Subarachnoid Haemorrhage

Incidence
1. 8/100,000/yr. Typically 35-65yrs
Causes
1. Rupture of saccular aneurysms (80%), AV malformations (15%), no cause found <15%.
2. Risk factors: Smoking, alcohol misuse, hypertension, bleeding disorders, mycotic aneurysm post-SBE, possibly lack of oestrogen (post menopausal), F:M >1:1, FH – close relatives have 3-5x increased risk
3. Berry aneurysms: Common sites: junction of posterior communicating with internal carotid, junction of anterior communicating with anterior cerebral artery, junction of anterior communicating with bifurcation of middle cerebral artery. 15% are multiple. Some are hereditary. Associations: Polycystic kidneys, COA, Ehlers-Danlos syndrome (hypermobile joints/increased skin elasticity)
Symptoms & Signs
1. Symptoms: Sudden (within seconds), devastating, typically occipital headache. Vomiting, collapse (+/- seizures), coma. Coma/drowsiness often last for days. 6% have earlier sentinel headache perhaps due to small warning leak from offending aneurysm. Signs: Neck stiffness, Kernigs sign takes 6hrs to develop, retinal and subhyaloid haemorrhage. Focal neurology at presentation may suggest site of aneurysm ie pupil changes indicating CNIII nerve palsy with a posterior communicating artery aneurysm or intracerebral haematoma. Later deficits suggest ischaemia from vasospasm, rebleeding or hydrocephalus.
Differential Diagnosis
1. Meningitis, migraine, intracerebral bleeds, cerebral venous thrombosis, in 50-60% of those with ‘thunderclap’ headache no cause is found
Investigations
1. CT – detects >90% within the first 48hrs. Older scanners may miss more. If CT –ve but strong clinical suspicion do LP >12hrs after headache onset. In SAH CSF will be bloody early on and xanthochromic (yellow) after a few hrs supernatant from spun CSF is looked at photometrically to find breakdown products of Hb. Finding bilirubin confirms SAH and shows CSF not just a ‘bloody tap’
Management
1. Get neurosurgical help in all cases. Immediately if reduced consciousness, progressive focal deficit or cerebellar haemotoma is suspected. Bed rest, chart BP, pupils, coma level. Repeat CT if deteriorating. Re-examine CNS often. Prevent need for straining with stool softeners.
  1. Surgical
    1. Craniotomy and clipping aneuryms can prevent re-bleeds. Best in those with few/no symptoms. If surgery likely do prompt angiography. Intraluminal platinum coils are an alternative with less mortality. Intracranial stents and balloon remodelling used for wide-necked aneurysms. Microcatheters can now reach previously unreachable lesions and AV malformations and fistulae may also benefit from this procedure
  2. Medical
    1. Cautiously control hypertension, analgesia for headache, bed rest +/- sedation for 4 weeks, keep hydrated (dehydration worsens vasospasm). Vasospasm – nimodipine (calcium antagonist) for 3 wks if BP allows
Rebleeding is common mode of death and occurs in 30% often in first few days. Vascular spasm follows a bleed often causing ischaemia +/- permanent CNS deficit. If this happens surgery is not helpful at time but may be so later. Most mortality occurs in first month, of those surviving first month 90% survive a year or more.
1. Grade I: no signs: 0% mortality, Grade II: neck stiffness and CN palsies: 11% mortality, Grade III: drowsiness: 37%, Grade IV: drowsiness with hemiplegia: 71%, Grade V: prolongued coma: 100%

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Subarachnoid Haemorrhage

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	Created by emailk8 almost 11 years ago