SESSION TITLE: Critical Care Student/Resident Case Report Posters IV
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 29, 2013 at 01:30 PM - 02:30 PM
INTRODUCTION: Stress-induced cardiomyopathy (SICM) is characterized by transient left ventricular wall motion abnormality associated with excessive catecholamine production. SICM occurring during the perioperative period has been reported (1). We report a case of an atypical SICM associated with negative pressure pulmonary edema (NPPE)
CASE PRESENTATION: A 23-year-old woman athlete with history of mild asthma underwent an uneventful septorhinoplasty under general anesthesia. Immediately following extubation, she developed severe dyspnea with stridor, hypertension and tachycardia. On lung auscultation, rales were present bilaterally. She was given furosemide and reintubated. A chest radiograph showed bilateral pulmonary edema. Electrocardiogram (EKG) revealed sinus tachycardia without ST-T changes. Echocardiography showed ejection fraction (EF) of 10% and globally dilated left ventricle. Three successive troponin levels were 0.44, 0.60 and 0.39 (normal<0.11). The patient was treated with IV furosemide. Her oxygenation and chest radiograph rapidly improved and she was extubated the next morning. Cardiac MRI on day 3 revealed EF of 44% with mild global hypokinesis, normal size chambers and no evidence of myocardial scarring. A month after the incident, the patient was completely asymptomatic with her usual exercise capacity.
DISCUSSION: NPPE is an uncommon complication of extubation, thought to be a result of the generation of markedly negative intrathoracic pressure due to forced inspiration against a closed glottis. Patients are usually young and athletic, capable of generating profound negative intra-thoracic pressure. It is well known that surgical procedures involving the upper airway tract have a high risk of NPPE. Our patient’s clinical presentation and her quick recovery are highly suggestive of NPPE. However, she also had features of SICM, with a highly adrenergic clinical state, echocardiographic and troponin abnormalities, and a rapidly improving myocardial dysfunction. We postulate that excessive catecholamine production due to airway obstruction has led to the occurrence of SICM.
CONCLUSIONS: A literature review revealed a similar case of SICM associated with NPPE with classic features of apical ballooning and electrocardiogram abnormalities (2). To our knowledge, our case is the first post-extubation SICM with atypical echocadiographic and EKG features. SICM should be considered in differential diagnosis of post-extubation pulmonary edema.
Reference #1: Wong AK, Vernick WJ, Wiegers SE, Howell JA, Sinha AS. Preoperative Takotsubo Cardiomyopathy identified in the operating room before induction of anesthesia. Anesthesia-Analgesia 2010;110:712-5
Reference #2: Lee SH, Chang CH, Park JS, Nam SB. Stress-induced cardiomyopathy after negative pressure pulmonary edema during emergence from anesthesia. Korean J Anesthesiol. 2012 January; 62(1): 79-82.
DISCLOSURE: The following authors have nothing to disclose: Hussein Hussein, Aydin Uzunpinar
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