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Increased Risk of Adrenal Insufficiency Following Etomidate Exposure in Critically Injured Patients—Invited Critique
Timothy R. Billiar, MD
Arch Surg. 2008;143(1):67.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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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, . . . [Full Text of this Article] AUTHOR INFORMATION
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Increased Risk of Adrenal Insufficiency Following Etomidate Exposure in Critically Injured Patients
Bryan A. Cotton, Oscar D. Guillamondegui, Sloan B. Fleming, Robert O. Carpenter, Shivani H. Patel, John A. Morris, Jr, and Patrick G. Arbogast
Arch Surg. 2008;143(1):62-67.
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