Klinische Wochenschrift
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Klinische Wochenschrift · Nov 1984
Randomized Controlled Trial Comparative Study Clinical TrialAdrenocortical suppression by a single induction dose of etomidate.
In a prospective controlled trial we studied the effect of a single induction dose of etomidate or thiopentone on the adrenocortical function in 29 patients undergoing elective surgery. During anesthesia and in the recovery period serum cortisol rose significantly in the thiopentone group only. ⋯ Moreover, plasma ACTH increased significantly more after etomidate than after thiopentone (p less than 0.02) indicating relative unresponsiveness of the adrenal cortex to stimulation by endogenous ACTH. We conclude that a single i.v. bolus of etomidate (0.26 mg/kg) leads to significant adrenal insufficiency in patients without preexisting endocrine abnormalities.
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Klinische Wochenschrift · Nov 1984
Case ReportsEtomidate: a selective adrenocortical 11 beta-hydroxylase inhibitor.
To investigate the adrenocortical suppression caused by the anesthetic etomidate, plasma levels of progesterone (P), 17-hydroxyprogesterone (17-OHP), 11-deoxycorticosterone (DOC), corticosterone (B), aldosterone (Aldo), 11-deoxycortisol (S), cortisol (F), and cortisone (E) were measured simultaneously before and after a short-term ACTH stimulation test in a 6.5-year-old boy whose convulsions could be kept under control only with constant etomidate infusions. During etomidate therapy, plasma levels of DOC and S were extremely elevated, the progestins P and 17-OHP were slightly elevated, whereas B and Aldo were in the lower normal range, and F and E were markedly decreased. A short-term ACTH stimulation test during etomidate infusion gave a blunted response of B, Aldo, F and E, whereas the level of DOC remained high and S even further increased. ⋯ In contrast, the ratios of DOC/P and S/17-OHP, which reflect 21-hydroxylase activity, were elevated and remained elevated after ACTH stimulation. After discontinuation of etomidate therapy, all the baseline steroid levels were somewhat elevated, but responded normally to ACTH. These results demonstrate that etomidate causes a specific and reversible blockade of the 11 beta-hydroxylation of adrenal steroid synthesis.