Amniotic fluid embolism (AFE) is a rare and severe complication of pregnancy or delivery that occurs suddenly and without warning. Estimated to occur in 2 to 8 cases per 100,000 deliveries, this life-threatening event is characterized by the rapid onset of cardiopulmonary collapse and severe bleeding. AFE is not caused by physical blockage, but rather a profound systemic reaction to the entry of foreign material into the mother’s circulation. Its unpredictable nature and rapid progression make it one of the most challenging obstetric emergencies to manage.
The Mechanical Entry of Fetal Material
The process begins with a breach in the physical barrier separating the mother’s blood from the contents of the womb. This separation is normally maintained by the intact walls of the uterus and the placental attachment site. A tear or rupture in the maternal-fetal interface allows the amniotic fluid and its components to enter the mother’s bloodstream. This breach typically occurs during labor, delivery, or immediately postpartum, often through exposed uterine veins at the placental site. The material that enters the circulation includes components of the amniotic fluid, such as fetal cells, hair (lanugo), and fatty skin secretions (vernix caseosa).
The Body’s Inflammatory Response
Once the foreign fetal material enters the mother’s blood, it triggers a massive and dysfunctional immune reaction. This response is considered an anaphylactoid syndrome of pregnancy, meaning it mimics a severe allergic reaction without requiring prior sensitization. The body recognizes the fetal components as foreign substances, initiating a catastrophic chemical cascade that releases potent inflammatory mediators (prostaglandins, thromboxanes, and various cytokines). The sudden release of these vasoactive substances immediately affects the mother’s heart and lungs, causing severe pulmonary vasoconstriction and bronchospasm. This intense reaction leads to acute respiratory distress and profound shock, and the severity of this inflammatory response drives the clinical course of AFE.
Immediate Cardiopulmonary and Hemorrhagic Collapse
The systemic chemical shock manifests in two rapidly occurring phases of collapse. The first phase is immediate cardiopulmonary failure, driven by severe pulmonary vasoconstriction, which causes the right side of the heart to fail, leading to acute hypoxia and respiratory arrest. The second phase is the onset of massive, uncontrollable bleeding, known as coagulopathy. The inflammatory cascade sets off Disseminated Intravascular Coagulation (DIC), rapidly consuming clotting factors and platelets. This consumption leaves the mother unable to form stable clots, resulting in massive hemorrhage from the uterus, surgical incisions, or intravenous sites, making the event extremely high-mortality.
Identifying Factors That Increase Risk
While AFE is largely a random and unpredictable event, certain factors are statistically associated with increased risk. These often include conditions that compromise the integrity of the maternal-fetal barrier or increase pressure in the womb. Advanced maternal age, typically considered over 35 years, is a recurring factor in studies of AFE incidence. Abnormalities of the placenta, such as placenta previa or placental abruption, also increase the likelihood. Other obstetric risk factors include the induction of labor, instrumental delivery, or Cesarean section, though AFE can still occur in low-risk pregnancies.