Approach to TIA and Management of Stroke after 4.5 hours - PowerPoint Presentation

Approach to TIA and Management of Stroke after 4.5 hours Robert Altman R4 McGill University August 25 th 2010 Summer Emergency Lecture Series

What to take out of today. Everything I’m presenting is evidence basedWhere 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 DefinitionTIADdx and TIA mimics Review of ABCD 2 score 48 hr cerebrovascular risk stratificationWho to admit and who can be dischargedSubacute management of ischaemic arterial stroke (and TIA for that matter)Practical aspects and highlights of frequently cited studiesTopics: 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 diagnosisDelays intervention in cases of true brain ischemiaDiverges 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. >7 days indicate infarction and received the designation stroke1970s Great preponderance of events lasting 24hrs-7d were a/w infarction, rendering the RIND obsoleteMore 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) These findings highlight an inconsistency between the concept of TIA (ischemia causing symptoms but no infarction) and the traditional definition of TIA

Transient Ischemic Attack Tides have turnedTime (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 monthshalf occurring within 48 hoursWhen recurrent TIAs, myocardial infarction and death from any cause are considered, the risk is more than 25% over the first 3 months. Mortality5-6 % annually, mainly by MI Early recognition of TIA and subsequent timely intervention is of critical and obvious importance.

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 NeurologicalFocalSuddenLocalizable to an anatomical structure in the CNS or retina

Immediate Management Get a real historyCarefully 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 recoveryHusband 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. IntubatedExam 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 MHx 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-upWhat is the critical information to garner from a TIA evaluation Age, sex PmHx : afib or PAF, prior TIA or CVA, CAD or recent MI, smoker, famHx of premature CVASymptoms: only motor, sensory, speech or bothBP and ECG rythm Total duration of symptoms (5 min?, 25 min? 24 hrs?)When? (today, yesterday, 6 months ago?)

=ABCD2 Criteria Points 48 hour stroke risk 90 day stroke risk A ge > 60 1 0-1 = 0% 2-3 = 1.3% 4-5= 4.1% 6-7 = 8.1% Approx 25% if score 6-7 B P = sBP > 140 or dBP > 90 1 C linical Unilateral weakness Speech, without weakness 2 1 D uration 0-10 min 10-59 min >59 min 0 1 2 D iabetes Mellitus 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. 2Expedited 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

Lancet. 2007 Oct 20;370(9596):1432-42 Statin Clopidogrel 1 anti-HTN Rx 2 anti-HTN Rx’s Cumulative proportions of patients prescribed new medication

What is the Recommended TIA Work-Up?

FYI TOAST classification systemAcute 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-) Vascular imaging ( extracranial & intracranial)*CUSCTA (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 *local strengths in that expertise in vascular imaging dictate what to select as first line (also other medical conditions i.e. PM or RF)

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 onsetFocal L hemiparesisDysarthria 45 min ago Anti-platelet?

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 ]Canadian Stroke Strategy

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 weeks ago hours ago Duration sec – few minutes >10 min Frequency multiple one to few Sensory yes alone no Motor no yes Speech no yes Risk factors no HTN, DM, Deficit dynamics Mild at onset Severe at onset Benign Malignant

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 3 rd most important cause of death after heart disease and cancerMost important cause of adult disability 30% of survivors require daily assistance.

Clinical Presentation SuddenFocal weakness, language impairment, gaze deviation, hemianopiaNeuroanatomically based Search for warning symptoms in week prior Amaurosis fugaxSentinel TIA’s

Modifiable Risk Factors for Ischemic Stroke Stroke Risk Factors Estimated RR Estimated Prevalence Hypertension 3.0-5.0 25-40% Cardiac Disease 2.0-4.0 10-20% Atrial Fibrillation 4.0-18.0 1-2% Diabetes Mellitus 1.5-3.0 4-8% Smoking 1.5-2.5 20-40% Alcohol Abuse 1.0-4.0 5-30% Hyperlipidemia 1.0-2.0 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 ) diseaseLV dysfunction and AfibUntreated HTN increases stroke risk 3-4 times. Treatment can reduce stroke risk and fatalities ~40%.Most patients require 2 or more agentsCHEP 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 Ischemic PENUMBRA

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 DiureticsACE-IACE-I + DiureticHOPE (2001 NEJM) PROGRESS (2001 Lancet) ARB ARB+diuretic Unlike patients with heart failure, the combination of an ACE inhibitor and ARB is not recommended for patients with strokeCCBAmlodipine (Norvasc)Alpha-blocker Use whatever it takes, it’s not how you get there, but that you get there.

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 non-fatal). 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 outInternal hemmorage, sepsis, MI, arrythmia, aortic dissectionDO NOT admit until explanation found Hypovolemia should be corrected with normal saline, and cardiac arrhythmias that might be reducing cardiac output should be correctedInvolve the appropriate services: medicine, vascular surgery, ICUCan 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 HgACE 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

Patients with TIA or minor stroke and atrial fibrillation should begin anticoagulation using warfarin immediately after brain imaging has excluded intracranial hemorrhage , aiming for a target therapeutic international normalized ratio of 2 to 3. [Evidence Level A] Canadian Stroke Strategy: afib My interpretation : The utility of CHADS score lies outside he realm of neurology (i.e. Target GP’s, cardiologists, internists). All patient’s with afib need to be on coumadin after their first ischemic event. 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 aloneUFH aloneNeitherDeath 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 Lancet,2004 Pooled analysis NASCET, ECST of subgroups. n=5,893

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

Sacco R et al. N Engl J Med 2008;10.1056/NEJMoa0805002 PROFESS Frequency of Types of Recurrent Stroke among the Study Patients, According to Treatment Group

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 hemorrhageThe 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 Plavix 75 mg ASA Allergic Acute MI/Angina PVD DM Dr. T. Wein , Montreal General Hospital

Practical Treatment Algorithm On ASA ASA/ Dipyridamole or Plavix Unstable Angina PVD Frequent Headaches Acute MI DM Dr. T. Wein , Montreal General Hospital 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 *Load or 5d overlap with ASA

Lipids 2x increased risk of stroke. Risk for CAD (which independently also increases stroke risk). Lipid assessment Do it (FLP) Lipid managementIschemic 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 ) Secondary target: CT/HDL < 4.0 mmol /L

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 double-blind 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

Stroke 2008;39;1647-1652 100m/ dL = 2.586 mmol /L 70 mg/ dL = 1.81 mmol /L

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 visitDiabetes managementTarget 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 Smoking2 –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 therapyconsider nicotine replacement therapy, nortriptyline, nicotine receptor partial agonist

Metabolic Syndrome2-6x increased stroke risk

Lifestyle and risk factor management Healthy balanced dietSodiumFor 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].ExerciseModerate 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

Components of acute inpatient care (new for 2008)Venous thromboembolism prophylaxisEveryoneMobilize 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)OxygenationDrops within 48hrs of stroke (multifactorial: central and peripheral reasons)Maintain >92%OSA Screen for and treatTemperatureTreat if >38C and search for sourceMobilization Early and frequent, with PT Continence Screen for UI, FI. Nutrition, oral care, swallowing assessment Canadian Stroke Strategy

Rick Swartz ,U of T

Rick Swartz ,U of T

Bottom Line Recognize the severity TIAMaximize 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 Postural dizziness alone Tingling of all 4 extremities Syncopal events Momentary word finding trouble that is not new Positional and recurrent numbness of one limbScintillating or flashing visual disturbances Almost anything with hyperventilation or chest pain

Top 6 symptoms likely to be TIA Vertigo only if present with brainstem symptoms Hemibody numbness Double vision, crossed numbness or weakness, slurred speech, ataxia of gait Monocular or hemifield visual loss (not blurring of entire visual field)Speech disturbance for a defined period of time (definite dysarthria, muteness or marked word finding difficulty, paraphasic speech)Hemibody weakness

Special Thanks Dr. M. KeezerDr. M. Ziller Dr. T. Wein Dr. Minuk Dr. CôtéCanadian Resident’s Review Course in StrokeAll particpantsSee References on each slide

Potential End-Points for TIA SEMINARS IN NEUROLOGY/VOLUME 25, NUMBER 4 2005

FYI TOAST classification systemIt 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.

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. ASPECTS : Alberta Stroke Programme Early CT Score Increased death & disability if ASPECTS ≤ 7 Increased death & disability if initial NIHSS >15.

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 56MNo 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 hoursNo neck pain, and no chiropractic manipulationNo tinnitusNo motor deficitsOn exam has a left L superior quadrantinopia (binocular)What’s going on?Is this a TIA/Stroke?