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Post Partum Management of Amniotic Fluid Embolism
Abstract Number: F3D-5
Abstract Type: Case Report/Case Series
Amniotic fluid embolism (AFE) was thought to be due to amniotic fluid emboli causing mechanical obstruction of the maternal cardiopulmonary circulation. Current proposed mechanism suggests that fetal material in the maternal circulation activate an inflammatory immunologic cascade resulting in cardiopulmonary collapse and disseminated intravascular coagulation (DIC).
A 35 y G2P1 female at 24w5d was admitted for induction termination for fetal hydrops of unknown etiology. She was induced with misoprostol and an epidural was placed for pain control. Her labor course was uncomplicated and the neonate was delivered without difficulty. Uterine tone was moderate and persistent uterine bleeding was noted with EBL of 700 mL requiring oxytocin 40 units and methergine 200 ug IM. Within 10 minutes of delivery, patient was hypoxic to 84%. Labs revealed hematocrit of 25, platelets of 82, INR 2.0 and fibrinogen 43 consistent with DIC. She was transfused 2 units FFP and 10 units cryoprecipitate. While receiving the FFP she was noted to have urticaria and puritis concerning for transfusion reaction. She received 25 mg IV diphenhydramine and 20 mg IV famotidine. Given concern for pulmonary embolism (PE) and AFE, a chest CT was performed which only showed groundglass opacification and pulmonary edema. She desaturated to the 70s and was transferred to the ICU. She was bradycardic to the 50s but her blood pressures were in 100s/60s. A transthoracic echocardiogram showed LVH, LV EF 70-75% and elevated RV pressures. She received 2 units of PRBC for hematocrit of 16.7. Her DIC improved and epidural catheter was removed POD1. She had non-oliguric acute kidney injury (AKI) thought to be due to her acute hemorrhage, AFE and contrast exposure. She was discharged home on POD6.
Our pt had several risk factors for AFE including age >35, induction of labor and concern for pre-eclampsia with elevated BP. AFE is a clinical diagnosis of exclusion based on a constellation of clinical sequelae. Our pt exhibited many of the signs and symptoms of AFE including worsening hypoxemia, coagulopathy, pulmonary edema and increased RV pressures. Treatment of AFE continues to be supportive: maintenance of oxygenation, cardiac output and correction of coagulopathy. Assessment and escalation of care to ICU should take place as soon as possible.
Abenhaim HA, Azoulay L, Kramer MS, Leduc L. Incidence and risk factors of amniotic fluid embolisms: a population-based study on 3 million births in the United States. Am J Obstet Gynecol. 2008;199:49.e1–8.
Chestnut DH, Wong CA, Tsen LC, Lee WDN, Beilin Y, Mhyre JM. Chestnut’s Obstetric Anesthesia: Principles and Practice, 5th ed. Saunders, Philadelphia, PA, 2014.
Kramer MS, Rouleau J, Baskett TF, Joseph KS. Amniotic-fluid embolism and medical induction of labour: a retrospective, population-based cohort study. Maternal Health Study Group of the Canadian Perinatal Surveillance System. Lancet. 2006 Oct 21; 368(9545):1444-8.