Adrenal inhibition following a single dose of etomidate in intubated traumatic brain injury victims

Abstract

Etomidate is frequently used to intubate traumatic brain injury (TBI) victims, even though it has been linked to adrenal insufficiency (AI) in some populations. Few studies have explored the risk of prolonged etomidate-induced AI among TBI victims. To determine the risk and the length of AI induced by etomidate in patients intubated for moderate and severe TBI. Participants in this observational study were moderate to severe intubated TBI victims aged ≥ 16 years. The anesthetic used (etomidate versus others) was determined solely by the treating emergency physician. Adrenocorticotropic hormone (ACTH) stimulation tests (250 μg) were performed 24, 48, and 168 hours after intubation. AI was defined as an increase in serum cortisol 1 hour post-ACTH test (delta cortisol) of less than 248.4 nmol/L. Forty subjects (participation 42.6%) underwent ACTH testing. Fifteen received etomidate, and 25 received another anesthetic. There were no statistically significant differences between groups as to the cumulative incidence of AI at any measurement time. However, at 24 hours, exploratory post hoc analyses showed a significant decrease in delta cortisol (adjusted means: etomidate group: 305.1 nmol/L, 95% CI 214.7-384.8 versus other anesthetics: 500.5 nmol/L, 95% CI 441.8-565.7). This decrease was not present at 48 and 168 hours. In TBI victims, although a single dose of etomidate does not increase the cumulative incidence of AI as defined, it seems to decrease the adrenal response to an ACTH test for 24 hours. The clinical impacts of this finding remain to be determined.