Management of Amniotic Fluid Embolism

Abstract

Amniotic fluid embolism (AFE) is a rare clinical syndrome that occurs intrapartum or immediately postpartum. The exact cause of this syndrome is not known although it is widely suspected that there may be an immune etiology causing an anaphylactoid-like reaction with complement activation. The syndrome occurs with greater frequency in parturients who are older and multiparous, have twin pregnancies, and experience difficult labors. It is also seen more frequently in preeclamptic patients and in women who have Cesarean sections. The classic presentation of this syndrome is cardiopulmonary collapse usually complicated by respiratory failure, cardiogenic shock, disseminated intravascular coagulation (DIC), and neurologic changes including seizures and coma. Severe and refractory hypoxemia results from significant ventilation/perfusion mismatching as well as from both cardiogenic pulmonary edema associated with acute left heart failure and noncardiogenic pulmonary edema (adult respiratory distress syndrome). The diagnosis of this syndrome is difficult and AFE remains a diagnosis of exclusion since there are no laboratory or radiographic tests which definitively confirm the diagnosis. The constellation of signs and symptoms in a pregnant woman who experiences the typical symptomology and a high degree of suspicion usually are sufficient to make the diagnosis of AFE.

The management of amniotic fluid embolism syndrome is supportive care. Correcting hypoxemia and hypotension is paramount to prevent further sequelae to the mother and the fetus. If AFE presents intrapartum, the fetus should be delivered immediately to support maternal hemodynamics. Specific therapies such as diuresis and inotropic support should be implemented if there is evidence of left heart failure and congestion. Intra-aortic balloon pump counterpulsation and extracorporeal membrane oxygenation have also been utilized. Refractory hypotension is managed with vasopressor support. Mechanical ventilation is usually required for severe respiratory failure regardless of the exact cause of the respiratory compromise. DIC is treated with appropriate blood products and recombinant human factor VIIa based on laboratory testing. Most recently, there has been some interest in the use of fresh frozen plasma as a source of C1 esterase since low levels of C1 esterase inhibitor have been detected in survivors of AFE.