GLUCOCORTICOID EXCESS
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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