The exact etiology of AFE remains poorly understood, but it is believed to occur when amniotic fluid, fetal cells, or other debris enter the maternal circulation through breaks in the uteroplacental barrier. This may happen during labor, delivery, or even following cesarean section, abortion, or trauma. Once these substances reach the maternal bloodstream, they trigger an abnormal systemic inflammatory response. This response is thought to be an immune-mediated process, similar to an anaphylactoid reaction, causing widespread vasoconstriction, pulmonary vasospasm, and activation of the coagulation cascade. Despite its name, AFE is not a mechanical embolic obstruction: fetal material enters the maternal circulation in many uneventful deliveries, fetal squamous cells have been recovered from the pulmonary blood of pregnant women who never developed the syndrome, and the amount of fluid involved can be trivial. The picture is better explained by an abnormal host response to fetal antigens, with complement activation and release of endothelin, leukotrienes, thromboxane and platelet-activating factor, which is why the term "anaphylactoid syndrome of pregnancy" has been proposed.
Several factors may predispose women to AFE, though it often occurs unpredictably. Known risk factors include advanced maternal age (35 years or older), induction of labor, cesarean delivery, instrumental vaginal delivery, placenta previa and placental abruption, multiple pregnancy, polyhydramnios, eclampsia, and uterine rupture or cervical laceration; multiparity appears in older series but is inconsistent in population studies. However, AFE can also occur in the absence of these risk factors, making it difficult to predict or prevent. The combination of its sudden onset, severe clinical presentation, and poorly understood pathogenesis contributes to the high mortality and morbidity associated with AFE.
