South West Stroke Project

Case-Based Stroke Education Series

January 26, 2017

Moderator: Dr. Shanil Narayan

Consultant: Dr. G. Bryan Young

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

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

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 of 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

South West Stroke Project

Stroke Rounds Case 1

Dr Shanil Narayan

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

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

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

Patient A

What are our thoughts and concerns?

Patient A

Differential Diagnosis; Stoke (ischemic or hemorrhagic) vs. Seizure

What is time of Stroke onset?

What are high risk features?

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

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.

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 onset.

However, this probably excludes many wake-up stroke (WAS) patients from recanalization therapy.

BY’s Comments

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.

MR angio with Gadolium

Drop in signal intensity Deriving Flow Measure

MRA in Left Hemisphere Ischemic Stroke

CTA in Left Hemisphere Stroke

DW ADC FLAIR and CT perfusion in WUS

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

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

Hemorrhage after Thrombolysis (HAT score)

South West Stroke Project

Stroke Rounds Case 2

Dr Tom Haffner

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

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

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 on CT)

Plan?

Patient B

Apixiban 5mg BID started

Rosuvastatin 40mg started

Aphasia improves but doesn’t completely resolve

Further tests?

MRI

CT angio

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?

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?

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?

Risk factors for intracranial stenosis

Black, Hispanic, Asian

Age

Hypertension

Hyperlipidemia/dyslipidemia

Smoking

Diabetes

Mgmt of intracranial stenosis

ASA + plavix x 90 days

Statin

Lower BP

No role for stenting (SAMMPRIS trial)

Case discussed with neuro

ASA + Plavix x 2 months then,

• Risk stroke from stenosis > risk from afib?

ASA + apixiban for how long?

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-occluding 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

Symptomatic Intracranial Arterial Stenosis

• SAMMPRIS study (NEJM 2011) showed worse outcome 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.

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 of 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

South West Stroke Project

Stroke Rounds Case 3

Dr. Ali Alnoor Kara

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

Medications:

Atorvastatin 40mg PO Daily

Gliclazide MR 60mg PO Daily

Allergies: NKDA

SHx: Retired RN

Smoking: nil

Alcohol: occasional glass of wine

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

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

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

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

Reviewed case with TeleStroke Consultant

Felt that there was an occlusion in M2 branch on 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.

Patient C’s face distraught when she was told that she would not receive tPA

Patient C was absolutely beside herself when she heard.

Dilemma

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

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.

Discussion

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 of hemorrhagic transformation, we could safely administer tPA.

Timeline

Symptom Onset: 1530h

Arrival to SGH: 1650h

TeleStroke Activation: 1700h

CT Head: 1708h

Initial Discussion with TeleStroke: 1733h

tPA Administration Time: 1754h

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).

I fully agree with thrombolysing: the stroke was too remote to worry about hemorrhagic transformation (our guidelines are 3 months or 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

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

A S P E C T S SCORE

28/02/2014 Grand Rounds

What is the ASPECTS score?

TIAs and Nondisabling Strokes

Transient Ischemic Attack Definition

• “Brief episode of neurologic dysfunction caused by focal brain or 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”

MRI in Acute Ischemic Stroke

South West Stroke Project

Case-Based Stroke Education Series

January 26, 2017

Moderator: Dr. Shanil Narayan

Consultant: Dr. G. Bryan Young