Download Approach to TIA and Management of Stroke after

Approach to TIA and Management
of Stroke after 4.5 hours
Robert Altman R4
McGill University
August 25th 2010
Summer Emergency Lecture Series
What to take out of today.
• Everything I’m presenting is evidence based
– Where no data or consensus exists, will have to resort
to ‘expert opinion’
• Tried to make this as user friendly and practical
so as to be able to refer back to at a future date
– Basic standards of practice
• know the guidelines, or where to find them; especially the
Canadian ones.
– Know the terminology and classification systems that
exist to facilitate your readings and assist in critically
appraising studies.
Outline
• Definition
– TIA
• Ddx and TIA mimics
• Review of ABCD2 score
– 48 hr cerebrovascular risk stratification
• Who to admit and who can be discharged
• Subacute management of ischaemic arterial stroke (and
TIA for that matter)
– Practical aspects and highlights of frequently cited studies
– Topics: CEA, BP, lipids, oxygenation, mobilization, swallowing,
speech, VTE prophylaxis
Next week...
AHA/ASA Guidelines
What is a TIA?
TIA
• Old definition
– “Sudden, focal neurological deficit of presumed
vascular origin lasting ≤ 24 hours”
• Suggests transient ischemic symptoms are benign
• Diagnosis on the basis of temporal course rather than
pathophysiological basis (tissue)
• Delays and obfuscates diagnosis
• Delays intervention in cases of true brain ischemia
• Diverges from the notion that TIA is to stroke what
angina is the MI
History
• 24-hour threshold arose in the mid-1960s.
– Assumption was that no permanent brain injury if symptoms
dissipated.
• Reversible ischemic neurological deficit (RIND) was applied to
events lasting 24 hours to 7 days.
findingsand
highlight
an inconsistency
• >7 days indicateThese
infarction
received
the designation stroke
between the concept of TIA (ischemia causing
• 1970s
symptoms but no infarction) and the traditional
– Great preponderance
of events lasting 24hrs-7d were a/w
of TIA
infarction, rendering thedefinition
RIND obsolete
• More recently, Hi-Res CT and diffusion-weighted MR studies
demonstrate symptoms lasting 24 hours also are associated with
new infarction.
– 30% to 50% of classically defined TIAs show brain injury on
diffusion-weighted magnetic resonance (MR) imaging (MRI)
Transient Ischemic Attack
• Tides have turned
• Time (old) vs. Tissue based
definition (new)
• AHA/ASA 2009 definition
– “Transient ischemic attack
(TIA): a transient episode of
neurological dysfunction
caused by focal brain, spinal
cord, or retinal ischemia,
without acute infarction.”
– No infarction on MRI
– ‘acute neurovascular
syndrome’ if no imaging
available
N Engl J Med, Vol. 347, No. 21
Transient Ischemic Attack
• Diagnostic certainty will
depend on the extent of
evaluation the individual
patient receives.
– This concept is not unique to
brain ischemia; it is typical of
most medical diagnoses.
– Brain imaging currently and
serum diagnostic studies likely
in the future (equivalent to
trops) increase diagnostic
certainty regarding whether a
particular episode of focal
ischemic deficits was a TIA or a
cerebral infarction.
TIA
• TIA is a very serious warning sign
• Among patients presenting to the ER with a TIA
– 10 to 15% of patients have a stroke within 3 months
Early recognition
of TIA and
– half occurring
within 48 hours
subsequent
timely
intervention
– When
recurrent TIAs,
myocardial
infarction and
death from
anycritical
cause are
considered,
is of
and
obviousthe risk is
more than 25% importance.
over the first 3 months.
– Mortality
• 5-6 % annually, mainly by MI
TIA Risk
Gladstone D et al. CMAJ. 2004 Mar 30;170(7):1099-104.
Epidemiology
• In the US, incidence is approx. 200 000 to 500 000
per year, with a population prevalence of 2.3% that
translates into 5 million individuals
• Lack of recognition by both the public and healthcare
systems (including physicians), thus current #’s:
– grossly underestimated
Signs / Symptoms
•
•
•
•
Neurological
Focal
Sudden
Localizable to an anatomical structure in the
CNS or retina
Immediate Management
• Get a real history
• Carefully examine the patient for residual
deficits and try to localize anatomically to
guide your work-up
• Construct a differential diagnosis based on
history
– Recognize the mimics
TIA/Stroke Mimics
CMAJ 2004;170(7):1134-7
Example: Real case
• 76F remote CVA, 6 months prior, R MCA territory, near full
recovery
• Husband heard thump on the floor this AM 10:30, now 12:00
• Went to see wife, panicked, unresponsive, called ambulance.
Ambulance note states pt had urinary incontinence (new)
• In ER, staff notes patient was awake, but not really responding
to commands, then eyes began deviating L then became
obtunded and comatose.
– Intubated
• Exam shows flaccid plegia on L, minimal to no response to pain,
withdraws, varying degrees on R. Both plantars upgoing. CT
head shows nil acute, old R MCA infarct.
• What is going on here?
• Is this a TIA/Stroke? NO
Example #2
• 36 M
• Hx of paranoid schizophrenia, morbidly obese,
HTN, dyslipidemia, and CAD with angina
• Called for code stroke
• Patient’s neck forced into sideflexion, mouth an
tongue stuck open, unable to speak but follows
commands well, no obvious other neurologic
deficits.
• What’s going on?
• Is this a TIA/Stroke? NO
Example #3
• Mr. P, a 76-year-old man, presents to the
emergency department after experiencing a
sudden onset of slurred speech associated with
tingling and clumsiness of his right hand.
• Symptoms lasted about 30 minutes and have
completely resolved.
• His examination is now unremarkable.
• He has a history of hypertension (controlled on
medication) and dyslipidemia.
• What’s going on?
• Is this a TIA/Stroke? Indeed
Triage – Risk Stratification
• Establishes who you will admit for expedited work-up
• What is the critical information to garner from a TIA
evaluation
1. Age, sex
2. PmHx: afib or PAF, prior TIA or CVA, CAD or recent MI,
smoker, famHx of premature CVA
3. Symptoms: only motor, sensory, speech or both
4. BP and ECG rythm
5. Total duration of symptoms (5 min?, 25 min? 24 hrs?)
6. When? (today, yesterday, 6 months ago?)
=ABCD2
Criteria
Points
48 hour
stroke
risk
Age > 60
1
BP = sBP > 140 or dBP > 90
1
0-1 = 0%
Clinical
•Unilateral weakness
•Speech, without weakness
2
1
2-3 = 1.3%
Duration
• 0-10 min
•10-59 min
•>59 min
0
1
2
4-5= 4.1%
Diabetes Mellitus
1
90 day
stroke
risk
Approx 25%
if score 6-7
6-7 = 8.1%
Lancet 2007; 370: 1432–42
Lancet 2007; 370: 1432–42
• Concentrate on duration, focality to weakness, DM and BP
Lancet 2007; 370: 1432–42
When to intervene?
Express
• Phase 1 vs. 2
• Expedited medical and surgical
management rather than give
recommendations to primary
care practitioner
• Conclusion: Urgent
assessment and early initiation
of a combination of existing
preventive treatments can
reduce the risk of early
recurrent stroke after TIA or
minor stroke by about 80%,
and reduce the total number
of all early recurrent strokes in
the whole population by over
half
Rothwell et al. Lancet 2007; 370: 1432–42
Cumulative proportions of patients prescribed new medication
Statin
Clopidogrel
1 anti-HTN Rx
2 anti-HTN Rx’s
Lancet. 2007 Oct 20;370(9596):1432-42
What is the Recommended TIA
Work-Up?
FYI
• TOAST classification system
– Acute and preventive treatments can and should be tailored to the
underlying mechanism implicated.
Stroke 1993;24;35-41
What is an expedited work-up? (AHA, CSC)
• Neuroimaging
– MRI with DWI, PWI
– CT (C-)
*local strengths in that expertise in vascular
imaging dictate what to select as first line
(also other medical conditions i.e. PM or RF)
• Vascular imaging (extracranial & intracranial)*
– CUS
– CTA (results comparable to CUS and MRA).
• NPV of excluding >70% carotid stenosis of 100%
– MRA (2D TOF) or MRA with contrast (superior resolution– has even supplanted
catheter angiography in some centers, but limited utility if renal disease)
– TCD (microembolic signals)
– Conventional angiography
• Cardiac and ‘other’ testing
– ECG (r/o afib, SSS, arrythmia, LVH)
– TTE, TEE
– Holter
• Routine bloodwork
– CBC, SMA7, Coags, E+, FLP, CK, LFT’s
– Hypercoagulable work-up depending on age / cryptogenicity of stroke-TIA
Clinical Case
• Sudden onset
dysarthria,
mild R
hemiparesis
after a fall, or
was it before
the fall?
• 60 min ago
• Would you
give this pt
clopidogrel?
• Sudden onset
– Focal L
hemiparesis
– Dysarthria
– 45 min ago
• Anti-platelet?
Canadian Stroke Strategy
• Carotid imaging should be performed within 24 hours of a
carotid territory transient ischemic attack or nondisabling
ischemic stroke (if not done as part of the original
assessment) unless the patient is clearly not a candidate for
carotid endarterectomy [Evidence Level B]
What about the echo? (AHA, CSC)
• Should you hold the patient overnight for an echo?
– “TIAs require urgent evaluation, but there is little evidence that
early echocardiographic evaluation has a higher yield.”
• The echocardiographic method used is important.
– TEE is more sensitive than TTE for atheroma of the aortic arch
and abnormalities of the interatrial septum (eg, atrial septal
aneurysm, PFO, atrial septal defect), atrial thrombi, and
valvular disease.
• Holter monitoring is abnormal in a minority of unselected
patients with TIA.
– However, prolonged cardiac monitoring (inpatient telemetry or
Holter monitor) is useful in patients with an unclear origin after
initial evaluation.
• The longer you can obtain the better
Stroke 2009;40;2276-2293
Stroke 2009;40;2276-2293
TIA Prognosis (summary)
Timing
Duration
Frequency
Sensory
Motor
Speech
Risk factors
Deficit dynamics
Benign
weeks ago
sec – few minutes
multiple
yes alone
no
no
no
Malignant
hours ago
>10 min
one to few
no
yes
yes
HTN, DM,
Mild at onset
Severe at onset
What are the other modifiable
cerebrovascular risk factors?
Part 2
Treatment of acute stroke after 4.5 hrs
Drowning in a Sea of Strokes
• Dr. Charles Miller Fisher
– House officers and students learn neurology “stroke by stroke”
• >50% of neurological admissions
• 50,000 new /year in Canada
• 3rd most important cause of death
– after heart disease and cancer
• Most important cause of adult disability
– 30% of survivors require daily assistance.
Clinical Presentation
• Sudden
• Focal weakness, language impairment, gaze
deviation, hemianopia
• Neuroanatomically based
• Search for warning symptoms in week prior
– Amaurosis fugax
– Sentinel TIA’s
Modifiable Risk Factors for Ischemic Stroke
Stroke Risk Factors
Hypertension
Cardiac Disease
Atrial Fibrillation
Diabetes Mellitus
Smoking
Alcohol Abuse
Hyperlipidemia
Estimated
RR
3.0-5.0
2.0-4.0
4.0-18.0
1.5-3.0
1.5-2.5
1.0-4.0
1.0-2.0
Estimated
Prevalence
25-40%
10-20%
1-2%
4-8%
20-40%
5-30%
6-40%
Sacco R. In Gorelick P, Alber M. handbook of Neuroepidemiology, New York, NY, Marcel Dekker Inc, 1994:77-19
G. Gubitz
High Blood Pressure
• The most important modifiable risk factor (2-5 x)
• Ischemic (primary and secondary), bleeding, “silent
strokes”
• Contributes to:
– Large-vessel atherosclerotic disease
– Small-vessel (lacunar) disease
– LV dysfunction and Afib
• Untreated HTN increases stroke risk 3-4 times. Treatment
can reduce stroke risk and fatalities ~40%.
• Most patients require 2 or more agents
• CHEP guidelines
– <140/90 (or if diabetes <130/80)
Acute BP Therapy
•Randomized controlled trials have not defined the
optimal time to initiate blood pressure lowering
therapy after stroke or transient ischemic attack.
•It is recommended that blood pressure lowering
treatment be initiated (or modified) prior to
discharge from hospital.
– For patients with nondisabling stroke TIA not requiring hospitalization, blood
pressure lowering treatment should be initiated (or modified) at the time of
the first medical assessment
Acute Hypertension Management
• AHA guidelines
– Lower only if > 220/120 mmHg
• or 185/110 for rt-PA
– Labetalol 10-20 mg IV q 10-20 min (or
nitroprusside infusion)
– Goal is 15-25% reduction within first 24hrs
Adams et al. Guidelines for the early management of adults with ischemic stroke. A guideline from the AHA/ASA stroke council… Stroke 2007;38:1655-1711.
Acute Hypertension Management
• But remember, impaired auto-regulation is
relative
– If I’ve been walking around for 5 yrs with a BP
210/140, be careful about dropping it too much
• Your ischemic penumbra is depending on that pressure
• Use the AHA 15% rule!
Pathophysiology
 Metabolically active tissue
 15-20% CO
 Complete arrest of flow:
 15 sec: suppression of electric activity
 2-4 min: inhibition of synaptic excitability
 4-6 min: inhibition of electric excitability
 Normal CBF > 55ml/min/100 g
 CBF<18 ml/min/100 g: electric failure
 CBF < 8 ml/min/100g: membrane failure
Acute, not-catastrophic HTN
•Hold all antihypertensives for first 24 hours!
•Permissive hypertension
•Avoid holding anti-HTN those that will give rebound
hypertension or tachycardia (beta blockers).
•Can generally restart after 24-36 hrs, but be cautious about it
•Don’t restart them all at once
•Gradual reintroduction
BP Management
• Diuretics
• ACE-I
– ACE-I + Diuretic
– HOPE (2001 NEJM)
– PROGRESS (2001 Lancet)
• ARB Use
whatever it takes, it’s not how you
get there,
butfailure,
thatthe
you
get there.
Unlike patients
with heart
combination
of an ACE
– ARB+diuretic
•
inhibitor and ARB is not recommended for patients with stroke
• CCB
– Amlodipine (Norvasc)
• Alpha-blocker
• 6105 individuals from 172 centres in Asia, Australasia,
and Europe were randomly assigned active treatment
(n=3051) or placebo (n=3054).
• Active treatment comprised a flexible regimen based
on the ACE-I perindopril (4 mg daily), with the addition
of the diuretic indapamide at the discretion of treating
physicians.
• The primary outcome was total stroke (fatal or nonfatal). Analysis was by intention to treat.
Lancet 2001; 358: 1033–41
Lancet 2001; 358: 1033–41
PROGRESS (Lancet 2001)
• Conclusion: This blood-pressure-lowering regimen
reduced the risk of stroke among both hypertensive
and nonhypertensive individuals with a history of
stroke or transient ischaemic attack.
– Combination therapy with perindopril and indapamide
produced larger blood pressure reductions and larger risk
reductions than did single drug therapy with perindopril
alone.
– Treatment with these two agents should now be
considered routinely for patients with a history of stroke or
transient ischaemic attack, irrespective of their blood
pressure.
Arterial Hypotension in Acute Ischemic Stroke
• Luckily very rare
– ‘associated with an increased likelihood of an unfavorable outcome’
(AHA)
• If present, be very suspicious as there is usually an underlying
medical reason and actively search it out
– Internal hemmorage, sepsis, MI, arrythmia, aortic dissection
– DO NOT admit until explanation found
– Hypovolemia should be corrected with normal saline, and cardiac
arrhythmias that might be reducing cardiac output should be corrected
• Involve the appropriate services: medicine, vascular surgery, ICU
• Can consider dopamine as vasopressor agent, however,
1. If drug induced hypertension is used, close neurological and cardiac
monitoring is recommended (Class I, Level of Evidence C).
2. Drug-induced hypertension, outside the setting of clinical trials, is not
recommended for treatment of most patients with acute ischemic
stroke (Class III, Level of Evidence B).
BP Targets in Primary and
Secondary Prevention
• Primary prevention sBP <140 mm Hg , dBP < 90 mm Hg
• Secondary prevention BP target of less than 140/90 mm Hg
– ACE inhibitor + diuretic is preferred [Evidence Level B].
• BP lowering treatment is recommended for the prevention of
first or recurrent stroke in patients with DM sBP< 130 mm Hg
and dBP<80 mm Hg.
• BP lowering treatment is recommended for the prevention of
first or recurrent stroke in patients with nondiabetic chronic
kidney disease to < 130/80 mm Hg
ENOUGH WITH BLOOD PRESSURE...
Atrial Fibrillation: CHADS2
Atrial Fibrillation: CHADS2
JAMA, June 13, 2001—Vol 285, No. 22
Lancet Neurol 2007; 6: 981–93
Canadian Stroke Strategy: afib
• Patients with TIA or minor stroke and atrial
fibrillation should begin anticoagulation using
My
interpretation:
The utility
CHADS
score lies
outside he
warfarin
immediately
afterofbrain
imaging
has
realm
of neurology
(i.e. Target
GP’s, cardiologists,
excluded
intracranial
hemorrhage,
aiming for a target
internists).
All international
patient’s with afib
need to beratio
on coumadin
therapeutic
normalized
of 2 to 3.
after their first ischemic event.
[Evidence
Level
A]
•No distinction for afib vs. Flutter
•No difference if PAF vs continual afib with controlled
ventricular response.
WHAT ABOUT HEPARIN FOR ACUTE
STROKE? OR CRESCENDO TIA’S?
Anticoagulation
• International Stroke Trial
– 19,435 pts
•
•
•
•
ASA (300mg qd) + UFH (5000 or 12,500 U bid)
ASA alone
UFH alone
Neither
– Death at 14 days, death or dependency at 6 months
– Heparin led to fewer recurrent strokes at 14 days (2.9% vs 3.8%)
• Offset by an increase in ICH (1.2% vs 0.4%)
• No significant difference in death or non-fatal recurrent stroke (11.7%
vs 12.0%)
• AHA does not recommend its use, even in the setting of worsening
stroke.
IST Collaborative Group. The IST: a randomised trial of aspirin, subcutaneous heparin, both, or neither among 19 435 patients with acute ischemic
stroke. The Lancet 1997;349:1569-1581.
Carotid Stenosis
• Only if symptomatic from ipsilateral
carotid, and 70-99% stenosis, ideally
within 2 weeks (NNT = 3)
– Evidence Level A
• Carotid endarterectomy should be
performed by a surgeon with a known
perioperative morbidity and mortality of <
6% [Evidence Level A].
‘2 concordant noninvasive
imaging modalities’ before OR
Time Frame of Benefit for CEA
Pooled analysis
NASCET, ECST of
subgroups.
n=5,893
Lancet,2004
Symptomatic carotid stenosis
i. Carotid endartarectomy is recommended for selected patients
with moderate (50%–69%) symptomatic stenosis, and these
patients should be evaluated by a physician with expertise in
stroke management [Evidence Level A].
iii. Carotid stenting may be considered for patients who are not
operative candidates for technical, anatomic or medical
reasons [Evidence Level C].
iv. Carotid endarterectomy is contraindicated for patients with
mild (< 50%) stenosis [Evidence Level A]
Asymptomatic carotid stenosis
• Carotid endarterectomy may be considered for
selected patients with asymptomatic 60%–99%
carotid stenosis.
– Patients should be less than 75 years old with a surgical
risk of < 3%, a life expectancy of > 5 years and be evaluated
by a physician with expertise in stroke management
[Evidence Level A]
• Dr. Cote & Minuk: maximal medical therapy.
– Don’t touch them!
Anti-Platelets
• Low-dose ASA prevention in people at risk
– increases GI bleed & hemorrhagic stroke risk.
– 75–160 mg daily as effective as higher doses.
• MATCH: bleeding higher w/ combined
ASA/Plavix (risk increases with long-term use)
• PROFESS: Aggrenox is not statistically
superior to Plavix
PROFESS
Frequency of Types of Recurrent Stroke among the Study Patients, According to Treatment
Group
Sacco R et al. N Engl J Med 2008;10.1056/NEJMoa0805002
Stroke 2008;39;1647-1652
Canadian Stroke Strategy
• All patients with transient ischemic attack or minor
stroke not on an antiplatelet agent at time of
presentation should be started on antiplatelet
therapy immediately [Evidence Level A]
• after brain imaging has excluded intracranial hemorrhage
– The initial dose of ASA should be at least 160 mg.
– For clopidogrel the loading dose is 300 mg.
• Conclusion:
Adding aspirin to clopidogrel in
high-risk patients with recent
ischaemic stroke or transient
ischaemic attack is associated
with a non-significant
difference in reducing major
vascular events.
However, the risk of
lifethreatening or major
bleeding is increased by the
addition of aspirin
Lancet 2004; 364: 331–37
Practical Treatment Algorithm
Not on anti-platelet
Plavix/Aggrenox > ASA 50-325 mg
ASA Allergic
Acute MI/Angina
PVD
DM
Plavix 75 mg
Dr. T. Wein, Montreal General Hospital
Practical Treatment Algorithm
On ASA
*Load or 5d
overlap with ASA
ASA/Dipyridamole
or
•If you want ASA + Clopidogrel (despite no st.
significant evidence for added protection), not
more than 3 months please [level B]
•No evidence for added protection in adding
an anti-platelet to someone on coumadin
•Subjecting them to added risk of life
threatening hemorrage
•Different stroke mechanism altogether
Plavix
Unstable Angina
PVD
Frequent Headaches
Acute MI
DM
Dr. T. Wein, Montreal General Hospital
Lipids
• 2x increased risk of stroke.
• Risk for CAD (which independently also increases
stroke risk).
• Lipid assessment
– Do it (FLP)
• Lipid management
Secondary target: CT/HDL < 4.0 mmol/L
– Ischemic stroke patients with LDL cholesterol of > 2.0 mmol/ L
should be managed with lifestyle modification and dietary
guidelines [Evidence Level A]
– Statin agents should be prescribed for most patients who have
had an ischemic stroke or TIA to achieve current recommended
lipid levels [Evidence Level A]
• SPARCL (NNT = 50)
• Randomly assigned 4731 patients who had a stroke or TIA
within 1-6 months before study entry, had LDL 2.6 to 4.9
mmol/L, and had no known coronary heart disease to doubleblind treatment with 80 mg of atorvastatin per day or
placebo.
• The primary end point was a first nonfatal or fatal stroke.
N Engl J Med 2006;355:549-59.
N Engl J Med 2006;355:549-59.
Conclusions from SPARCL
• In patients with recent stroke or TIA and without
known coronary heart disease, 80 mg of atorvastatin
per day reduced the overall incidence of strokes and
of cardiovascular events, despite a small increase in
the incidence of hemorrhagic stroke.
• LDL’s decreased by 50% in the atorvastatin group
compared to the placebo.
– Baseline = 3.43 (ator) vs. 3.45 (placebo)
– 1.89 vs. 3.32 mmol/L
100m/dL = 2.586 mmol/L
70 mg/dL = 1.81 mmol/L
Stroke 2008;39;1647-1652
Diabetes
• ~2x increased risk of stroke.
• Diabetes assessment [Evidence Level C]
– Test for it (fasting plasma glucose), or OGTT, HbA1c
• In ER, cerebrovascular clinic etc.
– Check lipids and BP at every visit
• Diabetes management
– Target HbA1c < 7% [Evidence Level A]
• Reduces microvascular complications > macrovascular
(DM1).
• Aim for fasting plasma glucose or preprandial plasma
glucose targets of 4.0 to 7.0 mmol/L
Other Modifiable Risk Factors
Smoking
• 2 –6 x risk (2x with second hand smoke only);
• One-time advice from physician results in 2% of smokers
quitting for >1 yr
• Strongly counselled to quit immediately, and be provided with
the pharmacologic and nonpharmacologic means to do so
[Evidence Level B]
– Nicotine replacement therapy and behavioural therapy
– consider nicotine replacement therapy, nortriptyline, nicotine
receptor partial agonist
Metabolic Syndrome
2-6x increased stroke risk
Lifestyle and risk factor management
• Healthy balanced diet
• Sodium
– For persons 9–50 years, the adequate Intake is 1500 mg.
Adequate Intake decreases to 1300 mg for persons 50–70
years and to 1200 mg for persons > 70 years. A daily upper
consumption limit of 2300 mg should not be exceeded by
any age group [Evidence Level B].
• Exercise
– Moderate exercise (an accumulation of 30 to 60 minutes)
of walking (ideally risk walking), jogging, cycling,
swimming or other dynamic exercise 4 to 7 days each
week in addition to routine activities of daily living
[Evidence Level A].
Lifestyle and risk factor management
• Alcohol consumption
– ≤ 2 standard drinks per day; and < 14 (M); and < 9
(F)drinks per week
Canadian Stroke Strategy
Components of acute inpatient care (new for 2008)
• Venous thromboembolism prophylaxis
–
Everyone
•
•
Oxygenation
–
–
•
Early and frequent, with PT
Continence
–
•
Treat if >38C and search for source
Mobilization
–
•
Screen for and treat
Temperature
–
•
Drops within 48hrs of stroke (multifactorial: central and peripheral reasons)
Maintain >92%
OSA
–
•
Mobilize early, maintain hydration, optimize anti-plt, compression stockings (no difference if pt using grduated
compression stockings or not according to CLOTS Lancet. 2009;373:1958-65), anticoagulants (LMWH, UFH)
Screen for UI, FI.
Nutrition, oral care, swallowing assessment
Rick Swartz ,U of T
Rick Swartz ,U of T
Bottom Line
• Recognize the severity TIA
–
–
–
–
Maximize medical therapy wherever you see the patient
Treat what is treatable / or correctible in the acute phase
Ensure appropriate follow-up
Be fluent with the major organizational guidelines and a few
landmark papers
• Try and standardize routine stroke care based on the
evidence (EBM)
• There is plenty to accomplish in stroke care after 4.5
hours, don’t be sad.
Top 7 symptoms unlikely to be TIA
1.
2.
3.
4.
5.
6.
7.
Postural dizziness alone
Tingling of all 4 extremities
Syncopal events
Momentary word finding trouble that is not new
Positional and recurrent numbness of one limb
Scintillating or flashing visual disturbances
Almost anything with hyperventilation or chest pain
Top 6 symptoms likely to be TIA
1. Vertigo only if present with brainstem symptoms
2. Hemibody numbness
3. Double vision, crossed numbness or weakness,
slurred speech, ataxia of gait
4. Monocular or hemifield visual loss (not blurring of
entire visual field)
5. Speech disturbance for a defined period of time
(definite dysarthria, muteness or marked word
finding difficulty, paraphasic speech)
6. Hemibody weakness
Special Thanks
•
•
•
•
•
•
Dr. M. Keezer
Dr. M. Ziller
Dr. T. Wein
Dr. Minuk
Dr. Côté
Canadian Resident’s Review Course in Stroke
– All particpants
• See References on each slide
Potential End-Points for TIA
SEMINARS IN NEUROLOGY/VOLUME 25, NUMBER 4 2005
FYI
• TOAST classification system
– It is logical to believe that both acute and preventive treatments can
and should be tailored to the underlying mechanism implicated.
ASPECTS:
Alberta Stroke Program Early CT scoring American
Journal of Neuroradiology 22:1534-1542 (9 2001)
Normal: 10 points. Substract one point for each area of
attenuation. Increased disability < 7.
• ▼stroke severity .
ASPECTS: Alberta Stroke Programme Early CT Score
• Quantitative alternative to 1/3 MCA exclusion criterion for rt-PA
(greater sensitivity and specificity for poor outcome)
– Normal: 10 points; -1 point for each area of hypoattenuation or focal swelling
• Increased disability ≤ 7.
Barber et al. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic
therapy. Lancet 2000;355:1670-1674.
ASPECTS: Alberta Stroke Programme Early CT Score
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Increased death & disability if ASPECTS ≤ 7
Increased death & disability if initial NIHSS >15.
Barber et al. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy.
The Lancet 2000;355:1670-1674.
BP and Long Term Outcome
Leonardi-Bee et al. Blood pressure and clinical outcomes in the International Stroke Trial. Stroke 2002; 33: 1315-1320.
Example #3
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56M
No PmHx
Non-smoker, no fam Hx
Last week while dragon-boating transiently described a
blurring / greying out of vision in L eye, followed by
moderate R sided pulsatile headache.
Visual disturbance resolved, as did H/A after 6 hours
No neck pain, and no chiropractic manipulation
No tinnitus
No motor deficits
On exam has a left L superior quadrantinopia (binocular)
What’s going on?
Is this a TIA/Stroke?