Write a short note on subarachnoid haemorrhage.

Definition

Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space between the arachnoid and pia mater. It accounts for about 5% of strokes but affects younger patients and carries very high mortality — roughly a third die before reaching hospital, and overall case fatality approaches 40–50%.

Aetiology

• Ruptured saccular ("berry") aneurysm — 80–85%, arising at the branch points of the circle of Willis: anterior communicating artery (commonest), posterior communicating artery, and middle cerebral artery bifurcation.
• Non-aneurysmal perimesencephalic haemorrhage (10%) — benign course, excellent prognosis, angiographically negative.
• Arteriovenous malformation, arterial dissection, mycotic aneurysm, vasculitis, coagulopathy, cocaine and amphetamine use, and trauma (the commonest cause of subarachnoid blood overall, though managed differently).

Risk factors: hypertension, smoking, excess alcohol, female sex, family history, autosomal dominant polycystic kidney disease, Ehlers–Danlos and Marfan syndromes, and coarctation of the aorta.

Clinical Features

• Sudden, severe "thunderclap" headache — "the worst headache of my life", reaching maximum intensity within seconds to a minute. This history alone mandates investigation.
• Vomiting, photophobia, neck stiffness (developing over hours as blood irritates the meninges), and transient or persistent loss of consciousness at onset in about half.
• Seizures at onset in 10%.
• Focal deficits: third nerve palsy with a dilated pupil suggests a posterior communicating artery aneurysm; hemiparesis or aphasia from intracerebral extension or vasospasm.
• Subhyaloid (preretinal) haemorrhage on fundoscopy — highly suggestive; Terson syndrome is associated vitreous haemorrhage.
• Sentinel ("warning") headache — a smaller herald bleed days to weeks before, present in a substantial minority and frequently dismissed as migraine or tension headache, representing the single greatest missed opportunity.
• The patient may be fully alert with a normal neurological examination — normality does not exclude SAH.

Grading

The Hunt and Hess and World Federation of Neurosurgical Societies (WFNS) scales grade severity from headache alone (grade 1) to deep coma (grade 5), and correlate strongly with outcome. The modified Fisher scale grades the amount of blood on CT and predicts vasospasm risk.

Investigations

• Urgent non-contrast CT brain — the first test. Sensitivity is over 95% within 6 hours of onset but falls progressively with time as blood is cleared. Blood appears hyperdense in the basal cisterns, sylvian fissures and sulci.
• Lumbar puncture if the CT is negative but suspicion persists — perform after at least 12 hours from onset to allow xanthochromia (yellow discoloration from bilirubin) to develop. Xanthochromia by spectrophotometry distinguishes true SAH from a traumatic tap; the three-tube test (persistent uniform blood across sequential tubes) is supportive but less reliable.
• CT angiography (and digital subtraction angiography, the gold standard) to identify and characterise the aneurysm for treatment planning.
• MRI with FLAIR and gradient echo is useful in the subacute phase when CT has become insensitive.
• ECG changes (deep T-wave inversion, QT prolongation, arrhythmia) and troponin rise are common and reflect neurogenic myocardial stunning, not primary cardiac disease.
• Electrolytes — hyponatraemia is very common from SIADH or cerebral salt wasting.

Management

1. Immediate

• Airway, breathing, circulation; admit to a neurosurgical or neurocritical care unit; bed rest with the head elevated; analgesia and antiemetics; avoid straining (stool softeners).
• Blood pressure control — lower extreme hypertension to reduce rebleeding risk while maintaining cerebral perfusion.
• Reverse anticoagulation; treat seizures.

2. Secure the aneurysm — the definitive treatment, and urgently

Endovascular coiling or surgical clipping, performed as early as possible (ideally within 24–72 hours). Rebleeding is the greatest early hazard, with peak risk in the first 24 hours and very high mortality. Coiling is preferred where the anatomy is suitable.

3. Prevent and treat delayed cerebral ischaemia (vasospasm)

• Vasospasm typically occurs between days 4 and 14, peaking around day 7, and is a leading cause of death and disability in those who survive the initial bleed.
• Oral nimodipine for 21 days in every patient — the only pharmacological measure with proven benefit in reducing poor outcome.
• Maintain euvolaemia and normal blood pressure; the older "triple-H" therapy (hypertension, hypervolaemia, haemodilution) has given way to induced hypertension with euvolaemia for established deficits.
• Transcranial Doppler and clinical monitoring for detection; endovascular angioplasty or intra-arterial vasodilators for refractory symptomatic vasospasm.

4. Manage complications

• Rebleeding — prevented by early securing of the aneurysm.
• Hydrocephalus — acute obstructive (external ventricular drain) or communicating (may require shunt).
• Hyponatraemia — distinguish SIADH from cerebral salt wasting; in SAH, cerebral salt wasting is common and fluid restriction is dangerous because hypovolaemia worsens vasospasm. Treat with salt and volume replacement.
• Seizures, neurogenic pulmonary oedema, cardiac dysfunction, DVT, and infection.

5. Long-term

Blood pressure control, smoking cessation, follow-up imaging, and screening of first-degree relatives where there are two or more affected family members or an associated condition such as polycystic kidney disease. Cognitive impairment, fatigue and mood disturbance are common in survivors and need rehabilitation.