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Chapter: Clinical Anesthesiology: Anesthetic Management: Obstetric Anesthesia

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Anesthesia for Amniotic Fluid Embolism

Amniotic fluid embolism is a rare (1:20,000 deliver-ies) but often lethal complication (86% mortality rate in some series) that can occur during labor, delivery, cesarean section, or postpartum.

AMNIOTIC FLUID EMBOLISM

 

Amniotic fluid embolism is a rare (1:20,000 deliver-ies) but often lethal complication (86% mortality rate in some series) that can occur during labor, deliv-ery, cesarean section, or postpartum. Mortality may exceed 50% in the first hour. Entry of amniotic fluid into the maternal circulation can occur through any break in the uteroplacental membranes. Such breaks may occur during normal delivery or cesarean sec-tion or following placental abruption, placenta pre-via, or uterine rupture. In addition to fetal debris, amniotic fluid contains various prostaglandins and leukotrienes, which appear to play an important role in the genesis of this syndrome. The alternate term anaphylactoid syndrome of pregnancy has been sug-gested to emphasize the role of chemical mediators in this syndrome.

Patients typically present with sudden tachy-pnea, cyanosis, shock, and generalized bleeding. Three major pathophysiological manifestations are responsible: (1) acute pulmonary embolism,disseminated intravascular coagulation (DIC), and (3) uterine atony. Mental status changes, includ-ing seizures, and pulmonary edema may develop; the latter has both cardiogenic and noncardiogenic com-ponents. Acute left ventricular dysfunction is com-mon. Although 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 cath-eter), amniotic fluid embolism should always be sug-gested by sudden respiratory distress and circulatory collapse. The presentation may initially mimic acute pulmonary thromboembolism, venous air embolism, overwhelming septicemia, or hepatic rupture or cere-bral hemorrhage in a patient with toxemia.

 

Treatment consists of cardiopulmonary resus-citation and supportive care. When cardiac arrest occurs prior to delivery of the fetus, the efficacy of closed-chest compressions may be marginal at best. Aortocaval compression impairs resuscitation in the supine position, whereas chest compressions are less effective in a lateral tilt position. Moreover, expeditious delivery appears to improve maternal and fetal outcome; immediate (cesarean) delivery should therefore be carried out. Once the patient is resuscitated, mechanical ventilation, fluid resus-citation, and inotropes are best provided under the guidance of invasive hemodynamic monitoring. Uterine atony is treated with oxytocin, methylergo-novine, and prostaglandin F2α, whereas significant coagulopathies are treated with platelets and coagu-lation factors based on laboratory findings.

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