ischaemic stroke

1. Ischaemic
Stroke
Siti Aishah Mohd Zameri

2. WHO Definition of Stroke
“Rapidly developing clinical signs of focal (or
global) disturbance of cerebral function, with
symptoms lasting 24 hours or longer or
leading to death, with no apparent cause
other than of vascular origin[1].”
By this definition ,TIA, which lasts <24 hours, and patients
with stroke symptoms caused by subdural hemorrhage, tumors,
poisoning, or trauma are excluded.
1.WHO MONICA Project Investigators. The World Health Organization MONICA Project (Monitoring trends
and determinants in cardiovascular disease). J Clin Epidemiol 41, 105-114. 1988

3. Classification of Stroke
Ischemic Stroke — three subtypes:
 Thrombosis : In situ obstruction of an artery.
 Embolism : Particles of debris originating elsewhere
that block arterial access to a particular brain region.
 Systemic hypoperfusion : More general circulatory
problem, manifesting itself in the brain and perhaps
other organs.
Hemorrhagic Stroke due to intracerebral hemorrhage
or subarachnoid hemorrhage
Data compiled by AHA show that strokes due to
ischemia, intracerebral hemorrhage and subarachnoid
hemorrhage are 87%, 10%, and 3 %respectively[8]
8. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics--2011 update: a
report from the American Heart Association. Circulation 2011; 123:e18.

4. Risk Factors for Ischemic Stroke

5. Clinical symptoms of stroke
 Middle cerebral artery:
-Aphasia
-Hemiparesis/plegia
-Hemisensory loss/ disturbance
-Homonymous hemianopia
-Parietal lobe dysfunction:sensory& visual inattention,
acalculia
•Anterior Cerebral Artery:
-Weakness of lower limb more than upper
limb

6. Clinical symptoms
 Posterior (vertebrobasilar) Cerebral
Artery circulation:
-Cortical blindness
-Ataxia
-Dizziness & vertigo
-Dysarthria
-Diplopia
-Dysphagia
-Horner’s Syndrome
-Hemiparesis/hemisensory loss contralateral to the
cranial nerve palsy
- Cerebellar sign

7. Causes of Ischaemic stroke
1)Atherothromboembolism (50%)
- atherothrombotic plaque can grow to
obstruct a vessel with intraluminal
propagation of the thrombus to cause
occlusion
2)Intracranial small vessel disease
(25%)
- is due to lipohyalinosis , microatheroma,
or thromboembolism from a larger artery
3)Cardiogenic embolism (20%)
- Most common causes: AF and valvular
heart disease

8. Investigation
 FBC- exclude anaemia, thrombocytopenia
 RP- hydration status
 RBS- exclude hypoglycaemia
 FLP & FBS
 12 lead ECG
 CXR
 CT Brain- differentiate haemorrhage or
ischaemic stroke, confirm site of lesion n
extent of brain affected
 ECHO- for suspected cardioembolism,
assess cardiac function.

9. Management
 Oxygen and airway support: prevent
hypoxia and worsening of neurological injury.
Elective intubation to secure airway meybe
needed.
 Observation: V/S monitoring, GCS charting
 Mobilisation: limb physiotherapy,
occupational therapy
 BP: Mild hypertension is desirable at 160-
180/90-100. BP reduction should not be
drastic. Proposed substance: Labetolol 10-20
mg boluses @ 10min interval up to 150-300
mg, rate of labetolol infusion:1-3mg/min, or T.
Captopril 6.25-12.5mg.

10. Management
 Blood Glucose: If hyperglycaemia, to treat with
insulin, if hypoglycaemia, treat with glucose
infusion
 Nutrition: perform swallowing test, if fail, to
insert RT.
 Raised ICP: IV Mannitol (0.25-0.5g/kg) over
20min, can be given every 6 hr. If hydrocephalus
is present, to drain using intraventricular
catheter. Hemicraniectomy and surgical
decompressive therapy with 48H after symptom
onset is recommended to prevent herniation.
Ventriculostomy & suboccipital craniectomy is
effective in relieving hydrocephalus & brainstem

11. Reperfusion of Ischaemic
Brain
 IV thrombolysis with rt-PA: 0.9mg/kg,
max 90mg. 10% of the dose given as
bolus, followed by 60min infusion.
Recommended within 4.5hr of onset of
ischaemic stroke
 Aspirin: Start within 48Hr of onset. Use
of aspirin within 24Hr of rt-PA is not
recommended.
 Anticoagulant: use of heparins is not
routinely recommended.
 Use of streptokinase is contraindicated in
acute ischaemic stroke due to poor
clinical outcome.

12. Primary Prevention
 HPT: tx if BP>140/90, target BP for
diabetics <130/80.
 DM: maintain tight glycaemic control
 Hyperlipidaemia: High risk group: keep
LDL<2.6, if no risk factor LDL<4.2
 Aspirin therapy: 100mg OD is useful for
female age >65
 Smoking cessation.

13. Secondary Prevention
 Aspirin: recommended:75-350mg OD
 Clopidogrel: 75mg OD.
 Ticlopidine: 250mg BD
 Double therapy: combination of aspirin &
clopidogrel.
 Anti-hypertensive treatment: ACE-i is
useful to reduce recurrent stroke in
normotensive & hypertensive pt.
 Lipid-lowering: should be considered in pt
with previous ischaemic stroke
 Diabetic control: good glycaemic control

14. Antiplatelet for acute
cardioembolic stroke
 Warfarin: adjusted dose may be
commenced within 2-4 days after patient
is neurologically & medically stable.
 Heparin(unfractionated): adjusted dose
may be started if pt at high risk of
embolism.
 Anticoalation may be delayed for 1-2
weeks if there has been substantial
haemorrhage. Urgent anticoagulation in
pt with moderate-to-large cerebral infarct
is not recommended as high risk of ICB
complication.

15. Cardiac condition predisposing to
ischaemic stroke:
 Atrial fibrillation: assess by CHA2DS2Vasc score.
Aspirin (75-325) is enough for pt<65 yrs with lone AF.
Dabigatran etexilate (110-150) is as effective compare
to warfarin in non-valvular AF.
 Prosthetic heart valves: Life-long warfarin, target
INR:2.5-3.5
 Bioprosthetic heart valve: if high risk, consider
warfarin 3-12 months or longer. For all other pt, give
warfarin for 3 months then aspirin (75-150) OD
 Mitral stenosis: if risk factor present, consider long
term warfarin. All other pt, start aspirin.
 MI & LV dysfunction: If LV thrombus is present,
consider 6-12mths warfarin. If LV clot not present but
has risk factor, consider warfarin 3-6 mths then
aspirin. If dilated cardiomyopathy consider life-long
warfarin.

16. Revascularisation Procedure
 Carotid endarterectomy: Indicated for
stenosis 70-99% after a recent
ischaemic event.Early intervention within
2 weeks is more beneficial. Not
recommended for stenosis <50%. Pt
should remain on antiplatelet before &
after surgery.
 Carotid angioplasty & stenting:
alternative to CEA if surgery is
undesirable, technically difficult or
inaccessible. Use of dual antiplatelet at
least 4 weeks after procedure.

17. Conclusion
 Over last few decades, advances has been made in
management of acute ischaemic stroke. This occurred
along with advances of imaging methods as well as
primary and secondary prevention.
 General care of stroke patient in ward still plays a vital
role to achieve better outcome. Many complication can
be anticipated and avoided in acute stroke setting.
 Management of stroke is to recognise as acute medical
emergency and for therapeutic nihilism is to be
abolished as standard practice.
 Education of general population regarding symptoms of
stroke and urgency to arrive in hospital for treatment
early will change the outlook for stroke survivors.