Sub-arachnoid Haemorrhage

 

• Background

  Pathophysiology

  • Bleeding in the subarachnoid space, causing brain injury through local pressure, toxicity from bleeding, and global ↑ICP.
  • 80% are due to the rupture of a berry (aka saccular) aneurysm in the circle of Willis.
  • Most of the rest are due to arteriovenous malformations.
  • If it results in a neurological deficit lasting ≥24 hours, can be considered a type of haemorrhagic stroke, though in clinical practice this term is rarely applied to SAH.

  Epidemiology

  • Peak onset 40-60 years old. Onset in men slightly earlier.
  • 1/200 lifetime risk. 1/5000 if no risk factors, 1/15 if several major risk factors present.

• Signs and symptoms

  Symptoms:

  • Thunderclap headache: sudden, devastating, occipital. Though the cardinal symptom of SAH, it is absent in 25%.
  • Sentinel headache (30%). Milder headache in the preceding days to weeks, reflecting small aneurysmal leaks.
  • Vomiting, seizures.
  • Collapse, loss of consciousness (40% at onset), coma.
  • Onset timing: ⅓ during daily activities, ⅓ during sleep, ⅓ during exertion.

  Signs:

  • Meningism: stiff neck, Kernig's (after 6 hours).
  • Retinal and subhyoid haemorrhage.
  • Focal neurological signs.

• Risk factors

  • Smoking
  • HTN
  • Family history
  • ↑Cholesterol
  • Autosomal dominant polycystic kidney disease.
  • Coagulopathy
  • Ehlers Danlos and Marfan's.

• Investigations

  Initial

  • FBC
  • Clotting: may show coagulopathy.
  • U&E: may show ↓Na+ due to cerebral salt wasting.
  • Glucose may be elevated.
  • ECG: SAH can cause cardiac abnormalities e.g. long QT.

  Diagnosis

  Non-contrast CT head:

  • Most sensitive in first 6 hours.

  LP after 12 hours if CT -ve:

  • Allows time for development of xanthochromia, a yellowing of the CSF from Hb breakdown.
  • Xanthochromia is detected with spectrophotometry of the last (of 4) CSF bottles, as there may be RBCs in the first bottle(s) from a traumatic tap.
  • Take simultaneous venous blood to check serum BR, protein, and glucose for comparison.
  • Will detect SAH in only 1 in 500 patients who've had a -ve CT in first 6 hours.

  If CT or LP +ve, confirm diagnosis with digital subtraction angiography (DSA) or CT angiogram.

• Management

  Medical:

  • Requires close specialist care, often ITU.
  • Regular neuro obs: GCS, pupils, neurological signs.
  • Aim SBP <180.
  • Nimodipine: calcium channel blocker to reduce vasospasm.
  • Analgesia for headache.

  Refer to neurosurgery. Possible interventions:

  • Clipping
  • Endovascular coil embolisation.

• Complications and prognosis

  Acute complications:

  • Neuro: obstructive hydrocephalus, rebleed, vasospasm in the circle of Willis (after 3-15 days).
  • Others: arrhythmias, pulmonary oedema.

  Outcomes:

  • 25% die, usually within 1 month. Due to initial bleed, rebleed, or vasospasm.
  • 50% left with long-term disability or neurological impairment.