Synopsis
Recognise acute haemorrhage or infarction within a pituitary lesion, give life-saving cortisol support, document neuro-ophthalmic severity and coordinate urgent MRI and specialist decompression decisions.
- Pituitary apoplexy is a clinical emergency caused by haemorrhage or infarction in the pituitary, usually within an adenoma; imaging haemorrhage without an acute syndrome is not synonymous with apoplexy.
- Think of it in sudden severe headache with visual acuity or field loss, diplopia, ptosis, vomiting, meningism, photophobia or reduced consciousness, even when no pituitary tumour was previously known.
- Exclude subarachnoid haemorrhage and meningitis in parallel, but do not let an unrevealing routine head CT close the diagnosis because pituitary MRI is more sensitive.
- Draw cortisol and the broader pituitary panel before glucocorticoid only when this creates no treatment delay; haemodynamic instability or major neuro-ophthalmic compromise requires empirical hydrocortisone.
- Society for Endocrinology emergency guidance supports hydrocortisone 100 to 200 mg intravenously as an adult bolus followed by infusion or divided parenteral treatment under the acute protocol.
- Record acuity, colour, pupils, ocular movements and fields serially; deterioration, severe persistent visual deficit or reduced consciousness strengthens the case for urgent transsphenoidal decompression.
- Stabilise fluid, sodium and glucose carefully because ACTH deficiency, vomiting and posterior-pituitary disturbance can all complicate the neurological presentation.
- Every patient needs ongoing endocrine and neurosurgical follow-up, with repeat pituitary and visual assessment at four to six weeks and longer surveillance for tumour and hormonal outcomes.
Key red flags
Haemodynamic instability, altered consciousness, reduced visual acuity or severe field defects are explicit indications for immediate empirical glucocorticoid in suspected apoplexy.
A fixed dilated pupil, rapidly declining vision or new dense ophthalmoplegia requires urgent neuro-ophthalmic and neurosurgical reassessment rather than waiting for the next ward round.
Meningism, fever or petechiae still requires antimicrobial and lumbar-puncture decision-making for meningitis; a pituitary lesion does not exclude infection.
Thunderclap headache needs the appropriate subarachnoid haemorrhage pathway in parallel because missing an aneurysmal bleed is catastrophic.
Polyuria, rising sodium or impaired thirst after steroid treatment signals emerging water-balance failure and requires closely supervised fluid and desmopressin decisions.
Investigation priorities
Confirm sellar haemorrhage or infarction and show compression of optic, cavernous and hypothalamic structures.
Management branches
Acute severe headache is accompanied by visual, ocular-motor, meningeal or consciousness change.
- Perform ABCDE assessment, bedside glucose, neurological and focused visual examination while establishing intravenous access and monitoring.
- Draw cortisol and other pituitary samples if immediately available, then give empirical parenteral hydrocortisone for instability or significant neuro-ophthalmic features.
- Correct circulatory and glucose disturbance, assess sodium and pursue emergency subarachnoid haemorrhage or meningitis treatment in parallel when indicated.
- Contact the regional endocrine-neurosurgical team early and obtain urgent pituitary MRI, using dedicated CT if MRI cannot be performed.
The patient is stable with preserved or improving vision and no deteriorating consciousness.
- Admit where frequent neurological, visual, fluid and electrolyte observation can be delivered with immediate specialist access.
- Continue glucocorticoid and supportive therapy, recording formal baseline and repeated visual findings rather than relying on subjective improvement.
- Review MRI, tumour type, comorbidity and patient preference jointly between endocrinology, neurosurgery and ophthalmology.