Succinyl choline apnea
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succinylcholine apnea pseudocholinesterase deficiency management authoritative guidance
Succinylcholine apnea is prolonged respiratory muscle paralysis after succinylcholine, most often due to inherited or acquired butyrylcholinesterase (pseudocholinesterase) deficiency. The enzyme normally rapidly hydrolyzes succinylcholine.
- Normal paralysis lasts about 5-10 minutes.
- With an atypical enzyme, apnea and paralysis may persist for hours, especially in homozygous inherited deficiency.
- The patient is conscious if anesthesia/sedation wears off, but cannot breathe or move. This is an airway and ventilation emergency, not a failure of oxygenation treatment alone.
Management
- Continue intubation and controlled ventilation with oxygen.
- Maintain adequate sedation/amnesia until neuromuscular function fully recovers.
- Monitor with a peripheral nerve stimulator if available.
- Avoid giving further succinylcholine, mivacurium, or empiric neostigmine. Anticholinesterases may worsen or prolong the block.
- Fresh frozen plasma is generally not routine treatment because supportive ventilation is safer and recovery is spontaneous.
- Confirm later with plasma butyrylcholinesterase activity and dibucaine number testing. Document the reaction and advise the patient and close relatives.
For later anesthetics, use alternatives such as rocuronium, with appropriate reversal strategy if needed. The OpenAnesthesia review similarly recommends sedation and ventilatory support until spontaneous recovery.
A 2026 systematic review describes the genotype-phenotype variation in butyrylcholinesterase deficiency (PMID 42120224).
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