Stillbirth, by definition, involves death of the fetus; it increases the risk of death of the fetus in subsequent pregnancies (see High-Risk Pregnancy).
Etiology
Fetal death during late pregnancy may have maternal, placental, or fetal anatomic or genetic causes (see table Common Causes of Stillbirth).
Common Causes of Stillbirth
Type |
Examples |
|
Maternal |
Diabetes mellitus if uncontrolled Morbid obesity (body mass index [BMI] ≥ 40 kg/m2) Trauma |
|
Placental |
Intra-amniotic infection (chorioamnionitis) Fetomaternal hemorrhage Twin-twin transfusion Umbilical cord accidents (eg, prolapse, knots) Uteroplacental vascular insufficiency |
|
Fetal |
Alloimmune thrombocytopenia Fetal alloimmune or inherited anemia Infection Major congenital malformations (particularly of the heart or brain) Nonimmune hydrops fetalis Single-gene disorders |
Complications
If a fetus dies during late pregnancy or near term but remains in the uterus for weeks, consumptive coagulopathy or even disseminated intravascular coagulation (DIC) may occur.
Diagnosis
The diagnosis of stillbirth is clinical.
Tests to determine the cause of stillbirth include the following:
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General examination of the stillborn fetus (eg, physical appearance, weight, length, head circumference [1])
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Fetal karyotype
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Maternal complete blood count (CBC) for evidence of anemia or leukocytosis
-
Kleihauer-Betke test
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Directed screening for acquired thrombotic disorders, including tests for antiphospholipid antibodies (lupus anticoagulant, anticardiolipin [IgG and IgM], anti-beta2 glycoprotein I [IgG and IgM])
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TORCH test (toxoplasmosis [with IgG and IgM], other pathogens [eg, human parvovirus B19, varicella-zoster viruses], rubella, cytomegalovirus, herpes simplex)
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Rapid plasma reagin (RPR)
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Thyroid-stimulating hormone (TSH), and if abnormal, free T4 (thyroxine)
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Diabetes testing (HbA1C)
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Examination of the placenta
Testing for hereditary thrombophilia is controversial and is not routinely recommended. The association between stillbirth and hereditary thrombophilia is not clear but does not appear to be strong, except for possibly factor V Leiden mutation. Testing (eg, for factor V Leiden) can be considered when severe abnormalities are detected in the placenta, intrauterine growth restriction occurs, or the woman has a personal or family history of thromboembolic disorders (1).
Often, cause cannot be determined.
Diagnosis reference
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1. American College of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine: Management of stillbirth. Obstetric Care Consensus No. 10, 2020.
Treatment
Uterine evacuation may have spontaneously occurred. If not, evacuation should be done using drugs (eg, oxytocin) or a surgical procedure (eg, dilation and evacuation [D & E], preceded by preabortion osmotic dilators to prepare the cervix, with or without misoprostol), depending on the gestational age.
After the products of conception are expelled, curettage may be needed to remove any retained placental fragments. Fragments are more likely to remain when stillbirth occurs very early in the pregnancy.
If DIC develops, coagulopathy should be promptly and aggressively managed by replacing blood or blood products as needed.
Postdelivery management is similar to that for live birth.
Parents typically feel significant grief and require emotional support and sometimes require formal counseling. Risks with future pregnancies, which are related to the presumed cause, should be discussed with patients.
Key Points
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There are many causes of stillbirth (maternal, fetal, or placental).
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Disseminated intravascular coagulation may develop secondarily.
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Do tests to determine the cause; however, the cause often cannot be determined.
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Evacuate the uterus using drugs or D & E, and provide emotional support to the parents.
