Stroke Diagnosis, Evaluation, And Treatment of

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    2 broad categories of stroke:

    Ischemia

    Inadequate blood supply (oxygen & nutrients) to an areaof the brain

    Hemorrhage-

    Leakage of blood into the closed cranial cavity

    Direct damage to tissue by compression/edema

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    Incidence

    ~700K per year (~200K are recurrent)

    80-90% are ischemic Male:Female ratio 1.25:1

    Ratio reverses after age 80

    Higher rates in Blacks, Hispanics, & NativeAmericans

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    Heart disease

    AFib, Valvular Dz, MI, endocarditis

    Hypertension

    Smoking Diabetes/Metabolic Syndrome Dyslipidemia Pregnancy Drug Abuse/Meds Bleeding Disorders/Anticoagulant Use

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    Thrombosis In situ arterial obstruction

    Arteriosclerosis, dissection, FMD

    Superimposed thrombosis

    Embolism Arterial obstruction from debris from another

    source Systemic Hypoperfusion

    Circulatory collapse

    Multiorgan involvement

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    Large Vessel Disease

    Common & InternalCarotids

    Circle of Willis & proximalbranches

    Small Vessel Disease

    Penetrating arteries

    Lacunar Stroke

    Stuttering course

    http://en.wikipedia.org/wiki/Image:Gray513.png
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    Cardiac Atrial fibrillation

    Heart valves, atrial thrombus, recent MI, dilatedCM, endocarditis, recent CABG Aortic Arterial (e.g. carotids)

    Other/Unknown DVT- Paradoxical embolus

    Abrupt onset, rapid improvement

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    Shock

    Cardiogenic, septic, hypovolemic

    Sx are more diffuse/nonfocal Border-zone regions

    Cortical blindness

    Stupor Proximal Weakness

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    IntracerebralHemorrhage (ICH) Bleeding within the brain

    tissue Forms a hematoma

    Growth stopped bytamponade or leaking intothe ventricles or CSF

    Headache, vomiting,delirium

    Progressive sx

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    HTN Trauma Bleeding Disorder

    Inherited Acquired, i.e. meds

    Amyloid

    Drug use

    Cocaine

    Amphetamines

    AVMs Bleeding into tumor Vasculitis

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    SubarachnoidHemorrhage (SAH)

    Bleeding into CSF on outer

    aspect of brain Quick rise in ICP

    Sudden onset headache in97%

    Aneurysm & AVMs aremost common cause

    http://www.strokecenter.org/pat/viewer/sah/sah_coronal_berry_2_500.jpg
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    Seizure with ToddsParalysis

    Syncope

    Migraine Head Trauma Brain tumor

    Metabolic Causes

    Hypoglycemia

    Hyponatremia

    Intoxication Uremia/ARF

    Hepatic Encephalopathy

    Conversion Disorder

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    Vital signs

    Temperature, Pulse, Blood Pressure

    Pulses Carotid Bruit Cardiac Exam Funduscopic exam Skin exam Signs of trauma

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    Neurologic Exam

    Level of consciousness/GCS

    Language/Speech Cranial nerves

    Vertigo, diplopia, ataxia

    Visual deficits Weakness/Paralysis

    Reflexes/ Babinski

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    Patients are awarded points based on eye opening, best verbal response,and best motor response. The patient's GCS score can range from 3/15 to15/15

    Eye opening score: 4, eyes open; 3, eyes open to speech; 2, eyes open inresponse to pain; 1, no eye opening

    Best verbal response score: 5, alert and oriented; 4, confused; 3,responds with inappropriate words; 2, makes incomprehensible sounds;1, no verbal response

    Best motor response score: 6, obeys commands; 5, localizes pain; 4,responds to pain with normal flexion/withdrawal; 3, responds to pain

    with abnormal flexion; 2, extends in response to pain; 1, no response topain

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    CBC with platelets Electrolytes, Bun, Cr Glucose

    LFTs PT/PTT O2 Sat ECG Chest XRay

    ESR Blood Cultures ANA

    Tox screen Alcohol level Blood type & cross Urine/Serum HCG Hypercoaguability Profile

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    CT Scan

    R/O Bleed

    Sensitivity much better after 24 hrs forischemic stroke

    Early signs (

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    MRI

    T1/T2 images, DWI

    Provides immediate

    evaluation of ischemia Not available for

    emergency use in manysettings

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    Carotid U/S for stenosis If ASVD, but no stenosis

    Risk Factor Modification If stenosis, consider

    Carotid Endarterectomy

    ?Carotid Stenting Vertigo & Syncope are not considered

    symptomatic

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    100% occlusion

    No treatment

    70-99% occlusion

    If good 5-yr survival & risks

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    Sudden onset of neurologic dysfunction thatlasts less than 24 hrs, brought on bypresumed transient ischemia to a portion ofthe brain

    May be better to describe as sx

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    Transient Sx Associated with Infarction No established diagnostic criteria

    In one case series, 15% of TSI pts had arecurrent stroke in-hospital vs. 0% in TIAgroup.

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    Could consider home if able to expediteurgent outpatient work-up

    AHA does not make a recommendation re:hospitalization One study suggested cost-effective if 24-hr

    stroke risk is >5%

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    NASCET trial suggested 90-day stroke risk of 20% with non-retinal TIAs (higher than for true stroke)

    2000 JAMA study

    5% risk w/in 2 days 11% risk w/in 90 days

    Higher risk with age >60, DM, sx >10 min, weakness, speechimpairment

    2004 Neurology study: 21% risk of stroke/MI/death within 1

    year of TIA

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    Age >60 = 1 pt Blood Pressure >140/90 = 1 Clinical Features

    Unilateral weakness = 2 Isolated speech deficit = 1

    Other = 0

    Duration

    >60 minutes = 2

    10-59 minutes = 1

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    Risk factor modification Antithrombotic therapy

    Anticoagulant therapy

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    Hypertension

    Goal 80 may not benefit as much & aggressive BP

    lowering may increase mortality

    Diuretic +/- ACEI as 1st line

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    Smoking

    Stop it

    Diabetes

    Goal A1c

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    Dyslipidemia

    Evidence not as strong as may think, but still a

    good idea, especially given other vascular disease SPARCL Study

    Atorvastatin 80 mg/day in pts 1-6 months from CVA/TIA

    Mean LDL reduction 56

    Endpoint was stroke: 16% RRR, but only 2.2% ARR (NNT~50)

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    Dyslipidemia, continued

    For average-risk patient, goal LDL

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    Lifestyle Modification

    Weight loss

    Exercise Dietary changes

    Reduce alcohol intake, especially heavydrinkers

    ?Homocysteine

    Consider B12, B6, Folate (MVI doses OK)

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    Aspirin

    20-25% reduction in stroke (& MI or other vascular

    death) Standard doses of 81-325 mg as good as higher

    doses

    81 mg dose just as good and less risk of bleeding

    ASA-non-responders?

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    Clopidogrel (Plavix)

    8% RRR vs. ASA for stroke/MI/Vasc death

    5.3% vs. 5.8%: NNT ~200 All for only $100+/month

    ?2nd-line therapy or ASA-allergic patients

    No increased bleeding vs. ASA, but combo should

    be avoided

    No neutropenia (like ticlopidine)

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    Dipyridamole

    Alone 50-100 mg TID

    Aggrenox (200mg ER-DP & 25mg ASA) BID 2 studies have shown ~3% ARR (NNT 33) over ASA

    alone for stroke prevention

    Some guidelines are suggesting this a 1st line

    therapy over ASA alone for stroke prevention

    Cost >$100/month

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    Warfarin has only been proven effective inprimary prevention of stroke in the setting ofatrial fibrillation

    AF is responsible for 1/6th of all strokes inpatients older than 60

    Risk reduction

    Warfarin about 3 times as effective as ASA Absolute annual risk reduction of ~3%

    Low Risk patients may consider ASA rx

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    Highest Risk: Prior Stroke or TIA High Risk: Any of the following

    Prior thromboembolism Female >75 yo

    SBP >160

    Heart failure

    Moderate Risk: None of above, but HTN Low Risk: None of the above, no HTN

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    Thrombolysis Blood Pressure Management

    Antithrombotic Therapy Management of Medical Complications

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    Time-sensitive

    Studies show that thrombolytics must be given

    within 3 hours of symptom onset

    Effective

    NINDS- Complete or near-complete recovery at 3

    months post-event (38% vs. 21%, NNT=6)

    No difference in mortality

    Harmful

    At least 6% risk of ICH

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    Alteplase (tPA) 0.9 mg/kg dose up to 90 mg

    10% as IV bolus, then 60 min infusion Multiple exclusion criteria Obtain informed consent (if possible)

    "There is a treatment for your stroke called alteplase that must be given within three hours

    after the stroke started. It is a 'clot-buster' drug that can lead to a complete or near-completereversal of a stroke in about one of every three patients treated. However, it has a major risk,since it can cause severe bleeding in the brain in about one of every 15 patients. If bleedingoccurs in the brain, it can be fatal. When used to treat large numbers of stroke patients, onaverage the potential benefits of this treatment outweigh the risks; however, in anyindividual patient it is a very personal decision."

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    Stroke/head trauma

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    Guidelines for In-Hospital Evaluation Physician Evaluation: 10 minutes

    Stroke Team Contact: 15 minutes

    Imaging: 25 minutes

    Interpretation: 45 minutes

    Thrombolysis Started: 60 minutes

    ?Coagulopathy- Dont wait for labs unless onCoumadin, Heparin, or Dialysis

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    Early Treatment

    Less severe symptoms

    Younger Age Lack of systolic HTN Normoglycemia

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    Blood flow in dilated, post-obstructive bloodvessels is BP-dependent

    Aggressive BP lowering canincrease

    mortality In one study, a fall in SBP >20 in first 24 hrs

    was the most likely factor associated with

    neurologic deterioration This does NOT apply to hemorrhagic stroke

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    Do not treat BP unless >220/120, unless Given thrombolytics (goal

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    ASA

    IST- ASA 300 mg within 48 hrs

    Reduced 14 day recurrent stroke (NNT=100)

    Reduced nonfatal stroke & death (NNT=100)

    CAST- ASA 160 mg within 48 hrs

    Reduced mortality at 4 weeks (NNT=166)

    Slight increased risk of hemorrhagic stroke

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    Heparin (LMWH) No clear benefit over ASA alone

    Reduced recurrent ischemic strokes by 9/1000 patients,

    but increased hemorrhagic strokes by same number

    ?Effective in some subsets

    Stroke-in-evolution or Progressive Stroke

    Many patients show neurologic deterioration in 1st

    24hrs

    No studies effectively define this population or prove abenefit

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    Acute Coronary Syndromes/Heart Failure Infections

    Aspiration pneumonia UTI

    Venous thromboembolism Consider DVT prophylaxis for all patients

    SCDs for pts with bleeds Heparin or Lovenox SQ for others

    Malnutrition/Dehydration (consider Adv Directives) Decubitus ulcers Contractures

    CONSIDER EARLY MOBILIZATION IN ALL PATIENTS!

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    Accounts for ~8% of all strokes Presenting sx

    Headache (~50%) Seizures (7-9%)

    Delirium/Altered LOC

    Focal neuro sx (depends on area of brain)

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    Mortality 35-50%

    Half of deaths in 1st 24 hours

    Prognosis Size & location of hemorrhage

    Age

    Glasgow Coma Score

    Comorbid conditions

    Prior antiplatelet/anticoagulant therapy

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    Neurosurgery Constant monitoring

    Bedrest Pain control Reverse coagulopathies

    Vitamin K, Fresh Frozen Plasma, Platelets

    ICP control

    Mannitol, Induced Coma, Hyperventilation

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    Blood pressure management Surgery

    Indicated for cerebellar bleeds >3 cm Supratentorial bleeds more controversial

    Depends on size, location, LOC, comorbidities

    Recombinant activated factor VII

    (rFVIIa) therapy Small studies show promise, but concern for pro-

    thrombotic effects

    http://www.ncbi.nlm.nih.gov/pubmed/16972833http://www.ncbi.nlm.nih.gov/pubmed/16972833http://www.ncbi.nlm.nih.gov/pubmed/16972833http://www.ncbi.nlm.nih.gov/pubmed/16972833http://www.ncbi.nlm.nih.gov/pubmed/16972833http://www.ncbi.nlm.nih.gov/pubmed/16972833http://www.ncbi.nlm.nih.gov/pubmed/16972833
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    High mortality rate, ~50%

    10% pre-hospital

    25% within 24 hrs 45% within 30 days

    Prognostic Factors

    Level of consciousness

    Age

    Amount of blood on CT

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    Diagnosis

    Head CT

    (+) in 92% of cases w/in 24 hrs

    Most sensitive in first 12 hrs

    Lumbar Puncture

    Not necessary for diagnosis but consider if clinical

    suspicion & negative head CT Elevated pressure & RBCs

    Xanthochromia: pink/yellow tint due to RBC breakdown

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    Neurosurgical ICU Constant monitoring Bedrest Pain control Reverse coagulopathies DVT Prophylaxis (SCDs)

    Blood Pressure Management Management of Aneurysms/AVMs