A patient with pseudocholinesterase deficiency receives succinylcholine during anaesthesia. Which of the following best explains the prolonged paralysis observed?

Explanation

## Pseudocholinesterase Deficiency and Succinylcholine Metabolism **Key Point:** Succinylcholine is rapidly hydrolysed by plasma pseudocholinesterase (butyrylcholinesterase). In patients with pseudocholinesterase deficiency (genetic or acquired), the drug is not metabolised efficiently, leading to prolonged neuromuscular blockade. ### Normal Metabolism of Succinylcholine 1. Succinylcholine is a depolarising agent with a very short duration (5–10 min) in healthy individuals 2. Plasma pseudocholinesterase rapidly hydrolyses the drug into succinylmonocholine and choline 3. This rapid metabolism is why succinylcholine is ideal for RSI 4. In pseudocholinesterase deficiency, hydrolysis is severely delayed 5. The drug remains at the neuromuscular junction, causing prolonged paralysis (hours) ### Pseudocholinesterase Deficiency: Causes and Types **Genetic variants:** - Atypical (abnormal) pseudocholinesterase: autosomal recessive - Prevalence: 1 in 3,500 (heterozygous); 1 in 100,000 (homozygous) **Acquired deficiency:** - Liver disease (cirrhosis, hepatitis) - Malnutrition - Pregnancy - Renal failure - Organophosphate poisoning **High-Yield:** The **dibucaine number** (or fluoride number) is used to diagnose pseudocholinesterase deficiency. A normal dibucaine number is >70% (normal enzyme inhibits dibucaine); abnormal variants show <20% inhibition. **Clinical Pearl:** Patients with pseudocholinesterase deficiency require prolonged mechanical ventilation and monitoring after succinylcholine administration. Neostigmine (an anticholinesterase) is NOT effective because the problem is lack of enzyme, not excess ACh. **Mnemonic:** **PSEUDOCHOLINESTERASE DEFICIENCY** — **P**rolonged **P**aralysis after **S**uccinylcholine. ### Why Other Options Are Wrong | Option | Why Incorrect | |--------|---------------| | Phase II block | Phase II block (desensitisation) occurs with prolonged succinylcholine exposure in normal patients, but the primary mechanism of prolonged paralysis in deficiency is delayed metabolism, not Phase II conversion. | | Non-depolarising metabolites | Succinylcholine metabolites (succinylmonocholine, choline) do not cause significant non-depolarising blockade. | | Hofmann elimination | Hofmann elimination is a temperature- and pH-dependent process used by atracurium and cisatracurium, not succinylcholine. |