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Chapter: Clinical Anesthesiology: Anesthetic Management: Anesthesia for Patients with Endocrine Disease

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Anesthesia for Glucocorticoid Deficiency

Primary adrenal insufficiency (Addison’s disease) is caused by destruction of the adrenal gland, which results in a combined mineralocorticoid and gluco-corticoid deficiency.

GLUCOCORTICOID DEFICIENCY

Clinical Manifestations

 

Primary adrenal insufficiency (Addison’s disease) is caused by destruction of the adrenal gland, which results in a combined mineralocorticoid and gluco-corticoid deficiency. Clinical manifestations are due to aldosterone deficiency (hyponatremia, hypovo-lemia, hypotension, hyperkalemia, and metabolic acidosis) and cortisol deficiency (weakness, fatigue, hypoglycemia, hypotension, and weight loss).

 

Secondary adrenal insufficiency is a result of inadequate ACTH secretion by the pituitary. The most common cause of secondary adrenal insuf-ficiency is iatrogenic, the result of prior admin-istration of exogenous glucocorticoids. Because mineralocorticoid secretion is usually adequate in secondary adrenal insufficiency, fluid and electrolyte disturbances are not present. Acute adrenal insuffi-ciency (addisonian crisis), however, can be triggered in steroid-dependent patients who do not receive appropriate glucocorticoid doses during periods of stress (eg, infection, trauma, surgery), and in patients who receive infusions of etomidate. The clinical features of this medical emergency include fever, abdominal pain, orthostatic hypotension, and hypovolemia that may progress to circulatory shock unresponsive to resuscitation.

Anesthetic Considerations

Patients with glucocorticoid deficiency must receive adequate steroid replacement therapyduring the perioperative period. All patients who have received potentially suppressive doses of ste-roids (eg, the daily equivalent of 5 mg of prednisone) by any route of administration (topical, inhalational, or oral) for a period of more than 2 weeks any time in the previous 12 months may be unable to respondappropriately to surgical stress and should receive perioperative glucocorticoid supplementation.

 

What represents adequate steroid coverage is controversial, and there are those who advocate variable dosing based on the extent of the surgery. Although adults normally secrete 20 mg of corti-sol daily, this may increase to over 300 mg under conditions of maximal stress. Thus, a traditional recommendation was to administer 100 mg of hydrocortisone phosphate every 8 h beginning on the morning of surgery. An alternative low-dose regimen (25 mg of hydrocortisone at the time of induction followed by an infusion of 100 mg during the subsequent 24 h) maintains plasma cortisol lev-els equal to or higher than those reported in healthy patients undergoing similar elective surgery. This second regimen might be particularly appropriate for diabetic patients, in whom glucocorticoid adminis-tration often interferes with control of blood glucose.

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