There is lack of evidence that succinylcholine should be avoided in patients on statin therapy.

P ARAPHRASING that an old soldier never dies, he just fades away, this author has written of succinylcholine, “A drug capable of generating so many controversies, surviving so many crises, so uniquely short acting and rapid in onset, and inexpensive, will not just die.” Indeed, succinylcholine still invites attention. In this issue of ANESTHESIOLOGY, Turan et al. skillfully document that patients who were receiving statin medications for hypercholesterolemia had greater myoglobinemia and fasciculation after intravenous administration of 1.5 mg/kg succinylcholine than did similar patients not taking statin medications. Because the myoglobinemia remained well below its normal renal toxicity threshold, the authors suggested that the muscular injury probably is of limited clinical consequences. Nevertheless, this new finding should provoke a timely reassessment of the role of succinylcholine. First of all, quantification of the succinylcholine-statin interaction is timely and important, considering the widespread, ever-increasing use of statin drugs in our health-conscious aging population and considering that both succinylcholine and the statin drugs frequently cause muscle damage. Turan et al. appropriately excluded from their study patients with American Society of Anesthesiologists status greater than III and those undergoing orthopedic and spinal surgeries and surgeries involving extensive muscle manipulations. They also excluded patients with hepatic, renal, or neuromuscular pathologies and those with chronic pain and risk of malignant hyperthermia. I have no qualms with a conclusion that absent other concerns, statin therapy per se may not necessarily contraindicate succinylcholine. I am, however, concerned with patients disqualified from this study, especially the vulnerable seniors with reduced functional reserves. Other unanswered questions remain because statinsvary in theirpropensity tocause muscle damage, and patients vary in their existing muscle damage and in the succinylcholine interaction. Indications for succinylcholine, or any drug, must be reevaluated periodically as more is learned about it. When they introduced succinylcholine to the United States 59 yr ago, Foldes et al. concluded in their 1952 publication that succinylcholine approximated most closely the definition of ideal relaxant. Upon reevaluation, however, Savarese and Kitz called for a major effort to replace succinylcholine with a “nondepolarizing succinylcholine,” and Savarese et al. immediately launched that effort in 1975. Lee classified the disadvantages of succinylcholine and noted that the list kept growing, whereas the drug’s specific indications kept dwindling. Many short-acting compounds intended to replace succinylcholine, including rapacuronium and TAAC3, have proved promising. Unfortunately, none have succeeded. Vecuronium, rocuronium, and cisatracurium excelled on their own virtues and gained wide clinical acceptance, but they also failed to completely retire succinylcholine. Currently, the rocuronium-sugammadex combination beats succinylcholine in practically all outcome measures. Unfortunately, sugammadex is still unavailable in the United States. Another series of compounds, the CW002-related neuromuscular blocking agents, are promising but remain experimental. Meanwhile, the advantages and disadvantages of succinylcholine and its indications should be updated in light of the current study by Turan et al. Photograph: J. P. Rathmell.