• Marc Vinclair, Christophe Broux, Patrice Faure, Julien Brun, Céline Genty, Claude Jacquot, Olivier Chabre, and Jean-François Payen.
• Department of Anesthesiology and Critical Care, Albert Michallon Hospital, BP 217, 38043, Grenoble, France.
• Intensive Care Med. 2008 Apr 1; 34 (4): 714-9.

ObjectiveTo determine the incidence and duration of adrenal inhibition induced by a single dose of etomidate in critically ill patients.DesignProspective, observational cohort study.SettingThree intensive care units in a university hospital.PatientsForty critically ill patients without sepsis who received a single dose of etomidate for facilitating endotracheal intubation.Measurements And Main ResultsSerial serum cortisol and 11beta-deoxycortisol samples were taken at baseline and 60 min after corticotropin stimulation test (250 microg 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 microg/dl) after ACTH stimulation and an excessive accumulation of serum 11beta-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 11beta-deoxycortisol ratio (F/S ratio), reflecting the intensity of the 11beta-hydroxylase enzyme blockade, improved significantly over time.ConclusionsA 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 11beta-deoxycortisol dosages are needed to provide evidence for adrenal insufficiency induced by etomidate in critically ill patients.

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