Abstract
Amniotic fluid embolism (AFE) is one of the leading causes of maternal mortality and morbidity in developed countries. Current thinking about pathophysiology has shifted away from embolism toward a maternal immune response to the fetus. Two immunologic mechanisms have been studied to date. Anaphylaxis appears to be doubtful while the available evidence supports a role for complement activation. With the mechanism remaining to be elucidated, AFE remains a clinical diagnosis. It is diagnosed based on one or more of four key signs/symptoms: cardiovascular collapse, respiratory distress, coagulopathy, and/or coma/seizures. The only laboratory test that reliably supports the diagnosis is the finding of fetal material in the maternal pulmonary circulation at autopsy. Perhaps the most compelling mystery surrounding AFE is not why one in 20,000 parturients are afflicted, but rather how the vast majority of women can tolerate the foreign antigenic presence of their fetus both within their uterus and circulation?
Highlights
When first described in the first half of the 20th century, amniotic fluid embolism was presumed to be the result of the physical obstruction of the maternal pulmonary circulation by fetal material contained within amniotic fluid [1, 2]
Much has been published about amniotic fluid embolism that, in light of current evidence, needs to be revised
The only laboratory test that is diagnostic at this time is the finding of fetal material in the maternal pulmonary circulation at autopsy
Summary
When first described in the first half of the 20th century, amniotic fluid embolism was presumed to be the result of the physical obstruction of the maternal pulmonary circulation by fetal material contained within amniotic fluid [1, 2]. Perhaps an equal concern is the significant maternal morbidity that results in survivors. A rare complication of pregnancy, the high rates of injury for both mother and newborn provide compelling arguments for a better understanding of the mechanism of disease. Mechanical obstruction of pulmonary blood flow is not reliably seen in AFE [10]. Clinical events, common in AFE, coagulopathy, adult respiratory distress syndrome, and neurological symptoms, are not typical in pulmonary embolism. Autologous amniotic fluid introduced into the maternal circulation in monkeys seems to be entirely benign [12, 13]
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