Pituitary tumours For PG ophthalmology Theory question Reference kanski ak khurana

Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Reading File
Reading File
Reading File
Reading File
Reading File
Reading File
Finding Sources
Reading File
Searching Images

bitemporal hemianopia visual field defect pituitary tumor chiasmal compression

Pituitary Tumours — Neuro-ophthalmology (PG Ophthalmology)

1. Anatomical basis

The pituitary gland sits in the sella turcica, roofed by the diaphragma sellae (a dural fold running from anterior to posterior clinoids). The optic nerves and chiasm lie just above this diaphragma, continuous posteriorly with the optic tracts, forming the anterior wall of the third ventricle.
Key exam point: A visual field defect in a patient with a pituitary tumour generally indicates suprasellar extension - tumours <10 mm (microadenomas) stay confined to the sella; those >10 mm (macroadenomas) extend beyond it and compress the chiasm - Kanski's Clinical Ophthalmology, p. 811-812.
Laterally, the cavernous sinuses flank the sella - a horizontally expanding tumour can involve the intracavernous III, IV and VI nerves. Conversely, an intracavernous carotid aneurysm can erode into the sella and mimic a pituitary tumour.
Chiasmal position variants (clinically important):
  • Prefixed chiasm - lies more anteriorly; a pituitary adenoma preferentially compresses the posterior chiasm (where macular decussating fibres are concentrated) → central/paracentral bitemporal defects.
  • Postfixed chiasm - lies more posteriorly; anterior chiasmal/optic nerve compression → junctional scotoma (central/paracentral scotoma in one eye + contralateral superotemporal defect, from involvement of contralateral inferonasal fibres looping into "Wilbrand's knee").

2. Classification of pituitary adenomas

Old histological classification (acidophil/basophil/chromophobe) is now replaced by a hormonal/functional classification:
TypeHormoneClinical syndrome
Lactotroph (prolactinoma)ProlactinMost common adenoma; amenorrhoea-galactorrhoea-infertility in women; hypogonadism, impotence, gynaecomastia in men. ~95% remain microadenomas
CorticotrophACTHCushing disease - moon face, central obesity, striae, hypertension
SomatotrophGHAcromegaly (adults) / gigantism (children)
Non-functioning ("chromophobe")None secretedPresents late, often with mass effect/visual loss rather than endocrine symptoms
(Kanski's Clinical Ophthalmology, p. 813-816)

3. Ophthalmic features

Symptoms: Vague, gradual visual loss (often unnoticed until advanced); headache without the classic features of raised ICP, so diagnostic delay is common.
Visual fields - the classic teaching:
  • Inferonasal fibres cross the chiasm anteriorly and inferiorly → affected first by an expanding pituitary lesion pressing from below → bitemporal superior quadrantanopia progressing to bitemporal hemianopia (the hallmark chiasmal field defect).
  • Field loss is commonly asymmetrical between the two eyes.
  • Contrast this with craniopharyngioma, which compresses the chiasm from above and behind (upper nasal fibres first) → inferotemporal quadrantanopia as the initial defect - a useful differentiator in exams.
  • Optic atrophy (band or diffuse) present in ~50% of cases with field defects; worsens visual prognosis after decompression.
  • Early sign: colour desaturation across the vertical midline on comparing a red target moved from nasal to temporal field, or comparing symmetrical nasal/temporal targets.
Other effects of extensive bitemporal loss:
  • Loss of sensory fusion → decompensated phoria, diplopia ("hemifield slide" phenomenon).
  • "Postfixation blindness" - a non-seeing zone beyond the fixation point from overlapping blind hemifields; causes difficulty with fine near tasks (threading a needle).
Ocular motility/cranial nerve involvement: Lateral (cavernous sinus) extension can cause III, IV, VI nerve palsies. See-saw nystagmus is a rare associated sign.
Differential diagnosis of a bitemporal-type defect (non-compressive mimics): dermatochalasis, tilted discs, optic disc coloboma, nasal retinoschisis, nasal retinitis pigmentosa, and non-organic (functional) visual loss.

4. Pituitary apoplexy

Acute haemorrhage into, or infarction of, a (usually previously undiagnosed) adenoma. Sheehan syndrome is the postpartum variant from peripartum haemorrhage/hypotension.
Presentation: sudden severe headache, nausea/vomiting, meningism, occasionally reduced consciousness or stroke-like features, sudden reduced VA and/or bitemporal hemianopia, and diplopia from ocular motor nerve compromise. Can precipitate an Addisonian crisis from acute hormonal insufficiency - a genuine ophthalmic/medical emergency requiring urgent MRI, visual fields, hormonal assessment, steroid replacement, and often surgical decompression - Kanski's Clinical Ophthalmology, p. 817.

5. Investigations

  • MRI with gadolinium (multiple planes, thin sections) is the imaging of choice - shows the relationship of the mass to the chiasm; adenomas are typically T1-hypointense, T2-hyperintense.
  • CT - shows sellar enlargement/erosion.
  • Formal visual field perimetry - essential baseline and for monitoring; low threshold for testing in any patient with unexplained unilateral central visual loss and chronic headache.
  • Endocrine work-up (by endocrinology) - combined over- and under-secretion patterns can coexist.

6. Management (standard teaching)

  • Prolactinoma: first-line medical therapy with dopamine agonists (cabergoline/bromocriptine) - often shrinks the tumour and can improve visual fields without surgery.
  • Other functioning/non-functioning macroadenomas with chiasmal compression: transsphenoidal surgical decompression is the mainstay; visual recovery is better when optic atrophy is absent.
  • Radiotherapy: adjunct for residual/recurrent tumour.
  • Apoplexy: acute steroid replacement +/- urgent surgical decompression.

7. Related lesions often asked together (for comparison)

  • Craniopharyngioma - Rathke pouch remnant; children present with dwarfism/delayed puberty/obesity, adults with visual loss; compresses chiasm from above/behind → inferotemporal field loss first; MRI shows mixed solid-cystic mass; surgical treatment but high recurrence.
  • Meningioma (tuberculum sellae, sphenoid ridge, olfactory groove) - middle-aged women; tuberculum sellae type classically produces a junctional scotoma.

High-yield exam one-liners:
  • "Visual field defect + pituitary tumour = suprasellar extension."
  • "Classic chiasmal defect = bitemporal hemianopia, asymmetrical, superior quadrants first."
  • "Pituitary adenoma compresses from below → superior bitemporal defect first; craniopharyngioma compresses from above → inferior bitemporal defect first."
  • "Junctional scotoma = ipsilateral central scotoma + contralateral superotemporal defect (anterior chiasm/optic nerve junction lesion)."
This aligns with the standard teaching found in both Kanski's Clinical Ophthalmology (Neuro-ophthalmology chapter, "Chiasm" section) and AK Khurana's Comprehensive Ophthalmology neuro-ophthalmology chapter, which covers the same chiasmal anatomy, field defect patterns and pituitary adenoma classification in near-identical fashion - useful to cross-reference both for viva preparation since examiners often draw the bitemporal hemianopia progression diagram and ask you to explain the fibre anatomy behind it.
This is a shared conversation. Sign in to Orris to start your own chat.