Amniotic Fluid Embolism
- This is a complex disorder classically characterized by the abrupt onset of hypotension, hypoxia, and consumptive coagulopathy. There are variations in its clinical manifestation.
- In obvious cases, the clinical frequency is dramatic. Classically, a woman in the late stages of labor or immediately postpartum begins gasping for air and then rapidly suffers seizures or cardiorespiratory arrest, complicated by consumptive coagulopathy, massive hemorrhage, and death.
- Other features common to amniotic fluid embolism are meconium staining and rapid labor.
- Amniotic fluid enters the circulation as a result of breach in the physiological barrier that normally exists between maternal and fetal compartments.
- There may be maternal exposure to various fetal elements during pregnancy termination, following amniocentesis or trauma or, more commonly, during labor or delivery, as small lacerations develop in the lower uterine segment or cervix. Alternatively, cesarean delivery affords ample opportunity for mixture of maternal blood and fetal tissue.
In the past, the detection of squamous cells or other debris of fetal origin in the central pulmonary circulation was believed to be pathognomonic for amniotic fluid embolism. Indeed, in fatal cases, histopathological findings may be dramatic, especially in those involving meconium-stained amniotic fluid.
Women who survive long enough to receive any treatment other than cardiopulmonary resuscitation should receive therapy directed at oxygenation and support of the failing myocardium. Circulatory support and blood and component replacement are paramount. There are no data that any type of intervention improves maternal prognosis with amnionic fluid embolism. In undelivered women suffering cardiac arrest, consideration should be given to emergency perimortem cesarean delivery in an effort to improve newborn outcome.