Subarachnoid Haemorrhage

Question 1

Definition of SAH

Answer 1

Arterial bleeding into the subarachnoid space.
• Often catastrophic and is an emergency

Question 2

Aetiology of SAH

Answer 2

• 80% of SAH are caused by a Berry aneurysm rupture in the Circle of Willis (leading cause of non-traumatic SAH
◦ Common sites are at the junctions of the posterior communicating artery with the internal carotid, at bifurcation of the middle cerebral artery and junction between anterior cerebral artery and anterior communicating artery

• The rest are due to non-aneurysmal perimesencephalic SAH, AV malformations and arterial dissections

Question 3

Risk factors for SAH

Answer 3

‣ Smoking
‣ Hypertension
‣ Alcohol abuse
‣ Previous aneurysmal SAH increases risk of new aneurysm formation
‣ Ehlers-Danlos, Marfan’s syndrome and Polycystic kidney disease increases risk of aneurysm formation

Question 4

History and Examination of SAH

Answer 4

• Severe sudden-onset headache:
◦ Typically described as a thunderclap headache.
◦ Peaks writhing 1-5min and can last over an hour
• Nausea/Vomiting: due to irritation of the cerebral cortex
• Depressed consciousness/LOC: caused by blockage of flow of CSF by the blood
• Neck stiffness and muscle aches (meningismus):
• Photophobia: due to irritation of the meninges
• Eyelid drooping, Diplopia etc: May have compression of the third nerve, leading to palsy. Likely a posterior communicating artery aneurysm
• Confusion

• Kernig’s sign: raise leg to test for meningism

Question 5

Investigations for SAH

Answer 5

• Emergency non-contrast CT head: Standard diagnostic test for SAH. Would see hyperdense (white areas) areas in the subarachnoid space (within first 24 hours)
• CT angiography: when confirmed SAH, use to identify location of bleed/aneurysm
• Neuro exam, GCS etc
• FBC
• Serum electrolytes: hyponatraemia is most common electrolyte abnormality in SAH
• Baseline clotting profile
• ECG: request in all patients

• Lumbar puncture: Only need to do if CT comes back -ve but signs are suggestive of SAH. Wait at least 12 hours for RBC to lyse so you can see xanthochromia (yellow colour due to bilirubin)

Question 6

Treatment for SAH if GCS score <8 or falling (severe):

Answer 6

1) Cardiopulmonary support: ABCDE, protect the airway, call neurosurgeon for transfer to neuroscience centre, HDU or ICU. Controlled O2 therapy, fluids if needed to maintain cerebral perfusion

+ Supportive care: monitor GCS, reexamine CNS, pupils, BP and sodium. Stop anticoagulants

+ Nimodipine: 60mg orally every 4 hours. Is a calcium channel blocker that would reduce risk of vasospasm and hence reduce risk of delayed cerebral ischaemia

CONSIDER endovascular coiling or surgical clipping: Coiling is preferred

Question 7

Treatment of SAH if GCS score >9:

Answer 7

1) Supportive care and monitoring
+ Nimodipine
+ Analgesia: start with paracetamol, avoid aspirin or NSAIDs before aneurysm occlusion

CONSIDER endovascular coiling or surgical clipping of aneurysm

Question 8

Prevention of SAH

Answer 8

For those at risk, treat the hypertension and help with smoking cessation

Question 9

Complications of SAH

Answer 9

• Neuropsychiatric problems: 50% of survivors report cognitive impairment (mood and memory problems)
• Hydrocephalus: due to blockage of arachnoid granulations
• Re bleeding: commonest cause of death
• Cerebral ischaemia: due to vasospasm can cause permanent CNS damage
• Hyponatraemia

Question 10

Prognosis of SAH

Answer 10

Use of endovascular techniques have led to a decrease in case-fatality and better prognosis
Survivors may not survive very long after, or may develop neurological deficits