EndocrinologyTier 1Disease (DEADMAN)

Acute metabolic derangements - pituitary apoplexy

Description

Haemorrhage or infarction of the pituitary - almost always into an adenoma
- ~80% the first presentation of a previously unknown adenoma
Endocrine emergency + neurosurgical emergency + ophthalmic emergency
Sudden severe headache is the near-universal opening symptom

Why it is dangerous

Expanding sellar mass in a bony box
- Up -> optic chiasm -> bitemporal field loss
- Lateral -> cavernous sinus -> CN III, IV, VI, V1/V2
- -> acute ACTH deficiency -> adrenal crisis
Death is from unrecognised cortisol deficiency, not from the bleed

Sheehan syndrome = the postpartum variant (infarction of a physiologically enlarged gland after obstetric haemorrhage)

2-12% of pituitary adenomas over their lifetime
Peak 5th-6th decade; M>F ~2:1
Non-functioning macroadenoma is the commonest substrate
Incidence of subclinical haemorrhage on imaging far higher than clinical apoplexy

Adenoma outgrows a fragile, low-pressure portal blood supply
- -> ischaemia +/- haemorrhagic transformation

Precipitants (~25-40%; the rest spontaneous)

Clinical

Headache - sudden, severe, retro-orbital (>90%)
- Thunderclap -> commonly misdiagnosed as SAH
Visual field defect (bitemporal hemianopia) ~60-70%
Ophthalmoplegia ~50% - CN III commonest (ptosis, mydriasis, down-and-out)
Nausea/vomiting, meningism, photophobia, fever, dec GCS
Hypotension, hyponatraemia, hypoglycaemia = cortisol deficiency

Imaging

MRI pituitary with contrast is the test - sensitivity ~90%
- Blood products in the sella, fluid level, deviated stalk
CT misses it in up to 80% early - a normal CT does not exclude apoplexy

Bloods - take before steroids, do not wait for them

Random cortisol + ACTH
TSH + fT4, prolactin, LH/FSH, testosterone/oestradiol, IGF-1
UEC (hyponatraemia), BGL, FBE, coags
Low/normal prolactin with a macroadenoma suggests infarcted lactotrophs and correlates with worse outcome

Mimics

SAH, bacterial meningitis, basilar migraine, cavernous sinus thrombosis, posterior communicating artery aneurysm

1. Steroid first - before imaging, before endocrine results

Hydrocortisone 100 mg IV stat, then 50 mg IV q6h (or 200 mg/24 hr infusion)
Indications for immediate steroid: haemodynamic instability, dec conscious state, visual loss, or any apoplexy until cortisol excluded
Do not give levothyroxine before hydrocortisone - precipitates adrenal crisis

2. Resuscitate

3. Decide surgery vs conservative - by deficit, not by imaging

Urgent transsphenoidal decompression (ideally <7 days) if:
- Severe or deteriorating visual acuity/field loss, OR
- Deteriorating conscious state
Conservative if: isolated ophthalmoplegia, no field deficit, stable GCS
- Ocular palsies recover in most without surgery
UK Pituitary Apoplexy Score (0-10; GCS, visual acuity, visual fields, ocular palsy) used to stratify - higher score favours surgery, but it is a guide, not a rule

4. Replace what is missing, long-term

Hydrocortisone taper to physiological replacement; reassess axis at 4-6 weeks
Levothyroxine after glucocorticoid cover
Sex steroids, GH later
Desmopressin if diabetes insipidus (uncommon - more a post-op problem)
Formal perimetry, MRI and full pituitary function testing at 4-8 weeks then annually
Steroid education: sick-day doubling, MedicAlert, emergency IM hydrocortisone

Long-term hypopituitarism is the rule, not the exception

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