Occasionally, directing 

the needle a little cephalad or a little deeper will locate the vein, but do not make 

misguided attempts in all directions, because of the danger of penetrating nearby 

structures such as the lung or the subclavian artery. Seek assistance if 3 or 4 attempts 

to locate the vein fail. If assistance is not obtainable, attempt catheterization on the 

other side (obtain a chest x-ray first to rule out pneumothorax), or insert an internal 

jugular venous catheter instead. 

13. After the vein has been entered, rotate the needle so that the bevel faces caudally 

(toward the patient's feet), and make sure that there is free flow of blood. Occasionally, 

if the tip of the needle lies against the wall of the vein, blood will flow if the bevel is 

facing cephalad but not when the bevel is rotated. If this is the case, advance or 

withdraw the needle a short distance, and check it again for blood flow. 

14. When the needle is properly located in the lumen of the vein, hold it in place with the 

thumb and forefinger of one hand, remove the syringe, and immediately occlude the hub 

of the needle to prevent any air from entering the vein. (If a hypovolemic patient takes a 

deep breath just as the syringe is disconnected, air may be sucked into the vein, 

possibly causing air embolism.) If the needle is properly positioned, blood should flow 

freely from it. 

15. The catheter can now be inserted using the Seldinger technique described earlier. 

16. Evacuate the insertion syringe of all blood clots, attach it to the catheter hub, and 

withdraw some blood to make sure that the catheter is in the vein. The blood should 

flow freely. Remove the syringe. An assistant should then insert the intravenous tubing 

into the catheter hub and check for rapid flow. 

17. Take the patient out of the Trendelenburg position. 

18. Secure the catheter at the insertion site by placing the skin suture through the skin, 

tying it, and then looping it around the catheter 3 times and tying it again. Make sure 

that the lumen of the catheter is not constricted by the tie. 

19. Position the needle and the needle guard on the patient's chest, making sure there 

are no kinks in the tubing or catheter. Apply a small amount of antibacterial ointment to 

the insertion site, cover it and the needle with a folded 10- × 10-cm (4- × 4-in) sterile 

gauze sponge, and tape the sponge in place after applying tincture of benzoin to the 

skin to help secure the tape to the skin and the catheter. 

20. Make sure that all connections are tight and patent, and tape all connections.

21. Obtain a chest x-ray immediately to check placement of the catheter and to detect 

possible pneumothorax. 

FEMORAL VEIN PHLEBOTOMY OR CATHETERIZATION 

Femoral vein catheterization is an easy way to gain rapid access to the central venous 

system, for example, during CPR. Because infection is common at this site, the femoral 

vein should not be used for procedures requiring elective long-term venous access (eg, 

parenteral nutrition). Femoral vein phlebotomy is useful in patients in whom peripheral 

veins of the extremities are not palpable (eg, intravenous drug abusers). However, this 

route should not be used to obtain blood for culture. 

Indications 

Femoral vein phlebotomy is used to obtain venous blood samples in patients in whom 

other sites cannot be used for venipuncture. Femoral vein catheterization is performed 

to gain central venous access. 


Contraindications to femoral vein phlebotomy or catheterization are as follows: 

• Previous surgery in the groin. 

• Prosthetic graft placement in the groin. 

• Venous occlusive disease of the extremities. 

• Acquired or congenital bleeding disorder. 

• Cellulitis or burn over the proposed site of insertion. 


One operator can perform femoral vein phlebotomy or catheterization unaided if the 

patient is cooperative, but it is helpful to have an assistant. 


A. Femoral Vein Phlebotomy 

• Materials for skin cleansing. 

• Syringe (20- to 30-mL) with 18- or 20-gauge needle. 


• Specimen tubes for blood.


B. Femoral Vein Catheterization 




• Catheter-clad needle (eg, Angiocath), 16- to 18-gauge and 12.5-20.5 cm (5-8 in) long; 

or a central venous catheter kit. 

• Container of intravenous infusion fluid with connecting tubing. All equipment should be 

flushed and fully assembled ready for use. 

• Nylon or silk suture (size 3-0) on a cutting needle. 



• Antibacterial ointment and dressings. 

• Drapes. 


• Tape. 


The patient should be supine, with the leg externally rotated on the side selected for 

phlebotomy or catheterization. 


The femoral vein normally lies 1-2 cm (3/8-3/4 in) medial to the readily palpable femoral 

artery (Figure 6-14). In a patient without a palpable femoral pulse, the approximate 

position of the vein can be determined by dividing the distance from the anterior 

superior iliac spine to the pubic tubercle into 3 equal segments. The artery lies at the 

junction of the medial segment and the middle segment. The vein is about 1.5 cm (5/8 

in) medial to this point and to the artery. 

Procedure 

A. Femoral Vein Phlebotomy 

1. Cleanse the skin. 

2. Locate the femoral artery with the nondominant hand.

3. Using the 20- to 30-mL syringe and the 18- or 22-gauge needle in the dominant hand, 

hold the needle at an angle of 90 degrees to the long axis of the vein. 

4. Insert the needle under the skin about 0.5 cm (3/16 in) medial to the artery, and pull 

the plunger back gently to create a slight vacuum as the needle is advanced. 

5. When the needle enters the vein, dark venous blood will flow back into the syringe. 

The blood should flow freely. 

6. After obtaining the desired amount of blood, remove the needle quickly, and apply 

direct pressure over the puncture site. 

7. Fill the specimen tubes as described under Upper Extremity Venipuncture, above. 

B. Femoral Vein Catheterization 

1. Assemble all equipment, and make sure that it is readily at hand. 

2. If necessary, shave the side of the groin chosen for insertion. 


4. Sterilize the skin around the groin, and drape the area. 

5. Locate the femoral artery. Infiltrate the skin 1.5 cm (5/8 in) medial to the artery with 

the 1% lidocaine. Omit this step if the patient is comatose. 

6. Using the catheter insertion needle attached to a syringe, insert the needle just under 

the skin, and pull the plunger back gently to crate a slight vacuum. Then advance the 

needle at an angle of 45 degrees to the long axis of the vein; when the needle enters 

the vein, dark venous blood will flow back into the syringe. The blood should flow freely. 

7. Advance the catheter into the vein. Once the catheter is in place, check to make 

certain that the blood flows freely. A central venous catheter could be inserted instead, 

using the Seldinger technique described earlier. 

8. Obtain an x-ray immediately in order to check the position of the catheter. 

9. If the femoral artery instead of the femoral vein is entered, brighter red blood will flow 

into the syringe under systemic arterial pressure. A patient in shock or cardiac arrest 

may have desaturated blood, with little arterial pressure, so that differentiation between 

arterial and venous puncture may be difficult. If the catheter is to be used solely for 

infusion of fluid or medication during emergency treatment (eg, CPR), temporary 

placement in the femoral artery is probably not harmful. If central venous access is 

required, withdraw the needle and catheter from the artery, maintain direct pressure 

over the area for 5 minutes, and then either try again on the same side or attempt 

catheterization on the opposite side.

SAPHENOUS VEIN CUTDOWN 

Indications 

Saphenous vein cutdown is performed to gain emergency venous access when other 

sites are not available or when multiple intravenous lines are required. 


Contraindications to saphenous vein cutdown are as follows: 

• Previous use of the saphenous vein for a surgical procedure (eg, cutdown, vein 

stripping, coronary artery bypass surgery). 

• Phlebitis. 

• Evidence of severe venous obstructive disease. 

• Cellulitis over the proposed site of insertion. 

• Significant trauma to the legs. 


One person can perform saphenous vein cutdown unaided; however, an assistant is 

helpful. 


A. Materials 





• Expanded gauze roll and tape. 



required: 

• Drapes. 


• Silk ligatures (size 3-0) (2).

• Nylon or polypropylene skin suture (size 3-0) on a cutting needle. 


• No. 15 and No. 11 scalpel blades, both mounted. 

• Kelly clamps (2). 

• Mosquito clamps (2). 

• Dissection tissue scissors and straight scissors. 

• Self-retaining retractors or right-angle retractors (2). 

• Pediatric feeding tubes, sizes 5F and 10F (1 each), cut to the proper length sufficient 

to extend to the knee is usually satisfactory). 

• Toothed and smooth forceps. 

• Plastic-coated absorbent pad to place beneath the patient's leg. 

C. Other Materials 

• Suitable intravenous infusion set (including blood pump and filter, if desired). 

• Container of intravenous fluid with connecting tubing. 


The patient should be supine. The foot selected for the procedure should be externally 

rotated to expose the medial malleolus, and the plastic-coated absorbent pad should be 

placed underneath the patient's leg. 


The saphenous vein runs anterior to the medial malleolus, under the skin and 

subcutaneous tissue, but superficial to the malleolus (Figure 6-15). At this site, the vein 

is usually 4-5 mm (1/8-3/16 in) in diameter in adults. 

Procedure 


connecting tubing, and make sure that the tubing has been flushed to remove all air. 

2. Place a tourniquet around the lower extremity proximal to the venotomy site to 

occlude venous return and dilate the saphenous vein. 

3. Sterilize the skin around the medial malleolus.

4. Drape the skin. 

5. Anesthetize the area with the 1% lidocaine with the 10-mL syringe and 25-gauge 

needle. Omit this step if the patient is comatose. 

6. With the No. 15 scalpel blade, make a 2-cm (3/4-in) superficial transverse incision 

(the dotted line in Figure 6-15), just anterior to the medial malleolus, being careful not to 

cut through the vein. 

7. Using a mosquito clamp, dissect the tissues in the long axis of the leg to isolate the 

vein. Pass the clamp under the vein and dissect the underlying tissue. Place a silk 

suture under the vein, and tie off the distal part of the vein. Maintain exposure with 

retractors. 

8. Supporting the vein with an open Kelly clamp, perform a venotomy with the No. 11 

scalpel blade: Hold the scalpel parallel to the long axis of the vein with the blade in a 

horizontal position, and pass it through the midportion of the superficial (or anterior) wall 

of the vein. Then turn the cutting edge of the blade upward, and open the top of the vein 

(see Figure 6-2). Take care not to transect the vein or puncture its outer wall. 

9. Dilate the vein with the closed point of the Kelly clamp. 

10. Insert the catheter (see Figure 6-3), and pass it 10-12.5 cm (4-5 in) proximally up 

the vein (it is unnecessary to pass it farther). Allow blood to fill the catheter, and then 

remove the tourniquet. 

11. Connect the intravenous tubing to the catheter, and begin the infusion. 

12. Now pass the second silk suture under and around the proximal portion of the vein 

(which now encloses the catheter). Tie this second suture around the vein and catheter 

proximal to the venotomy. Make it snug but not too tight, or it will cut through the vein, 

leaving the catheter loose. 

13. Close the skin with the nylon or polypropylene suture using a simple running stitch. 

Secure the catheter to the skin with a skin stitch. 

14. Apply antibacterial ointment to the wound, and wrap the ankle with an expanded 

gauze roll. 

INTRAOSSEOUS INFUSION 

Indications 

Intraosseous infusion is a temporary means of intravenous access in children to be 

replaced with conventional venous access as soon as possible. It is performed when 

other techniques of venous cannulation have failed or would be too time-consuming (eg, 

in the presence of cardiac arrest, trauma, shock). Complications are infrequent (0.6%) 

and consist mostly of osteomyelitis and infection in adjacent tissues.

Site Selection 

Several sites are suitable for infusion. In children under age 3 years, the proximal tibia 

or distal femur is preferred, but these sites should not be used in patients beyond age 5 

years, because the red marrow is replaced by fat beyond this age. The sternum is more 

suitable in older children; it may be too thin and inadequately ossified in infants. The 

iliac crest is also acceptable. 


Cutaneous infection or burn overlying the insertion site or major injury to the extremity 

proximal to the insertion site are contraindications. 


One person can perform the procedure. An assistant is helpful. 





• Sterile gloves. 

• Short, large-bore bone marrow needle or 18-gauge spinal needle. (Intraosseous 

infusion needles are commercially available.) 

• 10-mL syringe. 

• Intravenous infusion set, including sterile tubing and appropriate fluids for 

administration. 

• Gauze sponges (eg, 10 × 10 cm [4 × 4 in]). 

• Adhesive tape. 


The patient should be supine. If the proximal tibia is selected, the leg should be rotated 

slightly externally. 


The ideal insertion site on the tibia lies 1-2 cm distal to the tibial tuberosity on the 

anterior medial surface. On the femur it is 2-3 cm proximal to the lateral epicondyle in

the midline. 

Procedure 

1. Sterilize the skin. 

2. Drape the area. 

3. Using sterile technique, locate the desired insertion site and infiltrate the skin with 1% 

lidocaine over a 2- to 3-cm area. Lidocaine should also be infiltrated along the 

anticipated course of insertion, down to and including the periosteum. 

4. Using the bone marrow needle, spinal needle, or intraosseous infusion needle, 

penetrate the skin perpendicularly. Advance the needle toward the bone at a 6-degree 

angle (directed away from the growth plate; caudal at the tibia, and rostral at the femur). 

5. Use firm pressure to penetrate the cortex, employing a rotating or twisting motion. 

Upon entry into the marrow space, a sudden "give" will be felt. Caution: Errant 

placement of the needle can cause injury to the growth plate with resultant growth 

deformity. 

6. Remove the trocar from the needle and attach a 10-mL syringe. Aspiration of blood 

and marrow contents confirms needle-tip placement in the marrow. 

7. Connect a fluid-filled syringe or intravenous tubing to the needle and infuse under 

pressure. 

8. Apply gauze 10- × 10-cm (4- × 4-in) sponges (cut midway) against the skin at the 

entry site, surrounding the needle. Occasionally, deep penetration of the needle through 

the bone cortex on the opposite side can occur, with delivery of infusion into 

surrounding tissue spaces. This can also occur if the needle becomes dislodged and 

withdrawn from its intramedullary position; tape the needle firmly in place. 

(Commercially available intraosseous infusion needles may have a lip to which tape can 

be attached or a screw mechanism, for securing the needle to the skin surface.) If a 

spinal needle is used, a Styrofoam cup may be placed over the needle to protect it from 

being bumped. 

RADIAL ARTERY PUNCTURE (For Blood Gas & pH Analysis) 

Indications 

Indications for radial artery punctures are as follows: 

• Need to obtain arterial blood for blood gas and pH determinations. 

• Need to perform phlebotomy when other sites are inaccessible. 

Contraindications

Contraindications to radial artery puncture are as follows: 

• Positive Allen test (see below), indicating that only one artery supplies the hand. 

• Absence of palpable radial artery pulse. 

• Cellulitis or other infection over the radial artery. 

• Coagulation defects (relative contraindication). 


One person can perform radial artery puncture unaided, but it is helpful to have an 

assistant to maintain pressure over the puncture site while the operator prepares the 

sample for transport to the laboratory. 



• Lidocaine, 1%, with 5-mL syringe and 23- to 25-gauge, 1.5-cm (1/2-in) needle. 

• Heparinized syringe, 3- to 5-mL, preferably of glass or of siliconized plastic made 

especially for arterial blood sampling. To heparinize the syringe, aspirate 0.5 mL of 

heparin (100-1000 units/mL) into the syringe, hold the syringe upright, pull the plunger 

all the way out to the end, and then return all of the heparin to the original container. 

This procedure ensures that a small amount of heparin is in the tip of the syringe and 

needle hub that is adequate to heparinize the arterial blood gas sample but not enough 

to affect the accuracy of blood gas determinations. 

• Needle for arterial puncture, 23- to 25-gauge (depending on the size of the artery), 

1.5-cm (1/2-in) long. 

• Ice for transport. 


The patient should be in a comfortable position, either supine or sitting. If respiratory 

difficulties require that the patient sit upright, the upper extremity selected should be 

extended on a stable surface such as a bedside table or on the side of the bed. The arm 

should be positioned with the volar side up. 


The radial artery runs along the lateral aspect of the volar forearm deep to the 

superficial fascia. The artery runs between the styloid process of the radius and the 

flexor carpi radialis tendon. The point of maximum pulsation of the radial artery can 

usually be palpated just proximal to the wrist.

Allen Test 

The Allen test should be performed to confirm the patency of the ulnar artery before any 

attempt is made to obtain a blood sample from the radial artery. 

While the patient is elevating the arm and making a tight fist, occlude both radial and 

ulnar arterial flow with firm pressure over both the radial and the ulnar aspects of the 

volar forearm just proximal to the wrist. Allow a few minutes for the blood to drain from 

the hand, and then lower the arm to waist level and have the patient open the hand. 

Release the pressure on the ulnar artery while keeping the radial artery occluded. 

Normal skin color should return to the ulnar side of the palm in 1-2 seconds, followed by 

quick restoration of normal color to the entire palm. A hand that remains white indicates 

either absence or occlusion of the ulnar artery, in which case radial artery puncture is 

contraindicated. Failure to perform this test may result in a gangrenous finger or loss of 

the hand from a spasm or clotting of the radial artery where there is no collateral flow 

through the ulnar artery. 

Procedure 

1. Palpate the radial artery just proximal to the wrist, and determine where the pulse is 

most prominent. 

2. Locate the approximate position of the artery under the pad of the index finger by 

slowly rolling the finger from side to side. This maneuver causes the pulse to become 

alternately stronger and weaker and further helps to locate the relatively small artery. 

3. Cleanse the skin over the proposed site of puncture. 

4. Anesthetize the skin over the proposed site of puncture with 1% lidocaine using the 3- 

to 5-mL syringe and 23- to 25-gauge needle. 

5. Using the index and middle fingers of the nondominant hand, identify again the point 

of maximal pulsation of the radial artery (Figure 6-16). 

6. Attach the 23- to 25-gauge needle to the heparinized syringe, and holding the needle 

perpendicular to the arm, insert the needle into the skin in the anesthetized area. The 

smaller the needle, the less the risk of injury to the artery and the less painful the 

procedure to the patient. 

7. Guide the needle toward the point of maximum pulsation, and watch for a sudden 

gush of arterial blood into the hub of the needle or the lower part of the syringe. Once 

the needle has entered the lumen of the radial artery, the force of arterial pulsation 

should fill the syringe if it is specially designed for arterial puncture (glass or siliconized 

plastic). If an ordinary plastic syringe is used, a small amount of suction may be required 

to obtain an adequate blood sample (only 1-2 mL of blood is required for blood gas and 

pH analysis). 

8. If no blood is obtained with these maneuvers, it is possible that the needle has

completely passed through the radial artery. Advance the needle until it meets the 

periosteum of the radius. Slowly withdraw the syringe and needle, and look for the gush 

of arterial blood into the hub of the needle. 

9. If this attempt is still unsuccessful, withdraw the needle to a position just under the 

skin, move it 1 mm (1/16 in) to ether side of the previous attempt, and try again. Make at 

least 3 attempts before giving up and trying another site or seeking assistance. 

10. Remove the needle from the artery with a smooth, swift motion, and apply 

immediate direct pressure over the puncture site for 10 minutes. An assistant is helpful 

to apply pressure on the artery. 

11. Evacuate all air bubbles from the sample by holding the syringe upright and allowing 

the bubbles to collect near the needle hub. Gently tapping the syringe with the end of a 

finger will help dislodge bubbles from the walls of the syringe. Once all of the air has 

been confined to the tip of the syringe, evacuate it by pushing on the plunger. Then, cap 

the needle with a rubber stopper, label the tube with the patient's name and number, 

and place the sample on ice for transport to the laboratory. 

12. Return in 15 minutes, and check for adequate perfusion of the hand and for possible 

hematoma formation in the patient's wrist. 

DIRECT LARYNGOSCOPY, OROTRACHEAL INTUBATION, & NASOTRACHEAL 

INTUBATION 

Please see Chapter 8 for a complete discussion of airway management. 

Indications 

A. Orotracheal Intubation 

Indications for orotracheal intubation area as follows: 

• Inadequate oxygenation (eg, decreased arterial PO 2 ) that is not corrected by 

supplemental oxygen supplied by mask or nasal cannula. 

• Inadequate ventilation (increased arterial PCO 2 ). 

• Need to control and remove pulmonary secretions (bronchial toilet). 

• Need to provide airway protection in an obtunded patient or a patient with a depressed 

gag reflex. 

• Need to perform urgent or emergent diagnostic studies in a multiply injured or 

intoxicated patient or in an uncooperative patient with head injury. 

B. Nasotracheal Intubation 

Nasotracheal intubation is used for long-term intubation because it is more comfortable 

for the patient than orotracheal intubation. It is also used when access to the trachea

through the oropharynx is difficult and emergency cricothyrotomy is not indicated. The 

advantages of nasotracheal intubation are greater comfort for the patient and greater 

ease in communicating with the intubated patient through lip reading. Disadvantages 

include need for a smaller airway, which results in increased airway resistance; need for 

a more skilled operator, because the tube is usually inserted without direct vision; 

possible bleeding caused by passage of the nasotracheal tube through the 

nasopharynx; and sinusitis that may result owing to obstruction of the ostia of the 

sinuses. 


The following are only relative contraindications to tracheal intubation: 

• Severe airway trauma or obstruction that does not permit safe passage of an 

endotracheal tube. Emergency cricothyrotomy is indicated in such cases. 

• Cervical spine injury is no longer considered a contraindication to intubation. Rapid 

sequence induction followed by orotracheal intubation optimizes intubating conditions 

and with careful maintenance of in-line cervical immobilization has not been shown to 

lead to iatrogenic cervical spinal cord injury. 

• Nasotracheal intubation is still performed by those with significant experience with the 

technique but is contraindicated in the apneic patient. 


One person can perform direct laryngoscopy or tracheal intubation unaided in 

nontrauma patients. An assistant is required to maintain cervical spine immobilization 

for any patient with a history of trauma who requires intubation. 


• Self-refilling bag-valve-mask combination (eg, Ambu bag) or bag-valve unit (Ayres 

bag), connector, tubing, end-tidal CO 2 (ETCO 2 ) detector, and oxygen source. Assemble 

all items before attempting intubation. 

• Laryngoscope with curved and straight blades of a size appropriate for the patient. 

• Endotracheal tubes of several different sizes (Table 6-1). Low-pressure, high-flow 

cuffed balloons are preferred. Tracheal tubes used in nasotracheal intubation should be 

smaller than those used for orotracheal intubation (see Table 6-1). 

• Oral and nasal airways. 

• Tincture of benzoin and precut tape. 

• Introducer (stylets or Magill forceps). 

• Suction apparatus (tonsil tip and catheter suction).

• Syringe, 10-mL, to inflate the cuff. 

• Mucosal anesthetics and astringents (eg, 1% lidocaine jelly and phenylephrine nasal 

spray). 

• Water-soluble sterile lubricant. 


Unless contraindicated as in the trauma patient, the sniffing position—patient supine, 

with the neck extended, the occiput elevated, and the head tilted backward—permits 

visualization of the glottis and vocal cords and allows passage of the endotracheal tube. 

A towel rolled under the head usually makes it easier for the patient to maintain this 

position. 

In infants under age 1 month, the head and neck should be in a neutral position. 

Procedure 

A. Mask Ventilation 

Oxygen is delivered with a face mask at a rate of 10-15 L/min. 

1. Select the proper-sized mask; it should cover the mouth and nose and fit snugly 

against the cheeks. 

2. Place the nontrauma patient in the sniffing position. 

3. Place the mask over the patient's mouth and nose with the right hand. 

4. With the left hand, place the small and ring fingers under the patient's mandible, and 

lift up to open the airway. Grasp the mask with the thumb and index finger, and press it 

to the patient's face while lifting the mandible with the ring and small fingers. 

5. Compress the bag with the right hand. 

6. The chest should rise with each breath, and airflow should be unimpeded. If not, 

reposition the mask, and try again. Occasionally, insertion of an oral or nasal airway 

facilitates ventilation by mask. Because of the lack of support for the lips, elderly 

edentulous patients may be especially hard to ventilate using a mask. 

B. Topical Anesthesia 

Anesthetize the mucosa of the nose, oropharynx, and upper airway with cocaine, 4%, or 

lidocaine, 2%, if time permits and the patient is awake. 

C. Direct Laryngoscopy 

1. Place the patient in the sniffing position.

2. Check the laryngoscope and blade for proper fit, and make sure that the light works. 

3. Make sure that all materials are assembled and close at hand. 

4. Curved blade technique: (a) Open the patient's mouth with the right hand, and 

remove any dentures. (b) Grasp the laryngoscope in the left hand (Figure 6-17). (c) 

Spread the patient's lips, and insert the blade between the teeth, being careful not to 

break a tooth. (d) Pass the blade to the right of the tongue and advance the blade into 

the hypopharynx, pushing the tongue to the left and placing the tip of the blade into the 

vallecula. (e) Lift the laryngoscope upward and forward, without changing the angle of 

the blade, to expose the vocal cords. 

5. Straight blade technique: Follow the steps outlined for curved blade technique, but 

advance the blade down the hypopharynx, and lift the epiglottis with the tip of the blade 

to expose the vocal cords. The tip of the laryngoscope blade fits below the epiglottis, 

which is no longer visible with the blade in position. 

D. Orotracheal Intubation 

1. Select the proper-sized tube (see Table 6-1). Most adult men take an endotracheal 

tube that has an inside diameter of 8-9 mm. Most adult women take an endotracheal 

tube that is 7-8 mm internal diameter. For children, a general rule is that the external 

diameter of the tube is equal to the diameter of the child's fifth digit fingernail. 

2. With the 10-mL syringe, inflate the balloon with 5-8 mL of air. Make sure that the 

balloon is functional and intact. 

3. Lubricate the end of the tube (optional). 

4. Insert the stylet, and bend the tube and stylet gently into a crescent shape so that the 

tip of the stylet is at least 1 cm ( 3/8 in) proximal to the end of the orotracheal tube. 

5. Be sure that the syringe and the bag-valve combination are within easy reach. 

6. Ventilate the patient with the bag-valve combination for 1-2 minutes with 100% 

oxygen. 

7. Open the patient's mouth, remove dentures, and suction secretions or vomitus from 

the mouth. 

8. Visualize the glottis and vocal cords and, by direct laryngoscopy, gently pass the tube 

through the vocal cords into the trachea. Occasionally, having an assistant press 

posteriorly on the anterior neck at the level of the cricoid cartilage will help to bring an 

anteriorly placed larynx into view and facilitate intubation. This is known as the Sellick 

maneuver; it also helps reduce reflux of gastric contents into the hypopharynx. 

9. Gently pass the tube next to the laryngoscope blade, through the vocal cords, and far 

enough so that the balloon is just beyond the cords.

10. Withdraw the stylet, and inflate the cuff. 

11. Connect the bag-valve combination and ETCO 2 detector, and begin ventilation with 

100% oxygen. 

12. Confirm the tube is properly positioned by several methods. ETCO 2 -detector color 

change confirms endotracheal intubation in the patient with spontaneous circulation but 

the color may not change in patients who have had cardiac arrest. Next, it is important 

to use auscultation to confirm appropriate placement. First, listen over the stomach with 

a stethoscope while ventilating the patient. If sounds of airflow are heard or if distention 

of the stomach occurs, the tube is in the esophagus. If the esophagus has been 

intubated instead of the trachea, remove the tube, ventilate the patient with a mask, and 

try again. 

Next, listen to each side of the chest, including the axilla, to be sure that the breath 

sounds are equal. If the left chest has more distant breath sounds than the right chest, 

try withdrawing the tube 1-2 cm (3/8-3/4 in) and ventilating again. This maneuver helps 

to correct intubation of the right main-stem bronchus as a cause of unequal ventilation. 

Airway anatomy makes intubation of the right main-stem bronchus more likely than 

intubation of the left. When breath sounds are equal on both sides and the thorax rises 

equally on both sides with each inspiration, note the position of the tube (eg, mark the 

tube at the patient's mouth). 

13. Secure the tube in place with tracheostomy ribbon or tape. 

14. Obtain a chest x-ray immediately to check tube placement. 

15. Obtain arterial blood gas measurements to assess the adequacy of ventilation. 

E. Nasotracheal Intubation 

6. Steps 1-6 are the same as those for orotracheal intubation, except no stylet is 

needed. The tube must be checked and lubricated, and all materials must be readily at 

hand. 

7. Examine the patient's nose, and determine if one nasal passage is larger than the 

other. Insert the lubricated nasotracheal tube in the external naris, and pass it directly 

posteriorly until it meets the floor of the nasopharynx. The technique is similar to that 

used to pass a nasogastric tube (see Nasogastric Intubation, below). 

8. Make sure that the natural bend in the tube (without the stylet in place) corresponds 

to the direction of passage, and with gentle, steady pressure, continue to advance the 

nasotracheal tube into the posterior pharynx. At this point, the tube may meet with 

obstruction. If the tube fails to pass into the posterior pharynx under gentle, steady 

pressure, withdraw the tube, and attempt insertion in the opposite nostril. 

9. Once the nasotracheal tube is in the pharynx, the patient's head may be flexed by 

lifting the occiput if no concern for cervical spine injury exists. This helps to guide the 

tube through the vocal cords anteriorly into the larynx. The patient may start to cough

when the tube passes through the vocal cords. 

10. If the patient is breathing spontaneously, listen at the external end of the tube. If the 

tube is properly positioned over the larynx, air should be heard coming in and out of the 

tube. If no air is heard, the tube has slipped posteriorly and is in the esophagus. Place 

the index finger and thumb on each side of the larynx. This allows for external palpation 

of the endotracheal tube if it deviates to either piriform fossa. Using the digits flanking 

the trachea, manually deviate the trachea toward the intubated nares to facilitate better 

alignment and allow for easier intubation. 

11. When ventilation is heard, steady the patient's head in that position, and when 

inspiration begins, advance the tube into the trachea. 

12. Once the tube is in the trachea, inflate the balloon and listen again to make sure that 

air is coming from the nasotracheal tube, and look at the tube to see the condensation 

of water vapor with exhalation. 

13. Have an assistant steady the nasotracheal tube. Connect an air reservoir bag (eg, 

Ayers or Ambu bag) and ETCO 2 detector to the tube, ventilate the patient, and check 

for elevation of both sides of the chest on inspiration and the presence of breath sounds 

at each axilla in addition to color change on the ETCO 2 detector. As with orotracheal 

intubation, inadvertent intubation of the right main-stem bronchus (with poor ventilation 

of the left lung) occurs more commonly than intubation of the left bronchus. 

14. When proper positioning of the tube in the trachea has been achieved, secure the 

tube in place with tracheostomy ribbon or tape. Make sure that there is no pressure on 

the external naris that might cause necrosis. 

F. Removal of the Endotracheal Tube 

1. Ventilate the patient with a bag-valve combination for 1-2 minutes with 100% oxygen. 

2. Suction the patient's trachea, mouth, and hypopharynx before removing the tube. 

3. Deflate the cuff by withdrawing all air with the 10-mL syringe. 

4. Have the patient take a deep breath, and remove the tube at the midpoint of 

expiration. 

5. Suction the patient's mouth a second time to remove any remaining secretions. 

6. Begin oxygen, 5 L/min, by mask. Obtain a sample of arterial blood to assess 

respiratory function. 

NASOGASTRIC INTUBATION (For Gastric Evacuation or Lavage) 

Indications 

Indications for nasogastric intubation are as follows:

• Need to suppress vomiting caused by gastric distention or paralytic ileus. 

• Need to perform gastric lavage (therapeutic or diagnostic). 

• Need to perform gastric decompression. 

• Need to perform gastric evacuation. 


Important contraindications to nasogastric intubation are as follows: 

• Choanal atresia. 

• Massive facial trauma or basilar skull fracture. 

• Esophageal atresia or stricture. 

• Ingestion of a caustic substance (eg, acid, lye)-unless nasogastric intubation can be 

performed under direct vision. 

Relative contraindications to nasogastric intubation are as follows: 

• Recent gastric or esophageal surgery. 

• Recent oropharyngeal or nasal surgery. 

• Esophageal stricture. 

• Esophageal burn. 

• Zenker diverticulum. 


One person can perform nasogastric intubation unaided, but an assistant is helpful. 


• Nasogastric tube of the proper diameter. There are 2 main types of tubes: straight 

suction tubes and sump suction tubes (with 2 lumens). The sump tube is less likely to 

be sucked against the stomach wall and become plugged. The only disadvantage is that 

because of the second air-inlet port, it has a slightly smaller lumen for suction than a 

similarly sized straight suction tube. Most adults require a 16-18F sump tube. The 

limiting factor is the size of the naris. Children usually require a 10F nasogastric tube 

and infants an 8F tube. (Nasogastric size can be estimated by multiplying endotracheal 

tube size by 2.)

• Lubricant. 

• Suction syringe with catheter tip. 

• Connector (usually supplied with the nasogastric tube). 

• Suction tube and suction device (wall suction, intermittent wall suction, or portable 

intermittent suction). 

• Phenylephrine nasal spray, 0.5%, and benzocaine-tetracaine spray. 


• Tape. 


The patient should be in a comfortable, supported sitting position. Unconscious patients 

should either be supine and flat or supine with the head slightly elevated. Children or 

unusually overreactive adults may be asked to sit on their hands as a reminder to keep 

them away from the nose and the tube as it is being passed into the stomach. 

Procedure 

1. Explain exactly what the steps of the procedure will be, and explain the need for the 

patient's help at certain points. 

2. Determine the length of tubing necessary by measuring the distance between the ear 

and the umbilicus. 

3. Lubricate the end of the tube with lubricant. 

4. Apply 0.5% phenylephrine nasal spray to both nostrils to prevent epistaxis. If 

intractable gagging is a problem, Benzocaine-tetracaine spray applied to the pharynx 

will help. 

5. Insert the tube into the nostril at a 60- to 90-degree angle to the plane of the face, 

and advance it straight back until it meets resistance (the patient usually signs when this 

happens). 

6. Using the gentle pressure and pushing posteriorly and perpendicularly to the long 

axis of the head, advance the tip of the tube inferiorly and into the nasopharynx (Figure 

6-18). 

7. Have the patient take a small sip of water through the straw and hold it in the mouth 

without swallowing. Then have the patient swallow, and advance the tube into the 

esophagus simultaneously. If this maneuver is successful, the patient will gag. If it fails 

and the tube slips into the trachea, violent coughing will usually ensue. Withdraw the 

tube into the oropharynx, and try again. The most important step is timing the

advancement of the tube to coincide with the swallow. Patients with an altered 

sensorium sometimes tolerate tracheal intubation without any reflex coughing. The tube 

is improperly positioned if air exchange is heard. 

8. When the tube is in the esophagus, advance it into the stomach. In adults, the tube is 

usually in the stomach when it is advanced to the next-to-the-last mark on the sump 

tube. 

9. Once the nasogastric tube is in the stomach, withdraw some gastric juice, and with a 

suction syringe inject air down the tube while listening over the left upper quadrant for 

the sound of air leaving the tube and bubbling in the stomach. If no sound is heard, 

reposition the tube, and inject more air. If several attempts fail, check to make sure that 

the tube is not in the trachea or curled in the patient's mouth. Obtain a chest x-ray to 

check the position of the tube. Injecting a small amount of water-soluble contrast 

medium down the tube and visualizing its position with fluoroscopy or standard x-ray is 

the definitive confirmatory procedure. Never assume that the tube is in the correct 

position without performing some confirming maneuver. Nasogastric tubes have been 

left in the peripheral lung, cranial vault, extraesophageal mediastinum, and peritoneal 

cavity. 

10. Apply tincture of benzoin to the nose before securing the tube to the nose with tape, 

and make sure that the tube does not exert pressure on the external naris, which can 

result in pressure necrosis and sloughing of the naris. 

Special Problems 

A. Intubated Patients 

Inserting a nasogastric tube in an intubated patient can be difficult. Follow the steps 

outlined above, and remember to deflate the cuff of the endotracheal tube if the 

nasogastric tube becomes stuck in the upper esophagus. In an unresponsive intubated 

patient, it may occasionally be necessary to use Magill forceps and a laryngoscope to 

advance the tube into the esophagus under direct vision. 

B. Comatose Patients 

A comatose or obtunded patient cannot swallow at the right time to facilitate passage of 

the tube. The natural bend of the tube as it passes into the pharynx from the naris is 

anterior; the tube therefore tends to enter the trachea. Any one of the following 

maneuvers may be helpful (they should be performed in the order given here): 

1. Flex the patient's head when passing the tube. Make sure the patient does not have a 

cervical spine injury if this is attempted in the emergency department. 

2. After the tube passes into the hypopharynx, rotate the tube to direct the natural curve 

posteriorly and continue to advance it. 

3. Pass the tube through the nostril and into the nasopharynx, and insert a finger into 

the patient's mouth to manually guide the tube posteriorly into the esophagus. 

4. Use a laryngoscope and Magill forceps to pass the tube into the esophagus under

direct vision. 

INSERTION OF SENGSTAKEN-BLAKEMORE OR MINNESOTA TUBE 

Minnesota and Sengstaken-Blakemore tubes (Figure 6-19) are used to control 

hemorrhage from esophageal varices and the esophagogastric junction. The 

Sengstaken-Blakemore tube is a triple-lumen rubber tube with 2 balloons: one that is 

inflated in the lumen of the stomach and pressed against the esophagogastric junction, 

and one that is inflated in the lumen of the esophagus to press directly against the 

varices. Two of the lumens are used to inflate the balloons; the third opens into a port 

on the distal tip of the tube and is used to irrigate and drain the stomach. 

The Minnesota tube is currently preferable to the other tubes that are available. This 

tube has 4 lumens: 2 for filling the balloons, one that permits aspiration of gastric 

contents, and a fourth to aspirate the esophagus above the balloon. If a tube without an 

esophageal port is used (eg, a Sengstaken-Blakemore tube), a nasogastric tube must 

be tied to the Sengstaken-Blakemore tube just above the esophageal balloon in order to 

remove secretions collecting there. 

Effective use of the Sengstaken-Blakemore or Minnesota tube requires close attention 

to the pressure in each balloon and monitoring for continued bleeding from the 

esophagogastric varices (blood aspirated through the gastric aspiration port of the 

Sengstaken-Blakemore tube or above the esophageal balloon through a nasogastric 

tube or the esophageal port of the Minnesota tube). Proper insertion will also ensure 

that the gastric balloon is not inflated in the esophagus, which may lead to esophageal 

rupture. 

With either tube, patients may require orotracheal or nasotracheal intubation first to 

protect the airway before balloon tamponade is attempted. Intubation must always be 

done in comatose patients. 

Indications 

Indications for insertion of a Sengstaken-Blakemore tube are as follows: 

• Need to control massive upper gastrointestinal tract hemorrhage presumed to be from 

esophageal varices in a patient with hypovolemic shock. 

• Need to control documented esophagovariceal hemorrhage in a patient with or without 

hemodynamic compromise. 


Insertion of a Sengstaken-Blakemore tube is contraindicated in patients who have 

undergone previous gastroesophageal surgery. 


The operator will require an assistant.


• Sengstaken-Blakemore tube or Minnesota tube. 

• No. 18 Salem sump tube if Sengstaken-Blakemore tube is used. 

• Constant or intermittent wall or portable suction device. 

• Mercury manometer or aneroid pressure gauge. 

• Y connector. 

• Rubber-clad clamps (3). 

• Water-soluble lubricating jelly. 

• Cocaine spray, 4%. 

• Glass of water and a straw. 

• Manometer-grade rubber tubing, 0.6-1 m (2-3 ft). 

• Irrigating syringe, 50-mL; water, basin. 

• Football helmet with a face mask, if available. 

• Sponge rubber to act as cuff around the tube. 


The patient should be supine, with the head of the bed elevated 30-45 degrees if 

possible. It is difficult to insert the tube with the patient in the Trendelenburg position. 


Esophageal varices result form portal hypertension. When the distal esophageal veins 

become distended, they become susceptible to erosion, and the overlying mucosa 

becomes thinner. Mechanical or chemical (reflux of gastric acid) irritation may rupture 

the varices, causing hemorrhage. 

Procedure 

1. Protect the airway. In stuporous patients or those with a diminished gag reflex, 

endotracheal intubation should be performed before passage of a Minnesota or 

Sengstaken-Blakemore tube. 

2. Inflate the balloons to test for air leaks, and lubricate the distal end of the tube and 

balloons.

3. Make sure that all necessary equipment is readily at hand. 

4 .Deflate the balloons completely. 

5. Anesthetize the patient's nasal passages, pharynx, and hypopharynx with the 4% 

cocaine spray or benzocaine-tetracaine spray and wait 2-3 minutes. 

6. Pass the tube through one nostril with steady pressure until the tip of the tube is in 

the posterior pharynx. 

7. Advance the tube into the esophagus as the patient swallows. 

8. Advance the tube to at least the 50-cm mark. (In the typical adult, the tube should be 

in the stomach at this point.) 

9. Fill the irrigating syringe with air, and listen over the patient's stomach with a 

stethoscope while injecting air through the gastric aspiration port. If the tube is properly 

positioned, a gurgling sound will be heard in the stomach as air escapes from the tube. 

If no air is heard, withdraw the tube, and insert it again. Do not inflate either balloon until 

the tube is known to be in the stomach. 

10. When proper placement of the tube in the stomach has been confirmed, inflate the 

gastric balloon with air (250-275 mL for the Sengstaken-Blakemore tube; 450-500 mL 

for the Minnesota tube), and clamp the gastric balloon port with a rubber-clad clamp. If 

the patient develops substernal pain while the gastric balloon is being inflated, the 

balloon may be in the esophagus. Stop immediately, deflate the balloon, and push the 

tube farther into the stomach before attempting reinflation of the gastric balloon. 

11. Pull back on the tube until resistance is felt, showing that tamponade of the 

gastroesophageal junction has been achieved. Secure the tube with a minimum of 

tension (about 0.45 kg [1 lb]) by taping a cuff of sponge rubber to the tube just distal to 

the patient's nostril. 

12. Construct a pressure-reading mechanism by connecting the esophageal balloon 

port to a Y connector. Use part of the manometer-grade rubber tubing if needed. 

Connect the manometer or aneroid pressure gauge to one port of the Y connector and 

an inflating bulb of the 50-mL syringe to the other. 

13. If inflation of the gastric balloon fails to stop the bleeding, inflate the esophageal 

balloon to 35-50 mm Hg of pressure, using manometer control. Use the lowest pressure 

possible that will control hemorrhage. 

14. Aspirate through the gastric port of the tube, and evacuate the stomach of all blood 

and water. Irrigate and aspirate the stomach, if necessary, to completely evacuate all 

contents. 

15. Continue gastric lavage for 30 minutes, and check for bright red blood. If bleeding

continues, increase the esophageal balloon pressure by 5-mm Hg increments. Continue 

lavage to determine the exact pressure at which bleeding stops. Occlude the 

esophageal and gastric ports with a rubber-clad clamp proximal to the Y connector. 

16. Record the pressures in the gastric and esophageal balloons, and transport the 

patient to an intensive care unit with one-on-one nursing. 

17. Obtain a portable chest x-ray and abdominal film immediately to check for proper 

placement of the tube. 

18. If a football helmet is available, secure the tube to the face mask instead of using 

pressure against the nostril to hold the tube in place. 

19. If a Sengstaken-Blakemore tube is being used, pass a standard nasogastric Salem 

sump tube through the other nostril to evacuate all secretions that accumulate above 

the esophageal balloon. If a Minnesota tube is being used, attach the esophageal port 

to a suction device set to intermittent high suction. 

20. If the patient is comatose and the tube cannot be passed through the nose, insert it 

through the mouth, and guide it into the esophagus with a finger. An alternative is to use 

direct laryngoscopy and Magill forceps to guide the tube into the esophagus. Be careful 

not to puncture the balloon with the forceps. 

21 .Secure the tube as shown in Figure 6-20. 

22. The pressure in both balloons should be checked every 30 minutes by releasing the 

rubber-clad clamps on the tube proximal to the Y connector while the tube used for 

inflation is occluded. This connects the balloon to the manometer for pressure 

measurement, and air leaks in the balloon can be quickly detected before bleeding 

recurs. Periodically irrigate and aspirate through the gastric port and through the 

esophageal port (Minnesota tube) or Salem sump tube (Sengstaken-Blakemore tube) to 

make sure that no gastric or esophageal bleeding goes undetected. 

CRICOTHYROTOMY 

Indications 

Cricothyrotomy is performed when the airway must be secured or maintained and when 

attempts at orotracheal or nasotracheal intubation have failed. Transection or fracture of 

the trachea, larynx, or cricoid cartilage are contraindications. The procedure should not 

be performed in children younger than age 12 years. Transtracheal jet ventilation (also 

known as needle cricothyrotomy) is the preferred method for this age group. 


Cricothyrotomy is contraindicated when any other less radical means of securing an 

airway is feasible. 

Personnel Required

One person can perform cricothyrotomy unaided, but an assistant is helpful. 


Because cricothyrotomy is almost always performed when speed is essential to save 

the patient's life, presterilized kits containing the required materials should be available 

in all hospital emergency departments. The following items are required: 




• Sponges, 10 × 10 cm (4 × 4 in). 

• Drapes and rolled bath towel. 

• No. 11 scalpel blade, mounted. 

• Mosquito clamps (2). 

• Kelly clamps (2). 

• Self-retaining skin retractors. 

• Low-pressure, high-flow orotracheal tube sized to the patient (usually a small [4- to 

6-mm] tube is used to fit the small opening) or, if available, low-pressure cuffed 

tracheostomy tubes of various sizes. 

• Syringe, 10-mL, to inflate the balloon on the orotracheal tube. 

• Self-refilling bag-valve-mask combination (eg, Ambu bag) or bag-valve unit (eg, Ayres 

bag), connector, tubing, and oxygen source. 


• Tape. 


The patient should be supine, with a rolled bath towel under the shoulders, and the neck 

hyperextended. 


The cricothyroid membrane (conus elasticus and cricothyroid ligament) lies between the 

thyroid cartilage superiorly and the cricoid cartilage inferiorly (Figure 6-21). The

membrane is a poorly vascularized ligamentous structure that lies under the 

subcutaneous tissue between the laterally placed cricothyroid muscles. 

Procedure 

1. Assemble all necessary equipment. 


3. Sterilize the skin of the neck from the chin to the sternal notch and laterally to the 

base of the neck, if time permits. 

4. Observe sterile technique (don cap, mask, gloves, and gown) if time permits. 

5. Check the endotracheal tube or tracheostomy tube for cuff leaks by inflating the tube 

with air from a syringe. 

6. Identify the cricothyroid membrane. Using the 10-mL syringe with the 25-gauge 

needle, infiltrate the skin and underlying cricothyroid membrane with the 1% lidocaine in 

a line across the membrane while steadying the thyroid cartilage with the left hand. Omit 

this step if complete airway obstruction is present or if the patient is comatose. 

7. Using the No. 11 blade, make a vertical incision in the skin overlying the cricothyroid 

membrane. Retract the skin with self-retaining retractors and relocate the cricothyroid 

membrane by palpation. 

8. Make a horizontal incision through the cricothyroid membrane. Extend the incision in 

the cricothyroid membrane for approximately 1 cm on each side of the midline. 

9. Using a mosquito or Kelly clamp in the left hand (with the point downward), insert the 

clamp into the incision and spread it. This maneuver alone is sufficient to provide an 

airway for a patient with supraglottic airway obstruction. 

10. Grasp the endotracheal tube or tracheostomy tube with the right hand, and insert 

the tube through the incision into the trachea, directing it caudally. 

11. Connect the bag-valve unit to the tube, and immediately ventilate the patient with 

100% oxygen. Check for respiratory movement of the chest and the presence of 

bilaterally symmetric breath sounds. 

12. Inflate the balloon just enough to stop any audible air leak during the inspiratory 

phase of positive-pressure ventilation. 

13. Cut a 10- × 10-cm (4- × 4-in) gauze sponge halfway down the middle, and wrap it 

around the tube. If an orotracheal tube is being used, fashion a necklace of adhesive 

tape, apply tincture of benzoin to the tube, and tape it in place. If a tracheostomy tube is 

being used, secure the wings of the tube by tying the tapes around the patient's neck, 

leaving enough slack so that an index finger can easily slide under the tape. Tying the

tape too tightly can cause erosion of the skin and venous congestion above the tie, 

whereas tying it too loosely invites dislodging of the tube. 

14. Suction the trachea. 

15. Obtain a chest x-ray immediately to check the position of the tube. 

TRANSTRACHEAL JET VENTILATION 

Indications 

Transtracheal jet ventilation (TTJV) is an alternative to cricothyrotomy in patients who 

require emergency assisted ventilation when conventional methods of endotracheal 

intubation are not possible. 


TTJV is contraindicated if conventional methods of endotracheal intubation can be 

successfully employed or if the proper equipment for TTJV is not available. 


One person can perform the procedure unaided, although it is helpful to have an 

assistant to position the patient's head and handle equipment. 




• Intravenous catheter, 12- or 14-gauge, or 13-gauge cannula designed specifically for 

TTJV that has lateral flanges to which tape may be attached. 

• Bag-valve mask set. 

• 50-psi Oxygen source. 

• Demand valve device or Y adapter with connectors and tubing that connects to the 

50-psi oxygen source. 

• Adapter (eg, Luer-Lok) for connecting the demand valve outflow tubing to the catheter 

(Figure 6-22). 

• Tape for securing catheter in place. 

• Syringe, 3-mL. 

Positioning of the Patient

The patient is positioned supine with the head in the midline. It is helpful to have the 

neck slightly extended unless cervical spine injury is suspected. 


The cricothyroid membrane is a 1- to 1.5-cm membrane that lies inferior to the thyroid 

cartilage and superior to the cricoid cartilage. It can be located easily by palpating the 

protuberant midline portion of the thyroid cartilage ("Adams apple") and then moving the 

fingertip inferiorly 1.5 cm until it rests in a soft, flat depression between the thyroid 

cartilage and the cricoid cartilage. The examining fingertip will then be on the 

cricothyroid membrane. 

Procedure 

1. Position the head as described above. Have an assistant hold the patient's head or 

use the tape across the forehead to prevent unexpected motion. If the patient requires 

assisted ventilation, provide it by a bag-valve-mask device. 

2. Prepare the anterior surface of the neck with povidone-iodine. 

3. Using sterile gloves, locate the cricothyroid membrane. It may be helpful to place the 

thumb and index finger of the nondominant hand on either side of the cricothyroid 

membrane to stabilize the trachea and anchor and stretch the skin slightly. 

4. Connect the catheter or cannula to the 3-mL syringe. With the catheter or cannula 

and syringe in the dominant hand, pierce the skin and cricothyroid membrane at a 

45-degree angle, directing the catheter tip inferiorly (Figure 6-23). When the catheter tip 

enters the tracheal lumen, a slight "give" will be felt. The patient may also cough when 

the catheter stimulates the tracheal wall. Traction in the syringe plunger during the entry 

will confirm lumen entry when air is withdrawn freely. 

5. Slide the catheter sheath forward until it is snug against the skin, and then withdraw 

the needle. 

6. Connect the inflow tubing on the demand valve or Y adapter to the 50-psi oxygen 

source and the outflow tubing to the catheter via the adapter. (Note: 50 psi may be 

obtained from a step-down regulator that supplies oxygen to a demand valve or from a 

venturi flow regulator opened wide to deliver 15 L/min.) 

7. Begin ventilation at a rate of 20 breaths per minute, by pressing the button on the 

demand valve, or occluding the open port on the Y adapter, and inflating for 1 second, 

followed by a 2-second relaxation phase during which the patient will exhale passively 

through the oropharynx. Be prepared for secretions to be expelled during inflation as 

well as exhalation. 

8. Tape the catheter firmly in place, with the hub of the catheter snug against the neck.

THORACENTESIS 

Indications 

Indications for thoracentesis are as follows: 

• To relieve dyspnea or respiratory distress caused by accumulation of fluid in the 

pleural space. 

• To obtain pleural fluid for diagnostic tests. 


Contraindications to thoracentesis are as follows: 

• Severe coagulopathy (should be corrected before thoracentesis, unless severe 

respiratory failure is present, as determined by arterial blood gas analysis). 



One person can perform thoracentesis unaided. 




• Lidocaine, 1%, with 5-ml syringe and 25- or 27-gauge needle. 

• Sterile towels (4) or sterile paper drapes. 


• Catheter-clad needle (eg, Angiocath), 16- to 18-gauge, 30.5 cm (12 in) long; and 

30-mL syringe to aid in insertion. 

• Three-way stopcock. 

• Luer-Lok syringe, 30-mL. 

• Sterile connecting tubing and empty intravenous bottle, or vacuum bottle specially 

designed for thoracentesis (if removal of more than a few hundred milliliters of fluid is 

anticipated). The connecting tube should not have a drip chamber. 

• Collection vessels and culture media for laboratory analysis.


Thoracentesis is usually performed with the operator positioned behind the seated 

patient. Occasionally, thoracentesis must be performed in the lateral position when the 

patient cannot sit. 

For the posterior approach, the patient should be sitting on the edge of the bed or 

gurney with arms and trunk bent forward over a bedside stand and supported by the 

elbows or a pillow. 

If the lateral approach must be used, have the patient lie at the edge of the bed on the 

affected side with the ipsilateral arm extended over the head. The midposterior line must 

be accessible for insertion of the needle. Elevating the head of the bed 30 degrees is 

sometimes helpful. 


Access to the pleural space is gained through the intercostal spaces (Figure 6-24). 

Remember that nerves and blood vessels run on the underside of the rib, and that the 

domes of the diaphragm are highest posteriorly, occasionally as high as the 7th 

intercostal space. 

Procedure 

Position the patient, and prepare all equipment. 

A. Initial Preparation 

1. If removing a large volume of fluid, assemble the connecting tubing and a collection 

vessel. 

2. Observe sterile technique (don cap, mask, gloves, and gown) if time permits. 

3. Arrange all of the equipment on a sterile field on a Mayo stand or bedside table. 

4. Select the thoracentesis site by localizing the level of pleural fluid either by 

percussion (area of dullness) or ultrasonography. Insert the needle in the intercostal 

space below the level of fluid in the midposterior line (posterior insertion) or the 

midaxillary line (lateral insertion). 

5. Sterilize a wide area of skin around the proposed insertion site. 

6. Drape the patient (this may be impossible if the patient is sitting). 

7. Anesthetize the skin over the insertion site with the 1% lidocaine with the 25- or 

27-gauge needle and 5-mL syringe. Then anesthetize the superior surface of the rib and 

the parietal pleura. 

B. Catheter-Clad Needle (eg, Angiocath) Insertion

1. Attach a 30-mL syringe to the catheter-clad needle, and insert the needle through the 

skin over the rib selected. Advance the needle until it hits the rib. 

2. Move the tip of the needle cephalad over the edge of the rib until it encounters the 

superior aspect of the rib. 

3. Have the patient take a deep breath and hold it against a closed glottis. 

4. Advance the needle over the superior surface of the rib and through the pleura into 

the pleural space. Maintain constant suction on the syringe so that the pleural fluid will 

enter the syringe instantly when the pleural space is entered. Apply controlled, gentle, 

steady pressure with both hands steadied on the patient's back to keep from suddenly 

spearing the lung. Do not use a Kelly clamp to grip a catheter-clad needle. 

5. When the catheter has entered the pleural space, angle the needle caudally, and 

push the catheter off the needle and into the base of the pleural space. 

6. Occlude the lumen of the catheter, and have the patient exhale and breathe normally. 

7. Have the patient take a deep breath again and hold it; insert the 3-way stopcock into 

the catheter hub. Make sure that the stopcock valve is set to occlude the catheter port. 

Have the patient resume normal breathing. 

8. Connect the 30-mL Luer-Lok syringe to one port of the 3-way stopcock and (if 

needed) the intravenous tubing to the other. 

9. Turn the stopcock valve to connect the syringe with the catheter, and withdraw fluid 

from the pleural space. Then turn the stopcock so as to connect the syringe to the 

intravenous tubing, and empty the syringe through the tubing into the intravenous bag or 

bottle. The first syringeful of fluid may be reserved for diagnostic tests. 

10. Withdraw as much fluid as possible but no more than 1 L at one time. In order to 

completely evacuate the pleural space, the patient may have to be rocked from side to 

side while fluid is being withdrawn. 

11. When no more fluid can be withdrawn, the patient should take a deep breath and 

hold it while the catheter is quickly withdrawn. Cover the insertion site with a sterile 

occlusive dressing. 

12. Obtain an upright portable chest x-ray to check for possible pneumothorax and 

residual fluid. 

TUBE THORACOSTOMY (Insertion of a Chest Tube) 

Indications 

Tube thoracostomy is performed in order to drain air or fluid from the pleural space.


There are no absolute contraindications to chest tube insertion. Usually, the patient is in 

distress, and any relative contraindication (eg, coagulopathy) is superseded by the need 

to reinflate a compressed lung or drain fluid from the lungs. 


One operator can insert a chest tube alone; however, an assistant is helpful. 


Most hospitals have sterile thoracostomy trays ready for use. If a tray is not available, 

assemble the following instruments and materials: 





• Chest tube of the appropriate size and style to suit the clinical situation (see below). 

• No. 11 surgical blade, mounted. 

• Mayo clamp. 

• Kelly clamp. 

• Surgical silk suture (size 0) with large curved cutting needle. 


• Petrolatum-impregnated gauze. 

• Sterile gauze sponges, 10 × 10 cm (4 × 4 in). 

• Plastic adhesive tape, 5 cm (2 in) wide. 

• Suction apparatus, 3-bottle, with water-seal, collection, and water-column sections 

(Figure 6-25). In the United States, this device is usually supplied as a unit with tall 

connectors and tubes included (eg, Pleur-evac). 

• Sterile Y connector (if 2 chest tubes are to be connected to the same suction 

apparatus). 

Positioning of the Patient

Tubes are usually inserted laterally when fluid, pus, or blood is drained, irrespective of 

whether air is also being removed. The patient should lie with the affected side up, and 

the ipsilateral arm extended over the head and grasping the top of the bed or the 

guardrail for security. 

Rarely, chest tubes are inserted anteriorly to evacuate a pure pneumothorax. The 

patient should be supine, with the head raised about 10 degrees. Position the bed or 

gurney at a comfortable height to prevent back strain for the operator. 


See Anatomy Review under Thoracentesis, above. Remember that the intercostal 

arteries and veins follow the inferior border of the rib. 

Procedure 

1. Prepare all necessary equipment, and arrange it on a sterile towel placed on a Mayo 

stand or bedside table. 

2. Select the proper chest tube for insertion. In patients with trauma, insert the largest 

tube available (usually 36-40F). In patients without trauma, use a 26-32F chest tube, 

either straight or curved. In a patient with pure pneumothorax, a smaller chest tube 

(12-20F) is usually sufficient. A general rule is that a large tube effectively drains any 

substance from the pleural space and thus is preferred in emergencies, when the 

diagnosis may be unclear. 

3. Assemble the suction apparatus according to the manufacturer's directions. 

4. Connect the suction apparatus to a wall suction outlet, and adjust the suction so that 

a steady stream of bubbles is produced in the water column. 


6. Determine the insertion site. Most tubes are inserted in the lateral thorax at the 

anterior axillary line, just lateral to the nipple. This places the tube in the 4th or 5th 

intercostal space, ensuring that it is above the dome of the diaphragm. Palpate the 

nearest rib, and double-check the position; liver or spleen laceration can occur if the 

patient is not properly positioned. 

7. Observing sterile technique, open the sterile instrument tray, arrange all necessary 

instruments, and make sure that everything is present. 

8. Sterilize the skin over the insertion site and a wide area around it. 

9. Again locate the rib for the insertion site, and anesthetize the skin over the mid to 

inferior aspect of the rib with the 1% lidocaine with the 10-mL syringe and 25-gauge 

needle. Then anesthetize the surface of the rib and the tissue superior to it with the 

22-gauge needle.

10. Drape the area around the insertion site. 

11. Using the No. 11 blade, make a horizontal incision through the skin along the inferior 

aspect of the rib. The incision should be about 11/2 times as wide as the tube selected. 

Incise the skin down to the subcutaneous tissue. 

12. Use the Mayo clamp with the tips down as a dissector. Spread the tips to open 

tissue planes, and create a tunnel aiming toward the superior aspect of the rib. Make 

sure the clamp stays next to the rib. 

13. When the Mayo clamp is just over the superior edge of the rib, close the clamp, and 

push it with steady pressure through the parietal pleura and into the chest. This 

maneuver requires more pressure than might be anticipated. Use steady, even, 

controlled pressure to provide control of the clamp after it has perforated the pleura. A 

lunging motion may cause a hole in the lung, liver, or spleen. 

Once the clamp has penetrated the pleural space, air, fluid, blood, or pus may escape 

during expiration. Tension pneumothorax will whistle as air escapes under pressure, 

and the lung will collapse further during inspiration, because free air has access to the 

pleural space. 

14. Widen the hole in the parietal pleura by spreading the Mayo clamp. 

15. If a tube of large diameter is to be inserted, use the index finger to dilate the tract 

and hole in the pleura. This maneuver also ensures that entry has been made into the 

pleural space and not into a space inadvertently created between the parietal pleural 

and the chest wall. 

16. Grasp the end of the chest tube along the index finger and guide the tube down the 

tract into the pleural space, making sure that the last hole in the chest tube is within the 

pleural space. If a curved tube is being used, direct it inferiorly so that it lies along the 

base of the pleural space. A straight tube may be positioned inferiorly, laterally, or 

superiorly, depending on the clinical situation. 

17. Connect the chest tube to the suction apparatus, and make sure that the level in the 

water column varies with respiration. Usually, fluid, blood, or pus drains from the tube, a 

sign that the tube is properly positioned in the pleural space (unless the tube was 

inserted for pure pneumothorax). Note: If the tube has been inadvertently inserted 

between the parietal pleural and the chest wall, no fluid will drain from the tube, and the 

level in the water column will not vary with respiration. 

18. Sew the tube to the chest wall with the silk suture. Partially close the incision with a 

mattress stitch, and use one throw of a square knot to close the skin around the tube. 

Then, wind both ends of the suture around the tube, starting at the bottom and working 

toward the top (as if lacing up a shoe). Tie the ends of the suture snugly around the top 

of the tube. 

19. Wrap Xeroform or petrolatum-impregnated gauze around the tube to seal it to the

skin. Cover the tube with two 10- × 10-cm (4- × 4-in) sterile gauze sponges, cut so that 

they fit around the tube. Tape the sponges and the tube in place. Tape connections of 

the chest tube to the suction tube, and tape the chest tube to the patient's side below 

the insertion site. 

20. Obtain a portable upright chest x-ray to check the position of the tube and to make 

sure that the lung is expanded and that all fluid has been evacuated. 

Emergency Thoracotomy (See Chapter 24.) 

Emergency thoracotomy is performed to gain access to the heart and great vessels. It 

can occasionally be life saving, although controversy exists over the indications and the 

location where it should be performed. It should be performed only when the patient can 

be taken immediately afterward to the operating room. 

Indications 

1. Traumatic cardiac arrest following penetrating chest trauma with signs of life in the 

prehospital setting (survival rate up to 40%). 

2. Traumatic cardiac arrest following penetrating or blunt trauma with signs of life in the 

emergency department (low survival rate for blunt trauma victims). 

3. Cardiac tamponade with profound shock; patient is unresponsive to rapid volume 

expansion, is deteriorating, and is unlikely to survive until operation. 

4. Blunt or penetrating trauma to the chest or abdomen with profound shock; patient is 

unresponsive to rapid volume expansion, is deteriorating, and is unlikely to survive until 

operation. 

5. Massive chest or abdominal bleeding with profound shock; patient is unresponsive to 

rapid volume expansion, is deteriorating, and is unlikely to survive until operation. 


1. Traumatic cardiac arrest with no signs of life in the prehospital setting (survival rate 

virtually nil). 

2. Appropriate operating facilities and personnel not immediately available. 

3. Patient immediately responsive to volume expansion or decompression of tension 

pneumothorax. 


One individual experienced in the technique is required to perform the procedure, 

another to maintain an airway and assist ventilation, and, ideally, a third to prepare and 

hand equipment to the operator. In most cases, patients have multiple, concomitant 

needs that are best met by a team.




• Scalpel with No. 10 blades. 

• Rib spreaders. 

• Vascular clamps. 

• Nonvascular clamps. 

• Suture scissors. 

• Metzenbaum scissors (long). 

• Needle holder (long). 

• Suture (2-0 silk or comparable) on cutting needle. 

• 10-in DeBakey tangential occlusion clamp. 

• Suction catheter. 

• Tissue forceps. 

• Bone rongeur. 

• Rib approximator. 


The patient should be supine. Place rolled sheet under the left scapula and lower ribs, 

and elevate the left arm above the head to expose the left chest and axilla. The patient 

should be intubated and ventilated with positive pressure (manual bag-valve method or 

mechanical ventilator). Advance the endotracheal tube to selectively intubate the right 

main-stem bronchus. This allows the left lung to be manually collapsed providing access 

to the heart. Remember to decrease tidal volumes by half and increase the respiratory 

rate to compensate for ventilation of a single lung. 


The favored approach to the heart in an emergency setting is through a left 

thoracotomy. The incision follows the rib interspace, with care taken to avoid the 

intercostal vessels that run beneath each rib. The internal mammary artery runs parallel 

to the lateral margin of the sternum and must be ligated should hemorrhage from this

vessel occur. 

Procedure 

1. Prepare the anterior thoracic surface generously on both sides with skin-sterilizing 

solution, and cover it with sterile drapes to the extent that time allows. 

2. Using the No. 10 scalpel blade, make a horizontal incision in the left 4th or 5th 

intercostal space, extending from the sternum to the posterior axillary line. It should be 

deep enough to expose the intercostal muscles and should follow the superior rib 

margin to avoid injury to the intercostal vascular bundle beneath the rib above. In 

women, make the incision beneath the breast. 

3. With a scalpel or scissors, make a small opening through the intercostal muscles into 

the pleural space. Using Metzenbaum scissors, divide the intercostal muscles the entire 

length of the incision, remaining close to the superior margin of the rib. Ligate the 

internal mammary artery above and below. Using the scalpel or heavy scissors, cut 

through 2 sternocostal cartilages above the interspace. 

4. Insert a rib spreader and spread the ribs as widely apart as possible. If necessary 

(eg, in penetrating trauma to the right chest), the incision may be extended across the 

sternum and into the right chest to increase exposure. 

5. Inspect the heart. It will appear to be bluish if cardiac tamponade is present. To 

relieve tamponade or perform cardiac massage, open the pericardium. Pick up the 

pericardium with forceps and incise it from apex to base, using Metzenbaum scissors. 

Be careful to avoid the phrenic nerve, which courses longitudinally along the lateral 

heart margin. Remove any clotted blood; suction excess blood as needed. 

6. If observable cardiac contractions are inadequate, or if cardiac arrest has occurred, 

perform internal cardiac massage by gently compressing the heart with both hands. If 

ventricular fibrillation is present, a quivering motion will be observed. Perform 

defibrillation using the internal paddles, at an energy level of 5-50 J. If a myocardial 

laceration is present, it can be temporarily controlled with a fingertip or with a 3-0 

polypropylene suture. Horizontal mattress sutures through Teflon pledgets will help 

prevent further laceration of the myocardium. Place sutures through the epicardium and 

myocardium only. Avoid the coronary arteries. Atrial wounds can be repaired with 

simple interrupted sutures. 

7. Control massive bleeding from the lung or pulmonary vessels by cross-clamping the 

hilum of the involved lung. 

8. If the patient fails to respond rapidly to volume administration, or if intra-abdominal 

bleeding is suspected, incise the overlying pleural and cross-clamp the aorta above the 

point where it enters the diaphragm. Be careful to avoid clamping the esophagus. As a 

temporary measure during internal cardiac massage, the aorta may be occluded with 

the index and long fingers placed behind the heart. 

9. If resuscitation is successful, immediately transport the patient to the operating room

for definitive care. 

PERICARDIOCENTESIS 

Blind aspiration of the pericardium was formerly the only way to detect and treat a 

pericardial effusion. Complications of this technique included pneumothorax, myocardial 

or coronary artery laceration, and iatrogenic pericardial tamponade. Many emergency 

departments currently utilize bedside ultrasound to detect pericardial effusion. 

Ultrasound is quick, noninvasive, and can even provide guidance for pericardiocentesis 

in the symptomatic patient with pericardial effusion. Blind pericardiocentesis should be 

reserved for those situations in which a critically ill patient is suspected of having 

tamponade and no diagnostic tests are rapidly available to assist in the diagnosis or 

treatment. 

Indications 

The following description of pericardiocentesis assumes bedside emergency ultrasound 

or echocardiography are not rapidly available to evaluate and treat a suspected 

pericardial tamponade. 


In a patient who requires pericardiocentesis for decompensated or rapidly 

decompensating cardiac tamponade, there are no contraindications. In other patients, 

the following conditions are contraindications: 

• Infection along the proposed course of pericardiocentesis. 

• Bleeding diathesis (relative contraindication, especially if it can be corrected). 


Three people are required to perform pericardiocentesis: the operator and an assistant 

to monitor the electrocardiograph, and another physician besides the operator. A 

cardiothoracic surgeon should be available in case complications occur. 


Many hospitals have prepackaged sterile pericardiocentesis trays that contain many of 

the required items. If these are not available, the following instruments and materials are 

required: 




• Pericardiocentesis needle: 17-gauge, 12.5-cm (5-in) thin-walled steel needle (usually a

spinal needle) for aspiration. It is possible to use 16-gauge and even 14-gauge needles 

with plastic outer cannulas. 

• Syringes: assorted sizes, including 50-mL (2), 30-mL (2), 10-mL (2), and 5-mL (1). 


• Sterile conductive monitoring cable with alligator clamps at each end. 


• Silk suture (5-0) on a cutting needle. 

• Straight clamp and needle holder. 

• Needles: assorted sizes, including 25-gauge, 1.5-cm (5/8-in) (1); 22-gauge, 2.5-cm 

(1-in) (2); and 19-gauge, 4-cm (11/2-in) (5), for transferring specimens. 

• Drapes. 

• Sterile, capped, 15-mL specimen tubes (10). 

• Heparin, to lightly heparinize cytologic specimen tubes. 

• Specimen tubes, 1 purple-topped and 3 red-topped. 

• Clean glass microscope slides. 

• Microhematocrit centrifuge tubes with occlusive sealant. 

• Ice bucket to hold cytologic specimens. 

• Sterile dressing for entry and exit sites. 

• CPR cart and equipment and electrocardiograph. 


The patient should be supine, and if time permits, the thorax should be elevated 30 

degrees. Optimize bed height and lighting for the operator. 

Procedure 

A. Patient Preparation 

Take the following steps, if time permits: 

1. The patient should be in a bed where cardiac monitoring is available, preferably in a 

cardiac catheterization laboratory.

2. Position the patient, as described above. 

3. Begin electrocardiographic monitoring with limb leads. 

4. Gain secure intravenous access. 

5. Give atropine, 0.6-1 mg intramuscularly or subcutaneously, before pericardiocentesis, 

because vagal responses during cardiac tamponade may be devastating. 

6. Narcotics may be used as long as they do not depress consciousness or respiration. 

7. Supplemental oxygen, 5-10 L/min, by mask or nasal cannula is advisable. 

B. Observe Sterile Technique 

1. Don cap, mask gloves, and gown. 

2. Sterilize the skin in a wide area around the xiphoid process. 

3. Drape the field widely with sterile towels if time permits. 

C. Begin Pericardiocentesis 

1. Locate the appropriate site to the right of and below the xiphoid process (Figure 

6-26), and anesthetize the skin with the 1% lidocaine with the 10-mL syringe and 

25-gauge needle. Switch to the 22-gauge needle, and anesthetize the tissue beneath 

the xiphoid process along the track of the pericardiocentesis needle. Omit this step if the 

patient is comatose. 

2. A small incision in the skin with the No. 11 scalpel blade may facilitate entry of the 

pericardiocentesis needle. 

3. With the help of an assistant, attach the conductive monitoring cable to the chest 

terminal lead of the electrocardiograph using one of the alligator clamps. Attach the 

other end to the hub of the pericardiocentesis needle. Operate the electrocardiograph 

on the V lead setting. The pericardiocentesis needle then becomes a probing 

electrocardiographic lead. 

4. With the alligator clamp and conductive monitoring cable mounted, attach the 

pericardiocentesis needle to a 30-mL syringe. 

5. Perform pericardiocentesis. If this procedure is being done during active CPR, make 

sure that everything is ready beforehand, work rapidly, and stop CPR for only as long as 

necessary. Enter the selected site, just caudal and to the right of the xiphoid process, 

and direct the needle at an angle of 30-45 degrees to the skin. Aim toward the patient's 

right shoulder. Advance the needle slowly, and aspirate the fluid continuously. There is 

usually a palpable feeling of resistance when the needle pierces the parietal 

pericardium. 

If the attempt to penetrate the pericardium is unsuccessful and no fluid is aspirated,

ing the needle back to the subcutaneous tissue, and direct it more medially. Continue 

either until fluid is aspirated or until the needle hits the right side of the sternum, at 

which point it is safer to use fluoroscopic or echocardiographic guidance. 

Pericardial aspiration by an anterior left intercostal approach (usually the 4th left 

intercostal space just left of the sternum) is less satisfactory because it penetrates the 

pleural space and has a potential for laceration of the left anterior descending coronary 

artery or a branch of the internal mammary artery. This approach may be used as a last 

resort in a dying patient. 

6. Have an assistant continuously monitoring the electrocardiograph during the 

procedure. When fluid is aspirated and is flowing freely, the needle can be anchored at 

the chest wall with a surgical clamp to keep it from penetrating any farther. A myocardial 

current of injury or precipitation of arrhythmias on the electrocardiograph is a sign to 

slowly withdraw the needle until fluid is aspirated. In cardiac tamponade due to 

pericardial hemorrhage, the fact that pericardial blood does not clot (whereas 

intracardiac blood does) may be a helpful diagnostic clue. 

7. Aspirate until the pericardium is dry by slowly withdrawing fluid under constant 

electrocardiographic monitoring. Secure any specimens that are required for diagnostic 

tests. In the presence of decompensated cardiac tamponade, removal of even a small 

amount of pericardial fluid should result in a dramatic improvement in the patient's 

hemodynamic status. 

8. After aspiration is completed, withdraw the needle, and gain hemostasis with 

pressure. A single suture may be required. 

9. Cover the entry site with a sterile dressing. 

FOCUSED ASSESSMENT WITH SONOGRAPHY FOR TRAUMA 

Focused assessment with sonography for trauma (FAST) is a rapid, noninvasive 

technique for determining the presence of intra-abdominal fluid (eg, blood or urine) in 

the trauma victim. It does not detect retroperitoneal fluid collections or hollow viscus 

injury such as bowel perforation. The FAST exam is a quick screening tool and should 

be performed after the primary survey of the trauma victim. 

Indications 

• Blunt thoracoabdominal trauma. 

• Penetrating thoracoabdominal trauma. 

• Suspected pericardial tamponade. 

• Undetermined origin of hypotension in trauma patient. 

Contraindications

The FAST exam is contraindicated in the unstable trauma victim who requires 

immediate surgery. 


One operator can perform a FAST exam unaided. 


• Ultrasound transmission gel (hypoallergenic). 

• Ultrasound machine with 2.5- to 7.0-MHz transducer. Higher frequency allows for 

better resolution; however, a 3.5-MHz transducer is usually adequate for FAST exams 

performed on the adult trauma victim. 

• An attached printer that allows images viewed to be transferred to photographic paper 

for documentation. 


The patient should be supine on a level surface. Reverse-Trendelenburg position 

increases the sensitivity in the suprapubic view. 


FAST exams evaluate fluid collections in 4 anatomic locations. In the chest, the 

pericardial sac is viewed. In the abdomen, the Morison pouch in the right upper 

quadrant, the splenorenal recess in the left upper quadrant, and the pouch of Douglas in 

the suprapubic area are viewed. To optimally view the pelvis, a full bladder is required. 

When a Foley catheter is inserted before or during the FAST exam, remember to have 

the Foley drainage tubing clamped so as not to decompress the bladder. The distended 

bladder provides a good "acoustic window" to identify free fluid in the pelvis. 

Procedure 

1. Set up the ultrasound machine for FAST exams as instructed by the machine's 

manufacturer. 

2. Enter the patient's name and medical record number using the machine's annotation 

keys. 

3. Expose the patient's thoracoabdominal area and place ultrasound transmission gel in 

the following 4 locations: pericardial area, right upper quadrant, left upper quadrant, and 

suprapubic area (Figure 6-27). 

4. Orient the transducer for sagittal sections of the body and place it in the subxiphoid 

region. This view identifies pericardial fluid collections. 

5. Next, place the transducer on the right midaxillary region between the 4th and 5th ribs

to view the Morison pouch. Keep the transducer in the intercostal space to avoid 

shadows created by the ribs. 

6. Move the transducer, still in the sagittal plane, to the left posterior axillary line 

between the 9th and 11th ribs to view the splenorenal recess. 

7. Finally, place the transducer, now oriented for the transverse view, about 4-5 cm 

superior to the pubic symphysis in the midline to view the pouch of Douglas. 

8. Each view should be frozen on screen and printed. This documentation should be 

placed with the patient's medical record. Performing and interpreting FAST exams is not 

a difficult procedure, but it requires hands-on training, which should be undertaken by 

any emergency physician wishing to become prolific in its use. 

Limitations 

A FAST exam is helpful when the findings are positive; however, a negative study must 

be evaluated further (eg, with computed tomography [CT] scan, repeat evaluations, 

observation). A falsely negative FAST exam can result from several factors: 

• Too little time has elapsed since the trauma for the blood to accumulate. 

• Bleeding may be retroperitoneal and not visible on FAST exam. 

• Solid organ injury with encapsulated bleeding is present. 

• Hollow viscus injury is present. 

• Inadequate volume of fluid. As little as 50 cc of fluid can be detected; however, it may 

take up to 250 cc of fluid to create an unequivocally positive FAST exam. 

ABDOMINAL PARACENTESIS 

Indications 

Indications for abdominal paracentesis are as follows: 

• To determine the cause of ascites, including suspected intra-abdominal hemorrhage 

from trauma. 

• To lower intra-abdominal pressure in tense ascites (rarely indicated in the emergency 

department). 

• To obtain fluid for analysis and culture in patients with ascites who are thought to have 

an infection. 


The following conditions are relative contraindications to abdominal paracentesis, and

most can be corrected or circumvented if paracentesis must be performed: 

• Bleeding diathesis (coagulopathy or thrombocytopenia). Correct severe bleeding 

diathesis before performing paracentesis. Cautious paracentesis with a 22-gauge 

needle may be safely performed in patients with mild to moderate bleeding tendencies. 

• Previous abdominal surgery. 

• Severe bowel distention (correct with nasogastric suction and a rectal tube before 

performing paracentesis). 


One person can perform paracentesis unaided if the patient is cooperative. An assistant 

may be helpful if the patient is obese. 





• Needles in various sizes, including a longer 20- or 22-gauge spinal needle and a 

19-gauge catheter-clad needle (eg, Angiocath). Use a 22-gauge, 4-cm (11/2-in) needle 

or spinal needle in patients with severe bleeding diathesis. 


• Drapes. 

• Specimen tubes, both with and without anticoagulant, and a blood culture bottle. 

• Ice bucket for cytology specimens. 



• Tape and dressing material. 

• Three-way stopcock, connector tubing, and 500-mL collection bottle (if therapeutic 

paracentesis is planned). 


Have the patient supine at the edge of the bed nearest the operator (right side of the 

bed for a right-handed operator), with the trunk elevated 45 degrees. Allow 10 minutes

for ascites to pool in the dependent portion of the abdomen and for air-filled bowel to 

float up away from the puncture site. Be sure the bladder has been emptied by voiding 

or catheterization. 

The patient can be tipped 30 degrees to either side if paracentesis of the lower 

quadrants is necessary. Limited ascites can be aspirated successfully by having the 

patient bridge 2 beds or a bed and a chair on hands and knees. The approach in this 

case (a somewhat cramped one for the operator) is from below upward into the 

dependent abdomen. 

Procedure 


2. Sterilize the skin between the umbilicus and symphysis pubica and both lower 

quadrants. 

3. Drape the field widely. 

4. Using the 25-gauge needle, anesthetize the skin with the 1% lidocaine in the 10-mL 

syringe at the selected puncture site. The preferred site is on the poorly vascularized 

linea alba, about halfway between the symphysis pubica and the umbilicus (Figure 

6-28). Change to the 22-gauge needle, and anesthetize down to and including the 

peritoneum. 

5. Attach the 19-gauge catheter-clad needle to a 50-mL syringe. In patients with severe 

coagulopathy and thrombocytopenia, use a 22-gauge needle. In markedly obese 

patients, use a 20-gauge spinal needle. 

6. Puncture the skin. Keeping the needle perpendicular to the abdominal wall, maintain 

continuous negative suction in the syringe while slowly advancing the needle. In tense 

ascites, it may be useful to try Z-tracking the needle to minimize persistent leaking of 

ascitic fluid; that is, after penetrating the skin, move the needle and syringe 1-2 cm ( 3/8 

-3/4 in) before piercing the subcutaneous tissue, but maintain the perpendicular 

approach. Repeat this maneuver at the level of the peritoneum, thus describing an 

oblique Z pattern through the various layers of tissue. In this manner, the track of the 

needle from the skin to the peritoneal space will not be a continuous line when the 

needle is removed. 

7. The dense connective tissue of the peritoneum will yield a noticeable "pop" when 

pierced. 

8. Fluid should flow freely into the syringe. To avoid bowel or visceral trauma, 

particularly in patients with bleeding tendencies, it is preferable to remove the steel 

needle, leaving the plastic catheter in place while specimens are collected. The patient 

can be safely moved into more dependent positions with the plastic catheter in place to 

facilitate draining of sufficient fluid for analysis. In most cases of diagnostic 

paracentesis, a single collection of 50 mL is adequate. At a minimum, fluid should be 

sent to the laboratory for cell count, tests for protein, cultures, and staining with Gram

stain. For suspected neoplasia or for therapeutic relief of tense ascites, up to 1 L may 

be removed, although 750 mL is a more prudent upper limit in order to avoid adverse 

effects on intravascular volume. A 3-way stopcock can be used to minimize leakage 

while the operator is continually aspirating with a syringe. Alternatively, drainage can go 

directly into sterile 250- to 500-mL vacuum containers using connecting tubing. 

9. After samples have been collected, remove the catheter or needle, and apply firm 

pressure to the site for 5 minutes. 

10. Apply topical antibacterial ointment, and dress the site with a pressure dressing. 

11. If leaking of ascitic fluid persists despite a pressure dressing, close the paracentesis 

tract with a mattress stitch. 

PERITONEAL CATHETER INSERTION & PERITONEAL LAVAGE 

Indications 

Peritoneal lavage is performed to determine if intraperitoneal hemorrhage has occurred. 

With the proliferation of CT scanning and FAST exams, peritoneal lavage is used less 

frequently; however, it continues to have a role in evaluation of the trauma victim when 

the victim is too unstable to be sent for CT scan or if ultrasound is inconclusive. 


Contraindications to peritoneal lavage are as follows: 

• Previous intra-abdominal surgery of any kind. 

• Pregnancy. 

• Unstable patient who requires immediate surgery. 


One operator and an assistant are required for peritoneal lavage using the 

percutaneous approach. Alternatively, one operator and two assistants are required for 

peritoneal lavage using the operative approach. 


Prepackaged trays with the necessary equipment are available commercially, or they 

can be made up by the hospital. The following items are required: 



• Sterile towels (4) or sterile paper drapes.



• Peritoneal lavage catheter (11-18F) and introducing stylet. 

• Sterile bottle containing 1 L of lactated Ringer's injection or normal saline, with 

intravenous connector tubing. 

• Nylon suture (size 4-0) on a cutting needle (percutaneous approach); chromic catgut 

(size 3-0) plus silk, nylon, or polypropylene sutures (size 3-0) (operative approach). 

BR>• Needle holder and straight scissors. 


• For operative technique only: 2 Allis or Kocher clamps, 1 Kelly clamp, and 2 small 

right-angle retractors. 


The patient should be supine on a level surface. Examine the abdomen for scars; do not 

perform peritoneal lavage if abdominal surgery has been performed previously. Take 

diagnostic abdominal x-rays before performing peritoneal lavage (the procedure may 

produce artifacts on the x-ray [eg, ileus or intraperitoneal air]). 

Procedure 

A. Preparatory Measures 

1. Drain the bladder (by urination or catheterization, as required). Place nasogastric 

tube. 

2. Position the patient, and check to see that all equipment is at hand. 

3. Sterilize the skin of the anterior abdominal wall from the umbilicus to the symphysis 

pubica. 

4. Drape the operative site. 



skin about 2 cm (3/4 in) caudal to the umbilicus in the midline. Then, directing the 

needle perpendicularly to the anterior abdominal wall, infiltrate the fascia (linea alba), 

preperitoneal space (between peritoneum and fascia), and parietal peritoneum. The 

needle will encounter resistance when it reaches the peritoneum. 

B. Percutaneous Approach 

1. Using the No. 11 blade, make a 0.5-cm (1/4-in) transverse incision through the skin

and fascia to allow easy passage of the catheter and stylet. 

2. Carefully insert the catheter and stylet into the anesthetized tract with gentle, steady, 

controlled pressure. (Caution: The abdominal aorta lies in the path of the catheter.) 

Control is best achieved by making sure that both hands are comfortably placed on the 

patient's abdomen and by advancing the catheter with steady pressure applied by the 

thumb and forefinger. Advance the catheter through the peritoneum and into the 

peritoneal cavity. There will be a definite give ("pop") as the catheter penetrates the 

peritoneum. 

3. Once the catheter has penetrated the peritoneal cavity, slide it off the stylet and into 

the peritoneal cavity. The catheter should slide easily. If any resistance is encountered, 

withdraw the catheter and stylet together, and attempt insertion again. Difficulty in 

advancing the catheter may indicate that the stylet has not entered the peritoneal cavity 

and that the catheter is being inserted into the space between the peritoneum and the 

fascia; alternatively, there may be adhesions in the peritoneal cavity that have fixed the 

intraperitoneal structures. Failure to make this important distinction may result in 

false-positive or false-negative findings or perforation of intraperitoneal structures. 

C. Operative Approach 

With this approach, a superficial laparotomy is performed to permit direct visualization of 

the peritoneum when the catheter is inserted. The advantage of this approach is that 

inadvertent insertion of the catheter into the preperitoneal space is unlikely to occur; 

however, more personnel are required to perform the procedure. 

1. After the area has been anesthetized, use the No. 11 blade to make a 3-cm (13/16-in) 

vertical incision in the midline about 1 cm ( 3/8 in) inferior to the umbilicus. 

2. Using the Kelly clamp, bluntly dissect through subcutaneous tissue to the fascia of 

the abdominal wall. Then incise the fascia for the length of the incision. Again using a 

Kelly clamp, spread the preperitoneal fat, and expose the parietal peritoneum. 

3. Using 2 Allis or Kocher clamps, grasp the peritoneum, and lift it up to free it from any 

underlying visceral structures. (Grasp a bit of peritoneum with one clamp, grasp another 

bit with the second clamp about 1-2 cm [ 3/8 -3/4 in] away, and release the first clamp. 

Repeat as needed. This method of alternately grasping and releasing the peritoneum 

separates it from underlying structures.) 

4. Holding the peritoneum up between 2 clamps (Allis or Kocher), make a small stab 

wound through the peritoneum with a No. 11 scalpel blade. 

5. Insert the catheter into the peritoneal cavity under direct vision. 

D. Results 

With either approach, gross blood may return after the catheter has been placed and 

the stylet has been removed. This finding signifies extensive intraperitoneal 

hemorrhage, and the patient should be prepared for surgery. 

1. If blood does not return immediately, connect the intravenous tubing to the catheter,

and instill 1 L of sterile, warm Ringer's lactate or normal saline (Figure 6-29). Gently 

massage the abdomen to spread the fluid, and roll the patient from side to side to make 

sure that the lavage fluid reaches all areas of the peritoneal cavity. Lower the 

intravenous bottle to the floor. The fluid in the peritoneal cavity should flow out of the 

cavity and back into the bottle. Again, roll the patient from side to side to return as much 

fluid as possible to the bottle. 

2. After as much of the fluid as possible has been removed from the peritoneal cavity (a 

reasonable return is 75-80% of the fluid instilled), remove the catheter, and close the 

incision. Use the size 4-0 nylon skin suture if the percutaneous approach was used, and 

cover it with an adhesive dressing. To close the incision made for the operative 

approach, close the peritoneum with chromic catgut sutures; close the anterior 

abdominal fascia with interrupted silk, polypropylene, or nylon sutures; approximate the 

subcutaneous tissue with absorbable sutures; and close the skin. 

If immediate laparotomy is necessary, leave the incision open, and cover it with a sterile 

dressing that has been soaked in saline. 

3. Make sure to record the amount of any excess fluid left in the patient's peritoneal 

cavity as fluid input on the fluid intake and output computation sheet. 

Interpretation 

Significant intraperitoneal hemorrhage is indicated by grossly bloody lavage fluid or 

gross blood coming from the catheter. Lavage fluid with a hematocrit of 1% or higher 

also indicates significant intraperitoneal hemorrhage and suggests the need for 

laparotomy. Completely clear fluid indicates lack of significant intraperitoneal bleeding. 

INSERTION OF INDWELLING (FOLEY) URINARY CATHETER 

Indications 

Indications for insertion of an indwelling urinary catheter are as follows: 

• Diagnostic or therapeutic drainage of the urinary bladder. 

• Need for a reliable and frequent assessment of urine output (eg, for treatment of 

shock). 

• Need to perform retrograde cystography. 


The following are only relative contraindications to insertion of an indwelling urinary 

catheter: 

• Previous urethral surgery. 

• Suspected or known urethra trauma (free-floating prostate, blood issuing from urethra

meatus). In this case, perform a urethrogram before urethral catheterization is 

attempted. 


One person can insert an indwelling urinary catheter unaided. An assistant is helpful if 

the patient is uncooperative. 


Note: Most hospitals have disposable Foley insertion trays that contain most of the 

items listed below except for the catheter. It is important to check to see that the tray 

contains all of the needed materials and that the catheter, if it is supplied with the set, is 

of the proper size and desired material and has a balloon of the proper size. 

• Foley catheter of the appropriate size, material, and contour (different catheters are 

discussed below). 

• Urinary drainage bag and connecting tube. 

• Sterile lubricant. 

• Antiseptic solution and sterile cotton balls to sterilize the male urethral meatus and the 

female perineum. 

• Sterile syringe, 5- to 10-mL, filled with enough sterile water to inflate the balloon on the 

catheter. The size of the balloon is usually printed on the catheter (usually 5 mL). 

• Sterile gloves and drapes. 

Selecting a Catheter 

The Foley catheter is used in almost all cases when an indwelling urinary catheter is 

required. It consists of a double-lumen rubber tube with a terminal retaining balloon. The 

larger channel is for drainage of urine, and the smaller is for inflation of the balloon. 

Some indwelling catheters have a third lumen, for constant bladder irrigation. Foley 

catheters are of standard length (46 cm [18 in]) but come in varying diameters that are 

numerically graded (French system), with the larger number indicating a larger 

diameter. Two sizes of balloon are commonly available: 5-mL balloons for routine 

catheterizations and 30-mL balloons for special situations. Most Foley catheters are 

made of rubber. Teflon or Silastic is sometimes used for long-term, indwelling catheters. 

(Specialized shapes and contours are not discussed here, because they should be 

inserted by a urologist.) 

• For routine, short-term catheterization in males or females, a 14F or 18F rubber 

catheter with a 5-mL balloon is satisfactory. Smaller sizes are required for children. 

• Men with prostatic hypertrophy may require larger catheters (eg, 20-22F).


A. Females 

The patient should be in the lithotomy position. If she is comatose or under anesthesia, 

flex her knees and hips, and allow the legs to abduct. If the soles of the feet are pressed 

together, this position can easily be held by the patient without assistance. 

B. Males 

The patient should be supine. 


A. Females 

The female urethra is short, and because there is no prostate gland, passage of a 

catheter is relatively easy. The only difficulty is locating the urethral meatus, which lies 

in the superior fornix of the vulva, above the vaginal opening and below the clitoris. It 

appears as a small dimple or slit in the midline. 

B. Males 

The urethra leaves the bladder at the trigone, passes through the prostate, and then 

runs the length of the penis to exit at the meatus at the tip of the glans. 

Procedure 

A. Catheterization of Females 


2. Open the catheter tray and selected catheter, and position them on a sterile field 

placed on a bedside table or stand so that all required materials are readily accessible. 

3. Place a generous amount of lubricant on the sterile field. 

4. Put on sterile gloves, and drape the perineal area. 

5. Make sure that the catheter is open and the lubricating jelly is accessible. 

6. Open the antiseptic packet, and moisten the cotton swabs provided with antiseptic. 

7. Be sure that the syringe is filled with enough sterile water to inflate the balloon being 

used. 

8. Using the left hand (standing on the patient's right side), spread the labia and identify 

the superior fornix with the clitoris at the apex. Thoroughly cleanse the entire area with 

4-5 swabs soaked in antiseptic. Clean the labia with front to back strokes with 2 

successive swabs; then cleanse the urethral meatus with another 2 successive swabs. 

9. The left hand continues to hold the labia spread apart from the rest of the procedure.

10. Make a loop in the Foley catheter for easier handling. Grasp the catheter with the 

right hand, coat the tip and proximal portion with lubricating jelly, and insert the catheter 

into the urethral meatus, which lies just below the clitoris. Advance the catheter until 

urine returns. Then advance it 4-5 cm (15/8-2 in) farther to make sure that the balloon is 

well within the bladder. 

11. Inflate the balloon with the appropriate amount of sterile water (usually 5 mL; the 

balloon volume is usually printed on the catheter), and withdraw the catheter gently until 

the balloon is pulled snugly against the trigone (Figure 6-30). 

12. Collect a small amount of urine in a sterile container for appropriate studies 

(urinalysis should be obtained routinely), and then connect the catheter to the urinary 

drainage bag. 

13. Tape the Foley catheter and the urinary drainage tube to the upper thigh, leaving 

enough slack so that abduction of the legs will not put tension on the catheter. 

14. Note: The most common mistake in catheterization of the female bladder is to miss 

the urethral meatus and inadvertently slip the catheter into the vagina. No urine will 

return. Leave the catheter in place in the vagina as a marker. Obtain a new, sterile 

catheter, and try again. Remove the other catheter. 

B. Catheterization of Males 

7. Steps 1-7 are the same as those described under Catheterization of Females, above. 

8. Using the left hand (standing on the patient's right side), grasp the penis so that the 

shaft lies in the palm and the glans of the penis is free but secure. The penis should be 

held at a right angle to the abdomen. The left hand should remain in this position for the 

remainder of the procedure; it is no longer sterile. 

9. Sterilize the glans and urethral meatus with 3-4 swabs dipped in antiseptic. 

10. Put a single loop in the Foley catheter for easier handling, grasp the catheter in the 

right hand, and coat the tip of the catheter with lubricating jelly. It is often helpful to place 

some on the meatus as well. 

11. Insert the catheter into the urethral meatus, and advance it down the penile urethra 

to the base of the penis with successive, steady movements. 

12. Advance the catheter through the membranous and prostatic urethra into the 

bladder. 

13. Advance the catheter to the hilt (even if urine is obtained earlier) to ensure that the 

balloon is not inflated in the urethra. As soon as the catheter has been advanced to the 

hilt, release the penis to free both hands for inflation of the balloon. 

14. Inflate the balloon with the proper amount of sterile water for its size (usually 5 mL), 

and withdraw the catheter until the balloon is pulled snugly against the trigone.

15. Obtain a specimen for appropriate tests (at a minimum, routine urinalysis should be 

performed). Connect the urinary drainage system bag to the catheter, and tape the 

catheter to the upper thigh, leaving sufficient slack so that movement of the leg will not 

pull on the catheter. 

Problem Solving 

A. Males with Prostatic Enlargement or False Urethral Passages 

Conventional technique usually fails in patients with significant prostatic hypertrophy or 

false urethral passage. Listed below are a few techniques that have proved successful 

in catheterizing these patients. Caution: Reasonable persistence in attempting 

catheterization is acceptable; however, there comes a time when further manipulations 

may rupture the urethra or create new false passages. If attempts using the guidelines 

outlined below are still unsuccessful, consult a urologist, or insert a suprapubic catheter 

instead (see below). 

1. Increase the size of the catheter—Large catheters are stiffer and provide more 

forceful dilatation of the prostatic urethra. The larger, blunt tip tends to follow the true 

urethra rather than smaller false passages. 

2. Lubricate the urethra—Fill a 30- to 50-mL sterile catheter-tipped syringe with the 

lubricating jelly and inject the jelly down the urethra with gentle pressure until no more 

can be injected. Then insert the catheter. 

3. Inject lubricating jelly while the catheter is being passed—Fill the syringe as 

outlined above, insert the tip into the catheter, and fill the catheter with jelly. As the 

catheter is being passed, slowly inject more lubricant to ensure that the entire length of 

the catheter is lubricated and to help dilate the urethra just ahead of the catheter tip. 

4. Use a Coude catheter—A Coude catheter has an upwardly deflected tip, which may 

navigate through a narrowed prostatic urethra more successfully than a standard Foley 

catheter. 

B. Traumatized Patients 

Most patients with major trauma have a Foley catheter inserted during resuscitation. A 

rectal examination must be performed before a catheter is inserted in a male patient 

with major blunt trauma. Feel for the prostate and make sure that it is firmly attached to 

the surrounding tissues. A free-floating prostate or gross blood escaping from the 

urethra signifies urethral rupture until proved otherwise. In either case, Foley 

catheterization is contraindicated, and a suprapubic catheter should be inserted instead. 

PERCUTANEOUS SUPRAPUBIC CYSTOTOMY 

Suprapubic bladder cystostomy is a means of bypassing the urethra to provide drainage 

of the urinary bladder. 

Indications

Suprapubic bladder cystostomy is performed to provide bladder drainage when 

transurethral drainage is unsuccessful or contraindicated. 


Contraindications to suprapubic cystostomy are as follows: 

• Nondistended, nonpalpable bladder. 

• Carcinoma of the bladder, because percutaneous catheterization of the bladder might 

lead to seeding of the cancer along the track of the catheter. 

• Gross hematuria, which would require a tube of large diameter to drain clots from the 

bladder. 

• Recent cystostomy (the percutaneous technique might disrupt suture lines). 


One person can perform percutaneous suprapubic cystostomy unaided, although an 

assistant may be helpful, particularly if the patient is uncooperative. 


Many prepackaged commercial kits are available for percutaneous suprapubic 

cystostomy. The following items are required: 



• Lidocaine, 1%, with 10-mL syringe and 25-gauge, 1-cm (1/2-in) and 22-gauge, 4-cm 

(11/2-in) needles. 


• Razor. 


• Catheter-clad needle (eg, Angiocath), 14-gauge, 30-cm (12-in); or other commercially 

manufactured percutaneous suprapubic catheter set. A central venous catheter kit can 

also be used if no other equipment is available. 


• Closed urinary drainage system (sterile intravenous tubing and empty intravenous bag 

or bottle).

• Silk suture (size 3-0) on a curved cutting needle. 


• Suture scissors. 

• Antibacterial ointment. 

• Sterile gauze sponges, 5 × 5 cm (2 × 2 in), and tape. 

• Rolled bath towel for placement under the patient's hips. 


The patient should be supine, with a rolled-up towel placed under the hips. 


The urinary bladder lies in the midline of the lower abdomen. When it is distended, its 

position can be detected by palpation or percussion. 

Procedure 

1. Locate the distended bladder by palpation, percussion, or ultrasonography. If the 

bladder cannot be located, percutaneous suprapubic cystostomy should not be 

performed. If the bladder is not distended, it can usually be filled by oral or intravenous 

hydration. 

2. Prepare the area just above the symphysis pubica by shaving the pubic hair and 

sterilizing the skin. Extend the sterile field with drapes. 



5. Determine the insertion point by measuring cephalad 1-2 cm ( 3/8 -3/4 in) from the 

superior edge of the symphysis pubica in the midline (Figure 6-31). 


skin at the point of insertion. Then switch to the 22-gauge needle to anesthetize the 

subcutaneous tissue and anterior wall of the bladder. If the position of the needle is 

correct, urine can be aspirated through the needle. Remove the needle. 

7. Make a 0.5-cm (3/16-in) transverse incision in the skin over the anesthetized area 

with the No. 11 scalpel blade. 

8. The technique for placing the catheter depends on the type of catheter used:

a. Catheter-clad needle: 

(1) Attach a 50-mL syringe to the 14-gauge, 30-cm (12-in) catheter-clad needle. 

(2) Insert the catheter unit through the skin incision. 

(3) Advance the catheter caudally at a 50- to 60-degree angle to the abdominal surface. 

Advance the catheter with a smooth, deliberate motion, and steady the guiding hands 

on the patient's abdomen as necessary. A "give" is felt as the catheter and needle 

penetrate each successive layer of the fascia and bladder wall. Maintaining gentle 

suction with the syringe will cause aspiration of urine as soon as the bladder cavity has 

been entered. 

(4) Once the bladder has been entered, slip the catheter tip off the needle by holding 

the hub of the needle in the left hand and advancing the catheter with the right. 

(5) Advance the catheter about 6-8 cm (23/8-31/8 in) to make sure that enough of it is 

within the bladder. 

(6) Attach the sterile intravenous tubing to the catheter hub. If no assistant is available, 

reattach the 50-mL syringe to the tubing to keep the system closed. Otherwise, have an 

assistant attach the end of the tubing to the empty intravenous bag or bottle that is to 

receive the urine. 

(7) Suture the catheter in place at the insertion site with the size 3-0 silk suture. Wind 

the ends of the suture around the catheter at least 3 times to make sure that it is 

secured to the abdominal wall. 

(8) Apply antibacterial ointment to the insertion site, cover it with sterile 5- × 5-cm (2- × 

2-in) gauze sponges, and tape the sponges in place. 

(9) If not done earlier, attach the end of the tubing to the empty intravenous bag or 

bottle that is to receive the urine. 

(10) Tape all connections. 

b. Central venous catheter kit. Use the Seldinger technique, as previously discussed, to 

insert the catheter. 

c. Percutaneous suprapubic catheter. Follow the manufacturer's instructions for use. 

LUMBAR PUNCTURE 

Indications 

Lumbar puncture is performed to obtain cerebrospinal fluid for diagnostic tests (eg, 

suspected meningitis, subarachnoid hemorrhage).


Contraindications to lumbar puncture are as follows: 

• Local infection of the lumbar area. Cervical or cisternal puncture should be performed 

instead. 

• Suspected intracranial mass lesion (brain abscess, tumor, any posterior fossa lesion, 

subdural hematoma). Papilledema or focal cerebral defects (excluding ophthalmoplegia) 

suggest a mass lesion of the central nervous system. CT scan of the head should 

precede lumbar puncture in these circumstances. 

• Bleeding diathesis (relative contraindication; should be corrected if time permits). 

• Suspected spinal cord mass lesion (eg, epidural abscess, hematoma, or tumor). 

Myelography should be performed in consultation with a neurosurgeon to define the 

lower limit of the spinal block. 


One person can perform lumbar puncture unaided if the patient is cooperative. An 

assistant can help with positioning of the patient, lighting, handling of samples, and the 

like, and is essential if the patient is uncooperative. 


Prepackaged sterile disposable lumbar puncture trays are commercially available. If the 

tray is to be assembled at the hospital, the following items are required: 


• Materials for sterile techniques (gloves and mask; cap and gown are optional). 

• Spinal needles, 20- and 22-gauge (shorter, smaller-gauge needles are required for 

children). 

• Manometer. 


• Cerebrospinal fluid collection tubes (5). 

• Sponges, 10 × 10 cm (4 × 4 in). 



• Adhesive dressing.

• Ice bucket for specimens that must be put on ice immediately. 


A. Lateral Decubitus 

Place the patient in the lateral decubitus position lying on the edge of the bed and facing 

away from the operator. The patient should flex the lumbar spine as much as possible 

by assuming the fetal position (forehead bent toward knees and knees drawn up to 

abdomen). The patient's head should rest on a pillow, so that the entire craniospinal 

axis is parallel to the bed. Positioning is the most crucial aspect of successful lumbar 

puncture, and the 3 key elements of proper positioning are achieving maximal lumbar 

flexion (to open the intervertebral spaces), keeping the patient's spine parallel to the 

bed, and having the line of the patient's shoulders and pelvis be perpendicular to the 

bed (to facilitate orientation of the needle track). Prevent pelvic rotation by keeping the 

patient's knees and ankles aligned. An assistant is useful to help the patient maintain 

the proper position. 

B. Sitting 

The patient sits facing away from the operator and bends over a bedside table to 

maximize lumbar flexion. This position is useful when cerebrospinal fluid pressure is low 

(eg, dehydration) or when the patient is obese. Cerebrospinal fluid pressure can be 

determined by having the patient lie in the decubitus position after the needle is in place. 

After the patient has been properly positioned, raise the bed until the patient's lower 

lumbar spine is at the mid chest level of the operator, who should be seated. Adjust the 

lighting for optimal effect. 


Lumbar puncture should enter the subarachnoid space below the level of the conus 

medullaris, which extends to L1-L2 in most adults and L2-L3 in children. The L3-L4 

interspace, the most commonly used site for lumbar puncture, is at the level of the 

posterior iliac crests (Figure 6-32). The L4-L5 interspace may be preferable, however, 

because a traumatic spinal tap at this level may leave cerebrospinal fluid obtained at the 

higher interspace uncontaminated with red blood cells (because of the caudal direction 

of flow of cerebrospinal fluid). 

With the patient properly positioned, find the posterior iliac crest, and palpate the spine 

at this level for the L3-L4 interspace. Other interspaces are counted from this landmark. 

The needle should enter the exact midpoint of the interspace between the spinous 

processes. Mark the point on the patient's skin with the end of a ballpoint pen or the 

indentation from a fingernail to facilitate locating the landmark after the skin has been 

sterilized. 

It may be difficult to palpate the spinous processes in obese patients. Using the gluteal 

cleft to mark the midline, locate the sacral promontory, which is palpable even in obese 

patients. Move cephalad until the promontory ends, indicating the L5-S1 interspace; the 

L4-L5 interspace is then easily identified.

Procedure 

1. Observe sterile technique (don mask and gloves; cap and gown are optional). 

2. Prepare all equipment. Assemble the manometer and stopcock (the channel from the 

spinal needle to the manometer should be open), open the specimen tubes, and draw 

up the 1% lidocaine into the 5-mL syringe with the 25-gauge needle. 

3. Sterilize the skin in a wide field around the L2-L3 to L4-L5 interspaces. 

4. Place a sterile drape under the patient that extends over the edge of the bed. 

Contamination of gloves may be avoided by folding the edge of the drape back over the 

gloves, pushing the edge beneath the patient's back, and carefully removing the gloved 

hands. 

5. Place a second sterile drape over the top side of the patient, leaving only sterilized 

skin between the edges of the drapes. Although a drape with a center hole is preferred 

by some, it obscures the rest of the spine (a valuable landmark) and makes shifting to 

another interspace difficult. 

6. Locate the puncture site, and anesthetize the skin using the 1% lidocaine in the 5-mL 

syringe with the 25-gauge needle. Change to the 22-gauge needle before anesthetizing 

between the spinous processes. Be sure to apply vacuum to the syringe to make sure 

that the needle has not entered a blood vessel (blood in the syringe). 

7. Hold the spinal needle between the index and middle fingers, with the thumb over the 

stylet. It may be held with 2 hands, if necessary, for stability. Avoid touching the tip and 

shaft of the needle, because starch granules from the gloves may be introduced into the 

subarachnoid space and can cause sterile arachnoiditis. The 20-gauge needle is better 

for transmitting pressure changes in cerebrospinal fluid, but the 22-gauge needle is 

adequate in most cases; smaller needles should be used in children. 

8. Introduce the needle in the midline perpendicular to a line connecting the iliac crests, 

aiming about 30 degrees rostrally toward the umbilicus. Be sure the long axis of the 

needle is parallel to the bed and that the plane of the patient's back is perpendicular to 

the bed. In infants, the entry angle is nearer to the perpendicular, whereas in elderly 

patients, the angle may approach 45 degrees rostrally to pass beneath the osteophytic 

lipping of the spinous processes. The bevel of the needle should be facing up (parallel 

to the spine) if the patient is in the lateral decubitus position, so that the fibers of the 

dura are split longitudinally. 

9. Advance the needle slowly. There will be a "pop" as the needle passes through the 

ligamentum flavum and the spinal arachnoid membrane. Since the spinal venous plexus 

is anterior to the spinal canal, the chance of a traumatic spinal tap can be minimized by 

frequent checking of the position of the needle (withdraw the stylet). 

10. If the needle hits bone deep in the penetration, withdraw to the ligamentum flavum, 

and redirect the tip in a more caudal direction. (The needle will follow the same course

unless it is drawn back through the ligamentum flavum.) Pain radiating to the leg or 

buttock is an obvious indication to direct the needle toward the midline and away from 

the involved side. 

11. When cerebrospinal fluid begins to flow from the needle, discard the first few drops. 

Establish free flow of cerebrospinal fluid—rotating the bevel of the needle may be 

helpful. Do not aspirate cerebrospinal fluid unless it cannot be obtained by other means, 

because a nerve root may be trapped against the needle and injured. Replace the stylet 

halfway in the shaft of the needle to prevent leakage. If the patient is in a seated 

position and if cerebrospinal fluid pressures are to be obtained, have an assistant help 

the patient into the decubitus position, taking care not to move the needle. 

12. Remove the stylet, and attach the stopcock and the manometer to the needle. 

13 .If not already done, rotate the stopcock lever to open the channel between the 

needle and the manometer. Cerebrospinal fluid will rise into the manometer, and the 

opening cerebrospinal fluid pressure can be measured. Normal pressure is between 

780 and 180 mm H 2 0. If pressure is elevated, make sure that the patient's position is 

not causing jugular or abdominal compression. Have the patient slowly relax and uncurl 

from the fetal position (if in the lateral decubitus position) and then inhale deeply. 

Cerebrospinal fluid pressure falls with inspiration and rises with expiration. Check 

pressure changes with the patient's head first flexed and then extended. To detect mass 

lesions in the spinal canal, look for a block to cerebrospinal fluid that is present only on 

either extension or flexion. Abnormally low pressures may be caused by dehydration. 

14. Remove the manometer, and begin collecting samples of cerebrospinal fluid in the 

specimen tubes. This is most easily achieved by removing the 3-way stopcock and 

using the stylet to block flow between samples by replacing the stylet halfway in the 

shaft of the needle. Three tubes are routinely collected: tube 1 (0.5-1 mL), tube 2 (2-3 

mL), and tube 3 (2-4 mL) in adults (smaller amounts are collected in children). 

Frequently, however, further information is desired, and more samples are collected in 

the extra tubes (see section on specimen collection, below). If in doubt, collect extra 

fluid in additional tubes. 

15. Replace the manometer, and obtain a closing pressure if spinal subarachnoid block 

is suspected. 

16. Remove the needle, and place a small adhesive bandage over the puncture site. 

17. Draw venous blood for determination of glucose concentration. The radio of blood 

glucose to cerebrospinal fluid glucose is helpful in the diagnosis of inflammatory 

disease. 

18. Recommendations to have the patient lie supine after the procedure do not appear 

to affect the incidence of post-dural puncture headache. 

Special Problems Encountered in Lumbar Puncture

A. Massive Obesity 

If the patient is obese, landmarks are difficult to locate, and alternative methods for 

locating the L4-L5 interspace must be used (see Anatomy Review, above). Lumbar 

puncture with the patient sitting may be tried if attempts fail with the patient in the lateral 

decubitus position. The sitting position makes the midline easier to locate and increases 

lumbar flexion. A 12.5-cm (5-in) needle may be required. The patient must be 

cooperative. Cerebrospinal fluid pressures are not measured in this position, but the 

patient may be carefully repositioned in the lateral decubitus position after the needle is 

in place to record cerebrospinal fluid pressures. If lumbar puncture in the sitting position 

is unsuccessful, a neurosurgeon can use the cervical approach (done at the bedside), 

or a neuroradiologist can attempt a fluoroscopically guided approach (performed in the 

radiology department). 

B. Osteoarthritis 

As the body ages, desiccation of the nucleus pulposus of the intervertebral disk occurs, 

with subsequent narrowing of the disk space. This change, together with osteophytic 

"lipping" of the spinous process and calcification of the interspinous ligament and 

ligamentum flavum, combine to make lumbar puncture difficult. A larger-gauge needle 

(eg, 18- to 19-gauge) facilitates passage through calcified posterior ligaments. It may 

occasionally be necessary to resort to an oblique approach performed by a radiologist 

using fluoroscopy. 

C. Previous Lumbar Surgery 

Lumbosacral spine films assist in defining the extent of surgery and fusion. If all of the 

posterior approaches are unavailable for lumbar puncture, obtain neurologic or 

neurosurgical consultation. 

D. Inadvertent Arterial Puncture 

If arterial blood is obtained during lumbar puncture, completely withdraw the needle. 

Obtain a fresh spinal needle for the next attempt, because clotted blood makes 

replacement of the stylet difficult and also contaminates the sample. If the patient has 

an underlying coagulopathy, it should be corrected and the patient observed for signs of 

compressive spinal epidural or subdural hematoma (Chapter 16). 

E. High Opening Pressure 

If high cerebrospinal pressures are unsuspected before lumbar puncture is performed, 

use the smallest needle possible. Collect the minimum amount of fluid necessary 

(usually that in the manometer is sufficient), and withdraw the needle. Watch the patient 

carefully for signs of impending herniation, and treat accordingly (Chapter 16). Obtain a 

closing cerebrospinal fluid pressure; remove only as much fluid as causes the initial 

pressure to drop by one-half. A rapid drop in cerebrospinal fluid pressure to low levels 

with removal of only a small amount of fluid may be an ominous sign indicating 

impending herniation. Obtain urgent neurosurgical consultation. 

F. Hypotension 

Cerebrospinal fluid pressure is proportionate to venous pressure and PCO 2 . Severe 

hypotension may decrease the volume of the subarachnoid space and make it difficult 

to penetrate. Slowly advance the needle, and each time the stylet is removed, attach a 

tuberculin syringe with a small air bubble in the hub, relying on the negative pressure in

the epidural space to help define location (the bubble is sucked into the needle when 

the needle is in the epidural rather than the arachnoid space). Advancing the needle a 

few millimeters will place the tip within the subarachnoid space, permitting aspiration of 

cerebrospinal fluid. 

The sitting position may be helpful in the patient with severe hypotension, provided that 

arterial blood pressure is sufficient to enable the patient to tolerate the upright position. 

The sitting position takes advantage of gravity to help raise cerebrospinal fluid pressure 

in the lumbar space. 

G. Post-Lumbar Puncture Headache 

Headache following lumbar puncture is unfortunately a relatively common complication 

of the procedure. It does not appear to be related to the duration that a patient remains 

supine after the procedure. Smaller, less traumatic (pencil point) needles may reduce 

the incidence. Medications such as oral or intravenous caffeine may be of benefit for 

headaches that continue despite bed rest. For persistent headaches, an epidural blood 

patch is usually effective in resolving the headache. 

H. Blood in Cerebrospinal Fluid 

Features that point to a traumatic spinal tap rather than to subarachnoid hemorrhage 

include (1) normal cerebrospinal fluid pressure, (2) absence of xanthochromia after 

centrifugation, (3) blood sample followed by clearer samples or bloodier samples, (4) 

white cell count proportionate to red cell count (700-1000 red blood cells per white blood 

cell; 1 mg/dL of protein per 1000 red blood cells), (5) changing red cell count in 

successive tubes, or (6) clot formation (rare). A repeat lumbar puncture at a higher 

interspace yields cerebrospinal fluid that is usually clear if the fluid was bloody owing to 

traumatic tap at a lower level. The presence or absence of crenated red cells is of no 

diagnostic value. 

Specimens 

At a minimum, collect 3 tubes: tube 1 (0.5-1 mL) for cell count, tube 2 (2-3 mL) for 

culture and Gram stain, and tube 3 for protein and glucose determinations and for 

chemistry studies (2-4 mL). Most authorities recommend another 0.5 mL for a VDRL 

study. There is no harm in collecting extra tubes, because a variety of other diagnostic 

tests may be indicated. If the specimen is bloody, perform comparison counts in tubes 1 

and 3. 

If subarachnoid hemorrhage is suspected, the supernatant in the tube should be 

examined for xanthochromia. Centrifuge 2-3 mL of cerebrospinal fluid at 1000 rpm for 5 

minutes in a clinical centrifuge, and then examine the supernatant for the characteristic 

yellowish pigmentation of oxyhemoglobin and bilirubin. Xanthochromia does not appear 

until about 2-4 hours after hemorrhage, reaches a maximum around 6-48 hours, and 

may persist for 2-4 weeks (Table 6-2). Jaundice, hypercarotenemia, and elevated 

cerebrospinal fluid protein (> 150 mg/dL) may also cause xanthochromic spinal fluid. 

Xanthochromia does not occur in the supernatant after a traumatic spinal tap, because 

the bloody cerebrospinal fluid is not exposed to the enzyme in the subarachnoid space 

that converts hemoglobin to bilirubin.

ANTERIOR & POSTERIOR NASAL PACKING FOR CONTROL OF EPISTAXIS 

Bleeding from the anterior or posterior nasal passages is a commonly encountered 

emergency. The patient may present with bleeding ranging from mild epistaxis that is 

easily controlled by local pressure to exsanguinating hemorrhage causing hemorrhagic 

shock. 

Successful treatment of epistaxis requires careful identification of the bleeding source. 

To accomplish this, proper positioning of the patient, proper instruments, and a bright, 

hand-directed light source are a necessity. 

Bleeding in the anterior nares occurs most commonly in children and can be controlled 

by local measures such as direct pressure or cautery. Bleeding in adults usually occurs 

more posteriorly in the anterior nares and often requires anterior nasal packing; 

epistaxis in the elderly often requires both anterior and posterior nasal packing because 

the site of bleeding is in the posterior nares. 

Indications 

Nasal packing (Figure 6-33) is performed to control hemorrhage that cannot be 

controlled by local measures. 


The patient's ability or inability to cooperate during the procedure is the only limiting 

factor in performing nasal packing. Occasionally, direct control of the bleeding site under 

general anesthesia in the operating room is required. 


One person can perform nasal packing unaided, although it is helpful to have an 

assistant to position the patient and handle instruments. 


A. Anterior Packing 

• Cocaine solution, 4% (10 mL); benzocaine-tetracaine spray or tetracaine liquid; 

phenylephrine nasal spray, 0.5-1%. 

• Lidocaine, 1%, with epinephrine (10 mL). 

• Syringe, 5-mL, with 25-gauge needle. 

• Cotton-tipped swabs. 

• Silver nitrate-tipped sticks for coagulation. 

• Portable electrocautery device.

• Nasal speculum. 

• Headlamp, or reflective eye mirror with suitable light source. 

• Continuous suction device with nasal suction tips. 

• Petrolatum-impregnated gauze packing (continuous strip). 

• Nasal packing forceps. 

• Cotton pledgets. 

B. Posterior Nasal Packing 

The materials and equipment listed for anterior nasal packing are required for posterior 

nasal packing. The following additional items are required: 

• Occluding balloon catheter (specially designed for tamponade of the bleeding site) (2). 

• Absorbent cotton (4 × 5 cm [15/8 × 2 in]), with 3 pieces of size 0 silk suture material 

tied around the middle (alternative to balloon catheterization). 

• No. 12 or No. 14 red rubber catheter. 

• Scissors. 

• Kelly clamp. 


The patient should be either seated in an ENT chair or lying on a gurney with a back 

rest in the full upright position. The patient's head should also be supported. 


Bleeding from the anterior nares most commonly occurs in the Kiesselbach area, 

located anteriorly along the nasal septum (see Figure 32-1). Bleeding that occurs more 

posteriorly in the anterior nares (a common occurrence in adults) may originate in the 

nasal turbinates. Posterior epistaxis usually occurs in elderly patients with calcified 

arteriosclerotic vessels, which are refractory to the normal vasospastic control 

mechanism in response to bleeding and which may therefore bleed briskly. These 

posterior vessels are not accessible in a routine nasal examination, and control of 

epistaxis therefore requires tamponade with a balloon or pack. 

Procedure 

Commercial devices such as nasal tampons and anterior nasal balloons are available 

and are very effective. The nasal balloons usually have a central cannula that allows for 

air passage.

A. Anterior Nasal Pack 

1. Assemble and arrange all necessary equipment so that it is within easy reach. 

2. Position the patient as described above, and make sure that the patient is 

comfortable but well supported and immobile. 

3. Make sure that suction and adequate lighting are available. 

4. While the operator is arranging equipment, an assistant can pinch the nose to stop 

bleeding from the septum. 

5. Spread the patient's nostrils apart using the nasal speculum, and remove all blood 

with the suction device. Check the anterior septum for bleeding. Then examine the 

turbinates and the oropharynx to determine whether bleeding is occurring posteriorly. 

6.If an anterior bleeding vessel is identified (eg, vessel in the Kiesselbach area), 

bleeding can be controlled in one of 3 ways: 

a. Local vasoconstriction. Saturate cotton pledgets with tetracaine liquid mixed with 

phenylephrine nasal spray, place one in each nostril, and have an assistant or the 

patient firmly pinch the nostrils together for 5 minutes. The mixture will shrink the nasal 

mucosa and cause vasoconstriction, which, along with the pressure, often controls 

bleeding. An alternative method using 0.5-1% phenylephrine nasal spray and 

benzocaine-tetracaine spray in a similar manner is also effective. 

b. Silver nitrate-tipped sticks. After the bleeding site has been identified, cauterize the 

bleeding vessels using silver nitrate-tipped applicators. It is important to localize the site 

of cauterization precisely over the bleeding site. Overzealous cauterization of large 

areas of the nasal septum may cause septal necrosis with perforation. 

c. Electrocautery. A single anterior bleeding vessel may be cauterized using an 

electrocautery device. Exercise the same discretion required with chemical cautery. 

7. Bleeding that is occurring more posteriorly in the anterior nasal passage, which 

cannot be controlled by local measures, requires anterior nasal packing. Using nasal 

forceps, pack the petrolatum-impregnated gauze in successive, tightly packed layers 

(accordion pleating), starting in the most posterior part of the accessible portion of the 

nose and working anteriorly. Insert only a small quantity of gauze at a time to ensure 

that the anterior naris is completely packed. 

8. After the entire anterior nasal passage has been packed, check the oropharynx to 

see if bleeding is continuing posteriorly; if it is, insertion of a posterior pack is indicated 

(the anterior pack will have to be removed before this can be done). The anterior pack 

must then be replaced after posterior packing is completed. 

B. Posterior Nasal Pack 

1. Sedate the patient (for adults, diazepam, 10 mg orally; or morphine, 5-10 mg 

intramuscularly).

2. Anesthetize the anterior nose with cocaine-saturated cotton pledgets or 

benzocaine-tetracaine and phenylephrine sprays before inserting the posterior nasal 

pack using either of the methods outlined below. 

a. Balloon occlusion technique: 

(1) Balloon catheters made specifically to pack the posterior nasopharynx are available 

commercially. They work on the same principle as a Foley catheter, with an air inflation 

port to inflate the balloon. 

(2) The balloon-tipped distal end is inserted through the anterior naris into the posterior 

naris by guiding it directly posteriorly with gentle, steady pressure. After the catheter 

enters the posterior naris, inflate the balloon with the appropriate amount of air (the 

amount is printed on the balloon). Exert traction on the catheter to pull the balloon 

snugly up against the posterior nasal chamber, and secure the catheter at the external 

naris with gauze packing tied around the tube. Some nasal catheters have a small 

proximal balloon that, when inflated, will serve the same function as the gauze 

packing—to maintain tension on the distal intranasal balloon. 

(3) After inserting the balloon catheter, check the anterior naris for coexisting anterior 

bleeding and the oropharynx to determine if posterior bleeding is continuing. If bleeding 

is occurring from both sides, a second balloon catheter may be placed. Insert an 

anterior nasal pack. 

b. Gauze technique: 

(1) If a balloon catheter is not available, posterior packing can be accomplished using a 

4- × 5-cm (15/8 - × 2-in) piece of absorbent cotton or gauze. Tie the gauze around the 

middle with 3 strands of size 0 silk suture material. Two of the strands will be passed 

through the nasal passage and tied at the anterior naris. The third strand will be cut and 

allowed to hang down in the throat to facilitate removal of the pack after bleeding has 

been controlled. 

(2) Pass the No. 12 rubber catheter through the external naris until the catheter is 

visible in the patient's throat. 

(3) Using a Kelly clamp, grasp the end of the catheter in the throat, and bring it out 

through the patient's mouth (Figure 6-33A). 

(4) Take the 2 ends of the size 0 silk suture material securing the gauze pack and tie 

them to the catheter. 

(5) Pull the other end of the catheter through the patient's nose so that the sutures 

follow as the pack passes from the mouth to the posterior nasopharynx. This maneuver 

helps the pack fit snugly in the posterior nostril. 

(6) Repeat the process for the other nostril. Tie the 4 silk strands (2 from each nostril) 

across a gauze sponge placed under the nose to prevent pressure on the nares from

the septum. 

(7) After the posterior packs are in place, pack the anterior nares, and check the 

oropharynx again to make sure that hemorrhage is controlled. 

(8) In patients with preexisting cardiac or respiratory disease, draw blood for arterial 

blood gas determinations, because a significant drop in PO 2 may be seen. 

All patients with posterior nasal packs should be hospitalized for monitoring of the 

airway. If the external gauze wrapping around the catheter slips, the balloon may be 

displaced posteriorly into the hypopharynx and may obstruct the airway. Antimicrobial 

prophylaxis (to prevent sinusitis) is recommended by many authorities, although its 

benefit is unproved. Give ampicillin, 150 mg/kg/d intravenously in 4-6 divided doses. 

ARTHROCENTESIS (Knee, Shoulder, Elbow, Ankle, Wrist, Hand, & Foot Joints) 

The major peripheral joints can be aspirated safely in the emergency department. 

Aspiration of the hip and other joints of the axial skeleton usually requires the aid of 

specialists (orthopedic surgeons or rheumatologists) and the use of ancillary techniques 

(fluoroscopy and radionuclide scans); therefore, it is not discussed here. 

Indications 

Indications for arthrocentesis are as follows: 

• Need to obtain synovial fluid for diagnosis. 

• Drainage of hemarthrosis when conservative management is unsuccessful. 

• Instillation of local analgesic and anti-inflammatory agents into a joint. 


Contraindications to arthrocentesis are as follows: 

• Soft tissue infection overlying proposed site of aspiration. 

• Uncooperative patient (relative contraindication). 

• Severe bleeding diathesis or anticoagulant therapy. 


One person can perform arthrocentesis unaided if the patient is cooperative, although 

an assistant is helpful for handling samples and holding young children. 


• Materials for skin sterilization.

• Materials for sterile technique (mask and gloves; cap and gown are optional). 


• Needles: 25-gauge, 1.5-cm (5/8-in) (2); 22-gauge, 4-cm (11/2-in) (2); 20-gauge, 4-cm 

(11/2-in) (2); 27-gauge, 1.5-cm (1/2-in) (1). Select a needle size appropriate to the joint 

to be aspirated. 

• Syringes: 10-mL (2), 2-mL (2), 30-mL (1). 


• Drapes. 

• Gauze pads, 10 × 10 cm (4 × 4 in) (2); 5 × 5 cm (2 × 2 in) (2). 


• Sterile capped specimen tubes (2-3). 

• Containers for synovial fluid: purple-topped or green-topped (EDTA or heparin 

anticoagulant, respectively, for cell count and differential and examination for crystals) 

(2); gray-topped (fluoride inhibitor for glucose) (1); red-topped (no anticoagulant) (3). 

• Clean glass microscope slides and coverslips. 


See Procedure for Specific Joints, below. 

Procedure 

1. Stabilize the joint to be aspirated. Identify landmarks, and mark the entry point with a 

scratch or indentation on the skin. 

2. Sterilize the skin in a wide field around the puncture site. 


4. Observe sterile technique (don mask and gloves; cap and gown are optional). 

5. Anesthetize the skin with the 1% lidocaine with the 10-mL syringe and 22- to 

27-gauge needle; continue down to the joint capsule. 

6. Select an appropriate needle (usually 20-gauge for knee, shoulder, elbow, ankle, or 

wrist; 25- or 27-gauge for small hand joints) and syringe (10-mL for knee, shoulder, 

elbow, ankle, or wrist; 2-mL for hand joints). A large-bore needle (eg, 18-gauge) may be 

required for aspiration of pus in larger joints. Use the 30-mL syringe for large effusions.

7. Penetrate the skin at the selected site, and cautiously advance the needle into the 

joint space; a "pop" will be felt when the needle passes through the synovium into the 

joint space. Aspirate continuously. Stop advancing the needle when joint fluid flows 

freely into the syringe. 

8. Remove as much fluid as possible, but do not drain the joint dry if synovial biopsy is 

planned. 

9. If joint fluid fails to flow freely, bring the needle all the way back to the subcutaneous 

tissue before redirecting it, in order to avoid joint trauma that might occur with deep 

probing. 

10. After samples of fluid have been obtained, withdraw the needle, and apply firm 

pressure over the site for 1-2 minutes. 

11. Cover the site with an adhesive dressing. 

Procedure for Specific Joints 

A. Knee 

The joint space of the knee may be entered either medially or laterally (Figure 6-34). In 

either case, the leg should be fully extended, with the patient supine. Pressure on the 

opposite side of the joint will make the synovium bulge more prominently and assist in 

directing the needle. 

From the lateral aspect, the entrance site is at the intersection of lines (extended from 

the upper and lateral margins of the patella). A 22-gauge, 4-cm (11/2-in) needle held 

parallel to the bed is directed medially and just deep to the patella and into the 

suprapatellar space. 

From the medial aspect, the needle is introduced anteromedially in the space between 

the patella and the medial condyle. The needle (held parallel to the bed) is advanced 

upward (toward the undersurface of the patella) and laterally, beneath the patella and 

into the joint space. 

B. Shoulder 

The shoulder joint can be aspirated from either an anterior or a posterior approach. The 

latter has the advantage of being out of the patient's line of vision. 

For the posterior approach, the patient should sit in a chair and face backward (chest 

against the back of the chair). To open up the joint space and facilitate entry of the 

needle, the patient should put the arm of the site to be aspirated up against the chest 

and touch the opposite shoulder. This will adduct and internally rotate the arm. The 

head of the humerus is palpable posterolaterally. Use a 20- or 22-gauge, 4-cm (11/2-in) 

needle, and keep it parallel to the floor. Direct it about 30 degrees medially into the joint 

space from a point just under the posterior inferior border of the acromion (Figure 6-35). 

For the anterior approach, the patient should sit in a chair, facing forward, with the arm

comfortably supported in the lap. Using a 20- or 22-gauge, 4-cm (11/2in) needle, enter 

the joint space at a spot medial to the head of the humerus and just below the palpable 

tip of the coracoid process (Figure 6-36). Direct the needle slightly laterally and 

superiorly into the scapulohumeral joint space. 

C. Elbow 

Be certain to differentiate olecranon bursitis that does not involve the elbow joint from 

bulging synovium. 

Have the patient sit with the forearm supported from the elbow to the hand on a table, 

with the elbow joint in about 10-30 degrees of flexion. With significant effusion, the 

bulging synovium should be evident laterally. Introduce the needle (usually a 20- or 

22-gauge, 4-cm [11/2-in] needle) just below the lateral epicondyle and proximal to the 

olecranon process of the ulna (Figure 6-37). Advance the needle medially and slightly 

proximally into the joint space. 

D. Ankle 

Arthrocentesis of the ankle is more difficult than that of the other joints discussed here. 

The most common approach is anteromedial. Have the patient lie supine, with the knee 

extended and the foot slightly plantar-flexed. Identify the extensor hallucis longus 

tendon by having the patient extend the great toe. Just anterior (1 cm [@3/8 in]) and 

inferior (1 cm [@3/8 in]) to the medial malleolus and lateral to the extensor tendon is a 

small depression. Introduce the needle in this depression, and direct it toward the 

tibiotalar articulation (Figure 6-38). If swelling and pain are most severe on the side of 

the ankle, use a similar approach but from the anterolateral aspect of the joint. When 

subtalar disease is suspected (eg, pain on pronation and supination of the foot), the 

needle is introduced more distally, at the talonavicular articulation. Although fluid is 

seldom obtained at the talonavicular joint, injection of anti-inflammatory agents may be 

readily accomplished. 

E. Wrist 

A bulging, inflamed joint space at the wrist can be entered dorsally at prominent areas 

of swelling; such areas are invariably found on the radial or ulnar aspects. Use a 20- or 

22-gauge, 4-cm (11/2-in) needle. 

For the radial (lateral) entry, position the hand with the palmar surface down, and flex it 

over a rolled towel at the wrist. Aspirate the joint at the midpoint of the distal articulation 

of the radius, just medial to the extensor tendon of the thumb. The needle should be 

perpendicular to the skin during aspiration. 

The ulnar, or medial, approach is made in the middle of the palpable depression 

between the lateral aspect of the tip of the ulna and carpus. Position the hand as for a 

radial approach. Direct the needle ventrally toward the palmar surface and proximally 

into the joint space. 

To administer corticosteroids into the carpal tunnel (to treat compression of the median 

nerve), place the needle between flexor creases of the wrist just lateral to the palmaris 

longus tendon (or medial to the flexor carpi radialis), and advance it distally until 

resistance to injection is minimal. (See Chapter 29 for details.)

F. Small Joints of the Hands and Feet 

Systemic arthritides frequently involve the proximal and distal interphalangeal joints and 

the first metatarsophalangeal joint. Enter the joint in the midline just lateral to the 

extensor tendon on the dorsolateral aspect, and gently work a 25- or 27-gauge needle 

into the joint space. A 2-mL syringe suffices for aspiration and is easier to handle than 

larger ones. Maintain a slight vacuum in the syringe, so that any trauma to digital 

vessels will be recognized immediately (blood will appear in the syringe). Traction on 

the distal portion of the phalanx helps open the joint space, allowing easier access for 

the needle. 

Synovial Fluid Analysis 

If minimal fluid is available, priorities must be established for processing the sample. If 

pyogenic arthritis is a diagnostic possibility, an appropriate approach would be to place 

one drop of fluid on a microscope slide for Gram stain, another into a hemacytometer for 

cell count, and the remainder of the sample for culture. If 10-20 mL or more of synovial 

fluid is obtained, complete synovianalysis can be performed, as outlined below; partial 

analysis is possible on even as little as 1 mL of fluid. 

A. Physical Characteristics 

1. Determine the total volume of fluid removed. 

2. Assess color and clarity of fluid (normally a crystal-clear yellowish fluid through which 

print can be easily read). 

3. Note viscosity by allowing a drop to fall from the needle. Normal joint fluid has high 

viscosity and easily forms a cord several inches long. 

4. Perform the mucin clot test (Ropes test) by adding 1 mL of synovial fluid to diluted 

acetic acid (about 5%). Normally, the mucin in the fluid congeals within minutes, forming 

a gel (commonly called a clot) that remains firm for hours. In the case of infection or 

chronic inflammation, unstable gel forms that is easily broken up by gentle agitation. 

Examine the gel again at 1 hour for friability; normal mucin gel should be unchanged 

after 1 hour. 

B. Laboratory Studies 

The choice of studies is guided by clinical circumstances. Gram stain and culture, cell 

count, and examination for crystal formation should always be performed when fluid 

from an acutely inflamed joint is being evaluated. 

1. Cell count and differential—Place 2-10 mL of synovial fluid in a purple-topped 

(EDTA anticoagulant) or green-topped (heparin anticoagulant) tube for laboratory 

examination. If fluid is scanty, use 1-2 drops counterstained with methylene blue, and 

perform a cell count in the emergency department with a hemacytometer. Normal 

synovial fluid contains fewer than 200 white cells per microliter, of which less than 25% 

are polymorphonuclear neutrophils. 

2. Special stains—All joint fluid should be stained with Gram stain and examined by

microscopy. Special stains for fungi and acid-fast bacilli should also be performed when 

chronic monarticular arthritis is being evaluated. These tests are specific but not 

sensitive for detection of fungal or mycobacterial arthritis. 

3. Examination for crystals—Place a drop of synovial fluid on a clean glass 

microscope slide under a coverslip. Examine the specimen immediately; if this is 

impossible, slow the evaporation of joint fluid by sealing the edges of the coverslip with 

nail polish or petrolatum. Crystals can be detected using light microscopy and tentatively 

identified on the basis of morphologic characteristics seen at × 400 magnification. Urate 

crystals are needle-shaped; calcium pyrophosphate crystals are more 

rhomboid-shaped; and cholesterol crystals are flat, with notched corners. Polarized light 

microscopy demonstrates the negative birefringence of urate crystals and the positive 

birefringence of calcium pyrophosphate. The presence of crystals both free in fluid and 

within leukocytes is pathognomonic of crystal-induced arthropathy. If the laboratory is 

doing the examination, collect 1-2 mL of fluid in a purple-topped (EDTA anticoagulant) 

or green-topped (heparin anticoagulant) tube. 

4. Culture—Sterile, capped specimen tubes should be filled with 1-10 mL of fluid for 

bacterial cultures and, if indicated, mycobacterial and fungal cultures. In suspected 

gonococcal disease, chocolate agar should be inoculated with some of the fluid (in the 

emergency department if possible). When a potentially infected prosthetic joint is being 

evaluated, a jar of anaerobic transport media should also be inoculated. 

5. Glucose determination—Place 0.5-1 mL of synovial fluid in a gray-topped (fluoride 

anticoagulant) tube. The sample must be compared with a simultaneously drawn blood 

sample. Blood glucose that is more than 40 mg/dL higher than synovial fluid glucose 

suggests infection. 

6. Protein—Place 0.5-1 mL of synovial joint fluid in a red-topped (no anticoagulant) 

tube. Determine the total serum protein of a simultaneously drawn blood sample. 

Normal joint protein is about one third that of serum. 

7. Other studies—Less commonly indicated studies include cytology studies in 

possible pigmented villonodular synovitis or metastatic disease (5-10 mL in a lightly 

heparinized specimen tube); pH determinations (1-2 mL in a sealed heparinized 

syringe); complement levels; and tests for rheumatoid factor, antinuclear antibody, 

immunoglobulins, and various enzymes. 

The presence of fat globules (often with blood) suggests intra-articular fracture. 

INCISION & DRAINAGE OF SUPERFICIAL ABSCESS 

Indications 

A superficial abscess is incised in order to drain it. 


There are no contraindications to incision and drainage of a superficial abscess.


One person can usually incise and drain a superficial abscess unaided, although an 

assistant may be helpful to restrain an uncooperative patient. 


Many incision and drainage kits are commercially available. The following items are 

required: 


• Protective gown or apron and gloves. 


• Drapes. 

• Curved Kelly and mosquito clamps. 

• Forceps. 

• Packing material, such as gauze strip packing. 

• Sterile gauze sponges, 10 × 10 cm (4 × 4 in), and tape. 

• Ethyl chloride skin-freezing solution (optional). 

• Lidocaine, 1%, with 25-gauge needle and 5-mL syringe. 

• Culture tube and slides. 

• Sterile saline for irrigation. 

• Irrigating syringe and basin. 

• Needle, 18-gauge, with 5-mL syringe. 

• Plastic-coated absorbent pad. 


The patient should be lying on a firm surface in a comfortable position, with the area to 

be drained in full view and firmly supported. 

Procedure 

Anesthesia is the main difficulty in incision and drainage. Superficial abscesses suitable

for drainage at the bedside are painful, and the patient should be assured that pain will 

decrease after the pressure is relieved and the pus is drained. Incising the skin and 

draining the pus are painful, however, and little relief can be obtained short of general or 

block anesthesia, both of which require an anesthesiologist and an operating room. 

Spraying the area with ethyl chloride to freeze the skin will prevent some but not all 

pain. Infiltrating the thick layer of skin over the pointing abscess with lidocaine is 

impossible, and injecting lidocaine into the abscess cavity is ineffective and may create 

more pain from increased pressure. Narcotic analgesics (eg, morphine, 2-10 mg 

intramuscularly or subcutaneously) may take the edge off the pain and relieve some of 

the patient's anxiety, but they will not provide total relief. 

If an abscess is too large to be adequately drained at the bedside or if it appears that 

the patient may experience too much pain to be able to cooperate effectively, incision 

and drainage in the operating room is always an alternative. 

A. Simple Abscess Not Involving a Vital Structure 

1. Assemble the necessary equipment, and arrange it on a table or bedside stand. 

2. Position the patient. Place the plastic-coated absorbent pad under the body part with 

the abscess to be drained. 

3. Don sterile gloves and put on a gown to protect clothing. Cleanse the skin over the 

area being drained. Drape the area, and have extra absorbent materials ready to catch 

any pus not absorbed by the drape. 

4. If there is any doubt whether an abscess is actually present, take the 18-gauge 

needle and the 5-mL syringe, and aspirate the suspected abscess at the point of 

maximum fluctuance. If no pus is found, reassess the clinical situation, and proceed with 

incision and draining if it is deemed appropriate. 

5. If ethyl chloride or lidocaine is being used, it should be given at this time. 

6. Using the No. 11 blade, open the abscess at the point of maximum fluctuance, and 

allow the pus to drain under its own pressure. Using a quick, decisive motion minimizes 

the patient's discomfort. Collect the first portion of pus for Gram stain and culture and 

sensitivity testing. 

7. After the pressure has been relieved, insert the Kelly or mosquito clamp and find the 

longest axis of the abscess. Point the curve of the clamp up at the farthest point from 

the central incision and determine the shortest possible length to be incised so that the 

abscess is completely drained. Incise the skin to that point, using swift upward motion of 

the No. 11 blade. If it is necessary to make a long incision to completely drain the 

abscess, infiltrate the skin in the most lateral aspect with lidocaine. Repeat the 

procedure in the opposite direction. Allow any further pus to drain. Note: It is important 

to obtain an opening in the abscess wide enough to allow complete drainage of all pus. 

If the abscess is not opened completely, complete drainage cannot occur, and 

resolution of the abscess will be delayed. 

8. Using the clamp, break up any loculated pus in the cavity.

9. Irrigate the abscess with saline until all pus is removed. 

10. Pack the abscess cavity with iodoform or plain gauze packing. Fill the cavity tightly 

enough to cause hemostasis but not so tightly that it causes pain. 

11. Dress the area with the sterile 10- × 10-cm (4- × 4-in) sponge and tape. On the 

extremities or in areas where there is movement, consider dressing the site with an 

expanded bandage around the extremity. 

12. Begin antimicrobial therapy, if indicated (eg, for facial abscesses, cellulitis). 

Dicloxacillin, 20 mg/kg/d orally in 4 divided doses, is usually satisfactory. 

13. Schedule a follow-up appointment in 1-2 days. 

B. Incision and Drainage of Abscesses Over Special Areas 

1. Face, head, and neck abscesses—The clinical situation in these anatomic areas 

must be carefully considered before incision and drainage is performed, because the 

large scar left by complete incision and drainage may be cosmetically unacceptable and 

because of the possibility of injuring vital structures beneath the skin. In small superficial 

abscesses on the face, drainage can be accomplished by making a small incision at the 

lower part of the abscess, removing all pus, and leaving a gauze wick in the incision to 

keep the wound from closing. Frequent irrigation will be needed during follow-up to keep 

the cavity clean and promote healing. Any abscess that is large or that might involve 

vital structures should be drained in the operating room by personnel experienced in this 

procedure. 

2. Abscesses around joints—Make sure that the abscess does not involve the joint 

space. (Consult an orthopedic surgeon if there is any doubt.) If the abscess is superficial 

and does not involve the joint space, proceed with incision and drainage. Remember 

that splinting of the joint is necessary for adequate healing. 

3. Abscesses around the anus—Differentiate pilonidal abscesses from perianal 

abscesses caused by anal fistulas. Perianal of abscesses require surgical consultation 

and possibly drainage in the operating room. 

4. Abscesses of the hands, wrists, ankles, and feet—The compact arrangement of 

many vital structures in the hand, wrist, ankle, and foot makes drainage of abscesses in 

these areas difficult to perform in the emergency department. It is recommended that 

any abscess around these structures be drained in the operating room by experienced 

personnel. Surgical consultation is advisable in all cases of abscesses in these areas. 

TRANSCUTANEOUS CARDIAC PACING 

Transcutaneous cardiac pacing is a safe, rapid, noninvasive method of temporarily 

treating symptomatic bradyarrhythmias and asystole. Recent advances in technology 

have led to the development of defibrillators that are also capable of transcutaneous 

pacing. With these devices, transcutaneous pacing can be initiated in the prehospital 

setting or in the emergency department and is the procedure of choice in the treatment

of asystole and bradycardic cardiac arrest. 

Indications 

• Asystole. 

• Symptomatic bradycardia (< 40 beats/min) unresponsive to atropine. 

• Overdrive pacing for tachyarrhythmias (atrial, ventricular, torsade de pointes) 

unresponsive to medical and electrical cardioversion. 

• Transvenous pacing is difficult or contraindicated (eg, heart block in myocardial 

infarction treated with thrombolytic therapy). 

Complications 

The main complications associated with transcutaneous pacing are pain and local skin 

erythema due to first-degree burns. With the newer devices, pain from cutaneous nerve 

and muscle stimulation is now reported as tolerable. The energy levels used for pacing 

have not been shown to produce any significant myocardial damage. Other persons 

coming into contact with the pacing impulses may experience mild tingling. The risk of 

inducing ventricular fibrillation during transcutaneous pacing is negligible. 


One person can initiate transcutaneous pacing unaided. 

Equipment Required 

• Transcutaneous pacing device, 2 pacing electrodes, and connecting cable. 

• Optional electrodes and connecting cable for electrocardiographic monitoring are 

available with some models. 

Procedure 

1. Place one pacing electrode over the left anterior chest. Place the other electrode 

posteriorly in the interscapular area. Attach the connecting cables as indicated on the 

labels. 

2. If the pacing device is equipped for electrocardiographic monitoring, attach monitor 

leads to both shoulders and the left upper abdomen. Note: Standard 

electrocardiographic monitor results are usually uninterpretable owing to the strong 

pacing stimulus and movement artifact. 

3. Set rate at 80 beats/min; select synchronous mode for bradycardia or asynchronous 

mode for asystole. (Depending on the model, rate and mode may be fixed and not 

operator-selected.) Turn on power; turn on pacing.

4. Begin at 70-80 mA current output. 

5. Check for presence of a femoral pulse. Check the monitor for evidence of electrical 

capture (pacer spike before each QRS complex). If no pulse is detected, gradually 

increase the current output until pulse appears or highest current setting is reached. 

Caution: The carotid pulse is usually difficult to detect owing to muscle contractions. A 

Doppler stethoscope may be needed to ascertain the presence or absence of a pulse. 

6. Reduce current output to the lowest setting associated with a palpable pulse, and 

determine blood pressure. 

7. If transcutaneous pacing is successful, interrupt pacing intermittently to check for 

return of spontaneous electrical activity. As soon as the patient is stable, if pacing is still 

needed, insert a transvenous pacemaker. 

8. If transcutaneous pacing is unsuccessful and pacing is still required, attempt 

transvenous pacing. 





GENERAL INSTRUCTIONS FOR SKIN PREPARATION & STERILE 

TECHNIQUE

Table 6-1. Guidelines for endotracheal tube selection. 

Orotracheal 

Tube 1 

Premature Not applicable 

2.5 3-18 months Not applicable 

4-5 3-5 years 5 

6-6.5 8-14 years 6-7 

Female 7 

7-9 

1 

Inside diameter in 

millimeters. 





TABLES 

Table 6-1. Guidelines for endotracheal tube selection.

Table 6-2. Pigmentation of the cerebrospinal fluid following hemorrhage. 

Appearance Disappearance 

1/2-4 hours 7-10 days 

8-12 hours 2-3 weeks (yellow) 





TABLES 

Table 6-2. Pigmentation of the cerebrospinal fluid following hemorrhage.

Figure 6-1. Technique of percutaneous venipuncture. The needle should be inserted 

into the lumen of the vein at an angle of about 10-20 degrees, and the bevel should be 

facing up. (Reproduced, with permission, from Krupp MA et al: Physician's Handbook, 

21st ed. Lange, 1985.) 





FIGURES 

Figure 6-1

Figure 6-2. Venotomy technique. Exerting distal traction on the distal vein ligature, 

insert a No. 11 scalpel blade through the vein, and cut laterally. Open the venotomy 

incision with a mosquito clamp. (Reproduced, with permission, from Dunphy JE, Way 

LW [editors]: Current Surgical Diagnosis & Treatment, 5th ed. Lange, 1981.) 





FIGURES 

Figure 6-2

Figure 6-3. Technique of cutdown insertion. After exposing the vein and making the 

venotomy incisions (see Figure 6-2), elevate and stabilize the vein with a straight clamp 

while inserting the tip of the catheter in the venotomy incision. As soon as the tip of the 

catheter is within the lumen of the vein, remove the clamp, slide the catheter the 

required distance up the vein, and tie the vein proximally and distally. 





FIGURES 

Figure 6-3

Figure 6-4. A: Technique of removing the needle from the catheter-clad needle. B: 

Connecting the intravenous tubing. 





FIGURES 

Figure 6-4

Figure 6-5. Technique of securing an intravenous catheter to the skin with tape after 

insertion. 





FIGURES 

Figure 6-5

Figure 6-6. A: Scalp vein needle in an infant. B: Technique of inserting a butterfly 

needle. With the bevel of the needle facing up, oppose the 2 plastic "wings," and grip 

them between the thumb and forefinger while performing venipuncture. 





FIGURES 

Figure 6-6

Figure 6-7. Technique of securing a butterfly needle to the skin with tape after insertion. 





FIGURES 

Figure 6-7

Figure 6-8. Anatomic relationships of the external jugular vein. The external jugular vein 

originates at the level of the angle of the mandible in the parotid gland, and it courses 

caudally and anteriorly across the sternocleidomastoid muscle. It enters the subclavian 

vein near the subclavian triangle. 





FIGURES 

Figure 6-8

Figure 6-9. Technique of securing an external or internal jugular vein catheter to the 

skin with tape after insertion. 





FIGURES 

Figure 6-9

Figure 6-10. Internal jugular vein catheterization—middle approach. (Reproduced, with 

permission, from Dunphy JE, Way LW [editors]: Current Surgical Diagnosis & 

Treatment, 5th ed. Lange, 1981.) 





FIGURES 

Figure 6-10

Figure 6-11. Internal jugular vein catheterization—posterior approach. (Reproduced, 

with permission, from Dunphy JE, Way LW [editors]: Current Surgical Diagnosis & 






FIGURES 

Figure 6-11

Figure 6-12. Anatomic relationships of the subclavian vein. 





FIGURES 

Figure 6-12

Figure 6-13. Technique of subclavian vein catheterization. With the index finger in the 

suprasternal notch and the thumb marking the costoclavicular ligament, insert the 

needle just medial to the thumb. 





FIGURES 

Figure 6-13

Figure 6-14. Anatomic relationships of the femoral vein at the inguinal ligament. 





FIGURES 

Figure 6-14

Figure 6-15. Anatomic relationships of the saphenous vein. (Reproduced, with 







FIGURES 

Figure 6-15

Figure 6-16. Technique of radial artery puncture. The index and middle fingers are used 

to identify the point of maximum pulsation. 





FIGURES 

Figure 6-16

Figure 6-17. Technique of direct laryngoscopy and orotracheal intubation. A: The 

straight laryngoscope blade is passed behind the tongue and deep to the tip of the 

epiglottis. B: Lateral view showing straight laryngoscope blade deep to the tip of the 

epiglottis exposing glottic opening. C: View of glottis as seen through a laryngoscope 

with a curved blade. D: Insertion of endotracheal tube. (Parts A, B, and D reproduced, 

with permission, from Way LW [editor]: Current Surgical Diagnosis & Treatment, 3rd ed. 

Lange, 1977. Part C reproduced, with permission, from Kempe CH, Silver HK, O'Brien D 

[editors]: Current Pediatric Diagnosis & Treatment, 4th ed. Lange, 1976.) 





FIGURES 

Figure 6-17

Figure 6-18. Technique of nasogastric intubation. 





FIGURES 

Figure 6-18

Figure 6-19. Balloon tamponade for bleeding varices. A: The Sengstaken-Blakemore 

tube has a small gastric balloon (arrow) that can be inflated to 250 mL with air. B: The 

4-lumen Minnesota tube has a much larger gastric balloon that inflates to 450 mL and a 

series of aspirating ports (arrow) for removing secretions above the esophageal balloon. 





FIGURES 

Figure 6-19

Figure 6-20. Securing tamponade tube using crossed tongue blades. The insertion tube 

is secured to the corner of the mouth as shown. Foam or gauze may be placed between 

the triangle and the patient's mouth to prevent damage to gingival mucosa. 





FIGURES 

Figure 6-20

Figure 6-21. Anatomic relationships of cricothyroid membrane. (Reproduced, with 







FIGURES 

Figure 6-21

Figure 6-22. 50-psi oxygen source is connected via a demand valve to the transtracheal 

jet ventilator. 





FIGURES 

Figure 6-22

Figure 6-23. Proper orientation for introducing transtracheal catheter. The trachea is 

stabilized with the hand. 





FIGURES 

Figure 6-23

Figure 6-24. Technique of thoracentesis using a regular steel needle (not 

catheter-clad). A: Successful tap, with fluid obtained. Note the position of the needle in 

relation to the intercostal neurovascular bundle, and the use of the clamp to steady the 

needle at skin level (do not use a clamp with a catheter-clad needle). B: Air is obtained 

if the position of the needle tip is too high (lung is punctured, or preexisting 

pneumothorax is entered, as in illustration). C: A bloody tap may result from excessively 

low position of the needle with puncture of the liver. (Reproduced, with permission, from 

Wilson JL [editor]: Handbook of Surgery, 5th ed. Lange, 1973. Redrawn from GE 

Lindskog and AE Liebow.) 





FIGURES 

Figure 6-24

Figure 6-25. Diagram of tube thoracostomy and 3-bottle suction apparatus. Bottle A is 

connected to the thoracostomy tube and collects pleural drainage for inspection and 

measurement of volume. Bottle B acts as a simple valve to prevent collapse of the lung 

if tubing distal to this point is opened to atmospheric pressure. Pulmonary air leak can 

be detected by the escape of bubbles from the submerged tube. Bottle C is a system 

for regulating the negative pressure delivered to the pleural space. Wall suction should 

be regulated to maintain continuous vigorous bubbling from the middle open tube in 

bottle C. The resulting negative pressure (in cm H 2 0) is equal to the difference in the 

height of the fluid levels in bottles B and C. The Pleur-evac system works in a similar 

manner. One end is attached to the chest tube and the other end is attached to suction. 

Each chamber of the Pleur-Evac is filled with sterile water to the level noted in the 

manufacturer's instructions. (Reproduced, with permission, from Dunphy JE, Way LW 

[editors]: Current Surgical Diagnosis & Treatment, 5th ed. Lange, 1981.) 





FIGURES 

Figure 6-25

Figure 6-26. Diagram of pericardiocentesis showing position of needle and anatomic 

relationships. (Reproduced, with permission, from Way LW [editor]: Current Surgical 

Diagnosis & Treatment, 9th ed. Appleton & Lange, 1991.) 





FIGURES 

Figure 6-26

Figure 6-27. Illustration of the 4 views for the FAST exam and where fluid would be 

seen in each view. A = atrium; B = bladder; F = fluid; K = kidney; L = liver; S = spleen; V 

= ventricle. 





FIGURES 

Figure 6-27

Figure 6-28. Insertion site for abdominal paracentesis. (Reproduced, with permission, 

from Dunphy JE, Way LW [editors]: Current Surgical Diagnosis & Treatment, 5th ed. 

Lange, 1981.) 





FIGURES 

Figure 6-28

Figure 6-29. Technique of peritoneal lavage. (Reproduced, with permission, from 

Dunphy JE, Way LW [editors]: Current Surgical Diagnosis & Treatment, 5th ed. Lange, 

1981.) 





FIGURES 

Figure 6-29

Figure 6-30. Sagittal section of female bladder showing balloon of Foley catheter fitting 

snugly against the trigone. 





FIGURES 

Figure 6-30

Figure 6-31. Suprapubic cystostomy. Sagittal section of distended bladder showing 

insertion site for catheter. 





FIGURES 

Figure 6-31

Figure 6-32. Decubitus position for lumbar puncture. (Reproduced, with permission, 

from Krupp MA et al: Physician's Handbook, 21st ed. Lange, 1985.) 





FIGURES 

Figure 6-32

Figure 6-33. Packing to control bleeding from the posterior nose. A: Catheter inserted 

and pack attached. B: Pack drawn into position as catheter is removed. C: Strip tied 

over a bolster to hold pack in place with anterior pack installed "accordion pleating" 

style. D: Alternative method using balloon catheter instead of gauze pack. Anterior 

packing should follow placement of all posterior packs. (Reproduced, with permission, 

from Way LW [editor]: Current Surgical Diagnosis & Treatment, 9th ed. Appleton & 

Lange, 1991.) 





FIGURES 

Figure 6-33

Figure 6-34. Aspiration of the knee joint. 





FIGURES 

Figure 6-34

Figure 6-35. Posterior approach to shoulder joint aspiration. 





FIGURES 

Figure 6-35

Figure 6-36. Anterior approach to shoulder joint aspiration. 





FIGURES 

Figure 6-36

Figure 6-37. Aspiration of the elbow joint. 





FIGURES 

Figure 6-37

Figure 6-38. Determination of the needle entry site for ankle joint aspiration. A small 

depression can be palpated about 1 cm (1/2 in) anterior and inferior to the medial 

malleolus and lateral to the extensor hallucis longus. 





FIGURES 

Figure 6-38

SECTION II - MANAGEMENT OF COMMON EMERGENCY 

PROBLEMS 

7. Basic & Advanced Cardiac Life Support - Eric M. Sergienko, MD, & 


OVERVIEW OF CARDIAC ARREST 

EPIDEMIOLOGY OF CARDIAC ARREST 

Cardiac disease is the most common cause of death in the United States. The majority 

of cardiac deaths occur suddenly. There are more than 300,000 cardiac arrests each 

year in the United States. About two thirds of these occur in the prehospital setting. 

Survival to discharge varies dramatically from region to region and system to system 

with rates ranging from 1.4% in New York City to 49% in King County, Washington. A 

meta-analysis of defibrillator-capable emergency medical services (EMS) showed a 

median survival to discharge rate of 6.4%. Of note, resuscitation within critical care 

areas has similar success rates. Sudden cardiac death is associated with an underlying 

history of coronary artery disease, but an acute thrombotic event is associated with only 

20-40% of cardiac arrests. Twenty-five percent of cardiac arrests have a noncardiac 

origin (eg, massive pulmonary embolism, renal failure, malignancy). The most common 

presenting rhythm to prehospital care providers is ventricular fibrillation, which occurs in 

about a third of all patients. Asystole and pulseless electrical activity (PEA, formerly 

electromechanical dissociation) are the second and third most common rhythms, 

respectively, at time of first intervention. 

DETERMINANTS OF CARDIAC ARREST SURVIVAL 

The single most important factor for survival in the undifferentiated adult cardiac arrest 

victim is the elapsed time from patient collapse until the first defibrillation shock is 

delivered. Other factors related to a positive outcome include witnessed cardiac arrest, 

early bystander cardiopulmonary resuscitation (CPR), and chest pain as the presenting 

complaint. Early provision of advanced life support (ALS) has been shown to be of 

benefit, but its value in addition to defibrillation is of some debate. Factors associated 

with poor prognosis include dyspnea as the presenting complaint, malignancy or sepsis 

as the underlying cause of cardiac arrest, coexistence of pneumonia, presence of 

hypotension prior to cardiac arrest, and a homebound lifestyle. 

A patient who is not resuscitated in the field is unlikely to be resuscitated in the 

emergency department. Forty-six percent of patients are deemed dead in the field, and 

another 16% are declared dead upon arrival in the emergency department or shortly 

thereafter. The risks of transporting a patient who remains in cardiac arrest after ALS 

procedures have been performed in the field often outweigh the likelihood of a 

successful resuscitation with good neurologic outcome. Medical directors should 

consider protocols to determine death and termination of resuscitative efforts in the field.

THE TEAM APPROACH TO CARDIAC ARREST 

There are many pivotal participants in a cardiac arrest—first responder, prehospital 

EMS personnel, emergency department resuscitation team leader, emergency 

department resuscitation team members, and ancillary personnel. A successful 

resuscitation depends on a functional team. Roles should be identified prior to a 

resuscitation. Team behaviors and expectations can be established and used on a daily 

basis and during real-time resuscitations. 

The composition of the resuscitation team is based largely on resource availability and 

institutional preferences. Intuitively, there must be a team leader who is responsible for 

the overall direction of the resuscitation. A designated team member must manage the 

airway, and a second, or even third, team member can assist with airway functions, 

including ventilation, suctioning, and gathering and assembly of airway equipment. 

Multiple team members will rotate through providing chest compressions. The team 

leader must ensure that these providers do not become fatigued, providing for relief 

every 5-10 minutes. Vascular access must be obtained, and the team member 

performing this role can also administer medications. If a medication dispenser (eg, 

Pyxis) is being used, it is helpful to designate one person to manage it. Finally, it is 

helpful to have a recorder to record events, provide cues, track laboratory results, and 

communicate with areas outside of the resuscitation. The team leader must also control 

the number of people involved in the resuscitation. Too often the scene becomes 

chaotic because of those wanting to help or just take a look. 

Care providers are often trained as individuals, even though they most often respond as 

an integrated team. Utilization of team behaviors can minimize the number of errors, 

duplication of efforts, and loss of information that can occur during the confusion of a 

resuscitation. Maintaining situational awareness is the key to being an essential team 

member. Reinforcing situational awareness in others (ie, cross monitoring) emphasizes 

the team construct. Some mechanisms to enhance cross monitoring include call outs, 

check backs, and hand offs. Call outs involve information that must be shared with the 

entire team (eg, calling out vital signs). Check backs are means to avoid order 

errors—the recipient of the order repeats the order verbatim, and then the orderer 

confirms that order verbatim. Hand offs are positive transfer of control of aspects of 

patient care. These techniques sustain dynamic situational awareness and allow for an 

organized, integrated team approach to comprehensive resuscitative care. 

FAMILY PRESENCE DURING RESUSCITATION 

An often vexing issue in a resuscitation is the presence of family members. The default 

has been to exclude the family from the resuscitation. Most surveys of family members 

show they would prefer to be present at resuscitations. This is true for both adult and 

pediatric resuscitations. Most providers who work at facilities that allow family members 

to be present during resuscitation feel it is beneficial. Those who work at facilities that 

do not allow family members to be present feel that it is not beneficial and may interfere 

with the resuscitation. Programs that have implemented family presence during 

resuscitations dedicate a staff member to be at the family's side to answer questions, 

provide support, and act as a liaison between the family and the resuscitation team.

Clarke JR et al: An objective analysis of process errors in trauma resuscitations. Acad 

Emerg Med 2000;7(11):1303. [PMID: 11073483] 

Cooper S, Wakelam A: Leadership of resuscitation teams: "Lighthouse Leadership." 

Resuscitation 1999;42(1):27. [PMID: 10524729] 

de Vreede-Swagemakers et al: Circumstances and causes of out-of-hospital cardiac 

arrest in sudden death survivors. Heart 1998;79(4):356. [PMID: 9616342] 

Dickinson ET, Schneider RM, Verdile VP: The impact of pre-hospital physicians on 

out-of-hospital nonasystolic cardiac arrest. Prehosp Emerg Care 1997;1(3):132. [PMID: 

9709354] 

Hillman K et al: Redefining in-hospital resuscitation: the concept of the medical 

emergency team. Resuscitation 2001;48(2): 105. [PMID: 11426471] 

Soar J, Absalom A: Survival after cardiac arrest outside hospital. Heart 2000;83(1):103. 

[PMID: 10671071] 

Soo LH et al: Resuscitation from out-of-hospital cardiac arrest: is survival dependent on 

who is available at the scene? Heart 1999;81(1):47. [PMID: 10220544] 

Stiell IG et al: Modifiable factors associated with improved cardiac arrest survival in a 

multicenter basic life support/defibrillation system: OPALS Study phase I results. 

Ontario Prehospital Advanced Life Support. Ann Emerg Med 1999;33(1):44. [PMID: 

9867885] 

Tsai E: Should family members be present during cardiopulmonary resuscitation? N 

Engl J Med 2002;346(13):1019. [PMID: 11919313] 

Weston CF, Wilson RJ, Jones SD: Predicting survival from out-of-hospital cardiac 

arrest: a multivariate analysis. Resuscitation 1997;34(1):27. [PMID: 9051821] 

ADULT BASIC LIFE SUPPORT (See Figure 7-1.) 

THE CHAIN OF SURVIVAL 

The American Heart Association (AHA) first proposed the phrase "the chain of survival" 

to describe the interrelated series of interventions that must be in place to maximize 

functional survival from sudden cardiac death. Any failure to implement a single link in 

the chain will lead to a decrease in survival. As depicted by the AHA, there are 4 links in 

the chain of survival: early access, early basic life support (BLS), early defibrillation, and 

early advanced cardiac life support (ACLS). Some authors propose a total of 7 links, to 

include early prevention prior to the event and definitive care and rehabilitation after the 

event. The framework of ACLS and BLS interventions focuses on maintaining the links 

of this chain. 

TECHNIQUES OF BASIC LIFE SUPPORT

Early Prevention 

Early prevention involves both primary prevention, including lifestyle modification, and 

secondary prevention, including medical therapy. More pertinent, the patient and family 

should be taught the signs and symptoms of chest pain related to cardiac ischemia. 

Patients with known cardiac disease should attempt to treat the pain with sublingual 

nitroglycerin. If, after taking 3 doses of nitroglycerin, there is no relief, the patient should 

call the emergency number for his or her area. Patients without known disease should 

contact the emergency number if unremitting chest pain is present for more than 5 

minutes. In the hospital setting, an early, organized approach to chest pain, dyspnea, 

and abnormal vital signs including pulse oximetry can decrease the number of cardiac 

arrests. 

Early Access 

The first responder should call the appropriate emergency number (eg, 9-1-1) after 

coming upon an unresponsive patient. In the adult victim, after opening the airway and 

confirming apnea, "phone first." In the community setting, call the emergency number 

(eg, 9-1-1) to initiate an organized response to the cardiac arrest. In the hospital setting, 

initiate the hospital's emergency response or "code" system. Early access into the 

system is imperative to minimize the time delay until defibrillation. 

Early Basic Life Support 

Upon finding an unresponsive patient, activate the EMS system and then return to the 

patient to provide BLS until further help arrives. Assume a position alongside the patient 

so that rescue breathing and chest compressions can be done without repositioning 

one's body. Position the patient on a hard surface to allow for efficient chest 

compressions. This is achieved by placing a CPR board under the patient's chest or 

modifying the bed to provide a firmer surface. Anticipate the arrival of a defibrillator, 

which is usually positioned on the left side, next to the patient's ear. 

The ABCs 

A. Airway 

Open the patient's airway using the head-tilt and chin-lift method (Figure 7-2). Place one 

hand firmly on the patient's forehead; apply firm downward, backward pressure to tilt the 

head. Hook the fingers of the other hand under the bony part of the chin, lifting up the 

chin. In the event of trauma, use the jaw thrust without head tilt (Figure 7-3A). 

B. Breathing 

Assess breathing by leaning over the patient's open mouth and looking down at the 

chest for any rise or fall of breathing. Place an ear near the patient's mouth, listening for 

breathing or feeling the flow of air over the cheek (see Figure 7-2D). This should take no 

more than 10 seconds. 

In the absence of breathing, perform mouth-to-mouth, mouth-to-mask, or bag-mask 

ventilation. Health care professionals should be familiar with all of these techniques. A

mask with a one-way valve should be readily available in all health care settings to 

minimize the risk of contamination from the patient's oral secretions. A bag-mask should 

be available in all critical care areas and on crash carts. 

1. Mouth to mouth—The airway is maintained by using the head-tilt and chin-lift 

method. Pinch the patient's nose shut. Seal your lips around the patient's mouth (see 

Figure 7-2E). Give 2 slow breaths initially. There should be good chest rise and fall. If 

not, reposition the patient's airway and attempt to ventilate again. If there is still no 

movement of air, presume that the patient has a foreign body airway obstruction (see 

"Foreign Body Airway Obstruction" section, below) and attempt to clear it. 

2. Mouth to mask—A clear mask with or without a one-way valve (often called a pocket 

mask) can be used as an adjunct to mouth-to-mouth ventilation (see Figure 7-3C). 

Ventilations are provided in the same way as for mouth to mouth. It is often easier and 

more effective for the inexperienced provider to adequately ventilate the patient with the 

pocket-mask than with the bag-mask. When possible the mask should be attached to 

supplemental oxygen. There are 2 techniques to achieve an effective seal with the 

mask. 

a. Cephalic technique—The cephalic technique is used when there is more than 1 

provider. The provider ventilating the patient is positioned at the head of the bed. The 

mask is applied in one of two ways, either with the thumbs and thenar eminences 

providing a seal, while the fingers are used to perform jaw thrust, or with the thumbs and 

index fingers providing a seal, while the remaining fingers provide a jaw thrust (Figure 

7-4). 

b. Lateral technique—When there is only 1 provider, the lateral technique must be 

used to allow the provider to perform 1-person CPR. With the provider at the patient's 

side, a head tilt-chin lift is applied. The hand closer to the top of the patient's head 

performs a head tilt while creating a seal on the upper part of the mask with index finger 

and thumb. The lower hand performs a chin lift with the fingers while creating a seal on 

the lower part of the mask with the thumb and thenar eminence. 

3. Bag-mask ventilation—When ventilating a patient, use supplemental oxygen 

whenever possible, to provide up to a 100% concentration. The adult bag-mask is 

usually a 1600-mL self-inflating bag with a nonrebreathing valve attached to a face 

mask. There should be a reservoir for oxygen and tubing to connect to an oxygen 

source. 

When 2 providers are available to manage the patient's airway, the mask is applied as 

with the cephalic technique of the pocket-mask. Ventilations are then administered by 

the second provider squeezing the bag over 2 seconds and then releasing for 3 

seconds. If only one provider is available for airway management, he or she must 

provide an adequate seal with one hand, using the index finger and thumb while 

providing a chin lift with the other 3 fingers. The other hand is used to squeeze the 

bag-mask. Optimizing the head tilt by positioning towels underneath the patient's 

shoulders may help, especially if the patient is obese. Ventilation can be improved by 

squeezing the bag against the provider's body.

4. Cricoid pressure application—Cricoid pressure (Sellick maneuver) can be used to 

minimize gastric insufflation associated with ventilation. The cricoid cartilage is the only 

complete ring in the trachea. Posterior displacement of the cricoid cartilage closes off 

the esophagus. This should be done only in the unconscious patient. The cricoid 

cartilage is found by first locating the thyroid cartilage with the index finger, then moving 

down the neck over the cricothyroid membrane. The first cartilage ring below the 

membrane is the cricoid cartilage. Moderate pressure (5-10 pounds) is applied, pressing 

the cartilage with the thumb and index finger posteriorly toward the cervical spine. 

C. Circulation 

Assess circulation by checking for the carotid pulse. The carotid pulse is located in the 

groove lateral to the trachea. Check the pulse for no more than 10 seconds. If a pulse is 

present, rescue breathing can continue with 1 breath every 4-5 seconds. If a pulse is 

absent, start chest compressions. 

Chest compressions are performed on the lower half of the sternum. Identify the 

location by tracing the fingers of the hand nearest to the patient's feet along the costal 

margin to the xiphisternal junction (Figure 7-5). Place the heel of the other hand on the 

sternum just cephalad to the fingers of the first hand. Place the first hand on top of the 

other hand. The long axis of the heels of both hands should be parallel to the long axis 

of the sternum. Fingers may be interlaced or extended but must be kept off the chest. 

The provider is positioned with the knees as close to the patient as possible; the 

provider's shoulders, elbows, and heels of the hands are in a vertical line with the 

patient's sternum and chest. Provide compressions by rocking back and forth on the 

heels. If the patient is on a gurney, do compressions by rocking back and forth at the 

hips. The elbows should remain locked. Compressions should depress the sternum 

11/2-2 inches. Compressions should be rhythmic; the same amount of time should be 

spent on each phase of the cycle. The hands should not leave the chest. Give 100 

compressions per minute. Until the patient is intubated, the ratio of compressions to 

ventilations is 15 to 2. This ratio applies to all BLS providers. It allows for greater 

coronary perfusion pressures than the 5:1 ratio used previously by health care 

providers. Once an airway is established, ventilations and compressions can be 

performed asynchronously. 

COMPLICATIONS OF BASIC LIFE SUPPORT 

The key complication associated with ventilation is gastric insufflation. Air forced into the 

stomach can lead to gastric distention, which can cause regurgitation of stomach 

contents, diminished lung volumes, and decreased effectiveness of chest 

compressions. Complications occurring with chest compressions are numerous but can 

be minimized with correct technique. Even with correctly performed chest 

compressions, rib fractures can occur. Additional complications include lacerations of 

liver and spleen, pneumothorax, and hemothorax. 

FOREIGN BODY AIRWAY OBSTRUCTION 

Foreign body airway obstruction occurs in adults with ingestion of alcohol or other drugs 

(which result in an altered level of consciousness), in patients who have difficulty

chewing or swallowing secondary to stroke or other disease process, and in denture 

wearers. Foreign body airway obstruction can be recognized in the conscious patient 

when difficulty breathing, coughing, or the universal "I'm choking" sign—clutching 

fingers around the throat (Figure 7-6)—is seen. 

Ask the patient if he or she is choking. If the patient nods, ask if he or she can speak. If 

the patient has a strong cough, is not cyanotic, does not have labored breathing or 

retractions, and can speak, then a partial obstruction with good air exchange exists. 

Observe the patient, but do not intervene initially. Allow the patient to attempt to clear 

the obstruction by him- or herself. If the patient has a weak cough, is cyanotic, has 

labored breathing or stridor, or has difficulty speaking, then a partial obstruction with 

poor air exchange exists. Prompt intervention is indicated. If the airway is obstructed 

completely, the patient is unable to speak or cough and may become cyanotic. Rapid 

intervention is essential. 

The Heimlich maneuver, or abdominal thrust, is used in the conscious choking patient 

(see Figure 7-6). While standing behind the patient, position the fist with the thumb 

facing up over the umbilicus. Roll the fist so that the thumb is against the abdominal 

wall. Grasp the fist with the other hand. Apply sharp upward thrusts until the foreign 

body is cleared or the patient collapses and becomes unconscious. 

The Heimlich maneuver can be performed on a sitting patient by kneeling and reaching 

around the chair. 

If the patient collapses, position him or her on the floor. Perform a tongue-jaw lift by 

grasping the jaw and tongue with one hand (Figure 7-7A). With the other hand, perform 

a blind finger sweep. Attempt to ventilate. If the first attempt does not succeed, 

reposition the airway and attempt to ventilate again. If the second attempt fails, perform 

the Heimlich maneuver by straddling the patient (Figure 7-7B and C). Place the heel of 

one hand in the same location as that used for the standing abdominal thrust. Place the 

other hand over the top of the first. Provide five sharp upward thrusts. Repeat the 

sequence of finger sweep, ventilation, and thrusts until the obstruction is relieved or until 

alternative means of clearing the airway arrive (eg, Magill forceps, surgical or needle 

cricothyroidotomy). 

DEFIBRILLATION 

Defibrillation is the intervention for the heart in ventricular fibrillation. When a critical 

level of energy reaches the myocardium, the ventricles become depolarized. This 

provides an opportunity for the sinoatrial node or another pacemaker to restore an 

organized perfusing rhythm. To succeed, the defibrillator must overcome the resistance, 

or impedance, encountered going through the chest. To minimize transthoracic 

impedance the provider must select the proper size paddles or self-adhesive pads; 

apply them in the correct position (Figure 7-8); use conductive gel, pregelled conductive 

pads, or saline-soaked-gauze to minimize skin resistance; and apply 25 pounds of 

pressure to the paddles. Increasing the energy selected will increase the energy 

delivered. Repeated shocks will decrease transthoracic impedance successively. 

The same techniques for defibrillation are used for synchronized cardioversion. The

defibrillator must be placed in the synchronized mode. This is done by activating the 

"SYNCH" button on most defibrillators. This coordinates the shock so that it is not 

delivered during the relative refractory period (a shock during this period could result in 

ventricular fibrillation). Most defibrillators will revert to an unsynchronized mode after 

delivering a synchronized shock. This allows for rapid defibrillation if ventricular 

fibrillation occurs. For repeated synchronized cardioversion, the defibrillator must be 

resynchronized. A patient should be adequately sedated and receive analgesia prior to 

cardioversion, if circumstances permit. 

Defibrillation Waveforms 

Waveforms indicate the flow of energy between the two paddles or pads of the 

defibrillator. A monophasic waveform travels in one direction, whereas a biphasic 

waveform travels initially in one direction and then reverses flow. Old defibrillators used 

the monophasic waveform. The biphasic defibrillator was first used in implanted 

defibrillators because it required less energy to successfully defibrillate; therefore, a 

smaller battery was needed. This technology was transferred to the AED (Figure 7-9), 

which required a small battery with a long shelf life. Compared to monophasic 

waveforms, biphasic waveforms have the same rate of defibrillation, with less damage 

to the myocardium. Theoretically the biphasic waveform should be more effective at 

defibrillating than the monophasic waveform, but this has not been shown in a clinical 

trial. Most manufacturers are making the transition to a biphasic waveform for their 

manual defibrillators. Although these manufacturers have differing biphasic waveforms, 

they all require less energy—in the range of 150-200 J per shock. Some defibrillators 

have escalating levels of energy, whereas others are fixed. Providers must be familiar 

with their defibrillator. 

Automated External Defibrillation 

(See Figure 7-9.) Manual defibrillation was first performed in the 1960s. With the 

development of waveform recognition software, it has been possible to program a 

defibrillator to deliver a shock in the event of ventricular fibrillation. The first defibrillators 

designed to deliver a shock without human interpretation of the waveform were 

manufactured in the late 1970s. Several trials have shown a significant increase in 

survival to hospital discharge with a community automated external defibrillator (AED) 

program. This is true regardless of what type of first responder (emergency medical 

technician, firefighter, or police) used the AED. 

Before applying the AED, the rescuer should initiate airway management and 

ventilations. If the patient has no pulse, an AED should be brought to the patient's side. 

If two rescuers are available, one can perform CPR while the AED is sought, but 

obtaining the AED is the critical action. The AED requires the rescuer to power on the 

device, apply the self-adhesive pads to the patient's chest, press the Analyze button, 

and, if an electrical shock is indicated, press the Shock button. The current algorithm for 

AED use is shown in Figure 7-10. 

The medical direction of an AED program is crucial and is discussed in Chapter 2. 

Public Access Defibrillation

With the marked success of AEDs used by trained rescuers, the concept of providing 

public access defibrillators (PADs) evolved. PADs have a role in cardiac arrest in 

settings where an AED is used once in 5 years, when rescuers would take greater than 

5 minutes to respond from time of collapse, and when it would be likely a lay rescuer 

could use the AED in less than 5 minutes. Suggested venues for PADs include sports 

arenas, shopping malls, and airports. Where PADs have been established, there have 

been numerous reports of positive outcomes, with no adverse outcomes related to an 

improperly used AED. AED malfunction is most likely to occur secondary to lack of 

maintenance. Many manufacturers have created AEDs that perform daily self-checks 

that minimize this risk. Like the AED used by first responders, the PAD requires medical 

direction. 

Bang A, Herlitz J, Holmberg S: Possibilities of implementing dispatcher-assisted 

cardiopulmonary resuscitation in the community. An evaluation of 99 consecutive 

out-of-hospital cardiac arrests. Resuscitation 2000;44(1):19. [PMID: 10699696] 

De Maio VJ et al: CPR-only survivors of out-of-hospital cardiac arrest: implications for 

out-of-hospital care and cardiac arrest research methodology. Ann Emerg Med 

2001;37(6):602. [PMID: 11385328] 

Ewy GA: Cardiopulmonary resuscitation—strengthening the links in the chain of 

survival. N Engl J Med 2000;342(21):1599. [PMID: 10824080] 

Ginsburg W: Prepare to be shocked: the evolving standard of care in treating sudden 

cardiac arrest. Am J Emerg Med 1998; 16(3): 315. [PMID: 9596443] 

Ho J et al: Automatic external defibrillation and its effects on neurologic outcome in 

cardiac arrest patients in an urban, two-tiered EMS system. Pre-hospital Disaster 

Medicine 1997; 12(4):284. [PMID: 10179208] 

Jacobs I et al: The chain of survival. Ann Emerg Med 2001;37(4 Suppl):S5. [PMID: 

11290965] 

Niemann JT: Defibrillation waveforms. Ann Emerg Med 2001;37: 59. [PMID: 11145773] 

White RD, Hankins DG, Bugliosi TF: Seven years' experience with early defibrillation by 

police and paramedics in an emergency medical services system. Resuscitation 

1998;39(3):145. [PMID: 10078803] 

ADULT ADVANCED LIFE SUPPORT 

If a patient does not respond to initial CPR and defibrillation, further interventions are 

required. With the success of early interventions in restoring a perfusing rhythm, the 

patient may still require ALS (ie, airway, medications, and further evaluation) to optimize 

outcome. 

ADVANCED AIRWAY MANAGEMENT

Advanced airway techniques include endotracheal intubation, the use of the laryngeal 

mask airway, or the use of a double lumen tube such as the Combitube or 

pharyngotracheal lumen airway. 

Endotracheal intubation provides the best means of securing the airway; however, 

intubation should be attempted only by providers who are skilled in the procedure and 

who perform it at least 6-12 times per year. Placement of the tube should be confirmed 

by colorimetric end-tidal CO 2 detectors (although unreliable in prolonged cardiac arrest), 

esophageal detector devices, or capnography in addition to more traditional techniques. 

The details of endotracheal intubation are discussed in Chapters 6 and 8. A commercial 

tracheal tube holder may be more beneficial than regular tape in securing the 

endotracheal tube. Because of the risk of accidental and unrecognized dislodgment in 

the prehospital setting, it is recommended that the patient be placed in a cervical collar 

and on a backboard to minimize neck movement. When unable to secure an airway 

(either manually with advanced airway techniques or surgically) or unable to ventilate 

the patient using a bag-mask, the trained provider must perform a surgical or needle 

cricothyroidotomy. 

SPECIFIC RHYTHMS (See Figure 7-1.) 

Ventricular Fibrillation or Pulseless Ventricular Tachycardia 

As mentioned above, early defibrillation is the key to successful resuscitation in the 

patient with ventricular fibrillation. The first 3 shocks are given as stacked, sequential 

shocks. The paddles do not leave the chest, and the pulse is not checked between 

shocks. The monitor is checked between each shock. If a rhythm other than ventricular 

fibrillation (or ventricular tachycardia [VT] that was originally without a pulse) is noted, 

then a pulse check is performed. Shocks continue to be delivered between other 

interventions. It is acceptable to stack further shocks. 

Enhancing cardiac output and blood pressure improves both coronary and cerebral 

perfusion. This improves the outcome of subsequent defibrillation and helps to mitigate 

neurologic injury. In ventricular fibrillation, vasopressin (40 units) may be used as an 

alternative to the first dose of epinephrine. This is a 1-time dose; epinephrine may then 

be used starting 10 minutes after the vasopressin (see "Pharmacologic Therapy" 

section, below). 

Antidysrhythmics may prove beneficial in return of spontaneous circulation (ROSC). 

Both lidocaine and amiodarone are acceptable alternatives. Magnesium can be 

considered in torsade de pointes. Procainamide can be effective in recurring ventricular 

fibrillation. 

Pulseless Electrical Activity 

The key to successfully resuscitating the patient with PEA is identifying and treating the 

underlying cause. Assessment for these conditions can be facilitated by history, vital 

signs including temperature, electrocardiogram (ECG), blood gas analysis, electrolytes, 

and a focused physical examination. Initial interventions can be performed concurrently 

to address hypoxemia and hypovolemia.

Asystole 

Asystole usually is a preterminal rhythm. As with PEA, the underlying causes must be 

addressed. Transcutaneous pacing may be considered early on, but it should be used 

only if the patient was witnessed entering asystole from a perfusing rhythm. If an 

asystolic patient does not respond to ALS interventions in the field, terminate 

resuscitation efforts in the field and do not consider urgent transport. 

Tachydysrhythmia with a Pulse 

If a patient has a tachydysrhythmia with evidence of poor perfusion (where the 

tachydysrhythmia is the likely source), prompt cardioversion is indicated. Chest pain, 

dyspnea, altered level of consciousness, hypotension, and new-onset congestive heart 

failure are all indications of instability. Quickly perform synchronized cardioversion. Give 

the patient analgesic and sedative agents if circumstances permit. 

In a hemodynamically stable patient with a tachydysrhythmia, clinical evaluation is 

needed to determine the source of the dysrhythmia. History and ECG are the 2 key 

diagnostic aids. The most difficult differentiation is with the regular wide-complex 

tachycardias. The diagnostic dilemma is to decide whether the rhythm is 

supraventricular in origin with aberrant conduction or a true VT (Chapter 35). Table 7-1 

indicates findings suggestive of VT versus supraventricular tachycardia (SVT). If the 

rhythm cannot be confirmed as SVT, the patient should be presumed to have a VT, and 

appropriate treatment should be rendered. Treating a VT as an SVT can have 

disastrous results. The use of adenosine as a diagnostic aid in distinguishing between 

SVT with aberrant conduction and VT is also discouraged. The conversion of VT with 

adenosine has been reported, most often in young, otherwise healthy patients. 

Bradycardia 

As with tachydysrhythmia, a slow rhythm with signs of inadequate perfusion needs 

immediate intervention, regardless of the underlying pathology. A relative bradycardia 

with good perfusion may be observed while preparations are made to treat the 

underlying cause. Atropine can be beneficial if parasympathetic tone is excessive. This 

is typically the case in depressed sinus node automaticity and in atrioventricular (AV) 

block secondary to acute myocardial infarction. Bradycardias secondary to degeneration 

of the conduction system (or disruption, as in a transplanted heart), or due to 

pharmacologic or metabolic causes, generally do not respond to atropine. 

Transcutaneous or transvenous pacing can be used as a bridge to a more permanent 

pacing mechanism. 

PHARMACOLOGIC THERAPY (See Table 7-2.) 

Vasoactive Agents 

A. Epinephrine 

Epinephrine is a mixed a and ß agonist. It has been shown to increase diastolic aortic 

blood pressure and coronary perfusion pressure. As such, it has been the mainstay of

pharmacologic therapy in the pulseless patient, regardless of the underlying rhythm. 

High-dose epinephrine in adults has largely been abandoned. Although it resulted in a 

greater rate of ROSC and admission to hospital, higher dose epinephrine did not lead to 

an increase in hospital discharge. Its advantageous properties are related to its a 

receptor stimulation, whereas its ß properties may adversely lead to increased 

myocardial oxygen consumption. This has led researchers to seek a drug with more 

pure a properties. 

B. Vasopressin 

Vasopressin is an endogenous hormone also known as antidiuretic hormone. It evokes 

more prominent vasoconstriction in the skin, skeletal muscle, and intestinal tract, while 

causing relatively less vasoconstriction in the coronary, cerebral, and renal vasculature. 

It is potentially useful as an alternative to epinephrine in ventricular fibrillation. It has 

been shown to have a higher rate of ROSC in the porcine model, although the results of 

human trials have been mixed. Vasopressin has not been shown to be useful in either 

asystole or PEA. Vasopressin has not been shown to be beneficial in pediatric patients. 

C. Dopamine 

Dopamine has mixed a, ß, and dopaminergic effects that manifest in a dose-dependent 

fashion. At low doses of 2-4 ug/kg/min there is no inotropic effect, nor is there increased 

renal and splanchnic perfusion. At doses of 5-10 ug/kg/min, ß-1 and ß-2 inotropic 

effects predominate. At doses greater than 10 ug/kg/min there is a substantial 

predominance of a effects with a resultant decreased perfusion of the splanchnic bed. 

For this reason, high-dose dopamine should not be used. If hypotension remains after 

optimization of filling pressures, dobutamine (as an inotropic agent) or norepinephrine 

(as a vasopressor) should be considered. 

D. Norepinephrine 

Norepinephrine has predominantly a effects but has some ß effects as well. Its role is in 

the postresuscitation management of hypotension when systolic pressures are less than 

70 mm Hg. 

E. Dobutamine 

Dobutamine is a synthetic predominantly ß-1 agonist with little ß-2 or a effects. As such, 

it can improve myocardial contractility and increase cardiac output. It is the initial agent 

of choice in patients with systolic blood pressure of 70-100 mm Hg and no signs or 

symptoms of shock. Paradoxically it can worsen hypotension in patients with inadequate 

preload. Dobutamine can provoke tachyarrhythmias. It is run as an intravenous infusion 

of 2.5-15 ug/kg/min. 

F. Phenylephrine 

Phenylephrine is a pure a agonist that can be used in the postresuscitation phase to 

maintain diastolic blood pressure. Once blood pressure has been stabilized, an 

intravenous drip of 40-60 ug/min should be started and then titrated to effect. 

Antidysrhythmics 

A. Adenosine 

Adenosine is an endogenous nucleoside that is a potent but short-lived AV nodal

locking agent. Along with vagal maneuvers, it is considered first-line therapy in 

paroxysmal supraventricular tachycardia (PSVT) secondary to a reentrant-type 

conduction defect. Adenosine should be considered only when a supraventricular 

rhythm is suspected. It should not be used as an aid in differentiating between PSVT 

with aberrant conduction and VT. It is associated with a prolonged sinus pause. The 

patient will often experience transient flushing, dyspnea, or chest pain. BR> 

B. Amiodarone 

Amiodarone is predominantly a class III antidysrhythmic (potassium channel blocker), 

but it also has some properties of class I (sodium channel blockade), class II 

(ß-blockade), and class IV (calcium channel blockade) antidysrhythmics. This wide 

variety of effects makes amiodarone useful in treating both supraventricular and 

ventricular tachydysrhythmias. There is good evidence supporting its use in PSVT for 

both rate control and rhythm conversion. The same dosing regimen is used for 

hemodynamically stable VT, but this recommendation is extrapolated from unstable VT 

and ventricular fibrillation studies. In ventricular fibrillation or pulseless VT, 2 prospective 

prehospital trials have shown a significant increase in ROSC and survival to hospital 

admission. This has not, however, resulted in an increase in survival to hospital 

discharge. 

C. Atropine 

Atropine is a parasympatholytic agent useful in the treatment of bradycardias due to 

increased parasympathetic tone (second- and third-degree AV blocks). Its use can be 

considered in asystole and bradycardic PEA. Dosing in the perfusing patient is 0.5 mg 

IV every 5 minutes up to a total of 3 mg. In the pulseless patient, the dose is 1 mg IV 

every 5 minutes to a total dose of 3 mg. 

D. ß-Blockers 

ß-Blockers (ie, atenolol, metoprolol, esmolol) are indicated for SVT for rate control in 

patients with preserved left ventricular function. Atenolol and metoprolol are ß-1 

(cardioselective) blocking agents available in both intravenous and oral formulations. 

Esmolol is a short-acting ß-1 agent that must be given in a bolus and then maintained 

through a continuous infusion. This may be advantageous in patients who may respond 

negatively to ß-blockade (for example, patients with chronic obstructive pulmonary 

disease). If an adequate response is not achieved after 5 minutes, the loading dose may 

be repeated and the infusion rate doubled. 

E. Calcium Channel Blockers 

Calcium channel blockers (ie, diltiazem and verapamil) are also indicated for rate control 

in SVT. They slow AV nodal conduction and prolong the AV nodal refractory period. 

Calcium channel blockers are contraindicated in atrial fibrillation or atrial flutter with 

rapid ventricular response when an accessory pathway such as Wolf-Parkinson-White 

syndrome exists because it could lead to a life-threatening increase in the ventricular 

heart rate. Diltiazem is better tolerated in patients with impaired left ventricular function. 

F. Lidocaine 

Lidocaine is a class IB antidysrhythmic. It is the most commonly used agent for 

ventricular rhythms, both stable and unstable. The only large-scale observational study 

involving lidocaine demonstrated an increased survival to hospital admission but not to 

discharge. This study was confounded by the fact that the patients who were given

lidocaine received treatment from ALS providers (ie, registered nurses), whereas those 

who were not given lidocaine received treatment from prehospital technicians. Other 

smaller studies have not shown a clear benefit for lidocaine. 

G. Magnesium 

Magnesium is indicated for patients who are known or suspected to have a low 

magnesium level or recurrent ventricular dysrhythmias and for those with torsades de 

pointes. It has been used in the past for SVTs that have been unresponsive to 

adenosine, but no clinical trials to date support this use. 

H. Procainamide 

Procainamide is a second-line agent for stable VT. It is also indicated for pulseless VT 

and ventricular fibrillation, but there is less support for these uses. It is a class IA 

antiarrhythmic that is more effective than lidocaine in converting VT, but it is hindered by 

the time required to administer the medication as a continuous infusion. Also, 

procainamide can provoke hypotension, and its use should be avoided in patients with 

long QT intervals or when drugs that prolong the QT interval, such as amiodarone, have 

already been administered. 

POSTRESUSCITATION STABILIZATION 

After successful ROSC, continued evaluation and management are required. Initial data 

gathering is needed to address the patient's history, underlying condition, and current 

physiologic status. Cull the patient's history from friends, family, witnesses, and 

prehospital care providers. Evaluate evidence of the patient's prearrest condition from 

the history and physical examination. Evaluate the patient's status by physical 

examination, laboratory and radiologic studies, and continuous hemodynamic 

monitoring. Routine postresuscitation studies include complete blood count, electrolytes, 

glucose, cardiac enzymes, arterial blood gas, and a portable chest x-ray. Additional 

studies might include bedside echocardiography, pulmonary artery catheterization, heart 

catheterization, and computed tomography. Direct initial interventions toward 

maintaining stable hemodynamic parameters. The primary goal at this juncture is to 

restore adequate perfusion to peripheral organ systems, specifically the renal and 

splanchnic beds. Attach full monitoring equipment, if not done previously. Place a Foley 

catheter to monitor urine output. Secure intravenous lines, and replace any hastily 

placed lines. Provide a definitive airway if it is otherwise unsecured. If the patient 

requires ongoing ventilatory support, set up a mechanical ventilator. 

Hyperventilation is not indicated, because this can lead to decreased cerebral perfusion. 

Acidemia secondary to metabolic acidosis should resolve through adequate ventilation 

and increased organ system perfusion. 

Address postresuscitation hypotension initially with small-volume (250-500 cc) boluses 

of crystalloid solution. Reassess the patient and consider other causes of hypotension, 

such as pneumothorax and pericardial tamponade. If bolus fluid therapy fails, add 

vasoactive agents. The use of dopamine as a single-use agent is discouraged. 

Dobutamine should be used for inotropic support. Phenylephrine or norepinephrine can 

be used as a vasopressor.

Hyperthermia must be avoided, because this increases the cerebral metabolic rate, 

which creates an imbalance between delivered oxygen and demand. This can lead to 

anoxic cell death and can initiate a subsequent systemic inflammatory response. 

Hypothermia, in contrast, can be beneficial to the patient. Although studies have not 

shown the benefit of induced hypothermia, spontaneous mild hypothermia (34-36 °C 

[94-97 °F]) in the postresuscitation phase has been associated with an improved 

outcome. 

TERMINATION OF RESUSCITATION 

If there has been no response to the collective interventions in a resuscitation, the 

decision must be made to cease further efforts. An appropriate trial of electricity, 

vasoactive agents, and antidysrhythmics without any perfusing rhythm after 20-30 

minutes should prompt the termination of the resuscitation. In addition, bedside 

echocardiography can be used to evaluate wall motion and the presence of a gel-like 

echo in the ventricles. Wall motion suggests the possibility that PEA has been 

inadequately resuscitated. A gel-like echo in the ventricle is uniformly associated with 

death. One exception to the standard guidelines for termination of resuscitation is 

hypothermic cardiac arrest, which may occur from severe exposure or cold water 

drowning. Because of the protective effects of hypothermia, several cases of good 

neurologic recovery after prolonged resuscitation from hypothermic cardiac arrest have 

been documented. In general, continue resuscitation efforts until the patient has been 

rewarmed to a core temperature of 30-32 °C (86-90 °F). 

Abramson N et al: Ethics in emergency cardiac care. Ann Emerg Med 2001;37(4 

Suppl):S196. [PMID: 11290981] 

Cummins RO et al: In-hospital resuscitation: a statement for healthcare professionals 

from the American Heart Association Emergency Cardiac Care Committee and the 

Advanced Cardiac Life Support, Basic Life Support, Pediatric Resuscitation, and 

Program Administration Subcommittees. Circulation 1997;95(8):2211. [PMID: 9133536] 

Glazer S, Gray WA: Futile care. What is the endpoint of unsuccessful field 

resuscitation? Emerg Med Serv 1995;24(7):65. [PMID: 10143873] 

Herlitz J et al: Lidocaine in out-of-hospital ventricular fibrillation. Does it improve 

survival? Resuscitation 1997;33(3):199. [PMID: 9044490] 

Jaslow D et al: Termination of nontraumatic cardiac arrest resuscitative efforts in the 

field: a national survey. Acad Emerg Med 1997;4(9):904. [PMID: 9305433] 

Kapp MB: Evolving clinical practices and legal standards of care: softening the shock. 

Am J Emerg Med 1998;16(3):325. [PMID: 9596445] 

Kern KB, Halperin HR, Field J: New guidelines for cardiopulmonary resuscitation and 

emergency cardiac care: changes in the management of cardiac arrest. JAMA 

2001;285(10): 1267. [PMID: 11255370] 

Koster RW: Lidocaine: work still in progress. Resuscitation 1997;33(3):197. [PMID:

9044489] 

Kulkarni RG, Thomas SH: Severe accidental hypothermia: the need for prolonged 

aggressive resuscitative efforts. Prehosp Emerg Care 1999;3(3):254. [PMID: 10424866] 

Marco CA et al: Ethical issues of cardiopulmonary resuscitation: current practice among 

emergency physicians. Acad Emerg Med 1997;4(9):898. [PMID: 9305432] 

Morris DC et al: Vasopressin can increase coronary perfusion pressure during human 

cardiopulmonary resuscitation. Acad Emerg Med 1997;4(9):878. [PMID: 9305429] 

Nakatani K et al: Utility of colorimetric end-tidal carbon dioxide detector for monitoring 

during pre-hospital cardiopulmonary resuscitation. Am J Emerg Med 1999;17(2):203. 

[PMID: 10102328] 

Part 1: Introduction to the International Guidelines 2000 for CPR and ECC: a consensus 

on science. Resuscitation 2000;46:3. [PMID: 10978786] 

Proceedings of the Guidelines 2000 Conference for Cardiopulmonary Resuscitation and 

Emergency Cardiovascular Care: An international consensus on science. Ann Emerg 

Med 2001:37(4 Suppl):S1. [PMID: 11290963] 

Sanders AB: When are resuscitation attempts futile? Acad Emerg Med 1997;4(9):852. 

[PMID: 9305424] 

Stapleton ER: International guidelines 2000 for CPR and ECC: what do they mean for 

you? Emerg Med Serv 2001;30(9):45. [PMID: 11563344] 

Streger MR, Kelley K: Cardiac care 2000. Field termination of cardiac arrest 

resuscitation. Emerg Med Serv 2000;29(9):53. [PMID: 11143036] 

CARDIOPULMONARY RESUSCITATION IN INFANTS & CHILDREN 

Epidemiologic studies of cardiac arrest in children are fraught with methodologic 

problems that make it difficult to ascertain the true scope of incidence. In the United 

States, some 16,000 children each year die of unexpected cardiopulmonary arrest. 

Trauma remains the leading cause of death in the pediatric population. In pediatric 

patients under age 1 year, sudden infant death syndrome (SIDS) is the leading 

nontraumatic cause of death. Lesser causes include submersion injury, pulmonary 

disease, asphyxia, aspiration, and primary cardiac disease. 

Cardiac arrest in the pediatric population is most often secondary to respiratory arrest. 

Treatment prior to cardiac arrest is essential. Primary prevention has been shown to be 

effective in SIDS (ie, the "Back to Sleep" initiative) and with swimming pool safety 

education. 

The pediatric patient who experiences cardiopulmonary arrest in an out-of-hospital 

setting uniformly has a poor outcome. A prospective study in an urban EMS system

demonstrated a 2% survival rate with only 1 patient out of the 6 survivors having a good 

neurologic outcome. Patients not resuscitated in the field did not survive to hospital 

admission. 

The following terms apply to the pediatric patient: 

• Newborn: first 24 hours of life, wherein the patient transitions from a fetal to a neonatal 

circulation 

• Neonate: first 28 days of life 

• Infant: first year of life 

• Child: ages 1-8 years 

For the purposes of basic life support, an adult is someone older than age 8 years. 

There can be significant overlap across the age lines, in that it may be necessary to 

perform infant CPR on a toddler or adult chest compressions on a large child. 

PEDIATRIC BASIC LIFE SUPPORT 

Pediatric BLS utilizes the same basic techniques as adult BLS, but it is appropriately 

adapted for the size and physiology of infants and children. The first significant 

difference between adult and pediatric BLS is the "phone fast" rather than "phone first" 

rule. Because the predominant cause of pediatric cardiac arrest is respiratory arrest, in 

the event that help cannot be obtained simultaneously with initiating CPR (ie, the lone 

rescuer situation), CPR should be performed for 1 minute prior to interrupting to phone 

for help. 

A. Airway 

Opening the airway in a pediatric patient is similar to the procedure followed for adults. 

The head-tilt and chin-lift method is used for the patient not suspected of having trauma. 

The jaw thrust is used when cervical spine injury secondary to trauma is a possibility. In 

the event of loss of consciousness secondary to foreign body airway obstruction, the 

rescuer may use the tongue-jaw lift to visualize the oropharynx and remove any foreign 

bodies. 

B. Breathing 

Ventilations are provided in a manner similar to adults. In infants, the mouth-to-mouth 

and nose technique can be used. The rescuer's mouth is placed over the infant's mouth 

and nose to create an effective seal. In children, mouth-to-mouth ventilation is 

performed. Mouth-to-nose ventilation is an alternative when the rescuer is unable to 

obtain an effective seal with the preferred technique. Ventilations should be delivered 

over 1-1.5 seconds. Initially, 2 ventilations should be delivered. An effective ventilation 

occurs when there is enough force and volume provided to make the chest rise. An 

appropriately sized bag-mask may be used by the trained provider (250-mL bag for 

neonates, 500-mL bag for infants and children). Supplemental oxygen should be used 

with the bag-mask when available. An anesthesia bag may be used, but this requires a 

provider who routinely uses this with pediatric patients. In addition, the anesthesia bag

equires a continual flow of oxygen. Cricoid pressure should be applied when giving a 

child rescue breaths prior to the insertion of an endotracheal tube. (Cuffed tubes are not 

recommended for infants or children.) 


The rate of compressions should be performed faster in pediatric patients than in adults. 

In the infant, give at least 100 compressions per minute (newborn, 120 per minute). In 

the child, give 100 compressions per minute. In the infant, the preferred method for 

chest compressions is both hands encircling the chest with both thumbs providing 

compressions on the sternum (2-thumbs/encircling-hands technique). The alternative 

technique is using 2 fingers (either the index and middle finger or the middle and ring 

finger) from 1 hand to provide compressions. This technique may be more practical with 

a single rescuer. In children, the heel of 1 hand is used, but the technique is similar to 

the 2-handed method used for adults. In all patients, the depth of compression is one 

third to one half the depth of the chest. 

Five compressions are delivered, followed by a single ventilation. This is in contrast to 

the adult compression-to-ventilation ratio, which is 15:2 until the adult patient has been 

intubated. 

PEDIATRIC ADVANCED LIFE SUPPORT 

Pediatric ALS is directed toward the same goals of ALS in the adult: ROSC with 

preserved neurologic function. Hence, much of the underlying theory and algorithms are 

similar. Several important differences are noted below. As with adults, preparation is 

crucial, and in larger emergency departments, a dedicated pediatric crash cart should 

be assembled. Accordingly, in the prehospital arena, it may be useful to have a 

dedicated pediatric bag or kit on hand. These carts and kits should have 

age-appropriate equipment and medications. A means of estimating approximate 

weight, vital signs, and drug doses should be utilized. The Broselow-Luten length-based 

tapes are an excellent example. If these guides are unavailable, the endotracheal tube 

size can be estimated in children over age 1 year as follows: tube size = 1/4(age) + 4. 

Endotracheal intubation provides another route to deliver some resuscitation 

medications (eg, lidocaine, epinephrine, atropine). However, in one study, endotracheal 

intubation in the pediatric patient in the out-of-hospital setting did not improve survival 

over bag-valve-mask technique. 

Nonperfusing ventricular rhythms occur in up to 10% of pediatric cardiac arrests. If SIDS 

deaths are excluded, this rate increases to 19%. The chance of ROSC increases from 

about 5% in all patients to 30% in patients who present in ventricular fibrillation or 

pulseless VT. Appropriate paddles are 4.5 cm for infants up to age 1 year or 10 kg, and 

adult paddles for all others. Paddle positioning is the same as for adults. Defibrillation 

for ventricular fibrillation or pulseless VT is initially 2 J/kg, followed by 2-4 and then 4 

J/kg. Currently, AEDs provide shocks at a fixed energy level appropriate only for adults. 

This energy level delivers 6-8 J/kg in the average 8 year old. This energy level would 

deliver too much energy to a smaller patient. Because of this, AEDs are currently not 

recommended for children younger than age 8 years. The other significant concern in 

the pediatric patient is the potential misdiagnosis of rapid sinus tachycardia as VT, 

leading to delivery of an inappropriate shock. Pediatric AEDs are currently in

development. Any identifiably treatable causes, such as a toxic ingestion, electrolyte 

abnormalities, or asthmatic exacerbations, should be addressed appropriately. 

Vascular access in the pediatric patient in cardiac arrest should be achieved as rapidly 

as possible. The most rapid means of securing such access is through the use of an 

intraosseous catheter. The intraosseous needle can be placed in 30-60 seconds. It can 

be placed in any large bone containing marrow, although the proximal tibia is most 

recommended. High-dose epinephrine, which had been endorsed previously in pediatric 

patients, has not been shown to lead to an increase in survival to discharge. 

Gausche M et al: Effect of out of hospital pediatric endotracheal intubation on survival 

and neurological outcome: a controlled clinical trial. JAMA 2000;283:783. [PMID: 

10683058] 

Niermeyer S et al: International Guidelines for Neonatal Resuscitation: an excerpt from 

the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular 

Care: International Consensus on Science. Pediatrics 2000;106(3): E29. [PMID: 

10969113] 

Sirbaugh PE et al: A prospective, population based study of the demographics, 

epidemiology, management, and outcome of out of hospital pediatric cardiopulmonary 

arrest. Ann Emerg Med 1999;33(2):174. [PMID: 9922413] 

NOVEL APPROACHES IN CARDIAC ARREST MANAGEMENT 

ALTERNATIVE BASIC LIFE SUPPORT TECHNIQUES 

Several alternatives to the basic chest compression described in the "Adult Basic Life 

Support" section have been developed since Kouwenhoven's original proposal in 1960. 

Currently, 3 forms of alternative CPR remain as potential improvements over the basic 

chest compression. 

Active Compression/Decompression CPR 

Active compression/decompression (ACD) CPR requires a suction cup device, which 

adheres to the chest. This technique actively decompresses the chest, resulting in 

increased preload. This leads to greater cardiac output. Most trials of ACD have not 

demonstrated a significant increase in the number of patients who survive to hospital 

discharge. A study of 750 patients did show a significant increase in the number of 

patients surviving to discharge but not to 1-year survival. 

Interposed Abdominal Compressions 

Interposed abdominal compressions (IACs) apply positive pressure to the abdomen 

during the chest compressions relaxation phase. This increases the return of blood to 

the right ventricle, which leads to an increase in cardiac output and systemic perfusion 

pressure. Prospective trials have shown an increase in survival to discharge when IACs 

were performed in an in-hospital cardiac arrest. These results have not been seen in 

prehospital trials.

"Lifestick" CPR 

A combination of the other 2 techniques, referred to as "Lifestick" CPR (after the device 

used to perform the technique), provides improved hemodynamics over either technique 

alone. It has shown a significant increase in survival in the porcine model. Results of 

prehospital trials are pending. 

THE SCALING EXPONENT 

Intuitively, it was believed that the "coarser" the ventricular fibrillation, the more likely 

resuscitation was to be successful. Multiple studies have attempted to find a measure of 

this coarseness. Amplitude has a high correlation with successful defibrillation; however, 

patient movement, chest compressions, and other factors complicate calculation of 

amplitude during resuscitation. The scaling exponent is an estimate of the "roughness" 

or "smoothness" of the ECG waveform. It is a fractal measure that is independent of the 

amplitude or frequency of the waveform. Its value lies in identifying those patients who 

would benefit from immediate defibrillation. The calculation of the exponent is complex 

but can be performed in real time. Retrospective prehospital studies have identified a 

scaling exponent value at which CPR and pharmacologic therapy would result in a 

greater rate of ROSC. Animal studies have validated this value, although prospective 

prehospital trials are pending. 

FIBRINOLYTIC THERAPY 

Between 50% and 70% of patients experience sudden cardiac death secondary to 

intravascular thrombosis (20-40% due to an intracoronary thrombus; 20-30% related to 

a massive pulmonary embolus). Fibrinolytic therapy has been proposed as a means to 

treat these underlying causes. Multiple case reports and case series through the 1980s 

and 1990s showed a high rate of ROSC with a good neurologic outcome. The only 

prospective trial to date has supported good neurologic outcomes (Bottiger et al, 2001). 

Patients given tissue-type plasminogen activator had an odds ratio of 2.65 (95% CI, 

1.11-6.25) for ROSC and an odds ratio of 3.11 (95% CI, 1.32-7.69) for admission to the 

intensive care unit. The trial was stopped early due to the significantly improved 

outcome of the treatment group. This study also demonstrated the safety of fibrinolytics 

during CPR, with no significant bleeding complications related to CPR. 

The mechanism by which fibrinolysis may provide benefit in cardiac arrest is unclear. 

Changes in cardiac function occur within 2-12 minutes after the administration of 

fibrinolytics. This is not long enough to reestablish TIMI (trials in myocardial infarction) 

grade 3 flow. It is possible that only a small amount of flow is necessary to eliminate the 

insult causing the dysrhythmia or that the microvascular disease that is readily treated is 

the source of the insult. The neuroprotective effects of fibrinolysis are thought to be due 

to the reversal of an unopposed clotting cascade initiated during the cardiac arrest. 

Dosing of fibrinolytics is unchanged during cardiac arrest. Unfractionated heparin was 

administered to the patients in the largest case series and in one prospective study. 

Arntz HR et al: Phased chest and abdominal compression-decompression versus 

conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest. Circulation

2001;104(7): 768. [PMID: 11502700] 

Bottiger BW et al; Efficacy and safety of thrombolytic therapy after initially unsuccessful 

cardiopulmonary resuscitation: a prospective clinical trial. Lancet 2001;357(9268):1583. 

[PMID: 11377646] 

Callaway CW et al: Scaling exponent predicts defibrillation success for out of hospital 

ventricular fibrillation cardiac arrest. Circulation 2001;103(12):1656. [PMID: 11273993] 

Dickinson ET et al: Effectiveness of mechanical versus manual chest compressions in 

out-of-hospital cardiac arrest resuscitation: a pilot study. Am J Emerg Med 

1998;16(3):289. [PMID: 9596436] 

Kern KB: Thrombolytic therapy during cardiopulmonary resuscitation. Lancet 

2001;357(9268):1549. [PMID: 11377640] 

Plaisance P et al: A comparison of standard cardiopulmonary resuscitation and active 

compression-decompression resuscitation for out-of-hospital cardiac arrest. N Engl J 

Med 1999;341(8): 569. [PMID: 10451462] 

Plaisance P et al: Benefit of active compression-decompression cardiopulmonary 

resuscitation as a pre-hospital advanced cardiac life support. A randomized multicenter 

study. Circulation 1997;18;95(4):955. [PMID: 9054757] 

Skogvoll E, Wik L: Active compression-decompression cardiopulmonary resuscitation: a 

population-based, prospective randomized clinical trial in out-of-hospital cardiac arrest. 

Resuscitation 1999;42(3):163. [PMID: 10625156] 






OVERVIEW OF CARDIAC ARREST

Table 7-1. Differentiating ventricular tachycardia (VT) from supraventricular 

tachycardia (SVT) with aberrancy. 

Factors Favoring VT 

Atrioventricular dissociation 

qRS in lead V6 Response to carotid sin

Table 7-2. Pharmacotherapy in advanced cardiac life support. 1 

1 mg IV 

Adult Dose Indications Effects 

OR 

2-5 mg IV via ETT 

Any pulseless rhythms Increases perfusion to myocardium an 

brain by increasing peripheral vascula 

resistance. 

40 units IV VF, pulseless VT Increases peripheral vascular resistan 

For VF or pulseless VT: 

300 mg IV push 

VF, pulseless VT, VT with a pulse, 

SVT 

Predominately class III antiarrhythmic, 

has sodium, potassium channel, and a 

ß receptor blockade. 

1.0-1.5 mg/kg IV push VF, pulseless VT, VT with a pulse Class IB antiarrhythmic; suppresses 

ventricular automatically and electrical 

conduction. 

1-2 g IV slow push Torsade de pointes, known 

hypomagnesemia 

17 mg/kg IV slow bolus at 

maximum rate of 50 

mg/min 

Perfusing patients: 0.5 mg 

IV push q 5 min, to 

maximum of 3 mg 

Pulseless patients: 1.0 mg 

IV push q 5 min, to 

maximum of 3 mg 

6 mg rapid IV push through 

proximal peripheral line; 

central line dose is 

one-half 

0.25 mg/kg to a maximum 

dose of 20 mg IV push 

over 2 min 

Can cause cutaneous flush, apnea, an 

hyporeflexia, if given too quickly. 

VT with a pulse Decreases myocardial excitability and 

conduction velocity. 

Bradycardia, asystole. Parasympatholytic, eliminates vagal to 

SVT Endogenous nucleoside causing brief 

asystole allowing dominant pacemake 

resume function. 

SVT Calcium channel blocker. 

500 µg/kg bolus over 1 min SVT ß-Blocker (short acting). 

5 mg IV over 5 min SVT, myocardial infarction ß-Blocker (ß-1 selective). 

5 mg IV push SVT, myocardial infarction ß-Blocker (ß-1 selective). 

2-20 µg/kg/min Hypotension Inotropic agent/vasopressor (combine 

and ß agonists). 

2-20 µg/kg/min Hypotension Inotropic agent (ß agonist).

Start at 8-12 µg/min, then 

titrate to 2-4 µg/min for 

maintenance; maximum 

dose of 30 µg/min if 

hypotension unresponsive 

to lower doses. 

Hypotension. Vasopressor (predominately an a agon 

100-500 µg bolus IV. Hypotension. Vasopressor (pure a agonist). 

1 Agents are listed from most effective (and most commonly used) to least. 






TABLES 

Table 7-2. Pharmacotherapy in advanced cardiac life support.

Figure 7-1. Management of suspected cardiac arrest. 






FIGURES 

Figure 7-1

Figure 7-2. Opening the airway and providing ventilation. A: Obstruction of airway by 

posterior displacement of tongue (arrow) in resting, supine position. B and C: Relief of 

lingual airway obstruction in supine position by forward displacement of mandible 

(head-tilt and chin-lift method). D: Rescuer checks for spontaneous breathing by 

listening and feeling for exhaled air while looking for chest movement. E: 

Mouth-to-mouth ventilation. While maintaining head tilt and chin lift, the rescuer uses his 

or her fingers to seal the victim's nose shut; rescuer takes a deep breath, seals mouth 

over victim's mouth, and exhales, watching for chest movement. Look, listen, and feel 

for passive exhalation. 






FIGURES 

Figure 7-2

Figure 7-3. Jaw-thrust maneuver. A: If cervical spine injury is suspected, open airway 

by grasping and lifting angles of victim's lower jaw without tilting the head. B and C: 

Ventilation is best provided with the aid of a second rescuer or a pocket mask. 






FIGURES 

Figure 7-3

Figure 7-4. Ventilation technique using face mask and positive pressure ventilation (bag 

or valve). As in mouth-to-mouth ventilation, head must be tilted to keep airway open. 

Seal mask to face with one hand, with fingers under chin to maintain open airway. Use 

other hand to operate bag or valve. 






FIGURES 

Figure 7-4

Figure 7-5. Hand placement for closed chest compression. Locate xiphoid, and place 

heel of one hand 2 fingerwidths cephalad to the xiphisternal notch. Only the heel of the 

bottom hand should touch the chest wall—not the palm or fingers. 






FIGURES 

Figure 7-5

Figure 7-6. Clearing airway in conscious victim (Heimlich maneuver). Reach around the 

victim from the back, and deliver a sharp thrust to the epigastrium with the clenched fist, 

thumb-side toward the abdomen. 






FIGURES 

Figure 7-6

Figure 7-7. Clearing the obstructed airway. A: Finger sweep. Using a partially flexed 

index finger, sweep through far side of victim's mouth along cheek, deeply into back of 

the throat, and then out the near side. B and C: Supine Heimlich maneuver 

(subdiaphragmatic thrust). With victim level (or head down) and head turned to the side, 

rescuer kneels astride victim's thighs. Rescuer places heel of one hand midway 

between navel and xiphoid (well away from tip of xiphoid) and the other hand directly on 

top of the first. Deliver as many as 10 vigorous thrusts to victim's epigastrium. 






FIGURES 

Figure 7-7

Figure 7-8. Contact points for defibrillation electrodes (solid circles). Place one paddle 

electrode to the right of the sternum in the second or third interspace; the other paddle 

should be at the cardiac apex. In children and thin adults, paddles may be placed 

directly over the heart in anteroposterior orientation. 






FIGURES 

Figure 7-8

Figure 7-9. Use of the automated external defibrillator. 






FIGURES 

Figure 7-9

Figure 7-10. Algorithm for usage of automated external defibrillator (AED). ACLS = 

advanced cardiac life support. 






FIGURES 

Figure 7-10

8. Compromised Airway 1 - Harriet L. Boozer, MD, & Melissa M. 

Cheeseman, MD 

IMMEDIATE MANAGEMENT OF THE COMPROMISED AIRWAY (See 

Figure 8-1.) 

1 This chapter is a revision of the chapter by Julia Nathan, MD, from the 4th edition. 

Securing the airway and assuring adequate ventilation are the first priorities in the 

resuscitation of any acutely ill or injured patient. Without a patent airway and adequate 

gas exchange, other resuscitative measures will usually be futile. Thus attention to the 

airway must precede or occur simultaneously with any other type of management. The 

exception is the initial defibrillation in cardiac arrest due to ventricular fibrillation, if 

defibrillation can be performed immediately. 

Assess the Airway 

Determine the patient's level of consciousness, and note the presence of any 

respiratory effort. In patients with known or suspected cervical spine injury, all 

assessments and maneuvers should be undertaken with the cervical spine immobilized 

in a neutral position to prevent cord injury. 

A. Apneic, Unconscious Patients 

Open the airway with a chin-lift or jaw-thrust maneuver. If the cervical spine is not 

injured, place the head in the sniffing position (Figure 8-2). Clear the airway of 

obstructions, using a rigid suction catheter to remove any blood, vomitus, or secretions 

from the oropharynx. Remove any large obstructing foreign bodies from the oropharynx 

manually or with Magill forceps (see Chapter 7). 

If the patient remains apneic, assist ventilation using a bag-valve-mask device (eg, 

Ambu bag) or mouth-to-mouth breathing (see Chapter 7). If adequate personnel and 

equipment are available, immediately perform endotracheal intubation. Administer 

high-flow oxygen. 

B. Patients with Respiratory Effort 

Administer high-flow oxygen. Clear and position the airway as described above. Identify 

evidence of upper airway obstruction. Prolapse of the tongue and accumulation of 

secretions, blood, or vomitus are common causes of obstruction. Signs may include 

wheezing, sonorous respirations, stridor, cough, and dysphonia. Upper airway 

obstruction should be removed if present. Back blows or the Heimlich maneuver may 

clear the obstruction. If not, use suction or direct visualization and a Magill forceps or 

finger. Blind sweep is contraindicated. Obstructions that recur or persist require 

endotracheal intubation, either orotracheally or via cricothyroidotomy, tracheostomy, or 

percutaneous transtracheal jet ventilation (PTTJV) (see also Chapters 6, 7, and 48). 

Evaluate the effectiveness of the patient's respiratory effort. Helpful signs include

espiratory rate, tidal volume, accessory muscle use, level of consciousness, skin color, 

upper airway sounds, and auscultated lung sounds. Further assessment may include 

pulse oximetry, arterial blood gas measurement, and chest radiography. 

If intubation is indicated (Table 8-1), continue high-flow oxygen and assist ventilation as 

needed. Assemble all items necessary for the appropriate method of intubation (Tables 

8-2 and 8-3). Check for equipment malfunction. If the patient is alert, inform him or her 

of your plan. 

Prepare for Intubation 

A. High-Flow Oxygen 

All patients with airway or ventilatory compromise require high-flow oxygen. Oxygen 

through a nasal cannula at flow rates up to 6 L/min provides a patient with 20-40% 

inspired oxygen concentration. A variety of masks are available that can accept oxygen 

flow rates of 5-15 L/min. Masks equipped with reservoirs and nonrebreathing valves can 

deliver oxygen concentrations close to 100% at flow rates of 10 L/min if an adequate 

seal can be maintained between the mask and face. 

Before attempting intubation, preoxygenate the patient with 100% oxygen for 2-3 

minutes. In a ventilating patient, this provides 6-7 minutes of protection against hypoxia 

should the patient become apneic. In an apneic patient, preoxygenation with a 

bag-valve-mask unit provides 2-3 minutes of protection against hypoxia. Unsuccessful 

attempts at intubation should be stopped at 30 seconds so that the patient may be 

reoxygenated. 

B. Suction 

A rigid-tipped suction catheter should be available at all times to keep the airway clear 

of blood and secretions. The suction device should be set at 120 mm Hg. After 

intubation, suction the tracheobronchial tree with a sterile, flexible catheter as described 

in the "Care of the Intubated Patient—Pulmonary Toilet" section, below. 

C. Oral and Nasal Airways 

When the jaw thrust or chin lift is ineffective in airway opening, a nasal or oral airway 

may support collapsed oropharyngeal tissues and permit adequate ventilation. A range 

of sizes should be readily available in all areas of the emergency department (Figure 

8-3). 

The oral airway is best used in an obtunded patient. It may be inserted over a tongue 

blade or positioned backward as it enters the mouth and rotated after the tongue is 

cleared. Positioned correctly, it retracts the tongue upward and anteriorly. Care must be 

taken not to push the tongue backward into the pharynx, worsening the obstruction. An 

overly long oral airway can push the epiglottis over the larynx, causing complete 

obstruction. 

The soft, rubber, noncuffed nasopharyngeal tube tends to be better tolerated in a 

semiobtunded patient. Lubricate the tube with anesthetic jelly before insertion. Insert it 

through the least obstructed nostril, advancing it posteriorly along the floor of the nostril 

until it bypasses the tongue. If it is too long, it may enter the esophagus, resulting in

ineffective positive-pressure ventilation and gastric distention. Epistaxis may occur 

during insertion, and suction should be available. 

In patients with intact airway reflexes, placement of either device may cause emesis, 

gagging, or laryngospasm. During and after placement, head position should be 

maintained to optimize airway patency. Where indicated, spinal precautions must be 

maintained. Evaluate breath sounds after placement of either device to ensure that 

obstruction has not occurred. Care must be taken to avoid trauma during placement. 

D. Positive-Pressure Ventilation 

Following airway opening, positive-pressure ventilation may be used to preoxygenate a 

patient before intubation. Occasionally it may be the only form of ventilation in an apneic 

patient when an airway cannot be secured, or when a patient responds rapidly to other 

therapy. In general, however, it is not recommended for prolonged ventilation owing to 

gastric dilatation and technical difficulty. 

The bag-valve-mask unit is the device most commonly used to provide 

positive-pressure ventilation in the emergency department. The bag-valve-mask unit 

has a self-inflating bag that accepts 15-L/min oxygen flows. A nonrebreathing valve 

permits reservoir air to enter through a separate port from expired air. At these flow 

rates, inspired air will approach 100% oxygen. The self-filling bag permits use with 

spontaneously breathing patients. The unit can usually be attached to an endotracheal 

tube after intubation for manual bag-assisted tracheal ventilation. 

The procedure for using the bag-valve-mask unit is described in Chapter 6. Use of this 

device is difficult in the hands of a single operator because effective bag-valve-mask 

ventilation depends on a tight seal between the mask and face. Often this requires 2 

hands and a second operator to compress the bag. Many circumstances of anatomic 

variation or maxillofacial trauma make a tight seal impossible. During bag-valve-mask 

ventilation, proper head position must be maintained to preserve airway patency. 

Monitor the effectiveness of ventilation closely by frequent assessments of chest wall 

movement, lung sounds, and gastric dilatation. 

The positive pressure generated by bag-valve-mask ventilation leads to gastric 

dilatation and abdominal distention. This results in decreased lung compliance and 

significant risk of emesis and aspiration. A clear mask is recommended to reveal 

emesis. Suction equipment must be available. In patients with unprotected airways, 

cricoid pressure (the Sellick maneuver) is recommended (Figure 8-4). To perform the 

Sellick maneuver, apply firm, direct pressure on the circumferential cricoid cartilage. 

This will compress the esophagus posteriorly, decreasing gastric dilatation and reflux. If 

emesis occurs, release pressure on the cricoid to prevent esophageal rupture. If 

bag-valve-mask ventilation must be prolonged for any reason, place a nasogastric tube 

to reduce gastric dilatation and its consequences. 

Because of operational difficulties and risks of aspiration, the bag-valve-mask is a 

temporizing measure under most circumstances. Patients who require bag-assisted 

ventilation should generally be intubated as soon as it can be accomplished safely and 

practically.

The mouth-to-mask technique is another method of providing positive-pressure 

ventilation. This method may be easier for a single operator, because both hands can 

be used to seat the mask. Supplemental oxygen is provided via a port in the mask or via 

a nasal cannula worn by the operator. 

E. Esophageal Obturators and Related Devices 

An esophageal obturator airway (EOA) or similar device may be placed in the 

prehospital setting. These tubes are designed to provide airway protection and 

ventilation. The EOA has become mainly a device of historical interest because of a 

high rate of complications and uneven efficacy. The use of this device in the prehospital 

setting is not recommended. There are no indications for the EOA in the emergency 

department. 

Since introduction of this device, several modifications have been made. The 

esophageal gastric tube (EGT) airway has a hollow esophageal tube that permits 

passage of a nasogastric tube for gastric decompression. The esophageal tracheal 

Combitube (ETC) may be used as an endotracheal tube if blind insertion results in 

tracheal placement. Similarly, the pharyngeal tracheal lumen airway (PTLA) may be 

ventilated through either a long or short tube depending on the tube position after 

placement. 

The ETC has found favor in prehospital and emergency department settings. It 

comprises 2 tubes that form a single double-lumen tube. A proximal balloon isolates the 

hypopharynx, whereas the distal balloon occludes the esophagus or the trachea, 

depending on its location. The tube is inserted blindly and is fairly stiff, so that it usually 

enters the esophagus. Tube 1 is closed distally with side holes for ventilation. Tube 2 is 

open distally and gives a direct route to either the lungs or the stomach. Tube 1 is 

always ventilated first, when confirming placement of the tube. Advantages of the ETC 

include ease of placement, airway protection from aspiration, and lack of manipulation 

of the cervical spine in the trauma patient. 

Esophageal tubes are contraindicated in awake and semiobtunded patients and in 

infants, children, and patients less than 120 cm in height. Do not use them when there is 

known esophageal injury or ingestion of caustic substances. Complications are listed in 

Table 8-4. Because of reports of esophageal trauma, some authors recommend 

Gastrografin swallow or endoscopy after use of an EOA-like device. 

Patients intubated with an EOA in the field will need endotracheal intubation upon arrival 

in the emergency department. If an ETC or PTLA is in place, it may be used for 

continued resuscitation. The ETC is an effective device for prolonged mechanical 

ventilation. 

F. Cuffed Oropharyngeal Airway 

The cuffed oropharyngeal airway is a modified oropharyngeal airway with a large distal 

inflatable cuff. It is inserted like a traditional oral airway, and the cuff is then inflated in 

the supraglottic space. This device is useful in resuscitation because of its ease of 

insertion and the low level of skill required to place it. 

Agro F et al: Associated techniques for tracheal intubation. Resuscitation 2000;47:343.

[PMID: 11114469] (Review of different techniques for establishing a patent airway.) 

Foley LJ et al: Managing the airway in the critically ill patient—bridges to establish an 

emergency airway and alternate intubating techniques. Crit Care Clin 2000;16:429. 

[PMID: 10941582] (Review of alternative airway management techniques.) 

Levitan RM et al: Airway management and direct laryngoscopy—a review and update. 

Crit Care Clin 2000;16:373. [PMID: 10941579] (Review of airway management 

techniques.) 

Orebraugh SL: Difficult airway management in the emergency department. J Emerg 

Med 2002;22:31. [PMID: 11809554] (Review of techniques for managing the difficult 

airway.) 

Shuster M et al: Airway and ventilation management. Cardiol Clin 2002;20:23. [PMID: 

11845543] (Review of airway management techniques.) 

PRINCIPLES OF INTUBATION 

These principles of intubation management apply to all methods of airway management 

described in this chapter. Airway positioning, suction, and administration of 100% 

oxygen must precede any attempt at advanced airway control. Keep protective gear 

with the airway equipment, and use it routinely. 

Choice of Method 

Most patients can be intubated orally by direct laryngoscopic visualization of the cords. 

This is the method of choice, because the best assurance of correct tube placement is 

seeing the tube pass through the cords into the trachea. When direct visualization is not 

possible (Table 8-5), airway control can be achieved using a wide variety of special 

equipment and alternative methods described below (Table 8-6). 

Choice of a blind or surgical technique depends on the patient's condition, availability of 

equipment, and operator experience. Advantages, indications, and problems associated 

with each technique are summarized below. Most alternative procedures require some 

training and expertise. Become comfortable with several techniques, and be sure that 

the emergency department stocks the appropriate equipment. 

Intubation by any method carries risks of hypoxia, aspiration, laryngospasm, 

unrecognized esophageal intubation, bleeding, airway trauma, spinal cord trauma, right 

or left main-stem intubation, arrhythmia, and death. Delayed complications include soft 

tissue infection, mediastinitis, tracheal stenosis, and dysphonia. 

Any blind technique (nasal, digital, lighted stylet) carries increased risk of unrecognized 

esophageal tube placement and trauma to the hypopharynx and airway. These methods 

should be used only when direct visualization is dangerous or cannot be successfully 

completed. 

Surgical and needle techniques are generally rapid but in inexperienced hands may lead

to massive bleeding or trauma that makes control of the airway impossible. They share 

the relative contraindications of coagulopathy, goiter, overlying tumor, or overlying skin 

infection. There are no absolute contraindications other than the ability to obtain an 

airway by less invasive means. Although each invasive method of airway control has 

unique complications, as a group they share an increased risk of bleeding, extratracheal 

tube placement, and trauma to the airway and surrounding tissues over less invasive 

routes. Loss of integrity of the tissues of the neck may result in barotrauma and 

significant soft tissue infection. Delayed complications include hoarseness and 

subglottic stenosis. 

Universal Precautions 

Airway management presents many opportunities for exposure to patient secretions. 

Wear adequate protective clothing, including a gown, gloves, mask, and either a face 

shield or goggles, any time the airway is manipulated. When the intubator's fingers are 

in the patient's mouth (eg, digital intubation, lighted stylet), care must be taken to 

prevent bite wounds. Place a bite block or dental prod before initiating intubation. 

Alternatively, place several layers of gauze between the intubator's hand and the 

patient's teeth. If the patient wears dentures, remove them before airway manipulation. 

Laryngoscopy & Oral & Nasal Intubation 

See Chapter 6. 

Postintubation 

After intubation, assess the position of the endotracheal tube by observing the chest 

wall for expansion. Auscultate both lung fields and the abdomen while ventilating. 

Inaudible lung sounds or the presence of abdominal sounds suggest esophageal 

placement. If breath sounds are louder on the right than the left, suspect right 

main-stem intubation. Withdraw the tube 1-2 cm, and auscultate again. Confirm the tube 

position by chest x-ray. 

Levitan RM et al: Airway management and direct laryngoscopy—a review and update. 

Crit Care Clin 2000;16:373. [PMID: 10941579] (Review of airway management 

techniques.) 

NONSURGICAL ALTERNATIVES FOR MANAGING THE DIFFICULT 

AIRWAY 

Laryngeal Mask Airway 

The laryngeal mask airway (LMA) is a device that has been proved useful as an 

alternative for bag-valve-mask ventilation and as a rescue option in the difficult airway. 

The LMA is a semirigid tube with a distal inflatable mask that is inserted blindly into the 

hypopharynx. The mask lies over the larynx and seals around the glottic opening. The 

LMA does not protect against aspiration. This device has been demonstrated to be easy 

to insert with limited prior training. The LMA is appropriate for use in adults and 

pediatrics, including neonates weighing more than 2 kg. The intubating LMA (I-LMA) is a

modification of the LMA that has been developed to act as a conduit to allow passage of 

the endotracheal tube through the glottis. 

Digital Intubation 

This method has been used successfully when the cords cannot be visualized because 

of anatomic features or copious secretions. In the hands of experienced clinicians, it is 

rapid and can be achieved with little movement of the cervical spine. There are no 

absolute contraindications to this method, but it is a blind method and should not be 

used when direct visualization of the cords can be safely done. Because of the risk of 

being bitten, use this method only in deeply comatose patients. 

If necessary, one person can perform digital intubation unaided. No special equipment 

is necessary beyond an oxygen delivery system, suction, and an appropriately sized 

endotracheal tube with stylet. Lubrication may aid passage of the tube. Take 

precautions against the accidental or reflex bite. Place a stylet into the lubricated tube 

as far as the side hole, and bend the tube into a gentle hook at the end. 

To perform digital intubation, stand at the patients' right shoulder. Insert the index and 

middle fingers into the patient's mouth, and advance along the midline of the tongue 

until the epiglottis is palpated. Pass the endotracheal tube along the fingers until the tip 

reaches the epiglottis. Move the 2 fingers posteriorly, and advance the tube past the 

epiglottis while exerting gentle anterior pressure to guide the tip of the tube into the 

trachea. Once past the cords, remove the stylet before further advancement to prevent 

damage to the anterior trachea. After removing the stylet, adjust the final tube position, 

secure the tube, and verify its placement in the usual way. Never advance the tube 

against resistance. Cricoid pressure may be used until the endotracheal cuff is inflated. 

Complications are similar to those described for other methods of blind intubation. 

Variations on Basic Equipment 

Several variations on the basic equipment have been developed for managing the 

difficult intubation. Use of these devices may be helpful under some circumstances. 

Flexible-tipped endotracheal tubes (Endotrol, others) have a built-in thread that extends 

from the distal tip to the proximal end, where it attaches to a plastic ring. Traction on the 

ring flexes the tip of the tube, directing the tube more anteriorly, simulating the function 

of a flexible stylet. 

Specialized laryngoscope blades and handles are produced but are not widely available 

in most emergency departments. Several variations of the rigid fiberoptic laryngoscope 

also exist. These devices allow for indirect visualization of the airway through an 

eyepiece. The endotracheal tube is advanced off the stylet into the glottis under 

visualization. 

Fiberoptic Techniques 

A. Lighted Stylet

Lighted stylet and light wand devices have been developed to aid in blind intubation. 

This method can be used when blood, secretions, or vomitus fill the hypopharynx. 

Because laryngoscopy need not be used, lighted stylets may be advantageous when 

the cervical spine must remain immobilized. Blind intubation with a lighted stylet is most 

suitable for deeply comatose or apneic patients when there is little risk of stimulating 

protective reflexes or biting of the intubator's hand. Use a bite block or dental prod for 

protection. A lighted stylet can also be combined with direct laryngoscopy. Although 

there are no absolute contraindications to this technique, ambient lighting must be low 

to maximize its benefit. Obesity may diminish the intensity of transillumination. As for 

other blind techniques, avoid this method when direct laryngoscopy can be performed. 

If necessary, one person can perform this technique unaided. These devices have a 

battery-powered light source at the top of a semiflexible stylet. A longer, floppy stylet is 

available for nasal intubations. The stylet is threaded into an endotracheal tube. Aside 

from the lighted stylet, no special equipment is required. 

Form the assembly of stylet and endotracheal tube into a hook of slightly greater than 

90 degrees. The patient may be approached from the head if laryngoscopy is used. 

Otherwise, approach the patient from the right shoulder. While placing gentle traction on 

the tongue, pass the assembly into the mouth. When the epiglottis is reached, use a 

scooping or ladling motion to place the tip into the glottis. The appearance of 

transillumination at the neck indicates the position of the tube. Tracheal placement 

results in a bright, well-circumscribed area of transillumination at the cricothyroid 

membrane. The endotracheal tube can then be advanced over the stylet into the 

trachea. Transillumination lateral to the midline indicates piriform sinus placement and 

need for repositioning. Esophageal placement causes little or no transillumination. The 

procedure is essentially the same for nasal intubation with a lighted stylet. 

This procedure shares the same complications as other blind techniques: inadvertent 

malpositioning of the tube, hypoxia, and tissue damage. 

B. Fiberoptic Bronchoscope 

Fiberoptic bronchoscopes may be used to locate the opening of the glottis when direct 

laryngoscopy cannot be used or is unsuccessful. The endotracheal tube can then be 

advanced over the endoscope into the trachea. Although this procedure can be carried 

out without movement of the cervical spine, it requires skill and practice. It may be time 

consuming when the hypopharynx is filled with blood or secretions. In addition, the 

equipment is expensive and easily damaged. 

Foley LJ et al: Managing the airway in the critically ill patient—bridges to establish an 

emergency airway and alternate intubating techniques. Crit Care Clin 2000;16:429. 

[PMID: 10941582] (Review of alternative airway management techniques.) 

Levitan RM et al: Devices for difficult airway management in academic emergency 

departments—results of a national survey. Ann Emerg Med 1999;33:694. [PMID: 

10339685] (National survey of emergency medicine residency program directors and 

their use of alternative airway devices.) 

Orebraugh SL: Difficult airway management in the emergency department. J Emerg


airway.) 

Pollack CV: The laryngeal mask airway—a comprehensive review for the emergency 

physician. J Emerg Med 2001;20:53. [PMID: 11165839] (Review of the laryngeal mask 

airway indications, complications, and limitations.) 

Rodricks MB et al: Emergent airway management—indications and methods in the face 

of confounding conditions. Crit Care Clin 2000;16:389. [PMID: 10941580] (Review of 

management of the difficult airway, which includes review of current medications used in 

rapid-sequence protocols.) 



NEEDLE CRICOTHYROIDOTOMY BR> 

Cricothyroidotomy is the standard approach to creating an emergent surgical airway. 

Two methods using needle penetration of the cricothyroid membrane are described 

below. They are acceptable alternatives to cricothyroidotomy in selected cases and may 

be easier and less invasive than emergent cricothyroidotomy for inexperienced 

operators. 

Identification of the cricothyroid membrane is critical to performing either needle or 

surgical cricothyroidotomy (Figure 8-5). Palpation of the tracheal midline will identify the 

hyoid bone superiorly. Below this, the thyrohyoid space leads to the laryngeal 

prominence of the thyroid cartilage. The vocal cords lie behind the thyroid cartilage. The 

cricothyroid membrane is about 1.5 fingerwidths below the prominence and is bounded 

caudally by the cricoid cartilage. It is approximately 10 mm high and 22 mm wide. Each 

landmark must be clearly identified by palpation in the caudal and cephalad directions to 

prevent incision of the thyrohyoid space with entry into the hypopharynx, above the 

cords. Penetration of the cricothyroid membrane will enter the trachea about 1 cm below 

the vocal cords. Penetrate the cricothyroid membrane in the lower third of the 

membrane to avoid the superior cricothyroid vessels that run transversely across the 

upper third of the cricothyroid membrane. When subcutaneous air, trauma, or body 

habitus obscure the usual landmarks, the approximate position of the cricothyroid 

membrane may be determined by placing the small finger of the right hand in the sternal 

notch while the hand is held in neutral position. The cricothyroid membrane will lie 

approximately 4 fingerwidths above the sternal notch. If time allows, prepare the skin 

with an iodine skin disinfectant, and raise a wheal of local anesthetic over the 

cricothyroid membrane before inserting the needle. 

Percutaneous Transtracheal Jet Ventilation 

(See also Chapter 6.) PTTJV is an alternative technique for oxygenating and ventilating 

a patient who cannot be intubated in a more standard fashion. It is unique in that 

positive pressure is generated by high-pressure oxygen delivered as an intermittent jet 

through high-pressure tubing and a percutaneously placed large-bore tracheal catheter. 

No bag reservoir or nonrebreathing valve is employed. PTTJV is less invasive than 

cricothyroidotomy and less time consuming than retrograde intubation (see below). It is

elatively easily learned. With attention to detail, there are few complications. It can be 

used in awake or obtunded patients. Other advantages include presumed protection of 

the cervical spine and possible expulsion of a pharyngeal foreign body by expired air. In 

the emergency department it is regarded as a temporizing measure while other methods 

of airway control can be established. Indications for PTTJV are the same as for 

cricothyroidotomy. PTTJV has been proved useful in the pediatric population. 

Disadvantages include the need for either makeshift or commercially available special 

equipment. With prolonged use, retention of carbon dioxide may develop. 

Contraindications include anterior neck trauma, where high delivered pressures may 

lead to severe tissue disruption, and complete airway obstruction, where expired air 

cannot escape through the glottis. PTTJV shares the relative contraindications 

mentioned above for all invasive methods of airway control. Prior unsuccessful attempts 

at catheter placement may lead to air leak or subcutaneous emphysema after a second, 

successful attempt. 

The materials required for PTTJV are listed in Table 8-7. The system may be built out of 

items normally stocked in the emergency department and operating room. Several 

companies now produce specialized delivery systems and cannulas for PTTJV. The 

components of the system must be immediately available to be useful in emergency 

department airway management. 

To obtain the 50 psi of pressure necessary to generate adequate volume to expand the 

patient's chest, the high-pressure tubing must be attached to the oxygen tank through a 

step-down regulator (or demand valve). A wall oxygen outlet or the flush valve of the 

anesthesia machine are also potential sources of high-pressure oxygen. A 

bag-valve-mask unit cannot generate adequate pressure to ventilate a patient with this 

system. 

The high-pressure tubing is fitted with an interrupt valve along its length. If an interrupt 

valve is not available, a Y connector or side port in the oxygen tubing can be used as an 

alternate port. It is then attached directly to the tracheal catheter via a Luer-Lok adapter. 

If necessary, an adapter can be constructed using the male end from intravenous 

tubing, a 3-way stopcock, or the barrel of a 3-mL syringe. All connections should be 

reinforced with plastic ties to prevent separation under pressure (Chapter 6). 

The over-the-needle catheter must be kink-resistant and meet the specifications noted 

in Table 8-7. The commercially available catheters have distal side holes that diffuse the 

jet of air entering the trachea, preventing focal trauma. They also have a proximal flange 

for securing the catheter to the neck. 

Significant deviations from recommended equipment may lead to inadequate ventilatory 

volumes, hypoxia, and hypercapnia. 

To place the catheter, prepare the neck and locate the cricothyroid membrane as 

described above. Insert the over-the-needle catheter and needle into the lower third of 

the cricothyroid membrane in a caudal direction at an angle of 30-45 degrees. 

Aspiration of air should confirm catheter position. Advance the catheter, and remove the 

needle. In its final position, the tip of the catheter should be near the carina. Secure the

catheter at the neck, attach the oxygen delivery system to the catheter, and begin 

ventilation. 

When the alternate port is covered with a finger, oxygen is delivered to the patient, 

generating about 20 cm H 2 O pressure in the airway. Much of the 50-psi pressure is lost 

through the glottis during oxygen delivery. When the alternate port is released, there is a 

period of passive exhalation while the patient's chest wall and diaphragm recoil. 

Recommended ventilatory rates vary from 12 to 20 cycles per minute with an inspiratory 

to expiratory ratio of 1:2 (eg, 1 second with the alternate port covered leading to 

ventilation, 2 seconds with the alternate port opened allowing passive exhalation). 

During ventilation, the chest wall will rise and a significant volume of oxygen will be 

expelled from the glottis. This produces a spray of blood and secretions through the 

patient's mouth and nose, creating potential for hazardous exposure. During passive 

exhalation, the chest wall muscles recoil, expelling (less forcefully) some of the volume, 

and the chest wall should fall. Monitor the rise and fall of the chest wall closely, because 

without chest wall recoil and passive exhalation, hypercapnia, acidosis, and barotrauma 

may develop quickly. 

Complications include all those noted above for needle placement. Needle 

misplacement may cause perforation of the trachea or esophagus, leading to tissue 

disruption and emphysema of the deep tissues or mediastinitis owing to the high 

pressures of ventilation. Local subcutaneous emphysema is common. Inadequate 

monitoring may lead to hypoxia, hypercapnia, and acidosis as noted above. The awake 

patient may experience cough during the procedure. Even with good technique, 

prolonged ventilation using PTTJV will result in respiratory acidosis and hypoxia. 

Retrograde Intubation 

Retrograde intubation is indicated when oral or nasal intubation is contraindicated or 

technically impossible owing to anatomic, pathologic, or traumatic abnormalities. The 

advantages of this technique include maintenance of the cervical spine in a neutral 

position and the benefits of any blind technique. In addition, it requires less skill than 

fiberoptic intubation. Disadvantages include its time-consuming nature and the need to 

have the patient ventilating adequately throughout. This method is contraindicated when 

the airway is obstructed at or above the level of the cords. If the patient is unable to 

open the mouth, the retrograde wire must be passed out the nose for nasal intubation, 

which can be difficult and suboptimal in some settings. Contraindications include apnea 

and those described above, in the "Choice of Methods" section. 

Retrograde intubation can be performed by one operator, although an assistant is 

extremely helpful. Special equipment includes a needle large enough to accept a 

catheter or guide wire and a wire or catheter, approximately 70 cm in length. Local 

anesthetic is recommended. A small clamp is useful. 

The principle of retrograde intubation involves entering the trachea at the cricothyroid 

membrane with a guide wire that is threaded out the mouth or nose and used as a guide 

for blind oral or nasal intubation. After appropriate preparation of the neck, identify the 

cricothyroid membrane and surrounding landmarks. Pass a needle through the skin, 

and puncture the inferior third of the cricothyroid membrane with the needle directed

about 30 degrees caudad. Aspiration of air confirms tracheal placement. Rotate the 

needle to about 30 degrees cephalad, and reaspirate to confirm tracheal position. 

Introduce the wire through the needle. As the wire is threaded through the needle, it 

often exits spontaneously through the mouth. Occasionally, however, it must be 

retrieved with fingers or forceps. When the wire is in hand at the lips or nares, the 

needle is removed. Fix the wire at the cricothyroid membrane with fingers or a small 

clamp. Thread the proximal end of the wire into the endotracheal tube through the side 

hole (Murphy's eye). It should pass up through the lumen of the tube, exiting at its 

proximal end. Advance the lubricated tube along the wire until resistance is met, 

indicating that the tube is in the trachea, below the cords, pulled tight against the fixed 

wire. Release the wire at the skin, and pull it out through the proximal end of the tube. 

Advance the tube to the appropriate position, and confirm placement in the usual 

manner. 

Only a small number of cases of retrograde intubation have been described. Few 

serious complications have been reported. 

Orebraugh SL: Difficult airway management in the emergency department. J Emerg 


airway.) 

Soriano SG et al: The difficult pediatric airway—surgical airway, rigid bronchoscopy, and 

transtracheal jet ventilation in the pediatric patient. Anesthesiol Clin North Am 

1998:16:827. (Review of alternative methods for airway control in the pediatric patient.} 

SURGICAL AIRWAYS 

Cricothyroidotomy 

When there is complete upper airway obstruction or massive facial trauma that prohibits 

intubation from above, immediate access to the trachea can be obtained with 

cricothyroidotomy. In experienced hands, it is a rapid technique that maintains 

immobilization of the cervical spine. It is a radical procedure with risk of significant short- 

and long-term negative outcomes. It is contraindicated whenever the airway can be 

secured by less invasive means. In children, cricothyroidotomy becomes technically 

more difficult as the landmarks become smaller. Patient age less than 10 years is a 

relative contraindication for inexperienced practitioners. In children under age 5 years, 

PTTJV or a tracheostomy is preferable if possible. Other relative contraindications 

include preexisting laryngeal disease, coagulopathy, anatomic deformities of the neck 

due to trauma or other causes, and lack of familiarity with the procedure. 

The equipment and technique for cricothyroidotomy are described in Chapter 6. Kits are 

available that use over-the-wire techniques, progressive dilatation, and trocar 

placement. 

Early and delayed complications of cricothyroidotomy are the same as for other invasive 

techniques (see above). 

Tracheostomy

Tracheostomy has little indication in emergency department management of the airway. 

Its only true indication is severe blunt trauma to the neck with fracture of the thyroid or 

cricoid cartilage, preventing access to the cricothyroid membrane. Tracheostomy is the 

preferred method of surgical airway management in the very small child when PTTJV is 

not possible. Because of the proximity of vascular, nerve, and visceral tissue, the risk of 

negative sequelae is high. A thorough knowledge of anatomy and careful surgical 

technique are critical to success. It should be performed only by surgeons experienced 

with the procedure. 

Walls RM: Management of the difficult airway in the trauma patient. Emerg Med Clin 

North Am 1998;16:45. [PMID: 11809554] (Review of airway techniques in the trauma 

patient.) 

USE OF DRUGS TO ASSIST IN INTUBATION 

Many patients in the emergency department can be intubated without the use of 

pharmacologic intervention other than oxygen. However, when pharmacologic adjuncts 

are indicated, their use may dramatically reduce the difficulty of intubation and speed 

control of the airway. The patient's overall condition and the goal of intubation determine 

the choice of agent. 

Oral or nasal intubations in awake patients are best carried out under local, topical, or 

regional anesthesia. Occasionally, sedation alone may be useful in preparing for 

intubation. For a semiobtunded or combative patient, use of neuromuscular blockade 

with sedation, usually in a rapid-sequence intubation (RSI) protocol, provides rapid 

control of the airway while protecting against aspiration of gastric contents. 

Drugs that induce apnea must be used by or under the direct supervision of 

experienced clinicians prepared to obtain a surgical airway in the event of failed 

intubation. Equipment necessary for intubation and surgical airway must be prepared in 

advance and be available at the bedside before the patient is sedated or anesthetized. 

Topical Anesthesia 


Awake intubation presumes a patient with enough ventilatory effort to allow time to 

anesthetize the airway. The patient must be able to cooperate with, or at least tolerate, 

the noxious process of passing an endotracheal tube. Anesthesia of the airway causes 

loss of the normal protective airway reflexes, with concomitant risk of aspiration. 

Absorption of topical agents occurs more readily from tracheal tissues than from oral or 

nasal mucosa, increasing the risk of systemic toxicity if excessive doses are used. 

B. Choice of Agent 

Common choices for topical anesthesia of the airway are lidocaine and cocaine (Table 

8-8). All local anesthetics have central nervous system toxicities including confusion, 

coma, and seizures. All local anesthetics also have cardiovascular effects including 

slowed conduction, myocardial depression, arrhythmogenesis, and peripheral 

vasodilation. Hypotension and cardiac arrest may occur.

1. Lidocaine—Topical lidocaine may be administered as a gargle of 10-mL aliquots 

repeated 3 times. The drug must be spat out, not swallowed, between each dose to 

avoid toxic systemic levels. To aerosolize, 4 mL of a 4% solution may be administered 

through a standard nebulizer at 8 L/min with either a mouth piece or face mask. 

2. Cocaine—Topical cocaine combines anesthetic and vasoconstrictive properties. A 

local vasoconstrictor is unnecessary with cocaine and can be dangerous. Owing to risks 

associated with cocaine, its use has fallen out of favor in the emergency department. Its 

use is now generally limited to nasal anesthesia in the operating room (see Table 8-8). 

C. Topical Vasoconstrictors 

If nasal intubation is planned, addition of a local vasoconstrictor is necessary to 

decrease the risk of epistaxis (unless topical cocaine is used). The best drugs for this 

purpose are phenylephrine, 0.005-0.15%, or ephedrine, 1%. Topical epinephrine is 

ineffective. 

D. Topical Laryngeal Anesthesia 

After nasal and oropharyngeal anesthesia is induced, the posterior pharynx and larynx 

may require additional local anesthesia. Gentle direct laryngoscopy will permit local 

anesthesia of more distal tissues with a spray. Tracheal anesthesia can also be 

obtained by direct injection of 2-3 mL of 1-2% lidocaine through the cricothyroid 

membrane. 

Superior Laryngeal Nerve Block 

Sensory innervation of the larynx, epiglottis, and lower pharynx is supplied by the 

internal branch of the superior laryngeal nerve that branches from the vagus bilaterally. 

It pierces the thyrohyoid membrane between the thyroid cartilage and the hyoid bone 

below the greater horn of the hyoid, and runs in the submucosa of the piriform fossa. It 

may be blocked in the sitting patient by inserting the needle laterally just above the 

thyroid cartilage below the greater horn and injecting 2-3 mL of 2% lidocaine. The 

injection is then repeated on the other side. A median approach with the needle directed 

laterally and upward toward the greater horn of the hyoid bone on either side also will be 

effective (Figure 8-6). 

Rapid-Sequence Intubation 


Use of sedation alone to intubate a patient in the emergency department can be difficult 

and risky. Titration of a narcotic or sedative to an intubating dose is time consuming. 

Delays in airway control can delay other care. Unwanted central nervous system or 

cardiovascular side effects can persist, complicating the patient's postintubation course. 

Hypoventilation often occurs before the patient is adequately relaxed for intubation, and 

prolonged bag-valve-mask ventilation may be required. Many emergency department 

patients present with a full stomach. These factors, combined with gastric distention due 

to bag-valve-mask ventilation, depressed airway reflexes, and the emetic effects of 

sedatives, raise the risk of aspiration.

The RSI protocol diminishes these difficulties in the awake patient who is agitated or 

who has altered mental status and requires oral intubation. A rapid-acting 

neuromuscular blocker is given to paralyze the patient. Though controversial, some 

protocols recommend a priming dose of a nondepolarizing neuromuscular blocker (such 

as vecuronium) to facilitate paralysis, reduce fasciculations, and limit elevations in 

intracranial pressure during laryngoscopy. Prior to administration of the paralytic, a 

short-acting sedative is added to decrease agitation and the noxious sensations 

associated with paralysis and intubation in awake or semi-conscious patients. The 

patient is intubated immediately after paralysis. Further sedation or paralysis may then 

be effected as indicated. 

During the short period when the patient is paralyzed and not intubated, the airway must 

be protected from aspiration with cricoid pressure. 

The RSI protocol is generally unnecessary in a completely obtunded, relaxed patient; 

however, if the patient has retained enough muscle tone to make intubation without 

paralytics difficult, RSI may facilitate a more rapid intubation. Contraindications include 

contraindications to the specific drugs that will be used. Do not induce apnea if there are 

contraindications to oral intubation or evidence that it is not likely to be successful and 

bag-valve-mask ventilation will be difficult. Because the RSI protocol will obscure the 

neurologic examination and physical manifestations of status epilepticus, alternative 

plans to follow the neurologic condition of the patient must be made before inducing 

paralysis. 

B. Equipment and Personnel Required 

At least 2 individuals must be available to safely initiate the RSI protocol. Other than the 

drugs, no special equipment is required to induce neuromuscular blockade. Before 

giving any sedative or neuromuscular blocking agent, review the checklist in Table 8-9. 

The choice of sedative or anesthetic and neuromuscular blocking agent depends on the 

indication for intubation, patient condition, and user familiarity. 

C. Procedure 

Table 8-10 outlines the steps of the RSI protocol. The characteristics of the 

recommended drugs are mentioned in the "Drugs Used During Intubation" section, 

below. 

D. Additional Drugs 

Several agents may be added to the RSI protocol under specific circumstances. 

1. Vecuronium—Vecuronium, 0.01 mg/kg priming dose given 3-5 minutes before 

succinylcholine, will abolish fasciculations. Fasciculations may cause muscle pain, 

increased intragastric pressure, increased intraocular pressure, and increased 

intracranial pressure and may displace bony fractures. Although vecuronium can 

attenuate these effects, many physicians use fasciculations as an indicator that 

paralysis is being initiated and intubate immediately upon cessation of fasciculation. 

2. Atropine—Atropine, 0.01-0.02 mg/kg given immediately before the sedative, 

attenuates the vagal bradycardia associated with succinylcholine. Children, who tend to 

be more sensitive to the bradycardic and hypotensive effects of succinylcholine, benefit

from pretreatment with atropine. Pretreat adults with bradycardia and those receiving a 

second dose of succinylcholine. 

3. Lidocaine—Lidocaine, 1.5 mg/kg given 1 minute before intubation, may attenuate 

elevations in intracranial pressure associated with succinylcholine and intubation. It may 

have some protective effect against laryngeal spasm and ventricular arrhythmias during 

intubation. 

4. Analgesics—If pain control is part of the management plan, a narcotic such as 

morphine sulfate, 0.1 mg/kg; fentanyl, 1-2 ug/kg intravenously; or other analgesic should 

be added after intubation, because barbiturates have little analgesic effect and 

neuromuscular blockers have none. 

5. Anticonvulsant agents—If status epilepticus is present before intubation, load the 

patient with anticonvulsant medications such as phenytoin, 15 mg/kg, after intubation. 

The neuromuscular blockers used in the RSI protocol mask, but do not stop, central 

nervous system seizure activity. 

Drugs Used During Intubation 

A. Succinylcholine 

Succinylcholine is a depolarizing neuromuscular blocking agent. 

1. Dose—1.0-1.5 mg/kg in adults, 1.5-2.0 mg/kg in children. 

2. Onset—60 seconds to complete relaxation. 

3. Duration—5-10 minutes. 

4. Metabolism—Degraded by pseudocholinesterase. 

5. Indications and advantages— 

a. Drug of choice for the RSI protocol under most circumstances owing to rapid onset, 

complete muscular relaxation, and short duration. 

b. Single dose in emergency department setting usually well tolerated if appropriate 

precautions are taken (see below). 

6. Contraindications— 

a. Risk factors for hyperkalemia (see "Adverse effects and precautions," below). 

b. Hereditary pseudocholinesterase deficiency (1 in 2800 patients). 

c. Penetrating ocular trauma or glaucoma. 

d. Known family or personal history of malignant hyperthermia.

e. Hypersensitivity to succinylcholine. 

7. Adverse effects and precautions— 

a. Cardiovascular effects include bradycardia and hypotension, ventricular arrhythmias, 

and tachycardia or hypertension. Use with care in setting of irritable myocardium. 

b. Fasciculations (see above for sequelae). 

c. Hyperkalemia occurs in settings of subacute burns, subacute crush injuries, upper 

and lower motor neuron disease, and tetanus. Levels in excess of 9 mEq/L have been 

reported, and cardiac arrest may occur. Use may worsen hyperkalemia in renal failure 

patients. 

d. Pseudocholinesterase inhibition may occur in pregnancy, in renal or hepatic 

insufficiency, and with a variety of drugs. 

e. Malignant hyperthermia occurs in 1 in 50,000 patients. 

f. Histamine release may cause bronchospasm or anaphylactoid reaction. 

g. Intraocular pressure is elevated during fasciculations. 

h. Intracranial pressure may increase. 

i. Intragastric pressure may increase; use cricoid pressure until endotracheal tube cuff is 

inflated. 

j. Always use sedation with alert patients; succinylcholine has no intrinsic analgesic or 

sedative effect. 

B. Vecuronium 

Vecuronium is a nondepolarizing neuromuscular blocking agent (NDNMB). 

1. Dose—Standard dose is 0.1 mg/kg. To achieve rapid intubating conditions, 0.25 

mg/kg may be used. 

2. Onset—Dose dependent; standard doses achieve paralysis in 3-5 minutes, larger 

doses in 1-1.5 min. 

3. Duration—Dose dependent; standard doses last 20-40 minutes, and larger does 

may prolong paralysis 2-3 times the usual duration. 

4. Metabolism—Hepatic metabolism with renal excretion. No dose changes 

recommended in patients with congestive heart failure or hepatic or renal insufficiency. 

5. Indications and advantages—

a. One of the NDMBDs that can be used when succinylcholine is contraindicated. 

b. Short duration allows neurologic reevaluation and provides satisfactory paralysis for 

procedures such as computed tomography scan in emergent setting. 

c. Minimal cardiovascular effects at usual doses. 

d. Reversible after partial recovery (evidence of head lift, respiratory effort, or muscle 

twitch response) with neostigmine, 0.04 mg/kg intravenously. Atropine, 0.02 mg/kg 

intravenously, must also be administered to prevent muscarinic side effects. 

e. Does not cause fasciculations or elevate intracranial pressure. 

6. Contraindication—Know hypersensitivity to vecuronium. 


a. Reduce dosage in patients with myasthenia gravis to avoid prolonged blockade. 

b. Maintain cricoid pressure until inflation of endotracheal tube cuff. 

c. Must use sedation or anesthesia in awake patients. 

d. Block is prolonged by aminoglycosides, lithium, quinidine, lidocaine, and propranolol 

and in hypermagnesemia, hyperkalemia, dehydration, hypothermia, and respiratory 

acidosis. 

e. Use during pregnancy only if clearly indicated. 

C. Rocuronium 

Rocuronium is a rapid onset, short-acting NDNMB. 

1. Dose—0.6 mg/kg. 

2. Onset—1-2 minutes. 

3. Duration—30 minutes. 

4. Metabolism—Minimally hepatic with excretion in stool. 

5. Indications and advantages—Excellent choice for nondepolarizing neuromuscular 

blockade. Good alternative for use when succinylcholine is contraindicated. 

6. Contraindication— Known hypersensitivity to rocuronium. 

7. Adverse effects and precautions—

a. Effects potentiated by electrolyte disturbances, neuromuscular diseases, and renal or 

hepatic failure. 

b. Use in pregnancy only if clearly indicated. 

D. Pancuronium 

Pancuronium is a longer-acting NDNMB. 

1. Dose—0.05-0.2 mg/kg. 

2. Onset—1-3 minutes. 

3. Duration—Dose dependent, averaging 60-90 minutes. 

4. Metabolism—Hepatic metabolism with renal excretion. Dosage adjustments are 

indicated. 


a. Main use is prolonged blockade after intubation is complete. 

b. Does not promote bronchospasm. 

c. Reversible after partial recovery (see discussion of vecuronium, above). 

d. No elevated intracranial pressure or fasciculations. 


a. Known hypersensitivity to pancuronium. 

b. Cardiovascular instability or history of congestive heart failure. 


a. History of myasthenia gravis (see section on vecuronium, above). 

b. Cardiovascular effects include increased heart rate, increased afterload, and 

ventricular arrhythmias. Use with caution in the setting of irritable myocardium. 

c. Blockade is prolonged by multiple drugs (see section on vecuronium, above). 

d. Onset and duration profile are not optimal for use with the RSI protocol. 

e. Maintain cricoid pressure until inflation of endotracheal tube cuff. 

f. Always use sedation or anesthesia in awake patients.

g. Use in pregnancy only if clearly indicated. 

E. Thiopental 

Thiopental is a short-acting, highly lipid-soluble barbiturate sedative. 

1. Dose—1-4 mg/kg. 

2. Onset—60 seconds. 


4. Metabolism—Hepatic metabolism. 


a. Historically popular choice for the RSI protocol owing to rapid onset and short 

duration. 

b. Decreases intracranial pressure and cerebral oxygen consumption. 

c. Produces amnesia. 


a. Known sensitivity to barbiturates. 

b. Variegate or acute intermittent porphyria. 


a. Respiratory depression and apnea. 

b. Cardiovascular effects include myocardial depression, dilation of veins, tachycardia, 

and hypotension. Dehydrated patients are at greatest risk for hypotension. Use with 

care in cardiovascular disease and shock and in hypotensive patients. 

c. Cough, laryngospasm, bronchospasm, and hiccups. Consider an alternative drug for 

status asthmaticus. 

d. Nausea and vomiting. 

e. Pain on injection and local necrosis with extravasation. 

f. Anaphylactoid reactions. 

g. Effect prolonged or intensified by other sedatives, narcotics, probenecid, advanced 

age, Addison disease, renal or hepatic insufficiency, myasthenia gravis, and anemia.

h. Effect antagonized by aminophylline. 

i. Consider an alternative drug in pregnancy. 

F. Methohexital 

Methohexital is a rapid-, ultra-short-acting barbiturate anesthetic. 

1. Dose—0.5-1.5 mg/kg. 

2. Onset—Less than 60 seconds. 


4. Metabolism—Hepatic metabolism with renal excretion. 


a. Slightly shorter acting alternative to thiopental in the RSI protocol. 

b. See section on thiopental, above. 

6. Contraindications—See section on thiopental, above. 

7. Adverse effects and precautions—See section on thiopental, above. 

G. Etomidate 

Etomidate is a short-acting sedative-hypnotic. 

1. Dose—0.3 mg/kg intravenously. 

2. Onset—Within 1 minute. 


4. Metabolism—Hepatic metabolism with delayed elimination in end-stage liver 

disease. 


a. Alternative drug for sedation in RSI. 

b. Little to no cardiovascular side effects. 

c. Lowers intracranial and intraocular pressures. 

6. Contraindication—Known hypersensitivity to etomidate. 

7. Adverse effects and precautions—

a. May cause hypotension in the hypovolemic patient. 

b. May cause apnea, laryngospasm, hiccough, and cough. 

c. Decreases plasma cortisol and aldosterone. 

d. Local pain on injection. 

e. Skeletal muscle movements such as myoclonus. 

f. No recommendations for dosing in children younger than age 10 years. 

g. May cause fetal malformation in pregnancy. 

H. Midazolam 

Midazolam is a short-acting benzodiazepine central nervous system depressant. 

1. Dose—0.1-0.3 mg/kg. 

2. Onset—Approximately 30 seconds, depending on rate of injection when given 

intravenously. 


4. Metabolism—Hepatic metabolism with delayed elimination in congestive heart 

failure, renal insufficiency, and old age. 


a. Alternative induction agent for sedation in the RSI protocol (may have prolonged 

sedative effect). 

b. Minimal cardiovascular effects. 

c. May produce amnesia for several hours. 

d. Blunt intracranial pressure responses at high doses. 


a. Known sensitivity to midazolam or benzodiazepines. 

b. Acute narrow-angle glaucoma. 


a. Respiratory depression or arrest.

. Cardiovascular effects usually minimal with bigeminy, premature ventricular 

contractions, and nodal rhythms. 

c. Laryngospasm and bronchospasm, cough, and hives. 

d. Local irritation at injection site. 

e. Nausea and vomiting. 

f. Potentiated by other central nervous system depressants; dose modifications 

recommended. 

g. Dose modifications recommended in patients with chronic obstructive pulmonary 

disease or congestive heart failure, in elderly patients, and in patients with renal failure. 

h. Possible increase in fetal malformations with pregnancy. 

I. Fentanyl 

Fentanyl is a short-acting narcotic anesthetic. 

1. Dose—1-5 ug/kg intravenously. 





a. Alternative drug for sedation in the RSI protocol (sedation may be prolonged with 

thiopental). 

b. Both analgesic and sedative effects. 

c. No histamine release. 

d. Blunts intracranial pressure response to intubation. 

e. Reversible with naloxone, 1-4 mg intravenously. 

6. Contraindication—Known sensitivity to fentanyl. 


a. Respiratory depression and apnea. Respiratory depression may persist beyond 

analgesic and sedative effects.

. Muscle rigidity, which may occur with rapid injection of high doses. 

c. Rare bradycardia or cardiovascular depression. 


e. Effects potentiated by other central nervous system or respiratory depressants. 

f. Dose modifications recommended in patients with chronic obstructive pulmonary 

disease or congestive heart failure, in elderly patients, and in patients with renal failure. 

g. Possible increase in fetal malformations. Consider alternative drugs in pregnancy. 

J. Ketamine 

Ketamine is a dissociative anesthetic agent. 

1. Dose—1-2 mg/kg. 





a. Alternative drug for sedation and analgesia during the RSI protocol, particularly in 

hypotension. 

b. Sedative of choice in status asthmaticus patients because it may cause 

bronchodilation. 

c. Airway reflexes are usually maintained. Respiratory depression is usually minimal 

and transient. 

d. Myocardial depression is uncommon. 

e. Prominent analgesic effects. 


a. Hypersensitivity to ketamine. 

b. Head injury. 

c. Severe hypertension.


a. Elevated blood pressure and pulse rate are the most common cardiovascular effects. 

Hypotension, bradycardia, and arrhythmias have been reported. Use with caution if 

irritable myocardium is present or when hypertension would adversely affect patient 

course. 

b. Respiratory stimulation and maintained airway most common, but apnea, respiratory 

arrest, and laryngospasm also have been reported. 

c. Dysphoric emergence reactions. 


e. Local irritation at injection site. 

f. Increased intracranial pressure. 

g. Intraocular pressure may be increased. 

h. Muscle rigidity or myoclonus. 

i. Increased secretions. Consider pretreatment with atropine. 

j. Possible prolonged recovery when used concurrently with narcotics or barbiturates. 

k. Consider alternative drug in pregnancy and for patients below 2 months of age. 

Li J et al: Complications of emergency intubation with and without paralysis. Am J 

Emerg Med 1999;17:141. [PMID: 10102312] (Retrospective chart review of intubation 

complications with and without paralytics.) 

Rodricks MB et al: Emergent airway management—indications and methods in the face 

of confounding conditions. Crit Care Clin 2000;16:389. [PMID: 10941580] (Review of 

management of the difficult airway, which includes review of current medications used in 

rapid-sequence protocols.) 

Wadbrook PS: Advances in airway pharmacology—emerging trends and evolving 

controversy. Emerg Med Clin North Am 2000;18:767. [PMID: 11130938] (Review of 

drugs used for RSI protocol.) 

SPECIAL CASES 

Management of the Pediatric Airway 

Basic principles of airway management are similar for all age groups. However, 

anatomic and physiologic differences affect the emergency physician's equipment 

needs and management decisions when confronted with a pediatric airway emergency.

A. Unique Features 

• In infants, the head is relatively larger in proportion to the body. 

• The neck is more supple owing to a greater proportion of cartilaginous support tissue. 

• The airway is smaller, resulting in increased resistance and susceptibility to obstruction 

due to edema, blood, or secretions. 

• The mucosa is looser, permitting obstruction due to positioning and greater, faster 

distention from blood or edema. 

• The adenoidal and tonsillar lymphatic tissues are larger and more friable than those of 

adults. 

• The larynx is more cephalad and anterior. 

• The epiglottis is larger and more floppy and protrudes into the airway more 

prominently. 

• The narrowest portion of the airway in children younger than age 5 years is the cricoid 

cartilage rather than the larynx, as in adults. 

• The cricothyroid membrane is very small and does not lend itself to surgical 

manipulation. 

• The carina branches symmetrically at 45 degrees. 

• The chest wall is thinner, and both airway and gastric sounds radiate easily, making 

auscultation less reliable. 

• The chest wall is more pliable, and ventilation depends significantly on diaphragmatic 

movement. 

• Oxygen consumption is 6-8 mL/kg/min in children, whereas adults usually consume 

about 3-4 mL/kg/ min. Hypoxemia can occur more rapidly and is tolerated less well. 

• Apnea occurs suddenly during a wide range of illnesses and injuries. 

• Normal vital signs vary for different age groups (Table 8-11). 

B. Equipment Required 

All essential equipment (oxygen delivery systems, face masks, bag-valve-mask units, 

oral and nasal airways, laryngoscope blades, endotracheal tubes, stylets, and suction 

devices) should be stocked in a variety of sizes to accommodate the anticipated 

population served by the facility (see Table 8-11). Oxygen should be humidified and 

warmed to prevent drying of secretions and subsequent airway obstruction. 

Endotracheal tubes for children younger than age 8 years should be noncuffed to 

prevent damage to the cricoid ring. Correct tube size may be obtained from a table or

gauged based on one of the 3 following methods: 

1. The tube size should closely approximate the size of the child's small finger at the 

distal interphalangeal joint. 

2. The tube size should closely approximate the size of the child's nares. 

3. The tube size in millimeters is equal to (16 + patient's age in years) ÷ 4. 

For patients under age 4 years, a straight blade is preferred owing to the tendency of 

the epiglottis to protrude and cover the airway. In emergency departments where 

pediatric resuscitation is rare, precalculate the doses of commonly needed drugs, based 

on weights, and post them clearly in the resuscitation area or utilize length-based charts 

such as the Broselow-Luten tape. 

C. Decision and Techniques 

Evaluate for respiratory distress by assessing vital signs, skin signs, overall patient 

condition, use of accessory muscles, retractions, nasal flaring, and arterial blood gases 

or pulse oximetry. Supplemental oxygen must be given. Children often cannot tolerate a 

face mask. Adequate oxygen supplementation can frequently be achieved by directing a 

stream of humidified 100% oxygen across the patient's face. 

Airway positioning is essential. Alert patients will often choose the position of greatest 

airway patency and should not be forced to lie down. Infants and obtunded patients 

must be placed in the sniffing position (see Figure 8-2) unless cervical spine injury is 

suspected or present. In this position, the neck is flexed slightly, and the head is 

extended on the neck. The jaw thrust or chin lift is then used to lift the soft tissues out of 

the airway. Obstruction should be cleared. 

Oral and nasal airways are less useful in children because they frequently stimulate 

laryngospasm or emesis when reflexes are intact. In addition, placement may 

traumatize the adenoidal or tonsillar soft tissues, resulting in significant bleeding, which 

can be difficult to control and further complicate airway management. 

In obtunded or paralyzed children, cricoid pressure should be used during 

positive-pressure ventilation until intubation is confirmed. 

Bag-valve-mask ventilation is used initially for emergent oxygenation and ventilation in 

children because of the ease of attaining a seal and the smaller size of the chest cavity. 

Adequacy of ventilation is best assessed by observing chest wall motion; auscultation is 

less reliable. Nasogastric tube placement should accompany bag-valve-mask ventilation 

when safe to decrease the risk of emesis and aspiration. Care should be taken to 

coordinate breaths with the bag-valve-mask unit with spontaneous ventilations, when 

present. 

Definitive airway control involves oral endotracheal intubation. Blind nasal intubation is 

technically more difficult in children and is contraindicated in the emergency department. 

The increased adenoidal tissue is at risk for bleeding, and the anterior position of the 

larynx with the overlying epiglottis makes nasal tube placement more difficult.

Until age 10 years, children should be premedicated with atropine, 0.01-0.02 mg/kg, to 

prevent bradycardia with intubation. 

Because auscultation can be unreliable, tube placement should be confirmed by a 

colorimetric end tidal CO 2 detector, observation of chest wall movement, skin color, and 

radiographs. 

When a cervical fracture is suspected and immediate airway control is essential, RSI 

may be used with in-line traction; other options include PTTJV. PTTJV has been shown 

to be effective in the pediatric model. Perform needle cricothyroidotomy as described for 

adults. The smaller size of the airways should be taken into account. The possibility of 

obstruction at the cricoid cartilage must be considered, because ventilation at the level 

of the cricothyroid membrane would be ineffective in that situation. 

Surgical airways in young children and infants are extremely difficult. They should be 

performed only as a last resort by surgeons with experience in pediatric head and neck 

surgery. There are high failure and complication rates. Most airways will be adequately 

managed by bag-valve-mask or oral intubation techniques. 

D. Epiglottitis and Croup 

These illnesses may cause severe airway edema and sudden obstruction. Diagnosis is 

based on clinical features and, when necessary, anteroposterior and lateral neck soft 

tissue views. 

1. Croup—Croup progresses more slowly than epiglottitis, causes subglottic swelling 

and a barking cough, and is often accompanied by signs of viral upper respiratory 

infection. Croup rarely requires intubation. Treatment includes intravenous fluids, 

humidified air, steroids, and racemic epinephrine. 

2. Epiglottitis—Epiglottitis progresses rapidly with a toxic-appearing, drooling child 

sitting in the upright position with the neck hyperextended. Abrupt, complete airway 

obstruction can occur with minimal stimulation of the patient. When suspicion is high for 

epiglottitis, supplemental oxygen should be supplied and the patient transported with 

minimal disturbance to the operating room, where the epiglottis can be directly 

visualized. More than half of patients with epiglottitis will require intubation, which is best 

done in the operating room by the most experienced intubator before airway obstruction 

occurs. If intubation fails, an emergent tracheostomy must be performed, preferably by 

a pediatric otorhinolaryngologist. Treatment includes antibiotics and intravenous fluids 

after the airway is secured (see Chapter 48). 

Management of Foreign Bodies in the Airway 

Management of foreign bodies in the airway is dictated by the location of the object and 

the patient's age and condition. Most airway obstructions due to foreign bodies occur 

between the ages of 1 and 5 years. More than 3000 deaths annually are due to this 

disorder. 

Assessment begins with observation for tachypnea, air movement, stridor, retraction,

agitation or lethargy, and cyanosis. Auscultation and chest x-ray may be helpful. 

Examination of the oropharynx may reveal the foreign body. 

If the foreign body is visible, the airway may be cleared with a manual sweep. Blind 

sweep is not recommended. If the patient is coughing, do not interfere; the normal 

reflexes often clear the airway. Oxygen should be administered to all patients with 

foreign body aspiration. 

If there is total obstruction, attempt the Heimlich maneuver in patients older than 1 year; 

in younger children, back blows and chest thrusts are recommended. If these methods 

are unsuccessful, position the airway to optimize patency. Attempt to remove the object 

under direct observation with a laryngoscope. If this is unsuccessful, a surgical airway is 

necessary. Subglottic obstructions may not be relieved by cricothyroidotomy or 

tracheostomy. Removal in the operating room with rigid bronchoscope may be the only 

option. 

Management of the partially obstructed airway must be individualized. Bronchial 

obstructions often do not require intubation, and compromise may be subacute. If there 

is air movement and the object cannot be visualized on direct observation, the safest 

method for removal is under general anesthesia with the rigid bronchoscope. Take care 

not to cause complete obstruction while inserting the laryngoscope or bronchoscope. 

Management of Airway in Status Asthmaticus 

The asthmatic patient requires intubation when clinical evidence of fatigue is 

accompanied by increasing respiratory acidosis due to carbon dioxide retention and 

increasing hypoxia in the face of aggressive therapy. Intubation is dangerous for 

asthmatic patients. These patients are susceptible to barotrauma while intubated, and 

intubation does not ensure bronchodilation or adequate ventilation and oxygenation. 

Because of the difficulties of bag-valve-mask ventilation in status asthmaticus, many 

practitioners prefer awake nasal intubations with topical anesthetic. The asthmatic 

patient's active respiratory effort helps tube placement through the cords, but agitation 

often complicates this procedure. If the RSI protocol is used, succinylcholine is relatively 

contraindicated owing to histamine-induced bronchospasm. Similarly, thiopental may 

worsen the condition. Better choices include vecuronium, midazolam, fentanyl, and 

ketamine. Unlike other choices for sedation, ketamine also has bronchodilating effects. 

Management of Airway in Trauma Patients 

A. Patients with Unstable Cervical Spines or Facial Injuries 

When airway control must precede definitive stabilization of the spine, oral intubation 

with RSI and in-line maintenance of the cervical spine has been proved safe and 

effective. It is the method of choice in the trauma patient with suspected spinal injury. 

However, most large series report no bad neurologic outcomes with any technique that 

is carefully done. Other options for airway control include blind techniques such as nasal 

or digital intubation, use of lighted accessories, and transtracheal methods. The 

decision must be individualized based on the patient's level of consciousness and 

injuries, the urgency of the need for airway control, and the intubator's skill with various 

techniques.

Patients with severe facial and upper neck trauma present significant challenges to the 

emergency physician. If RSI techniques are attempted, the emergency physician should 

be prepared to switch immediately to a surgical airway or a bridge device to allow 

ventilation in the event that bag-valve-mask ventilation proves difficult or ineffective. If 

the airway is predicted from the beginning to be difficult, an awake intubation using 

topical anesthetics and intravenous sedation may be the best approach. 

B. Patients with Head Trauma 

Intubation of patients with severe head trauma is indicated to treat hypoventilation and 

hypoxia and to protect and control the airway in patients who are unstable or combative 

and agitated enough to require paralysis for necessary studies and procedures. 

Additionally, it is the only way to hyperventilate the patient to a lower PCO 2 as part of 

the treatment for elevated intracranial pressure. Approach to the airway must take into 

account other potential traumatic injuries to the mid face, cervical spine, soft tissues of 

the neck, and respiratory tract. Oral intubation with the RSI protocol is generally 

recommended. If the RSI protocol is used, lidocaine, 1.5 mg/kg intravenously, may 

attenuate the rise in intracranial pressure. Although succinylcholine is reported to raise 

intracranial pressure, it remains the recommended agent for neuromuscular blockade in 

the setting of head trauma because it allows for rapid control of the airway and initiation 

of treatment. Other sedative options available to attenuate the rise in intracranial 

pressure associated with laryngoscopy include fentanyl and etomidate. Vecuronium, an 

NDNMB, is administered at 0.01 mg/kg as a small priming dose to eliminate muscle 

fasciculations associated with succinylcholine use. Digital intubation or light-assisted or 

surgical airways may be used as indicated if oral intubation is unsuccessful. 

Cummins RO et al: Guidelines 2000 for cardiopulmonary resuscitation and emergency 

cardiovascular care. American Heart Association Currents 2000;Fall:1. (Update of 

advanced cardiac life support guidelines.) 

Levy RJ et al: Managing the airway in the critically ill patient—pediatric issues. Crit Care 

Clin 2000;16:489. [PMID: 10941587] (Review of the management of the difficult airway 

in the pediatric patient.) 

Soriano SG et al: The difficult pediatric airway—surgical airway, rigid bronchoscopy, and 

transtracheal jet ventilation in the pediatric patient. Anesthesiol Clin North Am 

1998;16:827. (Review of alternative methods for airway control in the pediatric patient.) 


North Am 1998;16:45. [PMID: 11809554] (Review of airway techniques in the trauma 

patient.) 

CARE OF THE INTUBATED PATIENT 

Adjunctive Drugs 

Intubated patients often require sedation to prevent coughing or "bucking" the 

endotracheal tube and to reduce agitation. Prolonged paralysis may be indicated during 

procedures or during early stages of management. In general, neuromuscular blockade

should be accompanied by sedation to blunt the noxious sensation of paralysis. 

Paralysis may mask the manifestations of status epilepticus. Patients with ongoing 

status epilepticus must have full anticonvulsant loading before, during, or immediately 

after paralysis. If the patient remains paralyzed, control of seizures must be 

demonstrated with electroencephalographic recording. 

Pulmonary Toilet 

After the endotracheal tube position is confirmed by clinical evaluation and x-ray, it is 

secured by taping about the head or neck to prevent accidental extubation. All intubated 

patients require regular suctioning. The frequency of suctioning depends on the amount 

of secretion produced. Indicators of the need to suction may include visible secretions 

welling up in the endotracheal tube, hypoxia, agitation, and increased difficulty with 

bagging. In the emergency department, most patients will be manually ventilated with a 

bag-valve-mask unit, at least initially. If on a mechanical ventilator, a patient should be 

preoxygenated with several minutes of bag-valve ventilation at 100% oxygen to ensure 

against hypoxia during suctioning. Disposable, sterile, narrow-gauge, flexible suction 

catheters are available for suctioning the endotracheal tube. The diameter of the 

catheter should be less than half the internal diameter of the endotracheal tube. Insert 

the catheter with the side port open. When the catheter is in the trachea, apply suction 

by covering the side port. Rotate the catheter several times to suction both right and left 

main stems. Continue suction and rotary movement during catheter removal. The 

patient is then reoxygenated. No single suctioning episode should last longer than 10-15 

seconds. Preoxygenate for 30-60 seconds before reinserting the catheter. Suctioning 

may be aided by administering 1-2 mL of sterile normal saline down the tube to moisten 

secretions. Complications of suctioning include hypoxia, arrhythmias, hypotension, 

mucosal trauma, and pulmonary collapse. There is also a surge in intracranial pressure 

during suctioning, which may be blunted by the use of tracheal or intravenous lidocaine. 

Occasionally the oropharynx must be suctioned with the rigid-tipped catheter to control 

oral secretions or blood. 

Endotracheal Medication 

Medications that are safe and probably effective when given endotracheally include 

epinephrine, atropine, lidocaine, diazepam, and naloxone. Because of erratic 

absorption, some authors recommend administering 2-10 times the normal intravenous 

dose for epinephrine endotracheally. Delivery is enhanced if the drugs are diluted in 10 

mL of normal saline before administration and aerosolized during administration by 

rapid injection through a pediatric feeding tube positioned in the trachea. 

Monitoring 

A. Observation 

Any patient intubated in the emergency department requires close observation. A 

respiratory technician, nurse, or physician should be present at all times. In addition to 

contributing critical clinical observation to the data obtained by monitoring devices, they 

may note complications of intubation and positive-pressure ventilation and address 

them before these complications compromise the patient.

Complications that may occur while a patient is intubated include barotrauma with 

tension pneumothorax, atelectasis, and obstructions or disconnections in the ventilatory 

circuit. In critically ill patients, continuous observation for changes in the patient's 

hemodynamic or mental status is the standard of care. 

B. Pulse Oximetry 

A pulse oximetry sensor can be clipped over the tip of a digit or an earlobe to detect the 

oxygen saturation of arterial blood. Oximetry reflects trends in oxygenation before, 

during, and after intubation. When the PaO 2 is greater than 60-80 mm Hg, a large 

change in PaO 2 may result in only a small change in oxygen saturation measured by 

the pulse oximeter. Oxygenation can also be maintained to some degree by 

hyperventilation (PCO 2 declines); however, pulse oximetry provides no information 

about the adequacy of ventilation. Consequently the pulse oximeter cannot substitute 

for arterial blood gas determinations in many clinical settings. The presence of nail 

polish, skin pigmentation, methemoglobin, carboxyhemoglobin, intravascular dye, 

hypothermia, and hypoperfusion all may reduce the accuracy of the pulse oximeter. 

C. Capnography 

Capnometers may be attached to the expired air circuit to monitor the end-tidal carbon 

dioxide tension (P et CO 2 ). In healthy patients, the plateau P et CO 2 is usually 1 mm Hg 

less than the PCO 2 . Because the absence of P et CO 2 indicates esophageal intubation, 

disposable devices are helpful to indicate successful endotracheal tube placement in 

patients with perfusing rhythms. 

D. Esophageal Detection Device 

An esophageal detection device is used to detect esophageal versus tracheal 

intubation. It consists of a large syringe or self-inflating bulb, which will easily aspirate 

air if the tube is in the trachea. Resistance to aspiration will be noted if the tube is in the 

esophagus. This device is useful in patients with or without perfusing rhythms. The 

device may be unreliable in morbidly obese, pregnant, or asthmatic patients. 

E. Arterial Blood Gases 

The measured pH, PaCO 2 , and PaO 2 remain the standard for monitoring respiratory 

status. The method for obtaining a sample is described in Chapter 6. The main 

disadvantage of using the arterial blood gas measurement is the discontinuous nature of 

the data. Transient changes and trends may be missed. Overall, however, it remains the 

best indicator of gas exchange and acid-base balance. 

F. Cardiac Monitoring 

Most intubated patients require continuous cardiac monitoring and frequent checks of 

blood pressure and heart rate. Hypoxia and other complications of intubation are often 

reflected early in changes in vital signs. 

G. Other Monitoring Methods 

Several other devices may assist in monitoring an intubated patient. Some are useful 

only in specific settings and others when intubated patients must be held for prolonged 

periods in the emergency department while awaiting a bed in an intensive care unit.

Transcutaneous PO 2 devices are available for neonates in whom P tc O 2 correlates well 

with PaO 2 . Arterial lines and pulmonary artery catheters allow intra-arterial 

measurement of PaO 2 and measurement of mixed venous oxygen saturation. 

Pulmonary functions may be monitored, particularly in patients who are likely to be 

extubated in the emergency department. 

General Care 

Paralyzed patients are unable to shift their weight from pressure points at will. 

Consequently, they must be turned every hour, and particular pressure points must be 

padded. If they are in a cool environment, they must be adequately covered. Lubricate 

and tape the eyes to prevent corneal ulceration. 

Mechanical Ventilation 

If mechanical ventilation is used in the emergency department, the choice of ventilator 

and ventilator settings must be individualized to the patient's condition. In many 

circumstances, a tidal volume of 15 mL/kg, a rate of 12, and the "assist control" mode 

are reasonable settings. For hyperventilation, start with a rate of 20 and check an 

arterial blood gas measurement for confirmation. The use of a ventilator does not 

obviate the need for close observation of the patient's condition by a physician or 

qualified nurse. 

Extubation 

In several circumstances, a patient may require extubation in the emergency 

department. Before electing to extubate, be certain that the patient has spontaneous 

ventilation and is able to generate a vital capacity of 15 mL/kg. The indication for 

intubation must be resolved, and airway reflexes should be intact. Optimally the patient 

should be able to follow commands and understand the planned procedure. If possible, 

decompress the stomach with nasogastric suction. Assemble equipment for suctioning 

and reintubation. Suction the oropharynx and tracheobronchial tree, manually 

oxygenate with 100% oxygen, release the cuff, and withdraw the tube at the end of 

inspiration. Ventilate with a mask, and observe for laryngospasm or respiratory 

insufficiency. If laryngospasm occurs, continue bag-valve-mask ventilation with 100% 

oxygen. Consider racemic epinephrine, 0.5 mL of 2.25% in 4 mL of normal saline via 

nebulizer. If these methods fail, reintubation or a surgical airway may be necessary. 

Cummins RO et al: Guidelines 2000 for cardiopulmonary resuscitation and emergency 

cardiovascular care. American Heart Association Currents 2000;Fall;1. 




CURRENT EMERGENCY DIAGNOSIS & TREATMENT - 5th Ed. (2004)



MD 

IMMEDIATE MANAGEMENT OF THE COMPROMISED AIRWAY (See 

Figure 8-1.)

Table 8-1. Indications for intubation. 





MD 

TABLES 

Table 8-1. Indications for intubation.

Table 8-2. Essential airway management equipment. 





MD 

TABLES 

Table 8-2. Essential airway management equipment.

Table 8-3. Optional equipment and rescue devices for 

difficult intubations. 

1 

Either commercially available or preassembled in a 

sterile tray. 





MD 

TABLES 

Table 8-3. Optional equipment and rescue devices for difficult intubations.

Table 8-4. Complications of esophageal airways. 





MD 

TABLES 

Table 8-4. Complications of esophageal airways.

Table 8-5. Relative contraindications for 

orotracheal intubation. 





MD 

TABLES 

Table 8-5. Relative contraindications for orotracheal intubation.

Table 8-6. Alternative methods of intubation. 





MD 

TABLES 

Table 8-6. Alternative methods of intubation.

Table 8-7. Equipment required for percutaneous transtracheal 

ventilation (PTTJV). 





MD 

TABLES 

Table 8-7. Equipment required for percutaneous transtracheal ventilation 

(PTTJV).

Table 8-8. Properties of local anesthetics. 

Lidocaine Available concentration 4-11% 

Gargle, spray, or 

atomizer 

Time to onset 5-10 minutes 

30-45 minutes 

Seizure, coma, 

confusion, respiratory 

arrest, cardiovascular 

depression 

Toxic doses > 3-4 mg/kg (toxicity has been 

reported with therapeutic doses) 





MD 

TABLES 

Table 8-8. Properties of local anesthetics.

Table 8-9. Checklist for initiation of RSI. 





MD 

TABLES 

Table 8-9. Checklist for initiation of RSI.

Table 8-10. Rapid-sequence induction protocol. 

1 

Sedative drug choices: 

Etomidate, 0.3 mg/kg 

Methohexital, 0.5-1 mg/kg 

Midazolam, 0.1-0.3 mg/kg 

Fentanyl, 1-5 µg/kg 

Ketamine, 1-2 mg/kg 

Thiopental, 1-4 mg/kg 

2 

Alternative neuromuscular blocker: 

Vecuronium, 0.1-0.25 mg/kg 

Rocuronium, 0.6 mg/kg 

(Use only when succinycholine is contraindicated). 





MD 

TABLES 

Table 8-10. Rapid-sequence induction protocol.

Table 8-11. Pediatric vital signs and airway equipment. 

Premature 1 mo 1 yr 5 yr 

1 4 10 16-18 

145 120 125 100 

30-40 25-35 20-30 12-25 

2.5-3.0 

Uncuffed 

3.5 4 5-6 

8 12 12 16 

0 1 1-2 

Straight 

2 

5 6-8 8 10 





MD 

TABLES 

Table 8-11. Pediatric vital signs and airway equipment.

Figure 8-1. Management of the compromised airway. I-LMA = intubating laryngeal 

mask airway; LMA = laryngeal mask airway; PTTJV = percutaneous transtracheal jet 

ventilation; RSI = rapid-sequence induction. 





MD 

FIGURES 

Figure 8-1

Figure 8-2. In the sniffing position, the head is slightly extended and the neck is flexed 

on the shoulders. This aligns the axis of the airway with the mouth and pharynx, 

facilitating direct visualization of the cords during intubation. It is particularly important in 

young children and infants, in whom the larynx is considerably more anterior. A pad 

beneath the occiput improves flexion of the neck. This position cannot be used when 

there is cervical spine injury. 





MD 

FIGURES 

Figure 8-2

Figure 8-3. A: Oral airway. B: Nasal airway. 





MD 

FIGURES 

Figure 8-3

Figure 8-4. The Sellick maneuver. Firm pressure on the cricoid cartilage compresses 

the esophagus, preventing aspiration of gastric contents when airway reflexes are 

absent. 





MD 

FIGURES 

Figure 8-4

Figure 8-5. Landmarks for locating the cricothyroid membrane. 





MD 

FIGURES 

Figure 8-5

Figure 8-6. The superior laryngeal nerve block. 





MD 

FIGURES 

Figure 8-6


IMMEDIATE MANAGEMENT OF SHOCK (See Figure 9-1.) 

1 This chapter is a revision of the chapter by Donald D. Trunkey, MD, Patricia R. Salber, 

MD, FACEP, FACP, & John Mills, MD, from the 4th edition. 

Essentials of Diagnosis 

• Early (compensated): Tachycardia, anxiety, restlessness, apprehension, delayed 

capillary refill, diaphoresis, widened pulse pressure. 

•Late (decompensated): Hypotension, confusion, loss of consciousness, oliguria, 

acidemia. 

Shock is a state of metabolic failure. In shock, tissues do not metabolize energy 

properly. This may be caused either by inadequate delivery of oxygen to the tissues or 

by the inability of tissues to properly metabolize oxygen once it is delivered. Clinical 

shock is a final common pathway for a diverse group of profound physiologic 

disturbances. Untreated, shock leads to multiple organ system failure and death. The 

mortality rate among patients in shock may be as high as 70%, depending on the 

underlying cause. Appropriate shock management involves early recognition of the 

condition in addition to treatment of both the underlying causes of shock and the 

physiologic abnormalities associated with the shock state (Table 9-1). 

Causes of Shock 

Shock can be caused by qualitative defects (in which blood flow, and therefore oxygen 

delivery, to tissues is depleted) or quantitative defects (in which cellular oxidative 

metabolism is primarily affected). The goal of shock therapy, regardless of cause, is to 

restore homeostasis before irreversible system dysfunction develops. 

On a cellular level, tissues deprived of blood flow receive insufficient oxygen and 

undergo a buildup of toxic metabolic byproducts. Left uncorrected, this situation leads to 

metabolic dysfunction severe enough that the tissue will fail to recover even if adequate 

oxygen flow is restored. 

Cellular dysfunction plays a particularly important role in septic shock, in which a toxic 

stimulus (such as endotoxin) triggers an inflammatory cascade, including the release of 

proinflammatory monokines, cytokines, prostaglandins, leukotrienes, histamine, nitric 

oxide, and proteases. These chemical mediators have differing regulatory functions on a 

wide variety of receptors, and differing functions on the same receptors in different 

locations. The presence of these mediators leads to a condition known as the systemic 

inflammatory response syndrome. Clinically, this syndrome is defined as two or more of 

the following:

• Temperature > 38 °C or < 36 °C 

• Pulse > 90 

• Respiratory rate > 20 or PaCO 2 < 32 mm Hg 

• White blood count > 11,000 or < 4000 or > 10% band forms 

In septic shock, the release of these mediators coincides with mitochondrial dysfunction 

leading to impaired oxygen utilization. 

A similar impairment occurs later in the other forms of shock. As the shock state 

progresses, normal cellular ionic concentration gradients deteriorate due to inadequate 

energy production. Intracellular calcium concentrations increase, leading to further 

inability of mitochondria to produce adenosine triphosphate, and causing muscle to lose 

its ability to relax normally. Intracellular CO 2 and H + increase, and a generalized 

catabolic state, accompanied by decreased cell membrane function, leads to cellular 

edema by osmotic flow of water. 

In shock from any cause, there comes a point at which restoration of adequate 

oxygenation will no longer restore tissue function and the evolution of multiple organ 

system dysfunction syndrome, and most likely death, will occur. 

Classification of Shock 

There are a variety of classification schemes for shock. Classically the causes of shock 

have been divided into four categories (Table 9-2). 

A. Hypovolemic Shock 

The chief abnormality in hypovolemic shock is decreased intravascular volume, which 

may occur as a result of loss of blood or plasma or of fluid and electrolytes. These 

losses may be exogenous (eg, gastrointestinal tract bleeding, diarrhea) or endogenous 

(eg, retroperitoneal hematomas or "third spacing" associated with bowel obstruction or 

pancreatitis). 

B. Cardiogenic Shock 

The chief abnormality in cardiogenic shock is abnormal cardiac function due to 

arrhythmia, "pump failure," myocardial depressant factors, or valvular dysfunction. 

C. Obstructive Shock 

The chief abnormality in obstructive shock is an impediment to filling of the right or left 

ventricle (decreased preload). If decreased filling is sufficiently severe, the resulting fall 

in cardiac output causes shock. Obstruction may occur in the systemic circulation (eg, 

obstruction of the vena cava) or pulmonary circulation (eg, massive pulmonary embolus) 

or may be due to pericardial disease (eg, cardiac tamponade) or cardiac disease (eg, 

atrial myxoma).

D. Distributive Shock 

The chief abnormality in distributive shock is abnormal distribution of vascular volume 

due to changes in vascular resistance or permeability. This can be thought of as an 

increase in the size of the vascular compartment. The end result is a decrease in 

ventricular filling that leads to inadequate cardiac output. The derangement of vascular 

volume characterizing distributive shock may occur as a result of sepsis, anaphylaxis, or 

neurogenic shock. 

Physical Diagnosis of Shock 

The first step in the diagnosis of shock is to suspect its presence. The most useful 

therapeutic interventions in shock may be those that take place in early compensated 

shock, when its presence may be difficult to determine. 

A. Signs of Shock 

(See Table 9-1.) 

1. Hypotension—Although hypotension is often mentioned first, it is a late sign of 

shock. Waiting for hypotension to develop before beginning treatment of shock is a 

potentially fatal error. Hypotension is a particularly late sign in children. In general, if a 

child's blood pressure is less than 2 times the child's age, plus 70, hypotension is 

present. 

2. Tachycardia—An elevated heart rate may be one of the earliest signs that shock is 

present. 

3. Adrenergic responses—The patient may be restless, agitated, or diaphoretic or may 

be cool in the extremities (due to peripheral vasoconstriction). The same mechanism 

may cause livedo reticularis (mottled skin) and capillary refill greater than 2 seconds. 

4. Altered mental status—The patient in shock may demonstrate normal mental status 

but also may have restlessness, anxiety, agitation, confusion, lethargy, or more 

profound alterations in consciousness. These changes may be an early finding. 

5. Orthostatic vital signs—The patient in early shock may evidence tachycardia or 

hypotension only in the standing position. If there are no contraindications to doing so, a 

set of vital signs taken 3 minutes after standing can be compared to a set previously 

taken lying down. An elevation in the heart rate, or a decrease in the blood pressure in a 

standing position, may indicate inadequate intravascular volume. 

B. Determination of Shock Severity 

1. Compensated shock—The body attempts to continue to perfuse vital organs as a 

shock state develops. Blood is preferentially shunted away from the skin, fat, skeletal 

muscle, and bone. As shock deepens, the liver and gut are deprived of oxygen, then the 

kidneys. Urine output is decreased. The body preserves blood flow to the most vital 

organs, the brain and heart, longest. As shock becomes severe, mental status 

deteriorates and arrhythmias and signs of cardiac ischemia may develop. 

2. Decompensated shock—The byproducts of inadequate cellular energy metabolism

eventually overwhelm the vasculature's ability to continue shunting blood to the vital 

organs. At this point, mental status is severely impaired, the patient is hypotensive, and 

the shock state is likely to lead to death even with aggressive supportive care. 

Initial Treatment of Shock 

There are common initial therapy points for shock of all types. These same points apply 

to very ill patients regardless of cause of disease. A cause of shock must be identified to 

provide more specific therapy. Obtain a brief history from the patient, family, friends, 

bystanders, police, or ambulance personnel. Use the examination to help provide clues 

to the cause (eg, circular erythema may indicate the prior use of "cupping" as a folk 

remedy to remove infectious illness). 

The ABCs (and D) 

A. Airway 

Open or maintain the airway. Is the patient speaking? If not, are sonorous respirations 

or stridor present, which might indicate an inadequate airway? Will suctioning or 

placement of a nasal airway improve the airway? If the patient tolerates an 

oropharyngeal airway (OPA), put it in place. A patient who tolerates an OPA has an 

inadequate gag reflex and will need to be intubated. Ventilate and intubate the patient if 

respiratory status is inadequate. For airway protection, intubate all trauma patients who 

have severely impaired mental status (use a Glasgow Coma Scale score of 8 or less as 

a guide). Avoid nasotracheal intubation if head trauma is present. 

B. Breathing 

Provide supplemental oxygen at 10-15 L/min via a non-rebreathing mask. Respirations 

of less than 12 or greater than 30 are unlikely to be sufficient. Pulse oximetry and 

arterial blood gas measurements may aid in the diagnosis of respiratory insufficiency 

when it is not clinically apparent. Sources of respiratory insufficiency, such as 

pneumothorax and loss of integrity of the chest wall (flail chest), should be sought and 

corrected. 


Stop obvious external hemorrhage. Obtain vascular access. Use large-bore peripheral 

catheters if hypovolemic shock is suspected. Administer fluids as is appropriate for the 

type of shock. Obtain an electrocardiogram (ECG) early if a cardiac cause is within the 

differential diagnosis. Patients with suspected shock should be on a cardiac monitor. If 

trauma is present, or if the patient is at risk for pericardial effusions (ie, history of renal 

failure, cancer, or pericarditis), consider bedside emergency department 

ultrasonography to rapidly identify correctable causes of shock such as pericardial 

tamponade or hemoperitoneum. Obtain a complete blood count (CBC), electrolytes, and 

renal function tests; and if trauma is present or hemorrhagic shock suspected, type and 

cross-match blood. Cultures of blood, urine, and possibly sputum should be obtained 

(prior to the administration of antibiotics) if septic shock is a possibility. Foley catheter 

insertion is necessary to monitor urine output and response to fluid therapy in 

hypovolemic shock. 

D. Disability

If trauma is present, the above steps should take place with protection of the cervical 

spine using a rigid collar and long spine board. Test and document the patient's 

Glasgow Coma Scale response. Evaluate distal motor and sensory function. Assess 

pupils for evidence of cerebral herniation. Rapidly check the fingerstick blood glucose 

and administer thiamine and naloxone if the patient has an altered mental status. 

Fink MP: Cytopathic hypoxia. Mitochondrial dysfunction as a mechanism contributing to 

organ dysfunction in sepsis. Crit Care Clin 2001;17(1):219. [PMID: 11219231] (A 

discussion of the metabolic deficits that develop with sepsis and their implications for 

sepsis therapy.) 

DETERMINATION OF THE CAUSE OF SHOCK 

Perform a rapid assessment of the most likely cause of shock in order to provide more 

specific and definitive therapy. Obtain a brief history from the patient, family, friends, 

bystanders, police, or ambulance attendants. Pay careful attention to clues available 

from the physical examination (eg, obvious trauma, melena, fever, or diarrhea). 

APPROACH TO SHOCK WITH A HISTORY OF TRAUMA (See also Chapter 10.) 

Is There Obvious External Blood Loss or Penetrating Injury? 

Turn the patient to examine his or her back (logroll the patient to maintain axial 

immobilization if cervical spine injury is suspected). 

Has There Been Chest Trauma? 

Chest trauma may be due to obvious penetrating injury or to blunt trauma causing 

hemothorax, tension pneumothorax, cardiac tamponade or rupture, or myocardial 

contusion. Carefully examine the patient for distended neck veins, indicating pericardial 

tamponade or tension pneumothorax. Tracheal deviation and unilaterally absent breath 

sounds are commonly noted when a tension pneumothorax is present. When tension 

pneumothorax is clinically suspected, needle decompression (Chapter 6) can be life 

saving and should not be delayed while waiting for chest x-ray confirmation. Bedside 

emergency department sonography enables the emergency physician to quickly assess 

for the presence of hemodynamically significant hemothorax or pericardial effusion. 

Has There Been Abdominal Trauma? 

Intra-abdominal or retroperitoneal bleeding may result from visceral or vascular injuries. 

Note: Intra-abdominal or retroperitoneal bleeding must be assumed to be present in any 

injured patient with severe shock, a normal chest x-ray, and no signs of significant 

external bleeding. Focused Assessment with Sonography for Trauma (FAST) exams 

(Chapter 6) can rapidly identify hemoperitoneum. In hemodynamically unstable patients 

with intra-abdominal free fluid, early exploratory laparotomy is required to reverse 

hemorrhagic shock. If emergency department sonography is not immediately available 

or if the results are equivocal, diagnostic peritoneal lavage should be performed to 

determine the patient's need for immediate laparotomy. In a more stable patient, 

abdominal computed tomography (CT) scan may be useful for diagnosing

intra-abdominal bleeding. 

Has There Been Deceleration Injury? 

Deceleration injury may be associated with lacerations of the aorta, especially in the 

region of the isthmus. A widened mediastinum may be visible on chest x-ray, but 

high-resolution contrast CT, transesophageal echocardiography, or aortic angiography 

is required for definitive diagnosis. 

Have There Been Pelvic or Thigh Injuries? 

Injuries to the pelvis or thigh may be associated with a large volume of concealed blood 

loss. Significant pelvic injuries are suspected when anteroposterior or lateral 

compression of the iliac wings indicates an unstable pelvis. If pelvic instability is 

apparent on the primary survey, repeated testing by other physicians could exacerbate 

ongoing pelvic hemorrhage and should be discouraged. A portable anteroposterior 

radiograph of the pelvis may demonstrate pubic symphysis diastasis and widening of 

the sacroiliac joints. MAST trousers may be used to close the volume and stabilize the 

pelvis in an attempt to limit intrapelvic hemorrhage. Alternatively, a bed sheet can be 

tightly wrapped around the pelvis and tied in a knot to stabilize the pelvis. 

Is There Evidence of Significant Spinal Cord Injury? 

Neurogenic shock may occur after traumatic quadriplegia or paraplegia. However, 

severe shock with the patient in the supine position is usually due to other concomitant 

causes of shock, such as blood loss. Do not confuse neurogenic shock with spinal 

shock. Spinal shock is a transient dysfunction of the spinal cord associated with 

traumatic injury. Neurogenic shock refers to the loss of vasomotor tone leading to 

diffuse vasodilation and hypotension. 

Did a Preexisting Medical Condition Cause Trauma? 

An example of a preexisting condition that results in trauma is an acute myocardial 

infarction that causes a motor vehicle accident. 

APPROACH TO SHOCK WITHOUT HISTORY OF TRAUMA 

Is This Hemorrhagic Shock? 

Blood loss may be difficult to recognize if there is preexisting anemia or if not enough 

time has elapsed for compensatory mechanisms to cause hemodilution. Serial 

hematocrit measurements are needed to rule out hemorrhagic causes of shock. Do not 

be reassured by the initial hematocrit being normal. 

A. Seek Evidence of Gastrointestinal Tract Blood Loss 

(See Chapter 14.) Ask about prior hematemesis, melena, or abdominal pain. Perform a 

test for occult blood on a sample of feces, and insert a nasogastric tube to search for 

blood loss in the gastrointestinal tract.

B. Seek Evidence of Aortic Dissection or Ruptured Abdominal Aortic Aneurysm 

(See Chapter 32.) The sudden onset of severe back or abdominal pain in a patient with 

a history of hypertension should suggest contained aortic dissection. Hematuria, 

neurologic deficit, or diminished peripheral pulses may be present. Abdominal pain with 

a palpable abdominal mass or abdominal tenderness and distention suggests rupture of 

an abdominal aortic aneurysm. Note: Severe hemorrhagic shock in a patient without an 

obvious source of blood loss should be considered to be caused by a ruptured 

abdominal aortic aneurysm, and exploratory laparotomy should be performed 

immediately. Patients with aneurysms that have been repaired with aortoiliac grafts may 

occasionally present with massive gastrointestinal tract bleeding resulting from rupture 

at the suture site into the colon or duodenum. 

C. Seek Evidence of Ectopic Pregnancy 

Consider ruptured ectopic pregnancy in a woman of childbearing age who presents in 

shock, especially if there is a history of pelvic pain, vaginal bleeding, or amenorrhea. An 

emergency bedside ultrasound of the right upper quadrant demonstrating free fluid in 

the hepatorenal (Morrison) space is frequently seen in patients in shock who have 

ruptured ectopic pregnancies. Transvaginal ultrasound yielding no intrauterine 

pregnancy when the serum human chorionic gonadotropin (hCG) level is greater than 

1600, or at greater than 4 weeks' gestation based on dates, should be assumed to 

indicate ectopic pregnancy in the setting of shock. Shock may be caused by ectopic 

pregnancy even when the quantified hCG is very low. Culdocentesis, blind aspiration of 

the rectouterine pouch, has largely been replaced by sonography. However, 

culdocentesis should be performed if pelvic sonography is not immediately available in 

the evaluation of a pregnant patient presenting in shock. 

Is This Nonhemorrhagic Hypovolemic Shock? 

Fluid or fluid and electrolyte loss may be the cause of hypovolemic shock in a patient 

with no evidence of external hemorrhage in whom serial hematocrit measurements 

remain stable (Table 9-2). 

Is There a Cardiac Cause of Shock? 

Cardiac causes of shock include arrhythmias, acute valvular dysfunction, rupture of the 

ventricular septum or free ventricular wall, or "pump failure" (cardiogenic shock). Pump 

failure can be caused by vascular obstruction, tamponade, or muscular dysfunction 

secondary to myocardial depressant factors. Ask about a history of hypertension, chest 

pain, or cardiac disease. Perform a careful physical examination, and pay special 

attention to the presence of distended neck veins, rales, and abnormal cardiac sounds 

(S 3 gallop, murmurs, rubs). An ECG may show arrhythmias or ischemic changes such 

as ST segment abnormalities. 

Is There Evidence of Pericardial Disease? 

Cardiac tamponade may occur in the patient with aortic dissection, pericarditis, uremia, 

or recent myocardial infarction. Occasionally patients with constrictive pericarditis 

present in shock. Assess the patient for pulsus paradoxus, Kussmaul sign, or distended

neck veins without evidence of pump failure (clear lung fields on chest x-ray, no S 3 

gallop). With bedside sonography in the emergency department, the clinician can rapidly 

detect significant pericardial effusions. Ultrasound can also be used to percutaneously 

drain pericardial effusions. If ultrasound or echocardiography is not immediately 

available, blind pericardiocentesis (Chapter 6) may be a life-saving procedure in 

patients with pericardial tamponade. If the patient is stable, obtain an echocardiogram to 

confirm the presence of pericardial fluid and to assist in pericardiocentesis. 

Is There Evidence of Sepsis? 

Fever or hypothermia, rigors, leukocytosis, or petechiae suggest septic shock. Infants, 

the elderly, and immunocompromised or severely leukopenic patients may lack 

symptoms that localize the site of infection. Consider the possibility of toxic shock 

syndrome in young women, especially if there is a history of tampon use or recent 

menses. 

Does the History Suggest Anaphylactic Shock? 

A history of a bee or wasp sting, recent administration of drugs, or ingestion of certain 

foodstuffs should raise a suspicion of anaphylactic shock. Urticaria, laryngeal edema, 

and bronchospasm often (but not invariably) accompany anaphylaxis. Because most 

cases of anaphylaxis are due to parenteral administration of medications and occur 

within minutes of exposure to the inciting agent, the diagnosis usually is readily 

apparent. 

Is This Obstructive Shock? 

Tension pneumothorax, an obstructive cause of shock, should be considered in a 

setting of chest or upper abdominal trauma when diminished breath sounds are present 

unilaterally with tracheal deviation. Other causes of obstructive shock, resulting from 

obstruction to filling of the right or left ventricle, are difficult to diagnose rapidly in the 

emergency department. Obstructive shock may be due to such diverse conditions as 

massive pulmonary embolus, mural thrombus, or atrial myxoma. (Although diseases of 

the pericardium such as tamponade and constriction are also obstructive disorders, 

symptoms and signs often permit early specific diagnosis.) Pulmonary embolus should 

be suspected in the patient who presents in shock with signs of right heart failure 

(distended neck veins, right-sided S 3 gallop), refractory hypoxemia (especially if there is 

evidence of decreased pulmonary compliance as manifested by difficulty in ventilating 

the patient with a bag-valve-mask), and an ECG that shows evidence of right heart 

strain (large R wave in lead V1, right axis deviation, or incomplete right bundle branch 

block or the classic S in lead I, Q in lead III, and T wave inversion in lead III.). 

Are There Other Causes of Shock? 

Unusual and infrequently encountered causes of shock include pheochromocytoma, 

addisonian crisis, and severe hypothyroidism (Chapter 41). Drug or toxins may also 

produce shock through a variety of mechanisms, including vasodilatation (eg, 

phenothiazines) and direct cardiac effects (eg, tricyclic antidepressants).

EMERGENCY TREATMENT OF SPECIFIC CAUSES OF SHOCK 

HYPOVOLEMIC SHOCK 


• Shock in the setting of massive blood, fluid, or electrolyte losses (eg, from burns, 

vomiting and diarrhea, trauma, internal hemorrhage). 


Hypovolemic shock may result from loss of whole blood, plasma, or fluid and 

electrolytes (Table 9-2). In many patients with hypovolemic shock who are seen in the 

emergency department, the cause of shock will be immediately apparent (eg, obvious 

bleeding or history of severe diarrhea). Common causes that may not be readily 

apparent include ruptured abdominal aortic aneurysm, aortic dissection, splenic rupture 

(which may occur after seemingly inconsequential trauma), intestinal obstruction, and 

peritonitis. 


The clinical features of shock are present. In addition, there may be signs suggesting 

hypovolemia as the cause, for example, obvious hemorrhage or clinical features 

associated with volume loss due to burns, peritonitis, bowel obstruction, or ruptured 

abdominal aneurysm. Central venous pressure is low, and both venous and arterial 

pressures improve rapidly with intravascular volume replacement. 

Treatment 

Perform the ABCDs as previously noted. 

A. Gain Intravascular Access 

The number of intravenous cannulas required depends on the severity of shock. For 

adults, catheters inserted should be 16 gauge or larger. During insertion of the 

intravenous line, blood should be obtained for CBC, electrolytes, blood urea nitrogen 

and creatinine, and prothrombin time. If hemorrhage is suspected, blood should be sent 

for blood typing and cross-matching. Arterial blood gas and lactate measurement may 

help in determining the severity of hypoperfusion and acidosis. Two large-bore 

(16-gauge or larger) peripheral catheters are sufficient for initial management. If 

peripheral access cannot be obtained, central access or venous cutdown might be 

considered. 

1. Long saphenous vein—The safest site for a venous cutdown is the long saphenous 

vein at the ankle (Chapter 6). If shock is not severe and the vein is not collapsed, insert 

a 16-gauge percutaneous catheter. 

2. Basilic vein—The basilic vein in the antecubital fossa is also a good site for a

large-gauge percutaneous catheter or venous cutdown. It can be used to achieve 

central venous pressure monitoring (Chapter 6). 

3. Femoral vein—A temporary percutaneous catheter inserted in the femoral vein may 

permit rapid access to the circulation without major complications (Chapter 6). 

4. Central veins—Avoid percutaneous catheterization of the subclavian or jugular veins 

for treatment of hypovolemic shock, because the great veins are usually collapsed, and 

the chances of complications such as hemothorax and pneumothorax are greatly 

increased. (For a patient in hypovolemic shock, the additional physiologic insult of 

hemothorax or tension pneumothorax may be rapidly fatal.) 

5. Intraosseous infusion—In infants and young children, rapid access for fluid 

administration can be gained through intraosseous infusion (Chapter 6). 

B. Administer Intravenous Fluids 

Administer intravenous fluids at once to restore adequate intravascular volume. The 

goal is normal cardiac output and tissue perfusion. 

1. Types of fluids— Table 9-3 lists various solutions used in resuscitation of patients in 

shock. These solutions may be divided into 2 main types: crystalloids and colloids. 

a. Crystalloids—Crystalloid solutions include isotonic (0.9%, or normal) saline and 

balanced salt solutions (eg, lactated Ringer's injection, Plasma-Lyte, Isolyte). Balanced 

salt solutions contain varying amounts of acetate or lactate (or both) that are 

metabolized to bicarbonate when perfusion of the liver is adequate. Crystalloids are 

readily available and relatively inexpensive. 

Hypertonic sodium chloride (7.5%) has been employed experimentally for hypovolemic 

shock due to hemorrhage (some preparations also include 6% dextran). These fluids 

osmotically draw water from extravascular spaces and can quickly expand blood 

volume. However, their safety has not yet been established, and there is growing 

concern over the value of rapidly expanding intravascular volume before hemorrhage is 

controlled surgically. Otherwise, hemorrhage may actually increase, accompanied by 

progressive hemodilution. 

b. Colloids—It has been advocated that colloid (high molecular weight) solutions draw 

water into the pulmonary vascular space and therefore out of the interstitium. This is 

most likely false. There is no proven benefit to using colloids over crystalloid in the 

setting of shock. 

c. Blood—Blood is most commonly available as packed red blood cells or whole blood. 

In patients in mild hemorrhagic shock, especially if blood pressure can be maintained 

with asanguineous fluids, typed and cross-matched packed red blood cells are 

preferred. Because it may take 45 minutes or longer to type and cross-match blood, 

patients with moderate to severe hemorrhagic shock may require type-specific, 

Rh-negative blood or universal donor blood (O-negative blood with low antibody titers to 

erythrocyte antigens) if shock persists after administration of more than 2-3 L of 

crystalloid solutions in adults or 20-40 mL/kg in children. Whole blood should be used as

soon as possible in patients with moderate to severe hemorrhagic shock. Because 

hypothermia is a frequent side effect of transfusion of large amounts of blood stored at 

4°C, blood should be administered through blood warmers. Critically ill patients with 

hematocrit less than 30% benefit from the administration of blood. 

(1) Plasma or albumin solutions—Plasma or albumin solutions are effective volume 

expanders; however, they may be harmful if they enter the pulmonary interstitium as a 

result of capillary leakage. 

(2) Plasma substitutes—Plasma substitutes such as dextrans have been used for initial 

volume replacement in hypovolemic shock, but their use is not widely accepted. 

2. Choice of fluids—The choice of fluid for resuscitation depends on the type of 

hypovolemic shock present (hemorrhagic versus nonhemorrhagic) and on the severity 

of shock. 

a. Mild shock—Normal saline, lactated or acetated Ringer's injection, and plasma or 

other blood products are equally effective in treating mild shock. Crystalloid solutions 

are strongly preferred because of their low cost, lack of adverse effects, and ready 

availability. 

b. Moderate to severe shock—There has been considerable controversy regarding the 

correct fluid to use in patients in moderate to severe shock. Current accepted therapy is 

to use crystalloids as a first-line agent. Blood should be used if bleeding is extensive or 

ongoing. With low hematocrit and controlled bleeding, there is some debate about what 

constitutes an appropriate transfusion threshold. It would be prudent to transfuse if the 

hematocrit is less than 30%. Assume that 3 L of crystalloid are required to achieve the 

same intravascular volume expansion as 1 L of blood. 

E. Evaluate the Effectiveness of Resuscitation 

1. Monitor indices of resuscitation (Table 9-4)—Indicators of successful resuscitation 

include improved blood pressure and urine output, diminished tachycardia, improved 

mental status, falling lactate, and normalizing pH. Additional guidelines include 

improved state of consciousness and peripheral perfusion (as measured by clinical 

criteria, including arterial blood pH). In an intensive care setting, measurements of 

cardiac output are also useful. 

a. Atrial filling pressure—The only estimate of atrial filling pressure available in most 

emergency departments is the central venous (right atrial) pressure. New, noninvasive 

measures of cardiac output, such as thoracic bioimpedance or real-time transnasal 

esophageal echocardiography, may prove useful in emergency department 

resuscitation management. Central venous O 2 saturation is being used by some groups 

as a measurement to approximate cardiac output in order to help guide emergency 

department fluid and pressor therapy without necessitating a pulmonary artery catheter. 

It is generally a good measure of intravascular volume but may be unreliable in patients 

with cardiac or pulmonary disease or in those who require mechanical ventilatory 

support. Such patients require measurement of pulmonary capillary wedge pressure.

Normal central venous pressure is 3-8 cm H 2 O. As a general rule of thumb, maintaining 

central venous pressure at 8-12 cm H 2 O when managing shock is prudent. A growing 

body of literature suggests that supranormal values of cardiac indices may reduce 

mortality in perioperative patients. This also may be true early in septic shock. 

b. Urine output—Urine output is a good index of visceral blood flow (specifically, renal 

blood flow) and should be maintained at more than 0.5 mL/kg/h in adults, 1 mL/kg/h in 

children, and more than 2 mL/kg/h in infants. This measurement is unreliable in patients 

with preexisting serious renal damage or when renal damage has occurred as a result 

of prolonged shock (eg, acute tubular necrosis). 

2. Record progress of resuscitation—Documentation, preferably entered on an 

emergency department critical care flow sheet, is essential both for emergency 

department management and for later management once the patient has been 

transferred to an intensive care unit or operating room. The following information should 

be systematically recorded: 

a. Vital signs—Record blood pressure, pulse, and respiration rate every 5-15 minutes. 

b. Fluids—Note the quantity and type of fluid administered. 

c. Central venous pressure—If central venous access has been obtained, measure 

and record central venous pressure every 30-60 minutes or as dictated by the progress 

of resuscitation. 

d. Urine output—Measure and record urine output every 30-60 minutes (use an 

indwelling catheter). 

e. Other factors—Obtain and record serial hematocrits, arterial blood gas 

determinations, electrolyte measurements, and renal function tests as indicated. 

F. Aggressively Search for the Cause of Persistent Shock 

Persistent shock or recurrence of shock in a patient who initially responded to treatment 

suggests ongoing, often occult hemorrhage. Obtain serial hematocrit measurements, 

give blood, and search for hidden sources of blood loss. Patients with severe, refractory 

shock may require immediate surgery (eg, left thoracotomy to cross-clamp the aorta, 

exploratory laparotomy). Possible sources of blood loss include the following: 

1. Thorax—Each hemithorax may contain up to 2 L of blood; therefore, a quick upright 

or lateral decubitus chest x-ray should always be obtained before surgery is considered. 

2. Abdomen—Hidden blood loss in the abdomen is common. Distention is a late and 

unreliable sign. Intra-abdominal hemorrhage must be assumed to be present in any 

patient in shock who has a normal chest x-ray and no external signs of significant 

bleeding. Bedside sonogram of the abdomen has become the preferred imaging 

modality to detect intra-abdominal free fluid, which can be assumed to be blood in the 

presence of trauma-induced shock. In an unstable patient, free fluid is an indication for 

emergent exploratory laparotomy. Diagnostic peritoneal lavage (Chapter 6) may be

helpful if gross blood is found or if a hematocrit of 2% or more is noted on the lavage 

sample. Absence of these signs does not exclude the possibility of intra-abdominal 

bleeding. A CT scan may demonstrate intraperitoneal fluid and help identify injury to 

specific solid organs. Its use should be restricted to patients who are relatively stable 

and for whom it can be obtained rapidly. 

3. Retroperitoneum—Bleeding in the retroperitoneum cannot be diagnosed with 

routine studies. A CT scan is a helpful diagnostic tool, if the patient's condition is stable 

enough to permit this delay. 

4. Pelvis—The pelvis may conceal a large amount of blood; hemorrhagic shock is a 

common sequela of pelvic fracture. 

5. Thigh—The thigh may contain 3-4 L of blood after a major fracture or crush injury. 

Disposition 

All patients in hypovolemic shock must be hospitalized. 

Felbinger TW, Suchner U, Goetz AE: Treating patients with severe sepsis. N Engl J 

Med 1999;341(1):56. [PMID: 10391763] (A current review of sepsis care.) 

Hebert PC: Transfusion requirements in critical care (TRICC): a multicentre, 

randomized, controlled clinical study. Transfusion Requirements in Critical Care 

Investigators and the Canadian Critical Care Trials Group. Br J Anaesth 1998;81(Suppl 

1):25. [PMID: 10318985] (A prospective randomized trial of transfusion in critically ill 

patients that shows lower mortality rates during hospitalization in a group randomized to 

a restrictive transfusion threshold.) 

Kohli-Seth R, Oropello JM: The future of bedside monitoring. Crit Care Clin 

2000;16(4):557. [PMID: 11070805] (A discussion of technology under development that 

may expand the information available to the bedside physician.) 

Wu WC et al: Blood transfusion in elderly patients with acute myocardial infarction. N 

Engl J Med 2001;345(17):1230. [PMID: 11680442] (A retrospective observational study 

of 79,000 patients with myocardial infarction, demonstrating much higher mortality rates 

in patients with lower hematocrit.) 

CARDIOGENIC SHOCK 


• Shock in the setting of cardiac outflow obstruction (eg, hypertrophic subaortic stenosis) 

or pump failure (eg, massive myocardial infarction, severe myocardial disease, 

arrhythmia). 

General Considerations

Broadly defined, the term cardiogenic shock denotes a shock syndrome resulting from 

some abnormal cardiac function, such as arrhythmias, valvular disease, or pericardial 

disease (eg, cardiac tamponade), as well as shock resulting from severe myocardial 

dysfunction (pump failure). This section considers mainly pump failure. Shock due to 

pericardial disease or cardiac tumors is discussed in the "Obstructive Shock" section, 

below. Further discussion of the diagnosis and treatment of arrhythmias, valvular 

disease, and pericardial disease is found in Chapters 34 and 35. 

Cardiogenic shock due to pump failure is often associated with acute myocardial 

infarction but may also result from end-stage cardiac disease of any cause, including 

valvular heart disease or cardiomyopathy. Cardiogenic shock is a complication of acute 

myocardial infarction in about 10% of patients and carries a grave prognosis (mortality 

rate > 50%) even with appropriate therapy. Potentially correctable myocardial—and 

nonmyocardial—factors may contribute to, or be the sole cause of, shock in a patient 

with myocardial infarction (Table 9-5). These factors must be sought and treated 

vigorously. 



@text_first;The hallmark of cardiogenic shock is hypotension (systolic blood pressure 

usually < 90 mm Hg, although it may be higher accompanied by clinical signs of 

increased peripheral vascular resistance (weak, thready pulse; cool, clammy skin) and 

inadequate organ perfusion (altered mental status, decreased urine output). The patient 

also shows signs of acute myocardial infarction or preexisting severe cardiac disease. 

1. Early signs—Tachycardia and decreased pulse pressure (due to elevated systemic 

vascular resistance) are early signs of decreased cardiac output and should alert the 

physician to potential problems even if systolic blood pressure is normal. Diaphoresis or 

other signs of an increase in circulating catecholamines may be present. Restlessness, 

agitation, or confusion is an early manifestation of decreased cerebral blood flow. 

2. Central venous pressure—Central venous pressure (assessed by examination of 

the patient's neck veins) varies in cardiogenic shock depending on intravascular volume 

and the degree of associated right ventricular failure. Central venous pressure is not a 

reliable means of diagnosing severe left ventricular failure. 

B. Imaging Studies 

Transthoracic echocardiography (TTE) can be a useful diagnostic modality, allowing 

visualization of hypodynamic myocardium. Determination of dilated right ventricle with 

TTE may point to a diagnosis of pulmonary embolus. TTE can also elucidate valve 

dysfunction. 

Treatment 

Initial treatment of cardiogenic shock should be started in the emergency department, 

definitive therapy often requires hemodynamic monitoring using pulmonary and other 

systemic pressure catheters.

An intra-aortic balloon pump may provide stabilization for patients in profound 

cardiogenic shock. If cardiogenic shock is from an acute coronary occlusion, reperfusion 

by percutaneous transluminal coronary angioplasty may improve survival, although 

overall mortality still remains high. Reperfusion by fibrinolytic therapy has not been 

shown to be beneficial in cardiogenic shock. 

A. Airway 

Using arterial blood gas measurements as guidelines, establish adequate ventilation 

and oxygenation. Give supplemental oxygen, 2-5 L/min, by nasal cannula, pending the 

results of blood gas determinations; adjust oxygen supplementation to maintain arterial 

PO 2 at 65 mm Hg or higher. Pulse oximetry may also be used to maintain oxygen 

saturation (= 90%). If hypercapnia and acidosis are present, tracheal intubation may be 

necessary (Chapter 6). 

B. Position 

Place the patient supine or supine with the legs elevated if systolic blood pressure is 

less than 70-80 mm Hg. Conversely, a patient with pulmonary edema and a normal or 

low normal blood pressure should be seated upright. 

C. Intravenous Access 

If hypotension is profound (systolic blood pressure < 70 mm Hg) and there is no 

evidence of pulmonary edema, gain intravenous access and infuse a crystalloid solution 

(normal saline or lactated Ringer's injection). 

D. Blood Work 

Draw a sample of venous blood for CBC, electrolyte measurements, renal function test, 

cardiac enzymes (assays may include CK, CK-MB isoenzymes, troponin, and 

myoglobin). Coagulation studies (prothrombin and partial thromboplastin times and 

platelet count) are essential if invasive monitoring or placement of a central venous 

catheter is anticipated. 

E. Cardiac Monitoring 

Obtain a 12-lead ECG, and begin continuous cardiac monitoring. 

F. Urine Output 

Monitor urine output hourly. Bladder catheterization may be necessary. 

G. Nonmyocardial Factors 

Search for and treat nonmyocardial factors that may be causing or contributing to shock. 

1. Acidosis—(See Chapter 42.) Respiratory acidosis (low arterial blood pH, high PCO 2 ) 

in cardiogenic shock is due to hypoperfusion, with production of lactic acid. In addition to 

measures to improve cardiac output, sodium bicarbonate may be given if the blood pH 

is less than 7.1 and the acidosis is metabolic. Give 0.5-1.0 mEq/kg over 5-10 minutes, 

and repeat as needed, using arterial blood gas determinations as a guideline. Caution: 

Do not administer sodium bicarbonate through the same intravenous line as 

catecholamines.

2. Arrhythmias—(See Chapter 35.) Cardioversion is the treatment of choice for 

tachyarrhythmias causing hypotension. Initial treatment for bradyarrhythmias causing 

hypotension is atropine, 0.5 mg intravenously every 5 minutes up to a total dose of 2 mg 

for adults; in children, give 0.02 mg/kg, with a minimum single dose of 0.1 mg and a 

maximum total dose of 1 mg. A transcutaneous pacemaker should be put in place only 

until transvenous pacing becomes available. If the patient has responded to atropine, 

then the transcutaneous pacer should be left on the patient, in the "off" mode, so that it 

is readily available should the bradycardia reoccur or worsen. 

3. Hypovolemia—In the patient with acute myocardial infarction, recent use of diuretics, 

excessive sweating, vomiting, or diarrhea may cause hypovolemia. In the patient 

without supine hypotension, measurement of orthostatic vital signs may provide a 

valuable clue to possible depletion of intravascular volume. Cautious administration of 

intravenous fluid should be attempted in patients who have no evidence of pulmonary 

edema. Give intravenous fluids in 50- to 100-mL increments over 5-10 minutes, and 

watch closely for signs of improvement (decreased heart rate, increased blood 

pressure) or deterioration (increased dyspnea or decreased arterial PO 2 ). 

4. Tamponade—Rupture of the free ventricular wall or pericarditis with effusion may 

result in cardiac tamponade and may be confused with cardiogenic shock of myocardial 

origin. Perform a careful physical examination, and look for evidence of cardiac 

tamponade (elevated neck veins with clear lung fields on chest x-ray, pulsus paradoxus, 

pericardial friction rub, low voltage on the ECG). As mentioned previously, bedside 

sonography in the emergency department can be used, if available, to rapidly identify 

and drain pericardial effusions causing tamponade. If ultrasound is not available, 

emergent blind pericardiocentesis may be life saving. 

5. Acute valvular disease or ventricular septal rupture—Listen carefully for 

characteristic murmurs. Definitive diagnosis may require cardiac catheterization or 

echocardiography. Treatment with intra-aortic balloon pumping or drugs that reduce 

afterload may gain time to prepare the patient for life-saving surgery (Chapter 34). 

H. Pharmacologic Therapy 

If the patient fails to respond to intravenous fluids, give dopamine, 200 mg in 250 mL of 

5% dextrose in water (800 ug/mL) at the lowest rate that maintains adequate blood 

pressure (usually 4-15 ug/kg/min). 

Dobutamine may be the mainstay for therapy of cardiogenic shock. This is especially 

true if left-sided congestive heart failure with low blood pressure is present. Dobutamine 

can increase cardiac contraction (positive inotropy) without raising afterload. This results 

in improved cardiac output. Because dobutamine has minimal a-receptor activity, it has 

little effect on the systemic blood pressure, making dopamine, not dobutamine, the 

inotropic agent of choice in profound hypotension. Norepinephrine can be considered as 

a second-line agent after dopamine. It will raise the blood pressure but will also cause 

increased infarct size and must be delivered via a central line. 

Stabilization in the emergency department may require maintaining blood pressure by 

means of such vasoconstriction while the patient is awaiting transfer to the intensive 

care unit.

Digitalis glycosides have no role in the initial treatment of cardiogenic shock. 

I. Intensive Care Unit 

Assess the need for urgent transfer of the patient to an intensive care unit. A patient 

with frank pulmonary edema and hypotension is difficult to manage in the emergency 

department, and every effort should be made to transfer the patient as rapidly as 

possible to an intensive care unit for hemodynamic monitoring and drug therapy. 

J. Treatment for Pulmonary Edema 

If the patient's blood pressure is only slightly decreased and the major clinical findings 

suggest pulmonary edema (elevated neck veins, rales, and decreased oxygenation) 

rather than decreased tissue perfusion (hypotension, clammy skin, and the like), small 

doses of intravenous furosemide (adults, 20-40 mg; children, 0.5-1.0 mg/kg) or a 

preload reducing agent (nitroglycerin ointment, 1.5-2.0 cm under an occlusive dressing) 

may be tried. Pay close attention to the effect of these drugs on blood pressure and 

clinical signs of tissue perfusion. 

Disposition 

All patients in cardiogenic shock should be hospitalized in an intensive care unit. 

OBSTRUCTIVE SHOCK 

Obstructive shock results from impaired filling of the ventricles (decreased preload) that 

is severe enough to cause a significant fall in cardiac output (Table 9-2). With the 

exception of acute cardiac tamponade and tension pneumothorax, obstructive disorders 

are difficult to diagnose and even more difficult to treat in the emergency department. 

Knowledge of the patient's medical history can be crucial in management. Clues to the 

specific cause of shock are discussed below. 

1. Cardiac Tamponade (See also Chapter 34.) 

A history of cancer, uremia, or infectious illness should suggest the possibility of 

pericardial effusion; distended neck veins without evidence of pump failure (clear lung 

fields on chest x-ray, absent S 3 gallop) suggest cardiac tamponade. Pulsus paradoxus, 

a fall in systolic blood pressure of 12 mm Hg or more during inspiration, occurs in almost 

every case of cardiac tamponade. A pericardial friction rub may or may not be present. 

Distant heart sounds, an enlarged cardiac silhouette on chest x-ray, and low voltage on 

the ECG are additional (but insensitive) clues to the presence of pericardial effusion. 

Sudden onset of shock in a patient with recent myocardial infarction may be due to 

rupture of the free ventricular wall that causes cardiac tamponade. Bedside emergency 

ultrasound plays an important role in rapid identification and treatment of pericardial 

effusions causing cardiac tamponade. If ultrasound is unavailable, blind 

pericardiocentesis is required for suspected tamponade and may be a life-saving 

intervention. If the patient's condition permits, obtain an echocardiogram to confirm the 

diagnosis and to guide pericardiocentesis. In the desperately ill patient, blind 

pericardiocentesis (Chapter 6) may be life-saving. See Chapters 10 and 34 for a more 

complete discussion of the diagnosis and treatment of cardiac tamponade.

2. Massive Pulmonary Embolism (See also Chapter 33.) 

Ask about a history of thrombophlebitis, pulmonary emboli, or hypercoagulable state 

(use of oral contraceptives, pregnancy status, family history of thromboembolic disease, 

cancer). Search for evidence of lower extremity venous thrombosis or for some other 

predisposing factor (lower extremity injury, recent prolonged immobility). Pleuritic chest 

pain, dyspnea, apprehension, or cough occurs frequently in patients with massive 

pulmonary embolism; hemoptysis or syncope occurs less commonly. Accentuation of 

the pulmonary closure sound (P 2 ) may occur. Massive pulmonary embolism with acute 

pulmonary hypertension may result in signs of right ventricular overload, for example, 

jugular venous distention and a right-sided S 3 gallop. The ECG may show evidence of 

acute right heart strain, for example, R > S in lead V1, S1Q3T3 pattern (large S wave in 

lead I, Q wave in lead III, inverted T wave in lead III). Patients with massive pulmonary 

embolism typically are hypoxemic. Pulse oximetry does not improve much with the 

administration of O 2 (a pulmonary embolism acts physiologically like an atrioventricular 

shunt). Attempt to maintain blood pressure with intravenous fluids (an initial bolus of 

500-1000 mL of normal saline should be infused rapidly); if the patient fails to respond, 

give vasopressors as described above. Administration of thrombolytic agents such as 

streptokinase or tissue plasminogen activator is indicated for massive pulmonary 

embolization. Current indications include shock, recent cardiac arrest, and severe 

respiratory failure; however, the prognosis in patients with massive pulmonary embolism 

is poor. See Chapter 33 for further discussion. Emergency surgery (eg, Trendelenburg 

procedure) is rarely successful. 

Atrial myxoma, mitral thrombus, coarctation of the aorta, obstructive valvular disease, 

and pulmonary hypertension are rare causes of shock in patients presenting to the 

emergency department. Emergent decompression of tension pneumothorax is 

discussed in Chapters 12 and 24. Supportive treatment usually includes fluids, 

vasopressors, and oxygenation. Echocardiography and right heart catheterization may 

help to establish the diagnosis in obstructive shock. 

DISTRIBUTIVE SHOCK 

Distributive shock occurs when distribution of intravascular volume is markedly 

abnormal as a result of decreased vascular resistance (as occurs in fainting, when 

blood pools in the venous rather than the arterial portion of the circulation). Cardiac 

output may be increased, normal, or low in patients with this type of shock. The causes 

of distributive shock are diverse and include septic shock, anaphylactic shock, and 

neurogenic shock, which are discussed below; acute adrenal insufficiency is discussed 

in Chapter 41. Some drugs and toxins may produce vasodilation and may also result in 

distributive shock. See Chapter 45 for a discussion of drug overdose and poisoning. 

1. Septic Shock (See also Chapter 46.) 

Essentials of Diagnosis

Systemic Inflammatory Response Syndrome (SIRS) 

• Respiratory rate greater than 20 or PaCO 2 

• Temperature > 38 °C or < 36 °C. 

• White blood cell count > 12,000 or < 4000 or > 10% band forms. 

• Heart rate greater than 90 beats/min. 

Sepsis 

• Presence of SIRS and infection confirmed. 

Severe Sepsis 

• Sepsis associated with organ dysfunction, hypoperfusion abnormality, or 

sepsis-induced hypotension. 

Septic Shock 

• Sepsis-induced hypotension despite adequate fluid resuscitation. 

• Persistence of hypoperfusion abnormalities or organ dysfunction. 

• Includes patients needing pressor agents to maintain blood pressure. 


Septic shock is the number one cause of death in U.S. intensive care units. The 

incidence of septic shock continues to increase. Septic shock is usually caused by 

gram-negative bacteria that invade the bloodstream (endotoxic shock), although other 

bacteria and some fungi may produce a similar syndrome. Septic shock may occur 

without frank bacteremia if there is extensive local infection (eg, intra-abdominal 

abscess). Shock also occurs in toxic shock syndrome as a result of absorption of a 

staphylococcal toxin. 

Factors predisposing to development of septic shock include trauma, diabetes, 

leukemia, severe granulocytopenia, disease of the genitourinary tract, radiation 

treatment, and treatment with corticosteroids or immunosuppressive agents. Immediate 

precipitating causes may include surgical or other manipulation of the urinary, biliary, or 

gynecologic tracts. 

Hypotension results from multiple factors. There is a loss of vascular integrity, leading to 

third spacing of fluids. There is a loss of contractile ability of the vasculature, leading to 

increased size of the vascular compartment. Energy metabolism becomes impaired on 

the cellular level, and cardiac function is depressed by chemical mediators. 


Clinical features of shock and infection are present. 

A. Systemic Signs

Rigors, fever (hypothermia is noted in 5-10% of patients), petechiae, leukocytosis, or 

leukopenia with a shift to the left may be noted. 

B. Localized Signs 

Abdominal tenderness, perirectal abscess, and extensive pneumonia may be present. 

Localizing symptoms and signs may be absent, however, especially if the patient is 

immunocompromised, very young, or very old. Typical sites of occult infection include 

the urinary tract, biliary system, pelvis, retroperitoneum, and perirectal area. 

C. Other Signs 

Hyperventilation with hypocapnia is common. The presence of infection should be 

confirmed by microscopic examination, culture, or other definitive test. Samples of body 

fluids and tissues that may harbor infection should be submitted for culture, including 2 

or 3 blood cultures. 

In toxic shock syndrome, toxins from localized staphylococcal colonization or infection 

cause severe hypotension or shock associated with a diffuse red rash (which later 

desquamates) and other symptoms and signs (nausea and vomiting, diarrhea, 

thrombocytopenia). The incidence of toxic shock syndrome increased in the late 1980s 

due to the marketing of highly absorbent, occlusive tampons that facilitated an 

anaerobic vaginal environment. With the removal of these tampons from the market, the 

incidence of this disease has fallen. 

Treatment 

A. Medical Measures 

1. Pharmacologic therapy—Over a decade of pharmaceutical investigation and clinical 

trials of drugs designed to block various parts of the pro-inflammatory cascade of sepsis 

has failed to yield a drug with proven clinical benefit for septic shock. Drugs that have 

gone through clinical trials include antiendotoxin antibodies, anticytotoxin antibodies, 

interleukin therapy, and antibodies to tumor necrosis factor. One study demonstrated 

that early, aggressive therapy in the emergency department may confer some survival 

advantage. 

2. Volume replacement—The amount of fluid administered follows the same guidelines 

governing fluid replacement in severe hypovolemic shock (see above). In general, for 

adults, 1-2 L given over 30-60 minutes (children, 10-20 mL/kg) will improve blood 

pressure and urine output; further administration of fluid depends on clinical response 

(ie, urine output, blood pressure, and pulse). 

3. Inotropic agents—Give dopamine (with both inotropic and vasopressor properties), 

3-15 ug/kg/min, if the patient fails to respond to measures that raise central venous or 

pulmonary capillary wedge pressure to normal levels. Norepinephrine may also be used 

for this purpose. Follow the dosage guidelines given in the table on the inside front 

cover. Vasopressin may also be useful in the setting of septic shock. 

4. Antibiotic therapy—Antibiotic treatment should be specific for the causative 

organism, but the etiologic agent may not be known at the onset of shock. Prompt 

empiric treatment with antibiotics should be started. Antibiotic recommendations change

frequently and vary depending on host and local resistance patterns. Therapy decisions 

should be based on the likely source of the infection (see Table 40-1). Because the 

mortality rate of septic shock is 40-70%, empiric therapy should be broad and 

aggressive, and later tailored to the culture results. Evidence suggests that many 

patients ill enough to be admitted to the intensive care unit receive inadequate antibiotic 

therapy and that this inappropriate therapy may contribute to mortality. 

B. Surgical Measures 

Antibiotics and fluid replacement are much less effective if an abscess or other localized 

source of infection is not drained. It is therefore critical to identify as soon as possible 

any source of sepsis (eg, intra-abdominal abscess, biliary obstruction with cholangitis) 

or any other disorder requiring surgery. 

C. Special Measures 

1. Corticosteroids—Administration of pharmacologic doses of glucocorticoids has no 

beneficial effect in patients with septic shock and may even be harmful. Therefore, 

high-dose corticosteroids should not be used as adjunctive therapy in septic shock. It is 

still a matter of debate whether patients will benefit from physiologic doses of steroids. 

2. Heparin—Disseminated intravascular coagulation (Chapter 39) may occur in septic 

shock. If treatment of septic shock is successful, consumption of coagulation factors 

usually ceases and rapid regeneration of these factors occurs. If coagulation studies 

confirm the presence of persistent disseminated intravascular coagulation (prolonged 

prothrombin and partial thromboplastin times, decreased number of platelets, depressed 

fibrinogen levels, and the presence of fibrin degradation products) and if there is 

significant bleeding, give heparin, 100 units/kg intravenously to start, followed by 10-40 

units/kg/h by continuous intravenous administration (infusion pump preferred). 

Response to heparin is indicated by slowing of bleeding and a rise within 12 hours of 

the levels of fibrinogen and factors V and VII. Platelet counts may rise at a slower rate. 

Discontinue heparin therapy when the cause of disseminated intravascular coagulation 

has been corrected and coagulation factors have been restored to hemostatic levels. 

Disposition 

All patients should be hospitalized, preferably in an intensive care unit. 

Alia I et al: A randomized and controlled trial of the effect of treatment aimed at 

maximizing oxygen delivery in patients with severe sepsis or septic shock. Chest 

1999;115(2):453. [PMID: 10027447] (A prospective, randomized controlled trial of 

maximizing cardiac performance in septic shock that did not demonstrate any benefit to 

patients. Interventions in the intensive care unit may be too much, too late, when it 

comes to septic shock.) 

Fitch S, Gossage J: Optimal management of septic shock. Postgrad Med 

2002;111(3):53. [PMID: 11912997] (A review summarizing the diagnosis and treatment 

of septic shock.) 

Gossage J: Early intervention in massive pulmonary embolism. Postgrad Med 

2002;111(3):27. [PMID: 11912996] (A guide to the evaluation and triage in the first hour

of patients with suspected massive pulmonary embolism.) 

Holmes CL et al: Physiology of vasopressin relevant to management of septic shock. 

Chest 2001;120(3):989. [PMID: 11555538] (Discussion of the pathophysiology and 

therapeutic role of vasopressin in septic shock.) 

Kollef MH et al: Inadequate antimicrobial treatment of infections: a risk factor for hospital 

mortality among critically ill patients. Chest 1999;115(2):462. [PMID: 10027448] (A 

prospective surveillance study in which 9% of patients in the intensive care unit were 

administered inappropriate antibiotics. The mortality rate among these patients was 

more than double those receiving appropriate antibiotics.) 

Rivers E et al: Early goal-directed therapy in the treatment of severe sepsis and septic 

shock. N Engl J Med 2001;345(19):1368. [PMID: 11794169] (A prospective randomized 

trial of algorithm-based intensive care aimed at maximizing cardiac parameters in the 

emergency department in the treatment of septic shock that shows significant 

reductions in mortality and morbidity. There may be a narrow window of opportunity to 

treat sepsis before irreversible deficits are established.) 

2. Anaphylactic Shock 


• Shock in the presence of massive histamine release. 

• Uticaria, soft tissue edema, wheezing secondary to bronchospasm, stridor due to 

laryngeal edema, hypotension due to vasodilatation. 

• Cutaneous and extremity perfusion is maintained. 


Anaphylactic shock is a catastrophic and frequently fatal type of allergic reaction that 

occurs within minutes after parenteral (rarely oral) administration of drugs or nonhuman 

proteins, including foods, sera, or venoms. In cases obviously caused by injections of 

drugs or sera, there is seldom any reason for delayed treatment. 


Symptoms and signs include marked apprehension, generalized urticaria or edema, 

back pain, a choking sensation, cough, bronchospasm, or laryngeal edema. In severe 

cases, hypotension, loss of consciousness, dilatation of the pupils, incontinence, and 

convulsions may be present; sudden death may occur. 

Three modes of presentation of anaphylaxis (based on the most conspicuous 

presenting features) are recognized; however, any combination of these may occur: (1) 

urticaria or angioedema that may be associated with upper airway obstruction and 

laryngeal edema, (2) bronchospasm, or (3) vascular collapse (ie, severe hypotension).

Treatment 

Begin treatment as soon as anaphylaxis is suspected. Do not wait until it is fully 

developed. 

A. Position 

Place the conscious patient in a comfortable position and ensure unimpeded ventilation. 

The unconscious patient should be placed supine, in a level or slightly head-down 

position (do this as quickly as possible). 

B. Airway 

Keep the airway open (Chapter 8), and give supplemental oxygen by mask or nasal 

prongs at a rate of 5-10 L/min. If the patient is not breathing, assist ventilation with a 

bag-mask until endotracheal intubation can be performed (Chapters 6 and 8). If 

equipment for insertion of an endotracheal tube is not available or if intubation is 

unsuccessful because of airway obstruction by laryngeal edema, cricothyrotomy 

(Chapter 6) may be necessary. 

C. Intravenous Access 

Insert an intravenous catheter and begin infusion of a balanced salt solution or normal 

saline (adults, 0.5-1 L over 30 minutes; children, 5-15 mL/kg), with further administration 

governed by blood pressure and urine output. 

D. Pharmacologic Therapy 

Epinephrine administered intravenously or via an endotracheal tube is central to the 

initial therapy for the very ill patient with anaphylaxis. 

1. Aqueous epinephrine—For anaphylaxis with mild to moderate symptoms, give 

epinephrine (adults, 0.3- 0.5 mg [0.3-0.5 mL of 1:1000 solution] intramuscularly; 

children, 0.01 mL/kg/dose up to a maximum of 0.4 mL/dose). For severe anaphylaxis, 

epinephrine should be administered intravenously or via an endotracheal tube (1.0 mL 

of 1:10,000 solution). Repeat every 5-10 minutes if symptoms continue or recur. A 

continuous infusion may be necessary in some patients. Add 1 mg of a 1:1000 solution 

of epinephrine to 250 mL of 5% dextrose in water (10 ug/mL); for adults, begin the 

infusion at a rate of 1 ug/min (children, 0.1 ug/kg/min) and increase up to 10 ug/min as 

needed. Caution should be used in patients with cardiac or hypertensive histories. 

2. Diphenhydramine—Give diphenhydramine (adults, 50 mg; children, 2 mg/kg) 

intravenously or intramuscularly, early in treatment. 

3. Histamine blockers—Administer ranitidine, 50 mg, or famotidine, 20 mg, 

intravenously to additionally block receptors and ameliorate the histamine reaction. 

4. Glucocorticoids—A soluble glucocorticoid preparation should be given as an 

adjunct to epinephrine. Give hydrocortisone sodium succinate, 100-250 mg 

intravenously; or methylprednisolone sodium succinate, 50-100 mg intravenously. 

Benefit from glucocorticoids will not be seen for several hours. 

5. ß-Agonist aerosol—If bronchospasm is present, give albuterol or another ß-agonist

inhalant solutions, 0.5 mL in 2.5 mL normal saline, by nebulizer every 30-60 minutes. 

Prevention 

Inquire carefully about any history of drug allergy before giving drugs. In drunk, 

unconscious, or obtunded patients, search for a card, bracelet, or necklace specifying 

drug allergies or medical conditions (eg, diabetes) requiring special attention. Be 

cautious when administering parenteral medications to patients with a history of drug 

allergy. If there is a history of previous reaction to the agent to be injected, use an 

alternative drug whenever possible. Given intravenous injections slowly, and observe 

individuals who have received parenteral medication for at least 30 minutes after 

injection. Patients with a history of anaphylactic reactions to insect venoms or other 

environmental agents that cannot be easily avoided should be prescribed a kit with 

epinephrine for self-administration and should be advised to carry it at times of high risk 

of exposure. 

Disposition 

Recurrent episodes of anaphylaxis may occur 12-24 hours after the initial episode; 

therefore, patients who have experienced life-threatening anaphylaxis should be 

hospitalized for observation and treatment. Patients who have shown only mild 

manifestations of anaphylaxis (eg, urticaria) that have resolved with treatment may be 

discharged from the emergency department after treatment (Chapter 46) and 6 hours of 

symptom-free observation. Follow-up is based on the principles outlined in Chapter 46. 

3. Neurogenic Shock 


• Hypotension in the presence of spinal cord injury. 

• Cutaneous and extremity perfusion is maintained. 


Neurogenic shock is due to failure of vasomotor regulation that results in pooling of 

blood in dilated capacitance vessels and a subsequent fall in blood pressure. True 

neurogenic shock should be distinguished from vasovagal syncope (Chapter 17). 

Although the mechanism of hypotension is similar in both conditions—sudden failure of 

vasomotor regulation—the condition is not prolonged enough in vasovagal syncope to 

produce diffuse tissue ischemia and clinical features of shock. 

Neurogenic shock is rare. It is most commonly due to traumatic quadriplegia or 

paraplegia (spinal shock), although a similar syndrome can be induced by high spinal 

anesthesia and is occasionally seen in severe Guillain-Barre syndrome and other 

neuropathies. In patients with traumatic spine injuries, it is important to remember that 

hypovolemic shock (due to associated injuries) is still the most common cause of shock 

and must be presumed to be present until proved otherwise.


The symptoms and signs of neurogenic shock are similar to those of hypovolemic 

shock. Signs of neurologic disease often associated with neurogenic shock are also 

present (eg, traumatic quadriplegia or paraplegia). 

Treatment 

Place the patient supine and give oxygen. If blood pressure and peripheral perfusion are 

not rapidly restored, begin other measures. 

The treatment of choice is volume replacement with crystalloid solution to "fill up" the 

dilated capacitance vessels. For adults give 1 L (children, 10-20 mL/kg) of crystalloid 

solution intravenously over 20-40 minutes (depending on the severity of shock). If initial 

fluid therapy is insufficient to bring the mean arterial pressure to greater than 80, an 

intravenous vasopressor agent with a-agonist activity, such as dopamine in high doses 

(> 10-20 ug/kg/min) or norepinephrine (4 mg in 500 mL normal saline started at 1-1.5 

cc/min) should be started. 

Disposition 

All patients should be hospitalized, preferably in an intensive care unit. 





IMMEDIATE MANAGEMENT OF SHOCK (See Figure 9-1.)

Table 9-1. Clinical classification of shock. 1 

Pathophysiology Mild (40% of blood volume 

lost) 

Agitation, confusion, or 

obtundation. Supine hypotension 

and tachycardia are invariably 

present. Rapid, deep respiration.

Table 9-2. Classification of shock by mechanism and common causes. 





TABLES 

Table 9-2. Classification of shock by mechanism and common causes.

Table 9-3. Fluids used for resuscitation of the patient 

in shock. 

Acetated Ringer's injection 

Normosol, Plasma-Lyte, etc 





TABLES 

Table 9-3. Fluids used for resuscitation of the patient in shock.

Table 9-4. Indices of successful resuscitation. 





TABLES 

Table 9-4. Indices of successful resuscitation.

Table 9-5. Potential correctable causes of 

cardiogenic shock. 





TABLES 

Table 9-5. Potential correctable causes of cardiogenic shock.

Figure 9-1. Management of a clinical state potentially associated with shock. BUN = 

blood urea nitrogen; FAST = focused assessment with sonography for trauma; LR = 

lactated Ringer's; NS = normal saline; PT = prothrombin time; PTT = partial 

thromboplastin time. 





FIGURES

10. The Multiply Injured Patient - Julia Martin, MD, & Michael McClurg, 

MD 


(See Figure 10-1.) 

The primary goal in providing care to the trauma patient is effective resuscitation while 

minimizing the time from injury to definitive care. 

PREPARATION 

Trauma care begins at the scene of the accident. It is important for hospitals to have 

good working relationships with local fire departments and emergency medical services 

(EMS) to ensure that proper care is provided early. Preparation efforts should be 

coordinated between the emergency departments and the local EMS systems, including 

prehospital protocols related to the treatment and transport of trauma patients. 

Transport protocols should incorporate decision-making guidelines including information 

regarding transporting patients to the most appropriate facility and the proper use of air 

medical transport. Prehospital providers should be trained to detect specific injuries and 

know the mechanism of forces which could predict the possibility of severe injury (Table 

10-1). Prehospital personnel should provide early notification to the emergency 

department for all major trauma patients to allow emergency department preparedness. 

Injury-scoring systems such as the Glasgow Coma Scale (GCS), Trauma Score, and 

Revised Trauma Score may be used to help quantify the degree of injury (Figure 10-2). 

Maintain a high index of suspicion with pediatric, geriatric, and obstetric patients. Their 

physiologic responses to major trauma differs from that of other patients, and their 

injuries are often missed or delayed in diagnosis. Early transfer to definitive care 

improves outcomes in these patient groups. 

Emergency department response should include a stepwise notification system to alert 

local surgeons or trauma teams and ancillary services such as x-ray, computed 

tomography (CT) scan, laboratory, blood bank, and operating room personnel. Initial 

stabilization and resuscitation is done most effectively if a well-organized team approach 

is used. The key to an organized system is the designation of a person in charge to 

oversee the total care of the patient. The team leader should assign specific tasks to 

emergency department team members. It is important for everyone to understand their 

roles, know where equipment is located, adhere to universal precautions, and keep 

noise and extraneous conversation to a minimum. Constant reassessment of the patient 

and maintenance of a high index of suspicion for possible injuries are important in the 

evaluation and resuscitation of trauma patients. 

INITIAL ASSESSMENT 

The initial assessment consists of a rapid primary survey, initiation of resuscitative 

measures, followed by a secondary survey. The primary survey includes evaluation of

the airway, breathing, and circulation and a brief neurologic exam. Problems identified in 

the primary assessment should be corrected immediately. Several tasks should occur 

simultaneously such as assessing the patient; initiating resuscitation; placing the patient 

on the cardiac monitor, pulse oximetry, and supplemental oxygen; and initiating 

intravenous lines. Rapid stabilization of airway, breathing, circulation, and neurologic 

status is paramount for patient survival. 

1. Primary Survey 

Assessment of ABCs 

A. Airway 

(See also Chapter 8.) Airway management and maintenance of adequate oxygenation 

are extremely important in the multiply injured patient. Shock leads to an oxygen deficit, 

which increases the body's demands and necessitates the need for supplementary 

oxygen. Cervical spine immobilization is considered part of airway management in 

trauma patients. To open the airway, a modified jaw thrust should be used with cervical 

spine control. An oropharyngeal or nasopharyngeal tube is useful to help maintain an 

airway. The nasopharyngeal tube may be used in semiconscious patients with an intact 

gag reflex. The oropharyngeal airway should be used only in unconscious patients 

without a gag reflex; otherwise, it may induce vomiting. 

Obtain a definitive airway in any patient who is not breathing, has inadequate ventilation 

or oxygenation, has an unprotected airway without a gag reflex, or has a decreased 

level of consciousness with a GCS score less than 8. Emergency department providers 

should be knowledgeable about and skilled with a variety of surgical and nonsurgical 

methods of securing an airway. Patients with inadequate ventilation and oxygenation 

require bag-mask ventilation until intubation is accomplished. Tracheal intubation may 

be accomplished by 2 methods: nasotracheal or orotracheal. Both methods require 

good cervical spine immobilization including manual stabilization of the neck. With 

adequate training and experience, rapid sequence intubation (RSI) offers many 

advantages in the multiply injured trauma patient. RSI involves the use of paralytics to 

rapidly achieve muscle relaxation and sedatives to render the patient unconscious and 

unaware of laryngoscopy and intubation. Use of paralytics helps protect against a rise in 

intracranial pressure associated with laryngoscopy, and with good manual cervical spine 

stabilization there is less risk of additional cervical spine injury. The use of paralytics 

and sedation requires a good working knowledge of the medications' indications, their 

side effects, and their contraindications, in order to minimize complications associated 

with the procedure. Being well trained in backup airway maneuvers such as the 

laryngeal mask airway, lighted stylet, fiberoptic intubation, and surgical airway options is 

imperative prior to initiating RSI in a patient. RSI is relatively contraindicated in patients 

who cannot be ventilated with a bag-valve-mask if intubation proves difficult or 

impossible. If orotracheal or nasotracheal intubation is unsuccessful, a surgical airway 

such as a cricothyrotomy should be performed. 

B. Breathing 

Assess adequacy of ventilation by inspecting the chest wall for adequate expansion; 

looking for paradoxical rise of the chest, flail segments, and sucking wounds; and noting 

labored respirations or auxiliary muscle use. Auscultate the lungs for the presence of

symmetrical breath sounds. 

If breath sounds are unilaterally diminished and the patient is intubated, consider 

withdrawing the endotracheal tube 2-3 cm in case the tip is residing in a main-stem 

bronchus, and then recheck the breath sounds. Persistently diminished breath sounds 

imply pneumothorax. If the patient is hypotensive, in shock, or laboring to breathe, 

perform a tube thoracostomy immediately. Should a delay exist before this can occur, 

decompress the chest with a 14-gauge angiocatheter or other catheter-clad needle 

inserted in the 2nd intercostal space at the midclavicular line. A stable patient with 

diminished breath sounds may await a chest x-ray for confirmation prior to 

decompression with a needle or thoracostomy tube. 

Treat a sucking chest wound by sealing the wound with an occlusive dressing (eg, 

petrolatum-impregnated dressing) at 3 points and then performing a tube thoracostomy 

(not through the chest wall defect). Adequacy of ventilation can be confirmed with 

arterial blood gas measurements. 


Rapidly assess blood pressure and pulse. A narrowed pulse pressure suggests 

hypovolemic shock. Hypotension is evidence of severe intravascular depletion. Rapidly 

evaluate the abdomen because it is frequently a source of significant hemorrhage in the 

multiply injured patient. Severe pelvic fracture or pelvic ring disruptions can be 

associated with massive intrapelvic hemorrhage. Give the patient crystalloid initially and 

then blood, if needed, to improve perfusion. 

1. Traumatic arrest—If spontaneous cardiac activity is not detected by palpation of the 

carotid artery, begin cardiopulmonary resuscitation immediately. If the patient has blunt 

trauma and has been pulseless for less than 5 minutes, or if there is penetrating chest 

trauma and the patient has been pulseless for less than 15 minutes, consider emergent 

thoracotomy. Only experienced physicians trained in emergent thoracotomy should 

perform this procedure. If the patient has been pulseless longer than the above time 

limits, thoracotomy is not indicated and has not been shown to improve survival. Initiate 

closed chest compressions with volume resuscitation with crystalloids and cardiac drugs 

per advanced cardiac life support guidelines (Chapter 7). 

2. External hemorrhage—Stop obvious external hemorrhage using direct pressure with 

sterile dressings. Scalp wounds, even small ones, can produce significant blood loss if 

not controlled. Sometimes direct pressure and dressings are not sufficient. For 

uncontrolled scalp wound hemorrhage, the wound should be closed with sutures, 

staples, or, if available, Raney scalp clips, preferably using sterile technique. If a 

nonsterile technique is used, the wound should be inspected carefully, cleansed, and 

then definitively closed using sterile technique when the patient stabilizes. Bleeding 

vessels should not be clamped indiscriminately. Rarely will compression be insufficient 

to control an exsanguinating arterial hemorrhage from an extremity. A blood pressure 

cuff inflated proximal to the wound can serve as an effective tourniquet temporarily until 

surgical control of the bleeding can be achieved. Except as a last resort, avoid 

tourniquets. If a tourniquet is required, monitor and document the application time. 

3. Shock—(See also Chapter 9.) Shock is defined as inadequate tissue perfusion and is

further classified as mild, moderate, or severe, based primarily on clinical criteria. Cool, 

pale skin; diaphoresis; delayed capillary refill (> 2 sec); tachycardia; and mental status 

changes are reliable indicators of shock. Hypotension and oliguria are presumed to be 

due to shock until proved otherwise. Do not assume that perfusion is adequate on the 

basis of supine pulse and blood pressure alone, because these signs may not change 

until late in shock. This is particularly true in young healthy adults—who are the most 

common victims of multiple trauma. Patients taking ß-blockers (or other medications 

that blunt the normal response to adrenergic stimulation) may not exhibit tachycardia 

despite profound shock. 

Shock in the traumatized patient is due to hypovolemia from hemorrhage in the majority 

of the cases. Cardiac tamponade, tension pneumothorax, or spinal cord or brain injury 

may contribute to shock or (rarely) may cause shock without concurrent volume loss. In 

a trauma patient, shock should be treated as hypovolemic shock with volume infusions 

until other causes of shock are found. 

Brief Neurologic Exam 

A quick neurologic exam may be accomplished by using the GCS (see Figure 10-2). 

The GCS allows for quick assessment of the patient's level of responsiveness to 

determine if he or she is awake and alert; responds to verbal stimuli with eye opening or 

following of commands; responds to painful stimuli (eg, sternal rub, muscle or tendon 

squeeze) by appropriate movement, localization, or posturing; or is unresponsive. 

Assess the patient's pupils for symmetry, size, and reactivity. An asymmetrically 

enlarged pupil in a unresponsive patient may imply transtentorial herniation, which 

should be treated with endotracheal intubation. Among the other interventions to reduce 

intracranial pressure is short-term hyperventilation (Chapter 22). 

2. Initial Resuscitation 

Evaluation and treatment must proceed rapidly and simultaneously. During the primary 

survey, correct any identified problems immediately. Place the patient on a cardiac 

monitor, including pulse oximetry with supplemental oxygen administered. Initiate 

intravenous lines and order initial laboratory studies. Place a Foley catheter after 

examination of the perineal area and rectal exam. Do not insert a urethral catheter if 

there is obvious injury to the external genitalia, obvious urethral bleeding, scrotal 

hematoma, a malpositioned or high-riding prostate on rectal examination, or difficulty in 

passing the catheter. Monitoring of urine output is important in evaluating the patient's 

response to resuscitative efforts. Urinary output below 0.5 cc/kg/h indicates significant 

hypovolemia. 

Intravenous Access 

Insert multiple large-bore (= 16-gauge) catheters in a patient with profound shock. 

Initiate at least 2 intravenous lines. Consider a central line to administer large amounts 

of fluids rapidly or to monitor central venous pressure in patients with poor peripheral 

venous access in profound shock, in the elderly, and in patients with significant 

comorbid disease.

Laboratory Tests 

Obtain blood specimens for hematocrit or complete blood count, electrolyte 

measurements, renal function tests, and coagulation (prothrombin and partial 

thromboplastin times). Obtain a urine sample for gross blood. Obtain a pregnancy test 

from female patients of child-bearing age. If abdominal trauma is present, request 

laboratory studies for liver enzymes, amylase, and lipase. If severe shock is evident or 

suspected, type and cross-match for 4 units of packed red blood cells, and obtain an 

arterial blood gas and serum lactate. Trauma patients have high rates of alcohol and 

drug use, and a blood alcohol level or urine drug screen may be useful in evaluating 

patients with altered mental status. 

Fluid Resuscitation 

If clinical evidence of shock is present, initiate intravenous infusion of crystalloid 

solution. Give up to 2 L of crystalloid solution to support intravascular volume before 

giving blood. Give cross-matched or type-specific blood, if available, to a patient in 

persistent shock unresponsive to crystalloids. If typed and cross-matched blood is not 

available, then give type O blood. Reserve type O-negative blood for females under age 

50 years; all others should receive type O-positive. 

Initial Radiographic Studies 

During the acute phase of evaluation and resuscitation, the most valuable x-rays are of 

the chest and pelvis. These x-rays assist in the evaluation of potential injuries 

associated with a large amount of blood loss. Although spine x-rays are important, the 

spine can be protected from further injury by adhering strictly to spinal immobilization 

precautions during the initial evaluation and resuscitation. 

Large hemorrhages can also be found in the abdominal cavity. The abdomen can be 

rapidly evaluated in the unstable trauma patient by using bedside emergency ultrasound 

and performing a FAST (Focused Assessment with Sonography for Trauma) exam to 

look for free fluid. The more traditional approach to the unstable patient was the use of a 

diagnostic peritoneal lavage (DPL), which should be performed by the surgeon caring 

for the patient if ultrasound is unavailable. In stable trauma patients, a contrasted CT 

scan of the abdomen and pelvis provides useful information regarding the extent of 

specific organ injuries. Because ultrasound and CT scan are poor in evaluating bowel 

injuries, maintain a high index of suspicion so that this type of injury is not overlooked, 

especially in pediatric patients. 

Ongoing Evaluation & Resuscitation 

Frequently reassess a multiply injured trauma patient for evidence of new or ongoing 

signs of shock. In the multiply injured patient, hemorrhage is the most common cause of 

shock. Even so, it is important to conscientiously assess the patient for other underlying 

causes of shock. Early surgical consult is important for any trauma patient with signs of 

shock. Splint fractures, administer antibiotics and tetanus toxoid when needed, and 

keep patients warm. Pay close attention to the prevention of further injury. Avoiding

infection, hypothermia, coagulopathy, and ongoing blood loss is important for minimizing 

possible mortality and morbidity. 

Melio FR: Priorities in the multiple trauma patient. Emerg Med Clin North Am 

1998;16:29. [PMID: 9496313] (Overview of the initial approach to the multiply injured 

trauma patient.) 

HEMORRHAGIC SHOCK 


• Evidence of external blood loss. 

• Injuries with associated internal blood loss. 

• Tachycardia. 

• Decreased level of consciousness. 

• Decreased urine output. 

• Delayed capillary refill. 

• Hypotension (late sign). 


Defined as inadequate tissue perfusion due to decreased cardiac output secondary to 

blood loss, hemorrhagic shock accounts for the overwhelming majority of trauma 

patients in shock. Clinical signs are due to compensatory mechanisms. For example, 

excess sympathetic nervous system stimulation causes tachycardia and peripheral 

vasoconstriction, whereas decreased peripheral and renal blood flow result in 

decreased urine output, pallor, delayed capillary refill, and weak peripheral pulses. 


A. Obvious Sources of Blood Loss 

Identify and control external hemorrhage during the primary survey. Logroll trauma 

patients to examine their backs. A single hematocrit may provide a baseline but is not 

helpful in detecting acute occult hemorrhage. 

B. Hidden Sources of Internal Blood Loss 

Serial hematocrits over several hours are useful in determining continued blood loss, 

because a single initial value may be deceivingly normal. Major sources of occult blood 

loss are as follows: 

1. Thorax—Each hemithorax may contain 1-2 L of blood, primarily as a result of a 

pulmonary laceration or laceration of intercostal vessels or internal mammary artery due 

to either penetrating or blunt trauma. Suspect hemothorax in cases of shock associated 

with decreased or absent breath sounds or when dullness to percussion is present on 

the affected side. A supine chest x-ray may only show haziness over the hemithorax. 

2. Abdomen—Assume intra-abdominal hemorrhage in patients in shock with a normal

chest x-ray and no external sources of bleeding. Abdominal distention is a late and 

unreliable sign. Kehr sign is referred left shoulder pain due to diaphragmatic irritation 

associated with hemoperitoneum and splenic injuries. Cullen sign (periumbilical 

ecchymosis) is a late finding in intra-abdominal hemorrhage. Use a FAST exam or DPL 

to examine unstable patients. Stable patients should undergo CT scan of the abdomen. 

3. Retroperitoneum—The retroperitoneum can accumulate approximately 4 L of blood 

before tamponade occurs, and retroperitoneal hemorrhage may not be detected by 

abdominal ultrasound or DPL. Grey-Turner sign (flank ecchymosis) is a late finding on 

physical examination. CT scan of the abdomen and pelvis is necessary to confirm the 

diagnosis. 

4. Pelvis—Pelvic fractures may result in extensive bleeding from the bone itself or from 

disruption of the presacral venous plexus. The presence of blood can be identified with 

FAST exam or DPL; however, identification of the definitive source of bleeding requires 

CT scan, angiography, or laparotomy. 

5. Soft tissues (ie, thigh, upper arm, calf)—Between 1 and 4 L of blood can 

accumulate in the soft tissues due to long bone fractures and may not be immediately 

apparent on physical examination. 

Treatment 

A. Direct Pressure 

Obvious external hemorrhage can usually be controlled with direct pressure over the 

bleeding site or over a proximal artery. Tourniquets are rarely indicated. Never blindly 

place a clamp into a wound. 

B. Indirect Pressure or Pneumatic Antishock Garment 

Immediate temporary stabilization of an unstable pelvis fracture can decrease the pelvic 

volume and help tamponade bleeding. This can be accomplished by internally rotating 

the lower legs and tying them together with a sheet, followed by another sheet tied 

around the pelvis itself. Although they have not been shown to improve survival in 

patients with hemorrhagic shock, military antishock trousers (MAST) can be applied and 

inflated as a temporary measure to splint pelvic or femur fractures and help control 

hemorrhage. MAST are contraindicated in severe head or chest trauma, evisceration, 

diaphragmatic rupture, pulmonary edema, cardiogenic shock, or advanced pregnancy. 

C. Supportive Measures 

Guidelines for volume resuscitation are set forth in Chapter 9. 

1. Crystalloid solutions—As a general rule, administer 3 cc of crystalloids for every 1 

cc of estimated blood loss. Consider administering blood products if the patient's 

hemodynamic response is not favorable after the first 2 L of crystalloids. 

2. Blood products—The amount of blood or blood products given depends on the 

clinical situation and the patient's response to fluid resuscitation. Ideally the hematocrit 

should be kept at approximately 30% (35-40% in elderly patients and those with 

preexisting cardiopulmonary disease).

3. Autotransfusion—Autotransfusion is the administration of autologous blood 

collected from the patient's thoracic cavity. The blood is collected from chest tube 

drainage into containers with sodium citrate added as an anticoagulant. The blood can 

then be filtered and reinfused into the patient. Advantages include blood that is 

immediately available and already warm, with no risk of infectious disease transmission 

or transfusion reaction. 

4. Warming of blood—Hypothermia is a common side effect of transfusion of stored 

blood. New combination pressure infusers and fluid warmers are ideally designed to 

avoid hypothermia during aggressive fluid resuscitation of trauma patients. 

Disposition 

Admit patients for surgery or observation as indicated. 


INJURIES TO THE NECK REGION (See also Chapter 23.) 


• Immobilize to prevent further injury. 

• Examine neck for both blunt and penetrating trauma. 

• Evaluate neck for expanding hematoma, crepitus, subcutaneous air, external 

hemorrhage, trachea midline, and cervical spine tenderness or deformity. 

1. Cervical Spine 


(See Chapter 23.) 

Treatment 

Maintain in-line axial immobilization if a cervical spine injury is suspected (Chapter 23). 

Disposition 

Admit all patients with injury to neck structures, other than minor blunt or superficial 

penetrating injuries. 

2. Upper Airway 

Clinical Findings

Injury to the upper airway is characterized by hoarseness or aphonia, apnea or 

respiratory distress, stridor, subcutaneous emphysema, or bubbling of blood during 

inspiration and expiration in open neck wounds. 

Treatment & Disposition 

Early definitive airway management using RSI or cricothyrotomy may be life-saving if 

indicated. If the airway is exposed, intubate directly through the wound. If subcutaneous 

emphysema is present, assume a tracheobronchial injury is present and attempt to pass 

the endotracheal tube distal to the site of injury if possible. 

All patients with injuries to the upper airway require admission. 

3. Esophagus 


Esophageal injury is uncommon, even in penetrating trauma. Difficulty swallowing and 

neck pain are common, but overt clinical signs may be minimal initially. Chest x-ray may 

reveal pneumomediastinum, but definitive diagnosis requires esophagoscopy or 

contrasted swallowing studies. 


Insert a nasogastric tube and administer broad-spectrum antibiotics (ie, penicillin). 

Obtain surgical consultation. 

4. Vascular Injury 


The neck is divided into 3 anatomic zones. Zone I is below the cricoid cartilage, zone II 

is between the cricoid and the angle of the mandible, and zone III is above the angle of 

the mandible. Clinical findings of a vascular injury are variable and may be subtle or 

absent initially. Traditionally, surgical exploration was advocated for all zone II injuries 

deep to the platysma and for others with clinical indications (expanding hematoma, 

active bleeding, diminished carotid pulsation, hemoptysis, crepitus, dysphonia, 

hematemesis, dysphagia, or Horner syndrome). Some authors advocate selective 

management with angiography, Gastrografin swallow, and esophagoscopy. Because of 

difficulties in accessing the major vascular structures in zone III and especially zone I, 

arteriography (Table 10-2) and the other studies mentioned above continue to be 

utilized for evaluation of injuries in these zones. 


Treat hemorrhagic shock as indicated (Chapter 9). Prompt surgical consultation with or 

without arteriography is essential. 

TENSION PNEUMOTHORAX (See also Chapter 24.)


• Respiratory distress. 

• Asymmetrical lung sounds. 

• May or may not have external signs of trauma to chest wall. 

• Tracheal shift is late sign. 

• Distended neck veins may not be present in patients with hypovolemic shock. 


Tension pneumothorax interferes with venous return to the heart and thus decreases 

cardiac output and perfusion. Oxygenation is also impaired. A simple pneumothorax can 

be converted to a tension pneumothorax during positive pressure ventilation. 


Tension pneumothorax is manifested by respiratory distress, distended neck veins, 

contralateral tracheal shift, asymmetry of breath sounds, and percussion tympany. 

Chest x-ray confirms the diagnosis; however, tension pneumothorax is a clinical 

diagnosis and treatment should not be delayed while waiting for radiographs. Profound 

shock and cardiac arrest may be refractory to usual treatment unless the tension is 

relieved. Therefore, if a tension pneumothorax is clinically suspected, and an 

appropriate mechanism of injury is identified, emergent needle thoracostomy should be 

performed. 

Treatment 

Tension pneumothorax may be treated initially by inserting a large-bore (ie, 14-gauge) 

needle into the 2nd intercostal space, in the midclavicular line on the affected side. A 

rush of air confirms the diagnosis. If the tension pneumothorax is due to an open 

pneumothorax creating a 1-way valve (ie, sucking chest wound), then application of an 

occlusive dressing sealed on 3 sides can prevent the development of further tension. 

Definitive treatment is tube thoracostomy in the fifth intercostal space, in the midaxillary 

line, as soon as possible (Chapters 6 and 24). 

Disposition 

Hospitalization is required for all patients with tension pneumothorax. 

FLAIL CHEST (See also Chapter 24.) 


• Paradoxical chest wall motion.


• If signs of hypoxia or ventilatory failure are present, intubation is required. 


Flail chest is diagnosed clinically with careful inspection and palpation revealing 

paradoxical motion of the flail segment (inward movement with inspiration and outward 

movement with expiration). 

Treatment 

The goal is maintenance of adequate ventilation and careful fluid resuscitation, because 

the underlying injuries are sensitive to both inadequate resuscitation of shock and fluid 

overload. In some patients, flail chest can be managed without mechanical ventilation; 

however, intubation and mechanical ventilation may be necessary at the first sign of 

ventilatory failure or hypoxia. All patients with flail chest should receive supplemental 

oxygen. 

Disposition 

All patients with flail chest require hospitalization in an intensive care unit and may 

eventually require intubation as pulmonary contusions worsen and the increased work 

of breathing and pain contribute to poor respiratory function. 

PULMONARY CONTUSION (See also Chapter 24.) 



• Worsening hypoxia with time. 

• Radiographic findings often delayed in comparison to a rapid decline in respiratory 

function based on clinical examination. 

• Diffuse pulmonary opacities on chest x-ray. 


Pulmonary contusion is one of the most common potentially lethal injuries to the chest, 

with respiratory failure developing over time. The severity of injury generally peaks 

between 48 and 72 hours. 

Clinicial Findings 

The diagnosis of pulmonary contusion is based on chest x-ray findings of diffuse 

opacities following traumatic chest trauma. A high index of suspicion is required, 

because radiographic findings may be delayed more than 24 hours. CT scan of the 

chest can confirm the diagnosis earlier than chest x-ray.

Treatment 

Careful monitoring of oxygenation and ventilation (including oxygen saturation and 

arterial blood gases) is required. Administer supplemental oxygen as indicated. Any 

patient with significant hypoxia (PaO 2 < 65 or oxygen saturation < 90%) despite 

high-flow supplemental oxygen should be intubated and mechanically ventilated. 

Associated medical conditions (ie, chronic obstructive pulmonary disease, renal failure) 

increase the likelihood that a patient will require early intubation and ventilatory 

assistance. 

Disposition 

Hospitalize all patients for observation and monitoring. 

CARDIAC TAMPONADE (SEE ALSO CHAPTER 24.) 


• Hypotension. 

• Jugular venous distension may or may not be present. 

• Muffled heart sounds. 

• Electrical alternans on electrocardiogram. 

• Positive FAST exam for pericardial fluid. 


Cardiac tamponade most commonly results from penetrating injuries and interferes with 

diastolic filling, thus leading to inadequate cardiac output and end organ perfusion. 


The classic presentation consists of the Beck triad, although this is not always present. 

The triad includes hypotension, jugular venous distention, and muffled heart tones. 

However, jugular venous distention is common in supine patients without tamponade 

and may not be seen in hypovolemic patients with tamponade. In addition, muffled heart 

sounds are difficult to hear during a noisy resuscitation. Although not commonly seen, 

electrical alternans on electrocardiogram (ECG) (positive and negative QRS axis 

alternating with each beat) is pathognomonic for the condition. A FAST exam can 

rapidly confirm the diagnosis (Chapters 6 and 9). 

A. Penetrating Injury 

Suspect cardiac tamponade in any patient with penetrating trauma to one of the 

hemithoraces, because it has been estimated to occur in approximately 2% of patients 

with anterior penetrating chest injury. However, injury to the heart can occur even with 

remote wounds (ie, abdomen, back, and flank), and especially following gunshot 

injuries.

B. Blunt Trauma 

Blunt anterior chest trauma occasionally causes tamponade, with blood originating from 

injuries to the heart itself, the great vessels, or pericardial vessels. Associated 

myocardial contusion is common, and the clinical findings of tamponade may be 

delayed. 

Treatment 

If cardiac tamponade is suspected before the patient is in extremis, an emergency 

echocardiogram can be useful in confirming the diagnosis. Studies have shown 

transesophageal echocardiogram (TEE) to be nearly 100% accurate in diagnosis of 

posttraumatic pericardial tamponade. Pericardiocentesis (Chapter 24) may be beneficial 

as temporary treatment; however, all patients with a positive pericardiocentesis after 

trauma require open thoracotomy to further evaluate the heart and great vessels. 

If shock is rapidly progressive despite treatment or if cardiac arrest occurs due to 

tamponade, immediate emergency thoracotomy is required in order to decompress the 

pericardium (Chapter 24). 

Disposition 

Immediate hospitalization and operative thoracotomy are required. 

MYOCARDIAL CONTUSION (See also Chapter 24.) 


• High-velocity blunt chest trauma. 

• New conduction abnormalities on electrocardiogram. 


• Wall motion abnormalities on echocardiogram. 


Suspect myocardial contusion (also known as blunt cardiac injury) in any patient who 

sustains high-velocity blunt chest trauma. The classic mechanism is an unrestrained 

driver in a head-on motor vehicle collision, in which a bent steering wheel or deformed 

steering column results. Clinically important sequelae include hypotension and wall 

motion abnormalities on 2-dimensional echocardiography, although significant 

conduction abnormalities may be the most potentially lethal manifestations and usually 

occur in the first 12 hours following injury. Unlike myocardial infarction, the contused 

area usually heals completely; however, a significant number of patients may have a 

clinically significant decrease in cardiac output. The diagnosis is established via ECG; 

unexplained sinus tachycardia is the most common finding. Other ECG abnormalities 

associated with the condition include arrhythmias (both atrial and ventricular), ST and T 

wave changes, and heart blocks. Echocardiogram and elevated cardiac enzymes have 

also been used to evaluate myocardial contusion, although they are not usually

ecommended as screening tools because they are unreliable and do not predict 

complications. 

Treatment 

Treat arrhythmias as indicated (Chapter 35). Obtain serial ECGs to assess for changes 

(including premature ventricular contractions, atrial fibrillation, bundle branch block, and 

ST-segment abnormalities). 

Disposition 

There is evidence that hemodynamically stable patients younger than age 55 years, 

with normal ECGs and no significant medical history, can be discharged to home. 

However, all other patients with significant blunt chest trauma should be considered for 

admission with continuous cardiac monitoring and observation for 12-24 hours. 

TRAUMATIC AORTIC RUPTURE (See also Chapter 24.) 


• Mechanism of injury at risk for aortic rupture. 

• X-ray findings consistent with aortic rupture. 

• Positive definitive diagnostic study such as CT scan, aortography, or transesophageal 

echocardiogram. 


The diagnosis of traumatic aortic rupture requires a high index of suspicion, based on 

mechanism of injury (eg, deceleration injuries, pedestrian struck by a vehicle, falls > 30 

feet) and radiographic findings. Making the diagnosis can be difficult because specific 

signs and symptoms are frequently absent and the physical examination is neither 

sensitive nor specific. 


Pseudocoarctation, with blood pressure higher in the upper extremities than in the lower 

extremities; diminished femoral pulses; or a new harsh systolic murmur suggest the 

possibility of aortic injury. However, up to 50% of patients are without external evidence 

of chest trauma. 

B. X-ray Findings 

The following findings on chest x-ray indicate aortic injury: 

• Widened mediastinum (> 8 cm on supine x-ray) 

• Tracheal or nasogastric tube deviation to the right 

• Widening of the right paratracheal stripe (> 5 mm)

• Depression of the left main-stem bronchus 

• Indistinct aortic knob 

• Left apical capping 

C. Other Imaging Studies 

Although helical CT scanning of the chest with intravenous contrast is highly sensitive 

for aortic injury, aortography remains the gold standard for diagnosis. TEE has also 

been reported to have very high sensitivity and specificity for thoracic aortic injury. 

Although not widely practiced for evaluation of traumatic aortic injury, TEE can be 

performed in the unstable patient either in the emergency department or in the operating 

room. 


Patients with significant blunt chest trauma and possible aortic rupture should be 

hospitalized for surgical consultation, diagnostic studies, and immediate surgery if 

indicated. Unstable patients require immediate thoracotomy. Otherwise, support blood 

pressure with intravenous crystalloids and blood, and maintain hematocrit at greater 

than 30%. Maintain systolic blood pressure at 100-120, and use ß-blockade (ie, 

esmolol) and afterload reduction (ie, nitroprusside) to control hypertension. 

Zinck SE: Radiographic and CT findings in blunt chest trauma. J Thorac Imag 

2000;15:87. [PMID: 10798627] (Review of the use of CT scan to diagnose traumatic 

chest injuries. Includes incidence of common injuries and diagnostic criteria.) 

ABDOMINAL TRAUMA (See also Chapter 25.) 


• Mechanism of injury. 

• Abdominal tenderness, distension, rigidity, or bruising. 

• FAST exam, DPL, or CT scan is diagnostic. 

• Laboratory studies: CBC, amylase, lactate. 


Significant amounts of blood may be present in the abdominal cavity without any 

dramatic change in appearance or abdominal dimensions. Injuries may be blunt (related 

to compression or crushing injury or deceleration) or penetrating. In blunt injuries, the 

spleen is the most commonly injured organ, and in penetrating injuries, the liver and 

small bowel are the most commonly injured organs. 

Clinical Findings

History, including mechanism of injury, and physical examination (with involuntary 

muscle guarding as a reliable sign of peritoneal irritation) must be supported by further 

diagnostic studies, unless the patient has no history of abdominal injury, is alert and 

oriented, and has a completely unremarkable abdominal examination. Laboratory 

studies include complete blood count, electrolytes, lactate, serum alcohol, urine drug 

screen, and urine pregnancy test as indicated. Radiographic studies include FAST 

exam and CT scan of the abdomen with intravenous, oral, or occasionally rectal 

contrast. DPL may be required for evaluation of unstable patients when ultrasound is 

not available or the results are equivocal. 

A. Stable Patients 

Hemodynamically stable patients may be sent to the radiology suite for CT scanning of 

the abdomen, followed by DPL if the CT scan is negative and a strong suspicion for 

bowel injury remains. A negative CT scan may be followed by serial abdominal 

examinations or serial FAST exams. 

B. Unstable Patients 

Hemodynamically unstable patients should remain in the emergency department and 

undergo FAST examination. If the FAST exam is positive and the patient subsequently 

stabilizes, then CT scanning of the abdomen with intravenous or oral contrast can be 

performed for further diagnosis and assessment of the extent of injury. Otherwise, the 

unstable patient with a positive FAST exam requires laparotomy. If the initial FAST 

exam is negative, but a high index of suspicion for intra-abdominal injury remains, then 

DPL or serial FAST exams may be performed. A positive DPL is an unstable patient 

requires laparotomy. 


Treatment is determined by the results of the above-noted studies and may include 

operative or nonoperative treatment of specific organ injuries depending on the injury 

severity and the patient's stability. Serial abdominal examinations or serial FAST exams 

are indicated for patients undergoing nonoperative treatment of intra-abdominal organ 

injury. 

Boulanger BR, Rozycki GS, Rodriquez A: Sonographic assessment of traumatic injury. 

Surg Clin North Am 1999;79:6. [PMID: 10625980] (Review of the FAST examination in 

general, with historical perspectives and possible future applications.) 

Boulanger BR et al: The routine use of sonography in penetrating torso injury is 

beneficial. J Trauma 2001;51:2. [PMID: 11493792] (Description of the use of the FAST 

exam at a level I trauma center and its benefit in early identification of intraperitoneal 

injury.) 

Chiu WC et al: Abdominal injuries without hemoperitoneum: a potential limitation of 

focused abdominal sonography for trauma (FAST). J Trauma 1997;42:617. [PMID: 

9137247] (Article providing evidence as to why a negative FAST exam does not 

definitively rule out intraperitoneal injury.) 

HEAD TRAUMA (See also Chapter 22.)


• Evidence of external trauma. 

• Altered mental status with or without focal neurologic findings. 

• Hemotympanum, Battle sign, or raccoon eyes. 

• Unequal or unreactive pupils. 

• Decreasing Glasgow Coma Scale score. 



Suspect head injury in any trauma patient with cranial lacerations or hematomas, and in 

any patient with an altered mental status with or without focal neurologic findings. 

Examine the scalp and cranium for evidence of lacerations, hematomas, or other 

structural deformities (ie, depressions). Examine the nose and ears for any clear fluid, 

which must be assumed to be cerebrospinal fluid. 

Physical examination findings suggestive of a basilar skull fracture include 

hemotympanum, cerebrospinal fluid leakage from the nose or ears, a postauricular 

hematoma (Battle sign), bilateral periorbital ecchymosis (raccoon eyes), or 7th cranial 

nerve palsy. 

B. Neurologic Examination 

Perform a rapid and directed neurologic exam on all patients. The GCS is used to 

quantify neurologic findings and allows a uniformed, standardized description of head 

injury severity. It assesses eye opening and verbal and motor responses. This 

standardized format allows for rapid identification of changes in neurologic status on 

subsequent evaluation. In addition, the following factors should be evaluated: 

• Level of consciousness: a simplified approach uses the AVPU mnemonic (awake, 

responds to verbal or painful stimuli, and unresponsive). 

• Pupillary response, extraocular movements, and the presence or absence of 

decorticate or decerebrate posturing. 

• General motor function and motor response to painful stimuli. 

• Deep tendon reflexes, including assessment of Babinski reflex. 

Serial neurologic exams are used to identify changes in neurologic status. 

C. Imaging Studies 

CT scan of the head without contrast should be performed on all patients suspected of 

having a closed head injury following trauma, especially if there is a history of more than 

a momentary loss of consciousness, amnesia, persistent vomiting, or severe headache.

Treatment 

An initial goal is to achieve euvolemic fluid status, because fluid overload or dehydration 

can be detrimental. In addition, the goal is to maintain a PCO 2 of 35-40 mm Hg, with 

hyperventilation indicated only for impending uncal herniation. Even when 

hyperventilation is indicated, the PCO 2 needs to be maintained above 25 mm Hg. 

Mannitol may be given as an osmotic diuretic for signs of increasing intracranial 

pressure. Decompressive craniotomy or burr holes may be indicated for extremely rapid 

neurologic deterioration. 

GENITOURINARY TRAUMA (See also Chapter 26.) 


• Evidence of pelvic injury or fracture. 

• Blood at urinary meatus, scrotal or perineal hematoma, high-riding prostate, or vaginal 

lacerations. 


Injuries such as pelvic fractures are often associated with genitourinary injuries. Initial 

physical examination findings suggestive of genitourinary injury include blood at the 

urinary meatus, scrotal or perineal hematoma, or a high-riding, ballotable prostate on 

rectal examination in males. Patients with blood at the urinary meatus should undergo a 

retrograde urethrogram prior to insertion of an indwelling urinary catheter to identify 

injuries anterior to the urogenital diaphragm. If a catheter is placed and gross hematuria 

is identified, then obtain a cystogram to identify injuries posterior to the urogenital 

diaphragm. Renal or ureteral injuries in hemodynamically stable patients are evaluated 

by CT scan of the abdomen with intravenous contrast. 

Treatment 

Treat shock as indicated. 

Disposition 

Hospitalize patients as required. Obtain urologic consultation. Hematuria without 

identifiable genitourinary or renal structural abnormalities may be followed by a urologist 

on an outpatient basis. 

EXTREMITY TRAUMA (See also Chapters 28 & 29.) 


• Deformities. 

• Swelling, soft tissue ecchymosis. 

• Abnormal neurovascular examination. 

• Early splinting decreases further damage. 


The goal in the initial assessment and management of extremity injuries is to rapidly 

identify injuries that pose a threat to life or limb. Early definitive management can 

prevent or limit complications from extremity injuries that can lead to long-term loss of 

function. 


During the secondary survey, examine all bones and joints, and obtain x-rays at 

90-degree angles to one another of areas of suspected injury. 

Crush injuries are characterized by massive swelling and soft tissue ecchymosis, and 

are suggested by the mechanism of injury. They place the patient at risk for developing 

a compartment syndrome, with immediate or delayed neurovascular compromise. 

Treatment 

Splinting of fractures (Chapter 28) prevents excessive fracture site motion, which helps 

control blood loss, reduce pain, and prevent further soft tissue or neurovascular 

damage. Cover open fractures with sterile saline-moistened dressings. Administer 

intravenous antibiotics (ie, cefazolin, 1 g ± penicillin and aminoglycoside depending on 

the type and severity of contamination) and tetanus prophylaxis if indicated. Obtain 

orthopedic consultation. 

If compartment syndrome is suspected, compartment pressures should be measured (> 

35 mm Hg exceeds the tissue perfusion pressure and suggests impending 

neurovascular compromise). Fasciotomy may be required. Evaluate patients for 

rhabdomyolysis via measurement of creatinine kinase and urine myoglobin. Treatment 

of associated myoglobinuria consists of aggressive fluid resuscitation and osmotic 

diuresis to maintain high renal tubular volume and urine flow. Alkalinization of the urine 

with sodium bicarbonate reduces the precipitation of myoglobin in the renal tubules. 

Disposition 

Hospitalize patients for observation or surgery as indicated. 

SPINAL TRAUMA (See also Chapter 27.) 


• Immobilize to prevent further damage. 

• Direct spinal tenderness on physical examination. 

• Swelling or deformity over spine. 

• Neurologic deficits in extremities. 

• Sensory loss. 

• Decreased rectal sphincter tone or perineal sensation. 


Proper immobilization of the entire spine with a semirigid cervical collar, head blocks, 

and long spine board are required until vertebral or spinal cord injuries are excluded. 


Evaluation consists of logrolling the patient to examine the entire spine, including a 

rectal examination to evaluate rectal sphincter tone and perineal sensation. Evaluate 

any painful areas radiographically, and perform a detailed motor and sensory 

examination on all extremities. Neurologic deficits may or may not be present initially; 

therefore, a high index of suspicion must be maintained while in-line spinal 

immobilization is continued. 


Immobilization and hospitalization are required for patients with evidence of spinal 

trauma, with the exception of alert and oriented patients with a thoracolumbar strain or 

those with a cervical strain, who may be discharged to home in a cervical collar with 

outpatient follow-up in 1-2 weeks for reevaluation for possible ligamentous injury. 

Orthopedic or neurologic consultation is indicated for fractures or neurologic deficits. 

Grabber MA et al: Cervical spine radiographs in the trauma patient. Am Fam Phys 

1999;59(2):331. [PMID: 9930127] (Summary of the clinical and radiographic evaluation 

of the cervical spine. Includes useful tables, algorithms, and x-rays with accompanying 

drawings.) 






Figure 10-1.)

Table 10-1. Definitions of major trauma. 

Clinical Information 

Systolic blood pressure < 90 mm Hg 

Respiratory rate < 10/min or > 29/min 

Glasgow Coma Scale score < 10 

Penetrating trauma other than distal extremity 

Combination of 2nd- or 3rd- degree burns over > 15% of the body and 

multiple trauma 

Trauma score < 13 

Revised trauma score < 11 

Pelvic fractures 

Paralysis 





TABLES 

Table 10-1. Definitions of major trauma.

Table 10-2. Indications for arteriography following trauma. 





TABLES 

Table 10-2. Indications for arteriography following trauma.

Figure 10-1. Assessment of the patient with multiple injuries. DPL = diagnostic 

peritoneal lavage; FAST = focused assessment with sonography for trauma. 





FIGURES 

Figure 10-1

Figure 10-2. Trauma scores used to quantify degree of injury. A: Determine total on 

Glasgow Coma Scale. B: Convert Glasgow Coma Scale total to Revised Trauma Score 

points and determine Revised Trauma Score total. 





FIGURES 

Figure 10-2





Assess Severity & Give Immediate Necessary Care 

1 This chapter is a revision of the chapter by John Mills, MD, & John M. Luce, MD, from 

the 4th edition. 

The first step in the evaluation of the patient with suspected respiratory disease is to 

quickly assess the severity by noting the patient's general appearance and heart and 

respiratory rate. Rapidly perform a focused examination of skin color and temperature, 

oropharynx, neck, lungs, heart, chest, and extremities. Any patient with severe 

respiratory distress should receive immediate oxygen supplementation during 

assessment and treatment. If severe respiratory distress is present (eg, too short of 

breath for speech)—and especially if it has developed over a short period of time 

(minutes to hours) —proceed rapidly with simultaneous evaluation and therapy (see 

Figure 11-1). As in all life-threatening conditions, providing and maintaining an adequate 

airway is the first consideration. 

Assess Adequacy of Oxygenation 

In the patient with severe respiratory distress, assessment and management are 

concurrent. Clinical assessment of airway and ventilatory status drives the 

decision-making process. The clinical picture is augmented by immediately available 

data to allow rapid decisions and treatment interventions required by the critically ill 

patient. Signs including inability to speak, stridor, diaphoresis, accessory muscle use, 

tripod position, pulsus paradox, and altered mental status may be associated with 

severe respiratory distress. Pulse oximetry, waveform capnography, and rapid 

electrolyte and pH machines offer prompt, invaluable data on oxygenation, gas 

exchange, and acid-base status. This information will drive treatment decisions and 

urgency for interventions such as noninvasive or invasive mechanical ventilation, or 

surgical airway. Additional modalities such as imaging, arterial blood gas sampling, and 

other laboratory tests that require more time are used to refine the treatment plan 

following initial assessment and stabilization. 

Pulse oximetry measures the percent oxygen saturation of hemoglobin and provides a 

guide to the oxygenation of arterial blood. However, because hyperventilation can raise 

the PO 2 , a normal saturation may be observed despite an abnormal elevated 

alveolar-arterial PO 2 gradient. Pulse oximetry provides no information about PCO 2 

tension or adequacy of ventilation. It is inaccurate when carbon monoxide is present in 

the blood. Probes may not read properly in patients with hypotension, severe 

vasoconstriction, or severe peripheral vascular disease. Patients with severe hypoxemia

(eg, saturation < 90%) or ventilatory insufficiency should also have arterial blood gas 

determinations. Recall that a PaO 2 of 60 mm Hg is equivalent to a saturation of 90%. 

However, patients on supplemental oxygen with normal ventilation should have PaO 2 of 

greater than 40 mm Hg and so should have a saturation of 100%. Because oximetry 

readings begin to change only toward the lower end of this gradient, reading less than 

95% (particularly in patients receiving supplemental oxygen) should be addressed 

promptly, before the patient becomes hypoxic. 

CARDIAC ARREST 


In unresponsive patients, check for airway patency and properly position the head and 

jaw to open the airway (Chapter 7). Evaluate respiratory effort and assist ventilations if 

inadequate. Assess for presence of a carotid pulse. In cardiac arrest, terminal gasping 

respirations may simulate respiratory distress; conversely, conditions that produce 

severe respiratory distress may lead to hypoxic cardiac arrest. 


Start cardiopulmonary resuscitation (CPR) at once if the carotid pulse is not palpable, 

and continue with appropriate basic and advanced life support measures (Chapter 7). 

Hospitalization in an intensive care setting is mandatory for these patients if they survive 

initial resuscitation. 

SEVERE UPPER AIRWAY OBSTRUCTION (SEE ALSO CHAPTER 8.) 


Listen for inspiratory and expiratory stridor. Look for increased work of breathing, which 

may include suprasternal, supraclavicular, and intercostal retractions. When coupled 

with cyanosis, significant upper airway obstruction is present. Patients with complete 

upper airway obstruction are in extremis and will lose consciousness and progress to 

cardiac arrest quickly without definitive treatment. 

Treatment 

A. Away from Hospital 

(See also Chapter 7.) Remove possible obstructing foreign bodies by performing the 

Heimlich maneuver repeatedly until successful. If the victim loses consciousness, call 

for help to activate the Emergency Medical Services system, and perform 6-10 supine 

subdiaphragmatic thrusts (supine Heimlich), followed by a finger sweep and attempt to 

ventilate. Repeat these steps until the obstruction is cleared. If the victim is markedly 

obese or in the third trimester of pregnancy, use closed chest compressions instead of 

the Heimlich maneuver. A foreign body may be removed by trained rescue personnel 

under direct visualization using a laryngoscope and suction device or forceps. Rarely, 

cricothyrotomy may be necessary, but it should be performed by rescuers trained in the

technique. 

B. In a Hospital Emergency Department 

Immediate direct laryngoscopy is indicated if the obstruction cannot be removed quickly. 

This may be the first step in emergency department treatment. Foreign bodies may be 

removed under direct visualization using forceps. Obstruction caused by soft tissue 

swelling or local edema (as in anaphylaxis or angioedema) may be relieved by passage 

of an endotracheal tube. Anaphylaxis requires specific treatment (Chapter 9). Epiglottitis 

may cause upper airway obstruction in either children or adults; if this condition is 

suspected, avoid patient agitation or repositioning until prepared to provide a definitive 

airway (Chapter 32). A physician skilled in difficult airway management should care for 

these patients and may use adjuncts such as fiberoptic intubating bronchoscopy for 

diagnosis or securing the airway. If less invasive methods fail, immediate cricothyrotomy 

or tracheostomy is required (Chapter 6). 

Disposition 

Patients with easy, uncomplicated removal of an obstructing foreign body may be sent 

home following a period of observation with instructions to eat more slowly, chew more 

thoroughly, and swallow more carefully. Patients who lost consciousness but otherwise 

appear well should be examined and observed in the emergency department. Patients 

requiring intubation or surgery or who remain symptomatic should be hospitalized for 

treatment and observation. 

ALTERED MENTAL STATUS WITH SHALLOW BREATHING 


Altered mental status in a patient with obvious respiratory distress may be due to carbon 

dioxide retention or profound tissue hypoxia. However, the patient may have unlabored 

shallow respirations. Absence of a gag reflex (unprotected airway) or severe 

hypercapnia or hypoxemia on arterial blood gas studies (ie, respiratory failure) together 

with clinical assessment of underlying causes of altered mental status combine to 

support the necessity for endotracheal intubation in the emergency department. 

Treatment 

Ventilatory support should be given until endotracheal intubation can be accomplished. 

Provide high-flow (10-15 L/min) supplemental oxygen by nonrebreather mask or 

bag-valve-mask ventilation, as indicated. 

As soon as oxygenation and carbon dioxide exchange have been partially corrected by 

assisted ventilation, the patient should be intubated. An endotracheal tube provides a 

definitive airway by preventing aspiration and facilitating effective respiratory support. 

If there is doubt about the need for intubation, err on the side of intubation. Evaluation 

and treatment of other causes of altered mental status should follow airway 

management (Chapters 17, 18, and 20).

Disposition 

Hospitalize these patients for further diagnosis and treatment. 

TENSION PNEUMOTHORAX 


Severe respiratory distress associated with tension pneumothorax usually occurs 

following blunt or penetrating chest trauma (including chest compressions during CPR). 

Rarely, it may occur spontaneously in patients with spontaneous pneumothorax. 

Contralateral tracheal shift, ipsilateral hyperresonant hemithorax with markedly 

decreased or absent breath sounds, hypotension, and distended neck veins are 

classical signs, although they are not invariably present. Treatment should be based on 

findings of acute cardiorespiratory collapse in the appropriate clinical setting. 

Treatment 

Give oxygen, 10-15 L/min by nonrebreather mask. Perform tube thoracostomy (Chapter 

6). For immediate relief, perform needle thoracostomy in the 2nd intercostal space in 

the midclavicular line with a large-bore (14- to 16-gauge) needle if delay is anticipated in 

obtaining equipment for chest tube insertion. The risk of needle or tube thoracostomy 

without x-ray confirmation of tension pneumothorax must be weighed against the 

severity of respiratory distress or hemodynamic compromise and the likelihood of the 

clinical diagnosis. If the procedure is properly performed, the risks of tube thoracostomy 

are minimal even in a patient without pneumothorax. 

Disposition 

Hospitalize these patients for further treatment. 

MASSIVE ASPIRATION 


If the patient with severe respiratory distress has vomitus with particulate matter in the 

oropharynx, significant aspiration is likely. 

Treatment 

Clear the airway with a large-bore, hard-tipped suction device. Endotracheal intubation 

is often required because of depressed consciousness with hypercapnia and severe 

hypoxemia, or inability to protect the airway. Begin oxygen, 10-15 L/min by 

nonrebreather mask. 

Antibiotics and corticosteroids have been suggested by some authorities because of the 

risk of bacterial pneumonia. However, there is evidence that antibiotics are ineffective 

acutely in this situation, because the initial infiltrate appearing on chest x-ray is due to a 

chemical pneumonitis. Corticosteroids have also not been shown to be effective in

decreasing the death rate from aspiration pneumonitis. In addition, pneumonia due to 

gram-negative organisms is more likely to develop in patients who have received 

corticosteroids than in those who have not. 

Disposition 

Hospitalize these patients for definitive treatment. 

SEVERE PULMONARY EDEMA (See also Chapters 33 & 34.) 


Patients with severe pulmonary edema are extremely dyspneic, especially in the supine 

position, and may cough up frothy, pink sputum. Rales (crackles) are present, and the 

chest x-ray usually reveals bilateral interstitial infiltrates (Figure 11-2). Fever is 

uncommon. In cardiogenic pulmonary edema, other manifestations of heart failure are 

often present: tachycardia, distended neck veins or hepatojugular reflux, peripheral 

edema, cardiomegaly, or a ventricular (S 3 ) gallop. Wheezing may also be present 

(so-called cardiac asthma, probably caused by reflex bronchospasm). Patients with 

cardiogenic pulmonary edema often give a history of heart disease and have had 

pulmonary edema before. 

Noncardiac pulmonary edema has many causes. Drug overdose (especially from heroin 

and other narcotics), septic shock, pulmonary contusion, pancreatitis, and fat embolism 

are the most common causes. 

Treatment 

Aggressive early management can decrease the need for intubation as well as the 

length of stay in intensive care. All patients with severe pulmonary edema should 

receive supplemental oxygen, 10-15 L/min, by nonrebreather mask. If the patient 

remains hypoxic, noninvasive positive-pressure ventilation (NIPPV) via continuous 

positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) may allow 

adequate gas exchange for hours to days until pharmacologic interventions produce 

improvement. Endotracheal intubation rates in congestive heart failure are significantly 

decreased by NIPPV use. Endotracheal intubation with mechanical ventilation may be 

required if the patient does not tolerate NIPPV or has refractory hypoxia and respiratory 

acidosis. 

Morphine, 2-10 mg intravenously; and/or nitrates given sublingually (0.4 mg), 

cutaneously (1-2 inches of nitroglycerin ointment), or by intravenous infusion (begin at 

5-10 ug/min, and titrate to desired effect) cause peripheral vasodilation. Diuresis using 

furosemide, 40-80 mg intravenously, or bumetanide, 1-2 mg intravenously, will often 

improve respiratory function in patients with both cardiogenic and noncardiogenic 

pulmonary edema. Use caution with morphine, because its use is associated with 

increased endotracheal intubation rates. Angiotensin-converting enzyme inhibitors 

(ACE-I) have the opposite effect in congestive heart failure. 

Additional treatment depends on whether the edema is cardiogenic or noncardiogenic

(Chapters 33 and 34). Determination of a pulmonary artery wedge pressure is essential 

to the differential of these conditions. This procedure is usually not performed in the 

emergency department. Long-term ACE-I therapy decreases readmission rates in 

patients with congestive heart failure. 

Disposition 

Hospitalize these patients for further diagnosis and treatment. Some patients with a mild 

exacerbation of known cardiogenic pulmonary edema referable to an easily reversible 

cause such as medication or dietary noncompliance may be evaluated, diuresed, and 

observed in the emergency department. They may be discharged home with close 

follow-up when they return to baseline. 

SEVERE ASTHMA, CHRONIC OBSTRUCTIVE PULMONARY DISEASE, OR 

PULMONARY FIBROSIS (See also Chapter 33.) 


Patients with asthma, chronic obstructive pulmonary disease, or pulmonary fibrosis may 

present with severe dyspnea and respiratory distress similar to that found in patients 

with pulmonary edema. However, dyspnea in the former group of patients is less likely 

to be postural. Cough is common to the obstructive disorders, but sputum production is 

variable. Most important, patients with asthma, chronic obstructive pulmonary disease, 

or pulmonary fibrosis usually have wheezing on auscultation of the chest, unless tidal 

volume is inadequate. In such patients, the principal physical findings are tachypnea, 

tachycardia, cyanosis, chest hyperexpansion, and globally diminished breath sounds. In 

severe episodes, a pulsus paradoxus may be present. The use of the 

sternocleidomastoid muscles during inspiration is common, and intercostal retractions, 

nasal flaring, and tripod position may be noted. Chest x-ray shows only hyperexpanded 

lung fields unless another pathologic process such as bacterial pneumonia is present. 

These patients frequently do not have pneumonia; rather, viral or (rarely) bacterial 

tracheobronchitis or exposure to an allergen has exacerbated their chronic underlying 

disease. Multiple objective measures can be utilized to assess response to therapy. A 

visual analog scale or other validated dyspnea assessment tool, as well as peak 

expiratory flow rate or forced expiratory volume in 1 second, may be measured in the 

emergency department. These measurements can be used to follow improvement, 

compare the degree of obstruction to a known baseline, and guide treatment and 

disposition for a given patient. 

Treatment 

Several practice guidelines are available to help direct care. Further management of 

patients with these disorders is discussed in Chapter 33. 

A. Oxygen 

Give oxygen, 1-3 L/min to raise arterial saturation to at least 95% or PO 2 to between 60 

and 80 mm Hg without causing respiratory depression and a marked increase in arterial 

PCO 2 . Pulse oximetry is preferred, but arterial blood gas analysis may be indicated to

help direct therapy. Tracheal intubation and mechanical ventilation should be avoided 

but may be necessary if a patient is in acute respiratory failure. Do not withhold oxygen 

from the acutely hypoxic patient. 

B. ß-Adrenergic Sympathomimetic Bronchodilators 

In adults, ß-adrenergic sympathomimetic bronchodilators should be given in aerosol 

form if possible; otherwise, they may be given parenterally. A typical regimen is 

albuterol, 0.2-0.3 mL in 3 mL normal saline, delivered by nebulizer over 5 times every 

30 minutes. ß-agonists may be nebulized in combination with ipratropium bromide (0.5 

mg, up to 3 doses). For patients who are able to use them properly, metered-dose 

inhalers are as efficacious as nebulized therapy. 

In general, parenteral therapy offers little benefit over nebulization, except in the most 

extreme cases. If used, parenteral therapy includes epinephrine, 0.2- 0.3 mL (1:1000 

dilution) every 20-30 minutes subcutaneously, or terbutaline, 0.25 mg subcutaneously 

every 2-4 hours. Parenteral therapy may have value in younger patients with severe 

exacerbation. However, parenteral administration of sympathomimetics can produce 

marked tachycardia and may induce myocardial ischemia, especially in elderly patients 

or those with preexisting coronary artery disease. Therefore, they should be used 

cautiously in this group and be withheld if chest pain or extreme tachycardia develops. 

C. Corticosteroids 

Corticosteroids should be given within the first hour of treatment to patients who do not 

respond adequately to nebulized or parenteral ß-adrenergic agents alone. The 

recommended regimen is methylprednisolone, 125 mg intravenously initially, or 

prednisone, 60 mg orally. If the patient is to be discharged from the emergency 

department, a short course of oral steroids is warranted. 

D. Magnesium Sulfate 

Magnesium sulfate has a bronchodilating effect that may be of benefit in asthma. Its use 

should be reserved for life-threatening bronchospasm that is refractory to all other 

interventions. Adult dosing of magnesium sulfate is 1-2 g intravenously over 15-30 

minutes; pediatric dosage is 40 mg/kg intravenously. Effects are short-lived after the 

infusion is discontinued. Blood pressure should be monitored and the infusion stopped if 

hypotension occurs. Intravenous calcium should be immediately available to counteract 

cardiac dysrhythmias related to magnesium. Deep tendon reflexes will be lost once 

serum magnesium concentration reaches 7-10 mEq/L (normal concentration is 1.5-2.0 

mEq/L); the infusion should be stopped if reflexes are lost. At higher concentrations, 

respiratory depression and cardiac arrest may occur. However, the dose used for 

asthma is relatively low (approximately one-fourth the dose used in preeclampsia). 

Disposition 

Hospitalize patients with significant bronchospasm that does not respond promptly to 

treatment, or those with moderate bronchospasm that fails to improve after several 

hours of treatment. Discharged patients should receive short-term outpatient 

corticosteroid therapy such as prednisone, 40-60 mg/d with or without a taper over 6-10 

days.

Barton ED: Tension pneumothorax. Curr Opin Pulm Med 1999;5:269. [PMID: 10407699] 

(A review of the pathophysiology, diagnosis, and treatment of tension pneumothorax.) 

Emerman CL et al: Prospective multicenter study of relapse following treatment for 

acute asthma among adults presenting to the emergency department. Chest 

1999;115:919. [PMID: 10459087] (Study of patient factors associated with relapse 

following acute asthma treatment in the emergency department.) 

Howes DS et al: Triage and the initial evaluation of the oral facial emergency. Emerg 

Clin North Am 2000;18:371. [PMID: 10967730] (A review of initial evaluation of facial 

emergencies to include acute airway obstruction.) 

Hunt SA et al: ACC/AHA Guidelines for the Evaluation and Management of Chronic 

Heart Failure in the Adult: Executive Summary. A Report of the American College of 

Cardiology/American Heart Association Task Force on Practice Guidelines (Committee 

to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 

Circulation 2001;104:2996. [PMID: 11739319] (Provides evidence-based 

recommendations for prevention and treatment of heart failure in various stages.) 

Kosowsky JM et al: Continuous and bilevel positive airway pressure in the treatment of 

acute cardiogenic pulmonary edema. Am J Emerg Med 2000;18:91. [PMID: 10674543] 

(Review of literature regarding use of noninvasive ventilatory support in acute 

congestive heart failure.) 

Lee-Chiong TL Jr: Pulmonary aspiration. Compr Ther 1997;23: 371. [PMID: 9239486] (A 

comprehensive review of pulmonary aspiration.) 

Lerner DL et al: Prevention and treatment of upper airway obstruction in infants and 

children. Curr Opin Pediatr 1998;10:265. [PMID: 9716888] (A review of airway 

obstruction causes in the pediatric population.) 

FURTHER DIAGNOSTIC EVALUATION 

Diagnostic Information 

A. Data Base 

After supplemental oxygen has been started and life-threatening problems have been 

corrected, proceed as follows to construct an emergency cardiopulmonary data base: 

1. Obtain brief history directed toward cardiopulmonary disease and comorbidities, 

including potential triggers or causes, previous similar episodes, previous need for 

mechanical ventilation, and duration of this attack of dyspnea. 

2. Obtain complete list of prescribed and unprescribed medications (current and recent 

past), including most recent dosage history and history of steroid use. 

3. Conduct physical examination of the heart, lungs, abdomen, extremities, and other 

areas as indicated.

4. Obtain complete blood count, urinalysis, serum creatinine or blood urea nitrogen, 

serum electrolytes, and glucose, depending on the patient's history and examination 

findings. 

5. Monitor pulse oximetry and peak expiratory flow rate, and conduct dyspnea scale 

assessment. Arterial blood gas may be performed based on pulse oximetry or 

concomitant clinical findings. 

6. Order chest x-ray and electrocardiogram, if indicated. 

7. Order additional indicated tests such as D-dimer or other imaging studies (ie, chest 

computed tomography [CT] scan, angiogram, ventilation-perfusion scan). 

B. Interpretation of Diagnostic Data 

Information from this data base usually will allow the emergency physician to identify the 

cause of dyspnea (further discussed below and in Table 11-1). The basis of this 

categorization is discussed below and in greater detail in Chapter 33. 

Disposition 

(See also specific conditions, below.) If the emergency data base suggests a significant 

acute abnormality, but an exact diagnosis cannot be made that would permit specific 

therapy to be started, hospitalize the patient even if the clinical status would not 

otherwise warrant hospitalization. Sometimes more than one abnormality is present in 

the same patient (eg, acute exacerbation of chronic bronchitis and pneumonia). 


CHEST WALL DEFECTS 

1. Flail Chest 


Posttraumatic flail chest is usually apparent on physical examination as painful 

paradoxical motion of the rib cage or sternum (inward with inhalation and outward with 

exhalation). Crepitation or subcutaneous emphysema may be noted on examination 

together with decreased breath sounds on the affected side. 

Treatment 

Provide supplemental oxygen. Use a bag-mask to support ventilation of patients with 

obvious hypoventilation. Continuously monitor pulse oximetry. 

Intubation for respiratory support need not be performed immediately if saturation is 

greater than 90% or arterial blood gas levels are satisfactory (PO 2 > 65 mm Hg, PCO 2 

< 44 mm Hg). However, endotracheal intubation and positive-pressure ventilation are 

likely to be required, and prolonged saturations of less than 95% or hypoventilation due

to pain should trigger intervention. 

Provide analgesia (morphine, 1-4 mg intravenously, or fentanyl, 25-50 ug 

intravenously), and watch carefully for signs of respiratory depression. Do not use 

analgesia if respiratory failure is imminent. 

Disposition 

All patients with flail chest injuries require hospitalization for treatment and evaluation of 

this and potential associated injuries. 

2. Neuromuscular Diseases 


Patients with dyspnea or respiratory distress associated with progressive 

neuromuscular disease usually have hypoventilation (decreased pulse oximetry 

readings or arterial blood gases showing hypoxemia and hypercapnia) and objective 

weakness of other muscle groups, though the latter is not always present. Among many 

possible causes are Guillain-Barre syndrome, myasthenia gravis, periodic paralysis, 

botulism, and tick paralysis. 


Believe the patient's complaints of dyspnea, and evaluate respiratory status using pulse 

oximetry, arterial blood gas analysis, and pulmonary function tests (eg, vital capacity 

and maximal inspiratory force). Intubation may be postponed if initial blood gas levels 

are satisfactory. Specific therapy should focus on the neuromuscular disease (Chapter 

18). Immediate hospitalization is indicated. 

PULMONARY COLLAPSE 

Moderate degrees of pulmonary collapse that do not cause severe respiratory distress 

or obvious physical findings can be apparent on chest X-ray. Treatment depends on the 

specific cause as discussed below. 

1. Pneumothorax 


The patient often has chest pain and severe respiratory distress, with decreased breath 

sounds and tympany elicited by chest percussion of the affected side. The degree of 

dyspnea or respiratory distress depends on the amount of collapse and on the degree of 

pressure (ie, tension pneumothorax). Chest x-ray shows lung collapse and air in the 

pleural space (Figure 11-3). Small amounts of fluid may also be present in the pleural 

space. Tension pneumothorax presents in a similar manner, and late findings include 

shift of the mediastinum away from the involved side, distended neck veins, 

hypotension, and shock.

Treatment 

Immediate thoracostomy is indicated for bilateral pneumothoraces or unilateral tension 

pneumothorax, even if the patient appears stable, because sudden deterioration is 

likely. Unilateral large (> 20% of the pleural space) simple (nontension) pneumothoraces 

are also best treated by thoracostomy tube in the emergency department before 

hospitalization. Other types of pneumothoraces may be treated with a chest tube or, if 

the pneumothorax is simple and uncomplicated, by catheter aspiration or by observation 

of the patient in the emergency department with the catheter connected to a Heimlich 

valve for 6 hours. If a follow-up chest x-ray demonstrates persistent lung reexpansion or 

unchanged pneumothorax size, the patient may be discharged with close follow-up and 

instructions to return if symptoms reappear. 

Disposition 

Hospitalization is indicated for patients who have received tube thoracostomy, including 

all patients who present with tension pneumothorax or bilateral pneumothoraces of any 

type or who fail to maintain lung reexpansion after catheter aspiration. 

Patients with small to moderate-sized unilateral simple pneumothoraces of recent onset 

may be observed for a few days in the hospital without a chest tube to see if the 

condition is stable or improving. Those with recurrent pneumothorax should be admitted 

and considered for surgical intervention. 

Patients with first-time stable small spontaneous unilateral pneumothoraces that remain 

asymptomatic with stable repeat chest radiograph after 4-6 hours with no symptoms 

may be referred for follow-up on an outpatient basis. These patients should be seen 

within 1-2 days. 

2. Hydrothorax & Hemothorax (Pleural Fluid or Blood) 


Fluid in the pleural space results in pulmonary collapse. Small amounts of air may be 

present as well. The patient shows moderate dyspnea or respiratory distress and has 

dullness with chest percussion of the affected side. Chest x-ray is diagnostic (Figure 

11-4). 

Treatment 

A. Hydrothorax 

If dyspnea of acute onset is thought to be secondary to hydrothorax, immediate 

drainage in the emergency department is indicated. A needle or small-gauge catheter 

should be used if the fluid is watery. Viscous effusions may require tube thoracostomy. 

No more than 1-2 L should be removed at any one time because of the risk of 

expansion injury to the lung. The fluid should be sent for analysis (pH, specific gravity, 

cell count, glucose, protein, lactate dehydrogenase, and amylase), culture (for 

Mycobacterium tuberculosis and other bacteria), and cytologic studies.

B. Hemothorax 

In hemothorax due to penetrating trauma, autotransfusion may be indicated. Otherwise, 

thoracentesis or tube thoracostomy (or both) should be done, followed by investigation 

into the source of bleeding (eg, aortic angiography, exploration) as indicated (Chapter 

24). 

Disposition 

Hospitalization is required for all patients except those with chronic recurrent pleural 

effusions of known cause and without significant hypoxia or respiratory impairment. 

3. Massive Atelectasis 


Atelectasis is alveolar collapse that is not due to pneumothorax or hydrothorax (Chapter 

33). Decrease in chest motion on the affected side, dullness to percussion, and 

decreased to absent breath sounds are noted. Dyspnea, tachycardia, and cyanosis may 

be present. The disorder is evident radiologically as an increase in density of the 

collapsed lung, with reduced volume of the involved hemithorax (narrowed rib 

interspaces, elevated hemidiaphragm, and mediastinal shift to the side of involvement). 

Treatment 

In general, patients with atelectasis exhibit some degree of respiratory distress, which 

can be quite variable. In the rare patient with respiratory failure, respiratory support 

(administration of oxygen and usually also assisted ventilation) should be initiated in the 

emergency department. Administration of oxygen is indicated for patients with hypoxia 

on pulse oximetry while the underlying cause is determined. 

Disposition 

Hospitalization is required unless the process is known to be chronic and 

nonprogressive. 

LOSS OF FUNCTIONAL LUNG PARENCHYMA 

A number of conditions can produce acute or chronic dyspnea through loss of functional 

pulmonary parenchyma. 

The hallmarks of diseases causing loss of functional lung parenchyma are inspiratory 

rales (crackles) on physical examination, dullness to percussion, auscultatory pitch 

changes (eg, egobronchophony, bronchophony, and bronchial breath sounds), and one 

or more infiltrates on chest x-rays. 

These disorders may be divided into those associated with (1) pulmonary edema, (2) 

pneumonia (including aspiration pneumonia), and (3) interstitial disease. Pulmonary 

contusion following blunt chest trauma is covered in Chapter 24.

In patients with dyspnea, several processes may be occurring simultaneously. For 

example, aspiration pneumonia may be a combination of chemical pulmonary edema 

and bacterial pneumonia, with varying degrees of airway obstruction; viral pneumonias 

are often interstitial in their early phases; and cardiogenic pulmonary edema starts as 

interstitial edema before progressing to the alveolar filling stage. Additionally, it may be 

difficult to differentiate these conditions initially in the emergency department (eg, 

pneumonia from pulmonary edema). 

1. Pulmonary Edema 


The clinical presentation of less severe pulmonary edema is similar to that associated 

with the more severe form discussed above. Patients generally are less dyspneic and 

have a history of symptoms and signs such as paroxysmal nocturnal dyspnea, gradually 

increasing peripheral edema, and intermittent chest pain if the pulmonary edema is 

cardiogenic. Noncardiogenic edema usually begins more abruptly and is more severe 

than the cardiogenic form. Chest x-ray shows cephalization (Figure 11-5). 

Treatment 

Give oxygen as needed. Additional treatment depends on whether the diagnosis is 

cardiogenic or noncardiogenic pulmonary edema (Chapter 33 and 34). Endotracheal 

intubation may be required if hypoxemia cannot be corrected with high-flow oxygen by 

mask. 

Disposition 

Many patients with dyspnea from acute pulmonary edema require hospitalization. Some 

patients with chronic or recurrent pulmonary edema (usually cardiogenic) can be 

managed on an outpatient basis. 

2. Pneumonia (See also Chapter 40.) 


Patients with pneumonia generally give a history of fever and cough; dyspnea is a 

secondary or late symptom. Production of purulent sputum and pleuritic chest pain are 

common. 

Physical examination usually shows a febrile patient with localized rales and dullness on 

percussion, often associated with signs of consolidation (egobronchophony, bronchial 

breath, and vocal sounds). In children, fever and cough are the only constant 

symptoms. 

Chest x-ray (Figure 11-6) shows one or more infiltrates, except in patients with early 

pneumonia or concomitant dehydration, in whom observation and rehydration over 4-6 

hours generally will make the infiltrates visible on x-ray. Immunosuppressed patients 

may also have pneumonia without infiltrates.

Patients with AIDS may develop pneumonia due to Pneumocystis carinii. Despite 

cough, fever, dyspnea, and hypoxemia (or an elevated alveolar-arterial PO 2 gradient 

calculated from arterial blood gas data), the clinical findings may be few and x-ray 

findings extremely subtle or normal. However, typical x-ray findings, if present, are a 

diffuse heterogeneous alveolar or interstitial infiltrate. 

Treatment 

Begin antibiotics promptly based on the clinical situation, likely pathogen, and the 

results (if available) of a Gram-stained smear of sputum. (See Chapter 40 for a more 

extensive discussion of evaluation and treatment of pneumonia.) 

Disposition 

Hospitalization is warranted for all seriously ill patients, for very young or very old 

patients, for patients with significant concurrent illnesses, for unreliable patients, and for 

patients with pneumonia of unknown cause. Patients with Pneumocystis pneumonia 

should be admitted. 

Adolescents and young adults with mild viral, mycoplasmal, or pneumococcal 

pneumonia usually can be managed on an outpatient basis (Chapter 40). Practice 

guidelines for management of community-acquired pneumonia provide support for 

specific dispositions. 

3. Diffuse Interstitial Pulmonary Disease (See also Chapter 33.) 


Most patients with interstitial pulmonary disease have a history of chronic dyspnea, are 

aware of their diagnosis, and come to the emergency department because of recent 

worsening of symptoms. If the patient has not sought medical attention previously, 

interstitial pulmonary disease may be suspected if the physical examination shows 

diffuse "dry" rales, the chest x-ray shows interstitial infiltrates, and arterial PCO 2 and 

PO 2 are low. 

Treatment 

Supportive care is the only treatment recommended in the emergency department. 

Disposition 

Hospitalization should be considered for all newly diagnosed patients and for patients 

with known interstitial disease with significant recent increase in dyspnea or hypoxemia. 

4. Aspiration 

Clinical Findings

Aspiration may present clinically as pneumonia without obvious prior aspiration or as 

respiratory distress with obvious aspiration (vomitus in mouth and on clothing and 

elsewhere). This latter presentation is more common in patients with altered mental 

status. 

Treatment 

Supportive care should be given immediately in all cases. If obvious aspiration has 

occurred, clearing the airway is the most important emergency measure. This is best 

accomplished with a large-bore, hard-tipped suction device. Endotracheal intubation for 

better airway control and pulmonary toilet should be considered, as should emergency 

bronchoscopy. 

Disposition 

Hospitalize all patients. The patient's initial status is not a reliable guide to the need for 

hospitalization, because pulmonary function may worsen progressively for 24-72 hours 

after aspiration. 

AIRWAY DISEASE 

Obstruction to airflow (airway obstruction) is a principal manifestation of all types of 

airway disease. 

1. Upper Airway Obstruction 

Lesions of the oropharynx, larynx, or trachea may occlude the airway sufficiently to 

cause dyspnea. 


Upper airway obstruction usually causes pronounced stridor (obstruction of inspiratory 

airflow equal to or greater than expiratory airflow), which may be accentuated by forced 

ventilatory efforts. The stridor may be accompanied by intercostal, suprasternal, or 

supraclavicular retractions or other signs of increased respiratory effort. The diagnosis 

can be made with lateral soft-tissue x-rays of the neck. In some cases, fiberoptic 

laryngoscopy is helpful. 

Causes of upper airway obstruction include foreign bodies, tonsillar hypertrophy, croup, 

epiglottitis, anaphylaxis with laryngeal edema, retropharyngeal abscess, and tumors. If 

epiglottitis is suspected, obtain a lateral neck x-ray before attempting to visualize the 

upper airway directly (Chapter 32). Young children may aspirate small objects (eg, 

beads, coins, or peanuts) that lodge in the trachea or main-stem bronchus. Wheezing 

may be mistaken for bronchospastic disease. An expiratory chest x-ray is diagnostic, 

showing unilateral hyperexpansion on the affected side due to the ball-valve effect of 

the obstructing object (which may not be visible). 

Treatment

A foreign body should be removed if present. Anaphylaxis with laryngeal edema 

requires immediate intramuscular injection of epinephrine, 0.5-1.0 mg (0.5-1.0 mL of 

1:1000 solution). Alternatively, give 0.1-0.2 mg (1-2 mL of 1:10,000 solution) 

intravenously. Repeat in 3-10 minutes as needed (Chapter 9). Additionally, 

administration of diphenhydramine, 25-50 mg intramuscularly or intravenously, or 

selective histamine blockers such as famotidine, 20 mg intravenously, will block further 

histamine release. Discharged patients should receive diphenhydramine, 25 mg orally 

every 6 hours for 24-48 hours, to prevent recurrence. Surgical cricothyrotomy may be 

emergently required if obstruction progresses. Occasionally patients with hereditary 

angioedema (due to C1q esterase inhibitor deficiency) will present with signs and 

symptoms similar to those of allergic anaphylaxis. These patients are affected little by 

epinephrine and require C1q esterase inhibitor replacement (or fresh-frozen plasma if 

C1q esterase inhibitor is unavailable). 

Children with epiglottitis (Chapter 48) should not receive direct or indirect laryngoscopy 

in the emergency department, because laryngeal spasm may precipitate complete 

obstruction. They should be carefully intubated in the operating room with surgeons 

present who can perform an emergency tracheostomy if needed. Adults with epiglottitis 

are less prone to sudden airway obstruction but should be admitted and monitored 

closely. Both children and adults should receive intravenous antibiotics. 

Other disorders should be treated specifically to the extent possible. 

Disposition 

Patients with dyspnea from documented or suspected upper airway obstruction require 

hospitalization unless the problem is chronic, mild, and nonprogressive or is due to a 

foreign body that can be removed in the emergency department. Successfully treated 

upper airway obstruction due to anaphylaxis may recur when epinephrine wears off. 

Therefore, a 4- to 6-hour period of observation (or hospitalization) is advisable. 

2. Asthma, Chronic Obstructive Pulmonary Disease, & Pulmonary Fibrosis (See 

also Chapter 33.) 

In these disorders, expiratory airflow tends to be reduced proportionately more than 

inspiratory flow. Patients with dyspnea caused by these types of airway disease usually 

have a history of respiratory symptoms and are aware of their diagnosis. 


Cough is commonly a feature, although sputum production is variable. Most of these 

patients have wheezing on auscultation, accentuated during forced expiration. Other 

findings are similar to those discussed earlier in this chapter. 

Treatment 

The therapy discussed under treatment of severe forms of these disorders is also of 

value in less severe presentations.

Disposition 

Hospitalization is indicated for patients with severe or rapidly worsening dyspnea that 

does not respond to a few hours of treatment in the emergency department. Adult 

patients with asthma who are discharged home should receive corticosteroid therapy: 

oral for those with moderate symptoms, and oral or inhaled for those with minor 

symptoms. Children benefit from intramuscular steroids or high-dose inhaled steroids. 

PULMONARY VASCULAR DISEASE 

Dyspnea from pulmonary vascular disease may be one of the most difficult diagnostic 

problems confronting the emergency physician. The manifestations of pulmonary 

vascular disease are extremely varied in character and severity, and there is a 

significant risk of labeling patients with these illnesses as hysterical personalities or 

malingerers. 

1. Acute Pulmonary Embolism (See also Chapter 33.) 


Patients with acute pulmonary embolism and infarction usually have dyspnea, 

tachypnea, pleuritic chest pain, tachycardia, hypoxemia, and hypocapnia. Low-grade 

fever, cough, hemoptysis, and wheezing may also be present. Pulmonary infiltrates, 

occasionally with effusion, may be seen on x-ray. 

Patients with embolization without infarction have similar manifestations but often 

without pulmonary infiltrates, fever, and hemoptysis. 

In massive pulmonary embolization, crushing anterior chest pain, dyspnea, severe 

hypoxemia, syncope, shock, and cardiac arrest are common. 

Patients with right-sided endocarditis and other causes of septic pulmonary 

embolization usually have high fever and rigors associated with symptoms of 

embolization; the chest x-ray often shows multiple, scattered infiltrates that frequently 

cavitate after several days of illness. 

Progressive, noninvasive evaluation strategies that consider specific risk factors and 

physical findings have essentially replaced invasive methods of diagnosis. D-dimer, 

venous lower extremity Doppler ultrasound, spiral CT, CT angiography, and 

ventilation-perfusion scanning have significantly decreased the need for conventional 

pulmonary angiography in suspected pulmonary embolism. 

Treatment 

Give oxygen. Give morphine as necessary for pain. Treat shock if present. Heparin 

should be started (unless contraindicated) if embolization is strongly suspected. Do not 

give heparin to patients with suspected septic embolization. For adults, give a bolus of 

10,000 units per hour, adjusting the rate to maintain the prothrombin time at 1.5-2 times

control values. Selected patients may be appropriate for low-molecular-weight heparin 

therapy (enoxaparin sodium, 1 mg/kg subcutaneously every 12 hours). Thrombolytic 

therapy (Chapter 33) should generally be reserved for patients with moderate to severe 

right ventricular dysfunction. 

Disposition 

Patients with suspected or documented pulmonary embolization almost always require 

hospitalization. 

2. Chronic Pulmonary Vascular Obstruction (Repeated Small Pulmonary Emboli) 

A much more difficult problem is presented by patients with repeated small pulmonary 

emboli without infarction or with progressive pulmonary vascular occlusion from other 

causes (intravenous drug abuse, sickle cell anemia, vasculitis). 


These patients usually complain of dyspnea yet may have no abnormal findings in the 

emergency cardiorespiratory data base. Although significant hypoxemia and hypocapnia 

are often present, blood gas values are occasionally normal at rest. Evidence of 

pulmonary hypertension and right ventricular overload is found infrequently and then 

only in patients with advanced illness. A normal perfusion lung scan virtually excludes 

pulmonary emboli and is evidence against other types of pulmonary vascular disease. 

By contrast, abnormal ventilation lung scans can be produced by practically any type of 

pulmonary disease: asthma, bronchitis, and emphysema are the most common 

offenders in patients with normal chest x-rays. 


Obtain pulse oximetry and possibly an arterial blood gas sample for determination of 

PO 2 , PCO 2 , and pH before starting treatment. Start low-flow oxygen, 2 L/min by nasal 

cannula, and adjust the flow to maintain oxygen saturation at 95% or greater. 

Hospitalization is indicated for patients with respiratory failure or if symptoms are 

worsening rapidly. Dyspneic patients with unexplained hypoxemia should not be 

discharged home without arranging for home oxygen and an evaluation to exclude 

pulmonary vascular disease (screening pulmonary function tests with diffusing capacity, 

measurement of the alveolar-arterial PO 2 gradient during rest and exercise, perfusion 

lung scan, pulmonary arteriography, and the like). Furthermore, if a patient comes to the 

emergency department on 2 or 3 occasions with dyspnea, and no abnormalities are 

noted in the cardiopulmonary data base, referral to a pulmonologist is warranted for 

evaluation and complete pulmonary function testing. 

MISCELLANEOUS CONDITIONS 

1. Pleurisy


Pleurisy and pleuritic pain from any cause may produce a sensation of dyspnea. Even 

conditions such as rib fractures that produce pleuritic pain in the absence of significant 

underlying pulmonary parenchymal abnormalities may cause splinting and atelectasis 

sufficient to produce hypoxemia. When pleural fluid forms, the pain and friction rub may 

lessen or disappear. Pleurisy is often part of a viral syndrome (which may occasionally 

be accompanied by pericarditis). Fever, myalgias, headache, nasal congestion, or flulike 

symptoms may be present. A chest x-ray is required to exclude underlying lung disease, 

pleural effusion, or pneumothorax. 

Treatment 

Other than measures for relief of pain, therapy must be directed toward the underlying 

lesions. 

Disposition 

Hospitalization is required if the patient is severely hypoxemic (arterial PO 2 = 60 mm Hg 

as a new finding), if parenteral analgesia is required for pain relief, or if the underlying 

disease requires hospital treatment. 

2. Metabolic Acidosis 


Metabolic acidosis (eg, diabetic ketoacidosis, salicylate overdose) can produce 

secondary hyperventilation that may be taken for dyspnea or respiratory distress. 

Arterial blood gas analyses usually show a normal or high PO 2 , marked hypocapnia 

(PCO 2 of 10-20 mm Hg), and metabolic acidosis (low serum bicarbonate concentration). 


Treatment depends on the underlying condition. Patients almost always require 

hospitalization for management of the underlying cause of metabolic acidosis (Chapter 

42). 

3. Anemia, Pregnancy, & Thyrotoxicosis 

These 3 conditions may at times have accompanying dyspnea, and therapy for the 

underlying condition is all that is required. 

4. Neurologic Hyperventilation 

Primary central nervous system disease can produce a variety of abnormal breathing 

patterns, including central hyperventilation and Cheyne-Stokes respiration, any of which 

could be mistaken for respiratory distress. Cheyne-Stokes respiration may also occur 

when the circulation is slowed, as in heart failure.


The diagnosis is based on finding obvious neurologic or cardiac disease consistent with 

the respiratory pattern. The arterial PO 2 is usually normal; PCO 2 may be low or high. 

Treatment 

No treatment of the respiratory condition is required. 

Disposition 

Disposition depends on the underlying disease. 

5. Psychogenic Hyperventilation & Pulmonary Neurosis 


Patients with psychogenic hyperventilation usually present with a history of acute 

dyspnea and anxiety, often precipitated by personal or environmental factors. 

Hyperventilation to the point of tetany is diagnostic. Lightheadedness (due to cerebral 

vasoconstriction) and circumoral or limb paresthesias are often present. Another helpful 

feature is that the dyspnea often improves with exercise. Patients can be calmed 

enough to speak, whereas in organic dyspnea, patients may not be capable of speech. 

There are usually no abnormalities on the screening data base other than a low arterial 

PCO 2 , normal or high arterial PO 2 , and elevated pH. Most of these patients can be 

diagnosed in the emergency department as having neuroses, but the possibility of 

pulmonary vascular disease must be considered. 

Treatment 

There is no specific treatment. Reassurance is usually helpful. Patients with 

symptomatic hypocapnia (circumoral tingling, carpopedal spasm, tetany) or marked 

respiratory alkalosis (pH > 7.55) should breathe into an airtight bag for several minutes 

to relieve hypocapnia. 

Disposition 

The patient should be referred to a pulmonary clinic or internist for complete evaluation 

and reassurance. 

Guthrie R: Community-acquired lower respiratory tract infections: etiology and 

treatment. Chest 2001;120(6):2021. [PMID: 11742937] (A review of the cause and 

treatment of community-acquired pneumonia.) 

Jain SK et al: Spontaneous pneumothorax: determinants of surgical intervention. J 

Cardiovasc Surg 1998;39:107. [PMID: 9537545] (Describes success of varying levels of 

intervention in spontaneous pneumothorax.)

Karnik AM: Management of pneumothorax and barotraumas: current concepts. Compr 

Ther 2001;27:311. (A comprehensive review of all aspects of pneumothorax.) 

Kline JA et al: New diagnostic tests for pulmonary embolism. Ann Emerg Med 

2000;35:181. [PMID: 10650235] (Review of noninvasive methods of evaluation for 

pulmonary embolism with specific emphasis on emergency department assessment and 

management.) 

Pezzella AT, Silva WE, Lancey RA: Cardiothoracic trauma. Curr Probl Surg 

1998;35:647. [PMID: 9739342] (A review of cardiothoracic trauma.) 

Scribano PV et al: Provider adherence to a clinical practice guideline for acute asthma 

in a pediatric emergency department. Acad Emerg Med 2001;8:1147. [PMID: 11733292] 

(Describes a practice guideline and issues relating to adherence to the guideline.) 

Sivaloganathan M, Stephens R, Grocott M: Management of flail chest. Hosp Med 

2000;61:811. [PMID: 11198758] (A short review of cases and treatment of flail chest.) 

Smoller JE et al: State of the art: panic anxiety, dyspnea, and respiratory disease. 

Theoretical and clinical considerations. Am J Respir Crit Care Med 1996;154:6. [PMID: 

8680700] (A review of hyperventilation and panic disorders and their relationship.) 

Stollberger C et al: Multivariate analysis-based prediction rule for pulmonary embolism. 

Thrombosis Research 2000;97:267. [PMID: 10709901] (Offers and validates a 

prediction rule for pulmonary embolism based on rapidly obtainable patient-specific 

information.) 







Figure 11-1.)

Table 11-1. Essentials of diagnosis of diseases causing dyspnea and respiratory distress. 1 

Specific 

Condition 

Pneumoth-orax. Cough and chest pain 


Upper airway 

obstruction 


Symptoms Other 

Than Dyspnea Chest X-ray 

Gradual onset. Weakness of non-respiratory 

muscles 

Usually abrupt onset (hours 

to days). 

Previous dyspnea common. Often dry rales. 

Abrupt onset; history of 

vomiting 

Hoarseness or aphonia. Normal. 

Lung collapse; mediastinal shift 

if tension. 

Rales with or without dullness over 

affected areas; fever. 

Vomitus in oropharynx, or on 

endotracheal suction. 

Gradual onset. Hyperventilation. 

Previous attacks common; 

abrupt onset with stress 

Signs of cardiac or neurologic 

disease. 

Tetany. 





TABLES

Figure 11-1. Management of severe respiratory distress. 






FIGURES 

Figure 11-1

Figure 11-2. The radiographic appearance of severe pulmonary edema. 






FIGURES 

Figure 11-2

Figure 11-3. Small right-sided pneumothorax. 






FIGURES 

Figure 11-3

Figure 11-4. Large left-sided hemothorax. 






FIGURES 

Figure 11-4

Figure 11-5. Mild to moderate pulmonary edema with cephalization of pulmonary 

vasculature. 






FIGURES 

Figure 11-5

Figure 11-6. Radiographic appearance of a right lower lobe pneumonia. 






FIGURES 

Figure 11-6

12. Chest Pain 1 - Sean P. Barbabella, DO & William R. Dennis, Jr., 

MD 2,3 



1 Chest pain due to trauma is discussed in Chapter 24. 

2 This chapter is a revision of the chapter by Mary T. Ho, MD, MPH, & John Mills, MD, 


3 The views expressed in this article are those of the authors and do not reflect the 

official policy or position of the U.S. Department of the Navy, the U.S. Department of 

Defense, or the U.S. government. 

INITIAL MANAGEMENT 

Begin Supplemental Oxygen 

Give oxygen, 4 L/min, by nasal cannula or face mask, pending further evaluation. 

Begin Continuous Cardiac Monitoring 

Begin cardiac monitoring with pulse oximetry, and treat life-threatening arrhythmias 

(Chapters 7 and 35). 

Look for Markedly Abnormal Hemodynamics 

A. Shock 

Look for signs of shock. Arterial hypotension and poor peripheral perfusion cause 

altered sensorium; pale, clammy skin; oliguria; and, frequently, respiratory distress. 

B. Central Venous Hypervolemia 

Central venous hypervolemia is manifested initially by distended superficial veins (best 

seen in the neck); later, pulmonary edema (causing cough, dyspnea, rales, and frothy 

sputum) or peripheral edema may be seen, although peripheral edema is usually absent 

in conditions of acute onset. 

Central venous hypervolemia may be caused by conditions obstructing venous return 

(eg, tension pneumothorax, pulmonary embolization) or by cardiac disease (eg, 

infarction, tamponade). Pulmonary edema is usually not seen in conditions causing only 

interference with venous return. 

MANAGEMENT OF THE PATIENT WITH CHEST PAIN & ABNORMAL 

HEMODYNAMICS


The patient is in acute distress, and signs of abnormal hemodynamics are obvious on 

examination. 


A. Immediate Measures 

Insert 2 large-bore (= 16-gauge) intravenous catheters. Draw blood for complete blood 

count (CBC), serum electrolyte measurements, glucose, and tests for renal function; 

reserve 2 tubes for other studies that may be needed. Begin administration of 

intravenous fluids based on estimate of intravascular fluid volume. 

1. Hypotension or shock present—Infuse intravenous crystalloid solutions (eg, normal 

saline or lactated Ringer's), about 300-500 mL in 20 minutes. Monitor the response 

(blood pressure, urine output, sensorium). 

2. Central venous hypervolemia (with or without shock or hypotension)—Pending 

more precise diagnosis, infuse normal saline to keep the intravenous catheter patent. 

Briefly examine the pulmonary and cardiovascular systems, and palpate the abdomen 

for presence of a pulsatile mass. Obtain a 12-lead electrocardiogram (ECG). Obtain 

arterial blood for blood gas and pH determinations. Avoid unnecessary arterial 

punctures if the patient is a candidate for thrombolytic therapy for acute myocardial 

infarction. Arrange for a portable chest x-ray as soon as possible. Insert a urinary 

catheter. 

B. Life-Threatening Abnormalities 

1. Hypotension or shock present—Hypovolemia is manifested by collapsed neck 

veins, clear lung fields on physical examination or chest x-ray, and absence of 

peripheral edema. The central venous and pulmonary capillary wedge pressures are 

low. Table 12-1 lists the differentiating features of the 3 most important conditions 

causing chest pain with hypotension but without central venous hypervolemia. 

If the diagnosis is uncertain, treatment should be oriented primarily toward aortic 

dissection (Chapter 38). 

Type and cross-match for 6-10 units of whole blood. Expand intravascular volume with 

administration of intravenous crystalloid solution. Consider inserting a central venous 

catheter. For severe hypovolemia with shock, up to 3 L of crystalloid solution may be 

given rapidly (over 30-60 minutes) to restore normal hemodynamics until cross-matched 

blood is available. If blood is needed immediately, type-specific or universal donor blood 

(O-negative, low antibody titer or erythrocyte antigens) may be used (Chapter 39). 

Maintain blood pressure with continued infusion of blood and crystalloid solution. Blood 

should be given to keep the hematocrit above 30%. 

Obtain emergency vascular or thoracic surgical consultation. 

Reexamine the patient for pulse deficits or an abdominal mass, and check urine for

occult blood; these findings indicate aortic aneurysm or dissection. Obtain a portable 

chest x-ray and if the patient is stable consider computed tomography (CT) scan of the 

chest or abdomen and pelvis if indicated. 

Management of thoracic aortic dissection consists of ß-blockade to maintain heart rate 

less than 60-80 beats/min (esmolol, loading dose 500 ug/kg/min followed by an infusion 

at 50 ug/kg/min to maintain desired heart rate) and vasodilators to maintain a systolic 

blood pressure less than 120 mm Hg (nitroprusside, 0.3-10 ug/kg/min to desired blood 

pressure), establishing the ß-blockade first. 

Hospitalize the patient in an intensive care setting immediately for further evaluation and 

treatment. 

2. Central venous hypervolemia with hypotension or shock—Superficial veins 

(especially neck veins) are distended; pulmonary and peripheral edema may be 

present. See Table 12-2 for guidelines to differential diagnosis. Consider tension 

pneumothorax immediately, because this condition may be quickly and reliably 

differentiated from the others and is easy to treat. Look for marked respiratory distress, 

laterally deviated trachea away from the affected side, and a hyperresonant hemithorax 

with markedly decreased or absent breath sounds on the affected side. Chest x-ray 

confirms the diagnosis, but treatment should not be delayed to obtain a chest x-ray, 

because many patients require definitive treatment quickly. 

Cardiac tamponade should also be diagnosed early, because treatment is reasonably 

effective but differs markedly from that for cardiogenic shock, heart failure, or pulmonary 

embolism. Look for hypotension, jugular venous distension, and muffled heart sounds 

(Beck triad) and for low voltage on all leads of the ECG, electrical alternans, or diffuse 

ST-segment elevation typical of pericarditis. A narrow pulse pressure and pulsus 

paradoxus may also be present. Pulmonary edema is rare. Chest x-ray is not helpful, 

because acute tamponade does not cause a detectable increase in heart size. Definitive 

diagnosis by noninvasive methods is best done by bedside emergency ultrasound or 

formal echocardiography, but tamponade may be confirmed (and treated) by 

pericardiocentesis alone in desperate cases. 

a. Tension pneumothorax—(See Chapter 24.) Insert a thoracostomy tube if one is 

readily available (Chapter 6). Otherwise, a 14-gauge needle inserted in the 2nd 

intercostal space at the midclavicular line or in the 4th intercostal space at the anterior 

axillary line relieves tension in the chest until a thoracostomy tube can be inserted. 

Hospitalize the patient for further care. 

b. Cardiac tamponade—(See Chapter 24.) Attempt volume expansion with intravenous 

administration of 500-1000 mL of crystalloid solution over 20-30 minutes if the diagnosis 

is confirmed (this therapy is disastrous for cardiogenic shock). If the initial trial succeeds 

in elevating the blood pressure, volume expansion may be repeated once in a patient 

whose systolic blood pressure subsequently drops to less than 90 mm Hg. 

If time permits, obtain emergency cardiothoracic consultation for therapeutic 

pericardiocentesis, which should be performed in the operating room or under 

echocardiographic or fluoroscopic guidance. Otherwise, perform immediate

pericardiocentesis (under ultrasound guidance if available) (Chapter 6) if rapid, 

progressive hypotension develops and the patient fails to respond to volume expansion. 

Hospitalize the patient at once in an intensive care unit. 

c. Cardiogenic (arrhythmogenic) shock—See Chapter 35 for further details on the 

diagnosis and treatment of cardiac arrhythmias. 

(1) Severe bradyarrhythmia (heart rate usually < 40 beats/min)—Give atropine, 0.5 mg 

intravenously; if necessary, repeat every 5-10 minutes up to a total dose of 0.04 mg/kg. 

An external transcutaneous pacemaker (Chapter 6) may be applied to increase the 

heart rate until a percutaneous transvenous pacemaker can be inserted, if indicated. 

Dopamine can be used to support blood pressure and increase myocardial contractility. 

Mix 200 mg of dopamine in 250 mL of 5% dextrose in water for a solution of 800 ug/mL. 

Infuse at a rate of 5-12 ug/kg/min by continuous intravenous infusion, and observe the 

response. The dosage may be increased as needed but should not exceed 20 

ug/kg/min. If the response is inadequate with dopamine, start an epinephrine infusion. 

Mix 1 mg of 1:1000 epinephrine in 50 cc normal saline, begin the infusion at 2-10 

ug/min, and titrate to desired effect. 

Isoproterenol may be given as a last resort until a temporary pacemaker becomes 

available. Give 2-4 ug/min initially by continuous intravenous infusion, and increase as 

needed up to 20 ug/min. Isoproterenol must be used with extreme caution and only with 

continuous cardiac monitoring and frequent blood pressure readings, because it may 

cause arrhythmias. Because of the vasodilatory (ß 2 -adrenergic) effect of isoproterenol, 

blood pressure may fall if the heart rate does not increase. 

Occasionally patients will present with hypotension or shock due to severe 

bradyarrhythmia and without central venous hypervolemia. For these patients, fluid 

challenge may be given as described in the section on cardiac tamponade. If the patient 

does not respond to the above measures or if the patient develops left heart failure with 

fluid challenge, insert a percutaneous transvenous pacemaker, which is the treatment of 

choice. Hospitalize all patients in an intensive care unit. 

(2) Severe tachyarrhythmia (heart rate usually > 180 beats/min)—Immediate 

cardioversion is the treatment of choice. Deliver 50-100 J of synchronized direct current 

countershock initially, and increase the shock by 50- to 100-J increments if there is no 

response. 

d. Cardiogenic shock (myocardial infarction)—(See also Chapter 9). In patients with 

no evidence of pulmonary edema, ensure adequate intravascular volume; give 

intravenous crystalloid solution, 300- 500 mL over 30 minutes. If blood pressure 

improves, maintain the infusion at a rate of 100-200 mL/h. 

Give dobutamine, dopamine, or a combination of both if no change in blood pressure 

occurs or if severe shock or pulmonary edema is present initially. Mix 500 mg (2 vials) of 

dobutamine in 250 mL of 5% dextrose in water for a 2 mg/mL solution, and give at a 

rate of 2.0-20 ug/kg/min by continuous intravenous infusion. Begin at the lower dose, 

and increase as needed, guided by clinical response. Dobutamine is the drug of choice 

for treatment of cardiogenic shock due to pump failure. Caution: Observe for signs of

arrhythmia. 

Give morphine, 2-4 mg intravenously every 5- 20 minutes, until pain and dyspnea are 

controlled. If hypotension is a concern, then fentanyl may be used for pain. Carefully 

monitor the patient's respiratory status. Avoid unnecessary arterial punctures in patients 

who may be candidates for thrombolytic therapy. 

Nitroglycerin ointment, 1.25-2.5 cm (1/2-1 in) applied under an occlusive dressing, can 

be used for additional preload reduction. If the patient's condition worsens because of 

the effect of the ointment, it can be discontinued by simply wiping it off. 

Notify the cardiology consultant immediately if an acute infarction pattern is evident on 

the 12-lead ECG. Ideally, patients eligible for thrombolytic therapy (Chapter 34) should 

have treatment begun in the emergency department by the emergency physician, 

avoiding the delay necessitated by obtaining cardiologic consultation or transporting the 

patient to the coronary care unit. Emergency reperfusion therapy with thrombolytic 

agents or percutaneous transluminal coronary angioplasty has been shown to be of 

benefit in decreasing the mortality rate and the size of the infarct. 

Hospitalize the patient immediately in a coronary care or intensive care unit, and insert a 

pulmonary artery (Swan-Ganz) catheter and an arterial line as soon as possible to 

monitor blood pressure and cardiac output. 

e. Massive pulmonary embolism—(See Chapter 33.) Because massive pulmonary 

embolism is an uncommon diagnosis and is difficult to confirm rapidly, every attempt 

should be made to exclude other causes of chest pain with shock. Consider an 

emergent echocardiogram if available. Findings consistent with massive pulmonary 

embolism include right ventricular hypokinesis and dilation. Right ventricular dysfunction 

from pulmonary embolism predicts increased mortality. 

Attempt volume expansion with administration of 300-500 mL of normal saline over 

20-30 minutes to elevate systolic blood pressure. The dose may be repeated if the trial 

is successful and if heart failure does not develop. In the rare patient with hypotension 

without central venous hypervolemia, a fluid challenge should also be given, but a larger 

dose (500-1000 mL of normal saline instead of 300-500 mL) may be administered. 

Give dopamine (see above). If clinical signs strongly suggest pulmonary embolism and 

thoracic dissection has been ruled out, begin heparin (unfractionated or a 

low-molecular-weight heparin) (see Pulmonary Embolism, below, and Chapters 33 and 

34). Obtain pulmonary consultation, and consider thrombolytic therapy. 

3. Central venous hypervolemia with normal or elevated blood 

pressure—Superficial veins (especially neck veins) are distended. Pulmonary and 

peripheral edema is common. Blood pressure is normal or (more commonly) elevated. 

Acute congestive heart failure is the most common cause. It generally occurs as an 

exacerbation of preexisting disease but occasionally results from acute myocardial 

infarction (acute cardiogenic pulmonary edema), although acute myocarditis or 

pericardial effusion without frank tamponade may be present rarely.

a. Nitroglycerin—Give nitroglycerin, 0.4 mg sublingually, or use nitroglycerin ointment, 

1.25-2.5 cm (1/2-1 in) applied under an occlusive dressing. Nitroglycerin by intravenous 

infusion, beginning with a rate of 10 ug/min and increasing by 5-10 ug/min every 3- 5 

minutes as needed, can be started in the emergency department. Monitor the blood 

pressure closely, and if hypotension develops, place the patient in the Trendelenburg 

position and decrease the infusion rate. Do not give nitrates to patients taking sildenafil 

(Viagra). 

b. Furosemide—Give furosemide, 0.5-1.0 mg/kg by bolus intravenous injection. The 

initial effect of rapid preload reduction is of immediate benefit; diuresis occurs later. 

c. Morphine—Give morphine, 2-4 mg intravenous, and repeat every 5-10 minutes until 

pain and dyspnea are relieved. 

d. Aspirin—Give aspirin, 160-325 mg chewed, if not contraindicated. If the patient has 

an allergy to aspirin, use clopidogrel, 75 mg orally. 

e. Angiotensin-converting enzyme (ACE) inhibitors—Captopril or enalapril are 

associated with reduced admission rates to the intensive care unit and decreased 

endotracheal intubation rates. Acutely, a reduction in preload and afterload has been 

seen. For oral or sublingual captopril, a one-time dose of 12.5 mg or 25 mg is given; 

enalapril is given as a 1.25 mg intravenous infusion over 5 minutes. Avoid using ACE 

inhibitors in patients who are hypotensive, pregnant, or hyperkalemic or in those who 

are allergic to ACE inhibitors. 

f. Positive-pressure ventilation—If the patient continues to deteriorate, consider early 

noninvasive positive-pressure ventilation (BiPAP or CPAP); this approach may even 

prevent the need for endotracheal intubation. 

g. Inotropic agents—Short-term inotropic therapy can improve hemodynamic 

parameters. These agents may be beneficial for patients who are unable to receive 

conventional therapy. Milrinone may be administered as a 50 ug/kg bolus over 10 

minutes, followed by an infusion at 0.25-0.75 ug/kg/min. Another choice is dobutamine, 

at an infusion rate of 2.5-15.0 ug/kg/ min. 

h. Nesiritide—Nesiritide (human B-type natriuretic peptide) is now recommended for 

the treatment of severe decompensated congestive heart failure. It is administered as a 

bolus of 2 ug/kg over 1 minute, followed by a continuous infusion of 0.01 ug/kg/min. 

Hypotension is the major dose-limiting side effect. Nesiritide has been shown to improve 

both hemodynamic parameters such as pulmonary capillary wedge pressure and clinical 

variables such as dyspnea and fatigue in patients admitted with congestive heart failure. 

i. Hospitalization—Hospitalize the patient immediately in an intensive care setting, and 

monitor hemodynamic status with a pulmonary artery catheter and arterial catheter as 

needed. 

MANAGEMENT OF THE PATIENT WITH SEVERE CHEST PAIN & NORMAL 

HEMODYNAMICS


The patient is in acute distress because of chest pain but is neither hypotensive nor in 

shock. 

Treatment 

A. Oxygen 

Give oxygen, 4 L/min, by nasal cannula or mask. Begin continuous electrocardiographic 

monitoring. 

B. Venous Access 

Insert an intravenous catheter (18-gauge is satisfactory), and begin an infusion of 

normal saline as slowly as necessary to keep the catheter open. 

C. Electrocardiogram 

Obtain a 12-lead ECG within 10 minutes of the patient's arrival. If the ECG reveals 

evidence of acute myocardial infarction, evaluate the patient for possible thrombolytic 

therapy (Chapter 34). 


Give aspirin, 160-325 mg chewed, if not contraindicated. If the patient has an allergy to 

aspirin, give clopidogrel, 75 mg orally. 

Give nitroglycerin, 0.4 mg sublingually. Sublingual nitroglycerin may be repeated twice 

with 5 minutes between doses. If pain continues despite morphine and sublingual 

nitroglycerin and if acute myocardial infarction is suspected, begin nitroglycerin by 

intravenous infusion (see above). 

Give morphine, 2-4 mg slowly intravenously; morphine may be repeated every 10-20 

minutes until the patient is more comfortable. 

E. Laboratory Findings 

Send blood samples to the laboratory for CBC; renal function tests; and serum 

electrolyte, glucose, lipase, and amylase determinations. Send blood samples for 

cardiac enzyme measurements (CK-MB isoenzymes, troponin I/T, myoglobin) if 

myocardial infarction is suspected and the patient is to be hospitalized. 

F. Treatment of Arrhythmias 

Correct any significant cardiac arrhythmias (Chapter 35). 

G. History and Physical Examination 

Take a thorough medical history with emphasis on the quality, radiation, severity, timing, 

and duration of chest pain, and perform a complete physical examination (see below). 

H. Chest X-ray 

Obtain a chest x-ray. An anteroposterior view with portable equipment is satisfactory if 

the patient is too sick to tolerate a better examination.

I. Other Tests 

Obtain additional tests as indicated on the basis of the history, physical examination, 

and results of laboratory tests. 

Disposition 

Patients with chest pain severe enough to cause objective distress should be 

hospitalized or admitted to an observation unit for further evaluation. 

American Heart Association in collaboration with the International Liaison Committee on 

Resuscitation. Guidelines 2000 for cardiopulmonary resuscitation and emergency 

cardiovascular care. Circulation 2000;102(8 Suppl):1. [PMID: 10966667] 

Antonelli M et al: A comparison of noninvasive positive-pressure ventilation and 

conventional mechanical ventilation in patients with acute respiratory failure. N Engl J 

Med 1998; 339:429. [PMID: 9700176] 

Brady WJ, Harrigan RA: Evaluation and management of bradyarrhythmias in the 

emergency department. Emerg Med Clin North Am 1998;16(2):361. [PMID: 9621848] 

Colucci WS et al: Intravenous nesiritide in the treatment of decompensated congestive 

heart failure: Nesiritide Study Group. N Engl J Med 2000;343:246. [PMID: 10911006] 

Hollenberg, SM, Kavinsky CJ, Parillo JE: Cardiogenic shock. The pathophysiology and 

management. Ann Intern Med 1999; 131(1):47. [PMID: 10391815] 

Jouriles NJ: Atypical chest pain. Review of aortic dissection, pulmonary embolism, and 

pericarditis. Emerg Med Clin North Am 1998;16(4):717. [PMID: 9889737] 

Lee TH, Goldman L: Evaluation of the patient with acute chest pain. N Engl J Med 

2000;342:1187. [PMID: 10770985] 

Spodick DH: Pathophysiology of cardiac tamponade. Chest 1998; 113(5):1372. [PMID: 

9596321] 

Wiesenfarth J: Aortic dissection; the symptoms, diagnosis and treatment. eMedicine; 

www.emedicine.com 

Wigder HN et al: Pressure support noninvasive positive pressure ventilation treatment of 

acute cardiogenic pulmonary edema. Am J Emerg Med 2001;19:179. [PMID: 11326339] 

Zevitz ME et al: Heart failure. eMedicine; www.emedicine.com. 

FURTHER EVALUATION OF THE PATIENT WITH CHEST PAIN 

Differential Diagnosis by Location & Quality of Pain

Evaluation of patients who complain of chest pain but are not in severe distress should 

proceed in a systematic fashion. The single most useful means of evaluation is the 

carefully elicited history supplemented by examination of the heart, lungs, abdomen, 

and peripheral vessels in conjunction with electrocardiograhy, chest x-ray, and arterial 

blood gas measurements. Consider most of the diagnostic possibilities at least briefly in 

every patient who presents with chest pain (Table 12-3). 

A. Retrosternal Discomfort 

Retrosternal discomfort, especially if it is a tightness, pressure, or "squeezing" pain, 

should suggest serious underlying disease, for example, myocardial infarction, unstable 

angina due to atherosclerosis or valvular heart disease, pericarditis, dissection of the 

aorta, or pulmonary embolism. When the above diagnoses are excluded, esophageal 

disease (eg, spasm, esophagitis) is the most common cause of retrosternal distress 

(see below). Because esophageal disease is relatively benign and rarely requires 

hospitalization, the more serious causes of retrosternal discomfort must be excluded 

with a high degree of certainty before concluding that the pain is of esophageal origin. 

Consider hospitalization for all adult patients with retrosternal pain for observation 

unless a condition not requiring hospitalization is diagnosed with certainty. 

B. Pleuritic Pain 

Pain that is markedly worse on inspiration should suggest pleurisy associated with 

pneumonia, pulmonary embolism, or isolated pleuritis. The pain of pneumothorax, 

pneumomediastinum, ruptured esophagus, and pericarditis frequently has a pleuritic 

component. The fleeting pain of a "stitch in the side" is often pleuritic in nature as well. 

Chest pain due to myocardial infarction may have a pleuritic component. 

One of the most serious causes of pleuritic chest pain, pulmonary embolism, is also one 

of the most difficult to diagnose given the widely varied presentations of the disease with 

nonspecific history and physical examination findings. Because of the increased 

mortality associated with misdiagnosis, consider pulmonary embolism in all patients 

presenting with pleuritic chest pain (Chapters 33 and 34). 

C. Back or Abdominal Pain with Chest Pain 

Abdominal pain that is inferior to the xiphoid process and associated with chest pain 

should suggest intra-abdominal disease, dissecting aortic aneurysm, or possibly 

myocardial ischemia. In stable patients, CT scan of the chest and abdomen with 

intravenous contrast can reliably exclude the diagnosis of dissecting or ruptured aortic 

aneurysm. Even after aortic catastrophes are excluded, patients with chest pain often 

require hospitalization or admission to an observation unit to rule out myocardial 

ischemia. 

D. Musculoskeletal Discomfort 

Musculoskeletal disease with chest pain (Tietze syndrome, rib fracture) is usually 

associated with marked tenderness localized over the affected site. Patients with chest 

pain referred from intrathoracic structures may also have some associated tenderness 

of superficial structures. Most patients with chest pain from musculoskeletal disorders 

can receive treatment in the emergency department and be discharged for outpatient 

follow-up care.

MANAGEMENT OF SPECIFIC DISORDERS CAUSING CHEST PAIN 

CARDIOVASCULAR DISORDERS 

ACUTE CORONARY SYNDROME (See Chapter 34.) 

MYOCARDIAL INFARCTION (See Chapter 34.) 

Mitral Valve Prolapse 


• Has late systolic click. 

• Palpitations are the most frequent complaint. 


Consider mitral valve prolapse in any patient with a mitral regurgitation murmur or clicks 

(without other known heart disease or other cause of chest pain) who presents with 

recurring atypical chest pains. The ECG may show nonspecific T-wave abnormalities. 

Echocardiography is required for definitive diagnosis. 

Treatment 

No specific emergency therapy is required. Although life-threatening arrhythmias may 

occur, they are rare. ß-blocker therapy (eg, metoprolol, 50 mg orally twice daily) may be 

offered to patients who are uncomfortably symptomatic. 

Disposition 

Refer patients to a cardiologist or primary care physician for definitive evaluation and 

management. 

AORTIC STENOSIS & REGURGITATION 


• Classic triad: angina, syncope, and heart failure. 

• Crescendo-decrescendo systolic murmur is classic finding in aortic stenosis, loudest at 

2nd right intercostal space. 

• Aortic regurgitation is a high-pitched, blowing decrescendo diastolic murmur. 

Clinical Findings

Chest pain in patients with severe aortic stenosis or regurgitation is clinically similar to 

that of angina and is probably the result of a similar mechanism, that is, relative 

myocardial ischemia secondary to diminished coronary blood flow. 

Anginal pain in a patient with aortic valve disease may indicate that hemodynamically 

significant abnormalities of the valve are present, with a higher risk of impending sudden 

death. Murmurs of aortic stenosis or regurgitation are present on physical examination, 

often with adjunctive findings indicating severe valvular disease (eg, thrill over the 

carotid artery, wide pulse pressure; see Table 12-3). 

Treatment 

Provide symptomatic treatment pending further evaluation for definitive treatment. Begin 

oxygen, 4 L/min, by nasal cannula, and obtain an ECG. Insert an intravenous catheter 

(18- to 20-gauge) and begin an infusion of normal saline to keep the catheter open. 

Give nitroglycerin, 0.3-0.4 mg sublingually, for pain. If nitroglycerin is not effective, give 

morphine, 2-4 mg intravenously. Monitor the patient closely and discontinue medication 

if any signs of decompensation develop. 

Disposition 

Hospitalization is warranted because of the imminent risk of decompensation or sudden 

death. Patients should be evaluated for cardiac catheterization or valve replacement 

with or without coronary bypass. 

PERICARDITIS (See Chapter 34.) 

Aortic Dissection (SEE CHAPTER 38.) 

PULMONARY DISORDERS 

PLEURISY & PLEURODYNIA (See also Chapter 33.) 


• Coxsackievirus B is most common cause. 

• Sudden lancinating chest pain. 

• Associated with fever, malaise, and headaches. 


Patients with idiopathic pleurisy or pleurodynia are generally young, and the onset of 

illness is acute, with severe pleuritic chest pain. Apart from low-grade fever in some 

patients and possible friction rub, other findings on physical examination are usually 

normal. Chest x-ray may show a small pleural effusion, with or without a small 

pulmonary infiltrate. Viruses (especially enteroviruses) are the usual causative agents.

An accurate diagnosis of pleurisy is important because its symptoms are similar to those 

of pulmonary embolism. Pleurisy is often a diagnosis of exclusion. 

Treatment 

Pleurisy and pleurodynia are benign, self-limited diseases, and only symptomatic 

measures are necessary. Although aspirin is sufficient for most patients, indomethacin, 

25-50 mg orally 3 times daily, is reported to be more effective. 

Disposition 

Hospitalization is rarely indicated, and then only for relief of severe pain. Refer patients 

to an outpatient clinic for turberculin testing and repeat chest x-ray. 

SPONTANEOUS PNEUMOTHORAX (See Chapter 33.) 

Traumatic Pneumothorax (SEE CHAPTER 24.) 

Pneumomediastinum (SEE ALSO CHAPTER 33.) 


• "Crunch" of subcutaneous air is felt on exam. 

• Chest x-ray is diagnostic. 

• Retrosternal pain. 


Pneumomediastinum is frequently associated with pneumothorax. It is characterized by 

severe boring pain located retrosternally or in adjacent areas; the pain sometimes 

radiates to the back. Chills, fever, and shock may be present, especially if there is 

concurrent mediastinitis. A mediastinal "crunch" on auscultation or air in the 

mediastinum on chest x-ray is diagnostic. 

Treatment 

Give oxygen, 3-5 L/min, by nasal cannula or mask. Insert an intravenous line (= 

16-gauge), and keep it open with normal saline. Give morphine, 2-4 mg intravenously, 

for pain; the dose may be repeated. 

Treat pneumothorax with tube thoracostomy as indicated. Evaluate the patient 

thoroughly to rule out serious underlying disease, ruptured bronchus, or a ruptured 

esophagus. Rupture of the esophagus is invariably associated with mediastinitis. 

Disposition

Hospitalize patients for observation and examination to rule out serious precipitating 

factors such as rupture of the trachea, bronchus, or esophagus. Refer patients with 

chronic or recurrent pneumomediastinum for outpatient care. 

PULMONARY HYPERTENSION (See also Chapter 34.) 


• Dyspnea, exertional syncope, and exertional chest pain. 

• Evidence of right ventricular failure almost always present. 

• Prominent P2 (pulmonic) heart sound. 

• Doppler echocardiography can help make diagnosis. 


Severe or sudden onset of significant pulmonary hypertension may cause an oppressive 

retrosternal sensation or frank angina associated with dyspnea on exertion. A history of 

easy fatigability, weakness, syncope on exertion, and hemoptysis may be elicited. A 

loud P 2 and right ventricular lift on physical examination suggest pulmonary 

hypertension. The ECG may reveal strain in the right side of the heart or cor pulmonale 

(right axis deviation; depressed ST segment and inverted T waves in leads II, III, aVF, 

and V1-5; and tall, peaked P waves in leads II, III, and aVF). A large right ventricle or 

large pulmonary vessels on chest x-ray are diagnostic. 

Treatment 

No specific treatment is available for pulmonary hypertension. Administer oxygen for 

hypoxia and treat other abnormalities (bronchopulmonary infection, recurrent pulmonary 

emboli, heart failure) that may be exacerbating the pulmonary hypertension. 

Disposition 

Hospitalization is indicated for patients with severe pain, hypoxia, or severe heart 

failure. Refer patients to a cardiologist for complete evaluation to rule out repairable 

lesions and to evaluate patients for treatment with anticoagulants or other 

investigational treatments. 

PULMONARY EMBOLISM (See Chapter 33.) 

Pneumonia (SEE CHAPTER 40.) 


ESOPHAGEAL DISORDERS 

Clinical Findings

Esophageal disorders such as esophagitis, spasm, motility disorders, and 

gastroesophageal reflux frequently cause retrosternal chest pain that can be difficult to 

differentiate from pain due to cardiac causes. When cardiac disease is excluded, 

esophageal disorder is the most common cause of chest pain. Characteristic features of 

chest pain of esophageal origin include pain that is burning in nature, often radiates 

along the sternum, is made worse by lying down and relieved by sitting, may be induced 

by swallowing, and often persists for hours after a shorter episode of more intense pain. 

Rest, sublingual nitroglycerin, "GI cocktails," and calcium-channel blockers can relieve 

pain of both cardiac and esophageal origin and should not be used as diagnostic aids. 

Because cardiac disease is more life threatening, cardiac causes of chest pain must be 

excluded with a high degree of certainty before esophageal disorder is diagnosed as the 

cause of pain. 

Diagnostic tests include barium swallow, endoscopy, manometry, and pH monitoring. 

Definitive emergency diagnosis of the esophageal disorder is seldom warranted. 

Treatment 

General symptomatic treatment can be offered to patients who are in discomfort, 

because the specific esophageal disorder is not usually known at the time of the 

emergency visit. A trial of viscous lidocaine, 15 mL mixed with 15 mL of an antacid 

given orally, can be tried for acute relief. Clinicians are cautioned to avoid attributing 

chest pain symptoms to an esophageal cause based entirely on improvement in chest 

discomfort after a "GI cocktail." Other measures include eating frequent small meals, 

using antacids, avoiding food before sleep, and using bed blocks (10-15 cm [4-6 in] 

high) under the head of the bed. If gastroesophageal reflux is suspected, H 2 -receptor 

blocker or proton-pump inhibitor therapy may be tried. 

Disposition 

If esophageal disorder is diagnosed as the cause of chest pain and cardiac disease or 

other life-threatening conditions can be excluded with confidence, refer the patient for 

outpatient care within 1-2 weeks. 

PERFORATED ESOPHAGUS (See also Chapter 24.) 


• Severe chest pain. 

• Pain increased with swallowing or breathing. 

• Chest x-ray may reveal air within the mediastinum, pleural cavity, pericardium, or 

subcutaneous tissue. 


Esophageal perforation is marked by agonizing retrosternal chest pain associated with

pneumomediastinum, pneumothorax, pneumonia, or purulent pleural effusion. A recent 

history of severe retching, vomiting, or endoscopy is often present. The diagnosis is 

confirmed by an esophagogram using water-soluble contrast medium or 

esophagoscopy. 

Treatment 


Disposition 

Hospitalize the patient for evaluation for possible surgery. 

PERFORATED STOMACH OR DUODENUM (See also Chapter 13.) 


• Often a history of peptic ulcer disease. 

• Vomiting is common. 

• Acute distress. 

• Acute abdominal x-ray may reveal free air in the abdomen. 


Perforation distal to the esophagus is characterized by sudden onset of severe pain that 

is usually epigastric but may be retrosternal and may radiate to the back. A history of 

chronic epigastric pain or ulcer disease often is present. Epigastric tenderness and 

diminished or absent bowel sounds may be found. If peritonitis has supervened, 

rebound tenderness and a rigid abdomen are present. Air under the diaphragm may be 

seen on an x-ray. Serum amylase or lipase levels may be elevated as a result of 

posterior perforation into the pancreas. Leukocytosis with a shift to the left often is 

present. 

Treatment 

Insert a large-bore (= 16-gauge) intravenous catheter, and give crystalloid solutions 

intravenously to support blood pressure. Give morphine, 2-4 mg intravenously, for pain; 

the dose may be repeated. 

Insert a nasogastric tube, and begin continuous suction. Obtain urgent surgical 

consultation. Begin prophylactic intravenous antibiotics (cefoxitin, 2 g intravenously, and 

gentamicin, 2 mg/kg intravenously; see also Table 13-1). 

Disposition 

Hospitalize the patient at once for emergency surgery.

PANCREATITIS (See Chapter 13.) 

Cholecystitis (SEE CHAPTER 13.) 

MUSCULOSKELETAL DISORDERS 

COSTOCHONDRAL SEPARATION, RIB FRACTURES, & INTERCOSTAL MUSCLE 

STRAIN (See also Chapter 24.) 


• Pain associated with movement. 

• X-rays may reveal a fractured rib. 

• Often a history of trauma. 


In this group of musculoskeletal disorders, pain is usually worse with movement and 

breathing. A history of minor trauma, strenuous exercise, or severe coughing often is 

present. Pain is localized and elicited by palpation. Chest x-ray may be normal or may 

show rib fractures if they are present. 

Treatment 

Oral analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for 

analgesia. Local heat alone may provide relief. Narcotic analgesics may be required if 

respiratory effort is affected because of pain. Splinting is generally not recommended for 

rib fractures, because it may impair respiratory function and promote atelectasis or 

pneumonia. For patients with rib fractures, ensure that a pneumothorax is not present 

on x-ray. 

Disposition 

Refer the patient for outpatient follow-up if pain is severe or persistent. 

DISK DISEASE (Cervical & Thoracic) 


• Pain radiates from neck or back to arms. 

• Paresthesia in fingers. 

• Weakness in arm with decreased reflexes. 

Clinical Findings

Disk disease may cause paroxysmal pain radiating from the back of the neck into the 

arms and fingers. The pain is aggravated by coughing, sneezing, and straining. Neck 

movement is restricted by cervical muscle spasm. The patient may have paresthesias 

and pain in the fingers, weakness of hand and forearm muscles, and decreased biceps 

and triceps reflexes. Narrowing of the vertebral interspace is seen on a plain film, and 

magnetic resonance imaging confirms the diagnosis. 

Treatment 

Treatment is symptomatic. Local heat may be of value. In mild cases, a light cervical 

collar during the day may be helpful. 

Disposition 

Hospitalization is rarely required even for patients with severe disk disease. Outpatient 

follow-up by a spinal surgeon is recommended. Mild cases can be treated on an 

outpatient basis. 

TIETZE SYNDROME (COSTOCHONDRITIS) 


• Remember that cardiac pain also can be reproducible by palpation. 

• Pain is localized to a specific point. 


Tietze syndrome affects the costochondral or chondrosternal junctions, with visible 

swelling and erythema of the overyling skin and localized tenderness. 

Treatment 

Pain usually is relieved by NSAIDs or other oral analgesics. Injection of 

lidocaine-corticosteroid preparations into the joints also relieves pain. 

Disposition 

Refer the patient for outpatient follow-up if pain is severe or persistent. 

MUSCLE SPASM ("STITCH") 


• History of trauma or exercise.


The patient complains of aching pain, usually in localized areas but sometimes more 

generalized. Pain often increases with movement and palpation. A history of minor 

trauma or strenuous exercise may be present. 

Treatment 

Massage, heat, and other local treatments are effective. Aspirin or other NSAIDs are 

useful. 

Disposition 

Refer the patient for outpatient follow-up as needed. A search for more serious illnesses 

(eg, myositis, arthritis, Pancoast tumor) may be necessary in recurrent or persistent 

cases that have no obvious cause. 

MISCELLANEOUS DISORDERS 

INTRATHORACIC NEOPLASM 


• History of fever, night sweats, and weight loss. 

• Cough or hemoptysis. 

• Chest x-ray may reveal a mass. 


Intrathoracic neoplasm is suggested by a mass seen on chest x-ray with no other 

explanation for the chest pain. 

Treatment 

Give analgesics and other supportive measures as required. 

Disposition 

Depending on their general condition, patients with intrathoracic neoplasms should be 

either hospitalized or referred for timely evaluation by a pulmonologist. 

ZOSTER (See also Chapter 46.) 


• Vesicles in a dermatomal pattern. 

• Does not cross midline. 

• Pain may precede vesicles. 


In the preeruptive stage of zoster, pain felt on the skin surface in dermatomal 

distribution may occur several days before the characteristic skin lesions (clusters of 

clear, fluid-filled vesicles in a dermatomal distribution) appear. Pain is typically unilateral 

and does not cross the midline. Hypoesthesia in dermatomal distribution may also be 

present. 

The appearance of the skin lesions confirms the diagnosis. Rarely, patients may present 

with pain as the only manifestation of the disease; in such patients, a rise in antibody 

titer is diagnostic. 

Treatment 

Give analgesics as necessary; narcotics may be required for relief. Acyclovir, 800 mg 

orally 5 times daily for 7-10 days, or famciclovir, 500 mg orally 3 times a day for 7 days, 

if given within 72 hours of onset may alleviate symptoms, shorten the duration of illness, 

and reduce the incidence of postherpetic neuralgia, a special concern in elderly 

patients. Local nerve block with long-acting anesthetics (eg, bupivacain [Marcaine, 

Sensorcaine]) is effective and obviates the need for narcotics and their associated side 

effects. It may also decrease the incidence and severity of postherpetic neuralgia. 

Prednisone, 60 mg orally daily (tapered over 2 weeks), may also decrease the incidence 

and severity of postherpetic neuralgia in elderly patients. 

Disposition 

Patients with severe cases (extensive localized disease, dissemination) may require 

hospitalization for pain control and possible treatment with intravenous acyclovir. Other 

patients may be referred for outpatient evaluation and continued treatment (analgesia). 

Bonow RO et al: ACC/AHA guidelines for the management of patients with valvular 

heart disease. J Heart Valve Dis 1998;7: 672. [PMID: 9870202] 

Bouknight DP et al: Current management of mitral valve prolapse. Am Fam Physician 

2000;61:3343. [PMID: 10865929] 

Brady WJ et al: Electrocardiographic diagnosis of acute myocardial infarction. Emerg 

Med Clin North Am 2001;19(2):295. [PMID: 11373980] 

Jouriles NJ: Atypical chest pain. Review of aortic dissection, pulmonary embolism, and 

pericarditis. Emerg Med Clin North Am 1998;16(4):717. [PMID: 9889737] 

Kontos MC: Evaluation of the emergency department chest pain patient. Cardiol Rev 

2001;9(5):266. [PMID: 11520450]

Ng SM et al: Ninety-minute accelerated critical pathway for chest pain evaluation. Am J 

Cardiol 2001;88:611. [PMID: 11564382] 

Rubin LJ: Primary pulmonary hypertension, review of the treatments. N Engl J Med 

1997;336:111. [PMID: 8988890] 

Stankus SJ, Dlugopolski M, Packer D: Management of herpes zoster (shingles) and 

postherpetic neuralgia. Am Fam Physician 2000;61:2437. [PMID: 10794584] 

Zalenski RJ, Shamsa F, Pede KJ: Evaluation and risk stratification of patients with chest 

pain in the emergency department. Predictors of life-threatening events. Emerg Med 

Clin North Am 1998;16:495. [PMID: 9739772] 






Figure 12-1.)

Table 12-1. Differentiating features of conditions causing chest pain with hypovolemia. 

History ECG Myocardial infarction with 

vagotonia 

Tearing chest pain; back 

pain; often history of 

hypertension 

Nonspecific or may show 

ischemia or infarction 

pattern, left ventricular 

hypertrophy 

Leaking upper abdominal 

aortic aneurysm 

Bradycardia; st 

hypotension 

Tachycardia; p 

epigastric mass

Table 12-2. Distinguishing features of conditions causing chest pain, hypotension, 

or shock in association with distended neck veins. 

Helpful Distinguishing Features 

Hyperresonant hemithorax with decreased breath sounds; chest x-rays diagnostic, 

trachea deviates away from affected side. 

Faint heart sounds; ECG with diffuse low voltage or electrical alternans. Pulmonary 

edema rare. Echocardiography diagnostic. 

ECG or cardiac monitor shows severe bradycardia (ventricular rate < 50 beats/min, 

usually < 40 beats/ min, usually > 180 beats/min). Signs of myocardial ischemia 

may also be present. 

Pulmonary edema almost always present. ECG almost always shows pattern 

diagnostic of infarction. 

Physical examination, ECG, and chest x-ray show signs of right heart strain. Chest 

x-ray may show infiltrates, effusion, or truncation of pulmonary vasculature. Confirm 

diagnosis by ventilation-perfusion scanning, spiral CT scan of chest or pulmonary 

arteriography. 





TABLES 

Table 12-2. Distinguishing features of conditions causing chest pain, 

hypotension, or shock in association with distended neck veins.

Table 12-3. Diagnostic clues to cause of chest pain. 1 

History Previous 

Attacks of 

Similar Pain 

Usually Squeezing, dull ache 2-10 minutes up to 20-30 

minutes 

In some cases Squeezing, dull ache, increases 

with time. 

> 30 minutes 

Usually Variable Variable; usually hours 

May have occurred Like angina Like angina 

May have occurred Like angina May be prolonged 

May have occurred Variable; often pleuritic and 

relieved by sitting 

Hours to days 

No Tearing, maximal at onset Variable 

In some cases Pleuritic Variable 

May have occurred Variable often pleuritic Variable 

No Variable; often pleuritic Variable 

Usually Like angina Variable

May have occurred Usually strong pleuritic 

component 

Rare Pleuritic Variable 

Usually Changes with eating Variable 

No Severe Variable 

No, or milder pain of ulcer Severe Variable 

Minutes to hours 

May have occurred Variable Hours to days 

Usually Variable Hours to days 

Variable Pleuritic ache, "sticking" 

sensation 


Variable; fleeting for stitch 




TABLES 

Table 12-3. Diagnostic clues to cause of chest pain.

Figure 12-1. Management of complaints of chest pain. 





FIGURES

13. Abdominal Pain 1 - Roger Humphries, MD, & Jon Andrew Russell, 

MD 



Perform Brief Examination 

1 This chapter is a revision of the chapter by Richard A. Crass, MD, & Donald D. 

Trunkey, MD, from the 4th edition. 

Record complete vital signs, including blood pressure and pulse with the patient in the 

sitting (or standing) position if blood pressure is normal in the supine position. Assess 

peripheral perfusion (alertness; skin and extremity temperature). Gently examine the 

abdomen to find an obvious aortic aneurysm or the presence of an "acute" abdomen, ie, 

boardlike (involuntary) guarding. Perform a rectal examination, and check the stool for 

blood. A brief history may often be obtained simultaneously. (If there has been 

abdominal trauma, proceed as outlined in Chapter 25.) 

Caution: Patients with acute myocardial infarction, especially involving the inferior or 

posterior wall, may present with epigastric or upper abdominal pain. A carefully elicited 

history and an electrocardiogram (ECG) should be obtained, especially if no abdominal 

disorder is clearly identified. In addition, patients with diabetic ketoacidosis may present 

with severe abdominal pain and vomiting. 

Identify Candidates for Urgent Surgery 

If hypotension (supine or postural) without gastrointestinal bleeding, an aneurysm, or a 

rigid abdomen is present in the patient with abdominal pain, there is a strong possibility 

of underlying life-threatening disease requiring early surgical correction. The on-call 

surgeon and operating room personnel should be notified. 

Treat Shock 

Note: Persistent shock despite fluid resuscitation in the patient with acute abdominal 

pain requires urgent laparotomy. 

Treat hypotension or frank shock (Chapter 9). To reiterate— 

1. Insert 2 large-bore (= 16-gauge) intravenous catheters in an upper extremity. 

2. Obtain blood for complete blood count (CBC) with differential, serum electrolyte 

measurements, lipase determination, renal function tests, and a rapid bedside glucose 

determination. Send a tube of clotted blood for typing and cross-matching.

3. Immediately begin rapid infusion of crystalloid solution (eg, a balanced salt solution). 

Adjust the rate of infusion based on blood pressure; initially, give 1 L over 10-20 minutes 

(adult dose). 

4. Administer oxygen, 5-10 L/min, by nasal cannula or mask to keep oxygen saturation 

on pulse oximetry above 95%. 

5. Insert a urinary catheter to monitor urine output, which is a sensitive indicator of 

visceral blood flow. Send a urine sample for analysis and for pregnancy test in women 

of child-bearing age. 

6. Obtain arterial blood gas and pH measurements, because they are a useful guide to 

the patient's overall physiologic condition. 

7. Insert a nasogastric tube if the patient shows evidence of peritonitis, severe ileus, 

intestinal obstruction, or gastrointestinal bleeding. The tube should be inserted before 

other diagnostic measures are undertaken. 

8. Obtain a 12-lead ECG, and begin continuous cardiac monitoring. 

9. If bacterial peritonitis is suspected, begin antibiotics after appropriate cultures have 

been obtained (Table 13-1). 

Farber MS, Abrams JH: Abdominal emergencies: has anything changed? Antibiotics for 

the acute abdomen. Surg Clin North Am 1997;77:1396. [PMID: 9431346] 

FURTHER EVALUATION OF THE PATIENT WITH ABDOMINAL PAIN 

When vital functions have been normalized, reassess the patient as described below 

unless immediate surgery is required (Table 13-2). 

Pain is usually present in acute intra-abdominal disorders. Diagnosis depends on 

meticulous history taking and physical examination. The history is usually the most 

important diagnostic aid, though physical examination and laboratory and x-ray studies 

provide important confirmation data. In general, 85-90% of diagnoses may be based on 

history alone, whereas laboratory examination alone or physical examination alone 

accounts only for an additional 5-8% of diagnoses each. The physician's time should be 

allocated accordingly. 

Often it is impossible to diagnose abdominal pain definitively in the emergency 

department. If pain is significant, it is prudent to hospitalize the patient for observation 

and further diagnostic procedures. 

HISTORY 

If there is a history of abdominal trauma, the diagnostic approach differs from that for 

spontaneous abdominal pain and is discussed in Chapter 25. Pelvic pain in women is 

discussed in Chapter 36.

Mode of Onset of Abdominal Pain 

(See Figure 13-2 and Table 13-2.) 

A. Abrupt Onset 

If the patient was well one moment and seized with agonizing (explosive) pain the next, 

the most probable diagnosis is rupture of a hollow viscus or a vascular accident (eg, 

ruptured aortic aneurysm). In these instances, the pain is maximal or nearly maximal at 

time of onset. 

Pain that begins abruptly, is only moderately severe at first, and worsens rapidly 

suggests acute pancreatitis, mesenteric thrombosis, or small bowel strangulation. If 

pelvic pain is present, consider a possible ruptured ectopic pregnancy or ovarian follicle 

cyst (Chapter 36). 

B. Gradual Onset 

Gradual onset of slowly worsening pain is characteristic of peritoneal infection or 

inflammation. Patients with appendicitis or diverticulitis often report gradual onset of 

pain. 

Character of Pain 


A. Severe Pain 

Severe abdominal pain may be caused by several conditions including renal and biliary 

colic or vascular conditions such as myocardial infarction, rupture of an abdominal aortic 

aneurysm, or mesenteric ischemia. Other conditions associated with severe pain 

include acute pancreatitis, perforation of a hollow viscus, or peritonitis. 

B. Dull Pain 

Pain that is dull, vague, and poorly localized and does not require analgesia is also 

likely to have been gradual in onset. Such findings strongly suggest an inflammatory 

process or a low-grade infection. Appendicitis and diverticulitis are associated with this 

type of pain. 

C. Intermittent Pain with Cramps 

The clinical picture of intermittent pain with cramps is common in gastroenteritis. 

However, if the pain comes in regular cycles, rises in crescendo fashion, and then 

subsides to a pain-free interval, the most likely diagnosis is mechanical small bowel 

obstruction. Occasionally, this type of pain occurs in early subacute pancreatitis or in 

renal colic. 

D. Absence of Pain 

Occasionally, a patient presents with no abdominal pain but rather a sense of fullness 

and a feeling that a bowel movement would bring relief. A bowel movement, whether it 

is spontaneous or due to administration of cathartics or an enema, usually fails to 

relieve discomfort, however. This so-called gas stoppage sign is characteristic of 

retrocecal appendicitis but may be present when any inflammatory lesion is walled off

from the free peritoneal cavity. 

Location of Pain 

Generally, pain fibers within the abdominal cavity are confined to the visceral 

peritoneum, parietal peritoneum, and blood vessels. The parietal peritoneum is 

innervated by somatic nerve fibers and will therefore localize pain. Pain due to visceral 

peritoneal involvement alone is poorly localized. In conditions that do not involve the 

parietal peritoneum, the most common sources of pain are distention of a hollow viscus 

and visceral ischemia. These general principles are a useful guide to a systematic 

evaluation of the cause of abdominal pain. 

A. Localized Abdominal Pain 

(See Table 13-2.) In general, when abdominal pain becomes localized, it does so over 

or near the involved viscus, for example, epigastric or right upper quadrant pain of acute 

cholecystitis, or right lower quadrant pain of appendicitis. However, the physician must 

remember anatomic variants (eg, an inflamed retrocecal appendix produces flank pain 

or nonlocalizing abdominal pain) and must consider all structures that might cause pain 

(eg, vascular disease). 

B. Radiation of Pain or Shift in Localization 

Radiation of pain or shift in localization of pain has particular diagnostic significance. 

1. Shoulder pain—Shoulder pain may be due to ipsilateral diaphragmatic irritation from 

air, blood, or infection in the peritoneal cavity. For example, cholecystitis may be 

associated with referred right shoulder pain or even epigastric and left shoulder pain 

mimicking angina. 

2. Diffuse periumbilical and epigastric pain—Diffuse periumbilical and epigastric pain 

gradually localizing to the right lower quadrant is a classic sign of appendicitis. With 

early appendicitis, only the visceral peritoneum surrounding the appendix is involved in 

the inflammatory process, and localization is therefore poor. As inflammation spreads 

and involves the parietal peritoneum, pain then localizes to the right lower quadrant. If 

the appendix is retrocecal, however, as it is in 15% of cases, the parietal peritoneum is 

not involved, and then pain remains poorly localized. 

3. Pain radiating from the flank—Pain radiating from the flank to the groin or genitalia 

usually signifies ureteral colic, as seen in urolithiasis. 

Anorexia; Nausea & Vomiting 

Anorexia and nausea and vomiting occur more commonly in disease of the upper 

abdomen; however, advanced intra-abdominal disease may be present without any of 

these symptoms. If the peritoneum is well protected from infection or inflammation, as in 

retrocecal appendicitis or when the appendix is completely isolated by omentum, the 

patient may retain a normal appetite. 

If nausea and vomiting precede the onset of pain, an acute abdominal emergency 

requiring operation is unlikely. The most likely diagnoses are gastroenteritis and food

poisoning, acute gastritis, acute pancreatitis, and (much less frequently) common duct 

stone and high intestinal obstruction. In most acute surgical emergencies, nausea and 

vomiting are not dominant or early symptoms, although they may be present by the time 

the patient seeks medical attention. 

Severe vomiting with retching—particularly after a dietary indiscretion or an alcoholic 

bout—followed by abdominal pain with or without hematemesis should immediately 

suggest mucosal laceration of the gastroesophageal junction (Mallory-Weiss syndrome) 

or an esophageal perforation (Boerhaave syndrome). Massive hematemesis or severe 

pain radiating into the chest and left shoulder in association with severe vomiting and 

retching are classic symptoms of Boerhaave syndrome. The presence of pleural fluid on 

chest x-ray further supports the diagnosis. 

Fever & Rigors 

Fever is common with most causes of acute abdominal pain. In appendicitis, the 

temperature is usually not high, and rigors (shaking chills) are uncommon. High fever or 

rigors in suspected appendicitis strongly suggest diffuse peritonitis from perforation of a 

viscus, pylephlebitis (septic thrombophlebitis of the portal vein), or another disorder 

entirely (eg, pyelonephritis). High fever with peritoneal signs in a female patient with no 

apparent general systemic illness is characteristic of acute salpingitis with pelvic 

peritonitis. Repeated shaking chills and fever are most common in infections of the 

biliary or urinary tract. Patients with acute cholangitis or acute pyelonephritis usually 

present with intermittent rigors and fever. Chills, fever, rigors, jaundice, and hypotension 

suggest suppurative cholangitis, which is a surgical emergency. 

Diarrhea, Constipation, & Obstipation 

Diarrhea, constipation, and obstipation may occur in the acute abdomen patient but are 

not often major symptoms in acute intra-abdominal disease requiring surgery. Colitis 

(vascular or some other kind) usually is associated with early and severe diarrhea. 

Occasionally, patients with diverticulitis, appendicitis, or salpingitis may also experience 

diarrhea. 

PHYSICAL EXAMINATION 

The basic steps of the physical examination of the acute abdomen are outlined in Table 

13-3. Remember that physical findings may be subtle in elderly or immunocompromised 

patients. 

Inspection 

The physician should first inspect the abdomen and look for striking features such as 

the scaphoid, contracted abdomen of an early perforated viscus; the visible peristalsis 

and distention of mechanical obstruction; or the soft, doughy distention of early ileus. 

Auscultation 

A silent abdomen, with complete absence of audible peristalsis, usually signifies diffuse

peritonitis; however, peristalsis may persist in the face of established peritonitis. Other 

manifestations of diffuse peritonitis such as rigidity and distention are usually also 

present. It may be necessary to listen for as long as 2-3 minutes to establish absence of 

peristalsis, because peristalsis diminishes if the patient has not eaten. 

High-pitched, tinkling bowel sounds are suggestive of acute small bowel obstruction. 

There may also be intermittent peristaltic rushes that coincide with the onset of pain. 

These findings will usually be associated with abdominal distention. 

In gastroenteritis, dysentery, and active ulcerative colitis, there may be abnormal 

high-pitched peristalsis with rushes that are not synchronous with the episodes of pain. 

Palpation 

A. Examine Hernial Rings and Male Genitalia 

Examine the inguinal and femoral canals in both sexes and the genitalia in the male, 

and look for incarcerated hernias that may be causing intestinal obstruction. This must 

be done by asking the patient to cough but should be done gently so as to cause as little 

discomfort as possible. 

B. Elicit Cough Tenderness 

In most acute inflammatory conditions arising within the abdomen, coughing elicits pain 

in the involved area. Directing the patient to point one finger to the area of pain provides 

objective localization of the lesion. With this information, the examiner can proceed to 

examine the abdomen and deliberately examine last the area now known to be most 

tender. 

C. Feel for Spasm of Rectus Abdominis Muscle 

The next step is to establish the presence or absence of true muscle spasm by placing 

a hand gently over the rectus abdominis muscle and depressing it slightly and gently 

without causing pain. The patient is asked to take a long, slow breath. If the spasm is 

voluntary, the muscle will immediately relax underneath the gentle pressure of the 

palpating hand. If there is true spasm, however, the muscle will remain taut and rigid 

through the respiratory cycle. This maneuver alone may be sufficient to establish the 

presence of peritonitis. 

Except for rare neurologic disorders, renal colic, or rectus muscle injury, only peritoneal 

inflammation produces abdominal muscle rigidity (for reasons not understood). In renal 

colic, the spasm is confined to the entire rectus muscle on the involved side. This 

distinction is important, because marked rigidity of the entire length of one rectus 

muscle with relaxation of the opposite rectus cannot occur in peritonitis, because the 

peritoneal cavity is not compartmentalized. It is possible to have segmental spasm of a 

rectus muscle involving only the upper or lower portion of one side, or to have 

segmental spasm of both rectus muscles in upper or lower abdominal peritonitis. In 

generalized peritonitis, however, both muscles are usually involved to the same degree. 

D. Perform One-Finger Palpation 

Abdominal tenderness must be assessed with one finger, because it is impossible to 

localize peritoneal inflammation accurately if palpation or tenderness is done with the

entire hand. Careful one-finger palpation, beginning as far away as possible from the 

area of tenderness elicited by coughing and gradually working toward it, will usually 

enable the examiner to delineate the area of abdominal tenderness precisely. In early 

acute appendicitis, this area is often no larger than 3 cm (1 3/16 in) in diameter and 

sometimes smaller. Diffuse abdominal tenderness without associated involuntary rigidity 

of the muscles suggests gastroenteritis or some other inflammatory process of the 

intestines without peritonitis. 

Do not test for peritoneal inflammation by looking for classic rebound tenderness (deep 

palpation of the abdomen with abrupt release). This maneuver yields no additional 

information and is so painful in patients with significant abdominal tenderness that 

further examination may be impossible. 

E. Look for Costovertebral Angle Tenderness 

Palpation should be followed by gentle percussion of the costovertebral angles. This will 

cause pain in individuals with pyelonephritis, retroperitoneal abscesses, and retrocecal 

appendix. Avoid excessively vigorous percussion, because it is not helpful in localizing 

tenderness and the pain it causes will make further examination difficult. 

F. Perform Deep Palpation 

Having established the presence or absence of muscular rigidity and localized the area 

of tenderness, the examiner now palpates more deeply for the presence of abdominal 

masses. Often, it is difficult to perform a reliable physical examination of the abdomen in 

an anxious patient. Some patients are so anxious that they begin to guard with voluntary 

contraction of the abdominal musculature before the examiner performs even light 

palpation. This barrier to palpation can occasionally be overcome by palpating with a 

stethoscope while auscultating bowel sounds. 

Among the more common lesions identifiable by careful palpation in patients with acute 

abdominal pain are the distended, tender gallbladder found in acute cholecystitis; the 

right lower quadrant tender mass of appendicitis with early abscess formation; the left 

lower quadrant mass of sigmoid diverticulitis; and the midline pulsatile mass indicating a 

leaking abdominal aneurysm. 

Percussion 

In free perforation of a hollow viscus with air under the diaphragm, there may be 

diminished or absent liver dullness. Tympany located laterally in the midaxillary line, 5 

cm (2 in) or more above the costal margin, is due to free air; tympany located anteriorly 

over the liver may be due to air in distended loops of bowel. 

Special Signs 

Several maneuvers in physical examination may help localize an acute abdominal 

lesion. 

A. Iliopsoas Sign 

(See Figure 13-3. ) The patient flexes the thigh against the resistance of the examiner's 

hand. A painful response indicates an inflammatory process involving the psoas muscle.

B. Obturator Sign 

(See Figure 13-4. ) The patient's thigh is flexed to a right angle and gently rotated, first 

internally and then externally. If pain is elicited, an inflammatory lesion involving the 

obturator internus muscle (pelvic appendicitis, diverticulitis, pelvic inflammatory disease) 

is present. 

C. Murphy's Sign (Inspiratory Arrest) 

The patient is asked to take a slow, deep breath as the examiner gently palpates the 

right upper quadrant. With descent of the diaphragm with the liver and gallbladder, an 

acutely inflamed gallbladder comes in contact with the examining fingers, causing pain, 

and the patient stops inspiration in an attempt to avoid the pain. 

Pelvic & Rectal Examination 

The importance of pelvic and rectal examination cannot be overstressed. In men a 

rectal examination plus simultaneous lower abdominal palpation with the other hand 

often reveals masses or localized pain not disclosed by abdominal examination alone. 

Likewise, pelvic examination in women provides essential information not revealed by 

other maneuvers. Evaluation of lower abdominal pain in women is discussed further in 

Chapter 36. 

Examination of stool for occult blood must be performed in every patient with abdominal 

pain. Occult blood may result from intestinal tumors (possibly causing intestinal 

obstruction), inflammatory bowel disease, and ischemic bowel disease. 

LABORATORY EXAMINATION 

CBC with differential, lipase measurements, and urinalysis are called for in most cases. 

Electrolyte determinations and tests of renal function should be obtained if vomiting, 

diarrhea, hypotension, or shock are present or if there is a strong chance that surgery 

will be performed. 

Blood Count 

The hematocrit reflects changes both in plasma volume and in red cell volume. It is 

most useful diagnostically if it is markedly elevated (indicating dehydration) or 

depressed (indicating anemia). Additionally, the hematocrit should be corrected toward 

normal values (between 30% and 45% is usually satisfactory) in preparation for surgery 

in hemodynamically unstable patients. 

The white cell count may be helpful if it is significantly elevated. However, normal or 

even low counts can occur in established peritonitis or sepsis (although usually with a 

marked shift to the left), and elevated counts may occur in gastroenteritis. A normal or 

low white count, particularly with lymphocytosis, may suggest viral infection. A 

progressively rising white count is of considerable diagnostic value and usually indicates 

progression of an inflammatory or septic process. A shift to the left on a blood smear 

may be a clue to an inflammatory reaction in the presence of a normal or only 

moderately elevated white count.

Serum Amylase & Lipase 

Serum amylase and lipase levels require cautious evaluation. Patients with abdominal 

pain and elevated serum amylase or lipase usually have acute pancreatitis. However, 

some patients with severe hemorrhagic pancreatitis have normal or low serum amylase, 

and patients with persistent or chronic pancreatitis often have normal serum amylase 

levels. In the presence of pancreatic pseudocysts, however, serum amylase often 

remains elevated. 

Serum amylase may be elevated in mesenteric arterial thrombosis, intestinal 

obstruction, or perforated duodenal ulcer and occasionally in other conditions. It is also 

elevated in macroamylasemia, a common benign condition in which urinary amylase 

clearance is markedly reduced as a result of complex formation with other serum 

proteins. 

Lipase is a more specific marker for pancreatitis because it is found only in the 

pancreas. Vissers et al. (1999) have suggested using lipase as the more accurate 

screening test for patients with suspected pancreatitis and that there is no clinical utility 

to obtaining both amylase and lipase in the emergency department. In emergency 

department patients with abdominal pain, lipase sensitivity (100%) was better than 

amylase sensitivity (72%) for the diagnosis of pancreatitis. In addition, for patients with 

radiographically proven alcoholic pancreatitis, the sensitivity of lipase was superior to 

amylase (100% vs. 55%, respectively). Unfortunately, the degree to which either marker 

is elevated cannot predict the severity of the condition or any associated complications 

of pancreatitis. 

Vissers RJ, Abu-Labari RB, McHugh DF: Amylase and lipase in the emergency 

department evaluation of acute pancreatitis. J Emerg Med 1999;17(6):1027. [PMID: 

10595892] (Review.) 

Hepatic Function Tests 

Hepatic function testing is indicated for patients who have right upper quadrant pain or 

tenderness, jaundice, acholic stools, or tea-colored urine and for patients in whom 

hepatitis is a concern. 

Urine 

Urinalysis (including microscopic examination of the sediment) is critical in ruling out 

urinary tract infection, urolithiasis, and diabetes. Hematuria strongly suggests 

urolithiasis. Rarely, however, urolithiasis with complete obstruction of the ureter may be 

associated with normal results on urinalysis. Low urine specific gravity associated with 

severe vomiting may be the earliest clue to renal disease. Obtain a urine pregnancy test 

in all women of child-bearing age. 

Serum Electrolytes & Tests of Renal Function 

Serum electrolyte determinations and a test of renal function (blood urea nitrogen,

serum creatinine, or both) are required to document the nature and extent of fluid losses 

if vomiting or diarrhea has been significant or if the illness has lasted for more than 48 

hours with diminished oral intake. Abnormalities should be corrected as much as 

possible in preparation for surgery (Chapter 42). 

Pregnancy Test 

A urine pregnancy test should be obtained in all women of child-bearing age unless 

pregnancy is physically impossible (eg, complete hysterectomy, bilateral 

oophorectomy). Women with a history of pelvic infection, current intrauterine device use, 

prior ectopic pregnancy, and failed tubal ligation are at increased risk for ectopic 

pregnancy. 

Electrocardiogram 

A 12-lead ECG should be obtained in patients with epigastric or upper abdominal pain in 

whom no clear cause of the pain is identified and cardiac ischemia is a possibility. 

Peritoneal Fluid 

In peritoneal dialysis or chronic liver disease patients, examination of the peritoneal fluid 

is often warranted if abdominal pain, tenderness, or fever are present. 

RADIOLOGIC EXAMINATION 

Radiologic examination may provide important evidence for diagnosis of acute 

abdominal disease. Close cooperation between the radiologist and the physician caring 

for the patient is essential. 

Suggested Studies 

Abdominal radiographs are most helpful in the evaluation of patients with suspected 

bowel obstruction or hollow viscus perforation and in children or mentally handicapped 

adults with possible foreign body ingestion. An acute abdominal series consists of three 

films: an upright anteroposterior chest x-ray, a supine anteroposterior abdominal x-ray, 

and an upright or left lateral decubitus abdominal x-ray. To maximize the diagnostic 

utility and limit unnecessary abdominal x-rays, Bohner suggests limiting these studies to 

patients with two or more of the following findings: prior abdominal surgery, increased 

bowel sounds, abdominal distention, peritoneal signs, history of constipation or 

vomiting, and age over 50 years. 

Interpretation 

When the films are reviewed, the following questions should be asked: (1) Are the 

outlines of the liver, spleen, kidneys, and psoas muscles clearly defined? (2) Are the 

peritoneal fat lines identifiable? (3) Is the gas pattern in the stomach, small bowel, and 

colon within normal limits? (4) Is there evidence of air outside the bowel or beneath the 

diaphragm? (5) Is there air in the biliary ducts and ductules? (6) Are there abnormal 

opaque shadows such as gallstones; ureteral stones; fecaliths; or calcification in lymph

nodes, pancreas, aorta, or other soft tissue masses? 

On the basis of these observations, the following important pieces of evidence may be 

obtained: 

A. Psoas Shadow 

Obliteration of the psoas shadow may indicate a retroperitoneal hematoma or abscess 


B. Gas Patterns 

Gas patterns are of particular importance. Dilated loops of small bowel with air-fluid 

levels and no gas in the colon are indicative of small bowel obstruction (Figure 13-6). 

C. Cecum 

Marked dilatation and rotation of the cecum or sigmoid are typical of volvulus. 

D. Dilatations 

Marked dilatation of the entire colon suggests colonic obstruction. Massive dilatation of 

the colon in acute colitis indicates toxic megacolon. Distention of both the small and the 

large bowel is characteristic of ileus, peritonitis, and pseudo-obstruction of the bowel 

(Figure 13-7). The differentiation between distended small and large bowel may at times 

be difficult. In advanced cases, the clinical signs may be more reliable than x-rays in the 

differentiation between intestinal obstruction and peritonitis. 

E. Air in Abnormal Locations 

Except following laparotomy, laparoscopy, or recent percutaneous gastrotomy tube 

placement, free air under the diaphragm usually indicates a perforated viscus, most 

commonly seen in perforated duodenal or gastric ulcer (Figure 13-8). Massive amounts 

of air beneath the diaphragm suggest colonic perforation. An encapsulated air shadow 

outside the contours of small or large bowel may indicate localized perforation of the 

intestine. Air in the biliary tract is diagnostic of a free communication between some 

portion of the gastrointestinal tract and the biliary tree. If evidence of intestinal 

obstruction is present, this pattern is characteristic of gallstone ileus. Air in the portal 

venous system indicates pylephlebitis with a gas-forming organism but also occurs in 

pneumatosis cystoides intestinalis and has been described following the introduction of 

hydrogen peroxide into the rectum. Rarely, free air in the peritoneum may be seen in 

asymptomatic or minimally symptomatic women with no signs of apparent underlying 

disease. The free air has presumably entered the peritoneum from the genital tract. 

F. Calcifications and Opacities 

X-rays of the abdomen may establish the presence of gallstones, ureteral stones, 

pancreatic calcification, retroperitoneal calcification, and vascular calcification. Such 

findings must be carefully correlated with the history and physical examination to 

establish their significance. 

Special Studies 

(See Table 13-4. ) Special x-ray contrast studies, ultrasonography, or computed 

tomography (CT) scans may be helpful.

A. Barium Enema 

Avoid barium enema if possible in the presence of acute abdominal disease and 

peritonitis. In rare cases, a water-soluble contrast enema is necessary to establish a 

diagnosis of sigmoid volvulus or a low, partial colonic obstruction due to carcinoma. 

B. Ultrasonography 

Ultrasonography is a useful technique for evaluating the gallbladder, biliary ducts, 

pancreas, appendix, kidneys, and abdominal aorta. It is probably the best single 

diagnostic test for evaluating patients with right upper quadrant pain (see Table 13-4). 

C. CT Scan 

The CT scan of the abdomen with oral and intravenous contrast is frequently obtained 

to gain information about not only the solid organs and retroperitoneal structures but 

also the hollow organs of the abdomen. Abdominal CT scanning has taken a prominent 

role in the evaluation of many patients with right lower quadrant pain and suspected 

appendicitis. 

D. Angiograms 

Angiograms are used less frequently than before in trauma, because CT scan has been 

found to be more useful in cases of rupture of a solid viscus such as the spleen or 

kidney. Mesenteric angiography is the best way to identify the site of bleeding in 

massive lower gastrointestinal tract hemorrhage, although radionuclide blood pool 

scans are more sensitive in intermittent or less severe hemorrhage (Chapter 14). 

ADDITIONAL MEASURES FOR THE MANAGEMENT OF ACUTE 

ABDOMEN 

Repeated Examination 

When the diagnosis is in doubt and the patient is not critically ill, a period of active 

observation is in order. Frequent inquiries about progression or alteration of symptoms 

combined with repeated, gentle examinations of the abdomen and, occasionally, repeat 

laboratory tests will avoid many unnecessary operations without risking dangerous 

delays. If the physician feels that a diagnosis cannot be made within 6-12 hours, the 

patient should be hospitalized for observation. Observation in the emergency 

department for more than 4-6 hours is unwarranted for reasons of patient comfort, 

quality of care, and cost. Even in the absence of a tentative diagnosis, hospitalization is 

indicated for patients with severe pain and abdominal tenderness or peritoneal signs 

and for those with laboratory test abnormalities suggesting significant disease. 

Relief of Pain 

Although some surgical consultants may still oppose the administration of narcotics until 

a definitive diagnosis or plan for laparotomy has been established, parenteral narcotic 

analgesics should be given at once to relieve severe pain. Evaluation of acute 

abdominal disease can be performed more accurately after severe pain is relieved and 

the patient can cooperate. In addition, studies have demonstrated no adverse effects on

the ability to diagnose acute surgical conditions when patients with an acute abdomen 

receive narcotics. What at first appears to be diffuse tenderness may become better 

localized. Abdominal masses not palpable initially often become obvious after moderate 

sedation and relief of pain. 

Antimicrobials 

Antimicrobial agents should be withheld until the diagnosis is at least tentatively 

established, except in the presence of obvious signs of systemic infection (high fever, 

rigors, hypotension). In obscure cases, antibiotic therapy may mask progression of 

disease and lead to serious complications with increased illness (eg, appendicitis). 

Surgical Consultation 

Early surgical consultation is helpful for both the patient and the surgeon. Because the 

surgeon, like the emergency physician, must rely on repeated examinations for 

diagnosis, the earlier observation begins, the faster a definitive diagnosis can be made. 

Furthermore, delays in consultation may allow worsening of the condition, with possible 

disastrous sequelae. 

Cook C, Campbell-Smith TA, Hopkins R: The abdominal radiograph: a pictorial review. 

Hosp Med 2002;63:726. [PMID: 12512199] 

Thomas SH et al: Effects of morphine analgesia in diagnostic accuracy in emergency 

department patients with abdominal pain: a prospective, randomized trial. J Am Coll 

Surg 2003;196:18. [PMID: 12517545] 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING ABDOMINAL 

PAIN 

INTESTINAL DISORDERS 

1. Appendicitis 


The initial symptom is poorly localized abdominal pain around the umbilicus or 

epigastrium, rarely in the right lower quadrant over McBurney's point. Later, the pain 

shifts from the periumbilical region to the right lower quadrant. Anorexia and nausea and 

vomiting usually accompany the illness. Localized abdominal tenderness and guarding 

are noted on physical examination. Fever is low grade, and the white count may be 

moderately elevated. Variations from the classic clinical picture are common, especially 

in retrocecal appendicitis, where the pain commonly remains poorly localized. 

Abdominal CT with intravenous and water-soluble oral contrast has become a widely 

accepted tool in the evaluation of patients with possible appendicitis (see Figure 13-8). 

The sensitivity and specificity of abdominal CT scan in the evaluation of appendicitis are 

90-100% and 91-99%, respectively. In addition, when appendicitis is not present, the CT 

scan demonstrates an alternative diagnosis two thirds of the time. Ultrasonography of 

the appendix may be helpful if the diagnosis is uncertain.


The patient should be hospitalized and prepared for surgery within a few hours. 

Administer intravenous crystalloid solution to replace any volume deficits. Antimicrobial 

therapy generally is not used until the decision is made to operate. 

Paulson EK, Kalady MF, Pappas TN: Clinical practice. Suspected appendicitis. N Engl J 

Med 2003;348:236. [PMID: 12529465] (Review.) 

2. Intestinal Obstruction 


The patient usually complains of intermittent colicky abdominal pain of sudden onset 

that rises to a peak and then subsides. Bowel habits may be altered. Vomiting may 

occur and will be feculent if obstruction is distal and long-standing. The abdomen is 

distended and tender, and peristaltic rushes as well as high-pitched tinkling may be 

heard. Dilated loops of bowel with air-fluid levels on abdominal x-ray confirm the 

diagnosis (see Figure 13-6). Differentiation between small and large bowel is often 

based on the mucosal patterns demonstrated on the abdominal radiograph. In the small 

intestine, the valvulae conniventes cross the width of the lumen, and in the large 

intestine the haustra do not cross the entire width of the lumen. Occasionally, x-ray 

findings are absent, and the diagnosis is based on clinical suspicion or abdominal CT 

scan with contrast. 


Nasogastric suction and intravenous hydration should be initiated and the patient 

hospitalized for evaluation and possible surgery. Some cases resolve without surgery. 

3. Perforated Peptic Ulcer 


Perforation of a duodenal ulcer usually causes sudden severe upper abdominal pain. 

The pain of perforation subsides when gastric contents are diluted by peritoneal 

secretions but reappears later, with progressive worsening. Shoulder pain may occur 

owing to diaphragmatic irritation. The patient is usually in severe distress, with shallow 

breathing and knees drawn up to the chest in an effort to minimize pain. Upper 

abdominal tenderness is accompanied by boardlike rigidity of the abdomen. X-ray with 

the patient upright may show air under the diaphragm (Figure 13-9). When abdominal 

radiographs are nondiagnostic and perforation is suspected, abdominal CT scan with 

intravenous and water-soluble oral contrast can be diagnostic. 


Insert a nasogastric tube for drainage of gastric acid. Administer crystalloid solution 

intravenously to correct volume depletion. Initiate broad-spectrum intravenous

antibiotics. Immediate hospitalization for surgery is necessary. 

4. Perforation of the Bowel 


Perforation of the bowel is accompanied by sudden or explosive onset of severe, 

agonizing mid or lower abdominal pain. Shock may be present and can be profound. 

Nausea and vomiting are common. The abdomen is rigid and tender. The temperature 

may be high and is accompanied by leukocytosis. A history of diverticulitis can often be 

elicited. 


Treat shock with intravenous crystalloid solution. Insert a nasogastric tube for 

continuous gastric suction. Obtain blood and urine cultures. Begin antimicrobials (see 

Table 13-1). Hospitalize the patient, and prepare for surgery within 1-2 hours. 

Jamieson GG: Current status of indications for surgery in peptic ulcer disease. World J 

Surg 2000;24:256. [PMID: 10658057] (Review.) 

Svanes C: Trends in perforated peptic ulcer: incidence, etiology, treatment, and 

prognosis. World J Surg 2000;24:277. [PMID: 10658061] (Review.) 

5. Diverticulitis 


Diverticulitis is associated with lower abdominal pain that is usually gradual in onset and 

localized, predominantly in the left lower quadrant, but that may be midabdominal or in 

the right lower quadrant. A history of diverticulosis may be present. Fever is low grade, 

accompanied by slight leukocytosis. Other findings may include abdominal tenderness, 

a palpable abdominal mass, and alterations in bowel function (either constipation or 

frequent defecation). 


Most patients should be hospitalized for administration of intravenous fluids and 

antimicrobial drugs (see Table 13-1) and further observation. Patients without significant 

nausea or vomiting, fever, or other systemic signs of infection or any peritoneal signs 

may be candidates for outpatient treatment with oral antibiotics as long as the patient is 

reliable. Instructions should include a clear liquid diet initially and to return if vomiting, 

worsening pain, or fever develop. 

6. Intestinal Strangulation 


Intestinal strangulation occurs most frequently in volvulus or femoral hernia and

occasionally in inguinal hernia. Onset of pain is usually rapid. Pain increases in severity 

and may be intermittent and colicky. The patient may complain of an urge to defecate. 

The abdomen is distended, rigid, and diffusely tender. Exquisite tenderness is present in 

the region of strangulation. Shock appears early. Other findings usually include nausea 

and vomiting, high fever, and leukocytosis. In the case of volvulus, findings on 

abdominal x-ray may be diagnostic. 


The patient should be hospitalized and prepared for surgery within 1 hour. 

7. Gastroenteritis (See also Chapter 15.) 


The patient complains of mild to severe cramping and pain that may have come on 

gradually or abruptly. There may be nausea and vomiting, retching, and diarrhea, in any 

combination. These symptoms usually precede the onset of pain, in contrast to 

conditions requiring surgery, in which pain is usually the first symptom. Abdominal 

examination reveals generalized discomfort. In contrast to situations requiring surgery, 

involuntary guarding, localized tenderness, and peritoneal signs (eg, cough tenderness) 

are absent. Fever is generally absent or mild, although patients with shigellosis typically 

have high fever and rigors. The patient may be dehydrated. Stool should be tested for 

blood, examined microscopically for leukocytes, and sent for culture if the patient has 

prolonged or severe diarrhea associated with fever. 


Severely ill or dehydrated patients should be hospitalized. Mild to moderately ill patients 

can be sent home with instructions for rehydration. If symptoms persist or worsen, 

patients should receive follow-up evaluation. Bismuth subsalicylate (Pepto-Bismol, 

many others) may be used for symptomatic relief. Opiate-containing antidiarrheal 

agents (diphenoxylate with atropine [Lomotil, many others]) should be used, with 

caution, only in patients with mild diarrhea without evidence of dysentery. See Chapter 

15 for details. 

8. Idiopathic Inflammatory Bowel Disease 


The patient complains of abdominal cramps and intermittent bloody diarrhea and usually 

gives a history of previous episodes of the same symptoms. A long history of colitis may 

be present. Weight loss, fever, and anemia may be present. Cramps may come on 

gradually or suddenly. The abdomen is slightly tender. Infectious causes of colitis (eg, 

Shigella, Clostridium difficile, Campylobacter, Entamoeba histolytica) should be 

systematically ruled out. 

Treatment & Disposition

A. For the Seriously Ill Patient or for Uncertain Diagnosis 

Treat hypotension or shock with administration of intravenous crystalloid solution. Give 

nothing by mouth; nasogastric suction may be helpful if the patient is vomiting. 

Abdominal radiographs or CT scan may provide important information about possible 

complications of inflammatory bowel disease such as perforation, bowel obstruction, or 

intraperitoneal abscess. Hospitalize the patient for definitive diagnosis and treatment. 

Indications for hospitalization are uncertain diagnosis, shock, fever, toxic megacolon, 

anemia, or gross blood in the stool. 

B. For the Ambulatory Patient with Certain Diagnosis 

For patients under the care of a gastroenterologist, discuss the options with the patient's 

physician regarding outpatient treatment with oral antibiotics, steroids, and other 

anti-inflammatory medications such as sulfasalazine. 

Berg DF et al: Acute surgical emergencies in inflammatory bowel disease. Am J Surg 

2002;184:45. [PMID: 12135718] (Review.) 

Ferrell RJ, Peppercom MA: Ulcerative colitis. Lancet 2002;359: 331. [PMID: 11830216] 

(Review.) 

Marteau P: Inflammatory bowel disease. Endoscopy 2002;34:63. [PMID: 11778131] 

(Review.) 

HEPATOBILIARY DISORDERS 

1. Biliary Colic 


Biliary colic is due to intermittent obstruction of the biliary tree by stones, usually at the 

cystic duct. The pain occurs in discrete episodes (frequently after ingestion of food), 

which usually begin abruptly and subside gradually. During an attack, steady upper 

abdominal pain extends all the way across the abdomen but is more severe on the right. 

Pain may be referred to the scapula. A careful history often reveals prior attacks of 

similar pain. Abdominal examination shows right upper quadrant tenderness and, 

occasionally, a palpable gallbladder. A right upper quadrant sonogram is diagnostic and 

shows gallstones or a dilated gallbladder and cystic duct. Dilation of the common bile 

duct is commonly seen with choledocholithiasis. 

Treatment 

In the absence of acute cholecystitis, ascending cholangitis, choledocholithiasis, or 

pancreatitis, no specific emergency treatment is necessary. Provide adequate 

analgesia. 

Disposition 

Refer the patient for possible elective cholecystectomy. Outpatient treatment involves 

controlling the symptoms with oral analgesics and possibly antiemetics.

2. Acute Cholecystitis 


Acute cholecystitis is characterized by acute right upper quadrant pain and tenderness 

that may be referred to the right scapula. A history of similar episodes may be present. 

The discomfort may be moderate to severe and prostrating. Anorexia and nausea and 

vomiting usually occur also. Low-grade fever and leukocytosis are usually present. In 

some cases, the gallbladder is palpable. Elderly patients with acute cholecystitis are 

more likely than younger patients to have few localized right upper quadrant signs and 

symptoms. 

Ultrasonography of the abdomen demonstrating gallstones, dilatation of the intra- or 

extrahepatic bile ducts or thickening of the gallbladder wall, and pericholecystic fluid (if 

present) confirms the diagnosis. Ultrasonography is the preferred diagnostic technique, 

because it is sensitive, specific, rapid, inexpensive, and without adverse effects. A 

sonographic Murphy's sign, specific tenderness of the gallbladder noted during the 

ultrasound exam, has a sensitivity of 88% and a specificity of 80% for acute 

cholecystitis. Nonvisualization on nuclear imaging (HIDA) of the biliary tract is also 

diagnostic and remains the gold standard for acute cholecystitis. 

Treatment 

Give analgesics intravenously or intramuscularly. Insert a nasogastric tube and attach it 

to continuous suction if the patient is vomiting. Give crystalloid solution (lactated 

Ringer's injection or equivalent) intravenously if the patient is dehydrated. Administer 

empiric antibiotics if the patient has systemic signs of infection such as fever. A 

second-generation cephalosporin such as cefuroxime, 1.5 g every 8 hours, and 

metronidazole, 500 mg every 8 hours, are recommended. Give nothing by mouth. 

Disposition 

Hospitalize patients with cholecystitis, and obtain immediate surgical consultation. 

Indar AA, Beckingham IJ: Acute cholecystitis. Br Med J 2002; 325:639. [PMID: 

12242178] (Review.) 

Trowbridge RL, Rutkowski NK, Shojania KG: Does this patient have acute cholecystitis? 

JAMA 2003;289:80. [PMID: 12503981] (Review.) 

3. Acute Suppurative Cholangitis 


Acute suppurative cholangitis is a surgical emergency commonly accompanied by 

bacteremia and septic shock. Symptoms are abdominal pain, jaundice, fever and chills, 

mental confusion, and shock. Because of the overwhelming suppurative process, the 

biliary obstruction may not be apparent, and the diagnosis is sometimes missed. Right

upper quadrant sonography is the diagnostic procedure of choice and shows dilated, 

obstructed intrahepatic biliary ducts. Bile and blood cultures are often positive for 

aerobic organisms such as Escherichia coli, Klebsiella, enterococcus, Enterobacter, 

Pseudomonas, Serratia, and Proteus species. The most common anaerobe is 

Bacteroide fragilis. 

Treatment 

Treat shock with infusion of intravenous crystalloid solution. Insert a nasogastric tube 

and connect it to a continuous suction device if the patient is vomiting. Insert a Foley 

catheter to monitor urine output. 

Administer antimicrobials: classical treatment of cholangitis has included an 

aminoglycoside, a penicillin, and metronidazole. Less nephrotoxic regimens include 

monotherapy with imipenem, mezlocillin, ciprofloxacin, or ampicillin-sulbactam. 

In the case of acute cholecystitis complicated by choledocholithiasis, endoscopic 

retrograde cholangiopancreatography can retrieve obstructed stones to decompress the 

common bile duct. 

Disposition 

Hospitalize the patient, and prepare for surgery or endoscopic papillotomy within 1-2 

hours. 

Ahmed A, Cheung RC, Keeffe EB: Management of gallstones and their complications. 

Am Fam Physician 2000;61:1673. [PMID: 10750875] (Review.) 

Lillemoe KD: Surgical treatment of biliary tract infections. Am Surg 2000;66:138. [PMID: 

10695743] (Review.) 

4. Hepatic Abscess 


When liver abscess results from other intra-abdominal infections, increasing toxicity, 

high fever, jaundice, and a deteriorating clinical picture are seen. Right upper quadrant 

pain may be present. In primary liver abscess (eg, caused by Entamoeba histolytica), 

the onset is insidious, and it may be several weeks before the disease becomes 

fulminant. High fever and leukocytosis often accompany the abscess, and rigors occur 

in approximately one fourth of patients. The liver becomes enlarged and is often tender. 

Right upper quadrant sonography, CT scan, or liver scan is diagnostic. Obtain blood for 

culture and amebic serologic tests. Many patients with amebic liver abscesses do not 

have intestinal amebiasis; hence, stool examination for parasites is not helpful. 


Hospitalize the patient immediately for evaluation and treatment. Empiric antimicrobial 

therapy must be active against amebas, anaerobes, and coliform bacteria. CT-guided

aspiration can assist in diagnosis. Empiric antibiotics should include an aminoglycoside, 

a penicillin, and metronidazole. In elderly patients or those with impaired renal function, 

a third-generation cephalosporin can be substituted for the aminoglycoside. 

Metronidazole alone (800 mg 3 times a day for 5 days) will resolve 95% of 

uncomplicated amebic abscesses. 

Krige JE, Beckingham IJ: ABC of diseases of the liver, pancreas, and biliary system, 

liver abscesses and hydatid disease. Br Med J 2001;322:537. [PMID: 11230072] 

5. Hepatitis 


Hepatitis is manifested by anorexia, nausea and vomiting, malaise, symptoms of upper 

respiratory tract infection or flulike syndrome, and bilirubinuria. Fever, jaundice, and an 

enlarged, tender liver are usually present. The white cell count is low or normal, and 

liver function tests show elevated bilirubin and hepatic enzymes (AST [SGOT], ALT 

[SGPT], and alkaline phosphatase). 

The most common causes are viral infection (hepatitis viruses, yellow fever, 

cytomegalovirus, Epstein-Barr virus) and alcohol. Alcoholic hepatitis can often be 

distinguished from viral hepatitis by the history and physical examination (evidence of 

alcohol abuse) and by AST and ALT levels (usually < 100 IU/L in alcoholic hepatitis). In 

alcoholic hepatitis, AST (SGOT) levels are the same or higher than ALT (SGPT) levels; 

in viral hepatitis, the situation is reversed. 


Severely ill patients with persistent vomiting, dehydration, hypoglycemia, hepatic 

encephalopathy, or significant coagulopathy (prothrombin time > 15 seconds) should be 

hospitalized. Other patients can be referred to a primary care physician and receive 

treatment at home. The patient should be instructed to maintain hydration and strict 

hygiene and to avoid potential hepatotoxins (alcohol). Patients with viral hepatitis must 

avoid handling food that will be consumed by others. Tests that help in specific 

diagnosis (eg, HBsAg and hepatitis A IgM antibody) can be obtained in the emergency 

department if the physician so chooses. Close family contacts should be advised 

regarding appropriate immunizations if hepatitis viruses are suspected. 

Bondesson JD, Saperston AR: Hepatitis. Emerg Med Clin North Am 1996;14(4):695. 

[PMID: 8921765] (Review.) 

VASCULAR DISORDERS 

1. Ruptured Aortic Aneurysm 


Rupture of an abdominal aneurysm is accompanied by severe abdominal pain of 

sudden onset that may radiate into the back. In some patients, pain is confined to the

flank, low back, or groin. Faintness or syncope may occur as a result of blood loss. After 

the first hemorrhage, pain may lessen and faintness may disappear, but these 

symptoms recur and progress until shock finally supervenes. While dissection is 

occurring, a discrete pulsatile mass can be palpated in the abdomen. If rupture occurs in 

the retroperitoneum, a poorly defined midabdominal fullness can be felt, and shock 

becomes profound. Emergency department bedside ultrasound can rapidly confirm the 

diagnosis. Most patients with a leaking or ruptured abdominal aortic aneurysm are too 

unstable to be diagnosed by CT scan. A chest x-ray should also be obtained to evaluate 

the thoracic aorta. 

Treatment 

(See also Chapter 32.) Insert at least 2 large-bore (= 16-gauge) percutaneous catheters 

for vascular access. Consider a central venous catheter. Draw blood for CBC, 

electrolytes, PT and PTT, and tests of renal function. Type and cross-match for 8 units 

of whole blood. Treat shock with intravenous crystalloid solution followed by whole 

blood as soon as available. In patients who are exsanguinating, type-specific or 

universal donor blood may be used until cross-matched blood is available (Chapter 39). 

Obtain immediate vascular or general surgical consultation. Prepare the patient for 

surgery as rapidly as possible. 

Disposition 

All patients must be hospitalized; the mortality rate is virtually 100% without surgical 

treatment. 

Mancini MC: Abdominal aortic aneurysm. Emedicine.com; www. 

emedicine.com/med/topic3443.htm 

2. Ischemic Colitis 


Patients with ischemic colitis are usually elderly and have evidence of vascular disease 

elsewhere in the body. A history of similar attacks, abrupt in onset and of varying 

degrees of severity, is often present. The pain may be localized anywhere in the 

abdomen or may be diffuse. Severe colitis is usually accompanied by bloody diarrhea. 

Ischemic areas may progress to gangrene if the ischemia is sufficiently severe; if 

ischemia is milder, the areas may heal, often with strictures. Routine laboratory tests do 

not show specific abnormalities, although hemoconcentration and azotemia are 

common. Tests that confirm the diagnosis of ischemic colitis include sigmoidoscopy or 

colonoscopy, barium enema, and visceral angiography. 

Treatment 

Treat shock and hemoconcentration with intravenous crystalloid solution. Administer 

antimicrobials (see Table 13-1). 

Disposition

All patients with suspected or documented ischemic colitis should be hospitalized for 

further diagnostic tests and possible surgery. 

MacDonald PH: Ischaemic colitis. Best Pract Res Clin Gastroenterol 2002;16:51. [PMID: 

11977928] (Review.) 

3. Mesenteric Thrombosis 


The patient usually complains of the sudden onset of severe, diffuse abdominal pain in 

the mid or lower abdomen. The pain is poorly localized and severe, often not relieved by 

narcotics. It is constant rather than crampy. Nausea and vomiting and diarrhea, with 

gross or occult blood in the stool, may be present. Physical findings are absent initially. 

As the condition progresses, abdominal distention and tenderness appear and shock 

supervenes. Marked leukocytosis, hemoconcentration, azotemia, and acidosis are 

commonly associated with mesenteric thrombosis. 


Treat shock and hemoconcentration with intravenous crystalloid solutions, and 

administer antimicrobials (see Table 13-1). Hospitalize the patient and prepare for 

emergency surgery. Visceral angiography or abdominal CT scan with oral and 

intravenous contrast may be used to confirm the diagnosis. 

Kim AY, Ha HK: Evaluation of suspected mesenteric ischemia: efficacy of radiologic 

studies. Radiol Clin North Am 2003;41:327. [PMID: 12659341] (Review.) 

4. Rupture of the Spleen (See also Chapter 25.) 


Rupture of the spleen is usually caused by trauma to the lower left rib cage that is often 

associated with rib fractures. Occasionally, the spleen may rupture after trivial or 

overlooked injury, usually when pathologic enlargement has occurred (eg, infectious 

mononucleosis, AIDS, leukemia). Actual splenic rupture may occur several days after 

initial injury. Blood leaking into the peritoneal cavity causes abdominal pain and 

tenderness that may radiate to the left side of the neck or left shoulder. Tachycardia, 

hypotension, and falling hematocrit are present, and shock may develop. Occasionally, 

patients present with syncope, hypotension, or shock without abdominal symptoms. 

Palpation of the left upper quadrant may reveal tenderness, mild spasm, and distention. 

Tenderness over the 9th and 10th ribs on the left is a diagnostic clue. Emergent bedside 

ultrasound, specifically the FAST exam (Chapter 25) can rapidly identify intraperitoneal 

fluid, which in the setting of blunt trauma must be assumed to represent blood. The 

spleen is intra-abdominal solid organ most commonly injured in blunt trauma. CT scan 

of the abdomen is useful for diagnosis of splenic rupture in stable patients. 

Treatment

Insert at least 2 large-bore (= 16-gauge) percutaneous intravenous lines. Obtain a CBC, 

and type and cross-match for 6 units of whole blood. Treat shock initially with 

intravenous infusion of crystalloid solution. Administer whole blood as soon as available, 

using hematocrit, blood pressure, pulse, and urine output to gauge the effectiveness of 

resuscitation. 

Disposition 

All patients with suspected splenic rupture should be hospitalized. Hemodynamically 

stable patients with less severe splenic injuries may be observed nonoperatively. 

Patients with hypotension and shock require emergent splenectomy. 

Debnath D, Valerio D: Atraumatic rupture of the spleen in adults. J R Coll Surg Edinb 

2002;47:437. [PMID: 11874265] (Review.) 

5. Splenic Infarct 


Infarction of the spleen usually occurs in patients with abnormal spleens due to 

hematologic disease (eg, sickling hemoglobinopathies). Rarely, it occurs as a result of 

arterial embolization (eg, in patients with endocarditis). Left upper quadrant pain of 

variable degree, occasionally referred to the shoulder, is present. Left upper quadrant 

tenderness is usually present as well. CT scan is helpful in confirming the diagnosis. 

Treatment 

No specific treatment is necessary. Symptomatic measures (eg, relief of pain) and 

treatment of the underlying disease may be necessary. 

Disposition 

Hospitalization is advisable until the diagnosis is confirmed. Likewise, hospitalization 

may be required for pain relief or treatment of the underlying disease. 

URINARY DISORDERS 

1. Renal Colic (See also Chapter 37.) 


Sudden, severe flank pain followed by hematuria is characteristic of renal colic. A 

history of passage of stones may be present. Examination reveals costovertebral angle 

tenderness on the side of the stone, with the pain shifting anteriorly and inferiorly as the 

stone progresses down the ureter toward the bladder. The stone can usually be 

visualized on x-ray. Excretory urography confirms the diagnosis by demonstrating 

obstruction to urinary flow. In most centers, noncontrast CT scan of the abdomen has 

replaced the intravenous pyelogram as the preferred diagnostic modality for the

evaluation of renal colic (Figure 13-10). Noncontrast CT scan is helpful in identifying the 

size and location of ureteral stones. Another benefit of noncontrast CT scan is that 

alternative diagnoses such as appendicitis or diverticulitis may be identified and the 

treatment modified appropriately. Urinary tract infection may coexist, and urinalysis 

should be performed in every case along with urine culture for organisms if infection is 

suspected. 


A severe clinical picture requires hospitalization for administration of parenteral 

analgesia and maintenance of hydration. Patients with either renal insufficiency or 

pyelonephritis and ureterolithiasis generally require admission for possible operative 

intervention. Patient with small stones can receive treatment on an ambulatory basis, 

with appropriate oral analgesia, hydration, and follow-up care with a primary care 

physician or urologist. 

2. Pyelonephritis (See also Chapter 40.) 


Patients with pyelonephritis typically have dysuria, urinary urgency and frequency, fever, 

and sometimes rigors. Pain, if present, is usually over the costovertebral angle or 

occasionally the abdomen. The pain is dull and usually gradual in onset. Malaise and 

nausea and vomiting are commonly present as well. Many bacteria and leukocytes are 

seen on stained smears of the urinary sediment. 


A patient who is severely ill (vomiting, high fever, rigors), pregnant, very young or very 

old, or immunocompromised, or who has know anatomic abnormalities of the 

genitourinary tract, requires hospitalization for intravenous hydration and parenteral 

antibiotics. Gentamicin and ampicillin or monotherapy with ceftriaxone or a 

fluoroquinolone provide reasonable empiric coverage for pyelonephritis. Outpatient 

therapy is appropriate for some patients with pyelonephritis, including those tolerating 

oral intake, those with telephone access, and those reliable to return if their condition 

worsens. Sequential therapy utilizing an initial parenteral dose of an antibiotic followed 

by an oral regimen as an outpatient is often recommended. 

Miller O, Hemphill RR: Urinary tract infection and pyelonephritis. Emerg Med Clin North 

Am 2001;19:655. [PMID: 11554280] (Review.) 

3. Renal Infarct 


Infarction of the kidney usually occurs because of arterial embolization (eg, from 

endocarditis or atrial fibrillation). In addition to flank pain and tenderness, hematuria is 

usually present. The diagnosis may be confirmed by CT scan, renal scan, or 

angiography.

Treatment 

No specific treatment is required for renal infarct. However, anticoagulation or other 

measures may be required to treat the underlying disease. 

Disposition 

Hospitalization is advisable for definitive diagnosis, administration of appropriate 

analgesia, treatment of underlying disease, and rapid anticoagulation measures if 

indicated. 

ACUTE PANCREATITIS 


Acute pancreatitis is characterized by abrupt onset of severe, unrelenting epigastric pain 

radiating to the back, often accompanied by vomiting and retching. In severe cases, the 

patient may be in shock. A predisposing condition (alcoholism, glucocorticoid 

administration, diabetes mellitus) may be present. Abdominal examination reveals 

decreased or absent bowel sounds and tenderness usually localized to the epigastrium. 

Rarely, an abdominal mass is palpated in the epigastrium. Elevated serum amylase and 

lipase levels, mild fever, and leukocytosis are often present. As discussed previously, 

lipase has better specificity and sensitivity for pancreatitis than amylase. If the diagnosis 

is uncertain, abdominal CT scan can often demonstrate changes pathognomonic of 

pancreatitis (although CT scan can be normal initially in 30% of patients with 

pancreatitis). Patients may have a history of recurrent pancreatitis; alcohol abuse is a 

common predisposing factor. 

Treatment 

Send blood for CBC; serum electrolyte, glucose, calcium, and lipase measurements; 

and renal and hepatic function tests. Insert an intravenous catheter (= 18 gauge), and 

begin an infusion of crystalloid solution. Give morphine, 2-4 mg intravenously, for pain; 

the dose may be repeated. Insert a nasogastric tube attached to a suction device if the 

patient is vomiting or if the abdomen is distended, especially if ileus is present. Give 

nothing by mouth to patients who are more severely ill. 

Disposition 

Patients with severe pain or persistent vomiting should be hospitalized for analgesia, 

intravenous hydration, and correction of electrolyte abnormalities. Even if they are not 

acutely ill, patients with no history of pancreatitis should be hospitalized for evaluation 

and treatment. Patients with chronic and recurrent pancreatitis may not require 

hospitalization if they can take fluids by mouth and do not require parenteral analgesics. 

Patients with recurrent acute pancreatitis due to alcohol abuse may receive oral 

analgesics and hydration on an outpatient basis if they are not severely ill. 

GYNECOLOGIC DISORDERS (See also Chapter 36.)

1. Ectopic Pregnancy with Rupture 


In ectopic pregnancy with rupture, the patient experiences sudden, severe, unilateral 

abdominal or pelvic pain that may be referred to the shoulder. Prior to rupture, pain may 

be vague or intermittent. There may be occasional nausea and vomiting but usually no 

fever. Irregular menses or other symptoms of pregnancy may be present as well. 

Postural hypotension or shock may be found on initial examination. Pelvic examination 

often reveals a unilateral doughy mass and tenderness on movement of the cervix. 

Pelvic sonography reveals free fluid and an adnexal mass. A urine pregnancy test is 

positive in almost all cases. 


Treat shock or hypotension with intravenous crystalloid solution and blood if necessary. 

Hospitalize the patient at once for emergency surgery or for laparoscopy if the diagnosis 

is in doubt (Chapter 36). 

Dart RG: Role of pelvic ultrasonography in evaluation of symptomatic first-trimester 

pregnancy. Ann Emerg Med 1999;33: 310. [PMID: 10036346] 

Mateer JR et al: Outcome analysis of a protocol including bedside endovaginal 

sonography in patients at risk for ectopic pregnancy. Ann Emerg Med 1996;27:283. 

[PMID: 8599484] 

2. Acute Salpingitis (Pelvic Inflammatory Disease) (See also Chapter 40.) 


The patient with salpingitis experiences gradual onset of pelvic and lower abdominal 

pain that slowly increases in severity. There may be headache and lassitude with high 

fever and tachycardia. Nausea and vomiting may be present. The patient shows 

exquisite tenderness to vaginal examination and particularly to movement of the cervix. 

Adnexal fullness or mass (tubo-ovarian abscess) may be present. A pelvic sonogram is 

diagnostic for tubo-ovarian abscess. 


Hospitalization of patients with pelvic inflammatory disease is recommended for the 

following situations: diagnosis is uncertain (eg, cannot exclude appendicitis); patient has 

severe symptoms such as nausea, vomiting, or high fever; patient is an adolescent or is 

pregnant or has failed outpatient treatment; patient is unable to follow up; or patient is 

immunocompromised (eg, HIV with low CD4 count). Surgery may be necessary if 

abdominal symptoms persist or if the patient's condition deteriorates. 

Quentin R, Lansac J: Pelvic inflammatory disease: medical treatment. Eur J Obstet 

Gynecol Reprod Biol 2000;92:189. [PMID: 10996679]

3. Ruptured Ovarian Follicle Cyst 


Patients with ruptured ovarian follicle cyst experience sudden, moderately severe pelvic 

or lower abdominal pain. Gastrointestinal symptoms usually are absent, and the patient 

is afebrile without leukocytosis. Tenderness may be elicited over the affected ovary. 

There should be no masses on pelvic examination, and the serum pregnancy test 

should be negative. 


Keep the patient under observation in the hospital until the diagnosis is confirmed. 

Operation is not necessary. 

4. Ovarian Torsion 


Torsion of the ovary is characterized by sudden unilateral lower abdominal or pelvic 

pain precipitated by a change in position. The pain is often sudden onset, sharp or 

colicky in nature, radiating into the groin, back or flank of moderate to severe intensity. 

Gastrointestinal symptoms include nausea and vomiting. Patients with ovarian torsion 

may have a history of ovarian abnormalities such as cysts or masses. 


The patient should be hospitalized for observation and possible surgery. 

Houry D, Abbott JT: Ovarian torsion: a fifteen-year review. Ann Emerg Med 

2001;38:156. [PMID: 11468611] 

5. Endometriosis 


Patients with endometriosis usually have a history of infertility, dysmenorrhea, and 

previous cyclic attacks of cramps and pains in the lower abdomen and possibly in the 

flank. Pain is worse with menses. Onset of symptoms may be gradual or sudden if there 

is associated bleeding. Painful defecation and dyspareunia are present. Aching pelvic 

discomfort and general tenderness on pelvic examination suggest endometriosis. 

Acquired secondary dysmenorrhea should be attributed to endometriosis until proved 

otherwise. 


If symptoms are mild, give the patient analgesics and refer her to the obstetrics and 

gynecology department for follow-up. If pain is severe, the patient should be

hospitalized for evaluation and possible surgery. 

PRIMARY PERITONITIS 


Primary peritonitis occurs almost exclusively in patients with preexisting ascites, 

especially those with cirrhosis or nephrotic syndrome. (Peritonitis secondary to 

traumatic fecal soilage is discussed in Chapter 25.) The symptoms and signs vary, but 

fever and abdominal pain and tenderness are common. The most helpful tests are blood 

culture and abdominal paracentesis for Gram-stained smear, cell count, and culture. A 

polymorphonuclear (PMN) cell count of greater than 250/mm 3 is highly suspicious for 

spontaneous bacterial peritonitis and is an indication for initiation of empiric antibiotics. 

Most cases of primary bacterial peritonitis demonstrate positive blood cultures, 

peritoneal fluid leukocyte counts over 1000/mm 3 (with a predominance of PMNs), and 

bacteria on Gram-stained smears or culture. In 40% of cases, all of these findings are 

present except that peritoneal fluid smears and cultures are negative. Familial 

Mediterranean fever produces sterile peritonitis that is difficult to distinguish from 

bacterial peritonitis. 

Treatment 

Culture blood and peritoneal fluid (include a culture for Mycobacterium tuberculosis). 

Treat shock, if present, with intravenous crystalloid solution. Begin parenteral 

antimicrobials: administer a cephalosporin in full doses (eg, cefotaxime, 2 g every 8-12 

hours for 5 days). Alternatively, fluoroquinolones can be used. 

Disposition 

All patients with suspected or confirmed acute peritonitis should be hospitalized for 

diagnostic evaluation and treatment. 

Rimola A et al: Diagnosis, treatment and prophylaxis of spontaneous bacterial 

peritonitis: a consensus document. J Hepatol 2000;32:142. [PMID: 10673079] (Review.) 

RETROPERITONEAL HEMORRHAGE 


Retroperitoneal hemorrhage is a rare condition that may occur secondary to minor 

trauma in individuals with defective clotting factors resulting from medication or disease. 

Back pain and abdominal pain are present, and the psoas sign is often positive. 

Abdominal CT scan localizes the bleeding in most cases. 

Treatment 

Treat shock with intravenous crystalloid solution, followed by cross-matched whole 

blood as soon as available. Correct coagulation defects by administering platelets or

clotting factors as needed. 

Disposition 

Patients with copious hemorrhage, active bleeding, severe clotting abnormalities, or 

severe pain should be hospitalized. 

CONDITIONS CAUSING ACUTE ABDOMINAL PAIN THAT ARE NOT 

AMENABLE TO SURGERY 

A variety of conditions not amenable to surgery may cause abdominal pain. Aside from 

common conditions such as pyelonephritis, salpingitis, myocardial infarction, and lobar 

pneumonia, a number of these conditions are capable of mimicking abdominal disorders 

requiring surgery. Most of these conditions simulate acute diffuse peritonitis. Helpful 

differential diagnostic tests are listed in Table 13-4. 






Figure 13-1.)

Table 13-1. Antimicrobials for the acute abdomen. 

Dose 

150 mg/kg/d intravenously in 4-6 divided doses 

1-2 g every 12 hours 

1.5-3.0 g every 6-8 hours 

3.1 g every 4-6 hours 

2 g every 6 hours 

900 mg every 8 hours

Table 13-2. Differential diagnosis of the common causes of acute abdominal pain. 

Location of Pain 

and 

Prior Attacks 

Periumbilical or localized 

generally to right lower 

abdominal quadrant. 

Associated 


Symptoms 

Anorexia common; nausea and 

vomiting in some. 

Helpful Tests 

and 

Examinations 

Slight leukocytosis. CT scan of th 

abdomen or ultrasound of the app 

may be helpful if diagnosis is unce 

Diffuse. Vomiting common. Dilated, fluid-filled loops of bowel 

abdominal x-ray. 

Epigastric. History of ulcer in 

many. 

Left lower quadrant. History of 

previous attacks. 

Diffuse; primarily in lower 

abdomen. Prior attacks 


Epigastric or right upper 

quadrant; may be referred to 

right shoulder. 

Intermittent right upper 

quadrant. Prior attacks 


Epigastric; diffuse. Prior 

attacks common. 

Anorexia; nausea and vomiting Upright abdominal x-ray shows ai 

under diaphragm. CT scan. 

Mild diarrhea common. CT scan shows inflammatory mas 

Diarrhea common, oftenwith blood 

and mucus. 

Blood and leukocytes in stool. CT 

scan. Abnormal results on 

proctosigmoidoscopy or barium 

enema. 

Anorexia; nausea and vomiting. Right upper quadrant sonography 

shows gallstones 

Radionuclide scan shows 

nonvisualistones. zation of gallbla 

Anorexia; nausea and vomiting Sonography shows gallstones. 


Diarrhea, commonly bloody. Barium enema shows "thumbprint 

of mucosa. CT scan. Visceral 

angiography shows vascular 

obstruction. 

Epigastrium and back. Variable; may be none. Sonography, CT scan, or angiogr 

shows aneurysm. 

Left upper quadrant or diffuse. 

May be referred to left 

shoulder. History of trauma 


Costovertebral or along course 

of ureter. 

Epigastric penetrating to back. Anorexia; nausea and vomiting 


Bilateral adnexal; later, may be 

generalized. 

Unilateral early; may have 

shoulder pain after rupture. 

Usually none. CT scan or liver-spleen scan show 

rupture. 

Peritoneal lavage reveals blood. 

Frequently nausea and vomiting. Hematuria. Abnormal Noncontras 

scan of the abdomen or excretory 

urogram (obstruction, hydronephr 

Nausea and vomiting may be 

present. 

Elevated serum lipase. CT scan s 

pancreatic inflammation. 

Ultrasound can rule out tubo-ovar 

abscess. 

Frequently none. Pelvic ultrasound reveals adnexal 

mass or blood. Positive urine 

pregnancy test.





TABLES 

Table 13-2. Differential diagnosis of the common causes of acute 

abdominal pain.

Table 13-3. Routine for physical examination of acute 

abdomen. 





TABLES 

Table 13-3. Routine for physical examination of acute abdomen.

Table 13-4. Definitive diagnosis of conditions causing acute abdominal pain. 

Condition 

Right upper quadrant Right upper quadrant sonogram; ra 

scan 

Right upper quadrant sonogram 

Right upper quandrant sonogram 

Liver function tests, especially transaminases 

Right upper quadrant sonogram; CT scan; 

radionuclide liver scan 

Chest x-ray 

Peritonitis Pancreatitis Duodenal perforation 

CT scan 

Pyelonephritis 

Appendicitis 

Urinalysis; noncontrast CT scan of abdomen; 

excretory urogram 

Urinalysis; renal scan or angiography 

Diverticulitis Ectopic pregnancy 

History and examination; supine and upright 

abdominal x-ray 

Supine and upright abdominal x-ray 

Supine and upright abdominal x-ray; CT scan 

with intravenous and water-soluble oral contrast 

CT scan; visceral angiography; barium enema 

CT scan with intravenous and water-soluble oral 

contrast 

CT scan 

History and examination; visceral angiography; 

laparotomy; CT scan with intravenous and 

soluble oral water-contrast 

History; hirsutism; elevated urinary 

porphobilinogens 

History—patient and family 

Diabetes, previous attacks 

Presence of syphillis; previous attacks 

Unilateral dematomal distribution 

Diffuse or variable

Figure 13-1. Algorithmic approach to complaints of abdominal pain. 





FIGURES 

Figure 13-1

Figure 13-2. Correlation between nature of abdominal pain and underlying 

condition.(Reproduced, with permission, from Way LW [editor]: Current Surgical 

Diagnosis & Treatment, 9th ed. Lange, 1991.) 





FIGURES 

Figure 13-2

Figure 13-3. Performing the iliopsoas test.(Reproduced, with permission, from Way LW 

[editor]: Current Surgical Diagnosis & Treatment, 6th ed. Lange, 1983.) 





FIGURES 

Figure 13-3

Figure 13-4. Performing the obturator test.(Reproduced, with permission, from Way LW 






FIGURES 

Figure 13-4

Figure 13-5. Obliteration of the psoas shadow on the right by a subhepatic 

abscess.(Reproduced, with permission, from Way LW [editor]: Current Surgical 

Diagnosis & Treatment, 6th ed. Lange, 1983.) 





FIGURES 

Figure 13-5

Figure 13-6. Upright abdominal x-ray showing dilated loops of small bowel with air-fluid 

levels and no gas in the colon. Patient had small bowel obstruction.(Reproduced, with 

permission, from Way LW [editor]: Current Surgical Diagnosis & Treatment, 9th ed. 

Lange, 1991.) 





FIGURES 

Figure 13-6

Figure 13-7. Abdominal x-ray showing dilated loops of small and large bowel without 

air-fluid levels, typical of diffuse peritonitis. (Reproduced, with permission, from Way LW 






FIGURES 

Figure 13-7

Figure 13-8. CT scan of the abdomen with oral and intravenous contrast in a patient 

with right lower quadrant pain. The study demonstrates a calcified appendolith (A and B) 

with associated stranding in the right lower quadrant. A dilated, fluid-filled appendix is 

noted (C). 





FIGURES 

Figure 13-8

Figure 13-9. Upright anteroposterior chest x-ray demonstrating pneumoperitoneum 

from a perforated peptic ulcer. 





FIGURES 

Figure 13-9

Figure 13-10. Noncontrast CT scan of the abdomen in a patient with left flank pain. 

Study demonstrates a dense calcification (ureterolithiasis) involving the mid portion of 

the left ureter, confirming the diagnosis of renal colic. 





FIGURES 

Figure 13-10



INTRODUCTION 

1 This chapter is a revision of the chapter by Richard A. Crass, MD, John P. Cello, MD, 

& Donald D. Trunkey, MD, from the 4th edition. 

For the majority of patients presenting with gastrointestinal (GI) bleeding, hematemesis 

(vomiting of blood), hematochezia (passage of bright red stools), or melena (black and 

tarry stools caused from the breakdown of large amounts of blood) will be the chief 

complaint. Occasionally patients may present with only dizziness, weakness, or 

syncope. If no obvious cause of shock is present, gastric lavage and a rectal 

examination should be performed promptly as part of the initial assessment. The 

severity of blood loss must be assessed quickly so that life-saving therapeutic 

interventions can be instituted. 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING BLEEDING 


ASSESS THE RATE AND VOLUME OF BLEEDING 

Any patient presenting to the emergency department with ongoing hematemesis or 

hematochezia is at significant risk of exsanguination, and prompt volume resuscitation 

must begin at once. Proceed with initial stabilization procedures as described below. 

CONDUCT INITIAL ASSESSMENT 

Place the patient in a monitored bed and obtain temperature, pulse rate, blood pressure, 

respiratory rate, and oxygen saturation via pulse oximetry. If the initial systolic blood 

pressure is greater than 100, and the pulse is less than 100 beats/min in the supine 

position, consider obtaining orthostatic blood pressure and pulse rate measurements. 

Recognize Risk Factors for Severe Gastrointestinal Bleeding 

Signs, symptoms, or history that may indicate ongoing hemorrhage are as follows: 

• Profuse hematemesis or hematochezia 

• Hypotension, tachycardia, or signs of shock (see Table 9-1) 

• Postural hypotension, tachycardia, or lightheadedness 

• Possible aortoenteric fistula (history of abdominal aortic aneurysm repair, or palpable 

pulsating abdominal mass)

• Known or suspected varices 

• Previous history of GI bleeding 

• History of diverticulosis 

Initial Stabilization Procedures 

A. Obtain Venous Access 

Insert 2 intravenous catheters into peripheral veins, preferably 18 gauge or larger in an 

adult. If peripheral access cannot be obtained, consider placement of a central venous 

line. 

B. Assess Need for Airway Management 

If the patient is having ongoing hematemesis or if signs and symptoms of shock are 

present, consider securing the airway with an endotracheal tube via rapid sequence 

intubation (Chapter 8). If immediate airway control is not needed, give oxygen via nasal 

cannula or face mask as needed to maintain oxygen saturation at greater than 93%. 

C. Perform Laboratory Studies 

Send blood for complete blood count (CBC). Type and cross-match blood for 2-6 units, 

depending on the extent of bleeding and the patient's status. Measure prothrombin and 

partial thromboplastin time to assess for any coagulopathy. Measure serum electrolytes 

and renal and liver functions. Blood urea nitrogen is elevated in many patients with 

upper GI bleeding. Venous blood gas and lactate may be helpful in assessing tissue 

perfusion status. 

D. Begin Fluid Resuscitation 

Rapidly bolus either warmed lactated Ringer's or normal saline to restore intravascular 

volume. 

E. Assess the Need for Immediate Blood Transfusion 

For persistent hypotension despite the infusion of 2 L of crystalloid, consider immediate 

transfusion of cross-matched blood if available. If not, then transfuse O-negative blood 

until cross-matched blood is available. Continue transfusion to maintain systolic blood 

pressure at greater than 90. 

F. Perform Electrocardiogram 

Obtain an electrocardiogram (ECG) for any patient over 50 years of age; for any patient 

with a history of ischemic heart disease or significant anemia; and for any patient with 

chest pain, shortness of breath, or severe hypotension. If the initial ECG demonstrates 

ongoing ischemia in the face of ongoing GI bleeding, then consider immediate 

transfusion of packed red blood cells. If a patient's initial hematocrit is less than 30% 

and he or she has a history of ischemic heart disease, early transfusion is probably 

indicated. 

G: General Examination 

Assess the patient's general appearance; vital signs; mental status (including 

restlessness); and skin signs such as pallor, moisture, telangiectasia, and petechiae.

Also, perform a cardiac and pulmonary examination to assess for abnormal heart or 

lung sounds that indicate cardiac dysfunction. 

H. Perform Abdominal Examination 

Inspect the abdomen for any skin changes (ie, telangiectasia, ecchymoses, or old 

surgical scars). Auscultate for any bruits that may indicate an aneurysm. Palpate for 

tenderness, mass, or hepatosplenomegaly. 

I. Perform Rectal Examination 

Inspect the anus and rectum for evidence of hemorrhoids or fissure. Obtain stool for 

hemoccult testing. 

J. Perform Bladder Catheterization 

If a patient is in shock or has a history of cardiac or renal dysfunction, insert a Foley 

catheter into the bladder to monitor urinary output. Order a urine analysis to assess for 

hematuria, which may indicate an abdominal aneurysm. 

K. Insert Nasogastric or Orogastric Tube 

If hematemesis has not been documented, prepare the nasal passageway and posterior 

pharynx with topical anesthetic, place a nasogastric tube, and lavage with room 

temperature normal saline (cold fluids may impede normal coagulation) until aspirate is 

clear. Persistent bleeding during lavage indicates potential life-threatening upper GI 

bleeding, and immediate consultation with a gastroenterologist or surgeon should be 

obtained. 

If persistent bleeding is noted and the endoscopist gives instructions to do so, place an 

Ewald orogastric tube for gastric lavage with increments of 200-300 mL of either saline 

or tap water because the fluid does not have to be sterile. The patient should be in the 

left lateral decubitus position with the bed in the Trendelenburg position. Lavage until 

the return is clear. 

L. Withhold All Fluids and Antacids 

Patients waiting for endoscopy should receive nothing by mouth. Do not administer 

fluids or antacids because they may impair adequate visualization during endoscopy. 

M. Correct Coagulopathy 

Patients taking Coumadin or who show signs of hepatic failure (eg, jaundice) may 

require vitamin K and fresh frozen plasma to correct coagulopathy before bleeding can 

be controlled. 

N. Seek Early Consultation 

After initial stabilization of the patient, contact the on-call general surgeon or 

gastroenterologist for either immediate endoscopy and therapy or further instructions. If 

emergent endoscopic services are unavailable at the treating facility, the emergency 

physician should find an accepting physician at a facility capable of providing these 

services and arrange rapid transport. 

Disposition

Based on certain clinical criteria such as age, comorbid disease, presenting vital signs, 

laboratory data, and availability of next-day follow-up, a subgroup of patients with GI 

hemorrhage can be discharged home. This decision should be made with the 

gastroenterologist. Intensive care unit admission should be reserved for patients with 

continued bleeding, abnormal vital signs, significant comorbid disease, or need for 

transfusion therapy and for those at increased risk for rebleeding (ie, esophageal 

varices). 

DETERMINE SITE OF BLEEDING 

Once the patient is stabilized, attempt to determine the bleeding site if it is not already 

obvious. In 90% of patients presenting with GI hemorrhage, the bleeding has an upper 

GI source (ie, proximal to the ligament of Treitz); in only about 10% of patients is the 

source of bleeding distal to this proximal portion of the duodenum. In about 80-85% of 

patients with GI hemorrhage, the bleeding will cease prior to the patient's arrival in the 

emergency department. 

Diagnostic Characteristics of Upper Gastrointestinal Bleeding 

See Figure 14-2. 

A. Hematemesis 

Hematemesis (excluding hemoptysis or swallowed blood from epistaxis) is observed. 

Blood or material in the nasogastric lavage tests positive for blood. 

The aspirate will be negative in approximately 10% of patients with a duodenal source 

of GI hemorrhage. A duodenal source cannot be excluded unless gastric lavage 

contents reveal bile. Even if bile is returned, the bleeding may have resolved 

spontaneously prior to arrival. If a patient reports unwitnessed hematemesis and gastric 

lavage is inconclusive, consultation with a gastroenterologist for early endoscopy is 

warranted. 

B. Melena and Hematochezia 

Melena is usually due to bleeding from an upper GI source. Hematochezia from an 

upper source usually indicates severe hemorrhage and corresponds with significant 

increases in mortality, need for transfusion, complications, and need for surgery. 

C. Absence of Bleeding 

If nasogastric lavage reveals bile and no blood, then active bleeding from an upper GI 

source is less likely. Between 80% and 85% of bleeding resolves spontaneously prior to 

the patient's arrival; therefore, in otherwise stable patients, close follow-up with an 

endoscopist should be arranged. 

Diagnostic Characteristics of Lower Gastrointestinal Bleeding 

A. Hematochezia 

An upper GI source is found for suspected lower GI bleeding in up to 15% of patients 

presenting with hematochezia. In these instances, consider aortoenteric fistula (in 

patients with abdominal aortic aneurysm repair) or duodenal ulcer. Otherwise, bleeding

distal to the ligament of Treitz is usually associated with hematochezia. 

B. Melena 

Melena is rarely associated with lower GI bleeding except when motility in the intestinal 

tract is decreased. Melena occurs more commonly as a result of an upper GI bleed. 

C. Bright Red Blood 

When seen as streaks on stool or on toilet paper after wiping, bright red blood usually 

indicates a hemorrhoidal source of bleeding. Consider anal fissures as well if the patient 

complains of painful bowel movements and bright red blood on the stool. 

D. Absence of Bleeding 

Spontaneous cessation of bleeding occurs in about 80-85% of cases without 

intervention, although cessation can be intermittent, and bleeding can restart at any 

time. 

FURTHER EVALUATION OF GASTROINTESTINAL BLEEDING 

The unstable patient should be rapidly resuscitated and stabilized prior to completing a 

detailed history and physical examination. Once the patient's hemodynamic status has 

stabilized, a more thorough examination should be done. For the patient not in extremis 

and otherwise stable, this examination can performed during the initial assessment. 

History 

Inquire about history of GI bleeding, esophageal varices, alcohol or nonsteroidal 

anti-inflammatory drug (NSAID) use, oral anticoagulation, recent weight loss, change in 

caliber of stools, abdominal pain suggestive of ulcer or gastritis, abdominal aneurysm 

repair, liver disease, or abdominal surgery. Recent vigorous retching or vomiting prior to 

onset of hematemesis suggests the presence of Mallory-Weiss tears. 

Inquire about history of hemorrhoids, anal fissures, or rectal trauma (eg, rectal 

intercourse, placement of foreign objects in rectum). 

In patients with AIDS and in otherwise immunocompromised patients, bleeding may be 

related to Kaposi sarcoma, lymphoma, or cytomegalovirus ulcerations. Visceral Kaposi 

sarcoma is usually associated with cutaneous lesions with classical dusky violaceous 

nodules. 

Physical Examination 

A. Vital Signs 

Reassess vitals signs every 15 minutes or more frequently as needed. 

B. Cardiopulmonary Examination 

Evaluate the patient for any evidence of cardiac dysfunction (ie, murmurs, rubs, gallops, 

arrhythmias). Listen to the lungs for abnormal sounds that may be suggestive of heart 

failure or an infectious process.

C. Liver Disease 

Examine the patient for signs of chronic liver disease (eg, hepatosplenomegaly, ascites, 

spider angiomas, enlarged abdominal vessels, jaundice, hepatojugular reflex, asterixis, 

palmar erythema). Although the presence of liver disease constitutes a higher likelihood 

of esophageal varices, GI bleeding will be from another identifiable source in 50% of 

patients with varices who present with GI bleeding. 

D. Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia) 

The presence of telangiectasias of the skin (particularly the digits) and lips may indicate 

this disease, which causes GI bleeding secondary to vascular malformations. 

E. Surgical Scars 

Inspect the patient for surgical scars that indicate previous abdominal surgery or 

possible vascular repair. 

F. Pain or Tenderness 

Epigastric tenderness to palpation is common with gastritis or peptic ulcer disease. Any 

patient who has had multiple episodes of vomiting may also have diffuse tenderness of 

the abdomen. A patient whose complaints of abdominal pain are out of proportion to the 

examination and who also has melena should be considered at risk for mesenteric 

ischemia. Significant tenderness or peritoneal signs may indicate perforation and 

warrant immediate surgical consultation. 

G. Rectal Examination 

Obtain a stool sample for hemoccult testing, and check for evidence of hemorrhoids or 

anal fissures. 

Special Examinations 

A. Upper Gastrointestinal Bleeding 

1. Endoscopy—Endoscopy is the most accurate diagnostic tool for upper GI bleeding; 

it locates the source of bleeding in 75-95% of patients. If the patient is actively bleeding, 

endoscopy should be performed as soon as possible. If the patient is stable and has no 

active bleeding, endoscopy should be performed within 24 hours, according to most 

experts. Advances in endoscopy hemostasis techniques also make it of therapeutic 

benefit to the patient (sclerotherapy and banding for varices). 

2. Upper gastrointestinal series—Once used for initial evaluation of the patient who is 

not actively bleeding, an upper GI series is no longer recommended for evaluation of 

upper GI bleeding. If done prior to endoscopy, the contrast material may obscure the 

endoscopist's view. 

3. Angiography—Because endoscopy has been the mainstay for diagnosis, 

angiography is used in only about 1% of patients with upper GI bleeding. It may be 

useful if endoscopy cannot identify a bleeding source even when active bleeding is 

suspected. 

B. Lower Gastrointestinal Bleeding

1. Anoscopy/proctosigmoidoscopy—Examination of the rectum and distal sigmoid 

colon should be undertaken as soon as the patient has been stabilized. If there is 

evidence of hemorrhoidal bleeding and no blood is noted above the rectum, the 

bleeding source is in the rectum. The presence of blood above the rectum reliably 

indicates bleeding from a more proximal site. 

2. Barium enema—This radiographic study is no longer commonly used as a diagnostic 

study for lower GI bleeding. The barium would interfere not only with endoscopic 

visualization but also with visceral angiography, should that be necessary. 

3. Colonoscopy—Once considered of no value in the acute evaluation of lower GI 

bleeding, colonoscopy is now considered by many endoscopists to be the modality of 

choice for diagnosis as well as for therapeutic intervention. A definitive diagnosis is 

made in approximately 75% of cases. Epinephrine injection can be performed if active 

bleeding sites are identified. 

4. Mesenteric angiography—If the bleeding rate is estimated to be greater than 0.5-1 

mL/min, angiography allows for selective embolization or vasopressin infusion. 

Complications associated with angiography include dye-induced renal failure, arterial 

dissection, and bowel infarction. This test should be ordered only after consultation with 

a general surgeon or gastroenterologist. 

5. Technetium red cell scintigraphy—Technetium bleeding scans may be indicated if 

the bleeding rate is greater than 0.1 mL/min. A portion of the patient's red blood cells 

are labeled with technetium- 99 m and reinfused, followed by scanning. The scan can be 

repeated periodically to help localize the bleeding site within the GI tract. This testing 

modality can be used prior to angiography to increase the yield and decrease the risk 

associated with the procedure. These exams are usually performed after consultation 

with the on-call endoscopist. 

Monitoring for Rebleeding 

A. Gastric Lavage 

After placement of a nasogastric tube, continue reassessment for rebleeding by using 

intermittent low continuous suction. Continued bleeding or rebleeding is an indication for 

emergent endoscopy. 

B. Stool 

Record frequency, color, and approximate amount of stool passed by the patient. 

Continued passage of bright red, maroon, or melenic stools may indicate need for 

further studies or transfusion. 

C. Hemoglobin and Hematocrit 

Frequent checking of hemoglobin and hematocrit (every 4 hours) is essential in patients 

with active bleeding after they are hemodynamically stabilized. Often the initial 

hematocrit is normal. After fluid resuscitation and equilibration of intravascular volume, 

the hemoglobin and hematocrit should be rechecked.

Almela P et al: Outpatient management of upper digestive hemorrhage not associated 

with portal hypertension: a large prospective cohort. Am J Gastroenterol 2001;96:2341. 

[PMID: 11513172] 

Fallah MA et al: Acute gastrointestinal bleeding. Med Clin North Am 2000;84:1183. 

[PMID: 11026924] 

Jensen DM et al: Urgent colonoscopy for the diagnosis and treatment of severe 

diverticular hemorrhage. N Engl J Med 2000;342:78. [PMID: 10631275] 

Kollef MH et al: BLEED: a classification tool to predict outcomes in patients with acute 

and lower gastrointestinal hemorrhage. Crit Care Med 1997;25:1125. [PMID: 9233736] 

Lefkovitz Z: Radiology in the diagnosis and therapy of gastrointestinal bleeding. 

Gastroenterol Clin 2000;29:489. [PMID: 10836191] 

O'Neil BB et al: Cinematic nuclear scintigraphy reliably directs surgical intervention for 

patients with gastrointestinal bleeding. Arch Surg 2000;135:1076. [PMID: 10982513] 

Peter DJ et al: Evaluation of the patient with gastrointestinal bleeding: an evidence 

based approach. Emerg Med Clin North Am 1999;17:239. [PMID: 10101349] 

Podila PV et al: Managing patients with acute, nonvariceal gastrointestinal hemorrhage: 

development of a clinical care pathway. Am J Gastroenterol 2001;96:208. [PMID: 

11197254] 

Shetzline MA et al: Provocative angiography in obscure gastrointestinal bleeding. South 

Med J 2000;93:1205. [PMID: 11142458] 

Wilcox CM et al: Causes and outcomes of upper and lower gastrointestinal bleeding: 

The Grady Hospital. South Med J 1999;92:44. [PMID: 993282] 

EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING 

UPPER GASTROINTESTINAL BLEEDING 


• May present with hematemesis or melena; massive upper GI bleeding may have 

hematochezia. 

• Peptic ulcer disease accounts for 50% of upper GI bleeding; consider initiating 

proton-pump inhibitor therapy. 

• Endoscopy diagnostic and often therapeutic. 

Table 14-1 lists the most likely sites of upper GI bleeding. Figure 14-2 is an algorithm for 

identification of the bleeding site. Esophagogastroduodenoscopy (EGD) is the 

procedure of choice for either acute hemorrhage or in the stable patient without active 

bleeding. Specific conditions and their management are discussed below.

PEPTIC ULCER DISEASE 

Peptic ulcer disease accounts for approximately half of all episodes of upper GI 

bleeding (see Table 14-1). 


Patients with peptic ulcer disease usually present with epigastric pain that can be made 

worse or even better with food depending on the location of the ulcer. Many patients 

have had dyspeptic symptoms for years. Up to 40% of patients may not relate pain prior 

to onset of bleeding. 

The severity of bleeding determines the clinical presentation: 

• Acute: Sudden onset with massive hemorrhage with symptoms and signs suggestive 

of shock upon presentation. 

• Chronic: Increased fatigue, weakness, occult blood in stool, and anemia due to slow 

bleeding may be the only symptoms among elderly patients with ulcer disease. 

Treatment 

Provide emergent management as discussed above, in the "Immediate Management of 

Life-threatening Bleeding" section. All patients with known peptic ulcer disease should 

be given a proton-pump inhibitor such as omeprazole or rabeprazole. If the patient has 

suspected peptic ulcer disease, consider initiating treatment with a proton-pump 

inhibitor in the emergency department. 

Somatostatin is an endogenous peptide that reduces splanchnic blood flow and GI 

motility, inhibits acid secretion, and may have gastric cytoprotective effects. Octreotide 

is a synthetic analogue of somatostatin that, when used in the presence of upper GI 

hemorrhage, may reduce the risk of continued bleeding from actively bleeding peptic 

ulcer disease. With a very short half-life, it is typically given as an infusion of 25-50 ug/h. 

Patients should be instructed not to smoke, consume alcohol, or use NSAIDS or aspirin 

on a regular basis. Recurrent or persistent hemorrhage requires evaluation for surgical 

intervention. 

Disposition 

Patients with active bleeding, tachycardia, hypotension, anemia, age greater than 65 

years, or significant comorbid disease should be admitted for evaluation and 

observation. If none of the above risk factors is present, and close follow-up with a 

gastroenterologist can be arranged within 24-48 hours, the patient may be discharged 

home. All patients should be given a proton-pump inhibitor as an outpatient, if not 

already prescribed by their primary care physician. 

GASTRITIS

Gastritis is a more frequently recognized entity with the advent of upper endoscopy as 

the preferred diagnostic modality in the evaluation of upper GI bleeding. Gastritis is 

commonly associated with alcohol ingestion as well as aspirin and NSAID use. 

Esophagitis and duodenitis may also coexist as findings on endoscopy. The presence of 

esophagitis on endoscopy indicates dysfunction of the gastroesophageal sphincter with 

reflux of gastric secretions. 


Although gastritis is asymptomatic in many cases, patients may experience anorexia, 

nausea, dyspepsia, pain, and immediate postprandial emesis. The diagnosis is made by 

endoscopy and cannot be reliably made by an upper GI series. Gastritis rarely results in 

massive bleeding by itself, but it can occur in the presence of portal hypertension and 

coagulopathies. 

Treatment 

Provide therapy as directed above. Continue nasogastric lavage until brisk bleeding has 

resolved. 

For nonbleeding, clinically suspected gastritis, a trial of an antacid with viscous lidocaine 

("GI cocktail") may provide quick relief. Consider prescribing a proton-pump inhibitor or 

recommending any of the many over-the-counter histamine H 2 antagonists (eg, 

ranitidine, famotidine). 

Instruct patients to avoid aspirin, NSAIDS, and alcohol until reevaluated by their primary 

care physician. 

Disposition 

Patients with active bleeding should be hospitalized and receive treatment as outlined 

above. For patients who meet previously mentioned criteria for discharge, ensure timely 

follow-up with either their doctor or a gastroenterologist. 

MALLORY-WEISS SYNDROME 

Tears in the esophageal mucosa and submucosa that usually occur after forceful 

retching and vomiting are responsible for approximately 10% of acute upper GI 

bleeding. The majority of cases (75%) originate in the stomach; the rest occur at the 

gastroesophageal junction. Bleeding usually resolves spontaneously, but 3% of deaths 

from upper GI bleeding have been attributed to Mallory-Weiss tears. 


In addition to retching and vomiting, this disorder has been reported following chest 

compressions, coughing, sneezing, or even straining with bowel movement. Many 

cases have no discernible predisposing factor. Alcohol abuse is a significant risk factor. 

EGD is the diagnostic gold standard.

Treatment 

Provide emergency management as outlined earlier. Nasogastric lavage until clear. For 

persistent bleeding, consult with the on-call endoscopist for emergent EGD with 

possible therapeutic epinephrine injection, coagulation, or embolization of the vessel. 

Disposition 

For bleeding that does not resolve spontaneously, hospitalize the patient for observation 

and treatment. 

ESOPHAGEAL VARICES 

Patients with underlying liver disease and portal hypertension are at increased risk for 

esophageal or gastric variceal bleeding. Approximately 40% of these patients will 

experience a variceal bleed. The mortality rate for these patients is 30-50%. 

Alcohol-induced cirrhosis is the most common cause of esophageal varices in the 

United States, but parasitic infestations of the liver are a frequent cause of cirrhosis in 

underdeveloped countries. 


Upper GI bleeding secondary to varices cannot be clinically diagnosed based on signs 

and symptoms alone. As mentioned earlier, in approximately 50% of patients with 

known varices who present with GI bleeding, the bleeding is from a source other than 

the varices. Endoscopic verification is mandatory for accurate diagnosis and treatment. 

Treatment 

A. Emergency Measures 

Provide emergent resuscitative efforts as outlined above. 

B. Airway Management 

If the patient has altered mental status or profuse hematemesis, protective intubation is 


C. Monitor Cardiovascular Status 

If the patient is unstable and has significant comorbid disease, consider invasive 

monitoring of central venous pressure and arterial blood pressure. 

D. Medical Therapy 

The immediate use of octreotide has been proven effective in controlling bleeding. 

Octreotide decreases splanchnic and hepatic blood flow as well as transhepatic and 

variceal pressures. Vasopressin has fallen out of favor because of its systemic effects 

and risk of ischemia. 

E. Endoscopic Therapy 

Sclerotherapy involves the injection of various sclerosing agents to promote thrombus

formation. Band ligation uses endoscopically placed rubber bands, which block blood 

flow and promote thrombus formation. Both therapies work well in over 90% of patients, 

but band ligation is associated with fewer complications. 

F. Balloon Tamponade 

In rare circumstances it may be necessary to insert the Sengstaken-Blakemore tube 

(Chapter 6) to tamponade uncontrolled hemorrhage prior to endoscopic confirmation. 

Patients must be intubated prior to insertion of the tube. 

Disposition 

Essentially all patients with variceal bleeding are admitted to an intensive care area for 

further observation and treatment. 

HEMOBILIA 

Hemobilia can occur secondary to trauma, hepatic tumors, gallstones, and parasites. It 

can cause bleeding into the biliary tract, resulting in upper GI bleeding. 


Hemobilia presents as GI bleeding. During EGD, bleeding is noted from the ampulla of 

Vater. Bleeding is typically mild. Angiography can further delineate the bleeding site. 


Patients should be hospitalized for observation and treatment. Embolization via 

interventional radiographic technique is the therapy of choice. 

AORTIC ANEURYSM (Aortoenteric Fistula) 


Upper GI bleeding in the presence of an abdominal aortic aneurysm (or graft) should be 

assumed to be secondary to an aortoenteric fistula until proven otherwise. 

Bleeding may be moderate at first, but profuse hemorrhage will eventually occur unless 

proper treatment is given. If the patient has a GI bleed and a history of an abdominal 

aortic aneurysm or graft repair, or if the history and physical examination are suggestive 

of such, obtain immediate surgical consultation after performing initial resuscitation. If 

the patient is hemodynamically unstable, emergent surgery is indicated. Consider 

bedside ultrasonography followed by computed tomography scan for confirmation in the 

stable patient. 

Treatment 

Stabilize as previously outlined and obtain immediate surgical consultation. 

Disposition

All patients with the above diagnosis should be placed in an intensive care setting for 

close monitoring. 

Almela P et al: Outpatient management of upper digestive hemorrhage not associated 

with portal hypertension: a large prospective cohort. Am J Gastroenterol 2001;96:2341. 

[PMID: 11513172] 

Avgerinos A et al: Early administration of somatostatin and efficacy of sclerotherapy in 

acute oesophageal variceal bleeds: the European Acute Bleeding Oesophageal Variceal 

Episodes (ABOVE) randomized trial. Lancet 1997;350:1495. [PMID: 9388396] 


[PMID: 11026924] 

Imperiale TF et al: Somatostatin or octreotide compared with H2 antagonists and 

placebo in the management of acute nonvariceal upper gastrointestinal hemorrhage: a 

meta-analysis. Ann Intern Med 1997;127:1062. [PMID: 94122308] 

Peter DJ et al: Evaluation of the patient with gastrointestinal bleeding: an evidence 

based approach. Emerg Med Clin North Am 1999;17:239. [PMID: 10101349] 

Podila PV et al: Managing patients with acute, nonvariceal gastrointestinal hemorrhage: 

development of a clinical care pathway. Am J Gastroenterol 2001;96:208. [PMID: 

11197254] 

EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING 

LOWER GASTROINTESTINAL BLEEDING 


• Patients present with hematochezia; 10% may be from an upper GI source. 

• 80-85% of lower GI bleeding resolves spontaneously. 

• Sigmoidoscopy or colonoscopy can diagnose most sources of lower GI bleeding. 


Lower GI bleeding is most commonly a result of diverticular disease, followed by 

angiodysplasia, colonic ulcers, and other miscellaneous causes. The most common 

cause depends on the patient's age. In the adolescent or young adult, Meckel 

diverticulum, inflammatory bowel disease, and polyps are the most likely causes. In 

adults up to age 60 years, diverticula, inflammatory bowel disease, and neoplasms are 

the more common causes. In patients over age 60 years, angiodysplasia, diverticula, 

and neoplasms predominate. 

In 80-85% of patients with lower GI bleeding, the bleeding resolves spontaneously, 

often making it difficult to locate the source of bleeding. Massive bleeding can occur

from any site in the lower GI tract, although diverticular bleeding originates in the colon. 

DIVERTICULOSIS 


Although typically asymptomatic, patients with diverticulosis may present with cramping, 

lower abdominal pain, and left lower quadrant tenderness to palpation. Tenesmus, 

constipation, or diarrhea may be associated with diverticulosis. Massive bleeding may 

occur acutely without any signs or symptoms of diverticulitis. 


(See Figure 14-3. ) Perform emergency stabilization as outlined above. Colonoscopy is 

becoming the modality of choice for initial evaluation in many cases after bowel prep. If 

massive hemorrhage is present, surgery may be necessary. Selective angiography with 

embolization is also an option for bleeding control. Most patients should be admitted for 

further observation and treatment. 

ANGIODYSPLASIA 


Angiodysplasia is characterized by painless bleeding that may be mild or massive. 

Signs may range from occult blood in stools to melena to hematochezia. Most patients 

are elderly and have a history of cardiac or renal disease. 

For bleeding rates 0.1 mL/min or greater, technetium red cell scan is fairly reliable, 

although the diagnostic modality of choice may vary between consultants. Colonoscopy 

may reveal spider angioma-like lesions. 


Stabilize the patient as previously discussed. Electrocoagulation has shown good 

results for treatment of bleeding lesions visualized during colonoscopy. If bleeding is 

localized via radionucleotide scanning, then embolization through angiography can be 

curative in many cases. Angiography can also provide accurate localization of the 

bleeding when surgical intervention is necessary. 

Hospitalize patients for further work-up and observation as directed by the consultant. 

HEMORRHOIDS 


Bleeding is usually the first symptom of internal hemorrhoids. There may be a history of 

straining on defecation, and the patient will present with frank hematochezia often mixed 

with well-formed, normal-appearing stools. Occasionally, recurrent bleeding can result in 

marked anemia. Exsanguinating hemorrhage is rare unless portal hypertension is

present. The diagnosis should be confirmed by proctoscopy in the emergency 

department. Careful anoscopy must be done to fully visualize hemorrhoids. If a flexible 

fiberoptic sigmoidoscope is used, retroflexion of the insertion tube (bending the section 

back to examine the rectum from above) is necessary to ensure good visualization of 

the anorectal junction. 

Treatment 

A. Medical Measures 

Most early cases can be managed with high-roughage diet, local measures (sitz baths, 

suppositories for hemorrhoids [Anusol, many others]), and stool softeners (psyllium 

[Metamucil, many others], dioctyl sodium sulfosuccinate [Colace, many others]). 

B. Surgical Measures 

Surgery is required occasionally to arrest hemorrhage not controlled by medical 

measures. 

Disposition 

Hospitalize patients for surgery to arrest persistent brisk bleeding. It is prudent to 

hospitalize patients with portal hypertension as well. Otherwise, refer patients to an 

outpatient clinic for follow-up. 

COLONIC POLYPS 


Painless rectal bleeding and discovery of a polyp on sigmoidoscopy, colonoscopy, or 

barium enema confirm the diagnosis of colonic polyposis. 

Treatment 

For significant bleeding, see "Immediate Management of Life-Threatening Bleeding" 

section. If bleeding persists, the polyps should be removed immediately. If bleeding has 

stopped, patients can be referred for elective colonoscopic polypectomy. 

Disposition 

Hospitalization is necessary if bleeding persists; otherwise, refer patients for outpatient 

colonoscopic polypectomy. 

COLITIS 


The chief findings are abdominal cramps, diarrheal stools containing blood and 

mucopurulent material, fever, weight loss, and anemia. On sigmoidoscopy, the rectal 

mucosa is eroded and friable. Infectious causes of colitis (particularly Shigella, 

Campylobacter, Entamoeba histolytica, Clostridium difficile, and Salmonella) must be

uled out (Chapter 40). 

Occasionally, particularly in elderly patients, ischemic colitis can occur with brisk 

hematochezia. Differentiation from idiopathic or infectious colitis is often possible on 

sigmoidoscopy. Ischemic colitis rarely, if ever, involves the rectum, whereas other forms 

of colitis almost always involve the rectum. 

Treatment 

See "Emergency Management of Life-Threatening Bleeding" section. Medical measures 

can usually control most symptoms in mild to moderate cases. Surgery is reserved for 

severe problems. 

Disposition 

Severe cases are medical emergencies requiring immediate hospitalization. Mild cases 

can be referred to the proper clinic for further evaluation and treatment after stool 

samples have been collected for evaluation for enteric pathogens. 

CROHN DISEASE 


Frank blood is seen in about one third of patients with Crohn disease, but massive 

bleeding is unusual. Patients have abdominal pain and tenderness; diarrhea occurs but 

is rarely a prominent symptom. There may be fever and sepsis. 

Fistula formation, fissures, and hemorrhoids are common. However, Crohn disease may 

not involve the rectum or sigmoid. A normal proctosigmoidoscopic examination does not 

exclude Crohn disease. 

Treatment 

Chrohn disease should be managed medically. Surgery is indicated only rarely, when 

massive bleeding is not controlled by medical measures. Amebic disease must be 

excluded before corticosteroids are used. 

Disposition 

Patients with severe bleeding or systemic symptoms (eg, fever, weight loss) must be 

hospitalized for observation and treatment. Patients with mild Crohn disease can be 

referred for outpatient follow-up. 

SOLITARY RECTAL ULCER 

Clincial Findings 

Rectal ulcer is an unusual lesion associated with rectal prolapse. It may result from 

straining at stool. The patient passes blood and mucus per rectum. Many patients are

elderly and have chronic constipation. 


Offer general measures to aid defecation (eg, hydration, stool softeners). Surgery 

should be avoided. Refer the patient to the appropriate clinic for evaluation and 

follow-up. 

MECKEL DIVERTICULUM 


About 25% of patients with Meckel diverticulum become symptomatic, and 25% of these 

patients have lower GI bleeding. This disorder usually occurs before age 2 years and 

rarely after age 10 years. Symptoms may mimic acute appendicitis. Meckel diverticulum 

may be diagnosed by technetium pertechnetate scintigraphy or angiography. BR> 


Hospitalize patients for observation, because surgery may be required for severe 

bleeding. 

Billingham RP: The conundrum of lower gastrointestinal bleeding. Surg Clin North Am 

1997;77:241. [PMID: 9092113] 


[PMID: 11026924] 

Jensen DM et al: Urgent colonoscopy for the diagnosis and treatment of severe 

diverticular hemorrhage. N Engl J Med 2000;342:78. [PMID: 10631275] 

O'Neil BB et al: Cinematic nuclear scintigraphy reliably directs surgical intervention for 

patients with gastrointestinal bleeding. Arch Surg 2000;135:1076. [PMID: 10982513] 






INTRODUCTION

Table 14-1. Cause and severity of upper gastrointestinal tract hemorrhage in all patients 

undergoing diagnostic endoscopy at the San Francisco General Hospital over 3 years. 

Severity of Hemorrhage 

(%) 

Source of 

Hemorrhage 

Severe 

(n = 140 patients) 

12 2 

Gastric ulcer 14 

Prepyloric ulcer 4 

Pyloric channel ulcer 2 

Gastric erosions 0 

Gastritis 0 

Varices 2 

Portal-hypertensive 

gastropathy 

Gastric cancer 

Polyp 2 

Dieulafoy lesion 

Total, stomach 24 

31 8 






TABLES

Figure 14-1. Immediate management of life-threatening bleeding. BUN = blood urea 

nitrogen; FFP = fresh frozen plasma; PT = prothrombin time; PTT = partial 

thromboplastin time. 






FIGURES 

Figure 14-1

Figure 14-2. Hematemesis or suspected upper GI bleeding. 






FIGURES 

Figure 14-2

Figure 14-3. Hematochezia or suspected lower GI bleeding. 






FIGURES 

Figure 14-3

15. Diarrhea & Vomiting - Phillip A. Clement, MD, & Jason A. Gardiner, 

MD 

INTRODUCTION 

Diarrhea and vomiting are common reasons for emergency department visits. Although 

the majority of cases are of an infectious, self-limiting nature, the differential diagnosis is 

broad with the potential for significant morbidity and mortality. Many pathologic 

processes involve gastrointestinal symptoms. Included are intracranial pathology 

(trauma, masses, infections), cardiac disease (myocardial infarction, angina), toxic 

exposures (digoxin, carbon monoxide, heavy metals), acute abdominal pathology 

(intestinal obstruction, mesenteric ischemia), and endocrine abnormalities (diabetic 

ketoacidosis, adrenal insufficiency), among others. In addition, infectious causes of 

diarrhea and vomiting can cause significant harm, especially in the elderly, in infants, 

and in immunocompromised individuals (Figure 15-1). 


HYPOTENSION & SHOCK 


• Signs of decreased perfusion. 

• Hypotension, tachycardia, oliguria, and orthostasis. 

• Cool, pale skin; dry mucous membranes; and altered mentation. 


Obtain complete vital signs, including blood pressure, pulse and respiratory rate, pulse 

oximetry, and a rectal temperature. Look for signs of decreased perfusion (ie, cool, pale 

skin; altered mentation; decreased urinary output; dry mucous membranes). 

Hypotension (systolic pressure < 90 mm Hg), tachycardia, oliguria, and orthostasis may 

indicate impending hemodynamic instability. Look for evidence of sepsis, 

gastrointestinal bleed, cardiac pump dysfunction, surgical abdominal pathology, toxic 

exposures, endocrine abnormalities, or anaphylaxis. 


Insert a large-bore intravenous catheter and draw blood for a complete blood count 

(CBC), electrolytes, renal and liver function, serum lipase, and a pregnancy test, if 

indicated. Type and cross-match if blood loss is suspected. Start supplemental oxygen, 

cardiac monitoring, and pulse oximetry together with normal saline volume resuscitation 

while the underlying cause is sought. If appropriate, initiate empiric antibiotic therapy. 

Hospitalize the patient for continuous monitoring, supportive treatment, and further

investigation if the cause is uncertain. Initiate specific treatment once the cause is 

determined. 

ACUTE ABDOMINAL EMERGENCIES 


• Focal abdominal pain or signs of peritoneal inflammation (rebound). 

• Pain that precedes the vomiting or diarrhea. 

• Pain out of proportion to the physical examination. 


Patients with acute surgical abdominal pathology may present with diarrhea and 

vomiting and are at risk of being mislabeled as having gastroenteritis. Inquire about the 

nature and location of pain, the existence of upper gastrointestinal (GI) symptoms 

(vomiting) and lower GI symptoms (diarrhea). Determine which symptom began first and 

clarify the patient's understanding of the term diarrhea. Signs and symptoms suggestive 

of an acute abdominal emergency include focal abdominal pain, an exam consistent 

with peritoneal inflammation, pain that precedes the vomiting and diarrhea, protracted 

vomiting with nonspecific abdominal pain, or pain out of proportion to the physical 

examination. Consider entities such as acute appendicitis, intestinal obstruction, 

mesenteric ischemia, ectopic pregnancy, GI bleed, intussusception, and gonadal torsion 

(Table 15-1). Serial abdominal exams in the emergency department may help 

differentiate early acute abdominal emergencies with vomiting or diarrhea from 

gastroenteritis. In patients with arteriovascular disease who present with pain out of 

proportion to the exam, mesenteric ischemia must be ruled out. Consider 

intussusception in infants and children with abdominal pain, vomiting, and diarrhea 

(often bloody). 


Treatment ultimately depends on the cause of the symptoms. Obtain complete vital 

signs; gain intravenous access; and draw blood for a CBC, electrolytes, renal and liver 

function tests, serum lipase, pregnancy test if appropriate, and blood type and 

cross-match. An acute abdominal series may demonstrate a small or large bowel 

obstruction. A computed tomography (CT) scan or ultrasound may help identify the 

cause of the acute abdomen. If intussusception is suspected, an air contrast or barium 

enema can be both diagnostic and therapeutic. If the patient's condition is unstable, 

seek appropriate surgical consultation early. 

TOXIC EXPOSURES 


• Cholinergic or sympathomimetic syndromes. 

• Ingestion of mushrooms, herbal or plant preparations, or seafood. 

• Occupational exposures; exposure to heavy metals, pesticides, or carbon monoxide. 

• Medications: digoxin, salicylates, or others. 


Diarrhea and vomiting are often the presenting symptoms of toxic exposures. The list of 

toxins is extensive (Figure 15-1). Obtain key historical information including 

medications, occupational exposures, use of herbal preparations, consumption of 

mushrooms or plant products, ingestion of seafood, exposures to heavy metals, and a 

history of allergic reactions. Search for specific toxin-induced syndromes such as 

cholinergic or sympathomimetic reactions. Consider common toxins such as digoxin, 

salicylates, and carbon monoxide. If neurologic symptoms exist, consider botulism or 

shellfish poisoning. 


Begin treatment with the proper decontamination method. Give patients with toxic 

ingestions activated charcoal and a cathartic. Patients with cutaneous and inhalation 

exposures should be removed from the source and the contaminant diluted. Initiate 

supportive care and continuous monitoring. Administer specific antidotes if appropriate. 

OTHER EMERGENCIES 


• Chest pain, shortness of breath, diaphoresis, acute pump failure. 

• History of cardiac, central nervous system, endocrine disease or trauma. 

• Abnormal neurological exam, altered mentation, fevers, headache. 

• Laboratory and physical abnormalities. 


Cardiac, central nervous system, or endocrine disorders may include vomiting or 

diarrhea as presenting symptoms (Figure 15-2). Evidence of a cardiac-related disorder 

include chest pain, shortness of breath, diaphoresis, a history of cardiac disease, or 

evidence of acute pump failure. Indications of central nervous system pathology include 

a history of trauma, an abnormal neurological exam, altered mentation, fevers, 

cephalgia, and evidence of other toxic or metabolic pathology affecting the central 

nervous system. Search for historical, physical, and laboratory evidence of endocrine 

dysfunction. 


Patients with a suspected cardiac, central nervous system, or endocrine causes of 

vomiting or diarrhea should receive aggressive evaluation and management. This may

include an electrocardiogram, continuous cardiac monitoring, intravenous access, 

supplemental oxygen, pulse oximetry, and a complete set of labs including clotting 

studies and cardiac enzymes as indicated. Obtain x-rays, CT scans, and consultations 

as needed. 

FURTHER EVALUATION OF THE PATIENT WITH DIARRHEA & 

VOMITING 

Once life-threatening conditions have been sought and treatment begun, an attempt 

should be made to further identify the cause of vomiting and diarrhea. Consider the 

following historical, physical, and laboratory investigations (Table 15-2). 

History 

A. Features of the Present Illness 

Important features of the present illness include time of onset, the nature of symptoms, 

and duration of illness. Differentiate acute (less than 2 weeks) from chronic symptoms. 

Clarify the patient's use of the term diarrhea. Identify associated symptoms. Inquire 

about fever, abdominal pain, anorexia, diarrhea, constipation, tenesmus, myalgia, 

vomiting, cephalgia, and neurologic symptoms such as paresthesias, weakness, or 

cranial nerve palsies. Inquire about the presence of blood or mucus in the stool and 

about the character of the vomitus (bloody or bilious). Determine the onset and severity 

of diarrhea and vomiting in relation to other symptoms. Abdominal cramps after copious, 

watery diarrhea is consistent with gastroenteritis. However, abdominal pain followed by 

nausea and loose stool could represent appendicitis. The symptom complex of profuse 

diarrhea, fever, myalgias, and cephalgia is consistent with dysentery, whereas a 

symptom complex of sudden severe headache, nausea, vomiting, and loose stool could 

represent a process such as subarachnoid hemorrhage. 

B. Medical and Surgical History 

Inquire about the patient's medical and surgical history. Give special attention to 

immunocompetency. Inquire about a history of HIV, diabetes mellitus, GI bleed, 

abdominal surgeries, malignancies, and endocrine disease. Ask about recent 

chemotherapy or radiation therapy. 

C. Medications and Antibiotic Use 

Inquire about medications including prescription, over the counter, herbal preparations, 

and drugs of abuse. Give particular attention to recent antibiotic or laxative use. 

D. Exposure Risk; Similar Illness in Others 

Ask about common source exposures such as daycare or community outbreaks. Inquire 

about a history of hospitalization or institutionalization. 

E. Dietary History 

Inquire about unusual foods, dairy products, eggs, seafood, or unpasteurized or 

undercooked food. Ask about the ingestion of mushrooms or other plant products. 

F. Travel History

Inquire about recent international travel, especially to developing countries. Ask about 

recent domestic travel or outdoor activities, especially backpacking or exposure to new 

water sources. 

G. Toxin Exposures 

Assess the risk of exposure to toxins, including heavy metals, carbon monoxide, 

salicylates, and digoxin (see Figure 15-1). Ask about occupational history as it relates to 

toxin exposures. In farm workers, consider pesticides (organophosphate poisoning) and 

nicotine (green tobacco syndrome). Inquire about a history of allergic reactions. 

H. Sexual Exposures 

Inquire about sexual contacts. Amebiasis, giardiasis, campylobacteriosis, salmonellosis, 

and shigellosis can be transmitted by both heterosexual and homosexual contact. 

Chlamydia trachomatis, herpes simplex, and Neisseria gonorrhoeae are also possible 

causes of lower GI symptoms. HIV-positive and immunocompromised individuals are 

subject to infections with Cryptosporidium, cytomegalovirus, and Mycobacterium avium 

intracellulare. 


Use the physical examination to assess the patient's hydration status, evaluate for 

sepsis, rule out the acute abdomen, and determine the presence of blood in the stool. 

A. General Appearance 

Assess the patient's overall health. Look for evidence of volume depletion, a toxic 

appearance, or jaundice. 

B. Fever 

Fever is consistent with invasive bacterial or parasitic causes of gastroenteritis (ie, 

dysentery). Fever could also indicate a process requiring acute surgical intervention. 

Less commonly, fever may be associated with a viral or noninvasive bacterial 

gastroenteritis. Food poisoning should not be associated with fever. 

C. Blood Pressure and Pulse Rate 

Hypotension and tachycardia are typical responses to volume depletion. If the volume 

status is not apparent, evaluate for orthostasis with the patient supine, sitting, and 

standing to detect more subtle degrees of volume depletion (systolic pressure drop = 10 

mm Hg and pulse rise = 15 beats/min). Young, healthy adults may maintain normal vital 

signs even with significant dehydration. Look for a blunted response in patients who are 

taking atrioventricular nodal blockers. 

D. Abdominal Examination 

Significant abdominal pain should prompt the search for causes other than infectious 

gastroenteritis. If abdominal examination elicits focal tenderness, or if signs of peritoneal 

inflammation are present, consider acute surgical pathology. However, subjective, 

diffuse, and crampy abdominal pain or tenderness may occur after extensive vomiting or 

diarrhea. In addition, several infectious agents, most notably Yersinia enterocolitica and 

Campylobacter sp., may mimic appendicitis and cause right lower quadrant pain, 

anorexia, low grade fever, and vomiting preceding the onset of diarrhea. Appendicitis

must be ruled out in patients with this presentation. 

E. Rectal Examination 

Perform rectal examination to detect fecal impaction, melena, or hematochezia. 

Laboratory & Diagnostic Studies 

Laboratory and diagnostic tests are of limited value in the routine evaluation of diarrhea 

and vomiting. Testing should be carried out, as indicated, in patients with a suspected 

noninfectious cause of vomiting or diarrhea, in those who are hemodynamically 

unstable, the very young, the elderly, and immunosuppressed individuals. In addition, 

testing may be necessary in patients with a prolonged course or in those not responding 

to conservative management. 

A. Fecal Cell Count 

Fecal erythrocytes and, to a greater degree, leukocytes have been used as a guide to 

determine who should receive empiric antibiotics. Both findings are associated with 

inflammatory diarrhea, of which bacterial dysentery is a common cause. However, there 

are many noninfectious causes of inflammatory diarrhea, which may also produce fecal 

red and white cells. These include inflammatory bowel disease, chemotherapy and 

radiation therapy, hypersensitivity, and autoimmune disorders. Just as the presence of 

erythrocytes and leukocytes is not specific for a bacterial process, their absence by 

stool smear does not rule it out. Furthermore, the cell count has not been shown to be a 

good indicator of which patients will benefit from empiric antibiotic treatment. 

B. Bacterial Culture of Stool 

Consider bacterial culture of stool in patients experiencing a prolonged course, in 

infants, in the elderly, in immunocompromised patients, and in patients who appear 

toxic. 

C. Stool for Ova and Parasites 

Consider testing for ova and parasites in patients with chronic diarrhea, those with a 

history of travel to developing countries, patients with HIV infection, and those with 

exposure to infants in daycare. 

D. Clostridium difficile Toxin 

Consider testing for C difficile toxin if the patient reports recent antibiotic use. Diarrhea 

may be delayed as long as 12 weeks after antibiotic therapy. Clindamycin, penicillins, 

and cephalosporins are commonly implicated. 

E. Escherichia coli 0157:H7 Toxin 

Test patients with suspected hemolytic-uremic syndrome for E coli 0157:H7 toxin. 

F. Giardia Antigen 

Consider testing for Giardia antigen in HIV-infected patients, in those with a history of 

travel to developing countries or a history of backpacking, and in those with daycare 

exposure. 

G. CBC, Blood Urea Nitrogen/Creatinine, Glucose, Lipase, and Liver Function

Tests 

Order other blood tests as indicated, especially if significant dehydration is suspected. 

H. Urinalysis 

A urinalysis and a urine pregnancy test should be obtained if indicated. 

I. Radiographic Evaluation 

Radiographic evaluation is indicated for patients thought to have a surgical abdomen. If 

abnormal bowel sounds, bilious vomiting, or abdominal distention are present, consider 

an acute abdominal series. An abdominal CT scan or an ultrasound may be appropriate 

as indicated. 

J. Referral 

Referral to a gastroenterologist may be indicated in the evaluation of chronic diarrhea. 

EMERGENCY EVALUATION & MANAGEMENT OF INFECTIOUS 

CAUSES OF DIARRHEA & VOMITING 

The specific agent responsible for an episode of infectious gastroenteritis is difficult to 

identify in the acute setting. However, viral agents account for the majority of episodes, 

up to 70% by some estimates. Of the remaining infectious causes, bacterial agents 

account for approximately 24% and parasitic agents account for 6%. 

VIRAL GASTROENTERITIS 


• Mild systemic symptoms; generally no fever or abdominal pain. 

• Fecal erythrocytes and leukocytes are uncommon. 

• Dehydration may be mild to severe. 


Most viral agents produce a secretory diarrhea. Viral cytotoxins lead to an increased 

cellular permeability and result in the secretion of water and electrolytes into the 

intestinal lumen. Unlike invasive dysentery, viral gastroenteritis usually lacks significant 

systemic symptoms and is not generally associated with fever and abdominal pain. 

Fecal erythrocytes and leukocytes are uncommon. The most frequently identified agents 

are Norwalk virus and rotavirus. 


Like other causes of nondysenteric gastroenteritis (Table 15-3), viral gastroenteritis 

tends to be self-limiting and to require only supportive care. However, significant 

dehydration can occur and lead to severe illness, especially in those at the extremes of 

age or those with other compromising medical conditions.

BACTERIAL GASTROENTERITIS 


• Cytotoxin-mediated bacterial gastroenteritis is clinically similar to viral gastroenteritis. 

• Invasive bacterial enteritis produces dysentery with fever, diarrhea, abdominal cramps, 

and other systemic symptoms. 

• Fecal erythrocytes and leukocytes are common in invasive disease. 


Bacterial agents may produce either an inflammatory or a secretory diarrhea. Secretory 

diarrhea is cytotoxin mediated and may be caused by toxins that are preformed and are 

therefore rapid acting, as with Staphylococcus aureus food poisoning, or by toxins 

formed after bacterial colonization, as with Vibrio cholerae (see Table 15-3). 

Inflammatory diarrhea is caused by direct bacterial invasion of the intestinal mucosa. 

The result is release into the intestinal lumen of water, electrolytes, blood, proteins, and 

mucus. The clinical presentation is dysentery and may include fever, abdominal pain, 

bloody diarrhea, anorexia, myalgia, cephalgia, dehydration, and weight loss. With 

invasive enteritis, stool smears generally contain both erythrocytes and leukocytes. 


Among patients with gastroenteritis, those with dysentery tend to experience the 

greatest morbidity and mortality. Several invasive bacterial agents, most notably 

Salmonella and Shigella, may result in bacteremia, sepsis, and death. This is especially 

of concern in the elderly, infants, and the immunocompromised. However, any bacterial 

agent can cause significant harm in susceptible patients. Worldwide, V cholerae 

accounts for a significant number of deaths annually. Treatment depends on the 

causative agent; however, in the acute setting an empiric strategy is often required (see 

below). 

PARASITIC ENTERITIS 


• Acute amebic dysentery may be clinically similar to bacterial dysentery. 

• Consider parasitic causes in patients with chronic diarrhea, a travel history to 

developing countries, or a history of institutionalization or immunocompromise. 


Parasitic agents are rarely identified in the emergency department. Acute amebic 

dysentery, caused by Entamoeba histolytica, may be difficult to distinguish clinically

from dysentery of a bacterial cause. Consider parasitic causes in patients with a travel 

history to developing countries, in institutionalized patients, or in immunocompromised 

patients. Also consider parasitic causes in those with a prolonged course and in those 

not responding to conventional treatment. Laboratory analysis of stool may be of benefit 

for diagnosing suspected parasitic enteritis. 


Treatment is best determined by the results of stool analysis. In the acute setting, 

empiric treatment may be required (see next section). 

EMPIRIC MANAGEMENT & DISPOSITION OF PATIENTS WITH INFECTIOUS 

GASTROENTERITIS 

Supportive Care 

Initial treatment consists of supportive care with special attention to the patient's 

hydration status. For many patients, this may be the only treatment necessary. Oral 

rehydration may be used for mild to moderate dehydration. In pediatric patients, oral 

rehydration can be accomplished by giving 50-100 ml/kg of a glucose-electrolyte 

solution over 4 hours. 

In patients with evidence of more severe dehydration, initiate intravenous fluid 

resuscitation with normal saline or lactated Ringer's solution. Give pediatric patients a 

bolus of 20 mL/kg of normal saline, which may be repeated as needed. Because 

children are particularly susceptible to hypoglycemia after prolonged vomiting and poor 

oral intake, a rapid bedside glucose determination should be performed in ill-appearing 

pediatric patients. 

Empiric Chemotherapy 

Interruption of the fecal-oral pathway should be the initial treatment for infectious 

gastroenteritis and can be accomplished by adherence to strict hygiene. Viral and 

noninvasive bacterial gastroenteritis, as well as many cases of bacterial dysentery, tend 

to be self-limiting and to require only supportive therapy. Initiate empiric antibiotic 

treatment in patients with a suspected invasive bacterial process and severe diarrhea, 

systemic symptoms, fever, and abdominal pain or in those who appear toxic. Fecal cell 

count is of limited utility in deciding whom to treat. Admit patients with this presentation if 

they are immunocompromised, have complicating medical conditions, are elderly, or are 

infants. For these patients, base ultimate treatment on culture results. Young, healthy 

adults may be candidates for outpatient treatment. 

Because the results of cultures are usually unavailable in the acute setting, treatment 

must be empiric and guided by knowledge of common causes of dysentery (Table 15-4 

). Ciprofloxacin, 500 mg orally twice daily for 3-5 days, has been shown to be more 

effective than trimethoprim-sulfamethoxazole (TMP-SMZ). Use empiric treatment with 

caution in pediatric patients and the elderly because of an association with 

hemolytic-uremic syndrome. This association has been shown with both ciprofloxacin 

and TMP-SMZ and is most strongly associated with treatment of enterohemorrhagic E

coli 0157:H7. Salmonella and Shigella have also been implicated. If possible, therefore, 

treatment in these patients should be based on culture results. 

Because no broad empiric strategy exists for the treatment of parasitic agents, drug 

therapy is best guided by laboratory analysis. However, if amebic dysentery is of 

concern, treatment with metronidazole should be considered. A second agent, such as 

iodoquinol, is needed after initial treatment. In patients with a history of previous 

antibiotic use and suspected C difficile colitis, C difficile toxin assay followed by oral 

vancomycin or metronidazole is appropriate therapy. 

Symptomatic Treatment 

A. Antiemetics 

Intravenous hydration helps reduce emesis and should be used as initial therapy. Often 

this is the only therapy needed. For patients with uncontrollable, protracted vomiting, the 

use of an antiemetic can be considered. However, these agents may cause somnolence 

and complicate evaluation in a potentially septic population. In addition, side effects are 

common, especially dystonic reactions with the phenothiazines (prochlorperazine or 

promethazine). For patients with vomiting significant enough to require antiemetics, 

obtain intravenous access and give an initial fluid bolus. Administer antiemetics 

intravenously or as a suppository. Consider the following: 

• Prochlorperazine (Compazine): adults, 5-10 mg intravenously, or 25 mg rectally; 

children > 10 kg, 0.1 mg/kg rectally every 6 hours (use is contraindicated in children < 

10 kg). 

• Promethazine (Phenergan): adults, 12.5-25.0 mg intravenously or rectally; children, 

0.25-1.0 mg/kg rectally every 4-6 hours. 

• Metoclopramide (Reglan): adults, 5-10 mg intravenously; children, 0.1-0.2 mg/kg 

intravenously every 6-8 hours. 

B. Antidiarrheal Agents 

The literature remains divided over use of antimotility agents in treating acute enteritis. 

Most beneficial effects are modest with the possible introduction of adverse effects. Of 

concern is the association of morphine administration with Salmonella and Shigella 

bacteremia. An additional association has been suggested between the use of opiates, 

loperamide, or diphenoxylate with atropine and the precipitation of toxic megacolon in 

patients with ulcerative colitis or antibiotic-associated colitis. Therefore, the use of these 

agents should be limited in the acute setting. Commonly used agents and some 

associated risks are listed below: 

• Loperamide (Imodium): Avoid in patients with antibiotic-associated colitis, inflammatory 

bowel disease, or dysentery. 

• Bismuth subsalicylate suspension (Pepto-Bismol): Avoid in pediatric patients because 

of concern about Reye syndrome. It may cause salicylate toxicity. 

• Kaolin-pectin suspension (Kaopectate): May cause constipation, bloating. Avoid if

intestinal obstruction is suspected. 

• Diphenoxylate with atropine (Lomotil): Avoid in pediatrics patients. May precipitate 

toxic megacolon in patients with inflammatory bowel disease. May cause central 

nervous system depression. 

• Opiates: Avoid in patients with antibiotic-associated colitis, inflammatory bowel 

disease, or dysentery. 

Disposition 

Hospitalization is rarely required for vomiting or diarrhea due to food poisoning or viral 

gastroenteritis. Even though symptoms may be severe, the vomiting or diarrhea rarely 

persists long enough to require inpatient parenteral hydration. Patients with dysentery 

and a toxic appearance, severe dehydration, or persistent vomiting or diarrhea; those 

with complicating medical conditions; and the very young or elderly may require 

hospitalization. Hospitalization may be required in the following cases: 

• Extremes of age: newborns and the very elderly tolerate fluid depletion poorly. 

• Systemic toxemia, as indicated by high fever and rigors. 

• Possible toxic exposures requiring further evaluation or treatment. 

• Massive diarrhea or extreme dehydration. 

• Severe vomiting (preventing oral replenishment) with diarrhea. 

• For further evaluation of unexplained causes of vomiting or diarrhea. 

• Poor home environment where required support cannot be provided. 

Aranda-Michel J, Giannella RA: Acute diarrhea: a practical review. Am J Med 

1999;106(6):670. [PMID: 10378626] 

Besser RE et al: Escherichia coli O157:H7 gastroenteritis and the hemolytic uremic 

syndrome: an emerging infectious disease. Annu Rev Med 1999;50:355. [PMID: 

10073283] 

Cleary RK: Clostridium difficile-associated diarrhea and colitis: clinical manifestations, 

diagnosis, and treatment. Dis Colon Rectum 1998;41(11):1435. [PMID: 9823813] 

Daniels NA et al: Vibrio parahaemolyticus infections in the United States, 1973-1998. J 

Infect Dis 2000;181(5):1661. [PMID: 10823766] 

Dryden MS et al: Empirical treatment of severe acute community-acquired 

gastroenteritis with ciprofloxacin. Clin Infect Dis 1996;22:1019. [PMID: 8783703] 

Dupont HL: Guidelines on acute infectious diarrhea in adults. Am J Gastroenterol

1997;92(11):1962. [PMID: 9362174] 

Eliason BC, Lewan RB: Gastroenteritis in children: principles of diagnosis and 

treatment. Am Fam Physician 1998;58(8): 1769. [PMID: 9835852] 

Fine KD, Schiller LR: AGA technical review on the evaluation and management of 

chronic diarrhea. Gastroenterology 1999;116 (6):1464. [PMID: 10348832] 

Framm SR, Soave R: Agents of diarrhea. Med Clin North Am 1997;81(2):427. [PMID: 

9093236] 

Gomi H et al: In vitro antimicrobial susceptibility testing of bacterial enteropathogens 

causing traveler's diarrhea in four geographic regions. Antimicrob Agents Chemother 

2001;45(1): 212. [PMID: 11120968] 

Hogan DE: The emergency department approach to diarrhea. Emerg Med Clin North 

Am 1996;14(4):673. [PMID: 8921764] 

Kroser JA, Metz DC: Evaluation of the adult patient with diarrhea. Prim Care 

1996;23(3):629. [PMID: 8888349] 

MacFarlane AS et al: Morphine increases susceptibility to oral Salmonella typhimurium 

infection. J Infect Dis 2000;181(4): 1350. [PMID: 10762566] 

Manatsathit S et al: Guideline for the management of acute diarrhea in adults. J 

Gastroenterol Hepatol 2002;17(Suppl):S54. [PMID: 12000594] 

Mathan VI: Diarrhoeal diseases. Brit Med Bull 1998;54(2):407. [PMID: 9830206] 

McNeely WS et al: Occult blood versus fecal leukocytes in the diagnosis of bacterial 

diarrhea: a study of U.S. travelers to Mexico and Mexican children. Am J Trop Med Hyg 

1996;55(4): 430. [PMID: 8916801] 

Nazarian LF: A synopsis of the American Academy of Pediatrics' practice parameter on 

the management of acute gastroenteritis in young children. Pediatr Rev 1997;18(7):221. 

[PMID: 9203830] 

Oldfield EC et al: The role of antibiotics in the treatment of infectious diarrhea. 

Gastroenterol Clin North Am 2001;30(3): 817. [PMID: 11586559] 

Slutsker L et al: Escherichia coli 0157:H7 diarrhea in the United States: clinical and 

epidemiologic features. Ann Intern Med 1997;126:505. [PMID: 9092315] 



SECTION II - MANAGEMENT OF COMMON EMERGENCY PROBLEMS


INTRODUCTION

Table 15-1. Conditions that may cause 

peritoneal inflammation (surgical 

abdomen) in association with vomiting 

and diarrhea. 





TABLES 

Table 15-1. Conditions that may cause peritoneal inflammation (surgical 

abdomen) in association with vomiting and diarrhea.

Table 15-2. Evaluation of acute vomiting and diarrhea. 

Complete set of vital signs: blood pressure, heart rate, respiratory rate, pulse 

oximetry, rectal temperature 

Abdominal exam: focal tenderness, signs of peritoneal inflammation, pain out of 

proportion to the exam, distended abdomen 

Rectal exam: fecal impaction, melena, hematochezia, occult blood 

Laboratory and diagnostic studies 

Fecal cell count: limited clinical utility because fecal erythrocytes and leucocytes 

are associated with dysentery and noninfectious processes 

Stool cultures: in patients who appear toxic, patients who are 

immunocompromised, and those with chronic diarrhea 

Stool for ova and parasites: in patients with chronic diarrhea, those with history of 

international travel, HIV-infected patients, and daycare exposures 

C difficile toxin: consider if recent antibiotic use Giardia antigen: consider in 

HIV-infected patients, in patients with history of travel to developing countries, in 

those with a history of backpacking, and in daycare exposures 

Complete blood count, blood urea nitrogen, creatinine, glucose, lipase, liver 

function test, and blood cultures: as indicated 

Urinalysis: urinalysis and a urine pregnancy test if indicated 

Radiographic evaluation: consider an acute abdominal series in suspected bowel 

obstruction; abdominal CT scan or ultrasound as indicated

Table 15-3. Differential diagnostic features of common types of nondysenteric gastroenteritis. 

Mode of 

Transmission Comments 

Previously cooked 

meats, fried rice, 

vegetables, dried 

fruit and powdered 

milk 

Home-canned fruits 

and vegetables; 

commercial fish 

products 

Contaminated 

scombroid fish (tuna, 

bonito, mackerel); 

dolphin fish 

(mahi-mahi) 

Staphylococcus aureus 1-6 hours 

Abrupt onset of 

nausea and 

vomiting, mild 

diarrhea. Fever is 

rare. Induced by 

preformed 

enterotoxins. 

Clostridium perfringens 8-24 hours 

Very rare. Mild 

gastrointestinal 

symptoms, followed 

by weakness, 

malaise, fatigue, 

drymouth, diplopia, 

dysphagia, and 

muscle 

incoordination. 

Progressive cranial 

nerve palsies and 

muscle weakness 

may lead to 

respiratory failure. 

Enterotoxigenic Escherichia coli 12-72 hours 

Numbness and 

tingling of the 

mouth; dysphagia; 

headache; 

dizziness; diffuse 

flushing of the face, 

neck, and upper 

trunk. May develop 

palpitations, 

nausea, vomiting, 

abdominal pain, and 

diarrhea. 

Bronchospasm 

occurs rarely. 

Caused by 

histamine-like 

substance released 

form contaminated 

fish muscle. 

Paralytic shellfish poisoning Up to 1 hour

Fecal-oral, 

person-to-person 

transmission; 

contaminated food or 

water; daycare; 

cooler months 


Norwalk and 

rotavirus are the 

most common 

agents. Nausea, 

vomiting, and 

watery diarrhea. 

May have mild 

abdominal cramps 

and myalgias. 

Usually afebrile. 

Occasionally 

epidemics occur, 

especially in infants 

and small children. 

Giardia lamblia 1-4 weeks 




TABLES 

Table 15-3. Differential diagnostic features of common types of 

nondysenteric gastroenteritis.

Table 15-4. Differential diagnostic features of common types of dysentery. 

Mode of 

Transmission Comments 

Fecal-oral, 

person-to-person 

transmission, or 

contaminated food. 

Daycare and 

institutions. Poor 

sanitation. Highly 

contagious. 

Contaminated food or 

water. Raw or 

undercooked shellfish. 

Salmonella spp. 8-72 hours 

Very common. 

Children aged 1-5 

years, 

institutionalized 

patients. Fever, 

headache, 

abdominal pain, 

myalgia, diarrhea 

with little 

vomiting. Febrile 

seizures and a 

toxic appearance 

may prompt 

lumbar puncture. 

Diarrhea may 

begin during the 

procedure. Fecal 

RBCs common; 

sheets of WBCs. 

Campylobacter spp. 1-7 days 

Most common 

during the 

summer months 

and in adults. 

Common in 

Japan. Diarrhea, 

abdominal 

cramps, 

low-grade fever, 

headache and 

nausea with 

minimal vomiting. 

Bacteremia is 

rare. Fecal RBCs 

and WBCs 


Enterohemorrhagic Escherichia coli 

0157:H7 

3-8 days

Contaminated water. More common in 

the elderly or the 

compromised. 

More severe in 

children. Cause 

of 10-15% of 

cases of pediatric 

diarrhea. 

Diarrhea, 

vomiting, and 

abdominal 

cramps with or 

without fever. 

Chronic infection 

may mimic 

inflammatory 

bowel disease. 

Fecal RBCs and 

WBCs common. 

Recent antibiotic use. 

Clindamycin, penicillins, 

and cephalosporins are 

most commonly 

implicated. 

Contaminated food or 

water. Poor sanitation, 

institutions. Travel to 

developing countries. 

More common in 

adults. More 

severe in 

Strongyloides stercoralis Weeks to months 

Patients with RBCs = red blood cells; TMP-SMZ = 

acute amebic trimethoprim-sulfamethoxazole; WBCs 

dysentery present = white blood cells. 

with abrupt onset 

of fever, 

abdominal pain, 

tenesmus, and 

bloody diarrhea. 

Vomiting is rare. 

Chronic 

dysentery causes 

malaise, weight 

loss, bloating, 

and 

blood-streaked 

diarrhea. May 

develop an 

hepatic abscess. 

Fecal RBCs and 

WBCs common.

Figure 15-1. Approach to the patient with vomiting and diarrhea, part 1. NSAIDs = 

nonsteroidal anti-inflammatory drugs. 





FIGURES 

Figure 15-1

Figure 15-2. Approach to the patient with vomiting and diarrhea, part 2. 





FIGURES 

Figure 15-2



(See Figure 16-1 AND TABLE 16-1.) 

1 This chapter is a revision of the chapter by Roger P. Simon, MD, from the 4th edition. 

Evaluation of the comatose patient should progress as for any patient in the emergency 

department. (For coma in victims of trauma, see Chapter 10 and 22.) Priorities include 

the initial ABCs, monitoring, venous access, and high-flow oxygen. Maintain cervical 

spine stabilization if trauma cannot be ruled out. The patient should be completely 

undressed and his or her body inspected for signs of trauma or drug use (ie, needle 

marks). Examine pupils for reactivity to light and evaluate movement of extremities for 

rapid determination of cause (ie, diffuse versus structural). The "coma cocktail" is an 

empiric treatment for common conditions presenting as coma. It consists of thiamine, 

glucose, and naloxone and should be administered early to the comatose patient. 

Thiamine is an important cofactor for several enzymes, and its depletion can lead to 

Wernicke encephalopathy with associated mental confusion. Administer a 100-mg 

intravenous dose of thiamine in all cases of coma. Hypoglycemia is another common 

condition that may present as coma. Administer a 25-g intravenous dose of glucose (50 

cc 50% dextrose) unless fingerstick testing can be done immediately at the bedside and 

reveals a normal glucose level. The order of thiamine and glucose is not important. 

Intravenous naloxone, 0.4-2.0 mg, will temporarily reverse opiate narcosis. The half-life 

of naloxone is shorter than that of more commonly abused opiates and will require 

repeated doses or continuous infusion. 

Essential laboratory studies should be ordered, including complete blood count, 

prothrombin time, partial thromboplastin time, chemistry panel, toxicologic screen, and 

blood cultures. Flumazenil, a specific benzodiazepine receptor blocker that can reverse 

benzodiazepine-induced coma, is not included in the coma cocktail because of its ability 

to induce seizures and cardiac arrhythmias. It should be used only if coma is definitively 

caused by benzodiazepine use (ie, the iatrogenic cause of moderate sedation). 

Monitor Cardiac & Pulse Oximetry 

Place the patient on a cardiac monitor to rule out lethal arrhythmias and to monitor for 

change in cardiac status. Use a pulse oximeter to monitor the patient's oxygenation 

status. 

Obtain Venous Access 

Establish two large-bore (= 18-gauge) intravenous lines in an upper extremity. Secure 

them in place for later use. 

Obtain Arterial Blood Gas Measurements

Arterial blood gas levels help to assess the adequacy of ventilation (by PCO 2 and PO 2 ), 

and blood pH is a useful clue to some drug intoxications (eg, salicylates) or metabolic 

encephalopathies. 

Perform Brief Evaluation 

A. Obtain History from Relatives, Friends, or Others 

Obtain a description of the onset of coma and a history of any chronic illnesses, 

medications, allergies, or ingestions (eg, diabetes, hypertension, drug abuse, persistent 

headaches). 

B. Obtain Complete Vital Signs 

Include core body temperature in measurement of vital signs. If hypothermia is 

suspected, use a thermometer capable of measuring temperatures less than 33.3 °C 

(92 °F). 

C. Perform a Rapid Physical Examination 

Look for major abnormalities, especially traumatic injury (including injury of the back), 

cardiopulmonary disease, and meningismus. 

D. Monitor Cardiac Rhythm 

Rule out or treat life-threatening arrhythmias. Obtain an electrocardiogram as soon as 

possible. 

Continue Treatment of Specific Disorders 

A. Hypoglycemia 

The intravenous glucose given empirically should promptly lessen hypoglycemic coma 

unless irreversible brain damage has occurred. Note: Beware of rebound hypoglycemia 

from long-acting insulin and oral hypoglycemic agents. A repeat dose of glucose or a 

glucose infusion may be necessary. 

B. Wernicke Encephalopathy 

The intravenous thiamine given empirically usually protects against Wernicke disease 

and will reverse the abnormalities over hours to days. Repeat daily until the patient 

starts a normal diet. 

C. Opiate Overdose 

The naloxone given empirically should reverse abnormalities related to opiate overdose. 

Note: Symptoms of opiate intoxication may recur, particularly if the patient has taken a 

long-acting drug (eg, methadone), because naloxone has a short half-life. Repeat as 

necessary. 

D. Hypoxemia or Hypercapnia 

Severe hypoxemia or hypercapnia may present as coma. Generally, PCO 2 must rise 

acutely to greater than 80 mm Hg and PO 2 must fall to less than 40 mm Hg before 

coma occurs. Give assisted ventilation with supplemental oxygen at once if blood gas 

abnormalities are life-threatening (PCO 2 > 60 mm Hg, PO 2 < 60 mm Hg). Marked

elevation in PCO 2 levels that are chronic (ie, near-normal pH) should not be rapidly 

corrected. See Chapter 33 for further details. 

E. Status Epilepticus 

Nonconvulsive status epilepticus can be mistaken for coma and should be considered in 

the differential diagnosis. Patients with prolonged convulsive status epilepticus may 

have decreased motor activity that may disappear altogether but continue to seize 

unnoticed. They may also present with nonconvulsive complex or absence status 

epilepticus. On physical examination, patients should be scrutinized for subtle eye and 

motor movements. If anticonvulsants are to be given empirically, phenytoin, 

fosphenytoin, lorazepam, or diazepam are good choices. The diagnosis of 

nonconvulsive status epilepticus must be confirmed by electroencephalogram. See 

Chapter 17 for detailed management of seizures. 

F. Hypothermia or Hyperthermia 

(See Chapter 44.) Body temperatures above 41-42 °C (105.8-107.6 °F) or below 32 °C 

(89.6 °F) may cause coma. Hyperthermia in particular may cause rapid, irreversible 

brain injury and requires immediate corrective action. If body temperature is 41 °C 

(105.8 °F) or higher, strip the patient and spray him or her with cool water while using a 

fan to blow air onto the patient. 

Hypothermia is generally much better tolerated than hyperthermia, and the physician 

may start corrective measures at a more deliberate pace. 

G. Meningitis and Encephalitis 

Antibiotics given early in the course of meningitis or encephalitis can improve patient 

outcome and can be accomplished early in the evaluation of a comatose patient. Any 

comatose patient with a fever or nuchal rigidity should be given appropriate empiric 

antibiotic therapy (ceftriaxone, 2 g intravenously, and ampicillin, 2 g intravenously) 

immediately. It is prudent to wait to perform the lumbar puncture after a computed 

tomography (CT) scan of the head has been obtained to rule out intracranial mass 

lesion or mass effect. Early administration of antibiotics is of the utmost importance in 

this clinical situation. No patient should be transferred to the CT scanner without first 

receiving antibiotics. 

See Chapters 19 and 40 for further comments on the management of meningitis and 

Chapter 6 for the technique of lumbar puncture and evaluation of the cerebrospinal fluid. 

Assess for Increased Intracranial Pressure 

Increased intracranial pressure (ICP) should be considered if any head trauma is 

present or if the patient has a history of intracranial tumor or infection. Head trauma, 

papilledema, pupillary abnormalities, and decerebrate posturing suggestive of herniation 

should lead to prompt intervention in lowering ICP and obtaining a head CT scan. The 

most rapid method of decreasing elevated ICP is to hyperventilate the patient to a PCO 2 

of 30-35 mm Hg. Mannitol, 0.75-1.0 g/kg, can also be used and will begin lowering the 

ICP in about 30 minutes. In the emergency setting it is not necessary to restrict fluids; 

the cerebral perfusion pressure (CPP) must be maintained, and intravenous fluids may 

be needed to maintain adequate blood pressure in response to the increase in ICP

(CPP = mean arterial pressure [MAP] - ICP). Early neurosurgical consultation is 

recommended because more definitive surgical treatment may be required. 

H. Hypertensive Encephalopathy 

Hypertension in a patient with altered mental status can result from malignant 

hypertension or from elevated ICP with resultant papilledema and secondary elevation 

of the blood pressure. Patients with malignant hypertension are young to middle aged 

and will usually demonstrate findings of end organ damage, especially hypertrophic 

cardiomyopathy and renal insufficiency. If suspected, hypertensive encephalopathy 

should be treated immediately with nitroprusside, labetalol, or another fast-acting 

intravenous antihypertensive agent. 

Look for Pinpoint Pupils 

A. Opiate Overdose 

Repeat administration of a narcotic antagonist (naloxone, 0.4-2 mg intravenously), 

particularly if the history and physical examination (eg, sclerosed veins) suggest 

intravenous drug abuse. 

B. Cholinesterase Inhibitor Poisoning 

Consider cholinesterase inhibitor poisoning if the patient has a history of exposure to 

insecticides or nerve gas and if paralysis, salivation, bronchorrhea, sweating, 

spontaneous defecation, or muscle fasciculations are present. 

If cholinesterase inhibitor poisoning is suspected, give atropine, 1-2 mg intravenously 

(adult dose), at once. Repeat every 2-5 minutes until signs of atropine effect (dilated 

pupils, flushed face, tachycardia) occur. See Chapter 45 for further details on evaluation 

and treatment of poisoning. 

C. Factitious Pinpoint Pupils 

Occasionally pinpoint pupils are due to miotic eye drops used by the patient, and some 

other condition has caused the coma. This finding can be seriously misleading unless 

the use of miotic eye drops is considered and excluded (primarily on the basis of 

history). 

FURTHER EVALUATION OF THE COMATOSE PATIENT 

Definitions 

Coma has been defined as total or near total unresponsiveness with the inability to 

induce a purposeful response. Other terms used to describe decreased levels of 

consciousness are as follows: 

• Stupor: severely impaired arousal with some response to vigorous stimuli 

• Obtundation: a lesser state of decreased arousal with some response to touch or voice 

• Lethargy: a state in which arousal, though diminished, is spontaneously maintained or 

requires only light stimulation

• Confusion: a state of impaired attention; implies adequate arousal to perform mental 

status tests of this ability 

• Delirium: a state of confusion with periods of agitation and sometimes hypervigilance, 

irritability, and hallucinations typically with alternating periods of depressed level of 

arousal 

Up to 75% of patients in a comatose state, without obvious cause, will likely have a 

diffuse systemic disorder. Structural lesions make up the remaining causes of coma; 

supratentorial lesions are more common than subtentorial lesions (Table 16-2). 

History 

A history may be obtained from friends and family (at the hospital or by telephone), 

police, or ambulance technicians. Crucial points include the following: 

• Recent head trauma, even though seemingly trivial 

• Drug use (including alcohol), recent or past (ask for pill containers) 

• History of seizures, diabetes, hypertension, cirrhosis, or previous neurologic disease 

that might explain the comatose state 

• Precomatose activity and behavior (eg, headache, confusion preceding coma); sudden 

versus gradual onset of coma 

• Multiple patients with coma or confusion, suggesting carbon monoxide poisoning or 

exposure to some other common-source toxin 


Physical examination should include the following: 

• Obtain complete vital signs and rectal temperature along with pulse oximetry. Observe 

the respiratory pattern. 

• Search carefully for signs of head trauma. (Evidence of trauma elsewhere on the body 

is presumptive evidence of head trauma.) 

• Examine for signs of meningeal irritation (nuchal rigidity, Brudzinski sign). 

Neurologic Examination 

The neurologic examination will be the most useful in determining the nature of the 

patient's unconsciousness. It is essential to record the results of the exam accurately, 

because treatment decisions will depend on whether subsequent examinations show 

improvement or deterioration in the patient's condition. Evaluation of the following areas 

assists in determining involvement of the central nervous system (CNS).

A. Respiratory Pattern 

Cheyne-Stokes, hyperventilation, apneustic breathing, or Biot breathing may be present. 

Apneustic breathing is characterized by a prolonged pause at the end of inspiration and 

suggests a lesion in the mid to caudal pons. Biot breathing is characterized by a chaotic 

or ataxic pattern with loss of regularity and suggests a lesion in the medulla or lower 

pons. 

B. Pupils 

Pinpoint pupils suggest opiate intoxication, cholinergic toxicity, or lesions in the pontine 

tegmentum. Large pupils have many causes. Adrenergic stimulation is the most 

common cause and can be from stimulant drug toxicity (eg, cocaine, phencyclidine) or 

from drug withdrawal. Pupillary asymmetry is usually caused by third nerve palsies. 

Loss of pupillary response, irregularly shaped pupils, and asymmetric sizes can be 

caused by lesions in the midbrain. Because ocular surgery has become more frequent 

than in the past, care must be taken not to confuse postoperative pupil abnormalities 

with neurologic abnormalities. 

C. Eye Movements 

Observe the position of the eyes at rest. Note dysconjugate gaze and spontaneous 

movements. Voluntary eye movement occurs in "locked-in" syndrome. (Ask the patient 

to open their eyes and look at your finger. A positive reaction indicates the syndrome.) 

1. Ocular bobbing—These quick downward conjugate movements are associated with 

a caudal pontine lesion. 

2. Convergence and retraction nystagmus—These movements are associated with a 

midbrain lesion. 

3. Ping pong gaze—This type of gaze, with pauses at extremes of horizontal gaze, is 

associated with vermian and bilateral hemispheric lesions. 

4. See-saw nystagmus—One eye intorts and rises while the other extorts and falls; this 

movement is associated with a lesion in the rostral midbrain near the anterior third 

ventricle. 

5. Dissociated nystagmus—This movement is associated with posterior fossa lesions. 

6. Oculocephalic testing—Note movements in the horizontal and vertical planes. 

(Ensure that no cervical spine trauma is present.) 

7. Oculovestibular testing—If the patient does not respond to the doll's eye maneuver 

(in which movement of the head in one direction produces conjugate eye movement in 

the opposite direction), use cold water calorics (irrigation of the contralateral ear with ice 

water). Horizontal movements are elicited by irrigating each ear separately. Irrigating 

both ears simultaneously tests vertical movements. No response suggests a lesion in 

the brain stem. 

D. Other Cranial Nerves

Spontaneous blinking indicates intact facial nerve and nucleus. Intact blink in response 

to corneal stimulation indicates intact trigeminal input and facial nerve output. 

E. Motor Responses and Reflexes 

Symmetry and spontaneous movements may give clues to side of focal lesions. 

Decorticate and decerebrate posturing are usually caused by hemispheric lesions. Deep 

tendon reflexes and plantar responses may also suggest lateralized lesion. Note any 

subtle repetitive motions suggestive of nonconvulsive seizures. Check for motor 

responses to pain both centrally (pressure on the supraorbital ridge) and peripherally 

(pressure on the nail beds of feet or hands). 

Ancillary Studies 

A. Electrolytes 

Electrolyte studies may show abnormalities such as hyponatremia, hypernatremia, or 

hypocalcemia. 

B. Bicarbonate 

Bicarbonate studies may indicate the presence of metabolic acidosis or acid-base 

disorders. 

C. Creatinine and Blood Urea Nitrogen 

Creatinine and blood urea nitrogen studies will show worsening of renal function. 

D. Arterial Blood Gas 

Arterial blood gases may show acid-base disturbances and will usually include a 

carboxyhemoglobin level to diagnose carbon monoxide poisoning. 

E. Pulse Oximetry 

Pulse oximetry provides a fast and accurate measure of oxygen saturation to rule out 

hypoxemia. 

F. Complete Blood Count 

Rarely useful, the complete blood count (CBC) may show thrombocytopenia or elevated 

or depressed white blood cell count. 

G. Urinalysis 

Urine glucose suggests hyperglycemia and hyperosmolar coma. The presence of white 

blood cells, nitrite, or bacteria suggests urosepsis. Calcium oxalate crystals suggest 

ethylene glycol poisoning. Cultures should be obtained as well. 

H. Blood and Urine Toxicology Screen 

These tests rarely change management but should be ordered when no obvious cause 

of coma is found. 

I. Head CT Scan 

If no metabolic cause for coma can be found, a noncontrast head CT scan should be 

obtained.


SUPRATENTORIAL MASS LESIONS 


• Unilateral hemispheric dysfunction; progression of deficits from rostral to caudal. 

• Aphasia (nondominant cerebral hemisphere); agnosia (nondominant cerebral 

hemisphere). 

• Somnolence and coma (diencephalon). 

• Unilateral pupil dilation and impaired cranial nerve III function (early midbrain). 

• Marked unilateral pupillary dilatation, loss of light reactivity, and oculocephalogyric 

reflexes (midbrain herniation). 

• Midline unresponsive, dilated pupils, no extraocular movements (pons). 

• Most mass lesions will appear on noncontrast CT scan. Use angiography is CT scan 

or MRI is unavailable. 


In supratentorial mass lesions, symptoms and signs of unilateral hemispheric 

dysfunction are usually present before onset of coma. These symptoms and signs 

persist into the early stages of coma. Neurologic deficits follow a characteristic 

progression from rostral to caudal (cerebral hemisphere to medulla) involvement. 

Results on neurologic examination are consistent with the anatomic level of involvement 

of the brain (Figure 16-2). The lesion can usually be demonstrated by CT scan or 

angiography. 

A. Cerebral Hemispheres 

Patients are generally alert. Hemiparesis and hemihypesthesia are commonly present. 

Aphasia may also be present with involvement of the dominant hemisphere, or agnosia 

(denial of the deficit) with nondominant involvement. 

B. Diencephalon 

Somnolence and eventually coma occur because of bilateral cortical involvement or 

diencephalic compression. Asymmetric motor and sensory abnormalities usually persist 

because of prior involvement of the cortex. Surgical removal of the mass when 

involvement does not exceed the level of the diencephalon generally results in recovery 

of consciousness. 

C. Midbrain 

1. Early stage—Herniation of the medial portion of the temporal lobe (the uncus) across 

the cerebellar tentorium produces midbrain signs, including unilateral pupillary dilation 

and impaired medial rectus muscle (oculomotor nerve) function, which may occur prior 

to loss of consciousness. 

Results on the remainder of the neurologic examination may be normal. It is critical to 

recognize that these findings represent early involvement at the midbrain level and carry

the same serious prognosis as the more classic midbrain state resulting from 

transtentorial herniation (see Figure 16-2). 

2. Midbrain stage (fully developed)—Progressive uncal herniation causes loss of 

consciousness, and the fully developed midbrain stage appears rapidly. Marked 

ipsilateral pupillary dilatation and loss of reactivity to light are noted, and caloric testing 

fails to produce medial deviation of the eye ipsilateral to the lesion. Painful stimuli elicit 

decerebrate (extensor) posturing. If the patient's condition progresses to full midbrain 

dysfunction (absent oculocephalogyric reflexes), the chances of survival without severe 

neurologic impairment decrease rapidly, especially in adults. 

D. Pons 

Pupils remain in mid position and are unreactive to light. Extraocular movements (in 

response to the doll's eye maneuver and caloric testing) are absent. (Barbiturates and 

other drugs also abolish oculomotor reflexes.) Death is inevitable once the 

supratentorial mass lesion produces pontine-level dysfunction. 

Focal pontine lesions (eg, pontine or cerebellar hemorrhage or infarction), as distinct 

from transtentorial herniation to the pontine level, produce pinpoint pupils that react to 

light when viewed with a magnifying glass. (Pinpoint pupils induced by opiates and 

pilocarpine must be excluded.) Extraocular movements are not inducible. 

Treatment 


If a delay in surgery is unavoidable and the patient's neurologic status is worsening, 

hyperventilation to an arterial PCO 2 of 30-35 mm Hg and administration of mannitol and 

the most rapidly acting intravenous glucocorticoids to reduce cerebral edema (Table 

16-3) may delay progression of the neurologic deficit. 

B. Immediate Palliative Surgery 

If the patient's neurologic status is worsening rapidly (eg, from cerebral hemispheric to 

midbrain level in less than 1 or 2 hours), immediate exploratory/decompressive 

craniotomy may be indicated, even if it must be done in the emergency department and 

even if the available personnel are not fully trained in neurosurgery. 

C. Definitive Surgery for Removal of Mass 

If a supratentorial mass lesion is suspected, emergency neurosurgical consultation is 

mandatory. Hematomas, tumors, and abscesses are the most common lesions causing 

supratentorial compression, and all may be amenable to surgery. 

If neurologic signs and symptoms are stable and the lesion is at the diencephalic level 

or above, a CT scan or magnetic resonance imaging (MRI) scan should be done. If the 

routine CT scan is normal, contrast media should be used and the scan repeated. 

Angiography and radionuclide brain scanning are also valuable diagnostic aids if CT 

scanning or MRI is unavailable. 

Disposition

Immediate hospitalization is mandatory in all patients. 

1. Subdural Hematoma 


• Headache, vomiting. 

• Confusion, paresis, depressed consciousness. 

• Pupil asymmetry, motor asymmetry, memory loss. 

• CT scan or MRI findings. 


The possibility of subdural hematoma must be considered in any comatose patient. 

Trauma is the most common cause, but in about 25% of cases, there is no history or 

evidence of trauma. 


Symptoms and signs are notoriously nonspecific, nonlocalizing, or absent (Table 16-4) 

and may be either stable or rapidly progressive. The frequency of bilateral hematomas 

makes localization of the lesion even more difficult, as does the coexistence of 

associated cerebral contusion. Hemiparesis, when present, is contralateral to the lesion 

in approximately 60% of cases, and ipsilateral pupillary dilatation occurs in 

approximately 75% of cases. Seizures may occur. CT scan is the diagnostic study of 

choice, revealing a hyperdense extra-axial crescent-shaped collection of blood, which 

rarely crosses the faux or tentorium. Subacute lesions may appear as isodense, and 

MRI would be preferred. Skull x-rays are not helpful. 

Note: Lumbar puncture is contraindicated. Cerebrospinal fluid abnormalities are 

nonspecific and cannot differentiate subdural hematomas from cerebral contusion 

without hematoma. 


Immediate hospitalization and emergency neurosurgical consultation are mandatory in 

all cases. Seek radiologic confirmation of the diagnosis in stable patients and in those 

with slowly worsening mild neurologic dysfunction. Unstable patients with rapid 

worsening (minutes to hours) neurologic deficit thought to be due to an expanding 

subdural hematoma may require emergency exploratory craniotomy without benefit of 

preoperative radiologic diagnosis. 

Hyperventilation, mannitol, and glucocorticoids (see Table 16-3) may be used to 

minimize cerebral damage while the patient is awaiting surgery. 

2. Hypertensive Intracerebral Hemorrhage


Intracerebral hemorrhage nearly always begins when the patient is awake. There are no 

prodromal features. Obtundation is unremitting and worsens steadily over minutes to 

hours, most often progressing to stupor or coma. Almost all patients are hypertensive 

(blood pressure = 170/90 mm Hg) when seen, and high blood pressure persists even 

into the late stages of transtentorial herniation. 

The ocular fundi may show hemorrhages secondary to the acute increase in ICP. 

Conjugate deviation of the eyes is common, with gaze directed toward the side of the 

supratentorial (or away from the subtentorial) hemorrhage. 

Headache occurs in 30-50% of patients and may be moderately severe; it overlies the 

location of the lesion. Vomiting and nuchal rigidity may also occur. Hemiplegia 

(contralateral to the hemorrhage) is a common early sign, because the site of 

hemorrhage (basal ganglia, 50% of cases; thalamus, 10%) abuts the internal capsule in 

most cases. Seizures are rare. CT scan provides the definitive diagnosis. The 

cerebrospinal fluid is grossly bloody in 90% of cases, and the pressure usually is above 

200 mm H 2 O and often greater than 600 mm H 2 O. The total protein content is as high 

as 300-1200 mg/dL. The cerebrospinal fluid glucose level is normal initially but may fall 

later. The cerebrospinal fluid red blood cell count may be as high as 1 million/uL, and 

white cells are present in proportion (one white cell per thousand red cells). Peripheral 

blood leukocytosis (15,000- 20,000/uL) is often present. 

Treatment 

Lowering of the blood pressure can be accomplished using labetalol, a fast-, 

short-acting agent, with both a and ß adrenergic blocking ability. Dosing is a 10 mg 

bolus intravenously, followed by 10-20 mg every 10 minutes until the desired effect or 

maximum dose of 160 mg is achieved. Sodium nitroprusside can also be used at 2 

ug/kg/min titrated to a mean arterial pressure of 100-125 mm Hg or systolic blood 

pressure of 140-160 mm Hg. 

Methods of treatment are frustratingly limited, especially because the hemorrhage 

occurs over a brief period and then stops. Bleeding probably does not recur, but the 

patient's condition worsens because of secondary cerebral edema. Survivors of 

intracerebral hemorrhage may recover with minimal neurologic deficit as the clot 

resolves over a period of months. 

Elevated intracranial pressure may respond temporarily to mannitol (see Table 16-3). 

Glucocorticoids are not efficacious. 

For hemorrhages originating deep within the brain (eg, basal ganglia, thalamus), 

surgical attempts to evacuate the clot are as disappointing as supportive care alone. 

Surgery may be life saving, however, for patients with hemorrhage into cortical white 

matter (lobar hemorrhage). 

Disposition

Immediate hospitalization is required, primarily for supportive care. 

3. Brain Abscess 


• Stupor. 

• Elevated temperature (50% of patients have normal temperature). 

• Elevated white blood cell count (25% of patients have white blood cell count < 

10,000/ul). 

• CT scan or MRI findings. 


Brain abscess accounts for only 2% of intracranial masses. Progression to stupor and 

coma may be rapid, occurring over days or, rarely, hours. Often the usual signs of 

infection are absent. The temperature is normal in half of patients, and the white blood 

cell count is below 10,000/uL in over one fourth of patients. Brain abscess should be 

considered in patients with AIDS who develop changes in mentation (may be caused by 

Toxoplasma gondii). 

Lumbar puncture is contraindicated. The results are nondiagnostic, varying between 

normal findings and those suggestive of meningitis. CT scan, radionuclide brain scan, or 

MRI will demonstrate the lesions in over 90% of cases. Antibiotics should be initiated 

immediately without awaiting the results of a CT scan if meningitis is suspected. Begin 

intravenous therapy with nafcillin, 2 g every 4 hours, plus cefotaxime, 150-200 mg/ kg in 

4 divided doses, plus metronidazole, 30 mg/kg/d in 4 divided doses (Chapter 40). 

Treatment 

Neurologic and neurosurgical consultation are necessary. Hospitalize the patient for 

definitive diagnosis and treatment. 

4. Brain Tumor 


• Headache. 

• Focal weakness. 

• Altered or depressed consciousness. 

• Seizures. 

• Papilledema. 

• Chest x-ray (lung cancer metastasized to the brain), CT scan, MRI findings. 

Clinical Findings


Coma is seldom the presenting symptom in primary or metastatic tumors of the CNS, 

although coma may result from seizures induced by the tumors. The patient typically 

has a history of days to weeks of headache, focal weakness, and altered or depressed 

consciousness. Papilledema is present in 25% of cases. 


The chest x-ray is a useful screening test for brain tumors, because lung cancer that 

has metastasized to the brain is the most common intracranial tumor. Other common 

CNS metastases often involve the lung before they affect the brain. 


Treatment with glucocorticoids is often dramatically effective in reducing surrounding 

edema and improving the neurologic deficit (see Table 16-3). Hospitalize the patient for 

diagnosis and treatment. 

5. Cerebral Infarction (Stroke) (See also Chapter 18.) 


• Hemiparesis. 

• Hemisensory losses. 

• Aphasia (dominant side involvement). 

• CT scan findings. 


The brain swelling of cerebral edema following massive hemispheric infarction can 

produce contralateral hemispheric compression or transtentorial herniation that will 

result in coma. Such cerebral swelling becomes maximal 48-72 hours after the infarct. 


The principal findings are hemiparesis or hemisensory loss (and aphasia if the dominant 

hemisphere is involved). Evolving transtentorial herniation progresses slowly over many 

hours or several days to stupor and coma. Absence of blood in the cerebrospinal fluid or 

on CT scan of the brain rules out cerebral hemorrhage. 

Treatment 

Consider the use of thrombolytics if the patient meets the criteria. See Chapter 18 for 

specific treatment of stroke. 

Disposition

Hospitalization is indicated for all patients. 

SUBTENTORIAL MASS LESIONS 


• Coma (sudden onset). 

• Conjugate gaze toward lesion. 

• Disconjugate eye movement with doll's eye or caloric testing. 

• Internuclear ophthalmoplegia. 



Clinical findings depend on the anatomic level of brain involvement. Generally there is 

coma of sudden onset without antecedent hemispheric signs (eg, hemiparesis or 

hemihypesthesia). With conjugate gaze deviation, the eyes are directed away from the 

side of the lesion and toward the hemiparesis. Disconjugate eye 

movements—especially internuclear ophthalmoplegia (lateral deviation of one eye on 

doll's eye maneuver or caloric testing without concomitant medical deviation of the 

contralateral eye)—strongly suggest a subtentorial lesion. Motor responses are not 

helpful in differentiating subtentorial from supratentorial lesions, because decerebrate or 

flaccid responses to painful stimulation occur with supratentorial lesions that progress to 

involve subtentorial structures. Respiration may be ataxic, gasping, or agonal. 

Differentiating a primary subtentorial process from transtentorial herniation in the late 

stage may be impossible except by extrapolating from the history. 

In pontine or cerebellar hemorrhage or infarction, pinpoint pupils are often present. 

(Remember that intoxication with cholinesterase inhibitors or opiates also produces 

pinpoint pupils.) 

Treatment 

Emergency neurosurgical consultation is mandatory. If surgery must be delayed and 

neurologic abnormalities are progressive, use glucocorticoids, mannitol, and 

hyperventilation (reduce PCO 2 to 25-35 mm Hg) to try to control swelling of the brain 

(see Table 16-3). 

Disposition 

Immediate hospitalization is required in all cases. 

1. Basilar Artery Thrombosis or Embolic Occlusion 


• Coma, altered mental status. 

• Respiratory pattern irregular. 

• Pupillary abnormalities, absent or abnormal horizontal eye movements. 

• Hemiparesis, hyperreflexia, positive Babinski sign. 



Basilar artery thrombosis and embolic occlusion are relatively common vascular 

syndromes that cause coma because of direct involvement of the penetrating arteries 

supplying the central core of the brain stem. Patients are usually elderly and often have 

a history of hypertension or transient ischemic attacks or evidence of other 

atherosclerotic vascular disease. 


Basilar artery transient ischemic attacks are characterized by (in order of frequency of 

occurrence) dizziness (rarely the only symptom), diplopia, weakness and ataxia, slurred 

speech, and visceral sensations (nausea and vomiting). 

Basilar artery occlusion causes coma in half of affected patients, and almost all present 

with some alteration of consciousness. Focal subtentorial signs are present from the 

onset, and the respiratory pattern is irregular. Pupillary abnormalities vary with the site 

of the lesion and include poorly reactive pupils of normal size (3 mm), pupils fixed in mid 

position (5 mm), or pinpoint pupils. Skew deviation of the eyes is common. Horizontal 

eye movements are absent or asymmetric during the doll's eye maneuver or caloric 

testing. Conjugate eye deviation, if present, is directed away from the side of the lesion 

and toward the hemiparesis. Vertical eye movements in response to the doll's eye 

maneuver may be intact. Symmetric or asymmetric motor signs (hemiparesis, 

hyperreflexia, and Babinski sign) may be present. The cerebrospinal fluid is free of 

blood. 

Treatment 

Current opinion supports anticoagulation for progressive subtotal lesions, although 

evidence for the efficacy of this treatment is inconclusive. 

Disposition 

Hospitalize the patient for treatment and supportive care. The prognosis varies directly 

with the degree of brain stem injury. 

2. Pontine Hemorrhage 


• Coma. 

• Ocular bobbing, pinpoint pupils, loss of lateral eye movement. 

• Fever. 

• Lumbar puncture or CT scan findings. 


Coma of apoplectic onset is the hallmark of pontine hemorrhage. Physical examination 

reveals many of the findings noted in basilar artery infarction, but there is no history of 

transient ischemic episodes preceding pontine hemorrhage. Additional features 

especially suggestive of pontine involvement include ocular bobbing, pinpoint pupils, 

and loss of lateral eye movements. Fever greater than 39.5 °C (103 °F) may occur in 

patients surviving for more than several hours. The cerebrospinal fluid is grossly bloody 

and under increased pressure. CT scan of the brain is almost always diagnostic, 

demonstrating high density (blood) in the brain stem. 

Treatment 

There is no effective treatment, and the mortality rate is high. 

Disposition 

Hospitalize the patient for confirmation of the diagnosis and for supportive care. 

3. Intracerebellar Hemorrhage or Infarction 


• Sudden onset headache, nausea, vomiting. 

• Ataxia. 

• Small reactive pupils. 

• Ipsilateral facial nerve palsy, nuchal rigidity, ipsilateral cerebellar limb ataxia. 

• Lumbar puncture or CT scan findings. 


Hypertension is the cause of intracerebellar hemorrhage in approximate three fourths of 

patients. The remaining cases result from ruptured intracerebellar arteriovenous 

malformations. Most affected patients are over age 50 years. 


The clinical picture ranges from sudden brain stem compression progressing rapidly to 

death (a picture virtually indistinguishable from primary pontine hemorrhage) to a 

progressive syndrome developing over hours or even several days (as commonly seen 

with cerebellar infarction). The onset is sudden and characterized by headache and 

nausea and vomiting, with marked ataxia of gait that may progress to complete inability

to walk or stand. Caution: Early stages of cerebellar hemorrhage are sometimes 

misdiagnosed as drug or alcohol intoxication. 

Other features include small reactive pupils with conjugate gaze deviation away from 

the side of the lesion, preserved vertical eye movements, and an ipsilateral peripheral 

facial palsy in some cases. Nuchal rigidity is present in half of patients. Hemiparesis is 

rare and, if present, mild in degree. The incidence of ipsilateral cerebellar limb ataxia 

varies, but when this sign is present, it is of obvious value in locating the lesion. 

Cerebrospinal fluid becomes grossly bloody within several hours after intracerebellar 

hemorrhage. 

Prompt diagnosis, preferably with CT scan of the brain (in which increased density seen 

on the scan represents blood in the cerebellar hemisphere), is crucial. Surgical 

decompression may be life saving. 

Treatment 

The only treatment for symptomatic cerebellar hemorrhage is surgical decompression, 

which may dramatically reduce symptoms. Pharmacologic reduction of cerebral edema 

may briefly delay progression of symptoms until surgery can be performed (see Table 

16-3). 

If appropriate treatment is given, lethargic or even stuporous patients may survive with 

minimal or no residual damage and with intact intellect. If the patient is in a deep coma, 

the chances for meaningful survival are small. 

Disposition 

Hospitalize the patient immediately for emergency surgical decompression. 

4. Subdural & Epidural Hematoma (Subtentorial) 


• Vomiting. 

• Cerebellar signs. 

• Ataxia, progressive obtundation, nuchal rigidity. 

• Papilledema (chronic). 



Subtentorial subdural and epidural hematomas are rare lesions with similar clinical 

pictures. Prompt and accurate diagnosis is important, because these potentially fatal 

disorders may be treated effectively. Occipital trauma frequently precedes the onset of 

brain stem involvement by hours to weeks.


Physical findings are those of extrinsic compression of the brain stem: vomiting, 

cerebellar signs with ataxia, and progressive obtundation. Nuchal rigidity may be 

present. Papilledema may occur in chronic cases. 

In most patients, skull x-rays reveal a fracture line crossing the occipital venous sinuses. 

CT scan confirms the diagnosis. 


Hospitalize the patient immediately for an urgent surgical decompression. 

5. "Locked-In" Syndrome 


• Patient is awake and alert. 

• Patient is quadriplegic and unable to speak. 

• Decerebrate posturing, flexor spasms. 

• One or more voluntary movements is preserved: eye opening, vertical eye movement, 

convergence. 

• Physical exam, lumbar puncture, and CT scan findings. 


The portion of the reticular formation responsible for consciousness lies above the level 

of the mid pons. Therefore, "transection" of the low brain stem by basilar artery stroke, 

encephalitis, demyelinating disease, or an infiltrative tumor can produce an akinetic and 

mute state with preserved consciousness (hence the term locked-in). 


Patients with "locked-in" syndrome are in fact awakened and alert but appear comatose 

because they are quadriplegic and unable to speak. Decerebrate posturing or flexor 

spasms may be noted. However, one or more voluntary movements such as eye 

opening, vertical eye movement, or convergence are preserved. Therefore, always 

instruct an apparently comatose patient to "open your eyes" or "look up at my finger" at 

least once during the examination. Voluntary movement of any kind is inconsistent with 

true coma. 


Hospitalize the patient for treatment and rehabilitation. Some patients will recover 

significant function after a month or more. 

POSTICTAL STATE


• Patient is unresponsive to pain. 

• Nonfocal neurologic exam. 

• Babinski sign (transient). 

• Todd paralysis. 

• Signs of recent seizure: tongue trauma, incontinence, rapidly clearing anion gap lactic 

acidosis. 

• Study findings: electrolytes, calcium, magnesium, lumbar puncture, CT scan. 


Coma resulting from seizure disorders is usually not a difficult diagnostic problem, 

because recovery of consciousness is rapid following the end of the seizure. Prolonged 

postictal coma (several hours) followed by several days of confusion may occur after 

status epilepticus, in patients with brain damage (eg, multiple cerebral infarctions, head 

trauma, encephalitis, mental retardation), and in patients with metabolic encephalopathy 

that alters consciousness and induces seizures (eg, hyponatremia, hyperglycemia). 


Patients may initially be unresponsive to deep pain and exhibit sonorous respirations. 

The neurologic examination is usually nonfocal, although Babinski sign may be 

transiently present. Uncommonly, there may be focal abnormalities (Todd paralysis) 

referable anatomically to the focus of seizure activity in the brain. 

Other evidence of a recent seizure may be present, such as trauma to the tongue from 

biting, incontinence, or a rapidly clearing anion gap (lactic) acidosis. The rapid resolution 

of coma in a patient with a witnessed seizure or known seizure disorder should suggest 

the diagnosis of the postictal state as the cause of coma. Coma that is at first thought to 

be postictal but that fails to improve should prompt an investigation for underlying 

processes contributing to mental status depression, including metabolic 

encephalopathy, underlying diffuse brain damage, encephalitis, and structural lesion. 

Appropriate investigations should include measurements of serum electrolytes, calcium, 

and magnesium; CT scan; and lumbar puncture. 

Treatment 

Treatment depends on the underlying cause of the seizure. Be alert for metabolic 

causes and treat them appropriately. See Chapter 17 for details of management. 

Disposition 

Immediate hospitalization is required for all cases of status epilepticus and prolonged 

postictal coma and for seizures due to metabolic causes that are not quickly correctable. 

Outpatient management may be possible for stable patients.

METABOLIC ENCEPHALOPATHIES 


• Progressive somnolence. 

• Intoxication, toxic delirium. 

• Agitation, stupor, coma. 

• Headache. 

• Symmetric neurologic findings. 

• Reactive pupils. 

• Hypoventilation, abnormal respiratory pattern. 

• Study findings: serum glucose, CBC, arterial blood gas, alcohol level, liver function 

tests, serum osmolality, serum electrolytes, rectal temperature, lumbar puncture, CT 

scan, electroencephalogram, electrocardiogram. 

• Loss of extraocular movements. 


Metabolic encephalopathies are characterized by a period of progressive somnolence, 

intoxication, toxic delirium, or agitation, after which the patient gradually sinks into a 

stuporous and finally comatose state. Subarachnoid hemorrhage is an exception: loss of 

consciousness is rapid. Headache is not an initial symptom of metabolic 

encephalopathy except in the case of meningitis, subarachnoid hemorrhage, or 

poisoning due to organophosphate compounds or carbon monoxide. 

Neurologic examination fails to reveal focal hemispheric lesions (hemiparesis, 

hemisensory loss, aphasia) before loss of consciousness. Neurologic findings are 

symmetric except in some patients with hepatic encephalopathy and hypoglycemic 

coma, which may be accompanied by focal signs (especially hemiparesis) that may 

alternate sides. Myoclonus and, during consciousness, asterixis may be present. 

The hallmark of metabolic encephalopathy is reactive pupils (a midbrain function) in the 

presence of impaired function of the lower brain stem (eg, hypoventilation, loss of 

extraocular movements), an anatomically inconsistent set of abnormalities. Respiratory 

patterns in metabolic coma vary widely and may help establish the cause of coma (see 

Table 16-1). 


Treatment depends entirely on the cause of coma. All patients require hospitalization for 

supportive care and specific therapy. 

1. Hypoglycemia (See also Chapter 41.) 


Unlike other organs, the brain relies mainly on glucose to supply its energy 

requirements. Abrupt hypoglycemia rapidly interferes with brain metabolism and quickly 

produces symptoms. Insulin and oral hypoglycemic drug overdose are the most 

common causes of hypoglycemia. 


Signs of sympathetic nervous system activity (tachycardia, sweating, and anxiety) may 

warn patients of impending hypoglycemia, although these signs may be masked by 

propranolol and other ß-blockers and are absent in patients with diabetic autonomic 

neuropathy. Common neurologic abnormalities are delirium, seizures, focal signs that 

often alternate sides, stupor, and coma. Table 16-5 summarizes the symptoms and 

signs of insulin-induced hypoglycemic shock. 

Hypoglycemic coma may be tolerated for 60-90 minutes, but once the stage of flaccidity 

with hyporeflexia has been reached, glucose administration within 15 minutes is 

mandatory to avoid irreversible damage. 


Give glucose, 50 mL of 50% solution intravenously (adult dose). Once the diagnosis of 

hypoglycemia is confirmed by analysis of blood drawn before treatment, give an 

additional 50 mL as needed or begin an infusion of dextrose 5% in water. Patients 

should be observed for 1-2 hours after glucose supplementation has been discontinued 

to ensure that hypoglycemia does not recur before they are discharged from the 

hospital. In some cases, hospitalization may be necessary, especially if hypoglycemia 

recurs despite treatment or in the event of long-acting insulin or oral hypoglycemic agent 

overdose. 

2. Hypoxemia 


Hypoxemia produces brain damage only as a result of concomitant cerebral ischemia. 

Cerebral blood flow diminishes and brain ischemia occurs when the arterial PO 2 falls to 

20-45 mm Hg. In cerebral anoxia due to cardiac arrest, where the duration can be timed 

precisely, 4-6 minutes of asystole begins to result in permanent CNS damage. Following 

asystole, the pupils dilate rapidly and become fixed, and tonic posturing is observed. A 

few seizure-like tonic-clonic movements are common. 


Treatment of hypoxemia depends on the cause. Support cardiac output, and maintain 

arterial PO 2 above 60 mm Hg by supplemental oxygen or mechanical ventilation. 

Hospitalize all patients for diagnosis and treatment. 

3. Drug Overdose

Drug overdose is one of the most common causes of coma in patients presenting to the 

emergency department in coma. Many drugs may be implicated, including 

sedative-hypnotics, opiates, tricyclic antidepressants, and antiepileptics. Details of 

management can be found in Chapter 45. 

Alcohol Intoxication 

Alcohol intoxication produces a metabolic encephalopathy similar to that produced by 

sedative-hypnotic drugs, although nystagmus during wakefulness and early impairment 

of lateral eye movements are not as common. Peripheral vasodilatation is a prominent 

manifestation and produces tachycardia, hypotension, and hypothermia. 

In individuals who are not chronic alcoholics, stupor occurs when blood alcohol levels 

reach 250-300 mg/dL, and coma occurs when levels reach 300-400 mg/dL. Because 

alcohol has significant osmotic pressure (100 mg/dL = 22.4 mOsm), alcohol intoxication 

is one cause of hyperosmolality. 

Management is discussed in Chapter 45. Patients should be observed until 

improvement has occurred (normal orientation and judgment; satisfactory coordination). 

Hospitalize patients who have abnormalities that would usually require hospitalization 

(eg, metabolic abnormalities, Wernicke encephalopathy). 

Narcotic Overdose 

In narcotic overdose, hypoventilation is almost always present, along with pinpoint 

pupillary constriction and absent extraocular movements in response to the doll's eye 

maneuver. Pinpoint pupils are also associated with other disorders that must be ruled 

out: use of miotic eye drops, pontine hemorrhage, Argyll Robertson pupils from syphilis, 

and organophosphate insecticide poisoning. 

Narcotic intoxication is confirmed by rapid pupillary dilation and awakening after 

administration of a narcotic antagonist such as naloxone, 2 mg, by rapid intravenous 

injection. Note: Patients who have overdosed on certain narcotics (eg, propoxyphene 

[Darvon, many others]) may not respond to 2 mg and may require 4 mg or more. 

Patients intoxicated with alcohol may awaken briefly after administration of naloxone. 

The duration of action of naloxone varies with the dose and route of administration. 

Repeat doses are frequently necessary, especially following intoxication with long-acting 

narcotics (eg, methadone). 

Treatment of drug overdose and poisoning is outlined above and discussed more fully in 

Chapter 45. Hospitalization should be considered for patients who do not recover 

completely in the emergency department or who have taken long-acting narcotics. 

?-Hydroxybutyrate 

?-Hydroxybutyrate is a CNS depressant and can induce coma. The drug has become 

popular at rave parties and has also been called the "date rape drug." Detection of the 

drug is difficult, because most of it is eliminated through the lungs.

Treatment is primarily supportive and may involve endotracheal intubation. Some 

evidence indicates that physostigmine can be used as an antidote. Some patients 

require hospitalization for prolonged supportive care. 

4. Hepatic Encephalopathy 


Hepatic encephalopathy can occur in patients with severe acute or chronic liver disease. 

Jaundice need not be present. In the patient with preexisting liver disease, 

encephalopathy may develop rapidly following an acute insult such as gastrointestinal 

hemorrhage. Patients with surgical portacaval shunts are especially predisposed to 

encephalopathy. 

Mental status is altered and ranges from somnolence to delirium or coma. There is 

increased muscle tone; hyperreflexia is common. Prominent asterixis occurs in the 

somnolent patient. Seizures—generalized or focal—occur infrequently. Hyperventilation 

with respiratory alkalosis is nearly universal and may be demonstrated by measuring 

arterial blood pH. Cerebrospinal fluid is normal but may appear xanthochromic in 

patients with serum bilirubin levels higher than 4-6 mg/dL. 


The emergency department should provide initial supportive measures only. 

Hospitalization for definitive treatment is indicated for all patients. 

5. Disorders of Electrolytes & Osmolality 


A. Hyperosmolality and Hypoosmolality 

Coma with focal seizures is a common presentation of hyperosmolality. Consciousness 

is altered if serum osmolality is less than 260 mOsm/kg H 2 O or greater than 330-350 

mOsm/kg H 2 O. 

B. Hyponatremia 

Delirium and seizures are common presenting features of hyponatremia. Hyponatremia 

may cause neurologic symptoms when serum sodium levels are below 120 mEq/L, and 

symptoms are frequent with levels below 110 mEq/L. When the serum sodium level falls 

rapidly, symptoms occur at higher serum sodium levels. 


The diagnosis and treatment of these entities are discussed in Chapter 42. 

Hospitalization is mandatory. 

6. Hyperthermia & Hypothermia


Hyperthermia and hypothermia are associated with symmetric neurologic dysfunction 

that may progress to coma. All comatose patients must have rectal temperature taken 

with an extended-range thermometer if the standard thermometer fails to register. 

A. Hypothermia 

Internal body temperatures below 26 °C (78.8 °F) uniformly cause coma; hypothermia 

with core temperatures above 32 °C (89.6 °F) does not cause coma. Body temperatures 

of 26-32 °C (78.8-89.6 °F) are associated with varying degrees of obtundation. Pupillary 

reaction will be sluggish below 32 °C (89.6 °F) and lost below 26.5 °C (80 °F). 

B. Hyperthermia 

Internal body temperatures above 41-42 °C (105.8-107.6 °F) are associated with coma 

and may also rapidly cause permanent brain damage. Seizures are common, especially 

in children. 


If hyperthermia is present, begin to lower body temperature immediately by undressing 

the patient, spraying with cool water, and directing the breeze from a fan onto the 

patient. Further diagnostic and treatment measures are discussed in Chapter 44. 

Hospitalization is mandatory. 

7. Meningoencephalitis 


A. Prodromal Symptoms 

Prodromal symptoms such as fever, headache, malaise, or upper respiratory tract 

symptoms are present for hours to days; 20% of patients are in a coma when first seen 

by a physician. 

B. Headache 

Headache is a common and characteristic symptom, and stuporous patients should be 

aroused and asked if they have a headache. 

C. Meningeal Signs 

Look carefully for meningeal signs so that lumbar puncture can be performed if 

necessary and a diagnosis made as soon as possible. Can the neck be fully flexed so 

that the chin touches the chest (with the mouth closed), or is movement limited? Is there 

knee flexion, even slight, during passive neck flexion? Does the neck or contralateral 

knee flex during unilateral raising of the straight leg? These signs of meningeal irritation 

may be absent in deep coma or at the extremes of age. 

D. Cerebrospinal Fluid 

Cerebrospinal fluid pressure may be as high as 600 mm H 2 O. White cell counts can

ange from as few as 10 monocytes/mL in patients with viral meningoencephalitis to 

over 10,000 cells/mL, mainly polymorphonuclear neutrophils, in patients with purulent 

bacterial meningitis. Cerebrospinal fluid may be acellular on the first lumbar puncture in 

rare cases of viral encephalitis and in some cases of overwhelming bacterial meningitis, 

but in overwhelming bacterial meningitis, organisms may be seen on gram-stained 

slides. In patients with bacterial meningitis, cerebrospinal fluid glucose is commonly 

below 40 mg/dL (often in the range of 5-10 mg/dL) when blood glucose is normal; in 

viral encephalitis, cerebrospinal fluid glucose is almost always normal. 


Start antibiotic therapy immediately based on clinical findings and microscopic 

examination of cerebrospinal fluid (see Table 40-3). Hospitalization is indicated for all 

patients with meningitis who present in coma. 

8. Subarachnoid Hemorrhage 


Blood may be found in the cerebrospinal fluid of a patient with intracerebral hemorrhage 

or head trauma; however, the term subarachnoid hemorrhage normally implies bleeding 

from a ruptured cerebral aneurysm or, less commonly, hemorrhage from a cerebral 

arteriovenous malformation. Aneurysmal bleeding is uncommon before age 30 years, 

whereas arteriovenous malformations may bleed much earlier, even in childhood. 

Ruptured mycotic aneurysm from subacute infective endocarditis is rare but may be 

seen at any age. About one half of patients die within the first month following bleeding. 

Coma from subarachnoid hemorrhage is the result of many factors, including the 

contusive force of the bleeding, communicating hydrocephalus, cerebral vasospasm, 

altered critical metabolic activity, and transtentorial herniation. Risk factors for 

subarachnoid hemorrhage are smoking, female gender, African American race, alcohol 

abuse, and binge drinking. 


The onset of symptoms is abrupt and accompanied by headache that is unique in the 

patient's experience and not necessarily severe. Consciousness is often lost at the 

onset. Markedly elevated blood pressure (seen in 50% of patients) is a common result 

of the hemorrhage and is not an indication of preceding hypertension. Decerebrate 

posturing or, rarely, seizures may also occur early, and moderate to marked confusion 

is frequent if the patient is conscious. Prominent focal signs are uncommon; bilateral 

extensor plantar responses occur. Meningeal irritation (as shown by nuchal rigidity) may 

take several hours to develop and may disappear when the patient is in deep coma. 

Optic fundi may show acute hemorrhages secondary to suddenly increased ICP or the 

more classic superficial subhyaloid (preretinal) hemorrhages. 

CT scan has a 92% sensitivity within 24 hours of symptoms. If the CT is negative and 

subarachnoid bleed is still suspected, a lumbar puncture should be performed to confirm 

the diagnosis. Cerebrospinal fluid pressure is usually markedly elevated, often higher 

than 600 mm H 2 O, and the cerebrospinal fluid is grossly bloody and contains from

100,000 to more than 1 million red blood cells per microliter. In rare cases, fewer than 

100,000 red cells are seen. The white blood cell to erythrocyte ratio in cerebrospinal 

fluid is initially the same as in the peripheral blood. The noninfectious meningitis that 

results from blood in the subarachnoid space may produce a pleocytosis of several 

thousand white blood cells during the first 48 hours. A reduction in cerebrospinal fluid 

glucose resulting from this "chemical" meningitis may occur between the fourth and 

eighth days after hemorrhage. 

Useful radiologic aids include a CT scan (which shows blood in the subarachnoid space 

in more than 85% of patients) and cerebral angiography (which demonstrates the site of 

bleeding). 

Treatment 

Protect the airway. Establish the diagnosis by CT scan or, if CT scan is not diagnostic, 

by lumbar puncture. Sedate the patient with diazepam, 5-10 mg intravenously or orally, 

if needed. Avoid hypotension by correcting fluid imbalance with infusion of crystalloid 

solutions. Obtain emergency neurosurgical consultation. 

Disposition 

All patients require hospitalization. 

PSYCHOGENIC COMA 


• Patient is unresponsive. 

• Normal physical examination. 

• Flaccid symmetric decreased muscle tone. 

• Normal and symmetric reflexes; normal Babinski sign. 

• Ice water calorics. 

• L Electroencephalogram findings. 


Coma is a diagnosis of exclusion that should be made only after careful documentation. 

The general physical examination should elicit no abnormalities; neurologic examination 

generally reveals flaccid, symmetrically decreased muscle tone, normal and symmetric 

reflexes, and the normal downward response to Babinski plantar stimulation. The pupils 

are normal in size (2-3 mm) or occasionally larger and respond briskly to light. Lateral 

eye movements elicited with the doll's eye maneuver may or may not be present, 

because visual fixation can suppress this reflex. 

Differentiating Psychogenic Coma from Organic Coma 

A. Eye Movements

The slow, conjugate roving eye movements of patients in metabolic coma cannot be 

imitated and, if present, are incompatible with a diagnosis of psychogenic 

unconsciousness. 

B. Eyelid Tone 

The slow, often asymmetric and incomplete eyelid closure commonly seen in organic 

forms of coma following passive opening of the lids cannot be mimicked. In addition, the 

patient with psychogenic coma usually shows some voluntary muscle tone of the eyelids 

during passive opening by the examiner. 

C. Ice-Water Caloric Response 

A helpful objective test in diagnosing psychogenic unconsciousness is the caloric test: 

there is no response at all or tonic deviation to the side of the irrigation in organic coma, 

but nystagmus occurs in psychogenic coma. Because the quick (return) phase of 

nystagmus requires an intact cortex, its presence is incompatible with a diagnosis of 

true coma. 

D. Electroencephalogram 

The electroencephalogram in psychogenic coma is that of a normal, awake person. In 

coma due to other causes, it is invariably abnormal. 


Obtain psychiatric consultation. Hospitalization may be required. See Chapter 47 for 

details. 

CRITERIA FOR BRAIN DEATH 

Brain death is defined as the irreversible loss of function of the brain, including the brain 

stem. Before a patient may be evaluated for the diagnosis of brain death, the patient 

must meet certain criteria: 

• Clinical or neuroimaging evidence of catastrophic CNS event compatible with the 

clinical diagnosis of brain death. 

• Exclusion or correction of medical conditions that may confound clinical assessment: 

- Acid-base disorders 

- Severe electrolyte disorders 

- Endocrinopathies 

- Absence of drug intoxication/poisoning 

- Patient core temperature > 32 °C (90 °F) 

Once these criteria have been met, the patient can be tested for the diagnosis of brain 

death. If the patient meets the following criteria, the patient is observed for at least 6

hours and clinical testing is repeated. If patient testing remains unchanged, a diagnosis 

of brain death can be made. 

• Coma (unresponsiveness): no cerebral motor response to pain 

• Absence of brain stem reflexes (all of the below): 

- No pupillary response to light 

- No oculocephalic reflex (doll's eyes maneuver) 

- No response to cold water calorics 

- No corneal reflexes 

- No jaw reflex 

- No grimacing to painful stimulus 

- No gag reflex 

- No cough response to tracheal/bronchial stimulation 

- Apnea over 8 minutes with PCO 2 > 60 mm Hg 

Confirmatory testing may be used when complicating factors are present such as 

severe facial trauma, preexisting pupillary abnormalities, or toxic drug levels. 

Confirmatory tests result in findings that are consistent with brain death and are not 

diagnostic. The standard confirmatory tests include cerebral angiography, transcranial 

Doppler ultrasonography, technetium- 99 m hexamethylpropyleneamineoxime brain scan, 

and somatosensory-evoked potentials. In some cases these tests may aid in the 

diagnosis and in others they may confuse the picture. Documentation of the diagnosis of 

brain death should include the cause and irreversibility of the condition, the absence of 

brain stem reflexes, the absence of any motor response to pain, the formal apnea test 

results, and the justification for and results of any confirmatory tests. The initial and 

repeat exams should be included. Currently most authorities feel that the same criteria 

above can be used for full-term infants more than 7 days old. Criteria for premature and 

newborns are still unclear. 

American College of Emergency Physicians: Clinical policy for the initial approach to 

patients presenting with altered mental status. Ann Emerg Med 1999;33:251. 

Bialer PA: Designer drugs in general hospital. Psychiatr Clin North Am 2002;25:231. 

[PMID: 11912942] 

Caldicott DG, Kuhn M: Gamma-hydroxybutyrate overdose and physostigmine: teaching 

new tricks to an old drug. Ann Emerg Med 2001;37:99. [PMID: 11145779] 

Cantrill SV: Brain death. Emerg Med Clin North Am 1997; 15:713. [PMID: 9255142]

Feske SK: Coma and confusional states: emergency diagnosis and management. 

Neurol Clin 1998;16:237. [PMID: 9537961] 

Hoffman RS, Goldfrank LR: The poisoned patient with altered consciousness: 

controversies in the use of a coma cocktail. JAMA 1995;274:562. [PMID: 7629986] 

McCabe JM: Uniform Determination of Death Act. Health Law Vigil 1985;8:21. [PMID: 

10270263] 

Plum F, Posner JB: The Diagnosis of Stupor and Coma, 3rd ed. Davis, 1980. 

Qureshi AI, Suarez JI: Use of hypertonic saline solutions in treatment of cerebral edema 

and intracranial hypertension. Crit Care Med 2000;28:3301. [PMID: 11008996] 

Riggs JE: Neurologic manifestations of electrolyte disturbances. Neurol Clin 

2002;20:227. [PMID: 11754308] 

Stieg PE, Kase CS: Intracranial hemorrhage: diagnosis and emergency management. 

Neurol Clin 1998;16:373. [PMID: 9537967] 






Figure 16-1 AND TABLE 16-1.)

Table 16-1. Assessment and management of coma. 





TABLES 

Table 16-1. Assessment and management of coma.

Table 16-2. Differential diagnosis of coma. 

Focal 

Supratentorial Lesions 

Intracerebral hemorrhage 

Epidural hemorrhage 

Subdural hemorrhage 

Pituitary apoplexy 

Infarction 

Thrombotic arterial occlusion 

Embolic arterial occlusion 

Venous occlusion 

Tumors 

Abcesses 

Subtentorial Lesions 

Cerebellar hemorrhage 

Posterior fossa subdural/extradural hemorrhage 

Cerebellar infarct 

Cerebellar tumor 

Cerebellar abscess 

Basilar aneurysm 

Pontine hemorrhage 

Brainstem infarct 

Basilar migraine demyelination 





TABLES 

Table 16-2. Differential diagnosis of coma.

Table 16-3. Drug therapy for cerebral edema. 

Dose 

Indications/ 

Comments 

Dexamethasone Intravenous or oral Prednisone 

1-5 g/kg 

1.5-4 g/kg/d Effective orally. Nausea and vomiting 


40-120 mg Can be used as an adjunct to mannitol to 

reduce fluid in the brain and decrease 

intracranial pressure. 





TABLES 

Table 16-3. Drug therapy for cerebral edema.

Table 16-4. Common findings in patients with subdural hematomas. 1 

Acute 2 (82 

Cases) (%) 

Chronic 4 

(216 Cases) 

(%) 

Headache 44 Confusion 41 Vomiting 

44 41 

57 20 

17 27 

1 22 

6 11 

0 3 

0 3

Table 16-5. Signs and symptoms of hypoglycemia after insulin 

administration. 1 

Symptoms 

Perspiration 

Loss of contact with 

environment 

Comatose 

Decerebrate rigidity 

Small pupils 

Salivation 

Somnolence 

Excitement and restlessness 

Tachycardia if stimulated (bradycardia if 

somnolent) 

Myoclonus 

Primitive reflexes (grasping, sucking) 

Reactive, dilated pupils 

Depressed responses to pain 

Roving eye movements 

Tonic and torsional muscular spasms 

Extensor plantar response 

Bradycardia 

Flaccid tone 

Depressed reflexes

Figure 16-1. Approach to the unconscious patient. 





FIGURES 

Figure 16-1

Figure 16-2. Symptoms at various levels of anatomic involvement of the brain. (Adapted 

and reproduced, with permission, from Plum F, Posner JB: The Diagnosis of Stupor and 

Coma, 3rd ed. Davis, 1980.) 





FIGURES 

Figure 16-2

17. Syncope, Seizures, & Other Causes of Episodic Loss of 

Consciousness 1 - Adam Saperston, MD, MS 



STATUS EPILEPTICUS 



• A prolonged seizure lasting 10-15 minutes. 

• Continuous or multiple seizures without intervening periods of consciousness. 


A prolonged seizure (lasting more than 10-15 minutes), continuous seizures, or multiple 

seizure episodes without intervening periods of consciousness constitute status 

epilepticus. 

Search carefully for seizure activity in the comatose patient. Manifestations may be 

subtle (eg, deviation of head or eyes; repetitive jerking of fingers, hands, or one side of 

the face). 

Immediate Measures for Patient with Active Seizures 

Perform the following in the order given here: 

A. Protect the Airway 

Roll the patient onto one side if possible. Insert a nasopharyngeal airway. Administer 

100% oxygen by nasal cannula or nonrebreathing face mask and monitor with pulse 

oximetry. Prepare for possible endotracheal intubation in the event that anticonvulsants 

fail to terminate the seizure. Do not waste time trying to insert a bite block or tongue 

blade through clenched teeth, because it does not protect the airway and may cause 

broken teeth. 

B. Insert an Intravenous Catheter 

To start diagnostic evaluation (Table 17-1), obtain blood specimens for glucose, 

electrolytes, magnesium, and calcium determinations; hepatic and renal function tests; 

and complete blood count (CBC); as well as 3-4 tubes of blood for possible toxicology 

screen or drug levels (including anticonvulsants if patient is known or suspected to be 

taking them).

C. Rule Out Hypoglycemia 

Give glucose, 50 mL of 50% solution intravenously over 5 minutes. Note: If malnutrition 

is suspected, give thiamine, 100 mg intravenously, slowly prior to, or at the same time 

as, glucose. 

D. Give Lorazepam or Other Benzodiazepine 

Give lorazepam, 0.1 mg/kg intravenously at 1- 2 mg/min up to 10 mg total, or diazepam, 

0.2 mg/kg intravenously at 2 mg/min up to 20 mg total, as a one-time dose. These drugs 

have been shown to be equally effective as first-line choices. Diazepam has a faster 

onset than lorazepam (2 versus 3 minutes); however, lorazepam has a longer duration 

of action (12-24 hours) compared to diazepam (15-30 minutes). Because of this 

property, lorazepam is currently considered the drug of choice. If venous access cannot 

be obtained, diazepam can be given rectally, endotracheally, or intraosseously, or 

midazolam, 0.2 mg/kg, can be given intramuscularly. 

E. Administer a Loading Dose of Phenytoin or Fosphenytoin 

Regardless of the effect of the benzodiazepine, a maintenance drug is required. Give 

phenytoin in normal saline, 15-18 mg/kg by intravenous infusion at a rate of 50 mg/min 

or slower. Infusion of phenytoin at more rapid rates (especially if given into centrally 

placed intravenous lines) can precipitate cardiac arrhythmias or hypotension. These 

unwanted hemodynamic and cardiac side effects can be avoided by the use of 

fosphenytoin, a prodrug of phenytoin. Fosphenytoin dosages are expressed as 

phenytoin equivalents (PE). Advantages of fosphenytoin are that it can be administered 

faster than phenytoin (150 PE/min) and intramuscularly if needed. The standard dose is 

15-20 mg PE/kg intravenously. The disadvantage is that it is more expensive. Oral 

phenytoin loading is less expensive and safe and probably appropriate if the patient is 

awake on arrival, alert, not vomiting nor intubated, and has not had repeated seizures or 

status epilepticus after arrival in the emergency department. 

F. Measure Arterial Blood Gases and pH 

Arterial blood PCO 2 is a sensitive indicator of the adequacy of ventilation (hypercapnia 

is present in proportion to the degree of hypoventilation). Metabolic acidosis due to 

lactic acidosis resulting from status epilepticus is commonly present for as long as 1 

hour after a seizure, depending on the duration and vigor of muscular activity. This 

acidosis requires no treatment. Acidosis lasting longer than 1 hour should prompt a 

search for other causes of acidosis (Chapter 42). 

G. Maintain Ventilation 

Patients in status epilepticus or those given anticonvulsant medications that are strong 

respiratory depressants may require endotracheal intubation to protect the airway and 

maintain adequate ventilation. Monitor arterial blood gas measurements to assess 

adequacy of ventilation (PO 2 = 80 mm Hg and PCO 2 at an appropriate level). 

H. Rule Out Meningitis 

Perform lumbar puncture immediately to rule out meningitis if fever (body temperature > 

38.5 °C [> 101.2 °F]) or nuchal rigidity is present. However, the muscle activity of status 

epilepticus alone produces transient fever higher than 38.5 °C (> 101.2 °F) in up to 79% 

of patients. Hyperthermia should be treated with passive cooling measures. Status

epilepticus may also produce a mild transient cerebrospinal fluid pleocytosis(< 100 

cells/uL). 

I. Use Alternative Drugs If Necessary 

If a benzodiazepine and phenytoin fail to stop the convulsions, use alternative drugs 

(Table 17-2). 

J. Search for the Underlying Cause of Seizure 

Emergency evaluation of the patient should proceed as outlined in Table 17-1. Common 

causes of seizures of acute onset are listed in Table 17-3. 

Prevention of Injury 

Prevent injury to the patient during the seizure by padding the environment. Do not use 

rigid restraint (fractures may result) or insert objects into the patient's mouth during the 

seizure. 

Treatment During Postictal State 

Do not give lorazepam or diazepam if the patient has postictal stupor or coma rather 

than active seizures. Further evaluation of the patient in stupor or coma should proceed 

as described in Chapter 16. 

Phenytoin or fosphenytoin, 15-18 mg/kg loading dose orally or intravenously (Table 

17-4; see also Table 17-2), should be given to all patients except those who have a 

short-term metabolic condition known to cause seizures, such as alcohol withdrawal or 

hypoglycemia, which does not require or respond to phenytoin. 

Alldredge BK et al: A comparison of lorazepam, diazepam, and placebo for the 

treatment of out-of-hospital status epilepticus. N Engl J Med 2001;345:631. [PMID: 

11547716] 

DeToledo JC, Ramsay RE: Fosphenytoin and phenytoin in patients with status 

epilepticus: improved tolerability versus increased costs. Drug Saf 2000;22:459. [PMID: 

10877039] 

Johnson J, Wrenn K: Inappropriate fosphenytoin use in the ED. Am J Emerg Med 

2001;4:293. [PMID: 11447516] 

Lowenstein DH, Alldredge BK: Status epilepticus. N Engl J Med 1998;338:970. [PMID: 

9521986] 

Treiman DM et al: A comparison of four treatments for generalized convulsive status 

epilepticus. N Engl J Med 1998;339:792. [PMID: 9738086] 

II. EVALUATION OF THE CONSCIOUS PATIENT WITH A HISTORY 

OF SYNCOPE 

The emergency department evaluation of the patient presenting with syncope consists

of a careful history, a physical examination that includes orthostatic blood pressure 

measurements and a 12-lead electrocardiogram (ECG). This initial workup will provide a 

diagnosis approximately 50% of the time. The initial goal should be to identify 

life-threatening causes of syncope. 

Confirm that Loss of Consciousness Is Caused by Syncope 

Syncope is a symptom characterized by transient, self-limited loss of consciousness. It 

is associated with a loss of postural tone, usually resulting in falling. Syncope must be 

differentiated from other symptoms such as dizziness, presyncope, and vertigo, all of 

which do not result in loss of consciousness. Typically syncopal episodes are brief, 

lasting no longer than 20 seconds. Recovery from syncope is usually characterized by 

almost immediate restoration of appropriate behavior and orientation. Syncope should 

not be confused with other causes of loss of consciousness such as epilepsy, hypoxia, 

hyperventilation, hypoglycemia, cataplexy, and intoxications. 

Rule Out Blood Loss 

In the awake patient with a history of one or more episodes of loss of consciousness, 

rule out acute blood loss due to various causes. 

A. Measure Blood Pressure and Pulse 

Supine hypotension (systolic blood pressure < 90 mm Hg) or severe peripheral 

vasoconstriction should be considered evidence of hemorrhagic shock until proven 

otherwise (Chapter 9). 

Orthostatic vital signs should be obtained, though they may be contraindicated in 

patients who have supine hypotension; those in shock; and those with severe altered 

mental status, spinal injuries, or pelvic and lower extremity injuries. Measure blood 

pressure and pulse after the patient has been lying down for 3 minutes. Record blood 

pressure, pulse, and symptoms again after the patient has been standing for 1 minute. 

A positive test for orthostatic hypotension is an increase of pulse of 30 beats/min or 

more, or a decrease in systolic blood pressure of 20 mm Hg or a decrease in systolic 

blood pressure to less than 90 mm Hg. The presence of symptoms such as dizziness or 

syncope should also be noted as a positive test. Many conditions can produce postural 

hypotension in the absence of hypovolemia (Table 17-5). The utility of orthostatic vital 

signs in children is questionable. Also, paradoxical bradycardia may occur in the 

presence of blood loss. 

B. Gain Venous Access 

Use an intravenous catheter (= 18 gauge), and administer a crystallized solution (eg, 

normal saline) as needed. If blood loss is suspected and the hematocrit or hemoglobin 

is normal, a repeat determination after volume repletion may confirm blood loss. Serial 

CBCs may be helpful in detecting active bleeding, and a dextrose test may be helpful if 

the history or physical examination suggests hypoglycemia. However, obtaining routine 

blood tests (for electrolytes, renal function, blood sugar, and hemoglobin) is not 

recommended, because they rarely uncover the cause of syncope. 

C. Obtain Stool Sample

Check stool specimens for blood (gross and microscopic). 

D. Look for Possible Gastrointestinal Tract Bleeding 

Nasogastric intubation may be indicated in suspected gastrointestinal tract bleeding or 

in syncope with unexplained postural hypotension. Caution: Upper gastrointestinal tract 

bleeding cannot be ruled out unless the nasogastric tube aspirate contains bile. 

Otherwise, brisk bleeding distal to the pyloric sphincter (eg, duodenal ulcer) may be 

missed if the sphincter is closed (Chapter 14). 

E. Consider Other Possible Causes of Bleeding 

Consider pelvic bleeding (eg, ruptured ectopic pregnancy) or trauma, especially that 

which is not visually obvious, such as splenic, hepatic, retroperitoneal, or pelvic injury. 

Determine Presence or Absence of Related Symptoms 

A. Syncope Associated with Cardiac Arrhythmias or Conduction Abnormalities 

Obtain an ECG. This quick, easy, noninvasive test is indicated in all cases of syncope 

except those with an otherwise clear cause. ECG abnormalities suggesting an 

arrhythmic cause of syncope are listed in Table 17-6. 

B. Syncope Associated with Prominent Abdominal or Pelvic Pain 

Patients with abdominal or pelvic pain may have hypovolemic syncope secondary to 

gastrointestinal hemorrhage, leaking aortic aneurysm, or ruptured ectopic pregnancy. 

Aortic dissection and rupture of a viscus into the peritoneal cavity may also produce 

syncope initially by vagal stimulation or later as a result of blood loss. See Chapter 13 

for further evaluation. 

C. Syncope Associated with Chest Pain or Dyspnea 

Consider myocardial infarction, pulmonary embolism, tension pneumothorax, or 

dissecting aortic aneurysm. 

D. Syncope Associated with Neurologic Symptoms (eg, Headache, Vertigo, 

Diplopia) 

Obtain neurologic consultation for possible basilar artery insufficiency, migraine, and 

subclavian steal syndrome. Loss of consciousness as an isolated symptom is rarely if 

ever caused by basilar artery ischemia. 

Further Evaluation of Syncope 

A detailed, accurate history from the patient, family, observers, or ambulance attendants 

is the most important factor in making the diagnosis. A head computed tomography (CT) 

scan must be obtained in the emergency department if the patient has focal neurologic 

findings. In the fully recovered patient with a normal neurologic exam, the head CT scan 

can be obtained either in the emergency department or at a follow-up outpatient visit. 

The most helpful features are the following: 

A. Epileptic Aura 

History of an epileptic aura preceding the syncopal attack or a period of confusion 

(postictal state) upon regaining consciousness strongly suggests seizures as the

diagnosis. This aura must be differentiated from symptoms of decreased cerebral blood 

flow (eg, those occurring before a syncopal episode or as a result of orthostatic 

hypotension or cardiac arrhythmia). 

B. Position of the Patient at Time of Loss of Consciousness 

Episodes beginning when the patient is lying down suggest seizure or cardiac 

arrhythmia, whereas orthostatic hypotension and vasovagal syncope occur when the 

patient is standing or sitting up. 

C. Syncope Related to Active Physical Exertion 

Syncope following active physical exertion is frequently noted in cardiac outflow 

obstruction (eg, aortic stenosis, hypertrophic obstructive cardiomyopathy [idiopathic 

hypertrophic subaortic stenosis], myxoma) and is elicited occasionally in patients with 

cardiac arrhythmias or pulmonary vascular disease (rare). 

D. Other Causes of Syncope 

Micturition and coughing are associated with distinctive syncopal syndromes. Simple 

fainting may occur during the first trimester of pregnancy and must be differentiated 

from syncope due to blood loss from ectopic pregnancy. Rare causes of syncope 

include glossopharyngeal neuralgia (throat or neck pain), hyperventilation, psychiatric 

causes, and Meniere disease (look for associated deafness and vertigo). 

E. Disposition 

Deciding whether to admit the patient with syncope is based on 2 different objectives: 

for diagnosis or for treatment. When the cause of syncope remains unknown, a risk 

assessment can be used for the admission decision. The following risk factors warrant 

consideration for hospitalization: (1) suspected or known heart disease, (2) ECG 

abnormalities suspicious for arrhythmic syncope, (3) syncope with onset during 

exercise, (4) family history of sudden death, and (5) syncope causing severe injury. 

Reasons for admission for patients who require treatment include the following: (1) 

syncope due to cardiac arrhythmia, ischemia, or structural cardiac disease, (2) 

cerebrovascular accident or focal neurologic deficits, and (3) severe orthostatic 

hypotension. 

Clinical policy: critical issues in the evaluation and management of patients presenting 

with syncope. Ann Emerg Med 2001; 37:771. [PMID:11385356] 

Kapoor WN: Primary Care, Syncope. N Engl J Med 2000; 343: 1856. [PMID: 11117979] 

Meyer MD, Handler J: Evaluation of the patient with syncope: an evidence based 

approach. Emerg Med Clin North Am 1999;17:189. [PMID: 10101346] 

III. EMERGENCY TREATMENT OF SPECIFIC DISORDERS CAUSING 

EPISODIC LOSS OF CONSCIOUSNESS 

SEIZURES (Epilepsy) 


Seizures can result from a primary central nervous system disorder or may be a 

manifestation of a serious underlying metabolic or systemic disorder. The distinction is 

critical, because therapy must be directed at the underlying disorder as well as at 

control of the seizure. A list of common central nervous system, metabolic, and systemic 

disorders that may cause seizures is given in Table 17-3. 


Clinically, seizures are diagnosed by episodes of loss of consciousness (or depressed 

consciousness) associated with an aura preceding the seizure (50% of patients) and a 

period of confusion (postictal state) following it. The most common type of seizure is 

grand mal epilepsy (generalized major motor convulsions). Firm diagnosis of subtler 

types of seizure (partial seizures, eg, complex partial or temporal lobe attacks) may 

require an electroencephalogram. For alcohol and drug withdrawal seizures, see 

Chapter 20. 

Seizures, especially those of status epilepticus, are accompanied by the following 

clinical abnormalities: 

A. Fever 

Internal body temperatures as high as 42 °C (107.6 °F) may develop because of intense 

muscular activity. Temperatures higher than 40 °C (104 °F) should be corrected 

(Chapter 38). 

B. Leukocytosis 

The peripheral leukocyte count may reach 60,000/uL, perhaps as a result of 

demargination of leukocytes secondary to catecholamine release; band cells, however, 

are rare. 

C. Acidosis 

Lactic acidosis is universal after a single major motor seizure, owing to maximal muscle 

exertion; arterial blood pH may reach 6.8-7.1. Lactic acidosis due to seizures is transient 

(< 1 hour) and benign and need not be corrected. It is not associated with shifts in 

potassium or hyperkalemia. Acidosis does not follow psychogenic seizures. 

D. Trauma 

Trauma, especially tongue and cheek bites, occurs commonly during seizures. 

Fractures and joint dislocations may occur. 

E. Cerebrospinal Fluid Abnormalities 

Elevation of the cerebrospinal fluid leukocyte count (usually less than 50/uL, and 

predominantly polymorphonuclear neutrophils) may follow severe seizures. Infection 

must be ruled out by cultures. 

Treatment 

For treatment of status epilepticus, see preceding discussion and Table 17-2. 

Pharmacologic characteristics of the most commonly used anticonvulsant drugs are

listed in Table 17-4. 

Disposition 

Patients with abnormal head CT scans or persistent focal abnormalities should be 

hospitalized so that diagnostic studies can be performed and the patient observed. 

Patients with established seizure disorders may be sent home several hours after the 

seizures have ceased if no acute abnormalities are found. They should be referred to 

their regular source of medical care within a few days. Patients with alcohol withdrawal 

may have seizures for 6-12 hours following the first occurrence; 95% of any additional 

seizures occur during this period. No antiepileptic drugs have been shown to be 

effective in this syndrome. Phenytoin is clearly ineffective; phenobarbital and lorazepam, 

while useful in theory, have not demonstrated efficacy in controlled studies. Chronic 

anticonvulsant administration is not necessary for alcohol withdrawal seizures alone. 

Hospitalization for alcohol withdrawal seizures is usually not needed if the patient can 

be reliably observed (eg, at a detoxification center or by family or friends) and the 

seizures treated with benzodiazepines. 

VASOVAGAL SYNCOPE (Simple Faints) 


• Usually occurs when patient is standing or sitting. 

• Lasts 10 seconds to a few minutes. 

• Associated with lightheadedness, nausea, pallor, sweating, and blurred vision. 

• No postictal period. 


Vasovagal disorders account for most episodes of syncope. Examples of vasovagal 

syncope include situational syncope (eg, micturition, cough, or defecation), emotional 

fainting, and carotid-sinus massage. Common precipitating factors are shown in Table 

17-7. 

Physiologic decreases in both arterial pressure and heart rate mediated by the vagus 

nerve combine to produce central nervous system hypoperfusion and subsequent 

syncope. Prolonged cerebral hypoxia with resultant tonic-clonic movements is more 

likely to occur if the patient remains upright. 


Vasovagal episodes begin in a standing or sitting position and only rarely in a supine 

position. 

A. Prodrome 

The prodrome lasts from 10 seconds to a few minutes and includes weakness, 

lightheadedness, nausea, pallor, sweating, salivation, blurred vision, and tachycardia.

B. Syncope 

Brain hypoperfusion causes dimming of vision; the patient then loses consciousness 

and sinks to the ground. Examination reveals an unconscious individual who is pale and 

sweating and who has dilated pupils and a slow, weak pulse. With loss of 

consciousness, bradycardia replaces tachycardia. 

C. Associated Symptoms 

Abnormal movements may be noted during the period of unconsciousness. These are 

mainly tonic or opisthotonic, but tonic-clonic activity is occasionally manifested. Urinary 

incontinence may occur, but tongue biting is rare. 

D. Postsyncopal Findings 

The patient is lucid and awake seconds to less than a minute after sinking to a 

recumbent position; a postictal confusional state is absent unless a convulsion has 

occurred. However, nervousness, dizziness, headache, nausea and vomiting, pallor, 

perspiration, and an urge to defecate may persist for hours. 

E. Recurrence 

Syncope may recur, especially if the patient stands up within 30 minutes after the 

attack. Syncope due to a specific precipitating factor (eg, cough) can be reproduced in 

the emergency department. 

Treatment 

Reassurance and a recommendation to avoid precipitating factors are usually all that is 

necessary. Cough suppression and sitting down to urinate are helpful in posttussive and 

micturitional syncope. Adequate nutrition and hydration should be encouraged. 

Disposition 

Refer the patient to an outpatient clinic or primary care physician after a period of 

observation and confirmation of the diagnosis in the emergency department. 

CARDIOPULMONARY SYNCOPE 


A cardiovascular origin for syncope is suggested when it occurs during recumbency, 

during or following physical exertion, or in a patient with known heart disease. Loss of 

consciousness in cardiac disease is most often due to an abrupt decrease in cardiac 

output, with subsequent cerebral hypoperfusion producing symptoms identical to those 

of fainting. Such cardiac dysfunction may result from rhythm disturbances 

(bradyarrhythmias or tachyarrhythmias), cardiac inflow or outflow obstruction, acute 

myocardial infarction, intracardiac right-to-left shunts, leaking or dissecting aortic 

aneurysms, or acute pulmonary embolus. Table 17-6 lists some of the more common 

cardiopulmonary causes of syncope. 

CARDIAC ARREST (SEE ALSO CHAPTER 7.)


• Suspect cardiac arrest and arrhythmias as possible causes in syncope. 


Loss of consciousness due to cardiac arrest (ventricular fibrillation or asystole) from any 

cause occurs in 3-5 seconds if the patient is standing or within 15 seconds if the patient 

is recumbent. The patient usually rapidly regains consciousness if adequate cardiac 

output is restored promptly; most patients who regain consciousness within 12 hours will 

recover without neurologic sequelae. 

Seizures are uncommon but are more likely to occur the longer the cerebral 

hypoperfusion lasts. A postictal confusional state occurs in patients who have 

convulsed. 


Initiate cardiopulmonary resuscitation; see Chapter 7 for further details. Immediate 

hospitalization in an intensive care unit for evaluation and treatment is required. 

ACUTE MYOCARDIAL INFARCTION (SEE ALSO CHAPTER 34.) 

Rarely, myocardial infarction is manifested by syncope without chest pain. 

Hospitalization is required in every case. 

CARDIAC ARRHYTHMIAS (See also Chapter 35.) 


See Table 17-6 for arrhythmias associated with syncope. Palpitations, fatigue, dyspnea, 

or chest pain may precede loss of consciousness. Atypical chest pain (mainly 

nonexertional, left precordial, sharp, and of variable duration) suggests mitral valve 

prolapse. 

Rapid (= 160 beats/min), slow (= 50 beats/min), or irregular pulse must be carefully 

investigated. Tachycardia of 180-200 beats/min will produce syncope in half of healthy 

persons. In patients with underlying heart disease or atherosclerosis, tachycardia as 

slow as 135 beats/min or bradycardia as fast as 60 beats/min may result in loss of 

consciousness. 

Chest auscultation with the patient in various positions (eg, sitting, left lateral decubitus, 

squatting) may disclose abnormal murmurs and clicks in the case of mitral valve 

prolapse. 

The ECG may confirm the diagnosis of arrhythmia, heart block, sick sinus, or prolonged

QT interval. However, a single ECG, obtained when the patient is asymptomatic, is 

frequently normal or nondiagnostic of a rhythm abnormality responsible for the syncope. 

A diagnosis can be firmly established only by demonstrating arrhythmias during 

symptomatic periods. 


Patients with syncopal attacks thought to be due to structural cardiac disease or an 

arrhythmia should be hospitalized for further evaluation. 

CARDIAC INFLOW OBSTRUCTION (SEE ALSO CHAPTER 34.) 


• Suspect with syncope due to change in position. 

• Look for physical exam findings: cardiac findings, engorged neck veins, weak pulse, or 

hypotension. 


Patients with atrial or ventricular myxomas and atrial thrombi usually present with 

embolization but may also have sudden loss of cardiac output and syncope; syncope 

occurring with change in position is classic but uncommon. Left atrial myxoma often 

mimics mitral stenosis but is occasionally manifested by mitral regurgitation murmur. 

Mitral valve prolapse may also cause syncope. 

Constrictive pericarditis or cardiac tamponade causes reduced cardiac output and may 

result in syncope. Any maneuver or drug that decreases heart rate or venous return will 

further impair cardiac output. The diagnosis is suggested by the presence of engorged 

neck veins, clear lung fields on chest x-ray, weak pulse, and hypotension (Chapter 34). 

Tension pneumothorax reduces cardiac output by decreasing venous return and may 

produce syncope. There is usually a history of chest trauma or chronic pulmonary 

disease with bullae. Chest x-ray and physical examination confirm the diagnosis. See 

Chapter 24 for details. 


Patients with syncope thought to be due to cardiac inflow obstruction require immediate 

treatment and hospitalization. 

CARDIAC OUTFLOW OBSTRUCTION 


• Consider with syncope related to exertion. 

• Look for cardiac physical findings. 

1. Aortic Stenosis 

Loss of consciousness secondary to congenital or acquired severe stenosis may occur 

in all age groups. Exertional syncope occurs as a result of cerebral hypoperfusion due 

to exercise-induced vasodilation in the presence of a fixed cardiac output. Two other 

pathophysiologic events are recognized: (1) acute transient left ventricular failure with 

normal sinus rhythm and (2) transient arrhythmia or cardiac stand-still, causing an acute 

drop in cardiac output. Sudden death may result. Autonomic insufficiency also has been 

reported in these patients. Reflex peripheral vascular vasodilation (presumably due to 

left ventricular baroreceptor activity) has been demonstrated in the absence of cardiac 

arrhythmia. 


Syncope usually follows exercise and is often associated with dyspnea, anginal chest 

pain, and sweating. Physical findings that occur with hemodynamically severe aortic 

stenosis include the following: 

• Characteristic midsystolic ejection murmur (often associated with a palpable thrill) 

• Sustained and prolonged left ventricular lift 

• Paradoxically split second sound 

• Delayed upstroke and reduced amplitude (pulsus parvus et tardus) on the carotid 

pulse 


Promptly hospitalize all patients with symptomatic aortic stenosis (angina, congestive 

heart failure, or syncope) to evaluate them for possible valve replacement. Median 

survival time following the initial episode of syncope due to aortic stenosis in the patient 

who does not receive a prosthesis is 1.5-3 years. 

2. Pulmonary Stenosis 


Severe pulmonary stenosis may produce syncope, especially following exertion. A 

hemodynamic process similar to that of aortic stenosis is responsible. Physical findings 

include right parasternal lift, systolic ejection murmur at the upper left sternal border, a 

prominent S 4 , and a conspicuous a wave in the jugular venous pulse. 


Immediate hospitalization is required, because the pathophysiology and prognosis of

this condition are similar to those of aortic stenosis. 

3. Hypertrophic Obstructive Cardiomyopathy 2 


• Syncope with exercise, dyspnea on exertion, and chest pain. 

• Cardiac findings including systolic ejection murmur, S 4 , and perhaps a thrill. 

2 Hypertrophic obstructive cardiomyopathy is also known as asymmetric septal 

hypertrophy or idiopathic hypertrophic subaortic stenosis. 


Symptoms include syncope with exercise, dyspnea on exertion, and chest pain. 

Physical findings include a prominent fourth heart sound, ventricular lift, transient 

arrhythmias, and systolic ejection murmur and perhaps a thrill, both of which increase 

with exertion and with decreased left ventricular chamber size (eg, as produced during 

the Valsalva maneuver). Echocardiography confirms the diagnosis. 


Hospitalize the patient for further evaluation and treatment. 

PULMONARY VASCULAR DISEASE (See also Chapter 27.) 


Pulmonary Embolism 

• Suspect pulmonary embolism as a cause of syncope. 

• Complaints of dyspnea and pleuritic chest pain when awake. 

• Look for tachypnea and tachycardia. 


A. Pulmonary Hypertension 

Syncope, often exertional, can be the presenting symptom of pulmonary hypertension. 

A history of dyspnea is invariably obtained as well. Signs of right ventricular failure 

(parasternal lift, increased pulmonary second sound, right-sided S 4 , and murmurs of 

pulmonary and tricuspid valvular insufficiency), electrocardiographic evidence of right 

ventricular hypertrophy, and tachypnea are often found. 

B. Massive Pulmonary Embolism

Syncope is the presenting symptom in approximately 20% of patients experiencing 

massive pulmonary embolism. When the patient regains consciousness after syncope, 

pleuritic chest pain, dyspnea, and apprehension are present. Hypotension, tachycardia, 

tachypnea, and significant hypoxemia frequently accompany large embolism, and death 

may occur. Syncope or sudden altered mental status was noted (retrospectively) as a 

prodrome in 60% of cadavers diagnosed with massive pulmonary embolism at autopsy. 


Provide supplemental oxygen (10 L/min) and assisted ventilation where necessary. See 

Chapter 27 for further evaluation and treatment. Hospitalization is usually required. 

CEREBROVASCULAR SYNCOPE 

Although syncope resulting from cerebrovascular disease is often diagnosed, such an 

association is in fact uncommon, because consciousness is lost only when the function 

of both cerebral hemispheres or the brain-stem reticular formation is compromised (see 

Table 17-6 and Chapter 16). 

BASILAR ARTERY INSUFFICIENCY (See also Chapter 18.) 


Basilar artery transient ischemic attacks (TIAs) usually occur after age 65 years. Loss of 

consciousness is a rare manifestation. 

Diplopia, vertigo, dysphagia, dysarthria, lateralized sensory or motor symptoms, and 

sudden bilateral leg weakness suggest brain-stem ischemia. Syncope is rarely if ever 

the initial or isolated symptom. 

TIAs typically are of sudden onset and brief duration (seconds to minutes), but when 

loss of consciousness has occurred, recovery is frequently prolonged (30-60 minutes or 

longer). 


Accurate diagnosis of basilar artery insufficiency is often difficult, and neurologic referral 

is recommended. Hospitalization is indicated, especially when syncope has occurred. 

Treatment with aspirin should be started; the specific effective dose has not yet been 

clarified. 

SUBCLAVIAN STEAL SYNDROME 


Patients with subclavian steal syndrome present with symptoms of vertebrobasilar 

artery insufficiency combined with symptoms of ipsilateral upper extremity ischemia. 

The diagnosis is confirmed by the episodic signs and symptoms of basilar artery

ischemia, syncope, vertigo, diplopia, limb paresis, paresthesias, and ataxia. Brain-stem 

infarction (stroke) has not been reported to result from subclavian steal syndrome alone. 

Blood pressures measured in the upper extremities are nearly always unequal. The 

average difference is a 45-mm Hg decrease in systolic pressure in the arm supplied by 

the stenotic vessel. 


If subclavian steal syndrome is suspected, elective hospitalization for arteriography and 

perhaps surgical correction is indicated. 

MIGRAINE (See also Chapter 19.) 

Syncope occurs in 10% of patient with migraine when they stand up suddenly. The 

timing of attacks suggests that loss of consciousness is due to orthostatic hypotension. 

CAROTID SINUS SYNCOPE 


Carotid sinus syncope classically results from pressure on an abnormally sensitive 

carotid sinus by a tight collar, neck mass, enlarged cervical nodes, or tumor. This 

pressure causes vagal stimulation that slows the sinoatrial and atrioventricular nodes 

and inhabits sympathetic vascular tone. The resulting bradycardia and systemic 

hypotension may then produce syncope. Bradycardia or hypotension may also occur 

without syncope. The syndrome may be reproduced in the emergency department by 

pressure on the carotid sinus for 5-10 seconds while the patient is both supine and 

erect; cardiac monitoring or ECG documents the induced bradyarrhythmia. Such 

pressure may also produce syncope resulting from cerebral ischemia if the examiner 

compresses the artery contralateral to an occluded carotid artery. Syncope is then due 

to cerebral hypoperfusion secondary to cerebrovascular disease and not to 

hypersensitivity of the carotid sinus. 

Treatment 

The patient with syncope should be placed supine and pressure on the carotid sinus 

relieved (eg, by loosening a tight collar). Further therapy is seldom required. Unusually 

severe or persistent bradycardia can be abolished in some cases by administration of 

atropine, 0.5 mg intravenously. 

Disposition 

Refer the patient to an outpatient clinic or primary care physician for evaluation. The 

patient should be told to avoid possible causes of the attacks (eg, tight collars). 

ORTHOSTATIC HYPOTENSION 

Orthostatic hypotension occurs more often in men than in women and is most common

in the sixth and seventh decades, although it may occur even in teenagers. Orthostatic 

hypotension may result from multiple disorders; the more common causes are listed in 

Table 17-5. 


Syncope often occurs following rapid change in the upright position, that is, from lying to 

sitting or from sitting to standing. Prolonged motionless standing, especially after 

exercise, or standing after prolonged bed rest, may also cause syncope. Patients 

usually describe lightheadedness, dimming of vision, weakness, and a fainting 

sensation. True vertigo does not occur. 

Blood pressure that is significantly lower (> 20 mm Hg systolic difference) when the 

patient is standing than when he or she is supine is diagnostic. Orthostatic tachycardia 

may be present as well. 

A stool sample should be evaluated for the presence of blood. CBC may reveal anemia 

or hemoconcentration due to blood loss or dehydration, respectively. Electrolyte 

determinations should be made to detect abnormalities produced by dehydration or 

drugs. Serum drug levels should be obtained as indicated. 

Treatment 

Discontinue any offending medication. Encourage oral fluid intake, or administer 

intravenous fluids to maintain hydration. Replace blood if acute blood loss is significant, 

and locate the source of bleeding. Instruct patients to stand up gradually, elevate the 

head of the bed on blocks, and use elasticized support stockings. 

Disposition 

Hospitalize the patient (1) if postural hypotension is currently producing symptoms and 

cannot be corrected easily in the emergency department, or (2) if an acute underlying 

cause of hypotension persists (eg, vomiting, diarrhea) or warrants hospitalization in any 

case (eg, gastrointestinal bleeding). Otherwise, refer the patient to an outpatient clinic or 

primary care physician. 

MISCELLANEOUS RARE CAUSES OF STATES OF ALTERED CONSCIOUSNESS 

HYPERVENTILATION 


• Diagnosis of exclusion. 

• Numbness and tingling (especially circumoral). 

• Muscle twitching and carpal pedal spasm. 


Psychogenic hyperventilation is a frequent cause of altered consciousness (eg, 

faintness, lightheadedness) but rarely culminates in syncope. Acute anxiety is the usual 

cause. The disorder is usually benign, but serious cardiopulmonary causes of 

hyperventilation or subjective dyspnea must be ruled out (Chapter 11). 


Common symptoms include lightheadedness, shortness of breath, numbness and 

tingling (especially circumoral or acral), muscular twitching, and in severe cases, carpal 

pedal spasm. Positive Chvostek and Trousseau tests are noted during the acute stage. 

Respiratory alkalosis without other abnormalities (eg, metabolic acidosis) is noted on 

arterial blood gas analysis. Symptoms are reproduced by hyperventilating in a controlled 

setting (eg, emergency department). 


Reassure the patient, and alleviate underlying anxiety. If the patient is acutely 

hyperventilating, ask the patient to count to 3 slowly between breaths. Patients 

experiencing a panic attack may benefit from alprazolam, 0.25-0.5 mg orally. 

Rebreathing from a paper bag is no longer recommended because of the potential risk 

of hypoxia. 

PSYCHIATRIC CAUSES 


• Diagnosis can be made only after careful exclusion of other causes. 

• Presence of bizarre postures or movements. 


Psychiatric causes of syncope include major depression, general anxiety disorder, and 

panic disorder. Fainting is a known manifestation of somatization disorder. Alcohol or 

drug abuse can lead to syncopal episodes. Malingering may be a factor; patients may 

use the episodes of feigned unconsciousness to manipulate other people for secondary 

gain. Patients with factitious disorder also may fake unconsciousness, but they do so for 

psychological reasons. 


Features that suggest psychiatric causes of syncope are lack of any prodrome, 

presence of bizarre postures or movements, lack of pallor, and prolonged 

unconsciousness. Most patients are young and have a well-documented history of 

psychiatric responses to stress; without such a history, a psychogenic cause in a patient 

over 30 years of age can be made only after thorough evaluation has excluded other 

causes of syncope.

While the patient is unconscious, caloric testing may be used to distinguish coma due to 

psychiatric causes from coma due to structural lesions or metabolic causes. In coma of 

organic cause, when ice water is directed against the tympanic membrane, the eyes will 

remain in mid position or will tonically deviate to the side of the irrigation. In psychogenic 

coma, the caloric test induces brisk nystagmus, or the patient awakens because of 

discomfort (Chapter 16). 


Refer the patient to an outpatient clinic or primary care physician for follow-up. 

MENIERE DISEASE (See also Chapter 32.) 


• Recurrent attacks of vertigo. 

• Associated with tinnitus. 

• Progressive hearing loss. 


Recurrent attacks of severe vertigo persisting for several hours associated with tinnitus 

and progressive hearing loss are diagnostic of Meniere disease. A few patients 

experience loss of consciousness for a few seconds at the onset of an attack. 


Meclizine, 50 mg orally once or twice daily, is often helpful. Refer the patient to an 

otolaryngologist. See Chapter 32 for details. 

Basilico FC: Cardiovascular disease in athletes. Am J Sports Med 1999;27:108. [PMID: 

9934429] 

Bloomfield DM: Strategy for the management of vasovagal syncope. Drugs Aging 

2002;19:179. [PMID: 12027777] 

Fedderly RT: Left ventricular outflow obstruction. Pediatr Clin North Am 1999;46:369. 

[PMID: 10218081] 

Fenton AM et al: Vasovagal syncope. Ann Intern Med 2000; 133:714. [PMID: 11074905] 

Grubb BP et al: Syncope resulting from autonomic insufficiency syndromes associated 

with orthostatic intolerance. Med Clin North Am 2001;85:457. [PMID: 11233955] 

Kenny RA: Neurally mediated syncope. Clin Geriatr Med 2002; 18:191. [PMID:

12180243] 

Mack G, Silberbach M: Aortic and pulmonary stenosis. Pediatr Rev 2000;21:79. [PMID: 

10702320] 

Martin PJ: Vertebrobasilar ischaemia. QJM 1998;91:799. [PMID: 10024945] 

Martinon-Torres F et al: The relation between hyperventilation and pediatric syncope. J 

Pediatr 2001;138:894. [PMID: 11391335] 

Roth HL et al: Seizures. Neurol Clin 1998;16:257. [PMID: 9537962] 

Schnipper JL, Kapoor WN: Diagnostic evaluation and management of patients with 

syncope. Med Clin North Am 2001; 85:423. [PMID: 11233954] 

Taylor CL et al: Steal affecting the central nervous system. Neurosurgery 2002;50:679. 

[PMID: 11904017] 

Wood KE: Major pulmonary embolism: review of a pathophysiologic approach to the 

golden hour of hemodynamically significant pulmonary embolism. Chest 2002;121:877. 

[PMID: 11888976] 






I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS (See 

Figure 17-1.)

Table 17-1. Emergency evaluation of the patient with seizures. 






TABLES 

Table 17-1. Emergency evaluation of the patient with seizures.

Table 17-2. Drug treatment of status epilepticus. 

Dose and Route 

Diazepam (Valium, others) 

or 

Lorazepam (Ativan, others) 

or 

Midazolam (Versed) 

Phenytoin (Dilantin, others) 

or 

Fosphenytoin 

Phenobarbital (Luminal, 

many others) 

First-line drug: 

Fast acting (lipid-soluble), short half-life 

intravenously (1Ãš2-4 hours for diazepam; up to 

16 hours for lorazepam). Respiratory depression 

occurs, especially if barbiturates must be added. 

Other complications are bradycardia and 

hypotension. Note: Regardless of effectiveness of 

diazepam, maintenance drug (phenytoin or 

phenobarbital) must be added to prevent 

recurrence of seizures. 

No respiratory depression. Therapeutic drug 

levels in the brain are achieved by the time the 

infusion has been completed. Effective as 

maintenance drug. Hypotension and cardiac 

arrhythmias may occur, especially in elderly 

patients. infusion rate of 100 mg/min is safe 

during active seizures. 

Respiratory depression and hypotension common 

with increasing doses (intubation and ventilatory 

support should be immediately available). 

Effective as maintenance drug. 

Paraldehyde Decomposes with storage; can cause metabolic 

acidosis, pulmonary hemorrhage, cardiovascular 

depression, and proctitis (if given rectally). Use 

glass syringe (paraldehyde causes plastic to 

break down); safely administered intravenously in 

4% solution. Absorption is rapid following 

intramuscular administration but slow with the 

rectal route. 

50 mg intravenously. If 

effective, then 50-100 mg 

diluted in 250 mL of 5% 

dextrose and infused at a 

rate of 1-2 mg/min. 

200-1000 mg slowly 



If the above is ineffective, proceed 

immediately to general anesthesia. 

PE = phenytoin equivalents. 

15 mg/kg slowly intrav 

mg/kg/h.





TABLES 

Table 17-2. Drug treatment of status epilepticus.

Table 17-3. Common causes of seizures of acute onset. 

Comment 

Idiopathic epilepsy Head trauma 

Acute or chonic; bacterial, viral, 

fungal, parasitic, etc. (Chapter 40). 

Serum sodium usually less than 120 

and often less than 110 mEq/L 

(Chapter 42). 

Serum glucose usually less than 40 

mg/dL (Chapter 41). 

Serum osmolalty usually greater than 

300 mOsm/L (Chapter 42). 

Blood pressure usually greater than 

250/150 mm Hg; seizures may occur 

at lower pressures (usually > 160/100 

mm Hg) when hypertension occurs 

suddently (eg, in children with acute 

renal failure) (Chapter 34). 

Respiratory alkalosis nearly always 

present. 

Develop and utilize a protocol for 

managing pregnancy-related 

seizures. 

Especially with tricyclic 

antidepressants, theophylline 

(aminophylline), phencyclidine (PCP), 

lidocaine, phenothiazines, isoniazid 

(Chapter 45 ). 

Anticonvulsants, ethanol, or 

sedative-hypnotic drugs (with 

habituation to daily doses of 600-800 

mg secobarbital or its equivalent. 

Do not occur after age 5; always 

consider other causes. 

Internal body temperature usually 

above 41-42 °C (105.8-107.6 °F); 

immediate reduction of body 

temperature to 39 °C (102.2 °F) is 

mandatory (Chapter 44).






TABLES 

Table 17-3. Common causes of seizures of acute onset.

Table 17-4. Summary of anticonvulsant drug therapy. 

Dose 

Serum Levels (µg/mL) 

Drug Oral Loading 

1000-1500 mg (15-18 

mg/kg) directly into a 

large vein, not 

exceeding 50 mg/min. 

Continuous 

electrocardiographic 

monitoring is mandatory. 

Cannot be infused in 

dextrose solutions (eg, 

5% dextrose in water). 

No intravenous 

preparation. 

300-400 mg/d in a single dose or 

23 divided doses. 

10-20. 

400 mg 2-3 times a day 4-8. 

Serum Half-Life 

(Normal Renal and 

Hepatic Function)

Table 17-5. Causes of orthostatic hypotension. 






TABLES 

Table 17-5. Causes of orthostatic hypotension.

Table 17-6. Common causes of syncope due to cardiopulmonary and 

cerebrovascular disease. 






TABLES 

Table 17-6. Common causes of syncope due to cardiopulmonary and 

cerebrovascular disease.

Table 17-7. Common factors 

precipitating vasovagal syncope 

(fainting). 






TABLES 

Table 17-7. Common factors precipitating vasovagal syncope (fainting).

Figure 17-1. Assessment of patients with seizure, syncope, or loss of consciousness. 






FIGURES


INTRODUCTION 

1 This chapter is a revision of the chapter by Roger P. Simon, MD, & Mary T. Ho, MD, 

MPH, from the 4th edition. 

The term weakness is broad and encompasses a diverse spectrum of disease 

processes. There is a great deal of overlap in the various clinical manifestations of 

muscle weakness. It can range from a primary muscular disorder to a neurologic 

dysfunction. Disorders characterized by rapid onset of loss of motor function are 

discussed in this chapter. With the exception of some stroke syndromes, consciousness 

is not impaired by the primary disease process, although secondary respiratory 

insufficiency may cause hypercapnia leading to obtundation. 

Caution: The major error to be avoided in dealing with patients presenting with acute 

weakness is misinterpreting the symptoms as psychogenic or hysterical. These patients 

usually are awake and alert and may not appear critically ill. They may be able to walk. 

Complaints of weakness of recent onset require careful evaluation before judgments are 

made about the cause of symptoms. 


ASSOCIATED WITH WEAKNESS (See Figure 18-1.) 

Stabilize Ventilation 

Treat dyspnea or objective respiratory distress in a patient with weakness as a potential 

life-threatening emergency. Respiratory muscles may be affected even though strength 

in the extremities is relatively unimpaired. 

A. Oxygen 

Give oxygen, 5 L/min by mask or nasal cannula, if breathing is labored, if there is 

obvious hypoventilation (patient is barely able to speak), or if there is evidence of 

hypoxemia (eg, cyanosis of digits). Distal extremity paresthesias and increased 

respiratory effort associated with the basic disease process (eg, Guillain-Barre 

syndrome) may support the impression of psychogenic hyperventilation. 

B. Laboratory Tests 

Arterial blood gases, vital capacity, and maximum inspiratory force should be measured 

immediately. Measurements of vital capacity and maximum inspiratory force will be 

abnormal even before alterations in arterial blood gases occur. 

C. Supported Ventilation 

Frank hypoventilation (PCO 2 > 50 mm Hg) is an indication for emergency supported 

ventilation (eg, bag-valve-mask), followed as quickly as possible by endotracheal

intubation and mechanical ventilation. 

Even if arterial blood gas measurements are normal or nearly normal, a markedly 

diminished vital capacity (

Caution: In case of suspected spinal cord compression, do not perform lumbar 

puncture in the emergency department, because it may worsen symptoms and make 

more difficult subsequent attempts to enter the subarachnoid space (eg, for 

myelography). 

II. FURTHER EVALUATION OF THE PATIENT WITH WEAKNESS 

After the immediate measures described above have been taken, further evaluation 

should proceed so as to localize the anatomic site of weakness into one of the following 

categories (see Table 18-1 and detailed discussions of specific disorders). 

SPINAL CORD DISEASE 


• Traumatic causes: concussion, incomplete cord (anterior cord, Brown-Sequard 

syndrome, central cord, conus medullaris, cauda equina), complete cord. 

• Nontraumatic (infectious) causes: epidural abscess, meningitis, subdural abscess, 

intramedullary abscess. 


Spinal cord disease should be suspected if weakness and sensory loss are found 

caudad to a horizontal plane in the body. Cranial nerve examination should be normal. 

The most common disorders producing rapidly progressive weakness or involvement of 

the nervous system at the spinal cord level are essentially confined to 4 processes: (1) 

disk protrusion (Chapter 21), (2) spinal epidural metastases, (3) transverse myelitis, and 

(4) spinal epidural abscess. Other causes such as radiation myelitis and ruptured 

arteriovenous malformations are rare. A diagnosis of suspected spinal cord 

compression by abscess or tumor demands immediate confirmation by MRI or 

myelography and prompt surgical decompression and antibiotics for abscess and 

emergency radiation therapy or surgical decompression for tumor. In transverse 

myelitis, no such mechanical compression of the spinal cord exists, and surgery only 

increases the morbidity. 

A. Imaging 

MRI is the study of choice; if it is unavailable, myelography is done. Obtain 

cerebrospinal fluid only at the time of myelography, because the subarachnoid space 

may be difficult to enter a second time. Remove only a small amount of cerebrospinal 

fluid for study, and use small volumes of contrast media (


Hospitalize the patient, and seek immediate neurologic or neurosurgical consultation. 

ANTERIOR HORN CELL INVOLVEMENT (Poliomyelitis) 



Poliomyelitis should be suspected if several of the following are present with weakness: 

• Asymmetric weakness with intact sensation. This asymmetry of motor involvement is 

virtually unique to poliomyelitis in patients who have not been vaccinated or in 

immunocompromised patients. 

• Gastrointestinal signs or symptoms. 

• Fever, headache, photophobia. 

• Meningeal signs. 

B. Imaging 

MRI scan may show localized inflammation to the anterior horn cells. 

C. Lumbar Puncture 

Perform lumbar puncture if poliomyelitis is suspected. Spinal cord compression 

(abscess), transverse myelitis, and poliomyelitis are the only conditions commonly 

producing acute weakness associated with cerebrospinal fluid pleocytosis. 

D. Differential Diagnosis 

Spinal cord compression and myelitis will produce a sensory deficit. Peripheral 

neuropathies may spare sensory nerves; motor involvement is usually symmetric. 


Treatment is primarily supportive. The prognosis is poor in the bulbar form of the 

disease, with a mortality rate of approximately 50%. Hospitalize all patients who have a 

clinical diagnosis of poliomyelitis. If bulbar involvement has produced respiratory failure, 

support respiration with supplemental oxygen and assisted ventilation (bag-valve-mask 

or endotracheal intubation). 

NEUROMUSCULAR BLOCKAGE 



Diseases affecting the neuromuscular junction are marked by early and prominent 

involvement of cranial nerves, causing difficulty in speaking and swallowing, facial

weakness, blurred vision, diplopia, and ptosis. Involvement of respiratory and extremity 

muscles follows. There are no sensory abnormalities, and reflexes are preserved, 

though responses may be depressed in proportion to the degree of weakness. 

B. Causes 

Diseases causing neuromuscular blockage include organophosphate (insecticide or 

nerve gas) poisoning, botulism, myasthenia gravis, and envenomations. Certain 

antibiotics (eg, aminoglycosides) may rarely cause neuromuscular blockade, but this 

occurs only in hospitalized patients with contributory conditions (eg, myasthenia gravis). 

Differential Diagnosis 

It is important to make a rapid diagnosis, because both botulism and organophosphate 

poisoning require immediate specific therapy. 

A. Organophosphate Poisoning 

Poisoning with organophosphates causes marked miosis and prominent glandular 

hypersecretion (sweating, salivation, lacrimation, and bronchorrhea). Most patients have 

been recently exposed to insecticide spraying, a fact easily elicited by questioning. 

B. Botulism 

Botulism affects the neuromuscular junction and causes nausea and vomiting followed 

by paralysis of muscles of accommodation, respiratory muscles, extraocular muscles, 

extremity muscles, and the lower bulbar muscles. Glandular secretion is not affected. 

C. Myasthenia Gravis 

Patients with myasthenia gravis usually know their diagnosis. The rare patient with 

undiagnosed acute myasthenia gravis should improve in response to edrophonium 

(Tensilon, others). Give 2 mg intravenously over 15-30 seconds; if no reaction occurs 

within 1 minute, give 8 mg more. Edrophonium has a rapid onset but brief duration of 

action, both of which permit quick assessment of cranial nerve weakness. Testing of 

limb muscles may require use of the longer-acting cholinesterase inhibitor neostigmine 

(1.5 mg intramuscularly, together with atropine, 0.5 mg intramuscularly). Edrophonium 

and neostigmine will not affect symptoms due to botulinum toxin or organophosphate 

poisoning. 

D. Venomous Animal Injuries 

(See also Chapter 44.) Certain bites can also produce acute symptoms, including 

weakness. 

1. Snakes—Compounds can be found in a poisonous snake's venom that can cause a 

variety of reactions depending on the species involved. For example, the bite of the pit 

viper (the most common poisonous snake in the United States) can cause many 

systemic symptoms, including weakness, tingling, muscle fasciculations, and metallic 

taste. Coral snake venom contains compounds that block neuromuscular transmission 

at the acetylcholine receptor site, thereby inhibiting cardiac and skeletal muscle. The 

first appreciated sign is ptosis of the eyes; other signs include proximal muscle 

weakness, slurred speech, and dysphagia.

2. Gila monsters—Gila monster bites are associated with weakness, pain, and edema. 

They are rarely fatal. 

3. Black widow spider—Black widow spider neurotoxin depletes acetylcholine from 

presynaptic nerve channels, thereby destabilizing the membranes. The patient 

complains of weakness, ptosis, difficulty speaking, and muscle cramps. 

4. Brown recluse spider—Bites from this spider can produce weakness, nausea, and 

vomiting. 

5. Scorpions—Toxicity varies within the species. The more dangerous type will have 

the more toxic effect. Systemic reactions include muscle spasms, hemiplegia, blurred 

vision, pseudoseizures, cardiac dysrhythmias, and respiratory arrest. 

Disposition 

Hospitalization is mandatory for all patients with suspected neuromuscular blockade. 

PERIPHERAL NEUROPATHY 


Disorders involving the peripheral nerves can produce sensory or motor symptoms or 

(most often) both. 


Weakness may preferentially involve either the distal or, rarely, the proximal 

musculature. Sensory loss is usually restricted to a distal (ie, stocking-glove) 

distribution. Weakness owing to cranial nerve involvement may occur but is not a 

common presenting feature. 

Reflexes are markedly depressed or absent early; this is helpful in identifying peripheral 

nerve impairment even before objective weakness can be documented. 

B. Laboratory Findings 

Cerebrospinal fluid protein is commonly elevated, but this may not occur until days after 

onset. The cell count is usually normal. 

Treatment 

Provide supportive care (eg, respiratory support as required). None of the illnesses 

causing peripheral neuropathy are relieved by specific emergency therapy except for 

tick paralysis, which responds to the removal of the tick (usually found in the hair). 

Disposition 

Hospitalization may be necessary for further evaluation and treatment.

MUSCLE DISEASE (Acute Myopathy) 


• Causes vary. 

• Malaise, fatigue, and symmetric proximal weakness. 

• Atrophy, hyporeflexia. 

• Dark urine. 

• No sensory complaints. 


Prompt diagnosis of primary muscle disease is important, because effective specific 

therapy is available for some of the conditions causing muscular weakness. 


Weakness is characteristically more proximal than distal, and lower extremity weakness 

is often greater than that in the upper extremities. Cranial nerve and respiratory 

abnormalities occur in severe cases; eye movements are spared. Objective sensory 

loss does not occur. Deep tendon reflexes are depressed in proportion to the muscle 

weakness. 


Collect urine for myoglobin testing (positive test for hemoglobin on dipstick in the 

absence of erythrocytes on microscopy; confirm by chemical assay) and blood for 

determination of muscle enzymes (CK, AST [SGOT]) and potassium in serum. 


Hospitalization is generally required, although mild attacks of recurrent familial hypo- or 

hyperkalemic paralysis may be treated adequately in the emergency department. If 

hypokalemia is present, give potassium chloride, 1-2 mEq/kg (equivalent to 5-10 g of 

potassium chloride) orally, and repeat once or twice at hourly intervals until strength is 

regained. Treat hyperkalemia associated with muscular weakness by infusing glucose 

and insulin (Chapter 42). 

HYSTERIA 


• Conversion disorder can suggest a neurologic disease, but no explanation can be 

found despite physical and diagnostic testing. 

• Complete and comprehensive psychosocial history is important. 

Hysteria as a cause of weakness can be diagnosed only after all other causes have

een eliminated. A history of hysteria or psychosomatic illnesses may be helpful, but 

one must also search for and eliminate other causes of weakness, because organic 

causes of weakness are frequently misdiagnosed initially as hysteria. Psychiatric 

evaluation should be obtained. 

Arce D et al: Recognizing spinal cord emergencies. Am Fam Physician 2001;64:631. 

[PMID: 11529262] (A review of spinal cord emergencies.) 

Della-Giustina DA: Emergency department evaluation and treatment of back pain. 

Emerg Med Clin North Am 1999;17:877. [PMID: 10584107] (A review of emergency 

diagnosis and management of back pain.) 

III. EMERGENCY MANAGEMENT OF SPECIFIC WEAKNESS 

DISORDERS 

DISORDERS OF THE SPINAL CORD 

METASTATIC TUMOR 


• Slowly progressive. 

• Stuttering neurologic deficit. 


The most common primary malignant neoplasms producing epidural metastases and 

spinal cord compression are breast cancer (20%), lung cancer (10%), Hodgkin disease 

(10%), and prostate cancer (7%). 


Local vertebral column pain at the level of the spinal cord lesion is the presenting 

symptom in the vast majority of patients. This symptom usually precedes neurologic 

deterioration by weeks to months, but occasionally it may be present for only a few 

hours. 

Onset of radicular radiation of the pain (involvement of the territory of a nerve root) 

heralds progression. Radiation of the pain may be bilateral, especially when the thoracic 

spine is involved. This is followed by weakness, paresthesias, and sensory impairment 

(especially to vibration) of the distal lower extremity. Bladder and bowel dysfunction 

occurs with rapid progression of symptoms over hours to days. Sensory and motor 

impairment soon ascends to a spinal cord level just below the site of the lesion. 

B. Imaging 

X-rays of the spine will usually reveal bony destruction by the tumor at the involved 

vertebral level. Demonstrate the extent of the lesion by MRI. If a myelogram is 

necessary, access to the subarachnoid space above the lesion is most easily obtained

via a lateral C1-C2 puncture. 


Patients with this diagnosis should be given corticosteroids immediately to reduce 

peritumoral edema (eg, dexamethasone, 10 mg intravenously, followed by 4 mg every 6 

hours intravenously or orally). Obtain emergency neurosurgical and neurologic 

consultation. 

Hospitalization is required for decompression by laminectomy or local radiotherapy. The 

latter is as effective as surgery (regardless of the tumor type) and is associated with 

fewer side effects. 

TRANSVERSE MYELITIS 


• Rapid onset of motor and sensory loss. 

• Sphincter disturbances. 


Transverse myelitis is a poorly defined entity that is usually idiopathic but may be a 

manifestation of a known systemic disease (eg, multiple sclerosis, systemic lupus 

erythematosus, vitamin B 12 deficiency). It may also result from acute hyperextension 

injury of the cervical spine (central cord syndrome). 



The presenting symptoms are equally divided between motor weakness, sensory loss or 

paresthesia, and back and radicular pain. Symptoms and signs of transverse (bilateral) 

cord involvement may progress to a maximum level within hours. Vertebral tenderness 

to percussion is noted in about half of cases. 

B. Imaging 

An MRI or myelogram is required to exclude a compressive lesion; myelography will 

almost always demonstrate free flow of contrast material. 


Treatment is supportive only. Partial to full recovery may occur over a period of weeks 

to months. Hospitalization is recommended for diagnosis and supportive care. Steroid 

treatment is frequently used, but its benefit is uncertain. 

SPINAL EPIDURAL ABSCESS


• Majority located along spinal neuraxis. 

• Hematogenous spread with seeding of epidural space (eg, intravenous drug use, 

infected indwelling catheters, urinary tract infection, abdominal infection). 

• Extension of adjacent vertebral osteomyelitis, penetrating trauma, or recent 

neurosurgery. 

• Fever, localized back pain; maybe subtle, radiating pain (along nerve root); sensory 

disturbances. 

• Tenderness to percussion or palpation. 

• Reflexes may be hypoactive, absent, brisk, or spastic. 

• Immediate imaging: MRI (procedure of choice), CT scan myelography, conventional 

myelography. 

• Lumbar puncture relatively contraindicated. 

Spinal epidural abscess is one eighth as common as transverse myelitis, but it may be 

associated with remarkably similar signs and symptoms. 


The most common predisposing conditions include local staphylococcal infections of the 

skin and surgical wounds (including intravenous sites), bacteremia, vertebral 

osteomyelitis, and intravenous drug abuse. 


Patients are usually febrile and appear acutely ill on presentation. Focal pain and 

localized tenderness over the abscess are nearly consistent findings. Classically, 

symptoms progress over a few days from local vertebral column pain to radiating 

radicular pain. Cord compression with weakness and sensory loss below the level of the 

lesion follows. 

B. Imaging 

Plain x-rays of the spine reveal osteomyelitic lesions in about 85% of cases, especially 

in patients with symptoms of long duration (weeks). MRI or myelography will show a 

complete block of cerebrospinal fluid flow in over 80% of cases. 

C. Laboratory Findings 

Lumbar puncture (only at the time of myelography) should be done with great care; the 

operator should aspirate frequently to make certain that the needle is not advanced 

through the abscess, allowing pus to enter the subarachnoid space. Culture of 

cerebrospinal fluid is usually negative, but Gram-stained smears and cultures of pus 

from the abscess reveal the causative organism in almost all cases. The cerebrospinal 

fluid cell count, glucose, and protein content are listed in Table 18-2. 


Hospitalization is required for emergency surgical decompression by laminectomy,

abscess drainage, and intravenous antimicrobial therapy. Selected patients without 

significant weakness can be managed with antibiotics alone. 

DISEASE OF ANTERIOR HORN CELLS 

POLIOMYELITIS 


Nonparalytic 

• Headache, fever, sore throat, nausea, vomiting, muscle aches. 

Paralytic 

• Severe muscle pain, spasms, weakness. 

• Asymmetric: lower limbs affected more than upper limbs. 

• Flaccid muscle tone. 

• Brisk to absent reflexes. 

• Patient complains of paresthesias but with no sensory loss. 

Bulbar Form 

• Involves spinal cord. 

• Dysphagia, dysphasia. 

• Shallow respirations, hiccups. 

• Diaphragm paralysis. 

• Autonomic dysfunction. 


Although now uncommon in the western world, poliomyelitis continues to occur in single 

cases or isolated epidemics in unimmunized populations. Other enteroviruses and 

attenuated (vaccine) strains of poliovirus may cause a similar syndrome. 



Poliomyelitis begins as a viral syndrome with fever, myalgias, headache, and upper 

respiratory or gastrointestinal symptoms. Nuchal rigidity and photophobia are common. 

Neurologic involvement follows this prodrome in about 1% of cases, with rapid onset of 

weakness that progresses over 3-5 days. Flaccid paralysis then occurs, is usually 

asymmetric or even unilateral, and more commonly involves the legs than the arms. 

Sensation is unimpaired. Cranial nerves are involved in 10-20% of cases (bulbar 

poliomyelitis); the most common manifestations are facial and pharyngeal weakness, 

which can be unilateral. Diaphragmatic and intercostal muscle involvement may lead to 

respiratory failure.


Lumbar puncture will show a cerebrospinal fluid cell count of 25-500 cells/uL. 

Neutrophils predominate early, and lymphocytes predominate later. Cerebrospinal fluid 

protein and glucose are normal early. The diagnosis can be confirmed by recovery of 

virus (from stool, cerebrospinal fluid, or throat washings) or by demonstration of a 4-fold 

rise in antibody titer against the virus. 


Hospitalization is mandatory, and public health associates should be notified promptly 

(by telephone, fax machine, or e-mail). No specific therapy is available. 

POSTPOLIOMYELITIS SYNDROME 


Postpoliomyelitis syndrome is characterized by the onset of new, slowly progressive 

weakness, fatigue, and pain in patients with a history of paralytic poliomyelitis years 

previously. Symptoms are the result of ongoing denervation of muscles involved in the 

prior attack that had subsequently reinnervated. Electromyography and muscle biopsy 

confirm active denervation. 


Hospitalization is rarely needed, because progression of dysfunction is slow. No specific 

treatment is available, but physical therapy may be beneficial. 

PERIPHERAL NEUROPATHIES 

MONONEUROPATHIES 

1. Bell Palsy (Facial Weakness) (See also Chapter 32.) 


• Cranial nerve VII paralysis. 

• Abrupt, isolated, unilateral, peripheral facial paralysis. 

• Diagnosis of exclusion; unknown cause. 

• Entire face is involved on affected side (unlike in cortical stroke, where upper third of 

face is spared). 

• Clinical findings determine tests to be ordered. 


Bell palsy is a common condition of unknown cause (although some authorities suggest 

a link with herpes simplex infection). Although manifestations of the disorder are

dramatic, recovery usually begins within 1 month, and complete resolution of symptoms 

occurs in 70-85% of patients. All patients with initial subtotal facial paralysis will make a 

cosmetically complete functional recovery. 


Diagnostic features include the following: 

• Development of symptoms over less than 24- 48 hours 

• Unilateral involvement of the facial nerve 

• No signs of other nervous system involvement 

• Postauricular pain (not required for diagnosis) 


The major differential diagnostic possibilities—and those of most concern to 

patients—are stroke and tumor. Tumors in the region of the facial nerve rarely cause 

sudden onset of symptoms and usually produce abnormalities of other facial nerves, 

resulting in nystagmus, decreased hearing, and ataxia. Facial numbness may suggest 

involvement of the trigeminal nerve, but patients with Bell palsy often describe pure 

facial weakness in sensory terms (eg, "My face is numb."). 

Stroke with facial weakness is associated with weakness of the ipsilateral arm and 

probably the ipsilateral leg also (most easily detectable in the extensors of the arm and 

the flexors of the leg). Stroke produces an upper motor neuron lesion, thereby sparing 

the muscles of the forehead. Bell palsy, however, involves the facial nerve itself and 

produces unilateral weakness of all facial muscles (those of the forehead, those 

responsible for eye closure, and those around the mouth). Other facial nerve functions 

may be involved, such as unilateral decrease of lacrimation and taste and increase in 

apparent intensity of sounds (eg, when talking on the telephone). 

Laboratory Tests & Other Examinations 

When the diagnosis is clear on clinical grounds, no further evaluation or radiographic 

studies (CT scans or MRI) are indicated. 


Although Bell palsy is cosmetically disfiguring during the acute phase, the more serious 

concern is the risk for eye injury owing to inability to close the eyelid completely. 

Artificial tears should be instilled frequently during waking hours, and the lid should be 

taped closed (under careful instruction) when the patient is asleep to prevent corneal 

abrasions and ulcers. Corticosteroids may affect the ultimate recovery of motor function; 

corticosteroids such as prednisone, 40-60 mg/d orally for 10 days, decrease the 

postauricular pain often associated with acute Bell palsy. Acyclovir, 400 mg 5 times 

daily for 10 days with steroids, has been shown to provide a faster recovery. All patients

should be referred to a neurologist, otolaryngologist, or primary care physician within a 

few days, regardless of whether corticosteroids have been given. Hospitalization is not 

required. 

2. Compressive Mononeuropathies 


Compressive mononeuropathies usually occur because prolonged compression of a 

superficial peripheral nerve interrupts blood flow, producing ischemic injury. This may 

result from sleep in an unusual position or from prolonged fixed position of a limb due to 

drug intoxication or general anesthesia. 

Radial Nerve Palsy 

Paralysis of the radial nerve produces complete but isolated wrist and finger drop 

(inability to extend the wrist or fingers) with inconsistent sensory loss over the radial 

portion of the dorsum of the hand. Such injuries occur from compression of the nerve 

against the humerus in patients sedated with alcohol or other drugs (Saturday night 

palsy) or during sleep with a partner (bridegroom's palsy). If the radial nerve is 

compressed in the axilla, as occurs in crutch palsy, the triceps muscle is affected as 

well, resulting in the additional finding of weakness of extension at the elbow. 

Complete recovery over weeks to months is the rule. Immediate treatment measures 

include splinting of the wrist or application of a sling and referral to a primary care 

physician, hand specialist, or neurologist. 

Ulnar Palsy 

Acute injury of the ulnar nerve occurs at the elbow following fracture or dislocation. 

Delayed ("tardy") ulnar nerve palsies result from repeated trauma, such as resting of 

upper body weight on the elbows. Wasting and weakness of the hands ultimately 

produce a claw posture (hyperextension at the metacarpophalangeal joint and flexion at 

the interphalangeal joints that are maximal in the fourth and fifth digits). Sensory loss 

occurs in the ulnar border of the dorsal and palmar aspects of the hand below the wrist, 

extending to involve the fourth and fifth fingers. Injury to the ulnar nerve in the palm (eg, 

cycle-racing palsy) spares the sensory fibers. 

Initial management consists of padding of the elbow and referral to a primary care 

physician, hand specialist, or neurologist. 

Peroneal Nerve Palsy 

Nerve compression occurs at the head of the fibula as a result of acute trauma (eg, 

fibular fracture, or sleeping or sitting with the legs crossed). The resulting footdrop 

produces a high-stepping gait in the involved limb, with inability to dorsiflex or evert the 

foot on examination. Some sensory loss may be found over the dorsum of the foot and 

the lateral aspects of the leg.

Lesions at the root of L5 (eg, disk disease) also produce footdrop but involve other 

muscles innervated by L5 as well (eg, foot invertors and knee flexors). 

Immediate management in the emergency department or upon referral to an 

orthopedist, primary care physician, neurologist, or physical medicine specialist consists 

of splinting the foot at a right angle (cock-up splint) to normalize the gait. 

POLYNEUROPATHIES 

1. Guillain-Barre Syndrome (Infectious Polyneuritis) 


• Most common acute neuromuscular paralytic syndrome in the United States. 

• Acute ascending progressive neuropathy starting in lower extremities; weakness is 

symmetric. 

• Paresthesias, hyporeflexia. 

• Muscle weakness may lead to respiratory failure (25% of cases). 

• Labile autonomic dysfunction (labile vital signs). 

• Pain in low back, buttocks, thighs, shoulders. 

• Facial weakness, dysphasia, or dysarthria may be present. 

• Anhidrosis, paralytic ileus, urinary hesitancy. 

• Decreased to absent reflexes. 

• History of gastrointestinal or respiratory infection (approximately 1-3 weeks prior to 

onset of weakness). 


Guillain-Barre syndrome is a common disease of uncertain cause involving the 

peripheral nerves and occurring in both sexes and all age groups, although the disease 

seems milder in children. 

In one half to two thirds of cases, a mild upper respiratory infection or gastroenteritis 

precedes the onset of the neurologic disease by 1-3 weeks. Well-documented cases 

have also been recorded following surgery, other viral infections, immunization (eg, 

influenza vaccine), and acute glomerulonephritis or as an acute seroconversion reaction 

to HIV infection. Marked hypophosphatemia can produce a nearly identical syndrome. 



Symmetric weakness is the major symptom. It may be either proximal or distal at onset 

and usually begins in the lower extremities. The weakness classically progresses in an 

ascending manner, involving first the lower and then the upper extremities and finally 

the cranial nerves within 1-3 days of symptom onset. The weakness does not ascend in 

all cases, however.

Subjective and objective sensory disturbances (numbness or paresthesias) of brief 

duration are common initially and may be the presenting complaint. These dysesthesias 

most commonly occur in a distal (stocking-glove) distribution. Muscle pain or tenderness 

is also an early symptom in about half of cases. 

Absence of the deep tendon reflexes (or, rarely, only distal areflexia with definite 

hyporeflexia of biceps and knee jerks) almost always occurs by the time of presentation 

to a physician. Note: This loss of reflexes is the most important clue to diagnosis and is 

found even in muscles that cannot yet be shown to be weak by objective testing. 

Cranial nerve (CN) involvement is common; involvement of every nerve except CNs I 

and II (olfactory and optic) has been described. The nerve most commonly affected is 

CN VII (facial); facial weakness (usually bilateral) occurs in half of cases. Cranial nerve 

palsies may be the most prominent feature of the illness, as in the Guillain-Barre variant 

of ophthalmoplegia, ataxia, and areflexia. 

Peripheral autonomic nervous system involvement also occurs and may be manifested 

by hypertension, tachycardia, facial flushing, postural hypotension, and 

electrocardiographic changes. Respiratory musculature weakness requiring assisted 

ventilation occurs in 25% of cases. 


Increased spinal fluid pressure is seen only in severe cases. The cerebrospinal fluid cell 

count is normal initially in most patients; less than 10% of patients have more than 10 

leukocytes per microliter. The classic elevation in cerebrospinal fluid protein to levels as 

high as 100-400 mg/dL in the absence of significant pleocytosis (so-called 

albuminocytologic dissociation) may not be seen until several days after the onset of 

symptoms. These cerebrospinal fluid findings support the diagnosis of Guillain-Barre 

syndrome, but they are not specific and may be seen occasionally in any acute or 

chronic polyneuritis. 


Endotracheal intubation and ventilatory support should be considered in the emergency 

department for patients in respiratory failure. Plasmapheresis begun within 10 days of 

the first symptoms in the severely affected patient may shorten the need for mechanical 

ventilation. Corticosteroids are ineffective and may prolong the disease in elderly 

patients. All patients should be hospitalized. 

2. Arsenical Neuropathy 


• Arsenic is found in certain water supplies and seafood; used in production of glass and 

semiconductors (industrial exposure). 

• Painful peripheral neuropathy. 

• Acute poisoning: vomiting and severe diarrhea leading to dehydration and shock.

• Chronic poisoning: classical dermatitis, peripheral neuropathy, chronic renal and 

hepatic damage. 

• Arsenic gas: acute hemolytic anemia and chills, hemoglobinuria (black urine). 


The neuropathy of arsenic poisoning is a rapidly progressive sensorimotor 

polyneuropathy that in many ways mimics Guillain-Barre syndrome. Common sources 

of arsenic include rat and ant poison and the copper acetoarsenite contained in 

insecticides (eg, Paris green). Fowler's solution, once used for psoriasis, also contains 

arsenic. Patients with chronic symptoms may represent attempted murder. 



Abdominal pain, nausea and vomiting, and diarrhea occur minutes to hours following 

ingestion. A rapidly progressive polyneuropathy ensues 7-14 days later. Symmetric 

ascending paresthesias, initially distal, begin in the lower extremities and progress to 

overt sensory loss. 

Diffuse muscle aches and tenderness are common, as is a burning pain on the soles of 

the feet that is markedly aggravated by touching the skin. Deep tendon reflexes are 

depressed early and in the same distribution as the sensory loss. 

Symmetric motor impairment follows as the neuropathy progresses over days to a few 

weeks and is typically more severe distally and in the lower extremities and can lead to 

flaccid paralysis. The cranial nerves, rectal sphincter, and respiratory muscles are 

unaffected. 

Cutaneous stigmata of arsenical poisoning include increased skin pigmentation and 

marked exfoliation (especially of the hands and feet). Mees's lines (transverse white, 

nonpalpable lines on the nails) are especially suggestive of arsenic poisoning but do not 

appear until 40-60 days after ingestion because of the slow rate of nail growth. 


Cerebrospinal fluid findings are similar to those seen with Guillain-Barre syndrome: 

glucose and cell counts are normal, and protein is elevated, although usually less than 

100 mg/dL. 

The diagnosis is established by documenting elevated concentrations of arsenic in urine 

(upper limits of normal: 0.1 mg/24 h) or hair protected from external contamination, most 

commonly pubic hair (upper limits of normal: 0.1 mg/100 g of hair). 

C. Imaging 

If continued ingestion of arsenic is suspected, abdominal x-ray may be helpful, because 

arsenic is radiopaque. 

Treatment

(See also Chapter 45.) Symptomatic patients should be given a chelating agent to 

facilitate excretion of arsenic. Treatment must be started within 24 hours after ingestion 

to influence the course of the neuropathy. Give dimercaprol, 3-4 mg/kg/dose 

intramuscularly every 4 hours for 48 hours, then 3 mg/kg every 12 hours for a total of 10 

days; or penicillamine, 100 mg/kg/d orally (maximum: 1 g/d) divided into 4 doses for 5 

days. Either course may be repeated if the patient is still symptomatic. Follow urine 

arsenic levels, because hair and nail levels do not reflect acute changes. 

Disposition 

If arsenic poisoning is diagnosed or suspected, hospitalization is indicated for evaluation 

and treatment. 

3. Acute Intermittent Porphyria 


• More common in 18- to 40-year-old age group. 

• Autonomic neuropathy: constipation, colicky abdominal pain, vomiting, hypertension. 

• Peripheral neuropathy. 

• Seizure, delirium, coma. 

• Depression. 

• Areflexia. 

• Any nerve can be involved. 


Acute intermittent porphyria (the most common form) is recognized as an autosomal 

dominant with variable penetrance disorder. It involves porphyrin metabolism producing 

episodic clinical symptoms, most commonly in the third to sixth decades. Women are 

affected much more frequently than men. Attacks are often precipitated by drugs that 

affect porphyrin metabolism (especially barbiturates and sulfonamides; see Table 18-3), 

infection, or fasting. 



Abdominal pain is the most common manifestation of porphyria (85% of cases). The 

abdominal pain is severe, often colicky, and may be generalized or localized. Onset of 

pain may precede development of other signs or symptoms by several weeks. Vomiting, 

constipation, and abdominal distention often lead to exploratory laparotomy, even 

though these signs are manifestations of an autonomic peripheral neuropathy. 

Weakness due to a predominantly motor polyneuropathy is the major neurologic 

manifestation. It is usually symmetric, beginning in the upper or lower extremities and 

most often proximally rather than distally. The neuropathy usually progresses slowly 

over days to weeks and is believed to result from axonal degeneration. Occasionally,

completed flaccid quadriparesis with associated respiratory paralysis requiring 

mechanical ventilation occurs over a few days. 

Cranial nerve involvement is common, especially CN VII, the vagus nerve (CN X), and 

the nerves to the extraocular muscles. Deep tendon reflexes are depressed or absent, 

except for a curious preservation of the ankle jerks in some patients. Signs of sensory or 

autonomic neurologic involvement are usually less prominent. 

Seizures, acute psychosis, hypotension, oliguria, and hyponatremia also occur. 

Tachycardia (> 100 beats/ min) is nearly always present because of catecholamine 

release during acute attacks. 


Cerebrospinal fluid pressure and glucose concentration are normal; protein 

concentration is slightly elevated (not over 100 mg/dL), and there may be a modest 

pleocytosis (

Cerebrospinal fluid and peripheral blood examinations are normal. 

Treatment 

The tick may be attached to any portion of the body but is most commonly hidden in 

long hair about the head and neck. Removal of the entire tick by application of ether, 

gasoline, or petroleum is followed by symptomatic improvement within hours. Complete 

resolution of symptoms occurs within a few days to a week. 

Disposition 

Patients in the acute phase must be hospitalized for supportive management. 

5. Diphtheritic Polyneuritis 


• Patients may present with nonspecific symptoms (fever, malaise, hoarseness, nausea 

and vomiting). 

• Neurologic exam includes cranial nerve and peripheral nerve palsies in lower 

extremities. 

• Progressive proximal to distal weakness. 



In diphtheritic polyneuritis, the cranial and peripheral nerves are affected 2-3 weeks 

following infection—the cranial nerves first, especially the palate and the muscles of 

ocular accommodation. The patient complains of inability to focus secondary to impaired 

visual accommodation paresis of the ocular muscles. Although this disease is rare in the 

United States, it is still seen elsewhere. Involvement of the nerve supply to the pharynx, 

larynx, face, extraocular muscles, and extremities occurs as the illness progresses over 

days to weeks. Reflexes are lost early. Sensory signs are not prominent, although distal 

paresthesias may be noted. 

Symptoms are usually maximal within 1-2 weeks. Gradual (usually complete) 

improvement then follows over months, although associated myocarditis may produce a 

significant number of deaths. 


Cerebrospinal fluid protein is elevated to 100-400 mg/dL. Recovery of the organisms 

from the pharynx or wound confirms the diagnosis, although such cultures may be 

negative by the time neuropathy is manifested. 


There is no specific treatment. Administration of diphtheria antitoxin will not abort the

neuropathy once symptoms have appeared. Patients must be hospitalized for 

supportive care. 

6. Paralytic Seafood Poisoning (See also Chapter 44.) 


• One of four distinct shellfish poisonings. 

• Paresthesias of lips, tongue, gums within 30 minutes of ingestion. 

• Muscle weakness, paralysis, cranial nerve dysfunction. 

• Nausea, vomiting, diarrhea. 

• Airway support required. 


Saxitoxin may be present in Atlantic and Pacific shellfish, especially between May and 

October, and can produce a fulminating sensorimotor polyneuropathy. Numbness and 

tingling of the fingers, toes, and perioral region are associated with a rapidly ascending 

motor paralysis that can begin within minutes following ingestion. Bizarre dysesthesias 

(eg, sensation that teeth are loose in their sockets; reversal of hot and cold sensation) 

are common and specific to saxitoxin or ciguatoxin poisoning. Ingestion of puffer fish 

containing tetrodotoxin may produce the same symptoms. 


There is no available antitoxin. Supportive care (including mechanical ventilation if 

indicated) is followed by complete recovery. Hospitalization is indicated for infants and 

elderly victims and for patients with respiratory insufficiency or objective weakness. 

DISEASES OF THE NEUROMUSCULAR JUNCTION 

BOTULISM 


• Afebrile (unless other infection is present). 

• Symmetric neurologic symptomatology. 

• Patient remains responsive. 

• Heart rate is normal or bradycardic; hypotension is absent. 

• Progressive, symmetric, descending weakness, first in muscles innervated by cranial 

nerves, then neck, arms, and legs. 

• Dry mouth, diplopia, dysarthria, generalized weakness. 


Clostridium botulinum toxin attacks the neuromuscular junction by impairing the release 

of acetylcholine at all peripheral synapses. Paralysis occurs mainly following the 

ingestion of foods contaminated with the toxin and only rarely from infected wounds. In 

infants, cases have resulted from colonization of the gastrointestinal tract by C 

botulinum (originating, in some cases, from ingested honey). Although commercially 

canned foods have caused epidemics, most cases have been due to improperly 

home-canned vegetables, fruits, meat, and fish. Ingestion of even a few drops of 

contaminated food may cause botulism. The distribution of the toxin in the contaminated 

vehicle may not be uniform. Fruits or vegetables contaminated with type A or B toxin will 

taste spoiled; other foods may not. Contaminated foods must be boiled for over 10 

minutes in order for the toxin to be reliably inactivated. 



Symptoms usually begin 12-48 hours following toxin ingestion and may progress over 

hours to days (Table 18-4). The shorter the interval between ingestion and the 

appearance of symptoms, the more severe the disease. The nervous system is involved 

in descending fashion, beginning with the muscles innervated by the cranial nerves. 

This contrasts with Guillain-Barre syndrome, in which there is usually ascending 

involvement. 

Nausea and vomiting are the initial symptoms in one third of cases (prominent with type 

E toxin). Blurring of vision (due to paralysis of muscles of accommodation) is the most 

common initial neurologic symptom. Diplopia, dysphagia, and dysphonia come on in 

sequence as lower bulbar muscles become involved. Weakness of respiratory and 

extremity muscles follows as the paralysis descends. Ptosis, extraocular muscle 

paralysis, and pupillary dilatation and fixation follow, and then weakness of jaw and 

palate function. Some deep tendon reflex activity remains until muscle paralysis is 

complete. 

Dryness of mucous membranes and orthostatic hypotension have been prominent 

features in some patients. Sweating, salivation, and bronchorrhea (seen in 

cholinesterase inhibitor poisoning) do not occur. There are no sensory abnormalities. 

Infant botulism is characterized by poor feeding, poor muscle tone, episodes of 

aspiration, and constipation. 


Examination of cerebrospinal fluid and peripheral blood smears is not helpful unless a 

superimposed condition develops (eg, aspiration pneumonia). Specimens of blood or 

contaminated food should be saved for laboratory assay for botulinum toxins (available 

through local public health departments). Blood samples should consist of 30 mL of 

clotted, nonheparinized blood, which need not be centrifuged or separated but must be 

collected before the antitoxin is started. In infants, save a sample of stool for culture for 

C botulinum (consult the local public health department for details). 

C. Electrocardiographic Findings 

T wave inversions, conduction abnormalities, and ventricular arrhythmias may occur.

Treatment 

A. Antitoxin 

Bivalent or trivalent antitoxin should be given as soon as possible after diagnosis. Skin 

testing should be performed before administration of antitoxin because of the risk of 

anaphylaxis. The current recommended dose of licensed botulinum antitoxin is a single 

10 mL vial (per patient), diluted 1:10 in a 0.9% saline solution and given in a slow 

intravenous infusion. Antitoxin and consultation may be obtained in the United States by 

telephoning the Centers for Disease Control in Atlanta: (404) 639-2206 (days) or (404) 

639-2888 (nights, weekends, and holidays). The local health department should be 

notified immediately as well (by any telecommunications method). Although the mortality 

rate has been reported to be as high as 60-70%, rapid diagnosis and adequate 

respiratory support should improve the outlook. Recovery of neurologic function occurs 

over weeks to months; complete recovery is common. 

Serum sickness may develop as a result of administration of antitoxin. Neostigmine and 

other drugs effective in treating myasthenia gravis are not helpful in botulism. 

B. Antibiotics 

The treatment of wound botulism is debridement and penicillin, 300,000 units/kg/d 

intravenously, in addition to other measures described above. Clindamycin, 30 mg/kg/d 

intravenously, or chloramphenicol, 50 mg/ kg/d intravenously, may be used in 

penicillin-allergic patients. Aminoglycosides may worsen neuromuscular blockade and 

should be avoided. 

C. Additional Measures 

Careful monitoring of vital capacity, maximum inspiratory force, and arterial blood gases 

is mandatory, because respiratory insufficiency may develop rapidly. Cathartics and 

enemas must be given early to remove any toxin remaining in the bowel. Emesis or 

gastric lavage is indicated if the contaminated food was ingested less than 6-8 hours 

before arrival at the emergency department. All other persons who have also eaten the 

suspected food should be given antitoxin, emetics, and cathartics even if they are 

asymptomatic. 

Disposition 

The patient must be hospitalized for observation and treatment. 

ORGANOPHOSPHATE POISONING (See also Chapter 45.) 


• DUMBELS: diarrhea, urination, miosis, bronchospasm, emesis, lacrimation, salivation. 

• Organophosphates can be absorbed through lungs, skin, gastrointestinal tract, 

mucous membranes. 

• Symptoms appear within hours of exposure (but immediately with large doses).

• Respiratory paresis. 


Organophosphates exert their toxic effect by inhibiting acetylcholinesterase, producing 

stimulation and then inhibition at the myoneural junction by the uncatabolized 

acetylcholine. Poisoning is most commonly due to insecticides (eg, parathion, 

malathion) and occurs during spraying or dusting of crops. Certain poison gases used in 

war have a similar action. 


Rapidity of onset and severity of symptoms vary with the dose and route of 

administration; symptoms of poisoning may occur within 5 minutes to 12 hours after 

exposure. 


(See Table 18-5.) Initial symptoms are fatigue, headache, dizziness, nausea and 

vomiting, and increased salivary and sweat production. Weakness of skeletal and bulbar 

muscles with marked fasciculations follows, and finally loss of consciousness occurs. 

Examination often reveals the characteristic garlic odor of the organophosphate 

compound. Lacrimation is common, and pupils are pinpoint and may be unreactive to 

light. Muscle fasciculations and complete motor paralysis may be present. 


Hyperglycemia with prominent glycosuria may occur. Polymorphonuclear leukocytosis is 

common. Laboratory demonstration of depressed plasma and erythrocyte 

cholinesterase activity confirms the clinical diagnosis. 

Treatment 

See also Chapter 39. 


Maintain airway and respiratory function, and remove residual organophosphate by 

washing the skin and removing exposed clothing. Ingested organophosphates should 

be removed by lavage and catharsis. Induction of emesis is usually contraindicated 

because of the early onset of drowsiness and risk of aspiration. In this case, protect the 

airway and perform gastric lavage. 

B. Specific Measures 

Atropine, a specific antidote, is the treatment of choice; however, it does not reverse 

paralytic symptoms. Large doses may be required. Start with 2 mg intravenously 

(children, 0.5 mg), followed by repeated doses of 2- 4 mg every 5-10 minutes (children 

< age 12 years, 0.05-0.10 mg/kg every 15 minutes, repeated as needed for symptom 

control) until signs of atropinization occur: flushing, mydriasis, drying of secretions, and 

tachycardia. The use of up to 50 mg in 24 hours is not unusual.

Pralidoxime (Protopam, 2-Pam) releases organophosphates from acetylcholinesterase 

and should be given to all patients with significant poisoning. It should not be used for 

carbamate poisoning, because carbamates are not irreversibly bound to 

acetylcholinesterase. The dose is 20-40 mg/kg in saline intravenously over 20-30 

minutes. The dose may be repeated in 1-2 hours. Adequate renal function is a 

prerequisite for use of pralidoxime, because it is excreted in the urine. 

Benzodiazepines may be used for seizure control. 

Disposition 

All patients except for the very mildly ill with stable or improving symptoms require 

hospitalization. The earlier treatment is instituted, the lower the mortality rate. 

MYASTHENIA GRAVIS 


• Rare, autoimmune disorder. 

• Bulbar muscles most common and severe (ptosis, diplopia, blurred vision, difficulty 

swallowing, dysarthria). 

• Muscle weakness provoked by repetitive use of muscles involved (eg, climbing stairs) 

with recovery during rest. 

• Decreased ability to clear secretions or generate adequate respirations. 


Musculature innervated by the cranial nerves is commonly the earliest and most 

severely involved in myasthenia gravis, as manifested by ptosis and by impaired eye 

movements, facial expressions, chewing, swallowing, and speaking. Pupillary 

responsiveness is preserved. There is increasing weakness on repetitive muscle use 

("fatigability"). Sensory abnormalities are absent. The diagnosis in previously untreated 

myasthenia gravis is confirmed by objective and unequivocal improvement following 

anticholinesterase drugs, for example, edrophonium (Tensilon, others) (for dosage, see 

differential diagnosis in "Neuromuscular Blockade" section, above) or the longer-acting 

neostigmine (Prostigmin) (1-1.5 mg intramuscularly; effect in 45-90 minutes). Stable 

patients with myasthenia gravis will be following one of the drug regimens listed in Table 

18-6. 

The acute occurrence of respiratory insufficiency or the inability to handle oropharyngeal 

secretions in a previously stable myasthenic patient constitutes a myasthenic crisis. 

Crises may be precipitated by intercurrent infection or surgery or may have no obvious 

cause. The subjective complaint of dyspnea in such patients demands immediate and 

careful evaluation. 

The difference between myasthenic and cholinergic crisis is of little practical importance; 

the latter, however, appears to be uncommon.

Treatment 

Immediately evaluate the need for respiratory assistance and endotracheal intubation, 

as described above. Temporizing with drug therapy may have disastrous 

consequences, because the patient may worsen within minutes. Discontinue 

anticholinesterase therapy in the intubated patient. Treat precipitating causes if present 

(eg, infection), but avoid aminoglycoside antibiotics because they may worsen 

myasthenia gravis. Plasmapheresis may temporarily reduce symptoms or help the 

patient to get over the crisis. Intravenous immunoglobulin appears to have a role in 

acute treatment intervention when other modalities have failed. 

Disposition 

All patients in myasthenic crisis require immediate hospitalization. Stable patients 

without any respiratory symptoms (not in crisis) may receive medical treatment (Table 

18-6) and be referred for outpatient care. Patients newly diagnosed as having 

myasthenia gravis may be hospitalized for evaluation and treatment or started on a 

medical regimen (Table 18-6) and referred to a clinic or private medical care. 

PRIMARY ACUTE MYOPATHIES 

HYPOKALEMIC PERIODIC PARALYSIS 


• May occur up to age 30 years, rare after age 50 years. 

• Severe symmetric complete weakness. 

• Symptoms can last up to 1 week. 

• Exacerbated by high carbohydrate meals, cold temperatures. 

• Potassium may be decreased but is not necessarily below normal. 

• Increased urinary sodium, potassium, chloride. 

• Decreased serum phosphorous. 


Hypokalemic periodic paralysis is characterized by episodes of profound weakness that 

may occur at intervals ranging from a day to years. Episodes are often precipitated by a 

large carbohydrate meal or a period of strenuous exercise, especially when followed by 

rest or sleep. 



An attack of weakness usually lasts 2-24 hours. The weakness is painless and 

generalized, often beginning in the lower extremities and becoming more severe 

proximally. Paralysis of cranial and respiratory musculature is rare, and for this reason

fatal episodes are uncommon. Extremity musculature is hypotonic during attacks. 

Reflexes are reduced in proportion to the muscle weakness. Sensory examination is 

normal. 


A markedly reduced serum potassium level (usually 2- 3 mEq/L) during the attack, with 

normal potassium levels and physical examination between episodes, confirms the 

diagnosis. 

Treatment 

Give potassium chloride, about 1 mEq/kg orally at hourly intervals, until improvement 

occurs (usually within 3-4 hours). Many patients will require intravenous potassium 

chloride, with the rate of administration not exceeding 20 mEq/h. The frequency and 

severity of attacks can be reduced with acetazolamide, 250 mg orally 2 or 3 times a day. 

Disposition 

Patients having acute attacks can usually receive treatment in the emergency 

department and be sent home. 

ACUTE ELECTROLYTE ABNORMALITIES 

Profound magnesium and phosphate depletion can cause acute muscle weakness and 

in particular must be considered in alcoholic patients. However, the vast majority of 

acute clinical syndromes of muscle weakness are due to high or low serum potassium 

concentrations (Table 18-7). Although the onset of weakness is not well correlated with 

serum potassium levels, values below 3 mEq/L or above 7.5 mEq/L are most commonly 

associated with symptoms. Specific therapy is dictated by the cause, but the potential 

for life-threatening cardiac arrhythmias from severe hypokalemia or hyperkalemia 

demands immediate therapy (see Chapter 42). 

RHABDOMYOLYSIS 


• Myalgias and muscle weakness. 

• Dark urine. 

• Tenderness, decreased muscle strength, swelling, soft extremities (vs. compartment 

syndrome) may be present. 

• May be secondary to infection. 


Release of myoglobin from the body musculature may be due to many causes (Table 

18-8). Weakness presumably results from loss of this contractile protein from muscle 

cells. Important consequences of rhabdomyolysis with myoglobinuria are acute renal

failure and marked elevations of serum potassium. 



Pain and swelling of the involved muscles and weakness of the limbs occur, especially 

in proximal distribution. Reflexes are depressed in proportion to muscle weakness. 

Sensory examination is normal. 


The urine is red-tinged and turns dark brown on standing. Myoglobinuria may be 

suggested by a heme-positive (dipstick) test in erythrocyte-free urine and confirmed by 

specific chemical testing. Muscle enzymes (CK) are massively elevated in most cases. 

Treatment 

Treatment consists of hydration to ensure high urine volumes and prevent precipitation 

of myoglobin in renal tubules. If anuria is present, fluids should be administered 

cautiously. A recommended regimen is normal saline at a rate of 1.5 L/h. Maintain urine 

output at 300 mL/h. Consider mannitol and sodium bicarbonate to alkalinize the urine. 

Neither, however, has been shown to be superior to saline alone. Monitor urine output 

closely. 

Disposition 

Hospitalization is mandatory. Serum potassium levels should be followed closely. The 

prognosis of this disorder is good even with profound muscle necrosis and renal failure. 

Arnon SS et al: Botulinum toxin as a biological weapon: Medical and public health 

management. JAMA 2001;285:1059. [PMID: 11209178]. (A review on how to recognize, 

diagnose and treat botulinum.) 

Bella I et al: Neuromuscular disorders and acute respiratory failure. Neurol Clin 

1998;16:391. [PMID: 9537968] (A review of neuromuscular disorders.) 

Chao D et al: Spinal epidural abscess: A diagnostic challenge. Am Fam Physician 

2002;65:1341. [PMID: 11996416] (A review on all aspects of epidural abscess.) 

Dellon AL: Management of peripheral nerve problems in the upper and lower extremity 

using quantitative sensory testing. Hand Clin 1999;15:697. [PMID: 10563271] (A review 

of management of peripheral nerve problems.) 

Greenstein P: Tick paralysis. Med Clin North Am 2002;86(2):441. [PMID: 11982312] (A 

compressive review of tick paralysis.) 

Gutmann L: Periodic paralyses. Neurol Clin 2000;18:195. [PMID: 10658175] (A review 

of metabolic myopathies.) 

Howard JF et al: Intravenous immunoglobulin for the treatment of acquired myasthenia

gravis. Neurology 1998;51:S30. [PMID: 9851728] (Consensus of an expert panel on 

acute treatment interventions in the rapidly progressive weakness or as chronic 

maintenance therapy for myasthenia gravis.) 

Hu H: Exposure to metals. Prim Care 2000;27:983. [PMID: 11072295] (A review of the 

diagnosis and treatment of heavy metal poisoning.) 

Jackson CG et al: The facial nerve. Current trends in diagnosis, treatment, and 

rehabilitation. Med Clin North Am 1999;83: 179. [PMID: 9927969] (A comprehensive 

review of the diagnosis and treatment of facial nerve disorders including Bell palsy.) 

Mines D et al: Poisonings: food, fish, shellfish. Emerg Med Clin North Am 1997;15:157. 

[PMID: 9056574] (A review of seafood-associated poisoning.) 

Posner MA: Compressive ulnar neuropathies at the elbow: I. Etiology and diagnosis. J 

Am Acad Orthop Surg 1998;6:282. [PMID: 9753755] (A review of the diagnosis of ulnar 

neuropathies.) 

Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 

2002;59:499. [PMID: 12236201] (A review of transverse myelitis.) 

Reid RL: Radial nerve palsy. Hand Clin 1988;4:179. [PMID: 3294243] (A review article 

on radial nerve palsy.) 

Ross MA: Acquired motor neuron disorders. Neurol Clin 1997;15:481. [PMID: 9227949] 

(A review article discussing acquired motor disease including poliomyelitis.) 

Sauret JM et al: Rhabdomyolysis. Am Fam Physician 2002;65:907. [PMID: 11898964] 

(A comprehensive review on the diagnosis and treatment of rhabdomyolysis.) 

Simpson et al: Recognition and management of acute pesticide poisoning. Am Fam 

Physician 2002;65:1599. [PMID: 11998835] (A review of pesticide poisoning 

management.) 

Suarez JI et al: Acute intermittent porphyria: Clinicopathologic correlation. Report of a 

case and review of the literature. Neurology 1997;48:1678. [PMID: 9191786] (A review 

of intermittent porphyria.) 

Wetzel FT et al: Management of metastatic disease of the spine. Orthop Clin North Am 

2000;31:611. [PMID: 11043100] (A review of the management of metastatic diseases of 

the spine.) 

IV. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS 

ASSOCIATED WITH STROKE 

Stroke is a cerebrovascular disorder resulting from impairment of cerebral blood supply 

by occlusion (eg, by thrombi or emboli) or hemorrhage. It is characterized by the abrupt 

onset of focal neurologic deficits. The clinical manifestation depends on the area of the 

brain served by the involved blood vessel. Stroke is the most common serious

neurologic disorder in adults and occurs most frequently after age 60 years. The 

mortality rate is 40% within the first month, and 50% of patients who survive will require 

long-term special care. 

Stabilize Ventilation 

A. Establish Airway 

Assess adequacy of airway and ventilation in all stroke patients, especially in the 

presence of depressed level of consciousness, absent gag reflex, respiratory difficulty, 

or difficulty managing secretions. 

B. Consider Intubation 

Patients with inadequate ventilation (respiratory acidosis) or difficulty managing 

secretions will require intubation. 

Search for Head Trauma 

Stroke patients may sustain head injury due to incoordination or weakness. Conversely, 

patients with focal neurologic findings due to head trauma may be mistakenly diagnosed 

as suffering from stroke. If head injury is suspected from the history or clinical findings, 

immobilize the cervical spine. Refer to Chapter 22 for management. 

Treat Cerebral Edema 

Deterioration of neurologic deficits or the presence of brainstem involvement (depressed 

sensorium, pupillary or extraocular movement abnormality, decorticate or decerebrate 

posturing) suggests significant cerebral edema and impending herniation. With the 

exception of temporizing measures prior to surgical decompression in cerebellar or 

superficial lobar hemorrhage, medical therapy for cerebral edema (see Table 16-3) 

associated with ischemic stroke does not alter the outcome. 

Treat Seizures 

(See Chapter 17 for management of seizures.) Consider prophylaxis for acute seizure in 

patients with embolic stroke or subarachnoid hemorrhage. Give intravenous phenytoin, 

15-18 mg/kg at a rate not greater than 50 mg/min, or fosphenytoin, 15—20 mg/kg PE 

(phenytoin equivalents) intravenously. 

Treat Hypoglycemia 

Occasionally patients with hypoglycemia may have focal neurologic deficits that may 

mimic a stroke. Confirm the presence of hypoglycemia using a glucometer or reagent 

strips before giving 50 mL of 50% dextrose solution. Stroke patients with elevated 

serum glucose may have a worsened outcome. 

Obtain Emergency CT Scan 

Emergency CT scan of the head should be obtained early. This is the most readily 

available method for reliably detecting the presence of hemorrhage and focal cerebral

edema. MRI, especially diffusion weighted, has enhanced the diagnosis of ischemic 

stroke. 

V. FURTHER EVALUATION OF THE PATIENT WITH STROKE 

Accurate diagnosis and identification of the underlying cause of the stroke are important 

for appropriate evaluation and treatment. Conditions that predispose to strokes should 

be sought and corrected. A systematic approach to the evaluation of the patient with 

stroke is detailed below and can be modified depending on the urgency of the patient's 

condition. 

History 

A. Determine Time Course of Deficits 

Transient ischemic attacks (TIAs) and deficits progressive in a stepwise pattern over 

hours to days suggest thrombotic vascular occlusion. Abrupt onset of full neurologic 

deficit is characteristic of embolic stroke. Abrupt onset and rapid evolution of deficits are 

associated with intracerebral hemorrhage. Rapid response to stroke can result in little 

apparent damage. Contrarily, a stroke left undiagnosed or untreated for too long can 

result in neurologic damage or even death. The goal is to determine the exact time of 

onset of symptoms because the current recommended window of opportunity for 

thrombolytic therapy is 3 hours. 

B. Identify Risk Factors 

Hypertension, diabetes mellitus, TIAs, hyperlipidemia, smoking, family history, and use 

of oral contraceptives predispose to atherosclerotic disease. Cardiac disorders such as 

changing cardiac rhythms (especially atrial fibrillation), dyskinetic myocardium, and 

valvular heart disease are associated with increased risk for embolic strokes (Table 

18-9). Bleeding dyscrasias, hypercoagulable states, blood disorders (especially sickle 

cell disease), and vascular disorders are also associated with a risk for stroke. Carotid 

artery bruits in patients with TIAs or stroke suggest the possibility of emboli derived from 

atheromatous plaques. Acute stroke syndromes, especially intracerebral hemorrhages, 

have been associated with cocaine and, less commonly, amphetamine use. 

C. Identify Other Associated Symptoms 

Severe headache and vomiting often accompany intracerebral hemorrhage. Patients 

with migraine headaches rarely may suffer strokes due to vascular spasm. 


A. General 

A thorough examination may reveal the underlying cause for the stroke and direct 

treatment. 

1. Vital signs—Record the body temperature. Hypertension is a risk factor for stroke, 

and systolic pressure above 200 mm Hg may require treatment. 

2. Head—Arteriovenous malformations may be detected by auscultation of the head for 

bruits. Palpate the temporal arteries for tenderness, nodularity, or absence of pulse

suggestive of giant cell arteritis. Search for any evidence of trauma. 

3. Eyes—Examination of the retina may reveal visible emboli in the retinal vessels. 

Subhyaloid hemorrhage is diagnostic for subarachnoid hemorrhage. 

4. Neck—The carotid arteries should be examined (one at a time) for presence of bruits 

and reduction of pulsation. Although these findings are not specific for carotid disease, 

further carotid studies may be warranted to evaluate for possible carotid 

endarterectomy. 

5. Heart—Changing cardiac rhythms and murmurs or valvular disease are associated 

with increased risk of embolization from the heart. 

6. Skin—Ecchymosis and petechiae may suggest blood disorders or vasculitis as 

causative factors. Presence of recent needle tracks or subungual splinter hemorrhages 

suggest the possibility of septic emboli derived from infected heart values. 

7. Lung sounds—Ausculate for possible aspiration pneumonia or pulmonary edema. 

B. Neurologic Examination 

A rapid neurologic examination should be performed in the emergency department and 

should focus on (1) localizing the anatomic site of deficit as an aid in determining the 

specific stroke syndrome (which dictates treatment) and (2) assessing the degree of 

neurologic impairment, from which improvement or worsening can be assessed. 

1. Level of alertness—Reduced mental alertness can be a sign of extensive injury from 

hemorrhage, brain-stem infarction or herniation, or metabolic changes. 

2. Cognitive—Assess response to commands and fluency of speech. Aphasia and 

apraxia are associated with involvement of the cerebral cortex and anterior (carotid) 

circulation; lacunar infarction or disturbance of posterior (vertebrobasilar) circulation is 

unlikely. 

3. Cranial nerves—Visual field abnormalities exclude lacunar infarction. Abnormal 

pupillary reflexes and ocular palsies are brain-stem findings and are associated with 

disturbance of posterior circulation or impending brain herniation. 

4. Motor—Hemiparesis can be associated with disturbance of the anterior or posterior 

circulation. Generally, in anterior circulation strokes, the face, hand, and arm are 

affected more than the leg. In lacunar infarction and posterior circulation strokes, this 

pattern is less common. Hemiparesis involving one side of the face and the other side of 

the body is due to disturbance of posterior circulation. 

5. Sensory—Hemisensory deficits without associated motor involvement are usually 

due to lacunar infarcts. Astereognosis (inability to identify objects by touch) and 

agraphesthesia (inability to recognize figures traced on the skin) are cortical sensory 

deficits and are due to disturbance of anterior circulation.

6. Cerebellar—Hemiataxia suggests involvement of the cerebellum or the brain stem, 

or lacunar infarction deep in white matter. 


A. Blood Tests 

The following blood tests should be obtained in most patients with focal neurologic 

deficits: 

• Complete blood count and platelet count (to detect blood dyscrasias), and prothrombin 

time and partial thromboplastin time for coagulation disorders 

• Glucose level, because both hyperglycemia and hypoglycemia may cause focal 

neurologic findings that can mimic stroke 

• Erythrocyte sedimentation rate to detect vasculitis or arteritis 

• Serologic test for syphilis 

• Toxicologic screen if drug use is suspected 

B. Electrocardiogram 

An electrocardiogram may reveal new arrhythmias or reversion to a normal rhythm, both 

of which are associated with increased risk for emboli. Presence of myocardial infarction 

or persistent changes suggestive of a ventricular aneurysm also increase the risk for 

stroke. 

C. CT or MRI Scan 

These studies are essential for localizing the lesion; distinguishing hemorrhagic from 

occlusive stroke; and identifying other intracranial disease, such as tumor or abscess, 

that can be confused with strokes. A CT or MRI scan should be obtained in any 

suspected stroke patient. 

D. Lumbar Puncture 

Occasionally, in patients suspected of having subarachnoid hemorrhage but whose CT 

scan is negative or equivocal, a lumbar puncture may be diagnostic (the cerebrospinal 

fluid is bloody or the supernatant is xanthochromic [yellow]). Lumbar puncture is often 

useful in patients with meningoencephalitis and vasculitis. 

Caution: In patients with focal neurologic findings, a CT or MRI scan should be 

performed prior to lumbar puncture. 

E. Vascular Studies 

Cerebral angiography may be indicated in patients suspected of having a surgically 

correctable condition such as cerebral aneurysm, arteriovenous malformation, and 

carotid atherosclerosis or stenosis. Noninvasive vascular studies such as 

ophthalmodynamometry, Doppler sonography, thermography, and ultrasonic studies 

may be useful to identify patients with suspected carotid atherosclerotic disease who 

may need angiography.

Bella I et al: Neuromuscular disorders and acute respiratory failure. Neurol Clin 

1998;16:391. [PMID: 9537968] (A review of neuromuscular disorders.) 

Chalk CH: Acquired peripheral neuropathy. Neurol Clin 1997;15:501. [PMID: 9227950] 

(A review of acquired peripheral neuropathies.) 

Ross MA: Acquired motor neuron disorders. Neurol Clin 1997; 15:481. [PMID: 9227949] 

(A review article discussing acquired motor disease including poliomyelitis.) 

Simpson et al: Recognition and management of acute pesticide poisoning. Am Fam 

Physician 2002;65:1599. [PMID: 11998835] (A review of pesticide poisoning 

management.) 

Walter FG et al: Envenomations. Crit Care Clin 1999;15:353. [PMID: 10331133] (A 

review article on management of envenomations.) 

Younger DS et al: Diagnosis in neuromuscular diseases. Neurol Clin 1996;14:135. 

[PMID: 8676841] (A review of acute myopathies.) 

VI. MANAGEMENT OF SPECIFIC STROKE SYNDROMES 

HEMORRHAGIC STROKE 

SUBARACHNOID HEMORRHAGE (See also Chapter 16.) 


• Sudden onset of severe headache. 

• Sentinel headache may be warning for aneurysmal subarachnoid hemorrhage. 

• Nausea and vomiting, low back pain, bilateral leg pain. 

• Photophobia, visual changes. 

• Loss of consciousness. 


Subarachnoid hemorrhage occurs secondary to bleeding in the subarachnoid space. It 

is a medical emergency. Approximately 80% are due to saccular or berry aneurysms. 

The rest may be due to 

• Trauma 

• Arteriovenous malformation (which usually bleeds earlier than aneurysms, often 

becoming symptomatic in childhood or before age 30 years) 

• Sickle cell disease

• Coagulopathies 

• Central nervous system vasculitis 

• Cocaine use 

• Amphetamine use 

• Moyamoya disease 

• Intracranial neoplasm or metastatic disease 


Patients usually complain of "the worst headache of my life" or "thunderclap" headache. 

Commonly associated symptoms include nausea and vomiting, neck stiffness, 

photophobia, back pain, and leg pain. Patients who present with stupor (localizing to 

pain) or coma are at high risk for mortality. 

A high index of suspicion must be raised in patients presenting with early warning signs 

of a sentinel leak, because they are frequently missed in the diagnosis of subarachnoid 

hemorrhage, and early diagnosis can be life saving. Grading of subarachnoid bleeds is 

based on the patient's condition on presentation. The grading scale is as follows: 

Grade Neurologic Status 

I Asymptomatic 

II Severe headache or meningismus, cranial nerve palsy 

III Drowsy; confused, minimal neurologic deficits 

IV Stuporous; moderate to severe hemiparesis 

V Deep coma; decerebrate posturing; no motor response 

A CT scan should be performed as the first diagnostic study (Figure 18-2). CT scan is 

up to 95% accurate within the first 24 hours; sensitivity decreases to 80% after 3 days 

and to 50% after 1 week. Selective catheter cerebral angiography aids in diagnosing 

cerebral aneurysms as the cause of subarachnoid hemorrhage. Lumbar puncture 

should be performed if the CT scan does not demonstrate blood but the suspicion for 

subarachnoid hemorrhage remains high. Lumbar puncture may demonstrate 

xanthochromic fluid or may even be bloody. 

Complications & Treatment 

The American Heart Association Special Writing Group of the Stroke Council has made 

various recommendations for subarachnoid hemorrhage: 

A. Aneurysmal Rebleeding

Aneurysmal rebleeding may be secondary to uncontrolled hypertension or aneurysmal 

clot fibrinolysis. Surgical clipping is strongly recommended to reduce the rate of 

rebleeding. 

B. Seizure 

Because seizures increase the risk of rebleeding after a subarachnoid hemorrhage, 

prophylactic use of an anticonvulsant for example, intravenous fosphenytoin or 

phenytoin, 15-20 mg/kg, is recommended. 

C. Hypovolemia and Hyponatremia 

Hypovolemia and hyponatremia can occur secondary to the syndrome of inappropriate 

secretion of antidiuretic hormone. Treatment involves intravenous hydration with 

isotonic crystalloid. A central intravenous monitor is desirable. 

D. Hydrocephalus 

1. Acute obstructive hydrocephalus—This form of hydrocephalus occurs in about 

20% of patients after subarachnoid hemorrhage. Ventriculostomy is recommended, 

although it may increase the risk of rebleeding or infection. 

2. Chronic communicating hydrocephalus—This form of hydrocephalus is a frequent 

occurrence after subarachnoid hemorrhage. A temporary or permanent cerebrospinal 

fluid diversion is recommended in symptomatic patients. 

E. Vasospasm 

Vasospasm, or delayed cerebral ischemia, remains a frequent complication with high 

morbidity and mortality rates. Nimodipine, 60 mg orally every 4 hours, is strongly 


F. Neurosurgical Consultation 

Seek neurosurgical consultation for definitive management. 

INTRACEREBRAL HEMORRHAGE (See also Chapter 16.) 


• No specific signs or symptoms reliably distinguish between intracerebral hemorrhage 

and ischemic stroke. 

• Symptoms vary depending on affected area and extent of bleeding. 

• Patients are more likely to exhibit signs of increased intracranial pressure; seizures 

more common. 

• Headache often severe and sudden. 

• Nausea and vomiting, hypertension, altered sensorium. 


Intracerebral hemorrhage is twice as common as subarachnoid hemorrhage and even 

more likely to result in a major disability or death. Bleeding occurs primarily in the brain

parenchyma, although blood appears in the cerebrospinal fluid in the majority of 

patients. Symptoms are due to mass effect of the hematoma with displacement and 

compression of adjacent brain tissue. The most common cause is advancing age and 

damage of intracerebral arterioles by long-standing systemic hypertension. Other 

causes include anticoagulation, drug and alcohol abuse, thrombolytic therapy, bleeding 

diathesis, neoplasms, cerebral amyloid angiopathy, infections, and arteriovenous 

malformations. 


Clinical findings depend on the site of the hemorrhage but occur abruptly and progress 

within minutes to a few hours. Headache and vomiting are frequent symptoms. Focal 

neurologic deficits are prominent, because most bleeding sites abut the basal ganglia, 

thalamus, and internal capsule. Abrupt onset of coma and prominent brain-stem findings 

(pinpoint pupils, absent extraocular movements) are characteristic of pontine 

hemorrhage. A CT scan is diagnostic and is the imaging study of choice. MRI and 

magnetic resonance angiography are useful in detecting structural abnormalities such 

as malformations and aneurysms (Figure 18-3). 

Ataxia and cerebellar abnormalities, with absent or mild hemiparesis, are characteristic 

of cerebellar hemorrhage. It is particularly important to diagnose hypertensive 

intracerebellar hemorrhage rapidly, because fatal brain-stem compression may occur 

rapidly; emergency surgical decompression can be life saving. Because the clinical 

differentiation from acute vestibular dysfunction may be difficult, patients with sudden 

onset of disequilibrium and vomiting may need a CT scan of the brain to exclude 

cerebellar hemorrhage. 


As with all other emergencies, initial management of a patient with intracerebral 

hemorrhage is directed toward airway, breathing, and circulation. A directed history and 

physical examination are essential to assess for underlying clues and deficits. If the 

patient exhibits need for airway protection, orotracheal intubation should be performed. 

Blood pressure management is based on a theoretical rationale: lower the blood 

pressure and decrease the risk of ongoing bleeding from ruptured small arterioles. The 

converse theory therefore holds that aggressive treatment of blood pressure may 

decrease cerebral perfusion pressure and worsen brain injury. The American Heart 

Association Special Writing Group of the Stroke Council recommends that blood 

pressure levels be maintained below a mean arterial pressure of 130 mm Hg in persons 

with a history of hypertension. 

Neurosurgical consultation should be obtained. The decision about whether and when 

to operate remains controversial. 

ISCHEMIC STROKE


• Secondary to thrombosis or embolism. 

• Consider in acute neurologic deficit (focal or global) or altered level of consciousness. 

• No historical feature distinguishes ischemic from intracerebral stroke, although 

headache, nausea and vomiting, and altered level of consciousness are more common 

in intracerebral stroke. 

• Abrupt onset of hemiparesis, monoparesis, or quadriparesis; dysarthria, ataxia, 

vertigo; monocular or binocular visual loss, visual field deficits, diplopia. 

• Symptoms occur alone or in combination. 

• Establish time of onset. 

• Beware of stroke mimics. 


Stroke is the third leading cause of death in the United States. It is also the leading 

cause of severe neurologic disability. Many significant advances in medical and surgical 

technologies for patients with TIAs and acute ischemic strokes have occurred, and 

research is ongoing. 

Ischemic strokes, comprising thrombotic, embolic, and lacunar occlusions, account for 

over 75% of all strokes and result in cerebral ischemia or infarction. A variety of 

disorders of blood, blood vessels, and heart can cause occlusive strokes, but the most 

common by far are atherosclerotic disease (especially of the carotid and vertebrobasilar 

arteries) and cardiac abnormalities. Risk factors for atherosclerosis are listed in Table 

18-10. 


Occurrence of TIAs preceding the stroke is the hallmark of stroke. The neurologic 

deficits may evolve over minutes to hours or days and are typical for a specific vascular 

distribution. Motor and sensory pathways are impaired. Headache and vomiting are 

rare. The diagnosis is made on the basis of the clinical findings and exclusion of 

hemorrhage by CT scan. MRI and repeat CT scan at 48-72 hours will often confirm the 

diagnosis when the initial study is normal. 


In 1996, the U.S. Food and Drug Administration approved the use of thrombolytic 

therapy for acute ischemic stroke, and the American Heart Association and the 

American Academy of Neurology published guidelines for its use. Management of acute 

ischemic stroke is handled on a case-by-case basis. Intravenous tissue plasminogen 

activator (t-PA) can be used if the following criteria are met: 

• The time of onset of the stroke is clearly defined, and treatment is started within 3 

hours after the onset of symptoms.

• A noncontrast CT scan has excluded hemorrhage prior to treatment. 

• Systolic blood pressure is less than 185 mm Hg, and diastolic blood pressure is less 

than 110 mm Hg. 

• The patient has no history of intracranial hemorrhage, head injury in the preceding 3 

months, or gastrointestinal or urinary tract hemorrhage in the past 3 weeks. 

Dosage and administration of t-PA: 

• Give 0.9 mg/kg body weight of intravenous t-PA up to a maximum of 90 mg. 

• Give 10% of the dose as a bolus and then administer the rest of the dose as a 

continuous infusion over 1 hour. 

• Do not give anticoagulants or antiplatelet drugs for 24 hours after treatment. 

Acute stroke patients should be admitted to stroke units (which have demonstrated 

improved outcomes). 

LACUNAR STROKE 


• Most frequent in basal ganglia and internal capsule. 

• Five classical lacunar syndromes: 

Pure Motor Stroke/Hemiparesis 

• Most common syndrome. 

• Affects face, arm, leg equally. 

• Dysarthria, dysphagia. 

• Transient sensory symptoms (but not signs) may be present. 

Ataxic Hemiparesis 

• Second most common syndrome. 

• Weakness and clumsiness on one side of body; legs affected more commonly than 

arms (homolateral ataxia and crural paresis). 

• Onset over hours to days. 

Dysarthria/Clumsy Hand 

• Variant of ataxic hemiparesis. 

Pure Sensory Stroke (Thalamus)

• Persistent numbness or tingling on one side of the body (face, arm, leg, trunk). 

• Unpleasant sensation. 

Mixed Sensorimotor Stroke 

• Hemiparesis or hemiplegia noted. 

• Ipsilateral sensory impairment. 


Lacunar stroke results from occlusion of the small penetrating arteries of the brain by 

lipohyalinotic deposits, which are a product of long-standing hypertension. The areas of 

infarction are generally small, and multiple old infarct sites may also be identified on CT 

scan. The clinical findings are distinct and may range from pure motor or pure sensory 

deficits to incoordination and clumsiness of the hand or ataxia of the arm or leg. CT 

scan is often normal or may show small lucencies in the affected areas, usually in the 

internal capsule, pons, cerebellum, or subcortical white matter. 


Treatment is supportive and consists mainly of blood pressure control. The prognosis is 

generally good. Patients should usually be hospitalized for observation. 

ARTERIAL DISSECTION 


• Nonspecific presenting signs and symptoms, neurologic deficits. 

• Headache, facial pain, neck swelling, amaurosis fugax, pulsatile tinnitus. 

• More common in young adults. 

• May follow traumatic event or simple manipulation of the neck, or may be 

spontaneous. 

• Horner syndrome/bruit. 


An acute progressive syndrome of carotid or vertebral artery ischemia almost invariably 

associated with anterior or posterior neck pain suggests carotid or vertebral artery 

dissection, respectively. A history of recent neck trauma is frequent and may be 

relatively trivial, such as chiropractic manipulation. Angiography is diagnostic and shows 

the markedly reduced intravascular lumen caused by dissection of the intimal layer, 

producing the characteristic "string sign." 


Surgical intervention is not indicated. Vessels recanalize spontaneously over months. 

Current opinion favors anticoagulation acutely and for several months thereafter to

educe the potential for distal embolization of platelet aggregates formed on the 

damaged vessel wall. 

TRANSIENT ISCHEMIC ATTACKS 


• Rapid onset. 

• Manifestations are variable, lasting 2-15 minutes and rarely up to 24 hours. 

• Review history and medications. 


Neurologic deficits occur suddenly and persist from minutes to hours but resolve 

completely within 24 hours. The National Stroke Association estimates that 40% of 

patients who had a TIA are likely to have a major stroke at some point in the future. A 

TIA should therefore be promptly evaluated to institute therapy to decrease the risk of 

stroke. These episodes are caused by small platelet, fibrin, or atheromatous emboli 

originating in extracranial vessels or the heart. Clinical findings depend on the area of 

the brain affected. Transient monocular blindness due to embolus in the retinal artery 

(amaurosis fugax) usually signifies ipsilateral carotid artery disease, but unlike 

hemispheric TIA, amaurosis fugax is associated with less risk for subsequent carotid 

stroke. 

Treatment 

Treatment is directed at identifying and correcting the underlying cause (eg, treat 

hypertension, evaluate for carotid endarterectomy). Antiplatelet agents are typically the 

treatment of choice for prevention of future strokes in patients who have experienced a 

TIA of presumed atherosclerotic origin. The selection of a specific agent is typically 

based on interpretation of the results of randomized trials that have tested these agents 

in populations of patients who have had a recent TIA or stroke. 

Four different antiplatelet agents have shown efficacy in preventing stroke or other 

vascular events in patients with cerebrovascular disease: 

A. Aspirin 

Aspirin is the most economical and frequently chosen (except in intolerant patients) 

antiplatelet regimen in patients with TIA. The U.S. Food and Drug Administration 

advocates the use of aspirin in doses of 50- 325 mg/d for the prevention of stroke. 

B. Ticlopidine 

Ticlopidine prevents platelet aggregation induced by adenosine diphosphate. Its use 

has been approved in the United States for prevention of stroke in patients with TIA or 

minor stroke. Typically used in patients who are intolerant to aspirin or who have had an 

ischemic event despite taking aspirin, its usefulness is limited by its side effects. The 

recommended dosage is 250 mg 2 times a day.

C. Clopidogrel 

Clopidogrel works by inhibiting platelet aggregation by adenosine diphosphate. It offers 

another alternative to patients intolerant to aspirin or who have had an ischemic event 

despite taking aspirin. It has a good safety profile. The recommended dosage is 75 

mg/d. 

D. Dipyridamole and Aspirin 

A combination of a cyclic nucleotide phosphodiesterase inhibitor and a cyclooxygenase 

inhibitor has been found to be effective. This medication contains 200 mg 

extended-release dipyridamole and 25 mg aspirin. The recommended dose is 1 capsule 

2 times a day. 

E. Anticoagulation 

Oral anticoagulation with warfarin continues to be the therapy of choice for stroke 

prevention in atrial fibrillation in patients who have had a TIA and in primary prevention 

of stroke in patients with atrial fibrillation. In patients in whom oral anticoagulation is 

contraindicated, aspirin is recommended. Current recommendations suggest a target 

range international normalized ratio of 2.0-3.0 for most indications for oral 

anticoagulation. 

F. Surgical Interventions 

1. Carotid endarterectomy—This intervention is used to remove atherosclerotic plaque 

from a carotid artery when the vessel is blocked. It has proved beneficial in preventing 

future strokes in certain patients with minor strokes or TIAs. The procedure is indicated 

when the vessel has a 70-99% blockage. When the vessel is 50-69% blocked, carotid 

endarterectomy is recommended; and when the vessel is less than 50% stenosed, there 

is no benefit from the procedure and medical management is recommended. 

2. Stereotactic microsurgery of arteriovenous malformations and 

aneurysms—This technique involves the use of computer technology and geometric 

principles to pinpoint the precise location of the arteriovenous malformation, allowing 

neurosurgeons to use microscope-enhanced methods and delicate instruments without 

affecting normal brain tissue. 

3. Stereotactic radiosurgery for arteriovenous malformations—This technique uses 

the same basic principle as microsurgery. Once located, the arteriovenous malformation 

can be obliterated by focusing a beam of radiation that causes it to clot and then 

disappear. 

4. Revascularization of the blood supply—This technique is used to treat aneurysms 

or blocked cerebral arteries. It provides a new route of blood to the brain by grafting 

another vessel to a cerebral artery or providing a new source of blood to the brain. 

5. Carotid angioplasty and stent placement—This method has had a high degree of 

technical success, and low complication rates have been reported. 

6. Decompressive hemicraniectomy—This technique is performed in patients with 

massive nondominant infarcts, who would otherwise succumb to herniation.

Disposition 

Most patients with TIAs should be hospitalized. Patients who have had recent thorough 

evaluation for TIAs or who are not candidates for therapy may be referred to their 

primary care physician for outpatient follow-up. 

Adams HP et al: Guidelines for thrombolytic therapy for acute stroke: A supplement to 

the guidelines for the management of patients with acute ischemic stroke: A statement 

for healthcare professionals from a special writing group of the Stroke Council, 

American Heart Association. Circulation 1996;94:1167. [PMID: 8790069] (Provides 

updated recommendations for use of thrombolytic therapy in clinical practice as 

approved by the American Heart Association Science Advisory and Coordinating 

Committee.) 

Albers GW et al: Supplement to the guidelines for the management of transient 

ischemic attacks. A statement from the Ad Hoc Committee on Guidelines for the 

Management of Transient Ischemic Attacks, Stroke Council, American Heart 

Association. Stroke 1999;30:2502. [PMID: 10548693] (Provides updated advances in 

medical and surgical therapies for patients with TIAs along with new data regarding 

underlying risk factors, as approved by the American Heart Association Science 

Advisory and Coordinating Committee.) 

Broderick JP et al: Guidelines for the management of spontaneous intracerebral 

hemorrhage. A statement for healthcare professionals from a special writing group of 

the Stroke Council, American Heart Association. Stroke 1999;30:905. [PMID: 10187901] 

(Addresses this common stroke subtype and stresses the fact that there are a limited 

number of randomized controlled studies for treatment of intracerebral hemorrhage.) 

Culebras A et al: Practice guidelines for the use of imaging in transient ischemic attacks 

and acute stroke. A report of the Stroke Council, American Heart Association. Stroke 

1997;28(7): 1480. [PMID: 9227705] (Provides useful recommendations regarding 

various diagnostic imaging studies for cerebrovascular disease.) 

Gorelick P et al: Prevention of first stroke. A review of guidelines and a multidisciplinary 

consensus statement from the National Stroke Association. JAMA 1999;281(12):1112. 

[PMID: 10188663] (A panel of experts convened to provide this consensus report to 

identify and modify cardiovascular and cerebrovascular risk factors to help prevent first 

stroke.) 

Hinton RC: Thrombosis and cerebrovascular disease. Med Clin North Am 

1998;82(3):523. [PMID: 9646778] (A review on acute thrombotic stroke.) 

Lewandowski C et al: Treatment of acute ischemic stroke. Ann Emerg Med 

2001;37:202. [PMID: 11174240] (A state-of-the-art article on all aspects of treatment of 

acute ischemic stroke in the emergency department.) 

Moonis M et al: Considering the role of heparin and low-molecular-weight heparins in 

acute ischemic stroke. Stroke 2002;33:1927. [PMID: 12105378] (A review on the use of

heparin in acute ischemic stroke.) 

Rabb CH et al: Surgical treatment strategies in ischemic stroke. Neuroimaging Clin N 

Am 1999;9:527. [PMID: 10433643] (Addresses current indications and techniques for 

the surgical treatment of ischemic stroke.) 

Stahmer SA, Raps EC, Mines DI: Carotid and vertebral artery dissections. Emerg Med 

Clin North Am 1997;15:677. [PMID: 9255140] (A review of management of carotid and 

vertebral dissections.) 

Stieg PE et al: Intracranial hemorrhage: Diagnosis and emergency management. Neurol 

Clin 1998;16:373. [PMID: 9537967] (A review of emergency management of intracranial 

hemorrhage.) 

Tuhrim S: Management of hemorrhagic stroke. Curr Cardiol Rep 2002;4:158. [PMID: 

11827640] 

Wolf PA et al: Preventing ischemic stroke in patients with prior stroke and transient 

ischemic attack. A statement for healthcare professionals from the Stroke Council of the 

American Heart Association. Stroke 1999;30:1991. [PMID: 10471455] (A review of 

factors placing patients at higher risk of developing stroke recurrence.) 





INTRODUCTION

Table 18-1. Differential diagnosis of acute weakness by anatomic localization. 

Disease State 

Compression by 

tumor or abscess; 

protruding disk or 

transverse myelitis. 

Guillain-Barre 

syndrome, arsenical 

neuropathy, 

diphtheritic 

neuropathy, 

porphyria, tick 

paralysis. 

Hypokalemia, 

hyperkalemia, 

periodic paralysis, 

myoglobinuria, 

hypophosphatemia, 

hypermagnesemia. 


Cranial Nerve 

Involvement Meningeal Signs 

None. Present in one third to 

one half of patients 

Common in 

Guillain-Barre syndrome, 

especially facial muscles 

(seventh nerve). 

Prominent. 

Rare. None. 

None. None. None. 




TABLES 

Table 18-1. Differential diagnosis of acute weakness by anatomic 

localization. 

Bladder 

Paralysis

Table 18-2. Differential diagnosis of acute weakness at the spinal cord level. 1 

Epidural 

Abscess 

11-77 1-65 

100% 36% 

100% 58% 

86% 51% 

62% 32% 

2-720 0-8800 

36-2000 18-216 

Normal Normal 

Days to months Minutes to weeks 

86% 7% 

30-83% 0% 

Transverse 

Myelitis

Table 18-3. Contraindicated and accepted drugs in treatment 

of acute intermittent porphyria. 





TABLES 

Table 18-3. Contraindicated and accepted drugs in treatment of acute 

intermittent porphyria.

Table 18-4. Symptoms and signs of botulism in approximate order of frequency. 

Extraocular muscle weakness 

Ptosis 

Bilateally dilated and unreactive pupils 

Dry mucous membranes 

Limb weakness 

Respiratory impairment 

Postural hypotension 


Signs 




TABLES 

Table 18-4. Symptoms and signs of botulism in approximate order of 

frequency.

Table 18-5. Manifestations of organophosphate poisoning. 1,2 

Severity of Poisoning 

Symptoms and Signs 

Moderate 

(%) 

Weakness 100 Headache 

2 Modified and reproduced, with permission, from Namba T et al: Poisoning due to 

organophosphate insecticides. Am J Med 1971;50:475. 





TABLES 

Table 18-5. Manifestations of organophosphate poisoning.

Table 18-6. Drug therapy of stable myasthenia gravis. 

Preparation 

60-mg tablets 3-5 hours 

180-mg sustained release capsules 6-12 hours 

15-mg tablets 2-4 hours 

Solution for injection; 1:1000, 1:2000, 1:4000 2-4 hours 





TABLES 

Table 18-6. Drug therapy of stable myasthenia gravis. 

Duration 

of Action

Table 18-7. Disorders of serum potassium causing acute muscle weakness. 





TABLES 

Table 18-7. Disorders of serum potassium causing acute muscle 

weakness.

Table 18-8. Common causes of rhabdomyolysis. 





TABLES 

Table 18-8. Common causes of rhabdomyolysis.

Table 18-9. Sources of emboli. 





TABLES 

Table 18-9. Sources of emboli.

Table 18-10. Risk factors for atherosclerosis 





TABLES 

Table 18-10. Risk factors for atherosclerosis

Figure 18-1. Assessment of complaints of weakness with or without dyspnea. 





FIGURES 

Figure 18-1

Figure 18-2. A noncontrast head CT scan demonstrating diffuse subarachnoid blood. 





FIGURES 

Figure 18-2

Figure 18-3. A noncontrast head CT scan demonstrating a large frontal intercerebral 

hemorrhage. 





FIGURES 

Figure 18-3


IMMEDIATE EVALUATION & MANAGEMENT OF HEADACHE 

CAUSED BY LIFE-THREATENING CONDITIONS (See Figure 19-1.) 

Has Head Trauma Occurred? 


If recent head trauma has occurred, evaluation of this problem takes precedence 

(Chapter 22). 

Have Seizures Occurred? 

Patients may have headache following one or more grand mal seizures. However, 

because the seizures may themselves be due to serious underlying disease (eg, 

subdural hematoma), evaluation of this problem takes precedence (Chapter 17). 

Are There Focal Neurologic Abnormalities? 

The presence of new focal neurologic abnormalities with headache, especially if 

papilledema is present as well, is strongly suggestive of a mass lesion (tumor, 

hematoma, abscess). Computed tomography (CT) scan or magnetic resonance imaging 

(MRI) should be done as soon as practical to make the diagnosis. Further evaluation is 

discussed in Chapter 18. 

Is Headache New or of Recent Origin? 

The single most important item of information to obtain from a patient with headache is 

whether the headache is new. A new headache is one occurring in a patient without a 

history of headaches, or a novel pattern or quality of pain in a patient with a history of 

headaches. New headaches demand immediate careful evaluation. 

Is the Complaint Consistent with Meningitis or Meningeal Irritation? 

If the headache is acute (sudden) or subacute (hours to days) in onset, subarachnoid 

hemorrhage (with resultant irritative [chemical] meningitis) or meningitis must be 

suspected. The usual manifestations are signs of meningeal irritation (stiff neck; positive 

Kernig and Brudzinski signs) and fever (usually absent in subarachnoid hemorrhage). 

These findings may be minimal or even absent in very young or very old patients. 

Seizures, confusion, or coma may be present as well. Subarachnoid hemorrhage should 

be strongly suspected in a patient with abrupt onset of headache that is unique to the 

patient's experience, especially if meningeal irritation or focal neurologic findings are 

present. An emergency CT scan is required; if the diagnosis is still unclear, lumbar 

puncture should be performed. If meningitis is also a possibility, antibiotic therapy 

should be started as soon as possible (based on microorganisms most common for

each age group) and before the CT scan is obtained (Chapter 40). 

Meningitis should be strongly suspected in a patient who presents with headache 

accompanied by fever, especially if signs of meningeal irritation are present. A lumbar 

puncture should be performed immediately and antibiotics begun as soon as possible 

(Chapter 40). 

If there are signs of altered mental status or if there are focal neurologic findings in a 

patient with fever, a brain abscess should be suspected. Lumbar puncture should be 

delayed until a CT scan is performed. 

Is Headache Due to Hypertensive Encephalopathy or Preeclampsia-Eclampsia? 

Moderate elevations of blood pressure alone seldom cause headache; however, severe 

hypertension as seen in hypertensive crises and eclampsia is associated with 

headache. If hypertension is present and the patient is pregnant or has signs of cerebral 

dysfunction (confusion, obtundation, or coma) or other end-organ damage (retinitis; 

nephritis with proteinuria), a life-threatening emergency exists. Note: In pregnancy, a 

slight increase in blood pressure may be more significant than in the nonpregnant 

patient. See Chapter 34 (hypertensive crisis) or Chapter 36 (eclampsia). 

Is This Temporal Arteritis? 

Temporal arteritis is a rare but treatable disease with serious sequelae that must be 

considered in every elderly patient with new headache. The principal manifestations are 

headache with temporal artery tenderness (not found in every case) and a markedly 

elevated erythrocyte sedimentation rate. Sudden monocular blindness may occur. If this 

condition is suspected, hospitalization is warranted to confirm the diagnosis by means of 

temporal artery biopsy and to begin therapy. For details of diagnosis and management, 

see later in this chapter. 

Is Headache Due to Disease in Paracranial Structures? 

New or acute headaches are often caused by disease in the eyes, ears, sinuses, or 

teeth. Look carefully for iritis or acute glaucoma (Chapter 31) or for sinusitis, otitis 

media, or dental caries or abscess (Chapter 32). Treatment should be focused on the 

primary condition. 

Are There Multiple Patients from the Same Vicinity? 

Multiple patients from the same vicinity with complaint of headache suggest carbon 

monoxide poisoning or other toxin exposure. Patients should be questioned specifically 

about heating sources (eg, gas heat or oven), burning materials (eg, charcoal) in poorly 

ventilated areas, use of household cleaners, or other chemical exposure. Specific 

treatment of carbon monoxide poisoning and other toxin exposure is discussed in 

Chapter 45. 

Disposition

Even after careful initial history and physical examination, the diagnosis may not be 

apparent in the patient with new headache. Patients with recent onset of new headache 

should be hospitalized if there is any suspicion of a life-threatening process. Increasing 

severity of subacute headache over days or weeks, even without focal signs, suggests 

serious intracranial disease, and the patient should undergo appropriate diagnostic 

procedures. Subacute headaches without progressive symptoms and chronic 

headaches may be evaluated on a nonemergency basis. 

Godwin SA, Villa J: Acute headache in the ED: Evidence-based evaluation and 

treatment options. Emergency Medicine Practice 2001;3:1. (A comprehensive review 

article on the diagnosis and management of acute headaches in the emergency 

department.) 

APPROACH TO THE DIAGNOSIS OF HEADACHE 

Pain-Sensitive Structures & Their Projections 

Headache is caused by traction, displacement, inflammation, or distention of 

pain-sensitive structures in the head or neck. Disorders of the scalp, teeth, eyes, and 

ears and of the mucous membranes of the nose, sinuses, and oropharynx can produce 

pain. Pain-sensitive structures about the calvarium include the scalp and its blood 

vessels, the neck muscles, and the upper cervical nerves. The skull, brain, and most of 

the dura are not pain-sensitive. In general, discrete intracranial lesions above the 

cerebellar tentorium produce pain in trigeminal distribution (anterior to ears), whereas 

lesions in the posterior fossa project pain to the second and third cervical dermatomes 

(posterior to ears). 

History 

A. Time of Onset 

Chronic headache (duration of months or more) is usually not due to a serious disorder, 

but headache of acute onset or of a changing pain pattern demands prompt evaluation 

in the emergency department. If the patient has a chronic headache disorder, determine 

whether the present headache differs from or is identical to the patient's chronic 

problem. 

Although the sudden onset of pain or "the worst headache I ever had in my life" typifies 

subarachnoid hemorrhage, the associated headache will be unique but need not be 

severe. 

B. Precipitating Factors 

1. Tension headache—Tension, emotional stress, and fatigue. 

2. Migraine—Hunger, nitrite-containing foods (hot dogs, salami, sausage), chocolate, 

aged cheeses, bright lights, menses, alcohol, caffeine, monosodium glutamate, 

aspartame, and insomnia. 

3. Cluster variant of migraine—Alcohol.

4. Trigeminal neuralgia and the jaw claudication of temporal arteritis—Chewing 

and eating. 

C. Location of Pain 

1. Migraine or the cluster variant—Hemicranial or retroocular pain. 

2. Tension headache—Commonly diffuse, occipital, or bandlike pain. 

3. Mass lesion headache—Often focal ("right here"). 

4. Trigeminal neuralgia—Stabbing pain localized to the second or third division of the 

trigeminal nerve. 

D. Quality of Pain 

1. Migraine or the cluster variant—Commonly described as throbbing and often 

preceded by prodromal symptoms or auras, for example, scintillating scotomas or other 

visual changes. 

2. Tension headache and mass lesion headache—Usually steady pain. 

3. Trigeminal neuralgia—A shooting or stabbing character. 

E. Timing 

1. Mass lesion headache—Commonly maximal on awakening. 

2. Cluster variant of migraine—Frequently awaken patients from sleep and often recur 

at the same time of day or night. 

3. Tension headache—May develop at regular intervals, especially with recurrent 

stressful situations. 

F. Factors Influencing Severity 

1. Migraine or the cluster variant—Frequently relieved by pressure on the ipsilateral 

temporal or carotid artery; by darkness, sleep, or vomiting; or during pregnancy. 

2. Mass lesion headache—Often exacerbated by events such as coughing and 

sneezing that transiently raise intracranial pressure. 

G. Associated Symptoms 

Nausea or vomiting is common with migraine and posttraumatic headache syndromes 

and may be seen late in the course of mass lesions. Photophobia is prominent with 

migraine headache but occurs also with meningitis, especially viral (aseptic) meningitis. 

Myalgias of pericranial muscles (eg, posterior neck muscles) often accompany tension 

headaches and viral syndromes. Rhinorrhea and lacrimation during headache typify the 

cluster variant of migraine and are ipsilateral to the pain. 

Physical Examination

A. Vital Signs 

1. Fever—The presence of fever supports a diagnosis of meningitis, encephalitis, or 

headache associated with viral infection. A low-grade fever may also occur in temporal 

arteritis. 

2. Blood pressure—Hypertension per se rarely causes headache, but chronic 

hypertension is the major risk factor for stroke, especially intracerebral hemorrhage, and 

stroke may be associated with acute headache. Blood pressure may be markedly 

elevated during hypertensive encephalopathy or as a result of preeclampsia-eclampsia, 

subarachnoid hemorrhage, or brain-stem stroke. 

B. Skin 

Neurofibromas or cafe au lait spots of Recklinghausen disease may be associated with 

benign or malignant intracranial tumors. 

Cutaneous angiomas sometimes accompany arteriovenous malformations of the central 

nervous system; rupture results in subarachnoid hemorrhage and acute headache. 

C. Scalp and Head 

1. Temporal arteries—Note nodularity or tenderness compatible with temporal arteritis. 

2. Sinuses—Note tenderness, erythema of overlying skin, or nasal discharge. 

3. Temporomandibular joints—Look for tenderness or limitation of motion. 

4. Orbits—A bruit heard when the stethoscope is placed on the eyeball over closed 

eyelids may suggest intracranial arteriovenous malformation. 

D. Neck and Back 

1. Muscle spasm—Cervical muscle spasm may be a sign of tension or may occur with 

migraine. 

2. Meningeal signs—Can the patient touch chin to sternum? If not, is the limitation of 

motion mainly in the anteroposterior direction, suggesting meningeal irritation, or in all 

directions, as is common with cervical spine disorders? Is there any discomfort, neck 

flexion, or contralateral knee flexion during straight leg raising (Kernig sign)? Most 

important, is there even slight flexion of the knee (Brudzinski sign) during passive neck 

flexion? 

a. Lumbar puncture—Any evidence of meningeal irritation in a patient with acute 

headache demands lumbar puncture to rule out meningitis and subarachnoid 

hemorrhage. The only exception to this rule is the presence of obvious lateralizing 

findings suggesting a mass lesion (brain abscess, tumor), in which case confirmatory 

studies (CT scan or MRI) should be done first. If there will be a delay (>1 hour) in 

obtaining the CT scan, begin antimicrobials (see Table 40-3). 

b. Absence of meningeal signs—Meningeal signs may be absent or difficult to 

demonstrate in the early stages of subacute meningitis (eg, tuberculous meningitis),

several hours may elapse before evidence of meningeal irritation develops after 

subarachnoid hemorrhage, and these signs disappear if the patient lapses into deep 

coma. Meningeal signs may also be minimal in the very young or very old. 

E. Neurologic Examination 

Unilateral cranial nerve, cerebellar, motor, or reflex abnormalities suggest a diagnosis of 

intracranial mass lesion. 

F. Miscellaneous Physical Findings 

Papilledema, the hallmark of increased intracranial pressure, should always be sought. 

Acute confusion or altered consciousness is common after subarachnoid hemorrhage 

and with purulent meningitis. 

G. Special Signs 

It is helpful to observe the patient for diagnostic signs during a headache. Ipsilateral 

conjunctival injection, lacrimation, and rhinorrhea support a diagnosis of cluster 

headache. Scalp tenderness is characteristic of migraine headache, subdural 

hematoma, and temporal arteritis. 

Clinch CR: Evaluation of acute headaches in adults. Am Fam Phys 2001;63:685. [PMID 

11237083] (A review article on the evaluation of headaches in adults.) 

Headaches: Treatments vary with the type. Mayo Clin Health Lett 2001;19:1. [PMID: 

11547602] (Review on the diagnosis and treatment of tension, migraine, and cluster 

headaches.) 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING ACUTE 

HEADACHE 

SUBARACHNOID HEMORRHAGE 

Subarachnoid hemorrhage is a life-threatening cause of acute headache. Patients 

typically present with a sudden onset of severe headache and most will go on to have 

focal neurologic signs. Diagnosis is best made with CT scan or MRI. Lumbar puncture is 

recommended for patients with negative neuroimaging. A detailed discussion of 

subarachnoid hemorrhage is found in Chapters 16 and 18. 

van Gijn J, Rinkel GJ: Subarachnoid haemorrhage: Diagnosis, causes and 

management. Brain 2001;124:249. [PMID: 11157554] (A comprehensive review article 

on the diagnosis, cause, and treatment of subarachnoid hemorrhage.) 

CEREBROVASCULAR ACCIDENT (STROKE) (See also Chapter 18.) 


• Sudden-onset focal neurologic deficit.

• Symptoms related to vasculature involved. 


Thrombotic or embolic strokes may be associated with mild to moderate nonthrobbing 

headaches that are mainly contralateral to the paralysis. The headache may precede or 

accompany the stroke. 


Treat stroke as described in Chapter 18. Hospitalize the patient for evaluation and 

treatment. 

Godwin SA, Villa J: Acute headache in the ED: Evidence-based evaluation and 

treatment options. Emergency Medicine Practice 2001;3:1. (A comprehensive review 

article on the diagnosis and management of acute headaches in the emergency 

department.) 

MENINGITIS & MENINGOENCEPHALITIS (See also Chapter 40.) 


• Headache, fever. 

• Nuchal rigidity. 


Headache, confusion, and nuchal rigidity developing over hours to days are classic 

features of meningitis (infectious, carcinomatous, or irritative [chemical]). However, in 

rapidly progressive pyogenic meningitis, fever and altered consciousness are the most 

prominent presenting signs. In patients with subacute meningitis (eg, cryptococcosis, 

tuberculosis), headache is an early symptom that may precede nuchal rigidity and other 

meningeal signs. The headache of meningitis is continuous and throbbing and, although 

generalized, usually most prominent over the occiput. The pain is increased by head 

shaking, jugular vein compression, or any other maneuver that increases intracranial 

pressure (eg, coughing, sneezing, straining at stool). Pain is not relieved by changes in 

posture. Neck stiffness and other signs of meningeal irritation must be sought with care, 

because they may not be obvious early. 

If meningitis or meningoencephalitis is suspected, perform lumbar puncture (Chapter 6) 

and obtain blood for culture. Relative contraindications to lumbar puncture are (1) 

papilledema and (2) prominent focal neurologic findings, suggesting mass lesion. 

Treatment 

A. Antimicrobials 

Begin antibiotics immediately after taking samples of blood and cerebrospinal fluid for

culture if bacterial meningitis is suspected. If lumbar puncture must be delayed for 

anatomic studies (CT scan), obtain 2 blood culture samples, and begin antimicrobials; 

perform lumbar puncture and culture cerebrospinal fluid as soon as possible. The 

choice of drug depends on the clinical circumstances and the results of Gram stain and 

culture of cerebrospinal fluid (see Table 40-3). 


General supportive care should be initiated in the emergency department. Protect the 

patient's airway, and provide padded bed rails or restraints for agitated or delirious 

patients. If seizures have occurred, start anticonvulsant therapy (Chapter 17). 

Concomitant corticosteroid treatment in purulent meningitis has been shown in children 

to decrease the incidence of residual hearing impairment. 

Disposition 

Immediate hospitalization is warranted except perhaps in the case of a patient with 

aseptic (viral) meningitis who appears well and can be observed at home by a third 

party and has close follow-up within 24 hours for reexamination. 

Williams AJ, Nadel S: Bacterial meningitis: Current controversies in approaches to 

treatment. CNS Drugs 2001;15:909. [PMID: 11735611] (A comprehensive review article 

on the treatment of bacterial meningitis.) 

POSTURAL (POST-LUMBAR PUNCTURE) HEADACHE 


• Follows lumbar puncture. 

• Headache exacerbated by the upright position. 

• Headache relieved by recumbency. 


Postural headache may follow lumbar puncture, especially if a large needle is used. 

This type of headache is worse in the upright position and nearly absent in recumbency. 

The onset of headache is usually within the first 24-48 hours and rarely occurs later. 

The site of the headache may be bifrontal, occipital, or in the neck and upper shoulders. 


Recumbency for 18-24 hours, good hydration, and analgesics are usually sufficient 

management. For more persistent cases, refer the patient to an anesthesiologist for an 

epidural blood patch at the site of the puncture (epidural injection of autologous blood at 

the site of the puncture will clot to seal the dural opening and prevent further leakage of 

cerebrospinal fluid). 

Chordas C: Post-dural puncture headache and other complications after lumbar

puncture. J Pediatr Oncol Nurs 2001;18:244. [PMID: 11719905] (A review article on the 

pathophysiology, diagnosis, treatment, and prevention of post-lumbar puncture 

complications.) 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING SUBACUTE 

HEADACHE 

POSTTRAUMATIC HEADACHE 


• History of head trauma. 

• May have associated dizziness, vertigo, insomnia. 


Headache caused by head injury may begin immediately or within weeks after trauma. 

Chronic posttraumatic headache is defined as a headache that continues for greater 

than 8 weeks after the trauma occurs. The symptoms are not necessarily proportionate 

to the severity of the traumatic event. Persistent worsening of headache, particularly 

after trauma, suggests subdural hematoma (Chapter 22). Associated dizziness, vertigo, 

insomnia, depression, and personality change may occur. This constellation of 

symptoms is referred to as posttraumatic syndrome. Posttraumatic headache usually 

presents no special diagnostic or distinguishing features, although it may be suggestive 

of tension headache or migraine. Pain usually remits after days to weeks but 

occasionally persists for years. 


The character of the headache dictates the treatment of posttraumatic headache. The 

pharmacologic treatments used for migraine and tension headache are appropriate for 

posttraumatic headache and should be chosen by the constellation of the patient's 

symptoms. Hospitalization is not indicated for posttraumatic headache, although referral 

for prophylactic therapy is indicated if symptoms persist. 

Solomon S: Posttraumatic headache. Med Clin North Am 2001;85:987. [PMID: 

11480269] (A review of the classification, clinical features, pathophysiology, diagnosis, 

and management of posttraumatic headache.) 

TRIGEMINAL NEURALGIA 


• Excruciating, stabbing, facial pain. 

• Pain in the distribution of the trigeminal nerve.


In trigeminal neuralgia, lightninglike stabs of excruciating pain characteristically recur 

over seconds to minutes and spontaneously abate. Occurrence during sleep is rare. 

Sensory stimulation (eg, touch, cold, wind, talking, chewing) of trigger zones about the 

cheek, nose, or mouth precipitates paroxysms of pain. 

Trigeminal neuralgia usually develops after the fourth decade. Pain-free intervals may 

last minutes to weeks, but permanent spontaneous remission is rare. Pain is confined 

mainly to areas supplied by the second or third divisions of the trigeminal nerve 

(maxillary and mandibular areas of the face). Physical examination must show no 

abnormalities of trigeminal nerve function (facial sensation, muscles of mastication, 

corneal reflex) that would support a diagnosis of posterior fossa lesions. Involvement of 

the first division of the trigeminal nerve (the forehead) or bilateral disease occurs in less 

than 5% of cases. 

Treatment 

Phenytoin, 250 mg intravenously over 5-10 minutes, may abort an acute attack. 

Remission of symptoms with carbamazepine (Tegretol, others) occurs in so many 

patients that it has been used as a diagnostic test. Begin with 100 mg orally twice daily, 

and increase by 100 mg every other day until the patient is pain-free or side effects 

develop. 

Baclofen (Lioresal, others) is also beneficial and has synergistic effects when used with 

carbamazepine or phenytoin. Begin with 5 mg orally 3 times daily, and increase by 5 mg 

every other day until the patient is pain-free or side effects (eg, dizziness, 

gastrointestinal upset) occur. Abrupt cessation of baclofen can cause seizures or 

hallucinations; the dosage should be decreased gradually. Lamotrigine (Lamictal) has 

also been shown to be useful in the treatment of trigeminal neuralgia, with a starting 

dose of 25 mg daily with an increase of 25 mg each week until a maintenance dose is 

reached. 

Disposition 

Neurologic referral for evaluation and treatment is appropriate. Hospitalization is not 

usually indicated. 

Sindrup SH, Jensen TS: Pharmacotherapy of trigeminal neuralgia. Clin J Pain 

2002;18:22. [PMID: 11803299] (An evidence-based review of the pharmacologic 

treatment of trigeminal neuralgia.) 

Zakrzewska JM: Diagnosis and differential diagnosis of trigeminal neuralgia. Clin J Pain 

2002;18:14. [PMID: 11803298] (A review article on the diagnosis and differential 

diagnosis of trigeminal neuralgia.) 

INTRACRANIAL MASS (Brain Tumor)


• Mild to moderate headache increasing in frequency or duration. 

• Becomes associated with a focal neurologic deficit. 


Headache due to primary or metastatic intracranial tumor is usually mild to moderate in 

severity and described as deep, aching, and initially intermittent. Pain is maximal on 

awakening and during episodes of increased intracranial pressure (eg, coughing, 

sneezing, or straining at stool). Headaches increase in frequency and duration over 

weeks to months and become associated with focal neurologic signs. One third to one 

half of patients with brain tumor present with this classic history. A CT scan obtained 

with intravenous contrast will usually confirm the diagnosis. MRI, which is more 

sensitive, may be used as well. 


If an intracranial mass lesion is found to be the cause of headache, urgent neurologic or 

neurosurgical consultation is indicated. Hospitalization may be required for initiation of 

treatment. The distinction between primary and metastatic tumor is essential, because 

treatment differs. 

Macarthur DC, Buxton N: The management of brain tumours. J R Coll Surg Edinb 

2001;46:341. [PMID: 11768575] (A review of the presentation, diagnosis, and surgical 

management of brain tumors.) 

PSEUDOTUMOR CEREBRI (Idiopathic Intracranial Hypertension) 


• Papilledema. 

• Increased intracranial pressure with normal cerebrospinal fluid. 

• Normal brain imaging study. 


Pseduotumor cerebri is a syndrome characterized by papilledema, increased 

intracranial pressure (with normal cerebrospinal fluid), and a normal brain imaging study 

demonstrating normal or small-sized ventricles. Women are affected much more 

commonly than men; the peak incidence occurs in the third decade. Diffuse headache is 

almost invariably a presenting symptom. Complaints of diplopia and blurred vision or 

transient visual obscuration occur in greater than 60% of cases. Moderate to severe 

papilledema is seen in over 40% of affected persons. The course in idiopathic cases is 

generally self-limited over several months, but visual loss may occur. Differentiation

from space-occupying intracerebral mass lesions is critical and can be achieved by CT 

scan. 


Hospitalization is necessary for evaluation and treatment in patients with newly 

diagnosed pseudotumor cerebri in the emergency department. Appropriate treatments 

include repetitive lumbar punctures, carbonic anhydrate inhibitors (acetazolamide), 

thiazide diuretics, and corticosteroids. Surgical maneuvers, including shunt or optic 

nerve sheath decompression, may be required. Patients who present to the emergency 

department with a known diagnosis of pseudotumor cerebri should receive treatment in 

consultation with the patient's neurologist, neurosurgeon, or ophthalmologist. 

Kosmorsky G: Pseudotumor cerebri. Neurosurg Clin North Am 2001;12:775. [PMID: 

11524298] (An exhaustive review of the physiology, pathogenesis, epidemiology, 

clinical manifestations, and treatment of pseudotumor cerebri.) 

TEMPORAL ARTERITIS (Giant Cell Arteritis) 


• Age greater than 50 years. 

• Unilateral headache. 

• Usually tender over the temporal artery. 

• Elevated erythrocyte sedimentation rate. 

• Unilateral vision loss if treatment is delayed. 


Temporal arteritis, although uncommon in the general population, is the most common 

form of systemic vasculitis. The disease preferentially involves large- to medium-sized 

arteries. It affects women twice as often as men and is rarely seen before the age of 50 

years. Nonspecific signs and symptoms are typical: malaise, myalgia, weight loss, 

arthralgia, and fever. The headache is classically of rapid onset, unremitting, and 

located over the temporal arteries. It is often unilateral. Associated scalp tenderness 

may be a prominent complaint, especially when patients lie with their head on a pillow or 

brush their hair. Pain during chewing (jaw claudication) is strongly suggestive of 

temporal arteritis. Permanent unilateral blindness, usually sudden in onset, occurs in 

about half of patients if treatment is delayed; half of patients so affected go on to 

develop bilateral blindness. 

The temporal arteries may be normal on examination, although focal tenderness, 

thickening, nodularity, or decreased pulsation may be found. The diagnosis should be 

suspected if the erythrocyte sedimentation rate is greater than 50 mm/h. 

The diagnosis can be established by demonstration of vasculitis in biopsy specimens of 

an affected artery. The biopsy specimens must be carefully examined (multiple

sections) because involvement is segmental. 

Treatment 

Temporal arteritis responds dramatically to corticosteroid treatment. Begin prednisone, 

40-60 mg/d orally, as soon as the diagnosis is suspected. Biopsy should be obtained 

within 2-3 days after beginning corticosteroids. Patients presenting with visual loss 

warrant immediate ophthalmology consult and should receive intravenous steroids in 

the emergency department. 

Disposition 

For patients with severe symptoms or visual loss, hospital admission is urgently 

indicated for evaluation and treatment with intravenous steroids. Patients with minimal 

symptoms may be discharged with oral prednisone but should make arrangements for 

close follow-up and biopsy within 3 days. 

Levine SM, Hillmann DB: Giant cell arteritis. Curr Opin Rheumatol 2002;14:3. [PMID: 

11790989] (A comprehensive review of the epidemiology, pathophysiology, diagnosis, 

and treatment of temporal arteritis.) 

Smetana GW, Shmerling RH: Does this patient have temporal arthritis? JAMA 

2002;287:92. [PMID: 11754714] (A literature review to assess accuracy of clinical signs 

and symptoms in the diagnosis of temporal arteritis.) 

MANAGEMENT OF SPECIFIC DISORDERS CAUSING CHRONIC 

HEADACHE 

TENSION HEADACHE 


• Gradual onset. 

• Band or pressure pain about the head. 

• Constant, nonthrobbing-type pain. 


Tension headache, although the most prevalent form of headache, is not the most 

severe. However, it has significant societal impact with lost workdays and reduced 

effectiveness when at work. Women are affected three times as commonly as men, and 

the age at onset is usually between the third and fifth decades. Headaches are often 

associated with emotional stress and have no prodrome. The pain typically comes on 

gradually; is bilateral, occipital, or frontal in location; and is described as a tight band or 

pressure about the head. The pain is constant and nonthrobbing and persists for hours 

or for the entire day. Nausea and photophobia are frequent accompanying symptoms 

but are milder than with migraine. Muscle spasm or tension, especially nuchal-occipital,

is usually present. About half of patients have headaches 10-30 times a month, and 

about one fifth are never completely free of headache. Results on neurologic 

examination are normal. 

Treatment 

The treatment approach for tension headaches in the emergency department is 

pharmacotherapy. Nonsteroidal anti-inflammatory drugs remain the therapy of choice in 

abortive treatment of tension headache. Combination medications that contain caffeine, 

analgesics, and sedatives have been found to be effective. Muscle relaxants 

(cyclobenzaprine, methocarbamol) may also be appropriate when muscle tension 

appears to play a strong role. Referral for prophylactic treatment with antidepressants 

(amitriptyline) and incorporation of a "wellness" component is appropriate for patients 

expressing depression or anxiety as precipitants to their headaches. 

Disposition 

If simple measures are not successful, neurologic referral may be necessary. 

Hospitalization is not indicated. 

Schulman EA: Overview of tension-type headache. Curr Pain Headache Rep 

2001;5:454. [PMID: 11560811] (A review of classification, causes, and treatment of 

tension headaches.) 

MIGRAINE 


• Throbbing-type pain. 

• Associated nausea, vomiting, and photophobia are common. 

• May have associated neurologic symptoms. 


Migraine headache is a primary brain disorder in which neural events result in 

vasodilation of blood vessels that causes pain and further nerve activation. Most cases 

occur in women, there is an inherited predisposition, and onset may be as early as the 

first decade. Recurrent vomiting during childhood may be the earliest manifestation of 

migraine. A family history of migraine is commonly present. 


Migraine headaches are classified as being with aura (formerly called classic migraine) 

or without aura (formerly called common migraine). 

Migraine with aura is preceded by transient neurologic symptoms (the aura). The most 

common auras are visual disturbances: hemianopic field defects, scotomas, and

scintillations that enlarge and spread peripherally. As the aura fades, vasodilatation 

occurs, producing the headache; however, aura can occur without headache. Migraine 

is said to be hemicranial, but half of migraine headaches are bilateral, and some are 

occipital. Migraine without aura lacks the classic aura and is bilateral in over half of 

cases. 

The pain is throbbing in most cases. Associated symptoms include nausea and 

vomiting, photophobia, and, less often, fluid retention, diarrhea, lightheadedness, and 

fainting. Continuing pain may cause cervical muscle contraction, leading to an 

erroneous diagnosis of tension headaches. Scalp tenderness may occur. 

Attacks may be precipitated by certain foods such as tyramine-containing cheeses, 

wine, meats with nitrite preservatives, chocolate containing phenylethylamine, and 

monosodium glutamate (a flavor enhancer). Fasting, emotion, menses, drugs 

(especially oral contraceptive agents and vasodilators such as nitroglycerin), and bright 

lights may also trigger attacks. Over half of patients experience no more than one attack 

a week lasting less than a day. Remissions are common during pregnancy and after 

menopause. 

Treatment 

A. Analgesics and Analgesic Combinations 

These drugs remain appropriate first-line therapy for acute migraine attacks. Commonly 

patient will have tried at least one or several analgesics prior to presentation to the 

emergency department. Appropriate analgesics include aspirin, nonsteroidal 

anti-inflammatory drugs and combination medications that contain caffeine, analgesics, 

and sedatives. Opiates should be avoided because they can exacerbate gastrointestinal 

symptoms and have a high abuse potential. 

B. Dopamine Antagonists (Antiemetics) 

Several dopamine antagonist have been shown to be effective in aborting acute 

migraine headaches. Prochlorperazine and metoclopramide are most widely used. 

Prochlorperazine dosing is 10 mg intravenously. Side effects included hypotension and 

akathisia. Metoclopramide is also effective in doses of 10 mg intravenously. 

C. Triptans 

The triptans have an advantage of being selective pharmacologic agents for the 

treatment of migraine headaches. These compounds are serotonin 5-HT receptor 

agonists. All of these drugs have been shown to be effective in aborting acute migraine 

headaches. However, they have significant side effects and cannot be used in patients 

with a history of cardiovascular disease. The following triptans can be used in the 

treatment of migraines in the emergency department: 

• Sumatriptan, 6 mg subcutaneously, which may be repeated after 1 hour; or 25-100 mg 

orally, which may be repeated after 2 hours 

• Naratriptan, 1-2.5 mg orally, which may be repeated after 4 hours 

• Almotriptan, 6.25-12.5 mg orally, which may be repeated after 2 hours

• Rizatriptan, 5-10 mg orally, which may be repeated after 2 hours 

• Zolmitriptan, 1.25-2.5 mg orally, which may be repeated after 2 hours 

D. Ergot Derivatives 

Ergot preparations have been used widely in the past for the acute treatment of 

migraine headaches. These drugs have complex pharmacology, and there is little 

evidence to support their use. With the effectiveness of dopamine agonists and triptans, 

ergot preparations should be abandoned for abortive therapy in the emergency 

department. 

E. Prophylactic Drugs 

Prophylatic therapy may be useful in preventing migraine headaches, but it should not 

be initiated in the emergency department. Patients should be referred to a neurologist 

for evaluation for preventive treatment. 

Disposition 

Referral to a neurologist or primary care physician is indicated. Hospitalization (other 

than a brief stay in the emergency department for parenteral medication) is rarely 

needed. 

Ducharme G: Canadian Association of Emergency Physicians guidelines for the acute 

management of migraine headache. J Emerg Med 1999;17:137. [PMID: 96650404] (A 

review of emergency department treatment of acute migraine headaches.) 

Elrington G: Modern management of migraine. Hosp Med 2001;62:687. [PMID: 

11762100] (Examines diagnostic as well as therapeutic and prevention strategies for 

migraine headaches.) 

Goadsby PJ, Lipton RB, Ferrari MD: Migraine—current understanding and treatment. N 

Engl J Med 2002;346:257. [PMID: 11807151] (Review of current understanding of the 

epidemiology, pathophysiology, and treatment of migraine.) 

CLUSTER HEADACHE 


• Clusters of daily attacks separated by week to months of pain-free intervals. 

• Attacks consist of severe unilateral headache. 

• Associated cranial autonomic symptoms include lacrimation, miosis, conjunctival 

injection, nasal congestion, and rhinorrhea. 


Cluster headache is a syndrome of distinct attacks of severe, unilateral headache with

ipsilateral cranial autonomic symptoms. The autonomic symptoms may include ptosis, 

lacrimation, miosis, conjunctival injection, nasal congestion, and rhinorrhea. It is more 

common in men than in women and begins later in life than migraine headaches. There 

is often no family history of similar headaches. 

Pain occurs in distribution of the trigeminal nerve and most commonly in the ocular, 

frontal, and temporal areas. Each attack builds in intensity over 10- 15 minutes and may 

last up to 3 hours. Attacks recur 1-3 times daily, often at nearly the same time for 

periods of weeks to 2-3 months that may be separated by headache-free interval 

remission periods that usually last for months or years. A subset of patients experience 

chronic cluster headaches without remission. These patients have attacks for greater 

than 1 year without remission or with remissions lasting less than 14 days. 

Episodes may be precipitated by alcohol or vasodilator-type drugs. Nitroglycerin 

challenge can be diagnostic, producing a typical headache in 30-60 minutes. 

Treatment 

Standard treatment for acute attacks is oxygen (7 L/min for 15 min) delivered by face 

mask; this treatment has a reported 70% response rate. Sumatriptan, 6 mg 

subcutaneously, although contraindicated in patients with known cardiovascular 

disease, has proved effective: 80% of patients experience complete or near complete 

relief. Less effective agents such as dihydroergotamine and ergotamine are also 

commonly used. Lidocaine, 20- 60 mg given intranasally, provides some relief within 10 

minutes in most patients, but complete relief is rare. 

Due to the severity, reoccurrence, and chronicity of attacks, prophylaxis should follow 

treatment for the acute headache. Prophylactic treatment should be initiated at the first 

sign of an attack and continued for 2 weeks past the last attack. Prophylactic agents 

include verapamil, ergotamine, lithium, methylsergide, and steroids. Verapamil is 

considered the agent of choice at dosages of 240-480 mg/d. Higher dosages (up to 

1200 mg/day) may be given to patients with chronic cluster headache. Surgical 

intervention has been recommended for intractable chronic cluster headaches that have 

become resistant to medical management. 

Disposition 

Neurologic referral is indicated. 

Ekbom K, Hardebo JE: Cluster headache: aetiology, diagnosis and management. Drugs 

2002;62:61. [PMID: 11790156] (Review of the pathophysiology, diagnosis, and 

management of cluster headaches.) 

Newman LC, Goadsby P, Lipton RB: Cluster and related headaches. Med Clin North 

Am 2001;85:997. [PMID: 11480270] (Review of the etiology, diagnosis, and treatment of 

cluster headaches with emphasis on differentiation between cluster headaches and 

related disorders.) 

Zakrzewska JM: Cluster headache: review of the literature. Br J Oral Maxillofac Surg

2001;39:103. [PMID: 11286443] (Literature review of papers on cluster headaches 

using the Cochrane systematic review guidelines; treatment and guidelines proposed 

based on evidence of this review.) 

HEADACHE DUE TO HYPERTENSION 

Headache is not a prominent feature of chronic hypertension. Research has shown that 

patients with hypertension and complaints of headache did not have blood pressure 

levels different than those during their headache-free periods. In addition, blood 

pressures preceding the headache pain were not significantly different than those 

measured at the onset of pain, and the majority of patients had their maximal blood 

pressures during headache-free periods. 

The acute onset of headache and severe blood pressure elevation are components of 

hypertensive crisis (Chapter 34) and also are commonly present following subarachnoid 

hemorrhage. As a result, patients presenting with headache and a history of 

hypertension should undergo a full evaluation, and the headache should not be 

presumed due to elevation of blood pressure. 

Kruszewski P et al: Headache in patients with mild to moderate hypertension is 

generally not associated with simultaneous blood pressure elevation. J Hypertens 

2000;18:437. [PMID: 10779095] (A study looking at the correlation of headaches and 

blood pressure in patients with mild to moderate hypertension.) 





IMMEDIATE EVALUATION & MANAGEMENT OF HEADACHE CAUSED 

BY LIFE-THREATENING CONDITIONS (See Figure 19-1.)

Figure 19-1. Management of complaints of headache. 





FIGURES

20. Delirium & Acute Confusional States - Eric W. Flach, MD, Timothy 

A. Coakley, MD, & James J. Mensching, MD, DO, FACEP 1,2 




2 The views expressed in this chapter are those of the authors and do not reflect the 

official policy or position of the Department of the Navy, Department of Defense, or the 

U.S. government. 

Delirium and acute confusional states are among the most difficult problems confronting 

the emergency physician. The patient's mental status can be assessed quickly using a 

classification scheme. Such schemes classify patients according to whether or not they 

are alert, their ability to attend, and their memory capability, allowing the physician to 

differentiate among coma, delirium, and dementia. These are the 3 main categorizations 

of a patient with an acutely altered mental status. This chapter focuses on delirium and 

acute confusional states. 

Confused patients are often uncooperative or combative, making evaluation difficult. 

Signs and symptoms may be manifestations of a life-threatening underlying condition 

demanding prompt diagnosis and treatment to prevent irreversible brain damage (Table 

20-1). Although evaluation may be difficult, every patient with an acutely altered state of 

consciousness must be examined and a history taken so that the cause can be 

established, if possible, in the emergency department. If the diagnosis cannot be 

established with certainty, the patient should be hospitalized. 

Immediate Measures 

A. Maintain Airway 

Clear secretions as needed. Begin oxygen, if necessary, 5-10 L/min, by mask or nasal 

cannula. Restrain the patient only if necessary. 

B. Gain Intravenous Access 

Insert a large-bore (= 18-gauge) intravenous catheter. Draw blood for complete blood 

count (CBC); serum glucose, electrolyte, calcium, and magnesium determinations; and 

hepatic and renal function tests. Obtain urine for urinalysis and toxicology screen. 

Administer the following intravenously: (1) thiamine, 100 mg by slow bolus injection; (2) 

50% dextrose in water, 50 mL over 3-5 minutes, if the patient is hypoglycemic by 

bedside fingerstick glucose testing; and (3) naloxone (Narcan, others), 2 mg by bolus 

injection. Caution: Administration of glucose may worsen brain injury by increasing 

lactate in ischemic areas. Do not give glucose to patients during the acute phases of 

stroke or after cardiac arrest if serum glucose is normal.

C. Treat Shock 

Hypotension and shock with associated peripheral hypoperfusion may be associated 

with delirium or confusion. Treat shock with immediate intravenous administration of 

crystalloid solutions unless the patient is in cardiogenic shock, and follow with more 

specific measures (Chapter 9). 

D. Correct Respiratory Failure 

Hypoxemia or hypercapnia that develops abruptly may be associated with delirium. 

Assess ventilatory status by means of arterial blood gases, and correct hypoxemia or 

hypercapnia by administration of oxygen, assisted ventilation, or both, as needed 

(Chapter 11). 

E. Treat Hyperthermia or Hypothermia 

Markedly elevated body temperatures (40.6 °C [105 °F]) may be associated with 

delirium or acute confusional states. Hypothermia is likely to produce confusion at body 

temperatures below 32.2 °C (90 °F) and unconsciousness at temperatures below 26.6 

°C (80 °F). Treat by lowering or raising core temperature, as needed (Chapter 44). 

F. Treat Severe Hypertension 

Severe hypertension (when associated with papilledema and encephalopathy) is a 

medical emergency requiring rapid reduction of diastolic pressure toward 100 mm Hg 

(Chapter 34). The diagnosis of hypertensive encephalopathy must be firmly established 

before antihypertensive therapy is started, however, because reduction of blood 

pressure when cerebral ischemia is present can severely exacerbate ischemic brain 

injury. 

Initial Evaluation 

1. Obtain complete vital signs, including temperature. 

2. Assess for shock (peripheral hypoperfusion). 

3. Obtain results of arterial blood gas and pH determinations. 

4. Does the delirium lighten after administration of intravenous glucose, thiamine, and 

naloxone? If so, consider the following possibilities: 

• Hypoglycemia (diagnosis is confirmed by finding of low serum glucose) 

• Wernicke encephalopathy (look for associated alcoholism, malnutrition, ataxia, 

ophthalmoplegia, and peripheral neuropathy) 

• Opiate overdose (diagnosis is confirmed by positive response to naloxone and 

toxicology screen) 

Further Evaluation 

See Table 20-2.

A. Examination and Diagnostic Tests 

1. History—Obtain a brief history from the patient, family, friends, neighbors, 

ambulance attendants, or bystanders. Ask in particular about prior episodes of 

confusion or delirium, duration and other features of the present episode, drug usage, 

and previous illness. 

2. Physical and neurologic examination—Perform a general physical examination, 

and look especially for signs of trauma, meningeal irritation, and cardiac disease. 

Complete a basic neurologic examination, including tests of orientation and memory. 

3. Laboratory studies—Send blood to the laboratory for CBC; serum electrolyte, 

glucose, calcium, and magnesium determinations; renal and liver function tests; 

carboxyhemoglobin level; and toxicology studies. Obtain urine for urinalysis and 

toxicology studies. 

4. Electrocardiogram—Obtain an electrocardiogram in order to seek any abnormalities 

that might suggest a cardiac cause of the confusional state (eg, myocardial infarction, 

cardiac arrhythmias, prolonged intervals). T-wave changes, however, are nonspecific 

and may be seen with acute intracranial events. 

5. Special studies—Special studies may be indicated based on the results of history 

and physical examination (eg, lumbar puncture for cerebrospinal fluid in the patient with 

confusion and fever or signs of meningeal irritation). 

6. Gastric contents evaluation—Administer an activated charcoal slurry (50-100 mg of 

activated charcoal admixed with water or sorbitol) and consider gastric lavage if 

ingestion or overdose of a toxin is a diagnostic possibility. 

B. Trauma 

If there is evidence of trauma—even if the head itself appears uninjured—consider the 

possibility of traumatic brain damage (eg, subdural or epidural hematomas). Computed 

tomography (CT) scan may be indicated (Chapter 22). Hospitalization is required even if 

no specific abnormality is found. 

C. Meningeal Irritation 

Look first for signs of meningitis due to infection or subarachnoid hemorrhage. 

Headache is common and may not be severe. Fever is common in infectious meningitis 

but is absent in the initial stage of subarachnoid hemorrhage. Signs of meningeal 

irritation (meningismus: stiff neck, positive Kernig and Brudzinski signs) are almost 

invariably present in meningitis or subarachnoid hemorrhage except in very young or 

very old patients. The most helpful diagnostic maneuver is passive flexion of the 

patient's neck, which elicits reflex knee flexion (usually unilateral) if meningeal irritation 

is present (positive Brudzinski sign). Perform lumbar puncture immediately in patients 

with meningismus in the absence of signs of increased intracranial pressure 

(papilledema, focal neurologic findings) for evaluation of cerebrospinal fluid (Chapter 

19). Bacterial meningitis requires urgent treatment (Chapter 40). 

D. Focal Neurologic Findings 

(See Table 20-2.) Although focal signs may be found in metabolic brain disease (notably

the fluctuating hemiparesis that may occur with hypoglycemia and hepatic 

encephalopathy), such asymmetric findings should be assumed to reflect a structural 

brain lesion until proved otherwise; appropriate neurologic or neurosurgical consultation 

should be obtained. 

The principal differential diagnostic considerations are cerebrovascular accidents 

(thrombotic or embolic) and mass lesions. Lumbar puncture is contraindicated, and the 

patient should be evaluated with CT scan. 

In patients with fever and focal neurologic findings, a brain abscess must be considered 

along with meningitis and encephalitis. A lumbar puncture is contraindicated until a CT 

scan has eliminated the possibility of a mass lesion. To avoid delay of needed treatment 

for possible meningitis while awaiting the results of the CT scan, obtain blood cultures, 

and begin antibiotics immediately (Chapter 40). 

E. Other Causes of Delirium or Confusion 

Once life-threatening conditions have been ruled out, a more specific diagnosis can be 

attempted. Main causes are shown in Table 20-2 and described below. Delirium or 

confusion occurring in patients with AIDS is discussed in Chapter 40. 

Johnson J: Identifying and recognizing delirium. Dement Geriatr Cogn Disord 

1999;10:353. [PMID: 10473939] 

Liptzin B: What criteria should be used for the diagnosis of delirium? Dement Geriatr 

Cogn Disord 1999;10:364. [PMID: 1047394] 

EMERGENCY MANAGEMENT OF SPECIFIC DISORDERS 

SEIZURE DISORDERS (See Chapter 17.) 


• Present in patients who have known seizure or have an underlying seizure disorder. 

• Mental status abnormalities and focal neurologic symptoms are usually present. 

• May be associated with psychiatric symptoms. 

• Administer appropriate anticonvulsant treatment as necessary. 

1. Postictal Confusion 


Postictal confusion is a fairly common phenomenon with seizures. It is usually 

diagnosed after a witnessed seizure in a patient who has an underlying seizure 

disorder. This confusion may be associated with psychiatric symptoms such as 

delusions, hallucinations, and behavioral changes. Although the psychiatric symptoms 

are usually brief, the patient may remain in a confusional state for some time.


Hospitalize the patient and give appropriate treatment if the cause of the psychiatric and 

confusional symptoms is not identified or the symptoms fail to resolve. 

2. Interictal & Postictal Psychosis 


Interictal psychosis is the presence of confusion and psychiatric symptoms (eg, apathy 

and diminished affect) in seizure patients that are unrelated to their seizures. Because 

these symptoms are not related to the seizure episode, this is a difficult diagnosis and 

should be considered in the delirious or confused patient who has an underlying seizure 

disorder. 

Postictal psychosis occurs predominately after a repeated number of seizures. Patients 

present with mood changes and psychiatric symptoms, mainly paranoid delusions. 

Hallucinations occur less frequently. 


Hospitalize the patient, administer the necessary anticonvulsant therapy, and monitor 

appropriately. 

Bostwick JM: The many faces of confusion. Timing and collateral history often hold the 

key to diagnosis. Postgrad Med 2000; 108:60. [PMID: 11098259] 

Kaplan PW: Assessing the outcomes in patients with nonconvulsive status epilepticus: 

nonconvulsive status epilepticus is underdiagnosed potentially overtreated, and 

confounded by comorbidity. J Clin Neurophysiol 1999;16:341. [PMID: 10478707] 

Lancman M: Psychosis and peri-ictal confusional states. Neurology 1999;53:S33. 

[PMID: 9139290] 

Murphy BA: Delirium. Emerg Med Clin North Am 2000;18:243. [PMID: 10767881] 

METABOLIC ENCEPHALOPATHIES 


• Will see changes in patient's mental status with lucid intervals and no focal 

abnormalities. 

• Patient tends to remain oriented to person but not place or time. 

• Similar withdrawal profile is seen with alcohol, barbiturates, and other 

sedative-hypnotic drugs. 

• Delirium tremens is life threatening and must be treated promptly. 

• Patients with Wernicke encephalopathy present with ophthalmoplegia, ataxia, and

confusion. Wernicke encephalopathy is a medical emergency and should be treated 

promptly with thiamine. 

1. Systemic Metabolic Disorders 

Systemic metabolic disease, acute drug intoxication, or sedative-hypnotic drug 

withdrawal can produce an altered mental status ranging from florid, agitated delirium to 

lethargy or coma. 


Marked fluctuation in the patient's mental state with intermittent periods of lucidity, 

without focal abnormalities, is characteristic of metabolic encephalopathy. A history of 

systemic illness (Table 20-3) or drug ingestion should be sought in every patient with a 

confusional state. Helpful clinical findings include the following: 

• Symmetric nystagmus is found in sedative-hypnotic drug and phencyclidine ingestion. 

• Asterixis is most commonly associated with hepatic or renal insufficiency. 

• Hallucinations occur in metabolic disorders and are typically visual, as exemplified by 

delirium tremens. 

• Orientation as to time is lost early in metabolic encephalopathy and is followed later by 

loss of orientation as to place, but orientation as to person is almost invariably 

preserved. This characteristic pattern of metabolic brain disease contrasts with that of 

psychiatric disorders, in which patients may know the correct day and date but are 

uncertain who or where they are. 

• Arterial blood gas and pH measurements may suggest a metabolic cause for acute 

confusional states and are useful in distinguishing the metabolic causes of coma. 


Seek and correct the cause of the metabolic disorder. Hospitalize the patient for 

treatment and diagnosis as indicated. 

2. Drug Withdrawal Syndromes (Ethanol & Other Sedative-Hypnotic Drugs) 


Several well-recognized syndromes are associated with acute withdrawal from alcohol, 

barbiturates, or other sedative-hypnotic drugs (Table 20-4). Manifestations of acute 

alcohol withdrawal are as follows: 

• Acute alcoholic tremulousness 

• Acute intoxication (inebriation, stupor, or combative states)

• Alcohol withdrawal seizures 

• Tremor and transitory hallucinations 

• Typical delirium tremens 

• Atypical delirious-hallucinatory states 

• Acute auditory hallucinations 

• Other miscellaneous manifestations, including Wernicke-Korsakoff syndrome 

Acute tremulous and hallucinatory states that are distinct from delirium tremens are 

more common and less serious than delirium tremens and are seen within the first 6-36 

hours following relative or absolute abstinence from alcohol, whereas classic delirium 

tremens syndrome typically appears after 3-4 days of abstinence (range: 24 hours to 5 

days or more). 


A. Delirium Tremens 

Note: Delirium tremens is an uncommon but life-threatening illness that requires prompt 

recognition and treatment for the best outcome. Symptoms and signs include the 

following: 

• Profoundly delirious state associated with tremulousness and agitation. 

• Excessive motor activity (most notable as a tremor that affects the face, tongue, and 

extremities but that may also involve speech) and purposeless activity such as picking 

at the bedclothes. 

• Hallucinations, classically visual rather than auditory, are a prominent feature, 

especially if patients are specifically asked, "What do you see? What's over there? Is 

there anything frightening you?" These patients may be quite suggestible and may be 

persuaded to light an imaginary cigarette or identify the color of a nonexistent piece of 

string. 

• Autonomic nervous system hyperactivity: tachycardia, dilated pupils, fever, and 

hyperhidrosis. 

• Loss of orientation as to time and place. Such patients are often oblivious to the most 

obvious features of the surrounding environment (eg, they do not know whether they are 

in bed or on a chair or wearing a suit or pajamas). 

Duration of delirium tremens is less than 24 hours in 15% of cases and less than 3 days 

in over 80%. 

B. Withdrawal Seizures 

Withdrawal seizures, a syndrome distinct from delirium tremens, may result from abrupt

decrease or cessation of alcohol consumption. About 90% of such convulsions occur 

6-48 hours after abstinence. 

Because delirium tremens requires a longer period of abstinence than withdrawal 

seizures, pure withdrawal seizures (ie, those occurring only during periods of 

withdrawal) always occur before delirium tremens. Therefore, any seizures occurring 

after delirium tremens must be assumed to be due to some cause other than alcohol 

withdrawal, and further evaluation is required. 

C. Sedative-Hypnotic Drug Withdrawal 

A syndrome nearly identical to delirium tremens but somewhat more protracted may 

follow withdrawal from short-acting barbiturates or other sedative-hypnotic drugs (Table 

20-4) in habituated patients. These drug-induced withdrawal reactions occur only when 

the patient has become habituated to large doses of the drug. 

D. ?-Hydroxybutyrate 

Since the early 1990s, a prolonged withdrawal syndrome has emerged with chronic 

frequent use of ?-hydroxybutyrate (GHB). GHB is an increasingly popular drug of abuse 

owing to its euphoric effects. It has been used in the past as an anesthetic agent, 

bodybuilding supplement, or sexual enhancer or to incapacitate victims for assault. Its 

precursor is readily available for purchase on the Internet. 

The onset of symptoms is typically between 1- 6 hours after the last use of GHB, and 

symptoms can last from 5 to 15 days. Initially patients experience anxiety, insomnia, 

and tremor. These symptoms progress rapidly to severe delirium with psychosis and 

agitation, and patients may require physical restraint and sedation. Autonomic instability 

and death can occur. 

Treatment 

A. Delirium Tremens 

Note temperature, pulse, and blood pressure, and record results twice hourly to monitor 

for hyperpyrexia and hypotension. Consider lumbar puncture to rule out meningitis if 

fever or meningismus is present. 

1. Fluids—Fluid requirements on the first day of treatment may be as high as 4-10 L 

because of profound dehydration. Intravenous fluid should contain glucose to prevent 

hypoglycemia. 

2. Thiamine—Thiamine, 100 mg/d, prevents Wernicke encephalopathy. Other 

water-soluble vitamins (B complex and C) should also be given. 

3. Sedatives—Judicious use of sedative drugs does not eliminate established delirium 

but does protect the patient against self-induced trauma and permit continued 

treatment. Sedatives (eg, benzodiazepines) may also prevent patients with impending 

delirium tremens from developing a full-blown case. 

a. Initial dose—A suggested regimen is diazepam (Valium, others), 10 mg 

intravenously given over at least 2 minutes, followed by 5 mg intravenously every 5

minutes until the patient is calm. The total dose required to calm a patient may be as 

high as 200 mg (rarely, even 700 mg or more). Drug-induced hypotension and 

respiratory depression during administration of diazepam for delirium tremens are 

uncommon if adequate hydration is maintained and overzealous treatment avoided. 

After delirium tremens has been controlled, the patient may sleep without interruption for 

up to 36 hours but can nonetheless be easily aroused. 

b. Maintenance doses—Administer diazepam, 5-10 mg, intravenously or orally as 

needed. Avoid intramuscular administration, because absorption by this route is erratic. 

Sedation is achieved within a few minutes following intravenous injection but may be 

delayed for 3 hours or longer following intramuscular injection if associated obesity, 

hyperpyrexia, or complicating illness (eg, pneumonia) is present. 

4. ACTH or corticosteroids—Do not administer ACTH or corticosteroids for delirium 

tremens; they are ineffective and potentially harmful. 

5. Phenothiazines—Phenothiazines have been used and may promptly control 

hallucinatory symptoms; however, these drugs are not recommended, because they 

may cause hypotension or precipitate seizures. 

6. ß-Blockers—The concomitant administration of ß-blocking drugs decreases the 

associated autonomic hyperactivity. 

B. Withdrawal Seizures 

Pure withdrawal seizures are self-limited and usually do not require anticonvulsant 

therapy. Observation is necessary, because about 60% of patients will have more than 

one seizure, 95% of which will occur within 12 hours after the initial seizure and 80% 

within 6 hours. Repetitive alcohol withdrawal seizures can be controlled 

pharmacologically with a single loading dose of phenobarbital (750 mg, intravenously 

slowly); phenytoin is ineffective. Patients with withdrawal seizures, unless previously 

investigated, should receive outpatient follow-up. Most should be investigated at least 

once for structural causes. Hospitalization is rarely required. 

C. Sedative-Hypnotic Drug Withdrawal 

Supportive care is usually all that is necessary for sedative-hypnotic withdrawal 

syndromes. This may entail short-term airway protection (about 8 hours) via 

endotracheal intubation. Associated delirium requires benzodiazepine treatment as 

outlined above in treatment of delirium tremens. 

Treatment 

The most important therapeutic aspect of care is attention to management of the airway. 

Effort should also be given to protecting the patient from harming him- or herself. 

Specific side effects from withdrawal are treated accordingly, as described above. 

Disposition 

Hospitalization is indicated for all patients with sedative-hypnotic drug withdrawal who 

have active delirium tremens or possible impending delirium tremens (tremor,

tachycardia, and agitation). Patients with more benign withdrawal states (tremulousness 

alone, hallucinatory states other than delirium tremens, withdrawal seizures) may be 

sent home after 6-12 hours of observation and treatment in the emergency department. 

3. Wernicke Encephalopathy (Acute Thiamine Deficiency) 


Wernicke encephalopathy is a medical emergency characterized by ophthalmoplegia, 

ataxia, and confusion. Most cases are associated with alcoholism, malnutrition, or both. 

Failure to initiate prompt thiamine therapy in a patient with any of these features may 

result either in death or in permanent neuropathy or loss of cognitive function. 

A. Ocular Abnormalities 

Nystagmus (horizontal alone or horizontal and vertical) may occur. Isolated vertical 

nystagmus is rare. Bilateral lateral rectus muscle (sixth cranial nerve) palsies and 

conjugate gaze palsies may be present. Other types of ophthalmoplegia may occur. The 

response to irrigation of the external ear canal with ice water (caloric test) is invariably 

abnormal and reveals unilateral or bilateral absence of ocular movement. 

B. Ataxia 

Ataxia is similar to that associated with alcoholic cerebellar degeneration. Truncal ataxia 

is most common, with a wide-based, unsteady gait as the major finding. Limb ataxia is 

less common than ataxia of gait and affects the lower extremities much more than the 

upper extremities. 

C. Confusion 

Frank delirium occurs in about 20% of cases. Blatant apathy, manifested as inattention, 

drowsiness, and decreased spontaneous speech, is present in most cases. In the 

recovery phase, Korsakoff psychosis may become more prominent, with marked 

impairment of recent memory and inability to retain new information. Confabulation is 


D. Cardiovascular Abnormalities 

Tachycardia, exertional dyspnea, minor electrocardiographic abnormalities, and 

orthostatic hypotension are common. Overt beriberi heart disease with heart failure is 

rare. 

E. Neuropathy 

Peripheral neuropathy is associated with Wernicke encephalopathy in approximately 

80% of cases. 

Treatment 

A. Vitamins 

Give thiamine, 100 mg intravenously, immediately upon diagnosis of Wernicke 

encephalopathy. Patients should be hospitalized and thiamine continued in doses of 50 

mg/d intravenously until adequate diet and bowel function are reestablished. Other 

water-soluble vitamins (B complex and C) should be given, because multiple

deficiencies are common in these patients. The need for folate or vitamin B 12 should be 

assessed based on the CBC (presence of hypersegmented polymorphonuclear 

leukocytes, and macrocytosis). Deficiencies of fat-soluble vitamins (A, D, and E) are 

rare. 

Magnesium deficiency is common in alcohol withdrawal states, and magnesium should 

be replaced based on blood levels (Chapter 42). 

B. Bed Rest 

Bed rest is necessary because of the patient's fragile cardiovascular status (deaths 

have been reported following trivial physical exertion). 

C. Outcome 

With thiamine therapy, oculomotor abnormalities may begin to improve within minutes to 

hours, and complete recovery will occur within 1-4 weeks, except for persistent lateral 

gaze nystagmus. Global confusional state, ataxia, peripheral neuropathies, and 

Korsakoff psychosis in particular clear much less quickly, and permanent disability is 


Disposition 

All patients with thiamine deficiency syndromes should be hospitalized for supportive 

care and continued administration of thiamine. 

4. Drug Intoxication 

Centrally Acting Anticholinergic Drugs 

Intoxication with a wide variety of anticholinergic medications that penetrate the central 

nervous system may produce agitated and confusional states. Table 20-5 lists 

representative prescription and over-the-counter medications. 

Delirium, psychosis, anxiety, hallucinations, breathlessness, hyperactivity, 

disorientation, seizures, and coma are typically associated with signs of peripheral 

cholinergic blockade: tachycardia, mydriasis, hyperpyrexia, urinary retention, decreased 

bowel motility, decreased sweating, and decreased bronchial, pharyngeal, and salivary 

secretions. The patient is hot, dry, red, and "mad as a hatter." 

Treatment is discussed in Chapter 45. Hospitalization is required for supportive care. 

Stimulants & Hallucinogenic Drugs 

Some commonly abused drugs, for example, cocaine, amphetamine, LSD (lysergic acid 

ethylamide), jimsonweed, and PCP (phencyclidine), can cause an agitated confusional 

state. Cocaine is currently the most frequent culprit and can produce agitation, anxiety, 

depression, psychosis, paranoia, suicidal ideation, or any combination of these 

conditions. Symptoms are independent of the route of drug administration. Treatment is 

discussed in Chapter 45. Short-term psychiatric admission often is required.

Beaver TM et al: Treatment of acute anticholinergic poisoning with physostigmine. Am J 

Emerg Med 1998;16:505. [PMID: 9725967] 

Brown TM: Drug-induced delirium. Semin Clin Neuropsychiatry 2000;5(2):113. PMID: 

10837100 

Dyer JE: Gamma-hydroxybutyrate withdrawal syndrome. Ann Emerg Med 2001;37:147. 

[PMID: 11174231] 

Myrick H et al: New developments in the pharmacotherapy of alcohol dependence. Am 

J Addict 2001;10:3. [PMID: 11268820] 

Olmedo R et al: Withdrawal syndromes. Emerg Med Clin North Am 2000;18:273. 

[PMID: 10767884] 

Talbot-Stern JK et al: Psychiatric manifestations of systemic illness. Emerg Med Clin 

North Am 2000;199. [PMID: 10767878] 

REYE'S SYNDROME 


• Associated with fatty degeneration of the liver. 

• A link exists between viruses, specifically chickenpox and influenza, and salicylates. 

• Extremely rare in individuals over age 20 years. 


Reye syndrome, an encephalopathy associated with fatty degeneration of the liver, is a 

major cause of delirium progressing to coma in infants and children. The degree of 

central nervous system impairment does not correlate well with the degree of hepatic 

dysfunction. The disease is extremely rare in individuals over age 20 years. Seasonal 

occurrence from November to April with a peak incidence in February has been noted. 

There may be a history of a preceding viral illness. Epidemiologic evidence has firmly 

linked Reye syndrome with chickenpox and influenza virus infections. An association 

between Reye syndrome and the use of salicylates during an antecedent illness has 

been demonstrated. 

The number of cases has dropped dramatically since the 1980s. Several authors have 

noted a correlation between the decrease in reported cases to almost zero and the 

discovery of many new metabolic disorders that have a common pathophysiology. New 

diagnostic techniques to identify these inborn errors of metabolism have revealed that 

many cases of Reye syndrome mimicked these disorders. It is now recommended that 

any infant or child suspected of having Reye syndrome undergo extensive testing to rule 

out the treatable inborn metabolic disorders. 

Clinical Findings

Illness begins with protracted vomiting and delirium that progresses to coma within 2 

days. Seizures are common but are usually self-limited. Decerebrate posturing is 

common, but focal neurologic signs are rare once coma is established. Sustained 

hyperventilation and hepatomegaly are usually noted. Cerebrospinal fluid examination 

reveals normal protein and cell count. Blood glucose is frequently reduced because of 

hepatic failure and may be reflected in low levels of cerebrospinal fluid glucose. Serum 

transaminase and blood ammonia levels are characteristically elevated. Prothrombin 

time is prolonged. Serum bilirubin is normal, so that icterus makes the diagnosis of 

Reye syndrome doubtful. 


Hospitalization is invariably required for control of intracranial pressure and supportive 

care. Early placement of an intracranial pressure monitor and measures to lower 

intracranial pressure may be helpful. There is no specific treatment. 

Orlowski JP: What ever happened to Reye's syndrome? Did it ever really exist? Crit 

Care Med 1999;27:1674. [PMID: 10470768] 

AMNESTIC SYNDROMES 


• Recall must be specifically tested for the identification of memory loss. 

• Amnestic syndromes are identified by their onset and duration; then a specific cause 

can be found. 

1. Amnestic Episodes 


The neurologic abnormality of memory loss is easily missed unless recall is specifically 

tested. Confused patients may present with only memory loss and no alteration of 

consciousness; the general physical examination may be entirely normal. Such patients 

have markedly abnormal recent memory (eg, they cannot remember 3 objects after 60 

seconds or even 30 seconds). Other cognitive functions and past memory are relatively 

intact. Such patients are confused about where they are and what they are doing. 

The causes and differential diagnosis of the amnestic syndromes are presented in Table 

20-6. The history, cerebrospinal fluid examination, CT or magnetic resonance imaging 

(MRI) scan, clinical course, or associated findings establish the cause in most cases. 


Administer thiamine, 100 mg intravenously, because Wernicke syndrome is a diagnostic 

possibility. All patients with new onset of memory loss should be hospitalized for

evaluation. 

2. Transient Global Amnesia 


Transient global amnesia occurs suddenly in previously normal middle-aged or elderly 

patients. Men are affected more frequently than women. Episodes of amnesia occur 

without warning and without associated headache or findings suggesting epilepsy. 

Cerebrovascular disease affecting thalamic or temporal lobe structures is the most likely 

cause. The results of laboratory studies are completely normal. 

During an attack, agitation is not a feature. Patients' responses to the illness are 

variable: some may be unaware of their deficit, but most realize that something is 

wrong; a few may recognize that their memory is impaired. During these episodes, 

patients may repeatedly ask the same questions regarding their current condition. 

The period of retrograde amnesia varies from a day to a few months or even years. 

Recovery usually occurs within hours, but amnesia for the entire episode is total and 

permanent. 


No specific treatment is available. Hospitalization is indicated, in part to prevent injury. 

Lewis SL: Aetiology of transient global amnesia. Lancet 1998;352: 397. [PMID: 

9717945] 

ACUTE STROKES (Cerebrovascular Accidents) 


• When the possibility of stroke is present, the appropriate cerebrovascular accident 

protocol should be followed (Chapter 18). 

• Sudden onset, seen most commonly in the elderly and in those with valvular or 

ischemic disease. 

• These patients tend to have acute onset of confusion with an associated fluent 

aphasia. 

1. Fluent Aphasia 


Lesions of the dominant posterior frontal lobe may produce a nonfluent (expressive) 

aphasia and prominent tight hemiparesis. Lesions in a more posterior location may 

partially or completely spare motor function but produce a fluent (receptive) aphasia 

easily mistaken for confusion or delirium. Such lesions occur suddenly and are usually

caused by embolic strokes in patients at risk of stroke (eg, the elderly or those with 

valvular or ischemic heart disease predisposing to embolization). 


Patients talk volubly. Their speech is well-articulated and grammatically correct but has 

little content. Sentences are characterized by word substitutions (eg, glass instead of 

clock), replacement of real words by nonsense words (eg, dreislen for finger), and 

substitution of explanatory phrases for words that cannot be recalled (eg, "the thing you 

write with" for pen). 

Deficits of comprehension are evident. Patients are unable, for example, to carry out the 

command, "Put your left hand on your right ear," or to repeat the simple phrase, "No 

ands, ifs, or buts." 

The isolated inability to name objects (anomia) without deficits of comprehension and 

repetition may represent a form of fluent aphasia due to a structural lesion but most 

commonly occurs with metabolic encephalopathies of any cause. 


Hospitalization is indicated for new cases to provide supportive care and determine the 

cause of the aphasia. A CT scan should be obtained. Emboli with an origin in the heart 

are a common cause and require short-term treatment with anticoagulants. Chronic 

cases do not require hospitalization. 

2. Agitated Confusion 


The acute onset of an agitated confusional state may occur with infarctions of the 

inferior division of the right middle cerebral artery. Such strokes spare motor cortex, so 

that localizing signs (eg, hemiparesis) are mild or absent. A homonymous hemianopia 

may be present on examination. The diagnosis is suggested by the abrupt onset of 

agitated confusion and is confirmed by CT or MRI scan. Embolus with an origin in the 

heart is common. 


Hospitalize the patient for treatment and observation. Evaluation for the source of the 

embolus and treatment with anticoagulants may be indicated. 

Hankey GJ: Management of the first-time transient ischemic attack. Emerg Med 

2001;13:70. [PMID: 11476418] 

Lewandowski C et al: Treatment of acute ischemic stroke. Ann Emerg Med 

2001;37:202. [PMID: 11174240] 

CONFUSION ASSOCIATED WITH PSYCHIATRIC DISEASE


• All forms of organic causes must be evaluated and ruled out prior to considering the 

possibility of psychiatric disease. 

• Patients tend to be fully oriented to place and time, and disorientation tends to be to 

person. 

• Short-term memory is preserved, and hallucinations are auditory in nature. 


Differentiation between organic and psychiatric causes of confusion (psychosis or 

hysteria) may be difficult. If careful evaluation (described below) is performed, few 

patients with metabolic diseases will be improperly diagnosed as having psychiatric 

illness. Additional useful differential features are outlined in Table 20-7. 

1. Psychotic Confusional States 


The presentation of patients with psychotic confusional states differs from that of 

patients with confusional states due to organic causes. The classic psychotic state is 

schizophrenia. Psychiatric causes of confusion have varying characteristics from 

organic as demonstrated below: 

• Psychotic patients may be fully oriented or, if disoriented, exhibit disorientation as to 

person that is at least as great as or greater than their disorientation to time and place. 

In organic brain disease, by contrast, disorientation as to time and place is invariably 

greater than to person. 

• Psychotic patients usually retain recent memory and are able to perform simple 

calculations and other cognitive tasks adequately. In contrast, these functions are rarely 

preserved in organic confusional states. 

• Auditory hallucinations are the mainstay with psychotic states, as opposed to the 

visual hallucinations seen in organic confusional states. 


Obtain psychiatric consultation. Hospitalization in a secure ward is required for patients 

with acute psychosis or abrupt worsening of chronic psychosis. Parenteral 

antipsychotics, for example, haloperidol (Haldol, others), 5-10 mg intramuscularly every 

30 minutes to 1 hour, should be given until the patient shows improvement. 

Chlorpromazine (Thorazine, many others), 25-50 mg intramuscularly, is equally effective 

but is less commonly used because of side effects of sedation and postural 

hypotension.

2. Hysteria 


Hysteria is a diagnosis of exclusion and should be made only after all other possibilities 

have been ruled out. The differential features listed in Table 20-7 are helpful, but few 

guidelines are absolute. It is useful to remember that amnesia is probably the most 

common hysterical disturbance of mental function. Hysterical amnesia usually includes 

the inability both to form new memories and especially to recall any past experience 

with certainty. For example, such patients often deny knowledge of their own name, a 

finding that in an awake and alert person is essentially restricted to the hysterical 

personality. The disparity between alleged mental incapacity and the ability to function 

in the immediate surroundings is often quite striking. 

The most helpful differentiating features on physical examination are asterixis and 

myoclonus, which, when present, point to a metabolic cause of the symptoms. Asterixis 

and myoclonus do not occur as features of psychiatric or hysterical illness. 

An electroencephalogram is often helpful in diagnosis, because it is nearly always 

normal in psychiatric disease and is frequently abnormal (usually slowed) in organic or 

metabolic disease. The presence of very fast ß-wave activity on the tracing may be 

seen with sedative-hypnotic drug intoxication and provides a helpful clue to proper 

diagnosis. 


Refer the patient for psychiatric consultation. Anxiolytics, for example, diazepam 

(Valium, others), 5-10 mg orally, may be helpful. Hospitalization may be required if a 

protected home environment is not available. 

CONFUSIONAL STATES OF UNCERTAIN CAUSE 

Even after all the above diagnoses have been considered, for many patients in 

confusional states, no clear diagnosis can be established in the emergency department. 

These patients, especially the elderly, are often found to have subclinical mild metabolic 

or drug-induced abnormalities or infection, and correction of the underlying disorder may 

restore patients to their customary normal state. Hyperthyroidism or hypothyroidism 

must be considered, especially in elderly patients. 

Hospitalization is indicated for further evaluation of all patients with confusional states of 

uncertain cause. 

Fisher CM: Hysteria: a delusional state. Med Hypotheses 1999; 53:152. [PMID: 

10532711] 

Marsh CM: Psychiatric presentations of medical illness. Psychiatr Clin North Am 

1997;20:181. [PMID: 9139290]







Figure 20-1.)

Table 20-1. Conditions associated with acute confusion or delirium 

that may cause rapid cerebral damage. 






TABLES 

Table 20-1. Conditions associated with acute confusion or delirium that 

may cause rapid cerebral damage.

Table 20-2. Differential diagnosis of conditions causing delirium or confusion. 


Somnolence; neurologic examination shows focal or asymmetric abnormality. Posterior 

nondominant parietal lobe strokes present with an agitated delirium, without hemiparesis. 

Headache, fever, meningeal signs, cerebrospinal fluid pleocytosis. 

History or evidence of seizures, especially seen in seizure patients with superimposed 

metabolic abnormality, encephalitis, or diffuse cerebral damage, in whom postictal state may 

be prolonged. 

Findings confined to recent memory loss. 

Sudden onset; patient alert; mild right hemiparesis (may be absent). Excessive speech with 

frequent word substitutions and nonsense phrases. 

Paranoia prominent; auditory hallucinations common; disorientation as to person, which is 

greater than that as to place, which is greater than that as to time. Recent memory preserved. 

Recent history or evidence of head trauma. 

Fluctuations in mental status (lucid intervals); asterixis; myoclonus; tremor; visual 

hallucinations; disorientation as to time, which is greater than that as to place, which is 

greater than that as to person; nystagmus. 






TABLES 

Table 20-2. Differential diagnosis of conditions causing delirium or 

confusion.

Table 20-3. Systemic illnesses associated with confusion due to metabolic 


Respiratory 

Hypercapnia 

Hypoxemia 

Cardiac 

Heart failure 

Endocarditis 

Other 

Sepsis 

Shock 

Drug ingestion 

Thiamine deficiency 

(eg, Wernicke-Korsakoff syndrome) 

Hyperthyroidism 

Hypothyroidism 






TABLES 

Table 20-3. Systemic illnesses associated with confusion due to metabolic 

encephalopathy.

Table 20-4. Sedative drugs reportedly followed by 

clinical abstinence syndromes after withdrawal from 

excessive dosage. 






TABLES 

Table 20-4. Sedative drugs reportedly followed by clinical abstinence 

syndromes after withdrawal from excessive dosage.

Table 20-5. Drugs that may cause a central anticholinergic 

syndrome. 1 

Tricyclic antidepressants 

Amitriptyline (Elavil, many others) 

Doxepin (Adapin, Sinequan, others) 

Imipramine (Tofranil, many others) 

Antihistamines 

Chlorpheniramine (Omade, Teldrin, many others) 

Diphenhydramine (Benadryl, many others) 

Promethazine (Phenergan, many others) 

Antispasmodics 

Methantheline (Banthine) 

Propantheline (Pro-Banthine, others) 

Over-the-counter drugs (hypnotics, analgesics) 

Sominex (diphenhydramine) 

Sleep-Eze (diphenhydramine) 

Contac (chlorpheniramine) 

Dristan (chlorpheniramine)

Table 20-6. Causes of amnestic syndromes. 1 

1 Modified and reproduced, with permission, from Victor M: The 

amnesic syndrome and its anatomical basis. Can Med Assoc J 

1969;100:1115. 






TABLES 

Table 20-6. Causes of amnestic syndromes.

Table 20-7. Differentiating features of organic and psychiatric disorders of mentation. 

Organic 

Age Younger; puberty to mid 30s. 

Any. Onset Usually gradual and insidious. 

Rare. Level of awareness Usually consistent. 

Common; predominantly 

visual, tactile, and 

olfactory. 

Usually affected; recent 

memory more affected 

than remote memory. 

Frequently abnormal, 

usually slow. 

Orientation Impaired: disorientation to person is 

greater than that as to place, which 

is greater than that as to time; may 

be unimpaired, however. 

Other evidence of organic central Usually absent. 

nervous system disease 

Asterixis and multifocal myoclonus Never seen.

Figure 20-1. Assessment of delirium or confusional states. 






FIGURES

21. Arthritis & Back Pain 1 - Roger L. Humphries, MD, & David O'Keefe, 

MD 

I. EVALUATION OF THE PATIENT WITH ACUTE ARTHRITIS (See 

Figure 21-1.) 

Is the Patient Systemically Ill? 

1 This chapter is a revision of the chapter by Peter G. Trafton, MD, from the 4th edition. 

Whenever a patient with acute joint pain also presents with fever, rigors, systemic 

symptoms, or signs of involvement of additional organ systems, careful evaluation is 

necessary to rule out potentially life-threatening processes such as infection or diffuse 

vasculitis. 

Hospitalization and consultation for evaluation of rheumatic or infectious disease are 

usually required for patients with arthritis and systemic symptoms. Obtain blood 

cultures, and perform the evaluation outlined below. 

Is This Disseminated Gonococcal Infection? 

In young adults, hematogenous gonococcal infection is one of the most common causes 

of acute arthritis. Arthritis may be the sole manifestation of disseminated gonococcal 

infection. Skin lesions are few and are found on the extremities, frequently around a 

joint, and are pustular or hemorrhagic, rarely bullous. Gram-stained smears of material 

contained in the pustules may reveal gram-negative diplococci within 

polymorphonuclear neutrophils. Tenosynovitis classically involves tendons of the hand 

or foot. The primary (mucosal) site of gonococcal infection is often asymptomatic. If 

disseminated gonococcal infection is suspected, culture of blood and secretions from 

the pharynx, rectum, and urethra or cervix should be obtained. 

Is There Arthritis on Joint Examination? 

Ascertain by careful examination whether acute joint pain is due to an intra-articular 

process. Is there redness, diffuse warmth, effusion, or painful limitation of active and 

passive motion? If the joint is not involved, consider cellulitis, tenosynovitis, bursitis, or 

other periarticular lesions. 

If It Is Not Arthritis, What Is It? 

The shoulders and upper extremities are frequent sites of acute painful extra-articular 

processes. Table 21-1 lists the common syndromes of nonarticular rheumatism. These 

disorders are described more fully later in this chapter. 

Is the Process Oligoarticular or Polyarticular?

Involvement of 1-3 joints in an asymmetric pattern is generally considered characteristic 

of oligoarthritis, although this asymmetric involvement may occur early in some 

polyarticular conditions such as juvenile rheumatoid arthritis. Common causes of 

oligoarthritis include infection, crystal deposition (eg, gout), and trauma. The polyarthritis 

syndromes involve many joints, usually in a symmetric fashion. 

Perform Arthrocentesis 

If one of the affected joints is acrally located (eg, wrist, elbow, knee, ankle), 

arthrocentesis should be attempted in the emergency department, using local 

anesthesia (Chapter 6). Arthrocentesis of shoulders and hips is best done by a 

specialist. The joint fluid should be analyzed and the results used to classify the arthritis 

according to the scheme in Table 21-2. 

Classification of Arthritis 

See Table 21-2. 

A. Noninflammatory (Class I) 

Acute arthritis in the presence of normal joint fluid usually indicates trauma, or 

osteoarthritis. Rarely, early joint aspiration in inflammatory arthritis produces a similar 

result. 

B. Inflammatory (Class II) 

Inflammatory arthritis may be present in acute gout, pseudogout, Reiter syndrome, 

rheumatoid arthritis, and rheumatic fever. Gram stain and culture of synovial fluid should 

be done to rule out early infectious arthritis. 

C. Septic (Class III) 

Purulent joint fluid (class III) is seen almost exclusively in bacterial and fungal infections. 

Gram stain of joint fluid may help to identify the causative organism before cultures 

become positive. 

D. Hemorrhagic (Class IV) 

Hemorrhagic joint fluid is seen in trauma with or without fracture; the presence of fat 

globules suggests fracture. A tear in the anterior cruciate ligament is the most common 

cause of hemarthrosis in the knee when no fracture is present. Also frequent are 

peripheral meniscus tears and patellar dislocations (with medial retinaculum tears). 

Hemorrhagic effusion is more likely to be associated with acute pain than is the 

noninflammatory effusion that can occur with minor joint trauma, because blood within 

the joint space generally causes an inflammatory reaction. Hemorrhagic fluid is also 

seen in hemophilia and in synovial neoplasms. 

II. EMERGENCY TREATMENT OF SPECIFIC CONDITIONS CAUSING 

ACUTE ARTHRITIS 

MONARTHRITIS OR OLIGOARTHRITIS

TRAUMATIC ARTHRITIS 


• Effusions often develop immediately after trauma. 

•Fever or other systemic signs or symptoms are not present. 


Severe joint pain associated with trauma is usually related temporally to an obvious 

injury. Mild pain may occur some time after the injury. Fever and other systemic signs 

usually are not present. The presence of noninflammatory or hemorrhagic synovial fluid 

confirms the diagnosis. Because patients with septic arthritis may also give a history of 

recent trauma, Gram stain and culture of fluid should be performed. 

The presence of many small fat globules in hemorrhagic joint fluid strongly suggests 

intra-articular fracture; x-rays should be carefully scrutinized to locate occult fractures. 

Well-localized tenderness over a bone is an important sign of fracture (Chapter 28). 

Scaphoid fractures are particularly difficult to locate and require careful correlation with 

clinical findings (eg, localized tenderness in the anatomic snuffbox). X-rays that show 

only joint effusion or periarticular soft tissue swelling are consistent with occult fractures 

or other joint injuries such as spontaneously reduced dislocations, ligamentous injuries, 

meniscus tears, avulsion fractures, and osteochondral fractures. 

Joint effusions that accumulate immediately following trauma are uniformly hemorrhagic 

and usually do not require arthrocentesis for diagnostic purposes. 


Splinting, protection from weight bearing, and follow-up care are essential. Analgesia 

may be needed. See Chapter 28 for more specific details and guidelines for treatment 

and disposition. 

ACUTE GOUTY ARTHRITIS 


• Presence of negative birefringent urate crystals in joint fluid and a negative Gram stain 

and culture. 

• Uric acid level is not helpful for diagnosis in an acute attack. 


Patients with acute gouty arthritis have monarthritis or oligoarthritis with class II or class 

III joint fluid, urate crystals in the synovial fluid, and a negative synovial culture.


There is sudden onset of warmth, hyperemia, induration, and extreme pain in a joint, 

most commonly the metatarsophalangeal joint of the great toe. The next most 

commonly involved joint is the knee. Although most patients present with only one 

painful joint, several joints may be involved. 


Elevated serum uric acid concentration is supporting evidence of gouty arthritis, 

although during an acute attack the serum urate level may be normal. Therefore, a uric 

acid level should not be ordered. Definitive diagnosis requires use of a polarizing 

microscope to demonstrate characteristic negative birefringence of urate crystals in the 

synovial fluid. 

Treatment 

A. Nonsteroidal Anti-Inflammatory Drugs 

Indomethacin or other nonsteroidal anti-inflammatory drugs (NSAIDs) may be indicated 

if a diagnosis of gout is well established. Aspirin is contraindicated, because small 

doses may cause hyperuricemia. 

1. Indomethacin—Give 50 mg orally every 8 hours for 2 days. Then reduce the dosage 

to 25 mg 3-4 times daily for 3 days. Peptic ulcer disease is a contraindication to 

indomethacin. 

2. Other drugs—Ibuprofen, 600 mg orally every 6 hours, or naproxen, 500 mg orally 

every 12 hours, may be used. Other NSAIDs in appropriate doses can be effective in 

acute gout. 

B. Colchicine 

Oral or intravenous colchicine, if administered within 24 hours of acute arthritis, can 

provide dramatic relief. Colchicine should not be used in patients with renal or hepatic 

dysfunction. Response to colchicine also strongly supports a diagnosis of gout. 

1. Oral treatment—Give colchicine, 0.6 mg every hour until pain has resolved, a 

maximum dose of 4- 6 mg is reached, or side effects of nausea and diarrhea cannot be 

tolerated. 

2. Intravenous treatment—Gastrointestinal toxicity can be reduced by giving 

colchicine, 1-2 mg intravenously in 50 mL of normal saline over 20 minutes; repeat this 

dose every 6 hours until the patient is asymptomatic or to a total dose of 4 mg. After a 

full course of colchicine, no further doses should be administered for 1 week. 

C. Corticosteroids 

Corticosteroids are useful in patients who cannot take NSAIDs or colchicine. 

Prednisone, 40 mg daily for 1-3 days followed by a slow taper over 1-2 weeks, is 

recommended. Alternatively, a single dose of adrenocorticotropic hormone (ACTH) or 

corticotrophin, 40 units intramuscularly, boosts the patient's endogenous steroid 

production and can provide relief from a gouty flare-up.

Disposition 

Hospitalization is rarely necessary. The patient should receive follow-up evaluation in a 

few days. 

ACUTE PSEUDOGOUT 


• Calcium pyrophosphate crystals in the joint. 


Patients with acute pseudogout have acute oligoarthritis with class II joint fluid and 

calcium pyrophosphate crystals in the synovial fluid. Pseudogout simulates gout in 

middle-aged or elderly patients. It differs from gout in that the knee is the most 

commonly involved joint. 

Serum uric acid levels are usually normal. Chondrocalcinosis may be present although 

not necessarily in the acutely involved joint. The presence of chondrocalcinosis, 

however, regardless of location, is not diagnostic. Definitive diagnosis depends on the 

presence of calcium dihydrate (pyrophosphate) crystals in synovial fluid. 

Treatment 

Aspiration of the joint is often adequate for relief of symptoms. NSAIDs may be helpful 

(see Acute Gouty Arthritis, above). Unlike patients with gouty arthritis, patients with 

acute pseudogout do not respond as well to colchicine. 

Disposition 

Hospitalization is rarely necessary. Refer the patient to a primary care physician. 

SEPTIC ARTHRITIS 


• Joint is painful, erythematous, and tender. 

• Systemic symptoms: fever and chills are common. 

• Definitive diagnosis by aspiration of the joint. Fluid may demonstrate the infecting 

organism by Gram stain or culture. 


Septic arthritis is one of the more common causes of oligoarthritis, but often only one 

joint is affected. The most frequent pathogen in septic oligoarthritis is the gonococcus, 

which, although difficult to demonstrate in joint fluid, often produces typical pustular skin 

lesions or tenosynovitis. The most common pathogen in monarticular septic arthritis is 

Staphylococcus aureus. Another common pathogen is Streptococcus spp. In 

intravenous drug users and immunocompromised hosts, gram-negative and anaerobic 

organisms may be seen. 


Patients with septic arthritis show evidence of infection in the joint (bacteria on 

Gram-stained smear or culture, or rapid response to antimicrobial therapy). Class III 

joint fluid is usually present. 


Patients with septic arthritis usually present with a severe monarticular process 

characterized by marked pain, erythema, and tenderness. The onset of septic arthritis is 

usually less precipitous than that of gout. A few patients with staphylococcal or 

gonococcal arthritis may present with 2 or more involved joints. Acute migratory 

oligoarthritis followed in 1-2 days by acute arthritis localized to 1 or 2 joints is especially 

suggestive of gonococcal arthritis. If multiple joints are involved in septic arthritis, the 

distribution is usually asymmetric. Systemic symptoms and signs of infection (eg, fever, 

chills, leukocytosis) are common. 


A definitive diagnosis is established by demonstrating the infecting organism in synovial 

tissue or joint fluid. Joint fluid shows high leukocyte counts, usually over 50,000/uL. The 

higher the white blood cell count in joint fluid, the greater the likelihood of bacterial or 

fungal arthritis. The glucose content of synovial fluid is usually reduced. If no 

antimicrobial therapy has been given, smears and cultures of joint fluid usually reveal 

organisms. 

In gonococcal arthritis, however, Gram-stained smears and even cultures of joint fluid 

are frequently negative, although in most cases, cultures of exudate from the cervix, 

urethra, pharynx, or rectum demonstrate gonococci. In gonococcal arthritis, the 

diagnosis may also be confirmed by prompt response to antimicrobial therapy (Chapter 

40). 

Treatment 

A. Joint Aspiration 

Aspiration of the joint is essential. Obtain cultures of blood and joint fluid. If gonococcal 

arthritis is suspected, cervical, urethral, and possibly pharyngeal and rectal cultures 

should be obtained. If sepsis is considered likely, as much fluid as possible should be 

removed from the joint. 


Begin an antibiotic deemed appropriate based on clinical findings and Gram-stained 

smears. Narrow the antibiotic coverage once results of Gram stain, culture, and

sensitivities are reported. The treatment of gonococcal arthritis is discussed in more 

detail in Chapter 40. 

Disposition 

Hospitalize all patients with suspected or documented septic arthritis and start them on 

intravenous antibiotics. Consult an orthopedic surgeon for possible incision and 

drainage of the infected joint. Patients with mild gonococcal arthritis often can be 

discharged early and given antibiotics to be taken orally, provided that they are reliable 

patients and careful follow-up can be ensured. 

Brusch JL: Septic arthritis. eMedicine; http://www.emedicine.com/ med/topic3394.htm 

OLIGOARTHRITIS OR POLYARTHRITIS 

OSTEOARTHRITIS (Degenerative Joint Disease) 


• Usually polyarticular involvement. Most commonly involves hips, knees, spine, and 

distal and proximal interphalangeal joints. 

• Systemic signs and symptoms (fever and chills) should be absent. 

• Radiographs usually demonstrate cartilage changes with osteophytes. 


Osteoarthritis is a chronic, progressive disease in which the smooth hyaline cartilage 

develops irregularities due to mechanical and cellular alterations. The adjacent bone 

then develops irregularities and osteophytes. Diagnosis is made by the clinical features 

of pain, decreased movement, and muscle wasting combined with radiographic findings 

of joint space narrowing, osteophytes, irregular joint surfaces, and bony sclerosis. 

Osteoarthritis is usually polyarticular but can be monarticular. The most commonly 

infected joints are knee, hip, cervical and lumbar spine, and distal and proximal 

interphalangeal joints. 


In the emergency department, newly diagnosed osteoarthritis must be carefully 

distinguished from the septic joint. Once osteoarthritis is diagnosed, patients should be 

discharged with medication and exercise instructions. First-line treatment is 

acetaminophen, 4000 mg every 24 hours in divided doses. Acetaminophen is as 

effective for osteoarthritis as NSAIDs and has fewer side effects. If NSAIDs are 

prescribed, select ibuprofen, 600 mg every 6 hours, as initial therapy. If patients are at 

high risk for gastrointestinal bleeding, select a COX-2 inhibitor instead of NSAIDs. 

Aerobic exercise, walking, and range of motion exercises have all shown benefits in 

knee and hip osteoarthritis. Patients should follow-up with their primary care physician 

within 1 week.

RHEUMATIC FEVER & POSTSTREPTOCOCCAL REACTIVE ARTHRITIS 


• Evidence of recent strep infection. 

• Constitutional symptoms: fever, malaise. 

• Often oligoarthritis with associated cardiac involvement, subcutaneous nodules, and 

erythema marginatum. 

Rheumatic fever or poststreptococcal reactive arthritis may present early as acute 

monarticular joint pain. Acute rheumatic fever is diagnosed using the Jones criteria 

found in Table 21-3. Poststreptococcal reactive arthritis will have only some of the 

Jones criteria and is usually oligoarticular. Carditis is rare, and the arthritis tends to be 

severe. Patients should be hospitalized if rheumatic fever is suspected. Initial treatment 

is penicillin and salicylates. 

Jansen TL et al: Acute rheumatic fever or post-streptococcal reactive arthritis: a clinical 

problem revisited, Br J Rheumatol 1998;37:335. [PMID: 9566678] 

POLYARTHRITIS 

RHEUMATOID ARTHRITIS 


• Often subacute joint pain. 

• Usually symmetric polyarthritis. 

• Radiographs demonstrate juxta-articular osteoporosis and later cartilage erosions. 


Rheumatoid arthritis generally presents as a symmetric, chronic polyarthritis with 

prominent involvement of proximal interphalangeal and metacarpophalangeal joints, 

often with ulnar deviation. Distal interphalangeal joints are not involved. 


Rheumatoid arthritis is a common cause of subacute joint pain involving multiple joints 

in adults. Although symmetric involvement is classic, the disease may begin with 

asymmetric involvement. In a typical acute presentation, joints may only be warm, 

tender, or swollen. 


Rheumatoid factor is positive in 85% of patients; therefore, a negative test does not rule 

out rheumatoid arthritis. Elevated erythrocyte sedimentation rate and C-reactive protein

are also common but nonspecific findings. 

C. X-ray Findings 

Early x-ray examination generally reveals soft tissue swelling and juxta-articular 

osteoporosis. Erosions are seen later. 

Treatment 

Aspirin and other NSAIDs have proven effective for the initial treatment of rheumatoid 

arthritis. However, the simultaneous administration of other drug classes in addition to 

NSAIDs is now common. For example, steroids, gold, penicillamine, methotrexate, 

cyclosporine, and sulfasalazine are being used. Initial management in the emergency 

department should consist of aspirin or NSAIDs in appropriate doses with urgent 

rheumatologist follow-up or consultation for additional prescriptions if indicated. 

Disposition 

The patient should be referred early to a rheumatologist or primary care physician. 

Consider admission for patients with severe systemic involvement (eg, disabling 

polyarthritis, fever, or weight loss) or vasculitis. 

SPONDYLOARTHROPATHIES 

Spondyloarthropathies are a cluster of chronic inflammatory rheumatic diseases that 

include psoriatic and intestinal arthritis, Reiter syndrome, and ankylosing spondylitis. 

They are not associated with rheumatoid factor but have a strong association with 

HLA-B27. Anatomic sites include the following: the entheses (sites of ligament and 

tendon insertion into bone), the sacroiliac joints, limb joints, and nonarticular sites (eg, 

gut, skin, and eye). 

1. Psoriatic Arthritis & Intestinal Arthritis 


• Common in patients with psoriasis or inflammatory bowel disease. 


Psoriatic arthritis is an inflammatory arthritis seen in 10% of patients with psoriasis. Nail 

involvement (pitting, dystrophy, or onycholysis) is a clue to the diagnosis. The arthritis 

occurs before psoriasis is seen in 15% of patients. 

Intestinal arthritis is an inflammatory arthritis seen in patients with ulcerative colitis or 

Crohn disease. In one study, this form of arthritis occurred in approximately 40% of 

these patients. The arthritis can be in the limb joints or the sacroiliac. 


Initial treatment is with NSAIDs. Sulfasalazine should be added if the patient cannot 

take or does not respond to NSAIDs. 

2. Reiter Syndrome 


• Usually affects young males. 

• Arthritis, conjunctivitis, and urethritis. 

• Arthritis is polyarticular and asymmetric, developing after chlamydial or bacterial 

gastroenteritis. 


Reiter syndrome is a reactive arthritis with the classic triad of arthritis, conjunctivitis, and 

urethritis. It is most commonly seen in men aged 15-35 years. The arthritis affects 

primarily the weight-bearing joints of the lower extremities. 

Reactive arthritis occurs within 1 month of a genitourinary (Chlamydia trachomatis) or 

enteral (Shigella, Salmonella, Yersinia, Campylobacter) infection. It is asymmetric and 

polyarticular. Arthrocentesis reveals a class II inflammatory joint fluid. 


NSAIDs are the mainstay of treatment. Tetracycline improves recovery time for reactive 

arthritis due to Chlamydia but not for enteral causes. The typical reactive arthritis lasts 

4-5 months, but patients can develop chronic or recurrent arthritis. 

3. Ankylosing Spondylitis 


• Patients under age 40 years. 

• Back pain of gradual onset. 

• Stiffness worse in morning. 

• X-rays show sacroiliitis. 


Ankylosing spondylitis is the most common spondyloarthropathy. Its classic findings 

include the following: gradual onset, age less than 40 years, back pain and morning 

stiffness worse with inactivity and made better with exercise, at least 3 months' duration, 

and radiographic evidence of sacroiliitis. Often a history of uveitis can be elicited.

An asymmetrical arthritis is manifested in peripheral joints because areas of enthesitis 

(Achilles and plantar fascia) are commonly involved. Arthrocentesis reveals a class II 

inflammatory joint fluid. Some patients will have constitutional complaints of malaise, 

decreased appetite, and fever. 


NSAIDs and strengthening exercises are used for treatment. Follow-up with a 

rheumatologist should be arranged. 

VIRAL ARTHRITIS 


Viral arthritis is acute, symmetric, and polyarticular. The two most common viruses 

causing secondary arthritis are rubella and hepatitis B. Mumps, adenoviruses, 

enteroviruses, and Epstein-Barr viruses have also been implicated. The arthritis is 

caused by deposition of immune complexes that cause an inflammatory reaction. 


Diagnosis is made by history. Recent viral infection or vaccination aid in diagnosis. The 

most frequently affected joints are the proximal interphalangeal joints, 

metacarpophalangeal joints, knee, and ankle. The symptoms are usually self-limiting 

after several weeks but can last years. 


Treatment is symptomatic and includes NSAIDs. Refer patients to their primary care 

physician. 

SYSTEMIC LUPUS ERYTHEMATOSUS 


• Arthritis associated with other systemic symptoms: rash, fever. 

• Positive anti-double-stranded DNA or positive antinuclear antibody test. 


Almost all patients with systemic lupus erythematosus will have arthritis. Patients 

usually also have fever, rash, or other features of the disease. Diagnosis in patients who 

present only with arthritis requires demonstration of a positive antinuclear antibody test 

or anti-double-stranded DNA along with other criteria set forth by the American 

Rheumatism Association. 


The acute arthritis of systemic lupus erythematosus is treated with NSAIDs. Patients 

should be referred to a rheumatologist for diagnostic evaluation and appropriate care. 

NONARTICULAR RHEUMATISM 

In the emergency evaluation of joint pain, it is important to distinguish between true 

articular (arthritis) and extraarticular (tendonitis and bursitis) causes. The clinical 

features of the common tendonitis and bursitis syndromes are set forth in Table 21-1. 

TENDONITIS 


• Pain and tenderness more localized to the tendon. 

• Although rare, always consider infectious causes of inflammation. 


In contrast to diffuse pain, warmth, and tenderness across an arthritic joint, tendonitis 

generally produces more localized pain that is reproduced with stretching of the affected 

tendon. Tendonitis is thought to be caused by repetitive overuse resulting in damage 

and inflammation to the tendon and surrounding structures. If the history reveals a 

puncture or laceration over a tendon with erythema, pain along the tendon, fever, and 

severe pain on minimal passive tendon motion, an infectious process must be ruled out. 

Treatment 

A. Adjunctive Measures 

Relative rest from exacerbating activities, effective splinting, and ice as needed are the 

mainstays of treatment. NSAIDs and an exercise program to maintain joint motion and 

build muscle strength are helpful. 

B. Local Injection 

Local injection of anesthetic and depot glucocorticoid preparations may be appropriate 

for some patients (see Bursitis, below). However, this procedure should be performed 

only by an individual skilled in the procedure, because complications (eg, local atrophy 

and rupture of the tendon) can result if corticosteroids are errantly injected into a 

weight-bearing tendon. 

C. Antimicrobials 

Suspicion of an infectious tendonitis requires orthopedic consultation for possible 

incision and debridement and hospital admission for appropriate intravenous antibiotics 

to cover presumptive staphylococcal and streptococcal species. 

Disposition

Most patients with tendonitis can receive treatment on an outpatient basis, with referral 

to an orthopedist if necessary. 

BURSITIS 


• Inflammation localized to the bursa, not the entire joint. 

• Common sites involved are elbow and prepatellar area. 

• Consider infection as cause of inflammation, especially if systemic symptoms such as 

fever and chills are present. 


A bursa is a sac normally containing a thin film of synovial fluid that cushions the 

interface between bone with ligaments and the overlying skin. Bursitis is inflammation of 

the bursa. Like tendonitis, bursitis may be due to trauma or infection (most commonly 

found in the olecranon and prepatellar bursa) or may be idiopathic. Clinical findings are 

pain, tenderness, and swelling of the involved bursa. 

Treatment 

A. Aspiration 

The olecranon and prepatellar bursa should be aspirated for diagnosis and treatment if 

fluctuance and infectious signs are present. 


Septic bursitis is usually due to S aureus and, pending results of culture and 

susceptibility testing, should be treated with a penicillinase-resistant, 

ß-lactamase-resistant antimicrobial (eg, nafcillin, 150 mg/kg/d intravenously in 4-6 

divided doses; or cefazolin, 60 mg/kg/d intramuscularly or intravenously in 3 divided 

doses). 

C. Anti-inflammatory Agents 

NSAIDs, combined with rest, are most effective. 

D. Corticosteroid Injection 

Locally injected corticosteroids are useful in treatment of aseptic bursitis. However, 

injections should be given only by physicians skilled in the procedure because 

complications can include infection. 

E. Surgery 

Septic bursitis rarely requires incision and debridement. 

Disposition 

Patients with septic bursitis require intravenous antibiotics either via home parenteral

therapy or in the hospital. Patients with aseptic bursitis may be discharged with primary 

care follow-up within 1 week. 

Almekinders LC, Temple JD: Etiology, diagnosis, and treatment of tendonitis: an 

analysis of the literature. Medicine and Science in Sports and Exercise 1998;30:1183. 

[PMID: 9710855] 

Barth WF, Kinim S: Reactive arthritis (Reiter's syndrome). Am Fam Physician 

1999;60:499. [PMID: 10465225] 

Brent LH: Ankylosing spondylitis and undifferentiated spondyloarthropathy. eMedicine; 

http://www.emedicine.com/med/ topic2700.htm 

Easton BT: Evaluation and treatment of the patient with osteoarthritis. J Fam Pract 

2001;50:791. [PMID: 11674913] 

Jansen TL et al: Acute rheumatic fever or post-streptococcal reactive arthritis: a clinical 

problem revisited. Br J Rheumatol 1998;37:335. [PMID: 9566678] 

Kaplan J: Gout and pseudogout. eMedicine; 

http://www.emedicine.com/emerg/topic221.htm 

Khan MA: Update on spondyloarthropathies. Ann Intern Med 2002;136:896. [PMID: 

12069564] 

Laupland KB, Davies HD: Olecranon septic bursitis managed in an ambulatory setting. 

The Calgary Home Parenteral Therapy Program Study Group. Clin Invest Med 

2001;24:171. [PMID: 11558851] 

Meader RJ: Acute rheumatic fever. eMedicine; 

http://www.emedicine.com/med/topic2922.htm 

Sack K: Monoarthritis: differential diagnosis. Am J Med 1997; 102(Suppl 1A):30S. 

[PMID: 9217557] 

Smith HR: Rheumatoid arthritis. eMedicine; emedicine.com/med/ topic2024.htm 

III. EVALUATION OF THE PATIENT WITH ACUTE BACK PAIN (See 

Figure 21-2.) 

Perform Baseline Evaluation 

An established routine for evaluating patients with acute back pain will ensure that 

life-threatening disease is not missed. Patients who do not fit into the categories below 

have acute back pain due to a nonemergent cause (eg, disk disease, facet syndrome, 

strains, and sprains) without underlying disease. 

A. History 

1. Is trauma present or did a precipitating event occur?—Often the patient reports

trauma or a precipitating event causing acute back pain. In patients with chronic back 

problems, even minor trauma such as a cough can cause acute back pain. 

2. Is visceral disease present?—The emergency physician's first goal should be to 

identify emergent causes of back pain and to exclude nonorthopedic causes (Table 

21-4). Evaluation and treatment should focus then on the organ thought to be involved. 

3. Are red flags present?—Red flags in the history will help the emergency physician 

recognize associated life threats. In patients younger than age 18 years, consider 

spondylolysis, spondylolisthesis, infection, tumor, and developmental disorders. In 

patients older than age 50 years consider aortic abdominal aneurysm, fracture, and 

malignancy first. A history of trauma or chronic steroid use increases the possibility that 

back pain is related to a vertebral fracture. If bowel or bladder incontinence, saddle 

anesthesia, or bilateral neurologic defect is reported, then an epidural compression 

syndrome (ie, spinal cord compression, cauda equina, or conus medullaris syndrome) is 

likely and must be investigated emergently. Weight loss, night pain, fever, chills, history 

of cancer, or intravenous drug use is concerning for malignant or infectious causes of 

back pain. 

4. Is associated arthritis present?—When back pain is associated with arthritis 

(oligoarthritis or polyarthritis), both disorders are usually due to the same cause. For 

example, ankylosing spondylitis commonly causes peripheral and vertebral arthritis 

concurrently. Evaluate these patients and provide treatment as if they had acute 

arthritis. 

5. Is a neurologic deficit present?—A new neurologic deficit in association with back 

pain, saddle anesthesia, or decreased rectal tone may indicate an epidural compression 

syndrome due to infection, tumor, or disk disease and calls for emergent management. 

Seek consultation with a neurosurgeon immediately, and consider magnetic resonance 

imaging (MRI). These patients may require hospitalization for diagnosis and treatment. 

6. Does the pain have a radicular distribution?—Unilateral back pain in a nerve root 

distribution suggests preeruptive zoster or nerve root compression. Refer the patient for 

follow-up care after providing appropriate analgesics. 

B. Examination 

Examine the back for deformity, tenderness, and range of motion; test for limitation of 

straight-leg raising and evaluate gait. Examine the heart, peripheral pulses, lungs, and 

abdomen. Perform a neurologic evaluation that includes reflexes, muscle strength, 

sensory examination of the legs and perineum, and assessment of rectal sphincter 

strength. Pay particular attention to vital signs because fever, tachycardia, or 

hypotension suggest a serious or possibly life-threatening cause of back pain. A rectal 

examination does not have to be performed in every patient with back pain, but it must 

be performed in all patients who have neurologic complaints or deficits. Red flags in the 

physical examination include decreased rectal tone, saddle anesthesia, motor 

weakness, and absent reflexes. These findings indicate possible epidural compression 

syndrome. A herniated disc is strongly suggested in the setting of diminished reflexes 

and positive straight-leg and crossed straight-leg raise tests.

C. X-ray and Laboratory Findings 

Obtain plain x-rays of the spine for patients with trauma and spinal tenderness, for 

children or adolescents with atraumatic back pain, and when red flags for infection or 

malignancy are present. MRI may be indicated to rule out an epidural compression 

syndrome. Laboratory studies such as complete blood count (CBC) with differential, 

erythrocyte sedimentation rate, and urinalysis should be performed if red flags are 

present. Patients with uncomplicated acute lumbosacral strains of less than 1 month's 

duration usually do not require imaging or laboratory testing. 

D. Disposition 

See below under specific conditions. 

IV. EMERGENCY TREATMENT OF SPECIFIC CONDITIONS CAUSING 

BACK PAIN 

TRAUMATIC BACK PAIN 

Back pain associated with trauma may imply a fracture or dislocation of the thoracic or 

lumbar spine. The patient should remain flat on his or her back and be moved only by 

logroll. Perform a careful examination for other injuries. After the examination is 

completed, logroll the patient, maintaining in-line spinal immobilization. If a spine board 

is present, remove it at this time to avoid soft tissue injury. With the patient on his or her 

side, carefully palpate the thoracic and lumbar spine for tenderness and deformity, and 

perform a rectal exam. Roll the patient back to a supine position, and obtain a careful 

neurologic exam. Order thoracic and lumbar spine x-rays if appropriate. Other 

evaluation and treatment should proceed as indicated depending on the injuries present 

(Chapters 10 and 27). 

ACUTE LUMBOSACRAL STRAIN & CHRONIC DEGENERATIVE DISK DISEASE 


• Often pain develops after lifting or twisting. 

• No associated constitutional symptoms (such as fever or weight loss). 

• Normal neurologic examination. 

• X-rays may show evidence of chronic degenerative disk disease. 



Acute lumbosacral strain and chronic degenerative disk disease differ only in their 

chronicity. The pain is typically a deep steady pain in the mid or low back that may be 

episodic. It is commonly unilateral and may radiate into the buttocks and posterior thigh. 

Pain is relieved by bed rest and aggravated by activity. There should be no red flags in 

the history or physical exam.

B. Physical Examination 

The physical examination may show normal results or may disclose one or more of the 

following: increased lumbar lordosis, scoliosis, limited back motion, asymmetric lateral 

bending, local deep tenderness, or tight hamstring muscles. Red flags, including 

positive stretch tests, are not present. 


CBC, urinalysis, and erythrocyte sedimentation rate are not indicated. If obtained, they 

are normal. 

D. X-ray Findings 

X-rays are not indicated. If obtained, they may be normal or may show one or more of 

the following signs of degenerative disk disease: disk space narrowing, horizontal 

anterior osteophytes, spondylolisthesis, posterior facet subluxation, sclerosis, or spurs. 

Treatment 

A. Analgesics 

Give drugs (NSAIDs or acetaminophen). Consider the COX-2 inhibitors or muscle 

relaxers for patients who cannot tolerate NSAIDS. If opioids are required, limit duration 

to less than 1 week and arrange close follow-up. If adequate pain control is not possible 

in the emergency department, consider hospitalization. 

B. Bed Rest 

Bed rest is no longer indicated. Patients should resume normal activities as tolerated by 

pain. Research indicates that back exercises are not beneficial in the acute setting, and 

patients who perform activities as tolerated recover more quickly than those who are on 

bed rest. 

C. Muscle Relaxers 

If spasm of the lumbar musculature is present, muscle relaxers for the first several days 

may be helpful. These agents may cause sedation. 

D. Diet 

Weight loss is important if obesity is a causative factor in acute lumbosacral strain. 

Disposition 

Hospitalization is rarely required. Refer the patient to a primary care physician or 

orthopedist if symptoms do not improve within 2 weeks. Patients must have instructions 

to return to the emergency department or their physician if any of the following red flags 

develop: new neurologic symptoms, bowel or bladder incontinence, worsening pain, 

fever, or night pain. 

SCIATICA 


• Often acute on chronic flare-ups of pain. 

• Radiation of pain in radicular fashion along the distribution of the sciatic nerve. 

• Positive straight- and crossed-leg raise tests. 

Sciatica usually represents an acute episode in a chronic degenerative process. 

Patients may have a history of chronic episodic low back pain. 


Pain usually begins abruptly, often with trivial trauma such as sneezing. The pain is 

often described as stabbing or shooting; is worse with coughing, Valsalva maneuver, or 

sitting; and is often incapacitating. Radiation in the distribution of the sciatic nerve is 

common. The main distinguishing feature of sciatica is radicular pain that extends below 

the knee. It affects 2% of patients with acute low back pain. In most cases it is caused 

by herniation of the nucleus pulposus, known most commonly as a herniated disc, that 

compresses a nerve root. Sciatica is 88% specific for a herniated disc. Other causes 

include intraspinal tumor or infection, foraminal stenosis, piriformis syndrome, and 

lumbar spinal stenosis. 

The radicular pain is usually only in one leg and may be characterized by paresthesias, 

loss of sensation, or motor weakness (Table 21-5); 95% of herniated discs occur at the 

L4-L5 or L5-S1 levels. The most common pathologic findings of the L5 nerve root are 

foot drop, loss of dorsiflexion of the great toe, and pain in the great toe. Findings in S1 

include heel pain, decreased plantar flexion of the great toe, and decreased ankle jerk. 

The difference between lumbosacral strain and sciatica is the presence of abnormal 

neurologic findings, pain below the knee, and positive straight-leg and crossed 

straight-leg raise tests in the latter case. Plain x-rays and laboratory evaluation are not 

indicated for sciatica unless associated red flags for fracture, malignancy, infection, or 

epidural compression syndrome are present. 


Treatment is nearly the same as that for lumbosacral strain, including instructions for 

activity as limited only by pain. Opioids may need to be used more frequently in the 

short term. The only treatment difference is that selected patients with sciatica may 

need epidural steroid injections. Systemic steroids have no proven benefit. 

Approximately 80% of patients with a herniated disc improve without surgery. Only 

5-10% will require surgery. More than 50% will improve within 6 weeks with 

conservative therapy. Therefore, patients meeting the criteria for sciatica alone may be 

safely discharged to follow up with their primary physician in 2 weeks and return to the 

emergency department for the same reasons as listed under lumbosacral strain. 

Back Pain in Children 

A child who presents with back pain should be evaluated carefully. Red flags include 

decreased activity secondary to pain, fever, and nocturnal pain. These are possible

indicators of tumor or infection. If the child has recently been involved in strenuous 

sports or exercise programs, consider spondylolysis and spondylolisthesis. Bacteremia 

increases the risk of spinal infections. Therefore, a history of recent febrile illness is 

important. Spine x-rays should be taken of virtually every child who presents with back 

pain. Consider obtaining CBC, urinalysis, and erythrocyte sedimentation rate if any red 

flags are raised. Consider admission for further workup and observation. 

EPIDURAL COMPRESSION SYNDROME 


• Bowel or bladder incontinence. 

• Saddle anesthesia, decreased or absent rectal sphincter tone, lower extremity deficits. 


Epidural compression syndrome is a true emergency. Consider this possibility in every 

patient who presents with back pain. Red flags in the history and physical examination 

are used to screen for this syndrome. The hallmark symptoms include urinary retention 

marked by overflow incontinence, saddle anesthesia, decreased rectal tone, and 

bilateral motor and sensory deficits. If any of these red flags is present, obtain a urinary 

postvoid residual. If the postvoid residual is less than 50-100 mL, then cauda equina 

syndrome can usually be ruled out (negative predictive value is 99.99%). However, if a 

patient has other significant red flags, pursue an epidural compression syndrome with 

imaging regardless of a normal postvoid residual. Causes include a large central disc 

herniation, tumors, trauma, epidural abscess, and hematomas. 


If an epidural compression syndrome is likely, start steroid therapy immediately before 

waiting for confirmatory MRI results. Dexamethasone is usually given in doses ranging 

between 10 mg and 100 mg intravenously depending on severity and rapidity of 

presentation and progression. The next step is to consult a neurosurgeon while ordering 

an emergent MRI. If unable to obtain an MRI scan, order a CT (computed tomography) 

scan with myelography. 

FACET SYNDROME 

Excessive overriding of lumbar or thoracic facets usually occurs as a consequence of 

disk space narrowing associated with degenerative disk disease. Facet syndrome is 

unusual and episodic and is characterized by the onset of acute scoliosis after 

asymmetric lifting. The diagnosis is usually made by exclusion. Patients should be 

instructed in the fundamentals of proper back care. 

SPINAL INFECTIONS (See also Chapter 40.)


• Usually occurs in patients with predisposition for infections: diabetic patients, 

intravenous drug users, transplant patients, cancer patients. 

• Fever and back pain are the hallmarks. 

• MRI or CT scan of the spine is essential. 


Disk space infections today are most commonly seen in intravenous drug users, 

diabetics, transplant patients, and cancer patients. Vertebral osteomyelitis should be 

suspected in patients who have recently undergone spinal surgery and present with red 

flags for infection. Epidural abscess and vertebral osteomyelitis are the most common 

spinal infections. The organism most commonly implicated is S aureus. 


Red flags for disk space infections are night pain, cough pain, night sweats, fever, and 

an elevated erythrocyte sedimentation rate. Be alert for the rare low-grade presentations 

of tuberculous and fungal diskitis. Systemic evidence of infection is usually present. 

The typical x-ray changes of disk space narrowing with adjacent vertebral end-plate 

destruction do not appear until 10-14 days after onset of symptoms. Bone scans are 

usually positive early in the illness before x-ray changes appear. Epidural or 

paraspinous abscess may appear as an ill-defined mass on x-ray. If a spinal infection is 

suspected, an MRI scan (gold standard) or CT scan must be ordered. Blood and urine 

cultures should also be collected. 


Spinal infections require hospitalization and orthopedic consultation, needle aspiration 

for bacteriologic diagnosis, and appropriate antibiotics. Occasionally surgical drainage is 

required. 

A neurologic deficit in association with signs of spinal infection often means that an 

epidural or paraspinous abscess is present. This is a major emergency demanding 

immediate MRI or CT myelography, consultation, hospitalization, and possibly emergent 

decompression. 

ANKYLOSING SPONDYLITIS 

See above for details of diagnosis, treatment, and disposition. 

NEOPLASM 

Metastatic tumor is the most common neoplastic process causing back pain. Bone 

marrow tumors such as multiple myeloma are second in frequency. Primary tumors of

the spinal column or spinal cord are rare. 

Fifty percent of bone must be lost before a lesion is evident on plain x-rays. Multiple 

lesions are common. Bone scan is more sensitive for early diagnosis. 

Red flags are weight loss; night pain in the absence of day pain; and a history of 

insidious and progressive pain that has not responded to conservative measures, 

especially in elderly patients. Laboratory findings may include an elevated erythrocyte 

sedimentation rate, significant anemia, proteinemia, and findings in other organ systems 

that suggest neoplasm. 

ZOSTER 

Preeruptive zoster may mimic degenerative disk disease. The pain of zoster is burning 

and dysesthetic, with striking unilateral radicular distribution that does not cross the 

midline. Skin hyperesthesia over the painful area is the earliest physical finding. See 

Chapter 46 for details. 

Aree D et al: Recognizing spinal cord emergencies. Am Fam Physician 2001;64:631. 

[PMID: 11529262] 

Della-Giustina D et al: Back pain: cost-effective strategies for distinguishing between 

benign and life-threatening causes. Emergency Medicine Practice 2000;2(2):1. 

Della-Giustina DA: Emergency department evaluation and treatment of back pain. 

Emerg Med Clin North Am 1999;17: 877. [PMID: 10584107] 





I. EVALUATION OF THE PATIENT WITH ACUTE ARTHRITIS (See Figure 

21-1.)

Table 21-1. Some common syndromes of nonarticular rheumatism. 

History X-Rays Treatment 1 

Severe pain, 

subacromial 

with or 

without 

midarm pain, 

worse with 

abduction. 

Moderate 

pain with use 

of thumb and 

grip on radial 

side of wrist. 

Pain over hip 

and thigh. 

Swollen 

knee; pain 

occasionally. 

Negative, or calcific deposit 

overlying greater tuberosity 

Local infiltration of 

corticosteroid. Physical 

therapy to preserve motion. 

Resistance to elbow flexion 

and extension reproduces pain. 

Point tenderness over bicipital 

groove. 

Bicipital tendinitis Elbow 

Negative Usually responds to local 

corticosteroid injection. Splint 

early; then mobilize. 

Negative Rest. Local corticosteroid 

infiltration. 

Negative Rest. Local injection of 

corticosteroids for resistant 

cases. 

Tenderness of patella. Patellofemoral 

chondromalacia 

TABLES 

Table 21-1. Some common syndromes of nonarticular rheumatism. 

1 Nonsteroidal anti-inflam 

agents such as ibuprofe 

naproxen may be useful 

of these conditions.

Table 21-2. Classification of abnormal synovial fluid. 

Viscosity Color 

Gram Stain 

and Culture 

Normal 

High Light yellow Negative Inflammatory 

Low Dark yellow Usually positive 1 Hemorrhagic (class IV) 

2 Many red cells also found. 





TABLES 

Table 21-2. Classification of abnormal synovial fluid.

Table 21-3. Revised Jones criteria for diagnosis of rheumatic fever. 1 

1 The presence of 2 major or 1 major and 2 minor criteria with 

supporting evidence of recent infection with group A streptococcus 

indicates a high probability of rheumatic fever. 





TABLES 

Table 21-3. Revised Jones criteria for diagnosis of rheumatic fever.

Table 21-4. Nonorthopedic (visceral) causes of acute back pain. 

Common Clinical Findings 

Flank pain, fever, pyuria, dysuria 

Flank pain, hematuria 

Hypotension, pulsatile mass, abnormal emergency bedside 

ultrasound or CT, scan 

Absent pulses, hematuria, abnormal chest x-ray 

Elevated serum amylase; tender abdomen, pancreatic calcification 

Tender abdomen, air under diaphragm 





TABLES 

Table 21-4. Nonorthopedic (visceral) causes of acute back pain.

Table 21-5. Neurologic findings in herniated lumbosacral disk. 

Root Sensory Findings 

Sc 

Stretc 

S1 Decreased response on lateral side of foot and 

leg 

Strongly positive 

L5 Decreased response on mid dorsum of foot Moderately positive 

L4 Decreased response on medial foot and 

anteromedial leg 

May be negative 





TABLES 

Table 21-5. Neurologic findings in herniated lumbosacral disk.

Figure 21-1. Assessment of patients with acute joint pain. 





FIGURES 

Figure 21-1

Figure 21-2. Assessment of patients with acute back pain. 





FIGURES 

Figure 21-2


22. Head Injuries - Stephen C. Ausband, MD, FACEP, & Ritu Sahni, MD, 

MPH 


Cervical Spine Immobilization 

Any patient with blunt force injury to the head should be suspected of having cervical 

spine injury until proven otherwise. Penetrating injuries to the torso and extremities not 

associated with blunt force are rarely associated with cervical spine injury. Cervical 

spine injury is associated with 5% of all blunt force injuries to the head; the greater the 

force, the greater the incidence of associated cervical spine injury. Immobilization of the 

cervical spine must include an appropriately sized and fitted cervical collar; head blocks; 

and a long, rigid spine board to which the patient is secured. Immobilize the cervical 

spine during evaluation by manual stabilization and logrolling the patient. Do not apply 

traction to the cervical spine. 

Airway 

Hypoxia is associated with increased morbidity and mortality in trauma patients. 

Hypoxia must be avoided or corrected immediately. All patients with traumatic head 

injury should receive 100% oxygen by high-flow nonrebreathing mask as initial therapy. 

Keep the airway clear by suctioning of blood and secretions as needed. Remove foreign 

bodies, avulsed teeth, and dental appliances. Loss of gag reflex, inability to adequately 

clear secretions, or GCS score of 8 or less are all indications to secure the airway with 

an endotracheal tube. Use clinical judgment to determine if a patient needs to be 

intubated in other situations, with priority on maintaining the airway during resuscitation, 

evaluation, and transport. Ventilate apneic or hypoventilating patients with an Ambu bag 

and 100% oxygen until intubation can be accomplished. Avoid using a bag to provide 

positive-pressure ventilation to an actively breathing patient because this induces 

gastric distention. 

Perform intubation while maintaining manual in-line cervical immobilization without 

applying traction. Rapid sequence intubation should be strongly considered for all 

patients. Once sedatives and paralytics have taken effect, remove the cervical collar 

and maintain manual stabilization. After intubation, replace the cervical collar. 

Orotracheal intubation is preferred because of the technical difficulty of nasotracheal 

intubation as well as the complications of bleeding, elevated intracranial pressure, and 

possible passage of the endotracheal tube through a fractured cribiform plate into the 

cranium. If orotracheal intubation is not successful, intubate the patient using a 

retrograde Seldinger technique, fiberoptic-guided intubation, or cricothyroidotomy 

depending on the equipment available immediately and the procedures with which the 

physician is most skilled. In addition, consider a temporizing device, such as a laryngeal

mask airway, in the patient who is difficult to intubate. After intubation, confirm 

endotracheal tube position by auscultation over the lung fields and epigastrium. 

Additional devices, such as color capnometers and aspiration devices may be used to 

confirm tube placement. Data show that any single test of endotracheal tube position is 

substantially less accurate than using 2 tests of position. Immediate portable chest 

X-ray must also be used to visualize endotracheal tube position. After successful 

intubation, place an orogastric tube. Avoid nasogastric tubes in patients with head 

trauma for the same reasons that nasotracheal intubation is to be avoided. 

Any change in the patient's condition or oxygen saturation and any substantial 

movement of the patient, such as to or from a computed tomography (CT) gantry, 

necessitates reevaluation of the endotracheal tube position by auscultation. 

The emergency physician must be familiar with advanced airway techniques to be able 

to perform rapid sequence intubation and guarantee definitive airway access in any 

patient. 

Breathing 

Once the airway is secured by intubation, assess the patient's respiratory status with an 

arterial blood gas. Use serial arterial blood gases or end-tidal carbon dioxide monitoring 

to maintain arterial PCO 2 level in the normal physiologic range. Hypercapnia is 

associated with increased morbidity and mortality. Hypocapnia is associated with 

decreased cerebral blood flow and decreased cerebral oxygen perfusion. Patients 

should not be hyperventilated in order to decrease PCO 2 levels, and PCO 2 should be 

maintained at 35 mm Hg or more. Frequently reassess the respiratory status of patients 

who do not require intubation. All patients with head trauma should be monitored with 

transcutaneous pulse oximetry during evaluation. 

Circulation 

Hypotension is associated with increased morbidity and mortality in trauma patients. 

Care should be taken to maintain an adequate blood pressure, defined as a mean 

arterial pressure greater than 90 mm Hg. Treat shock aggressively with warmed 

intravenous lactated Ringer's or normal saline and blood products as needed. Avoid 

hypotonic fluids. Avoid glucose-containing fluids because of the risk of hyperglycemia, 

which is deleterious to the injured brain. Do not attribute hypotension to head injury 

alone. Elevated blood pressure associated with bradycardia is a sign of increased 

intracranial pressure. 

Disability 

Establish a Glasgow Coma Scale (GCS) for any patient with a head injury. Repeat the 

GCS periodically during reassessment. In addition, measure pupillary response and 

symmetry and also consider doll's eye (oculocephalic) movements and caloric 

stimulation (oculovestibular) tests, if needed, to gauge the patient's level of cortical and 

brain-stem functioning. Note any asymmetry in neurologic examination or focal 

neurologic findings. In an unresponsive patient, motor response may be elicited by 

nailbed pressure. If motor responses are asymmetric, the best response is a more

accurate predictor of outcome and should be used for calculating the GCS. Document 

initial neurologic examination findings prior to administering sedative or paralytic agents, 

if possible. 

As for any patient with altered mental status, the clinician is advised to check for and 

treat any easily reversible causes of decreased level of consciousness, including 

hypoglycemia (bedside fingerstick blood glucose); hypoxemia (pulse oximetry); narcotic 

overdose (naloxone administration); and, in malnourished or alcoholic patients, 

Wernicke encephalopathy (thiamine administration). 

Exposure 

As with all trauma patients, the patient should be completely undressed and the entire 

body examined, including the back. Once initial examination is complete, cover the 

patient with warm blankets. Take care to avoid hypothermia by warming the 

examination room and using warm blankets and warm fluids. Rewarm the patient if he 

or she is already hypothermic. 

MANAGEMENT OF OTHER SYMPTOMS 

Seizures 

Seizure prophylaxis should be considered in patients with an initial GCS of 8 or less and 

in those with cerebral contusion, depressed skull fracture, intracranial hematoma, or 

penetrating head wound. In adults, phenytoin, phosphenytoin, or carbamazepine are the 

prophylactic drugs of choice. In children, phenobarbital has been used prophylactically. 

Treat any acute posttraumatic seizure rapidly with lorazepam, phenytoin, 

phosphenytoin, or phenobarbital to prevent worsening hypoxemia associated with the 

seizure and to limit secondary brain injury. 

Combativeness 

Evaluate a combative patient first for hypoxia, hypotension, hypoglycemia, and pain. 

Avoid physical restraints if possible, or, if needed, use them only long enough to allow 

for proper sedation and analgesic administration. Patients should never be allowed to 

struggle against restraints. Occasionally, patients who cannot be controlled with 

sedation and analgesia alone will require paralysis and endotracheal intubation for 

protection of the spine and to accomplish diagnostic studies. 

Pain Control 

After initial evaluation, do not withhold sedatives and analgesics. Narcotics and 

benzodiazepines are safe and effective medications for sedation and analgesia and 

should be used in doses high enough to be effective. Care must be taken to ensure that 

patients who are paralyzed and intubated have sufficient analgesic and sedative 

medications. 

Systemic Hypertension

If blood pressures are elevated, evaluate the patient for adequate sedation and 

analgesia. Hypertension associated with bradycardia is a sign of elevated intracranial 

pressures. Isolated systemic hypertension that is high enough to constitute a 

hypertensive urgency or emergency is rare. If present, systemic hypertension should be 

treated with caution to avoid rapid decrease in blood pressure or decrease in blood 

pressure below 10% of initial values. 

Intracranial Hypertension 

Elevations of intracranial pressure are heralded by bradycardia and hypertension, signs 

of transtentorial herniation, or progressive neurologic deterioration without other 

attributable cause. Mannitol is the drug of choice for treating elevated intracranial 

pressure. It is vitally important to maintain serum osmolality below 320 mOsm and to 

maintain euvolemia with intravenous fluid replacement during mannitol administration. 

Elevation of serum osmolality above 320 mOsm can lead to a reversal of the osmotic 

gradient with subsequent increase in cerebral edema. Mannitol administration should be 

initiated in consultation with a neurosurgeon, if possible. 

Gruen P, Liu C: Current trends in the management of head injury. Emerg Med Clin 

North Am 1998;16:63. [PMID: 9496315] 

EMERGENCY TREATMENT OF SPECIFIC HEAD INJURIES 

SOFT TISSUE INJURIES 

Although often dramatic in nature, soft tissue injuries of the head cause little long-term 

sequelae and most can be easily managed in the emergency department. However, soft 

tissue injuries of the head can be an indicator of possible significant intracranial injury. 

For example, one study found that any sign of trauma above the clavicles is an 

independent predicator of possible intracranial abnormality on CT scan. BR> 

1. Scalp Lacerations 


• Diagnosed through thorough inspection and palpation. 

• May be significant source of blood loss. 

• Evaluate for underlying skull fracture. 


Scalp lacerations are primarily diagnosed by palpation and a visual inspection of the 

patient's scalp. A complete and thorough examination of the scalp must be performed to 

find any evidence of laceration or hematoma. Once a laceration is located, palpate the 

area thoroughly to determine if any signs of skull fracture are present. Because the 

scalp has tremendous vascularity, scalp lacerations can be a source of significant blood 

loss.

Treatment 

Most scalp lacerations can be easily closed with either staples or simple interrupted 

sutures. Clipping of the hair may facilitate easier closure. Alternatively, water-soluble 

lubricating jelly (eg, Surgilube) may be used to keep hair out of the laceration during 

closure. Shaving of the scalp may lead to increased risk of infection. The scalp is highly 

vascular and may be closed up to 12 hours after initial injury. Any patient with a scalp 

laceration and significant traumatic mechanism or alteration of consciousness should 

undergo CT scanning prior to closure of the scalp laceration. The wound should be 

copiously irrigated with normal saline before closure. Occasionally, layered closure with 

absorbent sutures may be required (Chapter 30). 

Disposition 

Patients with scalp lacerations and no other complications may be discharged safely to 

home. Follow-up should occur in 3-5 days for recheck; the staples or sutures may be 

removed in 10-14 days. 

2. Hematoma 


• Diagnosed by inspection and palpation. 

• Strongly consider CT scan. 


Scalp hematoma is diagnosed by palpation and visual inspection. A hematoma has little 

long-term significance on its own but may be an indicator of more serious intracranial 

abnormality. Patients with scalp hematoma and significant mechanism of injury or 

alteration in level of consciousness should undergo CT scanning. 

Treatment 

A scalp hematoma is treated primarily like a hematoma or contusion in any other part of 

the body. Ice, elevation, and nonsteroidal anti-inflammatory drugs should be the 

mainstay of treatment. Aspiration of a scalp hematoma has little, if any, benefit and 

should rarely be attempted. 

Disposition 

Patients with only a scalp hematoma may be safely discharged home and referred for 

standard follow-up. 

SKULL FRACTURES 

Skull fracture is strongly associated with other more serious intracranial abnormalities.

Studies have shown that 40-100% of all intracranial abnormalities are associated with 

skull fracture. The skull fracture itself, however, is typically of little clinical consequence 

to the patient. 

1. Closed Skull Fractures 


• Use CT scan for diagnosis because CT shows fractures and other associated injuries. 

• Admit for observation. 


Closed fractures of the skull are detected primarily on noncontrast CT scan. Because 

these fractures are often associated with more serious injury, it is prudent to evaluate 

the injury with CT scan rather than plain skull x-rays. 

Treatment 

There is no specific treatment for linear skull fractures. Close observation is 

recommended to detect the development of an epidural hematoma after an initially 

negative CT scan. 

Disposition 

Patients with isolated closed skull fractures with no evidence of brain injury require 

admission to the hospital for a minimum of 24 hours of observation. 

2. Open Skull Fractures 



• Underlie scalp lacerations. 

• High risk of infection. 


Open fractures underlie scalp lacerations and are often palpated during evaluation of 

the scalp laceration. These fractures have a serious risk of infection. Definitive diagnosis 

is made with noncontrast CT scan, and more serious intracranial abnormality should be 

ruled out. Open skull fracture is likely if pneumocephalus is noted on CT scan (Figure 

22-1). 

Treatment

Initiate intravenous antibiotics such as cefazolin, and refer the patient to the appropriate 

surgical subspecialty for possible operative debridement. 

Disposition 

Hospitalize all patients with open skull fracture. 

3. Depressed Skull Fractures 


• Often found with inspection or palpation. 



Depressed skull fractures are often palpable or visible during examination. However, 

swelling around the area of the injury can mask a depressed skull fracture and make it 

appear to be a simple hematoma. Like all skull fractures, depressed skull fractures are 

often associated with more serious intracranial injury, and patients need to be evaluated 

accordingly. Noncontrast CT scan is the test of choice to determine whether the patient 

has intracranial injury or depressed skull fracture (Figure 22-2). 

Treatment 

Depressed skull fractures without intracranial injury represent a cosmetic situation. 

Open depressed skull fractures are at high risk of infection, similar to open 

nondepressed skull fractures. 

Disposition 

Patients should be admitted to the hospital for observation and referred to the 

appropriate surgical subspecialist for possible elevation of the depression and 

debridement if the fracture is open. 

4. Basilar Skull Fractures 


• Use CT scan for diagnosis because CT shows fractures and other associated injuries; 

may be missed on CT. 

• Associated with hemotympanum, Battle sign, raccoon's eyes, cerebrospinal fluid 

leaking from ear or nose, or hearing loss.


Basilar skull fractures are skull fractures at the base of the skull, typically at the petrous 

portion of the temporal bone. Clinical signs include hemotympanum, Battle sign 

(ecchymosis along the mastoid area of the skull), raccoon's eyes (periorbital 

ecchymosis), cerebrospinal fluid leak from the nose or ear, or hearing loss. Patients with 

any of these signs should undergo noncontrast CT evaluation for possible basilar skull 

fracture and to rule out more serious intracranial abnormality. 

Treatment 

Initiate intravenous antibiotics such as cefazolin. 

Disposition 

Patients with documented basilar skull fracture or significant signs of a basilar skull 

fracture should be admitted for observation. If a more serious intracranial abnormality is 

present, obtain neurosurgical consultation. 

INTRACRANIAL INJURY 

The primary goal in evaluating patients with potential head injury is to determine if an 

intracranial abnormality is present and then to determine if that injury requires surgical 

intervention. There has long been controversy as to which patients require CT scanning. 

Of patients presenting to the emergency department with head injury and a GCS of 15, 

6-8% have an intracranial abnormality. The vast majority of these injuries are 

nonsurgical, but they may have long-term cognitive implications for the patient. There 

are currently few recommendations as to when a patient requires CT scanning. The 

emerging practice is to obtain a CT scan whenever a patient has had an alteration in the 

level of consciousness at any time or amnesia to the event of injury. There have been 

some prospective validations of criteria that may allow CT scan to be safely foregone in 

a small percentage of these patients. However, it is difficult to determine which patients 

with a GCS of 15 will have intracranial abnormalities. 

1. Epidural Hematoma 


• Brief loss of consciousness followed by transient lucid interval. 

• Arterial bleeding source. 

• Diagnosis made by CT scan, which shows a biconvex hematoma. 

• Requires rapid neurologic evaluation for decompression. 

An epidural hematoma is a collection of blood and clot between the dura mater and the 

bones of the skull. Sources of bleeding from epidural hematoma include the meningeal 

arteries (often the middle meningeal artery) or occasionally the dural venous sinuses. 

These bleeds generally have a lenticular (biconvex) shape. Patients with epidural

hematoma may have an initial, brief loss of consciousness followed by a lucid interval 

during which they may be neurologically intact. This interval is then followed by rapid 

clinical deterioration. All patients with epidural hematoma typically require rapid 

intervention by a neurosurgical specialist. An epidural hematoma represents a 

space-occupying lesion to the brain, often from a high-pressure arterial source. 

Therefore, rapid expansion of this hematoma can lead to herniation of brain contents. 

Patient outcome is related directly to the patient's level of consciousness on 

presentation and to the time until decompression of potential space-occupying lesions 


2. Subdural Hematoma 


• Venous bleeding source. 

• Diagnosis made by CT scan, which shows concave hematoma. 

• May be chronic, acute, or acute on chronic. 

• Admit for neurosurgical evaluation. 

A subdural hematoma also represents a space-occupying lesion. This lesion, however, 

lies in the space between the dura mater and the arachnoid mater and usually conforms 

to the convexity of underlying cerebral cortex (Figure 22-4). The source of bleeding is 

often the bridging veins, which are more likely to tear in patients with significant brain 

atrophy (eg, elderly or alcoholic patients). These patients can develop large chronic 

subdural hematomas with minimal neurologic deficit. A subdural hematoma may or may 

not require surgical drainage. Acute bleeds can develop in areas of chronic subdural 

hematoma (often from new trauma) and cause neurologic deterioration (Figure 22-5). All 

patients with subdural hematoma should receive prompt neurosurgical evaluation. 

3. Cerebral Contusion 


• Diagnosis made by CT scan. 

• Associated edema may require intervention. 

Cerebral contusion represents a non-space-occupying discrete lesion within the brain 

matter itself. These lesions are less likely to lead to herniation than are other types of 

intracranial lesions. Significant edema can occur around areas of cerebral contusion, 

which can lead to increased intracranial pressure and midline shift. Typically no surgical 

intervention is required for cerebral contusion. However, if the contusion is large enough 

and significant shift occurs, then intracranial pressure monitoring may be instituted by 

the neurosurgical specialist. 

4. Traumatic Subarachnoid Hemorrhage


• Diagnosis made by CT scan. 

• Can lead to elevated intracranial pressure owing to cerebrospinal fluid obstruction. 

It was once thought that subarachnoid hemorrhage was relatively rare and had a poor 

outcome. However, it appears now that subarachnoid hemorrhage in a traumatic setting 

is much more common than previously believed. Traumatic subarachnoid hemorrhage 

is not a space-occupying lesion but can lead to increasing intracranial pressure, 

primarily by blocking the outflow of cerebrospinal fluid from the 3rd and 4th ventricles in 

the brain. Patients with asymptomatic subarachnoid hemorrhage may be admitted for 

observation and no further intervention. Patients with altered level of consciousness or 

other neurologic findings may require intracranial pressure monitoring in the critical care 

unit setting (Figure 22-6). 

5. Diffuse Axonal Injury 


• Diagnosis made by burring of gray- to white-matter margin, punctate cerebral 

hemorrhages, or cerebral edema. 

• Associated with posttraumatic coma. 

Shearing forces from sudden deceleration during blunt trauma can cause severe 

intracranial injury. Diffuse axonal injury is a frequent cause of posttraumatic coma. This 

injury is typically manifested on noncontrast CT by a blurring of the margin between the 

gray and white matter, punctate hemorrhages often in the internal capsule, and cerebral 

edema (Figure 22-7). 

MINOR HEAD INJURIES 

The vast majority of patients with head injury who present to the emergency department 

have minor head injuries. One study found no significant intracranial injuries in the 

absence of all of the following findings: headache, vomiting, age greater than 60 years, 

intoxication, deficits in short-term memory (anterograde amnesia), physical evidence of 

trauma above the clavicles, and seizure. The negative predictive value of the absence 

of these clinical variables was 100%. 

The first goal in caring for a patient with a head injury is to determine if a significant or 

serious intracranial mass lesion is present. Once serious injury is ruled out by 

examination, history, or CT scan, the patient falls into the category of minor head injury. 

Remember that any patient with amnesia to the event or any history of alteration of level 

of consciousness or loss of consciousness should undergo CT scanning. Patients who 

present with minor head injury complaints and have a negative CT scan and are

neurologically completely normal may be discharged to home, especially if in the care of 

a responsible adult. 

A significant question often arises regarding whether the injury is a concussion and what 

type of postconcussion restrictions are needed. Concussion is often wrongly thought of 

as transient loss of consciousness if CT findings are negative. Most current precaution 

guidelines, of which there are many, consider concussion to be a trauma-induced 

alteration in mental status that may or may not include loss of consciousness. The 

primary hallmarks of concussion are confusion and amnesia. Concussion is of 

significant importance because long-term neuropsychiatric testing on athletes who have 

sustained frequent concussions has shown that multiple concussions over a lifetime can 

lead to cognitive impairment. As a result, guidelines have been developed that grade 

concussion and recommend activity level by an athlete who undergoes concussion. 

Although these guidelines have not been fully used with non-athlete patients, some of 

these guidelines can be used to guide the outcome of non-athlete patients. Current 

guidelines have divided concussions into three grades (Table 22-1). The length of time 

the athlete or patient should refrain from strenuous activity is based on both the grade of 

the concussion and the history of prior concussions. Patients with a history of prior 

concussions have longer restrictions. Current recommendations for immediate 

treatment and restrictions are also available. 

Postconcussion syndrome is characterized by headache, dizziness, and cognitive 

impairment (memory) and occurs acutely in 50% of patients experiencing a mild 

traumatic brain injury. These symptoms can occur singly or with other symptoms, and 

they generally resolve over the initial weeks to months after a concussion. 

SPECIAL CONSIDERATIONS FOR PEDIATRICS 

Although it is difficult to determine when adult patients need further workup, the question 

is even more difficult to resolve for pediatric patients. Smaller children (younger than 

age 2 years) are even more difficult to evaluate for possible loss of consciousness, 

transient confusion, and amnesia. Some conservative guidelines favor obtaining 

noncontrast CT scan on any child under age 2 years with any sign of trauma to the 

head, including minor hematomas and scratches. A more traditional approach has been 

to obtain imaging studies only for children with a history of loss of consciousness, 

altered mental status, vomiting, seizures, or focal neurologic deficits after a traumatic 

event. 

INDICATIONS FOR HOSPITALIZATION 

In general, patients with minor head injury who have no clinical history findings that 

suggest neurologic injury, no neurologic abnormality on examination, and a normal CT 

scan can be discharged to home. Patients who have persistent amnesia, persistent 

alteration in level of consciousness, or any abnormality on CT scan should be admitted 

for observation. Patients with significant mass or space-occupying lesions should 

receive immediate neurosurgical consultation. 

DISCHARGE INSTRUCTIONS

Various methods have been proposed for ongoing evaluation after discharge of patients 

with minor head injury. These methods have ranged from having the patient's caregiver 

evaluate the patient every 30 minutes to once per night. None of these discharge 

instructions has been validated in any prospective manner. Currently, with relatively 

liberal use of CT scan, the possibility of return for worsening head injury is unlikely. It is 

not unusual, however, for patients to present with postconcussive symptoms days or 

weeks after a minor head injury. Discharge instructions for these patients should include 

being aware of any nausea or vomiting, alteration in level of consciousness, and any 

seizure activity. 

The interval at which patients should be reevaluated is unclear. Patients with minimal 

clinical findings or negative CT scan and a history not suggestive of or not including loss 

of consciousness or amnesia are unlikely to have a significant space-occupying lesion. 

The exception may be the patient with an epidural hematoma during the lucid interval. 

Therefore, patients with minor head injury should be observed for some period of time in 

the emergency department before discharge home. 

INTOXICATED PATIENTS 

Intoxicated patients frequently present to the emergency department after being found 

unresponsive or with a decreased level of consciousness. Alcoholic patients are at 

increased risk of obtaining a head injury secondary to ataxia, frequent falls, and other 

types of trauma. A detailed examination looking for signs of head trauma, pupillary 

abnormalities, or other lateralizing neurologic deficits is critical in early identification of 

head injuries in intoxicated patients. Frequent reexamination is also important to ensure 

that an intoxicated patient's level of consciousness is improving over time. Any 

deterioration in the level of consciousness or the development of new deficits should 

prompt an emergent noncontrast CT scan for further evaluation. 

American Academy of Neurology: Practice parameter: the management of concussion 

in sports (summary statement). Neurology 1997;48:581. [PMID: 9065530] 

Committee on Quality Improvement, American Academy of Pediatrics. Commission on 

Clinical Policies and Research, American Academy of Family Physicians: The 

management of minor closed head injury in children. Pediatrics 1999;104: 1407. [PMID: 

10585999] 

Coombs JB, Davis RL: A synopsis of the American Academy of Pediatrics' practice 

parameter on the management of minor closed head injury in children. Pediatr Rev 

2000;21:413. [PMID: 11121498] 

Haydel MJ et al: Indications for computed tomography in patients with minor head injury. 

N Engl J Med 2000;343:100. [PMID: 10891517] 

Jogoda AS et al: Clinical policy: neuroimaging and decision-making in adult mild 

traumatic brain injury in the acute setting. Ann Emerg Med 2002;40:231. [PMID: 

12140504] 

Kelly JP, Rosenberg JH: The development of guidelines for the management of

concussion in sports. J Head Trauma Rehabil 1998;13:53. [PMID: 9575257] 

Preboth M: AAFP and AAP issue a practice parameter on the management of minor 

closed head injury in children. Am Fam Physician 1999;60:2698. [PMID: 10606000] 

Schutzman SA et al: Evaluation and management of children younger than two years 

old with apparently minor head trauma: proposed guidelines. Pediatrics 2001;107:983. 

[PMID: 11331675] 

Servadel F et al: Defining acute mild head injury in adults: a proposal based on 

prognostic factors, diagnosis and management. J Neurotrauma 2001;18:657. [PMID: 

11497092] 

Simon B et al: Pediatric minor head trauma: indications for computed tomographic 

scanning revisited. J Trauma 2001;51: 231. [PMID: 11493779] 

Smally AJ: Management of minor closed head injury in children. Pediatrics 

2001;107:1231. [PMID: 11388318] 

Woodcock RJ, Davis PC, Hopkins KL: Imaging of head trauma in infancy and childhood. 

Semin Ultrasound CT MR 2001;22: 162. [PMID: 11327530] 





IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS

Table 22-1. Concussion grading and outcomes for a first concussion (American Academy of Neurolog 

Grade 

2 Symptoms Transient confusion 

of consciousness; 

concussion sympto 

more than 15 minu

Figure 22-1. Depressed right temporal and nondepressed left frontal skull fractures not 

well visualized on typical brain windows (A and B) but clearly seen on bone windows 

(C). Also note the associated frontal pneumocephalus. 





FIGURES 

Figure 22-1

Figure 22-2. Severely depressed frontal skull fracture with significant impingement on 

the frontal lobes. 





FIGURES 

Figure 22-2

Figure 22-3. Large acute right frontal epidural hematoma with associated mass effect 

on the frontal lobes and slight midline shift. 





FIGURES 

Figure 22-3

Figure 22-4. Small left subdural hematoma with effacement of the left lateral ventricle. 





FIGURES 

Figure 22-4

Figure 22-5. Bilateral acute on chronic subdural hematoma with significant mass effect 

compressing both cerebral hemispheres. Note the acute component of the hematoma 

layering posteriorly (dependent position). 





FIGURES 

Figure 22-5

Figure 22-6. Right temporal subarachnoid hemorrhage (A-D) with extension into basal 

cistern (A), third ventricle (B) and lateral ventricles (C and D). Also note the moderate 

sized left frontotemporal subdural prominently seen on B-D. 





FIGURES 

Figure 22-6

Figure 22-7. Diffuse axonal injury with punctate hemorrhages (mainly right frontal), 

changes of generalized edema with poor gray-white matter discrimination in the right 

hemisphere, and mass effect on the right lateral ventricle. 





FIGURES 

Figure 22-7

23. Maxillofacial & Neck Trauma 1 - Fermin S. Godinez, DO, & Susan J. 

Letterle, MD 


1 This chapter is a revision of the chapter by Roger L. Crumley, MD, from the 4th edition. 

Emergency management of life-threatening associated conditions is described in 

Chapter 10. 

ENSURE AIRWAY 

Evaluate the pharyngeal, laryngeal, and tracheal components of the airway in patients 

with head and neck trauma. Stabilize the head and axial spine with a cervical collar and 

full spine board immobilization until cervical spine injury can be excluded. 

Caution: Any patient with injury to the neck should be managed and monitored 

conservatively in anticipation of rapid airway obstruction. If acute airway obstruction is a 

reasonable expectation (eg, in the presence of expanding hematoma, edema, 

hoarseness, subcutaneous emphysema, or persistent laryngeal pain), serious 

consideration should be given to rapid sequence intubation (RSI). At times 

controversial, RSI by a skilled laryngoscopist with in-line cervical stabilization in a 

patient with a cervical spine injury has a high degree of success. Emergency physicians 

should be cautioned to avoid RSI techniques in patients with airway injuries that would 

preclude bag-valve-mask ventilation should intubation prove unsuccessful. 

In some circumstances, intubation while the patient is awake, using topical anesthetic 

and intravenous sedation, may be a better approach. If time permits, fiber optic 

bronchoscopy-assisted intubation can be an excellent alternative. A surgical airway 

should be immediately available at bedside and should be the next intervention if 

attempts at oral intubation are unsuccessful. Patients with an altered level of 

consciousness and no evidence of craniofacial injury, should have a nasogastric tube 

inserted after intubation to empty stomach contents. In patients with contraindications to 

nasogastric tube insertion, orogastric placement is recommended. 

Pharyngeal Airway Injury 

Massive injuries of the tongue or mandible may compromise or obliterate the 

pharyngeal airway. Because of this distorted anatomy, intubation may be difficult. The 

base of the tongue may be used as a landmark to help locate the epiglottis and secure 

the airway. 

If there is no air exchange, immediately perform a jaw thrust and clear the oral cavity 

and pharynx of blood and loose teeth while preparing a laryngoscope for emergency 

intubation (Chapter 6).

Laryngeal Airway Injury 

If there is evidence of injury below the level of the hyoid bone with compromise of the 

airway, assume that laryngeal fracture or laryngotracheal crush injury is present. 

Cricothyrotomy (Chapter 6) should be performed to secure the airway in patients with 

pharyngeal or laryngeal airway obstruction when laryngoscopy is difficult, delayed, or 

contraindicated. After a small-bore endotracheal tube is inserted through the 

cricothyrotomy, a standard tracheotomy should be performed. 

Tracheal Airway Injury 

If there is injury below the cricothyroid membrane, a standard tracheotomy will be 

necessary to bypass the obstructive lesion. 

In patients with no air exchange, it is permissible to attempt orotracheal intubation for 60 

seconds, but preparations for cricothyrotomy or tracheotomy must be initiated 

simultaneously. 

Intubation of the Trachea Through a Traumatic Opening 

Occasionally, patients will come to the emergency department with impending asphyxia 

and with a gaping wound of the lower anterior neck. In some of these patients, removal 

of dressings and clots in the wound exposes a traumatic defect of the trachea that can 

be intubated. Patients with dashboard injuries or "clothesline-fence" snowmobile or 

motorcycle injuries often present with laryngotracheal separation immediately above or 

below the cricoid cartilage. If there is no open wound, immediate tracheotomy is the 

preferred method of airway management. Oral intubation or paralysis may precipitate 

airway obstruction and cause death. Direct intubation of the trachea is sometimes 

possible through an open wound on the anterior neck. 

STOP BLEEDING 

Control Hemorrhage 

Patients with neck trauma (penetrating or blunt) may have rapidly expanding cervical 

hematomas from arterial or venous bleeding. Hematomas may cause airway obstruction 

and death if not recognized and treated. Facial and neck wounds may also be 

associated with external arterial or venous bleeding. Do not remove penetrating objects 

from the wound; they may be tamponading vessels at the site of injury. 

A. Pressure 

If venous oozing occurs, apply a pressure dressing in the emergency department. Do 

not wrap the neck with a circumferential dressing because it may increase intracranial 

pressure and act as a noose if edema or a cervical hematoma worsens. 

B. Pressure and Clamping 

If major arterial bleeding occurs in an open wound, try applying pressure first. If that 

fails—and only then—hemostats may be applied carefully under direct vision. Clamping

of large amounts of soft tissue without good visualization is contraindicated, because 

the vagus nerve or phrenic nerve may be included in the clamp (Figure 23-1). A firm 

pressure dressing is the safest hemostatic agent. 

C. Tracheotomy 

Exsanguinating oral hemorrhage after penetrating trauma may be controlled by 

endotracheal intubation through a cricothyrotomy or tracheotomy (with immediate 

inflation of the cuff to prevent aspiration), followed by pharyngeal packing. 

Treat Shock 

If hypovolemic shock is present as a result of bleeding from face or neck injuries, it is 

managed with infusion of intravenous crystalloid solution or blood as described in 

Chapter 9. Management of shock may be described briefly as follows: 

Insert 2 or more large-bore (= 16-gauge) intravenous catheters. Draw blood for a 

complete blood count, electrolytes, renal function tests, serum glucose, prothrombin and 

partial thromboplastin times, and blood clot for typing and cross-matching blood 

products. If the patient is hemodynamically unstable after initial crystalloid bolus of 1-2 

liters, 2 units of packed red blood cells (cross-matched if available) should be infused. 

Infuse crystalloid solution (up to 2-3 L in 30-60 minutes) to support blood pressure and 

urine output. Insert a urinary catheter to monitor urine output if no urethral injury exists. 

STABILIZE CERVICAL SPINE 

While the airway and bleeding are being managed, the emergency physician should be 

thinking about the cervical spine. Unless the physician is certain that the cervical spine 

is intact, the patient's head should not be moved. The head, axial spine, and lower 

extremities should be routinely immobilized until a reliable clinical exam, cervical spine 

radiographs, or computed tomography (CT) scan have excluded obvious injury. In-line 

cervical immobilization must be maintained by an assistant during intubation attempts. If 

unable to obtain a definitive airway with RSI, then a surgical airway is required. Once 

the airway is established and the patient is hemodynamically stable, anteroposterior, 

lateral, and odontoid cervical spine films or CT scans should be obtained whenever 

blunt head or neck trauma are present or if uncertainty exists due to the influence of 

drugs or alcohol. See Chapter 27 for further evaluation and management. 

Mandavia DP et al: Emergency airway management in penetrating neck injury. Ann 

Emerg Med 2000;35(3):221. [PMID: 10692187] (A retrospective study examining the 

approach to penetrating neck trauma, initial airway management, and their relative 

effectiveness from an urban level-1 trauma center and emergency medicine training 

program.) 

Desjardins G et al: Airway management for penetrating neck injuries: the Miami 

experience. Resuscitation 2001;48(1):71. [PMID: 11162884] (Review.) 

Tayal VS et al: Rapid-sequence intubation at an emergency medicine residency: 

success rate and adverse events during a two-year period. Acad Emerg Med

1999;6(1):31. [PMID: 9928974] (An observational study of a large cohort of RSI patients 

at an urban level-1 trauma center and emergency medicine training program.) 


North Am 1998;16(1):45. [PMID: 9496314] (Review of management of the difficult 

airway in the trauma patient, available devices for management, and rescue 

maneuvers.) 

II. FURTHER DIAGNOSIS & EVALUATION 

NECK TRAUMA 

Type of Trauma 

A. Penetrating Injury 

1. Knife wounds—If the penetrating instrument is still in situ, leave it there and obtain 

posteroanterior and lateral neck films or CT scan to determine its exact location (Figure 

23-2). Even if the weapon or object causing the injury has been removed, it is still useful 

to know the length and shape of the penetrating object, as well as the direction of entry. 

Knowing the direction and depth of the injury provides information about what structures 

may have been injured. 

2. Bullet wounds—Trauma from high-velocity missiles cannot be accurately assessed 

externally. Bullets frequently do not travel in a straight line. They may be deflected or 

fragmented as they pass through various tissues or strike bone. Bullets with high kinetic 

energy cause cavitation and tissue injury remote from the missile track. High-velocity 

missile injuries may require surgical intervention after evaluation by CT scan, 

angiography, 2-dimensional Doppler, or esophagoscopy. 


Blunt trauma to the neck is associated primarily with injury to the cervical spine and 

airway. Vascular and esophageal injuries are rare. Thus, careful assessment in the 

emergency department can identify the need for surgical exploration. 

Anatomic Location 

The neck may be divided into 3 zones: Zone I is the area bordered by the suprasternal 

notch, clavicles, and inferior aspect of the cricoid cartilage. Zone II is the area between 

the inferior cricoid cartilage and the angle of the mandible. Zone III is the area between 

the angle of the mandible and the base of the skull. The anatomical division of the neck 

into zones is relevant to the management of neck injuries because of the difficulty 

establishing proximal and distal control of vascular structures surgically in zones I and 

III. 

Wounds that penetrate the platysma should not be probed in the emergency 

department; they should be explored in the operating room. 

Airway Injury

Airway injury may be manifested by an air leak, subcutaneous or mediastinal 

emphysema, or pneumothorax, indicating frank airway laceration. Stridor, hoarseness, 

painful phonation, and hemoptysis and hemothorax may also indicate airway injury 

(pharynx, larynx, or trachea). Posteroanterior and lateral neck and chest x-rays or CT 

scans should be considered during evaluation of neck injury. Direct or indirect 

laryngoscopy must be performed before surgery to determine the exact nature of the 

airway injury. 

Esophageal Injury 

Injuries to the upper esophagus are associated with soft tissue crepitus, dysphagia, 

odynophagia, and drooling. An esophagogram with water-soluble contrast may 

demonstrate dye extravasation indicating perforation. However, esophagoscopy is 

virtually always necessary if the esophagram does not demonstrate an injury. 

Vascular Injury 

(See also Chapter 38.) Vascular injury may be immediately apparent if there is external 

bleeding, a bruit or thrill, or a cervical hematoma, or it may be hidden if bleeding occurs 

into the pleural space. Neurologic deficit may indicate intracranial vascular insufficiency. 

Suspected vascular injuries may be managed operatively once specific injuries are 

identified by 2-dimensional Doppler, angiography, esophagoscopy, or dynamic CT scan 

(Chapter 38). Injuries occurring in zone I or zone III usually require angiography. Zone I 

injuries may require thoracotomy to control hemorrhage. 

Nerve Injury 

(See Figure 23-1.) Assess the nerves in the neck that are susceptible to injury. 

A. Vagus, Recurrent Laryngeal 

Record the character of the patient's voice, and examine the vocal cords via indirect 

(mirror) or fiberoptic laryngoscopy. 

B. Spinal Accessory 

Test for function of the sternocleidomastoid and trapezius muscles. 

C. Hypoglossal 

Test for deviation of the protruded tongue to the side of the injury. 

D. Phrenic 

Assess movement of the diaphragm on chest examination or by x-ray. 

Disposition 

Patients with penetrating trauma of the neck should be hospitalized unless local 

exploration of the wound shows it to be superficial to the platysma. Patients with blunt 

trauma with no evidence of significant injury (by physical examination and x-rays of the 

neck and chest) may be safely discharged.

FACIAL TRAUMA 

Type of Injury 

Most facial injuries consist of blunt trauma or cutting injury of the superficial soft tissue 

(eg, lacerations). High-velocity missile injuries of the face usually involve the central 

nervous system, and such injuries take priority for management (Chapter 22). 

Airway Injury 

Severe trauma to the lower face may compromise the airway. If obvious measures such 

as suction or pulling the tongue forward do not correct the problem, diverting the airway 

around the injury by performing endotracheal intubation, cricothyrotomy, or tracheotomy 

is preferred. 

Vascular Injury 

Bleeding from facial injuries typically is profuse but rarely causes hypovolemia or shock. 

Control bleeding by direct pressure only; hemostatic clamping may injure important 

nonvascular structures. 

Nerve Injury 

Blunt or penetrating trauma may injure branches of the trigeminal, facial, auditory, 

lingual, or hypoglossal nerves. The best chance to diagnose such injuries is often in the 

emergency department before edema and pain worsen. A careful assessment of both 

motor and sensory function of these nerves, especially the facial nerve, is imperative. 

A. Facial Nerve 

Branches of the facial nerve can be tested by these maneuvers: 

1. Temporal branch (to the frontalis muscle)—Ask patient to wrinkle forehead. 

2. Zygomatic branch (to the orbicularis oculi muscles)—Ask patient to squeeze 

eyes shut tightly. 

3. Buccal branch (to the smile muscles)—Ask patient to wrinkle nose, elevate upper 

lip, smile, and "show your teeth." 

4. Marginal mandibular branch (to the lower lip depressors)—Ask patient to pucker 

or whistle. 

5. Cervical branch—Ask patient to wrinkle the neck. 

B. Trigeminal Nerve 

Test for sensation over the entire face and upper neck.

C. Auditory Nerve 

Test hearing in both ears. 

D. Lingual Nerve 

Test for sensation on both sides of the anterior tongue. 

E. Hypoglossal Nerve 

Test for ability to protrude tongue in midline and to both sides. 

Parotid Gland Injury 

An irregular quadrilateral area connecting the tragus, the angle of the mandible, the 

lateral commissure of the mouth, and the lateral canthus of the eye bounds an area 

where lacerations are most apt to injure Stensen's duct or branches of the facial nerve 

(Figure 23-3). Stensen's (parotid) duct courses anteriorly from the parotid gland in the 

preauricular area through the cheek to enter the buccal mucosa near the maxillary 

(upper) molar teeth. The initial evaluation of Stensen's duct requires only gentle probing 

with lacrimal probes, entering through the buccal surface. If the end of the probe 

appears in the cheek lacerations, Stensen's duct has been disrupted and requires 

surgical repair. If lacerated and unrepaired, the duct will spill saliva into the cheek or 

externally, creating a troublesome salivary fistula. This complication is easy to prevent 

but difficult to treat. 

Mouth Injuries 

Test for pain on jaw movement or biting, feel for crepitus on movement of upper or lower 

teeth, and look for obvious malocclusion indicating fracture of the mandible or maxilla. 

Look for loose or fractured teeth. Inspect the buccal mucosa, tongue, floor of mouth, 

teeth, palate, and pharynx for evidence of injury. Grasp the upper alveolar bone, and 

check for movement that suggests a maxillary fracture. Carefully palpate the remainder 

of the face to determine if other areas are potentially fractured. Obtain x-rays, a 

mandibular Panorex, or CT scan of the face to determine the extent of injury. 

Eye Injury 

(See also Chapter 31.) Look for obvious injury to the globe. Either enophthalmos or 

complaints of diplopia should arouse suspicion of orbital bone fracture. 

Bilateral periorbital hematomas ("raccoon eyes") are a sign of anterior basilar skull or 

ethmoid bone fracture, and a search for cerebrospinal fluid rhinorrhea should be made. 

Cerebrospinal fluid rhinorrhea may accompany closed head or maxillofacial injury. It 

should be suspected whenever clear fluid or watery bloodstained fluid drains from the 

nose. If cerebrospinal fluid rhinorrhea is suspected, a CT scan followed by 

otolaryngologic and neurosurgical consultation is indicated. There is no reliable method 

available in the emergency department for distinguishing cerebrospinal fluid from nasal 

mucus. 

Nasal Injury

Inspect the nose for obvious deformity or septal hematoma. Palpate for the presence of 

nondisplaced fracture. If active epistaxis is present, use packing or cautery to control the 

bleeding. Look for cerebrospinal fluid rhinorrhea (see above), which, if present, would 

require a CT scan of the brain and face with otolaryngologic or neurosurgical 

consultation. 

Ear Injury 

Inspect the external ear, ear canal, and tympanic membrane. Test hearing if possible. A 

direct blow to the external ear may produce otohematoma, auricular laceration, 

ossicular disruption, or perforated tympanic membrane (conductive hearing loss). Blunt 

head trauma may fracture the temporal bone (basilar skull fracture; Chapter 22), which 

is associated with hemotympanum, blood in the external canal, postauricular hematoma 

(Battle sign), cerebrospinal fluid otorrhea, facial nerve palsies, or sensorineural hearing 

loss. 

Disposition 

Most patients with extensive or open fractures or with serious injuries of the eye, ear, or 

salivary gland should be hospitalized. Uncomplicated fractures of the mandible, maxilla, 

and nasal bone—as well as contusions or lacerations of the skin—may be managed 

without hospitalization. (See discussion of specific injuries for details.) 

Hernandez JJ et al: Penetrating neck trauma. E-medicine Journal 2001;2(9). 

http://www.emedicine.com/med/topic2802.htm (Review of the relevant anatomy of the 

neck, image modalities for evaluation of neck injuries, and future and current 

controversies in the management of penetrating neck trauma.) 

Kendall JL et al: Penetrating neck trauma. Emerg Med Clin North Am 1998;16(1):85. 

[PMID: 9496316] (Review of the anatomy of the neck, methods for obtaining airway 

control, and management issues related to penetrating neck trauma.) 

Kim MK et al: Penetrating neck trauma in children: an urban hospital's experience. 

Otolaryngol Head Neck Surg 2000;123(4): 439. [PMID: 11020182]. (Chart review of the 

selective management of head and neck trauma in children.) 

III. EMERGENCY MANAGEMENT OF SPECIFIC INJURIES 

FACIAL FRACTURES 

MANDIBULAR FRACTURES 


• Note any obvious facial swelling or asymmetry. 

• Ask the awake and alert patient some simple questions: (1) "Do your teeth feel 

normal?" (2) "Does your bite feel normal?" (3) "Do you have any pain in your mouth,

jaw, or ears? Point to where it hurts." 


With the exception of the nasal bones, the mandible is by far the most frequently 

fractured facial bone. Initial evaluation of the patient with mandibular fracture should be 

thorough and include a detailed evaluation of sensory and motor function of the oral 

cavity. The oral cavity must be cleaned and suctioned of foreign bodies and debris, and 

a patent airway ensured. Laryngeal, cervical spine, and intracranial injuries must be 

sought first and treated. Failure to recognize a mandibular fracture may result in serious 

sequelae such as osteomyelitis, permanent malocclusion, or nonunion. 



Mandibular fractures may be detected simply by the presence of gross facial asymmetry 

on inspection or by malocclusion. If the patient has a sensation of dental malocclusion, 

mandibular or maxillary fractures should be strongly suspected. The body, condyles, 

and angle of the mandible and symphysis are common sites for fracture. In some 

studies, multiple fractures were present in almost half of patients with mandibular 

fractures. 

Pain is always present following mandibular fracture and may be so severe that the 

patient will refuse to open or close the jaw. The patient will usually point to the fracture 

site when asked to localize pain associated with mandibular movement. The "tongue 

blade test" is performed for each side of the mouth by having the patient bite down on a 

tongue blade between the molars. If the patient can stabilize the tongue blade between 

the molars on each side of the mouth while the examiner twists the stick until it breaks, 

the patient is unlikely to have a mandibular fracture. The sensitivity of this test is 95%. 

Tenderness is best ascertained by bidigital examination with the examiner's thumbs in 

the mouth on the teeth or dental alveoli (in edentulous patients). The fingers then 

palpate externally along the lower border of the mandible. By "rocking" the mandible 

from side to side, the physician can sense mobility in the midline area. 

B. Imaging 

X-ray evaluation for mandibular fracture should include a Panorex examination (Figure 

23-4), which gives a panoramic view of the entire mandible on one film and will usually 

show all fractures present. If Panorex technology is unavailable (or if patients with 

multiple injuries cannot be positioned properly), a coronal facial CT scan will be a more 

useful imaging study and offer better visualization of the condylar processes. 

Treatment 

Once the diagnosis of mandibular fracture has been established, the following 

measures should be carried out: 

A. Tetanus Prophylaxis 

Give tetanus toxoid or tetanus-diphtheria toxoid as needed (Chapter 30).


Choice of antibiotic should provide adequate coverage for oral aerobes and anaerobes. 

Penicillin G intravenously or penicillin VK orally will be sufficient. Clindamycin should be 

used in penicillin-allergic patients. 

C. Barton Bandage 

To provide comfort and initial stabilization of the fracture, a Barton bandage should be 

applied. This is simply a wrap-around gauze or Kerlix dressing that passes under the 

mandible and over the top of the head so as to close the mandible. Care must be taken, 

however, to maintain airway patency. 

Disposition 

Ideally, patients with mandibular fractures should be treated definitively in the 

emergency department before discharge. If necessary, however, patients with simple 

mandibular fractures may be discharged and referred to an otolaryngologist, plastic 

surgeon, or oral surgeon within a few days for definitive treatment. Provide adequate 

analgesics and antibiotics, and instruct the patient to drink plenty of liquids through a 

straw. 

Patients with open or severely displaced mandibular fractures should be seen by the 

maxillofacial consultant and hospitalized for treatment. 

MAXILLARY (LE FORT) FRACTURES 


Rene Le Fort, a French surgeon, identified and described patterns of injuries and 

fractures of the midface. The maxilla and associated structures of the middle third of the 

face are injured more often as a result of blunt trauma. Although this classification 

system is beneficial, it does not include unilateral Le Fort injuries, combinations of Le 

Fort types, or more extensive fractures and intracranial injuries. However, this system is 

still useful in providing the examiner with potential sites and patterns of injury. Using this 

knowledge the clinician can pay particular attention during physical examination and 

determine the necessity and utility of diagnostic imaging. 


The most helpful clinical findings are malocclusion, local tenderness, and maxillary 

mobility. The latter finding is elicited by grasping and rocking the anterior portion of the 

maxilla intraorally with one hand while stabilizing the head with the other hand. Motion is 

elicited in bilateral maxillary fractures if they are not seriously impacted. Diagnosis is 

confirmed by a facial CT scan. Le Fort fractures can be classified into 3 types (Figure 

23-5). 

1. Le Fort I Fracture 

Clinical Findings

Le Fort I is a fracture parallel to the alveolar process and hard palate of the maxilla. The 

fracture extends posteriorly behind the maxillary molars, and across the lateral wall of 

the maxillary sinus anterior to the piriform aperture (Figure 23-5A). This fracture 

essentially separates the maxillary teeth and alveolar bone from the rest of the maxilla 

and face. There are usually no airway complications associated with such a fracture. 

Treatment 

After completion of a careful evaluation and reasonable exclusion of any other serious 

injuries, no specific emergency treatment is indicated. Provide the patient with adequate 

pain control. 

Disposition 

Patients with uncomplicated Le Fort I type injuries may be managed as outpatients after 

maxillofacial consultation (otolaryngologist, plastic surgeon, or oral and maxillofacial 

surgeon). Patients with more complex or open fractures should be hospitalized. 

2. Le Fort II Fracture 


Le Fort II fracture is a pyramidal fracture involving the bony nasal skeleton and the 

middle third of the face, and it includes the fracture lines of Le Fort I injury (Figure 

23-5B). Displacement of the maxillary dentition due to fracture may cause malocclusion. 

Examination usually reveals ecchymosis of the nasal dorsum, the lower eyelids, and the 

maxillary gingival buccal sulcus. This injury pattern includes the infraorbital nerve canal, 

potentially causing nerve injury and a sensory deficit inferior to the involved lower eyelid. 

The face may appear elongated, and the anterior portion of the mid face will be mobile 

relative to the forehead. A CT scan of the face is the preferred imaging modality. If CT is 

not immediately available, a Waters view x-ray may demonstrate these fractures. 

Treatment 

No specific immediate treatment is necessary. Provide adequate analgesics. 

Disposition 

Consultation with a maxillofacial consultant (otolaryngologist, plastic surgeon, or oral 

and maxillofacial surgeon) should be obtained in the emergency department. The 

consultant should determine the final disposition based on the extent of the patient's 

injuries and the timing of any planned operative intervention. 

3. Le Fort III Fracture (Cranial Dysjunction) 


A LeFort III fracture, or craniofacial dysjunction, involves separation of all the facial

ones (including the zygoma, maxilla, and nasal bones) from the cranial base. The Le 

Fort III injury pattern includes fracture lines extending through the ethmoid bones and 

orbits and into the sphenopalatine fossa. The lines then pass medially across the 

glabellar region (bridge of nose). In some patients, the zygoma may become completely 

separated by fracture lines (Figure 23-5C, left side). Patients with Le Fort III fracture 

tend to have massive facial edema and ecchymosis and occasionally airway obstruction 

secondary to dissection of hematoma into the palate, pharyngeal walls, or tonsillar 

pillars. Patients frequently have associated mandibular fractures with posterior prolapse 

of the tongue and hematoma formation. 

Treatment 

If airway obstruction is present or impending, secure a definitive airway with orotracheal 

intubation. If orotracheal intubation is unsuccessful, cricothyrotomy is indicated for 

impending rapid airway obstruction. Nasotracheal intubation is contraindicated due to 

the possibility of intracranial passage of the endotracheal tube. Provide adequate 

analgesics. 

Disposition 

In virtually all cases, a maxillofacial consultant should examine the patient in the 

emergency department to determine the need for hospitalization. 

ZYGOMATICOMAXILLARY COMPLEX (ZMC) FRACTURES 


• Lower eyelid swelling and ecchymoses. 

• Flattened arch and decreased sensation of intraorbital nerve distribution. 

• Double vision with upward gaze. 

• Trismus. 


Malar (zygomaticomaxillary complex) fracture most commonly results from 

lateral-to-medial blunt force applied to the face. Three fracture lines are associated with 

ZMC fractures (Figure 23-6). The lateral orbital rim is fractured at the zygomaticofrontal 

suture. The orbital floor is disrupted, with the anterior end of the fracture line passing 

across through the zygomaticomaxillary suture line or the infraorbital foramen. The third 

fracture is through the zygomaticotemporal suture. When associated with ZMC fracture, 

the orbital floor fracture line is not a blowout fracture and should not be confused with 

one. 


Epistaxis occurs, because the bony floor of the orbit is also the roof of the maxillary 

sinus. Periorbital edema and ecchymosis are present. Examination and palpation show

flattening of the normal malar prominence and depression or separation of the lateral or 

inferior orbital rim. 

Facial paresthesias or hypesthesias of the upper lip and cheek occur if the infraorbital 

nerve is damaged at the infraorbital foramen or more posteriorly in the orbital floor. 

Diplopia may be present as a result of orbital hematoma or slight displacement of the 

eyeball. Herniation of orbital contents into the antrum (maxillary sinus) is less common 

in ZMC fracture than in orbital blowout fracture. Subcutaneous emphysema of the face 

indicates that the fracture has extended into the paranasal sinuses. Make sure there is 

no evidence of retrobulbar hematoma or a tense globe requiring immediate intervention. 

X-ray confirmation is readily obtained with a facial CT scan. Three-dimensional CT 

scanning provides a much more detailed view of the displacement of fracture fragments 


Treatment 

Control epistaxis with nasal packing or cautery, and provide adequate analgesics. 

Administer antimicrobials if the fracture extends into the sinuses. Penicillin or amoxicillin 

may be used. Fluoroquinolones, doxycycline, or clindamycin may be other alternatives 

for penicillin-allergic patients, if antibiotic therapy is indicated. 

Disposition 

Before being discharged from the emergency department, the patient should be 

examined by a maxillofacial consultant to determine the need for hospitalization. 

Ophthalmologic consultation is also recommended. 

In general, simple closed fractures of the zygomatic arch alone do not require further 

specific treatment or hospitalization. True ZMC fractures—especially those that are 

open or displaced, or with displacement of orbital contents—require open reduction 

under general anesthesia. Final disposition after the patient has been examined by a 

maxillofacial consultant should be determined based on the extent of injuries in addition 

to the method and timing of any planned surgical interventions. 

ORBITAL FLOOR ("BLOWOUT") FRACTURES 


• Decreased eye movement. 

• Limitation of eye movement. 

• Decreased sensation of the infraorbital nerve distribution. 

• Enophthalmos. 

• Double vision, especially with upward gaze. 


A. Pure Blowout Fracture 

Pure blowout fracture results from blunt anteroposterior force directed against the 

eyeball. Intraocular pressure rises markedly and is exerted in all directions. The orbital 

floor gives way because it is the weakest component of the orbital skeleton. Orbital fat, 

bone from the orbital floor, and occasionally extraocular muscles may be forced into the 

maxillary antrum. For this reason, ocular injuries and complications are more extensive 

with this fracture than with any other fracture. Because the infraorbital rim is not 

involved, tenderness may not be palpable on the face, and the diagnosis may be 

missed if the physician is not aware of the fracture and its mechanism. Unrepaired 

blowout fractures may result in permanent diplopia or disfiguring enophthalmos. 

B. Impure Blowout Fracture 

Impure blowout fracture results from anteroposterior blunt force similar to that causing 

pure blowout fracture, but in this instance the force is also exerted against the 

infraorbital rim, producing a fracture. Impure blowout fracture is more common than pure 

blowout fracture. Because the force is dissipated by the rim fracture, the globe usually 

sustains less trauma, resulting in fewer ocular complications (eg, hyphema, retinal 

detachment, commotion retinae, lens dislocation) than in pure blowout fractures. 


Suspect blowout fracture in any patient who has sustained blunt ocular or periorbital 

trauma. Diplopia and restricted upward gaze may confirm ocular muscle entrapment as 

a result of the fracture. Infraorbital nerve injury with infraorbital hypesthesia is common 

in both pure and impure blowout fractures. Epistaxis may be present from laceration of 

the mucosa of the roof of the maxillary sinus. 

Ocular injuries are usually associated with pure blowout fractures. Palpable fracture of 

the infraorbital rim occurs with impure blowout fractures and is absent in pure blowout 

fractures. 

Coronal CT scans of the orbital floor are often helpful in delineating the extent of the 

fracture (Figure 23-8). 


Consult with an otolaryngologist and ophthalmologist before discharging the patient 

from the emergency department. 

Patients with blowout fractures and orbital entrapment (ie, diplopia or limitation of ocular 

mobility) should be hospitalized for exploration of the orbital floor, under general 

anesthesia. Reduction and internal fixation of associated facial fractures may have to be 

performed simultaneously. 

Patients with orbital floor or rim fractures with no limitation of ocular mobility and without 

associated injury of the globe (Chapter 31) may be discharged from the emergency 

department and referred to an otolaryngologist to be seen within a few days. 

NASAL FRACTURES


The nasal bones are sometimes fractured laterally in one fragment, but more commonly 

there is impaction of the nasal skeleton into the piriform aperture (bony nasal vault), 

requiring that the septum and nasal bones be disimpacted anteriorly before they can be 

reduced laterally. Open nasal fractures are rare. 


There is a history of a blow to the nose, often associated with epistaxis. Tenderness, 

crepitation, or movement of nasal bones on palpation is present. Septal hematoma may 

be found on examination. 

X-rays of the nasal bones seldom provide additional information and are not 

recommended for routine use. 

Treatment 

Nasal fractures without deformity or septal hematoma may be treated with analgesics. If 

airflow obstruction develops in nasal passages or if obvious deformity is revealed when 

the swelling subsides, the patient should be referred to an otolaryngologist. Ideally, 

nasal fractures with deformity but no associated soft tissue swelling should be reduced 

immediately before swelling develops. If swelling develops, reduction should be delayed 

until the swelling subsides. Reduction should occur after consultation with an 

otolaryngologist. Instruct the patient on preventing reinjury. Provide adequate 

analgesics and a nasal decongestant spray for the first 3 days to provide some 

symptomatic relief. 

A. Provide Anesthesia 

Most fractures can be reduced following topical intranasal anesthesia with cocaine. Roll 

cotton pledgets into a cylindric shape, and soak in 4% cocaine solution. Insert with nasal 

forceps into the upper and lower nasal cavities, and leave in place for about 15 minutes. 

Occasionally, topical anesthesia must be supplemented by injected local anesthetic. 

B. Reduce Fracture 

Simple, laterally displaced fractures may be reduced by exerting thumb pressure on the 

nose in the direction opposite to the initial fracture force. 

Comminuted fractures must be manipulated anteriorly and laterally. This is most easily 

done with a Kelly clamp or Asch septal forceps inserted in the nose up the fracture site 

(Figure 23-9). If the nose then has normal external configuration, reduction is successful 

and should be maintained by applying tape over the nose, perhaps supplemented by an 

anterior nasal pack of petrolatum-impregnated gauze. 

If the fracture has been reduced or if it was nondisplaced, arrange for otolaryngologic 

consultation. If the emergency physician cannot achieve adequate reduction of a nasal 

fracture, an otolaryngologist should be consulted immediately. Simple lacerations 

without associated septal dislocation should be copiously irrigated and closed primarily.

Antimicrobial prophylaxis (see below) should be given. Deep or complex lacerations or 

those associated with septal deviation, nasal deformity, or dislocated cartilage should 

not be repaired until the otolaryngologist or plastic surgeon has examined the patient. 

C. Drain Hematomas 

Septal hematomas should be drained by incision through the anterior nasal mucosa at 

the time of fracture reduction. If septal hematoma is allowed to persist and results in 

abscess formation, the entire septal cartilage may be lost, resulting in a disfiguring 

"saddle" deformity of the nose. Give antimicrobial prophylaxis (eg, amoxicillin or 

erythromycin). 

Disposition 

Hospitalization is rarely required for nasal fractures. Patients should be told that the 

nasal air passages may become narrowed on one side or the other, thereby requiring 

septorhinoplasty at a later date. 

FRONTAL SINUS FRACTURES 


• Facial trauma; think about the mechanism of injury. 

• Rare in children; unlikely in early teens. 

• Consider intracranial injury. 


Frontal sinus fractures most commonly result from motor vehicle trauma in which the 

patient's head strikes the dashboard. Patients with frontal sinus fractures require 

thorough head, neck, and neurologic examination, including ophthalmologic 

consultation. If there are variations in the level of consciousness, neurosurgical 

consultation should be obtained immediately. Fractures of the posterior wall of the 

frontal sinus may cause dural tears or brain injury, whereas fractures of the floor of the 

sinus often injure the nasofrontal duct. 


There will usually be a history as well as evidence of trauma to the forehead. 

Cerebrospinal fluid rhinorrhea is common following fractures of the posterior wall of the 

frontal sinus, and a specific note about its presence or absence should be entered in the 

emergency department record. Epistaxis may represent associated direct nasal trauma 

or frontal sinus hemorrhage. 

Axial and coronal CT scan of the face and CT scan of the head will provide the most 

important information on the extent of injury and potential for further intervention. 

Associated injuries frequently include other facial fractures, depressed skull fractures,

and orbital fractures. 

Treatment 

When brisk hemorrhage from the nasal cavity accompanies these fractures, it is 

acceptable to pack the anterior nasal vault tightly with 1.25-cm (1/2-in) iodoform gauze. 

Elevation of the head will reduce venous pressure and bleeding while the patient's 

condition stabilizes or arrangements are made for surgery. Obtain urgent 

otolaryngologic and neurosurgical consultation. 

If the fracture is open, the wound should be covered with saline-soaked gauze. Avoid 

manipulation of bony fragments in the emergency department, because this may 

produce further dural injury. 

Antibiotics are needed because the fracture lines cross the contaminated mucosal 

surfaces of the nose and sinus. Prior to surgical intervention by the neurosurgeon or 

otolaryngologist, vancomycin or a third-generation cephalosporin may be used. 

Surgery is indicated for cerebrospinal fluid rhinorrhea, open fractures, markedly 

displaced fractures, and fractures involving the posterior wall or floor of the sinus. 

Disposition 

All patients with frontal sinus fractures should be hospitalized. 

TEMPORAL BONE FRACTURES (Basilar Skull Fracture) 


Most basilar skull fractures include temporal bone fractures. The temporal bone is 

shaped like a pyramid with its base directed laterally and its apex medially. Because it 

houses the cochlea, vestibule, facial nerve canal, jugular vein, and internal carotid 

artery, fractures through the temporal bone may have serious sequelae. 

Diagnosis is based on the history of trauma and the presence of bleeding; ecchymosis 

of the external ear, mastoid tip (Battle sign), or ear canal; bilateral, periorbital 

ecchymoses ("raccoon eyes"); hemotympanum; hearing loss (conductive or 

sensorineural); or anosmia. 

Clinical features depend on the type of fracture. Because basilar skull fractures may be 

associated with intracranial bleeding, brain injury, or subsequent meningitis, 

neurosurgical consultation, in addition to otolaryngologic consultation, should be 

obtained for all patients with suspected temporal bone fracture. 

1. Tympanic Bone Fractures 


The anterior face of the tympanic bone is the glenoid fossa of the temporomandibular

joint. Hence, the mandibular condyle may be driven posteriorly into the middle ear or the 

external auditory canal. Patients with facial trauma who have ecchymosis, bleeding, or 

lacerations of the anterior external auditory canal often have such a fracture. A CT scan 

confirms the diagnosis. 

Treatment 

The ear canal is anesthetized by injection of a local anesthetic, and tympanic bone 

displacement is reduced by means of a metal speculum in the ear canal. This procedure 

is usually performed by an otolaryngologist. 

Disposition 

Hospitalization is not usually necessary unless associated injuries are present. 

2. Longitudinal Fractures 


Longitudinal fractures are so named because the fracture line parallels the long axis of 

the temporal bone (petrous pyramid). These fractures account for 80% of all fractures of 

the temporal bone. The tympanic membrane is frequently torn, and a step-off may be 

seen in the roof of the external auditory canal. Ossicular chain dislocation with 

conductive hearing loss is frequent. The hearing loss in longitudinal fractures is usually 

conductive rather than sensorineural, because the fracture line does not traverse the 

cochlea. When facial nerve paralysis is present, it is usually delayed. Delayed facial 

paralysis implies a better prognosis than does immediate paralysis, which indicates 

lacerations or other disruption of the nerve trunk and thus requires surgical exploration 

of the bony nerve canal as soon as the patient's condition permits. 


Obtain immediate otolaryngologic consultation. All patients with this injury require 


3. Transverse Fractures 


Although less frequent than longitudinal fractures, the transverse fracture causes more 

severe injuries to the contents of the temporal bone. It usually starts near the internal 

auditory canal and runs a course perpendicular to the longitudinal axis of the temporal 

bone. Consequently, these fractures frequently traverse the cochlea, resulting in 

complete sensorineural hearing loss. Facial nerve injuries occur in over half of patients, 

and paralysis is commonly immediate, requiring exploration of the facial nerve canal. 


Patients with suspected transverse temporal bone fractures require hospitalization for

evaluation and surgery. Immediate otolaryngologic consultation should be obtained. 

TOOTH INJURIES 

AVULSION OF TEETH 

Stop gingival bleeding with pressure. While holding the tooth by the crown so as not to 

damage the periodontal ligaments, wash it with saline and replace it immediately in the 

tooth socket. Obtain emergency oral surgical consultation, because avulsed teeth can 

be successfully reimplanted in some cases. For this reason, an attempt should be made 

to retrieve avulsed teeth from the scene of the accident. 

SUBLUXATION OF TEETH 

Gently manipulate the tooth back into its proper position. Obtain oral surgical 

consultation, because the loose tooth will have to be immobilized with a splint until it has 

reattached to periodontal and gingival tissues. 

TOOTH FRACTURES 

Exposure of the pulp or dentin is exquisitely painful, and a dentist should cover the tooth 

with a temporary plastic crown affixed with zinc oxide-eugenol paste. Follow-up care 

should be provided by the patient's regular dentist within a few days. 

EXTERNAL EAR TRAUMA 

OTOHEMATOMA 


Bleeding between the auricular cartilage and the perichondrium frequently follows 

contusions or other injuries to the auricle. Such injuries are frequent in boxers and 

wrestlers. If untreated, they will result in cauliflower ear deformity, because blood under 

the perichondrium results in proliferative scarring and new cartilage formation. 

Treatment 

Treatment consists of aspiration or incision and drainage of hematomas, followed by 

application of saline-soaked cotton balls that conform to the auricular formation. A firm 

compression dressing should be wrapped around the head to prevent further hematoma 

formation. 

Disposition 

The patient should be seen by an otolaryngologist within 1-2 days. No specific 

instructions need be given. Hospitalization is not required. 

LACERATIONS OF THE AURICLE

Treatment 

Lacerations of the auricle result in deformity if they are not meticulously repaired. 

Debridement of devitalized tissue is important. Approximation of lacerated cartilage and 

perichondrium should be performed with a single layer of synthetic absorbable sutures. 

This layer is followed by 6-0 nylon skin sutures or skin tapes. Apply a petrolatum gauze 

dressing under slight pressure. 

Disposition 

Patients with extensive lacerations of the auricle should be hospitalized for surgical 

repair. Smaller lacerations repaired in the emergency department should be inspected 

by an otolaryngologist or plastic surgeon in 1-2 days. 

MIDDLE & INNER EAR DISORDERS FOLLOWING HEAD TRAUMA 

CEREBROSPINAL FLUID OTORRHEA 


Cerebrospinal fluid otorrhea often results from minimal head injuries. Small cracks in the 

tegmen tympani (roof of the middle ear) provide a route for leakage of cerebrospinal 

fluid into the middle ear cavity. If the eardrum has a chronic perforation or has been torn 

at the time of injury, such leaks will result in cerebrospinal fluid otorrhea. This flow is 

best demonstrated in the head-down position. If the eardrum is intact, however, the fluid 

may pass through the auditory tube and produce cerebrospinal fluid rhinorrhea. In either 

case, meningitis is a potential complication. A CT scan will help diagnose the injury and 

eliminate the possibility of associated intracranial bleeding or brain injury. 


Hospitalization and neurosurgical consultation are indicated for all patients with 

suspected leakage of cerebrospinal fluid. Prophylactic antibiotics have not been shown 

to be of benefit and are not recommended. 

FACIAL NERVE PARALYSIS 


Facial nerve paralysis may result from a small temporal bone fracture. The facial nerve 

passes through the middle ear cavity, where it is exposed to risk of injury from fractures 

and from foreign bodies introduced through the ear canal. Complete assessment of 

facial nerve integrity should be performed. Lost or decreased movements of the face, 

decreased tear production, or altered taste sensation on the affected side may indicate 

facial nerve paralysis or injury. An otolaryngologist should be consulted to evaluate the 

patient. 


Patients with temporal bone fractures and immediate facial paralysis should be 

hospitalized and otolaryngologic consultation obtained immediately. 

CONDUCTIVE HEARING LOSS 


Disarticulation of the ossicular chain may result from head injuries with or without 

temporal bone fracture. One or more of the tiny ossicles may be jarred free from 

attachments and prevent normal function of the middle ear conduction mechanism. 

Patients with such injuries complain of acute hearing loss. Evidence of temporal bone 

fracture may or may not be present. If a step-off is seen at 12 o'clock at the medial end 

of the ear canal, it is further evidence of such an injury. Bone conduction is greater than 

air conduction in tuning fork tests. Audiometric examination reveals whether a coexisting 

sensorineural hearing loss is present. 


Patients should be referred to an otolaryngologist within a few days for surgical 

reconstruction of the ossicular chain in the middle ear. Immediate hospitalization is not 

required. 

SENSORINEURAL HEARING LOSS 


More severe temporal bone fractures may produce sensorineural hearing loss. Such 

hearing losses are often total, and patients have severe vertigo during the first few days 

following injury. 


Intravenous diazepam, 2-5 mg over 5-10 minutes, is an effective labyrinthine 

suppressant for control of vertigo. Patients should be hospitalized for evaluation and 

urgent otolaryngologic consultation. 

VERTIGO 


Some patients with head injuries complain of vertigo even though a CT scan of the head 

shows the temporal bone to be intact. These symptoms are thought to result from 

jarring of the delicate membranous inner ear structures within the bony labyrinth. In 

most instances, the vertigo is described as difficulty in walking or as a floating 

sensation. Occasionally, vertigo is so severe as to be associated with nystagmus. 


Symptoms diminish over time. Reassurance and sedation with diazepam, 2-5 mg orally

2-4 times daily, or meclizine, 25 mg orally 3-4 times daily, are usually all that is required. 

Hospitalization is rarely necessary. The patient may be referred to an otolaryngologist 

for follow-up. 

CARE OF FACIAL LACERATIONS (See also Chapter 30.) 

Closure of Lacerations 

Facial laceration repair requires attention to detail. Excellent wound preparation and 

precise tissue edge approximation with fine suture material are needed for the best 

possible restoration of anatomic structures and lines. If complex or extensive facial 

wounds are present, request assistance from the most appropriate consultant (eg, 

otolaryngologist, ophthalmologist, oral and maxillofacial, or plastic surgeon). 

Injuries to the upper and lower lip are extremely common and likewise require precise 

repair. A soaking wet gauze sponge should be used to clean the lip of all blood and 

foreign debris. The vermilion border can be seen most easily if left wet. Closure of 

lacerations of this area should begin with placement of a small "sentinel" suture to align 

this border. The repair then progresses in either direction from it. 

Replacement of Avulsed Tissue 

Debridement of devitalized pieces of tissue should be done with caution and 

conservatism. Likewise, small avulsed pieces of external ear, nose, or facial soft tissue 

with skin may be cleaned, debrided, and replaced with a reasonable chance for survival. 

Larger pieces, as in total or subtotal avulsion of the external ear or scalp, are best 

reattached by microvascular techniques in the operating room. The physician should 

ask the patient with an avulsion injury if a friend or relative can return to the scene of the 

accident to retrieve lost fragments of tissue. 

Delay in Closing Lacerations 

In general, lacerations of the eyelids, lateral orbital region, nasal dorsum, and 

mandibular region should not be closed until x-rays of the facial bones have been taken. 

The otolaryngologist or maxillofacial consultant may prefer reduction and fixation of the 

fracture fragments through these lacerations. 

Because of the rich blood supply of the area, it is acceptable to close facial lacerations 

as much as 12-24 hours after injury when necessary. When delayed closure is 

necessary, the wound should be packed open with saline sponges. Antibiotics (eg, 

dicloxacillin, cephalexin, or erythromycin for penicillin-allergic patients) may be 

considered for delayed closure. Pressure dressings can be used to control hemorrhage, 

or hemostats may be applied if bleeding vessels can be identified. 

Repair Technique 

Once more extensive injuries have been excluded (ie, facial nerve or parotid duct 

transections), local anesthetic can be infiltrated in the wound edges, or a regional block 

(supraorbital, infraorbital, or mental) should be employed. After the wound has been

irrigated completely and conservatively debrided, the laceration should be further 

explored to remove any foreign debris and wound closure may proceed. Careful 

approximation with a fine suture material will provide the best result. The extent of the 

injury, number of layers or structures involved, and experience with repair of facial 

wounds will dictate choice of suture. Synthetic absorbable suture (eg, polyglycolic acid, 

polydioxanone, polyglactic acid, polytrimethylene carbonate, or polyglecaprone) may be 

used to close subcutaneous structures. These sutures have various periods of complete 

absorption, good tensile strength, and minimal inflammatory response compared to 

natural products. 

Subcutaneous tissue should be sutured using a "buried knot" (see Figure 30-9). 

Synthetic nonabsorbable monofilament sutures (eg, polypropylene, polybutester, or 

nylon) are a good choice for skin closure; they have high tensile strength and minimal 

inflammatory response but require attention to securing knots. During repair, care 

should be taken to avoid injury of nerves or vessels. The superficial passage of the 

needle should be very close to the skin edge, so that after this layer is complete, the 

skin is already approximated and the skin sutures serve only to ensure accuracy of 

repair. 

Facial skin should be sutured with 6-0 nylon or polypropylene on a nontraumatic reverse 

cutting needle. An important aspect of plastic closure of such lacerations is the angle of 

entry of the needle into the skin and the eversion produced by each suture (see Figure 

30-10). Because the subcuticular layer has already approximated the skin, the skin 

sutures need not be tied tightly. A surgeon's knot (2 loops) should be tied and pulled 

down loosely so that the skin edges just touch. The next loop of suture should be tied 

with the opposite twist, so that a square knot results. If this second loop is not tied down 

tightly, a small loop results between the first (surgeon's) knot and the second loop; this 

is thought to reduce tissue strangulation when wound edema causes the skin edges to 

swell against the sutures. At least 2 additional knot loops should be tied on top of this 

second knot. 

For linear lacerations, a running (uninterrupted) suture is acceptable. The same 

important principles of an everting needle angle and gentle tension will give the most 

cosmetic repair. Cyanoacrylate tissue adhesive provides a liquid alternative for 5-0 

suture or smaller for selective wound closures. Avoid mucous membranes and the eyes 

during application. Do not use it in areas of high tension and where hair is present. Prior 

to application, if no local anesthetic is used, warn the patient that this liquid may cause 

increased pain or an intense burning sensation. 

Facial skin sutures should be removed not later than the fourth day. An ophthalmic 

suture scissor or a No. 11 Bard-Parker blade is best for removing these fine sutures. 

After suture removal, both sides of the laceration should be painted with tincture of 

benzoin and the wound closed with adhesive dressings (eg, Steri-Strips) so that the 

opposing edges of the wound are pulled together. This will eliminate any tension on the 

closure and minimize widening and hypertrophy of the scar. The patient should be told 

that facial scars mature for 12 months and that facial scar revision may be done after 

that time. 

Bruns TB et al: Using tissue adhesive for wound repair: a practical guide to Dermabond.

Am Fam Physician 2000;61:1383 [PMID: 10735344] (Provides practical information 

regarding the use of cyanoacrylate for wound repair.) 

Dale RA: Dentoalveolar trauma. Emerg Med Clin North Am 2000;18(3):521. [PMID: 

10967737] (This review provides the emergency physician with an understanding of the 

initial evaluation and treatment of dentoalveolar trauma.) 

Druelinger L et al: Radiographic evaluation of the facial complex. Emerg Med Clin North 

Am 2000;18(3):393. [PMID: 10967732] (A review of imaging modalities of use in the 

clinical assessment of maxillofacial trauma.) 

Ellis E III et al: Assessment of patients with facial fractures. Emerg Med Clin North Am 

2000;18(3):411. [PMID: 10967733] (This review provides emergency physicians with a 

fundamental understanding of the evaluation and treatment of a variety of facial 

fractures.) 

Hollander JE et al: Laceration management. Ann Emerg Med 1999;34(3):356. [PMID: 

10459093] (This review presents current management and treatment options available 

for the repair of lacerations seen in the emergency department.) 

Laskin DM et al: Current trends in the treatment of maxillofacial injuries in the United 

States. J Oral Maxillofac Surg 2000;58(2):207. [PMID: 10670601] (This article presents 

the results of a survey questionnaire of oral and maxillofacial surgeons to assess 

regional and national trends in the management of maxillofacial trauma.) 

Parsa T et al: Initial evaluation and management of maxillofacial injuries. eMedicine 

Journal 2001;2(11). http://www.emedicine.com/med/topic3222.htm (This article 

discusses the clinical presentation, classifications, and approach to patients with 

maxillofacial trauma.) 

Schwab RA, Genners K, Robinson W: Clinical predictors of mandibular fractures. Am J 

Emerg Med 1998;16(3):304. [PMID: 9596439] (Prospective study in an urban 

emergency department of 119 patients presenting with mandibular trauma.) 

Segal Z et al: Facial trauma, zygomatic complex fractures. eMedicine Journal 2002;3(1). 

http://www.emedicine.com/plastic/ topic531.htm (This article presents historical, 

anatomic, and biomechanical information related to the evaluation and treatment of 

ZMC fractures.) 





Letterle, MD 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS

Figure 23-1. Location of nerves passing through the anterior neck that are susceptible 

to injury from penetrating trauma. 





Letterle, MD 

FIGURES 

Figure 23-1

Figure 23-2. Cross section of the anterior neck at the level of C6, looking down from 

above, showing structures that may be injured. 





Letterle, MD 

FIGURES 

Figure 23-2

Figure 23-3. Area of the face where facial lacerations may injure the parotid gland, 

Stensen's duct, or facial nerve branches. 





Letterle, MD 

FIGURES 

Figure 23-3

Figure 23-4. Panorex of the mandible, demonstrating a right ramus fracture (A) and a 

left parasymphyseal fracture (B). 





Letterle, MD 

FIGURES 

Figure 23-4

Figure 23-5. Anterior (left) and lateral (right) views of Le Fort maxillary fracture sites. A: 

Le Fort I. B: Le Fort II. C: Le Fort III. 





Letterle, MD 

FIGURES 

Figure 23-5

Figure 23-6. Diagram of a zygomaticomaxillary complex (ZMC) fracture. Note disruption 

of both the lateral orbital rim and the orbital floor, as well as the zygomatic arch. 





Letterle, MD 

FIGURES 

Figure 23-6

Figure 23-7. Three-dimensionally reconstructed facial CT scan. A. Left parasymphyseal 

mandibular fracture. B. Right zygomaticomaxillary complex (ZMC) fracture with inferior 

and lateral displacement of the ZMC. 





Letterle, MD 

FIGURES 

Figure 23-7

Figure 23-8. Orbital blowout fracture (impure type) on CT scan. Sequential horizontal 

cuts through the mid skull show blowout fracture of the right orbit, with rupture of the 

orbital contents into the maxillary sinus (upper left frame). Edema of the orbital contents 

is causing protrusion of the right eyeball (lower left frame). 





Letterle, MD 

FIGURES 

Figure 23-8

Figure 23-9. Reduction of nasal fracture by anterior traction with forceps. (Redrawn and 

reproduced, with permission, from Wang MK, Macomber WB: Maxillofacial injuries. 

Chapter 14 in: Echert C [editor]: Emergency Room Care, 4th ed. Little, Brown, 1981.) 





Letterle, MD 

FIGURES 

Figure 23-9


INTRODUCTION 

Up to half of all trauma patients sustain some degree of thoracic injury. Between 20% 

and 25% of all trauma deaths are directly attributable to chest trauma. Thoracic trauma 

is a contributing factor in another 25% of trauma deaths. 


ESTABLISH ABCS 

Address the ABCs as previously outlined in Chapters 9 and 10. Specific issues must be 

considered in evaluating the ABCs in the patient with blunt or penetrating chest trauma. 

The airway can be obstructed at any level from the pharynx to the trachea. 

Abnormalities in breathing can be caused by several mechanisms: (1) impairments in 

the chest wall or musculature, for example, secondary to pain or because chest wall 

motion is not coordinated, (2) impairments in gas exchange secondary to atelectasis, 

contusion, or disruption of the respiratory tract, or (3) central nervous system (CNS) 

impairments secondary to drugs or head trauma. Hypoxia is the most important feature 

of chest injury. Early interventions should attempt to ensure that an adequate amount of 

oxygen is delivered to the portions of the lung capable of normal ventilation and 

perfusion. Abnormalities in circulation can be caused by blood loss, increased 

intrapleural pressure, blood in the pericardial sac, vascular disruption, or myocardial 

dysfunction. Because shock will most often be caused by blood loss, the first step is to 

ensure adequate fluid resuscitation. 

EMERGENCY DEPARTMENT THORACOTOMY 

The role of emergency department thoracotomy is controversial. Indications for 

thoracotomy are (1) penetrating thoracic wound with agonal state or recent loss of vital 

signs, deterioration or cardiac arrest after care has been initiated, or uncontrolled 

hemorrhage from the thoracic inlet or out of a chest tube, (2) need for open cardiac 

massage or occlusion of the descending thoracic aorta before laparotomy, or (3) 

suspected subclavian vessel injury with intrapleural exsanguination. Contraindications to 

thoracotomy include penetrating trauma with no signs of life in the field or blunt trauma 

with no signs of life on arrival in the emergency department. Perform thoracotomy only if 

immediate surgical backup is available. 

Aihara R et al: Emergency room thoracotomy for penetrating chest injury: effect of an 

institutional protocol. J Trauma 2001; 50(6):1027. [PMID: 11426116] 

Feliciano DV, Rozycki GS: Advances in the diagnosis and treatment of thoracic trauma. 

Surg Clin North Am 1999;79 (6):1417. [PMID: 10625986] (Review.) 

PAIN CONTROL

Pain may impair chest wall expansion and impede oxygenation. Pain should be relieved 

with small, frequent doses of narcotic medications (eg, 1-5 mg morphine, or 50-100 ug 

fentanyl, every 5-10 minutes). Reassess the patient's pain level constantly to ensure 

adequate analgesia. 

IMMEDIATELY LIFE-THREATENING THORACIC INJURIES 

IDENTIFIED ON PRIMARY SURVEY 

Several injuries need to be considered in the patient with chest trauma. These entities 

can cause severe hypoxia or shock. The diagnoses are made clinically and need to be 

addressed without waiting for any diagnostic testing. Patients presenting with any one of 

these entities should receive treatment as outlined below and be admitted to the 

hospital for further care. 

TENSION PNEUMOTHORAX 


• Absent or decreased breath sounds. 

• Hyperresonance to chest wall percussion on the affected side. 

• Tracheal deviation away from the pneumothorax in the setting of respiratory distress 

and hypotension. 


Tension pneumothorax develops when a one-way valve air leak occurs from either the 

lung or the chest wall. Air enters the pleural space but cannot escape, leading to 

increased intrapleural pressure, collapse of the lung, and shift of the mediastinal 

contents to the opposite side. Tension pneumothorax can result from blunt chest injury 

with resultant parenchymal lung injury but can also be secondary to positive pressure 

ventilation. Occasionally a small penetrating wound can cause a valve-like effect that 

allows air to enter the pleural space on inspiration but not exit on expiration. The 

collapse of the lung leads to right-to-left pulmonary shunting and resultant hypoxia. In 

addition, increased intrathoracic pressure and pressure on the vena cava can reduce 

venous return to the heart and lead to decreased cardiac output and shock. 


Pneumothorax is characterized by respiratory distress, tachypnea, and hypoxia. There 

will be hyperresonance to percussion and decreased or absent breath sounds on the 

affected side. With tension pneumothorax, the trachea will be deviated away from the 

affected side. Neck veins may be distended, but this sign may be absent if the patient is 

hypovolemic. The diagnosis of tension pneumothorax is made clinically. Patients with a 

tension pneumothorax need immediate treatment and should not wait for x-ray. Figure 

24-1 is a chest x-ray of a patient whose physical exam findings should have led the 

physician to perform a needle decompression instead of an x-ray. For stable patients, in 

whom a pneumothorax is suspected, diagnosis is confirmed with chest x-ray (Figure

24-2). 

Treatment 

Treatment for a tension pneumothorax is immediate tube thoracostomy (Chapter 6). If a 

chest tube is not immediately available, needle thoracostomy with a large-bore (= 

16-gauge) needle in the second intercostal space in the midclavicular line will convert 

the tension pneumothorax into a simple pneumothorax until a tube can be placed. In this 

instance, leave the needle in until a definitive chest tube can be placed. Opening the 

wound further with a gloved finger or a clamp can relieve a tension pneumothorax 

associated with a penetrating injury. For patients with simple pneumothoraces 

secondary to trauma, traditional teaching has been to drain the pneumothorax through a 

tube thoracostomy and admit the patient for observation. However, it has been shown 

that patients with small pneumothoraces detected on computed tomography (CT) scan 

appear at low risk for complications and may not require drainage. In addition, serial 

observations or simple aspiration have been shown to be safe in patients presenting 

later or with small simple pneumothoraces. 

Di Bartolomeo S et al: A population-based study on pneumothorax in severely 

traumatized patients. J Trauma 2001;51(4):677. [PMID: 11586158] 

Miller A: Management of pneumothorax. Practitioner 2002;246 (1631):108. [PMID: 

11852618] (Review.) 

OPEN PNEUMOTHORAX 


Large penetrating wounds of the thorax result in an immediate pneumothorax. Because 

there is equilibration between intrathoracic and atmospheric pressure, negative 

intrathoracic pressure cannot be generated. Effective ventilation is thus impaired 

because air goes through the chest wall rather than into the lung, resulting in severe 

hypoxia. The diagnosis is obvious, and therapy should be instituted immediately. 

Treatment 

Cover the chest wound with an occlusive dressing (eg, petrolatum gauze) taped on 

three sides. This temporarily seals the wound and prevents development of a tension 

pneumothorax. More definitive treatment involves placing a large-bore chest tube on the 

affected side and closing the wound. 

MASSIVE HEMOTHORAX 


• Decreased breath sounds and dullness to chest wall percussion on the affected side. 

• Respiratory distress and hypotension.


Injury to the chest wall, great vessels, or lung can result in intrapleural bleeding or 

hemothorax. Most commonly these are secondary to penetrating injury disrupting 

pulmonary or systemic blood vessels. In hemothorax associated with great vessel injury, 

50% of patients die immediately, 25% live 5-10 minutes, and 25% live 30 minutes or 

longer. Respiratory insufficiency depends on how much blood is lost. In massive injury, 

the affected lung is collapsed, producing a right-to-left shunt. The loss of blood also 

leads to circulatory compromise. 



Respiratory distress, tachypnea, and a variable degree of hypoxia are present. There is 

dullness to percussion and decreased breath sounds on the affected side. Depending 

on the degree of blood loss, hypotension and flat neck veins may be present. Pulse 

pressure is narrow. Small hemothoraces may be difficult to detect in supine patients. 

B. Imaging 

Diagnosis is confirmed by chest x-ray (Figure 24-3 ). Small hemothoraces ( 1500 mL) have a ground-glass appearance on the supine film. 

Treatment 

For massive hemothorax, perform tube thoracostomy immediately without waiting for 

diagnostic tests. For smaller hemothoraces, diagnosis can be confirmed before 

instituting therapy. Tube thoracostomy using one or two large-bore chest tubes allows 

for accurate assessment of current and ongoing blood loss. Consider autotransfusion 

for patients with large bleeds (> 1 L). Initial blood loss of more than 1-1.5 L or ongoing 

continuing loss of more than 250 mL/h requires surgery. 

McGhee A, Swinton S, Watt M: Use of autologous transfusion in the management of 

acute traumatic haemothorax in the accident and emergency department. J Accid 

Emerg Med 1999;16(6):451. [PMID: 10572824] 

CARDIAC TAMPONADE 


• Signs and symptoms include dyspnea, narrow pulse pressure, hypotension, and 

tachycardia. 

• Bedside focused assessment with sonography for trauma (FAST) exams can be 

diagnostic.


Cardiac tamponade occurs when arterial, ventricular, or atrial injury causes blood to 

leak into the pericardium. True tamponade is rare and is most often associated with 

penetrating injuries. The pericardium is acutely not very distensible, and tamponade can 

occur even with a small amount (200 mL) of blood. The increased intrapericardial 

pressure compresses the heart and decreases cardiac output. In addition, venous return 

and cardiac filling decrease. Increased pressure may also lead to a decrease in 

myocardial perfusion. These factors lead to a decrease in cardiac output. Hypotension 

and shock then can result. 



Symptoms and signs of tamponade are nonspecific. Tachycardia and narrow pulse 

pressure are usually present. Beck's triad of hypotension, muffled heart tones, and 

distended neck veins is present in a minority of patients with tamponade from blunt 

trauma. Jugular venous distension may be absent because of coexisting hypovolemia. 

B. Imaging 

No specific findings on chest x-ray will confirm the diagnosis. Because tamponade can 

occur with a small effusion, heart size may not be significantly increased. Bedside 

focused assessment with sonography for trauma (FAST) exams (Chapters 6 and 25) 

are performed in many emergency departments to quickly identify pericardial effusions 

in patients with blunt or penetrating trauma. FAST exams allow rapid detection of 

pericardial fluid, with high sensitivity and specificity. An emergent thoracotomy can be 

life saving in an unstable patient with a pericardial effusion. In a stable patient, the 

diagnosis of pericardial effusion can be confirmed with transthoracic or transesophageal 

echocardiogram. Echocardiography can also define the hemodynamic impact of the 

effusion on cardiac function. When ultrasound or echocardiography is not available, for 

the stable patient, CT scan is sensitive for detection of pericardial fluid. However, CT 

scan does not allow assessment of cardiac dynamics. 

Treatment 

Pericardiocentesis has been advocated in the past as both a diagnostic and a 

therapeutic modality. However, there are serious limitations. Pericardiocentesis has 

been reported to result in up to 80% false negatives and 35% false positives. In acute 

injury a large part of the pericardial blood may be clotted and so will not be aspirated 

through even a large-bore needle. Pericardiocentesis may injure the heart or other 

organs and may cause delays in definitive care. With these caveats, in a stable patient, 

ultrasound-guided pericardiocentesis has been shown to be safe and reliable. In 

patients who are unstable or in severe shock with signs and symptoms consistent with 

cardiac tamponade, immediate thoracotomy allows relief of the tamponade and control 

of myocardial injury. 

Exadaktylos AK et al: Do we really need routine computed tomographic scanning in the 

primary evaluation of blunt chest trauma in patients with "normal" chest radiograph? J 

Trauma 2001;51(6):1173. [PMID: 11740271]

Salem K, Mulji A, Lonn E: Echocardiographically guided pericardiocentesis—the gold 

standard for the management of pericardial effusion and cardiac tamponade. Can J 

Cardiol 1999;15(11):1251. [PMID: 10579740] 

Tsang TS et al: Diagnostic value of echocardiography in cardiac tamponade. Herz 

2000;25(8):734. [PMID: 11200121] 

FLAIL CHEST 

Flail chest occurs when a segment of the chest does not have bony contiguity with the 

rest of the thoracic cage. When negative intrathoracic pressure is generated on 

inspiration, the flail segment moves inward, thus reducing tidal volume. Usually a 

significant blunt force is required (eg, motor vehicle collision or a fall from a height). The 

major complication is respiratory failure due to the underlying pulmonary injury. 


The two major symptoms of flail chest are pain and respiratory distress. Tachypnea with 

shallow respirations secondary to pain will be seen. Paradoxical chest wall movement 

may not occur in a conscious patient due to splinting of the chest wall. Crepitus is often 

present. Even with marked flail chest, the patient may be able to compensate initially for 

the reduced tidal volume by hyperventilating. When fatigue or underlying pulmonary 

injury develops, frank respiratory failure may supervene. 

Treatment 

Supplemental oxygen is the first-line treatment. Pain control with intravenous morphine 

or fentanyl should be instituted early. Epidural or intercostal nerve blocks have also 

been used but usually not in the immediate management of these injuries. Consider 

early intubation and mechanical ventilation. Approximately 50% of patients will need 

immediate intubation. Indications for early ventilation include marked hypoxia or 

inadequate breathing. External chest wall supports (taping, sandbags) reduce pain with 

movement of the flail segment, but they also reduce vital capacity and may worsen 

respiratory function; therefore, they are not indicated. 

Albaugh G et al: Age-adjusted outcomes in traumatic flail chest injuries in the elderly. 

Am Surg 2000;66(10):978. [PMID: 11261629] 

Sivaloganathan M, Stephens R, Grocott M: Management of flail chest. Hosp Med 

2000;61(11):811. [PMID: 11198758] (Review.) 

POTENTIALLY LIFE-THREATENING INJURIES IDENTIFIED ON 

SECONDARY SURVEY 

A careful and thorough secondary survey will identify multiple non-life-threatening chest 

injuries. Their prompt recognition and treatment may lead to an overall reduction in 

morbidity and mortality.

PULMONARY CONTUSION 


• Signs and symptoms include dyspnea, hemoptysis, tachycardia, palpable rib fractures, 

chest wall bruising, decreased breath sounds, or crackles on pulmonary auscultation. 

• Initially a pulmonary contusion may not be well visualized by chest radiograph. 


Pulmonary contusions are injuries of the lung parenchyma with hemorrhage and edema 

without associated laceration. They are the most frequent intrathoracic injuries in 

nonpenetrating chest trauma. They occur in approximately 30-75% of patients with 

significant blunt chest trauma. Pulmonary contusions typically occur at the site of impact 

and are often associated with other thoracic injuries such as rib fractures and flail chest, 

although they may occur alone. Pneumonia is the most common complication of 

pulmonary contusions, but their presence is a risk factor for the development of acute 

respiratory distress syndrome and long-term disability. 



Pulmonary contusion is often silent during the initial trauma evaluation. Significant 

trauma as well as the presence of other associated thoracic and extrathoracic injuries 

should raise the clinician's suspicion that pulmonary contusion is present. The most 

important sign of pulmonary contusion is hypoxia. The degree of hypoxemia correlates 

directly with the size of the contusion. Large contusions lead to significant respiratory 

distress. Other clinical findings suggestive of pulmonary contusion include dyspnea, 

hemoptysis, tachycardia, and other evidence of chest injury such as palpable rib 

fractures, chest wall bruising, decreased breath sounds, or crackles on pulmonary 

auscultation. 

B. Imaging 

Chest x-ray findings may range from patchy interstitial infiltrates to complete lobar 

opacification. Chest x-ray will initially miss a substantial number of pulmonary 

contusions, but as a result of ongoing hemorrhage and edema, radiographic evidence of 

contusion is usually apparent within 6 hours of injury. Because the size of the contusion 

may help predict the clinical course, a thoracic CT scan may provide additional useful 

information. Animal studies suggest that CT scans will identify contusions in 100% of 

those with experimentally induced pulmonary injury. Therefore, chest x-ray should be 

followed by CT scan when the likelihood of undetected injury is high and identification of 

the injury will alter its management. 

Treatment 

Early recognition and treatment of pulmonary contusion is essential to prevent long-term 

complications. The mainstay of treatment is supportive care and consists of the careful

use of intravenous fluids to ensure euvolemia, supplemental oxygen, chest 

physiotherapy, and if severe, the use of mechanical ventilation with positive 

end-expiratory pressure (PEEP). 

Disposition 

All patients with radiographic evidence of pulmonary contusion or clinical findings 

suggestive of pulmonary contusion should be admitted for monitoring and respiratory 

support. 

Greenberg MD, Rosen CL: Evaluation of the patient with blunt chest trauma: an 

evidence based approach. Emerg Med Clin North Am 1999;17(1):41. [PMID: 10101340] 

(Review.) 

Miller PR et al: ARDS after pulmonary contusion: accurate measurement of contusion 

volume identifies high-risk patients. J Trauma 2001;51(2):223; discussion, 229. [PMID: 

11493778] 

Moomey CB Jr et al: Cardiopulmonary function after pulmonary contusion and partial 

liquid ventilation. J Trauma 1998;45 (2):283. [PMID: 9715185] 

MYOCARDIAL CONTUSION 

Between 15% and 20% of patients sustaining significant thoracic trauma have some 

degree of cardiac involvement. Myocardial contusions are distinct areas of hemorrhage 

that are typically subendocardial but may extend transmurally. The right ventricle is 

most commonly involved due to its proximity to the sternum. Contusions of the 

myocardium typically produce wall motion abnormalities that may lead to conduction 

defects, dysrhythmias, or a decrease in cardiac output leading to cardiogenic shock. 


The clinical presentation of myocardial contusion is nonspecific. Patients are often 

asymptomatic but may complain of chest pain, have subtle electrocardiographic 

changes, or present with hypotension secondary to cardiac dysmotility. Specific 

standardized criteria for the diagnosis of myocardial contusion do not exist. Studies that 

have been used to make the diagnosis include the following: 

A. Electrocardiogram 

A normal electrocardiogram (ECG) does not exclude the possibility of myocardial 

contusion, but it is the best screening tool. Obtain an ECG whenever significant thoracic 

trauma is present, particularly if concomitant injuries such as flail chest, rib fractures, or 

pulmonary contusion are present. Similarly, obtain an ECG for trauma patients 

complaining of chest pain, for those with unexplained hypotension, and for those with a 

history of coronary artery disease. The most common finding by ECG in myocardial 

contusion is sinus tachycardia followed by nonspecific ST and T wave changes. A range 

of dysrhythmias and conduction disturbances may be evident, however, including ST 

elevation, atrial fibrillation, atrial flutter, premature ventricular contractions, ventricular 

tachycardia, ventricular fibrillation, first-degree heart block, and right bundle branch

lock. Although a normal ECG cannot exclude the presence of a myocardial contusion, 

the literature suggests that very few patients with normal ECGs develop complications. 

B. Biochemical Markers 

There is much debate in the literature regarding the value of obtaining cardiac enzymes 

in the evaluation of the patient with potential myocardial contusion. Although troponin 

and CK-MB are specific markers for myocardial injury in myocardial infarction, they 

should not be obtained routinely in the evaluation of these patients. Cardiac enzymes 

have not been shown to diagnose clinically significant contusions or predict the 

development of complications or need for hospital admission. 

C. Echocardiography 

Transthoracic and transesophageal echocardiography should not be used as screening 

tools for myocardial contusion. They are best used in the evaluation of patients with 

unexplained hypotension or persistent electrocardiographic abnormalities to exclude 

other potential cardiac injuries such as pericardial tamponade and ventricular rupture. 

Although both studies will identify wall motion abnormalities consistent with myocardial 

contusion, they have not been shown to predict or prevent clinical complications. 

Treatment 

There is no particular treatment for myocardial contusion other than to treat the potential 

complications as they arise. Monitor patients at all times. Treat dysrhythmias as 

discussed in Chapter 35. There is no role for the administration of prophylactic 

antidysrhythmics. Patients who subsequently develop myocardial infarction should 

receive appropriate treatment, but thrombolytics should not be given to trauma patients. 

Disposition 

Asymptomatic stable patients with normal ECGs and no evidence of other thoracic 

injury may be safely discharged from the emergency department. Elderly patients and 

those with a history of coronary artery disease, significant blunt thoracic trauma, ECG 

changes, or hypotension should be admitted for monitoring. 

Bertinchant JP et al: Evaluation of incidence, clinical significance, and prognostic value 

of circulating cardiac troponin I and T elevation in hemodynamically stable patients with 

suspected myocardial contusion after blunt chest trauma. J Trauma 2000;48(5):924. 

[PMID: 10823538] 


Surg Clin North Am 1999:79 (6):1417-29. [PMID: 10625986] (Review.) 



(Review.) 

DIAPHRAGMATIC HERNIA


• Delayed presentation is common. 

• A chest radiograph demonstrating a nasogastric tube above the diaphragm is 

diagnostic. 


Diaphragmatic hernias have been reported in 1-5% of patients sustaining blunt chest or 

abdominal trauma. They result either from direct violation of the diaphragm or from 

significant intra-abdominal or intrathoracic pressure applied to the diaphragm resulting 

in its rupture. The right side is affected up to three times less often than the left because 

it is relatively well protected by the liver. Up to 50% of these injuries are missed on the 

initial trauma evaluation, and their delayed presentation may not be clinically significant 

until herniation of abdominal contents through the diaphragm results in obstruction, 

incarceration, strangulation, perforation, or even death. Once a tear in the diaphragm 

occurs, it will not heal spontaneously, allowing for the herniation of abdominal contents 

into the chest cavity. Delayed presentations of patients with blunt diaphragmatic rupture 

have been reported up to 50 years after the primary traumatic event. 



Patients with diaphragmatic hernias may be asymptomatic, particularly in the acute 

phase, or may present with symptoms of bowel obstruction. Delayed presentation is 

common with nonspecific respiratory or bowel complaints, given that early diagnosis is 

difficult to establish and often missed. 

B. Imaging 

The chest x-ray is a valuable screening tool in detecting blunt diaphragmatic rupture. 

The initial x-ray is interpreted as normal in up to 50% of acute cases but will be 

abnormal in almost 100% of delayed presentations. Findings on an upright chest x-ray 

suggestive of diaphragmatic rupture include elevation or irregularity of the 

diaphragmatic border, unilateral pleural thickening, obvious herniation of abdominal 

contents into the chest cavity, and the presence of a nasogastric tube in the chest cavity 

(Figure 24-4). CT scans are often used preoperatively in the hemodynamically stable 

patients but have had less than satisfactory results in reporting isolated diaphragmatic 

injuries. Right-sided lesions are often missed because the contour of the right 

diaphragm is difficult to discern from the contour of the liver. 

Treatment 

Surgical reduction of the hernia and repair of the diaphragm is mandatory in all patients 

with diaphragmatic rupture. Care should be taken to avoid abdominal injury when 

placing a chest tube in patients with concomitant hemothorax or pneumothorax. 

Nursal TZ et al: Traumatic diaphragmatic hernias: a report of 26 cases. Hernia

2001;5(1):25. [PMID: 11387719] 

Shanmuganathan K, and Mirvis SE: Imaging diagnosis of nonaortic thoracic injury. 

Radiol Clin North Am 1999;37(3)533. [PMID: 10361545] (Review.) 

Singh S et al: Diaphragmatic rupture presenting 50 years after the traumatic event. J 

Trauma 2000;49(1):156. [PMID: 10912874] (Review.) 

ESOPHAGEAL DISRUPTION 

Esophageal disruption or perforation is an infrequent injury sustained secondary to blunt 

trauma. The mechanism of injury is unclear, but most occur during high-speed motor 

vehicle collisions and are typically associated with other serious thoracic injuries. 

Although their occurrence is rare, the reported mortality is more than 20% because of 

resultant complications of mediastinitis, which include pericarditis, pneumonitis, 

empyema, and even aortic erosion. 



Esophageal injuries are difficult to diagnose. The symptoms and signs are often 

nonspecific and masked by other serious injuries. It should always be suspected in the 

patient with evidence of serious neck, thoracic, back, or abdominal injury. Patients may 

complain of throat pain, dysphagia, odynophagia, hoarseness, choking, chest pain, 

hematemesis, dyspnea, or continued neck pain despite appropriate treatment and 

immobilization. Neck redness, swelling, unexplained tachycardia, subcutaneous 

emphysema of the neck or chest, and bloody nasogastric tube contents may be found 

on physical exam. 

B. Imaging 

Chest x-ray findings suggestive of esophageal injury include pneumomediastinum, 

widened mediastinum, and left pleural effusion. Gastrografin followed by barium swallow 

and esophagoscopy are probably the best diagnostic tools available for the detection of 

esophageal perforation; however, detailed exploratory surgery may be necessary for 

definitive diagnosis. 

Treatment 

Treatment of esophageal perforations depends on the location and the extent of the 

injury. Nonoperative management with drainage, antibiotics, and nutritional support may 

be appropriate for some injuries, but most require aggressive surgical management to 

prevent extensive spread of infection to the mediastinal and pleural cavities. 

Monzon JR, Ryan B: Thoracic esophageal perforation secondary to blunt trauma. J 

Trauma 2000;49(6):1129. [PMID: 11843720] 

Nakai S et al: Esophageal injury secondary to thoracic spinal trauma: the need for early 

diagnosis and aggressive surgical treatment. J Trauma 1998;44(6):1086. [PMID: 

9637167]

Shanmuganathan K, Mirvis SE: Imaging diagnosis of nonaortic thoracic injury. Radiol 

Clin North Am 1999;37(3)533. [PMID: 10361545] (Review.) 

AORTIC DISRUPTION 


• Consider the diagnosis in all patients with rapid deceleration injuries. 

• Signs and symptoms include chest pain, back pain, dyspnea, intrascapular murmur, 

and extremity pain caused by ischemia. 


Traumatic aortic rupture is a common cause of death in blunt trauma. Injury is typically 

caused by rapid deceleration and shearing forces sustained in motor vehicle collisions, 

falls, and crush injuries and most commonly involves the descending segment of the 

aorta just past the origin of the left subclavian artery. More than 80% of patients die at 

the scene. Another 10-20% of patients with aortic disruption will die within the first hour. 

Rapid diagnosis and treatment are essential to limit the mortality associated with these 

injuries. 



Consider aortic injury in all patients involved in rapid deceleration accidents. Clinical 

signs and symptoms suggestive of aortic injury include chest pain, back pain, dyspnea, 

intrascapular murmur, and extremity pain caused by ischemia. Patients may be 

hypertensive or hypotensive or may present with pseudocoarctation in which the upper 

extremities are hypertensive and the lower extremities have minimal blood pressure and 

pulse deficits. Fewer than 50% of patients have external signs of trauma. 

B. Imaging 

Chest x-ray is an excellent screening tool for blunt aortic injury and is commonly used to 

determine the need for further studies. Mediastinal widening greater than 8 cm is the 

chest x-ray abnormality that most commonly leads to further workup. Other findings 

suggestive of aortic injury include indistinct aortic knob, left mainstem bronchus 

depression, tracheal deviation to the right, nasogastric tube deviation, widening of the 

right paratracheal stripe (> 5 mm), apical capping, and obliteration of the space between 

the pulmonary artery and the aorta (Figure 24-5). Despite its use as a screening tool, 

chest x-rays are normal in 2-7% of patients with aortic injury. 

Angiography remains the gold standard for diagnosis of aortic injury. Angiography is 

expensive, time consuming, invasive, and requires a large dye load. Because the 

clinical indicators for blunt aortic injury are often nonspecific, a large number of 

aortograms have been performed in patients with normal aortas.

More recently, CT scan of the chest has been utilized in the evaluation of aortic injury 

and angiography is saved for those patients with abnormal findings by CT. CT is less 

expensive than angiography and can be performed much more quickly. With the 

newer-generation scanners and the use of intravenous contrast and consistent 

protocols, the sensitivity and specificity for aortic injury approaches 100%, particularly 

when criteria for positive scans include periaortic hematoma along with direct signs of 

aortic injury. 

Treatment 

Treatment of blunt aortic injury includes pharmacologic management of blood pressure 

and prompt surgical repair. 

Dyer DS et al: Thoracic aortic injury: how predictive is mechanism and is chest 

computed tomography a reliable screening tool? A prospective study of 1,561 patients. 

J Trauma 2000;48 (4):673. [PMID: 10780601] 


Surg Clin North Am 1999;79(6): 1417. [PMID: 10625986] (Review.) 



(Review.) 

Nagy K et al: Guidelines for the diagnosis and management of blunt aortic injury: an 

EAST Practice Management Guidelines Work Group. J Trauma 2000;48(6):1128. 

[PMID: 10866262] 

TRACHEOBRONCHIAL INJURY 


• Signs and symptoms include dyspnea, subcutaneous emphysema of the neck or 

upper thoracic region, hemoptysis, and hypoxia. 

• Suspect tracheobronchial injury if pneumothorax persists despite appropriate tube 

thoracostomy. 


Injury to the trachea or bronchus as a result of blunt trauma is relatively uncommon but 

can be quite severe. Approximately 80% of patients with tracheobronchial injuries die 

before reaching a hospital. Tracheobronchial injuries are usually the result of motor 

vehicle collisions and crush injuries. Right-sided bronchial injuries occur more 

commonly and are typically more severe; almost 80% occur within 2 cm of the carina. 

The diagnosis of tracheobronchial injury is missed in at least 25% of patients during the 

initial trauma evaluation.



Patients may be comfortable on room air or may present in acute respiratory distress. 

The most common clinical symptoms and signs suggestive of injury to the trachea or 

bronchus are dyspnea and subcutaneous emphysema of the neck or upper thoracic 

region but may also include hoarseness, hemoptysis, hypoxia, and persistent 

pneumothorax despite appropriate tube thoracostomy. 

B. Imaging 

Chest x-ray findings indicative of tracheobronchial injury include subcutaneous 

emphysema, pneumomediastinum, pneumothorax, and peribronchial air. 

Treatment 

Patients in respiratory distress with suspected tracheobronchial injury should be 

endotracheally intubated, preferably over a bronchoscope if time allows. Blind intubation 

is discouraged because it may result in the complete disruption of small tracheal 

lacerations. Stable patients with suspected trauma to the trachea or bronchi should 

undergo immediate bronchoscopy for definitive evaluation and localization of the injury 

followed by operative repair. 

Cassada DC et al: Acute injuries of the trachea and major bronchi: importance of early 

diagnosis. Ann Thorac Surg 2000;69(5): 1563. [PMID: 10881842] (Review.) 

Kiser AC et al: Blunt tracheobronchial injuries: treatment and outcomes. Ann Thoracic 

Surg 2001;71(6):2059. [PMID: 11426809] (Review.) 

Shanmuganathan K, Mirvis SE: Imaging diagnosis of nonaortic thoracic injury. Radiol 

Clin North Am 1999;37(3)533. [PMID: 10361545] (Review.) 

OTHER INJURIES 

RIB FRACTURES 

Rib fractures are the most common injury sustained in blunt thoracic trauma. They are 

usually sustained in motor vehicle collisions. Fractures of the first rib usually indicate 

severe trauma because of the force necessary to produce such an injury. Fractures may 

cause localized pain, crepitus, pain with inspiration, and dyspnea and may even cause 

pneumothorax or hemothorax. Mortality increases with the number of ribs involved. The 

pain associated with rib fractures may lead to hypoventilation, atelectasis, retained 

secretions, and finally pneumonia. 


Chest x-ray is the screening tool of choice for the detection of rib fractures, although up 

to 50% of rib fractures cannot be detected on chest x-ray. They may also be identified 

by specific rib x-rays and CT scan.

Treatment 

Rapid mobilization, respiratory support, and pain management are the mainstays of 

treatment for multiple rib fractures. Continuous body positioning and oscillation therapy 

prevent hypoventilation and atelectasis by promoting redistribution of ventilation and 

perfusion to various lung segments. Mechanical ventilation allows for healing of the ribs 

and prevention of complications in the patient with respiratory failure. Incentive 

spirometry is excellent supportive therapy in stable patients. Pain control is paramount 

in facilitating adequate ventilation. Epidural anesthesia with bupivacaine controls pain 

without causing sedation and impairing the cough reflex. 

Disposition 

Treatment of isolated rib fractures in young, healthy patients without evidence of other 

serious underlying injury involves pain medications and deep breathing exercises with 

incentive spirometry. These patients do not require routine admittance or serial 

radiographic studies. Consider admitting elderly or other patients with serious underlying 

lung disease and isolated rib fractures. These patients have a higher complication rate 

due to a higher prevalence of hypoventilation, atelectasis, and pneumonia. 

Easter A: Management of patients with multiple rib fractures. Am J Crit Care 

2001;10(5):320. [PMID: 11548565] (Review.) 

STERNAL FRACTURE 

Most sternal fractures are associated with blunt trauma (eg, motor vehicle collisions). 

They are most common in postmenopausal females. 


Pleuritic midline chest pain with focal tenderness over the sternum. There may be some 

pain with respiration, but there should be no pulmonary compromise. Because sternal 

fractures can be associated with myocardial contusions, evaluate patients for any 

evidence of myocardial injury as outlined previously. 

Treatment 

In the absence of complications, therapy for sternal fractures is mainly symptomatic. 

Give adequate analgesia with narcotics as necessary. 

Disposition 

Patients who have isolated sternal fractures and no evidence of other injuries can be 

safely sent home. Admit patients who have cardiovascular complications. Consider 

admission for patients who require more than standard doses of narcotics for analgesia 

or for patients who have limited social support. 

Sadaba JR, Oswal D, Munsch CM: Management of isolated sternal fractures: 

determining the risk of blunt cardiac injury. Ann R Coll Surg Engl 2000;82(3):162.

[PMID: 10858676] (Review.) 

SYSTEMIC AIR EMBOLISM 

Lung trauma in which air passages, lung parenchyma, or blood vessels are lacerated 

may result in a direct communication between these structures. Air can enter the 

pulmonary venous system as a result of a gradient caused by low pulmonary venous 

pressure (hypovolemia) or increased airway pressure (positive pressure ventilation, 

tension pneumothorax). Pulmonary venous air embolizes systemically, including 

coronary and cerebral circulation. Air embolization occurs most commonly after 

penetrating trauma. 


Hemoptysis, circulatory, and CNS dysfunction immediately after initiation of positive 

pressure ventilation suggest air embolism. Focal neurologic abnormalities in the 

absence of head injury are common. Circulatory arrest after the initiation of mechanical 

ventilation suggests air embolism. Funduscopic examination may reveal air in the retinal 

vessels. Air in arterial blood gases (not due to froth) is diagnostic. Transesophageal 

echocardiography has been suggested as a diagnostic tool. 

Treatment 

Oxygenation is the first-line treatment. Selective lung ventilation has been advocated as 

a means of isolating the affected lung and stopping or minimizing the flow of gas into the 

circulation. Alternatively, high-frequency ventilation has been shown to be effective by 

allowing decreased ventilatory volumes and pressures. For moribund patients, 

thoracotomy and clamping of the hilum of the affected lung has been advocated. 

Cerebral air embolism has been treated with hyperbaric oxygen therapy, but other 

priorities may preclude or delay its use. 

Ho AM, Ling E: Systemic air embolism after lung trauma. Anesthesiology 

1999;90(2):564. [PMID: 9952165] (Review.) 

TRAUMATIC ASPHYXIA 

Severe crush injury of the thorax or abdomen can cause retrograde flow of blood from 

the right heart into the great veins of the head and neck. 


The face and neck are a purplish-bluish color. Subconjunctival and retinal hemorrhages 

are common. Intracerebral bleeds are uncommon, but loss of consciousness or 

neurologic abnormalities can be caused by cerebral hypoxia. Traumatic asphyxia can 

indicate the possibility of other intrathoracic injuries associated with the severe crushing 

force. 


There is no specific therapy except oxygenation. Treat other injuries appropriately. 

Hospitalize patients for observation. 

COMMOTIO CORDIS 

Commotio cordis is the condition of sudden cardiac death or near sudden cardiac death 

after blunt, low-impact chest wall trauma in the absence of structural cardiac 

abnormality. Ventricular fibrillation is the most commonly reported arrhythmia induced in 

commotio cordis. Young male athletes aged 5-18 years are particularly at risk for this 

catastrophe. It has been described after blows to the chest from baseballs, softballs, 

hockey pucks, and other objects. Death is usually instantaneous, and successful 

resuscitation is uncommon. 

Link MS et al: What is commotio cordis? Cardiol Rev 1999;7 (5):265. [PMID: 11208236] 

(Review.) 

PENETRATING TRAUMA 

Penetrating trauma to the chest is usually inflicted by stabbing or gunshot but can 

include other foreign bodies or impalement injuries. Stab wounds commonly injure the 

ascending aorta, whereas gunshot wounds more typically injure the descending thoracic 

aorta, although laceration of the pericardium and any of the thoracic great vessels may 

occur. 


Information regarding the type of weapon, length or caliber of weapon, distance from the 

weapon, and amount of hemorrhage at the scene can be helpful when evaluating the 

patient with penetrating thoracic trauma. Most patients are hemodynamically unstable, 

and a rapid but thorough examination is essential. Address the ABCs first. 


During the secondary survey, evaluate patients for signs of vascular injury including 

unequal blood pressures of the extremities, new vascular bruits, and the classic signs of 

pericardial tamponade: distended neck veins, muffled heart sounds, and hypotension. 

Obtain a chest x-ray immediately to identify pneumothorax, hemothorax, or foreign 

body. Placing radioopaque markers at the sites of wound entry and exit can be helpful in 

the interpretation of the chest x-ray. Bedside emergency FAST exams for the evaluation 

of pericardial tamponade can be extremely helpful in identifying the need for 

thoracotomy in the penetrating trauma patient with signs of shock. The same 

life-threatening and potentially life-threatening injuries described in blunt trauma can 

occur with penetrating trauma to the chest and should be managed as discussed in 

those sections. 

Treatment 

Address significant shock immediately with intravenous fluid boluses and blood 

transfusion, although some data suggest that aggressive fluid resuscitation may

increase the amount of uncontrolled hemorrhage and subsequent mortality. Patients 

with pericardial tamponade require emergent pericardial window or thoracotomy. 

Perform tube thoracostomy in patients with evidence of pneumothorax or hemothorax. 

Autotransfusion is indicated in patients with large hemothoraces. Patients with initial 

chest tube blood loss exceeding 1500 mL, significant ongoing hemorrhage of more than 

250 mL/h, or persistent hypotension should be taken directly to the operating room. 

Never remove impaled objects in the emergency department because they may provide 

tamponade to surrounding vascular structures. The patient should be stabilized and the 

object removed in the operating room. Angiography is the gold standard for the 

evaluation of hemodynamically stable patients at high risk for great vessel injury based 

on the trajectory of the wound, although CT angiography has increasingly demonstrated 

reliability. 

Disposition 

Asymptomatic patients sustaining low-risk peripheral wounds with normal physical 

examinations and negative initial chest x-rays may be safely discharged to home after a 

3-hour observation and repeat negative chest x-ray. Patients who develop delayed 

pneumothorax during this observation period require tube thoracostomy and admission. 

Role of Emergency Department Thoracotomy in Penetrating Injuries 

Emergency department thoracotomy is best utilized in patients sustaining penetrating 

thoracic injuries who have a witnessed cardiopulmonary arrest in the emergency 

department or lose signs of life during a short transport to the emergency department. 

Survival rates for cardiac injuries and stab wounds are typically better than noncardiac 

injuries and gunshot wounds. Thoracotomy for penetrating injuries yields an overall 

survival rate of approximately 11%. 

Practice management guidelines for emergency department thoracotomy. Working 

Group, Ad Hoc Subcommittee on Outcomes, American College of Surgeons-Committee 

on Trauma. J Am Coll Surg 2001;193(3):303. [PMID: 11548801] 

Shatz DV et al: Efficacy of follow-up evaluation in penetrating thoracic injuries: 3- v. 

6-hour radiographs of the chest. J Emerg Med 2001;20(3):281. [PMID: 11267818] 

Stern SA: Low-volume fluid resuscitation for presumed hemorrhagic shock: helpful or 

harmful? Curr Opin Crit Care 2001; 7(6):422. [PMID: 11805545] 

Wall MJ Jr et al: Thoracic aortic and thoracic vascular injuries. Surg Clin North Am 

2001;81(6):1375. [PMID: 11766181] (Review.) 



SECTION III - TRAUMA EMERGENCIES


INTRODUCTION

Figure 24-1. An ill-advised chest x-ray demonstrating tension pneumothorax. Clinical 

signs alone should be sufficient to diagnose this condition and avoid the life-threatening 

delay involved in obtaining an x-ray. 





FIGURES 

Figure 24-1

Figure 24-2. The chest x-ray demonstrates a large right pneumothorax with widening 

and deepening of the right costophrenic angle, also known as the deep sulcus sign. 

Occasionally this sign is the only radiographic indication of a pneumothorax in a supine 

patient. 





FIGURES 

Figure 24-2

Figure 24-3. Blunt trauma patient with left hemothorax. 





FIGURES 

Figure 24-3

Figure 24-4. Adult female with blunt thoracoabdominal trauma from a motor vehicle 

collision. Chest x-ray demonstrates the nasogastric tube in the chest indicative of a 

ruptured left hemidiaphragm. 





FIGURES 

Figure 24-4

Figure 24-5. A: Chest x-ray of hypotensive adult male injured in a high-speed motor 

vehicle collision. Findings: (1) widened mediastinum, (2) deviation of the trachea to the 

right, (3) widening of the right paratracheal stripe, (4) left apical cap, (5) blurring of the 

aortic knob, (6) deviation of the nasogastric tube to the right, and (7) obliteration of the 

aorto-pulmonary window. B: Computed tomography (CT) scan of the chest 

demonstrates (1) periaortic hematoma and (2) a true and false aortic lumen; widening of 

the right paratracheal stripe is also noted. C: (1) Periaortic hematoma is present with (2) 

a small left hemothorax. 





FIGURES 

Figure 24-5

25. Abdominal Trauma - Luis E. Rodriguez, MD, & John E. Gough, MD, 

FACEP 


Abdominal injuries may be life threatening and should be approached cautiously. After 

trauma, the abdomen may be a sanctuary for occult bleeding that, if not discovered and 

corrected expeditiously, may lead to deleterious consequences. Traditionally these 

injuries are classified as either blunt trauma, the majority of which are from motor 

vehicle collisions, and penetrating injuries, which are predominantly secondary to 

gunshot or stab wounds. Rapid assessment, stabilization, and early surgical 

consultation are recommended. 

Assessment 

Initial management of patients with abdominal trauma is the same as for all other 

trauma patients. Begin the assessment with a rapid primary survey, including evaluation 

of the airway, breathing, circulation, disability, and exposure. 

A. Airway 

Administer high-flow oxygen, and intubate the patient if necessary. Maintain cervical 

spine immobilization until potential injury is ruled out. 

B. Breathing 

Auscultate for breath sounds. Inspect for asymmetry of chest wall movement, open 

wounds, or flail segments. Pulse oximetry and capnography may be useful. Perform 

needle decompression or tube thoracostomy if tension pneumothorax is suspected. 


Stop gross external hemorrhage with direct pressure. Assess pulses, capillary refill, and 

blood pressure. Obtain intravenous access with at least 2 large-bore (= 16-gauge) 

catheters. If peripheral intravenous access is inadequate, place a central venous 

catheter. Fluid resuscitation is an area of controversy (see below). 

D. Disability 

Complete a brief, focused neurologic examination to document the patient's baseline. 

The examination should include an assessment of pupillary size and reactivity, a 

determination of the patient's Glasgow Coma Scale score, and notation of any focal 

neurologic deficits such as unilateral weakness or poor muscle tone. Ideally, perform the 

examination before administering pain medications, sedatives, or paralytics. 

E. Exposure 

Completely undress the patient. Begin a more thorough secondary survey, including 

logrolling the patient and examining all skin folds, the back, and axillas for occult 

penetrating injuries. Identify any puncture wounds and document their location. To help 

identify the trajectory of bullets, place a radiopaque marker (eg, paper clip) at the wound

site prior to obtaining x-rays. Do not remove impaled foreign bodies because they may 

be providing hemostasis from a vascular injury. Foreign body removal should be 

performed with surgical consultation in a more controlled setting. Avoid using terms 

such as entrance or exit wound on initial presentation, because it is often difficult to 

correctly make this assessment visually. These determinations are best left to a forensic 

pathologist. 

Any penetrating injury below the level of the nipple line warrants evaluation for 

intra-abdominal injury. In patients in motor vehicle collisions, look for ecchymosis or 

erythema in the area of the clavicles or across the abdomen. The classic "seatbelt sign" 

may indicate intra-abdominal trauma. 

Examine the abdomen for any tenderness, rigidity, or guarding. It is often difficult to 

assess bowel sounds at this stage of the exam. Evaluate the pelvis for anteroposterior 

or lateral instability with gentle pressure; this does not require much force. Examine the 

genitalia and look for blood at the urethral meatus, especially in males. Perform digital 

rectal examination in any patient with abdominal trauma. Look for gross blood, assess 

sphincter tone, and note any other evidence of trauma. There is no role for occult blood 

testing acutely in a trauma. If blood at the urethral meatus or a high-riding prostate is 

present, placement of a urinary catheter is contraindicated and a retrograde 

urethrogram is required to evaluate for potential urethral injury. 

Treatment 

A. Fluid Resuscitation 

The concept of acute fluid resuscitation has evolved and may represent an area of 

some controversy. Animal and human studies have demonstrated deleterious effects of 

aggressive fluid resuscitation, particularly if penetrating trauma is present. Rapid 

infusion of large amounts of crystalloids may disrupt the formation of the soft clot and 

dilute the clotting factors, leading to increased bleeding. The results are less clear in the 

setting of blunt trauma. Also, blood pressure alone is not the best indicator of the level 

of shock. Attempts to make the patient normotensive are not recommended. A more 

reasonable goal may be to obtain systolic blood pressure of 80-90 mm Hg or a mean 

arterial pressure of 70 mm Hg. Crystalloids remain first-line fluids, followed by infusions 

of packed red blood cells. Other blood products may be indicated on an individual basis. 

Synthetic hemoglobin preparations are under evaluation. 

B. Indications for Emergency Laparotomy 

Patients with gunshot wounds that have an intra-abdominal trajectory require 

exploratory laparotomy. Most other patients with penetrating abdominal injuries will also 

require laparotomy given the high incidence of intra-abdominal injury once the fascia 

has been violated. Hemodynamically unstable patients sustaining blunt or penetrating 

trauma with a positive screening test (such as focused assessment with sonography for 

trauma [FAST] exam or diagnostic peritoneal lavage [DPL]) require laparotomy to 

control hemorrhage and evaluate for intra-abdominal injuries. Patients with obvious 

diaphragmatic injury noted on chest x-ray require emergent laparotomy. 

C. Surgical Consultation 

Seek surgical consultation early in the management of patients with abdominal trauma,

especially if the patient is hemodynamically unstable. 

Pepe PE, Mosesso VN, Falk JL: Prehospital fluid resuscitation of the patient with major 

trauma. Prehosp Emerg Care 2002; 6:81. [PMID: 11789657] 

Velmahos GC, Tatevossian R, Demetriades D: The "seat belt" sign: a call for increased 

vigilance among physicians treating victims of motor vehicle accidents. Am Surg 

1999;65:181. [PMID: 9926756] 

Wotherspoon S, Chu K, Brown AF: Abdominal injury and the seat-belt sign. Emerg Med 

2001;13:61. [PMID: 11476415] 

Diagnostic Testing 

A. Laboratory Evaluation 

Initial laboratory evaluation should include hemoglobin and hematocrit to establish a 

baseline, and a blood-type and screen in case transfusion of packed red cells is 

needed. A lactate level may be obtained and, if elevated, is an excellent indicator of 

shock. Base deficit is another indicator of shock. The role of amylase in abdominal 

trauma is uncertain. Examination of the urine may reveal gross hematuria, which 

suggests significant injury to the urogenital tract (Chapter 26). 

B. Other Diagnostic Modalities 

1. Plain radiography—Almost all major trauma patients require plain x-rays of the 

chest, pelvis, and cervical spine. Although rarely utilized today, a one-shot intravenous 

pyelogram may be useful in patients with flank wounds or gross hematuria who are 

unable to undergo further diagnostic testing prior to operative intervention. Plain 

radiography of the abdomen is generally not helpful. 

2. Diagnostic peritoneal lavage—Although DPL is still used occasionally, concern has 

been raised that DPL is overly sensitive, leading to nontherapeutic laparotomies. Recent 

literature has advocated the use of DPL in conjunction with computed tomography (CT) 

scanning or laparoscopy, particularly in low-velocity penetrating trauma (ie, stab 

wounds), to decrease the number of negative or nontherapeutic laparotomies. If DPL is 

considered, it should be performed only after consultation with the trauma surgeon, who 

should perform this diagnostic study in most cases. 

3. CT scanning—In the hemodynamically stable patient, CT scanning is an excellent 

diagnostic modality that is easy to perform. If significant intra-abdominal injury is 

suspected and the hospital is not equipped to manage such patients, it is unwise to 

delay transfer in order to obtain a CT scan, assuming a reasonably expeditious transfer 

is possible. 

4. Ultrasonography—Emergency ultrasonography has been studied extensively and is 

accurate. Also, it is safe in special patient populations (eg, pediatrics, obstetrics). FAST 

exam (see Chapter 6) is a bedside test that has demonstrated good accuracy with 

minimal experience (at least 30 examinations). The FAST exam consists of an initial 

subxiphoid view of the pericardium, followed by examination of the right upper quadrant 

looking for the Morison pouch (hepatorenal space). The Morison pouch is one of the

most dependent parts of the abdomen and often shows the first signs of intraperitoneal 

fluid collection (blood). Subsequently the splenorenal interface in the left upper quadrant 

(Figure 25-1) is evaluated, followed by the pelvis. Unlike CT, a FAST exam is rapid, can 

be performed bedside in the emergency department, and is easily repeatable. 

5. Laparoscopy—The use of laparoscopy, with or without CT scanning or DPL, is being 

studied. It is less invasive than traditional laparotomies and may shorten hospital stays 

and decrease patient costs, although it requires surgical consultation. The role of 

laparoscopy is not well defined at this time. 

DeMaria EJ et al: Complementary roles of laparoscopic abdominal exploration and 

diagnostic peritoneal lavage for evaluating abdominal stab wounds: a prospective study. 

J Lapraroendosc Adv Surg Tech A 2000;10:131. [PMID: 10883989] 

Gonzales RP et al: Abdominal stab wounds: diagnostic peritoneal lavage criteria for 

emergency room discharge. J Trauma 2001;51:939. [PMID: 11706344] 

Gonzales RP, Ickler J, Gachassin P: Complementary roles of diagnostic peritoneal 

lavage and computed tomography in the evaluation of blunt trauma patients. J Trauma 

2001;51:1134. [PMID: 11740265] 

Goodwin H, Holmes JF, Wisner DH: Abdominal ultrasound examination in pregnant 

blunt trauma patients. J Trauma 2001;50:689. [PMID: 11303166] 

Gracias VH et al: Defining the learning for the focused abdominal sonogram for trauma 

(FAST) examination: implications for credentialing. Am Surg 2001;67:364. [PMID: 

11308006] 

Nagy KK, Roberts RR, Joseph KT: Experience with over 2500 diagnostic peritoneal 

lavages. Injury 2000;31:479. [PMID: 10908739] 

Patel JC, Tepas JJ: The efficacy of focused abdominal sonography for trauma (FAST) 

as a screening tool in the assessment of injured children. J Pediatr Surg 1999;34:44. 

[PMID: 10022141] 

Taner AS et al: Diagnostic laparoscopy decreases the rate of unnecessary laparotomies 

and reduces hospital costs in trauma patients. J Laparoendosc Adv Surg Tech A 

2001;11:207. [PMID: 11569509] 

Types of Injury 

A. Blunt Abdominal Injury 

Blunt injury occurs most frequently with motor vehicle collisions. Injuries occur 

secondary to shearing, tearing, or direct impact forces. The presence of a seatbelt sign 

is indicative of intra-abdominal injury in at least 25% of cases. Ascertain if only a lap belt 

was used, especially in children. Lap-only restraints in children predispose them to 

intra-abdominal injuries such as intestinal perforations. These injuries may be 

associated with transverse lumbar spine fractures (Chance fractures).

B. Penetrating Injuries 

Any wound inferior to a line drawn transversely between the nipples should be treated 

as having the potential for intra-abdominal trajectory. As noted earlier, intravenous fluids 

should be used judiciously in the prehospital setting. Before arrival at the emergency 

department, patients may be given enough fluids to maintain a systolic blood pressure 

of 90 mm Hg, rather than a multiliter resuscitation. If penetrating injuries are present, 

initiate antibiotic therapy and administer a tetanus booster early in treatment. 

1. Gunshot wounds—All gunshot wounds with an intra-abdominal trajectory require 

exploratory laparotomy. Patients presenting with hypotension despite crystalloid 

resuscitation will need immediate exploratory laparotomy, antibiotics to cover abdominal 

flora, and a tetanus booster. Once intraperitoneal invasion has been ruled out, 

conservative management of wounds that are superficial and tangential to the abdomen 

may be used. Seek surgical consultation in all cases of abdominal gunshot wounds. 

2. Stab wounds—Patients with stab wounds require resuscitation as well as tetanus 

booster and antibiotics if intraperitoneal violation is suspected. Stab wounds differ from 

gunshot wounds in that the former may be locally explored to determine if the 

peritoneum has been violated. A surgeon should conduct this procedure for all but the 

most superficial wounds, and adequate staff and lighting are required. DPL, CT 

scanning, and laparoscopy may be utilized. If peritoneal violation has been ruled out, 

patients may be safely discharged with local wound care instructions. If the peritoneum 

has been violated, exploratory laparotomy is required. 


SPLENIC INJURIES 


• Most common in blunt trauma. 

• Left upper quadrant pain and tenderness, often with radiation to left shoulder. 

• May cause significant hemodynamic instability. 

• CT scan is noninvasive and sensitive in stable patients; use FAST exam or laparotomy 

for unstable patients. 

• Delayed rupture may occur. 


Splenic injuries commonly occur secondary to blunt injury. Patients may present with 

small hematomas, lacerations, devascularization, or complete rupture (Figure 25-2). 

There are numerous classifications of splenic injury. Most classifications range from 

simple lacerations to complete rupture. 


Management of splenic injury has evolved. Not all injuries require splenectomy.

Hemodynamically stable patients with low-grade lesions may be observed. Children are 

excellent candidates for conservative therapy. Elderly patients are poor candidates, 

particularly if they have high-grade injuries or if CT scan demonstrates free fluid. If 

hypotension unresponsive to 2 L of intravenous crystalloid infusion is present, blood 

transfusion should be given and the patient prepared for surgery. All splenic injuries 

require consultation with a trauma surgeon. Consider admission for patients with any 

splenic injury. 

DIAPHRAGMATIC INJURIES (See also Chapter 24) 


• May be secondary to blunt or penetrating forces. 

• Rupture occurs predominantly on left side. 

• Often difficult to visualize on initial chest x-ray (nasogastric tube may enhance 

diagnosis). 

• CT scan or laparoscopy more sensitive. 

• Delays in diagnosis lead to increased morbidity and mortality. 

Diaphragmatic injuries are frequently difficult to detect initially. The presence of 

abdominal contents in the thorax may not be obvious on initial chest x-ray. Insertion of a 

nasogastric tube may facilitate the diagnosis (Figure 25-3). However, diaphragmatic 

ruptures may be missed even on initial CT scan. If abdominal viscera are seen in the 

thoracic cavity, then the diagnosis is made easy. Undiagnosed diaphragmatic injuries 

are a significant cause of morbidity and mortality. 

LIVER INJURIES 


• Most common in blunt trauma. 

• Right upper quadrant pain and tenderness, often with radiation to right shoulder. 

• May cause significant hemodynamic instability. 

• CT scan is noninvasive and sensitive in stable patients; use FAST exam or laparotomy 

for unstable patients. 

Most liver injuries are managed with observation and conservative management. Liver 

injuries include lacerations, hematomas, or rupture (Figure 25-4). Because of the 

significant blood supply from the hepatic artery and portal vein, large defects are 

technically difficult to manage and may result in exsanguination and death. 

PANCREATIC INJURIES


• Uncommon, usually seen after blunt trauma. 

• Patients may present with epigastric or back pain. 

• Serum pancreatic enzyme levels are not sensitive or specific for injury. 

• CT scan is noninvasive and sensitive. 

Pancreatic injuries are rare and often difficult to diagnose. The pancreas may be 

lacerated or contused. Amylase levels are not specific and often are not helpful, 

particularly early in the evaluation of the patient. CT scan or radiologist-performed 

ultrasound may be helpful. Patients with pancreatic injuries should be admitted. 

RENAL INJURIES (See also Chapter 26) 


• Hematuria should raise suspicion for injury. 

• CT scan is noninvasive and sensitive in stable patients; one-shot intravenous 

pyelogram may be used in unstable patients, but it has limited sensitivity. 

The kidney may sustain lacerations, contusions, shattering, or devascularization 

injuries. After a urinary catheter is inserted during the initial assessment, determine 

whether gross hematuria is present. Microscopic analysis is not needed in adults. In 

children, the presence of at least 5 red blood cells per high-power field on microscopic 

examination indicates possible urinary tract injury. These findings warrant urologic 

consultation in the emergency department (see Figure 26-5). 

BLADDER INJURIES (See also Chapter 26) 


• Most commonly seen with pelvic fractures. 

• Hematuria should raise suspicion for injury. 

• Retrograde cystogram may identify injury (as well as associated urethral injury). 

• CT scan may also be utilized with cystogram. 

Bladder injuries may be either intraperitoneal or extraperitoneal. The diagnosis is 

suspected in a patient with abdominal pain and hematuria and is confirmed with a 

retrograde cystogram. Patients with intraperitoneal rupture require immediate surgery 

(see Figures 26-6 and 26-7). 

INTESTINAL INJURIES


• May occur with blunt and penetrating injuries. 

• Peritoneal signs may be delayed. 

• May be missed on initial plain x-rays and CT scans. 

• May have delayed presentation (eg, duodenal hematomas). 

Both penetrating and blunt injuries can cause intestinal perforations. These perforations 

may be subtle initially and may be missed on CT scan (Figure 25-5). Such injury may be 

present even if the patient can tolerate a trial of fluids by mouth in the emergency 

department. The emergency physician should be cautious if this diagnosis is suspected. 

Give patients who are to be discharged thorough instructions, including for follow-up 

care. Patients have been able to walk out of the emergency department only to return 

later with fever and a rigid abdomen. Rare cases of traumatic appendicitis have been 

reported in the literature. If injuries involving impact, or "spearing," with bicycle 

handlebars are present, consider evaluating the patient for a duodenal hematoma, 

which can be managed conservatively. 

FLANK INJURIES 


• May be associated with renal injuries. 

• Retroperitoneal hematoma may be false positive on diagnostic peritoneal lavage or 

ultrasound. 

• CT scan is noninvasive and sensitive in stable patients. 

Flank injuries are more difficult to manage than other types of injuries because 

differentiating intraperitoneal from retroperitoneal involvement can be difficult. An 

abdominal CT scan or one-shot intravenous pyelogram may be beneficial to diagnose 

ureteral or retroperitoneal injury. These studies should be performed in consultation with 

the trauma surgeon. 

Albrecht RM, Schermer CR, Morris A: Nonoperative management of blunt splenic 

injuries: factors influencing success in age > 55 years. Am Surg 2002;68:227. [PMID: 

11893099] 

Carlin AM et al: Factors affecting the outcome of patients with splenic trauma. Am Surg 

2002;68:232. [PMID: 11893100] 

Livingston DH et al: Admission or observation is not necessary after negative abdominal 

computed tomographic scan in patients with suspected blunt abdominal trauma: results 

of a prospective, multi-institutional trial. J Trauma 1998;44:273. [PMID: 9498497] 

Nagy KK et al: Routine preoperative "one-shot" intravenous pyelography is not indicated

in all patients with penetrating abdominal trauma. J Am Coll Surg 1997;185:530. [PMID: 

9404875] 





FACEP 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES

Figure 25-1. Positive FAST exam demonstrating a large amount of fluid surrounding the 

spleen. 





FACEP 

FIGURES 

Figure 25-1

Figure 25-2. Adult male blunt trauma patient with splenic injury. Multiple large 

lacerations of the spleen are noted with associated perisplenic hematoma. Perihepatic 

free fluid is also noted. Images A and B were obtained shortly after the initial bolus of 

intravenous contrast. Note the compression of the left kidney by the perisplenic 

hematoma. Image C was obtained after the initial bolus of intravenous had cleared the 

spleen. A large laceration on the posterior surface of the spleen is more clearly 

visualized extending anteriorly to the hilum. 





FACEP 

FIGURES 

Figure 25-2

Figure 25-3. Adult female blunt trauma patient with blurring of the left hemidiaphragm 

and an abnormal nasogastric tube and stomach bubble location, representing a left 

diaphragmatic injury. 





FACEP 

FIGURES 

Figure 25-3

Figure 25-4. Adult male blunt trauma patient with a large posterior hepatic contusion 

with associated perihepatic and perisplenic hemorrhage. 





FACEP 

FIGURES 

Figure 25-4

Figure 25-5. Adult male blunt trauma patient with left-sided intra-abdominal free fluid, 

small bowel wall thickening, and stranding in the mesenteric fat planes. Patient 

underwent exploratory laparotomy and was found to have a mesenteric tear with 

perforated and devascularized jejunum. 





FACEP 

FIGURES 

Figure 25-5

26. Genitourinary Trauma - Geoffrey A. Wiss, MD, Claudia Whitaker, 

MD, & Robert K. Dunne, MD, FACEP 


Genitourinary injuries occur in 10-20% of major trauma patients. Most of these injuries, 

with the exception of renal hilar disruption or shattered kidney, are not immediately life 

threatening. Because they are often accompanied by potentially life-threatening injuries 

to other organ systems, however, it is easy for the emergency physician to overlook and 

therefore miss signs or symptoms of urologic injury. Failure to diagnose and treat these 

injuries properly can result in significant long-term morbidity. Therefore, while evaluating 

the trauma patient, the physician needs to be aware of clues to genitourinary injury. 

These clues include (1) lumbar vertebral or lower rib fractures, (2) pelvic fractures, (3) 

flank pain or hematoma, (4) abnormal prostate on rectal exam, (5) blood at the urethral 

meatus, and (6) gross hematuria. 

Immediate Treatment 

For all patients with blunt or penetrating trauma, evaluate airway, breathing, circulation, 

and disability during the primary survey as per advanced trauma life support protocol 

(Chapter 10). During the secondary survey, evaluate for a boggy or high-riding prostate 

on rectal exam, perineal or scrotal hematoma, and any evidence of blood at the urethral 

meatus. If any of these signs is present, perform a retrograde urethrogram before 

inserting a Foley catheter. If the signs are absent, insert a Foley catheter if indicated (ie, 

in unstable patients or those unable to urinate). Urethral studies should never delay 

diagnostic studies of, or treatment for, potentially life-threatening injuries. Figures 26-1, 

26-2, and 26-3 provide algorithms for managing blunt, penetrating, and pediatric 

urologic injury. 

Special Examinations & Procedures 

Evaluation of the genitourinary system should be performed in a retrograde fashion: rule 

out urethral injury before bladder, then bladder before ureteral or renal injury. 

A. Catheterization 

A Foley catheter may be placed once physical examination supports the integrity of the 

urethra. If any signs of urethral injury are present, perform retrograde urethrogram first. 

If urethrogram is negative or not indicated, a 14-16F catheter should be placed using 

copious amounts of lubricating jelly and sterile technique. A folded 4- × 4-in gauze pad 

may be used to retract the foreskin in uncircumcised patients to prevent repeated 

unintended reduction of the foreskin over the glans with subsequent field and catheter 

contamination during placement. Any difficulty during placement warrants retrograde 

urethrography if urethral injury is a possibility. Gross or microscopic hematuria indicates 

possible urologic trauma, although the degree of microscopic hematuria does not 

correlate with the degree or location of injury.

In 1989, a 10-year prospective study established guidelines for evaluation and treatment 

of blunt renal trauma. Patients with gross hematuria require an imaging study. Patients 

with microscopic hematuria and a history of shock (systolic blood pressure < 90 mm Hg) 

or sudden deceleration injury should also have an imaging study performed. Those 

without shock or deceleration injury may be discharged home with outpatient urology 

follow-up to ensure that hematuria has cleared. Patients with penetrating injuries and 

more than 5 red blood cells per high-power field should undergo an imaging study, 

although the absence of hematuria does not eliminate the need for a study. With regard 

to penetrating trauma, the location of the wound is more important than the presence of 

hematuria for predicting injury, because significant injuries (9% of patients in one study) 

can be present even in the absence of hematuria. In pediatric patients, the kidney is the 

most commonly injured intra-abdominal organ. As a result, even microscopic hematuria 

from trauma requires further workup (usually by computed tomography [CT] scan) in 

pediatric patients. Likewise, further evaluation is required for all patients with penetrating 

trauma and any degree of hematuria. 

B. Suprapubic Catheter Placement 

Suprapubic catheter placement is indicated in trauma situations when Foley catheter 

placement is contraindicated, usually because urethral injury is suspected and cannot 

be confirmed with urethrogram or while awaiting surgical repair of a damaged urethra. 

Several commercial kits are available. Most of these kits utilize placement over a 

guidewire. If kits are unavailable, a single-lumen central venous catheter may be used. 

C. Intravenous Pyelogram 

No longer the study of choice, the intravenous pyelogram (IVP) has been replaced by 

the helical CT scan, although it is useful at institutions not equipped with CT scanners. 

These studies should be performed with an intravenous bolus of contrast followed by 

serial nephrotomograms. "One-shot" IVP studies in the trauma room are no longer 

recommended as a screening exam because of an unacceptably high level of false 

positives and negatives. If verification of 2 functioning kidneys is needed prior to surgical 

repair of a kidney, a simple IVP may be performed in the operating room. 

D. Retrograde Urethrography 

If urethral injury is suspected (eg, blood at the meatus, boggy or high-riding prostate, 

scrotal or perineal hematoma), urethrography should be performed prior to Foley 

catheter placement. After a preinjection abdominal x-ray is obtained, a Cooke adapter 

on a 60-cc syringe is gently inserted into the urethra and 60 cc of full- or half-strength 

water-soluble contrast is injected over 60 seconds; the x-ray is taken during the last 10 

seconds of injection. Extravasation with bladder filling denotes partial urethral tear, and 

extravasation with no bladder filling denotes complete urethral tear. 

E. Retrograde Cystography 

Bladder evaluation is required for gross hematuria or microscopic hematuria with pelvic 

fractures or penetrating injury. After a preliminary KUB, up to 400 cc of full-strength 

water-soluble contrast is instilled under gravity through a urethral catheter to the point of 

bladder contraction; x-rays are taken with the bladder full and after complete voiding. 

These x-rays may show either intra- or extraperitoneal extravasation. Because of the 

effective sealing capabilities of the 3-layered bladder wall, false negatives may be 

encountered if less than the recommended age-appropriate amount of contrast is

instilled. 

F. CT Scan 

Helical CT scan with intravenous contrast is the study of choice for evaluating ureteral 

or renal trauma. CT scan may also be used for retrograde cystography, although the 

same procedure outlined above should be followed. Clamping the Foley catheter during 

an intravenous contrast pelvic CT scan is not adequate to eliminate bladder injury, 

because of inadequate bladder pressures and dilute dye. 

G. Ultrasound 

Although used frequently in trauma situations to detect peritoneal blood, ultrasound 

does not have the sensitivity to reliably detect specific renal injuries and, therefore, is 

not recommended in the workup of renal trauma. 

Ahn JH, Morey AF, McAninch JW: Workup and management of traumatic hematuria. 

Emerg Med Clin North Am 1998; 16:145. [PMID: 9496319] 

Carlin BI, Resnick MI: Indications and techniques for urologic evaluation of the trauma 

patient with suspected urologic injury. Semin Urol 1995;13:9. [PMID: 7597359] 

Dreitlein DA, Suner S, Basler J: Genitourinary trauma. Emerg Med Clin North Am 

2001;19:569. [PMID: 11554276] 

Goff CD, Collin GR: Management of renal trauma at a rural, level I trauma center. Am 

Surg 1998;64:226. [PMID: 9520811] 

McAleer IM, Kaplan GW: Pediatric genitourinary trauma. Urol Clin North Am 

1995;22:177. [PMID: 7855953] 

McGahan JP et al: Use of ultrasonography in the patient with acute abdominal trauma. J 

Ultrasound Med 1997;16:653. [PMID: 9323670] 

Miller KS, McAninch JW: Radiographic assessment of renal trauma: our 15-year 

experience. J Urol 1995;154:352. [PMID: 7609096] 

Nagy KK et al: Routine preoperative "one-shot" intravenous pyelography is not indicated 

in all patients with penetrating abdominal trauma. J Am Coll Surg 1997;185:530. [PMID: 

9404875] 

Rubin GD, Silverman SG: Helical (spiral) CT of the retroperitoneum. Radiol Clin North 

Am 1995;33:903. [PMID: 7676014] 


RENAL INJURIES 


• Often accompanied by other abdominal injuries in blunt trauma. 

• Nausea, vomiting, flank ecchymosis, lower rib or lumbar fractures suggest injury. 

• No reliable markers for diagnosis, including hematuria. 

• CT scan is study of choice. 


Renal injuries are the most common urologic injuries. The kidneys are not fixed in place 

but hang from their vascular attachments and perirenal fat and move with the 

diaphragm. They are susceptible to deceleration injury, with blunt injury 5 times more 

common than penetrating injury. Kidneys with preexisting abnormalities such as tumors 

or hydronephrosis may be damaged by seemingly inconsequential mechanisms. 

The diagnosis of renal trauma is complicated by the frequent presence of other 

peritoneal injuries, as well as the absence of any accurate markers for renal injury. 

Hematuria may be absent with significant renal injury, and the degree of hematuria does 

not correlate with the degree of injury when present. Renal injuries are graded on a 

scale of 1 to 5 (Figure 26-4). Following a general trend for the nonoperative 

management of many solid organ intra-abdominal injuries, many renal injuries are 

increasingly being managed without routine surgical exploration. However, only a 

special subset of patients with high-grade renal injuries are candidates for observation 

without surgical repair or nephrectomy. 



Pain may be localized to one flank or over the abdomen, but visceral injury or pelvic 

fracture may obscure symptoms of renal injury. Nausea and vomiting, flank ecchymosis, 

lower rib fractures, or lumbar vertebral (especially transverse process) fractures may be 

noted. Urologic injury should be suspected in any penetrating wound to the flank or 

whose trajectory potentially crosses the paravertebral gutter. Extensive blood loss and 

shock may result from retroperitoneal bleeding. A palpable mass may indicate 

retroperitoneal hematoma or urinoma. If the retroperitoneum has been torn, 

hemoperitoneum will cause diffuse abdominal tenderness and ileus. 


Hematuria may or may not be present. 

C. Imaging 

The study of choice is helical CT scan of the abdomen and pelvis with intravenous 

contrast and immediate as well as delayed images (Figure 26-5). Under no 

circumstances should imaging delay necessary operative intervention. Surgical 

exploration should replace radiographic imaging in unstable patients who require 

immediate surgery. IVP is useful for diagnosing major renal injuries, although it will miss 

some smaller contusions and renal lacerations. 

Treatment

Renal contusions (85% of blunt trauma renal injuries) and minor renal lacerations (12% 

of such injuries) can be managed expectantly and rarely require operative intervention. 

Outpatient urology follow-up is necessary to ensure that hematuria has cleared. Major 

lacerations (3% of blunt trauma renal injuries) may require operative intervention, 

although the trend is to manage these injuries conservatively when possible. Renal 

pedicle injuries, representing 1-2% of blunt injuries, often result in nephrectomy. 

Penetrating renal trauma usually requires surgical intervention. Absolute indications for 

surgical exploration include uncontrollable renal hemorrhage and shattered kidney or 

avulsion of the main renal vessels. 

Goldman SM, Sandler CM: Upper urinary tract trauma—current concepts. World J Urol 

1998;16:62. [PMID: 9542017] 

Matthew LA, Smith EM, Spirnak JP: Nonoperative treatment of major blunt renal 

lacerations with urinary extravasation. J Urol 1997;157:2056. [PMID: 9146579] 

Mee SL et al: Radiographic assessment of renal trauma: 10-year prospective study of 

patient selection. J Urol 1989;141:1095. [PMID: 2709493] 

URETERAL INJURIES 


• Usually from penetrating trauma. 

• Patients with missed injuries may present with fever, abdominal pain, and mass. 

• CT scan or retrograde pyelography are studies of choice. 


The least frequently injured portion of the genitourinary system is the ureter. The 

majority of these injuries (80-90%) result from penetrating trauma, although blunt 

trauma may cause injuries often accompanied by injuries to nonurologic systems. In 

children, ureteral injuries occur more commonly at the ureteropelvic junction, because of 

the increased mobility of the spine as well as the intra-abdominal rather than intrapelvic 

location of the bladder. Ureteral injuries are often diagnosed either intraoperatively or 

when complications arise later, because such injuries are infrequent, are difficult to 

diagnose, and frequently occur in the presence of other injuries. 



Physical examination findings are nonspecific and usually related to associated 

intra-abdominal injuries, although pain similar to renal colic and a flank mass may be 

seen. Hematuria may be present but is often absent if complete ureteral transection has 

occurred. Use of intravenous indigo carmine dye during surgical exploration may help in 

the diagnosis of ureteral injury. Patients with a delay in diagnosis may present with 

abdominal pain, urinary urgency and frequency, fever, pyuria, and a palpable mass

containing urine (urinoma) or blood. 

B. Imaging 

Both IVP and CT scan may miss ureteral injuries. If performed soon after injury and 

associated administration of resuscitative fluids, the extravasation of contrast from the 

ureter may show up only as a hazy, ground-glass appearance. If injuries are near the 

ureteropelvic junction, extension of fluid around the kidney may incorrectly lead to 

diagnosis of renal rather than ureteral injury. Because retrograde pyelography uses a 

more concentrated dye and fluoroscopy, this modality may pick up injuries missed by 

other methods. 

Treatment 

All ureteral injuries require operative repair. Delayed repair, although associated with 

increased incidence of infections, does not lead to increased rate of renal function loss. 

Azimuddin K et al: Penetrating ureteric injuries. Injury 1998; 29:363. [PMID: 9813680] 

Kotkin L, Brock JW: Isolated ureteral injury caused by blunt trauma. Urology 

1996;47:111. [PMID: 8560642] 

Medina D et al: Ureteral trauma: preoperative studies neither predict injury nor prevent 

missed injuries. J Am Coll Surg 1998;186:641. [PMID: 9632150] 

BLADDER INJURIES 


• Usually due to blunt trauma or pelvic fractures. 

• Gross hematuria and abdominal pain often present. 

• Extraperitoneal rupture treated conservatively with Foley catheter. 

• Intraperitoneal rupture requires surgical intervention. 

• Retrograde cystogram is diagnostic study of choice. 


Bladder rupture most commonly occurs in association with blunt trauma and pelvic 

fractures, especially when the bladder is full. The rupture may occur into the 

intraperitoneal (Figure 26-6) or extraperitoneal space (Figure 26-7). The majority of 

ruptures (85%) occur into the extraperitoneal space and are often associated with pelvic 

fractures. Intraperitoneal ruptures are often caused by motor vehicle collisions during 

which a patient has a full bladder and are more likely to occur in patients with recent 

alcohol intake (predisposes to full bladders), women (thinner bladder musculature), and 

children (bladder not as protected by pelvis). Intraperitoneal bladder rupture generally 

occurs at the dome, the weakest area of the bladder. 

Clinical Findings


Gross hematuria is the most frequent finding (98%), along with lower abdominal pain 

and inability to void. 

B. Imaging 

Diagnosis of bladder injury is made by retrograde cystogram after urethral injury is ruled 

out by retrograde urethrogram. The bladder should be completely distended with 

300-400 cc of water-soluble contrast material instilled through a Foley catheter. 

Radiographs are taken after complete distention is obtained and then repeated after the 

bladder has been drained completely. Intraperitoneal rupture will show contrast material 

extending into the abdomen, outlining loops of bowel wall with extension into the 

paracolic gutters. Extraperitoneal rupture will show a coarse, streaked pattern of 

extravasation adjacent to the bladder. A postvoid view should always be obtained and is 

helpful in diagnosing subtle injuries that may have been obscured on initial films. 

Treatment 

Intraperitoneal ruptures and all penetrating injuries to the bladder require surgical 

intervention. Extraperitoneal injuries can usually be managed nonsurgically with Foley 

catheter drainage, followed by repeat cystogram in 10-14 days. Simple contusions or 

incomplete lacerations can also be managed conservatively, with Foley catheter 

drainage and early urologic follow-up. 

Ahn JH, Morey AF, McAninch: Workup and management of traumatic hematuria. Emerg 


URETHRAL INJURIES 


• Significant injury because of frequent complications. 

• Blood at urethral meatus and inability to void often seen. 

• High-riding prostate on digital rectal exam. 

• Retrograde urethrogram is best study. 


Urethral injuries are uncommon but are potentially the most debilitating because of the 

high rate of complications, such as incontinence, stricture formation, impotence, and 

chronic urinary tract infections. They occur most often in men secondary to blunt 

trauma. Urethral injuries in women are extremely rare and are usually associated with 

pelvic fractures. 

If urethral injury is suspected, placement of a Foley catheter before a retrograde 

urethrogram is obtained is contraindicated, because it may cause further injury and 

worsen a partial tear. If a catheter has already been placed, it should not be removed,

and a urethrogram should be performed around the catheter using a pediatric feeding 

tube and occluding the distal urethral meatus with gentle pressure on the glans. 

A special injury of note is the traumatic removal of a Foley catheter, either while moving 

the patient or occasionally by the patient stepping on the catheter while ambulating. 

Significant injury can occur by this mechanism, and a urethrogram should be performed 

prior to reinsertion of any catheters. 

1. Posterior Urethra 


The posterior urethra, consisting of the prostatic and membranous portions, is injured 

most commonly during blunt trauma associated with bony pelvic injuries. The urethra is 

usually sheared off proximal to the urogenital diaphragm. The prostate then becomes 

displaced superiorly by the developing hematoma (Figure 26-8). Concomitant bladder 

injuries are associated with 35% of posterior urethral injuries. 



Patients will complain of abdominal or perineal pain and an inability to void. Blood at the 

meatus is the most frequent sign of urethral injury. The prostate will be high-riding or 

boggy on rectal examination. 

B. Imaging 

Retrograde urethrogram will show extravasation of contrast material superior to the 

urogenital diaphragm (Figure 26-9). 

Treatment 

Initial management includes suprapubic cystostomy to provide urinary drainage. 

Definitive treatment options vary, and urologic consultation is essential. 

2. Anterior Urethra 


The anterior urethra, consisting of the bulbous and penile portions, is located below the 

urogenital diaphragm. Trauma to the anterior urethra is typically due to straddle injuries 

or a direct blow to the perineum, as well as from instrumentation or improper Foley 

catheter placement (Figure 26-10). 



If Buck's fascia remains intact, extravasation of blood and urine will be confined to the 

penile shaft and perineum. With rupture of the Buck fascia, extravasation will extend 

along the abdominal wall, confined only by Colles' fascia, with resultant perineal

"butterfly" hematoma. 

B. Imaging 

Contrast extravasation will be seen on urethrogram (Figure 26-11). 

Treatment 

Long-term catheter drainage or direct reanastomosis are the most common treatment 

options. 

Ahmed S, Neel KF: Urethral injury in girls with fractured pelvis following blunt abdominal 

trauma. Br J Urol 1996;78:450. [PMID: 8881960] 

Boon TA, Van der Werken C: Urethral injuries revisited. Injury 1996;27:533. [PMID: 

8994555] 

Goldman SM et al: Blunt urethral trauma: a unified, anatomical mechanical 

classification. J Urol 1997;157:85. [PMID: 8976222] 

Koraitim MM: Pelvic fracture urethral injuries: evaluation of various methods of 

management. J Urol 1996;156:1288. [PMID: 8808856] 

EXTERNAL GENITAL INJURIES 


• Blunt trauma to erect penis may cause rupture with pain and deforming hematoma; 

evaluate for surgical repair. 

• Blunt scrotal injuries require Doppler ultrasound studies. 

• Genital burn injures require early Foley catheter placement to prevent edematous 

urethral obstruction. 

• Consider pelvic floor penetration and sexual assault with all vaginal lacerations. 

1. Penile Rupture 

Penile fractures occur from blunt trauma to the erect penis causing rupture of the corpus 

cavernosum. The patient typically reports a loud "cracking" sound, immediate pain, and 

loss of erection. 



A large hematoma will be visible on the shaft of the penis, and the axis of the shaft may 

be deviated. 

B. Imaging 

Retrograde urethrogram may show extravasation if urethral injury is present.

Treatment 

Immediate urologic consultation is indicated for surgical repair. 

2. Constriction Injuries 

Constriction injuries can occur from objects placed circumferentially around the penile 

shaft. Occasionally these injuries are from obstructive rings placed during sexual play in 

adults. They require immediate removal to prevent urethral injury or neurovascular 

compromise. In circumcised male infants, hair is a common culprit. 

3. Testicular Injuries 

Blunt trauma to the scrotum may result in testicular rupture by forcefully compressing 

the testis against the symphysis pubis or medial thigh. 



Patients present with severe pain, nausea, vomiting, and extensive swelling due to 

hematoma formation, all of which make testicular examination difficult. 

B. Imaging 

The diagnostic study of choice is ultrasound examination with Doppler flow studies. 

Treatment 

Simple hematomas can be managed conservatively with scrotal elevation and sitz 

baths. Larger hematomas may require surgical drainage. Testicular rupture and 

penetrating injuries should be explored and repaired surgically. 

4. Skin Injuries 

A degloving injury usually requires extensive surgical debridement and repair, and may 

require skin grafting. With zipper injuries, the trapped skin can be released by cutting 

the sliding portion of the zipper. Scrotal lacerations can be repaired in a layered fashion 

once testicular injury has been ruled out. Burn injuries deserve special consideration 

because of the massive edema that may develop, resulting in urethral obstruction. A 

urethral or suprapubic catheter should be placed early during the initial resuscitative 

phase. 

5. Female Genital Injuries 

If vaginal bleeding is present, perform a speculum examination to evaluate for vaginal 

lacerations in addition to any injuries noted to the external genitalia. Simple lacerations 

can be repaired using absorbable sutures. If unable to obtain hemostasis, operative 

repair is indicated. In all vaginal lacerations, it is important to rule out penetration of the 

pelvic floor, which may indicate significant organ and vascular damage. The possibility

of sexual assault must always be considered, and follow-up with a gynecologist is 


Goldman HB, Dmochowski RR, Cox CE: Penetrating trauma to the penis: functional 

results. J Urol 1996;155:551. [PMID: 8558658] 

Goldman HB, Idom CB Jr, Dmochowski RR: Traumatic injuries of the female external 

genitalia and their association with urological injuries. J Urol 1998;159:956. [PMID: 

9474191] 

Kadish HA, Schunk JE, Britton H: Pediatric male rectal and genital trauma: accidental 

and nonaccidental injuries. Pediatr Emerg Care 1998;14:95. [PMID: 9583387] 

Pantuck AJ, Kraus SL, Barone JG: Hair strangulation injury of the penis. Pediatr Emerg 

Care 1997;13:423. [PMID: 9435009] 






IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES

Figure 26-1. Algorithm for staging blunt trauma in the adult. IVP = intravenous 

pyelogram; RBC/HPF = red blood cells per high-power field; SBP = systolic blood 

pressure. (Modified and reproduced, with permission, from Tanagho EA, McAninch JW: 

Smith's General Urology, 13th ed. Appleton & Lange, 1992.) 






FIGURES 

Figure 26-1

Figure 26-2. Algorithm for staging penetrating trauma in the adult. (Modified and 

reproduced, with permission, from Tanagho EA, McAninch JW: Smith's General 

Urology, 13th ed. Appleton & Lange, 1992.) 






FIGURES 

Figure 26-2

Figure 26-3. Algorithm for the evaluation of blunt trauma in children. IVP = intravenous 

pyelogram. (Modified and reproduced, with permission, from Tanagho EA, McAninch 

JW: Smith's General Urology, 13th ed. Appleton & Lange, 1992.) 






FIGURES 

Figure 26-3

Figure 26-4. Classification of renal injuries. Grades I and II are minor. Grades III, IV, 

and V are major. A: Grade I—microscopic or gross hematuria; normal findings on 

radiographic studies; contusion or contained subcapsular hematoma without 

parenchymal laceration. B: Grade II—nonexpanding, confined perirenal hematoma or 

cortical laceration less than 1 cm deep without urinary extravasation. C: Grade 

III—parenchymal laceration extending more than 1 cm into the cortex without urinary 

extravasation. D: Grade IV—parenchymal laceration extending through the 

corticomedullary junction and into the collecting system. A laceration at a segmental 

vessel may also be present. E: Grade IV—thrombosis of a segmental renal artery 

without a parenchymal laceration. Note the corresponding parenchymal ischemia. F: 

Grade V—thrombosis of the main renal artery. The inset shows the intimal tear and 

distal thrombosis. G: Grade V—multiple major lacerations, resulting in a "shattered" 

kidney. H: Grade V—avulsion of the main renal artery and/or vein. (Reproduced, with 

permission, from Tanagho EA, McAninch JW: Smith's General Urology, 16th ed. 

McGraw-Hill, 2004.) 






FIGURES 

Figure 26-4

Figure 26-5. Adult blunt trauma patient with high-grade right renal laceration and 

perinephric hematoma. (Note the normal appearing left kidney.) 






FIGURES 

Figure 26-5

Figure 26-6. Mechanism of vesical injury. A direct blow over the full bladder causes 

increased intravesical pressure and intraperitoneal rupture. (Reproduced, with 








FIGURES 

Figure 26-6

Figure 26-7. Adult blunt trauma patient with extraperitoneal bladder rupture. Note the 

contrast extravasation in the pelvis and along the left anterior abdominal wall. As 

evidence of significant pelvic trauma, note the right sacroiliac joint disruption (A) and the 

left acetabular fracture (B). 






FIGURES 

Figure 26-7

Figure 26-8. Injury to the posterior (membranous) urethra. The prostate has been 

avulsed from the membranous urethra secondary to fracture of the pelvis. Extravasation 

occurs above the triangular ligament and is periprostatic and perivesical. (Reproduced, 

with permission, from Tanagho EA, McAninch JW: Smith's General Urology, 16th ed. 







FIGURES 

Figure 26-8

Figure 26-9. Adult male blunt trauma patient with prostatomembranous urethral injury. 

Pubic symphysis diastasis is noted (A). Free extravasation and failure of contrast to fill 

the bladder indicate a posterior urethral disruption (B). 






FIGURES 

Figure 26-9

Figure 26-10. Injury to the bulbous urethra. Left: Mechanism: usually a perineal blow or 

fall astride an object; crushing of the urethra against inferior edge of pubic symphysis. 

Right: Extravasation of blood and urine enclosed within Colles' fascia. (Reproduced, 

with permission, from Tanagho EA, McAninch JW: Smith's General Urology, 13th ed. 

Appleton & Lange, 1992.) 






FIGURES 

Figure 26-10

Figure 26-11. Adult male patient with straddle injury to perineum and blood at the 

urethral meatus. This positive retrograde urethrogram reveals extravasation in the 

bulbous portion of the urethra indicative of urethral injury. 






FIGURES 

Figure 26-11

27. Vertebral Column & Spinal Cord Trauma 1 - Robert Casey Wilson, 

MD, & Louis J. Kroot, MD 

IMMEDIATE MANAGEMENT OF THE PATIENT WITH SUSPECTED 

SPINAL INJURY 

Suspect Spinal Cord Injury 

1 This chapter is a revision of the chapter by Henry M. Bartkowski, MD, PhD, from the 

4th edition. 

Patients with blunt head injury or multiple injuries from blunt or penetrating trauma 

should be assumed to have cervical or thoracolumbar spine injuries until proved 

otherwise, unless they are fully alert and have no evidence of midline tenderness, focal 

neurologic defect, intoxication, or painful, distracting injury. 

Immobilize Vertebral Spine 

Immobilization of the vertebral spine is essential to prevent further injury to the spinal 

cord. 

A. Supine Position 

Optimal immobilization is obtained by placing the patient supine (face up) on a firm, flat 

surface (eg, rigid, long spine board) without a pillow and with lateral motion of the neck 

restricted by a rigid cervical collar (Philadelphia) and lateral neck rolls connected with 

tape across the forehead. 

B. Lateral Position 

If the patient cannot lie supine for any reason (eg, vomiting), the lateral position with 

careful in-line cervical stabilization is acceptable. This immobilization should be 

maintained throughout resuscitation procedures, physical examination, and x-ray 

evaluation. 

C. Technique for Moving the Patient 

If the patient must be moved, in-line spinal stabilization should be maintained and the 

head and trunk lifted or rolled as one unit (logroll). 

Establish Airway & Maintain Ventilation 

(See also Chapter 8.) Airway obstruction may be manifested by gurgling or sonorous 

respirations, ineffective respiration (chest movement without movement of air), apnea, 

or cyanosis. High cervical cord transection (above C2 or C3) results in apnea due to 

intercostal muscle and diaphragmatic paralysis; cervical cord transection (above C6) or 

injury at a lower level may still result in respiratory failure because of intercostal muscle 

weakness or paralysis.

Note: Neck alignment and immobility must be maintained during attempts to establish 

adequate ventilation. 

A. General Measures 

Using a tonsil tip sucker, clear mouth and upper airway of obvious foreign material. 

Position the head in neutral position, avoiding motion of the cervical spine. Insert nasal 

or oropharyngeal airway. 

Provide supplemental oxygen by nasal cannula or mask if the patient is breathing, or 

support respiration with bag-mask combination (with supplemental oxygen) if 

hypoventilation is suspected. 

Measure arterial blood gases as soon as possible to assess adequacy of ventilation, 

and monitor oxygen saturation using pulse oximetry, if available. Both the intercostal 

muscles and the diaphragm contribute to normal ventilation. In patients with cervical 

spinal cord injuries, loss of the intercostal muscle innervation may cause patients to tire 

easily, causing ineffective ventilation and progressively worsening hypoxemia and 

hypercapnia. Repeated arterial blood gas measurements are therefore essential to 

monitor any changes in ventilatory status. 

B. Endotracheal Intubation 

If the measures described above fail to provide adequate ventilation or if hypoventilation 

or apnea is present, perform endotracheal intubation (Chapter 6). Endotracheal 

intubation should also be considered for airway control in the unconscious or obtunded 

patient with depressed gag and cough reflexes even if ventilation is adequate. If severe 

neck injury is accompanied by tracheal laceration, the trachea may be intubated directly 

through the wound. 

When patients with suspected cervical spinal injuries require an emergent definitive 

airway, perform oral endotracheal intubation with in-line cervical immobilization. 

Designate an assistant to maintain this immobilization from the time the cervical collar is 

removed until it is replaced after the endotracheal tube has been taped in place. In 

general, rapid sequence intubation (unless contraindicated [Chapter 8]) is preferred as 

the least traumatic and most efficient method of achieving intubation. Cadaver studies 

have shown no significant movement of the cervical spine during orotracheal intubation 

using in-line cervical stabilization in contrast to simple cervical collar immobilization, in 

which significant movement occurs. 

Nasotracheal intubation is an option only in the spontaneously ventilating patient. 

Because it is a blind technique, it occurs under less controlled intubating conditions that 

may predispose to emesis in patients with high likelihood of ileus or gastric atony. If time 

allows, fiberoptic intubation is a good alternative nontraumatic method in experienced 

hands. 

C. Cricothyrotomy 

Rarely, in a patient with severe craniofacial trauma resulting in distorted normal 

anatomic relationships, it may be impossible to establish an orotracheal or nasotracheal 

airway. Also, conventional means of intubation are sometimes unsuccessful in the

otherwise normal patient. In such cases, direct intubation of the trachea through 

cricothyrotomy or tracheostomy is indicated (Chapter 6). 

D. Suctioning of Secretions 

Patients with weak intercostal or diaphragmatic muscles cannot produce a strong cough 

and are therefore predisposed to progressive airway obstruction without any change in 

neurologic deficit. Frequent suctioning should be performed. An endotracheal airway 

may be required for patients with voluminous secretions. 

Treat Pneumothorax & Tension Pneumothorax 


Establish Satisfactory Circulation 

A. Cardiac Arrest 

If no pulse is detected, begin cardiopulmonary resuscitation (Chapter 7). 

B. Shock or Hypotension 

(See Chapter 9.) Shock (cool, pale skin; hypotension; abnormal mentation) or 

hypotension (systolic blood pressure < 90 mm Hg in an adult) may be due either to poor 

sympathetic tone below the level of the spinal cord lesion or to hypovolemia from other 

injuries. In most instances, hypovolemia is the cause. Sources of hypovolemia include 

hemorrhage into several compartments, such as the chest and the pelvis (evaluated by 

portable chest x-ray and anteroposterior view of the pelvis), the abdomen (evaluated by 

a focused assessment with sonography for trauma [FAST] exam [Chapters 6, 9, and 

25], diagnostic peritoneal lavage [DPL], or computed tomography [CT] scan of the 

abdomen), or the femur (hemorrhage is usually obvious clinically). If open wounds are 

present, significant external hemorrhage may have occurred at the scene of the injury. 

1. Hypovolemia—(See Chapter 9.) Insert 2 or more large-bore (= 16-gauge) 

intravenous catheters in an upper extremity; obtain blood for hematocrit, typing and 

cross-matching, electrolyte determinations, and renal function tests; and begin 

intravenous infusion of crystalloid solution to support blood pressure. Up to 3 L of 

crystalloid solution may be given before blood is required. Caution: Exercise care in 

fluid replacement, because patients with spinal cord injuries are at greater risk of heart 

failure than normal individuals. 

If hypotension or shock is not quickly corrected by these methods, search for bleeding 

from other injuries (Chapter 10). 

2. Poor sympathetic tone—Keep the patient supine and horizontal. Blood pressure in 

the normovolemic patient with spinal injury is usually normal as long as the patient is 

supine, because minimal sympathetic tone is required in this position. The use of 

low-dose dopamine, 5-10 ug/kg/min, may be necessary if no other source of 

hypotension has been identified and poor sympathetic tone is responsible for persistent 

hypotension despite supine patient positioning and crystalloid infusion. 

C. Normal Blood Pressure

Avoid excess fluid administration, which may increase spinal cord swelling or precipitate 

heart failure. 

D. Hypertension 

Although hypertension is rarely caused by spinal cord injury itself, the resulting bladder 

or bowel distention and subsequent autonomic discharge of the mass reflex may cause 

hypertension. Rule out more likely causes, such as severe head injury or drug ingestion, 

before attributing hypertension to an injured spinal cord. 

E. Head Injuries 

Patients with altered mental status, seizures, or cranial nerve or other focal neurologic 

deficits require emergent imaging of the brain after the initial assessment and 

stabilization of the ABCs. A noncontrast CT scan of the head is the study of choice to 

identify intracranial injuries. If the patient has only a history of loss of consciousness and 

is alert and oriented in the emergency department, head CT scan can be delayed and 

accomplished in conjunction with other CT scans that may be required to evaluate the 

patient with possible spinal injury. 

Minimize Neurologic Injury 

A. Reduce Spinal Cord Swelling 

Corticosteroids are useful in early treatment of spinal cord injury from blunt trauma, but 

only if begun within the first 8 hours after injury. Give methylprednisolone, 30 mg/kg as 

an intravenous bolus over 15 minutes; after a 45-minute delay, begin a maintenance 

infusion of 5.4 mg/kg/h for 24 hours in patients receiving treatment within the first 3 

hours after injury. Patients receiving treatment 3-8 hours after injury should be 

maintained on steroid therapy for 48 hours. Initiation of steroid treatment greater than 8 

hours after injury is probably of limited value and may increase morbidity and mortality 

secondary to nosocomial infections. Because of the often-limited information regarding 

time of injury in the initial emergency department evaluation, therapy should be 

instituted until injury time has been confirmed. Obtain neurosurgical consultation as 

soon as possible. Steroids play no role in the treatment of penetrating spinal cord 

injuries. 

B. Give Antibiotics for Penetrating Injuries 

Patients with penetrating spinal cord injury (eg, gunshot wound) should receive 

prophylactic antimicrobials. Nafcillin, 200 mg/kg/d intravenously in 4-6 divided doses, is 

widely recommended. 

Treat Complications 

A. Urinary Incontinence or Retention 

Patients may not note bladder dysfunction after spinal trauma because of loss of 

sensation below the lesion. Insert an indwelling catheter whenever spinal trauma is 

verified, to prevent urinary retention and to aid in monitoring urine output. 

B. Ileus 

Paralytic ileus and gastric atony are common after spinal trauma. Give the patient 

nothing by mouth, and insert a nasogastric tube connected to intermittent low-pressure

suction. 

Take Additional Measures as Needed 

A patient with spinal cord injury requires the same resuscitative measures customarily 

employed in major trauma. Insert an intravenous catheter and administer fluids and 

blood as required. Patients with spinal cord injury are particularly susceptible to 

exposure and should be covered with warm blankets in the emergency department to 

prevent hypothermia. 

Perform a baseline laboratory evaluation, including complete blood count (CBC) with 

platelet estimate, coagulation panel, serum electrolyte concentrations, renal function 

tests, blood glucose concentration, blood typing and cross-matching, and urinalysis. 

Treat other injuries. Evaluate and treat head injury and life-threatening conditions (eg, 

tension pneumothorax, cardiac tamponade, hemorrhagic shock) that take precedence 

over definitive treatment of vertebral and spinal cord trauma (Chapter 10). Maintain 

in-line spinal immobilization during resuscitation and treatment. If feasible, obtain 

cervical spine x-rays (anteroposterior and lateral) when the patient's condition permits. 

Even if no fractures are apparent, the spine may be unstable due to severe ligamentous 

injury. Maintain in-line immobilization until the patient can be reexamined free of 

distracting injury, intoxicants, or altered mental status. 

Bracken MB et al: Administration of methylprednisolone for 24 or 48 hours or tirilazad 

mesylate for 48 hours in the treatment of acute spinal cord injury. JAMA 1997;277:1597. 

[PMID: 9168289] 

Frohna WJ: Emergency department evaluation and treatment of the neck and cervical 

spine injuries. Emerg Med Clin North Am 1999;17:739. [PMID: 10584102] 

Gerling MC et al: Effects of cervical spine immobilization technique and laryngoscope 

blade selection on an unstable cervical spine in a cadaver model for intubation. Ann 

Emerg Med 2000;36:293. [PMID: 11020675] 

Goldberg W et al: Distribution and patterns of blunt traumatic cervical spine injury. Ann 

Emerg Med 2001;38:17. [PMID: 11423806] 

FURTHER EVALUATION OF THE PATIENT WITH SPINAL INJURY 

History 

Patients with spinal cord injuries can usually provide an accurate history of the injury. 

For example, auto collisions often result in cervical spine injuries that are frequently 

associated with head injuries; people who fall from heights often land on their feet and 

sustain fractures of the feet, hips, thoracolumbar spine; and so on. 

Complaints of back or neck pain should arouse a suspicion of spine injury. Stretching of 

the neck muscles, larynx, or esophagus in a hyperextension injury similar to whiplash 

may cause neck muscle pain and tenderness, hoarseness, or dysphagia. However, the

absence of spinal pain does not eliminate the possibility of spinal injury, especially if the 

patient is under the influence of alcohol or other mind-altering drugs. Consider spinal 

injury in any patient with blunt head injury; a neurologic deficit anatomically consistent 

with injury at a particular spinal level; or a penetrating injury to the neck, chest, or 

abdomen. 

General Physical Examination 

A brief general physical examination should precede specific assessment of neurologic 

function. Obtain complete vital signs, including core temperature. 

Carefully examine the head, chest, heart, abdomen, and extremities for other 

abnormalities. Remember that patients with spinal cord injuries may show few if any 

signs or symptoms of coexisting major injury because of anesthesia below the level of 

the lesion. Pain, guarding, rebound tenderness, and other signs may be absent despite 

the presence of fractured ribs, hemothorax, hemoperitoneum, peritonitis, and other 

major injuries. Examination of the genitals, rectum, and perineum may reveal priapism, 

decreased or absent rectal sphincter tone, or perineal sensation suggestive of spinal 

cord injury. Diligent, repeated examinations and laboratory tests (eg, CBC with 

differential, FAST exam, abdominal CT scan, DPL) are necessary to detect 

unsuspected injury. 

Gently but thoroughly examine the neck and spine for deformity, edema, ecchymosis, 

muscle spasm, or tenderness indicating possible vertebral fracture; a palpable defect in 

the posterior neck ligaments may be the only clue to major spinal injury. 

Neurologic Examination 

The emergency department neurologic examination for spinal trauma must be more 

thorough than that for head injury, although the complete trauma evaluation and initial 

assessment of the Glasgow Coma Scale score remain mainstays of the evaluation 

(Chapter 10). Neurologic examination assesses the following functions: mentation, 

motor function, sensation, and brain-stem and spinal reflexes. 

A. Mentation 

The spectrum of mentation includes all levels of consciousness ranging from alert to 

comatose: 

1. An alert patient demonstrates an immediate and appropriate response to all external 

stimuli. 

2. A patient in coma fails to respond normally to any external stimuli, including deep 

pain. 

3. Gradation between these extremes is best described by specific responses to specific 

questions or sensory stimuli, for example, "Patient is sleepy but arouses to loud voice. 

Knows name and location, but not time or reason for being in the hospital." Avoid vague 

terms to describe states of consciousness (eg, obtunded, semicoma, semistupor, 

lethargy) in individual patients, because these terms may be subjective and less

eliable, particularly when repeated examinations are performed by different people. 

B. Motor Function 

(See Tables 27-1, 27-2 and 27-3.) Movement of extremities should be carefully 

assessed and graded as follows: 

1. Normal movement means that the patient moves all extremities spontaneously, 

purposefully (ie, in response to specific commands), and with full strength and range of 

motion. 

2. Paralysis denotes no movement of the extremity or muscle group, either 

spontaneously or in response to painful stimuli. (Stimuli should be applied both directly 

to the extremity and to the trunk, because failure to move may be secondary to 

hypesthesia of the extremity.) Failure to move at all, either spontaneously or in response 

to an unpleasant stimulus, may indicate paralysis due to a structural lesion (eg, fracture) 

or metabolic causes (eg, drug overdose). Often, failure to respond is simply due to an 

inadequately painful stimulus. 

3. Gradation between these extremes should be described precisely, for example, 

"Patient extends right arm and leg, flexes left arm, and extends left leg in response to 

supraorbital pressure." Avoid broad descriptive terms such as "paraparesis" or 

"decerebrate posturing." Grade muscle strength from 0 (no movement) to 5 (full 

strength). 

4. Psychogenic paralysis rarely enters into the differential diagnosis of paralysis 

associated with trauma. See Chapter 16 for distinguishing features. 

C. Sensation 

(See Figures 27-1 and 27-2 and Table 27-4. ) Test as many sensory functions as 

possible in a patient with suspected spinal cord injury (in contrast to the more simple 

examination required for head trauma). Loss of some or all sensory functions below the 

lesion permits its precise anatomic localization. Perianal sensation should be tested; its 

presence eliminates the possibility of complete spinal cord transection and implies an 

improved prognosis. 

1. Position, vibration, and light touch—The dorsal columns can be tested by 

determining response to vibration, light touch, and changes in position. 

2. Pain and temperature—The ventral columns are tested by evaluating sensitivity to 

pain (pinprick) and temperature. 

3. Impaired mentation—When mentation is impaired, a pinprick or deep painful 

stimulation may be the only reliable sensory test. 

D. Brain-Stem Reflexes 

Brain-stem reflexes are usually intact except in the case of high cervical spinal cord 

injury, when nystagmus (midbrain, pons), facial hypalgesia (spinal nucleus of the 

trigeminal nerve), and hypoventilation (phrenic nerve, intercostals) may be present.

Note: The presence of brain-stem signs should not be attributed to spinal cord injury 

until an intracranial lesion has been excluded. 

E. Spinal Reflexes 

Tendon jerks and plantar responses are usually absent below the level of an acute 

complete spinal cord transection (Table 27-5); asymmetry is also common. Spasticity or 

increased tone in muscle groups may occur with partial spinal cord injuries. Anal 

sphincter tone (reflex and voluntary) becomes flaccid following complete spinal cord 

transection. Priapism occurring soon after injury suggests immediate complete spinal 

cord lesion. Onset at a later time may indicate that the lesion has progressed from an 

incomplete to a complete stage. Sweating and skin vasomotor tone are absent below 

the level of a spinal cord lesion. 

The bulbocavernosus reflex is dependent on an intact S1 and S2 spinal reflex. If the 

bulbocavernosus reflex is preserved in the presence of complete perineal sensory loss 

and flaccid paralysis of the lower extremities, it indicates that the period of spinal shock 

has passed and that the neurologic deficit is due to a lesion above the S1 segment. 

Absence of the bulbocavernosus reflex may indicate either the presence of spinal shock 

or a spinal cord lesion including the S1 and S2 segments. Spinal shock usually resolves 

within 24 hours and is accompanied by return of the bulbocavernosus reflex if the S1 

and S2 segments are not directly involved in the spinal cord lesion. 

Spinal Cord Syndromes 

A. Complete Spinal Cord Lesion 

The absence of sacral sparing (perianal sensation, rectal sphincter tone) indicates a 

complete spinal cord lesion, with recovery unlikely if the condition persists longer than 

24 hours. Sacral sparing suggests an improved prognosis. 

B. Partial Spinal Cord Lesions 

1. Brown-Sequard syndrome—This syndrome is usually caused by penetrating 

injuries resulting in hemisection of the spinal cord. The findings include loss of distal 

ipsilateral position and vibration sense, distal ipsilateral motor loss and vasomotor 

paralysis, distal loss of pain and temperature sense below T12 on the contralateral side 

(including the genitals and perineum). 

2. Central cord syndrome—This syndrome is usually due to cervical hyperextension, 

involving the central gray matter and the central parts of the lateral spinothalamic tracts. 

Quadriplegia may result, with minimal sacral sparing. The upper extremities are more 

involved than the lower extremities. 

3. Anterior cord syndrome—This syndrome results from cervical hyperflexion injuries. 

Position and vibration (posterior column functions) are preserved, but motor function, 

temperature, and pain sensation are lost bilaterally below the lesion. 

Reexamination 

Neurologic examination is helpful only if it is repeated often enough to establish a 

diagnosis, suggest further diagnostic steps, or clearly establish a trend in neurologic

function. The results of each examination may be seen as a point in a curve showing 

neurologic function with time. If successive examinations indicate improvement, further 

specialized testing may not be necessary. Failure to improve—verified by repeated 

examinations—indicates that additional studies are necessary, as does progressive 

deterioration from a baseline established by examination done on arrival in the 

emergency department. It is particularly important to note progressive neurologic 

dysfunction if injury involves the cervical spinal cord, because respiratory failure may 

result. 

Laboratory Examination 

Baseline studies required for all patients with suspected spinal cord injury include the 

following: CBC, urinalysis (specimen obtained by bladder catheterization), blood 

glucose concentration, serum electrolyte determinations, and renal function tests. 

Arterial blood gas measurements are necessary if ventilation is impaired or potentially 

threatened. 

Imaging 

Careful and correct interpretation of x-ray films is critically important in the treatment of 

spinal cord injury. Most spine abnormalities (eg, minor facet fractures and nondisplaced 

fractures) are more easily recognized by a radiologist, whose help should be sought in 

all cases. In a large study of blunt trauma patients, cervical spine injuries were identified 

in 2.4% of patients. Three-view cervical spine radiographs identified a cervical spine 

injury in 1.5% of the patients. Approximately 65% of all cervical spinal fractures and 

subluxations involve the lower vertebra (C5, C6, and C7). Radiographs were interpreted 

as normal in 0.9% of patients later found to have a cervical spine injury. Note: Normal 

spine x-rays do not exclude the presence of spinal cord injury. Spinal cord injury without 

radiographic abnormality is an uncommon but well-described condition, especially in 

children with flexible spinal columns and relatively larger head-to-body size ratios. In the 

NEXUS study, a large, observational, multicenter study, these injuries occurred in 

0.07% of all blunt trauma patients and in 6% of all the patients with spinal injuries. 

Central cord syndrome (central hemorrhage) and spontaneously reduced dislocations 

can be associated with normal x-rays, as can ligamentous tears resulting from 

flexion-extension injuries (whiplash). A thorough physical examination and a careful 

repeated neurologic evaluation are therefore essential in all cases. 

A. Chest, Skull, and Pelvis 

Portable chest and pelvis radiographs are standard in the initial evaluation of the patient 

with blunt spinal injury. Associated head injuries are common, and spinal injury patients 

often require CT scan of the head to evaluate intracranial injuries. 

B. Cervical Spine 

Anteroposterior and lateral views of the cervical spine extending from C1 to T1 and an 

odontoid (open mouth) view are required if cervical cord injury is suspected. The lateral 

cervical spine view alone is only 79% sensitive in detecting cervical spine injuries. If the 

segments from C6 to T1 are not visible, a "swimmer's" view should be obtained by 

having the patient supine, with one upper extremity abducted and extended (arm raised 

above head) and the opposite upper extremity adducted and extended (arm kept at side

of body). The shoulder of the adducted and extended extremity is then depressed by 

having a person stand at the foot of the bed and pull on the patient's hand. The x-ray is 

shot upward through the axilla of the abducted, extended extremity. Oblique views 

increase the sensitivity of the cervical spine series and are recommended by some in 

the evaluation of suspected cervical spinal injury. Standard oblique views require neck 

rotation; this can be avoided by performing a trauma oblique view, which is a 

modification of the oblique view. The trauma oblique view is obtained by aiming the 

x-ray beam at a 60-degree angle to the plane of the table with the patient supine (and 

immobilized). 

Other diagnostic modalities must be used if all of the cervical vertebrae cannot be seen 

adequately with these techniques. 

Flexion-extension views of the cervical spine have been recommended to evaluate 

ligamentous injuries in obtunded patients or in patients with persistent neck pain despite 

normal cervical spine radiographs. Recent studies have suggested little utility for 

flexion-extension views in children with normal initial cervical spine radiographs. In 

addition, flexion-extension views are discouraged for the acute evaluation of cervical 

instability because cervical spasm may temporarily stabilize the cervical spine despite 

significant ligamentous injuries. 

Magnetic resonance imaging (MRI), with superior ability to visualize soft tissues, may 

begin to play a significant role in the evaluation of cervical spine ligamentous injuries. If 

a patient is suspected of having a ligamentous cervical spine injury, continuous 

immobilization with a well-padded, rigid cervical collar is recommended for 14-28 days 

until follow-up studies such as flexion-extension radiographs or MRI can be performed. 

C. Thoracic and Lumbosacral Spine 

Indications for x-rays of the thoracic and lumbar spine follow the same criteria as those 

for the cervical spine. These criteria mandate that full radiographic evaluation be 

performed unless the patient is fully alert and has no evidence of midline bony 

tenderness; focal neurologic defect; intoxication; or painful, distracting injury. In addition, 

if a patient has a fracture in one portion of the spinal column, the entire spinal column 

must be imaged because the occurrence of an associated fracture at another level is 

relatively common. 

D. Special Studies 

1. CT scan—If a body scanner is available, the CT scan is the easiest and perhaps the 

best method of looking for vertebral column and spinal cord injury. MRI may be required 

for better visualization of the relationships between the spinal cord and the vertebral 

canal. 

2. Tomography—Tomograms provide excellent detail of the spine, but they are more 

difficult to interpret (and no easier to perform) than CT scans. 

3. MRI—MRI is indicated in patients with suspected spinal cord injuries and in patients 

with documented cord injuries. MRI provides a detailed view of the spinal cord, 

associated edema or hemorrhage, and surrounding soft tissues. With information 

obtained from MRI scans, injuries can be followed or operative interventions for cord

decompression and spinal stabilization can be planned. 

Hospitalization 

Hospitalization is required for patients with neurologic deficit, an unstable or potentially 

unstable vertebral column (with or without fracture), fractures or subluxation of vertebral 

bodies, or severe pain requiring parenteral analgesics for relief. 

Patients with uncomplicated fractures (ie, linear and undisplaced) of the transverse 

processes, sacrum, or coccyx and with normal results on neurologic evaluation and 

otherwise normal imaging studies do not require hospitalization. Provide symptomatic 

therapy as needed. 

EMERGENCY TREATMENT OF SPECIFIC SPINAL INJURIES 

Table 27-6 summarizes the mechanisms and common findings in many of the 

radiographically identifiable cervical spine injury patterns. 

VERTEBRAL FRACTURES WITHOUT SPINAL CORD INJURY 


In vertebral fractures without spinal cord injury, there is focal pain and tenderness over 

the vertebral column. Coughing or axial percussion of the head or feet may also cause 

pain that is referred to the fractured vertebral body. X-rays show fractures that may be 

in the vertebral body, the transverse processes, or the spinous processes. Coexisting 

dislocation or instability may be present. The neurologic examination is normal. 

Treatment 

Immobilize the patient on a firm surface (eg, rigid spine board), and use tape and lateral 

restraints (sandbags) or traction. Administer analgesia as needed. 

Disposition 

The only patients who do not require hospitalization are those with mildly symptomatic 

or asymptomatic, linear, nondisplaced, stable fractures of the spinous or transverse 

processes, or similar fractures of the sacrum or coccyx. Such patients may be given 

analgesics and a cervical collar for immobilization (if fractures are in the cervical 

vertebrae). A return visit should be scheduled within 1 week with an orthopedist or 

neurosurgeon. 

All other patients should be hospitalized—specifically, those with displaced or unstable 

fractures; fractures of cervical, thoracic, or lumbar vertebral bodies; open fractures; or 

multiple fractures. 

SPINAL CORD INJURY WITH OR WITHOUT VERTEBRAL FRACTURES 

Clinical Findings

Spinal cord injury with or without vertebral fractures is associated with neurologic 

symptoms and neurologic deficit. Findings are consistent with injury to the spinal cord 

(eg, sensory deficit ending circumferentially at T8). Bony injury to the vertebrae 

demonstrable on x-ray may or may not be apparent, because severe flexion-extension 

injuries and bony instability from ligamentous tears may cause serious or even fatal 

spinal cord injury without radiologically demonstrable abnormalities. 

Treatment 

A. ABCs 

Check the airway, gag reflex, and adequacy of ventilation, because high cervical cord 

lesions may cause death from respiratory insufficiency. Provide ventilatory support with 

a bag-mask combination or endotracheal intubation, if necessary. 

B. Vertebral Column Stabilization 

Stabilize the vertebral column using a rigid cervical collar and lateral restraints 

(sandbags or head blocks) to minimize further injury to the spinal cord. 

C. Hypotension and Blood Loss 

Correct hypotension and evaluate sources of blood loss such as hemorrhage into the 

chest, abdomen, pelvis, or femur. If no sources of hemorrhage are identified, judicious 

administration of intravenous crystalloid solutions (2-3 L) is indicated. If hypotension 

persists, low-dose dopamine, 5-10 ug/kg/min, is warranted to restore vasomotor tone. 

D. Other Measures 

Insert an indwelling urinary catheter and a nasogastric tube. Give nothing by mouth. 

E. Drug Therapy 

Spinal cord swelling from blunt trauma may be reduced by administering corticosteroids; 

however, the success of this treatment has not been proved. Give methylprednisolone 

in the dosing regimen previously discussed in this chapter. 

F. Consultation 

Obtain emergency neurosurgical consultation. 

Evaluation 

Obtain standard radiograph of the entire spine and CT scans of the vertebrae likely to 

be injured based on the sensory level in a patient with a probable spinal cord injury. To 

further evaluate the specific spinal cord injury and to make decisions regarding 

operative treatment, MRI of the spine is indicated. 

Disposition 

Hospitalize all patients with neurologic deficit caused by spinal cord injury. 

WHIPLASH (HYPEREXTENSION) INJURIES (Cervical Spine Sprain)


Patients with whiplash have a history of abrupt hyperextension of the neck (usually from 

a motor vehicle accident), usually without loss of consciousness. Injury from 

hyperflexion often occurs as well. Symptoms such as neck pain or muscle spasm, 

headache, hoarseness, and dysphagia often do not appear until 12-24 hours after 

injury. Neck pain may be referred to the arms or chest. Physical examination may show 

tenderness of anterior neck muscles and limited range of motion. Specifically, there is 

no evidence of neurologic deficit. By definition, whiplash does not cause fractures that 

are evident on cervical x-rays, although severe injuries may rupture the anterior disk 

fibers and result in widened disk spaces. X-rays are usually normal but may show 

reversal of the normal cervical lordosis. As previously mentioned, patients may have 

ligamentous instability despite normal cervical spine radiographs. For this reason, 

patients with persistent midline cervical spine tenderness should be immobilized in a 

well-padded, rigid collar 24 hours per day for 7-14 days until reexamined by a primary 

care physician or spine surgeon. 

Treatment 

Treatment consists of a rigid cervical collar, heat, and analgesics (narcotics are often 

required). Muscle relaxants may be indicated. At the time of reexamination, if a 

ligamentous injury is present, flexion-extension views will detect subluxation. MRI can 

be useful to identify ligamentous injuries in patients with possible cervical spine 

instability. If flexion-extension radiographs or MRI are abnormal, the patient should 

remain in the cervical collar and be referred to a spine surgeon to determine the 

significance of any subluxation. 

Disposition 

Hospitalization is rarely required. Refer the patient to a primary care physician or 

neurosurgeon for further evaluation. 

Frohna WJ: Emergency department evaluation and treatment of the neck and cervical 

spine injuries. Emerg Med Clin North Am 1999;17:739. [PMID: 10584102] 

Hoffman JR et al: Validity of a set of clinical criteria to rule out injury to the cervical spine 

in patients with blunt trauma. N Engl J Med 2000;343:94. [PMID: 10891516] 

Mahadevan S et al: Interrater reliability of cervical spine injury criteria in patients with 

blunt trauma. Ann Emerg Med 1998; 31:197. [PMID: 9472180] 

Mower WR et al: Use of plain radiography to screen for cervical spine injuries. Ann 

Emerg Med 2001;38:1. [PMID: 11423803] 

Panacek EA et al: Test performance of the individual NEXUS low-risk clinical screening 

criteria for cervical spine injury. Ann Emerg Med 2001;38:22. [PMID: 11423807] 

Pollack CV et al: Use of flexion-extension radiographs of the cervical spine in blunt 

trauma. Ann Emerg Med 2001;38:8. [PMID: 11423804]

Ralston ME et al: Role of flexion-extension radiographs in blunt pediatric cervical spine 

injury. Acad Emerg Med 2001;8:237. [PMID: 11229945] 






IMMEDIATE MANAGEMENT OF THE PATIENT WITH SUSPECTED 

SPINAL INJURY






TABLES 

Table 27-1. Segmental motor innervation: upper extremity.






TABLES 

Table 27-2. Segmental motor innervation: lower extremity.

Table 27-3. Motor function chart. 1 

Muscle Nerves 

Shoulder Girdle and Upper 

Extremity 

Deep neck muscles 

(sternocleidomastoid and 

trapezius also participate) 

Cervical Extension of neck 

Lateral bending of neck 

Scaleni Phrenic Inspiration 

Pectoralis major and minor Pectoral (thoracic; from 

medial 

Forward thrust of shoulder 

Levator scapulae Dorsal scapular Medial adduction and elevation 

of scapula 

Supraspinatus Suprascapular Lateral rotation of arm 

Latissimus dorsi, teres major, Subscapular (from Adduction of arm from front to 

and subscapularis 

posteriorcord of plexus) back 

Deltoid Axillary (from posterior 

cord of plexus) 

Lateral rotation of arm 

Biceps brachii Musculocutaneous (from 

lateral cord of plexus) 

Supination of forearm 

Coracobrachialis Flexion of forearm 

Brachialis Ulnar flexion of hand 

Flexor digitorum profundus 

Adduction of metacarpal of 

(ulnar portion) 

thumb 

Abductor digiti quinti Opposition of little finger 

Flexor digiti quinti Flexion of proximal phalanx, 

extension of 2 distal phalanges, 

adduction and abduction of 

fingers 

Pronator teres Median (C6, 7 from lateral Radial flexion of hand 

cord of plexus; C8, T1 

from medial cord of 

plexus) 

Palmaris longus Flexion of middle phalanx of 

index, middle, ring, or little 

finger 

Flexion of terminal phalanx of 

thumb 

Flexor digitorum profundus 

(radial portion) 

Flexion of hand

Abductor pollicis brevis Median (C7, 8 from lateral 

cord of plexus; C8, T1 

from medial cord of 

plexus) 

Flexion of proximal phalanx of 

thumb 

Opponens pollicis Flexion of proximal phalanx and 

extension of the 2 distal 

phalanges of index, middle, 

ring, or little finger 

C8, T1 

Extension of forearm C6-8 

Brachioradialis Radial extension of hand 

Extensor digitorum Extension of hand 

Extensor digiti quinti proprius Extension of hand 

Extensor carpi ulnaris Supination of forearm 

Abductor pollicis longus Radial extension of hand 

Extensor pollicis brevis Radial extension of hand 

Extensor indicis proprius Extension of hand 

Elevation of ribs 

Contraction of abdomen 

Lateral flexion of trunk 

Flexion of hip 

Sartorius Extension of leg 

Pectineus Obturator Adductor longus 

Piriformis . . . 

Abduction of thigh 

Flexion of thigh 

Abduction of thigh 

Obturator intemus Muscular branches form 

sacral plexus 

L4, 5; S1 

L4, 5; S1 

Gemeli 

Tibialis anterior Deep peroneal Supination of foot 

xtensor digitorum lingus Dorsal flexion of foot 

Extensor hallucis longus Dorsal flexion of foot 

Extensor digitorum brevis nbsp; 

L5, S1, 2 

Plantar flexion of foot in 

pronation 

Tibialis posterior and triceps 

surae 


supination


supination 

Flexion of middle phalanx of 

toes II-V 

Flexor hallucis brevis Spreading and closing of toes 

Voluntary control of pelvic floor

Table 27-4. Commonly used landmarks for 

testing dermatomal sensation. 

Dermatome 

C4-T2 

Nipple T7-8 

Umbilicus T12-L1 






TABLES 

Table 27-4. Commonly used landmarks for testing dermatomal sensation.

Table 27-5. Summary of reflexes. 1 

Afferent Nerve Efferent Nerve 

Corneal Pons Nasal (sneeze) 

Musculocutaneous Musculocutaneous 

Radial Radial 

Radial Radial 

Median Median 

Radial Radial 

Femoral Femoral 

Tibial Tibial 

Light Midbrain Accomodation 






TABLES 

Table 27-5. Summary of reflexes.

Table 27-6. Cervical spine injuries. 1 

Injury Characteristics 

Simple wedge compression Anterior loss of height; intact posterior column; stable fracture. 

fracture 

Flexion teardrop fracture Fracture of the anteroinferior aspect of the vertebral body; 

disruption of anterior, middle, and posterior columns; highly 

unstable injury. 

Anterior subluxation Disruption of posterior ligamentous complexes; potentially 

unstable. 

Bilateral facet dislocation Anterior displacement of more than half of the anteroposterior 

diameter of the vertebral body; highly unstable injury. 

Clay shoveler's fracture Fracture or avulsion of the spinous process; commonly seen in 

lower cervical vertebrae; stable injury. 

Flexion-rotation injuries 

Unilateral facet dislocation Anterior displacement of less than half of the anteroposterior 

diameter of the vertebral body; neurologic deficits can occur; 

rotation may be noted by malaligned spinous processes on 

anteroposterior film or off-set overlap of facets ("bow-tie sign") 

on lateral view; usually stable. 

Rotary atlantoaxial dislocation Type of unilateral facet dislocation; odontoid shows asymmetry 

of the lateral masses; unstable injury. 

Extension-type injuries 

Hangman fracture Fracture through pedicles of C2 secondary to hyperextension; 

spinolaminar disruption; unstable fracture. 

Extension teardrop fracture Displaced anteroinferior bony fragment; avulsion secondary to 

traction on anterior longitudinal ligament; highly unstable 

fracture. 

Fracture of the posterior arch of 

C1 

Axial compression injuries 

Odontoid view demonstrates no displacement of the lateral 

masses; stable injury. 

Jefferson fracture Lateral mass displacement of C1; significant prevertebral soft 

tissue edema; possibly unstable injury. 

Burst fracture of the vertebral 

body 

Disruption of the anterior and middle columns; mandates CT 

scan or MRI to evaluate retropulsion; if loss of height > 25%, 

neurologic deficit, or retropulsion occurs, then consider it to be 

an unstable fracture. 

Complex mechanism injuries 

Atlantoaxial subluxation Transverse ligament disruption; injury suspected if the 

predental space is > 3.5 mm (5 mm in children); unstable injury.

Atlanto-occipital dislocation Complete disruption of all ligamentous relationships between 

atlas and occiput; death often occurs immediately; highly 

unstable. 

Odontoid process fractures Type I: Avulsion of tip of dens; stable fracture. 

Type II: Fracture at base of dens; unstable fracture. 

Type III: Fracture extends into body of C2; unstable fracture.

Figure 27-1. Cutaneous innervation. (Reproduced, with permission, from Greenberg 

DA, Aminoff MJ, Simon RP: Clinical Neurology, 5th ed. McGraw-Hill, 2002.) 






FIGURES 

Figure 27-1

Figure 27-2. Cutaneous innervation. (Reproduced, with permission, from Greenberg 

DA, Aminoff MJ, Simon RP: Clinical Neurology, 5th ed. McGraw-Hill, 2002.) 






FIGURES 

Figure 27-2

28. Orthopedic Emergencies - Luis E. Rodriguez, MD, & John E. 

Gough, MD, FACEP 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES 

All trauma patients presenting to the emergency department should be managed initially 

in the same manner, regardless of their underlying injuries. Orthopedic injuries may at 

times be grotesque in nature and can draw attention away from more critical elements 

of initial patient assessment and treatment. The emergency physician must remain 

objective and proceed with the primary survey, which consists of evaluating the airway, 

breathing, circulation, disability, and exposure (ABCDEs). Even some closed fractures 

can be associated with significant blood loss (Table 28-1). 

Once the primary survey has been addressed (eg, intubation, tube thoracostomy), 

proceed to the secondary survey, which should be a thorough physical examination 

from head to toe with no system left unexamined. With cervical spine precautions in 

place, logroll the patient, assess the posterior scalp, and examine the entire spine for 

tenderness or step-off deformities. Perform a digital rectal examination to evaluate for 

sphincter tone, gross blood, or abnormal prostate position. When evaluating the pelvis 

for stability, apply gentle anteroposterior and lateral compression. Visualize and go 

through range of motion of all joints and document all lacerations, abrasions, and 

contusions. At this time, consider reduction of certain orthopedic emergencies such as a 

dislocated hip, knee, or any fracture or dislocation in which vascular compromise is 

present (Figure 28-1). Reduction should be done early, because complications such as 

avascular necrosis increase as time elapses. If possible, reduce fractures and 

dislocations with neurovascular compromise before transferring the patient to a trauma 

center for multisystem or severe injuries. If no immediate vascular compromise exists, 

the orthopedist may arrange to go to the operating room and reduce fractures or 

dislocations under general anesthesia. 

II. IMMEDIATE MANAGEMENT OF LIMB-THREATENING INJURIES 

TRAUMATIC AMPUTATIONS 


• Sharp, guillotine injuries are best candidates for reimplantation. 

• Keep amputated part clean, moisten with saline, and put on ice. 

• Do not allow part to freeze. 

• Cooling will help increase viability of amputated part up to 12-24 hours. 


Patients incurring traumatic amputations should be considered for reimplantation

surgery. Young healthy patients with sharp, guillotine injuries without crushing or 

avulsion damage are the best candidates for successful reimplantation. However, it is 

best to consider all patients as potential candidates, care for the amputated part, and 

make appropriate consultations or arrange for transfer. 



The patient presents with an amputated digit or limb. 


Although this diagnosis is made clinically, x-rays often help delineate exactly where the 

injury occurred, or if underlying fractures or dislocations exist. 

Treatment 

The amputated part should be kept clean, wrapped in a sterile dressing, moistened with 

sterile saline, placed in a plastic bag, and put on ice. Do not use dry ice or allow the 

amputated part to freeze. Cooling the amputated part will increase the viability from 6-8 

hours to approximately 12-24 hours. The injury should be treated as an open fracture, 

with appropriate use of antibiotics and tetanus prophylaxis. 

Disposition 

Patients with limb amputations usually require consultation with an orthopedic, plastic, 

or trauma surgeon. These patients should be admitted for further surgical management, 

neurologic and vascular evaluation, and monitoring of blood loss. Patients with small 

digit amputations may be managed in the emergency department and discharged with 

appropriate close follow-up. 

COMPARTMENT SYNDROME 


A potentially harmful complication of orthopedic injuries is the development of a 

compartment syndrome. Although predominantly occurring in the lower extremities, a 

compartment syndrome can potentially occur anywhere in the body including the 

abdomen and the orbits. The lower leg has four compartments: anterior, lateral, 

posterior, and deep posterior. Trauma below the knee can lead to progressive swelling 

with eventual decreased blood flow from vascular compression as well as neurologic 

compromise. 


Classically the findings associated with compartment syndrome are pallor, 

pulselessness, pain, paresthesias, and poikilothermia. Decreased or absent pulses are 

a late finding, and the presence of a pulse does not exclude compartment syndrome. 

Due to alteration of normal mental status, delays in recognition of compartment 

syndrome are more likely to occur in sedated patients or in those with head injuries than

in other patients. The diagnosis can be confirmed by measuring intracompartmental 

pressures with a Stryker needle or with a needle connected to an arterial line pressure 

monitor. Levels above 30 mm Hg are abnormal. 

Treatment 

Initially immobilization, elevation, cooling, and removal of any constricting bandages or 

splints are indicated. Intracompartmental pressures greater than 30 mm Hg generally 

require immediate intervention with fasciotomy. It is preferable to have a surgeon 

perform this procedure, if possible. 

Disposition 

Patients with compartment syndrome require hospitalization for definitive surgical 

management. 

III. GENERAL ORTHOPEDIC PRINCIPLES 

FRACTURES & DISLOCATIONS 

Fractures are disruptions in the continuity of bone and should be described with 

appropriate terminology. The terms closed or open designate important differences in 

the degree of skin breakdown at the fracture site. Degrees of displacement and 

angulation should be described in terms of the distal structure's relationship to the more 

proximal part of the body. For example, a posterior elbow dislocation describes the ulna 

in a posterior position relative to the distal humerus. Other descriptive terminology 

should be used, such as comminuted (fracture in more than two pieces), impacted 

(collapse of one fragment of bone onto another), transverse (fracture line at right angle 

to long axis of the bone), oblique (fracture line with angle other than right angle), and 

spiral (fracture line encircles bone secondary to rotational forces, often associated with 

child abuse). An avulsion fracture occurs when a ligament pulls a fragment of bone 

away. Pathologic fractures occur in weakened areas of bone as seen with osteomalacia, 

cysts, carcinomas, and Paget disease. When fractures occur with minimal trauma, 

consider the possibility of a pathologic fracture. Stress fractures occur most commonly 

in the lower extremity and are seen with repetitive trauma (eg, from prolonged marching 

or running). Stress fractures may be subtle and missed on initial radiographs. A bone 

scan may be necessary to make the diagnosis. 

Dislocations are disruptions in the normal relationship of the articular surfaces of the 

bones making up a joint. They may be associated with fractures. Dislocations should be 

described by the relationship of the distal bone to the more proximal bone (ie, 

anterior-posterior, medial-lateral). A subluxation is an incomplete dislocation. 

When pediatric fractures are evaluated, specific descriptions such as greenstick, torus 

or buckle, and plastic deformity may need to be used. Growth plate injuries in children 

are described by the Salter-Harris classification (Figure 28-2). 

Type I Injuries

The epiphysis is separated from the metaphysis without radiographic evidence of 

metaphyseal or epiphyseal fracture. Type I injuries are more common in younger 

children and may be seen with birth trauma. Historically these lesions were associated 

with scurvy and rickets. If significant displacement is not present, Type I injuries may be 

difficult to diagnose on initial radiographs. Thickening of the growth plate and soft tissue 

swelling may be the only signs evident on x-rays. If an injury is suspected but cannot be 

identified on the initial films, immobilization and orthopedic follow-up are recommended. 

Type II Injuries 

Type II injuries are the most common physeal injuries and are most often seen in older 

children (> age 10 years). The fracture line travels through the physis and is associated 

with an oblique fracture of the metaphysis on the opposite side from where the force 

was applied. The metaphyseal fragment is referred to as the Thurston-Holland sign. 

Type III Injuries 

Type III injuries comprise a vertical fracture of the epiphysis perpendicular to the physis, 

extending into the growth plate. This type of injury is uncommon and most frequently 

occurs at the distal tibial epiphysis. To avoid the potential of growth plate arrest, the 

fracture must be appropriately reduced to maintain proper blood supply. Reduction is 

accomplished most commonly with operative fixation. If surgery is not performed, 

frequent rechecks and follow-up radiographs are recommended to ensure that the 

fracture does not become displaced after immobilization. 

Type IV Injuries 

Unlike Types I-III, Type IV injuries are the result of compressive rather than rotational or 

shearing forces. Vertical splitting of the epiphysis occurs, extending through the physis 

and metaphysis. Type IV injuries require surgical repair, and growth plate arrest may 

occur even with operative fixation. 

Type V Injuries 

Type V injuries, which are rare, are the result of severe crushing forces applied to the 

epiphysis at the area of the physis. When seen, they occur most often at the distal tibia 

and the knee. Because no fracture is visible, these injuries are frequently missed on 

initial radiographs. Often they are diagnosed on follow-up visits after the shortening and 

angular deformity secondary to growth plate arrest is evident. Nontraumatic causes 

include osteomyelitis and epiphyseal aseptic necrosis. 

Eponyms 

Even though emergency physicians are likely to be comfortable using the many 

eponyms that exist to describe fractures (eg, Colles, Monteggia, Galeazzi), it is probably 

more efficient to provide orthopedic consultants with an anatomic description using the 

above terminology. For example, merely stating that the patient has a Colles' fracture 

does not convey whether the injury requires simple splinting and follow-up versus acute 

open or closed reduction.

SPRAINS & STRAINS 

Sprains are injuries to ligaments and may be associated with a fracture. The following 

grading system is used to describe the severity of the injury: 

• Grade I: incomplete tear. Swelling and ecchymosis may be present. Immobilization 

and conservative care are indicated. 

• Grade II: significant incomplete tear. Swelling and ecchymosis are usually present as 

is some laxity in the joint. Immobilization and orthopedic follow-up are indicated. 

• Grade III: complete disruption. The joint is unstable. Orthopedic consultation is 

indicated for possible surgical repair. 

When assessing joint instability, remember that joint effusions, guarding, and muscle 

contractions may complicate the initial clinical exam. If there is any question, a period of 

immobilization and follow-up examination are indicated. A strain is an injury to the 

muscle-musculotendinous unit. Strains are also graded according to severity. Most 

require immobilization and conservative management; however, surgical repair may be 

necessary, and orthopedic consultation or referral should be obtained if indicated. 

SPLINTING 

Splints are a basic part of orthopedic care. They are used to stabilize the injury, provide 

some amount of pain relief, and help prevent further injury. Some splints are designed 

to be temporary, such as those applied in the field by emergency medical services 

personnel. These splints should ideally stabilize the joint above and below the 

suspected injury. Emergency medical services personnel are generally taught to "splint 

it as it lies," and this concept also should apply initially in the emergency department. 

Attempting to correct deformities before obtaining radiographs is not recommended, 

unless vascular compromise is suspected. 

Splints are often applied in the emergency department before the patient is discharged 

or admitted and are left in place until more definitive orthopedic care is instituted. All 

physicians should be experienced in splinting. Even if the splint is to be applied by a 

technician, the physician should ensure that the splint is adequately padded and the 

limb is stabilized in an appropriate position before the patient is discharged. In addition, 

the physician should reevaluate and document the limb's neurovascular status after any 

reduction or splinting procedure. Use of circumferential plaster (ie, casts) is greatly 

discouraged in the emergency department. In almost all orthopedic injuries, soft tissue 

swelling worsens after discharge, potentially leading to significant neurovascular 

compromise if a cast has been applied in the emergency department. Specific splinting 

instructions are provided below for each injury. 

PROCEDURAL SEDATION 

Before a fracture or dislocation is reduced, adequate analgesia and muscle relaxation 

must be provided. The best way to accomplish fracture or dislocation reduction is with

sedation using either intravenous or intramuscular agents. Emergency departments 

should have specific policies in place for the administration and monitoring of patients 

undergoing sedation. The goal is to provide sufficient sedation for the procedure without 

having to administer general anesthesia. 

Before sedating a patient, ensure that the patient has fasted for 4-6 hours prior to the 

procedure. Necessary equipment includes at least one functioning venous catheter, 

continuous pulse oximetry, a suction catheter, airway intubation equipment, and a 

bag-valve-mask. Mallampati oropharynx assessment and consideration of the patient's 

American Society of Anesthesiologists (ASA) categorization should be determined 

before beginning the procedure to ensure that the emergency physician can manage 

any potential airway complications resulting from sedation. In general, only ASA Class I 

or II patients (those without serious systemic comorbid diseases) should undergo 

procedural sedation in the emergency department. ASA Class III or IV patients should 

optimally receive treatment in the operating room. 

Patients being sedated in the emergency department should receive supplemental 

oxygen regardless of initial oxygen saturation, and saturations should be maintained 

above 90% at all times. Medications should be short acting. Numerous medication 

combinations are available. We prefer using etomidate, 0.15 mg/kg intravenously. 

Etomidate has a profound and short-lived action, which should be sufficient for most 

procedures. Etomidate is currently not approved for use in children. It has been reported 

to cause adrenal suppression, the clinical significance of which is unknown. As with any 

sedative, airway support through airway maneuvers or assisted ventilation may be 

needed. An alternative is the combination of agents such as midazolam and fentanyl. 

Be aware that a potential side effect of fentanyl is chest wall rigidity (at higher doses or 

with rapid boluses), which may prohibit bag-mask ventilation and may necessitate 

paralyzation and intubation. Adequate documentation by trained nursing staff is a must, 

and sedated patients should be monitored until they can ambulate and tolerate fluids by 

mouth. 

CHILD ABUSE 

Unfortunately, child abuse remains a major problem in our society, with physical abuse 

affecting 2-5% of children in the United States. Skeletal injuries sometimes occur with 

abuse and may represent significant morbidity to the patient. Abuse should remain high 

on the list of differential diagnoses whenever injured children receive treatment, 

particularly if fractures are found in very young patients (ie, younger than age 3 years). 


The approach to diagnosis should be the same as for all trauma patients. Keys to 

potential abuse may be evident in the history, such as history inconsistent with the 

injuries seen or delays in seeking care (may be evidenced by callus formation at a 

fracture site seen on x-rays). Physical findings may include pattern injuries, old bruises, 

and multiple fractures in various stages of healing. 

Remember that significant force is required to produce fractures in the spine, scapula, 

and sternum. Rib fractures are uncommon in children except in the setting of abuse,

and chest radiographs should be examined carefully to identify these injuries. Spiral 

fractures have long been identified as red flags to alert the emergency physician of 

possible abuse. This is particularly true of humeral and femoral fractures (particularly in 

patients less than age 3 years); however, spiral fractures of the tibia may be seen with 

accidental injuries. Pulling and twisting forces may also result in a tearing of the 

periosteum and cartilage at the growth plate of long bones, scapulae, and clavicles. 

These corner fractures may also have a "bucket-handle" loop associated with them, 

which may be seen on plain x-rays. 

Treatment 

Treatment of specific injuries is described below. Careful documentation is encouraged. 

Disposition 

Obtain appropriate pediatric, orthopedic, and social services consultations while the 

patient is still in the emergency department. All physicians are required to report 

suspected child abuse. 

IV. MANAGEMENT OF SPECIFIC ORTHOPEDIC INJURIES 

SHOULDER GIRDLE INJURIES 

STERNOCLAVICULAR JOINT DISLOCATIONS 


• Chest wall deformity. 

• Sternoclavicular tenderness. 

• Sternal x-rays or computed tomography aids in diagnosis. 

• May be associated with mediastinal injuries. 


Dislocations of the sternoclavicular joint (SCJ) are the least common dislocations of a 

major joint. SCJ dislocations are frequently associated with motor vehicle collisions but 

also occur from sports injuries (eg, football, rugby). Anterior dislocations are most 

common and occur secondary to anterolateral force applied to the shoulder. Posterior 

dislocations are associated with crushing forces applied to the chest, and 25% of 

posterior dislocations are associated with injuries to the superior mediastinal structures. 

The severity of the injury may be graded as follows: 

• Grade I: mild sprain of the sternoclavicular and costoclavicular ligaments. May be 

treated with analgesia and sling and swathe. 

• Grade II: subluxation of the SCJ, may be anterior or posterior. Associated with rupture 

of the sternoclavicular ligament. Treatment is the same as with Grade I injury; however,

the joint must be immobilized for a longer period of time. 

• Grade III: complete dislocation. 



The diagnosis can often be made clinically. Tenderness, swelling, and deformity to the 

SCJ will be present. Patients typically use the unaffected arm to support the affected 

arm across the chest. 


Plain radiographs, including anteroposterior, oblique, and 40-degree cephalic tilt views 

aid in the diagnosis. A computed tomography (CT) scan may be necessary and is 

indicated in all cases of posterior dislocations to evaluate for mediastinal injuries. 

Treatment 

Obtain orthopedic consultation for both anterior and posterior dislocations. Anterior 

dislocations may be reduced in the emergency department using procedural sedation by 

placing a rolled towel or sheet between the scapulae and applying traction to the 

affected arm. A posterior dislocation may need operative repair, and early orthopedic or 

trauma surgery consultation is appropriate because compression of critical upper 

mediastinal structures such as the great vessels and trachea may occur. 

Disposition 

Patients with anterior dislocations may be discharged in a sling and swathe. Even if the 

reduction is successful, the joint is often unstable and the clavicular head may dislocate 

again. However, because the purpose of the reduction is often more cosmetic than 

functional, even if reduction is unsuccessful the patient may be discharged with 

immobilization in a sling and orthopedic follow-up. Posterior dislocations may be 

reduced with traction and adduction; however, patients with posterior dislocations 

should be managed in consultation with a specialist and most likely will require 

admission. 

CLAVICLE FRACTURES 


• Clavicle deformity. 

• X-rays confirm diagnosis. 

• Most heal with conservative management. 


A. Symptoms and Signs

Often the clavicle is deformed, and some swelling, tenderness, and occasionally 

crepitus are present. 

X-ray Findings 

Most clavicle fractures are easily seen with a clavicle series. 

Treatment 

Treat open fractures with antibiotics and orthopedic consultation. For closed clavicle 

fractures, treatment typically involves a sling, or sling and swathe. 

Disposition 

Patients with closed fractures may be discharged with orthopedic follow-up. Patients 

with open fractures require hospitalization for further management. 

ACROMIOCLAVICULAR JOINT INJURIES 


• Deformed and tender acromioclavicular joint. 

• May be confused with clavicle injury. 

• X-ray confirms diagnosis. 


Acromioclavicular joint (ACJ) injuries most commonly result from a direct fall onto the 

shoulder. ACJ injuries account for 25% of all dislocations within the shoulder girdle. 

These injuries are graded according to severity: 

• Grade I: sprain, minimal tear of the acromioclavicular (AC) ligament 

• Grade II: small tear of AC ligament, no change with weight bearing 

• Grade III: complete disruption of AC ligament, coracoclavicular ligament, and muscle 

attachments 



Patients should be examined in the sitting position. Often a deformity at the AC joint will 

be present, with swelling, tenderness, and occasionally crepitus. 


X-rays should include anteroposterior, axillary, and 15-degree cephalic tilt views. Stress 

views are no longer recommended. Classically, separation between the acromion and 

the clavicle is seen.

Treatment 

Type I and II injuries are treated conservatively with a sling. Type III injuries have 

traditionally been treated with surgical repair; however, conservative management has 

been used more recently with good results. 

Disposition 

Most patients may be discharged home. All patients should receive orthopedic referral 

for follow-up examination. 

SCAPULA FRACTURES 


• Pain and tenderness over scapula. 

• May be associated with more severe intrathoracic injuries. 

• X-ray (with axillary views) confirms diagnosis. 


Fractures of the scapula are uncommon, accounting for approximately 1% of all 

fractures. Fractures usually are secondary to direct blows (eg, falls, motor vehicle 

collisions) or to crush injuries. Because the scapula is well protected by muscle, the 

presence of a fracture indicates a significant mechanism of injury and warrants 

evaluation for other potential injuries. Associated injuries to the lung, chest wall, 

humerus, and clavicle often are present. Scapula fractures can be classified as follows: 

• Type I: fracture of coracoid process, acromion process, or scapular spine 

• Type II: fracture of the scapular neck 

• Type III: intra-articular fracture involving the glenoid fossa 

• Type IV: fracture of the body of the scapula (most common) 



The patient will present with pain and tenderness over the scapula. A hematoma and 

crepitus may also be appreciated. The patient will usually hold the affected arm close to 

the body. 


Fractures may be subtle on plain radiographs. Always obtain an axillary view to help 

identify fractures involving the glenoid, acromion, and coracoid processes. In some

instances CT scanning may be necessary to identify subtle or intra-articular fractures. In 

children, the physis of the acromion may be seen on x-rays. In approximately 3% of 

individuals this structure remains unfused (os acromiale) and can be mistaken for a 

fracture. 

Treatment 

The majority of isolated scapula fractures are managed conservatively with a sling and 

swathe and pain management. 

Disposition 

Significantly displaced fractures rarely may require surgical repair; patients with such 

fractures should be admitted. Patients with isolated scapular fractures may be 

discharged with close follow-up. 

ROTATOR CUFF INJURIES 


• Pain and decreased motion of shoulder. 

• Positive drop-arm test. 

• Plain X-ray of little value. 

• Arthrogram or magnetic resonance imaging will confirm diagnosis. 


The rotator cuff comprises four muscles: the subscapularis (internal rotation), the 

infraspinatus and teres minor (external rotation), and the supraspinatus (adduction). 

Acute tears are commonly seen with falls, either directly onto the shoulder or on an 

outstretched hand, but may also occur in the setting of lifting heavy objects. Tears occur 

more commonly in middle-aged to elderly males and usually involve the dominant arm. 



The patient complains of pain and decreased motion. Point tenderness over the greater 

tuberosity or a palpable defect may be seen. Tears may be evaluated by passively 

abducting the arm to 90 degrees and then applying pressure to the distal forearm. With 

significant acute tears, this will cause the patient to drop his or her arm (drop-arm test). 


Plain radiographs are usually of little use but should be obtained to rule out occult 

fractures. Superior displacement of the humeral head may be seen but is not diagnostic. 

Treatment

Provide adequate analgesia and a sling for comfort. 

Disposition 

Outpatient follow-up with scheduling of an arthrogram or magnetic resonance imaging 

(MRI) scan may be necessary to confirm the diagnosis. Patients may be discharged 

with orthopedic follow-up. 

SHOULDER DISLOCATIONS 


• Shoulder deformity, pain, and decreased movement. 

• Majority are anterior dislocations. 

• Anteroposterior, Y and axillary view X-rays confirm diagnosis. 

• Perform thorough nerve exam. 


The shoulder is the most commonly dislocated major joint in the body. Most (~95%) of 

these injuries are anterior dislocations and are often easily diagnosed clinically; 

however, in muscular individuals the clinical presentation may be less obvious. Posterior 

dislocations are much less common and are usually associated with violent muscle 

contractions as seen with seizures and electrocutions but may also occur with falls on a 

flexed, internally rotated arm. Posterior dislocations are often missed clinically and may 

also be difficult to identify on standard anteroposterior x-rays. 



The patient usually holds the arm in adduction and the elbow flexed close to the body. 

Pain occurs with the least amount of movement. The glenoid fossa may be palpable. A 

complete neurologic and vascular exam of the extremity is of paramount importance. 

Assess the lateral aspect of the shoulder for sensation in the distribution of the axillary 

nerve. Examine radial, ulnar, and median nerve distributions thoroughly prior to sedation 

and reduction. Document brachial and radial pulses. Luxatio erecta is an uncommon 

form of anterior dislocation in which the humeral head is forced out of the glenoid fossa 

secondary to a hyperadduction injury and comes to rest against the coracoid or 

subglenoid fossa. Clinically, the arm will be adjacent to the head with the forearm flexed 

over the head. Luxatio erecta may also be associated with injury to the axillary artery. 

With posterior dislocations the affected arm is usually held against the chest in 

adduction and is internally rotated. Abduction and external rotation are severely limited. 

The posterior shoulder may be prominent when viewed from above; however, this 

finding may be difficult to recognize, particularly in muscular individuals. 

B. X-ray Findings

Obtain a shoulder series, including a Y-view (Figure 28-3), which can help diagnose the 

direction of dislocation. Axillary views are often the most helpful if any doubt exists 

about the diagnosis. X-rays will also help identify associated fractures. A Hill-Sachs 

deformity (impaction of the posterolateral humeral head) may occur with dislocation. A 

fracture of the anteroinferior glenoid rim (Bankart fracture) may be seen with anterior 

dislocations. Bankart fractures may be subtle and identified only on CT scans. 

Treatment 

Some controversy exists over the need to obtain x-rays prior to reduction of shoulder 

dislocations. We do not generally recommend bypassing x-rays at this time unless 

vascular compromise is present. In patients with chronic recurrent dislocations, the 

dislocations may occur without significant trauma (eg, reaching backward, rolling over in 

bed); in this setting, consider reducing the shoulder before obtaining radiographs. 

Emergency physicians should be comfortable with numerous reduction methods. The 

patient will often require sedation prior to the procedure. We prefer the external 

rotation-adduction technique for reduction. With the patient in an upright position, the 

extremity is externally rotated while gentle traction and adduction are applied at the 

elbow. This technique is associated with a low risk of injury and does not require a great 

deal of force, as do the other methods. The traction-countertraction method—in which 

an assistant applies countertraction with a sheet and inline traction of the upper 

extremity—requires some physical strength (Figure 28-4). Do not try to pull the humerus 

into place. Instead place traction on the arm until the muscles fatigue and the humeral 

head slides in. After reduction, reevaluate neurovascular status and immobilize the 

shoulder with a sling and swathe. Obtain postreduction x-rays. 

Disposition 

Discharge patients with adequate analgesia such as nonsteroidal anti-inflammatory 

drugs or opiates and orthopedic follow-up in 2-3 days. If any neurologic findings are 

present, such as a wrist drop, obtain orthopedic consultation while the patient is still in 

the emergency department. Most of these neurologic findings are caused by a 

neuropraxia and usually improve over time. 

Kocher MS, Waters PM, Micheli LJ: Upper extremity injuries in the pediatric athlete. 

Sports Med 2000;30(2):117. [PMID: 10966151] 

Owens S, Itamura JM: Differential diagnosis of shoulder injuries in sports. Orthop Clin 

North Am 2001;32(3):393. [PMID: 11888134] 

Ruotolo C, Nottage WM: Surgical and nonsurgical management of rotator cuff tears. 

Arthroscopy 2002;18(5):527. [PMID: 11987065] 

UPPER EXTREMITY INJURIES 

HUMERUS FRACTURES


• Frequent in elderly patients. 

• Pain, deformity, and decreased mobility at shoulder. 

• X-ray confirms diagnosis. 

• Conservative management. 


Humerus fractures frequently occur in elderly women with a history of osteoporosis who 

fall on an outstretched hand (FOOSH). Consider pathologic fractures in younger 

patients without significant mechanisms, such as a 20-year-old baseball player who 

develops shoulder pain after pitching. 



The patient usually presents with deformity at the shoulder and ecchymosis. It is 

important to assess vascular status because the brachial artery lies in proximity to the 

distal humeral shaft and associated arterial injury may be present. Assess for radial 

nerve injury and wrist drop, particularly with humeral shaft fractures. Children who 

FOOSH usually sustain supracondylar humeral fractures, which are described below. 


X-rays show these injuries clearly. Proximal humerus fractures with some impaction are 

the most common type. In younger patients, look for signs of a unicameral cyst or other 

pathologic causes of fracture. 

Treatment 

Conservative management is generally the rule, especially in the elderly. These patients 

do well with a splint, sling, and swathe (Figure 28-5), or sling and swathe alone, and 

adequate analgesia. 

Disposition 

Patients should have orthopedic follow-up in 3-4 days. We recommend obtaining 

orthopedic consultation for any young person with humeral or humeral shaft fractures 

while the patient is still in the emergency department. If there is displacement of a 

humeral shaft fracture, a hanging or gravity splint may be applied. Occasionally these 

patients may undergo open reduction and internal fixation (ORIF). 

SUPRACONDYLAR FRACTURES 


• Occurs after FOOSH. 

• Elbow deformity, pain, and decreased mobility. 

• Posterior fat pad on lateral x-ray is highly suggestive. 

• May have high morbidity. BR> • Mandatory orthopedic consultation. 


Supracondylar fractures are of the distal humerus and classically occur in children. They 

are usually the result of a FOOSH. If not managed properly, supracondylar fractures 

may predispose to serious morbidity, including complications such as Volkmann 

ischemic contracture. 



Patients usually present complaining of elbow pain and arm swelling. A neurologic and 

vascular exam is important and must include notation of the anterior interosseous nerve 

sensory distribution. 


Supracondylar fractures may be subtle and at times may be suspected only by the 

presence of a posterior fat pad sign on a lateral elbow x-ray. Comparison views of the 

uninjured elbow may be of benefit if a fracture is suspected but not immediately 

apparent. 

Treatment 

All supracondylar fractures require orthopedic consultation. We recommend that these 

fractures not be reduced by emergency physicians. 

Disposition 

Disposition is as per orthopedic consultation. 

ELBOW INJURIES 


• Deformity, pain, and decreased range of motion. 

• Assess for ulnar nerve injury. 

• Anteroposterior and lateral x-rays are confirmatory. 

• Consider fracture if posterior fat pad is present. 

• No x-ray needed for a simple nursemaid's elbow. 


Elbow injuries usually occur from a direct blow to the elbow, causing immobility at the 

elbow joint. The patient generally holds the arm in flexion, and a moderate amount of 

swelling is present. Both fractures and dislocations may occur. It is important to assess 

neurologic function of the hand (especially in the ulnar nerve distribution because of its 

proximity to the elbow). 

X-rays should include anteroposterior and lateral views. Always look for the presence of 

fat pads. A small anterior fat pad can sometimes be normal; however, the presence of a 

posterior fat pad is abnormal and should alert the clinician to a fracture, such as a radial 

head fracture in adults or a supracondylar fracture in children. Even if a fracture is not 

visualized, treat the injury as though an occult fracture is present. 

1. Olecranon Fractures 

Olecranon fractures may occur by direct trauma or less commonly by contraction of the 

triceps while the elbow is flexed. 



Pain, limited range of motion, and a palpable defect or crepitus may be present. 


Plain x-rays should be sufficient to confirm the diagnosis. 

Treatment 

Most fractures may be treated with a splint, sling, and orthopedic follow-up. Displaced 

fractures (greater than 2 mm separation) or the presence of an ulnar nerve injury 

mandates acute orthopedic consultation. 

Disposition 

Patients who do not meet criteria for surgery may be discharged home as long as 

orthopedic follow-up can be obtained in 1-2 days. 

2. Radial Head Fractures 

Radial head fractures may occur by either direct trauma or more commonly by an 

indirect mechanism such as a FOOSH. 



The patient presents with pain, particularly on supination or pronation, and with limited 

range of motion. Elbow extension may be limited by joint effusion. 


It is often difficult to see a definitive fracture on plain x-rays. As mentioned previously,

the presence of a fat pad (especially posterior) should raise suspicion for an occult 

fracture. 

Treatment 

Simple radial head fractures are treated conservatively with analgesics and a simple 

sling. We recommend contacting an orthopedist for comminuted radial head fractures. 

Disposition 

Patients may be discharged with orthopedic follow-up in 3-5 days. 

3. Elbow Dislocations 

The elbow is second only to the shoulder as the most commonly dislocated major joint. 

Generally the radius and ulna are displaced together and the dislocation is described as 

the relationship of the ulna to the humerus (ie, posterior [most common], anterior, 

medial, or lateral). The most common mechanism is a fall, and associated fractures 

occur frequently. 



The patient often holds the elbow in 45 degrees of flexion, and a deformity at the 

olecranon is usually visible. Because of the location of the brachial artery and median 

nerve, the patient's neurovascular status should be assessed and documented initially 

and reassessed frequently. 


Examine plain radiographs for the presence of associated fractures. 

Treatment 

If neurovascular compromise is present, perform reduction as soon as possible. 

Dislocations may be reduced by applying traction to the wrist while the humerus is 

stabilized (Figure 28-6). Another technique involves applying traction at the wrist while 

the patient lies on his or her abdomen with the affected limb hanging off the bed. After 

appropriate analgesia and sedation, most dislocations can be reduced in a few minutes. 

These injuries should be reassessed for neurovascular injury and then placed in a long 

arm splint and sling (see Figure 28-5). 

Disposition 

Most patients may be discharged with adequate analgesia and orthopedic follow-up 

within 48 hours. 

4. Subluxation of the Radial Head 

Radial head subluxation (nursemaid's elbow) is a common injury, accounting for as

many as 25% of elbow injuries in children. This injury usually occurs in the 1- to 

3-year-old age group but may be seen up to school age and rarely in early teenagers. 

Subluxation occurs secondary to longitudinal traction on the arm while the elbow is 

extended and the arm pronated. This allows fibers of the annular ligament to slip 

between the radial head and the capitellum. 



Generally no deformity is seen. Some tenderness is present over the radial head, and 

the child characteristically refuses to use the arm. Although subluxation of the radial 

head is a common injury, obtain a thorough history to allay concerns about potential 

child abuse. 


Some authors suggest that if the clinician is confident with the mechanism of injury and 

the physical exam, radiographs need not be obtained prior to reduction. However, 

others assert that x-rays should always be obtained to rule out other potential injuries. 

Treatment 

Once the diagnosis is made, reduction is usually easily performed by stabilizing the 

elbow with one hand and, while applying gentle pressure on the radial head, supinating 

the forearm and flexing the elbow. Often a click or snap will be heard. The majority of 

patients regain normal use of the arm within minutes. Immobilization with a sling has 

been suggested; however, most patients will not comply, and if the reduction is 

successful, the sling likely will not make much difference. 

Disposition 

Unsuccessful or recurrent subluxations require outpatient orthopedic consultation. 

FOREARM FRACTURES 


• Pain and deformity present. 

• X-rays are confirmatory. 

• Assess for concomitant dislocations. 


Forearm fractures may occur secondary to varied mechanisms but are commonly seen 

with direct blows or a FOOSH. The site of injury determines the physical findings. 

Carefully examine the patient for function of the radial, median, and ulnar nerves. 

Assess, document, and later reassess distal pulses and tendon function. Development 

of a compartment syndrome should always be suspected and appropriate assessment

performed. As noted earlier in this chapter, it is probably more useful to describe the 

injury anatomically; however, the forearm is an area where many common eponyms for 

fractures exist, for example, 

• Colles' fracture: transverse fracture of distal radius with dorsal angulation 

• Smith fracture: transverse fracture of distal radius with volar displacement 

• Barton fracture: oblique, intra-articular fracture of the distal radius, with dorsal 

displacement of the distal fragment along with dorsal carpus subluxation 

• Hutchinson (chauffeur's) fracture: intra-articular fracture of the radial styloid 

• Monteggia fracture: ulna fracture with radial head dislocation 

• Galeazzi fracture: fracture of distal third of radius associated with dislocation of the 

distal radioulnar joint 

Treatment 

Nondisplaced fractures are generally treated conservatively with a sugar-tong 

(U-shaped) splint (volar and dorsal splint from distal metacarpals going around the 

elbow) and orthopedic follow-up. 

Disposition 

Displaced fractures warrant orthopedic consultation to determine the appropriate 

method (open versus closed) and timetable for reduction. Displaced forearm fractures in 

children should be seen by the orthopedist in the emergency department. 

Ring D, Jupiter JB, Zilberfarb J: Posterior dislocation of the elbow with fractures of the 

radial head and coronoid. J Bone Joint Surg Am 2002;84-A(4):547. [PMID: 11940613] 

WRIST & HAND INJURIES 

1. Lunate or Perilunate Dislocations 


• Occurs after FOOSH. 

• Wrist swelling, pain, and tenderness. 

• Anteroposterior and lateral x-rays of wrist are confirmatory. 

• Look for "piece-of-pie" and "spilled teacup" signs. 


Lunate or perilunate dislocations usually occur from a fall on an outstretched upper

extremity. It is believed to be part of a spectrum of injury associated with perilunate 

dislocation and occasionally a fracture. 



Usually the patient presents with a swollen wrist, decreased mobility, and severe pain. 

Median nerve injuries may be seen on exam. 


The lateral wrist view is the most important x-ray with these injuries. A line drawn 

through the center shaft of the radius normally bisects the lunate and capitate (Figure 

28-7A). In a lunate dislocation the radius and capitate are bisected and the lunate is 

displaced either dorsal or volar, giving what is sometimes referred to as a spilled teacup 

appearance (Figure 28-7B and C). The anteroposterior view shows a triangular-shaped 

lunate bone with the apex pointing toward the fingers, which is commonly referred to as 

the piece-of-pie sign. A perilunate dislocation occurs when the line drawn through the 

radius bisects the lunate only and the capitate is displaced. 

Treatment 

This injury should be managed by providing analgesia and splinting temporarily for 

comfort in the emergency department. Consult with an orthopedic surgeon for anatomic 

realignment. 

Disposition 

Patients undergoing ORIF should be admitted until the surgeon addresses the injury. 

Patients with reducible injuries may be given a long arm splint and sent home after 

arranging a treatment plan in conjunction with a surgeon. 

2. Scapholunate Dislocations 


• Frequently missed injury. 

• Anteroposterior hand x-ray confirms diagnosis. 

• "Terry Thomas" sign (greater than 3-mm scapholunate joint space). 


Usually occurring from a FOOSH, a scapholunate dislocation is a commonly missed 

hand injury. 



The patient may present with wrist swelling and decreased mobility. Tenderness over 

the wrist may be present. 


An anteroposterior view of the hand normally reveals a space between the scaphoid 

and lunate bone of less than 3 mm. If the distance is greater than 3 mm, then a 

dislocation injury is present. 

Treatment 

A scapholunate dislocation may temporarily be treated with analgesics and a radial 

gutter splint. 

Disposition 

Refer the patient to an orthopedic surgeon for definitive repair. 

3. Carpal Bone Fractures 


• Maintain high index of suspicion. 

• Consider scaphoid view x-rays. 

• Treat as fracture based on clinical findings even if x-ray findings are negative. 


Carpal bone fractures are often missed in the emergency department and require a high 

index of suspicion. Usually they occur after a fall on an outstretched upper extremity. 

Often, even if a fracture is not seen, the injury should be treated as a fracture in order to 

prevent long-term sequelae such as avascular necrosis seen with scaphoid or lunate 

(Kienbock disease) fractures due to the tenuous blood supply of these bones. 



Carpal bone fractures usually lead to wrist and hand swelling with decreased mobility 

and pain. Tenderness is often seen over the injured area. If tenderness is present in the 

anatomic snuffbox, consider a scaphoid fracture, regardless of x-ray findings, and treat 

the injury appropriately. 


Scaphoid and other carpal fractures may be seen on anteroposterior or dedicated 

scaphoid views. A triquetral fracture can often be seen on a lateral hand view as a small 

dorsal avulsion. Repeat x-rays in 1-2 weeks may often reveal a fracture that was not 

initially seen.

Treatment 

Scaphoid fractures may be treated with a thumb spica splint (Figure 28-8); other 

fractures may be treated with a volar wrist splint (Figure 28-9). 

Disposition 

Patients may be discharged with analgesics and follow-up with an orthopedist in 2-3 

days. 

4. Metacarpal Fractures 


• Hand swelling and pain. 

• Anteroposterior and lateral hand x-rays confirm diagnosis. 

• Assess for angulation and rotation. 


The most common metacarpal fracture, known as a boxer's fracture, is through the neck 

of the 5th metacarpal and occurs from punching an object or person. A Bennet fracture 

refers to an intra-articular fracture at the base of the first metacarpal. If the fracture is 

comminuted, then it is usually called a Rolando fracture. 



The patient presents with hand swelling, particularly over the dorsal surface, and 

tenderness over the affected bone. Assess for rotational injury by having the patient 

attempt to close his or her fist. The presence of open wounds should raise the suspicion 

that the injury resulted from hitting teeth. These wounds should be treated as human 

bites, with copious irrigation and antibiotics. 


Most metacarpal fractures should be visible on an anteroposterior or lateral view of the 

hand. Angulation of the fracture must be assessed in order to determine management. 

Treatment 

If any manipulation is needed, give the patient appropriate analgesics; local lidocaine 

infiltration may suffice. Correct any rotational deformity by gentle traction. If angulation 

of the metacarpal neck requires correction, it may be accomplished with gentle traction. 

The easiest way to remember angulation is the 10-20-30-40 rule. These are the 

maximum permissible degrees that may be tolerated in the 2nd, 3rd, 4th, and 5th 

metacarpals, respectively. Fractures involving the 2nd, 3rd, and 4th metacarpals may be 

treated with a volar wrist splint (Figure 28-10). After reduction, boxer's fractures may be

placed in an ulnar gutter splint (Figure 28-11) and Bennet fractures in a thumb spica 

splint (see Figure 28-8). 

Disposition 

After the injury is splinted, the patient may be sent home with adequate analgesia. We 

recommend arranging follow-up specifically for 1st metacarpal base fractures because 

they require operative repair. 

5. Phalanx Fractures & Dislocations 


• Finger pain, deformity, and limited mobility. 

• Finger x-rays are confirmatory. 


Phalanx fractures and dislocations often result from a direct blow to the affected digit. 

They may have rotational deformities as well as angulation. 



With dislocations, an obvious deformity usually is seen. Patients with fractures may 

present with swelling, pain, decreased mobility, ecchymosis, and tenderness. Assess for 

capillary refill and sensation with 2-point discrimination as well as for rotational injury. 


Plain x-rays of the hand, including anteroposterior and lateral views, often suffice. 

Occasionally a specific finger x-ray may be performed. 

Treatment 

Local anesthesia or digital blocks may be administered before manipulation. Reduction 

of dislocations and fractures can be managed with simple gentle traction. Splint these 

injuries with aluminum finger splints. 

Disposition 

The patient may be discharged with analgesics and hand surgeon follow-up in 3-4 days. 

6. Subungual Hematoma (See also Chapter 29.) 


• Painful fingernail and hematoma under nail. 

• May be associated with tuft fracture. 


Subungual hematomas usually occur from a direct blow to the nail, such as from a 

hammer. 



The patient presents with a painful digit. A hematoma is easily seen under the nail. 


Anterioposterior and lateral views of the affected digit often show a distal tuft fracture. 

Treatment 

If the hematoma is in excess of 25% of the nail surface, consider removing the nail for 

inspection of the nail bed. If less than 25% is present, then simple nail trephination may 

be performed for immediate relief of pain. Trephination is performed by using an electric 

cautery device or a heated paper clip perpendicular to the nail. 

Disposition 

Antibiotics are needed if a nailbed injury is present with an open fracture; orthopedic 

follow-up should occur in 2-3 days. Simple hematomas may be followed up by a primary 

care provider in 1 week. 

7. Boutonniere Deformity (See also Chapter 29.) 


• Swan neck deformity of finger. 

• May have avulsion fracture on x-ray. 


A boutonniere deformity often occurs from forced flexion at the proximal interphalangeal 

joint with rupture of the central slip of the extensor tendon, causing the classic deformity. 



The patient presents with obvious swan neck deformity. Decreased mobility and pain 

may also be present.


Occasionally an avulsion fracture of the middle phalanx may be seen on a lateral finger 

view. 

Treatment 

Splint the proximal interphalangeal joint in full extension for 4 weeks. Do not immobilize 

the distal joint. 

Disposition 

Discharge the patient with follow-up with a hand surgeon in 1 week. Give analgesics as 

needed. 

8. Mallet Finger (See also Chapter 29.) 


• Flexion of distal phalanx. 

• May have small avulsion fracture. 


Mallet finger often occurs as a sports-related injury when the distal phalanx receives a 

direct blow. The injury is a disruption of the extensor tendon at the site of insertion on 

the distal phalanx, with subsequently unopposed flexion of the distal phalanx. 



Pain is present at the distal interphalangeal joint, and the classic mallet deformity 

occurs, in which the distal phalanx is flexed. 


Occasionally a small avulsion fracture of the dorsal surface of the distal phalanx may be 

seen. 

Treatment 

Finger splint the distal interphalangeal joint in slight hyperextension. Commercially 

available splints can be used to reproduce this alignment. Splinting is required for at 

least 4-8 weeks. 

Disposition 

Discharge the patient with orthopedic follow-up within 3-4 days.

9. Ulnar Collateral Ligament Rupture 


• Consider in a fall while holding a ski pole. 

• Pain and swelling at 1st metacarpophalangeal joint. 

• X-ray may show small avulsion fracture of proximal phalanx. 


Also known as gamekeeper's or skier's thumb, ulnar collateral ligament rupture occurs 

after a forceful dislocation radially of the proximal phalanx of the thumb with 

spontaneous relocation that results in rupture of the ulnar collateral ligament. This injury 

most commonly results from falling with a ski pole in hand. 



Pain and swelling are present over the ulnar aspect of the proximal phalanx and 

metacarpal of the thumb. Weak pinching ability may be present. On exam there is 

tenderness with no end point on stress testing of the metacarpophalangeal joint (Figure 

28-12). Stress testing in the emergency department is usually not possible in an acute 

injury. 


Occasionally an avulsion fracture of the proximal phalanx may be seen. 

Treatment 

Apply a thumb spica splint and provide analgesics. Complete tears ultimately require 

surgical repair. 

Disposition 

Discharge the patient after immobilization; orthopedic follow-up is needed in 3-4 days 

for further repair. 

PELVIC GIRDLE INJURIES 

PELVIC FRACTURES 


• High degree of mortality.

• May have large amount of bleeding. 

• Consider if scrotal hematoma, urethra blood, or abnormal prostate are present. 

• Anteroposterior films are usually confirmatory. 


Pelvic fractures can be devastating injuries associated with significant mortality. The 

mechanism of injury in the majority of fractures is a high-velocity trauma as seen in 

motor vehicle collisions or when pedestrians are struck by cars. Fractures may also 

occur with low-velocity trauma such as crush injuries and simple falls, often seen in 

elderly individuals with osteoporosis. Much of the high degree of mortality may be 

related to the incidence of significant associated injuries (eg, head, thoracic, abdominal 

trauma). High-energy injuries that significantly disrupt the pelvic ring commonly tear 

pelvic veins and arteries. Bleeding associated with these injuries is frequently massive 

with the potential for exsanguination (see Table 28-1). The mortality rate for patients 

presenting with hypotension associated with pelvic fractures is approximately 50%. The 

mechanism and associated injuries determine the patient's presentation. 



All patients should receive a digital rectal examination to look for the presence of blood, 

to determine the position of the prostate, and for palpation of obvious fractures. 

Examination of the penis and testes or the vagina is necessary to evaluate for 

associated urologic and gynecologic injuries. If a urethral injury is suspected, do not 

place a urinary catheter; obtain a retrograde cystogram. If a urethral injury is present, 

consult with a urologist to place a suprapubic or Foley catheter (see Chapter 26). 

Compression to determine pelvic stability should be accomplished with gentle 

anteroposterior and lateral pressure (Figure 28-13). 


X-rays should initially include an anteroposterior view. Inlet and outlet views may be 

helpful; however, CT scanning should be obtained to classify the extent of injury and to 

plan for treatment. 

Treatment 

Fractures associated with disruption of the symphysis pubis (open book fractures) are 

frequently associated with massive bleeding into the pelvis. The patient should be 

monitored continuously with attention to the circulatory status and adequate volume 

replacement. Application of military antishock trousers may be initiated in the 

prehospital setting and needs to be continued in the emergency department. A sheet 

wrapped around the pelvis may also be used in an attempt to stabilize the fracture, 

decrease the volume of the pelvis, and help tamponade bleeding. In some cases the 

orthopedist may opt to place an external fixator device in the emergency department. 

Some patients may need emergent ORIF or need to be transferred to radiology for 

arteriography and embolization. 

Disposition

Obtain orthopedic consultation in all cases. Most patients will require hospitalization. 

Simple nondisplaced fractures of the pubic rami may be managed conservatively on an 

outpatient basis. Consultation with trauma surgery, urology, and gynecology may also 

be necessary. 

HIP INJURIES 


Hip injuries include various fractures and dislocations. As with pelvic fractures, hip 

injuries in young individuals are associated with high-energy trauma (eg, motor vehicle 

collisions, falls from height) and may be seen with direct (falls) or indirect 

(knee-to-dashboard) forces. Elderly patients frequently sustain hip injuries with lower 

forces such as a fall from standing. 

1. Hip Fractures 


• Frequent in elderly patients. 

• Hip pain and tenderness. 

• Frequently limb is shortened and externally rotated. 

• Anteroposterior and lateral films are usually confirmatory. 

• Consider CT scan or MRI if x-rays are negative and diagnosis is still suspected. 


Hip fractures are described anatomically as they may occur through the femoral neck, 

intertrochanteric, or subtrochanteric. 



The patient usually complains of groin pain. Shortening of the affected leg, with 

abduction and external rotation, is common but may not be obvious in cases of 

nondisplaced fractures. 


Radiographs should include anteroposterior (with the legs in internal rotation) and lateral 

views. CT scanning may be necessary, particularly if acetabular involvement is 

suspected. 

Treatment 

Immobilize the affected leg. If the fracture is closed and no neurologic deficits are 

present, inline traction may be applied. This immobilization is often initiated in the

prehospital setting. 

Disposition 

Monitor the patient for potential ongoing blood loss. Because of the risk of avascular 

necrosis of the femoral head, which occurs in 20% of these injuries, early orthopedic 

consultation is needed. Orthopedic consultation and admission for ORIF is warranted in 

the evaluation of all hip fractures. 

2. Hip Dislocations 


• Pain and deformity at hip. 

• Posterior dislocation is most common. 

• Hip or pelvic x-rays are confirmatory. 

• Patient's lower extremity is usually internally rotated and shortened. 


Hip dislocations are described by the relationship of the femoral head to the 

acetabulum. Dislocations may be accompanied by fractures of the acetabulum or 

femoral head. The vast majority (80-90%) of dislocations are posterior and are typically 

seen by indirect forces such as knee-to-dashboard injuries in motor vehicle collisions. 

Anterior dislocations are less common (10-15%) and may be seen slightly more 

frequently in patients with hip prostheses. Central dislocation refers to the femoral head 

being forced through a comminuted fracture of the acetabulum. Inferior dislocations are 

rare and occur almost exclusively in young children. Dislocations of the hip are generally 

the result of significant force, and potential associated injuries should be sought. 



Clinical examination in posterior dislocations generally reveals a slightly shortened 

extremity, adduction, and internal rotation, with the hip and knee in flexion. With anterior 

dislocations, findings include abduction, external rotation, and flexion of the hip. 


Obtain anteroposterior and lateral views to confirm the diagnosis and rule out 

associated fractures. 

Treatment 

Hip dislocations require urgent reduction to decrease the risk of avascular necrosis and 

neurologic sequelae. Posterior hip dislocations are commonly reduced by the Allis 

technique (Figure 28-14). After adequate sedation, the patient is placed supine and an 

assistant stabilizes the pelvis. The hip and knee are flexed to 90 degrees while upward

traction and slight rotation are applied. Once the dislocation is reduced, the leg is 

extended. 

An alternative method is the Stimson technique. The patient is placed prone with the leg 

extended over the edge of the bed. With an assistant stabilizing the pelvis, downward 

traction is applied with gentle rotation. The assistant then applies pressure over the 

greater trochanter toward the acetabulum. 

Disposition 

Once the dislocation is reduced by either method, the leg should be extended and 

placed in traction until postreduction x-rays can be obtained. Obtain orthopedic 

consultation for all hip dislocations. 

Brooks RA, Ribbans WJ: Diagnosis and imaging studies of traumatic hip dislocations in 

the adult. Clin Orthop 2000; 377:15. [PMID: 10943181] 

Yang EC, Cornwall R: Initial treatment of traumatic hip dislocations in the adult. Clin 

Orthop 2000;377:24. [PMID: 10943182] 

LOWER EXTREMITY INJURIES 

FEMORAL SHAFT FRACTURES 


• Pain and deformity of femur. 

• May lose large amount of blood in thigh. 

• Anteroposterior and lateral x-rays of femur are confirmatory. 


Fractures of the femoral shaft occur most commonly with high-energy trauma. Fractures 

occurring with minimal trauma should alert the emergency physician to the possibility of 

a pathologic fracture. 


As noted earlier, significant bleeding may occur secondary to femoral shaft fractures 

(see Table 28-1). The patient typically presents with tenderness and deformity of the 

thigh. Evaluate and document the neurovascular status. Although not as common as 

with lower leg fractures, significant soft tissue swelling can occur; therefore, frequent 

reexaminations should be performed to assess for the development of compartment 

syndrome. 


Anteroposterior and lateral views should confirm the diagnosis. Adequate visualization 

of the knee and hip on these films is important because associated fractures are


Treatment 

Adequate pain control and fluid resuscitation is indicated. Inline traction, either skeletal 

traction or an external traction device, should be applied to the leg. 

Disposition 

Obtain orthopedic consultation for admission and ORIF (usually with an intramedullary 

rod). 

KNEE JOINT INJURIES 

The knee is a large synovial hinge joint and is the most commonly involved joint in 

orthopedic injuries seen in the emergency department. The knee has a complex 

architecture of bone, muscle, ligament, and cartilage. The bones of the knee joint 

include the distal femur, proximal tibia, and patella. The fibula is not a part of the knee 

joint but serves as the attachment point for the lateral collateral ligament. The bones 

offer little stability to the joint, and the knee relies on the soft tissue components for 

proper function. 

The medial collateral ligament originates from the medial femoral epicondyle and inserts 

on the medial aspect of the tibia just distal to the tibiofemoral joint. The medial collateral 

ligament provides stability to valgus stresses (Figure 28-15A) and helps stabilize the 

medial meniscus. The lateral collateral ligament originates from the lateral femoral 

epicondyle and inserts onto the proximal fibula, providing resistance to varus forces 

(Figure 28-15B). The cruciate ligaments are located within the intercondylar notch and 

are named anterior and posterior by their attachment to the tibia at the tibial spines. The 

cruciate ligaments protect against anterior and posterior displacement of the knee. 

The menisci are cartilages positioned on the tibia. The menisci help dissipate forces 

within the knee joint and help prevent abnormal movement of the tibia and femur. The 

hamstring muscles (semitendinous, semimembranous, and the two heads of the biceps 

femoris) are the main flexors of the knee. The quadriceps muscles (vastus medialis, 

vastus lateralis, vastus intermedius, rectus femoris) combine to form the quadriceps 

tendon, which inserts onto the superior patella and the retinaculum of the joint capsule 

and functions in extension of the knee joint. 

The vasculature around the knee joint merits special attention. The collateral circulation 

is tenuous, and the popliteal artery is responsible for the blood supply to the lower leg. 

The popliteal artery is tethered above at the hiatus of the adductor magnus and below at 

the soleus muscle. This tethering makes the popliteal artery susceptible to injury from 

traction forces as seen with dislocations as well as disruption from fractures or 

penetrating wounds. 

The emergency department evaluation of an acute knee injury frequently involves 

obtaining plain x-rays, with anteroposterior, lateral, and sunrise view. Several clinical 

decision rules exist to aid the emergency physician in determining which patients need

x-rays acutely. The Pittsburgh rules note that mechanism of injury (such as blunt trauma 

and falls), patient age (greater than 55 years or less than 12 years), and inability to walk 

at least 4 weight-bearing steps are predictors of fractures that require radiographic 

evaluation. The Ottawa rules identify 5 indications for radiographs of the knee: age 

greater than 55 years, isolated tenderness of the patella, tenderness of the head of the 

fibula, inability to flex the knee to 90 degrees, and inability to transfer weight for 4 steps. 

Both sets of rules have demonstrated high sensitivity in predicting injuries and may be 

helpful to the emergency physician in the evaluation of the acutely injured knee. 

1. Patella Fractures 


• May be secondary to direct blow or traction injury. 

• Pain and tenderness are commonly seen. 

• May disrupt extensor mechanism. 

• Plain x-rays are usually sufficient. 

• Bipartite patella may be misinterpreted as fracture. 


The patella is the largest sesamoid bone in the body and may be fractured by direct 

forces such as falls and by indirect forces. Forceful contraction of the quadriceps 

muscles may result in a transverse fracture of the patella. Significant fractures of the 

patella may disrupt the extensor mechanism of the knee. 



Examination of the patient reveals pain and tenderness over the patella. A joint effusion 

may be present. If the patella is displaced significantly, a patellar defect may be 

palpable. 


Plain radiographs including anteroposterior, lateral, and sunrise views are usually 

sufficient to identify the fracture; however, CT scanning or MRI may be necessary to 

identify occult injuries. Bipartite or multipartite patellae are congenital findings that may 

be confused with acute fracture. 

Treatment 

Obtain orthopedic consultation. Simple fractures may be treated with immobilization of 

the knee in extension. 

Disposition 

Patients with simple fractures may be discharged with outpatient follow-up. Open and

displaced fractures require surgical repair. 

2. Patella Dislocations 


• Common in adolescents. 

• Almost always displaces laterally. 

• Obvious deformity, restriction of motion. 

• Plain x-rays are usually sufficient for diagnosis. 


The patella may be dislocated or subluxed by direct forces or a hyperflexion injury. The 

patella almost always displaces laterally. This injury occurs most commonly in 

adolescents. Often the patient gives a history of prior subluxations that resolved 

spontaneously. 



Tenderness is present on physical examination, and a deformity is usually easily seen. 

A joint effusion may be present. 


Plain radiographs are usually sufficient to confirm the injury. 

Treatment 

Management consists of closed reduction with appropriate sedation. This is 

accomplished by applying medial force to the patella while the knee is being extended. 

Disposition 

Immobilize the knee, give the patient crutches, and provide orthopedic referral for 

follow-up. Recurrent subluxations or dislocations may require surgical repair. 

3. Distal Femur Fractures 


• Generally represent high-energy injuries. 

• Associated hip and patella injuries are common. 

• Plain x-rays are usually sufficient. 

• Obtain arteriogram if vascular injury is suspected.


Fractures in the distal one third of the femur are typically described by the relationship of 

the fracture line to the femoral condyles. Distal femur fractures generally represent 

high-energy injuries. 



Pain and deformity are usually present. Associated patella and hip injuries sometimes 

occur. 


Diagnosis can usually be made with standard anteroposterior and lateral views. Oblique 

views and CT scanning may also be needed. If vascular compromise is suspected, 

obtain an arteriogram. 

Disposition 

Distal femur fractures are significant injuries that require orthopedic consultation in the 

emergency department. Skeletal traction and surgical repair are frequently required. 

4. Tibial Plateau Fractures 


• Usually occur to lateral aspect. 

• May be associated with peroneal nerve and popliteal artery injuries. 

• CT scan is helpful in planning treatment. 

• High suspicion for compartment syndrome. 


Tibial plateau fractures may result from axial loading and varus or valgus forces. The 

lateral portion of the tibia is most commonly involved. The fracture significantly impairs 

the function of the knee joint. Popliteal artery and peroneal nerve injuries may be seen, 

and the neurovascular status should be monitored continuously and documented. 



Pain and tenderness are usually easily elicited. A hemarthrosis may be present, and the 

incidence of associated ligamentous injuries is significant. 


Diagnosis is usually made on anteroposterior and lateral x-rays. CT scanning is often

used to delineate the extent of the injury. Tomograms and MRI may also be used. If 

vascular injury is suspected, obtain an arteriogram. 


Obtain orthopedic consultation to determine appropriate management. A compartment 

syndrome may accompany tibial plateau fractures, and compartment pressures should 

be measured if indicated. 

5. Tibial Tuberosity Fractures & Osgood Schlatter Disease 


• Usually avulsion fracture of patella tendon. 

• Obtain orthopedic consultation to determine treatment. 


These fractures generally occur secondary to strong flexion or extension of the knee 

against resistance. Fractures usually occur prior to closure of the epiphysis and 

represent an avulsion fracture caused by the patella tendon. 


Tenderness is present and, based on the mechanism of injury, an effusion may be 

seen. Diagnosis is confirmed with plain radiographs. In adolescents, Osgood-Schlatter 

disease must be in the differential diagnosis. Osgood-Schlatter disease is most 

commonly seen in males aged 10-13 years. It represents a chronic traction injury to the 

tibial tuberosity and commonly occurs in adolescents engaging in sporting activities. 

Radiographic findings may be difficult to differentiate from an acute fracture. A careful 

history and exam will help delineate an acute injury. A hemarthrosis is not associated 

with Osgood-Schlatter. 


Orthopedic consultation is necessary because tibial tuberosity fractures may require 

open reduction. Osgood-Schlatter disease is treated with immobilization and, in rare 

cases, surgery. 

6. Tibial Spine Fractures 


• Not common; usually seen in children. 

• Usually avulsion injury from cruciate ligament.

• Suspect associate ligament injury. 


Fractures of the tibial spines are not commonly seen. These fractures usually represent 

an avulsion injury by one of the cruciate ligaments. They are more commonly seen in 

children and most often involve the anterior tibial spine. 



Localized pain and a hemarthrosis may be present. If a significant ligamentous injury 

has occurred, instability of the knee may be seen. 


The presentation may be subtle and may be noted only as an incidental finding on the 

x-ray. Plain films will usually identify the injury. CT scanning, MRI, or arthroscopy may 

be needed to identify associated injuries such as cruciate ligament ruptures. 

Treatment 

Simple fractures are usually treated with immobilization. 

Disposition 

If significant ligamentous injury is present, surgery may be necessary. BR> 

7. Knee Dislocations 


• May be seen with high- or low-velocity injuries. 

• Tenderness and joint effusion are usually present. 

• Assess for associated popliteal artery injury. 


Dislocations involving the tibiofemoral joint (as opposed to patellar dislocations) are an 

orthopedic emergency and may represent a limb-threatening injury. They are commonly 

seen in high-energy trauma but may also be seen with low-velocity injuries such as from 

falls or jumping on a trampoline. The presence of a dislocation represents significant 

trauma to the soft tissues (ie, ligaments, menisci, and joint capsule). As noted above, 

the location and anatomy of the popliteal artery places it at significant risk of injury, 

particularly with posterior dislocations. Tenderness and joint effusion are generally 

present. 

Clinical Findings


Visual deformity may be obvious, but some dislocations may reduce prior to evaluation. 

Careful attention to the neurovascular status is indicated, and the presence of a pulse 

does not rule out an arterial injury. 


Plain radiographs help confirm the diagnosis. Traditionally, arteriography was 

recommended in all cases to identify arterial injuries such as intimal tears, which may be 

clinically subtle but progress to occlusion and ischemia. Some authors recommend that 

serial exams may be sufficient in low-velocity trauma. However, if arterial trauma is a 

possibility, arteriography or Doppler studies should be obtained. 

Treatment 

Management includes emergent reduction by inline longitudinal traction. The 

neurovascular status should be monitored continuously and reassessed frequently. 

Disposition 

Orthopedic consultation is necessary, and vascular surgical consultation may be 

needed. Patients for whom arteriography has not been obtained should be admitted for 

observation. 

8. Knee Ligament Injuries: General Considerations 


• Guarding and joint effusions may make diagnosis difficult in acute setting. 

• Patient may need immobilization and follow-up examination. 

Knee ligament injuries may range from minor sprains to complete disruptions. The more 

subtle injuries may be difficult to assess acutely because guarding and joint effusions 

may make determination of joint instability problematic. If possible, the unaffected knee 

should be examined before the injured knee in order to determine the patient's baseline, 

because some degree of laxity may be normal for an individual. After initial clinical and 

radiographic assessment, it is often prudent to treat the injury with a period of 

immobilization and crutches and to arrange for a follow-up examination. Depending on 

the patient's clinical situation and associated injuries, it is sometimes helpful to have the 

orthopedic consultant examine the patient under general anesthesia. 

9. Knee Ligament Injuries: Collateral Ligaments 

The medial collateral ligament is the most commonly injured ligament in the knee. The 

mechanism of injury often involves sporting events. The lateral collateral ligament is less 

commonly involved and occurs more often in high-energy trauma such as motor vehicle 

collisions.



The patient usually presents with tenderness along the distribution of the ligament. 

Evaluate the ligament's stability by placing varus and valgus stresses (see Figure 28-15) 

with the knee in extension and with 30 degrees flexion. 


Plain radiography is of limited use but should be obtained initially to rule out associated 

fractures. MRI has emerged as a useful modality to evaluate these injuries. Orthopedic 

follow-up should be arranged. 

Treatment 

Simple strains may be treated conservatively with immobilization and follow-up 

examination. 

Disposition 

Unstable joints will need further evaluation (eg, MRI, arthroscopy) and eventual surgical 

repair. 

10. Knee Ligament Injuries: Cruciate Ligaments 

Injuries to the cruciate ligaments usually result from direct anterior or posterior forces to 

the knee. Rotational forces may also injure the cruciate ligaments and are usually 

associated with other injuries (ie, menisci, collateral ligaments). Injuries may be 

associated with high- or low-energy trauma. The anterior cruciate ligament is the one 

most commonly injured. 



Joint effusions are common, and hemarthrosis may be seen particularly with anterior 

cruciate ligament injuries. Stability of the anterior cruciate ligament is assessed clinically 

by the Lachman (Figure 28-16), pivot shift, or anterior drawer tests. Stability of the 

posterior cruciate ligament is evaluated by Sag sign (Figure 28-17). 


Plain radiography may be unrevealing. Avulsion fractures of the tibial spines suggest a 

cruciate ligament tear. If the clinical examination does not reveal significant instability, 

outpatient follow-up examination may include MRI. 

Treatment 

Immobilize the knee and give the patient crutches and non-weight-bearing status 

instructions. 

Disposition

Orthopedic follow-up is indicated for all significant injuries, and arthroscopy may be 

performed for both diagnosis and treatment. 

11. Meniscal Tears 


• Medial meniscus most commonly affected. 

• Patient may complain of knee locking. 

• MRI or arthroscopy may be necessary for diagnosis. 


Meniscal tears usually occur when a rotational force is applied to the knee while the foot 

is planted. Because of degenerative process, the injury producing the acute tear may 

not be significant. The medial meniscus is most commonly affected. 



The patient may complain of hearing a pop, but this finding is not specific. Joint line 

tenderness is usually present, and the patient may complain that the knee "locks." This 

locking is usually seen with a "bucket-handle" tear of the meniscus when the free central 

portion becomes lodged in the intercondylar notch. Clinical diagnosis is evaluated by 

use of the McMurray and Apley tests. 


Plain films will not identify the tear but may be useful if associated bony injuries are 

suspected. 

Treatment 

Treatment involves knee immobilization, crutches, and pain control. 

Disposition 

Patients may be discharged from the emergency department with immobilization and 

orthopedic follow-up. Outpatient MRI is commonly used to make the diagnosis. 

Arthroscopy may be diagnostic and used to perform meniscectomy. 

Roberts DM, Stallard TC: Emergency department evaluation and treatment of knee and 

leg injuries. Emerg Med Clin North Am 2000;18(1):67. [PMID: 10678160] 

Seaburg DC et al: Multicenter comparison of two clinical decision rules for the use of 

radiography in acute, high-risk knee injuries. Ann Emerg Med 1998;32(1):8. [PMID: 

9656942]

Swenson TM: Physical diagnosis of the multiple-ligament-injured knee. Clin Sports Med 

2000;19(3):415. [PMID: 10918957] 

12. Tendon Ruptures 


• May disrupt extensor mechanism. 

• Quadriceps tendon is more commonly affected. 

• CT scan or MRI may be needed to confirm diagnosis. 


Complete rupture of the quadriceps or patella tendon will disrupt the extensor 

mechanism of the knee. Injuries can occur with high-energy injuries or may be seen with 

low-energy trauma, particularly in the elderly. The quadriceps tendon is more commonly 

ruptured compared to the patella tendon. 



The patient presents with a swollen and tender knee and is unable to extend the knee 

against resistance. A palpable defect may be appreciated. 


Plain films may demonstrate an abnormal position of the patella. CT scanning and MRI 

confirm the diagnosis. 

Treatment 

Place the patient in a knee immobilizer until consultation is obtained. 

Disposition 

Management depends on the extent of the injury. Complete ruptures require surgical 

repair. 

TIBIAL SHAFT FRACTURES 


• Most common long bone fracture. 

• Open fractures sometimes occur. 

• Plain x-rays are usually sufficient for diagnosis.

• Assess for compartment syndrome. 


The tibia is the most common site of long bone fractures. The majority of these fractures 

will occur with associated fracture of the fibula. The tibia can be injured by a variety of 

forces. 



Because little soft tissue is found around the tibia anteriorly, open fractures are 

common. Pain, swelling, and deformity are usually present. Compartment syndrome 

sometimes occurs with tibial injuries, and frequent reassessments should be performed. 


Plain films are usually adequate to identify the fracture. As with all suspected long bone 

injuries, the joints above and below should be adequately visualized on the radiographs. 

Treatment 

Measure compartment pressure if a compartment syndrome is suspected clinically. 

Simple nondisplaced fractures may be treated with a long leg posterior splint and 

crutches with orthopedic follow-up. 

Disposition 

Open, displaced, and comminuted fractures require orthopedic consultation because 

they require operative management. 

FIBULA FRACTURES 


• Isolated fibula fractures are uncommon. 

• Patient may be able to bear weight. 

• Assess for Maisonneuve fracture. 


Isolated fibular fractures are uncommon because they are usually seen with an 

associated tibia fracture. They may occur by direct blow or with rotational forces. Of 

particular importance is a Maisonneuve fracture, which is a fracture of the proximal 

fibula with an associated medial malleolus ankle fracture or ligamentous disruption of 

the ankle without a fracture. 

Clinical Findings


The patient usually complains of pain and tenderness, and a deformity can usually be 

palpated. If the fracture is an isolated fibular shaft fracture, the patient may be able to 

walk. 


Plain x-rays should be sufficient for the diagnosis. 

Treatment 

Splints or compressive dressing may be applied for comfort. A Maisonneuve fracture 

represents an unstable ankle injury, and orthopedic consultation is needed to determine 

definitive management. 

Disposition 

With isolated, uncomplicated fibula fractures, the patient may be discharged with 

instructions to advance from non-weight-bearing status to weight-bearing status as 

tolerated. 

ANKLE JOINT INJURIES 

The bones of the ankle include the distal tibia, distal fibula, and the talus. The ankle 

mortise is formed by the medial and lateral malleoli and the plafond (the articular 

surface of the distal tibia). As with the knee, the ankle relies on articular cartilage, joint 

capsule, and ligaments to provide joint stability. Management of ankle injuries is based 

largely on the joint's stability. 

The ligaments are divided into three sets: the syndesmotic (anterior and posterior 

tibiofibular ligaments); the lateral collateral (calcaneofibular, anterior talofibular, and 

lateral tibiocalcaneal ligaments); and the medial collateral or deltoid ligaments, which 

are further divided into four parts (posterior tibiotalar, tibiocalcaneal, anterior tibiotalar, 

and tibionavicular). Ankle injuries are common and often involve a combination of bony 

and ligamentous injuries. 

As with knee injuries, clinical decision rules aid the emergency physician in determining 

whether plain radiography is needed in the evaluation of ankle or foot injuries. The 

Ottawa ankle rules state that ankle x-rays should be obtained if there is pain at the 

malleoli, inability to bear weight for 4 steps, and tenderness posteriorly or inferiorly at 

the malleoli. Ottawa foot rules recommend that x-rays be obtained if there is inability to 

bear weight for 4 steps and tenderness at the base of the fifth metatarsal or over the 

navicular bone. The sensitivity of the Ottawa ankle rules is 98-100%. 

Pijnenburg AC et al: Radiography in acute ankle injuries: The Ottawa ankle rules versus 

local diagnostic decision rules. Ann Emerg Med 2002;39:599. [PMID: 12023701] 

1. Lateral Malleolar Fractures


• Inversion injury. 

• May include minor avulsion fractures to complete joint disruption. 



Lateral malleolar fractures may range from simple avulsion fractures seen with inversion 

to displaced fractures with mortise disruption. 



The patient usually presents with point tenderness, swelling, and difficulty ambulating. 


Plain radiographs are usually sufficient to make the diagnosis. 

Treatment 

Simple fractures may be treated with a posterior short leg splint with stirrups (Figure 

28-18), crutches with no weight bearing, and orthopedic follow-up. 

Disposition 

Open or displaced fractures require orthopedic consultation for operative management. 

2. Medial Malleolar Fractures 


• Eversion injury. 

• Often associated with deltoid ligament injury. 



Medial malleolar fractures result from eversion injuries or external rotation. These 

fractures are frequently associated with injuries to the deltoid ligament. 


BR>A. Symptoms and Signs 

Pain, swelling, and difficulty in ambulating are usually present. Palpate the proximal 

fibula to determine whether a Maisonneuve fracture is present.


Plain films will usually suffice for the diagnosis. 

Treatment 

Management is similar to that for lateral malleolar fractures; however, if significant injury 

to the deltoid ligament has occurred, the rehabilitation period will be longer. 

Disposition 

Patients with closed injuries may be discharged with a posterior short leg splint with 

stirrups (Fig 28-18), crutches with no weight bearing, and orthopedic follow up in 2-3 

days. 

3. Posterior Malleolar Fractures 


• Rare injury. 

• Usually avulsion from posterior talofibular ligament. 

• May represent significant joint instability. 


Fractures involving only the posterior malleoli are rare. They usually result from an 

avulsion injury involving the posterior tibiofibular ligament. If isolated they may be 

managed conservatively as above. If these fractures are associated with other injuries 

or joint instability, orthopedic consultation is indicated. Bimalleolar and trimalleolar 

fractures should be considered unstable and mandate orthopedic consultation for 

surgical management. 

4. Achilles Tendon Injuries 


• May occur from direct or indirect forces. 

• Use Thompson test. 

• Orthopedic consultation is necessary. 

BR>General Considerations 

Rupture of the Achilles tendon is often seen in middle-aged individuals participating in 

sporting activities. It may be secondary to a direct blow or can occur with indirect forces 

as with forced dorsiflexion. The patient frequently reports hearing a pop.



Localized pain and weakness in plantarflexion are present, and a deformity may be 

appreciated. The clinical diagnosis is based on history and clinical examination. To 

determine if the tendon has been ruptured, the emergency physician can squeeze the 

calf muscles with the patient prone and the knee flexed to 90 degrees (Thompson test) 

or alternatively squeeze the calf muscles with the patient kneeling on a chair with both 

knees flexed (Figure 28-19). Absence of plantarflexion or decreased plantarflexion 

compared to the unaffected side suggests rupture. 


X-rays may show thickening of the tendon. MRI will confirm the diagnosis. 

Treatment 

A temporary long leg or stirrup splint may be placed until consultation with orthopedics. 

Disposition 

Orthopedic consultation should be obtained because Achilles tendon injuries may be 

managed surgically or nonoperatively. 

5. Peroneal Tendon Injuries 


• Usually results from forced dorsiflexion. 

• Tenderness posterior to lateral malleolus. 

• CT scan or MRI may be needed to confirm diagnosis. 


The peroneal tendons function in eversion, pronation, and plantarflexion. These tendons 

can become subluxed or dislocated by tearing of the superior retinaculum attachment 

on the fibula. The injury usually results from forced dorsiflexion. 



The patient presents with pain, swelling, and weakness on eversion. Tenderness 

posterior to the lateral malleolus is present. 


A small avulsion fracture of the lateral malleolus is pathognomonic of this injury. A CT or 

MRI scan may be needed to confirm the diagnosis.

Treatment 

Treatment involves use of a posterior mold, crutches with no weight bearing, and 

analgesics. 

Disposition 

Orthopedic consultation is necessary to determine appropriate management. Patients 

with these injuries may be discharged with appropriate follow-up, but peroneal tendon 

injuries often need surgical repair. 

Kibler WB: Diagnosis, treatment and rehabilitation principles in complete tendon 

ruptures in sports. Scand J Med Sci Sports 1997;7:119. [PMID: 9211613] 

6. Ankle Dislocations 


• Associated fracture often present. 

• Assess neurovascular status. 

• Dislocation may require reduction before x-rays are obtained. 


An ankle dislocation represents displacement of the talus and foot from the tibia. 

Dislocations are described by the relationship of the talus to the tibia. They may be open 

or closed, and an associated fracture frequently occurs. Dislocations occur from axial 

loading to the foot in plantarflexion and are seen in sporting injuries and in high-energy 

trauma such as motor vehicle collisions. 



The neurovascular status should be determined quickly. The patient will have gross 

deformity of the ankle joint. 


Reduction is often performed prior to obtaining radiographs. 

Treatment 

Once the dislocation has been reduced, reassess the neurovascular status, splint the 

ankle, and obtain radiographs and orthopedic consultation. 

Disposition 

These patients will frequently be admitted and should not be discharged without

consultation from an orthopedist. 

7. Ankle Sprains 


• Anterior talofibular ligament is affected most commonly. 

• Swelling, ecchymosis, point tenderness. 

• Assess for instability of ligaments. 

• Ankle rules may help in determining need for x-rays. 

• Most are managed conservatively. 


Ankle sprains most often occur secondary to significant force applied as inversion and 

plantarflexion. The ligament most commonly affected is the anterior talofibular ligament, 

accounting for approximately two thirds of ankle sprains. The next most commonly 

affected ligament is the calcaneofibular ligament, and in 20% of cases the 

calcaneofibular and anterior talofibular are involved. The deltoid ligament located 

medially is injured less often (~5% of sprains). Eversion forces may initiate this injury, 

and sprains of the deltoid ligament typically require extended rehabilitation periods 

compared to the more common anterior talofibular or calcaneofibular ligament sprains. 

Deltoid ligament ruptures may be seen with medial malleolar fractures. 



The patient typically presents with a history of a fall or twisting injury. Often swelling, 

ecchymosis, and point tenderness are present. Grading of sprains is described earlier in 

this chapter. Always assess for associated injuries such as a Maisonneuve fracture or 

Achilles tendon rupture. 

Physical examination may include the anterior drawer test. With the patient seated, the 

knee flexed to 90 degrees, and the ankle in neutral position or 10 degrees of 

plantarflexion, gently pull forward on the heel while pushing the lower leg posteriorly. 

Visualize for any deformity or feel for a clunk. This test examines the integrity of the 

anterior talofibular ligament. The talar tilt-test assesses the anterior talofibular and 

calcaneofibular ligaments. With the knee flexed to 90 degrees and the ankle in a neutral 

position, invert the heel and assess for displacement of the talar head or laxity. The 

external rotation test is used to evaluate the distal talar syndesmotic ligaments. With the 

foot in neutral position and the knee flexed to 90 degrees, rotate the foot and assess for 

laxity and pain laterally. 


Use history, physical findings, and Ottawa ankle rules to determine whether radiographs 

are necessary. X-rays will be negative for fracture but may demonstrate soft tissue 

swelling. In significant ligament sprains and ruptures, the mortise may be affected.

Treatment 

Most ankle sprains may be treated conservatively on an outpatient basis. The RICE 

(rest, ice, crutches, and immobilization) treatment is usually indicated. For minor 

injuries, immobilization with an elastic bandage and crutches may be all that is 

necessary. For more significant injuries, a sugar-tong or posterior plaster splint may be 

applied. A plaster cast should never be applied acutely because of the risk of further 

swelling leading to increased pain and vascular compromise. Aircasts and other 

commercial devices may be useful. Crutches should be used (with no weight bearing 

initially and progressing to weight-bearing status as tolerated). Prescribe appropriate 

analgesics. Depending on the severity of injury, the patient may return to normal 

function in as little as a few days; however, it may be several weeks until proper function 

is restored. 

Disposition 

For minor injuries, treatment should be initiated as above. Follow-up may not be 

necessary. Patients may consider follow-up with a primary care provider for further 

evaluation in minor cases. Patients with significant sprains should receive treatment with 

immobilization and crutches as above and should be referred to an orthopedist within 1 

week. 

CALCANEAL FRACTURES 


• Most common tarsal bone fractures. 

• Axial loading, often associated with vertebral fractures. 

• The Boehler angle may detect subtle fractures. 

• Orthopedic consultation is necessary. 


The calcaneus is the largest of the tarsal bones and the one most commonly fractured. 

The most common mechanism is axial loading from a fall. A high association exists 

between calcaneal fractures and other lower extremity and vertebral fractures. 



The patient complains of severe pain in the heel and inability to bear weight. 

Ecchymosis and deformity may be present. 


Obtain plain radiographs including anteroposterior, lateral, and axial views. 

Measurement of the Boehler angle on the lateral view may help to identify subtle

fractures. The Boehler angle is formed by the intersection of lines drawn from the 

anterior and posterior elements of the superior portion of the calcaneus. The normal 

angle is 20-40 degrees; an angle of less than 20 degrees suggests a calcaneal fracture. 

Treatment 

A posterior leg splint or Jones wrap may be applied and the patient given crutches and 

non-weight-bearing status instructions. 

Disposition 

Orthopedic consultation is necessary to determine operative versus nonoperative 

management. 

TALAR FRACTURES 


• No muscle attachment on talus. 

• Tenuous blood supply. 

• CT scan or MRI may be necessary to detect subtle fractures. 


The talus is the second largest tarsal bone and is the second most commonly injured 

bone after the calcaneus. The talus is the only bone in the foot with no muscle 

attachment; it is held in place by the malleoli and ligaments. The talus has a somewhat 

tenuous blood supply, and avascular necrosis is a potential with significant fractures. 

Fractures may result from plantarflexion, dorsiflexion, or inversion forces. Talus 

fractures usually result from high-energy trauma, and associated injuries are common. 



Pain and swelling are common. Inversion and eversion are usually quite painful. 


Plain radiographs may miss subtle fractures, and CT scanning or MRI may be 

necessary. 

Treatment 

Simple fractures are treated conservatively. Major fractures often require open reduction 

or prolonged non-weight-bearing immobilization. 

Disposition

Patients should be admitted for further operative management. 

SUBTALAR DISLOCATIONS 


• Uncommon injury. 

• Associated with talocalcaneal and talonavicular ligament ruptures. 

• Plain x-rays should be sufficient for diagnosis. 

• Rapid reduction is indicated. 


Subtalar dislocations are rare injuries and occur secondary to severe rotational forces 

that rupture the talocalcaneal and talonavicular ligaments. The dislocation is usually 

lateral or medial, although anterior and posterior dislocations may occur. 



A deformity is usually visible. 


Plain radiographs including an anteroposterior view of the foot should determine the 

diagnosis. 

Treatment 

The dislocation should be reduced quickly, usually via closed reduction under adequate 

sedation. Inline longitudinal traction should be applied to the foot and then appropriate 

directional force applied to correct the deformity. 

Disposition 

After reduction, immobilization in a splint and orthopedic referral are indicated. 

TARSAL INJURIES 


• Isolated dislocations are rare. 

• Navicular fractures are most common, after calcaneal and talar fractures. 

• Local tenderness and swelling are common. 

• Plain x-rays are usually sufficient for diagnosis.


Fractures and dislocations can occur in the other tarsal bones (ie, navicular, cuboid, and 

the cuneiforms). Isolated dislocations are rare injuries. Fractures of the navicular are the 

most common in this portion of the foot. Avulsion fractures of the navicular occur when 

eversion stresses are exerted on the deltoid and talonavicular ligaments. 


Local pain and swelling are common. Plain radiographs may identify the injury; bone 

scans and tomography may be used to identify subtle injuries. 

Treatment 

Immobilization with a posterior short leg splint and orthopedic referral are indicated. 

TARSOMETATARSAL INJURIES (Lisfranc Injuries) 


• Uncommon injury; large amount of force is required. 

• Lisfranc joint. 



The tarsometatarsal joint comprises the articulation of the first 3 metatarsals with the 

medial, middle, and lateral cuneiform bones, as well as the articulation of the 4th and 

5th metatarsals with the cuboid. The tarsometatarsal joint separates the forefoot from 

the midfoot and is commonly referred to as the Lisfranc joint. It functions in supination 

and pronation of the foot. Injuries to this joint are uncommon and generally are the result 

of a large force applied to the foot. Dislocations can occur in part or all of this joint and 

are frequently associated with metatarsal and tarsal fractures. 



Pain and obvious deformity over the joint are generally present. 


Plain films usually suffice; a lateral weight-bearing view may detect subtle injuries but is 

not indicated in the emergency department. 

Treatment 

These injuries are often managed with closed reduction and percutaneous wires.

Disposition 

Orthopedic consultation is necessary. 

Perron AD, Brady WJ, Keats TE: Orthopedic pitfalls in the ED: Lisfranc 

fracture-dislocation. Am J Emerg Med 2001;19:71. [PMID: 11146025] 

METATARSAL FRACTURES 


• Common; result from crush or twisting injuries. 

• Most common at base of 5th metatarsal (Jones fracture). 

• Treat with posterior splint. 


Metatarsal fractures are common, accounting for approximately one third of foot 

fractures. They may occur as a result of crush injuries or twisting forces. 



A visible deformity may be present, along with tenderness and swelling. 


A fracture involving the base of the 5th metatarsal is the most common fracture. Plain 

radiographs should be sufficient to make the diagnosis. Care should be taken to 

examine the x-rays for subtle abnormalities in the Lisfranc joint. 

Treatment 

Avulsion fractures involving the tuberosity of the proximal 5th metatarsal can be splinted 

for comfort, or the patient may be allowed to bear weight in a hard-soled shoe. 

Fractures involving the metaphysis of the proximal 5th metatarsal are more prone to 

complication (ie, nonunion) and should be immobilized in a posterior splint (see Figure 

28-18). 

Disposition 

Discharge the patient with orthopedic follow-up within a few days. 

PHALANGEAL INJURIES 


• Fractures and dislocations are common. 

• Pain, obvious deformity. 

• X-rays may be bypassed in minor injuries. 

• Treatment involves buddy taping. 


Injuries to the toes are common and include both fractures and dislocations. Fractures 

of the phalanges are the most common fractures in the foot and frequently involve the 

5th phalanx. Dislocations are rare; when seen, they most commonly occur in the 

metatarsophalangeal joint of the great toe. 



Pain, swelling, and deformity are usually seen. 


X-rays usually reveal the injury. Radiographs may not be obtained for minor injuries. 

Treatment 

Conservative management and immobilization by taping to the adjacent toe (buddy 

taping) are instituted. Dislocations are usually easily reduced with adequate sedation or 

a digital nerve block. 

Disposition 

Patients with simple fractures do not require orthopedic follow-up. Complicated fractures 

and dislocations should be immobilized with buddy taping; patients with complicated 

fractures and dislocations should be referred for outpatient orthopedic follow-up. 

SESAMOID FRACTURES 


• Seen most commonly in flexor hallucis brevis tendon. 

• May be difficult to see on plain x-rays. 


Sesamoid bones commonly occur in the tendon of the flexor hallucis brevis. Fractures 

are not common and are usually the result of direct forces or hyperextension of the 

great toe. 

Clinical Findings


Local pain is present. 


Sesamoid bones are frequently unexpected findings on radiographs obtained to rule out 

other injuries. Sesamoid bones are not of uniform appearance, and sometimes fractures 

are difficult to recognize. 

Treatment 

Treatment is with immobilization, analgesia, and weight bearing as tolerated. 

Disposition 

These fractures generally do not require orthopedic evaluation; patients may be 

discharged to home. 

V. COMMON PITFALLS 

Missed orthopedic injuries are among the common malpractice claims in emergency 

medicine. Commonly missed injuries are carpal bone fractures, especially of the 

scaphoid. Other frequently missed injuries are posterior shoulder dislocations, hip and 

pelvic fractures in elderly patients, tarsometatarsal fracture dislocations, patellar tendon 

injuries, and compartment syndromes. Children may sustain injuries to growth plates 

with no radiographic evidence of injury on initial presentation. For this reason, 

emergency physicians should have a low threshold for immobilizing children with pain or 

tenderness near joints despite initially negative radiographs. Follow-up in 7-10 days 

should be arranged for reexamination out of the splint and possibly repeat x-rays. 

Patients should be advised that some nondisplaced fractures are not evident on initial 

radiographs and that outpatient follow-up and repeat radiographs may be indicated if 

pain or tenderness persists. 





FACEP 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING INJURIES

Table 28-1. Potential blood loss 

from closed fractures. 

Amount 

(in L) 

1-5+ 

Femur 1-2 

Leg 0.5-0.75 





FACEP 

TABLES

Figure 28-1. Technique of manual traction to align an angulated fracture and correct 

deformity. 





FACEP 

FIGURES 

Figure 28-1

Figure 28-2. Salter-Harris classification of growth plate injuries. 





FACEP 

FIGURES 

Figure 28-2

Figure 28-3. Sketch of view on tangential lateral x-ray shows the body of the scapula in 

its narrowest aspect. If the patient is poorly positioned, the medial and lateral borders 

are not superimposed. Normally the humeral head shadow lies directly over that of the 

glenoid, which may be hard to see. The position of the glenoid is indicated by the 

confluence of the scapular spine, the body of the scapula, and the coracoid process. A 

dislocated humeral head lies anterior or posterior to this point. 





FACEP 

FIGURES 

Figure 28-3

Figure 28-5. Posterior plaster splint with sling and swathe for immobilization of elbow or 

forearm injuries. Abundant cast padding is first wrapped around the arm. The posterior 

plaster must be reinforced medially and laterally to the elbow, but neither padding nor 

plaster should constrict the antecubital fossa. 





FACEP 

FIGURES 

Figure 28-5

Figure 28-4. Method of producing traction on dislocated humerus and countertraction 

on thorax for reduction of shoulder dislocation. 





FACEP 

FIGURES 

Figure 28-4

Figure 28-6. Reduction of posterior elbow dislocation by applying manual traction on the 

forearm while an assistant stabilizes the humerus. If radial or lateral displacement is 

present, it must be corrected before reduction is completed by flexion of the elbow. 





FACEP 

FIGURES 

Figure 28-6

Figure 28-7. A: Normal anatomy of the wrist. Note that the proximal end of the capitate 

rests in the lunate concavity. A straight line drawn through the metacarpal and capitate 

into the radius should bisect the lunate. The scaphoid makes an angle of 45 degrees 

with the long axis of the radius. B: Lunate dislocation. Lunate dislocates volarly. The 

angle between the scaphoid and the long axis of the radius is 90 degrees instead of the 

normal angle of 45 degrees. C: X-ray of volar dislocation of lunate. (Reproduced, with 

permission, from Way LW [editor]:Current Surgical Diagnosis & Treatment, 9th ed. 






FACEP 

FIGURES 

Figure 28-7

Figure 28-9. Volar splint for immobilization of wrist injuries. 





FACEP 

FIGURES 

Figure 28-9

Figure 28-8. Thumb spica splint: A slab of plaster is applied over adequate padding and 

secured with a loose elastic bandage. 





FACEP 

FIGURES 

Figure 28-8

Figure 28-10. Volar wrist and hand splint for immobilization of metacarpal shaft 

fractures and wrist injuries. A plaster slab is applied over adequate padding and secured 

with a loose elastic bandage. 





FACEP 

FIGURES 

Figure 28-10

Figure 28-11. Ulnar gutter splint for immobilization of injuries to the metacarpals of the 

4th and 5th fingers. A plaster slab is applied to the ulnar border of the forearm and hand 

over adequate padding and is then secured with a loose elastic bandage. 





FACEP 

FIGURES 

Figure 28-11

Figure 28-12. Stress examination of the thumb metacarpophalangeal collateral 

ligament. The ulnar side is injured more frequently. Test both sides in extension and 30 

degrees of flexion. Compare the injured digit with the uninjured thumb. Feel for a firm 

end point and absence of excessive laxity. 





FACEP 

FIGURES 

Figure 28-12

Figure 28-13. Compression-distraction test for stability of the pelvic ring. If the iliac 

crests can be pressed together or pulled apart, the pelvis is unstable. With more severe 

instability, one hemipelvis may be displaced proximally. 





FACEP 

FIGURES 

Figure 28-13

Figure 28-14. The Allis technique for reduction of posterior hip dislocation. Both hip and 

knee are flexed 90 degrees. An assistant stabilizes the pelvis while the operator pulls 

the femur anteriorly, rotating it slightly internally and externally to aid reduction, which is 

achieved mainly by deliberate, steady traction. 





FACEP 

FIGURES 

Figure 28-14

Figure 28-15. Valgus (A) and varus (B) stress tests for rupture of the medial and lateral 

collateral ligaments of the knee. More laxity than in the uninjured knee or lack of a firm 

end point constitutes a positive test. Pain and muscle guarding may make interpretation 

difficult. 





FACEP 

FIGURES 

Figure 28-15

Figure 28-16. The Lachman test for rupture of the anterior cruciate ligament. Attempt to 

pull the tibia forward relative to the femur while the knee is slightly flexed. Any increase 

in laxity compared with the uninjured knee signifies injury. 





FACEP 

FIGURES 

Figure 28-16

Figure 28-17. Rupture of the posterior cruciate ligament is a likely diagnosis when the 

tibia of the injured knee sags posteriorly below the distal femur when the legs are held 

flexed 90 degrees at the hip and knee. 





FACEP 

FIGURES 

Figure 28-17

Figure 28-18. Combined sugar-tong splint and posterior-plantar plaster slab with 

padding for ambulatory (non-weight-bearing) patient with foot injuries. 





FACEP 

FIGURES 

Figure 28-18

Figure 28-19. Test for Achilles tendon continuity. Squeeze the relaxed calf while 

observing the amount of ankle plantarflexion thus produced. If the tendon is ruptured, 

less motion occurs compared with that on the uninjured side. 





FACEP 

FIGURES 

Figure 28-19


EMERGENCY EVALUATION & TREATMENT 

1 This chapter is a revision of the chapter by Eugene S. Kilgore, Jr, MD, FACS, & 

William L. Newmeyer, MD, from the 4th edition. 

CM Carpometacarpal 

DIP Distal interphalangeal 

IP Interphalangeal 

LET Lateral extensor tendon 

MET Middle extensor tendon 

MP Metacarpophalangeal 

PIP Proximal interphalangeal 

TET Terminal extensor tendon 

Hand injuries are one of the more common reasons for emergency department visits. 

Hand injuries may be isolated or part of multiple trauma. These injuries are seldom life 

threatening but can result in significant disability, threatening a patient's livelihood and 

lifestyle. These injuries can have significant economic impact with possible loss of 

occupation and lost time from work. Systematic examination and initial care has a direct 

effect on the ultimate consequence of any hand injury. Overall it is far better to 

undertreat and refer than to overtreat and cause avoidable iatrogenic injury or disability. 

The course of recovery depends on initial management. 

Position the Patient 

Ideally the patient can be seated facing directly opposite the examiner, or the patient 

may be placed supine. The hand should be placed on a firm support that can be 

positioned against or attached to the table. Clothing around the arm should be removed 

to the shoulder. Lighting should be good, preferably wall or ceiling mounted. 

Control Bleeding 

Bleeding is controlled by direct pressure with sterile gauze packs, elevation, and, if 

necessary, an arterial tourniquet (eg, blood pressure cuff inflated above systolic blood 

pressure). Do not use clamps unless all other measures fail. Blind clamping of vessels 

can lead to further injury. 

Obtain History 

A. Current Injuries 

Ascertain the mechanism of injury by questioning the patient or others. An exact

description of how the injury occurred will help determine the need for x-ray, antibiotics, 

urgent consultation, or no consultation. It is important to document the mechanism of 

injury, the time at which it occurred, and the environment in which it occurred. Ask about 

the following details associated with the mechanism of injury: 

• Type of injury: crush, exploding, or simple amputation 

• Lacerations: exactly what device was involved and how the lacerations were caused 

• Position of the hand at the time of the injury (ie, fingers extended or flexed) 

• Presence of pain, numbness, paresthesias, weakness, discoloration, coldness, 

clumsiness or poor coordination, or crepitus 

• Circumstances surrounding open wounds: environment, whether inflicted in a dirty 

environment (ie, sewer or barnyard) or in a specific situation (ie, fight-clenched fist) 

B. Relevant History 

• History of prior or existing hand or upper extremity injuries or disorders. Dupuytren 

fasciitis, arthritis, and benign tumors are the most common nontraumatic problems 

noted. 

• Bleeding disorders likely to influence hemostasis (eg, hemophilia). 

• Factors that might impair wound healing (eg, use of corticosteroids). 

• Tetanus immunization status (Chapter 30). 

• Any allergies. 

• General state of health, medications, and ongoing treatments. 

Examine the Hand 

Examination of the hand is started while the history is being taken. In the event of an 

open wound, proper instruments and sutures must be made ready. Sterile technique is 

essential at all stages of the examination and early treatment of hand injuries. A sensory 

examination should be done with a fine needle before anesthesia is used. Before 

beginning active examination, anesthetize the injured area of the hand, and apply and 

inflate a tourniquet. 

A. Anesthesia 

Anesthesia must be used if a wound is to be explored or sutured. The preferred 

anesthetic is 1% lidocaine without epinephrine. Never use epinephrine with local 

anesthetics in hand injury, because it may constrict the vessels and interfere with blood 

flow. 

1. Digital block or wrist block—(See Figures 29-1 and 29-2. ) Digital blocks are 

preferred for procedures done distal to the PIP joint. Half-inch (1.5-cm) needles of 25,

27, or 30 gauge should be used with small volumes of 1% lidocaine. In a digital block, 

use about 0.5-1.0 mL around the digital nerve. The injection should never render the 

tissues tense nor be circumferential. 

In blocking peripheral nerves, the surgeon must be familiar with the anatomy of nerve 

distribution and the surrounding tissues. To avoid intravascular injection, always 

aspirate before injecting the anesthetic agent. 

2. Local infiltration—(See Chapter 30; Figure 30-1.) Wounds can be infiltrated locally 

as long as the amount of anesthetic injected does not make the tissues tense. 

3. Amount of solution—Systemic toxicity from overdosage may occur when large 

areas are anesthetized. This can be avoided by calculating the number of milligrams of 

drug in the volume of solution that may be required and then limiting the volume of 

injection so as to avoid giving a toxic dose (see Table 30-1). 

4. Inflamed areas—Anesthetic solutions should not be injected into inflamed areas 

unless these directly overlie an abscess that is to be drained. Such injections impair 

local tissue resistance to infection, may result in rapid systemic absorption because of 

the increased vascularity of inflamed tissues, and may be ineffective if the local tissue 

pH is low enough to reduce the anesthetic agent's ionic dissociation, which is essential 

for anesthetic activity. 

B. Application of Tourniquet 

An arm tourniquet should always be in place on the arm when hand wounds are 

examined or treated. A blood pressure cuff can be used but should be inverted so that 

the tubes extend cephalad and out of the way. When the cuff is in place, it should be 

wrapped with cast padding to keep it from unwrapping when inflated. 

When the anesthetic has taken effect and examination of the wound is about to start, 

the arm is elevated for 30 seconds and held there while the cuff is inflated to 275-300 

mm Hg and the tubes clamped with Kelly clamps to prevent deflation. This procedure is 

well tolerated by most patients for at least 15-20 minutes. 

C. Examination Sequence 

By dividing the examination into 4 distinct steps, much useful information can be gained 

rapidly. 

1. Observe the posture of the hand lying supine and at rest upon the examining table. 

Any marked variation from the normal stance should alert the examiner to the possibility 

of deforming injury. 

2. Observe active function of the various musculotendinous units and skeletal structures 

within the areas of injury. 

3. Assess loss of sensibility by testing for sweat and for awareness of pain by using a 

fine needle in areas of suspected nerve injury. Two-point discrimination is a sensitive, 

objective measure of sensory deficit. This may be difficult to do accurately, and the 

character and location of a wound may be more helpful than sensory nerve testing in

determining nerve injury. Sensory testing must be performed before application of a 

tourniquet and administration of anesthetics. 

4. Inspect the wound, in a sterile, bloodless field with a simple 2-power magnifying 

loupe, if available. A tourniquet should be in place but should not be inflated until the 

anesthetic has become effective unless there is uncontrollable hemorrhage (see above). 

The examination must proceed concurrently with early treatment such as cleansing and 

debridement (Chapter 30) before definitive emergency treatment and suturing are done. 

Note: In handling and examining tissue, remember that removal of blood clots and 

careful manipulation of tissues to preserve the microcirculation are far more important in 

avoiding infection than the type of antiseptic wound preparation used. 

EXAMINATION OF THE HAND & ASSESSMENT OF FUNCTION (See 

Figures 29-3 & 29-4. ) 

The hand is a highly mobile organ of extraordinary sensibility and remarkable 

adaptability, but it can be rendered useless or worse than useless by injury causing 

permanent stiffness, pain, or loss of sensibility. Prevention of permanent damage 

requires a sound knowledge of functional hand anatomy. 

Terminology 

(See Figure 29-5.) The hand and each finger have ulnar and radial sides and palmar 

and dorsal surfaces. There are 5 digits numbered and named as follows: I (thumb), II 

(index), III (long or middle), IV (ring), and V (small [little]). Commonly used abbreviations 

for the joints of the hand are shown in the box at the beginning of the chapter. Always 

specify which hand is injured, and note whether it is the dominant or nondominant hand. 

Skin & Circulation 

The skin of the palm sweats freely and is thick, tough, tethered by fascia, highly 

innervated, and well cushioned by fat. The dorsal skin, by contrast, is thin, very mobile, 

and less well supplied with sensory nerves. The arterial supply is mainly palmar. 

Venous and lymphatic drainage is mainly dorsal and can be impeded by dorsal injury, 

constriction, or taut skin. 

Twelve Extrinsic Flexors 


A. Anatomy 

1. Wrist flexors—There are 3 wrist flexors: the flexor carpi ulnaris (innervated by the 

ulnar nerve), the palmaris longus (median nerve), and the flexor carpi radialis (median 

nerve). 

2. Digital flexors—There are 9 digital flexors (one for each IP joint). The flexor pollicis 

longus (innervated by the median nerve) flexes the thumb IP joint. Flexor digitorum 

superficialis (sublimis) moves each PIP joint (all median nerve). Each superficialis is

generally able to contract independently, because the muscles are independent for each 

digit. 

A flexor digitorum profundus moves each DIP joint (median nerve to index and long 

fingers; ulnar nerve to ring and small fingers). The 3 ulnar profundi have a common 

muscle mass, and therefore one cannot contract and move one of these digit tips 

independently. 

B. Testing of Flexors 

1. Flexor carpi radialis—The flexor carpi radialis is tested by having the patient flex the 

wrist; the flexor carpi ulnaris is tested by spreading the fingers. The palmaris longus is 

tested by having the patient spread the fingers while flexing the wrist. 

2. Superficialis flexors—The superficialis flexors are tested by holding 3 digits not 

being tested in full extension and directing the patient to flex the fourth one. PIP flexion 

indicates an intact superficialis to that finger. 

3. Profundus flexors—The profundus flexors are tested by asking the patient to 

actively flex all of the fingers so that the distal pads of the fingers meet the distal palm. 

4. Flexor pollicis longus—The flexor pollicis longus is tested by having the patient 

actively flex the terminal phalanx of the thumb. 

Twelve Extrinsic Extensors 

(See Figure 29-4.) All extensors are innervated by the radial nerve. 

A. Anatomy 

1. Central wrist extensors—The extensor carpi radialis longus and extensor carpi 

radialis brevis insert into the bases of the second and third metacarpals, respectively. 

2. Extensor and ulnar deviator—The extensor carpi ulnaris inserts into the base of the 

fifth metacarpal. 

3. Abductor pollicis longus—The abductor pollicis longus deviates the wrist radially 

and stabilizes the base of the thumb (first metacarpal). It is tested by abducting the 

thumb radially. 

4. Two thumb extensors—The extensor pollicis brevis acts mainly at the MP joint; the 

extensor pollicis longus acts at the IP joint in concert with the intrinsics but, unlike the 

intrinsics, can extend the joint with much force and can even hyperextend it. 

5. Four finger extensors—An extensor digitorum communis to each finger forms the 

central slip (middle extensor tendon) of the extensor hood. 

6. Index and small fingers—The index and small fingers have independent (proprius) 

extensor tendons as well. These extend these fingers when the long and ring fingers are 

flexed.

B. Testing of Extensors 

Test the extensors by asking the patient to extend the fingers at the MP joint and to 

extend the IP joints. The latter is achieved by action of the extensor in conjunction with 

the intrinsic tendons in the extensor hood. The proprius tendons of the index and small 

fingers always lie ulnar to the extensor digitorum communis of each. 

Twenty Intrinsic Muscles 

A. Anatomy 

Of 20 intrinsics, 15 are innervated by the ulnar nerve and 5 by the median nerve. In 

conjunction with the extensor tendon, they form the extensor hood mechanism, which is 

a proximally based triangular sheet of 3 interconnected tendons. The lateral margins 

("lateral bands") are the small lateral extensor tendons (LETs) from the intrinsic 

muscles. The central large tendon ("central slip") from the extrinsic extensors is called 

the middle extensor tendon (MET), which inserts on the middle phalanx of each finger. 

The terminal extensor tendon (TET) is made up of a coalescence of METs and LETs 

into a very thin tendon that inserts on the distal phalanx. In the case of the thumb, which 

has only 2 phalanges, the equivalent of the MET is the extensor pollicis brevis; the 

equivalent of the TET is the extensor pollicis longus. The intrinsics flex the MP and 

extend the IP joints and abduct and adduct the digits. Working all together, they cup the 

palm. 

B. Testing of Intrinsics 

1. Thenar and hypothenar intrinsics—The thenar and hypothenar intrinsics act to 

pronate the thumb and little finger and thereby cup the palm. Have the patient make the 

distal fat pads of the thumb and small finger meet. 

2. Other intrinsics—Have the patient abduct the extended second through fifth digits; 

then flex these digits at the MP joints while extending the PIP and DIP joints. 

Examination of Nerve Injuries 

The 3 major nerves to the hand are the radial, median, and ulnar nerves. 

A. Radial Nerve 

The radial nerve innervates all extensors. 

1. Motor testing—Muscle testing is done by having the patient extend the wrist and 

digits (Figure 29-6C). 

2. Sensory examination—The radial nerve gives off a sensory branch that provides 

sensibility for the dorsal-radial aspect of the hand (Figure 29-6A and B). 

B. Median Nerve 

The median nerve innervates 9 of 12 extrinsic flexors, the lumbricals to the index and 

long fingers, and the 3 muscles of the thenar eminence, which are mainly concerned 

with opposition.

1. Motor testing— 

a. High median nerve—Testing for high median nerve injuries is done by flexing the 

DIP joint of the index finger and the IP joint of the thumb (Figure 29-7). 

Have the patient passively hold the fourth and fifth fingers fully flexed into the palm and 

follow this by full active flexion of the second and third fingers (Figure 29-7C). 

Have the patient flex the thumb to touch the distal palm at the base of the fifth finger 

(Figure 29-7D). 

b. Low median nerve—To test for low median nerve loss (eg, at the wrist), have the 

patient pronate the thumb, pressing the distal fat pad of the thumb against that of the 

ring finger. Then feel for a firm, contracted adductor pollicis brevis alongside the thumb 

metacarpal. 

2. Sensory examination—The median nerve provides sensibility to the radial two-thirds 

of the palm and the palmar surfaces of the thumb, the index and long fingers, the radial 

side of the ring finger, and the dorsal surface of the middle and distal phalanges of 

these fingers (Figure 29-7A and B). Because of the importance of this zone of 

sensibility, the median nerve is called the "eye of the hand." 

C. Ulnar Nerve 

The ulnar nerve innervates 15 of the 20 intrinsic muscles and only 3 extrinsic muscles. 

1. Motor testing—The intrinsics are tested by any of the following maneuvers: With the 

palm flat on the table, have the patient abduct and adduct the fingers, cross the fingers, 

or forcefully move the pointed index finger in a radial direction. 

The extrinsics are tested as follows: Forcefully flex the tips of the ring and small fingers 

to meet the distal palm to evaluate their profundi (Figure 29-8C); then forcefully spread 

the fingers apart and palpate for a tensed flexor carpi ulnaris tendon at the wrist. 

2. Sensory examination—The ulnar innervates the radial and ulnar halves of the pads 

of the small finger, the ulnar half of the pads of the ring finger, and the ulnar side of the 

hand (Figure 29-8A and B). The additional loss of sensibility on the dorsoulnar aspect of 

the body of the hand signifies a high lesion well proximal to the wrist. 

X-ray Examination 

Any severe injury to the hand requires x-rays to detect fractures, dislocation, and 

opaque foreign material or gas. Special positions should be requested, depending on 

the site and direction of trauma. If there is any doubt about the normalcy of the skeleton, 

comparable views of the opposite side should be taken for comparison. 

EQUIPMENT & MATERIALS FOR TREATMENT 

Instruments, Antiseptic Solutions, & Sutures

A. Needles 

Suturing should be carefully done with fine-pointed and very sharp cutting needles (eg, 

Ethicon P-1, P-3). 

B. Suturing Material 

Fine (4-0, 5-0, or 6-0) monofilament polypropylene suture material is preferred for skin 

closure. Only in infants and children should an absorbable suture such as 5-0 or 6-0 

chromic or plain catgut be used. 

C. Instruments 

Fine plastic surgery forceps, retractors, clamps, and needle holders are required. 

D. Skin and Wound Preparation 

The skin around the wound may be sterilized as described in Chapter 30. Take care not 

to splash disinfectants in the wound itself. The hand and wound may be irrigated with 

normal saline or even tap water (hydrogen peroxide can be toxic and is less preferable). 

Avoid prolonged soaking. 

Dressings, Splints, & Antibiotics 

A. Inner Dressings 

Petrolatum-impregnated gauze followed by a surgical gauze sponge saturated with 

water (tap water or sterile saline solution) is applied over the wound as the "core" 

dressing. The wetness draws blood from the wound and prevents dead space. None of 

this goes circumferentially around the digit, hand, or forearm. 

A foam pad such as a Reston pad with an adherent surface on one side (or comparable 

substitute) is then applied over the core dressing. 

Soft elastic gauze (Kerlix, Kling) or cast padding to form a soft, well-padded dressing is 

applied over the foam pad and may go circumferentially around the part. 

B. Splint 

The wrist is the most important joint to splint for all major hand injuries, even if only one 

digit is injured. Well-padded plaster as a splint protects the hand. 

For isolated pain-free dorsal injuries at the DIP or PIP joint, a tongue blade cut to the 

length of 2 phalanges and padded with gauze or foam rubber makes an excellent splint. 

If there is a wound over the joint, such a splint should be placed on the palmar side; if 

not, it is placed on the dorsum. 

The most useful palmar splint consists of 10-12 layers of plaster cut to fit the involved 

digit or digits and extending halfway up the volar surface of the forearm. It is padded 

with a thin foam pad (eg, Reston) and held in place with a loosely wrapped roll of plaster 

of paris, bias-cut stockinet, or elastic bandage. The hand generally should be in the 

"position of function," that is, slight wrist extension and MP flexion, with the PIP and DIP 

joints in partial extension and the thumb web open (Figure 29-9). Modification must be 

applied to take tension off a specific wound.

C. Sling 

No patient should leave the emergency department without a sling to hold the hand at 

the level of the heart or higher to promote venous and lymphatic drainage. Slings that 

hold the hand lower than the heart encourage the development of tissue edema. To 

avoid a tourniquet effect, the extremity should usually be outside of a sleeve. 

MANAGEMENT OF SPECIFIC TYPES OF HAND INJURIES 

LACERATIONS 

Small Lacerations 

Simple lacerations (superficial lacerations not extending into subcutaneous fat and not 

perpendicular to skin tension lines) can be closed by sterile surgical tapes (ie, 

Steri-Strips) or tissue adhesives. Wounds that require sutures (lacerations that are 

parallel to skin tension lines or into subcutaneous fat) should be evaluated in a sterile, 

bloodless field. Splinting and elevation of the limb can help healing and reduce pain. 

Splinting is also important for wounds that cross joints to prevent joint stiffness or 

contracture from wound scarring. Follow-up with a primary care physician in 7-10 days 

for suture removal is appropriate. 

Extensive Lacerations 

Wounds should be carefully evaluated in a sterile, bloodless field. Irrigation and cleaning 

with tap water or sterile saline is the next step. Careful handling of tissues is essential. 

Approximate the wound margins with sutures. If the wound is dirty, do not close under 

tension. If the edges cannot be easily approximated, the wound may be left open and 

the patient referred to a hand surgeon for primary or delayed split-thickness grafting. 

Consider the need for local and systemic antibiotics and tetanus prophylaxis. 

FINGERTIP INJURIES 

1. Fingertip Amputations 


Fingertip amputations are the most common type of amputation of the upper extremity. 

The location and size of the defect have to be considered. Depending on the location of 

the amputation, fingertip injuries can be classified into 4 zones. The zones have been 

designed to define the type of pulp damage and the existence of associated lesions of 

the nail bed and bone. The Zone 1 lesion is a distal amputation located far from the 

distal phalanx tubercle. Usually the lesion is less than 1 cm in area and does not affect 

the nail bed or bone. Zone 2 lesions involve the nail bed and usually partial phalangeal 

bone disruption and exposure. In Zone 3 the nail matrix is involved so that the nail 

growth will be followed by curved deformation. Zone 4 defines an amputation at the 

level of the distal phalanx, near the distal interphalangeal joint. Despite the intact distal 

attachment of the extensor and flexor tendons at the distal phalanx, the active motion of 

the distal remnant is limited.

Important information to be obtained from the patient includes age, the digit injured, 

mechanism and time of injury, occupation, location of the wound, and hand dominance. 

The digit injured influences management. Most hand surgeons want to maintain length 

of the thumb. The index finger is considered the next priority before other fingers. An 

intact pulp-to-pulp pinch mechanism is the goal. 


For Zone 1 injuries with pad loss of less than 1 cm, healing by secondary intention is the 

simplest and often best approach. Large dorsal wounds also heal well with this 

technique. It is the treatment of choice for pediatric fingertip amputations, especially 

when there is no bone exposure. Initial treatment includes wound cleansing, a 

nonadherent sterile dressing, appropriate tetanus prophylaxis, splinting, and a bulky 

dressing to protect the tip. Amputations that expose the distal phalanx are usually 

treated as contaminated open fractures with an initial intravenous dose of a 

cephalosporin followed by an oral course. Patients should have appropriate follow-up 

care in 1-3 days for wound care check. 

Fingertip amputations that have significant pad loss or bone loss (Zones 2-4) usually 

require the expertise of a hand surgeon. Surgical options include primary closure, full- or 

partial-thickness skin grafts, composite grafts, flaps, and replantation. If the amputated 

fingertip pad has been retained, is clean, and is in good condition, it may be reattached 

as a full-thickness skin graft. 

2. Subungual Hematoma 


Hematoma from blunt trauma (ie, a hammer blow) or crush injury that ruptures 

subungual blood vessels causes pain and dark red to black discoloration of the nail bed. 

An x-ray will rule out a fractured phalanx. 

Treatment 

Large subungual hematomas cause significant pain and should be evacuated via nail 

trephination (making a hole in the nail) with a high-temperature microcautery device or 

an 18-gauge needle or via complete removal of the nail. Use of heated paper clips may 

introduce carbon particles known as "lampblack" into the nail bed. Anesthesia is not 

usually required for trephination, and pain relief is immediate following decompression. 

Large subungual hematomas are often associated with significant nailbed lacerations. 

Many authors recommend removal of the nail and repair of nail bed lacerations for large 

subungual hematomas to promote optimal healing and normal nail growth. When the 

nail is removed, it should be cleaned and placed back into position, secured with 

sutures to function as a splint for the nail bed and to keep the proximal nail fold open. 

A fracture of the distal phalanx on radiographs may technically be called an open 

fracture, although these injuries usually heal without complication. Osteomyelitis is not 

often associated with ungual tuft fractures. The risk of infection with an open fracture of

the phalanx proper should be considered, and a broad-spectrum antibiotic and close 

follow-up are recommended. 

Disposition 

Patients with a subungual hematoma may be discharged from the emergency 

department after treatment (trephination, nail removal with or without nail bed repair). All 

patients with subungual hematoma should be informed about the possibility of nail loss 

or deformity. Antibiotics are recommended for hematomas associated with tuft fractures. 

3. Avulsion of Nail 


Avulsion of the nail results from a force elevating the tip of the nail and ripping it off its 

bed, or from a downward crushing force sufficient to tear the base of the nail out of the 

eponychial sulcus, ripping open the nail bed, and carrying the nail plate on a 

palmar-based pedicle flap. 

Treatment 

Nails avulsed at the base should be completely removed. If such a nail is left in place, a 

badly lacerated nail bed that requires repair may inadvertently be overlooked. The nail 

also creates a dead space that promotes scarring and infection. 

A. Removal of Nail 

Anesthetize by digital block. Remove the avulsed nail by inserting a clamp under the 

distal attached portion of the nail and advancing it proximally, removing the nail by 

spreading the clamp. The exposed nail bed should be covered with either the original 

nail (as described above) or with sterile petrolatum gauze and a portion of the gauze 

tucked into the nail sulcus. A lacerated nail bed should be meticulously closed with 5-0 

or 6-0 absorbable suture. 

B. Reattachment of Distal Torn Finger Flap 

If the distal portion of the finger has been torn off with the nail and has been left 

attached to the finger by a volar pedicle, the flap should be anatomically reduced and 

held with strips of paper tape (eg, Steri-Strips), or it should be sutured back in position 

with 6-0 absorbable suture. Antibiotics should be administered. 

C. Management of Fractures 

Open fractures of the distal phalanx are reduced and held by soft tissue suturing. If the 

fracture is displaced, internal fixation with a Kirschner wire may be necessary. 

Disposition 

The patient should follow up in 2-3 days for wound check and dressing change. 

Complicated problems should be referred to a hand surgeon and an immediate 

appointment made.

DISTAL EXTENSOR TENDON INJURIES 2 

1. Laceration of Extensor Tendons 


Dorsal finger and hand wounds frequently result in a partially or completely lacerated 

extensor tendon or extensor tendon hood mechanism. The extent of injury can be 

determined only by adequate exposure and direct examination. Accurate assessment of 

a tendon can be difficult because a 90%-lacerated tendon can still retain function. A 

partial tendon laceration can often be discovered by testing the tendon against 

resistance. Strength against resistance is diminished if a partial tendon laceration exists. 

Description using the 8 zones of extensor tendon injuries will help assess and guide 

treatment (Figure 29-10). 

2 Flexor and proximal extensor tendon injuries are discussed with flexor tendon injuries 

later in this chapter. 

Treatment 

Treatment of a partial tendon laceration that is less than 50% requires no repair and is 

treated with a protective splint. Extensor tendon repair can be performed in the 

emergency department after careful irrigation, inspection, and debridement or later by 

the consultant. 

If the tendon ends can be retrieved easily with minimal extension of the wound or by 

slight stretching of the skin, the tendon should be repaired in the emergency department 

by a simple figure-of-eight suture or a crisscross suture technique with 4-0 or 5-0 suture 

(in infants, 6-0 nylon) (Figure 29-11). A padded plaster forearm splint is then applied 

with the digit and hand positioned so that the repair is relaxed as much as possible. No 

individual joint should be hyperextended, nor should all joints be simultaneously 

extended. The MP joint should not be immobilized in full extension, because contraction 

of collateral ligaments may result in fixation of the joint in extension. One or more 

neighboring fingers should always be immobilized with the injured digit. 

Disposition 

If the tendon ends are not easily retrieved, notify a hand surgeon immediately and make 

arrangements for repair as soon as possible. 

In the interim, administer antibiotics for 2-3 days (see discussion of cellulitis, below). 

2. Mallet Finger 


• Suspect if bruising is present at DIP joint. 

• X-ray may be normal or show an avulsed chip at DIP joint. 

• Carefully test extension of DIP joint. 

• If left untreated, swan neck deformity will occur. 


Mallet finger is caused by laceration or avulsion of the extensor tendon at its insertion at 

the dorsum of the distal phalanx. A mallet finger commonly occurs after the distal finger 

is forcibly flexed such as from a sudden blow to the tip of the extended finger. Clinically, 

there may be ecchymosis at the DIP joint, but tenderness and swelling may be absent. 

An x-ray may be normal or demonstrate an avulsed chip fragment at the dorsum of the 

DIP joint. If the articular fracture involves more than 40% of the joint surface, referral to 

a hand specialist for open reduction is required. The extensor lag may not be present on 

the initial emergency department evaluation. Careful testing of extension at the DIP is 

important in identifying this problem. If left untreated, a flexion deformity at the DIP joint 

will develop followed by hyperextension at the PIP joint (swan neck deformity) (Figure 

29-12). 

Treatment 

A. Open Mallet Injuries 

Open injures are treated by tenorrhaphy and intramedullary fixation of the DIP joint by a 

hand surgeon. Give prophylactic antibiotics (see discussion of cellulitis, below). 

B. Closed Mallet Injuries 

Closed injuries may be treated by continuous dorsal external padded splint fixation of 

the DIP joint in full extension for 6-8 weeks. During splint changes the joint should be 

held up in extension. The digit should be kept dry to prevent maceration of the skin. 

Disposition 

The patient should follow up with a hand surgeon. 

3. Boutonniere Deformity 


• Suspect when trauma causes a painful, swollen PIP joint. 

• X-rays are usually normal. 

• Deformity is rarely clinically identifiable immediately after the event. 


Early diagnosis of a closed middle extensor tendon rupture or avulsion is difficult before 

the boutonniere (buttonhole) deformity has occurred. High suspicion is needed when the 

patient presents with trauma and a painful, swollen PIP joint. Although uncommon, volar

dislocations of the PIP joint can cause MET rupture. Unless a dislocation is present, 

radiographs are usually normal. 

In boutonniere deformity, the distal joint is hyperextended and the PIP joint of the finger 

(the MP joint of the thumb) is flexed (Figure 29-13). Extensor hood integrity is lost at the 

apex of the PIP joint of the finger (MP joint of the thumb) as a result of laceration or 

blunt trauma to the dorsum of the joint. The deformity is rarely manifest immediately 

after trauma and comes on insidiously as a result of gradual stretching of the injured 

hood. The underlying head of the bone protrudes through the hood, pushing aside the 

MET (extensor pollicis brevis of the thumb), which recedes, and the LETs, which slip 

volarly to become flexors of the joint and hyperextensors of the distal joint. 

Treatment 

A. Open Injuries 

Open injuries should be repaired (by a hand surgeon) as soon as possible with 

figure-of-eight nylon sutures and the joint splinted in full extension for 4 weeks with a 

palmar digital splint. 

B. Closed Injuries 

Closed injuries must be suspected if there is a history of a direct blow to the dorsum of 

the joint followed by swelling. Treatment consists of 4 weeks of PIP (thumb MP) 

splinting in extension to avoid boutonniere deformity, which rarely occurs if prompt 

treatment is provided. 

Secondary reconstruction of this deformity is very difficult and may never restore full 

motion of the IP joints. 

Disposition 

Open injuries should be irrigated and covered and the patient sent to a hand surgeon at 

once. Patients with suspected closed middle extensor tendon injuries should get early 

referral to a hand surgeon. The hand should be splinted with the PIP joint in extension, 

leaving the MP and DIP joints mobile. 

BONE & JOINT INJURIES 

Bone and joint injuries are discussed in more detail in Chapter 28, but a few general 

principles are emphasized here. 


If there is any question of bone or joint injury on x-ray, obtaining added views in other 

planes and identical views of the opposite extremity or a follow-up view in 7-10 days 

may resolve the issue. 

Treatment 

A. Splinting

The wrist joint is the principal joint governing movement and comfort of an immobilized 

fracture. Therefore, it should be splinted initially. In addition, to splint one finger well, an 

adjacent finger should be splinted with it. The thumb may be immobilized alone. The 

preferred position should be that of wrist extension, functional finger flexion, and 

opposition of the thumb. If there is throbbing pain at any time, it must be relieved 

promptly by loosening the bandages that secure the splint. 

B. Stable Injuries 

Stable dislocations or fractures can usually be treated in the emergency department by 

reduction and splinting, with appropriate anesthesia. Force should never be used. In lieu 

of force, open reduction is preferred. 

C. Open or Unstable Injuries 

Open or unstable injuries require a specialist's skill. The patient should be given a 

temporary splint and dressing and referred to a hand surgeon immediately. Give 

prophylactic antibiotics (see discussion of cellulitis, below). 

Disposition 

Patients with closed, stable injuries should follow up with an orthopedic surgeon or hand 

specialist in 7-10 days for assessment of comfort and integrity of the splint. Patients with 

open joint injuries, unstable injuries, or injuries that cannot be reduced easily must be 

referred early to a specialist experienced in hand surgery. 

Aronowitz E, Leddy J: Closed tendon injuries of the hand and wrist in athletes. Clin 

Sports Med 1998;17(3):449. [PMID: 9700414] 

Harrison BJ, Hilliard MW: Emergency department evaluation and treatment of hand 

injuries. Emerg Med Clin North Am 1999;17(4):793. [PMID: 10584103] 

Patel J et al: Hand lacerations—an audit of clinical examination. J Hand Surg [Br] 

1998;23(4):482. [PMID: 9726549] 

Perron AD et al: Orthopedic pitfalls in the emergency department: Closed tendon 

injuries of the hand. Am J Emerg Med 2001;19:76. [PMID: 11146026] 

Roser S, Gellman H: Comparison of nail bed repair versus nail trephination for 

subungual hematomas in children. J Hand Surg [Am] 1999;24(6):1166. [PMID: 

10584937] 

Wilhelmi B et al: Epinephrine in digital blocks: revisited. Ann Plast Surg 1999;43(5):572. 

[PMID: 10560879] 

INFECTIONS 

Infections of the hand are frequently encountered in emergency departments. Nearly all 

infections result from neglect following trauma and are fostered by venous congestion 

and tissue edema.

Careful handling of tissue, elimination of dead space, immobilization and elevation of 

the arm immediately after injury, and avoidance of constriction by snug clothing or 

jewelry are far more important in preventing infection than any type of wound 

preparation or antibiotic prophylaxis. The objective of treatment of all infections is to 

reverse congestion and restore normal circulation. If there is a possibility of serious 

infection, immobilize the hand in a splint. Applying zinc oxide ointment next to the skin in 

the inner (core) dressing promotes drainage by preventing drying, caking, and sealing 

off of the wound. 

All existing or potential infections should be monitored closely, for example, hourly or 

daily depending on the severity. Infections that may be treated in the emergency 

department include those of the nail folds, felons, simple abscesses, and cellulitis. 

Patients with other infections should be immediately referred. 

1. Paronychia & Eponychia 


• Swelling and collection of pus inside or around nail fold. 

• Consider X-ray to rule out foreign body or osteomyelitis. 

• Consider antibiotics if extensive cellulitis or lymphangitis is present. 


Inflammation leading to a collection of pus inside the nail fold is seen after trauma and 

often as a consequence of stress (Figure 29-14A). If neglected, it may extend around 

the entire nail margin and cause a floating nail. The usual cause is Staphylococcus 

aureus. Cultures are rarely necessary. Chronic paronychia is found in patients with 

occupational exposure to moisture or cleaning solutions (ie, housekeepers or 

dishwashers) and is most often caused by Candida albicans. 

An x-ray should be considered to rule out the presence of a foreign body or distal 

phalangeal osteomyelitis. 

Treatment 

Treatment consists of simple elevation of the nail fold with a No. 11 scalpel at the site of 

maximum tenderness or pus (Figure 29-14B). Generally, there is no pain if an abscess 

is already pointing and no blood is drawn with the scalpel. If the scalpel causes any 

pain, administer a digital block anesthetic. 

Antimicrobial agents are not indicated unless extensive cellulitis or lymphangitis is 

present. Chronic paronychia treatment may require nail removal, marsupialization of the 

eponychial fold, oral antibiotic, and topical antifungal ointment. 

Disposition

As with any hand infection, the patient should keep the hand elevated and follow up in 

24-48 hours. A common complication is osteomyelitis of the distal phalanx. Chronic 

paronychia requires referral to a hand surgeon for possible marsupialization. 

2. Herpetic Whitlow 


• Collection of grouped vesicles with erythematous base on the fingertip. 

• Use oral acyclovir in immunocompromised individuals. 

Herpetic whitlow is the most common viral infection of the hand, a self-limited herpes 

simplex viral infection of the distal finger. It classically presents as grouped vesicles with 

an erythematous base on the fingertip. Treatment is supportive; oral acyclovir is used in 

immunocompromised patients. 

3. Felon 


• Patient has a painful and swollen distal phalanx fat pad. 

• Staphylococcus aureus is the most common cause. 

• Most felons can be drained where the abscess points—usually mid pad with a central 

longitudinal incision. 


A felon is an abscess of the distal phalanx fat pad. S aureus is the most common 

pathogen. The patient usually presents with a painful and swollen distal pulp space. 


Classic treatment of felons emphasized the need for early and complete incision 

through the septa via fishmouth incisions to provide adequate drainage and to relieve 

pressure (Figure 29-15). But complications include damage to nerves and blood vessels 

as well as unstable finger pads, and painful neuromas or anesthetic fingertips may 

result. Most felons can be drained where they point—usually in the mid pad—by a 

central longitudinal incision that does not cross the distal flexion crease. Felons can also 

be drained by a single lateral incision. The incision should be made along the ulnar 

aspect of digits II-IV and the radial aspects of digits I and V, avoiding pincher surfaces. 

The incision is started 0.5 cm distal to the DIP joint crease and dorsal to the 

neurovascular bundle of the fingertip. Irrigate and loosely pack the wound, and then 

immobilize the finger. Treat empirically with antistaphylococcal oral antibiotics for 5 days 

and arrange follow-up in 1-3 days for wound care check.

4. Deep Fascial Space Infections 


• All deep space abscesses require referral to a hand surgeon. 

• Antibiotics should be started in the emergency department. 

The 4 potential deep fascial space infections of the hand are the subfascial web space, 

the dorsal subaponeurotic space (collar button abscess), a midpalmar space abscess, 

and the thenar space. Deep space abscesses are frequently seeded with S aureus, 

streptococci, and coliforms. All deep space infections require referral to a hand surgeon 

for operative exploration and drainage. Antibiotics should be initiated in the emergency 

department. 

5. Cellulitis (Including Human & Animal Bites) 


• A progressive cellulitis caused by Pasteurella multocida is easily seen in the first 24 

hours. 

• Cellulitis due to other pathogens usually takes 2-3 days to become clinically evident. 

• Another pathogen, Capnocytophaga canimorsus, associated with animal bites, can 

cause overwhelming sepsis in immunocompromised individuals. 

• Have a high suspicion for closed-fist bite wound when caring for patient with open 

wound over the MP joint following an altercation. Patients with these seemingly small 

wounds often present later with significant infections. 

Treatment 

A. Uncomplicated Cellulitis and Antibiotic Prophylaxis 

Wounds with an increased risk of infection (ie, human or animal bites, crush wounds, or 

contaminated wounds) should have antibiotic coverage for S aureus or Streptococcus 

pyogenes. Treatment recommendations include a first-generation cephalosporin such 

as cephalexin for oral use or cefazolin for intravenous use, or a penicillinase-resistant 

penicillin such as dicloxacillin for oral use or nafcillin or oxacillin for intravenous use. 

Trimethoprim-sulfamethoxazole (TMP-SMZ) or erythromycin may be effective in 

penicillin-allergic patients. Special consideration for polymicrobial coverage and possible 

admission are needed for diabetic patients and drug abusers. 

B. Animal Bites 

Infections caused by animal bites (ie, dog or cat) are often caused by P multocida, 

which causes a rapidly progressive cellulitis, easily identifiable in 24 hours. Infections 

from other pathogens are not usually evident for 2-3 days. Another common pathogen, 

C canimorsus (formerly known as DF-2), is a fastidious gram-negative rod that can

cause overwhelming sepsis in immunocompromised individuals. Treatment for animal 

bites includes amoxicillin-clavulanate, clindamycin plus a fluoroquinolone in 

penicillin-allergic adults, or clindamycin plus TMP-SMZ in children. Do not close these 

wounds. 

C. Human Bites 

A wound over the MCP joint (especially of the dominant hand) is likely to represent a 

closed-fist bite wound sustained during an altercation. These wounds have a high 

likelihood for infection. Patients often present with infected "fight-bite" wounds several 

days after suffering a seemingly minor injury during a fight. Perform a thorough 

examination of these wounds, looking for injuries to the extensor tendon or joint 

capsule. Any violation of these structures mandates orthopedic consultation. Wounds 

that do not involve the joint capsule or the extensor tendon should be thoroughly 

irrigated and any devitalized tissue debrided. 

Some authors have recommended mandatory admission at the time of initial evaluation 

even without any signs of infection or tendon or joint involvement, whereas others 

advocate outpatient therapy with oral antibiotics and close follow-up. Infections from 

human bites involve mixed anaerobes, streptococci, S aureus, and Eikenella corrodens 

and should be treated in the hospital. Antibiotic treatment options include 

amoxicillin-sulbactam, cefoxitin, and ticarcillin-clavulanate. Penicillin-allergic patients 

may receive clindamycin plus TMP-SMZ, or clindamycin plus fluoroquinolone. 

Prophylactic antibiotics for human bite wounds include amoxicillin-clavulanate or a 

second-generation cephalosporin. Given the propensity of these wounds to become 

infected, fight bites should never be sutured. 

Disposition 

Hospitalization under the care of a hand specialist is required for severe cases 

(extensive cellulitis, involvement of tendons or joints, infections of the palmar space, 

systemic symptoms, or unusual pathogens) or if the patient is unreliable or unable to 

take oral antibiotics. Patients with cellulitis managed as outpatients should be seen 

every day and hospitalized if the process continues. 

6. Suppurative Tenosynovitis 


• Swelling, erythema, and tenderness along the tendon sheath. 

• Exquisite pain on passive movement of tendon. 

• Consider gonococcal infection in young adults without an open wound. 


Suppurative tenosynovitis (nongonococcal) is characterized by swelling, erythema, and 

tenderness along the tendon sheath and, most important, exquisite pain on passive 

movement of the flexor tendon in the digit or the extensor tendon crossing the wrist. In

flexor tenosynovitis, passive movement is definitely achieved by holding the fingernail 

alone and prying it dorsally to extend the distal joint. The infection may have occurred 

because of an open wound contiguous to the involved tendon. 


In selected reliable patients with a confirmed diagnosis, outpatient therapy with close 

follow-up may be possible. Whenever there is inflammation with significant swelling, 

immediate hospitalization under the care of a hand specialist is required for open 

surgical drainage and parenteral antibiotic therapy. After obtaining appropriate 

specimens for culture, begin a cephalosporin (eg, cefazolin, 100 mg/kg/d in 3 divided 

doses) intravenously without waiting for the results of cultures. Immobilize the wrist and 

hand in a splint, and support the arm in a sling until operation can be performed. 

7. Disseminated (Hematogenous) Gonococcal Infection 

The diagnosis and treatment of gonococcal infection are discussed in Chapter 40. In 

young adults, tenosynovitis is often caused by gonococcal infection. The tenosynovitis is 

not associated with an open wound near the involved tendon sheath but is frequently 

associated with pustular skin lesions typical of gonococcal infection. Hospitalization for 

intravenous antibiotic therapy is usually indicated. In selected reliable patients whose 

diagnosis is confirmed, outpatient therapy with close follow-up may be possible. See 

Chapter 40 for recommended treatment. 

Perron AD, Miller MD, Brady WJ: Orthopedic pitfalls in the ED: fight bite. Am J Emerg 

Med 2002;20(2):114. [PMID: 11880877] 

Talan DA et al: Bacteriologic analysis of infected dog and cat bites. New Engl J Med 

1999;340(2):85. [PMID: 9887159] 

MINOR CONSTRICTIVE PROBLEMS 


The 3 common constrictive problems described here are often seen in the emergency 

department. Only the first is usually a true emergency. 

A. Carpal Tunnel Syndrome (Compression of the Median Nerve) 

Carpal tunnel syndrome is characterized by aching and numbness over the distribution 

of the median nerve (see Figure 29-7), with sparing of the small finger. These symptoms 

often awaken the patient from sleep and may be elicited by full flexion of the wrist for 30 

seconds (Phalen maneuver). Tapping over the median nerve at the wrist crease may 

feel like an electric shock (Tinel sign). Patients with this nerve compression may present 

with rapid onset of acute edema and progressive loss of feeling after trauma, 

inflammation, or allergy, and it requires urgent consultation with a hand specialist. 

B. Stenosing Flexor Tenosynovitis (Trigger Thumb or Trigger Finger) 

Stenosing flexor tenosynovitis is characterized by local tenderness over the proximal 

tendon pulley at the MP joint, with pain referred to the PIP joint and a snapping when

the finger or thumb goes through an active range of motion. Usually a history of 

repetitive strain is involved. 

C. De Quervain Tenosynovitis 

De Quervain tenosynovitis is characterized by pain and tenderness when tendons in the 

first dorsal compartment on the radial side of the wrist are actively or passively 

stretched; specifically, when the fist is clenched over the thumb while the wrist is put into 

marked ulnar deviation (Finkelstein test). 

Treatment 

A. Carpal Tunnel Syndrome 

Initial treatment involves wrist splinting and the use of nonsteroidal anti-inflammatory 

drugs. Activity modification and therapeutic exercises may also improve symptoms. The 

next step in treatment is injection of the carpal canal using 1 mL of steroid and 2-3 mL of 

lidocaine. Never inject into the substance of median or ulnar nerves. 

B. Flexor Tenosynovitis 

Administration of nonsteroidal anti-inflammatory agents may be started in lieu of 

injection therapy. Steroids should not be injected if an infectious process is suspected. 

About 0.5 mL each of steroid and lidocaine should be injected into the synovial bursa 

through the tendon flexor pulley at the base of the digit. The finger should be splinted in 

extension. 

C. De Quervain Tenosynovitis 

Nonsurgical treatment involves rest, splinting with a thumb spica splint, 

anti-inflammatory medications, stretching exercises, and corticosteroid injections. If 

injecting, use about 0.5 mL each of steroid and lidocaine at the radial styloid process but 

avoid the radial nerve. 

Disposition 

Referral to a hand surgeon is advised because multiple injections or surgical release of 

the tight ligament or sheath may be required. 

THERMAL INJURIES (See also Chapter 43.) 

1. First-Degree Burns 

Clinical Findings & Treatment 

Simple burns (redness without blistering) are treated with cold tap water rinse and 

analgesia. Comfort may be augmented by a soft nonirritative wrap to protect and 

immobilize the hand. Elevation and avoidance of constriction by snug garments are also 

advised. 

Disposition 

The patient should return or telephone for follow-up after 1-2 days.

2. Second-Degree Burns 


Blisters signify partial-thickness (second-degree) burns, which always retain cutaneous 

sensation even though they are variable in depth. Although this treatment is 

controversial, large blisters should be aspirated or unroofed and debrided. Small blisters 

may be left intact. Silver sulfadiazine (Silvadene) cream may be applied topically. For 

sulfa-allergic patients, bacitracin may be used instead. Second-degree burns may be 

dressed with a bulky dressing and the hand splinted in the position of function. Tetanus 

prophylaxis must be current (Chapter 30). In the case of burns caused by hot tar, the tar 

may be removed as described in Chapter 43. 

Disposition 

Patients with extensive burns or marked edema should be immediately referred to a 

hand specialist for evaluation and possible hospitalization. Patients with lesser 

involvement should be seen every 1-3 days for a dressing change, especially once 

blister debridement is started. 

3. Third-Degree Burns 


Full-thickness (third-degree) burns require bulky, loose sterile dressings with an 

anti-infective agent such as silver sulfadiazine. Appropriate elevation and splinting are 

also advised. Tetanus prophylaxis must be current (Chapter 30). 

Disposition 

If the burn is extensive (eg, > 1-2 cm 2 [3/8-3/4 in 2 ]) or is over the dorsum of a joint, refer 

the patient immediately to a hand specialist for decisions about the need for 

debridement and grafting. 

4. Electrical Burns (See also Chapter 44.) 

Burns from electricity are of 2 kinds: crossed circuit, producing arc heat; and conduction 

of high-voltage current within the tissues. Arc heat is often more frightening than 

extensively injurious to tissues. There is generally blackening of the skin owing to 

deposit of carbon. The burn may be anywhere from first-degree to third-degree in 

severity but is usually localized. The treatment of arc heat burns is the same as that of 

other thermal burns. 

High-voltage conduction burns involve a point of entry and another point of exit. The 

deep tissues are often coagulated out of proportion to surface skin changes. Blood 

vessels and nerves are the pathways of conduction and therefore most vulnerable. 

Immediate irreversible ischemia and paralysis are common. Such cases require 

hospitalization under the care of a hand specialist for urgent fasciotomy where

prophylactically indicated and for observation for systemic effects of the electrical shock. 

Appropriate debridement (even amputation), grafting, and reconstruction will follow. 

Extremity destruction is sometimes overwhelming. 

If the electrical conduction pathway within the body is not limited to the hand but also 

involves other areas, consideration should be given to possible myocardial injury. An 

electrocardiogram and cardiac isoenzymes (CK-MB and troponin) measurement should 

be obtained. Cardiac monitoring is necessary if myocardial injury is suspected. 

5. Frostbite (See also Chapter 44.) 

Exposure to cold may result in superficial or deep frostbite depending on the windchill 

factor and duration of exposure. Measures to prevent this vasoconstrictive disorder and 

the irreversible microvascular thrombotic events that lead to gangrene include the 

following: (1) avoiding exposure to wind, cold metal, snow, and ice by wearing protective 

gloves; (2) preserving the total body heat by wearing suitable clothing and head gear 

and avoiding sweat-producing physical effort or alcohol consumption; (3) ensuring 

adequate caloric intake, high in fat and carbohydrate; and (4) refraining from smoking. 

Superficial frostbite is limited to the skin. It exists when the discomfort of fingers 

exposed to cold is replaced by numbness. Reversal by warming is urgently required and 

is usually heralded by a warm tingling sensation. 

Deep frostbite is signaled by pain and swelling of the entire hand, followed by extensive 

blister formation and dysesthesia. Deep frostbite requires hospitalization under the care 

of a hand specialist. Cryofibrinogenemia aggravates the problem and is worsened by 

the use of heparin, which facilitates precipitation of cryofibrinogen. Treatment consists of 

rest and warming the patient and the hands. Immersion in water at 37-40 °C (98.6-104 

°F) for a short time (eg, 20 minutes) may be beneficial. Blisters must be debrided and 

dressed with sterile dressings. Sympathetic blockade should be considered. 

Luce E: The acute and subacute management of the burned hand. Clin Plast Surg 

2000;27(1):49. [PMID: 10665355] 

Smith MA, Munster AM, Spence RJ: Burns of the hand and upper limb—a review. Burns 

1998;24(6):493. [PMID: 9776087] 

FOREIGN BODIES 

Fishhooks, splinters, and other objects may have barbs or barblike projections that 

prevent withdrawal from the wound in the normal retrograde way. Removal is possible 

by pushing the foreign body along the direction of entry and removing it via a 

counterincision where it presents under the tented skin. Nerve block or other anesthesia 

and tourniquet ischemia are necessary before extraction is attempted. Prophylactic 

antibiotics and tetanus immunization are often necessary. 

Foreign bodies embedded in the hand may be difficult to locate and remove. The 

diagnosis is based on the history and examination, and x-rays are almost always useful 

in the case of glass or metal. Modalities such as computed tomography, magnetic

esonance imaging, and ultrasound can be helpful in finding nonradiopaque foreign 

bodies. If immediate accessibility and easy removal seem possible, an attempt can be 

made to remove the foreign body using regional anesthesia, a tourniquet, and sterile 

technique with loupe magnification. Typically, however, the discoloration of tissues by 

blood precludes the immediate search for a foreign body, which will be found much 

more easily after 3-4 weeks when phagocytosis has cleared the blood. Before starting 

the procedure, tell the patient that if search and removal prove at all difficult (eg, longer 

than 10-15 minutes), the procedure will be abandoned and referral made to a hand 

specialist. 

Consider leaving an entry wound open by inserting a loose drain, applying an 

appropriate dressing, and elevating and immobilizing the part. Give prophylactic local or 

systemic antibiotics and tetanus prophylaxis (Chapter 30). The patient can usually be 

assured that retrieval of small deep foreign bodies is not urgent, because they do not 

travel in the body, and that it is often contraindicated by the difficulty and risk of removal. 

Blankstein A et al: Localization, detection and guided removal of soft tissue foreign 

bodies in the hands using sonography. Arch Orthop Trauma Surg 2000;120(9):514. 

[PMID: 11011671] 

COMPLEX HAND INJURIES 

Classification 

Complex injuries include the following: amputations, serious tendon injuries, nerve 

injuries, high-pressure injection injuries, closed compartment syndromes, mangling 

injuries, and gunshot wounds. 

Evaluation & Initial Management 

In complex injuries, emphasis should be placed on early, rapid diagnosis and institution 

of supportive therapy. Many complex injuries require referral to a hand specialist 

immediately or early. In all cases, use conservative measures as outlined below. 

A. Avoid Manipulation 

Once the decision has been made to transfer or hospitalize the patient, the extremity 

should not be handled, probed, manipulated, or otherwise disturbed unless absolutely 

necessary. Foreign material that can be easily lifted out should be removed. Protect with 

a sterile dressing and, if necessary, a loosely applied splint pending definitive 

management. 

B. Prepare for Possible Urgent Surgery 

If there is a reasonable likelihood of surgery within 8-10 hours, give nothing by mouth. 

An intravenous infusion should be started in the uninjured limb and laboratory work 

ordered. 

C. Give Antibiotics 

In the case of open or penetrating wounds, antibiotics should be given parenterally 

(preferably intravenously in the uninjured extremity) as soon as possible; the earlier they

are started, the more effective they are. Give cefazolin, 1-2 g intramuscularly or 

intravenously every 6-8 hours (adult dose) or 25-100 mg/kg/d intramuscularly or 

intravenously, divided every 4-8 hours (for children aged > 1 month). 

1. Amputations 


Amputations account for about 1% of hand injuries. The diagnosis of amputation is 

obvious on inspection of the part. Amputations are generally classified as partial 

(incompletely severed part) or complete. 

Generally, tidy amputations at the level of the middle phalanx or the wrist or distal 

forearm have the best chance of functionally successful replantation. In the case of 

single-digit amputation, surgeons are much more inclined to favor replantation of a 

thumb than of a single finger. Discussions with the patient or relatives regarding the 

feasibility of replantation should be left to the hand surgeon. 


A. Replantation Possible 

Place the amputated member in gauze moistened with saline and then place it in a 

sealed plastic bag or container that is maintained at 4 °C (39.2 °F) (eg, on wet ice). Do 

not freeze the amputated part, because this destroys its viability. 

After starting appropriate supportive measures, if the treating facility is not capable of 

providing the microsurgical specialized care required for replantation, arrange promptly 

for referral to a capable facility. The treating physician must contact a microsurgical 

specialist at the hospital to which he or she would like to refer the patient in order to 

obtain the specialist's permission for transfer. Failure to do so could be considered a 

violation of the law (COBRA-EMTLA; see Chapter 5) and might subject the referring 

physician and hospital to significant financial penalties. 

B. Replantation Impossible 

If the amputated member either is not recovered or is clearly not salvageable, 

appropriate in-house or emergency department surgery should be undertaken to close 

the stump. Except for the simple fingertip pad amputation (discussed above), these 

injuries should almost always be referred to a hand specialist. 

2. Flexor & Proximal Extensor Tendon Injuries 


• First suspect that tendon injury may exist; impairment may not become evident until 

hours, days, or weeks later. 

• Check strength of digit against resistance. 

• Direct visualization and examination of open wound in sterile, bloodless field is

indicated. 


Almost all flexor tendon injuries, and those extensor injuries in which the proximal 

tendon has retracted out of reach, are considered complex injuries. Management of 

easily accessible extensor tendon injuries is discussed earlier in this chapter. 


A crucial step in the emergency management of any flexor or proximal extensor tendon 

injury is to suspect that it may exist and make the proper diagnosis. Impairment of a 

partially divided tendon (sometimes subtotally or even totally divided) may be 

functionally masked at the outset, only to become evident hours, days, or weeks later. 

In open injuries, tendon lacerations can often be diagnosed by the abnormal stance of 

the involved part of the hand and almost always by careful functional examination. If the 

diagnosis is not obvious, but the location of the wound raises the possibility of tendon 

injury, direct examination of the wound is indicated. Visualization of flexors can be 

difficult anywhere, whereas visualization of extensors is difficult mainly when they lie 

proximal to the metacarpal necks. 

Occasionally the emergency physician will see a closed profundus tendon rupture. Such 

an injury almost always follows sudden violent stretch of the flexor, after which the 

patient is unable to flex the distal phalanx. 

Treatment 

Obtain immediate consultation with a hand specialist. Dress the wound after irrigation, 

and splint the wrist and hand. Remove jewelry and snug garments, and elevate the 

extremity until definitive treatment can be given. Flexor tendon repair may be delayed as 

long as 10 days without compromising the eventual outcome. If tendon repair is to be 

delayed, the wound should be sutured and appropriate antibiotics administered (eg, 

cefazolin, 1-2 g intravenously, followed by cephalexin, 500 mg orally 4 times daily for 

3-5 days). 

Disposition 

Visualization of a lacerated tendon sheath is reason for referral unless the entire course 

of the tendon gliding beneath the laceration is observed to be intact. If in doubt, refer 

immediately, because neglected partial tendon lacerations can go on to rupture. 

3. Nerve Injuries 


Early diagnosis is crucial. The cause and nature of injury, the symptoms, or the location 

and depth of a laceration may suggest possible nerve injury. If careful motor, sweat, and 

sensory examination is performed and sometimes repeated more than once for the sake

of consistency in appropriate cases (Figures 29-16 and 29-17), few significant nerve 

injuries will be missed. 

Treatment 

Appropriate dressing and splinting should be applied when indicated and the patient 

warned about injury to anesthetized skin until definitive treatment can be given. 

Disposition 

Refer the patient to a hand surgeon, and determine when the patient is to be transferred 

for definitive care. 

4. High-Pressure Injection Injuries 


• Initial appearance of hand may show only pinpoint portal of entry and look deceptively 

normal. 

• Obtain an X-ray. 

• Ask about the type, amount, and velocity of the injected material. 


High-pressure jets of a variety of hot and cold fluids (eg, grease, water, plastics, organic 

solvents) and gases are widely used in industry. Accidental penetration of the skin 

through a pinpoint portal of entry may result in devastating damage, even though the 

initial (postinjection) appearance of the hand or other body part is usually deceptively 

normal. This is because the foreign material spreads instantly along tissue planes and is 

widely distributed in the hand or other part. Spread of material up a flexor tendon sheath 

after penetration of a digital pad is quite common. An x-ray should be obtained, because 

some injected materials are radiopaque (eg, lead-based paint). When a chemical, 

inflammatory, or thermal response becomes manifest 4-12 hours after injury, extensive 

ischemia and tissue necrosis may be seen. Important historical factors are the type, 

amount, and velocity of the injected material and the anatomic location. The type of 

material injected is the most important clue to the severity of the injury. 


Give analgesics for pain if necessary, and splint the extremity in a sling for comfort. 

Digital blocks are contraindicated due to the possibility of increased tissue pressure and 

vascular compromise. Obtain x-rays. 

Give nothing by mouth, and consult a hand surgeon immediately regarding referral. 

Prompt tetanus prophylaxis, systemic antibiotics, and decompressive surgery (eg, 

fasciotomy) must be arranged in most cases. Even so, the prognosis for maintaining 

circulation and salvaging function is often dismal.

5. Closed Compartment Syndromes 


• History of progressive pain and rock-hard compartment. 

• Pain on passive movement. 

• Hypoesthesia or paralysis of the digits. 


A compartment syndrome (eg, congestion progressing to various degrees of ischemia) 

can occur in any space of the digit, hand, forearm, or arm. It may involve a single space 

(eg, extensor and flexor compartments of the forearm and intrinsic muscle 

compartments of the hand). Obstructed venous flow leads to microvascular stagnation 

and death of muscle, fat, and nerves. Compartment syndrome may result from external 

compression (eg, a tight cast, prolonged pressure against an extremity of a comatose 

patient) or from internal swelling (eg, from severe bleeding, crush injury, burn, fracture, 

allergy, or infectious inflammatory reaction). The fate of a neglected case in which 

surgical decompression has not been performed is late fibrosis and severe functional 

impairment. 


The typical patient presents with a history of progressive severe pain (eg, throbbing) 

and a rock-hard compartment. When the whole forearm and hand are involved, there is 

hypoesthesia, reluctance or inability to move the digits, and pain on passive extension 

of flexed digits. Pain perception may be lost as pressure on the nerves destroys their 

conducting ability. 

Treatment 

Treatment is supportive until definitive surgical decompression can be performed. 

Support the limb in a sling, and give analgesics for pain. 

Disposition 

Urgent hospitalization for surgical decompression under the care of a hand specialist is 

indicated. 

6. Mangling Injuries 


Mangling injuries include gunshot and blast wounds, severe open crush wounds, severe 

bites by large animals, and a large variety of ripping or tearing injuries (ie, lawnmower- 

or snowblower-associated injuries). The common denominator is multitissue

involvement, distortion, and significant wound contamination. 

Treatment 

Rapid initiation of supportive measures; loose, bulky, sterile dressing and splinting; 

immediate administration of antibiotics (eg, cefazolin, 50-100 mg/kg/d intravenously or 

intramuscularly in 2-3 divided doses); and definitive surgical treatment are important to a 

successful outcome. 

Disposition 

All such injuries require immediate hospitalization and referral to a hand specialist for 

operative debridement and repair. 

Arellano A, Wegener E, Freeland A: Mutilating injuries to the hand: early amputation or 

repair and reconstruction. Orthopedics 1999;22(7):683. [PMID: 10418865] 

Chin G et al: Snowblower injuries to the hand. Ann Plast Surg 41(4):390, 1998. [PMID: 

9788219] 

Lewis HG et al: A 10-year review of high-pressure injection injuries to the hand. J Hand 

Surg [Br] 1998;23(4):479. [PMID: 9726548] 

Martin C, Gonzalez del Pino J: Controversies in the treatment of fingertip amputations. 

Clin Orthop 1998;353:63. [PMID: 9728160] 

Vasilevski D et al: High-pressure injection injuries to the hand. Am J Emerg Med 

2000;18:820. [PMID: 11103737] 

SPECIAL EMERGENCY DEPARTMENT PROBLEMS 

1. Removal of Rings 

All rings, bracelets, wristwatches, and snug shirt sleeves and coat sleeves should be 

prophylactically removed whenever injury, surgery, infection, or other cause of acute 

swelling of any part of the hand exists. Failure to do so may lead to serious congestion 

and unnecessary complications. 

A ring on a swollen finger can be removed in 3 ways: 

1. Lubricate the skin with soap, and carefully slip off the ring. 

2. Wrap the digit snugly with a string from the distal tip to just below the ring, and in that 

way "milk" edema out of the digit so that the ring can be removed over the string. 

3. Cut the ring with a commercial ring cutter, spread it with 2 pairs of pliers, and remove 

it. This is the preferred method when there is significant digital injury or swelling distal to 

the ring.

2. Snakebite 

See Chapter 44 for treatment. 





EMERGENCY EVALUATION & TREATMENT

Figure 29-1. Digital block. (1) Use 1/2-inch (1.5-cm) needles of 25, 27, or 30 gauge with 

small volume of 1% lidocaine. (2) Use about 0.5-1.0 mL around the digital nerve. (3) 

The injection should never render the tissues tense nor be circumferential. 





FIGURES 

Figure 29-1

Figure 29-2. A: Median and ulnar nerve block. B: Radial and ulnar sensory nerve block. 





FIGURES 

Figure 29-2

Figure 29-3. Palmar hand with skin removed reveals flexor tendons with their sheaths 

and the median and ulnar nerves with their terminal sensory branches. (Modified and 

reproduced, with permission, from Way LW [editor]: Current Surgical Diagnosis & 

Treatment, 9th ed. Appleton & Lange, 1991.) 





FIGURES 

Figure 29-3

Figure 29-4. Cutaway view of the dorsal hand demonstrates that the extensor tendons 

are ensheathed only at wrist level. (Modified and reproduced, with permission, from 

Way LW [editor]: Current Surgical Diagnosis & Treatment, 9th ed. Appleton & Lange, 

1991.) 





FIGURES 

Figure 29-4

Figure 29-5. Terminology of bones and joints of the hand. 





FIGURES 

Figure 29-5

Figure 29-6. Palmar (A) and dorsal (B) areas of autogenous radial nerve sensibility. 

Loss of radial sensibility is not critical. A simple test for main trunk radial paresis is 

shown in C. 





FIGURES 

Figure 29-6

Figure 29-8. A and B: The shaded area is innervated by the ulnar nerve. C: Terminal 

phalangeal flexion of ring and small fingers is by profundi innervated by the ulnar nerve. 





FIGURES 

Figure 29-8

Figure 29-7. A and B: Autogenous median nerve sensibility is indicated by the shaded 

areas. The profundi of the index and long fingers (C) are innervated by the median 

nerve, as is the flexor pollicis longus (D). 





FIGURES 

Figure 29-7

Figure 29-9. Position of function of the hand. Note graded flexion of fingers and slight 

dorsiflexion of wrist. 





FIGURES 

Figure 29-9

Figure 29-10. Zones of extensor tendon injury. 





FIGURES 

Figure 29-10

Figure 29-11. Methods of tenorrhaphy. A: For large-caliber tendons. B: These suture 

techniques are best for thin tendons with limited separation of stumps (eg, digital 

extensors). (Reproduced, with permission, from Schrok TR [editor]: Handbook of 

Surgery, 7th ed. Jones Medical Publications, 1982.) 





FIGURES 

Figure 29-11

Figure 29-12. Mallet finger with swan-neck deformity. Rupture, laceration, or avulsion of 

the insertion of the extensor mechanism results in mallet finger. (Modified and 

reproduced, with permission, from Way LW [editor]: Current Surgical Diagnosis & 






FIGURES 

Figure 29-12

Figure 29-13. Boutonniere deformity. Avulsion or laceration of the central extensor 

mechanism results in a flexion deformity at the PIP joint and hyperextension of the DIP 

joint—the boutonniere, or buttonhole, deformity. (Modified and reproduced, with 







FIGURES 

Figure 29-13

Figure 29-14. Incision and drainage of paronychia. (Modified and reproduced, with 







FIGURES 

Figure 29-14

Figure 29-15. Incision and drainage of felon. A: Central longitudinal incision—the 

recommended approach. B: Classic lateral or fishmouth incision, which has greater risk 

of complication. 





FIGURES 

Figure 29-15

Figure 29-16. Assessing nerve injury. A: Wrist drop in radial injury. B: Forceful 

extension of thumb tip is lost in radial nerve injury. C: "Ape hand" deformity in median 

nerve injury. D: Forceful flexion of tip of index finger is lost in high median nerve injury. 

E and F: Thumb web atrophy and clawing of ring and small fingers, and loss of 

abduction and adduction in ulnar nerve injury. (Reproduced, with permission, from 

Schrok TR [editor]: Handbook of Surgery, 7th ed. Jones Medical Publications, 1982.) 





FIGURES 

Figure 29-16

Figure 29-17. Sensory distribution of the hand. 





FIGURES 

Figure 29-17


EMERGENCY MANAGEMENT OF LIFE-THREATENING PROBLEMS 

1 This chapter is a revision of the chapter by Robert L. Walton, MD, W. Earle Matory, Jr., 

MD, FACS, & Steven H. Turkeltaub, MD. 

All patients with open wounds should be examined thoroughly for evidence of serious or 

life-threatening injuries that may not be obvious on initial presentation. Treat 

life-threatening conditions immediately. If necessary, institute cardiopulmonary 

resuscitation (CPR) at once (Chapter 7). Ensure adequate ventilatory status, and treat 

shock (Chapter 9) and hemorrhage prior to wound assessment. Consider the possibility 

of internal bleeding. 

When facial and scalp injuries are present, look closely for evidence of intracranial or 

cervical spine injury. If cervical spine injury is suspected, immobilize the neck before 

performing radiologic evaluation. Serial neurologic examinations are crucial to the 

evaluation of any head injury. 

HEMOSTASIS 

Prior to wound closure, establish absolute hemostasis to prevent hematoma formation 

and further blood volume depletion. Hemostasis is accomplished by direct and indirect 

methods. The use of indirect methods first is preferred in order to carefully assess the 

wound, avoid possible injury to important structures, and allow time for replacement of 

significant blood loss. 

Indirect Hemostasis 

Indirect methods of achieving hemostasis in the acute wound include elevation, 

pressure, application of vasoconstrictive agents, and chemical promoters of clotting. 

These methods are usually effective in the control of diffuse vascular oozing and lymph 

extravasation. 

A. Elevation 

Elevation of the injured part above the level of the heart is least damaging to the tissues 

and markedly diminishes capillary oozing. Caution is required in elderly patients with 

arteriosclerotic vascular disease, because elevation of the lower extremity may induce 

tissue hypoxia. 

B. Pressure 

Pressure can be used in various ways to effect hemostasis. Direct pressure over a 

vigorously bleeding wound is perhaps the most common method for rapid control of 

blood loss. In extremity wounds, a proximally placed blood pressure cuff is frequently 

used to control bleeding of distal wounds. In either case, take care to avoid the potential 

sequelae arising from excessive pressure.

Simple cutaneous lacerations are usually manifested by a diffuse capillary ooze that can 

be an annoying interference with inspection and repair. A simple pressure dressing 

applied to the wound for 20 minutes will usually control oozing. Ideally, pressure should 

not exceed capillary pressure (30 mm Hg) and should not impede vascular flow to distal 

parts. For proximal extremity wounds, apply pressure in graded fashion from the distal 

aspect of the extremity to the wound to avoid the tourniquet effect of the dressing. The 

graded pressure is accomplished with bulky dressings and elastic bandages. Assess 

capillary flow and sensibility of distal parts frequently to avoid ischemic injury. 

Reserve the use of tourniquets for isolated digital injuries or for complex injuries 

associated with excessive blood loss or requiring specialized examination. The 

tourniquet is placed proximal to the wound (usually the upper arm) and is inflated to 

20-30 mm Hg above systolic pressure. Most patients can tolerate the ischemia resulting 

from this maneuver for 15-20 minutes. However, the ischemia produces a reactive 

vasodilatation upon release of the tourniquet and may result in resumption of bloody 

oozing or hematoma formation. 

C. Vasoconstriction 

Epinephrine-containing solutions are frequently used in acute wounds to control 

capillary oozing. Concentrations of 1:400,000-1:100,000 units are used for these 

purposes. After infiltration, a full 7 minutes is required for maximal vasoconstrictive 

effect. Caution: Epinephrine decreases local wound defense mechanisms and should 

not be used in contaminated wounds because of the increased risk of infection. 

Although it will not affect the viability of acute random cutaneous flaps, epinephrine can 

induce vasospasm that may lead to necrosis of tissues supplied by an end-arterial 

circulation. For this reason, epinephrine is contraindicated in the management of 

wounds of the penis, of any digit, of the tip of the nose, or in any tissue with circulation 

compromised by the trauma. 

D. Chemical Hemostatic Agents 

Avoid using hemostatic agents, such as Avitene, Gelfoam, or Surgicel, in the 

emergency department setting; these agents have been shown to potentiate infections 

in contaminated wounds. 

Topical bovine thrombin can cause an allergic or anaphylactic reaction, intravascular 

coagulation, or death. 

Direct Hemostasis 

Direct methods of hemostasis include ligation and electrocauterization of the cut vessel 

ends. Use direct hemostasis for bleeding that cannot be controlled by indirect methods. 

An exception to this rule is injury to major vascular tributaries (eg, ulnar, femoral, 

brachial artery). Further injury to the cut vessel end resulting from attempts at direct 

hemostasis may preclude successful repair. In these situations, it is wise to apply firm 

pressure to the wound and consult a vascular surgeon. 

A. Ligation 

Simple tying or suture ligation is indicated for most vessels more than 2 mm (1/16 in) in

external diameter. To avoid excessive tissue trauma, one must precisely identify and 

clamp the vessel end prior to ligation. Cut arteries usually require only simple tying. 

Veins, however, do not hold ligatures well, and suture ligation is preferable. Suture 

ligation may be performed by passing the suture needle through a portion of the vessel 

wall and then circumferentially tying the vessel. This method prevents slippage of the 

ligature. Caution: Do not ligate arteries and veins en masse, because this may 

predispose to arteriovenous fistula formation. Absorbable sutures are preferred for tying 

and suture ligation in the acute wound. Synthetic absorbable sutures (polyglycolic acid 

[Dexon] and polyglactin [Vicryl]) are advantageous because of their low reactivity and 

high friction coefficients. Chromic catgut is also satisfactory. 

B. Electrocautery 

Damped electric current is effective in coagulating small vessel ends. Monopolar 

cautery causes approximately 3 times as much tissue necrosis as bipolar coagulation. 

Pinpoint coagulation is preferred, with delivery of the least amount of current needed for 

vessel thrombosis. Caution: Some surgeons use undamped electric current for cutting 

tissues during debridement of the acute wound. Although quite effective in diminishing 

blood loss, cutting current inflicts significant thermal injury to the surrounding tissues 

and increases their susceptibility to infection. This technique is not recommended for 

wound debridement or hemostasis. 

C. Chemical Cautery 

Caution: Silver nitrate and other caustics achieve hemostasis through tissue 

coagulation but are not recommended for wound hemostasis because of the amount of 

tissue necrosis they produce. 

WOUND ASSESSMENT 

HISTORY 

A detailed, thorough history is essential for assessing the extent of injury and for 

organizing appropriate wound management. Three basic questions are used to 

reconstruct the history of the injury. 

A. When Did the Injury Occur? 

The time of injury is important for determining the interval between injury and treatment. 

Most civilian injuries contain fewer than 10 5 bacteria per gram of tissue in the first 6 

hours and are therefore relatively safe to close. After the first 6 hours, bacteria may 

proliferate and increase the risk of infection if the wound is surgically closed. Exceptions 

to the 6-hour limit vary depending on the degree of wound contamination, the 

mechanism of injury, and the location of the wound. As a rule, local tissue resistance is 

directly proportionate to blood supply. Facial lacerations may often be closed safely 

within 24 hours of injury, owing to the abundant blood supply in that area. 

B. Where Did the Injury Occur? 

What were the possible contaminants associated with the injury? Contact with feces, 

pus, saliva, or soil greatly increases the risk of infection and precludes primary closure.

C. How Did the Injury Occur? 

The mechanism of injury and the type of instrument inflicting the wound influence 

subsequent management. Knowing the type of instrument that inflicted the wound will 

aid in assessing the extent of injury as well as the need for further diagnostic studies. 

The degree of wound contamination depends in part of the state of cleanliness of the 

instrument inflicting the injury. 

Types of Injuries 

A. Lacerations 

Lacerations cause minimal tissue injury and are relatively resistant to infection. 

B. Puncture Wounds 

Puncture wounds may become infected, especially if they are contaminated or if a 

foreign body is present. 

C. Stretch Injuries 

Stretch injuries can produce damage to blood vessels, nerves, ligaments, or tendons 

that is not visible superficially. 

D. Compression or Crush Injuries 

Compression or crush injuries result in the greatest amount of tissue necrosis. 

Hemorrhage into the soft tissues is common, resulting in ecchymosis and hematoma 

formation. The crushed tissue has a markedly impaired ability to heal and resist 

infection. 

E. Bites 

Bites are heavily contaminated and may require delayed closure. 

Tetanus Immunization Status 

It is important to ascertain the tetanus immunization status of patients who have 

sustained open wounds. Determine the date of the patient's most recent booster shot. 

Allergies 

The existence of any allergies or adverse reactions should always be elicited before 

treatment is started. Ask the patient specifically about past problems with anesthetics, 

antibiotics, or analgesics. Such questioning may remind the patient of a forgotten 

allergic or adverse reaction. 

EXAMINATION 

Careful inspection of the wound is imperative for proper management. Inspection should 

be conducted in an emergency care or surgical facility where adequate lighting and 

equipment are available. Sterile technique and gentle handling of tissues are mandatory 

to avoid additional tissue injury or contamination. 

Definitive wound evaluation requires a cooperative patient. If the patient is

uncooperative, it is perhaps wise to consider restraints, sedation, or local (see below) or 

general anesthesia—or even to postpone the examination, if possible, until more 

favorable conditions exist. 

Assess Type & Extent of Injury 

In assessing the type and extent of injury, consider the following questions: 

• Is there loss of function in the injured part? 

• Are important underlying structures involved, such as nerves, major blood vessels, 

ducts, ligaments, bones, or joints? 

• What is the level of contamination in the wound? 

• Are any foreign bodies present? 

• What is the viability of the injured parts? Are any parts missing? 

Examine for Avulsion Flaps 

Avulsion flaps may result in a sizable amount of nonviable tissue that may not be 

apparent initially. Distally located flaps result in greater tissue destruction than do 

proximally located flaps. Venous congestion is a sure sign of ultimate tissue death. 

Amputated tissue may be reattached in some cases. Seal the parts in a dry, sterile 

container and cool them on ice. If replantation is considered a possibility, consult a 

microsurgeon or appropriate specialist immediately. 

Consider Location of Wound 

A. Head and Neck 

Deep injuries to the head and neck frequently involve important underlying structures 

(Chapter 23). These complex anatomic areas cannot be extensively debrided without 

major functional or cosmetic loss. Wound evaluation and repair are often best done in 

the operating room by a maxillofacial or general surgeon. The importance of serial 

evaluations of the central nervous system and cervical spine in the presence of major 

head and neck trauma cannot be overemphasized. 

B. Chest and Abdomen 

Wounds of the chest and abdomen must be evaluated for possible communication with 

a body cavity as well as internal organ injury (Chapters 24 and 25). 

C. Extremities 

Deep wounds in the extremities must be carefully examined and anatomic landmarks 

visualized. Pulse deficits or bruits may be present, and an arteriogram may be indicated 

if the path of injury passes close to a major blood vessel (Chapter 38). Injuries to the 

extremities require detailed examination of nerve, tendon, and circulatory function 

(Chapter 29). Avoid extending the injury by inadvertent manipulation or haphazard

probing. Make sure that no tourniquet is inadvertently left in place where a dressing is 

applied. Adequate lighting, exposure, and selection of instruments are mandatory. Most 

tendon and nerve repairs and all vascular repairs should be performed in an operating 

room. 

Prepare for Definitive Care 

After initial assessment, cover the wound with a sterile dressing until definitive 

management or further evaluation can be performed. Obtain any necessary x-rays only 

after the wound has been protected from the possibility of additional contamination. If 

considerable delay in definitive evaluation and management is anticipated, the wound 

should be cleaned, conservatively debrided, and temporarily closed or covered. 

Extensive wounds—or minor ones involving major structures—are best evaluated and 

managed in the operating room. 

ANESTHESIA 

Preliminary Examination 

Perform a careful sensory and motor neurologic examination before administering 

anesthetic. 

Choice of Agent 

Local and infiltrative anesthetics have varying attributes with regard to safety, potency, 

duration of action, and effects on the local wound milieu (Table 30-1). Lidocaine is 

perhaps the safest local anesthetic, because allergic reactions are rare. The major 

problem with all local anesthetics is systemic absorption resulting in cardiovascular and 

central nervous system toxicity. For an adult, the maximum safe dose of 1% lidocaine 

without epinephrine is 5 mg/kg (do not exceed 300 mg); for 1% lidocaine with 

epinephrine, 7 mg/kg (do not exceed 500 mg). For children, the safety and efficacy of 

lidocaine and mepivacaine are known; child safety and efficacy of the other drugs in 

Table 30-1 are not known. 

Topical Anesthesia 

Topical anesthesia is especially useful in the management of small wounds in children 

who do not tolerate local infiltration. A commonly used combination solution is LET 

(lidocaine, epinephrine, and tetracaine). To apply the solution, soak a gauze pad in it 

and place the pad directly over the wound for 20 minutes. Do not use over mucous 

membranes or areas with end-arterial circulation (fingers, toes, nose, penis). Anesthesia 

can often be judged by the appearance of blanching at the wound site. Use the minimal 

amount of anesthetic necessary. 

Inhalation Anesthesia 

Inhalation anesthesia with nitrous oxide administered by experienced personnel can be 

a useful adjunct, especially for children.

Local Infiltration 

A. Method of Injection 

Infiltration of a local anesthetic agent is performed gently near the edge of the wound or 

directly into the wound with a small (No. 25-30) needle (Figure 30-1). Pain associated 

with local infiltration is partly due to the stretching of sensitive nerve endings in the 

dermis and may also be due in part to the difference in acidity of some anesthetics (the 

pH of commercial preparations of lidocaine is 5.0-7.0). Associated pain can be reduced 

by using smaller amounts of more concentrated anesthetic solutions and slower 

infiltration rates or, in the case of lidocaine, by preparing it as a buffered solution (9 mL 

of 1% lidocaine, to which 1 mL of sodium bicarbonate solution, 44 mEq/50 mL, is 

added). Restrict the dose of anesthetic to the least amount that will provide adequate 

anesthesia. This is particularly true for facial lacerations, where infiltration distorts 

important landmarks and makes precise matching of wound edges difficult. Infiltration of 

anesthetic directly into the wound is less painful but may spread infection in heavily 

contaminated wounds. 

B. Epinephrine Hemostasis 

Lidocaine and similar agents cause relaxation of spastic vessels, and bleeding may start 

again following local anesthesia. Addition of epinephrine overcomes this tendency and 

also prolongs the anesthetic effect. The concentration of epinephrine does not need to 

be higher than 1:400,000, and at least 7 minutes should be allowed for the full 

vasoconstrictive effect. Use a fresh vial of 1:1000 epinephrine, and dilute it with plain 

1% or 2% lidocaine. Premixed solutions of epinephrine-containing local anesthetics may 

lose their potency during prolonged storage. 

Although epinephrine has been shown to have little adverse effect on survival of 

experimental cutaneous flaps, its use in patients with traumatically elevated skin flaps or 

in tissues with questionable viability is not recommended. Never administer epinephrine 

in areas where segmental blood supply is critical (eg, fingers and toes). Epinephrine is 

contraindicated in heavily contaminated wounds, because it severely compromises local 

wound defense mechanisms. Consider the systemic side effects of epinephrine in 

patients with cardiovascular and peripheral vascular disease. 

Regional Anesthesia 

Regional anesthesia (sensory nerve blockage at a site proximal to the wound) is more 

difficult to achieve than local anesthesia, but it provides a larger anesthetic area and 

allows more extensive exploration and manipulation of the tissues. Because local wound 

anatomy is not distorted by regional block, more precise alignment of wound edges is 

possible. Onset of anesthesia is a function of the type of agent used and how close to 

the nerves the agent is injected. The duration of anesthesia can be prolonged with 

epinephrine; however, epinephrine should not be used for digital nerve blocks. Regional 

anesthesia is particularly applicable in extremity injuries complicated by heavy 

contamination or in extensive injury requiring long operating times for repair. It is also 

used in patients who are not good candidates for general anesthesia. 

A. Examples 

Examples of regional nerve blocks include axillary block; isolated ulnar, median, and

adial nerve blocks; digital nerve blocks; trigeminal nerve blocks; sciatic and femoral 

nerve blocks; and spinal anesthesia. Digital, infraorbital, and submental blocks are 

commonly performed in the emergency department. Isolated ulnar, median, and radial 

nerve blocks should be performed only by an experienced physician. 

B. Pitfalls 

Pitfalls of regional anesthesia include difficulty in placing the anesthetic close to the 

supplying sensory nerve; loss of valuable time in waiting for it to take effect; and risk of 

permanent injury to the nerve from direct infiltration of anesthetic into the nerve. 

Common Regional Blocks for Hand Surgery 

Several techniques for regional blocks in hand surgery are described below. Whatever 

the method used, a thorough understanding of anatomy is crucial. Avoid probing for 

paresthesias. Attempt to infiltrate the anesthetic without penetrating the nerve sheath, 

because this may injure the nerve. 

Use a 25- or 27-gauge needle; larger needles may cause significant nerve injury. Wait 

about 10 minutes for the full anesthetic effect in digital blocks and 20 minutes for wrist 

blocks. 

A. Digital Block 

The technique requires 2 separate needle sticks with 4 injections of 1 mL of 1% 

lidocaine next to the nerve bundle of all 4 digital nerves. The needle is first inserted 

dorsally to block the dorsal digital nerve and is then redirected without removal toward 

the volar nerve and the anesthetic is injected. The procedure is repeated on the 

opposite side of the digit. 

B. Radial Nerve Block 

The radial sensory nerve emerges beneath the brachioradialis tendon (Figure 30-2) 

about 6 cm (23/8 in) above the Lister tubercle. Inject about 4 mL of lidocaine in a 2-cm 

(3/4-in) wide band 4 cm (19/16 in) above the Lister tubercle. 

C. Median Nerve Block 

The median nerve at the wrist lies just radial and deep to the palmaris longus tendon 

and the transverse carpal ligament (Figure 30-3). The palmaris longus, when present, is 

easily identified by having the patient make a fist and flex the wrist. Insert the needle 

dorsally and distally between the palmaris longus and flexor carpi radialis, and inject 4 

mL. The lidocaine can be milked into the carpal tunnel to achieve the maximum blocking 

effect. 

D. Ulnar Nerve Block 

The ulnar nerve and artery course just dorsal to the flexor carpi ulnaris at the wrist 

(Figure 30-4). Avoid inadvertent injection of anesthetic into the artery by aspirating as 

the needle is advanced. Inject 2 mL on the ulnar side of the flexor carpi ulnaris. An 

additional 2 mL should be injected on the radial side to achieve a total block. 

Common Regional Blocks for Facial Surgery

A. Infraorbital Nerve Block 

The infraorbital foramen can be easily palpated along the anterior maxilla and lies along 

a line drawn between the pupil and the maxillary canine. Inject about 1-2 mL as the 

needle is advanced from a lateral to a medial direction (Figure 30-5). Avoid penetrating 

the nerve by being careful not to enter the foramen. An intraoral approach may also be 

used. Wait for symptoms of numbness of the upper lip. Infraorbital nerve block provides 

anesthesia of the cheek, upper lip, and parts of the nose. 

B. Supraorbital Nerve Block 

The exit of the supraorbital nerve from the orbit is readily identified by palpating the 

supraorbital notch. Inject a total of 1-2 mL of anesthetic about 0.5 cm (3/16 in) above 

the orbital rim (Figure 30-6). Advance the needle from a lateral to a medial direction, 

and avoid penetrating the nerve. If both supraorbital and infratrochlear blocks are 

needed, the wheal should be extended medially toward the midline. Supraorbital block 

is helpful in anesthetizing the forehead. 

CLEANING & DEBRIDEMENT 

Hair Removal 

Wounds in hairy areas are difficult to debride and suture, and hair in a wound acts as a 

foreign body, delaying healing and promoting infection. Shaving hair around wound 

edges facilitates management but invites wound infection if the infundibulum of the hair 

follicle is injured. 

Contamination can be minimized by clipping the hair 1-2 mm (1/16 in) above the level of 

the skin. Depilatory agents and special razors equipped with recessed blades also allow 

safe removal of hair without infundibular injury. 

Caution: Eyebrow and eyelash hair should never be removed, because removal 

destroys critical landmarks and makes accurate alignment of wound edges difficult. 

Misalignments may cause notch or step-off deformities in the brow line. Eyebrow hair 

also regrows slowly, creating a cosmetic problem. 

Mechanical Cleansing 

As an adjunct to surgical debridement, mechanical cleansing of the wound by irrigation 

or scrubbing is quite effective. Soaps and detergents should not be used in the open 

wound in conjunction with mechanical cleaning. 

A. Irrigation 

To be effective, irrigating solutions must be delivered under pressure. The danger of 

tissue injury with high-pressure irrigation must be weighed against the benefits of 

decontamination. 

Numerous devices are available for high-pressure irrigation, but the simplest and least 

expensive is syringe irrigation. A 35- or 50-mL syringe and a 19-gauge or blunt needle 

connected to a reservoir of irrigating fluid by a 3-way stopcock are most suitable. Bulb 

syringe irrigation has been shown to be no more effective in preventing wound infection

than no irrigation at all. 

Normal saline (or similar balanced crystalloid solution) is forcefully injected close to the 

wound surface and perpendicular to the surface of the skin. The amount of irrigant used 

depends on the size of the wound and the suspected extent of contamination. 

B. Mechanical Scrubbing 

1. Sponge—Mechanical scrubbing of the wound surface is usually best performed with 

a highly porous sponge. Sponges routinely used for hand washing work well. Brushes 

and low-porosity sponges decrease the wound's resistance to infection. 

2. Brush—"Abrasion tattooing," in which debris is embedded in the skin, requires 

vigorous scrubbing or dermabrasion to remove embedded debris. Soaps and detergents 

should not be used. 

Skin & Wound Cleansers 

Cleanse the wound and surrounding skin to remove transient microflora, gross debris, 

coagulated blood, and the like. 

A. Normal Saline 

In most instances, simply washing the open wound with saline under pressure (see 

above) removes most of the surface bacteria. 

B. Nonionic Surfactant 

The nonionic surfactant Pluronic polyol F-68 has been shown to be effective as a wound 

cleansing agent without demonstrably impairing resistance to infection or wound 

healing. 

C. Hydrogen Peroxide 

The foaming action of hydrogen peroxide is frequently used to remove particulate debris 

and recently clotted blood from wounds. Caution: For these purposes, dilute solutions 

of hydrogen peroxide (1% or less) must be used to reduce the potential for tissue injury 

associated with oxidation. In most cases, a less toxic means of wound cleansing may be 

preferred. 

D. Ionic Soaps and Detergents 

Ionic soaps and detergents (eg, pHisoHex) should not be used for wound cleansing, 

because they are extremely irritating to tissues and increase the potential for infection if 

used directly on the wound. They may be used for cleansing of intact skin surrounding 

the wound, although they have not been shown to be superior to ordinary soap or other 

agents for this purpose. After application, they should be removed by thorough rinsing 

with water. Prolonged use of agents containing hexachlorophene (particularly in 

children) is associated with severe toxicity, including neurologic damage and even 

death. 

E. Skin Disinfectants and Antimicrobials 

Skin disinfectants and antimicrobials vary in their microbicidal effects in wounds. Most 

are irritating to normal tissues, and some may cause severe toxicity by their systemic

absorption (eg, chlorhexidine, antimicrobial powders). Although a 1% solution of 

povidone-iodide is considered nontoxic, there is conflicting evidence regarding its 

efficacy in preventing wound infection. Tincture of iodine has been shown to potentiate 

wound infection, and its use can also result in elevation of blood iodine levels. Irrigation 

of wounds with antibiotic solutions is associated with a decreased rate of wound 

infection. 

Debridement 

Remove retained debris and devitalized tissue by surgical excision and mechanical 

cleansing. 

Surgical debridement consists of excising devitalized or severely contaminated tissues 

and irregular areas that interfere with wound closure. Use a stainless steel scalpel blade 

for debridement. 

A. Total Excision of the Wound 

The simplest method of debridement is total excision of the wound, creating a surgically 

clean area. Caution: Total excision is appropriate only for wounds that do not involve 

specialized structures (eg, injuries of the abdominal wall and thighs). More selective 

debridement is indicated for wounds on the hand or face. 

1. Special gauze pack and closure—It is often helpful to pack the wound with gauze, 

close with sutures, and excise the entire mass as a tumor, leaving a cuff of normal 

tissue attached. Take care to avoid exposure of the gauze during dissection. 

2. Vital staining—An alternative method of debridement is to stain the wound with a 

vital dye such as methylene blue, close, and excise the entire stained area. 

B. Selective Debridement 

In most situations, it is best to mechanically cleanse the wound (see above) and then 

perform selective debridement of all grossly nonviable tissue. Because a reliable 

laboratory test for tissue viability is not available, tissue viability must be assessed by 

careful inspection. Signs of tissue necrosis include gray or black color and lack of 

bleeding when the tissue is incised. Remove all nonviable portions except certain 

fibrous tissue remnants. Mangled, irregular wound edges imply severe local tissue injury 

and should be sharply debrided. If, on initial or subsequent evaluation, it appears that 

adequate debridement would prevent tension-free simple closure, consult an 

experienced surgeon for wound management. 

The potential viability of attached soft tissue parts depends on vascular supply and on 

the extent of injury. Venous effluent is the most critical component of vascularization. 

Assess traumatically elevated skin flaps for capillary refill and the presence of venous 

congestion. Rapid capillary refill or cyanosis in the flap indicates venous obstruction. If a 

sharp demarcation is seen between normal and abnormal perfusion of the flap, excision 

of the abnormal portion is indicated. If the area of perfusion is not well demarcated, 

clean and closely observe the wound. Consultation with a surgeon may be warranted. 

Excision procedures on the face, particularly of specialized structures such as the ear or

nose, require a conservative approach. The facial area has an abundant blood supply 

that enables tissues to survive on surprisingly small pedicles. In these cases, 

observation and expectant treatment are warranted. Obtain surgical consultation before 

performing any major debridement or debridement of a specialized part. 

WOUND CLOSURE 

After the wound has been examined, anesthetized, cleaned and debrided, and 

reexamined, the physician must decide whether to close it. Primary wound closure is 

preferable because of faster healing, less scarring, improved hemostasis, and better 

aesthetic and functional results. All foreign bodies should be removed to minimize the 

chance of infection. 

Contraindications to Wound Closure 

Several factors affect the risk of infection with wound closure and determine whether 

closure is justified. 

A. Heavy Bacterial Colonization 

A prolonged interval (more than 6 hours) between injury and attempted closure is 

usually a contraindication to wound closure. In a generously vascularized area such as 

the face, wound closure may be attempted up to 24 hours after injury. 

Heavily contaminated wounds (eg, bites) should be left open. Active wound infection at 

the time of the emergency department visit contraindicates closure of the wound. 

B. Major Tissue Defects 

Closure is contraindicated if the wound cannot be closed without excessive tension. 

C. Other Factors 

Closure is contraindicated if there are retained foreign bodies, devitalized tissue, or 

tissue with borderline adequate perfusion (high likelihood of infection). 

Primary Closure 

A. Objectives 

The objectives of primary wound closure are (1) precise alignment of injured parts to 

facilitate rapid healing, return of function, and a good cosmetic result; and (2) avoidance 

of tissue injury (eg, excessive electrocautery, strangulating sutures), hematoma 

formation, and wound tension. 

B. Delayed Primary Closure 

Contaminated wounds, if properly debrided, will gain resistance to infection if left open. 

After 48-96 hours, these wounds can then be closed with essentially no loss in wound 

healing time. Consider delayed primary closure in the case of wounds contaminated by 

feces, pus, a foreign body, or saliva in the case of bite wounds. Crush and blast injuries 

and avulsion injuries are markedly susceptible to infection and necrosis and should also 

be considered for delayed closure.

After initial debridement, dress the open wound with fine-mesh gauze and a sterile 

dressing. It should be left undisturbed for the next 4 days unless unexplained fever 

develops. After this time, the wound is closed using sterile technique. 

If delayed closure is elected, the patient should be hospitalized (for large or serious 

wounds) or seen daily on an outpatient basis. 

1. Suture Selection 

All sutures represent foreign bodies in the wound. For this reason, use the smallest size 

and the least amount of suture that will achieve adequate tissue apposition. Do not use 

sutures in contaminated wounds unless they are absolutely necessary to maintain 

alignment of tissue parts. 

The choice of needle and suture size is generally dictated by the size and location of the 

wound and the desired precision of closure. 

Atraumatic needles (round, tapered) are used for closing fascia, muscle, and 

subcutaneous tissues as well as for repairing lacerated vessels and nerves. Cutting 

needles are used primarily for dermal and epidermal closure, where the tough collagen 

fibers must be "cut" by the needle to allow easy passage of the suture. 

Large-diameter suture materials (2-0, 3-0) are best for closing major fascial layers and 

tissues subjected to strong tensile forces (eg, knee and elbow wounds). The effective 

strength of a suture material is only as great as the strength of the tissue being sutured: 

fine sutures placed in wounds subject to mechanical stresses may result in disruption of 

the wound if the fine suture material pulls through the wound. 

Generally, fine sutures are used in wounds (or their parts) requiring precise alignment; 

5-0 and 6-0 sutures are preferred for closure of facial lacerations. Layered closure 

(fascia, dermis) of any wound allows placement of fine epidermal sutures anywhere on 

the body. The epidermis itself has little tensile strength, and sutures are placed in this 

layer only to achieve accurate alignment of wound edges. 

Percutaneous closure of the epidermis and dermis in regions other than the face is best 

managed by the use of 3-0 or 4-0 suture material. Suture marks are the result of tension 

in the tied suture and the length of time the suture is left in place. 

Absorbable Sutures 

Absorbable sutures are biodegraded and lose their tensile strength in 2-6 weeks. 

A. Gut Sutures 

Sutures derived from sheep submucosa or beef serosa are digested by proteolytic 

enzymes in the wound. They are more rapidly degraded in the presence of infection. 

The knot-holding ability of plain gut is rather inconsistent; chromic gut seems to be 

better in this regard. 

1. Plain gut—Plain gut incites an intense inflammatory reaction in the wound and loses

its tensile strength within 2 weeks. 

2. Chromic gut—Treatment of gut with chromium salts decreases its tissue reactivity 

and prolongs its survival to about double that of plain gut. In some studies, however, it 

has been shown to potentiate infection more than plain gut. 

B. Synthetic Sutures 

Polyglycolic acid (Dexon), polyglactin (Vicryl), and polydioxanone (PDS) produce 

minimal tissue reaction in the wound and are most commonly used for dermal and 

subcutaneous closures and vascular ligation. 

1. Degradation—Polyglycolic acid and polyglactin are degraded by hydrolysis and lose 

50% of their tensile strength in 14-20 days and about 90% by the fourth week 

(comparable to chromic catgut). Polydioxanone, a third-generation synthetic absorbable 

suture, loses 50% of its tensile strength in 5 weeks and 90% at 2 months. 

2. Tying qualities—Although similar to silk in their handling characteristics, polyglycolic 

acid and polyglactin sutures do not hold knots quite as well. Polydioxanone looks, feels, 

and handles like monofilament nylon or polypropylene. 

3. Use in acute wounds—Absorbable synthetic sutures are probably superior to gut 

sutures in acute wounds because of their low tissue reactivity and resistance to 

degradation in the presence of infection. The monofilament characteristics of 

polydioxanone make it almost the ideal synthetic absorbable suture. 

Nonabsorbable Sutures 

Nonabsorbable sutures are degraded very slowly or not at all in the tissues. 

A. Silk 

Silk sutures represent the most common type of natural fiber suture. Silk gradually loses 

its tensile strength and is classified as a slowly absorbable suture material. The tissue 

reactivity of silk is the greatest of all nonabsorbable sutures, and its use in acute 

wounds has generally been abandoned. 

B. Stainless Steel and Metallic Clips or Staples 

Stainless steel sutures and metallic clips have been used for years because of their 

presumed inertness. These materials have been shown to increase infection rates 

significantly in contaminated wounds. The increase is probably the result of mechanical 

irritation resulting from their rigidity and not to corrosion. The stiffness of metallic sutures 

makes tying quite cumbersome. 

Many types of disposable skin staple devices are available. The staple configurations 

vary but are primarily designed to approximate wound edges with minimal tissue 

trauma. Some staples project above the skin surface to avoid staple marks. As with 

wound tapes, precise epidermal alignment is difficult to achieve with a skin staple, and 

these devices should not be used for cosmetic skin closures. Because a stapled wound 

usually does not contain dermal sutures, its tensile strength depends on the presence of 

the staple, and this must be kept in mind when considering staple closure of wounds

subjected to increased tension (eg, joint surfaces, mobile parts). If early removal of the 

staple is contemplated, the wound should be supported by skin tapes until the wound 

gains sufficient tensile strength to withstand local biomechanical forces. The time 

required varies from 1 to 2 weeks depending on the wound's location. 

C. Synthetic Sutures 

1. Dacron—Dacron is a polyester that elicits less tissue reaction than silk. Because of 

its high friction coefficient, it is as difficult to handle as a suture. The friction injury 

imposed on the tissues by Dacron can be overcome by coating it with Teflon. 

2. Nylon—Nylon causes less tissue reactivity than Dacron, and its use in contaminated 

wounds results in lower wound infection rates. Monofilament nylon sutures lose 

approximately 20% of their tensile strength within a year after placement in a wound. 

The monofilament form of nylon is quite stiff and does not hold knots well. Multifilament 

nylon sutures completely lose their tensile strength in the wound after 6 months, but 

they are easier to tie than monofilament sutures. 

3. Polypropylene and polyester—Polypropylene and polyester materials cause the 

least reactivity of all suture materials. They maintain their tensile strength indefinitely 

and are the suture material of choice for closure of contaminated wounds. These 

materials are used most commonly for fascia and skin closure. They are also 

advantageous in the repair of vascular, nerve, and tendon injuries. Because of their 

softer consistency, these materials generally hold knots better than does nylon. 

2. Wound Tapes 

Sutureless closure of the acute wound provides maximum resistance to infection. 

Various tape materials have been used and have resulted in significantly diminished 

wound infection rates compared to those in suture closure. Tape closure is most 

advantageous in the contaminated wound but is also useful in superficial clean and tidy 

wounds, wounds in children, and wounds in obese patients. 

Tape closure is inferior to suture closure in maintaining precise wound edge alignment 

and eversion, requisites for cosmetically acceptable closure. However, tape closure is 

often used after early removal of sutures in order to minimize suture marks and to 

provide additional splinting of the wound until tensile strength is sufficient to resist local 

forces tending to pull the edges of the wound apart. 

Attributes of Wound Tapes 

A. Strength 

To be effective, skin tapes must be strong enough to support the wound edges in close 

apposition until sufficient healing has occurred. 

B. Adherence 

The tapes must have excellent skin adherence and should not macerate the underlying 

skin surface. Removing all moisture and using a defatting agent (eg, acetone) enhances 

adhesiveness to the skin, and tapes so applied will adhere for up to 2 weeks. Although 

tincture of benzoin is occasionally used to increase adhesiveness and may initially

enhance tape adhesion, it is solubilized by skin oils and rapidly loses its effectiveness. 

C. Types 

Microporous, rayon-reinforced wound tapes satisfy the requirements for wound tapes 

quite well and are used most often (eg, Steri-Strips; Figure 30-7). Simple wound tapes 

can be fashioned from plain microporous 1.25-cm (1/2-in) paper tape and should be 

sterilized by applying iodine to the central area of the tape touching the wound. 

Wound Tapes over Deep Sutures 

Suture closure in irregular lacerations and crush injuries allows for better approximation 

of skin edges than does tape closure. Moreover, tape only approximates the superficial 

portion of the wound, leaving the deeper wound layers more vulnerable to local 

biomechanical stresses and resulting in a weak, unsightly scar. In clean wounds, it is 

sometimes preferable to close the deeper layers with sutures and then approximate the 

superficial layers with tape. 

3. Wound Staples 

Stainless steel wound staples (Ethicon, 3M, Deknatel, others) are occasionally used in 

the emergency department. Wounds—especially long, linear lacerations—can be closed 

more quickly with staples than with sutures. In some cases, when the costs of suture 

instrument sets, suture material, and labor are considered, stapling a wound may be 

considerably less costly. However, crushed or ischemic tissue may cause point necrosis 

and infection at the staple tip and produce a less cosmetically satisfactory result. Thus, 

staples should probably be limited to areas of less cosmetic importance, such as on the 

scalp or trunk. 

4. Tissue Adhesives 

Cyanoacrylate tissue adhesives (Dermabond) are now available for use in the United 

States. Cyanoacrylate adhesives polymerize rapidly when applied to tissues and form 

an adhesive layer on top of intact epithelium to hold the wound edges together. These 

adhesives cause an intense inflammatory reaction and should be used only on minor 

superficial lacerations. They should not be used near the eye, on mucous membranes 

or mucosal surfaces, on moist areas, or on areas with dense hair. Tissue adhesives 

should not be used for infected wounds. 

Tissue adhesives are useful for minor wounds, those less than 5 cm in length and with 

separated wound edges less than 0.5 cm; they are most beneficial for wounds that 

would close spontaneously. Wounds greater than 5 cm in length and 0.5 cm in 

separation have increased tensile forces that may lead to poor wound edge 

approximation and a poor cosmetic outcome. Subcutaneous sutures may be useful in 

decreasing wound edge tension and may lead to a far better cosmetic result. 

Preparation of wounds for closure with tissue adhesives is the same as for sutures. 

Thoroughly cleanse the wound and control bleeding before applying tissue adhesive. 

Hold the wound edges together and slightly everted with tissue forceps. Apply the 

adhesive by lightly wiping the applicator tip in the direction of the long axis. Apply a few

layers quickly and then hold the wound edges together for about 60 seconds to ensure 

adequate bonding. Once applied, tissue adhesives should not be covered with ointment 

or dressing. If any adhesive is applied to unwanted areas, it can be removed with 

petroleum jelly or acetone (nail polish remover). Many tissue adhesives are 

commercially available, with many different applicator sizes and applicator tips. Also 

available are accessories to assist with the entire procedure, from wound cleansing 

devices to tissue forceps of various sizes and shapes for any size or shape wound. 

Among the benefits of tissue adhesives is better cosmetic appearance, if used 

appropriately. Even more beneficial is the decreased risk of wound infection. The 

manufacturer of Dermabond states that the incidence of wound infection with this 

product is 3.6% and the incidence of dehiscence requiring retreatment is 2.2%; neither 

finding was statistically different by comparison with wounds closed with sutures. 

5. Choice of Closure Technique 

The choice of an appropriate material for wound closure is based on biologic and 

mechanical properties of the material and the characteristics of the wound. Decisions 

about layers to be closed are based on several factors, the most important of which are 

stress, dead space, and skin approximation. 

Fascia 

In soft tissue wounds that do not involve the face, the strength of closure depends on 

the fascia. Because fascia heals slowly, the suture material should be capable of 

maintaining its strength for a long time. Synthetic nonabsorbable sutures are best for 

this purpose. 

Muscle & Fat 

Muscle and fat do not hold sutures well, and closure is performed primarily to obliterate 

dead space. Dead space results from traumatic tissue loss, debridement, or gaping of 

subcutaneous layers. Suturing of dead space invariably produces additional tissue 

trauma and necrosis and is contraindicated in the closure of contaminated wounds. 

When such suturing is performed, it should be accomplished with the fewest possible 

loosely placed sutures. Chromic gut or one of the synthetic absorbable sutures should 

be used for this purpose. 

Skin 

Skin closure may be accomplished by layers, full-thickness percutaneous sutures, skin 

tapes, or a combination of these methods. The type of skin closure method chosen 

depends on the forces tending to open the wound and how good a cosmetic result is 

desired. The width of the scar that will result from healing will be influenced by the local 

stresses of the surrounding tissues. The direction of maximum force of skin tension is 

usually parallel to the skin wrinkles. Wounds oriented in the same direction as local 

stresses are subjected to less tension during healing and consequently produce a less 

visible scar. Examples include transverse lacerations of the forehead and vertical 

lacerations of the upper lip. Wounds that cross lines of maximal skin stress will be

subjected to increased tension during healing. These wounds frequently widen with time 

and have a tendency to form hypertrophic scars. Examples are transverse lacerations of 

the cheek and axial lacerations over the elbows. 

The propensity of a scar to hypertrophy is also influenced by factors unrelated to its 

location or technique of closure. The tendency of children and adolescents to form 

hypertrophic scars is notorious and is probably influenced by elevated levels of growth 

hormone or other growth factors. Pregnant women have an increased incidence of 

hypertrophic scar formation that decreases with the resumption of normal menses after 

delivery; this tendency is often associated with a parallel increase in pigmentation 

coinciding with pregnancy. Some investigators have postulated that hypertrophic scars 

and pigmentation are under similar hormonal influences. An increased incidence of 

hypertrophic scar and keloid formation is also found in blacks and other dark-skinned 

races. These specific groups of patients will demonstrate an exaggerated scar formation 

response that can be controlled only by manipulation of the wound in ways beyond the 

technical aspects of closure. Not all patients in these groups will form hypertrophic 

scars, however, and it is impossible to predict which patients might, except perhaps in 

the case of patients who have a history of hypertrophic scar formation. In these patients, 

precise wound closure using fine suture materials and atraumatic technique may lessen 

the degree of hypertrophic scarring that might otherwise result. Other methods of wound 

control include prolonged splinting, pressure bandages, corticosteroid therapy, and 

radiation therapy. In the acute wound, however, primary consideration is given to the 

location and orientation of the wound and its method of closure. 

A. High-Stress Wounds 

Layered wound closure is used to support wounds subjected to high skin tensions. The 

dermis is approximated with interrupted sutures, usually absorbable synthetics (Figure 

30-8A-C). These sutures should not involve the epidermis, because of the risk of 

epithelial cyst formation. The epidermal layers are then adjusted with fine 

nonabsorbable sutures or tapes (Figure 30-8D and E). This method of skin closure is 

commonly used for facial lacerations. 

B. Low-Stress Wounds 

Percutaneous sutures are used for most other sites. It is important to evert the wound 

edges and to effect precise epidermal approximation to achieve the best results (Figure 

30-9). Monofilament synthetic nonabsorbable sutures are the materials of choice for this 

type of closure. The size of suture material is not as important as the tightness of 

closure and the length of time the suture is left in place. These sutures should be 

removed by the seventh day to avoid epithelialization of the suture tracts. If additional 

support of the closure is required, as in wounds subjected to increased tension, skin 

tapes can be applied. 

6. Drainage of the Wound 

Drains constitute foreign bodies, produce tissue necrosis, serve as conduits for bacterial 

contamination of the wound, and are not very effective in preventing hematoma 

formation. If sound principles of management have been carefully followed, drains are 

usually unnecessary in the acute wound. If oozing cannot be controlled, it is preferable 

to delay wound closure. Drains, however, may be effective in evacuating pus and

necrotic exudates that might be found in heavily contaminated or already infected 

wounds. 

POSTOPERATIVE WOUND CARE & DRESSINGS 

Postoperative wound care should provide an ideal environment for wound healing. This 

is accomplished primarily through the use of dressings. A dressing serves one or more 

of 7 different functions: protection, immobilization, control of edema (compression), 

absorption, debridement, delivery of topical medications (antibiotics), and cosmetic 

appearance. 

Protection 

Wounds closed by percutaneous sutures are susceptible to surface bacterial invasion 

for the first 48 hours after closure. During this time, the wound should be protected with 

sterile dressings or frequent suture line care. 

A. Dressings 

If dressings are used, nonadherent materials (eg, Telfa, petrolatum-impregnated gauze) 

are favored because removal is easy and does not disturb sutures or coated wound 

edges. 

Petrolatum-impregnated dressings have been shown to decrease the rate of 

epithelialization in partial-thickness wounds. For this reason, ointment-impregnated 

dressings (eg, bacitracin, combined neomycin sulfate and polymyxin B sulfate 

[Neosporin]) or nonadherent occlusive dressings (Op-Site) are preferred for this 

particular type of wound. 

Occlusive or semiocclusive polyurethane, methacrylate, silicone polymer, or gel 

dressings provide excellent protection, and most do not alter the rate of normal 

epithelialization. If the wound contains residual necrotic debris or significant levels of 

bacterial contamination, however, the risk of wound infection is increased with these 

dressings. 

B. Undressed Wounds 

Suture line care without a dressing is commonly used for facial wounds and involves 

frequent meticulous cleansing with saline or dilute hydrogen peroxide solution. 

Cleansing removes the adherent coagulum from the suture-skin juncture, decreasing 

the likelihood of stitch abscess formation. After cleansing, the wound is dressed with an 

antibiotic cream or ointment (eg, bacitracin-neomycin). 

C. Tape Dressings 

Taped wounds are quite resistant to surface bacterial contamination. They usually 

require no protection other than that provided by the tape itself. These wounds should 

be checked frequently for wound drainage beneath the tape. Excessive drainage can 

cause maceration of the wound edge and thereby provide an excellent medium for 

bacterial proliferation. 

Immobilization

Immobilization of the wound enhances resistance to infection and may accelerate 

healing. 

A. Materials 

Immobilization is accomplished with splints, bulky dressings, skin tapes, or 

combinations of these methods. 

B. Duration of Immobilization 

Ideally, immobilization of the wound should be continued until it is no longer vulnerable 

to infection and has gained sufficient strength to withstand the stresses of motion and 

skin tension. Wounds become resistant to infection within a week, but development of 

maximal strength requires about 6 weeks. Protracted immobilization will defeat its 

possible advantages, for example, possibly producing permanent joint contractures in 

elderly persons. The advantages of wound immobilization must be weighed against the 

undesirable consequences. Extended immobilization is advisable for wounds of the face 

or whenever a good cosmetic result is desired. Areas such as the jaw line, chin, 

shoulder, and knee are subjected to more severe tissue stresses than are other areas 

and frequently require support for up to 3 months to achieve the best result. Extended 

wound support is also necessary in patients with neoplasms or immunodeficiency. 

Control of Edema 

Edema slows down the repair mechanisms and increases fibrous tissue proliferation. 

The wound with minimal edema will proceed to earlier complete healing and return of 

function. Peak wound edema occurs by 48 hours and gradually resolves over the next 

4-6 days. Persistent tissue edema after 7 days suggests inflammation or infection. In 

most cases, a compression dressing is beneficial during the first week of wound healing. 

In wounds that are prone to hypertrophic scarring, edema persists locally for up to 2 

years. In these wounds, continued pressure may be beneficial in controlling the extent 

of hypertrophic scarring. Custom-made elastic pressure garments are excellent adjuncts 

in this regard; otherwise, simple elastic bandages are equally effective. 

A. Elevation 

Elevation of the wound above the level of the heart is the simplest way to limit the 

amount of excess tissue fluid in the wound. In the ambulatory patient, the common 

triangular bandage sling or "yoke" sling serves these purposes well. Slings, like any 

other dressing, are only as good as patient compliance; instruction in their use is 

important if the goal is to be achieved. 

B. Pressure Dressing 

In certain situations, it is advantageous to apply pressure over the wound along with 

elevation by using bulky pressure dressings. 

Caution: Compression dressings should not be used in crush injuries or in injuries that 

tend to develop into compartment syndromes (eg, severe injuries of the forearm or leg). 

Continued pain or diminished sensitivity necessitates removal of the dressing and 

careful examination of the wound. Although these dressings are often used to absorb 

bloody oozing at the operative site, they should not be used as a substitute for diligent

hemostasis. 

Avoid constriction of proximal parts with these dressings, because venous and 

lymphatic congestion will occur as result of the tourniquet effect. 

Bony prominences must be carefully padded, with generous use of bulk. To ensure 

uniform compression throughout and to avoid constriction and pressure-point injury, 

smooth, even wrapping that avoids lumps is necessary when compression dressing is 

applied. 

In managing hand wounds, it is important to place 1 or 2 layers of gauze between the 

fingers to prevent maceration by sweat. The toes and fingertips should be exposed so 

that the physician can assess sensibility and capillary refill. 

Rolled gauze or bias-cut stockinet is preferred over elastic bandages, which are often 

too constricting. The finished dressing should be firm but not strangulating. 

In extremity injuries, compression dressing should extend proximally from the most 

distal point. For example, a wound of the forearm requiring a compression dressing is 

managed by applying the dressing starting from the fingers to above the wound. 

Absorption 

The absorptive capabilities of a dressing are used to remove bloody and serous ooze 

from the wound or drainage site. 

A. Closed Wounds 

In closed wounds, dry dressings are preferable, because moist ones will cause 

maceration of the skin and invite bacterial invasion. 

B. Open Wounds 

In open wounds, it is preferable to apply moist dressings to the open wound surface and 

back them with dry dressings to achieve a capillary effect. The exception to this principle 

is deep, tunnel-shaped wounds, where surface evaporation is limited, thus diminishing 

the capillary effect. These wounds are best managed by packing with dry gauze to 

achieve maximum absorption. 

C. Materials 

In all instances, absorptive dressings should be composed of fine-mesh gauze or spun 

fabric. 

Caution: Cotton meshes and synthetic equivalents become incorporated into the wound 

as foreign bodies that incite tissue inflammation and cause subsequent bacterial 

proliferation. 

Dextran polymers (eg, Debrisan wound-cleaning beads) have remarkable hygroscopic 

properties and serve well as absorbent dressings. They are quite effective in removing 

bacterial toxins and serous effluents from the wound surface. Wound healing is not 

significantly altered by their use.

Debridement 

Dressings are frequently used for mechanical debridement of the open wound. The 

traditional wet-to-dry method utilizes avulsion of adherent tissues to remove devitalized 

remnants from the wound surface. Unfortunately, this method does not discriminate 

between viable and nonviable elements and reinjures the wound with each dressing 

change. Although painful and detrimental to wound healing, this method is effective in 

removing fine tenacious material from the wound surface. It should be discontinued as 

soon as the desired effect has been achieved. 

The technique is as follows: Several layers of moist gauze are applied to the wound 

surface and allowed to dry. After about 4 hours, the adherent dressing is removed. 

Moistening the dry dressing before removal to loosen the dressing and lessen the pain 

of removal (as may be done by a sympathetic hospital attendant) defeats the purpose. 

Delivery of Topical Antibiotics 

The most common medicaments used in a dressing are antibacterials. Topical 

antibacterials are used to control bacteria that cannot be reached by systemic agents. 

They are not a substitute for adequate debridement. 

A. Agents 

Mafenide (Sulfamylon) and silver sulfadiazine (Silvadene) are most effective in this 

regard. These agents are also useful in partial-thickness injuries or marginally viable 

tissues (eg, abrasions, burns, crush injuries). By decreasing the potential for bacterial 

invasion, they diminish the likelihood of infection and the resulting tissue necrosis. 

B. Adverse Reactions 

Use of these agents must be monitored closely, because excessive amounts may cause 

acid-base imbalances (mafenide) or leukopenia (silver sulfadiazine). Both agents retard 

wound epithelialization and should be discontinued when the necrotic debris has been 

removed and wound bacterial counts are fewer than 10 5 organisms per gram of tissue. 

Cosmetic Appearance 

To the patient or casual observer, the sight of a wound is abhorrent and may be an 

occasion for adverse response. A dressing hides the wound and allows the patient to 

proceed with the process of rehabilitation without that distraction. In addition, a carefully 

applied, neat-appearing dressing reassures the patient that good wound care has been 

provided. 

1. Potential Infections & Antimicrobials 

Antimicrobials may be effective in preventing wound infection, particularly when the 

wound has fewer than 10 6 organisms per gram of tissue before treatment is started. 

Wounds with more than 10 6 organisms per gram of tissue often become infected 

despite antibiotic prophylaxis and should be left open. Systemic antibiotics, to be

effective, must be started as soon as possible following injury, preferably within 4 hours. 

Topical antibiotics are commonly used to suppress bacterial growth, although their 

efficacy at preventing subsequent infection is probably low. 

The likelihood of wound infection must be judged by the mechanism of injury, the level 

of contamination, the adequacy of debridement, and the patient's general status. 

Small inocula will result in infection if necrotic debris, foreign bodies, or altered tissue 

defense mechanisms (as occur in crush or contused wounds) are present. If adequate 

wound management must be delayed for any reason, then consider systemic 

antimicrobial prophylaxis. 

Sharp lacerations are markedly resistant to infection and in most instances will not 

require chemoprophylaxis. Open wounds, by virtue of their inflammatory response and 

resistance to bacterial dissemination, rarely become infected unless the initial level of 

contamination is great and cannot be reduced by cleansing and debridement. 

Furthermore, the fibrinous coagulum in these wounds limits the possible effectiveness of 

systemic antimicrobials on bacterial contaminants, thus making their use impractical. 

Deep wounds or those that involve poorly vascularized structures such as bone, tendon, 

ligament, or fascia should be treated with systemic antibiotics prophylactically. 

Oral mucosal lacerations rarely require systemic antibiotic prophylaxis, because the 

infection rate is low and randomized trials have not demonstrated a benefit from such 

treatment. 

Grossly contaminated wounds such as those that come in contact with feces, pus, or 

saliva should not be closed. Systemic antimicrobial therapy is mandatory. The choice of 

drug is based on the suspected predominant pathogen (Table 30-2). 

2. Tetanus Prophylaxis 

Tetanus prophylaxis is virtually 100% effective if used properly. Overuse of tetanus 

toxoid may induce serious allergic reactions. 

Investigate Previous Active Immunization 

A history of standard primary immunization with tetanus toxoid (or 

diphtheria-tetanus-pertussis vaccination) followed by boosters every 10 years virtually 

guarantees immunity from tetanus. In the United States, nearly all individuals over age 2 

years have had primary immunization (3 doses at 4-week intervals followed by one 

booster), and this too nearly guarantees immunity. Even individuals with only 2 previous 

tetanus toxoid immunizations will develop antibody rapidly enough following a tetanus 

toxoid booster so that passive immunization will be unnecessary in most cases. Patients 

over age 50 years, foreign-born patients, or patients unable to provide a history of 

tetanus immunization must be assumed to have incomplete immunization and should be 

given tetanus prophylaxis (Table 30-3). 

Determine Risk of Tetanus

The risk of tetanus is greater with wounds that are heavily contaminated by soil or feces, 

those involving crush injury of surrounding tissue, and those coming to medical attention 

after a delay of more than 24 hours. 

Select Active or Passive Immunizations 

Table 30-3 shows the U.S. Public Health Service recommended tetanus immunization 

schedules. Td (tetanus toxoid combined with adult-dose diphtheria toxoid) is preferable 

to tetanus toxoid alone. If passive immunization is required, human tetanus immune 

globulin is preferred over horse serum. The recommended dose is 250 units 

intramuscularly. If equine tetanus antitoxin must be used, inquire about and test for 

horse serum allergy before administering. The usual dose is 3000-5000 units. If both Td 

and tetanus immune globulin or antitoxin are given, they should be administered in 

separate sites using separate syringes. 

3. Rabies Prophylaxis 

Assess Risk of Rabies Exposure 


A. Species of Biting Animal 

Carnivorous animals (especially skunks, foxes, badgers, bobcats, coyotes, raccoons, 

dogs, and cats) and bats are more likely to be infected. Rabbits, squirrels, hamsters, 

guinea pigs, gerbils, chipmunks, rats, mice, and other rodents rarely transmit rabies in 

the United States. 

B. Determine if Animal Is Rabid (if Possible) 

(Note: Behavior is not a reliable sign of the rabid state.) If examination of the animal's 

brain for rabies is negative, it can be assumed that the animal's saliva did not contain 

rabies virus. 

Healthy domestic dogs and cats should be observed for 10 days by a veterinarian. If 

signs of rabies develop, the animal should be killed and its brain examined for rabies 

virus at the local public health laboratory. 

Stray or unwanted dogs and cats that cause bites should be killed immediately and 

examined for rabies. Wild animals that cause bites should be killed immediately and the 

brain examined for rabies. 

C. Circumstances of Biting Incident 

Unprovoked attacks are more likely to mean that the animal is rabid. Bites from 

apparently healthy animals that are fighting or feeding or that have been picked up or 

petted should be considered provoked and so have a low likelihood of causing rabies. 

D. Types of Exposure 

Any penetration of skin by teeth is regarded as a bite. Nonbite exposure consists of 

contamination of scratches, abrasions, mucous membranes, or previous wounds with

infected animal saliva. 

E. Rabies Immunization Status of Animal 

Vaccines are effective for cats and dogs but are not effective in preventing rabies in 

other animals, especially wild animals that have been domesticated (eg, pet skunks, 

foxes). 

F. Prevalence of Rabies in Region 

Certain areas are devoid of rabies (eg, San Francisco, Great Britain). Some rural areas 

are considered at high risk for rabies (eg, Texas-Mexico border). 

Management of Patients at High Risk 

Provide tetanus prophylaxis (see above), and give antibiotics if indicated (see above). 

Quickly administer appropriate postexposure rabies prophylaxis (see Figure 30-10 and 

Tables 30-4 and 30-5). 

Act quickly! The sooner antirabies measures are instituted, the more effective they are. 

A. Wound Care 

(This is the most important step.) Wash the wound copiously with 20% green soap 

tincture and water. Note: Quaternary ammonium compounds and alcohol are no longer 


B. Passive Immunization 

1. Rabies immune globulin USP—This neutralizing antibody should be given to all 

patients except those previously immunized who have documented antibody titers or 

those who have received preexposure human diploid cell rabies vaccine prophylaxis or 

a full course of human diploid cell rabies vaccine. Give 20 IU/kg at the onset of rabies 

therapy; rabies immune globulin can be given as late as the eighth day if necessary. 

Recommendations from the CDC in 1999 indicate that, if anatomically feasible, the full 

dose of rabies immune globulin should be thoroughly infiltrated in and around the 

wound; any remaining rabies immune globulin should be injected intramuscularly at a 

site distant from vaccine administration. Because rabies immune globulin may partially 

suppress the antibody response to vaccine, no more than the recommended dose 

should be given. 

2. Equine rabies immune globulin—This preparation should be used only when the 

human (USP) product is not available. Check for allergy to horse serum. The product 

contains 1000 IU/vial (about 5 mL). The dose is 40 IU/kg. 

C. Active Immunization 

Human diploid cell rabies vaccine is an inactivated virus vaccine prepared from rabies 

virus grown on human diploid fibroblasts. Give five 1-mL doses intramuscularly on 

specified days. The first dose is given as soon as possible after the bite; subsequent 

doses are given on days 3, 7, 14, and 28. No booster dose is needed. 

If preexposure human diploid cell rabies vaccine prophylaxis and adequate booster 

doses have been given (because of occupation as a veterinarian, for example), only two

1-mL intramuscular doses of human diploid cell rabies vaccine are needed, one as soon 

as possible after the bite and the other 3 days later. 

Routine serologic testing after treatment with human diploid cell rabies vaccine is not 

necessary unless the patient is immunocompromised or is taking corticosteroids. 

Individuals taking steroids should discontinue the medication while receiving antirabies 

treatment. 

4. Follow-up Care of the Wound 

After initial wound management, provisions must be made for follow-up and local wound 

care. Instruct the patient in how to recognize signs and symptoms of wound 

complications. A specific appointment for return should be made before discharge from 

the emergency department. It is helpful to supply patients with a printed list of danger 

signals and directions on wound care. 

Simple instructions giving specific details about wound care are useful in these 

situations. Patients want to know about limitations on activity, when they can bathe or 

shower, the type and frequency of dressing changes, when sutures will be removed, 

and precautions after suture removal. 

The changes that occur in a wound during the course of normal wound healing may 

cause anxiety, particularly if the wound is on the face and other exposed areas. The 

patient should be told that thickening of the area surrounding a scar usually abates by 3 

months. Redness of the scar usually persists for 3-6 months. The scar may assume 

various shades of blue depending on the environmental conditions. If the patient is 

prone to develop hypertrophic scars or keloids, it is wise to mention this possibility 

(particularly in children, adolescents, individuals of more heavily pigmented races, and 

pregnant women and in wounds of the shoulders, anterior chest, elbows, and knees). 

The fate of any wound as forming a "good" or "bad" scar is unpredictable. It is best to 

advise the patient that the ultimate appearance of the scar will not be known for at least 

9 months. Evaluation for possible scar revision should be delayed until after that time. 

5. Suture Removal 

The timing of suture removal depends on many factors such as location; type of wound 

closure; presence of infection; and the patient's age, health, and compliance. Table 30-6 

is a general guideline for suture removal in healthy adults with uncomplicated wounds. 

Modifications of these recommendations should be tailored to individual patterns. 

Abenavoli FM: Using Dermabond. Plast Reconstr Surg 2001; 108:269. [PMID: 

11420548] 

Bruns TB et al: Using tissue adhesive for wound repair: a practical guide to Dermabond. 

Am Fam Physician 2000;61:1383. [PMID: 10735344] 

Diphtheria, tetanus, and pertussis: recommendations for vaccine use and other 

preventive measures. Recommendations of the Immunization Practices Advisory

Committee (ACIP). MMWR Recomm Rep 1991;40(RR-10):1. [PMID: 1865873] 

Hollander JE: Laceration management. Ann Emerg Med 1999; 34:356. [PMID: 

10459093] 

Hsu SS et al. Tetanus in the emergency department: a current review. J Emerg Med 

2001;20:357. [PMID: 113488] 

Human rabies prevention—United States, 1999. Recommendations of the Advisory 

Committee on Immunization Practices (ACIP). MMWR Recomm Rep 1999;48(RR-1):1. 

[PMID: 10077411] 

Leach J: Proper handling of soft tissue in the acute phase. Facial Plast Surg 

2001;17:227. [PMID: 11735055] 

Thompson WL et al: Peripheral nerve blocks and anesthesia of the hand. Mil Med 

2002;167:478. [PMID: 12099083] 

Singer AJ et al: Closure of lacerations and incisions with octylcyanoacrylate: a 

multicenter randomized controlled trial. Surgery 2002;131:270. [PMID:1189403] 

EMERGENCY TREATMENT OF SPECIFIC TYPES OF WOUNDS 

FACIAL LACERATIONS (See Chapter 23.) 

INTRAORAL LACERATIONS 

Lacerations of the oral mucosa and tongue may not require closure if they are small. 

The rich blood supply promotes rapid healing, and cosmetic considerations are minimal. 

However, large or gaping wounds, through-and-through lacerations, and lacerations 

involving important deep structures, such as muscle or bone, require repair. In such 

wounds, after irrigation with saline, disrupted muscle should first be approximated with 

absorbable suture (eg, 5-0 Vicryl) and the mucosa closed with absorbable suture (eg, 

5-0 chromic gut or Vicryl). It is best to use the minimum number of sutures that will allow 

approximation of the wound edges. 

Through-and-through lacerations of the lip merit special attention: 

1. Irrigate the wound thoroughly, inside and out. A dry gauze roll between the lip and 

teeth will help prevent recontamination of the irrigated wound. 

2. Close the mucosal laceration with absorbable suture (eg, 5-0 chromic gut or Vicryl). 

3. Irrigate the wound again from the outside. The sutured mucosa will prevent reentry of 

saliva. 

4. If the orbicularis oris muscle is disrupted, approximate it with absorbable suture (eg, 

5-0 Vicryl).

5. Close the external skin with interrupted sutures of 6-0 monofilament nylon. Take 

extreme care to line up the opposing vermilion borders of the lip. 

6. Examine the adjacent teeth that produced the wound; they may be fractured or 

avulsed. 

BLAST INJURIES 


Wounds resulting from high-velocity missiles and shotgun blasts are among the most 

severe wounds encountered in civilian practice. Extensive tissue destruction is incurred 

locally, with loss or disruption of the wound parts to form a cavity. Sites distant from the 

point of impact may be injured as a result of shock waves transmitted through tissues. 

The extent of injury of these complex wounds is difficult to assess. 

Treatment 

Initial care is directed at hemostasis, cleansing, and minimal debridement. It is wise not 

to close the wound primarily. 

Repeated staged exploration at first presentation and then again 24 hours and 48 hours 

apart is used to remove necrotic or devitalized tissues. 

Antibiotic prophylaxis is recommended. Cefazolin, 1 g intravenously every 8 hours, is 

satisfactory. 

The wound is then closed secondarily, with priority given to reestablishment of bony 

relationships, followed by soft tissue coverage. 

Disposition 

Hospitalize all patients for management. 

HIGH-PRESSURE INJECTION INJURIES 


High-pressure injection equipment is used in industry to force liquids such as paint, 

paint thinner, oil, or grease through a small nozzle under high pressure, sometimes at 

pressure exceeding several thousand psi. If the nozzle is held against or close to the 

skin, it is possible for the liquid stream to be injected through the skin and into the 

subcutaneous tissues. 


These injuries have the potential for severe sequelae usually resulting from direct 

trauma and intense inflammation incited by the injected liquid. The edema that develops 

from the resulting inflammation can lead to increased tissue compartment pressures

and may lead to compartment syndrome. The type of injected material and amount and 

pressure velocity will determine the degree of inflammation and severity of injury. 

Patients with these types of injuries usually have small puncture wounds that are usually 

isolated to the extremities. Patients often present with pain out of proportion to the 

appearance of the wound and, if early, often with only minimal swelling. Because the 

material is injected at great force, the distance it can be injected into the tissues from 

injection site can be significant. 


Carefully assess neurovascular function at the time of presentation and attempt 

appropriate pain control via parenteral analgesics. Avoid digital blocks because of the 

resulting increase in pressure. Parenteral antibiotics should also be initiated at first 

presentation, directed at normal skin flora (Staphylococcus and Streptococcus). 

Appropriate radiographs should be obtained because some materials are radiopaque 

and may demonstrate the extent of subcutaneous spread and may also show the 

presence of subcutaneous emphysema. Early consultation with a hand specialist or 

other surgical specialist for early surgical debridement and follow-up is recommended. 

DEGLOVING INJURIES 


Separation of the skin and subcutaneous tissues from the underlying musculofascial 

planes constitutes a degloving injury. For flaps attached by a pedicle, the determinant of 

survival is their circulation. 


All but trivial degloving injuries require hospitalization. Plastic surgical consultation is 

advisable. 

AMPUTATIONS 


The greater the degree of ischemic injury resulting from interruption of blood flow, the 

less the chances for survival of the amputated part. Six hours is probably the longest 

time an amputated part can be deprived of its blood supply without cooling and still 

survive. Immediate cooling increases the tolerable ischemic time of the amputated part 

to 12-24 hours. This is particularly important when replantation must be delayed while 

the patient is transferred to a hospital where a surgical team skilled in replantation is 

available. 

Contraindications to replantation are the presence of significant associated injuries that 

may be life threatening, severe degloving or crush injuries of the amputated part, and 

major systemic disease.

Treatment 

To ensure the most expeditious management, every emergency department should 

know the location of the nearest microvascular replantation center before arranging for 

patient transfer. Initial treatment is outlined here: 

1. Gently cleanse the amputated part of gross contaminants; dry it; and place it in a 

clean, dry polyethylene bag. Place the bag in regular (wet) ice or in a refrigerator at 4 °C 

(about 40 °F). 

2. Control hemorrhage by pressure or elevation, or by tourniquet if the other methods 

are not successful. Gently cleanse the wound and cover it with a sterile dressing. 

3. Consider antimicrobial and tetanus prophylaxis in most instances. A parenteral 

cephalosporin is commonly used for these purposes (eg, cefazolin, 1 g intravenously). 

4. Reestablish normal blood volume. Blood transfusion may be necessary, because 

these injuries are occasionally associated with major blood loss. 

Disposition 

Immediately refer the patient to a facility where limb replantation can be done by experts 

in that procedure. 

BITES 

Most nonprimate mammalian bite wounds are minor, and only about 10% require 

suturing. The rare patient with major injuries sustained in an animal attack should be 

evaluated and receive treatment as any other patient with severe trauma. 

Meticulous wound care is the cornerstone of therapy for bite wounds and is the most 

important factor in preventing infection. The wound should be cleansed, debrided, and 

copiously irrigated. Treat all bite wounds on the extremities aggressively, with antibiotics 

and elevation and immobilization of the affected part. 

Routine cultures in the absence of infection need not be obtained, because there is no 

useful correlation between positive cultures and wounds that later develop clinical signs 

of infection. 

Antimicrobial prophylaxis (see Table 30-2) is recommended for all human and most cat 

bites but only for high-risk dog bites (below). The need for tetanus and rabies 

prophylaxis (Tables 30-3 and 30-4) should also be evaluated. 

1. Dog Bites 

Dog bites cause open wounds, often with tissue necrosis secondary to crush injury. 

Treat by prompt excisional debridement within 6 hours. If the extent of the wound or the 

length of time since injury precludes primary closure, the wounds should be irrigated, 

debrided, and left open or loosely sutured. Infection is unusual, and antimicrobial

prophylaxis is not indicated in routine cases. 

Dog bites associated with a high risk of infection are those of the hand, puncture 

wounds, and injuries more than 6-12 hours old. These wounds should be treated with 

vigorous local care and left unsutured. Antibiotic prophylaxis is recommended; 

amoxicillin/ clavulante 875/125 mg BID is the treatment of choice. An alternative is 

clindamycin 150-450 mg QID plus ciprofloxacin 500 mg BID. A three to five-day course 

is recommended. Low-risk bites do not require prophylactic antibiotics and may be 

sutured after appropriate wound care. Hospitalization is rarely indicated unless injuries 

are multiple or extensive or infection is present. 

Infected bites should be cleansed and debrided and the affected limb immobilized and 

elevated. A parenteral dose of a first-generation cephalosporin (eg, cefazolin, 1 g for 

adults, 8-17 mg/kg for children, intravenously) should be administered in the emergency 

department and the patient discharged with oral antibiotics (same as those for 

prophylaxis, above) for 7-10 days. Patients should receive follow-up care within 1-2 

days and be instructed to return earlier if their condition worsens. Hospitalize patients 

who have symptoms of sepsis. 

2. Cat Bites 

Cat bites cause deep puncture wounds with little crush injury and are associated with a 

high risk of infection, mainly with Pasteurella multocida. Wounds caused by cat claws 

are considered equivalent to bites. Treatment includes local cleansing, debridement, 

and prophylactic antibiotics for all significant bites. Amoxicillin-clavulanate is the 

treatment of choice (Table 30-2). 

Cat bite infections occurring within 24 hours are due to P multocida and should be 

treated as above. Wounds becoming infected after 24 hours should be treated with a 

first-generation cephalosporin or amoxicillin/clavulante (see Dog Bites, above) for 7-10 

days. 

Hospitalization is rarely indicated unless infection is severe or involves the hand. 

Primary closure should not be performed except in low-risk, cosmetically disfiguring 

facial bites. 

3. Human Bites 


Adult human bites are more serious than dog or cat bites. They are characterized by 

crush and tear injuries and are commonly located over the knuckles or the dorsum of 

the hand, frequently involving the tendons or joints. Inoculation of large numbers of 

bacteria from dental plaque also occurs. (Bites by children appear to carry a low risk of 

infection because of fewer mouth bacteria and less biting force.) Despite their rather 

innocuous initial appearance, these wounds are extremely dangerous, because they are 

prone to severe necrotizing infection. 


Hospitalize patients with suspected tendon, joint, or cartilage involvement (eg, bites of 

the hand or ear) for vigorous irrigation, debridement, and parenteral antimicrobials 

(high-dose penicillin or clindamycin). Wounds of this type are never closed. Bites of 

other structures may be treated with vigorous irrigation and debridement in the 

emergency department, followed by antimicrobial prophylaxis (see Table 30-2). The 

injured part should be elevated, immobilized, and checked frequently to assess the 

possible spread of infection. The patient should be reexamined within 6-18 hours and 

subsequently at 1- to 2-day intervals for a week. 

Signs of necrotizing infection are progressive erythema, blistering, and frank necrosis. If 

these signs are already present at the time of initial evaluation, hospitalization is 

indicated for wide debridement of the involved parts and parenteral antimicrobial 

therapy. 

PUNCTURE WOUNDS 


Puncture wounds are at risk of becoming infected, especially if dirty, contaminated, or 

containing foreign materials. Wounds associated with penetration through the soles of 

shoes (especially sneakers) often contain particles of debris and are particularly 

susceptible to infection. If joint capsule or bone is penetrated, septic arthritis and 

osteomyelitis can occur. Pseudomonas species are common pathogens. 

All puncture wounds should be probed gently with forceps or a long (6.5-cm or 2.5-in), 

22-gauge needle for the presence of foreign bodies; control pain as needed with 1% 

lidocaine anesthetic. Obtain soft-tissue x-rays of all wounds for which the history or 

mechanism of injury suggests retention of a foreign body (eg, broken glass, flying piece 

of metal), even if results of the wound probe are negative. 


A. Wound Cleansing and Exploration 

Irrigate the wound with normal saline under pressure and cleanse it with 1% 

povidone-iodine solution. Probe gently and remove foreign materials. Local infiltration 

with 1% lidocaine and slight enlargement of the wound may be necessary for adequate 

exploration. Extensive dissection in the emergency department to search for small or 

deeply embedded objects is not recommended. 

B. Tetanus and Antibiotics Prophylaxis 

Ensure that tetanus prophylaxis is up to date (see Table 30-3). Treat dirty or deep 

wounds (especially those with possible joint or bone involvement) with prophylactic 

antibiotics (Table 30-2). If penetration occurred through the sole of a sneaker (unless 

very superficial), consider prophylaxis against the high risk of Pseudomonas infection 

with antipseudomonal cephalosporin as a single parenteral dose (eg, ceftazidime, 1 g 

intramuscularly) or ciprofloxacin 500 mg BID for 3-5 days. 

C. Elevation and Follow-up

Instruct patients to elevate any involved extremity and, in foot injuries, to bear no weight 

for 3-5 days. Except in the case of superficial punctures, patients should be reexamined 

in 5-7 days or earlier if increased pain, redness, red streaking, or pus is noted. 

D. Osteomyelitis 

Patients with pain persisting longer than 5-7 days or with an abnormal erythrocyte 

sedimentation rate may have osteomyelitis. In either case, obtain x-rays of the affected 

area and, if normal, consider limited bone scan of the area. Refer patients with 

osteomyelitis to the specialist appropriate to the area of involvement. 

E. Retained Foreign Bodies 

Retained foreign bodies in critical areas (eg, eye) require urgent specialty consultation. 

Refer patients with possible retained foreign bodies in noncritical areas for outpatient 

surgical removal in 2-3 weeks. 

Armstrong BD: Lacerations of the mouth. Emerg Med Clin North Am 2000;18:471. 

[PMID: 10967735] 

Baldwin G et al: Puncture wounds. Pediatr Rev 1999;20:21. [PMID: 9919048] 

Bower MG: Evaluating and managing bite wounds. Adv Skin Wound Care 2002;15:88. 

[PMID: 11984053] 

Chrisodoulou L et al: Functional outcome of high-pressure injection injuries of the hand. 

J Trauma 2001;50:717. [PMID: 1303170] 

Goldstein EJ: Current concepts on animal bites: bacteriology and therapy. Curr Clin Top 

Infect Dis 1999;19:99. [PMID: 10472482] 

Howes DS et al: Triage and initial evaluation of the oral facial emergency. Emerg Med 


Lewis HG et al: A 10-year review of high-pressure injection injuries to the hand. J Hand 

Surg [Br] 1998;23:479. [PMID: 9726548] 

Markal N et al: Compression neuropathy of the hand after high-pressure air injection. 

Ann Plast Surg 2000;44:680. [PMID: 10884095] 

Mizani MR et al: High-pressure injection injury of the hand. The potential for disastrous 

results. Postgrad Med 2000;108:183. [PMID: 0914127] 

Presutti RJ: Prevention and treatment of dog bites. Am Fam Physician 2001;63:1567. 

[PMID: 11327433] 

Schnall SB et al: High-pressure injection injuries to the hand. Hand Clin 1999;15:245. 

[PMID: 10361635] 

Soucacos PN: Indications and selection for digital amputation and replantation. J Hand 

Surg [Br] 2001;26:572. [PMID: 11884116]

Vasilevski D et al: High-pressure injection injuries to the hand. Am J Emerg Med 

2000;18(7):820. [PMID: 11103737] 

Wrightman JM et al: Explosions and blast injuries. Ann Emerg Med 2001;37:664. 

[PMID: 11385339] 





EMERGENCY MANAGEMENT OF LIFE-THREATENING PROBLEMS

Table 30-1. Drugs used for local anesthesia. 1 

Cocaine 

Tetracaine 2 

(Pontocaine) 

Bupivacaine 2 

(Marcaine, 

Sensoricaine) 

Potency (compared 

to procaine) 

4 10 4-6 Stability at sterilizing 

temperature 

100-200 mg 50-100 mg 175 mg Total maximum 

pediatric dose 

. . . 

Concentration 3 1-2% 1-2% 1-2% 

Onset of action 5-15 min 5-10 min 5-10 min 

Duration 

2 

Not recommended for children. 

45-60 min 1-1 1/2 h 1 1/4-2 1/2h 

3 0.5% solution = 5 mg/mL; 1% solution = 10 mg/mL; 2% solution = 20 mg/mL. 





TABLES 

Table 30-1. Drugs used for local anesthesia.

Table 30-2. Choice of antimicrobials for prevention of infection in specific types 

of wounds. 1 

Antimicrobial Human bite Cefuroxime 

of Choice 

250-500 mg BID 

Amoxicillin/Clavulanate 

875/125 mg BID 

Other wounds Clindamycin 

150-450 mg QID 

or 

Cephalexin 

500 mg QID

Table 30-3. Guide to tetanus prophylaxis in wound management. 1 

Clean Minor 

Wounds 

Td 2 

Td 2 

Yes Yes 2 No No 3 

No 4 1 Adapted 

from MMWR 

1991;40:1. 

2 

Td = tetanus and diphtheria toxoids, adult type, for persons over 7 years 

of age. DTP for children under 7 years of age. TIG = tetanus immune 

globulin. 

3 

Unless wound is more than 24 hours old. 

No 4 

4 Unless it has been more than 10 years since last dose. 


Uncertain No 




TABLES 

Table 30-3. Guide to tetanus prophylaxis in wound management.

Table 30-4. Rabies postexposure prophylaxis guide. 1 

Animal Species 

Healthy and available for 10 

days of observation. 

Unknown (escaped). Wild 

Skunk, bat, fox, coyote, 

raccoon, bobcat, and other 

carnivores 

RIG 4 and HDCV. 5 

Consider individually. Local and 

state public health officials 

should be consulted on 

questions about the need for 

rabies prophylaxis. Bites of 

squirrels, hamsters, guinea pigs, 

gerbils, chipmunks, rats, mice, 

other rodents, rabbits, and hares 

almost never call for antirabies 

prophylaxis.

Table 30-5. Rabies immunization regimens. 1 

Preexposure rabies prophylaxis for persons with special risks of exposure to rabies, such as animal 

care and control personnel and selected laboratory workers, consists of immunization with either 

human diploid cell rabies vaccine (HDCV) or duck embryo vaccine (DEV), according to the following 

schedule, followed by a booster dose every 2 years. 

Number 

of 1-mL 

Doses 

Intervals 

Between Doses 

HDCV Intramuscular 1 booster dose. 3 

Postexposure rabies prophylaxis for persons exposed to rabies consists of the immediate, thorough 

cleansing of all wounds with soap and water, administration of rabies immune globulin (RIG) or, if 

RIG is not available, antirabies serum, equine (ARS), and the initiation of either HDCV or DEV, 

according to the following schedule. 

Number 

of 1-mL 

Doses 

Intervals 

Between Doses 

HDCV Intramuscular An additional booster 

dose. 5

Table 30-6. Timing of suture removal. 

Time (Days) 

3 

Cheek 5 

Ear, scalp 7-10+ 

Chest, back, abdomen

Figure 30-1. Injection of local anesthetic for wound closure. (Reproduced, with 

permission, from Dunphy JE, Way LE [editors]: Current Surgical Diagnosis & Treatment, 

5th ed. Lange, 1981.) 





FIGURES 

Figure 30-1

Figure 30-2. Radial nerve block, in which anesthetic is injected in a 2-cm (3/4-in) wide 

band 4 cm (19/16 in) proximal to the Lister tubercle on the radial aspect of the forearm. 

(Modified and reproduced, with permission, from Newmeyer WL: Care of Hand Injuries. 

Lea & Febiger, 1979.) 





FIGURES 

Figure 30-2

Figure 30-3. Median nerve block. Inject anesthetic around the median nerve just 

proximal to the wrist. The nerve is located between the tendons and the palmaris longus 

and flexor carpi radialis. (Modified and reproduced, with permission, from Newmeyer 

WL: Care of Hand Injuries. Lea & Febiger, 1979.) 





FIGURES 

Figure 30-3

Figure 30-5. Infraorbital nerve block. Intraoral or percutaneous injection around the 

palpable infraorbital foramina will result in anesthesia within the stippled area. 





FIGURES 

Figure 30-5

Figure 30-4. Ulnar nerve block. Inject anesthetic around the ulnar nerve just proximal to 

the wrist on either side of the flexor carpi ulnaris. (Modified and reproduced, with 

permission, from Newmeyer WL: Care of Hand Injuries. Lea & Febiger, 1979.) 





FIGURES 

Figure 30-4

Figure 30-6. Supraorbital nerve block. Inject anesthetic slightly superior to the orbital 

ridge at the supraorbital notch. Stippling shows area of anesthesia from ipsilateral 

injection. 





FIGURES 

Figure 30-6

Figure 30-7. Epidermal closure with tape. Top: Gentle traction is applied on the 

Steri-Strip to approximate the edges. Bottom: Closure of the wound. (Reproduced, with 

permission, from Dunphy JE, Way LE [editors]: Current Surgical Diagnosis & Treatment, 

5th ed. Lange, 1981.) 





FIGURES 

Figure 30-7

Figure 30-8. Layered cutaneous closure. 





FIGURES 

Figure 30-8

Figure 30-9. Percutaneous suture. Ideal placement of the suture everts the wound 

margins. This is accomplished by directing the needle away from the wound margin at 

the entrance point and toward the wound margin at the exit point. The path of a properly 

placed percutaneous suture will be wider at its base than at the skin entry and exit 

points. 





FIGURES 

Figure 30-9

Figure 30-10. Algorithm for management of possible rabies exposure. 





FIGURES 

Figure 30-10


31. Eye Emergencies 1 - William R. Dennis, Jr, MD, & Alia M. Dennis, 

MD 

I. EMERGENCY EVALUATION OF IMPORTANT OCULAR SYMPTOMS 

EVALUATION OF THE RED OR PAINFUL EYE (See Figure 31-1 and Table 31-1.) 

History & Examination 

1 This chapter is a revision of the chapter by Kalid F. Tabbara, MD, from the 4th edition. 

Historical factors are important in determining the cause of ocular complaints. History, 

when correlated with characteristic ocular findings, usually makes the diagnosis. A 

complete eye examination includes the following: 

A. Visual Acuity 

Test corrected visual acuity using a standard acuity chart (Snellen). Abnormal acuity in 

a patient who normally has 20/20 vision usually indicates disease of the eyeball or 

visual pathway. Pain and decreased acuity indicate corneal disease, acute 

angle-closure glaucoma, or iritis. 

B. Inspection 

Inspect external lids, lashes, lacrimal ducts, orbit, and periorbital area for any signs of 

trauma, infection, exudate, and the like. 

C. Pupillary Function 

Check for symmetrical pupils and reactivity to light and accommodation. 

D. Extraocular Motility 

Check for integrity of extraocular muscles and note any abnormalities. 

E. Visual Fields 

Check for abnormalities in the visual fields. 

F. Slit Lamp Examination 

Slit lamp examination should be done before and after fluorescein staining. 

G. Intraocular Pressure 

Intraocular pressure can be tested with a Tono-Pen or Schiotz tonometer (described 

later in this chapter). 

H. Funduscopy

Funduscopy is used to check the retinal field. 

I. Other Studies 

Further diagnostic studies including laboratory specimens, plain x-rays, computed 

tomography (CT) scan, or magnetic resonance imaging of the orbits may be needed to 

establish the diagnosis. 

Disposition 

Patients thought to have ocular conditions that may permanently decrease visual acuity 

(eg, acute angle-closure glaucoma) should be hospitalized. Patients with other 

conditions may receive treatment and be discharged if close follow-up evaluation is 

ensured. 

EVALUATION OF ACUTE UNILATERAL VISUAL LOSS (See Figure 31-2. ) 

Look for Trauma 

Exclude trauma as a cause of visual loss. Both blunt and penetrating ocular injuries may 

result in blindness. 

History & Examination 

Obtain a history from the patient (rate of onset of visual loss; whether it is unilateral or 

bilateral, painful or painless, with or without redness). Ophthalmologic examination 

should emphasize visual acuity and visual field testing. 

A. Inability to Visualize Retina 

Cloudy media will completely obscure the retina (red reflex absent) or will make it 

impossible to visualize retinal landmarks such as the optic disk. Chronic causes of hazy 

media are common (eg, cataracts) and should not be confused with whatever is causing 

acute visual loss. 

B. Abnormal Visual Fields 

Grossly abnormal visual fields are usually caused by central nervous system disease 

and thus generally affect both eyes (not always to the same degree). The retinas are 

usually normal on ophthalmoscopic examination. 

1. Hemianopia—Hemianopia is usually due to postchiasmal neurologic disorders (eg, 

tumor, aneurysm, migraine, stroke), in which case other acute neurologic lesions are 

present as well. Rarely, it is psychogenic in origin. 

2. Central scotoma—A central scotoma indicates isolate macular involvement typical of 

retrobulbar neuritis and may or may not be associated with pain. 

3. Tubular vision—Tubular vision not in conformity with the laws of optics is 

characteristic of psychogenic visual loss. 

C. Abnormal Retina

An abnormal retina, usually in the eye with visual loss, is characteristic of several rare 

but serious conditions. 

1. Central retinal artery occlusion—In central retinal artery occlusion, the fundus is 

usually pale with a cherry-red fovea. This is a medical emergency. (See below.) 

2. Central retinal vein occlusion—Central retinal vein occlusion is associated with 

multiple widespread retinal hemorrhages. 

3. Retinal hemorrhage—Retinal hemorrhage from other causes (eg, anticoagulation) 

may produce visual loss. 

4. Retinal detachment—Retinal detachment produces visual loss preceded by visual 

flashes. If visual acuity is affected, detachment is large and easily visible on direct 

ophthalmoscopy; however, small detachments may require indirect ophthalmoscopy for 

visualization. Flashes of light may also occur in patients with migraine or as a result of 

posterior vitreous detachment. 


Causes of acute visual loss are listed below and discussed on subsequent pages. 

A. Acute Angle-Closure Glaucoma 

Acute angle-closure glaucoma causes corneal edema, but the more striking findings are 

eye pain; pupils fixed in mid position or dilated, often with irregular margins; a shallow 

anterior chamber angle (Figure 31-3); and greatly increased intraocular pressure. Acute 

angle-closure glaucoma is a medical emergency. (See below.) 

B. Corneal Edema 

Severe corneal edema of diverse causes (eg, abrasion, keratitis) may cause visual loss 

with eye pain. 

C. Hyphema 

Hyphema is associated with blood in the anterior chamber on inspection. 

D. Vitreous Hemorrhage 

Vitreous hemorrhage causes painless visual loss, which is often total. The anterior 

chamber is clear. The red reflex is often absent. 

E. Endophthalmitis 

Endophthalmitis (intraocular infection) is a rare condition usually associated with eye 

pain and decreased visual acuity. Eye examination will disclose pus in the anterior 

chamber or vitreous. 

Disposition 

All patients with sudden visual loss due to ocular disease should be seen by an 

ophthalmologist before being discharged from the emergency department.

Leibowitz HM: The red eye. N Engl J Med 2000;343:345. [PMID: 10922425] 

Markoff DD et al: Common ophthalmologic emergencies: examination, differential 

diagnosis, and therapeutic management. Emerg Med Rep 1999;20:1. 

II. OCULAR CONDITIONS REQUIRING IMMEDIATE TREATMENT 

ACUTE ANGLE-CLOSURE GLAUCOMA 


• Severe pain, blurred vision, nausea and vomiting. 

• Red, nonreactive mid-dilated pupil. 

• Increased intraocular pressure confirms diagnosis. 


Acute angle-closure glaucoma results from sudden increase in intraocular pressure 

owing to blockage of the outflow channels in the anterior chamber angle by the iris root. 

The sudden rise in intraocular pressure causes intraocular vascular insufficiency, which 

may lead to optic nerve or retinal ischemia. If the acute attack of angle-closure 

glaucoma is not managed promptly, permanent vision loss may result. 


Acute angle-closure glaucoma is characterized by severe pain, halos around lights, 

blurred vision, photophobia, and nausea and vomiting. The affected eye is red, with a 

nonreactive middilated pupil (often with irregular margins), a hazy cornea, and a shallow 

anterior chamber angle. Intraocular pressure is usually markedly increased (see below 

for the technique of tonometry). The patient may have hyperopia (farsightedness). 


See Figure 31-2 and Table 31-1. In iridocyclitis (iritis), intraocular pressure is normal 

and the pupil is small and constricted. In conjunctivitis, intraocular pressure is normal 

and the pupil is not affected. Corneal ulcer is diagnosed by fluorescein staining of the 

cornea. 

Treatment 

Acute angle-closure glaucoma is an emergency. Failure to provide prompt treatment 

may result in permanent blindness. Hospitalize the patient, and obtain immediate 

ophthalmologic consultation for management. 

Reduce the intraocular pressure by one or more of the following means: 

• Timolol, 0.5%, 1 drop in the affected eye

• Pilocarpine, 2% eye drops, 2 drops every 15 minutes for 2-3 hours 

• Mannitol, 20%, 250-500 mL intravenously over 2-3 hours 

• Acetazolamide, 500 mg orally or 250 mg intravenously 

• Glycerin, 1g/kg orally in cold 50% solution mixed with chilled lemon juice 

Give sedation and analgesics as necessary to control pain and agitation. 

Disposition 

Acute angle-closure glaucoma calls for urgent referral to an ophthalmologist and 

hospitalization for initial medical treatment, followed by definitive surgical therapy. 

CENTRAL RETINAL ARTERY OCCLUSION 


• Sudden, painless complete loss of vision. 

• Exam shows pallor of disk, retinal edema, and "boxcar" appearance of retinal veins. 

• Treatment must be initiated immediately. 


Central retinal artery occlusion is most commonly embolic in origin. The retina is 

completely without blood as long as the artery is occluded, and visual receptors in the 

retina will degenerate within 30-60 minutes if blood flow is not restored. BR> 


There is a typical history of sudden, complete, painless loss of vision in one eye, usually 

in an older person. Ophthalmoscopic examination discloses pallor of the optic disk, 

edema of the retina, cherry-red fovea, bloodless constricted arterioles that may be 

difficult to detect, and "boxcar" segmentation of blood in the retinal veins. 

Treatment 

Central retinal artery occlusion is an emergency. If occlusion has persisted for over 1 

hour without treatment, vision has most likely been lost permanently; however, 

aggressive treatment should still be started. Visual recovery has occurred up to 3 days 

after central retinal artery occlusion. It is recommended that treatment be started if the 

patient is seen within 24 hours after onset of symptoms. 

Treatment measures consist of ocular massage (moderate pressure for 10 seconds and 

release for 5 seconds), anterior chamber paracentesis, intravenous acetazolamide, or 

inhaled carbogen (oxygen-carbon dioxide mixture of 95% oxygen and 5% carbon

dioxide). Other modalities to be considered by ophthalmology are direct infusion of 

tissue plasminogen activator (t-PA) or urokinase in the ophthalmic artery. 

Disposition 

All patients should be hospitalized on an emergent basis for treatment by an 

ophthalmologist. 

ORBITAL CELLULITIS 


• Redness around the orbit. 

• Pain with extraocular movement. 

• Intravenous antibiotics and emergent consultation for admission. 


Acute infection of the orbital tissues is commonly caused by Streptococcus 

pneumoniae, other streptococci, Staphylococcus aureus, and (chiefly in children) 

Haemophilus influenzae. Less frequently, certain fungi of the Phycomycetes group may 

cause orbital infections in diabetic patients (rhinoorbitocerebral mucormycosis). Most 

causative organisms enter the orbit by direct extension from the paranasal sinuses 

(especially through the ethmoid sinus) or through the vascular channels draining the 

periorbital tissues. Rarely, infection may spread to the cavernous sinus or meninges. 


There is a history of sinusitis or periorbital injury, pain in and around the eye, and 

sometimes reduced visual acuity. Examination discloses swelling and redness of the 

eyelids and periorbital tissues, chemosis of the conjunctiva, exophthalmos, and 

limitation of movement of the eye in all fields of gaze. Disk margins may be blurred, and 

fever is commonly present. There may be x-ray evidence of sinusitis. CT scan shows 

soft tissue orbital infiltration. 

Patients with invasive infection due to fungi of the Phycomycetes group (Mucor, 

Rhizopus, and other genera) may present with rapidly progressive orbital cellulitis, often 

with cavernous sinus thrombosis. Diabetic and immunocompromised patients are at 

increased risk. Examination often reveals coexisting maxillary and/or ethmoid sinusitis 

and palatal or nasal mucosal ulceration. 


Obtain cultures of blood and periorbital tissue fluid. Patients should be admitted and 

appropriate broad-spectrum intravenous antibiotics started (clindamycin and 

ceftazidime). Obtain immediate otolaryngologic (ENT) or ophthalmologic consultation. 

Obtain CT scan of the orbit to rule out orbital abscess and intracranial involvement.

Patients with orbital phycomycosis are given intravenous amphotericin B and require 

surgical intervention for debridement of infected tissue. Neurosurgical consultation is 

required to rule out intracranial involvement. 

CAVERNOUS SINUS THROMBOSIS 


• Complication from facial or sinus infections. 

• Headache, nausea, pain, and decreased vision are nonspecific symptoms. 

• Intravenous antibiotics early. 


Cavernous sinus thrombosis is usually associated with orbital and ocular signs and 

symptoms. The disease results from hematogenous spread of infection from a distant 

focus or from extension from a throat, facial, paranasal sinus, or orbital infection. 

Cavernous sinus thrombosis starts as a unilateral infection and commonly spreads to 

involve the other cavernous sinus. 


The patient complains of chills, headache, lethargy, nausea, pain, and decreased vision. 

Fever, vomiting, and other systemic signs of infection are present. Ophthalmologic 

examination discloses unilateral or bilateral exophthalmos, absent pupillary reflexes, 

and papilledema. Involvement of the third, fourth, and sixth cranial nerves or of the 

ophthalmic branch of the fifth nerve leads to limitation of ocular movement and decrease 

in the corneal sensation. 


Hospitalize the patient immediately, and send blood to the laboratory for culture and 

sensitivity studies and start appropriate antibiotics. Seek ophthalmologic, neurologic, 

and medical consultation early. Obtain CT scan of the head and orbit. 

ENDOPHTHALMITIS 


• Pus in anterior chamber is diagnostic. 

• Obtain emergent ophthalmology consultation for drainage and antibiotic treatment. 


Endophthalmitis is an acute microbial infection confined within the globe. Infection

involving the sclera as well as other intraocular structures is called panophthalmitis. 

Infections of the globe can be exogenous or endogenous. Exogenous infection results 

from penetrating injury or may follow intraocular surgery or a ruptured corneal ulcer. 

Endogenous infection by the hematogenous route is less common and may be 

accompanied by fever and chills. 


The patient complains of pain, blurred vision, and photophobia. Examination discloses 

redness of the eye, chemosis of the conjunctiva, swelling of the eyelid, hypopyon (pus in 

the anterior chamber), and cloudy media (fundus hazily seen, or absent red reflex). 


Send blood (2 specimens) for culture and sensitivity studies. Obtain emergent 

ophthalmologic consultation. Give sedation and analgesics. 

The patient may have to undergo anterior chamber tap and vitreous aspiration (by an 

ophthalmologist). Send specimens thus obtained for staining with Giemsa and Gram 

stains and for cultures on appropriate media. 

Check stained smears of ocular fluid, and if no organisms are seen, give empiric 

subconjunctival and systemic antibiotics while results of culture are pending. 

RETINAL DETACHMENT 


• Painless decrease in vision. 

• History of flashes of light, then "curtain" in front of eye. 

• Urgent consultation for surgical repair. 


Detachment of the retina is actually separation of the neurosensory layer from the 

retinal pigment epithelium. Subretinal fluid accumulates under the neurosensory layer. 

Detachment may become bilateral in one fourth of cases. Retinal detachment is more 

common in older people and in those who are highly myopic. Hereditary factors may 

also play a role. Three types of primary retinal detachment are recognized: (1) 

rhegmatogenous detachment, from retinal holes or breaks, (2) exudative detachment, 

usually from inflammation, and (3) traction detachment, which occurs when vitreous 

bands pull on the retina. Minimal to moderate trauma to the eye may cause retinal 

detachment, but in such cases predisposing factors such as changes in the vitreous, 

retina, and choroid play an important role in pathogenesis. Severe trauma may cause 

retinal tears and detachment even if there are no predisposing factors. 

Clinical Findings

The patient complains of painless decrease in vision and may give a history of flashes 

of lights or sparks. Loss of vision may be described as a curtain in front of the eye or as 

cloudy or smoky. Central vision may not be affected if the macular area is not involved; 

this frequently causes a delay in seeking treatment. Patients in whom the macula is 

detached present to the emergency department with sudden deterioration of vision. 

Intraocular pressure is normal or low. The detached retina appears gray, with white 

folds and globular bullae. Round holes or horseshoe-shaped tears may be seen by 

indirect ophthalmoscopy in the rhegmatogenous detachment. Vitreous bands or other 

changes may be seen in the traction type of detachment. 


Primary retinal detachment should be differentiated from detachment secondary to other 

causes, for example, from preeclampsia-eclampsia or tumors of the choroid. 


Arrange for immediate referral to an ophthalmologist. If the macula is attached and 

central visual acuity is normal, the condition should be urgently treated by an 


Retinal reattachment can be accomplished only by surgery, which is successful in about 

80% of cases. If the macula is detached or threatened, operation should be scheduled 

on an urgent basis, because prolonged detachment of the macula results in permanent 

loss of central vision. 

TOXIC CAUSES OF BLINDNESS 

A wide variety of organic chemicals may lead to visual deterioration. Ingestion of 

chemicals that cause corneal or lenticular opacities usually leads to insidious onset of 

visual loss. Ingestion of compounds that cause damage to nervous tissue may lead to 

slow or rapid deterioration of vision. Exposure to toxic doses of methanol, halogenated 

hydrocarbons (eg, methyl chloride), arsenic, and lead may cause permanent visual 

damage. Acute or chronic administration of drugs such as ethambutol, chloramphenicol, 

quinine, and salicylates may also cause optic neuritis and loss of vision. 

By far the most common toxic cause of blindness is methanol (methyl alcohol). 

Ingestion of only a few milliliters may cause permanent blindness. Acute methanol 

poisoning causes nausea and vomiting and abdominal pain. Headache, dizziness, and 

delirium may occur. Loss of vision may be complete and sudden a few hours after 

drinking methanol or may occasionally be noted about 3 days after exposure. Pupillary 

reflexes are sluggish. Ophthalmoscopic examination shows swelling and hyperemia of 

the optic nerve head, distention of the veins, and peripapillary edema of the retina. 

Hospitalize the patient immediately. See Chapter 45 for details of evaluation and 

treatment.

Banker AS et al: Retinal detachment. Ophthalmol Clin North Am 2001;14:695. [PMID: 

11787748] 

Beatty S et al: Acute occlusion of the retinal arteries: current concepts and recent 

advances in diagnosis and management. J Accid Emerg Med 2000;17:324. [PMID: 

11005400] 

Danis RP: Endophthalmitis. Ophthalmol Clin North Am 2002;15:243. [PMID: 12229241] 

Hitchings RA: Glaucoma in the new millennium. Ophthalmol Clin North Am 

1999;12:519. 

Jain A et al: Orbital cellulitis in children. Int Ophthalmol Clin 2001;41:71. [PMID: 

11698739] 

McGuigan ME: Poisoning potpourri. Pediatr Rev 2001;22:295. [PMID: 11533378] 

Migirov L, Eyal A, Kronenberg J: Treatment of cavernous sinus thrombosis. Isr Med 

Assoc J 2002;4:468. [PMID: 12073429] 

Sharma S et al: Retinal artery occlusions. Ophthalmol Clin North Am 1998;11:591. 

III. NONTRAUMATIC OCULAR EMERGENCIES 

ACUTE DACRYOCYSTITIS 


• Swelling, redness, and tenderness over the lacrimal sac. 

• Warm compresses and systemic antibiotics for treatment. 


Acute infection of the lacrimal sac occurs in children and adults as a complication of 

nasolacrimal duct obstruction. The most frequently encountered causative organism is S 

pneumoniae. 


The patient complains of pain. There may be a history of tearing and discharge. 

Examination discloses swelling, redness, and tenderness over the lacrimal sac (Figure 

31-4). 

Pus should be collected, for Gram-stained smear and culture, by applying pressure over 

the lacrimal sac. 

Treatment

Prescribe warm compresses 3-4 times daily. Begin appropriate systemic antibiotic 

therapy with first-generation cephalosporin or amoxicillin-clavulanate, until culture 

results are reported. Results of Gram-stained smears of purulent exudate may be 

helpful in guiding empiric therapy. Topical sulfacetamide, 10% eye drops, may be given 

every 2 hours, and erythromycin ophthalmic ointment, 0.5% (5 mg/g), may be used at 

bedtime. 

Massage of the nasolacrimal sac to express purulent discharge through the punctum is 

helpful in infants. The technique is to apply pressure over the lacrimal sac with a cotton 

swab (Q-tip). Irrigation of the lacrimal sac with diluted antibiotics should be done by an 


Disposition 

The patient can be discharged to home care with a prescription for systemic antibiotics 

and instruction in how to apply warm local compresses. Consult an ophthalmologist for 

consideration of surgical correction. The patient should be seen again within 3-4 days. 

ACUTE DACRYOADENITIS 


• Swelling and pain over temporal aspect of upper eyelid. 


Infection and inflammation of the lacrimal gland is characterized by swelling, pain and 

tenderness, and redness over the upper temporal aspect of the upper eyelid. 


Acute dacryoadenitis must be differentiated from viral infection (mumps), sarcoidosis, 

Sjogren syndrome, tumors, leukemia, and lymphoma. 

Treatment 

Purulent bacterial infections should be treated by incision and drainage of localized pus 

collections, antibiotics, warm compresses, and systemic analgesics. Viral dacryoadenitis 

(mumps) is treated conservatively. 

Disposition 

The patient should be referred to an ophthalmologist for follow-up care in 2-3 days. 

ACUTE HORDEOLUM (Stye)


• Pain and redness with swelling over the eyelid. 

• Warm compresses and topical antibiotic 3 times daily are key to treatment. 


Acute hordeolum is a common infection of the lid glands: the meibomian glands (internal 

hordeolum) and the glands of Zeis or Moll (external hordeolum). The most frequent 

causative organism is S aureus. 


A stye is characterized by pain and redness with variable swelling over the eyelid. A 

large hordeolum may rarely be associated with swelling of the preauricular lymph node 

on the affected side, fever, and leukocytosis. 

Treatment 

If pus is localized and pointing out to the skin or conjunctiva, a horizontal incision is 

made through the skin or a vertical incision through the conjunctiva. (This procedure 

should be performed by an ophthalmologist.) 

Disposition 

The patient can be discharged to continue treatment with warm compresses 3 times 

daily and topical antibiotic ointment (erythromycin or tetracycline) twice daily at home. 

EYELID INFECTIONS (Preseptal Cellulitis) 


• Tenderness and pain with erythema surrounding the eye. 

• Key to diagnosis is no pain with ocular movement. 

• Antibiotic treatment and daily follow-up to ensure the infection doesn't progress to 

orbital cellulitis. 


Preseptal cellulitis is an infectious or inflammatory process of the eyelid. Common 

causative organisms are S aureus, streptococci, and H influenzae. Viral causes should 

be considered if associated with a skin rash (eg, herpes zoster). 

Clinical Findings

There is tenderness, erythema, and edema of the eyelid. No proptosis, no pain with 

ocular movement, and no restriction of extraocular motility is present. If any of these are 

present, consider orbital cellulitis. 

Treatment 

Give amoxicillin-clavulanate for 10 days. Antivirals may be considered if herpes zoster is 

suspected. Incision and drainage may be needed in more severe cases. 

Disposition 

The patient can be discharged with daily follow-up with ophthalmology or 

otolaryngology. If the patient returns with failure of antibiotics or worsening symptoms, 

start intravenous antibiotics and obtain emergent ophthalmology or ENT consult. 

SPONTANEOUS SUBCONJUNCTIVAL HEMORRHAGE 


• Painless. 

• Vision is not affected. 


Rupture of conjunctival or episcleral blood vessels may occur spontaneously or in 

association with minimal trauma, violent coughing, or retching. The possibility of 

coagulopathies and systemic hypertension must be investigated in recurrent 

subconjunctival hemorrhage. 


The conjunctiva suddenly becomes bright red in blotchy distribution. There is no pain, 

and vision is not affected. Severe cases may be characterized by chemosis and 

subconjunctival accumulation of blood clots. Check for hypertension, and obtain a 

complete blood count with differential and coagulation panel (prothrombin time, partial 

thromboplastin time, and platelet count) if hemorrhage recurs or if there is any other 

evidence of bleeding diathesis. 


Treat with cold compresses within the first 12 hours after onset; later, use warm 

compresses for 10-15 minutes 3 times daily. The patient can be discharged to private 

care or a clinic and should be seen within 2-3 days for follow-up examination and care if 

needed. 

CONJUNCTIVITIS


• Most frequent cause of red eye. 

• Purulent drainage and conjunctival hyperemia help with diagnosis. 


Conjunctivitis is a frequent cause of red eye. It should be dealt with as an urgent 

medical problem until it is certain that the process is under control. 

Causes of Acute Conjunctivitis 

A. Infection 

Acute conjunctivitis may be caused by bacterial, viral, parasitic, fungal, or chlamydial 

infection. 

B. Chemical Irritation 

Chemical irritations causing acute conjunctivitis include chlorine gas and tear gas. 

C. Allergy 

Allergic causes of acute conjunctivitis include vernal keratoconjunctivitis and hay fever. 

D. Skin Disorders 

Skin disorders such as Stevens-Johnson syndrome, acne rosacea, Lyell disease, 

Kawasaki disease, and psoriasis may cause acute conjunctivitis. 

E. Systemic Disorders 

Sjogren syndrome and vitamin A deficiency may cause acute conjunctivitis. 


See Table 31-2. The patient complains of a "scratchy" sensation or pain, with 

conjunctival discharge. One or both eyes may be affected. Adherence of the eyelids 

upon awakening is common in bacterial conjunctivitis. 

Examination discloses conjunctival hyperemia, purulent or mucopurulent discharge, and 

variable degrees of lid swelling. Material should be taken from the conjunctival sac for 

smear (Gram and Giemsa stains) and for culture on blood and chocolate agar. Viral 

cultures may also be indicated. 

Treatment 

Until laboratory reports are received, prescribe topical sulfacetamide, 10% eye drops, or 

ciprofloxacin, 0.3% eyedrops (an alternative to ciprofloxacin is ofloxacin), 4 times daily; 

and erythromycin or tetracycline ophthalmic ointment at bedtime for suspected bacterial 

conjunctivitis.

For suspected chlamydial infection (eg, history of urethritis), prescribe topical and 

systemic tetracycline or erythromycin. Give 0.5 g 4 times daily for 21 days (adult dose). 

Doxycycline, 100 mg twice daily, may be substituted for tetracycline. Consider treatment 

for gonorrhea. 

Disposition 

Discharge patients to home care with instructions to return for follow-up in 48-72 hours. 

Patients who do not respond to treatment should be referred to an ophthalmologist. 

BACTERIAL CORNEAL ULCER 


• Exam with fluorescein aids in diagnosis. 

• Antibiotic treatment and close follow-up are mandatory. 

• Common in contact lens wearers. 


Corneal infections may be due to bacteria, viruses, chlamydiae, or fungi. The 

conjunctiva may or may not be involved. Bacterial corneal ulcers are serious, because 

rapid perforation of the cornea and loss of aqueous humor may occur; bacterial 

endophthalmitis may occur if bacterial ulcers are not properly treated. 


The patient complains of pain and photophobia, blurring of vision, and eye irritation. 

Examination discloses conjunctival hyperemia and chemosis, corneal ulceration, or 

whitish-yellowish infiltration. The examination is facilitated by fluorescein staining and 

inspection with ultraviolet light. Hypopyon may be present. Scrapings from the cornea 

should be taken for culture and staining with Gram and Giemsa stains. 

BR>Differential Diagnosis 



Management of bacterial corneal infections causing corneal ulcers must be instituted as 

early as possible. The patient should be seen by an ophthalmologist before discharge 

from the emergency department. Hospitalization may be necessary, especially if 

hypopyon is present. 

VIRAL KERATOCONJUNCTIVITIS


• Redness and pain with palpebral conjunctival follicles in one eye. 

• Adenovirus is most common; however, sulfacetamide is used. 


Viral keratoconjunctivitis is an acute conjunctivitis and keratitis caused most frequently 

by adenovirus (types 8 and 19). The patient complains of redness of the eye associated 

with tearing and moderate pain. The onset is often in one eye only, and this eye is more 

severely affected. Sensitivity to light (photophobia) may be noted 5-14 days after onset. 

Examination discloses swelling of the eyelids and bulbar conjunctival hyperemia, with 

follicles noted over the palpebral conjunctiva. A pseudomembrane may be noted over 

the palpebral conjunctiva. A tender preauricular lymph node can be palpated. 

Subconjunctival hemorrhage may occur within 48 hours. Corneal epithelial keratitis 

accompanies the conjunctivitis, but subepithelial opacities are not seen until 5-14 days 

after onset of symptoms. 

In adults, the disease is confined to the external eye. Children may have fever, 

pharyngitis, and diarrhea (pharyngoconjunctival fever). Staining of conjunctival 

scrapings with Giemsa stain demonstrates a predominantly mononuclear inflammatory 

reaction. When pseudomembranes occur, polymorphonuclear neutrophils may be seen. 

Culture for adenovirus is usually positive in the first 2 weeks after onset. Chlamydial 

conjunctivitis should always be considered in the differential diagnosis. 

Treatment 

Treatment is symptomatic. Topical decongestants may be helpful. Dark glasses may 

relieve photophobia. If the diagnosis is uncertain, send material for culture for bacteria, 

and start sulfacetamide, 10% eye drops, 4 times daily; and tetracycline, 1% (10 mg/g) 

ointment twice daily, while awaiting laboratory results. 

Because epidemics have been caused by spread of the viral agent by physicians and 

nurses, handwashing between examinations and complete sterilization of tonometer 

footplates are mandatory preventive measures. 

Disposition 

The patient should be discharged with instructions to seek a medical appointment in 2-3 

days. Patients should take care to avoid spread of virus from ocular secretions to other 

family members, and they should preferably stay home from work for a few days to 

avoid spread of the infection. 

ACUTE HYDROPS OF THE CORNEA


• Sudden, painless decrease in vision. 

• Unaffected eye shows keratoconus. 

• Follow-up with ophthalmologist in 24-72 hours. 


Acute hydrops of the cornea may occur in patients with keratoconus who develop 

rupture of Descemet's membrane, with resulting infiltration of the corneal stroma by 

aqueous humor. This may occur suddenly, resulting in corneal clouding. 


The typical presentation is of sudden, painless, marked decrease in visual acuity in a 

patient with keratoconus. There may be mild eye irritation, and the cornea is cloudy as a 

result of corneal edema. The patient usually has keratoconus in the other eye. Bacterial 

or viral keratitis must be ruled out. 

Treatment 

Hypertonic eye drops, for example, sodium chloride, 2% or 5% solution, should be 

instilled 4 times daily for 1 week. Apply a stream of hot air twice daily by hair dryer to 

speed dehydration of the cornea. Avoid rubbing the eye. 

Disposition 

Refer the patient to an ophthalmologist within 24-72 hours. 

HYPHEMA 


• Sudden decrease in visual acuity. 

• Sitting the patient up can aid in the diagnosis, because blood will accumulate inferiorly. 

• Must check intraocular pressure. 


Hyphema (blood in the anterior chamber) is usually caused by nonperforating trauma to 

the eye. In rare instances, hyphema may occur spontaneously as a complication of an 

ocular or systemic disorder. 

Clinical Findings

Hyphema is characterized by sudden decrease in visual acuity. If the intraocular 

pressure is elevated, there may be pain in the eye with or without headache. 

The whole anterior chamber may be filled with blood, or a blood level may be seen. The 

conjunctiva is hyperemic with perilimbal injection. 

Treatment 

Elevate the patient's head 30 degrees. Cover the affected eye with a shield. If 

intraocular pressure is elevated, immediate ophthalmologic consultation is needed for 

surgical evacuation of blood. 

Recently, intracameral injection (performed by an ophthalmologist) of 25 ug of t-PA has 

been shown to expedite the resorption of blood clots in the anterior chamber. 

Aminocaproic acid can be used topically to stabilize the clot and decrease the rate of 

rebleeding. 

Disposition 

Acute care and evaluation by an ophthalmologist is essential. Operative evacuation of 

nonabsorbed blood clots may be required. Recurrence of bleeding on the third to fifth 

days following injury is not uncommon. Disposition should be determined by the 

ophthalmologist. All patients with hyphema should be examined every day for 5 days 

and then as directed by the ophthalmologist. 

UVEITIS (Iritis & Iridocyclitis) 


• Photophobia, pain, and constricted pupil secondary to ciliary spasm. 

• Mydriatics are key to treatment. 


The uvea consists of the iris, ciliary body, and choroid. Anterior uveitis is inflammation of 

the iris and ciliary body, or iridocyclitis. Inflammation of all 3 structures is called 

panuveitis. 


See Table 31-1. The patient complains of blurred vision, photophobia, and headache or 

ocular pain. Ciliary injection may be present around the limbus, and conjunctival 

injection may be minimal. Intraocular pressure may be elevated. There is no 

conjunctival discharge. 

Treatment

Instill prednisolone acetate, 1% eye drops, 5 times daily. More frequent applications 

may be required in certain severe cases of anterior uveitis. Instill a cycloplegic mydriatic 

agent, such as tropicamide or cyclopentolate, 1% eye drops, 1 drop every 8 hours. If 

intraocular pressure is elevated, give acetazolamide, 250 mg orally every 6 hours. 

Disposition 

Patients with uveitis should be seen the next day for follow-up care. Continuing care 

should be by an ophthalmologist. The cause of uveitis should be investigated. 

VITREOUS HEMORRHAGE 


• Sudden, painless loss of vision. 

• Patient complains of seeing "floaters." 

• Secondary to trauma, retinal detachment, or diabetic retinopathy. 

• Urgent ophthalmology consultation is needed. 


Spontaneous hemorrhage into the vitreous body may result from local factors in the eye 

(eg, retinal tears, tumors, inflammation, venous occlusion, retinal detachment) or from 

associated systemic disorders (eg, hematopoietic diseases, diabetes mellitus, 

hypertension) (Table 31-3). Blood in the vitreous body clots rapidly, and removal of red 

blood cells is retarded because of the network of collagen fibers and hyaluronic acid. 


Vitreous hemorrhage is characterized by sudden, painless loss or deterioration of vision 

in the affected eye. The eye is not red. The red reflex of the fundus is hazy or faint or 

becomes black. Details of the retina and optic nerve are obscured by the cloudy 

vitreous. 


The patient should be evaluated immediately by an ophthalmologist. Partial or total 

vitrectomy may have to be considered later if absorption of blood does not occur or if 

vitreous clouding occurs secondary to organization of the blood clot. Photocoagulation 

of the neovascular network (ie, new blood vessel formation, as occurs in diabetic or 

sickle cell retinopathy), when present, may be considered in some cases as a 

prophylactic measure. 

Recent studies have shown that intravitreal injection of 25 ug of t-PA may be considered 

in selected patients with traumatic vitreous hemorrhage. 

RETINAL HEMORRHAGE


• Painless loss of vision occurs if the hemorrhage is in the macular area. 

• May have no symptoms. 


Retinal hemorrhage may be due to trauma, local ocular disease, or systemic disorders 

(Table 31-4). Hemorrhages may occur in superficial or deep layers of the retina or in the 

preretinal or subhyaloid space. 


The patient may complain of sudden decrease in vision when hemorrhage occurs in the 

macular or perimacular area. Small peripheral retinal hemorrhages cause no symptoms. 

Superficial retinal hemorrhages occurring in the nerve fiber layer are bright red and 

flame-shaped on ophthalmoscopic examination. Deep retinal hemorrhages are round 

and have a dark red color. Subhyaloid hemorrhage occurs in the space between the 

vitreous body and the internal limiting membrane and may have a boat-shaped 

appearance. A neovascular network may rupture and cause retinal or vitreous 

hemorrhage. 


Treatment depends on the cause; there is no specific treatment. The patient should be 

referred to an ophthalmologist for further care, for example, photocoagulation of new 

vessels associated with local or systemic conditions (eg, diabetes) to prevent 

recurrences. 

CENTRAL RETINAL VEIN OCCLUSION 


• Unilateral, painless loss of vision. 

• Often in elderly with glaucoma or hypertension. 


Central retinal vein occlusion occurs most frequently in elderly patients with glaucoma or 

hypertension. The incidence is increased also in diabetes mellitus, autoimmune 

diseases, Waldenstrom macroglobulinemia, cryoglobulinemia, sickle cell disease, 

polycythemia vera, and leukemia. 

Clinical Findings

The patient complains of sudden painless loss of vision in one eye. Ophthalmoscopy 

reveals dilated and tortuous veins, retinal and macular edema, multiple or diffuse retinal 

hemorrhages, and attenuated arterioles. 


There is no specific therapy. Refer the patient to an ophthalmologist within 24 hours for 

assessment of possible glaucoma or associated systemic disease. If local predisposing 

factors such as glaucoma are ruled out, patients with occlusion should have a complete 

medical evaluation. 

OPTIC NEURITIS 


• Painful unilaterally, especially with movement. 

• Afferent pupillary defect. 

• Many causes: case should be discussed with ophthalmology or neurology consult. 


Optic neuritis may be due to a variety of causes, including demyelinating diseases; 

systemic infections; nutritional and metabolic disorders; exposure to toxic substances 

(eg, arsenic, methanol, lead, tobacco); vascular insufficiency; and local extension of 

infection from intraocular structures, sinuses, or meninges. Optic neuritis includes 

retrobulbar neuritis (inflammation of the optic nerve posterior to the globe), in which 

there are by definition no ophthalmoscopic findings. 


The patient complains of decreased vision in one eye and sometimes pain on moving 

the eye. The pupillary reflex is sluggish. Ophthalmoscopic examination in optic neuritis 

shows hyperemia of the optic nerve head (may not be present in retrobulbar neuritis), 

congestion of the large veins, blurring of the disk margin, peripapillary retinal edema, 

and flame-shaped hemorrhages near the optic nerve head. Visual field testing discloses 

a central scotoma. 


Treatment depends on the cause. Systemic corticosteroids may be helpful in cases 

associated with demyelinating disease. The patient should be referred to an 

ophthalmologist or neurologist for further care within 1-2 days. 

Benson WH, Lanier JD: Current diagnosis and treatment of corneal ulcers. Curr Opin 

Ophthalmol 1998;9:45. [PMID: 10387468]

Bhagat N: Central retinal vein occlusion: review of management. Eur J Ophthalmol 

1999;9:165. [PMID: 10544972] 

Crouch ER: Topical aminocaproic acid in the treatment of traumatic hyphema. Arch 

Opthalmol 1997;115:1106. [PMID: 9298049] 

Curl A: Seeing red. A review of subconjunctival hemorrhage. Adv Nurse Pract 

1999;7:77. [PMID: 10373806] 

Grewal S et al: Acute hydrops in the corneal ectasias: associated factors and outcomes. 

Trans Am Ophthalmol Soc 1999;97:187. [PMID: 10703124] 

Hamill MB: Current concepts in the treatment of traumatic injury to the anterior segment. 

Ophthalmol Clin North Am 1999; 12:457. 

Hochman MA et al: Pathophysiology and management of subretinal hemorrhage. Surv 

Ophthalmol 1997;42:195. [PMID: 9406367] 

Kaufman HE: Treatment of viral diseases of the cornea and external eye. Prog Retin 

Eye Res 2000;19:69. [PMID: 10614681] 

Lederman C et al: Hordeola and chalazia. Pediatr Rev 1999;20: 283. [PMID: 10429150] 

Mawn LA et al: Preseptal and orbital cellulitis. Opthalmol Clin North Am 2000;13:633. 

Shields SR: Managing eye disease in primary care. Part 2. How to recognize and treat 

common eye problems. Postgrad Med 2000;108:83. [PMID: 11043082] 

Spraul CW et al: Vitreous hemorrhage. Surv Ophthalmol 1997; 42:3. [PMID: 9265701] 

Tolls DB: Peripheral retinal hemorrhages: a literature review and report on thirty-three 

patients. J Am Optom Assoc 1998;69: 563. [PMID: 9785731] 

Van Stavern GP: Management of optic neuritis and multiple sclerosis. Curr Opin 

Ophthalmol 2001;12:400. [PMID: 11734679] 

Weinberg RS: Uveitis. Update on therapy. Ophthalmol Clin North Am 1999;12:71. 

Yeatts RP: Acquired nasolacrimal duct obstruction. Ophthalmol Clin North Am 

2000;13:719. 

IV. OCULAR BURNS & TRAUMA 

OCULAR BURNS 


• History and physical examination. 

• Copious irrigation with normal saline, lactated Ringer's, or water after topical 

anesthetic is placed. 

• Check pH after irrigation; should be 6.8-7.4. 

• Immediate ophthalmology consultation is needed. 


Apart from the history, the diagnosis of chemical burns is usually based on the presence 

of swollen eyelids with marked conjunctival hyperemia and chemosis. The limbus may 

show patchy balanced areas with conjunctival sloughing, especially in the interpalpebral 

area. There is usually corneal haze and diffuse edema, with wide areas of epithelial cell 

loss and corneal ulcerations. Corneal ulcerations can be better visualized with blue light 

following instillation of fluorescein. 

ALKALI BURNS 


Alkali burns (especially particulate alkali such as lime) are very serious, because even 

after apparent removal of the offending agent, tiny particles may remain lodged within 

the cul-de-sac and cause progressive damage to the eye. 

Treatment 

Instill a topical anesthetic immediately (proparacaine, 0.5%; or tetracaine, 0.5%), and 

then copiously irrigate the eye with 2-3 L isotonic saline solution, water, or lactated 

Ringer's solution. A lid retractor may be useful. 

Double eversion of the eyelids (Figure 31-5) should be performed to look for and 

remove material lodged in the cul-de-sac. Solid particles of alkali should be removed 

with forceps or a moist cotton swab. After particles have been removed, irrigate again. 

Do not attempt to neutralize the alkali with acid, because the heat generated by the 

chemical reaction may cause further injury. 

Instill topical mydriatic eye drops and antibiotic ointment. After irrigation, the pH of the 

eye should be checked and the range should be 6.8-7.4. If the pH is still high, continue 

with irrigation. Parenteral narcotic analgesia is often required for pain relief (eg, 

morphine, 10 mg subcutaneously). 

Disposition 

Obtain immediate ophthalmologic consultation. 

ACID BURNS 

Clinical Findings

Acid burns as a rule cause damage more rapidly but are generally less serious than 

alkali burns, because they do not cause progressive destruction of ocular tissues (as do 

alkali burns). 

Treatment 

Immediately after exposure, irrigate the eyes copiously with sterile isotonic saline 

solution, lactated Ringer's, or tap water. Topical anesthetic (proparacaine, 0.5%) may 

be instilled to minimize pain during irrigation. Do not attempt to neutralize the acid with 

alkali. 

Parenteral or oral narcotic analgesics may be necessary. Patch the eye if corneal 

defects are present. 

Disposition 

Obtain immediate ophthalmologic consultation. 

THERMAL BURNS 


Injury due to thermal burns of the eyelids, cornea, and conjunctiva may range from 

minimal to extensive. Superficial corneal burns have a good prognosis, though corneal 

ulcers may occur as a result of loss of corneal epithelium. 

Thermal burns of the skin of the eyelids may be first, second, or third degree. 

Conjunctival hyperemia is noted. The cornea may show diffuse necrosis of the exposed 

corneal epithelium in the interpalpebral area. Corneal haze due to corneal edema is 

frequently seen in thermal burns of the cornea and may lead to decrease in vision. 

Treatment 

The treatment of ocular burns is similar to the treatment of burns occurring elsewhere 

on the body (Chapter 43). Provide systemic analgesia. Instill proparacaine, 0.5%, or 

tetracaine, 0.5%, to minimize pain during manipulation. In cases of corneal burns, instill 

a mydriatic agent. 

Disposition 

Hospitalize patients with severe burns for local care and administration of systemic 

analgesia. Obtain ophthalmologic consultation. 

BURNS DUE TO ULTRAVIOLET RADIATION 

Destruction of the corneal epithelium by ultraviolet light is know as actinic keratitis, snow 

blindness, and welder's arc burn (flash burn), depending on the source of ultraviolet 

radiation.


The patient complains of pain and gives a history of exposure to ultraviolet light 6-12 

hours earlier (eg, skiing, sunlamp). Examination discloses tearing, conjunctival 

hyperemia, and corneal haziness. There may be a superficial punctate staining of the 

cornea seen with fluorescein and with magnification (eg, slit lamp). Exposure to a 

welder's arc without protective filters produces keratitis similar to that resulting from 

ultraviolet radiation. 

Treatment 

Topical anesthetic should be instilled during the eye examination only. Do not give the 

patient a topical anesthetic to use at home. Instill a mydriatic agent and an antibiotic 

ointment. Recovery occurs within 12-36 hours. Provide systemic analgesics for pain 

(aspirin and codeine or equivalent). 

Disposition 

Patients with severe burns should be hospitalized. All other patients should be seen for 

follow-up the next day (by an ophthalmologist, if possible). 

MECHANICAL TRAUMA TO THE EYE 


• History is key to diagnosis. 

• Full exam is paramount to treatment and diagnosis. 


Ocular trauma may be classified as penetrating or nonpenetrating. Trauma can lead to 

serious damage and loss of vision. Eye injuries are common in spite of the protection 

afforded by the bony orbit and the cushioning effect of orbital fat. More widespread use 

of safety goggles would prevent most serious injuries to the eye. 

Evaluation 

Obtain a history of the injury from the patient or someone who knows what happened. 

Measure and record visual acuity with and without eyeglasses and through a pinhole 

aperture. Inspect the eyelids, conjunctiva, cornea, anterior chamber, pupils, lens, 

vitreous, and fundus for breaks in tissue and hemorrhage. Search for corneal lesions 

(eg, abrasion) by instilling fluorescein dye and examining the eye using a light with a 

light-blue filter. 

X-ray examination (orbital soft tissue film with contact lens localizer) or CT scan may be 

indicated to rule out radiopaque foreign bodies and to look for fractures of orbital bones.


Hospitalize patients with severe injuries, and consult an ophthalmologist immediately. 

Avoid causing further damage by manipulation. For more detailed discussion of 

treatment and disposition, see below under the specific type of injury. 

For severe pain, photophobia, or foreign body sensation, instill a topical anesthetic (eg, 

proparacaine, 0.5%, 1-2 drops once or twice). Systemic analgesics may be required. 

Cover the eye with an eye shield. 

PENETRATING OR PERFORATING INJURIES 


Penetrating or perforating ocular injuries require immediate careful attention and prompt 

surgical repair to prevent possible loss of the eye. 

Many facial injuries, especially those occurring in automobile accidents, are associated 

with penetrating ocular trauma. Some injuries may be concealed and inapparent 

because of eyelid swelling or because the patient's other injuries have dominated the 

attentions of the emergency department team. Such injuries, if not promptly attended to 

and adequately managed by an ophthalmologist, may lead to loss of vision. 

Evaluation 

Obtain and record a description of how the injury occurred. Examine the eye and ocular 

adnexa, including vision testing if the patient's condition permits. Do not apply pressure 

on the globe. CT scan is indicated to rule out intraocular radiopaque foreign body and to 

look for fractures of orbital bones. 


Penetrating injuries are those that cause disruption of the outer coats of the eye (sclera, 

cornea) without interrupting the anatomic continuity of that layer, thus preventing 

prolapse or loss of ocular contents. Perforating injuries are those resulting in complete 

anatomic disruption (laceration) of the sclera or cornea. Such wounds may or may not 

be associated with prolapse of uveal structures. Wounds of the sclera or cornea are 

often associated with intraocular or intraorbital foreign bodies. 

Treatment 

The objectives of emergency management of ocular penetrating or perforating injuries 

are to relieve pain, preserve or restore vision, and achieve a good cosmetic result. 

Avoid needless examination. 

Relieve pain with systemic analgesia, as needed. A sedative may be required. Cover 

the eye with an eye shield. Patch the uninjured eye also to minimize ocular movements. 

Do not manipulate the eye, instill eye drops, or apply antibiotic treatment.

Give tetanus prophylaxis if needed (Chapter 30.) Prohibit oral intake until the patient is 

examined by an ophthalmologist, because urgent surgery may be required. Provide 

hydration with intravenous fluids (eg, 5% dextrose in half-normal saline given at a rate of 

125 mL/h for an adult). 

Give parenteral antibiotics directed against gram-negative and gram-positive organisms. 

Give antiemetic agents to prevent further injury from intraocular pressure increase. 

Disposition 

The patient should be seen by an ophthalmologist for management of severe injuries, 

investigation of intraocular foreign bodies, and immediate surgical repair as required. 

Prompt repair of uveal prolapse decreases the risk of sympathetic ophthalmia in the 

uninjured eye. Delay in management of corneal lacerations may increase the risk of 

surgical and postoperative complications. 

BLUNT TRAUMA TO THE EYE, ADNEXA, & ORBIT 

Contusions of the eyeball and ocular adnexa result from blunt trauma. The outcome of 

such an injury cannot always be determined, and the extent of damage may not be 

obvious upon superficial examination. Careful eye examination is needed, along with 

x-ray examination or CT scan when indicated. 

Types of Injury 

A. Eyelids 

Check the eyelids for ecchymosis (see below), swelling, laceration, and abrasions. 

B. Conjunctiva 

Check the conjunctiva for subconjunctival hemorrhages or laceration of the conjunctiva. 

C. Cornea 

Check the cornea for edema, laceration, or rupture. 

D. Anterior Chamber 

Check the anterior chamber for hyphema, recession of angle, or secondary glaucoma. 

E. Iris 

Check the iris for iridodialysis, iridoplegia, rupture of iris sphincter, iris prolapse through 

corneal or scleral lacerations, or iris atrophy (later). 

F. Ciliary Body 

Check the ciliary body for hyposecretion of aqueous humor or for ciliary body prolapse 

through scleral lacerations. 

G. Lens 

Check the lens for dislocation or cataract (later). 

H. Vitreous

Check the vitreous for hemorrhage or prolapse. 

I. Ciliary Muscle 

Check the ciliary muscle for paralysis or spasm. 


Injury severe enough to cause intraocular hemorrhage (eg, vitreous hemorrhage or 

hyphema) involves the danger of delayed secondary hemorrhage from a damaged 

uveal vessel, which may cause intractable glaucoma and permanent damage to the 

eyeball. In such cases, immediate ophthalmologic consultation is necessary to rule out 

other eye injuries. 

Except for rupture of the eyeball itself, contusions do not usually require immediate 

definitive treatment. Apply an eye shield if the globe has been perforated and consult 

ophthalmology immediately. 

Use atropine, 1% eye drops, twice daily. Acetazolamide, mannitol, or other systemic 

agents may be necessary to lower intraocular pressure. Give systemic analgesia. 

Refer all patients to an ophthalmologist. 

1. Ecchymosis of the Eyelids (Black Eye) 


Blood in the periorbital tissues may occur from direct trauma or a blow to adjacent areas 

(eg, nose). The loose subcutaneous tissue around the eye permits blood to spread 

extensively. The diagnosis is usually obvious. Always rule out trauma to the eye itself 

(hyphema, blowout fracture, or retinal detachment). 

Treatment 

Apply cold compresses to decrease swelling and help stop bleeding. Twenty-four hours 

later, apply warm compresses to accelerate absorption of the hematoma. Exclude more 

serious ocular injury by careful examination. 

Disposition 

If the eye itself is uninjured, no follow-up contact is necessary. 

2. Lacerations of the Eyelids 


Lacerations or other wounds of the eyelids may be associated with serious ocular 

injuries not apparent at first examination, for example, injury to the lacrimal system, 

levator muscle, or optic nerve. A meticulous search for such injuries is mandatory in 

every patient with eyelid lacerations.


Patients with lacerations of the eyelids require suturing and then complete 

ophthalmologic evaluation. Lacerations involving the tarsal plate, the upper eyelids, or 

medial canthal area should be repaired by an ophthalmologist. 

3. Orbital Hemorrhage 


Exophthalmos and subconjunctival hemorrhage in a patient with a history of blunt 

trauma to the face suggest rupture of orbital blood vessels. There may be conjunctival 

chemosis or ecchymosis of the eyelids. 


Apply cold compresses, and obtain urgent ophthalmologic consultation. Hospitalize the 

patient for observation if severe injury has occurred. 

4. Fracture of the Ethmoid Bone 

The ethmoid bone is part of the medial wall of the orbit. Fracture of the ethmoid bone 

most frequently occurs with blunt trauma to the orbit. 


Fracture of the ethmoid bone is manifested by subcutaneous emphysema of the eyelids. 

There may or may not be ecchymosis of the eyelids. X-ray reveals air in the orbit. 

Fractures of other orbital bones should be ruled out by radiography. 

Treatment 

Fractures of the ethmoid bone usually do not require operative reduction. Provide 

analgesia as needed. Apply cold compresses. Give systemic antibiotic. Instruct the 

patient to avoid sneezing or blowing the nose. 

Disposition 

Refer the patient to an ophthalmologist within 1-2 days. 

5. Blowout Fractures of the Floor of the Orbit 


Blowout fracture may be associated with enophthalmos and hypotropia (visual axis of 

the injured eye is displaced downward in comparison to that of the sound eye), diplopia 

in the primary position or in upward gaze, limitation of ocular movement in upward gaze, 

and decreased or absent sensation over the maxilla. CT scan of the orbit shows orbital

floor displacement. 

Treatment 

Provide analgesia as needed. Apply a topical antibiotic ointment such as gentamicin, 

0.3%. Apply cold compresses and a sterile eye patch. 

Disposition 

Hospitalize the patient, and seek early consultation with an ophthalmologist and 

otolaryngologist because of possible fractures of the maxilla or zygoma. Obtain CT scan 

of the orbit. 

6. Corneal Abrasions 


• Pain, photophobia, blurring vision. 

• Fluorescein stain is key to diagnosis. 

• Always rule out globe perforation. 


The patient complains of pain, photophobia, and blurring of vision. There is usually a 

history of trivial trauma. Patients with severe pain and blepharospasm may require 

proparacaine, 0.5%, instilled in the eye to facilitate eye examination. In severe cases, 

the eye is red and the corneal surface is irregular and loses its normal luster. Staining 

with fluorescein reveals a defect in the corneal epithelium. Always rule out infection or 

perforation of the globe. 

Treatment 

Irrigate the eye gently with sterile saline solution to remove the debris and loose foreign 

bodies. In severe cases, instill 2 drops of either atropine, 1%, or homatropine, 5%, to 

relax the ciliary muscle and relieve pain. Instill ophthalmic antibiotic ointment. Caution: 

Do not use ointment containing corticosteroids. 

Provide analgesia as needed, for example, acetaminophen with codeine, 30 mg, orally. 

Avoid giving the patient topical anesthetics, which may lead to irreversible corneal 

damage. 

Disposition 

Refer patients for daily outpatient follow-up care. Ophthalmologic consultation should be 

obtained for corneal abrasions that fail to resolve in 48-72 hours. 

7. Corneal & Conjunctival Foreign Bodies


• Pain, foreign body sensation. 

• Use fluorescein; make sure to look under lids. 

• May need to rule out intraocular foreign body. 


There may be a history of working with high-speed tempered steel tools (eg, drilling), or 

there may be no history of trauma to the eye and the patient may even be unaware of a 

foreign body in the eye. In most cases, however, the patient complains of a foreign body 

sensation in the eye or under the eyelid, or just irritation in the eye. A corneal foreign 

body can be seen with the aid of a loupe and well-focused diffuse light. Conjunctival 

foreign bodies often become embedded in the conjunctiva under the upper eyelid. The 

lid must be everted (see Figure 31-5) to facilitate inspection and removal. 

Sterile fluorescein should be instilled to visualize minute foreign bodies not readily 

visible with the naked eye or loupe. Rule out intraocular foreign body (in certain cases, 

soft tissue x-ray or CT scan may be required for this purpose). 

Treatment 

Some loose foreign bodies can be removed with a moist cotton swab. Foreign bodies 

superficially embedded can be removed with the tip of a hypodermic needle or blunt 

spud. Anesthetize the cornea first with proparacaine or tetracaine solution, 0.5%. Instill 

ophthalmic antibiotic ointment (gentamicin, 0.3%; or sulfacetamide, 10%). 

Disposition 

After the foreign body has been removed, the patient should be seen again in 24 hours 

to make certain that infection has not occurred. Refer the patient to an ophthalmologist if 

foreign bodies are deeply embedded in the cornea, because they may have to be 

removed in the operating room under magnification. 

Brady SM et al: The diagnosis and management of orbital blowout fractures: Update 

2001. Am J Emerg Med 2001;19:147. [PMID: 11239261] 

Hamill MB: Current concepts in the treatment of traumatic injury to the anterior segment. 

Ophthalmol Clin North Am 1999; 12:457. 

Harlan JB Jr et al: Evaluation of patients with ocular trauma. Ophthalmol Clin North Am 

2002;15:153. [PMID: 12229230] 

Kuckelkorn R: Emergency treatment of chemical and thermal eye burns. Acta 

Ophthalmol Scand 2002;80:4. [PMID: 11906296]

Mester V et al: Intraocular foreign bodies. Ophthalmol Clin North Am 2002;15:235. 

[PMID: 12229240] 

Reich J: Investigating a foreign body. Part 1—Where and how to look. Aust Fam 

Physician 2000;29:974. [PMID: 11059088] 

Reich J: Investigating a foreign body. Part 2—Removal. Aust Fam Physician 

2000;29:1086. [PMID: 11127070] 

Reppucci VS et al: Current concepts in the treatment of traumatic injury to the posterior 

segment. Ophthalmol Clin North Am 1999;12:465. 

Schrage RF: Eye burns: an emergency and continuing problem. Burns 2000;26:689. 

[PMID: 11024601] 

V. EQUIPMENT & SUPPLIES 

Basic Equipment 

A great many specialized instruments have been devised for the investigation of eye 

disorders. Most emergency conditions can be diagnosed with the aid of a few relatively 

simple instruments. The following should be available in the emergency department: 

• Hand flashlight with fresh batteries 

• Slit lamp 

• Ophthalmoscope (preferably with lens that has a blue filter) 

• Visual acuity chart (Snellen) 

• Tonometer 

• Pinhole and occluder 

• Eye shield (plastic or metal) and tape 

Basic Medications 


A. Local Anesthetics 

Proparacaine, 0.5%, or tetracaine, 0.5%, may be used. 

B. Dyes 

Sterile fluorescein papers should be on hand. 

C. Mydriatics 

Tropicamide ophthalmic solution, 0.5% or 1%, is a satisfactory mydriatic when the

examiner wishes to obtain a clear view of the lens, vitreous, or ocular fundus. Eye drops 

(atropine, 1%; or homatropine, 5%) may be used in patients with iritis. 

D. Miotics 

The miotic agent pilocarpine, 1% or 2%, should be on hand. 

E. Antibacterial Agents 

Antibacterial agents include tetracycline, 1% ophthalmic ointment; polymyxin 

B-bacitracin ophthalmic ointment; sulfacetamide, 10% ophthalmic solution or ointment; 

or gentamicin, 0.3% ointment. 

VI. COMMON TECHNIQUES FOR TREATMENT OF OCULAR 

DISORDERS 

Eversion of the Upper Eyelid 

See Figure 31-5. The patient is instructed to look down. Grasp the eyelashes at the 

outer margin of the lid with the thumb and forefinger of one hand, and gently and slowly 

draw the lid downward and outward. Using a cotton swab, press against the upper edge 

of the tarsus over the center of the lid while turning the lid margin rapidly outward and 

upward over the applicator. With the lashes thus held against the upper orbital rim, the 

exposed palpebral conjunctiva can be inspected closely. After the examination is 

completed and the foreign body removed (if possible), when the patient looks up, the lid 

returns to its normal position. 

Eye Drops 

The patient should sit with both eyes open and looking up. Pull down slightly on the 

lower lid, and place 2 drops in the lower cul-de-sac. The patient is then asked to look 

down while finger contact on the lower lid is maintained. Do not let the patient squeeze 

the eye shut. Do not touch the eye or the eyelid with the applicator; likewise, do not 

instill eye drops with the dropper held far away from the eye. 

Ointments 

Ointments are instilled in the same way as liquids. While the patient is looking up, lift out 

the lower lid to trap the medication in the conjunctival sac. The lids should be kept 

closed for at least 1 minute to allow the ointment to melt. Tubes of ointment may be 

warmed with warm water before the ointment is instilled in the lower fornix. 

Warm Compresses 

Use a clean towel or washcloth soaked in warm tap water well below the temperature 

that will burn the thin skin covering the eyelids. Warm compresses are usually applied to 

the area for 15 minutes 4 times daily. The therapeutic rational is to increase blood flow 

to the affected area and decrease pain and inflammation. 

Removal of Superficial Corneal Foreign Body

The main considerations are good illumination, magnification, anesthesia, proper 

positioning of the patient, and sterile technique. If possible, the patient's visual acuity 

should be recorded first. 

The patient may be sitting or supine. A loupe should be used unless a slit lamp is 

available. (A loupe must be used if the patient is supine.) An assistant should direct a 

strong flashlight into the eye at an oblique angle. The examiner may then see the 

corneal foreign body and remove it with a moist cotton swab. If this is not successful, 

the foreign body may be removed with a metal spud while the lids are held apart with 

the other hand to prevent blinking. An antibacterial ointment is instilled after the foreign 

body has been removed. 

Note: It is essential to see the patient the next day to be certain infection has not 

occurred and healing is under way. 

Home Medication 

At home, the same techniques should be used as described above except that drops 

should be instilled with the patient lying supine. Experienced patients (eg, those with 

glaucoma) are usually quite skillful in self-administration of eye drops. 

Tonometry 

Tonometry is the determination of intraocular pressure using a special instrument that 

measures the amount of corneal indentation produced by a given weight. Tonometry 

readings should be taken on any patient suspected of having increased intraocular 

pressure. 

A. Precautions 

Tonometry should be done with great caution on patients with corneal ulcers. It is 

extremely important to clean the tonometer before each use by carefully wiping the 

footplate with a cotton swab moistened with sterile solution (be sure it is dry before 

using) and to sterilize the instrument once a day (dry heat). The tonometer should be 

sterilized by flame or in a hot-air tonometer sterilizer after use on an inflamed eye. 

Corneal abrasions are rarely caused by tonometry. Epidemic keratoconjunctivitis can be 

spread by tonometry, and this can be prevented if the tonometer is cleaned before each 

use and the principle of handwashing between patients is meticulously observed. 

B. Technique 

Anesthetic solution (tetracaine, 0.5%; or proparacaine, 0.5%) is instilled into each eye. 

The patient lies supine and is asked to stare at a spot on the ceiling with both eyes or at 

a finger held directly in the line of gaze overhead. The lids are held open without 

applying pressure on the globe. The tonometer is then placed on the corneal surface of 

each eye and the scale reading taken from the tonometer. The intraocular pressure is 

determined by referring to a chart that converts the scale reading to millimeters of 

mercury for a Schiotz tonometer. If the scale reading is 4 or less, the 7.5-g and 10-g 

weights are added separately to gain further information concerning the intraocular

pressure. Normal intraocular pressure is 12-20 mm Hg. 

C. Interpretation of Abnormalities 

If the intraocular pressure is 20 mm Hg or more, further investigation is indicated to 

determine whether glaucoma is present. Tonometry is an effective screening device to 

select patients for glaucoma testing. Visual field testing and ophthalmoscopic 

examination should be done and tonometry repeated several times at different hours of 

the day or on different days before a diagnosis of glaucoma is warranted. If the pressure 

remains high on successive readings and there is a visual field defect or cupping of the 

optic disks, the diagnosis of glaucoma is established. In borderline cases, tonography 

may be helpful in establishing the presence or absence of glaucoma. 

Corneal Staining 

Corneal staining consists of instillation of fluorescein into the conjunctival sac to outline 

irregularities of the corneal surface. Staining is indicated in corneal trauma or other 

corneal disorders (eg, herpes simplex keratitis) when examination with a loupe or slit 

lamp in the absence of a stain has not been satisfactory. 

A. Precautions 

Because the corneal epithelium—the chief barrier to corneal infection—is usually 

interrupted when corneal staining is indicated, be certain that whatever dye is used 

(particularly fluorescein) is sterile. 

B. Equipment and Materials 

Note: Fluorescein must be sterile. Fluorescein papers or sterile individual dropper units 

are safest. Fluorescein solution from a dropper bottle may be used, but there is a 

substantial risk of contamination. 

C. Technique 

The individually wrapped fluorescein paper is wetted with sterile saline or touched to the 

wet conjunctiva so that a thin film of fluorescein spreads over the corneal surface. Any 

irregularity in the cornea is stained by the fluorescein and is thus more easily visualized 

using a light with a blue filter. 

D. Normal and Abnormal Findings 

If there is no superficial corneal irregularity, a uniform film of dye covers the cornea. If 

the corneal surface has been altered, the affected area absorbs more of the dye and will 

stain a deeper green. It is customary to sketch the staining area on the patient's record 

for later comparison to show the progress of healing. 

Estimation of Anterior Chamber Depth 

See Figure 31-3. Using a hand flashlight, shine the light obliquely and parallel to the 

plane of the iris across the cornea and anterior chamber. A normal anterior chamber will 

be fully illuminated. With a shallow anterior chamber (as in angle-closure glaucoma), the 

anteriorly displaced iris will cast a shadow. 

VII. COMMON PITFALLS TO BE AVOIDED IN THE MANAGEMENT OF

OCULAR DISORDERS 

Dangers in the Use of Local Anesthetics 

Unsupervised self-administration of local anesthetics is dangerous, because the patient 

may further injure an anesthetized eye without knowing it. Furthermore, most 

anesthetics delay healing. This is particularly true of butacaine, which also elicits a high 

incidence of allergic responses. Therefore, patients should not be given local 

anesthetics to take home. Eye pain should be controlled by systemic analgesics. 

Errors in Diagnosis 

The most common mistaken ophthalmologic diagnosis is conjunctivitis when the correct 

diagnosis should be iritis (anterior uveitis), glaucoma, or corneal ulcer (especially herpes 

simplex ulcer). The differentiation between iritis and acute glaucoma may be difficult 

also. 

Misuse of Atropine 

Atropine must never be used in routine diagnosis. It causes cycloplegia (paralysis of the 

ciliary muscle) of about 14 days' duration and can precipitate an attack of glaucoma if 

the patient has a narrow anterior chamber angle. 

Dangers of Local Corticosteroid Therapy 

Local ophthalmologic corticosteroid preparations (eg, prednisolone) are often used for 

their anti-inflammatory effect on the conjunctiva, cornea, and iris. Although a patient with 

conjunctivitis, corneal inflammation, or iritis can be made more comfortable with topical 

corticosteroids, it must be stressed that the corticosteroids are associated with 4 very 

serious complications when used in the eye: herpes simplex keratitis, open-angle 

glaucoma, cataract formation, and fungal infection. 

The most common complications are herpes simplex keratitis and glaucoma. 

Corticosteroids enhance the pathogenicity of herpes simplex virus, apparently by 

increasing the destructive effect of collagenase on the collagen of the cornea. This is 

evidenced by the fact that perforation of the cornea occasionally occurs when 

corticosteroids are used during the more active stage of herpes simplex cornea 

infection. Corneal perforation was a rare complication of dendritic keratitis before 

corticosteroids came into general use. In the treatment of any corneal inflammation, 

particularly if the corneal epithelium is not intact, the prolonged use of corticosteroids is 

sometimes complicated by fungal infection, and this may lead to loss of the eye. Topical 

corticosteroids can cause or aggravate open-angle glaucoma and, less commonly, can 

produce cataracts. 

For these reasons, although corticosteroids are valuable in the treatment of ocular 

disease, any patient on whom they are being used should be watched carefully for the 

development of complications. Corticosteroids should not be used unless specifically 

indicated (eg, in iritis, certain types of keratitis, and acute allergic disorders), and 

patients using prescribed topical corticosteroids should always see an ophthalmologist

for follow-up examination. 

Use of Contaminated Eye Medications 

The external coats of the eye, including the sclera and the corneal epithelium, are 

resistant to infection. However, once the corneal epithelium or sclera is broken by 

trauma, the tissues become markedly susceptible to bacterial infection. For this reason, 

ophthalmic solutions that may be used in injured eyes must be prepared with the same 

degree of caution as fluids intended for intravenous administration. 

Sterile, single-use disposable units of the common ophthalmic solutions should be used 

whenever liquid medication is instilled into an injured eye. For routine use in intact eyes, 

nearly all eye medications are now available in small plastic containers. It is safe to use 

these medications provided they are not kept a long time after opening (eg, > 1 month) 

and are not contaminated accidentally. 

Overtreatment 

Some patients with chronic conjunctivitis or keratitis may be made worse by 

overtreatment with topical medications. These patients should be evaluated by an 


Liu GT et al: The neuro-ophthalmologic examination (including coma). Ophthalmol Clin 

North Am 2001;14:23. [PMID: 11370569] 





I. EMERGENCY EVALUATION OF IMPORTANT OCULAR SYMPTOMS

Table 31-1. Differential diagnosis of unilateral acute redness and pain of the eye not associated with 

trauma. 1 

Conjunctivitis Glaucoma Corneal Erosion 

Extremely common. Common. Common. 

Insidious. Sudden. Sudden. 

Normal. Markedly blurred. Blurred. 

None to moderate. Severe. Severe. 

None to mild. Minimal. Moderate. 

None. Occasional. None. 

Moderate to copious. None. Watery. 

Absent. Present. Present. 

Severe; diffuse in fornices. Minimal, diffuse. Mild to moderate. 

Clear. Steamy. Hazy. 

Absent. Absent. Present. 

Absent. Absent. Absent. 

Normal. Middilated, fixed, and 

irregular. 

Normal or constricted. 

Normal. Elevated. Normal. 

Variable; depending on cause. No organisms. No organisms. 

Normal. None. Poor to normal. 

2 Acute anterior uveitis. 





TABLES 

Table 31-1. Differential diagnosis of unilateral acute redness and pain of 

the eye not associated with trauma.

Table 31-2. Differential diagnosis of conjunctivitis. 

Bacterial Viral Irritant 

Acute. Acute or subacute. Acute. 

Moderate. Mild to moderate. None to mild. 

Copious, purulent. Moderate, seropurulent. Minimal, clear. 

PMNs, bacteria. PMNs, monocytes, no bacteria. Negative. 

Usually Staphylococcus aureus, 

pneumococci. 

Negative. Negative. 

. . . Adenoviruses; occasionally 

enteroviruses; rarely others. 

Negative. 

Common. Common. Rare. 





TABLES 

Table 31-2. Differential diagnosis of conjunctivitis.

Table 31-3. Some known causes of 

spontaneous vitreous hemorrhage not 

associated with trauma. 





TABLES 

Table 31-3. Some known causes of spontaneous vitreous hemorrhage not 

associated with trauma.

Table 31-4. Systemic conditions associated with 

retinal hemorrhage. 





TABLES 

Table 31-4. Systemic conditions associated with retinal hemorrhage.

Table 31-5. Commonly used ophthalmic medications. 

Uses Bacitracin 

Polysporin (bacitracin and polymyxin B) 

Gram-positive and 

gram-negative organisms 

Gram-positive organisms, 

Chlamydia 

Gram-positive and 

gram-negative organisms; 

does not cover 

Pseudomonas 

Ciprofloxacin (Ciloxan) 

Norfloxacin (Chibroxin) 

Ofloxacin (Ocuflox) 

Ophthalmic ointment: place 

times daily for 7-10 days. 

0.3% solutions for conjuncti 

every 2 hours for 2 days, th 

hours for 5 days. For ulcer, 

15 minutes for 6 hours, then 

30 minutes for the next 18 h 

use 2 drops every hour; day 

drops every 4 hours. 

Gentamicin (Genoptic, Garamycin) Gentamicin and tobramycin 

solution and 0.3% ointment 

Polymyxin B & trimethoprim (Polytrim) Ophthalmic solution: 1 drop 

for 7-10 days. 

Trifluridine (Viroptic) 1% solution: 1 drop every 2 

awake with maximum 9 dro 

After reepithelialization, dec 

every 4 hours for 7 days. 

Dilation, uveitis, cycloplegia Cyclopentolate (Cyclogyl) 

Dilation, no cycloplegia Scopolamine (Hyoscine) 0.25% solution; lasts 7 days 

Local anesthesia Tetracaine (Pontocaine)

Figure 31-1. Assessment of the red or painful eye. 





FIGURES 

Figure 31-1

Figure 31-2. Assessment of acute partial or complete loss of vision. 





FIGURES 

Figure 31-2

Figure 31-3. Estimation of depth of anterior chamber by oblique illumination. (Courtesy 

of R Shaffer.) (Reproduced, with permission, from Riordan-Eva P, Whitcher JP: 

Vaughan & Asbury's General Ophthalmology, 16th ed. McGraw-Hill, 2004.) 





FIGURES 

Figure 31-3

Figure 31-4. Acute dacryocystitis. (Reproduced, with permission, from Vaughan D, 

Asbury T, Tabbara KF: General Ophthalmology, 12th ed. Appleton & Lange, 1989.) 





FIGURES 

Figure 31-4

Figure 31-5. Eversion of the upper lid. A: The patient looks downward. B: The fingers 

pull the lid down, and a rod is placed on the upper tarsal border. C: The lid is pulled up 

over the rod. D: The lid is everted. (Redrawn and reproduced, with permission, from 

Liebman SD, Gellis SS [editors]: The Pediatrician's Ophthalmology. Mosby, 1966.) 





FIGURES 

Figure 31-5

32. ENT Emergencies: Disorders of the Ear, Nose, Sinuses, 

Oropharynx, & Mouth - David C. Van, MD, MS 

I. IMMEDIATE MANAGEMENT OF POTENTIALLY HARMFUL 

DISORDERS 

EAR PAIN 

The complaint of ear pain is more common among children than adults and usually 

relates to an infectious process. Though some conditions are serious, patients with most 

ear pain conditions can receive treatment and be discharged by the emergency 

physician without consultation (Table 32-1). 


A. History 

Ask patients about history of trauma, surgery, or recurrent infections involving the ear. 

Also ask about specific symptoms (eg, recent fever, upper respiratory infection, or canal 

discharge) and pain quality (eg, pain, pressure, itching, or "buzzing" sounds). Have the 

patient identify the exact location of the pain. A narrow differential diagnosis can be 

explored based on these historical characteristics. 


Palpate the area surrounding the ear to identify lymph nodes or a bony prominence. 

Tender nodes are common in infections of the middle and external ear. Pain, swelling, 

and erythema at the mastoid process should prompt the clinician to consider mastoiditis. 

If the pain relates to the canal, examine its external orifice for evidence of discharge. 

Next, view the canal and tympanic membrane. Make careful note of the appearance of 

the tympanic membrane regarding color; reflectivity; visibility of landmarks; and 

presence of fluid, air bubbles behind the membrane, or perforations. Check tympanic 

membrane motility by insufflation. Compare to the normal ear. If the ear exam is normal, 

look to the upper teeth and temporomandibular joint as possible causes. 

C. Other Studies 

If history and physical examination suggest mastoiditis, computed tomography (CT) 

scan should be obtained. 

Treatment 

Each condition requires a specific treatment (see Table 32-1). 

HEARING LOSS 

Sudden hearing loss is a deficit of less than 3 days duration and may be partial or 

complete. Diagnoses can be categorized as conductive (external or middle ear cause) 

or sensorineuronal (inner ear or cochlear nerve-central nervous system cause).

Medication-related injuries are usually dose and duration related, which should be 

considered when determining which patients are at risk for this complication. Many 

potential causes must be considered (Table 32-2). 


A. History 

The patient's account of precipitating events (trauma or recent activities) and the 

duration of symptom onset (seconds, hours, days) should help narrow the focus on 

possible causes. Unilateral deafness should increase the suspicion for a conductive 

process (or acoustic neuroma), whereas bilateral symptoms would suggest a systemic 

(metabolic or drug-related) problem. Take a careful medication history. Severity (partial 

versus complete loss of hearing) also should be assessed. Finally, the presence of 

tinnitus, vertigo, or neurologic symptoms should alert the clinician to the likelihood of a 

sensorineuronal cause. 


Look at the canals and tympanic membranes to rule out foreign body obstruction, 

infection, or injury. The cranial nerves should be examined. Weber and Rinne tests are 

useful for differentiating between conductive and sensorineuronal causes. The Webber 

test is performed by placing a vibrating 512-Hz tuning fork on the midparietal head 

(Figure 32-1). In unilateral conductive hearing loss, sound is heard more loudly in the 

impaired ear (it is more sensitized from previous decreased stimulus from the air). The 

Rinne test requires the base of a vibrating fork to be placed on the mastoid process. At 

the point when the patient cannot hear the sound, it is quickly moved off the bone and 

the tines placed at the ear canal (Figure 32-2). Repeat on each side. Normally, the 

patient can hear through the air longer than with bone conduction, but a pronounced 

difference indicates sensorineuronal loss. A conductive deficit in either ear will make 

bone conduction louder than air on the affected side. 


Bloodwork is helpful if infectious or metabolic causes are being considered. CT scan is 

appropriate for a suspected acoustic neuroma. 

Treatment 

Treatment should be directed toward the underlying disorder. Rapid follow-up by the 

appropriate provider (ie, otolaryngologist, neurologist) is recommended. 

VERTIGO 

True vertigo (room spinning, exaggerated or fictitious sensation of motion) can be quite 

disconcerting to patients, some of whom present in dramatic discomfort. 


A. History 

The most important determination is between central (central nervous system) and 

peripheral (relating to the 8th cranial nerve or the inner ear apparatus) causes. This

classification usually can be resolved on the basis of history alone (Table 32-3). 

Symptoms that are severe, of recent or sudden onset, and related to head movement 

typically relate to a peripheral disorder. Ask about recent use of potentially vestibulotoxic 

drugs: aminoglycosides, vancomycin, phenytoin, quinidine, and minocycline have been 

implicated. Caffeine, nicotine, and alcohol are known to exacerbate symptoms. Head 

trauma can occasionally lead to semichronic symptoms (lasting months to years). 

Specific causes of peripheral vertigo are described in Table 32-4. 


Examine the ear canal, tympanic membrane, cranial nerves, and cerebellar function. All 

patients with vertigo may have difficulty with the tandem walk exercise, but the presence 

of focal cerebellar exam findings (rapid alternating movements, heel-shin slide, or 

finger-to-nose pointing tests) should raise suspicion for a central cause. Indentifying 

nystagmus, especially with head movement and extreme left and right lateral gaze, is a 

crucial part of narrowing the differential diagnosis. The Dix-Hallpike test can help elicit 

the vertigo symptoms and nystagmus if they are not present at rest. In this test, the 

examiner places a hand on the patient's occiput, and the patient is rapidly reclined from 

an upright position onto a flat surface. The head should extend off the back edge so that 

the neck can be somewhat hyperextended. The test can be repeated with the head 

rotated to each side. A positive result occurs when nystagmus is observed after the 

movement, or if the patient reports an acute worsening of the vertigo. Nystagmus 

relating to a peripheral cause typically starts 1-3 seconds and diminishes over 5-30 

seconds after head movement. The examiner must quickly observe the eyes after 

moving the patient. On occasion the symptoms improve by the time of evaluation, and 

these characteristic signs may be difficult to elicit. Ask family members if they observed 

unusual eye movements during earlier attacks. 


Imaging (by CT scan or magnetic resonance imaging [MRI]) is warranted for patients 

with a suspected central cause or elderly patients with equivocal findings. MRI provides 

superior resolution of the cerebellum, though CT scan will typically rule out large 

lesions. 

Treatment 

Patients with prolonged nausea and poor fluid intake will often require intravenous 

hydration. Pharmacotherapy is more successful in peripheral-type vertigo. It is directed 

at relief of symptoms and does not affect the duration of the illness. The first-line agent 

is oral meclizine, 25-50 mg every 8-12 hours, but patients unable to manage oral fluids 

are better off with intravenous normal saline and diazepam, 5-10 mg intravenously (2-4 

mg intravenously for the elderly), or transdermal scopolamine (0.5-mg patch). In 

general, drugs with anticholinergic effects are useful. These include diphenhydramine, 

50 mg intramuscularly or orally every 6-8 hours; dimenhydrinate, 50-100 mg 

intramuscularly or orally every 4 hours; cyclizine, 50 mg orally every 6 hours; 

promethazine, 25 mg orally, rectally, or intravenously every 6-8 hours; or droperidol, 

2.5-5 mg intravenously. Patients with peripheral vertigo can be discharged after 

moderate improvement of symptoms and ability to take oral liquids. Depending on the 

cause, symptoms are likely to last several hours to 1 week but may persist for 4-5 

weeks. Many patients with central vertigo will require inpatient management targeted at

the underlying cause, though those who are comfortable after treatment and have firm 

follow-up can be discharged. 

Alternatively, the particle repositioning (Epley) maneuver can be tried if positional 

vertigo is suspected. It is based on the belief that moving the canalith to the utricle area 

of the inner ear will prevent it from stimulating the sensory mechanism. After 

determining the affected side (this is the nystagmus fast-component direction), perform 

the Dix-Hallpike test if necessary. It involves rather extreme extension and rotational 

movements of the neck, and its success depends partly on the patient's ability to 

tolerate these positions. All motions should be done slowly, such that each full cycle of 

the maneuver takes 2 minutes. Place the patient in a sitting position, turn the head 45 

degrees toward the affected side, lay the patient down and allow the head to extend 45 

degrees beyond neutral while hanging off the top edge of the bed. Rotate the extended 

head to the midline and then 90 degrees away from the affected side (total rotation: 135 

degrees). Then flex the neck to neutral, sit the patient up and rotate the head back to 

midline. The maneuver often must be repeated several times to be successful. 

EPISTAXIS 

Most episodes of epistaxis do not result in significant blood loss, are not life threatening, 

and can be managed with minimally invasive measures. However, the clinician will 

generally be well advised to start with an assessment of hemodynamic stability and 

provide support (intravenous fluids or blood products) when appropriate. The typical 

bleeding site is the Kiesselbach area of the anteromedial nostril, an area at risk due to 

the anastomoses of three separate arteries (Figure 32-3). Though predominantly due to 

trauma or environmental exposure, epistaxis can rarely be the first symptom of a 

growing nasal or sinus malignancy. 


A. History 

Many patients will be predisposed to bleeding, due to warfarin, platelet-inhibiting 

medications, renal failure, or hemophilia. These conditions require early identification so 

that a workup can be initiated. Blunt nose trauma or nose picking are common causes 

of bleeding. In cold seasons, the dry conditions created by noncirculated, heated indoor 

air can dehydrate the airways, predisposing the nasal mucosa to cracking. The repeated 

blowing and wiping of a nose in the setting of upper respiratory infection or allergic 

rhinitis can abrade and injure the mucosal surface. The absence of a sensation of blood 

in the oropharynx suggests anterior bleeding. Finally, epistaxis risk is increased in 

pregnancy, and identification of possible pregnancy is relevant for selection of 

pharmacologic adjuncts to treat the epistaxis. 


Hemodynamically stable patients are best examined sitting upright. In this position, most 

blood will exit the anterior nose and ingestion or aspiration will be minimized. If the 

bleeding is active, the patient should be told to clear each nostril of clots and then be 

shown how to pinch the entire cartilaginous portion of the nose for 15 minutes. This is 

sometimes all that is required to stop the bleeding (however, the nose should always be 

reexamined to confirm hemostasis). During this time, the clinician should don protective

clothing and eyewear and set up a headlamp illuminator, a nasal speculum, and a 

Frazier suction device. The nasal speculum is inserted such that squeezing the handle 

pushes on the upper and lower margins of the nostril. Both sides of the nose should be 

examined for bleeding and the integrity of the septum confirmed. Observe the posterior 

oropharynx for 10-15 seconds to confirm whether fresh blood is flowing down the back 

wall. A predominance of fresh blood in the oropharynx compared to the anterior nose 

suggests a posterior source. 

Treatment 

A. Anterior Epistaxis 

Epistaxis from an anterior source can usually be controlled without otolaryngologic 

(ENT) consultation. In general, minimally invasive and technically simple methods are 

preferred, but refractory bleeding requires escalation to more invasive procedures. 

Some patients may benefit from gentle opiate or benzodiazepine sedation. While using 

the Frazier suction device to keep the field clear of blood, apply 1% phenylephrine, 4% 

cocaine, or 2% lidocaine-epinephrine solution with a cotton swab or pledget for 

vasoconstriction and local anesthesia. Alternatively these solutions may be sprayed 

onto the mucosal surface. When the bleeding site can be seen, simple cautery with 

silver nitrate is often all that is required (see Figure 32-3). Exercise care to use only 

unilateral, brief applications only to the bleeding site. Rolling the material a short 

distance from above and over the bleeding site will prevent too much interference from 

blood flowing downward. 

Bleeding that persists should be treated with packing. Several options are available. 

Lidocaine-epinephrine-, phenylephrine-, or cocaine-soaked pledgets (dilute the latter 2 

agents 1:1 with normal saline to minimize systemic effects) can be placed in the inferior 

nostril via narrow forceps, then successively pushed superiorly until the nostril is 

packed. Commercial nasal tampons (Merocel) are simple to place after lubrication with 

a petrolatum-based ointment (Figure 32-4A). They are inserted blindly along the inferior 

(floor) surface of the nostril to a depth of 8 cm and then expanded with the application of 

saline or 1:1 dilutions of the vasoconstricting agent. Take care not to injure the lateral 

turbinates. As the material expands, pressure is uniformly applied to the inner walls, 

tamponading bleeding. Pro-coagulant products (Surgicel, Gelfoam) may be used alone 

or in conjunction with other materials to augment the hemostatic effect. 

If none of these methods is successful, a formal anterior pack with petroleum jelly gauze 

strip material may be necessary. It is placed in a similar fashion to the pledgets: the end 

of a continuous strip is placed inferiorly and far back in the nose, then pushed up to 

tamponade the upper surfaces and make room for successive strips. The nostril must 

be fairly tightly packed, and most clinicians repeat the procedure on the other side if 

bleeding persists. All patients with nasal packs should receive prophylaxis against 

bacterial sinusitis: amoxicillin-clavulanate, 875 mg twice daily for adults, 40 mg/kg/d 

divided 2-3 times daily for children. Packing material should be removed by an 

otolaryngologist in 3-5 days. Patients with anterior packs can be discharged to home. 

B. Posterior Epistaxis 

Posterior bleeding more typically arises from an arterial source and will not respond to 

the methods described above. Treatment of this entity requires the use of a Foley

catheter or nasal balloon device (Epistat, Nasostat) (Figure 32-4B). In addition to a 

posterior balloon, the specialized devices have an anterior tamponade apparatus 

(balloon or expanding tampon) that can be inflated or expanded independently. To 

prevent ischemia of the anterior nasal mucosa, the anterior portion is intended to exert 

less pressure than the posterior balloon. Insert it into the nostril such that the balloon is 

in the posterior portion of the nose. Then inflate the posterior balloon with saline until the 

point of discomfort. Properly placed, the posterior balloon may be all that is required to 

stop the bleeding. Usually, though, the anterior nose should be packed with petrolatum 

gauze (or the anterior balloon or tampon inflated to low pressure with the commercial 

devices) for tamponade. Patients with posterior packs should be admitted for airway 

observation, prophylactic antibiotics, and ENT consultation. 

NASAL OBSTRUCTION 

Most patients who present to the emergency department will have an acute obstruction 

(foreign body, trauma). Rarely, the problem is a complication of a chronic obstructive 

condition, such as an infection relating to a tumor or deviated septum. 


A. History 

Ask the patient how long the symptoms have been present and whether there were any 

precipitating events. In children, the most common cause of obstruction is a foreign 

body, often a colorful bead or a piece of food, and the history and diagnosis will be 

straightforward. Patients should also be queried regarding presence of a discharge. 

Purulent or foul-smelling liquids suggest an infection component—possible 

accompanying an established foreign body. Nearly all cases of nasal obstruction will 

involve one side, negating the risk of airway compromise and allowing for outpatient 

workup of cases that defy emergency department management. 


Look into each nostril with the otoscope or a nasal speculum. Most conditions can be 

characterized and treatment initiated based on direct inspection (Table 32-5). 

SORE THROAT 

Many conditions lead to the common symptom of throat pain, and although most are 

relatively benign, several can result in airway compromise and require heroic 

interventions. The patient who presents with drooling, severe difficulty swallowing, 

stridor, or difficulty moving air should be examined in a setting where airway equipment 

is close by. The evaluation of persons with obstructive airway symptoms requires 

balancing the need for examination and imaging studies with their safety, because 

certain conditions may worsen with time. If a lateral soft tissue neck x-ray can be safely 

obtained, it should precede the examination of pediatric patients. It will help rule out 

epiglottitis and pharyngeal abscess. In some cases, it may be prudent for a person 

skilled in airway management to observe the patient while x-rays are obtained. In 

general, children with these symptoms should remain with a parent throughout the 

preliminary workup, because any distress from parental separation may worsen the 

condition.


A. History 

In children, a careful immunization history may help identify those at risk for 

Haemophilus influenzae type B (Hib) infections. Although the incidence of pediatric 

epiglottitis has fallen dramatically as a result of the Hib vaccine, it is not zero. Over what 

time course did the problem develop? The rapid development of severe symptoms 

requires a prompt workup and treatment. Is there associated odynophagia (pain with 

swallowing) or dysphagia (difficulty swallowing)? These symptoms should prompt the 

examiner to consider imaging the neck. Fever, cough, or sputum should prompt 

consideration of infectious causes, and widespread symptoms (eg, headache, body 

aches, chest and joint pains, diarrhea) suggest a viral source. Sore throat without a 

cough is more likely to be from a bacterial infection. 


Patients with significant airway swelling and compromise (epiglottitis, abscesses) 

voluntarily sit straight up with the neck slightly extended. Such a general appearance is 

ominous. Examine the floor of the mouth, looking for focal elevations and tongue 

displacement. Look at the gingiva for evidence of abscess. Examine the uvula, tonsillar 

pillars, and entrance of the oropharynx for swelling, exudate, or erythema. Asymmetry 

should increase the suspicion for an abscess (Figure 32-5). Examine the anterior neck 

for evidence of lymph node enlargement, other masses, or asymmetry. 


Lateral and anteroposterior soft tissue neck x-rays can be useful for identifying epiglottis 

or retropharyngeal abscesses (Figure 32-6). Stable patients will benefit from intravenous 

contrast CT scan to delineate the exact location and extent of any mass or abscess. 

Treatment 

Each condition requires specific treatment (Table 32-6). Simple pharyngitis is by far the 

most common cause of sore throat among children and adults, and viral infections 

predominate (90%). Recent investigations suggest that differentiating bacterial from viral 

causes is difficult to accomplish by appearance alone. Yet untreated pediatric group A 

streptococcal infections are associated with acute rheumatic fever and valvular heart 

disease. The broad application of antibiotics will inevitably lead to emergence of 

resistant strains. The combination of throat pain, fever, and tender anterior cervical 

lymph nodes and the absence of a cough suggest strep and might reasonably be 

treated immediately. Otherwise, astute clinicians often rely on rapid strep tests or culture 

to determine which patients need antibiotics. This approach requires a reliable follow-up 

mechanism to be successful. Anxious parents can usually be convinced of the wisdom 

of this strategy because it avoids unnecessary antibiotics and their occasional 

concomitant allergic reaction and other side effects. Among sicker children and adults, 

the need for admission will in many cases depend on serial assessment of breathing 

comfort and ability to take oral liquids. 

Refer to the "Oropharynx" section, below, for specific details related to peritonsillitis 

(peritonsillar cellulitis and abscess) and epiglottitis.

TOOTH FRACTURE 

Tooth fractures are graded by the Ellis classification system (Figure 32-7). Fractures of 

the enamel alone (Ellis class I) require no urgent treatment (save gentle smoothing of 

any rough edges with sandpaper). An office dentist can fill in the defect later to satisfy 

cosmetic needs, but there is no risk of long-term damage to the tooth. Class II fractures 

are deeper and expose the dentin. Such injuries are characterized by a patch of yellow 

in the middle of the tooth defect. The dentin is vulnerable to bacteria, and prompt 

covering is essential for long-term preservation of the tooth. The wound should be 

irrigated with sterile saline, dried, and covered with calcium hydroxide paste or a foil or 

equivalent dressing. Because the permanent teeth in children have relatively thin dentin 

layers, bacterial penetration to the pulp is a greater risk in Ellis II fractures and dental 

consultation is appropriate. If unavailable, apply a dressing and refer the patient for 

prompt follow-up. Identification of blood or a pink spot in the defect indicates exposure 

of the pulp and an Ellis class III injury. Typically, this portion of the tooth is quite 

sensitive, making most class III fractures quite painful. Sterile saline irrigation and 

emergency department dental consultation are standard. Consider applying a local 

anesthetic block for management of pain. 

TOOTH SUBLUXATION OR AVULSION 

Subluxation is a traumatic injury, and results in a tooth that is, to varying degrees, loose 

in the socket. Gentle pressure alternating from the lingual and buccal aspects of the 

tooth with a cotton swab will demonstrate the extent of movement and is a necessary 

part of the evaluation. Primary teeth require no treatment. Patients with minimal laxity 

(up to 2 mm at tip) can be discharged with advice to eat only liquid or soft foods and 

follow-up with a dentist. Moderate mobility (more than 2 mm) or teeth that appear partly 

extruded from the socket depth will require socket reseating and a splint to prevent 

further injury to the vascular supply and fibrous cementum connections with the 

underlying alveolar bone. Immobilizing the tooth will maximize its long-term viability. 

Various materials are available for this purpose, and are generally placed by the dentist 

in the emergency department. If the emergency physician has access to these 

materials, he or she may apply the splint and discharge the patient with dental follow-up. 

At the very least, a foil-like material can be pressed over the loose tooth and its 

neighbors to anchor it. 

Total avulsion is a somewhat more urgent matter, because the chance for tooth survival 

falls with every minute it is out of the socket. If the tooth cannot be found, the possibility 

of tracheal aspiration should be investigated. Hanks' solution is the ideal storage and 

transportation medium for avulsed teeth, but because it is rarely available outside the 

hospital, patients who call ahead should be told to put the teeth in milk. Saliva and 

normal saline are less ideal options, and plain water or a dry surface are to be avoided 

for reasons of osmolality and cellular desiccation. Dry teeth will benefit from a brief soak 

in Hanks' Balanced Salt Solution (HBSS) or normal saline, but there should be little 

delay before replanting them directly into the socket. This procedure cannot wait for the 

dental consultant and can be done by the first clinician to make contact with the patient. 

When handling the tooth, touch only the crown (enamel) surface, because the 

cementum is fragile. After irrigation with HBSS or saline, place the tooth firmly into the

socket. Compare to the shape of mirror-image teeth on the other side of the mouth to 

clarify proper orientation if multiple teeth are out. Splinting (see above) will ensure that 

the tooth remains securely in place. This may require consulting the dentist. A short 

course (5 days) of prophylactic antibiotics should be given and dental follow-up 

arranged. 

POSTEXTRACTION TOOTH HEMORRHAGE 

Bleeding from the site of a recently extracted tooth may result from the simple 

dislodgment of clot from the base of the socket or may be a sign of an underlying blood 

dyscrasia. Patients should be asked about a history of hemophilia or use of antiplatelet 

or anticoagulant drugs. Laboratory testing may be necessary to evaluate the 

coagulation status. Initial management should entail placing rolled cotton gauze in the 

socket and asking the patient to bite down for 20 minutes. As an adjunct, 

lidocaine-epinephrine can be injected into the gingiva at the bleeding site prior to gauze 

pressure. Bleeding that does not respond to these measures will require dental 

consultation for revision of the socket. 

Barrett EJ et al: Avulsed permanent teeth: a review of the literature and treatment 

guidelines. Endod Dent Traumatol 1997; 13:153. [PMID: 9550040] (A primer aimed at 

primary care dentists for optimal care of tooth avulsion.) 

Bisno AL: Acute pharyngitis. N Engl J Med 2001;18:205. [PMID: 11172144] (Review of 

current recommendations of expert advisory committees.) 

Bluestone CD: Clinical course, complications and sequelae of acute otitis media. Pediatr 

Infect Dis J 2000;19(5 Suppl):S37. [PMID: 10821471] (Description of the uncommon but 

malignant bony and intracranial extensions of suppurative middle ear infections.) 

Chopra R: Epistaxis: A review. J R Soc Health 2000;120:31. [PMID: 10918781] (Review 

of epistaxis and its management.) 

Corneli HM: Rapid strep tests in the emergency department: an evidence-based 

approach. Pediatr Emerg Care 2001;17:272. [PMID: 11493831] (Discussion of 

integration of various forms of the rapid strep test commonly used in emergency and 

primary care settings into a logical diagnostic strategy.) 

Dewhurst SN et al: Emergency treatment of orodental injuries: a review. Br J Oral 

Maxillofac Surg 1998;36:165. [PMID: 9678879] (Review of treatment strategies for a 

variety of traumatic situations, with an emphasis on management in children.) 

Donly KJ: Management of sports-related crown fractures. Dent Clin North Am 

2000;44:85. [PMID: 10635470] (Discussion specific to the problem of tooth fracture.) 

Hilton M et al: The Epley (canalith repositioning) manoeuvre for benign paroxysmal 

positional vertigo. Cochrane Database Syst Rev 2002;CD003162. [PMID: 11869655] 

(Review of randomized trials evaluating the efficacy of the canalith repositioning [Epley] 

maneuver.)

Jacobs RF: Judicious use of antibiotics for common pediatric respiratory infections. 

Pediatr Infect Dis J 2000;19:938. [PMID: 11001130] (Outlines recommendations of a 

CDC/American Academy of Pediatrics panel on treatment of common pediatric 

respiratory infections including the common cold, otitis media, sinusitis, and 

tonsillopharyngitis. Addresses principles for containment of antimicrobial resistance.) 

Kalan A et al: Foreign bodies in the nasal cavities: a comprehensive review of the 

aetiology, diagnostic pointers, and therapeutic measures. Postgrad Med J 2000;76:484. 

[PMID: 10908376] 

Klein JO: Review of consensus reports on management of acute otitis media. Pediatr 

Infect Dis J 1999;18:1152. [PMID: 10608648] (Two comprehensive summaries of 

practice guidelines for this commonly overtreated condition.) 

Layug ML et al: Interim storage of avulsed permanent teeth. J Can Dent Assoc 

1998;64:357. [PMID: 9648418] (Review of the evidence for various preservation 

techniques. A literature review leads to debunking of various myths regarding treatment 

of the avulsed tooth.) 

Lippincott LH et al: ENT issues in pregnancy. J La State Med Soc 1999;151:350. [PMID: 

10474980] (Addresses common ENT disorders and the physiologic changes in 

pregnancy that may predispose patients to develop them. Outlines safe treatments for 

epistaxis and other common ENT conditions.) 

Marais J et al: Bullous myringitis: a review. Clin Otolaryngol 1997;22:497. [PMID: 

9466056] (Review of the treatment of bullous myringitis.) 

McCracken GH Jr: Diagnosis and management of acute otitis media in the urgent care 

setting. Ann Emerg Med 2002; 39:413. [PMID: 11919528] 

Osguthorpe JD et al: Frontal sinus malignancies. Otolaryngol Clin North Am 

2001;34:269. [PMID: 11344078] (Review of paranasal tumors and their management.) 

Peyvandi F et al: Rare coagulation disorders. Thromb Haemost 1999;82:1207. [PMID: 

10544899] (Review of the presentation and management of various factor-deficiency 

conditions that may complicate epistaxis.) 

Pichichero ME et al: Controversies in the medical management of persistent and 

recurrent acute otitis media. Recommendations of a clinical advisory committee. Ann 

Otol Rhinol Laryngol (Suppl) 2000;183:1. [PMID: 10963616] (Review of 

recommendations for management of chronic otitis media.) 

Pond F et al: Epistaxis: strategies for management. Aust Fam Physician 2000;29:933. 

[PMID: 11059081] (Review of epistaxis and its management.) 

Schapowal A: Otitis externa: a clinical overview. Ear Nose Throat J 2002;81:21. [PMID: 

12199185] 

Schulze SL et al: Pediatric external auditory canal foreign bodies: a review of 698

cases. Otolaryngol Head Neck Surg 2002; 127:73. [PMID: 12161734] 

Stollerman GH: Rheumatic fever in the 21st century. Clin Infect Dis 2001;33:806. 

[PMID: 11512086] (Review of the pathogenesis of acute rheumatic fever and acute 

glomerulonephritis, with diagnosis and treatment recommendations.) 

Thompson LD et al: Extracranial sinonasal tract meningiomas: a clinicopathologic study 

of 30 cases with a review of the literature. Am J Surg Pathol 2000;24:640. [PMID: 

10800982] (Review of paranasal tumors and their management.) 

Tusa RJ: Vertigo. Neurol Clin 2001;19:23. [PMID: 11471767] (Thorough review of 

diagnostic and management strategies for vertigo. Includes discussion of 

nonpharmacologic modalities.) 

Wang NE et al: Mastoiditis: a case-based review. Pediatr Emerg Care 1998;14:290. 

[PMID: 9733257] (Review.) 

Zadeh MH et al: Evaluation of hearing impairment. Compr Ther 2001;27:302. [PMID: 

11765688] (Review of the approach to identifying and treating causes of sudden and 

semiacute hearing loss.) 


DISORDERS OF THE EAR 

Please refer to the "Immediate Management" section and Table 32-1 for discussion of 

the following conditions: otitis externa, malignant otitis externa, foreign body or insect in 

canal, infected sebaceous cyst, chondritis, perichondritis, suppurative and serous otitis 

media, bullous myringitis, and acute mastoiditis. 

CERUMEN IMPACTION 


• Readily apparent by direct otoscope inspection. 


The walls of the ear canal possess a secretory mechanism that results in a coating of 

the familiar waxy substance, cerumen. Over months, this material can collect and result 

in canal obstruction. Rarely does the material need to be emergently removed, but its 

presence can lead to mild pressure, vertigo, or hearing loss symptoms, and it may 

obscure inspection of the tympanic membrane. 

Treatment 

Two methods are available for evacuation: blunt removal and irrigation. Blunt removal

entails use of a plastic curette, and care must be taken not to puncture the drum or 

injure the walls of the canal. Large, hard impactions may defy easy removal by this 

method and are better suited to removal by irrigation. Blunt removal should be 

discontinued if it becomes clear that the drum is perforated. For irrigation, a warm 

solution of equal parts 3% hydrogen peroxide and water is directed at the mass with a 

flexible catheter. Cut the catheter of a butterfly needle and attach the remaining tubing 

to a 30 cc syringe. The flexible tubing can be inserted directly into the canal by the 

patient or clinician with little risk of injuring the walls or tympanic membrane. Repeated 

emergency department irrigation at 15-minute intervals will remove all but the hardest 

masses. If this method does not work, continued home treatments (5-10 per day) will 

soften and clear the remaining obstruction within a few days. Care should be taken with 

either method in elderly or diabetic patients because canal trauma may predispose the 

patient to malignant otitis externa. 

FROSTBITE 


• Protruding appendages (ie, nose, ears, fingers, toes) are affected most often. 

• Pale color, insensate. 

• Injury borders may not be apparent for several hours. 


The nose and auricle are particularly vulnerable to injury from cold exposure. Superficial 

skin injuries are red and tender in the emergency department, but moderate and severe 

cases will appear pale and lack sensation prior to warming. Pain may not develop until 

later. After warming, the skin appearance will provide clues to the severity and extent of 

the damage. In the emergency department, the affected areas should be warmed with 

saline of slightly more than body temperature (100-105 °F). Inspect the lips, nose, and 

auricle regarding shape and contours, sensation, edema, skin color, and lesions. It may 

be helpful to draw a diagram showing the borders of injury. The distal edges of the 

auricle and tip of the nose are typically the first to be affected by cold exposure, with 

injury progressing proximally after prolonged exposure. 

Grading the Injury 

Accurate grading of cold exposure injuries can be attempted 1-2 hours after rewarming, 

but serious cases may require 1-2 days of observation for full assessment. Frostnip is a 

mild form of injury, characterized by pain, pallor, and numbness and resolves with no 

permanent injury after rewarming. Frostbite is graded in 4 levels of severity: 

1. First-degree injuries demonstrate hyperemia and edema, with eventual return of most 

sensation. 

2. Second-degree injuries are similar to first-degree injuries but involve blisters. 

Recovery of sensation is variable.

3. Third-degree injuries exhibit deeper skin and cartilaginous tissue damage, with 

smaller, hemorrhagic, blisters. There is significant permanent sensory deficit. 

4. Fourth-degree injuries remain pale, insensate, develop no blisters, and have 

permanent skin and cartilage breakdown. There is eventual full-thickness necrosis and 

deformity. 

Patients should be assessed for systemic cold injury and receive treatment for core 

hypothermia if necessary. Significant cold exposure causes a physiologic diuresis, and 

persons with prolonged exposure should receive warmed intravenous fluids. The ear 

should be covered (usually with a head wrap) with care taken to preserve the inherent 

shape and projection of the pinna. Gauze padding may be loosely placed in and behind 

the ear to preserve its shape until it has healed. The full extent of injury may take days 

to become apparent, and hospitalization for wound care is appropriate for severe (third- 

or fourth-degree) injuries. Update the tetanus toxoid. Recovered areas will remain 

abnormally cold-sensitive and prone to injury, because the tissues rarely heal 

completely. Encourage patients to avoid future cold exposure. 

CHRONIC (SUPPURATIVE) OTITIS MEDIA 


• Persistent ear pain and discharge despite antibiotics. 

Chronic otitis media refers to persistent discharge of purulent fluid through a tympanic 

membrane perforation. Ordinary ruptures of the tympanic membrane heal in 1-2 weeks, 

and persistent defects should prompt close scrutiny. Accumulations of keratin result in 

formation of a cholesteatoma, which can contribute to injury to the bony structures of 

the middle ear. Persistent infections of the middle ear have a low incidence association 

with meningitis (from hematogenous spread) as well as mastoiditis. CT scan will reveal 

the latter condition, and clinical judgment should be used to determine which patients 

need a lumbar puncture. Management of mastoiditis is usually surgical. Infections 

limited to the middle ear should be treated with antibiotics (see Table 32-1) and prompt 

outpatient ENT evaluation. 

DISORDERS OF THE SINUSES (SINUSITIS) 


• Midface pain associated with fever and purulent nasal discharge. 

• Often recurrent. 


The paranasal sinuses (maxillary, frontal, ethmoid, and sphenoid) are ordinarily air filled 

and communicate with the nasal passages through small ostia. Most bacterial infections 

occur in the setting of functional or anatomic obstruction, inflammation, impaired 

drainage, and bacterial overgrowth. The sinus fills with purulent fluid. Chronic sinusitis 

occurs with infections that persist for more than 3 months—often in a setting of 

irreversible obstruction or resistant bacteria and sometimes requires surgical drainage. 


A. History 

Sinusitis universally causes pain and pressure to the upper face, which may be 

perceived as a frontal headache. Fever, chills, and nasal discharge are common. When 

nasal discharge is present, determine the side of the discharge. Maxillary sinusitis 

commonly causes pain in the upper teeth. Symptoms typically worsen over 1-3 days 

and may follow an upper respiratory infection. Some patients with structural anomalies 

are predisposed to these infections and may give a history of similar previous episodes. 


Fever may be present. Classically, pressure or gentle tapping over the affected sinus 

will reveal tenderness on one side. The maxillary sinus is most often affected and can 

be examined by applying bilateral thumb pressure to the inferior aspect of the zygotic 

prominence above the corners of the mouth. Transillumination of the maxillary sinus can 

be accomplished in a darkened room by placing the otoscope light source directly 

against the zygoma and observing transmission of light through the anterior hard palate 

(behind the upper incisors). Though this test is less sensitive than x-ray, the presence of 

purulent fluid in the maxillary sinus will often obscure the light on one side. Plain sinus 

x-rays will reveal the presence of large sinus fluid collections (Figure 32-8A and B), but 

CT scan is the most sensitive test and will reveal anatomic anomalies such as small 

tumors or a deviated septum (Figure 32-8C). Typically this study can be done on an 

outpatient basis if the diagnosis remains in question or if the infection has failed to 

improve with a course of antibiotics. 

Treatment 

Culturing the sinus fluid directly is not practical in the emergency department. Empiric 

antimicrobial therapy should cover H influenzae, Moraxella catarrhalis, and 

gram-positive bacteria. Therapy should be continued for 12 days. 

Amoxicillin-clavulanate, 875 mg twice daily, covers ß-lactamase-resistant strains and 

the mixed flora typical of these infections. Trimethoprim-sulfamethoxazole and 

cefuroxime are alternatives for penicillin-allergic patients. Nasal decongestant pills and 

sprays can sometimes reduce swelling around the sinus ostia and promote drainage. 

Often the infection in the sinus is related to a mass (tumor, polyp, deviated septum, 

turbinate anomaly) or inadequate drainage (middle meatus obstruction), and patients 

should be referred to a primary care clinician or otolaryngologist for an evaluation after 

resolution of the acute episode. Occasionally surgical correction may be necessary. 

Chronic sinusitis has been associated with Staphylococcus aureus infections, but lasting 

resolution will often follow only surgical drainage and correction of the anatomic 

obstruction. Immunocompromised persons are at risk for Pseudomonas aeruginosa and

fungal infections. Treatment recommendations continue to evolve for chronic, recurrent 

sinusitis, largely in response to poor long-term success rates among some patient 

groups. 

Complications 

Several conditions related to sinus infection have been described. Direct extension of 

the infection to surrounding tissues can lead to frontal osteomyelitis, facial cellulitis, 

periorbital cellulitis, or periorbital abscess. For this reason, high fever, ocular movement 

problems, enophthalmos, diplopia, facial skin swelling, erythema, or extreme tenderness 

should be studied by CT scan. Intracranial extension can lead to meningitis, cavernous 

sinus thrombosis, brain abscess, or subdural empyema. Therefore, prominence of a 

headache or neurologic findings should prompt examination with CT scan or lumbar 

puncture. 

DISORDERS OF THE OROPHARYNX 

Please refer to the "Immediate Management" section and Table 32-6 for discussion of 

epiglottitis, Ludwig angina, and other causes of throat pain. What follows is a more 

detailed discussion regarding the pathophysiology and treatment of airway deep space 

infections. 

PERITONSILLITIS (PERITONSILLAR CELLULITIS & ABSCESS) 


• Extensive swelling does not typically obstruct the airway. 

• "Hot potato" voice. 

• Fever, severe pain. 

• Systemic dehydration typical. 


Peritonsillitis, peritonsillar cellulitis, and abscess (also known collectively as quinsy) are 

extensions of mixed-flora bacterial infections of the tonsils. The differentiation between 

cellulitis and abscess is difficult to make on clinical grounds and is determined by 

identification of an abscess by intravenous contrast CT scan or more commonly by 

drainage of pus after aspirating or incising the mass. Therefore, the initial treatment of 

each is the same. See Table 32-6 for a review of typical symptoms and a differential 

diagnosis. Once the diagnosis is made, most peritonsillar masses should be treated with 

intravenous antibiotics and a drainage procedure in the emergency department. 

Drainage Procedure 

A. Preparation 

First, make certain that the patient does not have obstructive airway issues. Patients 

with impending airway collapse should receive an emergency artificial airway prior to

decompression of the mass. The patient should be placed sitting upright in a dental 

chair with a headrest supporting the occiput. The upright position makes handling of oral 

secretions easier, and the headrest helps the patient relax and restricts movement 

during the procedure. The tonsillar mass should be palpated gently with a cotton swab 

to confirm fluctuance. A pulsatile mass should prompt the clinician to order an 

intravenous contrast enhanced CT scan to confirm the diagnosis and rule out the 

possibility of carotid artery aneurysm. For the drainage procedure to be successful, 

patients must not have extreme trismus and they should be cooperative and well 

anesthetized. Patients will generally be more cooperative when premedicated with a 

moderate dose of intravenous or oral opiate analgesic. Next, use a topical anesthetic 

spray such as Benzocaine-tetracaine, followed by an injection of 1-2 ml of 2% 

lidocaine-epinephrine into the mucosal layer of the abscess. Frazier suction should be 

made ready for control of secretions and any pus or blood that result from the 

procedure. 

B. Needle Drainage 

Place an 18-gauge needle on a 10-mL syringe. The tip of the plastic needle cap should 

be cut off such that when placed back on the needle, 0.5 cm of the needle protrudes 

beyond the end. This will prevent accidental deep penetration of the mass. Insert the 

needle on an axis level with the tongue into the superior pole of the peritonsillar mass 

(the most common site for fluid) and aspirate (Figure 32-9). Remove and culture as 

much fluid as possible. Next, aspirate from the middle pole, then the inferior pole. Take 

care to avoid directing the needle in a lateral direction, so as to avoid puncturing the 

carotid artery. Because the needle may have missed the pocket of fluid, or the fluid may 

have been too thick to flow through the needle, a negative aspirate procedure does not 

rule out an abscess. Opening the pocket with a scalpel blade (see below) at the location 

where pus was aspirated is optional but will minimize the risk of recurrence. 

C. Open Drainage 

Though many clinicians advocate needle aspiration (with antibiotics) as a safer and 

more comfortable method, incision and drainage with a scalpel blade appears to 

minimize recurrence risk. Some authors have suggested incising the mass at the 

location where pus has been aspirated by needle to minimize risk of both injury and 

infection recurrence. After anesthetizing the upper pole of the mass (see above), tape 

should be wrapped around the proximal aspect of the blade to prevent it from being 

inserted deeper than 0.5 cm. A single stab of depth 0.5 cm is made into the superior 

pole and extended no more than 0.5 cm in an inferolateral direction. Place the suction 

device tip into the incised area to remove any pus. Any bleeding that develops will 

usually resolve after the patient gargles with diluted hydrogen peroxide or salt water. 

Patients should be observed for at least 1 hour following the procedure. Most are 

dehydrated and will benefit from intravenous fluids. Those able to take oral fluids and 

pills can be discharged with oral antibiotics. The preferred regimen is penicillin, 2-4 

million units intravenously followed by 500 mg orally 4 times daily, or cephalosporins 

(eg, cefazolin, 1 g intravenously, followed by cephalexin, 500 mg 4 times daily for 10 

days). Most patients will need oral nonsteroidal anti-inflammatory agents and opiate 

analgesics for pain control. ENT follow-up in 2-3 days should be arranged. Patients with 

high fever, those unable to take oral fluids, and immunocompromised patients should be 

admitted for intravenous fluids and antibiotics. Some authors have advocated admitting

patients with negative aspirates as well, for intravenous antibiotics and close 

observation. 

EPIGLOTTITIS 


• Fever, throat pain, swallowing pain. 

• Decreased prevalence in children. 

• Adults appear nontoxic. 

• Definitive diagnosis by endoscopy. 

Due to widespread use of the Hib vaccine, epiglottitis is now more common among 

adults than children. Children with epiglottitis have high fever and varying levels of 

toxicity by appearance (see Table 32-6). In children suspected of having epiglottitis, 

flexible fiberoptic or direct laryngoscopy must be done to make or rule out the diagnosis. 

First, a skilled pediatric airway specialist must be called (this may be the emergency 

physician, otolaryngologist, or anesthesiologist). If patient stability permits, this clinician 

can accompany the child and parent while a lateral soft tissue neck x-ray is obtained. 

This, alone, may demonstrate the enlarged epiglottis (see Figure 32-6C). If the 

diagnosis remains uncertain, or the child is too unstable to have an x-ray, the patient 

should be accompanied to the operating room, where laryngoscopy or endotracheal 

intubation can be accomplished in a setting where a surgical airway can be easily done 

if the orotracheal method fails. All pediatric patients found to have epiglottitis should 

ultimately be intubated for airway protection and admitted. 

Adults with epiglottitis usually present with 2-3 days of steadily worsening throat pain, 

difficulty swallowing, and fever. The potential for rapid loss of airway patency is lower 

among adults, and most patients can have x-ray and emergency department flexible 

fiberoptic laryngoscopy without concern for rapid airway collapse. Those with epiglottitis 

should be admitted and receive intravenous antibiotics such as ceftriaxone, 1 g 

intravenously or intramuscularly every 24 hours. 

CROUP 


• Associated with a recent upper respiratory infection. 

• "Barking" cough. 

• Often quick resolution. 


Croup (laryngotracheobronchitis) is exclusively a disease of children, affecting mainly 

those aged 6 months to 3 years. It is the most common cause of stridor among young

children presenting to the emergency department. Unlike the supraglottic swelling of 

epiglottitis, croup leads to obstruction of the subglottic trachea (below the cords, mainly 

at the level of the cricoid cartilage). 


A. History 

The predominant cause is parainfluenza virus, and its peak incidence is fall and winter. 

The children are typically brought in at night, having recently developed a barking cough 

preceded by 2-3 days of a viral-type respiratory infection. The stridulous breathing is 

noisy and high-pitched, a result of air traveling through a severely narrowed airway. On 

occasion the symptoms will have improved by the time of arrival at the emergency 

department—possibly related to cold or moist night air. Because an aspirated airway 

foreign body could mimic the symptoms of croup, parents should be questioned 

regarding this possibility. 


Children with croup usually appear nontoxic. When present, fever is usually low grade, 

reflecting an underlying viral infection. With exertion or crying, rapid air movement 

through the small subglottic aperture becomes difficult and respiratory distress worsens. 

In extreme cases, cyanosis may occur. Because the lungs are not affected, the oxygen 

saturation is typically normal. Oropharyngeal exam is normal or may reveal the bilateral 

nonspecific erythema and swelling associated with a viral upper respiratory infection. 

Any unilateral swelling or tonsillar exudates should prompt consideration of bacterial 

surface or closed-space infections. Transmitted airway noise may obscure auscultation 

of lung sounds, which are normal in croup. An anteroposterior soft tissue neck x-ray will 

demonstrate the steeple sign of upper tracheal narrowing (Figure 32-10A). The serum 

white blood count may be elevated, but this is not specific for croup and has little value 

for differentiating croup from other processes. Occasionally, older children will present 

with a barking cough and the appearance of croup. An anteroposterior soft tissue neck 

x-ray will confirm the diagnosis (Figure 32-10B). The underlying cause is more likely to 

be bacterial among children older than 6 years. 

Treatment 

Consideration should be given to the stability of the patient's airway. Croup rarely leads 

to complete airway obstruction, and mild epiglottitis can present with symptoms similar 

to croup (see "Epiglottitis" section, above). The initial therapy is nebulized saline, which 

can be delivered by face mask or by having the parent direct the mist at the child's 

mouth ("blow-by"). Nebulized racemic epinephrine should be used for patients who do 

not improve promptly: place 10 drops of 2.25% solution and 2-3 mL of saline in a 

nebulizer. The treatment may be repeated every 20-30 minutes. Dexamethasone, 0.6 

mg/kg intramuscularly, is a useful adjunct for refractory croup. Serial clinical evaluations 

of patient comfort will help identify the small percentage of children who will require 

admission for observation and further therapy. Typically the symptoms improve within 

1-2 hours in the emergency department, and the children can be discharged. 

DISORDERS OF THE MOUTH

Though myriad disorders involve the teeth and periodontal tissues, patients typically 

present to the emergency department with acute processes in the mouth such as pain. 

Careful examination of the mouth is the key to correct diagnosis. 

TOOTH ANATOMY 

Teeth consist of a central pulp tissue, which is innervated by pain fibers and produces 

dentin (Figure 32-11). The dentin surrounds the pulp; makes up the bulk of the tooth 

mass; and is coated with enamel, a hard material that forms the outer surface of the 

tooth. The tooth surface of the root portion comprises cementum, which is less dense 

than enamel and not designed to withstand exposure to mouth flora and acids. Each 

tooth is embedded in periodontium, which consists of a bony support (alveolar bone) 

that is contiguous with underlying mandible and maxilla. The gingiva is the highly 

vascular mucosal tissue (gums) that covers the alveolar bone. 

TOOTH PAIN (See Table 32-7. ) 


• Commonly associated with prior tooth injury or cavity. 

• Differentiate simple infection from abscess. 


A. History 

Because dental caries are the most common source of tooth pain, ask patients about 

their cleaning habits and frequency of dentist visits. Duration and rate of pain onset may 

be useful clues to a subacute process, whereas recent trauma or dental instrumentation 

would suggest a noninfectious problem. Is the pain limited to one tooth or a particular 

area of the mouth? Pain that worsens with chewing implicates a local tooth problem. 


The focus of the examination should be the area said to be painful. Tap on suspect 

teeth with a tongue blade: This will elicit tenderness from infections inside the tooth 

(pulpitis) and at the tooth root (periapical abscesses). A high degree of tenderness 

suggests the latter, and a Panorex film is useful for confirming the diagnosis. A thorough 

viewing of the tooth and surrounding periodontium from all sides (use a warmed mirror 

to look at the lingual aspect) may demonstrate the cavity or any swelling. Focal 

erythema, swelling, and fluctuance would suggest a periodontal abscess. Examine the 

gingiva for ulcerations and pseudomembranes (acute necrotizing ulcerative gingivitis). 

The presence of blood can indicate poor periodontal health or may have resulted from 

recent trauma or instrumentation. Examine the tongue and floor of the mouth. Extension 

of dental infections into the soft tissues of the mandible can lead to Ludwig angina, 

characterized by a firm, boardlike mouth floor and tongue elevation (see Table 32-6). 

Treatment

Because most conditions are best treated definitively in a fully equipped dental office, 

oral analgesics and discharge with dental follow-up are usually indicated. Most patients 

benefit from anti-inflammatory agents such as ibuprofen or naproxen, or oral opiate 

analgesics such as codeine or hydrocodone as an adjunct. Application of a tooth block 

with a long-acting local anesthetic can provide hours of relief for those with severe pain 

and can reduce the reliance on oral analgesics. The anesthetic must be injected to the 

depth of the root tip to be effective. Place a block by injecting a 25-gauge needle parallel 

to the tooth to a depth of 0.5-0.8 cm (from the tooth-gingival interface) and infiltrate with 

0.75% bupivacaine. 

Because dental pain is a favored complaint of drug seekers, a small portion of those 

presenting with toothache will have fictitious pain. Short courses (2-3 days) of opiates 

are advisable when the presentation seems implausible. Some authors have suggested 

that the absence of relief from a well-placed block suggests an ulterior motive. 

Most painful tooth conditions also require therapy with an antibiotic. Oral penicillin, 500 

mg 4 times daily, is the treatment of choice for typical tooth and periodontal infections, 

but immunocompromised patients and those with high fever or severe illness should 

have parenteral penicillin, 15-20 million units/d, or a cephalosporin as well as 

clindamycin for anaerobic (mainly Bacteroides fragilis) coverage. Amoxicillin-clavulanate 

is a single oral agent that covers these organisms. 

TMJ PAIN 

TMJ pain (also broadly labeled temporomandibular disorder) is an inflammatory process 

of the temporomandibular joint, which often relates to overuse, trauma, or various 

arthritides. 


The joint area is tender to pressure on one or both sides, and pain is elicited with biting 

down on a tongue blade and mandible manipulation. The examiner can grip the chin 

and lower incisors and gently rock the mandible from side to side to elicit TMJ 

tenderness. Except in cases of recent trauma, x-ray images are rarely indicated in the 

acute setting. 


The usual therapy is for the patient to reduce the forceful use of the joint by avoiding 

hard foods and to use anti-inflammatory medications for 1-2 weeks. Follow-up with a 

dental professional for persistent pain is recommended, at which point chewing and 

biting habits can be explored. Occasionally, corrective appliances are used to promote 

correct positioning and use of the jaw. 

TMJ DISLOCATION 


• Inability to close mouth. 

• Onset sudden, associated with a "click." 

One of the most satisfying procedures encountered in the emergency department is 

reduction of a TMJ dislocation. Typically the patient gives a history of wide mouth 

opening (typically a yawn or laughter) followed by an inability to close the mouth after 

feeling a click. Often, these patients are intoxicated. They present with mouth open, are 

unable to speak clearly, and are sometimes distressed due to masseter spasm and 

pain. If the examination reveals deviation of the mandible to one side, the dislocation 

may be unilateral. 

The solution is easy and elegant. The clinician sits the patient on a stretcher with the 

back up to support the head (alternatively, the patient can be placed sitting on the floor 

with his or her back against the wall). The clinician faces the patient, and after padding 

the thumbs with layers of gauze, places them on the posterior lower molars and grips 

the underside of the mandible angle with the fingers. Steady, forceful downward 

pressure is applied onto the rear molars. Successful reduction is characterized by a 

sudden snapping of the mandible back into place, which can put the examiner's digits at 

risk of a bite injury if he or she is not prepared. The patient will have immediate relief. If 

severe masseter spasm is present, a muscle relaxant (eg, diazepam or midazolam 

intravenously) will make for an easier reduction. Patients who sustain this injury are at 

increased risk for developing it again and should be warned to avoid wide mouth 

openings in the future. 

American Academy of Pediatrics Subcommittee on Management of Sinusitis and 

Committee on Quality Improvement: Clinical practice guideline: Management of 

sinusitis. Pediatrics 2001; 108:798. [PMID: 11533355] (Practice guidelines addressing 

the choice of optimal antibiotics and the identification of patients who will require them.) 

Blotter JW et al: Otolaryngology consultation for peritonsillar abscess in the pediatric 

population. Laryngoscope 2000;110: 1698. [PMID: 11037828] (Review of 102 pediatric 

peritonsillitis cases treated with admission, intravenous antibiotics, and either discharge 

or tonsillectomy in the operating room, depending on response to 24 hours of therapy.) 

Hartmann RW Jr: Ludwig's angina in children. Am Fam Physician 1999;60:109. [PMID: 

10414632] (Review.) 

Hebert PC et al: Adult epiglottitis in a Canadian setting. Laryngoscope 1998;108:64. 

[PMID: 9432069] (Retrospective review of 813 cases in 2 centers reveals a case fatality 

rate of 1.2%.) 

Luhmann JD et al: Sedation for peritonsillar abscess drainage in the pediatric 

emergency department. Pediatr Emerg Care 2002; 18:1. [PMID: 11862127] (Review of 

an institutional experience with conscious sedation for incision and drainage treatment 

in 42 children over a 3.5-year time period.) 

Murphy JV et al: Frostbite: pathogenesis and treatment. J Trauma 2000;48:171. [PMID: 

10647591] (Review of recent developments in the understanding of pathophysiology

and treatment of cold-induced injury.) 

Newton-John T et al: Chronic idiopathic orofacial pain: II. What can the general dental 

practitioner do? Br Dent J 2001;191: 72. [PMID: 11508414] (Review of the scope of 

treatment options for new and chronic temporomandibular disorder pain.) 

Reamy BV: Frostbite: review and current concepts. J Am Board Fam Pract 1998;11:34. 

[PMID: 9456445] (Review of recent developments in the understanding of 

pathophysiology and treatment of cold-induced injury.) 

Rosekrans JA: Viral croup: current diagnosis and treatment. Mayo Clin Proc 

1998;73:1102. [PMID: 9818047] (Review.) 

Snow V et al: Principles of appropriate antibiotic use for acute sinusitis in adults. Ann 

Intern Med 2001;134:495. [PMID: 11255527] (Review of appropriate antibiotic use in 

sinusitis.) 

Steed PA et al: Temporomandibular disorders—traumatic etiology vs. nontraumatic 

etiology: a clinical and methodological inquiry into symptomatology and treatment 

outcomes. Cranio 2001;19:188. [PMID: 11482831] (Multicenter observational study 

evaluating the demographic distribution, symptom characteristics, and outcomes of 

1842 patients with temporomandibular disorders.) 

Stroud RH et al: An update on inflammatory disorders of the pediatric airway: epiglottitis, 

croup, and tracheitis. Am J Otolaryngol 2001;22:268. [PMID: 11464324] (Review of 

pediatric airway conditions requiring management in the emergency department.) 






I. IMMEDIATE MANAGEMENT OF POTENTIALLY HARMFUL 

DISORDERS

Table 32-1. Diagnosis and treatment of ear pain. 

Diagnostic Clues Comments 

Fever or chills; pain, 

swelling, and erythema 

at mastoid process. 

Typically an extension 

of acute otitis media. 

Normal canal and 

findings of concurrent 

otitis media. 

Severe ear pain. TM: 

bullae on TM surface, 

with surrounding 

erythema. Middle ear 

space not affected. 

Pain or swelling to the 

external (cartilaginous) 

ear. Recent ear trauma. 

Warm, erythematous, 

tender auricle, pinna 

skin. Evidence of recent 

trauma or piercing. If 

ear is deformed, 

suspect chondritis 

(cartilage infection). 

Usually young child, 

witnessed insertion. 

Foreign body in canal. 

Pain in canal. No 

discharge. 

Erythematous, cystic 

canal surface. Pain with 

pinna traction. 

Buzzing or movement 

sensation. Insect in 

canal or on TM. 

Relatively rare. Usually S pneumoniae, 

S pyogenes, S. aureus. If it develops 

after resolved otitis media: acute 

coalescent mastoiditis. 

Mycoplasma (or viral). 

If canal trauma is present, treat as for 

otitis externa, outpatient follow-up. 

May prevent recurrence with selenium 

sulfide (Selsun) or ketoconazole/steroid 

shampoo. 

Alternatively, may remove a large insect 

with narrow alligator forceps through the 

otoscope. 

Place a cotton wick through an 

obstructed or near-obstructed canal. 

Treat with topical steroid and antibiotic 

preparations: 

hydrocortisone-polymyxinneomycin 

(Cortisporin Otic), 4 drops qid, or 

hydrocortisone-ciprofloxacin (Cipro HC 

Otic), 3 drops bid. 

Otitis externa (malignant)

Common in children. 

Preceding upper 

respiratory infection. 

May lead to TM rupture 

(severe pain followed 

by rapid, spontaneous 

relief). Normal canal. 

TM is erythematous, 

dull light reflex, limited 

motility (most specific), 

landmarks not visible. 

Compare to other side. 

Make note of TM 

rupture, if present. 

Decreased hearing on 

affected side. 

Typical organisms: S pneumonia, H 

influenzae (children). Ruptured TM will 

require follow-up every 2-4 weeks to 

ensure healing.

Table 32-2. Causes of sudden hearing loss. 

Note: All are sensorineuronal except in the conductive 

category. U = unilateral; B = bilateral (typically). 






TABLES 

Table 32-2. Causes of sudden hearing loss.

Table 32-3. Central versus peripheral vertigo. 

Peripheral Causes 

Duration of onset Weeks to months. 

Severe. Nausea, vomiting Often absent. 

Movement exacerbates 

symptoms. 

Patient age Usually elderly. 

Always horizontal or Cranial nerve or cerebellar 

rotatory. Worse with head deficits 

movements and fatigues 

over 5-30 seconds. 

Often decreased 

(unilateral) or with 

tinnitus. 

Often present (especially 

ataxia—usually with slow onset; 

sudden onset suggests cerebellar 

hemorrhage). 

Causes Drugs. 

Cerebellar mass or stroke. 

Encephalitis or brain abscess. 

Vertebral basilar artery 

insufficiency. 

Temporal lobe epilepsy. 

Multiple sclerosis.

Table 32-4. Causes of peripheral vertigo. 

Diagnosis Acoustic neuroma Schwann cell tumor. Recovery correla 

with early surgery. 

Symptoms and nystagmus 

associated with head 

movement—often subsiding 

gradually several minutes 

after movement. 

Prominent hearing loss and 

vertigo. Temporally related 

to recent bacterial infection 

of middle or inner ear. 

Diagnosis by CT scan. 

Meniere disease (paroxysmal 

labyrinthine vertigo) 

Sometimes associated with high salt 

intake; may improve with low-sodium d 

Vestibular neuronitis Lasts 3-7 days, but mild symptoms ma 

persist for weeks. Thought to be relate 

viral labyrinthitis.

Table 32-5. Diagnosis and treatment of nasal obstruction. 

Diagnostic Clues Abscess Incise, drain, place temporary wick, or 

pack inside to prevent recurrence. 

Neonates only. Nasal Deviated septum 

tube will be difficult to 

pass on affected side. 

Treat sinusitis, if present. ENT referral. 

Typically infants, 

small children. 

Objects evident by 

inspection of the 

nostril. Purulent 

discharge may 

indicate concurrent 

sinusitis. 

Hematoma Incise, drain completely, pack loosely to 

ensure that mucosal layer is in contact 

with underlying cartilage. 

Usually painless, Rhinitis (allergic, viral) Symptomatic: decongestants, 

small. Cause minimal 

obstruction. May be 

directly visible through 

nostrils. 

Gradually progressive 

symptoms to critical 

point of emergency 

department 

presentation. 

Discharge may be 

blood streaked. Mass 

is nonfluctuant. 

antihistamines. 






TABLES 

Table 32-5. Diagnosis and treatment of nasal obstruction.

Table 32-6. Diagnosis and treatment of sore throat. 


Often history of recent food intake. May 

progress over 5-30 minutes, when severe. 

Quality of voice may help identify location of 

the swelling (hoarse: supraglottic airway; 

muffled or nasal: oropharynx). Edematous 

mucosa (uvula, soft palate) may be visible by 

direct oropharynx inspection. 

May involve mouth and pharynx, associated 

with poor oral hygiene. Mucosal ulceration, 

pseudomembranes, foul breath. 

Common. Fever; sore throat without cough; 

bilateral tonsillar swelling; and white, tender 

cervical lympha-denopathy. Often difficult to 

differentiate from viral pharyngitis on clinical 

grounds. Culture. 

Ill appearing. Fever, dysphagia common. 

Prominent gray pseudomembrane over 

tonsillar pillars. Diphtheria culture of throat 

swabs. 

Fever, voice hoarseness, severe pain, worse 

with swallowing. Drooling and sniffing position 

when swelling is severe. Condition is now as 

or more prevalent in adults, who may have lss 

acute presentations. Useful studies: soft tissue 

neck x-ray (enlarged epiglottis—"thumbprint" 

sign), fiberoptic laryngoscopy (red, swollen 

only at bedside in stable adults). 

Variable exudate, symptoms sometimes mild. 

Culture of DNA testing of oropharyngeal 

swabs. Requires genital exam and testing. 


Multiple possible routes of antigen entry, though most 

ingestion or inhalation. May be accompanied by hives 

anaphylaxis. Throat pain may be the minor complaint. 

Clinical diagnosis. 

Consider epiglottitis. Uncommonly causes airway 

obstruction, but admit patient if oral secretions are diff 

to control. Penicillin has a 10-20% failure rate. Use 

erythromycin or equivalent if treatment failure. Untreat 

group A streptococcal infection is associated with acu 

rheumatic fever. 

Uncommon in United States. Occasional toxic system 

sequelae. 

Routine use of the H influenzae vaccine has sharply 

decreased the incidence among children. Epiglottitis in 

vaccinated individual should prompt consideration of a 

antibiotic with S aureus and streptococci coverage. 

Results from orogenital contact. Symptoms may be m 

and chronic. 





TABLES 

Table 32-6. Diagnosis and treatment of sore throat.

Table 32-7. Diagnosis and treatment of tooth pain. 


Diffuse gingival pain, tenderness. May be 

accompanied by fever. Gingival tissues are 

ulcerated and may be covered with a gray 

pseudomembrane. Mouth has a foul odor. 

Formation of small (2-3 mm) white plaques on 

mucosal surfaces of the mouth. Tender to 

touch, may bleed if scraped. Surrounding 

erythema suggests secondary infection. 

Signs and symptoms of simple caries but with 

fever and extreme sensitivity to tooth 

percussion. Panorex film to demonstrate 

abscesses. 

Focal gingival swelling, erythema, fluctuance. 

Tender to pressure. 

Pain immediately following removal of a tooth. 

Rarely, pain will develop 3 days following the 

procedure, and examination of the socket 

reveals the foul odor and localized erythema 

consistent with a periodontal socket infection. 


Represents an infection of the gingiva by native mout 

flora. More common in immunocompromised persons 

mostly associated with poor oral hygiene. 

Onset often relates to stress or poor nutrition. 

Extension of the pulp infection into the root and 

periodontium, with resultant formation of an abscess. 

Advisable to suture a small piece of Penrose drain or 

iodoform tape into the cavity to keep open for 2-3 day 

(until follow-up). Frequent saltwater rinses. 

If dental consultation is not available in the socket infe 

should be referred to the dentist for prompt follow-up. 





TABLES 

Table 32-7. Diagnosis and treatment of tooth pain.

Figure 32-1. In the Webber test, vibrations are louder on the side with a conductive 

deficit. 






FIGURES 

Figure 32-1

Figure 32-2. Bone vibration that is longer than air vibration indicates a conductive 

problem. In a sensorineuronal deficit, air conduction is significantly longer than bone 

conduction. 






FIGURES 

Figure 32-2

Figure 32-3. Cauterization of bleeding at the Kiesselbach plexus. 






FIGURES 

Figure 32-3

Figure 32-4. The Xomed Merocel Pope (A) and Epistat II (B) products. 






FIGURES 

Figure 32-4

Figure 32-5. Asymmetric tonsillar pillar swelling and uvular displacement are typical of 

peritonsillitis. 






FIGURES 

Figure 32-5

Figure 32-6. Soft-tissue lateral x-rays. A: A normal soft tissue lateral x-ray 

demonstrating no enlargement of the epiglottis or tissues between the airway and 

cervical vertebrae. B: Retropharyngeal abscess in an adult. The airway is displaced 

anteriorly by a mass that contains an air-fluid level. C: Epiglottitis in a child. The 

epiglottis is enlarged and has a "thumbprint" shape. 






FIGURES 

Figure 32-6

Figure 32-7. The Ellis tooth fracture classification system. 






FIGURES 

Figure 32-7

Figure 32-8. Sinus imaging. A: Frontal sinusitis. B: Maxillary sinusitis. The affected air 

spaces are opacified due to being filled with fluid. C: CT scan demonstrating bilateral 

maxillary sinus and one ethmoid sinus opacification consistent with sinusitis. 






FIGURES 

Figure 32-8

Figure 32-9. Needle drainage sites for peritonsillar abscess. 






FIGURES 

Figure 32-9

Figure 32-10. The "steeple" sign of croup in a 1-year-old (A) and a 12-year-old (B). 






FIGURES 

Figure 32-10

Figure 32-11. Tooth anatomy. 






FIGURES 

Figure 32-11

33. Pulmonary Emergencies 1 - Christopher R. Pund, MD, & C. Keith 

Stone, MD 


(See also Chapter 11.) 

HEMOPTYSIS 


1 Portions of this chapter were revised from the chapter by John Mills, MD, & John M. 

Luce, MD, from the 4th edition. 

Hemoptysis is the expectoration of blood originating from the bronchopulmonary tree. It 

is a common condition with diverse causes ranging from benign to life-threatening 

disorders (Table 33-1). Morbidity and mortality depend primarily on the cause and 

severity of the bleeding. Massive hemoptysis is defined as coughing up of more than 

200 mL of blood in a 24-hour period or, more practically, as any amount that becomes 

hemodynamically significant or threatens ventilation. Massive hemoptysis requires 

prompt evaluation and treatment in order to prevent death from asphyxiation or 

hypovolemic shock. If a patient has active moderate hemoptysis, consisting of small 

volumes (less than 20 mL) of gross blood, or hemoptysis by history alone, management 

can proceed in a similar but more leisurely manner. 


History and physical examination are vitally important in identifying patients at high risk 

for pulmonary hemoptysis and to rule out nonpulmonary sources of hemorrhage (see 

Table 33-1). 

A. History 

Inquire about associated signs and symptoms. Hemoptysis can occur with an acute 

onset of fever, productive cough (pneumonia or bronchitis), a chronic productive cough 

(bronchiectasis or chronic bronchitis), or an acute onset of dyspnea and pleuritic chest 

pain (pulmonary embolism). Ask about weight loss, fevers, and night sweats 

(tuberculosis); underlying chronic lung disease (Goodpasture syndrome or vasculitis); 

and especially a history of tobacco use (cancer). 


Evaluate vital signs and assess patient for possible hemodynamic instability. Any 

significant hypoxia, tachypnea, tachycardia, or hypotension should be considered 

crucial in these patients. Do not continue the physical examination until the airway, 

breathing, and circulation (ABCs) have been stabilized. The examination should be 

aimed at grossly localizing the hemoptysis to a cardiac, pulmonary, or otolaryngologic 

source. Evaluate the lungs for evidence of disease, such as wheezing, rales, rhonchi, 

egophony, or hyperresonance of the chest wall. Also, assess the nose and mouth for

possible nonpulmonary sources of bleeding and perform careful cardiac auscultation for 

the opening snap or diastolic rumble associated with mitral stenosis. 

C. Laboratory Evaluation 

The laboratory evaluation should include complete blood count with differential, 

prothrombin and partial thromboplastin times, chest x-ray, electrocardiogram, and 

arterial blood gases (if severe bleeding or respiratory difficulties are present). Type and 

cross-match blood if anemia or hypotension is present. Occasionally renal function 

studies and urinalysis may be appropriate. As time permits, it may be reasonable to 

send sputum for bacterial and fungal cultures and for an acid fast bacillus stain for 

tuberculosis if suspected. 

Treatment 

Treatment depends primarily on severity and duration of hemoptysis. Immediate 

attention must be given to the ABCs. 

A. Maintain Airway, Oxygenation, and Ventilation 

Emergently protect the airway with vigorous suctioning, postural drainage, and 

endotracheal intubation as necessary to prevent asphyxiation. A large, 8.0-mm 

endotracheal tube should be used to facilitate suctioning and allow bronchoscopy as 

needed. Supplemental oxygen should be given to maintain oxygen saturation at greater 

than 95% by applied pulse oximetry. The hemithorax suspected as the source of 

bleeding should be kept in a decubitus and dependent position. In this position, the 

contralateral, well-ventilated lung field is kept free from any obstruction by blood. 

Monitor ventilation periodically with repeat arterial blood gases. 

B. Maintain Circulation 

After airway and breathing are secured, 2 large-bore (= 16-gauge) intravenous 

catheters should be placed along with cardiac monitoring and a noninvasive blood 

pressure cuff. Initiate infusion of crystalloid solution (normal saline or lactated Ringer's). 

Assess the patient for signs and symptoms of hypovolemic shock (ie, pale, cool skin; 

altered mental status; hypotension; tachycardia). Treat shock with rapid intravenous 

crystalloid infusion (up to 2 L) followed by packed red blood cells as needed. Patients 

who have thrombocytopenia should receive platelets. Patients with coagulopathy or who 

are taking Coumadin should receive fresh frozen plasma. Place a Foley catheter to 

monitor urine output if the patient is showing signs of hypovolemic shock. 

C. Provide Other Treatments 

If the bleeding continues and the patient remains unstable, urgent bronchoscopy should 

be performed. This allows suctioning of the airway, visualization of the bleeding, and 

temporary endobronchial tamponade through a balloon-tip catheter. If the bleeding 

source is clearly identified and the patient appears to be an acceptable surgical 

candidate, surgical resection can be considered by the cardiothoracic surgeon. 

However, if the patient is a poor surgical candidate, selective arteriography followed by 

bronchial artery embolization can be used. This procedure can be performed with or 

without bronchoscopy and is considered significantly safer than surgical resection, with 

much lower morbidity and mortality rates.

Disposition 

Admit all patients with massive, moderate, or ongoing hemoptysis, and seek immediate 

consultation with either a pulmonologist or a thoracic surgeon to discuss immediate 

diagnostic and therapeutic options. These patients are most often admitted to the 

intensive care unit for close observation until bleeding resolves and hemodynamic 

status is stabilized. Hospitalize other patients if initial evaluation discloses severe 

disorders requiring prompt treatment and evaluation (eg, heart failure, tuberculosis). 

Most patients with minimal hemoptysis can be discharged to home with internist or 

specialist follow-up in 3-7 days. Treat any underlying conditions (eg, pneumonia, 

bronchitis) as deemed necessary. 

Haponik EF, Fein A, Chin R: Managing life-threatening hemoptysis: has anything really 

changed? Chest 2000;118:1431. [PMID: 11083697] (Results of a survey on clinicians' 

approaches to management of life-threatening hemoptysis. Respondents were 

physicians attending the 1998 American College of Chest Physicians Annual Scientific 

Assembly.) 

Jean-Baptiste E: Clinical assessment and management of massive hemoptysis. Crit 

Care Med 2000;28(5):1642. [PMID: 10834728] (Overview of current evaluation and 

treatment of massive hemoptysis.) 

Lee TW et al: Management of massive hemoptysis: a single institution experience. Ann 

Thorac Cardiovasc Surg 2000;6:232. [PMID: 11042478] (Retrospective study evaluating 

the outcome of conservative and surgical treatment for patients presenting with massive 

hemoptysis.) 

PNEUMOTHORAX (See also Chapters 11 and 24.) 


• Acute-onset dyspnea, pleuritic chest pain. 

• Hyperresonance on percussion, decreased breath sounds on affected side. 

• Triad of tension pneumothorax: decreased breath sounds, hypotension, jugular venous 

distension. 


Pneumothorax is the abnormal collection of air within the pleural space. This condition 

may be classified as either spontaneous (primary or secondary) or traumatic 

(penetrating or blunt chest trauma, iatrogenic). 

Primary spontaneous pneumothoraces occur in patients without clinically apparent lung 

disease (often young, tall men, aged 20-40 years, who usually smoke). Secondary 

pneumothoraces are a complication of preexisting underlying pulmonary disease 

(usually chronic obstructive pulmonary disease [COPD], pneumonia, cystic fibrosis, 

asthma, tuberculosis, or Pneumocystis carinii pneumonia infection).

Traumatic pneumothoraces are common and must always be considered in trauma 

patients or in patients following any invasive procedure such as subclavian line 

placement, thoracocentesis, lung or pleural biopsies, or even barotrauma from 

positive-pressure ventilation. Tension pneumothorax is produced if air continues to enter 

the pleural space through a defect acting as a one-way valve. As this pressure within 

the pleural space becomes greater than atmospheric pressure, it can cause a shift of 

the mediastinum toward the contralateral side. This shift leads to compression on the 

vena cava with resultant decreased venous return to the heart, hypoxia, decreased 

cardiac output, and ultimately death if not treated quickly. 



Patients may be asymptomatic but usually present with any combination of pleuritic 

chest pain, tachypnea, and tachycardia. Percussion and auscultation will reveal 

hyperresonance and decreased breath sounds, respectively, on the affected side of the 

chest. In a tension pneumothorax with a significant amount of accumulated air, the 

trachea may be shifted away from the collapsed side with severe tachycardia, 

hypotension, cyanosis, and distended neck veins. 

B. Imaging and Laboratory Findings 

Chest x-ray will reveal most significant pneumothoraces except those localized to the 

anterior pleural space in supine patients. An upright chest x-ray or expiratory film may 

help with the diagnosis in these cases. Chest computed tomography (CT) scan is not 

routinely recommended for patients with first-time pneumothorax but may be indicated 

to evaluate suspected pulmonary disorders, trauma, and recurrent pneumothorax or 

while managing persistent air leaks. Assess the degree of respiratory insufficiency with 

arterial blood gases (PCO 2 , PO 2 ). 


Immediately ensure that the patient has an intact airway. If the airway is not intact, 

perform suctioning and endotracheal intubation as necessary. Provide supplemental 

oxygen if intubation is not needed. Treatment and management options depend 

primarily on the cause and size of the pneumothorax and on the patient's stability. 

Patients are generally considered stable if their respiratory rate is less than 24 

breaths/min, heart rate is between 60 and 120 beats/min with normal blood pressure, 

and oxygen saturation is greater than 90% and if the patient can speak in whole 

sentences between breaths. Otherwise, patients may be deemed unstable. 

A. Primary Spontaneous Pneumothorax 

Clinically stable patients with small pneumothoraces may be observed in the emergency 

department for 3-6 hours and discharged to home if repeat chest x-ray excludes 

progression of the pneumothorax. Aspiration is appropriate only if the pneumothorax 

enlarges. Admission is indicated for patients who cannot reliably have follow-up within 

12-48 hours with repeat chest x-ray. Patients who are unstable or stable with a large 

pneumothorax should undergo reexpansion of the lung with a 16-22F catheter (pigtail) 

attached to a Heimlich valve-water seal device or undergo tube thoracostomy and be

hospitalized. If a bronchopleural fistula is suspected or the patient may require 

positive-pressure ventilation, a 24-28F standard chest tube may be used. 

B. Secondary Spontaneous Pneumothorax 

Although somewhat controversial, it is now recommended that even clinically stable 

patients with small secondary pneumothoraces should be admitted rather than 

managed in the emergency department and discharged to home. Patients should be 

stabilized with simple aspiration or tube thoracostomy and hospitalized. Clinically stable 

patients with large pneumothoraces or unstable patients should undergo chest tube 

placement and be hospitalized. Refer these patients for medical or surgical intervention 

to prevent recurrence. 

C. Tension Pneumothorax 

Immediate needle thoracostomy (with a 14- to 16-gauge needle in the second 

intercostal space at the midclavicular line) should be performed if tension pneumothorax 

is suspected clinically. Do not wait for x-ray confirmation if the patient is unstable. 

Definitive tube thoracostomy should then be performed as soon as possible. The patient 

should be admitted for symptomatic treatment of chest pain and cough with serial chest 

x-rays until the pneumothorax resolves. 

D. Traumatic Pneumothorax 

Immediately assess for and treat tension pneumothorax if suspected as noted above. If 

the pneumothorax is secondary to blunt or penetrating injury with a high suspicion of 

hemothorax, a large-bore (32-36F) chest tube should be used to allow drainage of air 

and blood. If the pneumothorax is not highly suspect for hemothorax, a tube sized 28F 

or greater is appropriate. 

Baumann MH et al: Management of spontaneous pneumothorax. An American College 

of Chest Physicians Delphi consensus statement. Chest 2001;119(2):590. [PMID: 

11555554] (Evidence-based multidisciplinary expert panel consensus recommendations 

for management of adults with primary and secondary pneumothoraces.) 

ASTHMA & CHRONIC OBSTRUCTIVE PULMONARY DISEASE 

Asthma 


• Cough, wheezing, chest tightness, often worse at night. 

• Physical exam: prolonged expiratory phase or bilateral wheezing, tachypnea, 

tachycardia, hypoxia. 

• Reversible with bronchodilators. 

Chronic Obstructive Pulmonary Disease 

• Smoker with chronic productive cough complains of dyspnea. 

• Increased sputum production, bilateral wheezing, rales, rhonchi.


COPD is an umbrella term used to describe a group of lung conditions characterized 

primarily by chronic or recurrent airflow obstruction. The individual conditions are 

chronic bronchitis, emphysema, and asthma. Although each entity varies in its distinct 

anatomic and clinical features, patients share a common major complaint of dyspnea. 

Patients with these disorders present to the emergency department with severe 

respiratory distress, life-threatening hypoxia, and a need for emergent management. 

Because of the underlying airflow obstruction, these entities are evaluated in a similar 

manner to one another and share some basic treatment strategies. 

Asthma is a chronic but reversible inflammatory disorder of both the large and small 

airways. It is characterized by airway obstruction caused by periodic bronchospasm and 

hypersecretion of mucus. With chronic disease and prolonged attacks, smaller airways 

can become blocked secondary to increased hypertrophy of bronchial smooth muscle or 

mucus glands, progressive mast cell activation, and inflammatory cell infiltration. This 

clinical picture leads to air trapping, ventilation-perfusion mismatches, and resultant 

hypoxemia and respiratory failure. 

Chronic bronchitis and emphysema are both partially reversible but generally 

progressive diseases of airway obstruction. Both entities are highly correlated with 

tobacco smoking and are often associated with bronchospastic coughing, wheezing, 

and severe airway hyperreactivity. Chronic bronchitis is a clinical diagnosis and is 

present in any patient with a daily productive cough for at least 3 months in at least 2 

consecutive years. Its hallmark is hypersecretion of mucus in the large airways resulting 

from chronic irritation of inhaled substances and chronic infections. Emphysema is 

defined as destruction of lung parenchyma with abnormal coalescence of the airways 

distal to the terminal bronchioles. 

Many conditions are commonly associated with asthma and COPD exacerbations and 

are listed in Table 33-2. Some of these conditions are treatable, and the clinician should 

ask about them specifically while taking the patient's history. 


A. Asthma 

1. History—The most common clinical characteristics include chronic or episodic 

wheezing, cough, and dyspnea. Diagnosis depends on a prolonged history of asthmatic 

symptoms (as described above) associated with known precipitating factors (see Table 

33-2) and a sufficient, often immediate, response to bronchodilators. There may be 

associated chest tightness or pain, allergic symptoms (such as rhinitis, sneezing, nasal 

obstruction, conjunctivitis) or symptoms of purulent bronchitis or sinusitis. Presentations, 

signs, and symptoms vary widely and can change over time. Although diffuse wheezing 

is the hallmark of asthma, nonproductive cough may occur without wheezing. Asthma 

attacks can occur spontaneously without known precipitating factors. 

2. Physical examination—Patients will show some degree of respiratory distress and 

usually demonstrate periodic symptoms of coughing.

a. Mild exacerbations—Patients with mild exacerbations typically present with 

tachypnea, normal mental status, oxygen saturation greater than 95%, the ability to 

speak in full sentences, and only expiratory wheezing with prolonged expiratory phase 

on auscultation. 

b. Moderate exacerbations—Patients with moderate exacerbations get breathless 

while talking in short phrases, prefer sitting up, may appear somewhat agitated, 

commonly have increased respiratory rate with moderate use of accessory respiratory 

muscles, are tachycardic with oxygen saturation of 91-95% and a near normal PCO 2 , 

and have both inspiratory and expiratory wheezing. 

c. Severe exacerbations—Patients with severe exacerbations present with 

breathlessness at rest, ability to say only occasional words, inability to recline, 

respiratory rate greater than 30 breaths/min, oxygen saturation less than 91%, PaO 2 

less than 60 mm Hg, PaCO 2 greater than 40, significant use of accessory muscles with 

nasal flaring, heart rate greater than 120 beats/min, pulsus paradoxus often greater than 

10-20 mm Hg, agitation, and poor air movement with nearly inaudible breath sounds. 

d. Impending respiratory failure—Patients with impending respiratory failure are 

unable to speak, have paradoxical thoracoabdominal movements, relative bradycardia, 

little air movement, and are confused or drowsy secondary to increasing levels of 

carbon dioxide. 

Although an obvious relationship exists between symptoms and airflow obstruction, 

clinical findings alone are not reliable indicators of severity. Because many patients and 

physicians will underestimate the severity of airflow limitations, objective measurements 

such as peak expiratory flow (PEF) measurements should be obtained when feasible. 

B. Chronic Bronchitis 

1. History—Patients with acute exacerbations of chronic bronchitis are smokers who 

complain of increased sputum production in addition to worsening dyspnea on exertion. 

They come to the emergency department for treatment of worsening symptoms and any 

underlying complications (eg, pneumonia, congestive heart failure, pneumothorax). 

2. Physical examination—These patients were labeled in the past as "blue bloaters," 

meaning they are frequently cyanotic and overweight, with peripheral edema, but often 

appear comfortable at rest. These patients begin to present in their late 30s or early 40s 

with a history of multiple past lung infections. The dyspnea is usually mild, whereas 

peripheral edema may be marked, and the patient quickly notes limitations with 

exercising. Examination of the chest reveals bilateral wheezing, rales, and rhonchi. 

C. Emphysema 

1. History—These patients always have an extensive smoking history and complaints 

of worsening dyspnea on exertion, often with more severe coughing. As the severity and 

duration of disease progress, dyspnea may also occur at rest. 

2. Physical examination—These patients have been called "pink puffers." They are

typically thin smokers who are not cyanotic but appear quite uncomfortable and have 

significant complaints of dyspnea. They are usually over age 50 and have a chronic 

hacking cough (usually productive of scant, clear sputum). Dyspnea is often severe with 

obvious use of accessory muscles of respiration. The chest walls are barrel shaped and 

very quiet on examination, without adventitious sounds noted. 

Evaluation 

A. Medical History 

Duration, severity, and comparison with previous attacks (ie, more or less severe than 

usual) should be sought, along with recent exposure to common precipitating factors of 

disease. Identify precisely all medications being taken, with dosages and times of 

administration. Document any past or current home oxygen use; any recent completion 

of corticosteroids; and any previous hospitalizations including intensive care unit stays 

and especially intubations. 

B. Laboratory and Other Findings 

1. Arterial blood gases—An arterial blood gas is a direct measure of cardiopulmonary 

function. Although not routinely necessary for asthma patients, arterial blood gases 

should be part of the evaluation of every severe asthma attack and are virtually 

mandatory for patients with exacerbations of COPD. Symptoms and physical findings 

cannot be used to predict blood gas values accurately. All patients with acute 

exacerbations of asthma and COPD will have some degree of hypoxemia, even those 

with minimal bronchospasm undetectable by auscultation. Most asthma patients are 

hypocapnic as a result of reflex hyperventilation, whereas COPD patients may have low, 

normal, or even elevated arterial PCO 2 . 

During a severe asthma attack, as airway resistance increases significantly, poor gas 

exchange develops with worsening hypoxemia and rising PCO 2 levels. Thus, a normal 

or elevated PCO 2 with concomitant respiratory acidosis indicates a very sick patient 

with impending respiratory failure. 

Patients with chronic bronchitis and emphysema compensate for the acid load of 

chronic hypercapnia by bicarbonate retention (chronic respiratory acidosis with 

metabolic compensation), producing a relatively normal arterial blood pH. Therefore, a 

markedly lowered arterial blood pH in conjunction with hypercapnia indicates that the 

carbon dioxide retention is probably of recent onset (within 1-2 days) or that acidosis 

has a metabolic component. The new arterial blood gas must be compared with prior 

blood gas values and the current clinical condition to accurately evaluate the 

significance of the test. 

2. Chest x-ray—The chest x-ray in routine cases of asthma will be normal or 

demonstrate mild thoracic hyperinflation. However, it may be beneficial in revealing 

complications such as pneumonia, pneumothorax, or foreign body in young children 

(unilateral hyperinflation). In general, unless there is a reason to suspect another 

diagnosis or complications of asthma, a chest x-ray is not necessary for mild to 

moderate asthma.

By contrast, patients with COPD will often have chest x-ray findings, which may lead to 

changes in patient management. These findings include complications of COPD and 

findings consistent with congestive heart failure, lung cancer, tuberculosis, and pleural 

effusions. Therefore, it is recommended that a chest x-ray be ordered for all patients 

evaluated in the emergency department for an acute exacerbation of COPD. 

3. Peak expiratory flow measurement—Physicians and patients often underestimate 

the severity of asthmatic disease. PEF is a useful measurement for judging severity and 

monitoring the response to therapy in cases of mild to moderate asthma exacerbations. 

However, it is not helpful in severe asthma attacks, young children, or other difficult 

patients who are often unable or unwilling to cooperate. PEF should be compared with 

the patient's personal best or predicted peak flow values, which are based on age, sex, 

and height. PEF less than 50% of predicted indicates a severe exacerbation. 

Initially considered extremely helpful for COPD exacerbations, it is now recommended 

that PEF should not be used to diagnosis exacerbations nor determine their severity. 

4. Pulse oximetry—Pulse oximetry is used primarily to evaluate for hypoxemia. It is 

useful for monitoring oxygenation but provides no information on ventilation, hence, 

arterial blood gases are needed. 

5. Electrocardiogram—Look for evidence of supraventricular and ventricular 

arrhythmias, myocardial ischemia or infarct, and cor pulmonale (right ventricular 

hypertrophy, right atrial hypertrophy). 

6. Complete blood count and differential—Leukocytosis is common (especially in 

children) as a result of demargination induced by endogenous and exogenous 

epinephrine and corticosteroid use. Therefore, the white blood cell count is not a reliable 

indicator of infection; however, a shift to the left (to more immature leukocytes) may 

suggest infection. Marked eosinophilia occurs in some patients and does not indicate 

that asthma is due to allergy. 

7. Electrolytes—Serum electrolytes are of little benefit but may demonstrate 

hypokalemia (especially if the patient is taking diuretics) or dehydration. 

8. Microscopic examination of sputum—Sputum examination is usually not helpful in 

asthma patients unless an associated pneumonia triggered the exacerbation. 

Patients with COPD have chronically infected airways, but the amount of sputum and 

degree of purulence often increase during these exacerbations. Gram-stain samples 

may confirm the presence of significant infection (abundant polymorphonuclear 

neutrophils) and may help guide antimicrobial therapy, if needed. 

9. Theophylline levels—Serum concentrations should be obtained if the patient is 

currently taking theophylline. Theophylline has a narrow therapeutic index, and even 

when levels are toxic, the clinical examination cannot predict the level. 

Differential Diagnosis

Patients with many other conditions can present with wheezing, cough, shortness of 

breath, or any combination of the 3. 

A. Adults 

Adults can present with wheezing with many other conditions besides asthma and 

COPD. Some of these conditions include pulmonary embolus (tachycardia, tachypnea, 

hypoxia, chest pain), anaphylaxis (new medications, fish, allergens, angioedema), 

inhalation injury (history of exposure), uncompensated congestive heart failure (rales, 

distended neck veins, dependent edema, dyspnea), pneumonia (fever, cough, chills, 

infiltrate on x-ray), foreign body (elderly patients, oropharyngeal cancer, stroke), 

bronchiolitis obliterans, laryngotracheal masses, or vocal cord paralysis and 

dysfunction. 

B. Children 

In young patients with a long history of recurrent wheezing, there is little doubt about the 

diagnosis. In patients with their first attack of wheezing, look closely for other causes 

such as epiglottitis (any age, abrupt onset of fever, sore throat, inspiratory stridor, 

dysphagia, drooling, toxic appearance), croup (usually aged 6 months to 3 years, 2-3 

days of upper respiratory symptoms, "barking" cough worse at night, fever), bronchiolitis 

(usually respiratory syncytial virus, younger than age 2 years), foreign body aspiration 

(no previous history of wheezing, unilateral wheezing, unilateral atelectasis on chest 

x-ray, no response to bronchodilators). Other possibilities include cystic fibrosis, 

bronchopulmonary dysplasia, immunodeficiency syndromes, or congenital 

cardiovascular anomalies. 

Treatment 

The initial approach to treatment of asthma and COPD exacerbations revolves around 3 

goals: (1) correcting hypoxemia rapidly, (2) reversing airway obstruction, and (3) taking 

steps to reduce recurrence of airflow obstruction. These goals can be accomplished by 

providing supplemental oxygen, bronchodilators, and systemic corticosteroids as 

needed. The level of care is determined by the severity of disease. All patients should 

be placed on noninvasive blood pressure monitoring and pulse oximetry. Any patient 

having a moderate to severe attack also must be placed on a cardiac monitor, and 

peripheral venous access should be established as soon as possible. 

A. Mild Exacerbations 

1. Respiratory support—Correct hypoxemia with supplemental oxygen by nasal 

cannula. Maintain oxygen saturations greater than 90%. In asthma patients, obtain PEF 

(usually greater than 50% predicted). 

2. ß-Adrenergic agonists—These medications are the mainstay of treatment for 

asthma and COPD. The ones most commonly used are the short-acting ß 2 -selective 

agents. These agents cause rapid relaxation of bronchial smooth muscles, resulting in 

bronchodilation and reducing airflow obstruction. Albuterol, levalbuterol (the R-isomer of 

albuterol), and metaproterenol are used most often. Inhalation, through metered-dose 

inhalers (MDIs) or nebulizers, has been shown to be faster and to deliver higher 

concentrations of medication to the lungs with fewer systemic side effects than oral 

preparations. However, MDIs require coordination and a cooperative, alert patient who

can hold his or her breath for 5-10 seconds. Therefore, passive nebulized ß 2 -agonists 

are more often used in moderate and severe exacerbations. For mild disease, albuterol 

MDI dosing is 4-6 puffs every 20 minutes (up to 4 hours), and nebulized solutions 

should be given at 2.5 mg every 20-30 minutes for 3 doses as needed for dyspnea. 

Monitor patients for side effects such as tachycardia, especially if a history of underlying 

cardiovascular disease is present. An inhaled ß 2 -adrenergic agonists may need to be 

continued every 4 hours for 24-48 hours. 

3. Systemic corticosteroids—Steroids are well known to inhibit both inflammatory cell 

recruitment and the release of inflammatory mediators into the airways. Many patients 

with moderate to severe obstructive airway disease take chronic steroids. Although 

steroids do not initially change emergency department management, these medications 

are crucial to reduce the rate of relapse in moderate to severe exacerbations. They can 

also be helpful in mild attacks if the patient is not responding well to initial bronchodilator 

treatments. Consider steroids if the patient is taking oral or inhaled steroids, has had 

prolonged symptoms, or recently completed a steroid taper. The patient should continue 

steroids for 3-10 days after discharge to prevent a recurrence (adults: prednisone, 60 

mg first day, then 40 mg/d after discharge; children: prednisone, 2 mg/kg first day, then 

1 mg/kg/d after discharge). 

4. Anticholinergics—Ipratropium bromide, an atropine-like compound, is available as a 

MDI (Atrovent) and can be used to reverse vagally mediated bronchospasm without the 

unwanted anticholinergic side effects. If the asthma patient has known previous 

improvement with Atrovent, it should be added to initial therapy. Otherwise, it should be 

reserved for more severe disease. COPD patients, by contrast, should be started on 

anticholinergic nebulized or MDI treatment. Anticholinergics have proven additive 

bronchodilatory effects when used with ß 2 -adrenergic medications in this population. 

5. Antibiotics—Antibiotics are typically not indicated for mild asthma or COPD 

exacerbations unless evidence of infection is present on physical examination or chest 

x-ray. Patients with an acute exacerbation of COPD, presenting with worsening dyspnea 

and increased cough and sputum production, may have underlying pneumonia and 

should receive antibiotics. 

B. Moderate Exacerbations 

1. Respiratory support—Give supplemental oxygen by nasal cannula. Titrate to keep 

oxygen saturation greater than 90%. Higher levels of functional inspired oxygen 

concentration (FIO 2 ) in patients with COPD may be associated with worsening 

hypercapnia or apnea. This occurs because they tend to have baseline carbon dioxide 

elevations with a hypoxic ventilatory drive, and as they lose this hypoxic drive, apnea 

can occur. If the patient appears to be deteriorating, repeat arterial blood gases should 

be obtained after 30 minutes to reassess ventilation. However, clinical examination of 

the patient, not the arterial blood gas level, should direct the need for intubation. 

2. ß-Adrenergic agonists—Give albuterol, nebulized solution 2.5 mg every 20-30 

minutes for 3 doses, or MDI with spacer 6-12 puffs every 20 minutes (up to 4 hours as 

needed).

3. Systemic corticosteroids—Adults: prednisone, 60 mg orally, or methylprednisolone, 

60-125 mg intramuscularly or intravenously (if patient is unable to tolerate oral form); 

children: prednisone, 2 mg/kg first dose should be administered immediately. Discharge 

the patient to home with a steroid burst (adults: prednisone, 40 mg/d; children: 1 mg/kg, 

for 3-5 days) or taper (10-14 days) depending on severity. 

4. Anticholinergics—Ipratropium MDI or nebulized treatment should be given to 

asthma patients with known response to this medication. All COPD patients should 

receive ipratropium MDI (2-6 puffs every 4-6 hours) with albuterol or via nebulized 

treatment if unable to cooperate with inhalers. 

5. Antibiotics—Antibiotics are not indicated for patients with moderately severe asthma 

exacerbations unless evidence of infection is present on physical examination or chest 

x-ray. However, antibiotics are recommended for patients with an acute exacerbation of 

COPD. The macrolides and newer fluoroquinolones provide excellent monodrug 

therapy. 

6. Positive airway pressure—If the patient continues to deteriorate without significant 

improvement from the above measures, bilevel positive airway pressure (BiPAP) or 

continuous positive airway pressure (CPAP) can be administered in an attempt to avoid 

intubation. 

C. Severe or Life-Threatening Exacerbations 

1. Respiratory support—These patients can decompensate quickly; therefore, 

treatment should precede history taking. These patients often present with near-fatal 

asthma or COPD (evidence of respiratory failure or respiratory arrest), status 

asthmaticus (severe bronchospasm that does not respond to aggressive therapies 

within 30-60 minutes), or lethargy and disorientation. Immediate attention should be 

given to rapid correction of hypoxemia with 100% supplemental oxygen by face mask to 

keep saturations greater than 90%. 

2. Intubation and mechanical ventilation—Because patients may die without assisted 

ventilation, consider intubation if the patient appears exhausted, confused, or cyanotic. 

The clinical evaluation over time will dictate the need for intubation. Rapid-sequence 

intubation may need to be performed, but overwhelming exhaustion often makes this 

step unnecessary. Large endotracheal tubes should be used that facilitate suctioning 

and bronchoscopy, if needed. Ventilatory settings should allow an FIO 2 of 100% with 

hypoventilation (respiratory rate = 8-10 breaths/min), known as permissive hypercapnia. 

This hypercapnia, along with lower tidal volumes (6-8 mL/kg), helps to decrease 

overdistention, air trapping, and resultant barotrauma. 

3. ß-Adrenergic agonists—Give continuous albuterol nebulized treatment for 1 hour at 

high doses (5 mg every 20-30 minutes for 3 doses) to maximize results. 

4. Systemic corticosteroids—Methylprednisolone, 60-125 mg intravenously for adults, 

or 2 mg/kg for first pediatric dose, should be administered immediately. Lower doses 

(0.5 mg/kg-1.0 mg/kg) can continue, scheduled every 6-8 hours during hospitalization, 

with a 10- to 14-day oral taper on discharge.

5. Anticholinergics—Ipratropium nebulized solution, 0.5 mg every 20-30 minutes for 3 

doses, mixed with albuterol nebulized treatment should be given and then scheduled 

every 4-6 hours during hospitalization. 

6. Antibiotics—For patients with COPD, start intravenous antibiotics in the emergency 

department if they cannot tolerate oral antibiotics. Inpatient antibiotic coverage for 

pneumonia will include a combination of a fluoroquinolone, a ß-lactam/ß-lactamase 

inhibitor, a macrolide, or a third-generation cephalosporin. If the exacerbation is due 

primarily to asthma, antibiotics may be withheld. 

D. Other Known Treatment Modalities 

1. Magnesium sulfate—Magnesium has a direct relaxing effect on bronchial smooth 

muscle and also helps to stabilize many inflammatory mediators. For patients with 

severe asthma, magnesium (in conjunction with ongoing treatment) may help improve 

airway obstruction and avoid intubation. The dosing is 2-3 g intravenously, infused at 1 

g/min, with close monitoring of blood pressure. The infusion should stop if hypotension, 

respiratory depression, or decreased deep tendon reflexes occurs. 

2. Methylxanthines—Theophylline (oral) or aminophylline (intravenous) are moderately 

effective bronchodilators that may be considered in severe asthma in conjunction with 

other treatments if the disease is refractory. However, they have a very narrow 

therapeutic margin. Toxicity may be manifested by tachydysrhythmias, gastrointestinal 

upset, and central nervous system irritability. These medications are no longer 

recommended for the treatment of acute exacerbations of COPD. 

3. Ketamine—Ketamine has been shown to be a significant bronchodilator and should 

be the agent of choice during sedation for intubation of severely agitated patients with 

refractory disease (status asthmaticus). Usual anesthetic induction dose is 1-2 mg/kg 

intravenously or 4 mg/kg intramuscularly. 

Disposition 

A. Asthma 

Asthma patients who demonstrate a good response (PEF > 70% of predicted) and 

whose symptoms resolve can be discharged home. Those with an incomplete response 

to treatment (PEF 50-70% of predicted) with improved symptoms and no hypoxia can 

be discharged if close follow-up and correct use of inhalers can be demonstrated. All 

others, including patients seen in an emergency department within the past 3 days, 

those with a change in mental status, or those having a significant complication should 

be hospitalized for further treatment and observation for deterioration. Severe attacks 

should be treated in the intensive care unit. 

B. Acute Exacerbations of COPD 

Acute exacerbations of COPD should be treated with admission in patients who remain 

symptomatic, have significant comorbidities, develop mental status changes, are unable 

to perform activities of daily living without assistance, are unresponsive to treatment, or 

have a treatable complication such as congestive heart failure or pneumothorax. 

Patients with impending respiratory failure should receive treatment in the intensive care

unit. If these patients have responded to emergency department treatment, are reliable 

with good follow-up, and feel they are back to their baselines, they can be discharged to 

home. 

Li JT et al: Algorithm for the diagnosis and management of asthma: a practice 

parameter update: Joint Task Force on Practice Parameters, representing the American 

Academy of Allergy, Asthma, and Immunology, the American College of Allergy, 

Asthma, and Immunology, and the Joint Council of Allergy, Asthma, and Immunology. 

Ann Allergy Asthma Immunol 1998;81:415. [PMID: 9860033] (A thorough and complete 

update of the previously published practice parameters for the diagnosis and treatment 

of asthma.) 

National Asthma Education and Prevention Program: Practical Guide for the Diagnosis 

and Management of Asthma Based on the Expert Panel Report 2: Guidelines for the 

Diagnosis and Management of Asthma. National Institutes of Health Consensus 

Development Conference Consensus Statement. 1997;(Suppl. 4). [PMID: 974051] 

(Evidence-based, expert panel consensus recommendations for the diagnosis and 

management of asthma.) 

Snow V et al: The evidence base for management of acute exacerbations of COPD: 

clinical practice guidelines, part 1. Chest 2001;119(4):1185. [PMID: 11296188] (A joint 

expert panel formed by the American College of Physicians, American Society of 

Internal Medicine, and American College of Chest Physicians has developed 

evidence-based management recommendations for acute exacerbations of COPD from 

research centered primarily on emergency department and inpatient treatment settings.) 

ACUTE PULMONARY EMBOLISM 


• Acute onset of dyspnea, pleuritic chest pain, tachypnea, tachycardia. 

• Hypoxemia with widened A-a gradient. 

• Pulmonary angiogram is gold standard. 


A variety of clinical conditions may cause clots to form in the venous system that when 

dislodged will cause pulmonary emboli (Table 33-3). Venous thrombosis may result 

from a generalized hypercoagulable state, venous endothelial injury, or local stasis 

(Virchow triad). Clots that cause clinically significant pulmonary emboli form most 

commonly in the iliofemoral and pelvic venous beds. Pulmonary embolization, from 

veins of the upper extremities or distal lower extremities, is rare. 

When embolization occurs, the consequences and manifestations depend on the size of 

the embolism, the patient's underlying cardiorespiratory status, and whether subsequent 

infarction of pulmonary tissue occurs. With small- to medium-sized emboli, obstruction 

of a localized portion of the pulmonary vascular tree causes local atelectasis with

esulting ventilation-perfusion (V/Q) abnormalities and hypoxemia. Reflex 

hyperventilation with resultant hypocapnia and tachycardia also occurs. With massive 

embolization (obstructing over 60% of the vascular bed), acute pulmonary hypertension, 

right heart strain, systemic hypotension, and shock may also occur. Fragmentation of 

large emboli with distal migration of clot or further embolization may result in stepwise 

changes in clinical status. Death may occur suddenly. 


Patients should initially be categorized into pretest clinical categories (low, moderate, or 

high risk) following the history, physical examination, and clinical findings. This pretest 

probability will aid in directing further evaluation. 


The illness often begins abruptly, and a predisposing underlying condition is almost 

always present (see Table 33-3). Dyspnea, cough, anxiety, and chest pain occur in 

varying combinations. Hemoptysis may occur, and syncope is rare. Tachycardia and 

tachypnea are commonly noted on examination. Low-grade fever, hypotension, 

cyanosis, signs of deep venous thrombosis, pleural friction rub, and signs of pulmonary 

consolidation may be present. 


1. Chest x-ray—Although the chest x-ray is abnormal in most patients with pulmonary 

embolization with infarction, the abnormalities are often nonspecific (eg, atelectasis, 

pleural effusions, small infiltrates). The Westermark sign (dilated pulmonary vasculature 

proximal to embolus with oligemia distal) and Hampton's Hump (a pleural-based density 

with a rounded border facing the hilum) are specific though uncommon findings in 

pulmonary emboli. 

2. Electrocardiogram—The electrocardiogram is often abnormal, usually 

demonstrating tachycardia or diffuse nonspecific ST-T abnormalities. The classic finding 

of acute right heart strain (S1/Q3/T3; T-wave inversion in leads V1-V3) is more specific 

but somewhat uncommon. In massive pulmonary emboli, there may be findings of 

myocardial ischemia (leading to mistaken diagnosis of myocardial infarction without 

realization of the underlying cause). 

3. Arterial blood gases—A clinically significant pulmonary embolism is almost always 

associated with hypoxemia (oxygen saturation < 90%; PO 2 < 80 mm Hg); however, this 

finding may be partially obscured by the reflex hyperventilation and hypocapnia that 

occur in most patients. 

4. D-Dimer—The serum levels of D-Dimer (a degradation product of cross-linked fibrin) 

measured via an enzyme-linked immunoassay (ELISA) technique have been shown to 

be a highly sensitive (95%) screening examination in the assessment for acute 

thrombus formation. Therefore, if ELISA D-Dimer is negative, it can be helpful to avoid 

invasive procedures such as pulmonary angiogram or CT angiography in low-risk 

patients. However, be cautious with this test. If the patient has been given a moderate to 

high pretest probability for pulmonary embolus, then a definitive test (CT scan or 

angiogram) must be performed. Also, many hospitals have only the latex agglutination

D-Dimer assay, which has not been shown to have the same sensitivity and should not 

be used alone (or with indeterminate V/Q scans) to rule out acute thrombus. For this 

reason, the test remains controversial, and many institutions do not incorporate D-Dimer 

testing into their management strategies. 

C. Diagnostic Imaging 

1. Ventilation-perfusion radionuclide lung scans— 

a. Normal V/Q scan—A normal scan excludes significant embolization and the need for 

further testing because it is a highly sensitive screening examination in patients without 

known cardiopulmonary disease. However, a variety of other conditions (most 

commonly COPD) can result in an abnormal V/Q scan, making many results nonspecific 

(indeterminate). Therefore, in patients with known cardiopulmonary disease, a spiral CT 

angiogram may be a wiser first step in the evaluation of pulmonary emboli. 

b. High probability V/Q scan—A high probability V/Q scan is defined as a large 

perfusion defect in areas of normal ventilation and is highly specific (but insensitive) for 

acute pulmonary emboli. As a result, a high probability scan is sufficient to confirm 

diagnosis of pulmonary emboli. 

c. Indeterminate V/Q scan—An indeterminate V/Q scan (also reported as 

nondiagnostic, low probability, or intermediate probability) is more difficult to use 

clinically (and more confusing) and requires previously assessed pretest clinical 

suspicion. 

If the V/Q scan was indeterminate with a low to moderate clinical suspicion of 

pulmonary embolism, then perform ELISA D-Dimer (if negative: seek alternative cause; 

if positive: perform spiral CT angiography or duplex Doppler ultrasound—some hospitals 

go directly to spiral CT or Doppler without D-Dimer). 

Alternatively, if the V/Q scan was indeterminate with a high clinical suspicion of 

pulmonary embolism, perform a lower extremity venous Doppler ultrasound (if positive: 

treat pulmonary embolism or deep venous thrombosis, if negative: perform spiral CT 

angiography; if CT is positive: treat pulmonary embolism or deep venous thrombosis, if 

CT is negative: obtain pulmonary angiogram). 

2. Helicospiral CT angiography—Contrast-enhanced spiral CT scan allows for rapid 

evaluation but requires proper technique and expert radiographic interpretation. 

Although it is a very sensitive test for central pulmonary emboli, it may miss isolated 

subsegmental emboli. A spiral CT can also offer clues to alternative diagnoses if there is 

no evidence of pulmonary emboli. Most protocols for pulmonary emboli evaluation will 

also scan the pelvis and lower extremities as well as the chest in order to 

simultaneously evaluate for deep venous thrombosis (therefore, duplex Doppler may be 

unnecessary). Spiral CT scan is the initial study of choice to evaluate for pulmonary 

emboli in patients with underlying cardiopulmonary disease or an abnormal chest x-ray. 

If the spiral CT scan is positive for pulmonary emboli or demonstrates an alternative 

diagnosis, then provide treatment as indicated. If the CT scan is negative or 

indeterminate with symptoms of deep venous thrombosis or moderate to high pretest

clinical suspicion, then a Doppler ultrasound of the lower extremities is indicated (if 

positive: treat deep venous thrombosis or pulmonary emboli; if negative: obtain 

pulmonary angiogram for definitive diagnosis). If the CT scan is negative with low 

pretest clinical suspicion, then seek an alternative cause for the symptoms. 

3. Venous Doppler ultrasound—Doppler ultrasound is a noninvasive test used to 

evaluate for deep venous thrombosis. It is an operator-dependent procedure, and the 

results are often difficult to assess in patients with previous deep venous thrombosis. It 

is otherwise highly sensitive and specific for the diagnosis of deep venous thrombosis. 

This test is most useful in patients without evidence of deep venous thrombosis but with 

high clinical suspicion for acute pulmonary emboli or indeterminate V/Q or spiral CT 

scans. 

If the duplex Doppler is positive, use anticoagulation to treat for acute deep venous 

thrombosis or pulmonary emboli. If the test is negative in low-risk patients, then repeat it 

in 5-7 days. If the test is negative in moderate- to high-risk patients, then perform spiral 

CT angiography or pulmonary angiogram for a definitive diagnosis. 

4. Pulmonary angiogram—Pulmonary angiogram is the gold standard because of its 

high sensitivity and specificity. It is expensive and invasive, difficult to obtain, requires 

radiographic expertise, and can be associated with severe complications. Angiogram is 

most effective when diagnosis of pulmonary emboli must be established with certainty 

(eg, in patients in whom anticoagulation carries a high risk of adverse effects, in patients 

who will receive long-term anticoagulation, and in patients who will receive thrombolytic 

therapy). 

Treatment 

A. Respiratory Support 

Correct hypoxemia with oxygen, 5-10 L/min, by nasal cannula or mask. If hypercapnia is 

present on admission, arterial blood gas measurements should be repeated within 

15-20 minutes. Continuously monitor oxygen saturation by pulse oximetry. Worsening 

hypercapnia with progressive obtundation is an indication for emergent intubation. 

B. Anticoagulation Therapy 

Use unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) as soon as 

possible to prevent further clot formation in patients with high clinical likelihood for 

pulmonary emboli or with diagnosed pulmonary emboli. Use UFH with an initial 80 IU/kg 

bolus followed by 18 IU/kg/h infusion or LMWH (enoxaparin or dalteparin) to initiate 

anticoagulation. LMWH is at least as effective and safe as UFH and is more convenient. 

Compared with UFH, LMWH is more expensive but may reduce the total hospital cost 

and length of stay because activated partial thromboplastin time levels need not be 

followed in these patients. Evaluate patients for contraindications to anticoagulation 

prior to administration. 

C. Thrombolytic Therapy 

Although anticoagulation is sufficient treatment for most patients with pulmonary emboli, 

a few patients present with right heart dysfunction, hemodynamic compromise, or 

cardiogenic shock and may benefit from clot removal from the pulmonary artery.

Thrombolytic agents such as streptokinase, urokinase, and tissue plasminogen activator 

achieve such lysis and may also may prevent damage to the pulmonary vascular bed 

and decrease the morbidity and mortality associated with pulmonary emboli. 

Thrombolytic therapy may be associated with severe bleeding and cannot be used in 

patients with recent trauma, cerebral vascular accident, or gastrointestinal tract 

hemorrhage (see contraindications to thrombolytic therapy in Chapter 34). Before 

thrombolytic therapy is started, standard protocol must be followed: discontinue heparin 

and ensure that the thrombin time, prothrombin time, or activated partial thromboplastin 

time is less than twice the normal value. For the strict dosing and administration criteria 

of these thrombolytic agents, consult the package inserts. Thrombolytic agents should 

be discontinued if significant bleeding occurs; the actions of these drugs can be 

reversed with fresh frozen plasma. Reinstate heparin treatment after thrombolytic 

therapy has been completed. 

D. Surgical Treatment 

A transvenous catheter embolectomy or open surgical embolectomy may be a 

life-saving maneuver in a patient with massive emboli and refractory hypotension or in 

patients with contraindications to or failure of thrombolytics. A Greenfield filter may also 

be introduced to capture further emboli. 

Disposition 

Hospitalize all patients for continued anticoagulation and supportive care. Patients with 

large emboli or hemodynamic impairment, or those receiving thrombolytics, should be 

monitored in the intensive care unit. Patients in whom pulmonary embolism is strongly 

suspected should be hospitalized for anticoagulation (if no contraindications are 

present) until a definitive diagnosis can be made. 

Arcasoy SM: Thrombolytic therapy of pulmonary embolism: a comprehensive review of 

current evidence. Chest 1999;115 (6):1695. [PMID: 10378570] (Extensive review of 

medical research from 1966 to 1998 with the development of evidence-based guidelines 

for the use of thrombolytics in the treatment of acute pulmonary emboli.) 

Bloomgarden DC: Newer diagnostic modalities for pulmonary embolism. Pulmonary 

angiography using CT and MR imaging compared with conventional angiography. 

Emerg Med Clin North Am 2001;19(4)975. [PMID: 11762283] (Provides an in-depth, 

evidence-based review of the benefits of CT pulmonary angiography as a first-line 

diagnostic modality in evaluation for pulmonary emboli and a brief overview of the future 

use of magnetic resonance angiography.) 

Edlow JA: Emergency department management of pulmonary embolism. Emerg Med 

Clin North Am 2001;19(4):995. [PMID: 11762284] (Thorough evidence-based review of 

current evaluation, diagnosis, and treatment of acute pulmonary embolism in the 

emergency department.) 

Holbert JM: Role of spiral computed tomography in the diagnosis of pulmonary 

embolism in the emergency department. Ann Emerg Med 1999;33(5):520. [PMID: 

10216328] (Reviews advantages and disadvantages of all current diagnostic modalities 

for acute pulmonary emboli with a suggested algorithm for emergency department

evaluation.) 

Wolfe TR, Hartsell SC: Pulmonary embolism: making sense of the diagnostic 

evaluation. Ann Emerg Med 2001;37(5):504. [PMID: 11326187] (Review of large 

prospective studies with a proposed evidence-based diagnostic algorithm for the 

evaluation of suspected pulmonary embolism.) 

EMERGENCY MANAGEMENT OF SPECIFIC CONDITIONS 

PNEUMOMEDIASTINUM & SUBCUTANEOUS EMPHYSEMA 


• Soft tissue swelling, subcutaneous emphysema. 

• Hamman's crunch, air in the mediastinum on chest x-ray. 


Pneumomediastinum is commonly associated with pneumothorax (air in the 

mediastinum). It most commonly occurs from rupture of an overdistended alveolus or a 

collection of such alveoli ("bleb") into the peribronchovascular interstitial space with 

dissection backward along the bronchi to the mediastinum (Macklin effect). Because the 

mediastinal pleura is weaker than the pleura surrounding the lung, air may dissect into 

the mediastinum before entering the pleural space. 

Pneumomediastinum may occur without pneumothorax; air also may dissect through 

contiguous fascial planes into the neck and other soft tissues, causing subcutaneous 

emphysema. Occasionally pneumomediastinum is due to rupture of the esophagus 

(Boerhaave syndrome), and this diagnosis should be considered if the patient is acutely 

ill and has a history of vomiting. Pneumomediastinum also may have iatrogenic 

(mechanical ventilation, laparoscopy, biopsy) or posttraumatic causes or may result 

from asthma, Valsalva maneuver (smoking crack cocaine or marijuana, active labor, 

coughing), gas-producing bacterial mediastinitis, oral trauma (hypopharynx), or acute 

decompression injury (diving). 


Chest pain, aggravated by respiration, moving, and position changes, is a common 

symptom of pneumomediastinum. Diagnosis is made by hearing a mediastinal "crunch" 

(Hamman's crunch, a crunching sound heard over the heart during systole) on 

auscultation and seeing air in the mediastinum on chest x-ray. Subcutaneous 

emphysema presents as soft tissue swelling, especially in the neck. A crackling sound is 

heard when the tissues are compressed. 


No specific treatment is indicated unless esophageal rupture is present (Chapter 24).

Associated conditions such as pneumothorax should be corrected. Analgesics may be 

required. 

Hospitalize patients with severe pneumomediastinum with cardiovascular compromise 

(extensive spread of mediastinal air), for patients with pneumomediastinum complicated 

by other disorders (eg, mediastinitis, systemic air embolus, or pneumopericardium), or 

for patients who require narcotics for pain relief. 

McHugh TP: Pneumomediastinum following penetrating oral trauma. Pediatr Emerg 

Care 1997;13(3):211. [PMID: 9220508] (A review of the pathophysiology and treatment 

of pneumomediastinum with a case report of a toddler developing pneumomediastinum 

after falling with a spoon in his mouth.) 

Richard HM III et al: Pneumothorax and pneumomediastinum after laparoscopic 

surgery. Clin Imaging 1997;21(5):337. [PMID: 9316753] (Study evaluating the incidence 

and significance of pneumomediastinum after laparoscopic surgeries, noting this finding 

was not associated with significant morbidity and mortality.) 

Wintermark M, Schnyder P: The Macklin effect: a frequent etiology for 

pneumomediastinum in severe blunt chest trauma. Chest 2001;120(2):543. [PMID: 

11502656] (A review of the pathophysiology of pneumomediastinum with a retrospective 

analysis of patients with this diagnosis in one hospital, directly relating the presence of 

the Macklin effect to the length of intensive care unit stay.) 

PLEURODYNIA 


• Self-limited viral illness of skeletal muscle. 

• Severe pleuritic pain in ribs. 

• Low-grade fever, malaise. 


Pleurodynia (pleura, side; odyne, pain) is an acute, self-limited, and benign (though 

uncomfortable) viral illness of the skeletal muscle, not of the pleura or peritoneum. Most 

cases occur in epidemics during summer or early fall in young adults and children. It is 

caused primarily by group B coxsackieviruses and echoviruses. 


Systemic symptoms are mild (low-grade fever, malaise), but pleuritic pain in the lower 

ribs is severe (hence the name "devil's grip"). Examination may disclose low-grade fever 

and a pleural rub in some cases, although the physical examination is normal in many 

patients. Chest x-ray usually shows no abnormalities, but there may be a small amount 

of pleural friction fluid, a small pulmonary infiltrate, or both. The leukocyte count and the 

erythrocyte sedimentation rate are usually normal or only minimally elevated.

Pleurodynia may sometimes be accompanied by pericarditis, which may be diagnosed 

by a friction rub on auscultation or an enlarged cardiac silhouette on chest x-ray. 

Serious thoracic and abdominal pathology must also be ruled out. 

Treatment 

No specific therapy is available. For symptomatic relief, nonsteroidal anti-inflammatory 

agents may be effective. Aspirin is said to be less effective. Narcotic analgesics may be 

needed. 

Disposition 

Hospitalization is necessary only for patients who require parenteral analgesics or who 

also have pericarditis. 

Pichichero ME et al: Clinical and economic impact of enterovirus illness in private 

pediatric practice. Pediatrics 1998;102(5): 1126. [PMID: 9794944] (Prospective 

multicenter study from pediatric practices in New York, Arizona, and California 

evaluating the diagnosis and morbidity of enterovirus infections [including pleurodynia] 

for patients and its direct economic impact on the medical community, including the 

emergency department.) 

PLEURAL EFFUSION 


• Pleuritic chest pain, dyspnea with or without fever, cough. 

• Decreased breath sounds, decreased tactile fremitus on affected side. 

• Thoracentesis is definitive diagnostic and often therapeutic procedure. 


Pleural effusions are an abnormal collection of fluid between the parietal and visceral 

pleura as a result of a local disease process or inflammation. Normally 5-15 mL of 

serous fluid is present in the pleural space. An effusion can be classified as either an 

exudate or transudate to help in differential diagnosis. Exudative fluid analysis reveals 

(1) pleural fluid protein-to-serum protein ratio greater than 0.5, (2) pleural fluid lactate 

dehydrogenase (LDH)-to-serum LDH ratio greater than 0.6, and (3) pleural fluid LDH 

greater than two thirds of the upper limit of normal serum LDH. Exudates are associated 

with direct disease of the pleura itself usually from infection, inflammation, or 

malignancy. Transudates do not have the above characteristics and are most commonly 

caused by congestive heart failure, cirrhosis with ascites, or nephrotic syndrome. Every 

patient with a newly diagnosed pleural effusion requires prompt evaluation to determine 

the cause so that early and appropriate therapy can be given. 

Clinical Findings


The patient may complain of pleuritic or nonpleuritic chest pain or dyspnea. Chest 

examination discloses dullness, decreased breath sounds, and decreased tactile 

fremitus on the involved side. 

B. Imaging 

Upright posteroanterior and lateral chest x-rays can demonstrate pleural fluid in most 

cases if more than 250 mL of fluid is present (eg, blunting of costophrenic angles). 

Decubitus films are useful to differentiate pleural fluid from pleural scarring and to 

determine whether the fluid is loculated. Bilateral decubitus films may be necessary to 

demonstrate fluid in the case of very small effusions. X-rays or CT scans may be helpful 

in differentiating effusions from lung abscess adjacent to the pleura. 

Treatment 

A. Oxygen 

If dyspnea is present, obtain pulse oximetry or arterial blood gas measurements, and 

begin supplemental oxygen by mask or nasal cannula. 

B. Thoracentesis 

If chest examination or chest x-ray shows a massive fluid accumulation (ie, most of one 

hemithorax), or the patient is in respiratory distress, prompt thoracentesis with removal 

of 500-1000 mL of fluid should be considered for relief of symptoms. Remove the fluid 

over 30-90 minutes to prevent pulmonary edema in the reinflated lung. Recovered fluid 

should be sent for differential white blood cell count; determination of protein, LDH, and 

glucose content; cytologic study; cultures; and pleural fluid pH. If the patient is not in 

distress, thoracentesis should be deferred until after hospital admission. 

Disposition 

All patients with unexplained pleural fluid accumulations should be hospitalized for 

diagnosis and treatment. Stable patients with recurrent fluid of known cause (eg, 

metastatic cancer or heart failure) should be referred to their regular source of medical 

care or given treatment in the emergency department (eg, by thoracentesis) and 

discharged unless the underlying illness requires hospitalization. 

Light RW: Management of pleural effusions. J Formos Med Assoc 2000;99(7):523. 

[PMID: 10925561] (Review of current diagnostic, therapeutic, and prognostic strategies 

for pleural effusions.) 

ATELECTASIS 


• Decreased breath sounds or dullness to percussion over affected lung fields. 

• Evidence of lung collapse on chest x-ray.


Collapse of alveoli and small airways in a portion of the lung may result from extrinsic 

compression (pneumothorax, hydrothorax) or intrinsic abnormalities (hypoventilation, 

bronchial obstruction). Only intrinsic (resorption) atelectasis is discussed here. In the 

emergency department, intrinsic atelectasis may be seen in conditions causing 

hypoventilation (secondary to drug overdose or severe pleuritic pain from blunt chest 

trauma, tracheal trauma, or pulmonary embolism) or bronchial obstruction (asthma, 

foreign body, bronchial tumor, or aspiration). 



There are usually no findings other than those of the underlying disease, although 

patients with extensive atelectasis may experience chest pain, cough, or dyspnea. 

Physical findings may be absent but when present are nonspecific dry crackles, 

decreased breath sounds, or dullness to percussion over the affected lung. History of 

recurrent pneumonia in the same lobe may suggest airway obstruction. 


Chest x-ray shows areas of lung collapse. Coexisting signs may include depression or 

elevation of the hilum, elevation of a hemidiaphragm, or compensatory hyperinflation of 

other parts of the involved lung (often seen only on forced expiratory chest x-rays). CT 

scan may demonstrate location of an obstruction. Bronchoscopy is the definitive study, 

especially if tumor or foreign body is suspected. 

Arterial blood gases should be measured to assess respiratory function; hypoxemia and 

hypocapnia may be present. 

Treatment 

Emergency treatment should include hemodynamic monitoring with supplemental 

oxygen, chest physical therapy, meticulous pulmonary toilet, and treatment of 

underlying conditions (eg, aspiration of gastric contents, drug overdose, pain). 

Disposition 

Almost all patients with atelectasis must be hospitalized for evaluation and treatment of 

the underlying cause. The only exceptions are patients with chronic atelectasis of known 

cause who have not responded to vigorous therapy in the past (eg, carcinomatous 

bronchial obstruction) and those with very mild degrees of atelectasis (subsegmental) 

clearly due to self-limited disease (drug overdose, pleurisy). 

Rabinowitz RP: Management of infections in the trauma patient. Surg Clin North Am 

1999;79(6):1373. [PMID: 10625984] (Thorough discussion of the common types of 

infection in the trauma patient and the initial approach to the febrile trauma patient.) 

van der Jagt EW: Contemporary issues in the emergency care of children with asthma. 

Immunology and Allergy Clinics of North America 1998;18(1). (Extensive literature

eview including pathophysiology and treatment of asthma and its complications.) 

PNEUMONIA & BRONCHITIS 


Pneumonia 

• Fever, productive cough, dyspnea, pleuritic chest pain. 

• Rales, rhonchi, wheezing, or hemoptysis. 

• Decreased breath sounds or dullness to percussion over affected lobe. 

• Infiltrate on chest radiograph. 

Bronchitis 

• Cough associated with midline chest pain or burning. 

• Fever, dyspnea. 


Pneumonia and acute bronchitis are common emergency department entities, and they 

can be difficult to differentiate from one another. Suspect pneumonia or bronchitis in any 

patient presenting with fever, cough (with or without productive sputum), or dyspnea. 

Differentiation is important because treatment, disposition, and prognosis can differ 

significantly. 


A. Acute Bronchitis 

Diagnosis is based primarily on history and physical examination. Patients complain of 

cough, fever, and constitutional symptoms. The cough is initially dry (due to 

bronchospasms) but can become productive and is often associated with a midline 

chest pain or burning. Hemoptysis, wheezing, rhonchi, and rales may also be present. 

Laboratory tests are typically not helpful in making the diagnosis. Chest x-ray will show 

no evidence of infiltrate and is not indicated unless patients are dyspneic, hypoxic, or 

have significant comorbidities (eg, COPD, dementia). The cause is primarily viral (90%). 

B. Pneumonia 

Patients present with fever, dyspnea, cough, pleuritic chest pain, and increased sputum 

production. Evidence of an infiltrate will appear on the chest x-ray. Other signs noted on 

physical examination include rales or rhonchi on chest auscultation, often with locally 

decreased breath sounds and dullness to percussion. 

The primary goal of the history and physical examination should be to identify patients 

at high risk for significant morbidity and mortality. If pneumonia is suspected, check 

pulse oximetry and obtain a chest x-ray to aid in diagnosis and help rule out other 

conditions. Use clinical judgment to determine the need for further testing. The

necessity of blood and sputum cultures and Gram stains in patients well enough to be 

discharged has been debated, but these tests should always be obtained in patients 

who will be admitted. Microbiologic testing will not change the initial emergency 

department treatment of community-acquired pneumonia but in a small number of cases 

may alter the choice of antimicrobials after admission. The leukocyte count is not 

associated with increased morbidity and mortality and therefore should not be used in 

guiding patient management. 

Some helpful tests may include arterial blood gas measurements (hypoxia), hemoglobin 

and hematocrit (anemia), and a basic metabolic panel (dehydration, renal insufficiency) 

and may also include HIV screening, tuberculosis screening, and screening for 

Legionella and Mycoplasma pneumonia for hospitalized patients at high risk for these 

diseases. 

Treatment 

A. Acute Bronchitis 

This condition rarely needs aggressive management in the emergency department. 

Administer supplemental oxygen to hypoxic patients or intravenous fluids to patients 

who appear to be dehydrated. Otherwise, use symptomatic treatment with antipyretics 

and cough suppressants as needed. ß-Adrenergic MDIs (albuterol) are used to 

suppress cough secondary to bronchospasm. Antibiotics are not recommended 

because the primary cause is likely viral (unless the course is prolonged or the patient 

has significant underlying comorbidities). 

B. Pneumonia 

Patients well enough to be discharged home should be given instructions for antipyretic 

use and cough suppressants as needed, and they should be started on antibiotics. 

Doxycycline, a newer-generation fluoroquinolone, or a macrolide are equally appropriate 

antimicrobial choices. Each should be given for 7-10 days (except azithromycin, which 

is used for only 5 days). Patients who will be admitted can be started on initial 

antibiotics, which include (1) a newer-generation fluoroquinolone or (2) a macrolide plus 

a ß-lactam/ß-lactamase inhibitor. 

The initial antibiotic choices for patients admitted to the intensive care unit typically 

include either a newer-generation fluoroquinolone or macrolide plus either cefotaxime or 

a ß-lactam/ß-lactamase inhibitor. All patients should receive supplemental oxygen and 

intravenous fluids if dehydrated. See Chapter 40 for more specific pneumonia treatment 

recommendations. 

Disposition 

Patients with acute bronchitis can be discharged home with the above treatment if they 

are not hypoxic and do not have significant underlying cardiopulmonary disease. 

Pneumonia patients who are younger than age 50 years without comorbidities or altered 

physical examination findings can be safely discharged to home with antibiotics and 

follow-up in 72 hours unless they are immunocompromised, are unable to tolerate oral 

intake, have psychiatric illness, are alcohol or drug abusers, are homeless, or lack 

social support. Most patients who fall into one of these categories will be hospitalized. If

the patient has significant comorbidities, has altered mental status, or is 

hemodynamically unstable, intensive care unit admission and possible intubation are 

appropriate. Although cultures should be drawn expeditiously, they should not delay 

administration of antibiotics. 

Bartlett JG et al: Practice guidelines for the management of community-acquired 

pneumonia in adults. Infectious Diseases Society of America. Clin Infect Dis 

2000;31(2):347. [PMID: 10987697] (Evidence-based practice guidelines for the 

diagnosis and treatment of community-acquired pneumonia in adults.) 

DeBlieux PM, Slaven EM: Community-acquired pneumonia: deciding whom to admit 

and which antibiotics to use. Emergency Medicine Practice 1999;1(4):1. (Review of the 

most recent published guidelines for the management of community-acquired 

pneumonia with specific indications for admission and recommendations for antibiotic 

choice in the emergency department.) 

Fine MJ et al: A prediction rule to identify low-risk patients with community-acquired 

pneumonia. N Engl J Med 1997;336 (4):243. [PMID: 8995086] (Based on an extensive 

analysis of nearly 15,000 inpatients and validated by the pneumonia PORT cohort 

study, the authors have developed a 2-step algorithm for risk stratification of patients 

with community-acquired pneumonia that is used to help physicians make 

evidence-based decisions regarding hospitalization.) 

Gonzales R et al: Principles of appropriate antibiotic use for treatment of uncomplicated 

acute bronchitis: background. Ann Emerg Med 2001;37(6):720. [PMID: 11385346] 

(Multidisciplinary expert panel formed by the Centers for Disease Control and 

Prevention, which developed evidence-based recommendations on the management of 

patients with acute bronchitis.) 

PULMONARY TUBERCULOSIS 


• Fever, weight loss, hemoptysis, night sweats. 

• Chest x-ray notes hilar adenopathy with parenchymal infiltrates, often upper lobes or 

apical. 

• Positive purified protein derivative (PPD) skin test with positive acid fast bacilli on 

sputum smear. 

• Sputum culture for M tuberculosis is definitive diagnosis. 


Tuberculosis remains the world's leading infectious cause of death and reestablished 

itself as a major concern in the mid 1980s as the incidence rose sharply in the United 

States. Since 1993, the incidence has once again declined after significant federal 

funding was released for statewide tuberculosis control programs. These programs are 

aimed at controlling the major causes for this initial resurgence, including the HIV

epidemic, immigrants with undiagnosed tuberculosis from high-risk countries (ie, those 

with multidrug-resistant tuberculosis), previously established suboptimal antimicrobial 

regimens, and patient noncompliance. HIV is the most important risk factor for infection 

with tuberculosis. 

Pulmonary infection is caused when susceptible individuals inhale aerosolized droplets 

infected with Mycobacterium tuberculosis. Susceptible populations include HIV-positive 

individuals; those with close exposure to known infected persons; immigrants from Asia, 

Africa, or Latin America; medically underserved urban populations; the elderly; residents 

of nursing homes or correctional facilities; homeless populations; and health care 

workers. 

In immunocompetent hosts, primary tuberculosis is usually asymptomatic and is often 

identified only when a patient has a positive tuberculosis skin test. Initially the organisms 

either are killed by alveolar macrophages or persist and replicate within inactivated 

macrophages that can gain access to regional lymph nodes and disseminate into the 

bloodstream. Dissemination to the lungs (miliary tuberculosis) or to the kidneys, 

lymphatics, pleura, meninges, or bone (extrapulmonary tuberculosis) can also rarely 

occur. Eventually the organism lies dormant, walled off within granulomas, and may 

never again cause infection. However, depending on the host immune response, 

dormant organisms may become reactivated (reactivation tuberculosis). Risk factors for 

reactivation tuberculosis include HIV, recent tuberculosis infection (within 2 years), 

intravenous drug abuse, diabetes mellitus, prolonged steroid use, endstage renal 

disease, or chronic malabsorption syndromes. The goal in the emergency department is 

to recognize patients at high risk for disease; initiate early diagnosis, treatment, and 

referral for these patients; and protect hospital staff via early patient isolation. 


Many patients will know if they have had or been exposed to tuberculosis in the past. All 

patients with pulmonary symptoms should be questioned about the above-stated known 

risk factors for tuberculosis. 


The most common symptom of tuberculosis is cough, initially dry, often becoming 

purulent with or without hemoptysis. Fever is also very common, especially during the 

day with resolution at bedtime; night sweats are a major complaint. Fatigue, malaise, 

weight loss with anorexia, and occasionally pleuritic chest pain may be reported. 

Patients may appear chronically ill, with mental status changes (central nervous system 

disease), lymphadenopathy, rales on chest auscultation, and often a normal chest 

examination. 


Primary tuberculosis may appear on chest x-ray as parenchymal consolidation, 

atelectasis, pleural effusion, or possible paratracheal lymphadenopathy. A calcified 

Ghon complex may be evidence of healed primary infection. Reactivation tuberculosis 

often has a predilection for the upper lobes. Immunocompromised patients, especially 

HIV patients, may present with myriad changes on the chest x-ray.


1. Cultures and serologic testing—Many new methods (direct amplification tests, 

high-performance liquid chromatography, DNA fingerprinting with polymerase chain 

reaction technique, and serologic tests using ELISA) have been used to more rapidly 

identify M. tuberculosis. However, definitive diagnosis still depends on sputum cultures 

(which may take weeks). Now, with the emergence of multidrug-resistant tuberculosis, 

cultures are the standard of care because proper treatment depends on the 

susceptibility results. In the emergency department, acid fast staining of sputum can be 

performed and may be helpful in aiding diagnosis. 

2. Tuberculosis skin testing—If a patient is suspected of having tuberculosis, an 

intradermal purified protein derivative (PPD) skin test should be administered. Because 

these tests are not completed and read until 48-72 hours after administration, they are 

not very useful in the emergency department. A positive test (varying diameters of 

circumferential skin induration depending on risk factors for the disease) indicates 

previous infection or active tuberculosis infection. Positive PPD tests should be followed 

with chest x-ray to evaluate for new or active disease. Severely immunocompromised 

patients or HIV patients may be anergic and require an anergy skin test panel. 

Treatment 

A. Confirmed or Suspected Tuberculosis 

Because more than 4% of isolates are resistant to isoniazid in most of the United 

States, it is now recommended that all patients with confirmed or suspected tuberculosis 

be started on 4-drug therapy. The initial regimen consists of the following drugs: 

isoniazid, rifampin, pyrazinamide, and either ethambutol or streptomycin. All drugs 

should be continued until the susceptibility results from the sputum cultures are 

available. If the isolates are susceptible to isoniazid, rifampin, and pyrazinamide, then 

the fourth drug can be discontinued. A 6-month treatment course has been proven to be 

effective. Isoniazid and rifampin should be continued throughout this period, whereas 

pyrazinamide and ethambutol or streptomycin can usually be discontinued after 2 

months, if there is no evidence of multidrug-resistant, miliary, or extrapulmonary 

tuberculosis. If any of these forms are present, a 12-month treatment course should 

continue. 

B. Latent Tuberculosis 

Patients who have had positive PPD tests but negative chest x-ray and sputum (latent 

tuberculosis) and are at risk of reactivation tuberculosis should be given 9 months of 

isoniazid or 2 months of rifampin plus pyrazinamide. In children, only 9 months of 

isoniazid is recommended. Isoniazid is not recommended for pregnant patients. Patients 

with latent tuberculosis do not need treatment if they can prove or are certain that they 

already received treatment. 

C. Reporting Requirements 

The local health department must be informed of all cases of tuberculosis to ensure 

adequate care, availability of treatment resources, and compliance with therapy. 

D. Respiratory Isolation 

Any patient suspected or known to have tuberculosis must be immediately placed in

designated respiratory isolation rooms designed for the emergency department and 

hospital wards. Emergency department staff should quickly assess and triage these 

individuals and apply masks to patients and distribute respirators approved by the 

Occupational Safety and Health Administration to physicians and nursing teams. 

Patients should remain in isolation, either within the hospital setting, or in their own 

house, until proven to be noninfectious. 

E. HIV Testing 

All patients with newly diagnosed tuberculosis should be offered HIV testing because a 

significant number of patients are coinfected and have an increased risk of opportunistic 

infections and death. 

F. Infants, Children, and Adolescents 

This population of patients with active, culture-proven M. tuberculosis should receive 

essentially the same treatment as adults. Latent tuberculosis in children is treated with 9 

months of isoniazid only. Diseases are more likely to disseminate in children younger 

age 4 years. Avoid ethambutol in children because of secondary ocular toxicity. 

G. Pregnant Patients 

Pregnant women with tuberculosis can still receive rifampin, isoniazid, and 

pyrazinamide. However, ethambutol and streptomycin should be avoided because of 

the risk of ocular toxicity and congenital deafness, respectively. Mothers can still breast 

feed if taking these medications. 

Disposition 

Most patients are usually admitted for full work-up and evaluation after the initial 

diagnosis is confirmed. However, many patients can safely receive treatment at home 

with specific home isolation precautions along with screening and prophylactic treatment 

for family members and household contacts. Patients must fully understand the 

importance of adherence to their therapeutic regimens. If adherence cannot be 

confirmed, directly observed therapy will be provided and enforced by a public health 

official. Report all new diagnoses to the health department and ensure immediate 

primary care or infectious disease follow-up. 

All patients with multidrug-resistant tuberculosis, patients who are significantly ill or 

immunocompromised, those who are unable to care for themselves, homeless patients, 

those living in an institution (eg, nursing home, prison), the elderly, those with multiple 

comorbidities, and those coinfected with HIV should be hospitalized with respiratory 

droplet precautions. Hospitalization ensures that these patients remain in respiratory 

isolation, receive therapy daily, and are observed closely for adverse effects of 

antituberculosis medications. 

Advisory Council for the Elimination of Tuberculosis (ACET). Tuberculosis elimination 

revisited: obstacles, opportunities, and a renewal commitment. MMWR 

1999;48(RR-9):1. [PMID: 10485562] (The Centers for Disease Control and Prevention 

and ACET have reviewed their 1989 strategic plan to eradicate tuberculosis and have 

added new recommendations for diagnosis, treatment, and prevention based on the 

latest technology.)

PULMONARY ASPIRATION SYNDROME 


• High-risk patients with drug or alcohol intoxication, seizures, or swallowing disorders; 

obtunded patients. 

• Immediate respiratory difficulty due to chemical burn, hypoxemia, rales, wheezing 

(often unilateral). 

• Chest x-ray can be negative initially. 


Acute aspiration of gastric contents (Mendelson syndrome) may produce significant lung 

injury by acid corrosion, bronchial obstruction with food particles, or induction of 

chemical pneumonitis that is later complicated by bacterial pneumonia. Aspiration of 

gastric acid (pH < 2) produces immediate pulmonary injury that pathophysiologically is a 

form of acute respiratory distress syndrome. Aspiration of neutral gastric secretions 

admixed with food produces a more delayed injury; retained food particles may cause 

bronchial obstruction with atelectasis. All of these conditions are included in the term 

pulmonary aspiration syndrome. 

By contrast, aspiration of oropharyngeal secretions, especially in individuals with poor 

dental hygiene and large amounts of dental plaque, causes bacterial pneumonia 

(so-called aspiration pneumonia). This necrotizing process may be acute or subacute in 

onset and commonly results in lung abscess. 


Pulmonary aspiration occurring in the hospital may occur during anesthesia, 

cardiopulmonary resuscitation, or other procedures. Community-acquired cases are 

usually associated with drug (including alcohol) intoxication, seizures, disorders of 

swallowing, or gastroesophageal sphincteric incompetence. Within minutes to hours 

after aspiration, the patient develops productive cough; dyspnea; fever; leukocytosis; 

and signs of consolidation, pulmonary rales, or dullness. Chest x-ray shows pulmonary 

infiltrate without a characteristic pattern, although dependent segments of the lung 

(especially the right lower lobe) are more commonly involved. 

Sputum shows abundant leukocytes but no bacteria (or scant normal flora) on 

microscopic examination. Cultures are sterile or show scant normal flora. Food particles 

may be present on gross examination of sputum. 

Arterial blood gas and pH measurements must be made to assess ventilatory status. 

Pulse oximetry may suffice as a guide to arterial oxygenation if the saturation is high (> 

90%). 

Treatment

Provide respiratory support (eg, supplemental oxygen) as necessary on the basis of 

arterial blood gas measurements (or pulse oximetry) and clinical findings (Chapter 11). If 

the patient has significant dyspnea or respiratory distress, immediately establish airway 

control with intubation and mechanical ventilation. 

Witnessed aspirations should be treated by prompt oropharyngeal and tracheal 

suctioning. Acute obstruction of the upper airway should be treated immediately with the 

Heimlich maneuver. Retained, aspirated foreign bodies (greatest risk in children) often 

necessitate bronchoscopy for final diagnosis and removal. 

Corticosteroids have not been demonstrated to be helpful and may increase 

susceptibility to infection. Antibiotics for aspiration pneumonia should be given only if 

infection occurs and not as prophylaxis following an episode of aspiration. 

Disposition 

All patients should be hospitalized for observation and treatment as necessary. 

Young MA, Reynolds JC: Respiratory complications of gastrointestinal diseases. 

Gastroenterol Clin North Am 1998;27(4): 721. [PMID: 9890112] (Evidence-based review 

of gastroesophageal reflux disease and the management of the extraesophageal 

manifestations of the disease, including pulmonary aspiration.) 

ACUTE LUNG INJURY & ACUTE RESPIRATORY DISTRESS SYNDROME (See 

Table 33-4. ) 


• Recent known exposure to high-risk systemic or pulmonary etiologic agent. 

• Acute-onset respiratory failure (PaO 2 < 60 mm Hg with FIO 2 > 50%). 

• No chemical evidence of cardiogenic or volume overload pulmonary edema 

(pulmonary capillary wedge pressures < 18 mm Hg). 

• Chest x-ray shows diffuse bilateral infiltrates with normal heart size. 


Acute lung injury is a clinical syndrome composed of acute respiratory failure with 

impaired oxygenation secondary to overwhelming noncardiogenic pulmonary edema 

(bilateral pulmonary infiltrates on chest x-ray without clinical evidence of cardiogenic or 

volume overload pulmonary edema). Acute respiratory distress syndrome (ARDS), 

formerly called adult respiratory distress syndrome, is the most severe form of acute 

lung injury. Both entities are associated with significant mortality (30-40% or much 

higher if associated with sepsis) and are characterized by diffuse pulmonary capillary 

endothelial cell and alveolar epithelial cell damage with resultant pulmonary edema. 

Diverse specific pulmonary and extrapulmonary insults have been associated with the 

development of acute lung injury and ARDS (see Table 33-4). Without early diagnosis,

intervention, and treatment of the underlying cause, most patients will die of multiorgan 

system failure. 



Patients will present with dyspnea (usually 12-48 hours after the inciting event), which 

can rapidly progress to respiratory failure requiring intubation and positive-pressure 

ventilation. Symptoms of the underlying disorder may also be present (fever, trauma, 

burns), and some patients may have wheezing or cough productive of frothy or 

blood-tinged nonpurulent sputum. Rales are almost always present. 


Hypoxemia is universal and early arterial blood gases may demonstrate decreased 

PCO 2 secondary to hyperventilation. As impending respiratory failure and fatigue set in, 

resultant hypercapnia develops. Chest x-ray will demonstrate diffuse bilateral infiltrates 

but may be variable in patients with underlying pulmonary disease. Although not 

routinely recommended for diagnosis, a pulmonary artery catheter may be required to 

help differentiate noncardiac pulmonary edema from a cardiac cause. Pulmonary artery 

occlusion pressures (pulmonary capillary wedge pressures) less than or equal to 18 mm 

Hg are consistent with acute lung injury. 

Treatment 

A. Provide Respiratory Support 

1. Supplemental oxygen—Provide high initial oxygen concentration (FIO 2 = 50-100%), 

continue to monitor oxygen saturation with pulse oximetry, and titrate to the lowest 

possible FIO 2 to keep oxygen saturation greater than 90%. 

2. Intubation and mechanical ventilation—Mechanical ventilation is the central 

supportive intervention. Clinicians have implemented numerous ventilation strategies, 

but most support the use of high positive end-expiratory pressure (PEEP) with low tidal 

volumes to limit peak airway pressures and resultant barotraumas. Besides PEEP, other 

maneuvers are also used to help open collapsed alveoli. The most important of these 

maneuvers is prone positioning, which redistributes blood flow and ventilation, 

decreases atelectasis, and therefore improves oxygenation. 

B. Maintain Circulation 

Avoid both dehydration and vigorous hydration. Keep the pulmonary capillary wedge 

pressure as low as possible while maintaining an adequate cardiac index. This may be 

extremely difficult and may require internal monitoring via a Swan Ganz catheter. 

C. Treat Underlying Clinical Cause 

Prompt evaluation with rapid identification of the underlying cause is paramount for the 

survival of these patients. Specific treatment for the inciting disorder (most commonly 

sepsis) should begin as soon as possible in the emergency department. See Table 33-4 

for causes, and refer to listed chapters for specific therapies of each cause.

Disposition 

Hospitalize all patients for therapy in the intensive care unit. Very rarely noncardiac 

pulmonary edema due to a specifically treatable condition (eg, high altitude, narcotics) 

will resolve rapidly and completely in a few hours, allowing the patient to be discharged 

from the emergency department. 

Brower RG: Treatment of ARDS. Chest 2001;120(4):1347. [PMID: 11591581] (An 

exhaustive review of the currently published literature and a summary of past, present, 

and future evidence-based management options for patients with acute lung injury or 

ARDS.) 

Steinberg KP: Acute lung injury and acute respiratory distress syndrome. The clinical 

syndrome. Clin Chest Med 2000;21(3): 401. [PMID: 11019717] (A thorough review of 

definitions, pathophysiology, risk factors, clinical manifestations, and prognosis of acute 

lung injury or ARDS.) 

Weinacker AB: Acute respiratory distress syndrome: physiology and new management 

strategies. Annu Rev Med 2001;52:221. [PMID: 21091756] (Review of the clinical and 

pathologic features of ARDS and current treatment strategies to prevent lung injury and 

improve survival.) 

CYSTIC FIBROSIS 


Cystic fibrosis is an autosomal recessive disease with an abnormal transmembrane 

protein, which causes thick and viscous mucus with subsequent obstruction and 

damage to organs with exocrine function. Patients will have a history of chronic lung 

disease (especially bronchiectasis), pancreatic insufficiency, and gastrointestinal 

complaints. Most symptoms of disease and many complications develop at an early age 

(2-20 years), often with a history of cystic fibrosis in relatives. Other common findings 

include increased sweat chloride tests, failure to thrive (infants), ileus, azoospermia 

(male infertility), gallstones, biliary cirrhosis, intussusception, steatorrhea, nasal polyps, 

sinusitis, recurrent pneumonia with digital clubbing, and eventually cor pulmonale. 

Treatment 

A. Pulmonary Infections 

Cystic fibrosis patients are often hospitalized for acute pulmonary infections. They 

require supplemental oxygen, vigorous hydration (to mobilize mucus plugs), chest 

physiotherapy (percussion and postural drainage), and antimicrobial treatment. 

Antibiotics should be based on initial Gram stain of sputum and culture. Because 

Staphylococcus aureus (even multidrug-resistant S. aureus) and Pseudomonas 

aeruginosa are commonly present, combination therapy with an antipseudomonal 

penicillin (eg, ticarcillin) and an aminoglycoside (tobramycin) can be used. 

B. Complications 

All complications should also be treated, including pneumothorax (thoracostomy),

intussusception (barium enema), right heart failure (diuretics), and hyperglycemia 

(insulin). 

C. Future Treatments 

The most promising future treatments for cystic fibrosis include multiple gene therapy 

vectors used to replace the patient's defective copy for the abnormal protein. 

Disposition 

Hospitalization is often required for evaluation and treatment of new respiratory 

symptoms or complications of disease. However, because nosocomial infections can be 

detrimental to these patients and many patients are already taking chronic maintenance 

antibiotics, consultation with the pulmonologist should be obtained to assist with the final 

treatment decision. 

Koch C, Hoiby N: Diagnosis and treatment of cystic fibrosis. Respiration 

2000;67(3):239. [PMID: 10867591] (Review of current diagnostic aspects of cystic 

fibrosis and treatment with both intensive antimicrobial regimens and anti-inflammatory 

medications.) 

Lees CM, Smyth RL: The current management of cystic fibrosis. Int J Clin Pract 

2000;54(3):171. [PMID: 10829360] (Evidence-based review of the most current 

treatment strategies for patients with cystic fibrosis.) 

INTERSTITIAL PULMONARY DISEASE 


A variety of conditions may produce diffuse progressive pulmonary interstitial 

inflammation and fibrosis, including drugs, pneumoconioses, collagen diseases, 

sarcoidosis, organic and inorganic dusts, and illnesses of unknown cause with 

pathologic features involving chiefly the lungs (eg, idiopathic interstitial fibrosis). Aside 

from the pneumoconioses and sarcoidosis, these illnesses are relatively uncommon. 

The principal feature of all of them is that dyspnea begins gradually and seldom occurs 

acutely without a background of increasing shortness of breath. When dyspnea of acute 

onset does occur, it is often due to intercurrent illness (eg, pulmonary infection). 

Patients also have pulmonary function tests that demonstrate restrictive lung 

dysfunction and impaired gas exchange. 


Many patients with interstitial pulmonary disease will know their diagnosis; if not, it can 

seldom be made with certainty in the emergency department setting, because lung 

biopsy or bronchoalveolar lavage are often required. 


Gradually increasing dyspnea, especially on exertion, is the only reliable symptom. 

Chest pain, cough, sputum production, and other symptoms may occur but are 

inconsistent. Physical findings are variable, but dry crackles (rales) at the bases of the

lungs are common. Cyanosis and clubbing may be present as well. 

B. Imaging 

Chest x-ray usually shows interstitial infiltrates, although this may be a subtle finding. 

High-definition CT scans of the chest are also helpful in assessing these patients. Other 

changes may be present depending on the disease process (eg, hilar adenopathy in 

sarcoidosis, conglomerate fibrosis in silicosis). 


Provide respiratory support as needed, and treat intercurrent disease (eg, infection). 

Hospitalize patients with respiratory failure or recent marked worsening of symptoms or 

those in whom acute infection is suspected. Refer all patients not already under care to 

a pulmonary disease specialist. Early lung transplantation offers a surgical therapeutic 

option for selected patients. 

Gross TJ, Hunninghake GW: Idiopathic pulmonary fibrosis. N Engl J Med 

2001;345(7):517. [PMID: 11519507] (Review of the pathophysiology, current 

symptomatic and investigational treatments, and need for early referral of patients with 

interstitial pulmonary fibrosis to specialists for enrollment in clinical trials or for lung 

transplantation.) 




33. Pulmonary Emergencies 1 - Christopher R. Pund, MD, & C. Keith Stone, 

MD 


also Chapter 11.)

Table 33-1. Conditions causing hemoptysis. 

Extrapulmonary disease 

Thrombocytopenia 

Other coagulopathies 

Heart failure 

Mitral stenosis 

Nonpulmonary hemoptysis 

Aspiration of blood from nasal, oropharyngeal, gastrointestinal, 

or other bleeding site 

Pseudohemoptysis 

Production of red-tinged sputum not due to blood

Table 33-2. Common precipitating factors in acute asthma and exacerbations 

of chronic obstructive pulmonary disease. 





MD 

TABLES 

Table 33-2. Common precipitating factors in acute asthma and 

exacerbations of chronic obstructive pulmonary disease.

Table 33-3. Conditions that predispose to pulmonary 

embolization. 





MD 

TABLES 

Table 33-3. Conditions that predispose to pulmonary embolization.

Table 33-4. Selected clinical causes of acute lung injury and acute 

respiratory distress syndrome. 





MD 

TABLES 

Table 33-4. Selected clinical causes of acute lung injury and acute 

respiratory distress syndrome.

34. Cardiac Emergencies 21 - Roger L. Humphries, MD, & C. Keith 

Stone, MD 

Immediate Management 

1 See also Chapter 35 for emergencies due to cardiac arrhythmias. 

2 This chapter is a revision of the chapter by Melvin D. Cheitlin, MD, & Joseph A. Abbott, 

MD, from the 4th edition. 

Cardiac disease is usually manifested by symptoms of chest pain, dyspnea or 

respiratory distress, cardiac arrest or syncope, or shock. Because these symptoms are 

so commonly encountered in the emergency department and because they may result 

from disease in many organs other than the heart, they are discussed separately 

(Chapters 7, 9, 11, 12, and 17). Because almost any cardiac disease is at least 

potentially life threatening, no attempt has been made in this chapter to categorize 

disorders on the basis of severity or to assign priorities in treatment. 

ACUTE CORONARY SYNDROME 

Acute coronary syndrome refers to a spectrum of conditions that develop from blood 

flow that is insufficient to meet the metabolic needs of the myocardium. Patients with an 

acute coronary syndrome exist on a clinical continuum from unstable angina to 

non-ST-segment-elevation myocardial infarction to ST-segment- elevation myocardial 

infarction. 

ACUTE MYOCARDIAL INFARCTION (Coronary Occlusion) 

Myocardial infarction results when arterial blood flow to the myocardium is suddenly 

decreased or interrupted. It is usually due to atherosclerotic coronary artery disease with 

plaque rupture and sudden occlusion by thrombus; vasculitis or emboli are less 

common causes. Complete occlusion, most often with thrombus, is found in 80-90% of 

patients with chest pain and ST segment elevation who are studied by coronary 

angioplasty within several hours of onset. Rarely, patients dying of myocardial infarction 

are found to have normal coronary arteries, and infarction in such cases is presumably 

due to spasm of a coronary artery or thrombosis with complete lysis. Cocaine use has 

been associated with acute myocardial infarction, probably as a result of coronary 

spasm with or without intravascular thrombus formation. In myocardial infarction, 

severely ischemic and infarcted muscle contracts and relaxes poorly or not at all; if 

infarction is extensive, decreased cardiac output with heart failure or shock may result. 

After myocardial infarction, the ventricle may become aneurysmal or may even rupture. 

If conducting tissue is ischemic or infarcted, conduction abnormalities may occur. The 

infarcted endocardium attracts platelets and fibrin that may form mural clots, which can 

subsequently embolize. During acute myocardial infarction, the myocardium is 

electrically unstable, resulting in ventricular arrhythmias that are frequently life 

threatening.

Upon occlusion of a coronary artery, necrosis occurs in a time-dependent course, 

proceeding from endocardium to epicardium, generally over 4-6 hours. When residual 

perfusion by collateral vessels is present or lysis or thrombus occurs—either 

spontaneously or as a result of therapy—there will be salvage of myocardium. The 

earlier the reperfusion, the more myocardium is salvaged. 



Most patients with myocardial infarction have chest discomfort that is typically 

substernal and may radiate to the neck or left arm. Occasionally, pain occurs in atypical 

areas such as the right arm, shoulders, back, or epigastrium. The pain is usually 

oppressive or squeezing in character and may be associated with anxiety, restlessness, 

nausea and vomiting, abdominal bloating, dyspnea, and diaphoresis. It commonly 

begins at rest, worsens gradually, and frequently persists for hours. Occasionally, 

myocardial infarction is painless—especially in elderly or diabetic patients—and is 

manifested by the acute onset of left heart failure, hypotension, or cardiac arrhythmias. 

Up to 25% of patients with an acute myocardial infarction may not develop any 

significant symptoms that would prompt the patient to seek medical attention. 

Physical findings vary, and none are specific or diagnostic of myocardial infarction. An 

S 4 gallop or at times an S 3 gallop may be present. Occasionally, an apical systolic 

murmur or mitral insufficiency due to papillary muscle and left ventricular dysfunction is 

present. In patients with uncomplicated myocardial infarction, there may be no abnormal 

findings on physical examination. When cardiopulmonary physical findings are present, 

they tend to reflect the presence of complications (see below). 

B. Electrocardiographic Findings 

The electrocardiogram (ECG) shows signs of infarction (eg, high-voltage T waves, 

elevated ST segments, ST-segment-elevation myocardial infarction, abnormal Q waves) 

in about half of patients. Other patients may have T wave inversions 

(non-ST-segment-elevation myocardial infarction). In the remainder, the initial ECG 

shows only nonspecific ST or T wave changes, or may be normal. Note: A normal ECG 

does not rule out the possibility of myocardial infarction. Continuous ST segment 

monitoring or serial ECGs provide additional information and may demonstrate an 

evolving acute coronary syndrome in patients with initially nondiagnostic ECGs. 


A detailed discussion of all markers of cardiac ischemia is beyond the scope of this 

chapter. Elevation of the CK-MB isoenzyme is still considered by the World Heath 

Organization as one of the criteria used to diagnosis acute myocardial infarction. 

Because CK-MB is found not only in the myocardium but also in brain and skeletal 

muscle, it is less specific for a myocardial ischemic event than are some other markers. 

The CK-MB serum level elevates usually within 4-6 hours after the onset of an acute 

myocardial infarction and peaks within 12-24 hours. Levels return to baseline generally 

within 2-3 days of an acute myocardial infarction. Within 6 hours of an acute myocardial 

infarction, the sensitivity and specificity of elevations in the serum CK-MB levels are 

17-62% and 92-100%, respectively.

Troponin is a complex of three specific proteins found in striated muscle. Two of the 

subunits, cardiac troponin T (cTnt) and I (cTni), are useful as clinical markers of 

myocardial injury. Because these cardiac proteins are genetically unique, cTnt and cTni 

are the most cardiac-specific biochemical markers. With recent improvements in the 

assay, microinfarctions are diagnosed when elevations in cTnt or cTni occur without 

elevations in the CK-MB levels. After an acute myocardial infarction, cardiac troponin 

serum levels generally elevate within 2-6 hours, peak at 12-24 hours, and may stay 

elevated for 7-10 days. The sensitivities of elevations of cTnt and cTni within 6 hours of 

an acute myocardial infarction are 50-59% and 6-44%, respectively. The specificities of 

elevations of cTnt and cTni within 6 hours of an acute myocardial infarction are 74-96% 

and 93-99%, respectively. 

One of the first cardiac markers used clinically, myoglobin, is still used by some today. 

Myoglobin is the most sensitive early marker of cardiac injury. After an acute myocardial 

infarction, elevations occurs within 1-3 hours, levels peak within 4-12 hours, and levels 

remain elevated for 12-36 hours. The sensitivity and specificity of myoglobin for 

detecting myocardial infarction within 6 hours of symptom onset are 55-100% and 

76-98%, respectively. 


For a complete differential diagnosis of chest pain, see Chapter 12. Aortic dissection, 

pericarditis, and gastrointestinal disorders (eg, peptic ulcer disease, pancreatitis) must 

be excluded in patients being considered for thrombolytic therapy. 

Note: The diagnosis of myocardial infarction is suggested by the history, and a decision 

to admit the patient to the coronary care unit immediately should be based on this 

information alone. Because of the relatively benign course of patients admitted with a 

good history suggesting myocardial infarction and a normal initial ECG, in some 

institutions these patients are admitted to a monitored intermediate care unit rather than 

a coronary care unit. No amount of laboratory data obtained in the emergency 

department will definitely rule out myocardial infarction. 

Treatment 

Patients experiencing acute cardiac syndrome should receive aggressive treatment with 

the goal of rapidly reperfusing ischemic myocardium. The two methods currently 

available are pharmacologic thrombolysis via plasminogen activators and procedural 

coronary intervention. The effectiveness of either modality in reducing mortality and 

myocardial damage depends on how early it is given after the onset of symptoms. 


Begin intravenous infusion of 0.9% normal saline through a secure intravenous catheter. 

Use microdrip infusion to minimize volume overload. Start 2-3 peripheral venous lines in 

patients receiving thrombolytic agents. Begin oxygen, 2-5 L/min, by nasal cannula or 

mask. 

Start electrocardiographic monitoring, and obtain a 12-lead ECG. If chest pain is 

present, give nitroglycerin, 0.5 mg sublingually or one puff delivered to the oral mucosa.

Repeat if no effect occurs in 5 minutes. If chest pain returns and systolic blood pressure 

is above 100 mm Hg, start intravenous nitroglycerin at 10 ug/ min and increase by 5 

ug/min every 3-5 minutes until systolic blood pressure falls by 10% or chest pain is 

relieved. The systolic blood pressure should not drop below 90 mm Hg. 

Give a narcotic analgesic (eg, morphine, 2-8 mg intravenously) if chest pain persists. 

Give furosemide, 40 mg by intravenous bolus injections, if the patient has pulmonary 

edema. Give the patient a 160- to 325-mg non-enteric-coated aspirin tablet to chew. 

In the absence of contraindications for ß-blockers (heart rate < 55/min, systolic blood 

pressure < 90 mm Hg, moist rales above the lower third of the lung fields, advanced 

atrioventricular block, or history of asthma), give 15 mg of metoprolol in three 5-mg 

intravenous injections at 2-minute intervals. 

B. Additional Measures 

Establish a laboratory test data base: complete blood count (CBC) with differential, 

serum creatinine and electrolyte measurements, blood urea nitrogen determinations, 

enzyme levels (preferably CK isoenzymes, cTni or cTnt, etc). Platelet count, 

prothrombin time, partial thromboplastin time, and blood for typing (and cross-matching 

if needed) should be obtained for patients to be given thrombolytic therapy. Monitor 

urine output. 

C. Option 1: Thrombolytic Therapy 

If the duration of chest discomfort is at least 30 minutes and less than 4-6 hours and no 

contraindications are present, pharmacologic revascularization is indicated. Many 

thrombolytic agents are available, including streptokinase, anistreplase (APSAC), 

alteplase (tissue plasminogen activator: t-PA), reteplase (r-PA), and tenecteplase 

(TNK). Thrombolytics should be initiated in the emergency department because the 

benefit of pharmacologic thrombolysis decreases with each passing hour after 

myocardial infarction. Some patients with myocardial infarction may benefit from 

thrombolytics up to 12 hours after the onset of chest pain, although 6 hours is generally 

considered the cutoff. Alteplase administration over 90 minutes improved survival when 

compared to streptokinase or 3-hour alteplase infusion. Even though intracranial 

bleeding events increased, alteplase demonstrated a long-term survival advantage 

presumably secondary to earlier thrombolysis and reperfusion of thrombosed coronary 

arteries. Compared to alteplase, TNK may offer advantages of a single bolus 

administration and fewer intracranial hemorrhage complications. Intracranial 

hemorrhage is the most devastating complication of thrombolytic therapy, occurring in 

0.5-3.3% of patients. 

1. Indications—The indications for pharmacologic revascularization are as follows: 

• ST segment elevation of at least 0.1 mV in 2 or more leads (II, III, aVF or V1-V6, I, 

aVL) suggests acute injury in the absence of left bundle branch block. An acute true 

posterior myocardial infarction (with ST depression in leads V1-V4) is also an indication 

for thrombolysis. Patients with ongoing chest pain and a new (or not known to be old) 

left bundle branch block should also be considered for pharmacologic reperfusion. 

• Both chest pain and ST elevation are not relieved by 2-3 sublingual nitroglycerin

tablets. 

• Patient is alert and oriented, or a family member or friend familiar with the patient's 

medical history is present. 

• No contraindications to thrombolytic therapy or anticoagulation therapy are present 

(see below). 


a. Absolute contraindications—Absolute contraindications are as follows: 

• History of any hemorrhagic cerebrovascular event (stroke, arteriovenous malformation, 

or aneurysm) or any nonhemorrhagic cerebrovascular event or transient ischemic attack 

(within the last year) 

• Any intracranial neoplasm 

• Active, internal bleeding (eg, serious gastrointestinal bleeding) excluding menses 

• Suspected aortic dissection 

b. Relative contraindications—In the following conditions, the risks associated with 

thrombolytic therapy may be increased, and clinical judgment should be used in 

evaluating expected benefits: 

• Recent (within 10 days) puncture of a noncompressible blood vessel 

• Poorly controlled hypertension of several years' duration or severe, uncontrolled 

arterial hypertension (diastolic blood pressure greater than 110 mm Hg or systolic blood 

pressure greater than 180 mm Hg) 

• Diabetic hemorrhagic retinopathy or hemorrhagic ophthalmic condition 

• Current treatment with an anticoagulant with international normalized ratio greater than 

2-3 or other bleeding diathesis 

• Pregnancy 

• Any other condition associated with a predisposition to bleeding (eg, ulcerative colitis, 

active peptic ulcer disease, polycystic kidneys, gastrointestinal arteriovenous 

malformation, vascular tumors) or bleeding within 4 weeks 

• Prolonged (> 5 minutes) or traumatic external cardiac compression or traumatic 

endotracheal intubation 

• History of nonhemorrhagic cerebrovascular accident beyond 1 year 

• Recent (within 4 weeks) trauma or major surgery at a noncompressible site (eg,

coronary artery bypass surgery, organ biopsy, intra-abdominal surgery, or obstetric 

delivery) 

3. Dosages—If indicated, the following dosage regimens are recommended: 

a. Streptokinase—The recommended dosage is 1.5 million units in 250 mL of 5% 

dextrose in water, given intravenously over 1 hour. Because of the risk of serious 

allergic reactions, streptokinase is contraindicated in patients who have ever received 

streptokinase previously. 

b. Alteplase—The recommended dosage is 15 mg intravenous bolus followed by 0.75 

mg/kg (maximum 50 mg) intravenous infusion over 30 minutes and then 0.5 mg/kg 

(maximum 35 mg) over 60 minutes. Alteplase has a very short half-life (5 minutes); 

therefore, unfractionated heparin must be used to prevent reocclusion. Heparin should 

be started as a bolus of 60 units/kg at the start of the alteplase infusion followed by a 

maintenance dose of 12 units/kg. The reduction in mortality with alteplase thrombolysis 

(if used within 6 hours of symptom onset) is 23-30%. 

c. APSAC—The recommended dosage is 30 mg intravenously infused slowly over 5 

minutes. Because of the risk of serious allergic reaction, patients who have received 

streptokinase or APSAC previously cannot be given the drug again. 

d. Urokinase—The recommended dosage is a loading dose of 0.5 million units over a 

10-minute period. This is followed by infusion doses of 1.6-4.5 million units over 18-24 

hours. 

e. Reteplase—r-PA, a variation of t-PA, has a half-life of 13-16 minutes and is simpler 

to administer than t-PA. The dose is two 10-unit intravenous boluses over 2 minutes, 

with 30 minutes between each dose. 

f. Tenecteplase—TNK is a third-generation variation of t-PA. It has improved fibrin 

specificity and a longer half-life, allowing single bolus administration. The dose is based 

on weight, ranging from 30 mg to 50 mg rapid bolus. Overall mortality compared to t-PA 

was equal; however, in patients presenting later in the course of an acute myocardial 

infarction, those given TNK had fewer episodes of nonintracranial bleeding. 

Excellent evidence indicates that myocardial reperfusion salvages 

myocardium—resulting in better ventricular function than conventional 

management—and improves survival if reperfusion occurs within 6 hours after the onset 

of symptoms of myocardial infarction. Thrombolytic therapy may be beneficial in patients 

with persistent chest pain for up to 24 hours after onset of symptoms. t-PA results in a 

higher percentage of vessel patency (60-80%) than does streptokinase (30-60%) within 

the first hour with an associated improvement in survival. 

4. Heparin—Heparin should be used in conjunction with any thrombin-specific 

thrombolytic agent such as alteplase. Because of the systemic fibrinolysis achieved by 

streptokinase or APSAC, anticoagulation with heparin is not indicated. Intravenous 

heparin, 60 units/kg bolus followed by 12 units/kg/h, should be given in a separate line 

while alteplase is infusing because of the short half-life of alteplase and because of the

danger of recurring thrombosis. Heparin should be continued for 48 hours or longer, 

maintaining activated partial thromboplastin time at twice normal. 

5. Monitoring—Transfer patients given thrombolytic therapy to an intensive care unit as 

soon as possible after initiation of treatment. Monitor the following: 

• Blood pressure every 15 minutes during infusion and every 30-60 minutes thereafter. 

• ECG rhythm strip for reperfusion arrhythmias and ST segment changes. 

• Bleeding complications and changes in neurologic status. Avoid venous or arterial 

punctures and unnecessary trauma. 

• Twelve-lead ECG 4 hours after the start of therapy and as needed (eg, for recurrence 

of chest pain). 

• CK with isoenzymes and cTni or cTnt 4 hours after initiation of treatment and at 4-hour 

intervals for 24 hours. 

D. Option 2: Percutaneous Coronary Intervention 

Formerly termed angioplasty, percutaneous coronary intervention (PCI) involves cardiac 

catheterization and various techniques to assess and restore vessel patency 

emergently. Coronary artery stenting has become the procedure of choice. When 

performed early in the course of an acute myocardial infarction, PCI has demonstrated 

improved survival rates over pharmacologic thrombolysis. Increased rates of normal 

flow and decreased rates of reocclusion in the infarct-related artery are much more 

likely when PCI is chosen over pharmacologic thrombolysis. In addition, early definition 

of coronary anatomy can be used to tailor therapy and improve risk stratification. One 

study comparing PCI with t-PA found a reduction in mortality of 4% with PCI. Major 

complications associated with thrombolytics such as intracranial bleeding do not occur 

with PCI. In patients with contraindications to thrombolytics, PCI is the only option 

available to restore perfusion and salvage myocardium. Rescue PCI is useful for 

patients who have received thrombolytics but whose chest pain or ST segment 

elevation has failed to resolve. Unfortunately, PCI is not widely available; fewer than 

18% of U.S. hospitals are equipped to perform the procedure. 

Disposition 

Hospitalize all patients with clinical histories suggesting myocardial infarction, and start 

electrocardiographic monitoring (in a coronary care unit, if possible). Patients with 

suspected myocardial infarction and normal initial ECGs and initial cardiac enzymes 

may be admitted to a monitored intermediate care unit. 

COMPLICATIONS OF MYOCARDIAL INFARCTION 

About 10-15% of patients reaching the hospital with myocardial infarction die during 

hospitalization. One or more complications occur in over half of all patients with 

myocardial infarction.

1. Shock (Cardiogenic Shock) 

Shock complicating myocardial infarction occurs in 7-8% of patients and may be caused 

by extensive myocardial infarction with decreased cardiac output (most common), 

inappropriate reflex peripheral vasodilatation, arrhythmias, hypovolemia, right ventricular 

infarction, and mechanical complications such as ruptured ventricular septum and 

severe mitral regurgitation. Free-wall myocardial rupture results in tamponade and 

shock. The mortality rate is as high as 70-80% among patients with cardiogenic shock 

as a complication of acute myocardial infarction. 


Hypotension accompanied by confusion, obtundation or restlessness, cool skin, oliguria, 

and metabolic acidosis suggests shock. Mild to moderate hypotension alone is common 

in myocardial infarction and does not itself indicate shock. Shock in myocardial 

infarction may be due to many causes (see Table 9-1), which may be difficult to 

differentiate noninvasively (Table 34-1). 

Treatment 

Use any or all of the measures discussed here as necessary. (See also Chapter 9.) 

A. Airway Management 

Give oxygen, 5-10 L/min, by mask or nasal cannula. Patients in shock with respiratory 

failure require endotracheal intubation. 

B. Venous Pressure Monitoring 

Monitor central pressure with a Swan-Ganz pulmonary artery catheter (or, far less 

desirably, a central venous pressure catheter, since in acute myocardial infarction, left 

ventricular filling pressure can be markedly elevated with normal right ventricular filling 

pressure, and vice versa). Use an arterial line to measure blood pressure. If possible, 

defer insertion of these catheters until the patient has been hospitalized. 

C. Other Measures 

Give a fluid challenge (200 mL of saline intravenously over 20 minutes) if the patient is 

not in congestive heart failure (ie, no rales, no pulmonary edema on chest x-ray). 

Repeat as needed if congestive heart failure does not develop. Correct arrhythmias (see 

below). Insert a Foley catheter, and measure urine output hourly. 


Give dopamine (or dobutamine), 2.5-20 ug/kg/min by continuous intravenous infusion. 

Use the smallest effective dose, guided by hemodynamic response. When shock is 

caused by inappropriate vasodilatation (rare), a-adrenergic drugs such as 

norepinephrine are useful. 

E. Percutaneous Coronary Intervention 

Evidence indicates that acute revascularization by PCI might be particularly effective in 

patients who develop cardiogenic shock early (within 3-6 hours) after onset of 

myocardial infarction. PCI acutely should be seriously considered in such patients

ecause thrombolytics are ineffective in cardiogenic shock associated with an acute 

myocardial infarction. 

Disposition 

All patients with cardiogenic shock must be hospitalized, preferably in an intensive care 

unit. Therapy is directed at the likely causes of shock (eg, fluid administration to patients 

with right ventricular infarction). Intra-aortic balloon pump (IABP) counterpulsation can 

increase cardiac output and improve both coronary and systemic perfusion. IABP 

counterpulsation is most commonly used to support the patient with cardiogenic shock 

during PCI. 

2. Congestive Heart Failure 

Congestive heart failure is caused by extensive myocardial infarction, volume overload, 

arrhythmias, acute mitral regurgitation, or ventricular septal rupture. 


Symptoms and signs of congestive heart failure include dyspnea, anxiety, tachypnea, 

tachycardia, pulmonary rales or frank pulmonary edema, jugular venous distention, 

hypoxemia, and typical findings on chest x-ray (cardiomegaly, pulmonary vascular 

plethora, Kerley B lines, pleural effusion, or pulmonary infiltrates consistent with 

pulmonary edema). Wheezing may also be a sign of congestive heart failure (cardiac 

asthma). Suspect right ventricular infarction in inferior myocardial infarction if signs of 

right heart failure (right ventricular gallops, elevated central venous pressure, 

hepatomegaly, peripheral edema) are prominent in the absence of signs of left heart 

failure (dyspnea, rales, pulmonary congestion on chest x-ray). 

Treatment 

A. Airway Management 

Give oxygen, 5-10 L/min, by mask or nasal cannula. Obtain arterial blood gas 

measurements. Treat respiratory failure if present. 

B. Drug Therapy 

1. Furosemide—Give furosemide, as an intravenous bolus of at least the patient's 

normal total daily dose. If the patient is not already taking furosemide, administer a 

40-mg intravenous bolus initially, and observe the diuretic response by monitoring the 

patient's symptoms and urine output. Diuretics are contraindicated if right ventricular 

infarction is suspected. 

2. Morphine—Give morphine, 2-8 mg intravenously. 

3. Nitroglycerin—Apply nitroglycerin ointment, 1.25-2.5 cm (1/2-1 in), under an 

occlusive dressing if symptoms are mild. For severely symptomatic patients, a 

nitroglycerin infusion will benefit patients because both preload and afterload are 

reduced. In patients with inferior or right ventricular acute myocardial infarction, nitrates 

are relatively contraindicated because they may precipitate profound hypotension.

Hypotension related to nitrates is treated with reduction or discontinuation of the infusion 

depending on the degree of symptomatic hypotension. Intravascular volume expansion 

with intravenous fluid infusions will often quickly correct hypotension. 

Disposition 

Treatment of congestive heart failure in the emergency department is directed at 

reducing the intravascular volume through diuretics or vasodilation. Patients with 

respiratory failure may require intubation in the emergency department. Hemodynamic 

monitoring with a pulmonary artery catheter may assist in assessing volume status. In 

the setting of an acute myocardial infarction, patients with congestive heart failure 

should be closely monitored in an intensive care unit. 

3. Acute Mitral Regurgitation & Ventricular Septal Rupture 

Mechanical failure of infarcted tissue (eg, rupture of the ventricular septum or of 

papillary muscle supporting the chordae tendineae) is a common cause of acute mitral 

regurgitation and ventricular septal rupture. Minimal-to-moderate mitral regurgitation is 

common after myocardial infarction as a result of papillary muscle and left ventricular 

wall dysfunction. Severe degrees of mitral regurgitation can result from marked 

ischemia with little or no infarction and can be completely reversed with 

revascularization. 


Abrupt, severe congestive heart failure with pansystolic regurgitation murmur suggests 

acute mitral regurgitation or ventricular septal rupture. Echocardiography to detect mitral 

regurgitation or the abnormal velocity jet of a ventricular septal defect can establish the 

diagnosis. 

Treatment 


To be truly effective the following measures must be instituted in an intensive care unit: 

• Treat heart failure with diuretics, morphine, and nitroglycerin ointment (usually of 

minimal effectiveness). 

• Obtain urgent cardiologic and cardiac surgical consultation. 

• IABP is a useful temporizing measure while the patient is being prepared for surgery. 

B. Follow-Up Measures 

The only life-saving treatment for most patients is emergency cardiac catheterization 

followed by surgery. 

Disposition 

Hospitalize all patients for treatment and surgery.

4. Myocardial Rupture 

The chief cause of myocardial rupture is mechanical failure of an infarcted ventricular 

wall. 


Myocardial rupture is an uncommon cause of sudden death during acute myocardial 

infarction; it is responsible for only about 5% of deaths. Myocardial rupture is suggested 

by abrupt onset of hypotension with increased venous pressure (ie, cardiac 

tamponade). Pulseless electrical activity often occurs. 


If echocardiography or bedside emergency ultrasound demonstrates a pericardial 

effusion, pericardiocentesis is indicated and can be performed under ultrasound 

guidance (Chapter 6). When emergent ultrasound is not available to assess a patient for 

possible pericardial tamponade, blind pericardiocentesis may be life saving. 

Obtain emergency cardiac surgical consultation for immediate cardiac surgery. This is 

successful in the few cases in which rupture has been minimal with slow intrapericardial 

hemorrhage. 

5. Systemic or Pulmonary Embolization (See also Chapter 33.) 

Systemic or pulmonary embolization is commonly caused by intracardiac mural 

thrombosis or phlebothrombosis. 


The most common findings in pulmonary embolism are sudden unexplained dyspnea 

and tachycardia. Occasionally, pleuritic pain, signs of right heart strain, or abnormal 

chest x-ray may occur. Patients at greatest risk are those with thrombus visualized in 

the left or right ventricle by 2-dimensional echocardiography. The diagnosis may be 

confirmed by computed tomography (CT) scan of the chest, lung scan, or arteriography 

(Chapter 33). Systemic embolization is suspected when symptoms and signs of arterial 

occlusion occur. The clinical picture depends on the artery occluded, for example, flank 

pain and hematuria with renal artery embolism; pallor, pain, and loss of pulse with 

brachial or femoral artery embolism; stroke with cerebral artery embolism. 


Give oxygen, draw blood for determination of prothrombin and partial thromboplastin 

times, and then begin systemic anticoagulation with heparin, 80 units/ kg bolus followed 

by 18 units/kg/h infusion, or a low-molecular-weight heparin such as enoxaparin, 1 

mg/kg subcutaneous administration every 12 hours. Pericarditis is a relative 

contraindication to anticoagulation because of the risk of bleeding into the pericardial 

sac, with resulting cardiac tamponade. Heparin is also contraindicated in patients with

ecent stroke, active duodenal ulcer, or active bleeding that cannot be controlled by 

direct pressure. Even though it does not cross the placenta, heparin must be used with 

caution in pregnant patients, especially during the third trimester. (Acute myocardial 

infarction during pregnancy is quite rare.) 

With a massive pulmonary embolism with right heart failure or shock, intravenous 

fibrinolysis with streptokinase, urokinase, or t-PA has been recommended in doses 

similar to those given for acute myocardial infarction. Occasionally, mechanical 

disruption of the embolic thrombus by a catheter has been life saving. 

Seek appropriate surgical consultation (with a thoracic, general, or vascular surgeon) for 

patients with persistent hypotension, contraindications to thrombolytic therapy, or 

systemic embolization who may benefit from surgical intervention (eg, angioplasty and 

embolectomy for a pulseless and ischemic extremity). 

All patients should be hospitalized in the coronary care unit. 

6. Pericarditis 

When transmural myocardial infarction causes pericardial inflammation over the area of 

necrosis, pericarditis may occur within the first week. Pericarditis occurring more than 1 

week after myocardial infarction may be the result of Dressler syndrome, an 

autoimmune reaction. 


Pericarditis usually does not appear until 2-3 days after the onset of myocardial 

infarction. The appearance of a friction rub is often the only manifestation; pain and 

electrocardiographic changes are often absent. Frequently, a small pericardial effusion 

may be detected by echocardiography. If a pericardial friction rub is heard in the first 24 

hours after onset, suspect pericarditis as a primary diagnosis rather than as being due 

to acute myocardial infarction. Early ECG signs of pericarditis include diffuse ST 

segment elevation (with a concave upslope and indistinct J point) and diffuse PR 

segment depression (except in AVR, where the PR segment is elevated). 

Treatment 

Treat pain with a nonsteroidal anti-inflammatory agent such as indomethacin, 25-50 mg 

orally 3 times a day. If pain is severe, give morphine, 2-4 mg intravenously every 5-10 

minutes, and repeat as necessary. 

Disposition 

Hospitalize the patient in a coronary care unit for pain control and monitoring for 

possible cardiac tamponade (rare). 

ANGINA PECTORIS 


Myocardial ischemia (with attendant angina pectoris) results from an imbalance 

between myocardial oxygen supply and demand. Clinical findings vary depending on the 

severity of ischemia and on the frequency, duration, and rapidity of onset of ischemic 

episodes. If the demand for myocardial blood flow exceeds the capacity of the 

obstructed coronary arterial tree to supply it, the discomfort (angina pectoris) lasts until 

the excessive demand for coronary flow is reduced. 

Discomfort is more intense and lasts longer when coronary blood flow decreases 

markedly, as occurs with sudden marked increase in coronary artery obstruction 

resulting from abrupt development of thrombus over an atherosclerotic plaque, 

embolization to a coronary artery, or sudden occlusion by coronary artery spasm. If 

myocardial necrosis then occurs, the condition is termed myocardial infarction; 

otherwise, the episode is one of acute coronary insufficiency, or preinfarction angina. 

If obstruction is so severe that coronary blood flow is barely adequate to meet resting 

demands, even small increases in myocardial oxygen demand may cause angina. In 

addition, small aggregations of platelets on a ruptured plaque, spasm, or increased 

vasomotor tone can cause minor changes in the caliber of the severely obstructed 

coronary artery and precipitate angina. 

Myocardial ischemia can exist in the absence of any chest discomfort. In patients with 

severe ischemia, 24-hour electrocardiographic monitoring shows that 80% of the 

episodes of ST segment depression lasting for a minute or more are present without 

angina (so-called silent ischemia). Painless myocardial infarction is not unusual in 

elderly or diabetic patients. 


A. Stable Angina (Angina of Effort) 

By definition, the pattern of discomfort, its frequency of occurrence, and precipitating 

factors have remained the same for 3 or more months. 

Discomfort is usually substernal but may originate in other areas (eg, elbow, forearm, 

shoulder, neck interscapular region, or jaw), although substernal discomfort eventually 

occurs. It is usually precipitated by activities that increase myocardial oxygen 

consumption (eg, exercise, eating, or emotional upset), lasts longer than 1 minute and 

usually less than 15 minutes, and is usually relieved by rest or nitroglycerin. Pain that 

meets these criteria usually indicates the presence of fixed coronary obstruction. The 

most important feature suggesting the diagnosis of angina pectoris is discomfort 

precipitated by exercise or emotion. 

B. Unstable Angina 

Anginal pain that begins in a patient previously free of pain (ie, pain of less than 1 

month's duration) is called new-onset angina. Unstable angina is that which has 

changed in pattern, becoming more frequent (crescendo angina) and longer lasting. It is 

precipitated by a lesser degree of activity and may respond less to rest and nitroglycerin 

than does stable angina. Angina that occurs at rest without any obvious precipitating 

factor (rest angina) is the most serious form of unstable angina.

Sudden changes in angina not associated with increased myocardial oxygen demand 

(eg, increased blood pressure or heart rate) are presumed to be caused by a change in 

the anatomy of the coronary artery, for example, new vessel obstruction caused by 

progression of heart disease, development of thrombus, or other factors such as platelet 

aggregation or coronary spasm. 

C. Atypical Angina, or Prinzmetal (Variant) Angina 

Prinzmetal angina occurs as a result of a sudden, reversible, severe coronary artery 

obstruction (coronary artery spasm). It may occur in patients with fixed atherosclerotic 

coronary lesions and less often in those with minimal or no fixed coronary obstruction. 

Chest discomfort usually occurs without a precipitating cause. It frequently occurs at 

rest or awakens the patient at night. The discomfort frequently lasts longer than the 

usual episode of angina and is often accompanied by ST segment elevation (current of 

injury) that is transient and reversed in minutes after administration of nitroglycerin. With 

lesser degrees of spasm, ST segment depression may occur. Ventricular ectopy and 

ventricular tachyarrhythmias may also occur. 




A. Stable Angina 

Nitroglycerin, 0.4 mg sublingually, is the drug of choice when pain starts. It may also be 

taken prophylactically several minutes before activities that regularly precipitate angina. 

Pain is usually relieved in 1-2 minutes. Nitroglycerin tablets deteriorate in about 6 

months; headache and sublingual tingling are common side effects of active tablets. 

Patients with stable angina that has exhibited a set pattern of frequency and 

precipitating factors over 3 or more months do not require hospitalization and should be 

referred for evaluation on an outpatient basis. 

B. Unstable Angina, Rest Angina, and Prinzmetal Angina 

1. Immediate measures—Give oxygen, 5-10 L/min, by mask or nasal cannula. 

Hospitalize the patient immediately in the coronary care unit, and obtain daily ECGs and 

myocardial enzyme determinations (CK isoenzymes and cTni or cTnt) to detect possible 

myocardial infarction. 

2. Morphine—Give morphine, 2-3 mg intravenously every 5-10 minutes, to relieve 

prolonged pain. Monitor blood pressure. 

3. Nitroglycerin—Apply nitroglycerin paste, 1.25 cm (1/2 in), to the skin under an 

occlusive dressing every 4 hours, or transdermal nitroglycerin patches may be 

substituted. Topical nitroglycerin can be used if the patient is pain free. If the pain 

persists, an intravenous infusion of nitroglycerin is indicated at an initial rate of 10 

ug/min.

4. ß-Blockers—Add a ß-adrenergic blocking agent (eg, metoprolol, 5 mg intravenously 

over 2 minutes, every 5-10 minutes until a total dose of 15 mg has been administered) 

unless contraindicated (heart rate less than 60 beats/min, atrioventricular block, severe 

asthma, or chronic obstructive pulmonary disease). 

5. Aspirin—Start non-enteric-coated aspirin, 160- 325 mg orally. Aspirin has been 

shown to reduce the incidence of myocardial infarction and death by about 50%. 

6. Anticoagulation—Antiocoagulation may also be helpful in these patients. Use 

unfractionated heparin at 80 units/kg intravenous bolus followed by 18 units/ kg/h 

intravenous infusion or a low-molecular-weight heparin such as enoxaparin, 1 mg/kg 

administered subcutaneously every 12 hours. Compared to unfractionated heparin, 

enoxaparin was associated with decreased mortality in patients with acute myocardial 

infarction or recurrent angina. 

7. Other drug therapies—Glycoprotein IIB/IIIA receptor antagonists such as tirofiban 

and eptifibatide are the newest agents to be approved for use in patients with unstable 

angina. These agents block platelet binding at the receptor site that cross links 

fibrinogen to the platelets. Although these agents have shown promise when used in 

conjunction with PCI, their role in unstable angina is still being defined. 

8. Percutaneous coronary intervention—If pain continues despite treatment, consider 

PCI. If acute myocardial infarction has occurred and pain continues despite optimal 

medical management or thrombolytics, PCI must be considered. Percutaneous aortic 

balloon counterpulsation may also be useful in patients with cardiogenic shock. 

American College of Cardiology: 1999 Update: ACC/AHA guidelines for the 

management of patients with acute myocardial injury. Accessed at 

http://www.acc.org/clinical/guidelines/ nov96/1999/index.htm 

Antman EM: Decision making with cardiac troponin tests. N Engl J Med 2002;346:2079. 

[PMID: 12087146] 

Braunwald E et al: ACC/AHA 2002 guidelines update for the management of patients 

with unstable angina and non-ST-segment elevation myocardial infarction—summary 

article. J Am Coll Cardiol 2002;40:1366. [PMID: 12383588] 

Brown M et al: Acute interventions for myocardial reperfusion. Emerg Med Clin North 

Am 1998;16:565. [PMID: 9739775] 

Char DM, Israel E, Ladenson J: Early laboratory indicators of acute myocardial 

infarction. Emerg Med Clin North Am 1998; 16:519. [PMID: 9739773] 

Diop D, Aghababian RV: Definition, classification, and pathophysiology of acute 

coronary ischemic syndromes. Emerg Med Clin North Am 2001;19:259. [PMID: 

11373977] 

Hayes OW: Emergency management of acute myocardial infarction: focus on 

pharmacologic therapy. Emerg Med Clin North Am 1998;16:541. [PMID: 9739774]

Karras DJ, Kane DL: Serum markers in the emergency department diagnosis of acute 

myocardial infarction. Emerg Med Clin North Am 2001;19:321. [PMID: 11373981] 

Lee TH, Goldman L: Evaluation of the patient with acute chest pain. N Engl J Med 

2000;342:1187. [PMID: 10770985] 

Llevadot J, Giugliano RP, Antman EM: Bolus fibrinolytic therapy in acute myocardial 

infarction. JAMA 2001;286:442. [PMID: 11466123] 

McPherson JA, Gibson RS: Reperfusion therapy for acute myocardial infarction. Emerg 


Shannon AW, Harrigan RA: General pharmacologic treatment of acute myocardial 

infarction. Emerg Med Clin North Am 2001;19:417. [PMID: 11373987] 

HEART FAILURE 

Heart failure is the expected outcome of many cardiac diseases. The basic abnormality 

is inability of the heart to maintain cardiac output sufficient to meet systemic demands. 

Compensatory mechanisms include (1) dilatation of the ventricle to maintain normal 

stroke volume (Frank-Starling mechanism); (2) retention of sodium and water by the 

kidneys to maintain intravascular volume; (3) increased activity of the sympathetic 

nervous system, leading to tachycardia and increased systemic vascular resistance; 

and (4) increased serum renin and angiotensin, which stimulate aldosterone output and 

cause retention of sodium and water as well as increased systemic vascular resistance. 

Cardiac output is usually maintained at normal levels or below, but at the expense of 

increased ventricular volume and filling pressure. The increased ventricular filling or 

diastolic pressures result in increased pulmonary or systemic venous pressures, with 

consequent pulmonary or peripheral edema. Tissue and organ dysfunction may result 

from increased venous pressure, decreased cardiac output, and edema. 

Recently, it has been recognized that heart failure may occur primarily because of 

diastolic dysfunction where the ventricle appears to be noncompliant; therefore, even 

with normal diastolic volumes the high filling pressure results in pulmonary congestion. 

This type of heart failure is seen in hypertension, especially in elderly patients; in 

hypertrophic cardiomyopathy; and in myocardial ischemia. In many patients, both 

systolic and diastolic dysfunction are present. An echocardiographic-Doppler study 

should be performed in all patients with congestive heart failure to help determine the 

cause of the failure and the degree of systolic and diastolic dysfunction. The 

echocardiographic-Doppler study need not be done in the emergency department or at 

the first visit. 

Although the distinction between mild to moderate heart failure and severe heart failure 

is not absolute, it has practical therapeutic implications. 

SEVERE HEART FAILURE, INCLUDING PULMONARY EDEMA 

Clinical Findings


Frank pulmonary edema may occur with severe left heart failure. Patients experience 

dyspnea at rest (Chapter 11) and in severe cases may be cyanotic and cough up frothy 

sputum. Peripheral edema may or may not be present; edema may be severe 

(anasarca) in severe right heart failure. Pulmonary edema may be accompanied by 

wheezing, and a loud S 3 sound is usually present. Loud rhonchi and rales may interfere 

with more detailed evaluation. 


Chest x-ray may show pulmonary edema, pleural effusions, or cardiomegaly. 


Arterial blood gas measurements show hypoxemia; pH and PCO 2 vary, but hypocapnia 

and metabolic acidosis are common. With exhaustion, hypercapnia may occur, in which 

case intubation and mechanical ventilation are required. Recently the serum level of a 

neuropeptide, B-type natriuretic peptide (BNP), has been used clinically as a good 

marker for congestive heart failure. BNP is released from the ventricular myocardium in 

response to increases in ventricular wall tension. Above a BNP cutoff level of 100 

pg/mL, the sensitivity and specificity are 90% and 76%, respectively, for differentiating 

congestive heart failure from other causes of dyspnea. 

D. Electrocardiographic Findings 

Sinus tachycardia is common in patients with severe heart failure. In patients with 

hypertensive heart disease, left ventricular hypertrophy may be evident. In addition, 

obtain an ECG to detect the presence of ischemia. 

The differential diagnosis is discussed in Chapters 11 and 12. 

Of paramount importance is the establishment of the cause of the heart failure. Specific 

causes have specific therapies, for example, valve replacement for pulmonary edema 

from severe aortic stenosis, or lowering of blood pressure for hypertension. 

Note: Acute myocardial infarction or ischemia must be considered in all patients with 

sudden onset of congestive heart failure. 

Treatment 

A. Oxygenation and Venous Access 

Begin oxygen, 2-4 L/min, by mask or nasal cannula while awaiting the results of blood 

gas measurements. Insert a peripheral intravenous catheter, and give 0.9% normal 

saline by microdrip infusion to keep the catheter patent. 

B. Morphine 

Give morphine, 2-4 mg intravenously. Repeat every 20-30 minutes as needed for 

dyspnea, but stop if somnolence or hypercapnia supervenes. 

C. Furosemide

Give furosemide, 40 mg as an intravenous bolus. If the patient is not already taking oral 

furosemide, 40 mg intravenously is a common initial dose. For patients already taking 

oral furosemide, administer at least the daily dose as an intravenous bolus. If the patient 

fails to respond in 10 minutes, repeat the dose once. 

C. Nitroglycerin 

Nitroglycerin, being a potent vasodilator, is useful in severe congestive heart failure 

because it reduces preload and afterload. The dose is 10 ug/min initially. Severe 

hypotension can develop, especially in the setting of an acute inferior or right ventricular 

infarction. 

D. Nitroprusside 

If the cause of severe congestive heart failure is directly related to hypertensive 

emergency, administer nitroprusside, 2-20 ug/kg/min as a continuous infusion. While the 

patient is monitored carefully (arterial pressure monitor is recommended), the dose can 

be titrated to achieve the desired blood pressure. 

E. Nesiritide 

Just as the measurement of BNP is useful for the diagnosis of congestive heart failure, 

the administration of BNP (nesiritide) improves hemodynamics and dyspnea in patients 

with severe decompensated congestive heart failure. Nesiritide is administered as a 2 

ug/kg bolus over 1 minute, followed by a continuous infusion of 0.01 ug/kg/min generally 

for 12-24 hours. The major side effect of nesiritide is hypotension, which generally 

resolves quickly when the infusion is reduced or stopped. 

Disposition 

Hospitalize all patients with severe heart failure. Search for the reason behind the 

recurrent pulmonary edema, for example, noncompliance with regard to prescribed diet 

and medications, paroxysmal arrhythmias, institution of a medication with a negative 

inotropic effect, pulmonary emboli, or complicating disease. 

MILD TO MODERATE HEART FAILURE 



Nocturnal cough or dyspnea, orthopnea, dyspnea on exertion, and ankle swelling are 

common. The patient is not in distress at rest. Cardiomegaly is almost always found and 

is usually associated with some symptoms or sign of underlying cardiac disease (eg, 

angina or findings characteristic of aortic stenosis). Other important signs include 

increased venous pressure, hepatojugular reflux, pulmonary rales or pleural effusion, 

sacral or peripheral edema, and S 3 gallop. 

Because hypertension is one of the most common causes of heart failure, record the 

blood pressure reading in both arms with the patient supine and sitting. 


Chest x-ray may demonstrate cardiomegaly and pulmonary congestion.


Although there are no specific electrocardiographic manifestations of heart failure, it is 

nonetheless helpful to obtain an ECG. 

D. Laboratory Findings 

Obtain serum electrolyte determinations, renal function tests, and blood urea nitrogen 

and serum creatinine measurements. When renal blood flow is decreased, a rise in 

blood urea nitrogen out of proportion to the rise in serum creatinine is common (prerenal 

azotemia). Recently, measurement of serum BNP (as mentioned in the previous 

section) has been shown to improve accuracy in the diagnosis of congestive heart 

failure. 

Treatment 

Provide the patient with instructions for a low-sodium (1-2 g/d) diet. Prescribe a diuretic. 

A thiazide diuretic (eg, hydrochlorothiazide, 25 mg orally twice daily with potassium 

supplementation) should be sufficient initial therapy for most patients. Control 

hypertension if present (see below). 

Disposition 

By definition, hospitalization is not required for patients with mild heart failure per se, 

although it may be prudent to hospitalize some patients (eg, unreliable patients, those 

with other underlying illnesses or new-onset symptoms). All patients should be referred 

for long-term care and should be seen again within 1 week after their visit to the 

emergency department. Most of these patients will be candidates for medical therapy 

with angiotensin-converting enzyme inhibitors (eg, captopril or enalapril) or ß-blockers. 

These agents have been shown to improve symptoms in patients with moderate 

congestive heart failure. 

Colucci WS et al: Intravenous nesiritide in the treatment of decompensated congestive 

heart failure: Nesiritide Study Group. N Engl J Med 2000;343:246. [PMID: 10911006] 

HYPERTENSION & HYPERTENSIVE CRISIS 


The emergency physician evaluates patients with elevated blood pressures on a daily 

basis. The urge exists to treat all abnormal vital signs. Emergency physicians should 

avoid reflexly treating all elevated blood pressures without considering the patient in 

light of the clinical setting. For example, a patient experiencing pain or anxiety may be 

hypertensive in the emergency department simply as an adrenergic reflex. Aggressive 

treatment of asymptomatic hypertension in the emergency department may not be 

benign because it may lead to hypoperfusion and precipitate cerebrovascular ischemic 

events. When hypertension acutely causes symptoms, the organs most commonly 

affected include the brain, heart, and kidneys. Two categories of hypertension seen in 

emergency department patients merit further discussion: hypertensive urgency and 

hypertensive emergency.

A. Hypertensive Urgency 

Hypertensive urgency is classically defined as a severely elevated blood pressure in a 

patient with no symptoms, signs, or laboratory findings of end organ damage. Typical 

screening studies include serum creatinine (acute elevation), urinalysis (proteinuria, red 

blood cells, or red cell casts), chest x-ray (pulmonary edema or thoracic aortic 

dissection), and ECG (cardiac ischemia). 

B. Hypertensive Emergency 

Hypertensive emergency occurs when elevated blood pressure is responsible for 

symptoms, signs, or laboratory evidence of end organ damage, such as mental status 

changes (hypertensive encephalopathy), cardiac ischemia or congestive heart failure, or 

acute renal failure. 

Treatment 

A. Categories of Management 

1. Hypertensive urgency—If history, physical exam, and screening tests do not reveal 

any end organ damage, blood pressure should be controlled within 24-48 hours. 

Reliable patients can be discharged home with rapid follow-up with a primary care 

physician for blood pressure recheck and initiation or adjustment of antihypertensive 

therapy if blood pressure remains elevated. If therapy is used, oral agents are 

appropriate. Clonidine, 0.2 mg by mouth followed by 0.1 mg every hour until the blood 

pressure is adequately controlled; captopril, 12.5-25 mg by mouth; or sublingual or oral 

labetalol, 200-400 mg, may be used. 

2. Hypertensive emergency—Treatment involves rapid but controlled reduction in 

blood pressure using intravenous medications. The goal is to reduce the mean blood 

pressure by 25% within 1 hour of presentation. If the initial reduction is well tolerated by 

the patient, reduction to normal levels can be achieved over the ensuing 24 hours. 

B. Drugs Used to Treat Hypertensive Emergencies 

Caution: Avoid rapid, severe drops in blood pressure, because watershed cerebral 

infarction can occur. Blood pressure should be lowered gradually to the 160- 180 mm 

Hg range acutely and then lowered further only gradually over a period of days with oral 

therapy. 

1. Nitroprusside—Nitroprusside is a potent vasodilator. Give by continuous intravenous 

infusion at a rate of 2-20 ug/kg/min. This drug lowers blood pressure in seconds; 

stopping the infusion results in rapid return of blood pressure to the previous level. 

Hospitalization in an intensive care unit and intra-arterial pressure monitoring are 

usually required. 

2. Labetalol—Labetalol is a combination a- and ß-blocker useful in hypertensive 

emergency. The dose is 20 mg intravenously over 2 minutes. The dose can be doubled 

every 10 minutes until blood pressure reduction is achieved. The maximum total dose is 

300 mg. 

3. Hydralazine—Hydralazine is a vasodilator used mainly in pregnancy because it also

increases uterine blood flow. The dose is 10-40 mg intravenously every 15-30 minutes. 

If a continuous infusion is required, the dose is 1.5-5.0 ug/kg/min. 

4. Fenoldopam—Fenoldopam is particularly useful in patients with renal insufficiency or 

failure as an alternative to nitroprusside, which has been associated with cyanide 

toxicity. The initial dose is 0.1-1.6 ug/kg/min. 

5. Enalaprilat—Enalaprilat is an intravenous angiotensin-converting enzyme inhibitor. It 

is useful in congestive heart failure or for stroke patients as an alternative to 

nitroprusside. The dose is 1.25-5.0 mg per dose over 5 minutes every 6 hours. 

Disposition 

Patients with hypertensive crisis require immediate hospitalization. Patients with 

hypertensive urgency should be referred to a primary care physician within 12-24 hours. 

Evidence-based recommendations do not exist for the optimal timing and degree of 

blood pressure control in hypertensive urgency patients. 

Bisognomo JD: Malignant hypertension. Emedicine; 

www.emedicine.com/med/topic1107.html 

Cherney D, Straus S: Management of patients with hypertensive urgencies and 

emergencies. J Gen Intern Med 2002;17:937. [PMID: 12472930] 

Vidt DG: Emergency room management of hypertensive urgencies and emergencies. J 

Clin Hypertens 2001;17:158. [PMID: 11416701] 

PERICARDITIS, PERICARDIAL EFFUSION, & CARDIAC 

TAMPONADE 

PERICARDITIS & PERICARDIAL EFFUSION 


Acute pericarditis may result from viral or bacterial infections (including tuberculosis), 

collage vascular diseases (especially rheumatic fever and disseminated lupus 

erythematosus), uremia, penetrating and nonpenetrating trauma, or myocardial 

infarction, and it may develop after pericardiotomy or irradiation of the mediastinum. It 

also may be associated with neoplasm (especially lymphomas such as Hodgkin 

disease). Pericarditis may also develop from annular or myocardial abscesses due to 

infective endocarditis. Pericardial effusion, and even cardiac tamponade, may develop 

in patients with acquired immunodeficiency syndrome (AIDS). Occasionally, drugs such 

as hydralazine or procainamide can cause an immune-response pericarditis. Varying 

degrees of myocarditis usually accompany pericarditis and account for the 

electrocardiographic changes. It is important to make an accurate etiologic diagnosis of 

pericarditis, if possible, because the specific cause may dictate the type of treatment 

required.



Fever and symptoms of the underlying disease may be present. Acute pericarditis 

usually causes persistent anterior chest pain that is frequently made worse by lying 

down and made better by sitting up and leaning forward. A pleuritic component is 

common. Radiation of pain to the neck, left shoulder, or arm occurs frequently. 

1. Pericardial friction rub—The most common and most important diagnostic finding is 

pericardial friction rub with 2 or 3 components. The rub is frequently accentuated by 

having the patient breathe deeply or lean forward on hands and knees. A pericardial rub 

is absent in some cases, however. 

2. Pleural friction rub—A pleural friction rub may be present as well. 

3. Pericardial effusion—Pericardial effusion is rarely revealed on physical examination 

and is usually suspected on chest x-ray and confirmed by echocardiogram. With large 

effusions, heart sounds may be diminished, and pulmonary consolidation, rales at the 

base of the left lung, and dullness to percussion below the left scapula (Ewart's sign) 

may be present. Pericardial rub may lessen or disappear as pericardial effusion 

develops or may persist in the face of a large effusion. A rapidly accumulating effusion 

may cause cardiac tamponade (see below). 

B. X-ray and Other Findings 

1. Electrocardiogram—The ECG is usually abnormal in pericarditis, but the most 

common findings are nonspecific ST and T wave abnormalities. Initially, changes 

relatively specific for pericarditis are ST segment elevation in many leads (usually I, II, 

aVF, and V2-V6), with preservation of the normal concavity of the ST segment. Return 

of ST segments to the baseline on the ECG in a few days is followed by symmetric T 

wave inversion. Occasionally, the J junction elevation of ST segments seen as a normal 

variant may be confused with the electrocardiographic changes of pericarditis; however, 

in the normal variant, these changes do not evolve further. In pericarditis, moreover, the 

ST segment elevation is usually 25% or more of the T wave height in leads V5 or V6. 

Depression of the PR segment is highly indicative of pericarditis. 

2. X-rays—No chest x-ray changes are specific for pericarditis. In some patients, 

hypoventilation resulting from pleuritic pain may be sufficiently severe to cause 

atelectasis. The chest x-ray is also an insensitive indicator of pericardial effusion, 

especially in the case of rapidly developing effusions that only minimally distend the 

pericardial sac. An enlarged cardiac silhouette with a "water-flask" contour may be seen 

in the case of large effusions that have developed gradually. At times, the presence of 

pericardial fluid may be suspected if a radiolucent line representing epicardial fat is seen 

on the lateral chest x-ray well inside the cardiac silhouette and separated from the 

sternum by pericardial fluid. 

3. Echocardiography—Echocardiography is the most sensitive and specific 

noninvasive test for pericardial fluid and should be performed in all cases of suspected 

pericardial effusion or pericarditis.

Treatment 

Begin electrocardiographic monitoring. Monitor blood pressure every 5-15 minutes. In 

patients with hemodynamic instability, insert a central venous pressure catheter 

(Chapter 6), and monitor central venous pressure to detect signs of possible cardiac 

tamponade (Table 34-2). 

Draw blood for CBC, serum electrolyte measurements, and renal function tests. Relieve 

pain with morphine, 2-4 mg intravenously every 5-10 minutes, until pain is relieved; 

repeat as needed. 

Obtain an echocardiogram as soon as possible to look for signs of pericardial effusion. 

Consider consultation with a cardiologist. 

Consider pericardiocentesis (Chapter 6) to aid in etiologic diagnosis, especially if signs 

of infection (eg, fever) are present, suggesting pyogenic pericarditis or possible 

malignant pericarditis. If indicated, pericardiocentesis should be performed in an 

intensive care unit, cardiac catheterization lab with fluoroscopic guidance, or in the 

operating room. Pericardiocentesis in the emergency department should be done only 

to relieve decompensated cardiac tamponade and not to assist in etiologic diagnosis. 

Disposition 

Hospitalize most patients with acute pericarditis (with or without effusion), preferably in 

an intensive care or monitored intermediate care unit. Young patients with pericarditis 

who have had symptoms of several days' duration, who are hemodynamically stable 

with normal laboratory tests, and who are reliable often can be discharged with close 

follow-up in 1-3 days. 

CARDIAC TAMPONADE 


Accumulation of fluid in the pericardial space faster than the pericardium can 

accommodate it by distention results in compression of the heart, or cardiac tamponade. 

Pathophysiologic changes similar to tamponade may also result from constrictive 

pericarditis, although they are much more slowly progressive than tamponade resulting 

from rapidly accumulating pericardial fluid. The principal result of the cardiac tamponade 

is reduced diastolic filling of the ventricles, with resulting reduced cardiac output. 

Ultimately, shock and death supervene. 



1. Coexisting or antecedent findings—There may be coexisting or antecedent signs 

or symptoms of pericarditis or pericardial effusion or of the disease process causing 

effusion. However, some patients develop cardiac tamponade without coexisting 

findings.

2. Tachycardia and hypotension—If cardiac tamponade progresses so that central 

venous pressure rises higher than 18 mm Hg, right ventricular filing decreases, causing 

subsequent decreases first in right ventricular and then in left ventricular stroke volume. 

Reflex tachycardia and increased systemic vascular resistance result to support 

systemic blood pressure. As cardiac tamponade worsens, these compensations fail, 

resulting in a sharp drop in cardiac output and blood pressure (decompensated cardiac 

tamponade). Because death follows rapidly if decompensated tamponade is not 

relieved, even slight hypotension or tachycardia occurring in patients with suspected 

pericardial effusion must be carefully monitored. 

3. Pulsus paradoxus—In the normal healthy individual, systolic blood pressure drops 

no more than 8- 10 mm Hg on normal inspiration. This change is exaggerated in cardiac 

tamponade, and palpable pulse volume may also decrease on inspiration. Pulsus 

paradoxus is common in cardiac tamponade resulting from pericardial effusion but is 

less common in tamponade associated with constrictive pericarditis. 

4. Kussmaul's sign—During inspiration in cardiac tamponade there may be an 

increase in estimated central venous pressure (eg, by observation of jugular venous 

pulsation) rather than the normal decrease. 

B. X-ray and Other Findings 

1. Echocardiography—Echocardiography is the most sensitive and specific 

noninvasive test for the presence of pericardial fluid and should be performed as soon 

as possible in all patients with suspected cardiac tamponade. With cardiac tamponade, 

there is marked swinging of the heart and collapse of the right atrial and ventricular 

chamber on expiration. In addition, diastolic collapse of the right ventricle is diagnostic 

of pericardial tamponade. 

2. X-rays—Findings on chest x-ray usually are not helpful in the diagnosis of cardiac 

tamponade. A sudden marked increase in apparent heart size should suggest the 

possibility of pericardial effusion. 

3. Electrocardiogram—In cardiac tamponade, the ECG may show electrical alternates 

either of the QRS complex alone or of the entire complex (P, QRS, and T waves). This 

finding is rare in pericardial effusion without tamponade. 

C. Classification of Cardiac Tamponade 

The severity of cardiac tamponade may be classified as set forth in Table 34-2. 

Treatment 

A. Decompensated Cardiac Tamponade 

Note: Decompensated cardiac tamponade is an immediate threat to life and requires 

emergent treatment. 

1. Oxygenation and blood pressure support—Give oxygen, 5-10 L/min, by mask or 

nasal cannula. Insert a large-bore (= 16-gauge) peripheral intravenous catheter, and 

infuse crystalloid solution to support blood pressure. In an adult, give 300-500 mL in

10-20 minutes, and then continue the infusion based on the blood pressure response. 

2. Dopamine—Give dopamine, 2-20 ug/kg/min intravenously. Adjust dosage based on 

the blood pressure. 

3. Pericardiocentesis—If available, emergent echocardiography or emergent bedside 

sonography in the emergency department can be diagnostic. In addition, 

pericardiocentesis can be performed under ultrasound guidance (Chapter 6). If 

ultrasound is not available and the patient is in extremis, blind pericardiocentesis can be 

life saving. 

B. Compensated Cardiac Tamponade 

Give oxygen, as described above. Monitor blood pressure every 5-15 minutes. Start 

continuous electrocardiographic monitoring. Insert a central venous pressure catheter, 

and monitor central venous pressure. 

Insert a large-bore (= 16-gauge) peripheral intravenous catheter, and keep it patent with 

crystalloid solution. Confirm the presence of pericardial fluid or (rarely) pericardial 

thickening by bedside emergency ultrasound or echocardiography within 1 hour. 

Caution: Do not administer diuretics or preload reduction (eg, nitrates) to control 

venous plethora (hypotension will result). Treatment of the pericardial tamponade is 

recommended before administering any general anesthetic. Anesthesia will cause 

withdrawal of sympathetic support to the heart and venous bed and will result in severe 

hypotension. 

Disposition 

Hospitalize all patients with suspected or documented cardiac tamponade, preferably in 

an intensive care unit, and obtain urgent cardiologic and cardiothoracic surgical 

consultation. 

Bogolioubov A et al: Circulatory shock. Crit Care Clin 2001;17: 697. [PMID: 11525054] 

Goyle KK, Walling AD: Diagnosing pericarditis. Am Fam Physician 2002;66:1695. 

[PMID: 12449268] 

Soler-Soler J et al: Management of pericardial effusion. Heart 2001; 86(2):235. [PMID: 

11454853] 

MYOCARDITIS & CARDIOMYOPATHY 

Many diseases affecting the myocardial muscle have heart failure as their ultimate 

outcome. Secondary cardiomyopathies may be classified as shown in Table 34-3. 

In most patients, the cause is unknown. The most common cause of acute myocardial 

injury and heart failure is coronary artery disease with ischemia or infarction, and this 

diagnostic possibility must be considered in every patient who has sudden onset of 

congestive heart failure. Infectious causes of myocarditis include viruses (mainly

enteroviruses, especially coxsackievirus B), bacteria, protozoa (Trypanosoma cruzi and 

Borrelia burgdorferi), and parasites (Trichinella). 


Symptoms and signs may mimic those of almost any form of heart disease. Chest pain 

is common. Mild myocarditis or cardiomyopathy is frequently asymptomatic; severe 

cases are associated with heart failure, arrhythmias, and systemic embolization. 

Manifestations of the underlying disease (eg, Chagas disease) may be prominent. Most 

patients with biopsy-proven myocarditis report a recent viral prodrome preceding 

cardiovascular symptoms. 

Electrocardiographic abnormalities are often present, although the changes are 

frequently nonspecific. A pattern characteristic of left ventricular hypertrophy may be 

present. Flat or inverted T waves are most common, often with low-voltage QRS 

complexes. Intraventricular conduction defects and bundle branch block, especially left 

bundle branch block, are also common. An echocardiogram is useful to detect wall 

motion abnormalities or a pericardial effusion. Chest radiographs can be normal or show 

evidence of congestive heart failure with pulmonary edema or cardiomegaly. 

In acute myocarditis, cardiac enzymes (CK-MB, cTni, or cTnt) may be elevated. 

Endomyocardial biopsy is diagnostic. 

Treatment 

Bed rest is widely recommended, and there is some evidence supporting its benefits. If 

the cause of the disease is known (eg, trichinosis, acute rheumatic fever), begin therapy 

recommended for the underlying disease. Complications of myocarditis include chest 

pain, arrhythmias, embolization, and heart failure; these should be treated appropriately. 

Disposition 

Hospitalization is indicated unless the condition is chronic and stable. 

Pawsat DE, Lee JY: Inflammatory disorders of the heart: pericarditis, myocarditis and 

endocarditis. Emerg Med Clin North Am 1998;16:665. [PMID: 9739781] 

AORTIC ANEURYSMS & DISSECTIONS 


CONGENITAL HEART DISEASE 

The differential diagnosis of congenital heart disease is beyond the scope of this book. 

The general principles of management are outlined below as a guide for emergency 

physicians. 

Classification

Classification of congenital heart disease is based on the hemodynamic effects 

produced or on specific anatomic abnormalities: 

• Left-to-right shunts: interatrial septal defect, interventricular septal defect, patent 

ductus arteriosus 

• Right-to-left shunts: cyanotic heart disease (eg, transposition of the great vessels, 

tetralogy of Fallot, pulmonary atresia, tricuspid atresia) 

• Valvular stenosis, hypoplasia, and atresia: pulmonary valve and aortic valve stenosis, 

tricuspid atresia, pulmonary atresia, mitral and aortic atresia 

• Abnormalities of position: dextrocardia, transposition of the great vessels, corrected 

transposition 

• Abnormalities of great vessels: coarctation of the aorta, patent ductus arteriosus, 

arterial rings 

Obviously, individual lesions may combine attributes from 2 or more categories. For 

example, tricuspid atresia is both a right-to-left shunt (owing to interatrial 

communication) and an atretic lesion. 

Pathophysiology 

Large left-to-right shunts cause increased blood flow through the lungs and volume 

overload of one or both ventricles. Right-to-left shunts cause systemic venous return to 

bypass the lungs and go directly into the arterial circulation. The resulting arterial 

desaturation (if severe) may cause cyanosis. 

Valvular obstruction (aortic or pulmonary stenosis) and aortic obstruction (coarctation of 

the aorta) cause afterload abnormalities of the involved ventricles. Vascular rings 

around the trachea and esophagus cause symptoms resulting from obstruction (eg, 

dyspnea, cough, dysphagia). 

CYANOSIS 

All infants (under age 1 year) who have cyanotic heart disease are at risk for potential 

serious illness with sudden life-threatening complications. Lesions producing right-to-left 

shunts are frequently undetected until after the newborn period, because pulmonary 

blood flow is maintained by a patent ductus arteriosus. When the ductus arteriosus 

begins to close, cyanosis becomes manifest. If the ductus arteriosus is the major source 

of pulmonary blood flow—as may be the case in pulmonary atresia—the patient may 

become markedly cyanotic and die rapidly after the ductus arteriosus closes. 

No matter how well these children do or how asymptomatic they appear, their entire 

ability to oxygenate blood may depend on the presence of a patent ductus arteriosus, 

which may close unpredictably at any time. 

Clinical Findings

Cyanosis is most apparent in highly vascularized areas with superficial capillaries, for 

example, lips, oral and conjunctival mucosa, and nail beds. With more severe 

hypoxemia and desaturation, other areas of skin may appear cyanotic. The diagnosis 

may be confirmed by arterial blood PO 2 measurements. 


All infants with cyanosis (intermittent or constant) should be hospitalized for immediate 

evaluation by a pediatric cardiologist, because emergency catheterization and 

angiocardiography may be necessary. Frequently, definitive diagnosis can be made by 

2-dimensional echocardiography, with and without Doppler ultrasound. 

Older children with stable cyanotic heart disease do not require emergency 

hospitalization but should be referred for evaluation. If other signs of cardiac disease are 

present (eg, heart failure, arrhythmias), hospitalization or treatment is indicated as 

appropriate. 

ANOXIC SPELLS 


Anoxic spells are common in patients with cyanotic heart disease and usually start after 

the infant is aged 3 months or older. They rarely occur after age 4-5 years. The spells 

frequently start with the infant becoming fussy and developing increasing cyanosis and 

tachypnea. The infant then suddenly goes limp. These spells often occur in the morning 

after a good night's rest or when the child becomes more active, usually during feeding 

or straining at stool, and they are associated with sudden marked increases in 

right-to-left shunting. 

Treatment 

Place the child in the knee-chest position, and quickly give morphine, 0.2 mg/kg 

intramuscularly or subcutaneously. Give 100% oxygen by face mask, and be prepared 

to perform immediate intubation. If pH is 7.1 or lower, give sodium bicarbonate, 1-2 

mEq/kg, intravenously to correct acidosis. If hypoglycemia is present or suspected, give 

10% glucose solution intravenously at a rate of 5-10 mL/kg/h, and monitor blood 

glucose concentration. 

In children with anoxic spells and tetralogy of Fallot, propranolol, 0.01 mg/kg slowly 

intravenously, has been helpful. The dose may be repeated in 5 minutes. 

Disposition 

An unexplained episode of syncope, "lip spell," or convulsions in any child with known 

cyanotic heart disease should suggest anoxic spells. The child should be hospitalized 

immediately. 

HEART FAILURE

Congestive heart failure in infancy is usually associated with large left-to-right shunts at 

the ventricular level (eg, ventricular septal defect) or arterial level (eg, patent ductus 

arteriosus). It may also be associated with obstructive lesions such as aortic stenosis, 

aortic or mitral atresia, and coarctation of the aorta. Rarely, the cause can be 

anomalous origin of the left coronary artery from the pulmonary artery. Congestive heart 

failure may occur in the infant with atrial tachycardia or atrial flutter with rapid ventricular 

response, with or without preexcitation syndromes. Underlying heart disease need not 

be present. 

BR>Clinical Findings 

Congestive heart failure in infants is manifested by dyspnea on exertion just as it is in 

adults. Because the most common strenuous activity in which an infant engages is 

feeding, an infant with congestive heart failure will have to stop and breathe at the end 

of each swallow. Difficulty in taking the entire bottle in the usual 15-20 minutes may 

therefore be the principal manifestation of heart failure. In addition, the baby may be 

sluggish and fussy and have a weak cry. 

Physical findings in these infants are those of the underlying lesion as well as those 

associated with congestive heart failure. 

A. Aortic Murmurs 

In aortic murmurs (eg, pulmonary stenosis and coarctation of the aorta), systolic ejection 

murmurs are heard. They are frequently accompanied by ejection clicks. Patent ductus 

arteriosus or aortopulmonary windows are associated with continuous murmurs heard at 

the base of the heart. If stenosis is severe or if cardiac output is severely decreased, the 

murmur may not be loud. 

B. Tachypnea and Tachycardia 

Tachypnea and tachycardia are usually present. 

C. Sweating 

Because of the increased activity of the sympathetic nervous system in children with 

congestive heart failure, profuse sweating is common. 

D. Biventricular Failure 

Isolated left heart failure is unusual in infants. Biventricular failure with ventricular 

gallops, rales, hepatomegaly, and edema is more common. 

E. Venous Distention 

Because of the short neck in infants, venous distention frequently cannot be detected. 

F. Hepatomegaly 

Hepatomegaly may develop within a few hours after the onset of congestive heart 

failure and may resolve just as quickly with therapy. 

Disposition 

A. Immediate Hospitalization

Any infant or child with newly diagnosed congestive heart failure—especially if it is 

associated with a systolic ejection murmur—must be hospitalized for immediate 

evaluation. The murmur may be due to aortic stenosis, pulmonary stenosis, or 

coarctation of the aorta, each of which requires prompt diagnosis and treatment. 

B. Outpatient Care 

Children with mild congestive heart failure due to stable, previously diagnosed 

congenital heart disease may be managed on an outpatient basis. Diuretics and digitalis 

(in older infants and children) are frequently effective. 

PULMONARY HYPERTENSION 

The child with a large ventricular septal defect or patent ductus arteriosus can develop 

significant irreversible changes in the pulmonary vascular bed within 2 years and must 

therefore be evaluated as soon as the problem is discovered. 

Linear growth and weight gain may be slow. After age 2 years, compensatory 

mechanisms that decrease the size of the left-to-right shunt are frequent: for example, 

increased pulmonary vascular resistance, decreased pulmonary blood flow because of 

decreasing size of the ventricular septal defect, or development of infundibular 

pulmonary stenosis because of hypertrophy of the crista supraventricularis. 

Prompt referral to a pediatric cardiologist is indicated if previously undiagnosed 

ventricular septal defect or patent ductus arteriosus is detected. 

COARCTATION OF THE AORTA 

The diagnosis of coarctation of the aorta is made by finding femoral pulses that are 

decreased or absent when compared to brachial pulses. If femoral pulses are present 

but faint, blood pressure taken with a cuff of the appropriate size in the upper and lower 

extremities should show lower blood pressure in the legs than in the arm if coarctation 

of the aorta exists. Prompt referral to a cardiologist is indicated. 

Grifka RG: Cyanotic congenital heart disease with increased pulmonary blood flow. 

Pediatr Clin North Am 1999;46:405. [PMID: 10218083] 

Nouri S: Congenital heart defects: cyanotic and acyanotic. Pediatr Ann 1997;26:92. 

[PMID: 9121846] 

Waldman JD, Wernly JA: Cyanotic congenital heart disease with decreased pulmonary 

blood flow in children. Pediatr Clin North Am 1999;46:385. [PMID: 10218082] 




34. Cardiac Emergencies 21 - Roger L. Humphries, MD, & C. Keith Stone, MD

Immediate Management

Table 34-1. Differential diagnosis by hemodynamics of heart failure and hypotension after myocardial 

infarction. 

Central 

Venous 

Pressure 

Stroke 

Volume 

Index Treatment 

? or ? ? or ? Diuretics; preload and afterload 

reduction 

? or ? ? Saline volume loading 

? ? or ? Ventilation/perfusion scan; saline o 

dextran; volume loading; no diureti 

? or ? ? Inotropic agents; diuretics; preload 

afterload reduction if arterial press 

can be maintained; counterpulsatio

Table 34-2. Classification of cardiac tamponade. 

Blood Pressure 

Pulsus 

Paradoxus 1 

Normal Present (> 10 mm 

Hg) 

Normal 

hemodynamics 

(ie, pericardial 

effusion without 

cardiac 

tamponade) 

Decompensated 

cardiac 

tamponade 

Normal to increased 

Increased

Table 34-3. Classification of causes of secondary 

cardiomyopathy, with examples. 




34. Cardiac Emergencies 21 - Roger L. Humphries, MD, & C. Keith Stone, MD 

TABLES 

Table 34-3. Classification of causes of secondary cardiomyopathy, with 

examples.


INTRODUCTION 

Patients with cardiac arrhythmias often present to the emergency department. The 

patient's hemodynamic status determines the urgency with which the assessment and 

management should proceed. Patients with serious signs and symptoms (ie, shock, 

hypotension, congestive heart failure [CHF], severe shortness of breath, altered level of 

consciousness, ischemic chest pain, or acute myocardial infarction) require immediate 

treatment. With stable patients, more time is afforded for review of the 12-lead 

electrocardiogram (ECG) and rhythm strip to diagnose the cardiac arrhythmia. Review 

of available medical records, especially a prior ECG, may also assist in arrhythmia 

diagnosis. Examples of commonly encountered arrhythmias are presented in the 

appendix to this chapter. 

TACHYARRHYTHMIAS 

Immediate synchronized direct current (DC) cardioversion should be performed on all 

patients presenting with serious signs and symptoms. In the unstable patient, specific 

arrhythmia diagnosis (supraventricular or ventricular) does not need to be made 

immediately because the initial management is the same. Patients with polymorphic 

ventricular tachycardia (PMVT) of 30 seconds or more and all unstable patients should 

be treated with immediate asynchronous defibrillation. 

In stable patients, the initial medical management will be guided by the underlying 

rhythm and findings of a detailed history and physical examination. In recent years, the 

more traditional approach to categorize patients as either stable or unstable has been 

modified. Hemodynamically stable patients can be further subdivided into those with 

preserved or impaired cardiac function. Findings of impaired cardiac function in a patient 

who is otherwise stable may alter the pharmacologic treatment. 

SUPRAVENTRICULAR ARRHYTHMIAS 

1. Sinus Tachycardia 

Clinical Findings (See Appendix, Figure 35-3.) 

Sinus tachycardia occurs when the sinus rate is faster than 100 beats/min. Usually the 

rate is 101-160 beats/min. Young, healthy adults can accelerate their heart rate up to 

180-200 beats/min, particularly during exercise. Young children have been noted to 

have sinus rates up to 220 beats/min. Sinus tachycardia should not be viewed as a 

primary arrhythmia but more as a response to an underlying illness or condition. It is 

often normal in infancy and early childhood but can occur as a result of a number of 

conditions including pain, fever, stress, other hyperadrenergic states, anemia, 

hypovolemia, hypoxia, myocardial ischemia, pulmonary edema, shock, and 

hyperthyroidism. Certain medications and illicit drugs can also cause tachycardia.


The treatment of sinus tachycardia is directed at the underlying cause. This may include 

correction of dehydration with intravenous fluids, analgesic or antipyretic administration, 

or supplemental oxygen to correct hypoxia. Treatment aimed at correcting the heart rate 

may be harmful if the tachycardia is compensatory and is supporting the cardiac output. 

Gradual slowing of the heart rate during carotid sinus massage may help to differentiate 

sinus tachycardia from other supraventricular arrhythmias. Further management, 

including the need for hospitalization, depends on the underlying condition. 

2. Paroxysmal Supraventricular Tachycardia 

Clinical Findings (See Appendix, Figures 35-6, 35-7, 35-8, 35-9, 35-10 and 35-11.) 

Paroxysmal supraventricular tachycardia (PSVT) is a general term that refers to a 

number of tachyarrhythmias that arise from above the bifurcation of the His bundle. 

Approximately 90% of these arrhythmias occur as a result of a reentrant mechanism; 

the remaining 10% occur as a result of increased automaticity. 

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of 

PSVT, accounting for 50-60% of cases. The heart rate is usually 180-200 beats/min and 

is characterized by sudden onset and sudden termination. Because the reentrant 

mechanism occurs within the AV node itself, virtually simultaneous excitation of the atria 

and ventricles occurs. As a result, the P waves occur concurrent with the QRS 

complexes and are difficult to visualize on the ECG. Often, patients with AVNRT do not 

have underlying heart disease. Common precipitating factors include alcohol, caffeine, 

and sympathomimetic amines. Patients with AVNRT usually present in their third or 

fourth decade of life, and the majority (approximately 70%) are female. 

Atrioventricular reciprocating tachycardia (AVRT) accounts for 30-40% of PSVT. In most 

cases, the impulse travels down the AV node and follows a retrograde path up the 

accessory bypass tract. Because activation of the ventricles occurs through normal 

conduction pathways, the accessory pathway is concealed, and the QRS morphology is 

normal. Consider AVRT if the heart rate is faster than 200 beats/min or if P waves are 

seen following the QRS complex. 

Sinus node reentry and intra-atrial reentry are uncommon causes of PSVT, each 

accounting for approximately 5% of cases. In these arrhythmias, the heart rate is usually 

130-140 beats/min. More often, patients with these arrhythmias have underlying heart 

disease. 

Automatic atrial tachycardia is another uncommon arrhythmia, accounting for less than 

5% of cases of PSVT. The heart rate is usually 160-250 beats/min but may be as slow 

as 140 beats/min. In this case, the underlying mechanism is increased automaticity 

rather than reentry. Automatic atrial tachycardia is commonly associated with underlying 

heart disease. This arrhythmia is difficult to treat and may be refractory to standard 

measures including cardioversion. 

PSVT can be classified as AV nodal dependent or independent. This strategy may

prove useful in formulating treatment options. AVNRT and AVRT are AV nodal 

dependent, meaning that the AV node is involved in the reentrant circuit. For these 

rhythms, pharmacologic management is designed to decrease conduction through the 

AV node. 

Treatment 

A. Unstable Patients 

Patients with PSVT who are hemodynamically unstable require immediate synchronized 

DC cardioversion. Recommendations are to start with low energy levels (50 joules [J]) 

and then to increase the initial dose by 50 J as needed until sinus rhythm is restored. If 

clinical circumstances permit, administer intravenous sedatives. Avoid the common 

error of delaying emergent cardioversion to perform other patient care activities. 

If immediate cardioversion is unavailable, physical maneuvers that cause vagal 

stimulation can be attempted. If unsuccessful, a trial dose of adenosine or a 

calcium-channel blocker may be administered. Note that calcium-channel blockers are 

contraindicated in patients with hypotension or severe CHF. 

B. Stable Patients 

Tachycardia associated with PSVT is usually well tolerated unless the patient has 

underlying heart disease or left ventricular dysfunction. 

1. Physical maneuvers—In stable patients, physical maneuvers causing vagal 

stimulation can be attempted prior to medication administration. Maneuvers that 

stimulate the vagus nerve such as the Valsalva maneuver (expiration against a closed 

glottis), Mueller maneuver (deep inspiration against a closed glottis), cold water facial 

immersion, gagging, and carotid sinus massage are at times effective in terminating 

PSVT that results from AV nodal and sinoatrial (SA) nodal dependent mechanisms. 

Eyeball pressure may also cause vagal stimulation but is not recommended because of 

the possibility of ocular injury. Perform carotid sinus massage only after auscultation for 

carotid bruits. 

2. Pharmacologic treatment—If vagal stimulation is ineffective, adenosine is 

considered first-line medical therapy for conversion of PSVT. In general, pharmacologic 

agents with AV nodal blocking properties such as adenosine, ß-blockers, 

calcium-channel blockers, and digoxin are used for the acute management and 

prevention of AV nodal dependent PSVT. Other antiarrhythmic agents, such as 

procainamide and amiodarone, that exert effects at various levels of the cardiac 

conduction system are used for the management and prevention of AV nodal 

independent PSVT. Antiarrhythmic medications may be considered for conversion of 

PSVT when AV nodal blocking agents are unsuccessful. 

a. Adenosine—Adenosine is an endogenous nucleoside that slows conduction through 

the AV node and is successful in terminating more than 90% of PSVTs resulting from 

AV nodal reentry mechanisms (AVNRT and AVRT). Adenosine may also be effective in 

terminating sinus node reentry tachycardia but is usually ineffective in terminating 

automatic atrial tachycardia. Often adenosine will cause a transient AV block, briefly 

exposing the underlying atrial activity. Administration of a medication with more

prolonged effect on the AV node (ß-blockers or calcium-channel blockers) may provide 

a more sustained reduction in ventricular rate. 

Administer adenosine rapidly, and follow each dose immediately with a 20-cc saline 

flush. Administer an initial intravenous dose of 6 mg over 1-3 seconds. If this does not 

terminate the PSVT, a 12-mg dose can be administered in 2 minutes. The 12-mg dose 

can be repeated one additional time if necessary. Common side effects include facial 

flushing, hyperventilation, dyspnea, and chest pain. These side effects are often 

transient owing to the short half-life of adenosine (less than 5 seconds). The effects of 

adenosine are antagonized by caffeine and theophylline and potentiated by 

dipyridamole and carbamazepine. Heart transplant patients may be overly sensitive to 

the effects of adenosine; if necessary, use smaller doses. Because adenosine can 

provoke bronchospasm, use caution if it is being administered to patients with a history 

of reactive airway disease. 

Adenosine can also be administered to a stable patient with a wide QRS complex 

tachycardia suspected to be supraventricular in origin. Adenosine is preferred over 

calcium-channel blockers in patients with hypotension or impaired cardiac function and 

in patients concomitantly receiving ß-adrenergic blocking agents. 

b. ß-Adrenergic Blocking Agents—ß-Blockers such as propanolol or esmolol slow SA 

node impulse formation and slow conduction through the AV node. These medications 

should be used with caution in patients with a history of reactive airway disease and 

CHF. 

c. Propanolol—Propranolol is a nonselective ß-adrenergic blocking agent. As an 

alternative to calcium-channel blockers, propranolol is administered intravenously at a 

dose of 1-3 mg over 1-3 minutes. If necessary, an additional dose can be administered 

in 2 minutes to a total dose of 0.1 mg/kg. Esmolol is an ultra-short-acting ß 1 -selective 

ß-blocker that has the advantage of a brief half-life (~10 minutes) and a rapid onset of 

action. Administer a loading dose of 0.5 mg/kg over 1 minute. This is followed by a 

maintenance infusion of 50 ug/kg/min. If the response is inadequate, another dose of 

0.5 mg/kg can be administered after 4 minutes and the maintenance infusion increased 

to 100 ug/kg/min. When heart rate control is achieved, reduce the maintenance infusion 

to 25 ug/kg/min. 

d. Calcium-channel blockers—Calcium-channel blockers such as diltiazem or 

verapamil are effective in converting PSVT to sinus rhythm. The efficacy of diltiazem 

and verapamil in terms of conversion rates, rapidity of response, and safety profile 

appear similar. These medications decrease SA and AV node conduction and cause 

prolongation of the AV node refractory period. Calcium-channel blockers also decrease 

myocardial contractility and peripheral vascular resistance. Use calcium-channel 

blockers with caution in patients with left ventricular dysfunction or CHF. Avoid these 

medications in patients with wide complex tachycardia of unknown origin, ventricular 

tachycardia, or tachycardia with ventricular preexcitation. Hypotension is the most 

concerning side effect of intravenous administration and occurs in 10-15% of patients. 

Pretreatment with intravenous calcium has been recommended for patients with 

borderline hypotension as pretreatment to prevent further decline in the blood pressure 

after administration of intravenous calcium-channel blockers.

(1) Verapamil—The initial dose of verapamil is 5-10 mg administered intravenously over 

1-2 minutes. Additional doses of 5-10 mg can be administered every 15 minutes as 

needed until the desired effect is achieved or a total of 30 mg has been administered. 

(2) Diltiazem—The initial dose of diltiazem is 0.25 mg/kg administered intravenously 

over 2 minutes (20 mg for the average adult). If necessary, a dose of 0.35 mg/kg can be 

administered in 15 minutes. After conversion, a maintenance infusion can be started at 

5-10 mg/h and can be increased to a maximum of 15 mg/h if needed. The 

hemodynamic effects of diltiazem are often less pronounced than those of verapamil. 

e. Digoxin—Digoxin administration will increase vagal tone while reducing sympathetic 

activity. As a result, conduction through the AV node is slowed. Digoxin may be 

administered as an intravenous bolus dose of 0.5 mg. Additional doses of 0.25 mg may 

be given as needed every 2-4 hours, with a total dose not to exceed 1.25 mg in 24 

hours. The immediate benefit of digoxin is lessened by its slow onset of action. When 

used in combination, digoxin may allow for lower doses of subsequently administered 

antiarrhythmic agents. Avoid digoxin in patients with atrial fibrillation with ventricular 

preexcitation. 

f. Amiodarone—Amiodarone is a class III antiarrhythmic agent with sodium- and 

potassium-channel blocking properties and ß-blocking and calcium-channel blocking 

properties. By virtue of its ß-blocking and calcium-channel blocking properties, 

amiodarone slows conduction through the AV node. In patients with impaired cardiac 

function or CHF, treatment options narrow. Amiodarone has a solid safety profile and 

may be an effective alternative agent in this situation. Amiodarone can be administered 

as a slow intravenous infusion of 150 mg over 10 minutes. This is followed by a 

maintenance infusion of 1 mg/min for 6 hours and then 0.5 mg/min. Additional bolus 

doses of 150 mg can be repeated as needed for resistant or recurrent PSVT up to a 

total daily dose of 2 g. 

g. Procainamide—Procainamide is a class IA antiarrhythmic agent with 

sodium-channel blocking properties. Procainamide will slow conduction through both the 

AV node and, if present, an accessory bypass tract. Procainamide can be considered 

for patients with PSVT refractory to AV nodal blocking agents. The recommended 

loading dose of procainamide is 17 mg/kg administered as a slow intravenous infusion 

at a rate of 20-30 mg/min (1 g for an average adult). Stop the initial infusion if the 

arrhythmia is suppressed, hypotension develops, or the QRS complex widens by more 

than 50% of its original duration. After arrhythmia suppression, start a maintenance 

infusion at 1-4 mg/min. 

Disposition 

Hospitalization is recommended for patients in PSVT with accompanying serious signs 

and symptoms, patients requiring emergent cardioversion, patients in PSVT with 

ventricular preexcitation, and patients with arrhythmias refractory to standard treatment. 

Outpatient follow-up care should be provided for the otherwise healthy patient with a 

transient episode of PSVT converted to sinus rhythm in the emergency department.

3. Atrial Fibrillation 

Clinical Findings (See Appendix, Figures 35-12 & 35-13.) 

In atrial fibrillation (AF), the atrial rate is disorganized and is 400-650 beats/min. AF is 

characterized by an irregularly irregular ventricular rate with the absence of discernible 

P waves. 

AF is the most common sustained cardiac arrhythmia in adults; the incidence is about 

10-20 times that of atrial flutter. It is estimated that AF affects more than 2 million 

persons in the United States; its prevalence increases with age, approaching 10% in 

those over age 80 years. AF can occur in the absence of underlying heart disease or 

may be associated with a number of conditions, including chronic hypertension, valvular 

disease, cardiomyopathy, myocardial ischemia, myocarditis, pericarditis, or congenital 

heart disease. AF may also occur in the presence of other systemic disorders, including 

hyperthyroidism, pulmonary embolism, hypoxia, and excess consumption of alcohol or 

caffeine. 

Patients with nonvalvular AF have approximately a 5% annual incidence of stroke as a 

result of a thromboembolic event. This risk increases 4-fold in patients with mitral 

stenosis and increases dramatically in older patients, approaching 30% in patients aged 

80-89 years. 

Treatment 

Acute management of AF includes ventricular rate control and prevention of 

thromboembolic complications. Additional management considerations include 

restoration and maintenance of sinus rhythm. 


Patients in AF with a rapid ventricular response who are hemodynamically unstable 

require immediate synchronized DC cardioversion. Recommendations are to start with 

100 J and then to increase the dose by 50 J as needed until sinus rhythm is restored. 


In stable patients with a rapid ventricular response, the initial goal is rate control. This 

can usually be achieved with ß-blockers, calcium-channel blockers, or digoxin. 

ß-Blockers may prove most helpful in patients with hyperthyroidism but are relatively 

contraindicated in patients with CHF. Diltiazem and verapamil can often slow the 

ventricular rate and have the added benefit of antianginal effects and blood pressure 

control in hypertensive patients. In more than 90% of patients, a reduction in heart rate 

of at least 20% is noted. Diltiazem appears to be safe for use in patients with mild CHF. 

Digoxin can also help control the ventricular rate in patients with AF and may be useful 

in patients with left ventricular dysfunction. Its slower onset of action as compared to 

other agents makes it less useful for acute rate control. In patients with mild to moderate 

CHF, the administration of amiodarone may prove useful. Intravenous amiodarone can 

also be considered an alternative agent for rate control when the above agents fail. The 

specific medication choice will often be dictated by the urgency of the situation, the 

medication profile, physician preference, and the patient's underlying condition.

1. Anticoagulants—Prophylactic anticoagulation with warfarin has been shown to 

significantly reduce the incidence of stroke in patients with AF. If new-onset AF is of 

undetermined duration or greater than 48 hours' duration, initiation of anticoagulation is 

necessary. Current recommendations include anticoagulation for 3 weeks, followed by 

elective cardioversion and then continued outpatient anticoagulation for 4 more weeks. 

An alternative strategy is initial anticoagulation with unfractionated or 

low-molecular-weight heparin followed by transesophageal echocardiography to 

evaluate the left atrial appendage for the presence of clot. If no clot is identified, the 

patient may safely undergo cardioversion, followed by anticoagulation for 4 weeks. If a 

left atrial appendage clot is identified by transesophageal echocardiography, 

recommendations include anticoagulation for 3 weeks, followed by cardioversion and 

then continued anticoagulation for 4 additional weeks. In patients with AF of less than 

48 hours' duration, anticoagulation is not recommended. 

2. Antiarrhythmics—Various antiarrhythmic agents including amiodarone, 

procainamide, quinidine (class Ia), sotolol (class III), and ibutilide (class III) are used to 

chemically convert AF. Pharmacologic or electrical cardioversion may be considered in 

selected stable emergency department patients with AF of less than 48 hours' duration. 

Postponing cardioversion could lead to an increased resistance to attempts at 

conversion. 

Disposition 

Patients with chronic rate-controlled AF do not require hospital admission. In patients 

with new-onset AF, hospitalization is often required for ventricular rate control, initiation 

of anticoagulation, and sometimes for initiation of antiarrhythmic therapy. If a patient 

presents with thromboembolic complications, hospital admission will also be necessary. 

4. Atrial Flutter 


In atrial flutter, the atrial rate is usually 250-350 beats/min. At times, the characteristic 

sawtooth flutter waves may be seen on ECG, particularly in lead II. Typically, atrial 

flutter will present with 2:1 atrioventricular (AV) conduction. For this reason, it is 

important to consider atrial flutter in the differential diagnosis of a regular tachycardia at 

approximately 150 beats/min even in the absence of flutter waves. Atrial flutter occurs 

less commonly than AF but is more often associated with underlying heart disease. 

If atrial flutter is suspected in a patient with a nondiagnostic ECG, several options are 

available to better identify atrial activity. Vagal maneuvers or administration of an AV 

nodal blocking agent may briefly slow conduction through the AV node and unmask the 

flutter waves. At times, obtaining Lewis leads may also aid in uncovering P waves. To 

perform Lewis leads, the left and right arm electrodes are moved from the upper 

extremities to different positions on the anterior chest wall as lead I is monitored for 

evidence of P waves. 

Treatment

Acute management of atrial flutter includes ventricular rate control and prevention of 

thromboembolic complications. Additional management considerations include 

restoration and maintenance of sinus rhythm. 


Patients in atrial flutter with a rapid ventricular response who are hemodynamically 

unstable require immediate synchronized DC cardioversion. Recommendations are to 

start with 50 J and then increase the initial dose by 50 J as needed until sinus rhythm is 

restored. 


In stable patients with a rapid ventricular response, the initial goal is rate control. 

Adequate heart rate control can be achieved with the administration of either ß-blockers 

or calcium-channel blockers. Digoxin is often less effective acutely because of its slow 

onset of action. Amiodarone or diltiazem are alternatives for rate control in the stable 

patient with impaired cardiac function or CHF. 

The stroke risk for patients in atrial flutter appears to be similar to that of AF. Although 

controversial, some authors suggest using the same anticoagulation guidelines for atrial 

flutter as in AF. 

Disposition 

Patients with chronic rate-controlled atrial flutter do not require hospital admission. In 

patients with new-onset atrial flutter, hospitalization is often required for ventricular rate 

control, initiation of anticoagulation, and sometimes for initiation of antiarrhythmic 

therapy. 

5. Multifocal Atrial Tachycardia 


In multifocal atrial tachycardia (MAT) the heart rate is typically 100-130 beats/min. The 

characteristic ECG finding is at least 3 different P wave morphologies. The rhythm often 

appears irregular and can at times be confused with AF. Varying PR intervals may also 

be noted. When the rate is slower than 100 beats/min, the term wandering atrial 

pacemaker is applied. Unless underlying aberrant conduction is present, the QRS 

complexes are narrow. Severe underlying chronic obstructive pulmonary disease 

accounts for approximately 60-85% of cases. Other causes include CHF, hypokalemia, 

hypomagnesemia, pulmonary hypertension, hypoxia, hypercapnia, and methylxanthine 

toxicity. 

Treatment 

The initial treatment of MAT is directed at correcting the underlying cause. As with AF, 

the initial goal of therapy is to achieve heart rate control. Because MAT does not 

respond to electrical cardioversion, pharmacologic intervention may be required.

Metoprolol can be a first-line agent for symptomatic patients who do not have 

contraindications to ß-blockers. Metoprolol is a ß 1 -selective ß-adrenergic blocking agent 

that slows conduction through the AV node. It is administered as a 5-to 10-mg 

intravenous bolus over 3 minutes. If necessary, the dose can be repeated in 10-15 

minutes. Esmolol may be a reasonable alternative because of its short half-life. 

Magnesium may be effective in converting MAT and can be administered as a 2-g 

intravenous bolus over 1 minute. This is followed by a 2 g/h infusion for 5 hours. 

Magnesium can still be effective if serum magnesium levels are in the normal range. 

Potassium repletion may be helpful in patients who are hypokalemic. 

Amiodarone, digoxin, or diltiazem may be considered as alternative agents for rate 

control, especially when the patient exhibits findings of CHF. 

Disposition 

Patients with a new diagnosis of MAT do not necessarily require hospital admission. 

Patients may require hospitalization for MAT if the heart rate is difficult to control or for 

further management of the underlying condition. 

6. Preexcitation Arrhythmias 


Preexcitation refers to ventricular preexcitation that occurs as a result of impulse 

conduction through an accessory AV pathway. The Wolf-Parkinson-White (WPW) 

syndrome is the most common form of ventricular preexcitation. On the ECG, a short 

PR interval (less than 120 ms) and the presence of a d wave (initial upward slurring of 

the QRS complex) signify ventricular preexcitation. The Lown-Ganong-Levine syndrome 

is also considered in the class of preexcitation arrhythmias. This syndrome is 

characterized by a short PR interval, normal QRS morphology, and associated episodes 

of PSVT. 

A variety of arrhythmias may occur in patients with WPW syndrome; the most common 

is orthodromic AVRT. In this case, the cardiac impulse travels down the AV node 

(antegrade conduction) and stimulates the ventricles through the normal conduction 

pathways. The accessory AV bypass tract serves as the retrograde limb of the circuit. In 

the absence of aberrant ventricular conduction or a fixed bundle branch block, the 

morphology of the QRS complex is narrow without evidence of ventricular preexcitation 

(absent d wave). 

Rarely, antidromic AVRT occurs whereby the accessory AV pathway acts as the 

antegrade limb of the circuit and the AV node as the retrograde limb. Antidromic AVRT 

will produce a wide QRS complex tachycardia and may masquerade as ventricular 

tachycardia (VT). The tachycardia may be extremely rapid, leading to ventricular 

fibrillation (VF) as a result of an R-on-T phenomenon. 

AF is the second most common arrhythmia associated with WPW syndrome. AF with 

ventricular preexcitation has a high potential to precipitate hemodynamic compromise.

AF with a rapid ventricular rate is characterized by an irregular tachycardia and a wide 

QRS complex resulting from ventricular preexcitation. 

Treatment 

Patients with orthodromic AVRT who are hemodynamically unstable require immediate 

synchronized DC cardioversion. Recommendations are to start with 50 J and then to 

increase the initial dose by 50 J as needed until sinus rhythm is restored. In patients 

with known WPW syndrome presenting with a narrow complex regular tachycardia, 

orthodromic AVRT can be assumed. In stable patients, the medical treatment will be the 

same as in AVNRT. Pharmacologic treatment with adenosine, ß-adrenergic blocking 

agents, or calcium-channel blockers can be administered as deemed necessary and 

appropriate for the individual case. In general, the treatment of orthodromic AVRT with 

AV nodal blocking agents is safe. The risk of enhancing antegrade conduction down the 

bypass tract is very low. 

Treatment of AF with ventricular preexcitation is different from that of orthodromic 

AVRT. If the patient is hemodynamically unstable, immediate synchronized DC 

cardioversion starting at 100 J is warranted. The use of AV nodal blocking agents, 

specifically ß-blockers, calcium-channel blockers, and digoxin is contraindicated. If 

conduction through the AV node is slowed, conduction down the accessory pathway 

may be enhanced, possibly degenerating to VF. Because procainamide will slow 

conduction through both the AV node and the accessory pathway, it is the medication of 

choice when AF with a rapid ventricular response is associated with ventricular 

preexcitation. Procainamide is also the medication of choice in antidromic AVRT. 

Amiodarone can be used as an alternative agent in treating AF with ventricular 

preexcitation and findings of CHF. 

Disposition 

Hospitalization is not required for patients who are asymptomatic with evidence of 

ventricular preexcitation on the ECG (sinus rhythm, short PR, and a d wave). 

Hospitalize all patients who have serious signs and symptoms or those requiring 

cardioversion. In addition, hospitalization is recommended for patients with AF and 

ventricular preexcitation or antidromic AVRT. Patients who present with stable 

orthodromic AVRT may be discharged with close outpatient follow-up after 

pharmacologic conversion in the emergency department. 

Applegate TE: Atrial arrhythmias. Prim Care 2000;27:677. [PMID: 10918675] 

(Evaluation and management of atrial arrhythmias.) 

Atkins DL et al: Treatment of tachyarrhythmias. Ann Emerg Med 2001;37:S91. [PMID: 

11290974] (Overview and guidelines for the treatment of tachyarrhythmias.) 

Chauhan VS et al: Supraventricular tachycardia. Med Clin North Am 2001;85:193. 

[PMID: 11233949] (Classification, mechanism, clinical presentation, and therapy of 

supraventricular tachycardia.) 

Li H et al: Evaluation and management of atrial fibrillation in the emergency department.

Emerg Med Clin North Am 1998;16:389. [PMID: 9621849] 

Pelosi F et al: Evaluation and management of atrial fibrillation. Med Clin North Am 

2001;85:225. [PMID: 11233947] 

Trohman RG: Supraventricular tachycardia: implications for the intensivist. Crit Care 

Med 2000;28:129. [PMID: 11055681] (Diagnosis and management of supraventricular 

tachycardia.) 

Xie B et al: Clinical difference of narrow complex QRS tachycardias. Emerg Med Clin 

North Am 1998;16:295. [PMID: 9621846] (Diagnostic approach to narrow complex QRS 

tachycardias.) 

VENTRICULAR ARRHYTHMIAS 

1. Ventricular Tachycardia 


VT is the most common cause of wide QRS complex tachycardia. The term VT is used 

when 6 or more consecutive ventricular beats occur. The ventricular rate is usually 

180-250 beats/min, although rates slower than 160 beats/min may occur. Nonsustained 

VT is characterized by an episode lasting less than 30 seconds. Sustained VT is 

characterized by an episode lasting longer than 30 seconds, associated with 

hemodynamic compromise, or requiring therapeutic intervention for termination. Wide 

complex tachycardia (WCT) refers to a regular tachycardia with a QRS complex greater 

than 0.12 seconds (120 ms) in duration. WCT most often occurs as a result of either VT 

or SVT with aberrant conduction (underlying or rate-dependent bundle branch block). 

Very rarely, WCT will occur as a result of antidromic AVRT. 

In approximately 85% of patients presenting in the emergency department with WCT, 

the underlying arrhythmia is VT. The presence of structural heart disease, coronary 

artery disease, prior myocardial infarction, or CHF strongly suggests VT. Certain ECG 

findings favor VT over SVT with aberrant conduction. These findings include a QRS 

complex wider than 160 ms, the presence of fusion beats, and evidence of AV 

dissociation. AV dissociation occurs in about 50% of patients with VT and confirms the 

diagnosis. An algorithm has been developed to assist clinicians in distinguishing VT 

from SVT with aberrant conduction (Figure 35-1). Proper application of this diagnostic 

tool may help decrease misclassification of WCT. A common clinical error that must be 

avoided is to assume that WCT is SVT with aberrant conduction. All cases of WCT of 

unknown origin should be managed as VT. 

Treatment 


Patients with VT or WCT of unknown origin who are hemodynamically unstable with 

serious signs and symptoms require immediate synchronized DC cardioversion. 

Recommendations are to start with 50-100 J and then increase the initial dose by 50 J 

as needed until sinus rhythm is restored. Some authors advocate for cardioversion as

an alternative to medical management in the patient with stable VT. 


Traditionally, patients with stable VT are administered an antiarrhythmic agent for 

chemical cardioversion. A number of medications are available. The choice for a 

particular patient is often based on physician preference and experience, findings of 

preserved or impaired cardiac function, and the underlying cause of the VT. 

1. Lidocaine—Lidocaine is a class Ib antiarrhythmic with sodium-channel blocking 

properties. Because it can be administered rapidly with few side effects, some authors 

consider it the agent of choice for ventricular arrhythmias associated with acute 

myocardial ischemia or infarction. The recommended intravenous loading dose is 

1.0-1.5 mg/kg. If required, a second bolus dose of 0.75-1.5 mg/kg can be administered 

in 5-10 minutes. If ventricular ectopy persists, an additional bolus dose of 0.5-0.75 

mg/kg can be administered every 5-10 minutes to a maximum dose of 3 mg/kg. After 

rhythm suppression, start a maintenance infusion at 2-4 mg/min. Lidocaine has the 

lowest incidence of toxicity of all currently used antiarrhythmic medications. 

2. Other drugs—Procainamide is an alternative agent to lidocaine for the treatment of 

stable monomorphic VT. Bretylium is a class III antiarrhythmic that recently has become 

unavailable for use in the United States. Amiodarone may be preferable to other 

antiarrhythmic agents for ventricular tachycardia in patients with CHF. In comparison to 

other antiarrhythmic agents, amiodarone has greater efficacy and a lower incidence of 

proarrhythmic side effects. Dosing guidelines for amiodarone and procainamide are 

discussed in the section on PSVT. 

Disposition 

Hospitalization is recommended for all patients who present with VT. 

2. Proarrhythmic Ventricular Arrhythmias 


Proarrhythmia refers to the exacerbation of an existing arrhythmia or the development of 

a new arrhythmia during antiarrhythmic therapy. Most proarrhythmic episodes occur 

shortly after the initiation of antiarrhythmic therapy and can range from ventricular 

ectopy to intractable VT or VF. 

Numerous medications have been implicated in causing ventricular arrhythmias. Digoxin 

toxicity has been associated with VT and carries a 60-65% mortality rate. Type I 

antiarrhythmic agents with sodium-channel blocking activity are associated with a 

5-10% incidence of proarrhythmia. In addition, other medications that have 

sodium-channel blocking properties may be proarrhythmic in toxic doses. These 

medications include diphenhydramine, phenothiazines, propoxyphene, tricyclic 

antidepressants, and cocaine. 

Treatment

Early recognition and discontinuation of the offending agent is an important aspect of 

care. As with other tachyarrhythmias, synchronized DC cardioversion is indicated for 

patients who are hemodynamically unstable. 

Pharmacologic management of ventricular arrhythmias associated with sodium-channel 

blocking agents (ie, tricyclic antidepressants) is undertaken with sodium bicarbonate. 

Three ampules (150 mEq) of sodium bicarbonate can be added to 1 L of 5% dextrose in 

water. The solution can be administered intravenously at a rate of 2 mL/kg/h and titrated 

to a serum pH of 7.5-7.55. If VT occurs secondary to digoxin toxicity, the use of digoxin 

Fab fragments (Digibind) is indicated. Additional therapy may be warranted in specific 

clinical circumstances. 

Disposition 

Although uncommonly encountered in the emergency department, patients with 

proarrhythmic ventricular arrhythmias should be hospitalized for cardiac monitoring. 

3. Polymorphic Ventricular Tachycardia (Including Torsades de Pointes) 


Polymorphic ventricular tachycardia (PMVT) is a form of VT with varying QRS complex 

morphology. The rhythm is often irregular and hemodynamically unstable, and it can 

degenerate to VF. 

Torsades de pointes is a form of PMVT associated with a prolonged QT interval on the 

baseline ECG. The rhythm is often described as having a twisting-on-point appearance 

and can be either paroxysmal or sustained. The heart rate is usually 200-250 beats/min. 

Long QT syndromes associated with torsades de pointes include Lange-Nielsen 

syndrome and Romano-Ward syndrome. Torsades de pointes may also occur as a 

result of numerous medication interactions. A complete list of medications that have 

been reported to prolong the QT interval is available at www.qtdrugs.org. 

PMVT can also occur in the absence of a prolonged QT interval. In this case, cardiac 

ischemia or underlying structural heart disease is often the cause. 


Patients with PMVT who are hemodynamically unstable with serious signs and 

symptoms require immediate defibrillation. Recommendations are to start with 200 J. To 

prevent recurrence, discontinue all agents that can prolong the QT interval. 

Magnesium is the medication of choice for the management of torsades de pointes 

associated with congenital and acquired forms of long QT syndrome. It may be effective 

even when serum levels are normal. A 2-g intravenous dose can be administered as a 

slow push over 5 minutes. Follow the bolus dose by a maintenance infusion of 1-2 g/h. 

Consider supplemental potassium as an adjunctive therapy to maintain serum 

potassium levels in the high normal range. Temporary transvenous pacing at rates 

around 100 beats/min may be useful to prevent recurrences, especially in patients with

adycardia or pauses. 

Hospitalization is recommended for all patients who present with PMVT. 

4. Ventricular Fibrillation 


VF is characterized by an irregular ventricular rhythm with no discernible distinction 

between the QRS complex, ST segment, and T waves. VF is a common cause of 

sudden cardiac death and remains a significant contributor to mortality in the first 24 

hours after an acute myocardial infarction. In the absence of early bystander 

cardiopulmonary resuscitation and initiation of advanced cardiac life support, including 

defibrillation, survival rates are poor. 


Upon recognition of VF or pulseless VT, the immediate treatment is asynchronous 

defibrillation with 200 J. If required, administer a second shock with 200-300 J and a 

third at 360 J. Secure the patient's airway with endotracheal intubation. Pharmacologic 

therapy advocated in the 2000 American Heart Association guidelines includes 

vasopressin or epinephrine for persistent VF or pulseless VT after 3 stacked 

defibrillations. The antiarrhythmics, amiodarone or lidocaine, are used if the arrhythmia 

persists after 3 additional stacked defibrillations. All patients who have been 

successfully resuscitated from VF or pulseless VT should be started on a drip of the last 

antiarrhythmic administered and admitted to the intensive care unit for close 

observation. If an acute coronary syndrome is suspected as the cause of the arrest, the 

patient may require cardiac catheterization for evaluation and treatment. Chapter 7 

offers a more in-depth discussion of the management of cardiac arrest. 

Brady WJ et al: Wide QRS complex tachycardia: ECG differential diagnosis. Am J 

Emerg Med 1999;17:376. [PMID: 10452438] (Case presentations and discussion of 

wide QRS complex tachycardias.) 

Brugada P et al: A new approach to the differential diagnosis of a regular tachycardia 

with a wide QRS complex. Circulation 1991;83:1649. [PMID: 2022022] (An algorithmic 

approach to the diagnosis of ventricular tachycardia.) 

Chaudhry GM: Antiarrhythmic agents and proarrhythmia. Crit Care Med 2000;28:158. 

[PMID: 11055686] (Classes of antiarrhythmic agents and their proarrhythmic side 

effects.) 

Flinders DC et al: Ventricular arrhythmias. Prim Care 2000;27: 709. [PMID: 10918676] 

(Pathophysiology and clinical presentation of ventricular arrhythmias.) 

Gupta AK et al: Wide complex tachycardias. Med Clin North Am 2001;85:245. [PMID: 

11233948] (Differential diagnosis and management of WCTs.) 

Miller MB: Arrhythmias associated with drug toxicity. Emerg Med Clin North Am

1998;16:405. [PMID: 9621850] (Complications and arrhythmias associated with 

medication toxicity.) 

Passman R et al: Polymorphic ventricular tachycardia, long Q-T syndrome, and 

torsades de pointes. Med Clin North Am 2001;85:321. [PMID: 11233951] (Diagnosis 

and management of various forms of PMVT.) 

Shah CP et al: Clinical approach to wide QRS complex tachycardias. Emerg Med Clin 

North Am 1998;16:331. [PMID: 9621847] (Diagnostic approach to wide QRS complex 

tachycardias.) 

BRADYARRHYTHMIAS, CONDUCTION DISTURBANCES, & ESCAPE 

RHYTHMS 

As in tachycardia management, if a bradycardic patient is hemodynamically unstable, 

immediate intervention is required regardless of the origin of the underlying arrhythmia 

(eg, SA block, AV block, ventricular escape rhythm). Transcutaneous cardiac pacing is 

the initial intervention of choice for patients with serious signs and symptoms that occur 

as a result of a bradyarrhythmia. In stable patients, or in patients with mild symptoms 

(eg, dizziness, lightheadedness), pharmacologic treatment is often initiated with or 

without standby pacing. Medical management can be initiated in patients with 

symptomatic bradycardia as a bridge to cardiac pacing, or may be initiated if emergency 

cardiac pacing is unavailable. 

Primary conduction system disturbances account for 15% of bradyarrhythmias 

encountered in the emergency department setting. The remaining 85% occur as a result 

of various secondary causes such as acute coronary ischemia (40%), medications or 

toxicologic causes (20%), metabolic causes (5%), neurologic causes (5%), permanent 

pacemaker failure (2%), and other miscellaneous causes (13%). Symptomatic 

bradycardia resulting from AV conduction disturbances or sick sinus syndrome is more 

common in the elderly; the majority of patients present at age 65 years or older. 

SINUS BRADYCARDIA 


Sinus bradycardia occurs when the sinus rate is slower than 60 beats/min. Usually the 

rate is 45-59 beats/min, but on rare occasion it may be as slow as 35 beats/min. Sinus 

bradycardia is commonly associated with sinus arrhythmia and is often a normal finding 

in young, healthy, athletic individuals. Sinus bradycardia is often benign and does not 

necessarily indicate sinus node dysfunction. Although commonly physiologic, sinus 

bradycardia may be pathologic when patients experience symptoms of cerebral 

hypoperfusion or when the heart rate does not increase appropriately with activity or 

exercise. Certain underlying conditions have been associated with a slowing of the heart 

rate, including hypothermia, hypothyroidism, and increased intracranial pressure. In 

addition, a number of different medications, including ß-blockers, calcium-channel 

blockers, clonidine, digoxin, and lithium, can cause bradycardia. 


Usually no treatment is required for asymptomatic sinus bradycardia. When serious 

signs and symptoms are present, medical management, pacemaker placement, and 

hospital admission are indicated. 

SINUS ARREST 

Sinus arrest is defined as a failure of sinus node impulse formation. On the ECG, 

random periods of absent cardiac activity may be noted. Unless escape beats occur, 

lengthy pauses are noted. When pauses occur, patients may complain of dizziness or 

lightheadedness or may have syncope. If untreated, pauses longer than 2.5 seconds 

may progress to asystole. 

SINOATRIAL BLOCK 

SA block differs from sinus arrest in that SA block is a form of exit block rather than 

failure of impulse formation. Like sinus arrest, SA block may occur as a result of a 

number of conditions, including acute myocardial infarction, myocarditis, fibrosis of the 

SA node, excessive vagal tone, and digoxin toxicity. Analogous to AV block, SA block 

can be classified into first-, second-, and third-degree heart block. 

1. First-Degree Sinoatrial Block 

First-degree SA block does not produce any ECG changes. The diagnosis can be made 

only through electrophysiologic testing. 

2. Second-Degree Sinoatrial Block (Mobitz Type I) (See Appendix, Figure 35-24.) 

Second-degree Mobitz type I SA block, also known as SA Wenckebach, is 

characterized by PP intervals that gradually shorten while the PR interval remains 

constant. This cycle terminates with a blocked P wave. The length of the pause is 

shorter than twice the preceding PP cycle. 

3. Second-Degree Sinoatrial Block (Mobitz Type II) 

Second-degree Mobitz type II SA block is characterized by fixed pauses. On the ECG, 

the PP interval remains constant and is then followed by a blocked P wave. The PP 

interval, including the blocked P wave, will be twice the length of the normal PP interval. 

4. Third-Degree Sinoatrial Block 

Third-degree SA block may be difficult to distinguish from sinus arrest. Patients with 

either conduction disturbance present with variable pauses on the ECG until an escape 

rhythm occurs or sinus rhythm is restored. 

5. Sick Sinus Syndrome 

Clinical Findings

Sick sinus syndrome is a manifestation of sinus node dysfunction. Patients with the 

syndrome may present with a wide range of bradyarrhythmias. Numerous arrhythmias 

are associated with sick sinus syndrome, including marked sinus bradycardia, sinus 

pause, sinus arrest, and SA block. On occasion, patients may also present with 

ventricular or atrial tachyarrhythmias. 


Treatment may be indicated when pauses of more than 2-3 seconds occur or if the 

patient is symptomatic. Administration of atropine or initiation of temporary cardiac 

pacing may be required. Symptomatic patients will require hospital admission, often for 

permanent pacemaker placement. 

ATRIOVENTRICULAR BLOCK 

AV block refers to a group of conduction disturbances within the AV junctional tissue. In 

general, AV block is characterized by prolonged conduction time or a failure to conduct 

impulses through the AV node. The conduction disturbance can be partial (first- or 

second-degree AV block) or complete (third-degree AV block). In general, the 

hemodynamic effects will depend on the ventricular rate and the presence of underlying 

heart disease. AV conduction blocks are traditionally classified as first-, second-, or 

third-degree heart block. 

1. First-Degree Atrioventricular Block (See Appendix, Figure 35-25.) 

First-degree AV block is the most common conduction disturbance and is characterized 

by a PR interval that is prolonged greater than 0.2 seconds. In general, the PR interval 

is constant, and each atrial impulse is conducted to the ventricles. First-degree AV block 

can be a normal variant in young or athletic individuals due to excessive vagal tone. 

First-degree AV block is also common in elderly patients without underlying heart 

disease. It may occur in patients with myocarditis, mild digoxin toxicity, and inferior wall 

myocardial infarction secondary to AV nodal ischemia. 

2. Second-Degree Atrioventricular Block (Mobitz Type I) (See Appendix, Figure 

35-26.) 

Second-degree Mobitz type I AV block is also known as Wenckebach AV block. This 

type of block is characterized by a progressive lengthening of the PR interval followed 

by a nonconducted P wave leading to a dropped QRS complex. Classically, the PP 

interval remains constant except when sinus arrhythmia is present. The RR interval will 

have a characteristic cycle throughout the conduction disturbance. The RR interval that 

includes the blocked P wave is the longest in duration. This is then followed by RR 

intervals that subsequently become shorter until the next P wave is blocked. 

On a rhythm strip, grouped beating is often evident and can further help distinguish 

second-degree from third-degree AV block. The blocked P waves may occur frequently 

or periodically, and may or may not occur with regularity. Because Mobitz type I AV 

block is at the level of the AV node, the QRS complex is normal in configuration unless 

aberrant ventricular conduction or an underlying bundle branch block exists. In general,

Mobitz type I AV block does not usually produce hemodynamically significant 

symptoms. It can be seen in patients with acute myocardial infarction (usually inferior 

wall) and does not commonly progress to complete heart block (CHB). If CHB does 

occur, the escape rhythm pacemaker is usually located in the AV junctional tissue and is 

often fast enough to maintain an adequate cardiac output. 

3. Second-Degree Atrioventricular Block (Mobitz Type II) (See Appendix, Figure 

35-28.) 

Second-degree Mobitz type II AV block is characterized by a constant PR interval, either 

normal or prolonged, that is followed by a nonconducted P wave. In Mobitz type II AV 

block, the QRS complex is usually wide. This occurs because Mobitz type II AV block 

represents an infranodal block. At times, every other P wave is blocked. This is 

described as 2:1 AV conduction. When this occurs, one cannot distinguish between 

Mobitz type I or type II AV block (see Appendix, Figure 35-27). Mobitz type II AV block 

is common in patients with acute myocardial infarction (usually anterior wall) and can 

suddenly progress to CHB resulting in syncope. 

4. Third-Degree Atrioventricular Block (Complete Heart Block) 

Clinical Findings (See Appendix, Figures 35-29, 35-30 and 35-31.) 

Third-degree AV block, or CHB, is characterized by independent atrial and ventricular 

activity. As a result of complete AV block, no atrial impulses are conducted through the 

AV node. The ventricular rate is determined by the intrinsic escape rhythm, AV 

junctional escape (usually 45-60 beats/min), or an idioventricular escape rhythm 

(usually 30-40 beats/min). The atrial rate may be sinus in origin or may be from an 

ectopic atrial focus. In CHB the atrial rate is typically faster than the ventricular rate. As 

noted with second-degree AV block, the hemodynamic consequences depend on the 

ventricular rate and the presence of underlying heart disease. Syncope or CHF 

commonly accompany acute acquired CHB. Complete AV block is most commonly 

caused by coronary artery disease or by degeneration of the cardiac conduction system. 



Emergency cardiac pacing is indicated for patients with hemodynamically unstable 

bradycardia, especially for patients who have failed medical therapy, patients with 

malignant escape rhythms, and patients in bradyasystolic arrest. Transcutaneous 

cardiac pacing is the initial intervention because of its ease of application, compared to 

temporary transvenous pacing. In unstable patients, medical management can be 

initiated, although at times its utility is only temporary. 


1. Atropine—Atropine is an anticholinergic medication with parasympatholytic 

properties leading to enhanced SA node automaticity and AV node conduction. The 

initial intravenous dose of atropine is 0.5- 1.0 mg, which can be repeated every 5 

minutes to a total dose of 0.04 mg/kg (3 mg for the average adult). The maximal dose 

produces complete vagal blockade. Atropine is recommended for, but not limited to,

patients with symptomatic bradycardia or relative bradycardia, bradycardia with 

malignant escape rhythms, and asystole. 

Rarely, a paradoxic reduction in heart rate has been observed in patients with advanced 

AV block after administration of atropine. Therefore, use atropine with caution in 

patients with infranodal AV block (Mobitz type II, and CHB with wide QRS complexes). 

Other rarely encountered side effects of atropine administration include worsening of 

cardiac ischemia in patients with an acute myocardial infarction, or the development of a 

ventricular tachyarrhythmia. These adverse effects are uncommon, but knowledge of 

such responses may assist with proper patient selection. Atropine is not effective in the 

management of the heart transplant patient with symptomatic bradycardia because of 

surgical denervation of the vagus nerve. 

2. Isoproterenol—Isoproterenol is a nonspecific ß-adrenergic agonist that causes an 

increase in heart rate and cardiac contractility. The combined effects lead to increases 

in cardiac output and systolic blood pressure and decreases in systemic and pulmonary 

vascular resistance and diastolic blood pressure. As a result, no significant change in 

mean arterial pressure occurs. Myocardial oxygen demand is increased as a result of 

the increased heart rate and contractility. In addition, isoproterenol causes smooth 

muscle relaxation and bronchodilation. Isoproterenol may be used to treat symptomatic 

bradycardia in heart transplant patients. The initial intravenous dose of isoproterenol is 1 

ug/min, titrated slowly until the desired hemodynamic effects are achieved. The 

maximum infusion rate is 4 ug/min. 

3. Dopamine—Dopamine is an endogenous catecholamine with dose-related effects. At 

doses of 3.0- 7.5 ug/kg/min, it has ß-agonist properties resulting in increased heart rate 

and cardiac output. The ß-agonist effects are less pronounced than those of 

isoproterenol. Dopamine is the preferred catecholamine for symptomatic bradycardia 

refractory to atropine. 

4. Aminophylline—Aminophylline, a methylxanthine derivative, is a competitive 

antagonist of adenosine. Conduction disturbances during an acute myocardial infarction 

may be partially mediated by the endogenous release of adenosine. Aminophylline can 

be administered intravenously at a dose of 5-6 mg/kg infused over 5 minutes. A 

maintenance infusion may be required and can be initiated at 0.5 mg/kg/h. 

5. Glucagon—Glucagon stimulates cyclic adenosine monophosphate production. It 

may be beneficial in the treatment of bradycardia associated with ß-blocker or 

calcium-channel blocker toxicity. An initial intravenous dose of 0.05-0.15 mg/kg is 

recommended, although optimal doses have not been determined. 

Disposition 

Hospitalize all patients who have symptomatic bradycardia. Discontinue medications 

with AV nodal blocking properties. Although some patients with advanced AV 

conduction blocks will be asymptomatic, it is recommended that all patients with newly 

diagnosed second-degree Mobitz type II AV block and CHB be hospitalized. 

Often patients with Wenckebach AV block will be asymptomatic. Treatment is usually

not necessary unless symptoms occur. In general, no treatment is necessary for 

patients with first-degree AV block. At times, hospitalization will be necessary to treat 

the underlying condition such as myocardial ischemia or digoxin toxicity. 

IDIOVENTRICULAR RHYTHM 


Idioventricular rhythm refers to the occurrence of 6 or more consecutive ventricular 

escape beats. The rate of an idioventricular escape rhythm is usually 30-40 beats/min. 

The duration of the QRS complex often exceeds 0.16 seconds. The morphology of the 

QRS complex is similar to that in premature ventricular contractions (PVCs) but varies 

depending on the location of the ectopic ventricular focus. Escape rhythms often 

develop in response to severe bradycardia or an advanced AV block. If the rate is 

50-100 beats/min, the rhythm is called accelerated idioventricular rhythm (AIVR). AIVR 

can also be seen after administration of thrombolytic therapy for acute myocardial 

infarction and may serve as a marker of reperfusion. 


Treatment may be indicated if the ventricular escape rhythm is unable to maintain 

adequate cerebral perfusion or if the patient is unstable. If ventricular escape beats 

occur in response to advanced AV block, it could be dangerous to abolish the escape 

rhythm. In this case, the escape rhythm may be helping to maintain adequate perfusion. 

Management is directed at treating the underlying AV block. If AIVR occurs secondary 

to reperfusion, no treatment is generally needed. Because an idioventricular escape 

rhythm often occurs as a result of advanced AV block, the majority of patients will 

require hospitalization. 

ATRIOVENTRICULAR JUNCTIONAL RHYTHM 


AV junctional escape rhythm refers to the occurrence of 6 or more consecutive 

junctional escape beats. The ventricular rate is usually 45-60 beats/min. AV junctional 

rhythm, like AV junctional premature beats, may originate from any location in the AV 

junctional tissue. Because the origin of the rhythm is the AV junctional tissue, the QRS 

complex is narrow unless the patient has a preexisting bundle branch block. If the 

junctional escape rhythm is faster than 60 beats/minute, the term AV junctional 

tachycardia is applied. If this rhythm is present, digoxin toxicity should be ruled out. 


Patients with sinus bradycardia and occasional or intermittent AV junctional escape 

beats do not generally require intervention. Treatment including hospitalization will 

depend on the underlying cause of the cardiac arrhythmia. 

Brady WJ: Diagnosis and management of bradycardia and atrioventricular block 

associated with acute cardiac ischemia. Emerg Med Clin North Am 2001;19:371. [PMID:

1137398] (Diagnosis and management of bradycardia and conduction disturbances.) 

Brady WJ et al: Evaluation and management of bradyarrhythmias in the emergency 

department. Emerg Med Clin North Am 1998;16:361. [PMID: 9621848] 

Kaushik V et al: Bradyarrhythmias, temporary and permanent pacing. Crit Care Med 

2000;28:121. [PMID: 11055680] (Diagnosis of bradyarrhythmias and indications for 

cardiac pacing.) 

PERMANENT CARDIAC PACEMAKERS (See Appendix, Figures 

35-32, 35-33, 35-34, 35-35, 35-36 and 35-37.) 

It is estimated that more than 150,000 new patients have permanent cardiac 

pacemakers implanted in the United States annually. Emergency medicine physicians 

should be familiar with normal pacemaker function and be knowledgeable about 

common pacemaker malfunctions. It is estimated that permanent pacemakers have a 

6% yearly incidence of malfunction. Although many of these malfunctions will be 

identified during routine evaluation, some malfunctions will occur unexpectedly, resulting 

in an emergency department visit. 

Types of Pacemakers 

Pacemakers are either single-chamber (atrium or ventricle) or dual-chamber (atrium and 

ventricle) devices. In single-chamber pacemakers, a single lead paces and senses in 

the same chamber, most often the right ventricle. In dual-chamber pacemakers, one 

pacing and sensing lead is in the right atrium, and the other is in the right ventricle. 

Some newer, more advanced devices have a third pacing lead placed in the coronary 

sinus enabling biventricular pacing. 

Since 1990, almost all pacemaker leads are bipolar. Bipolar leads have 2 electrodes on 

the same pacing lead, a distal cathode, and a proximal anode located approximately 1 

cm apart near the distal tip of the pacemaker lead. Bipolar leads produce a small 

electrical field between the 2 electrodes. This produces a small, sometimes barely 

noticeable pacing spike on the ECG. Older pacemaker leads were unipolar in design. 

The cathode was located at the distal end of the lead, and the pulse generator served 

as the anode. Unipolar leads produce a larger electrical field and give rise to larger 

pacemaker spikes on the ECG. Unipolar leads are more likely to sense noncardiac 

electrical events such as pectoralis muscle activity. This can result in inappropriate 

inhibition of pacemaker activity (myopotential inhibition). The introduction of bipolar 

leads has virtually eliminated this type of oversensing malfunction. 

Pacemaker Codes & Settings 

In April 2001, the North American Society of Pacing and Electrophysiology (NASPE) 

and the British Pacing and Electrophysiology Group (BPEG) revised and updated the 

generic pacemaker code (Table 35-1). The first position identifies which chambers are 

paced. The second position identifies the chambers in which the pacemaker senses 

cardiac depolarizations. The letter designation for the first and second positions is the 

same. The third position represents the pacemaker's response to a sensed cardiac

event. In general, when a pacemaker senses spontaneous cardiac activity, it is either 

inhibited from firing or a pacemaker spike is triggered. The fourth position designates 

whether the pacemaker has the ability for rate-responsive (rate-modulation) functions. 

Pacemakers with this function can increase the pacemaker discharge rate during 

exercise or movement in an attempt to meet metabolic demands. The fifth position 

indicates the presence and location of multisite pacing (ie, biventricular pacing). 

Although pacemakers may be programmed for many different modes, 4 common 

settings are likely to be encountered by the emergency physician: VVI, VVIR, DDD, and 

DDDR (Table 35-2). In patients with single-chamber pacemakers, VVI is the most 

commonly programmed pacing mode. In this mode, the pacemaker will pace and sense 

the right ventricle. If the pacemaker senses intrinsic ventricular activity, the pacemaker 

is inhibited from firing. If the intrinsic ventricular rate is slower than the programmed 

rate, ventricular pacing occurs at a fixed rate. A disadvantage of VVI pacing is its 

inability to increase the pacemaker rate when the patient is physically active. Patients 

with single-chamber ventricular pacemakers may develop pacemaker syndrome. This 

can occur as a result of the loss of AV synchrony, retrograde VA conduction, or an 

inability to increase the pacemaker rate with activity. Common symptoms include 

malaise, fatigue, shortness of breath, chest pain, dizziness, and near syncope. VVIR 

pacing provides for rate-responsive demand ventricular pacing. 

Dual-chamber pacing can be used to counteract the effects of pacemaker syndrome by 

preventing the loss of AV synchrony. Dual-chamber pacemakers may function in a 

variety of modes depending on the underlying intrinsic rhythm. DDD pacing is the most 

common mode for dual-chamber pacemakers. This allows for dual-chamber pacing and 

sensing. The pacing stimulus can be inhibited or triggered depending on the intrinsic 

rhythm. Dual-chamber pacemakers will be programmed with both a lower rate limit and 

an upper rate limit. DDDR pacing provides for rate-responsive demand AV sequential 

pacing. 

COMPLICATIONS OF IMPLANTABLE CARDIAC PACEMAKERS 

Venous Access 

Although uncommon, the majority of venous access complications occur early after 

implantation. Venous access complications include bleeding, pneumothorax, 

hemothorax, and rarely air embolism. Venous thrombosis is another rare complication of 

pacemaker placement. Patients may present with unilateral upper extremity pain and 

swelling. 

Pacemaker Pocket Site 

Early pacemaker pocket site complications include bleeding with hematoma formation, 

wound dehiscence, or infection. Early pocket site infections are usually caused by 

Staphylococcus aureus. Late complications (greater than 30 days after implantation) 

can include pacemaker site erosion, keloid formation, pacemaker migration, and 

infection. Late infections are usually caused by Staphylococcus epidermidis. 

Approximately 6% of patients with permanent pacemakers develop pocket site 

infections.

Lead Complications 

A number of complications can occur with endocardial pacemaker leads. Lead 

dislodgment is uncommon; rates are less than 2% for ventricular leads and less than 

5% for atrial leads. If lead dislodgment is suspected, obtain posteroanterior and lateral 

chest radiographs and compare them with a prior chest x-ray. Lead fracture or insulation 

break may also occur. Lead fractures generally occur at three sites: (1) close to the 

pulse generator, (2) at the venous entry site, and (3) within the heart. Lead fractures 

may be diagnosed by chest x-ray or by pacemaker interrogation. 

Cardiac perforation is another uncommon but potentially serious lead complication. 

Suspect perforation in the patient with a new paced right bundle branch block pattern on 

ECG, intercostal muscle or diaphragmatic contractions (hiccups), pericardial effusion, or 

tamponade. Cardiac perforation may also be identified by a plain chest radiograph 

demonstrating the tip of the pacemaker lead outside the cardiac silhouette. 

Echocardiography may be invaluable in diagnosing a pericardial effusion. Most cases 

(80%) of perforation occur within the first 4 days of pacemaker insertion. Another 

uncommon lead complication is Twiddler syndrome. This occurs when a patient wiggles 

or rotates the pacemaker generator, eventually dislodging the pacemaker leads. 

PACEMAKER MALFUNCTION (See Appendix, Figure 35-37A and B) 


The most common pacemaker malfunctions are sensing abnormalities. Sensing 

malfunctions are further subdivided into undersensing or oversensing. Undersensing 

occurs when the pacemaker fails to sense intrinsic electrical cardiac activity (P wave or 

QRS complex). On the ECG, a pacing spike is preceded by an intrinsic P wave or QRS 

complex. Oversensing is the inappropriate inhibition of a pacing stimulus. On the ECG, 

this is evident by a pause that is longer than the programmed pacemaker rate. 

Other pacemaker malfunctions include failure to pace and failure to capture. Failure to 

pace is characterized by an absence of an appropriate pacing stimulus. Failure to 

capture occurs when a pacing stimulus fails to depolarize the myocardium. Physiologic 

failure to capture may occur if the pacing stimulus occurs during the ventricular 

refractory period (within 300 ms after a native depolarization). This is not a malfunction, 

but reprogramming may still be necessary. 

Lead complications are common causes of pacemaker malfunction. An increase in the 

pacing threshold may also cause sensing malfunctions and failure to capture. This can 

occur as a result of fibrosis at the lead tip, hyperkalemia, hypoxemia, myocardial 

ischemia, and antiarrhythmic drug toxicity. Battery depletion or component failure may 

result in failure to pace or undersensing. Electromagnetic interference from 

electrocautery or magnetic resonance imaging (MRI) can lead to oversensing. Patients 

with implantable cardiac pacemakers should not undergo MRI. Variable effects have 

been documented, including pacemaker motion, function modification, heating of the 

pacemaker generator, and induction of voltage or current in the pacing leads.

Pacemaker mediated tachycardia (PMT) is an uncommon complication that can occur 

with dual-chamber pacemakers. PMT can be triggered by a PVC with 

ventricular-to-atrial (VA) conduction. Retrograde atrial activity triggers a ventricular 

paced beat. As the ventricular paced beat undergoes VA conduction, another ventricular 

paced beat is triggered and the cycle continues. PMT will be evident by sustained 

pacing at the upper limit of the programmed pacing rate (100- 140 beats/min). The ECG 

will characteristically reveal a wide complex paced tachycardia. PMT is often not life 

threatening because the heart rate does not usually result in hemodynamic instability. 

Runaway pacemaker is another rare cause of a wide QRS complex paced tachycardia. 

In this case, the malfunctioning pulse generator discharges at a rate above its preset 

upper limit. 


Patients may present with a number of symptoms suggestive of pacemaker malfunction. 

These include dizziness, lightheadedness, near syncope, syncope, palpitations, 

shortness of breath, or chest pain. The symptoms most concerning are those 

associated with cerebral hypoperfusion. Patients may present after blunt chest trauma 

or external defibrillation leading to pacemaker malfunction. Bradycardia may be an 

indicator of malfunction because the lower limit of fixed rate pacing is typically 50-60 

beats/min. This may occur as a result of oversensing or failure to pace. The upper limit 

of rate responsive pacemakers is generally 100-140 beats/min. A paced rhythm at this 

rate may or may not be pacemaker malfunction. 

Evaluation of the patient suspected of having pacemaker malfunction includes a 12-lead 

ECG and rhythm strip. If available, a comparison ECG may be helpful. A chest 

radiograph should also be obtained. Serum electrolyte and antiarrhythmic levels may 

also be necessary. 

A systematic approach to the evaluation of the 12-lead ECG and rhythm strip may help 

to identify pacemaker malfunction. The ECG should be evaluated to determine the 

presence or absence of appropriate pacing spikes. A normally functioning pacemaker 

should be inhibited from firing when the patient's intrinsic rate is faster than the 

programmed rate. Pacemaker function cannot be evaluated when the intrinsic rate is 

faster than the programmed rate. When properly inhibited, no pacing spikes are seen on 

the ECG. 

Magnet application may provide information regarding battery depletion or malfunction. 

When applied correctly over the pacemaker generator, the magnet triggers a reed 

switch, which inactivates the sensing function. The pacemaker should revert to an 

asynchronous pacing mode at a rate (magnet rate) preset by the manufacturer (VOO or 

DOO mode). A magnet rate that is slower than the manufacturer's preset rate suggests 

battery depletion. If no pacemaker spikes occur after magnet application, lead fracture 

or another malfunction may be the cause. Because there is no industry standard, the 

response of a particular brand of pacemaker may be variable when a magnet is applied. 


Treat venous access complications accordingly. Admit for parenteral antibiotics any 

patients suspected of having pocket site infections. 

For patients presenting with pacemaker malfunction leading to symptomatic 

bradycardia, institute pharmacologic treatment or emergency pacing measures. If 

transcutaneous cardiac pacing is initiated, place the anterior pacing pad as far away 

from the pacemaker generator as possible. In the setting of symptomatic bradycardia, a 

magnet can also be applied to revert to asynchronous pacing. If a patient requires 

synchronized DC cardioversion or defibrillation, place the paddles or pads as far from 

the pulse generator as possible. 

In the emergency department, treatment of PMT may be undertaken by a number of 

different maneuvers. First, a magnet may be applied to terminate the tachycardia. If a 

magnet is unavailable or unsuccessful, chest wall stimulation using a transcutaneous 

pacemaker can be attempted. The required stimulus is usually 10-20 ma. This is less 

than the stimulus generally required for transcutaneous pacing. If unsuccessful, 

isometric exercises can be tried. Finally, chest thumps have had success in terminating 

PMT; no more than two are recommended. Each of the above techniques is designed to 

affect the sensing function of the pacemaker, inhibit ventricular pacing, and terminate 

PMT. If the above are unsuccessful, cardiology consultation for pacemaker interrogation 

and reprogramming will be necessary. 

Runaway pacemaker is a rarely encountered problem. Pharmacologic intervention or 

magnet application can be attempted but will most likely be unsuccessful. Definitive 

treatment may require disconnecting the pacemaker leads or removal of the pulse 

generator. 

Obtain cardiology consultation for patients suspected of having pacemaker malfunction. 

Unless the pacemaker can be interrogated in the emergency department, the majority of 

patients with suspected pacemaker malfunction will require hospitalization. 

Bernstein AD et al: The revised NASPE/BPEG generic code for antibradycardia, 

adaptive-rate, and multisite pacing. Pacing Clin Electrophysiol 2002;25:260. [PMID: 

11916002] (Position statement revising the pacemaker code.) 

Cardiac pacemakers and EKG recordings. Online Journal of Cardiology; 

www.mmi.mcgill.ca/heart/ecgPindex.html 

Glickson M et al: Cardiac pacing: a review. Med Clin North Am 2001;85:323. [PMID: 

11233953] 

Griffin J et al: Runaway pacemaker: a case report and review. J Emerg Med 

2000;19:177. [PMID: 10903469] 

Weinberger B et al: Pacemaker and automated internal cardiac defibrillator. eMedicine; 

http://www.emedicine.com/emerg/ topic805.htm (Review of cardiac pacing and 

automated internal cardiac defibrillator.) 

Xie B et al: Permanent cardiac pacing. Emerg Med Clin North Am 1998;16:419. [PMID:

96218551] (Review of cardiac pacing and its complications.) 

IMPLANTABLE CARDIOVERTER DEFIBRILLATORS 

Despite access to prehospital emergency care and early defibrillation, sudden cardiac 

death remains a significant health problem. It is estimated that more than 400,000 

people have sudden cardiac death in the United States annually. Implantable 

cardioverter defibrillators (ICD) have dramatically reduced the incidence of sudden 

cardiac death resulting from life-threatening ventricular arrhythmias. Since becoming 

commercially available in the late 1980s, more than 250,000 ICDs have been implanted 

worldwide. 

Since receiving U.S. Food and Drug Administration approval in 1985, ICDs have 

undergone significant technologic advances. Initially, devices were implanted in the 

abdominal wall and epicardial patches were sewn in place via a median sternotomy. 

Newer third-generation devices are smaller, and most are implanted in the subpectoral 

fascia using a transvenous lead system, similar to permanent pacemaker systems. As 

compared to earlier models, third-generation devices have more advanced tachycardia 

detection and termination features with longer battery life (7-8 years). The advanced 

tachycardia termination features include antitachycardia pacing, low-energy 

cardioversion, and high-energy defibrillation. Newer ICDs are also capable of 

rate-responsive dual-chamber back-up pacing. 

COMPLICATIONS OF IMPLANTABLE CARDIOVERTER DEFIBRILLATORS 

Venous access, ICD pocket site, and lead complications are all similar to the 

complications associated with permanent cardiac pacemaker systems. The most 

common lead complication is dislodgement, which is estimated to occur in up to 10% of 

cases. 

IMPLANTABLE CARDIOVERTER DEFIBRILLATOR MALFUNCTION 


Although uncommon, frequent or recurrent shocks may represent an ICD malfunction. 

An increased frequency of shocks may be caused by a number of conditions including 

an increased frequency of ventricular arrhythmias, device inefficacy, or an ICD sensing 

malfunction. The most common cause of an increased frequency of ICD shocks is an 

increased frequency of VT or VF. Ventricular arrhythmias can occur as a result of 

worsening left ventricular dysfunction, myocardial ischemia, or changes in 

antiarrhythmic therapy. An ICD sensing malfunction may lead to double counting of the 

T waves or inappropriate recognition of SVT as VT. Lead complications may also cause 

inappropriate ICD shocks. 

Occasionally a patient may present with a sustained ventricular arrhythmia without ICD 

intervention. Although rare, this may occur as a result of a failure to detect the 

arrhythmia or exhaustion of therapies. In patients with ICDs, antibradycardia pacing 

malfunctions will be similar to those experienced by patients with implantable cardiac 

pacemakers.

MRI is contraindicated in patients with an ICD. The strong magnetic field may damage 

the ICD generator and interfere with antitachycardia therapy. 


Temporary device deactivation may be necessary when frequent shocks occur. Similar 

to cardiac pacemakers, magnet application should trigger a magnetically activated reed 

switch. This disables all antitachycardia functions (antitachycardia pacing and shock 

therapies). Antibradycardia pacing functions are unaffected. Although most ICDs are 

immediately deactivated when a magnet is applied correctly, responses are somewhat 

manufacturer-dependent. Deactivation is not commonly performed, however, because 

the most common reason for frequent shocks is an increase in the frequency of VT or 

VF. 

If recurrent ventricular arrhythmias result in frequent ICD shocks, antiarrhythmic 

administration and sedation may be necessary. If the ventricular arrhythmia is 

incessant, external cardioversion or defibrillation may be needed. Place the defibrillator 

pads or paddles as far from the ICD generator as possible. Older ICDs with epicardial 

electrodes have been reported to increase the defibrillation threshold by preventing 

externally applied current from passing into the myocardium. This may decrease the 

likelihood of successful defibrillation. 

Pinski SL: Emergencies related to implantable cardioverter-defibrillators. Crit Care Med 

2000;28:174. [PMID: 11055688] (Review of the complications of implantable 

cardioverter defibrillators.) 

Shah CP et al: Implantable cardioverter defibrillators. Emerg Med Clin North Am 

1998;16:463. [PMID: 9621852] (Review of implantable cardioverter defibrillators.) 

GENERAL REFERENCES 

Emergency cardiac care guidelines. Part 6: Advanced cardiac life support. Section 5: 

Pharmacology I: Agents for arrhythmias. Circulation 2000;102:112. [PMID: 10966669] 

(Pharmacology review of advanced cardiac life support medications.) 

Emergency cardiac care guidelines. Part 6: Advanced cardiac life support. Section 7: 

Algorithm approach to ACLS emergencies. Circulation 2000;102:136. [PMID: 10966671] 

(Advanced cardiac life support guidelines.) 

Wald DA: Therapeutic procedures in the emergency department patient with acute 

myocardial infarction. Emerg Med Clin North Am 2001;19:451. [PMID: 11373989] 

(Review of cardioversion, defibrillation, and temporary cardiac pacing.) 

APPENDIX: COMMONLY ENCOUNTERED CARDIAC ARRHYTHMIAS 

Normal Sinus Rhythm (Figure 35-2) 

The heart rate is 60-100 beats/min. There is a constant and normal PR interval, and the

P wave will be upright in lead II and inverted in lead aVR. 

Sinus Tachycardia (Figure 35-3) 

The heart rate is faster than 100 beats/min. Usually the rate is 101-160 beats/min. The 

P wave morphology is the same as in normal sinus rhythm. 

Sinus Bradycardia (Figure 35-4) 

The heart rate is slower than 60 beats/minute. Usually the rate is 45-59 beats/min. 

Sinus bradycardia is commonly associated with sinus arrhythmia. The P wave 

morphology is the same as in normal sinus rhythm. 

Sinus Arrhythmia (Figure 35-5) 

The heart rate is usually 45-100 beats/min. The P wave morphology is the same as in 

normal sinus rhythm. The PP or RR cycles vary by 0.16 s or more. Most commonly, 

sinus arrhythmia occurs in relation to the respiratory cycle. The sinus rate will gradually 

increase with inspiration and slow with expiration. 

Automatic Atrial Tachycardia (Figure 35-6) 

The heart rate is usually 160-250 beats/min but may be as slow as 140 beats/min. The 

P wave morphology is usually different from that of normal sinus rhythm. The PP and 

RR cycles are regular in most cases. When the atrial rate is slower than 200 beats/min, 

1:1 AV conduction is commonly noted. When the atrial rate is faster than 200 beats/min, 

the ventricular rate is often half the atrial rate because of the refractoriness of the AV 

node. 

Atrioventricular Nodal Reentrant Tachycardia (Figures 35-7, 35-8, 35-9 and 35-10) 

The heart rate is usually 180-200 beats/min. The P waves occur concurrent with the 

QRS complex and are often difficult to visualize on the ECG. 

Atrioventricular Reciprocating Tachycardia (Figure 35-11) 

The heart rate is usually faster than 200 beats/min. Because activation of the ventricle 

occurs through normal conduction pathways, the accessory pathway is concealed, and 

the QRS morphology is normal. 

Atrial Fibrillation (Figures 35-12 & 35-13) 

The atrial rate is disorganized and is 400-650 beats/min. The ventricular rate is 

irregularly irregular. No P waves are discernible on ECG. 

Atrial Flutter (Figure 35-14) 

The atrial rate is usually 250-350 beats/min. Characteristic sawtooth flutter waves may 

be seen on the ECG, particularly in lead II. Variable AV conduction may be noted.

Typically, 2:1 AV conduction occurs, resulting in a ventricular rate of approximately 150 

beats/min. 

Multifocal Atrial Tachycardia (Figure 35-15) 

The heart rate is typically 100-130 beats/min. The characteristic ECG finding is at least 

3 different P wave morphologies. Varying PR intervals may also be noted. 

Ventricular Tachycardia (Figures 35-16 & 35-17) 

The ventricular rate is usually 180-250 beats/min, although rates slower than 160 

beats/min may occur. The QRS complex is wide (greater than 0.12 s in duration) and 

often bizarre in appearance. Fusion beats or AV dissociation may be noted. If AV 

dissociation is present, the diagnosis of VT is confirmed. 

Polymorphic Ventricular Tachycardia (Torsades de Pointes) (Figure 35-18) 

The heart rate is usually 200-250 beats/min. Torsades de pointes is described as having 

a twisting-on-point appearance. 

Ventricular Fibrillation (Figure 35-19) 

VF is characterized by an irregularly irregular ventricular rhythm with no discernible 

distinction between the QRS complex, the ST segment, and T waves. 

Premature Atrial Contractions (Figure 35-20) 

A premature atrial contraction (PAC) may originate from anywhere in the atria except 

the sinus node. The P wave morphology is usually different from that of normal sinus 

rhythm. It is common to see a postectopic pause after a PAC. The QRS complex is 

narrow unless aberrantly conducted. 

Premature Ventricular Contractions (Figure 35-21) 

A PVC may originate from anywhere in the ventricles. The QRS complex is 0.12 s or 

longer in duration and resembles either a left or right bundle branch block. Uniform 

PVCs originate from the same foci and have the same appearance. Multiform PVCs 

have different morphology because they originate from different ventricular foci. 

Idioventricular Rhythm (Figure 35-22) 

The ventricular rate is usually 30-40 beats/min. The morphology of the QRS complexes 

will be similar to premature ventricular contractions but will vary depending on the 

location of the ventricular foci. If the ventricular rate is 50-100 beats/min, the rhythm is 

called accelerated idioventricular rhythm. 

Atrioventricular Junctional Rhythm (Figure 35-23) 

The ventricular rate is usually 45-60 beats/min. The QRS complex is narrow unless

aberrantly conducted. If the junctional rhythm is faster than 60 beats/min, the term AV 

junctional tachycardia is applied. 

Sinoatrial Block (Figure 35-24) 

SA block is characterized by blocked P waves, evident by a long PP interval. The PP 

intervals before the blocked P wave may gradually shorten (SA Wenckebach), or the PP 

intervals may be constant (second-degree Mobitz type II SA block). 

First-Degree Atrioventricular Block (Figure 35-25) 

The PR interval is constant but characteristically prolonged greater than 0.2 s. 

Second-Degree Atrioventricular Block (Mobitz Type I) (Figure 35-26) 

There is progressive lengthening of the PR interval followed by a nonconducted P wave 

leading to a dropped QRS complex. Classically, the PP interval remains constant. The 

RR interval that includes the blocked P wave is the longest in duration. 

Second-Degree Atrioventricular Block (Figure 35-27) 

When every other P wave is blocked, one cannot distinguish between Mobitz type I or 

Mobitz type II AV block. This is described as 2:1 AV conduction. 

Second-Degree Atrioventricular Block (Mobitz Type II) (Figure 35-28) 

The PR interval is regular and can be either normal or prolonged. Periodically, a P wave 

is not conducted, leading to a dropped QRS complex. 

Third-Degree Atrioventricular Block (Complete Heart Block) (Figures 35-29, 35-30 

and 35-31) 

The PP interval (atrial rate) is usually shorter (faster) than the RR interval (ventricular 

rate). Because no atrial impulses are conducted through the AV node, no relationship 

exists between the atrial and ventricular activity. 

Single-Chamber Ventricular Pacing (Figures 35-32 & 35-33) 

When the intrinsic heart rate is faster than the programmed pacemaker rate, the 

pacemaker is inhibited from firing. When the intrinsic rate is slower, the pacemaker is 

triggered, taking over as the dominant pacemaker of the heart. 

Dual-Chamber Atrioventricular Pacing (Figures 35-34 & 35-35) 

The pacemaker is capable of pacing and sensing the atria and ventricles. Depending on 

the intrinsic rate, the pacemaker can either be triggered or inhibited. 

Failure to Capture (Figure 35-36)

Failure to capture occurs when an appropriate pacemaker discharge fails to depolarize 

the myocardium. Physiologic failure to capture can occur if the pacing stimulus occurs 

during the ventricular refractory period. 

Failure to Sense (Undersensing) (Figure 35-37A) 

Undersensing occurs when the pacemaker fails to detect intrinsic electrical cardiac 

activity. On the ECG, a P wave or QRS complex is inappropriately followed by a pacing 

spike. 

Oversensing (Figure 35-37B) 

Oversensing is the inappropriate inhibition of a pacing stimulus. On the ECG, it is 

evident by a pause that is longer than the programmed pacemaker rate. 





INTRODUCTION

Table 35-1. The 2001 revised NASPE/BPEG pacemaker code. 1 

Chamber(s) 

Sensed 

Rate 

Modulation 

O (None) O O 

A R (Rate modulation) V (Ventricle) I (Inhibited) V 

D 1 Reproduced, 

with permission, 

from Bernstein 

AD et al: The 

revised 

NASPE/BPEG 

generic code for 

antibradycardia, 

adaptive-rate, 

and multisite 

pacing. Pacing 

Clin 

Electrophysiol 

2002;25:260-264. 





TABLES 

Table 35-1. The 2001 revised NASPE/BPEG pacemaker code.

Table 35-2. Commonly used pacing codes. 

Chamber 

Paced Pacemaker Function 

Ventricle Demand ventricular pacing. If the intrinsic 

ventricular rate is faster than the programmed 

rate, the pacing stimuli is inhibited. If the intrinsic 

rate if slower than the programmed rate, 

asynchronous pacing occurs. 

Ventricle Demand ventricular pacing with the added 

feature of rate responsiveness. 

Atrium + ventricle Dual-chamber atrioventricular pacing. Both atria 

and ventricle are paced and sensed. 

Atrium + ventricle Dual-chamber atrioventricular pacing with the 

added feature of rate responsiveness. 

Ventricle In this mode, the dual-chamber pacemaker 

senses the atrial activity, then proceeds to pace 

the ventricles at the same rate with an 

appropriate atrioventricular interval. 

Ventricle Asynchronous ventricular pacing. This is the 

mode that a single-chamber ventricular 

pacemaker reverts to when a magnet is applied. 

Atrium + ventricle Asynchronous atrioventricular pacing. This is the 

mode that a dual-chamber pacemaker reverts to 

when a magnet is applied. 





TABLES 

Table 35-2. Commonly used pacing codes.

Figure 35-1. Algorithm for the diagnosis of tachycardia with a wide QRS complex. 

(Reproduced, with permission, from Brugada P et al: A new approach to the differential 

diagnosis of a regular tachycardia with a wide QRS complex. Circulation 

1991;83:1649-1659. [PMID: 2022022]) 





FIGURES 

Figure 35-1

Figure 35-2. Normal sinus rhythm at a rate of 90 beats/min. 





FIGURES 

Figure 35-2

Figure 35-3. Sinus tachycardia at a rate of 130 beats/min. 





FIGURES 

Figure 35-3

Figure 35-4. Sinus bradycardia at a rate of 45 beats/min. 





FIGURES 

Figure 35-4

Figure 35-5. Sinus arrhythmia. The heart rate varies between 60 and 80 beats/min. 





FIGURES 

Figure 35-5

Figure 35-6. Automatic atrial tachycardia at a rate of 140 beats/min. 





FIGURES 

Figure 35-6

Figure 35-7. Atrioventricular nodal reentrant tachycardia at a rate of 175 beats/min. 

Note the absence of clearly discernible P waves. 





FIGURES 

Figure 35-7

Figure 35-8. A: AV nodal reentrant tachycardia with a left bundle branch block (LBBB) 

at a rate of 155 beats/min. B: The baseline ECG in the same patient showing sinus 

rhythm with a LBBB at a rate of 95 beats/min. Note that the 11th beat is a premature 

ventricular contraction. 





FIGURES 

Figure 35-8

Figure 35-9. A: AV nodal reentrant tachycardia at a rate of 150 beats/min. B: Seconds 

later after the administration of adenosine, the same patient converts to sinus rhythm. 





FIGURES 

Figure 35-9

Figure 35-10. Paroxysmal supraventricular tachycardia at a rate of 150 beats/min in a 

patient who is hemodynamically unstable. After the 7th beat, the patient is cardioverted 

with 50 J to sinus rhythm. 





FIGURES 

Figure 35-10

Figure 35-11. A: AV reciprocating tachycardia at a rate of 250 beats/min. B: The same 

patient after pharmacologic conversion showing sinus rhythm with ventricular 

preexcitation. 





FIGURES 

Figure 35-11

Figure 35-12. A: Atrial fibrillation with a controlled ventricular response. B: Atrial 

fibrillation at a ventricular rate of 130 beats/min. 





FIGURES 

Figure 35-12

Figure 35-13. A: Atrial fibrillation with ventricular preexcitation. B: The same patient 

after pharmacologic conversion showing sinus rhythm with ventricular preexcitation. 





FIGURES 

Figure 35-13

Figure 35-14. A: Atrial flutter with 4:1 AV conduction. B: Atrial flutter with 2:1 AV 

conduction. The ventricular rate is 145 beats/min. 





FIGURES 

Figure 35-14

Figure 35-15. Multifocal atrial tachycardia at a rate of 145 beats/min. Note the different 

P wave morphologies. 





FIGURES 

Figure 35-15

Figure 35-16. The rhythm strip shows a run of ventricular tachycardia; the rate is 150 

beats/min. After 16 beats the ventricular tachycardia spontaneously converts to sinus 

tachycardia. 





FIGURES 

Figure 35-16

Figure 35-17. Ventricular tachycardia at a rate of 145 beats/min. 





FIGURES 

Figure 35-17

Figure 35-18. Polymorphic ventricular tachycardia. 





FIGURES 

Figure 35-18

Figure 35-19. Ventricular fibrillation. After 6 beats, sinus rhythm degenerates into 

ventricular fibrillation. 





FIGURES 

Figure 35-19

Figure 35-20. Sinus rhythm with premature atrial contractions in a bigeminal pattern. 

The configuration of the P waves of the premature atrial contractions are different from 

that of normal sinus rhythm. 





FIGURES 

Figure 35-20

Figure 35-21. A: Sinus rhythm with frequent premature ventricular complexes in a 

pattern of bigeminy. B: Sinus rhythm with frequent premature ventricular complexes in a 

pattern of trigeminy. 





FIGURES 

Figure 35-21

Figure 35-22. A: Atrial fibrillation with an idioventricular escape rhythm. B: Accelerated 

idioventricular rhythm at a rate of 50 beats/min. 





FIGURES 

Figure 35-22

Figure 35-23. AV junctional rhythm at a rate of 40 beats/min. 





FIGURES 

Figure 35-23

Figure 35-24. Sinus rhythm with second-degree Mobitz type I SA block. Note that the 

PP intervals gradually shorten, whereas the PR intervals remains constant. The cycle 

terminates with a blocked P wave. The length of the pause is shorter than twice the 

preceding PP cycle. 





FIGURES 

Figure 35-24

Figure 35-25. Sinus rhythm with first-degree AV block. The PR interval is 0.44 s. 





FIGURES 

Figure 35-25

Figure 35-26. Sinus bradycardia with second-degree Mobitz type I AV block. Note the 

progressive lengthening of the PR interval until a QRS complex is dropped. 





FIGURES 

Figure 35-26

Figure 35-27. Sinus rhythm with second-degree AV block. 





FIGURES 

Figure 35-27

Figure 35-28. Sinus rhythm with second-degree Mobitz type II AV block. Note the 

variable AV conduction. 





FIGURES 

Figure 35-28

Figure 35-29. Third-degree AV block. The atrial rate is 92 beats/min, and the ventricular 

rate is 50 beats/min. 





FIGURES 

Figure 35-29

Figure 35-30. Third-degree AV block. The atrial rate is 88 beats/min, and the ventricular 

rate is 30 beats/min. 





FIGURES 

Figure 35-30

Figure 35-31. Third-degree AV block with an accelerated idioventricular escape rhythm 

with a ventricular rate of 60 beats/min. 





FIGURES 

Figure 35-31

Figure 35-32. Asynchronous ventricular pacing. In this case, the intrinsic heart rate is 

slower than the programmed pacemaker rate. When this occurs, the pacemaker is 

triggered, taking over as the dominant pacemaker of the heart. 





FIGURES 

Figure 35-32

Figure 35-33. VVI pacing. Although the pacemaker spikes are difficult to appreciate, 

beats 3-8 are ventricular paced beats. When the intrinsic heart rate is faster than the 

programmed rate, the pacemaker is inhibited from firing. 





FIGURES 

Figure 35-33

Figure 35-34. AV sequential pacing in a dual-chamber pacemaker. In this case, the 

pacemaker will pace both the atria and ventricles when no intrinsic cardiac activity is 

sensed. 





FIGURES 

Figure 35-34

Figure 35-35. Dual-chamber pacemaker functioning in the VAT mode. The pacemaker 

paces the ventricles and senses the atria. If intrinsic atrial depolarizations are sensed, a 

ventricular pacing spike is triggered. This is evident on the ECG by the presence of 

atrial tracking. 





FIGURES 

Figure 35-35

Figure 35-36. A: Single-chamber ventricular pacemaker showing failure to capture. The 

underlying rhythm is second-degree Mobitz type I AV block. A ventricular pacing spike 

occurs after the 5th atrial complex (P wave). This pacing spike fails to depolarize the 

ventricular myocardium. B: Dual-chamber pacemaker showing failure to capture. Beat 3 

shows an atrial pacing spike that fails to depolarize the atrial myocardium. The 

pacemaker then proceeds to pace the ventricle. Beats 1, 2, and 4-9 show an atrial 

pacing spike with capture followed by normal AV conduction. (Part A reproduced, with 

permission, from Garson A: Stepwise approach to the unknown pacemaker ECG. Am 

Heart J 1990;119:924.) 





FIGURES 

Figure 35-36

Figure 35-37. A: Undersensing. The 5th beat is a premature ventricular contraction 

(PVC). The next beat is a ventricular paced beat. Note that the paced beat occurs soon 

after the PVC, indicating a failure to sense the preceding complex. B: The 1st and 2nd 

beats are paced, the 3rd and 4th beats show normal AV conduction. There is a longer 

than expected pause between the 4th and 5th beats. This occurs secondary to 

ventricular oversensing. (Reproduced, with permission, from Garson A: Stepwise 

approach to the unknown pacemaker ECG. Am Heart J 1990;119:924.) 





FIGURES 

Figure 35-37

36. Obstetric & Gynecologic Emergencies & Rape 1 - Melissa Platt, MD, 

& Mary Nan Mallory, MD, RDMS 


ABNORMAL VAGINAL BLEEDING (See Table 36-1.) 

1 This chapter is a revision of the chapter by Phillip J. Goldstein, MD, from the 4th 

edition. 

Patients with active vaginal bleeding are at risk of exsanguination and require 

immediate evaluation and treatment. 

Emergency Evaluation & Treatment 

A. Obtain Vital Signs 

Examine the patient for hypotension or tachycardia due to depletion of intravascular 

volume. 

1. Hypotension—If blood pressure and pulse are normal in the supine position, 

measure them in the sitting position. If they are still normal, measure them in the 

standing position to detect more subtle volume depletion. Supine or postural 

hypotension indicates life-threatening hemorrhage. 

2. Tachycardia—Tachycardia while the patient is resting or when she assumes the 

upright posture also may indicate vascular depletion. 

B. Treat Shock, if Present 

(See Chapter 9.) Briefly, 

1. Insert at least 1 large-bore (= 16-gauge) intravenous catheter. A central venous 

catheter may be preferable if peripheral venous access is not readily obtainable 

(Chapter 6). 

2. Determine the amount of blood loss, and draw blood for (a) typing and 

cross-matching (reserve 4 units of fresh-frozen plasma and 2-4 units of packed red 

cells), (b) platelet count, prothrombin time, and partial thromboplastin time to uncover 

any bleeding abnormality, (c) complete blood count (CBC), (d) renal function tests and 

measurement of serum electrolytes, and (e) arterial blood gas measurements and pH 

(useful in assessing adequacy of ventilation and perfusion). 

3. Insert a Foley catheter. 

4. If the patient is of child-bearing age, obtain a serum or urinary pregnancy test.

5. Begin rapid infusion of crystalloid solution (Ringer's injection or normal saline), the 

rate depending on vital signs (eg, 200-1000 mL/h), to restore intravascular volume and 

maintain blood pressure until compatible blood becomes available for transfusion. 

6. Infuse cross-matched blood as soon as possible. If the patient is unstable and 

cross-matched blood is unavailable, transfuse O-negative blood. Give 2 or more units 

depending on vital signs. 

C. Determine the Cause of Bleeding, and Stop It 

The measures described here should not be used in third-trimester pregnancy. 

1. Compression of uterus—Insert one hand in the vagina, elevate the uterus, and 

compress it against the abdominal wall and the other hand. 

2. Pelvic ultrasonography—In the evaluation of a pregnant patient with vaginal 

bleeding, ultrasound can be used to rapidly identify fluid in the pelvis or abdomen 

(presumed to be blood in the setting of shock), which is highly suggestive of ruptured 

ectopic pregnancy. In the setting of symptomatic vaginal hemorrhage in the first 

trimester of pregnancy, ultrasound may show retained intrauterine products of 

conception, indicative of an incomplete spontaneous abortion. For the nonpregnant 

patient, an ultrasound showing significant pelvic or intraabdominal fluid may be 

representative of a hemorrhagic ruptured ovarian cyst, which occasionally requires 

surgical intervention. 

D. Treat for Trauma 

If trauma has occurred, determine the extent of injury, and apply pressure to the 

bleeding site. 

E. Obtain Consultation 

Obtain urgent gynecologic or surgical consultation for possible emergent dilation and 

curettage, laparoscopy, or laparotomy. 

Disposition 

Patients with vaginal bleeding resulting in abnormal hemodynamics or anemia should 

be hospitalized. 

PELVIC PAIN WITH OR WITHOUT BLEEDING (See Table 36-2. ) 


A. History 

Obtain information about the following points: 

• Possible pregnancy (recent amenorrhea or abnormal period, intercourse without 

contraception, morning sickness, or tenderness of breasts of recent onset) 

• History of trauma, including rape or nontherapeutic abortion

• History of salpingitis 

• History of ectopic pregnancy 

• Duration of symptoms and relation to menses 

• Type of pain (cramping or constant) 

• Type and amount of vaginal bleeding or discharge 

• Use of intrauterine device (IUD) 

B. Symptoms and Signs 

Fever is often the first sign of infection, and pelvic warmth (from local inflammation) may 

be noted on bimanual examination. Pelvic organs are tender and engorged. 

C. Laboratory Tests and Special Examinations 

1. Blood tests—The white cell count, differential, and erythrocyte sedimentation rate 

may reflect inflammation. 

2. Pregnancy test—A pregnancy test is important if pain or bleeding is present (Table 

36-3). Qualitative tests of blood or urine are sensitive and may provide positive test 

results within 7 days of conception. They are also relatively inexpensive, easy to do, and 

can be performed in 5 minutes. Quantitative blood tests are more sensitive and may 

assist in the evaluation of gestational age. If the tests are performed using urine 

samples, false-positive results may rarely occur in the presence of psychotropic drugs, 

methadone, sperm, or proteinuria. 

3. Cultures—Obtain cervical swab cultures for gonococci and Chlamydia trachomatis if 

infection is a possible diagnosis. 

4. Ultrasound—Ultrasound may show an ectopic pregnancy, intrauterine pregnancy, 

inflamed fallopian tubes, ovarian cysts, or pelvic abscesses (Figures 36-1 and 36-2). 

5. Laparoscopy—Laparoscopy may be helpful when the diagnosis is uncertain. 


If the diagnosis is uncertain but either ectopic pregnancy or septic abortion is a 

possibility, consultation with a gynecologist for hospitalization or daily follow-up on an 

outpatient basis is mandatory. 

EMERGENCY MANAGEMENT OF GYNECOLOGIC DISORDERS 

ECTOPIC PREGNANCY


• Unilateral pelvic pain in early pregnancy. 

• Vaginal bleeding present or absent. 

• Risk factor assessment. 

• Unilateral adnexal tenderness or mass. 

• Uterine size less than dates. 

• Quantitative hCG and pelvic ultrasound. 


Ectopic pregnancy is the leading cause of pregnancy-related death in the first trimester. 

Patients with ectopic pregnancy are often encountered in the emergency department, 

and the disorder may be difficult to identify given the varied presentations that occur. 

Overall, of the pregnant patients who present with vaginal bleeding or abdominal pain, 

60% will have normally developing pregnancies, 30% will experience a miscarriage, and 

10% will have an ectopic pregnancy. Because ectopic pregnancy can be life 

threatening, it should be suspected in any patient presenting with menstrual 

irregularities, vaginal bleeding, and pelvic or lower abdominal pain. For some women, 

the initial presenting symptom of an ectopic pregnancy is syncope. The most common 

presenting complaint is vaginal bleeding, often scant at first, with cramping lower 

abdominal pain. 

The incidence of ectopic pregnancy is increased in women using an IUD and in those 

with a history of pelvic infection (eg, salpingitis), tubal surgery, infertility treatments, or 

previous tubal pregnancies. About 98% of ectopic pregnancies are tubal. 

The clinical presentation of ectopic pregnancy is variable, ranging from the 

asymptomatic patient to the patient with hemorrhagic shock. Rupture of the fallopian 

tube followed by free intraperitoneal bleeding from tubal vessels is the principal cause of 

illness and death. 

With improved resolution of ultrasound and rapidly available quantitative ß-human 

chorionic gonadotropin (ß-hCG) assays, the diagnosis of ectopic pregnancy can be 

made more accurately and earlier than in the past (Figure 36-3). 



Patients have a history of the following: (1) missed or abnormal menses or vaginal 

bleeding; however, 30% of patients with ectopic pregnancy have no vaginal bleeding; 

(2) pelvic pain, which may be unilateral, following amenorrhea; and (3) intermittent pain 

(occasionally). Rupture of the fallopian tube may bring temporary relief of pain. 

Symptoms of early pregnancy (eg, breast tenderness, nausea) may be present. 

Peritoneal pain may develop after tubal rupture with bleeding into the peritoneum. 

Unilateral abdominal or pelvic pain may persist or improve. Referred shoulder pain is

occasionally present. Syncope or lightheadedness may occur. 

In the early stages of ectopic pregnancy, the results of pelvic examination may be 

normal. Symptoms, if present, may be completely nonspecific initially, because the tubal 

pregnancy producing them may be in the early stages of development. In advanced 

cases, a tender adnexal mass, enlarged uterus, or blood in the peritoneal cavity (eg, 

doughy cul-de-sac) may occur. 

Obtain complete vital signs, including supine, sitting, and standing pulse and blood 

pressure measurements if these measures are normal in the supine position, to look for 

supine or orthostatic hypotension. 

B. Laboratory Tests and Special Examinations 

1. Pregnancy test—The qualitative urine and serum pregnancy test may be positive at 

levels as low as 10 mIU/mL. Check with the laboratory. The most specific and sensitive 

test is the serum quantitative ß-hCG. It may detect levels as low as 5 mIU/mL 

depending on laboratory assay. Quantitative ß-hCG values are invaluable in the 

interpretation of pelvic ultrasound in this setting. In a normal intrauterine first-trimester 

pregnancy, the ß subunit of hCG should double about every 1.5 days. 

2. Ultrasound—Endovaginal and transabdominal sonography have become key 

diagnostic tools in the differentiation of normal (see Figures 36-1 and 36-2) from 

abnormal early pregnancy (Figure 36-4). Occasionally, a mass can be seen in the 

adnexa or cul-de-sac, or products of conception can be visualized outside the uterine 

cavity, and ectopic pregnancy can be readily diagnosed (see Figure 36-4). 

Ultrasound is often useful in excluding an ectopic pregnancy by ruling-in an intrauterine 

pregnancy. If the patient reports a history of infertility treatments, avoid making 

premature conclusions because the possibility of a heterotopic pregnancy (ie, 

simultaneous intrauterine and ectopic) has been reported to be as low as 1 in 5000. 

With a ß-hCG of 6000-6500 mIU/mL, an intrauterine pregnancy can be visualized 

transabdominally 94% of the time. Likewise, a yolk sac can be identified at the 

discriminatory ß-hCG values of 1000-1500 mIU/mL. With endovaginal scanning, a small 

intrauterine collection of blood, or pseudosac, may be seen associated with an ectopic 

pregnancy. In very early pregnancy, at levels below the discriminatory values, the uterus 

may appear empty. Fluid in Morison's pouch on transabdominal scanning strongly 

suggests ruptured ectopic pregnancy in this clinical setting (Figure 36-5). 

3. Laparoscopy or laparotomy—Laparoscopy or laparotomy may be necessary to 

make a definitive diagnosis of ectopic pregnancy. 


Treatment of possible ectopic pregnancy is determined by the patient's risk factors for 

ectopic pregnancy (ie, infertility treatments, history of tubal ligation or pelvic 

inflammatory disease), hemodynamic stability, and physical examination findings. In 

addition, sonography is important in the evaluation of pregnant patients with either 

abdominal pain or vaginal bleeding (see Figure 36-3). Quantitative ß-hCG results may 

help in the interpretation of ultrasound findings.

A. High Probability of Ectopic Pregnancy 

Obtain emergent pelvic sonography if hemodynamic stability allows. If the quantitative 

ß-hCG value is greater than 1500-2000 mIU/mL in a patient with an empty uterine cavity 

on endovaginal ultrasound, ectopic pregnancy should be strongly suspected. An 

adnexal mass or extrauterine products of conception may or may not be readily 

identified. A large amount of pelvic or intraperitoneal fluid is highly suggestive of ectopic 

pregnancy (Figures 36-4C and 36-5). If ultrasound is unavailable for evaluation of a 

patient with a positive pregnancy test, physical findings worrisome for ectopic pregnancy 

include severe adnexal tenderness or an adnexal mass. 

Prevent or correct hemorrhagic shock by inserting a large-bore (= 16-gauge) 

intravenous catheter and infusing crystalloid solution for volume replacement. Type and 

cross-match for 2-3 units of packed red blood cells. Insert a Foley catheter, and send 

urine for analysis. 

Obtain emergency obstetric consultation, and prepare the patient for surgery. Obtain 

CBC; serum electrolyte, blood urea nitrogen, and creatinine determinations; coagulation 

profile; and other studies as required. 

B. Ectopic Pregnancy Equivocal 

Vaginal bleeding, pelvic pain, and tenderness without explanation may be present in a 

patient with a positive pregnancy test. 

Insert an intravenous catheter, and send blood for CBC and typing and cross-matching. 

Obtain pelvic sonogram. A transvaginal sonogram may not show definite evidence of an 

ectopic pregnancy, but worrisome signs include fluid in the cul-de-sac or an empty 

uterus with a quantitative ß-hCG at or above the discriminatory zone. Gynecologic 

consultation is recommended in these situations. 

C. Low Probability of Ectopic Pregnancy 

Vaginal bleeding or pelvic pain is present. The results of physical examination and 

laboratory studies are normal. Some authors have developed clinical criteria for 

prediction of ectopic pregnancy. Suggested low-risk clinical criteria (ectopic pregnancy 

risk < 1%) for patients with pain or bleeding include absence of signs of peritoneal 

irritation on palpation, no cervical motion, no adnexal or uterine tenderness, and no 

abdominal or pelvic pain other than in the midline. 

Send blood for quantitative ß-hCG. If a pelvic sonogram demonstrates an intrauterine 

pregnancy, and the patient is at low risk for a heterotopic pregnancy (ie, no fertility 

medications or procedures), discharge the patient with 48-hour follow-up. Other patients 

who can be managed as outpatients with close gynecologic follow-up include those with 

quantitative ß-hCG below the discriminatory zone (1000 mIU/mL) with an empty uterus 

and no abnormalities on endovaginal ultrasound suggestive of ectopic pregnancy. 

Patients with an isolated quantitative ß-hCG below 1000 are not necessarily low risk 

because nearly one third of patients with ectopic pregnancies have a quantitative ß-hCG 

level below 1000 mIU/mL. 

Discharge the patient from the emergency department to outpatient care with a definite

follow-up appointment for reevaluation within 1-2 days. Give the patient written 

instructions explaining that ectopic pregnancy is a possible diagnosis and that she must 

be alert to the following symptoms, which would require that she return to the hospital 

immediately: (1) increased vaginal bleeding, (2) increased pelvic or abdominal pain, or 

(3) syncope. 

SPONTANEOUS ABORTION 


• Vaginal bleeding in early pregnancy. 

• Pelvic and back pain common. 

• Variable pelvic exam findings. 

• Quantitative hCG and pelvic ultrasound. 

• Exclude ectopic pregnancy. 


At least 20% of all pregnancies terminate in abortion, usually because of serious defects 

in the ovum. Half of abortions occur before the 8th week of gestation and another 

quarter before the 16th week. Many of these early spontaneous abortions go unnoticed 

as a delayed menstrual period. Nevertheless, early spontaneous abortions are also a 

common cause of visits to the emergency department. 

If the fetus dies but is not expelled, a missed abortion occurs. If this state persists for 

longer than 4-6 weeks, disseminated intravascular coagulation may occur. Table 36-4 

describes the various types of spontaneous abortion. 



Almost all patients have a history suggesting possible pregnancy: 

• Sexual intercourse 

• Period of amenorrhea (absence of menses for a duration of 3 cycles or 6 months in 

women previously menstruating) 

• Nausea and vomiting; breast tenderness 

• Uterine cramps and vaginal bleeding 

• Passage of fetal or placental tissue (in inevitable, incomplete, or complete abortion) 

Caution: Pelvic examination should be performed on all patients with suspected 

abortion and on all pregnant patients with vaginal bleeding who have reached less than 

20 weeks' gestation. Extreme care, however, must be exercised in examining patients in

the second trimester; instruments should not be introduced into the cervical os. Beyond 

20 weeks' gestation, pelvic examination should be done by an obstetrician because of 

the increasing risk of placenta previa. 

B. Laboratory Tests and Special Examinations 

In the first trimester of pregnancy, a ß-hCG level that does not double in 48 hours 

suggests fetal demise. Real-time ultrasonography, using abdominal or vaginal probes, 

can be diagnostic, for example, demonstrating a fetus without heartbeat or movement. 

Pathologic examination of tissue expelled by the uterus confirms passage of the 

products of conception. 


Blood typing and antibody screening are required in all patients with abortion of any 

type. If patients are Rh-negative, give Rh o (D) immune globulin (RhoGAM, many others), 

1 vial, within 72 hours after any event in which fetal-maternal transfusion may occur, 

including abortion. 

A. Threatened Abortion 

Advise the patient to rest. Do not use hormones, douches, or tampons. The patient 

should not engage in coitus. Ultrasound scan may reveal a gestational sac or evidence 

of fetal cardiac activity. Discharge instructions must include follow-up instructions and 

indications for return to the emergency department, including passage of fetal tissue, 

severe vaginal bleeding greater than one pad per hour, significant abdominal or pelvic 

pain, or fever. The patient should also be given adequate narcotic analgesia for pain 

management. 

B. Incomplete or Inevitable Abortion 

Hospitalize the patient if hypovolemia or anemia is present or if the pregnancy is past 

the first trimester. Treat hypovolemia if present. An obstetrical or gynecological consult 

should be obtained to perform suction curettage or dilation and curettage as the 

treatment of choice. 

C. Complete Abortion 

The patient may be discharged to home care if vital signs and hematocrit are stable and 

if vaginal bleeding is clearly decreasing. Pain must also be clearly decreasing and the 

cervical os closed. A physician must differentiate a complete abortion from an 

incomplete abortion. Several clues can help the physician determine that a complete 

abortion has occurred: 

• A reliable history. 

• Ultrasound revealing a clean uterine stripe. 

• The products of conception are brought to the physician and confirmed by pathology. If 

pathology is not readily available, a physician can rub the specimen between a gauze 

pad; if the specimen is a blood clot it will dissolve. However, if the specimen is true 

products of conception, the specimen will not dissolve. A physician may also run the 

specimen under water; a blood clot will dissolve, whereas products of conception will

not. 

D. Missed Abortion (Retained Conceptus) 

Obtain CBC, differential, and coagulation panel (platelet count, prothrombin time, and 

partial thromboplastin time). Obtain disseminated intravascular coagulation screening 

tests if abnormal values are found. Hospitalize the patient, and prepare to perform 

dilation and curettage if evidence indicates infection or disseminated intravascular 

coagulation or if the products of conception have been retained more than 4 weeks. 

Outpatient management of early missed abortion is possible if the patient is closely 

monitored for possible spontaneous abortion and if fibrinogen levels are measured 

weekly. Levels below 150 mg/dL call for evacuation of the uterine contents. 

SEPTIC ABORTION 


• History of gynecologic procedure or abortion. 

• Pelvic pain. 

• Systemic signs of infection. 

• Tender uterus. 

• Profuse, malodorous vaginal discharge. 


Septic abortion is a rare complication after some obstetric-gynecologic procedures. 

Septic abortion may also arise as a result of nonsterile nontherapeutic abortion. The 

usual cause of sepsis is incomplete evacuation of the products of conception. Infection 

is usually due to mixed aerobic and anaerobic bacteria (bacteroides, Prevotella, group B 

streptococci, Enterobacteriaceae, and C trachomatis) and is rapidly progressive, 

extending quickly through the myometrium and involving the adnexa and pelvic 

peritoneum. Septic pelvic thrombophlebitis with or without septic pulmonary 

embolization is an uncommon but devastating complication. 



Symptoms and signs are consistent with a history of recent pregnancy and induced 

abortion followed by pelvic pain and symptoms of infection. Nonjudgmental questioning 

in a private setting by a physician may be necessary to elicit a history of nontherapeutic 

abortion; in some cases, such a history is never obtained. Clinical findings include signs 

of infection (eg, fever, leukocytosis); diffuse pelvic tenderness; and profuse, foul vaginal 

discharge in most cases. Frank septic shock may be present. 

B. Imaging 

Ultrasound or other imaging techniques (computed tomography [CT], magnetic 

resonance imaging) may show retained intrauterine material, uterine emphysema, or

intraperitoneal air from uterine perforation. 


Evacuation of the uterine contents is crucial and is the mainstay of treatment. It should 

be preceded by broad-spectrum antibiotic therapy (see below). 

Note: Although antibiotic therapy alone is effective in the earliest stage of infection, 

many patients require emergency hysterectomy. Death may occur despite the best 

treatment. 


Hospitalize the patient at once, and start general measures for septic shock (Chapters 9 

and 40). Obtain emergency surgical obstetric and gynecologic consultation. 


Obtain samples of blood and uterine discharge for culture. Draw blood for CBC, tests of 

hepatic and renal function, serum electrolyte determination, prothrombin time, partial 

thromboplastin time, platelet count, and disseminated intravascular coagulation 

screening tests if initial findings are abnormal. 

C. Antibiotics 

After taking specimens for culture of aerobic and anaerobic organisms, give antibiotics 

(eg, doxycycline, 100 mg every 12 hours intravenously and one of the following: 

cefoxitin, 2.0 g every 6-8 hours intravenously, ticarcillin-clavulanate, 3.1 g every 6 hours 

intravenously, or imipenem cilastatin, 0.5 g every 6 hours intravenously). 

CARCINOMA & OTHER TUMORS 

Although gynecologic cancers seldom present as emergency situations, the emergency 

physician should be aware of the various presenting symptoms and risk factors 

associated with gynecologic cancers. 

Carcinoma of the Vulva 

Vulvar cancers are rarely sudden in onset and usually occur in women over age 50 

years. They are more common in women with a history of cervical dysplasia or cancer. 

Patients seeking treatment for vulvar lesions in the emergency department should be 

advised to seek gynecologic consultation if any lesion initially thought to be due to 

infection or trauma fails to heal in a short time. Persistent unremitting vaginal pruritus is 

the single most common symptom of vulvar cancer and should never be dismissed as a 

frivolous complaint in the postmenopausal patient. 

Carcinoma of the vulva is not commonly seen in the emergency department. 

Carcinoma of the Vagina 

Vaginal cancers are rare. Bleeding is typically the presenting complaint. The patient is

usually age 50 years or older, but even teenagers have developed clear cell carcinoma 

(eg, girls whose mothers were given diethylstilbestrol during pregnancy). 

The source of the vaginal bleeding must be identified, and a speculum should be used 

to carefully inspect the vaginal walls. Careful digital examination of the vaginal mucosa 

is critical to detect submucosal infiltration by the tumor. 

Carcinoma of the Cervix 

Vaginal bleeding is the most common symptom in cervical cancer. Patients may be in 

their late 20s to (most commonly) early 40s. Patients often complain of persistent watery 

discharge. Speculum examination reveals a necrotic friable lesion on the cervix. 

Uncontrollable bleeding from the cervix may be treated with applications of ferric 

subsulfate solution or vaginal packing. Manipulation should be kept to a minimum. 

Biopsy of the lesion at its margin with normal tissue usually confirms the diagnosis, but 

this procedure should be performed only in an operating room. 

Carcinoma of the Endometrium 

Postmenopausal bleeding is the most common symptom of endometrial carcinoma. 

Risk factors associated with endometrial carcinoma include ingestion of exogenous 

estrogens, obesity, infertility, polycystic ovarian syndrome, and age over 50 years. 

The physician should not try to stop postmenopausal bleeding with administration of 

hormones (eg, estrogens or progesterone) without confirming the diagnosis beforehand. 

Consultation with a gynecologist should be obtained prior to discharge for further input. 

Carcinoma of the Ovaries 

Patients with ovarian cancer may have abdominal distention from ascites, intestinal 

obstruction, or rarely, acute abdominal pain. The possibility of ovarian cancer should be 

considered in any woman with abdominal or pelvic symptoms. Definitive diagnosis 

requires surgical or gynecologic consultation for laparotomy or laparoscopy. 

Other Tumors 

Patients with gestational trophoblastic disease may present with heavy vaginal bleeding 

and symptoms similar to those of early miscarriage, but the following symptoms and 

signs suggest trophoblastic disease: (1) heavy vaginal bleeding with or without passage 

of tissue, or great clusters of tissue aborted from the cervical os, (2) uterine size 

inappropriately large for dates, (3) profound anemia, (4) history of molar pregnancy, (5) 

first-trimester hypertension or preeclampsia, or (6) ß-hCG remarkably elevated over the 

expected values. The diagnosis can be confirmed by ultrasound examination. 

Any patient presenting with neurologic signs and with a recent history of molar 

pregnancy or trophoblastic disease may have cerebral metastasis. Central nervous 

system metastasis of trophoblastic disease represents a true oncologic emergency, 

because cerebral metastasis has the potential for cure as long as rapid growth or

hemorrhage does not occur. 

Patients with trophoblastic disease should be hospitalized for gynecologic consultation 

and possible referral to a regional trophoblastic disease center, where help is readily 

available. 

GENITAL TRAUMA 

Genital trauma in women almost always occurs as a result of sexual activity, either 

forced (rape) or voluntary (foreign bodies introduced into the vagina in sexual play). 

Penile thrusts rarely produce trauma unless it is the first sexual experience. 


The most common presenting complaints are vaginal bleeding and pain or dyspareunia. 

Examination usually reveals bleeding from a tear in the genital mucosa or skin. Bleeding 

is rarely brisk enough to produce signs of hypovolemia, but if these are present, replace 

volume losses, and provide supportive care (Chapter 9). In prepubertal patients, general 

anesthesia may be required for adequate examination. 


Determine whether rape has occurred, and proceed accordingly. Provide sedation or 

analgesia if necessary. 

Treat hypovolemia if present. Control vaginal bleeding temporarily with a vaginal pack 

or, if bleeding is from the external genitalia, with direct firm pressure (combined with an 

indwelling urinary catheter). 

Hospitalize the patient if bleeding cannot be easily and definitively controlled, and obtain 

gynecologic consultation. Small lesions at the introitus may be repaired in the 

emergency department under local anesthesia. However, small and seemingly minor 

vaginal tears may communicate with either the rectum or the peritoneum; consequently, 

such repairs are best performed by a gynecologist in an operating room with adequate 

anesthesia and good exposure. 

RUPTURED OVARIAN CYST 


• Sudden, moderate to severe unilateral pelvic pain. 

• Possible history of initial nausea, diaphoresis, near-syncope. 

• Lack of systemic signs of infection. 

• Negative pregnancy test. 

• Unilateral adnexal tenderness without mass. 

• Pelvic ultrasound excludes significant hemorrhage.


Ruptured ovarian cyst is associated with sudden, moderately severe pelvic or lower 

abdominal pain. There are no gastrointestinal symptoms. The patient is afebrile, and 

leukocytosis is variable. Tenderness is found over the affected ovary, and there are no 

masses. A pregnancy test should be obtained, because ectopic pregnancy is a possible 

diagnosis. Ultrasonography may show the presence of an ovarian cyst or free pelvic 

fluid and is useful to detect ectopic pregnancy. 


The physician should provide adequate analgesics, including narcotics if needed. The 

patient should be observed and may require hospitalization if the diagnosis is uncertain 

or if relief is required for severe pain not relieved by narcotics. Surgery is rarely required 

unless there is a significant hemoperitoneum from the rupture of a hemorrhagic corpus 

luteum cyst with hemodynamic instability. 

TORSION OF OVARIAN TUMOR 


• Extremes of age. 

• Single or recurrent moderate unilateral pelvic pain. 


• Pelvic mass. 

• Pelvic ultrasound. 


Torsion of ovarian tumor is associated with a history of attacks of cramps and pains, 

usually unilateral, in the lower abdomen and possibly in the flank. The symptoms, such 

as nausea, may be gradual, or they may occur suddenly if there is accompanying 

intraovarian bleeding. Discomfort is characterized by symptoms of pelvic mass (eg, 

painful defecation and dyspareunia). Ultrasonography may delineate the mass. Doppler 

studies may detect decreased or absent blood flow to the torsed ovary. 


Hospitalize the patient, and obtain urgent gynecologic consultation. Pelvic 

ultrasonography may be a useful diagnostic tool, but laparoscopy is frequently required. 

Laparotomy is indicated if the diagnosis is confirmed or if the patient's condition 

deteriorates. 

ENDOMETRIOSIS


• Recurrent pelvic, flank, or abdominal pain with menses. 



The patient with endometriosis gives a history of attacks of cramps and pains in the 

lower abdomen and possibly in the flank that are associated with menstruation. 

Symptoms may be gradual, or sudden if bleeding is present. Acquired dysmenorrhea is 

most commonly due to endometriosis. Other symptoms include painful defecation and 

dyspareunia. 


Refer the patient for further gynecologic evaluation. Definitive diagnosis usually requires 

laparoscopy. Provide oral analgesia as needed. 

DYSMENORRHEA 


• Painful menstruation. 


• Exclude pelvic infection. 


Many women experience painful menstruation (dysmenorrhea). The pain is cramping in 

nature, may be debilitating, and is usually relieved by release of menstrual contents 

from the uterus. The pain occurs because of elaboration of excessive quantities of 

prostaglandins by the endometrium with subsequent increased uterine tone. It is not 

psychological in origin. 

Idiopathic dysmenorrhea usually begins at menarche and is probably more common 

than the acquired form. Acquired dysmenorrhea, occurring in the late teens and early 

20s, may suggest endometriosis and is common in chronic pelvic inflammatory disease. 


Both types of dysmenorrhea may be seen by the emergency physician and may be 

treated by prostaglandin inhibitors (eg, ibuprofen, 400 mg orally every 6 hours; 

naproxen, 250-500 mg twice daily, or controlled release, 750-1000 mg every day). Local 

application of heat to the lower abdomen may be helpful.

MITTELSCHMERZ 

Midcycle pain (mittelschmerz) is common in women with regular menstrual periods who 

are not taking birth control pills. These patients may commonly have midcycle spotting 

caused by an estrogen surge. There is no fever and no other abnormal bleeding such 

as that resulting from trauma to the cervix (eg, coitus, douching). Pain usually occurs 

over several cycles. There is no history of intermittent lower abdominal pain. 

Examination at the time of mittelschmerz may reveal some lower quadrant tenderness 

with or without rebound. Bimanual examination may show localized tenderness. A 

palpable ovary may be present, but a history of regular menses, lack of fever, and 

negative pregnancy tests confirm the diagnosis. 

Mild analgesics and reassurance are usually adequate for these patients. 

UTERINE PROLAPSE 


• Prior vaginal deliveries. 

• History of pelvic heaviness, low back pain. 

• Patient may present with urinary retention. 

• Firm, muscular mass in or protruding from vagina. 


Uterine prolapse typically occurs because of muscular defects in the pelvic floor arising 

from childbirth. Prolapse is characterized by variable symptoms of pelvic heaviness or a 

dragging sensation and lower back pain. Urinary retention of sudden onset may be a 

presenting complaint. Examination reveals a firm, muscular mass in the vagina or 

protruding from the vagina (procidentia) and having the shape and size of the uterus 

and cervix. Cystocele, rectocele, and enterocele are commonly associated with 

procidentia. 


Acute postpartum prolapse is an emergency that requires immediate obstetric and 

gynecologic consultation. Patients with acute urinary retention or procidentia should 

have urgent gynecologic consultation. Patients with mild prolapse should be referred 

within 5-7 days for gynecologic evaluation and possible surgery. 

SALPINGITIS & TUBO-OVARIAN ABSCESS (See Chapter 40.) 

Rape (Men & Women) 

Proper care of the alleged rape victim requires concern for the social and emotional 

consequences of the event as well as for the medical sequelae. The best care fulfills the 

requirements of the law while providing proper support and reassurance to the patient.

Every state has its own laws and regulations concerning rape; however, some general 

principles apply. The physician's responsibilities include the following: 

• Recognizing and managing life-threatening trauma (eg, hemorrhagic shock). 

• Obtaining informed written consent for physical examination, collection of evidence, 

photographic documentation, and treatment. 

• Shielding the alleged rape victim from other patients, bystanders, and visitors. 

• Accurately diagnosing and treating all physical injuries, both genital and nongenital. 

• Recording a detailed and explicit history of the event in the patient's own words. 

• Carefully collecting specimens for evidence, with accurate documentation and 

protection of the chain of evidence. 

• Providing psychological support and follow-up. 

• Offering prophylaxis against pregnancy and sexually transmitted disease. 

• Avoiding a "diagnosis" of rape (it is not a medical diagnosis but a matter of 

jurisprudence). The physician should also avoid judgmental or conclusive language. 

• Being willing to testify in court. 

• Ensuring that discharge from the emergency department is to a safe place. 

• Encouraging a physical examination even if the patient declines forensic examination. 

Unless required to do so by statute, the emergency physician does not have a legal 

obligation to notify the police when providing treatment to a victim of alleged rape. 

Notifying the police is appropriate when the patient has consented (preferably in writing) 

to such notification. The physician may wish to refer the patient to a counseling 

organization that aids rape victims. 

The responsibilities described above are often best fulfilled by having teams 

experienced in working with rape victims perform the evaluation. Such teams should 

follow an established written protocol and document all findings in writing. 

1. Management of the Female Rape Victim 

Evaluation 

A. Initial Steps 

If required by law or with the patient's consent, inform the police (see below). Obtain 

written informed consent for examination. 

B. History

Obtain and record the history in the patient's own words. Obtain answers to other 

specific questions (if they have not already been answered). Record the victim's general 

appearance and demeanor, and note whether clothing is torn or stained. 

C. Evidence 

Collect and label relevant evidence, and protect the chain of evidence: 

1. Scrape under the fingernails, and also take trimmings from them. 

2. Comb pubic hair, and look for loose hairs from the assailant. 

3. Pull a few pubic hairs and save them. 

4. Collect any other loose hairs or dried blood. 

5. Examine the perineum and other suspect areas with a Woods light (prostatic 

secretions are fluorescent even when dry). 

6. Prepare 4 dried slides of vaginal contents (wash the vagina with saline if it is dry), and 

fix them with ether-alcohol. 

7. Collect vaginal aspirate or washings into a screw-topped specimen tube for acid 

phosphatase determination (a positive reaction indicates the presence of prostatic fluid 

ejaculate). 

8. Place a cotton swab of vaginal contents into a specimen tube (for typing of the blood 

group antigen in semen). 

9. Obtain material from the cervix for culture for gonococci and C trachomatis. 

10. Obtain urine for urinalysis (look for hematuria indicating genitourinary trauma). 

Perform a urine pregnancy test. 

11. Photograph all external lesions, but only with the patient's written consent. 

12. If oral or rectal penetration has occurred, steps 5-9 should be repeated with 

specimens from those sites. 

D. Physical Examination 

Thoroughly examine the patient for signs of trauma, discharge, or bleeding; record the 

results of the examination; and photograph all lesions (the last only with the patient's 

written consent). 

E. Pelvic Examination 

Look carefully for signs of trauma to the external genitalia. Note and record whether the 

hymen is intact and whether any hymenal tags are fresh (indicating trauma) or healed. 

Using a warm, water-moistened speculum, carefully examine the vagina for lacerations.

Topical application of toluidine blue may enhance identification of genital skin tears. 

Colposcopy enhances the identification of traumatic injury. Rarely, peritoneal perforation 

may occur. 

Evaluate the cervix for signs of preexisting pregnancy and trauma. Examine the rectal 

area. If penetration has occurred, proctoscopy may be advisable. 

F. Laboratory Tests 

Obtain blood for blood chemistry studies (if indicated), a serologic test for syphilis, and 

blood typing (to compare the alleged assailant's type with that of the victim). Blood 

sampling may also be used for hepatitis B and human immunodeficiency virus (HIV) 

serologic testing. 

Treatment 

The physician should be empathic and concerned, never skeptical or judgmental. 

A. Prevent Sexually Transmitted Disease 

Treatment for gonorrhea, C trachomatis, and syphilis (Chapter 40) should be offered but 

not forced on the patient. Only about 3% of rapes result in gonorrhea, and only about 

0.1% result in syphilis. Follow-up cultures for N. gonorrhoeae are essential. Perform 

follow-up serologic tests for syphilis 1 and 3 months after the rape. 

B. Prevent Infectious Diseases 

Offer the hepatitis B vaccine as well as follow-up in 3-4 weeks for repeat hepatitis 

vaccination and testing. HIV is also of concern. Start prophylactic medications based on 

risk factors with a follow-up for repeat HIV testing. 

C. Prevent Pregnancy 

Treatment for the prevention of pregnancy should be offered but not forced on the 

patient. Only about 1% of rapes result in pregnancy; the chances are much less if the 

victim is using an effective method of contraception. Give ethinyl estradiol, 200 ug, and 

norgestrel, 2 mg, orally over 12 hours in 2 divided doses (eg, norgestrel [Ovral], 2 

tablets orally, repeating in 12 hours), to prevent implantation if it is certain that the 

patient is not already pregnant. Advise the patient that nausea and vomiting may occur. 

Give an antiemetic 40 minutes prior to the oral contraceptives. 

Caution: Existing pregnancy is an absolute contraindication to the use of oral 

contraceptives. Warn the patient that this regimen may not be effective, and explain that 

a return visit within 1-2 weeks is essential for another pregnancy test. 

D. Report the Incident 

If required by law or if the patient consents, report the incident to the proper authorities 

before the patient leaves the emergency department, because the police will want to 

question her. If the alleged victim is a child, the incident may be child abuse and should 

be reported to the appropriate child welfare authorities (Chapter 48). 

E. Start Rape Counseling Immediately 

Preferably, counseling should be directed by experienced personnel who are part of an

established rape counseling program. 

F. Arrange Follow-up 

A definite appointment (time, place, and physician or clinic) should be made. 

2. Management of the Male Rape Victim 

Clinical Findings & Evaluation 


If required by law or with the patient's consent, inform the police (see below). Obtain 

written informed consent for examination. 

B. History 

Obtain and record the history as described above. 

C. Evidence 

Collect and label relevant evidence, and protect the chain of evidence: 

1. Scrape under the fingernails, and also take trimmings from them. 

2. Collect any loose hairs or dried blood. 

3. Using the techniques and preparations described in steps 5-9 under Management of 

the Female Rape Victim, examine samples of material from the mouth and rectum. 

D. Physical Examination 

Thoroughly examine the patient for signs of trauma, discharge, or bleeding; record the 

results of the examination. Photograph all lesions, but only with the patient's consent. 

Examine the mouth and the rectum for injuries. Proctoscopy may be advisable if 

penetration has occurred and if foreign objects were used, because peritoneal 

perforation may occur from rectal trauma. 

E. Laboratory Tests 

Obtain blood for blood chemistry studies (if indicated), a serologic test for syphilis, and 

blood typing (to compare the alleged assailant's type with that of the victim). 

Treatment 

A. Prevent Sexually Transmitted Disease 

Offer treatment and preventive therapy for sexually transmitted disease, as described 

above and in Chapter 40. 

B. Report the Incident 

If required by law or if the patient consents, report the incident to the proper authorities 

before the patient leaves the emergency department, because the police will want to 

question him. If the alleged victim is a child, the incident may represent child abuse and

should be reported to the appropriate child welfare authorities (Chapter 48). 

C. Start Rape Counseling Immediately 

Preferably, counseling should be directed by experienced personnel who are part of an 

established rape counseling program. Male victims of rape need counseling just as 

much as female victims. 

INTRAUTERINE DEVICES 

Problems with IUDs 

A. "Lost" IUD 

In the emergency department, the most common problem relating to these devices is 

the "lost" IUD. Check to see if the IUD is still properly placed by looking for the removal 

string protruding from the cervix (most women soon learn to feel for it with a finger). If 

no string can be found, the IUD may be located by uterine sonography or abdominal 

x-ray (for metallic IUDs). The IUD may be in an extrauterine position, in which case it 

should be removed surgically by laparoscopy or laparotomy, although this is usually not 

an emergency. 

B. Emergency Removal of IUD 

1. Infection—The principal indication for removal of an IUD in the emergency 

department is infection (salpingitis, endometritis, pyosalpinx, or pelvic peritonitis). The 

incidence of endometritis, salpingitis, and tubal abscess is increased in women using 

IUDs. Any of these conditions requires removal of the IUD so that infection can be 

completely cleared. If possible, the patient should be started on appropriate antibiotics 

before the device is removed in order to ensure adequate blood levels of the drug (see 

"Salpingitis" section in Chapter 40). 

2. Bleeding and pain—Persistent vaginal bleeding or pelvic pain usually requires 

removal of an IUD but not often on an emergency basis. Referral to the physician who 

inserted the device is preferable. 

If referral is impractical, grasp the string of the IUD with a Kelly clamp or other long 

grasping forceps, and pull with gentle but increasing force until the IUD emerges from 

the uterus. Do not jerk the string, because it may detach from the device and make 

removal more difficult. If the string is not easily seen after manipulation with a speculum, 

use a special IUD remover to locate and grasp the string. Alternatively, explore the 

endocervix with a crochet hook; this generally frees the string so that it can be easily 

grasped and the device removed. 

C. Serious but Rare Problems 

1. Perforation of the uterus—Perforation of the uterus is a probable diagnosis in 

patients with IUDs who have symptoms of endometritis, salpingitis, or peritonitis. 

Physical examination, an abdominal x-ray, and sonography show that the IUD is 

embedded in the uterine wall or free in the peritoneum. Emergency hospitalization is 

required. 

2. Pregnancy with IUD in place—If pregnancy is confirmed by a positive pregnancy

test, and an IUD is still in place, seek emergency obstetric consultation. Ectopic 

pregnancy is a distinct possibility in the pregnant patient with an IUD still in place. 

POSTCOITAL EMERGENCY CONTRACEPTION 

Postcoital emergency contraception, also known as the morning-after pill, can be given 

to prevent implantation. The U.S. Food and Drug Administration has approved 2 tablets, 

each containing 0.5 mg ethinyl estradiol and 0.5 mg DL-norgestrel, within 72 hours of 

intercourse and repeated again 12 hours later. Norgestrel [Ovral] has this combination; 

however, several prescriptive equivalents are available. Nausea and emesis frequently 

occur, and an antiemetic should be prescribed. Although the morning-after pill is 

reported to be 98% effective, a pregnancy test should be performed if menstruation 

does not occur within 21 days of treatment. 

DISORDERS OF THE VULVA & VAGINA 

Vaginal and vulvar cancers and other lesions are discussed earlier in this chapter. 

Vaginitis, gonorrhea, genital herpes virus infection, and genital abscesses are discussed 

in Chapter 40. 

A WARNING ABOUT DISCONTINUING CONTRACEPTION 

Treatment of gynecologic problems in the emergency department may require 

discontinuing the patient's current form of contraception. The emergency physician 

advising this course of action must warn the patient of the possibility of pregnancy and 

offer appropriate contraceptive advice. Discontinuation of oral contraceptives or IUD use 

because of treatment in the emergency department should not result in an unwanted 

pregnancy. 

American College of Emergency Physicians: ACEP emergency ultrasound 

guidelines—2001. Ann Emerg Med 2001;38:470. [PMID: 11574810] 

Ankum WM: Diagnosing suspected ectopic pregnancy: HCG monitoring and 

transvaginal ultrasound lead the way. [Editorial]. Br Med J 2000;321:1235. [PMID: 

1182067] 

Buckley RG et al: History and physical examination to estimate the risk of ectopic 

pregnancy: validation of a clinical prediction model. Ann Emerg Med 1999;34(5):589. 

[PMID: 10533005] 

Ciancone AC et al: Sexual assault nurse examiner programs in the United States. Ann 

Emerg Med 2000;35(4):353. [PMID: 10736121] 

Counselman FL et al: Quantitative B-HCG levels less than 1000 mIU/ML in patients with 

ectopic pregnancy: pelvic ultrasound still useful. J Emerg Med 1998;16:699. [PMID: 

9754920] 

Dart R et al: Normal intrauterine pregnancy is unlikely in emergency department 

patients with either menstrual days > 38 days or beta-HCG > 3,000 mIU/ml, but without

a gestational sac on ultrasonography. Acad Emerg Med 1997;4:967. [PMID: 9332628] 

Dart R, Dart L, Mitchell P: Normal intrauterine pregnancy is unlikely in patients who 

have echogenic material identified within the endometrial cavity at transvaginal 

ultrasonography. Acad Emerg Med 1999;6:116. [PMID: 10051902] 

Dart RG: Role of pelvic ultrasonography in evaluation of symptomatic first-trimester 

pregnancy. Ann Emerg Med 1999;33 (3):310. [PMID: 10036346] 

Durham B et al: Pelvic ultrasound performed by emergency physicians for the detection 

of ectopic pregnancy in complicated first-trimester pregnancies. Ann Emerg Med 

1997;29(3):338. [PMID: 9055772] 

Mateer JR et al: Outcome analysis of a protocol including bedside endovaginal 

sonography in patients at risk for ectopic pregnancy. Ann Emerg Med 1996;27(3):283. 

[PMID: 8599484] 

Rodrigues I, Grou F, Joly J: Effectiveness of emergency contraceptive pills between 72 

and 120 hours after unprotected sexual intercourse. Am J Obstet Gynecol 

2001;184:531. [PMID: 11262449] 

Shih CHY: Effect of emergency physician-performed pelvic sonography on length of 

stay in the emergency department. Ann Emerg Med 1997;29:348. [PMID: 9055773] 

Wilcox AJ et al: Natural limits of pregnancy testing in relation to the expected menstrual 

period. JAMA 2001;286:1759. [PMID: 11594902] 

EMERGENCY MANAGEMENT OF OBSTETRIC DISORDERS 

PREGNANCY 


The diagnosis and differential diagnosis of pregnancy are a critical skill in the 

emergency department, where many serious obstetric disorders (eg, abortion or ectopic 

implantation) may be seen. 

A. Early Symptoms and Signs 

Amenorrhea, nausea and vomiting, syncopal attacks, breast tenderness or tingling, and 

urinary symptoms (especially frequency) are early symptoms of pregnancy. Early signs 

of pregnancy include cervical cyanosis and softening, vaginal cyanosis, softening and 

enlargement of the uterus, and breast enlargement and tenderness. 


Urinary tests for pregnancy may occasionally be negative early in the pregnancy. 

False-positive results are rare at any time, unless trophoblastic tumors are present. 

Patients with trophoblastic tumors ranging from benign hydatidiform mole to 

choriocarcinoma can present with incomplete abortion or bleeding during the second

trimester of pregnancy without evidence of fetal activity. Serum hCG is often high 

(false-positive pregnancy test). 

Ectopic pregnancies and spontaneous abortions may rarely cause false-negative results 

on urine immunologic pregnancy tests. 

Differential Diagnosis of Pregnancy 

The differential diagnosis of pregnancy includes disorders producing secondary 

amenorrhea (endocrinopathies, emotional stress, drugs, malnutrition, and menopause) 

and those producing abdominal or uterine enlargement (obesity, tumors, 

pseudopregnancy [pseudocyesis]). 

DISCOMFORTS OF PREGNANCY 

Pregnant women are subject to many discomforts, any of which may cause a visit to the 

emergency department. If drug therapy of these complaints is contemplated, only drugs 

generally recognized as safe in pregnancy should be used, and the patient should be 

informed of potential benefits and risks. Common problems include vomiting, backache, 

syncopal attacks, urinary symptoms (with and without demonstrable urinary tract 

infection), heartburn, constipation, hemorrhoids, varicose veins, leg swelling, and 

cramps. 

Rarely, pregnant women may have severe abdominal pain localized to one or another 

quadrant. Patients with round ligament pain may present in this manner. The pain tends 

to be fairly constant, not cramping. Temperature and white blood cell count are usually 

normal. Treatment consists of oral analgesics and bed rest. 

Nausea and vomiting are common in the first trimester and usually occur in the morning. 

Patients with persistent vomiting (hyperemesis gravidarum) with dehydration, elevated 

specific gravity of urine, ketonuria, and hemoconcentration may require hospitalization 

for parenteral hydration and nutrition. Symptomatic treatment of nausea and vomiting is 

preferred, for example, eating soda crackers immediately on arising in the morning, or 

consuming small, frequent, low-fat meals. 

HYPEREMESIS GRAVIDARUM 


Hyperemesis gravidarum is usually easily diagnosed. However, other causes of 

vomiting, such as infection, diabetes mellitus, or abdominal disorders, must be 

excluded. 


Patients who are known to be pregnant or have symptoms and signs of pregnancy (see 

above) complain of persistent vomiting, often with postural dizziness, presyncope, 

weight loss, or other signs of dehydration. Hyperemesis gravidarum usually resolves 

early in the second trimester. Physical examination reveals signs of dehydration: 

hypotension or postural hypotension, tachycardia, dry mucous membranes, and

collapsed neck veins. Patients are rarely in severe shock. 


The test for pregnancy usually is positive, although rarely urinary tests may be negative 

early in pregnancy. Blood tests may show hemoconcentration, elevated blood urea 

nitrogen or creatinine, hypokalemia, or metabolic alkalosis. The urine usually appears 

concentrated with high specific gravity and ketonuria. 

Treatment 


Insert an 18-gauge intravenous catheter (a larger bore is rarely needed). Draw blood for 

CBC, electrolytes, and renal function. Infuse crystalloid solution containing glucose (eg, 

0.9% saline with 5% dextrose) to correct hypovolemia. (Glucose administration will 

inhibit ketogenesis.) The amount and rate of administration depends on the severity of 

dehydration. Replace potassium as needed. 

B. Antiemetics 

If emesis persists, administer an antiemetic. Use prochlorperazine, 5-10 mg 

intravenously (or intramuscularly); promethazine, 25 mg intravenously (or 

intramuscularly); or ondansetron, 8 mg orally twice daily. 

Medications should be avoided during the first 10 weeks of pregnancy because of fetal 

organogenesis, but a risk-to-benefit ratio must be weighed on a case-by-case basis. 

The patient should be made aware of such risks before being given antiemetics. 

Disposition 

Hospitalize patients who have persistent vomiting or ketonuria. Patients whose emesis 

is controlled and whose ketonuria resolves may be discharged with telephone follow-up 

in 1-2 days. Antiemetic tablets or suppositories may be prescribed for the patient to use 

only as needed. 

THIRD-TRIMESTER BLEEDING 


The most common causes of third-trimester bleeding are abruptio placentae, placenta 

previa, lower genital tract bleeding, or systemic coagulopathy. The least severe cause, 

lower genital tract bleeding, should be diagnosed only after the more severe conditions 

have been excluded systematically. 

Third-trimester bleeding must be treated as a grave emergency threatening the life of 

both mother and fetus. Vaginal, rectal, or speculum examination must never be done in 

the emergency department, because it may initiate hemorrhage. 


A. Placental Disorders

1. Abruptio placentae—Premature separation of the placenta from the endometrium is 

characterized by severe abdominal and pelvic pain and tenderness. The separation is 

associated with hemorrhage into the subplacental space (between the uterus and the 

placenta). In most cases, patients present with vaginal bleeding. Several risk factors are 

associated with abruptio placentae, including advanced maternal age, multiparity, 

smoking, hypertension, external abdominal trauma, cocaine use, or a history of previous 

abruption. Signs and symptoms include uterine tenderness, vaginal bleeding, back or 

abdominal pain, and an increase in contractions. In some cases, however, the 

subplacental hemorrhage may be concealed (occult abruption). 

Preeclampsia-eclampsia is common, and disseminated intravascular coagulation may 

occur. 

2. Placenta previa—A placenta implanted in the lower uterine wall usually causes 

painless bleeding in small volumes that occurs regularly over a short period of 

observation. Such seemingly small blood loss may produce a false sense of security, 

because sudden massive hemorrhage can occur at any time. Risk factors for placenta 

previa include increased age, increased parity, multiple gestations, and previous 

cesarean sections or abortions. 

B. Systemic Coagulopathies 

Coagulation disorders are uncommon as the sole cause of third-trimester bleeding. 

Diagnosis is confirmed by routine coagulation studies. 

Treatment 


Obtain emergency obstetric consultation. Evaluate the patient for hypovolemia (as 

shown by supine or postural hypotension), and if present, correct it with intravenous 

infusion of crystalloid solution or whole blood. 


Insert a large-bore (= 16-gauge) intravenous catheter. Draw blood for CBC, coagulation 

studies (prothrombin time, partial thromboplastin time, fibrinogen, and platelet count), 

and measurement of blood urea nitrogen and serum creatinine. Type and cross-match 

for 4 units of whole blood, preferably fresh. 

Monitor fetal heart tones and toxicology especially looking for the presence of cocaine. 

Obtain urine for urinalysis, and monitor urine output with an indwelling urinary catheter. 

C. Other Considerations 

Ultrasound should be used to determine the placental location, but this should not delay 

delivery if the fetus is in distress. 

The pregnant patient should never be maintained for any length of time in the supine, 

recumbent position (see Trauma in Pregnancy, below). 

Disposition 

Hospitalize the patient immediately, and move her to a delivery unit as soon as possible.

Fetal bradycardia increases the urgency of the need for cesarean section. 

TOXEMIA OF PREGNANCY (Preeclampsia-Eclampsia) 


Preeclampsia-eclampsia describes a condition that covers a spectrum of symptoms and 

a continuum of severity. The condition is characterized by pregnancy-induced 

hypertension, by proteinuria, and when severe (eclampsia), by seizures. Symptoms of 

preeclampsia and eclampsia are so variable that whenever a woman in the third 

trimester of pregnancy or early postpartum period comes to the emergency department 

with any complaint, her blood pressure should be checked and urinalysis performed to 

detect early signs of preeclampsia-eclampsia. 


Symptoms and signs are variable and may include headache, various visual symptoms, 

and vertigo. Nausea and vomiting, hyperreflexia, and abdominal pain may occur. 

Especially alarming is pain in the upper right quadrant and epigastrium (so-called 

hepatic pain), which is due to compression of the swelling liver by its capsule. 

Nervousness, irritability, and even frank seizures may occur. 

Hypertension or rising blood pressure relative to the patient's normal blood pressure is a 

significant sign. Note that blood pressure may not be sufficiently elevated to be 

considered abnormal because of the physiologic decline in blood pressure usually 

associated with pregnancy. 

Peripheral edema is usually present. Spasm of retinal arterioles and hemorrhage may 

occur. Hepatomegaly or hepatic tenderness (or both) may be present. 


Critical laboratory findings confirming the diagnosis of preeclampsia-eclampsia are 

decreased urine output, elevated blood urea nitrogen and serum creatinine levels, 

decreased creatine clearance, proteinuria, and evidence of disseminated intravascular 

coagulation. 


Patients with suspected preeclampsia-eclampsia should be evaluated by an obstetrician 

before they are discharged from the emergency department. 

A. Mild Preeclampsia 

Mild preeclampsia is characterized by diastolic blood pressure under 105 mm Hg, trace 

to 1+ proteinuria, good urinary output, and absence of other symptoms. The patient 

should rest in bed at home and must be closely monitored (eg, twice weekly). 

B. Moderate to Severe Eclampsia 

Moderate to severe eclampsia is characterized by proteinuria greater than 2+, diastolic 

blood pressure greater than 105 mm Hg, seizures, anuria, or severe edema. Hospitalize 

patients who are more than mildly ill or who worsen on bed rest at home. It is better to

err on the side of hospitalization, because eclampsia occurring out of the hospital 

greatly increases the chances of maternal or fetal death. 

Treat hyperreflexia with magnesium sulfate, 2-6 g in 50 mL half-normal or normal saline 

given over 30 minutes as an intravenous loading dose, followed by 2 g/h. 

Treat hypertension with intravenous hydralazine (Alazine, Apresoline), 20 mg in 50 mL 

of lactated Ringer's injection or 5% dextrose in water, infused at a rate of 1 mg every 2 

minutes. An infusion pump should be used if possible. When blood pressure falls below 

160/110 mm Hg, slow the infusion to a rate of about 1 mg/h, and adjust to maintain 

desired blood pressure. Do not reduce blood pressure to "normal" levels (120/80 mm 

Hg), because renal shutdown may result. Hypertension may also be controlled using 

nitroprusside or labetalol. Continued seizure activity raises the possibility of intracranial 

pathology such as a cerebral hemorrhage, and a CT scan of the head may be in order. 

Insert a Foley catheter. Monitor fluid intake and urinary output closely, and test urine for 

specific gravity and hematuria. 

When neurologic and cardiovascular status is stable, transfer the patient to a hospital 

equipped to manage high-risk obstetric patients. 

TRAUMA IN PREGNANCY 

Trauma due to gunshot wounds, assault, or automobile accident may cause abruptio 

placentae, ruptured fetal membranes, or direct fetal trauma. 

A. Normal Physiologic Changes 

An awareness of the normal physiologic changes in pregnancy is important in 

evaluating and providing treatment to the mother and fetus. 

• Systolic and diastolic blood pressure decreases approximately 10 mm Hg by the 

middle of the second trimester. 

• Resting heart rate increases by 10-15 beats. 

• Uterine blood flow increases to 17% of the cardiac output. 

• Hematocrit decreases to a range of 30-36%. 

• Tidal volume increases by 30-40%. 

• Residual volume and functional residual capacity decrease. 

• Leukocytosis is common by the second trimester. 

• PCO 2 decreases to approximately 35 mm Hg (mild respiratory alkalosis). 

B. Injuries 

1. Blunt abdominal trauma—Motor vehicle accidents account for most trauma. Be

aware of abruptio placentae or uterine rupture. 

2. Penetrating abdominal injuries—During pregnancy, the physical response to 

intraperitoneal irritation may be decreased. A cephalad and lateral displacement of 

maternal intraabdominal viscera occurs. 


The Kleihauer-Betke test detects fetal blood cells in the maternal circulation and is a 

helpful means of quantifying fetal bleeding; it may help identify fetal hypovolemia before 

obvious fetal distress occurs. 

Treatment 

A. Blunt Abdominal Trauma 

Beyond 24 weeks' gestation the patient should be placed in the left lateral decubitus 

position unless potential spinal injury is a concern. For the patient who is unable to have 

her spines cleared clinically, maintain spinal immobilization on a long, rigid spine board 

tilted slightly to the left. Ensure that ventilation and resuscitative measures are 

adequate. Anticipate rapid oxygen desaturation and aggressively treat any acidosis. A 

complete physical examination including a bimanual exam for evaluation of the cervical 

os should be completed. Maternal vital signs, vaginal bleeding, and any abdominal 

tenderness should be the focus of examination. 

For a pregnancy greater than 20 weeks' gestation, use a standard fetal monitor to 

monitor fetal heart tones and contractions. Fetal distress may precede maternal 

hemodynamic instability as an indicator of inadequately resuscitated shock. The need 

for aggressive resuscitation measures cannot be overemphasized because blood loss is 

easily underestimated. Early notification of surgical and obstetrical consultants is 

important. Radiologic studies should proceed as indicated. 

B. Penetrating Trauma 

Most gunshot wounds to the abdomen should be explored surgically. In a pregnant 

patient, unstable vital signs with any penetrating abdominal wound is an indication for a 

laparotomy. However, not all penetrating trauma requires surgery. For instance, stab 

wounds to the lower abdomen are less likely to cause visceral injuries than upper 

abdominal wounds and may not need exploratory laparotomy. Although generally 

considered contraindicated in pregnancy, diagnostic peritoneal lavage (Chapter 6) may 

help diagnose hemoperitoneum and the need for surgery. 

The decision to perform surgery with or without delivery should be made in conjunction 

with a surgeon and an obstetrician. Several factors are used to make interventional 

decision, including gestational age, penetration of amniotic cavity, and fetal injury. 

Perimortem Cesarean Delivery 

A. Indications 

A fetus may survive up to 30 minutes after maternal cardiac arrest, but the greatest 

likelihood for fetal survival is if delivery occurs within 4-5 minutes after maternal cardiac 

arrest. Another indication for a perimortem cesarean section is to improve the ability to

complete maternal cardiopulmonary resuscitation. 

B. Technique 

1. Cardiopulmonary resuscitation should continue throughout the procedure. 

2. Make an abdominal incision approximately 4-5 cm below the xiphoid to 2-3 cm above 

the pubis. 

3. Separate the rectus muscles bluntly in the midline and enter the peritoneum with a 

midline incision usually below the umbilicus. 

4. Make a vertical incision from the top of the uterine fundus to above the opaque 

insertion of the bladder. 

5. Remove the fetus. 

6. Remove the placenta. 

7. Close the uterus in one or two layers using large sutures. 

LABOR & DELIVERY 

In many hospitals, patients in active labor are seen initially in the emergency 

department. A calm and orderly approach to evaluation of these patients—as well as 

established policies for transfer of responsibility from emergency department staff to 

obstetric staff—is essential for proper management. 

Evaluation 

A. History 

If records from prenatal visits are not available, ask the patient about recent or 

intercurrent illness and risk factors such as diabetes mellitus, valvular heart disease, or 

previous cesarean section delivery. Ask whether the membranes have ruptured. 

Determine parity. Estimate the due date and gestational age of the fetus. 


Record complete maternal vital signs. Perform brief physical examination of the mother. 

Determine frequency and intensity of uterine contractions. 

Check for vaginal discharge by speculum examination (blood or meconium). The 

presence of amniotic fluid may be detected by an alkaline reaction (yellow turning to 

blue) with Nitrazine paper. 

Determine fetal position, and sketch it on an outline of the female figure. Determine the 

fetal heart rate during and between uterine contractions. 

Perform vaginal examination. Note: Do not perform digital examination if vaginal 

bleeding is present. Determine the presenting part and the degree of dilation and

effacement of the cervix by speculum. 


Progressive labor is characterized by uterine contractions occurring every 3 minutes 

and dilation of the cervical os. Abnormal signs requiring emergency obstetric 

consultation include fetal bradycardia (< 100 beats/min during or after uterine 

contractions, vaginal bleeding (on history or examination), transverse or breech 

presentations, and maternal illness (eg, eclampsia, coma, major trauma). 

Treatment 

A. Premature Birth 

Infants under 36 weeks' gestational age are likely to require neonatal intensive care. If 

there is no such nursery in the facility where the mother has sought treatment, consider 

transferring her to another facility unless she is in active labor and delivery is imminent 

or likely during transport (ie, baby is crowning or very low station). See Chapter 5 for 

further discussion. Children are better off being born at the site where the nursery exists 

than being transferred to the site after birth. 

Give crystalloid solution, 1000 mL over 3-4 hours, and monitor cardiovascular status 

carefully. In consultation with an obstetrician, decisions can be made about the use of 

tocolysis, administration of maternal betamethasone for fetal lung maturity, and 

prophylaxis against group B streptococci by administration of penicillin G. 

B. Routine Labor 

When delivery is imminent, give nothing (or sips of clear fluids only) by mouth. Maintain 

or reinstate adequate hydration with intravenous fluids. Give analgesia if there are no 

contraindications. Obtain a baby warmer, if available, and try to have a labor and 

delivery nurse present. Notify the patient's obstetric care provider that she is in the 

hospital and in active labor. 

C. Emergency Department Delivery 

If the examiner determines that the presenting part is in vertex position and is near the 

vulva, it is probably better to allow the patient to deliver in the emergency department 

than to rush her into elevators and through corridors to the delivery unit. 

1. Delivery—Analgesia may be given as needed to the mother with an uncomplicated 

term pregnancy. Delivery may be accomplished in either the lithotomy or the Sims 

position. Try to prepare a clean field (wash the vulva and perineum). Prevent sudden 

uncontrolled delivery of the fetal head. 

Clear the infant's nasal passages and airway. If thick meconium staining of the amniotic 

fluid is present, be prepared to clear the newborn's airway carefully and immediately, 

that is, clear the nostrils with a suction bulb (or DeLee suction trap, if available) after the 

head is delivered but before the body is delivered. Check for the umbilical cord. The 

physician may need to intubate the infant immediately, before spontaneous respirations 

occur, and apply suction to the trachea.

Cut the umbilical cord after ligating it about 2-3 in (5-7.5 cm) from the infant's abdomen. 

Deliver the placenta with gentle traction on the cord if it comes out easily. Massage the 

fundus to help obtain hemostasis and uterine tone. If the patient is not bleeding 

vigorously, the placenta may be left in place while the patient is sent to the delivery 

room for further measures (eg, suture of lacerations). 

2. Postpartum measures—Dry and examine the infant, and resuscitate if necessary. 

Keep the baby warm. 

Monitor the mother's blood pressure every 5 minutes for 15 minutes and then every 15 

minutes for 1 hour. A sample of the infant's clotted cord blood should be sent for ABO 

and Rh typing and a serologic test for syphilis. 

Disposition 

Hospitalize the newborn infant and mother for evaluation and supportive care. 

POSTPARTUM HEMORRHAGE 


• History of recent delivery. 

• Painless, sudden, brisk vaginal bleeding. 


Rarely, a patient returns to the hospital a few days after delivery with brisk vaginal 

bleeding that may or may not be associated with hemorrhagic shock. The usual causes 

of postpartum hemorrhage are uterine atony, retention of products of conception, or 

uterine rupture following cesarean section. Other possible causes are subinvolution of 

the placental site, vaginal tears, or bleeding from an episiotomy. Signs of postpartum 

hemorrhage may include an enlarged uterus suggestive of atony, a vaginal mass 

suggestive of an inverted uterus, or uterine bleeding with good uterine tone and a 

normal size suggestive of retained products of conception. 



Treat hemorrhagic shock, if present (Chapter 9). If bleeding is brisk, insert the fingers of 

one hand into the vagina, and compress the uterus against the abdominal wall. Insert a 

large-bore (= 16-gauge) intravenous catheter, and start infusion of crystalloid solution, 

followed by whole blood if the hematocrit falls. Monitor vital signs and urinary output. 


Draw blood for CBC, coagulation studies (prothrombin time, partial thromboplastin time, 

and platelet count), blood urea nitrogen, and serum creatinine. Type and cross-match

for 4 units of blood. 

C. Consultation 

Obtain emergency obstetric and gynecologic consultation. 

D. Medications 

Oxytocin, 20-30 mIU in 1 L of fluid given at 200 mL/h may be used for uterine atony. 

After an obstetrical consult is obtained, methylergonovine (Methergine) by mouth may 

be recommended prior to discharge. 

E. Definitive Treatment 

The definitive treatment is dilation and curettage, which should be performed by an 

obstetrician, because postpartum surgery may result in uterine perforation. 

Disposition 

If the cause of bleeding is definitively treated and the patient is otherwise stable, she 

can be discharged with close follow-up in 2-3 days. All other patients should be 

hospitalized and obstetric consultation obtained as needed. 

PUERPERAL SEPSIS & ENDOMETRITIS 


• History of recent delivery. 

• Systemic signs of infection. 

• Abdominal pain, vaginal discharge. 

• Peritoneal signs. 

• Boggy, tender uterus and purulent lochia. 


Symptoms of puerperal sepsis in the early postpartum period are fever, peritoneal pain, 

and vaginal discharge. Examination reveals abdominal tenderness, exquisite uterine 

tenderness, and purulent lochia with leukocytes and bacteria on Gram stain. 


If signs of sepsis are present, obtain obstetric and gynecologic consultation, and 

hospitalize the patient immediately. Patients with minimal symptoms may be managed 

as outpatients. Obtain samples of blood and discharge for diagnostic culture and 

sensitivity testing. Start antibiotics in accordance with the following recommendations: 

A. Severely Ill Patients 

Give cefotaxime, 1-2 g intravenously every 6-8 hours; or a combination of ampicillin, 1 g 

intravenously every 6 hours, and gentamicin, 1.5 mg/kg intravenously every 8 hours. 

Before beginning treatment with gentamicin, obtain baseline serum creatinine levels;

during treatment, obtain serum creatinine levels 1-2 times per week, and follow 

gentamicin peaks and troughs weekly. 

B. Mildly Ill Patients 

Doxycycline, 100 mg orally twice daily (or tetracycline, 500 mg orally 4 times daily), or 

ampicillin, 500 mg orally 4 times daily for 10-14 days, may be used for outpatients. 

Caution: Do not use doxycycline or tetracycline if the patient is breast feeding. 

PUERPERAL MASTITIS 


• Postpartum breast infection. 

• Increased localized breast pain. 

• Variable systemic signs of infection. 

• Localized tenderness, redness, induration, or warmth. 


Postpartum infection of the breast is almost always due to infection with Staphylococcus 

aureus. Pain, induration, redness, and warmth in the affected breast characterizes 

mastitis. Fever, chills, malaise, and axillary adenopathy may be present. 

The diagnosis of puerperal mastitis is based on systemic signs of infection, pain, and 

tenderness of the involved breast. Abscess formation may occur, and blood cultures are 

occasionally positive. 


A. Mild Cases (Afebrile) 

Apply warm compresses to the affected breast. The patient may continue to breast feed. 

The patient should be given dicloxacillin, 500 mg by mouth twice daily, or cephalexin, 

500 mg by mouth twice daily. Consultation with a lactation expert may be in order. Close 

follow-up with the obstetrician is recommended. 

B. Severe Cases (Suspected Abscess) 

Hospitalize the patient, and obtain surgical consultation. Give nafcillin or equivalent, 150 

mg/kg/d intravenously. Penicillin-allergic patients may be given clindamycin, 450 mg 

intravenously every 8 hours, or erythromycin, 0.5 g intravenously every 6 hours. 

American College of Obstetricians and Gynecologists: Trauma During Pregnancy. 

ACOG Technical Bulletin No. 161. American College of Obstetricians and 

Gynecologists, 1991. 

Chames MC et al: Late postpartum eclampsia: a preventable disease? Am J Obstet 

Gynecol 2002;186:1174. [PMID: 12066093]

Coleman MT, Trianfo VA, Rund DA: Nonobstetric emergencies in pregnancy: trauma 

and surgical conditions. Am J Obstet Gynecol 1997;177:497. [PMID: 9322613] 




36. Obstetric & Gynecologic Emergencies & Rape 1 - Melissa Platt, MD, & 

Mary Nan Mallory, MD, RDMS 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS

Table 36-1. Causes of abnormal vaginal bleeding. 






TABLES 

Table 36-1. Causes of abnormal vaginal bleeding.

Table 36-2. Differential diagnosis of pelvic pain. 

History and 

Symptoms 

Quality of Pain 

Laboratory Findings 

Type of 

Vaginal 

Discharge Cervix 

Adnexal 

Mass

Table 36-3. Clinical manifestations of common pelvic disorders. 

Possible Causes 

Trauma 

Postpartum hemorrhage 

Dysfunctional uterine bleeding 

Carcinoma 

Salpingitis and tubo-ovarian abscess 

Ruptured ovarian cyst 

Torsion of tube and ovary 

Mittelschmerz 

Abdominal disorders (appendicitis, etc.) 

Dysmenorrhea 

Endometriosis 

Endometritis 

Placenta previa 

Ectopic pregnancy 

Spontaneous abortion 

Abruptio placentae 


Degenerating fibroid (leiomyoma) 

Normal labor 

Labor with placenta previa 

Abruptio placentae 

Septic abortion 

Puerperal sepsis 







TABLES 

Table 36-3. Clinical manifestations of common pelvic disorders.

Table 36-4. Classification of spontaneous abortion. 

Symptoms and Signs 

Mild, transient uterine 

cramps with minimal 

transient vaginal bleeding. 

Uterine cramps and 

vaginal bleeding are 

persistent and excessive. 

Uterine cramps markedly 

diminish or stop. 

Uterine size is compatible with the presumed length of 

pregnancy. 1 

Inevitable abortion The cervical os is 

sponge stick pass 

Symptoms and signs of pregnancy disappear. 

Products of conception are noted in the vagina, or the 

patient gives a history of passage of tissue. 

The entire conceptus is expelled. 

Missed abortion Symptoms and si 

pregnancy tests c 

Uterine cramps are rare. Examination shows a small 

and irregularly softened uterus. 

1 

Uterine size in centimeters measured from the top of 

the symphysis pubica to the top of the uterine fundus is 

a useful approximation of gestational age in weeks from 

15-16 weeks through 32-33 weeks. A normal 20-week 

gestational age uterine size should be at the level of the 

umbilicus.

Figure 36-1. Bedside endovaginal ultrasound of an intrauterine pregnancy. An 

intrauterine gestational sac with a yolk sac is clearly visualized. 






FIGURES 

Figure 36-1

Figure 36-2. Bedside endovaginal ultrasound of an intrauterine pregnancy. An 

intrauterine gestational sac containing both a yolk sac and fetal pole is noted 






FIGURES 

Figure 36-2

Figure 36-3. Diagnostic algorithm for the patient with possible ectopic pregnancy. IUP = 

intrauterine pregnancy. 






FIGURES 

Figure 36-3

Figure 36-4. Endovaginal ultrasound clearly demonstrating an ectopic pregnancy. A: 

Longitudinal view of the uterus with a well-defined endometrial stripe and no intrauterine 

gestational sac. A gestational sac is noted posterior to the uterus. B: Transverse view of 

the uterus and right adnexa also demonstrating an extrauterine gestational sac. C: 

Longitudinal view demonstrating free fluid in the cul-de-sac. 






FIGURES 

Figure 36-4

Figure 36-5. Bedside transabdominal ultrasound of free fluid in Morison's pouch 

(hepatorenal space) secondary to a ruptured ectopic pregnancy. 






FIGURES 

Figure 36-5



CONDITIONS 

OLIGURIA OR ANURIA 


1 This chapter is a revision of the chapter by John Mills, MD, & Jack W. McAninch, MD, 


Decreased or absent urine output can occur from widely diverse disease states such as 

intravascular volume depletion or bladder outflow obstruction. In attempting to 

determine the cause of decreased urine output, it is helpful to categorize the mechanism 

as prerenal (eg, resulting from decreased or abnormal renal perfusion), renal (eg, 

resulting from intrinsic renal disease), or postrenal (eg, disease of the urinary collecting 

system distal to the renal parenchyma). 

A. Prerenal Causes 

Prerenal causes include hypovolemia, sepsis, and heart failure. 

B. Renal Causes 

Renal causes include tubular, glomerular, vascular, or interstitial disease. 

C. Postrenal Causes 

1. Supravesical obstruction—Supravesical obstruction rarely causes oliguria or 

anuria, because bilateral disease is required to reduce decreased urine flow. There are 

two types of supravesical obstruction: (1) ureteral obstruction (usually tumor) and (2) 

ureteropelvic or ureterovesical obstruction. 

2. Intravesical or infravesical obstruction—Intravesical or infravesical obstruction is 

more common than supravesical obstruction (Table 37-1). Causes include prostatic 

hypertrophy or carcinoma, drugs with atropinic or adrenergic effects, neurologic 

diseases, bladder stones or tumors, and urethral strictures or valves. 


A. History 

1. Obstruction—Differentiate between reduced urine output (with normal or nearly 

normal voiding patterns) and oliguria associated with difficult in voiding, feeling of 

incomplete voiding, diminished urinary stream, and the like. The latter findings suggest 

obstruction. 

2. Associated medical conditions—Ask about coexisting cardiac, pulmonary, renal, or

other underlying disease that might contribute to renal or prerenal oliguria. 

3. Drugs—The patient's medications might cause problems with urination or be 

nephrotoxic. Anticholinergics and sympathomimetics are most often the culprits of 

urinary retention. 


1. Vital signs—Obtain a complete set of vital signs and orthostatic vitals to determine if 

volume depletion is an issue. Correct volume depletion, if present (Chapter 9). 

2. General examination—Focus on signs of cardiac, pulmonary, renal, or hepatic 

disease that might contribute to oliguria of a prerenal or renal origin. Look for signs of 

volume depletion, such as dry mucous membranes or poor skin turgor. 

3. Distended bladder—Palpate the lower abdomen to determine whether a suprapubic 

mass, consistent with a distended bladder, is present. A distended bladder is 

manifested as a firm (but not hard) mass that is adjacent to the symphysis pubica and is 

dull to percussion. The diagnosis may be confirmed by passage of a Foley catheter; 

ultrasonography; radiologic studies (computed tomography [CT] scan, abdominal x-ray); 

or, if necessary, percutaneous needle aspiration in the event of a urethral stricture, 

stenosis, or injury. 

4. Prostate examination—Examine the prostate. Perform a rectal examination, looking 

especially for masses, prostatic hypertrophy, prostatic tenderness, or prostatic 

dislocation (associated with trauma). 

C. Detection of Bladder Outlet Obstruction 

Bladder outlet obstruction (complete or partial) is strongly suggested by a palpable 

bladder in a patient who is unable to void or who has a weak urinary stream or feeling of 

incomplete voiding. Whether lower abdominal pain is present depends on the rapidity of 

obstruction; acute obstruction causes rapid bladder distention and severe pain if 

sensation is intact. 

Diagnostic features of some of the common causes of bladder outlet obstruction are set 

forth in Table 37-1. 

Treatment 

A. Serious Underlying Disease 

If the patient is acutely ill or obviously in shock, is septic, or has heart failure or other 

serious coexisting conditions that might cause prerenal oliguria, these disorders must be 

evaluated and treated before those of the urinary tract. 

B. Distended Bladder (Presumed Bladder Outlet Obstruction) 

1. Gain intravenous access—Draw blood for complete blood count (CBC), electrolyte 

determination, and blood urea nitrogen and serum creatinine measurements. 

2. Drain the bladder—

a. Urethral catheter—Try to pass an indwelling urethral (Foley) catheter. If this 

maneuver is successful, drain the bladder, record the volume of urine obtained, and 

send a specimen for urinalysis and culture. Monitor the patient for postobstructive 

diuresis. Gradual bladder draining is not a proven method of decreasing bladder atony 

or mucosal hemorrhage. If bladder outlet obstruction is relieved by passage of a Foley 

catheter and is apparently due to a transient cause (eg, drugs), the catheter may be 

removed and the patient observed for ability to void after the effects of any drugs are 

presumed to have dissipated. In patients with fixed bladder outlet obstruction (eg, 

benign prostatic hypertrophy), leave the catheter in place, and obtain urologic 

consultation within 1 week. 

b. Suprapubic catheter—If a standard Foley catheter cannot be passed secondary to 

prostatic hypertrophy, reattempt passage using a coude catheter (which has a curved 

tip that usually allows passage beyond the enlarged prostate). If the coude catheter is 

unsuccessful and a urologist is not available, insert a suprapubic catheter for temporary 

drainage (Chapter 6). A large (16-gauge) needle-clad catheter (eg, Intracath) will 

provide satisfactory emergency bladder drainage. 

3. Treat cystitis and prostatitis, if present—See "Dysuria" section, below. 

4. Hospitalize patients as needed—Hospitalize patients who have systemic symptoms 

(fever, rigors, intractable emesis) and those who need additional diagnosis and 

treatment (eg, for management of postobstructive diuresis, azotemia, sepsis, or 

electrolyte abnormalities). 

C. Bladder Not Palpable; Patient Able to Void BR>If the patient can void on 

command but continues to have subjective or objective evidence of a weak urinary 

stream or if the patient experiences a feeling of incomplete voiding, partial bladder outlet 

obstruction is likely. 

Draw blood for CBC, electrolyte, blood urea nitrogen, and serum creatinine 

measurements. Send a urine specimen for urinalysis and culture. Treat cystitis or 

prostatitis, if present. 

If blood chemistry results and urinalysis are normal, refer the patient to a urologist. The 

presence of azotemia or electrolyte abnormalities indicates severe or long-standing 

obstructive uropathy, and the patient likely requires hospitalization. 

D. Bladder Not Palpable; Patient Unable to Void 

Consider the following in the differential diagnosis (1) intrinsic renal disease, (2) occult 

prerenal disease (unlikely, because most causes would be obvious on brief physical 

examination), (3) occult bladder outlet obstruction, or (4) supravesical obstructive 

uropathy (rare). 

Draw blood for CBC; serum glucose, electrolyte, calcium, and phosphorus; and tests of 

renal and hepatic function. Obtain chest and abdominal x-rays to help evaluate the size 

of the kidneys and bladder. Ultrasonography is the best noninvasive test for evaluating 

kidney and bladder size.

Ensure adequate hydration. In an adult without obvious volume overload (eg, pulmonary 

or peripheral edema), give 1-2 L of fluid orally or intravenously, and observe the patient 

for 1-2 hours. In an individual with normal kidneys, this amount should produce a brisk 

flow of urine. 

If anuria persists despite adequate hydration and if the bladder is not distended, the 

cause of the anuria is likely to be proximal to the bladder (prerenal, renal, or, rarely, 

bilateral ureteral obstruction). Bladder catheterization, with strict adherence to sterile 

technique, should be performed to confirm the lack of urine output. Hospitalize the 

patient for further evaluation. 

Disposition 

Hospitalization is required for patients with persistent unexplained anuria or severe 

oliguria (< 500 mL/d), those with systemic symptoms, and those with markedly 

abnormal electrolytes or renal function. 

Patients with partial bladder outlet obstruction (ie, weak urinary stream, with or without 

palpable bladder) should be referred to a urologist if renal function is normal or nearly 

normal. 

Asymptomatic patients with an indwelling urethral catheter should be reexamined or 

referred to a urologist within 1 week. 

SCROTAL PAIN (See Table 37-2. ) 


• Trauma is a common cause. 

• Infection accounts for orchitis and epididymitis. 

• Flank pain, hematuria, and scrotal pain usually indicate urolithiasis. 

• Incarcerated hernias cause scrotal pain. 

• Testicular torsion requires urgent diagnosis to salvage the testicle. A torsed testis may 

be high riding or horizontally lying; ultrasound will show diminished blood flow to the 

torsed testis. 


A. Trauma 

(See also Chapter 26.) Trauma commonly causes testicular or scrotal pain. Careful 

questioning may be required to elicit the circumstances under which the trauma 

occurred. 

B. Viral Orchitis 

Mumps virus and the enteroviruses may cause acute unilateral or bilateral orchitis. In 

orchitis due to mumps virus, associated parotitis is usually present.

C. Urolithiasis 

Rarely, patients with urolithiasis present with pain localized mainly in the scrotum; 

however, in most cases, back or flank pain has preceded the scrotal pain, or a history of 

nephrolithiasis is present. In such cases, the testicle and epididymis are normal to 

palpation. Hematuria is an important diagnostic clue. The diagnosis may be confirmed 

by unenhanced helical CT, intravenous pyelogram, or KUB (radiograph of the kidneys, 

urethras, and bladder). 

D. Incarcerated Hernia 

Inguinal hernias incarcerated in the scrotum may cause scrotal pain that may be 

confused with testicular pain. Bowel sounds are heard in the scrotum early in 

incarceration; if the hernia strangulates, bowel sounds are no longer audible. Intestinal 

hernia is almost always associated with clinical findings of intestinal obstruction 

(Chapter 13). Ultrasonography is diagnostic. 

E. Testicular Torsion, Epididymitis, and Torsion of the Testicular Appendages 

(See Table 37-2.) Torsion of a testicular appendage, epididymitis, and testicular torsion 

are the 3 most common causes of acute scrotal pain and account for approximately 

85-90% of cases. Because of the urgency to diagnose and treat testicular torsion within 

6 hours to prevent loss of the testis, testicular torsion must be promptly ruled out in all 

patients with scrotal pain. It may be difficult to distinguish from epididymitis or torsion of 

testicular appendages as edema and inflammation progress to involve the entire scrotal 

sac and contents. 

1. Testicular torsion—Testicular torsion tends to occur in young men and is rare in 

men over age 30 years; however, it can and does occur at all ages. There is often a 

history of episodes of similar scrotal pain, representing torsion with spontaneous 

repositioning of the testicle. The pain is abrupt in onset, severe, unilateral, and often 

associated with nausea and vomiting. Tenderness is initially noted only in the testicle; 

however, with persistent torsion and the resulting testicular hypoxia, pain and 

tenderness spread to involve contiguous intrascrotal structures. 

Examination early in the illness shows an elevated testicle that is apt to have a 

horizontal lie (Bell clapper deformity). The epididymis may be felt in an abnormal 

position (eg, anteriorly) in the early stages. Later, the entire scrotal contents become 

swollen and tender, making the examination extremely difficult and less informative 

because the epididymis becomes indistinguishable from the testis on palpation. 

2. Epididymitis—Epididymitis tends to occur in sexually active men over age 20 years 

and is the most common misdiagnosis for testicular torsion. There may be a history of 

urinary tract infection or urethritis. Pain begins gradually and is less severe than in 

testicular torsion. The Prehn sign is present if the pain is reduced when the scrotum is 

elevated. This finding is not specific to epididymitis nor is it a reliable discriminating 

clinical sign. Physical examination reveals a tender epididymis, often unilateral and 

often with erythema and edema of the scrotal skin. Early on, the testicle may be normal 

or minimally tender. However, as edema worsens, the epididymis becomes 

indistinguishable from the testicle on palpation, and a reactive hydrocele may develop, 

making it difficult to differentiate epididymitis from testicular torsion. Urinalysis frequently

shows pyuria and possibly bacteriuria if a concomitant urethritis or urinary tract infection 

is present. Doppler ultrasound shows increased blood flow to the affected testis, in 

contrast to the decreased blood flow seen in testicular torsion. 

3. Torsion of testicular or epididymal appendages—Of the 4 appendages, the 

appendix testis, located on the anterosuperior pole of the testis, is the most frequently 

(92%) torsed appendage followed by the appendix epididymis (7%), located on the head 

of the epididymis. Pain is usually sudden in onset and can be severe, with nausea and 

vomiting. Physical examination occasionally (21%) reveals a small, tender, firm nodule 

("blue dot" sign), representing the infarcted appendage in the anterosuperior pole of the 

testis. The scrotal skin and testicle are usually normal and minimally tender. In 

advanced cases, marked edema and appearance of a reactive hydrocele may obscure 

the diagnosis of testicular torsion. 

4. Specialized diagnostic tests for differentiating torsion from 

epididymitis—These tests should not delay emergent urologic consultation and 

surgical treatment of patients with high probability of testicular torsion (ie, patients under 

age 18 years with acute unilateral testicular pain and no signs or recent history of 

urinary tract infection). 

a. Spermatic cord block—Anesthetizing the scrotal contents may facilitate accurate 

examination but should be attempted only by the consulting urologist. Inject lidocaine 

without epinephrine (2%), 5-10 mL, around the spermatic cord at the external inguinal 

ring. 

b. Color-flow Doppler ultrasonography—Color-flow Doppler ultrasonography is the 

diagnostic study of choice at most institutions. It is widely available and has a sensitivity 

of 86-100% and a specificity of 100% as compared with a sensitivity of 80-100% and a 

specificity of 86-100% for radionucleotide imaging. The most frequent sonographic 

finding is absent or diminished blood flow to the affected testis, compared with the 

unaffected side. If the diagnosis is still unclear, then a nuclear study should be pursued. 

Ultrasound is more advantageous than nuclear scanning for elucidating other scrotal 

pathology including varicoceles, hydroceles, hernias, and masses. 

c. Radionuclide scan—In epididymitis, scanning of the scrotum after intravenous 

injection of technetium- 99 m sodium pertechnetate reveals increased scrotal uptake on 

the affected side, whereas torsion shows decreased uptake. 


(See Table 37-2.) If testicular torsion is present, obtain urgent urologic consultation, and 

prepare the patient for immediate surgery. Manual detorsion should be attempted if the 

urologist is not immediately available but should not delay definitive treatment. 

Detorsion of the testicle (either manual or surgical) must be accomplished within 6 hours 

to prevent testicular infarction. Torsion causes the patient's left testicle to rotate 

counterclockwise and the right to rotate clockwise (Figure 37-1); the affected testicle 

should be twisted in the opposite direction when detorsion is attempted. Because the 

testis affected by torsion is usually rotated a minimum of 360 degrees (one turn), the 

physician should initially attempt to untwist the testicle by counter-rotating it one turn.

The testis will usually return to normal position on its own after this maneuver, even if it 

was originally twisted more than one complete revolution. The urologist may choose to 

infiltrate the spermatic cord near the inguinal ring with lidocaine without epinephrine 

(2%), 5-10 mL, to facilitate the maneuver, and give analgesics as needed. Regardless 

of the result of manual detorsion, emergency surgery is indicated to perform 

detorsion—if necessary—and to secure the testicle. Without surgery, torsion may occur 

again at any time. 

In patients with suspected epididymitis or orchitis, urologic consultation should be 

sought if the diagnosis is in doubt. If epididymitis is present, see Chapter 40 for 

treatment. 

Torsion of the testicular appendage (after testicular torsion is excluded) is managed with 

bed rest, scrotal elevation, analgesics, and follow-up care within 1-2 days. Surgical 

excision is often needed for adequate pain control. 

PAINLESS SCROTAL MASS LESIONS (See Table 37-3. ) 


• Malignancy is often painless. 

• A tense hydrocele or a firm spermatocele must be differentiated from a tumor. 

Ultrasound is the diagnostic study of choice. 

• Sudden onset of a varicocele in an older male may be a late sign of a renal tumor. 


Conditions causing painless (relatively painless) scrotal swelling are not true 

emergencies, although testicular tumors are life threatening and require urgent 

evaluation (within a few days). 

Table 37-3 sets forth helpful diagnostic features of conditions associated with painless 

scrotal swelling. Patients with newly diagnosed testicular enlargement or mass lesions 

should be referred to a urologist. 

DYSURIA 


• Painful urination that represents acute inflammation of the urethra, bladder, or 

prostate. 

• Frequency and urgency may also be present. 

• Workup should be guided by other associated symptoms, ie, hematuria or discharge. 

• Urinalysis or sexually transmitted disease testing usually confirms the diagnosis.


Common causes of dysuria and their associated clinical findings are given in Table 

37-4. Urethral diverticula, urolithiasis, endocervical gonorrhea, balanitis, and urethral 

warts are uncommon causes of dysuria. 


A. Dysuria in Males 

1. Urethritis—In males, urethritis is a much more common cause of dysuria than is 

urinary tract infection. Attempt to express urethral discharge by milking the urethra, and 

send the material for culture and smear. If no discharge can be obtained, sample the 

anterior 2-3 cm (3/4-1 3/16 in) of the urethra with a calcium alginate, Dacron, or cotton 

swab, or wire loop; smear some of the urethral section obtained on a slide; and send the 

swab for culture for Neisseria gonorrhoeae. If facilities are available, also send a 

urethral swab in Chlamydia culture medium for culture and fluorescent antibody testing 

for Chlamydia infection. Do not use a wood-handled cotton swab, because wood is toxic 

to the Chlamydia organism. Smears should be stained with methylene blue or Gram 

stain and examined microscopically. The presence of more than 5 leukocytes per × 400 

field indicates urethritis; the presence of intracellular diplococci (gram-negative if a 

Gram stain was done)—especially without other bacteria—indicates gonococcal 

urethritis. See Chapter 40 for treatment of gonorrhea and nongonococcal urethritis. 

Dysuria without evidence of urethral or urinary tract inflammation (< 5 white blood cells 

per × 100 field, negative culture) is rare in men and may represent low-grade infection. 

Treatment for urethritis is usually indicated. 

2. Prostatitis—If no evidence of urethritis is found, obtain a midstream clean-voided 

urine specimen (supervise the patient so that the sample is collected properly). 

Polymorphonuclear neutrophils in the urine in the absence of urethritis are diagnostic of 

urinary tract inflammation. Prostatitis (either alone or associated with urinary tract 

infection) may be excluded by rectal examination. For further information on treatment, 

see Chapter 40. 

3. Urinary tract infection—Leukocytes, usually with bacteria, are found on microscopic 

examination of a midstream urine specimen. Urine dip reagent strips that test for the 

presence of leukocyte esterase and nitrite are equivalent to the urine sediment analysis 

at detecting pyuria when both are positive. They are increasingly being used as a 

screening tool and often eliminate the need for microscopic examination. Culture usually 

shows bacteria of a single species (usually > 10 5 colony-forming units per milliliter but 

occasionally only 10 2 -10 4 , especially with certain organisms [eg, Candida species or 

enterococci]). Note: Urinary tract infection is unusual in men under age 60 years unless 

associated urinary tract abnormalities are present or the patient engages in homosexual 

sexual activity. 

4. Local causes—Inspect the penis and urethral meatus for balanitis and intrameatal 

pathologic structures (warts, herpetic ulcers) that are commonly associated with dysuria. 

Urethral strictures often cause dysuria, and patients may describe a split or intermittent

urinary stream. 

B. Dysuria in Females 

1. Collection of urine—Obtain an uncontaminated urine specimen for microscopic 

analysis. Contamination of the specimen is usually indicated by the presence of 

squamous (vaginal) epithelial cells visible microscopically (eg, =5 cells per × 100 field); 

if these are seen, discard the specimen and obtain another, uncontaminated specimen. 

Proper collection techniques for adults are as follows: 

a. Midstream clean-voided urine—This method of collection is satisfactory in most 

cases but requires a cooperative patient and some coordination. 

b. Catheterization—A small, straight (9F) catheter should be used for quick "in and out" 

catheterization, because it is more comfortable than the 14-19F Foley-type catheter. 

Contamination may occur. 

c. Suprapubic aspiration—(See Chapter 6.) Suprapubic aspiration is useful in special 

situations (eg, for infants) and is associated with a very low contamination rate. 

2. Clinical differentiation of causes of dysuria in women— 

a. Dysuria-frequency syndrome (urethral syndrome) and urinary tract 

infection—These conditions are characterized by dysuria without vaginal symptoms 

(eg, discharge) and by pyuria (< 5 white cells per × 400 field). If bacteria are seen in the 

urinary sediment, urinary tract infection is a more likely diagnosis than urethral 

syndrome. Occasionally women with dysuria-frequency syndrome may have no pyuria. 

b. Local causes—If results on urinalysis are normal, if vaginal symptoms associated 

with dysuria are present, or if pain is felt outside the urinary tract (external dysuria), 

perform a pelvic examination to look for vaginitis, genital herpes, or a urethral caruncle. 

Urethral caruncle is found in postmenopausal woman and is a small, nontender red 

lesion resembling a strawberry on the dorsal aspect of the urethral meatus. In addition, 

it is helpful to culture endocervical mucus for gonococci, because gonococcal infection 

in women may be associated with dysuria. 

C. Dysuria Associated with Hematuria in Either Sex 

The presence of large numbers of erythrocytes in the urine in either sex should suggest 

hemorrhagic cystitis, concomitant urolithiasis, or urethral manipulation (see "Hematuria" 

section, below). 


Treat the various causes of dysuria as follows: 

A. Urinary Tract Infections 

For treatment of cystitis, pyelonephritis, and urethral syndrome, see Chapter 40. 

B. Gonorrhea


C. Vaginitis 


D. Prostatitis 


E. Other Conditions 

Patients with other conditions (eg, urethral stricture or diverticulum) should be referred 

to a urologist or gynecologist for evaluation. 

ATRAUMATIC HEMATURIA 


• Hematuria is often an early sign of genitourinary cancer. 

• Hematuria with associated flank or groin pain is suggestive of urolithiasis. 

• Dysuria and frequency may accompany hematuria of an infectious cause. 


Common causes of hematuria (microscopic defined as > 3 red blood cells per 

high-power field) and their associated clinical findings are set forth in Table 37-5. See 

Chapter 26 for management of hematuria associated with trauma or genitourinary 

manipulation. In all cases of atraumatic hematuria, nonglomerular diseases including 

infection account for 25% of cases, stones account for 20% of cases, and 10% of cases 

have an unknown cause. 

Renal vein thrombosis, renal arterial embolization, drug-induced (cyclophosphamide, 

penicillins) interstitial cystitis, glomerular diseases, abdominal aortic aneurysm, and 

malignancy are less common causes of hematuria. In the elderly, painless gross 

hematuria is malignancy until proven otherwise. 


A. History 

Hematuria associated with abdominal or flank pain and tenderness suggests urolithiasis 

or, less commonly, renovascular disease. Diagnostic clues may come from timing of the 

hematuria. Initial, terminal, or total stream hematuria suggests bleeding from the 

following respective areas: anterior urethral, posterior urethra to trigone, or bladder 

sources or beyond. 

Hematuria associated with dysuria and urinary urgency and frequency suggests 

hemorrhagic cystitis (drug-induced, infectious, or idiopathic). 

Systemic conditions associated with hematuria include thrombotic thrombocytopenic

purpura, Henoch-Schonlein purpura, sickling hemoglobinopathies, excessive 

anticoagulation therapy, or coagulopathies. 

Bleeding from other perineal areas, especially menstrual flow, may be mistaken for 

hematuria. 


Examine the external genitalia for local causes of hematuria (eg, intraurethral trauma). 

Examine the abdomen, back, and pelvis for tenderness and evidence of trauma. 

In males, perform a rectal examination for evaluation of the prostate after a urine 

specimen has been obtained, because prostatic manipulation can induce pyuria. 

C. Laboratory Examination 

1. Urinalysis—Perform urinalysis to confirm the diagnosis of hematuria. Carefully 

performed microscopic examination of a freshly voided midstream urine specimen is 

essential to the evaluation of hematuria; look especially for erythrocyte casts, which 

suggest glomerulonephritis. In men, fractionate urinalysis (initial, midstream, and 

terminal specimens) is also helpful in localizing the source of hematuria. 

2. Other laboratory tests—Further laboratory testing (except possibly urine culture) is 

not usually needed for bacterial hemorrhagic cystitis. Patients with urolithiasis should 

have baseline serum electrolyte determinations and renal function tests, especially prior 

to obtaining an intravenous pyelogram. Patients in whom a bleeding disorder is 

suspected or the cause of hematuria is unknown should have the following laboratory 

examinations: CBC with differential; prothrombin time, partial thromboplastin time, and 

international normalization ratio; serum electrolytes; and renal function. 

D. Special Studies 

An intravenous pyelogram may be necessary for the evaluation of urolithiasis, trauma, 

tumors, and other causes. However, compared with ultrasound, CT scanning is a better 

diagnostic study for evaluation of intra-abdominal pathology and tumors, especially 

those that are less than 3 cm in size. In pregnant females, ultrasound is the test of 

choice for evaluating hematuria. 

Cytoscopy is essential for evaluation of bladder or urethral hematuria due to tumors and 

other causes. It may also be helpful for localizing hematuria of the upper genitourinary 

tract to one side or the other. The need for cytoscopy should be determined by the 

consulting urologist. 

Other studies such as radionuclide scans or angiograms may be needed in special 

situations, but urologic consultation should be obtained before these studies are 

requested. 


Treat the various causes of hematuria as follows: 

A. Trauma


B. Urinary Tract Infection 


C. Suspected Tumor 

Refer the patient to a urologist for evaluation. Consider hospitalization in order to 

expedite diagnostic procedures. 

D. Urolithiasis 

See below. 

E. Glomerulonephritis 

Hospitalize the patient, and obtain consultation with a nephrologist. 

F. Prostatitis 


G. Urethral Strictures and Foreign Bodies 

Refer the patient to a urologist. 

H. Unknown Cause 

Patients with hematuria of an unknown cause need urgent urologic consultation. 

Agrawal M et al: Acute renal failure. Am Fam Physician 2000; 61:2077. [PMID: 

10779250] 

Anderson RU: Management of lower urinary tract infections and cystitis. Urol Clin North 

Am 1999;26:729. [PMID: 10584614] 

Curtis LA et al: Acute urinary retention and urinary incontinence. Emerg Med Clin North 

Am 2001;19:591. [PMID: 11554277] 

Farhat W et al: Urethral syndromes in children. Pediatr Rev 2001; 22:17. [PMID: 

11139643] 

Grossfeld GD et al: Evaluation of asymptomatic microscopic hematuria in adults: the 

American Urological Association best practice policy—part I: definition, detection, 

prevalence, and etiology. Urology 2001;57:599. [PMID: 11306356] 

Grossfeld GD et al: Evaluation of asymptomatic microscopic hematuria in adults: the 

American Urological Association best practice policy—part II: patient evaluation, 

cytology, voided markers, imaging, cystoscopy, nephrology evaluation, and follow-up. 

Urology 2001;57:604. [PMID: 11306357] 

Grossfeld GD et al: Evaluation of asymptomatic microscopic hematuria. Urol Clin North 

Am 1998;25:661. [PMID: 10026773] 

Kass EJ: The acute scrotum. Pediatr Clin North Am 1997; 44:1251. [PMID: 97467752]

Lummus WE et al: Prostatitis. Emerg Med Clin North Am 2001; 19:691. [PMID: 

11554282] 

Miller O et al: Urinary tract infection and pyelonephritis. Emerg Med Clin North Am 

2001;19:655. [PMID: 11554280] 

Sokolosky MC: Hematuria. Emerg Med Clin North Am 2001; 19:621. [PMID: 11554278] 

Strauss S et al: Torsion of the testicular appendages: sonographic appearance. J 

Ultrasound Med 1997;16:189. [PMID: 9166815] 


UROLITHIASIS (Renal Colic) 


• Patients usually present with sudden onset of unilateral flank pain that may radiate to 

the ipsilateral lower quadrant, groin, scrotum, or labia. 

• Hematuria is present in approximately 90% of cases. 

• Spiral CT scan is the diagnostic study of choice at most institutions, but KUB, 

intravenous pyelogram, and ultrasound may also be used. 


Patients with stones in the urinary tract commonly present to the emergency 

department. Stones usually form in the renal pelvis, and symptoms occur with passage 

of the stone into the ureter, as the result of infection, or both. The incidence of stones is 

highest amongst whites with a peak incidence between ages 20 and 50 years, and the 

male to female ratio is 3:1. Bladder stones are less common, and patients may present 

with hematuria or intermittent urinary obstruction. 



The initial symptom is usually acute, unilateral flank pain (stones near kidney) that 

rapidly becomes excruciating, radiating to the ipsilateral lower quadrant and often 

referred to the ipsilateral groin, testicle, or labia (stones near ureterovesicular). The pain 

may cause vasovagal syncope; occasionally patients are asymptomatic except for 

hematuria. Eliciting a history of pain that shifts anteriorly and inferiorly from the flank as 

the stone moves distally in the urinary tract may be helpful in differentiating renal colic 

from other types of abdominal pain. 

Some patients note gross hematuria. Nausea and vomiting are frequent. If complicating 

infection is present, signs and symptoms of pyelonephritis also may be present. Inquire 

about a history of similar attacks or a predisposing condition (eg, previous documented

urolithiasis, gout, hypercalcemia). 

Vital signs are usually normal in the absence of infection, although bradycardia from 

vagal hypertonicity or tachycardia from pain may be seen. Some degree of ileus is 

usually present. Tenderness over the affected kidney (costovertebral angle tenderness) 

and ureter can be elicited. 


Obtain a urinalysis. Hematuria (gross or microscopic) is present in approximately 90% 

of cases. Occasionally a patient presents with pain and no hematuria. 

A urine or serum human chorionic gonadotropin level should be obtained in all females 

of child-bearing age. Urine culture should be sent if an infected stone is suspected by 

bacteriuria and fever. 

Blood urea nitrogen and serum creatinine levels are usually normal. Although they will 

not change the emergency department management, calcium, magnesium, phosphorus, 

and uric acid levels may be helpful to the urologist in assessing for metabolic causes of 

stone formation. 

C. Imaging 

Imaging studies should be performed during the first episode of suspected renal colic or 

if the diagnosis is uncertain (see Figures 37-2 and 37-3). Patients with recurrent stones 

with typical historical and physical examination consistent with urolithiasis may be 

managed symptomatically without any diagnostic studies unless obstruction or infection 

is of concern. 

1. KUB—KUB, a study of the kidneys, urethras, and bladder, is useful because 90% of 

calculi are radiopaque. The sensitivity of this study is less than 70%. 

2. Ultrasound—Renal ultrasound may be useful to detect stones or hydronephrosis but 

is not as sensitive (64%) as helical CT or intravenous pyelogram, particularly for 

detection of small stones. It may be of value in patients with a history of hypersensitivity 

to intravenous contrast, with radiolucent stones, and especially in pregnant women. 

Pediatric and geriatric patients should also be evaluated with ultrasound as the first 

screening modality. 

3. Intravenous pyelogram—An intravenous pyelogram has a 90% sensitivity for 

detecting urolithiasis or the related obstruction as well as for assessing functional status 

and visualization of the entire urinary tract. Caution: This method is relatively 

contraindicated in the following settings: (1) patients with creatinine above 1.4 mg/dl, (2) 

elderly patients with proteinuria and elevated creatinine, and (3) patients with 

documented allergy to contrast media unless they are premedicated with antihistamines 

and steroids. 

4. Unenhanced helical (spiral) CT—Helical CT scan is widely used and currently the 

study of choice at many institutions for the diagnosis of renal colic. Not only is it 

accurate, but it is less time consuming, no contrast is required, and additional 

intra-abdominal information may be obtained. It has a sensitivity of 98%, a specificity of

97%, and positive and negative predictive values of 100% and 97%, respectively. It 

does not provide information regarding the functional status of the kidney. 

Treatment 

About 90% of renal stones are passed spontaneously. Basic treatment is as follows: 

A. Provide Analgesia 

Begin analgesics as soon as the diagnosis has been established with reasonable 

certainty. Opioids and antiemetics are mainstays of therapy. Ketorolac, the only 

injectable nonsteroidal anti-inflammatory agent, is as equipotent as mild narcotic 

analgesics. Ketorolac provides analgesia, and given its antiprostaglandin effects, it can 

decrease the inflammatory response, promote relaxation of the ureteral spasm, and 

alleviate capsular distention. For patients who are not hospitalized, an antiemetic, an 

anti-inflammatory agent, and a narcotic may be required for control of pain and emesis. 

B. Ensure Adequate Hydration 

Although authorities usually recommend drinking 2-3 L of fluid per day, this is probably 

of more value in preventing the formation of more stones than in facilitating passage of 

an existing stone. 

C. Strain Urine 

Patients with their first episode of urolithiasis or those who pass stones of unknown 

composition should strain their urine through a urine strainer or a coffee filter and submit 

the stone for chemical analysis. 

Prevention 

Specific preventive therapy can be recommended after the composition of the stone has 

been determined by chemical analysis. 

Disposition 

Patients with any of the following conditions require hospitalization: 

• Pain requiring parenteral analgesics 

• Intractable emesis 

• Coexisting pyelonephritis 

• Documented or suspected renal dysfunction (elevated blood urea nitrogen or serum 

creatinine levels, bilateral ureteral stones, oliguria or anuria, hydronephrosis) 

• Pain that persists for more than 2-3 days, suggesting persistent urinary obstruction 

Patients who do not require hospitalization should be referred to a urologist within 24-48 

hours for further evaluation and treatment.

DISEASES OF THE MALE GENITOURINARY SYSTEM 

1. Torsion of the Testicle 


• Testicular torsion, torsion of the testicular appendage, and epididymitis account for 

85-90% of all cases of scrotal pain. 

• Rare in males over age 30 years but occurs at all ages. 

• The testicle may be high riding with "bell clapper" deformity. 

• Detorsion must occur within 6 hours for testicular salvage. 

• Attempt manual detorsion. 

• Color-flow Doppler ultrasound demonstrates diminished blood flow to affected testis. 


Testicular torsion has a bimodal incidence with peaks occurring in neonates and 

pubescent males; however, it can occur in all age groups. Torsion of the testicular or 

epididymal appendages can also present as acute unilateral scrotal pain. Of the 4 

appendages, the appendix testis becomes torsed the most often (99%) and usually 

requires only supportive care. 

The history for testicular torsion is most often sudden onset of moderate to severe, 

unilateral scrotal pain. Patients may recount similar episodes that resolved 

spontaneously in the past. On physical examination, the testis can be high-riding with a 

transverse rather than vertical lie, slightly larger than the unaffected testis, and diffusely 

tender and erythematous. An absent cremasteric reflex on the affected side is the most 

sensitive physical finding. Nausea, vomiting, and abdominal pain may occur as a result 

of the ischemia. 

Epididymitis, orchitis, neoplasms, peritonitis, hernia, abdominal aortic aneurysm, 

Fournier gangrene, and other scrotal diseases need to be considered in the differential 

diagnosis (see Table 37-2). Urinalysis is usually normal. Color-flow Doppler 

ultrasonography or radionucleotide scanning may confirm the diagnosis. 

Epididymitis and orchitis may be confused with torsion of the testicle; helpful 

differentiating features are discussed in the section on scrotal pain and in Table 37-2. 

The diagnosis may be confirmed by Doppler ultrasound examination or radionuclide 

scanning. 


A. Provide Analgesia 

Parenteral narcotic analgesics usually are required. 

B. Prepare for Surgery 

Give nothing orally, obtain blood for CBC and renal function tests, and begin an

intravenous infusion. 

C. Obtain Immediate Urologic Surgical Consultation 

If a delay in urologic consultation is anticipated, attempt manual detorsion as discussed 

earlier in this chapter. Testicular salvage approaches 100% if detorsion (manual or 

surgical) is performed within 6 hours. 

2. Orchitis 

Orchitis is commonly associated with epididymitis. It usually has an infectious cause, for 

example, from viral, bacterial, or mycobacterial agents. Viral orchitis is most often due to 

mumps. The orchitis commonly presents 5 days after the parotitis. Mumps orchitis may 

result in atrophy. If the diagnosis is in doubt or specific treatment appears warranted, 

obtain urologic consultation. Symptomatic relief may be achieved with recumbency and 

analgesics. 

3. Priapism 


Priapism is a persistent involuntary, painful erection, unrelated to sexual stimulation and 

unrelieved by ejaculation. About 25% of cases are associated with leukemia, metastatic 

carcinoma, or sickling hemoglobinopathies. If the medical history is unclear, consider a 

CBC and sickling test. Alcohol, marijuana, cocaine, and now MDMA (Ecstasy) are 

among some of the recreational drugs known to induce priapism, but many prescriptions 

drugs are culprits as well. Regardless of treatment, there is a high incidence of corporal 

fibrosis and erectile dysfunction. 

Treatment 

Management is mainly to provide analgesia and hydration and to abort the erection to 

prevent permanent damage. Several modalities can be attempted, but success is often 

limited. Ice packs have limited success. Hydration, oxygenation, and sometimes 

exchange transfusion is necessary for sickle cell patients. Terbutaline has had some 

favorable results. Corporal aspiration and irrigation with a phenylephrine solution can be 

used but should be done in conjunction with urologic consultation. 

Disposition 

Hospitalize all patients with persistent priapism or those with serious underlying disease 

(sickling hemoglobinopathy, leukemia). Obtain urgent urologic consultation. 

4. Fournier Gangrene 


• Necrotizing fascitis of the perineum.

• Fever, pain, edema, and erythema of the scrotum are typically present. 

• Wide surgical debridement is crucial. 

• Mortality is approximately 60-70%. 

Fournier gangrene is a necrotizing fasciitis of the perineum that primarily affects diabetic 

males aged 20-50 years. Patients typically present with fever, pain, edema, and 

erythema of the scrotum or penis. The most common causes are infection and trauma. 

Aerobes or anaerobes may be the causative infectious agents. Treatment includes 

antibiotic therapy, wide surgical incision, and drainage. Mortality is approximately 

60-70%. 

5. Phimosis & Paraphimosis 


• Chronic balanoposthitis, due to a bacterial or fungal infection, is a risk factor for 

phimosis (inability to retract the foreskin). 

• Physiologic phimosis is normal in the first few years of life. 

• Paraphimosis (retracted, constricted foreskin proximal to the glans) may cause 

necrosis to the glans and urethra if not treated. 

Phimosis is a fibrous constriction of the foreskin preventing retraction; it is often 

associated with balanitis and may cause urinary retention. Phimosis or paraphimosis 

rarely results from chronic balanoposthitis, which is categorized as either irritant or 

infectious. Balanoposthitis is inflammation of the glans penis and the prepuce. 

Treatment for acute irritant balanoposthitis is sitz baths, cleansing with the foreskin 

retracted, and 0.5% hydrocortisone cream. Candidal infections are the most common 

infectious cause and are treated with good hygiene and topical antifungal cream. 

Phimosis without balanitis may be an indication for elective circumcision, but it is not an 

emergency. Surgical correction should not be attempted in the emergency department. 

Paraphimosis occurs when the retracted foreskin develops a fixed constriction proximal 

to the glans. The penis distal to the constricting foreskin may become swollen and 

painful, or even gangrenous, and urinary retention may result. Attempt manual 

reduction: Squeeze the glans firmly for 5-10 minutes to reduce its size. Then move the 

prepuce distally while the glans is pushed proximally. If manual reduction is 

unsuccessful, a dorsal slit of the foreskin is necessary (Figures 37-4 and 37-5). Refer 

the patient to a urologist for elective circumcision to reduce risk of recurrence. In 

addition, a complication of the Plastibell device for pediatric circumcision occurs if the 

ring inadvertently slips behind the glans, creating a paraphimosis and causing penile 

ischemia. The ring should be removed immediately. 

Abramson S et al: Impact in the emergency department of unenhanced CT on 

diagnostic confidence and therapeutic efficacy in patients with suspected renal colic: a 

prospective survey. 2000 ARRS President's Award. American Roentgen Ray Society. 

Am J Roentgenol 2000;175:1689. [PMID: 11090405]

Altman AL et al: Cocaine associated priapism. J Urol 1999;161: 1817. [PMID: 

10332443] 

Burgher SW: Acute scrotal pain. Emerg Med Clin North Am 1998;16:781. [PMID: 

9889740] 

Choe JM: Paraphimosis: current treatment options. Am Fam Physician 2000;62:2623. 

[PMID: 11142469] 

Dubin N et al: Priapism: Ecstasy related? Urology 2000;56:1057. [PMID: 11113767] 

Herbener TE: Ultrasound in the assessment of the acute scrotum. J Clin Ultrasound 

1996;24:405. [PMID: 8884519] 

Kassim AA et al: Acute priapism associated with the use of sildenafil in a patient with 

sickle cell trait. Blood 2000;95:1878. [PMID: 10744389] 

Langer JC et al: Circumcision and pediatric disorders of the penis. Pediatr Clin North 

Am 1998;45:801. [PMID: 9728187] 

Larkin GL et al: Efficacy of ketorolac tromethamine versus meperidine in the ED 

treatment of acute renal colic. Am J Emerg Med 1999;17:6. [PMID: 9928687] 

Lunquist ST et al: Diseases of the foreskin, penis, and urethra. Emerg Med Clin North 

Am 2001;19:529. [PMID: 11554274] 

Majeed S et al: Refractory priapism of unknown etiology in a pediatric patient. Pediatr 

Emerg Care 2000;16:347. [PMID: 11063367] 

Manthey DE et al: Nephrolithiasis. Emerg Med Clin North Am 2001;19:633. [PMID: 

11554279] 

Marcozzi D et al: The nontraumatic, acute scrotum. Emerg Med Clin North Am 

2001;19:547. [PMID: 11554275] 

Mulhall JP et al: Priapism: etiology and management. Acad Emerg Med 1996;3:810. 

[PMID: 8853679] 

Rekant EM et al: Emergency department time for evaluation of patients discharged with 

a diagnosis of renal colic: unenhanced helical computed tomography versus intravenous 

urography. J Emerg Med 2001;21:371. [PMID: 11728762] 

Siegel MJ: The acute scrotum. Radiol Clin North Am 1997; 35:959. [PMID: 9216633] 

Waugh MA: Balanitis. Dermatol Clin 1998;16:757. [PMID: 9891676] 

Location In Book:





CONDITIONS

Table 37-1. Diagnostic clues to the cause of bladder outlet obstruction. 

Frequency of 

Occurrence 


and Other Studies 

Common. Urethral catheterization may be difficult. 

Large amount of residual urine in bladder. 

Uncommon. Urethral catheterization often difficult. 

Large amounts of residual urine. Urethrogram or 

diagnostic. 

Uncommon. Urethral catheter is passed without difficulty. 

Cystogram or cystoscopy is diagnostic. 

Very uncommon. Urethral catheter passed without difficulty. 

Cystometrogram is diagnostic. 

Uncommon. Do not pass catheter. Retrograde urethrogram an 

cystogram are diagnostic. 





TABLES 

Table 37-1. Diagnostic clues to the cause of bladder outlet obstruction.

Table 37-2. Diagnostic clues to the cause of acute scrotal pain. 

History Urinalysis Results 

Treatment and 

Disposition 

History of injury. Variable; may have hematuria. Obtain urologic consultation (Ch 

26). 

Antecedent flank or back 

pain; occasionally 

abdominal pain. 

Hematuria. Obtain urologic consultation. 

Gradual onset, coexisting 

mumps parotitis common. 

Normal. Elevate and immobilize testicle ( 

with atheletic supporter), give 

analgesics, and discharge for 

follow-up care. 

Gradual onset; crampy pain. Normal. Obtain general surgical consulta 

hospitalize. 

Gradual onset; history of 

urethritis or urinary tract 

infection common; older 

men (> age 25 years). 

Abrupt onset (minutes to 

hours); history of testicular 

pain in some; boys and 

young men (< age 25 

years). 

Leukocytes; bacteriuria in some cases 

(coexisting urinary tract infection). 

1. Prescribe bed rest and elevat 

and scrotum, with analgesics as 

needed. 

2. Treat underlying urethritis or 

urinary tract infection with 

antimicrobials (Chapter40). 

3. Discharge all patients for follo 

care. 

Normal. Obtain emergency urologic 

consultation; hospitalize for surg 

Attempt manual detorsion (see t 

Abrupt onset. Normal. 1. Prescribed bedrest and eleva 

with analgesics as needed. 

2. Surgery is often needed to rel 

pain. 

3. Obtain urologic follow-up care 





TABLES 

Table 37-2. Diagnostic clues to the cause of acute scrotal pain.

Table 37-3. Diagnostic clues to the cause of common painless scrotal masses. 

History and 

Physical 

Examination 

Gradually 

enlarging 

painless cystic 

mass that 

transilluminates. 

Note: Hydrocele 

may complicate 

tumor. 

Patient often a 

young adult. 

Asymptomatic 

enlargement of 

testis, rarely 

painful. 

Examination 

shows firm, 

nontender mass 

that does not 

transilluminate. 

Gynecomastia, 

virilization, or 

feminization 

rarely occur. 


Varicocele Not usually required, physical examination i 

diagnostic. Ultrasonography also helpful in d 

enigmatic cases. 

Spermatocele Aspiration reveals white cloudy fluid with im 

sperm. Ultrasonography also helpful in diag 




TABLES 

Table 37-3. Diagnostic clues to the cause of common painless scrotal 

masses.

Table 37-4. Diagnostic clues to common causes of dysuria. 

Sex More 

Commonly 

Affected Diagnostic Studies 

Men. Leukocytes in urethral discharge or on urethral 

gonococcal or chlamydial infection are often po 

Men only. Prostatic massage produces leukocytes and ba 

discharge or urine ("3-glass test"). 

Men. Urethroscopy or urethrogram. 

Women (usually postmenopausal). Urethroscopy. 

Women only. Pyuria; leukocytes in urethral discharge or on u 

Women only. Vaginal smear or culture shows Candida, Gard 

or Trichomonas vaginalis. 

Women. Positive results on tests for herpes simplex. 

Mainly women. Pyuria and bacteriuria, urine culture shows mo 

bacteria/mL (often > 10 5 /mL). 

Either (mainly children). Hematuria occasionally. 

Either. Normal results on urinalysis. No leukocytes on 

Tests for gonococcal and chlamydial infection n 





TABLES 

Table 37-4. Diagnostic clues to common causes of dysuria.

Table 37-5. Diagnostic clues to common causes of hematuria. 

History and Physical 

Findings 

Often long-standing 

painless hematuria. 

Trauma See Chapter 26. 

Urolithiasis Intravenous pyelogram reveals u 

stone, obstruction, or postobstruc 

hydroureter; cystoscopy or cysto 

shows bladder stones. 

Dysuria common. Glomerulonephritis Urinalysis shows leukocytes, red 

and frequently proteinuria; blood 

nitrogen and serum creatinine ele 

Dysuria often present. 

Abnormal (large or 

tender) prostate. 

Urethral stricture, foreign body, or 

manipulation 

Urethroscopy reveals stricture or 

body. 

Intermittent hematuria 

that may be painless 

(trait) or painful (disease). 

Bleeding diathesis Coagulation tests show thromboc 

prolonged prothrombin time, etc 

39).

Figure 37-1. Torsion of the testicle. View of the testicles, epididymides, testicular 

appendages, and scrotum, showing direction of rotation of the testicles during torsion 

(as seen by the physician standing at the foot of the patient's bed and looking down at 

the patient). Manual detorsion should rotate the testicles in the opposite direction. 





FIGURES 

Figure 37-1

Figure 37-2. Stone in left upper ureter causing moderate obstruction. (Reproduced, with 







FIGURES 

Figure 37-2

Figure 37-3. Unenhanced helical CT scan demonstrating right-sided hydronephrosis 

(A), right nephrolithiasis (B), and stone in right ureter (C). 





FIGURES 

Figure 37-3

Figure 37-4. Method of performing a dorsal slit of the foreskin for balanitis and 

paraphimosis. An incision made through the tight band of skin as shown will relieve the 

paraphimosis. 





FIGURES 

Figure 37-4

Figure 37-5. Method of performing a dorsal slit of the foreskin for phimosis. 





FIGURES 

Figure 37-5

38. Vascular Emergencies 1 - Scott W. Hines, MD, & James J. 

Mensching, MD, DO, FACEP 

INTRODUCTION 

1 This chapter is a revision of the chapter by Carol A. Raviola, MD, & Donald D. Trunkey, 

MD, from the 4th edition. 

Most vascular emergencies are due either to disruption of the blood vessel wall with 

bleeding (eg, from penetrating trauma) or to occlusion of the blood vessel lumen (eg, by 

an embolus or thrombus). The major consequences of these events are blood loss or 

acute distal ischemia. If vascular injury is untreated, hypotension or tissue necrosis may 

occur. 

I. VASCULAR EMERGENCIES DUE TO TRAUMA 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING VASCULAR INJURIES 

Maintain Airway & Treat Associated Injuries 

(See Chapters 7 and 11.) Treat associated life-threatening head, thoracic, and 

abdominal injuries (Chapters 10, 22, 24, and 25). 

Stop Hemorrhage 

1. Stop active bleeding from arterial or venous hemorrhage by gentle manual 

compression. 

2. Avoid clamping the bleeding vessel, because this will cause further injury. 

3. Avoid the use of tourniquets. 

4. Do not remove embedded objects, because they may be preventing further bleeding. 

Treat or Prevent Shock 

(See also Chapter 9.) Insert 2 or more large-bore (= 16-gauge) intravenous catheters or 

perform venous cutdowns. Two intravenous access sites are preferable if the patient is 

already in shock or is bleeding profusely. 

While intravenous catheters are being inserted, draw blood for complete blood count 

(CBC), serum electrolytes, glucose and creatinine measurements, prothrombin time 

(PT), partial thromboplastin time (PTT), and typing and cross-matching (reserve 6-8 

units of packed red blood cells or whole blood).

Begin intravenous infusion of crystalloid solutions (eg, normal saline or lactated 

Ringer's) to support blood pressure. Up to 2-3 L of crystalloid solution may be given 

before blood products must be administered. 

Replace blood. The number of units administered depends on the severity of existing 

blood loss and on anticipated loss from projected surgery. Use fresh whole blood 

whenever possible. 

Prevent Further Vascular & Nerve Injury 

All fractures and joint dislocations associated with abnormal pulses should be carefully 

reduced and splinted to reduce further neurovascular damage. Control hemorrhage by 

pressure; avoid clamping vessels to stop hemorrhage. Consider adjunctive studies for 

further evaluation as appropriate (eg, computed tomography [CT] scan, angiography). 

Minimize Ischemia 

Keep ischemic limbs horizontal. Do not use tourniquets. 

Relieve Pain 

Provide adequate analgesia; if necessary, give narcotic analgesics. 

Obtain Surgical Consultation 

All documented or suspected vascular injuries should be examined promptly by a 

general or vascular surgeon before the patient is transferred from the emergency 

department. 

Hospitalize Patients as Required 

Hospitalize all patients with arterial or major venous injuries. 


Acute vascular injury may result in either hemorrhage or tissue ischemia. 

A. Arterial Injury 

1. Hemorrhage—Obvious external hemorrhage is present in many patients. Occult 

bleeding into soft tissue, the retroperitoneum, the pelvis, or body cavities may also 

occur. 

2. Ischemia—Ischemia from arterial injury must be recognized and treated promptly, 

because increased tissue pressure and swelling from ischemia further compromise 

arterial perfusion, and prolonged ischemia results in irreversible tissue damage. 

B. Venous Injury 

1. Hemorrhage—Obvious or occult bleeding usually occurs following venous injury. It is 

rarely life threatening except in the case of injuries to central veins (eg, vena cava) or

their immediate branches (eg, femoral vein). 

2. Ischemia—Tissue ischemia from venous trauma alone is rare, although venous 

obstruction and resultant tissue congestion may worsen preexisting tissue ischemia 

resulting from arterial injury. 

C. Causes of Vascular Injury 

1. Penetrating trauma—Penetrating trauma is the most common cause of peripheral 

vascular injury and ranges in severity from innocuous simple puncture wounds to 

extensive wounds caused by high-velocity missiles. Penetrating injuries to the central 

vessels may lead to massive hemorrhage and death. 

2. Blunt trauma—Blunt trauma may also cause vascular injury. Contusions or crushing 

injuries of an artery may cause either transmural disruption with hemorrhage, or partial 

disruption of the artery and elevation of the intima from an intramural hematoma (ie, 

dissection). Thrombosis of a segment of artery may also occur. Blunt trauma with 

dislocation of a joint may result in disruption of the arteries crossing that joint line, 

leading to ischemia distal to the site of injury (eg, disruption of the popliteal artery with 

posterior dislocation of the knee). Blunt trauma may also contribute indirectly to vascular 

occlusion by creating large hematomas near a blood vessel. Hematoma formation may 

lead to arterial spasm, distortion, or compartment syndromes, all of which may interfere 

with arterial flow. 

3. Chemicals—Chemical injury to blood vessels is increasing in frequency. It is 

generally iatrogenic or associated with parenteral drug abuse. Intra-arterial injection of 

drugs that are chemically irritating to tissues (eg, barbiturates) causes occlusion of small 

peripheral vessels. If occlusion is severe, all or part of the limb may be lost. 

Extravasation of an intravenously administered chemical may also cause associated 

arterial spasm or tissue necrosis. Barbiturates, phenytoin, vasopressors, and 

chemotherapeutic agents (eg, doxorubicin) are notable examples. High doses of certain 

intravenously administered vasopressors (eg, dopamine) can cause intense peripheral 

vasoconstriction with ultimate digital ischemic necrosis. 

D. Sequelae 

Late sequelae associated with major vascular injuries include the development of false 

aneurysms and arteriovenous fistulas. 

1. False aneurysms—False aneurysms do not contain all three layers of the vessel 

wall (intima, media, and adventitia). They result from walled-off disruptions of vessel 

walls. They enlarge over time, may compress adjacent veins or nerves, and may rupture 

without warning. 

2. Fistulas—Fistulas may occur after adjacent arteries and veins are injured 

simultaneously, usually as a result of stab wounds or missile injury. The fistula may 

enlarge over time and cause increased cardiac output if a large left-to-right shunting of 

blood is present. If the fistula involves the blood supply to an extremity, dilated veins 

may be observed in that extremity. Turbulent blood flow through the fistula results in an 

obvious thrill or bruit. Fistulas may also compress adjacent nerves or impede collateral 

circulation, or they may rupture, causing a severe hemorrhage.

Principles of Diagnosis 

A. Physical Examination 

If there is a wound in the vicinity of a major blood vessel, assume that vascular injury 

has occurred. The findings listed below may not appear for hours to days following a 

significant vascular injury, and absence of these findings does not rule out the possibility 

of vascular injury. 

1. Signs—Clinical manifestations of vascular injury include an expanding or pulsating 

hematoma, to-and-fro or continuous murmurs of arteriovenous fistulas, a false 

aneurysm, loss of pulses, progressive swelling of the injured part, unexplained ischemia 

or dysfunction, and unilateral cool or pale extremities. 

2. Pulses—Perform a complete vascular examination unless treatment of other 

life-threatening injuries precludes it. 

a. Palpation—Palpate all peripheral pulses: carotid, axillary, brachial, radial, femoral, 

popliteal, dorsalis pedis, and posterior tibial. 

b. Doppler ultrasound examination—The presence of blood flow in a peripheral 

vessel can be detected using a standard pocket Doppler apparatus. Any assessment of 

the normality of this flow requires concomitant pressure measurements or waveform 

analysis. 

3. Murmurs and bruits—Auscultate over injured areas to detect bruits or murmurs. 

4. Neurologic function—Assess neurologic function. Paresthesia may be an early sign 

of developing vascular problems (eg, compartment syndrome). 

B. Diagnostic Imaging 

Arteriography is the single best method of confirming suspected peripheral, mesenterial, 

and cervical vascular injury. In addition, arteriography defines the nature and extent of 

injury and is essential to the surgeon contemplating corrective surgery. CT scan with 

contrast has emerged as the diagnostic study of choice to evaluate central vascular 

injuries (eg, aortic injury or rupture) due to its ready availability. Ultrasonography and 

arteriography are also useful in specific circumstances (discussed below). 

Caution: Diagnostic imaging should not be performed in a patient whose condition is 

unstable and who needs emergency laparotomy or thoracotomy. The procedure should 

be delayed until after resuscitation and treatment of the life-threatening emergency, 

either in the emergency department or in the operating room. 

EMERGENCY MANAGEMENT OF SPECIFIC VASCULAR INJURIES 

NECK INJURIES (See also Chapter 23.)


• History of blunt or penetrating trauma. 

• Consider concomitant injury to nonvascular structures. 

• Arteriography, ultrasound, or CT scan confirm diagnosis. 


Vascular injury to the neck is most often due to penetrating injuries; however, blunt 

trauma to the cervical vessels can result in intimal disruption, dissection, and 

thrombosis. Concomitant injury to nonvascular structures of the neck (eg, trachea, 

esophagus, and spinal cord) may also occur. The cervical spine must be protected until 

injury is excluded. 

Penetrating Trauma 

In penetrating trauma to the neck, two immediate concerns are massive hemorrhage 

and airway compromise secondary to a rapidly expanding hematoma. 

A. Emergency Treatment 

Control hemorrhage, preferably with direct pressure. If this fails, balloon tamponade with 

a Foley catheter may act as a temporizing measure along with ongoing fluid 

resuscitation; neither of these measures should delay transport to the operating room 

for definitive repair. If a rapidly expanding hematoma is suspected, tracheal intubation 

via direct laryngoscopy or intubating bronchoscope should be conducted before 

compression of the trachea makes this procedure more difficult or impossible. 

Transtracheal jet insufflation and cricothyrotomy are methods of last resort; in this 

setting, emergent tracheostomy is preferable. 

B. Further Treatment 

Further management is a function of the patient's hemodynamic stability and the 

location of the wound. All actively bleeding, hemodynamically unstable patients are 

taken immediately to the operating room for surgical exploration. For stable patients with 

wounds that penetrate the platysma muscle, management is a function of the zone of 

the neck affected (Figure 38-1). Wounds should never be probed beyond the level of the 

platysma muscle in the emergency department. 

1. Zone I injuries—These wounds are frequently associated with injury to the great 

vessels and require imaging to exclude major arterial injury. 

2. Zone II injuries—These injuries may be further evaluated by surgical exploration or 

imaging of the vessels and nonvascular structures at the discretion of the attending 

surgeon. 

3. Zone III injuries—Because the relationship of the blood vessels to the base of the 

skull makes surgical exploration and distal control of hemorrhage difficult, preoperative 

imaging should be conducted to define the injury and help plan the surgical approach.

Blunt Trauma 

Blunt trauma to the carotid artery can result in intimal disruption, dissection, and 

thrombosis leading to acute cerebral ischemia manifest as a gross hemispheric 

neurologic deficit not explained by intracranial trauma. Conduct emergent imaging of the 

neck arteries. 

Diagnostic Imaging 

The gold standard for detecting vascular injury in the neck remains arteriography. 

However, both ultrasonography and helical CT scan can be used. 

Disposition 

Asymptomatic patients with mild neck injuries due to blunt trauma or penetrating injuries 

that do not cross the platysma muscle may be discharged from the emergency 

department. Hospitalize all other patients with neck injuries, and consult with a general 

or vascular surgeon. 

CHEST INJURIES (See also Chapter 24.) 


• Significant mechanism of thoracic trauma. 

• Tearing retrosternal or interscapular pain, dysphagia, hoarseness, or dyspnea. 

• In blunt trauma, less than half of patients will have visible signs of chest wall injury. 

• CT scan confirms diagnosis. 


Vascular injury to the chest occurs secondary to both penetrating and blunt trauma. If 

bleeding is not contained within fascial planes, these injuries can lead to exsanguination 

and death, often before the patient arrives in the emergency department. A high degree 

of suspicion for this type of injury must be maintained in any patient with a significant 

mechanism of thoracic trauma. With the evolution of helical (spiral) CT scan, CT with 

contrast has become the diagnostic study of choice in evaluating vascular injury in a 

hemodynamically stable patient with chest trauma. 

Thoracic Aortic Injury 

Penetrating and blunt trauma may cause thoracic aortic injury (TAI). Though penetrating 

TAI may be caused by any variety of objects or weapons, blunt TAI involves large, 

violent deceleration forces (eg, falls, motor vehicle collisions including occupant ejection 

or auto-pedestrian). The greatest risk of TAI in a motor vehicle collision exists when the 

impact occurs on the same side of the vehicle as the occupant, when there is greater 

than 15 inches of intrusion into the passenger compartment, and when the overall

change in velocity experienced by the vehicle and its occupants is greater than 20 miles 

per hour. A significant mechanism of injury should heighten suspicion of blunt TAI, 

because less than half of these patients will have visible signs of chest wall injury. 



Patients may complain of tearing retrosternal or interscapular pain. Less frequently, 

dysphagia, hoarseness, stridor, or shortness of breath is present. The physical 

examination often reveals no external evidence of chest wall injury. Classically, a 

difference in upper-extremity pulses and a harsh systolic murmur across the precordium 

and in the interscapular area are noted. Signs and symptoms of shock may be present. 

B. Imaging 

The chest x-ray is frequently the first imaging study obtained (Figure 38-2); the classic 

chest x-ray findings associated with TAI are listed in Table 38-1. However, 7% of 

patients with TAI can have a normal chest x-ray and further imaging studies may be 

warranted, based on clinical suspicion and mechanism of injury. In the past, 

aortography had been the study of choice in evaluating TAIs. However, helical CT scan 

has emerged as the study of choice after initial chest x-ray. It is more readily available 

than aortography and less invasive, and prospective clinical trials have shown spiral CT 

scan to be 100% sensitive and 99.7% specific in diagnosing TAI following blunt trauma. 

In centers where transesophageal echocardiography (TEE) is readily available, it is a 

highly sensitive (98%) and specific (100%) modality for diagnosing TAI. TEE can be 

done at the bedside, requires no contrast dye, and evaluates real-time cardiac function. 


Patients with TAI will require emergent consultation with a vascular or thoracic surgeon. 

In the emergency department it is important to maintain intravascular volume with 

crystalloid solutions and blood products. Systolic blood pressure should be lowered to 

less than 120 mm Hg. Exsanguinating hemorrhage may require emergency 

thoracotomy for the control of bleeding. 

PULMONARY VASCULAR INJURIES 


• Usually due to penetrating thoracic or abdominal injury. 

• Rapidly expanding hemothorax on chest x-ray. 



Most patients present with penetrating chest or abdominal trauma and rapidly 

expanding hemothorax, visible on chest x-ray. Rarely, blunt chest trauma is associated

with pulmonary vascular injury. 


Most patients can be managed with a chest tube that uses suction and allows the lung 

to reexpand and block the bleeding vessel. Continued massive bleeding requires 

prompt surgery. Consider the use of autotransfusion. Prompt consultation with a 

general, vascular, or thoracic surgeon is required, because exsanguination can occur 

rapidly. Hospitalization is indicated for all patients. 

ABDOMINAL INJURIES (See also Chapter 25.) 


• History of abdominal trauma. 

• Signs and symptoms of shock that fail to respond to resuscitation efforts. 


Patients with injuries to major vessels within the abdominal cavity present mainly with 

hemorrhagic shock that fails to respond to resuscitative efforts. Although arteriography 

is rarely required to diagnose vessel injury in the abdomen, it is useful both 

diagnostically and therapeutically in patients with severe pelvic trauma who have 

ongoing bleeding, because angiographic embolization can be effective treatment in 

certain injuries. Aortography is also useful in establishing the diagnosis of renovascular 

pedicle injury in trauma patients with nonvisualization of a kidney on urography. CT 

scan may also be helpful. 


Immediate operation is the only effective treatment for abdominal vascular injuries. 

Support blood pressure with infusion of intravenous fluids (colloid or crystalloid 

solutions) until surgery can be performed. Packed red blood cells or whole blood should 

be used as soon as available (Chapter 9). 

A portable chest x-ray (upright, if possible) should be obtained before laparotomy, to 

rule out unsuspected thoracic injuries. 

INJURIES TO THE EXTREMITIES 


• History of blunt or penetrating trauma. 

• Presence of a pulse does not rule out vessel injury. 

• Use arteriography to evaluate.


A. Penetrating Trauma 

Vascular injuries are present in 25-35% of patients with penetrating trauma to the 

extremities. Occasionally vascular trauma is present without the usual physical findings, 

and the presence of a pulse does not rule out injury to the vessel. Arteriography should 

be considered whenever the weapon's trajectory has passed close to major blood 

vessels. 


Vascular injury may also occur after blunt trauma, especially if fractures and joint 

dislocations are present. Even if the pulse is restored with splinting and traction, an 

arteriogram is necessary to rule out significant injury to the intima. 

C. Posterior Dislocation of the Knee 

Posterior dislocation of the knee is associated with popliteal artery injury in half of 

cases, and arteriography is therefore mandatory. 

Treatment 

Stabilize the patient, and stop hemorrhage as outlined above. Splint fractures. Do not 

clamp vessels or use a tourniquet unless injury is exsanguinating the patient and 

compression fails to control the hemorrhage. 

Disposition 

All patients with suspected vascular injury should be hospitalized for arteriography. 

Obtain general or vascular surgical consultation. 

MAJOR VENOUS TRAUMA 


• History of trauma. 

• Injuries to major venous structures manifested by progressive hemorrhagic shock (not 

ischemia). 

• Venography may aid diagnosis. 


Trauma to peripheral veins without associated arterial injury usually does not require 

operative correction; however, disruption of the central large veins (vena cava or its 

immediate branches, subclavian or iliac veins)—especially where they are not enclosed 

by dense fascia or muscles—requires prompt operation. 

Clinical Findings

Venous injury is usually manifested by hemorrhage, not ischemia. Patients with 

bleeding from the central veins present with progressive hemorrhagic shock (Chapter 

9). Superior vena cava and subclavian vein hemorrhage is usually associated with 

hemothorax visible on chest x-ray. 

In contrast, hemorrhage from the inferior vena cava and iliac vein is more difficult to 

detect. The only common finding is progressive hemorrhagic shock, and many of these 

injuries are not suspected before they are discovered at surgery. 

Diagnosis depends on venography (occasionally the lesion may be visible on the 

venous phase of an arteriogram) and on discovery at surgery, because most patients 

are too unstable to allow detailed radiologic evaluation. 


Surgical correction in the operating room is indicated. 

American College of Emergency Physicians: Clinical policy for the initial approach to 

patients presenting with penetrating extremity trauma. Ann Emerg Med 1999;33:612. 

[PMID: 10216346] 

Asensio JA et al: Multiinstitutional experience with the management of superior 

mesenteric artery injuries. Am Coll Surg 2001;193:354. [PMID: 11584962] 

Chen MY et al: Role of angiography in the detection of aortic branch vessel injury after 

blunt thoracic trauma. J Trauma 2001;51:1166. [PMID: 11740270] 

Cook AD et al: Chest radiographs of limited utility in the diagnosis of blunt traumatic 

aortic laceration. J Trauma 2001;50:843. [PMID: 11371839] 

Dyer DS et al: Thoracic aortic injury: how predictive is mechanism and is chest 

computed tomography a reliable screening tool? A prospective study of 1,561 patients. 

J Trauma 2000;48: 673. [PMID: 10780601] 

Exadaktylos AK et al: Do we really need routine computed tomographic scanning in the 

primary evaluation of blunt chest trauma in patients with "normal" chest radiograph? J 

Trauma 2001;51(6):1173. [PMID: 11740271] 

Fishman JE et al: Direct versus indirect signs of traumatic aortic injury revealed by 

helical CT: performance characteristics and interobserver agreement. Am J Roentgenol 

1999;172:1027. [PMID: 10587141] 

Goarin JP et al: Evaluation of transesophageal echocardiography for diagnosis of 

traumatic aortic injury. Anesthesiology 2000;93: 1373. [PMID: 11149428] 

Horton TG et al: Identification of trauma patients at risk of thoracic aortic tear by 

mechanism of injury. J Trauma 2000; 48:1008. [PMID: 10866244]

Ledbetter S et al: Helical (spiral) CT in the evaluation of emergent thoracic aortic 

syndromes: traumatic aortic rupture, aortic aneurysm, aortic dissection, intramural 

hematoma, and penetrating atherosclerotic ulcer. Radiol Clin North Am 1999; 37:575. 

[PMID: 10361547] 

Malhotra AK et al: Minimal aortic injury: a lesion associated with advancing diagnostic 

techniques. J Trauma 2001;51:1042. [PMID: 11740248] 

Mirvis SE et al: Use of spiral computed tomography for the assessment of blunt trauma 

patients with potential aortic injury. J Trauma 1998;45:922. [PMID: 9820704] 

Munera F et al: Diagnosis of arterial injuries caused by penetrating trauma to the neck: 

comparison of helical CT angiography and conventional angiography. Radiology 

2000;216:356. [PMID: 10924553] 

Novelline RA et al: Helical CT in emergency radiology. Radiology 1999;213:321. [PMID: 

10551209] 

Simon BJ et al: Factors predicting early in-hospital death in blunt thoracic aortic injury. J 

Trauma 2001;51:906. [PMID: 11706338] 

Thompson EC et al: Penetrating neck trauma: an overview of management. J Oral 

Maxillofac Surg 2002;60:918. [PMID: 12149739] 

II. VASCULAR EMERGENCIES NOT DUE TO TRAUMA 

Acute Ischemia 

ACUTE PERIPHERAL ISCHEMIA DUE TO MAJOR ARTERIAL OCCLUSION 


• History of arrhythmia, myocardial infarction, valvular disease, or atherosclerosis may 

be present. 

• Pain, paresthesias, and coolness of affected extremity. 

• Pale, mottled, cyanotic limb with decreased or absent pulses. 

• Angiography confirms diagnosis. 


Acute arterial occlusion may be caused by an embolus, thrombosis, or trauma to an 

artery. Occlusion leads to distal ischemia, which if not corrected can progress to 

irreversible tissue damage and necrosis. 

A. Embolic Occlusion 

Embolic occlusion is caused by the dislodgment of an intravascular thrombus which 

travels distally and occludes a smaller artery. The majority of thrombi originate in the

heart, but they may come from anywhere within the vascular system. A history of 

arrhythmia, myocardial infarction, or valvular heart disease suggests an embolic cause 

for acute peripheral ischemia. 

1. Cardiac emboli—Cardiac emboli generally originate in the left atrium in patients with 

atrial fibrillation or mitral valve disease and in the left ventricle in patients with recent 

myocardial infarction or ventricular aneurysm. 

2. Vascular emboli—Vascular emboli originate on irregular luminal surfaces of 

atherosclerotic vessels (eg, ulcerative plaques or aneurysms). These emboli may 

contain cholesterol in the clot. 

3. Tumor emboli—Tumor emboli are rare, the most common sources are atrial 

myxomas. 

B. Thrombotic Occlusion 

Thrombosis of an atherosclerotic artery resulting in acute ischemia is uncommon but 

may occur secondary to plaque disruption and resultant clot formation. A history of 

peripheral vascular disease, claudication, progressive rest pain, or nonhealing wounds 

of the distal extremities is suggestive of occlusion secondary to thrombosis, because 

these patients often lack sufficient collateral flow that can minimize ischemia. 

C. Consequences of Occlusion 

Acute occlusion of a previously patent major artery results in ischemia of the nerves, 

muscles, and skin distal to the occluded site. The severity of symptoms is a function of 

the adequacy of flow through collateral vascular channels. Within a few hours after 

persistent and severe occlusion, irreversible anesthesia, paralysis, and tissue infarction 

occur. During this time, the developing thrombus progressively occludes the distal 

vessels, reducing the likelihood of restoration of blood flow to distal parts. For these 

reasons, early recognition and appropriate treatment, before irreversible damage 

occurs, is critical. 



Patients typically present with extremity pain but may also complain of paresthesias and 

even paralysis of the affected limb. Physical examination may reveal a pale, mottled, 

cool, or cyanotic limb. Pulses will be reduced or absent, and there may be tenderness to 

palpation of affected muscle groups. 


A Doppler ultrasound may be useful in evaluating a suspected acute arterial occlusion. 

Angiography of the affected limb confirms the diagnosis and is useful for planning 

surgical intervention. 

Treatment 

Obtain an immediate general or vascular surgery consultation.

Insert a large-bore (= 16-gauge) intravenous catheter. Obtain baseline laboratory 

studies, including CBC, PT, PTT, and blood chemistries. Also send a blood sample for 

typing and cross-matching. Begin intravenous heparin at full anticoagulation dosage as 

soon as possible. 

Definitive treatment involves surgical thrombectomy or clot lysis through the use of 

localized intravascular thrombolytics. 

Disposition 

All patients with acute arterial insufficiency should be hospitalized for management. 

ACUTE PERIPHERAL ISCHEMIA DUE TO SMALL-VESSEL OCCLUSION ("Blue Toe 

Syndrome") 


• Abrupt onset of small painful area on affected digit. 

• Affected area is tender, cool, and cyanotic. 

• Asymmetric distribution. 

• Livedo reticularis may be present. 


Acute occlusion of a digital artery by microemboli results in ischemia of the affected 

digit. The most common sources of these microemboli are proximal atherosclerotic 

plaques or aneurysms. Debris consisting of cholesterol, calcium, and platelet 

aggregates breaks off from these areas, travels distally through the vasculature, and 

lodges in the small digital arteries. Other sources of microemboli are clots on prosthetic 

heart valves and septic emboli from infected heart valves. 


The diagnosis is based on clinical findings. Patients typically report the abrupt onset of a 

small painful area on the affected digit that is tender, cool, and cyanotic. If multiple 

areas are affected, the distribution of lesions is asymmetric. Pulses in the affected 

extremity are intact. A fine, lacelike rash (livedo reticularis) may be noted. If the patient 

presents late, gangrene may be present. 

Treatment 

Treatment is directed at identifying and treating the proximal source of the emboli 

because recurrence is likely if the source is not removed. Consult a vascular surgeon. 

Disposition 

Hospitalize the patient for evaluation and treatment of the source of the microemboli.

ACUTE PERIPHERAL ISCHEMIA DUE TO VENOUS OCCLUSION 


• Massive acute swelling of affected leg. 

• Leg has doughy consistency. 

• Cyanosis and gangrene may occur. 

• Color-flow Doppler ultrasound or contrast venography confirms diagnosis. 


Phlegmasia cerulea dolens (venous gangrene) is a severe form of iliofemoral 

thrombosis characterized by massive venous occlusion. Rapidly progressive venous 

hypertension results in diffuse limb swelling to the level of the groin. Distal ischemia 

occurs secondary to increased venous and tissue pressure. Cyanosis develops, and 

gangrene can occur. 


Massive acute swelling of the entire leg and cutaneous cyanosis occur early. Distal 

pulses are diminished or absent. The leg has a doughy consistency, and bullae may be 

present. Gangrene is a late finding. The diagnosis is confirmed by color-flow Doppler 

ultrasound or contrast venography. 

Treatment 

Obtain immediate general or vascular surgery consultation. Begin intravenous heparin 

at full anticoagulant dosage. The first step in definitive treatment is catheter-directed 

intrathrombus thrombolysis. If this approach fails, or if the use of thrombolytics is 

contraindicated, the treatment is thrombectomy. 

Disposition 

Hospitalize all patients for definitive management. 

ACUTE VISCERAL (INTESTINAL) ISCHEMIA 


• Severe, poorly localized abdominal pain. 

• May have history of intestinal angina. 

• Pain out of proportion to physical exam findings. 

• Gross or occult intestinal bleeding. 

• Mesenteric arteriography confirms diagnosis.


Significant arterial insufficiency can cause ischemia that results in necrosis of the bowel 

mucosa. This may progress to full-thickness involvement in 6-48 hours. The extent of 

necrosis depends on the vessel involved, the adequacy of collateral perfusion, and the 

degree of hypoperfusion. Untreated severe intestinal ischemia results in intestinal 

gangrene, diffuse peritonitis, cardiovascular collapse, and death. 

Causes 

A. Acute Mesenteric Vascular Occlusion 

Acute mesenteric vascular occlusion is the cause of acute visceral ischemia in two 

thirds of patients. Occlusion may be due to an embolus from a cardiac mural thrombus 

or to arterial thrombosis that is the end result of atherosclerotic stenosis of the involved 

vessel. Some patients give a history of intestinal angina (pain after eating, often relieved 

by vomiting). Rarely, arterial thrombosis is due to a dissecting aneurysm (aortic or 

mesenteric artery), connective tissue disease (eg, polyarteritis), or other conditions. 

Venous thrombosis occurs occasionally and is associated with portal hypertension, 

abdominal sepsis, hypercoagulable state, trauma, or use of oral contraceptives. 

B. Nonocclusive Arteriolar Intestinal Ischemia 

Nonocclusive arteriolar intestinal ischemia is the cause of acute visceral ischemia in one 

third of patients and can occur with cardiac arrhythmia, sepsis, or any prolonged 

hypotensive state. Splanchnic vasoconstriction causes ischemia secondary to a 

low-flow state. 


Obscure abdominal pain and intestinal bleeding in elderly patients should suggest the 

diagnosis of intestinal ischemia. 


Severe, poorly localized diffuse abdominal pain is invariable in intestinal ischemia. 

Classically the pain is out of proportion to that expected based on physical examination 

findings. See Chapter 13 for differential diagnosis of disorders causing acute abdominal 

pain. With major acute occlusion, the onset of pain is sudden. With nonocclusive 

ischemia, pain may develop more insidiously. 

Usually, few abdominal findings occur early in the disease; later, abdominal distention 

and tenderness generally occur. Gross or occult intestinal bleeding may be present. 

Systemic toxicity may precede abdominal findings. Shock and generalized peritonitis 

occur late. 


1. Laboratory tests—Laboratory tests show leukocytosis, metabolic acidosis, and 

elevated serum lactate.

2. X-ray findings—Upright plain films show ileus, absence of intestinal gas, or diffuse 

distention with an air-fluid level. Ischemia and intestinal necrosis are late findings. 

Abdominal plain films are abnormal in only 20% of cases. A barium enema (not 

recommended if vascular disease is strongly suspected) may show "thumbprinting" of 

the colonic mucosa. 

3. Mesenteric arteriography—When performed early in the course of the disease, 

mesenteric arteriography is the definitive diagnostic procedure, because it demonstrates 

major vascular occlusion, if present. If it is done later, it merely delays necessary 

surgery and permits development of more extensive bowel necrosis and peritonitis. The 

catheter inserted in the superior mesenteric artery may be used to infuse vasodilating 

agents when the cause of disease is nonocclusive arteriolar intestinal ischemia and 

after the primary occlusive lesion is corrected. 

Treatment 

Treat hypotension and shock with infusion of intravenous crystalloid solutions and 

blood, if bleeding is present. Notify a vascular or general surgeon immediately to 

prepare for surgery. Prompt operation is required to resect necrotic bowel. In some 

cases, the embolus can be removed or the arterial obstruction bypassed. 

Vasodilator drugs may be used as an adjunct to management of the vascular disease in 

selected cases of nonocclusive ischemia; however, operation is usually required to 

resect necrotic bowel. Begin parenteral administration of broad-spectrum antimicrobials. 

Disposition 

All patients with suspected or proved acute visceral ischemia should be hospitalized. 

ACUTE CEREBRAL ISCHEMIA DUE TO EMBOLI 


• Unilateral motor or sensory deficits, dysarthria, aphasia, ataxia, visual disturbance, or 

vertigo. 

• Noncontrast CT scan distinguishes between thrombotic or embolic etiologies and 

hemorrhagic etiologies. 


Cerebrovascular accident (CVA) (stroke) due to infarction is in many cases the result of 

embolization of thrombotic or atheromatous debris from an extracranial vascular source. 

The advent of thrombolytic therapy for ischemic CVA or stroke has dramatically 

changed emergency department evaluation and management of cerebral embolic 

events. 

Clinical Findings


Patients with CVA or transient ischemic attack (TIA) may present with unilateral motor 

or sensory deficits, dysarthria, aphasia, ataxia, visual disturbances, or vertigo, 

depending on the location of the insult. TIAs are classically defined as neurologic 

deficits spontaneously resolving within 24 hours. 

B. Imaging 

1. Emergent noncontrast cranial CT scanning—This diagnostic tool is vital to the 

evaluation of a patient presenting with a CVA within 3 hours of symptom onset; 

determining whether a CVA is ischemic or hemorrhagic may allow tissue plasminogen 

activator administration (provided no other contraindications are present and the 

hospital has a "brain attack" program involving emergency medical services, the 

emergency department, radiology, neurology, and neurosurgery). 

2. Noncontrast CT scanning—This imaging method may be helpful for patients with 

TIA; duplex scanning of the carotid arteries may reveal atherosclerotic lesions 

responsible for the TIA. 


For treatment and disposition of CVAs, see Chapter 18. Patients with TIAs should be 

started on antiplatelet therapy and referred to a neurologist. Certain patient 

characteristics (age > 60 years, diabetes, symptoms > 10 minutes, weakness, and 

speech impairment) are associated with a higher short-term risk of stroke and may 

warrant admission for an expeditious evaluation. 

American Heart Association: Guidelines 2000 for cardiopulmonary resuscitation and 

emergency cardiovascular care. Circulation 2000;102:I204. [PMID: 11001640] 

Centeno RF et al: An alternative approach: antegrade catheter-directed thrombolysis in 

a case of phlegmasia cerulea dolens. Am Surg 1999;65:229. [PMID 10075298] 

Choucair MM et al: Leg ulcer diagnosis and management. Dermatol Clin 2001;19:659. 

[PMID: 11705353] 

Eklof B et al: Indications for surgical treatment of iliofemoral vein thrombosis. Hematol 

Oncol Clin North Am 2000;14:471. [PMID: 10806568] 

Greenwald DA et al: Ischemic bowel disease in the elderly. Gastroenterol Clin North Am 

2001;30:445. [PMID: 11432300] 

Johnston SC et al: Short-term prognosis after emergency department diagnosis of TIA. 

JAMA 2000;284:2901. [PMID: 11147987] 

Novelline RA et al: Helical CT in emergency radiology. Radiology 1999;213:321. 

[PMID:10551209] 

Verstraete M et al: Thrombolysis in the management of lower limb peripheral arterial

occlusion—a consensus document. Am J Cardiol 1998;81:207. [PMID: 9591906] 

Arterial Aneurysms 

RUPTURED ABDOMINAL AORTIC ANEURYSM 


• Sudden onset of abdominal or flank pain, pulsatile abdominal mass, and hypotension. 

• CT scan with contrast confirms diagnosis. 


An artery is described as aneurysmal once it reaches more than twice its normal 

diameter. The exact mechanism behind the formation of an abdominal aortic aneurysm 

(AAA) is unknown and is likely multifactorial. The belief that aneurysms are due to 

atherosclerosis alone has undergone serious challenge in the past several years. Risk 

factors include a family history of AAA, male gender, age greater than 70 years, 

long-term smoking, and systemic hypertension. This condition is fairly common, 

affecting 2-5% of the population over age 60 years. The primary complication of AAA is 

spontaneous rupture, which carries a high mortality rate. The chance of rupture 

increases exponentially as the diameter of the aneurysm increases (Table 38-2). 

If the aneurysm ruptures into the peritoneal space, exsanguination and death occur 

rapidly, usually prior to arrival in the emergency department. When rupture occurs into 

the retroperitoneal space, a tamponade effect may temporarily control hemorrhage and 

allow time for diagnosis and treatment. 



The classic symptoms of AAA rupture include sudden-onset abdominal or flank pain, 

pulsatile abdominal mass, and hypotension. However, because this triad is seen in only 

50% of patients presenting with AAA rupture, a high level of suspicion must be 

maintained. This diagnosis must be considered in patients with hypotension and shock 

of uncertain cause and in patients presenting with myocardial ischemia or infarction. 

Additionally, patients who have undergone previous aortic bypass grafting can present 

with gastrointestinal bleeding caused by erosion of the graft into the duodenum and 

subsequent rupture. 


The hematocrit may be normal or low. 


The electrocardiogram (ECG) may show signs of myocardial ischemia. 

D. Imaging

CT scan with contrast is the diagnostic test of choice in evaluating symptomatic AAAs in 

normotensive, hemodynamically stable patients. Abdominal x-ray may reveal the 

presence of an AAA due to calcification of the wall of the aneurysm (70% of AAAs). 

Ultrasound is used to diagnose and follow progression of asymptomatic AAAs. 

Aortography is used to investigate the vascular anatomy in the workup for elective 

(nonemergent) AAA repair. 

Treatment 

Act quickly. Even if the patient appears hemodynamically stable at the time of initial 

evaluation, the contained rupture may progress rapidly to exsanguinating hemorrhage at 

any time. 

Treat hypotension and shock (see Chapter 9 for more detail): 

1. Begin oxygen, 4 L/min, by nasal cannula or mask. 

2. Insert 2 large-bore (= 16-gauge) intravenous catheters by venous cutdown. 

3. Obtain blood for CBC, electrolyte determinations, and renal function tests; and type 

and cross-match for 10 units of packed red blood cells or whole blood. Measure the 

hematocrit immediately and at frequent intervals thereafter. Remember that the delay in 

equilibration of blood volume may keep the hematocrit falsely elevated for 12-18 hours. 

4. Give 1-3 L of crystalloid solution intravenously to restore adequate blood pressure, 

and follow with cross-matched blood. If the initial hematocrit is below 20%, either 

"universal donor" blood or type-specific blood may be necessary. 

5. Insert a urinary catheter, send urine for analysis, and monitor urine output. 

Request urgent consultation with a general or vascular surgeon, because immediate 

surgery is the only definitive treatment. 

Disposition 

Hospitalize all patients with suspected or documented ruptured abdominal aortic 

aneurysm. 

VISCERAL & HYPOGASTRIC ARTERY ANEURYSMS 


• Abrupt onset of diffuse abdominal pain. 

• Signs and symptoms of shock may be present. 

• CT scan with contrast or visceral angiography confirms diagnosis. 


Congenital aneurysm occurs in younger patients, whereas atherosclerotic aneurysm 

occurs more commonly in older patients. The splenic artery is the most commonly 

involved vessel. Bleeding may be confined to the lesser sac of the peritoneal cavity for 

the first 24-48 hours. However, free rupture into the general peritoneal cavity invariably 

causes exsanguination. Rupture is most common during pregnancy. Hypogastric artery 

aneurysms may rupture into the retroperitoneum or erode into contiguous organs, in 

which case gastrointestinal bleeding or hematuria occurs. 


There is abrupt onset of diffuse abdominal pain. Hypotension occurs secondary to blood 

loss. The hematocrit is low if the bleeding is more than a few hours old. CT scan with 

contrast is an excellent tool for diagnosis in the hemodynamically stable patient. 

Peritoneal lavage may reveal gross blood. A plain film of the abdomen may show an 

aneurysm if it has calcified. 

The only definitive diagnostic procedure is selective visceral angiography, which should 

be performed in the hemodynamically stable patient in whom an aneurysm is not 

present on a plain film. 

Treatment 

Start resuscitative measures, including insertion of a large-bore (= 16-gauge) 

intravenous catheter, nasogastric tube, Foley catheter, and the like (see Treatment 

section for ruptured abdominal aortic aneurysm, above, and Chapter 9). Draw blood for 

CBC, and type and cross-match for 8 units of packed red blood cells or whole blood. 

Notify a vascular surgeon at once, because early operation is imperative. 

Disposition 

Immediately hospitalize all patients with suspected or documented visceral and 

hypogastric artery aneurysms. 

THORACIC AORTIC ANEURYSM (Aortic Dissection) 


• Sudden, severe, tearing chest pain radiating to the back or neck. 

• Chest x-ray may show widened mediastinum. 

• CT scan with contrast confirms diagnosis. 


Aortic dissection is defined as extraluminal blood entering and dissecting between the 

intima and media of the aortic wall. Aortic dissection is the most common aortic surgical

emergency with an annual incidence of 5-10 cases per 100,000 population. Several 

classifications of aortic dissections have been described (Table 38-3). Approximately 

65% of tears occur in the ascending aorta. Less frequently they occur in the aortic arch 

(10%) or descending thoracic aorta (20%). Nearly 5% of aortic dissections occur in the 

abdominal aorta. Untreated aortic dissections are associated with an overall mortality 

rate of 21% in the first 24 hours, 60% within the first 2 weeks, and over 90% in the first 3 

months. For dissection of the ascending aorta, the 24-hour mortality rate is 60% and the 

2-week mortality rate is nearly 80%. 

Aortic dissection typically occurs in men who are middle-aged or older. It is associated 

with hypertension in nearly 90% of cases. Other predisposing conditions include 

connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome, Turner 

syndrome, tuberous sclerosis), congenital aortic anomalies including the valve, cocaine 

use, pregnancy, and weightlifting. 



The classic symptoms of acute aortic dissection are a sudden, severe, sharp or tearing 

chest pain. Most patients are either normotensive or hypertensive; a murmur of aortic 

insufficiency is auscultated less than half the time. The pain may migrate and include 

the back, neck, and jaw as the dissection progresses. As the dissection advances it may 

occlude any of the branches of the involved section of the aorta, leading to coronary 

insufficiency, strokes, mesenteric ischemia, acute renal insufficiency, and neurologic 

deficits secondary to spinal cord ischemia. Patients may also present with cardiac 

tamponade, congestive heart failure, or Horner syndrome. 

Depending on which vessels have been compromised, there may be signs of CVA, 

acute myocardial infarction, clinical findings associated with arterial occlusion of an 

extremity (ischemia, absent pulses), abdominal or back pain with or without hematuria 

or ileus, or wide difference in blood pressure measurements in the 2 arms or in an arm 

and a leg on the same side. 

If the base of the aortic valve is involved, varying degrees of aortic insufficiency occur. 

The dissection may leak into the pleura or pericardium, causing a pericardial or pleural 

friction rub with effusion. 

When rupture starts, shock of sudden and catastrophic onset may occur as a result of 

cardiac tamponade, massive hemothorax, or hemomediastinum. The patient may have 

a history of one or more of the conditions listed above. 


Hematuria may be present; the hematocrit may be normal or low. 


Approximately 40% of patients with aortic dissection will have ST-segment or T-wave 

changes on their ECG. Only 30% of patients will have a normal ECG (Table 38-4). 

D. Imaging

Although the chest x-ray may show a widened mediastinum, abnormal aortic contour, or 

pleural effusion, these findings are inconsistent. According to the International Registry 

of Acute Aortic Dissection study, over 12% of patients presenting with an aortic 

dissection will have a normal chest x-ray (see Table 32-4). In recent years, CT scan with 

contrast has replaced aortography as the imaging mode of choice to diagnose aortic 

dissection. Although each method has a sensitivity and specificity approaching 100%, 

CT scan is noninvasive and is generally more available than arteriography. TEE has 

also been found to be highly reliable in the investigation of the thoracic aorta. Many 

authorities recommend TEE as the modality of choice when readily available, because 

of its expediency and accuracy. 

Goals of Treatment 

There are 3 main goals of treatment: 

A. Reduce Hypertension 

Hypertension must be controlled. The forces contributing to the development of 

dissection are a function of increased systolic blood pressure and the force generated 

with each systolic contraction of the left ventricle. Accordingly, once dissection is 

suspected, the essential first step is to reduce systolic pressure and the rate of rise of 

the left ventricular pressure wave (dp/dt) if the patient is not hypotensive. If the patient is 

hypotensive, treat for hypovolemic shock (Chapter 9). 

B. Manage Pain 

Use titrated narcotic analgesia to control the patient's pain. 

C. Obtain Surgical Consultation 

Obtain immediate vascular or thoracic surgery consultation for consideration of 

operative repair. 

Treatment 

A. All Patients 

1. Insert 2 or more large-bore (= 16-gauge) intravenous catheters or perform venous 

cutdowns. 

2. Draw blood for CBC, electrolyte measurements, tests of renal function, PT, PTT, and 

typing and cross-matching (reserve 10 units of packed red blood cells of whole blood). 

3. Insert a Foley catheter, send urine for urinalysis, and monitor urine output on an 

hourly basis. 

4. Give oxygen, 5 L/min, by mask or nasal cannula. 

5. Obtain immediate vascular or thoracic surgical consultation. 

B. Patients with Normotension, Hypotension, or Shock 

1. Assume that free rupture or cardiac tamponade has occurred.

2. Begin intravenous infusion of crystalloid solutions to support blood pressure; give 

packed red blood cells or whole blood as soon as available. 

3. Obtain chest x-ray (if possible) to confirm the diagnosis. 

4. Consult with the surgeon, who will decide whether immediate operation or 

confirmatory studies are necessary. 

5. Perform immediate surgery if cardiac tamponade or gross aortic insufficiency is 

present. 

C. Patients with Hypertension 

Institute emergency control of blood pressure with an intravenous infusion of 

nitroprusside and a ß-blocker. Nitroprusside reduces both preload and afterload by 

causing arterial and venous dilation. The ß-blocker counters the reflex tachycardia and 

increased contractility expected with preload and afterload reduction. 

1. Start an infusion of Esmolol (short-acting, intravenous ß-blocker). Give a loading dose 

of 500 ug/ kg followed by an infusion of 25-200 ug/kg/ min. Titrate the infusion to a goal 

heart rate of 60-70 beats/min. 

2. Start an infusion of nitroprusside at a rate of 0.5-10 ug/kg/min. Titrate the infusion to 

the lowest blood pressure compatible with adequate organ perfusion, typically a mean 

arterial pressure of 60-70 mm Hg. 

3. If intensive blood pressure monitoring is not available, labetalol hydrochloride, an a- 

and ß-adrenergic receptor-blocking agent, may be used effectively by itself to reduce 

blood pressure and left ventricular dp/dt. Give 20 mg over 2 minutes by intravenous 

injection. Additional doses of 40-80 mg can be given every 10 minutes (maximum dose 

300 mg) until the desired blood pressure has been reached. (Alternatively, 2 mg/min 

may be given by intravenous infusion, titrated to desired effect.) 

Disposition 

Hospitalize all patients without delay. Obtain urgent cardiothoracic surgical consultation 

for all patients, even those already receiving medical treatment. 

POPLITEAL & FEMORAL PERIPHERAL ANEURYSMS 


• Symptoms are due to thrombus, embolization, or pressure from an expanding 

aneurysm. 

• Pulsatile mass on physical examination (if not thrombosed). 

• Ultrasound confirms diagnosis. 

• Arteriography defines distal arterial circulation.


Occlusion or distal embolization of the friable lining of peripheral aneurysms results in 

symptoms of distal ischemia. Unlike AAA or visceral aneurysm, rupture is rare. The 

most common locations of peripheral aneurysms are the popliteal artery and, 

secondarily, the femoral artery. Popliteal aneurysms are often bilateral and are often 

associated with AAAs. 

Acute occlusion can result in severe distal ischemia. Distal embolization can also result 

in severe distal ischemia; however, it is often associated with episodes of moderate 

ischemia that decrease as collateral circulation improves. 



Symptoms are due to thrombosis, embolization, pressure from an expanding aneurysm, 

or (rarely) rupture. There may be an arterial mass in the popliteal fossa or the groin. The 

aneurysm is pulsatile unless it is thrombosed. Signs of acute arterial occlusion often 

coexist. 

Popliteal aneurysms can cause symptoms (eg, signs of venous obstruction, weakness, 

sensory defects) when they compress the popliteal vein or tibial nerve. Rupture of the 

aneurysm is rare. 

B. Imaging 

1. Plain x-ray—A rim of calcification may be apparent in the wall of the aneurysm. 

2. Arteriography—Arteriography may not demonstrate the aneurysm if it is 

thrombosed, but this procedure is generally advised to define the status of the arterial 

circulation distal to the aneurysm. 

3. Ultrasonography—Ultrasonography is helpful in identifying the presence of an 

aneurysm. 

Treatment 

Notify a vascular surgeon, because immediate operation is required when severe distal 

ischemia has occurred secondary either to acute thrombosis or to distal embolization. 

Elective operation is recommended for any aneurysm producing compression of 

adjacent structures as well as for most documented popliteal aneurysms, because the 

rate of complication is high if these are left untreated. 

Disposition 

All symptomatic patients should be hospitalized immediately. 

Dmowski AT et al: Aortic dissection. Am J Emerg Med 17;372. [PMID: 10452437]

Fikar CR et al: Etiologic factors of acute aortic dissection in children and young adults. 

Clin Pediatr 2000;39:71. [PMID: 10696543] 

Hagan PG et al: The international registry of acute aortic dissection (IRAD): new insight 

into an old disease. JAMA 2000; 283:897. [PMID: 10685714] 

Hallett JW: Management of abdominal aortic aneurysms. Mayo Clin Proc 2000;75:395 

[PMID: 10761495] 

Ledbetter S et al: Helical (spiral) CT in the evaluation of emergent thoracic aortic 

syndromes: traumatic aortic rupture, aortic aneurysm, aortic dissection, intramural 

hematoma, and penetrating atherosclerotic ulcer. Radiol Clin North Am 1999; 37:575. 

[PMID: 10361547] 


10551209] 

Sternbergh WC III et al: Abdominal and thoracoabdominal aortic aneurysm. Surg Clin 

North Am 1998;78:827. [PMID: 9891579] 

VENOUS DISEASE 

Lower-Extremity Deep Venous Thrombosis 


• Unilateral swelling, warmth, and redness of affected limb. 

• Physical examination is unreliable in diagnosing deep venous thrombosis. 

• Contrast venography or ultrasound confirms diagnosis. 


Deep venous thrombosis (DVT) results in 600,000 hospitalizations each year in the 

United States. If untreated, DVT commonly results in pulmonary embolism, thus making 

it a significant source of morbidity and mortality. 

As described by Virchow in 1856, venous thrombosis is predisposed by stasis of blood 

flow, hypercoagulopathy, and vascular endothelial injury. Specific conditions associated 

with development of DVT are shown in Table 38-5. 



Patients with symptomatic DVT typically complain of unilateral lower-extremity pain and 

swelling that begins gradually and progresses over days. The described sense of 

fullness may worsen with standing or walking. Physical examination is of little help in

diagnosing DVT and should not be used to exclude diagnosis. Possible findings include 

unilateral lower-extremity edema, warmth, or erythema. There may be tenderness along 

the course of the affected vessel, and rarely the clot will be palpable. The time-honored 

Homans sign (pain in posterior calf with passive dorsiflexion of the foot) has been 

shown to be unreliable in diagnosing DVT. Because the DVT results in a systemic 

inflammatory response, the patient may be febrile. Adjunctive testing is required 

because physical examination is unreliable in diagnosing DVT. 


1. Contrast venography—Although contrast venography remains the gold standard for 

diagnosing DVT, it has been largely replaced by ultrasonography in most institutions. 

The advantages of contrast venography include a sensitivity and specificity of nearly 

100% and the ability to detect DVTs of the calf, iliac vessels, and inferior vena cava that 

can be missed by ultrasound. Its primary disadvantages include its invasive nature, use 

of contrast material, and availability. Additionally, 5-15% of studies performed are 

technically inadequate. 

2. Ultrasonography—Ultrasonography is the most accurate noninvasive study for 

diagnosing lower-extremity DVT, with a sensitivity of 93-100% and a specificity of 

97-100% in detecting proximal DVTs. The limitations of ultrasonography are its ability to 

detect pelvic and calf DVTs (20% of which will extend into the popliteal vein and thigh). 

3. D-Dimer assay—D-dimer is formed when fibrin is degraded by plasmin. The testing 

for the presence of D-dimer is by latex agglutination (least sensitive), whole blood 

agglutination (bedside, qualitative), and enzyme-linked immunoassay (ELISA) (most 

accurate). When combined with ultrasound, the whole blood agglutination and ELISA 

have an almost 100% negative predictive value. 

Treatment 

For DVT of proximal veins of the thigh, put the patient on bed rest and elevate the limb. 

Catheter-directed thrombolytic therapy with streptokinase or urokinase is effective in 

treating acute DVT less than 7 days old and may prevent postphlebitic complications. 

Alternatively, start anticoagulation with intravenous heparin or SC low-molecular-weight 

heparin. Obtain consultation with a vascular surgeon in cases of massive iliofemoral 

thrombosis. Surgery may be required for certain patients. 

Management of calf DVT and the need for hospitalization are controversial. Isolated calf 

thrombi do not commonly produce pulmonary emboli, although they may propagate into 

proximal vessels. Traditional treatment has been low-dose heparin (eg, 5000 units 

subcutaneously twice a day), although some authors advocate serial noninvasive 

studies (eg, ultrasound) and treatment only if propagation occurs. 

Disposition 

All patients with proximal DVT should be hospitalized. Because of the association 

between DVT and malignancy, patients with a new diagnosis of DVT should be referred 

to a primary care provider for further evaluation.

SUPERFICIAL THROMBOPHLEBITIS 


• Pain, tenderness, induration, and erythema along course of affected vein. 

• Affected extremity shows only slight to no edema (no other signs of impaired venous 

return). 


Superficial venous thrombosis of the upper extremity is usually iatrogenic, occurring 

secondary to intravenous catheterization. Lower-extremity superficial venous 

thromboses may be associated with varicose veins, bacterial infection of surrounding 

tissues, trauma, or thromboangiitis obliterans. Trauma may play a part in the 

development of thrombi or may cause recurrences. 


Pain, tenderness, induration, and erythema are noted along the course of the involved 

vein, which may feel like a cord. The extremity shows only slight or no swelling, and 

there are no other signs of impaired venous return. 

Septic thrombophlebitis usually occurs following intravenous injections (especially 

among intravenous drug abusers) and at venous catheter sites. It should be suspected 

in the presence of the above symptoms or fluctuance along a superficial vein. Fever and 

rigors may be present. The diagnosis is confirmed if pus can be aspirated from the vein. 

Treatment 

A. Cases with No Complications 

For uncomplicated superficial venous thrombosis, only symptomatic treatment is 

required. Neither bed rest nor anticoagulation is indicated. An elastic bandage at and 

above the level of thrombosis helps to speed remission. Elevation of the leg when the 

patient is sitting and nonsteroidal anti-inflammatory drugs are also helpful. 

B. Cases with Complications 

Obtain general or vascular surgical consultation for all complications. If clinical 

examination suggests that the thrombosis is approaching the saphenofemoral junction, 

ligation and division of the saphenous vein are indicated, because pulmonary 

embolization can result from deep venous involvement. 

If septic thrombophlebitis occurs, parenteral antimicrobials are required, and the 

involved segment of vein must be excised or ligated and drained to prevent persistent 

bacteremia. 

Disposition

Patients with mild, localized superficial thrombosis may be discharged. Patients with 

more serious disease, including suspected or documented septic thrombophlebitis, 

should be hospitalized. 

UPPER-EXTREMITY VENOUS THROMBOSIS 


• Pain and swelling of affected limb. 

• Occurs in 3% of patients with a central venous catheter. 

• Examination reveals nonpitting edema, normal skin color, and intact distal pulses. 

• Contrast venography or ultrasonography confirms diagnosis. 


Upper-extremity deep venous thrombosis (UEDVT) is much less common than 

lower-extremity DVT but remains an important cause of morbidity because of its 

association with pulmonary embolism and postphlebitic sequelae (persistent 

upper-extremity pain and swelling). Nearly 12% of cases of UEDVT will be complicated 

by pulmonary embolism. Mortality from UEDVT is approximately 1%. 

The most common risk factor for UEDVT is central venous catheter placement, with 

clinically significant thrombus formation in 3% of patients with a central line. The second 

most common category of UEDVT is spontaneous (effort-related) thrombosis. Risk 

factors include repetitive activities involving hyperabduction of the shoulder and aberrant 

anatomy of the costoclavicular space. Other causes include intravenous drug use, 

thoracic tumors, and radiation. The most commonly affected site of thrombosis is the 

axillary-subclavian venous system. 



Patients typically present with pain and swelling of the affected limb. The risk factors 

discussed above may be present. Physical examination may reveal nonpitting edema of 

the affected side forearm (occasionally the whole arm), normal skin color, and intact 

distal pulses. Venous cords may be palpable. 

B. Imaging 

As with lower-extremity DVT, contrast venography remains the gold standard for 

diagnosis of UEDVT. However, it is slowly being replaced by ultrasonography, which 

has been shown to have a high degree of sensitivity and specificity for diagnosing 

UEDVT. 

Treatment 

Initial treatment involves immobilization, elevation, and the application of heat to the 

affected limb. This is followed by systemic anticoagulation with intravenous heparin or

SC low-molecular-weight heparin. Other options include catheter-directed thrombolysis 

and surgical thrombectomy. Frequently surgery is required to correct underlying 

anatomic defects to prevent recurrence. Consult a vascular surgeon. 

Disposition 

Hospitalize all patients for definitive management. 

RUPTURED VENOUS VARICOSITIES (Varicose Veins) 


• Bleeding from varicose veins, usually due to minor trauma. 


Rupture is an uncommon complication of varicose veins. The skin overlying varices can 

become thin, and erosion can occur spontaneously or with minor trauma. 


Bleeding from varicose veins is present and may be brisk. 

Treatment 

Gentle digital pressure over the bleeding site and elevation of the leg control the initial 

bleeding. Suture ligature of the ruptured vein may be necessary to definitively stop the 

bleeding. When the initial bleeding has been controlled, the leg should be wrapped in an 

elastic bandage or Unna's paste boot. Consult a vascular or general surgeon about 

elective stripping of varicose veins. 

Disposition 

Brief hospitalization may be advisable. 

PULMONARY EMBOLISM 

Pulmonary embolism is an occasional complication of venous thrombosis. It is 

discussed in Chapter 33. 

ARTERIOVENOUS FISTULA 


• Abnormal connection between arteries and veins.

• Constant systolic and diastolic (to-and-fro) murmur and palpable thrill at site. 

• Arteriography confirms diagnosis. 


Arteriovenus fistulas are abnormal connections between arteries and veins. They may 

be congenital or acquired. Congenital lesions tend to have more diffuse connections 

and may involve an extremity. Acquired arteriovenous fistulas—other than those 

constructed to gain access for dialysis—generally occur secondary to trauma and result 

from erosion of the artery into a contiguous vein. Other causes include malignancy, 

infection, and arterial aneurysm. The physiologic effect depends on the size of the 

communication. 


A constant systolic and diastolic (to-and-fro) murmur is heard, and a thrill is palpable 

over most arteriovenous fistulas. Cardiac output may be high if significant left-to-right 

shunting of blood exists. Patients with congenital arteriovenous fistulas may show 

increased muscle mass, increased bone length, clubbing, and cyanosis of the involved 

limb. Polycythemia may also be present. 

Complications 

Complications include cosmetic deformity due to limb disproportion, congestive heart 

failure, severe arterial insufficiency, expanding false aneurysm, and hemorrhage. 

Arteriography delineates the precise outlines of the lesion and may be used for 

therapeutic embolization. 


Patients with pain, expanding mass, heart failure, or obvious high cardiac output require 

hospitalization. Others may be discharged from the emergency department and referred 

to a vascular surgeon or general surgeon. 

Centeno RF et al: An alternative approach: antegrade catheter-directed thrombolysis in 

a case of phlegmasia cerulea dolens. Am Surg 1999;65:229. [PMID: 11705353] 

Choucair MM et al: Leg ulcer diagnosis and management. Dermatol Clin 2001;19:659. 

[PMID: 10075298] 

Dauzat M et al: Diagnosis of acute lower limb deep vein thrombosis with ultrasound: 

trends and controversies. J Clin Ultrasound 1997;25:343. [PMID: 9282799] 

Eklof B et al: Indications for surgical treatment of iliofemoral vein thrombosis. Hematol 

Oncol Clin North Am 2000;14:471. [PMID: 10806568] 

Heron E et al: Long-term sequelae of spontaneous axillary-subclavian venous 

thrombosis. Ann Int Med 1999;131:510. [PMID: 10507960]

Kennedy D et al: Physical examination findings in deep vein thrombosis. Emerg Med 



10551209] 

Rosen CL et al: The diagnosis of lower extremity deep vein thrombosis. Emerg Med Clin 

North Am 2001;19:895. [PMID: 11762272] 

Stephens MB: Deep venous thrombosis of the upper extremity. Am Fam Physician 

1997;55:533. [PMID: 9054222] 

OTHER VASCULAR SYNDROMES 

THORACIC OUTLET SYNDROME 


• Signs and symptoms caused by compression of the neural, arterial, or venous 

structures at the thoracic outlet. 

• Hand or arm fatigue with use, especially with abduction of the arm. 

• Elevated arm stress test may elicit symptoms. 


Thoracic outlet syndrome comprises a variety of disorders caused by abnormal 

compression of the neural, arterial, or venous structures at the superior aperture of the 

thorax (thoracic outlet); the most common is compression of nerve structures against 

the first rib. Symptoms of dysfunction of branches of the brachial plexus are far more 

common than symptoms secondary to compression of the axillary-subclavian artery or 

vein, accounting for approximately 95% of cases. Compression of the 8th cervical and 

1st thoracic nerve roots (C8 and T1) is most common. The second most common 

pattern is involvement of the 3 uppermost nerve roots of the brachial plexus, the 5th 

through 7th cervical nerve roots (C5-C7). Thoracic outlet syndrome is rarely an 

emergency. 


A. Symptoms 

The diagnosis is typically made on clinical grounds with patients complaining of hand or 

arm fatigue with use, especially with activities involving abduction of the arm. More 

subtly, patients may note wasting of the muscles of the hand. 

If symptoms are due to nerve compression, patients may complain of positional 

paresthesias in the distribution of one or more trunks of the brachial plexus. 

Compression of C8-T1 nerve roots results in paresthesias in the ulnar nerve distribution, 

whereas symptoms referable to C5-C7 compression may involve the ear, neck, upper

thorax, or lateral aspect of the shoulder. Raynaud symptoms, secondary to compression 

of sympathetic nerve fibers may also be reported. 

Symptoms of venous compression and thrombosis include pain and swelling of the 

affected limb. Patients with arterial thoracic outlet syndrome with resultant 

subclavian-axillary artery stenosis or aneurysm formation may present with symptoms of 

acute arterial occlusion or embolization. 

B. Signs 

Physical examination should include the elevated arm stress test (EAST test) in an 

attempt to provoke symptoms. In this test the patient externally rotates and abducts 

both arms to 90 degrees with elbows flexed 90 degrees and shoulders braced 

posteriorly. The patient then opens and closes both hands for a 3-minute period. 

Patients with thoracic outlet syndrome will complain of the rapid onset of fatigue and 

heaviness of the arms and are often unable to complete the entire test. Paresthesias 

may also be reproduced. 

In neurologic thoracic outlet syndrome, wasting of the lateral thenar muscles of the 

hand, weakness of the intrinsic muscles of the hand, and patchy sensory deficits in the 

distribution of the involved nerve roots may be seen. Reproducible paresthesias during 

the EAST test may be elicited. 

Findings in arterial thoracic outlet syndrome include a blood pressure differential in the 

upper extremities, a bruit with auscultation over the subclavian or axillary artery, and 

radial pulse deficit on the affected side during the EAST test. Findings of acute arterial 

occlusion or embolization may be found. Thoracic outlet syndrome secondary to venous 

occlusion or thrombosis may be associated with swelling of the affected extremity and 

normal pulses. 

C. Imaging 

1. X-rays—Plain film radiographs of the cervical spine or chest may reveal skeletal 

abnormalities predisposing to thoracic outlet syndrome (cervical rib, first rib, or clavicle 

deformity). 

2. Angiography—Angiography may be indicated for evaluation of acute arterial 

occlusion or embolization. 

3. Ultrasonography—Ultrasonography may be indicated for evaluation of arterial 

aneurysms or venous thrombosis. 

4. Venography—Venography may be indicated for evaluation of venous thrombosis. 


Patients with neurologic thoracic outlet syndrome can be discharged with a referral to a 

neurologist or thoracic surgeon. Patients with evidence of a venous or arterial 

abnormality and stable symptoms should be referred to a vascular or thoracic surgeon. 

If venous thrombosis or arterial occlusion or embolization is present, the patient should 

be hospitalized with immediate surgical consultation.

COMPLICATIONS OF PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY & 

RETROGRADE ANGIOGRAPHY 


• History of recent percutaneous procedure. 

• May see complications at puncture site or signs and symptoms due to thrombosis or 

embolization. 

An increasing number of patients are undergoing percutaneous transluminal angioplasty 

(balloon dilatation of the arteries) and angiography via the femoral artery. These 

patients are observed for the development of immediate complications but are usually 

discharged from the hospital within 24-48 hours and may subsequently present to the 

emergency department with complications (Table 38-6). 

Hospitalize the patient, and obtain prompt vascular or cardiothoracic surgical 

consultation, because many of these complications require surgical treatment. 

ERGOTISM 


• History of ergotamine use or exposure. 

• Mottled cyanosis of the thighs and lower legs with intense cyanosis of the feet. 


Ergotism is caused by ergotamine tartrate or other ergot derivatives or by consumption 

of rye contaminated by ergot fungus. The disease is characterized by profound 

vasoconstriction that is almost always limited to the lower extremities. 


There is mottled cyanosis of the thighs and lower legs, with intense cyanosis of the feet. 

Prolonged vasospasm may result in distal thrombosis. Secondary tissue loss may 

occur. Other findings include vomiting, diarrhea, cramps, and various central nervous 

system symptoms. 


Hospitalize the patient, and maintain adequate blood pressure and intravascular 

volume. Withdraw ergotamine medication. Vasodilators and heparin anticoagulation 

may be indicated. Hyperbaric oxygen therapy may be tried, although there is no 

evidence of benefit. Consult a general surgeon or vascular surgeon. Lumbar

sympathectomy may be required. 

INTRA-ARTERIAL INJECTION OF DRUGS 


• History of parenteral drug injection. 

• Severe burning pain distal to injection site. 


Inadvertent or intentional intra-arterial injection of drugs can cause intense vasospasm 

followed by arterial occlusion, with distal gangrene as a possible result. This is 

commonly known as a "hand trip" by intravenous drug abusers. Vasospasm may occur 

while the drug is being given, or the reaction may be delayed. Unfortunately, many 

patients with delayed reactions fail to seek medical attention until ischemia is advanced. 


There is a history of therapeutic or illicit drug injection by the parenteral route. Severe 

burning pain in distal arterial distribution is followed by intense vasospasm. If the 

vasospasm has been prolonged, gangrene of the fingers or entire hand may occur even 

though the arterial vasoconstriction subsequently resolves. 


Hospitalize the patient, and obtain vascular surgical consultation. If the needle is still in 

place, irrigate distally with heparinized saline. Start systemic anticoagulation with 

heparin. Systemic vasodilating agents may be necessary to treat the intense 

vasospasm. Intra-arterial injection of vasodilators (eg, reserpine) is not usually 

beneficial. If sympathetic nerve block is indicated because of persistent severe 

peripheral ischemia, consult an anesthesiologist or vascular surgeon. 

FROSTBITE 

Arterial injury is a major pathogenetic factor in frostbite injury. See Chapter 44 for details 

of diagnosis and treatment. 

Gelabert HA et al: Diagnosis and management of arterial compression at the thoracic 

outlet. Ann Vasc Surg 1997;11:359. [PMID: 9236991] 

Wilbourn AJ: Thoracic outlet syndromes. Neurol Clin 1999;17: 477. [PMID: 10393750] 

Location In Book:




DO, FACEP 

INTRODUCTION

Table 38-1. X-ray findings associated with traumatic rupture 

of the thoracic aorta. 





DO, FACEP 

TABLES 

Table 38-1. X-ray findings associated with traumatic rupture of the thoracic 

aorta.

Table 38-2. Annual risk of rupture of an abdominal aortic 

aneurysm as a function of the size of the aneurysm. 

Annual Risk of Rupture 

Rare 

4-5 cm 5-10% per year 

Greater than 7 cm

Table 38-3. Aortic dissection classification systems. 

Type I Stanford System 

Involves the 

ascending 

aorta 

Type B All others 





DO, FACEP 

TABLES 

Table 38-3. Aortic dissection classification systems.

Table 38-4. Chest radiography and electrocardiogram results for patients with acute aortic dissection. 

Present, No. 

Reported (%) 

427 (100) 171 (97.7) 

53 (12.4) 27 (15.8) 

91 (21.3) 47 (27.5) 

263 (61.6) 94 (56) 

212 (49.6) 88 (53) 

110 (25.8) 41 (24.0) 

60 (14.1) 31 (18.1) 

82 (19.2) 36 (21.8) 

139 (31.3) 54 (32.1) 

184 (41.4) 68 (42.8) 

116 (26.1) 498 (32.2) 

67 (15.1) 20 (13.2) 

34 (7.7) 15 (9.9) 

14 (3.2) 1 (0.7) 

277 (61.1) 132 (75.4) 

148 (32.7) 26 (14.9) 

20 (4.4) 8 (4.6) 

8 (1.8) 6 (3.4) 

1.83 (0.82) 2.15 (0.91) 

Classification 2 

Type B, No. (%)

Table 38-5. Factors predisposing to 

deep venous thrombosis. 

1 

Causes secondary protein S 

deficiency. 





DO, FACEP 

TABLES 

Table 38-5. Factors predisposing to deep venous thrombosis.

Table 38-6. Complications of percutaneous transluminal angioplasty. 





DO, FACEP 

TABLES 

Table 38-6. Complications of percutaneous transluminal angioplasty.

Figure 38-1. Zones of vascular injury in the neck. 





DO, FACEP 

FIGURES 

Figure 38-1

Figure 38-2. Chest x-ray from a patient with a traumatic aortic injury demonstrating a 

wide mediastinum, blurring of the aortic arch, left apical cap, and deviation of the 

nasogastric tube. 





DO, FACEP 

FIGURES 

Figure 38-2

39. Hematologic Emergencies - J. Stephan Stapczynski, MD, & 

Geoffrey A. Martin, MD 

I. HEMOSTATIC DISORDERS: GENERAL CONSIDERATIONS 

Most bleeding seen in the emergency department is due to trauma—the result of local 

wounds, lacerations, or other structural lesions—occurring in patients with normal 

hemostasis. Conversely, bleeding from multiple sites, bleeding from untraumatized 

sites, delayed bleeding several hours after trauma, and bleeding into deep tissues or 

joints suggests the possibility of a bleeding disorder. Historical data for the presence of 

a congenital bleeding disorder include the presence or absence of unusual or abnormal 

bleeding in the patient and other family members and the possible occurrence of 

excessive bleeding after dental extractions, surgical procedures, or trauma. Many 

patients with abnormal bleeding have an acquired disorder, commonly due to liver 

disease or drug use (particularly ethanol, aspirin, nonsteroidal anti-inflammatory drugs 

[NSAIDs], warfarin, and antibiotics). 

The site of bleeding may provide an indication of the hemostatic abnormality. 

Mucocutaneous bleeding—including petechiae; ecchymoses; epistaxis; or 

gastrointestinal, genitourinary, or heavy menstrual bleeding—is characteristic of 

qualitative or quantitative platelet disorders. Purpura is often associated with 

thrombocytopenia and commonly indicates a systemic illness. Bleeding into joints and 

potential spaces, such as between fascial planes and into the retroperitoneum, as well 

as delayed bleeding, is most commonly associated with coagulation factor deficiencies 

(Figure 39-1). Patients who demonstrate both mucocutaneous bleeding and bleeding in 

deep spaces may have disorders such as disseminated intravascular coagulation (DIC), 

in which both platelet abnormalities and coagulation factor abnormalities are present. 

Basic hemostatic tests and clinical evaluation are generally adequate for diagnosis 

(Table 39-1). Additional hemostatic studies are ordered as indicated (Table 39-2). 

II. HEMOSTATIC DISORDERS: PLATELET DISORDERS 

DISORDERS OF DECREASED PLATELET PRODUCTION 

Neonatal infections, such as cytomegalovirus (CMV) or rubella, may cause isolated 

thrombocytopenia. Many medications impair platelet production and produce 

thrombocytopenia (Table 39-3). Chronic alcohol use is a common cause of 

thrombocytopenia and will generally resolve if the patient abstains from drinking for 

longer than 7 days. If multiple cell lines are affected, the differential diagnosis includes 

aplastic anemia, marrow infiltration from lymphoma or leukemia, or myelofibrosis. 

Usually the history and physical examination determines the most likely source of 

thrombocytopenia; however, bone marrow biopsy is sometimes needed. 

IMMUNE THROMBOCYTOPENIA 

Antibody-mediated platelet destruction can be related to medications, infections, or

autoimmune diseases. Two of the more common antibody-mediated thrombocytopenic 

disorders are idiopathic thrombocytopenic purpura (ITP) and drug-induced immune 

thrombocytopenia. 

1. Idiopathic Thrombocytopenic Purpura 


ITP is an acquired autoimmune disease characterized by thrombocytopenia, the 

presence of purpura or petechiae, normal bone marrow, and no other identifiable cause 

for the thrombocytopenia. Platelet destruction is mediated by the production of 

autoantibodies that attach to circulating platelets, and the antibody-coated platelets are 

removed by the reticuloendothelial system. The bone marrow usually responds by 

increasing platelet production, but sometimes the same antibodies that bind to the 

platelets also bind to the megakaryocytes, limiting the bone marrow response. Despite 

the presence of antibodies, the circulating platelets function properly, and many people 

with ITP may not have significant bleeding despite low platelet counts. 

ITP occurs in all age groups and may have an acute or chronic course. Acute ITP is 

more common among younger children, affects males and females equally, and 

typically resolves in 1-2 months. Chronic ITP lasts more than 3 months, is more 

common in adults, has a female predilection, and rarely remits spontaneously. 

Additionally, patients with chronic ITP are more likely to exhibit an underlying disease or 

autoimmune disorder, such as HIV infection, systemic lupus, Graves disease, 

Hashimoto thyroiditis, or antiphospholipid antibody syndrome. 


The most common symptom of ITP is petechiae; mild bleeding may also be seen at 

mucosal surfaces, including epistaxis, gingival bleeding, and menorrhagia in women of 

child-bearing age. The physical examination is otherwise normal; the presence of 

lymphadenopathy, hepatosplenomegaly, anemia, or hyperbilirubinemia should suggest 

an alternative diagnosis, such as leukemia, lymphoma, systemic lupus erythematosus, 

infectious mononucleosis, or hemolytic anemia. The complete blood count (CBC) should 

be normal in all cell lines except for the platelets. In some patients with bleeding, a mild 

anemia may be present. The peripheral blood smear should show large, well-granulated 

platelets that are few in number. The diagnosis of ITP is based primarily on the history, 

physical examination, CBC, and peripheral smear. 

Treatment 

Minimize bleeding risks in patients with ITP, for example, by avoiding the use of 

antiplatelet medications (eg, aspirin and NSAIDs), avoiding unnecessary invasive 

procedures, maintaining good blood pressure control, treating exacerbating comorbid 

conditions (eg, liver disease, renal disease), and addressing fall risks. Treatment of ITP 

depends on severity, comorbid conditions, and presence of bleeding. Asymptomatic 

patients, who are otherwise healthy, with platelet counts greater than 50,000/uL require 

no treatment. Treatment is indicated for (1) nonbleeding patients with platelet counts 

less than 20,000/uL and (2) patients with bleeding or significant risk factors for bleeding

and platelet counts less than 50,000/uL. Initial therapy in adults is prednisone started at 

60-100 mg/d (children, 1-2 mg/d) and tapered after the platelet count reaches normal 

(usually requires 4-8 weeks). For patients who do not respond to steroids, the main 

alternative therapy is splenectomy. For life-threatening bleeding, the current 

recommendation is high-dose steroid therapy (methylprednisolone 1-2 g/d intravenously 

for 2-3 days) with or without intravenous immunoglobulin. Transfuse platelets as needed 

following the first dose of methylprednisolone or immunoglobulin; holding the platelet 

transfusion until the first dose of either is completed results in a better response. 

Conjugated estrogen, 25 mg intravenously one time, can be given for severe uterine 

bleeding. 

Disposition 

Hospitalization is required for ITP-related bleeding. Hospitalization is generally not 

required for asymptomatic patients with platelet counts greater than 20,000/uL. At 

counts below 20,000/uL, hospitalization may not be required if patients are 

asymptomatic or have only mild purpura. Hospitalization is prudent when arranging 

patient follow-up is difficult, when compliance is in doubt, or when significant additional 

bleeding risk factors are present. 

2. Drug-Induced Immune-Mediated Thrombocytopenia 

Heparin is the drug most commonly associated with drug-induced immune-mediated 

thrombocytopenia. Platelet counts typically fall after the 5th day of therapy, usually to 

below 100,000/uL; less than 10% of patients develop profound thrombocytopenia with 

counts less than 20,000/uL. Paradoxically, the complications from heparin-induced 

thrombocytopenia are usually thromboembolic (deep venous thrombosis, pulmonary 

embolism, stroke), the conditions heparin is used to treat. Immediate cessation of 

heparin therapy is indicated when the platelet count falls to below 100,000/uL or more 

than 50% from baseline. Substitute alternative agents (eg, danaparoid, hirudin, 

argatroban) for heparin. Avoid future exposure to either unfractionated heparin or the 

low-molecular-weight heparins. 

The platelet glycoprotein IIb/IIIa receptor antagonists are associated with a 3-7% 

incidence of modest thrombocytopenia (platelet counts of 50,000- 100,000/uL), typically 

occurring within the first 24 hours of treatment. Severe thrombocytopenia (below 

20,000/uL) occurs in less than 1% of patients. Petechiae, wound hematomas, mucosal 

bleeding, and hematuria are the most common hemorrhage complications. Platelet 

counts return to normal within 2-3 days after drug discontinuation. 

Other drugs rarely cause immune-mediated thrombocytopenia; the sulfonamide, 

penicillin, and cephalosporin antibiotics have been most commonly reported. In this 

circumstance, thrombocytopenia typically develops 7-10 days after start of the 

medications, platelet counts typically fall to below 20,000/uL, and the most common 

symptoms are petechiae and oral mucosal hemorrhagic blisters. 

THROMBOTIC THROMBOCYTOPENIC PURPURA & HEMOLYTIC UREMIC 

SYNDROME

Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) 

involve platelet aggregation in the microvascular circulation via the mediation of von 

Willebrand factor (vWF), leading to consumption thrombocytopenia and 

microangiopathic hemolytic anemia (MAHA) or schistocyte-forming hemolysis as red 

blood cells (RBCs) are fragmented during travel through these occluded arterioles and 

capillaries. TTP and HUS are clinical syndromes with characteristic features, but overlap 

between the syndromes makes differentiation sometimes difficult. TTP is traditionally 

more common in adults, whereas HUS is more common in children. TTP typically 

induces more prominent neurologic deficits with deposition of platelet aggregates in a 

broader, systemic distribution; HUS more specifically impairs the renal system. In 

general, adults presenting with clinical and laboratory evidence of MAHA accompanied 

by thrombocytopenia should receive treatment for TTP once other diagnoses have been 

excluded (eg, sepsis, metastatic cancer, systemic vasculitis, preeclampsia-eclampsia, 

Evans syndrome, heparin-induced thrombocytopenia with thrombosis, and malignant 

hypertension). Untreated TTP has an 80-90% mortality rate. 

Pallor, jaundice or scleral icterus, fatigue, and dyspnea on exertion are common 

because of the hemolytic anemia. With significant thrombocytopenia, purpura or 

mucosal bleeding may be evident. Focal neurologic deficits (often vacillating), aphasia, 

seizure, coma, visual disturbance, chest pain, cardiac conduction disorders, abdominal 

pain, oliguria, and hypertension indicate end-organ involvement. 

1. Thrombotic Thrombocytopenic Purpura 



TTP classically comprises the following pentad of symptoms and signs: (1) 

thrombocytopenia, (2) MAHA, (3) fever, (4) renal impairment, and (5) neurologic 

impairment. It is uncommon for all 5 features to occur in any one patient, but if they are, 

severe end-organ ischemia or damage has likely taken place. Thrombocytopenia and 

MAHA are the most common features, and fever is the least frequent finding. 

A common feature of acquired TTP is the development of autoantibodies to a 

vWF-cleaving metalloprotease termed ADAMTS-13. Pregnancy is the most common 

precipitating event for TTP. Preeclampsia has some features similar to TTP, but TTP 

usually presents earlier during pregnancy, around 23-24 weeks, and delivery does not 

affect the course of TTP. By contrast, preeclampsia more commonly occurs in the third 

trimester, and delivery is the treatment of preeclampsia. Other triggers of TTP include 

infection (particularly HIV), vaccination, and autoimmune disorders such as systemic 

lupus erythematosus. Several drugs have been associated with TTP, including 

quinidine, cyclosporine, tacrolimus, and the antiplatelet agents ticlopidine and 

clopidogrel. A particularly refractory form of TTP has been seen in post-bone marrow 

transplant patients after treatment with the cancer chemotherapeutic agents mitomycin, 

cisplatin, gemcitabine, and bleomycin. 


TTP is still a clinical diagnosis, but characteristic laboratory findings include severe 

anemia, thrombocytopenia (uL), schistocytes or helmet cells on peripheral smear,

decreased haptoglobin, elevated reticulocyte count, and elevated unconjugated 

(indirect) bilirubin seen with intravascular hemolysis. The direct Coombs test (DAT) is 

characteristically negative, because the hemolysis seen in TTP does not involve 

anti-RBC autoantibodies. Because TTP thrombi do not involve fibrin, TTP is 

distinguished from DIC based on normal coagulation studies. Compared with TTP, 

preeclampsia is associated with a reduced plasma antithrombin III level. 

Treatment 

Acquired TTP is treated with daily plasma exchange consisting of (1) plasmapheresis to 

remove large vWF multimers and autoantibodies and (2) plasma infusion to give the 

patient back one calculated daily volume of fresh frozen plasma (FFP) or 

cryoprecipitate-poor plasma (cryosupernatant). The use of plasma exchange has 

decreased TTP mortality rates from 90% to 10-20%. If plasmapheresis cannot be 

performed immediately, initial FFP infusion should be started but infusion should never 

replace exchange. Plasma exchange is performed daily until several days after 

remission is achieved. Remission usually occurs within 1 week but may require up to 4 

weeks. Remission is defined by normalization of the platelet count and lactate 

dehydrogenase (LDH) combined with clinical resolution of tissue ischemia and 

thrombosis. Corticosteroids (usually prednisone, 1-2 mg/kg/d) may be helpful in the 

presence of a high autoantibody titer and if plasma exchange does not provide the 

desired response. Splenectomy can induce long-term remission or cure in cases of 

plasma exchange failure by removing a site of autoantibody production and by removing 

a site of microvascular occlusion, which mitigates MAHA. 

Supportive measures may be needed to address systemic complications associated 

with TTP, including RBC transfusion for anemia, anticonvulsants for seizures, 

antihypertensives for hypertension, and hemodialysis for severe renal insufficiency. 

Avoid platelet transfusions, unless life-threatening bleeding or intracranial hemorrhage 

is present, because thrombosis may worsen acutely, leading to rapid renal failure and 

potentially death. Aspirin can worsen hemorrhagic complications in the setting of severe 

thrombocytopenia and also should be avoided. Heparin is not beneficial in TTP or HUS. 

Relapse rates after appropriate treatment may be as high as 30%, and maintenance 

therapies have not been shown to prevent relapse. 

2. Hemolytic Uremic Syndrome 


HUS is a disease primarily of early childhood, with a peak incidence between ages 6 

months and 4 years. The adult form of HUS may be very difficult to distinguish from 

TTP. The overall mortality rate is 5-15%; the prognosis is worse in older children and 

adults. HUS is characterized by acute renal failure, MAHA, fever, and moderate 

thrombocytopenia. HUS often follows a viral or bacterial illness. Although several 

infectious agents have been implicated, Escherichia coli serotype O157:H7 is a 

well-recognized factor. Between 20% and 40% of patients with E coli O157:H7 infection 

have bloody diarrhea; 15% of children and 5% of adults go on to develop HUS. Onset of 

HUS is typically 2-14 days after diarrhea develops. Other organisms implicated in HUS 

include Shigella, Yersinia, Campylobacter, Salmonella, Streptococcus pneumoniae,

varicella, echovirus, and coxsackievirus A and B. 

In HUS the microthrombi are confined mostly to the kidneys, whereas in TTP they occur 

throughout the microcirculation. Laboratory studies reflect the presence of MAHA, and 

thrombocytopenia may be present but generally not to the degree seen in TTP. The 

serum creatinine may be markedly elevated, and urine, if present, contains protein and 

RBCs (although the urine can be normal). 

Treatment 

Patients with mild HUS with less than 24 hours of urinary symptoms require only fluid 

and electrolyte correction and supportive care. Steroid therapy may be beneficial. In the 

setting of more severe disease, plasma exchange or infusion have been performed with 

equivocal results. Patients whose disease resembles TTP may respond to plasma 

exchange, but the overall low mortality of HUS makes use routine use of plasma 

exchange questionable. Hemodialysis may be required in the setting of acute renal 

failure, especially in adults, because acute renal failure tends to be more severe. A 

shorter duration of dialysis therapy is associated with increased likelihood of recovery 

from HUS. Do not treat infection with E coli O157:H7 with antimotility drugs because 

these agents appear to increase the risk of developing HUS. Antibiotic treatment of E 

coli O157:H7 dysentery is controversial, but meta-analysis has found no evidence that 

antibiotic treatment increases or decreases the risk of developing HUS. 

THROMBOCYTOPENIA DUE TO PLATELET SEQUESTRATION 

In patients with marked splenomegaly, splenic sequestration may commonly produce 

platelet counts as low as 40,000/uL. However, isolated splenomegaly rarely results in 

clinically significant hemorrhage without the presence of another concomitant 

hemorrhagic disorder, and splenectomy is rarely indicated. 

QUALITATIVE PLATELET ABNORMALITIES 

Several disease processes can cause acquired qualitative or functional platelet 

abnormalities (Table 39-4). In the myeloproliferative diseases, despite frequently 

elevated platelet counts, the platelets are often dysfunctional and patients can develop 

mucosal hemorrhages or clinically significant bleeding. To control acute bleeding, 

consider transfusion to raise the level of normal platelets to 50,000/uL. In 

macroglobulinemia and related disorders, the elevated serum proteins interfere with 

platelet function and patients with clinically significant bleeding may require 

plasmapheresis to reduce the protein level and correct hemostatic function. 

Many commonly used drugs can influence platelet function (see Table 39-3). Of these, 

the most commonly used are aspirin, the NSAIDs, and clopidogrel. Aspirin inhibits 

platelet function by acetylating and irreversibly inactivating platelet cyclooxygenase, 

which inhibits platelet aggregation. This antithrombotic effect can be seen in doses as 

small as 30 mg, occurs within 1 hour after ingestion, and continues for the lifespan of 

the platelets. Because the NSAIDs reversibly inhibit platelet cyclooxygenase, the 

impairment of platelet aggregation lasts only as long as the active drug is present in the 

circulation, usually less than 24 hours. An exception is the drug piroxicam, which has a

2-day half-life. Ticlopidine and clopidogrel are related substances that inhibit platelet 

function by impairing fibrinogen binding to glycoprotein IIb/IIIa receptors and by 

inhibiting platelet binding. Platelet inhibition occurs within 24-48 hours after ingestion 

and continues for approximately 4-10 days after discontinuation of therapy. 

THROMBOCYTOSIS 

Thrombocytosis, a platelet count above 500,000/uL, can be seen in many disorders, 

including inflammatory reactions, malignancy, polycythemia vera, and postsplenectomy. 

Platelet function can be normal or abnormal depending on the underlying condition. 

With abnormal platelet function, thrombocytosis can be associated with bleeding (eg, 

mucosal or gastrointestinal bleeding or ecchymoses) or thromboembolism (eg, deep 

venous thrombosis, portal or mesenteric thrombosis, splenic vein thrombosis). However, 

these events are unusual, even with platelet counts in excess of 1 million/uL. 

III. HEMOSTATIC DISORDERS: COAGULATION FACTOR 

DISORDERS 

HEMOPHILIA 


Hemophilia is a disorder of coagulation caused primarily by a deficiency or defect in one 

of two circulating plasma proteins. Hemophilia A, or classic hemophilia, is caused by a 

deficiency of factor VIII and is the most common cause of hemophilia in the United 

States, affecting 1 in 10,000 males. Hemophilia B, or Christmas disease, is caused by a 

deficiency of factor IX. This form of hemophilia is less common, affecting approximately 

1 in 25,000 to 35,000 males. Together these forms of hemophilia account for about 99% 

of patients with inherited coagulation factor deficiencies; the remaining individuals have 

rare forms of factor deficiencies. Hemophilia A and B are clinically indistinguishable from 

each other, and specific factor testing is required for diagnosis. Both hemophilia A and B 

are X-linked recessive disorders; therefore, hemophilia is a disease overwhelmingly of 

men, and women are asymptomatic carriers. Approximately one third of new cases of 

hemophilia A and one fifth of new cases of hemophilia B arise from a spontaneous gene 

mutation. 



Bleeding manifestations in patients with all forms of hemophilia are directly attributable 

to the decreased plasma levels of either factor VIII or IX (Table 39-5). Individuals with 

factor levels below 1% of normal are classified as having severe disease, and these 

people will experience severe spontaneous bleeding episodes and difficult-to-control 

bleeding related to traumatic events. Patients with factor levels of 1-5% of normal are 

classified as having moderate disease; although they may bleed spontaneously, more 

commonly their bleeding is related to a traumatic event. Patients with factor levels of 

5-25% of normal are classified as having mild disease and usually bleed only after 

trauma. Those with factor levels of 25-50% may never be aware that they have 

hemophilia, or they might manifest unusual bleeding only after major surgery or severe

trauma. Patients with hemophilia do not have problems with minor cuts and abrasions. 

As a result of exposure to blood products, many hemophiliacs have chronic viral 

hepatitis or are infected with HIV. Fortunately, as a result of newer viral inactivation 

procedures and recombinant technology, few seroconversions have resulted from the 

use of currently available factor replacement products. 


Routine coagulation studies (prothrombin time [PT] or activated partial thromboplastin 

time [aPTT]) require only 30% of normal factor VIII or IX level to be normal; therefore, 

patients with mild disease may have normal values. Coagulation studies are unlikely to 

yield new information in the known hemophiliac and are not routinely indicated when the 

patient presents with mild to moderate bleeding episodes. 

Treatment 

A general principle in managing major or life-threatening bleeding in a hemophilic 

patient is early and complete factor replacement, before or at the same time as other 

resuscitative and diagnostic maneuvers. Spontaneous or traumatic bleeding into the 

neck, tongue, retropharynx, or pharynx has a high potential for airway compromise. Any 

patient with hemophilia who complains of a new headache, localizing neurologic 

symptoms, or a blunt head injury requires immediate factor replacement therapy 

followed by urgent computed tomography scanning of the head. Hemophilic patients 

with complaints of back, thigh, groin, or abdominal pain may have bleeding into the 

retroperitoneum. At times the initial manifestations of bleeding can be subtle. Simple 

injuries such as ankle and wrist sprains may at first appear benign but can be 

complicated by bleeding. Compartment syndromes result from muscle bleeds within the 

fascial compartments of the extremities, both spontaneously and after minimal trauma to 

an extremity. 

One of the most common manifestations of hemophilia is hemarthrosis. Clinical 

evidence of an acute problem with the joint may or may not present, but these patients 

can reliably report when bleeding is occurring. Prompt treatment of hemarthroses can 

prevent or reduce the long-term sequelae of hemophilic arthropathy. Many patients and 

their families have a sophisticated understanding of the disease. These patients will 

know to seek treatment at the first sign of a problem, and as stated earlier, little outward 

evidence of pathology may be present initially. Despite minimal findings, take seriously 

the concerns of these patients. Additionally, many known hemophiliacs will have in their 

medical records a detailed treatment plan for how to manage acute bleeding episodes. 

Consult these records when they are available. 

Do not place central lines, including femoral lines and external jugular lines, in patients 

with hemophilia without giving factor replacement therapy. Similar rules apply to arterial 

blood gases or lumbar puncture. Patients with hemophilia should never receive 

intramuscular injections unless factor replacement is given and maintained for several 

days. Do not give compounds that contain aspirin for pain relief. 

Two different factor replacement types exist: recombinant or plasma derived (Table 

39-6). The highest level of purity comes from the recombinant factors, but these 

products cost 2-3 times more than plasma-derived products, and they are not available

everywhere. Another concern with the plasma-derived factors is that some of the 

preparations may contain other coagulation factors, some partially activated. Prolonged 

use of the less pure concentrates may increase the risk of DIC or, in some cases, cause 

paradoxical clotting. Safety, cost, and availability must be considered when choosing 

the product to use in replacement therapy, but because the recombinant forms are 

perceived to be safer, approximately 60% of patients with severe hemophilia in the 

United States receive these preparations. 

The dosing regimen used in the hemophilic patient is based on the clotting factor's 

volume of distribution, the factor's half-life, and the hemostatic level of factor required to 

control the bleeding (Table 39-7). Clotting factor is dosed in units (U) of activity; 1 unit of 

factor represents the amount of factor present in 1 mL of normal plasma. For hemophilia 

A, 1 unit of factor VIII per kilogram of body weight raises the plasma level by 

approximately 0.02 U/mL (2%) with a half-life of approximately 8-12 hours. For 

hemophilia B, 1 unit of factor IX per kilogram of body weight will raise the plasma level 

by approximately 0.01 U/mL (1%) with a half-life of approximately 16 hours. The amount 

of factor needed can be calculated using the patient's weight and the desired increase in 

factor activity (to avoid wasting factor, round off all doses to the closest vial): 

Bleeding from the mouth is common in hemophiliacs, particularly children. If an oral 

bleed is present, identify the area, clean it of inadequate clot, and place a dry topical 

thrombin on the bleeding site. In addition to factor replacement, antifibrinolytic agents 

such as epsilon-aminocaproic acid (EACA) and tranexamic acid are useful to prevent 

bleeding when the clot falls off. For superficial mucosal injuries, it may be possible to 

manage the bleeding with antifibrinolytic therapy alone. The dose of EACA is 75-100 

mg/kg for children (6 g for adults) every 6 hours, given orally or intravenously. Topical 

hemostatic agents used to help control oral or nasal bleeding include microfibrillar 

collagen hemostats, thrombin, and absorbable gelatin sponges. 

Patients with mild hemophilia A (factor levels of 5% or greater) who have mild bleeding 

may not always require factor replacement. Rather, these patients may be given 

desmopressin, which causes endothelial storage sites to release vWF that is capable of 

carrying additional amounts of factor VIII in the plasma. This medication is well 

tolerated, and patients can administer it at home by subcutaneous injection or intranasal 

spray. The dose of intravenous desmopressin is 0.3 ug/kg (maximum dose, 20 ug) over 

30 minutes. The concentrated intranasal form of desmopressin is an antidiuretic agent, 

and fluid restriction may be needed during use. For children older than age 5 years, a 

single spray in a single nostril (150 ug total dose) is adequate. For adolescents and 

adults, a single spray in each nostril is used (300 ug total dose). This dose of intranasal 

desmopressin increases the factor VIII level by 2-3 times. This treatment can be 

repeated in 8-12 hours, but the patient's stores of factor VIII will be depleted, and 

subsequent effect will be less.

In response to the clotting factors used to treat bleeding episodes, some people will 

develop inhibitors, or antibodies against the replacement factor. Inhibitors tend to occur 

most commonly in patients with severe hemophilia because of frequent factor 

replacement. These inhibitors not only interfere with the effectiveness of factor 

replacement therapy but also cause anaphylaxis to factor administration in patients with 

hemophilia B. Inhibitors occur in 10-25% of those with hemophilia A and in 1-2% of 

those with hemophilia B. The use of factor replacement in hemophilic patients with 

inhibitors is guided by the concentration of inhibitor (measured in Bethesda Inhibitor 

Assay [BIA] units) and by the type of response the patient has to factor concentrates. 

Bleeding episodes are more difficult to treat in these patients, but options do exist. 

Given the complexity of these patients, consultation or transfer to a center with 

hematology is recommended. 

Disposition 

Many patients with hemophilic bleeding episodes can receive factor replacement in the 

emergency department or clinic and then be discharged home with follow-up in 12-24 

hours. Hemophilic patients with bleeding episodes that require hospital admission 

include (1) those with bleeding involving the central nervous system, neck, pharynx, 

retropharynx, or retroperitoneum, (2) those with potential compartment syndrome, (3) 

those for whom treatment requires more than 3 doses (relative indication), (4) those 

unable to use, or lacking access to, factor replacement, or (5) those in whom pain 

cannot be controlled with oral analgesics. 

VON WILLEBRAND DISEASE 


Von Willebrand disease is the most common congenital bleeding disorder; it is present 

in 1% of the population. This disease is a group of disorders caused by abnormalities of 

vWF. The disease is heterogeneously inherited and expressed, and although multiple 

subtypes exist, these can be classified into 3 major groups (Table 39-8). Type I is the 

most common and is a partial quantitative disease, type II is a qualitative (abnormal 

function) disease, and type III is a severe and almost complete deficiency of vWF (this 

type is a rare autosomal recessive form). vWF is a glycoprotein that, as opposed to 

most other coagulation factors, is synthesized, stored, and then secreted by the 

vascular endothelial cells. It is a cofactor for platelet adhesion and the carrier protein for 

factor VIII. 



Bleeding symptoms are common in people with von Willebrand disease, particularly in 

children and adolescents. Symptoms includes recurrent epistaxis, gingival bleeding, 

unusual bruising, gastrointestinal bleeding, and menorrhagia in young women. 

Hemarthrosis is not typical unless severe disease is present. In mild cases of von 

Willebrand disease, patients may be unaware of the disease until they undergo a 

surgical procedure or experience a traumatic event. Von Willebrand disease is relatively

common, and its presence influences the treatment of other medical problems, because 

patients with this disease should not take medications with known antiplatelet effects, 

including aspirin, NSAIDs, antiplatelet agents, heparin, and some antibiotics. 


Common abnormalities on hemostatic testing include a prolonged bleeding time, low or 

normal vWF antigen, and low vWF activity. The PT is usually normal, but this can be 

variable, as can the factor VIII level. This variability sometimes makes von Willebrand 

disease difficult to differentiate from mild hemophilia A. The patient's blood type affects 

the vWF level; blood type O has as much as a 30% reduction in vWF levels compared 

to the other blood types. 

Treatment 

Desmopressin has become a mainstay of therapy for many patients with type I von 

Willebrand disease and may work in conjunction with other plasma products that contain 

vWF for types II and III. In responsive individuals, desmopressin causes a transient 2- to 

4-fold increase in vWF. It also seems to have an effect on the endothelium that 

promotes hemostasis. The dose is 0.3 ug/kg (maximum dose, 20 ug) administered 

subcutaneously or intravenously every 12 hours for a total of 3-4 doses; after 4 doses, 

tachyphylaxis develops. Desmopressin can also be used as an intranasal spray. For 

children older than age 5 years, a single spray in a single nostril is adequate (150 ug 

total dose). For adolescents and adults, administer a single spray in each nostril (300 ug 

total dose). 

Plasma derivatives that contain vWF are used for patients with type I disease that does 

not or no longer responds to desmopressin and for patients with type II or III disease. To 

be effective the chosen product must have vWF in the high molecular weight form. 

Cryoprecipitate meets this objective (contains factor VIII and vWF), but the potential for 

viral transmission is a concern. If cryoprecipitate is used, 10 bags every 12-24 hours will 

usually control bleeding. Humate-P is an intermediate-purity factor VIII concentrate that 

has significant amounts of vWF and can be used to treat bleeding episodes. Platelet 

transfusions may benefit patients with certain types of von Willebrand disease 

(especially type III) that do not respond to vWF-containing concentrates of 

cryoprecipitate. 

Local measures to control bleeding in von Willebrand disease include (1) intranasal 

application of porcine strips (e.g., Surgicel), porcine strips sprinkled with microfibrillar 

collagen (e.g., Avitene), or cauterization for epistaxis, (2) birth control pills to help raise 

vWF levels and limit the degree of menstrual bleeding, and (3) EACA for dental injury or 

planned intraoral procedures. 

LIVER DISEASE 


Acute and chronic diseases of the liver can be associated with many hemostatic 

abnormalities. Hepatocytes synthesize all of the coagulation factors and related 

regulatory proteins, with the exception of factor VIII. Malabsorption of vitamin K can

occur with processes that interfere with the absorption of fat-soluble vitamins, including 

impaired bile acid metabolism (ie, primary biliary cirrhosis), intrahepatic or extrahepatic 

cholestasis, and treatment with bile acid binders. Thrombocytopenia in severe liver 

disease is most often due to portal hypertension, which leads to congestive 

hypersplenism and splenic sequestration. Patients with significant liver disease have 

increased fibrinolysis due to decreased synthesis of a 2 -plasmin inhibitor. In some 

patients with liver disease, abnormal fibrinogen molecules are synthesized that, when 

cleaved to fibrin monomers, do not polymerize correctly. 

Patients with mild to moderate hepatic dysfunction frequently have subclinical 

hemostatic abnormalities. Patients with severe liver disease may have life-threatening 

bleeding. Laboratory studies should include a PT, aPTT, and platelet count. Also 

consider obtaining fibrinogen levels and measurement of fibrin degradation products 

(FDP) or D-dimer. In general, prolongation of the PT and a plasma fibrinogen level of 

less than 100 mg/dL is a poor prognostic sign in patients with liver disease. 


Patients who have liver disease and laboratory abnormalities without clinically significant 

bleeding usually require only close observation. If clinically significant bleeding is 

present or an invasive procedure or surgery is pending, the coagulopathic state will 

need to be treated. Transfuse packed RBCs to maintain an adequate hemoglobin level 

and to maintain hemodynamic stability. Give oral or intravenous vitamin K to all patients. 

FFP can be used to replace coagulation factors temporarily, but the volume needed to 

completely replenish the coagulation factors may limit the amount given. Cryoprecipitate 

may be used to replace fibrinogen in patients with fibrinogen levels less than 100 mg/dL. 

Platelet transfusions may be appropriate if platelet counts are low. Desmopressin (either 

0.3 ug/kg subcutaneously or intravenously [maximus dose, 20 ug], or 300 ug intranasal 

spray) shortens the prolonged bleeding time in some patients with liver disease. 

Although controlled trials are lacking, there are few side effects. 

RENAL DISEASE 

Hemostatic abnormalities commonly occurring in patients with renal disease include 

quantitative and qualitative platelet abnormalities and clotting factor abnormalities. 

Platelet counts are frequently normal, although mild thrombocytopenia may occur. 

Clinically significant bleeding may occasionally occur with dialysis-induced 

thrombocytopenia. Retention of uremic toxins causes inhibition of platelet aggregation. 

Preventive measures include optimizing nutrition with folate, vitamin B 12 , and iron 

repletion; optimizing dialysis; and correcting anemia with recombinant human 

erythropoietin. Acute bleeding can be treated with dialysis, transfusion of RBCs, 

desmopressin, and conjugated estrogens; cryoprecipitate transfusion and platelet 

transfusion are rarely used. Dialysis improves platelet function transiently, lasting for 1-2 

days. Platelet function is optimized when the hematocrit (percentage of RBC mass to 

blood volume) is maintained at 26-30% because anemia contributes to bleeding. In 

uremic patients with prolonged bleeding times, 50-75% will have shortening or 

normalization of the bleeding time when given desmopressin. Conjugated estrogen, 25 

mg intravenously, also improves both bleeding time and clinical bleeding in more than

80% of uremic patients. Cryoprecipitate carries the risk of viral transmission, and 

platelet transfusions are relatively ineffective because the infused platelets quickly 

acquire the uremic defect. Restrict the use of cryoprecipitate and platelet transfusions to 

life-threatening bleeding when used in combination with packed RBCs, desmopressin, 

and conjugated estrogens. 

WARFARIN & VITAMIN K DEFICIENCY 


The vitamin K-dependent coagulation factors produced in the liver are prothrombin 

(factor II), factor VII, IX, and X, as well as the anticoagulant proteins C and S. Nutritional 

deficiency of vitamin K is rare in adults. However, patients with liver disease can have 

vitamin K deficiency due to a combination of poor nutrition and malabsorption. 

Additionally, deficiency of the vitamin K-dependent factors can occur in patients 

receiving antibiotics, particularly the third-generation cephalosporins that contain the 

N-methylthiotetrazole side chain (ie, moxalactam, cefamandole, cefotaxime, 

cefoperazone). 

Warfarin, the major oral anticoagulant used in the United States, inhibits the production 

of the vitamin K-dependent coagulation factors. The half-life of warfarin is approximately 

36 hours with normal hepatic function. The standard starting dosage is usually 5 mg/d 

with subsequent dose adjustment guided by the international normalized ratio (INR). 

Observable anticoagulation effect is expected in 2-7 days. The goal INR is 2.0-3.0 for all 

indications except in patients with prosthetic mechanical valves and with 

antiphospholipid antibody syndrome; these patients require a higher INR of 2.5-3.5. 

Maintenance dosage can be influenced by different variables, including the patient's 

vitamin K stores, malnutrition, liver function, concurrent medical disorders, and 

numerous drug interactions. 


The major adverse effects associated with warfarin treatment include warfarin 

embryopathy, warfarin-induced skin necrosis, and bleeding. Warfarin interferes with a 

vitamin K-dependent protein used to build the bone matrix, resulting in fetal bone 

abnormalities. This toxicity occurs with warfarin exposure during the 6th to 12th weeks 

of gestation, but warfarin should be avoided during the entire pregnancy. 

Warfarin-induced skin necrosis is an uncommon complication occurring during the first 

week after initiating therapy. Some patients who develop this complication have a 

hereditary heterozygous protein C deficiency or protein S deficiency. 

Treatment 

Treatment of warfarin complications includes discontinuation of warfarin, heparinization 

if anticoagulation is required, vitamin K administration, and screening for protein C and 

protein S deficiencies. The fear of creating a hypercoagulable state in persons with 

undiagnosed protein C deficiency is unfounded, but persons with a known 

hypercoagulable state should receive anticoagulation therapy with heparin before 

starting warfarin.

Bleeding is the most common complication of warfarin treatment; the risk of bleeding is 

related directly to the degree of anticoagulation. Additionally, individual risk factors for 

bleeding include age greater than 65 years, hypertension, anemia, prior cerebrovascular 

disease, gastrointestinal lesions, and renal disease. Medications that increase warfarin 

activity and antiplatelet medications can also increase bleeding risks. Management of 

bleeding depends on the type of bleeding and the INR value. The anticoagulated state 

can be reduced in 3 ways: withhold warfarin, administer vitamin K, or transfuse FFP 

(Table 39-9). 

Recent studies suggest that subcutaneous administration of vitamin K has an 

unpredictable and delayed response, whereas oral vitamin K is convenient to 

administer, is effective, and produces less resistance to subsequent warfarin use. 

Additionally, hypersensitivity reactions and anaphylaxis are uncommon with the oral 

administration of vitamin K. Intravenous administration of vitamin K results in the rapid 

reversal of hypercoagulation but is associated with anaphylaxis or hypersensitivity 

reactions, including flushing, diaphoresis, hypotension, dyspnea, and chest pain. Doses 

of vitamin K above 10 mg are associated with overcorrection of hypercoagulation and 

warfarin resistance for up to 1 week upon reinstitution of anticoagulation. In general, 

restrict the intravenous use of vitamin K to patients with life-threatening bleeding or to 

those with an INR greater than 20. 

Superwarfarins with a prolonged duration of action are used as rodenticides; 

brodifacoum is the most widely available of these agents. Patients presenting with an 

overdose may develop severe coagulopathy with major mucosal bleeding and internal 

bleeding. Treatment with high doses of vitamin K, up to 100-125 mg/d for several 

weeks, may be required because of the long half-life of these products. 

DISSEMINATED INTRAVASCULAR COAGULATION 


DIC is an acquired syndrome characterized by both widespread activation of the 

coagulation system (resulting in fibrin formation and consumption of hemostatic factors) 

and activation of the fibrinolytic system (resulting in the breakdown of fibrin clots, 

consumption of coagulation factors, and bleeding). DIC is associated with a variety of 

disorders such as infection (usually bacterial and occasionally viral), malignancy 

(adenocarcinoma, acute leukemia, lymphoma), trauma (burns, fat embolism), liver 

disease, and environmental disorders (hyperthermia, envenomation). DIC may be acute 

and life threatening or chronic and compensated. 



Clinical features of DIC vary with the underlying precipitating medical illness. The clinical 

complications of DIC are bleeding, thrombosis, purpura fulminans, and multiple organ 

failure. Although hemorrhage and thrombosis may occur simultaneously, in an individual 

patient, one manifestation usually predominates and the most common one is bleeding. 

Bleeding can range from petechiae and ecchymoses to bleeding from the

gastrointestinal tract, genitourinary tract, surgical wounds, mucocutaneous sites, and 

venipuncture sites. Intravascular coagulation and fibrin deposition can cause multiple 

organ failure. Clinical signs include mental status changes, focal ischemia or gangrene, 

oliguria, renal cortical necrosis, and adult respiratory distress syndrome. Purpura 

fulminans results when widespread arterial and venous thromboses occur and is most 

commonly seen with significant bacteremia. In chronic DIC, the pathophysiology of 

disease is essentially the same, but the destruction of coagulation factors and platelets 

is balanced by hepatic and bone marrow production. 


The typical laboratory results in acute DIC include prolonged PT, low platelet count, and 

low fibrinogen level. The most commonly observed abnormality is thrombocytopenia. 

Fibrinogen levels may remain normal because fibrinogen is an acute-phase reactant. 

FDP and D-dimer may help differentiate DIC from other causes of prolonged 

coagulation times and low platelets; the D-dimer may be more specific than FDP in 

diagnosing DIC. Additional laboratory findings include increased LDH, decreased 

haptoglobin levels, and a peripheral smear with schistocytes. Patients with chronic DIC 

will have minor abnormalities on the screening assays, reflecting the limited 

consumption of coagulation factors that are being replaced by hepatic synthesis. 

Treatment 

Treatment of acute DIC rests on supportive measures and management of the 

underlying illness. Circulatory stabilization requires fluid, RBCs, and sometimes 

inotropic agents. If possible, the underlying cause of the DIC needs to be treated. 

Secondary treatment involves replacement therapy with platelets, fibrinogen, and 

coagulation factors. Many patients with DIC require no specific therapy if evidence of 

bleeding or thrombosis is lacking and laboratory study results are not deteriorating. 

Replacement therapy should be given only to patients with bleeding or an impending 

invasive procedure and should use specific replacement products: fibrinogen repletion 

with cryoprecipitate to raise the plasma fibrinogen level to 100-150 mg/dL, platelet 

concentrates to raise platelet count above 50,000/uL, and FFP to replace coagulation 

factors. Patients with DIC also should be given vitamin K and folate. 

Heparin administration usually has a limited role in the treatment of acute DIC. It is 

usually considered in patients with documented DIC in whom thromboembolic 

complications predominant the clinical picture (ie, purpura fulminans). Consider heparin 

for patients with chronic DIC and thrombosis (ie, solid tumors). Antifibrinolytic agents, 

including EACA, are used with great caution in treating DIC. Although these drugs may 

reduce bleeding, their use is associated with serious or fatal thromboembolic 

complications. Restrict antifibrinolytic agents to patients who have documented 

hypofibrinogenemia and fibrinolysis; these agents should be given with heparin to 

minimize the potential for thrombosis. 

Amitrano L et al: Coagulation disorders in liver disease. Semin Liver Dis 2002;22:83. 

[PMID: 11928081] 

Cines DB, Blanchette VS: Immune thrombocytopenic purpura. N Engl J Med 

2002;346:995. [PMID: 11919310]

Levi M, Ten Cate H: Disseminated intravascular coagulation. N Engl J Med 

1999;341:586. [PMID: 10451465] 

Levine MN et al: Hemorrhagic complications of anticoagulant treatment. Chest 

2001;119(1 Suppl):108S. [PMID: 1157645] 

Mannucci PM, Federici AB: Management of inherited von Willebrand disease. Best 

Pract Res Clin Haemtol 2001;14:455. [PMID: 11686109] 

McCrae KR et al: Platelets: an update on diagnosis and management of 

thrombocytopenic disorders. Hematology (Am Soc Hematol Educ Program) 2001:282. 

[PMID: 11722989] 

Moake JL: Thrombotic microangiopathies. N Engl J Med 2002; 347:589. [PMID: 

12192020] 

Opatrny K: Hemostasis disorders in chronic renal failure. Kidney Int Suppl 1997;62:S87. 

[PMID: 9350690] 

Petrini P: Treatment strategies in children with hemophilia. Paediatr Drugs 2002;4:427. 

[PMID: 12083971] 

Sallah S, Kato G: Evaluation of bleeding disorders. A detailed history and laboratory 

tests provide clues. Postgrad Med 1998; 103:209. [PMID: 9553596] 

IV. ANEMIA 

Anemia is a common problem, affecting an estimated one third of the world's 

population. Worldwide, the most common causes of anemia include iron deficiency, 

thalassemia, hemoglobinopathies, and folate deficiencies. Within the United States, the 

most common causes are iron deficiency, thalassemia, and anemia of chronic disease. 

Not only is anemia common in the general population, but also the prevalence of 

anemia increases with age. Given the ubiquity of this entity, some patients who present 

to the emergency department with anemia will be symptomatic, whereas anemia will be 

an incidental finding in other patients. 

Anemia is defined as a reduced concentration of RBCs. Erythropoiesis ensures that the 

number of RBCs present is adequate to meet the body's demand for oxygen and that 

RBC destruction equals production with an average lifespan of 120 days for circulating 

erythrocytes. Any process or condition that impairs the production, increases the rate of 

destruction, or increases the loss of erythrocytes will result in anemia if the body cannot 

produce enough new RBCs to keep up with the loss. 

Quantification of the RBC concentration is reflected in the RBC count per microliter, 

hemoglobin concentration, or hematocrit. Normal RBC values for adults vary slightly 

between males and females (Table 39-10). Based on RBC values, there are three 

categories of anemia (Table 39-11).

Regardless of the cause of anemia, many of the clinical manifestations are the same. 

The severity of symptoms and signs related to anemia depends on several factors: the 

rate of development of anemia, the extent of anemia present, the patient's age, the 

patient's general physical condition, and other existing comorbid illnesses. Patients with 

chronic and slowly developing anemia may have almost no complaints even with 

hemoglobin levels as low as 5-6 g/dL. More typically, most people will begin to be 

symptomatic with hemoglobin levels at about 7 g/dL. Patients with chronic anemia may 

complain of weakness, fatigue, lethargy, dyspnea with minimal exertion, palpitations, 

and orthostatic symptoms. Physical examination findings in patients with significant 

chronic anemia may include orthostatic hypotension; tachycardia; skin, nail bed, and 

mucosal pallor; systolic ejection murmur; bounding pulse; or widened pulse pressure. 

Patients who develop anemia in a rapid fashion frequently have more pronounced 

symptoms. Additionally, these patients may have hypotension, resting and exertional 

dyspnea, palpitations, diaphoresis, anxiety, severe weakness that may progress to 

lethargy, and altered mental status. Loss of more than 40% of blood volume leads to 

severe symptoms that are due more to intravascular volume depletion than to anemia. 

The diagnosis of anemia is established by the finding of a decreased RBC count, 

hemoglobin, or hematocrit on the routine CBC. A specific cause of anemia need not be 

established in the emergency department; however, appropriate workup should be 

initiated to help expedite a diagnosis and initial studies should be started before the 

transfusion of packed red blood cells. The basic evaluation of a patient newly diagnosed 

with anemia includes the following: RBC indices provided with the CBC, reticulocyte 

count, and peripheral blood smear. The mean cellular volume (MCV) is the most useful 

guide to the possible cause of an anemia. The reticulocyte count reflects activity in the 

bone marrow. The red cell distribution width (RDW) measures the size variability of the 

RBC population, and in early nutritional deficiency anemias (iron, vitamin B 12 , or folate) 

the RDW may be increased before the MCV becomes abnormal. As part of the general 

evaluation, the two most common sources of blood loss should be investigated: 

gastrointestinal (eg, checking the stool for occult blood) and uterine bleeding(eg, 

history). 

IRON-DEFICIENCY ANEMIA 

Iron-deficiency anemia occurs when body iron content is insufficient for erythropoiesis; it 

manifests as a microcytic, hypochromic anemia. Iron deficiency is seen with either 

inadequate iron intake (usually in undeveloped countries with little meat in the diet) or 

from a combination of iron loss (hemorrhage) and inadequate intake (in developed 

countries). Heme iron (as found in meat) is absorbed more efficiently than is nonheme 

iron (found in vegetables) and accounts for the higher incidence of iron deficiency in 

vegetarians. Total body iron content varies with age and gender at 35-60 mg/kg of body 

weight. Each gram of hemoglobin contains 3.47 mg of iron. The recommended daily 

intake of iron is about 7 mg in a man, 12-16 mg in a menstruating woman, and 5-7 mg in 

a postmenopausal woman. 



The symptoms of iron-deficiency anemia (fatigue and weakness) are generally due to

the anemia. Occasionally patients may describe a desire to chew ice or cold food 

(termed pagophagia) or leg cramps on climbing stairs. Gastrointestinal epithelial 

(angular stomatitis, glossitis, esophageal webs, and gastric atrophy) and nail 

(koilonychia) abnormalities have been described in iron deficiency, although their 

frequency varies and these findings are uncommon in the United States. 


Patients with iron-deficiency anemia have both microcytic (low MCV) and hypochromic 

(low MCHC) erythrocytes. The platelet count is often elevated. Examination of the 

peripheral smear is useful to exclude thalassemia; target cells are not seen in 

iron-deficiency anemia. Combined iron deficiency and folate deficiency produces 

variation in red cell size, some macrocytic and others microcytic, such that the 

measured MCV can be within the normal range. Iron-deficiency anemia produces a low 

serum ferritin, low serum iron, and elevated total iron-binding capacity. The absence of 

stainable iron on bone marrow aspirate establishes the diagnosis without other tests. 

Possible blood loss should be investigated in a patient with iron-deficiency anemia and 

often requires testing for occult blood loss from either the gastrointestinal tract (stool for 

occult blood) or the kidneys (hemoglobinuria or hemosiderinuria). 

Treatment 

Iron-deficiency anemia is treated effectively and economically with oral iron therapy 

using ferrous sulfate, 325 mg (children, 1-2 mg/kg) with each meal three times daily. A 

response with increased reticulocytes is seen within 3-4 days and peaks in 7-10 days, 

with the hemoglobin level increasing about 1 g/dL per week. Once normal hemoglobin 

levels are achieved, oral iron therapy should continue to replenish total body iron stores. 

Parenteral iron therapy is reserved for the rare patient who cannot absorb oral iron, but 

parenteral preparations are expensive and associated with adverse effects, including 

fatal anaphylactic reactions. The dose of parenteral iron preparations is calculated 

according to hemoglobin level and ideal body weight; the formula varies by specific 

product. Red cell transfusion is used for the patient with ongoing blood loss or acute 

symptoms of inadequate oxygen delivery to the brain or heart. 

ACUTE HEMOLYTIC ANEMIA 

The immune-mediated hemolytic anemias traditionally have been divided into 3 

categories: autoimmune, alloimmune, and drug related. 

AUTOIMMUNE HEMOLYTIC ANEMIA 


Individuals with autoimmune hemolytic anemia (AIHA) make antibodies against their 

own RBCs or against the body's higher-incidence antigens. The overall incidence of 

AIHA is approximately 1-3 cases per 100,000 population per year. The incidence of 

AIHA in infants and children is less, approximately 0.2 cases per 100,000 population per 

year in those under age 20 years. AIHA in children is commonly associated with viral or 

respiratory infections; is mediated by immunoglobulin G (IgG); and causes acute, 

fulminant hemolysis. Pregnant women have a 5 times greater risk of developing

autoantibodies, but significant RBC destruction is not common. 

Diagnosis of AIHA requires evidence of an autoantibody against RBCs in the form of (1) 

detection of the autoantibody on the patient's red cells (positive DAT) and (2) 

identification of an autoantibody, after either eluting (washing off) the antibodies from a 

patient's red cells or detecting the autoantibodies in the patient's serum (indirect 

Coombs test). To make the diagnosis of AIHA, serologic evidence of autoantibodies 

should be correlated with clinical and other routine laboratory evidence of hemolytic 

anemia, including decreased hemoglobin, decreased haptoglobin, elevated reticulocyte 

count, elevated unconjugated (indirect) bilirubin, elevated LDH, or hemoglobinuria. 

AIHA can be divided into primary and secondary varieties. Primary AIHA refers to cases 

without an underlying cause (idiopathic), and secondary AIHA refers to cases seen with 

an underlying disorder (Table 39-12). Primary AIHA is more common in women, with 

peak incidence during the 4th and 5th decades. The hemolytic process in AIHA can take 

place within the vascular space or in the liver or spleen. AIHA is also categorized 

according to autoantibody type: warm type, cold type, and mixed type. 

1. Warm-Type AIHA 


Warm-type AIHA comprises 70% of AIHA cases and is usually mediated by an IgG 

antibody directed against surface antigens of the RhD-erythrocyte system. 

Autoantibodies of the warm type react most strongly near 37 °C. These autoantibodies 

are usually pan-reactive and produce hemolysis both in the patient's RBCs and in 

transfused RBCs. Warm-type autoantibody-mediated hemolysis is predominantly 

extravascular, occurring in the spleen. Warm-type AIHA carries a 2:1 female preference 

but has no racial predilection. About half of warm-type AIHA cases can be labeled as 

primary or idiopathic. Secondary cases are most often associated with 

lymphoproliferative disorders (in about half) or a systemic autoimmune disease. 

Viral-induced or HIV-associated warm-type AIHA is often mild and self-limited. 

Treatment 

Warm-type AIHA is initially treated with oral prednisone, 1-1.5 mg/kg/d for 1-3 weeks. 

Improvement is usually noted within 1 week, and 70-80% of patients are better within 3 

weeks. Once the patient's hemoglobin level stabilizes, the steroids can be tapered. 

Complete remission is achieved in 15-20% of new-onset cases of warm-type AIHA, but 

half of patients will need low-dose prednisone for several months. 

Between 10% and 20% of steroid-treated patients will fail to respond adequately or will 

require unacceptably high doses to maintain the desired response. In such patients the 

AIHA is treated with either splenectomy or cytotoxic drugs. Splenectomy removes both 

the main site of extravascular hemolysis and a major site of general autoantibody 

production. Splenectomy produces a 65-70% response rate and has the potential for 

long-term remission or a complete cure. 

Cytotoxic drugs produce a 40-60% response rate and have been used for patients who

have not responded to steroids or splenectomy. Severe hemolysis in cases of 

warm-type AIHA may be treated with plasma exchange as a transient stabilizing 

measure while waiting for steroids or cytotoxic agents to take effect. Intravenous 

immunoglobulin may be used as adjunctive treatment in children who cannot tolerate 

the side effects of chronic high-dose steroids or cytotoxic agents. Danazol, an 

attenuated androgen with fewer side effects than glucocorticoids, can produce 

remission in occasional patients. 

For patients with life-threatening anemia, RBC transfusion of the least incompatible 

units may be transfused slowly with close monitoring. Transfusion may precipitate 

further production of autoantibodies as well as introduce a source for the production of 

allogeneic antibodies. 

2. Cold-Type AIHA: General Considerations 

Cold-type AIHA autoantibodies are usually immunoglobulin M (IgM) and are most 

strongly hemolytic at 0-4 °C. The presence of cold-type autoantibodies leads to 

clumping or agglutination of RBCs on peripheral smear at cooler temperatures. 

Hemolysis occurs in both the extravascular and intravascular spaces, and Kupffer cells 

in the liver are responsible for most of the extravascular RBC destruction. The two 

common cold-type AIHA disorders are cold agglutinin syndrome (CAS) and paroxysmal 

cold hemoglobinuria (PCH). Fifty percent of secondary cold-type AIHA cases are 

associated with lymphoproliferative disorders. 

3. Cold-Type AIHA: Cold Agglutinin Syndrome 

CAS accounts for up to one third of all AIHA cases and is typically IgM mediated and 

directed against the I/i blood group antigens. Primary CAS is seen in older adults, 

particularly females, with a peak incidence at age 70 years. The hemolysis associated 

with the primary and chronic secondary forms of CAS tends to be mild and stable with 

hemoglobin levels of 9-12 g/dL. Secondary CAS can also occur as an acute attack, 

such as that seen in patients who have preceding infectious illnesses, including from 

Mycoplasma pneumoniae, Epstein-Barr virus (EBV), adenovirus, CMV, influenza, 

varicella zoster virus (VZV), HIV, E coli, Listeria monocytogenes, and Treponema 

pallidum. 


Symptom onset corresponds with the peak antibody response to infection, usually 2-3 

weeks after the onset of illness. The triggered cold-type AIHA resolves approximately 

2-3 weeks later. Chronic cold-type AIHA associated with lymphoproliferative diseases, 

such as chronic lymphocytic leukemia, lymphomas, and Waldenstrom 

macroglobulinemia, produces high autoantibody levels with the potential for significant 

hemolysis. Cold weather exacerbates CAS; more episodes of acute hemolysis are seen 

during winter. Patients are apt to develop acrocyanosis because the peripheral 

circulation is typically cooler than the central circulation. Raynaud phenomenon, 

vascular occlusion, and tissue necrosis may complicate CAS. Clumping of cold 

agglutinins will elevate the MCV and decrease the RBC count. Peripheral smear 

findings include the spherocytosis caused by RBC membrane destruction, as well as

anisocytosis, poikilocytosis, polychromasia, and agglutination. As with other forms of 

hemolytic anemia, patients will have elevated LDH and unconjugated bilirubin with 

moderate disease, and decreased haptoglobin, hemoglobinemia, and hemoglobinuria 

with severe, intravascular hemolysis. 

Treatment 

In primary and chronic CAS with mild anemia, treatment is symptomatic and involves 

simply keeping extremities, noses, and ears warm in cold weather. Patients with CAS 

should take daily folate supplements. Treatment for severe hemolysis has been 

successful with immunosuppressive or cytotoxic agents, such as chlorambucil, 

cyclophosphamide, a-interferon, or fludarabine. As in warm-type AIHA, plasmapheresis 

may prove helpful as a temporizing measure by removing autoantibodies, particularly as 

auto-IgM has an intravascular distribution, but such therapy should be combined with 

immunosuppressive agents. Unlike warm-type AIHA, CAS rarely responds to steroids 

though such treatment may be considered in atypical cases. Because splenic 

macrophages play a lesser role in IgM-mediated cold-antibody disease, splenectomy is 

not as helpful for cold-antibody mediated extravascular hemolysis. RBC transfusion can 

be performed for patients at risk for significant cardiac or cerebrovascular ischemia, but 

transfused blood should be kept at 37 °C using a blood warmer. Transfusions should be 

limited because they may worsen ongoing hemolysis. In addition to the risk of producing 

alloantibodies to transfused RBCs, most cold antibodies act against the I group 

antigens, which are found on most donor RBCs. 

4. Cold-Type AIHA: Paroxysmal Cold Hemoglobinuria 

PCH is caused by a biphasic IgG autoantibody called the Donath-Landsteiner antibody. 

The PCH autoantibody is directed against the P antigen system found on most RBCs. 

Despite the name, hemolysis may occur at both cold and normal temperatures. 


Symptoms include high fever, chills, headache, abdominal cramps, nausea and 

vomiting, diarrhea, and leg and back pain that develops with cold exposure. Cold 

urticaria, extremity paresthesias, and Raynaud phenomenon may also develop. Primary 

PCH and PCH secondary to congenital or late-stage syphilis are characterized by 

chronic disease with cold-induced relapses. Secondary PCH caused by other infectious 

agents is most common in children and is one of the more common causes of childhood 

hemolytic anemia. Postinfection PCH is usually associated with measles, mumps, EBV, 

CMV, VZV, adenovirus, influenza A, M pneumoniae, Haemophilus influenzae, and E 

coli. Most cases of postinfectious PCH are self-limited, but severe cases may take 

weeks to resolve. With severe hemolysis, hemoglobinuria is common and 

methemoglobinuria may be seen. Acute renal failure may develop as a complication of 

PCH. 

Treatment 

Keep patients with PCH warm. Consider steroids in children with severe hemolytic 

anemia, but because infection-related PCH tends to be self-limited, the benefit is

uncertain. PCH secondary to syphilis responds to effective antibiotic treatment. 

Splenectomy is not helpful, and plasmapheresis should be used only as a temporizing 

measure in life-threatening cases. RBC transfusion using a blood warmer should be 

limited to patients with severe hemolysis, because most donor units are P antigen 

positive and may stimulate further production of PCH autoantibodies. 

5. Mixed-Type AIHA 

Mixed-type AIHA occurs as primary or secondary disease (usually lymphoproliferative or 

autoimmune diseases). The course of illness is usually chronic with severe 

exacerbations. Like warm-type AIHA, mixed-type AIHA is steroid responsive, can be 

treated with splenectomy, and responds to cytotoxic therapy. Because relapses are not 

triggered by cold exposure, acrocyanosis and the Raynaud phenomenon are not 

characteristically seen. As with any secondary AIHA, treatment of the underlying 

disorder will reduce hemolytic activity. 

ALLOIMMUNE HEMOLYTIC ANEMIA 

Alloimmune hemolytic anemia requires exposure to allogeneic RBCs with subsequent 

formation of alloantibodies that react specifically with the allogenic RBCs that triggered 

their production; these antibodies do not react against a patient's own RBCs. A 

well-known example of alloimmune hemolytic anemia is when the RhD-negative 

maternal immune system develops IgG alloantibodies on exposure to RhD-positive fetal 

RBCs. The maternal alloantibodies can then cross the placenta to inflict fetal RBC 

destruction in a condition termed hemolytic disease of the newborn. Anemia can range 

from mild to potentially fatal producing intrauterine fetal death. By still uncertain 

mechanisms, administration of anti-D IgG with any fetomaternal hemorrhage event and 

soon after delivery will suppress maternal alloantibody formation and prevent hemolytic 

disease of the newborn. Treatment of established disease employs intrauterine and 

intravascular fetal transfusion and may include plasma exchange or intravenous 

immunoglobulin therapy. 

Most adults who develop alloimmune hemolytic anemia have a history of RBC 

transfusion, which sensitizes patients to allogeneic RBC antigens. A subsequent 

transfusion can result in immediate alloantibody production, resulting in the fever, chest 

and flank pain, tachypnea, tachycardia, hypotension, hemoglobinuria, and oliguria seen 

in the hemolytic transfusion reaction. In patients with high alloantibody titers, the 

hemolytic reaction can be immediate, whereas patients with lower alloantibody levels 

develop delayed hemolysis occurring 3-7 days posttransfusion. 

DRUG-RELATED AIHA 

Drug-related AIHA can be divided into 3 types: autoimmune, drug adsorption, and 

neoantigen. Steroids can be used in cases of drug-related severe hemolysis. RBC 

transfusion will aggravate hemolysis if the recipient's serum contains antibodies against 

antigens found on the transfused RBCs. 

Autoimmune Drug-Related AIHA

Autoimmune drug-related AIHA results when the offending drug triggers formation of 

autoantibodies that bind with RBC self-antigens, leading to a hemolytic process 

serologically indistinct from that seen in warm-type AIHA. The diagnosis is proved when 

the hemolytic process abates on withdrawal of the offending drug. Drugs implicated 

include a-methyldopa, levodopa, mefenamic acid, procainamide, diclofenac, quinidine, 

phenacetin, and the second- and third-generation cephalosporins (particularly cefotetan 

and ceftriaxone). Up to 71 drugs have been associated with development of a positive 

DAT; however, significant hemolysis is seen only occasionally. An extended drug 

exposure is usually required for autoantibodies to form. A positive DAT does not 

indicate that hemolysis will occur or that a drug must be discontinued. Within days of 

stopping the offending drug, hemolysis usually stops, though it may take months to see 

full resolution of the process. 

Drug Adsorption-Type AIHA 

Drug adsorption-type AIHA requires that the drug incite the formation of antidrug 

antibodies and that the drug bind to the RBCs with significant affinity. Antibodies formed 

against the drug will react against the drug bound to the RBC surface, producing 

hemolysis. This type of hemolysis has also been called drug-requiring because the 

absence of the offending drug eliminates the hemolytic reaction completely. 

Neoantigen-Type Drug-Related AIHA 

Neoantigen-type drug-related AIHA involves weak binding of the offending drug to 

normal RBCs. The body's immune system, seeing the formed immune complexes as 

foreign, will generate an immune response, which then produces hemolytic disease. 

The classic causative agent is penicillin, and isolated cases of 

diphtheria-tetanus-pertussis vaccination in children have been associated with 

hemolysis, possibly via this neoantigen mechanism. 

SICKLE CELL ANEMIA 


Sickle cell anemia is caused by the substitution of the amino acid valine for glutamine at 

position 6 in the ß-globin chain producing an abnormal hemoglobin tetramer termed 

hemoglobin S (HbS). As a result of this mutation, deoxygenated HbS polymerizes, 

deforming the RBC and producing the characteristic sickled appearance. The distorted 

cell results in premature RBC destruction and also increases the viscosity of blood, 

leading to obstruction within the microvasculature. The overall effect is chronic ongoing 

hemolysis and episodic periods of vascular occlusion resulting in tissue ischemia 

affecting most organ systems. 

This defect is inherited as an autosomal recessive trait, and disease is seen in patients 

who are homozygous for the sickle gene (HbSS). People with sickle cell trait (HbAS; 

heterozygous with one gene for normal ß-globin chain and one gene for a ß-globin 

chain with the sickle mutation) have a normal lifespan and are usually asymptomatic 

except in rare cases of severe physiologic stress when they may have an acute pain 

crisis, splenic infarction, or cerebrovascular complications. Approximately 8% of the

African American population carries sickle cell trait (heterozygous for the sickle cell 

gene), and approximately 0.15-0.2% of African American newborns have sickle cell 

disease (homozygous for the sickle gene). A lesser percentage of individuals of Middle 

Eastern, eastern Mediterranean, and Indian descent may have the HbS gene. 



Patients with sickle cell disease typically present to the emergency department because 

of complications (Table 39-13). Acute painful (vasoocclusive) sickle cell crisis is a 

common problem, and the average patient with sickle cell disease has 1-4 severe 

attacks per year. The initiating event may not be identifiable, but stressors such as 

infection, cold, dehydration, and altitude have been implicated. As a result of 

intravascular sickling and small vessel occlusion, infarction of bone, viscera, and soft 

tissue occurs. Infarction manifests as diffuse bone, muscle, and joint pain and, in some 

cases, symptoms related to a specific affected organ. Initial management includes 

aggressive pain management and hydration, an assessment of the cause of the current 

crisis, and a search for additional complications. 


Generally a CBC and reticulocyte count help assess the degree of anemia and ensure 

that the marrow is still producing red cells. If the reticulocyte count is not available, the 

presence of polychromasia in the peripheral blood smear can indicate continued red cell 

production. Patients with sickle cell disease sometimes have a low-grade fever and an 

elevated white blood cell (WBC) count. This combination can make it difficult to 

determine whether an infection is present during a crisis. Consider infection if the WBC 

count has a left shift and is elevated above 20,000/uL. Because of the chronic 

hemolysis, mild elevations in bilirubin and serum LDH are common. 

Treatment 

Supplemental oxygen is commonly used for painful crises, but unless the patient is 

systemically hypoxemic, it has not proved to be of routine benefit. Treatment of acute 

pain requires opioids, and patients with severe pain should receive parenteral agents 

(commonly intravenously in the United States and subcutaneously in the United 

Kingdom). A potent opioid, such as morphine or diamorphine, is recommended, 

whereas meperidine, with the potential for neurotoxicity from the metabolite 

normeperidine, is not recommended. Some patients may be tolerant because of prior 

opioid treatment, and large doses may be required. Regular doses of analgesics for a 

few hours to several days are typically required. Patient-controlled analgesia can be 

used in selected patients. NSAIDs can be used for their additive effect in pain 

management of sickle cell crisis. Because patients with sickle cell disease with a painful 

crisis have an absolute or relative hypovolemia due to their disease (deficient renal 

concentrating ability) or crisis (anorexia, vomiting, fever), aggressive oral or intravenous 

rehydration is commonly carried out. Induced hyponatremia and purified poloxamer 188 

shorten the duration and severity of an acute crisis but the effect is small, and no 

approach to shortening the duration and severity of a painful sickle cell crisis has proved 

reliable, safe, and appropriate for routine use. A common and recommended practice is 

to develop an individualized assessment and treatment protocol for specific patients

who frequently present to the emergency department with painful crises. 

Simple or exchange transfusion to reduce the concentration of HbS-containing red cells 

to below 30% can prevent or reverse the vasoocclusive process. Transfusion should not 

raise the hematocrit above 36% in sickle cell patients. Transfusion carries significant 

expense, risk of blood-borne disease transmission, and the potential for iron-overload, 

and it exposes the patient to the minor red cell antigens with the potential to induce 

antibodies that prevent or complicate future transfusions. Transfusion for sickle cell 

crisis or complications is reserved for specific indications such as aplastic crisis, 

pregnancy, stroke, respiratory failure, general surgery, and priapism. Hydroxyurea has 

been used to reduce the frequency and severity of painful crises. The major side effect 

is bone marrow, hepatic, and renal toxicity, and hydroxyurea has not been approved for 

use in children. Daily prophylactic penicillin V reduces the incidence of infections and 

reduces mortality from sepsis in children. 

Sickle Cell Complications 

A. Bone Pain 

Bone pain is common during a sickle cell crisis and may include the back and the 

extremities. Usually the pain is diffuse, and no physical findings are present. However, 

redness, warmth, or swelling suggest infection (cellulitis or osteomyelitis). The complaint 

of localized pain to the hip with difficulty ambulating suggests the possibility of aseptic 

necrosis of the femoral head, and approximately 30% of those with sickle cell disease 

develop hip pathology by age 30 years. Bone infarctions may cause symptoms similar 

to osteomyelitis. Plain radiographs may show evidence of aseptic necrosis or 

osteomyelitis, whereas bone infarcts are not usually visible on radiographs. Joint 

effusions are occasionally seen as a complication of sickle cell crisis, but arthrocentesis 

is often necessary to determine if the joint is infected. 

B. Dactylitis 

In young children an early manifestation of sickle cell disease is dactylitis (hand-foot 

syndrome). The syndrome is thought to be due to infarction of the red marrow with 

associated periosteal inflammation. The syndrome manifests as fever and painful 

swelling of the hands, feet, or both, and some redness and warmth may be present. As 

the child grows, the hematopoietic tissue in the metacarpal and phalangeal marrow is 

replaced by fatty tissue, making this entity less likely. 

C. Chest Syndrome 

The acute chest syndrome is used to describe a sickle cell crisis with pulmonary 

symptoms and a new pulmonary infiltrate found on radiograph. The patient might have 

pleuritic chest pain, shortness of breath, fever, nonproductive cough, and tachypnea. 

The exact cause of the chest syndrome is unclear, but infection, infarction (ribs or lung), 

and pulmonary fat embolism (from ischemic marrow fat necrosis) have all been 

implicated. Although a chest radiograph is not routinely required in all patients with 

painful sickle cell crisis, it is indicated in those with pulmonary symptoms or signs of 

fever. The onset of acute chest syndrome may be associated with a fall in hemoglobin 

level from the normal baseline. Pulmonary infiltrates may be present in one lobe or be 

diffuse and bilateral, and pleural effusions may be present. Severe cases may progress 

rapidly to respiratory failure. Treatment involves close monitoring of fluid status, oxygen,

and pain control. Broad-spectrum antibiotics to cover S pneumoniae and M pneumoniae 

are recommended. In severe cases, simple transfusion or exchange transfusion can be 

done. Acute chest syndrome is currently the leading cause of death from sickle cell 

disease in the United States. 

D. Abdominal Pain 

Generalized and constant abdominal pain is a common complaint during an acute sickle 

cell crisis, and it may be difficult to distinguish between infarction of the abdominal and 

retroperitoneal organs associated with a sickle cell crisis and a focal abdominal problem 

such as cholecystitis or appendicitis. Frequently the patient can determine that the pain 

is similar to or different from prior episodes. Patients with a typical vasoocclusive 

episode should not have evidence of peritonitis (rebound). Hepatic infarction may cause 

the acute onset of jaundice and abdominal pain and can be difficult to distinguish from 

hepatitis or cholecystitis. Biliary disease is common because pigment-related 

cholelithiasis is seen in 30-70% of patients with sickle cell disease. Severe right upper 

quadrant pain and marked elevations of bilirubin may be due to intrahepatic cholestasis. 

E. Genitourinary System 

Vasoocclusive events involving the kidneys are common but often asymptomatic. 

Infarction in the renal medulla may cause flank pain, renal colic-type pain, and 

costovertebral angle tenderness, mimicking pyelonephritis. Papillary necrosis may result 

in either gross or microscopic hematuria, but red cell casts are uncommon. Renal 

imaging studies are generally necessary for correct diagnosis. Priapism occurs in up to 

30% of males with sickle cell disease. Initial treatment is fluid hydration, pain control, 

and transfusion. Urinary tract infections are more common in patients with sickle cell 

disease, and urinalysis is recommended. 

F. Splenic Infarction 

The spleen is particularly susceptible to the effects of sickled cells. During childhood, 

microinfarctions result in a nonfunctional spleen (in 14% of patients by age 6 months 

and 94% by age 5 years). Immunizations, prophylactic penicillin therapy, and parental 

education are critical to minimize the risk of infection and prompt early evaluation of 

fever in these patients. As sickle cell patients age, their risk of overwhelming sepsis 

decreases, but they remain predisposed to infection. 

G. Splenic Sequestration 

Splenic sequestration is more common in children than in adults, and it is a potential 

cause of death that can be averted with treatment. This syndrome is manifest by sudden 

enlargement of the spleen with an acute fall in the hemoglobin level due to 

sequestration of the blood volume within the spleen. Symptoms include tachycardia, 

hypotension, pallor, lethargy, and abdominal fullness. Left upper quadrant pain may or 

may not be present. The spleen is usually enlarged and firm. Platelets may also be 

sequestered, resulting in moderate thrombocytopenia. Therapy includes volume 

resuscitation, which may mobilize some of the red cells trapped within the spleen. 

Transfusion or exchange transfusion may be necessary; rarely, splenectomy is 

necessary. Unfortunately, recurrence of this syndrome is common. 

H. Hemolytic Anemia 

Patients with sickle cell disease have a chronic hemolytic process with a baseline

hemoglobin level usually between 6 and 9 g/dL; the reticulocyte count is 5-15%. With 

infections the hemolytic process may worsen and hemoglobin may drop from previous 

baseline. Typically, reticulocytosis will increase in response to the increased red cell 

destruction but may not be enough to compensate for the increased hemolysis. Acutely, 

the patient may notice symptoms of worsening fatigue, shortness of breath, dyspnea on 

exertion, and scleral icterus. The hemolysis is rarely severe enough to require 

transfusion. 

I. Aplastic Crisis 

Aplastic crisis results when the production of red cells declines significantly, producing a 

rapid decrease in the hemoglobin level with reticulocytopenia. The most common cause 

of aplastic crisis appears to be infection, specifically from parvovirus. Folate deficiency 

and bone marrow necrosis also may play a role. Aplastic crisis is more common in 

pediatric patients than in adults. The hemoglobin level will be unusually low, and few or 

no reticulocytes will be present (reticulocyte count typically < 0.5%. The WBC and 

platelet levels are usually normal. Generally this syndrome is self-limiting, and the 

marrow will begin producing red cells spontaneously within a week. Transfusion may be 

required in the interim. 

J. Neurologic Complications 

Complications of sickle cell disease include stroke and subarachnoid hemorrhage. The 

cause of strokes in most patients is cerebral infarction due to occlusion or narrowing of 

large cerebral vessels. Approximately 10% of patients with sickle cell disease 

experience a stroke before age 20 years. Acute treatment is emergent simple or partial 

exchange transfusion. Unfortunately, children who suffer a stroke are at 70-90% risk for 

recurrence. Chronic transfusion therapy is indicated to prevent recurrent stoke after the 

initial event. Cerebral aneurysms are also more common in sickle cell patients, perhaps 

due to local vessel occlusion or ischemia. 

K. Infections 

Patients with sickle cell disease are functionally asplenic after early childhood, making 

them susceptible to infections from encapsulated organisms, such as H influenzae and 

S pneumoniae. Other common infections associated with sickle cell disease include 

pneumonia caused by these organisms as well as M pneumoniae, meningitis, and 

osteomyelitis due to Salmonella typhimurium, Staphylococcus aureus, and E coli. 

Although low-grade fever sometimes occurs during an acute crisis, unexplained fevers 

of 38 °C (101 °F) or higher require evaluation for bacterial infection and consideration 

for early treatment with broad-spectrum antibiotics. 

L. Cardiac Complications 

Cardiomegaly is common and correlates with the degree of chronic anemia. 

Additionally, cardiac dysfunction may occur from microinfarcts and hemosiderin 

deposition from hemolysis and blood transfusion. Because of the chronic anemia, 

enhanced cardiac contractility is present to maintain adequate systemic oxygen delivery 

producing a widely radiating systolic ejection murmur. 

M. Dermatologic Complications 

Chronic, poorly healing leg ulcers around the malleoli are common in older patients with 

sickle cell disease. Minor injury, impaired microcirculation due to repeated sickling

episodes and microinfarcts, and infections all contribute to the development and 

persistence of these ulcers. 

Disposition 

Most sickle cell pain crises last 2-3 days. Patients with adequate clinical response and 

no indications for hospital admission can be discharged with oral pain medications and 

referred for follow-up with their primary care physician in the next 24-48 hours. The 

following are guidelines for hospital admission for sickle cell patients: (1) pulmonary or 

neurologic complications, (2) significant bacterial infection, (3) splenic sequestration or 

aplastic crisis, or (4) pain that remains poorly controlled or patients unable to maintain 

adequate hydration. 

THALASSEMIAS 

The thalassemias are a diverse group of disorders characterized by defective synthesis 

of globin chains that results in the inability to produce normal adult hemoglobin. The 

hallmark of these disorders is a microcytic, hypochromic, hemolytic anemia. These 

disorders are most common in individuals of Mediterranean, Middle Eastern, African, or 

Southeast Asian descent. Patients with the ß-thalassemias have diminished production 

of the ß-globin chain, which allows unmatched a-globin chains to accumulate as a 4 

tetramers in the immature red cell. These tetramers are insoluble, and their precipitation 

damages the developing erythroid precursor cells, resulting in early death. Patients with 

a-thalassemia develop an excess of ß-globin chains that accumulate as ß 4 tetramers 

called hemoglobin H (HbH). HbH is more soluble and stable so that, in the severe 

a-thalassemia, ineffective erythropoiesis is less of a problem and increased destruction 

of the cells due to structural abnormality is more prominent. Thalassemia red cells 

contain decreased hemoglobin, which accounts for the hypochromia and target cell 

formation. Individuals with either a- or ß-thalassemia can be minimally to severely 

affected due to the specific genotype and whether the mutation produces complete or 

partial reduction in globin chains. 

a-Thalassemia Carrier & Trait 

a-Thalassemia carriers have normal RBC size, shape, and number and have no clinical 

consequences from this inherited gene. Those with a-thalassemia trait are detected by 

the finding of microcytic RBCs and a normal hemoglobin level. 

HEMOGLOBIN H DISEASE 

Hemoglobin H disease is a disorder in which 1 out of 4 a-globin chain genes is 

functional. Patients with hemoglobin H disease usually present in the neonatal period 

with a severe hypochromic anemia. Later in life the clinical picture includes a 

hypochromic, microcytic anemia with jaundice and hepatosplenomegaly. These patients 

may not require regular transfusions, but a transfusion may be necessary in conditions 

of increased oxidative stress (which may cause precipitation of the unstable hemoglobin 

H resulting in hemolysis) or infection. Most of these patients will know their diagnosis, 

and the emergency physician need provide only supportive care and blood transfusion 

when necessary. Medications that may precipitate hemolysis should be avoided in this

population (Table 39-14). 

ß-Thalassemia Minor (ß-Thalassemia Trait) 

Patients with ß-thalassemia minor are heterozygous for the ß-globin mutation and have 

only mild microcystic anemia. Splenomegaly may be present. These patients may 

exhibit microcytosis, hypochromia, and basophilic stippling on blood smear. An elevated 

hemoglobin A 2 level, typically 4-6%, confirms the diagnosis. These patients will 

generally not have clinical manifestations, and this form of thalassemia may come to the 

clinician's attention only during an evaluation for a mild anemia. 

ß-Thalassemia Major (COOLEY ANEMIA) 

In patients with ß-thalassemia major, both ß-globin genes are defective and production 

of ß-globin chains is severely impaired. ß-Thalassemia major is characterized by a 

severe anemia that begins within the first year of life. These children develop 

hepatosplenomegaly, jaundice, expansion of the erythroid marrow (causing bone 

changes and osteoporosis), and increased susceptibility to infection. The anemia is 

severe and requires regular and lifelong blood transfusions. These transfusions and 

enhanced iron absorption eventually cause iron overload, which, if untreated, results in 

hemochromatosis with cardiac, hepatic, and endocrine dysfunction. The RBCs of these 

children show a low MCV with microcytic and hypochromic cells. Variation in size and 

shape of the RBCs will be notable (increased RDW) as will the presence of nucleated 

cells. Consider this diagnosis in any child with a severe microcytic anemia and the 

appropriate ethnic background. For those with a known diagnosis who present to the 

emergency department with significant symptoms related to anemia or hemolysis, 

consider transfusion and search for precipitating events. 

GLUCOSE-6-PHOSPHATE DEHYDROGENASE DEFICIENCY 

Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme responsible for preventing 

oxidative damage to intraerythrocytic hemoglobin. Over 300 variant mutations are 

described for G6PD; the highest prevalence is in individuals of African, Asian, or 

Mediterranean descent. Because the gene for G6PD is carried on the X chromosome, 

males are affected when they are hemizygous. Females must carry two defective genes 

to be severely affected, but because expression of this gene is variable, women with 

one dysfunctional gene may show some symptoms. The severity of G6PD disease is 

related to the magnitude of enzyme deficiency; patients with severe deficiencies have 

less than 10% of normal enzyme activity and patients with moderate deficiencies have 

10-60% of normal activity. G6PD deficiency is seen in approximately 10-15% of black 

males in the United States. 

Oxidization of the hemoglobin sulfhydryl groups causes hemoglobin to precipitate within 

the cell; it is recognized by the presence of Heinz bodies on the peripheral blood smear. 

The affected RBC is removed from the circulation by the spleen. Oxidant damage also 

occurs at the RBC membrane, producing both extravascular and intravascular 

hemolysis. 

A history of neonatal jaundice 1-4 days after birth is common. Patients with severe

variants may have a severe chronic hemolytic anemia. In the more common variants of 

G6PD deficiency, the patient is usually asymptomatic except for acute hemolytic crises 

that occur due to bacterial and viral infections, exposure to oxidant drugs (most 

commonly sulfonamides, antimalarials, and nitrofurantoin), metabolic acidosis (such as 

diabetic ketoacidosis), renal failure, and in some patients, ingestion of fava beans (see 

Table 39-14). These episodes are usually self-limited and well tolerated because only 

the older RBCs will hemolyze. The incidence of pigmented gallstones and splenomegaly 

is increased in patients with G6PD deficiency. Treatment for this disease is supportive 

and preventative. 

HEREDITARY SPHEROCYTOSIS 

Hereditary spherocytosis is the result of an erythrocyte membrane defect and is the 

most prevalent hereditary hemolytic anemia among people of northern European 

descent. The disease is typically inherited in an autosomal dominant pattern, although a 

less common autosomal recessive variant exists; in up to 20% of patients the disease is 

the result of an apparent spontaneous mutation. The abnormal shape of the RBC 

results from molecular abnormalities in the cytoskeleton of the cell membrane, resulting 

in red cells with a microspherocytic shape, which is not pliable enough to pass through 

the spleen, leading to an increased rate of destruction and a compensatory increase in 

RBC production. The clinical spectrum of hereditary spherocytosis includes (1) mild 

disease, occurring in 20-30% of cases, with an autosomal dominant inheritance, (2) 

moderate disease, occurring in 60-75% of cases, with primarily autosomal dominant 

inheritance, and (3) severe disease, in about 5% of cases, occurring with autosomal 

recessive inheritance. 

Neonatal jaundice during the first week of life occurs in 30-50% of hereditary 

spherocytosis patients. After the neonatal period, the symptoms and signs depend on 

the severity of ongoing hemolysis. Patients with mild disease usually have a normal 

hemoglobin level and little or no splenomegaly but are susceptible to hemolytic or 

aplastic episodes triggered by infection. Patients with moderate disease have mild to 

moderate anemia, modest splenomegaly, periodic episodes of hemolysis with jaundice, 

and an increased incidence of pigmented gallstones. The rare patient with severe 

hereditary spherocytosis has chronic jaundice, an enlarged spleen, and significant 

hemolytic anemia requiring episodic blood transfusions. 

The peripheral blood smear shows spherocytes with a normal to low MCV and 

increased MCHC (> 36%). The diagnosis of hereditary spherocytosis is established by 

the osmotic fragility test. In severe cases, splenectomy will generally reverse the anemia 

except in the unusual cases of autosomal recessive variants. After splenectomy, 

spherocytes are still present. 

Ballas SK: Sickle anaemia: progress in pathogenesis and treatment. Drugs 

2002;62:1143. [PMID: 12010077] 

Bolton-Maggs PH: The diagnosis and management of hereditary spherocytosis. 

Baillieres Best Pract Clin Haemtol 2000;13: 327. [PMID: 11030038] 

Gehrs BC, Friedberg RC: Autoimmune hemolytic anemia. Am J Hematol 2002;69:258.

[PMID: 11921020] 

Hermiston ML, Mentzer WC: A practical approach to the evaluation of the anemic child. 

Pediatr Clin North Am 2002; 49:877. [PMID: 12430617] 

Mehta A, Mason PJ, Vulliamy TJ: Glucose-6-phosphatase dehydrogenase deficiency. 

Baillieres Best Pract Clin Haemtol 2000;13:21. [PMID: 10916676] 

Scjroer SL: Pathophysiology of thalassemia. Curr Opin Hematol 2002;9:123. [PMID: 

11844995] 

Telen MJ: Principles and problems of transfusion in sickle cell disease. Semin Hematol 

2001;38:315. [PMID: 11605166] 

Vichinsky EP et al: Causes and outcomes of the acute chest syndrome in sickle cell 

disease. N Engl J Med 2000;342: 1855. [Erratum in N Engl J Med 2000;343:824.] 

[PMID: 10861320] 

Wonke B: Clinical management of beta-thalassemia major. Semin Hematol 

2001;38:350. [PMID: 11605170] 

Wright MS: Drug-induced hemolytic anemias: increasing complications to therapeutic 

interventions. Clin Lab Sci 1999;12: 115. [PMID: 10387489] 

V. POLYCYTHEMIA 

The term polycythemia means increased cellular components in peripheral 

blood—RBCs, WBCs, and platelets—but in common practice is used to describe 

increased red cells or erythrocythemia. Polycythemia can be a primary disorder due to 

malignant transformation of a hematopoietic stem cell (called polycythemia vera) or can 

be secondary to overstimulation of red cell production. Polycythemia is characterized by 

an increased red cell mass. In relative or false polycythemia, the red cell mass is normal 

but decreased plasma volume results in elevated hemoglobin and hematocrit values. 

PRIMARY POLYCYTHEMIA (Polycythemia Vera) 

Polycythemia vera is an unregulated neoplastic proliferation of red cells, usually 

accompanied by increased WBC and platelet production. Peak age at onset is 50-70 

years, although it can occur in young adults. 



Onset is gradual, and symptoms are usually due to hyperviscosity and impaired 

circulation in the brain (headache, dizziness), eyes (impaired vision), heart (chest pain), 

or peripheral circulation (claudication). Increased production of basophils and mast cells 

can lead to pruritus after a hot shower from histamine release. Hemorrhagic or 

thrombotic complications are rare. Physical findings include hypertension (common), 

plethora or ruddy complexion, splenomegaly (in about 75% of cases), and

hepatomegaly (in about 30% of cases). 


Determination of red cell mass with a radionuclide technique will show an elevated 

value (> 36 mL/kg in males or > 32 mL/kg in females) but is unnecessary when the 

hemoglobin value is above 20 g/dL or hematocrit is above 60% in males or above 56% 

in females; these values are always associated with an elevated red cell mass. The 

WBC and platelet counts are commonly elevated. 


Standard treatment for polycythemia vera is periodic phlebotomy to remove excess red 

cells, reduce blood viscosity, and improve microcirculation. Polycythemia vera patients 

with altered mentation should have emergent phlebotomy with 500 mL of blood 

removed. Myelosuppressive agents are occasionally used, generally when excessive 

platelet production causes thrombotic or hemorrhagic complications. 

SECONDARY POLYCYTHEMIA 

Secondary polycythemia is produced by erythropoietin stimulation of bone marrow red 

cell production. Systemic hypoxia (eg, from chronic obstructive pulmonary disease, 

right-to-left cardiac shunts) or local renal hypoxia (eg, atherosclerotic renal vascular 

disease) can lead to stimulation of erythropoietin production by the kidney. Because of 

the widespread use of cigarettes, chronic obstructive pulmonary disease is the most 

common cause of secondary polycythemia. Less common causes include chronic 

carbon monoxide exposure, renal tumors that secrete erythropoietin, use of androgenic 

steroids, and familial hemoglobinopathies associated with high oxygen affinity. 


Polycythemia should be suspected when the hematocrit is greater than 52% in males or 

47% in females. Confirmation of red cell mass and plasma volume requires 

measurement via radionuclide techniques. Systemic hypoxia (arterial oxygen saturation 

< 92%) or chronic carbon monoxide exposure (carboxyhemoglobin levels > 8%) should 

be considered. Blood viscosity increases and impairs microcirculation with hematocrit 

values above 60-65%. 


Symptomatic patients should undergo phlebotomy to reduce blood viscosity and 

improve microcirculation, and emergent phlebotomy may be necessary in the 

emergency department for patients with acute symptoms. Long-term management of 

secondary polycythemia depends on the primary disorder. 

Prchal JT: Molecular biology of polycythemias. Intern Med 2001;40:681. [PMID: 

11518102] 

Tefferi A: Polycythemia vera: a comprehensive review and clinical recommendations. 

Mayo Clin Proc 2003;78:174. [PMID: 12583529]

VI. WHITE CELL DISORDERS 

NEUTROPENIA 


Neutropenia is defined as a decrease in circulating neutrophils as detected by 

measuring the absolute neutrophil count (ANC) in the peripheral blood. The ANC is 

determined by multiplying the total WBC count by the percentage of neutrophils and 

bands from the WBC differential. The ANC is normally greater than 1500 cells/uL in 

individuals of European descent and greater than 1000 cells/uL in African Americans. 

Neutropenia produces an increased susceptibility to bacterial infections inversely related 

to the ANC. Severe neutropenia is defined as an ANC less than 500 cells/uL. 


Neutropenia can be congential, associated with inherited immune defects and 

phenotypic abnormalities. A form of congential neutropenia is chronic benign 

neutropenia, either familial with an autosomal dominant inheritance pattern, or 

nonfamilial. Patients with chronic benign neutropenia do not have significantly increased 

susceptibility to bacterial infections. Acquired neutropenia can be due to drugs, toxins, 

nutritional deficiencies, autoimmune disorders, or diseases that impair bone marrow 

granulocyte cell production. The list of drugs that can produce neutropenia is extensive, 

but the most likely agents are the cytotoxic chemotherapeutic agents used to treat 

malignancies. 

Neutropenia should be suspected when a cancer patient receiving chemotherapy 

presents with fever or when an otherwise healthy patient presents with an infection that 

has not responded as expected to antibiotic treatment. The evaluation of the febrile 

neutropenic patient requires a careful evaluation for clinically occult infection. Because 

of the neutropenia, the patient may not be able to generate pus in a local site or wound, 

an infiltrate on chest radiograph, or pyuria on urinalysis in response to infection. 

Carefully examine the mouth, sinuses, and rectal area for evidence of local infection. 

Obtain blood cultures, urine culture, and a chest radiograph. When present, culture 

other body secretions such as diarrhea, wound exudate, or sputum. 


The decision to initiate empiric antibiotic therapy is based on the estimated risk of 

serious bacterial infection as judged by the cause, severity, and expected duration of 

neutropenia and on the patient's clinical condition. The severely ill cancer patient with 

severe neutropenia (ANC ANC < 500 cells/uL) due to recent chemotherapy clearly 

requires broad-spectrum empiric antibiotic therapy and hospital admission. Conversely, 

a mildly ill cancer patient with mild neutropenia (ANC of 1000-1500 cells/uL) who has 

not received recent chemotherapy can likely be discharged home with symptomatic 

therapy and no antibiotic treatment as long as the evaluation does not find a specific 

bacterial infection requiring treatment. Consult with the hematologist-oncologist 

regarding treatment and admission decisions. If indicated, initiate empiric antibiotics in

the emergency department after obtaining appropriate cultures. Multiple antibiotic 

regimens are used, typically a broad-spectrum agent such as a third-generation 

cephalosporin (ceftazidime), or a fluoroquinolone (levofloxacin), or a carbapenem 

(imipenem and cilastatin) with or without a specific antistaphylococcal agent such as 

vancomycin. 

LEUKOCYTOSIS 

Elevated WBC counts may represent an appropriate response to infection or may 

constitute an autonomous proliferation of cells due to a primary hematologic disorder. 

Elevated WBC count is not a problem by itself except in the unusual case of leukemia 

associated with hyperleukocytosis, when WBC counts exceed 100,000- 300,000 

cells/uL, causing increased blood viscosity and circulatory compromise. This can lead to 

central nervous system impairment and respiratory insufficiency; urgent treatment with 

leukocytapheresis is indicated. As a temporizing measure, intravenous hydration and 

exchange transfusion can be performed. 

ACUTE LEUKEMIA 


Acute leukemia is a malignancy of hematopoietic stem cells in which the leukemic cell 

population replaces and suppresses normal bone marrow cells, resulting in bone 

marrow failure with anemia, functional or absolute neutropenia, and thrombocytopenia. 

The usual causes of illness and death are infection (related to neutropenia) or 

hemorrhage (related to thrombocytopenia). These rapidly progressive disorders are 

uniformly fatal without treatment. Fortunately, effective treatment is available for most 

patients with acute leukemia, and depending on cell type, 20-40% of adult patients and 

50-70% of pediatric patients with acute leukemia survive longer than 5 years with 

current therapy. Acute leukemias have historically been classified according to 

neoplastic cell morphology (acute lymphocytic leukemia, or ALL, and acute myelocytic 

leukemia, or AML), but immunologic analysis has found a wide diversity in neoplastic 

cell origin. 


Patients with acute leukemia typically develop symptoms over a few weeks and present 

with fatigue (due to anemia), fever (due to neutropenia), or bleeding problems (due to 

thrombocytopenia or DIC). Leukemic organ infiltration accounts for symptoms such as 

bone pain (ALL), swollen gums (AML), and abdominal pain due to splenomegaly (ALL 

and AML) 

The diagnosis of acute leukemia is suspected when the WBC count is elevated and the 

peripheral blood smear shows a large number of immature white cells (blast cells), 

along with anemia and thrombocytopenia. Uncommonly, blast cells may be absent from 

the peripheral blood (termed aleukemic leukemia) and the hemoglobin value and 

platelet count may be normal. Definitive diagnosis of acute leukemia is based on bone 

marrow examination showing more than 30% immature blast cells. Differentiation 

between the types of acute leukemia is made using morphologic, histochemical, and

immunochemical staining. 

Disposition 

Hospitalize patients with suspected acute leukemia. Evaluate fever, if present, and 

initiation of empiric antibiotic treatment in the neutropenic patient is prudent. Patients 

with hyperleukocytosis (> 300,000 cells/uL) may develop symptoms of impaired 

microcirculation and require emergent treatment. 

CHRONIC LEUKEMIA 

Chronic leukemias are indolent diseases, typically found in older adults and producing 

nonspecific systemic symptoms (malaise, fatigue, weight loss, low grade fever) and 

signs of leukemic organ infiltration (splenomegaly, lymphadenopathy). Chronic 

leukemias have historically been classified according to neoplastic cell morphology 

(chronic lymphocytic leukemia, or CLL, and chronic myelocytic leukemia, or CML), but 

immunologic analysis has found a wide diversity in neoplastic cell origin. 

1. Chronic Lymphocytic Leukemia 

CLL is the most common leukemia seen in the adult population of Western countries. 

Most cases of CLL are seen in patients older than 55 years, and the majority of cases 

have a slow progression lasting up to 10 years before they enter a final terminal stage. 

These patients commonly experience repeated infections such as pneumonia, herpes 

simplex, and herpes zoster because the lymphocytes are functionally incompetent. 

Patients often have fatigue, lymphadenopathy, mucosal surface bleeding, or 

hepatosplenomegaly. Diagnosis is suggested by a peripheral blood smear with absolute 

lymphocyte count exceeding 5000 cells/uL and confirmed with bone marrow 

examination. Patients with an initial diagnosis of CLL and without any of the 

complications can be followed up with a hematologist. Patients with any of the 

above-mentioned complications (bleeding, fever, symptoms of hyperviscosity, bone 

marrow failure) need hospitalization and prompt consultation with a hematologist. 

2. Chronic Myelocytic Leukemia 

CML is a clonal disorder of hematopoietic stem cells most commonly due to a reciprocal 

translocation between the long arms of chromosomes 22 and 9, resulting in a shortened 

chromosome 22, termed the Philadelphia chromosome. 

Patients typically present with fatigue, malaise, and weight loss. Often findings of 

leukocytosis and splenomegaly with or without hepatomegaly are found incidentally on 

routine examination. The CBC often shows a moderate leukocytosis of 20,000-60,000 

cells/uL, a mild anemia, and variable platelet counts. The peripheral blood smear shows 

a predominance of myeloid progenitor cells (myeloblasts, myelocytes, metamyelocytes) 

and nucleated red blood cells. 

Most patients are clinically stable and responsive to therapy for 3-5 years, then develop 

an acute blastic crisis (generally myeloid but occasionally lymphoid) that is refractory to 

treatment and progresses to death. A small subset of CML patients bypass the initial

chronic phase and enter a rapidly progressive leukemic phase wherein they have 

profound leukocytosis and thrombocytopenia as evidenced by bleeding, petechiae, and 

ecchymoses. A serious complication is the hyperviscosity syndrome in which WBC 

counts exceed 300,000 cells/uL or with a leukocrit greater than 10%. This is evidenced 

by neurologic and ophthalmologic manifestations and respiratory failure. 

Exchange transfusion can be a useful temporizing measure in the acute setting with 

severe stupor or seizure, but urgent leukocytapheresis is the most effective treatment. 

INFECTIOUS MONONUCLEOSIS 


Infectious mononucleosis is a primary infection with EBV characterized by fever, 

pharyngitis, adenopathy, and greater than 10% atypical lymphocytes in the peripheral 

smear. Only a minority of primary EBV infections come to medical attention; population 

studies indicate as many as 90% of young adults have serologic evidence of prior EBV 

infection, but only a minority of individuals describe a prior episode of infectious 

mononucleosis, supporting the concept that most primary EBV infections are mild or 

asymptomatic. 



The incubation period of infectious mononucleosis is 1-2 months. Initial symptoms are 

fatigue, malaise, and sore throat. Fever is usually low grade, and chills are uncommon. 

The pharyngitis of infectious mononucleosis may be exudative or nonexudative, and 

tonsillar enlargement is common. The lymphadenopathy is usually bilateral and in the 

posterior cervical nodes, although other lymph nodes may be affected and generalized 

lymphadenopathy is possible. Splenic tenderness is common early in the disease, 

whereas splenomegaly is a later finding. A variety of other symptoms or signs are well 

described in infectious mononucleosis: (1) an early, faint, evanescent generalized 

maculopapular rash, (2) early bilateral periorbital edema, (3) hepatitis with liver 

tenderness and jaundice, (4) uvular edema, and (5) neurologic disorders such as Bell 

palsy, optic neuritis, other cranial nerve mononeuropathies, aseptic meningitis, 

encephalitis, Guillain-Barre syndrome, and transverse myelitis. 


Common laboratory findings of infectious mononucleosis include (1) leukocytosis 

(usually 12,000-20,000 cells/uL), (2) lymphocytosis (usually > 60% on the white cell 

differential), (3) atypical lymphocytosis (> 10% and frequently > 30%), (4) mild 

elevations in serum transaminases, and (5) elevated erythrocyte sedimentation rate. 

EBV infection induces the production of host antibodies that form the basis for serologic 

diagnosis of infectious mononucleosis. Specific antibody testing in clinical use for 

infectious mononucleosis includes both IgM and IgG antibodies to either the viral capsid 

antigen found on the viral surface or the Epstein-Barr nuclear antigen found in the viral 

core. The most commonly used antibody test is the Monospot, which detects an IgM 

antibody to the viral capsid antigen (historically named heterophile antibody) that 

produces agglutination of horse red blood cells. The Monospot is considered to have

approximately 85% sensitivity and almost 100% specificity. However, the sensitivity of 

this test is lower early in the clinical disease (up to 6 weeks is required for maximal 

sensitivity) and in children under age 2 years, who are frequently Monospot negative. 

False-positive Monospot tests have been seen in patients with CMV, rubella, systemic 

lupus erythematosus, rheumatoid arthritis, HIV, and herpes simplex infections. 


The differential diagnosis of infectious mononucleosis includes (1) streptococcal 

pharyngitis (complicated by the observation that up to 30% of infectious mononucleosis 

patients have detectable group A streptococci in the oropharynx), (2) primary CMV 

infection (the closest clinical mimic of infectious mononucleosis), (3) acute 

toxoplasmosis (usually with unilateral lymphadenopathy), and (4) viral hepatitis. 

Treatment 

There is no effective antiviral therapy for infectious mononucleosis. For the patient with 

excessive tonsillar enlargement, a 5- to 7-day course of oral prednisone, 1 mg/kg/d, 

provides symptomatic benefit. Steroids are also used for rare patients with central 

nervous system involvement or hemolytic anemia. Antibiotic treatment of coexistent 

group A streptococci is controversial. Some clinicians recommend withholding antibiotic 

treatment because a positive throat culture or streptococcal antigen test represents 

colonization rather than infection and antibiotic treatment may induce a rash that, 

though due to the infectious mononucleosis and not the drug, may be judged as a drug 

allergy and complicate future antibiotic therapy. Patients should be instructed to refrain 

from strenuous physical activity and especially contact sports for 3 weeks. 

MULTIPLE MYELOMA 



Multiple myeloma is a disease of malignant plasma cell proliferation and excessive 

secretion of monoclonal paraproteins. Multiple myeloma usually presents during the 6th 

to 7th decades of life. The most common initial symptoms are bone pain (in up to 70% 

of patients; involving the lumbar region) sometimes with pathologic fractures; 

constipation, nausea, confusion, and somnolence from hypercalcemia; fatigue and 

pallor from anemia; infection with impaired immunity; bleeding from thrombocytopenia or 

hyperviscosity; and paresthesias from peripheral neuropathies. Complications of 

multiple myeloma include renal impairment, amyloidosis from paraproteinemia, 

hypercalcemia, and spinal cord compression from extradural compression. Physical 

examination findings include bony tenderness, soft tissue plasmacytoma masses, pallor 

from anemia, ecchymoses or petechiae, epistaxis, or findings of spinal cord 

compression (lower extremity weakness or dysesthesias with incontinence of bowel or 

bladder with associated decreased rectal tone or saddle anesthesia). 


The diagnosis is suspected when the serum globulin protein level is elevated and is 

confirmed with serum protein immunoelectrophoresis demonstrating a monoclonal

spike. Evaluate the patient's hematologic (CBC), hemostatic (PT, PTT), renal (blood 

urea nitrogen and creatinine), and metabolic (electrolytes, calcium, uric acid) status. 

Quantification of urinary protein excretion (Bence-Jones proteinuria; ie, lambda light 

chains) is sometimes useful for diagnosis and determining response to therapy. A 

skeletal series looking for sites of lytic lesions (commonly in the skull and long bones) 

can be helpful to identify potential pathologic fracture sites and to differentiate multiple 

myeloma from Waldenstrom macroglobulinemia (which does not typically have lytic 

bone lesions). Bone marrow examination typically finds sheets or clumps of plasma 

cells replacing normal marrow contents. 


Many patients with multiple myeloma are asymptomatic, and specific treatment can be 

delayed until the patient shows signs of disease progression without affecting efficacy of 

treatment. Treatment is usually with the chemotherapeutic agents melphalan and 

prednisone. In occasional patients, multiple myeloma is treated with irradiation and 

chemotherapy followed by autologous bone marrow or peripheral blood stem cell 

transplantation. Adjunctive therapy may include bisphosphonates to prevent 

hypercalcemia and pathologic fractures, erythropoietin to treat anemia, and radiation to 

lytic lesions to prevent pathologic fractures. Complications of hypercalcemia, 

hyperviscosity, pathologic fracture, or spinal cord compression necessitate admission 

and specific therapy. 

WALDENSTROM MACROGLOBULINEMIA 


Waldenstrom macroglobulinemia is a rare malignancy of B lymphocytes characterized 

by excessive production of monoclonal IgM. Symptoms and signs are due to the 

elevated serum viscosity (from the IgM) and infiltration of organs (bone marrow, spleen, 

liver, lymph nodes) from the neoplastic lymphocytes. The disease most commonly 

occurs in the elderly; median age at onset is approximately 60 years. 


The onset is typically gradual, and common symptoms are weakness, anorexia, and 

weight loss. Symptoms due to hyperviscosity include mental status changes, Raynaud 

phenomenon, peripheral neuropathy, and visual changes. Ocular signs of hyperviscosity 

include papilledema, enlarged retinal veins, and retinal hemorrhage. 

Hepatosplenomegaly and lymphadenopathy are common. Purpura can occur due to 

thrombocytopenia, and functional platelet impairment from the IgM paraproteinemia. 

The laboratory diagnosis of Waldenstrom macroglobulinemia is supported by (1) an IgM 

level above 3 g/dL and (2) hematologic abnormalities of anemia and thrombocytopenia 

and occasionally leukopenia. The malignant nature is identified with high-resolution 

serum protein immunoelectrophoresis or bone marrow biopsy with immunochemical 

staining. 


Consider hyperviscosity for any Waldenstrom macroglobulinemia patient who presents 

with mental status or visual changes. Measure the serum viscosity; if elevated, start 

urgent plasmapheresis. Chemotherapy with alkylating agents (chlorambucil, melphalan, 

or cyclophosphamide) is used to reduce production of the IgM paraprotein and control 

symptoms of neoplastic organ infiltration. Prednisone is used to control autoimmune 

symptoms such as digital ischemia from cryoglobulinemia or immune hemolysis from 

agglutination. Other chemotherapeutic agents are sometimes used, but no combination 

is superior or changes median survival. Stable, asymptomatic patients typically do not 

receive treatment. 

Aquino VM: Acute myelogenous leukemia. Curr Probl Pediatr Adolesc Health Care 

2002;32:50. [PMID: 11951090] 

Chan KW: Acute lymphoblastic leukemia. Curr Probl Pediatr Adolesc Health Care 

2002;32:40. [PMID: 11951089] 

Garcia-Sanz R et al: Waldenstrom macroglobulinaemia: presenting features and 

outcome in a series with 217 cases. Br J Haematol 2001;115:575. [PMID: 11736938] 

Kalidas M, Kantarjian H, Talpaz M: Chronic myelogenous leukemia. JAMA 

2001;286:895. [PMID: 11509034] 

Oscier D: Chronic lymphocytic leukemia. Br J Haematol 1999; 105(Suppl 1):1. [PMID: 

10330924] 

Papesch M, Watkins R: Epstein-Barr virus infectious mononucleosis. Clin Otolaryngol 

2001;26:3. [PMID: 11298158] 

Porcu P et al: Leukocytoreduction for acute leukemia. Ther Apher 2002;6:15. [PMID: 

11886572] 

Rajkumar SV et al: Current therapy for multiple myeloma. Mayo Clin Proc 2002;77:813. 

[PMID: 12173715] 

Viscoli C, Castagnola E: Treatment of febrile neutropenia: what is new? Curr Opin Infect 

Dis 2002;15:377. [PMID: 12130933] 

Wendtner CM et al: New aspects on the pathogenesis, diagnostic procedures, and 

therapeutic management of chronic lymphocytic leukemia. Int J Hematol 2001;73:32. 

[PMID: 11372752] 

VII. TRANSFUSION THERAPY 

Transfusion in the emergency department is typically used for acute blood loss and 

circulatory shock. As medical care is moved to outpatient settings and emergency 

departments become more crowded, emergency physicians may be responsible for 

transfusion therapy that was once relegated to inpatient settings. An understanding of 

the available blood products, their indications, and potential complications of 

transfusions is important for safe and effective transfusion practice.

PACKED RED BLOOD CELLS 

An adult's total blood volume is estimated to be 2.5 L/m 2 , 75 mL/kg, or approximately 5 

L in a 70-kg person. Fresh whole blood transfusion would be ideal to replace acute 

blood loss; however, during the storage of whole blood, platelets and other factors 

become inactive. In addition, the storage life of whole blood is less than that of individual 

components. Therefore, by necessity and convenience, whole blood is fractionated to its 

components for storage and transfusion. 

PRBCs are prepared by the centrifugation of whole blood to remove about 80% of the 

plasma. Then a preservative solution is added, most commonly 

citrate-phosphate-dextrose, with additional nutrients adenosine, glucose, and mannitol. 

Each unit of PRBCs has a hematocrit of 65-80% and a volume of approximately 

250-350 mL (Table 39-15). Transfusion of 1 unit of PRBCs into a typical adult will 

increase the hematocrit by 3% or the hemoglobin by 1 g/dL. 

The primary reason for emergency transfusion of PRBCs is acute blood loss or 

profound anemia with impaired oxygen delivery. Based on animal and human studies, 

lactic acid production increases, oxygen extraction ratio exceeds 50%, and the mortality 

rate starts to increase in otherwise stable patients with hemoglobin levels of 3.5-4.0 

g/dL. In an animal model of coronary stenosis, adverse cardiac effects are seen with 

hemoglobin levels of 6.0 g/dL. However, there are reports of Jehovah's Witnesses, who 

generally refuse blood products, tolerating surgery with hemoglobin levels below 6.0 

g/dL as long as intravascular volume is maintained. Patients with chronic anemia have 

developed compensation mechanisms so that chronic anemia is better tolerated than 

acute anemia. Various consensus panels have recommended transfusion for 

hemoglobin less than 7 g/dL, whereas patients with hemoglobin greater than 10 g/dL 

rarely will benefit from transfusion. Some patients with cardiac or vascular disease may 

benefit from transfusion when hemoglobin levels are 7-10 g/dL. Transfusion thresholds 

for children may be higher and depend on the cause of their anemia. 

Depending on the urgency of transfusion, most patients can be typed (ABO and RhD 

blood group type) and cross-matched against the blood intended for transfusion. The 

blood type can be determined in about 15 minutes, whereas typing and cross-matching 

takes approximately an hour. In critically ill patients, type O RhD negative (universal 

donor) may be transfused because it does not contain blood group antigens. Type O 

RhD-positive blood may also be used if type O RhD-negative blood is not available, but 

it is not the blood of choice for women of child-bearing potential. If an RhD-negative 

patient is transfused with 1 unit of RhD-positive PRBCs, approximately 80% will develop 

anti-D antibodies. Because the effect of 1 unit of PRBCs is small and clinically 

inconsequential, it is standard practice to transfuse a minimum of 2 units and raise the 

hematocrit by 6% and hemoglobin level by 2 g/dL. 

PRBCs may be further treated to meet specific uses, for example, leukocyte-reduced 

PRBCs, irradiated PRBCs, washed PRBCs, and frozen PRBCs. Leukocyte-reduced 

PRBCs have had 70-85% of the leukocytes removed. The advantages of 

leukocyte-reduced PRBCs is (1) to prevent or avoid nonhemolytic febrile reactions due 

to antibodies to WBC and platelets, if the patient has been exposed to previous

transfusions or pregnancies, (2) to prevent sensitization in patients who may be eligible 

for bone marrow transplantation, and (3) to minimize the risk of virus transmission such 

as HIV and CMV. The leukocytes can be reduced by filtration or other methods before 

storage of the PRBCs or during transfusion. Irradiation of PRBCs eliminates the 

capacity of T cells to proliferate, therefore preventing the donor's T cells from reacting to 

the recipient's cells and causing graft-versus-host disease. Consider using irradiated 

cells in transplant patients, neonates, and immunocompromised patients. Washed 

PRBCs are indicated in patients who have a hypersensitivity to plasma, such as IgA 

deficiency. For rare blood types, PRBCs may be frozen and saved for up to 10 years for 

later use. This process is more expensive than normal storage, and once thawed the 

blood must be washed and transfused within 24 hours. 

One unit of PRBCs, about 250-350 mL in volume, is generally transfused over 1-2 

hours. However, blood may be transfused more rapidly in patients with hemodynamic 

instability. During standard transfusions the initial rate is slower over the first 30 

minutes, so that if there is incompatibility, the transfusion may be stopped. 

PLATELETS 

Platelet transfusions may be used either prophylactically to prevent bleeding, or 

therapeutically when patients with thrombocytopenia are actively bleeding. Platelets are 

collected from whole blood donation or from single donors using apheresis techniques. 

One random-donor platelet concentrate prepared from 500 mL of donated whole blood 

contains an average of 7.5 × 10 10 platelets (see Table 39-15). One apheresis-collected 

single-donor platelet concentrate generally contains 3-6 × 10 11 platelets, depending on 

local collection practice. Platelets should be given according to ABO compatibility, if 

available. A dose of 1 random-donor platelet concentrate per 10 kilograms 

(approximately 6-8 random-donor platelet concentrates for an adult) or 1 

apheresis-collected single-donor platelet concentrate in an adult will increase the 

platelet count by about 50,000/uL. Response to platelet transfusions is variable; 

therefore, platelet levels should be checked at 1 hour and 24 hours. Failure of platelets 

to rise appropriately may be due to increased consumption of platelets from an 

underlying process, destruction due to platelet antibodies, or sequestration due to 

hypersplenism. Transfused platelets should survive 3-5 days, unless a consumptive 

process is present. 

The cause of thrombocytopenia is important in the decision to transfuse platelets. With 

ITP, an antiplatelet antibody-mediated consumptive process, the platelets are larger, 

younger, and more functional; therefore, prophylactic transfusion is rarely indicated 

despite very low platelet counts. However, with platelet hypoplasia, platelet function is 

impaired, making the risk of bleeding greater. Patients with comorbid diseases such as 

infection, fever, medications, and central nervous system involvement may be more 

likely to bleed or may be at higher risk if they bleed; therefore, the threshold for platelet 

transfusion is higher. 

The dose of platelets should reflect the indication. In general, spontaneous bleeding is 

possible, and prophylactic transfusion is indicated with platelet counts less than 

10,000/uL. Platelet counts of greater than 50,000/uL rarely cause significant bleeding. 

Indications for platelet transfusion include the following:

• Platelet count 10,000 uL in asymptomatic patients 

• Platelet count 15,000 uL and coagulation disorder or minor bleeding 

• Platelet count 20,000 uL and major bleeding 

• Platelet count 50,000 uL and invasive procedure (thoracentesis, paracentesis) or 

general surgery required, or during massive transfusion (1-2 blood volumes) 

• Platelet count 100,000 uL and neurologic or cardiac surgery required 

Like PRBCs, platelets can be leukocyte-reduced or washed. Patients who have had 

repeated transfusions may become alloimmunized and refractory to platelet transfusion, 

noted by the lack of expected rise of platelet count after transfusion. Such patients need 

HLA- or cross-matched platelets. Other disorders may affect the efficacy of platelet 

transfusion including duration of platelet storage, bacterial sepsis, antibiotics, 

graft-versus-host disease, DIC, and splenomegaly. 

Relative contraindications to platelet transfusion are consumptive processes such as 

TTP or heparin-induced thrombocytopenia, in which transfusion may worsen 

thrombosis. In these diseases, platelet transfusion should be performed in consultation 

with a hematologist. 

FRESH FROZEN PLASMA 

FFP is plasma obtained after the separation of whole blood from RBCs and platelets, 

and then frozen within 6 hours. Each unit of FFP is 200-250 mL and contains about 1 

unit of each coagulation factor and 2 mg of fibrinogen per mL (see Table 39-15). FFP is 

appropriate for rapid replacement of multiple coagulation deficiencies such as in liver 

failure, warfarin overdose, DIC, and massive transfusion in bleeding patients. 

Administration of FFP prophylactically to nonbleeding patients is not indicated, and 

prophylaxis is not always needed for some procedures in patients with a coagulopathy. 

For example, patients undergoing paracentesis and thoracentesis are not at increased 

risk of bleeding until the INR is greater than 2 times control. During massive transfusion 

with replacement of an entire blood volume, coagulation factor levels are about one third 

of normal, and although PT and PTT may be abnormal, clinical coagulopathy does not 

always occur. Indications for FFP transfusion include the following: 

• Rapid reversal of warfarin therapy 

• Bleeding and multiple coagulation defects as evidenced by prolonged PT, INR, and 

aPTT greater than 1.5 control (eg, liver disease, DIC) 

• Correction of coagulation defects for which no specific factor is available (specific 

factor replacement is safer and better but may not always be available) 

• Transfusion of more than one total blood volume with evidence of active bleeding and 

prolonged PT or PTT

Other possible indications for FFP in consultation with an appropriate specialist include 

TTP, antithrombin III deficiency, and hereditary angioedema (FFP contains C1 

esterase). 

Because the efficacy of transfused coagulation factors varies, the increase in specific 

coagulation factors seen after FFP infusion also varies. In general, 1 unit of FFP will 

increase most coagulation factors by 3-5% in a 70-kg adult. The common adult dose of 

7-8 mL/kg (or 2 units of FFP in a 70-kg individual) will increase coagulation factors by 

only 10%, a clinically inconsequential benefit in most circumstances. For clinically 

relevant correction of coagulation factor deficiencies, a dose of 15 mL/kg (or 4 units in a 

70-kg adult) is required (see Table 39-15). As indicated by the name, FFP is stored 

frozen and there may be a delay while it is thawed. FFP should be ABO compatible. 

After transfusion, reevaluate bleeding and coagulation studies. If consumption is 

present, repeated FFP transfusion should be guided by the PT, INR, and aPTT 

response. 

CRYOPRECIPITATE 

Cryoprecipitate is the cold-insoluble protein fraction of FFP. Each unit of cryoprecipitate 

is about 20-50 mL and contains about 225 mg of fibrinogen, 80 units of factor VIII, and 

variable amounts of von Willebrand factor (vWF) (see Table 39-15). It also contains 

some factor XIII and fibronectin. With the development of recombinant factor VIII 

products for use in hemophilia, the primary role of cryoprecipitate is now replacement of 

fibrinogen or vWF. Bleeding patients with fibrinogen levels below 100 mg/dL due to 

severe liver disease, DIC, and dilutional coagulopathy may benefit from cryoprecipitate. 

The dose of cryoprecipitate is 1 unit/5 kg (or 10 units in an adult), which will raise 

fibrinogen by about 75 mg/dL. 

OTHER PLASMA-DERIVED PRODUCTS 

Immunoglobulin for Intravenous Administration 

Immunoglobulin for intravenous administration is a pooled IgG product that has been 

virally attenuated. Labeled indications for its use are ITP, pediatric HIV infection, and 

primary humoral immunodeficiency; it is also indicated for several new and off-label 

treatments such as for Kawasaki disease and autoimmune disorders. Dose and 

administration varies by the indication. Adverse reactions include anaphylaxis especially 

in IgA deficiency (rare), febrile reactions, headache, and renal failure. Some patients 

develop transient positive serology to hepatitis C and CMV. 

Albumin 

Albumin is a virally inactivated purified plasma protein that usually accounts for 50% of 

circulating protein and 75% of plasma oncotic pressure. Albumin transfusion in patients 

with decreased oncotic pressures may transiently increase oncotic pressure; however, 

the albumin rapidly distributes to extravascular spaces. Therefore, because of its cost 

and the lack of proved efficacy over crystalloid, there is no advantage to using albumin.

Antithrombin III 

Antithrombin III is a serum coagulation inhibitory protein. Deficiency can be acquired or 

congenital and is usually associated with difficult-to-treat thrombosis. Antithrombin III 

replacement is indicated in antithrombin III deficiency-related thrombosis and for 

thrombosis prophylaxis. This product should be considered in antithrombin III-deficient 

patients when difficulty is encountered in achieving adequate heparinization or when 

recurrent thrombosis is observed despite adequate anticoagulation. It is also reasonable 

to give concentrate to antithrombin III-deficient subjects before major surgeries or in 

obstetric situations where the risks of bleeding from anticoagulation are unacceptable. 

Currently, antithrombin III therapy is under investigation in sepsis, DIC, and other 

thrombotic diseases. The dose depends on the indication. An infusion of 50 units (1 unit 

is the amount in 1 mL of pooled plasma) of antithrombin III concentrate per kilogram will 

usually raise the plasma antithrombin III level to about 120% of normal in a congenitally 

deficient individual. Monitor plasma antithrombin III levels to ensure that they remain 

above 80%. Subsequent administration of antithrombin III at 60% of the initial dose at 

24-hour intervals is recommended to maintain antithrombin III levels in the normal 

range. 

MASSIVE TRANSFUSION 

Massive transfusion is defined as the replacement of one blood volume or about 10 

units of PRBCs within a 24-hour period. Patients receiving less than one blood volume 

rarely need hemostatic factor (ie, FFP, platelets) replacement. In patients receiving two 

blood volumes or more than 20 units of PRBCs, transfusion of coagulation factors and 

platelets may be empirically helpful. For patients who receive 1-2 times total blood 

volume, hemostatic factor replacement should be guided by considerations noted 

above: (1) If the platelet count is less than 50,000/uL, platelet transfusion is warranted; 

(2) if the INR is greater than 1.5, FFP may be given; and (3) if fibrinogen levels are 

below 100 mg/dL, it may be replaced with cryoprecipitate. In massive transfusion, 

hypothermia is a risk and blood and crystalloid as well as the patient should be warmed. 

Hypocalcemia from the preservative citrate-chelating calcium is rare but should be 

considered in massive transfusion if symptoms or signs of hypocalcemia are present. 

COMPLICATIONS OF TRANSFUSION THERAPY 

Up to 20% of all transfusions may lead to some type of adverse reaction. Although most 

of these reactions are minor, some are life threatening (Table 39-16). In critically ill 

patients, transfusion reactions may be difficult to identify; therefore, attention should be 

paid to unexpected changes in patient status during a transfusion. 

Infectious Complications of Blood Transfusion 

Improved blood donor screening, serologic testing, safer handling of blood products, 

and viral inactivation of many blood products has reduced the risk of infection from 

blood transfusion (Table 39-17). Most cases of viral transmission are thought to occur 

during the window period between infection and antibody production in the donor. This 

window is reduced but not eliminated by the use of antigen testing. The prevalence of 

CMV-positive antibodies in the general population is 50-80%. Therefore, blood is not

outinely tested for CMV unless the recipient is seronegative and is (1) pregnant, (2) a 

potential or present transplant candidate, (3) immunocompromised, or (4) a premature 

infant. Use of leukocyte-reduced blood components further decreases the risk of CMV 

transmission to susceptible populations because most of the virus resides in the 

leukocytes. Bacterial sepsis resulting from RBC transfusion is most commonly due to 

Yersinia enterocolitica, which is able to grow easily in refrigerated blood. The risk of 

bacterial sepsis is highest with random-donor platelet concentrates. 

Acute Hemolytic Transfusion Reactions 

Hemolytic transfusion reactions occur when the recipient's antibodies recognize and 

induce hemolysis in the donor's RBCs. The reaction is usually acute when antibodies 

already exist in sufficient levels but can be delayed when an amnestic response occurs 

to a transfused RBC antigen to which the recipient is already sensitized. Acute 

transfusion reactions are most commonly caused by ABO incompatibility and are 

usually the result of technical errors made during the collection of blood, during 

pretransfusion testing, or in patient identification. The majority of transfusion-related 

fatalities are due to acute hemolytic reactions. 

The risk of acute hemolytic transfusion reaction due to incompatible blood is 1-4 per 

million units transfused; the fatality rate is approximately 50%. With acute hemolytic 

reaction, most of the transfused cells are destroyed, which may result in activation of the 

coagulation system with DIC and release of anaphylotoxins and other vasoactive 

amines. Evidence of this type of reaction includes back pain, pain at the site of the 

transfusion, headache, alteration of vital signs (fever, hypotension, dyspnea, 

tachycardia), chills, bronchospasm, pulmonary edema, bleeding due to developing 

coagulopathy, and evidence of new or worsening renal failure. Recognition of 

transfusion reactions in critically ill patients who may already be hypotensive and 

tachycardiac is difficult and requires a high degree of suspicion. Ongoing transfusion 

should be stopped immediately on first indication of potential problems. While laboratory 

confirmation is being performed, treat the sequelae of hemolysis supportively. Check 

renal function (serum creatinine, urinalysis), electrolytes, and coagulation status (PT, 

INR, aPTT). Maintain renal blood flow and urine output with fluids, mannitol, and 

furosemide as needed. Treat shock with volume and vasopressors to support blood 

pressure. Treat coagulopathy with FFP. Send the remaining donor blood, along with a 

posttransfusion blood specimen from the recipient, to the blood bank. Diagnosis is made 

by evidence of hemolysis (hemoglobinuria or hemoglobinemia) and by blood 

incompatibility. The blood bank will be able to test the blood, review records, confirm 

blood types, and determine if the patient's syndrome is from a transfusion reaction. 

Risk of morbidity and mortality is proportional to the amount of blood received prior to 

recognition of the transfusion reaction. Therefore, in nonemergent blood transfusions, 

the initial rate of blood transfusion is low for the first 30 minutes to allow for the 

identification of a transfusion reaction while minimizing the volume of blood transfused. 

The best medicine is prevention by strict adherence to detail in obtaining blood for 

cross-match and initiating transfusion. 

Extravascular Hemolytic Reactions

Extravascular hemolytic reactions occur in about 1 per 1000 PRBC units transfused. 

Hemolysis most commonly occurs in the spleen and occasionally in liver and bone 

marrow. This type of reaction is less serious than acute hemolytic transfusion reactions 

and is rarely fatal. It may be confirmed by a positive DAT, elevated unconjugated 

bilirubin, and poor response to transfusion. Treatment is supportive. 

Febrile Transfusion Reactions 

Febrile transfusion reactions are characterized by onset of fever during or within a few 

hours of a blood transfusion. This type of reaction is one of the more common 

transfusion-related complications and is more common in multiparous women or 

multiply transfused patients. The clinical presentation can range from a mild elevation in 

temperature to fever along with rigors, headache, myalgias, tachycardia, dyspnea, and 

chest pain. Initially it may be difficult to differentiate a febrile reaction from the more 

serious hemolytic transfusion reaction or sepsis. Febrile transfusions result from a 

combination of recipient antibody against donor leukocytes and the release of cytokines 

produced during storage. For non-leukocyte-reduced platelets the risk of fever during 

transfusion is about 20%, and with leukocyte reduction, the incidence of febrile reactions 

is about 2%. For the first-time febrile reaction, or in any severe reaction, the transfusion 

should be stopped and the product returned to the blood bank. Laboratory investigation 

similar to that done for possible hemolytic transfusion reaction should be done and 

blood cultures should be obtained. Febrile transfusion reactions are usually self-limited 

and respond to antipyretics. Premedication with diphenhydramine and acetaminophen 

may help prevent these reactions. For patients with recurrent febrile reactions, the use 

of leukocyte-reduced blood products and pretreatment with antipyretics may be helpful. 

Allergic Transfusion Reactions 

Allergic transfusion reactions are associated with onset of urticaria and pruritus during 

the transfusion and occur in approximately 1% of transfusions. Fortunately, only a small 

percentage of patients will have more severe reactions such as bronchospasm, 

wheezing, and anaphylaxis. These reactions are caused by an immune response to 

plasma proteins. Conservative therapy with an antihistamine usually controls the 

symptoms. The transfusion does not typically have to be stopped. For more severe 

symptoms the transfusion may need to be stopped and more aggressive management 

initiated. In patients with IgA deficiency, more severe anaphylactoid reactions can occur 

in response to exposure to the IgA in donor products. Washing the plasma from the 

cells minimizes this type of reaction. 

Alderson P et al: Human albumin solution for resuscitation and volume expansion in 

critically ill patients. Cochrane Database Syst Rev 2002;(1):CD001208. [PMID: 

11869596] 

Bianco C: Choice of human plasma preparations for transfusion. Transfus Med Rev 

1999;13:84. [PMID: 10218231] 

Carson JL et al: Transfusion triggers: a systematic review of the literature. Transfus Med 

Rev 2002;16:187. [PMID: 12075558]

Dodd RY: Current viral risks of blood and blood products. Ann Med 2000;32:469. 

[PMID: 11087167] 

Goodnough LT et al: Transfusion medicine. First of two parts—blood transfusion. N Engl 

J Med 1999;340:438. [PMID: 9971869] 

Goodnough LT et al: Transfusion medicine. Second of two parts—blood conservation. N 

Engl J Med 1999;340:525. [PMID: 10021474] 

Heddle NM: Pathophysiology of febrile nonhemolytic transfusion reactions. Curr Opin 

Hematol 1999;6:420. [PMID: 10546797] 

Kopko PM, Holland PV: Mechanisms for severe transfusion reactions. Transfus Clin Biol 

2001;8:278. [PMID: 11499977] 

Rebulla P: Platelet transfusion trigger in difficult patients. Transfus Clin Biol 2001;8:249. 

[Erratum in Transfus Clin Biol 2002; 9:109.] [PMID: 11499971] 

Rebulla P: Revisitation of the clinical indications for the transfusion of platelet 

concentrates. Rev Clin Exp Hematol 2001; 5:228. [PMID: 11703819] 

Wilkes MM, Navickis RJ: Patient survival after human albumin administration. A 

meta-analysis of randomized, controlled trials: Ann Intern Med 2001;135:149. [PMID: 

11487482] 





Martin, MD 

I. HEMOSTATIC DISORDERS: GENERAL CONSIDERATIONS

Table 39-1. Standard tests of hemostasis. 

Normal Value Platelet count Traumatic bleeding not a 

serious concern unless 

platelet count < 50,000/µL, 

and spontaneous bleeding 

unlikely unless platelet count 

< 10,000/µL. 

11-13 seconds, depending on 

reagent; INR 1.0 

Activated partial thromboplastin time Tests intrinsic and common 

pathways: factors XII, XI, IX, 

VIII, V, prothrombin, and 

fibrinogen. 

150-450 mg/dL Fibrin degradation products by latex 

agglutination 

< 500 µg/L, depending on 

assay methodology 


Breakdown products of 

fibrinogen and fibrin 

monomer. 




Martin, MD 

TABLES 

Table 39-1. Standard tests of hemostasis.

Table 39-2. Specialized tests of hemostasis. 

Normal Value Bleeding time Tests interaction betw 

platelets and 

subendothelium. 

10-12 seconds Mixing test 1:1 mixing of abnorm 

plasma with normal 

plasma will correct a 

single coagulation fa 

deficiency and norma 

PT or PTT. If mixing 

not normalize the PT 

PTT, a coagulation 

inhibitor is present. 

60-130% (0.6-1.3 

units/mL) 

Inhibitor screens Used to detect inhibit 

to coagulation factors 

lupus-anticoagulant)

Table 39-3. Drugs that impair platelet production or function. 

Impair Platelet Function 

(Prolonged Bleeding Time) 

Aspirin 

Gold salts 4+ Antiplatelet agents: ticlopidine and clopidogrel 

Quinine and quinidine 4+ Calcium channel blockers 

Aspirin 3+ Nitroglycerin 

Valproic acid 3+ Phenothiazines 

Thiazides 2+ 

Procainamide 2+ 

Cimetidine and ranitidine 2+ 

Penicillins/cephalosporins 1+ 

1 

The numerals following each drug indicate 

relative incidence based on case reports. 





Martin, MD 

TABLES 

Table 39-3. Drugs that impair platelet production or function.

Table 39-4. Conditions associated with 

functional platelet disorders. 





Martin, MD 

TABLES 

Table 39-4. Conditions associated with functional platelet disorders.

Table 39-5. Common bleeding locations in hemophilia patients. 

Comments 

Common, can lead to joint destruction and chronic arthropathy 

Can occur in any location, dangerous in the neck (asphyxia), limb (compartment 

syndrome), and retroperitoneum (hemorrhagic shock) 

Epistaxis, bleeding after dental extractions, gastrointestinal bleeding 

Can occur with minimal trauma, common cause of death 

Common, rarely serious 





Martin, MD 

TABLES 

Table 39-5. Common bleeding locations in hemophilia patients.

Table 39-6. Available products for hemophilia treatment. 

Available Products Hemophilia A All have a low risk of HIV and 

hepatitis transmission. 

Both products have reduced 

amounts of von Willebrand factor. 

Monoclate-P is highly purified source 

of factor VIII. 

Low to no risk of hepatitis or HIV. 

No evidence of porcine viral 

transmission to humans. 

Factor IX complex 

products: 

Koyne-80 factor IX 

complex 

Proplex T factor IX 

complex 

Profilnine SD 

Bebulin VH 


Activated factor IX complex products: 

Autoplex T 

Feiba VH 

Purified factor IX products: 

Alpha Nine SD 

Mononine 




Martin, MD 

TABLES 

Table 39-6. Available products for hemophilia treatment.

Table 39-7. Initial factor replacement guidelines. 

Minimum Initial 

Factor Level 

Hemophilia B 

Initial Dose 

30-50% 30-40 U/kg Epistaxis 

Deep muscle 

50% 50 U/kg Gastrointestinal bleeding 

100% 100 U/kg 





Martin, MD 

TABLES 

Table 39-7. Initial factor replacement guidelines.

Table 39-8. Classification of von Willebrand disease. 

Occurrence 

in 

Patients 

with von 

Willebrand 

Disease 

10-15% of 

patients 

I All multimeric forms are 

present, but their quantity is 

diminished. 

III Essentially no vWF is 

present.

Table 39-9. Warfarin reversal guidelines. 

Any elevation Withhold warfarin. 

Replace coagulation 

factors with FFP or 

Bleeding 

factor complex 

concentrates. 

Vitamin K, 5-10 mg IV 

(dose dependent on 

INR) 

Mild to moderate < 5 Withhold warfarin until 

INR therapeutic and 

then restart at same or 

lower dose. 

None > 9 Withhold warfarin until 

INR therapeutic and 

then restart at same or 

lower dose. 

Vitamin K, 2-4 mg PO

Table 39-10. Normal red blood cell (RBC) values for adults. 1 

Male RBC count 

(million/µL) 

14-17 Hematocrit 

(%) 

78-100 Mean cellular 

hemoglobin 

(pg/cell) 

32-36 Red cell 

distribution 

width (%) 

0.5-2.5 


1 Normal 

values may 

vary 

depending 

upon the 

equipment 

used, patient's 

age, and 

altitude. 

4.0-5.5 

36-48 

25-35 

11.5-14.5 




Martin, MD 

TABLES 

Table 39-10. Normal red blood cell (RBC) values for adults.

Table 39-11. Classification of anemias. 

Mean 

Corpuscular 

Volume (fL) Cause 

Microcytic 

Variable, but usually < 32 Elevated reticulocytes, target cells, normal or 

elevated serum ferritin and iron 

< 32 Basophilic red blood cell stippling 

Variable, but usually < 32 Elevated serum iron; ring sideroblasts in bone 

marrow 

80-100 Acute blood loss 80-100 

> 36 Decreased platelets

Table 39-12. Causes of secondary autoimmune hemolytic anemia. 





Martin, MD 

TABLES 

Table 39-12. Causes of secondary autoimmune hemolytic anemia.

Table 39-13. Emergencies in sickle cell disease. 

Specific Emergencies 

Musculoskeletal pain 

(typical painful crisis) 

Splenic sequestration 

Pneumonia 


Acute chest pain syndrome 

Priapism 

Hemolytic crisis 

Sepsis 

Urinary tract infections 




Martin, MD 

TABLES 

Table 39-13. Emergencies in sickle cell disease.

Table 39-14. Drugs that produce oxidative stress on 

red blood cells and may induce hemolysis. 

Drug 

Sulfacetamide 

Sulfanilamide 

Antimalarials Chloroquine 

Pentaquine 

Nitrofurantoin 

Phenazopyridine 

Ciprofloxacin 

niridazole 

Chloramphenicol 

Naphthalene 

Vitamin K analogs 

Acetanilid 

Isobutyl nitrite

Table 39-15. Characteristics of blood products and doses. 

Approximate 

Shelf Life 

Content/Unit 1 

21-42 days Red cells, 65-80% 

Plasma, 20-35% 

5 days Platelets, 7.5 × 10 10 

5 days Platelets, 3-6 × 10 11 

1 year frozen and 24 hours thawed Each coagulation factor, 200-250 units; and 

fibrinogen, 400-500 mg 

1 year frozen Factor VIII, 80 units; fibrinogen, 225 mg; 

von Willebrand factor, variable amounts

Table 39-16. Acute transfusion reactions. 

Symptoms and Signs Evaluation 

Fever, chills, low back pain, dyspnea, 

tachycardia, shock 

Retype and cross-match. Direct and indirect Coombs 

tests. Serum haptoglobin, free hemoglobin, and indire 

bilirubin. Urine hemoglobin. 

Low grade fever, but may be asymptomatic Retype and cross-match. Direct and indirect Coombs 

tests. Serum haptoglobin, free hemoglobin, and indire 

bilirubin. Urine hemglobin. 

Fever, chills Evaluate for intravascular hemolysis and infection. 

Mild: urticaria, pruritus 

Severe: dyspnea, wheezing, hypotension, 

tachycardia, shock 


For mild symptoms that resolve with antihistamines: n 

further evaluation. 

For severe symptoms: evaluate for intravascular 

hemolysis. 




Martin, MD 

TABLES 

Table 39-16. Acute transfusion reactions.

Table 39-17. Risk of infection from transfusion of blood products. 

Estimated Frequency 1 

1:1,000,000 (200,000-2,000,000) 

Unknown 

1:500,000 (250,000-2,000,000) 

1:40,000 (30,000-250,000) 

1:40,000 (30,000-150,000) 

1:10,000 

1:12,000 random donor platelet concentrates 

1:500,000 packed red blood cells

Figure 39-1. Coagulation cascade. Ca 2+ = calcium; fibrinogen is factor I; PL, 

phospholipid surface (often platelets); prothrombin is factor II. (Reprinted, with 

permission, from Eberst ME: Evaluation of anemia and the bleeding patient. Page 1368 

in Tintinalli JE, Kelen GD, Stapczynski JS (eds.): Emergency Medicine. A 

Comprehensive Study Guide, 5th edition. McGraw-Hill, 2000. 





Martin, MD 

FIGURES

40. Infectious Disease Emergencies - Brian Hawkins, MD, & Daniel F. 

Danzl, MD 


SEPTIC SHOCK 


• Fever. 

• Tachycardia, tachypnea. 

• Leukocytosis, leukopenia, elevated or low white blood cell count. 

• Left shift or bandemia. 


• Clinical suspicion of infection. 


Sepsis results from a complicated interplay between the immune system and an 

infectious source, leading to a release of inflammatory cytokines in a cascade that 

affects every organ system in the body. Response to endotoxin and other immune 

modulators leads to a release of prostaglandins, histamine, and bradykinins that leads 

to arterial and venous dilation and increased endothelial permeability. Systemic 

inflammatory response syndrome (SIRS) is a nonspecific term describing the 

inflammatory processes seen after trauma, infection, burns, and medical disease such 

as pancreatitis. Sepsis is a systemic response (a form of SIRS) to infection. Sepsis 

syndrome is defined by (1) clinical evidence of infection, (2) fever or hypothermia, (3) 

tachypnea, (4) tachycardia, and (5) impaired organ system function or perfusion (such 

as altered mentation, hypoxemia, elevated plasma lactate level, or oliguria). Septic 

shock is sepsis-associated hypotension. Sepsis is the 13th leading cause of death in the 

United States; more than 700,000 cases of severe sepsis occur each year. Excluding 

fungal sepsis (which has a mortality rate of 83%), the mortality rate for sepsis is 

28-50%. 

Patients especially susceptible to infections include immunocompromised individuals 

and those whose natural mechanical barriers of defense have been breached or 

manipulated through injury or surgery. The incidence of bacteremia and sepsis is 

increased in patients who are receiving corticosteroids, immunosuppressive agents, 

cancer chemotherapy, or radiation as well as in those with diabetes, leukemia, severe 

granulocytopenia, genitourinary tract diseases, and cirrhosis. The age extremes are at 

risk. 

Clinical Findings

The classical clinical pattern of abrupt onset of chills followed by fever and hypotension 

is present in only 30-40% of patients in septic shock. Other presenting symptoms 

include hypothermia, oliguria, alteration of mental function, unexplained hypotension, or 

metabolic acidosis. 

Immediate Measures 

A. Maintain Airway and Ventilation 

Initiate continuous pulse oximetry and oxygenate by nasal cannula or face mask. Listen 

for stridor or other evidence of upper airway obstruction. Ensure that equipment 

necessary for definitive airway management is readily available because a patient with 

altered mental status or hypoxemia may require intubation. 

Measure arterial blood gases (uncorrected for core temperature) and pH. Respiratory 

alkalosis may be present early in septic shock but usually progresses to a metabolic 

acidosis. The use of pulse oximetry can help as an overall indicator of perfusion and 

oxygenation but may be misleading if vasoconstriction is present. 

B. Establish Adequacy of Circulation 

Insert a large-bore catheter and obtain blood samples for laboratory studies. Two 

catheter sites will be necessary because of the large volumes of infusion and multiple 

medications necessary. 

A flotation tip catheter (PAC) may be necessary for hemodynamic monitoring, but the 

role of a PAC is controversial in adults because studies have shown limited benefit. In 

children the role of the PAC appears to be more clearly defined. Insertion of a PAC is 

usually an intensive care unit procedure. 

A central venous catheter will allow for infusion of inotropic agents as well as 

measurement of central venous pressure (CVP) and possibly central venous oxygen 

concentration (CVO 2 ), which may help guide patient management. 

Place the patient on a continuous blood pressure monitor and consider placing an 

arterial line because of the inaccuracies associated with traditional blood pressure 

measurements in shock. The presence of an arterial line will also make it easier to 

obtain blood and measure arterial blood gases. 

Monitor cardiac rhythm and obtain a 12-lead electrocardiogram because of the risk of 

precipitating ischemia in patients with preexisting coronary artery disease. Shock may 

also lead to arrhythmias secondary to electrolyte and acid-base abnormalities. 

Begin volume replacement with crystalloid (studies have shown no difference between 

crystalloid and colloid with respect to mortality or development of pulmonary edema). In 

an adult, 1-2 L of crystalloid will typically improve blood pressure and urine output. The 

use of early goal-directed therapy in the emergency department (ie, monitoring central 

venous oxygen saturation, lactate, base deficit, and pH and having clearly set goals for 

improvement in these parameters during a set period of resuscitation) is beneficial to 

patients in septic shock. Significant impact on the final outcome of sepsis can be made 

in the emergency department prior to intensive care unit admission. This is partially

ased on the failure of traditional methods such as mean arterial pressure and urinary 

output in assessing tissue hypoperfusion and hypoxia and increased utility of other 

methods such as CVO 2 . If a CVP catheter is available, a CVP of 15 suggests adequate 

volume unless the patient has acute respiratory distress syndrome, in which case the 

CVP should be maintained between 8 and 10. Large volumes of crystalloid (6-10 L) are 

usually required during the initial resuscitation, and in approximately 50% of patients, 

hypotension will reverse with fluid resuscitation alone. 

Insert an indwelling urinary catheter. 

C. Obtain Complete Vital Signs 

1. Signs of septic shock—Hypotension in sepsis is the endpoint of a vicious cycle of 

inflammation that, if left untreated, will lead to multiorgan failure. Cardiovascular effects 

of sepsis include vasculature changes due to vasodilation and capillary leak, and direct 

myocardial depressant effects on the myocardium. Patients in sepsis who are 

deteriorating have worsening cellular function due to sepsis-induced mitochondrial 

dysfunction. This leads to a process termed cytopathic hypoxia, which is diminished 

adenosine triphosphate production despite a normal PO 2 . Early in sepsis the extremities 

may be warm and dry and then progressively cool and clammy. Hypotension, 

tachycardia, tachypnea or hyperventilation, altered sensorium, and oliguria may be 

present. 

2. Fever or hypothermia—A core temperature is indicated with seriously ill patients. 

Use a low-reading probe in hypothermic patients. 

D. Regulate Blood Pressure 

Give inotropic agents and vasopressors to patients unresponsive to fluids. The goal 

mean arterial pressure is 60 mm Hg. 

1. Dopamine—Dopamine is the most commonly used initial agent for septic shock. It 

has dose-related a, ß, and dopaminergic sympathetic effects. The major side effects are 

increased heart rate, increased pulmonary artery wedge pressure, and decreased 

gastric pH. Acidosis is the most common cause of failure of this agent. 

2. Dobutamine—Dobutamine may be warranted after volume replacement and 

vasoconstrictor therapy have begun for low cardiac output states. This agent is mainly a 

ß agonist but has a activity as well and can cause peripheral vasodilation, pulmonary 

vasodilation, decreased pulmonary hypoxic vasoconstriction, and tachycardia. 

3. Epinephrine—Epinephrine acts as an a and ß agonist and increases cardiac output, 

blood pressure, heart rate, and blood lactate levels but decreases splanchnic blood flow 

and gastric pH. Consider using this agent if others fail. 

4. Norepinephrine—Norepinephrine acts as an a and ß agonist and has potent 

peripheral vasoconstrictor and inotropic effects. Its administration can lead to severe 

systemic, pulmonary, renal, and splanchnic vasoconstriction. Norepinephrine is useful in 

patients who respond to dopamine with excessive tachycardia or in patients who remain 

hypotensive. Note: Norepinephrine is gaining support in the management of sepsis

without serious organ dysfunction and may eventually replace dopamine as the initial 

agent of choice. 

5. Phenylephrine—Phenylephrine is a selective a-adrenergic agonist that lacks direct 

myocardial effects and may be indicated for patients with tachyarrhythmias. 

E. Correct Acidosis 

Correct acidosis by improving oxygen delivery and hemodynamic parameters. Patients 

with severe acidosis have a decreased response to catecholamines; nevertheless, 

bicarbonate therapy is recommended only for severe acidosis (eg, pH < 7.1) because 

bicarbonate may lead to diffusion of CO 2 into the cells, leading to intracellular acidosis. 

F. Correct Coagulopathy 

If the patient is coagulopathic or actively bleeding, administer fresh frozen plasma or 

packed red blood cells. The hemoglobin should be maintained between 8 and 10. 

G. Select Therapy 

Because sepsis is a heterogeneous entity, a one-therapy-for-all approach is not 

suitable. Therapy should be directed by specific metabolic or biochemical derangements 

that are present. 

1. Corticosteroids—Because the efficacy of steroids in treating sepsis is unclear, they 

are not recommended for acute sepsis. 

2. RhAPC (recombinant human activated protein C; drotrecogin a 

[Xigris])—RhAPC is approved for treatment of severe sepsis. Studies show 40% 

relative risk reduction in mortality at 28 days in patients given Xigris. In vitro studies 

have shown this drug to have anti-inflammatory action. 

3. Vasopressin—Vasopressin infusions can cause a pressor response and decrease 

the required doses of conventional catecholamines. 

4. Dopexamine—Dopexamine is a synthetic catecholamine, with ß-adrenergic and 

dopaminergic effects without a stimulation, that may be beneficial in septic shock. 

5. Other agents—Numerous studies have concluded that agents such as interleukin 

antagonists, monoclonal antibody against tumor necrosis factor a, and 

platelet-activating factor antagonists have no proven benefit. 

H. Search for Source of Infection 

Thoroughly but rapidly examine the patient for an obvious source of infection. Examine 

skin and nails, looking carefully for a rash, petechiae, purpura, abscesses, ulcers, an 

infected intravenous catheter insertion site, needle marks, and splinter hemorrhages. 

Examine the patient's scalp, back, perineum, mucosal surfaces, palms, and soles. 

Check for signs of meningeal irritation. Listen for heart murmurs or abnormal lung 

sounds. Examine the abdomen and perform a rectal examination because rectal 

abscesses are frequently overlooked on physical examination. Percuss and palpate all 

joints and vertebrae. Perform a bimanual pelvic examination on all female patients.

I. Perform Diagnostic Tests 

1. Blood cultures—Obtain 2 sets of blood cultures (aerobic and anaerobic) from 

separate sites on all seriously ill patients. 

2. Gram staining and culture—Obtain Gram-stained smears and cultures of all 

accessible body fluids, purulent material, and other potentially infected tissue. Typical 

sources of infection include urine, pulmonary secretions, cerebrospinal fluid (CSF), 

surgical wounds and drains, intravenous catheter sites, ascitic fluid, and decubiti. 

Microscopic examination of the buffy coat of a centrifuged blood sample may identify the 

organism, particularly in meningococcemia. 

3. Other laboratory studies—A complete blood count may display leukocytosis, 

leukopenia, or left shift as well as thrombocytopenia. Increased consumption and 

decreased hepatic production of clotting factors, as well as the possible development of 

disseminated intravascular coagulation, may lead to coagulation abnormalities. 

Hypotension and acute tubular necrosis may lead to acute renal failure. Elevated liver 

function tests may be seen in hepatic dysfunction. Electrolyte abnormalities include 

hypokalemia, hyponatremia, hypomagnesemia, and hypophosphatemia. A patient can 

present with either hyperglycemia (secondary to stress response) or hypoglycemia. 

4. Radiologic studies—Obtain chest x-ray, bone and soft tissue x-rays, and other 

studies as needed. 

J. Start Antibiotic Treatment 

Early antibiotic therapy is associated with decreased mortality. Ideally antibiotic 

treatment should be targeted at a specific organism, but the causative agent is 

frequently unknown. Empiric therapy must be used until the infectious agent is identified 

(Table 40-1). The most common route of entry for organisms is the genitourinary tract, 

followed by the respiratory tract, wounds, and the gastrointestinal tract. Gram-negative 

organisms are currently the most common organisms and include Escherichia coli, 

Klebsiella spp., Proteus spp., Enterobacter spp., and Pseudomonas spp. Gram-positive 

organisms include Staphylococcus aureus, pneumococci, enterococci, and 

Streptococcus viridans. Anaerobic organisms such as Bacteroides fragilis are 

increasingly common as causative organisms. 

Provide surgical treatment as needed: antibiotics and volume replacement will not 

provide much aid in the face of a surgical cause of sepsis that requires further surgery. 

Examples include intra-abdominal abscess, biliary obstruction with cholangitis, perirectal 

abscess, or septic abortion. 

Disposition 

Intensive care is required for all patients in septic shock and for those seriously ill with 

infection. 

Annane D: Corticosteroids for septic shock. Crit Care Med 2001;29:S117. [PMID: 

11445691]

Anonymous: Practice parameters for hemodynamic support of sepsis in adult patients in 

sepsis. Task Force of the American College of Critical Care Medicine, Society of Critical 

Care Medicine. Crit Care Med 1999;27(3):639. [PMID: 10199548] (Review.) 

Balk RA: Severe sepsis and septic shock: definitions, epidemiology and clinical 

manifestations. Crit Care Clin 2000;16(2):179. [PMID: 10768078] (Review.) 

Butt W: Pediatric critical care: a new millennium: septic shock. Pediatr Clin North Am 

2001;48(3):601. [PMID: 11411296] (Review.) 

Choi PT et al: Crystalloids vs. colloids in fluid resuscitation: a systematic review. Crit 

Care Med 1999;27(1):200. [PMID: 9934917] 

Cohen JC et al: UK Medical Research Council International Working Party. New 

strategies for clinical trials in patients with sepsis and septic shock. Crit Care Med 

2001;29(4):880. [PMID: 11373487] (Review.) 

Dellinger RP: Bacterial sepsis and septic shock: current therapy for sepsis. Infect Dis 

Clin North Am 1999;13(2):495. [PMID: 10340180] (Review.) 

Friedman G, Silva E, Vincent JL: Has the mortality of septic shock changed with time? 

Crit Care Med 1998;26:2078. [PMID: 9875924] 

Glauser MP: Pathophysiologic basis of sepsis: considerations for future strategies of 

intervention. Crit Care Med 2000;28 (9)(Suppl):S4. [PMID: 11007189] 

Holmes C et al: Physiology of vasopressin relevant to management of septic shock. 

Chest 2001;120(3):989. [PMID: 11555538] (Review.) 

Jindal NJ, Hollenberg SM, Dellinger RP: Pharmacologic issues in the management of 

septic shock. Crit Care Clin 2000;16 (2):233. [PMID: 10768081] (Review.) 

Lerosa SP: Sepsis: menu of new approaches replaces one therapy for all. Cleve Clin J 

Med 2002;69(1):65. [PMID: 11811722] 

Martin C et al: Effects of norepinephrine plus dobutamine alone on left ventricular 

performance of septic shock patients. Crit Care Med 1999;27(9):1708. [PMID: 

10507587] 

Mizock BA: Metabolic derangements in sepsis and septic shock. Crit Care Clin 

2000;16(2):319. [PMID: 10768084] (Review.) 

Opal S: Therapeutic rationale for antithrombin III in sepsis. Crit Care Med 

2000;28(9):1681. [PMID: 11007195] 

Opal S, Cross A: Bacterial sepsis and septic shock: clinical trials for severe sepsis; past 

failures and future hopes. 1999;13(2):285. [PMID: 10340167] (Review.) 

Rivers E et al: Early goal-directed therapy in the treatment of severe sepsis and septic

shock. N Engl J Med 2001;345:1368. [PMID: 11794169] 

Schexnayder SM: Pediatric septic shock. Pediatr Rev 1999;20 (9):303. [PMID: 

10473659] 

Simon D, Trenholme G: Sepsis and septic shock: antibiotic selection for patients with 

septic shock. Crit Care Clin 2000; 16(2):215. [PMID: 10768080] (Review.) 

Sriskandan S, Cohen J: Bacterial sepsis and septic shock: gram-positive sepsis; 

mechanisms and differences from gram-negative sepsis. Infect Dis Clin North Am 

1999;13(2):397. [PMID: 10340174] 

Turner A, Tsamitros M, Bellomo R: Myocardial cell injury in septic shock. Crit Care Med 

1999;27(9):1775. [PMID: 10507416] 

EVALUATION OF THE IMMUNOCOMPROMISED PATIENT WITH SUSPECTED 

INFECTION 

Classification of Immune Dysfunction 

Identification of the type of immune dysfunction will often enable the physician to predict 

the agent causing infection, so that the differential diagnosis and, in some cases, 

treatment may be started in the emergency department. Types of immune dysfunction 

include the following: 

1. Granulocytopenia—Patients with circulating granulocyte counts below 500 are 

especially susceptible to infections caused by gram-negative bacilli (including 

Pseudomonas aeruginosa) and staphylococci. Profound granulocytopenia is usually due 

to myelosuppressive therapy or irradiation, which in addition to causing toxic effects on 

the bone marrow, damages the mucosa of the alimentary canal. Bowel flora may 

thereby enter the bloodstream and cause septicemia and secondary pneumonia. 

Perirectal and perineal infections are also common. 

2. Cellular immune dysfunction—Defects in cell-mediated immunity may be due to 

underlying disease (eg, congenital defects in cell-mediated immunity, Hodgkin disease, 

AIDS) or may occur as a result of antineoplastic or immunosuppressive treatment (eg, 

treatment of lymphoma or transplant rejection). Patients with this type of immune 

dysfunction are especially susceptible to infections caused by intracellular pathogens 

such as Listeria monocytogenes, Mycobacterium spp., Cryptococcus neoformans and 

other fungi, and herpes viruses (herpes simplex virus [HSV], cytomegalovirus [CMV]), 

as well as Pneumocystis carinii. 

3. Humoral immune dysfunction—Defects in opsonizing antibody production occur in 

patients with untreated multiple myeloma and in patients who have undergone 

splenectomy. These patients are susceptible to infections caused by encapsulated 

organisms, particularly Streptococcus pneumonia and Haemophilus influenzae. Patients 

with multiple myeloma usually develop pneumonia; splenectomized patients may 

develop overwhelming sepsis.



Fever is the most reliable sign of infection in immunocompromised patients and must 

never be ascribed to an underlying disease until infection has been excluded. Localized 

collections of pus (abscesses or fluctuant areas) are generally absent in neutropenic 

patients, and the only sign of serious infection may be a localized area of redness or 

tenderness in a febrile patient. In all immunocompromised patients, careful examination 

of the lungs, skin, and mucous membranes for signs of infection is important. The lungs 

may show signs of pneumonia, and signs of disseminated infection may be found in the 

skin and mucous membranes (eg, the ulcerated pustules characteristic of ecthyma 

gangrenosum in patients with sepsis caused by P aeruginosa, and perirectal cellulitis in 

patients with neutropenia). 


Determination of the absolute number of circulating granulocytes is mandatory in the 

evaluation of immunocompromised patients. For example, if the patient's white cell 

count is 1500 with a total of 10% mature and immature polymorphonuclear neutrophil 

leukocytes (PMNs), then the granulocyte count is 150. For all immunocompromised 

patients, samples of blood, urine, and sputum should be sent for Gram stain and 

culture. A chest x-ray will often show signs of pneumonia, even in patients with very low 

white blood cell counts. Other studies (eg, sinus x-rays) should be obtained, depending 

on localized symptoms and signs. 

Treatment 


In febrile patients with granulocyte counts under 1000, antibiotic therapy should be 

started immediately after material for routine culture has been obtained. Circumstances 

that strengthen the directive for urgent empiric therapy include (1) a rapidly falling 

granulocyte count, (2) a very low granulocyte count (< 500 further increases the risk of 

infection; < 100 is frequently associated with fulminant infection), and (3) other clinical 

findings suggesting infection. 

(Current therapy for neutropenic fever involves monotherapy using ceftazidime, 

imipenem, and cefepime or dual therapy with an aminoglycoside plus an 

antipseudomonal penicillin, ticarcillin-clavulanic acid, piperacillin-tazobactam, or 

ceftazidime. 

B. Isolation 

Neutropenic patients should be hospitalized in private rooms, and strict hand-washing 

precautions observed. Protective isolation as usually practiced (ie, masks and gowns) 

does not appear to be effective. Patients should be prescribed a diet free of fresh fruits 

and vegetables, which are often heavily contaminated with gram-negative bacilli. 

Disposition 

All immunocompromised patients with new findings of fever or other signs of infection 

should be hospitalized.

Sumaraju V, Smith LG, Smith SM: Infectious complications in asplenic hosts. Infect Dis 


II. EMERGENCY MANAGEMENT OF SPECIFIC DISORDERS 

MENINGITIS & MENINGOENCEPHALITIS 


• Fever. 

• Nuchal rigidity. 

• Mental status change. 

• Photophobia. 

• Headache. 

• Cerebrospinal fluid findings. 


Meningitis is defined as inflammation of the meninges; it is the major infectious 

syndrome affecting the central nervous system (CNS). When meningitis is accompanied 

by parenchymal involvement, it is referred to as meningoencephalitis. The epidemiology 

of meningitis has changed drastically since H. influenzae immunizations became 

available. The incidence of meningitis caused by the agent has decreased by 94%. The 

average age of a meningitis patient has risen from 15 months to 25 years, and there is 

an increasing trend for adult meningitis to be nosocomial rather than community 

acquired (with a corresponding increase in gram-negative organisms). Acute bacterial 

meningitis is a life-threatening medical emergency. The current mortality rate is 25%, 

the morbidity rate is 60%, and survival depends on prompt recognition and early 

treatment. 



Patients with meningitis present with fever, headache, nuchal rigidity, and mental 

dysfunction. Seizures and cranial nerve deficits are also common. Infants with 

meningitis may present with only vomiting, lethargy, irritability, and poor feeding. Elderly 

patients may present with only low-grade fever and delirium. The headache associated 

with meningitis is continuous and throbbing and, although generalized, is usually most 

prominent over the occiput. The pain is increased by jugular vein compression or any 

other maneuver that increases intracranial pressure (eg, coughing, sneezing, straining 

at stool). Neck stiffness and other signs of meningeal irritation must be sought with care, 

because they may not be obvious early and may disappear during coma. (For 

contraindications to lumbar puncture, see Table 40-2). Patients with meningitis may be 

divided into 2 groups on the basis of the presentation of the disorder. 

1. Acute presentation (septic meningitis)—Symptoms and signs have been present

for less than 24 hours and are rapidly progressive. The causative organisms are usually 

pyogenic bacteria, and the mortality rate is approximately 50%. 

2. Subacute presentation—Symptoms and signs have been present for 1-7 days. 

Meningitis is due to bacteria, viruses, or fungi, and the death rate due to bacterial 

infection is much lower than in patients with acute presentation of disease. Aseptic 

meningitis is typically caused by viruses (enteroviruses, HSV, or Epstein-Barr virus 

identified by polymerase chain reaction [PCR] in 95% of patients). Suggestive features 

such as respiratory tract syndrome and hand-foot-mouth syndrome strengthen the 

diagnosis. Chronic meningitis is defined as meningitis present for more than 4 weeks; 

the major infectious causes are tuberculous meningitis and cryptococci. 


Perform lumbar puncture immediately in the absence of papilledema and focal 

neurologic findings (see Table 40-2). Interpretation of CSF findings is shown in Table 

40-3. Draw blood for serum glucose measurement and for culture. Gram staining of 

CSF will allow presumptive identification of the causative agent. Even if no organisms 

are seen on Gram-stained smears of CSF, bacterial meningitis is a likely diagnosis and 

warrants empiric antimicrobial therapy if total CSF leukocytes number more than 1000, 

if PMNs make up at least 85% of the white cells in CSF, or if the CSF glucose is less 

than 50% of the serum glucose level in a simultaneously drawn blood sample. The 

differential diagnosis in patients in whom PMNs are less than 85% of the CSF white 

count must include several possible causes of acute lymphocytic meningitis (Table 

40-4). Prior treatment with antibiotics could result in sterile cultures of CSF. 

Treatment 

A. Antimicrobial Therapy 

1. Acute presentation—When bacterial meningitis is suspected, begin administration 

of appropriate empiric antibiotics immediately (Table 40-5). Give the first dose as soon 

as samples of CSF and blood have been collected for tests; the goal is to begin 

intravenous administration of antimicrobials within 30 minutes after a patient with acute 

presentation of meningitis has sought treatment. If lumbar puncture must be delayed for 

computed tomography (CT) scan, obtain 2 blood samples for culture and begin 

appropriate antimicrobials. Perform lumbar puncture after mass lesion has been 

excluded and obtain CSF for microscopic examination as soon as possible. For 

pathogen-specific antibiotic therapy for bacterial meningitis, see Table 40-6. 

2. Subacute presentation—Treatment is based on results of Gram staining of CSF 

and other tests. If meningitis is likely but gram staining is negative, begin empiric 

treatment based on the patient's clinical characteristics pending the results of CSF 

studies. 

3. Suspected brain abscess—In patients thought to have a brain abscess, begin 

intravenous therapy with a combination of penicillin and metronidazole or a 

third-generation cephalosporin. Obtain an emergency CT scan. 


General supportive care measures should be started in the emergency department.

Protect the patient's airway, and provide padded rails or restraints for agitated or 

delirious patients. If seizures occur, begin anticonvulsant therapy. Avoid overhydration, 

which may worsen cerebral edema. In children older than age 2 months who have 

bacterial meningitis, dexamethasone reduces neurologic sequelae and hearing loss. 

Dexamethasone should preferably be given prior to antibiotic therapy. 

Disposition 

Immediate hospitalization is warranted for all patients, except those with aseptic (viral) 

meningitis who appear well and can be observed at home. 

Cartwright KAV: Early management of meningococcal disease. Infect Dis Clin North Am 

1999;13(3):661. [PMID: 10470561] (Review.) 

Coyle PK: Overview of acute and chronic meningitis. Neurol Clin 1999;17(4):691. 

[PMID: 10517924] (Review.) 

Kaplan SL: Clinical presentations, diagnosis, and prognostic factors of bacterial 

meningitis. Infect Dis Clin North Am 1999;13(3):579. [PMID: 10470556] (Review.) 

Saez-Llorens X, McCracken GH: Antimicrobial and anti-inflammatory treatment of 

bacterial meningitis. Infect Dis Clin North Am 1999;13(3):619. [PMID: 10470558] 

(Review.) 

Spach DH, Jackson LA: Bacterial meningitis. Neurol Clin 1999;177(4):711. [PMID: 

10517925] (Review.) 

Wubbel LW, McCracken GH: Management of bacterial meningitis: 1998. Pediatr Rev 

1998;19(3):78. [PMID: 9509854] (Review.) 

PNEUMONIA 

1. Pneumonia in Neonates (Aged < 2 Months) 


• Fever, cough, dyspnea. 

• Tachypnea. 

• Focal lung exam. 

• Sputum findings. 



Neonates with pneumonia often have widely disseminated infection caused by group B 

streptococci, gram-negative bacilli, viruses, or other pathogens. Patients present with 

fever or labile temperature, poor feeding, irritability, jaundice, and apneic spells.

Concurrent meningitis is frequent in bacterial infections. 


Draw samples of blood, urine, and CSF for culture for bacteria and viruses. Order 

routine blood tests and a chest x-ray. 


See "Treatment" and "Disposition" sections after discussion of pneumonia in teenagers 

and adults. 

2. Pneumonia in Infants & Children (Aged 2 Months to 5 Years) 



In infants, tachypnea out of proportion to fever is the most common sign of lower 

respiratory tract infection. Grunting respirations secondary to air trapping and expiratory 

obstruction suggest pneumonia. Localized findings (rales, decreased breath sounds) 

are more common in children over age 1 year. 


A peripheral leukocyte count over 15,000 suggests bacterial pneumonia, although lower 

blood counts do not exclude the diagnosis. Arterial blood gas analysis may be obtained 

to assess the adequacy of ventilation. Electrolyte levels and blood urea nitrogen are 

useful in assessing the degree of dehydration, the most frequent complication seen in 

this age group. When obtainable, Gram-stained smears of sputum may be diagnostic. 

Lobar consolidation, pneumatoceles, and pleural effusions suggest pneumonia. Blood 

cultures are frequently positive in pneumonia due to H. influenzae. Severely ill or 

immunocompromised patients may benefit from pneumocentesis. 



and adults. 

3. Pneumonia in Older Children (Aged 5-14 Years) 



Infection with Mycoplasma pneumoniae is the most common cause of pneumonia in this 

age group and usually develops insidiously with fever and malaise followed in 3-5 days 

by nonproductive cough, hoarseness, and sore throat, with or without chest pain. 

Physical examination may disclose pharyngeal erythema and areas of fine rales, 

wheezes, or dullness, especially in the lower lobes. Myringitis occurs in approximately 

15% of patients, occasionally with the development of tympanic bulla, and 

maculopapular rashes are common. Pneumonia due to S. pneumoniae, H. influenzae, 

and S. aureus usually follows a viral upper respiratory infection and is characterized by

abrupt onset of fever, chills, tachypnea, and cough accompanied by signs of lobar 

consolidation or bronchopneumonia. 


In pneumonia due to M. pneumoniae, the white cell count is usually normal or slightly 

elevated, and chest x-ray reveals scattered segmental infiltrates, atelectasis, interstitial 

disease, or, less frequently, lobar consolidation. 

In pneumonia due to bacteria other than M. pneumoniae, the white cell count usually 

exceeds 15,000. Chest x-ray abnormalities include patchy infiltrates, increased 

bronchovascular markings, lobar consolidation, cavitary infiltrates, and pleural effusions 

or empyema. Gram-stained smears of sputum may allow for a presumptive diagnosis if 

numerous PMNs, few epithelial cells, and a predominant microorganism are found. 

Pleural fluid should be examined if present. 



and adults. 

4. Pneumonia in Teenagers & Adults (Aged 15 Years & Older) 


In teenagers and young adults, M. pneumoniae and S. pneumoniae are the most 

common causative agents of pneumonia. In older adults, S. pneumoniae is the most 

common cause, although many other pathogens may also cause disease. Aspiration 

pneumonia due to mixed anaerobic and aerobic flora is common in patients with 

depressed consciousness. Alcoholic patients are predisposed to severe pneumonia due 

to Klebsiella pneumoniae and other gram-negative bacilli. Patients with chronic lung 

disease may develop pneumonia due to H. influenzae. Legionella spp. are an 

uncommon but important cause of community-acquired pneumonia in middle-aged 

adults; special diagnostic tests (sputum for direct fluorescent antibody) and treatment 

with erythromycin or azithromycin is required for successful management. 



The clinical signs of pneumonia due to M. pneumoniae are similar to those in younger 

patients. In pneumonia due to other bacteria, there is often abrupt onset of malaise, 

fever with or without rigors, productive cough, and pleuritic chest pain. Rales and signs 

of consolidation are noted on physical examination. Elderly or debilitated patients may 

manifest only fever and obtundation. In Legionnaire disease, high, spiking fevers, 

diarrhea, and delirium are especially common. Foul-smelling sputum and involvement of 

dependent parts of the lung suggest aspiration pneumonia due to mixed anaerobic and 

aerobic flora. 


Chest x-ray findings are similar to those described for mycoplasma and other bacterial

pneumonias in older children, except that pneumatoceles are rare in adults. Bilateral 

pneumonia indicates severe or atypical disease (eg, septic emboli due to endocarditis). 

In pneumonia due to M. pneumoniae, the white cell count is usually normal or only 

slightly elevated. In pneumonia due to other bacteria, leukocytosis commonly exceeds 

15,000. In elderly or critically ill patients, however, leukopenia with a shift to the left 

sometimes occurs and is a poor prognostic sign. Gram-stained smear of a good sputum 

sample (showing many PMNs, few epithelial cells) is the most important diagnostic test 

in acute pneumonia. In general, all but the smallest pleural effusions should be 

aspirated to rule out empyema. Send fluid to the laboratory for Gram staining and 

culture and for measurement of protein, lactate dehydrogenase, glucose, and pH. Blood 

cultures and arterial blood gas measurements should be obtained for all patients 

severely ill with pneumonia. Results of other laboratory tests are less specific: prerenal 

azotemia is common in elderly patients; in Legionnaire disease, hyponatremia, 

hypophosphatemia, and elevated liver enzyme levels are common enough to be 

important diagnostic clues. 

Treatment 

The correct choice of treatment for pneumonia is essential. The initial antibiotic choices 

given in the emergency department influence patient outcome and should be based on 

the patient's age and the probable causative organism (Table 40-7). Patients with 

nosocomial pneumonia who receive the appropriate antibiotic therapy are more than 

twice as likely to survive compared with patients who had inappropriate therapy 

selected. 

Disposition 

Neonates should be hospitalized. Severely ill infants (ie, with respiratory distress, 

hyperthermia, or PO 2 < 70) should be hospitalized. Hospitalization is indicated for most 

older patients with pneumonia, especially for patients with preexisting pulmonary 

disease, and is required for all patients with bilateral bacterial pneumonia. 

BRONCHIOLITIS 


• Wheezing, cough, low-grade fever. 

• Tachypnea. 


Bronchiolitis is an acute inflammation of the bronchioles, most commonly resulting from 

a viral infection. It typically affects children from birth to age 2 years and occurs mostly 

during the winter months (November to March). Respiratory syncytial virus (RSV) is the 

cause in 60-90% of cases; the remaining cases are caused by parainfluenza, 

adenovirus, rhinovirus, and influenza.



The child with bronchiolitis typically has a 4-day history of clear profuse rhinorrhea and 

congestion, usually accompanied by low grade fever followed by the development of a 

cough, tachypnea, and wheezing. Signs of respiratory distress including cyanosis and 

accessory muscle use may be evident, and inspiratory wheezing and crackles are 

typically heard on auscultation of the patient's lungs. Apnea can occur, and 

approximately 2-7% of children ill enough to require hospitalization develop respiratory 

failure and require intubation. 


A nasopharyngeal swab can be sent for viral culture and is the gold standard for 

diagnosis but is rarely indicated clinically. A chest x-ray is recommended for all patients 

and may show findings characteristic of bronchiolitis: hyperinflation, atelectasis, 

peribronchial thickening, and diffuse interstitial infiltrates. 

Treatment 

Oxygen rapidly relieves hypoxemia and is the most important therapeutic agent for 

bronchiolitis. The use of bronchodilators is controversial and does not decrease 

hospitalization rates. Racemic epinephrine is a potential agent for bronchiolitis; its use is 

associated with improvement in clinical scores and increase in oxygen saturations. 

Studies evaluating the use of glucocorticoids show no improvement in outcome. 

Ribavirin is a synthetic nucleoside analogue that has virostatic activity against RSV and 

is recommended for use in patients with a history of congenital heart disease or chronic 

lung disease, preterm infants, infants younger than age 6 weeks, and infants ventilated 

for RSV infection. 

Disposition 

Criteria suggestive of severe disease include the following: ill or toxic appearing, oxygen 

saturation less than 95%, gestational age less than 34 weeks, respiratory rate greater 

than 70 breaths/min, atelectasis on x-ray, and age less than 3 months. The infant's 

oxygen saturation while feeding is the single best objective measure of severe disease. 

Cross JT, Campbell GD: Drug-resistant pathogens in community and hospital-acquired 

pneumonia. Clin Chest Med 1999;20(3):499. [PMID: 10516899] (Review.) 

Cunha BA: Community-acquired pneumonia: diagnostic and therapeutic approach. Med 


Fiel S: Guidelines and pathways for hospital-acquired pneumonia. Chest 

2001;119(2):412S. [PMID: 11171778] (Review.) 

Mandell LA: Antibiotic therapy for community-acquired pneumonia. Clin Chest Med 

1999;20(3):589. [PMID: 10516906] (Review.) 

Wright RB, Pomerantz WJ, Luria JW: New approaches to respiratory infections in

children: bronchiolitis and croup. Emerg Med Clin North Am 2002;20(1):93. [PMID: 

11826639] (Review.) 



• Fever. 

• Painful joint. 

• Joint effusions. 

• Arthrocentesis findings. 


Left untreated, septic arthritis rapidly destroys articular cartilage, causing permanent 

joint damage. Delay between the onset of symptoms and treatment is the major 

determining factor for prognosis. Joint infection may occur by hematogenous route, 

direct inoculation, or spread of contiguous infections. The peak incidence occurs in 

children under age 3 years, and boys are affected twice as often as girls. Septic arthritis 

typically affects only one or a few asymmetrically distributed joints. Because joint 

infection superimposed on rheumatoid arthritis sometimes occurs, any joint that 

develops inflammation out of proportion to that in other affected joints should be 

aspirated to rule out the possibility of infection in patients with rheumatoid arthritis. 

Some studies have shown that up to 50% of cases of septic arthritis occur in patients 

with rheumatoid arthritis. Other groups at high risk include intravenous drug abusers 

and patients on hemodialysis. Rarely, acute arthritis is caused by fungi, mumps, or 

hepatitis B virus or, in women, may be due to wild or vaccine strains of rubella virus. 

Aspiration of the affected joint in the emergency department is often necessary to 

differentiate septic arthritis from other causes of synovitis, such as gout or pseudogout. 



Patients with septic arthritis usually have acute or subacute onset of pain, erythema, 

swelling, and limitation of motion in the affected joints. The arthritis more commonly 

affects the large joints, especially the knee. Systemic symptoms and signs of infection 

(malaise, fever, and leukocytosis) are common but not always present. In infants or 

neonates, failure to feed or pseudoparalysis of the extremity may be present. 


Definitive diagnosis is established by demonstration of the infecting organism in synovial 

tissue or joint fluid. Blood cultures may be positive even though cultures of joint fluid are 

negative and should be obtained for all patients thought to have septic arthritis. 

1. Joint fluid analysis—Joint fluid typically shows high leukocyte counts, usually over 

50,000, although the count may not be strikingly elevated in early disease. Synovial fluid 

should be considered inflammatory and possibly infectious if the count is above 7500.

The higher the white cell count in joint fluid, the greater the likelihood of bacterial or 

fungal arthritis. The glucose content of synovial fluid is usually lower than normal but 

occasionally may be normal. If no antimicrobial therapy has been given, smears and 

cultures often reveal the causative organism. The most common organisms are gram 

positive; S. aureus is the most common pathogen of this group. A synovial fluid lactic 

acid test may be useful in excluding septic arthritis; the test has a negative predictive 

value of 97%. Results of other laboratory tests are variable, and plain x-rays of affected 

joints are usually negative early in the disease. 

2. Gonococcal arthritis—In gonococcal arthritis, Gram-stained smears and cultures of 

joint fluid are negative in 50-75% of cases, although in 86% of patients, cultures of 

exudates from the cervix, urethra, pharynx, or rectum demonstrate gonococci. Because 

the gonococcus is a fastidious organism, demonstration of its growth in cultures 

depends on prompt processing of specimens by the laboratory. Because special 

handling is also required, all specimens submitted should bear the instruction "Rule out 

gonorrhea." Prompt response to antimicrobial therapy helps confirm the diagnosis of 

gonococcal arthritis. 

Treatment 

A. Aspiration 

Aspirate affected joints, and repeat aspiration as often as necessary to evacuate 

accumulating joint fluid. Aspiration is necessary except for infections in inaccessible 

joints, such as the hip. Open drainage is almost never required in gonococcal arthritis. 


High doses of intravenous antibiotics should be given (Table 40-8). Intra-articular 

instillation of antibiotics is unnecessary, because high antibiotic levels are attained in 

synovial fluid when drugs are given intravenously. If no organisms are seen on 

Gram-stained smears of synovial fluid, but other findings suggest septic arthritis, empiric 

antibiotic therapy based on the type of patient and clinical findings should be started 

pending results of culture and sensitivity. 

Disposition 

Hospitalize all patients with suspected or documented septic arthritis. 

OSTEOMYELITIS 


• Pain, fever. 

• Increased erythrocyte sedimentation rate. 

• Biopsy findings. 


Osteomylitis is an infection of bone that affects all age groups. The infecting organisms 

are bacteria, mycobacteria, or fungi. For purposes of discussion, osteomyelitis can be 

classified according to the pathogenic mechanism: (1) hematogenous osteomyelitis, (2) 

osteomyelitis secondary to contiguous focus of infection, and (3) osteomyelitis 

associated with peripheral vascular disease. Hematogenous osteomyelitis is common in 

children, although its incidence is increasing in older age groups. Hematogenous 

osteomyelitis in adults usually involves the vertebral bodies. Spread of disease from a 

contiguous focus of infection is the most common pathogenic mechanism in adults. 

Osteomyelitis associated with vascular insufficiency occurs almost exclusively in adults 

who have diabetes mellitus or severe peripheral vascular disease. 

In both children and adults, the most commonly involved bones are the long bones, 

especially those of the lower extremities; this is particularly true in children. Orthopedic 

procedures or traumatic wounds predispose to osteomyelitis of the extremities. 



1. Hematogenous osteomyelitis—In children, abrupt onset of high fever, systemic 

toxicity, and physical findings of local suppuration surrounding the involved bone (local 

pain, swelling, and tenderness) are typical. The child is often unwilling to move the 

affected extremity. The most common location is the metaphysis of long bones. 

In adults, the disease may be more indolent, particularly in patients with vertebral 

osteomyelitis. About half of patients may have pain, swelling, chills, and fever. Patients 

with vertebral osteomyelitis may have low-grade or intermittent fever or back pain that 

may be either severe or only nagging and may not cause extreme discomfort or 

immobility until late in the disease. Focal tenderness over the dorsal spines of the 

involved vertebral bodies may be the only physical finding. 

2. Osteomyelitis secondary to contiguous infection—The most common 

predisposing factor is postoperative infection, such as that following open reduction of 

fractures. Extension of soft tissue infections to bone from infected fingers and toes, 

infected teeth, or infected sinuses also occurs. Most patients are over age 50 years and 

may present with fever, swelling, and erythema in the initial episode. During 

recurrences, sinus formation and drainage are the major presenting signs. 

3. Osteomyelitis associated with vascular insufficiency—Patients with osteomyelitis 

associated with vascular insufficiency invariably have diabetes mellitus or severe 

peripheral vascular disease. The toes and small bones of the feet are usually affected. 

Local signs and symptoms such as pain, swelling, redness, or frank cellulitis with deep 

ulcers in the soft tissue are prominent. Pain is often absent because of diabetic 

neuropathy. 


Routine laboratory tests are of limited value in the diagnosis of osteomyelitis. The 

leukocyte count is often elevated in acute disease but may be normal in more chronic 

infection. The erythrocyte sedimentation rate is elevated in most patients. Radiographic 

procedures are the primary diagnostic tool, although plain x-rays may not show signs of

disease until 10-14 days after symptom onset. The earliest visible x-ray changes are 

adjacent soft tissue swelling and periosteal reaction. Lytic lesions and areas of sclerosis 

may then develop. If osteomyelitis is suspected and plain x-rays fail to reveal signs of 

disease, CT scan or technetium bone scan should be performed. The diagnosis is 

confirmed by culture and histologic examination of bone. Bacteriologic findings vary, 

and cultures should be obtained from bone (via needle aspiration or surgical biopsy) or 

blood (results are positive in 50% of cases in patients with acute hematogenous 

osteomyelitis). Magnetic resonance imaging (MRI) is an important imaging modality for 

detecting vertebral osteomyelitis. 

Treatment 

The most important therapeutic measures are systemic antibiotics and surgery to drain 

abscesses or for debridement of necrotic tissue. The selection of an antibiotic depends 

on identification of the causative organism. If the disease is uncomplicated (ie, involves 

a long bone in a patient without underlying medical problems), if the patient is a child, or 

if the patient is critically ill, then antistaphylococcal therapy should be initiated, because 

S. aureus is the most common infective organism. 

Surgery in acute osteomyelitis should be limited to biopsy for diagnosis, drainage of 

suppurative areas, and debridement of necrotic bone. Surgical drainage is also 

indicated if neurologic abnormalities are present or develop in patients with vertebral or 

cranial osteomyelitis or if infection spreads to the hip joint in a child. 

Disposition 

Patients with acute osteomyelitis should be hospitalized for intravenous antimicrobial 

therapy. 

Carek PC, Dickerson LM, Sack JL: Diagnosis and management of osteomyelitis. Am 

Fam Physician 2001;63(12):2413. [PMID: 11430456] 

Pioro MH, Mandell BF: Septic arthritis. Rheum Dis Clin North Am 1997;23(2):239. 

[PMID: 9156391] (Review.) 

Shitty AK, Gedalia AG: Septic arthritis in children. Rheum Dis Clin North Am 

1998;24(2):287. [PMID: 9606760] (Review.) 

PHARYNGITIS 


• Sore throat, fever. 

• Cervical lymphadenopathy. 

• Odynophagia. 

• Erythematous pharynx.


Acute pharyngitis is inflammation of the pharynx. It is often caused by viral or bacterial 

infections. The most important task in the evaluation of pharyngitis is to identify and 

treat group A streptococcal infection and to recognize less common causes of 

pharyngitis associated with more serious systemic illness. Viral infections (rhinovirus, 

adenovirus, and many others) are responsible for 90-95% of sore throats. 



1. Group A streptococcal infection—The most common cause of bacterial 

pharyngitis, presentations of group A streptococci vary and include fever, sore throat, 

anterior cervical lymphadenopathy, headache, beefy red pharynx, tonsillar exudates, 

lymphatic hyperplasia, and scarlatiniform rash. The so-called classic findings of high 

fever, pharyngeal exudates, and anterior cervical lymphadenopathy only suggest 

streptococcal pharyngitis and do not confirm the diagnosis. The three clinical features 

that are most helpful in differentiating streptococcal from viral pharyngitis are fever of 

38.9 °C or higher, painful cervical adenitis, and absence of flulike symptoms such as 

cough and coryza. 

2. Infectious mononucleosis—Acute infection by Epstein-Barr virus (the causative 

agent of infectious mononucleosis), by adenovirus, or by the human immunodeficiency 

virus (HIV) may produce an exudative pharyngitis with fever, posterior cervical 

adenopathy, malaise, and enlarged spleen. Patients with acute CMV infection may have 

pharyngeal soreness, but examination shows a few findings of note. 

3. Diphtheria—Diphtheria should be considered in patients with exudative or 

membranous pharyngitis in whom the status of immunization for diphtheria is either 

incomplete or in question. The characteristic tonsillar or pharyngeal membrane varies 

from light to dark gray and is firmly attached to the tonsillar and pharyngeal mucosa. 

Toxemia and tachycardia out of proportion to the degree of fever are other clues. 

4. Vincent angina—Vincent angina is a membranous pharyngitis caused by a mixture 

of aerobic and microaerophilic bacteria and spirochetes. It is generally encountered in 

children and young adults and is characterized by foul breath, cervical lymphadenitis, 

and low-grade fever in association with membranous pharyngitis. Removal of the 

necrotic gray pseudomembrane usually results in bleeding. 

5. Other causes—Other causes of bacterial pharyngitis include M. pneumoniae, N. 

gonorrhoeae, Chlamydia trachomatis, Arcanobacterium haemolyticus, groups C and G 

streptococci, and secondary syphilis. 


Definitive diagnosis of group A streptococcal pharyngitis can be made by results on 

culture of exudates from the throat and demonstration of a rise in titers to 

antistreptolysin-O or other streptococcal products, because many people are 

asymptomatic carriers of group A streptococci. Rapid streptococcal antigen tests are 

highly specific but not as sensitive as culture. The American Heart Association has

evised its recommendation for throat cultures before antibiotic therapy. Throat cultures 

are considered "valuable" for children and adolescents and "not as essential" for adults. 

They are indicated primarily to avoid the unnecessary use of antibiotics for the 70-80% 

of adult patients with pharyngitis due to virus. In the patient with culture-proved 

streptococcal pharyngitis, follow-up test-of-cure throat cultures are not indicated unless 

the patient remains symptomatic. Cultures of asymptomatic family members and 

contacts should be reserved for special circumstances—for example, if the patient has a 

history of rheumatic fever or if there is an epidemic of group A streptococcal pharyngitis. 

An elevated white cell count (> 12,000) suggests bacterial pharyngitis. Obtain a 

heterophil agglutination test or mononucleosis spot test for patients thought to have 

infectious mononucleosis. A complete blood count with differential may also reveal a 

lymphocytosis with atypical lymphocytes. 

Treatment 

Begin empiric treatment in children and young adults if the classic signs and symptoms 

of streptococcal pharyngitis, scarlatiniform rash, or a history of rheumatic fever or 

valvular heart disease are present, or if illness occurs during an epidemic of group A 

streptococcal infection. A throat culture is not necessary in most cases because its 

results would not influence the management strategy. Effective antibiotic regimens are 

penicillin V, 250 mg orally 4 times a day for 10 days, or benzathine penicillin G, 1.2 

million units intramuscularly (children < age 10 years, 600,000 units; children aged 

10-15 years, 900,000 units). For penicillin-allergic patients, erythromycin, 250 mg orally 

4 times a day for 10 days, is suggested. For both penicillin and erythromycin, a full 10 

days of therapy is necessary to eradicate infection and prevent rheumatic fever. 

Patients with a sore throat but no other features of streptococcal pharyngitis should 

receive symptomatic therapy (throat lozenges, saline gargles). A throat culture is not 

necessary. Patients with sore throat or one or two features (fever, exudates, or 

adenopathy) have an intermediate chance of having streptococcal pharyngitis. A throat 

culture may be useful to avoid unnecessary use of antibiotics and to reassure the 

patient. Antibiotic treatment should be withheld until the results of the culture are known. 

Disposition 

Patients with pharyngitis without complications may receive treatment on an outpatient 

basis. Patients thought to have diphtheria, Vincent angina, epiglottitis, or possible 

localized abscess should be hospitalized. 

Hayes CS, Williamson HW: Management of group A beta-hemolytic streptococcal 

pharyngitis. Am Fam Physician 2001;63(8):1557. [PMID: 1132743] (Review.) 

Richardson MA: Sore throat, tonsillitis, and adenoiditis. Med Clin North Am 

1999;83(1):75. [PMID: 9927961] (Review.) 

URINARY TRACT INFECTIONS 

ACUTE LOWER URINARY TRACT INFECTION (Uncomplicated Cystitis)


• Dysuria. 

• Frequency, urgency, resistancy. 

• Suprapubic pain. 

• Hematuria. 

• Pyuria. 


Uncomplicated bacterial cystitis is defined as a urinary tract infection confined to the 

bladder. It affects women more commonly than men and tends to recur even in the 

absence of anatomic abnormalities. Many patients with apparent lower urinary tract 

infection also have asymptomatic involvement of the upper urinary tract (absence of 

fever, chills, or flank pain). Children present with cystitis without the complaint of dysuria 

much more commonly than do adults. Conditions such as vesicoureteral reflux may 

predispose children to infections, and an aggressive workup to evaluate for these 

possibilities is required. Prior to age 1 year, the incidence is nearly equal in males and 

females, but after age 1 year, females are 30 times as likely to develop a urinary tract 

infection until age 50 years, when men begin developing an increased incidence of 

these infections. 

Most cystitis is caused by bacterial infection, usually E coli (80%) and other enteric 

gram-negative bacilli such as Proteus mirabilis, Klebsiella pneumonia, and P 

aeruginosa. Gram-positive bacteria such as Streptococcus faecalis, S. epidermis, and 

S. viridans are less common causes. Adenovirus is a common cause of hemorrhagic 

cystitis in children (typically males) and occasionally young adults. 



A history of urinary tract infections is frequently elicited. Dysuria and urinary frequency 

and urgency are the most common symptoms in adults, although they may be absent in 

children. Patients may report that their urine is cloudy, smelly, or dark. 

Suprapubic discomfort and tenderness are common. Patient are usually afebrile or have 

a low-grade fever. The presence of high fever (> 38.3 °C [101 °F]) or rigors is 

inconsistent with a diagnosis of uncomplicated cystitis and suggests pyelonephritis. 

Nausea and vomiting, though uncommon in adults, are not unusual in children with 

uncomplicated cystitis. 

Neonates may present with poor feeding, vomiting, jaundice, or irritability and may not 

always have fever. Young children may present with new bed-wetting or loss of bladder 

training. 


1. Urinalysis—Accurate diagnosis of urinary tract infection depends on obtaining a

urine specimen uncontaminated by perineal secretions. The presence of squamous 

epithelial cells or of mixed flora on Gram-stained smears suggests contamination, and 

the specimen should be discarded and a better one obtained. Urine should be examined 

while it is fresh (within 1 hour) or should be refrigerated if delay is expected. Urine 

should be obtained by catheter or clean-catch specimens only because bagged 

specimens are usually contaminated. 

a. Chemistry—Mild degrees of proteinuria and hematuria are common on dipstick tests 

of urine. If the infection is caused by a urea-splitting bacterium (eg, P. mirabilis), urinary 

pH may be abnormally high (eg, 6-8). The leukocyte esterase dipstick test is a reliable 

indicator of infection. Chemical tests for the presence of bacteria in urine (eg, nitrate 

reduction) are not sensitive and specific enough to be generally recommended. 

b. Sediment—Many leukocytes and often some erythrocytes are present. Clumps of 

leukocytes must be differentiated from white blood cell casts, which signify upper urinary 

tract involvement. In most cases, numerous bacteria are visible. 

c. Gram-stained smears—Microscopic examination of Gram-stained specimens of 

urinary sediment from centrifuged urine usually shows bacteria of a single morphologic 

type. If uncentrifuged urine is examined, and an average of one bacterium is found per 

oil-immersion field, there is about an 80% probability that there are 10 5 organisms per 

milliliter of urine (strongly indicative of infection). 

2. Urine culture—In women of child-bearing age with a history of recurrent cystitis (2-3 

times per year) who are otherwise healthy, treatment may be started on the basis of 

urinalysis results alone, and urine culture may be postponed until 1 week after treatment 

(test-of-cure culture) or may be omitted in patients who respond well to treatment. In all 

other patients, quantitative urine cultures should be obtained. Growth of at least 10 5 

organisms of a single species per milliliter of urine indicates a high probability of active 

urinary tract infection. A urine culture should be ordered for all febrile infants under age 

2 years, for children with a history of urinary tract infection, for children who are taking 

suppressive antibiotic therapy, and for children in whom antibiotic therapy is started 

regardless of urinalysis results. Smaller numbers (10 2 -10 4 /mL) of bacteria (especially of 

a single species) are significant and indicate the need for therapy (see 

"Dysuria-Frequency Syndrome" section, below). 

Treatment 


Nonpregnant women of child-bearing age who have a history of recurrent cystitis and 

findings compatible with uncomplicated cystitis may be given a short course (3 days) of 

therapy. Single-dose therapy has fallen into disfavor because of the frequency of 

relapse and because it requires that the patient be seen 2-4 days later for a test-of-cure 

urine culture. All other patients should receive multidose therapy for at least 7-10 days. 

Because men often harbor occult infection in the prostate or kidney, some authorities 

recommend that treatment be extended for at least 3 weeks in an effort to prevent 

relapse of infection. Current American Academy of Pediatrics guidelines recommend 

treatment for children for 7-14 days with coverage by antibiotics until radiologic studies

are completed and urologic referral conducted. 

Select an antimicrobial from those listed in Table 40-9. Trimethoprim-sulfamethoxazole 

(TMP-SMZ) and ciprofloxacin, because of their good penetration into the prostate and 

high level of activity against uropathogens, are recommended for men with urinary tract 

infection who have normal serum creatinine levels. 

There is an increasing trend of bacterial resistance in urinary tract pathogens; 40% are 

resistant to ampicillin or amoxicillin, 5% are resistant to TMP-SMZ, and 17% are 

resistant to cephalexin. 

B. Adjunctive Measures 

Phenazopyridine (Pyridium, many others), 200 mg orally 3 times a day, may help relieve 

severe dysuria. The drug should be taken for only 2-3 days. Warn patients that their 

urine will turn orange. 

C. Follow-up 

In uncomplicated cystitis, follow-up urine cultures are optional in patients who respond 

to therapy. Patients given single-dose or 3-day therapy and whose symptoms recur 

should have urine culture and be given a 10-day course of therapy. 

Disposition 

Infants, children, and men with diagnosed urinary tract infection should receive 

treatment and be referred to a urologist. Hospitalization is indicated for children younger 

than age 3 months and for children with dehydration, toxicity, vomiting, or failure of 

outpatient regimen. Urologic referral is also recommended for women with frequent 

recurrences of cystitis (monthly) and probably also for those who have had 3 or more 

infections in 1 year, although the latter recommendation is controversial. Hospitalization 

is not indicated for patients with uncomplicated cystitis. 

UPPER URINARY TRACT INFECTION (Pyelonephritis) 


Acute pyelonephritis is symptomatic inflammatory bacterial infection of the kidney. 

Because it most commonly results from spread of infection up the ureters from the 

bladder, it is usually caused by the same organisms that cause cystitis (ie, E. coli, P. 

mirabilis). In elderly men, pyelonephritis may be caused by S. faecalis. In patients who 

have received prior antimicrobial therapy (eg, during recent hospitalization, because of 

chronic indwelling Foley catheter), the infecting organisms may be resistant to 

commonly used antimicrobials. Note: Pregnant patients are especially prone to upper 

urinary tract infection. Because pyelonephritis in pregnancy is associated with an 

increased risk of premature delivery, pregnant patients with urinary tract infection should 

always receive multidose antimicrobial therapy. 

Between 15% and 25% of children and young adults with endstage renal failure have 

chronic pyelonephritis that results in renal scarring and decreased renal function, 

termed reflux nephropathy. This renal scarring can be prevented by avoiding urinary

tract infection. Emphysematous pyelonephritis is acute pyelonephritis associated with 

gas in the collecting system; it typically occurs in patients with diabetes. This disease 

has a 75% mortality rate, and emergency nephrectomy is required. 



Pyelonephritis is characterized by symptoms of cystitis (dysuria, urgency, and 

frequency) accompanied by flank pain and tenderness. Fever, rigors, and, in patients 

with complicating bacteremia or endotoxemia, systemic signs of sepsis (eg, 

hypotension, delirium) may be present. In young children, fever is the predominant 

symptom; only 32% of boys and 40% of girls display dysuria as a symptom, and flank 

pain is an even less common symptom. In pyelonephritis occurring as a complication of 

nephrolithiasis, severe flank pain radiating to the groin may be the most prominent 

symptom. In patients with sickle cell disease, diabetes, or nephropathy caused by 

analgesic abuse, necrosis of the renal papillae with sloughing into the ureters occurs as 

a complication of renal infection, and the patient may present with symptoms of ureteral 

obstruction that mimic nephrolithiasis. 


1. Urine—The findings on urinalysis, microscopic examination, and culture are the 

same as in cystitis (see above), except that leukocyte casts (granular casts) occur only 

with pyelonephritis. Gross hematuria and pain suggest pyelonephritis complicating 

urolithiasis. For all patients with suspected pyelonephritis, send urine for culture and 

susceptibility testing. 

2. Other laboratory studies—Serum electrolyte, blood urea nitrogen, and creatinine 

measurements should be obtained, because azotemia may be present. The white cell 

count is usually elevated. A normal or low white cell count with a shift to the left in a 

patient with suspected pyelonephritis is often a sign of sepsis, indicating the need for 


C. X-ray and Other Findings 

Some authorities suggest that excretory urography be performed in all nonpregnant 

women with pyelonephritis after the infection has cleared. In patients with pyelonephritis 

in whom urinary obstruction is suspected, radiologic and other examinations should be 

performed as soon as possible. Ultrasonography is a safe and sensitive means of 

assessing hydronephrosis and may reveal intrarenal and perinephric abscesses. 

Remember that in pregnancy some degree of ureteral dilatation (usually greater in the 

right ureter than the left) is normal. 

Treatment 


(See Table 40-9.) Patients with anatomic abnormalities of the urinary tract or 

concomitant prostatitis may require up to 6 weeks of therapy. In patients with suspected 

bacteremia or suspected infection due to antibiotic-resistant organisms, an 

aminoglycoside should be added.

B. General Measures 

If vomiting or dehydration is present, begin intravenous fluid replacement with crystalloid 

solutions. Provide analgesia for flank pain if needed. Give antipyretics for high fever 

regularly (rather than as needed) until the patient is afebrile. 

Disposition 

Patients who meet the criteria listed below or who have any of the following conditions 

should be hospitalized: 

• Inability to maintain oral hydration or take medications 

• Concern about compliance or follow-up 

• Diagnostic uncertainty 

• Severe illness with high fevers, severe pain, and marked debility 

• Comorbid illness (eg, diabetes, renal failure, immunosuppression) 

• Failure of outpatient therapy 

Patients who are not hospitalized should have a follow-up appointment within 1-2 days 

to assess their response to therapy. 

Some patients with pyelonephritis, especially young women, may not be sick enough for 

hospitalization but do not appear well enough to go home. For these patients, a 12- to 

24-hour period of intravenous antimicrobial therapy, intravenous hydration, and 

observation in the emergency department may be indicated. If rapid resolution of signs 

and symptoms occurs, the patient may be discharged with a prescription for oral 

antimicrobials and a follow-up appointment in 1-2 days. 

DYSURIA-FREQUENCY SYNDROME 


The dysuria-frequency syndrome (urethral syndrome) occurs by definition only in 

women, usually young women. These patients have symptoms of lower urinary tract 

infection but have urine cultures that are sterile or contain fewer than 10 5 organisms per 

milliliter of urine. Patients with dysuria-frequency syndrome may be divided into 2 

groups: those with accompanying pyuria (> 10 leukocytes per high power field) and 

those without. In women with pyuria, symptoms are usually due either to a low-grade 

bacterial cystitis (bacteriuria with < 100,000 organisms per milliliter of urine) or to 

chlamydial urethritis with or without accompanying chlamydial cervicitis. N. gonorrhoeae 

also causes urethritis. HSV causes urethritis during primary infection and, on occasion, 

during recurrent infection. In some patients with pyuria and in most patients who lack 

pyuria, no causative agent can be identified. 

Clinical Findings


The principal symptoms are those of cystitis: dysuria, urgency, and frequency. The 

dysuria is "internal" dysuria as opposed to the "external" dysuria occurring in vaginitis or 

genital HSV infection and results from urine coming into contact with denuded skin. 

Findings on physical examination are normal except that there may be urethral 

inflammation or mucopurulent cervical discharge and cervical edema in patients whose 

symptoms are due to gonococcal or chlamydial infection. Pelvic examination is 

important to diagnose vaginitis, which may also cause dysuria. 


The urine may be normal or may contain PMNs with few or no bacteria. Swabs of 

urethral discharge should be obtained for smear and culture for N. gonorrhoeae in 

patients with a history of gonorrhea, in those with multiple sexual partners, and in those 

whose recent sexual partner has had urethritis. Urine culture shows scant growth or no 

growth of organisms. A cervical swab for Chlamydia antigen (fluorescent or ELISA slide 

test) is indicated in sexually active women with cervicitis accompanying this syndrome, 

because this organism causes concurrent cervicitis and urethritis. 

Treatment 

Antimicrobial therapy is usually reserved for patients with pyuria. Tetracyclines and 

erythromycin are the most effective drugs for suspected chlamydial infection; other 

bacterial pathogens may be resistant to these drugs. Optimal treatment of chlamydial 

infection requires 7 days of therapy. Short-course, 3-day therapy may be tried initially in 

patients with low-grade bacteriuria. None of the single-dose regimens provides reliable 

empiric therapy for both chlamydial and bacterial infection. 

Disposition 

Because of the difficulties of empiric therapy in the urethral syndrome, a follow-up visit 

to a primary care physician should be arranged. If ordinary bacterial cultures of urine are 

sterile in patients with pyuria, the patient's sexual partners should be screened for 

urethritis and Chlamydia infection. 

Miller O, Hemphill RR: Urinary tract infection and pyelonephritis. Emerg Med Clin North 

Am 2001;19(3):655. [PMID: 11554280] (Review.) 

Orenstein R, Wong ES: Management of urinary tract infections in adults. Am Fam 

Physician 1999;59(5):1225. [PMID: 10088877] (Review.) 

Roberts JA: Management of pyelonephritis and upper urinary tract infections. Urol Clin 

North Am 1999;26(4):753. [PMID: 10584616] (Review.) 

Roberts KB: The AAP practice parameter on urinary tract infections in febrile infants and 

young children. Am Fam Physician 2000;62(8):1815. [PMID: 11057838] (Review.) 

Santen SA, Altieri MF: Pediatric urinary tract infection. Emerg Med Clin North Am 

2001;19(3):675. [PMID: 11554281] (Review.)

DISEASES OF THE FEMALE GENITOURINARY TRACT (See also "Sexually 

Transmitted Diseases" section.) 

PELVIC INFLAMMATORY DISEASE 


• Lower abdominal pain. 

• Vaginal discharge. 

• Fever. 

• Cervical motion tenderness. 

• Bilateral lower adnexal tenderness. 


Infection of the uterine tubes may be acute or chronic and unilateral or bilateral. It may 

lead to pyosalpinx or tuboovarian abscess. Pelvic peritonitis is frequently present. 

Causative agents include C. trachomatis, N. gonorrhoeae, anaerobic bacteria (which 

include Bacteroides and gram-positive cocci), facultative gram-negative bacilli (such as 

E. coli), Mycoplasma hominis, and rarely Actinomyces israelii. Because it is often 

impossible to differentiate among these agents in individual patients, treatment 

regimens that are active against the broadest possible range of these pathogens should 

be used. Risk factors for pelvic inflammatory disease (PID) include young age, multiple 

sexual partners, intrauterine device insertion, vaginal douching, tobacco smoking, 

chlamydial or gonococcal infection, and bacterial vaginosis. 



Patients are usually young (< age 30 years) and sexually active. Symptoms include 

fever (sometimes with rigors), severe pelvic pain that may be either continuous or 

crampy (pelvic pain is usually bilateral and is the most common presenting symptom), 

dyspareunia, menstrual disturbances, vaginal discharge, and gastrointestinal 

disturbances (anorexia, nausea and vomiting, constipation).Patients usually are 

menstruating or just finished their periods (risk of ascending infection is increased 

secondary to the loss of the cervical mucus plug during menses). 

Physical examination in acute cases discloses marked tenderness on manipulation of 

the cervix and palpation of the adnexa. There is a unilateral tender adnexal mass if 

tuboovarian abscess or pyosalpinx is present. The clinical spectrum in PID includes a 

gradual progression from subclinical endometritis to salpingitis to pyosalpinx to 

tuboovarian abscess to pelvic peritonitis to perihepatitis. A ruptured tuboovarian 

abscess carries with it a mortality rate of 7% and may require emergency surgery. Table 

40-10 presents physical examination criteria. 

B. Laboratory Tests and Special Examinations

There is usually leukocytosis or an elevated erythrocyte sedimentation rate or C reactive 

protein. Obtain a serum pregnancy test. Purulent fluid should be cultured for aerobic 

and anaerobic pathogens, specifically for N. gonorrhoeae and Chlamydia. 

Ultrasonography may be helpful in detecting or assessing the size of tuboovarian 

abscess. 

Treatment 

A. Antibiotic Therapy 

Table 40-11 presents treatment options. No single agent is active against the entire 

spectrum of pathogens. Several antibiotic combinations provide a broad spectrum of 

activity against the major pathogens, but none have been adequately evaluated. 

Treatment with penicillin, ampicillin, amoxicillin, or a cephalosporin alone is not 


B. Reevaluation 

Patients who are not hospitalized should be reevaluated in 2-4 days and hospitalized if 

their condition has not improved markedly. 

C. Adjunctive Measures 

Relieve pain. Narcotics are frequently required. If present, an intrauterine device should 

be removed as soon as adequate antibiotic levels are achieved in the blood. Surgery 

should be delayed at least 2-3 days, until the effect of antibiotic therapy can be 

assessed, even if pyosalpinx or tuboovarian abscess is present. Pelvic abscesses often 

regress with antibiotic therapy alone or may drain externally via the vagina or rectum. 

Repeated ultrasound examinations help to determine the patient's progress. 

Disposition 

There is an increasing trend toward the outpatient management of PID. Indications for 

admission include uncertain diagnosis, pelvic abscess, pregnancy, adolescence, severe 

illness, failure of outpatient management, an inability to arrange follow-up, and 

HIV-positive status. 

VAGINITIS 


• Abnormal vaginal discharge. 

• Pruritus, irritation, odor. 

• Inflamed cervix. 


Vaginitis is a common and annoying disorder that in the absence of other symptoms or 

signs rarely indicates serious disease. Common pathogens include Candida albicans, 

Trichomonas vaginalis, Gardnerella vaginalis with anaerobic bacteria (bacterial

vaginosis), and gonococci (in prepubertal girls). Other common causes are estrogen 

deficiency (atrophic vaginitis) and vaginal foreign body. Systemic antibiotics (especially 

tetracyclines), oral contraceptives, diabetes mellitus, primary genital HSV infection, and 

pregnancy predispose to the development of candidiasis. Less common causes include 

allergy, cervicitis, polyps, tumors, vaginal ulcer, shigellosis, irradiation for cancer, and 

certain bubble bath preparations. 



Vaginal discharge and pruritus are the chief symptoms. Vaginal discharge with varying 

degrees of inflammation of the vaginal wall (minimal in atrophic vaginitis) is usually 

found. Search for foreign bodies in the vagina, particularly in young girls, and examine 

for associated disorders (eg, salpingitis). 


1. Examination of smears— 

a. Gram stain—Look for Candida and G. vaginitis (small gram-negative rods usually 

adherent to epithelial cells; "clue cells"). Methylene blue stain also demonstrates clue 

cells. Vaginitis due to Candida or Trichomonas is usually associated with a 

polymorphonuclear exudate, whereas inflammatory cells are absent in bacterial 

vaginosis caused by G. vaginalis. In prepubertal girls with gonococcal vulvovaginitis, 

Gram stain of smears usually shows typical gram-negative intracellular diplococci, but 

cultures should be performed to confirm the diagnosis. 

b. Saline wet mount—Look for motile trichomonads. Candida and clue cells of G. 

vaginalis may also be seen. 

c. Potassium hydroxide wet mount—Addition of a few drops of potassium hydroxide 

to a sample of vaginal secretions releases a typical amine odor (fishy) in cases of 

bacterial vaginosis due to G. vaginalis. Microscopic examination reveals Candida in 

cases of Candida vaginitis, but Gram staining is more sensitive and specific. 

2. Urinalysis—Obtain a clean-catch urine specimen for analysis and culture if dysuria is 

present. 

3. Other tests—Obtain fasting blood glucose measurement in cases of recurrent 

candidiasis, to rule out diabetes mellitus. 

Treatment 

A. General Measures 

Avoid systemic antibiotic therapy, if possible. Advise patients regarding adequate 

perineal ventilation. Patients should wear loose-fitting cotton underpants with skirts and 

avoid tight-fitting constrictive clothing. Sitz baths may give relief. Occasional douches 

with white vinegar (2 tablespoons per quart of warm water) may provide symptomatic 

relief but seldom influence recovery. Advise patients to avoid intercourse for a few days 

after treatment. Partners also should receive treatment, as described below.

B. Specific Measures 

1. C albicans vaginitis— 

a. Imidazole regimens—(1) Miconazole nitrate (vaginal suppositories, 200 mg) or 

clotrimazole (vaginal suppositories, 200 mg), intravaginally at bedtime for 3 days, or (2) 

butoconazole (2% cream, 5 g), intravaginally at bedtime for 3 days, or (3) terconazole, 

80 mg suppository or 0.4% cream, intravaginally at bedtime for 3 days. 

b. Reinfection—The male partner should wear a condom, or both partners should 

abstain from intercourse for 2-3 days. Balanitis due to Candida occurs almost 

exclusively in uncircumcised men. Occasionally the patient's gastrointestinal tract is a 

reservoir for Candida, in which case oral nonabsorbable antifungal preparations (eg, 

nystatin), are necessary. 

2. T. vaginalis vaginitis—Give the patient and her sexual partner metronidazole, 2 g 

orally in a single dose (eight 250-mg tablets). This regimen is curative in about 95% of 

cases. An alternative regimen involves metronidazole, 250 mg orally 3 times daily for 7 

days. Resistance of T. vaginalis to metronidazole has been observed but is rare. If 

treatment fails, the patient should receive the same treatment regimen again. Address 

persistent treatment failure in consultation with an expert. 

3. Bacterial vaginosis—Several species of vaginal bacteria (including G. vaginalis) 

interact to produce this syndrome. Metronidazole, 500 mg orally 2 times daily for 7 days, 

is an effective treatment. Warn the patient about side effects. Clindamycin, 300 mg 

orally 2 times daily for 7 days, may be used in pregnant patients. Because bacterial 

vaginosis may be a factor in premature rupture of membranes and premature delivery, 

close clinical follow-up of pregnant women is essential. Treatment for male sexual 

partners does not reduce the risk of recurrence of bacterial vaginosis in the index case. 

4. Atrophic vaginitis—Prescribe estrogen suppositories or creams. Diethylstilbestrol, 

one 0.5-mg vaginal suppository every 3 days for 3 weeks, followed by 1 week without 

treatment, may be tried. 

5. Gonococcal vaginitis—See "Gonorrhea" section, below. 

Disposition 

Patients should have a follow-up appointment with a gynecologist or primary care 

physician in 7-10 days so that the results of treatment can be assessed and follow-up 

cultures obtained. 

GENITAL ABSCESSES 


• Labial pain, swelling.

• Fluctuant lesion. 


Vulvar abscesses may rise in a sebaceous gland or Bartholin gland (Bartholin cyst). 

Skene glands, adjacent to the urethra, may also be the site of abscess formation. N. 

gonorrhoeae is responsible for some vulvar abscesses: the remainder are caused by a 

variety of bacteria, often in mixed culture. 


The patient complains of tender swelling of the labia majora that is confirmed by 

examination. Gram stain and culture of pus from the abscess help to identify the 

causative organism. Endocervical culture for N. gonorrhoeae should be performed, if 

possible. 

Treatment 

A. Nonfluctuant Lesions 

If lesions are not fluctuant, incision and drainage is not indicated. If gonorrhea is 

suspected, give ceftriaxone, 250 mg intramuscularly. In addition, give a broad-spectrum 

antibiotic such as amoxicillin clavulanate, 500 mg 3 times daily. Prescribe sitz baths and 

application of warm compresses. Ask the patient to return in 1-2 days for reevaluation of 

the need for incision and drainage. 

B. Fluctuant Lesions 

When drainage is performed, pack the abscess. Administer antimicrobials as described 

above. Have the patient return in 2-3 days. 

Disposition 

Gynecologic follow-up is mandatory, because surgery may be necessary. Occasionally 

marsupialization may be performed at the time of diagnosis of acute bartholinitis. 

MUCOPURULENT CERVICITIS 


• Vaginal discharge. 

• Pruritus. 

• Cervical exudate. 


The presence of mucopurulent endocervical exudates strongly suggests cervicitis due to 

chlamydial or gonococcal infection.



Vaginal discharge and pruritus may be present. Mucopurulent endocervical exudate 

may be observed. 


1. Swab test—Mucopurulent secretion from the endocervix may appear yellow or green 

when viewed on a white cotton-tipped swab. Cervicitis is present if bleeding occurs 

when the first swab culture for gonococci is taken or if erythema or edema is present 

within a zone of cervical ectopy. 

2. Slide test—Flurorescent antibody or ELISA slide test should be used to diagnose 

Chlamydia. 

3. Gram stain—Gram-stained smears of endocervical secretions show greater than 10 

PMNs per microscopic oil-immersion field. The presence of gram-negative, diplococci 

suggest infection with N. gonorrhoeae but is not diagnostic. Culture is necessary to 

confirm infection with N. gonorrhoeae. 

Treatment 

If N. gonorrhoeae is suspected or found on Gram stain of endocervical or urethral 

discharge, treatment should be given as recommended for uncomplicated gonorrhea in 

adults. If N. gonorrhoeae is not suspected, treatment should be as recommended for 

chlamydial infection in adults. 

DISEASES OF THE MALE GENITOURINARY TRACT 

ACUTE BACTERIAL PROSTATITIS 


• Fever. 

• Low back pain. 

• Dysuria. 

• Urgency. 

• Prostatic tenderness. 



Patients with acute bacterial prostatitis often have chills, fever, low back and perineal 

pain or pressure, malaise, dysuria, urgency, and difficulty voiding or decreased urinary 

stream. Recurring attacks of acute prostatitis are common. Urethral discharge may be 

present if prostatitis is secondary to urethritis (uncommon). The prostate is tender and 

enlarged. Prostatic abscess should be suspected when localized prostatic tenderness,

swelling, or fluctuance is present. Prostatic massage is contraindicated in severe, acute 

prostatitis because it may induce bacteremia. A simple rectal examination may be 

performed, however. Prostatitis is the most common urologic diagnosis in men over age 

50 years; as many as 50% of men are affected in their lifetime. 


When acute bacterial prostatitis is suspected based on the patient's symptoms and on 

physical examination, presumptive diagnosis may be made based on the results of 

urinalysis and urine Gram stain and culture. The bacterial pathogen found in the urine 

will usually be the same as that infecting the prostate. The presence of bacteria should 

be confirmed by culture and susceptibility testing. Leukocytosis is common. Azotemia 

suggests obstructive uropathy. Obtain blood cultures for all patients who have high fever 

or rigors. 

Treatment 


Enterococcal prostatitis may require inpatient treatment with intravenous ampicillin and 

gentamicin. Fluoroquinolones are the first-line agents of choice for outpatient therapy. 

Other inpatient regimens include TMP-SMZ intravenously in 2 divided doses or an 

aminoglycoside. Gonococcal prostatitis is uncommon and should be managed in 

consultation with a urologist. 


Analgesics (often including a narcotic) should be provided. Hot sitz baths may provide 

relief. Bed rest is usually helpful. a-1-Blockers may be useful to decrease pain and 

recurrence rates. 

Disposition 

Patients with acute bacterial prostatitis causing systemic symptoms (high fever, rigors) 

or with suspected prostatic abscess should be hospitalized for treatment with parenteral 

antibiotics and consultation with a urologist. 

Patients who are not hospitalized should return for follow-up in 3-4 days to ensure that 

recovery is progressing and again 7-10 days after stopping antimicrobial therapy for a 

test-of-cure culture of expressed prostatic secretions or of urine. Refer the patient to a 

urologist or to a source of regular medical care. 

ACUTE EPIDIDYMITIS 


• Testicular pain. 

• Epididymal tenderness. 

General Conditions

Epididymitis usually results from retrograde spread of urethral or urinary tract infection 

into the epididymis. Epididymitis is therefore usually caused by the same pathogens 

causing urethritis (eg, gonococci, Chlamydia) or urinary tract infection (eg, E. coli). The 

former pathogens are found more commonly in men younger than age 35 years, and E. 

coli is seen more often in men over age 35 years. 



Pain and tenderness of the epididymis is present on one or both sides. Epididymitis 

must be differentiated from testicular torsion and from torsion of the testicular 

appendage. In orchitis the testicle is diffusely and tensely swollen, warm, firm, and 

tender. 

Urethritis or urinary tract infection usually coexists with epididymitis, and evidence of 

these conditions must be sought with appropriate laboratory tests. At a minimum, Gram 

or methylene blue stain of urethral exudates (or swab of material in the anterior urethra 

if no exudates can be obtained) and a clean-voided midstream urine specimen should 

be obtained for analysis. 

Treatment 


1. Epididymitis with urinary tract infection—Give TMP-SMZ for 10 days. 

2. Epididymitis in sexually active heterosexual men younger than age 35 

years—Regardless of whether N. gonorrhoeae is demonstrated, the Centers for 

Disease Control (CDC) recommends treatment for gonorrhea and Chlamydia. 

Administer ceftriaxone intramuscularly followed by doxycycline or tetracycline for 10 

days. 


Prescribe analgesics as needed. Hot sitz baths may be helpful. Bed rest and scrotal 

elevation for 1-2 days will provide symptomatic relief. If the patient must be ambulatory, 

an athletic supporter may be helpful. 

Disposition 

Refer the patient to a urologist or primary care physician within a few days. 

Hospitalization is indicated for orchitis that does not respond within 48 hours to oral 

therapy and adjunctive measures. 

SEXUALLY TRANSMITTED DISEASES 

The management of all sexually transmitted diseases should include counseling 

regarding safe sex practices and the performance of HIV antibody test in consenting 

patients.

GONORRHEA 

N. gonorrhoeae causes primary genitourinary tract infections, localized infections, and 

the disseminated arthritis-dermatitis syndrome. Approximately 600,000 new cases are 

diagnosed each year. 



In men, gonococcal urethritis is characterized by acute onset of dysuria, sometimes with 

hematuria, and a copious creamy urethral discharge. Less profuse urethral discharge 

requiring milking of the penile urethra may also occur. Local extension of infection may 

produce inflammation of preputial glands, epididymitis, seminal vasculitis, and 

prostatitis. In women, gonococcal cervicitis may be asymptomatic or patients may 

present with vaginal discharge or symptoms of accompanying urethritis (eg, dysuria, 

frequency). Occasionally a Bartholin gland abscess is the initial complaint. Patients with 

gonococcal salpingitis complain of lower abdominal pain (unilateral or bilateral), vaginal 

discharge, and metromenorrhagia. Pain on cervical motion and adnexal tenderness is 

usual; nausea and vomiting and marked abdominal tenderness or rebound suggest 

pelvic peritonitis. 

Rectal infection with N. gonorrhoeae is usually asymptomatic, although patients 

occasionally present with proctitis (rectal pain, discharge, tenesmus, and constipation). 

Pharyngeal infection is almost always asymptomatic. 

Patients with gonococcal conjunctivitis present with marked conjunctival erythema and 

purulent discharge, often unilateral. In adults, it usually follows contact between 

contaminated fingers and the eye. 


In men, obtain a Gram-stained smear of urethral discharge, examine it microscopically, 

and obtain culture and antimicrobial susceptibility testing. The presence of leukocytes 

(usually PMNs) and intracellular gram-negative diplococci on the smear is more than 

99% specific for gonorrhea. A smear showing only PMNs with no gram-negative 

diplococci is a predictor of a negative gonococcal culture in over 90% of patients, 

although culture for gonorrhea is generally recommended. These patients should 

receive treatment for nongonococcal urethritis. Culture of the pharynx and rectum is 

necessary if there is a history of oral or receptive rectal intercourse, because negative 

results on Gram-stained smears from these areas do not rule out gonorrhea. 

In women, findings on Gram-stained smears of cervical secretions may suggest 

gonorrhea (PMNs with intracellular gram-negative diplococci), but culture should be 

performed to confirm the diagnosis. Culture of rectal secretions is recommended in all 

women, because sometimes it is the only site yielding positive cultures. Culture of 

pharyngeal secretions is necessary in patients with a history of oral sexual intercourse. 

Express the exudates in purulent conjunctivitis, and examine a Gram-stained smear. 

Gram-negative diplococci confirm a diagnosis of gonococcal conjunctivitis. Send a 

sample of the exudates for culture.

Culture on Thayer-Martin media remains the gold standard for diagnosis. The PCR is 

97-99% sensitive, with specificity of 99%. A serologic test for syphilis (eg, VDRL) should 

be ordered for all patients. 

Treatment 

Because there has been worldwide spread of strains of N. gonorrhoeae that are 

resistant to penicillin, amoxicillin, and tetracycline, these agents are no longer 

recommended for empiric treatment of gonococcal infections. Use ceftriaxone, 150 mg 

intramuscularly, an oral fluoroquinolone (eg, ciprofloxacin, 500 mg, or ofloxacin, 400 mg, 

single dose), or azithromycin (2 g single dose). Because of the high frequency of 

coexisting chlamydial infection (up to 45%), a tetracycline, doxycycline, or azithromycin 

regimen should follow the treatment of gonococcal infections. 

Patients with gonococcal conjunctivitis must be hospitalized and should receive 

ophthalmologic consultation. Therapy consists of ceftriaxone, 1 g intramuscularly or 

intravenously once daily for at least 5 days, combined with immediate and at least 

hourly irrigation of the eye with saline or buffered ophthalmic solutions. Simultaneous 

ophthalmic infection with C. trachomatis can also occur. Careful ophthalmic follow-up is 

necessary to prevent ocular complications. 

Disposition 

Hospitalization is not required for patients with localized gonococcal infection, except for 

gonococcal conjunctivitis. Sexual partners with gonorrhea must be notified and receive 

treatment. Cases of gonorrhea must be reported to the local public health department. 

NONGONOCOCCAL URETHRITIS (Nonspecific Urethritis) 

Nongonococcal urethritis, or nonspecific urethritis, is due to infection with C. trachomatis 

in over half the cases. Genital Mycoplasmas (Ureaplasma), HSV, and Trichomonas are 

occasional causes. 



Most male patients have urethral discharge and dysuria. Symptoms are often insidious 

in onset, with urethral discharge that is scanty, mucoid, watery, and most prominent in 

the morning. Women may be asymptomatic or may complain of dysuria or frequency. 

Infection may involve the cervix as well and extend to the oviducts, producing low-grade 

fever. 


Urethral discharge should be stained with Gram stain and examined microscopically. 

The presence of more than 4 leukocytes per high-power field confirms the diagnosis of 

urethritis. If no organisms morphologically consistent with gonococci are found, then 

presumptive diagnosis of nongonococcal urethritis can be made. A Gram-stained smear 

with findings diagnostic of gonorrhea does not exclude nongonococcal urethritis,

ecause dual infection with Chlamydia and the gonococcus is common, particularly in a 

heterosexual population. The specimen should be sent for culture but because of 

difficulties in culturing this organism, culture is 80% sensitive. PCR testing is the most 

sensitive (93-99%), with specificity of 99-100%. A serologic test for syphilis should also 

be obtained. 

Treatment 

First-line agents recommended by the CDC include single-dose azithromycin or a 7-day 

course of doxycycline. If nongonococcal urethritis is suspected (negative or equivocal 

findings on Gram-stained smear with culture results pending) or documented (culture 

negative for nongonococcal urethritis), sexual partners should also receive treatment. 

Disposition 

Patients with nongonococcal urethritis can receive treatment on an outpatient basis. 

GENITAL HERPES SIMPLEX VIRUS INFECTION 


• Fever, adenopathy. 

• Vesicles on an erythematous base. 

• Pain. 


HSV is a major cause of recurrent genital lesions. The initial (primary) infection is the 

most severe, although it is sometimes asymptomatic. After the primary lesion has 

healed, the virus remains latent in the paraspinous ganglia, where it periodically causes 

reactivation of infection. Genital infection is usually caused by HSV type 2, and about 

99% of patients with recurrent disease will be infected by type 2 virus. Spread of 

infection is almost exclusively by sexual intercourse. 


Obtain a serologic test for syphilis (eg, VDRL) to rule out coexisting syphilis. 


1. First clinical episode of genital HSV—The first clinical attack of HSV is usually the 

most severe. Patients may present with fever, malaise, myalgias, and arthralgias. 

Aseptic meningitis occurs in 10-20% of cases, particularly in women. Associated 

symptoms may include dysuria, dyspareunia, and urinary retention. Successive crops of 

grouped vesicles on an erythematous base denude, form ulcers, and heal by secondary 

intention, usually in 2-3 weeks but sometimes not until after 6 weeks. Genital edema is 

common. Local pain and regional adenopathy are usually marked. In men, the glans 

and penile shaft are involved. In women, the vulva, vagina, and cervix are the usual

sites of involvement. Male or female patients with herpetic proctitis present with fever, 

tenesmus, constipation, and rectal pain. 

2. Recurrent HSV episodes—Recurrent infection is common and may be triggered by 

a variety of stimuli (eg, friction, menstruation, sexual intercourse, pregnancy, or stress). 

Recurrent attacks are frequently heralded by a prodrome consisting of local itching, 

pain, or aching in the buttocks or leg. Initially, a papule develops that rapidly vesiculates, 

breaks down into an ulcer, and then heals, usually within 7-10 days. The virus may be 

recovered as long as lesions are moist. Patients should avoid direct skin-to-skin contact 

until the area is completely dried and healed. 

The presence of HSV may be confirmed by the Tzanck test (about 60% sensitivity and 

80% specificity) or virus culture. Virus culture is recommended in most cases. 

Treatment 

Antipyretics and analgesics may help to relieve systemic symptoms. Antiviral regimens 

(Table 40-12) accelerate resolution of the signs and symptoms of herpetic eruptions but 

do not affect the subsequent risk, frequency, or severity of recurrences after the drug is 

discontinued. Immunocompromised patients (especially AIDS patients) with extensive, 

ulcerative, or progressive mucocutaneous herpes should receive oral therapy. 

Continuous therapy is necessary in some patients. Hospitalization for intravenous 

therapy may be warranted if the patient is unable to take medications orally or if the 

lesions are extensive. Antibiotics are not necessary unless Gram-stained smears 

suggest bacterial superinfection. Women with primary genital herpes frequently have 

associated Candida vaginitis, which should be treated as described above. The patient 

should bathe the exposed affected areas with warm tap water, or apply warm 

compresses every 4 hours. Because lesions shed infectious virus, patients should avoid 

manipulating lesions with their bare hands and should wash their hands after exposure 

(autoinoculation of the eye or other sites may occur). Any other contact with the lesions 

(eg, sexual) should be avoided until they have healed. 

Disposition 

Hospitalization is occasionally indicated for patients with primary HSV infection because 

of severe pain, systemic symptoms, and other complications (urinary retention, 

obstipation, aseptic meningitis, dehydration). Hospitalization is also required for patients 

with extensive, large, or rapidly progressive lesions. 

Patients with genital HSV infection are often frightened and confused about the nature 

and transmission of the disease and may suffer both physically and psychologically. 

Counseling should be initiated and provided in the emergency department, if possible, 

and patients should be referred to a gynecologist or primary care provider who is 

experienced in treating HSV infection and who can explain the disease, answer any 

questions, and provide information on various methods of treatment, so that the patient 

can make an informed evaluation of the associated efficacy, risks, and side effects. 

Obtain obstetric consultation for pregnant patients with HSV infection.

SYPHILIS 


• Chancre (painless). 

• Rash. 

• Positive VDRL, RPR, FTA-ABS. 


Disease following infection due to Treponema pallidum may be divided into primary, 

secondary, latent, and tertiary stages. Infection with T. pallidum has been identified as 

an important risk factor for HIV infection. An HIV antibody test should be obtained for all 

consenting patients with syphilis. 



1. Primary stage—A chancre develops at the site of entry of the spirochete between 10 

days and 6 weeks after exposure. The ulcer, located on the genitals or occasionally on 

extragenital sites (finger, mouth), is nontender and has a depressed center and rolled, 

pearly edges. Associated inguinal adenopathy, if present, is usually firm, hard, and 

nontender. 

2. Secondary stage—Secondary disease develops about 4 weeks after the 

appearance of the chancre. Clinical manifestations reflect the presence of spirochetes in 

the bloodstream. Most common is a rash that ranges from macular to maculopapular to 

plaques (condyloma lata). The rash is generally distributed over the thorax, abdomen, 

and extremities; it may involve the palms and soles; and it is nonpruritic. Associated 

findings may include low-grade fever, generalized lymphadenopathy, hepatitis, 

meningitis, alopecia, and weight loss. 

3. Latent stage—A positive serologic test is the only sign, and this stage may last from 

1 to 2 months up to more than 20 years. 

4. Tertiary stage—This stage is characterized by destructive lesions of the aorta, CNS, 

skeletal structures, and skin. 


The diagnosis of infectious syphilis is confirmed by serologic testing or by positive 

results on microscopic darkfield examination of scrapings from the chancre or lesions of 

secondary disease. Obtain blood for serologic testing (eg, VDRL or RPR); if results are 

positive, perform a treponemal antibody test (eg, FTA-ABS or MHA-TP). 

Treatment 

A. Infectious Syphilis

1. Benzathine penicillin G—The treatment of choice is benzathine penicillin G (2.4 

million units intramuscularly). Patients who claim to be allergic to penicillin should be 

tested (ie, skin testing) and desensitized, if necessary. 

2. Doxycycline—An alternative regimen for penicillin-allergic patients is doxycycline, 

100 mg orally twice daily, or tetracycline, 500 mg 4 times daily for 14 days. 

3. Erythromycin—Patients who cannot take penicillin, doxycycline, or tetracycline and 

who are reliable and can be followed closely can take erythromycin, 500 mg orally 4 

times daily for 14 days. 

B. Jarisch-Herxheimer Reaction 

Asprin or acetaminophen may be prescribed for the Jarisch-Herxheimer reaction that 

commonly occurs within a few hours after treatment for secondary syphilis has been 

started. The reaction is characterized by malaise, fever, faintness, and intensification of 

the rash. Patients with secondary syphilis who are released from the emergency 

department following penicillin therapy should be warned about the symptoms of the 

reaction and should be told that it is not due to penicillin allergy. 

C. Syphilis in HIV-Infected Patients 

A lumbar puncture should be performed in HIV-infected patients with early syphilis 

because of increased risk of treatment failure and CNS relapse. If the CSF cell count is 

normal and the VDRL test nonreactive, give 1-3 doses of benzathine penicillin G 

therapy. Serum VDRL testing must be repeated at monthly intervals for at least 3 

months. Tetracyclines are probably inadequate therapy for HIV-infected patients with 

syphilis. Ceftriaxone, 250 mg intramuscularly once daily for 10 days, can be tried. 

Disposition 

Patients may receive treatment on an outpatient basis. Cases of syphilis must be 

reported to the local public health department. Sexual partners of patients should be 

notified and receive treatment. Arrangements must be made for follow-up serologic 

testing. 

CHANCROID 


Chancroid is an ulcerating genital infection caused by Haemophilus ducreyi. It is 

common in tropical and subtropical regions and is believed to be underdiagnosed in the 

United States. 


Chancroid is manifested by the appearance of a small pustule that rapidly ulcerates with 

an irregular and purulent exudative base that is painful. It is associated with tender 

inguinal lymphadenopathy in 50% of cases. 

Definitive diagnosis requires growth on culture media, and the diagnosis should be

considered for any patient who has painful genital ulceration and for whom darkfield 

fluoroscopy and HSV testing are negative. 

Treatment 

Recommended treatments include azithromycin orally or ceftriaxone intramuscularly; 

ciprofloxacin and erythromycin are alternatives. 

TRICHOMONIASIS 


• Erythematous pustule. 

• Adenopathy. 

• Pain. 

• Gram stain or culture. 



Most men with T. vaginalis infections develop nongonococcal urethritis, but women 

typically develop malodorous yellow-green frothy discharge, dysuria, dyspareunia, 

vulvar irritation, and pruritus. 


Motile parasites are seen on a wet-mount smear. 

Treatment 

Single-dose metronidazole or metronidazole therapy for 7 days is the only treatment 

option. No effective alternatives are available. 

Lawson MA, Blythe MJ: Pelvic inflammatory disease in adolescents. Pediatr Clin North 

Am 1999;46(4):767. [PMID: 10494256] 

Lummus WE, Thompson I: Prostatitis. Emerg Med Clin North Am 2001;19(3):691. 

[PMID: 11554282] 

McKininzie J: Sexually transmitted diseases. Emerg Med Clin North Am 2001;19(3):723. 

[PMID: 11554284] 

SKIN & SOFT TISSUE INFECTIONS 

SUPERFICIAL SOFT TISSUE INFECTIONS


• Erythema, pain, edema. 

• Fever. 

• Elevated white blood cell count. 


Superficial soft tissue infections (eg, impetigo, erysipelas, cellulitis) are rarely 

emergencies. However, these infections may be potentially life- or limb-threatening in 3 

situations: (1) when infection is near the face or hand, (2) when cellulitis occurs in the 

presence of diabetes, peripheral vascular disease, or venous or lymphatic insufficiency, 

or (3) when local infection occurs in the presence of immunodeficiency, particularly 

leukopenia, leukemia, or AIDS. 



1. Impetigo—Impetigo is a superficial skin infection seen mainly in children. It is usually 

due to group A streptococci. Less commonly, staphylococci alone or in conjunction with 

streptococci may cause the disease. It has 2 forms: bullous (impetigo bullosa) and 

nonbullous (impetigo contagiosa). Nonbullous impetigo begins with small vesicles that 

rapidly pustulate and rupture easily. The purulent discharge dries, forming the 

characteristic thick, golden yellow (honey-crusted) appearance. Bullous impetigo is 

related to toxin formation and initially appears as a vesicle that rapidly enlarges to form 

a bulla, which then forms a dark brown crust. Exposed areas are the most common 

sites of lesions. Mild regional lymphadenopathy is common. The lesions are painless 

and often pruritic; systemic symptoms are minimal. 

2. Ecthyma—Ecthyma is a deeper form of impetigo that is associated with ulceration 

and scarring. It occurs frequently on the legs, often as a complication of debility or 

infestation with ectoparasites. 

3. Staphylococcal scalded skin syndrome—This is the most severe manifestation of 

skin disease caused by widespread bullae and exfoliation. It usually occurs in young 

children but may rarely develop in adults. It begins abruptly with fever, skin tenderness, 

and scarlatiniform rash. Large, flaccid, clear bullae form and promptly rupture, resulting 

in separation of sheets of skin. 

4. Erysipelas—Erysipelas is a distinctive superficial cellulitis characterized by 

prominent lymphatic involvement. It is almost always due to group A streptococci and is 

more common in infants, young children, and older adults than in younger adults. The 

face is most often involved. The lesion is painful and has a bright red, edematous, 

indurated appearance and an advancing raised border that is sharply demarcated from 

adjacent normal skin. A common form of the disease affects the bridge of the nose and 

cheeks. Fever is common. Erysipelas is usually limited to the dermis and lymphatics but 

can occasionally extend more deeply to produce cellulitis and bacteremia.

5. Cellulitis—Cellulitis is an acute spreading infection of the skin that extends deeper 

than erysipelas. Group A streptococci and S. aureus are the most common causative 

agents. Previous trauma or underlying skin lesions (eg, furuncle, ulcer) predispose to 

the development of cellulitis. Local tenderness, pain, and erythema develop within 

several days and intensify rapidly. The lesion has poorly demarcated borders, and the 

skin is red, hot, and edematous. Malaise, fever, and chills may develop. In older 

patients, cellulitis in the lower extremity may be complicated with thrombophlebitis. In 

patients with diabetes or peripheral vascular disease, cellulitis in the lower extremity 

may be caused by gram-negative bacilli and anaerobes, in addition to streptococci and 

staphylococci. 


Leukocytosis with a shift to the left may be present. Obtain a Gram-stained smear and 

culture of material from vesicles, bullae, or exudates. Examination of material aspirated 

at the leading edge of cellulitis may reveal the causative organism. Obtain blood 

cultures from patients with high fever, chills, or rapid progression of infection. 

Treatment 

A. Impetigo and Ecthyma 

Penicillin is the treatment of choice and is administered either as a single intramuscular 

injection of benzathine penicillin G (children, 300,000-600,00 units; adults, 1,200,000 

units) or as oral penicillin, 125-500 mg every 6 hours for 10 days. Erythromycin 

(children, 30-50 mg/kg/d orally in divided doses every 6 hours for 10 days; adults, 

250-500 mg orally every 6 hours). Erythromycin is an alternative for penicillin-allergic 

patients. Topical mupirocin can also be used for impetigo. It is helpful to remove the 

crust by soaking it in soap and water. 

Bullous impetigo responds to treatment with a penicillinase-resistant penicillin (eg, 

dicloxacillin); erythromycin may be substituted in penicillin-allergic patients. 

B. Staphylococcal Scalded Skin Syndrome 

Staphylococcal scalded skin syndrome is treated with a penicillinase-resistant penicillin 

(eg, nafcillin, 50- 100 mg/kg/d intravenously in newborns; 100-200 mg/ kg/d 

intravenously in older children). Topical treatment consists of application of cool saline 

compresses. Corticosteroids should not be used. 

C. Erysipelas 

Mild cases in adults may be treated with procaine penicillin G (600,000 units 

intramuscularly once or twice daily) or with oral penicillin, 250-500 mg orally every 6 

hours for 2 weeks. Erythromycin, 250-500 mg orally every 6 hours, is a suitable 

alternative. For more extensive erysipelas, hospitalization for treatment with parenterally 

administered aqueous penicillin G, 600,000- 2,000,000 units intramuscularly every 6 

hours, is required. 

D. Cellulitis 

Mild, early cellulitis may be treated with oral antibiotics. Because S. aureus may be 

involved, empiric therapy is with a penicillinase-resistant penicillin or first-generation

cephalosporin. For more severe infection thought to be caused by streptococci or 

staphylococci, give penicillinase-resistant penicillin intravenously with or without 

penicillin G. A first-generation cephalosporin equivalent to cefazolin (1-2 g/d 

intravenously) is an alternative for patients who are not critically ill. Vancomycin (1-2 g/d 

intravenously) is an alternative for penicillin-allergic patients. If superinfection with 

gram-negative bacteria is present or suspected, add an aminoglycoside such as 

gentamycin or amikacin. Local care includes immobilization and elevation of the 

involved limb. 

Disposition 

Patients with lymphangitis and patients with cellulitis that has progressed rapidly over 

the preceding 12 hours can be given parenteral antibiotic therapy in the emergency 

department if they are reliable for follow-up within 12-24 hours. Hospitalize patients who 

worsen despite parenteral antibiotic therapy, those who are unreliable, and those who 

cannot be closely followed in an outpatient setting. Cellulitis involving the face or hand 

usually requires hospitalization for parenteral antibiotic therapy. The presence of 

diabetes, venous or lymphatic insufficiency, or systemic symptoms usually requires 

inpatient or outpatient parenteral therapy. 

DEEP SOFT TISSUE INFECTIONS 

Deep soft tissue infections involve subcutaneous tissues and may also involve muscles 

and fascial planes. Classification of these infections is complicated by use of varied 

nomenclature. Most of these infections are due to anaerobic and aerobic gram-positive 

and gram-negative organisms. 

1. Infected Vascular Gangrene & Cellulitis 

Infected vascular gangrene and cellulitis is a mixed infection occurring mostly in the 

lower extremities in patients with peripheral vascular disease or diabetes. Anaerobic 

organisms, aerobic gram-negative bacilli, and staphylococci may be involved. 


An underlying ulcer is often the source of infection that may spread to involve not only 

superficial and deep soft tissue but also muscles or an entire limb. Gas formation may 

occur. Edema and foul-smelling pus are noticeable. Pain and tenderness may be 

present. 


Hospitalization is required for surgical debridement and intravenous therapy with a 

combination of antibiotics (eg, cefoxitin alone, or clindamycin plus gentamicin). 

Underlying osteomyelitis is common if an ulcer is present. Amputation is sometimes 

necessary. 

2. Clostridial Anaerobic Cellulitis


Clostridial anaerobic cellulitis is a necrotizing clostridial infection of devitalized 

subcutaneous tissue. The deep fascia is not appreciably involved, and there is ordinarily 

no associated myositis. Gas formation is common and often extensive. Onset of 

infection is gradual after an incubation period of several days. Local pain, swelling, and 

systemic toxicity are not prominent. A thick, dark, sometimes foul-smelling drainage is 

characteristic. Frank crepitus is present. Gram-stained smears of drainage material 

show numerous blunt-ended, thick, gram-positive bacilli. Soft tissue x-rays show 

abundant gas. Obtain cultures for aerobic and anaerobic organisms. 


Hospitalize patients for treatment with high doses of intravenous penicillin 

(chloramphenicol for penicillin-allergic patients) and surgery. 

3. Nonclostridial Anaerobic Cellulitis 


A clinical picture similar to clostridial cellulitis can be produced by nonclostridial 

anaerobic bacteria alone or in mixed infection with aerobic gram-negative and 

gram-positive organisms. 


Antimicrobial therapy is based on the findings on Gram-stained smears of drainage 

material. Because these are frequently mixed infections, several antibiotics may be 

needed (eg, cefoxitin, clindamycin, or penicillin plus an aminoglycoside). Surgical 

incision and drainage is necessary. 

4. Synergistic Necrotizing Cellulitis 


Synergistic necrotizing cellulitis is a rapidly progressive infection with high fever and 

systemic manifestations caused by infection with anaerobes and anaerobic 

gram-negative bacilli. It occurs most commonly on the perineum and lower extremities 

and is associated with a high mortality rate. The disease is first manifested as skin 

ulcers from which drains foul-smelling, reddish-brown ("dishwater") pus. Circumscribed 

areas of blue-gray gangrene surround these drainage sites, but intervening skin 

appears normal. Local pain and tenderness are marked. Tissue gas is noted in about 

one fourth of patients. 


Hospitalization for prompt surgical incision and drainage of necrotic tissue must be 

combined with antimicrobial therapy (eg, clindamycin plus gentamicin).

5. Necrotizing Fasciitis 


Necrotizing fasciitis is a mixed anaerobic and aerobic infection that rapidly dissects 

deep fascial planes and produces severe toxicity associated with a high mortality rate. It 

most commonly occurs on the extremities but may occur on the abdomen in patients 

with diabetes mellitus, especially after abdominal surgery, or on the perineum or 

scrotum (Fournier gangrene) in patients with diabetes mellitus, especially after urinary 

tract manipulation. The affected area is initially erythematous, swollen, and painful. 

Bullae containing serosanguineous material appear, and subcutaneous gas is common. 

Systemic toxicity with high fever is prominent. When a lesion is probed with a hemostat 

through a limited incision, the instrument passes easily along a plane just superficial to 

the deep fascia, a distinguishing feature that does not occur with ordinary cellulitis. 

Leukocytosis is present. About half the cases are due to group A streptococci alone; the 

remainder are due to mixtures of gram-positive and gram-negative bacteria, both 

aerobic and anaerobic. 


Hospitalization for prompt surgical therapy with extensive incision and excision of 

necrotic tissue is of paramount importance. The initial empiric antimicrobial therapy (eg, 

cefoxitin alone, or clindamycin and gentamicin) should be altered based on the results 

of Gram-stained smears and cultures of tissue biopsies. 

6. Clostridial Myonecrosis 

Clostridal myonecrosis (gas gangrene) is a necrotizing infection of fascia and muscle. 

Infection most commonly occurs following surgical procedures or as a result of 

contaminated wounds. Patients with peripheral vascular disease, diabetes, and 

neoplastic diseases are especially at risk for this infection. 


The incubation period is usually less than 3 days. Severe pain is the earliest symptom, 

followed by intense swelling and edema. A thin hemorrhagic exudate may be seen. The 

skin is exquisitely tender to touch and has a bronze to dusky discoloration that darkens 

with time. Bullae may appear and are filled with serosanguineous fluid. Crepitus is 

uncommon early in the disease. There may be a watery brown discharge with a peculiar 

sweet smell. Systemic symptoms of tachycardia and low-grade fever are usually 

present. Gram-stained smears may demonstrate Clostridium perfringens, but surgical 

exploration is necessary for confirmation of the diagnosis. 


Hospitalization for prompt, complete excision of necrotic muscle is mandatory. Penicillin 

G or chloramphenicol is recommended for the penicillin-allergic patient. Because some 

species of Clostridium are resistant to clindamycin and cefoxitin, these agents should 

not be used as initial empiric drugs in suspected cases of clostridial myonecrosis.

General supportive measures include administration of oxygen and adequate volume 

replacement to counteract shock. Hyperbaric oxygen, though useful, is not a substitute 

for immediate surgery. 

Callahan EF et al: Cutaneous infections. Dermatol Clin 2000;18 (3):497. [PMID: 

10943544] (Review.) 

Dong SL et al: ED management of cellulites: a review of five urban centers. Am J Emerg 

Med 2001;19(7):535. [PMID: 11698996] 

Rhody CR: Bacterial infections of the skin. Primary Care Clinics in Office Practice 

2000;27(2):459. 

Sadick NS: Current aspects of bacterial infections of the skin. Dermatol Clin 

1997;15(2):341. [PMID: 9098643] (Review.) 

Stone DR, Gorbach SL: Necrotizing fasciitis. Dermatol Clin 1997;15(12):213. [PMID: 

9098631] (Review.) 

III. MANAGEMENT OF INFECTIONS CAUSED BY SPECIFIC 

ORGANISMS 

ACUTE MENINGOCOCCEMIA 


• Fever. 

• Petechial rash. 

• Hypotension, shock. 

• Positive blood culture. 



Meningococcemia often follows a mild upper respiratory infection. Onset may be acute 

or subacute, with fever and malaise, with or without symptoms and signs of meningitis 

or septic shock. A petechial rash appears early in the course of the illness, usually on 

the trunk and lower portion of the body and over pressure points (eg, under elastic 

underwear or stockings). The petechiae are small (1-2 mm), irregular, gunmetal gray, 

and often palpable. Petechiae may become confluent (purpura) or may progress to form 

vasculitic ulcers. Mucosal petechiae (eg, on the palpebral conjunctiva) also occur. Early 

in the disease, the number of petechiae correlates with the degree of thrombocytopenia 

and with the probability of disseminated intravascular coagulation. A majority of patients 

with meningococcal disease (80-85%) present with meningitis and most of the 

remaining (15-20%) present with septicemia without meningitis. 

B. Laboratory Findings

Results of routine laboratory studies are consistent with the findings of bacteremia with 

or without sepsis. All patients should be evaluated for disseminated intravascular 

coagulation (prothrombin time, international normalized ratio, partial thromboplastin 

time, fibrinogen level, and fibrin degradation products). Always obtain blood cultures. 

The likelihood of a positive culture is 50% in patients prior to antibiotic treatment and 

only 5% after receiving antibiotics. Other special laboratory tests that may be helpful 

include the following: 

1. Bacteria on stained smear. Meningococci (gram-negative kidney bean-shaped 

diplococci) may be found on the stained smears of the buffy coat of a centrifuged blood 

sample or in material taken from petechial skin lesions. If meningitis has developed, 

meningococci and PMNs may often be seen on careful examination of gram-stained 

smears of CSF. 

2. Blood sample for PCR. 

3. CSF for microscopy, culture, PCR, and antigen detection. Contraindications to lumbar 

puncture include a Glasgow Coma Scale score of less than 13 or deteriorating scores, 

other signs of raised intracranial pressure, focal neurologic signs, impending or 

established septic shock, infection at the planned puncture site, or bleeding disorder. 

4. Throat (nasopharyngeal) swab culture. Throat culture is typically useful only in infants 

and young children. Results are not likely to be significant in an adult because of the 

high nasal carriage rate. 


Rickettsial infections, septicemia caused by organisms other than meningococci (eg, H. 

influenzae, S. pneumonia, S. aureus), and atypical measles may resemble 

meningococcemia. Bleeding diatheses (eg, idiopathic thrombocytopenia purpura) and 

cutaneous vasculitides (eg, Henoch-Schonlein purpura) may also be confused with 

meningococcemia. 

Complications 

A. Septic Shock 

Septic shock is a common complication of meningococcemia. Myocarditis is often found 

at autopsy and may contribute to vascular collapse. 

B. Disseminated Intravascular Coagulation 

Disseminated intravascular coagulation is frequently diagnosed in meningococcemia. 

Therapy is directed mainly at treating the underlying sepsis while giving supportive care. 

C. Adrenal Hemorrhage 

Waterhouse-Friderichsen syndrome is characterized by shock and vascular collapse 

caused by glucocorticoid deficiency due to adrenal hemorrhage. 

D. Metastatic Infection 

Meningitis, arthritis, and pericarditis are common complications.

Treatment 


Empiric treatment with ceftriaxone or cefotaxime is appropriate with a change to 

aqueous penicillin G when meningococcal disease is verified. Chloramphenicol may be 

used if the patient has a history of serious allergy to penicillin. 

B. Steroids 

Treat suspected adrenal insufficiency with doses of injectable hydrocortisone 

(Solu-Cortef) or methylprednisolone (Solu-Medrol). Dexamethasone should be used to 

treat meningococcal meningitis but not meningococcal septicemia without meningitis. 

Disposition 

Patients with meningitis should be hospitalized in an intensive care unit. 

Prophylaxis of Exposed Contacts 

Current recommendations include rifampin orally in 4 divided doses, a single dose of 

oral ciprofloxacin, or a single intramuscular dose of ceftriaxone. 

Cartwright KAV: Early management of meningococcal disease. Infect Dis Clin North Am 

1999;13(3):661. [PMID: 10470561] 

Cohen J: Meningococcal disease as a model to evaluate novel anti-sepsis strategies. 

Crit Care Med 2000;28:S64. [PMID: 11007201] 

ROCKY MOUNTAIN SPOTTED FEVER 


• Fever. 

• Headache. 

• Petechial rash (palms or soles). 


Rocky mountain spotted fever is an acute febrile tick-borne illness caused by Rickettsia 

rickettsii. Although it has been reported in most states in the United States, it is most 

common in the southern Atlantic and south central states and in Oklahoma. Most cases 

occur in warm months, when ticks are most active. Eighty percent of patients have a 

history of tick bite. 



Following an incubation period of about 1 week, there is sudden onset of fever, chills, 

malaise, myalgias, and severe frontal headache. On the 2nd to 5th day of illness, a pink 

macular rash 1-4 mm in diameter appears on the palms, soles, hands, feet, wrists, and 

ankles. Over the next 24-48 hours, the rash becomes petechial, purpuric, and even 

gangrenous and spreads centripetally to involve the rest of the body. (At this stage the 

rash may mimic the lesions of fulminant meningococcemia, although in 

meningococcemia, the skin eruption appears earlier in the disease.) There may be 

diffuse edema due to capillary leakage; hypotension, splenomegaly, and delirium may 

be seen. A common treatment error is to give the patient penicillin for streptococcal 

disease. 


Results on ordinary laboratory testing are not exceptional. The white cell count is 

usually not elevated. Hyponatremia, hypochloremia, and hypoalbuminemia may be 

present. Thrombocytopenia may occur as an isolated finding or in association with 

disseminated intravascular coagulation, which is common in Rocky Mountain spotted 

fever. The CSF is usually normal, but protein levels may be elevated and a few 

mononuclear cells may be present. No specific laboratory test is available for the 

diagnosis of Rocky Mountain spotted fever during the acute stage; therefore, the 

diagnosis must be made on clinical grounds. 

Treatment 

Give tetracycline or doxycycline to adults and older children. Give chloramphenicol to 

children younger than age 8 years. 

Disposition 

Hospitalization is required for all patients except those with the mildest symptoms. 

Severely ill patients should be in an intensive care unit. 

INFECTIVE ENDOCARDITIS 


• Fever, chills. 

• New or changing murmur. 

• Cutaneous lesions. 

General Consideration 

Infective endocarditis denotes infection of the endothelial surface of the heart, most 

often the cardiac valves. The disease may either be acute or subacute and may affect 

normal valves, previously damaged cardiac valves, or prosthetic valves. It is usually 

caused by bacteria, but fungi are also common pathogens in intravenous drug abusers 

with acute endocarditis. Seeding of bacterial emboli or deposition of immune complexes 

in the skin may cause characteristic skin lesions that can alert the physician to the

correct diagnosis before progressive damage to the heart leads to circulatory collapse. 

Common pathogenic organisms include S. viridans, Streptococcus bovis, and the 

HACEK group of gram-negative organisms (Haemophilus, Actinobacillus, 

Cardiobacterium, Eikenella, and Kingella). S. aureus is particularly virulent, and infection 

is associated with a high mortality rate. Staphylococcus epidermis and 

coagulase-negative staphylococci are the leading causes of infective endocarditis in 

patients with prosthetic valves. 



Patients usually present with fever and malaise. In subacute endocarditis, there may be 

a history of anorexia, night sweats, and weight loss. Patients may also present in 

cardiac failure, with a stroke due to cerebral embolism, or with a cold extremity due to 

arterial emboli. Patients with infective endocarditis of the tricuspid valve (usually seen in 

intravenous drug abusers) commonly present with acute, often bilateral, embolic 

pneumonia. Examination of the heart often reveals a murmur, although heart murmurs 

are commonly absent in right-sided endocarditis. 

Characteristic (but not specific) cutaneous and mucosal lesions in bacterial endocarditis 

include conjunctival and palatal petechiae, subungual (splinter) hemorrhages, Osler 

nodes, and Janeway lesions. Osler nodes are tender erythematous nodules with 

opaque centers that appear on the pulp of the fingertips and toes. Janeway lesions are 

nontender red or maroon macules or nodules that develop on the palms and soles. 

Careful ophthalmologic examination may also reveal Roth spots (pale oval areas 

surrounded by hemorrhage) near the optic disk. 

The Duke criteria were developed in 1994 to aid in the diagnosis of endocarditis. The 

diagnosis requires 2 major criteria or 1 major and 3 minor criteria or 5 minor criteria 

(Table 40-13). 


Laboratory findings are variable and nonspecific for infective endocarditis. A 

normochromic normocytic anemia may be present, especially for patients with subacute 

disease. The white cell count may be elevated, especially in acute disease. The 

erythrocyte sedimentation rate is usually elevated. Microscopic hematuria is present in 

30-50% of patients. Immune complex glomerulonephritis with renal failure may occur. 

Transthoracic echocardiography is 98% specific for endocarditis, but sensitivity may be 

less than 60%. Transesophageal echocardiography is close to 100% sensitive for 

examination of native valves and 84-94% sensitive for prosthetic valves. 

Definitive diagnosis depends on isolating the causative organisms in blood cultures; 

however, 5-20% of patients with clinical endocarditis have persistently negative blood 

cultures (termed culture-negative endocarditis). Gram-stained smears of aspirates from 

skin lesions (usually Janeway lesions) occasionally permit rapid diagnosis. In patients 

with embolic pneumonia, Gram-stained smears of sputum may demonstrate the 

causative agent (usually S. aureus); however, in intravenous drug abusers, possible 

concurrent infection with other organisms (streptococci, gram-negative bacilli) must be 

treated pending blood culture results.

Treatment 

In patients who are not acutely ill and in whom symptoms and signs of cardiac failure or 

major emboli are absent, antibiotic therapy may be withheld pending blood culture 

results. In all other patients, empiric antibiotic therapy should be initiated after samples 

of blood, urine, and (when present) sputum and aspirates from skin lesions have been 

obtained for culture. 

A. Abnormal Cardiac Valve or Congenital Heart Disease 

Usual pathogens in patients with abnormal cardiac valves or congenital heart disease 

are S. viridans and group D streptococci. Aqueous penicillin G intravenously is an 

acceptable empiric regimen. Vancomycin intravenously may be substituted for penicillin. 

B. Prosthetic Cardiac Valves 

Many pathogens cause prosthetic cardiac valve endocarditis. Infection occurring less 

than 6 months postoperatively may be caused by S. aureus, S. epidermidis, 

gram-negative aerobic bacilli, diphtheroids, or fungi. Infection occurring more than 6 

months after prosthetic valve insertion is usually caused by S. viridans, aerobic 

gram-negative bacilli, enterococci, or staphylococci. Because growth of some of these 

organisms requires multiple blood cultures using special techniques, it is best to avoid 

early empiric therapy whenever possible. In a patient who requires immediate surgery 

because of hemodynamic decompensation, empiric therapy may be started with 

vancomycin and gentamycin. 

C. Parenteral Drug Abuse 

The usual pathogens in intravenous drug abusers are S. aureus, Pseudomonas spp., 

and streptococci, including group D streptococci. Empiric treatment should include 

vancomycin and gentamicin with substitution for vancomycin with penicillin and nafcillin, 

oxacillin, or methicillin in patients with compromised renal function. 

Disposition 

Patients with suspected bacterial endocarditis should be hospitalized. Obtain 

cardiothoracic surgical consultation for patients with infected prosthetic heart valves, 

new onset of cardiac failure, or emboli in major vessels, because emergency valve 

replacement is often necessary. 

Brook MM: Pediatric bacterial endocarditis: treatment and prophylaxis. Pediatr Clin 

North Am 1999;46(2):275. [PMID: 10218075] 

Giessel BE et al: Management of bacterial endocarditis. Am Fam Physician 

2000;61(6):1725. [PMID: 10750879] 

Ryan EW, Bolger AF: Transesophageal echocardiography (TEE) in the evaluation of 

infective endocarditis. Cardiol Clin 2000;18(4):773. [PMID: 11236165] 

DISSEMINATED GONOCOCCEMIA


• Fever. 

• Skin lesions. 

• Septic arthritis. 

• Positive culture results. 


Gononoccal bacteremia occurs in 1-3% of patients with infections and is the leading 

cause of acute septic arthritis in adults. A presumptive diagnosis based on the 

characteristic clinical picture is usually possible in sexually active patients. 



Disseminated gonococcemia begins as a subacute febrile illness with migratory 

polyarthralgia. Typically, in the first week of illness, 5-40 discrete lesions develop on the 

extremities; the face and trunk are spared. Lesions vary and range from petechiae and 

erythematous, palpable purpura to vesiculopustules with an erythematous halo, and 

they often have necrotic centers. About one fourth of patients have tenosynovitis, 

usually affecting the wrist or ankle. Acute septic arthritis, affecting one or more large 

joints, may follow disseminated gonococcemia or may occur in its absence. 


The white cell count may be elevated. Blood cultures are often positive in disseminated 

gonococcemia. Although Gram stains and culture of skin lesions are generally negative, 

cultures of all sites are negative in as many as 50% of patients, and a presumptive 

diagnosis is based instead on the prompt response to ceftriaxone therapy. 

Treatment 


Give ceftriaxone (1 g intravenously or intramuscularly every 24 hours). 

B. Arthrocentesis 

Arthrocentesis should be performed as often as necessary to prevent accumulation of 

fluid in an infected joint. Open drainage is usually not necessary in gonococcal arthritis. 

Disposition 

Most patients with septic arthritis should be hospitalized, but outpatient treatment with 

daily visits for joint aspiration is an acceptable alternative for reliable patients. Many 

patients with only dermatitis or tenosynovitis may receive outpatient treatment with close 

follow-up. 

TOXIC SHOCK SYNDROME


Toxic shock syndrome results from absorption of toxin from localized S. aureus 

colonization or infection. In the past, most cases occurred in young women who had 

vaginal colonization with S aureus that produce toxic shock syndrome toxin-1 (TSST-1); 

however, nonmenstrual-related cases currently outnumber menstrual-related cases. 

Most of the nonmenstrual cases occur in the postoperative setting. The toxin functions 

as a superantigen that allows the antigen to bind directly to the MHC-II (major 

histocompatibility complex) receptor in a nonspecific fashion. This may result in 

activation of 5-30% of the total T cell population, leading to massive cytokine production. 

Streptococcal toxic shock syndrome (STSS) is similar in appearance to toxic shock 

syndrome but is associated with invasive streptococci infection. A majority of cases of 

STSS have occurred in young, otherwise healthy individuals aged 20-50 years. The 

initial presentation in STSS is localized pain in an extremity with cutaneous signs of a 

soft tissue infection. Toxic shock syndrome rarely shows the signs of cutaneous skin 

involvement commonly seen in STSS. 

The mortality rate in STSS is 5 times higher than in toxic shock syndrome. 


Menstrual-related toxic shock syndrome usually starts abruptly during menses. It occurs 

most commonly in women using tampons or contraceptive sponges. In nonmenstrual 

cases associated with postoperative infection, signs of localized infection in the wound 

may be absent. 


There is a short prodrome consisting of various combinations of the following symptoms 

and signs: fever, myalgias, vomiting, diarrhea, and pharyngitis. Patients then develop 

shock (systolic blood pressure < 80 mm Hg) with fever (> 39 °C) and signs of multiple 

organ dysfunction. At the time of presentation to the emergency department or within 24 

hours of admission to the hospital, a diffuse, blanching, macular erythema appears, 

accompanied by signs of mucous membrane inflammation (pharyngitis, conjunctivitis, 

vaginitis, and strawberry tongue). The rash fades in about 3 days, but desquamation of 

the hands and feet occurs in all patients 5-12 days after the rash disappears. Patients 

typically prefer to remain motionless in bed because of intense myalgias. Confusion and 

agitation occur in about half of patients. Pedal edema is common. 


Laboratory findings reflect dysfunction of several organ systems. There may be 

leukocytosis and thrombocytopenia, elevated blood urea nitrogen and creatinine levels, 

hyperbilirubinemia, elevated hepatic enzymes, or sterile pyuria. The prothrombin, INR, 

and partial thromboplastin times may be elevated, with or without thrombocytopenia. 

Other laboratory abnormalities include acidosis, elevated creatine kinase levels 

(indicating rhabdomyolysis), hypocalcemia, decreased serum albumin and total protein 

due to capillary leakage, and elevated liver enzyme levels. Cultures of material from the 

vagina or cervix are usually positive for S. aureus. Blood cultures are negative in 85% of 

patients with toxic shock syndrome and in 50% of patients with STSS.


Remove the vaginal tampon or nasal or wound packing if present. Begin volume 

replacement with saline or colloid solutions and with vasopressors, if necessary. Admit 

the patient to an intensive care unit, and monitor hemodynamic status. Start treatment 

with a first-generation cephalosporin, penicillinase-resistant synthetic penicillin, or 

vancomycin intravenously. Some studies have shown intravenous immunoglobulin to be 

useful in treating STSS. 

GROUP A STREPTOCOCCAL INFECTIONS ASSOCIATED WITH A TOXIC 

SHOCK-LIKE SYNDROME 

An infection with group A streptococci that is remarkable for severity of local tissue 

destruction, life-threatening systemic toxicity, and toxic shock-like syndrome has been 

described in adults. Clinical isolates frequently produce pyrogenic exotoxin A. The portal 

of entry may be the skin or the mucous membranes, or infection may occur subsequent 

to a surgical procedure, but many patients do not have obvious evidence of a portal of 

entry. 



Pain is the most common initial symptom and is frequently severe and abrupt in onset. 

The pain usually involves the extremity but may be intra-abdominal. Before symptom 

onset, some patients complain of an influenza-like syndrome characterized by fever, 

chills, myalgia, vomiting, and diarrhea. Patients often have oral temperatures above 37 

°C, may have confusion that rapidly deteriorates into coma, or may be combative. 

Shock is apparent at the time of presentation or within hours with evidence of 

hypotension, renal dysfunction, and respiratory failure. Most patients present with soft 

tissue infection, such as cellulitis or necrotizing fasciitis. Deeper infections may be 

present, including osteomyelitis, myometritis, peritonitis, suppurative phlebitis, or 

endophthalmitis. A major difference between these patients and patients with STSS is 

that the former have extensive soft tissue infection and bacteremia. The mortality rate is 

approximately 30%. 


Laboratory findings reflect dysfunction of several organ systems. There may be 

leukocytosis and thrombocytopenia. The hematocrit is initially normal but may drop 

within 48-72 hours. Serum creatinine and creatine kinase levels are elevated, but 

calcium and albumin levels are low. Microscopic hematuria is often present and 

correlates with the presence of renal impairment. Group A streptococci are cultured 

from the blood, body fluid, or tissues of all patients who have not received antibiotic 

therapy. 


Intensive fluid replacement, central venous or pulmonary capillary wedge pressure 

monitoring, and timely surgical debridement are essential. Start antibiotic therapy with

intravenous penicillin or a cephalosporin. Admit patients to the intensive care unit. 

Manders SM: Toxin-mediated streptococcal and staphylococcal disease. J Am Acad 

Dermatol 1998;39(3):1725. [PMID: 10750879] (Review.) 

LYME BORRELIOSIS 

Lyme borreliosis (Lyme disease, Lyme arthritis) is a chronic disease caused by the 

spirochete Borrelia burgdorferi. Transmission is by several tick vectors (Ixodes, 

Amblyomma, Rhipicephalus) and occurs throughout the United States; the highest 

prevalence is in the Northeast and Midwest. It has been recognized in Europe, Asia, 

and Australia. In stage 1, a rash is present, sometimes accompanied by fever. Timely 

treatment at this stage may prevent disease progression. 



Between 3 and 32 days following the tick bite, which the patient may not notice, a 

gradually expanding area of redness with clearing (erythema migrans) occurs at the bite 

site. The involved skin is warm but not particularly tender to touch. About half of affected 

patients will develop smaller lesions of similar morphology at areas remote from the bite 

site over ensuing days to weeks. 

In stage 1 disease (erythema migrans), often there are fever, chills, malaise, and 

regional lymphadenopathy. In stage 2 (days to weeks after infection), symptoms related 

to the multisystemic nature of Lyme borreliosis often appear, such as meningitis, 

hepatitis, sore throat, dry cough, heart block and other cardiac abnormalities, 

musculoskeletal pain, and neuropathy. Fatigue and lethargy are prominent and may 

persist for months after the skin lesions have disappeared. 

A persistent illness (stage 3) may linger for months to years and usually involves the 

musculoskeletal system (chronic arthritis), neurologic system (both central and 

peripheral), and skin (acrodermatitis chronica atrophicans). Stage 3 illness responds 

more slowly to treatment, and treatment at this stage has higher failure rates compared 

to stages 1 and 2. 


Laboratory testing is currently not reliable or standardized. Diagnosis depends on 

recognition of the pathognomonic rash. Serodiagnosis by either indirect 

immunofluorescence or ELISA may be negative in early infection. Nonspecific 

laboratory abnormalities include an elevated erythrocyte sedimentation rate, mild 

anemia, and transient elevations in SGOT (AST), SGPT (ALT), and lactate 

dehydrogenase enzyme levels. 


The treatment of choice for early Lyme borreliosis is tetracycline for at least 10 days, or 

for 20 or 30 days if symptoms persist or recur. For children under age 12 years, give 

amoxicillin or penicillin V. In pediatric patients with penicillin allergy, give erythromycin

for 15-30 days. For more serious disease (eg, Lyme carditis or meningitis), use 

intravenous therapy with ceftriaxone or penicillin G for 14-21 days. 

Edlow JA: Lyme disease and related tick-borne illnesses. Ann Emerg Med 

1999;33(6):680. [PMID: 10339684] (Review.) 

Gayle A: Tick-borne diseases. Am Fam Physician 64(3):1461. [PMID: 11515835] 

(Review.) 

IV. AIDS & HIV INFECTION (See Table 40-14. ) 


AIDS patients can present in extremis, with shock, acute respiratory distress syndrome, 

or multiple organ failure secondary to overwhelming infection. Acute adrenal failure can 

occur secondary to CMV and tuberculosis affecting the adrenals. AIDS and HIV can 

complicate virtually any organ system, and a detailed history and physical examination 

are necessary. AIDS is the end stage of chronic infection by HIV, a lymphotrophic 

retrovirus. Transmission occurs by sexual contact, perinatally, and by contact with 

infected blood. The virus causes slow destruction of the helper T cell subset and in most 

affected individuals leads to fatal immunosuppression. 


Assess mental status carefully because mental status changes may be early signs of 

CNS infection or neuropsychiatric problems such as HIV dementia. Examine the eyes 

carefully for retinal lesions such as yellowish exudates and large hemorrhages seen in 

CMV or toxoplasma retinitis. The presence of nuchal rigidity may not be a presenting 

symptom of meningitis in an HIV-positive patient but should be assessed. Examine the 

mouth for evidence of oral candida (thrush) or leukoplakia, herpes, and Kaposi 

sarcoma. Pulmonary examination could reveal tachypnea or unequal breath sounds. A 

cardiac examination is essential in evaluating for murmurs that could be secondary to 

an infectious endocarditis (especially in intravenous drug abusers). Examine genitalia 

for lesions such as the chancre of syphilis. An anorectal examination can reveal fissures 

or fistulas, perianal abscesses, or prostatitis. A careful neurologic examination can 

disclose a CNS lesion that could be either infectious or neoplastic in origin. 

Organ System-Specific Presentations 

A. Pulmonary 

The most common presenting complaint for an HIV-positive patient is pulmonary in 

origin. P. carinii pneumonia (PCP) is the most common identifiable cause of death in 

AIDS patients and remains common (70% of HIV-positive patients will get it, and 70% of 

those will get reinfected). PCP is typically associated with fever and nonproductive 

cough, in contrast to bacterial pneumonia, in which the cough tends to be productive. 

Other causes of pulmonary pathology include tuberculosis, CMV, Cryptococcus, 

Histoplasma, and neoplasms (Kaposi sarcoma, lymphoma). 

B. Neurologic

Ninety percent of patients with AIDS and 10-20% of HIV-positive patients will present 

with neurologic symptoms at some point (eg, seizure, mental status change, headache). 

It is crucial to rule out infectious causes (Cryptococcus, bacterial meningitis, 

Histoplasma, CMV, progressive multifocal leukoencephalopathy, HSV, neurosyphillis, 

tuberculosis) but also to consider HIV encephalopathy (also known as AIDS dementia or 

subacute encephalitis; occurring in up to 15% of AIDS patients), lymphoma, 

cerebrovascular accident, and metabolic encephalopathy. 

C. Gastrointestinal 

Fifty percent of HIV-positive patients will have a gastrointestinal complication, 

presenting with complaints such as odynophagia, abdominal pain, bleeding, or diarrhea. 

Common infections include Shigella, Salmonella, E. coli, Campylobacter, 

Cryptosporidium, Isospora, CMV, or Mycobacterium avium complex (MAV). Bacterial 

infection is typically fulminant. If bacterial infection is suspected, give a fluoroquinolone 

empirically. Hepatitis is commonly seen secondary to high rates of coinfection with 

hepatitis B and C but can also be due to CMV, Cryptosporidium, or MAV. Proctocolitis is 

common in HIV-positive patients, and unless a careful examination is carried out, this 

diagnosis is easily overlooked (common causative organisms include Campylobacter, 

Shigella, Salmonella, gonococcus, and Chlamydia). 

D. Systemic 

Acute HIV infection causes an acute flulike illness in 50-90% of patients. Patients may 

present with fever, weight loss, adenopathy, or fatigue. MAV causes disseminated 

disease in up to 50% of AIDS patients (with fever, weight loss, and diarrhea). Fever is a 

common symptom and, in the absence of organ-specific clues, needs to be evaluated 

carefully. It may be due to HIV infection itself or another infectious cause. Patients with 

PCP may present with fever in the absence of respiratory symptoms. Cryptococcal 

meningitis can begin as fever without headache. Also consider Mycobacterium 

tuberculosis, MAV, endocarditis (especially if the patient is an intravenous drug abuser), 

and fever associated with neoplasm (lymphoma). 

E. Ophthalmologic 

The most common ocular finding is retinal microvasculopathy ("cotton wool spots"). 

CMV retinitis is common, and patients with this disorder present with visual loss, 

blindness, photophobia, scotomata, and floaters. On examination, CMV retinitis appears 

as fluffy white perivascular lesions with hemorrhage. HSV ophthalmicus is a worrisome 

complication; patients present with conjunctivitis, episcleritis, iritis, and keratitis. 

F. Renal 

HIV-positive patients commonly display prerenal azotemia secondary to volume 

depletion but also must deal with the consequences of drug nephrotoxicity, HIV 

nephropathy (focal segmental glomerulosclerosis), and renal tubular acidosis 

(hyperchloremic metabolic acidosis non-anion-gap acidosis), which are common in HIV 

infection and AIDS. 

G. Skin 

Patients can display a multitude of symptomology related to the skin. Infections are 

common (eg, Staphylococcus, Pseudomonas, HSV, herpes zoster, syphilis, 

intertriginous Candida), as are xerosis or pruritus associated with HIV infection.

H. Drug Reactions 


Laboratory Data 

Obtain an arterial blood gas measurement to aid in investigating pulmonary complaints 

(PaO 2 < 60 or oxygen saturation < 90 is suggestive of pneumonitis). A fall in oxygen 

saturation of greater than 3% with activity is 80% sensitive for PCP. A chest x-ray can 

be useful in narrowing the differential diagnosis of pulmonary complaints based on 

appearance, but these findings are often nonspecific. Chest x-rays are read as negative 

in 15-20% of patients with documented PCP. Obtain blood and urine cultures 

(remember fungal and mycobacterial studies) as needed to evaluate systemic 

complaints or for focal complaints related to possible infection. Sputum culture and 

Gram stain are particularly useful for pulmonary complaints. 

A complete blood count is helpful as a general index to evaluate for infection and for 

hematologic complications of HIV infection. In the absence of a CD4 count, an absolute 

lymphocyte count can be helpful. If the total lymphocyte count is less than 1000, then 

the CD4 is likely less than 200. CMV or MAC usually do not occur unless CD4 is less 

than 50. CSF should be sent for typical studies such as opening-closing pressures, cell 

count, glucose, protein, Gram stain, and culture, as well as other studies in selected 

cases: India ink, viral culture, fungal culture, Toxoplasma and cryptococci antigens, and 

coccidioidomycosis titer. 

Evaluation of gastrointestinal complaints should proceed by sending stool for Wright 

stain, ova and parasite testing, acid-fast stain, and culture. Send standard stool cultures, 

Thayer-Martin culture, Chlamydia culture or immunoassay, and viral culture for HSV if 

proctocolitis is suspected on clinical examination. 

HIV-positive patients should receive a head CT scan prior to lumbar puncture if mental 

status changes are present. MRI scans are superior to CT scan for detection of cerebral 

toxoplasmosis and other lesions. 

Treatment 

Manifestations of HIV infection can range from asymptomatic to life-threatening and can 

affect any organ system. Because of the complexity of opportunistic infections and 

malignancies occurring in HIV-positive patients, the diagnosis often cannot be made in 

the emergency department. In general, admit patients if a fever of unknown source or 

CNS findings are present or in the event of seizure, suspected PCP, hypoxia worse than 

baseline, intractable diarrhea, disseminated Herpes zoster, marrow suppression, 

extreme weakness, or inability to care for self or obtain follow-up. 

Disposition 

Disposition depends on the organ system in question. Ensure that the patient is 

adequately resuscitated. Final diagnoses may require biopsy or complicated studies to 

obtain a final diagnosis.

Aftergut K, Cockerell CJ: Update on the cutaneous manifestations of HIV infection. 

Dermatol Clin 1999;17(3):445. [PMID: 10410852] (Review.) 

Barbaro G et al: HIV-associated cardiovascular complications: a new challenge for 

emergency physicians. Am J Emerg Med 2001;19(7):566. [PMID: 11699002] (Review.) 

Patton LL, van der Horst C: Oral infections and other manifestations of HIV disease. 

Infect Dis Clin North Am 1999;13(4)445. [PMID: 10410852] (Review.) 

Stone VE: Primary care of the patient with HIV/AIDS. Infect Dis Clin North Am 

2000;14(4):967. [PMID: 11144647] (Review.) 





MD 

I. IMMEDIATE MANAGEMENT OF LIFE-THREATENING PROBLEMS

Table 40-1. Organisms and empiric therapy for sepsis. 

Major 

Community- 

Acquired 

Pathogens 

Major 

Nosocomial 

Pathogens 

Escherichia coli Aerobic gram-negative rods 

Bacteroides fragilis Anaerobes 

Candida spp. 

Escherichia coli 

Klebsiella spp. 

Enterobacteria 

Proteus spp. 


Aerobic gram-negative 

enterococci 

Lung Macrolide and thi 

cephalosporin 

OR 

levofloxacin 

Skin and Soft Tissue Vancomycin ± im 

OR 

piperacillin-tazoba 




MD 

TABLES 

Table 40-1. Organisms and empiric therapy for sepsis.

Table 40-2. Contraindications to lumbar puncture. 





MD 

TABLES 

Table 40-2. Contraindications to lumbar puncture.

Table 40-3. Cerebrospinal fluid (CSF) findings in meningitis. 

Normal 

Viral 

Meningitis 

Tuberculous 

Meningitis 

WBC/mL > 1000 

0-15 < 50 < 50 Lymphocytes 

(%) 

< 50 

45-65 45-65 30-45 CSF/blood 

glucose ratio 

< 0.4 

20-45 50-100 100-500 Pressure > 25-30 





MD 

TABLES 

Table 40-3. Cerebrospinal fluid (CSF) findings in meningitis.

Table 40-4. Some causes of acute lymphocytic meningitis. 





MD 

TABLES 

Table 40-4. Some causes of acute lymphocytic meningitis.

Table 40-5. Recommended empiric antimicrobial therapy for bacterial meningitis based on age. 

Major Pathogens 

Neisseria meningitidis, 

Streptococcus pneumoniae, 

Haemophilus influenzae 

Alternative 

Regimens 

Meropenem or 

chloramphenicol 

Streptococcus pneumoniae, Ampicillin plus fluoroquinolone 

Listeria 

(ciprofloxacin, levofloxacin) 

monocytogenes,gram-negative 

bacilli 


18-50 years 

Less than 3 months 




MD 

TABLES 

Table 40-5. Recommended empiric antimicrobial therapy for bacterial 

meningitis based on age.

Table 40-6. Pathogen-specific therapy for patients who have bacterial meningitis. 

Preferred 

Regimen Duration 

Penicillin G (or ampicillin) 14-21 days 

Ceftriaxone (or cefotaxime) 7-10 days 

Ampicillin plus gentamicin 14-21 days 

Penicillin G (or ampicillin) 7-10 days 

Ceftriaxone (or cefotaxime) 10-14 days 

Vancomycin plus ceftriaxone (or cefotaxime) 10-14 days

Table 40-7. Treatment of pneumonia. 

Viruses 

Cytomegalovirus, rubella, herpes simplex virus 

Bacteria 

Group B streptococci 

Listeria spp. 

Coliforms 

Staphylococcus aureus 

Pseudomonas aeruginosa 

Other 

Chlamydia trachomatis 

Chlamydia trachomatis 

RSV and other respiratory viruses 

Bordetella spp. 

RSV and other respiratory viruses 

Streptococcus pneumoniae 


Chlamydia spp. 

Mycoplasma spp. 


Respiratory viruses 


Mycoplasma spp. 

Chlamydia spp. 

Cause Alte 

For chlamydial infection, use er 

Clarithromycin 

Intensive care unit admission 

Cefotaxime or ceftriaxone plus 

Hospitalization 

Cefuroxime plus azithromycin 

Mycoplasma spp. and respiratory viruses are most common Doxycycline or azithromycin 

Fluoroquinolone or Augmentin o 

Cefoxitin or ticarcillin clavulanat

Table 40-8. Treatment of septic arthritis. 

Cause 


Enterobacteriaceae 

Group B streptococci 

Neisseria gonorrhoeae 


Streptococcus pyogenes 



Alternative 

Treatment 

Antistaphylococcal penicillin + amino-glycosi 

Vancomycin + third-generation cephalospori 

Neisseria gonorrhoeae Nafcillin if gram-positive organisms are found 


Antistaphylococcal penicillin + ciprofloxacin 

Streptococci 

Gram-negative bacilli 

Neisseria gonorrhoeae 





MD 

TABLES 

Table 40-8. Treatment of septic arthritis.

Table 40-9. Empiric antibiotic therapy for urinary tract infection. 

First-Line Therapy Comments 

Fluoroquinolone 

Intravenous fluoroquinolone, ampicillin + gentamicin, 

third-generation cephalosporin, or antipseudomonal 

penicillin 

Ampicillin + gentamicin, piperacillin-tazobactam 

Ticarcillin-clavulanate, imipenem, or meropenem 


Rule out obstruction 




MD 

TABLES 

Table 40-9. Empiric antibiotic therapy for urinary tract infection.

Table 40-10. Criteria for diagnosis of pelvic inflammatory disease. 





MD 

TABLES 

Table 40-10. Criteria for diagnosis of pelvic inflammatory disease.

Table 40-11. Antimicrobial therapy for pelvic inflammatory disease. 

Inpatient Treatment 

Cefoxitin IV + doxycycline IV 

Cefotetan IV + doxycycline IV 

Clindamycin IV + gentamicin IV + doxycycline IV 





MD 

TABLES 

Table 40-11. Antimicrobial therapy for pelvic inflammatory disease.

Table 40-12. Outpatient treatment for herpes infections. 

Agent and Dosing 

Acyclovir, 200 mg PO 5 

times a day for 10 days 

Acyclovir, 200 mg PO 5 

times a day for 5 days 

Acyclovir, 400 mg PO 

bid 


Famciclovir, 250 mg PO tid for 5-10 

days 

Valacyclovir, 500 mg PO bid for 5 

days 

Valacyclovir, 1000 mg PO qd 




MD 

TABLES 

Table 40-12. Outpatient treatment for herpes infections.

Table 40-13. Duke criteria for diagnosis of infective endocarditis. 





MD 

TABLES 

Table 40-13. Duke criteria for diagnosis of infective endocarditis.

Table 40-14. Common HIV emergencies. 

Common Causes 

Pulmonary 

Cough, dyspnea, pulmonary 

infiltrates 

Toxoplasma gondii Seizures; focal neurologic deficit; 

encephalopathy, hydrocephalus 

Neutropenia with sepsis 

Cryptococcal infection 

Disseminated 

mycobacterial infection 

(several species) 

Sinusitis 

Pneumocystis carinii 

Cytomegalovirus 

Salmonella spp. 

Thrombocytopenia 

Intestinal or pulmonary 

Kaposi sarcoma (rare) 



Diarrhea, dehydration 

Arterial blood gas measurements 

Chest x-ray 

Giemsa, acid-fast, and 

gram-staining of sputum; culture 

Bronchoscopy with lavage with 

biopsy 

Lumbar puncture (after CT scan) 

Brain biopsy 

Culture of stool and microscopic 

examination for parasites 




MD 

TABLES 

Table 40-14. Common HIV emergencies.

Table 40-15. Side effects of HIV antiviral therapy. 

Side Effects 

Nausea, vomiting, fever, rash, dizziness 

Elevated LFTs, diarrhea, nausea 

Rash, nausea, headache, vomiting 

Rash, headache, fatigue 

Diarrhea, pancreatitis, neuropathy, elevated LFTs 

Central nervous system effects, rash, elevated LFTs 

Nausea, headache, stomatitis, white blood cells, platelets, 

hemoglobin 

Nephrolithiasis, elevated bilirubin, nausea, abdominal pain 

Headache, fatigue, nausea 

Diarrhea, nausea 

Rash, nausea, headache, elevated LFTs 

Nausea, headache, diarrhea, elevated LFTs 

Diarrhea, nausea, elevated LFTs 

Neuropathy, elevated LFTs 

Neuropathy, rash 

Headache, neutropenia, nausea, myalgias

41. Metabolic & Endocrine Emergencies - Micheal D. Rush, MD, & 

Wason W. S. Louie, MD 


METABOLISM 

Disorders of carbohydrate metabolism represent a broad category of emergent and 

potentially emergent conditions. Most are related to diabetes and associated 

complications. They may also occur as a result of or be mimicked by drug or alcohol 

toxicity, multisystem trauma, head injury, cardiovascular disease, cerebrovascular 

disease, and infection. Patients may present with coma or altered mental status or look 

remarkably well clinically yet be on the brink of metabolic decompensation. These 

disorders may be a challenge not only to diagnose early but also to treat in the most 

severe cases. Often they are precipitated by underlying illness or injury. Early diagnosis 

and effective treatment of these underlying entities is a crucial element in resolving the 

metabolic decompensation. 

DIABETIC KETOACIDOSIS 


• Signs and symptoms include fatigue, tachypnea (Kussmaul respiration), tachycardia, 

altered mental status, abdominal pain, vomiting, polyuria, and polydipsia. 

• Arterial pH < 7.3, serum glucose = 250 mg/dL, and serum bicarbonate = 15 mEq/L. 


Diabetic ketoacidosis (DKA) is the most common acute life-threatening complication of 

diabetes. It is more commonly seen in type 1 diabetes but may occur rarely in type 2 

diabetes. It is a result of insulin-producing ß cell failure in the islets of Langerhans 

located in the pancreas. This results in insulin deficiency, which then shifts the normal 

metabolic processes from using glucose for fuel to using lipids for fuel. Metabolic stress, 

most commonly from trauma or infection, may accelerate this process. The result is 

osmotic diuresis from severe hyperglycemia leading to dehydration, electrolyte loss, and 

metabolic acidosis, which results from a combination of dehydration and the 

overproduction of ketone bodies from fat metabolism, primarily ß-hydroxybutyrate and 

acetoacetate, which further acidify the blood. Eventually, hypovolemia leads to 

inadequate blood flow to the kidneys and limits renal excretion of glucose. As serum 

osmolality rises above 320 mOsm/L, lethargy and coma may ensue. If left untreated, 

severe metabolic acidosis from DKA can lead to depression of cardiovascular function, 

severe hyperkalemia, and potentially lethal cardiac dysrhythmias. 

Clinical Findings

A. History 

Determine if the patient has diabetes. Direct the history to ascertain potential 

precipitating causes of DKA: 

• Recent or current infection of any type (most common) 

• Injury or trauma 

• Acute coronary syndrome or myocardial infarction 

• Transient ischemic attack or stroke 

• Medications (corticosteroids, thiazides, or sympathomimetics) 

• Acute or acute-on-chronic pancreatitis 

• Alcohol or drug abuse 

• Psychosocial factors, such as depression or inability to afford medications, limiting 

compliance 

• Noncompliance with insulin regimen 


Symptoms and signs include general fatigue and weakness, abdominal pain (be aware 

of precipitating causes such as appendicitis, cholecystitis, pancreatitis, and pregnancy), 

and Kussmaul respirations (rapid deep respirations attempting to compensate for 

acidosis). Patients may have a fruity or acetone-like smell to the breath. Other findings 

include polyuria, polydipsia, and polyphagia (the body's attempt to compensate for 

inefficient use of fuel and water loss in excreting glucose); nausea and vomiting 

(hemorrhagic gastritis occurs in 25% of patients); altered mental status ranging from 

agitation to coma; hypothermia (may be fever equivalent; if present, prognosis is poor). 


1. Key findings—Key laboratory features include serum glucose = 250 mg/dL, 

ketonuria (ketonemia is unreliable unless ß-hydroxybutyrate is measured), serum 

bicarbonate = 15 mEq/L, and arterial pH < 7.3 (venous pH has been shown to be a 

consistent, acceptable substitute for arterial pH). Limit arterial blood gas analysis to 

patients in whom oxygenation or ventilation is a concern or when diagnosis may be 

uncertain. 

2. Serum potassium—Serum potassium is often elevated initially despite total body 

deficits estimated at 3-5 mEq/kg body weight. Additionally, potassium may be lost 

through vomiting or urinary losses. Metabolic acidosis shifts potassium out of the cells 

and into the extracellular fluid space. Because insulin therapy drives potassium back 

into the cells, serum potassium should be monitored every 2 hours during the first 8 

hours of treatment. Low initial serum potassium (< 3.2 mEq/L) represents a severe total 

body potassium deficit, and emergent repletion of potassium is essential to prevent 

life-threatening cardiac dysrhythmias.

3. Serum sodium—Serum sodium is usually low from losses in the urine and vomitus 

coupled with dilution effects of water being drawn out of the cells into the extracellular 

compartment by hyperglycemia. This effect can be corrected by adding 1.8 mEq/L to the 

serum sodium concentration for each 100 mg/dL the serum glucose concentration is 

above normal. Serum sodium may also be artificially lowered by severe 

hypertriglyceridemia. Although sodium deficits may approach 7-10 mEq/kg, sodium 

repletion must proceed gradually to avoid cerebral edema, especially in children. 

4. Serum phosphate—Serum phosphate is usually normal or elevated despite deficits 

approaching 1 mmol/kg body weight. Routine phosphate repletion has not been shown 

to improve clinical outcomes in DKA and is not indicated. There is significant potential to 

cause severe hypocalcemia, which may manifest without the typical finding of tetany. 

Severe hypophosphatemia (< 1 mg/dL) may cause skeletal, cardiac, and respiratory 

muscle depression; phosphate should be replaced in this circumstance. 

5. Other important laboratory findings— 

a. Anion gap—Anion gap is useful to assess severity of acidosis and to follow progress 

of therapy. The anion gap is obtained from the following formula: 

Normal values are = 10. Effective serum osmolality may be estimated from the following 

formula: 

Values of at least 320 mOsm/kg are associated with central nervous system 

involvement, usually lethargy or coma. Below this value, other causes for lethargy or 

coma such as head injury, subarachnoid hemorrhage, or cerebrovascular accident 

should be investigated. This value may also be used to diagnose hyperglycemic 

hyperosmolar nonketotic syndrome (HHNS) or ingestions of ethanol or other osmotically 

active substances such as ethylene glycol or other alcohols. 

b. Serum ketones—Standard laboratory tests measure only acetoacetate. The primary 

ketone body formed in DKA initially is ß-hydroxybutyrate, which is broken down into 

acetoacetate in the presence of insulin. Serum ketones are not reliable as a diagnostic 

test because initially they may be reassuringly negative even in a severely ill DKA 

patient. They are not useful to track therapy because in most cases they will increase as 

the patient improves. 

c. Blood urea nitrogen (BUN) and creatinine—These levels may be elevated because

of severe dehydration, even to the point at which acute tubular necrosis and renal failure 

occur. If these levels are elevated on initial chemistries, be sure to establish urine output 

prior to initiating potassium repletion. 

d. Electrocardiogram—The electrocardiogram (ECG) may reveal severe electrolyte 

disturbances or diagnose cardiac ischemia or myocardial infarction, a common 

precipitating cause of DKA or HHNS in older patients. History and physical examination 

should dictate whether to order cardiac enzymes. 


Given the similar nature of treatment for DKA and HHNS, treatment and patient 

disposition for these two entities are presented together in the discussion of HHNS, 

below. 

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME 


• Most symptoms relate to severe dehydration. 

• Kussmaul respirations and abdominal pain are unusual findings. 

• Absence of acidosis, small or absent serum ketones, and hyperglycemia usually = 600 

mg/dL. 


HHNS, formerly called hyperglycemic hyperosmolar nonketotic coma or hyperosmolar 

coma, is differentiated from DKA in that patients with HHNS have enough insulin activity 

to prevent lipolysis and ketogenesis. DKA often manifests suddenly over hours to a few 

days, whereas HHNS is more insidious, developing over several days to weeks. Also, in 

mild or early DKA, mental status is normal, whereas in HHNS, mental status is nearly 

always abnormal, ranging from confusion to stupor or coma. HHNS occurs most 

commonly in older (> 65 years) patients who may or may not have diagnosed diabetes 

and who are often residents in chronic care facilities. Symptoms of hyperglycemia such 

as frequent urination may be attributed to aging, and the thirst response may be 

depressed as normal physiology of aging or unrecognized secondary to dementia. 

Patients also may not have or be given proper access to fluids. 

Usually, a severe physiologic stressor, most commonly infection, is a precipitating 

cause. Myocardial infarction, cerebrovascular accident, trauma, and drug effects or 

interactions may also precipitate HHNS. Electrolyte deficits are similar in DKA and 

HHNS, and the free water loss is on the order of 9 L in HHNS compared with an 

average water loss of 6 L in DKA. 


A. History

Risk factors for HHNS include age of 65 years or older, residence in a chronic care 

facility or nursing home, change in diabetes regimen, addition of medications that may 

elevate glucose levels (eg, corticosteroids, thiazides, anticonvulsants, 

sympathomimetics), recent or current infection, and dementia. 


Symptoms and signs include polydipsia, polyuria, or polyphagia; generalized weakness; 

altered mental status (clouded thinking to confusion to lethargy or coma); dry mucous 

membranes; poor skin turgor; and delayed capillary refill. Kussmaul respiration is 

usually not present unless metabolic acidosis from sepsis or hypoperfusion occurs. 

Abdominal pain is not a typical finding in HHNS (in contrast to DKA); its presence merits 

aggressive investigation for precipitating causes. Acute cholecystitis and appendicitis 

may be insidious and occur atypically in elderly patients. 


1. Key laboratory findings—Key findings to diagnose HHNS and differentiate it from 

DKA include the following: 

• Serum glucose is usually = 600 mg/dL. 

• Urine or serum ketones are small or absent (a small amount of ketone may be 

detected secondary to starvation). Glucosuria is prominent. 

• Serum bicarbonate is usually > 15 mEq/L. 

• pH is usually > 7.30. 

• The anion gap may be variable depending on precipitating cause but is usually = 10 

• Effective serum osmolality is = 320 mOsm/kg. 

2. Serum sodium—In the early stages of HHNS, serum sodium findings are similar to 

those in patients with DKA. Urinary losses and fluid shifts out of the cell and into the 

extracellular compartment create hyponatremia usually in the 125-130 mg/dL range 

(remember to correct by adding 1.8 mg/dL for every 100 mg/dL glucose above normal). 

As water losses worsen, hypernatremia ensues and osmolality rises, leading to 

progressive lethargy and coma. 

3. Serum potassium—Potassium levels will most commonly be normal or low, unless 

renal failure is present. An associated metabolic acidosis driving potassium out of the 

cells is usually not present in HHNS. 

4. Blood urea nitrogen and creatinine—BUN is often markedly elevated. 

Gastrointestinal bleeding may also elevate BUN, and this is a possible precipitating 

cause of HHNS in elderly patients. 

5. Other studies—Other studies should be dictated by the history and physical 

examination findings, but have a low threshold to obtain serial ECGs and cardiac

enzymes to rule out cardiac ischemia or myocardial infarction, computed tomography 

(CT) scan of the head to rule out cerebrovascular accident or subdural hematoma, and 

rectal exam and nasogastric tube to look for gastrointestinal hemorrhage. Order an 

abdominal CT scan or ultrasound to work up abdominal pain if the patient is stable 

enough to leave the emergency department. 

Treatment 

Initial treatment for DKA and HHNS is similar. The various aspects of therapy should be 

initiated concurrently whenever possible. Differences in therapy of DKA and HHNS are 

noted when appropriate. Frequent reassessment of vital signs, mental status, and 

laboratory parameters are essential to successful therapy of DKA and HHNS. 

A. Resuscitation Issues 

Assess the airway and consider obtaining arterial blood gases for any patient who 

appears not to be oxygenating or ventilating properly or who is obtunded or comatose. 

Consider proceeding directly to rapid-sequence intubation in patients who are 

unresponsive or who have depressed gag or swallow reflexes. Avoid succinyl choline if 

hyperkalemia is suspected based on peaked T waves on ECG or rhythm strip. 

Oxygen therapy is indicated for all DKA or HHNS patients at flow rates adequate to 

maintain oxygen saturation above 96% or PO 2 = 70 mm Hg. Hypoxia should trigger an 

investigation for aspiration, pneumonia, or pulmonary edema in the differential diagnosis 

of precipitating causes. 

B. Fluid Therapy 

Fluid therapy is dictated by 3 parameters: vital signs, corrected serum sodium, and 

serum glucose. Overall fluid deficits approach 6-10 L in most patients, and daily 

maintenance fluid requirements must also be considered. Multiple, preferably large-bore 

(= 18-gauge), intravenous lines are essential. Central venous access should be strongly 

considered. 

Hypotension should prompt a bolus of 1 L of 0.9% NaCl solution to restore blood 

pressure to at least 90 mm Hg. 

Caution: Assess patients for cardiogenic shock and renal failure before giving large 

volumes of intravenous fluids. Reassess patients frequently for adequate urine output 

and absence of pulmonary edema or congestive heart failure. Hemodynamic monitoring 

(Swan-Ganz) is indicated to facilitate fluid management if cardiogenic shock is present. 

In the absence of hypotension, administer 1-1.5 L (~ 15-20 mL/kg) normal saline in the 

first hour of therapy. 

Using the serum sodium corrected for excess glucose: 

• If serum sodium is high or normal, give 0.45% NaCl or half normal saline at a rate of 

5-15 mL/kg for the next liter of fluids. 

• If serum sodium is low, give 0.9% NaCl or normal saline for next liter of fluids at a rate 

of 5-15 mL/kg.

• Once serum glucose reaches approximately 250 mg/dL, 5% dextrose in 0.45% NaCl is 

the fluid of choice at a rate of 250 mL/h; or use 5% dextrose in normal saline if the 

corrected serum sodium remains low. 

Follow serum electrolytes, venous pH, BUN and creatinine, and glucose, and calculate 

the osmolality frequently (every 2 hours in the first 8 hours) as measures of progress in 

therapy. The aim is a decrease in serum osmolality of no more than ~ 3 mOsm/kg/h. 

Urine output may be unreliable while glucose levels remain high secondary to osmotic 

diuresis. Once glucose levels approach normal, urine output may be used to guide 

therapy; 30-50 cc/h is considered adequate. 

C. Electrolyte Replacement 

1. Potassium—Potassium repletion may commence once urine output is confirmed and 

should be accomplished according to the following algorithm, with target levels of 

4.0-5.0 mEq/L: 

• If serum potassium is 3.3 mEq/L or less, hold insulin therapy and give 40 mEq/h 

intravenously as potassium chloride or as a mixture of two-thirds potassium chloride and 

one-third potassium phosphate (~ 5 mmol) if serum phosphate is less than 1 mmol/L. If 

patient is not vomiting, potassium chloride, 20-40 mEq, may also be given orally or by 

nasogastric tube. Assume a deficit of about 100 mEq potassium for each 1 mEq/L below 

normal. 

• If serum potassium is 3.3-5.0 mEq/L, give 20-30 mEq potassium chloride in each liter 

of intravenous fluid. 

• If serum potassium is 5.0 mEq/L or more, hold potassium repletion and recheck serum 

potassium in 2 hours. 

• Follow serum potassium every 2 hours during the first 8 hours of therapy. 

D. Insulin Therapy 

Insulin therapy for DKA and HHNS is generally accomplished intravenously using 

regular human insulin. Subcutaneous insulin may be absorbed erratically in severely 

volume-depleted patients. Begin therapy with a bolus of 0.1-0.15 U/kg body weight. In 

DKA this dose rapidly halts lipolysis and further ketogenesis. In HHNS it helps in rapidly 

lowering very high serum glucose and halting further water loss to osmotic diuresis. 

Start a continuous infusion at 0.1 U/kg body weight per hour, and monitor capillary blood 

glucose hourly. If glucose is not decreasing at least 50-70 mg/dL/h, insulin dosage may 

be doubled hourly until this rate of decline is achieved. Hold insulin therapy for any 

potassium level less than 3.3 mEq/L until repletion is undertaken and the level has risen 

on recheck in 2 hours. 

E. Sodium Bicarbonate Therapy 

Sodium bicarbonate therapy is generally indicated only for severe cases of DKA (arterial 

pH < 6.9). Bicarbonate therapy will seldom if ever be indicated for HHNS. At pH higher 

than 6.9, no benefit has been proved in controlled trials on DKA outcomes, whereas 

studies have shown aggressive bicarbonate therapy leading to increased rates of

cerebral edema, especially in children. No controlled data exist on bicarbonate therapy 

when pH is less than 6.9. Given the catastrophic potential of such severe acidosis on 

cellular metabolism, bicarbonate therapy is indicated in these patients and is 

accomplished by giving 100 mmol of NaHCO 3 diluted in a 500-cc bag of 5% dextrose in 

water given over 2 hours. This may be repeated every 2 hours until venous pH is 

greater than 7.0 

F. Treatment of Suspected or Known Precipitating Causes 

Infection is the most common precipitating cause of DKA and HHNS. Be sure to 

examine the patient's entire skin surface for wounds and cellulitis. Obtain a urine 

pregnancy test and conduct a pelvic examination in women of child-bearing age who 

have DKA to rule out pelvic inflammatory disease or pregnancy as sources of 

physiologic stress. Analysis and cultures of all appropriate body fluids (blood, sputum, 

urine, cerebrospinal fluid) should be obtained as dictated by the history and physical 

examination or broadly in obtunded or comatose patients. Consider empiric 

administration of broad-spectrum antibiotics until culture results are available. Treat 

other precipitating causes as they become known, for example, cardiac catheterization 

and percutaneous transluminal coronary angioplasty for myocardial infarction. 

G. Flow Sheet 

It is a good idea to organize vital signs, mental status findings, monitored laboratory 

values, intravenous fluid therapy types and rates, insulin dosages, electrolyte repletion, 

urine output, and bicarbonate administration (if any) into a flow sheet that can be 

included in the patient's chart. 

Disposition 

Patients with all but the mildest cases of DKA and all patients with HHNS should have 

cardiac monitoring and a higher level of nursing care for at least 24 hours. Whether the 

patient goes to an intermediate care or telemetry unit or the intensive care unit is based 

on severity of the case and response to initial therapy as judged by the treating 

physician. 

Kitabchi AE et al: Management of hyperglycemic crises in patients with diabetes 

mellitus. (Technical Review). Diabetes Care 2001;24:131. [PMID: 11194218] (Definitive 

and extremely comprehensive review on diagnosis and therapy of DKA and HHNS by 

the foremost authorities in these aspects of endocrinology and diabetes care. Contains 

helpful therapeutic algorithms.) 

Hyperglycemia without Ketoacidosis or Unrecognized Type 2 Diabetes 

Hyperglycemia in the absence of metabolic decompensation (DKA or HHNS) is an 

increasingly common finding in the emergency department. Obesity, pre-diabetes, and 

diabetes are epidemic in the United States. Sedentary lifestyles and high-carbohydrate 

and high-fat diets have contributed to the epidemic. Patients with diabetes may present 

with hyperglycemia from self-monitored blood glucose, or they may have no history of 

diabetes. Patients without diabetes may present with symptoms of hyperglycemia, most 

typically polydipsia, polyuria, fatigue, and blurred vision, or they may present with one or 

more complications of unrecognized diabetes, such as ischemic heart disease, cerebral

or peripheral vascular disease, nonhealing wounds, or persistent or recurrent infections 

(especially of the skin and genitourinary tract). Some patients present with unrelated 

complaints, and diabetes and hyperglycemia are found incidentally. The astute 

emergency clinician should know the risk factors for type 2 diabetes and recognize any 

of these symptomatic presentations as an indication to investigate the possibility of 

hyperglycemia or unrecognized diabetes. 


A. History 

Risk factors for hyperglycemia and unrecognized type 2 diabetes are listed in Table 

41-1. 


Symptoms of hyperglycemia may include polydipsia, polyuria, polyphagia, weakness, 

fatigue, headache, blurred vision, lightheadedness, or dizziness. When present, 

symptoms are generally mild to moderate. 

Superficial skin and skin structure infections (cellulitis, furuncles, abscesses, nonhealing 

wounds or ulcers), urinary tract infections, candidal genital infections, malignant otitis 

externa, and rhinocerebral mucormycosis all have epidemiologic associations to 

hyperglycemia and diabetes. Chronic hyperglycemia impairs neutrophil function and 

other cellular immune responses. Glycosuria is thought to contribute directly to urine 

bacterial colonization. 

To excrete excess glucose, large volumes of water are lost, and the patient rapidly 

becomes dehydrated if fluid intake is not keeping up. Symptoms may include weakness, 

dizziness, near-syncope, and headache. Signs are sunken eyes, poor skin turgor, and 

poor capillary refill. 


Random serum glucose of greater than 200 mg/dL in the setting of symptoms of 

hyperglycemia or metabolic decompensation (DKA or HHNS) or fasting serum glucose 

of greater than 126 mg/dL on repeat occasions are both diagnostic of diabetes. 

Impaired fasting glucose is defined as a fasting plasma glucose of 110- 126 mg/dL. 

Glycosylated hemoglobin, or A1C, is increasingly available as a rapid assay, and the 

role of A1C in diagnosing diabetes is evolving. Levels of 6.1% or more are about 80% 

sensitive in diagnosing diabetes; levels of 7.0% or more are nearly always consistent 

with diabetes. 

It is always prudent to assume that severe hyperglycemia (= 400 mg/dL) represents 

impending decompensation. An underlying cause should be sought aggressively, most 

commonly infection, but cardiac ischemia or myocardial infarction sometimes occur and 

an ECG plus cardiac enzymes may be helpful. Lack of compliance with antidiabetic 

regimen or diet should always be exclusionary. Have a low threshold in this setting to 

check electrolytes and BUN and creatinine to screen for metabolic decompensation, 

severe electrolyte imbalance, and renal insufficiency.

Treatment 

A growing body of literature suggests that hyperglycemia is a risk factor for adverse 

outcomes and that tight glucose control is a strong component of therapy for nearly 

every acute illness or injury experienced by diabetes patients. If hyperglycemia is mild 

(< 300 mg/dL), patients are not significantly volume-depleted, no specific cause is 

identified, and medical follow-up is readily available, no specific treatment is required 

other than to refer patients to primary care for diabetes testing (fasting plasma glucose 

is preferred over oral glucose tolerance test) or for adjustment of antidiabetic regimen in 

patients with known diabetes. When serum glucose is greater than 300 mg/dL, 

treatment is as follows: 

A. Fluids 

Normal saline or lactated Ringer's solution, 1 L given over 1 hour, may be adequate 

monotherapy for hyperglycemia. 

B. Insulin 

Mildly volume-depleted patients may be given 0.1 U/kg regular human insulin or insulin 

lispro (Humalog) or insulin aspart (Novolog) subcutaneously. Regular insulin at a dose 

of 0.1-0.15 U/kg should be given intravenously to dehydrated patients because 

subcutaneous insulin absorption may be erratic in these patients. Insulin may be 

rebolused intravenously if glucose does not decline by 50-75 mg/dL in the first hour. 

C. Oral Hypoglycemic Agents 

Oral hypoglycemic agents are generally not indicated for acute therapy of severe 

hyperglycemia, but if a patient is newly diagnosed with diabetes, the emergency 

physician may wish to prescribe an oral agent on discharge. Metformin, which inhibits 

fasting hepatic glucose production and promotes weight loss, is the oral agent least 

likely to cause hypoglycemia. Metformin can be safely started at 500 mg orally once per 

day; the dosage can be increased by 500 mg/d each week until 500 mg 4 times a day is 

reached. Metformin therapy may be initiated if serum creatinine levels are 1.4 mg/dL or 

lower. Above this level, the patient is at risk for developing lactic acidosis. Sulfonylurea 

or insulin therapy is best undertaken after the patient has received diabetes education 

and knows the symptoms of hypoglycemia, how to treat them, and when to call for help. 

If adjusting an existing oral agent or insulin dosage, it is a good rule of thumb not to 

increase insulin dosages by more than 10% or sulfonylurea dosage by more than about 

20%. Patients may also be taking insulin resistance-reduction agents such as 

thiazolidinediones or agents that inhibit breakdown of complex carbohydrates in the 

small intestine, such as a glucosidase inhibitors. 

D. Treatment of Underlying Causes 

Treat any underlying causes for hyperglycemia appropriately as they are discovered 

(eg, antibiotics for urinary tract infection). 

Disposition 

Most patients with hyperglycemia in the absence of metabolic decompensation can be 

safely discharged after thorough evaluation for underlying causes and therapy has 

reduced blood glucose to less than 250-300 mg/dL. Patients with serious underlying

causes or in whom hyperglycemia is resistant to treatment should be hospitalized for 

further workup and treatment. 

Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of 

the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes 

Care 2003;26(Suppl. 1):S5. [PMID:12502614] (Defines the various types of diabetes, 

their presentation, and diagnostic criteria.) 

Montori VM, Bistrian BR, McMahon MM: Hyperglycemia in acutely ill patients. JAMA 

2002;288:2167. [PMID: 12413377] (Outstanding brief review of the pathophysiology of 

hyperglycemia, its causes, and the rationale and literature supporting aggressive blood 

glucose control in acutely ill patients.) 

HYPOGLYCEMIA 


• Common signs and symptoms include irritability, diaphoresis, and tachycardia related 

to increased circulating catecholamines. 

• As hypoglycemia progresses, neuroglycopenic effects range from focal neurologic 

deficits such as diplopia and paresthesias to coma. 

• Always remember to check the fingerstick blood glucose on every patient presenting 

with altered mental status or who appears to be acutely ill. 

Causes 

Hypoglycemia may occur for many reasons. Most commonly hypoglycemia results from 

an excess of endogenous or exogenous insulin or oral hypoglycemic agents, such as 

sulfonylureas. Failure of other organs that either produce glucose or mediate the 

production of glucose and glucose homeostasis may also precipitate hypoglycemia. 

A. Exogenous Insulin 

In patients with known diabetes, hypoglycemia may occur as a result of the following: 

• Delay in eating after taking insulin, or general malnutrition or inadequate caloric intake 

from acute nausea and vomiting or gastroparesis 

• Increased or unusual physical exertion 

• Increased physiologic stress resulting from illness (most commonly infection or 

sepsis), injury, or emotional upset 

• Excessive dose of exogenous insulin (Note: Remember to check the patient's vision 

and confirm that he or she can read the syringe appropriately.) 

• Variable absorption from injection site

• Impaired counter-regulatory hormone axis (glucagon and epinephrine) secondary to 

autonomic failure caused by iatrogenic (insulin therapy-related) hypoglycemia 

• Excessive insulin release produced by sulfonylurea drugs, especially in the presence 

of renal insufficiency 

• Alterations in therapeutic regimen, particularly increases in insulin or oral agent 

dosages or the addition of new oral agents such as thiazolidinediones, which may 

reduce insulin resistance and improve therapeutic action of endogenous or exogenous 

insulin 

Rarely, insulin or sulfonylurea drugs have been given to nondiabetics with the intent to 

harm. Comprehensive toxicology, insulin, and C-peptide levels can help diagnose these 

problems. C-peptide is not present in manufactured insulin; therefore, a high insulin 

level without a correspondingly high C-peptide level is diagnostic of insulin overdose. 

B. Pancreatic ß Cell Tumor 

Tumor of the insulin-secreting ß cells in the islets of Langerhans may cause refractory 

hypoglycemia and even coma. C-peptide levels will elevate concurrently with insulin 

levels. 

C. Alcohol 

Excessive ethanol intake, especially without adequate caloric intake, may cause severe 

hypoglycemia. Alcohol abuse depletes hepatic glycogen production and storage and 

also reduces NADH-mediated gluconeogenesis. Caution: Administer thiamine, 100 mg, 

prior to giving large amounts of glucose to alcoholic patients with hypoglycemia to avoid 

Wernicke encephalopathy. 

D. Postprandial or Reactive Hypoglycemia 

The intake of large amounts of calories in nondiabetics may produce enough excess 

insulin to induce mildly symptomatic hypoglycemia. Seldom is the hypoglycemia severe 

enough or persistent enough to cause decreased level of consciousness or coma. 


A. History 

Try to obtain history of diabetes from emergency medical services; family; or Medic Alert 

bracelet, necklace, or wallet card. Emergency medical services or family may also be 

helpful in disclosing alcohol use, recent caloric intake, alterations of medication regimen, 

and recent illness or injury. 


Most early symptoms and signs are the result of increased catecholamine release 

(glucose usually 30-50 mg/dL): tachycardia, irritability, diaphoresis, paresthesias, 

hunger, decreased concentration. Later or more severe symptoms and signs of 

neuroglycopenia (glucose usually < 30 mg/dL) include confusion or bizarre behavior; 

visual disturbances (blurred vision, diplopia, hallucinations); hypothermia; seizurelike 

activity (myoclonus, tremor) and even seizures; focal neurologic deficits similar to Todd 

paralysis that resolve with glucose administration or remain transiently; and lethargy,

syncope, or coma. 


The capillary or fingerstick glucose test is the most rapid diagnostic method to test blood 

glucose levels. Because glucometers can become unreliable at readings less than 40 

mg/dL, always try to draw a serum or plasma sample for glucose before administration 

of glucose. 

Search for ancillary causes of hypoglycemia such as infection or sepsis, myocardial 

infarction, cerebrovascular accident, alcohol use, pregnancy, drug use (particularly 

stimulants), occult trauma, depression (poor caloric intake or insulin or oral agent 

overdose), other endocrinopathies (Addison disease, myxedema, thyrotoxicosis, 

pituitary insufficiency) as dictated by history and physical examination, and, when 

appropriate or if history is not available, laboratory studies. 

Treatment 

A. Airway 

Make sure the patient's tongue is not obstructing the airway and that the gag reflex and 

preferably the ability to phonate and swallow are present. 

B. Emergency Therapeutic Measures 

1. Intravenous glucose—If intravenous access is readily obtainable, administer 50 cc 

of 50% dextrose in water (containing approximately 25 g of glucose, which is enough to 

resolve most hypoglycemic episodes). Caution: Remember to give thiamine, 100 mg 

intravenously or intramuscularly, to alcoholic patients prior to administration of glucose 

to prevent Wernicke encephalopathy. Monitor the patient's mental status and recheck 

capillary blood glucose 30 minutes after glucose administration. Repeat dosages of 50% 

glucose or even infusion of glucose glucose-containing intravenous fluids (5-10%) may 

be necessary to maintain adequate blood glucose levels. Neuroglycopenia (altered level 

of consciousness, seizurelike activity, focal neurologic deficits) may take time to resolve 

completely; however, if abnormalities persist longer than 30 minutes after glucose 

administration and hypoglycemia has not recurred, other causes should be investigated 

with a head CT scan and appropriate laboratory studies. 

2. Oral feeding—As soon as the patient regains consciousness, clear fruit juice (eg, 

apple, grape; 6 oz = ~ 15 g glucose) is a good choice to maintain glucose levels, and if 

the patient has not eaten, a snack or meal is appropriate. 

3. Glucagon—If intravenous access is not readily available, 1 mg of glucagon may be 

given intramuscularly. The response time is typically 10-15 minutes, and nausea and 

vomiting along with overcorrection of glucose levels are common. Given that glucagon 

can be given intramuscularly, all patients with insulin-treated diabetes (or their families) 

should carry and be familiar with the use of glucagon emergency kits, which come with 

syringe, lyophilized glucagon, and diluent. 

4. Monitoring—Consider the duration of action of the insulin and/or oral agents taken 

by the patient. Hourly capillary glucose checks should be taken until glucose levels are 

stable. Generally the patient should be observed through the peak time of the

longest-acting insulin, typically 30 minutes to 1 hour after the dose with insulin lispro or 

insulin aspart, 2 hours with regular insulin, or 6 hours with NPH. Insulin glargine has no 

peak activity and does not generally cause hypoglycemia by itself. Patients taking 

long-acting insulins with peak activity, such as lente or ultralente, and patients taking 

sulfonylurea oral agents should generally be observed for a day in the hospital. 

Disposition 

Indications for admission include persistent or recurrent hypoglycemia despite 

appropriate therapy, hypoglycemia related to an oral agent or long-acting insulin, or 

serious ancillary cause (eg, severe infection, persistent nausea and vomiting). 

Conditions for discharge include availability of responsible adult to be with the patient for 

next 8-12 hours; ability to take oral fluids and food; medical follow-up available within 

24-48 hours; and ability to (and understanding of the need to) perform blood glucose 

checks, especially if changes are made in the therapeutic regimen. 

American Diabetes Association: Position Statement: Hospital admission guidelines for 

diabetes mellitus. Diabetes Care 2003;26(Suppl. 1):S118. [PMID: 12502634] (American 

Diabetes Association recommendations on when to admit patients with hypoglycemia.) 

Cryer PE: Hypoglycaemia: the limiting factor in the glycaemic management of type I and 

type II diabetes. Diabetologia 2002;45:937. [PMID: 12136392] (An excellent review of 

therapeutic hypoglycemia and the counter-regulatory response, both normal and 

pathologic.) 

McAulay V, Deary IJ, Frier BM: Symptoms of hypoglycaemia in people with diabetes. 

Diabet Med 2001;18:690. [PMID: 11606166] (Extensive review of literature on clinical 

presentation and symptomatology in diabetes-related hypoglycemia.) 

LACTIC ACIDOSIS 


Lactic acidosis is a common complication of critical illness. It is defined as serum lactic 

acid concentration greater than 5 mmol/L and arterial pH less than 7.35. Typically lactic 

acidosis results from the metabolism of glucose in the presence of inadequate tissue 

oxygenation or inadequate disposal of lactic acid by the liver. Severe acidosis can lead 

to impairment of cardiac contractility, increased pulmonary vascular resistance, 

sensitization of the myocardium to dysrhythmias, hyperkalemia, and inhibition of 

metabolism at the cellular or molecular level. The mortality rate is high, approaching 

40-60%. 

Causes 

Lactic acidosis may occur in any severe illness in which the combination of inadequate 

tissue oxygenation, inadequate tissue perfusion, and inadequate lactic acid disposal is 

present. Common underlying causes include the following:

• Respiratory, hepatic, renal, or heart failure 

• Sepsis 

• Shock 

• Cancer, especially leukemias 

• Acute infarction of lung, bowel, or extremities 

• Severe abdominal or multisystem trauma 

• Alcohol, methanol, or ethylene glycol poisoning 

• Drugs: cocaine, metformin, isoniazid 


Diagnostic efforts should focus on finding the underlying cause of the lactic acidosis. 

Treatment of the underlying cause is crucial to recovery. 


The clinical presentation varies according to the underlying illness or injury. Symptoms 

may include hyperventilation, generalized weakness, abdominal pain, or hypotension. 

Often there is a general lack of symptoms, especially in the early stages of the 

underlying pathology. As a result, diagnosis is frequently difficult in the period when the 

underlying illness and the acidosis itself are most treatable. A high index of suspicion is 

essential in older patients and in patients with the underlying illnesses identified above. 


Laboratory findings include pH less than 7.35 and often less than 7.2; anion gap greater 

than 15 mEq/L; and lack of explanation of acidosis by other causes—such as 

salicylates; alcohol, methanol, or ethylene glycol poisoning; or diabetic or alcoholic 

ketoacidosis. Hyperphosphatemia is a common finding secondary to anaerobic 

glycolysis or cellular disruption. Samples collected for lactate should be chilled 

immediately and centrifuged promptly to avoid continued lactic acid production by red 

and white blood cells, which can distort results. 

Treatment 

Detailed attention to resuscitation issues is essential in improving outcome. Improving 

tissue oxygenation through delivery of adequate oxygen through the lungs and 

adequate perfusion to carry the oxygen to the tissues via the circulatory system is 

critical. 

A. Oxygen 

High flow rates are indicated. Consider rapid-sequence intubation, mechanical 

ventilation, or noninvasive ventilation (eg, bilevel positive airway pressure) when arterial 

blood gas analysis indicates that oxygenation or ventilation is inadequate.

B. Fluids BR>Rapid infusion of 1 L of 0.9% saline is indicated to restore intravascular 

volume. Reassess the patient frequently to avoid volume overload in the setting of acute 

renal failure or cardiogenic shock and circulatory failure. 

C. Pressors 

Avoid vasoconstrictive pressors such as norepinephrine and higher doses of ß active 

pressors such as dopamine and dobutamine because they tend only to worsen tissue 

hypoxia. Low doses of dopamine and dobutamine may improve cardiac output and renal 

blood flow and are worth trying. 

D. Sodium Bicarbonate 

The use of sodium bicarbonate is one of the most controversial issues in the treatment 

of metabolic acidosis. The majority of data available suggest that at pH levels greater 

than 6.9, no benefit has been shown supporting the administration of sodium 

bicarbonate, at least in the clinical settings of severe metabolic acidosis resulting from 

DKA and sepsis. Significant risks of administering bicarbonate include hypernatremia 

and hyperosmolality, volume overload, paradoxical increase of intracellular acidosis 

secondary to excess carbon dioxide as a result of bicarbonate metabolism, and cerebral 

edema. If pH is less than 6.9, especially if the patient is exhibiting one or more 

complications of severe acidosis as listed above, consider administering 1-2 amps (~ 44 

mEq/amp) diluted in 1 L of 5% dextrose in water or 0.2% saline infused over 2 hours. 

Reassess pH after allowing at least 2 hours for equilibration. 

E. Treatment of Underlying Causes 

Treatment of underlying causes may include revascularization therapy or balloon pump 

support in patients with cardiogenic shock, antibiotics for suspected sepsis after 

appropriate culture material is obtained, amputation or revascularization of ischemic 

extremities, removal or revascularization of ischemic bowel, hemodialysis for renal 

failure, or removal of toxic components such as ethylene glycol or methanol. 

Disposition 

The prognosis is grim, and mortality is high. Prompt identification and treatment of the 

underlying root cause of lactic acidosis remains the best hope for a positive outcome. 

Adrogue HJ, Madias NE: Management of life-threatening acid-base disorders. N Engl J 

Med 1998;338:26. [PMID: 9414329] (Excellent overview of pathophysiology of severe 

acidosis and the management of several common causes.) 

Forsythe SM, Schmidt GA: Sodium bicarbonate for the treatment of lactic acidosis. 

Chest 2000;117:260. [PMID: 10631227] (An intelligent debate on the rationale, or more 

accurately lack thereof, for giving sodium bicarbonate as therapy for severe metabolic 

acidosis.) 

ALCOHOLIC KETOACIDOSIS


• Signs include tachypnea (Kussmaul respirations are common), tachycardia, abdominal 

tenderness, poor skin turgor, and delayed capillary refill. 

• In general, serum glucose < 250 mg/dL distinguishes alcoholic ketoacidosis from DKA. 


Alcoholic ketoacidosis (AKA) typically occurs in the alcoholic patient who is on a long 

drinking binge and either is unwilling or unable to take in food calories secondary to 

nausea and vomiting, gastritis, or pancreatitis. Lipolysis is driven by the lack of caloric 

intake and catecholamine release from alcohol intoxication or withdrawal. Acid-base 

disturbances are frequently mixed in these patients because volume depletion alkalosis 

and respiratory alkalosis frequently coincide. As in DKA, underlying causes and 

contributors such as infection, trauma, gastrointestinal hemorrhage, hepatic or renal 

failure, concurrent cocaine or methamphetamine use, and rhabdomyolysis must be 

investigated and treated as part of the overall diagnostic and therapeutic plan. 


A. History 

The patient's history most often includes a recent or ongoing alcohol binge with poor 

food intake, nausea and vomiting, and abdominal pain. 


The physical examination most often shows tachypnea (Kussmaul respirations are 

common), tachycardia, and abdominal tenderness to palpation. Poor skin turgor and 

delayed capillary refill are also common. Fever is not generally part of the syndrome, 

and causes of fever should be sought aggressively. 


1. Metabolic acidosis—Low pH (often < 7.2) and low serum bicarbonate are common. 

2. Plasma or urine ketones—Most of the ketone bodies produced in AKA are 

ß-hydroxybutyrate, which does not show up on the standard test for ketones in serum or 

urine. Negative initial ketone test does not rule out AKA. 

3. Electrolyte disorders—Hyponatremia, hyperkalemia, hypokalemia, 

hypophosphatemia, hypomagnesemia, and hypocalcemia are common findings in 

patients with AKA. 

4. Glucose—Glucose levels range from hypoglycemia to moderately elevated (up to 

250 mg/dL) in the absence of diabetes. 

5. Alcohol levels—Alcohol levels may not be elevated by time of presentation because 

the patient may not have been able to maintain oral intake of even alcohol for some 

time. Be alert for signs and symptoms of alcohol withdrawal or delirium tremens.

Treatment 

A. Glucose 

After giving thiamine, 100 mg intravenously or intramuscularly, give 5% dextrose 

solution in 0.9% normal saline, 1 L/h for the first 1-2 hours; 5% dextrose in 0.45% 

normal saline is then appropriate at 250 cc/h. 

B. Potassium 

Total body potassium levels are generally low secondary to losses from vomiting, but 

severe acidosis may elevate serum potassium levels and AKA patients may present 

with hyperkalemia. If urine output is established, up to 20 mEq/L of potassium chloride 

may be given per hour. If vomiting is controlled, consider supplementing with oral 

potassium chloride at up to 40 mEq every 2 hours. Assume a total body deficit of at 

least 100 mEq of potassium for each 1 mEq/L below normal. Potassium levels should 

be reevaluated every 2 hours for the first 4-8 hours of therapy. 

C. Insulin 

Generally, mild hyperglycemia will resolve with intravenous fluid therapy. Intravenous 

insulin, 0.1 units regular insulin/kg, may be required along with glucose to treat severe 

hyperkalemia (> 6.0 mEq/L) if changes such as peaked T waves, prolonged QRS 

interval, or loss of P waves are evident on the ECG. 

D. Magnesium 

Consider giving magnesium sulfate, 1-2 g, empirically in the first liter of fluid because 

magnesium deficiency is extremely common in alcoholic patients. This therapy makes 

the myocardium less susceptible to dysrhythmias and also helps restore calcium 

homeostasis. 

E. Bicarbonate 

Bicarbonate is indicated only as therapy for acute hyperkalemia; acidosis generally 

responds rapidly to volume repletion. 

F. Treatment of Underlying Causes 

Do not assume that severe abdominal pain is due to AKA alone; pancreatitis or upper 

gastrointestinal bleeding are often concurrent illnesses contributing to AKA. 

Disposition 

Although metabolic problems tend to correct reasonably rapidly with intravenous fluids 

and glucose administration, most AKA patients are extremely unreliable and would have 

difficulty complying with outpatient treatment and follow-up. Alcohol withdrawal may also 

complicate the course as the ketoacidosis improves. Hospitalization for observation is a 

prudent choice for patients with AKA. 

Fulop M: Alcoholic ketoacidosis. Endocrinol Metab Clin North Am 1993;22:209. [PMID: 

8325283] (Most recent comprehensive review on the topic in English.) 

Wrenn KD et al: The syndrome of alcoholic ketoacidosis. Am J Med 1991;91:119.

[PMID: 1867237] (Presents the only existing data on emergency department patients 

(retrospective) with AKA regarding clinical presentation, underlying illnesses, and 

laboratory findings.) 

EMERGENCY MANAGEMENT OF OTHER METABOLIC & 

ENDOCRINE ABNORMALITIES 

THYROID DISORDERS 

1. Thyroid Storm 


• Typical stigmata of hyperthyroidism, thyromegaly, ophthalmopathy, tremor, stare, 

diaphoresis, and agitation. 

• Fever (usually). 

• Tachycardia (out of proportion to fever) often with associated atrial arrhythmias. 

• Mental status changes ranging from confusion to coma. 


Thyroid storm represents a disorder of extreme thyrotoxicosis, or the overproduction of 

thyroid hormone. Thyroid storm, if not diagnosed and treated promptly, is a 

life-threatening emergency. The diagnosis is made clinically, and although laboratory 

testing may suggest the diagnosis, interpretation of thyroid function tests in the setting 

of acute illness may be difficult. No laboratory test is available that will confirm the 

diagnosis. The classic findings of thyroid storm include fever (> 38.5 °C [101.5 °F]); 

tachycardia out of proportion to fever; gastrointestinal symptoms; cardiovascular 

symptoms; and central nervous system abnormalities, most commonly confusion, 

agitation, or delirium rather than lethargy, obtundation, or coma. 

Causes 

Thyroid storm is frequently associated with serious concurrent illness or injury. Common 

factors that may trigger thyroid storm include infection, recent surgery, trauma, 

pregnancy, stroke, metabolic disorders such as diabetic ketoacidosis, radioiodine 

therapy, drug abuse (stimulants most commonly), alcohol abuse, iodinated contrast 

material, and discontinuation of antithyroid medications. 


The diagnosis of thyroid storm is made clinically. Laboratory results may be of little help 

because thyroid hormone secretion and metabolism may be altered by acute stress or 

illness and may not be significantly abnormal. Most patients who present with thyroid 

storm have had a history of partially treated hyperthyroidism or have signs and 

symptoms of antecedent thyroid disease, such as thyromegaly, proptosis, stare, 

myopathy, or myxedema. The diagnosis should be made empirically and treatment

initiated when a patient with prior or current thyroid disease decompensates rapidly in 

the setting of fever, tachycardia, central nervous system hyperactivity, and unexplained 

cardiac or gastrointestinal symptomatology. 


Fever is characteristic and may exceed 40 °C (104 °F). The fever may be primarily from 

thyrotoxicosis or may be secondary to a precipitating infection. Always assume infection 

is the primary cause, obtain appropriate cultures, and treat accordingly with empiric 

broad-spectrum antibiotics. 

Cardiac findings include sinus tachycardia, supraventricular tachycardia, atrial 

arrhythmias, and congestive heart failure. The tachycardia seen with a thyroid storm is 

usually out of proportion to the fever. Gastrointestinal symptoms include nausea, 

vomiting, diarrhea, abdominal pain, and in rare cases jaundice. Mental status changes 

are commonly seen. Patients may present with delirium, confusion, psychosis, or coma. 

Neuromuscular findings include agitation, tremor, generalized weakness (especially in 

the proximal muscles), and periodic paralysis. 

Findings consistent with prior thyroid disease include thyromegaly, orbitopathy, tremor, 

stare, pretibial myxedema and other integumentary changes such as coarse hair and 

thick, dry skin. Death may occur from hypovolemic shock, coma, congestive heart 

failure, tachydysrhythmias, or any combination of these. 

Apathetic hyperthyroidism is important to consider in the elderly population. Because of 

advanced age and other comorbid conditions, the classic signs and symptoms of thyroid 

storm and thyrotoxicosis may be subtle or absent. This may make diagnosis of 

thyrotoxicosis especially difficult in the elderly population. 


Thyroid function tests are frequently not helpful in diagnosing acute thyroid storm. 

Previous abnormal thyroid test may inform the clinician of a preexisting thyrotoxicosis 

but will not confirm the diagnosis of a thyroid storm. The most helpful thyroid function 

tests are thyroid-stimulating hormone (TSH), which will be markedly low in most patients 

with thyroid storm, and free thyroxine (T 4 ), which will be elevated. These studies may 

not be readily available in a timely manner to all emergency department clinicians. 

Electrolyte and glucose abnormalities may be present, most commonly resulting from 

gastrointestinal losses, dehydration, physiologic stress, and fever. 

Laboratory and imaging studies should be directed toward findings in the history and 

physical examination. Blood cultures, urine cultures, chest X-ray, complete blood count 

(CBC) with differential, chemistry panel, and ECG and cardiac enzymes are generally 

indicated to look for precipitating causes. Head CT scan is indicated for delirious or 

comatose patients. 


The ECG is usually abnormal; common findings are sinus tachycardia, increased QRS 

interval and P wave voltage, nonspecific ST-T wave changes and atrial dysrhythmias, 

usually atrial fibrillation or flutter. Conduction defects, most commonly first-degree AV 

block and nonspecific interventricular conduction delay, may occur. Ischemic findings or

myocardial infarction may be present, especially in older patients with concurrent illness 

such as diabetes or hypertension. 

Treatment 

A. Emergency Measures 

Maintain an airway. Consider rapid-sequence intubation for severely agitated or 

comatose patients, and give supplemental oxygen. Ensure adequate intravenous 

access, preferably with a large-bore (= 18-gauge) catheter. Draw blood samples for free 

T 4 and TSH radioimmunoassay, CBC, serum electrolytes and glucose measurements, 

renal and hepatic function tests, and arterial blood gas determination. 

Electrocardiographic monitoring is indicated. 

Initiate intravascular volume replacement with isotonic fluids, at least 1 L normal saline 

or lactated Ringer's in the first hour, and vasopressors as needed if the patient is 

hypotensive. Frequent reassessment is necessary to prevent fluid overload, especially 

in patients exhibiting signs of high output cardiac failure (tachycardia, dyspnea, wide 

pulse pressure). 

B. Hormone Synthesis Blockers 

Thionamides block thyroid hormone synthesis. They are not available in parenteral 

forms and should be administered orally or by nasogastric tube. Propylthiouracil, 

200-300 mg every 6 hours, is the drug of choice. In addition to blocking thyroid hormone 

synthesis, propylthiouracil has the ability to block peripheral conversion of T 4 to the 

more physiologically active triiodothyronine (T 3 ). 

C. Hormone Release Blockers 

Iodine therapy is a therapeutic adjunct to propylthiouracil. Iodide compounds should be 

given 2-4 hours after initial propylthiouracil dose. Potassium iodide (SSKI, 35 mg 

iodide/drop), 5 drops 3-4 times daily given orally or by nasogastric tube, will inhibit 

thyroid hormone release. 

Alternatively, Lugol's iodine solution (8 mg iodide/drop), 10 drops every 8 hours given 

orally or by nasogastric tube, may be used. Seriously ill patients may be given iodinated 

radiographic contrast agents such as sodium ipodate (Oragrafin) or sodium iopanoate 

(Telepaque). The dose for either is 1 g by mouth daily as a single dose or 500 mg twice 

daily. These medications can only be given orally. 

D. Hormone Action Blockers 

ß-Adrenergic antagonists such as propanolol block the peripheral effects or excess 

thyroid hormone and decrease conversion of T 4 to T 3 . A typical dose is 0.5-1.0 mg 

intravenously every 10-15 minutes until pulse reduction is achieved. In patients with 

bronchospastic disease, cautious use of esmolol, 0.05-0.1 mg/kg/min intravenously, or 

calcium channel blockers such as diltiazem, 5-15 mg/h intravenously, may be 

considered. 

E. Corticosteroids 

Corticosteroids inhibit peripheral conversion of T 4 to T 3 . In addition, they also treat the

elative adrenal insufficiency that may be present. Intravenous hydrocortisone, 100 mg 

every 8 hours, may be used; if concurrent adrenal insufficiency is in the differential 

diagnosis, dexamethasone, 0.1 mg/kg intravenously every 8 hours, may be given and 

an adrenocorticotropic hormone (ACTH) stimulation test of the adrenocortical axis may 

still be undertaken. 

Disposition 

Hospitalization in an intensive care unit is indicated for all patients with thyroid storm. A 

Swan-Ganz catheter may be necessary to facilitate fluid management and assess 

progress of therapy in cases complicated by cardiac failure. 

Dabon-Almirante CL, Surks MI: Clinical and laboratory diagnosis of thyrotoxicosis. 

Endocrinol Metab Clin North Am 1998; 27:25. [PMID: 9534025] (Good overview of 

thyrotoxicosis, outlining the clinical manifestations by organ systems.) 

Ringel MD: Management of hypothyroidism and hyperthyroidism in the intensive care 

unit. Crit Care Clin 2001;17:59. [PMID: 11219235] (Complete coverage of hyperthyroid 

treatments, detailing both medical and surgical options.) 

2. Myxedema Coma 


• A potentially lethal complication of severe hypothyroidism. 

• Look for typical stigmata: dry skin, delayed reflex relaxation, generalized weakness, 

edema, or a transverse scar across the low anterior neck. 

• Alteration in mental status (although coma is rare). 

• Often hypothermic (< 35.5 °C [95.9 °F]). 


Myxedema coma is a rare complication of hypothyroidism related to severe deficiency of 

thyroid hormone production resulting in encephalopathy. The most common causes for 

hypothyroidism include autoimmune disorders (Hashimoto thyroiditis), prior 

thyroidectomy, and radioactive iodine ablation of the thyroid. Myxedema coma typically 

occurs in the winter months often after cold exposure. Other predisposing factors 

include cerebrovascular accident, anesthesia or surgery, trauma, medications, and 

infections. Cardinal features include hypothermia, hyporeflexia, central nervous system 

depression, coma, bradycardia, and slow verbal responses. Oxygenation and ventilation 

may be impaired because of decreased respiratory drive and respiratory muscle 

weakness. Onset may be rapid or may be insidious, especially in the elderly. Mortality is 

estimated at up to 60-70%; the elderly population is at highest risk. When myxedema 

coma is recognized and treated appropriately, mortality drops to 15-20%. 

Clinical Findings

The presumptive diagnosis of myxedema coma should be made when clinical 

manifestations of hypothyroidism are accompanied by disturbances of consciousness, 

hypothermia, hypoventilation, and hypotension. 

A. History 

The history, if available, is usually that of classic hypothyroidism and may include 

discontinuation of thyroid medication, previous radioactive iodine treatment, 

thyroidectomy, or drug administration (sedatives, iodides, or amiodarone). 


Symptoms and signs of hypothyroidism include cold intolerance, dry skin, constipation, 

weight gain, irregular or absent menses, muscle cramps, paresthesias, angina, or 

seizures. Neurologic complaints such as generalized weakness, slow speech, 

disorientation, apathy, ataxia, inappropriate humor (myxedema wit), or psychosis are 

also common. As hypothyroidism worsens, neurologic symptoms progress to lethargy, 

disorientation, grand mal seizures, and myxedema coma. 

Hypothermia is found in approximately 80% of patients with myxedema coma. 

Hypoventilation often occurs secondary to decreased respiratory drive and generalized 

muscle weakness. Hypotension may be present. Gastrointestinal ileus or urinary 

retention are common. 

In comatose patients, the only data the clinician may have are physical findings: 

bradycardia; generalized puffiness; periorbital edema; ptosis; cutaneous myxedema; 

coarse, dry skin; macroglossia; delayed deep tendon reflexes; thyroidectomy scar or a 

goiter; or coarse, sparse hair. 


Thyroid studies typically reveal low serum free T 4 and T 3 levels. The serum TSH level is 

high in primary hypothyroidism and low or undetectable in secondary hypothyroidism. 

Secondary hypothyroidism represents a failure of the hypothalamus to secrete adequate 

thyrotropin-releasing hormone (TRH) or failure of the anterior pituitary to secrete TSH. 

Obtain routine blood cultures, urine cultures, chest radiography, and ECG in the search 

for a precipitating cause. Arterial blood gases may reveal hypoxemia, hypercapnia, and 

a respiratory or mixed respiratory-metabolic acidosis. Hyponatremia and hypoglycemia 

may be signs of concurrent adrenal insufficiency. These are also potential contributors 

to central nervous system depression. Serum creatine kinase may be elevated. 

Myocardial pathology or rhabdomyolysis must be excluded as causes. 

D. Imaging 

Chest radiography may show an enlarged heart from a pericardial effusion or other 

precipitating cause for the myxedema coma, such as pneumonia. A bedside 

echocardiogram can confirm a pericardial effusion. 

E. Electrocardiographic Findings 

The ECG shows bradycardia, low voltage of the QRS complex in all leads, flattening or 

inversion of the T waves, and conduction abnormalities.

Treatment 

A. General and Supportive Measures 

1. ABCs—Assess airway. Patients with myxedema coma may need rapid-sequence 

intubation and mechanical ventilation for hypoxemia and hypoventilation. Patients may 

need assistance with bag-valve-mask ventilation to achieve adequate preoxygenation. 

Electrocardiographic monitoring is indicated. 

2. Venous access—Establish large-bore (= 18-gauge) intravenous access. Draw blood 

samples for free T 4 , free T 3 , TSH, cortisol, CBC, renal and hepatic function tests, 

arterial blood gases, and electrolyte and glucose levels. 

3. Fluid replacement—Isotonic crystalloid solution (normal saline or lactated Ringer's) 

should be given for hypotension. Avoid hypotonic solutions because hyponatremia may 

be present. Avoid giving vasopressors because they may provoke dysrhythmias, 

especially when used with intravenous thyroid replacement therapy. In addition, 

vasopressors are not likely to be effective because of a reduced adrenergic receptor 

response. 

4. Treatment for hypothermia—Hypothermia is usually corrected by administration of 

thyroid hormone; however, passive rewarming methods may be used. Avoid external 

warming blankets. Active methods of rewarming may cause vasodilation and 

cardiovascular collapse. 

5. Treatment for hypoglycemia—Treat hypoglycemia with 50% dextrose initially, then 

by 5% dextrose infusion (in normal saline or lactated Ringer's). Treat gastrointestinal 

ileus and urinary retention with a nasogastric tube and Foley catheter, respectively. 

6. Other medications—Avoid unnecessary medications that may further exacerbate a 

myxedema coma such as central nervous system depressants. Treat severe 

hyponatremia (= 120 mEq/L) with isotonic intravenous fluids (normal saline); be careful 

not to correct too rapidly to avoid fluid overload. Thyroid replacement therapy and 

corticosteroids will generally correct mild hyponatremia. 

Intravenous corticosteroids (hydrocortisone sodium phosphate or sodium succinate), 

100 mg every 8 hours, are indicated as treatment for frequently concurrent adrenal 


7. Treatment of precipitating causes—Treat appropriately any identified precipitating 

cause for myxedema coma. Recovery from myxedema coma is slow because reversal 

of severe metabolic abnormalities is required. 


Although thyroid replacement therapy is indicated for myxedema coma, the method of 

replacement is controversial. T 3 has the advantage of being more physiologically active 

than T 4 ; however, it carries the increased risk of dysrhythmia and ischemic heart 

disease in susceptible populations such as the elderly. T 4 in low doses has not proved 

effective. A frequently used and generally safe method appears to be high-dose

intravenous T 4 therapy, 200-500 ug as an initial intravenous loading dose over the first 

hour, followed with 50-100 ug/d intravenously until oral intake is tolerated and the 

patient can begin taking an initial oral replacement dose of 50-100 ug/d. In younger 

comatose patients without comorbid coronary artery disease, T 3 at low intravenous 

doses of 10 ug every 8 hours may be given in addition to T 4 until the patient is 

conscious. All patients receiving any form of intravenous thyroid hormone therapy 

should have continuous cardiac monitoring. 

Disposition 

Hospitalization in an intensive care unit is indicated for all patients with myxedema 

coma. 

Ringel MD: Management of hypothyroidism and hyperthyroidism in the intensive care 

unit. Crit Care Clin 2001;17:59. [PMID: 11219235] (Good overview of thyroid pathology, 

diagnosis, and treatment. Details the rationale and various methods of thyroid hormone 

replacement.) 

Wall CR: Myxedema coma: diagnosis and treatment. Am Fam Physician 2000;11:2485. 

[PMID: 11130234] (Highlights the variable presentations of myxedema coma and 

emphasizes the need for a high index of suspicion.) 

ACUTE ADRENAL INSUFFICIENCY (Addisonian Crisis) 


• Consider addisonian crisis in patients with hypotension refractory to intravenous fluids 

or in acutely ill patients with typical stigmata of chronic glucocorticoid use such as moon 

facies and buffalo hump. 

• Common symptoms include orthostasis, weight loss, anorexia, lethargy, abdominal 

cramps, nausea, vomiting, diarrhea, and mental depression. 

• Classic electrolyte abnormalities include hyponatremia associated with hyperkalemia. 


The adrenal glands produce four different groups of hormones: glucocorticoids, 

mineralocorticoids, catecholamines, and sex hormones. Failure to produce all but the 

sex hormones may induce a life-threatening emergency because cardiovascular 

stability, extracellular fluid and electrolyte balance, glucose homeostasis, and the body's 

ability to deal with metabolic stress all depend on the other three classes of adrenal 

hormones. Recognizing the clinical manifestations of adrenal insufficiency requires a 

high index of suspicion because signs and symptoms are often nonspecific. 

Classification 

A. Primary Adrenocortical Insufficiency

Primary adrenocortical insufficiency (Addison disease) results from primary destruction 

of the adrenal glands. Causes include autoimmune insults (most common), infection, 

systemic inflammatory response, thrombosis, hemorrhage, malignant metastatic 

carcinoma (most commonly lung, breast, hematogenous), and medications (most 

commonly warfarin, antifungals, and corticosteroids). Etomidate, a medication used with 

increasing frequency in emergency medicine for rapid- sequence intubation and for 

procedural sedation, may also cause transient and occasionally serious primary adrenal 

insufficiency. Whereas tuberculosis was the most common infectious cause in the past, 

HIV and related opportunistic complications are now responsible for most infectious 

insults to the adrenal glands. The infection may be primary or secondary via an 

opportunistic infection, most commonly systemic fungal, protozoal, or herpes simplex or 

cytomegalovirus infections. Patients with coagulopathy or thromboembolic disease are 

at higher risk for bilateral adrenal hemorrhage. Waterhouse-Friderichsen syndrome 

related to Neisseria meningitidis or pneumococcal septicemia consists of bilateral 

adrenal hemorrhage and abrupt circulatory collapse. 

B. Secondary Adrenocortical Insufficiency 

Secondary adrenocortical insufficiency results from pathology of the hypothalamus and 

pituitary. Corticotropin-releasing hormone (CRH) and ACTH release are impaired 

causing dysfunction along the entire hypothalamus-pituitary-adrenal axis. Common 

causes include corticosteroid withdrawal and systemic inflammatory states such as 

sepsis. A primary pituitary or hypothalamic mass must also be considered. 



As with other endocrine disorders, signs and symptoms are typically nonspecific 

because a number of different organ symptoms are involved. Clinical findings are 

typically secondary to low glucocorticoid and mineralocorticoid levels. 

1. Glucocorticoid deficiency—Symptoms and signs include hypotension (particularly 

hypotension refractory to fluids), orthostasis, weight loss, anorexia, lethargy, abdominal 

cramps, nausea, vomiting, diarrhea, and mental depression. 

2. Mineralocorticoid deficiency (primary deficiency only)—Symptoms and signs 

include hypovolemia, orthostasis, hypotension, and salt craving. 

Acute bilateral adrenal hemorrhage is not accompanied by the above chronic 

manifestations but should be suspected in the following situations: 

• Patients with sepsis who have rapid or unexplained deterioration 

• Adults with major medical illnesses who have abdominal, flank, or chest pain; 

dehydration; hypotension; shock; or fever (especially if anticoagulants have been used) 

Patients with secondary adrenal insufficiency may present with acute adrenal 

insufficiency; in these patients it is preceded by one of the following: 

• History of or physical features characteristic of chronic glucocorticoid administration

(eg, moon facies, buffalo hump) 

• Symptoms of hypopituitarism (hypogonadism, hypothyroidism) and manifestations of a 

hypothalamic or pituitary tumor (including headache, bitemporal visual field defects, or 

enlargement of the sella turcica) in patients with hypothalamic or pituitary disorders 

3. Symptoms and signs of acute crisis—Rapid worsening of glucocorticoid-deficiency 

symptoms is associated with severe weakness. Symptoms of mineralocorticoid 

deficiency occur only with primary adrenal insufficiency: 

• Fever 

• Increased nausea and vomiting with nonspecific abdominal pain 

• Rapid dehydration and hypovolemia 

• Hypotension and shock 

• Altered mental status ranging from lethargy to obtundation and coma 


Mineralocorticoid deficiency causes a classic hyponatremia and hyperkalemia. The 

finding of the two together should suggest the diagnosis of primary adrenal insufficiency. 

Other findings may include anemia of chronic disease, elevated blood urea nitrogen, 

hypoglycemia, hypocalcemia, lymphocytosis, and eosinophilia. Hyperkalemia is typically 

not seen in secondary adrenal insufficiency because aldosterone production is usually 

preserved. 

C. Imaging 

Calcification of the adrenals may be present as a result of tuberculosis, histoplasmosis, 

or other disseminated fungal disease. Magnetic resonance imaging (MRI) of the head is 

usually the test of choice for secondary adrenal insufficiency to reveal sellar and 

hypothalamic-pituitary tumors, and CT scan of the abdomen is the test of choice in 

primary adrenal insufficiency to image the adrenal glands. Enlarged adrenal glands 

suggest tuberculosis, fungal disease, cancer, hemorrhage, or AIDS. Small adrenal 

glands suggest autoimmune disease, chronic infection, or chronic vascular 

abnormalities. 


The ECG may reveal low voltage in all leads and changes characteristic of electrolyte 

abnormalities, most commonly hyperkalemia with peaked T waves, prolongation of QRS 

interval, and loss of P waves in severe cases. 


Draw blood for serum cortisol level. A serum cortisol exceeding 20 ug/dL at any time of 

the day makes the diagnosis of adrenal insufficiency unlikely. Ideally the blood is drawn 

when the patient is under duress.

An ACTH stimulation test, however, is the study of choice. After the initial serum cortisol 

is drawn, 250 ug of synthetic ACTH (Cosyntropin) is given. Serum cortisol levels are 

drawn 30 and 60 minutes later. Failure of the adrenals to produce cortisol to levels of 

25-30 ug/dL suggests primary adrenal insufficiency. A normal response to the test does 

not rule out adrenal insufficiency because partial adrenal insufficiency may be present. 

Note: An ACTH stimulation test cannot be undertaken if hydrocortisone was given as 

initial therapy. Dexamethasone is a reasonable and effective alternative to 

hydrocortisone that will not disrupt the results. 

In addition, the 250 ug of Cosyntropin is thought to be supratherapeutic, being many 

times the normal physiologic levels seen in a stress situation. A low-dose ACTH test has 

been suggested that uses only 1-2 ug of the drug. The rest of the parameters of the 

test—including timing of cortisol levels and the cortisol levels of 25-30 ug/dL needed to 

suggest adequate adrenal function—remain the same, and the test is thought to be 

more sensitive with the lower dose of cosyntropin. 

Treatment 


Assess the airway, intubate as necessary for decreased mental status, and provide 

supplemental oxygen as needed. Establish large-bore intravenous access. Draw blood 

for CBC, electrolytes, glucose level, renal and hepatic function tests, and serum cortisol. 

Perform an ACTH stimulation test. 

Monitor body weight, fluid intake, and urine output. Check serum electrolytes, glucose, 

and renal function every 4-6 hours, then once or twice daily until these measures are 

stable. Monitor potassium levels carefully. Even though potassium levels may be high 

initially, total body deficits often exist and will appear in conjunction with hydrocortisone 

therapy. Replace fluid volume and correct electrolyte abnormalities as appropriate. 


Hydrocortisone, 100 mg intravenously every 8 hours, is the mainstay for treating adrenal 

insufficiency. Alternatively, dexamethasone, 0.1 mg/kg every 8 hours, may be used 

without disruption of diagnostic testing although it supports only glucocorticoid function. 

Once diagnostic testing has been done, hydrocortisone is the drug of choice because it 

has both glucocorticoid and mineralocorticoid functions. Once patients are stable, the 

dose may be tapered gradually over 1-2 weeks. 

Patients receiving less than 50 mg/d of hydrocortisone will likely need mineralocorticoid 

support as well. Fludrocortisone, 0.05-0.2 mg/d, is the drug of choice. Fludrocortisone 

therapy is necessary as transition to oral therapy begins. 

Disposition 

Admission to the hospital is indicated if an addisonian crisis is suspected or confirmed. 

Intensive care unit admission is warranted for hemodynamically unstable patients. 

Marik PE, Zaloga GP: Adrenal insufficiency in the critically ill. A new look at an old

problem. Chest 2002;5:1784. [PMID: 12426284] (Reviews adrenal insufficiency in light 

of modern causes.) 

Zolga GP, Marik P: Hypothalamic-pituitary-adrenal insufficiency. Crit Care Clin 

2001;17:25. [PMID: 11219233] (Comprehensive review of the pathophysiology and 

management of adrenal insufficiency emphasizing the need for a high index of 

suspicion.) 

PHEOCHROMOCYTOMA (Catecholamine Crisis) 


• Catecholamine crisis symptoms are headache, palpitations, flushing, or diaphoresis 

associated with hypertension. 

• Symptoms associated with pheochromocytoma are often intermittent (with 

asymptomatic periods in between episodes), whereas those of a monoamine oxidase 

inhibitor (MAOI) crisis or of sympathomimetic intoxication are not. 


A catecholamine crisis is typically caused by one of three entities (1) a 

pheochromocytoma, (2) a MAOI crisis, or (3) intoxication from cocaine or other similar 

sympathomimetics. Occasionally a catecholamine crisis may be induced by sudden 

cessation of clonidine therapy. Catecholamines bind to a-1 and ß receptors and in 

excess may cause various signs and symptoms such as headache, palpitations, 

diaphoresis, and often severe hypertension. A thorough history will usually lead to the 

cause of catecholamine crisis, except in the case of pheochromocytoma, which often 

remains an elusive cause because the symptoms are nonspecific and often intermittent. 

This section focuses on diagnosis and treatment of pheochromocytoma. 



Classic manifestations include headache, diaphoresis, pallor, palpitations, nervousness, 

apprehension, nausea, vomiting, and abdominal pain. Hypertension, often severe (= 

120 mm Hg diastolic), is a striking sign that usually prompts the clinician to include 

catecholamine crisis in the differential diagnosis. 

Hypertension is frequently intermittent and may not always be present at the time of 

examination. Labile hypertension is the hallmark of a pheochromocytoma. Recent 

reviews have placed the frequency of hypertension at 72.4% and sustained 

hypertension at only 47.9%. 

Complications that occur late in the course of the disease may cloud the diagnosis 

because they can be dramatic and distracting. Presentations in severe cases may 

include abdominal or chest pain, aortic dissection, encephalopathy, cardiomyopathy, 

pulmonary edema, fever, and anion gap metabolic acidosis.

Neurocutaneous syndromes such as neurofibromatosis, von Hippel-Lindau disease, 

ataxia-telangiectasia, tuberous sclerosis, and Sturge-Weber syndrome are sometimes 

associated with pheochromocytoma. Cutaneous findings (ie, cafe-au-lait spots, 

telangiectasias) may provide clues to a diagnosis. 

Mucosal neuromas and a marfanoid appearance suggest multiple endocrine neoplasia 

type IIB. Other findings include weight loss, heat intolerance, hyperglycemia, and 

tachycardia. 

B. Laboratory Findings and Special Tests 

The diagnosis of pheochromocytoma is made along two pathways. First, a biochemical 

diagnosis must be made. Second, the tumor must be defined by radiologic studies for 

possible surgical excision. 

The initial test of choice is a 24-hour urine collection for catecholamine and 

catecholamine metabolites (norepinephrine, epinephrine, dopamine, vanillylmandelic 

acid [VMA], and metanephrine). In the absence of grossly positive results, plasma 

catecholamine levels have been unreliable for diagnosis; however, new research has 

shown free plasma metanephrine to be useful as a diagnostic marker. 

Although 90% of pheochromocytomas arise from the adrenal glands, 10% are found in 

extra-adrenal sites. Localization of the tumor is performed by CT scan, MRI, and isotope 

scanning with metaiodobenzylguanidine. 

C. Cardiac Effects of a Catecholamine Crisis 

In addition to tachydysrhythmias, a prolonged QT interval, which can predispose the 

patient to more lethal arrhythmias, may be present on the ECG. Findings of cardiac 

ischemia and coronary artery disease (ST elevation or depression and T wave 

inversion) also complicate the diagnostic picture because many of these findings 

resolve after tumor removal. 

Treatment 


Assess airway, and provide supplemental oxygen as needed (5-10 L by nasal cannula 

or mask). Establish large-bore intravenous access. Draw blood for routine studies (CBC, 

serum electrolytes, glucose, hepatic and renal function). Replace volume deficits, and 

correct electrolyte abnormalities. Avoid drugs or procedures that may exacerbate a 

catecholamine crisis. Begin 24-hour urine collection for fractionated catecholamines, 

metanephrine, and VMA. 

BR>B. Specific Therapy 

1. Phentolamine—The a-adrenergic blockade of phentolamine has been the traditional 

cornerstone of acute therapy for pheochromocytoma. The dose is 1-2 mg intravenously 

every 5 minutes. Caution: Higher initial doses may cause sudden severe hypotension. 

If no response is seen, increase the dose to 5 mg intravenously every 5 minutes until 

adequate blood pressure control occurs. Orthostatic hypotension is a common side 

effect and can be managed by ensuring adequate hydration and keeping the patient 

recumbent.

2. Nitroprusside—Intravenous sodium nitroprusside infusion, 0.5-10 ug/kg/min, may be 

useful in a hypertensive crisis. Risks of cyanide toxicity with prolonged therapy and the 

need for careful continuous cardiovascular monitoring have prompted clinicians to 

switch to newer agents such as fenoldopam and labetalol to control blood pressure in 

hypertensive crisis. 

3. Fenoldopam—Fenoldopam, a dopamine-1 receptor agonist, is a promising 

alternative to nitroprusside. An intravenous infusion beginning at 0.1 ug/kg/min 

vasodilates renal, splanchnic, and coronary circulation. Improved renal blood flow, lack 

of a toxic metabolite, and a short half-life of 7-9 minutes are its major advantages. 

4. ß-Blockers—ß-Adrenergic blockade is usually reserved for patients with severe 

tachydysrhythmias. Propranolol, 1-2 mg intravenously at a rate of 1 mg/min repeated 

every 5 minutes to a total of 10 mg, may be used. ß-Blockade should begin only after 

a-blockade has been established to avoid unopposed peripheral a-receptor 

vasoconstriction. Mixed a-ß receptor antagonists are an excellent alternative to simple 

ß-blockade and significantly lessen the risk of unopposed a effects. Labetalol may be 

given in 10-20 mg intravenous boluses every 10 minutes until the desired blood 

pressure is achieved with maintenance intravenous infusion of 0.5-2.0 mg/min. 

5. Benzodiazepines—Benzodiazepines may also be useful in blunting the body's 

sympathetic response to excess catecholamines. Lorazepam, 1-2 mg intravenously, or 

diazepam, 5-10 mg intravenously, are common starting doses. Administer these drugs 

judiciously to avoid oversedation and hypotension, particularly if the patient is volume 

depleted. 

Disposition 

Hospitalization in an intensive care unit is indicated in all patients with 

pheochromocytoma. 

Elliott WJ: Hypertensive emergencies. Crit Care Clin 2001;17:435. [PMID: 11450325] 

(An excellent review of the literature on diagnosis and treatment of all causes of 

hypertensive emergency, including pheochromocytoma.) 

Liao WB et al: Cardiovascular manifestations of pheochromocytoma. Am J Emerg Med 

2000;18:622. [PMID: 10999582] (Focuses on the presentation and treatment of 

cardiovascular problems associated with pheochromocytoma.) 

Young WY: Pheochromocytoma and primary aldosteronism: diagnostic approaches. 

Endocrinol Metab Clin North Am 1997;26:801. [PMID: 9429861] (Emphasis of this 

article is on the diagnostic approach to pheochromocytoma.) 

PITUITARY APOPLEXY 


• Rare disease with variable presentation. 

• Patients often have headache. 

• Neurologic deficits including hemiparesis; cranial nerve defects including 

ophthalmoplegia and bitemporal hemianopsia. 


Pituitary apoplexy is a massive hemorrhagic infarction of the pituitary gland. Clinically 

the condition almost always occurs in the setting of a preexisting pituitary tumor or 

tumor in structures adjacent to the sella turcica. Pituitary adenomas are particularly 

prone to hemorrhage and necrosis. The symptoms seen in pituitary apoplexy result from 

(1) leakage of blood and necrotic material into the subarachnoid space, (2) development 

of a rapidly expanding hemorrhagic intrasellar mass lesion compressing the optic 

chiasm, cavernous sinuses, cranial nerves, and adjacent structures (hypothalamus and 

internal carotid arteries), and (3) acute hypopituitarism. 

Risk factors for pituitary apoplexy include head trauma, irradiation, estrogen, 

anticoagulation use, DKA, hypertension, diuretics, use of bromocriptine, and pregnancy 

(Sheehan syndrome, which occurs when massive intrapartum hemorrhage and shock 

occur, leading to vasospastic necrosis of the pituitary). 



Diagnosis is challenging, because pituitary apoplexy is a rare disease with variable 

presentation. Onset may be acute and dramatic or subacute, developing over days to 

weeks. Neurologic symptoms are most prominent and are usually the most striking 

features seen when a patient with pituitary apoplexy is examined. 

Headache is a common feature. Pituitary apoplexy should enter the differential 

whenever a pathologic headache is suspected. The quality of the headache has been 

described as subacute and worsening, as retroorbital, and as a sudden thunderclap. 

Meningeal irritation may be prominent feature. Nausea and vomiting may be present. 

Fever often is present from blood in the subarachnoid space or hypothalamic 

compression disturbing normal temperature regulation. Neurologic symptoms range 

from paresthesias to ataxia to unilateral weakness mimicking cerebrovascular accident. 

Ophthalmologic symptoms are also common. Compression of the optic chiasm from an 

expanding mass can cause visual disturbances, particularly bitemporal hemianopsia. 

Cranial nerve III compression can cause ophthalmoplegia. Further encroachment on the 

cavernous sinus can lead to dysfunction in cranial nerves IV, V, and VI (cavernous sinus 

syndrome). Compression of the internal carotid artery can lead to mental status 

changes ranging from mild lethargy to delirium to coma. Internal carotid artery 

compression can also cause hemispheric ischemia. 

With pituitary apoplexy, numerous endocrinopathies may be present. A history of 

pituitary hormone dysfunction may be helpful in making the diagnosis of pituitary 

apoplexy; however, adrenal insufficiency is the most life-threatening complication and

equires immediate attention in the emergency department. Respiratory failure may 

occur because of hypothalamic compression or increased intracranial pressure. 


Hypernatremia and hyponatremia may occur as a result of diabetes insipidus or 

inappropriate secretion of antidiuretic hormone. Obtain thyroid function tests, cortisol 

levels, growth hormone levels, and prolactin levels to assess global pituitary function. 

Cerebrospinal fluid will often be xanthochromic or grossly bloody, with elevated opening 

pressure. Analysis reveals elevated protein concentrations and increased numbers of 

red and white cells. Do not perform lumbar puncture if an intracranial mass is 

suspected. 

C. Imaging 

CT scan and MRI are the imaging studies of choice for diagnosis of pituitary apoplexy. 

Acute hemorrhage appears hyperdense on CT scan. Blood appears hypodense on 

T2-weighted MRI scans. MRI is helpful in detecting hemorrhage in the subacute setting. 

Because these patients are often unstable, exercise care in deciding to send the patient 

out of the emergency department for a prolonged period of time for an MRI. CT may 

miss small pituitary tumors, but CT scans are rapid and will pick up most clinically 

significant lesions in the sella turcica and surrounding structures. A negative CT scan 

does not necessarily exclude the diagnosis of pituitary apoplexy. 

Treatment 

Assess for a patent airway, consider rapid-sequence intubation and mechanical 

ventilation in obtunded or comatose patients, and provide supplemental oxygen as 

needed. Cardiac monitoring is indicated. 

Hydrocortisone sodium succinate or phosphate, 100 mg intravenously, should be given 

to all patients suspected of having pituitary apoplexy to treat frequently concurrent and 

potentially lethal acute adrenal insufficiency. 

Definitive treatment for pituitary apoplexy is neurosurgical decompression, generally 

accomplished by transsphenoidal approach. Indications for surgery are decreasing 

consciousness, progressive vision loss, or increasing extraocular motor palsy indicating 

cavernous sinus compression. 

Disposition 

Hospitalization and immediate neurosurgical consultation are indicated. Surgery is the 

definitive treatment, but not every patient will require an operation. Some patients 

recover without sequelae with conservative management alone. 

Inamasu J et al: Pituitary apoplexy without ocular/visual symptoms. Am J Emerg Med 

2001;19:88. [PMID: 11146033] (Covers the classic clinical presentation of pituitary 

apoplexy along with an unusual presentation.) 

Laws ER, Kamal T: Pituitary surgery. Endocrinol Metab Clin North Am 1999;28:119. 

[PMID: 10207687] (Good information on the medical management of pituitary apoplexy

prior to surgery. Also covers general surgical approaches.) 

Lee CC et al: Emergency department presentation of pituitary apoplexy. Am J Emerg 

Med 2000;18:328. [PMID: 10830692] (Good review on the presentation, diagnosis, and 

management of pituitary apoplexy.) 

INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE 


• Hyponatremia in the setting of a reduced plasma osmolality, persistent urinary 

secretion of sodium (> 20 mEq/L), and urine osmolality that is inappropriately high for 

the degree of hyponatremia and hypoosmolality found. 

• Mental status changes ranging from mild to severe dependent on the degree of 

hyponatremia. 


Antidiuretic hormone (ADH), also known as arginine vasopressin (AVP), is secreted 

from the posterior pituitary and acts on the collecting ducts in the nephron to induce 

water reabsorption. Inappropriate secretion of antidiuretic hormone (SIADH) is a state of 

pathological hormone excess. Classic diagnostic criteria include (1) hyponatremia with 

lower than normal plasma osmolality in the absence of dehydration or volume depletion, 

(2) failure of the kidney to dilute the urine in the presence of reduced serum osmolality 

(urine osmolality is frequently > 300 mOsm/kg), (3) continued sodium excretion (usually 

> 20 mEq/L) despite hyponatremia, and (4) absence of hyponatremia producing states 

such as hypothyroidism, adrenal insufficiency, congestive heart failure, cirrhosis, or 

renal disease. 

Causes 

Numerous diseases and drugs can cause SIADH. Of particular note are malignancies 

(small cell carcinoma of the lung, pancreatic carcinoma, thymoma, Hodgkin disease), 

central nervous system disorders, surgery, pulmonary disorders (tuberculosis, 

pneumonia, lung abscess, bronchiectasis). Several medications have been implicated in 

SIADH, most commonly antidepressants, antipsychotics, anticonvulsants, sulfonylureas, 

angiotensin-converting enzyme inhibitors, narcotics, and MDMA (Ecstasy). 

The elderly are at higher risk for SIADH because several physiologic effects of aging 

contribute to its pathogenesis, including an increased ADH response to osmotic 

stimulation; declining renal function; and decreased renin, angiotensin, and aldosterone 

production. 



The clinical presentation of SIADH depends on the level of hyponatremia and water

intoxication: 

• In mild cases (serum sodium = 120 mEq/L), patients are usually asymptomatic. 

• When serum sodium reaches 105-120 mEq/L, patients begin to experience neurologic 

manifestations such as anorexia, nausea, vomiting, personality changes, depressed 

tendon reflexes, and muscle weakness. 

• With severe hyponatremia (= 105 mEq/L), coma, seizures, delirium, cranial nerve 

palsies, hypothermia, and altered patterns of respiration (Cheyne-Stokes) may be 

evident. 

Because SIADH can be caused by various pathologic conditions, patients will also 

present with signs or symptoms of their underlying disease (eg, malignancy, pulmonary 

disease). Edema and other signs of volume overload are highly unusual even with 

severe hyponatremia and water intoxication. Signs of volume overload indicate an 

alternative diagnosis. 


Hyponatremia is the classic feature of SIADH. Other findings include a reduced plasma 

osmolality, persistent urinary secretion of sodium (> 20 mEq/L), and urine osmolality 

that is inappropriately high for the degree of hyponatremia and hypoosmolality found. 

Treatment 


Assess airway, protect the airway with endotracheal intubation in obtunded or comatose 

patients and initiate mechanical ventilation, and provide supplemental oxygen as 

needed. Establish large-bore intravenous access. Draw blood for measurement of 

serum sodium and other electrolytes, creatinine, blood urea nitrogen, osmolality, cortisol 

levels, and thyroid function studies (TSH and free T 4 ). Send urine for urinalysis and 

measurement of urinary osmolality, electrolytes, and specific gravity. 

Monitor carefully the patient's body weight, intravenous and oral intake, and urine 

output. Measure serum and urine electrolytes and osmolality every 4-6 hours during the 

acute phase and then once or twice daily until the patient's condition has stabilized. 

Assess the patient for evidence of renal, hepatic, or cardiac dysfunction. Obtain a 

history of drugs and medications used by the patient. Evaluate for manifestations of 

cancer, central nervous system disease, or pulmonary disease. 


Fluid restriction is the treatment of choice for the correction of hyponatremia. 

1. Mild SIADH (serum sodium = 120 mEq/L)—Restrict fluids to 800-1000 mL per 24 

hours. 

2. Moderate SIADH (serum sodium 105-120 mEq/L)—Restrict fluids to 500 mL per 24 

hour.

3. Severe SIADH (serum sodium < 105 mEq/L or at any level if the patient 

develops neurologic complications such as coma or seizures)—This is a medical 

emergency. Treatment is as follows: 

• Administer hypertonic saline, 3% solution, at 1-2 mL/kg/h for the first 3-4 hours. 

• Use intravenous furosemide, 1 mg/kg, to counteract volume overload. 

• Monitor sodium and potassium every 1-2 hours and adjust fluids and replace as 

needed. 

• Correct to a serum sodium level of 125 mEq/L or until central nervous system 

involvement resolves, then resume fluid restriction therapy as described previously. 

Serum sodium correction should average 0.5-2 mEq/L/h and no more than 12 mEq/L in 

the first 24 hours. Faster rates of sodium correction increase the risk for central pontine 

myelinolysis. Symptoms of tetraparesis and bulbar palsy are seen. Once central pontine 

myelinolysis occurs as a complication, there are no proved methods of treatment. 

Disposition 

Responsible patients with mild SIADH without any neurologic symptoms may be 

managed on an outpatient basis with fluid restriction and close follow-up. Patients with 

more severe symptoms of SIADH and those who may not follow proposed treatment 

recommendations should be hospitalized. Patients receiving hypertonic saline should be 

admitted to the intensive care unit. 

Miller M: Syndromes of excess antidiuretic hormone release. Crit Care Clin 2001;17:11. 

[PMID: 11219224] (Discusses the various causes, pathophysiology, and management 

options of SIADH.) 

Robertson GL: Antidiuretic hormone. Normal and disordered function. Endocrinol Metab 

Clin North Am 2001;30:671. [PMID: 11571936] (Covers antidiuretic hormone physiology 

in both normal and disease states.) 

CENTRAL DIABETES INSIPIDUS 


• Signs and symptoms include lethargy, altered mental status, irritability, hyperreflexia, 

and spasticity. 

• Urine osmolality of < 150 mOsm/kg in the setting of serum hypertonicity and polyuria is 

generally diagnostic of diabetes insipidus. 


Central diabetes insipidus can be defined by the abnormal excretion of large amounts of 

solute-free water in the urine. Urine volumes in patients with central diabetes insipidus 

have exceeded 45 mL/kg per 24 hours. The pathology behind central diabetes insipidus 

is ADH deficiency, usually resulting from an insult to the hypothalamic-posterior-pituitary 

axis. Most patients will have an intact thirst mechanism, and polydipsia (fluid intake > 

3.5 L/d) occurs in an attempt to maintain adequate hydration. If water intake does not 

keep up with urinary losses, extracellular volume depletion and hypernatremia soon 

develop. 

Causes 

Central diabetes insipidus can be acquired or caused by congenital factors. Acquired 

causes include head trauma, surgery, tumors (craniopharyngiomas, primary or 

metastatic hypothalamic tumors), infection (tuberculosis, syphilis, basilar meningitis, 

fungal infections), cerebrovascular events (cerebral aneurysms, cavernous sinus 

thrombosis, postpartum pituitary infarction, cerebrovascular accidents), granulomatous 

diseases (sarcoidosis, histiocytosis X, Wegener granulomatosis). Congenital forms of 

both central and nephrogenic diabetes insipidus exist. 



1. ADH deficiency—Profound polydipsia and polyuria are present. Polyuria may lead to 

associated nocturia, incontinence, or enuresis. Urine osmolality is typically less than 300 

mOsm/kg. 

2. Hypernatremia and hyperosmolality—Hypernatremia causes intracellular 

dehydration as water shifts to the more hypertonic extracellular fluid space. The organ 

most susceptible to these effects is the brain. Signs and symptoms include lethargy, 

altered mental status, irritability, hyperreflexia, and spasticity. 

Intracranial hemorrhage may occur as the brain shrinks and mechanical tension is 

placed on dural veins and venous sinuses. Patients with marked volume deficits 

typically have hypotension, tachypnea, tachycardia, and decreased level of 

consciousness. Fever may be present. With severe dehydration, hypovolemic shock 

and coma are common. Patients whose diabetes insipidus is caused by intracranial 

neoplasms may also have visual field defects and anterior pituitary insufficiency. 

Symptoms are milder in chronic hypernatremia because the brain has had a chance to 

produce its own osmotic components. In the patient presenting with polydipsia and 

polyuria, a number of pathologic processes can be present and the differential diagnosis 

is broad. As a general rule, a urine osmolality of less than 150 mOsm/kg in the setting of 

hypertonicity and polyuria is diagnostic of diabetes insipidus. A good history can identify 

drug-induced diabetes insipidus caused by lithium or demeclocycline. A trial of DDAVP 

(exogenous ADH) can also distinguish neurogenic from nephrogenic diabetes insipidus. 

Urine osmolality will increase and volume will decrease with DDAVP administration in 

central but not nephrogenic diabetes insipidus. 

B. Laboratory Findings

Hypernatremia and hyperosmolality are found in uncompensated patients. Serum 

sodium may be greater than 160 mEq/L in severe cases, and prerenal azotemia is 

common in these patients. Specific gravity and osmolality of urine are low in proportion 

to serum osmolality. 

C. Imaging 

Urgent MRI of the brain is indicated to rule out tumor, mass, or hemorrhage in the 

region of the hypothalamus or pituitary gland. CT scanning may help exclude other 

central nervous system lesions. 

Treatment 


Assess airway, consider rapid-sequence intubation and mechanical ventilation in 

obtunded or comatose patients, and provide supplemental oxygen as needed. Establish 

large-bore intravenous access. Draw blood samples for measurement of electrolytes, 

osmolality, glucose, calcium, serum cortisol levels, and renal and thyroid function tests. 

Measure plasma ADH; if very low, this may be diagnostic. 

Obtain urine specimens for routine urinalysis and specific gravity and osmolality 

measurements. Monitor volume status, body weight, fluid intake, and urine output and 

specific gravity. 

B. Volume and Electrolyte Deficits 

Water administration—whether orally, by nasogastric tube, or intravenously—is the 

treatment for hypernatremia. Whenever possible, the oral or nasogastric route is 

preferred because water absorption and resultant decline in serum sodium 

concentrations are more gradual. 

Free water deficit can be calculated by the following equation: 

Hypotonic saline (0.45% normal saline) or 5% dextrose in water may be given. The 

latter is given to patients who show severe signs of neurologic compromise from 

hypernatremia. Be wary of hyperglycemia when using dextrose-containing solutions; it 

may cause an osmotic diuresis and worsen the hypernatremia. 

Replace half the volume deficit within the first 12-24 hours. When serum sodium 

decreases to less than 150 mEq/L, 0.45% or 0.9% saline should be used. Decreasing 

the serum sodium greater than 1-2 mEq/L/h can cause fluid shifts back into the 

intracellular compartment causing cerebral edema. Neurologic deterioration after 

hydration therapy should raise serious concern and prompt action. 

C. Specific Therapy 

Desmopressin acetate or DDAVP, 1-2 ug every 12-24 hours subcutaneously or 

intravenously or 5-20 ug every 12 hours intranasally, is a synthetic AVP analogue that is

the drug of choice when treating central diabetes insipidus. It is preferred over other 

AVP preparations because it has a longer half-life and has almost no pressor effect. 

Disposition 

Patients with diabetes insipidus should be hospitalized for definitive diagnosis and 

initiation of treatment. Patients who are severely hypernatremic or who present in 

hypovolemic shock merit intensive care unit admission for at least the first 24 hours of 

treatment. 

Robertson GL: Antidiuretic hormone. Normal and disordered function. Endocrinol Metab 

Clin North Am 2001;30:671. [PMID: 11571936] (Excellent review of normal and 

pathologic antidiuretic hormone physiology.) 

Singer I, James OR, Fishman LM: The management of diabetes insipidus in adults. 

Arch Intern Med 1997;157:1293. [PMID: 9201003] (Discusses the various causes of 

diabetes insipidus, gives two case studies, and gives a comprehensive overview of 

initial and chronic treatment.) 




41. Metabolic & Endocrine Emergencies - Micheal D. Rush, MD, & Wason W. 

S. Louie, MD 


METABOLISM

Table 41-1. Risk factors for hyperglycemia and 

unrecognized diabetes mellitus. 




41. Metabolic & Endocrine Emergencies - Micheal D. Rush, MD, & Wason W. 

S. Louie, MD 

TABLES

42. Fluid, Electrolyte, & Acid-Base Emergencies - Michael E. Chansky, 

MD, FACEP, Andrew Nyce, MD, & Jason Friedman, MD 1 

I. DIAGNOSIS OF FLUID & ELECTROLYTE DISORDERS 

Variations in Total Body Water 

1 This chapter is a revision of the chapter by Michael H. Humphreys, MD, from the 4th 

edition. 

Variations in total body water can usually be detected on the basis of the history and 

physical examination. Intravascular volume and serum osmolarity are regulated by 

homeostatic mechanisms involving thirst, antidiuretic hormone (ADH), and renal sodium 

excretion and absorption. 

A. Volume Excess 

Volume excess is manifested as peripheral edema or circulatory overload (jugular 

venous distention, pleural effusion, ascites, cardiac gallop). 

B. Volume Depletion 

Volume depletion is shown by poor skin turgor, dry mucous membranes, or thirst. 

C. Circulatory Compromise and Decreased Intravascular Volume 

Compromised circulation and decreased intravascular volume are manifested by resting 

tachycardia, narrowed pressure, orthostatic hypotension, or shock. 

ELECTROLYTE ABNORMALITIES 

Disordered electrolyte concentrations produce vague symptoms that are referable 

primarily to the neuromuscular system and are often mistaken for primary neurologic or 

metabolic abnormalities. 

Detection of electrolyte abnormalities requires a high index of suspicion in the proper 

clinical setting and laboratory measurement of blood constituents (sodium, potassium, 

chloride, bicarbonate [HCO 3 - ], calcium, magnesium, and phosphorus). Serum glucose, 

blood urea nitrogen, and creatinine are also helpful. These tests are indicated for any 

patient with even vague neuromuscular symptoms and a pertinent history, examination, 

or medications. 

APPROACH TO THE PATIENT 

A. Normal Values 

Evaluation and treatment are based on (1) assessment of total body water and its 

distribution and (2) electrolyte concentrations.

1. Body water— Table 42-1 lists the normal volumes of various body fluid 

compartments both as fractions of body weight and as amounts in liters in a hypothetical 

man or woman. 

2. Electrolytes— Table 42-2 presents the normal ranges of serum electrolyte 

concentrations. 

3. Osmolality—The osmolality of fluid in any one compartment is identical to that in all 

other compartments; normally, it is about 290 mOsm/kg. 

B. History 

The history should include information about the following: 

• Salt and water retention 

- Symptoms of congestive heart failure 

- Recent weight gain 

- Peripheral edema or ascites 

- History of congestive heart failure or liver or renal disease 

• Volume depletion 

- Gastrointestinal losses from vomiting, diarrhea, or nasogastric tube 

- Urinary losses associated with renal disease, diuretics, or diabetes insipidus 

- Excessive insensible loss from skin associated with fever or sweating 

C. Physical Examination 

The physical examination supports the historical data. Particularly helpful are any 

documented changes in body weight, skin turgor, mucous membranes, or vital signs 

that have occurred over a short time. A decrease in blood pressure and an increase in 

pulse rate when the patient changes from the supine to an upright (sitting or standing) 

position is a relatively sensitive measure of intravascular hypovolemia. 

D. Laboratory Findings 

Laboratory measurements provide corroboration and quantification of abnormalities. 


DISORDERS OF SERUM SODIUM CONCENTRATION 

HYPONATREMIA (See Figure 42-1.)


• Hyponatremia is a disorder of impaired water excretion. 

• Assess volume status, measure urine osmolality, and review all medications and 

thyroid and adrenal function. 

• Symptoms relate to the rate of change. 

• Therapy is geared toward replacing volume and treating the underlying condition. 


Hyponatremia is commonly associated with many disease processes (Table 42-3) and 

use of certain drugs (Table 42-4). It is characterized by a serum sodium concentration 

under 130 mEq/L. Hyponatremia is a manifestation of decreased water excretion. 

Appropriate water excretion occurs only when the kidneys are adequately perfused, 

chloride is transported in the ascending loop, and ADH secretion is inhibited. Symptoms 

of hyponatremia vary but relate primarily to the rate of serum sodium change. 

Alterations in central nervous system function dominate the clinical presentation and 

include delirium, drowsiness, and lethargy progressing to coma and seizures. These 

symptoms may coexist with those caused by concurrent volume depletion: faintness 

and dizziness, orthostatic hypotension, tachycardia, dry mucous membranes, poor skin 

turgor, oliguria, and thirst. 

Rule out spurious hyponatremia arising from erroneous sampling, especially when the 

serum sodium concentration fails to correlate with the clinical scenario, (ie, sample 

drawn above an intravenous line of hypotonic fluid). In the following conditions, the 

measurement is accurate but does not represent a true hypoosmolar state 

(pseudohyponatremia): 

A. Hyperlipidemia and Hyperproteinemia 

In hyperlipidemia and hyperproteinemia, markedly increased amounts of lipid or protein 

occupy an increased portion of the plasma volume, resulting in decreased volume of 

water for electrolytes and other solutes. The sodium concentration in total plasma 

volume is decreased; however, if sodium concentration in plasma water is measured, it 

is normal. 

The plasma is turbid and milky if hyperlipidemia is present. Excess plasma proteins can 

be detected quickly in the laboratory using a protein refractometer. In each of these 

cases, a normal sodium concentration can be expected if serum osmolality is normal 

despite the measured hyponatremia. 

B. Hyperglycemia 

The increase in extracellular fluid osmolality produced by excess glucose molecules 

causes the transfer of water from the intracellular to the extracellular compartment, 

thereby increasing the volume of water there. Because sodium is confined principally in 

the extracellular space, serum sodium concentration falls. Correction of hyperglycemia 

usually corrects hyponatremia by approximately 1.6 mEq/L of sodium for every 

100-mg/dL fall in glucose concentration. Correction of hyperglycemia only shifts water

etween the intracellular and the extracellular spaces, so that the total body sodium 

does not change. 

Preliminary Evaluation 

A. Assess Urgency of Treatment 

1. Serious symptoms—Prompt therapy is indicated if muscle cramps, weakness, 

myoclonus, confusion, delirium, lethargy, seizures, coma, or increased deep tendon 

reflexes are associated with reliable laboratory evidence of severe hyponatremia (serum 

sodium < 120 mEq/L). Hyponatremia should be presumed to be the cause of symptoms 

until proved otherwise. 

2. Rapidity and intensity of treatment—These factors depend on the rate of 

development of hyponatremia, its severity, and any life-threatening complications (eg, 

seizures, altered mental status). Slowly developing chronic hyponatremia is well 

tolerated even to a serum sodium concentration as low as 120 mEq/L. An abrupt fall in 

serum sodium concentration, even though it is of lesser degree, may be poorly 

tolerated. 

B. Assess Extracellular Fluid Volume 

The history and physical examination may suggest increased or decreased extracellular 

fluid volume. This finding—as well as determination of the sodium concentration in a 

urine specimen obtained before treatment has been started—provides a basis for 

diagnosis. 

1. Hyponatremia with Hypovolemia 


Hyponatremia with hypovolemia occur because losses of water and salt have been 

partially replaced with water, via appropriate ADH secretion. Patients show signs of 

hypovolemia (postural hypotension or tachycardia; oliguria) and (occasionally) frank 

shock. 

A. With Renal Sodium Conservation 

(Urine sodium < 10 mEq/L unless diuretics have been given.) Hyponatremia is due to 

extrarenal losses of sodium with continued intake of water. Usual causes include 

gastrointestinal losses (vomiting, nasogastric tube, or diarrhea), severe sweating, or 

increase in volume of fluid sequestered from extracellular fluid ("third-spacing") (eg, 

from burns, pancreatitis, intestinal obstruction, or crush injuries). 

B. With Renal Sodium Wasting 

(Urine sodium > 20 mEq/L.) Hyponatremia is due at least in part to renal sodium 

wasting such as occurs with diuretic therapy or in patients with adrenal insufficiency. 

Patients with chronic renal disease may also present with this clinical picture. 

Treatment 

Restore depleted extracellular fluid volume with infusions of isotonic saline solutions

(eg, normal saline or lactated Ringer's injection). Hypertonic saline is rarely necessary to 

treat this form of hyponatremia. 

Disposition 

The need for hospitalization depends on the underlying cause and the need for 

prolonged treatment. 

2. Hyponatremia with Fluid Overload 


Hyponatremia with fluid overload occurs because of a relative decreased intravascular 

volume and ADH secretion. This results in an impaired ability to excrete water. Total 

body sodium is greater than normal. Signs of fluid overload (jugular venous distention, 

sacral or peripheral edema, pulmonary edema or pleural effusions, ascites, or anasarca) 

are present. Evidence of the underlying disease (eg, heart failure, cirrhosis) is usually 

apparent. The urine sodium concentration is characteristically less than 10 mEq/L 

unless the patient has been taking diuretics. 

Treatment 

A. Water Restriction 

Restrict salt and water intake (eg, 2 g of sodium; 1-2 L of water daily). Water restriction 

is necessary so that insensible water losses will produce slow correction of 

hyponatremia. 

B. Diuretics 

Loss of water may need to be accelerated in some patients (eg, those with pulmonary 

edema) by giving diuretics (eg, furosemide [Lasix], 0.5-1.0 mg/kg intravenously). If 

diuretics aggravate renal hypoperfusion, hyponatremia may worsen. 

C. Hypertonic Saline 

It may be advisable to administer small amounts of hypertonic saline (100-200 mL of 3% 

sodium chloride solution) to patients who already have expanded extracellular fluid 

volume if they have profound hyponatremia (serum sodium < 110 mEq/L) with serious 

manifestations (eg, coma or seizures). In such cases, monitoring of central venous 

pressure or pulmonary capillary wedge pressure in an intensive care unit setting is 

advisable, and concomitant administration of furosemide (as above) is usually 

necessary. 

D. Dialysis 

In patients with concurrent renal failure, emergency dialysis may be necessary to help 

correct hyponatremia. 

Disposition 

Hospitalization is required in most cases.

3. Hyponatremia with Isovolemia 


Occasionally, hyponatremia develops in euvolemic patients. In this setting, evaluation of 

urine osmolality in addition to determination of urine sodium may be helpful. 

Hyponatremic patients should have a urine osmolarity significantly less than serum 

osmolarity (ie, indicating appropriate excretion of water). 

A. Deficiency of Potassium 

The uncommon occurrence of hyponatremia resulting from a deficiency in total body 

potassium has been reported in patients who have taken diuretics without potassium 

supplementation. 

B. Inappropriate Antidiuretic Hormone Secretion 

In the syndrome of inappropriate secretion of ADH, mild hyponatremia is universal, and 

urine osmolality is usually over 300 mOsm/kg. Drugs other than diuretics have also 

been associated with hyponatremia (see Table 42-4). The mechanisms by which these 

drugs cause hyponatremia are not firmly established but may include inappropriate 

secretion or enhanced effect of ADH. 

C. Hypothyroidism 

Hypothyroidism may also be associated with isovolemic hyponatremia. 

D. Psychogenic Polydipsia 

Psychogenic polydipsia may produce mild to moderate hyponatremia caused by excess 

free-water intake. Euvolemia is maintained through the renal excretion of sodium. Urine 

sodium is typically elevated (> 20 mEq/L), and urine osmolality is low (< 300 mOsm/kg). 

Treatment 

Treatment depends entirely on the underlying cause. In patients with precarious 

hemodynamic status, monitoring of central venous pressure in an intensive care unit is 

essential. 

Inappropriate secretion of ADH is treated primarily by water restriction (eg, 1-2 L/d). 

Hypokalemic hyponatremia is corrected by restoring body potassium stores. Replace 

potassium by intravenous infusion at a rate not to exceed 10-15 mEq/h, via a central 

line in a monitored setting. Concentrations of solutions should seldom exceed 40 

mEq/L. Oral therapy is preferable to parenteral administration, if the patient's condition 

permits it. The usual dose for an adult is 40-120 mEq/d. 

Drugs associated with hyponatremia should be stopped. 

Severe hyponatremia (serum sodium < 120 mEq/L) without life-threatening symptoms 

may be treated by administration of isotonic saline with concomitant administration of 

potent diuretics (eg, furosemide, 0.5-1.0 mg/kg intravenously). Profound hyponatremia 

(serum sodium < 110 mEq/L) or severe hyponatremia with life-threatening

manifestations (eg, coma, seizures) should be corrected more rapidly by the infusion of 

100-200 mL of hypertonic (3%) sodium chloride solution (adult dose) along with a 

diuretic in an intensive care unit. 

Disposition 

Most patients with isovolemic hyponatremia and all patients with abrupt hyponatremia 

require hospitalization. Abrupt hyponatremia may be associated with permanent 

neurologic damage, as may rapid or overcorrection. 

HYPERNATREMIA 


• Hypernatremia is related to pure water loss, hypotonic fluid, or rarely salt gain. 

• Most common in infants and the elderly. 

• Symptoms are primarily neurologic and related to severe hypovolemia. 

• Measure urine osmolality. 

• Therapy is emergent and aimed toward restoring volume and water deficits. 

• Address the underlying condition. 


Hypernatremia is characterized by a serum sodium concentration over 150 mEq/L. 

Hypernatremia is much less common than hyponatremia but may also cause serious 

neuromuscular symptoms and signs. Hypertonicity normally stimulates ADH release 

and thirst. Hypernatremia arises from an inability either to concentrate the urine or to 

drink water. Excessive salt intake may rarely play a role. Thus, hypernatremia may arise 

from excessive water loss, decreased water intake, or salt gain. 

A. Excessive Water Loss 

Excessive water loss often occurs when the thirst mechanism is deficient (eg, in infants 

or when coma, intubation, or dementia are present). Causes can be classified as 

nonrenal or renal. 

1. Nonrenal—Nonrenal causes of excessive water loss include protracted fever, burns, 

and thyrotoxicosis. 

2. Renal—There are 5 main renal causes: 

• Tube feeding syndrome (ie, more water than sodium is lost in relation to intake of 

water and sodium, producing osmotic diuresis) 

• Diabetes insipidus 

• Hypercalcemia

• Renal failure 

• Drugs (eg, demeclocycline, lithium) 

B. Inadequate Water Intake 

Inadequate water intake may occur when coma is present or when the thirst mechanism 

is lost. 

C. Excessive Sodium Intake: Massive Salt Ingestion 

Excessive sodium intake may result from ingestion of salt pills, from ocean drowning, or 

from iatrogenic causes (eg, inadvertent hypertonic solution administration). 



Symptoms and signs of hypernatremia relate to the severity and rate of development. 

These include thirst, lethargy, and dehydrated appearance (eg, dry mucous 

membranes, poor skin turgor). Tachycardia, low blood pressure, and oliguria may be 

present. Fever, confusion, delirium, seizures, and coma are manifestations of severe 

hypernatremia. Intracerebral hemorrhage may occur in severe cases, perhaps 

secondary to tearing of bridging veins stretched by shrinking brain tissue. Elevated 

blood urea nitrogen level and hematocrit may also occur. 

B. Renal Conservation of Water 

The approach to the patient with hypernatremia depends primarily on urine osmolality. 

1. Urine osmolality greater than 400 mOsm/kg—If urine osmolality is greater than 

400 mOsm/kg, renal water-conserving mechanisms are operating. 

a. Nonrenal losses—Hypernatremia is due to nonrenal losses of water from skin, 

lungs, gut, or burn areas, with attendant failure of water intake to keep pace with water 

losses. In this situation, total body sodium deficits may also be present despite the 

hypernatremia. 

b. Tube feedings—Hypernatremia with concentrated urine also occurs with high-protein 

tube feedings with limited water intake. The increased urine urea concentration results 

in osmotic diuresis, with loss of more water than sodium. 

c. Diabetes mellitus—Osmotic diuresis from glycosuria in patients with diabetes 

mellitus may also result in hypernatremia (after correction for the elevated glucose 

concentration). 

2. Urine osmolality less than 250 mOsm/kg— 

a. Diabetes insipidus—Hypernatremia accompanied by a urine osmolality of less than 

250 mOsm/kg is characteristic of diabetes insipidus. 

b. Central diabetes insipidus—Impaired secretion of ADH from the pituitary may occur

following damage to or disease of the pituitary gland or the hypothalamus. 

c. Nephrogenic diabetes insipidus—Nephrogenic diabetes insipidus results from 

insensitivity of the renal distal tubule and collecting duct to ADH. Acquired nephrogenic 

diabetes insipidus may occur in patients taking lithium or demeclocycline or after relief 

of prolonged urinary tract obstruction. 

3. Urine osmolality approximately equal to plasma osmolality—Hypernatremia may 

also develop when urine osmolality is about the same as plasma osmolality. In this 

case, hypernatremia results from impaired renal water conservation, which may occur 

(1) in the diuretic phase of acute renal failure, (2) in certain cases of postobstructive 

diuresis, with severe potassium depletion, (3) in prolonged hypercalcemia, or (4) in 

some cases of chronic renal disease. 

Treatment 

Acute hypernatremia is a medical emergency because of the risk of brain damage and 

impaired ability to regulate water intake. 

A. Hypovolemia 

Hypernatremia in the presence of severe hypovolemia should be treated initially with 

isotonic saline to correct the volume deficit, followed by 5% dextrose in water to replace 

the free-water deficit. A mild volume deficit may be treated initially with 0.45% saline in 

5% dextrose in water. 

B. Water Deficit 

Replace water with intravenous dextrose solutions (eg, 5% dextrose in water). The 

amount of sodium excess and the amount of water required to restore serum sodium 

concentration to normal can be estimated from equations 6 and 7 (Appendix). For 

example, a 70-kg man with a serum sodium concentration of 155 mEq/L has an 

estimated total body water of 35 L and excess sodium of 525 mEq (15 mEq/L × 35). It 

would take 3.75 L of water to restore serum sodium to 140 mEq/L. In general, the rate 

of correction of hypernatremia should not exceed 1-2 mEq/L/h. 

C. Body Deficit of Sodium 

Because total body sodium deficits frequently exist with hypernatremia, fluid therapy 

often must include sodium in hypotonic replacement solutions. 

D. Correction of the Underlying Disorder 

After initiating therapy, it is important to address the cause of water loss, inadequate 

water intake, or salt intoxication. 

Disposition 

Patients with serum sodium over 150 mEq/L require hospitalization. Patients with lesser 

degrees of hypernatremia may be discharged from the emergency department with 

close follow-up. 

DISORDERS OF SERUM POTASSIUM CONCENTRATION

Potassium is the principal intracellular electrolyte; over 95% of the body's potassium is 

stored within cells. The body's potassium content is given in Table 42-5. Disorders of 

serum potassium concentration may not reflect accurately the condition of body 

potassium stores for the following reasons: 

• Serum pH alters the distribution of potassium between cells and plasma: acidosis 

promotes transfer of potassium from intracellular to extracellular fluid, causing 

hyperkalemia; alkalosis does the reverse, causing potassium to enter the cells. 

• Extensive cell injury (eg, from burns or crush injuries) may release large amounts of 

potassium into the extracellular fluid and cause hyperkalemia, because tissue cells 

contain most of the body's potassium. 

• Body potassium content and serum concentrations of potassium are regulated by the 

kidney; however, the kidneys adjust to alterations in serum potassium more slowly and 

with less efficiency than is the case with sodium. 

• Diuretic-induced potassium loss is one of the major causes of hypokalemia. 

Diminished food intake alone is rarely a cause of hypokalemia, because most foods 

contain large amounts of potassium. 

• Potassium distribution may be affected by circulating levels of hormones such as 

insulin (which causes potassium influx into cells) and catecholamines (which cause 

potassium influx via their ß-adrenergic effects). 

HYPOKALEMIA 


• Most commonly occurs in diuretic therapy and metabolic alkalosis. 

• Symptoms are primarily neuromuscular and cardiac. 

• Serum potassium represents only 2% of total body potassium. 

• Whenever possible, utilize oral replacement; never give more than 15 mEq/h 



Hypokalemia is defined as a serum potassium concentration of less than 3.5 mEq/L. It is 

a common complication of diuretic therapy. Other causes are listed in Table 42-6. Most 

cases of hypokalemia result from excessive potassium wasting. 



Clinical signs and symptoms suggestive of hypokalemia include varying degrees of 

weakness, including muscular paralysis; paralytic ileus; rhabdomyolysis; and cardiac

dysrhythmias, including A-V dissociation, ventricular tachycardia, and ventricular 

fibrillation. 


The most important laboratory tests to obtain are a basic chemistry panel and consider 

a venous pH. Hypokalemia can be seen in both acidosis and alkalosis. Determining 

whether a metabolic derangement exists, and what that derangement is, remains the 

key to correcting the electrolyte abnormality (Figure 42-2) . 


Typical electrocardiogram (ECG) changes seen with hypokalemia include ST 

depression, T wave flattening, and the appearance of U waves (Figure 42-3). 

Treatment 

A. Hypokalemia Due to Alkalosis 

If hypokalemia is not associated with depletion of body stores of potassium and is due 

solely to metabolic alkalosis, the initial goal of treatment is to correct the alkalosis or the 

condition causing it. Hypokalemia, however, may cause or exacerbate metabolic 

alkalosis (eg, prolonged gastric suction), thus necessitating potassium repletion. 

B. Hypokalemia Associated with Depletion of Body Potassium Stores 

Treat hypokalemia arising from depleted body potassium stores with oral or intravenous 

potassium salts, depending on severity and associated symptoms. 

Intravenous emergency replenishment of potassium stores is indicated for patients with 

severe hypokalemia (serum potassium < 2.5 mEq/L), especially if neuromuscular or 

ECG manifestations are present. 

If intravenous replenishment is necessary, the solution should be no more concentrated 

than 60 mEq/L and is generally infused at a rate of 10-15 mEq/h. The solution should be 

mixed in normal saline or other dextrose-free solutions, because the addition of 

dextrose will stimulate insulin release and lead to intracellular uptake of the cation. 

Potassium should always be infused as a drip, never pushed rapidly. Although there is 

some debate over the use of central versus peripheral venous access for the infusion, it 

appears that either is acceptable. However, peripheral infusion may be complicated by 

painful irritation, especially at faster infusion rates. 

If patients are able to take fluids orally, they can be given oral potassium, which is safe 

and rapidly absorbed. Give K + solution, 40 mEq orally every 3-4 hours, until 

hypokalemia is corrected. Avoid giving high doses of potassium-containing tablets or 

capsules for rapid potassium repletion, because esophageal injury has been reported if 

stricture is present. 

A good estimate for potassium repletion is that the administration of 20 mEq will cause a 

0.25 mEq/L rise in concentration. Therefore, a serum potassium of 2.5 mEq/L, or a 

potassium deficit of 1.0 mEq/L, will require approximately 80 mEq of oral or intravenous 

replacement. In general, the overall rate of intravenous potassium replacement should 

not exceed 5 mEq/kg/ 24 h (0.2 mEq/kg/h).

Occasionally patients may have hypokalemia and potassium depletion that are 

refractory to administration of potassium salts. Magnesium deficiency may contribute to 

this abnormality, and repletion of magnesium will be necessary to bring about full 

correction of the potassium depletion and hypokalemia. 

Disposition 

Patients with severe hypokalemia (serum potassium < 2.5 mEq/L) require 

hospitalization in a monitored setting for proper diagnosis and correction. Patients with 

lesser degrees of hypokalemia may be discharged from the emergency department but 

should have close follow-up and repeat testing within 1 week. 

HYPERKALEMIA (See Figure 42-2.) 


• A true life-threatening medical emergency. 

• Suspect in patients with renal disease, diabetic patients, or those taking potassium 

supplements. 

• Symptoms are primarily neuromuscular and cardiac. 

• ECG progression from hyperacute T waves to ventricular fibrillation may be rapid. 

• Beware of spurious hyperkalemia. 

• Therapy stabilizes cardiac membranes, shifts potassium into cells, and causes 

potassium elimination. 

• Always admit patients to monitored setting and address the underlying condition. 


Hyperkalemia is generally defined as a serum potassium concentration greater than 5.0. 

It is less common (Table 42-7), but more immediately life threatening, than 

hypokalemia. 



Clinical symptoms and signs of hyperkalemia include generalized weakness or 

paresthesias, diarrhea, and cardiac dysrhythmias. 


The ECG changes seen in hyperkalemia are varied and well-documented (see Figure 

42-3). A thorough understanding of these changes is crucial to the emergency 

physician, because they are often the first clinical indication of an abnormality. Tall, 

hyperacute, or "peaked" T waves are most often associated with mild hyperkalemia. As 

hyperkalemia worsens, prolongation of the PR interval and the QRS duration can be 

seen. Severe hyperkalemia can be manifest in many ways, including loss of P waves, 

intraventricular conduction delays, bundle branch blocks, bizarre QRS morphologies,

ventricular fibrillation, and asystole. 

In addition to these changes, ECG findings consistent with ischemia or infarction, 

including ST-segment changes and (less frequently) Q waves, can be seen in 

hyperkalemia. These changes will resolve with treatment of the underlying disorder. 

Because of the wide variety of possible ECG manifestations, hyperkalemia should be 

suspected in any high-risk patient (eg, with renal insufficiency or taking 

potassium-sparing diuretics) who has ECG abnormalities. 

C. Spurious Hyperkalemia 

Rule out spurious hyperkalemia caused by the following conditions: 

1. Hemolysis—If serum in the sample appears hemolyzed (pink), draw a new blood 

sample. Hemolysis is also associated with markedly elevated serum lactate 

dehydrogenase concentrations. 

2. Marked thrombocytosis—Platelet counts over 1 million/uL may result in liberation of 

significant amounts of potassium as clotting occurs. This effect may be avoided by 

measuring potassium concentrations or heparinized plasma rather than serum. 

3. Fist clenching during antecubital phlebotomy—This action can raise serum 

potassium concentration in the sample (but not in the body) by releasing potassium from 

the exercising forearm muscles. 

D. True Hyperkalemia 

If hyperkalemia is still present after acidosis has been corrected, the cause of 

hyperkalemia must be determined and treatment instituted accordingly. 

1. Renal disease—Renal disease associated with hyperkalemia is always manifested 

by decreased creatinine clearance and elevated serum creatinine. 

2. Mineralocorticoid deficiency—Mineralocorticoid deficiency (eg, Addison disease, 

acute adrenal insufficiency) may be manifested by hyperkalemia and hyponatremia. In 

severe cases, orthostatic hypotension or shock may also be present. 

In certain cases of renal insufficiency and type 4 renal tubular acidosis, hyporeninemic 

hypoaldosteronism may also be associated with hyperkalemia. In either case, serum 

sodium is usually low, which is unusual in other causes of hyperkalemia. 

3. Drug-induced hyperkalemia—Drug-induced hyperkalemia (eg, ingestion of 

aldosterone antagonists or large amounts of potassium) may be diagnosed from the 

history. Penicillin G, administered as a potassium salt in high doses, may be an 

iatrogenic cause of hyperkalemia. The use of potassium-containing salt substitutes in 

patients with sodium-retaining disorders may also predispose to hyperkalemia. Other 

medications that may cause hyperkalemia include potassium-sparing diuretics, 

nonsteroidal anti-inflammatory drugs, and digoxin. 

4. Crush injuries or burns—Rhabdomyolysis or burns sufficient to produce 

hyperkalemia are grossly apparent in most cases.

Treatment 

The speed with which treatment must be initiated depends on the degree of 

hyperkalemia and on symptoms, signs, and ECG abnormalities. Any unstable patient 

(serum potassium > 7.0 mEq/L, or with any degree of hyperkalemia and concurrent 

ECG changes) requires emergency stabilizing measures before further treatment, such 

as potassium elimination, is initiated. 

A. Emergent Stabilization 

Emergent stabilization is indicated for patients discussed above. Two amps of calcium 

gluconate, or 1 amp of calcium chloride, administered as an intravenous push, helps to 

decrease the irritability of cardiac myositic membranes. This can be repeated after 2-5 

minutes and followed by an infusion of 5 amps mixed in 500 mL of 5% dextrose in 

water, because the stabilizing effect of calcium is transient. Although calcium chloride 

provides a larger and more rapidly bioavailable source of calcium, it also carries a 

theoretical risk of worsening acidosis and should be used with caution in cases of 

hyperkalemia caused by acidosis. 

Insulin (10 units regular, intravenous push) can be administered to force a temporary 

influx of potassium into the cells. This should be given in concert with glucose to prevent 

iatrogenic hypoglycemia. Adding ß-2 agonists, either intravenously or via nebulization, 

can also enhance potassium influx. 

In patients with acidosis, sodium bicarbonate can be administered; however, this 

approach is not indicated in diabetic ketoacidosis (see "Acid-Base Disorders" section, 

below). 

B. Potassium Elimination 

Potassium elimination can be accomplished in one of two ways. Kayexalate (sodium 

polystyrene sulfate) is a potassium exchange resin that will bind the cation and enhance 

its elimination in the gastrointestinal tract. Hemodialysis is the definitive treatment and 

should be considered in patients with renal failure or following the above emergent 

measures in a severely unstable patient. 

C. Correction of the Underlying Disorder 

In almost all cases, correction of the underlying acidosis, or other secondary cause of 

the hyperkalemia, will resolve the electrolyte abnormality. This should be noted when 

undertaking corrective measures, because treatment of the underlying cause combined 

with emergent treatment of hyperkalemia may result in a hypokalemia. This is especially 

true in diabetic ketoacidosis, where patients often have depleted their total-body 

potassium stores, despite an apparent serum hyperkalemia. For this reason, treatment 

should be aimed at the underlying disorder, and chemistry panels should be checked 

every 1-2 hours until the patient has been stabilized. Serial blood gases may also be 

warranted. 

Disposition 

Patients with hyperkalemia require hospitalization in a monitored setting.

DISORDERS OF SERUM CALCIUM CONCENTRATION 

Calcium, the most abundant cation, is 99% bound to bone and 1% extracellular. Serum 

calcium is composed of 2 major fractions. About 55% of total serum calcium is bound to 

serum proteins (chiefly albumin) or complexed to organic anions such as citrate; the 

other 45% exists as free, or ionized, calcium. Symptoms and signs of disordered serum 

calcium concentration are due to changes in the ionized fraction. Proper interpretation of 

serum calcium concentration requires measure of serum albumin concentration. Serum 

calcium is usually reported in mg/dL; this unit is easily converted to mEq/L by dividing by 

2. The ionized calcium level in plasma is controlled chiefly by the action of parathyroid 

hormone, calcitonin, and vitamin D metabolites and is related to the patient's acid-base 

status. Acidosis increases the fraction of total calcium in the ionized form by displacing it 

from albumin, whereas alkalosis decreases it. As a result, symptomatic hypocalcemia 

may develop in patients who hyperventilate (acute respiratory alkalosis) or in those in 

whom metabolic acidosis has been rapidly corrected with infusion of sodium 

bicarbonate. 

HYPOCALCEMIA 


• May accompany shock, sepsis, or massive transfusion of blood products. 

• Neuromuscular and respiratory symptoms predominate. 

• Rarely life-threatening by itself and may be associated with disorders of magnesium 

and phosphate. 

• A prolonged QT interval may be only ECG manifestation. 

• Address the underlying cause. 


Hypocalcemia is defined as an ionized calcium concentration of less than 2.0 mEq/L. It 

may result from decreased intake or decreased absorption of calcium (eg, vitamin D 

deficiency, malabsorption syndromes), increased renal loss (eg, renal failure, diuretic 

therapy), endocrine disease (hypoparathyroidism), hypomagnesemia, or 

hyperphosphatemia. Hypocalcemia may accompany shock, hemorrhagic pancreatitis, 

sepsis, or massive transfusion of blood products (Table 42-8). 



Many patients with mild hypocalcemia are asymptomatic. Symptoms and signs of more 

severe hypocalcemia include tetany, weakness, fatigue, cramps, carpopedal spasm, 

convulsions, diplopia, and stridor and dyspnea due to laryngospasm. Positive 

Trousseau and Chvostek signs and fasciculations of skeletal muscle also occur. 

Cataracts may also occur with long-standing hypocalcemia.


An arterial or venous blood gas may be useful to identify (1) respiratory or metabolic 

alkalosis as a cause of transient tetany and (2) hypercapnia secondary to severe 

hypocalcemia. It is important to determine renal function and serum potassium and 

magnesium concentrations (coexisting abnormalities are common and may require 

treatment). 


A prolonged QT interval may be noted on the ECG without U waves (Figure 42-4). 

Treatment 

Hypocalcemia is rarely life threatening but must be addressed in conjunction with 

treating the primary disorder. Severe hypocalcemia can cause laryngeal stridor and 

grand mal seizures. Because of the potential for severe symptoms, even mild symptoms 

attributable to hypocalcemia should be treated. Asymptomatic patients require close 

outpatient follow-up and an appropriate workup. 

For initial treatment in a symptomatic adult, give calcium chloride (5%) or calcium 

gluconate (10%), one to two 10-mL ampules by intravenous infusion. Then give 1 

ampule in 500 mL of normal saline intravenously over 8 hours to provide 100-500 mg of 

calcium and maintain the serum calcium concentration at 7-8 mg/dL, the level at which 

symptoms are usually alleviated. During massive transfusions, 10 cc of calcium chloride 

should be given for every 4-6 units of blood. Long-term treatment of chronic 

hypocalcemia requires oral calcium supplements and vitamin D. Treat 

hypomagnesemia, if present (see below). 

Caution: Rarely, hypocalcemia requiring treatment is accompanied by markedly 

elevated phosphorus concentration (> 6 mg/dL). To prevent metastatic calcification, 

correct hyperphosphatemia before or while giving calcium. Give intravenous glucose 

and insulin (see "Hyperphosphatemia" section, below). 

Disposition 

Patients with acute symptomatic hypocalcemia require hospitalization in a closely 

monitored setting. Patients with less severe disease may be discharged from the 

emergency department but should have close follow-up. 

HYPERCALCEMIA 


• Usually caused by a malignancy or hyperparathyroidism. 

• Symptoms are primarily neuromuscular and renal. 

• Serum calcium above 12 mg/dL requires acute diagnosis and therapy. 

• Therapy is primarily volume repletion because natriuresis promotes renal calcium 

excretion.

• Bisphosphonates are effective osteoclast inhibitors. 

• Always admit symptomatic patients. 


Hypercalcemia is characterized by a serum calcium concentration over 11 mg/dL. It is 

commonly associated with numerous conditions (Table 42-9) and may have 

life-threatening consequences. The majority of patients with symptomatic hypercalcemia 

have either hyperparathyroidism or a malignancy. 



Symptoms of hypercalcemia usually begin at levels over 12 mg/dL and are nonspecific. 

The diagnosis may be missed unless it is suspected and serum calcium measured. 

Central nervous system depression, stupor, somnolence, weakness, psychosis, and 

coma may occur. Anorexia, vomiting, constipation, and abdominal pain may also be 

seen. Symptoms become severe at serum concentrations greater than 15 mg/dL. 

Renal damage may occur in chronic cases, for example, when impaired concentration 

ability of the kidney leads to polyuria, dehydration, hypernatremia, thirst, and finally 

azotemia. Band keratopathy may occur in long-standing hypercalcemia. 

Hypercalcemia reflects an increase in the concentration of the ionized fraction of 

calcium, because elevated levels of calcium-binding serum proteins (chiefly albumin) do 

not occur except in cases of extreme dehydration. 


ECG abnormalities include prolonged PR interval, shortened QT interval, and flattened 

T waves. 

Treatment 

Any serum calcium concentration above 12 mg/dL requires prompt treatment, especially 

if symptoms are present. The goal of treatment is to lower serum calcium by general 

measures and by measures appropriate to the specific cause of hypercalcemia. Avoid 

immobilization if at all possible. 

A. Promote Excretion of Calcium by the Kidney 

1. Fluids—Volume expansion with isotonic saline promotes a natriuresis and calcium 

excretion, and is the first step in treating hypercalcemia in patients with normal renal 

function. The vast majority of these patients are initially dehydrated. Infuse saline until 

the patient is clinically euvolemic and producing adequate urine. Rarely patients may 

require monitoring of central venous pressure. 

2. Diuretics—Furosemide is also effective in increasing excretion of calcium in patients 

in whom volume expansion with isotonic saline has been achieved. Do not use thiazide 

diuretics, because they may aggravate hypercalcemia. Give furosemide, 0.5-1.0 mg/kg 

intravenously, and monitor fluid status closely, because hypovolemia induced by

furosemide will diminish calcium excretion and prolong hypercalcemia. 

B. Increase Deposition of Calcium in Bone 

Another treatment approach is to promote deposition of calcium into bone or decrease 

the rate of resorption of calcium from bone. 

1. Bisphosphonates—These analogues of pyrophosphate are concentrated in areas of 

boney turnover and inhibit osteoclast activity. The first-generation bisphosphonate 

etidronate is poorly absorbed orally and is most effective intravenously (7.5 mg/kg 

intravenously each day for 3 days). It may cause hypophosphatemia through a renal 

mechanism. Second-generation pamidronate, 60-90 mg intravenously, infused over 24 

hours, has higher potency and prolonged duration of action. Fever is common and 

thought to be secondary to cytokine release from osteoclasts and macrophages. 

Pamidronate is the agent of choice in severe hypercalcemia associated with malignancy 

and is used with forced diuresis. 

2. Mithramycin—Given in an intravenous dose of 25 ug/kg, mithramycin lowers serum 

calcium concentration within 8-12 hours, and this effect may last several days. Close 

monitoring of serum calcium is necessary because toxicity is related to frequency and 

dose administered. Toxicity is unusual with only 1 or 2 doses. Mithramycin use has 

been displaced by the second-generation bisphosphonates in the treatment of 

malignancy-induced hypercalcemia. 

3. Calcitonin—Calcitonin may be effective in some cases of hypercalcemia; it should be 

reserved as adjunctive rather than primary therapy. Action is immediate, inhibiting 

calcium and phosphorus release at the osteoclast level. Therapy is short lived, most 

likely due to tachyphylaxis. The starting dose is 4 IU/kg intramuscularly or 

subcutaneously every 12 hours. Calcitonin should be reserved as a rapid modality in 

life-threatening hypercalcemia while waiting for more sustained therapies (eg, 

pamidronate) to work. Glucocorticoids may prolong the hypocalcemic effect of 

calcitonin. 

4. Phosphate—Caution: Hypercalcemia complicated by hypophosphatemia (common 

in primary hyperparathyroidism) will respond to slowly raising the patient's serum 

phosphate concentration to near normal. Although intravenous phosphate can 

dramatically lower serum calcium, there is significant risk of toxicity, including potentially 

fatal metastatic calcification. Use intravenous phosphate only in consultation with a 

nephrologist in a critical care setting. 

C. Decrease Absorption of Calcium by the Intestine 

Corticosteriods reduce any increase in gastrointestinal absorption of calcium, such as 

occurs in vitamin D intoxication and sarcoidosis. Steroids are also effective in 

hypercalcemia secondary to lymphoproliferative malignancies, due to antitumor effects. 

Hydrocortisone, 3-4 mg/kg/d orally or intravenously, should cause a fall in serum 

calcium concentration within 1-2 days. 

D. Perform Hemodialysis 

In patients with renal insufficiency or in whom the above measures are ineffective, 

hemodialysis with calcium-free dialysate effectively removes calcium from the

extracellular fluid. 

Disposition 

Patients with a serum calcium concentration over 12 mg/dL should be hospitalized. 

Those with lower levels may be discharged from the emergency department but require 

close follow-up and outpatient workup. 

DISORDERS OF SERUM PHOSPHORUS CONCENTRATION 

HYPOPHOSPHATEMIA 


Hypophosphatemia is characterized by a serum phosphorus concentration under 2 

mg/dL. It is a common condition with diverse causes (Table 42-10). An isolated serum 

phosphate level may not reflect total body stores, because phosphate is prone to 

shifting intracellularly. Phosphate is critical to many cellular functions, and severe 

hypophosphatemia has profound effects on multiple organ systems. 


Diagnosis of hypophosphatemia depends on laboratory measurement of serum 

phosphorus concentration, because clinical symptoms are usually vague and 

nonspecific. Acute respiratory alkalosis or a recent glucose load may lead to 

hypophosphatemia. Fatigue, neuromuscular weakness, irritability, paresthesias, 

dysarthria, confusion, convulsion, and coma may occur. At serum levels below 1 mg/dL, 

hemolysis and impaired neutrophil phagocytosis become evident. Erythrocyte 

2,3-disphosphoglycerate is lowered, resulting in decreased delivery of oxygen to the 

tissues. Rhabdomyolysis may occur. 

Treatment 

Treatment consists of replacing phosphorus by intravenous or oral phosphate 

supplements. All patients with a serum phosphorus concentration under 2 mg/dL should 

receive supplements. Milk is an excellent source of phosphate. Aluminum phosphate gel 

(Phosphaljel) or neutral phosphate salts (adults, 0.5-1.0 g/d of phosphate orally) can be 

given. 

Sodium or potassium phosphate may be carefully given intravenously in severe 

symptomatic hypophosphatemia, (usually phosphate < 1.0 mg/dL). Serum phosphate, 

calcium, potassium, and magnesium must be carefully monitored during therapy, 

because hypocalcemia and metastatic calcifications may occur during therapy. 

Intravenous therapy of severe hypophosphatemia should be given by experienced 

physicians in a monitored, critical care setting. Oral therapy is safer and should be used 

whenever possible. 

Disposition

Hospitalization is invariably necessary for patients with a serum phosphorus 

concentration under 1 mg/dL and is strongly advised for those whose serum 

phosphorus is under 2 mg/dL. Patients for whom hospitalization is not indicated require 

close follow-up. 

HYPERPHOSPHATEMIA 


Hyperphosphatemia is characterized by a serum phosphorus concentration over 7 

mg/dL. It may result from chronic or acute renal disease; hypoparathyroidism; growth 

hormone excess; cytolysis (rhabdomyolysis or chemotherapy of lymphoproliferative 

tumors); excessive enemas with phosphate-containing solutions; or ingestion of large 

amounts of phosphate, vitamin D, or laxatives. 


No signs are directly referable to hyperphosphatemia. However, hypocalcemia or 

hypomagnesemia may develop because of tissue deposition of calcium phosphate. 

Treatment 

A. Glucose and Insulin 

Administer 50% glucose and regular insulin as described above (see "Hyperkalemia" 

section) to produce an initial fall in serum phosphorus. 

B. Volume Expansion 

Infuse isotonic saline to achieve volume expansion and promote excretion of phosphate 

by the kidneys in patients with normal renal function. Acetazolamide (Diamox) will also 

facilitate urinary phosphate excretion. Give 500 mg every 6 hours, but monitor fluid 

balance closely. 

C. Phosphate-Binding Antacids 

Oral phosphate-binding antacids such as aluminum hydroxide will cause binding of 

phosphate in the gut and reduce phosphate absorption. 

D. Dialysis 

Dialysis is required to lower serum phosphorus concentration in patients with renal 

failure. 

Disposition 

Indications for hospitalization usually depend on factors other than hyperphosphatemia 

itself (eg, renal insufficiency, rhabdomyolysis). 

DISORDERS OF SERUM MAGNESIUM CONCENTRATION 

Magnesium, the most abundant intracellular divalent cation, is distributed approximately 

1% extracellularly, 30% intracellularly, and 69% in bone. Serum concentration may not

eflect total body stores. Magnesium is essential to life and plays an important role in 

regulating cellular adenosine triphosphate and maintaining intracellular potassium 

concentration. Green vegetables, nuts, peas, and beans are rich in magnesium. 

Excretion is via the kidneys and depends on glomerular filtration. Magnesium deficiency 

is usually caused by decreased intake (nutritional deficiency) or enhanced excretion 

(endocrine or renal disorders). 

HYPOMAGNESEMIA 


• Frequently associated with disorders of calcium, potassium, and phosphate. 

• Common in malnourished patients and in those with renal disease. 

• Symptoms are primarily neuromuscular and similar to those of hypocalcemia. 

• Utilize oral replacement whenever possible. 

• Symptomatic patients require admission. 

• Identify and treat the underlying cause. 


Hypomagnesemia is characterized by a serum magnesium concentration under 1 

mEq/L (< 1.2 mg/dL). It is commonly associated with several conditions (Table 42-11). It 

is frequently associated with hypocalcemia and disorders of potassium and phosphate, 

and should be suspected in high-risk patients and those with other electrolyte and 

elemental deficiencies. 


Carpopedal spasm, tetany, athetoid movements, jerking, coarse and flapping tremors, 

and hyperexcitability may occur. A positive Babinski sign, seizures, and weakness are 

seen. Hypertension and vasomotor changes as well as confusion, disorientation, and 

psychotic behavior can occur. Severe hypomagnesemia and hypokalemia may lead to 

significant prolongation of the QT interval and subsequent ventricular tachycardia and 

fibrillation. 

Treatment 

Hypocalcemia and hypokalemia associated with hypomagnesemia are characteristically 

resistant to calcium supplementation but respond quickly to magnesium replacement. 

Great caution must be used in patients with renal insufficiency. Monitor and correct 

associated electrolyte abnormalities. 

A. Oral Replacement 

The oral route is preferred in patients with long-standing magnesium deficiency. For 

adults, give magnesium oxide, 400 mg 4 times daily. 

B. Parenteral Replacement

Reserve parenteral administration of magnesium for patients with severe 

hypomagnesemia, usually those who have evidence of neuromuscular or cardiac 

dysfunction. 

1. Intramuscular route—Give magnesium sulfate, 1.0 g intramuscularly every 4-6 

hours. This route is painful. 

2. Intravenous route—Intravenous therapy is reserved for severe hypomagnesemia 

(usually in alcoholic patients). One cc of 50% magnesium sulfate contains 50 mg of 

magnesium. The usual recommended dose of intravenous magnesium is 1 g of 

magnesium sulfate every 6 hours. In the presence of ventricular tachycardia (torsade de 

pointes), 4 cc of 50% magnesium sulfate should be infused over 1-2 minutes. 

Disposition 

Patients with symptomatic hypomagnesemia require hospitalization. Patients with less 

severe magnesium depletion may require hospitalization because of associated 

conditions. 

HYPERMAGNESEMIA 


Hypermagnesemia is characterized by a serum magnesium concentration over 3 mEq/L 

(3.6 mg/dL). It is usually due to renal failure (acute or chronic) that is often associated 

with excessive magnesium intake (eg, from magnesium-containing antacids or 

magnesium sulfate). 



Symptoms and signs are uncommon and vary depending on the severity of 

hypermagnesemia. 

1. Serum concentration of 3-4 mEq/L—Peripheral vasodilatation may result in 

hypotension. Nausea and vomiting may also occur. 

2. Serum concentration of 5-7 mEq/L—Drowsiness, confusion, and lethargy develop, 

and deep tendon reflexes are depressed or absent. 

3. Serum concentration above 10 mEq/L—Coma and death occur, preceded by 

progressive weakness and skeletal muscle paralysis, with depression of the respiratory 

centers. 


ECG changes include a prolonged PR interval, widened QRS complexes, and elevated 

T waves.

Treatment 

A. Patients with Renal Insufficiency 

In patients with severe renal insufficiency, significant hypermagnesemia must be treated 

by dialysis using a magnesium-free dialysate. 

B. Patients with Normal Renal Function 

Infusion of isotonic saline solution for volume expansion promotes urinary excretion of 

magnesium. Potent diuretics such as furosemide, 0.5-1.0 mg/kg intravenously, may also 

be effective. Intravenous infusion of calcium will temporarily neutralize the 

neuromuscular effects of hypermagnesemia. 

Disposition 

All patients with hypermagnesemia require hospitalization. 

Adrogue HJ et al: Hypernatremia. N Engl J Med 2000;342 (20):1493. [PMID: 10816188] 

(A thorough review of hypernatremia, with an emphasis on, and examples of, 

recommended therapy.) 

Adrogue HJ et al: Hyponatremia. N Engl J Med 2000;342 (21):1581. [PMID: 10824078] 

(A thorough review of hyponatremia, with an emphasis on, and examples of, 

recommended therapy.) 

Agus ZS: Hypomagnesemia. J Am Soc Nephrol 1999;10:1616. [PMID: 10405219] 

(Signs and symptoms of hypomagnesemia are reviewed, as are the causes, approach 

to diagnosis, and therapy.) 

Carlstedt F, Lind L: Hypocalcemic syndromes. Crit Care Clin 2001;17:139. [PMID: 

11219226] (A review of calcium metabolism, hypocalcemia, and benefits of calcium 

replacement in the critically ill.) 

Dacey MJ: Hypomagnesemic disorders. Crit Care Clin 2001;17 (1):155. [PMID: 

11219227] (A review of the causes of hypomagnesemia as well as pathophysiology and 

therapeutics in critically ill patients.) 

Davidson T: Conventional treatment of hypercalcemia of malignancy. Am J Health Syst 

Pharm 2001;58(Suppl 3):S8. [PMID: 11757206] (A review of the pathophysiology of 

hypercalcemia of malignancy, comparing available treatments and suggesting treatment 

guidelines. An excellent review of all FDA-approved therapies.) 

Fulop M: Algorithms for diagnosing some electrolyte disorders. Am J Emerg Med 

1998;16:76. [PMID: 9451320] (Presents an algorithmic approach to differentiating the 

causes of abnormalities in serum sodium, potassium, and calcium.) 

Halperin ML et al: Potassium. Lancet 1998;352:135. [PMID: 9672294] (An overview of 

the pathophysiology of potassium disorders as well as a stepwise approach to the 

diagnosis and treatment of potassium disturbances.)

Kapoor et al: Fluid and electrolyte abnormalities. Crit Care Clin 2001;17:503. [PMID: 

11525047] (A comprehensive review of electrolyte abnormalities with a focus on critical 

care.) 

Mandal AK: Hypokalemia and hyperkalemia. Med Clin North Am 1997;81:611. [PMID: 

9167648] (A thorough review of the causes and effects of disturbances in potassium 

homeostasis.) 

Mattu A et al: Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 

2000;18:721. [PMID: 11043630] (A case-based review of the common ECG changes 

seen in hyperkalemia.) 

Singer FR: Medical management of nonparathyroid hypercalcemia and hypocalcemia. 

Otolaryngol Clin North Am 1996;29: 701. [PMID: 8844739] (A comprehensive review of 

the medical management of both hypocalcemia and hypercalcemia.) 

Ziegler R: Hypercalcemic crisis. J Am Soc Nephrol 2001;12(Suppl 17):S3. [PMID: 

11251025] (A comprehensive review of the pathophysiology, diagnosis, and treatment 

of hypercalcemia.) 

ACID-BASE DISORDERS 

An understanding of acid-base disorders is paramount to the emergency physician. 

These disorders are encountered on a daily basis, and command of this complex topic 

guides appropriate management in the emergency department. 

DEFINITIONS 

Although the hydrogen ion concentration [H + ] in humans is extremely low (normal level 

is 40 nmol/L), its regulation is vital to the function of many proteins and enzyme 

systems. Acid-base disorders are generally not characterized by [H + ], but rather by the 

pH of the disturbance. Normal pH in humans is 7.4 (range 7.36-7.44). Acidemia is a 

state in which the blood pH is less than 7.36, and alkalemia is a state in which the blood 

pH is greater than 7.44. The pH of any solution is determined by the 

Henderson-Hesselbach equation: 

According to this equation, pH equals the pK a (the pH at which one half of the 

compound is ionized) added to the ratio of the log of the concentration of base to its 

related acid. 

In humans the most important acid base buffer is the bicarbonate-carbonic acid system. 

CLASSIFICATION OF ACID-BASE DISORDERS 

An arterial blood gas and an electrolyte panel are essential tests needed to determine

the nature of the disorder(s) in patients with potential acid-base disorders. Acidosis is a 

process that tends to produce an acidemia, whereas alkalosis is a process that tends to 

produce an alkalemia. A metabolic or respiratory process alone (primary acid-base 

disorder) or a combination of the two processes (mixed acid-base disorder) may result 

in an alteration of blood pH. Metabolic processes involve a primary alteration in the 

HCO 3 - concentration, whereas respiratory disorders involve a primary alteration in the 

PaCO 2 . 

Primary processes that change pH from normal are generally only partially 

compensated; therefore, the primary acidosis or alkalosis is always evident by the 

acidemic (< 7.36) or alkalemic (> 7.44) pH. Patients with a primary respiratory alkalosis 

always have PCO 2 less than 35 mm Hg, whereas patients with a primary respiratory 

acidosis always have PCO 2 greater than 45 mm Hg. Patients with a primary metabolic 

alkalosis always have a HCO 3 - concentration greater than 28 mEq/L, whereas patients 

with a primary metabolic acidosis always have a HCO 3 - concentration less than 22 

mEq/L. 

COMPENSATION 

Many metabolic and respiratory processes can cause swings in pH, but pH homeostasis 

is maintained by the combination of physiologic buffers, the lungs, and the kidneys. The 

bicarbonate-carbonic anhydrase buffer system is the most important buffering system in 

the blood and interstitial fluid. Cell metabolism produces carbon dioxide that combines 

with water to form carbonic acid. Carbonic acid then dissociates to form HCO 3 - and H + : 

The normal concentration of carbonic acid is 1.2 mmol/L compared to the plasma 

HCO 3 - concentration of 24 mmol/L. 

Under physiologic stress, the lungs and kidneys play a vital role in maintaining 

near-normal pH by altering the concentrations of this buffer system. The respiratory 

system provides compensation for primary metabolic processes, whereas the kidneys 

compensate for primary respiratory processes. 

An alteration in blood pH secondary to a metabolic disturbance is sensed by 

chemoreceptors, which in turn signal the respiratory center. The generation of a 

metabolic acidosis (decrease in pH and HCO 3 - ) will stimulate the respiratory center, 

causing a decrease in the PaCO 2 and consequently increasing the blood pH. The 

generation of a metabolic alkalosis (increase in pH and HCO 3 - ) will inhibit the 

respiratory center, causing an increase in the PaCO 2 and consequently decreasing the 

blood pH.

In contrast to the almost immediate compensation provided by the respiratory system, 

the kidneys provide little compensation until after 6-12 hours of sustained alteration in 

blood pH. The kidneys maintain normal pH by excreting acids produced by normal 

metabolism in addition to adjusting HCO 3 - reabsorption in the proximal tubule. The 

kidneys respond to acidosis by stimulating renal synthesis and retention of HCO 3 - and 

actively excreting H + while retaining HCO 3 - . More than 6-12 hours of alkalemia 

stimulates the kidney to excrete HCO 3 - and retain H + . 

Table 42-12 displays the compensatory responses in primary acid-base disturbances. 

One should recognize the pattern in primary disturbances: the compensatory response 

of elevation versus lowering of the HCO 3 - or PaCO2 is in the same direction as the 

primary abnormality. Discordance between the direction of compensation and the 

primary abnormality indicates two primary disorders (see below). Generally, primary 

processes that change pH from normal are only partially compensated (the exception is 

chronic respiratory alkalosis); therefore, compensation does not approach total 

correction, nor can one overcompensate. 

CLINICAL ACID-BASE DISORDERS 

1. Respiratory Acidosis 


• Impairment in rate of alveolar ventilation generates a hypercapnic state. 

• Clinical feature is alteration of consciousness. 

• Treat the underlying disorder. 


Respiratory acidosis is defined as an elevated PaCO 2 (> 45 mm Hg) and a subsequent 

drop in serum pH below 7.35. This results from an impairment of the rate of alveolar 

ventilation. Respiratory acidosis can be caused by central nervous system disorders, 

diseases affecting the respiratory muscles directly, airway obstruction, or primary 

pulmonic processes (Table 42-13). 


The hallmark clinical finding of respiratory acidosis is an alteration in level of 

consciousness. The characteristic features of hypercapnia range from fatigue, irritability, 

headache, confusion, stupor, or obtundation to coma and depend on the severity and 

chronicity of this process. A PaCO 2 of 70mm Hg secondary to acute respiratory acidosis 

may result in a coma, whereas a person with a chronic respiratory acidosis may not 

progress into a coma until the PaCO 2 exceeds 100 mm Hg. Prolonged states of

hypercapnia may result in elevated intracranial pressure from cerebral vasodilatation. 

Physiology 

A. Acute Respiratory Acidosis 

An acute increase in the PaCO 2 results in a rise of [H + ] and subsequent drop in the 

serum pH. Within 10-15 minutes of an acute rise in PaCO 2 , intracellular proteins begin 

the buffering process, resulting in a 3- to 4-mEq/L increase in the HCO 3 - concentration. 

This immediate buffering will elevate the pH only slightly (0.05-0.10 units), and no 

further compensation occurs until the kidney responds to the sustained acidosis. In the 

acute setting, a 10 mm Hg increase in the PaCO 2 will decrease the pH by 0.08 and 

increase the HCO 3 - concentration by 1.0 mEq/L. 

B. Chronic Respiratory Acidosis 

Chronic obstructive pulmonary disease and extreme obesity are two common conditions 

that may produce chronic respiratory acidosis secondary to inadequate alveolar 

ventilation. With sustained acidosis from an elevated PaCO 2 , the kidneys begin 

compensation within the first 6-12 hours but may not reach a steady state for 2-3 days. 

The kidneys buffer the acidosis by increasing acid secretion in addition to excreting 

chloride in preference to HCO 3 - . This buffering results in the characteristic elevated 

HCO 3 - (usually not greater than 38 mEq/L), hypochloremia, and near normal pH of 

chronic respiratory acidosis. A 10 mm Hg increase in PaCO 2 will decrease the pH by 

0.03 and increase the HCO 3 - concentration by 3.5 mEq/L. 


The primary treatment goal must be focused on reversing or stabilizing the underlying 

process that generated the respiratory acidosis. Depending on the clinical scenario, 

naloxone, oxygen, or ß agonists may be needed to improve the patient's respiratory 

status. Additionally, a trial of bilevel positive airway pressure (BiPAP) or tracheal 

intubation may be required to improve alveolar ventilation, but avoid decreasing the 

PaCO 2 faster than 5 mm Hg/h in patients with chronic respiratory acidosis. Rapid 

correction of the pH can cause acute hypocalcemia and subsequent dysrhythmias and 

seizures. 

Patients with acute respiratory acidosis should be admitted, whereas patients with 

chronic respiratory acidosis may require hospitalization depending on the patient's 

clinical status (ie, hypoxemia). 

2. Metabolic Acidosis 


• Anion gap acidosis caused by ketones, lactate, toxins, uremia. 

• Non-anion-gap acidosis rarely life-threatening. 

• Use Winter's formula to identify respiratory compensation. 

• Treat the underlying cause. 


Metabolic acidosis occurs due to an imbalance between the plasma concentration of H + 

and HCO 3 - . This imbalance is caused by an overproduction of organic acids such as 

ketones or lactate, loss of HCO 3 - through intestinal or renal wasting, or by the inability to 

excrete normal acid production. These mechanisms result in a decrease in the plasma 

concentration of HCO 3 - to less than 22 mmol/L and a pH less than 7.35. 


The identification of a metabolic acidosis is made by laboratory values, but the 

diagnosis of the process generating the metabolic acidosis depends on the clinical 

situation and the anion gap (AG). 

The AG is a measure of the difference between the predominant cation, sodium, and 

the combination of the predominant anions, chloride and HCO 3 - . 

The normal AG is 8-14 mEq/L. The calculation of an increased versus normal AG is the 

key step in determining the cause of metabolic acidosis. 

A. Increased Anion Gap 

An elevated AG is synonymous with the presence of a metabolic acidosis and implies 

an overproduction of acids or a decrease in acid clearance by the kidney. The 

accumulation of acidic anions that are not measured by routine laboratory testing lowers 

the serum HCO 3 - via buffering, hence generating an increased AG. An increased AG is 

associated with the following conditions: 

• Ketoacidosis: in diabetic or alcoholic patients; starvation 

• Renal failure 

• Lactic acidosis 

• Exogenous toxins leading to lactic acidosis: cyanide, carbon monoxide, ibuprofen, 

isoniazid, iron, strychnine, toluene 

• Exogenous toxins metabolized to acids: aspirin, methanol, ethylene glycol, 

paraldehyde

B. Normal Anion Gap 

A metabolic acidosis with a normal AG is generated by the loss of bicarbonate with a 

reciprocal increase in the chloride concentration. Causes of normal AG (hyperchloremic) 

metabolic acidosis can be classified according to serum potassium concentration. 

Causes associated with hypokalemia include diarrhea, small bowel or pancreatic fistula, 

ureteral diversion, ileal loop (obstruction verus too long), type 1 renal tubular acidosis, 

and carbonic anhydrase inhibitors. Normal and hyperkalemic sources include type 4 

renal tubular acidosis, early renal failure, hydronephrosis, tubulointerstitial renal 

disease, and hypoaldosteronism. Other causes of a normal AG metabolic acidosis 

include rapid normal saline hydration and posttreatment of diabetic ketoacidosis. 

The urinary anion gap (UAG) is calculated as follows: 

The UAG grossly reflects urine ammonium excretion and can help differentiate the 

source of the normal AG metabolic acidosis. A negative value for the UAG indicates the 

acidosis and hypokalemia are generated from gastrointestinal sources (ie, diarrhea), 

whereas a near neutral or positive value for the UAG points toward a renal cause for the 

acidosis. 

Physiology 

The body buffers an acute metabolic acidosis by utilizing intracellular and extracellular 

proteins, increasing H + elimination by the kidney, and stimulating the respiratory drive. A 

decreased pH stimulates the chemoreceptors in the brain to increase the alveolar 

ventilation, which decreases the PaCO 2 . If appropriate compensation is occurring in 

response to the metabolic acidosis (gap or nongap), then the PaCO 2 should equal the 

value calculated by Winter's formula, or PaCO 2 = 1.5([HCO 3 - ]) + 8 ± 2. If the PaCO2 via 

arterial blood gas is higher than the calculated value, then the patient has a 

superimposed primary respiratory acidosis (hypoventilation). If the PaCO 2 via arterial 

blood gas is below the calculated range, the patient has a superimposed primary 

respiratory alkalosis (hyperventilation). Respiratory compensation will not decrease the 

PaCO 2 below 10-15 mm Hg, and it may take 12-24 hours of respiratory compensation 

to reach a steady state. 

Treatment 

Metabolic acidosis requires treatment of the underlying cause that generated the 

acidosis. The appropriate treatment depends on the underlying illness. For example, 

diabetic ketoacidosis is treated with hydration, insulin, and electrolyte supplementation 

as needed. The restoration of tissue perfusion by supporting the patient's respiratory 

and cardiovascular state is essential in the treatment of metabolic acidosis. These two 

measures will help correct the acidosis, but sometimes intravenous sodium bicarbonate 

is needed to correct the metabolic derangement. This is generally withheld from

treatment unless the pH falls below 7.1. The estimation of the HCO 3 - dose is as follows: 

As a general rule, initially correct the deficit with one half of the calculated HCO 3 - dose, 

followed by a recheck of the serum HCO 3 - and pH to guide further therapy. The dose of 

HCO 3 - should not exceed 0.5-1.0 mEq/kg at a time. Be careful with the administration of 

intravenous HCO 3 - because of potential complications of volume overload, 

hypokalemia, decreased ionized calcium, paradoxical cerebrospinal fluid acidosis, and 

serum alkalosis. 

3. Respiratory Alkalosis 


• Hypocapnia generated by many common causes. 

• Chronic state may result in near normal compensation. 

• Treat the underlying cause. 


Respiratory alkalosis is defined as a PaCO 2 concentration below 35 mm Hg and 

subsequent elevation in serum pH above 7.45. An acute respiratory alkalosis is caused 

by hyperventilation secondary to other causes. Common causes include early shock, 

early sepsis, trauma, fear, anxiety, pulmonary disease (congestive heart failure, asthma, 

pneumonia, pulmonary embolism), central nervous system infection, cerebrovascular 

accident, pregnancy, liver disease, hyperthyroidism, and acute salicylate ingestion. 

These causes generally decrease the PaCO 2 to 25-35 mm Hg, but further hypocapnia 

can result from metabolic acidosis or hypoxia. 


The clinical findings of respiratory alkalosis vary depending on the severity and acuity of 

the process. An acute respiratory alkalosis can produce circumoral and digital 

paresthesias in addition to carpopedal spasm and possibly tetany. These symptoms 

may be caused partly by a modest hypocalcemia secondary to the acute respiratory 

alkalosis. Severe hypocapnia causes cerebral vasoconstriction that in part produces the 

clinical symptoms of lightheadedness, dizziness, confusion, and possibly loss of 

consciousness. Chronic respiratory alkalosis may produce hypophosphatemia and 

lower the seizure threshold. 

Physiology 

A. Acute Respiratory Alkalosis

Acute hyperventilation lowers the PaCO 2 concentration, and within minutes 

compensation begins. H + ions attempt to buffer the hypocapnic state by moving from 

inside the cell to the extracellular space. A 10 mm Hg decrease in the PaCO 2 will lower 

the HCO 3 - concentration by 2.5 mEq/L and increase the pH by 0.8. There is no 

significant renal loss of HCO 3 - in the acute setting. 

B. Chronic Respiratory Alkalosis 

In response to chronic hypocapnia, the kidney decreases the H + secretion while 

retaining chloride in exchange for HCO 3 - . In chronic states, a 10 mm Hg decrease in 

PaCO 2 will increase the pH by 0.03 and decrease the HCO 3 - concentration by 5 

mmol/L. Additionally, mild hypokalemia is produced by potassium shifting into cells in 

exchange for H + . After 2 weeks, this compensation will bring the pH to normal levels. 


Treatment for respiratory alkalosis focuses on treating the underlying disorder. 

Symptomatic patients with respiratory alkalosis caused by anxiety or psychogenic 

hyperventilation may require a rebreathing device such as a paper bag in an attempt to 

increase the PaCO 2 concentration. Appropriate disposition of patients with respiratory 

alkalosis depends on the underlying process. 

4. Metabolic Alkalosis 


• Commonly results from vomiting or volume depletion secondary to diuretics. 

• Evaluate urine chloride concentration to help guide therapy. 


Metabolic alkalosis is defined as a primary elevation of plasma HCO 3 - above 28 

mmol/L, with a subsequent elevation of pH above 7.45. A primary metabolic alkalosis 

usually results from the loss of gastric acid contents (via vomiting or nasogastric tube) or 

from volume depletion secondary to diuretics. Although the majority of metabolic 

alkaloses are generated from volume depletion, various medical conditions can 

generate hyperbicarbonatemia (Table 42-14). The diagnosis of the process generating 

the metabolic alkalosis depends on the clinical situation and measurement of the urinary 

chloride. 


Metabolic alkalosis produces hypokalemia, hypocalcemia, and hypomagnesemia. 

Depending on the degree of alkalosis (usually pH > 7.55), increased neuromuscular 

activity can occur and become clinically apparent via positive Chvostek and Trousseau

signs, twitching, and tetany. Metabolic alkalosis can also produce cardiac 

tachyarrhythmias and reduce oxygen availability. 

Physiology 

The generation of a metabolic alkalosis is compensated in part by hypoventilation. A 1.0 

mEq/L increase in the HCO 3 - concentration will increase the pH by 0.015 and the 

PaCO 2 by 0.7 mm Hg. This compensatory increase in PaCO 2 from hypoventilation is 

usually limited to 55 mm Hg because the chemoreceptors will not allow the associated 

hypoxemia below a PaO 2 of 60 mm Hg. 

Many different physiologic processes can generate a metabolic alkalosis. 

Hyperbicarbonatemia can result from diuretics secondary to an excessive loss of 

chloride relative to HCO 3 - , resulting in a so-called contraction alkalosis. The loss of H + 

from excessive vomiting or from the enhanced renal excretion in a mineralocorticoid 

excess state can also generate a metabolic alkalosis. Additionally, massive blood 

transfusions can cause a metabolic alkalosis from the metabolism of sodium citrate into 

sodium bicarbonate. Hypokalemia causes hyperbicarbonatemia by causing a shift of H + 

into cells, and the kidney maintains the alkalosis by secreting H + while reabsorbing 

HCO 3 - . 

The kidneys compensate for a metabolic alkalosis initially by excreting some of the 

excess HCO 3 - in the urine. Under circumstances of severe volume depletion, the kidney 

actually maintains the alkalosis by reabsorbing HCO 3 - in an attempt to maintain plasma 

volume regardless of the acid-base status. As the kidney responds to the metabolic 

alkalosis, the urine chloride concentration can be evaluated. A level below 10 mEq/L 

indicates tubular reabsorption of chloride, signifying volume depletion. This urine 

chloride concentration can help guide subsequent therapy. 

Treatment 

Patients with a urine chloride concentration below 10 mEq/L require volume expansion. 

Normal saline infusion should correct the alkalosis by suppressing renal acid excretion 

and enhancing renal HCO 3 - excretion. The kidneys can correct for a metabolic alkalosis 

only if sufficient volume is replaced. Additionally, potassium replacement in the form of 

potassium chloride may be needed to correct the alkalosis. Depending on the clinical 

situation, generally 100-500 mEq of K + may be needed to correct the hypokalemia 

associated with the alkalosis. 

Patients with a urine chloride concentration above 20 mEq/L are not as responsive to 

volume expansion. Specific therapy should be guided toward the underlying processes 

generating the alkalosis. Patients with a mineralocorticoid excess state require 

potassium replacement. Patients with significant edema may require acetazolamide to 

enhance HCO 3 - secretion.

5. Mixed Acid-Base Disorders 


• Up to 3 disorders can coexist. 

• Approach in a stepwise fashion. 

• Metabolic acidosis and respiratory alkalosis commonly coexist. 

• Accurate evaluation of data will guide treatment. 


Whenever a primary disturbance exists, the lungs and kidneys begin to adjust their 

physiologic parameters in an attempt to bring the pH toward normal. If the degree of 

compensation is inadequate, or if an acid-base disorder causes no shift in arterial pH 

(except in chronic respiratory alkalosis), or if the clinical picture does not fit with a 

primary disturbance alone, then consider the presence of a second primary process. 

The presence of 2 or more primary processes occurring simultaneously is referred to as 

a mixed acid-base disorder. Respiratory acidosis and respiratory alkalosis can never be 

present simultaneously, but any other combination of processes can occur. 

Approach the patient with a mixed acid-base disorder in a stepwise fashion: 

1. A thorough history and physical examination can provide clues about the disorders. 

2. The predominant disorder (acidosis versus alkalosis) is reflected by the acidemic or 

alkalemic pH. Confirm the accuracy of the laboratory data via the 

Henderson-Hesselbach equation. 

3. Determine the predominant process altering the pH by interpreting the HCO 3 - 

concentration and PaCO 2 (see above). 

4. Always calculate the serum AG. 

5. Determine the degree of compensation (described below). 

6. Calculate the delta gap (described below). 

7. Interpret urine and serum electrolytes. 

Combined Metabolic Acidosis & Respiratory Acidosis 

Upon identification of a metabolic acidosis from the blood gas and electrolyte panel, 

determine whether the respiratory compensation to the metabolic acidosis is appropriate 

(see "Primary Metabolic Acidosis" section, above). If the PaCO 2 is higher than 

expected, then the patient has a superimposed primary respiratory acidosis. This is an 

ominous mixed disorder and is found in patients in cardiopulmonary arrest. In patients

with a chronic respiratory acidosis, HCO 3 - should be increased by 3.5 mEq/L for every 

10 mm Hg increase in PCO 2 . A smaller increase in HCO 3 - implies a superimposed 

primary metabolic acidosis or a compensation that is not complete. 

Combined Metabolic Acidosis & Respiratory Alkalosis 

If the respiratory compensation results in a lower PCO 2 than expected in response to a 

metabolic acidosis, the patient has a superimposed primary respiratory alkalosis. This 

mixed disorder is commonly encountered in the emergency department. Causes include 

congestive heart failure, early sepsis, early shock, liver disease, and salicylate 

ingestion. In patients with chronic respiratory alkalosis, HCO 3 - should be decreased by 

5 mEq/L for every 10 mm Hg decrease in PCO 2 . A greater decrease in HCO 3 - implies a 

superimposed primary metabolic acidosis. 

Combined Metabolic Alkalosis & Respiratory Acidosis 

Once an acute metabolic alkalosis is identified, the appropriate respiratory 

compensation should be an increase in the PCO 2 of 0.6 mm Hg for each 1 mEq/L 

increase in HCO 3 - concentration. A greater increase in PCO2 implies a superimposed 

primary respiratory acidosis. In patients with chronic respiratory acidosis, HCO 3 - 

concentration should be increased by 3.5 mEq/L for every 10 mm Hg increase in the 

PCO 2 . A greater increase in HCO 3 - implies a superimposed primary metabolic alkalosis. 

This mixed disorder can occur in patients with chronic respiratory acidosis who develop 

a metabolic alkalosis from diuretics for cor pulmonale. 

Combined Metabolic Alkalosis & Respiratory Alkalosis 

A smaller increase in the PCO 2 of 0.6 mm Hg for each 1 mEq/L increase in HCO 3 - 

secondary to an acute metabolic alkalosis implies a superimposed respiratory alkalosis. 

In patients with chronic respiratory alkalosis, HCO 3 - should be decreased by 5 mEq/L 

for every 10 mm Hg decrease in PCO 2 . A smaller decrease in HCO 3 - implies a 

superimposed primary metabolic alkalosis or a compensation that is not complete. This 

mixed disorder is present in patients with hepatic failure who are taking diuretics and in 

patients who require mechanical ventilation and are taking diuretics or given nasogastric 

suction. 

Triple Disturbances 

Patients may present with a maximum of three primary disturbances. For example, a 

55-year-old man with alcoholic liver disease presents to the emergency department with 

protracted vomiting and a blood pressure of 70/40. Laboratory values reveal an AG of 

25 (metabolic acidosis from lactate) and a HCO 3 - concentration of 22 mEq/L. The 

calculated PaCO 2 for appropriate respiratory compensation is 39-43 mm Hg [1.5(22) + 

8 ± 2]. The patient's PaCO 2 is 25 mm Hg, which clearly reflects a respiratory alkalosis

(hyperventilation) from liver disease. A third disturbance (metabolic alkalosis) should be 

suspected if laboratory values reveal a high AG with a HCO 3 - concentration close to 

normal. 

Determine the presence of a triple disturbance by calculating the delta gap. The delta 

gap is defined as the deviation of the AG from normal minus the deviation of the HCO 3 - 

from normal. Prior to calculating the delta gap, assume a normal AG of 10 mmol/L, and 

in a high AG acidosis every unit rise in the AG above 10 lowers the patient's HCO 3 - 

concentration by 1 unit via buffering. This patient's deviation in the AG is 15 (25 - 10), 

and the deviation in the HCO 3 - concentration is 2 (24 - 22). This difference of 13 (15 - 2) 

represents an elevated delta gap (normal range 0 ± 6). In this example, the presence of 

an elevated delta gap represents a higher than expected HCO 3 - level, hence a 

simultaneous third disorder: metabolic alkalosis from the protracted vomiting. 

Adrougue HJ, Madias NE: Management of life-threatening acid-base disorders. First of 

two parts. N Engl J Med 1998;338(1):26. [PMID: 9414329] (Discussion of the 

complications and management of severe metabolic and respiratory acidosis.) 

Adrougue HJ, Madias NE: Management of life-threatening acid-base disorders. Second 

of two parts. N Engl J Med 1998;338(2):107. [PMID: 9420343] (Discussion of the 

complications and management of severe metabolic and respiratory alkalosis.) 

Bia M, Their SO: Mixed acid base disturbances: a clinical approach. Med Clin North Am 

1981;65:347. [PMID: 7230962] (Classic article for the approach to mixed acid-base 

disturbances.) 

Fall PJ: A stepwise approach to acid-base disorders. Practical patient evaluation for 

metabolic acidosis and other conditions. Postgrad Med 2000;107(3):249. [PMID: 

10728149] (Stepwise approach to evaluation of acid-base disorders using a clinical 

example to guide discussion.) 

Fulop M: Flow diagrams for the diagnosis of acid-base disorders. J Emerg Med 

1998;16(1):97. [PMID: 9472767] (Approach to acid-base disorders using flow diagrams.) 

Gluck SL: Acid-base. Lancet 1998;352:474. [PMID: 9708769] (Discussion of acid-base 

disorders focused on metabolic processes.) 

Kraut JA, Madias NE: Approach to patients with acid-base disorders. Resp Care 

2001;46(4):392. [PMID: 11262558] (Practical approach to acid-base disturbances with 

case examples.) 

Laski ME, Kurtzman NA: Acid-base disorders in medicine. Disease-A-Month 

1996;42(2):51. [PMID: 8631223] (In-depth discussion of acid-base disorders.) 

Rutecki GW, Whittier FC: An approach to clinical acid-base problem solving. Compr 

Ther 1998;24(11-12):553. [PMID: 9847971] (Five-step approach to acid-base disorders 

including algorithms for metabolic acidosis.)

APPENDIX: USEFUL EQUATIONS & FORMULAS 

Osmolality 

P osm is in mOsm/L, [Na + ] in mEq/L, and [glucose] and [blood urea nitrogen] in mg/dL. 

When measured osmolality exceeds calculated osmolality by more than 10 mOsm/L, an 

osmolal gap exists owing to the presence of significant quantities of unmeasured solute: 

If the solute is alcohol, the blood alcohol concentration can be estimated: 

Hyponatremia 

To determine whether the cause of the serum sodium concentration ([Na + ] serum ) 

abnormality is due to total body sodium, potassium, or water abnormality, equation 4 

may be helpful. 

where TBW = total body water (in L), [Na + e] = total body Na + (in mEq), and [K + e] = total 

body K + (in mEq). TBW may be estimated using equation 5. (See also Table 42-1.) For 

example, if [Na + ] serum is low and TBW is estimated to be normal, total body sodium or 

potassium must be decreased, and sodium or potassium replacement is the necessary 

treatment. However, if TBW is increased and [Na + ] serum is low, diuresis is the necessary 

treatment.

The relationship between serum sodium concentration and serum glucose concentration 

is as follows: For each increase in serum glucose concentration of 100 mg/dL, there will 

be a reciprocal decrease of 1.6 mEq/dL in serum sodium concentration. 

Hypernatremia 

Plasma Calcium Concentration & Plasma Albumin Concentration 

For every fall in serum albumin of 1 g/dL, plasma calcium will fall about 0.8 mg/dL. This 

reduction does not reflect a change in free Ca 2+ (ionized) concentration and therefore 

does not represent true hypocalcemia. 






I. DIAGNOSIS OF FLUID & ELECTROLYTE DISORDERS

Table 42-1. Volume of body fluid compartments. 

Fraction of 

Body Weight 

Man (154 lg 

[70 kg]) 

0.5-0.6 42 L 

Intracellular fluid 20 L 0.15-0.2 14 L 

Plasma volume 3 L

Table 42-2. Normal serum electrolyte concentrations. 

136-146 mEq/L 

Potassium (K + ) 

Chloride (Cl - ) 

Bicarbonate (HCO 3 - ) 

Calcium (Ca 2+ ) 

Magnesium (Mg 2+ ) 

Phosphate (PO 4 3- ) 


3.5-5 mEq/L 

96-106 mEq/L 

24-28 mEq/L 

8.5-10.5 mg/dL (4.2-5.2 mEq/L) 

1.8-3 mg/dL (1.5-2.5 mEq/L) 

3-4.5 mg/dL (1-1.5 mmol/L) 





TABLES 

Table 42-2. Normal serum electrolyte concentrations.

Table 42-3. Conditions causing hyponatremia. 






TABLES 

Table 42-3. Conditions causing hyponatremia.

Table 42-4. Drugs implicated in the development of 

hyponatremia. 






TABLES 

Table 42-4. Drugs implicated in the development of hyponatremia.

Table 42-5. Potassium content of the body. 1 

0.4 

1 

0.4 

7.6 

1 

89.6 

Body Potassium (%)

Table 42-6. Causes of hypokalemia. 1 

Skin: Burns; excessive sweating 

Hypokalemia with no deficit (shift into cells) 

Insulin; ß-adrenergic agonists 

Athletic training; testosterone (anabolic agent) therapy 

Respiratory alkalosis 

Familial periodic paralysis 

Treatment of megaloblastic anemia

Table 42-7. Causes of hyperkalemia. 






TABLES 

Table 42-7. Causes of hyperkalemia.

Table 42-8. Causes of hypocalcemia. 1 

1 Reproduced, with permission, from Schroeder SA et al (editors): Current 

Medical Diagnosis & Treatment 1991. Appleton & Lange, 1991. 






TABLES 

Table 42-8. Causes of hypocalcemia.

Table 42-9. Causes of hypercalcemia. 1 

Hypophosphatasia 

Immobilization 

Familial hypocalciuric hypercalcemia 

Complications of renal transplantation Iatrogenic

Table 42-10. Causes of hypophosphatemia. 






TABLES 

Table 42-10. Causes of hypophosphatemia.

Table 42-11. Causes of hypomagnesemia. 1 

Associated with hypercalciuria 

Renal magnesium wasting 

Unexplained 

Hyperparathyroidism 

Postparathyroidectomy 

Vitamin D therapy 

Induced by aminoglycoside antibiotics, cisplatin

Table 42-12. Primary disorders and compensatory responses. 

Primary Abnormality Respiratory acidosis Increased bicarbonate 

Decreased bicarbonate Respiratory alkalosis Decreased bicarbonate 

Increased bicarbonate 






TABLES 

Table 42-12. Primary disorders and compensatory responses.

Table 42-13. Causes of respiratory acidosis. 






TABLES 

Table 42-13. Causes of respiratory acidosis.

Table 42-14. Causes of metabolic alkalosis. 

Saline Resistant 

(Urine [Cl - ] > 20 mEq/L) 

Gastrointestinal: vomiting, 

nasogastric suction, Cl - diarrhea, 

villous adenoma 

Diuretic therapy 

Cystic fibrosis 

Posthypercapnia 

Alkali syndrome 

Refeeding alkalosis 

Massive blood transfusion 

Hypercalcemia (bone metastases)

Figure 42-1. Emergency evaluation of hyponatremia. 






FIGURES 

Figure 42-1

Figure 42-2. Emergency evaluation of hyperkalemia. 






FIGURES 

Figure 42-2

Figure 42-3. Correlation between serum potassium concentration and ECG findings. 

The correlation is approximate and depends on serum pH and concentrations of other 

ions (Na + , Ca 2+ ). (Reproduced, with permission, from Schroeder SA [editor]: Current 

Medical Diagnosis & Treatment 1992. Appleton & Lange, 1992.) 






FIGURES 

Figure 42-3

Figure 42-4. The ECG in hypocalcemia. T waves are upright, but the QT interval is 

prolonged at 0.4 s (corrected for RR of 0.66 s, QT c = 0.48 s). The lengthening of the QT 

interval is due to a lengthening of the ST segment and not to any abnormality in the T 

wave itself. Blood calcium at the time the above recording was made was 6.8 mg/dL. 

(Reproduced, with permission, from Goldman MJ: Principles of Clinical 

Electrocardiography, 12th ed. Lange, 1986.) 






FIGURES 

Figure 42-4

43. Burns & Smoke Inhalation 1 - Melissa M. Cheeseman, MD, & Harriet 

L. Boozer, MD 



Begin CPR If Needed 

1 This chapter is a revision of the chapter by Anthony A. Meyer, MD, PhD, & Patricia R. 

Salver, MD, FACEP, FACP, from the 4th edition. 


Establish an Adequate Airway 

Severe burns to the lower face and neck may be associated with upper airway and 

laryngeal edema that cause airway obstruction. Inhalation of superheated air or steam 

in a confined space may also cause significant upper airway edema. Full-thickness 

chest wall burns, especially if they are circumferential, may limit chest wall movement 

and cause respiratory failure. Consider early endotracheal intubation in all patients with 

such injuries. When the burn size exceeds 60% total body surface area, including the 

face, early endotracheal intubation is advisable. If endotracheal intubation is impossible, 

cricothyrotomy may be necessary. 

Support Ventilation & Oxygenation 

Give oxygen, 2-12 L/min, by nasal cannula or face mask. If smoke inhalation might have 

occurred, give 100% oxygen by tight-fitting reservoir face mask or endotracheal tube. 

Monitor oxygen saturation by pulse oximetry. (Note that the actual oxygen saturation 

can be obtained by subtracting the percent of carboxyhemoglobin from the measured 

value.) Burn patients with inhalation injuries require frequent reevaluation because of 

possible progressive respiratory compromise. 

Gain Intravenous Access 

Patients with deep burns covering more than 15% of body surface area (Figure 43-2) 

require intravenous fluid resuscitation. Insert 1 or 2 large-bore (=16-gauge) peripheral 

intravenous catheters, preferably inserted through nonburned skin. Central venous 

access is needed only if large-bore peripheral access is impossible. 

Obtain Laboratory Data 

Arterial blood gas analysis is helpful if respiratory involvement is present. In addition, for 

assistance in overall patient management and resuscitation, submit blood for 

carboxyhemoglobin level, complete blood count, and electrolytes and urine for 

myoglobin. Obtain chest x-ray and electrocardiogram (ECG).

Begin Fluid Resuscitation 

Burns are associated with the loss of large volumes of intravascular fluid, electrolytes, 

and protein through capillaries with increased permeability. Loss begins soon after injury 

and is maximal during the first 6-8 hours. Several formulas may be used as guidelines 

to fluid resuscitation (Table 43-1). Most burn centers use only crystalloid for the first 

18-24 hours and use either the Parkland or the modified Brook formula. These formulas 

should be individualized for each patient on the basis of the patient's response to 

therapy. In general, infusion rates should be adjusted to maintain urine output at 0.5-1.0 

mL/kg/h for adults and 1.0 mL/kg/h for children under 10 kg. 

Obtain 12-Lead ECG & Monitor Cardiac Rhythm 

Hypoxemia, shock, electrolyte disturbances, or carbon monoxide poisoning in a burn 

patient may predispose to development of myocardial ischemia or cardiac arrhythmias. 

Evaluate for Possible Associated Injuries 

Burn patients frequently have other injuries in addition to the burn. Patients who have 

been burned in motor vehicle accidents or explosions should be evaluated as described 

in Chapter 10. Search for fractures and injuries of the hand, cervical spine, chest, and 

abdomen in patients who may have jumped or fallen from a burning building or been 

burned in a motor vehicle crash. 

Insert a Urinary Catheter 

Insert an indwelling urinary catheter to monitor urinary output and to obtain urine for 

urinalysis (including myoglobin determination if the patient has sustained an electrical 

burn). Patients with full-thickness burns of the penile glans or shaft may require 

suprapubic cystostomy. An indwelling urinary catheter is the most important monitoring 

device in burn patients. 

Insert a Nasogastric Tube 

Patients with deep burns covering more than 20% of their body surface will develop 

ileus. A nasogastric tube will decrease the risk of emesis and possible aspiration. If the 

patient is to be transported by air to a burn facility, a nasogastric tube is mandatory, 

because decreased cabin pressure may cause gastric distention and vomiting. The tube 

should be on suction or open to air and not clamped during transport. 

Provide Tetanus Prophylaxis 


Remove Jewelry 

Remove all rings, watches, and other jewelry, which could act as a tourniquet when 

edema develops.

Gueugniaud PY et al: Current advances in the initial management of major thermal 

burns. Intensive Care Med 2000;26:848. [PMID: 10990098] 

Ramzy PI et al: Thermal injury. Crit Care Clin 1999;15:333. [PMID: 10331132] 

Rose JK, Herndon DN: Advances in the treatment of burn patients. Burns 1997;23:S19. 

[PMID: 9177897] 

Yowler CJ, Fratianne RB: Current status of burn resuscitation. Clin Plast Surg 

2000;27:1. [PMID: 10665352] 

FURTHER EVALUATION OF THE PATIENT WITH BURNS OR 

INHALATION INJURY 

Obtain a History 

Ask the patient, witnesses, and family about the mechanism of injury (eg, explosion, 

spilled liquid, house fire) and about the possible presence of combustibles known to be 

toxic. Find out whether the patient was burned in an open space or in an enclosed 

space; the latter increases the risk of inhalation injury. Also ask about underlying 

medical problems, tetanus immunization status, and medication allergies. 

Determine the Severity of Injury 

An accurate estimate of the severity of injury is crucial in determining the need for 

hospital admission or referral to a burn center and in guiding initial fluid resuscitation 

and establishing a prognosis. Table 43-2 lists several important determinants of burn 

severity. Table 43-3 is the American Burn Association's classification of burns according 

to severity. In general, patients with minor burns may be managed as outpatients, 

patients with moderate uncomplicated burns should be hospitalized, and patients with 

major burns should be transferred to a burn center. If local personnel or facilities do not 

have experience in caring for burn patients, then patients with moderate or major burns 

should be referred to a burn center. 

A. Burn Size 

Accurate measurement of the burned area, expressed as a percentage of body surface 

area, should be performed in all burn patients. Burn size may be estimated by using an 

age-adjusted surface area chart (see Figure 43-2) or by using the "rule of nines" for 

adults or the "rules of fives" for infants and children (Table 43-4). The size of scattered 

small burns can be estimated by comparing them with the size of the patient's hand, 

which constitutes about 11/4% of body surface area. The extent of all burns should be 

recorded on a drawing (front and back views) on the patient's chart. 

B. Burn Depth 

Burns are typically described as first, second, third, or fourth degree. A more useful 

description, based on the wound's ability to heal, is partial-thickness (heals 

spontaneously) and full-thickness (requires skin grafting). Deep partial-thickness burns 

usually require grafting to expedite healing and decrease contractures and hypertrophic

scar. Figure 43-3 shows the level of skin involved with each type of burn. Table 43-5 

outlines the physical findings usually associated with each type of burn. The depth of 

burn should be recorded accurately on a drawing (front and back views) on the patient's 

chart. 

Several principles must be kept in mind when considering burn depth. First, because it 

is difficult to distinguish deep partial-thickness burns from full-thickness burns, these 

burns should be assumed to be full-thickness injuries and should be treated accordingly. 

Second, burn wounds change over 48-72 hours, and what may appear to be superficial 

injury on initial examination may progress to a deeper-level injury, especially if the 

patient has poor perfusion or the wound becomes desiccated or infected. 

C. Burn Site 

Burns in the following areas are considered major injuries: 

1. Hands and feet—Deep burns of the hands or feet cause scarring and may produce 

permanent disability. 

2. Face—Partial- or full-thickness facial burns may cause severe scarring, with profound 

physical and emotional impact. They are also often associated with inhalation injury and 

compromised airway. 

3. Eyes—Burns of the eyes may cause corneal scarring and eyelid dysfunction that may 

ultimately lead to blindness. Note: Patients with possible eye burns should be examined 

as quickly as possible, preferably in the emergency department, because massive 

periorbital edema often develops and hinders later examination. 

4. Ears—Deep burns of the ears predispose to development of pressure deformity and 

infection. Examine the tympanic membrane in patients with external ear injuries caused 

by hot liquids or chemicals. 

5. Perineum—Burns of the perineum are difficult to manage on an outpatient basis and 

are more susceptible to infection than are other types of burns. 

D. Presence of Circumferential Burns 

Any deep circumferential burn is a potential major injury. Circumferential deep burns of 

the neck may cause lymphatic and venous obstruction that leads to laryngeal edema 

and airway obstruction. Circumferential burns of the extremities may restrict blood flow, 

causing an increase in tissue pressure and ischemia. Circumferential chest wall injuries 

may impede chest wall movement and lead to respiratory failure. 

E. Inhalation Injury 

Inhalation injury (burn sustained in a confined space, singed nasal nares, soot around 

the nares, carbonaceous sputum, hoarseness, stridor, symptoms of respiratory distress, 

carboxyhemoglobin level > 10%) signifies a major burn. Diagnosis and management of 

inhalation injuries are discussed below. 

F. Electrical Injury 

Damage from electrical injury may be extensive, even though the outward signs of injury

are minimal. Cardiac arrhythmias and renal failure from myoglobinuria are possible 

complications. All electrical injuries should be considered major injuries. 

G. Age of Patient 

The mortality rate from burn injury is increased in very young or very old patients; these 

are also the age groups in which burns most commonly occur. Burns in a child under 

age 5 years or in an adult over age 55 years are more likely to be serious than are 

burns in other age groups. 

H. Associated Injuries 

Burns may occur in patients with other injuries, such as fractures or internal injuries due 

to vehicular accidents, falls, or explosions. The associated injuries often place the 

patient at increased risk of serious complications or death, even though the burns 

themselves are small. 

I. Major Underlying Medical Problems 

Major preexisting medical problems in a burn patient are associated with an increased 

rate of serious complications and death. Patients with a history of myocardial infarction, 

angina, significant pulmonary disease, diabetes mellitus, or renal failure are considered 

poor-risk patients even if their burns are not serious. Burned patients with a history of 

alcohol or other drug abuse are also at higher risk for complications following burn 

injury. 

Control Pain 

Patients with minor burns, especially of the extremities, may relieve pain by immersing 

the burned part in cool water; do not use this method in patients with larger burns, 

because of the risks of inducing hypothermia. Oral, subcutaneous, or intramuscular 

administration of narcotic analgesics may provide adequate pain relief for outpatients; 

however, intravenous morphine (in increments of 1-3 mg for adults or 0.1-0.2 mg/kg for 

children) should be used to control pain in patients with moderate or major burn injuries. 

Take care to avoid precipitating respiratory failure in a burn patient with compromised 

respiration. Ventilator support may be required in some patients to permit administration 

of adequate amounts of analgesics safely. 

Provide Appropriate Wound Care 

Gently remove clothing, dirt, and other foreign material adhering to the burn; irrigation 

with sterile saline (at room temperature) may be helpful. Do not scrub wounds or use 

harsh detergents or chemical disinfectants (eg, benzalkonium chloride, 

povidone-iodine). Little or no debridement of moderate or major wounds should be 

performed in the emergency department. Redundant skin from ruptured blisters of minor 

superficial partial-thickness burns may be removed. The wounds of patients with 

moderate or major burns, especially those who will be transferred to a burn facility, 

should not be treated with topical ointments or complex dressings in the emergency 

department, because these will have to be removed for evaluation upon arrival at the 

receiving facility. A simple nonadherent dressing such as petrolatum-impregnated gauze 

or sterile saline-soaked dressings should be applied instead. Outpatient management of 

minor burns is discussed in the "Emergency Treatment of Specific Types of Burns"

section, below. 

Transfer the Patient to a Burn Center 

All major burns and many moderate burn injuries are best treated in a burn center, 

which has the personnel, equipment, and experience needed to treat major burns 

effectively. When a patient with a serious burn is first evaluated, the closest burn center 

should be contacted immediately, so that recommendations for care can be obtained 

and plans made for transfer, if indicated. Transfer should be coordinated with the 

physician at the burn center, and unnecessary delays should be avoided. If transfer can 

be carried out quickly, escharotomy may be performed at the receiving facility in 

patients with circumferential burns of the extremities, chest, or neck who do not have 

signs of respiratory compromise or tissue ischemia. Fluid resuscitation and all other 

supportive measures should be continued during transport, and the patient should be 

kept warm. Complete medical records should be sent with the patient. 

Kao CC, Garner WL: Acute burns. Plast Reconstr Surg 2000; 105:2482. [PMID: 

10845306] 

Sheridan RL: Comprehensive treatment of burns. Curr Probl Surg 2001;38:641. [PMID: 

11568825] 

EMERGENCY TREATMENT OF SPECIFIC TYPES OF BURNS 

SMOKE INHALATION 


• Look for evidence of thermal injury (airway edema). 

• Consider signs of chemical injury including cyanide. 

• Evaluate for carbon monoxide intoxication. 

Mechanisms of Injury 

The mechanisms of injury in smoke inhalation may be divided into 3 categories: (1) 

thermal injury of the airways, (2) chemical injury of airways and lung parenchyma, and 

(3) systemic chemical poisoning. Although one type of injury may predominate in some 

patients, most patients have a combination of injuries. All victims of smoke inhalation 

should be examined carefully for the presence of any of these injuries. 

A. Thermal Injury 

Patients who have been trapped in a fire in a confined space inhale superheated gases 

and may also have direct flame injury of the face and neck, which is associated with 

development of marked upper airway edema and possible airway obstruction. Because 

of the efficient thermal exchange system of the upper airway, direct thermal injury to the 

lower respiratory tract is unusual; rarely, exposure to water or steam in the heated gas 

mixture may produce thermal damage in the lower trachea and bronchi.

B. Chemical Injury 

Chemical injury to the airways and lung parenchyma may be caused by noxious 

products of combustion of flammable materials (Table 43-6). Some of these products 

are directly toxic to the airways and lung parenchyma. Only the most commonly 

produced toxins are discussed below. 

1. Acrolein—Acrolein is a highly reactive aldehyde that results from combustion of 

wood and petroleum products. It rapidly reacts with lung and airway tissues, causing 

injury by protein denaturation. Prolonged inhalation or exposure to high concentrations 

(> 150 parts per million) for short periods of time (minutes) can be fatal. Lesser 

exposure causes pulmonary edema due to alveolar capillary leakage; bronchorrhea and 

bronchospasm, which may be severe; and ventilation-perfusion disturbances that cause 

hypoxemia that may persist even after the person is no longer exposed to smoke. 

Acrolein also causes conjunctivitis and ocular tearing even at low concentrations. 

2. Hydrochloric acid—Hydrochloric acid is one of the main products of combustion of 

polyvinyl chloride, a material commonly found in the structural components of houses 

and high-rise buildings as well as in furnishings and plastics. Hydrolysis occurs when 

hydrochloric acid comes in contact with the mucosa of the upper airway and 

tracheobronchial tree, causing protein denaturation and cell death. Even limited 

exposure may cause marked ocular irritation and tearing, although individuals with 

repeated or prolonged exposure may become desensitized to this effect. More severe 

exposure is associated with dyspnea, chest pain, and irritation of mucous membranes. 

Onset of pulmonary edema may be delayed for 2-12 hours after exposure, and the 

patient may appear asymptomatic in the interim. Toxic levels of hydrochloric acid gas 

may persist for as long as 1 hour after a fire has been extinguished. Patients exposed to 

products of combustion of polyvinyl chloride may also demonstrate premature 

ventricular contractions and may be at risk for development of lethal cardiac 

arrhythmias. 

3. Toluene diisocyanate—Toulene diisocyanate is a product of combustion of 

polyurethane, a synthetic material found in almost all homes and offices, where it is 

used in seat cushions, mattresses, and carpet backing. Toluene diisocyanate is also 

found in insulation material. Toluene diisocyanate may cause severe bronchospasm, 

especially in persons with underlying obstructive lung disease, and is also an ocular 

irritant. 

4. Nitrogen dioxide—Nitrogen dioxide is produced in fires involving automobiles or 

agricultural wastes. It is an uncommon though important toxin, because even brief 

exposures to high concentrations may cause severe bronchospasm, laryngospasm, and 

pulmonary edema. If the patient survives, late development of bronchiolitis fibrosa 

obliterans and chronic interstitial lung disease may occur. 

5. Other noxious products—Particulate matter in smoke may stimulate irritant 

receptors in the large airways and cause bronchoconstriction. 

C. Systemic Chemical Poisoning 

1. Carbon monoxide—(See Chapter 45.) The most widely recognized and most

common complication of smoke inhalation is carbon monoxide poisoning. Carbon 

monoxide is a product of incomplete combustion and is produced in varying amounts in 

all fires. Carbon monoxide binds to hemoglobin with an affinity that is 260 times greater 

than that of oxygen, forming carboxyhemoglobin. The presence of even small amounts 

of carboxyhemoglobin drastically alters the affinity of the remaining unbound 

hemoglobin. Thus, even small concentrations of carbon monoxide may markedly reduce 

the binding of oxygen to hemoglobin, and the carbon monoxide that is bound is not 

easily displaced by oxygen. The presence of carboxyhemoglobin shifts the 

oxyhemoglobin dissociation curve to the left, making it more difficult for hemoglobin to 

release bound oxygen to the tissues. The net result is tissue hypoxia and lactic acidosis 

due to cellular anaerobic metabolism. Carbon monoxide also binds to the cytochromes, 

interfering with intracellular energy production, but this binding is 9 times weaker than 

that to oxygen. In high concentrations, carbon monoxide is also bound to myoglobin; 

rhabdomyolysis with myoglobinuria and renal failure may occur. The half-life of 

carboxyhemoglobin is about 4 hours, which can be reduced to 40-50 minutes by 

administration of 100% oxygen. 

2. Cyanide—(See Chapter 45.) Reports have documented the presence of cyanide in 

the smoke of residential fires. Because of the difficulties in measuring cyanide levels in 

patients and because of the difficulty in recognizing smoke-related cyanide poisoning, 

the clinical relevance of cyanide poisoning in smoke inhalation is uncertain. Because 

there are risks associated with treating cyanide poisoning—which involves the 

production of methemoglobin by infusion of sodium nitrite—in a patient who also 

demonstrates carboxyhemoglobinemia, empiric therapy for cyanide poisoning is not 

recommended. The diagnosis and treatment of cyanide poisoning are discussed in 

Chapter 45. 


A. Thermal Injury 

Thermal injury to the upper airway should be suspected in any patient who has been in 

a fire occurring in a confined space, in patients with obvious face or neck burns, and in 

patients with soot around the nares and soot-tinged sputum or burned nasal or facial 

hairs. Patients may complain of dyspnea; there may be stridor, drooling, or dysphonia. 

The diagnosis is confirmed by direct visualization of the larynx by laryngoscopy or in 

some cases bronchoscopy. 

B. Chemical Injury 

Chemical injury to the airways and lung parenchyma is difficult to diagnose in the 

emergency department. Direct laryngoscopy or flexible fiberoptic bronchoscopy may 

reveal mucosal friability and edema of the airways. Initially the chest x-ray is often 

normal; noncardiogenic pulmonary edema may develop hours after exposure. Xenon 

lung scans, pulmonary function tests, and nitrogen washout studies have all been used 

to document the extent of pulmonary involvement, but they seldom provide more 

information than is obtainable by bronchoscopy. 

C. Carbon Monoxide Poisoning 

Systemic chemical poisoning due to carbon monoxide should be suspected in every 

victim of fire and may be confirmed by measuring the serum carboxyhemoglobin level.

The often-described cherry-red skin color is not a frequent or reliable finding in patients 

with carbon monoxide poisoning. Similarly, arterial blood gas measurements are not 

reliable determinants of carbon monoxide poisoning, because PO 2 and the calculated 

percentage of oxygen saturation of hemoglobin (the value that is routinely reported by 

clinical laboratories) are not affected by carboxyhemoglobin. The oxygen saturation 

measured by pulse oximetry does not distinguish oxyhemoglobin from 

carboxyhemoglobin. Hence, the actual saturation is obtained by subtracting the percent 

of carboxyhemoglobin from the measured saturation obtained from the pulse oximeter. 

Typical nonexposed, nonsmoking individuals may have serum carboxyhemoglobin 

levels of up to 1%; smokers usually have levels of 4-6%. Levels above 10% signify 

significant exposure and may be associated with symptoms as outlined in Table 45-11. 

Patients may be asymptomatic when carboxyhemoglobin levels are below 10-15%. 

Levels higher than 50-60% are associated with a high incidence of coma and seizures, 

and levels higher than 70% are frequently fatal. Myocardial ischemia or infarction and 

cardiac arrhythmias occur frequently, especially in patients with underlying 

atherosclerotic heart disease. Some patients who initially appear to have recovered may 

experience delayed onset of a neurologic syndrome characterized by dementia, ataxia, 

and other sensory and motor abnormalities. This syndrome may be due to infarcts in the 

globus pallidus. 

Treatment 

For the critically ill patient, proceed as outlined earlier in this chapter. If there are signs 

of thermal injury to the airway, endotracheal intubation is necessary. In patients with 

major burns, even if the airway is patent initially, edema frequently occurs minutes or 

hours later. Prophylactic intubation prevents later urgent, difficult intubation. 

Obtain arterial blood gas and carboxyhemoglobin determinations in all patients with 

possible smoke inhalation. While waiting for the results, give 100% oxygen by 

tight-fitting reservoir mask or, if indicated, by endotracheal tube. Avoid alkalosis and 

hypothermia, which decrease the dissociation of carbon monoxide from hemoglobin. 

Indications for hyperbaric oxygen therapy have been described as a carboxyhemoglobin 

level greater than 25%, neurologic symptoms, seizures, or depressed consciousness. 

The efficacy of hyperbaric oxygen in clinical management remains unproved. Although 

therapy shortens the half-life of carboxyhemoglobin to less than 30 minutes, the hazards 

and the length of time involved in transporting a critically ill patient to the nearest 

hyperbaric oxygen facility and the limits of resuscitating the patient in the chamber may 

outweigh the benefits of treatment. Hyperbaric oxygenation may be useful, however, in 

the severely poisoned patient who fails to respond to therapy with 100% oxygen. If 

carboxyhemoglobin levels are under 2% and if oxygenation is adequate, the inspired 

oxygen content can be decreased. 

In stable patients with suspected thermal or chemical injury of the airway, evaluate 

mucosa injury using direct laryngoscopy. 

Obtain an ECG, and monitor cardiac rhythm. Carbon monoxide poisoning is associated 

with myocardial ischemia and cardiac arrhythmias.

Obtain a chest x-ray to look for signs of lung injury if smoke inhalation has occurred and 

to serve as a baseline for further changes. 

Give inhaled and parenteral bronchodilators to patients with clinical evidence of 

bronchospasm. 

Obtain a urine specimen for assessment of myoglobinuria. If present, treat as described 

in Chapter 18. 

No evidence supports the use of prophylactic antibiotics or systemic corticosteroids in 

the treatment of inhalation injuries. 

Disposition 

Because victims of smoke inhalation may develop late respiratory failure, these patients 

should be hospitalized for 24 hours for observation. All patients with carboxyhemoglobin 

levels higher than 25% should be hospitalized. Patients who present to the emergency 

department with respiratory compromise or respiratory failure should be hospitalized in 

an intensive care unit. 

CHEMICAL BURNS 


Most chemical burns result from exposure of the skin to strong acids or alkalis. Other 

chemicals that may cause skin damage include phosphorus and phenol. Because full 

development of chemical burns is slower than that of other types, the size of chemical 

burns is usually underestimated during initial evaluation. 


Definitive diagnosis of chemical burns depends on the history. The physician should try 

to ascertain both the type of chemical involved and its concentration. Physical 

examination of a patient unable to give a history may aid in diagnosis. Alkali burns are 

frequently full-thickness injuries, appear pale, and feel leathery and slippery. Acid burns 

are usually partial-thickness injuries and are accompanied by erythema and erosion. 

Skin is stained black by hydrochloric acid, yellow by nitric acid, and brown by sulfuric 

acid. 

Treatment 

The mainstay of treatment of any chemical burn is copious irrigation with large amounts 

of tap water. To be most effective, treatment should be started immediately after 

exposure, preferably before arrival in the emergency department. 

Remove any contaminated clothing. Do not attempt to neutralize the burn with weak 

reciprocal chemicals (acids for alkali burns and alkali for acid burns), because the heat 

generated from the chemical reaction may cause severe thermal injury. Occasionally 

the leathery skin of an alkali burn may make it difficult to completely wash off the alkali,

and injury may continue; further irrigation and emergency excision of burned tissue by a 

surgeon experienced in this procedure may be indicated. 

After copious irrigation with water, the following treatment for specific types of chemical 

burns may be used: 

A. Hydrofluoric Acid 

Cover burns with calcium gluconate (2.5%) gel prepared by mixing 3.5 g of calcium 

gluconate powder in 150 cc of water-soluble lubricant, secured by an occlusive cover. In 

fingertip burns, the fluoride ion often penetrates under the nail bed and matrix, so that it 

is usually wise to remove the nail or make a large wedge. For persistent pain or more 

severe burns, the treatment of choice is subcutaneous and intradermal injections of 

calcium gluconate (10%), 0.5 mL/cm 2 of burned area by a 30-gauge needle. Larger 

volumes should not be used, especially in the fingers, because further damage may 

occur from compartment pressure or the intrinsic toxicity of calcium. For extremely 

severe burns, some authors recommend intra-arterial perfusion of calcium. 

B. Phenol 

After copious irrigation with water, enhance the removal of phenol by applying 

polyethylene glycol, which increases the solubility of phenol. Follow with additional water 

irrigation. 

C. Phosphorus 

Phosphorus, a potent oxidizing agent, ignites and melts on air contact and often leaves 

embedded deposits on the skin. Immersion in cool water is recommended, followed by 

attempts to remove embedded material. Some authors recommend applying a solution 

of copper sulfate (1-3%) in hydroxycellulose (1%) to inactivate the phosphorus and aid 

in its removal, but few studies of this treatment have been made, and systemic toxicity 

from copper absorption may occur if copper is used repeatedly or over large areas. 

Fluid resuscitation in the patient with large chemical burns is the same as that for 

patients with similar-size thermal burns. Because the size of chemical burns may be 

underestimated initially, reevaluate the patient after 24-48 hours. 

Disposition 

The choice between hospitalization or outpatient management of chemical burns should 

be made using the same criteria as for thermal burns. However, remember that the full 

extent of skin injury may not be readily apparent during the initial emergency 

department evaluation. 

TAR BURNS 


Roofing tar usually varies in temperature from 51.1 to 80 °C (124-176 °F). The hands, 

arms, head, and neck are the most commonly burned areas. 

Treatment

Cool the tar immediately with water, which often separates the tar from the skin. If the 

tar continues to adhere, either leave it in place or apply one of the commercially 

available cream- or oil-based solvents specially made for this purpose. If these are not 

available, use mayonnaise or mineral oil. Do not use hydrocarbon solvents, such as 

paint thinner, because they may further injure burned skin. Cover the wound with sterile 

dressings. When dressings are changed after 12-24 hours, much of the tar will have 

separated and will be removed with the dressings. 

Initial stabilization of the patient with large tar burns should follow the procedures 

outlined for thermal burns. 

Disposition 

The criteria for admission or transfer to a burn center for patients with tar burns are the 

same as for patients with thermal burns. 

SUNBURN 


Most sunburn is a first-degree (erythema) or superficial partial-thickness (blisters) burn. 

Skin changes from sunburn are maximal about 12-24 hours after exposure. Patients 

usually present to the emergency department for pain relief. Occasionally a patient with 

extensive superficial partial-thickness burns will require fluid resuscitation and 

parenteral analgesics for pain control. 


Diagnosis is based on a history of exposure to the sun (or to ultraviolet light in tanning 

booths) and physical findings of erythema and blistering. 

Treatment 

Sunburn can be difficult to treat. Saline-soaked dressings or calamine lotion may 

provide some relief from pain and itching. Aspirin or other nonsteroidal anti-inflammatory 

agents (eg, indomethacin, 25-50 mg orally 3-4 times a day) work by blocking the 

production of prostaglandins that are thought to be important mediators of pain in 

sunburned skin. More severe burns may benefit from the application of topical 

corticosteroid preparations such as triamcinolone acetonide, 0.1%, or a short course of 

systemic corticosteroids (prednisone, 40 mg orally to start, with the dose tapered over 

3-5 days). Patients with extensive partial-thickness sunburn should receive treatment 

according to the guidelines described for other thermal burns. 

Disposition 

Almost all patients with sunburn may receive treatment on an outpatient basis. If there 

are large blisters, the patient should be seen again in 2-3 days to make sure that 

secondary infection has not developed. Patients should be advised to avoid prolonged

exposure to the sun in the future and to use a sunscreen (eg, over-the-counter 

preparations containing PABA [p-aminobenzoic acid] or dioxybenzone) before 

exposure. Patients requiring fluid resuscitation or parenteral analgesics should be 

hospitalized. 

ELECTRICAL BURNS (See Chapter 44.) 

OCULAR BURNS (See also Chapter 31.) 


• High level of suspicion in patients with facial burns. 

• Evaluate for foreign bodies. 

• Examine eyes with fluorescein. 


Patients with facial burns may also have burns to the eyelid and the eye itself. Such 

burns are associated with the development of massive periorbital edema that makes 

delayed examination difficult. It is therefore important that patients with suspected ocular 

burns be examined promptly, preferably in the emergency department and by an 



Instill tetracaine, 0.5%, or proparacaine, 0.5%, in the conjunctival sac to decrease pain 

during examination. Retract the eyelids, and look for foreign bodies. Remove contact 

lenses to prevent injury to the cornea due to pressure from edematous lids. Corneal 

abrasions and thermal injury may be detected by instilling fluorescein in the conjunctival 

sac and examining the eye using the blue light on an ophthalmoscope or, if the patient's 

condition permits, a slit lamp. 

Treatment 

Irrigate any suspected chemical burn of the eye with large amounts (2 L) of sterile 

normal saline using a Morgan lens. Treat corneal abrasions and thermal injuries by 

instilling an ophthalmic antibiotic in the conjunctival sac. Alkali burns may require larger 

amounts of irrigating fluid, and irrigation should continue until the effluent pH is normal. 

Alkali burns require emergent ophthalmologic consultation. 

Disposition 

Burns of the eyes are major injuries. Hospitalize the patient, and obtain urgent 

ophthalmologic consultation. 

CIRCUMFERENTIAL BURNS OF NECK, CHEST, & EXTREMITIES


Circumferential deep burns of the neck may cause lymphatic and venous obstruction 

leading to laryngeal edema and airway obstruction. Circumferential chest wall injuries 

may impede chest wall movement and lead to respiratory failure. Circumferential burns 

of the extremities may restrict blood flow, causing increased tissue pressure with 

resultant ischemia. 


Patients with deep circumferential neck wounds should undergo direct visualization of 

the larynx by laryngoscopy. Because laryngeal edema may develop hours after initial 

examination, frequent reevaluation may be necessary. 

Monitor patients with circumferential chest wounds for signs of respiratory compromise 

(tachypnea, dyspnea, deteriorating arterial blood gas levels); measurement of forced 

vital capacity or peak airway pressure may be useful. 

Carefully examine the extremity distal to the wound in patients with circumferential 

burns of the extremities. Look for evidence of ischemia (diminished pulses, poor 

capillary refill, anesthesia); loss of vibratory sense is an early sign. If available, a 

Doppler ultrasound device is useful to assess distal blood flow. Because edema 

continues to develop during the first 6-8 hours after burn injury of the extremities, 

frequent reevaluation is important. 

Treatment 

Patients with deep circumferential burns of the neck are candidates for early 

endotracheal intubation. 

Elevate the injured extremity of patients with circumferential wounds of the extremities in 

order to minimize development of edema. Remove rings or other jewelry that could act 

as a tourniquet when edema develops. If evidence of distal ischemia develops, 

escharotomy is indicated. Ideally this should be performed in a burn center by a surgeon 

experienced in this procedure. Occasionally escharotomy must be performed in the 

emergency department before the patient is transported to a burn center for definitive 

care. Sterilize the overlying skin (Chapter 6), and make medial and lateral incisions 

through the eschar using a No. 20 scalpel or electrocautery. Incise deeply enough to cut 

entirely through the burned skin and release the constricting eschar (typically this occurs 

at the level of the subcutaneous fat). No anesthesia is required. Blood loss is seldom 

significant but can be controlled by cautery or suture if necessary. 

Patients with a circumferential chest wall burn may require escharotomy in the 

emergency department. Using sterile technique, incise the eschar along the anterior 

axillary line bilaterally to the costal margins, and then join these incisions with incisions 

along the costal margins and just below the clavicles. This releases a segment of chest 

wall eschar that can move with respiratory excursion. 

Disposition

All patients with deep circumferential burns of the neck, extremities, or chest wall should 

be hospitalized, preferably in a burn center. 

BURNS DUE TO CHILD ABUSE 


• High index of suspicion. 

• Discrepancy between the history and physical findings. 

• Err on the side of protecting the child. 


Burns represent 8-14% of child abuse injuries seen in the United States; about 15% of 

abused children have been intentionally burned at some time. 


Suspect child abuse if there is a delay in seeking medical care, if there is a history of 

other injuries, or if there is a discrepancy between the history and the physical findings. 

The injuries most commonly encountered in the emergency department are burns of the 

perineum caused by immersion in hot water in children who are being toilet-trained, and 

cigarette burns in children of any age. 


The treatment of burns in children is the same as that of a burn of comparable size in 

any other patient, but if there is any suspicion that the injury was due to abuse, the child 

must be hospitalized and the attending physician informed of the emergency physician's 

suspicions. By law, suspected child abuse must be reported to the appropriate child 

welfare authorities (Chapters 5 and 48). Obtain consultation with appropriate personnel 

as soon as possible (eg, social worker, nurse, psychologist, pediatrician). 

OUTPATIENT MANAGEMENT OF MINOR BURNS 


Burns that meet the criteria for outpatient management (described above) may be 

treated initially in the emergency department, after which arrangements should be made 

for close follow-up on an outpatient basis. 

Treatment 

First-degree burns (erythema only) are best treated with application of nonadherent 

dressings (eg, petrolatum-impregnated gauze). Clean deeper burns by gently irrigating 

them with sterile normal saline solution. Leave blisters intact, and perform only minimal

debridement. Wounds may be covered with a topical antibiotic such as silver 

sulfadiazine cream or triple antibiotic ointment and wrapped in a bulky dressing. Instruct 

the patient to keep the wound clean and to change dressings and apply topical antibiotic 

cream twice a day at home. A nonadherent, semipermeable, polyurethane dressing (eg, 

Epi-Lock), which is left in place for 5-7 days, may be an acceptable alternative for some 

patients. Such dressings should be covered with roll gauze, which is changed daily. 

Have the patient elevate affected extremities to minimize development of edema. All 

patients should receive tetanus prophylaxis as outlined in Chapter 30. Prophylactic 

systemic antibiotics are not indicated. Control pain with oral analgesics (eg, codeine, 

oxycodone). 

Disposition 

Patients should be seen on an outpatient basis in 1-2 days. Ruptured blisters or dead 

tissue may be debrided at that time. Promptly treat any minor infection with oral 

antistaphylococcal drugs (eg, dicloxacillin, 250- 500 mg orally 4 times a day [children < 

40 kg, 25-50 mg/kg/d orally divided into 4 equal doses]; or a first-generation 

cephalosporin such as cephalexin, 250-500 mg orally 4 times a day [children, 25-50 

mg/kg/d orally divided into 2 or 4 equal doses]). Patients who develop infections (fever, 

extensive cellulite, lymphadenitis), poor-risk patients (diabetics), and unreliable patients 

must be hospitalized for administration of parenteral antibiotics and continued wound 

care. 

Heimbach D: What's new in general surgery: burns and metabolism. J Am Coll Surg 

2002;194:156. [PMID: 11848634] 

Lee-Chiong TL Jr: Smoke inhalation injury. Postgrad Med 1999; 105:55. [PMID: 

10026703] 

Reilly DA, Garner WL: Management of chemical injuries to the upper extremity. Hand 

Clin 2000;16:215. [PMID: 10791168] (Review.) 

Schrage NF et al: Eye burns: an emergency and continuing problem. Burns 

2000;26:689. [PMID: 11024601] 

Smith ML: Pediatric burns: management of thermal, electrical, and chemical burns and 

burn-like dermatologic conditions. Pediatr Ann 2000;29:367. [PMID: 10868433] 

Wong L, Spence RJ: Escharotomy and fasciotomy of the burned upper extremity. Hand 

Clin 2000;16:165. [PMID: 10791164] 





Boozer, MD


Figure 43-1.)

Table 43-1. Formulas for fluid resuscitation in burn patients. 

Day 1 1 

Formula Parkland (Baxter) 

Lactated Ringer's 

injection 

Child: 3 mL/kg per percentage of body 

surface area burned

Table 43-2. Determinants of burn severity. 





Boozer, MD 

TABLES 

Table 43-2. Determinants of burn severity.

Table 43-3. Summary of American Burn Association burn severity 

categorization. 





Boozer, MD 

TABLES 

Table 43-3. Summary of American Burn Association burn severity 

categorization.

Table 43-4. Rule of nines (rapid means of estimating body surface area burned 

in adult patients) and rule of lives (rapid means of estimating body surface area 

burned in infants and children.) 

Percentage 

Area Infant Head and 20 Arm 

neck

Table 43-5. Characteristics of burns of different depth. 

Depth of Burn Skin Texture 

Superficial 

partial-thickness 

Involves 

underlying 

subcutaneous 

tissue, tendon, or 

bone 


Pinprick 

Sensation 

First-degree Red 

Edematous Yes Deep 

partial-thickness 

Variable No 




Boozer, MD 

TABLES 

Table 43-5. Characteristics of burns of different depth. 

Thick

Table 43-6. Common toxic products of combustion. 

Toxic Product 

Acrolein, acetaldehyde, formaldehyde, acetic acid, formic acid, nitrogen 

dioxide, carbon monoxide 

Hydrochloric acid, phosgene, chlorine 

Hydrocyanic acid, isocyanates (eg, toluene diisocyanate), carbon 

monoxide 

Acrolein, acetic acid, formic acid 

Nitrogen dioxide and other oxidesof nitrogen; acetic acid; formic acid; 

carbon monoxide 





Boozer, MD 

TABLES 

Table 43-6. Common toxic products of combustion.

Figure 43-1. Management of life-threatening burn or inhalation injury. 





Boozer, MD 

FIGURES 

Figure 43-1

Figure 43-2. Burn size may be estimated using an age-adjusted burn chart. 

(Reproduced, with permission, from Way LW, [editor]: Current Surgical Diagnosis & 






Boozer, MD 

FIGURES 

Figure 43-2

Figure 43-3. Layers of the skin, showing depth of first-, second-, and third-degree 

burns. (Reproduced, with permission, from Way LW [editor]: Current Surgical Diagnosis 

& Treatment, 9th ed. Appleton & Lange, 1991.) 





Boozer, MD 

FIGURES 

Figure 43-3

44. Disorders Due to Physical & Environmental Agents 1 - D. Shannon 

Waters, MD, & Rebecca C. Bowers, MD 

EMERGENCY TREATMENT OF DISORDERS DUE TO COLD 

1 This chapter is a revision of the chapter by Paul S. Auerbach, MD, from the 4th edition. 

Individuals vary considerably in their response to environmental cold. Factors that 

increase the possibility of injury due to cold include poor general physical condition, 

nonacclimatization, childhood or advanced age, systemic illness, anoxia, and the use of 

alcohol and other sedative drugs. High wind velocity (windchill factor) and moisture may 

markedly increase the propensity for cold injury at low temperatures. 

SYSTEMIC HYPOTHERMIA 


• Signs and symptoms depend on degree of hypothermia. 

• Rewarming methods include passive external active, external, and active internal 

rewarming. 


A. Healthy Persons BR>Accidental hypothermia occurs when an external cold 

challenge overwhelms an individual's capacity to produce or conserve heat. 

Hypothermia may occur in otherwise healthy individuals during occupational or 

recreational exposure to cold or as a result of accidents or other misfortunes. Alcohol 

abuse is a common predisposing cause. 

B. Persons with Predisposing Factors 

Systemic hypothermia may follow exposure to even slightly lowered temperatures when 

preexisting altered homeostasis exists as a result of debility or disease. Accidental 

hypothermia is more likely to occur in elderly or inactive people and those with 

cardiovascular, dermatologic, or cerebrovascular disease; mental retardation; 

myxedema; hypopituitarism; or alcoholism. The use of sedative-hypnotic or 

antidepressant drugs may be a contributing factor. 


Because lowered body temperature is the sole finding in some patients brought to the 

emergency department, making the diagnosis often depends on awareness of the 

possibility of hypothermia. 

A. Temperature

In the hypothermic patient, oral and axillary temperatures are not accurate. Infrared 

tympanic thermometers or rectal probes should be used. The temperature varies widely 

in hypothermia, and accurate monitoring is essential. 


At rectal temperatures of 35 °C (95 °F), hypothermia is classified as mild. Shivering is at 

a maximum and consciousness is normal. At 34 °C (93.2 °F), the victim develops 

apathy, drowsiness, slurred speech, and poor judgment. At 32 °C (89.6 °F), the 

hypothermia is profound with marked alteration in mental status, lethargy, and ataxia. At 

31 °C (87.8 °F), shivering stops and failure of the thermoregulatory mechanism is 

imminent. The patient soon becomes unresponsive; profound bradycardia, hypotension, 

and hypoventilation can occur; and fixed pupils may develop. The patient may appear to 

be in a state of rigor mortis. Ventricular fibrillation and asystole may occur 

spontaneously at core temperatures below 28 °C (82.4 °F). Note: For this reason, a 

hypothermic patient should not be considered dead until all reasonable resuscitative 

measures have failed. No one is dead until he or she is "warm and dead." 


Several laboratory findings are unique to hypothermia. The electrocardiogram (ECG) 

may demonstrate prolongation of any conduction interval; atrial fibrillation is common. A 

pathognomonic positive deflection in the RT segment is known as a J, or Osborne, 

wave (Figure 44-1). 

Hypoglycemia, hypomagnesemia, and hypophosphatemia are common in hypothermia, 

particularly in alcoholic individuals. Hyperglycemia may be seen as a result of 

hemorrhagic pancreatitis in patients with long-lasting exposure to the cold. Sodium and 

potassium levels may be elevated or depressed. Arterial blood gas samples drawn at 

cold temperatures are generally analyzed at 37 °C (98.6 °F), which causes lowering of 

pH and elevation of PO 2 and PCO 2 readings. However, clinical therapy is based on the 

uncorrected determinations recorded at 37 °C. 

D. Complications 

Metabolic acidosis, pneumonia, pancreatitis, renal failure, sepsis, and ventricular 

fibrillation may occur. Death due to systemic hypothermia usually results from cardiac 

arrest associated with ventricular fibrillation, which may occur during rewarming. 

E. Underlying Conditions 

Obtain a brief history from witnesses or relatives of a patient with hypothermia, and 

perform a general physical and laboratory examination to detect underlying conditions 

that might predispose to hypothermia. Examination should include an evaluation of renal 

function (uremia), thyroid function (myxedema), and adrenal function (Addison disease). 

If sepsis is a diagnostic possibility, obtain blood for culture. 

Treatment 

Bundle the victim of suspected hypothermia in dry, warm blankets at the scene of 

discovery, and transport the person to the nearest hospital as soon as possible. Note: 

Transport should be as gentle as possible because of the risk of cardiac arrhythmias 

due to increased myocardial irritability. Hospitalization and monitoring in an intensive

care unit are required for all victims with initial core temperatures below 32 °C (89.6 °F) 

or for those with complications of hypothermia. 

A. Cardiopulmonary Resuscitation 

Adequacy of ventilation and circulation must be ensured by careful clinical observation, 

continuous electrocardiographic monitoring, and serial determinations of arterial blood 

gases. If cardiac arrest occurs, start cardiopulmonary resuscitation (CPR) (Chapter 7). If 

the victim has any detectable pulse or breathing, no matter how slow, do not initiate 

CPR; unnecessary brisk closed chest compression may induce ventricular fibrillation. 

Because of the protective effects of hypothermia, bradycardia and hypotension are 

generally well tolerated. 

1. Establish an airway—Intubation of the unprotected airway and frequent suctioning 

may be required. 

2. Give warm, humidified oxygen—Depression of the respiratory center in 

hypothermia causes hypoxemia or hypercapnia, requiring controlled ventilation and 

supplemental oxygen. Avoid hyperventilation, because a rapid fall in PCO 2 may trigger 

ventricular fibrillation. 

3. If arterial blood pH is below 7.1, cautiously give bicarbonate—(See Chapter 42). 

Do not try to attain neutral pH, because sudden changes in acid-base equilibrium may 

cause cardiac arrhythmias. Mild acidosis (pH 7.25-7.35) due to hypothermia in the 

absence of sepsis is generally well tolerated. Management should be based on arterial 

blood gas measurements recorded at 37 °C (98.6 °F). 

4. Correct ventricular fibrillation—Electrical defibrillation is rarely successful at core 

temperatures below 30 °C (86 °F). Bretylium tosylate is the drug of choice in ventricular 

fibrillation; lidocaine and other class Ib agents are generally ineffective. Other 

pharmacologic measures to correct bradycardia and hypotension should generally be 

avoided. 

5. Correct fluid, electrolyte, and glucose abnormalities—Give thiamine, 100 mg 

intravenously; naloxone, 2.0 mg intravenously; and dextrose, 25 g intravenously, to all 

patients with altered mental status who are thought to be hypothermic. Volume 

expansion with warmed fluid generally helps the rewarming process. Avoid lactated 

Ringer's solution because the lactate is not metabolized efficiently by a cold liver. 

B. Treatment of Underlying Conditions 

Treat underlying and predisposing conditions as necessary (eg, heart disease, 

hypoglycemia, malnutrition, adrenocortical insufficiency [hydrocortisone, 200 mg 

intravenously], hypothyroidism [levothyroxine, 400 ug intravenously; plus 

hydrocortisone, 100 mg intravenously]). 

C. Rewarming 

Rewarming is essential but potentially harmful, because peripheral vasodilatation may 

divert blood flow from internal organs to the skin and shunt cooled blood to the central 

circulation, causing a brief drop in core temperature. Note: Rapid rewarming may be

hazardous, because hypothermic patients are particularly vulnerable to lethal cardiac 

arrhythmias. Core rewarming should be undertaken only if hypothermia is severe and 

the patient shows cardiovascular instability (eg, cardiac arrest, ventricular fibrillation). 

1. Mild hypothermia (core temperature = 33 °C [91.4 °F])—Passive rewarming to 

prevent further heat loss is sufficient for most patients with mild hypothermia, because 

their thermoregulatory mechanism is intact, and many of these patients are able to 

generate heat by shivering. Most patients should be wrapped in dry, heated blankets 

and carefully monitored. Patients with mild hypothermia who are otherwise healthy 

usually respond well to heated blankets and the administration of heated (45 °C [113 

°F]) intravenous solutions. Another conservative approach—often used with elderly or 

debilitated patients—is to wrap the patient in an electric blanket kept at 37 °C (98.6 °F). 

Patients must be carefully monitored when any of these rewarming methods are used. 

2. Moderate to severe hypothermia (core temperature < 33 °C [91.4 °F])—Moderate 

to severe hypothermia often requires additional rewarming measures, because 

thermoregulation is altered or absent. Individualized supportive care is mandatory, 

because active rewarming is hazardous. As mentioned previously, active core 

rewarming is necessary only for patients with cardiovascular instability. 

a. Active external rewarming methods—Heated blankets, forced-air blankets (Bair 

Hugger), or warm baths have been used, with a rate of rewarming of about 1-3 °C/h (up 

to 600 kcal/h using hydraulic pads at 45 °C). Because it is easier to monitor the patient 

and to carry out diagnostic and therapeutic procedures when heated blankets rather 

than warm baths are used for active rewarming, heated baths are not widely 

recommended. There is some potential risk with active external rewarming, because 

marked vasodilation may occur. Combining active external rewarming with active core 

rewarming may prevent the resultant hypotension and core temperature after-drop 

sometimes seen during rewarming. If active external rewarming is used, the patient 

should be carefully monitored and supported hemodynamically. The application of 

commercial heat packs directly to hypothermic skin may cause serious burns. 

b. Active internal (core) rewarming methods—Internal rewarming is suggested for 

patients with profound hypothermia of long duration in which there is suspected 

underlying debilitation, for patients with complications of cardiovascular or respiratory 

insufficiency, and for patients in cardiac arrest. 

Repeated peritoneal dialysis may be performed using warm (45 °C [113 °F]) 

potassium-free dialysate solution or normal saline. The usual exchange rate is 6 L/h, 

which can increase the core temperature 1-3 °C/h. 

Warm fluids (crystalloid solutions) administered by gastrointestinal, colonic, or bladder 

lavage may be employed. Placement of a nasogastric tube is less invasive but may run 

the risk of stimulating ventricular dysrhythmias owing to the irritability of the hypothermic 

heart. 

Administration of heated intravenous fluids contributes only 17 kcal/h, which accounts 

for an increase in body temperature of less than 1/3 °C/L. Microwave rewarming of 

crystalloid solutions to 40-42 °C (104- 107.6 °F) may be safely accomplished in about

2-3 minutes. This technique causes some hemolysis of erythrocytes, and if blood 

products are used they should be administered through a high-flow countercurrent fluid 

infuser or reconstituted with warmed normal saline. 

Heated humidified oxygen, either via a tight-fitting mask or by endotracheal tube, will 

raise the core temperature 1 °C/h or 1.5-2 °C/h, respectively. 

Thoracic cavity lavage may achieve rapid rewarming with the added advantage of 

warming the heart more quickly. Insert 2 thoracostomy tubes, and continuously infuse 

fluid warmed to 41 °C (105.8 °F) through one tube and drain it through the other. 

Extracorporeal blood rewarming methods including arteriovenous and venovenous 

rewarming as well as hemodialysis have been reported as treatment options but are 

limited to medical centers with the available resources. 

Negative pressure rewarming is a new technique based on the principle that 

thermoregulatory blood flow to certain skin areas is regulated by arteriovenous 

anastomosis. Negative pressure and a thermal device are used to increase local 

subcutaneous blood flow, allowing heat to be transferred directly from the skin to the 

critical body core despite the central drive for vasoconstriction. The devices have 

reported good rewarming rates, although more studies are needed. 

D. Antimicrobials 

Patients with severe hypothermia—especially those who are comatose—are at high risk 

for development of aspiration pneumonia; subsequent pulmonary, urinary tract, or 

intraperitoneal infections; and sepsis. If severe infection is suspected, obtain a chest 

x-ray and samples of blood and urine for culture, and take material for culture from any 

other appropriate sites (eg, cerebrospinal fluid). If sepsis is likely, administer 

broad-spectrum antibiotics. Prophylactic antimicrobial drugs are unnecessary if infection 

is unlikely. Many hypothermic alcoholic, debilitated, or elderly patients will have an 

underlying infection, and the cause should be aggressively sought and treatment 

initiated. 

E. Complications of Rewarming 

Observe the patient for signs of metabolic acidosis, cardiac arrhythmias, acute 

respiratory distress syndrome, pancreatitis, ischemic bowel, pneumonia, myoglobinuria 

with renal failure, or clotting abnormalities. 

Disposition 

Hospitalize all patients who present with core temperatures below 33 °C (91.4 °F), 

especially if the sensorium is altered. Patients with coexisting illness and core 

temperatures under 35 °C (95 °F) should be hospitalized. The mortality rates in 

hypothermia are variable and depend on the cause of hypothermia and the patient's 

underlying condition. 

COLD INJURY OF THE EXTREMITIES


• Tissue injury or death is caused by ischemia and thrombosis in capillaries or by 

formation of ice in the tissues. 

• Treatment of frostbite or chilblains depends on the severity of skin injury and includes 

rewarming by both passive and active measures. 

In the normal person, exposure of the extremities to cold produces immediate intense 

localized vasoconstriction followed by reflex generalized vasoconstriction. When skin 

temperature falls to 25 °C (77 °F), tissue metabolism is slowed but the relative demand 

for oxygen exceeds the supply from diminished circulation; thus, the area becomes 

cyanotic. At 15 °C (59 °F), tissue metabolism is markedly decreased and the 

dissociation of oxyhemoglobin is reduced, which may give the skin a pink, 

well-oxygenated appearance. Tissue damage occurs at this temperature. Tissue death 

may be caused either by ischemia and thrombosis in capillaries or by actual freezing. 

Freezing (frostbite) does not occur until the skin temperature drops to -10 to -4 °C 

(14-24.8 °F). The body's "hunting reaction," or alternating vasoconstriction and 

vasodilation of vessels in the frozen area, results in repetitive cycles of partial thawing 

with refreezing. This process causes the most damage. The incidence of frostbite 

depends on factors such as wind, moisture, mobility, venous stasis, trauma, 

malnutrition, and occlusive arterial disease. 

1. Chilblains (Pernio) 


Chilblains, a less severe form of cold injury than frostbite, is more common in children 

and women as well as people with any form of peripheral vascular disease. Chilblains 

are red or violaceous pruritic skin lesions, usually on the face or extremities, caused by 

exposure to cold and humidity without actual freezing of tissues. Lymphocytic vasculitis 

is common. Chilblains may be associated with edema or blistering and are subsequently 

aggravated by excessive warmth. With continued exposure, ulcerative or hemorrhagic 

lesions may appear and progress to scarring, fibrosis, and atrophy. 


Elevate the affected part on pillows or sheepskin, and allow it to warm gradually at room 

temperature. 

Do not rub or massage injured tissues or apply ice or heat. Protect the area from trauma 

and secondary infection. Refer the patient to a primary care physician or clinic for 

follow-up. 

2. Frostbite 

Clinical Findings

A. Classification 

Frostbite is injury of the tissues due to freezing. The classification of injury is applied 

after rewarming because most frostbite appears similar initially. 

1. First-degree—Freezing without blistering; peeling is occasionally present. 

2. Second-degree—Freezing with clear blistering. 

3. Third-degree—Freezing with death of skin, hemorrhagic blisters, and subcutaneous 

involvement. 

4. Fourth-degree—Freezing with full-thickness involvement (including bone); ultimate 

loss or deformity of body part. 

This classification scheme neither accurately predicts clinical outcome nor aids in initial 

management because a discrepancy exists between skin lesions and the extent of deep 

tissue injury, and demarcation is not complete for 3-5 weeks. 


Frostbitten tissue appears white or blue-white, is firm or hard (frozen), cool to the touch, 

and generally insensitive. Because cold injury produces anesthesia, many symptoms 

are not apparent until rewarming begins or the part is closely inspected. In patients with 

mild frostbite, the symptoms are numbness, paresthesias, pruritus, and lack of fine 

motor control. With increasing severity, decreased range of motion, blister formation, 

and prominent swelling are noted. Thawing unmasks local tenderness and throbbing 

pain. The tissue becomes discolored, loses its elasticity, and becomes immobile. 

Profound edema, hemorrhagic blisters, necrosis, and gangrene may occur. Long-term 

sequelae include cold sensitivity, loss of sensation, and hyperhidrosis. 

Treatment 

A. Systemic Hypothermia 

Treat moderate to severe associated systemic hypothermia before managing frostbite. 

B. Rewarming 

1. Superficial frostbite—Rewarm extremities affected by superficial frostbite (frostnip) 

by removing wet clothing and applying constant warmth, which can be accomplished by 

exerting gentle pressure with a warm hand. 

2. Full-thickness frostbite—Rapid rewarming is the most important aspect of 

management. It should not be attempted, however, until the risk of refreezing is gone. 

Once rewarming can begin, it should be performed with a waterbath containing an 

antimicrobial agent. Strict adherence to a narrow water temperature window of 40-42 °C 

(104-107.6 °F) is necessary. When a red-purple color appears and the skin becomes 

pliable, the rewarming may cease. 

C. Resuscitation 

Unless concomitant hypothermia exists, intravenous hydration is not usually necessary.

Severe cases of frostbite have led to subsequent rhabdomyolysis with renal failure, 

which then requires aggressive hydration. Intravenous narcotics are almost always 

necessary secondary to the severe pain associated with rewarming. 

D. Protection of the Injured Part 

In the prehospital setting, padding, splinting, and avoidance of rewarming are all that is 

necessary. Once in the secure hospital setting and after rewarming has been achieved, 

avoidance of further trauma is important. Affected body parts should be elevated and 

padded, uncovered or loosely dressed, and left at room temperature. Debride clear 

blisters because prostaglandins and thromboxane are present in the exudate. Leave 

hemorrhagic blisters intact. Apply aloe vera cream every 6 hours. Administer ibuprofen, 

400-600 mg every 8-12 hours for 72 hours. 

E. Anti-infective Measures 

Infection prevention is important after rewarming. Maintain a sterile environment. Protect 

skin blebs from physical contact. Whirlpool therapy at temperatures of 32-38 °C 

(89.6-100.4 °F) twice daily for 30 minutes for a period of 3 or more weeks helps to 

cleanse the skin and debride superficial dead tissue. Penicillin prophylaxis is highly 

recommended for severe cases. 

F. Adjunctive Therapies 

1. Anticoagulation—Consistent benefit from anticoagulation has not been 

demonstrated. 

2. Dextran—Animal experiments have shown promise, but human clinical trials have 

not been attempted. 

3. Vasodilators—Intra-arterial injections of reserpine reduce vasospasm but have not 

prevented tissue loss. 

4. Thrombolysis—Thrombolytics have been extremely successful in aiding tissue 

survival in the animal model. Small clinical studies with tissue plasminogen activator are 

also showing success in humans, but the results of larger, multicenter trials are needed. 

5. Surgery—Amputation or debridement should not be considered until it is definitely 

established that tissues are dead. Although rare, the development of a compartment 

syndrome necessitates fasciotomy. The line of demarcation between injured and normal 

tissue may not appear until 3-5 weeks after injury; mummification of the injured 

extremity may require the same length of time. Technetium- 99 pyrophosphate scanning 

accurately predicts the level of ultimate amputation. Magnetic resonance imaging and 

magnetic resonance angiography are under investigation as possible techniques for 

assessing demarcation lines much earlier. 

Regional sympathectomy performed 24-48 hours after injury has reportedly ameliorated 

the early sequelae of frostbite, including a reduction in edema and decreased 

subsequent tissue loss. Appropriate clinical studies have yet to be performed to support 

the use of this therapy.

6. Hyperbaric oxygen—Considerable disagreement exists as to the effectiveness of 

hyperbaric oxygen therapy. In animal models, early institution after rewarming, with 

subsequent daily therapy, decreased tissue loss. 

Disposition 

Hospitalize all patients with second- or third-degree frostbite and patients with extensive 

areas of first-degree frostbite. 

3. Immersion Syndrome (Immersion Foot; Trench Foot) 


• Caused by prolonged immersion in cold water. 

• Alternating vasospasm and vasodilatation results in initial cold and anesthetic feet 

followed by blistering and ulceration. 

• Treatment includes rewarming and wound care. 


Immersion foot (or hand) is caused by prolonged immersion in cool or cold water or mud 

that causes alternating arterial vasospasm and vasodilatation. The affected parts are 

first cold and anesthetic. Hyperemia follows after 24-48 hours, and the parts become 

warm, with intense burning and tingling pain. Blistering, swelling, redness, ecchymoses, 

and ulceration are noted. The posthyperemic phase occurs after 2-6 weeks and causes 

the limbs to become cyanotic, with increased sensitivity to cold. Complications include 

lymphangitis, cellulitis, thrombophlebitis, and wet gangrene. 

Prevention 

Changing out of wet socks and shoes as soon as possible is paramount to the 

prevention of immersion syndrome. In the military, individuals at risk for immersion foot 

apply silicone ointment to the bottoms of their feet twice daily as a preventive measure. 


Treatment is best started during or before the stage of reactive hyperemia. 

Immediate treatment consists of protecting the extremities from trauma and secondary 

infection. Rewarm the injured areas gradually by exposing them to air (not to ice or 

extreme heat). Do not soak or massage the skin. The patient should remain at bed rest 

until all ulcers have healed. Keep the affected parts elevated to aid in removal of edema 

fluid, and protect pressure sites (eg, heels) with pillows or booties lined with cotton 

batting. Give antimicrobials only if infection occurs. 

Hospitalize all patients with immersion syndrome.

Giesbrecht GG: Cold stress, near drowning and accidental hypothermia: a review. Aviat 

Space Environ Med 2000;71:733. [PMID: 10902937] (Review of therapy and new 

techniques in the treatment of hypothermia.) 

Humphrey W et al: Warm water immersion: still a threat to the soldier. Mil Med 

1997;162:610. [PMID: 9290296] (Case reports of soldiers with immersion foot 

syndrome.) 

Kulkarni RD et al: Severe accidental hypothermia: the need for prolonged aggressive 

resuscitative efforts. Prehosp Emerg Care 1999;3:254. [PMID: 10424866] (Case report 

and review of the treatment of hypothermia.) 

Lazar HL: The treatment of hypothermia. N Engl J Med 1997;337:1545. [PMID: 

9366589] (Review of the treatment of hypothermia and discussion about the findings of 

the Walpoth et al article [see below].) 

Murphy JV et al: Frostbite: pathogenesis and treatment. J Trauma 2000;48:171. [PMID: 

10647591] (Review article on frostbite.) 

Soreide E et al: A non-invasive means to effectively restore normothermia in cold 

stressed individuals: a preliminary report. J Emerg Med 1999;17:725. [PMID: 10431966] 

(A prospective study to evaluate the use of subatmospheric pressure and heat to 

restore normothermia.) 

Stavem K et al: Accuracy of infrared ear thermometry in adult patients. Intensive Care 

Med 1997;23:100. [PMID: 9037647] (Prospective comparison of infrared ear 

thermometry vs. core reference [pulmonary artery] temperature.) 

Vassal T et al: Severe accidental hypothermia treated in an ICU: prognosis and 

outcome. Chest 2001;120:1998. [PMID: 11742934] (A retrospective analysis of the 

characteristics and outcome of patients admitted to an intensive care unit with severe 

accidental hypothermia.) 

Walpoth BH et al: Outcome of survivors of accidental deep hypothermia and circulatory 

arrest treated with extracorporeal blood warming. N Engl J Med 1997;337:1500. [PMID: 

9366581] (An analysis and testing of survivors of severe hypothermia for residual 

deficits. Cardiopulmonary bypass is recommended as the rewarming method of choice.) 

Walsh S: More red toes. J Pediatr Health Care 2000;14:205. [PMID: 10900417] 

(Discussion of cold-induced skin disorders.) 

EMERGENCY TREATMENT OF DISORDERS DUE TO HEAT 

The 5 main disorders due to environmental heat stress are (1) heat edema, (2) heat 

syncope, (3) heat cramps, (4) heat exhaustion, and (5) heat stroke. 

Acclimatization usually results after 8-10 days of exposure to high temperatures, but 

even a fully acclimatized person may suffer a heat disorder when heat exposure is 

combined with excessive fatigue; severe infection; alcohol intoxication; use of

anticholinergic drugs; or failure to maintain hydration, salt intake, or caloric intake. 

Elderly or obese persons and those with chronic debilitating diseases are most 

susceptible to heat disorders due to circulatory failure or failure of the sweating 

mechanism. 

HEAT EDEMA 


• Swelling of feet and ankles due to vasodilatation and venous stasis. 

• Treatment is elevation of the limbs. 

Nonacclimatized individuals, particularly the elderly, may develop swelling of the feet 

and ankles that is generally associated with periods of prolonged sitting or standing. The 

edema is not complicated by manifestations of congestive heart failure or lymphatic 

disease. The cause of heat edema is muscular and cutaneous vasodilation combined 

with venous stasis. Interstitial fluid then accumulates in the lower extremities. Because 

the problem is self-limited, treatment involves use of support hose and simple elevation 

of the lower limbs. Diuretics are not indicated. 

HEAT SYNCOPE 


• Caused by peripheral pooling of the intravascular volume. 

• Patient responds promptly to rest, cooling, and rehydration. 

Simple fainting may occur suddenly after exertion in the heat. Cutaneous and muscular 

vasodilation redistributes intravascular volume to the periphery of the body. Volume loss 

and prolonged standing (pooling in the lower extremities) also contribute to the 

development of inadequate central venous return and insufficient cerebral perfusion. 

The patient's skin is cool and moist, the pulse is weak, and transient hypotension 

occurs. In general, core temperature is normal or mildly elevated. The patient usually 

responds promptly to rest in a recumbent position, cooling, and oral rehydration. 

Evaluate elderly people who experience syncopal episodes for hypoglycemia, 

arrhythmias, and fixed myocardial or cerebrovascular lesions. 

HEAT CRAMPS 


• Spasms of the voluntary muscles of the abdomen and extremities. 

• Caused by salt depletion.

• Treatment consists of fluid and salt replacement. 


Heat cramps are due primarily to salt depletion and are manifested by painful spasms of 

the voluntary muscles of the abdomen and extremities. The skin may be moist or dry, 

and cool or warm. Muscle fasciculations may be present. The core temperature is 

normal or only slightly elevated. Laboratory studies (rarely indicated) may reveal 

hemoconcentration and low serum sodium levels, although this is variable, and normal 

serum sodium levels are frequently noted. Hypokalemia occurs occasionally. 


Treatment includes oral fluid and salt replacement with 0.1-0.2% salt solution (1/4-1/2 

teaspoon table salt in 1 cup water) or, in severe cases, intravenous normal saline 

solution. Give supplementary potassium as dictated by measured serum levels. Replace 

glucose if needed. An alternative therapy for mild symptoms is a commercial electrolyte 

solution (eg, Gatorade). Place the patient in a cool place, and massage sore muscles 

gently. 

The patient should rest for 1-3 days, depending on the severity of the attack. 

Hospitalization is usually not required. 

HEAT EXHAUSTION 


• Caused by either primary water loss or primary sodium loss due to prolonged heat 

exposure. 

• Rapidly leads to heat stroke. 

• Symptoms of dehydration are present, but central nervous system symptoms are not 

seen. 

• Treatment includes rehydration and cooling. 


Heat exhaustion is a systemic reaction to prolonged heat exposure (hours to days) and 

is due to sodium depletion, dehydration, accumulation of metabolites, or a combination 

of these factors. It is a premonitory syndrome that rapidly evolves to heat stroke. Central 

nervous system symptoms are generally not present, and the core body temperature is 

usually less than 40 °C (104 °F). 


Two types of heat exhaustion have been described: hypernatremic (primary water loss) 

and hyponatremic (primary sodium loss). The hypernatremic form is seen in persons 

without access to free water and results from inadequate water replacement. The

hyponatremic form results from excessive thermal sweating with pure water 

replacement. It differs from heat cramps in that systemic symptoms are present. Pure 

forms of either type are rare, and most cases have a mixed salt and water depletion. 

The signs and symptoms of heat exhaustion are nonspecific and include headache, 

nausea, vomiting, malaise, muscle cramps, and dizziness. Dehydration is manifested by 

tachycardia, hypotension, and diaphoresis. In a hypernatremic patient, the water deficit 

can be calculated using the following formula: 

where TBW = total body water, calculated as follows: 

Measurement of serum electrolytes and renal function is advisable in most patients, 

because serum sodium concentration may be markedly low in patients with heat 

exhaustion. Myoglobinuria indicates subclinical rhabdomyolysis. 


Initial treatment includes placing the patient in a cool place and giving adequate cool 

water and salted (< 200 mOsm/L) fruit drinks or salt tablets according to the estimated 

amount of water and salt depletion. If the patient is unable to drink fluids, give normal 

saline or lactated Ringer's injection with 5% glucose supplementation intravenously in 

accordance with clinical and laboratory findings. If marked hyponatremia with water 

intoxication is present, administration of intravenous hypertonic saline may be required 

(Chapter 42). 

Hospitalize patients with moderate to severe symptoms and those who are elderly or 

have comorbid illnesses. 

HEAT STROKE 


• Extremely high body temperatures causing altered mental status and multiorgan 

dysfunction. 

• Rhabdomyolysis and severe hepatic damage occur. 

• Treatment is rapid reduction in body temperature. 


Heat stroke is characterized by dysfunction of the heat-regulating mechanism, with

altered mental status (ranging from confusion to coma) and elevated core body 

temperature in excess of 41 °C (105.8 °F). Sweating is variable. The extremely high 

body temperature rapidly causes widespread damage to body tissues, with significant 

rhabdomyolysis and multiorgan dysfunction. Illness and death result from destruction of 

cerebral, cardiovascular, hepatic, and renal tissue. 

Heat stroke usually follows excessive exposure to heat or strenuous physical activity 

under exceptionally hot environmental conditions, although it may develop in elderly, 

infirm, or otherwise susceptible individuals in the absence of unusual exposure to heat. 

Cardiovascular disease, diabetes, cystic fibrosis, alcoholism, obesity, recent febrile 

illness, and debility are predisposing factors. Anesthetics, paralyzing agents, diuretics, 

sedatives, antidepressants, and anticholinergic drugs may also be contributing factors. 



Premonitory findings include headache, dizziness, nausea, diarrhea, and visual 

disturbances. Most patients have profound central nervous system dysfunction including 

seizures, delirium, and coma. The skin is hot, flushed (cyanosis may be present), and 

usually dry (although sweating may be present). Prior to cardiovascular collapse, the 

pulse may be strong and rapid. Blood pressure is initially elevated, and hypotension is a 

late finding that signals circulatory collapse. Hyperventilation may cause initial 

respiratory alkalosis, which is generally followed by metabolic acidosis. Stigmas of 

coagulopathy may be present and include hematuria, hematemesis, bruising, petechiae, 

and oozing at sites of venipuncture. Core body temperatures as high as 46 °C (114.8 ° 

F) have been reported in some patients who have achieved full recovery. 


Laboratory findings include hemoconcentration, decreased blood coagulation, and 

evidence of disseminated intravascular coagulation. Hypoprothrombinemia, 

hypofibrinogenemia, or thrombocytopenia may be present. The white blood cell count is 

routinely elevated. Hypophosphatemia and hypokalemia sometimes occur. 

Hyperkalemia is associated with acute renal failure due to rhabdomyolysis. The patient 

has scantly concentrated urine ("machine oil urine") containing protein, tubular casts, 

and myoglobin. A consistent finding in patients with heatstroke is severe hepatic injury. 

Serum transaminase levels rise to tens of thousands, although complete recovery 

usually ensues if treatment is initiated quickly. 

Treatment 

Act quickly to prevent further inquiry. 

A. Airway and Ventilation 

Maintain an adequate airway and ventilation; monitor arterial blood gas levels. Give 

supplemental oxygen, 6-10 L/min, by mask or nasal cannula. 

B. Temperature Reduction 

Reduce body temperature promptly. As a first-aid measure, place the patient in a shady, 

cool place and remove his or her clothing. Sprinkle the patient's entire body with water,

and cool by fanning. Alcohol sponge baths are contraindicated and can result in alcohol 

toxicity. If the victim is near a cold stream, it may be helpful to immerse the patient in the 

water to facilitate cooling. 

In the emergency department, place the patient on a cooling blanket, and place ice 

packs on the axilla, posterior neck, and inguinal areas (do not apply ice directly to the 

skin). Water should be sprayed on the patient with a fan blowing on him or her to 

maximize evaporative cooling. If the temperature cannot be rapidly lowered, or if the 

victim is unresponsive and the initial core temperature exceeds 42 °C (107.6 °F), begin 

peritoneal lavage with cold potassium-free dialysate, 2 L every 10-15 minutes. When the 

rectal temperature drops to 39 °C (102.2 °F), discontinue active measures to lower 

temperature to avoid hypothermia, but continue temperature monitoring. Hyperthermia 

may recur due to thermoregulatory instability, and additional cooling may be required. 

Benzodiazepines may be given as needed to control shivering. Because the 

hypothalamic set point is not elevated as it is in fever, aspirin and acetaminophen are 

ineffective and should not be given. They may even worsen coagulopathy and liver 

damage. 

C. Maintenance of Urine Output 

Maintain adequate urinary output (30-50 mL/h). Insert an indwelling urinary catheter to 

monitor urine output. If myoglobinuria is present, alkalize the urine with intravenous 

administration of bicarbonate, and consider the use of mannitol, 0.25 g/kg intravenously, 

to promote diuresis. Maintain blood pressure and urine output with intravenous infusion 

of crystalloid solutions and inotropic agents as necessary (monitoring of central venous 

pressure or pulmonary capillary wedge pressure may be required). a-Adrenergic drugs 

are contraindicated because they produce vasoconstriction and decrease heat 

exchange. Dobutamine may be preferable to dopamine as an inotropic agent, because 

it does not have the a-adrenergic renal effects associated with dopamine at rapid rates 

of infusion. 

Disposition 

Hospitalize all patients whose core temperature has exceeded 41 °C (105.8 °F) for 

treatment of possible complications (disseminated intravascular coagulation, renal 

failure, hepatic failure, rhabdomyolysis, cardiac arrhythmias, myocardial infarction, and 

coma). 

With early diagnosis and proper care, 80-90% of previously healthy patients should 

survive. Extreme hyperpyrexia (rectal temperature > 42 °C [107.6 °F]), persistent coma 

after cooling, markedly elevated alanine aminotransferase (serum glutamic pyruvic 

transaminase) and aspartate aminotransferase (serum glutamic oxalacetic 

transaminase) levels, and hyperkalemia associated with extensive rhabdomyolysis are 

unfavorable prognostic signs. 

Backer HD et al: Exertional heat illness and hyponatremia in hikers. Am J Emerg Med 

1999;17:532. [PMID: 10530529] Retrospective analysis of the presentation of 

exercise-associated hyponatremia and heat disorders in hikers.

Khosla R et al: Heat-related illnesses. Crit Care Clin 1999;15:251. [PMID: 10331127] 

(Review of minor and major heat illnesses and temperature regulation.) 

Waters TA: Heat illness: tips for recognition and treatment. Cleve Clin J Med 

2001;68:685. [PMID: 11510526] (Review of heat exhaustion versus heat stroke.) 

EMERGENCY TREATMENT OF ELECTRICAL INJURIES 

LIGHTNING INJURIES 


• Lightning injuries can result not only in burns but also in multiorgan dysfunction. 

• Respiratory arrest is the most common cause of death; ventricular fibrillation and 

asystole are also seen in severe cases. 

• Management is the same as that for a person with blunt trauma. 


Lightning associated with thunderstorms strikes the earth more than 120 times per 

second. Although the number of lightning strikes in human beings is low, at least 

200-400 people are killed each year as a result of injuries caused by lightning. 

A stroke of lightning travels from a thundercloud to the ground at a speed of 10,000 

km/s (10 7 m/s), and it briefly attains voltages over 100 million V and temperatures of up 

to 3000 °C (5432 °F). Lightning is direct current (DC). The most common form of 

lightning is streak lightning. Injuries are caused by a direct strike, splash (eg, from trees, 

building, fences), step voltage, or blunt trauma. In step voltage, ground surface current 

is transmitted through a circuit created by the victim's legs (pathway of least resistance). 


Suspect lightning injury in a person found dazed, unconscious, or injured in the vicinity 

of a thunderstorm. Certain pathognomonic clinical signs help to establish the diagnosis. 

A. Burns 

Although enormous levels of electrical energy are generated in a lightning strike, burns 

are frequently superficial. The flashover phenomenon channels most of the current 

along the outside of the body (over the skin) rather than through the victim, as occurs in 

other types of electrical injury. As the current races over the body, it vaporizes moisture 

on the skin and may destroy clothing in an explosive manner. Burns of unusual patterns 

may be noted. 

1. Linear burns—Linear burns are first- and second-degree burns that begin at the 

head and neck and course in a branching pattern down the chest and legs. They tend to 

follow areas with a heavy concentration of sweat.

2. Punctate burns—Punctate burns are clusters of discrete, circular, partial- or 

full-thickness burns that form starburst patterns on the skin. 

3. Feathering burns—Feathering burns are not true burns but rather cutaneous 

imprints from electron showers that track through the skin. They create a fernlike pattern 

with delicate branching. These patterns are also called ferning, keraunographic 

markings, and Lichtenberg flowers or figures. 

4. Thermal burns—Thermal burns from clothing or heated metal are typical second- 

and third-degree burns. Cranial burns (direct or indirect head strike) and leg burns 

(ground current) are associated with increased death rates. 

B. Altered Mental Status 

Victims of lightning strikes are usually disoriented, combative, or comatose. Rarely they 

are alert, but they typically have amnesia for the event. 

C. Cardiac Arrest 

Cardiac arrest is a result of sudden cardiac standstill induced by the massive DC 

countershock of the lightning strike. Spontaneous resumption of normal cardiac function 

is the rule if cardiac standstill is not complicated by simultaneous respiratory arrest 

(brain-stem shock or contusion). Both asystole and ventricular fibrillation have been 

associated with lightning strike. Myocardial infarction is a potential acute complication. 

D. Neurologic Injuries 

Central nervous system injuries include epidural and subdural hematomas (due to 

associated falls), subarachnoid hemorrhage, coagulation burn injuries of brain, 

intraventricular hemorrhage, and respiratory paralysis. Seizures, loss of consciousness, 

and peripheral neurovascular instability are common. Anterograde amnesia and 

confusion are noted in most patients. Paraplegia and quadriplegia have also been 

described. 

E. Musculoskeletal Injuries 

Victims of lightning strikes are frequently thrown to the ground by tetanic muscle 

contractions, or they may be injured by falls from heights. Fractures of the skull, spine, 

ribs, and extremities may occur. Intrathoracic and abdominal injuries result from blunt 

trauma. 

F. Eye and Ear Injuries 

Eye injuries associated with lightning strikes include cataracts, corneal abrasions, 

hyphema, uveitis, vitreous hemorrhage, and iridocyclitis. Note: Dilated pupils should 

never be the sole criterion for termination of resuscitative efforts, because they may 

merely reflect transient autonomic sympathetic discharge or parasympathetic inhibition. 

Temporary sensorineural hearing loss with or without rupture of the tympanic membrane 

may result from the loud noise and physical shock wave. 

Treatment 

A. Maintain the Airway, and Begin Cardiopulmonary Resuscitation

Respiratory arrest is the most common cause of death in persons who have been struck 

by lightning. Artificial respiration should be continued until spontaneous respiration 

resumes or the rescuer cannot continue because of exhaustion. Begin closed chest 

compression if no pulse (carotid or femoral) is present (Chapter 7). Victims struck by 

lightning and apparently dead have been successfully resuscitated after prolonged 

efforts. 

B. Anticipate Traumatic Injury 

Management of the victim of lightning strike is the same as that for a person who has 

sustained severe blunt trauma. Examine the entire body for evidence of significant 

skeletal, muscular, or internal injury. Immobilize the spine. Obtain x-rays of the cervical 

spine and chest, an ECG, and appropriate laboratory tests (urinalysis; complete blood 

count; blood urea nitrogen and serum electrolyte and creatinine measurements; and 

CK-MB, lactic dehydrogenase, and aspartate aminotransferase enzyme 

determinations). If the patient's level of consciousness deteriorates, if focal neurologic 

signs are present, or if coma is prolonged, obtain a computed tomography (CT) scan of 

the brain. Fasciotomy of paralyzed or pulseless extremities should be guided by 

measurement of intracompartmental tissue pressures to avoid unnecessary surgery on 

limbs that are pulseless and cyanotic as the result of transient sympathetic overactivity 

with intense vasospasm. 

C. Begin Burn Therapy and Fluid Replacement 

Management of burn wounds follows standard procedures (Chapter 43). 

Rhabdomyolysis and myoglobinuria are rarely caused by lightning strike unless severe 

thermal injury or blunt trauma to muscle has occurred. Administration of intravenous 

fluids should be adjusted according to blood pressure readings and urine output. 

Alkalization of the urine and administration of mannitol are not necessary unless 

myoglobinuria is present. If significant brain injury is present, intracranial and pulmonary 

artery pressure monitoring may be necessary for proper evaluation of fluid replacement. 

Tetanus should be updated appropriately (Chapter 30). 

Disposition 

Prolonged cardiac monitoring and serial cardiac enzymes are required only if the patient 

has a history of cardiac arrest, loss of consciousness, cardiac arrhythmia, or abnormal 

ECG or if admission is considered for other reasons (burns, trauma). Screen the urine 

regularly for evidence of myoglobinuria. Record results of visual acuity and hearing tests 

to establish a baseline measurement. 

If the victim has experienced cardiopulmonary arrest and resuscitation efforts have been 

successful (resumption of spontaneous cardiac activity), allow a minimum of 12-24 

hours before weaning the patient from the ventilator to see if spontaneous respiratory 

activity resumes. If electroencephalographic abnormalities are present, they may clear 

over 24-72 hours. Dilated pupils cannot be used as an early diagnostic criterion for brain 

death. 

ELECTRIC SHOCK & BURNS


• Direct current is less dangerous than alternating current. 

• Alternating current (most house current) can cause ventricular fibrillation and 

respiratory arrest. 

• Burns can result from the electrical current and, although they may look mild, can 

indicate significant internal damage. 

• Treatment includes cardiopulmonary resuscitation, wound care, and possibly 

fasciotomy. 


Electric shock may result from carelessness or ignorance in working with electricity, 

faulty appliances and equipment, or severed electric power lines, or it may be an 

accident of nature (lightning). Dry skin offers high resistance to passage of ordinary 

levels of electric current. However, skin moistened with water, ointment, sweat, saline 

solution, or urine offers greatly reduced resistance to electric current. The amount and 

type of current, the duration and area of exposure, and the pathway of the current 

through the body determine the degree of damage. If current passes through the heart 

or the brain, death may be rapid. 

Direct current is much less dangerous than alternating current (AC) and is generally 

tolerated at much higher strengths. High-voltage AC current with a high number of 

cycles per second (hertz, Hz) may be less dangerous than low-voltage current with 

fewer cycles per second. 

Alternating current of 25-300 Hz and 25-200 V, a range that includes house current in 

most locales, tends to cause ventricular fibrillation if the pathway includes the heart. 

With voltages over 1000 V, respiratory paralysis often occurs. With intermediate 

voltages (220-1000 V), a mixed picture of respiratory insufficiency and arrhythmias is 

noted. 


A. Electric Shock 

Electric shock may produce momentary or prolonged loss of consciousness. Ventricular 

fibrillation is the most serious immediate arrhythmia, although ectopic beats, sinus 

tachycardia or bradycardia, atrial fibrillation, and asystole can occur. Respiration may 

continue for a few minutes after injury or be absent, with immediate respiratory 

paralysis. When respiratory failure occurs, the patient becomes unconscious. Although 

a pulse can be felt, the patient is cyanotic and has cool, clammy skin and marked 

hypotension. Seizures, deafness, blindness, aphasia, and neuropathy can also result 

from electric shock. Multiple orthopedic injuries may be seen, including posterior 

shoulder dislocations and femoral neck fractures. 

After recovery from mild to moderate electric shock, muscular pain, fatigue, headache, 

and generalized or focal nervous irritability occur. Physical signs vary according to the

sites of action of the current. 

B. Electrical Burns 

There are 3 distinct types of electrical burns: (1) flash (arc) burns, (2) flame burns, and 

(3) direct burning of the tissues by electric current. Direct burns cause entry wounds that 

are usually sharply demarcated, round or oval, painless gray areas with a surrounding 

inflammatory reaction. The exit wounds are more ragged looking, with an "exploded" 

appearance. Initial examination of the surface wound is often misleading, because the 

injury may appear relatively innocuous despite extensive deep tissue destruction. Little 

destruction may be evident for the first 7-10 days; ischemia and sloughing then occur 

slowly in severely affected areas. The temperature generated in an arc burn from 

household electric current (110-220 V) may reach 3000 °C (5432 °F). 

Common complications include cardiac arrhythmias or cardiac failure, circulatory shock, 

hemorrhage, and myoglobinuria. 

Treatment 

A. Electric Shock 

Free the victim from the current at once. This may be done in many ways, but the 

rescuer must be protected. Turn off the power, sever the wire with a dry 

wooden-handled ax, make a proper ground to divert the current, or drag the victim 

carefully away using dry clothing, a leather belt, rubber or other dry nonconductive 

materials. 

Check cardiac and ventilatory function. If the patient is apneic or pulseless, begin 

artificial ventilation or CPR (Chapter 7). 

B. Electrical Burns 

Treat tissue burns conservatively. The direction and extent of tissue injury may not be 

apparent for 7-10 days. Treat circulatory shock, if present, with intravenous infusion of 

crystalloid solutions. Locate entrance and exit wounds to help determine the pathway of 

the current. If current has passed through the chest, obtain an ECG. Serum CK-MB 

isoenzyme levels may be falsely elevated immediately after high-voltage electrical 

injuries and should not be considered a reliable indicator of myocardial damage. Monitor 

cardiac rhythm to detect rhythm disturbances in unconscious victims, those who have 

presented with cardiac arrhythmias, or those with an abnormal ECG. If myoglobinuria is 

present, monitor arterial blood pH at regular intervals to detect acidosis, which requires 

intravenous bicarbonate therapy to alkalize the urine and maintain blood pH above 7.45. 

Use intravenous mannitol, 2.5 g initially, to promote moderate diuresis. 

Assess the need for fasciotomy by measurement of intracompartmental tissue 

pressures. In children who have bitten electrical cords, be alert for delayed (up to 3 

weeks) erosion of the labial artery. 

Disposition 

Hospitalize all small children and patients who have lost consciousness or experienced 

cardiac or respiratory arrest, as well as those with ischemic chest pain, myoglobinuria,

or significant burn wounds. 

Fahmy FS et al: Lightning: the multisystem group injuries. J Trauma 1999;46:937. 

[PMID: 10338416] (Case presentation of a group lightning injury with description of 

clinical features.) 

Fish RM: Electric injury, part II: specific injuries. J Emerg Med 2000;18:27. [PMID: 

10645833] (Review of the diagnostic and treatment considerations for electric injuries.) 

Fish RM: Electric injury, part III: cardiac monitoring indications, the pregnant patient, and 

lightning. J Emerg Med 2000;18:181. [PMID: 10699519] (Review and analysis of 

publications about cardiac monitoring indications, pregnancy and electric injury, and 

lightning injury. 

Jain S et al: Electrical and lightning injuries. Crit Care Clin 1999;15:319. [PMID: 

10331131] (Review of pathophysiology and management of electrical and lightning 

injuries.) 

Lederer W et al: Electricity-associated injuries I: outdoor management of 

current-induced casualties. J Emerg Med 1999;43: 69. [PMID: 10636320] (Review 

article of epidemiology, clinical manifestations, and resuscitation in electric shock 

injuries.) 

EMERGENCY TREATMENT OF RADIATION INJURIES 

RADIATION INJURIES 


• Radiation exposure can cause damage to multiple organ systems. 

• Organ system damage depends on the dose of radiation delivered. 

• Treatment is supportive regardless of radiation dose. 


The effects of radiation have been observed in the clinical use of x-rays and radioactive 

agents, after occupational or accidental exposure, and following the use of atomic 

weapons. The harm derived depends on the quantity of radiation delivered to the body, 

the type of radiation (x-rays, neutrons, gamma rays, or alpha or beta particles), the site 

of exposure, and the duration of exposure. 

Tolerance to radiation is difficult to define, and there are no absolute standards for all 

types and levels of radiation. In the United States, the National Committee on Radiation 

Protection has set the maximum permissible limits of radiation exposure for 

occupationally exposed workers over age 18 years at 0.1 rem per week for the whole 

body (not to exceed 5 rems per year) and 1.5 rems per week for the hands. 2 (For 

purposes of comparison, routine chest x-rays deliver 0.1-0.2 rem). If recommended

limits are exceeded, radiation injury may occur. 

Death after acute lethal radiation exposure is usually due to destruction of 

hematopoietic organs, gastrointestinal mucosal damage, central nervous system 

damage, or widespread vascular injury. Vomiting within 1 hour after radiation exposure 

is often a sign of lethal exposure. 

2 In radiation terminology, a rad is the unit of absorbed dose and a rem is the unit of 

dose of any radiation to body tissue in terms of its estimated biologic effect. The gray 

(Gy) is a unit of measure for the dose of ionizing radiation equal to 1 J/kg of tissue. One 

gray is equal to 100 rad. 

A. 4-6 Gy (400-600 Rads) 

Doses of 4-6 Gy (400-600 rads) of x-ray or gamma radiation applied to the entire body 

at one time will kill more than half of exposed persons within 60 days; death is usually 

due to hemorrhage, anemia, and infection secondary to injured hematopoietic cells. 

B. 10-30 Gy (1000-3000 Rads) 

Doses of 10-30 Gy (1000-3000 rads) to the entire body are associated with a death rate 

of 100%. Destruction of gastrointestinal mucosa and bone marrow leads to death within 

2 weeks. Bloody diarrhea begins within 4-5 days and is followed by hemorrhage and 

sepsis. 

C. 30 Gy (3000 Rads) and Above 

Doses above 30 Gy (3000 rads) to the entire body cause widespread vascular damage, 

cerebral anoxia with seizures, ataxia, coma, hypotensive shock, and death within a few 

days. 


A. Injury to Skin and Mucous Membranes 

Irradiation causes erythema, epilation, destruction of fingernails, or epidermolysis, 

depending on the dose. 

B. Injury to Deep Structures 

1. Hematopoietic tissues—Injury to bone marrow may cause a decrease in production 

of blood elements. Lymphocytes are most sensitive, polymorphonuclear neutrophils 

next most sensitive, and erythrocytes least sensitive. Damage to blood-forming organs 

may vary from transient depression of one or more blood elements to pancytopenia. 

The degree of lymphocyte depression within the first 24-48 hours can be used to 

estimate the dose received. 

2. Cardiovascular system—Pericarditis with effusion or constrictive pericarditis may 

occur many months after exposure to ionizing radiation. Myocarditis is less common 

than pericarditis. Smaller vessels (capillaries and arterioles) are more readily damaged 

than larger blood vessels. If injury is mild, recovery of function occurs. 

3. Gonads—In males, small single doses of radiation (2-3 Gy; 200-300 rads) cause

transient aspermatogenesis, and larger doses (6-8 Gy; 600-800 rads) may cause 

sterility. In females, single doses of 2 Gy (200 rads) may produce sterility. Moderate to 

heavy irradiation of the embryo in utero results in injury to the fetus or causes embryonic 

death and abortion. 

4. Respiratory tract—High or repeated moderate doses of radiation may cause 

delayed pneumonitis (weeks or months). 

5. Mouth, pharynx, esophagus, and stomach—Mucositis with edema and painful 

swallowing of food may occur within hours to days after exposure to radiation. The 

salivary glands are relatively radioresistant. Gastric secretion may be temporarily 

(occasionally permanently) inhibited by moderately high doses of radiation. 

6. Intestines—Loss of mucosa with ulceration and inflammation may follow moderately 

large doses of radiation. 

7. Viscera and endocrine glands—Hepatitis and nephritis may be delayed 

complications of therapeutic irradiation. Normal thyroid, pituitary, pancreas, adrenals, 

and bladder are relatively resistant to low to moderate doses of radiation. 

8. Nervous system—High doses of radiation may damage the brain and spinal cord by 

impairing their blood supply. Peripheral and autonomic nerves are highly resistant to 

radiation. 

C. Systemic Reaction (Radiation Sickness) 

Symptoms vary with type and amount of exposure. Each phase will be shortened for 

increasing dosages. The prodromal phase consists of incapacitating vomiting and 

malaise. An asymptomatic latent phase then follows. A third phase then occurs with 

dose-dependent symptoms and findings. Bone marrow suppression may occur as early 

as 24 hours. A gastrointestinal syndrome involving massive fluid losses and bloody 

diarrhea will begin a few days to a week after exposure to higher doses. The 

neurovascular syndrome will occur with extremely high doses within a few hours to 1-3 

days. This syndrome includes seizures, coma, and eventual death. 

Treatment 

There is no specific treatment for the biologic effects of ionizing radiation. Safe and 

effective radioprotective drugs are not available. 


Decontamination in most instances will occur prior to arrival at a medical facility. If it 

does not, simple removal of clothing with placement in marked containers will achieve 

90% reduction in contamination. Bare skin and hair should be washed thoroughly and 

the effluent secured for disposal. Radioactive particles will not cause acute injury to 

medical personnel and should not interfere with emergency management. 

B. Local Treatment 

The success of treatment of local radiation injury depends on the extent, degree, and 

location of tissue injury. A victim exposed to more than 0.25-0.5 Gy (25-50 rads) of

adioactive iodine should receive potassium iodide, 130 mg (65 mg for children) orally 

every day for 10 days, to prevent uptake in the thyroid gland. The drug should be given 

in the first hour after exposure, because it is only 50% effective after a delay of 3 hours. 

C. Systemic Treatment 

Treatment of the systemic reaction following irradiation is symptomatic and supportive. 

No truly effective antiemetic is available for the distressing nausea that frequently 

occurs. Granisetron and ondansetron are the most effective. Massive fluid replacement 

will be necessary, as will nutrition replacement. Isolation and neutropenic precautions 

must be implemented. Blood products will be needed, and cytokines may be of benefit. 

Consider bone marrow transplantation for all victims with exposures exceeding 3 Gy 

(300 rads). Patients with neurovascular syndrome usually receive expectant treatment. 

Disposition 

All patients with signs or symptoms of radiation exposure must be hospitalized. Advice 

may be obtained from the Radiation Emergency Assistance Center/ Training Site 

(REAC/TS) in Oak Ridge, Tennessee ([865] 576-3131). The 24-hour emergency 

network telephone number is (865) 481-1000. 

Armed Forces Radiobiology Research Institute, Military Medical Operations Office: 

Military Manual of Medical Management of Radiological Casualties. 

http://www.afrri.usuhs.mil/www/ outreach/pdf/radiologicalhandbooksp99-2.pdf 

Goans RE: Early dose assessment following severe radiation accidents. Health Phys 

1997;72:513. [PMID: 9119674] (Early approximation of radiation exposure to guide initial 

medical management.) 

Goans RE: Early dose assessment in criticality accidents. Health Phys 2001;81:446. 

[PMID: 11569639] (Early approximation of radiation exposure to guide initial medical 

management.) 

EMERGENCY TREATMENT OF NEAR-DROWNING 


The asphyxia associated with drowning is usually due to aspiration of fluid, but it may 

result from airway obstruction caused by laryngeal spasm that occurs while the victim is 

gasping under water. About 10% of victims develop laryngospasm after the first gulp 

and never aspirate water ("dry drowning"). The rapid sequence of events after 

submersion—hypoxemia, laryngospasm, fluid aspiration, ineffective circulation, brain 

injury, and brain death—may occur within 5-10 minutes. This sequence may be delayed 

for longer periods if the victim, especially a child, has been submerged in very cold 

water or if the victim has ingested significant amounts of barbiturates. 

The differences in the pathophysiology of aspiration of fresh water (hypotonic) and 

seawater (hypertonic) usually have little clinical significance in humans, because the 

amount of fluid aspirated in most patients is small. The primary effect in both instances 

is disruption of the vascular endothelium and dilution of pulmonary surfactant, with

esulting atelectasis and perfusion of poorly ventilated alveoli (large physiologic shunt). 

Foreign materials such as sand, algae, microorganisms, oil, or chemicals in the 

aspirated fluid may cause additional pulmonary injury. Fresh water, when absorbed, 

may produce hemodilution and intravascular hemolysis. Aspiration of large amounts of 

seawater may result in hypovolemia and hemoconcentration. Clinical features in both 

types of drowning are similar, and prompt ventilatory management is mandatory. 

A number of initial factors may precede near-drowning and may need to be considered 

in management: (1) use of alcohol or other drugs (a contributing factor in an estimated 

25% of adult drownings), (2) extreme fatigue, (3) intentional hyperventilation just prior to 

diving or swimming under water ("shallow water blackout"), (4) sudden acute illness (eg, 

epilepsy, myocardial infarction), (5) head or spinal cord injury sustained in diving or 

surfing accidents, (6) venomous stings by aquatic animals, and (7) decompression 

illness or air embolism associated with scuba diving. 

Hypoxemia, acidosis, and hypoperfusion of vital organs are common factors accounting 

for the high incidence of illness and death associated with drowning. Other problems 

include variations in vascular volume, cardiac failure, renal insufficiency, electrolyte 

abnormalities, hematologic disturbances, and infection. 


The victim of near-drowning may present with a wide range of clinical manifestations. 

Spontaneous return of consciousness often occurs in otherwise healthy individuals 

when submersion is brief. Other patients respond promptly to immediate artificial 

ventilation. Vomiting is common. Patients with more severe near-drowning may 

experience frank pulmonary failure, pulmonary edema, shock, anoxic encephalopathy, 

cerebral edema, or cardiac arrest. A few patients may be deceptively asymptomatic 

during the recovery period, only to deteriorate as a result of acute respiratory failure in 

the ensuing 6-24 hours. 


The patient may be unconscious, semiconscious, or awake and apprehensive. 

Cyanosis, trismus, apnea, tachypnea, and wheezing may be present. A pink froth from 

the mouth and nose indicates pulmonary edema. Cardiovascular manifestations may 

include tachycardia, arrhythmias, hypotension, shock, and cardiac arrest. 


Urinalysis may show proteinuria, hemoglobinuria, and ketonuria. The white blood cell 

count is elevated because of leukocyte demargination induced by stress. The PO 2 is 

usually decreased and the PCO 2 increased or decreased. Metabolic acidosis is always 

present. 


Chest x-rays may show pneumonitis or pulmonary edema. Preliminary x-rays may 

appear normal in patients with mild symptoms. 

Treatment

Begin resuscitation immediately. Do not waste time attempting to drain water from the 

victim's lungs or stomach. (If, however, a tense, water-filled stomach prevents adequate 

lung expansion, place the victim supine, perform the Heimlich maneuver [Chapter 7], 

clear the victim's mouth with a finger sweep, and resume artificial ventilation.) Place the 

patient in a slightly head-down position (15 degrees) to allow fluid to drain from the 

mouth. 

A. Open Airway and Maintain Ventilation 

Open the airway, and ventilate the patient. If the victim is not breathing, clear the mouth 

and pharynx with the finger, open the victim's airway, and institute immediate 

mouth-to-mouth or mouth-to-nose breathing. Give oxygen in high concentrations by 

continuous positive airway pressure. 

Perform endotracheal intubation for assisted ventilation as soon as possible, and begin 

positive end-expiratory pressure breathing. Consider the possibility of cervical spine 

injury, particularly in a diving or surfing accident. 

B. Establish Circulation 

Check for a carotid or femoral pulse. If a pulse cannot be detected, start CPR without 

delay (Chapter 7). External chest compression cannot be performed effectively in the 

water; therefore, bring the victim ashore or out of the water as quickly as possible in 

order to attempt resuscitation. In the hospital setting, monitor the effectiveness of CPR 

with arterial blood gas measurements. 

C. Treat Hypothermia 

Measure the patient's core temperature and treat systemic hypothermia. Hypothermia 

improves the chances for survival. If the patient is in full cardiac arrest (ventricular 

fibrillation or pulseless ventricular tachycardia, asystole, or mechanical dissociation), 

use core rewarming techniques (see Systemic Hypothermia, above) to attain a core 

temperature of 33-35 °C (91.4-95 °F) before discontinuing CPR. If the patient shows 

signs of life (spontaneous respirations, detectable pulse), core rewarming techniques 

may not be necessary. Complete recovery has been reported after prolonged 

resuscitative efforts, even when victims have had dilated, fixed pupils. This is 

particularly true of infants and children, in whom the brain is protected by hypothermia. 

Studies have also shown that children involved in warm water near-drowning with initial 

signs and symptoms that portend a bad outcome can ultimately have a near or total 

recovery. Therefore, aggressive resuscitation efforts should be attempted after warm 

water incidents as well. 

Disposition 

Near-drowning victims who are initially asymptomatic must be monitored for "secondary 

drowning" or respiratory distress that develops later. Studies have shown that signs and 

symptoms of secondary drowning occur within 6-8 hours. If the patient has a normal 

physical examination and respiratory effort, a Glasgow Coma Scale score of 13 or 

greater, and a room air oxygen saturation of 95% or greater on presentation, he or she 

may be safely discharged home after 6-8 hours. 

Causey AL: Predicting discharge in uncomplicated near-drowning. Am J Emerg Med

2000;18:9. [PMID: 10674523] (Retrospective cohort study to determine if routine, 

noninvasive parameters could be used to predict early discharge.) 

Spack L: Failure of aggressive therapy to alter outcome in pediatric near-drowning. 

Pediatr Emerg Care 1997;13:98. [PMID: 9127416] (Retrospective chart analysis of 

pediatric drowning victims and their outcome.) 

Zuckerman GB: Predictors of death and neurologic impairment in pediatric submersion 

injuries. The pediatric risk of mortality score. Arch Pediatr Adolesc Med 1998;152:134. 

[PMID: 9491038] (Retrospective chart review of pediatric drowning victims and their 

outcome.) 

EMERGENCY TREATMENT OF DISORDERS DUE TO ATMOSPHERIC 

PRESSURE CHANGES 

DECOMPRESSION SICKNESS (Caisson Disease, "Bends") 


• Caused by release of nitrogen bubbles from plasma and tissues during ascent. 

• Type 1: joint pain; Type 2: cardiorespiratory or neurologic involvement. 

• Treatment is immediate recompression in a hyperbaric chamber. 


Decompression sickness has long been recognized as an occupational hazard for 

professional divers. In recent years, the popular sport of scuba diving has exposed a 

large number of variably trained individuals to the hazards of decompression sickness. 

Divers using conventional diving gear (scuba; self-contained underwater breathing 

apparatus) breathe air or other oxygen-containing gas mixtures that are at the same 

pressure as that of the surrounding water. Water pressure increases by 1 atmosphere 

for every 10 m (33 ft) below the surface. The increased pressure increases the amount 

of gas dissolved in plasma and tissues. During ascent, as external pressure decreases, 

the dissolved gases (predominantly nitrogen) escape from tissues as gas bubbles. A 

similar disorder occurs in persons who rapidly ascend to altitudes above 2000 m (6600 

ft) in unpressurized aircraft. The size and number of gas bubbles escaping from the 

tissues are functions of the depth and duration of the dive, the degree of physical 

exertion (exercise increases the amount of dissolved nitrogen), and the speed of ascent. 

The quantity and site of release of nitrogen bubbles determines the symptoms. 


Symptoms begin to appear within 6 hours but may be delayed up to 24 hours. The 

clinical picture varies and can be divided into 2 types of decompression sickness. Type 

1, or the minor symptom complex, includes deep, aching pain in the large joints of the 

extremities. This has been termed the bends. Type 2 involves any cardiorespiratory or

focal neurologic symptoms. Neurologic symptoms include ataxia, paralysis, vertigo, 

visual or speech disturbance, and cognitive deficits. A propensity for the spinal cord 

seems to be prevalent in many cases. Chest pain and shortness of breath occur with 

involvement of pulmonary artery circulation. 

Treatment 

A. Early Measures 

Give oxygen, 6-10 L/min, by mask. Give mild analgesics as needed. In the absence of 

congestive heart failure, give intravenous fluids (5% dextrose in normal saline or 

lactated Ringer's injection) to correct dehydration and maintain normal hydration. 

B. Recompression 

Immediate recompression is the only effective treatment. Rapid transport to a treatment 

facility for immediate recompression is necessary not only to relieve symptoms but also 

to prevent permanent impairment. Persistent symptoms may be treated successfully 

with hyperbaric oxygen up to 7 days after the onset of serious decompression sickness. 

All emergency department physicians should know the location of the nearest 

hyperbaric chamber. The local public health department or nearest naval facility may be 

able to provide such information. In the United States, clinical advice may be obtained 

rapidly by telephoning the National Diving Alert Network (DAN) at Duke University ([919] 

684-8111, or [919] 684-4326 after hours). A patient who is transported to a hyperbaric 

chamber by aircraft must not be exposed to a cabin altitude higher than 300 m (1000 ft). 

C. Complications 

Further measures may be necessary to relieve some of the complications associated 

with the bends (eg, shock, spinal cord injury, bladder paralysis, hemoconcentration, and 

disseminated intravascular coagulation). 

Disposition 

Transport the patient immediately to the nearest recompression center (hyperbaric 

chamber) for evaluation and treatment. Caution: Never attempt recompression in the 

water. 

ARTERIAL GAS EMBOLISM 


• Increased pressure in the lungs causing air to escape from alveoli. 

• Results in air in the interstitial space or in the pulmonary venous circulation. 

• Can result in pneumothorax or occlusion of the coronary or cerebrovascular systems. 

• Treatment is immediate recompression in a hyperbaric chamber. 


Diving regulators maintain the pressure of the gas being breathed and thereby enable

the diver to descend and maintain lung expansion against the pressure of the 

surrounding water. Because of the pressure-volume relationship (Boyle's law: P 1 V 1 - 

P 2 V 2 ), greater volume changes for a given change in depth occur near the surface than 

at a greater depth. 

If the breath is held on ascent (by closure of the glottis) or if air is trapped in the lung by 

bronchospasm during ascent, the volume of gas in the lung expands. When a pressure 

differential of about 80 mm Hg is reached, air will be forced from the alveoli through the 

pulmonary alveolocapillary membrane. The result will be air in the interstitial space 

(creating pneumothorax or mediastinal emphysema) or formation of bubbles in the 

pulmonary venous circulation. These bubbles travel through the left side of the heart 

into the systemic arterial circulation, where they may be trapped in smaller arteries and 

cause coronary artery or cerebrovascular occlusion. Larger bubbles may occlude the 

large vessels of the central circulation and become lodged in the heart, causing 

complete circulatory collapse. One study has found that this process may be the cause 

of death in most fatal cases of arterial gas embolism. 


A. Arterial Embolism 

Patients usually present with dramatic symptoms. If the symptoms occur more than 10 

minutes after the diver has surfaced, they are not due to air embolism. Many victims of 

arterial gas embolism die immediately upon surfacing. 

If air bubbles enter the cerebral circulation, the victim becomes unconscious or has a 

seizure during ascent or immediately upon surfacing. Other symptoms include 

blindness, confusion, or an apparent acute stroke. 

If the bubbles have entered the coronary arteries, the person presents with symptoms 

similar to those of acute myocardial infarction, with chest pain, arrhythmias, and 

collapse. Complete, sudden circulatory collapse occurs with occlusion of the central 

circulation. 

B. Pneumothorax 

Signs of pneumothorax or mediastinal emphysema develop more slowly and are not as 

life threatening; signs include shortness of breath, hyperresonance of the chest to 

percussion and decreased breath sounds on the affected side, and subcutaneous 

crepitus that may extend into the neck. 

Treatment 

A. Early Measures 

Give oxygen, 6-10 L/min, by mask. Position the victim head down (15-30 degrees) on 

the left side in the Trendelenburg position. Give 5% dextrose in normal saline or lactated 

Ringer's injection intravenously to maintain urine output at 1-2 mL/kg/h. 

B. Recompression 

Immediate recompression is the only effective treatment; the patient should be

transported to a hyperbaric chamber immediately (see Decompression Sickness, 

above). 

Disposition 

Transport the patient immediately to the nearest recompression center (hyperbaric 

chamber) for evaluation and treatment. Caution: Never attempt recompression in the 

water. 

Certain anatomic risk factors predispose divers to pulmonary barotrauma. A history of 

obstructive lung disease or an anatomic abnormality such as lung cysts may increase 

the likelihood of pulmonary barotrauma. A helical (spiral) CT scan of the chest may help 

assess future fitness to dive in survivors of pulmonary barotrauma by revealing 

previously undiagnosed lung pathology. 

HIGH-ALTITUDE SICKNESS (Mountain Sickness) 


Rapid means of modern transportation have increased the number of unacclimatized 

people who are exposed to the effects of high altitude. Lack of sufficient time for 

acclimatization, increased physical activity, and varying degrees of ill health may be 

responsible for the acute and chronic disturbances that result from hypoxemia at 

altitudes greater than 2000 m (6600 ft). Marked individual differences in tolerance to 

hypoxemia exist. Acclimatization involves a variety of changes that affect the 

respiratory, circulatory, hematopoietic, renal, and pulmonary systems. 

1. Acute Mountain Sickness 


• Flulike symptoms due to lack of acclimatization to higher altitudes. 

• Treatment is descent, oxygen, and antiemetics. 

• If descent is not possible, dexamethasone or acetazolamide can be used to aid 

acclimatization. 


Symptoms and signs include headache (the most common and usually the most 

prominent symptom), lassitude, difficulty in concentrating, sleep disturbances, 

drowsiness, dizziness, insomnia, anorexia, nausea and vomiting, dyspnea on exertion, 

and palpitations. 

Symptoms are often worse on the second and third day after ascent but usually clear 

completely within 5-7 days. Serious illness is rare; deaths from mountain sickness do 

not occur, by definition.

Treatment 

The most effective treatments are descent to lower altitude and administration of 

oxygen. Headache responds to analgesics. Use narcotics judiciously to avoid distorting 

sleep patterns or masking signs of altered mental status, which accompany impending 

high-altitude encephalopathy. Antiemetics are indicated for nausea and vomiting. By 

decreasing periodic breathing, acetazolamide has been useful in treating insomnia. 

Studies show that severe or rapidly progressive mountain sickness may respond 

favorably to dexamethasone, 4-6 mg orally every 6 hours, until signs of improvement 

occur; the dose is then tapered over 3-5 days. 

Prevention 

Preventive measures include gradual ascent, adequate rest, avoidance of alcohol and 

tobacco, and avoidance of strenuous exercise until acclimatization has been achieved. 

Acetazolamide, 125 mg twice a day before and during ascent, is the preferred drug for 

prophylaxis; dexamethasone is an alternative. Studies have also found Ginkgo biloba to 

reduce acute mountain sickness dramatically in both gradual and rapid ascent. 

Disposition 

If symptoms persist, returning to lower altitude is curative. 

2. Acute High-Altitude Pulmonary Edema 


• Pulmonary edema due to rapid ascent to altitudes above 2400 m (8000 ft). 

• Cough and dyspnea on exertion lead to pink, frothy sputum and dyspnea at rest. 

• Chest x-ray findings show patchy infiltrates but normal heart size. 

• Treatment is rapid descent, continuous positive-pressure ventilation, oxygen, and 

nifedipine. 


Acute high-altitude pulmonary edema is a serious disorder usually occurring at levels 

above 2400 m (8000 ft). High-altitude pulmonary edema is associated with exercise and 

rapid ascent and is commonly noted in young, previously healthy individuals who have 

not become properly acclimatized. Known risk factors for development of high-altitude 

pulmonary edema are previous episodes of the disease, congenital absence of one 

pulmonary artery, and brief sojourn at low altitude by persons acclimatized to living at 

high altitudes. 


Early symptoms of high-altitude pulmonary edema generally appear on the second night 

at a new altitude. Early symptoms include dry cough and dyspnea on exertion. As 

illness progresses, cough productive of pink, frothy sputum occurs as does dyspnea at

est. Orthopnea is uncommon. Extreme weakness and drowsiness ensue. 

Physical signs include tachycardia, tachypnea, cyanosis, rales, rhonchi, and confusion 

that progresses to coma. Tachycardia begins with exertion and progresses to 

tachycardia at rest. Rales most often originate in the right axilla and become bilateral as 

illness progresses. Death may occur in untreated high-altitude pulmonary edema. 


The white blood cell count and hematocrit are often slightly elevated. The erythrocyte 

sedimentation rate is usually normal. Fluid collected by bronchoalveolar lavage shows 

high protein and cellular content associated with the high-permeability vascular leak due 

to hypoxia and increased pulmonary vascular pressures. 


Findings on chest x-ray are variable. In mild disease, patchy infiltrates in a solitary lung 

field (commonly the right middle lobe) are noted. The infiltrates rarely coalesce and 

generally do not involve the base of the lungs. The central pulmonary arteries are 

dilated, but the cardiac shadow is of normal size. In severe illness, infiltrates are more 

generalized, but no left atrial enlargement or Kerley lines are noted. Unilateral 

pulmonary edema is consistent with unilateral atresia of the pulmonary artery. 


Transient, nonspecific electrocardiographic changes such as tachycardia, right axis 

deviation, right ventricular strain, and occasional right bundle branch block can occur. 

Treatment 

Early recognition of the disease is crucial. Persistent dry cough and dyspnea in a person 

who has recently arrived at high altitude should be considered high-altitude pulmonary 

edema until proved otherwise. 

A. Rest 

Limit the patient's physical activity as much as possible. The sitting or semi-Fowler 

position is usually the most comfortable. 

B. Oxygen 

Give oxygen, 4-6 L/min, by mask; otherwise, deliver the maximum amount possible with 

the equipment at hand. 

C. Continuous Positive-Pressure Ventilation 

Application of continuous positive pressure during spontaneous ventilation (which can 

be achieved with a portable apparatus) relieves symptoms and improves oxygenation in 

patients with high-altitude pulmonary edema and is a useful temporizing measure during 

descent. Portable hyperbaric chambers, or Gamow Bags, are also helpful if descent is 

impossible. 

D. Descent 

Development of high-altitude pulmonary edema is an automatic indication for descent to 

lower altitude as quickly as possible (a descent of 500-1000 m [1650-3300 ft] is usually

sufficient), although it is best to descend below an altitude of 1500 m [5000 ft]). 

Supplemental oxygen and descent to a lower altitude should bring about marked 

improvement within 12-72 hours. 

E. Drugs 

Acetazolamide, 250 mg every 6 hours, has been used, but its usefulness is still debated 

in acute illness. Nifedipine, 10 mg orally initially and then 30 mg of extended-release 

preparation every 12-24 hours, has been shown to be beneficial by lowering pulmonary 

artery pressures. 

Prevention 

Preventive measures include (1) education of prospective mountaineers about the 

possibility of serious pulmonary edema, (2) gradual ascent to permit acclimatization, 

and (3) rest and avoidance of strenuous exercise for 1-2 days after arrival at high 

altitudes. Medical attention should be sought promptly if respiratory symptoms develop. 

Patients with a history of high-altitude pulmonary edema have a 60% chance of the 

illness recurring with repeat ascents. Prophylaxis with nifedipine, 20-30 mg of the 

extended release form every 12-24 hours, is helpful. 

Mountaineering parties climbing at 2400 m (8000 ft) or higher should carry a supply of 

oxygen and equipment sufficient for several days if hospital facilities are not available. 

People with symptomatic cardiac or pulmonary disease should avoid high altitudes. 

Detection of a heart murmur and recurrent episodes of high-altitude pulmonary edema 

should prompt investigation for a previously existing valvular, shunt, or pulmonary 

hypertension problem. 

Disposition 

Hospitalization is generally recommended if symptoms persist for more than a few hours 

after return to lower altitudes. 

3. High-Altitude Cerebral Edema 


• Cerebral edema due to rapid ascent to altitudes above 2400 m (8000 ft). 

• Signs and symptoms include headache, ataxia, papilledema, and global 


• Treatment is immediate descent, oxygen, and dexamethasone. 


Acute high-altitude cerebral edema, a syndrome related to hypoxemia, occurs at 

elevations above 2400 m (8000 ft). Like its counterpart high-altitude pulmonary edema,

it is more common in unacclimatized individuals and is the end-stage form of acute 

mountain sickness. Death occurs from brain-stem herniation. 

Early symptoms include severe headache, ataxia, confusion, incoordination, and 

drunken behavior. Ataxia is usually the first sign of advancement to high-altitude 

cerebral edema in someone with acute mountain sickness. The physical examination 

may reveal papilledema, retinal hemorrhages, and occasionally a cranial nerve palsy. 

Patients with high-altitude cerebral edema typically present with global encephalopathy. 

Focal neurologic deficits are present only in the most severe forms of high-altitude 

cerebral edema and should prompt investigation into other causes of headache and 

mental status changes. Seizures are uncommon. Because high-altitude pulmonary 

edema commonly accompanies high-altitude cerebral edema, the patient may be 

lethargic and short of breath and may demonstrate tachycardia. 

Treatment 

It is crucial to recognize early manifestations. Because the symptoms of early 

high-altitude cerebral edema are similar to those of acute mountain sickness, anyone 

with headache and fatigue at high altitude must be watched closely for signs of 

deterioration. Inability to walk a straight line is a fairly sensitive test for incipient 

high-altitude cerebral edema. 

A. Oxygen 

Give oxygen, 6-10 L/min, by mask, or give 100% oxygen if possible. Keep the patient in 

a sitting position, with the head elevated. 

B. Descent 

Development of high-altitude cerebral edema is an automatic indication for descent to 

lower altitude as quickly as possible (a descent of 500-1000 m [1650-3300 ft] is usually 

sufficient, although it is best to descend below an altitude of 1500 m [5000 ft]). 

Dexamethasone, 8 mg orally or intramuscularly initially followed by 4-6 mg orally every 

6 hours, is recommended. Nifedipine for high-altitude pulmonary edema is 

contraindicated in patients with concomitant severe high-altitude cerebral edema. 

Disposition 

Hospitalization is generally recommended if symptoms persist for more than a few hours 

after return to lower altitudes. 

Cheshire WP Jr et al: Headache in divers. Headache 2001;41:235. [PMID: 11264683] 

(Review of decompression illness.) 

Erdmann J: Effects of exposure to altitude on men with coronary artery disease and 

impaired left ventricular function. Am J Cardiol 1998;81:266. [PMID: 9468065] 

(Prospective study evaluating the effect of exposure to high altitude in men with 

coronary artery disease.) 

Hackett PH et al: High altitude illness. N Engl J Med 2001;345:107. [PMID: 11450659] 

(Review of acute mountain sickness, high-altitude pulmonary edema, and high-altitude

cerebral edema.) 

Levine BD et al: Effect of high-altitude exposure in the elderly: the Tenth Mountain 

Division Study. Circulation 1997;96:1224. [PMID: 9286953] (Prospective study to 

evaluate the impact of high altitude on elderly patients.) 

Neuman TS: Arterial gas embolism and decompression sickness. News Physiol Sci 

2002;17:77. [PMID: 11909997] 

Neuman TS et al: Fatal pulmonary barotrauma due to obstruction of the central 

circulation with air. J Emerg Med 1998;16:413. [PMID: 9610969] (Case studies of 

patients with severe barotrauma and discussion of the treatment.) 

Reuter M et al: Computer tomography of the chest in diving-related pulmonary 

barotraumas. Br J Radiol 1997;70:440. [PMID: 9227223] (Retrospective chart analysis 

of patients diagnosed with pulmonary barotrauma who underwent a CT scan of the 

chest. 

Tetzlaff K et al: Risk factors for pulmonary barotrauma in divers. Chest 1997;112:654. 

[PMID: 9315797] (Retrospective chart analysis of patients with pulmonary barotrauma to 

determine potential risk factors for the development of barotraumas.) 

Yarnell PR et al: High-altitude cerebral edema (HACE): the Denver/Front Range 

experience. Semin Neurol 2000;20:209. [PMID: 10946741] (Retrospective case analysis 

and discussion of patients with high-altitude illness.) 

EMERGENCY TREATMENT OF DISORDERS DUE TO VENOMOUS 

ANIMALS 

SNAKE BITES 


• Venomous bites can result from either pit vipers or elapids. 

• Pit viper envenomation results in symptoms related to cytolysis, whereas elapid bites 

can result in neurotoxic symptoms. 

• Antivenin is available for both pit viper and elapid bites and should be administered for 

symptomatic envenomations. 


Snakes bite at least 50,000 humans each year in the United States. Most snake bites 

are from nonpoisonous snakes. There are 2 main types of poisonous snakes: crotalids, 

or pit vipers (rattlesnakes, cottonmouths [water moccasins]), and elapids (coral snakes, 

cobras). Among venomous bites in the United States, 95% are from pit vipers (mostly 

rattlesnakes). Envenomation occurs in only 15-20% of venomous bites.

Snake venom is a complex mixture of proteolytic enzymes and toxic proteins. In 

general, crotalid venom is mainly cytolytic, whereas elapid venom is mainly neurotoxic. 

Cytolytic venom lyses cells; enhances local spread of venom; and causes hemolysis, 

increased capillary permeability, and altered hemostasis. Neurotoxic venom can disrupt 

neuromuscular activity, causing paresthesias, weakness, and respiratory paralysis. 


Identify the snake if at all possible. Pit vipers have large triangular heads with pits 

between the eyes and the nose. Coral snakes have black and red circumferential bands 

separated by narrower yellow bands ("red on yellow, kill a fellow; red on black, venom 

lack"). If the identity of a snake is not obvious, obtain help from a herpetologist or a 

poison control center. 

Collect the snake, if possible, for positive identification; take care to avoid being bitten. 

Remember that the head of a decapitated snake may exhibit reflex actions for as long 

as 1 hour after it has been severed from the body. The predominantly cytolytic venom of 

crotalids can cause edema, hemorrhage, and necrosis around the bite site as well as 

distant from the site in severe envenomations. Systemic signs and symptoms consist of 

hemolysis, thrombocytopenia, disseminated intravascular coagulopathy, vomiting, and, 

rarely, respiratory failure with cardiovascular instability or collapse. 

The predominately neurotoxic venom of elapids and the Mojave green rattlesnake may 

produce few or no early local signs of envenomation, but neurologic symptoms 

(paresthesias, blurred vision, dysphagia, hypersalivation, ptosis, and respiratory 

depression) may appear after a delay of 2-6 hours. 

Treatment 

A. Emergency First-Aid Measures 

Many of the most well-known first-aid measures are no longer recommended. 

Cryotherapy, tourniquets, and incision and suction have not been shown to be helpful 

and in many cases cause more harm. The best management is to transport the patient 

to the nearest hospital. Immobilize the bitten part as if it were a fracture, and hold it 

below the level of the heart. Keep the patient on strict bed rest, if possible. If the patient 

has a severe envenomation with progression of symptoms, emergency medical service 

providers may place a constriction band over the site of the bite. A constriction band is a 

broad, flat band exerting 20 mm Hg of pressure that still permits 1-2 fingers under the 

band. However, if the patient is stable, application of a constriction band is not 

recommended, even if transport time is long. If a constriction band or suction device has 

been placed prior to the arrival of emergency medical services, it should be left in place 

for transport. Suction devices have been shown to cause injury themselves, however, 

and can be removed if no liquid is being extracted. 

B. Hospital Measures 

Assess the patient's respiratory and cardiovascular status. Determine if airway 

management or cardiovascular resuscitation with crystalloid or vasopressors is needed. 

Obtain intravenous access. Assess bite site for local progression. Determine species of

snake if possible. Check complete blood count, electrolytes, coagulation profile, and 

urine myoglobin. Type and cross-match blood. 

Antivenin is warranted if abnormalities are found in any of the above measures. 

Crotalidae polyvalent immune Fab, also known as CroFab or FabAV, has been 

approved by the U.S. Food and Drug Administration (FDA) and should be used as 

needed (Table 44-1). Antivenin must be reconstituted and then administered slowly 

intravenously for 10 minutes. If no signs or symptoms of anaphylaxis occur, then the 

infusion rate may be increased to be complete in 1 hour. No reports of anaphylaxis have 

occurred thus far with the use of FabAV, but vigilant monitoring must continue 

throughout infusion. For coral snake (Eastern or Texas variety) bites, give 3-6 vials of 

Eastern coral snake antivenin. Coral snake antivenin is not effective against the bites of 

the Arizona or Sonoran coral snake. 

Tetanus should be updated and antibiotics administered in severe bites. 

Surgical management of a snake bite is not needed in the acute phase unless evidence 

of compartment syndrome is present. Many of the signs and symptoms of compartment 

syndrome are present with snake bite, but it is extremely rare for intracompartmental 

pressures to be elevated. Fasciotomy should be reserved for patients with elevated 

pressure measurements. Delayed debridement of necrotic tissue may ultimately be 

necessary. 

Disposition 

Place patients requiring antivenin in the intensive care unit for monitoring. Asymptomatic 

patients with no local progression and normal laboratory values may be discharged after 

8 hours with close wound follow-up. 

Boyer LV: Recurrence phenomena after immunoglobin therapy for snake 

envenomations: part 2. Guidelines for clinical management with crotaline Fab 

antivenom. Ann Emerg Med 2001;37:196. [PMID: 11174239] (Review of the use of 

crotaline Fab antivenom at the time of presentation and with symptom recurrence.) 

Bush SP: Immediate removal of extractor is recommended. Ann Emerg Med 

2001;38:607. [PMID: 11679882] (Comment on the use of the extractor in snake bites 

and its complications.) 

Dart RC: Efficacy, safety, and use of snake antivenoms in the United States. Ann Emerg 

Med 2001;37:181. [PMID: 11174237] (Review of the use of Crotalidae and CroFab in 

snake envenomation.) 

Hall EL: Role of surgical intervention in the management of crotaline snake 

envenomation. Ann Emerg Med 2001;37:175. [PMID: 11174236] (Review of surgical 

techniques in the treatment of snake bites.) 

McKinney PE: Out-of-hospital and interhospital management of crotaline snakebite. Ann 

Emerg Med 2001;37:168. [PMID: 11174235] (Review of out-of-hospital management 

including constriction bands in the treatment of snake bites.)

Seifert SA: Recurrence phenomena after immunoglobulin therapy for snake 

envenomations: part I. Pharmacokinetics and pharmacodynamics of immunoglobulin 

antivenoms and related antibodies. Ann Emerg Med 2001;37:198. [PMID: 11174238] 

(Review of the use of antivenins and the recurrence of symptoms after their use.) 

BEES & WASP STINGS 


• Most people who experience a Hymenoptera envenomation have only a painful and 

urticarial lesion at the site of the sting; more severe reactions can occur and result in 

anaphylaxis and multiorgan dysfunction. 

• Oral pain control, tetanus prophylaxis, and diphenhydramine are generally the only 

treatment needed. In severe reactions, airway management, vasopressors, and even 

dialysis may be needed. 


Bees, wasps, and ants are members of the order Hymenoptera. In the United States, 

domesticated honey bees, feral bumblebees, paper wasps, yellow jackets, and fire ants 

are the most common attackers, although the aggressive, swarming Africanized bees 

have been present in the United States since the early 1990s. These insects inject 

venom through a stinger connected to a venom reservoir supplied by venom glands. 

The venom causes hemolysis and destruction of platelets and leukocytes. It is also 

capable of destroying vascular endothelium and necrosing skeletal muscle. 


Patients with Hymenoptera envenomation can present with a wide array of signs and 

symptoms. The most common effect of a sting is a small pruritic and urticarial-type 

lesion that also causes pain. Ten percent of people have a large local reaction greater 

than 5 cm in diameter. These reactions may last longer than the smaller lesions. Less 

than 1% of patients experience a systemic reaction. Some have a milder reaction with 

only nausea, vomiting, and diarrhea as well as pruritic urticarial lesions distant from the 

sting site. Rarely a victim will experience anaphylaxis. Persons who experience multiple 

stings or who are taking ß-adrenergic blocking drugs may experience more severe 

reactions. Immediate and delayed toxic reactions may occur with envenomation by 50 

or more stings. These reactions include hemolysis and rhabdomyolysis with subsequent 

renal failure, thrombocytopenia, disseminated intravascular coagulopathy, and liver 

dysfunction. 

Treatment 

Remove stings or fragments by scraping, not with forceps. Apply topical ice packs. Oral 

pain control, diphenhydramine, and tetanus prophylaxis are usually all that is necessary 

for small or large local reaction. Mild systemic reactions may require intravenous

diphenhydramine as well as intravenous corticosteroids and a short period of monitoring 

to allow early intervention for progression to anaphylaxis. Anaphylaxis requires 

intubation, intravenous access, aggressive fluid resuscitation, aerosolized ß-agonists for 

bronchospasm, subcutaneous or intravenous epinephrine, and possibly pressor agents. 

Toxic reactions will require the above measures with possible blood products, dialysis, 

and extensive hospital care. 

Disposition 

Patients with local reactions may be discharged home. Patients with severe systemic 

reactions require admission. The Phoenix Poison Control Center recommends 

mandatory 24-hour admission for children, the elderly, and patients with underlying 

medical problems or if 50 or more stings are sustained. Otherwise, young healthy 

individuals with massive envenomation require 6 hours of monitoring with initial and 

discharge laboratory evaluations of renal and liver function, coagulation studies, and red 

blood cell count; if no abnormalities are found, patients may be discharged to home. 

Studies of sensitized individuals have found that the vast majority never experience 

escalating symptoms with future stings; many have less severe reactions. Victims with 

less severe systemic reactions should undergo immunotherapy and carry an emergency 

epinephrine pen. 

BLACK WIDOW SPIDER BITES 


• Symptoms of envenomation include severe pain in the bitten extremity and muscle 

spasms of the abdomen and trunk. 

• Abdominal muscle spasms can mimic a surgical abdomen. 

• Severe hypertension and tachycardia can occur. 

• Treatment includes narcotic analgesics, intravenous calcium gluconate, and antivenin 

in the seriously ill. 


The female black widow spider (Latrodectus mactans) is shiny black, with a red 

hourglass marking on its abdomen. Only the female is dangerous. This spider is 

common in California and other parts of the United States. Other Latrodectus species 

may be found in other countries. The venom is a neurotoxin that acts on the myoneural 

junction. 

The bite itself is minor and often unnoticed at first. Characteristic symptoms of 

envenomation occur within 10-60 minutes, including severe pain in the bitten extremity 

and muscle spasms of the abdomen and trunk. Diffuse paresthesias are noted as well 

as muscle fasciculation, piloerection, and diaphoresis. Headache, nausea and vomiting, 

hyperactive deep tendon reflexes, and ptosis may be noted. Victims are in agonizing 

pain; the rigidity of abdominal muscles may mimic a surgical emergency. Severe 

hypertension and tachycardia may occur. Deaths are rare; at greatest risk are small

infants or older patients with preexisting cardiovascular disease. Symptoms peak at 2-3 

hours after the bite and may last up to 24 hours. 

Treatment 

Most patients respond to narcotic analgesics. Calcium gluconate, 0.1-0.2 mL/kg slowly 

intravenously, is often effective in alleviating muscle spasm. Methocarbamol, 1 g 

intravenously, infused at a rate no faster than 100 mg/min, is less effective. Local 

applications of ice should be used judiciously. Antivenin should be reserved for use in 

seriously ill infants and older patients and should be preceded by horse serum 

sensitivity testing. One vial of antivenin is sufficient for most patients; give 1 ampule (2.5 

mL) in 10-50 mL of normal saline by slow intravenous infusion. 

Disposition 

All patients who have been bitten by a black widow spider should be observed for 12-24 

hours, because hypertension and muscle spasm commonly recur. Hospitalization is 

necessary for all patients under age 14 years, those older than age 65 years, those with 

a history of hypertension, and those who present with severe symptoms. 

BROWN RECLUSE SPIDER BITES 


• The venom of the brown recluse spider is cytotoxic and causes local tissue 

destruction. 

• The bite progresses from an initial pustule to a bull's eye-like lesion to a larger 

craterlike ulcer (severe cases). 

• Most bites require only tetanus prophylaxis and local wound care; more symptomatic 

patients may require more aggressive wound care including dapsone, antivenin, and 

excision. 


The brown recluse spider (Loxosceles reclusa; other Loxosceles spp.) has a dark, 

violin-shaped area on its back. It is found in old wood piles, attics, closets, and clothes 

piles and prefers dark, undisturbed places. The venom, which contains 

sphingomyelinase D, is chiefly cytotoxic, causing local tissue destruction by destroying 

endothelial cells; it also has a hemolytic component, which on rare occasions may 

cause massive hemolysis. The enzyme may also disrupt nerve impulses, thus causing 

skin anesthesia at the bite site. 

The bite initially seems mild and often goes unnoticed. Pain at the site begins 1-4 hours 

later, and an erythematous area with a central pustule or hemorrhagic vesicle may be 

seen. The typical bull's-eye lesion is created when the red blister is encircled by a pale, 

irregularly shaped and ischemic halo, which in turn is surrounded by extravasated 

blood. The pustule may gradually grow to form a craterlike lesion over 3-4 days, with

associated lymphadenopathy and low-grade fever. Healing is slow, and large lesions 

may occasionally require skin grafting. Rarely, ulcerating skin lesions may appear years 

after a bite. A generalized systemic reaction termed loxoscelism may occur 24-48 hours 

after the bite, with fever, malaise, arthralgias, rash, and hemolysis. Rare fatalities have 

occurred in small children, who have shown massive intravascular hemolysis, 

accompanied by hemoglobinuria, jaundice, hypotension, renal failure, pulmonary 

edema, and disseminated intravascular coagulation. There appears to be little 

correlation between the development of a systemic reaction and the severity of the skin 

lesion. 

The bites of many other insects may be mistaken for brown recluse spider bites and 

lead to unnecessary treatment. One helpful clue (although not absolutely reliable) is that 

spiders tend to bite only once, whereas other insects leave multiple bites. 

Treatment 

Because of the progressive necrosis associated with many brown recluse bites, early 

surgical excision is not recommended. Excision of a necrotic area should occur only 

after the area has stabilized. Many recent studies have failed to show any significant 

benefit to corticosteroid therapy. Dapsone has been one of the more effective 

treatments if administered within 36 hours of the bite. The drug has severe side effects, 

however, and is not recommended for children. It should be reserved for rapidly 

progressing lesions and systemic illness. Hyperbaric oxygen therapy and wound 

coverage with nitroglycerin patches have failed to produce consistent effective reduction 

in progression of the necrosis. Brown recluse antivenin, if given within 24 hours, has 

been shown to be the most effective approach to limiting dermonecrosis. Many brown 

recluse spider bites are minor and heal without specific treatment other than tetanus 

prophylaxis (Chapter 30) and local wound care. 

Disposition 

Most brown recluse spider bites can be treated on an outpatient basis. Patients with 

large or infected wounds or those who have signs of a systemic reaction should be 

hospitalized. 

SCORPION STINGS 


• Most bites produce only local reactions including a painful sting site with or without 

erythema. 

• The bite of the Centruroides exilicauda scorpion can produce severe systemic 

symptoms including extreme restlessness, diaphoresis, seizures, and hypertension. 

• Severe reactions should be treated in the intensive care unit with neuroleptics, 

antihypertensives, and atropine; antivenin is available for treatment failures. 


Most scorpions are relatively harmless, producing only local envenomation reactions. 

However, C. exilicauda [sculpturatus] may produce severe systemic toxicity. 

This arthropod is small and yellowish, has a small tubercle (telson) at the base of its 

stinger, and is 2.5-7.5 cm (1-3 in) long. It is found mostly in the southwestern United 

States (Arizona, New Mexico, Texas, and along the Colorado River) but may rarely be 

transported in freight to distant states. Related arthropods are found in many other parts 

of the world. 

The venom of C. exilicauda contains a neurotoxin that may produce severe systemic 

symptoms. Other scorpion stings generally produce only local reactions. 


The initial sting is intensely painful with little or no erythema or swelling. Light 

percussion of the wound causes intense pain. Although pain and paresthesias generally 

resolve within 4 hours, local symptoms may persist for several days. 

Generalized reactions may occur within 60 minutes and include extreme restlessness, 

uncontrollable jerking, nystagmus, diaphoresis, diplopia, incontinence, hypersalivation, 

confusion, seizures, hypertension, and occasionally wheezing or stridor. 

Children under age 10 years are more likely to have severe or prolonged reactions; 

older children and adults usually recover in 10-12 hours. 

Treatment 

Periodic applications of ice may relieve local pain; avoid intense cooling. Immobilize the 

affected part. Do not apply a tourniquet. 

Most children recover with supportive care alone but should be observed in an intensive 

care unit. Strong depressants or tranquilizers do not appear to shorten the duration of 

symptoms and may produce respiratory depression; specifically, opiate analgesics 

seem to potentiate the toxicity of the venom. Diazepam or phenobarbital may be used to 

control seizures; sympatholytic antihypertensive agents may be required to control 

hypertension. Secondary to the adrenergic effects of most foreign scorpion stings, 

atropine has not been recommended for treatment of excessive oral secretion. 

Centruroides venom, however, has predominantly cholinergic-mediated neuromuscular 

effects and little to no adrenergic effect. Therefore, atropine use to dry oral secretions 

and prevent the necessity of intubation is becoming much more popular. 

Goat serum antivenin is available in Arizona (Arizona Poison and Drug Information 

Center [800] 222-1222 or [602] 495-6360) but has not been approved by the FDA. It is 

effective only for stings from C. exilicauda and is not of benefit for stings from scorpions 

from South America, Asia, or the Middle East. It is recommended only for use in severe 

envenomations with respiratory compromise unresolved by symptomatic treatment. 

Disposition

Hospitalize all patients with C. exilicauda stings for supportive care. 

Curtis J: Insect sting anaphylaxis. Pediatr Rev 2000;21:256. [PMID: 10922021] (Review 

of insect stings and their complications.) 

Forks TP: Brown recluse spider bites. J Am Board Fam Prac 2000;13:415. [PMID: 

11117338] (Review of the presentation and treatment of brown recluse spider bites.) 

Graudins A et al: Red-back spider (Latrodectus hasselti) antivenom prevents the toxicity 

of widow spider venoms. Ann Emerg Med 2001;37:154. [PMID: 11174232] (Study 

assessing the efficacy of the antivenin in preventing in vitro and in vivo toxicity of widow 

spider bites.) 

Jelinek GA: Widow spider envenomation (latrodectism): a worldwide problem. 

Wilderness Environ Med 1997;8:226. [PMID: 11990169] (Review of the problem of black 

widow spider envenomation.) 

Kolecki P: Delayed toxic reaction following massive bee envenomation. Ann Emerg Med 

1999;33:114. [PMID: 9867899] (Case report and review of massive bee envenomation.) 

Lowry BP et al: A controlled trial of topical nitroglycerin in a New Zealand white rabbit 

model of brown recluse spider envenomation. Ann Emerg Med 2001;37:161. [PMID: 

11174233] (Randomized, blinded controlled study assessing topical nitroglycerin 

treatment in brown recluse spider bites.) 

Suchard JR et al: Atropine use in Centruroides scorpion envenomation. J Toxicol Clin 

Toxicol 2001;39:595. [PMID: 11762667] (Case study series of the use of atropine in the 

scorpion bite.) 

Vetter RS et al: Mass envenomations by honey bees and wasps. West J Med 

1999;170:223. [PMID: 10344177] (Review of the literature on mass stinging events.) 

HAZARDOUS MARINE LIFE 

Many ocean-dwelling animals are potentially harmful to humans because of their ability 

to traumatize, envenom, or otherwise poison their victims with bites or stings. Most 

human injuries result from envenomation. 

1. Stingrays 


• Evenomation occurs when the tail of the stingray releases venom into its victim. 

• The sting causes intense local pain as well as nausea and vomiting, weakness, 

tachycardia, and muscle cramps. 

• Removal of any foreign material and irrigation with hot water are the mainstays of

treatment. 


Stingrays are the fish most commonly responsible for human envenomations; at least 

2000 stings occur annually in the United States. Stingrays are usually encountered in 

the waters off coastal regions, where they lie partially submerged in the sand. When 

disturbed, they splash upward with a muscular tail, which carries 1-4 venomous stings. 

Each sting is a retroserrate vasodentin spine containing multiple venom glands 

surrounded by an integumentary sheath. Injury due to stingrays therefore involves both 

a traumatic wound (which can be quite severe) and envenomation. The most common 

sites of injury are the lower extremities, followed by the upper extremities, abdomen, 

and chest. Wound necrosis is not uncommon. 


The sting is followed by immediate intense local pain and moderate swelling with 

bleeding. The pain radiates centrally and can be so severe that it causes disorientation. 

Systemic symptoms occur within 30 minutes of the sting and include nausea and 

vomiting, weakness, diaphoresis, vertigo, tachycardia, and muscle cramps. If 

envenomation has been severe, syncope, paralysis, hypotension, cardiac arrhythmias, 

and death may occur. 

Treatment 

A. Irrigate the Wound 

Irrigate the wound with whatever diluent is at hand (preferably sterile saline or water). 

Remove any obvious pieces of foreign matter. Immediate basic first aid is necessary to 

help prevent eventual necrosis, ulceration, and infection. 

B. Anesthetize the Wound 

Soak the wound in hot water to tolerance (45-50 °C [113-122 °F]) for 30-60 minutes. 

Stingray venom is heat labile and may be denatured in hot water. If heat fails to relieve 

the pain, infiltrate the wound with lidocaine, 1-2% without epinephrine; or perform 

regional nerve block. Do not apply ice to the wound. 

C. Explore the Wound 

Wound exploration and an x-ray should be performed so that all tissue fragments may 

be removed. Close the wound loosely around drains, or pack it open. 

D. Give Antibiotics 

Administer standard tetanus prophylaxis (Chapter 30), and start treatment with 

trimethoprim-sulfamethoxazole (160 mg and 800 mg, respectively, twice a day), 

ciprofloxacin (500 mg twice a day), or tetracycline (500 mg 4 times a day) for 7 days. 

E. Surgical Debridement 

If necrosis develops, early surgical debridement is recommended. Serial debridement 

may be necessary to stop any progression.

F. Hyperbaric Oxygen 

Hyperbaric oxygen has been used successfully in the setting of myonecrosis when 

serial debridement is required. If used, it should be instituted immediately after 

debridement takes place. 

Disposition 

Any patient with significant envenomation from a stingray sting should be observed for 

4-6 hours for appearance of systemic side effects. Patients who are discharged should 

have close outpatient follow-up for wound care. 

2. Sea Snakes 


• The initial bite is painless, but limb and respiratory paralysis as well as myolysis can 

occur with envenomation. 

• Treatment is the same as for land snake envenomation and includes sea snake 

antivenin if paralysis or myolysis is present. 


Sea snakes are present in all oceans except the Atlantic and are very similar to 

terrestrial snakes except for the shape of their tail. Although 90% of sea snake bites are 

dry, the venom is highly toxic to the nervous system and can cause significant myolysis. 

The sea snake is not aggressive, and some type of provocation is necessary to be 

bitten. 


The initial bite is relatively painless, but with significant envenomation comes rapid limb 

and respiratory muscle paralysis, ptosis, ophthalmoplegia, and myolysis. Renal failure 

can occur if myolysis is severe. The hemolysis and coagulopathy associated with U.S. 

snake bites is not seen. 

Treatment 

The same basic first-aid principles used for terrestrial envenomation still apply. Monitor 

respiratory status and prepare for intubation. Screen for signs of myolysis with CK, urine 

myoglobin, and renal function panel. Signs should be present by 6 hours. If paralysis or 

myolysis is present, administer sea snake antivenin. Between 1 and 3 ampules should 

be given initially, although more may be necessary. Tiger snake antivenin may be used 

if sea snake antivenin is not available. Polyvalent snake venin is the third-line choice. 

3. Jellyfish


• Jellyfish envenomations are associated with extreme pain both locally and distant from 

the sting site. 

• Extensive skin changes may be seen shortly after envenomation. 

• Systemic signs and symptoms include nausea and vomiting, autonomic changes, and 

paralysis. 

• Death is usually caused by respiratory paralysis or drowning secondary to limb 

paralysis. 


There are 3 types of jellyfish that cause the vast majority of the morbidity and mortality 

associated with jellyfish envenomation of humans: box jellyfish, Irukandji jellyfish, and 

Portuguese man-o-war. Jellyfish envenomate by touching prey or unsuspecting bathers 

with long tentacles containing hundreds of stinging cells called nematocysts. The 

jellyfish sting can cause a wide array of symptoms ranging from skin irritation to death. 


Most jellyfish stings cause only a localized inflammatory skin reaction and require only 

symptomatic care. A few jellyfish, however, can cause severe systemic envenomation 

syndromes. 

A. Box Jellyfish 

Severe incapacitating localized pain occurs immediately with the development of wide, 

erythematous bands on the skin. Confusion progressing to unconsciousness as well as 

respiratory failure and cardiac arrest can occur within 5 minutes. If the patient lives, skin 

changes occur over the next few hours with the development of blistering and necrosis 

that may cause permanent scarring. 

B. Irukandji Jellyfish 

The initial sting is hardly felt. Approximately 30 minutes later, the Irukandji syndrome 

begins. Unbearable pain generally begins in the sacral area and rapidly progresses to 

the rest of the body. The pain is always present but worsens in waves. Other symptoms 

include profuse diaphoresis, restlessness, headache, nausea and vomiting, severe 

hypertension, and tachycardia. Later complications include pulmonary edema, transient 

cardiomyopathy, and left ventricular dysfunction. 

C. Portuguese Man-o-War 

Portuguese man-o-war stings are very painful and leave a "string of beads" appearance. 

Shortly afterward, an Irukandji-like syndrome can occur, which consists of nausea and 

vomiting, and muscle cramps, particularly in the abdomen and chest. Pain may be so 

severe in the chest as to cause hypoxia. Death can occur. 

Treatment

A. Box Jellyfish 

Due to the rapidity of possible fatality, basic life support on the scene and advanced 

cardiac life support once in medical hands must be a priority. Vinegar application to the 

sting sites will inactivate venom. Compression bandages should be applied next. An 

antivenin exists and should be used if available. Intramuscular injection above the sting 

sites should be performed with 3 ampules. Intravenous pain control is always necessary 

in all but the most trivial stings. 

B. Irukandji Jellyfish 

Initial first aid is not usually necessary. The role of vinegar is uncertain because it is not 

known whether vinegar inactivates the nematocysts. Intravenous pain medication will be 

needed. Control of blood pressure with an a-adrenergic blocking agent will also be 

necessary. Monitoring for early signs of heart failure with echocardiography within the 

first 24 hours is recommended. Respiratory and cardiovascular support may ultimately 

be needed. Development of an antivenin is under way. 

C. Portuguese Man-o-War 

First aid consists of removing tentacles. Vinegar is not indicated. Rinsing with seawater, 

not fresh water, is the treatment of choice. Cold packs and intravenous pain medicine 

will ease pain. Rarely, respiratory support may be needed. 

Disposition 

Victims of envenomation should be monitored for 6-8 hours for systemic effects. The 

elderly or the very young should be monitored for 24 hours. 

4. Scorpion Fish 


• Extreme pain at sting site. 

• Wound sites commonly become ischemic or secondarily infected. 

• Systemic signs and symptoms include neurologic changes, respiratory failure, and 

autonomic dysfunction. 


Scorpion fish are divided into 3 groups on the basis of appearance and structure of the 

venom organ: zebra fish, scorpion fish, and stonefish. The venom apparatus consists of 

12 or 13 dorsal spines, 3 anal spines, and 3 pelvic spines, all of which can be erected 

upon stimulation. The venom can be highly toxic (stonefish) and contains chemical 

fractions analogous to those contained in stingray venom. 


Scorpion fish stings vary in intensity depending on the species. Most cause immediate 

pain, with central radiation of discomfort. Local ischemia at the wound site progresses

over days to marked swelling, erythema, and cellulitis. Prolonged indolent wound 

infections sometimes result. Systemic symptoms occur within the first few hours and 

include vomiting, weakness, diarrhea, delirium, seizures, paresthesias, fever, arthritis, 

hypertension, cardiac arrhythmias, respiratory failure, hypotension, and death. 

Treatment 

Manage systemic symptoms and dysfunctions supportively. An antivenin is available in 

Australia for management of stings by the Indo-Pacific stonefish. It is manufactured by 

Commonwealth Serum Laboratories, Melbourne, Australia. For scorpion fish stings 

occurring in coastal waters surrounding the United States, institute the following 

regimen: 

A. Provide Pain Relief 

Immerse the wound in hot water to tolerance (45-50 °C [113-122 °F]) for 30-60 minutes. 

If heat fails to relieve the pain, infiltrate the wound with lidocaine, 1-2% without 

epinephrine; or perform regional nerve block. Pain from a stonefish sting may be so 

severe that it causes delirium requiring parenteral narcotic analgesics for relief. 

B. Manage the Wound 

Debride and explore the wound, and remove all foreign material. If there is a chance 

that a spine may have entered a joint, these procedures should be performed in the 

operating room, and the surgeon should use magnifying loupes to explore the joint. Do 

not suture wounds tightly; allow adequate drainage. 

C. Give Antibiotics 

Administer standard tetanus prophylaxis (Chapter 30), and start treatment with 

trimethoprim-sulfamethoxazole (160 mg and 800 mg, respectively, twice a day), 

ciprofloxacin (500 mg twice a day), or tetracycline (500 mg 4 times a day) for 7 days. 

Disposition 

Patients who have sustained significant envenomation from a scorpion fish sting should 

be observed for 4-6 hours for development of systemic symptoms. All patients should 

be seen frequently on an outpatient basis for wound care after discharged. 

5. Sea Urchins 


• Extreme pain at sting site. 

• Skin changes at site. 

• May have retained spines. 

• Systemic signs and symptoms include neurologic changes and respiratory failure. 


Sea urchins are egg-shaped, globular, or flattened echinoderms found in areas ranging 

from the shallow intertidal zone to great oceanic depths. Some species are covered with 

sharp, brittle, venom-filled spines that readily break off. Most sea urchin venom contains 

several toxic fractions that may include cholinergic compounds and potent neurotoxins. 

Envenomation occurs when a victim inadvertently handles or falls on a sea urchin and 

the spines penetrate the skin. 


Injuries caused by sea urchin spines are associated with immediate intense burning 

pain, followed by erythema, edema, and aching. One or more spines typically break off 

in the skin. A purplish discoloration indicates penetration of the skin but does not 

necessarily mean that a spine remains. Multiple wounds may cause a systemic reaction, 

including nausea and vomiting, intense pain, paralysis, aphonia, respiratory distress, 

and death. Pain may subside within the first 2 hours, but paralysis may remain for 6-8 

hours. 

Treatment 

Systemic symptoms and dysfunctions are managed supportively. No antivenin is 

available for sea urchin venom. 

A. Relieve Pain 

Immerse the wound in hot water to tolerance (45- 50 °C [113-122 °F]) for 30-60 

minutes. If heat fails to relieve the pain, infiltrate the wound with lidocaine, 1-2% without 

epinephrine; or perform regional nerve block. 

B. Remove Embedded Spines 

Halt the envenomation process by carefully removing the spines (avoid fragmentation). 

Although some thin spines may be absorbed over 2-3 weeks, remove as many as 

possible. Remove all thick spines, because of the potential for foreign body reactions 

and infections. Many spines are radiopaque and can be visualized using soft tissue 

x-ray techniques. Obtain surgical consultation if there is a chance a spine may have 

entered a joint, if a spine is near a significant neurovascular structure, or if a spine has 

been lost in a closed space in the hand. In these cases, the spine should be removed in 

the operating room with the aid of magnifying loupes. Do not suture the wounds tightly; 

allow adequate drainage. 

Disposition 

Patients with significant sea urchin envenomation should be observed for 4-6 hours for 

appearance of systemic effects. Patients who are discharged should have frequent 

outpatient follow-up for wound care. 

INGESTION OF POISONOUS FISH 


• Consider ingestion of poisonous fish in anyone with gastroenteritis, neurologic 

symptoms, and respiratory compromise. 

The more intensive harvesting of marine plants and animals for food has increased the 

number of poisoning episodes due to ingestion of such items. Emergency physicians 

should obtain a dietary history from any patient who presents with gastroenteritis, 

respiratory compromise, confusing neurologic signs, or sudden unexplained systemic 

illness. 

1. Ciguatera Toxin Poisoning 


Ciguatera fish poisoning is caused by tropical and semitropical marine coral reef fish 

whose tissues accumulate toxins that originate in the toxic dinoflagellate Gambierdiscus 

toxicus. The toxin is ingested by small herbivorous fishes, which are eaten by larger 

carnivorous fishes. Humans are then the final consumer. Larger and older fish are more 

toxic in ciguatera-endemic areas. The most frequently implicated fishes in the United 

States include barracuda, jack, snapper, and grouper. 


Symptoms usually occur within 15-60 minutes of ingestion—almost always within 12 

hours—and increase in severity over the next 4-6 hours. Symptoms include abdominal 

pain, nausea and vomiting, diarrhea, chills, paresthesias, pruritus, dysphagia, 

odontalgia, pathognomonic reversal of the sensation of hot and cold, fatigue, athetosis, 

ataxia, vertigo, headache, myalgias, bradycardia, hypotension, central respiratory 

failure, and coma, with an overall death rate of 0.1-12%. More severe reactions often 

occur in persons previously poisoned by the toxin. Untreated, the gastroenteritis usually 

resolves in 24-48 hours, whereas the neurologic syndrome may last for weeks. The 

diagnosis is made on the basis of clinical findings; there is currently no test that 

indicates the presence of ciguatoxin in human blood. 


Treatment is largely supportive and symptomatic. Gastric emptying (via gastric lavage 

or emesis), catharsis, and instillation of activated charcoal may be of limited value if 

performed within 3 hours after ingestion. Avoid magnesium-based cathartics. Treat 

hypotension with intravenous infusion of crystalloid solutions and vasopressors. 

Mannitol infusion, 1 g/kg intravenously, has been reported to reverse cardiac depression 

and severe neurologic symptoms. Bradyarrhythmias generally respond well to atropine. 

Treat persistent myocardial failure with judicious administration of calcium gluconate, 

1-2 intravenously over 24 hours; the rationale is that the toxin occupies calcium receptor 

sites that affect the permeability to sodium of the pores in neural and myocardial 

membranes. Although many other drugs have been recommended, none have proven 

benefit. 

Admit patients with cardiovascular symptoms for observation.

2. Scombroid Poisoning 


Scombroid poisoning follows the ingestion of toxic fish of the families Scomberesocidae 

and Scombroidei, which include albacore, tuna, mackerel, bonito, kingfish, and wahoo. 

Scombroid poisoning can also be caused by nonscombroid fish such as dolphin, 

sardine, anchovy, amberjack, and ocean salmon. This pseudoallergic syndrome results 

from the improper preservation or refrigeration of dark-fleshed fish. These fish contain 

certain bacteria, most commonly Vibrio spp. Muscle tissue undergoes degradation 

induced by these bacteria that transforms histidine to histamine if not stored below 0 °C 

(32 °F). Histamine levels higher than 20-50 mg/100 mL are noted in toxic fish. It has 

been suggested that histamine alone is unlikely to be the sole toxin, because oral 

histamine is converted in the bowel to N-acetyl histamine. Cooking does not prevent the 

toxic effects. 

Clinical Findings BR> 

Symptoms occur within 15-90 minutes of ingestion and are the same as those caused 

by histamine (eg, flushing of the face, neck, and upper torso; sensation of warmth; 

urticaria; pruritus; angioneurotic edema; epigastric pain; abdominal cramps; diarrhea; 

nausea and vomiting; headache; thirst; pharyngitis; tachycardia; palpitations; 

bronchospasm; and hypotension). Untreated mild to moderate scombroid poisoning 

resolves within 6-12 hours. 


Treatment is directed at reversing the effects of histamine. Patients with minor poisoning 

without respiratory distress should receive diphenhydramine, 25-75 mg orally. If the 

reaction is severe, give epinephrine, 0.3-0.5 mL of 1:1000 solution subcutaneously. 

Nausea and vomiting are usually controlled by the antihistamine. In refractory cases, the 

histamine antagonists cimetidine, 300 mg intravenously, or ranitidine, 50 mg 

intravenously, may be given. Oral cimetidine, 300 mg every 6 hours, may be used to 

combat persistent headache. If the patient presents in the emergency department within 

1 hour of consuming a large amount of scombroid fish, it may be helpful to empty the 

stomach (via gastric lavage or emesis) and administer activated charcoal, 50-100 g in 

sorbitol. 

Admit patients with serious illness for observation. 

3. Puffer Fish (Tetrodotoxin) Poisoning 


Tetrodotoxin is one of the most potent nonprotein poisons found in nature and is 

characteristic of the order Tetraodontiformes. The poison is found in puffer fish, also 

known as toadfish, blowfish, blowfish, swellfish, balloonfish, and porcupine fish. The 

microbial flora of the fish produces the toxin. Some of these tropical and subtropical fish 

are prepared as delicacies (fugu) in Japan by trained and licensed chefs. The toxin is

distributed throughout the entire fish, with the greatest concentrations in the liver, 

gonads, intestine, and skin. The poison interferes with central and peripheral 

neuromuscular transmission, causing depression of the medullary respiratory 

mechanism, intracardiac conduction, and myocardial and skeletal muscle contractility. 

The toxin is water soluble but very difficult to remove from the fish by cooking. 


The onset of symptoms can be as rapid as 10 minutes or can be delayed for up to 5 

hours. Victims initially develop paresthesias, followed by hypersalivation, diaphoresis, 

lethargy, headache, nausea, vomiting, abdominal pain, diarrhea, weakness, ataxia, 

tremor, paralysis, respiratory failure, coma, and hypotension. Sixty percent of victims 

die, most within the first 6 hours. 

Treatment 

A. Manage the Airway 

If the victim is obtunded or evidence of dysphagia or respiratory insufficiency is present, 

endotracheal intubation should be performed and supplemental oxygen administered, 

guided by serial arterial blood gas measurements. Prompt ventilatory support in the 

setting of rapid paralysis is the most important intervention to prevent anoxic brain 

damage. 

B. Give Activated Charcoal 

If treatment is within 3 hours of ingestion, perform intragastric placement of 50-100 g of 

activated charcoal in 70% sorbitol solution. In the paralyzed or obtunded patient, protect 

the airway before giving charcoal. 

C. Provide Symptom-Based Life Support 

Hypotension may necessitate administration of crystalloid solutions or, rarely, the 

addition of a pressor agent. Bradyarrhythmias generally respond to atropine; heart block 

may necessitate temporary placement of a transvenous or transcutaneous pacemaker. 

Disposition 

Patients with respiratory difficulties, cardiovascular symptoms, or paralysis should be 

hospitalized in an intensive care unit. Patients with symptoms of a minor intoxication, 

which may be limited to paresthesias and mild dysphagia, should be observed in the 

emergency department or intensive care unit for at least 8 hours to detect deterioration. 

4. Paralytic Shellfish Poisoning 


Bivalve mollusks filter large quantities of water unselectively to gather plankton and 

extract oxygen. This action leads to concentration of bacteria, viruses, biologic toxins, 

and other substances in the tissues of such shellfish. Paralytic shellfish poisoning is 

induced by ingesting any of a variety of clams, oysters, scallops, mussels, chitons, 

limpets, murex, starfish, and sand crabs. The source of toxicity is the toxin elaborated

y various planktonic dinoflagellates and protozoan organisms. The most common 

dinoflagellates are Protogonyaulax (or Alexandrium) and Ptychodiscus spp, which are 

responsible for colored tides and enormous mortality in bird and marine populations. 

Saxitoxin, elaborated by Protogonyaulax, is found in greatest concentrations in the 

digestive organs, gills, and siphon. No physical characteristic distinguishes the carrier 

animal. A toxin concentration of greater than 75-80 ug/100 g of shellfish tissue is 

considered hazardous. The toxin blocks sodium conductance, inhibiting neuromuscular 

transmission at the axonal and muscle membrane levels. In humans, a lethal dose of 

purified saxitoxin is 0.1 mg. 


Within minutes to a few hours of ingestion of contaminated shellfish, intraoral and 

perioral paresthesias ensue. These rapidly involve the neck and distal extremities. Other 

symptoms include dizziness, incoordination, weakness, incoherence, dysarthria, 

sialorrhea, dysphagia, diarrhea, nausea, vomiting, dysmetria, headache, loss of vision, 

and tachycardia. Flaccid paralysis and respiratory insufficiency may follow. Unless a 

period of anoxia occurs, the victim will often remain awake and alert, although 

paralyzed. Death due to respiratory arrest occurs in up to 25% of victims within the first 

12 hours. 

Treatment 

A. Manage the Airway 

If the victim is obtunded or evidence of dysphagia or respiratory insufficiency is present, 

endotracheal intubation should be performed and supplemental oxygen administered, 

guided by serial arterial blood gas measurements. Prompt ventilatory support in the 

setting of rapid paralysis is the most important intervention to prevent anoxic brain 

damage. 

B. Perform Gastric Emptying 

If the victim shows any neurologic signs that indicate impending paralysis or respiratory 

difficulty, gastric emptying should be preceded by endotracheal intubation. The toxin is 

gastric acid stable and partially inactivated in alkaline solutions. If treatment is within 3 

hours of ingestion, perform gastric lavage with at least 2 L of 2% sodium bicarbonate 

solution in 200-mL aliquots, followed by intragastric placement of 50-100 g of activated 

charcoal in 70% sorbitol solution. 

C. Provide Symptom-Based Life Support 

Hypotension may necessitate administration of crystalloid solutions or, rarely, the 

addition of a pressor agent. Bradyarrhythmias generally respond to atropine; heart block 

may necessitate temporary placement of a transvenous or transcutaneous pacemaker. 

Disposition 

Patients with respiratory difficulties, cardiovascular symptoms, or paralysis should be 

hospitalized in an intensive care unit. Patients with symptoms of a minor intoxication, 

which may be limited to paresthesias and mild dysphagia, should be observed in the 

emergency department or intensive care unit for at least 8 hours to detect deterioration

Australian Venomous Research Unit at the University of Melbourne: Australian CSL 

Antivenom Handbook. http://www. wch.sa.gov.au/paedm/clintox/cslb_index.html 

Centers for Disease Control and Prevention: Scombroid fish poisoning—Pennsylvania 

1998. JAMA 2000;283:2927. [PMID: 10896527] (Morbidity and mortality weekly report 

on puffer fish poisoning.) 

Fenner PJ: Dangers in the ocean: the traveler and marine envenomation. I. Jellyfish. J 

Travel Med 1998;5:135. [PMID: 9772332] (Review of venomous jellyfish and treatment 

of envenomations.) 

Fenner PJ: Dangers in the ocean: the traveler and marine envenomation. II. Marine 

vertebrates. J Travel Med 1998:5:213. (PMID: 9876198) (Review of venomous marine 

vertebrates and treatment of envenomations.) 

Field J: Puffer fish poisoning. J Accid Emerg Med 1998;15:334. [PMID: 9785165] (Case 

report of puffer fish poisoning and review of the literature.) 

Hawdon GM et al: Venomous marine creatures. Aust Fam Physician 1997;26:1369. 

[PMID: 9470289] (Review of the features of envenomation by venomous marine 

creatures.) 

Lipp EK et al: The role of seafood in foodborne diseases in the United States of 

America. Rev Sci Tech 1997;16:620. [PMID: 9501377] (Review of seafood poisoning.) 

Rocca AF et al: Hyperbaric oxygen therapy in the treatment of soft tissue necrosis 

resulting from a stingray puncture. Foot Ankle Int 2001;22:318. [PMID: 11354445] (Case 

study of stingray puncture with resultant complications and treatments.) 






EMERGENCY TREATMENT OF DISORDERS DUE TO COLD

Table 44-1. Indications and dosages of Crotalidae Polyvalent Immune Fab (FabAV). 

Dosing None 

The patient should be given enough 

vials to achieve the goal. This 

generally ranges from 3 to 12 vials, 

although up to 25 vials have been 

used. 

Stabilization of signs and 

symptoms and no 

progression of signs and 

symptoms after FabAV 

given. 

Prevent recurrence.

Figure 44-1. Hypothermia. The patient is in atrial fibrillation with a slow ventricular 

response. The QRS complexes are narrow, and there is an additional positive slurred 

deflection, the J wave (Osborne wave), just prior to the ST segment. 






FIGURES


Sewalls, MD 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING CONDITIONS 

Victims of Poisoning with Coma, Seizures, or Marked Obtundation 

1 This chapter is a revision of the chapter by Kent R. Olson, MD, FACEP, & Charles E. 

Becker, MD, from the 4th edition. 

A. Keep Airway Open 

Establish and maintain an adequate airway and ventilation. Begin supplemental oxygen, 

12 L/min, by nonrebreathing mask. If the patient has no gag reflex, intubate for airway 

protection, to facilitate oxygenation, and to remove airway secretions. 

B. Obtain Arterial Blood Gas and pH Measurements 

Obtain arterial blood for blood gas and pH measurements to determine adequacy of 

ventilation and perfusion. 

C. Gain Intravenous Access 

Insert a large-bore (= 18-gauge) peripheral or central intravenous catheter, and draw 

blood for complete blood count, serum electrolyte and blood glucose measurements, 

and tests of renal and hepatic function. 

D. Treat Coma Promptly 

(See Chapter 16.) Give glucose, 50 mL of a 50% solution (25 g of glucose) 

intravenously over 3-4 minutes. 

Give naloxone (Narcan, others), 0.4-2 mg intravenously. If the patient's response is 

weak or if narcotic overdose is suspected, give repeated doses of 2 mg every 1-2 

minutes up to a total dosage of 10-20 mg. Note: The duration of action of naloxone (2-3 

hours) is shorter than that of many of the narcotics it reverses. Patients responding to 

naloxone must be observed for at least 3 hours after the last dose. 

If alcoholism or malnutrition is suspected, give thiamine, 100 mg intramuscularly or in 

intravenous solution with or prior to glucose administration. 

E. Maintain Circulation 

Maintain circulation, and treat shock by restoring intravascular volume with intravenous 

infusion of crystalloid solutions (Chapter 9). Caution: Fluid overload and pulmonary 

edema may occur with overly vigorous hydration. If administration of more than 20-30 

mL/ kg of crystalloid solution and usual doses of dopamine (ie, 5-15 ug/kg/min 

intravenously) fail to restore blood pressure, insert a pulmonary artery catheter to obtain 

pressure readings and help guide further therapy with fluids or pressor agents.

F. Treat Seizures 

(See Chapter 17.) If the patient is experiencing seizures, give diazepam, 0.1-0.2 mg/kg 

intravenously over 1-2 minutes. If this is not effective, give phenytoin, 15- 20 mg/kg, or 

fosphenytoin, 15-20 phenytoin equivalents per kilogram, at a rate no faster than 

100-150 mg/min. 

G. Start Electrocardiographic Monitoring 

Start cardiac monitoring. Obtain a 12-lead electrocardiogram (ECG), and note especially 

the rate; rhythm; presence of arrhythmias; and PR, QRS, and QT intervals. If overdose 

of tricyclic antidepressants is suspected, obtain serial ECGs. 

H. Perform Gastric Lavage 

Perform gastric lavage with a large-bore orogastric or nasogastric tube (Ewald tube) for 

any potentially lethal ingestion and in any patient with altered mental status who might 

have ingested a toxic substance within 1 hour prior to arrival (see section on 

decontamination, below). 

I. Search for Associated Illness 

Look for other causes of coma or seizures (Chapters 16 and 17). In particular, look for 

(1) head trauma (focal neurologic deficits or asymmetric seizures), (2) other trauma 

causing hemorrhage or shock, (3) infection (generalized or central nervous system), (4) 

metabolic disorders (hyponatremia, hypoglycemia, hyperglycemia), (5) hypothermia 

(use a rectal thermometer that can measure temperatures lower than 32 °C [89.6 °F]), 

or (6) hyperthermia. 

Victims of Poisoning with Intact Gag Reflex & Lethargy 

Management is the same as that outlined above for patients with absent gag reflex, 

except that endotracheal intubation may not be necessary before gastric lavage. The 

airway may be adequately protected by placing the patient in the lateral decubitus 

position with the head and trunk slightly lower than the feet (Trendelenburg position). 

FURTHER MANAGEMENT OF VICTIMS OF POISONING 

For assistance in identifying drugs and poisons and access to expert toxicologic 

consultation, refer to www.aapcc.com for appropriate poison center listings. Experts at 

the poison center can (1) provide immediate assistance in selecting appropriate 

laboratory or toxicity tests and in recommending preferred methods of gut 

decontamination or the use of antidotes and (2) advise on patient disposition. 

Obtain Brief History 

Obtain as much information as possible from paramedics, bystanders, police, family, 

and friends. Ask about recent use of drugs or medications, and find out whether any 

empty pill bottles, medications, or drug paraphernalia were found at the scene. If several 

patients present with similar symptoms of poisoning, consider carbon monoxide 

poisoning, food poisoning, or other toxins that can affect multiple victims simultaneously. 

Correlate the history with physical findings and results of laboratory tests, but do not be 

misled by the history. What the patient or friends say was ingested may differ from what

was actually swallowed, especially in suicide attempts. 

Decontaminate as Soon as Possible 

A. Inhaled Poisons 

Remove the patient from the source of poison, and give oxygen by mask. Inhalation of a 

water aerosol may help to dilute inhaled irritants in the nasopharynx. Check for 

hoarseness and singed nasal hairs (eg, after smoke inhalation), and be alert for delayed 

development of upper airway obstruction or pulmonary edema. 

B. Contaminated Eyes 

(See Chapter 31.) Wash the eyes immediately with copious amounts of plain water or 

normal saline; do not use neutralizing solutions. Hang a bottle containing 500-100 mL of 

normal saline above the patient, and dribble the solution slowly into the corner of the 

injured eye through the intravenous tubing. 

If the contaminating material was acidic or basic, tears may be checked with pH paper 

after the eyes have been washed to make sure that all toxic material has been removed. 

A careful eye examination is indicated following irrigation (Chapter 31). 

C. Contaminated Skin 

Wash the skin immediately with plenty of water and dilute soap solution. Discard 

contaminated clothes in a marked plastic bag. Certain toxins, such as 

organophosphates, are well absorbed through the skin and are difficult to remove. 

Remove all particulate matter prior to irrigation. 

Hydrofluoric acid burns are particularly penetrating and corrosive. Prompt immersion of 

the burn into quaternary ammonium salt solution or 10% calcium gluconate solution or 

2.5% gel, or subcutaneous injection of calcium gluconate deep to the burn (0.5 mL of 

10% solution per square centimeter of burn area) may be helpful. A plastic surgeon (or 

hand surgeon) should be consulted for injuries involving the fingers. 

D. Ingested Poisons 

The traditional approach has been to remove ingested toxins by emesis or gastric 

lavage, followed by activated charcoal and catharsis. However, recent evidence 

suggests that gastric emptying (particularly emesis) may have limited efficiency, 

especially if initiated more than 1 hour after the ingestion, and may delay the 

administration of charcoal. Gastric lavage is the preferred method of gastric emptying, 

particularly in patients who have taken a rapid-acting convulsant or those with a rapidly 

declining level of consciousness. 

1. Ipecac—Induced emesis is no longer recommended in the emergency department. 

Although controversial, ipecac may still have a role in the domestic setting (eg, 

mushroom poisoning). 

2. Gastric lavage—Use gastric lavage in patients with suspected serious poisonings 

who present to the emergency department within 1 hour of ingestion. Unless a patient is 

intubated, gastric lavage is contraindicated if airway protective reflexes are absent.

Gastric lavage is performed with a large-bore (at least 36F for adults) orogastric or 

nasogastric tube. (Pill fragments cannot be removed through standard-sized nasogastric 

tubes.) Use tap water or saline at body temperature in 250-mL increments, and continue 

lavage until fluid returns clear or free of pill fragments. 

3. Activated charcoal—Activated charcoal, 50-100 g as a slurry, can be given if a 

patient has ingested a potentially toxic amount of a poison. Unless a patient has an 

intact or protected airway, the administration of activated charcoal is contraindicated. 

For oral administration, charcoal can be made more palatable by adding a small amount 

of cherry, licorice, or chocolate flavoring just before administration. Mixing the charcoal 

with 1 mL/kg of 70% sorbitol improves taste and also provides cathartic action. Although 

routine use of a cathartic with activated charcoal is not endorsed, if used, it should be 

limited to a single dose in order to minimize adverse effects. As with gastric lavage, the 

effectiveness of activated charcoal decreases with time. 

Charcoal has great adsorptive properties and can bind most poisons (exceptions 

include alcohols, potassium, lithium, and iron). If the ingested dose of poison is known, 

attempt to give at least 10 times that weight of charcoal, in divided doses if necessary. 

4. Whole bowel irrigation—Whole bowel irrigation has been used successfully for 

removal of iron tablets and sustained-release and enteric-coated preparations. This 

technique utilizes a balanced electrolyte-polyethylene glycol solution (Colyte, 

GoLYTELY) to flush out the entire intestinal tract. It is given by nasogastric tube, 1-2 L/h 

(400-500 mL/min in children), until the rectal effluent is clear (3-5 hours or more). 

Perform Complete Physical Examination 

Look for characteristic physical signs of various kinds of poisoning while immediate 

treatment measures are being started. Physical signs associated with specific poisons 

are listed in Tables 45-1 and 45-2. 

Order Other Laboratory & X-ray Studies as Needed 

Appropriate laboratory evaluation of the patient is determined, in part, by the patient's 

clinical condition. 

A. Blood Tests 

Obtain arterial blood gas and pH measurements to determine adequacy of ventilation 

and circulation. Draw blood for measurement of serum electrolytes, blood urea nitrogen, 

blood glucose, and serum osmolality. Calculate anion and osmolar gaps (Tables 45-3 

and 45-4). 

B. Electrocardiogram 

Obtain an ECG, and look for widened QRS complexes or QT intervals, atrioventricular 

block, ventricular tachyarrhythmias, or evidence of ischemia (Table 45-5). 

C. X-ray Studies 

Obtain a chest x-ray to look for pulmonary edema (caused by narcotics, barbiturates, 

salicylates, ethchlorvynol, or corrosive chemicals) or infiltrates (due to aspiration of

gastric contents, inhalation of certain metal fumes, or hydrocarbon aspiration). Obtain 

an abdominal x-ray to look for radiopaque pills or toxins (Table 45-6). 

D. Urine Studies 

Obtain urine for toxicologic screening and routine analysis, and look for calcium oxalate 

crystals (ethylene glycol poisoning); positive test for occult blood (myoglobinuria, 

hemolysis); or positive test for phenylpyruvic acid (eg, Phenistix) in phenothiazine or 

salicylate overdose (may be negative in patients with acid urine). 

E. Toxicologic Studies 

Request toxicologic studies. Results of toxicologic studies may be useful in later 

confirmation of the diagnosis but are rarely helpful in the emergency department. It is 

more cost-effective to save serum and urine samples in the laboratory and analyze 

them later only if necessary. For certain types of poisoning, however, obtaining 

estimates of drug concentration quickly is valuable in determining the need for specific 

therapy. These drugs and their antidotes are discussed later in this chapter, under each 

specific poisoning. 

Accelerate Elimination of Poisons 

A. Toxicokinetics 

The rational management of drug overdose requires an understanding of the 

absorption, distribution, and elimination of the toxin. Most published kinetic parameters 

have been determined at normal doses, whereas pharmacokinetics in victims of 

poisoning are often more complex. 

Dissolution and absorption of toxin or gastric-emptying time may be altered in poisoned 

patients, so that the peak effects may be delayed (as occurs with anticholinergics). The 

gastrointestinal tract may be injured, allowing increased absorption of certain materials 

(eg, iron). If the finite capacity of the liver to metabolize a drug is exceeded, an 

increased amount of the drug may be delivered to the systemic circulation. If the 

concentration of the toxin in the bloodstream increases dramatically, protein binding 

may be saturated (eg, in salicylate poisoning), so that the fraction of free toxin 

increases. Circulatory insufficiency, hypothermia, and electrolyte and acid-base 

imbalance influence the metabolism and excretion of ingested drugs. Any of these 

factors may drastically alter normal kinetics and confuse calculations. Despite these 

limitations, pharmacokinetic principles may be useful in the management of drug 

overdose. Some terms commonly used in toxicology are defined below. 

1. Half-life—The half-life of a toxin is the time required to eliminate one half of the toxin 

from the body. This parameter is most meaningful for the many drugs (eg, barbiturates, 

theophylline) that exhibit first-order kinetics, in which a fixed percentage of the toxin is 

removed per unit of time. Other drugs (eg, alcohol) have zero-order kinetics, in which a 

fixed amount of toxin is removed per unit of time. In an overdose, pathways of 

elimination are often saturated, and first-order kinetics are replaced by fixed-rate, or 

zero-order, elimination. 

2. Volume of distribution—The volume of distribution (V d ) is the volume into which the 

toxin is distributed after absorption. If a drug is sequestered outside the blood and is

highly tissue bound, it will have a large volume of distribution. Table 45-7 gives the 

volumes of distribution for several common drugs. 

3. Clearance—Clearance is the volume of plasma that can be cleared of toxin per unit 

of time. Clearance includes both renal and metabolic components, and the proportion 

that each contributes to total clearance is important. For example, a toxin may be 95% 

metabolized and 5% renally excreted, in which case doubling the renal clearance of the 

toxin will not significantly enhance its total elimination from the body. 

Knowledge of these parameters is helpful when measures to increase drug elimination 

(eg, forced alkaline diuresis, hemodialysis, or hemoperfusion) are under consideration. 

For example, toxins with large volumes of distribution are present in only minute 

quantities in plasma and are not effectively removed by dialysis or diuresis. Measures to 

enhance elimination of drugs with rapid intrinsic clearance rates will not contribute 

significantly to the overall elimination rate. 

B. Methods to Enhance Drug Elimination 

The decision to use measures to improve drug elimination should be based on a rational 

understanding of the drug's properties and the patient's clinical condition. Most patients 

respond satisfactorily to appropriate supportive care. The risks, time, and expense 

involved in hemodialysis or hemoperfusion must be weighed against the possible 

benefits. In some patients, the severe potential toxicity of the poison warrants immediate 

hemodialysis (Table 45-8). With other poisons, dialysis is of no theoretic or proved 

benefit. 

1. Diuresis and pH manipulations—Because many toxins are weak acids or bases, 

they can be ionized in solutions of varying pH. In the ionized state, they are less likely to 

cross cell membranes, and their reabsorption to the renal tubular epithelium is 

decreased. The clinical significance of these measures depends on the contribution of 

renal elimination to total body clearance. It is also important to consider the possible 

adverse effects of overhydration, alkalemia, or acidemia. Note: Most studies have failed 

to show a significant effect of forced diuresis or pH manipulation on the outcome of 

poisoning. 

Weak acids such as salicylate and phenobarbital are more fully ionized in basic 

solutions, so that alkalizing the urine may serve to trap them in the tubular lumen, thus 

increasing excretion of the drug in the urine. 

Weak bases such as amphetamines, strychnine, and phencyclidine are more ionized in 

an acid medium; acidification of the urine has been proposed to enhance their removal. 

However, acidification may promote myoglobinuric renal failure in patients with 

rhabdomyolysis, a common complication of poisoning by these agents, and is no longer 


2. Hemodialysis—During hemodialysis, toxin is removed from the blood into a dialysate 

solution across a semipermeable membrane. The toxin must be relatively water soluble 

and not highly protein bound. It should have a small volume of distribution and slow rate 

of intrinsic elimination (ie, a long half-life). Hemodialysis is effective in removing 

methanol, ethylene glycol, salicylates, and lithium, among other drugs (see Table 45-8).

It is also of value in correcting pH and electrolyte imbalances, especially in anuric 

patients. 

3. Peritoneal dialysis—This method is much less efficient than hemodialysis in 

removing most drugs. 

4. Hemoperfusion—In hemoperfusion, blood is pumped through a column of adsorbent 

material (charcoal or resin) and returned to the patient's circulation. Vascular access 

similar to that for hemodialysis is required. The kinetic conditions required are the same 

as in hemodialysis; that is, the drug should have a small volume of distribution and a 

slow rate of intrinsic clearance. Hemoperfusion has the advantage that the drug or toxin 

is in direct contact with the adsorbent material; therefore, high molecular weight, poor 

water solubility, and even plasma protein binding are not limiting factors as they are in 

hemodialysis. Hemoperfusion is commonly associated with thrombocytopenia. 

Hemoperfusion will not correct pH or electrolyte imbalances. 

5. Repeated doses of activated charcoal—Repeated doses of charcoal given orally or 

via gastric tube (20-30 g every 3-4 hours without a cathartic) may enhance elimination 

of some drugs and toxins from the bloodstream by a type of so-called gut dialysis. 

Drugs for which this may be useful can be recalled by the mnemonic ABCD: 

antimalarials (quinine) and aminophylline, barbiturates (phenobarbital), b-blockers 

(nadolol), carbamazepine, and dapsone. 

C. Antidotes 

Table 45-9 sets forth several common useful antidotes. Their indications and dosages 

are discussed below in the sections on specific toxins. The half-life of the antidote 

relative to that of the toxin must be considered. Most important, antidotes should not be 

used indiscriminately and without regard for the patient's clinical condition. They may 

have serious side effects and in some cases may be more toxic than the poison. Note: 

Always treat the specific symptoms manifested by the patient, not those known to be 

associated with a certain poison. 

MANAGEMENT OF CONDITIONS ASSOCIATED WITH POISONING 

Airway Management 

It is essential to protect the lungs from aspiration and maintain adequate ventilation and 

oxygenation. In the patient with a depressed gag reflex, gastric lavage and 

administration of activated charcoal may result in significant aspiration. 

A. Patients in Coma or with Markedly Depressed Gag Reflex 

Endotracheal intubation should always be performed in these patients, especially before 

gastric lavage. 

B. Awake Patient with Normal Gag Reflex 

Gastric intubation and lavage may be performed without special precautions. 

C. Lethargic Patient

The lethargic patient with fluctuating mental status and a variable gag reflex poses a 

more difficult problem in management. If the gag reflex is intact, cautious gastric lavage 

may be performed with the patient in the left lateral decubitus position and with the head 

of the bed or stretcher tilted down at an angle of 10-20 degrees. Note: If there is any 

doubt about the patient's ability to protect the airway with a gag or cough reflex, gastric 

lavage must be preceded by intubation with a cuffed endotracheal tube. 

If intubation is not immediately performed, it is critical to monitor the status of the airway 

closely and to position the patient so as to preserve aspiration. An initially responsive 

patient may rapidly become more obtunded. Significant swelling and upper airway 

obstruction may be late developments after thermal, chemical, or caustic burns. 

Seizures 


A. General Management 

Management of drug-induced seizures is generally the same as that for seizures due to 

other causes, that is, protection of the airway; use of anticonvulsants; and correction of 

acidosis, hypoxemia, electrolyte abnormalities, and hyperthermia. Seizures unrelated to 

poisoning may also occur as a result of intracranial bleeding from trauma, 

hypoglycemia, or hyponatremia. Seizures caused by poisoning are rarely focal, nor are 

they associated with asymmetric neurologic findings. Meningitis may mimic metabolic or 

toxic encephalopathy and must be ruled out by lumbar puncture (Chapter 40). 


In certain types of poisoning, refractory seizures may require specific therapy: 

1. Seizures occurring as a result of theophylline, lithium, or salicylate overdose usually 

require hemodialysis or hemoperfusion to accelerate removal of the drug. 

2. In isoniazid poisoning with seizures refractory to diazepam, administer pyridoxine, 5 g 

(or 1 g per gram of isoniazid ingested) intravenously. 

3. Seizures due to organophosphate poisoning may respond to atropine and 

pralidoxime. (See "Organophosphates & Other Cholinesterase Inhibitors" section, 

below.) 

Hypotension 

(See Chapter 9.) Hypotension is a common associated condition in victims of poisoning. 

The mechanism of hypotension may be direct cardiac depression, peripheral 

vasodilation, or fluid defects or shifts that result in hypovolemia. Concurrent hypothermia 

may aggravate hypotension. Be alert for possible concurrent trauma with occult internal 

bleeding or concurrent infection with septic shock. 

In the absence of associated pulmonary edema, a fluid challenge should be given with 

intravenous boluses of 1 L of normal saline. A central venous or pulmonary artery 

catheter may need to be inserted to monitor fluid needs and response to therapy in

cases of refractory hypotension. Monitoring of urine output with an indwelling catheter is 

recommended. If hypotension and hypoperfusion are severe and unresponsive to 

administration of fluids and temperature correction, vasopressors may be of benefit. 

Thermodysregulation 

See Chapter 44 for further details of the management of hypothermia and hyperthermia. 

A. Hyperthermia 

1. Causes—Many drugs cause hyperthermia, either by direct toxic effects on 

temperature-regulating mechanisms or through associated hyperactivity or seizures. 

a. Salicylates—Salicylate intoxication causes hyperthermia by uncoupling of oxidative 

phosphorylation, resulting in inefficient (and therefore heat-generating) production of 

ATP. 

b. Phenothiazines—Phenothiazines inhibit the autoregulatory ability of the central 

nervous system, leading to environmentally induced hypothermia or hyperthermia. 

c. Seizures or hyperactivity—Hyperthermia may result from seizures or extreme 

hyperactivity (particularly if the patient has to be forcibly restrained) following poisoning 

by phencyclidine or amphetamines. 

d. Anticholinergic properties—The anticholinergic properties of many drugs (eg, 

antihistamines, tricyclic antidepressants) can aggravate hyperthermia by inhibiting 

sweating. 

2. Treatment—For dangerous core temperatures above 41 °C (105.8 °F), cool the 

patient rapidly by sponge bathing with evaporation accelerated by fanning and ice 

packs; treat seizures. Muscular hyperactivity is most effectively treated with 

benzodiazepines or neuromuscular paralysis and assisted ventilation. 

B. Hypothermia 

Hypothermia may be caused by certain drugs, exposure to cold, hypoglycemia, sepsis, 

or hypothyroidism. The diagnosis may be missed if a rectal thermometer capable of 

reading temperatures in the range of 24-32 °C (75.2-89.6 °F) is not used. 

For severe hypothermia, rapidly restore normal body temperature with warm 

intravenous fluids, warm gastric or peritoneal lavage, or ventilation with warmed, 

humidified air. Slow passive rewarming by external means is usually sufficient in milder 

cases. 

Delayed Severe Toxicity 

Initial evaluation may fail to reveal the seriousness of poisoning with some drugs. 

Severe, potentially preventable hepatic damage may occur after acetaminophen 

overdose unless the physician determines acetaminophen levels and administers the 

antidote acetylcysteine, when appropriate, early in treatment. Other poisons with 

characteristically delayed severe toxicity are listed in Table 45-10.

The development of sustained-release preparations has increased the chances of 

nearly normal results on initial evaluation. The possibility that a sustained-release 

preparation has been used must be considered in theophylline or salicylate poisoning, 

because with these drugs, serum or blood concentrations are used to evaluate the 

severity of intoxication. Under these circumstances, it is prudent to observe the patient 

longer and obtain a second blood-level reading before deciding on further treatment and 

disposition. 

Barceloux D, McGuigan M, Hartigan-Go K: Position statement: cathartics. American 

Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical 

Toxicologists. J Toxicol Clin Toxicol 1997;35:743. [PMID: 9482428] (Guidelines on the 

use of cathartics in overdose.) 

Bowden CA et al: Clinical applications of commonly used contemporary antidotes. Drug 

Saf 1997;16:9. [PMID: 9010641] (Review of commonly used antidotes in poisoning.) 

Chyka PA et al: Position statement: single-dose activated charcoal. American Academy 

of Clinical Toxicology; European Association of Poisons Centres and Clinical 

Toxicologists. J Toxicol Clin Toxicol 1997;35:721. [PMID: 9482427] (Guidelines on the 

use of charcoal in overdose.) 

Krenzelok EP et al: Position statement: ipecac syrup. American Academy of Clinical 

Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J 

Toxicol Clin Toxicol 1997;35:699. [PMID: 9482425] (Guidelines on the use of ipecac 

syrup in overdose.) 

Larsen LC et al: Oral poisoning: guidelines for initial evaluation and treatment. Am Fam 

Physician 1998;57:85. [PMID: 9447216] (Practical review of the evaluation and 

treatment of the poisoned patient.) 

Poisindex. http://www.micromedex.com/products/poisindex (Web site containing 

information on individual drugs and treatment for poisoning.) 

Proudfoot A: Practical management of the poisoned patient. Ther Drug Monit 

1998;20:498. [PMID: 9780125] (Review of the management of the poisoned patient.) 

Tenenbein M: Position statement: whole bowel irrigation. American Academy of Clinical 

Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J 

Toxicol Clin Toxicol 1997;35:753. [PMID: 9482429] (Guidelines on the use of whole 

bowel irrigation in overdose.) 

Vale JA: Position statement: gastric lavage. American Academy of Clinical Toxicology; 

European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin 

Toxicol 1997;35:711. [PMID: 9482426] (Guidelines on the use of gastric lavage in 

overdose.) 

Watson ID: Laboratory support for the poisoned patient. Ther Drug Monit 1998;20:490. 

[PMID: 9780124] (Discussion of the types of laboratory analysis available in the

evaluation of the poisoned patient.) 

EMERGENCY TREATMENT OF SPECIFIC POISONINGS 

ACETAMINOPHEN 


• Patient may be asymptomatic early after ingestion or present with anorexia, nausea, 

and right upper quadrant pain. 

• Draw 4-hour postingestion levels, and use the nomogram (Figure 45-1) to predict 

severity. 

• Acetylcysteine therapy is antidote if level of acetaminophen is above the possible 

toxicity line. 


Acetaminophen is a widely used ingredient in numerous over-the-counter and 

prescription preparations. One of the products of the normal metabolism of 

acetaminophen is hepatotoxic; at toxic levels, it saturates the glutathione detoxification 

system in the liver and accumulates, causing delayed hepatic injury (24-72 hours after 

ingestion). The toxic dose of acetaminophen is considered to be over 140 mg/kg. The 

margin of safety is probably lower in patients who are chronic alcohol abusers, those 

with liver disease who have been fasting, and those with induced microsomal enzymes 

(most commonly from other drugs). 


Caution: Shortly after ingestion of acetaminophen, there may be no symptoms or only 

anorexia or nausea; hepatic necrosis may not become clinically apparent until 24-48 

hours later, when nausea, jaundice, and markedly elevated results on liver function tests 

may appear. Hepatic failure may follow. 

Treatment 


Provide intensive supportive care and gastrointestinal decontamination as described 

previously. Administer activated charcoal regardless of the possibility that acetylcysteine 

may be administered (see below). 

B. Estimation of Severity 

Obtain a 4-hour postingestion acetaminophen serum concentration measurement, and 

use the nomogram (see Figure 45-1) to predict the range of severity. If the 4-hour level 

is over 150 ug/mL, or if a toxic dose (7.5 g) is suspected to have been ingested, begin 

treatment with acetylcysteine. Because acetaminophen and salicylate are often ingested 

simultaneously, a measurement of serum salicylate concentration should also be 

obtained immediately.

The Rumack-Matthew nomogram (see Figure 45-1) is not helpful in determining the 

need for N-acetylcysteine (NAC) in chronic or enteric-coated ingestions. In these cases, 

2 serum acetaminophen levels should be obtained 4-6 hours apart and treatment given 

if either level is above the possible toxicity line. 

C. Acetylcysteine Therapy 

Acetylcysteine (Mucomyst) substitutes for glutathione and binds the toxic metabolite of 

acetaminophen, thus inactivating and detoxifying it. Give 140 mg/kg orally of a 10% or 

20% solution diluted to 5% with citrus juice or soda. Follow with 70 mg/kg orally every 4 

hours for 18 doses. If the patient vomits a dose within 1 hour, it should be repeated; 

slow drip by nasogastric tube and administration of an antiemetic (eg, metoclopramide, 

10-20 mg intravenously) may be helpful. The intravenous dosing of NAC is used 

extensively in the United Kingdom and in Canada and is beginning to be used in the 

United States, although it has not been approved by the U.S. Food and Drug 

Administration (FDA). Intravenous NAC, 0.2 g/mL, is given after a 1:5 dilution in 5% 

dextrose in water over 1 hour. The initial dose is 140 mg/kg followed by 70 mg/kg every 

4 hours for an additional 12 doses. Anaphylactoid reactions have been reported with the 

use of intravenous NAC. Both the oral and intravenous routes have been demonstrated 

in multiple studies to be effective. 

The effectiveness of acetylcysteine depends on its use early in treatment; it must be 

given within 12-16 hours of ingestion of acetaminophen and preferably within 8-10 

hours. Do not delay treatment if a serum acetaminophen level is not readily available 

and a toxic dose may have been taken. Treat with NAC empirically and reevaluate 

treatment after the acetaminophen level has returned. NAC can be given in conjunction 

with activated charcoal without any change in dosing. NAC can also be safely given in 

pregnancy. 

Disposition 

Use serum concentration of acetaminophen as a guide to the severity of poisoning, and 

hospitalize all patients requiring acetylcysteine therapy and those with evidence of 

hepatotoxicity. 

Bailey B et al: Management of anaphylactoid reactions to intravenous N-acetylcysteine. 

Ann Emerg Med 1998;31:710. [PMID: 9624310] (Retrospective case study and literature 

review of patients who developed anaphylactoid reactions to intravenous NAC.) 

Cetaruk EW et al: Tylenol Extended Relief overdose. Ann Emerg Med 1997;30:104. 

[PMID: 9209234] (Retrospective case analysis of the evaluation and management of 

overdose with Tylenol Extended Relief.) 

Kozer E et al: Management of paracetamol overdose: current controversies. Drug Saf 

2001;24:503. [PMID: 11444723] (Review of both oral and intravenous NAC in 

acetaminophen overdose.) 

Woo OF et al: Shorter duration of oral N-acetylcysteine therapy for acute 

acetaminophen overdose. Ann Emergency Med 2000;35:363. [PMID: 10736123]

(Retrospective case series evaluating the safety and efficacy of a shorter NAC 

regimen.) 

AMPHETAMINES & OTHER RELATED STIMULANTS 


• All drugs in this class are central nervous system stimulants. 

• Predominant symptom is sympathetic hyperactivity. 

• Treatment is supportive; no specific antidote is available. 


Amphetamines and other stimulants are easily abused because of their wide availability, 

primarily through street sales of illicit drugs but also in the so-called legal-high diet 

preparations. These drug combinations may contain varying amounts of 

methamphetamine, methylene-dioxyamphetamine (MDA), caffeine, ephedrine, and 

phenylpropanolamine. Illicitly obtained stimulants may also contain phencyclidine. 

Cocaine is discussed later in this chapter. 

All of these drugs are central nervous system stimulants and cause sympathetic 

hyperactivity. Some may produce significant vasoconstriction, causing hypertension and 

bradycardia. Most of these drugs have short half-lives, and their peak effect and toxicity 

occur within 30 minutes after intravenous or intramuscular administration and 2-3 hours 

after oral ingestion. As a result, serum drug level measurements are of little value, and 

measures to enhance elimination generally do not alter the outcome. 


Significant amphetamine poisoning is always accompanied by symptoms. Euphoria, 

mydriasis, and restlessness progress in severe cases to toxic psychosis and seizures. 

Hypertension can be severe and associated with palpitations or arrhythmias. Seizures 

and hyperthermia may produce rhabdomyolysis and myoglobinuria. 

Phenylpropanolamine is no longer available because of documented cases of severe 

toxic encephalopathy and even cerebrovascular accidents. 

Treatment 



previously. For severe agitation or psychotic behavior, diazepam, 5-10 mg in adults 

(0.2-0.5 mg/kg intravenously in children), may be helpful; repeat every 5-10 minutes 

until sedation has been achieved. Lorazepam, 4-8 mg intravenously in adults (0.05-0.1 

mg/kg in children), or haloperidol, 0.1-0.2 mg/kg intramuscularly, is also effective. 

B. Treatment of Seizures 

Treat seizures with diazepam, followed by phenobarbital, phenytoin, or both if seizures

are uncontrollable or recur (Chapter 17.) 

C. Treatment of Hypertension 

Hypertension is generally transient and, unless severe, does not require treatment. 

Often the hypertension responds to benzodiazepine administration, but in severe cases 

(eg, diastolic blood pressure > 120 mm Hg, encephalopathy), intravenous nitroprusside, 

0.5-1.0 ug/ kg/min, is effective and easily titratable. Phentolamine, 0.1 mg/kg slowly 

intravenously, is an alternative drug. 

D. Treatment of Arrhythmias 

Tachycardia and ventricular tachyarrhythmias may respond to administration of 

propranolol, 0.05-0.1 mg/kg intravenously. 

E. Other Measures 

Monitor temperature, and start cooling measures if hyperthermia occurs. Check the 

urine for myoglobin. Acidification of the urine is not recommended. 

If chest pain is present, perform an ECG and cardiac enzymes, and consider 

hospitalization to rule out myocardial ischemia or infarction. 

Patients with seizures may require computed tomography (CT) scanning to rule out 

intracranial hemorrhage. 

Disposition 

Hospitalize patients with complications (psychotic behavior, hypertension, hyperthermia, 

chest pain, arrhythmias) or those with prolonged symptoms. 

Albertson TE et al: Methamphetamine and the expanding complications of 

amphetamines. West J Med 1999;170:214. [PMID: 10344175] (Review of the toxicity of 

methamphetamine use.) 

Chan TC et al: Drug-induced hyperthermia. Crit Care Clin 1997;13:785. [PMID: 

9330841] (Review of the pathophysiology, presentation, and treatment of 

sympathomimetic poisoning.) 

Mersfelder TL: Phenylpropanolamine and stroke: the study, the FDA ruling, the 

implications. Cleve Clin J Med 2001;68: 208. [PMID: 11263849] (Review of 

phenylpropanolamine side effects and toxicity.) 

Richards JR et al: Methamphetamine abuse and rhabdomyolysis in the ED: a 5-year 

study. Am J Emerg Med 1999;17:681. [PMID: 10597089] (Retrospective case review of 

patients with rhabdomyolysis and methamphetamine use.) 

ANTICHOLINERGICS 


• Ingestion produces many symptoms prompting the phrase "blind as a bat, hot as 

Hades, red as a beet, dry as a bone, and mad as a hatter." 

• Treatment is primarily supportive, although physostigmine can be used in 

life-threatening situations. 


Atropine, scopolamine, belladonna, many antihistamines, and tricyclic antidepressants 

are anticholinergics. Many plants (eg, jimsonweed [Datura stramonium], nightshade, 

Amanita muscaria mushrooms) also contain anticholinergic compounds. 


These drugs block cholinergic receptors both centrally and peripherally. Ingestion of a 

significant amount of an anticholinergic drug can produce many clinical effects. The 

popular phrase "blind as a bat, hot as Hades, red as a beet, dry as a bone, mad as a 

hatter" describes many of the manifestations of anticholinergic toxicity. Other signs and 

symptoms include tachycardia, gastrointestinal ileus, urinary retention, delirium, and 

hallucinations. Seizures can also occur. 

Treatment 


previously. Most patients can be managed with supportive measures alone, including 

sedation with benzodiazepines, cooling, and bladder emptying. If a patient develops 

life-threatening complications of anticholinergic toxicity (hemodynamically significant 

tachycardia, hyperthermia, or seizures resistant to benzodiazepines), physostigmine, 

1-2 mg intravenously over 2 minutes, can be given. Physostigmine works within 

minutes, and the duration of effect is 30-60 minutes. It has been associated with severe 

complications, including bradycardia, heart block, and seizures. Atropine should be 

readily available if the antidote is used, and ECG monitoring is necessary. Note: 

Physostigmine should never be used as a diagnostic test for patients with an altered 

mental status or hallucinations. Physostigmine is contraindicated in patients with an 

overdose of any drug that could delay intraventricular conduction (tricyclic 

antidepressants), asthma, or mechanical bowel or bladder obstruction. 

Disposition 

Hospitalize patients who have incapacitating signs or symptoms of anticholinergic 

poisoning. 

Chan TC et al: Drug-induced hyperthermia. Crit Care Clin 1997;13:785. [PMID: 

9330841] (Review of the pathophysiology, presentation, and treatment of anticholinergic 

poisoning.) 

Dewitt MS et al: The dangers of jimson weed and its abuse by teenagers in the 

Kanawha Valley of West Virginia. WV Med J 1997;93:182. [PMID: 9274142] (Case 

review of jimson weed ingestion evaluation and treatment.)

Grace RF: Benztropine abuse and overdose—case report and review. Adverse Drug 

React Toxicol Rev 1997;16:103. [PMID: 9359932] (Case report and review of the 

management of anticholinergic overdose.) 

Weiner AL et al: Anticholinergic poisoning with adulterated intranasal cocaine. Am J 

Emerg Med 1998;16:517. [PMID: 9725971] (Case report of the presentation of cocaine 

and anticholinergic toxicity.) 

ß-Adrenergic Blocking Agents 


• Ingestion of a large amount of ß-blockers primarily affects the cardiac system. 

• Symptoms of ingestion include hypotension, bradycardia, and bronchoconstriction. 

• Plasma levels are not useful. 

• Glucagon can be used to treat hypotension if fluids are unsuccessful; glucagon can 

also be used to treat arrhythmias, but cardiac pacing may be required in severe cases. 


ß-Adrenergic blocking agents are widely used in clinical medicine to treat hypertension, 

arrhythmias, angina pectoris, migraine headache, and thyrotoxicosis. ß-Blockers act by 

competing with catecholamines for a finite number of ß 1 and ß 2 receptor sites. The ß 1 

receptors are responsible for increasing the force and rate of cardiac contraction. The 

ß 2 receptors mediate vasodilatation; bronchial smooth muscle dilation; and a number of 

metabolic effects, including glycogenolysis. Excessive ß blockade can therefore cause 

hypoglycemia, bradycardia, bronchoconstriction, and hypoglycemia. In overdose, ß 1 

and ß 2 selectivity is lost, and generalized ß blockade is seen. Some agents (eg, 

pindolol) have partial intrinsic sympathomimetic activity and may cause hypertension 

and tachycardia in overdose. 


The main features of massive ß-blocker overdose are hypotension and bradycardia. 

Pulmonary edema or bronchospasm may also occur, especially in patients with 

preexisting congestive heart failure or asthma. Hypoglycemia and hyperkalemia are 

sometimes seen. Convulsions are common with propranolol and other agents (eg, 

oxprenolol) with high lipid solubility and marked membrane-depressant effects. Seizures 

have not been reported with atenolol, pindolol, or practolol. The ECG may show sinus 

bradycardia, atrioventricular blocks, or a prolonged QRS interval. In rare cases 

ventricular tachyarrhythmias may occur, especially with sotalol overdose. Death is 

usually due to profound myocardial depression, with advanced atrioventricular block or 

asystole. The heart may not respond to attempts at pacing, even with high currents. 

Plasma levels of ß-blockers are not clinically useful and are not routinely available.

Treatment 


General management of overdose, including airway protection, treatment of 

hypoglycemia, and gastrointestinal decontamination should be undertaken as outlined 

earlier. 

B. Treatment of Hypotension 

Treat hypotension initially with fluids. If this is unsuccessful, use glucagon, 5-10 mg 

(100-150 ug/kg) as an intravenous bolus, followed by an infusion of 2-5 mg/h. Glucagon 

increases intracellular cyclic AMP by a mechanism different from that of ß receptors. If 

the initial bolus is unsuccessful, a second bolus may be tried up to a maximum dosage 

of 10 mg. 

C. Treatment of Arrhythmias 

Advanced atrioventricular block or bradycardia resulting in hypotension can also be 

treated initially with glucagon; atropine, 0.01-0.03 mg/kg intravenously, or isoproterenol, 

0.05-0.3 ug/kg/min by intravenous infusion, may also be used. If these are 

unsuccessful, cardiac pacing may be necessary. 


Enhance elimination. Because of the relatively large volume of distribution and 

extensive protein binding, dialysis is not likely to be of value for propranolol overdose. 

Less lipophilic agents (eg, atenolol, nadolol) have much smaller volumes of distribution 

and may be eliminated by dialysis or hemoperfusion, but they are less likely to cause 

profound toxicity. 

Disposition 

Patients should remain under observation for at least 6-8 hours after ingestion. Patients 

with significant ß-blocker intoxication (eg, profound bradycardia, conduction 

abnormalities, hypotension, shock) should be hospitalized. 

Love JN et al: Characterization of fatal beta blocker ingestion: a review of the American 

Association of Poison Control Centers data from 1985-1995. J Toxicol Clin Toxicol 

1997;354:353. [PMID: 9204094] (Retrospective review of ß-blocker-related fatalities.) 

White CM: A review of potential cardiovascular uses of intravenous glucagon 

administration. J Clin Pharmacol 1999;39:442. [PMID: 10234590] (Review of the use of 

glucagon in the treatment of ß-blocker overdose.) 

CALCIUM-CHANNEL BLOCKING AGENTS 


• Ingestion of a large amount of calcium-channel blockers can cause hypotension,

adycardia, and central nervous system depression. 

• Treatment is primarily supportive, although both calcium and glucagon can be used to 

treat hypotension and bradycardia. 

• Levels of calcium-channel blockers are not useful. 


Calcium-channel blockers are being used with increasing frequency for supraventricular 

tachycardia, hypertension, rate control in atrial fibrillation or atrial flutter, angina, and 

vasospasm. These agents block the slow calcium channels and have the following 

cardiovascular effects: they depress sinus node activity, slow atrioventricular nodal 

conduction, cause coronary and peripheral vasodilatation, and depress myocardial 

contractility. Verapamil and diltiazem have the most marked myocardial effects and are 

especially dangerous in patients with sinus or atrioventricular nodal disease, 

Wolff-Parkinson-White syndrome, on digitalis therapy or in patients receiving ß-blockers, 

quinidine, disopyramide, or other myocardial depressant drugs. Nifedipine is especially 

dangerous in patients receiving nitrates or ß-blockers and in patients with obstructive 

valvular heart disease. Nifedipine is more likely than verapamil or diltiazem to be 

associated with increased heart rate and vasodilatation. Calcium-channel blockers may 

also block insulin release, resulting in hyperglycemia. 


The main manifestations of calcium-channel blocker overdose are hypotension, 

bradycardia, and depressed mental function. Bradydysrhythmias result from sinoatrial 

and atrioventricular nodal conduction dissociation. If the ingestion is a sustained-release 

preparation, toxicity and symptoms may be delayed for 6-8 hours. With regular-release 

preparations, toxicity is generally seen in 2-3 hours. Hyperkalemia and seizures, which 

are sometimes observed in overdoses of ß-blockers, are not prominent in overdoses of 

calcium-channel blockers. The ECG shows evidence of bradyarrhythmia with 

atrioventricular block. Death results from severe myocardial depression leading to 

asystole. 

Treatment 


General management includes airway protection and gastrointestinal decontamination. 

Give multidose activated charcoal and initiate whole bowel irrigation in a patient who 

may have ingested sustained-release preparations. 

B. Cardiac Care 

Constant cardiac monitoring is essential. Appropriate pharmacologic management in 

seriously ill patients may require placement of central intravenous lines. 

Leg elevation, Trendelenburg positioning, and fluid management may be required. 

Advanced atrioventricular block and bradycardia resulting in hypotension may be 

treated initially with atropine, 0.01-0.03 mg/kg intravenously. Cardiac pacing may be 

required.


In hypotensive patients not responding to the therapy outlined above, calcium solutions 

have sometimes been successful. Administer 10% calcium chloride, 10-20 mL for adults 

(10-30 mg/kg for children) intravenously, or 10% calcium gluconate, 10-20 mL for adults 

(0.2- 0.4 mL/kg for children), followed by repeated boluses or continuous intravenous 

infusion as necessary. Calcium administration improves the blood pressure more than 

the heart rate. As in ß-blocker overdose, glucagon may improve both heart rate and 

blood pressure. An initial bolus of 2-5 mg intravenously may be given and followed by 

up to a total of 10 mg if no response is seen. If glucagon improves the patient's 

hemodynamics, then an infusion should be started. Isoproterenol, epinephrine, 

phenylephrine, or amrinone may be required for severe, unresponsive hypotension. 

Disposition 

Asymptomatic patients should be observed for at least 8-10 hours. Patients with 

significant calcium-channel blocker overdose should be hospitalized for monitoring and 

observation. 

Adams BD et al: Amlodipine overdose causes prolonged calcium channel blocker 

toxicity. Am J Emerg Medi 1998;16:527. [PMID: 9725975] (Case report of amlodipine 

overdose with treatment overview.) 

Papadopoulos J et al: Utilization of a glucagon infusion in the management of a massive 

nifedipine overdose. J Emerg Med 2000;18:453. [PMID: 10802424] (Case report of 

nifedipine overdose with glucagon as the treatment.) 

White CM: A review of potential cardiovascular uses of intravenous glucagon 

administration. J Clin Pharmacol 1999;39:442. [PMID: 10234590]. (Review of the use of 

glucagon in the treatment of calcium-channel blocker overdose.) 

CARBON MONOXIDE 


• Carbon monoxide is a colorless and odorless gas that binds with great affinity to 

hemoglobin. 

• Severe tissue hypoxia results. 

• Carbon monoxide levels correlate with severity of symptoms and should be used to 

guide treatment. 

• Treatment is with 100% oxygen; hyperbaric oxygen can also be used in certain 

circumstances. 


Carbon monoxide, a colorless, odorless, and tasteless gas, is produced by incomplete 

combustion of organic materials and is found in engine exhaust, gas heaters, burning

charcoal briquettes, and solid alcohol (Sterno Canned Heat, many others). Any fire may 

also produce large quantities of carbon monoxide. 

Carbon monoxide binds to hemoglobin with an affinity about 200 times greater than that 

of oxygen. The resulting carboxyhemoglobin complex cannot transport oxygen, causing 

tissue hypoxia that can lead to death or permanent neurologic damage if untreated. 

Hemoglobin saturation and blood oxygen content are dangerously low despite adequate 

(or elevated) arterial PO 2 levels. 


The severity of symptoms usually correlates with carboxyhemoglobin levels (Table 

45-11). The carboxyhemoglobin level can be from either venous or arterial blood. The 

earliest reliable diagnostic symptom is headache. Usually, PO 2 is normal, although 

metabolic acidosis due to tissue hypoxia may be present. Using oxygen saturation 

calculated from PO 2 (based on assumption of normal hemoglobin) or measured by 

pulse oximetry will provide an incorrect estimate of oxygen-carrying capacity. Blood may 

be cherry-red, but the patient rarely appears pink. The ECG may show ischemia or 

infarction in a person with coronary disease. Delayed central nervous system effects 

such as parkinsonism, memory loss, and personality changes can occur after recovery. 

Treatment 

Note: Act quickly. Delay in treatment may worsen neurologic damage. 


Administer 100% oxygen by nonrebreathing face mask or endotracheal tube, not by 

nasal cannula or loose-fitting face mask. Oxygen competes with carbon monoxide for 

hemoglobin-binding sites. The half-life of carboxyhemoglobin in a person breathing 

room air is 5-6 hours; in 100% oxygen, it is only 1 hour. Hyperbaric 100% oxygen lowers 

the carboxyhemoglobin level even more rapidly (23 minutes), but it is seldom readily 

available and no studies have demonstrated a reduction in post-carbon monoxide 

poisoning neurologic deficits in patients receiving hyperbaric oxygen versus 100% 

oxygen. Consider hyperbaric oxygen for patients with major symptoms of carbon 

monoxide intoxication such as loss of consciousness or myocardial ischemia or if the 

patient is pregnant. 

B. Blood Tests 

Obtain arterial blood for measurement of carboxyhemoglobin content and arterial blood 

gases. 

C. Chest X-ray 

If carbon monoxide poisoning is associated with smoke inhalation, obtain a chest x-ray 

and consider hospitalization and monitoring for development of noncardiogenic 

pulmonary edema. 


The use of corticosteroids and mannitol for cerebral edema has been recommended,

ut their value in preventing late neurologic sequelae remains unproved. 

Disposition 

All patients with significant carbon monoxide poisoning (ie, with chest pain or other 

evidence of cardiac ischemia, neurologic signs, or carboxyhemoglobin concentrations 

above 25%) and pregnant patients must be hospitalized and given oxygen. Oxygen may 

be administered in a hyperbaric chamber, in the circumstances described earlier in this 

section. 

Gilmer B et al: Hyperbaric oxygen does not prevent neurologic sequelae after carbon 

monoxide poisoning. Acad Emerg Med 2002;9:1. [PMID: 11772662] (An animal model 

study evaluating the efficacy of hyperbaric oxygen to treat carbon monoxide poisoning.) 

Greingor JL et al: Acute carbon monoxide intoxication during pregnancy. One case 

report and review of the literature. Emerg Med J 2001;18:399. [PMID: 11559621] (Case 

report of carbon monoxide poisoning in pregnancy and review of the literature.) 

Juurlink DN et al: Hyperbaric oxygen for carbon monoxide poisoning. Cochrane 

Database System Review 2000;(2): CD002041. [PMID: 10796853] (Meta-analysis of 

hyperbaric oxygen for carbon monoxide poisoning.) 

Sheridan RL et al: Hyperbaric oxygen treatment: a brief overview of a controversial 

topic. J Trauma 1999;47:426. [PMID: 10452491] (Review of the use of hyperbaric 

oxygen in carbon monoxide poisoning.) 

CARDIAC GLYCOSIDES 


• These cardiotoxic drugs result in rhythm and conduction disturbances in the heart and 

occasionally severe hyperkalemia. 

• Digoxin levels are indicative of the degree of poisoning in the acute overdose. 

• Patients with severe arrhythmias or hyperkalemia may benefit from digitalis antibodies 

to reverse toxicity. 

• All patients with poisoning require hospitalization. 


Digoxin; digitoxin; and several plant digitalis derivatives including oleander, foxglove, 

and lily of the valley are the sources of digitalis and the cardiac glycosides. They are 

used therapeutically primarily for their ability to slow conduction through the 

atrioventricular node in disease states such as atrial fibrillation. They also increase the 

force of myocardial contractility and enhance automaticity. These therapeutic effects 

also mediate the severity of toxicity. 

Digoxin has a large volume of distribution (6-10 L/ kg) and a half-life of about 40 hours;

for the most part, it is excreted unchanged in the urine. Digitoxin, by contrast, has a 

small volume of distribution, is highly protein bound, and undergoes extensive 

enterohepatic recirculation; its half-life is 7 days. In the elderly, the half-life may be 

increased owing to decreased creatinine clearance. 


Blurred vision, color vision disturbance (especially with green or yellow vision), and 

neurologic symptoms may occur. The most serious toxic effects are those that cause 

rhythm and conduction disturbances in the heart, for example, third-degree 

atrioventricular block, bradycardia, ventricular ectopy, bidirectional ventricular 

tachycardia, and paroxysmal atrial tachycardia with atrioventricular block. In patients 

with chronic atrial fibrillation, digitalis toxicity may cause nonparoxysmal junctional 

tachycardia, which is characterized by a regular rhythm with narrow QRS complexes 

and a heart rate of 90-120 beats/min (Chapter 35). Although hypokalemia may 

aggravate digitalis toxicity in the patient receiving chronic therapy, acute ingestion of an 

overdose is often associated with hyperkalemia. The plasma potassium level in digoxin 

overdose is indicative of the degree of poisoning of the Na + -K + -ATPase pump; if the 

potassium is elevated, the toxicity is severe. Therapeutic serum levels of digoxin are 

0.5-2 ng/mL; for digitoxin, they are 18-22 ng/mL. 

Treatment 



previously. Gastric lavage may worsen bradycardia by enhancing vagal tone. 

B. Electrolyte Abnormalities 

If hypokalemia is present, replace potassium (Chapter 42). For severe hyperkalemia, 

measures to reduce the potassium level may be necessary (Chapter 42) in order to 

reduce the cardiotoxic effects of digitalis. Because the total body potassium is not high, 

potassium-binding resins (ie, Kayexalate) should not be used. Other measures such as 

insulin, glucose, and sodium bicarbonate can be attempted in addition to specific 

antidotal therapy. Avoid the use of calcium, which may potentiate the cardiac toxicity of 

digitalis. Magnesium replacement may be beneficial. 

C. Arrhythmias 

(See also Chapter 35.) For symptomatic bradycardia or second- or third-degree 

atrioventricular block, atropine, 0.5-1.0 mg intravenously, repeated every 5 minutes if 

there is no response, may be helpful. The total dose should not exceed 2 mg. A 

transcutaneous pacemaker may be used. 

For ventricular ectopic beats, both lidocaine and phenytoin are effective, although 

lidocaine is easier to use. Give 1 mg/kg as an intravenous bolus, followed by 1-4 

mg/min by continuous infusion. Phenytoin and the new prodrug fosphenytoin are also 

effective at suppressing atrial and ventricular ectopy. 

Avoid direct current (DC) countershock, because it may cause serious conduction and 

rhythm disturbances including asystole or ventricular fibrillation in patients with digitalis

toxicity. If countershock is unavoidable, use the lowest voltage that is effective. 

D. Drug Removal 

Dialysis or hemoperfusion is of no value for digoxin because of its large volume of 

distribution. Digitoxin may be effectively removed by hemoperfusion and by repeated 

doses of activated charcoal or cholestyramine, which interrupt enterohepatic 

recirculation. 

E. Digitalis Antibodies 

Digitalis-specific Fab fragment antibodies are extremely effective and are indicated for 

patients with serious arrhythmias or severe hyperkalemia. Each vial of Digibind binds 

0.6 mg of digoxin. Toxicity usually is reversed within 5-10 minutes, and the 

digoxin-antibody complex is excreted in the urine. After Digibind administration, serum 

digoxin levels are elevated owing to cross-reaction of the complex in the assay. For 

information on Digibind use and how to calculate the dosage, see Table 45-12. When 

the ingested amount is unknown, 5-10 vials may be given initially. 

Disposition 

All patients with digitalis and other cardiac glycoside poisoning require hospitalization in 

a cardiac-monitored unit for observation and treatment. Onset of cardiac toxicity may be 

delayed for 6-12 hours after acute ingestion. 

Barron SW et al: Advances in the management of digoxin toxicity in the older patient. 

Drugs Aging 1997;10:18. [PMID: 9111705] (Review of digoxin toxicity and treatment in 

the elderly.) 

DiDomenico RJ et al: Analysis of the use of digoxin immune Fab for the treatment of 

non-life-threatening digoxin toxicity. J Cardiovasc Pharmacol Ther 2000;5:77. [PMID: 

11150387] (Analysis of the use of digoxin immune Fab in the treatment of digoxin 

toxicity.) 

Gupta A et al: A case of nondigitalis cardiac glycoside toxicity. Ther Drug Monit 

1997;19:711. [PMID: 9421116] (Case study of cardiac glycoside poisoning from 

oleander.) 

Ma G et al: Electrocardiographic manifestations: digitalis toxicity. J Emerg Med 

2001;20:145. [PMID: 11207409] (Review of the electrocardiographic manifestations of 

digitalis toxicity.) 

CAUSTICS & CORROSIVES 


• Includes both acids and alkalis. 

• Ingestion can result in coagulative (acids) or liquefactive (alkalis) necrosis of tissue. 

• Treatment is supportive and includes dilution of the material with water, milk, or normal

saline. 

• Endoscopy is recommended to assess degree of damage. 


Corrosive agents include strong agents, alkalis (caustics), oxidizing agents, and other 

chemicals. They are commonly used in household cleaners (Table 45-13). 

A. Acids 

Toilet bowl cleaners, bleaches, battery acid, soldering flux (zinc chloride), and many 

industrial sources contain acids. 

B. Alkalis 

Lye (drain cleaners, reagent tablets used to detect glucose in urine [Clinitest, many 

others]), ammonia, and industrial-grade detergents contain caustic alkalis. 

The mechanism of toxicity is tissue destruction resulting from coagulative (acids) and 

liquefactive (alkali) necrosis and heat injury during neutralization of the chemical by 

water in body tissues. Most household bleaches and detergents are dilute and do not 

cause severe corrosive burns. Concentrated alkalis are common in the household, 

especially in granular form or strongly concentrated liquids (pH > 12.5), and these cause 

severe tissue damage. Corrosive burns may lead to airway or intestinal edema and 

obstruction, mucosal perforation, and (later) stricture formation. 


Symptoms are almost always present with significant ingestion and include mouth and 

throat pain, dysphagia, drooling, and substernal or abdominal pain. However, significant 

gastric or esophageal burns may be present without oral lesions. Skin and eye burns 

may also occur (Chapters 31 and 43). 

Treatment 


Dilute the corrosive material with water, normal saline, or milk (8 ounces for adults, 4 

ounces for children). Do not give neutralizers, because they may increase the heat of 

hydration and worsen subsequent tissue destruction. 

Do not induce vomiting, because this may produce further tissue damage. Activated 

charcoal is contraindicated because it can interfere with endoscopy. 

After liquid corrosive ingestion, careful insertion of a nasogastric tube and gastric lavage 

is recommended by some gastroenterologists. 

B. Endoscopy 

Diagnostic endoscopy should be performed in any symptomatic patient with or without 

oral burns. Endoscopy may not be necessary in asymptomatic patients, although this 

remains controversial.

C. Pharmacologic Treatment 

No studies support the efficacy of corticosteroids in preventing stricture formation, and 

the authors do not recommend them. Esophageal or gastric perforation is a 

contraindication to their use. Antibiotics are indicated for suspected perforation or 

infection. 

Disposition 

Hospitalize all patients known or thought to have ingested or inhaled (aspirated) caustic 

or corrosive agents with a potential for tissue damage. Skin burns may be managed on 

an outpatient basis if they are of mild to moderate severity (Chapter 43). Eye injuries 

should be copiously irrigated and evaluated by an ophthalmologist (Chapter 31). 

Gupta SK et al: Is esophagogastroduodenoscopy necessary in all caustic ingestions? J 

Pediatr Gastroenterol Nutr 2001;32:50. [PMID: 11176325] (Chart review of caustic 

ingestions evaluating the need for esophagogastroduodenoscopy depending on the 

initial presentation.) 

Millar AJ et al: Detection of caustic esophageal injury with technetium 99m-labelled 

sucralfate. J Pediatr Surg 2001;36:262. [PMID: 11172412] (Prospective study 

evaluating radiolabeled sucralfate in the evaluation of caustic injury.) 

COCAINE & LOCAL ANESTHETICS 


• Overdose of local anesthetics causes initial central nervous system excitement and 

seizures, followed by central nervous system depression. 

• Cocaine intoxication causes sympathetic hyperactivity and can result in severe 

hypertension, myocardial ischemia, and even aortic dissection. 

• Treatment is supportive and should address any resulting cardiac or central nervous 

system symptoms. 


Cocaine is a natural extract from coca leaves. It is a local anesthetic that also has 

sympathomimetic effects. Overdoses of all local anesthetics are manifested by initial 

excitement and seizures, followed by central nervous system depression. Peak effects 

occur rapidly, usually in less than 1 hour. 

A. Cocaine 

All significant overdoses are associated with symptoms. Intravenous injection of cocaine 

and inhalation (smoking) of freebase, or crack, cocaine may result in very high levels. 

Cocaine causes euphoria, excitement, and restlessness; toxic psychosis, seizures, 

hypertension, tachycardia, dysrhythmias, and hyperthermia may follow absorption of 

toxic amounts. Chest pain, myocardial ischemia and infarction, and aortic dissection 

have occurred. Blood cocaine and metabolite concentrations vary widely and do not

predict the development of clinical findings. 

B. Local Anesthetics 

Common local anesthetics such as lidocaine, mepivacaine, and procaine have no toxic 

effects in usual doses. With excessive doses, they cause tremors, anxiety, and 

restlessness, followed by seizures and then cardiorespiratory depression. Toxic doses 

for these drugs vary and depend on the route and duration of administration. Maximum 

recommended doses for infiltration anesthesia in adults are lidocaine, 4.5 mg/kg; 

bupivacaine, 2 mg/kg; and procaine, 7 mg/kg. Larger doses may be tolerated if 

epinephrine has been included in the preparation. 

Treatment 



previously. 

B. Treatment of Cocaine Overdose 

Treat manifestations of sympathetic hyperactivity in the same way as for amphetamine 

overdose. Because effects peak rapidly, measures to enhance elimination of the drug 

from the body are unnecessary. 

If a patient is thought to have ingested packets of cocaine (body packers), whole bowel 

irrigation should be instituted immediately and a surgical consult obtained for removal of 

the packets. 

Patients with chest pain suggestive of ischemia should be evaluated with a 12-lead 

ECG and considered for admission to rule out myocardial infarction. Myocardial 

infarction may be present even with a normal ECG. Patients with a new onset of 

seizures may need CT scanning to rule out intracranial hemorrhage. 

C. Treatment of Overdose with Common Local Anesthetics 

Treatment consists of supportive measures with particular attention to respiratory 

depression and hypotension. Seizures are usually brief and easily treatable with 

benzodiazepines and usually do not require other anticonvulsant therapy. 

Disposition 

Hospitalize patients with cocaine or local anesthetic poisoning manifested by multiple 

seizures, hyperthermia, ischemic chest pain, or severe hypertension. 

Blaho K et al: Blood cocaine and metabolite concentrations, clinical findings, and 

outcome of patients presenting to an ED. Am J Emerg Med 2000;18:593. [PMID: 

10999576] (Prospective study of cocaine and its metabolites correlated with clinical 

findings and outcome.) 

Dribben WH et al: A pilot study to assess the safety of dobutamine stress 

echocardiography in the emergency department evaluation of cocaine-associated chest 

pain. Ann Emerg Med 2001;38:42. [PMID: 11423811] (Prospective case series of

patients with cocaine-associated chest pain, evaluating the efficacy of dobutamine 

stress echocardiography.) 

Naguib M et al: Adverse effects and drug interactions associated with local and regional 

anaesthesia. Drug Saf 1998;18:221. [PMID: 9565736] (Review of the adverse effects 

with the use of local and regional anesthesia.) 

Olmedo R et al: Is surgical decontamination definitive treatment of "body-packers"? Am 

J Emerg Med 2001;19:593. [PMID: 11699007] (Case reports of body packers and their 

medical management.) 

Singh R et al: Local anaesthetics: an overview of current drugs. Hosp Med 1998;59:880. 

[PMID: 10197123] (Review of the pharmacology and side effects of local anesthetics.) 

Steinhauer JR et al: Spontaneous coronary artery dissection associated with cocaine 

use: a case report and brief review. Cardiovasc Pathol 2001;10:141. [PMID: 11485859] 

(Case report and literature review of coronary artery dissection associated with cocaine 

use.) 

CYANIDE 


• Cyanide acts as a cellular asphyxiant that inhibits the use of oxygen by the body's 

tissues. 

• Symptom onset is rapid and ultimately results in hypotension. 

• In mild cases, supportive care including 100% oxygen is adequate. 

• If poisoning is severe, a cyanide antidote kit of sodium nitrite, amyl nitrite, and sodium 

thiosulfate should be used. 

• Cyanide levels are not readily available and should not be used to determine 

treatment. 

• All patients with cyanide intoxication should be hospitalized. 


Fumigants, hydrocyanic acid gas used in industry, amygdalin (Laetrile) in fruit pits (eg, 

apricot, cherry, peach), and burning plastics and fabrics are sources of cyanide. Sodium 

nitroprusside used to treat severe hypertension undergoes a biotransformation to 

methemoglobin and cyanide and can be a source of poisoning. Cyanide poisoning has 

also resulted from metabolism of ingested acetonitrile in an artificial nail-removing 

solution. 

Cyanide is a rapidly absorbed cellular asphyxiant that inhibits the cytochrome oxidase 

system for oxygen utilization in cells. The inability of the body's tissues to use oxygen 

leads to anaerobic metabolism and a profound metabolic acidosis. Death may occur 

within minutes after a dose of 200 mg. In fatal poisoning, blood levels usually exceed 

1-2 ug/mL. Cyanide gas is much more toxic than salt forms because of its rapid

absorption, and its effects are usually immediate. 


Significant poisoning is associated with rapidly developing symptoms, including 

headache, nausea and vomiting, anxiety, confusion, and collapse. Initial hypertension 

and tachycardia progress to hypotension, bradycardia, and apnea. The smell of bitter 

almonds is present occasionally. The skin may appear pink. The measured oxygen 

saturation of venous blood may be elevated as a result of failure of oxygen uptake by 

the tissues. 

Treatment 

Note: Act quickly. To be successful, treatment must be started within 5-10 minutes in 

cases of severe poisoning. In witnessed cases of cyanide poisoning, begin therapy 

without waiting for symptoms. 


Supportive care only, including 100% oxygen, may be given to patients with mild to 

moderate symptoms. Close observation is needed because the antidote may need to be 

administered if the patient deteriorates. If activated charcoal is available, administer it at 

once. Although its binding affinity for cyanide is low, it can adsorb a lethal dose. 

B. Antidote Administration 

Every emergency department should have a prepackaged cyanide antidote kit 

containing sodium nitrite, 300 mg in 10-mL ampules (2); sodium thiosulfate, 12.5 g in 

50-mL ampules (2); amyl nitrite inhalant, 0.3 mL (12 Aspirols); and syringes and 

stomach tube (Table 45-14). 

1. Nitrites—Nitrites produce methemoglobin, which binds free cyanide. 

1. Break a capsule of amyl nitrite under the patient's nose for deep inhalation while 

starting an intravenous infusion of sodium nitrite and thiosulfate. A new ampule should 

be used every 3 minutes until intravenous medication has begun. 

2. Give sodium nitrite, 300 mg (10-mL ampule) intravenously for adults; for children, 

0.12- 0.33 mL/kg up to 10 mL with a normal hemoglobin concentration (for alternate 

dosing in a child with abnormal hemoglobin, consult Poisindex). Caution: Do not 

overtreat; fatal methemoglobinemia has resulted from overzealous use of nitrites. After 

initial therapy, guide subsequent treatment by monitoring symptoms and signs. The goal 

of nitrite therapy is a methemoglobin level of 25-30%. 

2. Thiosulfate—Sodium thiosulfate is a cofactor in the rhodanese enzyme conversion 

of cyanide to thiocyanate, which is less toxic and readily excreted. Give thiosulfate, 50 

mL of a 25% solution in adults and 1.65 mL/kg of a 25% solution in children, 


C. Vitamin B 12A

Vitamin B 12A (hydroxocobalamin) has been successfully used in Europe. 

Hydroxocobalamin reverses cyanide toxicity by combining with cyanide to form 

cyanocobalamin (Vitamin B 12A ). The usual dose is 50 mg/kg; a single dose of 5 g is 

usually sufficient. 

D. Hyperbaric Oxygen 

Hyperbaric oxygen may be considered in cases that are refractory to standard care, 

including use of the antidote kit. It has not been proven, however, to have any significant 

clinical advantage over 100% oxygen. 

E. Treatment for Persistent Symptoms 

If symptoms of cyanide poisoning persist, the sodium nitrite and sodium thiosulfate can 

be repeated at half of the original dose. 

Disposition 

All patients with suspected or documented cyanide poisoning should be hospitalized. 

Chin RG et al: Acute cyanide poisoning: a case report. J Emerg Med 2000;18:441. 

[PMID: 10802422] (Case report and review of the treatment of cyanide poisoning.) 

Mueller M et al: Delayed cyanide poisoning following acetonitrile ingestion. Postgrad 

Med J 1997;73:299. [PMID: 9196706] (Case report of cyanide toxicity from acetonitrile 

ingestion.) 

Sauer SW et al: Hydroxocobalamin: improved public health readiness for cyanide 

disasters. Ann Emerg Med 2001;37:635. [PMID: 11385334] (Review of the use of 

hydroxocobalamin to treat cyanide poisoning.) 

Suchard JR et al: Acute cyanide toxicity caused by apricot kernel ingestion. Ann Emerg 

Med 1998;32:742. [PMID: 9832674] (Case report of cyanide toxicity from ingestion of an 

apricot kernel.) 

DRUG-INDUCED METHEMOGLOBINEMIA 


• Methemoglobinemia cannot bind oxygen or carbon dioxide. 

• Symptoms correlate with the degree of methemoglobinemia and can include 

asymptomatic cyanosis, dyspnea, and severe central nervous system depression. 

• Treatment includes methylene blue, which can reduce methemoglobin levels in less 

than 1 hour. 


Hemoglobin becomes methemoglobin when iron is oxidized from the ferrous to the ferric 

form. Methemoglobin is a dark chocolate color and can no longer bind oxygen or carbon

dioxide. Conversion of hemoglobin to methemoglobin decreases both delivery of oxygen 

to the tissues and removal of carbon dioxide, and tissue hypoxia may result. 

Methemoglobin is produced endogenously in small quantities and is reduced by 

methemoglobin reductase; normally, less than 1-2% of hemoglobin is methemoglobin. 

Methemoglobinemia is caused by various oxidant drugs and poisons, including nitrites 

(food preservatives, some well water), nitrous gases, chloroquine and primaquine, 

phenazopyridine (Pyridium, others), sulfonamides, sulfones, aniline dye derivatives, 

phenacetin, dapsone, local anesthetics, and nitrobenzenes. 


Symptoms correlate with the degree of methemoglobinemia. At concentrations of 1.5 

g/dL (about 10% of the total hemoglobin), patients may seek care for cyanosis without 

any shortness of breath. When the level of methemoglobin exceeds 15% of total 

hemoglobin, blood appears chocolate brown when it is dripped onto filter paper. The 

exact concentration of methemoglobin in the blood may be determined 

spectrophotometrically. However, the PO 2 and calculated oxyhemoglobin on routine 

arterial blood gases are falsely normal, and the measured saturation by pulse oximetry 

is unreliable. 

Conversion of up to 25% of normal hemoglobin to methemoglobin is usually not 

associated with clinical findings other than peripheral and perioral cyanosis, although 

anxiety, headache, weakness, and lightheadedness can develop. At conversion levels 

of 35-40%, patients experience lassitude, fatigue, and dyspnea. At conversion levels 

exceeding 60%, coma and death may occur as a result of severe central nervous 

system depression. Anemia, acidosis, respiratory compromise (eg, chronic obstructive 

pulmonary disease), and cardiac disease may make patients more symptomatic than 

expected for a given methemoglobin level. 

Treatment 



previously. 

B. Oxygen 

Oxygen per se does not affect the methemoglobin level, but it should be given to 

improve tissue oxygenation pending the start of specific therapy. Give oxygen, 5-10 

L/min, by mask or nasal cannula; in comatose or severely acidotic patients, give 100% 

oxygen by rebreathing mask or endotracheal tube. Continue oxygen therapy for 1-2 

hours after giving methylene blue (see below). Always give oxygen if the percentage of 

methemoglobin is higher than 40% or if the patient has severe symptoms. 

C. Methylene Blue 

Methylene blue is a specific antidote for methemoglobinemia. The dose is 1-2 mg/kg, or 

0.1 mL/kg of a 1% solution, given intravenously over 5 minutes. The dose may be 

repeated at 1 mL/kg once after 1 hour, but the amount specified should not be 

exceeded, because an overdose of methylene blue can also cause

methemoglobinemia. Methylene blue should reduce methemoglobin levels significantly 

in less than 1 hour. Patients with glucose-6-phosphate dehydrogenase deficiency may 

not respond to methylene blue and may experience hemolysis. Exchange transfusions 

may be required in these patients. Note: Methylene blue is contraindicated in patients 

with methemoglobinemia associated with nitrite treatment of cyanide poisoning because 

it may cause release of cyanide, resulting in toxic concentrations. 

D. Removal of Source 

Discontinue the offending drug or chemical. 

Disposition 

Symptomatic patients with methemoglobinemia should be hospitalized for treatment. 

Some agents (eg, dapsone) may produce prolonged or recurrent methemoglobinemia 

over several days. 

Griffey RT et al: Cyanosis. J Emerg Med 2000;18:369. [PMID: 10729678] (Discussion of 

the diagnosis, evaluation, and management of methemoglobinemia.) 

Khan NA et al: Methemoglobinemia induced by topical anesthesia: a case report and 

review. Am J Med 1999;318:415. [PMID: 10616167] (Case report and overview of the 

treatment of methemoglobinemia caused by topical anesthesia.) 

Wright RO et al: Methemoglobinemia: etiology, pharmacology, and clinical 

management. Ann Emerg Med 1999;34:646. [PMID: 10533013] (Review of 

methemoglobinemia and its cause, pharmacology, and clinical management.) 

ETHANOL & OTHER ALCOHOLS 


• Ethanol, methanol, ethylene glycol, and isopropanol are all central nervous system 

depressants. Levels of all alcohols should be obtained, although the level may not 

predict the severity of the intoxication. 

• Treatment of ethanol intoxication is supportive and includes glucose and thiamine. 

• Treatment of methanol and ethylene glycol ingestions includes either fomepizole or an 

ethanol drip to inhibit the formation of toxic metabolites. 

• Treatment of isopropanol ingestion is supportive and may include dialysis if the level is 

greater than 400 mg/dL. 


Methanol, ethylene glycol, and even isopropanol have been used as cheap substitutes 

for ethanol, although this practice is less common now than formerly. These alcohols 

may also be ingested accidentally or in suicide attempts. All are capable of causing 

intoxication similar to that produced by ethanol, and all can widen the osmolar gap (see 

Table 45-4). Additional toxic effects can occur as a result of the metabolism of ethylene

glycol and methanol. 

1. Ethanol 

Ethanol is a central nervous system depressant. It is metabolized by alcohol 

dehydrogenase (in most cases by fixed-rate, zero-order kinetics) at a rate of about 7-10 

g/h, resulting in a decrease in blood alcohol concentration of 20-30 mg/dL/h. The rate of 

elimination among individuals varies, as does tolerance. In the United States, legal 

impairment for purposes of driving is generally defined as blood (or breath) ethanol 

concentrations above 80-100 mg/dL; coma usually occurs with levels exceeding 300 

mg/dL, except in chronic ethanol abusers who have developed tolerance. 


Symptoms of alcohol intoxication include ataxia, dysarthria, depressed sensorium, and 

nystagmus. The breath may smell of alcohol, but this finding is neither sensitive nor 

specific. Alcohol intoxication is frequently seen with trauma and can contribute 

significantly to morbidity and mortality. Coma and respiratory depression with 

subsequent pulmonary aspiration due to intoxication is also a common cause of illness 

and death. Laboratory diagnosis may be aided by direct determination of the blood 

ethanol concentration or by its estimation from the calculated osmolar gap (see Table 

45-4). 

Treatment 



previously. Supportive care is the primary mode of therapy. Special care should be 

taken to prevent aspiration. 

B. Thiamine and Glucose 

Give thiamine and glucose as needed. Give thiamine, 100 mg intramuscularly or 

intravenously, to prevent Wernicke syndrome. Check for hypoglycemia, because 

ethanol inhibits gluconeogenesis, and give glucose, 50 mL of a 50% solution (25 g of 

glucose) intravenously over 3-4 minutes, if needed. 


Diagnose and correct disorders such as hypovolemia, hypothermia, infection, trauma, or 

gastrointestinal tract bleeding. Do not use fructose therapy or forced diuresis. 

Disposition 

Hospitalize patients with ethanol poisoning if ethanol intoxication has caused 

abnormalities that would by themselves require hospitalization (eg, obtundation, 

seizures, refractory hypoglycemia). 

2. Methanol 

Methanol is a highly toxic alcohol found in a variety of commercial products, including

paint stripper, antifreeze, automobile windshield washer fluid, and solid alcohols (Sterno 

Canned Heat, many others). It is metabolized by alcohol dehydrogenase to 

formaldehyde and formic acid. An osmolar gap and metabolic acidosis with an anion 

gap result. Optic neuritis (caused by formate) that results in blindness has been 

described after overdose. Early diagnosis is essential, because permanent blindness or 

death may result if methanol intoxication is left untreated. 


The major clinical effect of methanol before it is metabolized is central nervous system 

depression. As the methanol is metabolized to formic acid (this may be delayed 6-18 

hours if ethanol has also been ingested), visual disturbances invariably occur (blurred 

vision or hazy, snowlike patterns), along with hyperemia of the optic disk, headache, 

dizziness, and breathlessness. In severe toxicity, seizures and coma may occur. 

Examination shows variable degrees of central nervous system dysfunction (agitation 

and intoxication to coma). Pupillary dysfunction has been shown to be a strong predictor 

of mortality. The retinas may appear suffused and bright red. Early after ingestion, the 

only finding may be inebriation with an elevated osmolar gap. Later, severe metabolic 

acidosis occurs. 

Treatment 

If serious intoxication is suspected, begin therapy even before receiving the results of 

blood methanol concentration determination. 



previously. The main objective of treatment is to limit the accumulation of formate by 

blocking the metabolism of methanol by alcohol dehydrogenase. Two drugs have been 

shown to be effective, fomepizole (Antizol) and ethanol. 

1. Fomepizole—Fomepizole is approved by the FDA for the treatment of ethylene 

glycol poisoning and is also effective in methanol intoxication. Fomepizole, like ethanol, 

inhibits alcohol dehydrogenase and the formation of toxic metabolites. Give a loading 

dose of 15 mg/ kg intravenously, followed by 10 mg/kg every 12 hours for 48 hours. 

After 48 hours the dose is increased to 15 mg/kg every 12 hours until the level of 

methanol is undetectable or both symptoms and acidosis resolve and the level is less 

than 20 mg/dL. Fomepizole has several advantages over ethanol infusion, including 

ease of dosing, lack of central nervous system depression, and no requirement for 

constant serum monitoring because of its reliable therapeutic concentration. Ethanol 

infusion can also be used if fomepizole is unavailable. 

2. Ethanol—Ethanol is metabolized in preference to methanol by alcohol 

dehydrogenase, thus blocking further metabolism of methanol. The loading dose of 

ethanol for an average 70-kg adult is 0.7 g/kg (2 mL/kg of 100-proof [50%] ethanol 

orally; or 7 mL/kg of 10% ethanol intravenously). Maintain continuous infusion of 

0.07-0.1 g/kg/h to keep blood concentration of ethanol between 100 and 200 mg/dL. 

These levels are sufficient to produce clinically evident intoxication. Ethanol may be

given intravenously or orally, but intravenous solutions must be at concentrations of 

10% or less to prevent hypertonicity of the solution. Monitor and maintain adequate 

ventilation during the infusion of ethanol. 

B. Other Measures 

Correct metabolic acidosis with sodium bicarbonate; keep the pH at 7.2 or higher. 

Because folate deficiency increases the toxicity of methanol (in animals), folate 

replacement may be helpful. It can be given as a 50-mg intravenous dose every 4 hours 

for 5 doses, then once a day. 

C. Hemodialysis 

Hemodialysis is indicated for methanol blood concentrations higher than 50 mg/dL and 

in patients with severe acidosis, high formate levels, seizures, optic changes, or mental 

status changes; it should be started as soon as possible. The ethanol infusion must be 

adjusted to replace ethanol lost in dialysis (increase ethanol to 0.15-0.2 g/kg/h). 

Fomepizole is also dialyzed, and dosing should be increased to every 4 hours during 

dialysis. 

Disposition 

Hospitalize all patients with suspected or documented methanol poisoning. If the 

osmolar gap and anion gap are both normal 1 hour after suspected injection, serious 

intoxication is unlikely. 

3. Ethylene Glycol 

Ethylene glycol is a common ingredient of deicers and antifreeze products. It is sweet 

tasting, and some preparations are attractively colored. Following ingestion, it is 

metabolized by alcohol dehydrogenase to glycolate and ultimately to oxalate, which 

precipitates with calcium to form calcium oxalate crystals. Symptoms may occur within 

30 minutes or after a delay of several hours. 


The clinical course of ethylene glycol intoxication can be divided into 3 phases. The first 

phase occurs less than 1 hour after ingestion and is characterized by central nervous 

system depression. The second phase affects the cardiopulmonary system, and heart 

failure or pulmonary edema can occur approximately 12 hours after ingestion. The final 

phase occurs 24-72 hours after ingestion and is characterized by renal tubule necrosis, 

flank pain, hematuria, and renal failure. Visual symptoms are usually not present, and 

the ocular fundi appear normal (as distinguished from their appearance in methanol 

poisoning). An osmolar gap is present, and after metabolism to toxic products, a severe 

acidosis usually occurs, and crystals of calcium oxalate may be seen in the urine. The 

urine may be fluorescent under an ultraviolet lamp owing to the fluorescent often added 

to commercial antifreeze products. 

Treatment 

Fomepizole is the treatment of choice, although ethanol can be used if fomepizole is

unavailable. The dosing is the same as in methanol poisoning. Hemodialysis is now 

indicated only in patients with severe acidosis or abnormal renal function; the ethylene 

glycol level by itself does not determine the need for dialysis. 

Disposition 

Hospitalize all patients with suspected or documented ethylene glycol intoxication. 

4. Isopropanol 

Isopropanol is a common ingredient in many household products, especially rubbing 

alcohol. It causes intoxication with central nervous system and cardiac depression; 

blood concentrations of 150 mg/dL are frequently associated with deep coma. It is 

metabolized by alcohol dehydrogenase to acetone, although most of the clinical effects 

of isopropanol intoxication are due to the parent compound. Both the alcohol and its 

metabolite cause an elevated osmolar gap, but acidosis is rare. The odor—and 

acetonemia without acidosis—is characteristic of isopropanol intoxication. 

Treatment 

Treatment is primarily supportive and similar to that for ethanol intoxication. 

Hemodialysis is indicated for patients with an isopropanol level greater than 400 mg/dL 

and significant central nervous system depression. 

Disposition 

Hospitalize patients with isopropanol intoxication who have significant signs (eg, stupor, 

coma, or hypotension). 

Abramson S et al: Treatment of the alcohol intoxications: ethylene glycol, methanol and 

isopropanol. Curr Opin Nephrol Hypertens 2000;9:695. [PMID: 11128434] (Review of 

diagnosis and treatment of intoxication with ethylene glycol, methanol, and isopropanol.) 

Barceloux DG et al: American Academy of Clinical Toxicology practice guidelines on the 

treatment of ethylene glycol poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol 1999; 

37:537. [PMID: 10497633] 

Brent J: Current management of ethylene glycol poisoning. Drugs 2001;61:979. [PMID: 

11434452] (Review of the treatment of ethylene glycol poisoning.) 

Sivilotti ML et al: Toxicokinetics of ethylene glycol during fomepizole therapy: 

implications for management. For the Methylpyrazole for Toxic Alcohols Study Group. 

Ann Emerg Med 2000;36:114. [PMID: 10918102] (Evaluation of drug concentration data 

obtained in the ethylene glycol arm of the Methylpyrazole for Toxic Alcohols trial.) 

HEAVY METALS


• Signs and symptoms of heavy metal ingestion can vary widely and include all major 

organ systems. 

• Levels can be obtained and in many cases guide treatment. 

• Chelation therapy is available for iron, lead, arsenic, and mercury poisoning. 

1. Iron 


Iron poisoning results primarily from ingestion of mineral supplements containing 

divalent iron: ferrous sulfate (20% elemental iron), ferrous fumarate (33%), and ferrous 

gluconate (12%). 

Absorption of iron is dose related and may increase dramatically with overdose levels, 

especially when the corrosive action of iron has damaged the intestinal mucosal barrier. 

Iron also causes vasodilatation and disruption of cellular electron transport. The 

elemental iron equivalent should be used when toxic doses are being estimated; an 

amount higher than 20-30 mg/kg causes toxicity, and amounts over 60 mg/kg are 

potentially lethal. Blood concentrations of iron may assist in the diagnosis of acute 

toxicity but may be unreliable owing to concurrent absorption of iron and distribution in 

the tissues. A peak concentration in serum often occurs 4-5 hours after ingestion. 

Serum concentrations over 400 ug/dL are potentially serious, and levels over 1000 

ug/dL are associated with severe poisoning. 


Four stages of intoxication are commonly described: 

1. Severe nausea and vomiting and abdominal pain occur within 1-4 hours. 

Hyperglycemia and leukocytosis are common. In severe cases, hemorrhagic 

gastroenteritis, shock, acidosis, and coma may follow. A plain film of the abdomen may 

show radiopaque iron tablets. 

2. During the next period, which lasts 6-12 hours and sometimes up to 24 hours, the 

patient may appear relatively well or may even improve. Patients with significant 

ingestions, however, can still have progressive, silent systemic deterioration. 

3. A stage of shock, acidosis, coagulopathy, and hypoglycemia may occur 12-24 hours 

after ingestion of significant amounts of iron and reflects a severe course and poor 

outlook. Serum iron concentration at this stage may be deceptively low, because most 

absorbed iron has been taken up by tissues. 

4. The last stage is characterized by hepatic poisoning with possible progression to 

hepatic failure.

Treatment 



previously. Empty the stomach by induced emesis with syrup of ipecac or gastric 

lavage. For serious or massive ingestion, enhance removal or iron from the 

gastrointestinal tract with whole bowel irrigation. Activated charcoal is not effective. 

B. Chelation Therapy 

Intravenous chelation with deferoxamine is the treatment of choice when symptoms of 

iron poisoning are evident or when the serum iron level is over 400 ug/dL (Table 45-15). 

The iron-deferoxamine complex is excreted in the urine and has a pink color. If urinary 

output is inadequate, the complex may be removed by peritoneal dialysis or 

hemodialysis. The deferoxamine intramuscular challenge is no longer recommended, 

and any patient with a significant ingestion who appears toxic or has a serum iron level 

greater than 400 mg/dL should receive treatment. 

Observe the patient for several hours when ingestion of significant amounts of iron is 

suspected, because symptoms in the initial phase may be deceptively mild. 

Disposition 

Hospitalize all patients with suspected or documented cases of iron poisoning. If 

patients remain asymptomatic, with a negative abdominal x-ray and no elevation of 

white blood cell count or blood glucose 6 hours after ingestion, they may be discharged 

to home care. 

2. Lead 


Inorganic lead is found in paint in older homes; pottery glazes containing lead (not used 

commercially in the United States); and fumes from welding, smelting, and battery 

manufacturing. Gasoline may contain organic lead (tetraethyl lead). Most adult cases of 

lead poisoning are due to inhalation exposure; chronic ingestion is the most common 

cause of lead poisoning in children. 

Lead is well absorbed from the respiratory tract and usually poorly absorbed from the 

gastrointestinal tract; target organs are bone, kidney, bone marrow, and the nervous 

system. Lead toxicity usually occurs with chronic absorption of more than 0.4-0.5 mg/dL; 

a single chip of lead-based paint may contain 50-100 mg of lead. Most lead poisoning 

results from chronic, subacute exposure rather than acute exposure to large amounts. 


Early symptoms of lead poisoning are nonspecific, for example, listlessness, irritability, 

headache, abdominal pain, and constipation. Subtle behavioral changes and intellectual 

impairment may occur in children. With severe toxicity, lethargy, clumsiness, ataxia, 

seizures, and coma occur. Peripheral neuropathy (lead palsy)—characterized chiefly by

extensor muscle weakness with minimal sensory loss—occurs after prolonged chronic 

exposure and occurs more frequently in adults than in children. Exposure to organic 

lead compounds produces a more dramatic acute encephalopathy than does exposure 

to inorganic lead. Delirium and hallucinations are associated symptoms. 

The best standard diagnostic tool is the concentration of lead in the blood. (The 

concentration in the hair is not useful.) Up to 25 ug/dL is considered normal but may in 

fact be toxic over long periods, especially in children. Over 70 ug/dL is serious and 

usually requires hospitalization. Plain films of the abdomen may show radiopaque 

(ingested) lead in the gastrointestinal tract. Microcytic anemia may be present, and 

when it is associated with basophilic stippling of red blood cells on the peripheral blood 

smear, it strongly suggests lead poisoning. In children, so-called lead lines can be 

visualized radiographically as opacities at the metaphyseal plate; these lines represent 

toxic effects of lead on bone growth rather than lead deposition in bone. 

Treatment 



previously. Consider whole bowel irrigation if a lead foreign body has been ingested. 


(See Tables 45-15 and 45-16.) Treatment depends on blood lead concentration; if the 

hematocrit is less than 20%, adjust the lead level as shown in the following equation: 

Proceed with treatment as outlined in Table 45-16. Because of concerns that lead may 

be redistributed to the brain with an edetate calcium disodium (EDTA) challenge, 

toxicologists no longer recommend this practice. Several chelating agents can be used 

to treat lead poisoning. 2,3-Dimercaptosuccinic acid (DMSA) (Succimer) is now FDA 

approved for oral chelation in children with lead levels greater than 45 mg/dL and can 

also be used in adults. Dimercaprol (BAL) and EDTA are still used as well; penicillamine 

is a less effective chelating agent, but is also less expensive. 

Disposition 

Hospitalize patients with symptoms of severe lead poisoning or blood lead 

concentrations higher than 70 ug/dL. 

3. Arsenic 


Many insecticides, rodenticides, and wood preservatives are sources of trivalent 

arsenic. The much less toxic pentavalent organic arsenic found in shellfish and other 

foods produces positive urine screens for arsenic but is not associated with clinical

toxicity. Highly toxic arsine gas is produced by burning arsenic-containing ores and is 

used in the electronics industry. 

Arsenic is absorbed mainly through the gastrointestinal tract but may be absorbed 

through intact skin or after inhalation, binds avidly to tissue proteins, and accumulates in 

tissue. The lethal dose of trivalent arsenic is about 100-300 mg in an adult; the 

pentavalent form is rapidly excreted and less toxic. 



1. Arsenic salt ingestion— 

a. Acute poisoning—Symptoms and signs include crampy abdominal pain, vomiting, 

profuse watery diarrhea, a burning sensation in mucous membranes, conjunctivitis, 

tremor, hypotension, tachycardia, and seizures. A garlic odor is sometimes noted on the 

breath. Abdominal plain films may show radiopaque material in the gut. Periorbital 

edema may occur after 1-2 days. 

b. Chronic poisoning—Symptoms include stocking-glove peripheral sensory and 

motor neuropathy, malaise, anorexia, alopecia, anemia, and stomatitis. These 

symptoms are also noted during recovery from an episode of acute poisoning. 

2. Arsine gas inhalation—Arsine gas is highly toxic and causes rapid intravascular 

hemolysis and renal failure. Other characteristics of arsenic toxicity are often not seen. 


Measurement of 24-hour urinary arsenic excretion levels is useful but can be 

misleading, because ingestion of shellfish containing nontoxic forms of arsenic may 

cause transient elevation of arsenic levels. The chief usefulness of this measurement 

lies in monitoring the response to chelation therapy. In chronic poisoning, arsenic 

concentrations are elevated in the hair and nails. 

Treatment 

A. Acute Poisoning 


previously. Perform gastric lavage. Give DMSA (if the patient can tolerate oral 

medications) or BAL (see Table 45-15), and continue until the urine arsenic level is less 

than 50 ug/24 h. 

B. Chronic Poisoning 

Management usually consists of prevention of further arsenic absorption and 

gastrointestinal decontamination. Penicillamine is no longer recommended. 

C. Arsine Gas Inhalation 

Blood transfusion may be necessary for severe hemolysis. Give adequate fluids to 

prevent renal hemoglobin deposition. Chelation therapy is of no value for acute 

exposure to arsine gas.

Disposition 

Hospitalize all patients with suspected or documented arsenic poisoning. 

4. Mercury 


Elemental mercury vapor is produced in the course of various manufacturing 

procedures, during repair of mercury-containing instruments, and when the liquid metal 

is heated (eg, home ore processing). Inorganic mercury salts are present in 

disinfectants and older cathartics and diuretics. Organic mercury is found in fungicides 

used in seed grain and in environmentally contaminated seafood. 

Mercury poisoning can result from ingestion (mercury salts), inhalation (elemental 

mercury), injection, and dermal absorption. Mercury is avidly bound to sulfhydryl groups 

and disrupts cellular enzyme and membrane function. 



1. Elemental mercury poisoning—Liquid mercury is nontoxic if swallowed, but 

mercury vapor is well absorbed by inhalation and rapidly enters the central nervous 

system. With large exposure, encephalopathy, gingivitis, and pneumonitis may occur. 

The predominant manifestations of chronic mercury poisoning are various 

neuropsychiatric symptoms (erethism): tremor, anxiety, incapacitating shyness, and 

irritability. 

2. Inorganic mercury poisoning—Salts of inorganic mercury are corrosive and 

irritating to the gastrointestinal tract. Mercurous salts (eg, calomel) are poorly absorbed 

and generally less toxic than mercuric salts, which cause gastroenteritis with bloody 

emesis and diarrhea. The target organ is the kidney; acute tubular necrosis is common. 

Chronic intoxication may cause gingivitis, salivation, dysarthria, intention tremor (mainly 

of the fingers, eyes, and tongue), nervousness, emotional outbursts, and memory loss. 

3. Organic mercury poisoning—Organic mercury (methyl mercury, ethyl mercury) has 

been implicated in epidemic poisonings resulting from ingestion of seed grain fumigated 

with mercury compounds or from consumption of heavily contaminated seafood. These 

compounds are well absorbed and reach high levels in the nervous system with 

devastating effects. They can also cross the placenta. 

Tremor and neuropsychiatric symptoms are similar to those occurring with exposure to 

the vapor of elemental mercury, but the development of peculiar sensory deficits is 

unique to this type of mercury poisoning. These distinctive symptoms include 

paresthesias; constriction of visual fields; loss of hearing, smell, and taste; 

incoordination; choreoathetosis; stupor; and incontinence. Uncontrollable crying and 

laughter are also seen. The developing fetus may concentrate mercury in the central 

nervous system, with resulting congenital cerebral palsy, mental retardation, and other

irth defects. 


Blood levels are not always reliable indicators of excessive mercury burdens because of 

its wide distribution; levels may even be elevated 2-3 days after a seafood meal. Whole 

blood levels are recommended for acute intoxications; normal levels are less than 5 

ug/dL. A 24-hour urine collection can be more helpful than a blood level, and a level 

greater than 20 ug/dL indicates meaningful exposure. 

Treatment 



previously. A kidney-ureter-bladder x-ray may be helpful in elemental mercury ingestion 

to document its presence and passage through the gastrointestinal tract. 


DMSA has been shown to lower mercury levels, although it is not FDA approved for this 

indication (see Table 45-15). BAL can also be used, although it is contraindicated in 

methyl mercury poisoning because it can exacerbate central nervous system symptoms. 

Penicillamine is rarely used. 

C. Supportive Treatment 

Renal failure, a common occurrence after poisoning with inorganic mercuric salts, is 

treated with general supportive measures, which may include dialysis. 

Disposition 

Hospitalize all patients with suspected or documented mercury poisoning. 

Gordon RA et al: Aggressive approach in the treatment of acute lead encephalopathy 

with an extraordinarily high concentration of lead. Arch Pediatr Adolesc Med 

1998;152:1100. [PMID: 9811288] (Case report and review of literature on the treatment 

of lead toxicity.) 

Graeme KA et al: Heavy metal toxicity, part I: arsenic and mercury. J Emerg Med 

1998;16:45. [PMID: 9472760] (Review of the toxicity of arsenic and mercury and the 

diagnosis and treatment of arsenic and mercury poisoning.) 

Graeme KA et al: Heavy metal toxicity, part II: lead and metal fume fever. J Emerg Med 

1998;16:171. [PMID: 9543397] (Review of the toxicity of lead and the diagnosis and 

treatment of lead poisoning.) 

Ioannides AS et al: Acute respiratory distress syndrome in children with acute iron 

poisoning: the role of intravenous desferrioxamine. Eur J Pediatr 2000;159:158. [PMID: 

10664227] (Case report of severe acute respiratory decompensation in a child given 

intravenous desferrioxamine.) 

Levin SM et al: Clinical evaluation and management of lead-exposed construction

workers. Am J Ind Med 2000;37:23. [PMID: 10573595] (Review of the adverse effects 

and treatment of lead exposure in industry and treatment guidelines.) 

Muckter H et al: Are we ready to replace dimercaprol (BAL) as an arsenic antidote? 

Hum Exp Toxicol 1997;16:460. [PMID: 9292286] (Animal model of the treatment of 

arsenic poisoning with BAL, DMSA, and 2,3-dimercaptopropane-1- sulfate.) 

Siff JE et al: Usefulness of the total iron binding capacity in the evaluation and treatment 

of acute iron overdose. Ann Emerg Med 1999;33:73. [PMID: 9867890] (Review of 

reported cases of iron overdose using total iron-binding capacity as part of the 

laboratory analysis.) 

Staudinger KC et al: Occupational lead poisoning. Am Fam Physician 1998;57:719. 

[PMID: 9490995] (Diagnosis and management of occupational lead exposure.) 

HYDROCARBONS 


• Choking, gagging, or gasping following ingestion. 

• Hypoxia. 

• Delayed (4-6 hours) physical findings. 

• Infiltrates on chest x-ray (chemical pneumonitis). 


Hydrocarbons—a large group of compounds that includes petroleum distillates—exert 

various toxic effects. They are classified by 2 characteristics: viscosity (low-viscosity 

products are more likely to cause chemical aspiration pneumonia) and their potential for 

systemic toxicity (central nervous system or cardiac toxicity). These properties are 

summarized in Table 45-17. 

The major complication following ingestion of petroleum distillates is aspiration 

pneumonitis, which may occur with poisoning caused by any of the low-viscosity 

compounds. 

Most cases of poisoning are accidental, and exposure is rarely more than a taste (5-10 

mL). As little as 1-2 mL of low-viscosity compounds may produce severe chemical 

pneumonitis if aspirated into the tracheobronchial tree. 

Accidental or intentional inhalation of hydrocarbon vapors may produce irritation, 

nausea, and headache. Exposure to volatile vapors in an enclosed area may result in 

hypoxia owing to displacement of oxygen from the atmosphere. Inhalation of aromatic 

(eg, toluene) or halogenated (eg, freon, trichloroethylene) hydrocarbon solvents may 

cause euphoria, confusion, hallucinations, coma, and cardiac arrhythmias. Chronic 

exposure to toluene may cause myopathy, hypokalemia, renal tubular acidosis, and 

neuropathy.


Symptoms suggesting aspiration are choking, coughing, or gasping immediately 

following ingestion of a toxic compound. Physical signs of aspiration are often present 

but may be delayed for up to 4-6 hours. For example, chest x-ray may reveal infiltrates 

before physical signs appear. Systemic signs of toxicity include narcosis, delirium, and 

for certain compounds, seizures. Some of these effects may result from hypoxemia due 

to pneumonitis. Hydrocarbons may sensitize the myocardium to the arrhythmogenic 

effects of endogenous catecholamines. 

Treatment 

Although gastric aspiration of any ingested hydrocarbon may increase the chances of 

aspiration, ingestion of even small amounts of low-viscosity compounds with known 

significant systemic toxicity requires gastric aspiration and administration of activated 

charcoal. For example, the camphor contained in 10 mL of Campho-Phenique is 

sufficient to cause seizures in a child. The toxic dose of benzene or toluene is unknown 

but may be less than 10 mL. 

A. High-Viscosity Lubricants 

No treatment is required. 

B. Low-Viscosity Compounds with No Known Systemic Toxicity 

If there are unequivocal signs of aspiration pneumonitis, protect the airway if necessary 

to prevent further aspiration, and give oxygen. However, there are case reports of pulse 

corticosteroid therapy used successfully in the treatment of late acute respiratory 

distress syndrome following hydrocarbon ingestion. 

If the patient is asymptomatic and has no history of coughing or choking after ingestion, 

aspiration is unlikely. Do not induce emesis, because it may increase the risk of 

aspiration. Observe the patient closely for 4-6 hours to detect signs of possible 

aspiration. Obtain a chest x-ray even in asymptomatic patients. 

C. Low-Viscosity Compounds with Unknown or Unproved Toxicity 

It is unclear whether these compounds have inherent systemic toxic effects apart from 

chemical pneumonitis, and controversy exists regarding the use of lavage to clear a 

compound of this group from the body. Evaluate the patient, and give treatment for 

possible pulmonary aspiration, as described above. 

D. Low-Viscosity Compounds with Known Systemic Toxicity 

Consider gastric emptying for ingestions of more than 30 mL of hydrocarbons with 

systemic toxicity, intentional overdoses, and mixed overdoses with other toxins. In the 

absence of the above scenarios, avoid gastric emptying. Activated charcoal should also 

be initiated under the same pretenses. Activated charcoal is especially useful if the toxin 

(eg, camphor) is known to produce coma or seizures abruptly. If lethargy, coma, or 

seizures are present, intubate the patient with a cuffed endotracheal tube, and perform 

gastric aspiration. Evaluate the patient for possible pulmonary aspiration.

Disposition 

Hospitalize patients who have ingested low-viscosity petroleum distillates if symptoms 

or signs of systemic toxicity (lethargy, seizures) or pneumonitis (coughing, choking, 

abnormal findings on chest x-ray) are present. Because delayed onset of pulmonary 

complications may occur after hydrocarbon poisoning, it is prudent to observe patients 

for 4-6 hours before discharging them from the emergency department. 

Kamijo Y et al: Pulse steroid therapy in adult respiratory distress syndrome following 

petroleum naphtha ingestion. J Toxicol Clin Toxicol 2000;38:59. [PMID: 10696927] 

(Case report and discussion of the treatment of hydrocarbon ingestion.) 

Mickiewicz M et al: Hydrocarbon toxicity: general review and management guidelines. 

Air Med J 2001;20:8. [PMID: 11331818] (Review of hydrocarbon toxicity and 

management guidelines.) 

INHALANTS (Toxic Gases & Vapors) 


• Hypoxia. 

• Irritation of upper airway and conjunctiva. 

• Chemical pneumonitis and pulmonary edema. 


Many toxic inhalants (eg, carbon monoxide, phosgene) are produced by combustion of 

household or industrial products in accidental fires or as byproducts of work activity (eg, 

welding). Many toxic chemicals exist in gaseous form (eg, chlorine, arsine), and 

exposure occurs during an accidental spill or leak. Toxic gases can be classified as (1) 

simple asphyxiants, (2) chemical asphyxiants and systemic poisons, and (3) irritants or 

corrosives (Table 45-18). 

A. Simple Asphyxiants 

Methane, propane, and inert gases cause toxicity by lowering the ambient oxygen 

concentration. 

B. Chemical Asphyxiants and Systemic Poisons 

Examples include carbon monoxide, cyanide, and hydrogen sulfide. These substances 

possess intrinsic systemic toxicity manifested after absorption into the circulation. 

C. Irritants or Corrosives 

These substances cause cellular destruction and inflammation when they come in 

contact with the tracheobronchial tree, usually by producing acids or alkali upon contact 

with moisture. Gases that are highly water soluble (eg, chlorine, ammonia) cause 

immediate irritation, mainly of the upper airway and conjunctiva, whereas gases that are 

poorly soluble in water (eg, nitrogen dioxide) may be more deeply inhaled, producing

delayed lower airway destruction with chemical pneumonitis and pulmonary edema. 


Symptoms and signs vary depending on the toxin. In an accidental fire, combinations of 

all classes of toxic inhalants may be responsible for symptoms of toxicity, for example, a 

burning sensation in the eyes and mouth, sore throat, brassy cough, dyspnea, and 

headache. Look for singed nasal hairs, carbonaceous deposits on the nose and face, 

upper airway swelling or obstruction, wheezing or signs of pulmonary edema, and 

manifestations of systemic toxicity. Obtain arterial blood gas determinations, 

carboxyhemoglobin level measurements, and chest x-ray. 

Treatment 

Remove the patient from the source of toxic gases, and begin supplemental oxygen, 10 

L/min, by mask. For victims of smoke inhalation or carbon monoxide poisoning, give 

100% oxygen. 

Treatment of poisoning caused by chemical asphyxiants and systemic toxins depends 

on the specific toxin. For cyanide, see previous discussion; for hydrogen sulfide 

poisoning, use sodium nitrate and hyperbaric oxygen, as outlined in the "Cyanide" 

section. Although unproved, nitrite therapy may decrease sulfide toxicity by binding it 

with methemoglobin. Do not give thiosulfate for hydrogen sulfide intoxication, because 

the enzyme rhodanese is not involved in elimination of sulfide. 

For upper airway irritation, humidified oxygen is often effective. Carefully observe the 

patient for stridor and other signs of progressive airway obstruction that would require 

endotracheal intubation. 

For bronchospasm, give nebulized bronchodilators (Chapter 33). 

Disposition 

Hospitalize for observation and treatment all patients with significant symptoms or signs 

of poisoning caused by inhalation of toxic gases. Patients exposed briefly to 

high-solubility irritant gases whose symptoms have resolved can be safely discharged; 

however, those exposed to low-solubility irritants such as nitrogen oxides or phosgene 

may experience delayed-onset pulmonary edema or chemical pneumonitis and should 

be admitted for 16-24 hours' observation. 

Brouette T et al: Clinical review of inhalants. Am J Addict 2001;10:79. [PMID: 11268830] 

(Epidemiology, pharmacology, and sequelae of inhalant abuse.) 

Lau FL et al: A fatal laboratory accident with toxic gases inhalation. Eur J Emerg Med 

1998;5:265. [PMID: 9486258] (Case reports and discussion of exposure of toxic gases.) 

Meng Y et al: Inhalation studies with drugs of abuse. NIDA Res Monogr 1997;173:201. 

[PMID: 9260190] (Review of inhalants and their pharmacology.)

ISONIAZID 


• Seizures, metabolic acidosis, and coma. 

• Seizures may be refractory to standard management (benzodiazepines). 

• Estimated acute toxic dose is 80-100 mg/kg. 


Isoniazid is a common antituberculosis drug often prescribed as a 3- to 6-month supply. 

The principal manifestations of isoniazid overdose are seizures, metabolic acidosis, and 

coma. Seizures may be due to depression of ?-aminobutyric acid levels in the central 

nervous system. Severe metabolic acidosis accompanies recurrent seizure activity. The 

estimated acute toxic dose is 80-100 mg/kg, although this range may be lower in 

patients with preexisting seizure disorders, vitamin B 6 deficiency, or chronic alcoholism. 


Symptoms occur 30 minutes to 3 hours following ingestion and include nausea and 

vomiting, slurred speech, dizziness, lethargy progressing to stupor, hyperreflexia, 

seizures, metabolic acidosis, hyperglycemia, and cardiovascular and respiratory 

depression. Symptoms and signs occur promptly after significant poisoning. 

Treatment 



previously. 

B. Treatment of Seizures 

Treat seizures with lorazepam or diazepam, as described in Chapter 17. If these 

medications are not effective, give pyridoxine (vitamin B 6 ) in doses equivalent to the 

amount ingested (gram for gram). If the amount ingested is unknown, start with 5 g (0.1 

g/kg) intravenously given over 3-5 minute, and repeat every 10-15 minutes until 

seizures are controlled. If the intravenous form of pyridoxine is not available, pyridoxine 

can be given as a slurry in a similar dose via a nasogastric tube. Unfortunately, many 

hospitals are ill-equipped and do not have the recommended 5-g aliquot available. 

C. Enhanced Elimination 

Consider hemodialysis for patients unresponsive to conventional therapy. 

Disposition 

Hospitalize all patients who have ingested more than 80 mg/kg of isoniazid and those 

who have signs or symptoms suggesting isoniazid poisoning.

Ramero JA et al: Isoniazid overdose: recognition and management. Am Fam Physician 

1998;57:749. [PMID: 9490997] (Case study and discussion of the treatment of isoniazid 

overdose.) 

Santucci KA et al: Acute isoniazid exposures and antidote availability. Pediatr Emerg 

Care 1999;15:99. [PMID: 10220077] (Prospective study to determine the availability of 

pyridoxine in emergency departments.) 

LITHIUM 


• Apathy, lethargy, tremor, slurred speech, and ataxia. 

• In severe overdose, choreoathetosis, seizures, and coma. 

• Toxicity often accidental and seen with diuretic therapy and dehydration. 

• Lithium levels > 2 mEq/L are usually toxic. 


Lithium is frequently used to treat bipolar disorder and other psychiatric disorders. It is a 

monovalent cation like sodium and potassium; unlike these cations, however, it has only 

a small gradient of distribution across cell membranes and cannot maintain membrane 

potentials. It is rapidly absorbed into extracellular fluid, with an initial volume of 

distribution of 0.1-0.2 L/kg. Its distribution into selected tissues then occurs slowly over 

several hours. Its final volume of distribution is about 1 L/kg. It is excreted unchanged in 

the urine and actively reabsorbed, with a half-life of approximately 22 hours (with normal 

renal function). Sodium and water depletion lead to marked increases in the 

reabsorption of lithium and to elevation of blood concentrations of lithium. 


Symptoms of lithium overdose include apathy, lethargy, tremor, slurred speech, ataxia, 

and fasciculations, which may progress in severe overdose to choreoathetosis, 

seizures, coma, and death. Persistent neurologic sequelae may occur. Toxicity is 

frequently accidental and occurs secondary to chronic sodium depletion, diuretic 

therapy, and dehydration. In these cases, the serum lithium level is a more reliable 

index to the severity of overdose, because adequate time has passed for distribution 

into the central nervous system. In such circumstances, blood concentrations of lithium 

higher than 2 mEq/L are usually associated with toxicity. 

In acute overdose, in contrast, initially elevated serum lithium concentrations may be 

misleading, because distribution into tissues occurs over several hours. For example, an 

initial toxic level of 4 mEq/L may easily fall to 1 mEq/L with final distribution. Thus, in 

acute overdose, repeated measurements of serum lithium levels and assessment of 

mental status (eg, every 4 hours) are more helpful than a single assessment in 

evaluating toxicity.

Treatment 

A. General Management and Prevention of Absorption 


previously. Whole bowel irrigation is an effective means of increasing lithium removal. 

Sodium polystyrene sulfonate is also effective in decreasing the lithium concentration, 

but the dose and effect on the potassium level have not been determined. 

B. Enhanced Elimination 

The treatment of choice for serious intoxication is hemodialysis. Specific indications for 

hemodialysis have not been well defined by careful studies, but dialysis should be 

considered for any patient with obtundation, seizures, or coma, or when serum levels at 

equilibrium exceed 4 mEq/L. However, many patients with high levels do not have 

serious clinical toxicity. Dialysis is the only route of elimination in patients with renal 

failure. Hemoperfusion is not effective. 

Because lithium is reabsorbed in the kidney when sodium and fluids are depleted, 

administration of intravenous saline may promote lithium excretion. Normal urine flow 

rates are adequate. The value of forced saline diuresis using large fluid volumes is 

unclear, and the authors do not recommend it. 

Activated charcoal does not adsorb lithium and is of no value. 

C. Prevention of Accidental Toxicity 

To prevent chronic (accidental) toxicity, frequent assessment of fluid and sodium 

balance and lithium levels is recommended for patients taking lithium. 

Disposition 

Hospitalize all patients with serum lithium concentrations above 2-3 mEq/L and those 

who show objective signs of lithium intoxication. 

Linakis JG et al: Use of sodium polystyrene sulfonate for reduction of plasma lithium 

concentrations after chronic lithium dosing in mice. J Toxicol Clin Toxicol 1998;36:309. 

[PMID: 9711196] (Placebo-controlled animal study to determine whether multiple oral 

doses of sodium polystyrene sulfonate are effective in reducing chronic lithium toxicity.) 

Micheli F et al: Blepharospasm and apraxia of eyelid opening in lithium intoxication. Clin 

Neuropharmacol 1999;22:176. [PMID: 10367183] (Case study and discussion of lithium 

overdose.) 

Newland KD: Hemodialysis reversal of lithium overdose cardiotoxicity. Am J Emerg Med 

2002;20:67. [PMID: 11781927] (Case study and discussion of the use of hemodialysis 

in lithium overdose.) 

Scharman EJ: Methods used to decrease lithium absorption or enhance elimination. J 

Toxicol Clin Toxicol 1997;35:601. [PMID: 9365427] (Meta-analysis of the methods used 

to decrease lithium absorption or enhance elimination.)

OPIATES 


• Sedation, hypotension, bradycardia, hypothermia, and respiratory depression. 

• Diagnosis is confirmed if patient regains consciousness after naloxone. 


Codeine, propoxyphene, and other opiates with varying potencies and durations of 

action are found in a wide range of prescription analgesic preparations. Some opiates, 

such as dextromethorphan, are found in nonprescription drugs. 

The opiates act on central nervous system receptors and cause sedation, hypotension, 

bradycardia, hypothermia, and respiratory depression. Most opiates have a half-life of 

3-6 hours; the major exceptions are methadone (15-20 hours) and propoxyphene (12-15 

hours). 


Consider opiate intoxication in any comatose or lethargic patient, especially when the 

clinical findings listed above are present. Pinpoint pupils are a typical sign, although in 

mixed overdoses, pupils may be in mid position. Signs of parenteral drug abuse may or 

may not be apparent. Pulmonary edema may occur. The diagnosis is confirmed if toxic 

concentrations of opiates are found in blood or urine or if the patient regains 

consciousness after administration of naloxone. 

Treatment 



previously. Maintain adequate airway and ventilation. 

B. Naloxone or Nalmefene 

1. Naloxone—Give naloxone (a specific narcotic antagonist) to all patients with 

suspected opiate overdose. Start with 0.4-2 mg intravenously. Repeat 3 or 4 times if no 

response occurs and narcotic overdose is suspected. Some authorities recommend up 

to 10-20 mg to treat suspected narcotic overdose. Propoxyphene poisoning seems to be 

particularly resistant to the usual doses of naloxone. Because naloxone has a half-life of 

1 hour and effects lasting only 2-3 hours (shorter than many opiates), its effects may 

wear off before those of the narcotic, permitting the patient to lapse into coma again. If 

relapse occurs after the first response to naloxone, a naloxone continuous infusion may 

be started, using approximately two thirds the dose required to initially awaken the 

patient given over each hour. 

2. Nalmefene—Another option in the busy emergency department is a long-acting

opioid antagonist such as nalmefene. Nalmefene, 2 mg, has been shown to last for as 

long as 8 hours, thereby reducing the need for any drips or repeated doses of naloxone. 

Naloxone is still the preferred initial antidote for comatose patients when the cause is 

uncertain because it will produce a shorter period of withdrawal in the chronically 

opioid-dependent patient. 

C. Prevention of Narcotic Withdrawal Symptom 

Watch carefully for withdrawal symptoms caused by naloxone or nalmefene. Chronic 

narcotic abusers who have developed tolerance to opiates may develop acute narcotic 

withdrawal when these agents are given. Although this syndrome is not life threatening, 

it is a management problem in the emergency department if the patient becomes 

combative or uncooperative or signs out of the hospital before adequate treatment can 

be given. Careful titration of the naloxone dose may help to prevent narcotic withdrawal 

syndrome. Some authors have even recommended the use of home-based supplies of 

naloxone to prevent opiate overdose death among misusers. 

Disposition 

Hospitalize and observe all patients thought or known to have ingested significant 

amounts of opiates and those who relapse after the initial response to naloxone. 

Patients with heroin overdose who respond to naloxone may be safely discharged if 

they are asymptomatic 3 hours after the last dose. 

Rice EK et al: Heroin overdose and myoglobinuric acute renal failure. Clin Nephrol 

2000;54:449. [PMID: 11140805] (Retrospective case analysis evaluating the use of 

heroin and the development of renal failure.) 

Sporer KA: Acute heroin overdose. Ann Intern Med 1999;130:584. [PMID: 10189329] 

(Literature review of the use and toxicity of heroin.) 

Stang J et al: Preventing opiate overdose fatalities with take-home naloxone: pre-launch 

study of possible impact and acceptability. Addiction 1999;94:199. [PMID: 10396785] 

(Structured interviews of a community and treatment sample of opiate-addicted 

individuals regarding the possible home use of naloxone.) 

Wang DS et al: Nalmefene: a long-acting opioid antagonist. Clinical applications in 

emergency medicine. J Emerg Med 1998;16:471. [PMID: 9610980] (Review of the 

pharmacology and clinical use of nalmefene.) 

Watson WA et al: Opioid toxicity recurrence after an initial response to naloxone. J 

Toxicol Clin Toxicol 1998;36:11. [PMID: 9541035] (Retrospective case-control study to 

determine the frequency and potential predictors of opioid toxicity recurrence after a 

response to naloxone.) 

ORGANOPHOSPHATES & OTHER CHOLINESTERASE INHIBITORS 


• Toxicity and potency vary widely. 

• DUMBELS (diarrhea; urination; miosis; bronchorrhea; excitation with muscle 

fasciculation, anxiety, and seizures; lacrimation; and seizures). Death is usually from 

respiratory depression. 

• Diagnosis usually confirmed with low plasma or red blood cell cholinesterase level. 


Cholinesterase inhibitors are found in a variety of insecticides (organophosphates and 

carbamates) available for home and commercial use (eg, crop sprays, bug bombs, flea 

collars). Some chemical warfare agents (nerve gases) are also cholinesterase inhibitors. 

These compounds inhibit acetylcholinesterase and therefore allow accumulation of 

acetylcholine at muscarinic and nicotinic receptors in nerve endings. Organophosphates 

bind irreversibly with the enzyme, whereas carbamates are considered reversible 

inhibitors. All are rapidly absorbed from the skin, gastrointestinal tract, and respiratory 

tract. Toxicity and potency vary widely. Workers constantly exposed to 

organophosphates and infants with underdeveloped cholinesterase activity are at 

greater risk for intoxication. 


Miosis, excessive salivation, bronchospasm, hyperactive bowel sounds, and lethargy 

typically occur shortly after exposure. Either bradycardia (muscarinic effect) or 

tachycardia (nicotinic effect) may be observed. QT-interval prolongation and 

pleomorphic ventricular tachyarrhythmias are a late consequence of poisoning. 

Symptoms of toxicity are easily remembered with the mnemonic DUMBELS (diarrhea; 

urination; miosis; bronchorrhea; excitation with muscle fasciculation, anxiety, and 

seizures; lacrimation; and salivation). Death is usually caused by respiratory 

depression. 

Measurement of the plasma or red blood cell cholinesterase level is helpful in confirming 

acute toxicity; cholinesterase levels become low soon after exposure. 

Treatment 



previously. Careful management of the airway is important, because significant 

bronchial secretions, bronchospasm, and hypoventilation may occur. Position the 

patient so as to avoid aspiration, and provide suction and oxygen as required. Early 

recognition of respiratory distress and subsequent intubation may decrease the mortality 

among these patients. 

Remove and isolate the patient's clothing, and carefully wash the skin with soap and 

water. Medical personnel should be careful to avoid cross-contamination. 

B. Pharmacologic Treatment

Atropine is a symptomatic treatment for muscarinic signs (salivation, bronchorrhea, 

bronchospasm, sweating). Large doses may be required. Start with 1-2 mg 

intravenously (0.5 mg in children), followed by repeated doses of 2-4 mg every 5-10 

minutes until signs of atropinization occur (ie, flushing, mydriasis, drying of secretions, 

and tachycardia). The use of up to 50 mg in 24 hours is not unusual. 

Pralidoxime (Protopam, 2-PAM) competitively inhibits binding of organophosphates to 

acetylcholinesterase and should be given to all patients with significant intoxication. It is 

not required for carbamate poisoning, because carbamate toxicity is transient. The dose 

is 1-2 g (25-50 mg/kg in children) in saline intravenously over 5-10 minutes. Continuous 

pralidoxime infusion has also been shown to improve the outcome in organophosphate 

poisoning. Adequate renal function is a prerequisite for use of pralidoxime, because it is 

excreted in the urine. 

C. Neurologic Sequelae 

Patients who receive prompt treatment usually recover from acute toxicity. However, 2 

neurologic sequelae of severe intoxication—organophosphate-induced delayed 

neuropathy and intermediate syndrome—may occur after significant exposure. 

Disposition 

Hospitalize all patients with suspected or documented serious organophosphate 

poisoning. Carbamate poisoning is usually transient, and patients who recover rapidly 

may be discharged. 

Kwong TC: Organophosphate pesticides: biochemistry and clinical toxicology. Ther 

Drug Monit 2002;24:144. [PMID: 11805735] (Review of the biochemistry and clinical 

toxicology of organophosphates.) 

Singh S et al: Aggressive atropinisation and continuous pralidoxime (2-PAM) infusion in 

patients with severe organophosphate poisoning: experience of a northwest Indian 

hospital. Hum Exp Toxicol 2001;20:15. [PMID: 11339619] (Noncontrolled study to 

determine if continuous pralidoxime infusion and atropine improved the outcome in 

patients with severe organophosphate poisoning.) 

Sungur M et al: Intensive care management of organophosphate insecticide poisoning. 

Crit Care 2001;5:211. [PMID: 11511334] (Retrospective case study analysis to evaluate 

the clinical course of organophosphate poisoning.) 

Wang MH et al: Q-T interval prolongation and pleomorphic ventricular tachyarrhythmia 

('Torsade de pointes') in organophosphate poisoning: a report of a case. Hum Exp 

Toxicol 1998;17:587. [PMID: 9821023] (Case report and discussion of organophosphate 

poisoning.) 

PHENCYCLIDINE 


• Rapid onset of action. 

• Vertical and horizontal nystagmus are common. 

• Symptoms may fluctuate, unpredictably, from severe agitation to quiet stupor. 

• Hyperthermia and rhabdomyolysis may lead to myoglobinuria and renal failure. 


Phencyclidine (PCP)—a common adulterant of marijuana, amphetamines, and street 

hallucinogens—is also called angel dust, crystal, supergrass, ozone, whack, rocket fuel, 

and peace pill by its users. It may be smoked, snorted, ingested, or injected. 

PCP is a sympathomimetic, hallucinogenic, dissociative agent originally used as a 

veterinary anesthetic. It has a rapid onset of action when smoked or snorted, causing 

euphoria and hallucinations. Serious overdose does not usually occur with smoking, 

because users can titrate the dose to achieve the desired effect. Ingestion of 20-25 mg 

of PCP can cause severe intoxication. PCP has a large volume of distribution (2-4 L/kg) 

and a half-life of several hours to days. As a weak base, it is ionized in acidic media 

such as the stomach and acidic urine. It is eliminated primarily by metabolism. Because 

only about 10% is excreted into the urine, increasing urinary output or urinary 

acidification (to cause ion trapping) is unlikely to increase elimination of the drug 

significantly. 


Symptoms typically fluctuate, with patients alternating unpredictably from severe 

agitation to quiet stupor. Bizarre, paranoid behavior and extreme violence may occur 

unexpectedly. Both vertical and horizontal nystagmus are common. The pupils may be 

large or small. Hypertension, tachycardia, and hyperthermia are common. Marked 

muscle rigidity, dystonias, and seizures may occur. Hyperthermia and rhabdomyolysis 

resulting in myoglobinuria and renal failure are a major cause of subsequent illness. The 

diagnosis is made primarily on clinical grounds but may be confirmed by demonstrating 

PCP in urine or gastric aspirate. Serum PCP concentrations are not of value in 

emergency management. 

Treatment 



previously. Most instances of PCP intoxication are mild and self-limited, and patients 

need no specific treatment other than to be in a quiet and supportive environment. 

B. Treatment of Moderate to Severe Poisoning 

Diazepam, 2-5 mg intravenously every 30 minutes until sedation is achieved, is effective 

in controlling moderate agitation or anxiety. 

Haloperidol, 5-10 mg intravenously, may also be effective in controlling toxic psychosis. 

The goal of treatment is to prevent complications stemming from muscular hyperactivity 

and subsequent hyperthermia and rhabdomyolysis.

C. Treatment of Rhabdomyolysis or Myoglobinuria 

If the patient has rhabdomyolysis or myoglobinuria, maintain urine output with 

intravenous fluids and mannitol. Alkalization of urine is recommended in order to 

minimize renal deposition of myoglobin. 

D. Enhanced Elimination 

Because PCP has a large volume of distribution, dialysis procedures are not useful. 

Acidification of the urine with ammonium chloride or hydrogen chloride has been used, 

but it does not significantly increase the total elimination rate, and it is not 

recommended. Evidence indicates that aciduria may worsen myoglobinuric renal 

toxicity. It is no longer recommended. 

Disposition 

Hospitalize patients who have moderate to severe PCP poisoning, particularly if 

hyperthermia, severe muscular rigidity, or evidence of rhabdomyolysis is an 

accompanying manifestation. 

Cruz R et al: Pulmonary manifestations of inhaled street drugs. Heart & Lung: The 

Journal of Acute and Critical Care 1998;27:297. [PMID: 9777375] (Review of the 

pulmonary manifestations of snorting or smoking PCP.) 

Piecuch S et al: Acute dystonic reactions that fail to respond to diphenhydramine: think 

of PCP. J Emerg Med 1999;17:527. [PMID: 10338254] (Case report of a presentation of 

PCP use initially thought to be due to phenothiazines.) 

PHENOTHIAZINES & OTHER ANTIPSYCHOTICS 


• Extrapyramidal side effects (eg, dystonia, orofacial spasms) 

• Sedation, miosis, and hypotension are common. 

• Coma, seizures, and ventricular arrhythmias may occur with large doses. 


Antipsychotic drugs include chlorpromazine (Thorazine, many others), prochlorperazine 

(Compazine), haloperidol (Haldol, others), and many other phenothiazines and 

butyrophenones. 

The mechanism of toxicity of the antipsychotics is complex. Antiadrenergic properties 

cause sedation and hypotension, anticholinergic effects are manifested by dry mouth 

and tachycardia, and antidopaminergic properties may produce extrapyramidal side 

effects (most commonly seen with haloperidol). The contribution of each of these effects 

in drug overdose depends on the specific drug and on the individual patient. Most of 

these compounds have large volumes of distribution (10-30 L/kg) and long half-lives

(12-30 hours); dialysis is not effective. 


Extrapyramidal side effects may occur even at therapeutic doses and include dystonic 

posturing, spasm of orofacial muscles, cogwheel rigidity, and spasticity. With acute 

overdose, sedation, miosis, and hypotension are common. Coma and seizures may 

occur with very large ingestions. Prolongation of the QT interval and ventricular 

arrhythmias may occur. Disruption of the temperature-regulating mechanism may lead 

to hyperthermia or hypothermia. Abdominal x-rays may show radiopaque tablets in the 

gut. 

Treatment 



previously. Treat hypotension with intravenous crystalloid solution; if a vasopressor is 

needed, norepinephrine is preferable. 

B. Treatment of Extrapyramidal Reactions 

Diphenhydramine (Benadryl, many others), 0.5-1 mg/ kg intravenously slowly; or 

benztropine (Cogentin), 1-2 mg intramuscularly for adults, is recommended for 

extrapyramidal reactions. Relapse may occur; dispense oral anticholinergics for 2-3 

days. Sophisticated drug-seeking patients have been known to simulate dystonias in 

order to receive these medicines. 

C. Treatment of Atypical Antipsychotic Overdose 

Patients who overdose on atypical antipsychotics (eg, risperidone, olanzapine) present 

in a manner similar to patients who overdose on the high-potency antipsychotics and 

should be managed similarly. 

Disposition 

Hospitalize patients with suspected or documented poisoning due to antipsychotics. In 

the acute period, close cardiac monitoring for arrhythmias and hypotension is 

warranted. Indications of significant poisoning include (1) a large number of pill 

fragments found in the stomach or intestines by means of lavage, emesis, or abdominal 

plain film, (2) rapidly worsening clinical findings, and (3) obtundation. Patients with 

extrapyramidal reactions who respond to anticholinergic therapy may be discharged. 

Catalano G et al: Atypical antipsychotic overdose in the pediatric population. J Child 

Adolesc Psychopharmacol 2001;11:425. [PMID: 11838825] (Case report and literature 

review of the treatment of risperidone overdose.) 

Chan-Tack KM: Neuroleptic malignant syndrome due to promethazine. South Med J 

1999;92:1017. [PMID: 10548178] (Case report and discussion of promethazine as a 

cause of neuroleptic malignant syndrome.) 

James LP et al: Phenothiazine, butyrophenone, and other psychotropic medication

poisonings in children and adolescents. J Toxicol Clin Toxicol 2000;38:615. [PMID: 

11185968] (Retrospective case analysis of phenothiazine and butyrophenone ingestions 

in children.) 

POISONOUS MUSHROOMS 


• Delayed onset of symptoms (gastrointestinal irritation) of 6-12 hours suggests a toxic 

mushroom ingestion. 

• Mushrooms containing amatoxin may produce fatal hepatic necrosis. 


Of the over 5000 varieties of mushrooms found in the United States, about 100 can be 

toxic. Most poisonous mushrooms act as gastrointestinal irritants. Table 45-19 lists 

several types of poisonous mushrooms, symptoms, and treatment. The most significant 

are Amanita phalloides and other mushrooms containing amatoxin, which may produce 

fatal hepatic necrosis. 

Assistance with identification of specimens can often be obtained from a university 

biology department or mycology society. Poisindex and regional poison control centers 

may also help with identification. However, because accurate identification of 

mushrooms is difficult without an experienced mycologist and impractical because many 

types of mushrooms are often ingested at one time, the best approach to mushroom 

ingestion is to assume that the most toxic types have been consumed. Delayed onset 

(6-12 hours) of gastrointestinal symptoms suggests amatoxin or monomethylhydrazine 

poisoning. 

Treatment 


previously. 

If the identity of the ingested mushrooms is not known, induce emesis at home or 

perform gastric lavage in the emergency department. This should be followed by 

activated charcoal every 2-4 hours. 

If poisoning with amatoxin is suspected, hospitalize the patient for observation and 

obtain baseline hepatic and renal function measurements. A variety of potential 

antidotes have been recommended, including corticosteroids, penicillin G, thioctic acid, 

silymarin, and NAC. No well-designed controlled human studies have addressed the 

efficacy of these antidotes. More important than specific antidotes is supportive care, 

including aggressive fluid replacement for massive gastroenteritis, supplemental 

glucose, and supportive treatment for hepatic encephalopathy. Early charcoal 

hemoperfusion or dialysis may be beneficial. Liver transplant has been successful in 

several patients with massive hepatic necrosis.

Table 45-19 describes specific treatment for various kinds of mushroom poisoning. 

Disposition 

Hospitalize patients thought or known to have ingested mushrooms known to cause 

serious poisoning (see Table 45-19). 

Broussard CN et al: Mushroom poisoning—from diarrhea to liver transplantation. Am J 

Gastroenterol 2001;96:3195. [PMID: 11721773] (Case study series and discussion of 

the toxicity of mushrooms.) 

Wellington K et al: Silymarin: a review of its clinical properties in the management of 

hepatic disorders. BioDrugs 2001;15: 465. [PMID: 11520257] (Literature review and 

discussion of the potential for silymarin use in hepatic disorders.) 

POISONOUS PLANTS 


• Identification of plant is often difficult but essential to diagnosis of toxicity. 

• Symptoms are dependent on plant toxin ingested (eg, cyanide, cardiac glycosides, 

anticholinergics). 


Several hundred species of plants in the United States contain toxic compounds. Tables 

45-20 and 45-21 give examples of nontoxic and toxic plants. Details about identification, 

mechanism of toxicity, and treatment are best obtained from a local poison control 

center or from Poisindex. If the identity of a plant is unknown, it is helpful to take along a 

sample to a local nursery or to a botanist. Gardening books are also useful sources of 

identification. Despite the potential for plants to cause serious toxicity, physicians have a 

general lack of knowledge about plant poisoning. 

Treat the specific symptoms manifested by the patient, not those thought to be 

associated with the type of poisonous plant believed to have been ingested. Many 

similar species of plants have widely varying potencies and combinations of toxins; the 

plant's age, the soil conditions, and other factors influence the severity of toxic 

symptoms. 

Classes of Toxins 

Some of the more common plant toxins are described below. The list is not complete. 

A. Oxalates 

Insoluble calcium oxalate crystals in the leaves and stems of some plants irritate the 

mucous membranes and can cause edema of the mouth, throat, and tongue. In rare

severe reactions, drooling, dysphagia, and airway obstruction may occur. Renal failure 

may occur if sufficient amounts of oxalates are absorbed. 

B. Amygdalin and Cyanogenic Glycosides 

Cyanide is produced by the gastrointestinal hydrolysis of chewed-up fruit pits or seeds. 

(Prunus species: cherry, apricot, peach) or leaves and stems (Hydrangea, elderberry). 

Severe poisoning is uncommon. See "Cyanide" section for symptoms and therapy. 

C. Cardiac Glycosides 

Digitalis and similar compounds are present in varying amounts in certain plants. Death 

after consumption of only one oleander leaf has been reported (see "Cardiac 

Glycosides" section). 

D. Anticholinergics 

The typical anticholinergic syndrome of dry mouth, tachycardia, delirium, urinary 

retention, and mydriasis is seen. Most poisonings are mild, and supportive treatment is 

sufficient (see "Anticholinergics" section). 

E. Nicotinelike Toxins 

These toxins include nicotine and aconitine. Symptoms include nausea and vomiting, 

salivation, diarrhea, restlessness, and seizures. Mydriasis may also occur. Following an 

initial phase of excitement, respiratory depression and hypotension may occur. 

F. Solanine 

Solanine has effects similar to those of nicotine. In addition, plants containing solanine 

often have significant amounts of atropinic alkaloids, so that the net effect is 

unpredictable. Onset of symptoms may be delayed several hours. 

G. Toxalbumins 

These highly toxic compounds (eg, abrin, ricin, phallin) can cause acute gastroenteritis, 

dehydration, and shock. Convulsions, hemolysis, and renal and hepatic injury can also 

occur. Oral and esophageal irritation or burns may be seen. 

Treatment 

In general, emesis is recommended after ingestion of any unidentified plants or those 

with known potentially serious toxic effects. Follow emesis with activated charcoal, a 

cathartic, and symptomatic treatment as needed. Keep the patient under observation. 

Begin specific treatment as indicated for the specific toxins involved. 

Disposition 

Disposition depends on the plant ingested and the symptoms experienced. 

Lawrence RA: Poisonous plants: when they are a threat to children. Pediatr Rev 

1997;18:162. [PMID: 9114716] 

Manriquez O et al: Analysis of 156 cases of plant intoxication received in the Toxicologic 

Information Center at Catholic University of Chile. Vet Hum Toxicol 2002;44:31. [PMID:

11824773] (Retrospective analysis of plant and mushroom ingestions.) 

SALICYLATES 


• Toxicity generally occurs at levels > 150 mg/kg. 

• Early manifestations include nausea, vomiting, and hyperventilation. 

• Initial respiratory alkalosis is often followed by a severe metabolic acidosis, creating a 

mixed acid-base status. 

• Hypoglycemia is prominent in children. 


Salicylates are present in numerous prescription and nonprescription medications, for 

example, analgesics, bismuth subsalicylate (Pepto-Bismol, many others), or oil of 

wintergreen (methyl salicylate). 

The mechanism of toxicity with salicylate poisoning is complex and includes direct 

central nervous system stimulation, uncoupling of oxidative phosphorylation, inhibition of 

Krebs cycle enzymes, and interference with hemostatic mechanisms. The volume of 

distribution is dose dependent and usually small; with significant ingestion, however, the 

drug is redistributed into the central nervous system. Because salicylate is a weak acid, 

acidemia increases its penetration of the central nervous system. The half-life may 

increase from 2 to 20 hours at overdose levels as a result of saturation of liver 

metabolism. The elimination of salicylate is increased in alkaline urine. The minimum 

acute toxic dose is 150 mg/kg, with severe toxicity occurring at doses over 300-500 

mg/kg. However, many cases of toxicity are a result of prolonged excessive treatment of 

minor illnesses (subacute or accidental overdose). The chronically ill and the elderly are 

at greater risk for subacute toxicity because of relative hypoalbuminemia and renal 



Early manifestations of overdose include nausea and vomiting, tinnitus, listlessness, 

and hyperventilation. Loss of fluid and electrolytes is common. Initial respiratory 

alkalosis is followed by severe metabolic acidosis, hypokalemia, and hypoglycemia. 

Seizures, hyperpyrexia, and coma occur as toxicity becomes more severe. 

Measurement of the blood salicylate concentration is essential for effective 

management, although it is not as reliable an indicator of the severity of illness if 

subacute toxicity is present. In cases of acute salicylate ingestion, the Done nomogram 

has been shown to have a poor predictive value and the prognosis and patient 

management should not be based solely on an aspirin level. Consider the patient's 

clinical presentation, age, aspirin level, and acid-base status in making treatment 

decisions. In the presence of acidosis, toxicity occurs with considerably lower levels. 

Salicylate determinations should be repeated every 4-5 hours. Repeated measurements 

are especially important for ingestion of sustained-release or enteric-coated

preparations, which are absorbed slowly and may result in delayed peak levels. 

With subacute (accidental) toxicity, severity of poisoning does not correlate well with 

serum salicylate concentration, but levels above 30 mg/dL (300 mg/L) are significant. 

Patients with subacute toxicity are frequently very young or very old, and they usually 

present with dehydration, obtundation, and acidosis. The diagnosis is often missed 

while the physician concentrates on the more prominent secondary complications. 

Cerebral and pulmonary edema and death are more common in patients with subacute 

toxicity. 

A Phenistix test of urine may be positive (purple or purple-brown) with salicylate toxicity, 

but false-negative results have been reported in patients with acid urine. 

Treatment 



previously. After acute overdose, give adequate charcoal to bind ingested salicylate. 

Multidose activated charcoal may be beneficial. For enteric-coated aspirin, toxicologists 

recommend lavage followed by activated charcoal, with further doses of activated 

charcoal and possibly even whole bowel irrigation if the salicylate level is rising. 

B. Correction of Acid-Base Status 

Correct dehydration, hypoglycemia, hypokalemia, and acidosis. For significant 

dehydration, start with 20 mL/ kg of an intravenous crystalloid solution given over 1-2 

hours, and then give 3-5 mL/kg/h to maintain the urine output at 2-3 mL/kg/h. To correct 

acidosis and promote excretion of salicylate in the urine, give sodium bicarbonate, 1 

mEq/kg/h. Concurrent correction of potassium deficit is mandatory. Urine pH should be 

maintained at 7-7.5. Alkalization of the urine is often unsuccessful in critically ill patients 

(especially the elderly), and it may aggravate pulmonary and cerebral edema. 

C. Enhanced Elimination 

Hemodialysis is recommended for critically ill patients with persistent seizures, acidosis 

that fails to respond to treatment, or cerebral or pulmonary edema. Although high 

salicylate concentrations (eg, > 120 mg/dL [1200 mg/L] at 6 hours) generally represent 

severe toxicity, hemodialysis should be based on the patient's complications and not the 

drug level. Hemodialysis is efficient in removing salicylate and can help to correct pH 

and electrolyte abnormalities. Consider early hemodialysis in ill patients with subacute 

overdose. Although there are no proved guidelines, elderly patients with serum 

salicylate levels over 60 mg/dL, and those with significant neurologic toxicity, should 

probably receive immediate hemodialysis. If the patient is hemodynamically unstable or 

hemodialysis is unavailable, continuous hemodiafiltration has been reported to be a 

viable alternative. 


Obtain measurements of serum salicylate every 4-6 hours to monitor adequacy of 

treatment. If evidence of salicylate-induced hypoprothrombinemia is present, give 

vitamin K, 10 mg intramuscularly.

Rehydration and rapid correction of acidemia are essential. Give glucose, and replace 

potassium deficits. 

Disposition 

Hospitalize all patients with known or suspected severe salicylate poisoning. Patients 

who have ingested enteric-coated tablets (eg, Ecotrin) may remain asymptomatic for 

several hours or even days; repeated blood levels and abdominal x-rays or even 

endoscopy may be necessary if a massive ingestion is suspected. 

Higgins RM et al: Alkalinization and hemodialysis in severe salicylate poisoning: 

comparison of elimination techniques in the same patient. Clin Nephrol 1998;50:178. 

[PMID: 9776422] 

Juurlink D et al: Gastrointestinal decontamination for the enteric-coated aspirin 

overdose: what to do depends on who you ask. J Toxicol Clin Toxicol 2000;38:465. 

[PMID: 10981955] (Survey of poison control centers and their individual 

recommendations for gastrointestinal decontamination in overdose with enteric-coated 

aspirin.) 

Wrathall G et al: Three case reports of the use of haemodiafiltration in the treatment of 

salicylate overdose. Hum Exp Toxicol 2001;20:491. [PMID: 11776412] (Case reports 

and discussion of the use of hemodiafiltration in the treatment of salicylate overdose.) 

SEDATIVE-HYPNOTICS 


• Symptoms include nystagmus, atonia, lethargy, somnolence, respiratory depression, 

hypotension, and hypothermia. 

• Sedative-hypnotics such as ?-hydroxybutyric acid may be associated with symptoms 

ranging from respiratory depression and coma to seizurelike activity with aggressive 

behavior. 


Sedative-hypnotics include a broad range of drugs used to treat anxiety or insomnia. 

They can induce tolerance and can cause a withdrawal syndrome similar to that 

associated with ethanol withdrawal (except for the time of onset and duration). These 

agents are found singly and in various drug combinations. Of note, one 

sedative-hypnotic, ?-hydroxybutyric acid (GHB), has become a relatively new drug of 

abuse. Effects range from respiratory depression, apnea, and coma to seizurelike 

activity along with aggressive behavior. 

Absorption, distribution, and elimination of sedative-hypnotics vary. In general, the 

mechanism of toxicity of these drugs is central nervous system depression similar to 

that caused by ethanol.


Clinical manifestations of overdose include nystagmus, ophthalmoplegia, ataxia, 

dysarthria, lethargy, somnolence, respiratory depression, hypotension, and 

hypothermia. With the onset of deep coma, oculocephalic reflexes are lost, and the 

pupils become nonreactive to light. The initial electroencephalogram may be flat, 

although the patient may subsequently recover completely. Serum drug levels may be 

misleading, because levels of intoxication and rates of elimination vary enormously from 

person to person, depending on prior drug use and the patient's physical state. 

Treatment 



previously. Treat shock and hypotension with an initial bolus of 200-1000 mL of 

intravenous crystalloid solution (Chapter 9). Restore the patient's core temperature to 

normal levels, because hypothermia will worsen hypotension. Monitoring the pulmonary 

capillary wedge pressure is helpful in avoiding fluid overload and determining the need 

for pressor agents. Vasopressors should be used only if adequate fluid replacement is 

ineffective (as determined by pulmonary capillary wedge pressure measurements). 

B. Enhanced Elimination 

Reserve hemodialysis or hemoperfusion for patients who remain hypotensive or 

otherwise unstable despite aggressive supportive care. These measures successfully 

remove only a few sedative-hypnotics (eg, phenobarbital, meprobamate, ethchlorvynol). 


The benzodiazepine antagonist flumazenil (Mazicon) should be used with extreme 

caution, if at all. The dose is 0.2 mg intravenously slowly repeated every 5-10 minutes 

as needed, up to a maximum 3-5 mg. Effects wear off in 1-3 hours, and repeated 

sedation is common. Contraindications include known seizure disorder, benzodiazepine 

addiction, and tricyclic antidepressant overdose. General supportive care usually 

suffices. 

Treatment of GHB toxicity is similar to the treatment of toxicity from all other 

sedative-hypnotics in that supportive care will usually suffice. However, flumazenil has 

no effect on GHB toxicity, but intravenous physostigmine (slowly over 2-3 minutes) has 

been found in some case studies to reverse the respiratory depression of GHB toxicity 

and obvert the need for intubation. The use of physostigmine should be discouraged, 

however, because of the potential for the development of life-threatening cardiac 


Disposition 

Hospitalize patients with sedative-hypnotic drug poisoning resulting in depression of 

vital reflexes (eg, respiration, gag reflex). 

James L et al: A tale of novel intoxication: a review of the effects of

gamma-hydroxybutyric acid with recommendations for management. Ann Emerg Med 

1998;31:729. [PMID: 9624313] (Literature review of the effects and management of 

GHB intoxication.) 

Rachel LC et al: Clinical course of gamma-hydroxybutyrate overdose. Ann Emerg Med 

1998;31:716. [PMID: 9624311] (Retrospective case analysis of patients with GHB 

overdose.) 

Yates SW et al: Physostigmine in the treatment of gamma-hydroxybutyric acid 

overdose. Mayo Clin Proc 200;75:401. [PMID: 10761496] (Case report of the use of 

physostigmine in the treatment of GHB overdose.) 

THEOPHYLLINE & METHYLXANTHINES 


• Minimum acute toxic dose is 10 mg/kg. 

• Mild symptoms include nausea and vomiting, tremor, anxiety, and abdominal 

cramping. 

• Severe symptoms include arrhythmias and seizures. 


Theophylline causes bronchodilatation; gastric, central nervous system, and cardiac 

stimulation; and vasodilatation. The half-life is 4-8 hours and is shortened in chronic 

smokers and prolonged in patients with congestive heart failure or cirrhosis. In acute 

overdose, the half-life may be markedly prolonged (up to 50 hours). 

The minimum acute toxic dose is over 10 mg/kg, or 700 mg, in the average adult. 

Because drug metabolism varies markedly depending on the patient's clinical status, 

careful monitoring of patients receiving therapeutic doses is necessary to avoid 

iatrogenic toxicity. 


Mild symptoms of toxicity are nausea and vomiting, abdominal cramps, tremor, and 

anxiety. Arrhythmias and seizures occur with more serious intoxication. Seizures are 

often refractory to treatment with standard anticonvulsants. The characteristics of acute 

single overdose differ from those of chronic, subacute overmedication. Acute overdose 

is characterized by hypotension, tachycardia, and hypokalemia. Seizures and serious 

arrhythmias are common with levels over 100 mg/L but rare with levels under 90 mg/L. 

By contrast, chronic intoxication more commonly results in seizures and arrhythmias 

with much lower serum levels (ie, 20-70 mg/L). Hypotension and hypokalemia are 

uncommon. The elderly are at highest risk for fatal outcome. 

Sustained-release theophylline preparations are now commonly used, so that after 

acute overdose, early blood concentrations of the drug may be low and gastrointestinal

symptoms absent. Obtain serial blood levels until the theophylline level begins to fall. 

Treatment 



previously. 

B. Gastrointestinal Decontamination 

Consider gastric lavage if a significant dose has been ingested within 1 hour of arrival at 

the emergency department. Administer multidose activated charcoal; consider whole 

bowel irrigation for sustained-release preparations. 

C. Treatment of Seizures 

Seizures (Chapter 17) are usually difficult to control with standard drugs. Start with 

diazepam, 0.1-0.2 mg/ kg as an intravenous bolus, followed by phenobarbital, 15 mg/kg, 

intravenously over 20-30 minutes. Perform hemoperfusion immediately if seizures are 

not controlled. 

D. Treatment of Hypotension 

Treat hypotension with intravenous fluids. Propranolol, 0.02-0.05 mg/kg, or esmolol, 

25-50 ug/kg/min, intravenously, may reverse hypotension associated with tachycardia, 

both of which are mediated by excessive ß-adrenergic stimulation. 

E. Treatment of Arrhythmias 

Ventricular tachyarrhythmias and rapid atrial fibrillation may be controlled with 

propranolol or esmolol intravenously(see above) or with standard antiarrhythmics. 

F. Enhanced Elimination 

Charcoal hemoperfusion, hemofiltration, or hemodialysis are the treatments of choice 

for severe poisoning. Hemoperfusion is the treatment of choice for severe poisoning 

(intractable seizures, acute overdose with serum level over 80-100 mg/L, and 

hemodynamic instability). Repeated doses of activated charcoal may be effective at 

lowering theophylline levels, obviating extracorporeal treatment. 

Disposition 

Hospitalize patients with significant theophylline poisoning (serum concentrations above 

30 ug/mL or signs or symptoms of toxicity). 

Henderson JH et al: Continuous venovenous haemofiltration for the treatment of 

theophylline toxicity. Thorax 2001;56:242. [PMID: 11182020] (Case study and 

discussion of the use of venovenous hemofiltration in theophylline toxicity.) 

Seiko O et al: Recovery from theophylline toxicity by continuous hemodialysis with 

filtration. Ann Intern Med 2000;133:922. [PMID: 11103070] (Case report of the use of 

hemodialysis with filtration to treat theophylline toxicity.) 

Shannon M: Life-threatening events after theophylline overdose. Arch Intern Med

1999;159:989. [PMID: 10326941] (Prospective longitudinal cohort study of patients with 

theophylline overdose.) 

TRICYCLIC ANTIDEPRESSANTS 


• Average toxic dose is 5 mg/kg. 

• Anticholinergic symptoms range from mydriasis, agitation, and tachycardia to seizures 

and coma. 

• Cardiovascular manifestations are often life threatening and include QRS widening, 

profound hypotension, atrioventricular blocks, and ventricular arrhythmias. 


Major tricyclic antidepressants include amitriptyline (Elavil, many others), imipramine 

(Tofranil, many others), and doxepin (Adapin, Sinequan). Maprotiline (Ludiomil) is a 

tetracyclic antidepressant with similar properties. 

The antidepressants are analogs of phenothiazines, with complex effects, including 

anticholinergic, a-adrenergic-receptor blocking, and quinidinelike activity on the heart. 

They are well absorbed and highly tissue bound, with volumes of distribution of 10-40 

L/kg. These drugs are eliminated primarily by metabolism in the liver, and the half-lives 

are 10-30 hours. The average toxic dose is more than 5 mg/kg, with severe poisoning 

occurring at doses of 10-20 mg/kg. 


Many symptoms are the result of the anticholinergic activity of these drugs, for example, 

mydriasis, dry mouth, tachycardia, agitation, and hallucinations. The onset of coma may 

be rapid, even precipitous. Twitching and myoclonic jerking have been noted, and 

seizures occur frequently and may be difficult to treat. 

Cardiovascular manifestations are the most dramatic and life threatening (Figure 45-2). 

Quinidinelike slowing of conduction is reflected by widening of the QRS complex (> 100 

ms) and prolonged QT and PR intervals. Varying degrees of atrioventricular block and 

ventricular tachycardia are common. Atypical (torsades de pointes) ventricular 

tachycardia may occur. Profound hypotension resulting from decreased contractility and 

vasodilatation may occur and is a frequent cause of death. Hypoxemia and acidosis 

aggravate the cardiovascular toxicity of tricyclic antidepressants. 

Diagnosis is generally based on history, relevant physical findings, widened QRS 

complexes, and prolonged QT intervals (3 C's: cardiac abnormalities, convulsions, and 

coma). The diagnosis may be confirmed by qualitative or quantitative tests for these 

drugs in the blood or urine. Plasma concentrations are rarely available and often lack 

sensitivity in detecting active metabolites. Prolongation of the QRS complex or the 

terminal axis in lead aVR is a better predictor of severity of poisoning than is the drug


Note: Some newer cyclic antidepressants (amoxapine) and antipsychotics (loxapine) 

can cause seizures and coma without associated cardiovascular toxicity or 

electrocardiographic changes. 

Treatment 



previously. Do not induce emesis because of the well-established risk of seizures and 

coma. Perform gastric lavage if the patient has ingested a toxic amount and is seen 

within 1 hour. Also, administer activated charcoal at the beginning and again at the end 

of the procedure. 

B. Cardiac Monitoring 

Constant monitoring of the ECG for at least 6 hours is mandatory. Progressive widening 

of the QRS complex indicates worsening toxicity. 

C. Treatment of Seizures 

Treat seizures with diazepam and phenytoin (Chapter 17). Do not use physostigmine to 

treat seizures, because it may cause seizures and other complications as described 

below. 

D. Treatment of Arrhythmias 

Sinus tachycardia is benign and usually does not require treatment. Physostigmine and 

propranolol may aggravate conduction abnormalities and should not be used. 

Ventricular arrhythmias and conduction defects may respond to sodium bicarbonate, 

50-100 mEq (1-2 mEq/kg) as an intravenous bolus. It is not clear whether the 

improvement is merely a result of correction of acidosis, a result of transient 

hypernatremia, or a result of a shift in the protein binding of the drug with alkalosis. 

Lidocaine, 1-2 mg/kg as an intravenous bolus (Chapter 35), is frequently effective. 

Phenytoin, 15- 18 mg/kg intravenously over 20-30 minutes, is the logical drug of choice 

because it enhances conduction while decreasing automaticity, but there is no proof that 

it is more effective. Quinidinelike drugs (eg, quinidine, procainamide, disopyramide) are 

contraindicated, because they worsen cardiotoxicity. 

E. Treatment of Hypotension 

Treat hypotension initially with intravenous infusion of sodium bicarbonate, 50-100 mEq 

(1-2 mEq/kg), and crystalloid solutions. If the patient fails to respond after 1-2 L have 

been infused, further therapy should be guided by measurement of pulmonary artery 

wedge pressures and cardiac output. Norepinephrine and epinephrine have been found 

to be more effective than dopamine in refractory hypotension. 

F. Other Measures 

Hemoperfusion has no role in tricyclic antidepressant poisoning. However, several new 

antidotes, including a-1 acid glycoprotein and hypertonic saline, are under investigation.

Disposition 

Hospitalize all symptomatic patients with overdose of tricyclic antidepressants. Use 

serial ECGs along with the patient's clinical appearance to predict impending toxicity. 

Observe asymptomatic patients for a minimum of 6-8 hours, taking repeated 

measurements of the vital signs and QRS interval. 

Kerr GW et al: Tricyclic antidepressant overdose: a review. Emerg Med J 2001;18:236. 

[PMID: 11435353] (Review of the pharmacokinetics, clinical presentation, and treatment 

of tricyclic antidepressant overdose.) 

Ma Y et al: The antidotal effect of alpha(1)-acid glycoprotein on amitriptyline toxicity in 

cardiac myocytes. Toxicology 2001;169:133. [PMID: 11718954] (Animal model study to 

evaluate the use of a-1 acid glycoprotein in the treatment of QRS prolongation caused 

by amitriptyline.) 

McCabe J et al: Experimental tricyclic antidepressant toxicity—a randomized, controlled 

comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation. Ann 

Emerg Med 1998;32:329. [PMID: 9737495] (Randomized, controlled animal-model 

comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation in 

severe tricyclic antidepressant overdose.) 

Mehta NJ et al: Tricyclic antidepressant overdose and electrocardiographic changes. J 

Emerg Med 2000;18:463. [PMID: 10802426] (Case report and discussion of ECG 

changes in tricyclic antidepressant overdose.) 

Singh N et al: Serial electrocardiographic changes as a predictor of cardiovascular 

toxicity in acute tricyclic antidepressant overdose. American Journal of Therapeutics 

2002;9:75. [PMID: 11782822] (Case report and discussion of the predictive value of 

ECG changes in acute tricyclic antidepressant overdose.) 

WARFARIN & OTHER ANTICOAGULANTS 


• A single overdose with warfarin usually does not cause significant bleeding. 

• May see ecchymosis, hematuria, melena, epistaxis, gingival bleeding, hematoma, and 

hematemesis. 

• Life-threatening cardiac tamponade and intracranial hemorrhage may occur. 


Dicumarol and other natural anticoagulants are found in sweet clover. Warfarin and 

other synthetic coumarinlike anticoagulants are used therapeutically and as 

rodenticides. 

Warfarin and other coumarinlike compounds inhibit blood clotting by interfering with the

synthesis of vitamin K-dependent clotting factors (II, VII, IX, X). Only the synthesis of 

new factors is affected, and the anticoagulation effect is delayed until currently 

circulating factors have degraded. Thus, effects may be seen within 8-12 hours after 

ingestion because factor II has only a 6-hour half-life, but peak effects are usually not 

observed until 1-2 days after ingestion because of the longer half-lives (24-60 hours) of 

the other clotting factors. 

The potency and pharmacokinetics of the different coumarin anticoagulants vary. 

Warfarin is highly bound to albumin and has a half-life of 35 hours. It is metabolized by 

the liver. Multiple drug interactions are known to increase or decrease the 

anticoagulation effect (Table 45-22). 

A single overdose with warfarin does not usually cause significant bleeding, because 

the half-life of warfarin is shorter than that of some of the clotting factors. Chronic 

warfarin administration carries a greater risk of excessive anticoagulation and bleeding. 

However, some newer, extremely potent and long-acting anticoagulants, also known as 

super-warfarins (brodifacoum, indanediones), may produce severe bleeding disturbance 

for several weeks to months following a single overdose. 


Excessive anticoagulation may result in ecchymoses, hematuria, uterine bleeding, 

melena, epistaxis, gingival bleeding, hemoptysis, or hematemesis. Hematomas may 

result in compression neuropathy or compartment syndrome. Life-threatening cardiac 

tamponade and intracranial hemorrhage have been reported. Such complications can 

be prevented if the international normalized ratio (INR) is carefully monitored and kept 

within the desired therapeutic range, if interacting drugs are avoided, and if antidotal 

therapy is begun promptly when necessary. 

Treatment 



previously. Gastric lavage and emesis are not recommended. Treatment is rarely 

required for acute single overdose of warfarin, because the dose involved (eg, from 

typical rodenticide) is small, and any anticoagulation effect is usually brief and mild. 

However, caution and careful follow-up are indicated after ingestion of the 

super-warfarins. Obtain a baseline prothrombin time, and repeat the measurement after 

24 and 48 hours. 

B. Treatment of Major Hemorrhage 

For major hemorrhage (eg, intracranial hemorrhage, aortic dissection, shock), control 

bleeding with fluid resuscitation and withhold further doses of warfarin. Vitamin K, 5-10 

mg intravenously, should be given along with fresh-frozen plasma, 15 mL/kg, or 

prothrombin complex concentrates. For patients with asymptomatic prolongation of the 

INR (> 10), give vitamin K, 2-5 mg orally, without fresh-frozen plasma. Recheck the INR 

in 6-12 hours. If the INR is between 6 and 10, give vitamin K, 2 mg, orally without 

fresh-frozen plasma and recheck the INR in 12-24 hours. In all the above cases, vitamin 

K should be given intravenously or orally, not intramuscularly, because of the risk of

erratic absorption and hematoma formation. 

Disposition 

Hospitalize all patients with significantly prolonged prothrombin times, evidence of 

bleeding, or history of ingestion of massive amounts of anticoagulants. Patients who 

have documented anticoagulant effect after ingestion of the super-warfarin rodenticides 

will need close follow-up and repeated vitamin K dosing for up to several weeks. 

Cruickshank J et al: Warfarin toxicity in the emergency department: recommendations 

for management. Emerg Med 2001;13:91. [PMID: 11476421] (Retrospective analysis of 

adult patients with warfarin toxicity and literature review of the treatment guidelines.) 

Walter-Michael H: Rational, high quality laboratory monitoring before, during and after 

infusion of prothrombin complex concentrates. Thrombosis Research 1999;95:S25. 

[PMID: 10499906] (Review of the use of prothrombin complex concentrates to treat 

warfarin overdose.) 

Weibert RT et al: Correction of excessive anticoagulation with low-dose oral vitamin K. 

Ann Intern Med 1997;126:959. [PMID: 9182473] (Case analysis of patients with 

excessive anticoagulation who received oral vitamin K.) 





Sewalls, MD 

IMMEDIATE MANAGEMENT OF LIFE-THREATENING CONDITIONS

Table 45-1. Physical findings associated with various types of poisons. 





Sewalls, MD 

TABLES 

Table 45-1. Physical findings associated with various types of poisons.

Table 45-2. Toxidromes. 1 

Representative 

Agent(s) 

Cocaine 

Amphetamine 

Scopolamine 

Atropine 

Sulfonylureas 

Insulin 

Additional Signs 

and Symptoms 

Seizures, rhabdomylosis, myocardial 

infarction 

Death may result from seizures, 

cardiac arrest, hyperthermia 

Seizures, dysrhythmias, 

rhabdomyolysis 

Death may result from hyperthermia 

and dysrhythmias 

Paralysis, slurring of speech, bizarre 

behavior, seizures 

Death may result from seizures, 

altered behavior 

Cholinergic 

Salicylates 

Serotinin syndrome 

Opioid 

1 Reproduced, with permission, from Tintinalli JE, Kelen GD, Stapczynski S: Emergency Medicine: A C 





Sewalls, MD 

TABLES 

Table 45-2. Toxidromes.

Table 45-3. Drugs causing metabolic acidosis associated 

with an elevated anion gap. 1 

1 

Anion gap = (Na 

+ 

+ K 

+ 

) - (HCO3- + Cl 

- 

) = 12-16 mEq/L. 





Sewalls, MD 

TABLES 

Table 45-3. Drugs causing metabolic acidosis associated with an elevated 

anion gap.

Table 45-4. Calculation of the osmolar gap in toxicology. 





Sewalls, MD 

TABLES 

Table 45-4. Calculation of the osmolar gap in toxicology. 

Lethal 

Concentration 

(mg/dL)

Table 45-5. Electrocardiographic manifestations of poisoning. 

Examples of Causes 

Hypocalcemia (ethylene glycol) 


Type I antiarrhythmic agents 

Phenothiazines (selected) 



Beta-adrenergic blockers 

Calcium-channel blocking agents 

Digitalis glycosides 



Amphetamines, cocaine 

Digitalis glycosides 

Theophylline 



Cellular, asphyxiants (cyanide, carbon monoxide) 

Hypoxemia (pneumonia) 

Hypotension 





Sewalls, MD 

TABLES 

Table 45-5. Electrocardiographic manifestations of poisoning.

Table 45-6. Drugs and toxins that may be radiopaque. 1 

Heavy metals (iron, arsenic) is 

Psychotropics (phenothiazines, tricyclic antidepressants) 

Enteric-coated tablets 

1 Caution: Recent 

studies suggest 

that these drugs 

are not routinely 

visible on x-ray. If 

tablets have 

dissolved, 

false-negative 

x-ray results may 

occur. Abdominal 

x-rays are 

therefore useful 

only if positive 

findings are seen. 





Sewalls, MD 

TABLES 

Table 45-6. Drugs and toxins that may be radiopaque.

Table 45-7. Volumes of distribution for some common drugs. 

Drugs with Small Volumes of Distribution 

10-20 L/kg 0.8 L/kg 

20-30 L/kg 0.5 L/kg 

> 40 L/kg 0.6 L/kg 

10-20 L/kg 0.6 L/kg 

6-10 L/kg 1.1 L/kg 

4 L/kg 0.6 L/kg 

5 L/kg 0.2 L/kg 

0.5 L/kg 





Sewalls, MD 

TABLES 

Table 45-7. Volumes of distribution for some common drugs.

Table 45-8. Indications for hemodialysis (HD) or hemoperfusion (HP) 

in the management of poisoned patients unresponsive to antidotal or 

supportive therapy. 





Sewalls, MD 

TABLES 

Table 45-8. Indications for hemodialysis (HD) or hemoperfusion (HP) in the 

management of poisoned patients unresponsive to antidotal or supportive therapy.

Table 45-9. Some poisons for which there are specific antidotes. 

Specific Antidote 

Acetylcysteine 

Physostigmine 

Atropine 

Pralidoxime (2-PAM) 

Flumazenil 

Glucagon 

Calcium 

100% Oxygen 

Sodium nitrite 

Sodium thiosulfate 

Vitamin B 12 (not yet approved for use in the United States) 

Digoxin-specific antibodies 

Chelating agents 

Pyridoxine (vitamin B 6 ) 

Ethanol, folate, 4-methyl pyrazole (not approved for use in the United States) 

Naloxone 

Sodium bicarbonate 





Sewalls, MD 

TABLES 

Table 45-9. Some poisons for which there are specific antidotes.

Table 45-10. Selected examples of poisons with delayed severe 

toxicity. 

Delayed Effect 

Hepatic necrosis 

Hepatic necrosis 

Hepatic and renal damage 

Blindness 

Pulmonary fibrosis 

Bleeding 

Peripheral neuropathy, hair loss 

Renal failure 





Sewalls, MD 

TABLES 

Table 45-10. Selected examples of poisons with delayed severe toxicity.

Table 45-11. Clinical findings in carbon monoxide poisoning. 

Carboxyhemoglobin 

(% of Total 

Hemoglobin) 

Less than 35 ppm (cigarette 

smoking) 

None, or mild headache 

10 0.01% (100 ppm) Throbbing headache, 

dyspnea with moderate 

exertion 

30 0.03-0.05% (300-500 ppm) Headache, tachycardia, 

confusion, lethargy, collaps 

60-70 0.19% (1900 ppm) Rapidly fatal

Table 45-12. Digoxin immune Fab dosing. 





Sewalls, MD 

TABLES 

Table 45-12. Digoxin immune Fab dosing.

Table 45-13. Common corrosive agents. 

Examples Concentrated alkali Penetrating liquefaction 

necrosis 

Pool disinfectants 

Toilet bowl 

cleaners 

Weaker cleaning agents Superficial burns and 

irritation; deep burns (rare)

Table 45-14. Prepackaged cyanide antidote kit. 1 

How Supplied Amyl nitrite Break 1-2 aspirols 

under patient's nose 

3 g/dL (300 mg in 10 mL 

[vials]) 

Sodium thiosulfate 500 mg intravenously

Table 45-15. Chelating agents. 

Chelating Agent Side Effects 

Deferoxamine Hypotension with rapid intravenous 

route of administration. 

Edetate 

calciumdisodium 

(EDTA) 

2,3-Dimercaptosuccinic 

acid (DMSA) 

(Succimer) 


Reversible acute tubular necrosis; zinc 

and vitamin B 6 depletion. Do not give 

orally. If urinary output inade-quate with 

administration, initiate hemodialysis. 

Nausea, vomiting, diarrhea, transient 

liver function enzyme elevation. 

3-5 mg/kg/dose IM q 4 h × 5 d Penicillamine 




Sewalls, MD 

TABLES 

Table 45-15. Chelating agents.

Table 45-16. Recommended treatment for lead poisoning by blood 


Treatment 

None. 

Stop further exposure to lead and monitor blood levels monthly. 

Children: Give DMSA (Succimer) in the absence of encephalopathy or 

protracted vomiting. BAL and EDTA can also be used. 

Adults: Give EDTA and BAL. Although not FDA-approved for adults, consider 

use of DMSA. 

Considered a medical emergency. Institute chelation with BAL, EDTA, and 

possibly DMSA immediately.

Table 45-17. Clinical features of hydrocarbon poisoning. 

Examples 

Furniture polish, 

mineral spirits, 

kerosene, lighter fluid 

CHAMP: Camphor, 

Halogenated or 

Aromatic hydrocarbons 

(benezene, toluene), 

Metals, Pesticides 


Risk of 

Systemic 

Toxicity 

High-viscosity Low 

Low Low-viscosity, unknown systemic 

toxicity 

High 




Sewalls, MD 

TABLES 

Table 45-17. Clinical features of hydrocarbon poisoning. 

High

Table 45-18. Clinical features of toxic gases and fumes. 

Toxin Clinical Features Simple asphyxiants Cooking gas 

Cooking gas 

All fires 

Industry (especially welding) 

Carbon monoxide Forms carboxyhemoglobin; 

inhibits oxygen transport. 

Headache is earliest 

symptom. 

High solubility in 

water 

Industry; swimming pool 

chemical; bleach mixed with 

acid at home 

Industry; burning fabrics 

Nitrogen dioxide Has sweet "electric" smell. 

Delayed onset (12-24 hours) 

of tracheobronchitis, 

pneumonitis, and pulmonary 

edema. Late chronic 

bronchitis. 

Zinc 

Copper 

Tin 

Teflon 


"Metal fumes fever." Chills, 

fever, myalgias, headache, 

nonproductive cough, 

leukocytosis (4-8 hours after 

exposure). 

Hydrocyanic acid Highly toxic ce 

asphyxiant (see 

cyanide). 

Humidified oxygen; 

bronchodilators; airway 

management. 

Ozone 

Arsine Highly toxic. He 

pulmonary ede 

failure; chronic 

toxicity. 




Sewalls, MD 

TABLES 

Table 45-18. Clinical features of toxic gases and fumes.

Table 45-19. Mushrooms: symptoms, toxicity, and treatment. 

Mushrooms Treatment 

Onset < 2 h Nausea, vomiting, diarrhea (occasional 

bloody) 

Initial: nausea, vomiting, diarrhea 

Inocybe 

Clitocybe 

Amanita muscaria 

Amanita pantherina 

Psilocybe 

Gymnopilus 

Supportive atropine, 0.01 mg/kg, 

repeated as needed for severe 

secretions. 

Supportive sedation with phenobarbital, 

30 mg IV, or diazepam, 2-5 mg IV, as 

needed for adults 

Supportive sedation with phenobarbital, 

0.5 mg/kg, or, for adults, 30-60 mg IV, or 

diazepam, 0.1 mg/kg or 5 mg IV, for 

adults 

Gyromitra esculenta: fall s 

Amanita phalloides, Aman 

Amanita virosa: spring sea 

Coprinus Supportive IV hydration 

Propranolol for supraventricular 

tachycardia 

Norepinephrine for refractory 

hypotension 

Reproduced, with permission, from Tintinalli JE, Keten GD, Stapczynski S: Emergency Medicine: A Co 





Sewalls, MD 

TABLES 

Table 45-19. Mushrooms: symptoms, toxicity, and treatment.

Table 45-20. Some nontoxic plants. 





Sewalls, MD 

TABLES 

Table 45-20. Some nontoxic plants.

Table 45-21. Some poisonous plants. 1 

Type of Toxin 

Andromedotoxin (nicotinelike and cardiotoxic) 

Solanine 

Oxalates 

Toxalbumin (ricin) 

Anticholinergic 

Nicotinelike 

Oxalates 

Cyanogenic (ripe berries nontoxic) 

Cardiac glycosides 

Cyanogenic 

Toxalbumin (a lectin) 

Solanine 




Nicotinelike 

Tyramine (hypertension; gastroenteritis) 

Andromedotoxin (nicotinelike and cardiotoxic) 


Oxalates 

Cyanogenic (amygdalin) 

Nicotinelike 

Oxalatelike 

Nicotine 

Cicutoxin (seizures) 

Taxine (gastrointeritis, cardiac toxicity)

Table 45-22. Interactions of warfarin and oral 

anticoagulants with selected drugs. 

Decreased 

Anticoagulation 

Effect 

Barbiturates 

Chloral hydrate Cholestyramine 

Disulfiram Oral contraceptives 

Quinidine 

Sulfonamides 





Sewalls, MD 

TABLES 

Table 45-22. Interactions of warfarin and oral anticoagulants with selected 

drugs.

Figure 45-1. Nomogram for prediction of acetaminophen hepatotoxicity following acute 

overdosage. The upper line defines serum acetaminophen concentrations known to be 

associated with hepatotoxicity. The lower line defines serum levels 25% below those 

expected to cause hepatotoxicity. To give a margin for error, the lower line should be 

used as a guide to treatment. (Modified and reproduced, with permission, from Rumack 

BM, Matthew M: Acetaminophen poisoning and toxicity. Pediatrics 1975;55:871.) 





Sewalls, MD 

FIGURES 

Figure 45-1

Figure 45-2. Supraventricular tachycardia with prolonged QT c and terminal right axis 

resulting from tricyclic antidepressant overdose. 





Sewalls, MD 

FIGURES 

Figure 45-2

46. Dermatologic Emergencies - Joseph A. Salomone III, MD, FAAEM, 

& Martha Ann Pratt, MD 

IMMEDIATE RECOGNITION & MANAGEMENT OF 

LIFE-THREATENING PROBLEMS 

To some observers, emergency medicine and dermatology may seem to be two of the 

most unrelated specialties in medicine, but the emergency physician will encounter 

many patients presenting with dermatologic complaints. The astute clinician will realize 

that, although rare, some of these problems can be life threatening. Some patients may 

even require emergent airway protection and vigorous resuscitation. This chapter 

reviews those special situations and discusses common and uncommon dermatologic 

complaints. 

Initial Evaluation 

The initial evaluation begins with the primary survey and vital signs. Always focus 

special attention on airway, breathing, and circulation (the ABCs). Note any abnormal 

vital signs and oxygen saturation, and be alert to subtle changes in mental status or 

behavior that may indicate impending airway or cardiovascular collapse. The ABCs 

apply to all clinical situations, and thorough histories and examinations are often the 

most helpful tools in arriving at any diagnosis. Early and appropriately aggressive airway 

management and fluid resuscitation may prevent morbidity or even death. 

History 

Parallel to the assessment of the ABCs is the beginning of a thorough history that 

includes potential recent exposures to foods, medications, plants, insects, and the like 

that may have triggered the condition. An AMPLE history, addressing the patient's 

allergies, medications, past medical and surgical history, last meal, and events leading 

up to the presentation may provide information necessary to begin appropriate 

management. 

ANGIOEDEMA & URTICARIA 

1. Angioedema 


• Swelling of face, lips, tongue. 

• May lead to airway compromise. 


Angioedema is edema that forms in the mucous membranes and subcutaneous tissues 

of the face and neck. Particularly dangerous is the involvement of the mouth, tongue, 

and lower airway, which can lead to severe airway compromise. Two subtypes exist, the 

rare hereditary form and the acquired form. The hereditary variant is usually due to 

C1-esterase deficiency. The acquired form is most commonly secondary to 

angiotensin-converting enzyme (ACE) inhibitors and has increased in prevalence 

because of widespread usage of these drugs. 

Treatment 

Emergent airway protection is mandated if airway compromise is impending or present. 

Treat shock if present. Discontinue any implicated medications or substances. Supply 

oxygen to maintain oxygen saturation at greater than 90%. In severe angioedema with 

airway compromise, administer epinephrine (0.3-0.5 mL of 1:1000 solution) 

subcutaneously or intramuscularly. This may be repeated every 10 minutes and is used 

to maintain a patent airway. Give antihistamines, such as diphenhydramine HCl, 1-2 

mg/kg or 25-50 mg parenterally. Methylprednisolone sodium succinate, 125 mg 

intravenously, may be repeated every 6 hours. This drug is used to help blunt or block 

any late-phase response. 

Disposition 

Admit patients to an intensive care unit if airway compromise is present; otherwise, they 

may need observation in the emergency department. If a patient is thought to have 

experienced a reaction to a medication, instruct the patient to discontinue that 

medication and contact his or her primary care physician to discuss an alternative 

medication. 

2. Urticaria 

Urticaria 


• Localized areas of dermal edema. 

• Intense itching. 

Anaphylaxis 

• May have urticaria. 

• Bronchospasm. 

• Angioedema. 

• Shock. 


Urticaria (hives) may be either acute or chronic and may appear in any age group. The

condition represents one end of a continuum, ranging from urticaria to anaphylactic 

shock. Because various medications and foods are most often implicated as causes, 

take a thorough history of possible exposures. The lesions themselves represent 

localized areas of edema in the dermis. They appear as intensely pruritic, sharply 

demarcated areas with either an erythematous or a blanched base and border. Their 

appearance may wax and wane, and individual lesions often resolve within an hour. 

With anaphylaxis, there may be an initial decrescendo of the presenting symptoms with 

early interventions. A late-phase response may occur hours later with a more severe 

presentation than the initial symptom complex. 

Treatment 

If airway compromise is not present, patients can be given H 1 -receptor blockers (see 

diphenhydramine dosing, above), steroids, and even epinephrine. H 2 -receptor blockers, 

such as ranitidine, may also be added. If airway compromise is present, treat 

emergently as for angioedema (see above). 

Disposition 

Disposition is the same as for angioedema (see above). Remember the 

sometimes-biphasic nature of anaphylactic reactions. Instruct patients to avoid any 

potentially responsible agents. Give any patient with a history of anaphylaxis a 

prescription for an auto-injector epinephrine device and instruct the patient on its proper 

use prior to discharge. 

Chin AG et al: Angiotensin-converting enzyme inhibitor-induced angioedema: a 

multicenter review and an algorithm for airway management. Ann Otol Rhinol Laryngol 

2001;110 (9):834. [PMID: 11558759] (A brief review with a focus on airway 

management and outcomes at two tertiary care centers.) 

Rusznak C et al: Anaphylaxis and anaphylactoid reactions. A guide to prevention, 

recognition, and emergent treatment. Postgrad Med 2002;111(5):101. [PMID: 

12040857] (A review of pathophysiology and emergent treatment of anaphylaxis with 

specific treatment recommendations.) 

STEVENS-JOHNSON SYNDROME & TOXIC EPIDERMAL NECROLYSIS 


• Epidermal detachment. 

• Drug-induced or post-viral illness. 

• Patients may be critically ill. 


A disorder of epidermal detachment was initially reported in 1922, when Stevens and 

Johnson published a description of two children with fever, erosive stomatitis, severe

conjunctivitis, and a disseminated cutaneous eruption. It is now known to be a 

drug-induced state or one that follows a viral illness. Stevens-Johnson syndrome (SJS) 

and toxic epidermal necrolysis (TEN) are now thought to represent ends of a spectrum 

of reactions involving detachment of the epidermis. Both conditions share inciting 

factors. The range of disorders has been classified into three categories: SJS, involving 

less than 10% of body surface area (BSA); transitional cases, involving 10-30% of BSA; 

and TEN, with greater than 30% of BSA with detached epidermis. Mortality rates for 

SJS are approximately 5%; rates are much higher (30%) with TEN. Death is most 

commonly from sepsis secondary to infections from S. aureus and P. aeruginosa. 


Patients with SJS present with severe, intensely painful bullae and mucosal ulcerations 

with a truncal distribution of target-like lesions. The skin lesions are typically purpuric 

macules. The Nikolsky sign may be elicited. This refers to easy separation of the upper 

layers of the epidermis from the lower layers with very minor trauma, such as lateral 

traction or gentle rubbing on the skin. Patients with TEN typically present with fever, 

pruritus, pharyngitis, and conjunctivitis. These symptoms and signs precede mucous 

membrane and skin involvement. Mucous membrane involvement usually occurs first, 

followed by skin involvement. The rash is painful and usually starts on the upper trunk or 

face. Affected skin may be erythematous or have bullae. There may be eroding of the 

bullae, or the affected skin may slough in large sheets. This may progress over hours to 

days. The sloughing may involve other organ systems, including the gastrointestinal 

tract and the respiratory tree. 

Treatment 

Discontinue any potentially responsible medications. This usually requires that all 

nonessential medicines be stopped, because no tests are available to identify culprit 

agents. Careful correction of electrolyte abnormalities and fluid replacement are critical, 

because significant fluid losses occur with loss of the protective skin barrier. In TEN, 

airway protection and mechanical ventilation may be necessary if the trachea and upper 

airway are involved. Sloughing and detachment of mucosa can lead to airway 

compromise. Antibiosis may be necessary to avoid sepsis-related complications. Pain 

control is essential. 

Disposition 

In severe cases, treatment in a burn center may be necessary. Guard carefully against 

infection. Avoid central lines if possible. Avoid steroids because they have not proved 

beneficial. 

Becker DS: Toxic epidermal necrolysis. Lancet 1998;351(9113): 1417. [PMID: 9593426] 

(A review of TEN with a practical focus on treatment strategies.) 

Revus J: New advances in severe adverse drug reactions. Dermatol Clin 

2001;19(4):697. [PMID: 11705355] This is an extensive review of various drug-related 

reactions.

Wolkenstein P et al: Toxic epidermal necrolysis. Dermatol Clin 2000;18(3):485. [PMID: 

10943543] (A thorough review of the diagnosis, cause, and treatment of TEN.) 

Wolkenstein PE et al: Drug-induced toxic epidermal necrolysis. Clin Dermatol 

1998;16(3):399. [PMID: 9642534] (A thorough review of TEN.) 

EXFOLIATION & ERYTHRODERMA 


• A diffuse, generalized erythema and scaling. 

• Occurs secondary to many disease states. 


Many cutaneous diseases present with exfoliative erythroderma, or generalized redness 

and scaling. This condition is associated with a high risk for morbidity and mortality, 

independent of the inherent risks of the disease process it represents. Most commonly, 

this condition occurs secondary to psoriasis, atopic dermatitis, cutaneous T-cell 

lymphoma, or reactions to any of a wide range of inciting drugs. The erythrodermic state 

usually has a slow progression, but an acute onset may occur in patients who have 

cutaneous dermatoses or severe drug reactions. 


Clues to the diagnosis may be from the underlying disease, such as psoriatic plaques or 

characteristic nail changes. Bullous pemphigoid typically exhibits tense bullae in addition 

to erythroderma. Long-standing erythroderma may be associated with keratoderma, 

alopecia, and ectropion. Peripheral edema occurs in 50% of patients. Patients with 

severe drug reactions may appear acutely ill with fever, malaise, and lymphadenopathy. 

A leukocytosis with eosinophilia, organomegaly, and hepatic or renal impairment may 

be present. In the most severe cases, high-output cardiac failure may occur. Severe 

alterations in fluid balance may occur, leading to shock. Sepsis may ensue, and hepatic 

necrosis may be fatal. 

Treatment 

Correction of derangements in fluid balance must begin early. Take care with the skin, 

applying moist dressings to weeping areas. Low-potency topical steroids may be used. 

Avoid high-potency preparations, because the large surface areas involved could lead 

to the absorption of large doses of steroids. Treat secondary infections. 

Disposition 

Hospital admission is often required, preferentially in an intensive care unit, depending 

on the needs of the patient.

Rothe MJ et al: Erythroderma. Dermatol Clin 2000;18(3):405. [PMID: 10943536] (A 

review of erythroderma with a focus on inciting agents, diagnosis, and treatment and 

includes excellent photographs of skin findings.) 

STAPHYLOCOCCAL SCALDED SKIN SYNDROME 


• Skin appears scalded and blistered. 

• Affects primarily children. 

• Skin barrier is broken and leads to S. aureus infection. 


Primarily a disease of children, staphylococcal scalded skin syndrome (SSSS) refers to 

a series of toxin-induced blistering dermatoses. The exfoliative toxins are primarily 

attributed to S. aureus, and all phage groups of the bacterium have now been 

implicated. Mortality rates are low (2-3%) in children but can reach as high as 60% in 

adults who have comorbidities or preexisting conditions. 


The clinical presentation ranges from a milder form with localized eruption of a few 

fragile fluid-filled bullae surrounded by normal skin, to a more involved state. The more 

widespread form is often associated with fever, generalized erythema, and poor feeding 

in infants. Subsequently, large bullae form with a predilection for sites of friction. Erosion 

can occur in large areas, resulting in open, painful lesions. The Nikolsky sign is present. 

Unlike in SJS or TEN, mucous membranes are spared in SSSS. This may be a helpful 

distinguishing factor. The process is thought to result from a break in the protective skin 

barrier, which leads to a S. aureus infection. Typical areas involved in the primary 

infection include the umbilicus in neonates, as well as the nasopharynx, urinary tract, 

and other sites. 

Treatment 

Cases of localized eruptions may be treated with oral antibiotics. The widespread form 

usually requires parenteral antibiotics to cover penicillin-resistant S. aureus. Treatment 

for adults is nafcillin, 1.5 g, or oxacillin, 2 g intravenously every 4 hours. For pediatric 

patients, treatment is nafcillin or oxacillin, 150 mg/kg/d intravenously in divided doses for 

5-7 days. If superinfection is suspected, an aminoglycoside may be needed. 

Rehydration and thermoregulation are essential, as is adequate pain control. 

Disposition 

Severe cases require treatment in an intensive care unit or burn center. Because the 

cleavage of the epidermis and exfoliation are extremely superficial, the lesions typically 

heal with little or no residual scarring.

Callahan EF et al: Cutaneous (non-HIV) infections. Dermatol Clin 2000;18(3):497. 

[PMID: 10943544] (A concise and thorough review of major cutaneous infections.) 

Ladhani S: Recent developments in staphylococcal scalded skin syndrome. Clin 

Microbiol Infect 2001;7(6):301. [PMID: 11442563] (A review of the latest knowledge 

regarding the pathophysiology and cause of SSSS, with a discussion of the diagnosis 

and treatment.) 

RECOGNITION & MANAGEMENT OF POTENTIALLY 

LIFE-THREATENING PROBLEMS 

CELLULITIS & ERYSIPELAS 

Cellulitis 


• Deeper infection. 

• Affects skin and subcutaneous tissues. 

Erysipelas 

• Well-demarcated, superficial, erythematous infection. 

• Often affects face and extremities. 


Cellulitis and erysipelas refer to infections of the subcutaneous tissues. Erysipelas 

involves the more superficial upper dermis, and cellulitis is deeper, with more extensive 

involvement of the subcutaneous tissues and fat. Both conditions are acute and are 

related to a breach in the skin's protective barrier function. This can be secondary to 

fissuring and maceration, burns, venous stasis, malnutrition, or any of a number of other 

factors. The primary causative agent is group A ß-hemolytic streptococcus. Other 

causes include streptococci B, C, and G and, less commonly, staphylococci infection. 

Causative organisms associated with cellulitis include S. aureus, H. influenzae, S. 

pneumoniae, Pseudomonas, and several others. If untreated, both conditions can lead 

to devastating complications such as local abscesses and gangrene with severe 

cellulitis. Facial erysipelas may lead to cavernous sinus thrombosis. Both cellulitis and 

erysipelas may lead to septicemia. 


Erysipelas is characterized by well-demarcated, erythematous, indurated plaques. The 

borders may be palpable. Primary sites include the face, scalp, and lower extremities. 

Patients are usually in the extremes of age. Cellulitis is usually associated with painful 

swelling and erythema of the involved area. The borders are usually less well defined,

and the affected area is typically warm. 

Treatment 

Although many cases can be managed on an outpatient basis, patients may have 

constitutional symptoms, and those with comorbid conditions may be quite ill and 

require hospitalization. Antibiotics are used empirically to cover streptococci and S. 

aureus. Recommended therapies include penicillin G, 600,000 to 2 million units 

intravenously every 6 hours, for streptococci; and nafcillin, 1.5-2 g intravenously every 4 

hours, for staphylococci. Treat methicillin-resistant cases with vancomycin. If H. 

influenzae is suspected, use ampicillin, 200-250 mg/kg intravenously divided into 6 

doses. Trimethoprim-sulfamethoxazole may be used in penicillin-allergic patients. 

Patients who appear well and without constitutional symptoms may be given oral 

therapy. This includes oxacillin, 0.5-1 g orally 4 times daily, or erythromycin, 0.25-0.5 g 

orally 4 times daily, in the penicillin-allergic patient. Simple measures may be helpful in 

both conditions, including rest, cool compresses, elevation of the affected part, and 

antibacterial soaks. Debridement is used in secondary abscesses. 

Callahan EF et al: Cutaneous (non-HIV) infections. Dermatol Clin 2000;18(3):497. 

[PMID: 10943544] (A concise and thorough review of major cutaneous infections.) 

Sadick NS: Current aspects of bacterial infections of the skin. Dermatol Clin 

1997;15(2):341. [PMID: 9098643] (A review of cutaneous infections with practical 

applications to diagnosis and treatment.) 

PUSTULAR PSORIASIS 


• Most patients have preexisting plaque psoriasis. 

• Patients are systemically ill and febrile. 

• Large areas of erythema with multiple pustules. 


This condition usually occurs in patients with the preexistent plaque variant of psoriasis 

(see later for a description). Patients typically appear ill or toxic. Constitutional 

symptoms are present, including fever and malaise. Patients are often bedridden. A 

thorough history often reveals a recent withdrawal from systemic corticosteroid therapy. 


Psoriatic plaques may be seen in conjunction with large areas of erythema. These are 

usually covered with small pustules. The pustules enlarge and merge to form large 

purulent collections on the skin. Patients become extremely ill and are usually febrile 

and experience arthralgias and gastrointestinal symptoms. A more localized variant may 

be seen on the palms and soles, without concomitant plaque psoriasis.


The generalized form of pustular psoriasis can be difficult to treat. It usually mandates 

inpatient treatment with the close collaboration of a dermatologist. 

Drew GS: Psoriasis. Prim Care 2000;27(2):385. [PMID: 10815050] (A thorough review 

of various types of psoriasis with a discussion of multiple treatment modalities.) 

PEMPHIGUS VULGARIS 


• Blistering of skin and mucous membranes. 

• Usually affects older adults. 


Pemphigus is one of several autoimmune diseases of the skin that present with 

blistering. The antibodies attack skin proteins and result in the inability of cells in the 

epidermis to hold together normally. Blisters form within the superficial epidermis. 

Although rare, pemphigus can be life threatening. Several subtypes exist, and 

pemphigus vulgaris is the most common and the most severe. Prior to newer 

developments in therapy, mortality rates were as high as 50% at 2 years and 100% at 5 

years. 


Pemphigus most often occurs in older adults. The skin and mucous membranes are 

usually affected, and oral lesions often appear first. All mucous membranes may 

eventually be affected. As described earlier, the blistering is superficial. This results in 

fragile, flaccid blisters. The underlying skin may be erythematous. In the oral cavity, the 

blisters often slough prior to presentation, and the clinician may find only ulcerations. 

Hoarseness may occur if the lower airway is involved. Oral involvement can be 

extremely painful, interfering with the patient's ability to tolerate oral intake. The blisters 

slough easily, and the erosions enlarge by extending their borders. The Nikolsky sign is 

present. These erosions often crust over, but scarring is not usually a problem. 

Treatment 

Patients may have only isolated lesions, but more commonly there is widespread 

involvement. Patients may appear ill or toxic. Initial management involves fluid 

resuscitation, because fluid losses from the blistering are significant. Institute antibiotic 

therapy if secondary infection is present. Causative organisms are usually streptococci 

or staphylococci. This chronic disease usually mandates lifelong immunosuppressive 

therapy. The advent of glucocorticoids has decreased the mortality rates to 

approximately 5%. Start steroid therapy immediately. The suggested doses are 1-2.5

mg/kg/d of prednisone. Prednisone doses of 60 mg/d are recommended for treating 

isolated oral lesions. Topical high-potency steroids, such as clobetasol propionate 

0.05%, can also be used in mild cases of skin involvement but should not be used on 

mucous membranes. Other immunosuppressive agents, such as azathioprine, are 

usually added to the oral steroid regimen later. 

Disposition 

Admit patients who appear ill to an intensive care unit for careful management of their 

fluid balance, with the close help of consultants to aid in the diagnosis. 

Cotell S et al: Autoimmune blistering skin diseases. Am J Emerg Med 2000;18(3):288. 

[PMID: 10830686] (A discussion of pemphigus and pemphigoid disorders from the 

perspective of the emergency physician.) 

Toth GG et al: Therapy of pemphigus. Clin Dermatol 2001; 19(6):761. [PMID: 

11705686] This is a review of current methods of treating pemphigus. 

RECOGNITION & MANAGEMENT OF NON-LIFE-THREATENING 

PROBLEMS 

CONTACT DERMATITIS & Rhus Dermatitis 


Rhus dermatitis 

• Intense itching. 

• Erythema with vesicles. 

• Linear distribution. 

• Lesions appear 8-48 hours after exposure to poison ivy, poison oak, or poison sumac. 


Contact dermatitis refers to a collection of disorders resulting from an inciting 

environmental agent that has contacted the skin. The usual manifestation is a 

papulosquamous eruption, but vesicles may also be present. 

A classic example is Rhus dermatitis, which is induced by plants in the Rhus genus 

(Toxicodendron). This collection of plants includes poison ivy, poison oak, and poison 

sumac. The culprit agent is the plant oil urushiol, and 50-70% of the U.S. population is 

sensitive to this substance. Factors affecting the clinical significance of any contact 

include the extent of exposure, the patient's age and activity level, and the patient's 

immunocompetence. Poison ivy, poison oak, and poison sumac are native plants of 

North America, rarely found at elevations above 4000 feet. Their appearance is quite 

variable, and they do not always exhibit the classic three-leaf morphology. The oil 

urushiol is widely distributed in almost all parts of the plant. The resultant dermatitis is

classically described as a form of delayed hypersensitivity (type IV) reaction. 


After the first exposure, lesions can erupt within 8-48 hours, and they may persist for up 

to 3 weeks. The presence of an intensely pruritic, erythematous, papulovesicular 

eruption after an environmental exposure is highly suggestive of Rhus dermatitis. The 

lesions are usually linear. Transfer of the allergenic urushiol can continue and produce 

more lesions if it is not completely removed. It must be cleansed from the fingernails, 

skin, and clothing and from pets. Transfer of the oil, not the vesicles or the vesicular 

fluid, is responsible for the development of new lesions. Immediate eruption after 

exposure is not consistent with Rhus dermatitis, because it takes at least 8 hours for the 

cell-mediated response to develop. The most common sites for eruptions are the face 

and extremities. The lesions may range from erythematous papules to large bullae. Any 

of the commonly used rules for estimation of body surface area of burns, such as the 

"rule of nines" or preprinted estimation sheets, may be used to estimate the percentage 

of body surface area involved. 

Treatment 

The condition is self-limiting, with resolution within 3 weeks if all of the urushiol is 

removed. The most important therapy is prevention of exposure, but if exposure occurs, 

the individual should attempt to remove the oil within 10-30 minutes of exposure. 

Treatment can decrease the severity of the symptoms, but it does not shorten the 

course. Oral antihistamines are effective symptomatic therapy for the intense pruritus. 

Topical preparations, including calamine, camphor, and cool compresses, are useful 

measures for comfort. Extreme caution must be used with topical antihistamines, 

zirconium, and benzocaine. These medications are no longer advocated, secondary to 

systemic absorption and sensitization. Over-the-counter steroid preparations are 

typically not helpful, because they contain too little steroid to be of benefit. 

The backbone of therapy is usually a moderate-potency topical corticosteroid, such as 

triamcinolone 0.1% cream or betamethasone 0.1% cream. If the case is more severe or 

widespread, high-potency preparations such as clobetasol propionate 0.05% may be 

used. Extreme caution must be used with these creams, because systemic effects can 

occur secondary to steroid absorption. Steroid therapy can also be used orally, but to be 

effective it must begin within 18 hours of exposure. Therapy must be tapered for 2-3 

weeks. If the dose is too low or the course is too brief, intense rebound flares will often 

occur. A single 40-mg intramuscular dose of triamcinolone will typically produce good 

results in adults. Superinfection of the lesions with staphylococci or streptococci is the 

most common complication. 

Disposition 

Outpatient therapy is sufficient in all but the most severe cases, which may require 

parenteral steroids. Systemic glucocorticoids may be used at doses starting with 1 

mg/kg/d and continuing until the symptoms resolve.

Tanner TL: Rhus (Toxicodendron) dermatitis. Prim Care 2000; 27(2):493. [PMID: 

10815057] (A thorough review of Rhus dermatitis with practical applications to diagnosis 

and treatment.) 

IMPETIGO 


• Infection due to Staphylococcus or Streptococcus species. 

• Lesions appear honey-crusted. 

• More common in children but may affect all ages. 


Impetigo is an infection of the skin primarily due to group A streptococci and, less 

commonly, S. aureus. The infection is classified into bullous and nonbullous forms; the 

nonbullous form comprises approximately 70% of cases. Young children are the 

predominant age group affected, but adults are not excluded. A break in the protective 

skin barrier is the inciting event. Conditions such as chickenpox, abrasions, and burns 

are typically associated with impetigo. Predisposing situations include crowded living 

conditions, poor hygiene, and contact sports. 


Impetigo is associated with the classic history of the emergence of a small vesicle or 

pustule. This is often in the context of one of the above-mentioned conditions. The 

vesicle or pustule develops into the classic honey-crusted lesion. These lesions are 

usually less than 2 cm in diameter and may be mildly pruritic. The lesions are usually 

not painful. Although in healthy individuals the lesions will usually heal spontaneously 

with little scarring, the potential complications can be life threatening. Complications 

include septicemia, pneumonia, osteomyelitis, and glomerulonephritis. 

Treatment 

Correction of predisposing environmental conditions is important. The honey-colored 

crust must be removed. Cleansing with antibacterial soaps and solutions is helpful. The 

only topical antibiotic therapy currently indicated for the treatment of localized lesions is 

mupirocin (Bactroban) ointment. Patients should apply the ointment until the lesions 

resolve. Scalp and oral lesions typically require oral therapy, as do disseminated cases. 

Effective oral therapies include cloxacillin, amoxicillin/clavulanate, or clindamycin. 

Cephalosporins may be used, such as cephalexin, cefaclor, cefadroxil, cefprozil, or 

cefpodoxime proxetil. Seven days of therapy has been demonstrated as effective. If 

symptoms persist beyond 7 days, cultures should be taken and further treatment based 

on the results. Treat lesions suspected of being due to S. aureus with a 

ß-lactamase-resistant penicillin such as oxacillin or nafcillin. 

Sadick NS: Current aspects of bacterial infections of the skin. Dermatol Clin

1997;15(2):341. [PMID: 9098643] (A review of cutaneous infections with practical 

applications to diagnosis and treatment.) 

HERPES ZOSTER 


• Most cases are very painful. 

• Prodrome of paresthesias may occur. 

• Rash appears as a bandlike distribution of vesicles. 

• Usually has a dermatomal distribution. 

• Usually does not cross the patient's midline. 


Herpes zoster (HZ), or shingles, is a painful condition that results from reactivation of a 

latent infection with the varicella zoster virus (VZV). A patient who is naive to the virus 

develops chickenpox after an initial exposure. After resolution of this primary infection, 

the VZV remains dormant in the satellite cells of the dorsal root ganglion of the sensory 

nerves. It remains there for the rest of the patient's life. The triggers of subsequent 

reactivation in certain patients are not fully understood. Events such as trauma and 

exposure to ultraviolet radiation have been implicated in provoking eruptions of shingles. 

The incidence of HZ is increased in the elderly population. This is thought to result from 

diminishing immune function with increasing age. Although usually a localized process, 

disseminated HZ can develop in immunocompromised individuals. 


The diagnosis is primarily clinical. Previous history of chickenpox and the progression of 

current symptoms are important points in the history. 

Three phases of HZ have been described. During the prodrome phase, 80% of patients 

feel altered sensations in the affected dermatome. These are typically described as 

pain, burning, or paresthesias. These feelings may be intense and will often be present 

several days before the appearance of any lesions. This can often make the diagnosis 

difficult during this phase. 

Patients in the acute phase present with the eruption of vesicles, usually in a band-like 

pattern, which follows a dermatomal distribution. Only rarely will the lesions cross the 

midline. The two most common sites are the trunk and face, respectively. The lesions 

will dry and form a crust within 7-10 days. The lesions usually resolve within 2-3 weeks. 

An unfortunate subset of patients will go on to develop the chronic phase of HZ, known 

as postherpetic neuralgia (PHN). This is an extremely painful condition, which persists 

at least 30 days after the eruption resolves. PHN can be quite difficult to treat and is 

much more likely in the older patient. It may occur in up to 50% of elderly patients with 

HZ.

Several dangerous complications can develop from HZ, including ophthalmic HZ. This 

condition occurs when the ophthalmic branch of the trigeminal nerve is involved. Up to 

half of these patients will have ocular HZ. A clue to the presence of ocular HZ can be 

involvement of the tip of the patient's nose. Conjunctivitis, uveitis, and ulcerative keratitis 

can occur as a result of HZ. These serious conditions can lead to blindness if not 

managed properly. A complete ocular examination and urgent ophthalmologic referral 

are essential. Other potential complications of HZ include the Ramsay Hunt syndrome 

(an acute facial paralysis), meningitis, and encephalitis. 

Treatment 

It is important to educate patients who have HZ. They must understand that they are 

contagious to those who are not immune to VZV and to those who have not had 

chickenpox. This infective state lasts until the vesicles have dried and crusted, or 

approximately 1 week from the onset of the rash. During this time, patients should avoid 

pregnant women, those who are immunocompromised, and those who have never had 

chickenpox. 

Pain relief is important and is usually achieved with short-term combinations of oral 

analgesics and narcotics. Antiviral drugs are of use in the treatment of HZ, if therapy is 

started within 72 hours of the eruption of the rash. Oral acyclovir, 800 mg 5 times daily, 

is effective in improving resolution of the rash and decreasing the incidence of PHN. 

Famciclovir and valacyclovir are other options, with similar efficacy to acyclovir. One 

study showed valacyclovir as having some superiority in pain control. Studies have 

shown that steroids do not prevent the development of PHN. Some authors suggest that 

steroids are beneficial in treating Ramsay Hunt syndrome. Treatment of ocular 

involvement requires the assistance of an ophthalmologist. 

Morgan R: Shingles: a review of diagnosis and management. Hosp Med 

1998;59(10):770. [PMID: 9850292] (A discussion of varicella zoster and herpes zoster 

with a good review of the diagnosis and treatment of shingles.) 

HERPES SIMPLEX 


• Vesicles on an erythematous base. 

• HSV-1: usually oral; HSV-2: usually genital. 

• Spread by direct contact. 


Herpes simplex virus (HSV) is a major cause of recurrent orofacial and genital lesions 

and causes other types of illness as well (eg, keratitis, encephalitis). Infection is spread 

by direct contact. Primary infection is often the most severe, although it may be 

asymptomatic. After the primary lesion has healed, the virus remains latent in sensory

neurons in ganglion tissue, where it periodically reactivates in response to diverse 

stimuli. 

HSV type 1 (HSV-1) tends to be associated with oral lesions and is spread through 

contact with saliva from an infected person, whereas HSV type 2 (HSV-2) causes 

mainly genital lesions and is spread primarily by sexual contact. 


A. Primary Herpes Simplex Infection 

The first clinical attack of HSV infection is usually the most severe. Patients may present 

with fever, malaise, and arthralgias. Infection is characterized at first by grouped 

vesicles and later by denudation, erosions, or punctate lesions on a swollen, tender, 

painful erythematous base. Local pain and regional adenopathy are usually marked. 

Gingivostomatitis is the most common manifestation of HSV-1 infection; patients with 

HSV-2 infection usually present with genital lesions (ie, of the vulva, vagina, penis, 

anus, or perineum). Patients (especially women) with genital herpes may have aseptic 

meningitis. The primary illness usually disappears in 2-3 weeks but may last as long as 

6 weeks. 

B. Recurrent HSV Infection 

Recurrence of infection is common and may be triggered by fever, exposure to 

ultraviolet light, friction or trauma associated with sexual intercourse, menstruation, and 

possibly stress or fatigue. Focal itching, pain, or aching may precede the appearance of 

vesicles by hours to a few days in some patients. Vesicles usually rupture 

spontaneously within a few days and heal within a week without scarring. The virus may 

be recovered as long as lesions are moist; until the area is completely dry and healed, 

the patient should avoid direct skin-to-skin contact with others. 

C. Specific Diagnosis 

For either primary or recurrent herpes simplex, especially genital herpes, confirm the 

diagnosis by culture or antigen detection. 

Treatment 

A. Primary Infection 

Antipyretics or analgesics may help to relieve systemic symptoms. Give oral acyclovir, 

valacyclovir, or famciclovir to all patients who have primary infection. Hospitalize 

severely ill patients for administration of intravenous acyclovir, 15 mg/kg/d in 2-3 divided 

doses. Give other patients oral acyclovir, 200 mg 5 times daily for 7-10 days; 

valacyclovir, 1 g twice a day for 7-10 days; or famciclovir, 250 mg 3 times daily for 5-10 

days. 

Antibiotics are not necessary unless local purulence or cultures or Gram-stained smears 

positive for bacteria suggest concomitant bacterial infection. Candida vaginitis occurs 

frequently in women with primary genital herpes. 

B. Recurrent Infection 

Patients should not touch or manipulate lesions and should avoid physical contact with

others around the area of moist or active lesions. Acyclovir, 200 mg orally twice daily for 

5 days; valacyclovir, 500 mg twice daily for 5 days; or famciclovir, 125-250 mg 3 times 

daily for 5 days, will somewhat reduce healing time and the duration of virus shedding if 

started within a day of lesion onset. 

Disposition 

Hospitalization is often indicated for patients with primary genital herpes, who may have 

severe pain, systemic symptoms, and other complications (eg, aseptic meningitis, 

neuropathic bladder). Hospitalization is also required for patients with large or rapidly 

progressive lesions, especially if the patient is immunocompromised. 

Refer pregnant patients with newly diagnosed genital herpes to an obstetrician. Order a 

serologic test for syphilis (eg, VDRL) for all patients to rule out coexisting syphilis. 

Consider testing for HIV if risk factors are present. 

Taylor TJ et al: Herpes simplex virus. Front Biosci 2002;7:d752. [PMID: 11861220] (A 

review of herpes simplex virology.) 

Whitley RJ, Roizman B: Herpes simplex virus infections. Lancet 2001;357:1513. [PMID: 

11377626] (A comprehensive review of pathophysiology, diagnosis, and treatment of 

herpes simplex infections.) 

PSORIASIS 


• Common disorder. 

• Well-circumscribed plaques. 

• Erythematous base with silvery scale. 

• Predilection for extensor surfaces. 


Psoriasis is a common skin condition affecting up to 2% of the U.S. population. It has 

been described among all age groups with a similar male-to-female ratio. Onset is 

usually in the third decade of life. The disease process is well described and 

understood, but its cause is still unknown. A family history is present in 30% of patients. 

Psoriasis significantly affects the patient's quality of life. It is chronic, and there is no 

known cure. The plaque variant of psoriasis, or psoriasis vulgaris, is the most common 

form. 


Thorough examination reveals the characteristic erythematous, raised, scaly plaques. 

These are often described as having a salmon-colored base with tightly adherent silvery 

scales. They are typically found on the extensor surfaces of major joints, such as

elbows and knees. Other sites of predilection include the scalp, ears, and umbilicus. 

Lesions are often found to be in various stages of plaque formation and healing. 

Potassium hydroxide preparations can be used to differentiate psoriasis from tinea. 

Classic nail findings, such as pitting and onycholysis, can also aid in the diagnosis. 

Cultures play no role in the diagnosis of psoriasis. 

Treatment 

Many remedies have been tried over the years, but no cure has been found for 

psoriasis. Therapies often merely decrease scaling and increase the patient's comfort. 

Tar preparations and shampoos are well-known effective keratolytics, which decrease 

scaling. Avoidance of skin trauma is helpful, because the Koebner phenomenon is 

associated with psoriasis. This phenomenon refers to a flare in symptoms and initiation 

of plaque formation after local skin trauma, including scratching and even surgical 

incisions. Judicious use of topical low-potency steroids may be helpful initially. 

Calcipotriene is a newer preparation that is a topical vitamin D 3 analogue. Applied twice 

daily, effects are typically seen within 8 weeks. Oral and parenteral steroids play little or 

no role in the treatment of plaque psoriasis. Their use has been demonstrated as 

harmful in certain situations, such as the exacerbation of the more serious pustular 

psoriasis. 

Disposition 

Outpatient therapy is sufficient, except in the most severe cases. Referral should be 

made to a primary care physician or a dermatologist for more involved therapies, 

including topical preparations, ultraviolet phototherapy, and systemic agents such as 

methotrexate. 

Drew GS: Psoriasis. Prim Care 2000;27(2):385. [PMID: 10815050] (A thorough review 

of various types of psoriasis with a discussion of multiple treatment modalities.) 

Feldman SR et al: Psoriasis. Med Clin North Am 1998;82(5):1135. [PMID: 9769796] (A 

concise review of psoriasis and its treatment.) 

SCABIES 


• Human parasite. 

• Causes intense itching. 

• Spread by contact. 

• May affect entire households. 


Scabies have been known to affect the human condition for thousands of years. The 

culprit organism in scabies is a mite, Sarcoptes scabiei. This mite is found in varying

stages of development in the epidermis of the infested individual. There it makes 

tunnels, leaving behind eggs and feces. The mites are obligate parasites of humans and 

are spread by skin-to-skin contact between persons. This includes both sexual and 

nonsexual interactions. 


The diagnosis of scabies is primarily a clinical one, with the usual history of intense 

pruritus that is especially worse at night. Consider scabies when entire households 

complain of the onset of pruritus. The classic physical findings are tiny burrows in the 

web spaces between the fingers, in intertriginous areas, and in flexural creases. 

Burrows may not always be seen. Only excoriations and impetiginization may be found. 

The lesions may be difficult to differentiate from atopic dermatitis. In the most extreme 

cases, heavy mite loads may result and lead to the crusted or Norwegian variant. This is 

usually limited to individuals with severe disabilities or in immunocompromised states. 

The diagnosis of scabies is confirmed by microscopic visualization of mites or eggs in 

skin scrapings. 

Treatment 

A. Adults 

The treatment for adults (except pregnant or lactating women) and older children 

includes permethrin 5% cream (Elimite). It should be applied after a shower or bath over 

the entire body from the neck down. It should be left on for 8 hours, after which it should 

be carefully washed off. A 60-g tube is usually sufficient to treat one to two people. All 

clothing and bed linens should be laundered in hot water to kill all remaining mites. 

Alternative regimens include lindane cream or lotion. Used for many years, it is effective 

but some strains of lindane-resistant scabies exist. Also, dangerous central nervous 

system side effects have occurred in the elderly and in immunocompromised patients, 

or in normal hosts after repeated uses. Sulfur in petrolatum 6% is another treatment 

option. It should be applied to the entire body from the neck down for three consecutive 

nights. Patients should bathe between applications and 24 hours after the final 

treatment. Although it has no dangerous systemic effects, this remedy has an 

unpleasant odor. Crotamiton 10% cream may be applied for two consecutive nights and 

then washed off 24 hours after the last application. 

B. Children 

The treatment for infants, children younger than 10 years of age, and pregnant or 

lactating women is permethrin 5% cream, crotamiton 10% cream, or sulfur and 

petroleum as described above. The lindane preparation should not be used. 

PEDICULOSIS 


• Lice infestation. 

• Different distributions: head, body, pubic area.

• Spread by direct contact or sharing of personal items. 


Pediculosis refers to infestation of the body with lice. Similar to scabies, pediculosis 

results from a parasite. These organisms feed on the blood of humans. Several variants 

exist, and the organisms are named in reference to the area of the body they inhabit. 

These include P. humanus var. capitis (head lice), P. humanus var. corporis (body lice), 

and P. pubis (pubic lice). Head lice are the most common, with the classic scenario of 

outbreaks in school children seen in all levels in society. The lice are transmitted by 

direct contact as well as by sharing of hats, brushes, and other personal items. Body 

lice predominantly affect adults of lower socioeconomic standing, such as the homeless 

and those in refugee situations. Pubic lice are spread by sexual contact, and they often 

occur in conjunction with other sexually transmitted diseases. 


Recognition of the lice as described above is essential in the diagnosis. Pruritus may 

lead to excoriations that may become secondarily infected. Infestation of head lice is 

diagnosed by visualizing live lice or nits (eggs) attached to the proximal portion of the 

hair shaft. Body lice and eggs are found in the clothing of the affected individual, with 

excoriations over the body. Pubic lice are intensely pruritic, and the lice themselves may 

be transferred to other hair-bearing areas of the body. Remember to screen these 

patients for other sexually transmitted diseases. When pubic lice are found in children, 

they have often resulted from nonsexual contact; however, abuse should be considered 

in the differential. 

Treatment 

For the treatment of pediculosis capitis, corporis, and pubis, permethrin 1% cream rinse 

can be used. It can be applied to the groin, armpit, or scalp for 10 minutes and then 

washed off. Lindane 1% shampoo may be used as an alternative regimen. It is applied 

as above but is left on for 8 hours before washing off. For pediculosis capitis, it may be 

used as a shampoo, left on for 4 minutes, and then rinsed. Lindane should never be 

used on pregnant or lactating women, or on children younger than 10 years of age. 

Chosidow O: Scabies and pediculosis. Lancet 2000;355(9206):819. [PMID: 10711939] 

(A thorough review of scabies and pediculosis with a discussion of treatment 

modalities.) 

CUTANEOUS DERMATOPHYTES/TINEA 


• Superficial fungal infections. 

• Flat, scaly patches.


Dermatophytes include a group of fungi that infect the skin. The organisms themselves 

survive on the dead keratin found in the uppermost layer of the epidermis. The 

infections are limited to this superficial distribution in immunocompetent individuals. The 

dermatophytoses are classified by the distribution of the lesions. 


A. Tinea Corporis 

Tinea corporis refers to tinea of the body. Some authors and clinicians include the face 

in this category, but the American Academy of Dermatology refers to tinea of the face 

separately as tinea faciei. The most common causative organisms are Trichophyton 

rubrum, Microsporum canis, and Trichophyton mentagrophytes. Classic ringworm (tinea 

circinata) is the most common form of tinea corporis. It usually begins as a flat scaly 

patch with a raised, palpable border. It enlarges by advancing its border outward, 

leaving an area of central clearing. 

B. Tinea Pedis 

Also known as athlete's foot, tinea pedis is a common condition. It affects up to 70% of 

adults. It is divided into three subtypes. The most prevalent is the interdigital type. It is 

chronic and occurs with fissuring and maceration between the toes. Moccasin-type tinea 

pedis has a plantar distribution. The plantar surface is tender and erythematous. It is 

usually covered with a silvery scale. The third type is the wet, vesicular type. 

C. Tinea Cruris 

Tinea cruris, commonly called "jock itch," affects the groin area, sparing the genitalia. 

Men are affected more commonly than women, and the condition has a predilection for 

summer months. 

D. Tinea Versicolor 

Tinea versicolor affects a deeper layer of the skin than the previously described tineas. 

It is caused by the yeast Malassezia furfur. It often is associated with multiple 

hypopigmented macular lesions distributed over the trunk and extremities. Exposure to 

sunlight accentuates the lesions, because they do not tan normally like the surrounding 

skin. A fine scale is often present. 

Treatment 

A. Tinea Corporis 

Mild cases of tinea corporis can usually be treated with over-the-counter topical 

preparations, such as miconazole nitrate or clotrimazole. Prescription agents include 

ketoconazole 2% cream or econazole nitrate. All topical remedies should be used for 

1-2 weeks after resolution of symptoms. Extensive disease or difficult cases may require 

oral therapy. Agents include griseofulvin, itraconazole, terbinafine, and fluconazole. 

B. Tinea Pedis 

Most mild cases of tinea pedis can be treated successfully with 1-4 weeks of therapy 

with an over-the-counter preparation, in conjunction with the use of drying powders.

Severe cases may require oral therapy. Drugs such as griseofulvin, fluconazole, and 

itraconazole are effective. Cases are often recurrent if concomitant nail disease is 

present. 

C. Tinea Cruris 

Tinea cruris can often be treated with topical antifungal therapies used for 2-3 weeks 

(see as for tinea corporis). The area should be kept dry, because moisture and 

maceration are problems with this disease. Antifungal powders and loose-fitting clothing 

are often useful adjuncts. A mild topical corticosteroid may be used cautiously for a 

short time to help relieve the pruritus, which is often severe. Corticosteroids may be 

used only for 48-72 hours; longer use is contraindicated. As with tinea corporis, resistant 

disease may require oral therapy. 

D. Tinea Versicolor 

Limited tinea versicolor can be treated with topical selenium sulfide 2.5%. Daily 

application of ketoconazole to the affected areas for 3 days is an alternative regimen. 

Recurrence of the disease may be prevented with the use of a once-monthly bedtime 

application of selenium sulfide 2.5%. 

Goldstein AO et al: Mycotic infections. Effective management of conditions involving the 

skin, hair, and nails. Geriatrics 2000;55(5):40. [PMID: 10826264] (A thorough review 

with an extensive discussion of treatment modalities and pharmaceutical regimens.) 

Rupke SJ: Fungal skin disorders. Prim Care 2000;27(2):407. [PMID: 10815051] (A 

review of various fungal disorders, including tinea, pityriasis, and candida.) 

PITYRIASIS ROSEA 


• Herald patch is initial lesion. 

• Rash is usually truncal and has a "Christmas tree" distribution. 

• May be pruritic. 


Pityriasis rosea is a common rash that may easily be confused with tinea corporis. It is a 

papulosquamous eruption that most commonly affects patients in the second to the 

fourth decades of life. Pityriasis rosea affects men and women equally. Although its 

cause is thought to be related to a viral process, the exact cause of pityriasis rosea is 

unknown. 


The classic progression of the exanthem begins with the appearance of a herald patch. 

This is an isolated lesion usually found on the trunk. It is typically oval shaped and can 

be as large as 10 cm in diameter. It usually has an erythematous border, and there may

e central clearing. The subsequent lesions usually develop within 1-2 weeks, and their 

distribution has been described as resembling the shape of a Christmas tree. The 

individual lesions are smaller than the herald patch, are usually a lighter shade, and 

have a scaly border. 

Treatment 

The lesions are self-limiting and usually disappear within 6-8 weeks. The initial lesions 

regress, and new lesions develop during this time. No effective treatment has been 

found for pityriasis rosea. If pruritus is present, it may be treated symptomatically with 

antihistamines or topical hydrocortisone 1% ointment. Patients should be reassured that 

recurrences are uncommon, occurring in only approximately 3% of cases. 

Hsu S et al: Differential diagnosis of annular lesions. Am Fam Physician 

2001;64(2):289. [PMID: 11476274] (A basic discussion comparing various skin lesions 

and their diagnoses.) 

Wyndham M: Pityriasis. Practitioner 1997;241(1575):358. [PMID: 9254391] (A brief 

discussion of pityriasis and its diagnosis and treatment.) 

MOLLUSCUM CONTAGIOSUM 


• Viral infection. 

• Pearly pink papules with central umbilication. 


Molluscum contagiosum is a viral infection of the skin. It is associated with multiple 

lesions, typically papules, spread over the skin. Molluscum contagiosum is present 

worldwide. In normal hosts, it is a self-limited disease and usually resolves within 8 

weeks. Recently there has been increased prevalence in the immunocompromised 

population, especially in patients with HIV. In this population the disease presentation 

can be dramatic, with large, widespread lesions and a longer duration. 


The diagnosis is made by the identification of the lesions. They are typically 

flesh-colored papules. The lesions may also appear pearly pink. The papules are 

rounded with a distinctive central umbilication and are firm to palpation. They usually are 

1-5 mm in diameter, but in certain situations they may be quite large. The lesions may 

be distributed anywhere on the body, but they are rarely found on the palms or soles. 

They are usually found in groups, and usually fewer than 20 lesions are present. 

Molluscum contagiosum is spread by close contact with infected persons, by contact 

with contaminated surfaces, or by autoinoculation with scratching or shaving. It can also 

be spread by sexual contact.

Treatment 

Most lesions resolve without treatment in immunocompetent patients. Lesions involving 

the perineum and genitalia should be treated to avoid spread via sexual contact. If 

lesions require treatment, the two most commonly used modalities are cryosurgery and 

curettage. Various topical therapies have had varying levels of success, including lactic 

acid, podophyllin, cantharidin, and silver nitrate. In pediatric patients, use of a topical 

anesthetic, such as lidocaine plus prilocaine, should be considered prior to curetting. 

Instruct patients to avoid contact sports, swimming pools, and other such activities until 

the lesions have resolved. 

Lewis EJ et al: An update on molluscum contagiosum. Cutis 1997; 60(1):29. [PMID: 

9252731] (A discussion of the latest information regarding the diagnosis and treatment 

of molluscum contagiosum, with a focus on the immunocompromised population.) 




46. Dermatologic Emergencies - Joseph A. Salomone III, MD, FAAEM, & 

Martha Ann Pratt, MD

47. Psychiatric Emergencies - Gregory Hall, MD, & Denis J. Fitzgerald, 

MD 

I. INTRODUCTION 

Psychiatric emergencies are acute changes in behavior that negatively impact a 

patient's ability to function in his or her environment. Often such patients are in a state 

of crisis in which their baseline coping mechanisms have been overwhelmed by real or 

perceived circumstances. In dealing with such emergencies, the emergency physician 

faces many challenges and must prioritize his or her clinical efforts toward four main 

concerns. 

First, the physician must ensure his or her own safety and the patient's well-being if 

violence or agitated behavior is present. Second, the physician must perform an 

effective screening assessment, probing for organic causes and completing a 

psychiatric safety check. The screening assessment ensures that there is no underlying 

medical cause for the patient's condition, either initially inducing the aberrant behavior or 

evolving as a consequence of that behavior (eg, malnutrition or dehydration). The 

screening assessment also involves a psychiatric safety check to explore for suicidal 

ideation, homicidal ideation, or the patient's inability to care for him- or herself. Third, the 

physician must ensure that the patient receives appropriate psychological support and 

medical treatment, even if that treatment needs to be provided without the patient's 

consent. Fourth, the physician must determine the appropriate disposition for the 

patient. 

The algorithm in Figure 47-1 provides a decision-making guide to the management of 

psychiatric emergencies. This algorithm reflects the four main priorities in patient care 

and provides a framework for this chapter. 

Frumin M et al: Psychotic and behavioral problems. Neurol Clin 1998;16:521. [PMID: 

9537973] 

Richards CF, Gurr DE: Psychosis. Emerg Med Clin North Am 2000;18:253. [PMID: 

10767882] 

II. THE S.A.F.E.S.T. APPROACH TO VIOLENT OR AGITATED 

PATIENTS 

The emergency physician may find him- or herself dealing with a patient who threatens 

or exhibits violent behavior toward staff. In these cases, it is important to recognize the 

early warning signs of impending violence and adopt an approach to management that 

reduces the likelihood of injury to staff and patient. Early warning signs of impending 

violence include threatening statements, clenched fists, loud vocalizations, shifting body 

position toward a fighting posture, agitated movements, and striking inanimate objects. 

If such behavior is detected, adopt the S.A.F.E.S.T. Approach:

Spacing—Maintain distance from the patient. Allow both the patient and you to have 

equal access to the door. Do not touch a violent person. 

Appearance—Maintain empathetic professional detachment. Use one primary contact 

person to build rapport. Have security staff available as a show of strength. 

Focus—Watch the patient's hands. Watch for potential weapons. Watch for escalating 

agitation. 

Exchange—Delay by calm, continuous talking is crucial to permit deescalation of the 

situation. Avoid punitive or judgmental statements. Use good listening skills. Target the 

current problem or situation in order to find face-saving alternatives for resolution and to 

elicit the patient's cooperation with treatment. 

Stabilization—If necessary, use three stabilization techniques to get control of the 

situation: physical restraint, sedation, and chemical restraint. 

1. Physical restraint—Once the situation permits, it is advisable to restrain any violent 

or agitated patient to ensure safety. This activity is best done by trained security 

personnel who should also search the patient for weapons. Implement documentation 

that indicates the need for restraints and provides a record of safety checks on the 

restrained patient. 

2. Sedation—If agitation persists, sedation is best achieved by administering 

lorazepam, 1-2 mg intramuscularly or intravenously. Dosing may be repeated every 30 

minutes for 4 doses maximum, if needed to achieve effect. 

3. Chemical restraint—Chemical restraint is best achieved with neuroleptics. For 

patients not responding to sedation, haloperidol may be administered (5 mg 

intramuscularly). In elderly patients, it is best to start with lower dosing and increase by 

1- to 2-mg increments. Dosing may be repeated every 30 minutes until the patient is 

more in control. Be alert for the emergence of extrapyramidal symptoms, seizure 

activity, or neuroleptic malignant syndrome (see below, in discussion of 

psychopharmacotherapy). 

Treatment—Once the patient is more manageable, initiate treatment based on the 

patient's symptoms. The patient may refuse treatment and may need to receive 

treatment involuntarily in order to ensure his or her safety. 

American College of Emergency Physicians: Use of patient restraints. Ann Emerg Med 

2001;38:619. [PMID: 11699510] 

Annas GJ: The last resort—the use of physical restraints in medical emergencies. N 

Engl J Med 1999;341:1408. [PMID: 10536135] 

Buckley PF: The role of typical and atypical antipsychotic medications in the 

management of agitation and aggression. J Clin Psychiatry 1999;60:52. [PMID: 

10340688]

Citrome L, Volavka J: Violent patients in the emergency setting. Psychiatr Clin North Am 

1999;22:789. [PMID: 10623971] 

FitzGerlad D: S.A.F.E.S.T. Approach. In: TIGER Coursebook (in press). 

http://www.ucemergencymedicine.com/pdfs/Tiger.pdf 

Hill S, Petit J: The violent patient. Emerg Med Clin North Am 2000;18:301. [PMID: 

10767886] 

Hillard JR: Emergency treatment of acute psychosis. J Clin Psychiatry 1998;59:57. 

[PMID: 9448670] 

Richards JR et al: Chemical restraint for the agitated patient in the emergency 

department: lorazepam versus droperidol. J Emerg Med 1998;16:567. [PMID: 9696171] 

III. EMERGENCY DEPARTMENT SCREENING ASSESSMENT 

TARGETED HISTORY 

Focus on precipitating causes and circumstances that brought the patient to the 

emergency department. It may be necessary to elicit information from multiple sources 

such as family, friends, or ambulance personnel. Other key topics include previous 

psychiatric treatment, seizure disorders, polysubstance abuse, and any recent suicidal 

attempts including possible ingestions. 

FOCUSED PHYSICAL EXAMINATION 

Perform a thorough physical examination, including neurologic assessment. Complete 

vital signs are essential. Look for physical clues to the source of an altered mental 

status, such as evidence of head injury, drug use, or toxidromes (constellation of 

symptoms produced by a toxic ingestion or exposure). Assess the patient for adverse 

consequences of his or her behavior such as malnutrition or dehydration. 

MENTAL STATUS EXAMINATION 

It is important to document the mental status examination in patients presenting with 

psychiatric emergencies. The mental status assessment should probe for global 

functioning, thought disorders, mood disorders, and personality disorders. 

A. Global Functioning 

Assess the patient for general orientation (person, place, time, reason for visit), memory 

(short and long-term), judgment, and concentration. 

B. Thought Disorders 

Assess the patient for abnormal thought content such as hearing voices, experiencing 

command hallucinations, or having paranoid thoughts. 

C. Mood Disorders 

Assess the patient for evidence of depression or mania. Compare the appropriateness

of the patient's stated mood with his or her overt affect. Look for clues such as 

emotional lability or unbalanced emotional extremes. 

D. Personality Disorders 

Try to assess whether the patient's current behavior is an acute psychiatric event that 

represents a decompensation in his or her normal functioning or a representative 

sample of a maladaptive pattern of behavior derived from an underlying socially 

inappropriate personality matrix. 

SCREENING LABORATORY TESTS 

The following studies are often helpful in the evaluation of patients presenting with 

psychiatric emergencies: 

• Electrolyte panel with glucose 

• Pulse oximetry 

• Toxicology screen 

• Liver function tests 

• Computed tomography (CT) scan of the head 

• Electrocardiogram (ECG) 

• Thyroid function tests 

DIAGNOSTIC FOCUS: ORGANIC VERSUS FUNCTIONAL CAUSE 

The emergency department is the first stop, in many instances, for patients with many 

different types of acute, and sometimes chronic, complaints. Often a patient presents 

with an alteration in his or her mental state, behavior, level of functioning, mood, or 

personality. The emergency physician must distinguish between those patients needing 

medical treatment for an organic problem (eg, delirium or dementia) and those 

individuals who would benefit from psychiatric treatment for a functional problem (eg, 

thought disorder, mood disorder, personality disorder). 

Functional disorders may be very difficult to differentiate from an acute mental status 

change caused by an organic condition. However, some factors may point to an organic 

cause of the behavioral change. Organic causes often are acute in onset, whereas 

functional disorders develop over time. Visual hallucinations are much more common 

with organic syndromes or medical illness than are auditory hallucinations. Age of onset 

may also be a clue. Patients presenting with functional etiologies are usually younger, 

typically 12-40 years of age. Exceptions are always possible, but older patients need 

special consideration when disease is being attributed to psychiatric origin, especially 

when no history of previous psychiatric disorder is present. Patients with organic 

disorders generally present with emotional lability, whereas patients with a flat affect 

usually have functional disease. Finally, any abnormality in vital signs or features of a

toxidrome should immediately point to an organic cause. 

PSYCHIATRIC SAFETY CHECK 


The emergency physician must directly assess for the presence of suicidal or homicidal 

ideation in all patients presenting with a psychiatric emergency. In general, the patient's 

ability to care for him- or herself is a cardinal component of the initial assessment. 

Suicidal Patients 

The management of suicidal ideation involves recognition of the problem, an 

assessment of risk, and development of a treatment plan. 

A. Recognition of Suicidal Ideation 

Patients with suicidal ideation may present with an obvious attempt to cause self-harm. 

However, such patients may present to the emergency department more indirectly, with 

suicidal ideation as the underlying cause behind other presentations, such as through 

an automobile accident. The best screening approach involves general questions about 

the patient's emotional state. Inappropriate, irrational, or dysphoric answers should 

prompt further investigation, culminating in direct questions about suicidal intent. 

B. Assessment of Risk 

Several factors increase the risk of suicide. Patients with prior suicide attempts are at 

increased risk. Patients who employ violent means are more serious about their intent. 

Existence of a detailed plan reflects significant commitment to following through with the 

suicide attempt, particularly when coupled with a depressed emotional state or altered 

mental status. Poor social support or inadequate coping mechanisms also puts patients 

at increased risk. 

C. Treatment 

Admit patients who have clear suicidal ideation, unless immediate psychiatric evaluation 

is an option. The admission may be directly to the psychiatry service or to the medical 

service with a psychiatry consult. It may be necessary to sign involuntary admission 

holds on patients who resist efforts to ensure their safety. Patients with suicidal ideation 

should be monitored closely at all times, ideally with a one-on-one sitter. They should be 

given emotional support throughout their stay, and their environment should be carefully 

screened for any potential means of suicide. 

Homicidal Patients 

Patients expressing homicidal intent require special measures to ensure staff safety and 

the safety of the third party threatened by the patient. The patient's threats should be 

believed, particularly if he or she has a specific plan. The third party, if specifically 

named, should be contacted through appropriate authorities to ensure his or her safety. 

The patient should be closely monitored by security personnel, with restraints, as 

indicated, in a setting devoid of potential weapons. Acute psychiatric consultation is 

mandatory.

IV. ORGANIC CAUSES FOR PSYCHIATRIC EMERGENCIES 

Patients with acute behavior, mood, or thought disturbances must be medically 

evaluated for the presence of dementia or delirium. Dementia is a chronic, progressive 

alteration in memory associated with cognitive decline and agnosia, apraxia, and 

aphasia. Alzheimer disease is the classic type of dementia. However, infections, such 

as HIV, and other neurologic conditions, such as stroke, can also cause dementia. 

Delirium, by contrast, is an acute disturbance in consciousness. It may also involve 

cognitive decline, but the patient's level of consciousness is decreased, unlike in 

dementia. Delirium has a short onset and usually a fluctuating course. 

DEMENTIA 

Alzheimer disease is the most common type of dementia. It starts with memory loss 

affecting recent memory. Long-term memory is usually preserved. As the disease 

progresses, more cognitive deficits become apparent until the patient is no longer able 

to function. History and physical exam are the most important contributors to the 

diagnosis. Magnetic resonance imaging (MRI) is an important adjunct. 

Acetylcholinesterase inhibitors (eg, tacrine, donepezil) are used to increase central 

nervous system (CNS) levels of acetylcholine. This treatment helps to delay the 

progression of the disease in some patients. However, no agent is currently available 

that can prevent the ultimate progression of Alzheimer disease. 

DELIRIUM 

Multiple medical problems can cause a delirious state, which may be confused with 

psychosis. Drug intoxication or withdrawal; infection; and endocrine, metabolic, 

neurologic, and cardiopulmonary disturbances are most often implicated. 

DRUG INTOXICATION & WITHDRAWAL 

Stimulants 

The stimulant drugs such as cocaine and amphetamines, including MDMA (Ecstasy), 

can cause symptoms of behavioral and personality disturbance. These drugs can also 

induce someone with a compensated psychiatric illness such as schizophrenia to 

decompensate. Therefore, when evaluating a patient with mental status changes and 

bizarre behavior, the physician should determine whether stimulant drugs are present. 

The diagnosis is based on history of substance abuse, characteristic signs, and a 

positive drug screen. Cocaine and amphetamines both cause a sympathetic rush. They 

cause hypertension, tachycardia, dilated pupils, and diaphoresis. MDMA causes less 

sympathetic hyperactivity and has more hallucinogenic properties. 

Psychological manifestations of stimulants include dysphoria, paranoid psychosis, and 

potentially a delirious state. Stimulants also cause a disinhibition leading to poor impulse 

control. As a result, patients with acute ingestion are more likely to be violent, homicidal, 

or suicidal. This property is seen especially in patients taking amphetamines. 

Management of patients with acute toxicity is supportive. Benzodiazepines are the

treatment of choice for the acutely agitated and violent person taking cocaine or 

amphetamines. 

Withdrawal from stimulants initially involves anxiety, anhedonia, depression, fatigue, 

and severe craving for the drug of abuse. Withdrawal does not cause a significant risk 

for death from cardiac or pulmonary disturbances. The withdrawal state may be a risk 

factor, however, for suicide. Patients receive supportive measures, usually lasting 1-2 

weeks until improvement in the anxiety and lethargy is seen. However, the anhedonia 

and cravings may continue for weeks. 

Depressants 

Alcohol and benzodiazepines are the classic depressants. The diagnosis is based on 

clinical findings coupled with a positive drug level. They cause a decrease in sensorium, 

lethargy, ataxic gait, nystagmus, and respiratory depression. Individuals presenting with 

symptoms of intoxication and lethargy warrant evaluation for depressant use. These 

chemicals, however, can inhibit impulse control, and some people have a paradoxical 

excitation when using depressants. Monitoring of airway and breathing status is crucial. 

Searching for any other cause of the behavior (eg, head injury) is also important. 

Alcohol withdrawal is noteworthy due to the continued morbidity and even mortality that 

occurs from such a widely used substance. Delirium tremens can cause a clinical 

picture very similar to that of an acute psychotic break. Patients with delirium tremens 

have stopped drinking for as little as a few hours to days. Patients clinically show signs 

of sympathetic overload, including hypertension and tachycardia. They are usually 

diaphoretic and, by definition, tremulous. This delirious state can be differentiated from 

functional psychosis due to the history, autonomic dysfunction, and visual 

hallucinations. Treatment is with benzodiazepines. A titrated lorazepam infusion may be 

needed to decrease the hypertension, tachycardia, and CNS symptoms. 

Opioids 

All opioid medications, such as morphine and heroin, can cause the classic triad of 

respiratory depression, miosis, and decreased mental status. Diagnosis is based on the 

clinical picture, positive drug screen, or response to naloxone. Usually the patient 

abusing opiates presents with lethargy and not bizarre behavior. However, if these 

chemicals are mixed with stimulants (eg, cocaine, amphetamines), the result may be 

any type of delirium that can mimic functional psychosis or mood disorder. 

Hallucinogens 

Lysergic acid diethylamide (LSD) and phencyclidine (PCP) are the traditional 

hallucinogenic drugs. LSD is absorbed through the oral mucosa and binds to 

postsynaptic serotonergic receptors. The patient may report kaleidoscopic 

hallucinations. However, the drug may also cause violence, suicidal ideation, and 

bizarre memories or flashbacks. PCP is a dissociative anesthetic. Patients are awake 

but exhibit bizarre behavior that can become suddenly violent. Patients may be 

hypertensive and tachycardic. Patients may also experience a host of behavioral and 

neurologic changes such as loss of concentration or the presence of illogical speech,

nystagmus, or ataxia. Diagnosis is based on the history of use, clinical findings, and 

drug screen results. Treatment for hallucinogens includes ruling out any other 

associated acute medical problem and providing supportive care in a calm, quiet 

environment. Benzodiazepines may be used in acutely agitated patients. 

INFECTION 

Systemic 

Many patients, especially the elderly, with systemic infections present with delirium. 

Sometimes the delirious state involves behavioral changes. Any elderly patient with 

acute mental status changes should be evaluated for systemic infection. Diagnosis is 

based on the clinical picture coupled with the source of infection on urinalysis, chest 

x-ray, or cultures. 

Central Nervous System 

Encephalopathy is an infectious process that causes inflammation around the brain. The 

etiology often is viral (eg, herpes, HIV). Clinical manifestations usually involve fever and 

headache. If the infection affects the limbic area of the brain, personality and behavioral 

changes can occur, including floridly psychotic behavior and aggression. Meningitis, 

likewise, may cause delirium and altered mental status. Therefore, if an infectious cause 

is suspected, especially in a patient with fever, the patient should receive a head CT 

scan and lumbar puncture. Diagnosis is based on these two tests in the appropriate 

clinical setting. Treatment is aimed at the underlying infectious or inflammatory process. 

If infection is suspected, initiate acyclovir and antibiotics as soon as possible. 

ENDOCRINE & METABOLIC DISORDERS 

Hepatic Encephalopathy 

Patients with stigmata of liver failure routinely present with altered mental status. These 

patients may be delirious. At times they may be violent or aggressive. Pathophysiology 

is debated, but there is a correlation with high ammonia levels. Therefore, in the context 

of liver failure, an ammonia level may be helpful in narrowing down the differential 

diagnosis to hepatic encephalopathy. Treatment is usually supportive along with 

lactulose to enterally clear toxins usually cleared by the liver. 

Electrolyte Abnormalities 

Hypercalcemia and alterations in sodium, either hyponatremia or hypernatremia, are the 

most common causes of altered mental status. Personality and behavioral changes are 

much less common than lethargy. Seizures, coma, and death are possible if the 

electrolyte abnormality is not corrected appropriately. Fortunately, the diagnosis is easily 

made with routine electrolyte chemistry panels. 

Hypoglycemia 

The brain requires glucose to function. A low blood glucose level can mimic any type of

CNS event. Patients may present with decreased consciousness or focal neurologic 

findings similar to a stroke. Blood glucose level should be checked as soon as possible 

in any patient with behavioral changes. Rapid correction of hypoglycemia can itself 

cause behavioral changes. Violence and aggression from the rapid correction are 

usually short in duration. However, if a patient continues to have symptoms after the 

glucose level has been corrected, further investigation into the cause is warranted. 

Thyroid Disease 

Hyperthyroidism and hypothyroidism have been implicated in acute behavioral changes 

mimicking psychiatric disorders. Hyperthyroidism may cause anxiety and tremor. These 

patients usually present with mild to moderate hypertension and tachycardia along with 

weight loss and heat intolerance. Patients with hypothyroidism can present with 

symptoms of fatigue all the way to delirium or coma. Other symptoms include 

gastrointestinal complaints such as constipation, cold intolerance, weight gain, and 

menstrual irregularities. Diagnosis can be reliably made based on laboratory levels of 

thyroid hormones. 

NEUROLOGIC DISORDERS 

Seizure Disorder 

Patients who have had a seizure may present with normal mental status or may have 

decreased consciousness from a postictal state. A history of seizure or witnessed 

seizure activity may guide the workup. Nonconvulsive status epilepticus is much more 

difficult to determine. These patients may present with decreased consciousness or may 

be awake and alert. Patients may even have behavioral changes from blank stare to 

aggression depending on the location of the seizure focus. Nonconvulsive status 

epilepticus should be considered in patients with behavioral or neurologic changes, 

especially if a history of epilepsy is present. If necessary, neurologic consultation and an 

electroencephalogram would be appropriate to confirm the diagnosis. 

Cerebral Vascular Accident 

Cerebral vascular accidents (CVAs) are usually associated with focal weakness and a 

variable level of consciousness. Depending on the area of the brain affected, patients 

may have significant cognitive deficits. Patients may present with bizarre behavior 

secondary to aphasia or neglect. Therefore, a CVA should be considered in patients 

with risk factors for vascular disease or cardioembolic phenomenon. CT scanning and 

MRI can be helpful in diagnosis. 

Wernicke-Korsakoff Syndrome 

A clinical diagnosis, Wernicke encephalopathy is secondary to thiamine deficiency and 

occurs mostly in alcoholic patients. The main features clinically are ataxia, 

ophthalmoplegia (either nystagmus or gaze palsy), and mental status changes. The 

mental status change involves anything from confusion to delirium or even coma. Thus, 

this entity should be considered in anyone with a history of alcohol abuse, eye changes, 

and mental status changes. The development of Korsakoff psychosis can accompany

these findings. Patients with malnutrition and alcohol abuse should be given thiamine. 

Theoretically, anyone with this history who is given dextrose should receive a thiamine 

supplement first although there is little evidence in the dogma that it must be given 

before the glucose. 

CARDIOPULMONARY DISEASE 

Diseases of the cardiopulmonary system can cause significant behavioral changes. 

Myocardial infarction, pulmonary edema, and pulmonary embolism can cause anxiety 

secondary to pain, shortness of breath, and a possible sense of doom. These disorders 

may elicit significant fear in patients, which may manifest itself as panic attack or even 

aggression. Patients may also be hypoxic or hypotensive, which may cause decreased 

consciousness and cognitive dysfunction. Diagnosis is based on clinical suspicion 

coupled with basic cardiac function evaluation (ECG, cardiac enzymes, pulse oximetry, 

chest x-ray). 

V. FUNCTIONAL CAUSES FOR PSYCHIATRIC EMERGENCIES 

Patients with psychiatric illness present to the emergency department with a disorder of 

behavior secondary to abnormal thought process, mood, or personality traits. The 

changes that result in the visit to the emergency department usually occur over a period 

of weeks. Patients may present with depressed mood, labile affect, paranoid delusions, 

auditory hallucinations, and psychomotor retardation, or they may be in a manic state. 

The clinical picture is quite variable, and organic cause for the decompensation should 

be investigated. 

COGNITIVE (THOUGHT) DISORDERS: SCHIZOPHRENIA 

Diagnosed clinically, schizophrenia is a common disorder. Most patients with 

schizophrenia are not institutionalized and routinely present to the emergency 

department for acute medical care. The visit may be due to medication noncompliance, 

ineffective medication, or substance abuse. Onset of disease is usually in the late teens 

or early adult years. The cause of schizophrenia is not fully understood, but it is 

heralded by a disturbance in thought process. Current medications work on 

dopaminergic and serotonergic receptors. 


Patients with schizophrenia present with positive symptoms (delusions, hallucinations, 

and bizarre behavior) and negative symptoms (withdrawal, blunted affect, catatonia). 

Organic causes of the behavior must be sought (eg, steroid toxicity, substance abuse or 

withdrawal, encephalitis, HIV encephalopathy). Common manifestations of disorganized 

thought include the following: 

• Social withdrawal, often with poor personal hygiene 

• Preoccupation with inner thoughts and auditory hallucinations, which are often violent, 

sexual, or religious in nature

• Labile affect, often presenting with flat emotionless affect but rapidly changing 

• Poor ability to focus on a topic, making it difficult to follow the patient in conversation 

• Flight of ideas 

• Hallucinations, often derogatory to the patient 

• Grandiose or persecutory delusions 

• Catatonia 

• Paranoia 

Treatment 

Provision of a safe and supportive environment is important, both for the patient and 

emergency department staff. Patients with aggression and grossly disruptive or 

dangerous behavior require antipsychotic agents such as haloperidol, 5-10 mg 

intramuscularly, for management. Patients who are unable to care for themselves or 

who pose a high risk of harm to themselves require psychiatric consultation and 

admission. Often patients present in a withdrawn state (catatonia). These patients are at 

high risk for dehydration, electrolyte imbalances, and malnutrition. Therefore, along with 

psychiatric consultation, evaluation for organic disease that results from the psychiatric 

condition is imperative. 

AFFECTIVE (MOOD) DISORDERS 

DEPRESSION 

Diagnosed based on a constellation of symptoms, depression is the most common 

mood disorder. Patients have variable presentations ranging from an acute depressive 

state lasting days after an emotionally taxing event to chronic depression lasting years. 


Depression is characterized by a change in mood. Patients commonly have intense 

feelings of sadness, guilt, and hopelessness. Patients are often anhedonic, with no 

interest in pleasurable activity. These patients also may have psychomotor retardation 

or agitation with variable sleeping patterns. Depressed patients routinely are evaluated 

in the emergency department for complaints of fatigue or decreased appetite, suicidal 

ideation or attempt, overdose, substance abuse, dehydration, or malnutrition. 

Patients with depression may present with delusions or frank psychosis. These patients 

may or may not have a diagnosis of schizoaffective disorder, which is a disorder of both 

thought and mood. The delusions are usually persecutory or somatic in nature. 

Treatment

Life-threatening medical conditions must be detected and treated. Dehydration, 

overdose, and illicit drug ingestion must be medically managed. Many general medical 

conditions may cause depression and must also be ruled out. Neurodegenerative 

disorders, stroke, thyroid disorders, epilepsy, metabolic disorders, and infection are just 

some of the conditions that may involve a depressed state. Once patients are medically 

stable, those at risk of harming themselves or others must receive psychiatric 

consultation and be admitted. 

MANIC STATES 

Mania is another type of mood disorder. Many patients with mania have bipolar affective 

disorder, alternating between episodes of mania and depression. Mania is diagnosed 

clinically and is characterized by variable degrees of heightened mood and activity. The 

symptoms may be mild, characterized by an overly friendly and talkative personality. 

This condition is called hypomania. Others may present with grandiose delusions, 

insomnia, and aggressive behavior. Caution must be used in the emergency department 

when dealing with a manic patient. The disorder can cause an increase in unpredictable 

behavior. 


The predominance of an infectious, inappropriate euphoria coupled with hyperactivity 

and talkativeness suggests the diagnosis. Mania is also characterized by decreased 

need to eat or sleep. Patients routinely are awake all hours of the night and may go for 

extended periods of time without a significant amount of sleep. The disorder is also 

characterized by flight of ideas, decreased ability to concentrate on a task, inappropriate 

laughing and joking, increased uninterrupted speech, and grandiose delusions. Patients 

with bipolar affective disorder may be rapid cycling. In this state, patients, over hours to 

days, alternate between severely depressed mood and a state of euphoria. When 

disorganization of thought process is a prominent feature, a diagnosis of schizoaffective 

disorder should be considered. 

Treatment 

Initially, evaluate patients for an organic cause or signs of organic disease resulting from 

the manic state. Illicit drug use, especially stimulants, may cause a clinical picture of 

mania. In addition, patients with mania may be dehydrated or have an electrolyte or 

nutritional disorder secondary to decreased consumption of food and water while in a 

manic state. 

Evaluate patients for toxicity from drugs used to treat mania, such as lithium or 

antiepileptics. Once patients are medically stable, evaluate them for risk of harming 

themselves or others. If a patient is found to be at risk, psychiatric consultation and 

admission are required. Treat acute hostile behavior medically as appropriate. Reducing 

the environmental stimuli in the emergency department is important. Place the patient in 

a safe and quiet room after ensuring that he or she has no objects that may be used to 

cause harm. If the patient continues to be agitated, medical management with 

lorazepam, 1-2 mg intravenously or intramuscularly, or haloperidol, 5-10 mg 

intramuscularly, is appropriate.

BORDERLINE PERSONALITY DISORDER 

Borderline personality disorder presents a special situation in the emergency 

department. Patients with this disorder regularly present to the emergency department 

and are usually well known for their frequent visits. The diagnosis is clinical, based on 

patient behavior. 


Patients with borderline personality disorder are characterized by their volatile 

interpersonal relationships. They can be very impulsive and have labile affect. Patients 

are usually very demanding, frequently presenting with suicide threats and other 

self-destructive behavior. They commonly experience paranoid thoughts and have other 

comorbid conditions such as substance abuse and affective disorders. 

Treatment 

Evaluation of the patient for medical illness is the first priority. Treat medical and 

surgical issues resulting from self-destructive behavior rapidly, and evaluate the patient 

for continued threat to self or others. If such a threat exists, seek psychiatric 

consultation for the patient and arrange for admission. 

Additional techniques for dealing with patients with borderline personality disorder 

involve contacting the patient's support structure (eg, family, friend, or therapist) and 

ensuring adequate follow-up. The number of visits to the emergency department is 

inversely proportional to the amount of social support the patient receives outside the 

hospital. Furthermore, emergency department staff should treat the patient's 

abrasiveness as a symptom of the disorder and avoid being abrasive toward the patient 

in response. Addressing the patient's complaints promptly may prevent escalation of 

symptoms. 

OTHER FUNCTIONAL CAUSES 

SOMATOFORM DISORDERS & HYSTERICAL STATES 

Somatoform disorders and hysterical states are psychiatric functional disorders 

diagnosed by exclusion of organic disorders. Patients present with physical complaints 

of different types. Patients perceive the complaints as real, even though no underlying 

physical organic cause is responsible. These disorders must be separated from 

malingering, which involves deliberate and conscious deception for secondary gain. 

1. Conversion Disorder 

Conversion disorder is characterized by motor or sensory dysfunction caused by 

psychological stress with no true physical dysfunction. These symptoms are not 

intentionally produced and frequently are seen in the emergency department after a 

traumatic event, especially if a loved one is injured or killed. Different types of 

conversion disorder involve motor symptoms, sensory symptoms, or seizures.


The most important factor for the emergency physician is to differentiate between 

somatic symptoms due solely to functional cause and true organic disease exacerbated 

by psychologic stress. Evaluate patients for disorders such as Guillain-Barre syndrome, 

botulism poisoning, herpes encephalitis, and CVAs. Obtain a thorough history, including 

history of psychiatric disease, and conduct a thorough physical exam. Pay close 

attention to discrepancies in the physical findings. A patient with hysterical blindness 

can be tested for nystagmus by running a strip of paper with multiple vertical lines on it 

(ECG paper) in front of the patient's eyes. Doing so will elicit tracking and nystagmus if 

the patient has vision (optokinetic reflex). The diagnosis of conversion disorder is 

strengthened by a fluctuating pattern of disability; a lack of concern about the disability; 

a pattern that does not follow known anatomic relationships; intact sphincter tone; and, 

when the complaint is paralysis, presence of the Hoover sign (in which counterpressure 

with the heel of the unaffected leg is absent when the patient is asked to lift the affected 

leg). 

Treatment 

Differentiating a conversion disorder from a true motor or sensory disorder is imperative. 

If the diagnosis is difficult, an elaborate workup may be initiated. If the diagnosis of 

conversion disorder is made, psychiatric consultation and counseling are appropriate. 

2. Somatization Disorder 

Somatization disorder is characterized by 4 or more different pain complaints along with 

at least 2 gastrointestinal complaints, a sexual complaint, and a neurologic complaint. 

Patients usually have a history of multiple surgeries, numerous emergency department 

visits, multiple medications, multiple reported allergies, and no relief from intractable 

chronic pain. The emergency physician must rule out significant medical disease and at 

the same time avoid elaborate workups. Evaluating available medical records and 

contacting the patient's other physicians or counselors is imperative. 

3. Hypochondria 

Hypochondria represents an anxious preoccupation with physical signs and symptoms. 

Patients have a fear of having a serious medical condition. Evaluation of the patient 

based on clinical reasoning is important, followed by reassurance and referral for 

psychiatric counseling. 

DISSOCIATIVE STATES: PSYCHOGENIC FUGUE 


Psychogenic fugue is the dissociative state most commonly encountered in the 

emergency department. The disorder is diagnosed clinically and characterized by the 

sudden loss of memory. It usually begins abruptly after a psychologically catastrophic 

event, such as the loss of a close family member. Patients are usually in good health

and able to communicate, but they are unable to answer personal questions, for 

example, regarding their name and address. Patients may travel long distances without 

recall and are often found in bus or train stations. Recovery of memory can occur within 

a few hours or take several weeks. Afterward, the patient often has amnesia for the 

period of dissociation. 

Treatment 

The emergency physician must rule out organic disorders. Alcohol abuse is the most 

common cause of blackouts, which may mimic psychogenic fugue. Malingering must 

also be considered, especially if the patient is confronted with legal problems. Once 

other etiologies have been ruled out, it is important to reassure the patient that the 

disorder is not permanent. Social support is important to help the patient emotionally 

cope until the problem resolves. 

DEVELOPMENTAL DISORDERS 

Patients with developmental disorders such as autism and mental retardation require 

special attention. Patients are usually diagnosed by the age of 3 years due to poor 

functional development and failure to reach milestones. These patients may present to 

the emergency department with hostility or a change from baseline functioning. It is 

imperative that the physician discuss the changes with the patient's parents or 

caregivers and then evaluate the patient for recent trauma, signs of infection, and 

comorbid medical conditions. The inciting event often is organic in cause and must be 

treated before the patient's symptoms will improve. 

Bair BD: Frequently missed diagnosis in geriatric psychiatry. Psychiatr Clin North Am 

1998;21:941. [PMID: 9890132] 

Broderick KB, et al: Emergency physician practices and requirements regarding the 

medical screening examination of psychiatric patients. Acad Emerg Med 2002;9:88. 

[PMID: 11772676] 

Brust JC: Acute neurologic complications of drug and alcohol abuse. Neurol Clin 

1998;16:503. [PMID: 9537972] 

Goldman LS: Medical illness in patients with schizophrenia. J Clin Psychiatry 

1999;60:10. [PMID: 10548136] 

Korn CS, Currier GW, Henderson SO: "Medical clearance" of psychiatric patients 

without medical complaints in the emergency department. J Emerg Med 2000;18:173. 

[PMID: 10699517] 

Perrone J, et al: Drug screening versus history in detection of substance use in ED 

psychiatric patients. Am J Emerg Med 2001;19:49. [PMID: 11146019] 

Radomsky ED, et al: Suicidal behavior in patients with schizophrenia and other 

psychotic disorders. Am J Psychiatry 1999; 156:1590. [PMID: 10518171]

Reeves RR, Pendarvis EJ, Kimble R: Unrecognized medical emergencies admitted to 

psychiatric units. Am J Emerg Med 2000;18:390. [PMID: 10919525] 

Richards CF, Gurr DE: Psychosis. Emerg Med Clin North Am 2000;18:253. [PMID: 

10767882] 

Tolbot-Stern JK, et al: Psychiatric manifestations of systemic illness. Emerg Med Clin 

North Am 2000:18:199. [PMID: 10767878] 

Tse SK, et al: How good are accident and emergency doctors in the evaluation of 

psychiatric patients? Eur J Emerg Med 1999; 6,297. [PMID: 10646916] 

Tueth MJ, Zuberi P: Life-threatening psychiatric emergencies in the elderly: overview. J 

Geriatr Psychiatry Neurol 1999;12: 60. [PMID: 10483926] 

Williams ER, Shepherd SM: Medical clearance of psychiatric patients. Emerg Med Clin 

North Am 2000;18:185. [PMID: 10767877] 

VI. PSYCHOPHARMACO- THERAPY 

Psychiatric medications have changed significantly in recent years. New atypical 

antipsychotics are being prescribed ever more frequently because of their more benign 

side-effect profiles. Psychiatrists and primary care providers are prescribing 

antidepressants to patients with symptoms of depression. Due to the rapid increase in 

the use of these medications, an understanding of their indications and potential 

toxicities is essential for an emergency physician faced with medically evaluating 

patients who are taking these drugs. Emergency physicians also need to be aware of 

potential uses for typical antipsychotic medications and the risks of using them. 

TRADITIONAL ANTIPSYCHOTICS 

Traditionally, high-potency antipsychotic agents such as haloperidol are used to treat 

agitation, violence, and acute psychosis in the emergency department. The 

high-potency agents are associated with less sedation, hypotension, and anticholinergic 

effects than are low-potency agents such as chlorpromazine or thioridazine. However, 

the high-potency agents are associated with a higher incidence of dystonic reactions 

and extrapyramidal side effects (EPS). 

For an acutely agitated patient, the intravenous or intramuscular route of administration 

is preferred. Haloperidol is thought to have less potential for EPS or dystonic reaction 

when given intravenously. These agents may be used in combination with minor 

tranquilizers such as benzodiazepines, but prolonged sedation is a risk. Like its closely 

related cousin droperidol, haloperidol has the potential, like many other psychoactive 

agents, to cause a prolonged QTc. This factor should be considered before such drugs 

are used, and appropriate cardiac monitoring should be established. The potential for 

cardiac conduction delays should be of particular concern when giving haloperidol to 

patients with overdose or toxin exposure. 

Any toxic overdose of typical antipsychotics should be treated with supportive care.

Dyskinesias are treated with diphenhydramine, 25-50 mg intravenously or 

intramuscularly, or benztropine, 1-2 mg intravenously or intramuscularly. The usual 

dose of haloperidol for agitation in a patient whose appearance does not appear to be 

due to overdose or toxicologic origin is 5-10 mg intravenously or intramuscularly. 

Escalating doses of haloperidol are no longer considered appropriate. Effects should 

start within 30 minutes and peak at 1-2 hours. 

NEUROLEPTIC MALIGNANT SYNDROME 


Neuroleptic malignant syndrome is an uncommon and potentially fatal reaction usually 

due to high-potency antipsychotic medications. The condition is characterized by 

hypertension, tachycardia, hyperthermia, and muscle rigidity. It may also occur in cases 

of acute delirium. Consider neuroleptic malignant syndrome in any patient who is known 

to have a psychiatric condition and who is taking neuroleptic medications. 

Treatment 

Treatment begins with management of airway, breathing, and circulation. Discontinue 

antipsychotic medication immediately. The patient should be cooled and rehydrated with 

crystalloid. Initiate muscle relaxation with intravenous benzodiazepines or dantrolene (1 

mg/ kg). Bromocriptine has also been used to help treat this condition because it is 

potentially caused by CNS depletion of dopamine. Further management includes 

supportive care and evaluation for rhabdomyolysis. 

ATYPICAL ANTIPSYCHOTICS 

In the 1990s, atypical antipsychotic medications (eg, risperidone, clozapine, quetiapine, 

olanzapine) started to replace the traditional antipsychotics in the treatment of 

schizophrenia. This trend is due to their improved efficacy for treating both positive and 

negative symptoms of schizophrenia. These agents have a much improved side-effect 

profile. EPS are minimal, if occurring at all. Tardive dyskinesia, likewise, is very rare 

even with long-term use. Overall, the medications have enhanced efficacy, fewer side 

effects, and greater patient compliance. 

Atypical agents appear to be relatively safe. Most patients who overdose on these 

medications have few if any signs of toxicity. Death is especially rare but is more 

commonly associated with pediatric overdose and in adults not accustomed to taking 

the medications. Toxic signs and symptoms depend on age and dose ingested. The 

effects usually range from CNS depression, slurred speech, and ataxia to coma and, 

rarely, seizure. Respiratory depression, hypotension, and anticholinergic symptoms also 

occur. Sinus tachycardia is the most common cardiac disturbance. Prolongation of QTc 

and dysrhythmias happen infrequently. Treatment for overdose is largely supportive, 

paying attention to airway, breathing, and cardiac monitoring. Hemodialysis is unlikely to 

be of any benefit secondary to the large volume of distribution of these agents. 

Some of the agents have more specific side effects. Clozapine has a higher risk of 

seizures as compared to the other agents. Risperidone is the one agent that can cause

EPS when used in higher doses. Finally, clozapine has a risk of agranulocytosis that 

usually becomes evident in the first few months of therapy. Therefore, a complete blood 

count should be routinely obtained in patients taking this medication. 

ANTIDEPRESSANTS 

Antidepressants have been around for decades. The older antidepressants such as 

tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) were 

effective, but they had the potential for serious side effects or death. Selective serotonin 

reuptake inhibitors (SSRIs) are now the predominant antidepressant agents. However, 

even newer agents are increasingly becoming available that combat depression and 

other disorders such as anxiety and obsessive-compulsive disorder. 

The SSRIs include fluoxetine, sertraline, paroxetine, and fluvoxamine. SSRIs are 

metabolized by cytochrome P450 enzymes. Of note, SSRIs can inhibit these enzymes, 

causing altered levels of other medications that are metabolized by the liver in the same 

way. Therefore, caution must be used when a patient is taking an SSRI and other 

medications such as theophylline or warfarin. 

SSRI overdoses usually cause minor symptoms but rarely death. The serotonin 

syndrome, marked by tremulousness and delirium, is also a risk. However, it occurs 

much less frequently than with MAOIs. Symptoms of SSRI overdose can include 

nausea, vomiting, tachycardia, dizziness, and drowsiness. Seizures, coma, and death 

are possible but rare. Treatment includes supportive measures and observation. Base 

the decision to use charcoal and gastric lavage on the time since ingestion and the 

patient's level of consciousness. 

Newer agents such as venlafaxine (Effexor) and mirtazapine (Remeron), like the SSRIs, 

are relatively safe agents. Common symptoms of overdose include drowsiness and 

sinus tachycardia. Patients who overdose on these agents usually require only 

observation and supportive care. However, two exceptions should be noted. Citalopram 

in doses greater than 600 mg has caused seizures and cardiac conduction 

abnormalities. A patient who has ingested a large quantity may require monitoring in an 

intensive care setting. Buproprion, likewise, has been associated with seizures in people 

with bulimia nervosa and in individuals who overdose on high doses. 

Buckley PF: Broad therapeutic uses of atypical antipsychotic medications. Biol 

Psychiatry 2001;50:912. [PMID: 11743945] 

Burns MJ: The pharmacology and toxicology of atypical antipsychotic agents. J Toxicol 

Clin Toxicol 2001;39:1. [PMID: 11327216] 

Goldberg JF: New drugs in psychiatry. Emerg Med Clin North Am 2000;18:211. [PMID: 

10767879] 

Welch R, Chue P: Antipsychotic agents and QT changes. J Psychiatry Neurosci 

2000;25:154. [PMID: 10740988] 

VII. DISPOSITION


Disposition is critical in patients with psychiatric emergencies. Patients should be 

admitted to the hospital if they meet any of the following criteria, which constitute a 

psychiatric crisis: 

• Unable to care for self 

• Actively suicidal 

• Actively homicidal 

• Unresolved symptoms with an organic cause 

Admit such patients to the psychiatric service or, alternatively, to the general medicine 

service with a psychiatry consult. Assign patients full-time sitters for their safety. 

Involuntary Procedures & Admission 

One of the unique aspects of managing patients with psychiatric disease is the potential 

need to initiate involuntary procedures or admission when such patients refuse 

life-saving intervention. Generally, patient care is conducted under the auspices of the 

patient's informed consent. However, care can be rendered without consent in four 

recognized situations: (1) if the patient is a minor, in which case consent must come 

from parents unless the treatment is immediately required to save the child's life, (2) if 

the patient lacks the current capacity to comprehend the choice or weigh the factors 

needed to make the decision, in which case the physician or significant other(s) may 

need to make the decision, (3) if the patient is unable to offer consent because of a 

life-threatening medical condition (such as a comatose state) that precludes the 

patient's ability to offer input into the decision, in which case consent is presumed for 

life-saving measures until the patient's wishes become known via advance directive or 

next of kin, or (4) if the patient is having an acute psychiatric crisis in which he or she is 

not exhibiting a rational pattern of behavior with regard to self-preservation and what 

reasonable individuals would consider to be consistent with the patient's best interests, 

in which case the physician is obligated by his or her oath to act to preserve the 

patient's life until the situation changes to permit the patient's consensual participation in 

the care. 

Patients experiencing an acute psychiatric crisis may therefore need procedures and 

admission performed for their safety without their consent. Involuntary procedures 

include physical or chemical restraint. Such patients may also require involuntary 

admission or 72-hour holds to permit psychiatric assessment. In most venues, this type 

of involuntary care may be authorized by a practicing physician, police officer, or social 

service worker who has reason to believe that the patient is a safety risk to him- or 

herself or another because of psychiatric illness. This individual must document 

evidence to support the decision, and it is good practice to seek the independent 

corroboration of two physicians if available. Under such circumstances, the patient may 

then receive treatment and be held against his or her will for up to 72 hours until the

psychiatric evaluation is completed to verify that the patient is no longer at risk of 

harming him- or herself or others due to psychiatric illness or other treatable cause. 





I. INTRODUCTION

Figure 47-1. Decision-making algorithm for psychiatric emergencies. 





FIGURES

48. Pediatric Emergencies - Roger L. Humphries, MD, Keith D. 

Bricking, MD, & Thomas M. Huhn, MD 1 


1 This chapter is a revision of the chapter by Ronald A. Dieckmann, MD, MPH, FAAP, 

FACEP, & Kevin Coulter, MD, FAAP, from the 4th edition. 

A. Epidemiology 

Children constitute the most diverse and challenging patient population facing the 

emergency physician. They represent approximately 10% of prehospital and 30% of 

emergency department patients. Critical illness and injury in children are less frequent 

than in the adult population and occur in only about 5% of emergency department 

pediatric patients. 

The epidemiology of pediatric emergency medicine changes with the clinical setting. In 

the prehospital environment, the common presenting complaints are trauma, seizures, 

respiratory distress, and toxicologic emergencies. In the emergency department, the 

most common complaints are either infections, including upper respiratory infections, 

gastroenteritis, and otitis media, or trauma. 

Injury is the leading cause of pediatric morbidity and mortality between the age of 1 year 

and adulthood. Illness also exacts a terrible toll on the childhood population, especially 

in the youngest age groups, even though many childhood maladies are preventable or 

their complications could be reduced through preventive measures or earlier recognition 

of distress. 

B. Assessment 

Assessment of the pediatric patient in the emergency department requires an 

age-specific approach. A calm, reassuring, and gentle manner on the physician's part 

will facilitate information collection and encourage patient cooperation in examination 

and testing. 

Knowledge of the child's growth and development often is required for the diagnosis, 

management, and disposition of the pediatric emergency department patient. 

Assessment of growth is most accurate when considered in terms of prior growth in the 

same individual. 

Severity of acute pediatric illness and injury is often difficult to discern. In contrast to the 

direct anatomic examination that underlies physical evaluation of the adult, 

observational methods of assessment may be more sensitive to illness and injury acuity 

in children (Table 48-1). Such observations appear to be more predictive of serious 

illness than anatomic physical examination using standard palpation, percussion, and 

auscultation techniques. 

Assessment and management of the distressed pediatric patient require appropriately

sized equipment. Table 48-2 itemizes emergency department equipment and supplies 

for children. Table 48-3 provides equipment sizes for invasive procedures in children of 

different age groups. 

Vital signs vary by age (Table 48-4). A rapid formula for estimating systolic blood 

pressure is 80 + (2 × age [in years]). The maximum effective heart rate in infants is 200 

beats/min; in young children, 150 beats/ min; and in school-aged children, 120 

beats/min. Respiratory rate decreases with advancing age, ranging from 50 breaths/min 

in the newborn period to 40 breaths/min at 1 year, 30 breaths/min at 2 years, 20 

breaths/min at 3 years, and 16 breaths/min throughout school ages. The use of vital 

signs to assess vital functions in pediatric patients, however, is hazardous. 

Appropriate-sized measuring equipment is imperative, techniques must be applied 

carefully, and interpretation must be age-related. Furthermore, even accurately 

obtained, age-adjusted vital signs may be insensitive. Instead, other objective measures 

of cardiopulmonary function—such as the pediatric observational scale (Table 

48-1)—and simple physical signs—such as skin color, temperature, and capillary 

refill—are often better triage and assessment tools. 

C. Concept of the Distressed Family 

The emergency department physician must appreciate the intimate relationship of the 

child to the family. Acute pediatric illness and injury are inextricably part of the family 

environment and dynamics. The child as well as the entire nuclear and extended family 

may experience major psychological, emotional, and financial consequences of 

pediatric emergencies. Effective care requires appropriate consideration of the child 

within the distressed family, enlistment of parental assistance in evaluation and 

management, and provision of psychological support. 

D. Pain and Sedation 

Too often, the inexperienced physician neglects pain control or procedural sedation 

because of misunderstanding about the significance of pain in the young child, 

unwarranted fear of addicting children to narcotic agents, or ignorance of appropriate 

agents. When a painful procedure is necessary, an effective approach integrates careful 

explanation directly to the child and enlistment of parental understanding and 

assistance. Whenever conscious or deep sedation procedures are performed, the 

emergency department physician must ensure the patient's safety by strict adherence to 

guidelines of monitoring. This includes preparation for any potential airway 

complications, such as aspiration or apnea. In general, only previously healthy or mildly 

chronically ill children should be considered as candidates for sedation procedures in 

the emergency department. Sometimes a restraint apparatus will facilitate the 

procedure. 

The following are guidelines for a variety of clinical situations: 

1. Topical anesthetics for wound repair—The formulation TAC (0.5% tetracaine, 

1:2000 epinephrine or adrenaline, and 11.8% cocaine) has been associated with 

seizures after systemic absorption of the cocaine component. Another topical 

anesthetic, LET (2% lidocaine, 1:1000 epinephrine, and 2% tetracaine), has a more 

favorable safety profile. However, because the onset of action of LET is about 30 

minutes, it should be applied early in the evaluation of wounds to avoid unnecessary

treatment delays. Any anesthetic containing epinephrine (such as LET or TAC) should 

be avoided on end-arterial structures, such as the ears, nose, digits, or penis. 

2. Sedation and analgesia for painful procedures—Use a combination of fentanyl, 

1.0-1.5 ug/kg intravenously every 3 minutes, and midazolam, 0.05- 0.075 mg/kg 

intravenously every 3-5 minutes. The reversal agents naloxone, 0.01-0.1 mg/kg 

intravenously, and flumazenil, 0.01 mg/kg to a maximum of 0.2 mg, should also be 

available at the bedside and can be administered for respiratory depression. Use pulse 

oximetry to monitor the child's respiratory status after administration. 

3. Sedation for imaging studies—For individuals requiring imaging studies such as 

computed tomography (CT) scan or magnetic resonance imaging (MRI), use 

pentobarbital, 5 mg/kg intramuscularly, midazolam, 0.5 mg/kg orally (maximum dose, 20 

mg), or methohexital, 1 mg/kg intravenously. 

4. Other drugs used for painful procedures— 

a. Inhaled nitrous oxide—Administration of inhaled nitrous oxide requires a reliable 

scavenging system to avoid exposure to staff as well as a careful regulatory method for 

oxygen delivery in the oxygen-nitrous oxide mix. 

b. Ketamine—Ketamine, 3-4 mg/kg intramuscularly, or 1 mg/kg intravenously, may be 

used for procedural situations involving children under 10 years, especially burn 

debridement, foreign body removal, deep wound care, abscess incision and drainage, 

sexual abuse evaluation, and interventions such as lumbar puncture or orthopedic 

reductions. Use atropine, 0.01 mg/kg (maximum, 0.5 mg), or glycopyrrolate, 0.005 

mg/kg (maximum 0.25 mg), as part of the same intramuscular injection to avoid 

hypersalivation. Intravenous administration is better for longer procedures. Ketamine 

may elevate intracranial and intraocular pressure, induce emesis, and occasionally 

precipitate laryngospasm; because ketamine use in older children may also cause an 

adverse behavioral reaction upon emergence from sedation, the concomitant use of 

midazolam, 0.025- 0.05 mg/kg intravenously, is recommended in children over age 5 

years. Nonetheless, it is an effective drug when used by trained personnel and with 

appropriate cardiopulmonary monitoring including vital signs and continuous pulse 

oximetry. 

5. Outpatient analgesia—Outpatient analgesia should ordinarily include a nonsteroidal, 

anti-inflammatory drug such as ibuprofen, 4-10 mg/kg every 6-8 hours. This drug can 

also be used in combination with oral narcotic agents for treatment of severe pain. 

Acetaminophen, 10-15 mg/kg/dose every 4-6 hours, can also be used for treatment of 

mild pain on an outpatient basis. 

E. Drug and Fluid Administration 

All parenterally and orally administered agents must be given strictly on a per-kilogram 

basis, until maximum adult doses and volumes are reached. Overdosing and 

overhydration are dangerous errors in emergency pediatrics. Underdosing is also 

frequent, especially in infants and small children. Initial treatment of dehydration should 

include isotonic fluids (normal saline or lactated Ringer's). Deaths due to acute 

hyponatremic cerebral edema have been reported with administration of as little as 40

mg/kg intravenous 5% dextrose in water. Physicians and nurses must meticulously 

review drug and fluid orders to ensure that they are age- and weight-corrected. 

Vascular access is often the rate-limiting step in provision of life-saving therapy to 

critically ill and injured children. The emergency department physician must be familiar 

with a variety of techniques for access into the cardiopulmonary system. 

1. Endotracheal tube—In critically ill, intubated patients, the endotracheal route is an 

effective conduit for administration of a variety of life-saving drugs, including 

epinephrine, atropine, lidocaine, naloxone, and diazepam. Epinephrine is by far the 

most commonly used. When administered through the endotracheal tube, higher doses 

of epinephrine, up to 10 times the intravenous dose, must be used to achieve adequate 

serum concentrations. The pharmacokinetics of endotracheal epinephrine 

administration may be optimized by delivering the drug directly into the highly vascular 

trachea and proximal tracheobronchial tree instead of directly into the endotracheal 

tube. The preferred technique requires insertion of a nasogastric tube or a size 5F 

umbilical catheter past the distal tip of the endotracheal tube with direct instillation of 

drugs through the tube. Because endotracheal drugs may be more effective if 

aerosolized, dilute the drug with normal saline to a maximum volume of 0.5-1 mL//kg, 

and then inject rapidly to achieve a partially aerosolized form. 

2. Intravenous access—In infants, the scalp is an ideal site for cannulation; use a size 

25 butterfly needle. In children past the neonatal period, the dorsal veins of the hand, 

antecubital fossa, or dorsum of the foot are usually accessible with a 24- or 22-gauge 

intravenous catheter. The external jugular vein is a large vein, usually easily visualized 

and readily cannulated with a 20-gauge catheter if the child is properly restrained and 

the head is held in a dependent position. 

3. Intraosseous infusion—(See also Chapter 6.) For patients under age 5 years in 

extremis and requiring life-saving drug and fluid administration, intraosseous infusion is 

an alternative method of administration. A short, thick needle with trocar tip is inserted 

into the intramedullary space of the bone. The richly vascularized intramedullary space 

allows for direct entry of drugs and fluids into the central circulation through emissary 

veins. The easiest insertion sites are the medial proximal tibia or the distal midline 

femur. Intraosseous infusion is a rapid and effective technique of achieving therapeutic 

serum concentrations of almost all important drugs; moreover, a large fluid volume can 

be rapidly administered in injured or dehydrated patients. When necessary, insert 

multiple intraosseous lines. The most common complication of this procedure is 

osteomyelitis. 

F. Medicolegal Considerations 

Most exposure to legal liability derives from the patient's status as a minor. Although 

state laws protecting children vary significantly, some common legal principles apply. 

Consent issues are frequent and often vexing problems in the emergency department. 

Consent may be difficult to obtain either because the legal guardian is absent or 

because the child's actual caregiver may be neither the legal guardian nor a legally 

authorized surrogate. If the child's legal guardian is unavailable, the health care provider 

must make and clearly document every effort to communicate directly with the child's

legal representative. 

If the child's condition allows, informed consent must be obtained from the legal 

representative. If the child's condition is life threatening, and permanent harm or 

physical disability will result from delay of appropriate medical interventions, treatment, 

including appropriate analgesia, must be implemented under the concept of implied 

consent. If the characteristics of this legal action are not clearly spelled out by 

emergency department policy, consultation with the hospital's legal authority is prudent. 

Whenever treatment is instituted without formal consent, the reasons for such action 

must be documented on the patient's medical record. 

Another dilemma occurs when a child presents to the emergency department with acute 

serious injury or illness, and the legal representative refuses appropriate medical 

assistance. If the patient's condition is such that permanent impairment or death may 

result from failure to treat, emergency legal recourse through the local juvenile court 

system may be required, especially if the legal representative is incompetent owing to 

substance abuse or other debilitating mental conditions. The hospital administrator, 

legal counsel, and social services should also be notified. 

In some circumstances, parental consent is not needed for emergency care. For 

example, "emancipated minors" are, by law, able to act as adults and consent to 

medical care, even though they have not obtained legal age of maturity. Emancipated 

minors include individuals who are married, pregnant, in active duty in the armed 

services, or declared emancipated by the Superior Court. Moreover, many states 

recognize "mature minors," a status whereby a minor also has the power to consent to 

medical care in situations involving substance abuse, mental disease, sexually 

transmitted disease, or pregnancy. 

G. Death in the Emergency Department 

The sudden and unexpected death of an infant or child in the emergency department 

constitutes one of the most difficult situations in emergency practice. Careful and 

compassionate dialogue between the physician and parents, and between the physician 

and emergency department staff, is essential to minimize chaos in the clinical setting 

and to reduce confusion and anger among bereaved families and department 

personnel. Debriefing for health care workers may also be appropriate within 48-72 

hours to alleviate stress that may impair work performance or cause psychological 

disability. 

CARDIOVASCULAR EMERGENCIES 

Evaluation of cardiopulmonary function in children, especially in infants and younger 

children, requires special techniques. Vital signs are generally insensitive and 

nonspecific. Blood pressure poorly reflects volume status. When perfusion is mistakenly 

equated with blood pressure, early signs of hypovolemia can be missed. Figure 48-1 

demonstrates the relationship of a child's blood volume to blood pressure during acute 

blood loss. In children, hypovolemia triggers compensatory tachycardia and intense 

peripheral vasoconstriction, which effectively maintains blood pressure until volume loss 

exceeds about 50% of intravascular volume.

Tachycardia, while sensitive to cardiopulmonary duress, is nonspecific. Normal heart 

rate also varies with age, and tachycardia is a common response to many types of 

stress (eg, fever, anxiety, hypoxia, hypovolemia). In children, assessment of volume 

status should focus primarily on skin signs (temperature, color, capillary refill, turgor) in 

combination with heart rate. Feeling the skin at the knee is an excellent first maneuver 

to assess warmth and skin perfusion. Rate of urine output may be the next best 

measure of core perfusion. Adequate core blood flow results in 1-2 mL/ kg/h of urine 

production. Therefore, in the unstable child with suspected perfusion abnormalities, a 

urinary bladder catheter is imperative to monitor output. 

Cardiac rhythm disturbances in children are unusual. The most common disturbance is 

bradycardia, usually secondary to hypoxia. Properly applied pulse oximetry, at the triage 

desk or as part of initial clinical assessment, is an easy and useful method for rapid 

evaluation of oxygen saturation in patients with slow or rapid heart rates. When a 

primary tachycardia occurs, it is usually supraventricular in origin. In the distressed 

child, electrocardiographic monitoring will assist in evaluating cardiovascular status and 

in judging response to therapy. 

DEHYDRATION 


• Commonly occurs after severe or prolonged episodes of diarrhea and vomiting. 

• Significant signs include acute weight loss, listlessness, sunken eyes, dry mucous 

membranes, poor capillary refill, and tachycardia. 


Acute dehydration is a common pediatric emergency. Diarrhea and vomiting are the 

most frequent causes. Other common causes are blood loss, burn wounds, open 

wounds, fever or hyperthermia, sweating, inadequate fluid intake, polyuria, and 

poisoning. 


Clinical evaluation of the dehydrated child requires assessment of hydration status. 

Comparison of presenting weight with recent weights may be useful. Management is 

dictated by degree of acuity (mild, 3-5% weight loss; moderate, 10%; severe, 15%). 

Formulate initial treatment on the basis of clinical evaluation of degree of dehydration. 

Dry or pasty mucous membranes, sunken eyes, doughy and cool peripheral skin with 

poor capillary refill, and listlessness signal severe dehydration. Laboratory assessment 

of type of dehydration assists the physician in later strategies for specific electrolyte 

replacement. Serum sodium concentration is the most important laboratory parameter. 

Serum sodium concentration does not indicate degree of hydration but does provide a 

useful measure for titrating sodium repletion (see below). 

Treatment

After rapid assessment of degree of dehydration, management must match severity of 

illness. 

A. Oxygen and Intravenous Access 

For severely dehydrated patients, provide supplemental oxygen, attach pulse oximeter 

and cardiac monitor, and establish intravenous or intraosseous access with one or two 

secure catheters. 

B. Volume Resuscitation 

For a severely dehydrated infant or young child, rapidly infuse a balanced isotonic 

solution (eg, normal saline or lactated Ringer's injection). Infants and children have 

limited glycogen stores and are prone to hypoglycemia when stressed; rapid blood 

glucose analysis (eg, fingerstick blood sugar) should be performed, and glucose should 

be replaced if less than 60 mg/dL. Administer 5 mL/kg 10% dextrose in water for infants 

and young children and 2 mL/kg 25% dextrose in water for older children. 

Administer a fluid bolus of 20 mL/kg, and then repeat boluses of 20 mL/kg until physical 

signs (heart rate, skin temperature, and capillary refill) indicate improved perfusion. After 

60 mL/kg of isotonic fluid have been administered, if vital signs have not normalized, 

consider administration of packed red blood cells, 10-20 mL/kg, fresh-frozen plasma, or 

occasionally 5% albuminated saline. 


After stabilizing the patient, slow the intravenous infusion to a maintenance rate (Table 

48-5) and devise a therapeutic plan. Insert a urinary bladder catheter if the child has 

uncertain volume replacement requirements. Send blood for complete blood count 

(CBC); electrolytes; and glucose, blood urea nitrogen (BUN), and creatinine 

measurements. Arterial blood gas determination is indicated for the child who remains 

unstable after 60 mL/kg of volume administration. 

When laboratory data are available, titrate sodium and water repletion accordingly. For 

hyponatremic and isotonic dehydration, replace the calculated volume deficit over 24 

hours, giving 50% of the deficit in the first 8 hours and the remaining 50% over the 

following 16 hours. Ongoing losses and maintenance requirements must also be 

included. Control fever, because insensitive water losses are significantly increased by 

temperature elevation. Add small amounts of potassium to the ongoing infusion, once 

urination is observed, and replace calculated potassium deficits over 48 hours. The 

minimum daily maintenance requirements for water, sodium, and potassium are noted 

in Table 48-5. For hypernatremic dehydration, divide fluid and electrolyte replacement 

evenly over 48 hours to avoid rapid osmolal shifts and central nervous system 


D. Oral Rehydration Therapy 

Use oral rehydration therapy (ORT) in most dehydrated patients. Children can usually 

take fluids by mouth. Vomiting does not contraindicate use of ORT. Unless shock, 

altered mental status, or severe weakness is present, ORT may be used as part of early 

emergency department and inpatient management for most dehydrated patients. Other 

patients not requiring hospitalization can be easily rehydrated using this technique. The

composition of ORT as set by the World Health Organization includes 90 mEq/L of 

sodium, 20 mEq/L of potassium, 30 mEq/L of citrate, and a 1-2% glucose concentration. 

Commercial preparations that provide approximately these electrolyte constituents 

include Pedialyte, Lytren, and Infalyte. Other commonly used clear liquids, such as 

colas, have too few electrolytes (Na + , K + , and Cl - ), and their high sugar content may 

contribute to worsening of osmotic diarrhea. If the child can be discharged, prescribe 

home fluid replacement that is appropriate for the age of the child, the calculated deficit, 

and ongoing losses. 

SHOCK 


• Altered mental status. 

• Tachypnea, tachycardia. 

• Hypotension is a late sign in children. 


Shock is inadequate oxygen delivery to tissues. Most causes of shock in children (eg, 

gastrointestinal fluid losses, burns, blood loss from acute injury) involve decreased 

stroke volume usually from hypovolemia (hypovolemic shock). Septic shock, a form of 

distributive shock, occurs usually in the patient under age 2 years and must always be 

considered in the sick-appearing, febrile child. Anaphylactic shock, another form of 

distributive shock, may develop after bee stings or after in-hospital use of parenteral 

drugs or contrast agents. Cardiogenic shock is extremely rare in children but may 

complicate congenital heart disease or toxicologic emergencies. 

Shock is not hypotension. Successful management includes early recognition of the 

compensated, normotensive phase of shock. During the compensated phase of 

hypovolemic shock, vital signs in the supine patient are usually normal, except for mild 

tachycardia. Skin signs of hypoperfusion are usually evident, and laboratory testing may 

disclose metabolic acidosis. Intervention is usually successful during this phase. When 

the hypotensive, decompensated phase develops in the absence of recognition and 

effective treatment, irreversible shock and death may result. 

Treatment 

Rapid clinical assessment should disclose a shock category, so that focused treatment 

can be immediately instituted (Chapter 9). Failure to act expeditiously and aggressively 

is a common error and may significantly increase mortality risk. Figure 48-2 is an 

algorithm for treatment of uncompensated shock in children. 


Consider immediate endotracheal intubation. In the ill-appearing child with signs of 

shock and sepsis or the frankly hypotensive child, intubation should be accomplished 

either immediately or after the patient fails to respond to first-line resuscitation with

oxygen and fluids. After intubation, insert a nasogastric tube. 

Apply supplemental oxygen, attach pulse oximeter and cardiac monitor, establish 2 

secure intravenous catheters, check fingerstick blood sugar, and insert urinary bladder 

catheter. 


Initiate volume resuscitation if indicated, or begin administration of an inotropic agent. 

When inotropic agents are used, the intravascular volume must be adequate. Inotropic 

infusions can then be titrated at the bedside, often using multiple infusions (dopamine, 

epinephrine, dobutamine), until perfusion is restored. Start with epinephrine at 0.1-1.0 

ug/kg/min, and then add a second inotropic agent if cardiovascular response does not 

occur. If physical examination is equivocal for hydration status, a chest x-ray may help: 

dehydration or overhydration is reflected in the appearance of pulmonary vessels. 


Obtain arterial blood gases, CBC, electrolytes, platelets, coagulation studies, blood 

cultures (if infection is suspected), and urinalysis, and consider a urine drug screen to 

help guide secondary treatment after stabilization. A chest x-ray is also necessary in 

most cases. 

Bardella IJ: Pediatric advanced life support: a review of the AHA recommendations. Am 

Fam Physician 1999;60:1743. [PMID: 10537389] (Review.) 

CONGESTIVE HEART FAILURE 


• Sweating during feeding or crying; failure to thrive. 

• Tachypnea, tachycardia. 

• Hepatomegaly. 


Congestive heart failure (CHF) is unusual in childhood. It usually presents in the first 

year of life in patients with congenital heart disease. Table 48-6 lists the structural 

conditions causing CHF at different times during infancy. Myocarditis and other 

cardiomyopathies, toxicologic conditions, and coronary artery disease are also included 

in the differential diagnosis of new heart failure in childhood. 

Treatment 

When congestive heart failure has progressed to frank pulmonary edema, treat as 

follows: 


Assess need for immediate endotracheal intubation in the severely distressed,

hypotensive, or hypoxic patient (pulse oximetry < 85% on 100% oxygen). 

Apply 100% oxygen, sometimes with positive-pressure ventilation through an 

endotracheal tube, and attach pulse oximeter and cardiac monitor. Insert urinary 

bladder catheter and check fingerstick blood sugar. 

Establish a secure intravenous line with 5% dextrose in water at a rate to keep the vein 

open. 

B. Pharmacologic Treatment 

Administer morphine sulfate, 0.1 mg/kg intravenously. Administer furosemide, 1-2 mg/kg 



Obtain arterial blood gas, CBC, electrolyte, BUN, creatinine, and digoxin levels if 

appropriate. Obtain an ECG. Order a chest x-ray in the room or with a nurse or 

physician in attendance in the radiology suite. 

Administer digoxin. Digitalization doses are 10 ug/ kg intravenous load, a second dose 

at 6 hours, and a third dose at 24 hours. Occasionally, patients with severe pulmonary 

edema unresponsive to initial therapy require dopamine, dobutamine, or both. 

McCollough M, Shafieff G: Common complaints in the first thirty days of life. Emerg Med 

Clin North Am 2002;20:27. [PMID: 11826636] (Review.) 

O'Laughlin MP: Congestive heart failure in children. Pediatr Clin North Am 1999;46:263. 

[PMID: 10218074] (Review.) 

CARDIAC DYSRHYTHMIAS 


Although uncommon, dysrhythmias sometimes occur in children with known congenital 

heart disease, acquired heart disease (eg, myocarditis), or secondary to other metabolic 

or toxicologic disorders. Therapy is aimed at the underlying condition. Evaluation of 

dysrhythmias includes clinical assessment of cardiopulmonary status and interpretation 

of the electrocardiogram (ECG). Key electrocardiographic features are heart rate and 

width of the QRS complex. These constituents must be evaluated against age-specific 

norms. 

Treatment 



Apply supplemental oxygen; attach pulse oximeter and cardiac monitor. Establish a 

secure intravenous line with 5% dextrose in water at a rate to keep the vein open. 

Obtain an ECG if the patient is hemodynamically stable.

B. Cardioversion 

Unstable patients with tachydysrhythmias require immediate electrical direct current 

countershock. Initial mode (synchronized or asynchronized) and exact energy levels are 

dictated by the nature of the dysrhythmia. (See Table 48-7.) 

If electrical conversion does not occur with initial shock, double electrical doses until 

conversion occurs or until the maximum electrical dose is 8 J/kg. If synchronized 

countershock fails at 4 J/kg, switch to asynchronized mode (defibrillation). Ensure that 

paddles are held firmly against chest wall and that a good conductive agent is 

employed. Standard 4.5-cm pediatric paddles are used for infants up to age 1 year. If 

standard 4.5-cm pediatric paddles are unavailable for sternoapical placement, use adult 

paddles in an anteroposterior configuration. 

Pretreat conscious patients requiring cardioversion with light anesthesia (diazepam, 0.1 

mg/kg), and be prepared to perform endotracheal intubation and full cardiopulmonary 

resuscitation. 

Fulton S, Jackimczyk KC: Antidysrhythmics. Emerg Med Clin North Am 2000;18:655. 

[PMID: 11130932] (Review.) 

RESPIRATORY DISTRESS 

In children, normal ventilation and oxygenation occurs with minimal visible effort. 

Evaluation of respiratory function includes assessment of rate, work of breathing, skin 

and mucous membrane color, and mental status. Respiratory rate alone is an 

insensitive indicator of respiratory distress, because rates vary significantly with age, 

excitement, anxiety, or fever. Tachypnea may be an early manifestation of respiratory 

distress, or it may result from respiratory compensation for metabolic acidosis caused 

by shock, diabetic ketoacidosis, inborn errors of metabolism, salicylism, or chronic renal 

insufficiency. A slow respiratory rate may indicate impending respiratory failure. 

Observation alone will usually disclose distress or increased work of breathing. A child 

with noisy breathing is especially worrisome, especially if inspiratory stridor is present. 

This denotes upper airway obstruction. Immediate therapy is indicated to relieve 

obstruction and improve oxygenation and ventilation. Increased work of breathing is 

also evidenced by nasal flaring and by suprasternal, intercostal, and subcostal 

retractions. Retractions become more pronounced cephalad to caudad with increasing 

hypoxia. Grunting is produced by premature glottic closure and usually represents 

alveolar collapse and loss of lung volume, which develop in patients with pulmonary 

edema, pneumonia, or atelectasis. Auscultation will provide further differentiation of 

disease possibilities. Wheezing, rales, or decreased breath sounds may be present. 

However, auscultation is often inaccurate in the busy, noisy emergency department 

setting. Cyanosis, when present, represents severe distress and is best seen on 

mucous membranes of the mouth and nail beds. Peripheral cyanosis is more likely due 

to circulatory failure than to pulmonary failure. Finally, mental status changes may be a 

clue to gas exchange abnormalities. Hypoxic patients are restless and agitated; 

hypercapnic patients are drowsy or even comatose. 

Rapid evaluation of respiratory function is imperative in all distressed emergency

department pediatric patients. Respiratory failure and respiratory arrest due to a wide 

spectrum of causes (eg, head trauma, coma, poisoning, pneumonia, asthma, foreign 

body aspiration) are the most common causes of cardiac arrest in childhood. Timely, 

aggressive intervention in early stages as well as meticulous respiratory monitoring by 

means of pulse oximetry and continuous observation will avert preventable adverse 

patient outcomes. Children with respiratory distress should not be sent for imaging 

studies without qualified personnel in attendance. Early hospital admission is usually 

warranted for such patients. 

Pulse oximetry must be used liberally in the emergency department setting in order to 

disclose undetected oxygen desaturation states. Pulse oximetry is noninvasive, simple, 

and reasonably accurate. Use this assessment modality in all cases of suspected 

respiratory distress, cardiopulmonary disease, or serious trauma. In selected patients, 

especially those with significant tachypnea or work of breathing, pulse oximetry may 

underestimate degree of distress, and it provides no indication of adequacy of 

ventilation (ie, PCO 2 ). In such patients, obtain arterial blood gas levels to help measure 

the severity and nature of the ventilation or oxygenation disturbance. 

APNEA 


Apnea means cessation of ventilation for 20 seconds or for 10-20 seconds in patients 

who also manifest bradycardia, cyanosis, or pallor. Ordinary sleep will sometimes cause 

breathing irregularities easily confused with apnea. There are 2 classifications of apnea: 

central and obstructive. Central apnea is characterized by an absence of respiratory 

effort secondary to diminished muscular activation. It occurs in newborn infants, often in 

preterm infants. Infection, metabolic abnormalities, anemia, hypoxia, or central nervous 

system injury may be associated with newborn apnea. Obstructive apnea occurs in later 

infancy and childhood and is related to obstructive upper airway conditions. This results 

in cessation of airflow despite respiratory effort, as can be seen with chest and 

abdominal movement. 

Treatment 

A. Apnea in Infants 

Apnea in infants may be symptomatic of life-threatening illness. Such patients ordinarily 

require hospital admission for observation and full workup for infections and for central 

nervous system, metabolic, and feeding problems. Initial management in the emergency 

department is discussed here. 

1. Oxygenation and ventilation—Place child on supplemental oxygen, and apply pulse 

oximeter and cardiac monitor or apnea monitor. 

2. Volume resuscitation—If evidence of dehydration is present, establish intravenous 

access with lactated Ringer's solution or isotonic normal saline. Otherwise, if the patient 

is euvolemic, begin 5% dextrose in quarter-normal saline at maintenance rate for weight 

(see Table 48-5).

3. Laboratory and imaging studies—Obtain blood for CBC with differential, 

electrolytes, BUN, creatinine, ionized calcium and magnesium, and cultures. Obtain 

clean urine for urinalysis, culture, and toxicology studies. Consider spinal fluid analysis 

in most infants and any young child with meningeal signs, toxicity, or altered mental 

status. CT scan can usually precede spinal fluid analysis in the child who does not 

appear acutely infected. 

Obtain a chest x-ray and respiratory syncytial virus (RSV) and pertussis studies. 

Consider an ECG. Consider an EEG if the patient has an altered mental status or if a 

seizure focus is suspected. 

4. Other measures—Admit for observation and further evaluation on an apnea monitor. 

B. Apnea in Children 

Obstructive apnea in slightly older patients may be serious. Focus evaluation on 

obstructive upper pharyngeal lesions such as tonsillitis and pharyngitis or 

laryngomalacia. Chest x-ray and lateral neck films, along with transnasal laryngoscopy, 

are often necessary. Emergency department evaluation may be insufficient to exclude a 

serious diagnosis, and hospital admission may be indicated. 

UPPER AIRWAY OBSTRUCTION 


• Inspiratory stridor. 

• Suspect foreign body aspiration if symptoms develop rapidly without associated signs 

of infection. 

• Anteroposterior and lateral neck x-rays are helpful to differentiate croup from 

epiglottitis. 


Upper airway obstruction is usually readily apparent. Inspiratory stridor is the hallmark. 

The child is dyspneic and shows signs of respiratory distress, including tachypnea; 

flaring; and supraclavicular, intercostal, and subcostal retractions. Ventilation and 

sometimes oxygenation abnormalities are present. If obstruction is severe, hypercapnia 

will be present, usually along with depressed mental status, cyanosis, and decreased air 

movement. Arterial blood gases will demonstrate carbon dioxide retention and often 

hypoxemia. Pulse oximetry will be abnormal in most advanced cases but normal in 

typical cases. 


In children, the common causes of stridor and upper airway obstruction are croup, 

epiglottitis, and foreign body aspiration. The epidemiologic and clinical characteristics of 

these entities are compared in Table 48-8. Other less common conditions producing 

stridor are bacterial tracheitis (usually Staphylococcus aureus or Haemophilus

influenzae), retropharyngeal or peritonsillar abscess, trauma, caustic ingestions, 

neoplasm, or angioneurotic edema. 

Treatment 

(See Figure 48-3.) Clear the airway using procedures recommended in Table 48-9 for 

the patient with complete airway obstruction. Avoid airway clearance maneuvers in the 

patient with incomplete or partial airway obstruction, because this may worsen 

obstruction. Allow the child to adopt a position of comfort, usually on the parent's lap. 

Apply supplemental oxygen, and attach pulse oximeter and cardiac monitor. 

A. Epiglottis 

If a child presents with clinical findings suggestive of epiglottitis, immediately arrange to 

establish a definitive airway, preferably by orotracheal intubation in the operating room. 

In the rare case in which abrupt airway obstruction occurs, first attempt bag-valve-mask 

ventilation and prepare for orotracheal intubation. If bag-valve-mask and orotracheal 

intubation fails, perform needle cricothyrotomy or surgical tracheostomy. Minimize all 

invasive interventions in order to avert patient agitation and potential precipitous airway 

obstruction. 

Once the airway is secured, obtain blood and throat cultures and begin antibiotic 

therapy. Intravenous cefuroxime, 50 mg/kg every 8 h; intravenous cefotaxime, 50 mg/kg 

every 8 h; or intravenous ceftriaxone, 50 mg/ kg every 24 h, may be used. Alternatives 

include trimethoprim-sulfamethoxazole (TMP-SMZ), 4-6 mg/ kg TMP and 20-30 mg/kg 

SMZ every 12 h, or ampicillin-sulbactam, 25-75 mg/kg every 6 h. 

In a patient with a lower likelihood of epiglottitis, a soft tissue lateral film of the neck may 

be useful to help demonstrate the swollen epiglottis (Figure 48-4). 

A physician should be at the patient's bedside at all times, including in the radiology 

suite, prepared to perform definitive airway maneuvers. 

B. Croup (Laryngotracheobronchitis) 

Croup is a clinical syndrome characterized by barking cough, inspiratory stridor, and 

hoarseness of voice. These symptoms are believed to be secondary to viral 

inflammation of the upper airway. If history and clinical assessment, sometimes in 

combination with lateral neck x-rays and chest x-rays, suggest croup, therapy includes 

the following: 

1. Initial steps—Apply humidified oxygen, and attach pulse oximeter and cardiac 

monitor. Rarely is immediate endotracheal intubation necessary before attempts at 

medical management. Keep the child in a position of comfort, usually on the parent's 

lap. 

2. Pharmacologic treatment—Give glucocorticoids to any child who presents with 

croup symptoms and demonstrates increased work of breathing. Give either nebulized 

budesonide, 2 mg, or oral or intramuscular dexamethasone, 0.15-0.6 mg/kg. 

For children who are moderately or severely distressed, consider nebulized racemic

epinephrine (0.5 mL of 2.25% racemic epinephrine) or nebulized L-epinephrine (5 mL of 

1:1000). Previously all children who received epinephrine were hospitalized because of 

concerns over severe rebound airway swelling. Current recommendations allow for 

discharge if the patient remains comfortable without stridor or signs of respiratory 

distress for 2-3 hours after 1 epinephrine nebulization. Patients who require a second 

epinephrine nebulization should be hospitalized for further observation and treatment. 

Discharged patients must have reliable guardians and be able to return if their 

symptoms worsen. 

3. Humidified oxygen with saline—For the minimally distressed child with no stridor at 

rest and pulse oximetry greater than 92% on room air, consider cool, humidified oxygen 

with nebulized saline. If this approach is effective in the emergency department at 

reducing upper airway obstruction, such patients may ordinarily be discharged and may 

use cool mist therapy at home. 

C. Foreign Body Aspiration 

The anatomic level and completeness of airway obstruction will dictate physical findings. 

The history is usually highly suggestive, with a brief asymptomatic interval followed by 

sudden dyspnea, coughing, and gagging, after the child has handled a small object 

such as jewelry, a toy, a pin, a peanut, or candy. In 20% of cases, the object is in the 

upper airway; in 80%, it is in the main-stem or lobar bronchus. Stridor is present if the 

object is lodged high, at the level of the larynx; wheezing and decreased breath sounds 

occur if is it lodged below the larynx. Mild tachypnea may be the only finding. Lateral 

neck x-rays may be helpful for radiopaque foreign bodies in the neck. When lower 

airway occlusion is suspected, chest x-rays taken in decubitus positions bilaterally 

(preferentially in expiration) will often reveal hyperinflation in the affected lung area. This 

finding is most visible in the dependent lung, which will be more radiolucent when 

compared with the superior lung in the same decubitus view or with the contralateral 

dependent lung in the other decubitus view. 

1. Complete obstruction—If obstruction is complete and airway clearance maneuvers 

(see Table 48-9) fail, perform laryngoscopy immediately, and attempt to remove the 

foreign body with Magill forceps under direct vision. After removal of the foreign body, 

insert a properly sized endotracheal tube to prevent later inflammatory obstruction. 

2. Partial obstruction—In most patients, obstruction is partial. Apply supplemental 

oxygen, and attach pulse oximeter and cardiac monitor. Do not attempt endotracheal 

intubation. 

Establish venous access and begin 5% dextrose in quarter-normal saline, at 

maintenance rate (see Table 48-5). Allow the patient to assume a position of comfort, 

usually on the parent's lap. 

Obtain chest x-rays (see above). Maintain constant observation of the patient by nurse 

or physician. Arrange for rigid bronchoscopy, under general anesthesia, to remove the 

foreign object. 

Wright RB, Pomerantz WJ, Luria JW: New approaches to respiratory infections in 

children. Bronchiolitis and Croup. Emerg Med Clin North Am 2002;20:93. [PMID:

11826639] (Review.) 

LOWER AIRWAY DISORDERS 

Lower airway disorders are a disparate group of conditions with varying clinical 

presentations that may affect oxygenation and ventilation. Lower airway disease 

includes both obstructive conditions and parenchymal or alveolar disease. The clinical 

hallmarks are dyspnea and tachypnea, often with cough. Wheezing denotes an 

obstructive process. 

In children, the most common causes of lower airway obstruction are bronchiolitis, 

asthma, and foreign body obstruction. In infants, congenital anomalies of the airway 

(tracheal web, cysts, vascular rings, lobar emphysema) must also be considered. 

Pneumonia is the most frequent pediatric alveolar disorder, although pulmonary edema, 

inhalation injury, and cystic fibrosis must also be excluded. 

1. Bronchiolitis 


Bronchiolitis is a wintertime acute lower airway respiratory disease, usually caused by 

RSV, that produces small airway obstruction. It primarily affects children under age 12 

months. Cough, coryza, and upper respiratory symptoms, usually with fever, precede 

wheezing and dyspnea. Clinical signs of respiratory distress are variable. The white 

blood cell count is normal, and the chest x-ray shows shifting patterns of hyperaeration 

and atelectasis. Hypercapnia, hypoxemia, or both may be present. 

Treatment 


Apply supplemental humidified oxygen, and attach pulse oximeter. Keep child on 

parent's lap. 

B. Bronchodilator Therapy 

If wheezing is present, a trial of nebulized epinephrine or albuterol (0.15 mg/kg of 0.5% 

solution or 0.03 mL/ kg by mask; maximum, 2.5 mg) is recommended. Albuterol can be 

repeated every 15-60 minutes depending on severity of disease and response to the 

medication. If bronchodilator therapy produces improvement, continue bronchodilator 

therapy as discussed below for asthma. 


Obtain a chest x-ray and nasopharyngeal swab for RSV viral culture. Rapid testing such 

as enzyme-linked immunoassay (ELISA) and fluorescent antibody testing may also be 

available. 

Disposition 

Admission is required for children who appear ill or toxic. Admission is recommended if 

any of the following are present: oxygen saturation less than 95%, respiratory rate

greater than 70 breaths/min, atelectasis on chest x-ray, gestational age less than 34 

weeks, or age less than 3 months. 

Klassen TP: Recent advances in the treatment of bronchiolitis and laryngitis. Pediatr 


2. Asthma 


The most common pediatric respiratory disease is reactive airway disease, or asthma. 

Dyspnea, cough, and wheezing are part of the usual presentation. In infancy, wheezing 

is typically associated with bronchiolitis, caused by RSV. The relationship of bronchiolitis 

in infancy to childhood asthma is not clear, although approximately one half of infants 

with bronchiolitis later develop asthma. Bronchiolitis may respond to bronchodilator 

therapy with albuterol or subcutaneous epinephrine, which indicates reversible smooth 

muscle spasm. In both conditions, mucus plugging of small airways, edema, and 

bronchial constriction are key pathophysiologic features. Asthma appears to be 

increasing in prevalence, and morbidity and mortality rates associated with this 

condition are rising. 

When a patient presents during an asthma exacerbation, important historical information 

includes recent steroid use, prior intensive care unit admissions, prior intubations 

secondary to asthma, preceding triggers, medications and frequency of their use, and 

baseline peak expiratory flow rates (PEFRs). 

PEFR is extremely useful in asthma evaluation, and handheld pediatric-sized devices 

should be available in the emergency department. PEFR is more sensitive than 

auscultation, pulsus paradoxus, or other physical signs in gauging severity of 

obstruction and response to therapy. Children aged 4-5 years can successfully use 

handheld peak flow meters. Comparison of presenting PEFR with known baseline 

values is especially helpful. Arterial blood gas measurements and chest x-ray are 

necessary in severe cases. Physical exam findings also guide the management and 

treatment of asthma. Inability to speak, cyanosis, accessory muscle use, pulsus 

paradoxus, or signs of infection may indicate more serious disease. 

Treatment 



Provide supplemental oxygen therapy, and attach pulse oximeter. Oxygen is 

recommended for all children with any sign of respiratory distress (eg, dyspnea, difficulty 

speaking, mental status changes, or accessory muscle use). 

B. Pharmacologic Therapy 

1. Inhaled ß 2 -agonists—Inhaled ß 2 -agonists are the drugs of choice for the treatment 

of acute bronchoconstriction. Nebulizers, metered-dose inhalers, and dry-powder 

inhalers are equally effective. Nebulized albuterol treatment (0.15 mg/kg; maximum, 5

mg) may be preferred by children who cannot adequately inspire medications from other 

routes. 

2. Glucocorticoids—Consider glucocorticoids for all children with asthma who present 

in an acute exacerbation. The initial dose of prednisone is 2 mg/kg, with a maximum of 

80 mg. 

3. Ipratropium bromide—Ipratropium bromide alone is not recommended and is not a 

first-line therapy. Although a dosing regimen has not been determined, when used as an 

adjunct with albuterol, ipratropium bromide has been shown to improve pulmonary 

function tests and to decrease emergency department time in an acute asthma 

exacerbation. 

4. Epinephrine or terbutaline—In general, subcutaneous epinephrine, 0.01 mg/kg up 

to 0.3-0.5 mg, or terbutaline intravenously or subcutaneously offers no advantage over 

an inhaled ß-agonist but should be considered in addition to inhaled albuterol for 

critically ill children with severe respiratory distress, poor air movement, or rapid 

decompensation. A terbutaline intravenous bolus of 2-10 ug/kg should be followed by an 

infusion starting at 0.4 ug/kg/min to a maximum of 5.0 ug/kg/min. 

5. Magnesium—The benefit of intravenous magnesium, 25-50 mg/kg (maximum, 2 g), 

is unclear and may be considered for moderate to severely ill patients who have not 

responded to other therapies. 

C. Intubation 

Absolute indications for intubation include apnea, respiratory failure, and coma. Relative 

indications include marked hypoxia, rapidly rising hypercarbia with respiratory acidosis, 

inability to speak, mental status changes, and exhaustion. 

Disposition 

There are no absolute guidelines for admission or discharge of a pediatric asthma 

patient. Intensive care unit admission is required for patients with an altered level of 

consciousness, hypotension, or respiratory failure. Hospitalization is strongly 

recommended for patients with a poor social situation, history of near fatal asthma, or 

inability to tolerate oral medications. If the clinical decision is made to discharge the 

patient home, an inhaled ß 2 -agonist should be prescribed. In addition, steroids (eg, 

prednisone, 2 mg/kg/d) should be strongly considered and follow-up within 3 days 

arranged. 

Baren JM, Zorc JJ: Contemporary approach to emergency department management of 

pediatric asthma. Emerg Med Clin North Am 2002;20:115. [PMID: 11831222] (Review.) 

Smith SR, Strunk RC: Acute asthma in the pediatric emergency department. Pediatr 


3. Pneumonia 

Clinical Findings

Patients with pneumonia present with symptoms of cough and dyspnea, with or without 

fever. Abdominal pain may be the presenting complaint. Nonspecific symptoms in a 

young child or infant may include irritability, poor feeding, decreased physical activity, 

vomiting, diarrhea, or apneic episodes. Signs of respiratory distress, including 

wheezing, rales, rhonchi, or focal absence of breath sounds, usually are present. 

Physical evaluation may be nonspecific. Tachypnea and respiratory distress may be 

present with a clear chest on auscultation or with discrete rales in affected lung 

segments. Chest x-rays show lobar or peribronchial perihilar patterns of infiltration, 

sometimes with pleural effusion. 

Pediatric pneumonia can be caused by bacteria, viruses, Mycoplasma, mycobacteria, or 

Chlamydia. Age is an important consideration in determining possible pathogens in 

children with pneumonia (Table 48-10). Certain clinical or laboratory features suggest 

specific causes: high fever, appearance of illness, significant leukocytosis, and pleural 

effusion suggest bacteria; afebrile pneumonia with eosinophilia in infancy suggests 

Chlamydia; extreme lymphocytosis in an unimmunized infant with whooping cough 

suggests pertussis; hilar adenopathy and upper lobe infiltration suggest primary 

tuberculosis. In younger children, rapid diagnostic testing for RSV (by 

immunofluorescent and ELISA antigen techniques performed on nasal or conjunctival 

specimens) may provide the cause. In older children, sputum Gram staining may guide 

initial therapy. 

Treatment 

Rapid evaluation of respiratory status, in combination with pulse oximetry and 

occasionally arterial blood gas determination, will direct the immediate therapy. 


Provide supplemental oxygen, and attach pulse oximeter and cardiac monitor. Evaluate 

degree of respiratory distress. Significant respiratory distress is best defined as pulse 

oximetry less than 92% on room air. 

B. Laboratory and Imaging Studies 

Obtain a chest x-ray (posteroanterior and lateral). Consider CBC with differential, 

absolute neutrophil count, C-reactive protein, RSV studies, and blood culture. 

C. Antimicrobial Therapy 

Administer antimicrobial therapy based on age and clinical appearance. See Table 

48-11 for guidelines. 

D. Treatment of Suspected Tuberculosis 

Arrange for in-hospital multiple drug therapy with isoniazid, rifampin, and pyrazinamide 

for children with clinical and epidemiologic evidence of primary pulmonary tuberculosis. 

Consider applying an intradermal PPD test and arrange 48-hour follow-up for patients at 

risk of having tuberculosis. 


Children with a parapneumonic pleural effusion require a thoracentesis and subsequent

hospital admission for observation and intravenous antibiotics after the procedure. 

Analysis of the fluid should include Gram stain, culture, cell count and differential, total 

protein, pH, and glucose. 

Disposition 

Most children can be discharged home with appropriate follow-up on antibiotics. 

Hospitalization is required if the patient demonstrates signs of toxicity, dehydration, 

significant respiratory distress, hypoxemia, or pleural effusion or if the patient is less 

than 20-30 days old. Consider hospitalization for children younger than age 3 months 

and for patients with preexisting pulmonary disease. Twenty-four hour follow-up is 

required for all children diagnosed with pneumonia and discharged. 

McCracken GH: Diagnosis and management of pneumonia in children. Pediatr Infect 

Dis J 2000;19:924. [PMID: 11001128] (Review.) 

McIntosh K: Community-acquired pneumonia in children. N Engl J Med 2002;346:429. 

[PMID: 11832532] (Review.) 

NEUROLOGIC EMERGENCIES 

Objective neurologic evaluation of the emergency department patient involves 

recognition of age-appropriate differences in cognitive function. For patients with altered 

mental status, an objective scale, such as the pediatric Glasgow Coma Scale (Table 

48-12) will help reduce interobserver differences in assessment and provide a measure 

for comparison during serial examinations. 

SEIZURES 


Seizures are common pediatric emergencies in both the prehospital environment and 

the emergency department. Approximately 5% of all children have one or more seizures 

before age 16 years. Epilepsy is a chronic condition of recurrent seizures that develops 

in only a small portion of patients who have single seizures. Most seizures in childhood 

are single, generalized tonic-clonic events lasting a few minutes. Seizures may be 

generalized or focal. Status epilepticus is defined as continuous seizure activity for 30 

minutes or as recurrent seizures without intervening return of consciousness. Seizures 

may be generalized or focal, or focal with secondary generalization. Patients with focal 

status epilepticus may present with or without preserved consciousness. Status 

epilepticus is often the first presentation of seizures in childhood. 

The causes of seizures and status epilepticus in children are multiple and 

age-dependent. Children under age 3 years presenting with status epilepticus are most 

likely to have serious conditions, for example, central nervous system infections or 

vascular disorders, anoxia, trauma, intoxications, or metabolic abnormalities. Many of 

these conditions are treatable. In older children, however, status epilepticus is usually 

the result of chronic epilepsy with noncompliance for anticonvulsive medications, 

chronic progressive encephalopathy, or idiopathic encephalopathy. The likelihood of

serious underlying disease in a child presenting with status epilepticus is inversely 

correlated with age. 

Febrile seizures are also common in childhood. The peak age is 8-20 months, although 

they may occur in children from approximately 6 months to 6 years of age. Often, 

underlying diseases are simply upper respiratory tract infections or gastroenteritis. 

Febrile seizures may be simple or complex. A simple febrile seizure typically occurs as 

a generalized self-limited tonic-clonic seizure of several minutes' duration. Complex 

febrile seizure denotes a seizure with high-risk features, including focal onset, postictal 

neurologic abnormalities, or duration greater than 15 minutes. Other high-risk features 

include prior neurologic or developmental abnormalities or a history of epilepsy in the 

nuclear family. The simple febrile seizure is usually benign and requires no therapy; 

however, children presenting with high-risk features are at greater risk for recurrent 

afebrile features. 


Many children will present in the postictal state. In such patients, search for a specific 

cause. Obtain a history from the parents beginning with a precise description of the 

seizure itself, including the nature of onset (focal or generalized), duration, and quality of 

motor features. Exclude syncope, hysteria, breath-holding, and night terrors. Other 

confusional states that may be difficult to distinguish from seizures include migraine 

headache, hereditary chin trembling, familiar choreoathetosis, and narcolepsy. Also 

exclude head trauma and alcohol and drug intoxication. Several drugs are well 

associated with seizure activity: cyclic antidepressants, sympathomimetics (cocaine, 

amphetamine, phencyclidine), theophylline, isoniazid, phenothiazines, camphor, 

anticholinergics, antihistamines, and lindane. Physical examination should specifically 

exclude head trauma, bulging fontanelle, papilledema, meningeal irritation, focal 

neurologic signs, cutaneous lesions, and systemic disease. 

Treatment 

A well-organized approach to seizure management minimizes the complications of the 

acute electrical and metabolic derangements and averts iatrogenic complications. 

Ensure adequate ventilation and oxygenation in the patient with active seizures, and 

then address termination of the seizure and reversal of metabolic imbalances. Finally, 

attempt to establish the cause in order to implement specific therapy. 


1. Initial steps—Open the airway, use suction to clear secretions or foreign bodies, and 

then administer oxygen. Ordinarily, reserve intubation for failure of medical 

management. 

Protect the child from injury by manually holding the head. Remove tight-fitting clothing 

from the child. 

2. Laboratory studies—Establish intravenous access, and draw blood for immediate 

bedside glucose determination and other appropriate laboratory investigations, including 

CBC; glucose, lead, calcium, and magnesium levels; liver and renal function; and

electrolytes, ammonia, and pertinent drug levels. Send urine for toxicologic screening. 

Consider obtaining an arterial blood gas if significant acidosis is suspected. The best 

alternative to intravenous access in children younger than age 5 years with prolonged 

refractory status epilepticus may be the intraosseous route. 

3. Volume resuscitation—If rapid bedside glucose determination is less than 90 

mg/dL, administer 25% dextrose in water, 2 mL/kg/dose slowly intravenously. In children 

over age 3 years, give 50% dextrose in water at 1 mL/kg. If evidence of dehydration is 

present, provide lactated Ringer's solution or isotonic normal saline. Otherwise, if the 

patient is euvolemic, start 5% dextrose in quarter-normal saline at maintenance rate for 

weight (see Table 48-5). 

4. Pharmacologic therapy—Consider naloxone, 0.1 mg/kg (max 2 mg) intravenously. 

If the child is febrile, administer rectal acetaminophen, 10-15 mg/kg. If fever fails to 

respond to acetaminophen, use tepid water baths to reduce temperature. 

5. Other measures—After a febrile seizure, children who appear toxic or do not return 

to baseline mental status (after a brief postictal period) should undergo a full septic 

workup including a lumbar puncture. 

B. Specific Management 

If seizures continue after first-line supportive care, consider immediate anticonvulsant 

therapy (Figure 48-6). Duration of seizure activity may be related to ultimate neurologic 

outcome, particularly in patients with severe underlying disease. 

Alternatives to intravenous lorazepam include rectal diazepam, 0.5 mg/kg administered 

by lubricated tuberculin syringe approximately 5 cm into the rectum, or intramuscular 

midazolam, 0.2 mg/kg. Phenytoin, barbiturates, and benzodiazepines may be given 

intraosseously. 

Hanhan UA, Fiallos MR, Orlowski: Status epilepticus. Pediatr Clin North Am 

2001;48:683. [PMID: 11411300] (Review.) 

Reuter D, Brownstein D: Common emergent pediatric neurologic problems. Emerg Med 


INFECTIOUS DISEASES 

FEVER 

The evaluation of febrile children is a common problem for the emergency physician. 

Although most of these children will have benign, self-limited viral infections, a few will 

have invasive disease with bacterial pathogens that may cause significant illness and 

even death. No source of infection will be evident after history and physical examination 

in 20% of febrile children. The ability to identify those children at increased risk for 

serious disease is the key to management. Because young children are at increased 

risk for more serious disease, the child's age frequently determines the extent of the 

evaluation.

1. Fever in Infants 


Management of fever in infants under age 3 months is complicated and controversial. 

Signs of disease at this age are frequently subtle and nonspecific, and there are multiple 

sources of infection. Relative to older infants, these infants uncommonly have febrile 

disease, and when present, it more likely reflects a serious invasive infection. Causes of 

fever at this age include (1) infections acquired in the household, (2) late onset of 

disease acquired in the nursery, at delivery, or in utero, and (3) infections secondary to 

anatomic or physiologic abnormalities. 

Household-acquired infections are the most likely cause of fever in this age group, 

particularly with an uncomplicated prenatal and delivery history. Respiratory and 

gastrointestinal infections are most common. The incidence of invasive disease caused 

by Streptococcus pneumoniae is significant in the first 2 months of life. Other causes 

include the late onset of signs of congenital infection, such as rubella, cytomegalovirus, 

or syphilis. In addition, the delayed onset of infection acquired at delivery, for example, 

group B streptococci, Escherichia coli, and Listeria, are potentially life-threatening 

infections in this age group. Disease acquired in the nursery before discharge (eg, S. 

aureus) may also become manifest during this time. Additionally, infections associated 

with an underlying anatomic abnormality, particularly those of the urinary tract, are 

potential sources of infection. 

The younger the infant, the greater the risk of disease. The incidence of bacterial 

disease in febrile infants under age 1 month with a temperature of at least 38 °C (100.4 

°F) is approximately 13%; in infants aged 1-2 months, the incidence is approximately 

10%. In infants under age 3 months with temperatures over 40 °C (104 °F), the 

incidence of serious disease may be as high as 30-40%. 


Evaluation includes a careful history of the pregnancy, delivery, and nursery course of 

the infant. Inquire about household infections. Look for general signs of illness, including 

lethargy and irritability. Otitis media can occur in infants under age 2 months. Other 

clues to the source of fever are (1) rash, jaundice, hepatosplenomegaly, macrocephaly 

(congenital infection), (2) direct hyperbilirubinemia (urinary tract infection), (3) 

pseudoparalysis, cellulitis, meningitis (group B streptococci), and (4) meningitis 

(Listeria). 

A. Laboratory Findings 

The laboratory evaluation of febrile infants under age 3 months includes the following: 

1. CBC with differential and blood culture—A white blood cell count less than 5000 

or greater than 15,000; absolute neutrophil count greater than 10,000; or band count 

greater than 1500 increases the probability of sepsis. 

2. Peripheral blood smear—Toxic granulation and vacuolization of white cells are 

sensitive indicators for invasive bacterial disease.

3. Lumbar puncture—Both bacterial and aseptic meningitis may be serious in febrile 

infants under age 3 months. Lumbar puncture is mandatory for infants under age 1 

month and is strongly recommended for infants aged 1-3 months. Spinal fluid studies 

include cell count and differential, glucose, protein, Gram stain, and culture and antigen 

detection by counterimmunoelectrophoresis or latex agglutination for group B 

streptococci, H. influenza, S. pneumoniae, and N. meningitidis. 

4. Urinalysis—Obtain urine dipstick and microscopic analysis. Positive findings are at 

least 5 white blood cells per high-power field or positive nitrite or leukocyte esterase. 

5. Urine culture—A bagged specimen is not adequate because of the high incidence of 

contamination. Suprapubic aspiration or bladder catheterization are the preferred 

methods of obtaining urine. 


Findings of pneumonia may be present on chest x-ray even in infants without cough, 

tachypnea, or rales. 

Treatment 



Management must be conservative. If evaluation discloses a local infection (eg, 

meningitis, pneumonia, or urinary tract infection), hospitalize the infant and promptly 

institute intravenous antibiotic therapy. 

1. Antimicrobials for infants birth to age 4 weeks—If the suspected causative 

organism is group B streptococci, Listeria, or E. coli, give ampicillin, 50 mg/kg every 6-8 

hours, and gentamicin, 2.5 mg/kg every 12 hours. 

2. Antimicrobials for infants aged 4-8 weeks—If the suspected causative organism is 

group B streptococci, Listeria, H. influenzae, or S. pneumoniae, give ampicillin, 50 

mg/kg every 6-8 hours, and either ceftriaxone, 100 mg/kg/d, or cefotaxime, 50 mg/kg 

every 6 hours. 

3. Other antimicrobials—The cephalosporins are not active against Listeria and thus 

are not recommended as the sole treatment for presumed sepsis in infants under age 8 

weeks. If S. aureus infection is possible, replace ampicillin with a penicillinase-resistant 

antibiotic such as nafcillin, 50-200 mg/kg/d, depending on the child's age. 

B. Treatment of Otitis Media 

The infant older than age 1 month with otitis media who clinically appears well may be 

discharged with antibiotics and careful follow-up. 

C. Treatment for Fever without Clear Cause 

Clinical and laboratory screening criteria have been developed for febrile infants under 

age 3 months without an evident source of infection after detailed history and physical

examination. These criteria attempt to classify infants into high- and low-risk categories. 

Infants meeting low-risk criteria (Philadelphia criteria) are considered safe to discharge 

home provided the parents are reliable and follow-up is assured at 24 hours. The 

Philadelphia criteria have demonstrated excellent sensitivity (100%) for identifying those 

infants aged 1-2 months with serious bacterial infections. These criteria, however, were 

not adequate when applied to infants under age 1 month. Therefore, all infants less than 

age 1 month with fever of 38 °C (100.4 °F) or higher require a full septic workup, 

intravenous antibiotics, and hospitalization until culture results are negative (see Figure 

48-7). 

2. Fever in Children 


Of emergency department visits for children aged 3-36 months, 8% are for fever. 

Differentiating serious illnesses such as bacterial diseases from self-limited viral 

infections can be difficult in febrile children in this age group. They are at increased risk 

for occult invasive bacterial diseases (eg, pneumonia, urinary tract infection, meningitis, 

occult bacteremia). Children with invasive bacterial disease may present with an 

undifferentiated febrile illness. 


Young children with pneumonia may present without auscultatory findings in the chest; 

occasionally, the only clues to diagnosis are a history of cough with fever and tachypnea 

on physical examination. Urinary tract infections are occult infections in young children 

because dysuria and urinary frequency are not clinically apparent in this age group. 

Although children with meningitis may present with significant obtundation, initially 

children show only high fever and irritability. 

Occult bacteremia is the presence of bacteremia in a young child who is only 

moderately ill-appearing. Risk factors appear to be the child's age and height of the 

fever at presentation. The incidence is greatest under age 3 years. Approximately 6% of 

children presenting to an emergency department with temperatures over 38.5 °C (101.3 

°F) have bacteremia. The likelihood of bacteremia increases with increasing fever and 

may exceed 10% in children with temperatures over 40 °C (104 °F). S. pneumoniae is 

the most common pathogen. A white blood cell count greater than 15,000 has been 

used for screening febrile children, but it lacks specificity. Almost 90% of children with 

occult bacteremia recover spontaneously. Sequelae such as meningitis, cellulitis, 

pneumonia, or sepsis may develop. Studies have shown the rates of occult bacteremia 

have been decreasing. Use of the H influenzae b (Hib) vaccine has drastically reduced 

the incidence of H influenza infection, which is now a rare cause of occult bacteremia 

and meningitis. 

Treatment 


Evaluate the child before administering acetaminophen and then again after the 

temperature has been lowered. Acetaminophen is equally effective in lowering the

temperature in both bacteremic and nonbacteremic febrile children. However, children 

with meningitis are less likely to be clinically improved after the use of antipyretics. If the 

examination discloses a source of infection, initiate appropriate laboratory studies and 

treatment. 

B. Fever with an Apparent Source 

A recognizable viral syndrome (eg, herpetic gingivostomatitis, hand-foot-and-mouth 

disease) can qualify as a source of a high fever in a child and may require no further 

ancillary studies. If a virus is suspected, treat the infection symptomatically with oral 

fluids and antipyretics, and follow up by telephone contact or reexamine the patient 

within 24 hours. 

C. Fever without an Apparent Source 

The treatment of febrile children younger than age 36 months with fever greater than 39 

°C (102.2 °F) and no apparent source of infection after appropriate laboratory screening 

(ie, urinalysis, stool studies, chest x-ray) remains controversial. In 1993, Baraff and 

others published guidelines recommending intramuscular antibiotics (ceftriaxone, 50 

mg/kg/d) for febrile children (= 39 °C [102.2 °F]) aged 3-36 months without a source of 

infection and a white blood cell count greater than 15,000. Follow-up in 24 hours is 

required, at which time cultures are checked and a second dose of antibiotic is 

administered. In 2000, Baraff modified the widely adopted recommendations, taking into 

account the 90% efficacy of the pneumococcal conjugate vaccine in reducing 

pneumococcal disease (Figure 48-8). 

D. Management of the Child Appearing Seriously Ill 

The young febrile child appearing seriously ill requires aggressive diagnostic evaluation 

and prompt institution of parenteral antibiotic therapy. Obtain cultures of blood, urine, 

and cerebrospinal fluid, and begin antibiotics. If physical examination or laboratory 

evaluation does not disclose a source of infection, use a second- or third-generation 

cephalosporin intravenously (eg, cefuroxime, ceftriaxone). Regardless of whether a 

source of infection is found, hospitalize seriously ill febrile children for continued 

antibiotic therapy and observation. 

Avner JR, Baker MD: Management of fever in infants and children. Emerg Med Clin 

North Am 2002;20:49. [PMID: 11826637] (Review article of the evaluation and 

management of fever in young children.) 

Baker MD, Bell LM, Avner JR: Outpatient management without antibiotics of fever in 

selected patients. N Engl J Med 1993;329:1437. [PMID: 8413453] (Controlled clinical 

trial.) 

Baraff LJ: Management of a fever without a source in infants and children. Ann Emerg 

Med 2000;36:605. [PMID: 11097701] 

Baraff LJ et al: Practice guideline for the management of infants and children 0 to 36 

months of age without source. Ann Emerg Med 1993;22:1198. [PMID: 8517575] 

(Practice guidelines for evaluation and management of febrile infants and children 

based on meta-analysis.)

Kramer MS: The young febrile child: evidence-based diagnostic and therapeutic 

strategies. Emergency Medicine Practice 2000;2:7 (revised edition). (Comprehensive 

clinical discussion of the evaluation and management of previously healthy febrile 

children aged 3-36 months.) 

Kuppermann N, Fleisher GR, Jaffe DM: Predictors of occult pneumococcal bacteremia 

in young febrile children. Ann Emerg Med 1998;31:679. [PMID: 9624306] (Prospective, 

multicenter, randomized trial of antibiotic use in young febrile children at risk for occult 

bacteremia.) 

Lee GM, Harper MB: Risk of bacteremia for febrile young children in the 

post-Haemophilus influenzae type b era. Arch Pediatr Adolesc Med 1998;152:624. 

[PMID: 9667531] (Prospective clinical trial.) 

MENINGITIS 


• Fever, headache, stiff neck, mental status changes or excessive irritability. 

• Cerebrospinal fluid Gram stain or culture may be diagnostic for a specific organism. 


Meningitis is an infection of the central nervous system characterized by fever, alteration 

in the level of consciousness, and in some instances a stiff neck. Acute bacterial 

meningitis is of particular concern to the emergency physician because failure to make a 

prompt diagnosis and institute antibiotic treatment may result in significant illness and 

possibly death. 

Meningitis occurs following invasion of the subarachnoid space by a pathogenic 

organism. In children, this occurs most commonly by hematogenous spread but may 

also occur by direct extension from a contiguous focus of infection such as sinusitis or 

mastoiditis. Disruption of the normal anatomic barriers to the cerebrospinal fluid 

secondary to a basilar skull fracture or a congenital sinus tract may also result in 

infection. Acute meningitis is usually of viral or bacterial origin (Table 48-13). The onset 

of meningitis in children usually follows one of 2 patterns: (1) The illness develops over 

several days as a nonspecific febrile illness, or (2) signs of central nervous infection 

develop over hours. 



In infants, the clinical findings may be nonspecific: restlessness, irritability, poor feeding, 

emesis, diarrhea, lethargy, decreased tone, respiratory distress, full fontanelle (late 

finding), and seizures. Obvious neck stiffness or other signs of meningeal irritation (eg, 

Kernig or Brudzinski signs) are not reliably present in infants under age 18 months. In 

children over age 18 months, headache, nausea, vomiting, signs of increased

intracranial pressure, focal neurologic signs, fever, lethargy, and photophobia are 

common. Infants and children with N meningitis infection often present with a petechial 

rash. 


1. Lumbar puncture—The diagnosis is established by evaluation of the cerebrospinal 

fluid by lumbar puncture. Contraindications to performing a lumbar puncture in children 

with suspected meningitis include (1) hemodynamic instability (child in shock or having 

respiratory difficulties), (2) evidence of mass lesion or increased intracranial pressure 

(eg, focal neurologic signs [hemiparesis, facial palsy, gaze preference], altered pupillary 

reactions, bradycardia, hypotension, apnea, posturing), (3) a bleeding disorder, and (4) 

infection overlying the lumbar puncture site (eg, cellulitis). If a contraindication exists in 

a patient with clinical suspicion of meningitis, give intravenous antibiotics immediately. 

The lumbar puncture may be performed when the child is stabilized or when the 

contraindication has resolved. 

Cerebrospinal fluid analysis should include cell count, Gram staining, protein and 

glucose determinations, and culture (Table 48-14). The cell count in the cerebrospinal 

fluid should be performed quickly because delay over 90 minutes will result in lysis of 

white blood cells. 

2. Other tests—Blood tests include peripheral white blood cell count and serum 

glucose determination. Ideally, these should be done before the lumbar puncture, 

because both will increase during a lumbar puncture. It takes approximately 30 minutes 

for serum glucose to equilibrate with spinal fluid. Blood culture should also be performed 

and serum electrolytes obtained. The syndrome of inappropriate secretion of antidiuretic 

hormone (SIADH) may occur in acute meningitis, with resulting hyponatremia and 

volume overload. Urinalysis should be performed. 

C. Imaging 

If a mass lesion or increased intracranial pressure is suspected, give antibiotics 

immediately and obtain an emergent CT scan. 

Treatment 


Assess the airway. In a child with significant central nervous system depression who 

has an impaired gag reflex or is hypoventilating, perform an elective orotracheal 

intubation. 

Apply oxygen. Use 100% nonrebreathing reservoir bag-mask if the child is severely ill. 

Monitor with pulse oximetry. Attach an electrocardiographic monitor, and watch closely 

for bradycardia. 


Assess the child's intravascular volume by means of blood pressure, heart rate, and 

capillary refill. Hypovolemia can compromise perfusion of the central nervous system. 

Aggressive rehydration is indicated if signs of hypovolemia are present. If the child is 

euvolemic, give fluids at two-thirds the normal maintenance rate until serum electrolyte

esults have been obtained. If evidence of SIADH is present, continue fluids at 

two-thirds the maintenance rate. If no SIADH is present, increase intravenous fluids to 

the normal maintenance rate (see Table 48-5). 

C. Steroid Therapy 

The administration of steroids (dexamethasone) in patients with bacterial meningitis is 

controversial. Studies have shown a benefit of steroids (although only statistically 

significant when the cause is H. influenzae) in reducing neurologic sequelae 

(sensorineural hearing loss) in patients with bacterial meningitis. In the post-Hib vaccine 

era, the current applicability of these results has been questioned because H. influenzae 

is now a rare cause of meningitis. Studies have suggested benefit for pneumococcal 

meningitis if steroids are commenced before or with antibiotics. Further complicating 

recommendations are concerns that steroids may decrease meningeal permeability, 

preventing adequate penetration of some antibiotics through the blood-brain barrier and 

resulting in subtherapeutic cerebrospinal fluid concentrations. Many authors still 

advocate steroids for children over age 2 months with bacterial meningitis. The 

recommended dose of dexamethasone is 0.15 mg/kg every 6 hours for 2-4 days, given 

before or concomitant with the initiation of antibiotic therapy. 

D. Antimicrobial Therapy 

Administer antimicrobial therapy based on the child's age and the most likely pathogens 

(see Table 48-13). In critically ill children suspected of having meningitis, administer 

antibiotics rapidly without delay prior to lumbar puncture. 


Treat seizures aggressively with anticonvulsants (see Figure 48-6). 

Disposition 

Children with proved or suspected bacterial meningitis require prompt hospitalization, 

ideally in an intensive care unit. 

McIntyre PB et al: Dexamethasone as adjunctive therapy in bacterial meningitis. A 

meta-analysis of randomized clinical trials since 1988. JAMA 1997;278:925. [PMID: 

9302246] (Meta-analysis.) 

Quagliarello VJ, Scheld WM: Treatment of bacterial meningitis. N Engl J Med 

1997;336:708. [PMID: 9041103] (Review.) 

Wubbel L, McCracken GH: Management of bacterial meningitis: 1998. Pediatr Rev 

1998;19:78. [PMID: 9509854] (Review.) 

ACUTE OTITIS MEDIA 


• Loss of light reflex or bulging tympanic membrane is suggestive of otitis media.

• Loss of mobility of the tympanic membrane with otitis media is sensitive and specific 

sign. 


After viral upper respiratory infection, otitis media is the next most common infectious 

pediatric disease. It accounts for up to one third of pediatric office visits and a high 

proportion of illness visits to the emergency department. 

Acute otitis media results from auditory (eustachian) tube dysfunction, usually following 

an upper respiratory infection. In infants and children, S. pneumoniae, H. influenzae, 

and Moraxella catarrhalis are the most common pathogens. 


The history is typically that of an infant or child who has had an upper respiratory 

infection for a few days and then presents with symptoms of ear pain. The pain of otitis 

media is typically acute in onset, severe, constant, and associated with hearing loss. 

Younger, preverbal children tend to have nonspecific symptoms of irritability, lethargy, 

gastrointestinal disturbances, and frequently poor sleeping. Children with acute otitis 

media may be afebrile or have only mild temperature elevation. High fever (> 40 °C [104 

°F]) should alert the physician to the possibility of a more serious underlying infection, 

such as meningitis or pneumonia. Older children can accurately describe the source of 

their pain. Pus may rupture through the tympanic membrane, producing a purulent 

discharge and a prompt decrease in pain. Otoscopy reveals an opaque white tympanic 

membrane bulging outward and loss of visible ossicles. Erythema of the tympanic 

membrane is a common finding but is not nearly as sensitive as loss of normal tympanic 

membrane landmarks. Decreased movement of the tympanic membrane, demonstrable 

by pneumatic otoscopy, is sensitive and specific. 

Occasionally, facial nerve paralysis develops acutely. Vertigo and sensorineural hearing 

loss may occur if inflammation spreads to the inner ear and causes serous or purulent 

labyrinthitis. Mastoiditis occurs with infection of the bony structure of these air cells. The 

mastoid area becomes red, tender, and swollen. Typically the auricle is pushed laterally 

and downward. 

No laboratory tests or x-rays are generally required. The bacteriology of otitis media has 

been clearly defined. Tympanocentesis is indicated only when unusual organisms may 

be present (eg, in neonates or immunosuppressed patients) or if acute otitis media is 

complicated by meningitis. If mastoiditis is a clinical concern, CT scan can detect small 

collections of fluid within the mastoid air cells as well as destruction of the bony septa. 

Treatment 


Begin antimicrobial therapy (Figures 48-9 and 48-10, and Table 48-15). Consider 

alternative antibiotics if a child is less than age 24 months, attends daycare, has 

received multiple antibiotic courses, or has received antibiotics in the past 30 days. 

Treat uncomplicated otitis media for up to 10 days, and arrange for reevaluation.

B. Treatment of Pain and Fever 

Treat associated pain and fever with acetaminophen or ibuprofen. A commercially 

available mixture of benzocaine, antipyrine, and oxyquinoline sulfate (Auralgan) applied 

topically into the ear canal may also provide pain relief. 

C. Treatment for Infants under Age 4 Weeks 

Infants under age 4 weeks with acute otitis media require hospitalization because of the 

risk of associated hematogenous spread of disease. If fever is present or an infant 

appears ill, a full evaluation for meningitis and sepsis is required. 

D. Management of Facial Nerve Paralysis 

If facial nerve paralysis accompanies acute otitis media, perform myringotomy, 

administer intravenous antibiotics, and hospitalize the patient. 

E. Treatment of Mastoiditis 

Treat mastoiditis like osteomyelitis. Perform myringotomy, culture, and Gram staining of 

middle ear fluid, and give antibiotics based on Gram-stain results. Drainage of the 

mastoid may be required. 

Disposition 

Modify risk factors for otitis media to improve resolution. For example, limit passive 

smoke exposure, control food and inhalant allergies, and treat sinusitis. The primary 

benefit of antibiotics in treating acute otitis media is to decrease the incidence of 

suppurative complications (ie, mastoiditis) and to shorten the duration of symptoms. 

A repeat ear examination should be performed at the end of therapy. Children should be 

reexamined if no clinical improvement occurs in 48 hours. 

Dowell SF et al: Acute otitis media: management and surveillance in an era of 

pneumococcal resistance—a report from the Drug-Resistant Streptococcus pneumoniae 

Therapeutic Working Group. Pediatr Infect Dis J 1999;18:1. [PMID: 9951971] (Review.) 

Hoberman A et al: Efficacy of Auralgan for treating ear pain in children with acute otitis 

media. Arch Pediatr Adolesc Med 1997;151:675. [PMID: 9232040] (Prospective 

randomized, controlled trial.) 

Klein JO: Review of consensus reports on management of acute otitis media. Pediatr 

Infect Dis J 1999;18:1152. [PMID: 10608648] (Review.) 

Louie JP, Bell LM: Appropriate use of antibiotics for common infections in an era of 

increasing resistance. Emerg Med Clin North Am 2002;20:69. [PMID: 11826638] 

(Review.) 

Takata GS et al: Evidence assessment of management of acute otitis media: I. The role 

of antibiotics in treatment of uncomplicated acute otitis media. Pediatrics 2001;108:239. 

[PMID: 11483783 ] 

(Mhttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=

eta-analysis.) 

&dopt=Abstract">eta-analysis.) 

PHARYNGITIS 


Infections of the pharynx cause mucosal inflammation and ulceration, resulting in pain 

that is exacerbated by swallowing. The most common causes of pharyngitis in children 

are viruses and group A streptococci. Enteroviruses, particularly coxsackievirus, cause 

erythematous and vesicular lesions on the soft palate and pharynx. Other viruses 

associated with pharyngitis include adenovirus, influenza virus, parainfluenza virus, 

rhinovirus, Epstein-Barr virus, and RSV. Bacteria other than group A streptococci 

occasionally cause pharyngitis. Corynebacterium diphtheriae is now a rare cause of 

membranous pharyngitis in the United States. Corynebacterium hemolyticum has been 

associated with pharyngitis and erythematous rash in adolescents. Sexually active 

teenagers and victims of sexual abuse may have pharyngeal infection with Neisseria 

gonorrhoeae. Mycoplasma pneumoniae may also cause pharyngitis, but this is usually 

associated with more prominent lower respiratory tract infections. Acute uvulitis has 

been associated with H. influenzae type B. 


Most cases of streptococcal pharyngitis are in school-aged children, but recent studies 

have suggested that disease can be found in all age groups including children younger 

than age 2 years. Common presenting signs and symptoms include fever, sore throat, 

pharyngeal hyperemia, exudate, or petechiae. The characteristic erythematous fine, 

raised, generalized "sandpaper" rash of scarlet fever supports the diagnosis of 

streptococcal infection (see Table 48-18). Abdominal pain and headache are frequent 

findings in children with streptococcal pharyngitis and may distract the physician from 

the diagnosis. 

Throat cultures remain the most practical and reliable means of diagnosing 

streptococcal pharyngitis. Rapid detection of streptococcal antigen from throat swabs is 

possible, but because the sensitivity is only 76-87%, a negative test should be followed 

by a throat culture. 

The white blood cell count may be elevated with streptococcal pharyngitis, but this is a 

nonspecific finding. White blood cell count may also be increased with Epstein-Barr 

virus infection, where the blood smear will show 10-20% atypical lymphocytes and a 

mononucleosis test (Monospot, many others) is positive. Children over age 4 years with 

infectious mononucleosis will develop heterophilic antibodies 1-2 weeks into the course 

of infection in 30% of cases. Heterophilic antibodies are less common in children under 

age 4 years. 

Tonsillar infections with group A streptococci may extend into surrounding tissues and 

result in peritonsillar cellulitis or abscess; the child will usually present with fever, 

toxicity, muffled voice, tender superior cervical lymphadenopathy, trismus, and drooling. 

Peritonsillar abscess is commonly unilateral. Initially there is edema and erythema of the

soft palate and tonsil and frequently but not invariably a whitish tonsillar exudate. 

Peritonsillar abscess is characterized by deviation of the tonsil and soft palate on the 

affected side medially, causing the uvula to point away from the side of the abscess. 

Retropharyngeal or lateral pharyngeal abscesses may also develop in concert with 

group A streptococcal pharyngitis and are often associated with stridor and signs similar 

to those of peritonsillar abscess. 

Treatment 

A. Symptomatic Therapy 

Use symptomatic therapy to decrease discomfort, including acetaminophen and 

saltwater gargles. 

B. Antimicrobial Therapy 

If streptococcal pharyngitis is likely, begin antibiotic therapy at the time of the 

examination. The duration of symptoms can be decreased if treatment is begun before 

culture results are available. 

Prescribe oral penicillin (or an alternative) for suspected streptococcal pharyngitis. If 

antibiotic therapy is initiated within 7-9 days of onset of illness, acute rheumatic fever 

can be prevented. 

1. Penicillin V—Dosing of penicillin V for children under age 12 years is 250 mg 2 or 3 

times daily for 10 days; dosing for adolescents is 500 mg 2 or 3 times daily for 10 days. 

2. Benzathine penicillin G—If compliance is a problem, benzathine penicillin G, 25,000 

units/kg intramuscularly (maximum, 1.2 million units), is a good alternative to the 

multiple-daily dosing of penicillin V. The pain may be lessened if it is used in a mixture 

with procaine penicillin G. The total dose is still based on the amount of benzathine 

penicillin G. 

3. Alternatives for penicillin-allergic patients—For children allergic to penicillin, the 

macrolides are the drug of choice. Erythromycin estolate, 40 mg/kg/d divided 2-4 times 

daily for 10 days; erythromycin ethylsuccinate, 40 mg/kg/d divided 2-4 times daily for 10 

days; clarithromycin, 15 mg/kg/d 2 times daily for 10 days; or azithromycin, 12 mg/kg/d 

for 5 days are all approved by the U.S. Food and Drug Administration. 

C. Rapid Antigen Test 

If the rapid antigen test is positive, begin treatment. A negative rapid antigen test should 

be followed up with a throat culture. 

D. Treatment for Peritonsillar Cellulitis 

Treat early stages of peritonsillar cellulitis on an outpatient basis with penicillin and 

follow-up. If the disease has progressed to deviation of the soft palate and uvula, 

hospitalize the child and initiate intravenous antibiotics with aqueous penicillin G, 

250,000 units/kg/d in divided doses every 4 hours, after needle aspiration. Consult an 

otorhinolaryngologist if the abscess cannot be aspirated easily and for consideration of 

definitive incision and drainage.

Disposition 

A repeat examination is indicated if no improvement occurs in 48 hours. Particularly in 

older children and adolescents, a mononucleosis test should then be done. Children 

with early signs of peritonsillar abscess must be reexamined in 12-24 hours. 

Berkovitch M et al: Group A streptococcal pharyngotonsillitis in children less than 2 

years of age—more common than thought. Clin Pediatr 1999;38:361. [PMID: 10378094] 

(Prospective randomized, controlled trial.) 

Hayes CS, Williamson H: Management of group A beta-hemolytic streptococcal 

pharyngitis. Am Fam Physician 2001;63:1557. [PMID: 11327431] (Review.) 

Louie JP, Bell LM: Appropriate use of antibiotics for common infections in an era of 

increasing resistance. Emerg Med Clin North Am 2002;20:69. [PMID: 11826638] 

(Review.) 

PERIORBITAL CELLULITIS 


• Erythema and swelling around the eye. 

• No pain with range of motion of the extraocular muscles. 

• No diplopia or proptosis. 


Periorbital swelling is a common problem in children. The primary task is to differentiate 

serious and life-threatening causes of this finding from those that are benign. Cellulitis 

restricted to the eyelid is preseptal or periorbital. Orbital cellulitis refers to infection 

involving orbital contents posterior to the septum. Differentiation of these 2 entities is 

essential to management. Table 48-16 lists the differential considerations of periorbital 

swelling. Periorbital cellulitis can be classified as secondary to sinusitis (group I), 

secondary to disruption of local skin integrity (group II), or secondary to bacteremia with 

no apparent predisposing focus (group III). 

A. Group I 

Periorbital swelling from sinusitis is usually subacute in onset, evolves over several 

days, and is neither tender nor indurated. Fever is typically absent or low grade. This 

condition can occur at any age, but it is rare in infancy. X-rays show sinus opacification. 

Blood cultures are almost always negative. This is the most common form of periorbital 

cellulitis and is caused by organisms that commonly cause sinusitis (ie, nontypeable H 

influenzae, S pneumoniae, M catarrhalis, S pyogenes, and anaerobic bacteria). 

B. Group II 

Primary skin infection about the eye may result from secondary infection, prior trauma, 

or insect bite. There is rapid onset of tender and indurated preseptal swelling with fever.

Blood cultures are typically negative. S aureus and group A streptococci are the most 

common pathogens. Human and animal bites may produce a polymicrobial infection. 

C. Group III 

Children with idiopathic periorbital cellulitis are generally younger than those in the 

previous 2 groups. These children have a history of a mild upper respiratory infection for 

1-5 days followed by rapid onset of high fever and preseptal swelling. Swelling is often 

tender and indurated. Prior to the institution of the Hib vaccine, H. influenzae was a 

common organism causing periorbital cellulitis as a complication of bacteremia. Current 

cases are most likely to be from S. pneumoniae. 

Orbital cellulitis can be distinguished clinically from periorbital cellulitis by the presence 

of proptosis, ophthalmoplegia, pain on eye movement, and loss of vision. Patients are 

usually febrile; blood cultures are usually negative. Orbital cellulitis is usually secondary 

to extension of pus from sinusitis (usually ethmoidal) into the orbit or due to penetrating 

orbital trauma. The most common bacterial organisms include S. pneumoniae, M. 

catarrhalis, S. aureus, H. influenzae (in nonimmunized patients), and anaerobes. 

Management of orbital cellulitis should include blood cultures and CBC if the patient is 

febrile or appears bacteremic. Infants under age 3 months with these symptoms should 

be worked up as outlined in Figure 48-7. Obtain a CT scan without contrast for all 

patients suspected of having orbital cellulitis. Mild cases may be managed with daily 

ceftriaxone injections. More severe cases should receive inpatient intravenous 

antibiotics (second- or third-generation cephalosporins). A nasal decongestant and 

warm compresses may also be beneficial to patients. 

Treatment 

A. Afebrile Patients 

Consider ambulatory therapy for children with early mild periorbital cellulitis who are 

afebrile and do not appear ill. Use ceftriaxone, 50-75 mg/kg/d intramuscularly for 5 days, 

or amoxicillin-clavulanate, 45 mg/kg/d divided twice daily for children weighing more 

than 40 kg, and perform a repeat evaluation in 24 hours. If contiguous skin infection is 

present, treat with dicloxacillin, 25 mg/kg/d divided 4 times daily. 

B. Febrile Patients 

Hospitalize any child with periorbital swelling who is febrile and appears ill. Begin 

intravenous antibiotic therapy. For young children whose periorbital cellulitis is not 

secondary to an external skin infection, give cefuroxime, 100 mg/kg/d divided 3 times 

daily, or ceftriaxone, 100 mg/kg/d divided twice daily. For children whose infection is 

secondary to an external skin source, use nafcillin, 50-200 mg/kg/d in divided doses 


Hospitalize children with orbital cellulitis secondary to direct extension from a contiguous 

sinus, or a subperiosteal abscess, for treatment with intravenous antibiotics. Coverage 

for H. influenzae, S. pneumoniae, S. aureus, and anaerobes must be included (ie, 

ceftriaxone, 50-100 mg/kg/d divided twice daily, and clindamycin, 15-40 mg/kg/d divided 

3 or 4 times daily). Consult an ophthalmologist whenever orbital cellulitis is suspected.

Disposition 

Children with acute onset of fever, toxicity, and periorbital swelling should be 

hospitalized promptly for intravenous antibiotic therapy. Children less acutely ill who 

receive outpatient treatment should be reexamined in 12-24 hours. 

Donahue SP, Schwartz G: Preseptal and orbital cellulitis in childhood. Ophthalmology 

1998;105:1902. [PMID: 9787362] (Retrospective chart review and discussion.) 

Mawn LA et al: Preseptal and orbital cellulitis. Ophthalmol Clin North Am 2000;13:633. 

(Review.) 

URINARY TRACT INFECTION 


Urinary tract infections are relatively common in children. Risk in the first 10 years of life 

for boys and girls is 1.1% and 3.5%, respectively. About 40% of these children will have 

recurrent infections. 

In children, E. coli is the predominant pathogen (approximately 95% of initial infections 

and 80% of all infections). Other organisms causing urinary tract infections are 

Klebsiella, Proteus mirabilis (particularly in males), coagulase-negative staphylococci (in 

adolescent females), adenovirus (hemorrhagic cystitis), Chlamydia trachomatis 

(frequency-dysuria syndrome), Pseudomonas, Streptococcus faecalis, Streptococcus 

viridans, N. gonorrhoeae, Ureaplasma urealyticum, herpes simplex virus, and H. 

influenzae (uncommon). 

Children with congenital anomalies of the urinary tract are at increased risk for infection. 

Vesicoureteral reflux is present in over 30% of children with urinary tract infection. Other 

abnormalities include obstruction at the level of the urethra, bladder, or ureter and 

duplication of the urinary tract and ureteroceles. In male infants, increased susceptibility 

to infection may be related to an uncircumcised penis. 

In the first months of life, urinary tract infections are most common in males. By age 4 

months, however, urinary tract infections are 10 times more common in females, and 

this female predominance continues through childhood and adolescence. Approximately 

one third of newborns with urinary tract infection are bacteremic. By age 1-3 months, the 

incidence of bacteremia with urinary tract infection is decreased to 18%; and by age 3-8 

months, the incidence is 6%. 


In the neonate, nonspecific symptoms predominate. Poor feeding, irritability, fever, 

vomiting, diarrhea, and slow weight gain are common symptoms. The neonate may also 

develop a direct hyperbilirubinemia. In infants aged 1 month to 2 years, nonspecific 

symptoms still predominate. Alert parents may note urinary frequency, dribbling, weak 

stream, and abdominal distress during voiding. Many young infants with urinary tract 

infection are febrile. In preschool and school-aged children, dysuria is a frequent

symptom and may be accompanied by abdominal and flank pain, frequency, urgency, 

enuresis, and fever. Dysuria is a nonspecific symptom in children, however. Dysuria in 

children often has causes other than urinary tract infection, such as chemical urethritis 

from strong soaps, diaper rash, herpes, or pinworm. In adolescent females, dysuria and 

frequency are common with urinary tract infection but may also be secondary to 

vaginitis or the acute urethral syndrome. 

The key to diagnosis is demonstration of bacteria in the urine. Methods of collecting 

urine in children include a urine bag taped to the perineum, clean-catch specimens, 

bladder catheterization, and suprapubic aspiration. The urine specimen collected by bag 

is helpful only if it proves to be negative. Most positive cultures from urine bag 

specimens in infants and newborns represent contamination. Febrile infants under age 

3 months who are likely to be admitted to the hospital should undergo either bladder 

catheterization (using an 8-10F pediatric feeding tube) or suprapubic aspiration. Older 

infants and children should undergo bladder catheterization if the bag urine specimen 

shows evidence of infection. Midstream clean-catch specimens are acceptable in 

children who can void on command. 

Urine test strips using a nitrite and leukocyte esterase indicator are helpful. Most urinary 

pathogens will convert nitrite to nitrate, and false-positive reactions are uncommon. 

However, false-negative results can occur with urinary pathogens unable to convert 

nitrite to nitrate (eg, Staphylococcus saprophyticus, enterococci). Therefore, if the urine 

test strip is negative for nitrite and clinical findings or history suggest possible urinary 

infection, other tests are still indicated. 

Urine collected by the clean-catch method is likely to be infected if more than 10 4 

colonies of a single organism are found. If urine is collected by bladder catheterization 

or suprapubic aspiration, 10 3 colonies or more of a single organism represents infection. 

More than 5 white blood cells per high-power field of urine sediment in a child who is 

symptomatic for urinary tract infection is highly suggestive. However, pyuria alone is not 

a reliable guide for identification of a urinary tract infection. Any bacterium present on 

Gram staining of unspun urine, when viewed under oil immersion, is a sensitive 

indicator of urinary tract infection. 

Obtain a blood culture in neonates, infants, and any child who is highly febrile. Assume 

that children with fever, back pain, and costovertebral angle tenderness have 

pyelonephritis. As many as 25% of children with urinary tract infections and no 

symptoms of pyelonephritis have upper tract disease. No effective noninvasive means 

exist to identify upper tract infections. 

Treatment 

A. Outpatient Treatment 

In children who are to receive outpatient treatment, use oral antibiotics effective against 

E. coli. Cystitis should be treated for 7 days, whereas pyelonephritis and febrile urinary 

tract infection should be treated for 10-14 days. Treatment options include the following: 

TMP-SMZ, 6-12 mg/kg/d TMP and 30-60 mg/kg/d SMZ; sulfisoxazole, 120-150 mg/kg/d; 

amoxicillin, 20-40 mg/kg/d; cephalexin, 50-100 mg/kg/d; or cefixime, 8 mg/kg/d. 

Phenazopyridine, 10 mg/kg/day divided every 8 hours, can be used for symptomatic

elief. 

Outpatient therapy can be instituted for febrile but nontoxic-appearing children older 

than age 3 months, provided they can tolerate fluids and medications by mouth. 

Follow-up should occur at 24-48 hours. It is advisable to administer a parenteral first 

dose of antibiotics (intravenous or intramuscular gentamicin or third-generation 

cephalosporin) in the emergency department, and start oral antibiotics at home. Any 

child, regardless of age, who appears toxic should be admitted for parenteral antibiotics. 

B. Inpatient Treatment 

Hospitalize neonates and young infants with urinary tract infections, and give 

intravenous antibiotics on the presumption of pyelonephritis. Use ampicillin, 100 mg/ 

kg/d in divided doses every 12 hours, and gentamicin, 7.5 mg/kg/d in divided doses 


C. Evaluation for Urinary Tract Anomalies 

Because of the frequency of urinary tract anomalies in children who have urinary tract 

infections, evaluation of the urinary tract by sonogram and voiding cystourethrogram are 

frequently indicated in boys of any age; girls aged 2 months to 2 years with their first 

culture-proven urinary tract infection; and children with febrile urinary tract infection or 

pyelonephritis. The sonogram can be done during the acute illness if necessary. Order a 

voiding cystourethrogram approximately 1 month after diagnosis. Postpubertal females 

with recurrent uncomplicated cystitis do not require imaging studies. 

Disposition 

Admit infants, febrile or not, under age 3 months with urinary tract infection for 

intravenous antibiotic administration. Nontoxic-appearing, febrile, older infants and 

children with urinary tract infection can receive treatment on an outpatient basis with 

follow-up at 24-48 hours. 

Children receiving outpatient treatment will require a repeat urine culture to document 

cure in 1 week. At 24- to 48-hour follow-up, check the urine culture to ensure 

appropriate antibiotic selection. If clinical improvement is not evident, consider 

hospitalization for parenteral antibiotics. Discharge instructions should caution parents 

to return if persistent vomiting, lethargy, or other worsening symptoms occur. 

Santen SA, Altieri MF: Pediatric urinary tract infections. Emerg Med Clin North Am 

2001;19:675. [PMID: 11554281] (Review.) 

Shaw K, Gorelick MH: Urinary tract infection in the pediatric patient. Pediatr Clin North 

Am 1999;46:1111. [PMID: 10629676] (Review.) 

GASTROENTERITIS 


Diarrhea is a common reason for bringing a child to medical attention. Dehydration 

frequently complicates diarrhea in children, particularly in young infants who experience

a greater net fluid and electrolyte loss. Acute diarrhea in children most commonly results 

from infectious gastroenteritis. Keys to management include identification of children 

who will benefit from antimicrobial therapy, prevention or treatment of dehydration, and 

identification of children with diarrhea secondary to other processes (eg, 

intussusception, hemolytic uremic syndrome). In the United States, rotavirus is the most 

common cause of acute diarrhea, particularly in winter months. 



Information regarding the duration of diarrhea, number of stools per day, frequency of 

urination, presence of tears when crying, and most recent weight of the child are helpful 

in assessing the risk of dehydration. A history of frequent vomiting, particularly early in 

the course of the disease, suggests a viral cause. High fever, lack of vomiting, 

abdominal pain with bowel movements, and the presence of gross blood and mucus in 

the stool suggest a bacterial cause. A history of recent antibiotic use suggests the 

possibility of pseudomembranous colitis. A history of recent travel suggests the 

possibility of a parasitic infection or traveler's diarrhea. Children in daycare are 

particularly susceptible to infections with Giardia lamblia. Inquire about a common 

outbreak of symptoms in family members that may suggest food poisoning. When more 

than one member of the family has symptoms of nausea, vomiting, or headache, 

explore the possibility of carbon monoxide poisoning. Assess the child's hydration 

status, and look for signs of appendicitis or intussusception. Serial abdominal 

examinations are recommended to rule out surgical conditions. Gastroenteritis is one of 

the most common diagnoses listed in cases of missed appendicitis. 


1. Stool culture—A stool culture is the most reliable means of identifying a bacterial 

cause. It is not cost effective, however, to culture the stool of every child with diarrhea. 

Obtain cultures from children at highest risk for bacterial disease. Stool cultures for 

Shigella, Salmonella, and Campylobacter should be obtained in the following 

circumstances: 

• If the child presents with obvious symptoms of acute bacterial dysentery (ie, fever, 

watery stool, fecal leukocytes, and gross blood in the stool). 

• If the child has abrupt onset of frequent stools without the initial vomiting common to 

viral gastroenteritis. Perform methylene blue slide examination for the presence of fecal 

leukocytes. A positive result (> 5 white blood cells per high-power field) is a sensitive 

indicator of a bacterial pathogen. Trophozoites of G. lamblia may also be identified. 

• If the child has hemoglobinopathies or immunodeficiencies. 

2. Peripheral white blood cell count—A peripheral white blood cell count may be 

helpful, because Salmonella and Shigella can cause leukocytosis. Some patients with 

Shigella infection may have a low white blood cell count with a marked shift to the left. 

3. Other laboratory tests—If the child appears dehydrated, check serum electrolytes, 

BUN, creatinine, and fingerstick blood sugar. Blood cultures are also indicated in young

infants with bloody diarrhea and any child who appears significantly ill. 

If the child is in daycare or has a history of recent travel, examine the stool examined for 

parasites. 

Treatment 

A. Rehydration 

The use of oral rehydration solutions for children with mild to moderate dehydration and 

of intravenous fluids for children with more severe dehydration is critical to prevent 

severe morbidity and mortality. Breast-feeding infants should continue to breast feed 

while taking oral rehydration. 

B. Antiemetics and Antidiarrheal Agents 

Antiemetic and antidiarrheal drugs occasionally worsen symptoms in children with 

gastroenteritis. 


The empiric use of antibiotic therapy is indicated for obvious symptoms of bacterial 

dysentery. TMP-SMZ (TMP, 8-12 mg/kg/d, and SMZ, 30-60 mg/kg/d, in divided doses 

every 12 hours) can be given empirically until culture results are available. 

Disposition 

Hospitalize children with moderate to severe dehydration, particularly if vomiting 

prohibits oral rehydration, and young infants with fever and bloody diarrhea. Young 

infants are at increased risk for Salmonella bacteremia. 

Instruct parents about the signs of dehydration and the proper use of oral rehydration 

solutions. Parents should encourage children to continue small but frequent amounts of 

liquids at home and to resume a normal diet as tolerated. 

Infants under 6 months of age should be followed up by telephone or be seen in 24 

hours. Reevaluate older children if diarrhea persists longer than 3 days. Children with 

bloody diarrhea should be reexamined in 24 hours. 



• Patient usually febrile. 

• Involved joint is tender, swollen, erythematous with painful range of motion. 

• Aspiration with fluid analysis is diagnostic. 


Septic arthritis is an acute bacterial infection of a joint. Delay in treatment may result in

permanent damage and loss of function of the infected joint. Septic arthritis in children 

usually occurs through hematogenous seeding. It may also result from contiguous 

spread of osteomyelitis or through a penetrating injury. The bacterial cause is age 

related (Table 48-17). Special clinical situations include N. gonorrhoeae joint infections 

in young children who have been sexually abused and patients with sickle cell disease, 

who are at a high risk for joint infections with Salmonella. 



Almost all patients have fever and malaise. Typically the infected joint is hot, painful, 

and swollen and has overlying erythema. Early in the disease, the child may present 

with an unexplained limp. In young infants with hip involvement, the obvious findings of 

swelling and erythema may be absent. More commonly the infant will not move the leg 

on the infected side and will keep the leg abducted and externally rotated. Movement of 

the hip causes pain. Patients with toxic synovitis may have similar complaints but in 

general have a lower-grade temperature and less pain on joint manipulation. 


1. Joint aspiration—Definitive diagnosis is established by joint aspiration. Examine 

joint fluid for cell count and differential, Gram staining and culture, protein and glucose 

determinations, and mucin clot. Synovial white blood cell count greater than 50,000 is 

considered positive for septic arthritis. Gram staining of joint fluid is important, because 

up to 33% of joint aspirates may be sterile. 

2. Blood tests—CBC, C-reactive protein, and erythrocyte sedimentation rate are 

helpful, particularly when considering noninfectious diagnoses. Perform a blood culture, 

because it may produce a pathogen even with a negative joint aspirate culture. 

C. Imaging 

Radiographic studies of the joint are of limited help in the older child with obvious joint 

infection. They usually demonstrate capsular swelling. Radiographic studies may be 

helpful in the evaluation of the hip, because the physical examination may not be 

definitive. Ultrasound may be able to identify small joint effusions. 

Radionuclide studies may show diffuse uptake within the joint. MRI may be helpful in 

differentiating septic arthritis from transient or toxic synovitis. 

Treatment 

Successful management depends on prompt antibiotic therapy (see Table 48-17) and 

surgical drainage as indicated. Gram staining may be helpful in guiding choice of 

antibiotics. 

Septic arthritis of the hip is a surgical emergency, and these patients should undergo 

prompt surgical drainage. Children with sickle cell disease should receive adequate 

therapy for Salmonella until culture results are known. 

Disposition

Hospitalize children with suspected septic arthritis for intravenous antibiotic therapy. 

Obtain orthopedic consultation to evaluate the need for surgical drainage of the involved 

joint. 

Leet AI, Skaggs DL: Evaluation of the acutely limping child. Am Fam Physician 

2000;61:1011. [PMID: 10706154] (Review.) 

ACUTE OSTEOMYELITIS 


• Usually warm, tender, swollen area. 

• Initially x-rays may be normal. 

• Bone scan may be diagnostic. 


Acute osteomyelitis is a pyogenic infection of bone that occurs in about 1 in 5000 

children before the age of 13 years. Although any bone may be involved, in children the 

long bones are more frequently infected. Infection usually is the result of seeding, 

although spread from a contiguous focus or through direct traumatic inoculation can 

also occur. 

Over 90% of cases of acute hematogenous osteomyelitis are caused by S. aureus. 

Group A streptococci and H. influenzae are less common causes. In neonates, 

osteomyelitis may also be caused by group B streptococci and gram-negative enteric 

organisms. Children with sickle cell disease are at risk for Salmonella and S. 

pneumoniae osteomyelitis. Puncture wounds to the plantar surface of the foot may 

result in Pseudomonas aeruginosa osteomyelitis. 



The clinical hallmarks are fever and well-localized bone tenderness. Chills, malaise, and 

appearance of illness are frequently present. Lower extremity disease will frequently 

result in a limp. Point tenderness is usually evident on careful examination. There may 

also be swelling, warmth, redness, and focal induration at the site of infection. The 

young infant is usually irritable when the affected extremity is touched or moved. 

Pseudoparalysis is common, and occasionally significant swelling of the extremity will 

occur. 


Draw blood for culture, CBC, C-reactive protein, and erythrocyte sedimentation rate. 

Blood cultures are positive in about 30-50% of patients with osteomyelitis. Obtain 

orthopedic consultation regarding aspiration of bone at the site of tenderness, because 

there may be some risk of epiphyseal damage.

C. Imaging 

Obtain plain x-rays of the affected extremity. Radiographic changes are usually not 

evident until 7-10 days after disease onset. However, soft tissue swelling and 

obliteration of the tissue planes may be the initial radiographic findings. Later findings 

include periosteal reaction and osteolysis. 

After the child has been admitted to the hospital, technetium bone scans may be helpful. 

Treatment 

The mainstay of treatment of acute bacterial hematogenous osteomyelitis is parenteral 

antibiotics (see Table 48-17). Because culture results are usually not available when the 

diagnosis is first made, empiric therapy depends on the patient's age. 

In children with puncture wound osteomyelitis of the foot, surgical debridement is an 

important part of therapy. Parenteral antibiotics active against Pseudomonas should be 

started. 

Disposition 

Hospitalize children in whom acute osteomyelitis is suspected. 

Kothari NA, Pelchovitz DJ, Meyer JS: Imaging of musculoskeletal infections. Radiol Clin 

North Am 2001;39:653. [PMID: 11549164] (Review.) 

EXANTHEMS (See Table 48-18. ) 

Important considerations are the child's age, the time of year, knowledge of illnesses 

currently present in the community, history of exposure to individuals with rashes, 

medication history, prodromal symptoms such as fever, and initial appearance and 

progression of the rash. Note how ill the child appears, the morphology and distribution 

of the rash, mucous membrane involvement, associated lymphadenopathy, and 

presence of hepatosplenomegaly. 

Gable EK, Liu G, Morrell DS: Pediatric exanthems. Prim Care 2000;27:353. [PMID: 

10815048] (Review.) 


ABDOMINAL PAIN 


Abdominal pain is a common complaint. Causes are many and include both 

intra-abdominal and systemic illnesses. The child presenting with acute severe 

abdominal pain may have an acute abdomen requiring immediate surgical intervention. 

Recognition of the acute abdomen in children may be difficult but is critical in reducing 

morbidity and mortality.

Abdominal pain can originate from 3 neural pathways. Visceral pain originates from 

distention of a viscus, which stimulates nerves locally that send impulses to the central 

nervous system through autonomic parasympathetic fibers. Because these nerve fibers 

from different organs overlap, visceral pain is not specific to the site of the viscus 

involved. Somatic pain is generally intense and well localized. It arises from irritation of 

the parietal perineum. Frequently there is abdominal muscle reflex spasm over the site 

of pain. Referred pain is somatic or visceral in origin but is felt elsewhere. 

Common causes of abdominal pain in infants are colic, constipation, gastroenteritis, 

intussusception, viral syndrome, and volvulus; in younger children, appendicitis, 

constipation, gastroenteritis, pneumonia, streptococcal pharyngitis, urinary tract 

infection, and viral syndrome; and in school-aged children, appendicitis, pregnancy, 

gastroenteritis, pneumonia, peptic ulcer, and pelvic inflammatory disease. Other more 

rare causes include pancreatitis, Henoch-Schonlein purpura, and hemolytic uremic 

syndrome. 




Note the nature of the pain, including time of onset, duration, severity, and location; 

associated gastrointestinal symptoms, including anorexia, vomiting, diarrhea, and 

constipation; associated systemic symptoms, including fever, cough, sore throat, 

dysuria, rash, and joint pain; and history of significant disease, particularly sickle cell 

disease, renal disease, and gynecologic disorders (for adolescents). Obtain a thorough 

menstrual, sexual, and medication history from the patient. 

Obtain accurate vital signs. Observe the child over a period of time. Children with 

colicky pain may appear quiet and even lethargic and then suddenly develop crampy 

pain. Perform a complete physical examination, and assess the child's state of hydration 

and perfusion. Group A streptococcal pharyngitis and lower lobe pneumonia are 2 

common sources of referred abdominal pain. Inspect the abdomen for signs of 

generalized distention or visible bowel loops. Auscultate the abdomen to evaluate the 

nature of the bowel sounds. Decreased or absent bowel sounds may signal an ileus, 

whereas sudden rushes of bowel sounds associated with crampy abdominal pain may 

indicate the presence of an intussusception. Gently seek out the areas of maximal 

tenderness. Careful percussion will determine areas of rebound pain. Perform a rectal 

examination. In boys, examine the testicles to rule out epididymitis or testicular torsion. 

In sexually active girls, rule out pelvic inflammatory disease. Appendicitis, which is the 

most common nontraumatic surgical emergency in the pediatric population, must be 

considered in all children who present with abdominal pain. Incidence peaks in 

adolescent years, but appendicitis has also been reported in neonates and infants. 

Perforation is nearly universal in children younger than age 3 years old compared to the 

less than 15% rate of perforation in adolescents. Common presenting symptoms in 

children younger than age 3 years include emesis, pain, diarrhea, and fever. Irritability, 

grunting respirations, cough, and right hip complaints may also be present. Localized 

tenderness to digital examination of the rectum may disclose a retrocecal appendix.


1. Urinalysis—Look for evidence of a urinary tract infection. More than 5 white or red 

blood cells per high-power field are occasionally seen in patients with appendicitis. 

2. Complete blood count with differential—CBC with differential may be useful in 

suggesting an infectious cause for abdominal pain. The white blood cell count is an 

insensitive and nonspecific test and cannot be used to rule out appendicitis. 

3. Other laboratory studies—Electrolytes, BUN, and creatinine measurements should 

be obtained for children who appear dehydrated after protracted vomiting or diarrhea. 

Consider lipase, and hepatic function tests if biliary disease, pancreatitis, or hepatitis are 

possible causes. Obtain a serum pregnancy test in adolescent girls. 

B. Imaging 

Obtain a chest x-ray for children with abdominal pain and respiratory symptoms (ie, 

cough, tachypnea). Lower lobe pneumonia in children may frequently result in referred 

pain to the abdomen that can mimic an acute abdomen. Obtain flat and upright, or 

decubitus, abdominal films for children with an acute abdomen to demonstrate 

obstruction, a radiopaque ureteral stone, an appendolith, or free air from a perforated 

viscus. 

CT scanning with oral and intravenous contrast is a sensitive test in the workup of 

appendicitis. Abdominal ultrasound is another modality commonly used at some centers 

instead of CT for detecting inflammation of the appendix. Ultrasound may also aid in 

diagnosing cholecystitis, hydronephrosis, appendiceal abscess, and ovarian torsion. 

Testicular ultrasound is indicated to rule out torsion. 

Barium or air-contrast enema may be used to look for intussusception in children with 

recurrent episodes of cramping abdominal pain, vomiting, and bloody stools. These 

tests are contraindicated if signs of peritonitis are present. 

Disposition 

Keep the patient on nothing-by-mouth status, and obtain surgical consultation. 

Broad-spectrum antibiotics should be started if obvious signs of perforation are present. 

If surgery is not immediately indicated, ensure close observation and follow-up. Admit 

the child to the hospital for frequent abdominal examinations. 

Outpatient management is indicated only when an acute abdomen appears unlikely and 

the physician is certain that the child will be returned for an examination within 12-24 

hours. 

D'Agostino JD: Common abdominal emergencies in children. Emerg Med Clin North Am 

2002;20:139. [PMID: 11826631] (Review.) 

Irish MS et al: The approach to common diagnoses in infants and children. Pediatr Clin 

North Am 1998;45:729. [PMID: 9728184] (Review.)

Pearl RH et al: The approach to common diagnoses in infants and children, part II. 

Pediatr Clin North Am 1998;45:1287. [PMID: 9889755] (Review.) 

Rothrock SG, Pagane J: Acute appendicitis in children: emergency department 

diagnosis and management. Ann Emerg Med 2000;36:39. [PMID: 10874234] (Review.) 

VOMITING 


Causes of vomiting in children may be categorized as due to direct irritation to the 

gastrointestinal tract, intestinal or gastric outlet obstruction, effect of a toxin or other 

noxious stimulus on the central nervous system, or elevated intracranial pressure. 


Look for precipitating factors including trauma, medications, feeding techniques, and 

recent illness. It is helpful to know the nature of the vomitus (eg, bilious bloody, coffee 

ground, bright red, or feculent), the relationship to eating and position, and whether 

projectile vomiting occurs. The absence of passage of stool or gas implies obstruction. 

Inspect the abdomen for signs of obstruction, and look for evidence of a systemic illness 

(eg, otitis media, urinary tract infection). 

A. Vomiting in the Newborn 

Infants commonly regurgitate a portion of feedings. Nonforceful regurgitation is usually 

benign. Forceful vomiting, however, often indicates serious disease. Causes of 

gastrointestinal obstruction in newborns include the following: 

1. Intestinal atresia—Vomiting begins shortly after birth. Abdominal x-rays reveal 

distention of the stomach and duodenum with an absence of colonic air. Early surgical 

intervention is necessary. 

2. Meconium ileus—Antenatal perforation of the intestines secondary to obstruction 

with meconium results in vomiting shortly after birth; 90% of patients have cystic 

fibrosis. 

3. Meconium plug syndrome—The distal colon becomes obstructed with a plug of 

meconium. A barium enema shows the plug and usually relieves the obstruction. This 

entity is suggestive of Hirschsprung disease. 

4. Midgut volvulus—This abdominal emergency usually presents in the first month of 

life with bile-stained vomiting and abdominal distention. An upper gastrointestinal series 

usually demonstrates obstruction. Immediate surgical management is essential because 

many of these obstructions are associated with vascular compromise. 

5. Hirschsprung disease—Delayed passage of meconium associated with abdominal 

distention and bilious vomiting is suggestive. A barium enema is helpful in diagnosis. 

6. Pyloric stenosis—Patients with muscular hypertrophy of the pylorus typically present

in the third week of life with nonbilious vomiting. Observe the infant during feeding to 

evaluate this event. Patients may present with altered consciousness if dehydrated. An 

olive-like mass may be palpable when examining the patient's mid-epigastrium. 

Ultrasound is the preferred diagnostic study. Pyloromyotomy is curative. 

B. Vomiting in Infants and Children 

Most infants and children who vomit have gastroenteritis. More serious causes of 

vomiting include the following: 

• Gastrointestinal obstruction in the young child, particularly intussusception, should be 

considered. Examine the abdomen for a sausage-shaped mass in the right upper 

quadrant and the rectum for "currant jelly stools" in the child presenting with intermittent 

crampy abdominal pain followed by vomiting. If a history of trauma is present, duodenal 

hematoma and traumatic pancreatitis should be considered. 

• Appendicitis may begin with a history of nausea and vomiting prior to the appearance 

of right lower quadrant abdominal pain. 

• Hepatitis in children is commonly associated with anorexia and vomiting. 

• In children with protracted vomiting and increasing lethargy, consider the diagnosis of 

Reye syndrome. Obtain blood for liver function tests and ammonia and glucose 

measurements. 

• Consider incarcerated inguinal hernia in a child with abdominal pain and vomiting. 

Treatment 

(See Figure 48-11.) Administer fluids if the child is dehydrated or if an obstruction is 

present. Insert a nasogastric tube if obstruction is suggested. 

Obtain upright and supine x-rays if signs of obstruction are present. A barium or 

air-contrast enema is indicated when considering the diagnosis of intussusception. 

Perform an upper gastrointestinal series emergently in the infant with bilious emesis 

who may have a midgut volvulus. 

Obtain urinalysis, CBC, platelet count, and electrolyte measurement as indicated by the 

child's clinical condition. 

Irish MS et al: The approach to common diagnoses in infants and children. Pediatr Clin 

North Am 1998;45:729. [PMID: 9728184] (Review.) 

BLEEDING 


Gastrointestinal hemorrhage in children usually results from ulceration of the bowel 

mucosal lining secondary to infection or ischemia. Subsequent bleeding into the 

gastrointestinal tract can be manifest in a number of ways. Hematemesis (vomiting of

lood) and melena (black stool) usually indicate that the site of bleeding is in the 

stomach or duodenum proximal to the ligament of Treitz. Hematochezia (red blood per 

rectum) usually indicates bleeding in the distal small bowel or colon. In children, 

however, rapid gastrointestinal transit may result in hematochezia following upper 

gastrointestinal bleeding. 


The patient's age and the amount and type of bleeding help determine the most likely 

cause. Bleeding in neonates is usually benign and self-limited. Profuse, painless 

bleeding may indicate Meckel diverticulum. Bleeding associated with pain may occur 

with intussusception. Diarrhea associated with bleeding per rectum usually indicates 

bacterial dysentery. 

Obtain vital signs to detect cardiovascular compromise. Clinical signs of liver disease 

may indicate a coagulopathy or esophageal varices as a possible cause of bleeding. 

Elicit a careful history for nonsteroidal anti-inflammatory drug use or exposure to 

warfarin-containing drugs. 

Occasionally what appears to be gastrointestinal hemorrhage is not truly from the 

gastrointestinal tract. Epistaxis, nasopharyngeal trauma, and hemoptysis may result in 

coffee-ground emesis. Some substances may color the emesis or stool red (eg, food 

colorings, beets, red gelatin, artificial fruit drinks, and antibiotic syrups). The stool should 

be routinely checked with a guaiac test for occult blood. 

A. Bleeding in the Newborn 

1. Swallowed maternal blood—Swallowed maternal blood at delivery or from a 

bleeding nipple can result in hematemesis or melena in the newborn. These infants 

usually appear otherwise healthy. An Apt-Downey test can differentiate infant from 

maternal blood by identifying fetal hemoglobin. 

2. Hemorrhagic disease—Newborns with hemorrhagic disease may present with 

melena or hematochezia. However, other evidence of a generalized bleeding disorder 

usually is present. Maternal medications such as aspirin or anticoagulants may result in 

neonatal hemorrhage. Consider vitamin K deficiency if the neonate did not receive an 

intramuscular injection after birth. 

3. Stress ulcers—In an infant with asphyxia or sepsis, stress ulcers may cause 

significant gastrointestinal bleeding. Stress ulcers can be secondary to sepsis, asphyxia, 

intracranial pathology, or heart disease. 

4. Other causes—Consider necrotizing enterocolitis, anal fissures, malrotation with 

midgut volvulus, and Hirschsprung disease with enterocolitis. 

B. Upper Gastrointestinal Bleeding in Infants and Children 

The most common cause of upper gastrointestinal bleeding is esophagitis or gastric and 

duodenal ulceration. Esophageal varices are an uncommon cause of bleeding in young 

children that may develop with severe liver disease. With forceful vomiting, tears of the 

distal esophagus (Mallory-Weiss syndrome) can occur in the esophagus, causing upper

gastrointestinal hemorrhage. 

C. Lower Gastrointestinal Bleeding in Infants and Children 

1. Anal fissures—Anal fissures are the most common cause of hematochezia in 

infants. 

2. Cow's milk sensitivity—Sensitivity to cow's milk protein can result in severe colitis 

with bloody stools. 

3. Intussusception—Always consider intussusception in a child who presents with 

colicky abdominal pain followed by vomiting. Typically these children may appear well 

between episodes of vomiting. Bloody stool helps establish the diagnosis. 

4. Meckel diverticulum—Patients with Meckel diverticulum may present with the 

painless appearance of bright red blood per rectum. Sufficient blood may be lost to 

result in cardiovascular compromise. The gastric mucosa within the diverticulum can be 

identified on technetium scan. 

5. Bacterial or viral infection—Fever and diarrhea associated with blood per rectum 

are usually secondary to an invasive bacterial infection of the colon. Culture stool for 

Campylobacter, Shigella, and Salmonella. Viral pathogens such as rotavirus and 

Norwalk virus must also be considered as possible causes. 

6. Hemolytic uremic syndrome—Hemolytic uremic syndrome is characterized by 

acute renal failure with thrombocytopenia, hemolytic anemia, and bloody diarrhea. 

Children with this syndrome are usually quite ill and require hospitalization and close 

observation. 

7. Intestinal polyps—Intestinal polyps are sometimes found in young children and may 

result in bright red blood per rectum. A diagnosis can be established by colonoscopy. 

8. Henoch-Schonlein purpura—This disorder is characterized by small vessel 

vasculitis of the skin, gastrointestinal tract, and kidneys. Patients will at times have 

palpable purpura of the skin, joint swelling and pain, and colicky abdominal pain. 

Gastrointestinal bleeding may be secondary to submucosal hemorrhage. These children 

are also at an increased risk for intussusception. 

9. Inflammatory bowel disease—Patients with inflammatory bowel disease may 

present with evidence of gastrointestinal bleeding associated with anemia, poor growth, 

abdominal pain, and diarrhea. 

Treatment 

(See Figures 48-12 and 48-13.) Evaluate cardiovascular status. Achieve intravenous 

access if significant blood loss has occurred. Send blood for CBC, platelet count, 

coagulation studies, and typing and cross-matching. Consider stool evaluation for fecal 

leukocytes, bacterial culture, ova and parasites. 

Infuse saline or Ringer's lactated injection initially if the child is in shock. Alternatively,

infuse type O, Rh-negative blood. 

Place a nasogastric tube to determine if the site of bleeding is in the upper 

gastrointestinal tract. Lavage with saline (10 mL/kg) until active bleeding stops. Unstable 

patients are at risk for aspiration and may require intubation. 

If blood loss is greater than 10 mL/kg/h, emergent surgical intervention may be 

necessary to control bleeding. 

Disposition 

Admit children with acute upper gastrointestinal bleeding to the hospital for stabilization 

and endoscopic evaluation. Children with lower gastrointestinal bleeding can be 

evaluated as outpatients as long as they appear well and are hemodynamically stable. 

Stabilize a hemodynamically unstable patient before performing diagnostic procedures. 

Emergent surgical intervention may be necessary to identify the site of bleeding. 

Pearl RH et al: The approach to common diagnoses in infants and children, part II. 

Pediatr Clin North Am 1998;45:1287. [PMID: 9889755] (Review.) 

FOREIGN BODY 

Esophageal Foreign Bodies 

Foreign bodies within the esophagus become lodged at the cervical esophagus, aortic 

arch, or lower esophageal sphincter. Esophageal obstruction secondary to a foreign 

body may result in substernal chest pain and increased salivation secondary to inability 

to swallow. The physical examination is usually normal unless perforation has occurred. 

X-ray examination of the chest will usually disclose the foreign body; in the esophagus it 

is best seen on an anteroposterior film (Figure 48-14). A radiolucent foreign body (eg, 

plastic) may not be visible on x-ray. 

Gastric & Small Bowel Foreign Bodies 

Most foreign bodies that successfully pass through the esophagus will navigate the 

remainder of the gastrointestinal tract without difficulty. The occasional object that is 

unable to pass through the stomach after a period of 3 days should be removed by 

endoscopy. Intestinal obstruction may occur if a foreign body becomes lodged in the 

region of the ileocecal valve. 

HEMATOLOGIC DISEASES 

ANEMIA 


In children, over 75% of anemias are due to iron deficiency or thalassemia minor, both 

of which are characterized by microcytosis. The most common cause of anemia in 

children aged 6 months to 2 years is nutritional iron deficiency. Typically this results

from excessive cow's milk intake. Less commonly iron deficiency anemia will occur 

secondary to chronic blood loss, usually from the gastrointestinal tract (eg, duodenal 

ulcer, Meckel diverticulum, and polyps). 

Anemias not due to iron deficiency are caused by one of 2 processes: (1) Decreased 

erythrocyte production or release from the bone marrow, for example, transient 

erythroblastopenia of childhood (TEC). TEC typically occurs in children aged 1-2 years. 

Severe anemia and reticulocytopenia spontaneously resolve in 1-2 months. (2) 

Increased destruction, sequestration, or acute loss of circulating red cells owing to sickle 

cell disease, autoimmune hemolytic anemia, or hemolytic uremic syndrome, or blood 

loss due to trauma, surgery, or peptic ulcer disease. 



With rapid onset of anemia from blood loss or hemolysis, signs of cardiovascular 

compromise as well as impending cardiac failure may be present. With slow onset of 

anemia, children typically show pallor and decreased exercise tolerance but no 

evidence of cardiovascular compromise even with extremely low levels of hemoglobin. 

Hemolytic anemias may cause jaundice and splenomegaly. Petechiae may indicate 

hemolytic uremic syndrome. 


Laboratory evaluation should include a complete blood count with hemoglobin, red 

blood cell indices, white blood cell and platelet counts, peripheral smear, and 

reticulocyte counts. Anemia with microcytosis in a young child strongly suggests iron 

deficiency. If the stool is negative for occult blood, further tests are not necessary if the 

child is not severely anemic. 

Treatment 

A. Iron Therapy 

Treat iron deficiency with elemental iron at 3-6 mg/ kg/d (ferrous sulfate, 75 mg/0.6 mL 

dropper, equivalent to 15 mg elemental iron/0.6 mL dropper) in 1-2 daily doses. 

Continue iron therapy for 2 months after the anemia is corrected. Restrict cow's milk 

intake. 

If anemia has developed slowly, patients can often tolerate remarkably low hemoglobin 

levels, even to 4-5 g/dL, without the need for transfusion if other effective therapy is 

available. 

B. Transfusion 

Transfuse children who experience a rapid decline in hemoglobin to less than 7, 

particularly if signs of cardiovascular compromise are present. 

In patients with gradual onset of anemia who require transfusion, slow transfusion is 

recommended, because these children are at risk for congestive heart failure with rapid 

transfusion. Administer a diuretic prior to transfusion to prevent circulatory overload (eg, 

furosemide, 1 mg/kg intravenously).

Disposition 

Obtain consultation with a hematologist for anemias requiring transfusion, anemias 

associated with hemolysis, and anemias without an obvious cause. 

Recheck the hemoglobin level in children receiving iron therapy in 2-4 weeks to 

document response. 

SICKLE CELL DISEASE 



Vasoocclusive events are associated with severe local pain, fever, leukocytosis, and 

impaired organ function. Abdominal pain may be severe and suggest appendicitis or 

cholecystitis. In young children, a common initial vasoocclusive episode is manifested 

by hand-foot syndrome, or dactylitis, with fever, acute swelling, and pain in one or both 

hands or feet. Bone and joint pain may be quite severe, and differentiation from skeletal 

infection may be difficult. 

Splenic infarcts may cause severe abdominal pain and lead to progressive atrophy of 

the spleen. Because of impaired splenic clearance of bacteria, children with sickle cell 

anemia are partially susceptible to infection by encapsulated organisms. Acute splenic 

sequestration, a severe vasoocclusive crisis, occurs in 10% of children aged 5 months 

to 2 years with sickle cell disease. Symptoms include left upper quadrant pain, massive 

splenomegaly, and hypovolemic shock. 

Vasoocclusive crises may involve the central nervous system and produce neurologic 

symptoms of severe headache, visual disturbances, coma, and seizures. Also in 10% of 

patients with sickle cell disease, cerebral vessel thrombosis during these crises may 

result in stroke. A combination of pulmonary infarcts and infection may lead to the acute 

chest syndrome manifested by chest pain, dyspnea, and tachypnea. These children 

may become severely hypoxic. Priapism is another complication of sickling and can be 

extremely uncomfortable to the child. 


Obtain a complete blood count and reticulocyte count. A decrease in hematocrit from 

baseline may indicate the need for transfusion. The absence of reticulocytosis indicates 

an aplastic crisis (often from parvovirus B19) and heralds an abrupt decrease in the 

hematocrit. 

Obtain cultures of blood and urine if fever is present. Obtain blood for electrolytes if 

dehydration is a concern. 

If bone pain is associated with high fever, chills, toxicity, and leukocytosis, bone 

aspiration is indicated to diagnose osteomyelitis. 

B. Imaging

Obtain x-rays of the chest if hypoxemia, cough, tachypnea, or dyspnea is present. 

Infiltrates may be present in patients with acute chest syndrome. 

Treatment 


Administer oxygen only if the patient is hypoxemic or in respiratory distress. Intravenous 

fluid hydration is important in reversing the sickling process if dehydration is present. 

B. Venous Access 

Begin an intravenous line if fluids or parenteral pain medications are anticipated. For 

patients with acute splenic sequestration, bolus with intravenous fluids and perform 

exchange transfusion when available. 


Children with sickle cell disease have an increased susceptibility to sepsis from 

encapsulated organisms. Figure 48-15 is an algorithm for the management of the febrile 

child with sickle cell disease without an obvious localizing source of infection. 

D. Pain Management 

Treatment of pain in a sickling crisis is important for the child's recovery. Ask the patient 

to use an objective scale (eg, 1-10) to grade pain severity. Use this scale to guide pain 

management. Do not hesitate to use parenteral narcotics for adequate pain control 

because of concerns about drug addiction. Acetaminophen with or without codeine can 

be used for mild pain. For severe pain, give intravenous morphine sulfate, 0.1 mg/kg 

every 2-4 hours, or meperidine, 1 mg/kg every 3-4 hours. 

E. Treatment of Acute Chest Syndrome 

Treatment of acute chest syndrome includes hospitalization, intravenous antibiotics, and 

supplemental oxygen to keep oxygen saturation above 95% on pulse oximetry. 

Administer intravenous fluids to maintain hydration. If hypoxemia worsens, exchange 

transfusion may be required. Consider vancomycin for patients not responding to initial 

antibiotics. 

Disposition 

Children who can maintain adequate oral fluid intake and whose pain is controlled with 

oral medication can be managed as outpatients with close follow-up. 

Hospitalize children who require continued parenteral therapy for pain, those who 

cannot maintain adequate oral hydration, or those who have required more than 2 visits 

for treatment of the same painful crisis. 

Freeman L: Sickle cell disease and other hemoglobinopathies: approach to emergency 

diagnosis and treatment. Emergency Medicine Practice 2001;3:11. 

Sadowitz P, Amanullah S, Souid AK: Hematologic emergencies in pediatric emergency 

room. Emerg Med Clin North Am 2002;20:177. [PMID: 11826633] (Review.)

Wethers DL: Sickle cell disease in children: part II. Diagnosis and treatment of major 

complications and recent advances in treatment. Am Fam Physician 2000;62:1309. 

[PMID: 11011859] (Review.) 

IDIOPATHIC THROMBOCYTOPENIC PURPURA 


• Usually children present with petechia, purpura, or spontaneous bleeding involving the 

mucous membranes. 

• Platelet counts usually less than 100,000. 


The differential diagnosis of thrombocytopenia involves one of 3 mechanisms: (1) 

increased destruction (idiopathic thrombocytopenia purpura [ITP], hemolytic uremic 

syndrome, or disseminated intravascular coagulopathy), (2) decreased production 

(aplastic crisis, marrow infiltrating neoplasms), and (3) splenic sequestration (sickle cell 

disease). ITP results from increased destruction of only platelets, causing severe 

isolated thrombocytopenia. It commonly follows a viral illness. It is usually benign and 

self-limited; approximately 80-90% of cases resolve within 6 months. 



Children usually present with the abrupt appearance of petechiae, purpura, and 

spontaneous bleeding of the skin and mucous membranes. They may also have 

epistaxis. Early in the disease, intracranial hemorrhage occurs in less than 1% of 

patients. These patients usually manifest severe headache or altered level of 

consciousness. Children with ITP typically appear in good health. They usually are not 

febrile and do not have splenomegaly. Children with platelet counts under 10,000/uL are 

at risk for life-threatening complications. 

B. Clinical Findings 

Obtain a CBC, blood smear, and platelet count. Typically the platelet count is less than 

100,000/uL and sometimes is less than 20,000/uL. 

Bone marrow examination may be recommended by the hematologist if the presentation 

is atypical. 

Treatment 


Observation is adequate for children with only moderately severe thrombocytopenia. 

B. Corticosteroid Therapy 

If the platelet count is less than 10,000-20,000/uL or if extensive bleeding is present,

consultation with a pediatric hematologist and corticosteroid therapy are recommended. 

Corticosteroids will usually cause the platelet count to increase to 20,000/uL within 

48-72 hours. 

C. Emergent Interventions 

Emergent intervention is needed for severe gastrointestinal bleeding, hematuria, or 

intracranial hemorrhage. Whole-blood transfusion may be required for severe anemia. 

Intravenous corticosteroids should be administered as methylprednisolone, 10-30 

mg/kg/d for 3-5 days (maximum, 1 g over 30 minutes). 

D. Gamma Globulin 

Intravenous infusion of gamma globulin, 1 g/kg/d for 2 consecutive days, or a single 

dose of anti-Rh D, 40-80 mg/kg over 5 minutes in Rh-positive patients, will also result in 

a rapid rise in platelet count. 

E. Platelet Transfusions 

Platelet transfusions are indicated for refractory ITP and life-threatening hemorrhage, 

but the half-life of transfused platelets is brief. Splenectomy may be indicated if medical 

treatments fail. 

Disposition 

Hospitalize children with ITP if the platelet count is less than 10,000/uL or if significant 

bleeding is present, particularly young children for whom avoidance of traumatic play is 

difficult. 

Advise older children to avoid all contact sports and vigorous playground activities 

during the acute phase of the disease. 

Obtain emergent neurosurgical consultation for any signs of intracranial hemorrhage. 

Obtain hematologic consultation and a bone marrow examination before corticosteroid 

therapy is initiated. 

Chu YW, Korb J, Sakamoto KM: Idiopathic thrombocytopenia purpura. Pediatr Rev 

2000;21:95. [PMID: 10702324] (Review.) 

Sadowitz P, Amanullah S, Souid AK: Hematologic emergencies in pediatric emergency 

room. Emerg Med Clin North Am 2002;20:177. [PMID: 11826633] (Review.) 

NEWBORN EMERGENCIES 


The need for resuscitation of the newborn infant is based on the Apgar score (Table 

48-20). Vital signs should be recorded frequently to monitor the success of 

resuscitation. Physical examination should establish the degree of maturity of the infant 

as well as the integrity of the infant's respiratory and cardiovascular functions. 

Treatment


The key to treatment in the newborn infant is to be prepared and use an organized team 

approach. A "code card" posted in the emergency department, or use of the Broselow 

tape, can help guide drug dosing and choice of equipment sizes. 

If time permits, alert the obstetric service and nursery staff prior to the birth of the baby. 

Electronic fetal monitoring is helpful if time and equipment availability permit. 

An overhead radiant warmer should be present and turned on. If one is not available, 

use heating lamps or warm blankets. Proper equipment should be available and 

functioning (Table 48-21). 

At birth the umbilical cord should be quickly clamped and then cut. The infant should be 

placed under the radiant warmer and immediately assessed, and an Apgar score should 

be assigned (see Table 48-20). The heart rate can be monitored by palpation of the 

umbilical arterial pulse. The oropharynx can be gently suctioned and the infant 

stimulated by rubbing its back. The infant should be towel-dried. Apgar scores should be 

assigned at 1 and 5 minutes. 

B. Neonatal Resuscitation 

Infants who are bradycardic, apneic, or significantly depressed require immediate 

resuscitative efforts (Figure 48-16). 

Epinephrine, atropine, or naloxone can be administered endotracheally during 

resuscitative efforts prior to the establishment of vascular access. When this route is 

used, double the usual intravenous dosages of these medications. 

Umbilical vein catheterization can also be used for emergent drug administration or 

volume expansion. Umbilical artery catheterization can be used for frequent arterial 

blood gas analysis and blood pressure readings. 

Continue to assign Apgar scores at 5-minute intervals to determine the need for 

continued resuscitative efforts. Be alert to complications particular to the newborn when 

resuscitation does not result in expected improvement (eg, meconium aspiration, 

respiratory distress syndrome, shock, maternal substance abuse, pneumothorax, 

choanal atresia, diaphragmatic hernia, tracheoesophageal fistula). As the Apgar score 

improves, prepare the infant for transport to the nursery for close monitoring and care 

as indicated. 

CHILD ABUSE 

PHYSICAL ABUSE 


In 2000, over 3 million referrals concerning child abuse or neglect were reported to child 

protective services in the United States. Almost 1 million children were found to be 

victims of maltreatment, which included neglect, medical neglect, physical abuse, sexual

abuse, and psychological abuse. The rate of child maltreatment was 12.2 victims per 

1000 children in the United States. Management of possible child abuse is one of the 

most difficult clinical problems facing the emergency physician. The initial presentation 

of a physically abused child frequently occurs in the emergency department. The 

physician's responsibilities are to (1) acknowledge that a problem exists, (2) maintain a 

high index of suspicion, (3) discuss concerns with the parents in a sensitive and 

compassionate manner, (4) ensure protection of the child, (5) perform a complete 

medical evaluation of injuries or neglect, including documentation and radiologic 

imaging if indicated, and (6) report suspicions to child protective services. 

The key to diagnosis of physical abuse is matching a carefully taken history with the 

extent of injury. Historical indicators of abuse include (1) a history that overestimates or 

underestimates the injury, (2) a history that suggests a lack of proper supervision, (3) 

inconsistencies or changes in the history, and (4) a delay in seeking medical care. 

Note the quality of the parent-child interaction. Note whether the parents appear to be 

under the influence of drugs or alcohol. 

Consider the child's motor skills and capabilities when evaluating the worthiness of the 

history. Injuries that could occur accidentally only in an older child with more advanced 

motor skills strongly suggest the possibility of nonaccidental injury. 

Physical indicators of abuse include (1) injuries that do not match the history, (2) 

specific pathognomonic injuries (eg, looped wire marks or cigarette burns), (3) multiple 

injuries in various stages of healing, (4) different types of injuries or disease (eg, burns 

and fractures), (5) overall evidence of poor care, and (6) evidence of failure to thrive. 



1. Bruises—The skin is the most commonly injured site. Injuries from physical abuse 

may be either nonspecific bruises or pathognomonic injuries that clearly reflect the 

instrument used to strike the child. The specific pattern of bruising may be indicative of 

nonaccidental trauma. Young children accidentally bruise themselves in predictable 

ways. A pattern of bruising significantly different from that of accidental bruises should 

raise suspicion of nonaccidental trauma. Locations of possible accidental cutaneous 

injuries in the young child are the shins and knees, hips (iliac crests), spinal 

prominences, chin, forehead, face (facial scratches in infants), lower arms, and elbows. 

Locations of injuries that probably are not accidental are the buttocks, inner thighs, 

genitalia, perineum, rectum, abdomen, chest, cheeks, neck, ears, and inner surface of 

upper arms. Be alert to specific abusive cutaneous injuries, for example, wire loop 

marks made by extension cords, belt marks, burns from hot objects such as silverware 

or heat vents, and belt buckle marks. 

2. Skeletal trauma—Skeletal trauma occurs in one fifth to one third of abuse cases. 

More than half of these fractures occur in children under age 1 year. Suspicious 

fractures include femoral, epiphyseal metaphyseal, and rib fractures. 

a. Femoral fractures—Femoral fractures (spiral or transverse) in children under age 3

years are suspicious. Minor falls, less than 30-60 cm, usually do not result in femoral 

fractures. 

b. Epiphyseal metaphyseal fractures—Epiphyseal metaphyseal fractures in young 

infants and children are virtually diagnostic of abuse because they usually do not occur 

with accidental falls. These fractures usually occur as a result of severe pulling, twisting, 

or shaking of a child's limbs. These activities produce severe acceleration-deceleration 

forces on the limbs, resulting in metaphyseal chip fractures. 

c. Rib fractures—Rib fractures in infants under age 2 years are extremely uncommon 

because the infant's rib cage is extremely pliant. Rib fractures in these children should 

always raise the possibility of nonaccidental trauma. 

3. Burns—Burn injuries should raise the possibility of abuse in young children when 

they do not fit the normal accidental pattern. Children may be held down in scalding 

water as a means of discipline. These immersion burns typically cause injury to the 

buttocks and to the hands and feet in a stocking-glove distribution. The line of 

demarcation between burned and normal skin is usually quite abrupt. The flexion 

creases of the legs are usually spared. Children may also be burned by hot objects such 

as heater grates, curling irons, or cigarettes. Cigarette burns typically cause a deep 

circular burn about 5-10 mm in diameter. They may be difficult to differentiate from 

impetigo or insect bites. 

4. Skin lesions—See Table 48-22. 

5. Head injuries—Head injuries carry the highest incidence of morbidity and mortality. 

Abusive head injuries either are due to direct impact with a fist or other object or are 

secondary to severe rotational forces during vigorous shaking. Many children with 

abusive intracranial injury suffer a combination of impact and shaking injuries. Both 

shaking and impact can cause severe acceleration-deceleration forces to the brain, 

resulting in shearing injury to the bridging vessels that connect the brain to the dura. 

Subdural hematomas can then occur with resulting cerebral compression. In addition, 

these forces can cause direct neuronal injury within the brain. Infants who are severely 

shaken can present with sudden onset of seizure or coma but have no signs of head 

trauma. Typically infants who are severely shaken will have bilateral retinal 

hemorrhages and on CT scan may have bilateral subdural hemorrhages. 

6. Abdominal injuries—Nonaccidental abdominal injury may produce severe injury to 

the viscera, including intramural hematomas of the small bowel, splenic or hepatic 

lacerations, traumatic pancreatitis, and renal contusions. 

B. Diagnostic Procedures 

The following diagnostic studies should be ordered: 

• CBC, platelet, and coagulation studies 

• Urinalysis (recommend urine pregnancy test for adolescent females) 

• A skeletal x-ray series, if indicated, of the skull, ribs, and long bones

Jain AM: Emergency department evaluation of child abuse. Emerg Med Clin North Am 

1999;17:575. [PMID: 10516839] (Review.) 

National Clearinghouse on Child Abuse and Neglect Information: 

http://www.calib.com/nccanch/pubs 

SEXUAL ABUSE 


Sexual abuse is involvement of children and adolescents in sexual activities they cannot 

comprehend because of their developmental level, activities to which they are unable to 

give informed consent, or activities that violate social taboos. These activities may 

physically injure the child and leave detectable patterns of trauma, but often sexual 

abuse may involve genital touching or fondling that does not cause detectable injury and 

may even be physically pleasurable to the child. Most victims of sexual abuse are 

female, and the mean age is approximately 7-8 years. Children are usually molested by 

males who are well known to them, either as a family member or trusted friend. 

Adolescents are more commonly molested by strangers. 


Various behavioral reactions may ensue following sexual abuse. In preschool children, 

these can be fear states (eg, fear of adult males), nightmares, precocious sexual 

behavior, enuresis, encopresis, or behavior regression. In school-aged children, 

indicators may be precocious sexual behavior, sexual aggression toward other children, 

cross-dressing, school failure, truancy, running away, or depression. Adolescents may 

demonstrate behavioral problems with drugs, promiscuity, prostitution, running away, 

sexual aggression toward other children, depression, somatic complaints, or school 

failure. 

Disclosures of sexual abuse often are incomplete and may later be retracted because 

the perpetrator is typically someone to whom the child feels great allegiance and on 

whom the child is dependent. 

Some children who are sexually abused show signs of abuse, including genital and 

nongenital trauma as well as the presence of sexually transmitted diseases (STDs). An 

STD may be the only indication of molestation (Table 48-23). Direct injuries to hymenal 

tissue are rarely accidental. Hymenal lacerations should always raise the possibility of 

sexual abuse. Typical straddle injuries do not cause hymenal lacerations. Anal 

penetration may result in erythema and swelling of the perianal tissue as well as 

lacerations, abrasions, and bruising. 

Children in whom sexual abuse is being considered should be evaluated at a center 

where health care providers accustomed to examining sexual abuse victims are located. 

The goals of the medical evaluation are to (1) treat any medical illness or injuries, (2) 

provide crisis counseling, (3) provide protection for the child if necessary, and (4) 

precisely document injuries and collect evidence for use by the legal system.

Approach the child in a compassionate, nonthreatening manner, and ask nonleading 

questions in an attempt to uncover whether sexual abuse has occurred. The physical 

examination should be performed immediately if sexual assault has occurred within 72 

hours or the child has signs or symptoms of genital injury or infection. Look for both 

nongenital and genital injuries. Many examiners employ a colposcope with a camera 

attachment to provide photographic documentation of genital injuries. A speculum 

examination in a prepubertal child is indicated only when symptoms of vaginal injury 

(eg, vaginal bleeding) are present. This is best done under general anesthesia. 

Laboratory tests in the diagnosis of STDs should be obtained routinely, including wet 

mount and Gram staining of genital or rectal discharge; genital and rectal cultures for N. 

gonorrhoeae and C. trachomatis; pharyngeal culture for N. gonorrhoeae; culture of 

lesions suspicious for herpes simplex; and serologic studies for hepatitis B, syphilis, and 

human immunodeficiency virus, if indicated. 

If the sexual assault has occurred within 72 hours of the examination, seminal fluid may 

be present on or within the child. The proper collection of this evidence is essential. 

Physicians who examine sexual abuse victims must be fully knowledgeable of the 

protocol for evidence collection in their locale. 

Treatment 

A. Treat Physical Injuries 

Treat physical injuries as necessary. Inspect vaginal lacerations for possible extension 

into the abdominal cavity. Significant perineal or vaginal lacerations are best examined 

under general anesthesia in the operating room. 

B. Treat Sexually Transmitted Diseases 

Because STDs are relatively uncommon in prepubertal victims of sexual abuse, empiric 

therapy is recommended only if the child has a vaginal or rectal discharge that on Gram 

staining is suggestive of gonorrhea. Adolescent victims of sexual assault should 

routinely be given treatment for STDs at the time of the examination, because the 

incidence of STDs in this group is significant. Give empiric treatment for both Chlamydia 

(doxycycline, 100 mg twice a day for 10 days) and gonorrhea (ceftriaxone, 125 mg 

intramuscularly). 

C. Offer Pregnancy Prevention 

After documentation of a negative urine pregnancy test, adolescent girls should be 

offered prophylaxis against conception with norgestrel (Ovral), 2 pills at the time of 

examination and 2 pills 12 hours later orally. 

D. Offer Counseling 

Pediatric and adolescent victims of sexual abuse should be offered counseling following 

the initial evaluation. Many children will require extensive counseling, particularly those 

who are victims of long-term incestuous relationships. 

Disposition 

Children and adolescents may be discharged home if their medical condition permits

and safety can be ensured. If the child is at risk for further sexual abuse, removal from 

parental custody and placement in shelter care is indicated. 




48. Pediatric Emergencies - Roger L. Humphries, MD, Keith D. Bricking, MD, 

& Thomas M. Huhn, MD 1 


Table 48-1. Predictive model: acute illness observational scale. 1 

1 

Normal 

3 

Severe 

Impairment 

Strong with normal tone, or content and not crying Weak or moaning or high pitched 

Cries briefly then stops, or content and not crying Continual cry or hardly responds 

If awake, stays awake, or if asleep and stimulated, 

wakes up quickly 

Falls to sleep or will not rouse 

Pink Pale or cyanotic or mottled or ashen 

Skin normal, eyes normal, and mucous membranes 

moist 

Skin doughy or tented, and dry mucous mem 

eyes 

Smiles or alerts (= 2 mo) No smile; face anxious, dull, expressionless; 

mo) 

1 

Reproduced, with permission, from McCarthy PL et al: Observational scales for febrile children. Pedia 






TABLES 

Table 48-1. Predictive model: acute illness observational scale.

Table 48-2. Guidelines for equipment and supplies for use in pediatric patients in the emergency 

department. 1 

1 

Adapted from Committee on Pediatric Equipment and Supplies for Emergency Departments, Nationa 

Emergency Medical Services for Children Resource Alliance. Reproduced, with permission, from ACE 

policy statement. Care of children in the emergency department: guidelines for preparedness. America 

College of Emergency Physicians, 2001. 

2 

Suitable for hypothermic and hyperthermic measurements with temperature capability from 25°C to 4 

3 

May be satisfied by a disposable CO2 detector of appropriate size for infants and children. For childre 

years or older who are = 20 kg in body weight, an esophageal detection bulb or syringe may be used 

additionally. 

4 

Equipment that is essential but may be shared with the nursery, pediatric ward, or other inpatient ser 

and is readily available to the emergency department. 

5 

Equipment or supplies that are desirable but not essential. 

6 

To regulate rate and volume. 

7 

Ensure availability of pediatric sizes within the hospital. 

8 

Available within hospital for burn care. 

9 

Many types of cervical immobilization devices are available, including wedges and collars. The type o 

device chosen depends on local preferences and policies and procedures. Chosen device should be 

stocked in sizes to fit infants, children, adolescents, and adults. Use of sandbags to meet this requirem 

is discouraged, because they may cause injury if the patient has to be turned. 






TABLES 

Table 48-2. Guidelines for equipment and supplies for use in pediatric 

patients in the emergency department.

Table 48-3. Equipment and sizes available for invasive procedures. 

Inner 

Diameter 

Endotracheal 

Tube (mm) 

Chest 

Tube (F) 

Newborn 0-1 5 

3.5 12 6 months 1 8 

4 20 2-3 years 1 8 

5-6 28 6-8 years 2 10 

7 32 14 years 3 12

Table 48-4. Age-related vital signs. 

Mean 

Weight 

(kg) 

Normal 

Heart 

Rate 

Premature 40 40-60 

3.5 100-170 3 months 50 30-50 

8 100-170 1 year 65 30-40 

13 100-160 4 years 70 20 

20 70-115 8 years 80 16 

30 60-105 12 years 90 16

Table 48-5. Daily maintenance requirements for fluids and electrolytes. 

Water 

Requirement 1 

100 mL/kg 

50 mL/kg + 1000 mL 2 mEq/kg 

20 mL/kg + 1500 mL 

Potassium 

Requirement 2

Table 48-6. Structural causes of congestive heart failure 

during infancy. 

1 

Reproduced, with permission, from Hoffman JIE: Congestive 

heart failure, Page 54 in: Pediatric Emergency Medicine: A 

Clinician's Reference. Grossman M, Dieckmann RA (editors). 

Lippincott, 1991. 






TABLES 

Table 48-6. Structural causes of congestive heart failure during infancy.

Table 48-7. Treatment of common pediatric dysrhythmias. 

Rate/min Initial Treatment Narrow complex tachycardias 

Sinus tachycardia < 0.10 Treatment of primary condition. 

300-500 If unstable, 

synchronized 

electrical DC 

cardioversion, 

0.25 J/kg. 

If stable, vagal 

maneuvers 

(rectal 

stimulation, ice 

water to face, 

Valsalva). 

Atrial fibrillation < 0.10 

120-300 As for atrial 

flutter. 

Wide complex tachycardias 

Ventricular tachycardia > 0.10 Lidocaine, 1.0-1.5 mg/kg, then 

20-50 µg/kg/min. 

150-300 As for ventricular Ventricular fibrillation 

tachycardia. 

Variable 

Age-related Oxygen, 

stimulation.

Table 48-8. Differential diagnosis of upper airway obstruction. 

Croup Foreign Body 

6 months to 3 years Under 3 years 

Parainfluenza Foreign body 

Fall or winter Any 

Night or morning Daytime 

Slow Abrupt 

Yes No 

Generally low grade None 

Mild No 

Possible No 

No No 

Inspiratory + expiratory Inspiratory + expiratory 

Variable Variable 

Yes No 

Normal Normal 

Steeple sign Hyperinflation 

Normal May show radiopaque body 






TABLES 

Table 48-8. Differential diagnosis of upper airway obstruction.

Table 48-9. Management of complete foreign body airway obstruction in infants and children. 

Infant (up to 

age 1 year) 

Open airway, 

perform 

tongue-jaw lift. 


Conscious Patient unable to ventilate: 

Perform Heimlich maneuver: abdominal thrusts 

above the umbilicus standing behind the victim. 

Continue thrusts until foreign body is expelled or 

victim becomes unconscious. 

If able to visual foreign body, remove it. If no spontaneous respiration 

breathing. 





TABLES 

Table 48-9. Management of complete foreign body airway obstruction in 

infants and children.

Table 48-10. Causes of pneumonia by age. 1 

Infecting Organism 

Bacteria 

Group B streptococcus 

Gram-negative bacilli 

Viruses 

Chlamydia 

Viruses 

Bacteria 

S pneumoniae 

S aureus 

H influenzae 

Viruses 

Bacteria 

S pneumoniae 

S aureus 

H influenzae 

Viruses 

Bacteria 

S pneumoniae 

M pneumoniae 

Viruses 

Bacteria 

S pneumoniae 

M pneumoniae

Table 48-11. Suggested drug treatment for community-acquired pneumonia in children, according to 

whether they are hospitalized. 1 

Inpatient, with Signs of 

Sepsis, Alveolar 

]Infiltrate, Large Pleural 

Outpatient 

Effusion, or All Three 

Admit patient. Administer IV ampicillin and gentamicin, with or without 

cefotaxime. 

If patient is afebrile, give oral erythromycin, 

30-40 mg/kg/d in 4 divided doses, or oral 

azithromycin, 1 dose of 10 mg/kg, then 5 

mg/kg/d for 4 days. Admit patient if fever or 

hypoxia is present. 

Administer oral amoxicillin, 80-100 mg/kg/d 

in 3 or 4 divided doses). 

Administer oral erythromycin, 30-40 mg/kg/d 

in 4 divided doses, oral clarithromycin, 15 

mg/kg/d in 2 divided doses), or oral 

azithromycin, 1 dose of 10 mg/kg, then 5 

mg/kg/d for 4 days. In children older than 8 

years of age, consider oral doxycycline, 4 

mg/kg/d in 2 divided doses. 

Administer IV cefotaxime, 200 mg/kg/d in 3 divided dose 

given 8 hours apart 2,4 

Administer IV cefotaxime, 200 mg/kg/d or IV cefuroxime 

mg/kg/d in 3 divided doses given 8 hours apart 2,4 

Administer IV cefotaxime, 200 mg/kg/d or IV cefuroxime 

mg/kg/d in 3 divided doses given 8 hours apart. 4 Consid 

adding IV azithromycin if patient is not doing well. 2 

2 Staphylococcal pneumonia is unusual; however, if cultures of blood or pleural fluid grow Staphylococ 

aureus or, in other exceptional circumstances, oxacillin or, in areas where methicillin-resistant S aureu 

reasonable possibility, vancomycin should be added. 

3 

In infants younger than 6 weeks of age, treatment with azithromycin, 5 mg/kg/d in 2 divided doses giv 

12 hours apart, should be considered in view of reports of hypertrophic pyloric stenosis in infants who 

received erythromycin. 

4 

Some experts suggest treatment with ampicillin, 200-300 mg/kg/d intravenously in 4 divided doses gi 

hours apart, in patients who have lobar, and therefore most likely pneumococcal, pneumonia. 






TABLES 

Table 48-11. Suggested drug treatment for community-acquired 

pneumonia in children, according to whether they are hospitalized.

Table 48-12. Pediatric Glascow Coma Scale. 1 

> 1 Year 

4 Spontaneously Spontaneously 

3 To verbal command To shout 

2 To pain To pain 

1 No response No response 

Best Motor 

Response 

> 1 Year 

6 Obeys Spontaneous 

5 Localizes pain Localizes pain 

4 Flexion-withdrawal Flexion-withdrawal 

3 Flexion-abnormal (decorticate 

rigidity) 

2 Extension (decerebrate 

rigidity) 

Flexion-abnormal 

(decerebrate rigidity) 

Extension (decorticate 

rigidity) 

1 No response No response 

Best Verbal 

Response 

> 5 years 0-23 Months 

5 Oriented and converses Appropriate words and 

phrases 

Smiles, coos 

appropriately 

4 Disoriented and converses Inappropriate words Cries, consolable 

3 Inappropriate words Persistent cries and/or 

screams 

Persistent, inappropria 

crying and/or screami 

2 Incomprehensible sounds Grunts Grunts, agitated/restle 

1 No response No response No response 

Total: 3-15

Table 48-13. Common causes of meningitis and empiric antibiotic therapy. 

Common Bacterial 

Causes 

Group B 

streptococcus 

E coli 

Listeria 

S pneumoniae 

N meningitidis 

H influenzae type B 

(rare) 

S pneumoniae 

N meningitidis 


Dose 

15 mg/kg q 6 h 


100 mg/kg q 24 h 



100 mg/kg q 24 h 

Preterm to < 1 month 

3 months-6 years 

Ampicillin plus cefotaxime or 

gentamicin 

Vancomycin plus cefotaxime 

ceftriaxone 





TABLES 

Table 48-13. Common causes of meningitis and empiric antibiotic therapy.

Table 48-14. Cerebrospinal fluid values in normal and disease states. 1 

White Blood Cell 

Count (%PMN) 

Protein 

(mg/dL) 

Intracranial 

Pressure 

(mm H 2 O) 

< 6 (0) < 35 < 180 

200-10,000 (80-100) 100-500 > 200 

200-10,000 (40-100) 100-500 > 200 

25-1000 (< 50) 50-100 < 180 

50-1000 (< 50) 50-300 > 200 

1 

Adapted from Tureen J: Meningitis. In: Pediatric Emergency Medicine: A Clinician's Reference. Gros 

M, Dieckmann RA (editors). Lippincott, 1991. 






TABLES 

Table 48-14. Cerebrospinal fluid values in normal and disease states.

Table 48-15. Drugs used for the treatment of acute otitis media. 

Dosage Amoxicillin (Amoxil) Standard dose for ch 

risk factors > age 24 

80-90 mg/kg/d (bid) × 10 d Amoxicillin-clavulanate (Augmentin) Alternative to high-do 

gastrointestinal intole 

10 mg/kg/d × 1 d then 5 mg/kg/d Cefdinir (Omnicef) 

× 4 d 

Alternative to high-do 

10 mg/kg/d (qd) × 10 d Cefprozil (Cefzil) 

50 mg/kg/d IM × 3 d Cefuroxime axetil (Ceftin) 

15 mg/kg/d (bid) × 10 d Clindamycin (Cleocin) No activity against H 

catarrhalis 

8 mg/kg/d TMP 

40 mg/kg/d SMZ (bid) × 10 d 


DRSP = drug resistant Streptococcus 

pneumoniae. 





TABLES 

Table 48-15. Drugs used for the treatment of acute otitis media.

Table 48-16. Differential diagnosis of periorbital swelling. 1 

Onset Other Features 

Rapid Usually unilateral 

Tender swelling with fever 

Variable Tense or soft nontender 

Swelling not associated with fever 

Variable Bite may be visible 

Rapid Bilateral, nontender, afebrile 

Days Unilateral or bilateral evidence of sinusitis

Table 48-17. Causes and antibiotic therapies for septic arthritis and osteomyelitis in infants and childre 

Possible Pathogen Therapy for Osteomyelitis 

Gram negative rods, group B streptococcus Ampicillin, 200 mg/kg/d, plus gentamicin, 7.5 mg/kg/d 

S aureus, rarely H influenzae Nafcillin, 100-200 mg/kg/d, plus cefotaxime, 150 mg/kg/d 

S aureus, group A streptococcus Nafcillin, 100-200 mg/kg/d

Table 48-18. Exanthems. 1 

Usual Age Prodrome Distribution Dia 

Adolescents/young adults Absent or low-grade 

fever, malaise, upper 

respiratory symptoms 

Begins on face and moves 

downward rapidly 

Young children Fever (occasional) Usually generalized, may be 

acral 

5 months to 5 years Fever, symptoms of upper 

respiratory infection 

Under 3 years High fever for 3-5 days 

prior to exanthem 

Any age Fever, malaise, 

headache, restlessness 

1-6 years Upper respiratory 

symptoms with 

generalized 

lymphadenopathy and 

hepatosplenomegaly 

Rubella IgM or 

acute/convales 

serologic test 

Usually clinical 

throat, rectal sw 

cases 

Generalized Viral isolation o 

acute/convales 

seroconversion 

Trunk, neck, may be 

generalized, lasts hour to 

days 

Wrists, ankles, plams, soles, 

later trunk 

Face, arms, legs, buttocks, 

spares the torso 

Under 5 years None Eruption with intensification in 

neck, face, axillae, and groin 

< 2 years Malaise, fever, symptoms 

of upper respiratory 

infection 

Any age Malaise, fever, itching, 

burning 


Trunk, extremities, palms, 

soles 

Clinical 

Serologic test 

Clinical; hepati 

Epstein-Barr se 

elevated liver f 

Clinical: culture 

systemic site (n 

Clinical, blood 

Palms, soles, back of hands Clinical 





TABLES 

Table 48-18. Exanthems.

Table 48-19. Common nontraumatic causes of abdominal pain. 

Clinical Entity 

and Demographics 

Meckel diverticulitis 

Mean: 2 years 


and Laboratory Findings 

Anemia, elevated blood urea nitrogen 

and creatinine 

Intussusception Fever, distension (late), right-sided 

mass; dehydration, anemia, 

leukocytosis (late) 

Malrotation/ midgut 

volvulus 

Normal (early), tenderness, possible 

distension, peritonitis (late); 

dehydration; anemia; leukocytosis 

(late) 

Hirschprung disease Asymptomatic (early), lethargy, fever, 

obtunded, shock (late), abdominal 

distension, normal or hyperactive 

bowel sounds 

Ectopic pregnancy Positive urine pregnancy test, lower 

quadrant pain and tenderness, 

amenorrhea, adnexal tenderness 

Influenza Altered breath sounds, low grade 

fever 

Cystitis Suprapubic tenderness, pyuria, 

bacteruria, varying degrees of 

hematuria 

99m recommended 



Ultrasound: pericolic or appendiceal 

fluid; edema 

Abdominal CT scan with intravenous 

contrast: enlarged appendix or right 

lower quadrant stranding or fluid 

5-9 months 

Abdominal CT scan with intravenous 

contrast: decreased enhancement, 

enlargement of kidney 





TABLES 

Table 48-19. Common nontraumatic causes of abdominal pain.

Table 48-20. Evaluation of the newborn infant using the APGAR score. 

Score 

1 Appearance (color) Pink trunk and 

pale limbs

Table 48-21. Equipment required for neonatal resuscitation. 1 

Prehospital/ 

Field 

Blankets (warm) 

Thermometer, 

temperature probe 

+ 

+ Lighting + 

+ Suction catheter 

with syringe 

± Face masks 

(preterm, term) 

+ 

+ Anesthesia bag, 

manometer 

+ 

+ Stylet ± 

+ Oral airways 

(000-0) 

± 

Spare bulbs and 

batteries 

+ 

+ Hemostat, 

forceps, scissors, 

scalpel 

+ 

Resuscitation 

drugs 

+ 

ECG monitor + 

Blood gas 

machine 

+ 

+ Defibrillator + 

Thoracostomy tray + 

Grossman M, Dieckmann RA (editors). Lippincott, 1991. 






TABLES 

Table 48-21. Equipment required for neonatal resuscitation.

Table 48-22. Differential diagnosis of skin lesions in child abuse. 

Diagnostic Procedure 

Trauma Hemophilia von Willebrand disea

Table 48-23. Sexually transmitted diseases in children. 1 

Nonabusive Transmission 

Organism Clinical Features 

Nonsexual 

Contact 

3-7 days Yes, neonatal conjunctivitis Chlamydia trachomatis 

5-7 days Yes Condyloma 

acuminatum, human 

papillomavirus 

3-28 days Yes, neonate may carry in the vagina for 

3-6 weeks after birth 

Grossman M, Dieckmann RA (editors). Lippincott, 1991. 

Syphilis

Figure 48-1. Relationship of blood volume to blood pressure in children during acute 

blood loss. (Reproduced, with permission, from Schwaitzberg SD, Bergman KS, Harris 

BH: A pediatric trauma model of continuous hemorrhage. J Pediatr Surg 1988;23:605.) 






FIGURES 

Figure 48-1

Figure 48-2. Treatment algorithm for pediatric uncompensated shock. 






FIGURES 

Figure 48-2

Figure 48-3. Treatment algorithm for pediatric stridor. 






FIGURES 

Figure 48-3

Figure 48-4. Lateral soft tissue x-ray of the neck, showing thumbprint sign of epiglottitis. 






FIGURES 

Figure 48-4

Figure 48-5. Management of asthma exacerbation: emergency department and 

hospital-based care. FEV 1 = forced expiratory volume in 1 second; PEFR = peak 

expiratory flow rate. (Reproduced from National Institutes of Health: National Asthma 

Education and Prevention: Practical Guide for the Diagnosis and Management of 

Asthma, p. 29. NIH Publication No. 97-4053. National Institutes of Health, 1997.) 






FIGURES 

Figure 48-5

Figure 48-6. Management of status epilepticus. ICP = intracranial pressure; ICU = 

intensive care unit; PE = phenytoin equivalent; PR = per rectum. (Reproduced, with 

permission, from Chiang VW: Seizures. Page 578 in: Fleisher G [editor]: Pediatric 

Emergency Medicine, 4th ed. Williams & Wilkins, 2000.) 






FIGURES 

Figure 48-6

Figure 48-7. Algorithm for the management of a previously healthy infant (birth to 90 

days) with fever without a source with a temperature of 38 °C (100.4 °F) or greater. CSF 

= cerebrospinal fluid; WBC = white blood cell. (Reproduced, with permission, from 

Baraff LJ: Management of fever without a source in infants and children. Ann Emerg 

Med 2000; 36:605.) 






FIGURES 

Figure 48-7

Figure 48-8. Algorithm for the management of a previously healthy child (3-36 months) 

with fever without a source. ANC = absolute neutrophil count; WBC = white blood cell. 

(Reproduced, with permission, from Baraff LJ: Management of fever without a source in 

infants and children. Ann Emerg Med 2000; 36:605.) 






FIGURES 

Figure 48-8

Figure 48-9. Antibiotic choices for acute otitis media. TPC = tympanocentesis with 

culture and susceptibility testing. Recommendations are for children aged 3-36 months 

with acute otitis media (AOM). 1 If fully vaccinated with pneumococcal conjugated 

heptavalent vaccine, cefixime can be used as an alternative second-line antibiotic. 2 

Azithromycin (5 days) may be an alternative for the older child with recurrent AOM who 

has (1) concomitant pneumonia suggestive of atypical pathogens or (2) significant 

gastroenteritis. Because azithromycin has limited coverage of Haemophilus influenza 

(~50%), some experts recommend adding trimethoprim-sulfamethoxazole. 3 Also AOM 

with concomitant conjunctivitis. 4 Also AOM with concomitant impetigo. 5 Augmentin 

ES-600 may be substituted. (Reproduced, with permission from Block SL, Harrison CJ: 

Diagnosis and Management of Acute Otitis Media, 1st ed. Professional 

Communications, 2001.) 






FIGURES 

Figure 48-9

Figure 48-10. Antibiotic choices for acute otitis media for the penicillin-allergic child. 

TMP-SMZ = trimethoprim-sulfamethoxazole; TPC = tympanocentesis with culture and 

susceptibility testing. Recommendations are for children aged 3-36 months with acute 

otitis media (AOM). 1 Because azithromycin has limited coverage of Haemophilus 

influenza (~50%), some experts recommend adding TMP-SMZ. Also AOM with 

concomitant pneumonia suggestive of atypical pathogens. 2 Also AOM with concomitant 

conjunctivitis. 3 With concomitant impetigo (Staphylococcus aureus). In AOM, coverage 

of ß-lactamase-positive H. influenza is 10-25%. (Reproduced, with permission from 

Block SL, Harrison CJ: Diagnosis and Management of Acute Otitis Media, 1st ed. 

Professional Communications, 2001.) 






FIGURES 

Figure 48-10

Figure 48-11. Algorithmic approach to vomiting in children. 






FIGURES 

Figure 48-11

Figure 48-12. Treatment algorithm for melena and hematemesis. 






FIGURES 

Figure 48-12

Figure 48-13. Treatment algorithm for hematochezia. 






FIGURES 

Figure 48-13

Figure 48-14. Posteroanterior (A) and lateral (B) chest x-rays, showing esophageal 

foreign body. 






FIGURES 

Figure 48-14

Figure 48-15. Clinical pathway: management of the febrile child with sickle cell disease. 

Give antibiotics emergently—before obtaining diagnostic studies—if signs of toxicity or 

sepsis are present. (May draw blood cultures if done expediently.) The evidence for 

recommendations is graded using the following scale: Class I = definitely 

recommended. Definitive, excellent evidence provides support. Class II = acceptable 

and useful. Good evidence provides support. Class III = may be acceptable, possibly 

useful. Fair-to-good evidence provides support. Indeterminate = continuing area of 

research. (Reproduced, with permission, from Freeman L: Sickle cell disease and other 

hemoglobinopathies: approaches to emergency diagnosis and treatment. Emerg Med 

Practice 2001;3[12]:14.) 






FIGURES 

Figure 48-15

Figure 48-16. Algorithmic guide to neonatal resuscitation. 






FIGURES 

Figure 48-16

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