Cardiac arrest with pulmonary edema in a non-parturient after ergonovine administration recovered with extracorporeal membrane oxygenation -A case report-
A 31-year-old woman with height of 164 cm and weight of 42 kg (BMI; 15.62, normal; 18.5-23) was admitted for hysteroscopic myomectomy, under general anesthesia. Except penicillin allergy, she had no history of cardiovascular diseases, nor did she have any coronary risk factors, including smoking, diabetes mellitus, hyperlipidemia, hypertension, coagulative disorder, oral contraceptive use, and/or family history of myocardial disease. Physical examination and routine preoperative laboratory tests, including chest X-ray, and electrocardiogram (ECG) were unremarkable with total cholesterol and high density lipoprotein within normal range.\nAfter arriving at the operating room, ECG, pulse oximetry, non-invasive blood pressure, and end-tidal carbon dioxide (EtCO2) monitoring were attached to the patient. For induction of general anesthesia, thiopental sodium 200 mg, followed by rocuronium 20 mg, were injected intravenously and classic laryngeal mask airway (No. 4) was inserted. Then, she was positioned to lithotomy for the operation. Anesthesia was maintained with desflurane 5.0-6.0 vol% in 50% nitrous oxide and oxygen. The operation was uneventful for 30 minutes, with stable vital signs, except slight tachycardia with heart rate 105 to 120 beats/min. Further, the estimated blood loss was negligible.\nAt the end of the surgery, ergonovine maleate 0.2 mg distilled with normal saline 10 ml was intravenously administered slowly for a minute at the request of the surgeon for the uterine contraction. About 2 minutes later, EtCO2 suddenly decreased to 20 mmHg from 33 mmHg, followed by a loss of plethysmographic wave. The patient was cyanotic, but anesthetic monitor showed no noticeable change in the airway pressure and expiratory tidal volume. The blood pressure, although measured at 119/89 mmHg a few minutes ago, was not checkable with un-palpable radial pulse, and ECG showed severe bradycardia, followed by asystole.\nImmediately, 1 mg epinephrine was injected intravenously, FiO2 increased to 100%, and thereafter, chest compression was started. Laryngeal mask airway was changed to endotracheal tube (No. 7), under direct laryngoscopy, right internal jugular vein cannulated and arterial line in the right radial artery established, while chest compression continued, inotropics infused and intermittent atropine and other drugs were administered. Even with these measures, the patient responded poorly and cardiac rhythm couldn't be detected. The patient was just showing low blood pressure of about 40/20 mmHg, which was observed via arterial line, probably due to chest compression. About 20 minutes after cardiac arrest, ECG returned to sinus rhythm but with tachycardia and ST elevation. Blood pressure increased to 60/20 mmHg, heart rate was at 130 beats/min, SpO2 85%, and arterial blood gas analysis with pH 7.2, PCO2 42.7 mmHg, PO2 54.3 mmHg, bicarbonate 18.2 mmol/L, base -8.2 mmol/L, and sO2 82%. Other hematologic and electrolyte were within normal limits and the results were as follows: Hemoglobin 12.2 g/dl, Hematocrit 39.7%, Na+ 136 mmol/L, K+ 3.1 mmol/L, Ca2+ 4.5 mg/dl, and Cl- 117 mg/dl. With continued intotropic support, nitroglycerin 100 µg was intravenously administered with the suspicion of myocardial ischemia. Within 5 minutes, blood pressure further increased to 123/80 mmHg, heart rate to 128 beats/min, SpO2 100%. However, afterwards, the systolic blood pressure decreased to 75 mmHg and SpO2 88% again, despite inotropic support.\nChest X-ray, taken immediately after arrival to the intensive care unit, showed bilateral diffuse pulmonary edema (). Even though ECG didn't show definite ST abnormalities, except sinus tachycardia (), cardiac enzymes were elevated as follows; troponin I 3.2 ng/ml (normal < 0.78), CK-MB 12.08 ng/ml (normal < 5). Transthoracic echocardiography showed the ejection fraction of only 22% (normal 56-78%), with severe hypokinesia in the inferior and septal area. Patient was unresponsive, blood pressure still low with systolic pressure below 80 mmHg and oxygen saturation around 75-82%. So, the patient was managed with the extracorporeal membrane oxygenation (Capiox SP Pump controller 101, Terumo, Japan) through left femoral veno-right femoral arterial route with initial blood flow of 2-2.5 L/min. After that, the hemodynamics and oxygenation became stable with blood pressure 100/47 mmHg, and SpO2 100%.\nShe regained consciousness at the night of the operative day, and endotracheal tube was removed the following day. Extracorporeal membrane oxygenation was weaned and inotrope infusion was stopped at the third postoperative day. Afterwards, she recovered and was discharged without cardiopulmonary complication.