Screening patients with prolonged neuromuscular blockade after succinylcholine and mivacurium

Patients with pseudocholinesterase (BChE) variants may exhibit markedly prolonged paralysis after the administration of succinylcholine or mivacurium. We sought to evaluate to what extent molecular biology may contribute to the biological assessment of such patients. We conducted a prospective cohort study in patients referred to our center between 1995 and 1999 for prolonged neuromuscular blockade after mivacurium or succinylcholine. For each patient, phenotyping was performed with a conventional biochemical technique and molecular biology for the detection of the atypical mutation (A variant). Among the 36 patients referred, 31 had low BChE activity, 26 had received mivacurium (BChE activity, 2.1 U/mL; 0.3-4.3 U/mL), and 5 had received succinylcholine (BChE activity, 1.9 U/mL; 1.1-3.2 U/mL) (mean; extreme values). The mean clinical duration of paralysis was 90 min (40-140 min) after succinylcholine and 301 min (120-720 min) after mivacurium. Thirty-two patients had a BChE deficiency of genetic origin: 20 were homozygous (AA), 10 were heterozygous (UA) for the A variant, and 2 did not have the A mutation (UU). One heterozygous UA patient had normal BChE activity. Nine among the heterozygous UA and the two homozygous UU patients probably carried a not-screened variant. In most cases, biochemical diagnosis was sufficient to confirm the existence of constitutional deficiency; molecular biology improved the accuracy of diagnosis in 11 patients (30%) but had few or no clinical implications for the patient him- or herself.

Systematic screening for the pseudocholinesterase atypical variant by biochemical and DNA analysis after a prolonged neuromuscular blocking effect of succinylcholine or mivacurium shows that molecular biology could improve the diagnosis in approximately one third of patients, but with few clinical implications, compared with biochemical testing.