01OverviewDefinition, clinical context and the essential points that orientate the chapter.
The sellar and suprasellar region contains the pituitary gland, stalk, optic nerves and chiasm, cavernous sinuses, hypothalamus and nearby carotid arteries. Pituitary neuroendocrine tumours are common causes of a sellar mass, but the differential also includes craniopharyngioma, Rathke cleft cyst, meningioma, metastasis, hypophysitis, aneurysm and other lesions. The clinical problem is therefore broader than “pituitary adenoma”: first define the visual, endocrine and vascular consequences, then establish the lesion with specialist imaging and laboratory assessment.
The nasal retinal fibres cross in the optic chiasm, so compression from below often produces temporal field loss in both eyes. Early disease may be subtle, asymmetrical or detected only on formal perimetry. More extensive compression can reduce central acuity, colour vision and eventually cause optic atrophy. Lateral extension into the cavernous sinus may disturb ocular motor nerves, especially the third nerve. A normal bedside confrontation test or preserved reading acuity does not exclude clinically important chiasmal dysfunction.
Mass effect and hormone function must be assessed together. A lesion may hypersecrete prolactin, growth hormone or ACTH, or compress normal gland tissue and cause deficiencies. Mild prolactin elevation can arise from stalk disconnection and must not automatically be labelled a prolactinoma. Central hypothyroidism is interpreted with free T4 rather than TSH alone. Most importantly, suspected cortisol deficiency changes immediate safety: thyroid hormone should not be started in an unstable patient until adrenal sufficiency has been addressed.
Pituitary apoplexy is acute haemorrhage or infarction, usually within a pituitary tumour. Around four-fifths of patients in the Society for Endocrinology emergency guidance had no known pituitary history. Acute headache, vomiting, field or acuity loss, ophthalmoplegia, meningism or reduced consciousness can mimic subarachnoid haemorrhage or meningitis. The guidance identifies haemodynamic instability, altered consciousness, reduced visual acuity and severe field defects as indications for empirical adult hydrocortisone; this is adrenal replacement and life-saving emergency treatment, not the dexamethasone strategy used for vasogenic oedema around many intracranial tumours.
Key points
- A pituitary-region mass may compress the optic chiasm, disturb anterior or posterior pituitary function, invade the cavernous sinus or be discovered incidentally; imaging appearance alone does not establish the lesion type.
- Chiasmal compression classically causes bitemporal field loss, but acuity can remain normal early and patterns vary with the direction of compression; test each eye formally rather than relying on confrontation alone.
- Pituitary apoplexy is an adult neuroendocrine emergency: acute headache plus neuro-ophthalmic or consciousness change requires resuscitation, urgent endocrine–neurosurgical contact, MRI and timely hydrocortisone when indicated.
- Investigate a stable mass with dedicated contrast pituitary MRI, formal automated perimetry when the lesion abuts or compresses the optic apparatus, and biochemical assessment for hormone hypersecretion and hypopituitarism.
- The cortisol axis takes priority in an unwell patient. Draw cortisol and other pituitary hormones before steroids if this is immediately feasible, but never delay life-saving glucocorticoid replacement for sampling.
- Treatment is lesion- and hormone-specific: visual compromise usually prompts surgical assessment, whereas prolactinoma, non-functioning adenoma, craniopharyngioma and other parasellar lesions do not share one management algorithm.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Pituitary neuroendocrine tumour
Functional or non-functioning adenohypophyseal tumours can enlarge upward toward the chiasm, laterally into cavernous sinuses and downward into the sphenoid region.
Non-adenoma sellar lesions
Craniopharyngioma, Rathke cleft cyst, meningioma, hypophysitis, metastasis and vascular lesions have different endocrine, imaging and treatment implications.
Apoplexy
Haemorrhage or infarction within pituitary tissue, often a tumour, abruptly expands sellar contents and can impair vision, consciousness and ACTH secretion.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Optic chiasm compression
Upward growth injures crossing nasal retinal fibres, commonly producing temporal field loss in both eyes before central acuity necessarily falls.
- 2Pituitary compression or destruction
Reduced ACTH, TSH and gonadotropin secretion causes central hormone deficiency; stalk disruption can raise prolactin and impair posterior pituitary signalling.
- 3Cavernous-sinus extension
Lateral disease can affect ocular motor nerves and trigeminal sensory fibres, producing diplopia, ptosis or facial sensory change.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Ask about bumping into doorframes, difficulty noticing traffic or people to either side, reading problems and loss of confidence driving. Check acuity, colour vision, pupils, confrontation fields, fundi and ocular movements; arrange formal perimetry because early bitemporal loss may escape bedside testing.
Consider apoplexy in acute severe headache with neuro-ophthalmic signs, known pituitary tumour, meningism or reduced consciousness. Do not wait for the entire syndrome: threatened vision or haemodynamic compromise is enough to activate emergency endocrine and neurosurgical care.
Seek fatigue, postural symptoms, weight change, menstrual disturbance, loss of libido, erectile dysfunction and reduced secondary sexual hair. Interpret these with illness severity and medication exposure; cortisol deficiency is the immediately dangerous deficit.
Look for galactorrhoea or hypogonadism, acral and facial change, sweating, diabetes or sleep apnoea suggesting acromegaly, and catabolic or cushingoid features suggesting ACTH excess. Biochemistry rather than appearance confirms a functional syndrome.
Polyuria, polydipsia and hypernatraemia suggest arginine-vasopressin deficiency. This pattern is unusual for an uncomplicated adenoma and broadens the differential toward stalk, inflammatory, metastatic or craniopharyngeal disease.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Formal visual acuity, colour vision and automated perimetryFirst step - Why
- Quantify optic nerve and chiasm function in each eye and create a baseline for urgent decisions and follow-up.
- Interpretation and limitations
- Bitemporal loss supports chiasmal compression, but junctional and asymmetric defects occur. The Endocrine Society recommends formal fields when a lesion abuts the optic nerves or chiasm; worsening acuity or severe field loss changes urgency.
- 02
Dedicated contrast-enhanced pituitary MRI - Why
- Define the sellar lesion, suprasellar extension, optic apparatus, cavernous sinuses, stalk and haemorrhage or infarction.
- Interpretation and limitations
- MRI is the investigation of choice in suspected apoplexy and confirms most cases; pituitary CT is used when MRI is contraindicated or impossible. Imaging distinguishes anatomy, not all histologies or hormonal function.
- 03
Urgent safety bloods and random cortisol in suspected apoplexy - Why
- Detect electrolyte, glucose, renal, haematological and coagulation abnormalities and preserve a pretreatment cortisol sample when feasible.
- Interpretation and limitations
- Take U&E, FBC, renal and liver tests, clotting and glucose; ideally sample cortisol before hydrocortisone. A result must not delay empirical steroids when haemodynamic, consciousness or severe visual criteria are present.
- 04
Pituitary hormone profile - Why
- Screen for hypersecretion and hypopituitarism using cortisol, free T4 with TSH, prolactin, IGF-1 and gonadal-axis tests selected for age, sex and context.
- Interpretation and limitations
- Dynamic testing and repeated specialist assays may be needed. Modest prolactin elevation may be stalk effect, free T4 can be low with an inappropriately normal TSH, and acute illness changes several axes.
- 05
Paired serum and urine osmolality with fluid balance - Why
- Investigate polyuria or hypernatraemia for posterior pituitary dysfunction while assessing volume state.
- Interpretation and limitations
- Inappropriately dilute urine despite hyperosmolar plasma supports AVP deficiency, but osmotic diuresis and excess fluid also cause polyuria. Water deprivation is unsafe in an acutely unwell or hypernatraemic patient.
- 06
Targeted CT/angiography or infection work-up - Why
- Exclude subarachnoid haemorrhage, aneurysm, meningitis or cavernous-sinus disease when presentation is not explained safely by a pituitary mass alone.
- Interpretation and limitations
- The acute differential remains active even if a sellar lesion is known. Lumbar puncture is not a routine apoplexy test and requires a separate safety decision after imaging and clinical assessment.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Intracranial aneurysm
Aneurysm near the sella can mimic a mass and may present with painful third-nerve palsy; vascular imaging is crucial before biopsy or surgery.
Meningitis or subarachnoid haemorrhage
Fever, photophobia, neck stiffness and thunderclap headache overlap with apoplexy and require parallel emergency investigation and treatment decisions.
Primary ophthalmic disease
Glaucoma, retinal disease and optic neuropathy can cause field loss, but the pattern and pituitary MRI relationship guide localisation.
Craniopharyngioma or stalk lesion
Posterior pituitary dysfunction, calcification and hypothalamic involvement make a simple pituitary adenoma less likely and broaden specialist investigation.
Additional chapter-specific clues
Painful ophthalmoplegia, ptosis, anisocoria and trigeminal sensory loss can reflect lateral tumour extension but also aneurysm, cavernous-sinus thrombosis or carotid pathology. Acute onset requires parallel vascular and infectious reasoning.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Emergency apoplexy pathwayAcute headache with visual compromiseFirst stepAn adult develops sudden severe headache, vomiting, a severe new field defect and hypotension with a sellar mass.+
- 1Resuscitate and check glucose, neurological state, acuity, fields and ocular movements; call the joint endocrine–neurosurgical service immediately and treat competing SAH or meningitis pathways when indicated.
- 2Draw urgent safety bloods and pituitary samples if immediately feasible, then give empirical adult hydrocortisone because haemodynamic instability and severe visual loss meet Society for Endocrinology criteria; do not wait for cortisol results.
- 3Obtain urgent pituitary MRI, or pituitary CT when MRI cannot be performed, and continue careful fluid and electrolyte assessment.
- 4Transfer after stabilisation to a unit with neurosurgical, endocrine and ophthalmic expertise; urgent decompression is considered for severe or worsening visual deficits or declining consciousness, while selected stable cases may be managed closely without immediate surgery.
- 5Reassess all pituitary axes, vision and imaging after the acute phase and provide steroid sick-day and emergency information when ongoing adrenal replacement is required.
02Stable mass pathwayProgressive bitemporal field lossA stable adult has several months of peripheral visual loss and MRI shows a suprasellar pituitary-region mass contacting the chiasm.+
- 1Document acuity, colour vision, pupils, ocular movements and formal fields, and screen explicitly for both hormone excess and deficiency.
- 2Review dedicated pituitary MRI and biochemical testing through a pituitary multidisciplinary team, keeping adenoma, craniopharyngioma, meningioma, cyst, inflammation, metastasis and aneurysm in the differential.
- 3Address threatened vision and cortisol safety first, then choose lesion-specific treatment: surgical decompression is commonly assessed for visual compromise, while a confirmed prolactinoma usually begins with specialist medical treatment.
- 4Use serial MRI, perimetry and endocrine review if observation is selected; any new apoplexy symptoms, visual progression or hormonal decompensation overrides the planned interval.
03Surveillance pathwayStable lesion without current surgical criteriaA pituitary-region lesion is stable, does not threaten the optic apparatus and has no uncontrolled hormone syndrome.+
- 1Confirm the baseline with dedicated imaging, pituitary hormone assessment and visual testing when anatomical proximity or symptoms warrant it.
- 2Agree lesion-size- and anatomy-aware MRI, endocrine and clinical follow-up with a named result owner rather than applying one interval to every mass.
- 3Bring review forward for new headache, visual change, ophthalmoplegia, polyuria, hormonal symptoms or radiological growth and reconsider specialist treatment.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Hydrocortisone for adult pituitary apoplexy
When empirical replacement is indicated, Society for Endocrinology guidance allows 100 mg IM followed by 50–100 mg IM every 6 hours, or 100–200 mg IV followed by a continuous infusion of 2–4 mg/hour.Do not delay for cortisol sampling in an unstable or visually threatened patient. Monitor glucose, sodium, potassium, fluid balance and haemodynamics, then obtain endocrine advice for conversion and taper; this regimen is not the dexamethasone regimen for tumour-related vasogenic oedema.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Permanent visual loss
Prolonged or severe optic pathway compression can progress from reversible dysfunction to optic atrophy and irreversible functional impairment.
Adrenal crisis
Acute ACTH deficiency causes hypotension, hypoglycaemia and electrolyte disturbance and is potentially fatal without glucocorticoid replacement.
Panhypopituitarism
Multiple anterior axes may fail and require specialist long-term replacement in the correct physiological sequence with ongoing monitoring.
Post-treatment fluid disorders
AVP deficiency and delayed hyponatraemia can follow pituitary surgery and demand structured sodium and fluid monitoring.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Track visual acuity and formal fields against a documented baseline; new or progressive loss triggers earlier pituitary, ophthalmic and neurosurgical review.
- Repeat pituitary MRI according to lesion size, proximity to the optic apparatus, growth and treatment; Endocrine Society incidentaloma guidance uses earlier imaging for macrolesions than microlesions.
- Reassess pituitary axes after surgery, apoplexy and during conservative follow-up because deficiencies or hypersecretion may evolve independently of size.
- Monitor fluid balance and sodium after apoplexy or pituitary intervention, recognising that AVP deficiency and delayed hyponatraemia require distinct evaluation.
- Ensure patients with adrenal insufficiency receive replacement education, sick-day rules and emergency steroid arrangements from the endocrine team.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Acuity is not the field
Central acuity may be preserved while temporal fields are substantially impaired. Formal perimetry therefore answers a different question from reading a chart.
Prolactin needs context
A large non-functioning lesion can mildly raise prolactin by interrupting hypothalamic dopamine delivery. Magnitude, assay behaviour and imaging must be interpreted by endocrinology.
Cortisol before thyroid
Giving thyroid hormone to a patient with untreated central adrenal insufficiency can precipitate decompensation. Establish or protect the cortisol axis first when clinically relevant.
Apoplexy can be first presentation
No previous pituitary diagnosis is reassuring: the Society guidance notes that most patients presenting with apoplexy have no known pituitary problem.
Not every sellar lesion is an adenoma
Stalk thickening, posterior pituitary dysfunction, calcification, dural attachment or vascular flow features should broaden the diagnostic discussion.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling normal central acuity a normal visual assessment and omitting formal fields when the chiasm is contacted.
- 02
Waiting for every hormone result before giving hydrocortisone to an unstable adult with suspected pituitary apoplexy.
- 03
Using tumour-oedema dexamethasone as if it were the Society for Endocrinology adrenal-replacement regimen.
- 04
Treating any prolactin elevation as proof of prolactinoma without considering stalk effect or assay limitations.
- 05
Starting thyroid replacement before addressing possible cortisol deficiency in an acutely unwell patient.