During ECT, succinylcholine is administered as a muscle relaxant. A patient develops prolonged apnoea lasting 45 minutes after a standard dose. The most likely explanation is:

• A Halothane anaesthesia inhibiting pseudocholinesterase activity
• B Succinylcholine-induced phase II (dual) block in a patient on lithium
• C Pseudocholinesterase (plasma cholinesterase) deficiency — either hereditary or drug-induced — delaying succinylcholine hydrolysis ✓
• D Malignant hyperthermia triggering sustained depolarisation

Explanation

Succinylcholine is normally hydrolysed within 3–5 minutes by plasma pseudocholinesterase (butyrylcholinesterase). Hereditary pseudocholinesterase deficiency (dibucaine-resistant variants, genetic: E1 locus mutations) or drug-induced inhibition (organophosphates, echothiophate eye drops, metoclopramide, cyclophosphamide) causes prolonged neuromuscular blockade (suxamethonium apnoea). Management is supportive ventilation; the Dibucaine number (normally 70–85; <30 in homozygous deficiency) confirms the diagnosis. Lithium may prolong neuromuscular blockade but does not cause 45-minute apnoea.

Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.