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UPDATE IN STROKE MANAGEMENT David Lee Gordon, M.D., FAHA Professor and Chairman Department of Neurology The University of Oklahoma Health Sciences Center DLG DISCLOSURES FINANCIAL DISCLOSURE I have no financial relationships or affiliations to disclose. UNLABELED/UNAPPROVED USES DISCLOSURE

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update in stroke management

UPDATE IN STROKE MANAGEMENT

David Lee Gordon, M.D., FAHA

Professor and Chairman

Department of Neurology

The University of Oklahoma Health Sciences Center

dlg disclosures
DLG DISCLOSURES
  • FINANCIAL DISCLOSURE
    • I have no financial relationships or affiliations to disclose.
  • UNLABELED/UNAPPROVED USES DISCLOSURE
    • I will reference the following off-label or investigational use of drugs or products: intra-arterial t-PA in stroke patients
stroke in the united states
STROKE IN THE UNITED STATES

Affects > 780,000 persons per year

Major cause of death (#3) & long-term disability

Oklahoma has 6th-highest stroke death rate

Estimated U.S. cost for 2008 = $65.5 billion

Mostly hospital (esp. LOS) & poststroke costs

Appropriate use of IV t-PA s long-term cost

DRG 559 for AIS w/ thrombolysis ( hospital reimbursement from $5k to $11.5k)

three stroke types
THREE STROKE TYPES

Focal Brain Dysfunction

Intracerebral Hemorrhage

Bleeding

into brain

Subarachnoid Hemorrhage

Bleeding around brain

Ischemic

Stroke

Clot occluding

artery

85%

10%

5%

Diffuse Brain Dysfunction

acute ischemic stroke ais tia low blood flow to focal area of brain
INFARCT

CLOT

ACUTE ISCHEMIC STROKE (AIS) & TIALOW BLOOD FLOW TO FOCAL AREA OF BRAIN
  • Pathophysiology:
    • Usually thromboembolism (blood clot forms in vascular system, travels downstream, plugs cerebral artery)
  • Acute therapy:
    • Thrombolysis (or thrombectomy)
    • Do NOT lower BP
    • Avoid aspiration / IV glucose
  • 2 prevention:
    • Antithrombotic therapy
    • Vascular risk factor therapy
    • Possible carotid endarterectomy (CEA) or angioplasty (CAS)

Ischemic stroke=

Infarction with sequelae

Transient ischemic attack=

No infarction and no sequelae

transient ischemic attack tia and acute neurovascular syndrome
TRANSIENT ISCHEMIC ATTACK (TIA) AND “ACUTE NEUROVASCULAR SYNDROME”
  • Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without infarction
  • Typically < 1 h, but time limit is no longer part of definition
  • Risk of stroke = 5% w/in 2 d, 10% w/in 3 m
  • Appropriate antithrombotic therapy based on cause
  • Urgently evaluate for cause
    • MRI w/ DWI, intracranial MRA, carotid duplex, echo
    • Can admit to “observation status”

Discover cause, determine therapy, decrease risk!

ischemic stroke pathophysiology the first few hours
Penumbra

Core

Clot in Artery

ISCHEMIC STROKE PATHOPHYSIOLOGYThe First Few Hours
  • “TIME IS BRAIN:
  • SAVE THE PENUMBRA”
  • Penumbra is zone of reversible ischemia around core of irreversible infarction—salvageable in first few hours after
  • ischemic stroke onset
  • Penumbra damaged by:
  • Hypoperfusion
  • Hyperglycemia
  • Fever
  • Seizure
ischemic penumbra pathophysiology of therapeutic window
Penumbra

Core

CEREBRAL

BLOOD

FLOW

(ml/100g/min)

Normal function

20

15

Neuronal dysfunction

CBF

8-18

PENUMBRA

10

Neuronal death

CBF

< 8

5

CORE

1

2

3

TIME (hours)

ISCHEMIC PENUMBRA: PATHOPHYSIOLOGYOF THERAPEUTIC WINDOW

Identification of penumbra through MRI perfusion-diffusion mismatch or perfusion CT may replace time as the major indication for emergency acute ischemic stroke therapies.

organized care of stroke patients performance improvement utilization review
ORGANIZED CARE OF STROKE PATIENTS:PERFORMANCE IMPROVEMENT / UTILIZATION REVIEW
  • Acute stroke team
  • Stroke multidisciplinary team
  • Stroke unit
  • Prewritten stroke orders
  • Address each aspect of care each day

Supportive medical care

Treatment of acute stroke

Rehabilitation

Outpatient planning

Keep away future strokes

Etiologic evaluation

An organized approach enables

emergency treatment, a thorough evaluation,

and improved patient outcome at decreased cost.

Stroke unit care results in decreased rate of aspiration pneumonia, decubiti, stroke progression or recurrence, and death.

stroke emergency brain imaging noncontrast ct scan
Acute (4 hours)

Infarction

Subacute (4 days) Infarction

R

L

L

R

Subtle blurring of gray-white junction & sulcal effacement

Obvious dark changes & “mass effect” (e.g., ventricle compression)

STROKE EMERGENCY BRAIN IMAGING:NONCONTRAST CT SCAN
stroke emergency brain imaging noncontrast ct scan11
STROKE EMERGENCY BRAIN IMAGING:NONCONTRAST CT SCAN

Intracerebral Hemorrhage

Subarachnoid Hemorrhage

CT detects 90% of SAHs;

if SAH suspected &

CT negative, must LP

CT detects all ICHs immediately

ais emergency therapy iv tissue plasminogen activator t pa
< 3.0 Hours

No upper age limit

No limit on stroke size

Can give if taking warfarin & INR < 1.7

3.0-4.5 Hours

Do NOT give if:

Pt > 80 yo

NIHSS > 25

DM w/ previous stroke

Taking warfarin at all

AIS EMERGENCY THERAPY: IV TISSUE PLASMINOGEN ACTIVATOR (T-PA)
  • Must give < 4.5 h—earlier you give it, better the outcome
  • Stroke onset = last time known to be normal
  • Do NOT give if glucose < 50
  • Do NOT give if BP > 185/110
  • Disability risk  30% despite ~5% symptomatic ICH risk
  • Lawsuits for not giving >>> lawsuits for giving
ais ed stroke care 24 7 1 h evaluation 1 h infusion
AIS ED STROKE CARE 24/7:1-H EVALUATION, 1-H INFUSION

I. Triage–10 min

Review t-PA criteria

Page acute stroke team

Draw pre t-PA labs*

II. Medical Care–25 min

Place O2 , 2 NS IVs

Obtain BP, weight, NIHSS

Obtain 12-lead ECG

Send patient to CT

III. CT & Labs–45 min

Obtain lab results

Read CT

Return pt to ED

IV. Treatment–60 min

Start IV t-PA

Monitor for ICH sxs

HTN, headache

N/V,  neuro status

*CBC, platelets, PT/INR, PTT, chem 7, cardiac panel

other ais therapies maybe ia yes asa no high dose heparin
OTHER AIS THERAPIES:MAYBE IA, YES ASA, NO HIGH-DOSE HEPARIN
  • Intra-arterial t-PA
    • Only preliminary evidence to date, not FDA approved
    • Theoretical window 6 h—but do NOT preclude IV t-PA w/in 4.5 h
    • Studies ongoing, esp. combined w/ IV t-PA
  • MERCI or Penumbra device
    • Mechanical embolectomy devices
    • Theoretical window 8 h
    • Both FDA approved, but controlled trial results pending
  • Aspirin
    • Aspirin 325 mg per day begun within 48 h of stroke onset decreases morbidity & mortality (may begin 24 h after t-PA)
  • Heparin(s)
    • Insufficient evidence to recommend routine use of high-dose IV heparin, LMW heparin, or heparinoid as Rx for AIS per se
the ais bp relationship
Penumbra

Core

Clot in Artery

THE AIS-BP RELATIONSHIP

In AIS, high BP is a response,

not a cause—don’t lower it!

  • BP increase is due to arterial occlusion (i.e., an effort to perfuse penumbra)
  • Failure to recanalize (w/ or w/o thrombolytic therapy) results in high BP and poor neuro outcomes
  • Lowering BP starves penumbra, worsens outcomes
ais is not a hypertensive emergency
AIS IS NOT A HYPERTENSIVE EMERGENCY!
  • ASA/AHA AIS Guidelines tables no longer include recs for BP Rx in non t-PA patients
  • Text of guidelines state “Do not Rx unless BP > 220/120,” but also state:
    • No data to suggest 220/120 is dangerous & requires Rx
    • Evidence that BP lowering worsens outcomes is concerning
    • Goal is to avoid overtreating pts until definitive data available
  • Only definite indications to  BP emergently in AIS:
    • AMI, CHF, Ao dissection, ARF, or HTN encephalopathy
    • Candidate for thrombolysis and BP > 185/110
may lower bp slightly pre t pa must pick an upper limit to treat 220 120 is one option
Lower BP

pre-t-PA

No BP med,

No t-PA

MAY LOWER BP SLIGHTLY PRE T-PAMUST PICK AN UPPER LIMIT TO TREAT—220/120 IS ONE OPTION

If all t-PA criteria met except sustained BP > 185/110:

  • Ensure 2 IVs (NS @ 75 cc/h, saline lock)
  • Calm patient, empty bladder
  • Recheck BP, lower slightly if necessary
    • SBP > 220 or

DBP > 120

    • SBP > 185 and < 220 or

DBP > 110 and < 120

Avoid excessive lowering of BP just to give t-PA—

“Don’t kill the penumbra to save the penumbra”

lowering bp in t pa patients
LOWERING BP IN T-PA PATIENTS
  • Nicardipine 5 mg/h IV infusion
    • Increase 2.5 mg/h q5min to max 15 mg/h
    • Easily titratable without an arterial line
  • Labetalol 10-20 mg IV
    • May repeat q 10-15 min
    • Pre-t-PA: only use a 2nd dose only if necessary

Note Different Target BPs Pre & Post T-PA

Pre t-PA: < 185/110

Post t-PA: < 180/105

worrying about the lungs aspiration dysphagia oxygen
WORRYING ABOUT THE LUNGS:ASPIRATION, DYSPHAGIA, & OXYGEN
  • Weak oropharyngeal muscles common
  • Neurogenic dysphagia: liquids worse than solids (purees best)
  • Stroke pts on ventilator: 2/3 mortality, most survivors disabled
  • Recommendations (science):
    • Keep pt 100% NPO until evaluation
    • Use NG feeding tube if necessary (& IV NS 75-125 cc/h)
    • Evaluate with video fluoroscopy whenever possible
    • Use continuous feed only if Dobhoff tip distal to pylorus
  • Recommendations (art):
    • Maintain HOB > 30°
    • Maintain O2 sat > 92 or 95% w/ 2-4L O2
hyperglycemia acute stroke diabetes 2 stroke prevention
HYPERGLYCEMIA & ACUTE STROKE /DIABETES & 2 STROKE PREVENTION
  • Acutely, peri-stroke hyperglycemia associated with worse clinical outcomes
  • Inpatient goal BG < 150
  • Chronically, each 1%  in Hgb A1C results in significant  in risk of death, MI, vascular complications, including 12%  in stroke risk
  • Outpatient goal Hgb A1C < 7.0
secondary stroke prevention risk factor modification
SECONDARY STROKE PREVENTION:RISK-FACTOR MODIFICATION
  • Hypertension
    • Day 1 poststroke, start low-dose ACE-I or ARB
    • Slowly (days to weeks)  dose, add diuretic, watch K+
    • Anti-HTN meds benefit those w/ and w/o HTN history
    • Evaluate for sleep apnea and treat w/ CPAP
    • Outpatient goal < 120/80—over weeks to months

*In stroke pts, ACE-Is & ARBs appear to decrease risk of stroke, MI, & vascular death beyond effect on BP alone. Based on theory and animal models, ARBs may be more effective than ACE-Is.

secondary stroke prevention mechanisms of ace i arb benefits
Vasoconstriction
  • Na retention
  • Vascular proliferation

 Endothelial function

  • Inflammation
  •  LDL transport

ANGIOTENSIN

CONVERTING

ENZYME

AT 1

The

Bad

ARB

ACE-I

ANGIOTENSIN I

ANGIOTENSIN II

  • Vasodilatation
  • Natriuresis

 Vascular proliferation

 Endothelial function

  • Apoptosis
  • No cholesterol effect

AT 2

The

Good

SECONDARY STROKE PREVENTION:MECHANISMS OF ACE-I/ARB BENEFITS

Based on animal studies and pathophysiologic considerations, ARBs may be superior to ACE-Is for stroke prevention, but ONTARGET found no difference between telmisartan & ramipril in reducing vascular risk.

secondary stroke prevention risk factor modification23
SECONDARY STROKE PREVENTION:RISK-FACTOR MODIFICATION
  • Hypercholesterolemia
    • Do not discontinue statins on admission
    • Obtain LDL w/in 48 of stroke onset
    • If LDL > 100, use hi-dose statin shown to stroke/MI/death risk
      • atorvastatin 20-80 mg/d
      • pravastatin 40-80 mg/d
      • simvastatin 40-80 mg/d
      • rosuvastatin 10-40 mg/d
    • If LDL < 100, use lower statin dose
    • Outpatient goal LDL < 70 (but give statin to all pts)
supportive medical care prevent complications
SUPPORTIVE MEDICAL CARE:PREVENT COMPLICATIONS
  • Aspiration (NPO until swallowing evaluation)
  • Deep-vein thrombosis
    • Sequential compression devices (if stroke < 48 h)
    • Heparin 5000 q8h or enoxaparin 40 mg/d
  • Urinary tract infection (avoid Foley catheters)
  • Constipation (docusate sodium for all)
  • Decubitus ulcers (move q2h, out of bed TID by day 2)
  • UGI bleed (H2B, but not cimetidine)
  • Fever (acetaminophen + antibiotics as indicated)
rehab outpatient planning begin on admission decrease length of stay
REHAB & OUTPATIENT PLANNING:BEGIN ON ADMISSION, DECREASE LENGTH OF STAY
  • SP—swallowing evaluation before oral feedings
  • PT, OT—bedside first, out of bed ASAP
  • Social worker—plan based on level of care, pay source, caregiver support
  • Communicate with primary-care clinician
  • Educate pt, caregiver daily (not just on discharge)
    • Call 911
    • Follow-up after discharge
    • Medications
    • Risk Factors
    • Stroke Symptoms
poststroke depression
POSTSTROKE DEPRESSION
  • Suspect if sxs persist 1-2 wks after stroke
  • Is an “organic,” not “reactive” depression
  • Occurs in ~ 50% of stroke pts
  • May affect rehab and recovery
  • Often resolves w/in one year
  • SSRIs equally effective, but if pt takes warfarin:
    • Escitalopram (Lexapro) 5-10 mg qAM
    • Citalopram (Celexa) 10-20 mg qAM
    • Sertraline (Zoloft) 25-50 mg qAM
causes etiologies of ischemic stroke six main categories
OLDER PATIENTS

(> 55)

YOUNGER PATIENTS

(< 55)

Hypercoagulable

states

Nonatherosclerotic

vasculopathies

Large-artery

atherosclerosis

Small-artery

disease

Cardioembolism

Hypotension

Correct therapy depends on cause of stroke!

“Cause” & “risk factor” are not synonymous—must Rx both!

CAUSES (ETIOLOGIES) OF ISCHEMIC STROKE:SIX MAIN CATEGORIES
etiologic evaluation identify stroke find source of clot
ETIOLOGIC EVALUATION:IDENTIFY STROKE, FIND SOURCE OF CLOT

NONINVASIVE

Day 1

INVASIVE

Day 2

ARTERIES

MRI & intracranial MRA

Carotid duplex (CD)

*Catheter

angiogram

HEART

ECG & monitor

Cardiac biomarkers

Transthoracic echo (TTE)

*TEE

BLOOD

*Hypercoagulable profile

*in select

patients

mri brain in hyperacute ischemic stroke
R

L

R

L

R

L

DWI

ADC

FLAIR

MRI BRAIN IN HYPERACUTE ISCHEMIC STROKE
  • DWI & ADC: Early infarction visible
  • FLAIR: No signal changes; possible sulcal effacement in area of infarction
intracranial mra ap views of anterior circulation
INTRACRANIAL MRA:AP VIEWS OF ANTERIOR CIRCULATION

Normal

Paucity of R MCA Branches

c/w Embolic Occlusions

RACA

LACA

RMCA

LMCA

RICA

LICA

RICA

LICA

carotid duplex
ECA

CCA

ICA

Plaque

CAROTID DUPLEX
  • Evaluates carotid arteries in neck (operable area)
  • Excellent screen in the right hands
  • May not differentiate 99 vs. 100% stenosis
  • Need contrast angiography for clinically relevant stenosis measurement
  • Carotid duplex =

Doppler (velocities) +

B-mode ultrasound

(echo picture)

echocardiography tte vs tee
ECHOCARDIOGRAPHY:TTE VS. TEE

TRANSTHORACIC ECHO

Left Ventricle

  • Thrombus
  • Dilatation
  • SEC/smoke
  • Dyskinesis
  • Aneurysm

TRANSESOPHAGEAL ECHO

Left Atrium

  • Thrombus
  • Dilatation
  • SEC/smoke
  • Tumor

PFO/IASA > 5 mm

Endocarditis

Aortic Arch

  • Athero > 4 mm
  • Thrombus
  • Tumor

LA

LV

SEC/EF 20%

PFO

Identifies

source in

37.2%

of pts in

NSR

Identifies

source in

30-40%

of pts with

unknown cause

hypercoagulable profile patients 55 years old
CBC w/ diff & platelets

PT/aPTT

Fibrinogen

Factor VIII

Factor VII

C-reactive protein

Antithrombin III

Protein C

Protein S (total & free)

Lipoprotein (a)

HYPERCOAGULABLE PROFILEPATIENTS < 55 YEARS OLD
  • Activated protein C resistance (APCR) (& Leiden factor V mutation if APCR -)
  • Prothrombin G20210A mutation
  • Antiphospholipid antibodies
    • Lupus anticoagulant
    • Anticardiolipin abs
    • Anti-β-2-glycoprotein I abs
    • Antiphosphatidylserine abs
  • Methyltetrahydrofolatereductase (MTHFR) C677T & A1298C mutations
  • Sickle cell screen
ct mri appearance cannot determine etiology of small cerebral infarcts
CT / MRI APPEARANCE CANNOT DETERMINE ETIOLOGY OF SMALL CEREBRAL INFARCTS

small-art. “occlusion” =

small-art. “disease”

  • Dx of small-artery “disease” requires:
    • Lacunar syndrome
      • e.g., pure motor, pure sensory,

pure sensorimotor

    • Medial, small (< 1.5 cm) infarct on CT or MRI
    • History of longstanding HTN or DM
    • Otherwise normal etiologic evaluation

Small L subcortical

infarction in 40 yo

woman w/ DM—due

to embolus from

aortic papilloma

Small-artery “disease” is a diagnosis of exclusion

secondary stroke prevention antithrombotic rx based on cause
SECONDARY STROKE PREVENTION:ANTITHROMBOTIC RX BASED ON CAUSE

High-flow states:

platelets cause clots

Platelets are like Velcro

sticking to bumpy walls

Low-flow & hypercoagulable states:

clotting factors cause clots

Clotting factors are like dissolved powdered gelatin

that forms clumps of Jello when liquid is static

large-artery

atherosclerosis

small-artery

disease

cardioembolism

hypercoagulable

state

ANTIPLATELET AGENT

aspirin 81-325/d

clopidogrel 75/d

aspirin + dipyridamole XR 25/200 twice/d

ANTICOAGULANT

warfarin

INR 2.0-3.0

or

INR 2.5-3.5

secondary stroke prevention antiplatelet agents for arterial disease
SECONDARY STROKE PREVENTION:ANTIPLATELET AGENTS FOR ARTERIAL DISEASE
  • Aspirin
    • Prevents MI & stroke
    • Stroke rec 50-365 mg/d, but MI rec 75-162 mg/d
    • Low dose with less side effects, > 1200 mg/d ineffective
    • Enteric coating, NSAIDs may lessen efficacy
  • Clopidogrel 75 mg per day
    • Prevents MI and stroke
    • Routine combination with aspirin not indicated in stroke pts, though not resolved for subset of pts with large-artery athero
    • PPIs lessen efficacy
  • Aspirin / dipyridamole XR 25/200 twice daily
    • Data regarding MI prophylaxis lacking
    • Headache common side effect of dipyridamole
    • Not superior to clopidogrel…with more bleeding side effects
secondary stroke prevention warfarin for cardioembolism
SECONDARY STROKE PREVENTION:WARFARIN FOR CARDIOEMBOLISM
  • Underused for a. fib./flutter, esp. blacks, Hispanics, elderly
  • Starting dose 5 mg qPM
  • INR monitoring
    • Target 2.5, range 2.0-3.0 (mechanical HVR 2.5-3.5)
    • Reflects dose 2-3 days ago, stabilizes in 10-14 days
    • Vitamin K (greens, NG feedings, Ensure, Slimfast, MVI)
    • Other meds, EtOH, cranberry juice
    • Dose and formulation changes
  • Limit holding for procedures (e.g., dental, GI, surgery)
secondary stroke prevention carotid stenosis procedures
Internal

Carotid

Artery

D

External

Carotid

Artery

N

stenosis

in ICA bulb

% stenosis

= (D-N)/D

by contrast

angiography

Common

Carotid

Artery

SECONDARY STROKE PREVENTION:CAROTID STENOSIS PROCEDURES
  • Carotid Endarterectomy (CEA)
    • Clear benefit if 70-99% stenosis
    • Some benefit if 50-69% stenosis
    • Accept complication rate < 6%
  • Carotid Angioplasty/Stenting (CAS)
    • Now, option only in high-risk pts
      • Restenosis after CEA
      • Radiation-induced stenosis
      • Increased medical risk for CEA
      • Contralateral carotid occlusion
    • Cerebral protection devices improving, trials continue
secondary stroke prevention risk factor modification39
SECONDARY STROKE PREVENTION:RISK-FACTOR MODIFICATION
  • Cigarette smoking cessation
    • Bupropion (Wellbutrin SR or XL, Zyban)
      • Start 150 mg daily x 3 days
      • Then 150 mg BID x 3 months
    • Nortriptyline (Pamelor)
      • Start 10-25 mg each night
      •  gradually to 75 mg each night
    • Nicotine patch/gum/inhaler
      • Concurrent with bupropion or nortriptyline
    • Varenicline (Chantix)
      • Start 0.5 mg daily x 3 days
      •  gradually to 1 mg BID x 11 wk
secondary stroke prevention risk factor modification40
SECONDARY STROKE PREVENTION:RISK-FACTOR MODIFICATION
  • Lifestyle
    • Alcohol: men < 2 oz / d, women < 1 oz / d
    • Diet: Low saturated fat, low Na+, high K+,

fruits > vegetables, Mediterranean diet

    • Exercise: > 20 min aerobic exercise, > 3 x / wk
    • Weight: maintain BMI 18.5-24.9 kg/m2
  • Drugs to Avoid
    • Estrogen (oral contraceptives, HRT)
    • Sympathomimetic agents (incl. decongestants, diet pills)
    • NSAIDs (if taking aspirin)
    • PPIs (if taking Plavix)
ischemic stroke tia 2 prevention summary 1 of 2
ISCHEMIC STROKE / TIA2 PREVENTION SUMMARY 1 OF 2
  • Prescribe:
    • Antithrombotic agent based on cause
    • ARB or ACE-I regardless of BP
    • Statin regardless of cholesterol
  • Maintain:
    • Hgb A1C < 7.0
    • BP < 120/80, including ARB or ACE-I
    • LDL < 70, including statin
    • Nutrition w/ fruits, Mediterranean diet
    • Alcohol intake < 2 oz/d (men) or < 1 oz/d (women)
    • BMI 18.5-24.9 kg/m2
    • Aerobic exercise > 20 min/d, > 3 d/wk
ischemic stroke tia 2 prevention summary 2 of 2
ISCHEMIC STROKE / TIA2 PREVENTION SUMMARY 2 OF 2
  • Discontinue:
    • Cigarette smoking
    • Sympathomimetic agents (incl. decongestants)
    • Estrogens
  • Treat:
    • Carotid stenosis 50/70-99% (CEA or CAS)
    • Sleep apnea (CPAP)
    • Sickle cell disease (monitor TCD, Hgb S < 30%)
ad