Spontaneous subarachnoid haemorrhage (SAH) — most commonly from rupture of a saccular (berry) aneurysm — is a life-threatening emergency. The characteristic presentation is a sudden-onset ‘thunderclap’ headache, described by patients as the worst headache of their life, occurring at peak intensity within seconds. This may be accompanied by loss of consciousness, meningism (neck stiffness, photophobia, vomiting), and focal neurological signs.

CT head is the first investigation and is positive in approximately 95% of cases within the first 12 hours. If the CT is negative but clinical suspicion remains high, lumbar puncture at 12 hours post-ictus is required to detect xanthochromia (the yellow discolouration of CSF caused by breakdown products of haemoglobin). CTA or formal catheter angiography is required to identify the causative aneurysm.

ICU Management of SAH

ICU admission is required for all patients with severe SAH (World Federation of Neurosurgical Societies grade 3–5 — characterised by GCS <14, focal neurological deficit, or coma). The priorities are securing the aneurysm as soon as possible (neurosurgical clipping or endovascular coiling, typically within 24 hours of presentation), and preventing and treating the secondary complications that cause the majority of morbidity and mortality in patients who survive the initial bleed.

The most feared secondary complication is delayed cerebral ischaemia (DCI), also known as vasospasm, which occurs typically between days 4 and 14 post-haemorrhage. SAH triggers release of oxyhemoglobin and other vasoactive substances into the subarachnoid space, causing sustained spasm of cerebral vessels and potentially precipitating stroke. Nimodipine — an L-type calcium channel blocker with preferential cerebrovascular activity — reduces the risk of DCI and is given orally at 60 mg every 4 hours for 21 days in all SAH patients.

Euvolaemia is the haemodynamic target in SAH — neither hypovolaemia (which reduces CPP and triggers compensatory vasospasm) nor aggressive hypervolaemia (the old ‘triple-H’ therapy of hypertension, hypervolaemia, and haemodilution is now largely abandoned as the hypervolaemia component is harmful). If clinical or radiological vasospasm develops, hypertensive therapy is used — raising MAP by 10–20 mmHg above the patient’s baseline may reverse ischaemic symptoms.

Other Complications of SAH

Hydrocephalus occurs acutely in approximately 20% of SAH patients due to obstruction of CSF drainage by blood in the subarachnoid space. It presents as worsening consciousness and requires external ventricular drain (EVD) insertion for immediate CSF drainage. Rebleeding before the aneurysm is secured carries a mortality of approximately 70% and is prevented by early aneurysm treatment. Cardiac complications — including ECG changes (deep T-wave inversions, QTc prolongation), regional wall motion abnormalities, and neurogenic pulmonary oedema — occur due to the massive catecholamine surge at the time of haemorrhage.