Pseudocholinesterase Deficiency
Updated On: July 21, 2026
Anesthesia Implications
Prolonged paralysis - A normal dose of succinylcholine or mivacurium can produce a block lasting hours instead of minutes. Suspect it when neuromuscular function doesn't return on schedule.
Keep them asleep and ventilated - The safe response is supportive: maintain sedation and mechanical ventilation until the block resolves on its own. Never extubate a still-weak patient.
Confirm with the twitch monitor - Track recovery with the nerve stimulator; an absent or fading train-of-four after succinylcholine that doesn't recover is the tell.
Sugammadex won't help - It reverses the aminosteroid agents (rocuronium, vecuronium), not succinylcholine or mivacurium. Don't reach for it expecting reversal.
Alternative relaxants - In a known deficiency, avoid succinylcholine and mivacurium and use a reversible non-depolarizer whose clearance doesn't depend on this enzyme.
Document and warn family - Flag the chart; the inherited form is heritable, so relatives should be told to mention it before any anesthetic.
Pathophysiology
Pseudocholinesterase (plasma cholinesterase or butyrylcholinesterase) is a liver-produced enzyme that hydrolyzes the ester-linked neuromuscular blockers succinylcholine and mivacurium.
When it is deficient — inherited (atypical or absent variants) or acquired (liver disease, pregnancy, malnutrition, certain drugs) — a standard dose of these agents is not broken down normally and produces a markedly prolonged block. A homozygous atypical patient can stay paralyzed for hours after a single dose of succinylcholine. The condition is otherwise silent and usually declares itself only when spontaneous ventilation fails to return.