Cerebro-Vascular Accident

Dr Pukar Ghimire
MBBS, MD
 Introduction
• 4rd most common cause of death
• Includes range of disorder of CNS
– Stroke
– SAH
– Cerebral venous thrombosis
 Pathophysiology
• 85% is due to infarction
• 15% due to hemorrhage
 Infarction
• mostly caused by thromboembolic disease
secondary to atherosclerosis in the major
extracranial arteries (carotid artery and aortic
arch)
– 20% of infarctions are due to cardioembolism
– further 20% are due to thrombosis in situ caused
by intrinsic disease of small perforating vessels
(lenticulostriate arteries), producing so-called
lacunar infarctions.
• Infarction occurs only when the homeostatic
mechanism fail that help to prevent infarction
even when a vessel is blocked
• Higher brain temperature, and higher blood
sugar have both been associated with a
greater volume of infarction
• Subsequent restoration of blood flow may
cause haemorrhage into the infarcted area
(‘haemorrhagic transformation’)
• This is particularly likely in patients given
antithrombotic or thrombolytic drugs, and in
patients with larger infarcts.
• The infarct swells with time and is at its
maximal size a couple of days after stroke onset.
• At this stage, it may be big enough to exert
mass effect both clinically and radiologically;
sometimes, decompressive craniectomy is
required
• After a few weeks, the oedema subsides and
the infarcted area is replaced by a sharply
defined fluid-filled cavity.
 Intracerebral hemorrhage
• It usually results from rupture of a blood
vessel within the brain parenchyma
• The explosive entry of blood into the brain parenchyma
causes immediate cessation of function in that area as
neurons are structurally disrupted and white-matter fibre
tracts are split apart.
• The haemorrhage itself may expand over the first minutes
or hours, or it may be associated with a rim of cerebral
oedema, which, along with the haematoma, acts like a mass
lesion to cause progression of the neurological deficit.
• If big enough, this can cause shift of the intracranial
contents, producing trans tentorial coning and sometimes
rapid death
 Clinical features
• Acute stroke and TIA are characterised by a
rapid-onset, focal deficit of brain function.
• The typical presentation occurs over minutes,
affects an identifiable area of the brain and is
‘negative’ in character
• Provided that there is a clear history of this,
the chance of a brain lesion being anything
other than vascular is 5% or less
• The clinical presentation of stroke depends
upon which arterial territory is involved and
the size of the lesion
• Reduced conscious level usually indicates a
large volume lesion in the cerebral
hemisphere but may result from a lesion in
the brainstem or complications such as
obstructive hydrocephalus, hypoxia or severe
systemic infection.
• The combination of severe headache and
vomiting at the onset of the focal deficit is
suggestive of intracerebral haemorrhage.
• General examination may provide clues to the
cause, and identify important comorbidities
and complications.
 Classification of stroke
• Transient ischaemic attack (TIA) describes a
stroke in which symptoms resolve within 24
hours with no defect seen in imaging
– The term TIA traditionally also includes patients
with amaurosis fugax, usually due to a vascular
occlusion in the retina.

• Stroke describes those events in which

symptoms last more than 24 hours.
• Progressing stroke (or stroke in evolution)
describes a stroke in which the focal
neurological deficit worsens after the patient
first presents. Such worsening may be due to
increasing volume of infarction, haemorrhagic
transformation or increasing cerebral oedema.

• Completed stroke describes a stroke in which

the focal deficit persists and is not progressing.
• Reversible ischemic neurological
defeicit(RIND)
– Event lasting for 24 hrs to 7 days
 Investigations
• Investigation of acute stroke aims to
– confirm the vascular nature of the lesion,
– distinguish cerebral infarction from haemorrhage
and
– identify the underlying vascular disease and risk
factors
• CT remains the most practical and widely available
method of imaging the brain.
• It will usually exclude non-stroke lesions, including
subdural haematomas and brain tumours, and will
demonstrate intracerebral haemorrhage within
minutes of stroke onset
• However, especially within the first few hours after
symptom onset, CT changes in cerebral infarction
may be completely absent or only very subtle.
• Changes often develop over time
• For most purposes, a CT scan performed
within 24 hours is adequate but there are
certain circumstances in which an immediate
CT scan is essential
• MRI has scanning times that are longer.
However, MRI diffusion weighted imaging
(DWI) can detect ischemia earlier than CT
• MRI is more sensitive than CT in detecting
strokes affecting the brainstem and
cerebellum and unlike CT, can reliably
distinguish haemorrhagic from ischaemic
stroke even several weeks after the onset.
 Vascular imaging
• Detection of extracranial vascular disease can help
establish why the patient has had an ischaemic
stroke and, in highly selected patients, may lead
on to specific treatments, including carotid
endarterectomy to reduce the risk of further
stroke
• Extracranial arterial disease can be non-invasively
identified with duplex ultrasound, MRA or CT
angiography or occasionally intra-arterial contrast
radiography
• Cardiac investigation
– Approximately 20% of ischaemic strokes are due to
embolism from the heart.
– The most common causes are atrial fibrillation,
prosthetic heart valves, other valvular abnormalities
and recent myocardial infarction.
– A transthoracic or transoesophageal echocardiogram is
required to confirm the presence of a clinically
apparent cardiac source or to identify an unsuspected
source such as endocarditis, atrial myxoma, intracardiac
thrombus or patent foramen ovale.
 Management
• Management is aimed at
– minimising the volume of brain that is irreversibly
damaged,
– preventing complications ,
– reducing the patient’s disability and handicap through
rehabilitation, and
– reducing the risk of recurrent stroke or other vascular
events.
• With TIA there is no brain damage and disability, so
the priority is to reduce the risk of further vascular
events.
 Supportive care
• Should begin at same time as acute medical
management
• If dysphagia– iv nutrition or NG feeding
• The patient’s neurological deficits may worsen
during the first few hours or days after their onset.
• This is most common in those with lacunar infarcts
but may occur in other patients, due to extension of
the area of infarction, haemorrhage transformation,
or the development of oedema with consequent
mass effect.
• Patients with cerebellar haematomas or infarcts with
mass effect may develop obstructive hydrocephalus
and some will benefit from insertion of a ventricular
drain and/or decompressive surgery
• Some patients with large haematomas or infarction
with massive oedema in the cerebral hemispheres
may benefit from anti-oedema agents, such as
mannitol or artificial ventilation.
• Surgical decompression to reduce intracranial
pressure should be considered in appropriate patients.
 Thrombolysis
• Intravenous thrombolysis with recombinant tissue
plasminogen activator (rt-PA) increases the risk of
haemorrhagic transformation of the cerebral infarct
with potentially fatal results.
• However, if it is given within 4.5 hours of symptom
onset to carefully selected patients, the
haemorrhagic risk is offset by an improvement in
overall outcome
• The earlier treatment is given, the greater the
benefit.
• IV rtPA (0.9 mg/kg to a 90-mg maximum; 10%
as a bolus, then the remainder over 60 min)
versus placebo in ischemic stroke within 3 h of
onset
 Aspirin
• In the absence of contraindications, aspirin
(300 mg daily) should be started immediately
after an ischaemic stroke unless rt-PA has
been given, in which case it should be
withheld for at least 24 hours.
• Aspirin reduces the risk of early recurrence
and has a small but clinically worthwhile effect
on long-term outcome.
 Heparin
• No use
• it increases the risk of both intracranial and
extracranial haemorrhage
• No long term benefit as well
 Coagulation abnormalities
• In those with intracerebral haemorrhage,
coagulation abnormalities should be reversed
as quickly as possible to reduce the likelihood
of the haematoma enlarging.
• This most commonly arises in those on
warfarin therapy.
• There is no evidence that clotting factors are
useful in the absence of a clotting defect.
Management of risk factors
 Carotid endarterectomy and angioplasty
• A small proportion of patients with a carotid territory ischaemic
stroke or TIA will have a greater than 50% stenosis of the carotid
artery on the side of the brain lesion.
• Such patients have a greater than average risk of stroke
recurrence.
• Removal of the stenosis has been shown to reduce the overall
risk of recurrence
• Surgery is most effective in patients with more severe stenoses
(70–99%) and in those in whom it is performed within the first
couple of weeks after the TIA or ischaemic stroke
• Endarterectomy of asymptomatic carotid stenosis is not routinely
justified.
SUBARACHNOID HEMORRHAGE
• Women are affected more commonly than
men and the condition usually presents before
the age of 65.
• The immediate mortality of aneurysmal SAH is
about 30%; survivors have a recurrence (or
rebleed) rate of about 40% in the first 4 weeks
and 3% annually thereafter.
• Eighty-five percent of SAH are caused by saccular
or ‘berry’ aneurysms arising from the bifurcation of
cerebral arteries particularly in the region of the
circle of Willis.
• The most common sites are in the anterior
communicating artery (30%), posterior
communicating artery (25%) or middle cerebral
artery (20%).
• Five percent of SAH are due to arteriovenous
malformations and vertebral artery dissection.
 Clinical features
• typically presents with a sudden, severe,
‘thunderclap’ headache (often occipital),
which lasts for hours or even days, often
accompanied by vomiting, raised blood
pressure and neck stiffness or pain.
• It commonly occurs on physical exertion,
straining and sexual excitement.
• On examination, the patient is usually
distressed and irritable, with photophobia.
There may be neck stiffness due to
subarachnoid blood but this may take some
hours to develop.
• Focal hemisphere signs, such as hemiparesis
or aphasia, may be present at onset if there is
an associated intracerebral haematoma.
 Investigation
• CT brain
• Lumbar Puncture
• The diagnosis of SAH can be made by CT, but a negative
result does not exclude it, since small amounts of blood in
the subarachnoid space cannot be detected by CT.
• Lumbar puncture should be performed 12 hours after
symptom onset if possible, to allow detection of
xanthochromia
• If either of these tests is positive, cerebral angiography is
required to determine the optimal approach to prevent
recurrent bleeding.
 Management
• Nimodipine (30–60 mg IV for 5–14 days,
followed by 360 mg orally for a further 7 days)
is usually given to prevent delayed ischaemia
in the acute phase.
• Insertion of platinum coils into an aneurysm
(via an endovascular procedure) or surgical
clipping of the aneurysm neck reduces the risk
of both early and late recurrence.
• Treatment may also be required for
complications of SAH, which include
– obstructive hydrocephalus (that may require
drainage via a shunt),
– delayed cerebral ischaemia due to vasospasm (which
may be treated with vasodilators),
– hyponatraemia (best managed by fluid restriction)
and
– systemic complications associated with immobility,
such as chest infection and venous thrombosis.