Placental Abnormalities
James Wong III
Megan C. Henn
Michelle D. Lall
OVERVIEW
The placenta is the lifeline of the growing fetus. Maternal blood enters the placenta through approximately 120 spiral arteries and pools in the intervillous space, exchanging oxygen and nutrients with fetal villi. A total of 600 to 700 mL of maternal blood passes through the placenta every minute, equating to the entirety of a mother’s circulating blood volume passing through the uterus every 10 minutes. Any compromise to this system can cause rapid exsanguination and lead to maternal or fetal death. Health care providers must be able to diagnose and manage the more common as well as rare, but potentially life-threatening, placental abnormalities.
ATRAUMATIC PLACENTAL ABRUPTION
Placental abruption, or abruptio placentae, is the premature separation of the normally implanted placenta. It is a serious obstetric complication associated with 12% of all perinatal deaths. Abruption occurs in 1% of all pregnancies, but overall incidence varies.1 An abruption starts as a hemorrhage into the decidua basalis, the area of the placenta adjacent to the uterine wall. The hemorrhage causes a split in the decidua and forms a hematoma. The hemorrhage may be self-limited and asymptomatic. An expanding hematoma can continue to grow, causing a separation of the decidua basalis that leads to a partial or complete separation of the placenta from the uterine wall (Figure 20.1). Depending on the extent of the separation, this can lead to life-threatening hemorrhage to the mother and inadequate gas exchange for the fetus, leading to fetal demise.
Etiology and Risk Factors
The etiology of placental abruption is not completely known but thought to be primarily a chronic vascular process starting early in pregnancy.2 Histologic studies reveal evidence of chronic infarcts on the placental-decidua interface that eventually lead to abruption later on in the pregnancy. An inflammatory process, either acute or chronic, is thought to be another potential cause supported by the histologic finding of macrophage and neutrophil infiltration throughout the placental abruption interface. A previous history of abruption carries the greatest association with a 15- to 20-fold increased risk. Maternal hypertension is another risk factor with a 3-fold increased risk. Additional risk factors include cocaine use, smoking, advanced maternal age, multiparity, autoimmune disease, thrombophilias, bicornuate uterus, and leiomyomas.3,4
 Figure 20.1: Types of placental abruption. (From Casanova R, Beckmann CRB, Ling FW, et al. Beckmann and Ling’s Obstetrics and Gynecology. 8th ed. Philadelphia, PA: Wolters Kluwer; 2018.) |
Clinical Features
Placental abruption classically presents as vaginal bleeding, abdominal pain (or back pain if attached to the posterior uterine wall), and uterine tenderness. In one study, 78% presented with vaginal bleeding, 66% with uterine or back pain, and 60% had nonreassuring fetal status.5 The physical examination may reveal evidence of maternal hypovolemia, uterine hypertonicity or tenderness, fetal bradycardia, or contractions.6 Uterine contractions are classically high frequency and low amplitude but vary considerably.7
The overall clinical picture must be considered as none of these findings are reliably found in all abruptions. Late pregnancy hemorrhage from placental abruption typically presents with painful bleeding, whereas placenta previa presents as painless bleeding; however, both may present atypically. Uterine bleeding may be concealed within the placental margins, termed a concealed abruption, and vaginal bleeding may not be present at all. Conversely, placenta previa occasionally presents during labor and, therefore, may also present with abdominal pain.
The degree of vaginal bleeding may not correspond to the severity of separation or the well-being of the fetus. A patient may present with profuse vaginal bleeding but have only a small partial abruption with no effect on the fetus, or conversely, the patient may present with scant bleeding but have a complete abruption and fetal demise. The fetal prognosis correlates more directly to the degree of placental separation. There is a 5.5-fold increased risk of preterm delivery with a 25% separation of the placenta, a 4-fold increased risk of stillbirth with a 50% separation, and a 31.5-fold increased risk with a 75% separation.8 The severity of abruption is based not only on the severity of symptoms but also on objective findings such as vital signs and evidence of fetal distress.
Classification System
Page’s clinical classification system for abruption is one of the most widely used and helps gauge the severity of an abruption in the acute setting9:
Class 0: asymptomatic but retroactively diagnosed postpartum
Class 1: none to minimal vaginal bleeding, no maternal or fetal distress, no vital sign abnormalities, slightly tender uterus
Class 2: none to moderate vaginal bleeding, moderate to severe uterine tenderness with contractions, maternal tachycardia, orthostatic blood pressure (BP) and heart rate (HR) changes, fetal distress, hypofibrinogenemia between 50 and 250 mg/dL
Class 3: none to heavy vaginal bleeding, very painful contractions, maternal shock, fibrinogen less than 150 mL/dL, coagulopathy, fetal death
Diagnostic Testing
The diagnosis of placental abruption is primarily clinical as there are no tests that can rule out abruption definitively. Moreover, the diagnosis of abruption is confounded by the physiologic
changes that occur in pregnancy, including lower BP, increased blood volume, and increased cardiac output. These physiologic changes may mask an otherwise obvious diagnosis of hypovolemic hypotension or hemodynamic instability through the increased circulatory reserve.
changes that occur in pregnancy, including lower BP, increased blood volume, and increased cardiac output. These physiologic changes may mask an otherwise obvious diagnosis of hypovolemic hypotension or hemodynamic instability through the increased circulatory reserve.
Laboratory Testing
Laboratory studies should include a complete blood count (CBC), blood type and screen, coagulation studies, complete metabolic panel (CMP) including liver function studies to assess for HELLP (Hemolysis, Elevated Liver enzymes, Low Platelet count) syndrome, urine drug screen (to assess for causes of abruption), and a Kleihauer-Betke test to evaluate for maternal-fetal hemorrhage. Certain laboratory values support a diagnosis of abruption if abnormal. A D-dimer is likely be elevated in an abruption. Studies suggest that a serum level of alpha-fetoprotein more than 280 µg/L has a strong association with abruption.10 A Kleihauer-Betke test has limited diagnostic utility but may support a diagnosis of abruption if positive.7,11 However, no laboratory value safely excludes abruption.
Ultrasound
Placental abruption hematomas have a variable appearance on ultrasound including hypo-, hyper-, or isoechoic compared to the placenta and can be both homogenous or heterogenous in consistency. The appearance of a hematoma on ultrasound depends on the amount of bleeding, the chronicity of bleeding, and to what extent the bleeding has escaped the uterus. If there is vaginal bleeding or uterine rupture, blood may not pool in the uterus and, therefore, will not be detectable by ultrasound. Placental positioning within the uterus plays a role in the likelihood of detecting intrauterine blood accumulation. Ultrasound is insensitive in the diagnosis of placental abruption with false-negative rates of 50% to 80%. In one study, ultrasound was only 24% sensitive in detecting placental abruption. Despite the poor sensitivity, ultrasound does have reliable positive predictive values of approximately 90%12; therefore, an ultrasound finding of a large hematoma dividing the placenta and the uterus with corresponding symptoms is likely to indicate placental abruption. The finding of a hematoma is associated with worse maternal and fetal outcomes; however, a severe abruption may be present despite no findings on ultrasound.
Despite its poor sensitivity for placental abruption, in clinical practice ultrasound is useful in undifferentiated vaginal bleeding in a pregnant patient to look for other causes, such as placenta previa, vasa previa, or molar gestation, all of which can be diagnosed via ultrasound. Additionally, because of its high positive predictive value, the finding of a retroplacental hematoma with symptoms consistent with abruption should be assumed to be placental abruption.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) is highly sensitive for placental abruption but is not appropriate for unstable patients. MRI is recommended for any patient that can tolerate the examination and if the findings will change management.13 Although MRI is not shown to be harmful to the fetus, there are concerns about energy deposition leading to fetal tissue heating as well as potential effects of acoustic noise. The American College of Radiology (ACR) recommends performing MRI on pregnant patients at magnetic field strengths of less than 1.5 Tesla and only using the minimal number of slices necessary.14,15 Intravenous (IV) gadolinium for MRI is relatively contraindicated as it is shown to produce adverse effects in animal models at doses higher than provided to humans. To date, there are no reported adverse effects to fetuses with the use of gadolinium. However, the theoretical risk is such that it should only be used in the rare circumstances of absolute necessity.
Fetal Monitoring
Fetal distress is one of the most concerning findings in the setting of abruption. This finding is the most useful tool for determining management and may also be the first indicator of maternal distress. Fetal hemodynamics are more sensitive to reductions in maternal blood flow and, therefore, may indicate warning signs prior to any hemodynamic instability in the mother. Prompt fetal monitoring for HR and contractions should be initiated soon after patient arrival. Signs of fetal distress include abnormal HR, reduced HR variability, and late decelerations.16 There is a close association between abnormal readings and fetal morbidity, so careful monitoring and prompt action is required.
A normal fetal heart rate (FHR) varies between 120 and 160 beats/min. A FHR outside of this range or trending toward the extremes of this range is cause for concern. HR variability is
important as beat-to-beat variability is an indicator of fetal autonomic nervous function and of fetal activity, and any reductions are concerning for fetal distress (Figure 20.2). Late decelerations are small-amplitude HR reductions that occur immediately after a uterine contraction and indicate fetal hypoxia. These differ from early decelerations that occur simultaneous to the contraction (due to fetal vagal response to head compression) and variable decelerations (umbilical cord compression) that are large in magnitude and occur at any time (Figure 20.3).
important as beat-to-beat variability is an indicator of fetal autonomic nervous function and of fetal activity, and any reductions are concerning for fetal distress (Figure 20.2). Late decelerations are small-amplitude HR reductions that occur immediately after a uterine contraction and indicate fetal hypoxia. These differ from early decelerations that occur simultaneous to the contraction (due to fetal vagal response to head compression) and variable decelerations (umbilical cord compression) that are large in magnitude and occur at any time (Figure 20.3).
 Figure 20.2: Fetal heart rate variability. A, Short-term variability absent, long-term variability absent—abnormal. B, Short-term variability present, long-term variability absent—abnormal. C, Short-term variability absent, long-term variability present—abnormal. D, Short-term variability present, long-term variability present—normal. (From Gibbs RS, Karlan BY, Haney AF, Nygaard IE. Danforth’s Obstetrics and Gynecology. 10th ed. Philadelphia, PA: Wolters Kluwer; 2008.) |
 Figure 20.3: Fetal heart rate decelerations. Late decelerations are an indicator of fetal distress and may warrant immediate cesarean delivery. (From Gibbs RS, Karlan BY, Haney AF, Nygaard IE. Danforth’s Obstetrics and Gynecology. 10th ed. Philadelphia, PA: Wolters Kluwer; 2008.) |
Management
The management priority for any placental abruption is to support the expectant mother. Continuous fetal monitoring including FHR and tocometer should be employed early in all viable pregnancies (>24 weeks or per hospital guidelines). The initial management strategy includes securing large-bore IV access, crystalloid fluids to maintain urine output greater than 30 mL/h, blood products as needed, displacing the uterus off the aorta and inferior vena cava, early obstetrics consultation, and close and early fetal monitoring as there may be limited time between fetal distress and the need for emergent cesarean section.
Provide Rh-negative mothers Rh immune globulin within 72 hours regardless of Kleihauer-Betke results as the test is not sensitive in detecting small quantities of bleeding. However, the Kleihauer-Betke test may reveal a significant fetal hemorrhage and additional Rh immune globulin may be indicated. Administer appropriate medications to patients in which delivery is likely including: group B strep prophylaxis, corticosteroids for pregnancies less than 34 weeks of gestation, and neuroprotective doses of magnesium sulfate for pregnancies less than 32 weeks of gestation. Do not provide tocolytic agents unless instructed by an obstetric consultant.
The decision between expectant management and delivery is largely based on gestational age, fetal status, and maternal status. At any given point during pregnancy, conservative management may be appropriate as long as both mother and fetus are stable. At less than 24 weeks’ gestation, stability is mainly focused on the mother. After 24 weeks’ gestation, both fetal and maternal stability are monitored closely, medications indicated for fetal prematurity are given, and the pregnancy is managed conservatively until early scheduled delivery at 37 to 38 weeks. Emergent cesarean delivery is warranted for any evidence of fetal or maternal instability.7
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