Ischaemic Stroke

Siti Aishah Mohd Zameri

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

Classification of StrokeIschemic 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.

Risk Factors for Ischemic Stroke

Clinical symptoms of strokeMiddle 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

Clinical symptomsPosterior (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

Causes of Ischaemic stroke1)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 artery3)Cardiogenic embolism (20%)- Most common causes: AF and valvular

heart disease

InvestigationFBC- exclude anaemia, thrombocytopeniaRP- hydration statusRBS- exclude hypoglycaemiaFLP & FBS12 lead ECGCXRCT Brain- differentiate haemorrhage or

ischaemic stroke, confirm site of lesion n extent of brain affected

ECHO- for suspected cardioembolism, assess cardiac function.

ManagementOxygen and airway support: prevent hypoxia

and worsening of neurological injury. Elective intubation to secure airway meybe needed.

Observation: V/S monitoring, GCS chartingMobilisation: limb physiotherapy, occupational

therapyBP: 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.

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 compression caused by large cerebellar infarction.

Reperfusion of Ischaemic BrainIV 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.

Primary PreventionHPT: tx if BP>140/90, target BP for

diabetics <130/80.DM: maintain tight glycaemic controlHyperlipidaemia: 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.

Secondary PreventionAspirin: recommended:75-350mg ODClopidogrel: 75mg OD.Ticlopidine: 250mg BDDouble 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

Antiplatelet for acute cardioembolic strokeWarfarin: 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.

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.

Revascularisation ProcedureCarotid 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.

ConclusionOver 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.