Pituitary Adenoma

Pituitary adenomas arise from the cells of the anterior pituitary. The 2022 WHO classification calls them pituitary neuroendocrine tumours (PitNETs) and classifies them by cell lineage, defined by transcription factors: PIT1 (somatotroph, lactotroph, thyrotroph and mammosomatotroph), TPIT (corticotroph) and SF1 (gonadotroph), with a small group of null-cell tumours^[1]. Some subtypes, such as sparsely granulated somatotroph, Crooke cell, silent corticotroph and immature PIT1-lineage tumours, are considered high-risk because they recur more often.

Clinically, tumours are described by size (microadenoma under 1 cm, macroadenoma 1 cm or more, giant over 4 cm), by hormone secretion (functioning or non-functioning) and by invasion of the cavernous sinus.

• Prolactinoma: amenorrhoea, galactorrhoea and infertility in women; hypogonadism, low libido and mass effect in men.
• Somatotroph adenoma: acromegaly (or gigantism in children), with cardiovascular, metabolic and joint disease.
• Corticotroph adenoma: Cushing disease.
• Thyrotroph adenoma: secondary hyperthyroidism (rare).
• Non-functioning macroadenoma: bitemporal hemianopia, hypopituitarism and headache.
• Pituitary apoplexy: sudden headache, visual loss and ophthalmoplegia from haemorrhage or infarction of a tumour, a medical and often surgical emergency.

Dynamic contrast-enhanced pituitary MRI identifies microadenomas as areas of delayed enhancement and shows macroadenoma extension above the diaphragm, into the sphenoid sinus and into the cavernous sinus. The Knosp classification grades cavernous sinus invasion by the relationship of the tumour to lines drawn between the cavernous and supraclinoid carotid artery on coronal MRI: grades 0–2 rarely invade, while grades 3 and 4 usually do^[2]. Micko and colleagues later split grade 3 into 3A (extension above the intracavernous carotid) and 3B (below), with different rates of true invasion^[3]. Endocrine testing covers all axes, including prolactin (diluted to avoid the “hook effect” in large tumours), IGF-1, morning cortisol and thyroid function. Formal visual fields are assessed.

Prolactinomas, including macroprolactinomas causing visual loss, are treated first with dopamine agonists such as cabergoline, which normalise prolactin and shrink most tumours; surgery is reserved for resistance, intolerance or patient preference^[4]. Other secreting tumours and symptomatic non-functioning macroadenomas are treated by surgery. Small, incidental non-functioning tumours can be observed. Radiotherapy, radiosurgery and medical therapy (somatostatin analogues, pegvisomant, steroidogenesis inhibitors) are used for residual or recurrent disease.

The endoscopic endonasal transsphenoidal approach is now the standard route for most pituitary tumours, providing a wide, panoramic view of the sella and parasellar region^[5,6].

• Open the sphenoid sinus widely; identify the sellar floor, carotid prominences, optic protuberances and the opticocarotid recesses.
• Open the dura and remove the tumour systematically, working from inferior to lateral and finally superior so that the diaphragma descends late.
• Look for a pseudocapsule; extracapsular dissection improves remission in functioning tumours.
• Identify and preserve the normal gland, which is usually displaced superiorly or posteriorly.
• Reconstruct according to the intraoperative CSF leak; use a nasoseptal flap for high-flow leaks^[7].

Vision improves in most patients with chiasmal compression. Endocrine remission depends on tumour type, size and invasion. Complications include diabetes insipidus and SIADH (often transient), new hypopituitarism, CSF leak, epistaxis, sinusitis and, rarely, carotid artery injury or visual worsening. Postoperative care includes checking cortisol, fluid balance and sodium, and endocrine follow-up.