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