Treatment: consists of aggressive cardiopulmonary resuscitation, stabilization, and supportive care. The diagnosis can be firmly established only by demonstrating fetal elements in the maternal circulation (usually at autopsy or less commonly by aspirating amniotic fluid from a central venous catheter However, it may also initially mimic acute pulmonary thromboembolism, venous air embolism, overwhelming septicemia, or hepatic rupture or cerebral hemorrhage in a patient with toxemia. Acute left ventricular dysfunction appears to be a common feature.ĭiagnosis: Sudden respiratory distress and circulatory collapse should cause you to strongly consider amniotic fluid embolism. Seizures and pulmonary edema may develop the latter has both cardiogenic and noncardiogenic components. Three major pathophysiological manifestations are responsible: (1) acute pulmonary embolism, (2) DIC, and (3) uterine atony.
Symptoms: Typically, patients will present with sudden tachypnea, cyanosis, shock, and generalized bleeding. The alternate term “anaphylactoid syndrome of pregnancy” has been suggested to emphasize the role of chemical mediators in this syndrome. In addition to desquamated fetal debris, amniotic fluid contains various prostaglandin and leukotrienes, which appear to play an important role in the genesis of this syndrome. These breaks may occur during normal delivery or cesarean section or following placental abruption, placenta previa, or uterine rupture. Mortality: Exceeds 50% in the first hour.Įtiology: Entry of amniotic fluid into the maternal circulation through any break in the uteroplacental membranes.
Time Frame: Amniotic fluid embolism can occur during labor, delivery, cesarean section, or postpartum. Epidemiology: rare (1:20,000 deliveries) but potentially lethal complication (86% mortality rate in some series)
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