Key Facts

SAH is a neurosurgical emergency with high mortality and morbidity. A high index of suspicion is essential — any thunderclap headache must be investigated to exclude SAH. The motto "CT-negative SAH" drives the need for LP if CT is non-diagnostic.

Epidemiology

Incidence ~8-10 per 100,000 per year in UK. Peak age 40-60 years. Female predominance (1.6:1). ~3,000 cases per year in UK. ~3% of all strokes. Mortality ~50% (15% die before reaching hospital, 25% die within 24 hours). 50% of survivors have significant disability.

Aetiology

• Berry (saccular) aneurysm: ~85% — arise at arterial bifurcations in the circle of Willis
• Non-aneurysmal perimesencephalic: ~10% — benign; venous origin; centred on midbrain cisterns; angiography negative; excellent prognosis
• Other: AVM, dissection, dural AV fistula, mycotic aneurysm, coagulopathy, cocaine, pituitary apoplexy
• Risk factors for aneurysm: family history (3× risk if first-degree relative), smoking, hypertension, alcohol excess, autosomal dominant polycystic kidney disease (ADPKD), Ehlers-Danlos type IV, coarctation of the aorta

Pathophysiology

Aneurysm rupture → blood enters subarachnoid space → immediate rise in ICP → global cerebral hypoperfusion → loss of consciousness. Blood in CSF causes meningeal irritation (headache, neck stiffness, photophobia). Complications: rebleeding (highest in first 24 hours), vasospasm/DCI (days 4-14), hydrocephalus (acute — blood obstructs CSF flow; chronic — impaired CSF resorption), seizures, hyponatraemia (SIADH or cerebral salt wasting).

Classic Presentation

• Thunderclap headache: sudden-onset, maximal intensity within seconds; severe; "worst headache of my life"
• Often occipital
• May occur during exertion, straining, or sexual intercourse
• Neck stiffness (meningism — may take hours to develop)
• Photophobia
• Nausea and vomiting
• Loss of consciousness (transient or prolonged)

Associated Signs

• CN III palsy (dilated pupil, ptosis, "down and out" eye): PComA aneurysm compressing CN III
• Focal neurological deficit (depending on location)
• Subhyaloid (pre-retinal) haemorrhage on fundoscopy (Terson syndrome)
• Seizures (~10%)

Red Flags

• Any thunderclap headache (SAH until proven otherwise)
• "Sentinel headache" — minor warning leak days/weeks before major SAH (~30% report preceding headache)
• CN III palsy (PComA aneurysm — may rupture imminently)
• GCS deterioration (rebleeding, hydrocephalus, vasospasm)

Immediate

• CT head (non-contrast): FIRST — sensitivity >95-98% within 6 hours (Fisher/modified Fisher grading); shows hyperdense blood in subarachnoid space, cisterns, fissures
• If CT positive → CT angiography: identify aneurysm (location, size, morphology) — sensitivity >95% for aneurysms >3 mm

If CT Negative (but Clinical Suspicion)

• Lumbar puncture at ≥12 hours post-symptom onset:
  • Xanthochromia on spectrophotometry (NOT visual inspection): presence of oxyhaemoglobin/bilirubin confirms SAH
  • Uniformly bloodied CSF (not decreasing across bottles) — less reliable
  • Opening pressure: may be raised

Further Investigation

• Digital subtraction angiography (DSA): gold standard for aneurysm detection; required if CTA inconclusive; also therapeutic (coiling)
• MRI/MRA: can detect aneurysm and old SAH (FLAIR sensitive to subarachnoid blood)
• Transcranial Doppler (TCD): monitor for vasospasm (MCA velocity >120 cm/s suspicious, >200 cm/s = severe vasospasm)

Bloods

• FBC, coagulation, U&Es: baseline
• Troponin: SAH can cause myocardial injury (neurogenic stunned myocardium)
• Sodium: monitor for hyponatraemia (SIADH or cerebral salt wasting)
• Group and save: for potential surgery

Grading

• WFNS grade (World Federation of Neurosurgical Societies): based on GCS + focal deficit
• Fisher/Modified Fisher grade: based on CT appearance — predicts vasospasm risk

Acute

• Admit to neurosurgical/neurocritical care unit
• Secure airway if GCS ≤8
• Analgesia: paracetamol 1 g QDS, codeine 30-60 mg QDS; avoid NSAIDs (platelet effect)
• Antiemetics: ondansetron 4 mg IV PRN
• Blood pressure: maintain SBP <160 mmHg pre-intervention (reduce rebleeding risk)
• Nimodipine 60 mg PO every 4 hours for 21 days: reduces DCI/vasospasm (British Aneurysm Nimodipine Trial; NICE NG128)
• VTE prophylaxis: pneumatic compression devices (NOT pharmacological until aneurysm secured)
• Stool softeners: prevent straining (lactulose)

Definitive Aneurysm Treatment

• Endovascular coiling: preferred for most aneurysms (ISAT trial — better outcomes than clipping at 1 year); performed by interventional neuroradiology; ideally within 48-72 hours
• Neurosurgical clipping: preferred for certain locations (MCA), wide-necked aneurysms, or failed coiling
• Flow diverters: for giant/complex aneurysms

Delayed Cerebral Ischaemia (Vasospasm)

• Days 4-14: monitor with TCD, clinical assessment
• Nimodipine (already started)
• Triple-H therapy: induced hypertension (vasopressors), haemodilution, hypervolaemia (IV fluids) — controversial but widely used
• Intra-arterial nimodipine/milrinone: via catheter if severe vasospasm
• Balloon angioplasty: for focal vasospasm refractory to medical therapy

Hydrocephalus

• Acute: EVD (external ventricular drain) insertion
• Chronic (weeks-months): VP shunt if persistent

Referral Criteria

• All confirmed SAH: immediate neurosurgical centre transfer
• All thunderclap headaches: urgent investigation (CT ± LP)

Overall mortality ~50% (15% die before hospital, 25% within 24 hours, further 25% within 30 days). Of survivors, ~50% have significant cognitive/neurological disability. Good-grade SAH (WFNS I-II): ~80% good outcome. Poor-grade SAH (WFNS IV-V): ~80% poor outcome. Rebleeding: 4% on day 1, ~1.5% per day for next 14 days without treatment. Vasospasm/DCI occurs in ~30% (peak day 7). Perimesencephalic SAH has excellent prognosis (no rebleeding, no vasospasm).

WFNS Grading

Modified Fisher Grading (Vasospasm Risk)

Common Aneurysm Sites