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Cerebral Vascular Accident PowerPoint Presentation

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Description : Stroke and its clinical manifestation. Types of stroke. Symptoms and management of stroke.

Tags : Cerebral Vascular Accident, CVA, Stroke, brain tissue, neurological function, Ischemic Stroke, Hemorrhagic Stroke

Published on : Apr 02, 2021 | Views : 4087 | Downloads : 51

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STROKE BY DR. SIBGHA BARI
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What is a Stroke? Brain tissue is damaged from a sudden loss of blood flow, resulting in a loss of neurological function Causes: Blockage (blood clot) occurring inside a blood vessel Blood vessel leaks blood due to rupture
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Types of Strokes Ischemic Stroke (85%) Hemorrhagic Stroke (15%)
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Ischemic Stroke Types of Ischemic Stroke: Embolic Stroke Blood clot travels to the brain Thrombotic Stroke Blood flow is blocked to the brain
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Hemorrhagic Stroke Bleeding occurs from vessels within the brain. High blood pressure or a rupture of a blood vessel or an aneurysm may be the cause.
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RISK FACTORS FOR STROKE Non modifiable Age- incidence ↑ with age until age 75. Race- higher in African Americans Gender- higher in men Heredity- family history increases risk Potentially Modifiable Lifestyle- excessive alcohol, cigarette smoking, obesity, high fat diet, drug abuse. Pathologic conditions- cardiac disease, DM, HTN, headaches, hypercoagulability states.
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ETIOLOGY AND PATHO: Extracranial factors- related to the circulatory system. Systemic blood pressure- <70 and >160 cardiac output- when reduced by 30% cerebral blood flow is reduced. Blood viscosity- anemia increases cerebral blood flow and polycythemia reduces it.
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Intracranial factors: Blood vessels The condition of the blood vessels supplying the brain is important!!! Potential problems- congenital anomalies (, kinking, and AV malformations). The malformations interfere with cerebral blood flow and contribute to atherosclerotic disease
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Intracranial factors, cont’d Intracranial pressure. Causes of ICP include: stroke, neoplasms, inflammation, trauma, and hydrocephalus. ICP compresses the brain and reduces cerebral blood flow, which may lead to infarct. Both extra cranial and intracranial factors may lead to stroke
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Atherosclerosis An abnormal accumulation and infiltration in the intima of the arteries. Plaques develop in an area of high turbulence; which may later damage the plaque. Platelets and fibrin aggregate or collect on the surface of the plaque. Parts of the plaque breaks off and travel to a narrower distal artery Cerebral infarct occurs.
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TYPES OF STROKE Ischemic: Most common type of stroke! Occurs due to decreased blood flow to an area of the brain due to partial or complete occlusion of an artery due to thrombosis. This lack of blood, oxygen and nutrients to an area of the brain causes necrosis of cerebral tissue. Two types: thrombotic and embolic
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Thrombotic stroke Most common cause of cerebral infarct! Cause: Due to formation of a blood clot or coagulation of blood that results in narrowing of blood vessel or occlusion. 2/3 of strokes due to HTN or DM. (accelerate the atherosclerotic process) May also be due to oral contraceptives, coagulation disorders, polycythemia, arteritis, chronic hypoxia and dehydration.
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Thrombotic Stroke Thrombotic strokes are usually proceded by prodromal episodes (warnings) called TIA’s (transient ischemic attacks). TIA’s last from 5 to 30 minutes. Include- paresis or decreased strength and motion of an extremity. Aphasia or disturbance of language function, Paralysis, mental confusion, or visual disturbances.
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EMBOLIC STROKE Cerebral embolism results from occlusion of cerebral artery by an embolus. Necrosis and cerebral edema results. Embolus is the second most common cause of stroke. Most emboli originate in the endocardium with plaques or tissue breaking off and entering circulation.
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Embolic Stroke Emboli are associated with heart conditions such as; A fib MI Infective endocarditis Rheumatic heart disease Valvular prostheses Most commonly related to head trauma High rate of recurrence if cause is not treated.
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Hemorrhagic stroke Intracerebral hemorrhage is bleeding within the brain caused by rupture of a blood vessel that lasts from minutes to days. Most commonly caused by HTN May be caused by brain tumors, trauma, thrombolytic drugs, and ruptured aneurysms.
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Hemorrhagic stroke Blood within the closed area of the brain imposes pressure on the brain tissue and displaces brain tissue and decreases blood flow to brain. Clinical manifestations depends on the site and amount of hemorrhage and resultant damage. Poor prognosis; 70% die
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Pathophysiology Hemorrhagic Stroke Changes in vasculature Tear or rupture Hemorrhage Decreased perfusion Clotting Edema Increased intracranial pressure
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Vessels of the Brain Right Side
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Subarachnoid stroke Caused by aneurysms, AV malformations, trauma, and HTN. May have prodromal symptoms if ballooning or dilation applies pressure to brain tissue. May suddenly rupture, causing neuro changes Majority of aneurysms are in the Circle of Willis
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Subarachnoid hemorrhage, cont’d If aneurysm leaks, patient may have a headache! Rupture of aneurysm causes pressure in subarachnoid space due to bleeding. Clinical manifestations: Headache, lethargy, confusion, nausea, vomiting, fever, neck pain, and backaches, paralysis, coma and death. Massive hemorrhage is defines as 30 to 50 ml of blood. Watch for re-bleeding when clot starts to dissolve. (usually within first 2 weeks post rupture). Reduce activity and prevent straining.
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Aneurysm Localized dilation of arterial lumen Degenerative vascular disease Bifurcations of circle of Willis 85% anterior 15% posterior
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Arteriovenous Malformations AVM Tangled mass of arteries and veins Seizure or ICH
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Stroke Symptoms include: SUDDEN numbness or weakness of face, arm or leg SUDDEN confusion, trouble speaking or understanding. SUDDEN trouble with vision. SUDDEN trouble walking, dizziness, loss of balance or coordination.
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Manifestations by Vessel Vertebral Artery Pain in face, nose, or eye Numbness and weakness of face (involved side) Gait disturbances Dysphagia Dysarthria (motor speech)
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Manifestations by Vessel Internal carotid artery Contralateral paralysis (arm, leg, face) Contralateral sensory deficits Aphasia, impairment of language (dominant hemisphere involvement) Apraxia inability to perform learned (familiar) movements (motor task), Agnosia the loss of the ability to recognize objects, faces, voices, or places (obj. recognition), Unilateral neglect (non-dominant hemisphere involvement) Homonymous hemianopia is a condition in which a person sees only one side―right or left―of the visual world of each eye
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Transient Ischemic Attack Warning sign for stroke Brief localized ischemia Common manifestations: Contralateral numbness/ weakness of hand, forearm, corner of mouth Aphasia Visual disturbances- blurring Deficits last less than 24 hours (usually less than 1 or 2 hrs.) Can occur due to: Inflammatory artery disorders Sickle cell anemia Atherosclerotic changes
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TYPES OF STROKE COMPLETE STROKE: when strokes evolves rapidly over a few minutes and reaches to maximum disability within an hour or two and the symptoms lasting longer than 24 hours is called complete stroke. The clinical features depend on the site and extent of disease. Hemiplegia Dysphasia Headache is common, vomiting and epileptic fits may also accompany. Disturbed consciousness with papilledema occur.
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TYPES OF STROKE Stroke affecting brain stem are more likely to cause loss of consciousness. The cardinal features of brain stem infarction are,sudden vertigo,vomiting,loss of consciousness, oculomotor palsy, weakness on the side of the lesion and loss of pain and temperature sensation on the opposite side.
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Stroke –In- Evolution A progressive stroke which develops over hours or days. Characteristic of an enlarging intra-arterial thrombus. A stepwise or intermittent progression of deterioration of neurological symptoms. Manifestations do not resolve and leave residual damage.
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Completed Stroke Neuro defects unchanged over 2 to 3 days. Usually embolic in nature Also called “stable stroke”.
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Clinical Manifestations All deficits are directly related to area of brain that is involved.
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Neuromotor Function Destruction of motor neurons in the pyramidal pathway causes following impairments: Mobility Respiratory function Swallowing and speech Gag reflex Self-care abilities
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Motor deficits Loss of skilled voluntary movement (akinesia). Impairment of integration of movements Alterations in muscle tones Alteration in reflexes Initial hypo-reflexia which progresses to hyper-reflexia for most patients.
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Patterns of deficits Contralateral deficits A lesion on one side of the brain affects the motor function on the other side of the brain. The arms and legs on the affected side may be weak or paralyzed to different degrees depending the degree of cerebral circulation compromised.
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The affected shoulder tends to rotate internally; the hip rotates externally. The affected foot is plantar flexed and inverted. An initial period of flaccidity may lasts for several days to weeks. Spasticity of muscles follows the flaccid stage and is related to interruption of upper neuron influence.
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Communication Aphasia- total loss of comprehension and use of language due to damage to the dominant hemisphere (left hemisphere). Dysphasia-dysfunction related to comprehension or use of language due to partial disruption or loss.
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Communication Conductive aphasia- mixture of both expressive and receptive aphasia Global aphasia- results from a massive lesion and there is virtual loss of all language ability.
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Communication, cont’d Wernicke’s area damage Receptive aphasia where neither the sound or speech or its meaning can be understood. Impaired comprehension of both spoken and written language. Boca’s area damage Expressive aphasia (difficulty speaking and writing) Dysarthria- disturbance in muscular control of speech. (pronunciation, articulation, phonation) DOES NOT AFFECT COMPREHENSION OF LANGUAGE.
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Affects: May be unable to control emotions May be depressed RT body image and loss of function May be frustrated RT immobility and communication issues
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Diagnostic Studies CT Scan- indicate size and location of lesion, differentiates between infarct and hemorrhage, effectiveness of treatment, and evaluate the course of healing. MRI- considered best method to differentiate between hemorrhage and infarct. LP may be done to detect blood or WBC’s (not done if increased ICP is suspected)
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Collaborative care PREVENTION Healthy diet Weight control Regular exercise No SMOKING Limiting alcohol Routine health assessment
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DRUG THERAPY Prophylactic low dose aspirin, daily. Persantine decreases platelet aggregation which helps to decrease risk of thrombus and embolus formation.
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Surgical Therapy Carotid endarterectomy (CEA)- the atheromatous lesion is removed from the carotid artery to improve blood flow Decreases stroke and death in patient with TIA’s. Done on patient with 70-99% occlusion
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Transluminal Angioplasty Insertion of balloon to open stenosed artery to permit blood flow. Patient with symptomatic stenosis of vertebrobasilar or carotid arteries Risk of dislodging emboli
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ACUTE CARE Abc Airway Breathing Circulation Hydration Nutrition Blood pressure Blood glucose Urinary infection Constipation Depression & anxiety Maintain patient warmth Reassure patient and family
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Treatment IV solutions with glucose and water are avoided. (hypertonic solutions may increase cerebral edema) Increased ICP from cerebral edema peaks in 72 hours and may cause brain herniation.
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How to manage ICP Enhance venous drainage by: Elevating HOB Maintain head and neck in alignment Avoidance of hip flexion Limit cerebral tissue metabolism and vasodilation by: avoiding hyperthermia, avoiding hypervolemia, manage constipation
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Medications Diuretics (decrease cerebral edema) Mannitol (Osmitrol) Lasix, (Furosemide) Dexamethasone for patients with vasogenic edema
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Drug Therapy Thrombolytic therapy Recombinant tissue plasminogen activator (t-PA)- to re-establish blood flow and prevent cell death for patients with ischemic strokes. Patients who receive t-PA within 3 hours after a stroke more likely to have 32% less injury three months after stroke. T-PA works by lysis thrombus/clot by binding and digesting the fibrin and fibrinogen.
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Drug therapy Calcium channel blockers are given for patients with hemorrhagic strokes. Excess intracellular calcium may be harmful to brain tissue. Nimodipine (Nimotop) decreases effects of vasospasm and minimizes tissue damage. Aspirin decreases platelet aggregation at site of plaque.
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Complications of stroke Chest infection Epileptic seizures Pain ful shoulder Deep venous thrombosis/embolism Pressure sores Urinary infections Constipation Depression and anxiety