Hypopituitarism

Incidence: 45.5:100,000.

30% of pituitary macroadenomas (>10 mm) cause one or more hormone deficiencies.

About 4.2 years after pituitary radiation therapy, some 50% of pts have hypopituitarism.

Less common causes include empty sella syndrome, head trauma, infiltrative disease, and expansive internal carotid artery aneurysm.

If hormone replacement is adequate, surgery presents no increased risk.

If due to secreting tumor, there is an increased risk of Cushing disease, acromegaly, SIADH, or hyperthyroidism.

Concerns regarding manifestations of disease process: Cushing disease (hypercortisolism secondary to an adrenocorticotropic hormone–secreting adenoma), acromegaly (secondary to a growth hormone–secreting adenoma), and hyperthyroidism in the setting of thyrotropic adenomas.

Operative risks: Bleeding, DI, and SIADH.

GH-secreting adenoma predisposing to acromegaly and subsequent airway abnormality and OSA.

Hypoglycemia.

Altered volume status due to increased urinary losses.

Adequacy of adrenal function.

Increased risk of CV disease.

Possible increase in ICP.

Partial or complete disruption of pituitary gland secretion. Symptoms result from end-organ hypofunction or dysfunction. Organs affected include adrenal and thyroid glands, reproductive system, and liver (glucose production) and kidneys.

Pt may manifest cortisol deficiency, hypothyroidism, amenorrhea, infertility, insulin-induced hypoglycemia, and/or DI.

Pituitary apoplexy is the abrupt destruction of pituitary tissue resulting from infarction or hemorrhage. Symptoms include sudden loss of pituitary function with hypotension, eye pain, blindness, and ophthalmoplegia.

61% secondary to tumors of the pituitary gland

9% due to other types of lesions

19% due to other causes (radiation, hemorrhage, infarct, head trauma, infiltrative diseases)

No cause identified in 11%