The kalaemic and neuromuscular effects of succinylcholine in centronuclear myopathy: A pilot investigation in a canine model.

BACKGROUND: Myopathies are generally considered to increase the risk for succinylcholine-induced hyperkalaemia and may affect the duration of action of neuromuscular blockers. Centronuclear (myotubular) myopathy (CNM) is congenital and produces various degrees of muscular weakness and associated complications such as respiratory failure. The effects of succinylcholine and the potentially lethal consequences of hyperkalaemia on patients with CNM are unknown due to its rarity. One source of information is the dog, as CNM occurs naturally in dogs. Because of its remarkable similarity with the disease in man, canine CNM can serve as a model to further our knowledge of the effects of succinylcholine. OBJECTIVES: We examined the kalaemic and neuromuscular effects of succinylcholine in dogs with and without autosomal-recessive CNM. DESIGN: A prospective, experimental study. SETTING: Anaesthesiology laboratory, College of Veterinary Medicine, Cornell University, New York, USA. PATIENTS: Six dogs with autosomal-recessive CNM and six control dogs. INTERVENTIONS: Dogs received succinylcholine 0.3 mg kg during isoflurane anaesthesia. MAIN OUTCOME MEASURES: Whole blood potassium concentration was measured 5 min before and after succinylcholine administration. Neuromuscular function was measured with acceleromyography and single twitch stimulation. RESULTS: All dogs recovered uneventfully from anaesthesia. The increase in potassium concentration [mean (SD)] following succinylcholine was similar between groups: CNM 0.5 (0.4) mmol l and control 0.7 (0.4) mmol l (P = 0.47). Recovery of the single twitch to 25, 75 and 90% was longer in the CNM group (all P < 0.001); 90% recovery took 35.5 (1.18) min for the CNM group and 23.3 (1.68) min for the control group. CONCLUSION: CNM did not exacerbate the increase in blood potassium that is ordinarily seen with succinylcholine. Recovery from succinylcholine was nearly 50% longer in dogs with CNM. Although our sample size is too small to evaluate the incidence of succinylcholine-induced hyperkalaemia, extrapolation of these findings suggests that increased duration of action should be expected if succinylcholine is given to a patient with autosomal-recessive CNM.