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Management of Fetal Demise caused by Abruption at Term

2/1/2016 - Shari M. Lawson, MD

Mentor: Nancy D. Gaba, MD

Placental abruption complicates 0.5 to 1% of pregnancies, but very rarely results in fetal demise.  Fetuses that survive are at increased risk of significant morbidity. Management must address the following: maternal and fetal status, severity of the abruption, and gestational age and viability of the fetus. When placental abruption results in fetal demise, there should be significant concern that the abruption is severe and potentially life threatening to the mother as well.

The initial evaluation needs to include a comprehensive history and physical exam to identify causes of abruption that could impact management like hypertensive disorders of pregnancy, abdominal trauma, or cocaine use. The mother’s hemodynamic status must be closely evaluated and monitored. Fetal demise should raise concern for significant hemorrhage. Two large-bore intravenous catheters should be placed and volume resuscitation initiated with crystalloid or uncrossmatched blood as clinically warranted. Blood samples should be sent for type and crossmatch, complete blood count, fibrinogen, and PT/aPTT to assess for acute blood loss anemia and coagulopathy. Elevated d-dimers may be associated with severe placental abruption, but are not diagnostic. Consumptive coagulopathy (disseminated intravascular coagulation) is more common with concealed abruption.

The patient should also be assessed for vaginal bleeding and for concealed retroplacental hemorrhage. Bleeding per vagina can be assessed objectively with either a volumetric container or by weighing items used to absorb blood such as underpads and linen. Concealed hemorrhage may be assessed serially by ultrasonography or measuring fundal height. Ultrasonography should not be used to exclude placental abruption, as the appearance of clot on ultrasound is similar to the echotexture of placenta. Ultrasonography should be performed to determine fetal presentation and confirm fetal demise.

Many patients who have experienced a severe abruption and fetal demise have regular contractions on tocodynamometer and may deliver spontaneously. Vaginal delivery is the preferred route as surgery is often complicated by coagulopathy. Prior classical cesarean is not an absolute contraindication for vaginal delivery, but the decision and counseling should weigh the risks of surgical hemorrhage due to coagulopathy against the risks of uterine rupture (4-9% with prior classical cesarean section). Amniotomy or oxytocin augmentation will usually result in a rapid vaginal delivery. During labor, ongoing blood losses should be noted and replaced as indicated.

If vaginal delivery is contraindicated for obstetric indications such as transverse lie, profound maternal hemorrhage with hypovolemia unresponsive to resuscitation, or a high clinical suspicion for uterine rupture, there is a significant risk of intraoperative hemorrhage due to atony or coagulopathy that can lead to peripartum hysterectomy. If surgical delivery is necessary, marked thrombocytopenia (platelets less than 50,000/µL) or hypofibrinogenemia (fibrinogen less than 100 mg/dL) should be corrected with platelet or cryoprecipitate infusion to mitigate the risks of intraoperative hemorrhage. Packed red blood cells should be transfused to maintain the hematocrit between 25 and 30%.  Massive transfusion protocols should be initiated if necessary.

Couvelaire uterus, widespread extravasation of blood into the myometrium and beneath the serosa, may be encountered but is not necessarily an indication for hysterectomy. Rh immunoglobulin should be administered per protocol.

Initial approval 11/2015; Reaffirmed 5/2017.

 

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