Etomidate is still a valid anesthetic for electroconvulsive therapy.

Abstract

Komatsu et al have recently written that the use of etomidate as an anesthetic induction agent for surgery is associated with increased 30-day mortality and cardiovascular morbidity, compared with propofol. Etomidate has long been recognized as suppressing adrenocortical function and, as an infusion over days, has been indicted in increasing intensive care unit patient mortality. Even in single doses, etomidate causes a reduction in cortisol production, although recovery from single-dose suppression is generally prompt. In prospectively evaluating etomidate as an anesthetic for electroconvulsive therapy, Lebowitz et al, in a pilot study, found that 3 times per week, etomidate did not cause adrenocortical suppression that lasted until the following treatment. The steroid responses did not differ from those of methohexital, and no patient demonstrated evidence of cortisol deficiency. Consequently, concerns raised by Komatsu et al about etomidate's safety seem unwarranted when used for electroconvulsive therapy, and their study's conclusions likely relate to issues with their retrospective methodology.