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  Vol. 143 No. 1, January 2008 TABLE OF CONTENTS
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Increased Risk of Adrenal Insufficiency Following Etomidate Exposure in Critically Injured Patients

Bryan A. Cotton, MD; Oscar D. Guillamondegui, MD; Sloan B. Fleming, PharmD; Robert O. Carpenter, MD; Shivani H. Patel, PharmD; John A. Morris Jr, MD; Patrick G. Arbogast, PhD

Arch Surg. 2008;143(1):62-67.

Background  Timely diagnosis and treatment of adrenal insufficiency (AI) dramatically reduces mortality in trauma patients. We sought to identify risk factors and populations with a high risk of developing AI.

Design  Retrospective registry study.

Setting  Academic level I trauma center.

Patients  All trauma patients in the intensive care unit who underwent cosyntropin stimulation testing (CST) for presumed AI from January 1, 2002, through December 31, 2004.

Interventions  Cosyntropin stimulation testing, in which response was defined as an increase of 9 µg/dL (248 nmol/L) or more in cortisol level.

Main Outcome Measures  Risk factors for developing AI in critically ill trauma patients.

Results  In 137 patients, CST was performed; 83 (60.6%) were nonresponders and 54 (39.4%) were responders. Age, sex, race, trauma mechanism, Injury Severity Score, and Revised Trauma Score were not statistically different between the groups. Rates of sepsis/septic shock, mechanical ventilation, and mortality were also similar between the 2 groups. However, rates of hemorrhagic shock on admission (45 [54%] vs 16 [30%]), requirement of vasopressor support (65 [78%] vs 28 [52%]), and etomidate exposure (59 [71%] vs 28 [52%]) were all significantly higher in the nonresponder group (P < .01). The increased risk of AI remained after controlling for potential confounding covariates (age, mechanism, Injury Severity Score, and Revised Trauma Score).

Conclusions  Exposure to etomidate is a modifiable risk factor for the development of AI in this sample of critically injured patients. The use of etomidate for procedural sedation and rapid-sequence intubation in this patient population should be reevaluated.


Author Affiliations: Division of Trauma and Surgical Critical Care, Department of Surgery (Drs Cotton, Guillamondegui, Carpenter, and Morris), and Departments of Clinical Pharmacology (Drs Fleming and Patel) and Biostatistics (Dr Arbogast), Vanderbilt University Medical Center, Nashville, Tennessee.



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RELATED LETTERS

Lack of Evidence for Adrenal Insufficiency After Single-Dose Etomidate
Michael E. Mullins and Daniel L. Theodoro
Arch Surg. 2008;143(8):808-809.
EXTRACT | FULL TEXT  

Lack of Evidence for Adrenal Insufficiency After Single-Dose Etomidate—Reply
Bryan A. Cotton and Oscar D. Guillamondegui
Arch Surg. 2008;143(8):809.
EXTRACT | FULL TEXT  

RELATED ARTICLE

Increased Risk of Adrenal Insufficiency Following Etomidate Exposure in Critically Injured Patients—Invited Critique
Timothy R. Billiar
Arch Surg. 2008;143(1):67.
EXTRACT | FULL TEXT  


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Rapid sequence induction in the emergency department: induction drug and outcome of patients admitted to the intensive care unit
Baird et al.
Emerg. Med. J. 2009;26:576-579.
ABSTRACT | FULL TEXT  

Opioid Contribution to Decreased Cortisol Levels in Critical Care Patients
Daniell
Arch Surg 2008;143:1147-1148.
FULL TEXT  

Lack of Evidence for Adrenal Insufficiency After Single-Dose Etomidate--Reply
Cotton and Guillamondegui
Arch Surg 2008;143:809-809.
FULL TEXT  

Lack of Evidence for Adrenal Insufficiency After Single-Dose Etomidate
Mullins and Theodoro
Arch Surg 2008;143:808-809.
FULL TEXT  

Etomidate and Adrenal Insufficiency: Another Retrospective Study
JWatch Emergency Med. 2008;2008:2-2.
FULL TEXT  





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