Cerebral Vasospasm After Subarachnoid Haemorrhage

Cerebral vasospasm after subarachnoid haemorrhage is delayed narrowing of the cerebral arteries beginning on days 3 to 4, peaking at days 7 to 10 and resolving by about day 21. It is a major cause of delayed cerebral ischaemia and poor outcome after aneurysmal haemorrhage.

Angiographic vasospasm occurs in about 60 to 70% of patients with aneurysmal subarachnoid haemorrhage, and delayed cerebral ischaemia in about 20 to 30%. It follows thick subarachnoid blood on CT (modified Fisher grade 3 and 4), higher clinical grade, smoking and hyperglycaemia.

Delayed cerebral ischaemia. A new focal deficit or fall of 2 or more points on the Glasgow Coma Scale lasting at least 1 hour, or a new infarct on imaging, not explained by rebleeding, hydrocephalus, seizure or metabolic disturbance.

Other contributors. Cortical spreading depolarisations, microthrombosis, microvascular constriction, inflammation and early brain injury, so vasospasm is not the only cause of delayed ischaemia.

Pathophysiology.

Blood breakdown products, mainly oxyhaemoglobin, impair nitric oxide signalling and increase endothelin and calcium mediated smooth muscle contraction, producing sustained arterial narrowing.

Reduced perfusion beyond the narrowed segment, with microcirculatory failure and impaired autoregulation, leads to infarction.

• Delayed onset, from day 3, of new focal deficits (hemiparesis, aphasia, neglect), confusion, drowsiness or falling Glasgow Coma Scale score.
• Fluctuating deficit with changes in blood pressure or volume status.
• Asymptomatic narrowing is common.

Red flags.

• New deficit or drop in consciousness from day 3 to day 14.
• Hypotension or hypovolaemia in the vasospasm window.
• Sudden severe headache (rebleeding).

• Daily neurological examination in the high risk window; urgent CT to exclude hydrocephalus, rebleeding and infarction when deterioration occurs.
• Transcranial Doppler: mean middle cerebral artery velocity over 120 cm/s suggests spasm, over 200 cm/s severe spasm, and a Lindegaard ratio over 3 (over 6 severe) separates spasm from hyperaemia.
• CT angiography and CT perfusion, or digital subtraction angiography, for confirmation and for intervention planning.
• Exclude other causes: electrolytes (sodium), glucose, infection, seizure (EEG), hydrocephalus.

Differential diagnosis. Rebleeding, acute hydrocephalus, seizures, hyponatraemia, infection, sedation, hypoxia and hypoperfusion from hypovolaemia or cardiac stunning.

• Nimodipine for all patients: 60 mg orally or by nasogastric tube every 4 hours, started within 96 hours of haemorrhage and given for 21 days. Maximum 360 mg daily. Monitor blood pressure closely; if systolic pressure falls, give 30 mg every 2 hours instead of stopping. Reduce to 30 mg every 4 hours in cirrhosis; no renal adjustment; avoid with strong CYP3A4 inhibitors and grapefruit juice; do not give intravenously unless the intravenous product is licensed, because of severe hypotension. Evidence supports improved outcomes rather than prevention of angiographic spasm.
• Maintain euvolaemia and normal sodium; avoid hypovolaemia and prophylactic hypervolaemia, and avoid hypotension.
• Delayed cerebral ischaemia: treat the cause, optimise volume and induce hypertension with a vasopressor while monitoring neurological response, adjusting to symptoms and cardiac function.
• Refractory deficits: endovascular treatment with intra-arterial vasodilator infusion or balloon angioplasty at a specialist centre.
• Avoid prophylactic induced hypertension, haemodilution and statin therapy, which lack proven benefit.
• Secure the aneurysm early, drain hydrocephalus, treat fever and seizures, and give thromboprophylaxis.

Monitoring. Neurological observations at least every 1 to 2 hours in the first 2 weeks; daily transcranial Doppler where available; daily sodium.

Referral and escalation. Neurosurgical or neurocritical care at all times; interventional neuroradiology for refractory deficit.

Special groups. Older adults and those with cardiac disease are at risk from induced hypertension; monitor cardiac function.