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Additional lab findings showed 170 a fibrinogen level of 399 mg/dL and a normal coagulation panel and platelet range. No evidence of venous thrombosis was noted. Chest X-ray showed severe airway disease, and chest CTA further demonstrated airspace opacities in both lungs. She was transferred to the ICU, where she was started on Levophed for refractory hypotension. Return of spontaneous circulation was achieved following CPR and administration of a single dose of epinephrine. She lost palpable pulses, and CPR was initiated as intubation was performed. Approximately 30 minutes following surgery, the patient developed sudden onset of shortness of breath, tachypnea, confusion, cyanosis, hypotension, brady-cardia, and hypoxemia with an oxygen saturation of 21% despite supplemental oxygen. Emergency cesarean section was required due to an umbilical cord prolapse. Her pregnancy was otherwise uncomplicated.

The following case describes the labor course of a patient with FVL+/- complicated by a postpartum AFE that did not progress to DIC.Ĭase Report: Patient is a 31-year-old G2P0 with a history of FVL+/- who presented for a scheduled induction of labor at 40 weeks and 5 days gestational age. Specifically, we ask if alterations in the coagulation cascade of heterozygous Factor V Leiden mutation (FVL+/-) can decrease mortality as seen in studies with severe sepsis. With similar theorized mechanisms, we suspect factors that may modify mortality in sepsis may also modify mortality in AFE. This often results in acute respiratory distress syndrome (ARDS), cardiopulmonary arrest, disseminated intravascular coagulation (DIC), and death. All rights reserved.Background: Amniotic fluid embolism (AFE) is a rare and commonly fatal obstetric emergency theorized to trigger an inflammatory reaction much like the systemic inflammatory response syndrome (SIRS) of sepsis, leading to vascular constriction and coagulation. In cases that require prolonged cardiopulmonary resuscitation or, after arrest, severe ventricular dysfunction refractory to medical management, consideration for venoarterial extracorporeal membrane oxygenation should be given.īlood product cardiac arrest coagulation cryoprecipitate dobutamine norepinephrine platelet right ventricular failure.Ĭopyright © 2019 Elsevier Inc. Amniotic fluid embolism-related coagulopathy should be managed with hemostatic resuscitation with the use of a 1:1:1 ratio of packed red cells, fresh frozen plasma, and platelets (with cryoprecipitate as needed to maintain a serum fibrinogen of >150-200 mg/dL). Blood pressure support with vasopressors is preferred over fluid infusion in the setting of severe right ventricular compromise. If such failure is identified, treatment that is tailored at improving right ventricular performance should be initiated with the use of inotropic agents and pulmonary vasodilators. Where available, we recommend performing transthoracic or transesophageal echocardiography as soon as possible because this is an easy and reliable method of identifying a failing right ventricle. We describe key features of initial treatment of patients with amniotic fluid embolism. Because amniotic fluid embolism usually is seen with cardiac arrest, the initial immediate response should be to provide high-quality cardiopulmonary resuscitation. Amniotic fluid embolism is an uncommon, but potentially lethal, complication of pregnancy.