Duration of adrenal inhibition following a single dose of etomidate in critically ill patients.

摘要

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