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stroke.pptx brain disorders ceredibro vascular
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- 3. Cerebrovascular accident or Brainattack is sudden loss of function resulting from disruption of blood supply to a part of the brain.
- 4. ETIOLOGY MODIFIABLE RISK FACTORS- •Hypertension • Smoking & alcoholism • Diabetes mellitus • Cardiovascular disease • Asymptomatic carotid stenosis • Transient ischemic attacks • Sickle cell anemia • Dyslipidemia • Obesity • Poor diet ( increased fat & sodium, decreased Potassium) • Physical inactivity • Postmenopausal hormone therapy NON- MODIFIABLE RISK FACTORS • Older age • Gender (males) • Heredity • Prior stroke or heart attack
- 5. S. NO COMPARISION ISCHEMIC STROKEHEMORRHAGIC STROKE 1. CAUSE •Large artery thrombosis • small penetrating artery thrombosis • Cardiogenic embolic • cryptogenic •others •Intracerebral hemorrhage •Subarachnoid hemorrhage •Cerebral aneurysm •Arteriovenous malformation 2. SYMPTOMS Numbness or weakness on one side of face especially arm & legs. Exploding headache. Decreased LOC 3. FUNCTIONAL RECOVERY Plateau at 6 months Plateau at 18 months
- 6. 1.Large artery thromboticstrokes- caused by atherosclerotic plaques in large arteries of brain , resulting in thrombus formation & occlusion. 2.Small penetrating artery thrombotic strokes- also called Lacunar stroke, most common.
- 7. 1.Embolic strokes- causedby valvular heart disease & thrombi in left ventricle, can be prevented by use of anticoagulants. 2.Cryptogenic strokes- no known cause. 3.Others- illicit drug use, coagulopathy, migraine &
- 9. •Due to obstructionof a blood vessel •Disruption in cerebral blood flow •Cellular metabolic events •Failure of neurons to maintain aerobic respiration •Mitochondria switch to anaerobic respiration •Production of lactic acid in large amounts •Change in ph (ACIDOSIS) •Inability of neuron to produce adequate energy •Insufficient fuel for depolarisation •Cessation of membrane pumps •Accumulation of calcium & release of glutamate •Activation of damaging pathways.
- 11. •Numbness or weaknessof face, arm or leg, especially on one side of body. •Confusion •Change in mental status •Trouble speaking or understanding speech •Visual disturbances •Difficulty in walking, dizziness or loss of balance •Sudden severe headache
- 12. •Hemiplegia, hemiparesis, flaccid paralysis •Dysarthria,dysphasia, aphasia (expressive, •receptive or global) •Apraxia •Hemianopsia •Disturbed visual spatial relationships •agnosia
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- 14. •Careful history •Complete physical& neurologic examination •NCCT (non contrast computed tomography)- whether ischemic or hemorrhagic •ECG •Carotid ultrasound •CT angiography •MRI or MRA •Transcranial Doppler flow studies •Echocardiography •SPECT
- 15. •Platelet inhibiting medications- aspirin,clopidogrel •Statins- 3- hydroxy 2-methyl glutaryl- coenzyme A , e.g. simvastatin • Anti- hypertensive drugs- ACE inhibitors, thiazides • Thrombolytic therapy- t-PA – Tissue plasminogen activator •Anticoagulant therapy- INR above 1.7
- 16. •DOSAGE- 0.9mg/kg with max.dose 90mg. •10% of the dose is administered IV bolus over 1 minute. •Remaining 90%is administered over 1 hour. •Obtain vital signs every 15 min for first 2 hours.
- 17. Anticoagulant administration- heparin Osmotic diuretics- mannitol Elevationof the head Endotracheal intubation Neurologic assessment Hemodynamic monitoring
- 18. •Endarterectomy- removal of atheroscleroticplaque from carotid artery. •Carotid stenting •with angioplasty. •Carotid stenting •without angioplasty.
- 19. Acute pain R/tHemiplegia & disuse Impaired physical motility R/t loss of balance & coordination Self care deficit R/t stroke sequalae Disturbed sensory perception R/t altered sensory reception Impaired urinary elimination R/t flaccid bladder Disturbed thought process R/t brain damage
- 20. PREVENTIVE MEASURES- •Leading ahealthy lifestyle. •Quitting smoking. •Maintaining a healthy weight. •Daily exercise •Following a healthy diet. •DASH (dietary approaches to stop hypertension)- high in fruits & vegetables, low fat dairy products, low in animal proteins.