Although a rare event, occurring in 1/25000–80000 deliveries, amniotic fluid embolism (AFE) is perhaps the most catastrophic of all obstetric complications. In the developed world, AFE accounts for approximately 10% of all direct maternal deaths, rating it among the top three causes. The prominence of AFE is accounted for by the fact that, although it is a rare condition, the mortality rate is 30–80% and, even among survivors, the hypoxic insult is so profound that many have permanent neurological damage. There is some evidence that prompt resuscitation and intensive care lead to improved intact survival.

Pathophysiology

The pathophysiology of AFE is poorly understood. It has been suggested that many of the hallmarks of AFE are similar to those of septic shock and anaphylaxis. Furthermore, it has been established that amniotic fluid commonly enters the maternal circulation without ill effect in most women. It is postulated that in certain susceptible women, fetal cells and other vasoactive substances, such as prostaglandins and leukotrienes, may initiate, via endogenous mediators, a complex pathophysiological cascade similar to that seen in anaphylactic and septic shock. The sequelae are as follows:

1. • Initially, there is acute pulmonary arteriolar obstruction and hypertension. This is transient and soon followed by left ventricular failure resulting in profound hypotension.

2. • Next, there is severe hypoxia as a result of ventilation–perfusion imbalance. This, together with the hypotension, produces a generalised hypoxia, often leading to seizures. It is this profound and sustained hypoxia that is responsible for the neurological damage in survivors.