Steroid replacement after etomidate: no benefit
More fuel for the etomidate debate…
- Etomidate has been a useful induction agent for RSI for many years due to its greater haemodynamic stability compared with thiopentone or propofol
- It is widely used in the USA
- It inhibits the 11β-hydroxylase enzyme that converts 11β-deoxycortisol into cortisol in the adrenal gland
- A single dose of etomidate has been demonstrated to inhibit cortisol production for up to 48 hrs
- This has led to concerns about its use in the critically ill, particular in patients with severe sepsis / septic shock
- This small study randomised patients receiving etomidate to hydrocortisone or placebo, with no significant difference in these patient-oriented outcomes: duration of mechanical ventilation, intensive care unit length of stay, or 28-day mortality
- This study suggests that replacement doses of hydrocortisone are not required after a single dose of etomidate
- No randomised study has conclusively demonstrated increased mortality due to etomidate; however while controversy and the possibility of harm remain, I personally see no reason not to use ketamine for RSI in haemodynamically compromised patients.
- Ketamine was compared with etomidate in a previous controlled trial
OBJECTIVE: To investigate the effects of moderate-dose hydrocortisone on hemodynamic status in critically ill patients throughout the period of etomidate-related adrenal insufficiency.
DESIGN: Randomized, controlled, double-blind trial (NCT00862381).
SETTING: University hospital emergency department and three intensive care units.
INTERVENTIONS: After single-dose etomidate (H0) for facilitating endotracheal intubation, patients without septic shock were randomly allocated at H6 to receive a 42-hr continuous infusion of either hydrocortisone at 200 mg/day (HC group; n = 49) or saline serum (control group; n = 50).
MEASUREMENTS AND MAIN RESULTS: After completion of a corticotrophin stimulation test, serum cortisol and 11β-deoxycortisol concentrations were subsequently assayed at H6, H12, H24, and H48. Forty-eight patients were analyzed in the HC group and 49 patients in the control group. Before treatment, the diagnostic criteria for etomidate-related adrenal insufficiency were fulfilled in 41 of 45 (91%) and 38 of 45 (84%) patients in the HC and control groups, respectively. The proportion of patients with a cardiovascular Sequential Organ Failure Assessment score of 3 or 4 declined comparably over time in both HC and control groups: 65% vs. 67% at H6, 65% vs. 69% at H12, 44% vs. 54% at H24, and 34% vs. 45% at H48, respectively. Required doses of norepinephrine decreased at a significantly higher rate in the HC group compared with the control group in patients treated with norepinephrine at H6. No intergroup differences were found regarding the duration of mechanical ventilation, intensive care unit length of stay, or 28-day mortality.
CONCLUSION: These findings suggest that critically ill patients without septic shock do not benefit from moderate-dose hydrocortisone administered to overcome etomidate-related adrenal insufficiency.
Corticosteroid after etomidate in critically ill patients: A randomized controlled trial
Crit Care Med. 2012 Jan;40(1):29-35