STROKE (ISCHAEMIC)
DEFINITION
The sudden or rapid onset of localised damage in a part of the brain lasting
greater than 24 hours, with motor, sensory, perceptual, or higher function
deficits, due to lack of oxygen reaching the tissue as a result of disruption
of blood supply.
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INCIDENCE
80-85% of all strokes are ischaemic.
Prevalence
800/100,000 population.
Incidence
7000 new strokes per year in NZ.
Age
Mostly elderly, however 30% <65 years.
Gender
M>F.
Ethnicity
Common in Maori and PI.
& Earlier onset - 56-60yrs compared with 73 years for Pakeha.
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AETIOLOGY
Local Factors
Consider Virchow's Triad:
Vessel wall, stasis, hypercoagulability.
Wall/ Stasis
IEMs - Marfan's, homocystinuria.
Vessel infections - HIV, syphilis.
Vasculitides & sieve.
Atheroma +/- thrombosis & embolus (up to 80%)
Dissection.
Hylinosis (from chronic hypertension) - 10%.
Fibromuscular dysplasia.
Hypercoagulable States
See topic for complete discussion.
Congenital hypercoag.
Polycythaemia & sieve.
DPT, eg the OCP.
Non-Local Factors
Distant Emboli
10-15% of all strokes from heart emboli.
Congenital cardiac disease.
Paradoxical emboli.
Bacterial endocarditis.
Cardiac tumours (e.g. atrial myxoma).
Arrhythmias, eg AF.
Valvular heart diseases (mitral/ aortic).
Prosthetic valves.
Post-MI stasis.
Cardiomyopathies & sieve.
Cardiac surgery, catheterisation,.
Global events
Hypoperfusion and sieve.
Global cerebral hypoxia.
Eg caused by:
Acute MI, shock, arrhythmias.
(refer individual cards).
Cerebral venous occlusions.
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BIOLOGICAL BEHAVIOUR
Pathophysiology
Only atheroma will be discussed.
See other individualcards for different causes.
Gruel builds up most often around the aortic arch, the origin of internal
carotid, bifurcations of this, the proximal middle cerebral and the basilar
arteries.
Mostly strokes result from emboli forming on unstable plaques of atheroma.
Focal brain damage is the cardinal issue, with symptoms related precisely
to the area damaged.
Refer functional anatomy at the end of bio behaviour.
However other clinical pictures are possible - multi infarct dementia and
global ischaemia - see below.
Natural history
Sudden onset neurological deficit.
Abrupt over a few seconds or minutes.
Rapidly progressive over 1-2 hours.
May be restricted at first, then followed by a period of worsening (see
below).
This is followed by a plateau, then a gradual improvement over months.
Worsening
Due to enlargement of the infarct, haemorrhage into the infracted brain,
or oedema and seizures.
Cerebral oedema can occur 2-5 days following the stroke.
Associated with poor prognosis.
Care must be taken not to exacerbate oedema when giving fluids, etc.
Swelling associated with the stroke can cause brainstem compression or
acute hydrocephalus.
Complications
Hypertension/ hypotension
Due to autoregulation.
This usually regulates intracerebral P between 40 and 150mmHg.
But is thrown out of kilter by stroke.
Hypotension may increase the size of the infarction.
Penumbra - area round ischaemia which has enough blood for cells to remain
viable.
Other
DVT - occurs in 50% pts with hemiplegia after a stroke.
Hyponatraemia - inappropriate ADH secretion.
Hyperglycaemia - associated with poor outcome.
Fever and infection (common cause of mortality in short term).
Classification
TACI
PACI
PoCI
LacI
Multi-infarct dementia
Global causes - tend to cause damage at the watershed areas between vascular
supply areas.
Prognosis
20% dead at 1 month.
5-10% per year thereafter.
55% dead or dependent at 1 year.
20,000 disabled in NZ.
Functional Anatomy
Vascular Areas
Circle of Willis
See anatomy book.
Crucial to know derivative arteries and what they supply.
Anterior Cerebral A.
Primary motor and sensory cortices - feet and lower limbs.
Sup parietal lobule - spatial skills, 3D recognition, shapes, faces, abstract
perception.
Part of frontal association cortex - intelligence, mood, personality, cognitive
functions.
Middle Cerebral A.
Primary motor and sensory - except the above.
Inferior parietal lobule - spatial skills, 3D recognition, abstract perception.
Angular gyrus and supramarginal angular gyrus - language areas important
for reading/ writing.
Exners area (dominant hemisphere) - motor production of writing.
Brocas area (dominant hemisphere) - motor production of speech.
Wernickes area (dominant hemisphere) - speech recognition.
Primary auditory cortex (transverse gyrus of Heschl).
Frontal association cortex - intelligence, mood, personality, cognitive
function.
Temporal association area - memory, mood, aggression.
Post Cerebral A.
Primary visual cortex.
Supplementary visual cortex.
Other Brain Areas
Discussed in further detail in relevant cards.
Integrative functions
Poorly understood.
Not readily localisable.
Eg learning, memory, consciousness.
Cerebellum
Learning and performing rapid, coordinated, highly skilled movements (e.g.
running, swimming).
Maintains posture and balance.
Brainstem
RAS (arousal) - cardiac centre & resp centre).
Cranial nerve nuclei.
Vestibular system.
Important to be able to map these blood supplies on a cortex to fully understand
the stroke.
White matter tracts
Coronal Plane
Coronal radiation - carries white tracts up from brainstem.
Sublenticular/ auditory - carrying tracts to & from auditory centres.
Transverse Plane
Retrolenticular radiation - visual radiation.
Posterior limb - corticospinal tracts.
Genu - corticonuclear tracts.
Anterior limb - basal ganglia and thalamus tracts.
Corticospinal Tracts
Fibres run from the cortex through the crus cerebri.
Spread out in the pars basilaris of the pons and reform as the pyramids
in the medulla, crossing at the pyramidal decussation.
Run as corticospinal tract in the lateral funiculus of the spinal cord.
Thalamus & Med Lemniscus
Gracile and cuneate fasciculus of the dorsal columns.
Carries touch, vibration sensation.
Synapse at the gracile and cuneate nuclei in the lower medulla.
Post-synaptic fibres then cross at the internal arcuate fibres and then
travel to the thalamus as the medial lemniscus.
Globus Pallidus
Complex learned movements.
Spinothalamic Tract
Fibres carry pain and temperature sensation.
Cross at the level of entry to the spinal cord and run as the spinothalamic
tract to the thalamus.
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MANIFESTATIONS
General Notes
Preceding TIA history in 15%.
Note other relevant history suggesting atheropathy (refer iCARD).
Ischaemic CANNOT be differentiated from haemorrhagic
strokes without a scan.
Symptoms
Local
As per syndromes / area of occlusion.
See TACI, PACI,
PoCI, LacI cards.
Systemic
LOC rare (comatose or stuporose patients are more likely haemorrhagic).
Pt may be drowsy, confused, amnesic, aphasic (can't speak) or having 'blackouts'.
Pt may deteriorate 2-5 days (see above).
Complications
As for complications above.
Commonly aspiration, pneumonia, DVT, depression.
Signs
Neuro exam
Be thorough!
CNs - suggests PoCI.
Tone - ?defect.
Initially flaccid, later UMN.
Power - ?weakness.
Coordination
?cerebellar signs - PoCI.
?RAMs (basal ganglia involvement).
Reflexes - ?UMN.
?Babinski
Sensory
?touch, pain, temp (sensory cortex).
Pain & temp normal (superficial lesion).
Pain and temp only (thalamic lesion).
Aetiological Causes
Thorough evaluation as for suspected causes.
Refer individual icards.
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INVESTIGATIONS
Imaging
Non-contrast CT is most important.
- essential to differentiate ischaemic and haemorrhagic strokes.
Normal in 30-40% of strokes.
- rest have low-density area of infarction.
- can be up to 1-2 days for signs of ischaemia to be seen.
CXR & ECG - ?cause.
Carotid scans if relevant (MRA / carotid Doppler USS).
Stenosis or occlusion possible.
Haematology
Usually normal
If ESR abnormal, look for a treatable cause.
- eg vasculitis, endocarditis.
Biochem
Atheroma risk factors.
Glucose up 10% frequently.
Others indicated as per causes.
Microbiology
?treatable causes.
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MANAGEMENT
Prevention
Primary prevention
Vascular risk factors.
Smoking esp (increases risk of stroke by 50%).
- stopping smoking reduces risk to level of non-smokers in 2-5 years.
Note statins reduce stroke risk in IHD pts.
Other
Warfarin in patients with prosthetic valves, rheumatic valvular disease
or atrial fibrillation.
Carotid endarterectomy for severe ipsilateral carotid stenosis (>70%
or ratio of internal carotid artery flow to common carotid >4) - controversial
if asymptomatic.
Aspirin has NOT been shown to be beneficial in the primary prevention of
strokes.
The Acute Event
Think!
Is it a stroke?
Where is it?
What sort is it?
Why has it occurred?
Supportive Treatment
1. Oxygen
- hypoxia worsens infarct.
2. ETT
- if airway under threat
3. Measure BSLs
- hyperglycaemic worsens outcome
- treat with insulin
4. Electrolytes
- hyponaetraemia worsens confusion / seizures
- occurs due to ADH secretion.
5. BP control
- High BP common after stroke
- Do not lower unless SBP>220 or DBP>130
- Seek specialist advice if concerned.
- Avoid precipitous falls - induce hypoxia
6. Be alert for infections, dehydration, aspiration, dvts.
- larger strokes, drooling, choking, absent gag, weak cough, dysphonia,
CN palsies show risk to swallow.
- test for safe swallowing with saliva, then small sips of water.
- after a sip ask to speak and check for cough.
- withhold for formal assessment if doubt.
- give TEDs and early mobilisation.
Reducing Infarct Size
Aspirin
If CT proven ischaemia.
300mg daily
Given within 24hrs of stroke prevents thrombus propagation and recurrence
(small benefit, NNT=100).
Early treatment is better for outcome.
Heparin subcut/ IV
Is sometimes used.
But no proven value on long-term outcome.
May benefit some in terms of early recurrent strokes.
May increase risk of intracranial haemorrhage.
- some say avoid for 48hrs in cardioembolic stroke or severe events.
IV tPA
Beneficial if started within 3hrs of definite onset point.
- not for mild or very severe strokes.
- not if any CT suspicion of mass / haemorrhage.
6% risk of further haemorrhage (60% fatal)
Only in hospitals with stroke unit / team backup for intensive monitoring
& a protocol.
Exclusion criteria:
- risk of bleeding.
- INR >1.7.
- heparin in last 48hrs / prolonged PTTK.
- platelets <100,000
- previous stroke / head injury <3mo.
- major surgery <14 days
- SBP >185; DBP>110
- rapidly improving neuro deficit
- prior intracerebral haemorrhage
- BSL <2.5 or >20
- Seizure at onset of stroke
Administration
- 0.9mg/kg up to max of 90mg
- 10% as bolus, then rest over one hour in infusion
- no antcoagulants / antiplatelets for 24hrs
Monitoring
All admit to ICU / stroke unit.
- no CVL, Art line, NG tube for 24 hrs
BP/pulse every 15mins for 2 hrs
- avoid hypo and hypertension.
- if SBP 180-230/DBP 105-120 (2 readings 5-10m apart) then 10mg IV labetalol
over 1-2mins.
- rpt every 5-10mins up to 150mg or targets achieved.
- add nitroprusside 0.5-10mcg/min if SBP remains >230 or DBP 120-140.
Then every 30mins for 6 hrs
Then hourly for 24 hrs
- any deterioration: assume haemorrhage until CT
--> Stop and get surgical consult if appropriate
--> Measure PCV, Hb, PTTK, INR, platelets, fibrinogen.
Long term
Rehabilitation (interdisciplinary).
Secondary prevention
Aspirin, low dose daily
Other antiplatelets (e.g. persantin (dipyridamole) - combination shown
to reduce the risk of stroke).
Anticoagulation to prevent embolic stroke if relevant.
Primary prevention as above.
No evidence of benefit for statins in patients with previous stroke.
Surgery
Carotid endarterectomy - for prevention (above).
NB - If completely occluded and asymptomatic - leave it.
Risk of stroke or death during operation is ~3%.
Risk of stroke reduced by 80%.
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