Case-Based Stroke Education Series January 26, 2017 Moderator: Dr. - - PowerPoint PPT Presentation

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Case-Based Stroke Education Series January 26, 2017 Moderator: Dr. - - PowerPoint PPT Presentation

South West Stroke Project Case-Based Stroke Education Series January 26, 2017 Moderator: Dr. Shanil Narayan Consultant: Dr. G. Bryan Young Faculty/Presenter Disclosure Faculty: Dr. Bryan Young, Dr. Shanil Narayan, Dr. Ali Kara, Dr. Tom


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South West Stroke Project

Case-Based Stroke Education Series

January 26, 2017 Moderator: Dr. Shanil Narayan Consultant: Dr. G. Bryan Young

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SLIDE 2

Faculty:

  • Dr. Bryan Young, Dr. Shanil Narayan, Dr. Ali Kara,
  • Dr. Tom Haffner

Relationships with commercial interests: No actual or potential conflicts of interest in relation to this educational program

Faculty/Presenter Disclosure

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SLIDE 3

This program has received financial support from:

South West Local Health Integration Network – Ontario Ministry of Health and Long-Term Care

Potential for conflict(s) of interest:

  • Planning committee member, Dr. Gord Schacter
  • Member of Lundbeck Advisory Board
  • Participated in the following clinical trials in the past two years:

Novartis, Sanofl Aventis, Bristol Myers Squib

  • Planning committee member, Dr. Paul Gill
  • Participated in the following clinical trial in the past two years: DETECT

study

Disclosure of Commercial Support

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SLIDE 4
  • The Planning Committee mitigated bias by ensuring there

was no industry involvement in the planning or the education content.

  • To comply with accreditation requirements of the College
  • f Family Physicians of Canada and The Royal College of

Physicians and Surgeons of Canada, speakers were provided with Declaration of Conflict of Interest forms, which were reviewed by the Regional Stroke Education Coordinator on behalf of the Planning Committee and submitted to the Western University’s CPD Office.

  • The Planning Committee reviewed the initial presentation

supplied by the speaker to ensure no evidence of bias.

Mitigating Potential Bias

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SLIDE 5

South West Stroke Project

Stroke Rounds Case 1

Dr Shanil Narayan

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SLIDE 6

Patient A

  • 84 M seen in ER for suspected R MCA infarct
  • PMH
  • Hyperchol, Afib. Prev CVA (2014)
  • L weakness previously “almost completely recovered”
  • MEDS
  • Coumadin
  • Ramipril, Lipitor
  • Non smoker
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SLIDE 7

Patient A

  • Initially described by paramedics as L sided.
  • Described by ER MD as minimally responsive and

unclear if focal weakness 0530

  • Awoke around 0300 “unwell” but nothing focal

described – Back to bed 0330

  • Wife checked on him at 0500 and unable to speak

and not moving L side. 911 activated

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SLIDE 8

Patient A

  • In ER Severe Expressive Aphasia + NIH 26
  • CT head
  • previous R MCA stroke with Encephalomalacia.
  • Old lacunar infact l. Lentiform nucleus.
  • No retrievable clot.
  • CBC N. INR 1.5. Glucose 8.7
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SLIDE 9

Patient A

  • What are our thoughts and concerns?
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SLIDE 10

Patient A

  • Differential Diagnosis; Stoke (ischemic or

hemorrhagic) vs. Seizure

  • What is time of Stroke onset?
  • What are high risk features?
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SLIDE 11

Risks of Thrombolysis

  • Complications related to intravenous r-tPA (average)
  • symptomatic intracranial hemorrhage 6%
  • major systemic hemorrhage 2%
  • angioedema 5%
  • 3 - 4.5 hour window “relative? contraindications”
  • Patient is < 80 years of age
  • Patient does not have a history of both diabetes AND stroke
  • Patient is not taking Warfarin (Coumadin) or any other anticoagulant regardless of

INR/coagulation results

  • NIHSS is < 25
  • Written informed consent obtained from patient and/or family – required when IV

tPA given within the 3-4.5 hour window.

  • Scoring systems?
  • HAT (Hemorrhage after Thrombolysis)
  • iScore
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SLIDE 12

Patient A

  • tPA 0630 (3 hours after last seen normal)
  • Rapid improvement
  • Day 1 family and patient thought “back to

normal”

  • Singular concern was some impulsivity
  • Strong family supports
  • Discharged home on Day 3 with community

stroke team.

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SLIDE 13
  • Whew! Controversial case. Dodged a bullet?
  • Of ischemic stroke patients about 20% waken

with the stroke.

  • Clinically we go with “last time seen well” or

“without any new deficits” for timing stroke

  • nset.
  • However, this probably excludes many wake-

up stroke (WAS) patients from recanalization therapy.

BY’s Comments

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SLIDE 14

Assessing Suitable WAS Patients if time of onset not clear

  • Requires neuro-imaging:
  • MR:
  • perfusion-diffusion mismatch
  • DWI/ADC vs. FLAIR
  • CT angiography: CT vs CBF/CT perfusion vs CBV.
  • Requires protocols and full cooperation of

radiology/neuroradiology and intervention (if EVT attempted)

  • Trials still ongoing – stay tuned.
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SLIDE 15

MR angio with Gadolium

Drop in signal intensity

Deriving Flow Measure

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SLIDE 16

MRA in Left Hemisphere Ischemic Stroke

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CTA in Left Hemisphere Stroke

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DW ADC FLAIR and CT perfusion in WUS

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  • Was he really in usual health at 0300h?
  • Neurological exam: expressive aphasia or

muteness (right hemisphere stroke)?

  • No absolute contraindication to tPA but very

close to the 3-4.5 hour window, for which he would be excluded: age, on anticoagulant (even with subtherapeutic INR).

In Patient A’s Case

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SLIDE 20

THROMBOLYSIS

Treatment expanded to 4.5h (NINDS

rtPA Stroke Study/ECASSIII)

For >3hrs thrombolysis is considered except for : age >80yr, NIHSS >25, any anticoagulation use; hx of previous stroke + diabetes m. Expansion of window provides modest yet clinically worthwhile improvements rtPA (alteplase) 0.9 mg/kg with 10% given in 1 minute and the remainder over 1 hour NIHSS

EARLIER TREATMENT = BETTER OUTCOME

Grand Rounds

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Hemorrhage after Thrombolysis (HAT score)

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South West Stroke Project

Stroke Rounds Case 2

Dr Tom Haffner

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Patient B

  • 68 Caucasian M seen in ER for suspected L MCA infarct

(outside of window)

  • Expressive aphasia, sudden onset 2 days ago
  • PMH
  • Afib, prev ablation (2014)
  • “complex migraine” presenting with aphasia 2014
  • MEDS
  • ASA
  • Propranolol (for “migraines”)
  • Non smoker
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Patient B

  • Expressive aphasia on exam
  • Neurological exam otherwise normal
  • Afib on the monitor and EKG
  • CT head (non-contrast):
  • No acute infarct
  • No old infarct
  • Small vessel ischemic changes
  • Carotid ultrasound
  • Stable mild plaque bilaterally
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SLIDE 25

Patient B

  • LDL 3.11 TC: 4.62 HDL 0.87
  • Echo:
  • Dilated LA
  • No thrombus
  • EF normal

CHADS = 3 (presumed TIA/small stroke not seen

  • n CT)

Plan?

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SLIDE 26

Patient B

  • Apixiban 5mg BID started
  • Rosuvastatin 40mg started
  • Aphasia improves but doesn’t completely

resolve Further tests?

  • MRI
  • CT angio
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SLIDE 27

Comes back …

  • 2 weeks later. Ongoing spells of sudden

worsening of expressive aphasia which resolve after 30min.

  • flashing lights preceding the events?
  • Pt convinced “complex migraine” but doesn’t get

better with propranolol + candesartan

  • Also, felt to have some right sided neglect by OT
  • Compliant with meds
  • CT head repeated
  • No acute infarct
  • Now what?
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SLIDE 28
  • Ophthamology removes foreign body in eye
  • MRI head
  • Acute infarction in territory of left MCA consistent

with embolic source

  • No other areas of infarction
  • Change mgmt?
  • Failure of apixiban?
  • Add ASA?
  • Alternative diagnosis?
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SLIDE 29
  • CT angiogram
  • Severe stenosis in M1 of left MCA (8mm x 4mm)
  • Discussion points:

1. Should I have ordered CT angio up front?

  • Carotids only mild dx.
  • Probable cause of stroke (afib)
  • Expensive to do CT angio for every stroke pt

2. When should you think about intracranial stenosis? 3. How do you manage intracranial stenosis + Afib and recent stroke

  • ASA + plavix?
  • Abixiban + ASA?
  • Stent?
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Risk factors for intracranial stenosis

  • Black, Hispanic, Asian
  • Age
  • Hypertension
  • Hyperlipidemia/dyslipidemia
  • Smoking
  • Diabetes
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Mgmt of intracranial stenosis

  • ASA + plavix x 90 days
  • Statin
  • Lower BP
  • No role for stenting (SAMMPRIS trial)
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  • Case discussed with neuro
  • ASA + Plavix x 2 months then,
  • Risk stroke from stenosis > risk from afib?
  • ASA + apixiban for how long?
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SLIDE 33
  • Migraine is always a diagnosis of exclusion with a

stroke syndrome.

  • DDx between cardioembolic vs artery origin. Was

the MCA stenosed or did it contain a non-

  • ccluding embolus (partly recanalized?)
  • Fairly low CHADS2 score: risk of stroke probably

about 1.9%/year if stroke not cardioembolic and >8%/year if its was.

  • Risk of stroke from intracranial MCA stenosis: 4-

9% at 3 months, 8-12% at 1 year with medical management (SAMMPRIS study)

Patient B: BY Comments

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SLIDE 34

Symptomatic Intracranial Arterial Stenosis

  • SAMMPRIS study (NEJM

2011) showed worse

  • utcome for stented

patients cf medically managed group.

  • Endarterectomy not

feasible.

  • EC-IC bypass was shown to

be futile (NEJM, 1985).

  • Therefore no procedural

intervention is of value.

  • Antiplatelets and control of

risk factors are indicated.

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SLIDE 35
  • Intracranial arterial stenosis carries a high risk

for ischemic stroke. Therefore, CTA (arch to vertex)or MRA is recommended for all ischemic strokes and TIAs.

  • Antiplatelets are indicated along with control
  • f risk factors (no stenting or EC-IC bypass!).
  • A fib is worrisome, especially since we cannot

be certain of source of stroke. Might anticoagulate as well.

Patient B: BY comments

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South West Stroke Project

Stroke Rounds Case 3

  • Dr. Ali Alnoor Kara
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Patient C

  • 71F from home with husband
  • RFR: Witnessed R sided facial droop and expressive

aphasia at 1530h by husband

  • PMHx:
  • T2DM
  • Dyslipidema
  • Previous Stroke in 2012 - no residual deficits
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SLIDE 38
  • Medications:
  • Atorvastatin 40mg PO Daily
  • Gliclazide MR 60mg PO Daily
  • Allergies: NKDA
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SLIDE 39
  • SHx: Retired RN
  • Smoking: nil
  • Alcohol: occasional glass of wine
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  • HPI: Sudden-onset R sided facial droop and

expressive aphasia at 1530h, witnessed by husband.

  • No antecedent symptoms or problems

reported.

  • EMS called and immediately brought to

SGH on Stroke Protocol

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SLIDE 41
  • Initial Assessment:
  • T 36.7; HR: 118 bpm (sinus tachycardia); BP:

174/97 mmHg; SpO2 97% (R/A); BG 8.9

  • NIHSS: 5
  • Right-sided facial droop
  • Expressive aphasia
  • Dysarthria
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SLIDE 42
  • Hyperacute CT Head:
  • No acute infarct;
  • No evidence of hemorrhage;
  • Remote infarct in L parietal-occipital region

(unchanged from 2013);

  • No identifiable clot amenable for endovascular

therapy (reported by Radiology)

  • No other contraindication for tPA

administration

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SLIDE 43
  • The remainder of the investigation were

within normal limits, and no other “absolute" contraindications to the administration of tPA were identified

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  • Reviewed case with TeleStroke Consultant
  • Felt that there was an occlusion in M2 branch
  • n L side (not amenable to endovascular

therapy) and evidence of an old posterior branch infarct.

  • Recomendation was not to proceed with tPA

because of the location of the old stroke (? related to new symptoms), and risk of hemorrhagic transformation.

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  • Patient C’s face distraught when she was

told that she would not receive tPA

  • Patient C was absolutely beside herself

when she heard.

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Dilemma

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  • I had reviewed with the patient and her

husband at bedside the risks/benefits of tPA

  • NIHSS score wasn’t terribly high
  • the deficits she had were extremely distressing

for her and would be a major disability for her.

  • Her husband said that “she would die if she would

never be able to speak again, Doc!”

  • Patient C emphatically nodded her head at that

statement, with tears streaming down her face

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SLIDE 48
  • If she had presented prior to the launch of

TeleStroke

  • based on what I was told by Radiology

regarding no absolute C/I to tPA

  • given the clinical context described
  • we would have proceeded with tPA

administration.

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SLIDE 49

Discussion

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  • I contacted the Consultant again to re-

review the case, and see if there was any chance she would be an acceptable candidate for tPA.

  • The Consultant had just finished re-

reviewing the images, and felt that as long as the family knew there was a higher risk

  • f hemorrhagic transformation, we could

safely administer tPA.

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Timeline

  • Symptom Onset: 1530h
  • Arrival to SGH: 1650h
  • TeleStroke Activation: 1700h
  • CT Head: 1708h
  • Initial Discussion with TeleStroke: 1733h
  • tPA Administration Time: 1754h
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Outcome

  • On discharge, she had resolution of her facial

droop with some degree of residual dysarthria, but was able to articulate intelligibly, and was safe to swallow all consistencies.

  • She preferred ongoing follow-up close to the

centre that she was from (who had Outpatient Stroke Rehab Capabilities).

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SLIDE 53
  • I fully agree with thrombolysing: the stroke

was too remote to worry about hemorrhagic transformation (our guidelines are 3 months

  • r less for contraindicating thrombolysis).
  • She was not “too good to thrombolyse”.

Aphasia is a serious disability. Don’t rely on NIHSS score alone in making decision.

Patient C: BY comments

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  • Relative contraindication: Previous stroke or

severe head injury within 3 months? (Original NINDS trail 1995)

  • Contraindication: For >3 hour time previous

stroke + DM (ECASS III)

  • Previous ICH – depends if vascular lesion

treated; microbleeds not a contraindication.

  • Territory and size of stroke (ASPECTS 7 or less)

Decisions re: Thrombolysis

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A S P E C T S SCORE

28/02/2014 Grand Rounds

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What is the ASPECTS score?

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TIAs and Nondisabling Strokes

Transient Ischemic Attack Definition

  • “Brief episode of

neurologic dysfunction caused by focal brain

  • r retinal ischemia, with

clinical symptoms typically lasting less than one-hour and without evidence of acute infarction”.

  • Risk of subsequent

stroke is similar for TIAs and nondisabling stroke. Many “TIAs” are “ministrokes”

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MRI in Acute Ischemic Stroke

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South West Stroke Project

Case-Based Stroke Education Series

January 26, 2017 Moderator: Dr. Shanil Narayan Consultant: Dr. G. Bryan Young