Subarachnoid Haemorrhage (SAH)

Definition | Aetiology | Pathophysiology | Risk Factors | Signs and Symptoms | Investigations | Management

Definition

A subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space, typically caused by the rupture of an intracranial aneurysm, leading to a sudden severe headache and neurological deficits.

Aetiology

SAH is most commonly caused by aneurysmal rupture but may also result from trauma or vascular malformations.

Common Causes:

  • Aneurysmal rupture (85%): most commonly from the anterior communicating artery.
  • Traumatic brain injury: leading to secondary SAH.
  • Arteriovenous malformations (AVMs): congenital vascular abnormalities.
  • Coagulopathy: including anticoagulant use or bleeding disorders.
  • Idiopathic: no clear source found in some cases.

Pathophysiology

  • Rupture of a cerebral artery leads to bleeding into the subarachnoid space.
  • Increased intracranial pressure (ICP) reduces cerebral perfusion.
  • Blood breakdown products trigger vasospasm, increasing the risk of secondary ischaemia.
  • Inflammatory response contributes to cerebral oedema and hydrocephalus.

Risk factors

  • Hypertension.
  • Smoking.
  • Family history of aneurysms.
  • Polycystic kidney disease (associated with aneurysms).
  • Excessive alcohol consumption.
  • Connective tissue disorders (e.g., Ehlers Danlos, Marfan syndrome).

Signs and symptoms

SAH presents with an abrupt onset of neurological symptoms.

Key Features:

  • Thunderclap headache: sudden, severe headache, often described as "the worst headache of my life."
  • Neck stiffness: due to meningeal irritation.
  • Photophobia: sensitivity to light.
  • Loss of consciousness: may occur at onset.
  • Seizures: can be an initial presentation.
  • Nausea and vomiting: common due to raised ICP.

Investigations

  • Urgent non-contrast CT brain: first line test; hyperdense blood in the subarachnoid space confirms diagnosis.
  • Lumbar puncture (LP): if CT is negative but suspicion remains, perform LP at least 12 hours post-onset to check for xanthochromia (bilirubin breakdown product).
  • CT angiography: identifies aneurysms or vascular malformations.
  • Magnetic resonance angiography (MRA): alternative vascular imaging.
  • Blood tests:
    • Full blood count (FBC): detects infection or anaemia.
    • Coagulation screen: assesses clotting abnormalities.
    • Renal function: essential before contrast imaging.

Management

1. Immediate Resuscitation:

  • Secure airway and maintain oxygenation.
  • Strict blood pressure control (aim for SBP <140 mmHg).
  • Fluid resuscitation to maintain cerebral perfusion.

2. Neurosurgical and Endovascular Treatment:

  • Aneurysm coiling (preferred): endovascular embolisation of the aneurysm.
  • Craniotomy with aneurysm clipping: if endovascular treatment is not suitable.

3. Medical Management:

  • Calcium channel blockers (Nimodipine 60 mg every 4 hours): reduces risk of vasospasm related stroke.
  • Analgesia: avoid NSAIDs due to bleeding risk; use paracetamol.
  • Seizure prophylaxis: if indicated in high risk cases.

4. Complication Management:

  • Vasospasm: treated with triple H therapy (hypertension, hypervolaemia, haemodilution).
  • Hydrocephalus: may require external ventricular drainage (EVD).
  • Rebleeding prevention: early intervention within 48 hours is preferred.

5. Long-Term Follow-Up:

  • Monitor for cognitive and functional impairments.
  • Encourage lifestyle modifications (smoking cessation, blood pressure control).
  • Screen family members if a genetic link is suspected.