Abstract
Succinylcholine (SCh) normally causes a small increase in serum potassium concentration, but certain conditions may predispose to severe hyperkalaemia. This is due to “up-regulation” of skeletal muscle acetylcholine receptors (AChR), which also results in resistance to non-depolarizing muscle relaxants (NDMR). Anticonvulsant therapy causes NDMR resistance because of sub-clinical blockade, and diminished release, of acetylcholine. We studied nine patients chronically receiving anticonvulsants (phenytoin and /or carbamazepine) and nine control patients. Anaesthesia was induced typically with thiopentone or propofol; isoflurane and N2O were used for maintenance. The ulnar nerve was supramaximally stimulated and mechanical twitch height was measured with a force transducer at the adductor pollicis, before and after SCh 1 mg · kg− 1, until return to baseline height. Plasma potassium concentration was measured 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 control group, P < 0.01. The normal potassium response coupled with prolonged duration suggests a hypersensitivity to SCh that is consistent with an anticonvulsant-induced mild upregulation of AChR.
Résumé
Normalement, la succinylcholine ne provoque qu’une légère augmentation du potassium sérique, mais certaines conditions peuvent favoriser une hyperkaliémie grave. Ceci est dû à la régulation «à la hausse» des récepteurs acétylcholinergiques des muscles squelettiques (AChR), qui produit aussi une résistance aux myo-relaxants non dépolarisants (MRND). Par un bloquage infraclinique, la thérapie anticonvulsivante produit une résistance aux MRND et une diminution de la libération d’acétylcholine. Nous avons étudié neuf patients sous thérapie anticonvulsivante (du phénytoin ou de la carbamazépine) et les avons comparés à neuf contrôles. L’anesthésie a été induite avec du thiopentone ou du propofol et maintenue à l’isofiurane et au N2O. Un stimulus supramaximal a été appliqué au nerf cubital et la force du twitch mesurée avec un transducteur à l’adducteur court du pouce, avant et après SCh 1 mg· kg− 1, jusqu’au retour à la ligne de base. La kaliémie a été mesurée avant, à trois, cinq, et dix minutes après SCh. L’augmentation moyenne maximale de potassium a été de 0.2 mEq · L− 1 dans chaque groupe. La durée de retour à la ligne de base a été de 14.3 ± 2.3 min (moyenne ± SD) dans le groupe anticonvulsivant et 10.0 ± 1.6 dans le groupe contrôle, P = 0.001. L’index de récupération (temps de récupération à 25% à 75%) a été de 2.6 ± 0.9 min dans le groupe anticonvulsivant et de 1.4 ± 0.3 min dans le groupe contrôle, P < 0.01. La normalité de la réponse kaliémique associée à une durée prolongée suggère une hypersensibilité à la SCh consistante avec une légère régulation «à la hausse» induite par la thérapie anticonvulsivante.
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Melton, A.T., Antognini, J.E. & Gronert, G.A. Prolonged duration of succinylcholine in patients receiving anticonvulsants: evidence for mild up-regulation of acetylcholine receptors?. Can J Anaesth 40, 939–942 (1993). https://doi.org/10.1007/BF03010096
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DOI: https://doi.org/10.1007/BF03010096