Recurrent pregnancy loss: Evaluation and discussion of the causes ...

MEDICAL PROBLEMS IN PREGNANCY 

ROBERT KIWI, MD 

Department of Obstetrics and Gynecology, 

Cleveland Clinic 

Recurrent pregnancy loss: 

Evaluation and discussion 

of the causes and their management 

■ ABSTRACT 

Women who miscarry two or more consecutive 

pregnancies deserve an evaluation to look for the cause, 

which sometimes can be treated. They can also be 

reassured that approximately 70% of women in this 

situation ultimately succeed in having a baby, even 

though the cause of recurrent miscarriage can be 

determined in only about half of cases. 

■ KEY POINTS 

Chromosomal abnormalities account for more than 50% 

of pregnancy losses. Some couples can overcome this 

problem by in vitro fertilization. 

Some uterine anomalies, such as a septate uterus, can be 

surgically corrected. 

Cerclage for cervical incompetence should be performed 

late in the first trimester. 

Luteal phase defect is generally treated with 

progesterone, although the benefit of this therapy is 

uncertain and it may cause hypospadias in the infant. 

Women with polycystic ovary disease should be treated 

with metformin until 12 to 20 weeks of gestation. 

If pregnancy loss is attributed to antiphospholipid 

antibodies or systemic lupus erythematosus, in 

subsequent pregnancies women can be treated with 

prednisone throughout the first trimester, as well as with 

aspirin and possibly heparin. 

M 

ANY THINGS can go wrong in pregnancy. 

The cause of a miscarriage can reside in 

one’s genes, anatomy, endocrine system, 

immune system, blood-clotting system, or 

environment—but in many cases no cause 

can be found. 

The experience can be painful for the 

couple, especially if they have lost several 

pregnancies in a row. Fortunately, most couples 

ultimately succeed in having a baby, 

regardless of the cause of their recurrent pregnancy 

loss or their treatment. 

This paper discusses known and suspected 

causes of recurrent pregnancy loss and how to 

evaluate and treat the problem. 

■ ‘RECURRENT’ MEANS THREE 

CONSECUTIVE LOSSES 

Recurrent pregnancy loss (also called recurrent 

abortion, recurrent spontaneous abortion, 

and recurrent miscarriage) is usually 

defined as three or more losses in a row. 

About 15% of couples lose one recognized 

pregnancy, and 2% lose two. The theoretical 

risk of three or more losses is only 0.34%. 

Only two consecutive losses is cause enough 

to evaluate some patients, particularly those 

who are older or who have a history of infertility. 

Most miscarriages occur within 12 

weeks of conception. 

The cause of recurrent pregnancy loss is 

often very difficult to assess. In fact, the cause 

The author has indicated that he has served on the speaker’s bureaus of 

the Adeza Biomedical and Aventis corporations. 

CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 73 • NUMBER 10 OCTOBER 2006 913 

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RECURRENT PREGNANCY LOSS 

KIWI 

Most 

miscarriages 

are in the first 

trimester 

can be determined in only about half of 

patients. 

■ CHROMOSOMAL ABNORMALITIES 

Chromosomal abnormalities account for more 

than half of recurrent pregnancy losses. Most 

of the losses are in the first trimester; about 2% 

to 5% of all fertilized ova contain chromosomal 

abnormalities at conception, but this 

number falls to fewer than 1% in fetuses at 

term. 1,2 

Aneuploidy 

Aneuploidy means having a different number 

of chromosomes than the 46 found in the normal 

(euploid) cell. 

Trisomy (having one additional whole or 

partial chromosome) accounts for 52% of all 

pregnancy losses due to chromosomal abnormalities. 

About 16% of losses due to chromosomal 

abnormalities are due to trisomy 16; trisomy 

13, 18, and 21 account for 9% and are 

found in 0.1% of live births, with trisomy 21 

being the most common. 3 

Monosomy (having only one chromosome 

of a normally diploid pair) accounts for 

18% of pregnancy losses due to chromosomal 

abnormalities; 98% of these losses are in the 

first trimester. 4 The 45,X genetic pattern is the 

most common genetic cause of recurrent pregnancy 

loss; nevertheless, this pattern is present 

in up to 7 of 10,000 live births. 

Triploidy (having three complete haploid 

sets of chromosomes instead of two, for a total of 

69 chromosomes) accounts for 17% of pregnancy 

losses due to chromosomal abnormalities. 

Mosaicism is more than one chromosomal 

pattern in a single person. The most common 

mosaic abnormality is 45,X/46,XX. 

Translocation 

In 6% to 7% of cases of recurrent pregnancy 

loss, one or both parents carry a chromosomal 

translocation. Of these, 35% are robertsonian 

translocations (the fusing of the two long arms 

of paired chromosomes into a single chromosome, 

usually followed by the loss of the short 

arms), and 65% are reciprocal translocations 

(reciprocal exchange of segments between 

nonhomologous chromosomes with no gain or 

loss of genetic material). 5 

Many translocations involve chromosomes 

13, 14, 15, 21, and 22. 1,2 

More women than men carry translocations, 

because many affected men are sterile. 6 If a man 

carries a translocation, the chance of passing it 

on to an offspring is 2% to 5%; a woman has a 

10% to 20% chance of passing on a translocation 

she carries. 5,7 If a parent has a balanced 

translocation, the risk of an unbalanced translocation 

occurring in the fetus is about 4%. 

Do chromosomal abnormalities recur? 

Evidence is mixed as to whether chromosomal 

abnormalities tend to recur in subsequent 

pregnancies. Hassold 8 studied 40 couples and 

found a 70% recurrence risk with a prior aneuploid 

pregnancy vs 20% with a prior euploid 

pregnancy. Warburton et al 9 found no 

increased risk of chromosomal abnormalities 

in subsequent pregnancies after spontaneous 

abortions if the fetus carried an aneuploidy 

that is always lethal in utero or if the parents 

had normal chromosomes. 

Carriers of a translocation in chromosome 

22 almost always miscarry; a woman with a 

translocation involving breaks in chromosome 

13 or 14 has a 25% risk of spontaneous abortion. 

Parity and older maternal age. Rates of 

pregnancy loss are higher in women who have 

had more children, possibly because these 

women tend to be older: the risk rises with 

maternal age, whether or not the fetus is normal. 

In older women, oocytes tend to have 

more chromosomal abnormalities and the 

endometrium is less receptive. 

Treatment of genetic problems 

Selected couples who have lost pregnancies 

because of aneuploidy can undergo in vitro 

fertilization. The blastocysts are examined, 

and they are implanted only if they are chromosomally 

normal. 10 

If the mother has poor oocytes, the procedure 

can be done with donated eggs from a 

younger woman or a woman with proven fertility; 

the rate of normal live births is high. 11 

■ UTERINE ABNORMALITIES 

From 10% to 15% of women who have lost 

multiple pregnancies have uterine anomalies 

such as a partial or complete septum. 12–14 

914 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 73 • NUMBER 10 OCTOBER 2006 


These anomalies can cause fetal loss in all 

trimesters 15 via poor implantation because 

of abnormal vascularization of the septum, 16 

uterine distention (possibly resulting in cervical 

incompetence), abnormal placentation, 

an abnormal lower uterine segment 

and cervix, or an increase in uterine contractility 

resulting in preterm birth or pregnancy 

loss. 

Congenital müllerian abnormalities 

The paired müllerian ducts develop into the 

fallopian tubes, uterus, cervix, and the upper 

two thirds of the vagina. 

The prevalence of congenital müllerian 

anomalies used to be estimated as 2% of 

women, but now that magnetic resonance 

imaging, ultrasonography, and laparoscopy are 

being performed more often, it is estimated to 

be as high as 6%. 

Septate uterus, resulting from failure of 

resorption of the septum between the two 

uterine horns, is associated with the greatest 

number of pregnancy losses, particularly if a 

complete septum remains. 16,17 Other anomalies 

include uterus didelphys (a double 

uterus, resulting from complete nonfusion of 

the müllerian ducts) and bicornuate uterus 

(from partial nonfusion of the müllerian 

ducts), but they are less likely to cause recurrent 

pregnancy loss. 17 

Women who have an untreated uterine 

septum have a fetal survival rate of only 6% to 

28%, and more than 60% have recurrent 

pregnancy loss. 18 Treatment with transcervical 

uteroplasty results in a high pregnancy success 

rate. 13 

Congenital müllerian anomalies are 

linked to renal anomalies: 67% to 75% of 

women with a unicornuate uterus also have 

an absent or a bifid kidney, and 15% to 20% 

of patients with unilateral renal agenesis have 

a major genital anomaly. 19 

Diethylstilbestrol exposure 

Diethylstilbestrol (DES) was used in the 

United States until 1971, and women exposed 

to DES in utero have high rates of recurrent 

pregnancy loss. 20 For many, the cause is an 

abnormal lower uterine segment and cervix, 

resulting in cervical incompetence and 

preterm labor and birth. This problem should 

become rare as women of the generation 

exposed to DES reach the end of their childbearing 

years. 

Asherman syndrome 

(intrauterine synechiae) 

The prevalence of intrauterine synechiae 

(adhesions) is difficult to determine. In a series 

of 200 patients with adhesions, 43% were sterile 

and 14% had recurrent pregnancy loss. 21 

Uterine leiomyomata 

Submucous leiomyomata or fibroids can distort 

the uterine cavity and impede implantation. 

The association of subserosal and intramural 

fibroids with recurrent pregnancy loss is 

less clear. 

Cervical incompetence 

Cervical incompetence classically causes losses 

in the second trimester (gestational weeks 

12 to 28). It is associated with painless cervical 

dilatation and expulsion of the fetus. The 

diagnosis requires two consecutive losses. 

Cervical incompetence can be caused by 

congenital factors (eg, DES exposure), trauma 

(including forceps delivery, especially if performed 

before dilatation is complete), and 

surgical procedures (eg, cervical cone biopsies, 

laser procedures, and loop electrocautery excision 

procedures). 

The chance of carrying the baby to term 

can be improved by placing a cervical cerclage 

at 10 to 14 weeks, after fetal viability has been 

confirmed. 

■ HORMONAL CAUSES 

OF PREGNANCY LOSS 

Luteal phase defect 

The reported prevalence of luteal phase defect 

in patients with recurrent pregnancy loss 

varies from 23% to 60%. 22 Whether and how 

it causes pregnancy loss is unclear. 23 

Epidemiologic studies suggest that low 

progesterone levels, possible due to impaired 

folliculogenesis, 24 play a role in recurrent 

pregnancy loss. Progesterone is essential for 

maintaining early pregnancy. Low levels of 

progesterone-associated endometrial protein 

have been reported in patients with luteal 

phase defects, and this abnormality may result 

The risk of 

pregnancy loss 

increases with 

parity and 

maternal age 




KIWI 

Septate uterus 

can be repaired 

transcervically 

in recurrent pregnancy loss. 25 Progesterone 

also has an immunosuppressive effect, which 

may help maintain pregnancy. It also relaxes 

uterine muscles, possibly by inhibiting 

prostaglandins, which may help keep the 

uterus from contracting prematurely. 26 On the 

other hand, serum progesterone levels are not 

predictive of pregnancy outcome. 27 

Progesterone supplements are often used 

to support early pregnancy in patients with 

recurrent pregnancy loss and luteal phase 

defect. Generally recommended are vaginal 

suppositories of progesterone 50 mg twice a 

day or newer once-a-day formulations such as 

progesterone gel (Crinone 8%). 

But two meta-analyses published simultaneously 

had conflicting findings on whether 

progesterone supplementation actually 

helps. 28,29 Moreover, it may cause birth 

defects: Carmichael et al, 30 in a case-control 

study involving 502 babies with severe 

hypospadias, found that taking progestins during 

pregnancy was associated with a significantly 

increased risk of this anomaly. 

Clomiphene citrate 50 mg on days 5 

through 9 of the menstrual cycle is usually prescribed 

for either irregular menstrual cycles or 

luteal phase defect. 

Thyroid hormone 

Thyroid abnormalities are infrequently diagnosed 

during pregnancy and are rare in women 

with recurrent loss. Patients with treated thyroid 

dysfunction do not have an increased risk 

of miscarriage. 31 More women with recurrent 

pregnancy loss have antithyroid antibodies 

than in the general population, but evidence 

that these antibodies actually cause pregnancy 

loss is lacking. 32 

Pregestational diabetes mellitus 

Women with poorly controlled diabetes (as 

reflected by hemoglobin A 1c levels greater 

than 8%) have higher rates of spontaneous 

abortion in early pregnancy than women 

without diabetes, and the children they carry 

to term have more congenital anomalies. 

However, these risks are not higher in women 

with subclinical diabetes or well-controlled 

disease. 33 Miodovnik et al 34 did not find an 

increased risk of recurrent pregnancy loss 

among diabetic women. 

Polycystic ovary disease 

From 20% to 40% of patients with recurrent 

pregnancy loss have polycystic ovary disease, 

compared with 10% to 20% of women in the 

general population. 35 

Abnormalities in polycystic ovary disease 

can include high levels of luteinizing hormone, 

glucose, and insulin, 36 the latter due to 

insulin resistance. Patients suspected of having 

polycystic ovary disease should have fasting 

insulin levels measured as part of their 

evaluation. 

Metformin 1,000 to 1,500 mg/day seems 

to reduce the rate of spontaneous abortions in 

the first trimester in patients with polycystic 

ovary disease. 37 It also improves ovulation 

cycles and increases the rate of conception. 

Treatment should be continued until 12 to 20 

weeks of gestation. 38 Metformin does not cross 

the placenta, and there is no evidence that it 

increases the incidence of congenital anomalies 

when taken throughout the first 

trimester. 

■ IMMUNOLOGIC FACTORS 

Immunologic factors have long been proposed 

as causes of recurrent pregnancy loss because 

the fetus contains paternal antigens, which are 

immunologically foreign. 39,40 Evidence suggests 

that the fetus and placenta are protected 

by local immunomodulating factors and that 

pregnancy loss may result from a breakdown of 

immune homeostasis. 

‘Blocking-factor deficiency’ 

One theory of recurrent pregnancy loss is that 

the mother’s immune system mounts a cellmediated 

response against the fetus, that antibodies 

develop in all successful pregnancies to 

block this response, and that without these 

blocking antibodies, abortions always occur. 

However, no direct evidence shows that the 

conceptus is immunologically attacked in the 

absence of blocking factors. 41 

Dysregulation of a normal immunologic 

mechanism that operates at the maternal-fetal 

interface may involve activity of natural killer 

cells in the endometrium, which appear to 

regulate effects that support pregnancy, such 

as promoting placental and trophoblast 

growth and trophoblast invasion and modulat- 



ing the immune system at a local level. 42 

The topic is ripe for investigation, but 

endometrial factors are impractical to evaluate 

in vivo. Many immunologic tests can be 

used only indirectly to try to define an 

immune dysfunction, especially for very early 

repeated failures or unsuccessful pregnancies 

by in vitro fertilization. 

Treatment. In the past, patients without 

blocking antibodies and with antipaternal 

antibodies were treated by immunization 

using white blood cells from the spouse, but 

this treatment is no longer available. 

Immunoglobulin G contains antibodies 

that block T cell receptors, which inhibit natural 

killer cell activity. Intravenous immunoglobulin 

infusions are still used in cases in which antibody 

test results are interpreted as being associated 

with recurrent pregnancy loss. However, 

the value of intravenous immunoglobulin G 

therapy is still controversial, and it should be 

considered experimental. 43,44 

Antiphospholipid antibody syndrome 

Antiphospholipid antibodies consist of anticardiolipin 

antibodies and lupus anticoagulant; 

one or the other is present in 5% to 15% 

of women with recurrent pregnancy loss. 45 

Recurrent pregnancy loss and late fetal death 

may occur because of placental infarction or 

impaired trophoblast function. 46 Another 

hypothesis is that complement activation is a 

central mechanism of pregnancy loss in 

antiphospholipid antibody syndrome. 47 

The diagnosis of antiphospholipid antibody 

syndrome requires at least one clinical 

criterion (arterial, venous, or small-vessel 

thrombosis in any organ or tissue, or recurrent 

pregnancy loss) plus at least one laboratory 

criterion (positive anticardiolipin antibody, 

lupus anticoagulant, or B2 glycoprotein-1 

antibodies on two or more occasions at least 6 

weeks apart). 

Patients with high levels of anticardiolipin 

antibodies who have had a fetal death 

seem to be at high risk of future loss. 

Systemic lupus erythematosus 

Systemic lupus erythematosus (SLE) is present 

in 1 in 5,000 pregnancies. 48 Spontaneous 

abortions occur in 10% to 40% of women 

with SLE. 49 Recurrent losses, particularly 

those that occur after 20 weeks of gestation, 

appear to be associated with a vasculopathy of 

the decidua (the inner wall of the uterus, 

which envelops the embryo). 50 

The risk of fetal loss is increased in 

patients with hypertension, active SLE, lupus 

nephritis, or abnormally low complement levels. 

51 Risk is also increased for patients with 

antiphospholipid antibodies: from 6% to 24% 

of patients with SLE are positive for lupus 

anticoagulant, 52 and 40% are positive for 

anticardiolipin antibodies. 49 

Treatment for antiphospholipid antibody 

syndrome and SLE 

Aspirin 80 mg per day can be used for 

patients with low-level antiphospholipid antibodies, 

lupus anticoagulant, or anticardiolipin 

antibodies, although there are no outcome 

data on this approach. 

Low-molecular-weight heparin is recommended 

for patients with recurrent pregnancy 

loss or early fetal demise associated with SLE, 

lupus anticoagulant, or antiphospholipid antibodies. 

Generally, enoxaparin (Lovenox) 1 

mg/kg or dalteparin sodium (Fragmin) 5,000 

units daily by subcutaneous injection is recommended. 

Antifactor Xa should be kept in the 

range of 0.5 to 1.0 IU/mL. Combined aspirin 

and heparin is recommended for managing 

recurrent or late pregnancy loss in patients with 

SLE or antiphospholipid antibodies. 

Prednisone. Patients with SLE with or 

without lupus anticoagulant and anticardiolipin 

antibody have been treated with prednisone 

and aspirin or heparin, or all three. 

Aspirin plus heparin appears to be the better 

approach for the management of both recurrent 

pregnancy loss and late pregnancy loss. 

Patients with active lupus should ideally 

be treated before the onset of pregnancy and 

should be in remission preferably for about 6 

months before attempting pregnancy. It 

should be noted that prednisone is used for 

treatment of the disease and not simply for 

patients with recurrent pregnancy loss with a 

positive antinuclear antibody titer. 

Patients with SLE in remission who are 

taking prednisone in a low dose at the onset of 

pregnancy should continue taking it at the 

same dose. Prednisone is often started in 

patients who are in a lupus flare at the onset of 

Data are mixed 

on whether 

progesterone 

supplements 

improve 

pregnancy 

outcomes 




KIWI 

The most 

common 

inherited 

thrombophilic 

disorders are 

factor V Leiden 

and 

prothrombin 

G20210A 

mutations 

pregnancy to control lupus activity and maximize 

the chance of a successful pregnancy. For 

patients with recurrent pregnancy loss, the 

dose should be maintained throughout the first 

trimester and then tapered. Often, patients 

with active SLE or with multiorgan involvement 

are co-managed by a rheumatologist. 

Prednisone has not been shown to be 

associated with congenital anomalies in 

humans, but intrauterine growth retardation 

and gestational diabetes may develop in 

patients who are maintained on prednisone 

throughout pregnancy. However, active SLE is 

also associated with poor fetal outcome. 

■ THROMBOPHILIAS 

Patients with an inherited thrombophilia may 

have recurrent pregnancy loss due to coagulopathy, 

especially in the second or third 

trimester. Thrombosis of the spiral arterioles 

in the intervillous space may impair placental 

perfusion and lead to abnormal uteroplacental 

circulation, causing late fetal loss, intrauterine 

growth retardation, and placental abruption. 

Whether pregnancy loss in the first trimester 

also occurs by this mechanism is uncertain. 53 

The most common inherited thrombophilic 

disorders are the factor V Leiden 

mutation and the prothrombin G20210A 

mutation. Factor V Leiden, an autosomaldominant 

mutation, is present in 5% of white 

people. Dizon-Townson et al, 54 in a case-control 

study, found that the prevalence of the 

factor V Leiden mutation was twice as high 

among the mothers of 139 spontaneously 

aborted fetuses compared with unselected 

pregnant women. On the other hand, 

Lockwood 55 states that whether this mutation 

is a factor in first-trimester pregnancy loss is 

uncertain. 

Other inherited thrombophilias include 

deficiencies of protein S, protein C, and 

antithrombin, which produce a hypercoagulable 

state that is associated with thromboembolic 

and other obstetrical complications during 

pregnancy. Whether they cause recurrent 

pregnancy loss is unclear. 

Low-molecular-weight heparin is recommended 

for patients with recurrent pregnancy 

loss or early fetal demise associated with 

thrombophilia. 

■ INFECTION 

No evidence suggests that infection causes 

recurrent pregnancy loss, although infections 

with Listeria monocytogenes, cytomegalovirus, 

and Toxoplasma gondii may cause sporadic losses. 

To plausibly cause repeated loss, an organism 

must persist in the genital tract, but possible 

culprits, including toxoplasmosis, rubella, 

cytomegalovirus, and herpes infections, do not 

fulfill the criteria for recurrent loss, ie, persistence 

or spontaneous recurrence of infection 

involving maternal, fetal, or placental tissues. 

56 

■ ENVIRONMENTAL AGENTS 

Data are limited linking recurrent pregnancy 

loss with environmental agents, occupational 

factors, or stress. Sporadic losses have been 

associated with anesthetic agents, 57 smoking, 

alcohol, and caffeine. 58 

■ CLINICAL EVALUATION 

Evaluation of a patient with recurrent pregnancy 

loss should include a detailed medical, 

surgical, family, genetic, and menstrual history. 

Patients should be questioned about their 

use of drugs, tobacco, alcohol, and caffeine, 

and whether they have been exposed to occupational 

hazards. 

All prior pregnancies should be examined 

in detail, with attention to gestational age at 

time of loss, complications, ultrasonography 

findings, pathology reports, and chromosomal 

analyses. 

Physical examination 

The physical examination should include 

evaluation of the thyroid for enlargement or 

goiter, evaluation of the breasts for galactorrhea, 

and examination for hirsutism, which 

could indicate the patient has thyroid dysfunction 

or hyperprolactinemia. 

The pelvic examination should include 

evaluation of the cervix if the patient may 

have been exposed to DES or has had cervical 

surgery. An enlarged uterus may be 

associated with fibroids, and enlarged 

ovaries may indicate polycystic ovary disease. 



Laboratory tests 

Laboratory tests should be selected on the 

basis of findings in each patient’s history and 

examination. 

Blood tests may include a complete blood 

cell count, antinuclear antibodies, anticardiolipin 

antibodies, lupus anticoagulant, prolactin 

levels, and thyrotropin levels. Chromosomes of 

both parents should be evaluated. 

Evaluation for thrombophilia includes 

testing for protein C, activated protein C, the 

factor V Leiden and prothrombin mutations, 

protein S, antithrombin, and the fasting 

homocysteine level. 

Timed endometrial biopsy can help confirm 

ovulation or evaluate a luteal phase 

defect. Although this procedure is controversial, 

it remains the best test for evaluating 

endometrial abnormalities. 

Testing for cytomegalovirus, Listeria, and 

toxoplasmosis is possible but is not generally 

recommended because these agents are associated 

with sporadic rather than recurrent pregnancy 

loss. 

Imaging tests 

Hysterosalpingography, three-dimensional 

saline ultrasonography, 59 and magnetic resonance 

imaging can help detect uterine 

abnormalities. 

Hysteroscopy and laparoscopy are useful if 

other tests have indicated abnormalities that 

should be confirmed, such as a uterine septum. 

In the future, these procedures are likely to be 

replaced by three-dimensional ultrasonography 

or magnetic resonance imaging. 

Review of pathology 

If possible, pathology slides from the aborted 

pregnancy should be reviewed by a placental 

pathologist, especially in cases in 

which no specific abnormalities were found 

during the evaluation or in the initial 

pathology report. 

Additional tests 

The usefulness of additional testing for natural 

killer cells, antipaternal antibodies, blocking 

antibodies, cytotoxic antibodies, and 

HLA antibody typing is questionable: 

whether these antibodies relate to pregnancy 

loss is doubtful. 

■ MONITORING THE PREGNANCY 

Human chorionic gonadotropin beta 

should be measured quantitatively starting at 

the patient’s missed period and be repeated 2 

or 3 times per week until fetal viability is 

established. 

Ultrasonography should be done at 6 to 

6-1/2 weeks and repeated every 10 to 14 days 

until approximately 12 weeks of gestation. 

Frequent and early ultrasonography has several 

advantages: a viable fetus is a good indicator 

that the pregnancy will be successful, seeing 

a viable fetus offers the mother significant 

psychological benefit, and an unsuccessful 

pregnancy can be detected quickly, increasing 

the chance that placental tissue can be 

obtained for chromosomal analysis. 

Genetic testing with chorionic villous 

sampling or amniocentesis should be offered. 

■ PSYCHOLOGICAL SUPPORT 

SHOULD BEGIN EARLY 

Psychological support and counseling should 

start before conception and continue 

throughout the first trimester and beyond. 

Patients should attend a reproductive loss 

clinic if available. 

Loss of a pregnancy at any gestational age 

can trigger a significant grief reaction. Early 

loss was once considered less traumatic than 

stillbirth or neonatal death, but a better predictor 

of the severity of a grief reaction may be 

the degree of attachment to the pregnancy. 60 

Women who suffer recurrent pregnancy 

loss may experience cumulative grief and 

increasing ambivalence during subsequent 

pregnancies. Patients may develop a protective 

emotional shield during pregnancy in an 

attempt to reduce the pain of impending loss. 

Seeing a healthy fetus with early ultrasonography 

may help a woman who has suffered 

recurrent pregnancy loss form an attachment 

during pregnancy. On the other hand, 

facilitating early bonding can backfire if the 

pregnancy is again unsuccessful. 61 

■ PROGNOSIS IS GOOD 

Various factors influence the risk of a recurrent 

loss, which increases from 14% to 21% after 

For couples 

with recurrent 

pregnancy loss, 

counseling 

should start 

before 

conception 




KIWI 

one miscarriage, to 24% to 29% after two losses, 

to 31% to 33% after three losses. The risk of 

miscarriage decreases after a pregnancy that 

results in a live birth. 

A positive attitude when managing couples 

with recurrent pregnancy loss is important 

and statistically justified: the chance of 

eventually having a successful pregnancy is 

about 70% regardless of evaluation findings 

and treatments. 18 

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