Disclosure Statement: Dr. Knoefel has nothing to disclose

Stroke Janice E. Knoefel, MD, MPH Professor of Medicine & Neurology University of New Mexico Geriatrics/Extended Care (retired) New Mexico VA Healthcare System Albuquerque, NM

Disclosure Statement: Dr. Knoefel has nothing to disclose

Learning Objectives: 1. Discuss prevention of stroke 2. Understand types of stroke 3. Review acute management

Stroke Facts > 700,000 new strokes/year in USA Third leading cause of death (~ 20%) Leading cause of chronic disability in adults (60-70% of survivors) Incidence increases dramatically with age Major public health problem BUT, the good news is the incidence has declined remarkably over the past 50-60 years due to management of risk factors

Prevention Modifiable risk factors Hypertension Cigarette Smoking Cardiac Health Diabetes Mellitus Carotid Artery Narrowing Hyperlipidemia Alcohol use

Prevention: Hypertension Hypertension is the strongest risk factor, it contributes to ALL types of stroke: Cerebral hemorrhage Small vessel lacunar stroke Thromboembolic stroke from carotid disease Cardiac disease leading to embolic stroke from atrial fibrillation, acute and chronic effects of MI and dilated cardiomyopathy

Prevention: Hypertension Of the modifiable risk factors: Hypertension still undertreated, especially in the elderly Best treatment target is home BP Patient/family education outcomes improved with home BP monitoring

Prevention: Smoking Of the modifiable risk factors: Increases stroke risk 3 fold The risk factor with the most immediate treatment benefit: Declines significantly after 2 years of cessation Returns to risk of nonsmoker after 5 years of cessation Stroke risk reduction starts within weeks Many cessation strategies available Cessation counseling at every clinical encounter: I am desperate to get you to stop smoking

Prevention: Heart Disease Heart disease risk factors: Coronary artery disease Left ventricular hypertrophy/clot Valvular heart disease Valvular replacement Atrial fibrilation Valvular Nonvalvular

Prevention: Diabetes Increases stroke risk 2-4 fold Tight control of diabetes might reduce risk Weaker evidence for reduction of other vascular complications Synergistic risk factor in presence of hypertension and hyperlipidemia

Acknowledgement of Unmodifiable Risk Factors Age: risk increases with age Sex: M>F middle age, F>M older age Race: increased in African Americans In most cases, as the risk factors go, so goes the risk for stroke Family History: as yet unknown increased risks in certain families

Question 1 Why is hypertension the most important risk factor which should be addressed for the prevention of stroke? A) Hypertension contributes to all stroke types B) Hypertension causes damage to organs other than the brain C) Medication is effective and generally has few and tolerable side effects D) It is the easiest factor to control with the most immediate benefit Answer: 1. A, B and C 2. A and C 3. B and D 4. D only

Current Recommendations American Stroke Association: Blood Pressure 120/80 or lower If atrial fibrillation is present, treat appropriately If you smoke, stop If you drink alcohol, do so in moderation

Current Recommendations Keep LDL below 200 Follow your doctor's advice carefully to control your diabetes Include exercise in your daily activities Enjoy a lower sodium, lower fat diet

Cerebral Circulation Anterior Circulation: MCA, ACA and branches Frontal and parietal lobes Part of temporal lobes Internal capsule, basal ganglia, thalamus Posterior circulation: Vertebral, Basilar and branches PCA, SCA, AICA, PICA Inferior temporal lobes, occipital lobes Brainstem Cerebellum Circle of Willis serves to control collateral flow Vascular anatomy variable

Transient Ischemic Attack Transient neurologic deficit lasting less than 24 hours, most lasting minutes to hour Most common symptoms are transient monocular blindness, focal motor or sensory deficit, transient aphasia or global amnesia TIA is a medical emergency 3 fold increased risk of stroke 50% of risk in the first 48 hours following TIA Urgent assessment and treatment indicated Presence of known stroke risk factors make the urgency even greater

Internal Carotid Artery Disease Symptoms reflect hemispheric dysfunction Hemiparesis Hemisensory loss Aphasia Apraxia Visual loss, usually hemianopsia May occasionally present with focal seizures

Internal Carotid Artery Disease Assessment should include: Neuroimaging study Noninvasive imaging of carotids Management should include: 70+% symptomatic stenosis -> endarterectomy, angioplasty, stenting, or medical management if extreme medical co-morbidities <70% symptomatic or asymptomatic stenosis needs to be highly individualized; options include endarterectomy, endovascular or medical treatment Medical management indicates control of BP, optimize lipids status and added antiplatelet therapy

Surgical Treatment in Carotid Stenosis Strong indication for > 90% (critical) stenosis Definite indication for >70% stenosis Slight benefit for 50-70% stenosis Clinician must weigh benefits vs definite risks of surgery Need to consider current function of individual, life expectency and experience of local surgeon/surgical center

Anti-platelet Trials For any anti-platelet treatment: Risk reduction 1/3 for non-fatal MI Risk reduction 1/2 non-fatal stroke Risk reduction 1/6 for any vascular death Which is the best anti-platelet treatment? The one that you will take!

Anti-Platelet Agents ASA 81-325mg daily, lower dose = fewer s/e >325mg has no added therapeutic effect Ticlopidine 6% added risk reduction over ASA Clopidogrel 7% added risk reduction over ASA Aspirin-extended release dipyridamole combination 13% added risk reduction Dipyridamole alone same as ASA Warfarin indicated only for prevention of cardioembolic, not thrombotic, events

Current Recommendations Anti-Platelet Agents ASA 81mg in high risk patients for secondary prevention Clopidogrel, dipyridamole or ASA-dipyridamole in aspirin failure or aspirin sensitive high risk patients Ticlopidine not recommended due to side effects and the availability of other effective agents Cost (160-350x) factor favors aspirin

Anticoagulation: Prevention Atrial arrhythmias Valve replacement (mechanical) Valve abnormality (severe) Ventricular clot or dilatation Carotid stenosis or ulcerated plaque pending surgery

Anticoagulation: Prevention The risks of anticoagulation need to be assessed individually, given the risk for primary stroke vs. secondary stroke The potential for falls with injury and adherence to treatment plan are the major considerations If anticoagulation is not feasible, then treatment with ASA or another anti-platelet agent should be considered

Vertebrobasilar Arterial Disease Posterior circulation disruptions result in disturbances of cranial nerves, descending motor or ascending sensory tracks in brainstem Brainstem is packed with many structures in a small space resulting in a myriad of signs, symptoms and syndromes Thalamus and posterior cerebral hemispheres also supplied by posterior circulation

Vertebrobasilar Arterial Disease Posterior circulation vascular lesions result in Disordered eye movements Horner s syndrome Unilateral/bilateral/crossed motor or sensory deficits Arm Leg Face Dysphagia Dysarthria Stupor or coma Visual disturbance Behavioral changes

Vertebrobasilar Arterial Disease Treatment of vertebrobasilar cerebrovascular disease is typically medical ASA 81mg in high risk patient Clopidogrel, dipyridamole or ASA-dipyridamole in aspirin failure or aspirin sensitive high risk patients Warfarin not indicated for treatment of thrombotic events, as it is no better than antiplatelet therapy and carries much higher risk, inconvenience and cost

Lacunar Cerebrovascular Disease Occurs secondary to occlusion of small penetrating vessels coming directly off the large cerebral arteries Results from lipid deposition and hyalinization (lipohyalinosis), so-called small vessel disease, as opposed to atherosclerosis of the large cerebral vessels, large vessel disease Risk factors include hypertension, diabetes, hyperlipidemia and smoking Best treatment is aggressive risk factor management and antiplatelet therapy

Lacunar Cerebrovascular Disease Well-defined clinical syndromes: Pure motor hemiplegia stroke Pure hemisensory stroke Ataxic hemiparesis Dysarthria-clumsy hand syndrome

Acute Stroke Issues Hydration status Blood pressure management Seizure prophylaxis Cardiovascular management Venous thromboembolic Assessment of nutrition Prevention of aspiration Thrombolytics

Acute Stroke: hydration Dehydration at presentation is very common Rehydration is indicated but should be gradual Need to prevent added contribution to cerebral edema caused by infarction Hypotension from dehydration at presentation unusual since hypertension following stroke is the rule rather than the exception

Acute Stroke: BP Blood pressure management in acute stroke is complicated by: Raised intracranial pressure Intracranial hemorrhage Thrombolysis treatment Acute arterial dissection Acute renal failure Acute MI or pulmonary edema

Acute Stroke: BP Hypertension is common in acute stroke presentation(physiologic) Improves spontaneously 1-4 days after onset No initial management of mild-moderate BP elevation needed Treatment needed in extreme BP >220/120 If needed, therapy must be gradual, ~15%/day More damage done by aggressively lowering BP elevations Systolic should not drop below 160 acutely BP drop worsens outcomes in studies at 5 days to 3 months post stroke

Acute Stroke: seizures Seizures occur in 4-8% stroke patients acutely Seizures occur in 10-15% stroke survivors at 1 year Incidence dependent upon location of stroke: cortical lesion>>>subcortical Prophylaxis not warranted for low yield Antiepileptic drugs may impair natural healing: phenytoin and phenobarbital AND may increase incidence of aspiration, falls, confusion, depression

Acute Stroke: cardiovascular Cardiac death accounts for 15% of stroke mortality Screen on admission for acute MI, CHF, arrhythmia, ventricular clot Treat acute problems with complete evaluation, consultation as needed Maintain previous CV therapy regimen Attend to CV risk factors = perfect intervention opportunity Anticoagulation for stroke does not protect heart, may need antiplatelet Rx

Acute Stroke: venous thromboembolism 17-42% prevalence in affected leg Exacerbated by bed rest Incidence of pulmonary emboli in acute stroke: 17-30% rate of PE with no prevention 3-7% of PE on prevention Pulmonary emboli result in increased mortality 13-25% of stroke deaths from PE Thromboprophylaxis needed universally Discontinue with successful ambulation Not recommended long term for plegic leg, may use passive range of motion and compression stockings

Acute Stroke: nutrition Strokes occur in elderly Strokes often occur in sick elderly: multiple meds/diagnoses Strokes occur in functionally impaired Obtain admission nutrition assessment Parameters: height, weight, IBW, albumin Dietitian calculates caloric, protein, fluid needs, HOWEVER

Acute Stroke: aspiration Need to assess for aspiration before attempting oral intake in acute stroke. Aspiration/pneumonia = 30 to 50% mortality in acute stroke Much aspiration is silent = low clinical suspicion Incidence of dysphagia in acute stroke is 30-85% = need for high suspicion Bedside swallowing assessment within 24 hours of admission May still need to go to fiberoptic endoscopic evaluation of swallowing (FEES)

Acute Stroke: aspiration Clinical signs of aspiration: Dysphonia Dysarthria Abnormal gag reflex Abnormal volitional cough Cough after swallowing Voice change following swallow Enteral feeding should be used liberally PEG is often temporary, 2-8 weeks NG tubes should be avoided if possible due to increased risk of aspiration

Secondary complications Level of nutrition predicts skin breakdown and pressure ulcer healing Fall prevention protocols in routine use Dx and Rx of confusion and agitation Dx and Rx of depression Complete review of pre-admission medications Early Dx and Rx of pain syndromes Treatment of constipation & incontinence

Question 2 Mortality in acute stroke is caused by a number of different mechanisms. What is/are the most preventable cause(s) of death in stroke? A) Seizures B) Pulmonary embolism C) Uncontrolled blood pressure D) Aspiration/pneumonia Answer: 1. A, B and C 2. A and C 3. B and D 4. D only

Acute Stroke: Thrombolytics Thrombolytics available at numerous hospitals Only FDA-approved therapy is recombinant tissue-plasminogen activator (rt-pa) Time is of the essence, no more than 3 hours from symptom onset to IV infusion of rtpa Acquaint patients and family with symptoms of stroke by public education programs Instruct staff, patient, family to call 911 EMTs trained to recognize stroke and to alert ER while on route with patient Joint Commission certifying Stroke Centers with stroke teams trained and on call for rt-pa

Acute Stroke: Thrombolytics Contraindications are many: History of or CT presence of intracranial hemorrhage Sustained BP above 185 / 110 History of major surgery within 2 weeks Bladder or GI bleeding Coagulopathy Thrombocytopenia INR> 1/7 Severe stroke Minor or improving stroke symptoms

Acute Stroke: intracerebral hemorrhage (ICH) Accounts for 15-20% of all strokes 80% occurs between ages of 40-70 Higher risk in African and Asian Americans Hypertension present in 75-80% of cases Excessive use of alcohol is a risk factor too Locations for bleeds: putamen thalamus cerebellar hemispheres pons cerebrum, mainly temporal lobe

Acute Stroke: intracerebral hemorrhage (ICH) Common cause of recurrent lobar hemorrhage in older adults is cerebral amyloid angiopathy ICH care complicated by prior use of anticoagulant and anti-platelet therapy Secondary causes of ICH: Trauma Arteriovenous malformation Aneurysm Treatment is supportive: Control of severe hypertension Discontinuation of antithrombotic medications May require neurosurgical intervention

Stroke Treatment Units Development of treatment protocols (order sets) have streamlined process of acute stroke treatment and acute rehabilitation Improved functional outcomes Lowered morbidity and mortality Improved coordination of inpatient care and outpatient referrals Reduced hospital stay and cost Improved patient and family satisfaction

Stroke Treatment Units AHA, Pan-European consensus guidelines: 10 RCTs, 1586 subjects treated for 3 weeks 28% and 21% reduction in mortality at 3 months and 1 year Another RCT: 220 subjects followed for 5 years Lower mortality and institutionalization, improved independence in ADLs and reduced need for assistance in home

Stroke Treatment Units Obstacles to appropriate stroke rehab: Referral bias 17% go to inpatient rehab(8-31%) 23% go to nursing facility(12-42%) 36% use home health rehab (10-62%) 14% use outpatient rehabilitation 27% receive no rehab services(9-55%) Patients more likely be referred to rehab from stroke units Every diagnosis of stroke warrants rehab

Stroke Rehabilitation NO person with CVA should be discharged without arrangements made for rehab Traditional rehabilitation may be carried out in a variety of settings rehab/stroke unit in acute care hospital rehabilitation hospital low intensity rehab in nursing care setting outpatient rehab with home discharge home rehabilitation

More Information www.aan.com/professionals/practi ce/ guideline/index www.strokeassociation.org

ACUTE CVA SYMPTOMS Call 911