# Pseudocholinesterase Deficiency in a Patient Undergoing Electroconvulsive Therapy: A Case Report

## TL;DR

A patient with pseudocholinesterase deficiency experienced prolonged paralysis during electroconvulsive therapy, highlighting the need for better monitoring.

## Contribution

This case report highlights the diagnostic challenge of pseudocholinesterase deficiency during ECT and emphasizes the importance of quantitative neuromuscular monitoring.

## Key findings

- Prolonged paralysis after succinylcholine during ECT was initially misattributed to psychotropic medications.
- Pseudocholinesterase deficiency was confirmed with reduced plasma pseudocholinesterase activity (3745 U/L).
- Switching to rocuronium and using sugammadex allowed safe and rapid recovery in subsequent sessions.

## Abstract

Pseudocholinesterase deficiency (PD) is a genetic or acquired condition that impairs the metabolism of succinylcholine, leading to unpredictable and potentially prolonged paralysis. Its recognition during electroconvulsive therapy (ECT) is particularly difficult because postictal physiology, psychotropic polypharmacy, and the frequent absence of quantitative neuromuscular monitoring may make residual paralysis difficult to detect. We report a 34-year-old woman with pharmacotherapy-resistant schizophrenia who developed consistently prolonged paralysis after succinylcholine during ECT. In the first session, anaesthesia with propofol (80 mg) and succinylcholine (60 mg) produced an adequate seizure, but recovery of spontaneous ventilation and motor function was delayed by approximately 24 minutes, with only mild tachycardia and hypertension; this was initially attributed to chronic psychotropic treatment. The same pattern recurred during the second session despite adequate hypnotic depth on bispectral index (BIS) monitoring and unreliable neuromuscular monitoring data. Laboratory testing subsequently revealed markedly reduced plasma pseudocholinesterase activity (3745 U/L), confirming PD. Succinylcholine was then replaced with rocuronium (40 mg), and reversal was performed with high-dose sugammadex (960 mg), resulting in immediate and uneventful recovery in all remaining sessions under continuous quantitative neuromuscular monitoring. This case illustrates that PD may go unrecognised in ECT when quantitative neuromuscular monitoring is unavailable or unreliable and reinforces the need for routine monitoring to detect atypical recovery patterns and reduce the risk of unrecognised awareness during anaesthesia.