Suxamethonium-induced myalgia.

Sir,—I read with interest the paper by Kahraman and colleagues on the effect of i.m. diclofenac on suxamethonium-induced myalgia [1]. Diclofenac, administered i.m. to conscious patients, is painful and has a tendency to cause sterile abscesses. Its use to ameliorate suxamethonium myalgia could be a case of a "remedy worse than the disease". Pretreatments have been tried previously but all have disadvantages. Pre-curarization complicates neuromuscular pharmacology [2] while other methods could cause complications, for example i.v. phenytoin, as advocated by Hatta, Saxena and Kaul [3] which, whilst effective, exposes the patient to a potentially toxic drug and substantially prolongs induction time. I believe that the incidence and severity of myalgia in the study of Kahraman and colleagues was high (thus providing better material for study) because they used the largest recommended dose of suxamethonium (1.5mgkg~')In an unpublished pilot study in 20 patients, I compared the effect of oral diclofenac 75 mg with placebo, using suxamethonium 1 mg kg"" for intubation and found no significant difference in myalgia assessed by visual analogue scores. Reducing the dose of suxamethonium prevents suxamethonium myalgia, is simple and.economical. Stewart, Hopkins and Dean [4], in their controlled trial used, respectively, suxamethonium 1.5 mg kg" and 0.5 mg kg". They found intubating conditions satisfactory in both their groups but the incidence and severity of myalgia was significantly reduced in the group receiving suxamethonium 0.5 mg kg". The answer may be to avoid the use of suxamethonium unless specifically indicated (i.e. rapid sequence induction). Beck and coworkers [5] and Alcock and colleagues [6] have shown that intubation is possible without neuromuscular block if laryngeal reflexes are sufficiently suppressed.