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Successful Management of Cardiac Arrest From Amniotic Fluid Embolism With Ondansetron, Metoclopramide, Atropine, and Ketorolac: A Case Report
Abstract Number: S 47
Abstract Type: Case Report/Case Series
Introduction: Amniotic fluid embolism (AFE), a rare obstetric event with high maternal and fetal mortality, consists of cardiac and pulmonary symptoms with consumptive coagulopathy. In animal models of pulmonary embolism, serotonin receptor blockers, cyclooxygenase inhibitors, and vagotomy improve cardiac function and decrease mortality.(1,2) Here we report a successful resuscitation of cardiac arrest from AFE using adult cardiac life support (ACLS) plus ondansetron, metoclopramide, atropine, and ketorolac.
Case: 41 yo G8P3043 woman presented at 39 weeks for labor induction. At complete cervical dilation, the patient complained of shortness of breath. Oxygen saturation decreased to 80% and within 1 minute she developed cardiac arrest. ACLS was initiated and the baby was quickly delivered via forceps. The patient was still pulseless after 40 minutes of ACLS. Atropine 1mg, ondansetron 8mg, metoclopramide 10mg, and ketorolac 30mg were then administered and the patient regained a pulse and stabilized within 2 minutes. A bedside echocardiogram one hour later showed a hyperdynamic left ventricle, a flat intraventricular septum, right ventricle pressure and volume overload, and preserved right ventricular function. Right heart failure improved quickly. The patient then developed consumptive coagulopathy. Profuse uterine bleeding requiring 13u PRBC, 6u FFP, 2u platelets, 30u cryoprecipitate, 2 doses of recombinant Factor VIIa, and an intrauterine Bakri balloon. She required hemodialysis for 5 days due to acute tubular necrosis. The patient developed speech and memory function difficulties which still persist. She was discharged to home on day 13.
Discussion: AFE treatment requires prompt resuscitative measures plus fetal delivery, yet maternal mortality is still high. Pulmonary hypertension and right-sided heart failure are seen with echocardiography in AFE cases.(3) Animal models suggest that significant embolism of any material is followed by platelet degranulation, pulmonary hypertension due to serotonin and thromboxane, and systemic hypotension due to vagal stimulation.(1,2) It was not until ondansetron (5-HT3 antagonist), metoclopramide (5-HT3 antagonist), atropine (vagolytic), and ketorolac (cyclooxygenase inhibitor) were given that the patient regained a pulse. It is likely that anti-serotonin, anti-thromboxane, and vagolytic therapy helped restore this patient’s circulation and ultimately helped her survive AFE.
1. Armstrong DJ, Miller SA. The role of platelets in the reflex tachypnoeic response to miliary pulmonary embolism in anaesthetized rabbits. Exp Physiol 1990;75:791-800.
2. Leanos OL, et al. Reflex circulatory collapse following intrapulmonary entrapment of activated platelets: Mediation via 5-HT3 receptor stimulation. Br J Pharmacol 1995;116:2048-52.
3. James CF, et al. Massive amniotic fluid embolism: Diagnosis aided by emergency transesophageal echocardiography. Int J Obstet Anesth 2004;13:279-83.