STROKE

Definition of stroke

1. Sudden onset of focal neurological deficit , lasting > 24 hours

due to cerebrovascular disturbances , either due to inadequate
blood supply to a part of the brain or hemorrhage

Risk factors for stroke

RISK FACTORS

Modifiable Non-modifiable
 Age >40 y.o  Hypertension
 M>F  DM- a/w lacunar stroke
 Afro carribean>  Hypercholesterolemia
Asian>Europe  A. fib, heart failure,
 Hereditary endocarditis
 Previous vascular  Obesity esp abdominal
event (MI, stroke) obesity
 Smoking
 Heavy alcohol use
 OCP
 polycythaemia

Classification of stroke
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 1. Based on pathogenesis
ISCHEMIC MECHANISMS OF STROKE HEMORRHAGIC

AH) Can only be differentiate with CT brain

CH)-rupture of a blood vessel within the brain parenchyma
ormation
headache, vomiting, LOC, very high BP

o brain parenchyma causes an interruption in blood supply, & at the same time, the flood of blood irritat
d over the first minutes or hours or may be associated with a rim of cerebral edema, which along with the
(cytotoxic edema) & release of glutamate into the ECFglutamate opens membrane channel, ↑influx of C
), particularly in patient after given antithrombotic & larger infarcts.

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 2. Based on type of blood vessels involved

Arterial Venous Watershed area

-see - venous - These areas are thin strips of in between the
below located at farthest end branches of two adjacent vascular
outer territories ( at borderzone area, between ACA & MCA
layer or MCA and PCA)
compare -adequate blood pressure must be maintained to
to artery ensure that enough blood is pumped into these areas.
-easily - are at high risk of developing ischemia during
affected extreme drops of BP
by the - triggers include extreme dehydration, MI, and sepsis
trauma - If ischemia to watershed areas is maintained > few
minutes the tissues begin to die, causing a stroke.
- Watershed areas are particularly vulnerable to low
BP in people who have advanced carotid stenosis.
3. Based on location

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 Lacunar
(arterioles, <
Anterior
Posterior
15mm)
circulation
circulation

1. Supply
1) Cortical
by
1) Supply
Anterior
signs
byCerebral
must
Artery (ACA)
be absent
posterior
& MCA
2. Supplies
2) LACI allcerebral
brain
(Lacunarlobes
artery,
(cortex)circulation
branch infarction)
of
3. 2 types– 22% vetebrobasilar
a) TACI/TACS
3) 4 types artery
(total anterior
circulation
a)
2) Pure
POCI infarct/
motor(60%)
(posterior
syndrome)--motor
circulation
17% are of
i) Hemiplegia
internal
infarct) d/t–capsule.
25%
damage
3) Dense
Supplyof upper
brainstempart
of4)cortical
hemiplegia,
Usuallyspinal
present
equal
tract
ii) Hemianopia
involvement
with ataxia, d/t of
damage
upper
diplopia,
to&optic
lwr
vertigo,
limb
nerve
b) Pure
or bilateral
sensory(5%)-
iii) Cortical
thalamus.
wekaness
deficitsPresent
(dysphasia
with on
dominant
heminumbness
hemisphere,
w/o significant
visospatial
weakness loss on
non-dominant
c) Mixed/sensorimo
hemisphere)
tor (20%)
b) PACI/PACS(partial
d) Ataxia
anteriorhemiparesis
circulation –
infarct/mild syndrome)
weakness - 36%
&
i) 2 ofataxia
the aboveon the /
cortical
same deficits
side ofalone
body

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Approach to history

1. Causes –risk factors

2. Current clinical features
a) Onset – must be sudden
b) Ask features based on site
3. Complications of stroke

acute chronic
 Aspiration pneumonia  Seizures d/t space occupying lesion
 UTI  Physical disability
 Septicaemia  Contractures, disuse atrophy
 Deep veins thrombosis  Loss of independence
 Bedsore  Psychological
 Depression
 Death
4. Rule out other differential diagnosis

Physical examination

1. Skin
a. Xanthelasma
b. Rashes(arteritis, splinter haemorrhages, livedoreticularis)
c. Limb ischaemia/deep venous thrombosis

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 2. Eyes
a. Diabetic changes
b. Retinal emboli
c. Hypertensive changes
d. Arcus senilis
3. Cardiovascular system
a. Blood pressure (hypertension, hypotension)
b. Heart rhythm (atrial fibrillation)
c. Murmurs (sources of embolism)
d. Jugular venous pressure (heart failure, hypovolaemia)
e. Peripheral pulses and bruits (generalised arteriopathy)
4. Respiratory system
a. Pulmonary oedema
b. Respiratory infection
5. Abdomen
a. Urinary retention(palpable bladder)
6. Locomotor
a. Injuries sustained during collapse with stroke
b. Comorbidities which influence functional abilities

Investigations

1. FBC
a) WBC – to look for infection (complications of stroke such as
UTI)
b) Platelet – to rule out bleeding disorder
c) Polycythemia
2. RFT – look for electrolyte imbalance
3. Coagulation profile - PT/APTT
4. ESR – to rule out vasculitis
5. FBS – to look for hypoglycaemia or DM, risk factor of stroke

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6. Fasting serum lipid – to look for risk factor of stroke, premature
athresclerosis
7. ECG - to look for cardiac source of embolism
8. CXR
9. CT scan
a) to exclude non-stroke lesion (not a stroke if not from vascular)
such as from subdural hematoma & brain tumour,
b) to differentiate ischemic & hemorrhagic stroke.
c) Usually done on 1st day of onset, but can be done within 7 days
of onset

Ischemic stroke Hemorrhagic

stroke
- Appears black - Appears
- LACI usually small areas, near basal ganglia, white
almost at central part
- PACI/TACI – usually larger area, involving
cortical part
- Can be seen as a lesion which comprises a
mixture of dead brain tissue that is already
undergoing autolysis and tissue that is
ischemic and swollen but recoverable
(penumbra). The infarct swells with time and
is at its max size few days after onset.
Craniectomy may be required to reduce mass
effect. As weeks go by, the edema subsides
and the infracted area is replaced by a
sharply defined fluid filled cavity.

10. MRI
a) if after 7 days of onset
b) Can detect ischemia earlier than CT
c) More sensitive than CT in detecting stroke affecting brainstem
and cerebellum
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11. Carotid Doppler
12. VDRL, HIV – to rule out neurovascular syphilis
13. Other additional investigations
a) Transesophageal echo(TEE), transthoracic echo (TTE) – 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. Such
findings may lead on to specific treatment
b) Autoimmune screen : ANA, antiDSDNA
c) Thrombophilia screen and lupus anticoagulants
d) CT / MR angiography – to detect extracranial arterial disease, if
suspect aneurysms
e) Fasting homocysteine
f) CRP

Management

Aims :

1. minimising the volume of brain that is irreversibly damaged,

2. preventing complications
3. reducing the patient's disability and handicap through
rehabilitation
4. reducing the risk of recurrent episodes

Acute management

1. Airway
a) Is the patient able to protect his/her airway?
b) Can the patient swallow without evidence of aspiration?
c) Perform a swallow screen and keep patient nil by mouth if
swallowing unsafe
2. Breathing

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 a) Is the patient breathing adequately?
b) Check oxygen saturation and give supplementary oxygen if
oxygen saturation < 95%
3. Circulation
a) Are peripheral perfusion, pulse and blood pressure adequate?
b) Treat with fluid replacement, anti-arrhythmics and inotropic
drugs as appropriate
4. Hydration
a) Is the patient dehydrated or unable to swallow?
b) Give fluids parenterally or by nasogastric tube if swallow is
unsafe
5. Nutrition
a) Assess nutritional status
b) Consider nutritional supplements
c) If dysphagia persists for a day or two, start feeding via a
nasogastric tube
6. Medication
a) If the patient is dysphagic, consider alternative routes for
essential medications
7. Blood pressure
a) Unless there is heart failure or renal failure, evidence of
hypertensive encephalopathy or aortic dissection, do not lower
the blood pressure in the first week since it will often return
towards the patient's normal level within the first few days
b) Early blood pressure reduction may decrease cerebral
perfusion and increase infarction to offset potential benefits.
8. Blood glucose
a) Is the blood glucose ≥11.1 mmol/l (200 mg/dl)?
b) Hyperglycaemia may increase infarct volume, therefore use
insulin (via infusion or glucose/potassium/insulin (GKI)) to
normalise levels but monitor closely to avoid hypoglycaemia
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9. Temperature
a) Is the patient pyrexial?
b) Raised brain temperature may increase infarct volume
c) Investigate and treat any cause but give antipyretics early
10. Pressure areas
a) These should be formally assessed and measures taken to
reduce the risk
b) Treat infection, maintain nutrition, provide a pressure-relieving
mattress and turn immobile patients regularly
11. Incontinence
a) Ensure the patient is not constipated or in urinary retention
b) Avoid urinary catheterisation unless the patient is in acute
urinary retention or incontinence is threatening pressure areas

Principles of management of stroke

1. Resuscitate if there is any hemodynamics instability

2. Thrombolysis
a) If patient present < 3 hours anf no CI
b) Eg : IV thrombolysis with recombinant tissue plasminogen
activator (rt-PA)
3. Secondary prevention with aspirin
a) 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.
b) Aspirin reduces the risk of early recurrence and has a small but
clinically worthwhile effect on long-term outcome
c) may be given by rectal suppository or by nasogastric tube in
dysphagic patients.
4. Risk factors identification and modification
a) Heparin - used in treating acute ischaemic stroke, Intracranial
haemorrhage must be excluded on brain imaging before
considering anticoagulation.
5. Supportive measures
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6. Anticipate, prevent and treat complications
7. Rehabilitation
a) Occupational therapy, physiotherapy, speech therapy
8. Surgery
a) Carotid endartectomy - A small proportion of patients with a
carotid territory ischaemic stroke or TIA will have a greater
than 70% stenosis of the carotid artery on the side of the brain
lesion. Such patients have a greater than average risk of stroke
recurrence. For those without major residual disability, removal
of the stenosis has been shown to reduce the overall risk of
recurrence, although the operation itself carries a 5% risk of
stroke
b) Carotid angioplasty and stenting are technically feasible but the
long-term effects on the risk of stroke are unclear
9. Others
a) routine use of corticosteroids, haemodilution, vasodilators and
'neuroprotective' agents should be avoided since they may all
have adverse effects and none has been shown to improve
patient outcomes.

Prognosis
1) 30% recurrence occur in the first 30 days

Differential diagnosis of stroke

1. Subdural hematoma
2. Trauma
3. Contusion
4. Brain abscess
5. Brain tumour

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