Download 4._Management_of_Stroke

UPDATE IN ACUTE
ISCHEMIC STROKE
MANAGEMENT
OU Neurology
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
OU Neurology
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)
OU Neurology
THREE STROKE TYPES
Focal Brain Dysfunction
Intracerebral
Hemorrhage
Ischemic
Stroke
85%
Clot occluding
artery
Subarachnoid
Hemorrhage
10%
Bleeding
into brain
5%
Bleeding
around brain
Diffuse Brain Dysfunction
OU Neurology
ACUTE ISCHEMIC STROKE (AIS) & TIA
LOW BLOOD FLOW TO FOCAL AREA OF BRAIN
 Pathophysiology:
INFARCT
 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
CLOT
Ischemic stroke =
Infarction with sequelae
Transient ischemic attack =
No infarction and no sequelae
 2 prevention:
 Antithrombotic therapy
 Vascular risk factor therapy
 Possible carotid endarterectomy
(CEA) or angioplasty (CAS)
OU Neurology
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!
OU Neurology
ISCHEMIC STROKE PATHOPHYSIOLOGY
The First Few Hours
“TIME IS BRAIN:
SAVE THE PENUMBRA”
Penumbra
Penumbra is zone of
reversible ischemia around
core of irreversible
infarction—salvageable in
first few hours after
ischemic stroke onset
Core
Penumbra damaged by:
• Hypoperfusion
• Hyperglycemia
• Fever
• Seizure
Clot in
Artery
OU Neurology
Penumbra
ISCHEMIC PENUMBRA: PATHOPHYSIOLOGY
OF THERAPEUTIC WINDOW
CEREBRAL
BLOOD
FLOW
20
(ml/100g/min)
15
10
Core
Normal
function
PENUMBRA
5
CORE
1
2
Neuronal
dysfunction
CBF
8-18
Neuronal
death
CBF
<8
3
TIME (hours)
Identification of penumbra through MRI perfusion-diffusion
mismatch or perfusion CT may replace time as the major
indication for emergency acute ischemic stroke therapies.
OU Neurology
ORGANIZED CARE OF STROKE PATIENTS:
PERFORMANCE IMPROVEMENT / UTILIZATION REVIEW
 Acute stroke team
 Stroke multidisciplinary team
 Stroke unit
 Prewritten stroke orders
Supportive medical care
Treatment of acute stroke
Rehabilitation
Outpatient planning
Keep away future strokes
Etiologic evaluation
 Address each aspect of care each day
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.
OU Neurology
STROKE EMERGENCY BRAIN IMAGING:
NONCONTRAST CT SCAN
Acute (4 hours)
Infarction
L
Subacute (4 days)
Infarction
L
R
Subtle blurring of graywhite junction & sulcal
effacement
Obvious dark changes
& “mass effect” (e.g.,
ventricle compression)
R
OU Neurology
STROKE EMERGENCY BRAIN IMAGING:
NONCONTRAST CT SCAN
Intracerebral Hemorrhage
CT detects all ICHs
immediately
Subarachnoid Hemorrhage
CT detects 90% of SAHs;
if SAH suspected &
CT negative, must LP
OU Neurology
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
< 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
OU Neurology
FAST Test
Use the FAST test for recognizing and responding to stroke
symptoms.
 Facial Droop:
Ask the person to smile. Does one side of the face droop?
 Arm Drift:
Ask the person to raise both arms. Does one arm drift downward?
 Slurred Speech:
Ask the person to repeat a simple sentence. Does the speech sound
slurred or strange?
 Time:
If you observe any of these signs, it’s time to call a senior doctor.
OU Neurology
The goal
the acute management of patients with
stroke is to stabilize the patient and
to complete initial evaluation and
assessment, including imaging and
laboratory studies, within 60 minutes of
patient arrival
OU Neurology
Time Target
Door to doctor 10 min
Access to neurologic expertise 15 min
Door to CT scan completion 25 min
Door to CT scan interpretation 45 min
Door to treatment 60 min
OU Neurology
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
OU Neurology
Inclusion Criteria
Diagnosis of ischemic stroke causing
measurable neurologic deficit
Onset of symptoms 3hours before
beginning of treatment.
The patient and family understand the
potential risks and benefits of therapy
Recent AHA/ASA guidelines recommend
extension of IV rtPA treatment window up to
4.5hours based on ECASS(III) trial
OU Neurology
Obslute contindications
 ICH (whenever the previous history)
 Acute MI
 Pericaditis
 Endocarditis
 Bleeding tendency
OU Neurology
Exclusion Criteria
 Neurologic signs are clearing spontaneously
 Neurologic signs are minor and isolated
 Systolic blood pressure >185 mm Hg, diastolic blood
pressure >110 mm Hg
 Head trauma or prior stroke in the past 3 months
 MI in the last 3 months
 GI/GU hemorrhage in previous 21 days
 Arterial puncture at a non-compressible site during prior
7 days
 Major surgery within the last 14 days
OU Neurology
 Taking any anticoagulant or if on anticoagulant INR >1.7
 Patient received heparin in the last 48 hours with
elevated partial thromboplastine time (aPTT)
 Platelet count of <100,000/μl
 Blood glucose less than 50 mg/dl or greater than 400mg
 Seizure with residual postictal focal impairments
 CT scan shows evidence of multi-lobar infarction (hypodensity greater than one third of MCA territory)
OU Neurology
Recent evidences suggest to expand the window time
for the administration of rtPA from 3 hrs to 4.5 hrs to
the above eligible patients excluding any one of the
following:
 *Patients older than 80 years
 * All patients taking oral anticoagulants are excluded
regardless of the (INR)
 *Patients with baseline NIHSS greater than 25
 * Patients with a history of stroke and diabetes
OU Neurology
No antiplatelet or anticoagulant therapy
should be administered for 24 hours
following tPA.
Obtain a repeat head CT scan or MRI 24
hours after tPA to rule out asymptomatic
hemorrhagic transformation prior to initiating
antithrombotic therapy.
OU Neurology
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
OU Neurology
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
Penumbra
Core
Clot in
Artery
OU Neurology
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
OU Neurology
MAY LOWER BP SLIGHTLY PRE T-PA
MUST 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
No BP med,
No t-PA
 SBP > 185 and < 220 or
DBP > 110 and < 120
Lower BP
pre-t-PA
Avoid excessive lowering of BP just to give t-PA—
“Don’t kill the penumbra to save the penumbra”
OU Neurology
 The aim is to maintain MAP = 70 - 130 mm Hg
 MAP = DP + 1/3 (SP-DP) OR {(2xDP) + SP}/3
 Labetalol Initial: 20 mg IV over 2 min, then 40-80 mg IV q10min to no more
than 300
 mg, OR 1-2 mg/min continuous IV infusion
 Nicardipine I V: Initial 5 mg/hr slowly, may increase q15min by 2.5 mg/hr;
maximum
 15 mg/h; when desired blood pressure reached, lower to 3 mg/h
 Enalapril 1.25 - 5 mg IVP every 6 h
 Esmolol 250 μg/kg IVP loading dose, then 25 - 300μ/kg/ min
 Hydralazine 5 - 20 mg IVP every 30 min OR 1.5 to 5 μg /kg/ min
 Nitroglycerin 20 - 400 μg/min
 Sodium nitroprusside (0.5 mcg/kg/min)
OU Neurology
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
OU Neurology
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
OU Neurology
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
OU Neurology
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.
OU Neurology
SECONDARY STROKE PREVENTION:
MECHANISMS OF ACE-I/ARB BENEFITS
ANGIOTENSIN
CONVERTING
ENZYME
ACE-I
ANGIOTENSIN I
AT 1
The
Bad
Vasoconstriction
Na retention
 Vascular proliferation
 Endothelial function
Inflammation
 LDL transport
AT 2
The
Good
Vasodilatation
Natriuresis
 Vascular proliferation
 Endothelial function
Apoptosis
No cholesterol effect
ARB
ANGIOTENSIN II
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.
OU Neurology
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)
OU Neurology
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)
OU Neurology
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
OU Neurology
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
OU Neurology
CAUSES (ETIOLOGIES) OF ISCHEMIC STROKE:
SIX MAIN CATEGORIES
OLDER PATIENTS
(> 55)
Large-artery
atherosclerosis
Small-artery
disease
YOUNGER PATIENTS
(< 55)
Cardioembolism
Hypotension
Hypercoagulable
states
Nonatherosclerotic
vasculopathies
Correct therapy depends on cause of stroke!
“Cause” & “risk factor” are not synonymous—must Rx both!
OU Neurology
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
OU Neurology
MRI BRAIN IN HYPERACUTE ISCHEMIC
STROKE
 DWI & ADC: Early infarction visible
 FLAIR: No signal changes; possible sulcal
effacement in area of infarction
R
L
DWI
R
L
ADC
R
L
FLAIR
OU Neurology
INTRACRANIAL MRA:
AP VIEWS OF ANTERIOR CIRCULATION
Normal
RACA
RMCA
RICA
Paucity of R MCA Branches
c/w Embolic Occlusions
LACA
LMCA
LICA
RICA
LICA
OU Neurology
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
ECA
 Carotid duplex =
Doppler (velocities) +
B-mode ultrasound
(echo picture)
CCA
ICA
Plaque
OU Neurology
ECHOCARDIOGRAPHY:
TTE VS. TEE
TRANSTHORACIC ECHO
LV
SEC/EF 20%
Identifies
source in
37.2%
of pts in
NSR
Left Ventricle
 Thrombus
 Dilatation
 SEC/smoke
 Dyskinesis
 Aneurysm
TRANSESOPHAGEAL ECHO
Left Atrium
 Thrombus
 Dilatation
 SEC/smoke
 Tumor
PFO/IASA > 5 mm
PFO
Endocarditis
Identifies
source in
Aortic Arch
30-40%
 Athero > 4 mm
of pts with
 Thrombus
unknown cause
 Tumor
LA
OU Neurology
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)
 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
OU Neurology
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
OU Neurology
SECONDARY STROKE PREVENTION:
ANTITHROMBOTIC RX BASED ON CAUSE
High-flow states:
platelets cause clots
Low-flow & hypercoagulable states:
clotting factors cause clots
Platelets are like Velcro
sticking to bumpy walls
Clotting factors are like dissolved powdered gelatin
that forms clumps of Jello when liquid is static
large-artery
small-artery
atherosclerosis
disease
cardioembolism
ANTIPLATELET AGENT
aspirin 81-325/d
clopidogrel 75/d
aspirin + dipyridamole XR 25/200 twice/d
hypercoagulable
state
ANTICOAGULANT
warfarin
INR 2.0-3.0
or
INR 2.5-3.5
OU Neurology
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
OU Neurology
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)
OU Neurology
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%
Internal
Carotid
Artery
External
Carotid
Artery
D
N
 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
stenosis
in ICA bulb
Common
Carotid
 Cerebral protection devices improving,
Artery
trials continue
% stenosis
= (D-N)/D
by contrast
angiography
OU Neurology
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
OU Neurology
SECONDARY STROKE PREVENTION:
RISK-FACTOR MODIFICATION
 Lifestyle
 Alcohol:
 Diet:
men < 2 oz / d, women < 1 oz / d
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)
OU Neurology
ISCHEMIC STROKE / TIA
2 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
OU Neurology
ISCHEMIC STROKE / TIA
2 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%)
OU Neurology
THE END
OU Neurology