Pituitary masses and visual-field defects

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The differential extends beyond adenoma to Rathke cleft cyst, craniopharyngioma, meningioma, hypophysitis, metastasis and rarer sellar lesions. Imaging morphology, tempo, age, cancer or pregnancy context and hormone pattern help classify the process, but tissue is sometimes required after safe endocrine stabilisation.

Visual anatomy predicts symptoms. Crossing nasal retinal fibres lie in the chiasm, so compression often removes temporal fields in both eyes. Extension into the cavernous sinus can affect ocular motor nerves, while posterior or lateral lesions may create less typical defects. Confrontation is a useful bedside screen but cannot replace formal perimetry for treatment decisions.

Hormone excess and deficiency can coexist. A macroadenoma can secrete one hormone while compressing normal tissue and impairing others. The immediate danger is cortisol deficiency; longer-term consequences include central hypothyroidism, hypogonadism, growth hormone deficiency and, after surgery or stalk injury, arginine vasopressin deficiency.

Key points

A sellar mass may present through visual loss, headache, cranial nerve palsy, hormone excess, pituitary deficiency or incidental imaging; size alone does not establish clinical significance.
Upward expansion compresses the optic chiasm classically causing bitemporal field loss, but junctional, asymmetric or central defects occur and patients may not notice gradual peripheral change.
New or progressive visual acuity loss, field deterioration, diplopia or reduced consciousness requires urgent pituitary, ophthalmology and neurosurgical assessment rather than routine clinic surveillance.
Obtain dedicated contrast pituitary MRI and formal visual acuity, colour and field testing when the lesion approaches the optic apparatus or symptoms suggest compression.
Assess the full anterior pituitary, placing cortisol safety first; replace suspected ACTH deficiency before starting levothyroxine for central hypothyroidism.
Measure prolactin early and request dilution when a very large lesion has only a modest reported value, because assay hook effect can disguise a macroprolactinoma.
Functioning tumours need disease-specific biochemical confirmation: IGF-1 for acromegaly and validated cortisol testing for Cushing disease, not random growth hormone or cortisol alone.
Most prolactinomas are treated medically even with a macroadenoma, whereas compressive non-functioning adenomas commonly require transsphenoidal surgery; decisions belong in a pituitary MDT.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Pituitary adenoma

A functioning or non-functioning adenoma can enlarge within the sella, secrete one hormone and compress normal pituitary and visual tissue.

Cystic or adjacent benign lesion

Rathke cleft cyst, craniopharyngioma and meningioma can mimic a pituitary adenoma when their sellar or suprasellar growth produces comparable mass effect.

Inflammatory or malignant disease

Hypophysitis, metastasis and infiltrative disorders are more likely in selected pregnancy, immune, cancer or systemic contexts.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Sellar tissue expands
A mass enlarges upward, laterally or posteriorly according to anatomy, sometimes before producing a recognisable hormone syndrome.
2
The optic chiasm is compressed
Pressure on crossing nasal retinal fibres commonly removes temporal visual fields in both eyes, while acuity may remain initially preserved.
3
Normal pituitary tissue is impaired
Compression reduces trophic hormone output, causing central cortisol, thyroid, gonadal or growth-hormone deficiency while the condition remains active.
4
Hormone excess may coexist
A secreting tumour can produce prolactin, growth hormone, ACTH or another hormone while simultaneously causing mass-related deficiency.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Chiasmal field loss

Bumping into doorframes, difficulty driving, missing people at the side or bitemporal defects on confrontation suggests optic-chiasm compression.

Acuity or colour change

Reduced central vision, washed-out colours or a relative afferent pupillary abnormality indicates significant optic pathway dysfunction and increases urgency.

Cavernous sinus extension

Diplopia, ptosis or impaired eye movements can result from third, fourth or sixth cranial nerve involvement beside the sella.

Pituitary failure

Fatigue, postural symptoms, amenorrhoea, low libido, erectile dysfunction, cold intolerance or reduced shaving frequency may reflect one or several deficient axes.

Hormone excess

Galactorrhoea, acromegalic change, Cushing features or thyrotoxicosis can identify a functioning adenoma and profoundly alter first-line treatment.

Stalk and posterior effects

Moderate hyperprolactinaemia can result from lost dopamine delivery, while polyuria and thirst suggests posterior or hypothalamic disease uncommon in a simple adenoma.

Red flags requiring action

Thunderclap headache with visual loss, ophthalmoplegia, meningism or altered consciousness suggests pituitary apoplexy and requires immediate emergency management.
Haemodynamic instability, vomiting, hyponatraemia or hypoglycaemia in a patient with a sellar lesion may represent secondary adrenal insufficiency; give hydrocortisone without waiting when crisis is suspected.
Rapidly worsening acuity, colour vision or formal field defect requires same-day specialist discussion because delayed decompression can leave permanent optic damage.
Polyuria with hypernatraemia, impaired thirst or reduced consciousness signals dangerous water-balance failure needing monitored endocrine management.
A sellar lesion in known cancer, pregnancy, recent immunotherapy or systemic inflammatory disease broadens the urgent differential beyond a routine benign adenoma.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

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
Dedicated contrast pituitary MRIFirst step
Why
Define lesion compartment, optic relationship, cavernous extension, haemorrhage and differential morphology.
Interpretation and limitations
Report dimensions and distance or contact with chiasm rather than macroadenoma alone; CT is an alternative when MRI is impossible but characterises soft tissue less well.
02
Formal visual assessment
Why
Measure acuity, colour discrimination, pupils, ocular motility, optic discs and reproducible visual fields.
Interpretation and limitations
Automated or Goldmann perimetry quantifies the defect for urgency and follow-up; bedside confrontation can miss early or central change.
03
Nine am cortisol and ACTH-axis assessment
Why
Identify life-threatening central adrenal insufficiency before other hormone replacement or surgery.
Interpretation and limitations
Interpret cortisol against illness, exogenous steroid and local assay; an unwell patient with suspected deficiency should receive empirical hydrocortisone before confirmatory testing.
04
Prolactin with dilution and macroprolactin context
Why
Distinguish prolactinoma, stalk disconnection, assay artefact, medicines and biologically inactive macroprolactin.
Interpretation and limitations
Very high prolactin supports prolactinoma; an unexpectedly modest result beside a giant lesion warrants dilution to exclude hook effect before surgery is chosen.
05
Free T4 TSH gonadotrophins and sex hormones
Why
Map central thyroid and gonadal function as part of complete pituitary assessment.
Interpretation and limitations
Low free T4 with an inappropriately normal or low TSH indicates central hypothyroidism; gonadotrophins must be interpreted for age, sex, cycle and current hormone therapy.
06
IGF-1 and targeted excess testing
Why
Screen for growth hormone excess and direct further Cushing or thyrotroph investigations from phenotype.
Interpretation and limitations
Age-adjusted IGF-1 is the acromegaly screen; abnormal cortisol or thyroid patterns need disease-specific confirmation rather than diagnosis from a single random value.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Glaucoma or retinal disease

Ocular pathology can cause field defects, but formal perimetry and ophthalmic examination show a pattern that does not localise to the chiasm.

Stroke or neurological lesion

Homonymous rather than bitemporal field loss, abrupt onset or focal neurological signs suggest a post-chiasmal cerebral cause.

Physiological pituitary enlargement

Pregnancy-related gland enlargement requires gestation-aware interpretation and lacks the same invasive or hormone-discordant features when supported by the history and examination.

Primary target-gland disease

Low target hormone with a raised trophic hormone indicates thyroid, adrenal or gonadal failure rather than pituitary compression.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01VISIONNew visual defect with sellar massFirst stepVisual field, acuity, colour or ocular-motor change suggests optic or cavernous compression.

1Document bedside acuity, pupils, fields, colour and eye movements, and ask specifically about sudden headache or altered consciousness.
2Check haemodynamics, glucose, sodium and urgent cortisol status, giving emergency hydrocortisone if apoplexy or adrenal failure is plausible.
3Arrange urgent pituitary MRI and formal neuro-ophthalmic testing while contacting the regional pituitary neurosurgical and endocrine team.
4Choose urgent decompression, dopamine agonist treatment or monitored conservative care according to apoplexy, tumour type and objective visual trajectory.

02FOUNDIncidentally discovered pituitary lesionSellar imaging abnormality is reported without an acute neurological presentation.

1Review the original scan, previous imaging, lesion size, chiasm proximity, symptoms, pregnancy and cancer or immunotherapy history.
2Obtain baseline pituitary hormone evaluation and formal fields when the lesion contacts or approaches the optic apparatus.
3Classify functioning status and differential in the pituitary MDT rather than assuming every lesion is a non-functioning adenoma.
4EscalationSet imaging, hormone and visual follow-up with explicit intervals and escalation thresholds, or refer for treatment when compression or secretion warrants it.

03DEFICITHormone deficiency from mass effectClinical or biochemical assessment shows loss of one or more anterior pituitary axes.

1Assess cortisol first and provide glucocorticoid replacement and sick-day education when ACTH deficiency is known or strongly suspected.
2Start levothyroxine only after cortisol safety is secured, titrating by free T4 rather than TSH in central disease.
3Address gonadal and growth hormone axes after tumour treatment, fertility goals, contraindications and recovery potential are clarified.
4Re-test axes after surgery, radiotherapy or major tumour shrinkage because requirements can recover or new deficits can emerge.

04TREATTumour-specific managementImaging, hormones and vision establish a lesion needing active therapy.

1First lineUse dopamine agonist as first-line for most prolactinomas, monitoring early visual and prolactin response in compressive macroadenomas.
2Refer non-prolactin compressive adenomas and appropriate functioning tumours for transsphenoidal surgical review by an experienced team.
3Consider radiotherapy or disease-specific medical therapy for residual, recurrent or unresectable disease under specialist commissioning.
4Continue lifelong surveillance of tumour, vision, hormone replacement and late radiotherapy or surgical effects at an interval matched to risk.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Replace ACTH-dependent cortisol before thyroid treatment, surgery and physiological stress in a pituitary patient.

Hydrocortisone for central adrenal insufficiency

Use a physiological divided oral replacement regimen when stable, or immediate parenteral stress dosing when apoplexy, shock or failed absorption is suspected.

Provide sick-day rules, card and emergency kit where indicated; do not use a reassuring TSH or normal potassium to exclude central cortisol deficiency.

Suppress prolactin and usually shrink a prolactinoma, often avoiding decompressive surgery even for macroadenoma.

Cabergoline

Begin the pituitary specialist's low weekly regimen with food and titrate against prolactin, visual recovery, tumour size and tolerability.

Review postural symptoms, nausea, sleepiness, impulse-control or psychiatric change and fibrotic-valve monitoring under the current SmPC and local protocol.

Replace deficient thyroid hormone when the pituitary cannot generate an appropriate TSH signal.

Levothyroxine for central hypothyroidism

Start only after cortisol sufficiency or glucocorticoid cover is established, then titrate using free T4 and clinical response.

TSH is not a valid dose target in established central hypothyroidism; over-rapid treatment can precipitate adrenal crisis or stress cardiovascular disease.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Irreversible visual impairment

Progressive chiasmal or optic-nerve compression can permanently reduce fields, colour vision and acuity without timely specialist management.

Adrenal crisis

Unrecognised ACTH deficiency can decompensate during illness, surgery or vomiting and is the immediate endocrine safety priority.

Pituitary apoplexy

Haemorrhage or infarction within the lesion causes sudden headache, visual deterioration, ophthalmoplegia and acute cortisol failure.

Long-term hormone deficiency

Mass effect and treatment can leave enduring thyroid, gonadal, growth-hormone or vasopressin deficits requiring lifelong review.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat formal visual fields, acuity and colour testing at an interval matched to chiasm contact, treatment choice and the rate of initial visual change.
Use comparable pituitary MRI sequences and expert measurements to distinguish true growth or shrinkage from protocol and slice variation.
Review cortisol, free T4, prolactin, gonadal status, IGF-1 and water balance after surgery or major tumour treatment on the local pituitary schedule.
Monitor headache pattern, diplopia and visual function between planned appointments, giving patients a same-day route for sudden deterioration.
During replacement, assess clinical adequacy and harm rather than relying on TSH for central thyroid disease or random cortisol while taking hydrocortisone.
Revisit fertility, pregnancy, driving, occupation and psychological effects because tumour control does not automatically restore these outcomes.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Patients fill in missing fields

Slow bitemporal loss may be compensated by eye and head movements, so a patient can deny symptoms despite substantial formal perimetry defects.

Prolactin changes the surgeon's queue

A large prolactinoma can recover vision rapidly with dopamine agonist treatment, making an urgent accurate diluted result management-defining.

Potassium stays normal centrally

ACTH deficiency usually preserves aldosterone, so absent hyperkalaemia should never reassure against dangerous secondary adrenal insufficiency.

Thyroxine can expose cortisol failure

Increasing metabolic demand and cortisol clearance before glucocorticoid protection may precipitate crisis in an unrecognised ACTH-deficient patient.

Polyuria is diagnostically useful

Arginine vasopressin deficiency at initial presentation is unusual for a simple adenoma and should broaden consideration to stalk, inflammatory or metastatic disease.

11Common pitfallsFrequent interpretation and management errors.

01
Do not call confrontation fields normal and omit formal perimetry when MRI shows optic contact or the patient reports functional peripheral loss.
02
Do not begin levothyroxine for low free T4 before assessing and protecting the cortisol axis.
03
Do not send a patient with an unexpectedly modest prolactin and huge mass directly to surgery without requesting assay dilution.
04
Do not assume every sellar lesion is an adenoma when diabetes insipidus, cancer, immunotherapy or inflammatory features suggest another process.
05
Do not defer rapidly deteriorating vision to a routine endocrine appointment; optic recovery depends on timely specialist action.
06
Do not stop follow-up after technically successful surgery, because residual growth, recurrence and late pituitary deficits remain possible.