Sharlette Lynch
Prolonged apnea after succinylcholine should prompt consideration of impaired drug metabolism, including reduced butyrylcholinesterase activity, while other causes of delayed emergence are evaluated. We report a 69-year-old, 72.7-kg man with severe systemic illness and hypoalbuminemia who underwent esophagogastroduodenoscopy and colonoscopy under total intravenous general anesthesia. Induction included propofol, fentanyl, and succinylcholine 100 mg. Approximately two hours after the initial succinylcholine dose, the patient was extubated but developed profound ventilatory weakness, with a respiratory rate of approximately three breaths per minute, tidal volumes of approximately 30 mL, and inability to sustain a head lift. Four qualitative train-of-four responses were present without subjectively detectable fade; no quantitative ratio was available. Naloxone improved alertness but did not restore adequate ventilation. Emergency reintubation was performed with an additional 80 mg of succinylcholine. Head computed tomography demonstrated no acute intracranial abnormality, and the patient was transferred to the intensive care unit for supportive ventilation. Respiratory strength returned gradually, and definitive extubation occurred at 21:25, approximately five hours and 37 minutes after reintubation. The profound weakness documented before the second succinylcholine dose raised concern for a prolonged effect of the initial dose. Severe hypoalbuminemia and systemic illness supported possible acquired reduction in butyrylcholinesterase activity, although inherited deficiency could not be excluded. Because enzyme activity, dibucaine inhibition, genetic testing, and quantitative neuromuscular monitoring were not obtained, the diagnosis remained presumptive. This case emphasizes that four qualitative twitches do not establish adequate neuromuscular recovery and that persistent ventilatory failure after improved consciousness warrants continued evaluation for neuromuscular blockade.