Amniotic Fluid Embolism
Apr 2013 – by M. Thiet, MD
Case: A 42 year-old multiparous female presents in active, advanced labor. The pregnancy had been complicated by diabetes and polyhydramnios. At the time of spontaneous rupture of membranes, copious clear fluid is noted and the cervical exam is 9/50%/-3. The patient complains of shortness of breath and appears agitated. There is a fetal bradycardia to 50 beats per minute without return to baseline. The patient is hypoxemic, tachycardic and has a respiratory arrest.
The above scenario is consistent with a diagnosis of amniotic fluid embolism (AFE) and the clinician needs to act rapidly to deliver the fetus and resuscitate the patient.
Amniotic Fluid Embolism (AFE) is an uncommon but catastrophic obstetric emergency, which needs to be high on the differential list when an obstetric patient experiences sudden, acute maternal cardiovascular collapse with evidence of respiratory compromise and/or coagulopathy. The incidence of AFE is 2-7 cases per 100,000 births with a maternal mortality rate of 20%. AFE is responsible for about 10% of maternal deaths in developed countries. If AFE occurs prior to delivery neonatal outcome is poor and associated with a neonatal mortality rate estimated at 10-50%. Although the pathophysiology of AFE is not known, it has beensuggested 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. Therefore, all clinicians who provide care to women during this period must be able to recognize symptoms and respond promptly with aggressive resuscitation and support to improve outcome.
The hallmark of AFE is cardiovascular collapse, often with acute dyspnea or cyanosis and tachycardia. Generalized tonic-clonic seizures are the first sign of AFE in 10-50% of patients. Risk factors for AFE include advanced maternal age, multiparity, pre-eclampsia/eclampsia, diabetes mellitus, and polyhydramnios, or 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 1st phase is characterized by respiratory distress and hypoxemia, which leads to altered mental status followed by hemodynamic collapse. The 2nd phase involves coagulopathy and bleeding which may include disseminated intravascular coagulation (DIC). The 3rd phase results from the tissue injury and end organ system failure seen in AFE with pulmonary vascular constriction often leading 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 Intensive Care Unit should be made available. Laboratory assessment includes arterial blood gas analysis to evaluate the level of hypoxemia, with 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), endotracheal intubation 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, usually abdominal delivery unless immediate operative vaginal delivery can occur.
Control of hemorrhage and correction of coagulopathy should be the goal of replacement therapy of blood products with possible use of recombinant factor VII if needed for DIC. 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.
Maternal and neonatal mortality due to AFE remains high, however it can be decreased by early recognition and aggressive resuscitation and therapy.
Dean LS, Rogers RP 3rd, Harley RA, Hood DD. Case scenario: amniotic fluid embolism. Anesthesiology. 2012 Jan; 116(1):186-92
Baldisseri MR. Amniotic fluid embolism syndrome. In: UpToDate, Basrow DS (Ed), UpToDate, Waltham, MA, 2012