Amniotic fluid embolism syndrome (also called anaphylactoid syndrome of pregnancy) is a catastrophic condition that occurs during pregnancy or shortly after delivery [1,2]. Although first reported in 1926, it was not widely recognized until 1941 when an autopsy series of eight women who had died from sudden shock during labor reported squamous cells and mucin of fetal origin in the maternal pulmonary vasculature [3,4]. Fetal squamous cells have also been described in the vascular beds of the maternal kidneys, liver, spleen, pancreas, and brain .
Amniotic fluid embolism syndrome is reviewed here. The management of critically ill obstetric patients is discussed separately, including those with venous thromboembolism. (See "Critical illness during pregnancy and the peripartum period" and "Deep vein thrombosis and pulmonary embolism in pregnancy: Treatment".)
Amniotic fluid embolism syndrome is rare. Most studies indicate that the incidence rate is between 1 and 12 cases per 100,000 deliveries [6-11].
Several factors have been associated with amniotic fluid embolism syndrome. They include precipitous or tumultuous labor, advanced maternal age, cesarean and instrumental delivery, placenta previa and abruption, grand multiparity (≥5 live births or stillbirths), cervical lacerations, fetal distress, eclampsia, and medical induction of labor [6,11,12]. Our understanding of the pathogenesis suggests that these factors probably are associated with amniotic fluid embolism syndrome, but not the direct cause. The syndrome is best considered unpredictable and unpreventable.
Amniotic fluid probably enters the maternal circulation through the endocervical veins, the placental insertion site, or a site of uterine trauma . Once it reaches the maternal circulation, it can precipitate cardiogenic shock, respiratory failure, and, most likely, an inflammatory and anaphylactoid response.