The prevalence and impact of AI in critical illness has gained considerable attention recently such that guidelines for the diagnosis and treatment of AI in sepsis have been established.1 Although AI is known to occur in critically ill trauma patients in the early postinjury period, its contribution to patient outcomes and its causes are not well understood. Also underappreciated is the potential contribution of commonly used pharmacologic agents on adrenal function. One such agent is etomidate, a sedative commonly used during rapid-sequence intubation in the initial treatment of severely injured patients. Etomidate has a known impact on adrenal function by blocking mitochondrial hydroxylase activity and, hence, steroidogenesis. This effect was thought to be short-lived after a single dose and therefore of little consequence in the trauma setting. In a retrospective study, the authors of this report have provided evidence that AI, assessed 48 hours after intubation, occurs more frequently in severely injured patients who received etomidate than in those who did not (54% vs 30%). Furthermore, AI was associated with longer hospital stay, more ventilator days, and longer stays in the intensive care unit. However, AI also occurred more frequently in the setting of hemorrhagic shock and in patients who developed coagulopathy. These observations raise intriguing questions. For example, does shock render patients more susceptible to prolonged adrenal dysfunction due to delayed recovery of the enzyme system inhibited by etomidate? Is the initial interpretation of refractory hemorrhagic shock actually a manifestation of early profound adrenal dysfunction?
Billiar TR. Increased Risk of Adrenal Insufficiency Following Etomidate Exposure in Critically Injured Patients—Invited Critique. Arch Surg. 2008;143(1):67. doi:10.1001/archsurg.2007.19
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