Review of: Hildreth AN, Mejia VA, Maxwell RA, et al: "Adrenal suppression following a single dose of etomidate for rapid sequence induction: A prospective randomized study." Journal of Trauma. 65(3):573 579, 2008.
The administration of etomidate has been linked to subsequent adrenocortical insufficiency in non-trauma patients but has not been well studied in the trauma population. These researches enrolled 30 multiple-trauma patients and randomized them to either receive etomidate (18 E patients) and succinylcholine, or a combination of fentanyl and midazolam (12 FM patients) with succinylcholine for RSI. They then measured their serum cortisol levels four to six hours afterward and performed a cortisol stimulation test by administering ACTH.
The patients reportedly had similar degrees of trauma and were aggressively resuscitated. They followed their clinical course and found the following. The serum cortisol levels of the 18 E patients was significantly lower than the FM patients and failed to respond to ACTH as well as the FM patients. This would consistent with suppression of the adrenal cortex.
Clinically, the patients in the E group required longer ICU stays (6.3 days versus 1.5 days,p< 0.05), more ventilator days (28 versus 17,p< 0.01), and longer hospital stays (11.6 days versus 6.4,p< 0.01) compared to the FM group.
The authors conclude that the use of etomidate for RSI in trauma patients let to chemical evidence of adrenocortical insufficiency and may have contributed to the clinical findings listed above. In the text of the article, the authors make this statement: "In light of our study, we recommend that other drugs should be used as first-line agents for RSI in trauma patients."
Just when you thought you had a handle on the RSI issue, someone comes along and throws another wrench in the works. The concern for adrenal insufficiency is why we abandoned high-dose steroids for suspected spinal injuries. Although I don't contest the cortisol levels the authors obtained in this study, I do question their conclusions.
First, the treating physicians were not blinded to which patients were in which group. They knew who was adrenosuppressed. Did this affect their treatment? The E group received significantly more intravenous fluids, blood and blood products. The authors state the patients had similar brain and lung injury severity scores, but we should take notice that the overall injury severity scores were higher (26 versus 19). Although not statistically significant, this may be due to the relatively low overall sample size of only 30 patients and the fact that 60% of the patients were in the E group.
The authors attempt to theorize that the adrenocortical insufficiency may have somehow altered the physiology of the E group in some way as to require their need for a greater need for volume replacement, but they do not provide us any supporting evidence for this theory. I would feel more confident if I knew more about the specific injuries of both groups. The injury severity score is simply not specific enough for such a small study group to make such generalizations.
Although this article sparks my interest, I'm not prepared to eliminate etomidate from my protocols just yet. More study is warranted, and I would ask future authors to be prepared to provide more details about the patient injuries so that we can attempt to determine what if any impact adrenocortical insufficiency, as it relates to etomidate administration, plays in the trauma victim.