- Affects an estimated 3 to 5 per 100,000 live births.
- Mortality rate among affected parturients is as high as 85% and accounts for up to 12% of all maternal deaths.
- Significant and permanent neurologic sequelae are common among survivors.
- Introduction of fetal cells, amniotic fluid, and inflammatory mediators in the maternal circulation are thought to be the cause.
- Presents during labor or the immediate postpartum period with acute hypoxia and hypotension.
Clinical Presentation of AFE:
- Hypotension is a key feature of the disease and is present in 100% of patients with severe disease.The initial transient physiologic response is pulmonary hypertension resulting in hypoxia and right heart failure. Patients who survive the initial insult develop a left heart failure and pulmonary edema
- Hypoxia is an early manifestation of AFE and is thought to arise from acute pulmonary hypertension and ventilation/perfusion mismatch. Pulmonary edema develops later in association with left ventricular dysfunction.
- Disruption of normal clotting cascade occurs in up to two thirds of patients.
Management of AFE:
- Oxygenation: Tracheal intubation, mechanical ventilation, and supplemental oxygen.
- Circulatory support: Fluid resuscitation and pressor support as needed.
- Lines and monitors: Normal ASA monitors plus invasive BP, and PA catheter and/or TEE to assess ventricular function.
- Regular lab studies to aggressively treat coagulopathy.