Risk factors include: advanced maternal age (>35 y); cesarean delivery; placenta previa; meconium; intrauterine fetal demise; placental abruption; meconium staining of the amniotic fluid; chorioamnionitis; and macrosomia.

True incidence is unknown but estimated to occur in 2 to 8 per 100,000 deliveries.

Amniotic fluid embolism accounts for approx 6% of maternal deaths in USA.

Mortality was once as high as 61% to 86%, but more recent registries have reported mortality between 11% and 44% of pts.

Morbidity is also high as it is suggested that up to 60% of pts have persisting neurologic deficits.

Amniotic fluid embolism accounts for approx 6% of maternal deaths in USA.

Mortality was once as high as 61% to 86%, but more recent registries have reported mortality between 11% and 44% of pts.

Morbidity is also high as it is suggested that up to 60% of pts have persisting neurologic deficits.

Hypoxia.

Hypotension/cardiopulmonary collapse.

Heart failure (can have both right and left ventricular failure).

DIC: Occurs in nearly all survivors of the initial catastrophic event.

Hemorrhage: 40% of amniotic fluid embolism-associated deaths are due to hemorrhage.

Altered mental status.

Seizures.

ARDS.

Acute pulm Htn.

Amniotic fluid going to central circulation.

There are three necessary conditions:

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  Amniotomy (breach in the barrier between the intact fetal membranes that isolate amniotic fluid from the maternal circulation).

  
  
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  Laceration of endocervical or uterine vessels or site of placental attachment.

  
  
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  Traditionally it was thought that a pressure gradient (intrauterine pressure > CVP or uterine venous pressure) was needed, but the presence of an electrochemical gradient can provide the means for mediators of AFE to inflict damage.

Immunologic factors also likely to be involved, and complement activation may play a role in the pathophysiology of AFE (e.g., SIRS).