A small, but growing body of evidence is starting to correlate the physiologic adrenal suppression of etomidate with worsening clinical outcomes. This study is a French prospective cohort that really likes etomidate for RSI, so, they decided to ask the question whether a continuous hydrocortisone infusion has any substantial effect on cardiovascular parameters in the setting of etomidate use.
Short answer, no.
Their randomized groups are awfully small – 45 patients in each group – so their power to detect a difference is not great. But, at the minimum, there’s no profoundly obvious difference or any seemingly clinically significant trend between the two groups.
I trained using etomidate for everyone, but I’ve almost completely moved to alternative agents, ketamine being the most prominent of those agents. Most significantly, ketamine differs from the other agents in terms of having analgesic properties as well, and I think it is reasonable to provide some treatment for the pain associated with laryngoscopy. There is evidence that ketamine is a myocardial depressant and may be deleterious in patients with limited cardiac reserve, but so far in limited literature it holds up clinically well against etomidate and midazolam.
“Corticosteroid after etomidate in critically ill patients: A randomized controlled trial”
http://www.ncbi.nlm.nih.gov/pubmed/21926601
“Intubating ICU patients with ketamine: adverse effects that can occur.”
http://www.ncbi.nlm.nih.gov/pubmed/18079246
One thing to consider about this study is they had an extremely small number of patients included who were septic (septic with no shock, 1 pt in control and 2 in the hydrocortisone group with septic shock patients being completely excluded). There are a few articles (tekwani et al, jabre et al and retrospective corticus review) suggesting that etomidate is associated with increased mortality in the subset of septic patients. The increase in mortality in both the jabre and tekwani study were around 6-8%.
This by no means is definitive and the evidence is weak at best, but this study basically demonstrates nothing that I think most er docs already didn't know. Adrenal suppression from etomidate in patients without sepsis is likely of no consequence.
The important point is the one that you make which is there are other agents that exists that may be superior.
Other agents exist that, at least, provide alternatives. We have an etomidate shortage at our facility, and the best thing is that it's giving our physicians an opportunity to experience different induction agents – and to learn that you can make an individualized decision for each patient which agent might be appropriate, rather than simply reaching for etomidate each time.