Hypopituitarism

Stress-dose steroids - Corticosteroid requirements rise with surgery, stress, and pregnancy. Confirm the usual hydrocortisone regimen, typically 10 to 20 mg in the morning plus 5 to 10 mg in the afternoon, and cover the case. Adrenal crisis from ACTH deficiency is the leading cause of acute decompensation in these patients.

Treat on suspicion, not on labs - Adrenal insufficiency should be treated on clinical suspicion without waiting for biochemical confirmation. A hypotensive hypopituitary patient not responding to fluid and pressor gets steroid.

Steroid before thyroid, always - Replacing thyroid hormone before corticosteroid precipitates adrenal crisis. If both are being started, the corticosteroid goes first.

Confirming the adrenal axis - An 8 AM serum cortisol with a paired ACTH level; equivocal results go to a cosyntropin stimulation test, 250 mcg IV or IM with cortisol drawn at 30, 60, and 90 minutes, where over 18 mcg/dL is a normal response. The insulin tolerance test is the best provocative test for both GH and ACTH but deliberately drives glucose to 40 mg/dL and should not be performed in patients with cardiac disease or epilepsy.

Read the T4, not the TSH - In central hypothyroidism the TSH is no longer a reliable marker. Order free or total T4 to judge thyroid status. Replacement starts low, levothyroxine 25 mcg daily, and is titrated up, particularly in the elderly and in cardiac disease.

Sodium and urine output - ADH deficiency shows up intraoperatively as polyuria with dilute urine. Follow serum sodium, urine specific gravity, and urine osmolality; desmopressin, intranasal or oral, is the replacement. Sodium can move in either direction in a patient already on desmopressin, so measure it rather than assume.

Watch the glucose - Cortisol and growth hormone are counterregulatory hormones. Without them the patient defends poorly against hypoglycemia - check point-of-care glucose during long cases and before emergence.

Mass effect and apoplexy - When a pituitary tumor is the cause, look for bitemporal hemianopsia and headache and confirm with gadolinium-enhanced MRI plus formal visual field testing. Sudden severe headache with visual loss in a known adenoma is apoplexy, an emergency rather than a case to postpone.

Downstream body effects - GH deficiency tracks with obesity, hypercholesterolemia, and metabolic syndrome; estradiol deficiency with osteoporosis, so pad and position carefully. In Sheehan syndrome, hypothyroid features such as bradycardia, hypotension, fatigue, and weight gain surface months after the index hemorrhage.

Hypopituitarism is deficiency of one or more pituitary hormones - anterior: GH, TSH, LH/FSH, ACTH, prolactin; posterior: ADH and oxytocin. About 75 percent of the gland has to be destroyed before deficiency appears, so the presentation is often subtle. Pituitary tumors cause roughly 61 percent of cases; the rest come from hypothalamic and parasellar tumors, traumatic brain injury, pituitary surgery or cranial irradiation, infiltrative disease (hemochromatosis, sarcoidosis, histiocytosis), hypophysitis, and pituitary apoplexy - acute infarction or hemorrhage of the gland, which is an emergency. Sheehan syndrome is infarction of the hyperplastic pituitary after severe postpartum hemorrhage.

What matters perioperatively is the downstream failure: no ACTH means no cortisol response to surgical stress, no TSH means central hypothyroidism and the risk of myxedema coma, and no ADH means uncontrolled free-water loss. Mortality is increased from cardiovascular and respiratory disease.