Maternal Cardiac Arrest During Cesarean Section in a Mobidly Obese Asthmatic with Undiagnosed Pheochromocytoma and Cardiomyopathy
Abstract Number: 215
Abstract Type: Case Report/Case Series
Case Report: A 36 yo term parturient with morbid obesity (167kg) and poorly controlled asthma was admitted to labor and delivery in active labor. The anesthesiology team was called for urgent CS because of fetal tachycardia with absent variability. The patient complained of pain with contractions and appeared anxious. Vital signs: BP 144/70, HR 116, RR 24, and SpO2 94% on 6L O2/min via CFM. Her mouth opening was small and only her soft palate was visible. Neck extension and thyromental distance were normal. She had end-expiratory wheezes throughout both lung fields and 2+ pitting edema. Jugular venous pressure was difficult to estimate. After inhaled albuterol she was brought to the OR without delay. She underwent combined spinal epidural anesthesia without difficulty and remained hemodynamically stable without need for vasopressors. After delivery of a vigorous infant her SpO2 decreased to 80-85% and she became combative. BP was 100/60, HR 130s (ST). GA was induced with propofol (130mg) and succinylcholine via RSI. After intubation, attempts to ventilate were minimally effective with PIPs greater than 70cm water. ETCO2 was present and persistent but decreased. Breath sounds were barely audible. A catheter was placed easily through the ETT and frothy sputum was suctioned. Ventilation through an ambubag was also ineffective. Despite escalating doses of intravenous epinephrine and inhaled albuterol for bronchospasm, further cardiopulmonary deterioration ensued and ACLS was initiated. After a total of 5mg of intravenous epinephrine and several defibrillations, ventilation became easier and circulation was restored. TTE demonstrated a greatly enlarged left ventricle and reduced LV function (EF 20-30%) consistent with dilated cardiomyopathy. CT revealed cardiomegaly and multiple areas of pulmonary atelectasis with a small right pleural effusion and a right adrenal mass with no evidence of PE. CT brain demonstrated cerebral edema consistent with ischemic encephalopathy. The patient died four weeks later in the ICU. Autopsy revealed dilated cardiomyopathy and a right adrenal pheochromocytoma.
Discussion: Comorbidities played a central role in this unfortunate maternal death, some of which were known (morbid obesity and asthma) and some of which were undiagnosed (dilated cardiomyopathy and pheochromocytoma.) Her poverty and homelessness limited her access to prenatal care which hampered effective evaluation and treatment of her symptoms, as did a non-reassuring fetal status in the early hours of the morning. Pheochromocytoma may mimic other diseases such as preeclampsia (1), may worsen bronchial asthma (2),and may cause cardiomyopathy, heart failure, cardiac asthma and pulmonary edema. Several of her disease processes played a role in her decompensation after delivery, though the relative contribution of each remains debatable.
References: 1. IJOA. July 2006: 15(3) 240-245
2. Eur Respir J. Sept 1991:4(8)1021-2