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Stroke
- 2. Definitions Stroke Clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death Transient Ischemic attack (TIA) Clinical syndrome of rapid onset of focal deficitsof brain function which resolves within24 hours Amaurosis fugax
- 5. Ischemic Stroke 80% of strokes Arterial occlusion of an intracranialvessel leads to hypoperfusion of thebrain region it supplies Two etiological types Thrombotic Embolic
- 6. IschemicPenumbra Tissue surrounding thecore region of infarction which is ischemic but reversibly dysfunctional Maintained by collaterals Can be salvaged if reperfused intime Primary goal of revascuralization therapies
- 7. HemorrhagicStroke Two types Intracerebral hemorrhage(ICH) Subarachnoid hemorrhage(SAH) Higher mortality rates when compared to ischemic stroke
- 8. Intracerebral Hemorrhage • Result of chronic hypertension • Small arteries are damaged due to hypertension • In advanced stages vessel wall is disrupted and leads to leakage • Other causes: amyloid angiopathy, anticoagulant therapy, cavernous hemangioma, cocaine, amphetamines
- 9. Subarachnoid Hemorrhage Most common cause is rupture of saccular or Berry aneurysms Other causes include arteriovenous malformations, angiomas, mycotic aneurysmal rupture etc. Associated with extremely severe headache
- 11. CLASSICALPRESENTATIONS THROMBOTIC H/O TIA STROKE IN EVOLUTION USUALLYHAPPENS EARLYMORNING EMBOLIC PATIENTS WITH KNOWN HEART DISEASE LIKE IHD, VALVULAR HEART DISEASE RAPID RECOVERY HAEMORRHAGIC STROKE IN HYPERTENSIVE PATIENTS ASSOCIATED WITH EMOTIONAL EXCITEMENT HEADACHE & VOMITING
- 12. DIFFERENTIALDIAGNOSIS SPACE OCCUPYING LESION(TUMOR) SEIZURE MIGRAINE SUBDURAL HAEMATOMA METABOLIC DISTURBANCE LIKE HYPOGLYCAEMIA
- 13. SUMMARY Rapid onset focal deficit of brain functionconfirms stroke Onset and progression will decide the aetiology Precise history of deficit will decide thesite of lesion
- 15. INVESTIGATIONOBJECTIVES To confirm the vascular nature of the lesion The pathological type of the vascular lesion The underlying vascular disease Risk factors present
- 16. INVESTIGATIONMODALITIES: BRAIN NON-INVASIVE CT Scan MRI Scan MR Angiography Doppler Ultrasound EEG PET SPECT INVASIVE Lumbar Puncture Contrast Angiography (Cerebral Arteriography) CT Angiography
- 17. CTSCAN Mandatory initial investigation Haemorrhage appears instantly as a hyperdense area Infarct appears as a hypodense area Infarct may not appear before 48 hrs MRI may be done instead but ct scan is more sensitive for detecting haemorrhage Diffusion weighted MRI is good for identifying ischaemic lesion
- 19. ISCHAEMICLESION
- 20. STROKE PATIENT CT SCAN/MRI VASCULAR NATURE CONFIRMED HAEMORRHAGE ISCHAEMIA Cont’d…
- 23. Carotid Artery Ultrasound Showing a Completely Calcified Atherosclerotic Plaque
- 25. MRangiogram showing giant aneurysm at the middle cerebral arterybifurcation
- 26. NORMAL CT SCAN HAEMORRHAGE SUSPECTED LUMBAR PUNCTURE CSF WITH BLOOD/ XANTHOCHROMIA HAEMORRHAGE CONFIRMED
- 27. TREATMENTOBJECTIVES 1. MINIMIZE VOLUME OF BRAIN IRREVERSIBLY DAMAGED 2. PREVENT COMPLICATIONS 3. REHABILITATION 4. REDUCE RISK OF RECCURENCE
- 28. MANAGEMENTOFATRANSIENT ISCHAEMICATTACK(TIA) MEDICAL MANAGEMENT (if diffuse atherosclerotic disease or pooroperative candidates) Stop smoking Concurrent medical problems tobe addressed: Emboli from heart and other parts of cardiovascular system (a) anti coagulants: Heparin(IV), Warfarin(oral) (b) anti platelet drugs: Aspirin(oral),Ticlopidine Diabetes, Hypertension, Hyperlipidemia
- 29. MANAGEMENTOFATRANSIENT ISCHAEMICATTACK(TIA)–Cont’d SURGICALMANAGEMENT CAROTID AND CEREBRALARTERIOGRAPHY STENOSIS Mild to Moderate Severe Regular Follow Up Carotid Endarterectomy All above can be done only if there is relatively little atherosclerosis elsewhere in cerebrovascular system.
- 30. MANAGEMENTOFANACUTE EPISODEOFSTROKE AIRWAY - Maintain airway, prevent aspiration, keep nil per oral BREATHING - Maintain oxygen saturation >97% - Supplementary oxygen CIRCULATION - Adequacy of pulse and BP - Fluid, Anti Arrhythmics, Ionotropes HYDRATION - Prevent dehydration ; give adequate fluids - Parenteral or via nasogastric tube NUTRITION - Nutritional supplements and Nasogatricfeeding MEDICATION - Administer medication also by routes other than oral
- 31. MANAGEMENTOFANACUTE EPISODEOFSTROKECont’d BLOOD PRESSURE - unless indicated (heart or renal failure,hypertensive encephalopathy or aortic dissection) it should not be lowered for the fear of expansion of infarct. Ischaemic stroke - maintain 180/110 mm Hg Haemorrhagic stroke – keep MAP <115 mm Hg BLOOD GLUCOSE - INSULIN to treat hyperglycaemia(can increase infarct size) - maintain < 200mg% TEMPERATURE - early use of antipyretics PRESSUREAREAS – To prevent occurrence of decubitus ulcers INCONTINENCE
- 32. ISCHAEMICSTROKE THROMBOLYTICS and REVASCULARISATION - - tPA (alteplase)-0.9mg/kg(max 90mg) 10%of dose – initial IV bolus remainder infused over one hour - to be used < 3 hrs of onset of symptoms (for maximum efficacy) - haemorrhage to be ruledout NEUROPROTECTIVE AGENTS
- 33. ANTIPLATELETTHERAPY Asprin, Clopidogrel - act by inhibiting platelet aggregation andadhesion. - aspirin 300mg single dose to be given immediately following diagnosis. - if alteplase given it can be with held for 24 hrs. - later aspirin at a dose of 75 mg in combination with clopidogrel 75 mg daily for about one yearduration.
- 34. ANTICOAGULANTS HEPARINS , WARFARIN -heparins act by accelerating the inhibition of factor II and factor Xof coagulation cascade -warfarin antagonises vitamin Kto prevent activation of clotting factors -decrease risk of recurrence andvenous thromboembolism -intra cranial haemorrhage to be excluded before therapy -more useful if stroke is evolving
- 35. ANTICOAGULANTS-Cont’d HYPEROSMOLAR AGENTS - reduce cerebral oedema - 20% mannitol IV – 100ml TID - oral glycerol if swallow is normal Concurrent medical problems such as atrial fibrillations to be tackled OTHERS: - PENTOXYPHYLLINE (hemorrheology modifier) to be used within 12hrs -NEUROPROTECTIVE AGENTS
- 36. HAEMORRHAGICSTROKE Control of hypertension Control coagulation abnormalities (esp due to oral anticoagulants) Surgical decompression Surgery for aneurysms and arterio-venousmalformations Anti platelet and anti coagulants are contraindicated
- 37. REHABILITATION PHYSIOTHERAPY - as early as possible - initially passive moments - later active movements - in every case early mobilization - prevents contractures, spasticity and atrophy OCCUPATIONAL THERAPY
- 38. REHABILITATION - Cont’d SPEECH THERAPY IMPROVE QUALITY OF LIFE WITH MOTOR AIDS -leg brace, toe spring , cane, walking stick
- 39. SECONDARYPREVENTION Blood pressure control Diabetes Management Lipid Management Smoking Cessation Alcohol Moderation Weight Reduction/Physic al Activity Anti platelet agents / Anti coagulants Statins Diuretics +/- ACE inhibitors
Editor's Notes
- Atherosclerosis is the most common pathology leading to thrombotic occlusion of blood vessels Hypercoagulable disorders – uncommon cause Antiphospholipid syndrome Sickle cell anemia Polycythemia vera Homocysteinemia Vasculitis: PAN, Wegener’s granulomatosis, giant cell arteritis