Prolonged neuromuscular paralysis following rapid-sequence intubation with succinylcholine

To report a case of severely prolonged succinylcholine-induced neuromuscular paralysis in a patient with previously undiagnosed butyrylcholinesterase deficiency.

A 54-year-old female was admitted for surgical drainage of a groin abscess. She was given propofol 200 mg and succinylcholine 160 mg (1 mg/kg) intravenously to induce sedation and paralysis for endotracheal intubation. Thirty minutes after the 19-minute procedure, the patient showed no evidence of spontaneous recovery of respiration. She was transferred to the intensive care unit and 11 hours later was successfully weaned from the ventilator and extubated. A butyrylcholinesterase level of 552 IU/L (reference range 2673-6592) confirmed butyrylcholinesterase deficiency. Six months later, in compliance with institutional review board/human subjects research requirements, the patient returned for a dibucaine inhibition test and second butyrylcholinesterase assay; the butyrylcholinesterase level in the second assay was 789 IU/L. The dibucaine inhibition test result was 61.1% (reference range 81.6-88.3), suggesting that the adverse drug effect had a pharmacogenetic basis. Use of the Naranjo probability scale indicated a probable relationship between the prolonged neuromuscular paralysis and succinylcholine therapy in this patient.

Succinylcholine remains the drug of choice to facilitate rapid-sequence endotracheal intubation during induction of anesthesia and in patients undergoing emergency procedures who are at risk for gastroesophageal regurgitation. Its short duration of action is due to rapid hydrolysis by the endogenous enzyme butyrylcholinesterase. Rarely, patients with butyrylcholinesterase deficiency may show marked sensitivity to succinylcholine, manifested clinically by severely prolonged neuromuscular paralysis and apnea.

Butyrylcholinesterase deficiency may go undiagnosed for decades until succinylcholine is used in a surgical procedure. When it does occur, a butyrylcholinesterase level should be obtained and a dibucaine inhibition test should be conducted to test for unrecognized hereditary butyrylcholinesterase deficiency. If a pharmacogenetic basis is confirmed, the patient should receive information about the condition, implications, inheritance, and need for family testing.