STROKE (HAEMORRHAGIC)
DEFINITION
AKA Intracerebral haemorrhage.
Bleed into the tissue of the brain, resulting in deficit of any brain function,
from higher processing of speech and language, to movement and sensation,
to total destruction of life-supporting vital centres, due to rupture of
an artery.
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INCIDENCE
Incidence
Account for ~10% of all strokes.
Common.
Age
Mostly >70 years.
40-70 years with severe vessel diseases.
<40 years with congenital malformations.
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AETIOLOGY
AVMs (2.2% risk/yr after age 20).
Cavernous angiomas.
Hereditary bleeding disorders.
Thrombocytopaenia & sieve.
Mycotic aneurysms.
Tumours (especially mets).
Hypertension & Charcot-Bouchard aneurysms.
Cerebral amyloid angiopathy.
- Especially in Alzheimer's & multi-infarct dementia.
DPT - Amphetamines, cocaine, ecstasy.
Iatrogenic - warfarin increases risk 8-11 times.
0.3-1.3% of patients with MI treated with anti-thrombolytics.
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BIOLOGICAL BEHAVIOUR
Pathophysiology
Bleed into the brain tissue, usually from rupture of a small artery.
May extend to the ventricles or subarachnoid space.
Damage is due to:
- Direct tissue damage.
- Interruption of blood supply.
- Compression of surrounding tissue.
- Raised ICP.
- Oedema.
- Extent and location of damage defines clinical outcome.
Prognosis
30-50% die within 30 days.
Complications
Neurological complications
Cerebral oedema
2-5 days following the stroke.
Associated with a poor prognosis.
Help by avoiding hypo-osmolar IV fluids, hypoxia, overhydration, increased
central venous pressure, agitation, carbon dioxide retention.
Hydrocephalus and brain stem compression
Swelling associated with a stroke can compress the brainstem or cause acute
hydrocephalus.
Seizures
Progressing ischaemic stroke
A progressive neurological deficit may be caused by:
Enlargement of the infarct.
Haemorrhage into the infarct.
Oedema.
Seizures.
Systemic complications
Hypertension
- avoid rapidly lowering BP.
Hypotension
- stop antihypertensive medications and prevent dehydration to avoid dropping
BP.
DVT
- occur in about 50% of patients with hemiplegia following a stroke, prevent
with stockings.
Hyponatremia
- due to inappropriate secretion of ADH. Treat with fluid restriction.
Hyperglycaemia
- associated with a poor outcome. Avoid glucose-containing fluids and treat
with insulin.
Hypoxia
- most commonly secondary to a pulmonary infection. Can make infarcted
area bigger.
Fever and Infection
- A common cause of mortality after the first week.
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MANIFESTATIONS
Symptoms
Local
No hx prodromal TIAs.
Rapid onset (faster than seen with an ischaemic stroke).
May be featurse of meningism - severe headache (ischaemic strokes may also
cause headache), stiff neck.
Vomiting, drowsiness
Focal deficits
Clinically indistinguishable from a type of cerebral infarction (refer iCARDs).
Signs
Refer ischaemic stroke
Clinically indistinguishable.
Observe
Fundi - ?hypertensive changes (& papilloedema).
Palpate
Neck for stiffness.
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INVESTIGATIONS
Imaging
CT / MRI to determine whether ischaemic / haemorrhagic.
If haemorrhagic, CT demonstrates blood in brain substance.
Appears dense - white.
Angiography may detect AVM or aneurisms in younger pts.
Haematology
Coag studies.
Microbiology
Do LP cultures if suspicion of endocarditis.
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MANAGEMENT
Conservative
Rehab.
Secondary Prevention
Correct haemostatic defects.
Treat hypertension and other risk factors.
Medical
Reduce ICP - mannitol.
Avoid early lowering of BP.
Protamine sulphate if caused by heparin.
Vit K and fresh frozen plasma if caused by warfarin.
Surgical
Evacuation - rarely done but if indicated, eg cerebellar haemorrhage 2-4cm,
with raised ICP and/or worsening LOC.
DVT prophylaxis.
AVMs and aneurisms may be operated on.
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