Th e pathophysiology of AFE syndrome is unclear. Previously, this syndrome was believed to result from embolization of amniotic fl uid into the pulmonary circulation. However, an anaphylactoid or hyper sensitivity reaction to the contents of this fl uid is more likely [17] . Th e presence of amniotic fl uid in the pulmonary circulation is neither sensitive nor specifi c, as this has been identifi ed in mothers who do not develop AFE syndrome. Patients may present with seizure-type activity or acute respiratory distress. Acute lung injury results in profound hypoxemia, intense hypoxic pulmonary vasoconstriction, and acute right heart failure (Table 4) , result ing in hemodynamic collapse. Bowing of the right ventricle into the left results in acute diastolic and then acute systolic failure of the left ventricle. Th ere is simultaneous DIC that may manifest with bleeding from the placental bed. Nausea, vomiting, headache, confusion, and seizures commonly follow. Death from AFE syndrome results from multi-organ failure, exsanguinations, or cardiac arrest. Neurologic injury is common in survivors.