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Cerebral Vascular Accident (CVA)/ Stroke
- 1. NEUROLOGICAL DISORDERS UNIT -XII CerebralVascular Accident (CVA) (stroke) COMPILED BY - Mr. Ashish Henjali Roy B.Sc Nursing(Nursing Tutor) Savitri Hospital And Paramedical Institute,Gorakhpur,UttarPradesh.
- 2. DEFINITION Cerebral vascular accident(CVA) is the disruption of the blood supply to the brain, due to ischemia and hemorrhage within the brain tissue is termed as cerebral vascular accident which is resulting in neurological dysfunction. It is also known as transient ischemic attack or stroke or brain attack.
- 3. Risk/Etiological Factors • Nonmodifiable: Age : 40 years Above Gender : More common in men Race : Africans and Americans have more chances Genetic : Family History Incidence rate : 119-145 /100,000 population in india • Modifiable: Previous History of attack ,Hypertension,Hyperlipdemia,Heart disease, smoking, excessive alcohol,use of excessive of birth control pills, obesity , sleep apnea, metabolic syndrome, lack of exercise, poor diet,drug abuse and diabetes mellitus.
- 4. Types There are twomajor types of CVA- 1) ISCHEMIC- causes 80% • Thrombotic--blood clot within a blood vessel in the brain or neck. • Cerebral embolism. (2) HEMMORRHAGIC - causes 20% • Intra-Cerebral hemorrhage - rupture of a cerebral blood vessel with bleeding/pressure into brain tissue. • Sub-archnoid Hemorrhage -Stenosis of an artery supplying to the brain • Intracranial bleeding occurs mainly in the case of aneurysm
- 5. Clinical Manifestations • Clinicalmanifestations vary depending on the vessel affected and the cerebral territories it perfuses. i. Early signs hemiparesis, loss of speech, nausea and vomiting, headache,vertigo,syncope(sudden temporary loss of consciousness). ii. Motor loss-hemiplegia (paralysis on one side of the side) or hemiparesis (motor weakness on one side of the body). iii. Communication loss : Dysarthria (a) Receptive aphasia (inability to understand the spoken word). (b) Expressive aphasia (inability to speak). iv. Dysphasia: difficulty in use of langauge
- 6. iv. Vision loss:homonymous hemianopia (loss in the same half visual field of each eye), horner’s syndrome (sinking of eyeball, ptosis) v. Sensory loss: decreased pain,touch, pressure and temperature sensations. vi. Bladder impairment: incontinence,retention vii. Impairment of mental activity. Unilateral neglect (attened to one side of the body. viii. Report to stimuli on one side of the body, use on extermity, orient the head and eye to one side. • (a) Level of consciousness may vary from lethargy, to mental confusion, to deep coma. • (b) Blood pressure may be severely elevated due to increased intracranial pressure.
- 7. PATHOPHYSIOLOGY i. Due tothe thrombosis, Cerebral embolism, Stenosis ,cerebral hemorrhage ii. In early stage due to disruption in blood flow but the cellular metabolism occurs iii. But due to further loss of blood supply the anaerobic metabolism in absence of oxygen and glucose occur and increase in latic acid and decrease in ATP iv. Due to cerebral ischemia brain hypoxia occur survival rate of cell tissue will be decrease and lactic acid cause irritation to brain cell. v. Temporary neurologic deficits or TIA (Trancient Ischemic Attack) vi. If it is not restore, permanent neurological deficits occur within the 4 minutes or brain cell death occur.
- 8. Diagnostic Evaluation • HistoryCollection • Physical Examination- Neurological Examintions • Carotid ultrasound: to detect carotid stenosis. • CT scan: to determine cause and location of stroke. • MRA (Magnetic Resonance Angiography of brain or CT angiography: noninvasive evaluation of cerebrovascular structures. • Cerebral angiography: to determine extent of cerebrovascular insufficiency and to evaluate for structural abnormalities. • PET, MRI with diffusion-weighted images to localize ischemic damage. • TCD(Trans Cranial Doppler Ultrasound) - noninvasive method used to evaluate cerebral perfusion. Useful in the bedside evaluation and to provide a means for ongoing monitoring of cerebral blood flow to document changes and trends. • Licox system Examination- to check the brain oxygenation.
- 9. Management Acute Treatment - •Support of vital functions: maintain airway, breathing, oxygenation, circulation. • Reperfusion and hemodilution with colloids and volume expanders (albumin). • Thrombolytic therapy : (tPA therapy)recombinant tissue plasminogen (tPA) given I.V. 0.9 mg/kg within 3 hours of onset of symptoms; transarterially within 6 hours of onset of symptoms • Abciximab (Repro): antiplatelet agent delivered intra-arterially • Antiplatelet agents such as ticlopidine (Ticlid), clopidogrel (Plavix), or aspirin. • Verapamil: vasodilator injected into intracranial vessel to treat acute spasm • Clot retrieval • Removal of hematoma
- 10. Management of systemichypertension with nitroprusside (Nipride) or alternative I.V. antihypertensive agents • Vasopressor agents to maintain SBP within prescribed range • Diuretic treatment to reduce cerebral edema, which peaks 3 to 5 days after infarction may be used, although this is controversial. • Calcium channel blockers, nimodipine (Nimotop), to reduce BP, promote vasodilatation, and prevent cerebral vasospasm. • Anti-epileptic - eg. Phenytoin Antispasmodic agents for spastic paralysis. A rehabilitation program, including physical therapy, occupational therapy,speech therapy (as soon as stable), and counseling as needed. Treatment of poststroke depression with antidepressants such as selective serotonin reuptake inhibitors (SSRI).
- 11. EXCLUSION • Head CTdemonstrates early signs of infarction or hemorrhage • Uncontrolled hypertensive nonresponsive to I.V. or oral agent (systolic > 185 or diastolic > 110 mm Hg) • Glucose level > 400 mg/dL • Coagulopathy • Heparin within past 48 hours – Patient on warfarin – Elevated PTT or PT – Platelet count < 100,000 • History of previous intracranial hemorrhage, head trauma, or stroke within last 3 months • Gastrointestinal or genitourinary tract hemorrhage in the past 3 weeks • History of major surgery in the past 2 weeks
- 12. Surgical Management ofCVA • Transluminal Anigoplasty • Balloon angioplasty to treat acute spasm • Stenting • MERCI (Mechanical Embolus Removal In Cerebral Ischemia) • Metal Clipping • AVMS (Arteriovenous Malformation Surgery)
- 13. Complications • Aspiration pneumonia •Dysphagia in 25% to 50% of patients after stroke • Spasticity(Flaccid movements), contractures(no clean movement) • Deep vein thrombosis, pulmonary embolism • Brain stem herniation • Post-stroke depression
- 14. Nursing Diagnosis • Riskfor Injury related to neurologic deficits • Preventing Falls and Other Injuries • Maintain bed rest during acute phase (24 to 48 hours after onset of stroke) with head of bed slightly elevated and side rails in place. • Administer oxygen as ordered during acute phase to maximize cerebral oxygenation. • Frequently assess respiratory status, vital signs, heart rate and rhythm, and urine output to maintain and support vital functions. • When patient becomes more alert after acute phase, maintain frequent vigilance and interactions aimed at orienting, assessing, and meeting the needs of the patient. • Try to allay confusion and agitation with calm reassurance and presence. • Assess patient for risk for fall status. • Impaired Physical Mobility related to motor deficits • Preventing Complications of Immobility
- 15. NURSING MANAGEMENT • Ischemicstroke with measurable deficits using the NIH stroke scale (lowest is 15 and 42 is the highest score,scoring in NIHSS is in this form 0 = no stroke, 1- 4= minor stroke, 5-15=mild stroke ,15-20= moderate, 21- 42=severe stroke • Interventions to improve functional recovery require active participation of the patient and repetitive training. Functional demand and intensive training are believed to trigger CNS reorganization responsible for late functional recovery after stroke. • Apply splints and braces as indicated to support flaccid extremities or on spastic extremities to decrease stretch stimulation and reduce spasticity. – Volar splint to support functional position of wrist – Sling to prevent shoulder of flaccid arm – High-top sneaker for ankle and foot support • Exercise the affected extremities passively through ROM four to five times • Daily to maintain joint mobility and enhance circulation; encourage active ROM exercise as able. • Teach patient to use unaffected extremity to move affected one.
- 16. • Maintain functionalposition of all extremities. – Apply a trochanter roll from the crest of the ilium to the midthigh to prevent external rotation of the hip. – Place a pillow in the axilla of the affected side when there is limited external rotation to keep arm away from chest and prevent adduction of the affected shoulder. – Place the affected upper extremity slightly flexed on pillow supports with each joint positioned higher than the preceding one to prevent edema and resultant fibrosis; alternate elbow extension. – Place the hand in slight supination with fingers slightly flexion. – Avoid excessive pressure on ball of foot after spasticity develops. – Do not allow top bedding to pull affected foot into plantar flexion; may use tennis shoes in bed. – Place the patient in a prone position for 15 to 30 minutes daily, and avoid sitting up in chair for long periods to prevent knee and hip flexion contractures. – Encourage neutral positioning of affected limbs to promote relaxation and to limit abnormal increases in muscular tone to enhance functional recovery (reflex-inhibiting positioning).
- 17. • Assist withambulation as needed with help of physical therapy as indicated. – Check for orthostatic hypotension when dangling and standing. – Graduate the patient from a reclining position to head elevated, and dangle legs at the bedside before transferring out of bed or ambulating; assess sitting balance in bed. – Assess the patient for excessive exertion. – Have patient wear walking shoes or tennis shoes. – Assess standing balance, and have patient practice standing. – Help patient begin ambulating as soon as standing balance is achieved; ensure safety with a patient waist belt. – Provide rest periods as patient will tired easily in this condition. • Encourage patient to drink small sips from a straw with chin tucked to the chest, strengthening effort to swallow while chin is tucked down. • Inspect mouth for food collection and pocketing before entry of each new bolus of food.
- 18. • Inspect oralmucosa for injury from biting tongue or cheek. • Encourage frequent oral hygiene. • Teach the family how to assist the patient with meals to facilitate chewing and swallowing. – Reduce environmental distractions to improve patient concentration. – Provide oral care before eating to improve aesthetics and afterward to remove food debris. – Position the patient so he is sitting with 90 degrees of flexion at the hips and 45 degrees of flexion at the neck. Use pillows to achieve correct position. – Maintain position for 30 to 45 minutes after meals to prevent regurgitation and aspiration. • Impaired Urinary Elimination related to motor/sensory deficits • Attaining Bladder Control • Insert indwelling bladder catheterization during acute stage for accurate fluid management; remove as soon as status stabilizes.
- 19. • Establish regularvoiding schedule every 2 to 3 hours, correlated with fluid intake when bladder tone returns. If patient is unable to void, intermittent catheterization can be used to empty bladder and prevent overstretching of bladder. The bladder scan device is useful in monitoring bladder capacity and identifying individuals at risk. • Assist with standing or sitting to void (especially males). • Disabled Family Coping related to catastrophic illness, cognitive and behavioral stroke, and caregiving burden. • Strengthening Family Coping • Encourage the family to maintain outside interests.
- 20. • Teach stressmanagement techniques, such as relaxation exercises, use of community and faith-based support networks. • Encourage participation in support group for family respite program for caregivers, or other available resources in area. • Involve as many family and friends in care as possible. • Provide information about stroke and expected outcome. • Teach family that stroke survivors do show depression in the first 3 months of recovery.
- 21. ;) THANKYOU SOMUCH FOR YOUR CAREFULL LISTENING AND KIND ATTENTION !!! ;)