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To determine the incidence and duration of adrenal inhibition induced by a single dose of etomidate in critically ill patients.Prospective, observational cohort study.Three intensive care units in a university hospital.Forty critically ill patients without sepsis who received a single dose of etomidate for facilitating endotracheal intubation.Serial serum cortisol and 11β-deoxycortisol samples were taken at baseline and 60 min after corticotropin stimulation test (250 μg 1–24 ACTH) at 12, 24, 48, and 72 h after etomidate administration. Etomidate-related adrenal inhibition was defined by the combination of a rise in cortisol less than 250 nmol/l (9 μg/dl) after ACTH stimulation and an excessive accumulation of serum 11β-deoxycortisol concentrations at baseline. At 12 h after etomidate administration, 32/40 (80%) patients fulfilled the diagnosis criteria for etomidate-related adrenal insufficiency. This incidence was significantly lower at 48 h (9%) and 72 h (7%). The cortisol to 11β-deoxycortisol ratio (F/S ratio), reflecting the intensity of the 11β-hydroxylase enzyme blockade, improved significantly over time.A single bolus infusion of etomidate resulted in wide adrenal inhibition in critically ill patients. However, this alteration was reversible by 48 h following the drug administration. The empirical use of steroid supplementation for 48 h following a single dose of etomidate in ICU patients without septic shock should thus be considered. Concomitant serum cortisol and 11β-deoxycortisol dosages are needed to provide evidence for adrenal insufficiency induced by etomidate in critically ill patients.