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TRANSCRIPT
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