PROLONGED DURATION OF SUCCINYLCHOLINE IN PATIENTS RECEIVING ANTICONVULSANTS - EVIDENCE FOR MILD UP-REGULATION OF ACETYLCHOLINE-RECEPTORS

Succinylcholine (SCh) normally causes a small increase in serum potass ium concentration, but certain conditions may predispose to severe hyp erkalaemia. This is due to ''up-regulation'' of skeletal muscle acetyl choline receptors (AChR), which also results in resistance to non-depo larizing muscle relaxants (NDMR). Anticonvulsant therapy causes NDMR r esistance because of sub-clinical blockade, and diminished release, of acetylcholine. We studied nine patients chronically receiving anticon vulsants (phenytoin and/or carbamazepine) and nine control patients. A naesthesia was induced typically with thiopentone or propofol, isoflur ane and N2O were used for maintenance. The ulnar nerve was supramaxima lly stimulated and mechanical twitch height was measured with a force transducer al the adductor pollicis, before and after SCh 1 mg . kg-1, until return to baseline height. Plasma potassium concentration was m easured before and at three, five, and ten minutes following SCh. Mean maximum potassium rise was 0.2 mEq . L-1 in each group. The time for return to baseline twitch height was 14.3 +/- 2.3 min (mean +/- SD) in the anticonvulsant group and 10.0 +/- 1.6 min in the control group, P = 0.001. The recovery index (time for 25% to 75% recovery) was 2.6 +/ - 0.9 min in the anticonvulsant group and 1.4 +/- 0.3 min in the contr ol group, P < 0.01. The normal potassium response coupled with prolong ed duration suggests a hypersensitivity to SCh that is consistent with an anticonvulsant-induced mild upregulation of AChR.