SAH

Aneurysmal SAH. 1

Perimesencephalic Bleeding. 1

Spontaneous Convexity SAH. 1

 

Aneurysmal SAH

Epidemiology

•   5% of strokes

•   50% mortality

•   10-15% die before reaching hospital

•   50% of patients are less than 55years old

Pathology

•   85% are aneurysmal

•   10% non-aneurysmal perimesencephalic

•   5% rare causes

o   Tumours

o   Inflammatory conditions

o   Dissection

o   Amyloid

o   Arterial malformations/fistula

•   Straining/physical activity is reported prior to 20% of ruptures

Aneurysms

 

 

 

Clinical

•   Sudden headache – onset with seconds (75%)

•   Often severe but sudden onset is more specific

•   Lateralized in 30%

•   Vomiting can occur, non-specific

•   Seizures – 1in 14 at onset

•   2/3 have decreased consciousness, 50% of which are in a coma

•   Neck stiffness common, takes 3-12hours to develop

•   Intraoccular haemorrhages – occur in 1 in 7.  Due to sustained increase in CSF pressure obstructing central retinal vein.

o   May cause visual disturbances/blobs in vision

•   Third nerve palsy

•   Other focal neurology can occur to infarction. 

•   Severe hypertension can occur

•   Cardiac arrest in 3% 

Complications

•   Re-bleeding

o   15% risk in first few hours

o   40% risk over first 4 weeks

o   Significantly worse prognosis, 80% die or disabled

•   Delayed brain ischaemia

o   Peak onset 5-14days

•   Hydrocephalus

o   Gradual reduction in consciousness

o   Downward deviation of the eyes and small unreactive pupils

Long-term complications

•   Late re-bleeding ~0.7% between 1month and 1year

•   Epilepsy

o   ~8% by 1 year, ~12% by 5 years (Neurology 2015)

•   Anosmia in 30%

•   Cognitive deficits common

•   Psychosocial dysfunction 60% reported changes in personality

•   Only 25% recover fully

 

Diagnosis

CT scan

•   95% will show extravasated blood on first day

•   Less on subsequent days

•   False positives can occur with diffuse brain swelling due to blood in congested subarachnoid vessels .

MRI

•   Probably similar sensitivity to CT initially

•   Better sensitivity than CT after a few days

LP

•   Picks up an additional 3% if negative CT

•   Wait 6-12hours after headache onset (sensitivity increases with time up to 12 hours)

•   Measure pressure (to exclude other diagnoses)

•   If CSF is spun down and supernatant yellow – this is indicative of bililrubin and SAH.

•   Formal testing for bilirubin usually done – xanthochromic index

 

Angiography

•   Catheter angiography is gold standard

o   Higher risks: 1.8% ischaemic complications, 1-2% aneurysm rerupture

•   CT angiography

o   95% sensitivity

o   Safer and quick

•   MRI angiography

o   Good sensitivity but often impractical.

Treatment

Large intracerebral haemorrhages or subdural extension

•   Evacuation or hemicraniotomy to allow cerebral expansion

Prevention of re-bleeding

•   Surgical clipping

o   ARR of poor outcome 10%

o   RRR of poor outcome 19%

•   Endovascular coiling

o   ISAT trial showed RRR of 24% and ARR of 7% compared with surgery.

Prevention of delayed cerebral ischaemia

•   Calcium channel antagonists

•   RRR 18%, ARR 5.1%

•   Nimodipine best studied

o   60mg PO Q4h for 3weeks

o   IV may be more harm than good

•   Magnesium sulphate may be useful

•   Maintain intravascular volume (no evidence)

Management of hydrocephalus

•   Lumbar puncture can improve consciousness

•   Need to determine if site of obstruction in the subarachnoid space or in the ventricular system.

•   Catheter insertion through burr hole.

 

Prevention

•   Incidental aneurysm

o   Need to consider many risk factors to make informed decision

o   Age, Size of lesion, Family history, Location

•    

•   Second aneurysms in patients who have had SAH

o   Higher risk of rupture

o   Higher psychological burden

o   Coiling usually offered

•   Screening

o   First degree relatives have 5-12x risk of SAH (2-5% lifetime risk)

o   Chance of finding lesion is 1.7x general population

o   Should screen:

o   People with >1first degree relative with SAH

o   ADPKD patients >20yrs old

o   Identical twins if one has SAH

o   After initial screen may be benefit in 5 yearly screening

o   No need to screen after an initial episode of SAH (with rare exceptions)

 

 

Non-aneurysmal SAH

•   Large single centre series (Stroke 2011;42:3055) of all SAH:

o   17% were non-aneurysmal

o   3% were convexity, non aneurysmal SAH

Perimesencephalic Bleeding

•   Blood confined to cisterns around midbrain – basal cisterns, quadrigeminal cistern

•   Some sedimentation of blood can occur but no frank extension of haemorrhage

•   Headache usually slower onset, less change in mental state.

•   Angiogram negative

•   Probably caused by rupture of vein in prepontine or interpeduncular cistern

•   Low risk of re-bleed

•   Good prognosis and normal life expectancy

 

Spontaneous Convexity SAH

•   Minimal data, two major cases series

o   Stroke 2011 – 25 cases

o   Neurology 2010

Aetiology

Causes identified (in order of frequency):

•   Cerebral amyloid angiopathy (especially >60years)

•   RCVS

•   PRES

•   Post CEA hyperperfusion

•   Dural sinus thrombosis

•   Amphetamine use

•   Cerebral vasculitis

•   Infective endocarditis

•   ITP/anticoagulation etc.

•   Moyamoya

 

Mimics on imaging

•   Thrombosed cortical vessel

•   Cluster of micobleeds

•   Calcification

•   Haemorrhagic transformation of infarct

Clinical

•   Headache (~40%)

•   Transient sensory/motor symptoms

o   Often observed to spread over several minutes

o   Often occur recurrently

o   ?Seizures vs cortical spreading depression – no epileptiform changes indentified in cases to date - ?therefore more likely cortical depression

•   Seizures

o   Frequency depends on series (Stroke 2011 - ~ 20%, Neurology 2010 – none)

Prognosis

•   Variable depending on series

•   Many cases of iscahemic stroke/ICH etc. on follow-up - ?a marker of vascular disease