Mon22November0925AM 4

Etomidate is known to cause suppression of hormone synthesis in the adrenal cortex even when a single dose has been given.

It has been associated with higher rates of mortality on intensive care units when administered by infusion.

Which one of the following is thought to be the best explanation for this?

(Please select 1 option)

Inhibition of pregnenolone synthesis

Inhibition of cholesterol desmolase

Inhibition of 11b-hydroxylase Correct

Inhibition of aldosterone synthesis

Inhibition of 11b/18-hydroxylase

Explanation

The mechanism of etomidate effects on the adrenal axis is through a reversible and concentration-dependent blockade of 11b-hydroxylase and, to a lesser extent, 11B/18-hydroxylase (aldosterone synthase, CYP11B2) and the cholesterol side-chain cleavage enzyme known as cholesterol desmolase, or P450scc (converts cholesterol to pregnenolone)

Etomidate was first introduced into clinical practice in Europe in 1972 and was approved for use in the United States in 1983. In early June 1983, and later that same month, letters to the editor were published in The Lancet describing increased mortality in the setting of continuous sedation for trauma patients after the introduction of etomidate. Since then etomidate was no longer used by infusion as a sedative.

Anaesthetists should consider treating selected patients with corticosteroids if etomidate is used for a single dose induction of anaesthesia. Decreased cortisol and aldosterone levels due to this adrenal suppression have been documented to occur approximately 30 minutes after a single induction dose of etomidate, with the duration of the effect being as long as 24 hours to 48 hours.

Answer Statistics

1

1%

2

5%

3

66%

4

10%

5

20%

Times answered: 268