Pituitary incidentaloma and pituitary apoplexy

• A pituitary incidentaloma is a sellar or parasellar finding discovered by chance on imaging done for another reason; pituitary adenomas are the commonest such finding, followed by Rathke cleft cyst and empty sella.
• Most microadenomas (under 10 mm) are truly incidental, hormonally inactive, and change little over years; macroadenomas (10 mm or more) are the ones that threaten vision.
• The work-up has three parts whatever the size: a dedicated pituitary MRI, baseline pituitary hormone testing, and visual field testing whenever the lesion sits near or abuts the optic chiasm.
• Pituitary apoplexy is sudden haemorrhage or infarction in the pituitary, usually in a previously unknown tumour; it presents with thunderclap headache, visual loss, ophthalmoplegia and acute hypopituitarism, and empiric hydrocortisone can be lifesaving.
• Management is team-based: acute stabilisation and steroids first, then a decision between conservative care and transsphenoidal decompression based on vision and consciousness, followed by long-term hormone and imaging follow-up.

By the end of this page you should be able to:

1. Define a pituitary incidentaloma and separate a micro- from a macro-adenoma, explaining why size and distance from the optic chiasm drive decisions. ^[1]
2. Plan the initial imaging, endocrine and visual assessment of a newly found sellar lesion, including which tests are done and when they are repeated.
3. Recognise pituitary apoplexy from its clinical picture, know which investigations confirm it and which other emergencies it mimics.
4. Give the acute medical management of apoplexy, including the hydrocortisone regimen, indications for surgery and the surgical approach.
5. Apply the Pituitary Society 2025 surveillance intervals for MRI and for visual fields to a chosen patient.
6. Counsel a patient on prognosis, and adapt care in pregnancy, in older adults and in low-resource settings.

These two topics are studied together because they describe the same anatomical problem at opposite speeds. An incidentaloma is found slowly and silently; apoplexy is the same region failing all at once. A patient with a known small incidentaloma is told "we will watch it"; a patient with apoplexy is told "we are resuscitating you now". Understanding both lets you decide, for every sellar mass, whether the next step is reassurance with surveillance, referral for planned surgery, or an emergency call to the neurosurgical team.

The newest dedicated guideline for the incidentaloma is the Pituitary Society international consensus guideline statement of 2025, built from a workshop of 40 experts from 21 countries. For the emergency, the Society for Endocrinology Endocrine Emergency Guidance of 2016 remains the referenced UK document, and an updated 2024 narrative review summarises the modern evidence on medical versus surgical care. Where these sources do not agree, both views are given rather than a false single answer. ^[1]

Clinically non-functioning pituitary adenomas dominate this group, and the words "pituitary incidentaloma" and "non-functioning pituitary adenoma (NFPA)" are often used interchangeably. Two size categories matter because they behave differently:

• Microadenoma: an adenoma with maximal diameter of less than 10 mm. These are nearly always detected without overt signs or symptoms, show no hormone secretory activity, and have a low likelihood of inducing hormonal deficits. ^[1]
• Macroadenoma: an adenoma of 10 mm or more. These are more likely than microadenomas to be associated with visual field changes or with cavernous sinus invasion at the time they are first identified. ^[1]

Classification is therefore not just academic. It sets the imaging interval, the intensity of endocrine monitoring and whether a neurosurgical referral is needed.

Pituitary apoplexy has a separate definition. It is a clinical syndrome of acute haemorrhage and, or, infarction of the pituitary gland, most often of a pituitary tumour. The word "apoplexy" was introduced in 1950 for sudden haemorrhagic necrosis in a pituitary tumour. ^[3] It can occur in a healthy gland (for example Sheehan syndrome after severe post-partum haemorrhage) or in a gland affected by inflammation, infection or tumour. It is rare in children and adolescents.

Pituitary incidentalomas are common at post-mortem but uncommon on routine imaging. Autopsy studies report the highest figures: a survey of 33 studies covering more than 19,000 autopsies found 2,084 lesions, a mean prevalence of 10.7 percent, with a range of 1.5 to 31.1 percent. ^[1] On MRI the figure is lower: a meta-analysis of 29 MRI studies covering 38,406 patients reported a crude estimate of 2.7 pituitary neoplasms per 1,000 scans. ^[1] Population studies estimate 78 to 94 clinically relevant pituitary adenomas per 100,000 people, with country-standardised incidence rising from about 0.59 to 0.73 cases per 100,000 up to 1.6 to 2.0 per 100,000 per year over 8 to 14 years. ^{[1] [3]}

In clinical series, pooled estimates from 18 studies covering more than 2,000 patients suggest that about 43 percent of imaging-detected incidentalomas are macroadenomas. ^[1] The proportion of incidentally detected micro- and macroadenomas that grow over time varies widely, and a systematic review of 11 studies found 3.3 per 100 person-years growth for microadenomas and 12.5 per 100 person-years for macroadenomas. ^[1] Such growth is not always dangerous: many lesions remain stable for years and some even shrink.

Pituitary apoplexy is far less common: an estimated incidence of about 0.17 episodes per 100,000 person-years and a prevalence of about 6.2 cases per 100,000 people. ^[3] Across published series the prevalence is 0.6 to 10 percent of surgically removed pituitary tumours, averaging 2 percent. ^[3] It develops more often in men (67.5 percent, aged 50 to 60), giving a male-to-female ratio of about 2 to 1. ^[3] Non-functioning adenomas account for about 45 percent of tumours that bleed. ^[3] Microadenoma apoplexy is rare (about 0.36 percent), and the risk of an apoplectic event in a patient with a non-functioning macro-adenoma or a known incidentaloma is 0.2 to 0.6 events per 100 person-years. ^[3] Precipitating factors are found in 30 to 40 percent of cases. ^[3]

Apoplexy in special populations follows its own epidemiology. In pregnancy it occurs in about 1 in 10,000 term pregnancies, most often around 24 weeks of gestation, with about 10 percent post-natal (Sheehan syndrome). ^[3] In children and adolescents it is reported in 1.8 to 7.5 percent of surgically treated pituitary tumours, occurs more in functioning than in non-functioning tumours (mainly prolactinomas, about 73.5 percent), and affects boys and girls equally. ^[3] Sheehan syndrome remains an important cause of hypopituitarism in regions where obstetric care is limited.

Incidentalomas arise from tissues native to the sella: pituitary adenomas, Rathke cleft cysts, craniopharyngiomas, meningiomas, arachnoid cysts, lipomas and empty sella, plus vascular, inflammatory and infiltrative lesions. No modifiable risk factor is known. Prolactinomas comprise 6 to 18 percent of incidentalomas in pooled series. ^[1] A young age at discovery, multiple tumours or extra-sellar extension should raise the possibility of an inherited syndrome and prompt endocrine and genetic assessment.

Apoplexy is thought to follow one of six mechanisms: intra-lesional haemorrhage; an acute increase in pituitary blood flow; ischaemia when a growing tumour outgrows its supply; ischaemia in low-flow states such as major surgery or shock; hormonal or pharmacological stimulation of the gland; or a coagulation disorder. ^[3] Estrogen therapy, somatostatin analogues and dopamine agonists (bromocriptine and cabergoline) have all been implicated, although dopamine agonist therapy can be continued after an apoplectic event to control prolactinoma size and secretion. ^[3] Growth hormone and ACTH secreting tumours are over-represented, and men have a higher risk than women.

The harm done by an incidental macroadenoma follows from its position: it is a firm, usually slow-growing mass in a small bony box. Superior growth pushes the optic chiasm from below, producing bitemporal hemianopia and, if severe, reduced visual acuity. Lateral growth enters the cavernous sinus and can produce cranial nerve palsies (third nerve, then fourth and sixth), or carotid compression. Downward growth erodes the sella floor. Sustained contact with the normal gland produces hypopituitarism. Hormone hypersecretion (prolactin, growth hormone or ACTH) is the other mode of presentation.

Apoplexy is a vascular event with mechanical consequences. Haemorrhage or infarction enlarges the gland abruptly, and the rigid sella has nowhere to yield, so intra-sellar pressure rises. Superior compression of the chiasm causes sudden visual loss; lateral compression of the cavernous sinus causes third, fourth and sixth nerve palsies, often with periorbital pain; inferior compression can leak cerebrospinal fluid. Haemorrhage may extend into the subarachnoid space and mimic meningitis or subarachnoid haemorrhage. Adenohypophyseal necrosis gives acute hypopituitarism within hours, and corticotroph failure is the most dangerous because cortisol loss produces hypotension, hyponatraemia and collapse. Hyponatraemia occurs in up to 40 percent of patients, from adrenal insufficiency, central hypothyroidism or the syndrome of inappropriate antidiuresis. ^[3] GH deficiency is almost universal at diagnosis but is not tested acutely.

An incidentaloma often announces itself through the reason the scan was requested: headache, head injury, syncope, stroke, ear disease or unrelated cancer staging. Many patients have no symptoms referable to it. A macroadenoma may produce subtle clues: bitemporal visual loss noticed only when driving, slowly progressive headache, or hypopituitarism (fatigue, cold intolerance, loss of libido, oligo- or amenorrhoea, erectile dysfunction). A minority secrete hormone and present in the usual way for that tumour.

The endocrine examination looks for the specific patterns of hormone excess (Cushingoid features, acral change, galactorrhoea) and for signs of hypopituitarism (pallor, fine wrinkled skin, loss of body hair, small testes, low blood pressure). Neuro-ophthalmic examination is the safety-critical part: visual acuity, visual fields to confrontation, pupillary reactions, and testing of ocular movements for a third, fourth or sixth nerve palsy. Cranial nerve signs point to cavernous sinus involvement and change both urgency and surgical planning.

Apoplexy presents differently and fast. The Society for Endocrinology describes it as a rare, potentially lethal endocrine emergency characterised by acute severe headache, visual defects and, or, reduced consciousness. ^[2] The clinical picture is:

• Headache in 89 percent, often sudden, retro-orbital or frontal, sometimes occipital, and severe. ^[3]
• Ophthalmoplegia in 78 percent, mainly third nerve palsy, then fourth or sixth. ^[3]
• Vomiting in 69 percent. ^[3]
• Campimetric (visual field) defects in 64 percent, usually a bitemporal hemianopia from chiasmal compression. ^[3]
• Reduced visual acuity in 52 percent. ^[3]
• Hypopituitarism in most patients: gonadotroph failure in about 75 percent, corticotroph failure in about 70 percent, thyrotroph failure in about 50 percent. ^[3]
• A reduced level of consciousness, from cortisol collapse or mass effect, and sometimes seizures or focal deficits.

The syndrome mimics more common emergencies: subarachnoid haemorrhage, bacterial or viral meningitis, brainstem infarct, cavernous sinus thrombosis, and adult optic neuritis. Fever, neck stiffness and photophobia can occur when blood leaks into the subarachnoid space. Therefore the first test in a patient with sudden severe headache is CT of the brain (with lumbar puncture when needed) to exclude haemorrhage and meningitis; once life-threatening causes are excluded, MRI confirms apoplexy. ^{[2] [3]}

Precipitating factors, when present, are hypertension, major surgery (especially coronary artery bypass), dynamic pituitary testing, anticoagulant or antiplatelet therapy, coagulopathy, pregnancy and head trauma. ^{[2] [3]}

The differential has two parts: mimics of the acute presentation, and mimics of the sellar mass on imaging.

A mass discovered incidentally on CT, brain MRI or PET-CT needs a dedicated pituitary MRI with gadolinium unless there is a contraindication. ^[1] The Pituitary Society 2025 recommendations are for a standardised protocol with T1-weighted spin echo images in coronal and sagittal planes before and after gadolinium, plus T2-weighted fast spin echo images in the coronal plane, with a slice thickness of 3 mm or less. ^[1] Routine CT is not recommended for characterising an adenoma because soft-tissue contrast and appreciation of cavernous sinus invasion are inferior; CT is used later to assess calcification and bony extension. ^[1] Apoplexy is best shown by MRI, which confirms the diagnosis in over 90 percent of patients; CT diagnoses less than 30 percent of apoplexies even though it shows a sellar mass in more than 80 percent. ^{[2] [3]} When MRI is contraindicated or unavailable, pituitary CT is acceptable. ^[2]

If an incidental sellar or parasellar lesion is under-characterised on the original scan, the dedicated MRI is mandatory before any endocrine or surgical plan is finalised.

Pituitary hormone testing is recommended at initial presentation for every incidental sellar lesion, irrespective of size, and for patients with incidentally discovered empty sella. ^[1] The baseline panel recommended by the 2025 guideline is: free thyroxine, TSH, morning cortisol, ACTH, luteinizing hormone, follicle-stimulating hormone and IGF-1, with testosterone in men and oestradiol in women; prolactin in all patients. ^[1] Dynamic testing of the hypothalamic-pituitary-adrenal axis is performed when morning cortisol suggests hypocortisolism, and dynamic testing for growth hormone deficiency may be required in selected patients after other deficiencies are corrected. ^[1] Screening for hypercortisolism is done only when clinically warranted. ^[1] Premenopausal women with regular menses do not need gonadal hormone testing. ^[1]

For apoplexy the same hormones are taken, but urgently: urea and electrolytes, full blood count, renal and liver function, clotting profile, and cortisol, prolactin, free thyroxine, TSH, IGF-1, growth hormone, LH, FSH and testosterone or oestradiol, so that any axis failure is defined after the patient is stabilised. ^{[2] [3]}

Visual assessment is essential because the optic chiasm is the structure the patient will actually notice failing. By confrontation, check visual acuity, visual fields, pupillary responses and eye movements in every patient with a macroadenoma or with symptoms.

Formal perimetry is preferred. Humphrey automated static perimetry (or Goldmann kinetic perimetry) should be performed whenever the lesion abuts or is within 5 mm of the optic chiasm, or when visual symptoms exist. ^{[1] [3]} In apoplexy, visual acuity, visual fields and ocular motility are assessed at the bedside during the first 48 hours and, if possible, with an instrument (Humphrey or Goldmann). ^[3]

The 2025 guideline sets the follow-up schedule for visual fields:

• Repeat visual field testing at 6 months in patients with suprasellar extension when surgery is not performed, because compression may progress before imaging shows it. ^[1]
• Repeat at 1 to 2 years in all patients with macroadenomas, since adenoma growth and baseline distance to the chiasm do not always predict visual deterioration. ^[1]
• For macroadenomas not compressing the chiasm that are followed with annual MRI, test visual fields every 6 to 12 months to catch early growth during the extended scan interval. ^[1]
• Patients with abnormal results are referred to a neuro-ophthalmologist. ^[1]

Timing of the first MRI after diagnosis is individualised. In the absence of new or worsening symptoms, the 2025 guideline accepts the following intervals if surgery is not undertaken: 2 to 3 years for microadenomas, 1 year for macroadenomas 5 mm or more away from the optic chiasm, and 6 to 12 months for macroadenomas less than 5 mm from the optic chiasm. ^[1] Slowly enlarging or stable macroadenomas less than 5 mm from the chiasm are rescanned every 1 to 2 years; stable macroadenomas 5 mm or more away every 2 to 3 years. ^[1] For microadenomas smaller than 5 mm that are stable on a repeat MRI performed 2 to 3 years after the initial scan, ongoing surveillance can be reconsidered, especially in patients with reduced life expectancy, poor functional status or a contraindication to surgery. ^[1]

Surveillance MRI alone is not enough; hormone testing is repeated at 1 to 2 years in micro- and macroadenomas (earlier if new symptoms occur), and whenever a lesion enlarges. ^[1] Documented hormone hypersecretion or hypopituitarism is then followed according to the relevant condition-specific guideline. ^[1]

There is no single blood test that diagnoses an incidentaloma; the diagnosis is radiological, the staging biochemical, and the management individualised. A mass is described by its size, its consistency (solid versus cystic), its T2 signal, stalk deviation and whether it invades the cavernous sinus. Multiple (double) incidentalomas are rare and usually comprise growth hormone and ACTH secreting tumours. ^[1]

Apoplexy is a clinical diagnosis supported by imaging, and two scoring systems are used to grade severity and guide the surgery decision:

• Pituitary Apoplexy Score (PAS), proposed by the UK group in 2011, scores level of consciousness (Glasgow Coma Scale: 15 gives 0, 8 to 14 gives 2, under 8 gives 4), visual acuity (normal 0, reduced unilateral 1, reduced bilateral 2), visual fields (normal 0, unilateral defect 1, bilateral defect 2) and ocular paresis (absent 0, unilateral 1, bilateral 2), giving a score built from those components. ^[3] Surgical patients in retrospective series had PAS 3 to 4 versus 1 to 2 in conservatively treated patients; a patient with a score around 3 to 4 is the one for whom surgery is most commonly chosen.
• Pituitary Apoplexy Grading System (PAGS) grades severity from 1 (asymptomatic, subclinical) through 2 (hypopituitarism only), 3 (headache), 4 (ophthalmoplegia) to 5 (visual deficits or low Glasgow score that precludes visual assessment). Higher grades tend towards earlier surgery and recover endocrine function less completely. ^[3]

Neither score is perfect and both are criticised for ignoring hormone status; prolactin level has been suggested as a predictor of recovery of pituitary function. ^[3]

The 2025 guideline adds explicit surgical referral criteria. Consult an endocrinologist (and a neurosurgeon when appropriate) when a pituitary incidentaloma is new and has one or more of: diameter 10 mm or more, or cavernous sinus invasion; 15 to 20 percent growth on previous imaging; visual field deficits or location abutting or near the chiasm or suprasellar space; ophthalmoplegia or severe headache; features of hypopituitarism or hormone hypersecretion; or pregnancy desired or diagnosed during pregnancy. ^[1]

Apoplexy is a medical emergency and the initial steps are identical wherever the patient is. Stabilise the patient first; only then treat the pituitary.

1. Resuscitation: airway, breathing, circulation, fluids; place on a monitored bed or in high-dependency care.
2. Empirical glucocorticoids are indicated in haemodynamic instability, altered consciousness, reduced visual acuity or severe visual field defects; the Society for Endocrinology calls steroid replacement potentially lifesaving in these patients. ^[2] The widely used regimen is hydrocortisone 100 to 200 mg intravenously as a bolus, followed by 2 to 4 mg per hour by continuous intravenous infusion, or 100 mg intramuscularly followed by 50 to 100 mg intramuscularly every six hours. ^{[2] [3]} Keep to the agreed regimen and the hospital's own apoplexy protocol rather than combining. Dexamethasone 2 to 16 mg per day orally or intravenously in divided doses may initially help reduce oedema when early decompression is not undertaken. ^[3]
3. Urgent bloods: urea and electrolytes, full blood count, renal and liver function, clotting profile, and (for later analysis) random cortisol, TSH, free T4, prolactin, IGF-1, LH, FSH and testosterone or oestradiol. ^{[2] [3]}
4. Careful fluid and electrolyte balance, with daily or more frequent monitoring; watch for hyponatraemia from adrenal insufficiency, central hypothyroidism or the syndrome of inappropriate antidiuresis. ^[3]
5. Visual bedside assessment in the first 48 hours: visual acuity, visual fields and ocular motility, repeated and, when possible, verified with Humphrey or Goldmann perimetry. ^[3]
6. Imaging: MRI is the investigation of choice; CT of the brain is performed (with lumbar puncture if needed) to exclude subarachnoid haemorrhage and meningitis first. ^[2]
7. Urgent referral and transfer to the joint neurosurgical and endocrine unit for definitive management, with transfer of the stabilised patient to a centre with neurosurgical high-dependency facilities and on-site endocrine and ophthalmology expertise. ^[2]

Monitoring during conservative care is clinical and frequent: assessment of neurological status initially every hour, lengthening to every 4 to 6 hours as the patient improves; daily visual acuity and visual fields until they improve; daily or more frequent renal function and electrolytes; and an urgent MRI (with a plan for decompression) if consciousness, visual acuity or visual fields deteriorate. ^[3] After initial improvement, hydrocortisone is rapidly tapered to 20 to 30 mg by mouth daily in three divided doses, or stopped if adrenal insufficiency is excluded. ^[3]

Once stabilised, the aim is to prevent secondary insult and to decide whether the patient needs decompression. In practical terms:

• Patients with severe and progressive visual loss, severe and persistent visual field defects, deteriorating consciousness (or sudden amaurosis or hypothalamic involvement) are offered surgery. ^{[2] [3]}
• Patients without neuro-ophthalmological symptoms, or with mild and stable findings, or with subacute apoplexy, can be treated conservatively, with close monitoring, intravenous glucocorticoids, hormone replacement, treatment of any functioning tumour, and reversal or management of precipitants. ^[3]
• Prolactinomas complicating apoplexy are managed conservatively with dopaminergic agonist therapy in addition. ^[3]
• In most reported series, transsphenoidal decompression is preferred because it relieves the visual apparatus and adjacent structures with lower morbidity and mortality than open surgery; endoscopic transsphenoidal surgery is the more commonly used approach, with craniotomy reserved for special cases. ^[3]
• Surgery is performed by a neurosurgeon experienced in pituitary pathology, and close postoperative monitoring (24 to 48 hours) covers water and electrolyte balance, plasma and urine osmolality, neurological status and visual deficits. ^[3]

The timing of surgery is debated. Older guidance, endorsed in 2016, states that patients who had surgery within 8 days showed significantly greater improvement in visual acuity and visual fields. ^[2] A more recent prospective multicentre observational study found no association between surgery within 2 to 4 days and outcomes at three months, and showed that apoplectic tumour volume fell significantly at 2 to 3 months even without surgery. ^[3] Both positions are defensible and are stated here honestly: treat imminent visual or neurological failure promptly, but do not treat the operation itself as an absolute emergency in a stable patient. ^{[2] [3]}

Outcome evidence is also mixed. A systematic review and meta-analysis found recovery rates for visual field, endocrine function and ophthalmoplegia of 76 percent, 23 percent and 81 percent after surgery versus 79 percent, 23 percent and 90 percent after conservative treatment. ^[3] In practice, patients who come to surgery tend to have worse visual deficits at presentation (selection bias), so the apparent similarity in outcomes should not be read as proof that the two strategies are equivalent for a given patient.

Surgical indication criteria from the 2016 guidance, still widely used, are: severely reduced visual acuity; severe and persistent visual field defects; deteriorating level of consciousness. ^[2] Pituitary surgery carries early complications in about 6 percent of patients within 30 days of discharge (CSF leak, hyponatraemia, epistaxis), plus possible diabetes insipidus, infection and hypopituitarism. ^[3]

For an incidental, hormonally inactive adenoma, the 2025 Pituitary Society consensus recommends:

• Surgery for hypersecreting (functioning) adenomas, as per their condition-specific guidelines. ^[1]
• Surgery for visual compromise, cranial neuropathy or any neurological deficit related to the tumour. ^[1]
• Surgery for an adenoma abutting the optic chiasm, after evaluation in a pituitary tumour centre of excellence; in patients over 65, or any age with poor functional status but intact vision, observation can be considered. ^[1]
• Individualised care when the adenoma is 5 mm or more from the chiasm: surgical consultation may be considered for macroadenomas in young patients, those growing on serial MRI or those with cavernous sinus invasion, and in women wishing to become pregnant. ^[1]
• Surgery for severe or progressive vision loss or diminished consciousness from apoplexy. ^[1]
• Risks and benefits of surgery for severe headache refractory to headache medication, after multidisciplinary review including a neurologist. ^[1]
• For asymptomatic macroadenomas, age and functional status guide the decision; in frail patients close observation may be preferable, and in the absence of driving clinical factors patient preference counts. ^[1]
• Surgery may be considered for progressively enlarging macroadenomas, especially near the chiasm, and for new-onset hypopituitarism, though recovery of pituitary deficits after surgery is not guaranteed. ^[1]

A consistent point across the consensus is the value of a pituitary tumour centre of excellence (multidisciplinary pituitary team: endocrinologist, neurosurgeon, neuroradiologist, ophthalmologist, pathologist, radiation oncologist) where available.

Small, stable, non-functioning lesions may simply be observed. Cystic lesions are handled individually: the consensus recommends surgery for enlarging cystic lesions associated with visual or hormonal dysfunction, with observation for small stable arachnoid cysts, and multidisciplinary discussion for small stable craniopharyngiomas. ^[1] Empty sella as an incidental finding means surveillance of any hormone deficit plus surveillance imaging; hormone testing is specifically repeated every 1 to 2 years because hypopituitarism can appear without concomitant growth. ^[1]

Follow-up is long and structured:

• MRI at the surveillance intervals above. ^[1]
• Hormone evaluation every 1 to 2 years in all micro- and macroadenomas, earlier if new symptoms or growth. ^[1]
• Visual fields per the schedule above. ^[1]
• Apoplexy survivors need endocrine and neurosurgical follow-up, with repeat assessment of pituitary and visual function at 4 to 6 weeks, then every 6 to 12 months to optimise replacement and monitor tumour progression or recurrence. ^[2]
• Patients with functioning tumours need the relevant condition-specific follow-up; tumour recurrence and new apoplectic events are rare but reported. ^[3]

• Visual compromise, from bitemporal hemianopia to monocular or binocular visual loss, if a large adenoma or an apoplexy compresses the chiasm.
• Cranial nerve palsies (third, fourth, sixth) from cavernous sinus involvement.
• Hypopituitarism: gonadotroph, corticotroph, thyrotroph and growth hormone axes singly or in combination.
• Acute collapse, hyponatraemia and cortisol crisis in apoplexy.
• Cerebrospinal fluid leak, diabetes insipidus, infection, epistaxis and hypopituitarism after surgery.
• Recurrence or progression of the underlying tumour, and a rare second apoplectic event.
• Permanent hypopituitarism in many apoplexy survivors, regardless of treatment modality.

For incidentalomas the outlook is generally good. Many microadenomas do not grow, and most macroadenomas that are 5 mm or more from the chiasm can be safely watched. Visual acuity and visual fields usually recover after timely surgical decompression, and ophthalmoplegia recovers in most patients after apoplexy. Complete biochemical remission sometimes occurs after apoplexy in GH or ACTH secreting tumours, but patients then commonly need long-term replacement.

Endocrine prognosis in apoplexy is less favourable: permanent hypopituitarism is common in both medically and surgically treated patients, and GH deficiency is present in almost all patients at diagnosis. A subgroup with very low prolactin may be less likely to recover pituitary function. ^[3] Recovery rates of 76 percent (visual field), 23 percent (endocrine) and 81 percent (ophthalmoplegia) after surgery do not differ greatly from 79 percent, 23 percent and 90 percent after conservative treatment. ^[3] In a series of pregnant women with apoplexy, maternal and fetal outcomes included preterm delivery in three cases and one maternal death, underlining the seriousness and the need for specialist teamwork.

Pregnancy. Diagnostic work-up in pregnancy is complicated by the normal enlargement of the pituitary and by increased lactotroph activity. MRI without gadolinium is preferred when possible; CT is avoided. Visual field testing is safe and important. Apoplexy in pregnancy usually presents around 24 weeks and carries high rates of hypopituitarism; management is by an experienced pituitary and obstetric team with induction of delivery when delivery is imminent. ^[3] Hormone replacement uses pregnancy-safe agents where accepted protocols allow.

Children and adolescents. Apoplexy in this age group is rare but is more often found in functioning tumours, mainly prolactinomas; hypopituitarism and visual disturbance occur in 40 to 45 percent. ^[3] Incidentalomas in the young may be part of familial disease and merit genetic evaluation. Surgical tumour recurrence rates around 14.7 percent have been reported. ^[3]

Older adults. Incidentalomas are common and apoplexy carries a higher risk from comorbidities (hypertension, diabetes, antiplatelet and anticoagulant use). Hypopituitarism may present non-specifically and mimic delirium or frailty; an incidentaloma near the chiasm in an older adult can safely be observed if vision is intact and function is poor, as the 2025 consensus recognises. ^[1] For older patients contraindicated for surgery, even with compressive symptoms such as ophthalmoplegia, conservative management with careful monitoring may be continued when it is effective. ^[3]

Functioning tumours. Apoplexy may produce spontaneous biochemical remission in acromegaly (GH and IGF-1 tend to fall) or Cushing disease (apoplexy is the most commonly reported event, in 91 percent, in spontaneous remission of Cushing disease), but careful long-term follow-up is needed because recurrence happens. ^[3]

• Dedicated pituitary MRI may not be available locally; a contrast-enhanced MRI done to the standard protocol, or CT if MRI is genuinely unavailable, still identifies the lesion in most patients, and CT specifically detects a sellar mass in more than 80 percent of apoplexy cases. ^{[2] [3]}
• Endocrine testing can be staged: morning cortisol and TSH first, then prolactin and IGF-1 if affordable, then dynamic tests only when clinically important.
• Visual fields require only a dark room, a tangent screen or a portable perimeter when automated perimetry is unavailable; even confrontation fields, repeated daily in the first 48 hours, will catch most deterioration in apoplexy.
• Treatment of apoplexy requires only hydrocortisone (cheap and widely available), intravenous fluids and a plan for urgent transfer, plus neurosurgical access.
• Long-term care of permanent hypopituitarism needs reliable, affordable hydrocortisone and levothyroxine and a steroid emergency card; these should be arranged before discharge.
• Expertise: image interpretation, surgical and radiotherapeutic access varies widely. Seek early liaison with the nearest pituitary or neurosurgical centre, and agree a shared care plan.

• A pituitary incidentaloma is a sellar or parasellar lesion found by chance on imaging; pituitary adenomas are the commonest, and about 43 percent of imaging-detected ones are macroadenomas.
• Microadenomas (under 10 mm) are usually hormonally inactive and very unlikely to cause hypopituitarism; macroadenomas (10 mm or more) threaten vision and the cavernous sinus.
• The initial work-up is the same regardless of size: dedicated MRI, baseline pituitary hormones and visual field testing when the lesion is near the chiasm.
• Visual changes, not image change alone, are the trigger for surgery in a conservatively managed lesion.
• Hormone testing is repeated every 1 to 2 years because new hypopituitarism can appear without tumour growth.
• Pituitary apoplexy is sudden haemorrhage or infarction, usually in a previously unknown adenoma, in about 0.17 people per 100,000 per year.
• Its signature is sudden severe headache (89 percent), ophthalmoplegia (78 percent), visual field defect (64 percent) or visual loss (52 percent), vomiting (69 percent) and acute hypopituitarism; it mimics subarachnoid haemorrhage and meningitis.
• Give empiric hydrocortisone (100 to 200 mg intravenous bolus, then 2 to 4 mg per hour, or 100 mg intramuscularly then 50 to 100 mg six-hourly) before the labs return in the sick patient, then taper to 20 to 30 mg daily. ^[3]
• Transsphenoidal decompression is preferred when indicated (severe visual loss, persistent severe field defects, deteriorating consciousness), ideally within 8 days by older criteria, though recent data have not confirmed a 2 to 4 day advantage.
• Surgery and conservative care produce similar recovery rates for visual field and ophthalmoplegia, but careful patient selection remains essential.
• Long-term follow-up means pituitary and visual function at 4 to 6 weeks, then every 6 to 12 months, plus MRI surveillance for the underlying tumour.
• Permanent hypopituitarism is common after apoplexy; arrange replacement and a steroid emergency card before discharge.
• Pregnant, very young and very old patients, and low-resource settings, each need the same principles applied with available tools and specialist liaison.

Related MedGrasp pages (plain text): hypopituitarism, acromegaly, Cushing syndrome, adrenal insufficiency, headache, subarachnoid haemorrhage, meningitis. (Prerequisites and related entries in front matter are left empty for this curriculum-gap topic.)