Etomidate is a well-known general
anesthetic most commonly used for procedural sedation or rapid sequence
intubation because of its quick onset, short duration of action, and
pharmacologic profile that does not generally does not cause clinically
significant hemodynamic instability. One side effect of etomidate is its
ability to inhibit or decrease the production of cortisol in the adrenal
glands. While in most patients this is of no clinical relevance, it could
be more detrimental in some patients with sepsis.
is able to decrease the production and secretion of cortisol from the adrenal gland
through a direct inhibition of the enzyme, 11-beta-hydroxylase. This
enzyme is required to convert the precursor, 11-deoxycortisol to cortisol
within the zona fasciculata with the adrenal cortex layer of the adrenal gland.
Fortunately, other hormones (aldosterone and testosterone) also produced within
the adrenal glands can still be made.
stated above, patients known to have sepsis or be in septic shock are known to be at
a higher risk for adrenal insufficiency. As such, some clinicians may elect to
use another sedative for procedural sedation or rapid sequence intubation in
patients known to have sepsis or be in septic shock. However, the
clinical relevance of this effect is still under some debate.
Jong FH, Mallios C, Jansen C et al. Etomidate suppresses adrenocortical function
by inhibition of 11 beta-hydroxylation. J Clin Endocrinol Metab
DE, Griffiths H. The inhibtion by etomidate of the 11 beta-hydroxylation
of cortisol. Clin Endocrinol 1984;20(5):625-9.
B, Dorr H, Stuttmann R et al. Effect of a single bolus of etomidate upon
eight major corticosteroid hormones and plasma ACTH. Clin Endocrinol
Z, Afessa B, Finkielman JD. The incidence of relative adrenal
insufficiency in patients with septic shock after the administration of
etomidate. Crit Care 2006;10(4):R105.
CM, Mitchell AL, Shorr AF. Etomidate is associated with mortality and
adrenal insufficiency in sepsis: a meta-analysis. Crit Care Med