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The Code
Stroke
Handbook
The Code Stroke
Handbook
Approach to the
Acute Stroke Patient
ANDREW MICIELI, MD
Senior Neurology Resident, University of Toronto, Toronto, ON, Canada

RAED JOUNDI, MD, DPhil, FRCPC

Neurologist and Stroke Fellow, University of Calgary, Calgary, AB, Canada

HOUMAN KHOSRAVANI, MD, PhD, FRCPC

Assistant Professor, Division of Neurology, Department of Medicine,
University of Toronto, Toronto, ON, Canada
Division of Neurology, Department of Medicine, Hurvitz Brain Sciences
Program, and Regional Stroke Centre, Sunnybrook Health Sciences Centre,
Neurology Quality and Innovation Lab (NQIL), Toronto, ON, Canada

JULIA HOPYAN, MBBS, FRACP, FRCPC

Assistant Professor, Division of Neurology, Department of Medicine,
University of Toronto, Toronto, ON, Canada
Division of Neurology, Department of Medicine, Hurvitz Brain Sciences
Program, and Regional Stroke Centre, Sunnybrook Health Sciences Centre,
Toronto, ON, Canada

DAVID J. GLADSTONE, BSc, MD, PhD, FRCPC

Associate Professor, Division of Neurology, Department of Medicine,
University of Toronto, Toronto, ON, Canada
Division of Neurology, Department of Medicine, Hurvitz Brain Sciences
Program, and Regional Stroke Centre, Sunnybrook Health Sciences Centre,
and Sunnybrook Research Institute, Toronto, ON, Canada
Academic Press is an imprint of Elsevier
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by the Publisher (other than as may be noted herein).

Notices
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experience broaden our understanding, changes in research methods, professional
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Practitioners and researchers must always rely on their own experience and knowledge
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ISBN: 978-0-12-820522-8

For information on all Academic Press publications

visit our website at https://www.elsevier.com/books-and-journals

Publisher: Nikki Levy

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Cover Image: Andrew Micieli

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Preface

A 65-year-old patient arrives at the Emergency

Department with stroke symptoms that began
45 min ago. You are called STAT!
Acute stroke management has changed dramatically
in recent years. Tremendous advances have been made in
acute treatments, diagnostic neuroimaging, and organized
systems of care, and are enabling better outcomes for pa-
tients. Stroke has evolved from a largely untreatable condi-
tion in the acute phase to a true medical emergency that
is potentially treatable—and sometimes curable. The Code
Stroke Emergency Response refers to a coordinated team-
based approach to stroke patient care that requires rapid
and accurate assessment, diagnosis, and treatment in an ef-
fort to save the brain and minimize permanent damage.
The Code Stroke Handbook contains the “­essentials”
of acute stroke to help clinicians provide best practice
patient care
Designed to assist frontline physicians, nurses, paramed-
ics, and medical learners at different levels of training, this
book highlights clinical pearls and pitfalls, guideline recom-
mendations, and other high-yield information not readily
available in standard textbooks. It is filled with practical tips
to prepare you for the next stroke emergency and reduce
the anxiety you may feel when the Code Stroke pager rings.
❏ An easy-to-read, practical clinical resource spread over
12 chapters covering the basics of code stroke consul-
tations—history taking, stroke mimics, neurological ex-
amination, acute stroke imaging (noncontrast CT/CT
ix
x Preface

angiography/CT perfusion), and treatment (thrombol-

ysis and endovascular therapy).
❏ Includes clinical pearls and pitfalls, neuroanatomy
­diagrams, and stroke syndromes, presented in an easily
digestible format and book size that is convenient to
carry around for quick reference when on-call at the
hospital.
❏ Provides foundational knowledge for medical students
and residents before starting their neurology, emer-
gency medicine, or internal medicine rotations.
This book is dedicated to our patients with stroke, their
families, and our colleagues, teachers, and mentors who
have taught us so much.
We hope you enjoy this book.

Andrew Micieli
Raed Joundi
Houman Khosravani
Julia Hopyan
David J. Gladstone
Acknowledgments

Andrew Micieli has no academic acknowledgments.

Dr. Joundi’s stroke fellowship is funded by the Canadian
Institutes of Health Research. Dr. Khosravani is supported
by the Department of Medicine, Sunnybrook Health
Sciences Centre; University of Toronto Centre for Quality
Improvement and Patient Safety; and Thrombosis Canada.
Dr. Hopyan is supported by the Department of Medicine,
Sunnybrook Health Sciences Centre. Dr. Gladstone is
­supported by the Department of Medicine, Sunnybrook
Health Sciences Centre; the Bastable-Potts Chair; the Tory
family; and a Mid-Career Investigator Award from the
Heart and Stroke Foundation of Canada.

xi
CHAPTER 1

History taking

Beep…Beep…Beep
CODE STROKE in the Emergency Department,
Acute zone bed 10.
Welcome to the code stroke; let’s get started.

The initial assessment of the code stroke patient involves

identifying whether the clinical presentation is compatible
with an acute stroke diagnosis or a stroke mimic. The first two
chapters of this book will help answer this question. Like a
good detective, you need to gather the important clues, ig-
nore distractions and red herrings, and eliminate the other
suspects—all in a timely manner. This chapter will provide
you with a stepwise approach to:
❏ Taking an appropriate and focused history by gathering
relevant clinical information from multiple sources.
❏ Identifying the common symptoms associated with (and
not associated with) acute stroke.
Chapter 2 will discuss various stroke mimics and how to clin-
ically differentiate them.

Early stroke symptom recognition is important

to facilitate rapid transfer to a stroke center. Regional
Emergency Medical Services (EMS) have protocols in
place to identify and prioritize potential stroke cases,

The Code Stroke Handbook © 2020 Elsevier Inc. All rights reserved.
https://doi.org/10.1016/B978-0-12-820522-8.00001-6 1
2 The Code Stroke Handbook

and try to minimize transportation time to the most

­appropriate stroke c­ enter. The mnemonic FAST, which
stands for Face (sudden facial droop), Arm (sudden uni-
lateral arm weakness), Speech (sudden speech difficulty),
and Time to call EMS, is being used to promote public
awareness. Most prehospital stroke screening tools involve
some combination of these cardinal symptoms.
It has been estimated that nearly two million neurons
die each minute that elapses during the evolution of
an average acute ischemic stroke. Each hour without
treatment the brain loses on average as many neurons as
3.6 years of normal aging. This is captured by a commonly
used phrase “time is brain.”

Ideal stroke treatment targets

❏ Door-to-needle time for intravenous tissue plasmin-
ogen activator (tPA): < 30 min
❏ Door-to-groin puncture time for endovascular therapy:
< 60 min
Disability decreases with quicker treatment; therefore, aim for
the fastest assessment for potential brain-saving or lifesaving
treatment.

For the resident physcian or medical student on call,

the first task is a simple one: write down the time you
first received the code stroke page. There are many other
time-related parameters that you may need to document
throughout the code stroke, including time of patient ar-
rival, time of the first CT scan slice, and time of tPA admin-
istration. This becomes important later when calculating
door-to-CT scan time or door-to-needle time. After all, the
quicker a stroke patient is treated, the more likely they are
to have a functionally independent outcome.
 History taking 3

Regional variations exist in terms of code stroke triage

in the emergency department (ED). Depending on the hos-
pital, the pager may notify you where the stroke patient is in
the ED (or on the inpatient hospital ward), or you may need
to call the number on the pager to confirm you received
the page, ask the location of the stroke patient, and their
estimated time of arrival if they are not already in the ED.
Sometimes the ED charge nurse will have some ad-
ditional information for you. This prenotification clini-
cal information can vary in terms of how detailed it is.
Sometimes it is very detailed with a high pretest probabil-
ity for stroke, such as:
We have a 76-year-old woman from home with a witnessed
onset at 1500 hours of aphasia and right face, arm and leg
weakness.

At other times, the clinical information is vague and

undifferentiated, such as:
“85-year-old man with confusion.” This could be a number
of neurological or non neurological conditions (more on
stroke mimics to come in Chapter 2).

Not all activated code strokes are from the ED.

Inhospital strokes (i.e., a patient admitted to the ward) also
occur, though with less frequency. Your approach to the
patient should be the same. Often, the patient's medical
comorbidities or recent surgery precludes the use of tPA.
Once the code stroke is activated, many different people
are set in motion (even before the stroke resident/staff make
their way to the patient). The first step is a rapid assessment
and rushing the patient to the CT scanner as quickly as pos-
sible. In some hospitals, prior to the CT scan, the nurses will
insert two cubital fossa IV lines, complete a 12-lead ECG, and
draw urgent bloods that are sent stat for: CBC, ­electrolytes,
4 The Code Stroke Handbook

creatinine, coagulation profile, random blood glucose level,

troponin and type and screen. This blood work will help
with treatment decisions and contraindications to tPA.
You have now made your way to the stroke patient in
the ED. Like any acute situation in medicine, do not forget
the basics: ABCs—Airway, Breathing, Circulation. Quickly
eyeball the patient and check the vital signs from the mon-
itors or from EMS or the triage nurse. Make sure that the
patient is protecting their airway and there are no imme-
diate life-threatening issues. Luckily, this is typically not
the case, although some patients have a depressed level of
consciousness either from a devastating intracranial event
or another systemic issue. If the patient looks unstable, do
not hesitate to request help from an ED physician, or rapid
response/ICU.

Important initial questions to ask

Make every effort to speak directly to the paramedics, the
patient, patient’s family, and any eyewitness to obtain the
most reliable medical history. There are 6 key questions
to ask first, before we get a more detailed history and un-
derstand exactly what happened (specific symptoms and
chronology):

1. Clarify the time the patient was “last seen normal” and
the exact time of onset of symptoms, or the time the
patient was found with symptoms.
2. What are the main neurological deficits? Did they
improve or worsen en route?
3. Relevant past medical history and medications (do
they have known atrial fibrillation? Are they taking
anticoagulant medications? Do they have an allergy to
contrast dye?).
 History taking 5

4. Baseline functional status and occupation.

5. If arriving by EMS: vitals en route, EMS cardiac
rhythm (normal sinus or atrial fibrillation or other?),
blood glucose.
6. Did they bypass a closer hospital en route?

(1) The most important initial question to clarify with the

patient, family, or witness is the stroke onset time and the
patient’s “last seen normal time,” as it starts the clock on
eligibility for acute treatment, i.e., thrombolytic therapy
with tPA and/or endovascular therapy. Sometimes the
exact time of onset is unknown/uncertain or difficult to
obtain, but try to really pin it down. Use clock time (i.e.,
23:00), rather than “2 h ago,” or “30 min ago.”
If the patient woke up with symptoms (i.e., a wake-up
stroke), when were they last seen well? Did they get up
in the middle of the night to use the washroom and were
they normal then? If the patient woke up with symptoms
in the morning without previous awakenings, we must
use their last seen normal time which is typically when
they went to bed. A common reason for ineligibility for
tPA is arrival at the hospital too late, beyond the time
window for treatment (although this is an evolving area
of clinical research, and advanced imaging may enable
the use of tPA outside the traditional time window).
(2) Now we need to clarify the neurological deficits.
Clinical features in favor of an acute arterial
stroke diagnosis:
❏ Sudden onset of persistent focal neurological
symptoms
❏ Symptoms compatible with a vascular territory
(see Chapter 4—stroke syndromes).
6 The Code Stroke Handbook

What is a transient ischemic attack (TIA)?

Definition: a clinical syndrome characterized by the
sudden onset of focal neurological symptoms that resolve
within 24 h (although typically lasting minutes) AND no
infarction is visualized on brain imaging.
The symptoms are transient as blood flow is tempo-
rarily blocked and then restored. Perfusion is dependent
on many local and systemic factors (migration of clot,
collateral circulation, cardiac output, blood pressure, etc.).
These patients are at risk of recurrent stroke—­
especially within the first week of symptom onset—and
require timely assessment and management.
Clinical pearl: Given the increasing availability of
MRI with diffusion weighted sequences, many clinical
events previously thought to be TIAs are in fact small
ischemic strokes.

Specifically, what are the neurological symptoms? Are

they acute? Are they stable, fluctuating, worsening, or im-
proving? Acute stroke is a dynamic condition and it is
important to ask EMS if the symptoms have improved
compared to their initial assessment.
Was there a loss of consciousness or evidence of seizure
(rhythmic activity, bitten tongue, bruising, incontinence)?
Focal deficits can occasionally follow a seizure (postic-
tal) and are transient (called Todd’s paresis). Are there as-
sociated fever or infectious symptoms, or other systemic
symptoms such as palpitations, chest pain, or shortness of
breath?
Time course and duration of symptoms is important.
Migraine auras by definition last between 5 and 60 min in
adults; however, typically they last 20–30 min. Seizures on
average occur for 30 s–3 min. Syncope is brief, lasting sec-
onds. More on stroke mimics in the next chapter.
 History taking 7

Clinical pearls—We will review examples

of neurological symptoms typically not
associated with stroke

Recurrent/stereotyped episodes of aphasia

Aphasia is a cortical phenomenon and repeated ischemia
to the same cortical area can be caused by TIAs if there
is ­
significant intracranial occlusive disease. However,
one should also consider focal seizures (ictal aphasia).
Another less likely e­ tiology is migraine aura which may
occur without headache.
Isolated dysphagia
When dysphagia is acute in onset, stroke should be
considered, although isolated dysphagia is rare. Often,
clarification of the history reveals a subacute or chronic
presentation in which case the differential diagnosis is
broad and includes neurological and non neurological
etiologies.
Lower motor neuron (“peripheral”) facial weak-
ness (i.e., Bell’s Palsy)
This pattern of weakness involves the forehead and is
usually due to a lesion in the ipsilateral facial nerve (sev-
enth cranial nerve). Rarely, a lesion in the brainstem fa-
cial nucleus or fascicle can also result in a lower motor
neuron CN 7 palsy, but is almost always accompanied
by a nuclear sixth nerve palsy or other symptoms in this
scenario.
Isolated anisocoria
You cannot attribute isolated anisocoria to a stroke with-
out associated ptosis to suggest a Horner’s syndrome (as-
sociated with carotid artery dissection), or ptosis with
some deficits in the rectus muscles innervated by the
third cranial nerve to suggest a third nerve palsy (assum-
ing the patient is not comatose).
8 The Code Stroke Handbook

(3) What is their past medical history? Do they have a

previous history of stroke/TIA?
Vascular risk factors include:
❏ Previous TIA/stroke
❏ Atrial fibrillation
❏ Hypertension
❏ Diabetes
❏ Dyslipidemia
❏ Coronary artery disease or congestive heart failure
❏ Valvular heart disease
❏ Smoking
❏ Obstructive sleep apnea
❏ Alcohol abuse
❏ Other less common factors: migraine, oral contra-
ceptive agents, hormone replacement therapy, anti-
phospholipid antibody syndrome, infection, cancer
❏ Rare genetic conditions such as (cerebral autosomal
dominant arteriopathy with subcortical infarcts and
leukoencephalopathy (CADASIL)) or Fabry disease.
Any recent surgery or invasive procedures? Recent
gastrointestinal bleeding, genitourinary bleeding, or other
adverse bleeding events? Any known kidney or liver dis-
ease or malignancy? Any recent myocardial infarction or
recent TIAs/strokes? Any prior intracranial hemorrhage?
History of seizures? Recent headaches, neck pain, whiplash
or trauma? Known allergies to drugs or X-ray contrast dye?
(4) What is their baseline functional status? What is their
occupation? What is their cognitive baseline, and what
are their goals of care/DNR status?
(5) Were they hyper/hypotensive en route? Does the
cardiac rhythm strip show an irregularly irregu-
lar rhythm or abnormalities relating to myocardial
­infarction (ST elevation)? Are they hypoglycemic?
 History taking 9

Severe hypoglycemia or hyperglycemia can result in

focal neurological signs and altered consciousness that
can mimic stroke and blood glucose should always be
checked on arrival at ED or obtained from EMS.
Look at the rhythm strip from EMS and telemetry
monitor in ED as it may identify atrial fibrillation.
(6) Did EMS bypass a hospital en route to your stroke
center? This is a practical question as it may be relevant
to local hospital repatriation policies at some centers.
The history is extremely important.This cannot be stressed
enough. You may not get all of it initially, but try to hit
the high-yield questions before you move on to quickly
examine the patient.

In summary, the most important questions are:

❏ Clarify the stroke onset time and/or last seen normal
time
❏ What are the main new deficits
❏ Baseline functional status
❏ Is the patient on anticoagulation or have a past med-
ical history of bleeding
❏ Vital signs and glucose

It is not possible to reliably predict an ischemic from a

hemorrhagic stroke type based on history or examination
alone, which is why patients are not recommended to take an-
tiplatelets or anticoagulants at onset of symptoms before a CT
head is done (approximately 15% of stroke events in North
America are hemorrhagic). Neuroimaging is necessary to
differentiate ischemic from hemorrhagic stroke.
Clinical clues for a hemorrhagic etiology include:
❏ Patient on anticoagulation
❏ Head trauma
❏ Progressive neurological deterioration
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