i schemic stroke

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ALISON SMOCK, MD DEPARTMENT OF NEUROLOGY MEDICAL UNIVERSITY OF SOUTH CAROLINA ischemic stroke

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i schemic stroke. Alison Smock, MD Department of Neurology Medical University of South Carolina. definitions. Transient ischemic attack A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction - PowerPoint PPT Presentation

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ALISON SMOCK, MDDEPARTMENT OF NEUROLOGY

MEDICAL UNIVERSITY OF SOUTH CAROLINA

ischemic stroke

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definitions

Transient ischemic attack A transient episode of neurological dysfunction caused by

focal brain, spinal cord, or retinal ischemia, without acute infarction

Tissue-based definition rather than time-based definition

Stroke Infarction of the central nervous system May be symptomatic or silent May not be evident by MRI

Stroke. 2009;40:2276-2293

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epidemiology

Transient Ischemic Attack Estimated prevalence of self-reported physician-

diagnosis TIA is approximately 2.3% (translates to ~5 million people)

Incidence of TIA increases with age and varies by sex and race/ethnicity Men, blacks, and Mexican Americans have higher rates

of TIA their their female and non-Hispanic white counterparts

Approximately 15% of all strokes are heralded by a TIA 10-15% of patients have a stroke within 3 months, with

half occurring within 48 hoursCirculation. 2013;127:e6-e245

Stroke. 2009;40:2276-2293

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epidemiology

TIA ABCD2 score

Clinical score to determine the risk for stroke within the first 2 days following a TIA

Age BP Clinical Features Duration Diabetes1 point ≥ 60 SBP ≥ 140

OR

DBP ≥ 90

Speech disturbance

without unilateral weakness

10-59 min Yes

2 points -- -- Unilateral weakness with or without speech

impairment

≥60 min --

Lancet. 2007;369:283-292.

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epidemiology

ABCD2 score 2-day stroke risk Comment

0-3 1.0% Hospital observation may be unnecessary without another indication (ie new onset Afib)

4-5 4.1% Hospital observation justified in most situations

6-7 8.1% Hospital observation worthwhile

Lancet. 207;369:283-292

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epidemiology

Stroke prevalence Estimated 6.8 million Americans ≥20 years of age

have had a stroke (2007-2010 data) Overall stroke prevalence during this period is an

estimated 2.8% Older adults, blacks, people with lower levels of

education, and people living in the southeastern United States had higher stroke prevalence

Circulation. 2013;127:e6-e245

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epidemiology

Stroke incidence Each year, ~795,000 people experience a new or

recurrent stroke (610,000 are first attacks, 185,000 are recurrent)

Of all strokes, 87% are ischemic, 10% are ICH, 3% are SAH

Each year, ~55,000 more women than men have a stroke Women have a higher lifetime risk of stroke than men Women have a lower age-adjusted stroke incidence than

men White women 45-84 yo have lower stroke risk than white

men, but women >85 yo have elevated risk compared to white men

Analysis of data from FHS and GCNKSS suggests that stroke incidence is declining over time Circulation. 2013;127:e6-e245

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epidemiology

Stroke mortality In 2009, stroke accounted for 1 of every 19 deaths in the US When considered separately from other CVDs, stroke ranks

No. 4 among all causes of death From 1999 to 2009, the annual stroke death rate decreased

36.9% and the actual number of stroke deaths declined 22.9%

Circulation. 2013;127:e6-e245

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epidemiology

Circulation. 2013;127:e6-e245

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http://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_319832.pdf

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Circulation. 2013;127:e6-e245

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so why does it matter?

Disability Stroke is the leading cause of serious long-term

disability in the United States In the NHLBI’s FHS, among ischemic stroke survivors

who were ≥65yo, the following disabilities were observed at 6 months after stroke: 50% had some hemiparesis 30% were unable to walk without some assistance 46% had cognitive deficits 35% had depressive symptoms 19% had aphasia 26% were dependent in ADLs 26% were institutionalized in a nursing home

Circulation. 2013;127:e6-e245

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etiology

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etiology of ischemic stroke

TOAST criteria Thrombosis or embolism due to atherosclerosis of a

large artery Embolism of cardiac origin Occlusion of a small blood vessel Other determined causes

Dissection Aneurysm Vasculitis

Undetermined cause (cryptogenic or incomplete investigation)

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traditional other

Hypertension Hyperlipidemia Diabetes mellitus Smoking Coronary artery disease Heart failure Cardiac arrhythmias Chronic kidney disease Physical inactivity Drug use History of prior stroke Family history

Underlying rheumatologic disease

Hypercoagulable states

CNS infectionSepsisSleep apnea

risk factors

Circulation. 2013;127:e6-e245

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etiology and presenting symptoms

Large vessel strokes (ICA, MCA, ACA, PCA) Cardio-embolic Atherosclerosis Artery-artery

embolism Dissections Aneurysms

Small vessel strokes Uncontrolled

hypertension Uncontrolled diabetes Uncontrolled

hyperlipidemia Smoking Sympathomimetics

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http://www.cixip.com/index.php/page/content/id/1007

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Carotids

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Internal Carotids and MCAs

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http://www.studyblue.com/notes/note/n/airway-77-93/deck/3078597

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Circle of Willis

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large vessel stroke syndromes – cortical

MCA – dominant hemisphere Contralateral hemiparesis (face/arm > leg) Contralateral hemisensory changes Head and eye deviation toward stroke Contralateral hemianopia Language difficulty Alexia Agraphia Acalculia Apraxia

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large vessel stroke syndromes – cortical

MCA – non-dominant hemisphere Contralateral hemiparesis (face/arm > leg) Contralateral hemisensory changes Neglect/extinction Anosognosia Loss of prosody of speech Flat affect

ACA Crural paresis > arm paresis Frontal signs (eg, abulia)

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large vessel stroke syndromes – cortical

Posterior Circulation ECVA/ICVA

Dizziness/Vertigo Cranial nerve lesions Cerebellar symptoms

PCA Homonymous hemianopia Hemisensory changes (lateral thalamus) Left PCA – alexia without agraphia, Gerstmann (acalculia,

agraphia, finger agnosia, R/L disorientation) Right PCA – prosopagnosia, visual neglect Bilateral – cortical blindness (Anton’s syndrome)

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http://www.neuropenews.org/?attachment_id=2010

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large vessel stroke syndromes – cortical

Basilar artery Typically presents as ischemia in the pons Asymmetric but bilateral motor and reflex

abnormalities Bulbar involvement Respiratory involvement “Tip of the Basilar”

Decreased LOC Oculomotor/pupillary abnormalities

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small vessel stroke syndromes – subcortical

Pure motor Corona radiata, posterior limb of the internal capsule,

pons, medullaPure sensory

ThalamusSensorimotor

Thalamus, basal gangliaAtaxic hemiparesis

Corona radiata, anterior limb of the internal capsuleDysarthria-clumsy hand syndrome

Upper pons, junction between CR and IC

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acute stroke

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FDA approved options

(r)tPA (recombinant) tissue plasminogen activator – Gold Standard Approved for use within 3 hours of onset of neurologic

deficits in a defined population of patients

Aspirin 325mg Approved for use in patients who do not receive tPA

who do not have any contraindications (drug allergy) and 24 hours after receiving tPA if there is no hemorrhage on 24h post-tPA CT/MRI scan

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tPA mechanism of action

http://www.cvpharmacology.com/thrombolytic/thrombolytic.htm

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tPA – evidence based medicine

National Institute of Neurological Disorders and Stroke (NINDS) tPA Trial NEJM.1995;333:1581-1587

European Cooperative Acute Stroke Study (ECASS) I JAMA 1995;274(13):1017-25

ECASS II Lancet. 1998;352(9136):1245-51

ECASS III NEJM. 2008;359:1317-1329

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tPA

What do you need to give IV tPA Last known normal Focal neurologic deficits by physical examination Non-contrasted head CT Finger stick blood glucose

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thrombectomy

Indications Large vessel strokes (even after receiving IV tPA) Outside of the window for IV tPA Imaging suggestive of penumbra

Contraindications Matched deficit on CTP

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stroke = brain attack

Why should you call a BAT Sudden development of focal neurologic findings

Why you should NOT call a BAT Altered mental status (without focal neurologic findings) To get a faster head CT

Who gets paged – it is an emergency after all… Neurology residents on call All vascular neurology attendings All NSICU attendings All neuroradiology attendings On call radiology residents All neurointerventional radiologists NIR techs and nurses CT techs NSICU, 9E and 9W charge nurses

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stroke = brain attack

What information is helpful to us? Last known normal Symptoms that prompted the BAT Reason for admission Current medications Current labs – including finger stick Recent vitals DNR/DNI status

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MUSC policy for calling a BAT

Altered mental status MET is called first, then the MET resident can

determine if a BAT is warranted

“If an in-patient is experiencing a change in mental status or confusion the Medical Emergency Team (MET) should be paged to the bedside to assess the patient – not the Brain Attack Team!”

“Once the Medical Emergency Team (MET) has assessed the patient and determines that a BAT should be called, at that time the BAT will respond.”

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VA policy for calling a BAT

Regular hours (730a-530p weekdays) There is always a neurology resident in house, simply

page them After hours

If there is an inpatient that has stroke-like symptoms, the upper level medicine resident is expected to evaluate the patient (ie NIHSS), speak with the neurology resident on call if there is concern for acute stroke and the neurology resident will help direct care while going over to the VA

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standard inpatient work up

Neuroimaging 24 hour post tPA scan MRI if indicated Vessel imaging

CTA vs MRA vs carotid dopplersLabs

A1c, lipids, UA, UDS When are TFTs indicated When is B12/folate/RPR indicated

TTE Agitated saline?

PT/OT/SLP consults

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primary prevention

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non-modifiable risk factors

Age Risk of ischemic stroke and ICH doubles for each successive

decade after age 55Gender

More prevalent in men than in womenLow Birth WeightRace/EthnicityGenetics

A meta-analysis of cohort studies showed that a positive family history of stroke increases risk of stroke by approximately 30% [OR 1.3; 95% CI, 1.2 to 1.5, P < 0.00001]

Cardioembolic stroke is the least heritable type of stroke compared with other ischemic stroke subtypes

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modifiable risk factors

HypertensionCigarette smokingDiabetesDyslipidemiaAtrial fibrillationOther cardiac conditionsAsymptomatic carotid stenosisSickle cell diseasePostmenopausal hormone therapyOral contraceptivesDiet and nutritionPhysical inactivityObesity and body fat distribution

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secondary prevention

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modifiable risk factors

Hypertension <120/80

Diabetes A1c <7%

Lipids LDL-c <70mg/dL Treatment with niacin or gemfibrozil in patients with low HDL-c

Cigarette smoking Advisement to quit Avoid environmental/passive smoking Cessation

Physical activity

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interventional approaches to patients with large artery atherosclerosis

Symptomatic extracranial carotid disease CEA recommended if:

Patients with recent TIA or ischemic stroke within the past 6 months and ipsilateral severe (70-99%) stenosis

Patients with recent TIA or ischemic stroke and ipsilateral moderate (50-69%) stenosis, depending on patient-specific risk factors (age, sex, comorbidities)

Indicated for patients with TIA or stroke, surgery within 2 weeks is reasonable rather than delaying surgery

CAS indicated if: Alternative to CEA for symptomatic patients at average

or low risk of complications associated with endovascular intervention with ICA stenosis >70%

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interventional approaches to patients with large artery atherosclerosis

Extracranial vertebrobasilar disease Optimal medical therapy Endovascular and surgical treatment of patients with

EVS may be considered if refractory to medical therapy

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interventional approaches to patients with large artery atherosclerosis

Intracranial atherosclerosis Stroke or TIA due to 50-99% stenosis of a major

intracranial artery, aspirin preferred over warfarin 90 days ASA 325mg and Plavix 75mg, then ASA

monotherapy thereafter No indication for dual antiplatelet therapy beyond 90 days ASA = Plavix = Aggrenox … except for side effect profile

and cost Aggressive medical management

BP <140/90 mmHg Total cholesterol <200 mg/dL

Angioplasty and/or stent placement is not warranted and considered investigational

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