Deficiency associated with prolonged apnea after succinylcholine?

• A. Acetylcholinesterase
• B. Butyrylcholinesterase
• C. Monoamine oxidase
• D. Catechol-O-methyltransferase

Answer: (B)

Prolonged apnea after succinylcholine happens when the body cannot rapidly inactivate the drug because the enzyme that hydrolyzes it is deficient. Succinylcholine is a depolarizing neuromuscular blocker, and its quick termination depends on hydrolysis by plasma cholinesterases. The enzyme mainly responsible for breaking down succinylcholine in the blood is butyrylcholinesterase (also called pseudocholinesterase). If someone has a genetic variant or other causes of butyrylcholinesterase deficiency, succinylcholine remains active longer, so muscles stay paralyzed for an extended period and ventilation is required until the drug wears off.

Acetylcholinesterase is the enzyme at the neuromuscular junction that mainly degrades acetylcholine, not succinylcholine, so its deficiency wouldn’t explain the prolonged apnea. Monoamine oxidase and catechol-O-methyltransferase metabolize monoamines, not neuromuscular blockers, so they aren’t involved here.