Amniotic Fluid Embolism

Abstract

Amniotic fluid embolism is one of the most catastrophic complications of pregnancy. First described in 1941, the condition is exceedingly rare and the exact pathophysiology is still unknown. The etiology was thought to be embolic in nature, but more recent evidence suggests an immunologic basis. Common presenting symptoms include dyspnea, nonreassuring fetal status, hypotension, seizures, and disseminated intravascular coagulation. Early recognition of amniotic fluid embolism is critical to a successful outcome. However, despite intensive resuscitation, outcomes are frequently poor for both infant and mother. Recently, aggressive and successful management of amniotic fluid embolism with recombinant factor VIIa and a ventricular assist device, inhaled nitric oxide, cardiopulmonary bypass and intraaortic balloon pump with extracorporeal membrane oxygenation have been reported and should be considered in select cases.

Amniotic fluid embolism in an HIV-positive parturient

“…6,7 The clinical scenario we describe in our report ts well with the presumptive diagnosis, namely peripartum acute collapse with cardiac arrest, hypoxia, neurological signs and coagulopathy, 8 and as such we made the diagnosis on clinical grounds. Laboratory investigations that served to con rm the diagnosis included the deranged INR and the low complement levels.…”

Cardiovascular emergencies and cardiac arrest in a pregnant woman

“…Maternal and fetal morbidity is high, with neurological sequelae in survivors [52]. AFE usually occurs intrapartum or in the immediate postpartum period, and typical symptoms are acute hypotension (or cardiac arrest), acute hypoxemia and coagulopathy [53].…”

Amniotic Fluid Embolism: An Update of the Evidence

“…Therefore, abnormally low levels of C3 and C4 detected in AFE cases are suggestive of complement activation, either through the classical or alternative pathway [9,10]. The susceptibility of women to develop AFE after the transfer of AF or its components may depend on allergic diatheses or previous sensitization to specific fetal antigens [11]. Nevertheless, no related theory based on reliable evidence has been widely accepted nor have amniotic fluid-specific markers been developed, so far.…”

“…In 30% to 45% of patients coagulopathy develops with severe bleeding resulting from disseminated intravascular coagulation (DIC). Such a phenomenon may develop in two alternative ways: on the one hand, the procoagulant substances contained in the AF may activate the extrinsic coagulation cascade on the other hand, urokinase-like plasminogen activator and plasminogen activator 1 contained in the AF may trigger massive hyperfibrinolysis [9,11,15].…”