A 70 kg, 28-year-old woman receives succinylcholine 100 mg for rapid sequence intubation. She does not fasciculate and appears to have prolonged neuromuscular blockade lasting 4 hours. Which enzyme deficiency MOST likely explains this?

• A Acetylcholinesterase deficiency at the motor endplate
• B Phase II block from excess succinylcholine
• C Pseudocholinesterase (plasma cholinesterase) deficiency ✓
• D Hepatic failure reducing succinylcholine redistribution

Explanation

Succinylcholine is normally hydrolysed within 3–5 minutes by pseudocholinesterase (butyrylcholinesterase) in the plasma. Genetic variants with reduced enzyme activity (homozygous atypical dibucaine-resistant enzyme) prevent this hydrolysis, resulting in prolonged neuromuscular blockade of 2–6 hours. Absence of fasciculations may indicate a very low enzyme activity since the drug cannot be metabolised quickly enough to produce the phase I activation-then-block sequence. The dibucaine number is used to identify the atypical enzyme variant. True acetylcholinesterase deficiency at the NMJ does not affect succinylcholine metabolism.

Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.