Pituitary Tumour / Apoplexy

Pituitary tumours are the most common intracranial neoplasm and are almost always benign adenomas (increasingly found on MRI). They present in three ways: hormone hypersecretion, hypopituitarism (see Hypopituitarism), or mass effect (headache, visual field loss). Non-functioning adenomas ≥10 mm usually cause hypopituitarism; functioning adenomas cause a hormone-specific syndrome.

Prolactinoma (most common functional adenoma)

• Features: women — galactorrhoea, menstrual disturbance, infertility; men — erectile dysfunction, reduced libido; children — pubertal delay. If >10 mm (macroadenoma), headache and visual field loss.
• Investigations: serum prolactin; MRI brain. Examine visual fields and for gynaecomastia.
• Management: endocrine referral; medical therapy is a dopamine agonist (cabergoline, bromocriptine, quinagolide). Ovulation may return quickly — counsel on contraception. Treat ~3 years then trial withdrawal if symptoms resolved, tumour shrunk, and prolactin well-controlled on a low dose. Restart and continue lifelong on relapse in men or with a macroadenoma. The COCP is an option for galactorrhoea/osteoporosis protection where fertility isn’t wanted. Macroadenomas need endocrine input before conception (risk of enlargement in pregnancy/breastfeeding).

Acromegaly (GH excess)

• Features: enlargement of hands/feet, coarsening of soft tissues (lips, nose, jaw, tongue), sweating, headaches, amenorrhoea/reduced libido, snoring/sleep apnoea, deepening voice. (Murtagh triad: nasal problems + ring/shoe fitting problems + sweating.)
• Investigations: GH that fails to suppress on OGTT and elevated IGF-1; MRI shows a pituitary adenoma.
• Management: aim IGF-1 into the normal range and GH <2.5 microgram/L. Transsphenoidal surgery is first-line; if unfit, medical therapy with a somatostatin analogue (lanreotide, octreotide), adding a dopamine agonist (cabergoline, bromocriptine) if inadequate.

Cushing’s disease (ACTH-secreting adenoma)

The pituitary cause of Cushing’s syndrome (~70% of endogenous cases), managed by transsphenoidal adenoma removal (remission >65%; glucocorticoid replacement for up to a year afterwards). For the full features, confirmation of cortisol excess, and ACTH-based localisation, see Cushing’s syndrome.

Pituitary apoplexy

Sudden haemorrhage or infarction of the pituitary (usually into an underlying adenoma).

• Presentation: severe headache (95% — may mimic subarachnoid haemorrhage), vomiting (~69%), visual field defects (~64%), reduced visual acuity (~52%), diplopia/ptosis (cranial nerve palsies), ± altered mental state; ACTH deficiency is the most common resulting hormone deficit.
• Precipitants: hypertension, major surgery, pregnancy, head injury.
• Management: an emergency — hospital transfer (differentials: SAH, meningitis, optic neuritis). IV hydrocortisone (100 mg stat then 50 mg 6-hourly) for glucocorticoid cover; dexamethasone for oedema; urgent endocrine and neurosurgical review for possible decompression.