One third of all antepartum bleeding is due to AP, with an incidence of 1 in 75 to 1 in 225 births. The incidence increases with maternal age.
AP recurs in 5% to 17% of pregnancies after one prior episode and up to 25% after two prior episodes.
There is a 7% incidence of stillbirth in future pregnancies after AP leading to fetal death.
Bleeding does not correlate with abruption size and may vary from scant to massive.
AP without vaginal bleeding can result in delayed diagnosis and consumptive coagulopathy.
Blood in the basalis layer stimulates forceful, classically tetanic, uterine contractions leading to ischemic abdominal pain.
AP is associated with maternal hypertension, advanced maternal age, multiparity, cocaine use, tobacco use, chorioamnionitis, preterm premature rupture of membranes, coagulopathy, and trauma. Many cases are idiopathic.
Patients with chronic hypertension, superimposed preeclampsia, or severe preeclampsia have fivefold increased risk of severe abruption compared to normotensive women. Antihypertensive medications do not reduce the risk.
Cigarette smoking increases the risk of stillbirth from AP by 2.5-fold. The risk increases by 40% for each pack per day smoked.
Rapid changes in intrauterine volume can lead to abruption, such as rupture of membranes, therapeutic amnioreduction for polyhydramnios, or during delivery of multiple gestations.
Abruption occurs more frequently when the placenta implants on abnormal uterine surfaces as with submucosal myomas or uterine anomalies.
Hyperhomocysteinemia, factor V Leiden, and prothrombin 20210 mutations (thrombophilias) are associated with an increased risk of abruption.
TABLE 10-1 Important Steps in the Diagnosis and Management of Third-Trimester Vaginal Bleeding | |
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Massive maternal blood loss may lead to hemorrhagic shock (see Chapter 3).
Maternal disseminated intravascular coagulation (DIC) can occur and is found in 10% to 20% of AP with stillbirth.
Extravasation of blood directly into the uterine muscle (Couvelaire uterus) can lead to uterine atony and massive postpartum hemorrhage.
Fetal hypoxia may occur, leading to acute fetal distress, hypoxic-ischemic encephalopathy, premature delivery, and fetal death. Milder chronic abruption may lead to growth restriction, major malformations, or anemia.
Classically presents late in pregnancy with vaginal bleeding and acute severe abdominal pain. Even slight clinical suspicion should prompt rapid investigation and close monitoring.
Maternal vital signs, fetal heart rate assessment, and uterine tone should be evaluated immediately.
Mark or record the fundal height to follow expansion of concealed hemorrhage. Blood may be sequestered between the uterus and placenta when the placental margins remain adherent. Membranes or the fetus itself may obstruct the cervical os and prevent accurate assessment of blood loss.
Defer digital cervical exam until PP and VP have been ruled out.
Ultrasound is insensitive in diagnosing AP, but large abruptions may be seen as hypoechoic areas underlying the placenta.
Perform a speculum exam to evaluate vaginal or cervical lacerations and the amount of bleeding.
Complete blood cell count with hematocrit and platelets (<100,000 plts/µL suggests severe abruption)
Blood type and screen (crossmatch should be strongly considered)
Prothrombin/activated partial thromboplastin time
Fibrinogen (<200 mg/dL suggests severe abruption)
Fibrin split products
Consider holding a whole blood specimen at the bedside while lab work is pending. If a clot does not form within 6 minutes or forms and lyses within 30 minutes, DIC may be present.
The Apt test can be performed to evaluate whether vaginal blood is from the mother or the fetus. The blood is collected and lysed in water to release hemoglobin. Sodium hydroxide is mixed with the supernatant. Fetal hemoglobin is resistant to the base and will remain pink, whereas maternal hemoglobin will oxidize and turn brown. In theory, this qualitative test could be used to identify bleeding from VP, but the short time to fetal distress after a ruptured umbilical vessel and the sensitivity of fetal heart monitoring make the test largely unnecessary.
The Kleihauer-Betke test for fetal hemoglobin in the maternal circulation is not valuable in diagnosing AP.
Large-bore intravenous access should be obtained.
Fluid resuscitation should be initiated and a Foley catheter placed to monitor urine output (>0.5 mL/kg/hr or at least 30 mL/hr should be observed).
Close monitoring of maternal vital signs and continuous fetal monitoring should be maintained.
Rh D immunoglobulin should be administered to Rh-negative individuals.
Further management depends on the gestational age and hemodynamic status of both mother and fetus.