*Relative to cortisol.
Data from Stoelting RK, Hillier SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2006:462.
A typical oral replacement dose for Addison’s disease may consist of prednisone, 5 mg in the morning and 2.5 mg in the evening, or hydrocortisone, 20 mg in the morning and 10 mg in the evening. If indicated, mineralocorticoid replacement may consist of 0.05 to 0.2 mg/day of fludrocortisone. Standard glucocorticoid doses should be supplemented during periods of surgical stress.
Anesthetic considerations
Anesthetic management for patients with primary adrenal insufficiency should provide for exogenous corticosteroid supplementation. Etomidate should be avoided because it transiently inhibits synthesis of cortisol in physiologically normal patients. Doses of anesthetic drugs should be minimized because these patients may be sensitive to drug-induced myocardial depression. Invasive monitoring (arterial line and pulmonary artery catheter) is indicated. Because of skeletal muscle weakness, the initial dose of muscle relaxant should be reduced, and further doses should be governed by peripheral nerve stimulator response. Plasma concentrations of glucose and electrolytes should be measured frequently during surgery.
Secondary adrenocortical insufficiency
Definition
Secondary adrenocortical insufficiency is caused by ACTH deficiency from two primary etiologies: (1) hypothalamic–pituitary–adrenal (HPA) axis suppression after exogenous glucocorticoid therapy and (2) ACTH deficiency secondary to hypothalamic or pituitary gland dysfunction (tumor, infection, surgical or radiologic ablation). Long-term treatment with glucocorticoids, for any cause, results in negative feedback to the hypothalamus and pituitary gland, decreased ACTH output, and eventual adrenal cortex atrophy. The longer the duration of glucocorticoid administration, the greater the likelihood of suppression, but the precise dose or duration of therapy that produces adrenal suppression is unknown. Sustained and clinically important adrenal suppression usually does not occur with treatment periods less than 14 days. Treatment periods long enough to provoke signs of Cushing syndrome are usually associated with adrenal suppression of clinically significant.
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