Glucocorticoid excess may be due to exogenous administration of steroid hormones, intrinsic hyper-function of the adrenal cortex (eg, adrenocortical adenoma), ACTH production by a nonpituitary tumor (ectopic ACTH syndrome), or hypersecre-tion by a pituitary adenoma (Cushing’s disease). Regardless of the cause, an excess of corticosteroids produces Cushing’s syndrome, characterized by muscle wasting and weakness, osteoporosis, central obesity, abdominal striae, glucose intolerance, men-strual irregularity, hypertension, and mental status changes.
Patients with Cushing’s syndrome may be volume overloaded and have hypokalemic metabolic alka-losis resulting from the mineralocorticoid activity of glucocorticoids. These abnormalities should be corrected preoperatively in the manner previously described. Patients with osteoporosis are at risk for fracture during positioning. If the cause of Cushing’s syndrome is exogenous glucocorticoids, the patient’s adrenal glands may not be able to respond to peri-operative stresses, and supplemental steroids are indicated (see the section on Glucocorticoid Deficiency). Likewise, patients undergoing adre-nalectomy require intraoperative glucocorticoid replacement (in adults, intravenous hydrocortisonesuccinate, 100 mg every 8 h). Other complications of adrenalectomy may include significant blood loss during resection of a highly vascularized tumor and unintentional pneumothorax. On the other hand, many adrenal tumors are removed uneventfully dur-ing laparoscopic surgery.
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