UMEM Educational Pearls

Category: Critical Care Literature Update

Title: Etomidate and adrenal suppression

Keywords: etomidate, adrenal insufficiency (PubMed Search)

Posted: 7/7/2008 by Mike Winters, MD (Updated: 9/29/2023)
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Recent Articles from the Critical Care Literature

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

Vinclair M, Broux C, Faure P, Brun J, Genty C, et al. Intensive Care Med 2008;34:714-9.

Etomidate has become a favored first-line induction agent for intubation in the emergency department. Given its excellent hemodynamic tolerance, etomidate is especially useful in hemodynamically unstable patients. A known side effect of etomidate is adrenal suppression, due to inhibition of 11β-hydroxylase, the enzyme that converts 11β-deoxycortisol into cortisol. As a result, recent literature has raised concerns that etomidate may worsen patient outcomes in those with relative adrenal insufficiency, namely those with septic shock.

The current study is a prospective, observational study conducted in France from October 2005 to January 2006. The purpose of the study was to assess the duration of adrenal suppression following a single dose of etomidate, given either in the field or in the emergency department for RSI. Importantly, patients with septic shock, or those with preexisting adrenal insufficiency, were excluded from this study. To diagnose adrenal insufficiency, the investigators measured total cortisol and 11β-deoxycortisol following a high-dose cosyntropin stimulation test (250 mcg). Values were obtained at 12, 24, 48, and 72 hours following etomidate administration. An accumulation of 11β-deoxycortisol with a lack of cortisol rise was used to establish etomidate-related adrenal insufficiency.

A total of 40 patients were included in this study. The majority of patients required intubation as a result of either trauma or subarachnoid hemorrhage. At hour 12, 80% of patients fulfilled the investigators definition of etomidate-related adrenal insufficiency, whereas by hour 48, only 9% met criteria. In addition, at hour 24, patients with etomidate-related adrenal suppression required larger doses of norepinephrine that those without adrenal inhibition. From their data, the authors conclude that a significant proportion of patients without septic shock have adrenal suppression for at least 12 hours following a single dose of etomidate. This effect, however, appeared reversible in that most patients recovered adrenal function by hour 48. Finally, the authors recommend that systemic steroid supplementation be considered during the first 48 hours in hemodynamically unstable patients who have received etomidate for intubation.

There are a number of limitations with this study. The most important limitation is, perhaps, the authors’ definition of etomidate-related adrenal insufficiency. Diagnosing adrenal insufficiency in critically ill patients remains controversial. The cosyntropin test (high- or low-dose) has many recognized limitations. In addition, measurement of 11β-deoxycortisol is difficult because reference values for critically ill patients are rare. The authors also chose to measure total serum cortisol, rather than the more biologically active free serum cortisol. Lastly, data for all 40 patients at 72 hours was not complete.

Take Home Points: This small, observational study found a high incidence of adrenal suppression for at least the first 12 hours in unstable patients receiving etomidate for intubation. Importantly, this study excluded patients with sepsis or septic shock. Given the limited number of patients and the difficulty in defining adrenal insufficiency in the critically ill, this study provides some interesting results and is hypothesis-generating at best. Their recommendation for systemic steroid supplementation during the first 48 hours following etomidate administration in unstable patients cannot be supported by this study.