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Amniotic Fluid Embolism

4/1/2013 - Mari-Paule Thiet, MD

Editor: Christopher M. Zahn, MD

Amniotic Fluid Embolism (AFE) is an uncommon but catastrophic obstetric emergency. The frequency of AFE is 2-7 cases per 100,000 births. It is responsible for approximately 10-15% of maternal deaths in developed countries. If AFE occurs prior to delivery, the neonatal mortality rate is estimated to be 10-50%. Many surviving neonates suffer neurologic impairment. Neurologic impairment is also common in women survivors, particularly those who suffer cardiac arrest associated with AFE. Although the pathophysiology of AFE is not known, it has been suggested that entry of amniotic fluid into the maternal circulation activates inflammatory mediators causing an anaphylactoid-like response.

Although AFE occurs most commonly during labor and delivery or the immediate postpartum period, it has been reported to occur as late as 48 hours postpartum. The hallmark of AFE is cardiovascular collapse, often with acute dyspnea or cyanosis and tachycardia. Patients may also present with acute severe consumptive coagulopathy without cardiorespiratory symptoms. Risk factors for AFE include advanced maternal age, multiparity, pre-eclampsia, eclampsia, diabetes mellitus, and polyhydramnios or other uterine over-distention. Labor abnormalities associated with an increased risk of AFE include precipitous labor, induction of labor, placental abruption, cervical laceration, and uterine rupture.

There are 3 phases which have been described during the clinical course of AFE. The first phase involves pulmonary and systemic hypertension with resultant severe pulmonary vasoconstriction, characterized by respiratory distress and hypoxemia, leading to altered mental status followed by hemodynamic collapse. The second phase involves decreased systemic vascular resistance and left ventricular stroke work index. The third phase involves lung injury and coagulopathy, which may include disseminated intravascular coagulation (DIC). The results from the tissue injury and end organ system failure seen in AFE with pulmonary vascular constriction often lead to pulmonary hypertension, right-sided heart failure, and global myocardial depression.

The management of AFE includes early recognition and prompt multidisciplinary management with anesthesia. Massive blood transfusion protocols should be activated. An operating room, interventional radiology and the Intensive Care Unit should be made available. Laboratory assessment includes arterial blood gas analysis to evaluate the level of hypoxemia, serial blood counts and coagulation studies. An arterial catheter to monitor blood pressure and a central venous pressure catheter can be helpful. The management should focus on oxygenation (airway and breathing) and circulatory support with blood products, judicious use of intravenous fluids, vasopressors, and even cardiopulmonary bypass. If AFE occurs prior to delivery, maternal resuscitation is aided by expeditious delivery.

Control of hemorrhage and correction of coagulopathy should be the goal of replacement therapy of blood products with the possible use of recombinant factor VII, if needed. Hysterectomy may be required to control hemorrhage. Support of maternal oxygenation often requires high oxygen flow rate and invasive mechanical ventilation with increasing levels of oxygen and increased positive end-expiratory pressures. The goal of therapy is to limit hypoxemia and hypotension to prevent ischemic consequences such as brain injury, acute renal damage, and myocardial ischemia.

Further Reading:

Dean LS, Rogers RP 3rd, Harley RA, Hood DD. Case scenario: amniotic fluid embolism. Anesthesiology. 2012 Jan; 116(1):186-92

Williams Obstetrics, 24th Edition (2014); pages 812-814

Initial Approval:  April 2013; Revised: September 2015; Reaffirmed March 2017


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