Postextubation Upper-Airway Obstruction Leading to Negative-Pressure Pulmonary Edema and Hypoxic Cardiac Arrest Despite Apparent Recovery After Sugammadex Reversal: A Case Report

Abstract Postextubation upper-airway obstruction may cause negative-pressure pulmonary edema (NPPE) and, rarely, life-threatening cardiovascular collapse. Apparent clinical recovery after neuromuscular blockade reversal does not necessarily ensure adequate upper-airway function. A 67-year-old woman underwent laparoscopic cholecystectomy under general anesthesia with induction of rocuronium. At the end of surgery, the train-of-four (TOF) count was 2, and sugammadex over 2 mg/kg was administered, after which four qualitative TOF responses subsequently returned. Before extubation, the patient opened her eyes and obeyed verbal commands, with breathing tidal volume of 6mL/kg. However, thoracoabdominal asynchrony subsequently developed, and the patient was noted to have a decreased level of consciousness at the point of approximately 5 minutes after extubation. Severe hypoxemia progressed to bradycardia and pulseless electrical activity. Return of spontaneous circulation was achieved after 3 minutes of cardiopulmonary resuscitation. Post-resuscitation lung ultrasonography and chest radiography demonstrated pulmonary edema, which markedly improved within 5 hours. This case highlights that clinically significant upper-airway obstruction may occur after apparent recovery from neuromuscular blockade with identification of qualitative TOF responses, despite administration of a clinically substantial dose of sugammadex. Such obstruction may rapidly progress to negative pressure pulmonary edema (NPPE) and hypoxic cardiac arrest.