Front Panel Painting:

LIFE
By: William T. Chua, MD
Past Director, Heart Institute
St. Lukes Medical Center
 5th REVISED EDITION

Guidelines for the

Prevention, Treatment and
Rehabilitation of
Stroke
 Copyright 2011 by the Stroke Society of the Philippines

All rights reserved.

No part of this book may be reproduced, distributed, or transmitted in any form or by
any means, or stored in a database or retrieval system, without the prior written
permission of the publisher.

Copyright No. A2010-2696

ISBN no. 978-971-94968-0-9

First Published 1999

Second Edition 2002
Third Edition 2004
Fourth Edition 2006
Fifth Printing 2007
Fifth Edition 2010
Fifth Revised Edition 2011

Editor-in-chief: Artemio A. Roxas Jr., MD, MSc, FPNA

Published by: The Stroke Society of the Philippines

For inquries please contact:

SSP Secretariat
Rm.1403 North Tower, Cathedral Heights Bldg. Complex
St. Luke's Medical Center, E. Rodriguez Ave., Quezon City
Email: ssp_secretariat@yahoo.com
Telephone: 723-0101 loc. 5143
Telefax: 722-5877
www.strokesocietyphil.org

Printed in the Philippines by: GoldenPages Publishing Company

 TABLE OF CONTENTS
Foreword
Message from the Founding President .............................................3
Message from the President ...............................................................4
World Stroke Day Declaration ...........................................................6

Chapter I. Overview of Stroke ......................................................................................9

Chapter II. Guidelines for Primary and Secondary Prevention of Stroke .....27
Preface to the Guidelines on Primary
and Secondary Prevention of Stroke
I. Hypertension ...............................................................................................29
II. Diabetes Mellitus ........................................................................................33
III. Atrial Fibrillation ........................................................................................40
..............40
IV. Acute MI, Left Ventricular Thrombus and Cardiomyopathy
Valvular Heart Disease ..............................................................................42
V.
Cholesterol ..................................................................................................49
VI.
Carotid Stenosis ..........................................................................................54
VII.
Intracranial Stenosis ...................................................................................58
VIII. Peripheral Arterial Disease ........................................................................61
IX. Smoking .......................................................................................................65
X. Excessive Alcohol .......................................................................................69
XI. Physical Inactivity........................................................................................70
XII. Obesity .........................................................................................................77
XIII. Special Section on Diet for Stroke ...........................................................81

Chapter III. Guidelines for Acute Stroke Treatment ...........................................89

SSP Classification of Acute Stroke Based on Clinical Severity ..........90
I. Guidelines for TIA and Mild Stroke .......................................................91
II. Guidelines for Moderate Stroke ..............................................................94
III. Guidelines for Severe Stroke ....................................................................96
IV. Early Specific Treatment for Ischemic Stroke .......................................98
V. A. Antithrombotic Therapy in Acute Stroke .................................98
B. Neuroprotection and Neuroprotectant Drugs .........................99
C. Anticoagulation in Acute Cardioembolic Stroke....................102
D. Administration of rt-PA in Acute Ischemic Stroke...............104
Blood Pressure Management After Acute Stroke ..............................108
VI. Management of Increased ICP...............................................................113
VII. Hemicraniectomy for Malignant MCA Infarction ..............................116
VIII. Stroke Scales ..............................................................................................123
IX. A. Glasgow Coma Scale ..................................................................123
B. NIH Stroke Scale.........................................................................123
C. Modified Rankin Scale................................................................126

1
Chapter IV. Guidelines for Transient Ischemic Attack
and Atrial Fibrillation ..........................................................................127
I. Transient Ischemic Attack ......................................................................128
II. Atrial Fibrillation ......................................................................................140

Chapter V. Guidelines for Hemorrhagic Stroke ..................................................149

I. Hypertensive Intracerebral Hemorrhage .............................................152
II. Aneurysmal Subarachnoid Hemorrhage ..............................................154
III. Arterio-Venous Malformation ...............................................................161

Chapter VI. Neuroimaging for Stroke ...................................................................167

Chapter VII. Guidelines for Stroke Units, Nursing Management ................185

and Stroke Rehabilitation
I. Guidelines on the Establishment and Operation of Stroke Units ...186
II. Guidelines for Nursing Management of Stroke Patients ..................190
III. Guidelines for Stroke Rehabilitation .....................................................204
IV. Strategy for Implementation of Guidelines ........................................216
V. Stroke Units in the Philippines ..............................................................218

Working Committees ...................................................................................220

SSP Board of Trustees .................................................................................222
SSP Conventions ............................................................................................223

2
 MESSAGE from the FOUNDING PRESIDENT
(from Guidelines for the Prevention, Treatment and Rehabilitation of Brain Attack, 4th edition)

These Guidelines for the Prevention, Treatment and Rehabilitation of Brain

Attack is the output of the seven Stroke Congresses on Brain Attack organized by the
Stroke Society of the Philippines.

Aware of the many advances in research toward the prevention, treatment

and rehabilitation of brain attack, the Stroke Society of the Philippines initiated the
First Congress with the theme, Thinking Globally, Acting Locally, in October 1999.
Since then, six more congresses have tackled the issue of organizing stroke services,
and subsequently, intracerebral and subarachnoid hemorrhage.

We worked on the principles that stroke is preventable through ways that

may be implemented across all levels of society; that stroke is a brain attack needing
emergency management where no allowance for worsening is tolerated; and that in the
Philippine setting, the treatment should be optimal through proven, affordable,
culturally acceptable and ethical means.

With the panel of experts of the Stroke Society of the Philippines consisting
of neurologists, internists, neurosurgeons, vascular surgeons and physiatrists, we
worked with the practitioners in the field, identified by the Department of Health.

The Guidelines were subjected to close scrutiny by experts and practitioners

in the field, whose recommendations and comments were embodied in the final
output.

We realize that this is not a perfect document, but the Society is proud to
present to our public these guidelines, which embody our best efforts to gather the
latest, evidence-based data, and the opinion of experts in the Philippines.

We continue to update the Guidelines as new knowledge comes to the

forefront. We dedicate the Guidelines to our patients, students, practitioners and our
health workers, that we may in our small way, contribute to the vision of Health for
All in our beloved country.

JOVEN R. CUANANG, MD
Founding President
Stroke Society of the Philippines

3
 MESSAGE from the PRESIDENT

Since the last revision of the Guidelines for the Prevention, Treatment and
Rehabilitation of Brain Attack in 2006, tremendous amount of new knowledge have
been published that needs revision of the 4th edition of the Guidelines. In the same
token, a different format has been followed in order to accommodate revisions and
modifications that would facilitate easy reading and ready source of information about
stroke. A new title was also given for this new edition because these guidelines not
only deal with acute treatment which is synonymous with brain attack but also with
prevention and rehabilitation of stroke. Furthermore, topics on arteriovenous
malformation and neuroimaging of stroke have also been added on this revised
edition. This concise compilation of prevention, treatment and rehabilitation of
stroke will undoubtedly serve as the immediate reference not only for specialists but
also for other physicians as well.

My personal gratitude goes to Artemio Roxas Jr., M.D. for leading the
revision and also to the members of the different groups that reviewed, contributed
and revised the different topics in order to come up with these 2010 Guidelines.

Jose C. Navarro, MD, FPNA

President
The Stroke Society of the Philippines

4
 STROKE: THINK GLOBALLY, ACT LOCALLY

Principles:

1. Stroke is a "brain attack

needing emergency management, including specific treatment and secondary and tertiary
prevention.

2. Stroke is an emergency

where virtually no allowances for worsening is tolerated.

3. Stroke is treatable

optimally, through proven, affordable, culturally acceptable and ethical means.

4. Stroke is preventable

in a manner that could be implemented across all levels of society.

For anyone experiencing stroke,

proceed immediately to a hospital,
preferably a facility that can provide stroke care.

Remember:
TIME is BRAIN

The recommendations contained in this document are intended to merely guide

practitioners in the prevention, treatment and rehabilitation of patients with stroke.
In no way should these recommendations be regarded as absolute rules,
since nuances and peculiarities in individual patients, situations or communities
may entail differences in specific approaches. The recommendations should supplement,
not replace, sound clinical judgments on a case-to-case basis.

5
 WORLD STROKE DAY PROCLAMATION

Cape Town, the 26th of October, 2006

STROKE: A PREVENTABLE AND TREATABLE CATASTROPHE

THE GROWING EPIDEMIC

STROKE IS PREVENTABLE but rising globally

?
Aging, unhealthy diets, tobacco use, and physical inactivity, fuel a growing
epidemic of high blood pressure, high cholesterol, obesity, diabetes, stroke,
heart disease and vascular cognitive impairment.
?
Worldwide, stroke accounts for 5.7 million deaths each year and ranks second
to ischemic heart disease as a cause of death; it is also a leading cause of
serious disability, sparing no age, sex, ethnic origin, or country.
?
Four out of five strokes occur in low and middle income countries who can
least afford to deal with the consequences of stroke.
?
If nothing is done, the predicted number of people who will die from stroke
will increase to 6.7 million each year by 2015.
?
Six million deaths could be averted over the next 10 years if what is already
known is applied.
?
Much can be done to prevent and treat stroke and rehabilitate those who
suffer the devastating consequences of stroke.

JOIN FORCES TO PREVENT STROKE

THE SAME FEW RISK FACTORS ACCOUNT FOR THE LEADING HEALTH
PROBLEMS OF THE WORLD but research about the common threat occurs in
isolation from other major chronic diseases.

?
The common risk factors, tobacco use, physical inactivity, and unhealthy diet,
contribute to stroke, heart disease, diabetes, chronic lung disease, cancer, and
pose a risk for Alzheimers disease.
Therefore we need to:
? Coordinate the efforts of all disease-oriented organizations working to
prevent the rise of these underlying risk factors.

ENSURE WHAT WE KNOW BECOMES WHAT IS DONE

PREVENTION IS THE MOST READILY APPLICABLE AND AFFORDABLE PART
OF OUR KNOWLEDGE but prevention is neglected.

Therefore we need to:

? Encourage healthy environments to support healthy habits and lifestyles.

6
 ?
Use effective drugs for both primary and secondary prevention. Regretfully
these drugs are neither accessible nor affordable in many developing
countries, nor used optimally in developed ones.
?
Discourage unproven, costly, or misdirected practices, which drain resources
from more cost effective approaches.
?
Educate health professionals at all levels through a common vocabulary, a
core curriculum, on-line materials, long distance mentoring, and opportunities
for learning in clinical practice settings.

RECOGNIZE THE UNIQUENESS OF STROKE

THE DIFFERENT TYPES OF STROKE HAVE SPECIFIC COURSES REQUIRING
SPECIAL TREATMENT AND REHABILITATION.

Therefore, we need to:

? Study their causes and understand their mechanisms
? Organize skilled teams of physicians, neurosurgeons, neurointerventionalists,
and rehabilitation specialists to deal with these special types of stroke.

RECOGNIZE, TREAT AND PREVENT VASCULAR COGNITIVE

IMPAIRMENT
SUBCLINICAL (SILENT) STROKES OCCUR FIVE TIMES AS OFTEN AS
CLINICAL (OBVIOUS) STROKES, AND MAY AFFECT THINKING, MOOD AND
PERSONALITY.

Therefore, we need to:

? Recognize that vascular cognitive impairment (VCI) occurs commonly and at
times hastens Alzheimers disease (AD)
? Manage the common risk factors for stroke, VCI and AD (tobacco use, high
blood pressure, high cholesterol, physical inactivity, obesity and diabetes).

BUILD TRANSDISCIPLINARY TEAMS FOR STROKE CARE AND

REHABILITATION
ORGANIZED STROKE CARE IMPROVES OUTCOMES but remains the exception
nearly everywhere.

Therefore we need to:

? Establish simple but comprehensive stroke units.
? Encourage transdisciplinary teams to develop expertise and translate evidence
into practice.
? Build a health care system that responds to the needs of each individual
dealing with the impact of stroke and rejoining society.

7
ACTIVELY ENGAGE THE PUBLIC AROUND THE WORLD
THE PUBLIC, ACTING AS INDIVIDUALS, VOTERS OR ADVOCATES, CAN BEST
INFLUENCE THEIR OWN FUTURE RISK AND CARE but not enough is being done.

Therefore we need to:

?
Increase awareness of the public, policymakers, and health professionals about
the causes and symptoms of stroke.
?
Send a unified, consistent message throughout the world:

STROKE IS A PREVENTABLE AND TREATABLE CATASTROPHE

Whereas; stroke is a global epidemic that threatens lives, health, and quality of life.
Whereas; much can be done to prevent and treat stroke, and rehabilitate those who suffer one.
Whereas; professional and public awareness is the first step to action.
We hereby proclaim an annual

WORLD STROKE DAY

October 29

8
Overview
 An Overview of Stroke
Overview

Stroke is a brain attack and should be considered as an emergency situation that is potentially
treatable and most importantly- preventable. These guidelines on stroke were written to help
attain the primary objective of the Stroke Society of the Philippines (SSP) to limit the burden of
stroke in the country. Awareness of accepted, updated, cost-effective and evidence-based
management for stroke is important and crucial.

Whereas the previous editions were mainly compilations of guidelines for management, this
edition has been reformatted for which basics on strokes and neuroimaging were included to
serve as a handbook on stroke. The different chapters of this handbook will help local health
personnel doctors, nurses, physical therapists, barangay health workers- to understand and
prepare them on their roles in the management of stroke patients from acute to the chronic
phase.

I. THE BURDEN OF STROKE

Diseases of the vascular system which include stroke are the second most common cause of
death worldwide and in the Philippines. The 1998 and 2005 health statistics from the Philippine
Department of Health (DOH) reported that diseases of the vascular system which include
cerebrovascular diseases (CeVD) or stroke were the second leading cause of mortality. The
World Health Organization (WHO) uses the term CVD or cardiovascular diseases to include
diseases involving the vascular system which include myocardial infarction (MI), stroke and
peripheral vascular disease.

Of the 58 million global deaths in 2005, 5.7 million were from stroke alone. Worldwide, 10% of
all deaths are attributed to strokes and the WHO predicts an impending epidemic of diseases of
the vascular system including stroke by the year 2020. It is predicted that there will be 6.5 million
deaths due to stroke in 2015 and 7.8 million in 2030.

The WHOs Global Burden of Stroke in 2005 reported that the prevalence in the Philippines is
14 per 1,000 people, more than the average of <5 per 1,000 in the industrialized world. Stroke is
also the leading cause of disability in adults with up to 32% of all stroke survivors permanently
disabled. In addition, stroke is also the second most important cause of dementia. The burden
of stroke will rise in the Asia-Pacific region to which the Philippines belongs due to longevity
and increasing prevalence of risk factors. Although epidemiologic data are sparse in Asian
populations, in some Asian countries like Korea and Japan, the rate of stroke is already higher
than the rate of MI.

Although incidence data for stroke in the Philippines is still being awaited, various prevalence
studies have already been done. The table below shows the different major community based
prevalence studies done locally. The wide variations in prevalence report are due to the different
age groups surveyed, different methods of sample collection and case ascertainment. The
National Nutrition and Health survey (NNHeS II) conducted by the Food and Nutrition
Institute (FNRI) of the Department of Science and Technology (DOST) with the DOH and 12
medical specialty organizations was national in scope. Using stratified muli-stage sampling, the
survey included all regions and provinces in the country. On the other hand, the Morong and

10
 Overview
Currimao studies utilized house-to-house surveys of the two communities. The three studies
for determining stroke prevalence utilized the Philippine Neurological Association (PNA)
Stroke Survey questionnaire validated by the PNA Stroke Council. In addition to using the
questionnaire, the PNA Morong stroke study did actual case verification of cases.

Stroke Prevalence Studies in the Philippines 1-3

Stroke Ascertainment
Study Population N Question on Previous
Questionnaire
History of Stroke
FNRI - NNHeS. 2005 Age 20 and over 4,753 1.9% 1.4%
PNA Community Stroke
Prevalence Study, All age group 19,113 0.5% __
Morong, Rizal. 2005
SSP Currimao Stroke
40 and above 1,400 1.6% 1.9%
Prevalence Study. 2009

II. STROKE AWARENESS

Public awareness about stroke has been a major advocacy of the Stroke Society of the
Philippines (SSP). A community survey done by SSP (SAGIP or Stroke Awareness Gap In the
Philippines) among 750 adults in Currimao, Ilocos Norte, showed that knowledge of what stroke is
was seen only in 34.4% of respondents with 20.5% confusing it with heart attack and 27.2% admitting they
dont know what stroke is. More than half mistook chest pain and shortness of breath as a
presentation of stroke. In general, there was poor knowledge on risk factors of stroke.4

The awareness programs of SSP thru its COBRA committee (Committee On BRain Attack)
include distribution of educational posters, flyers, videos and teaching the public the warning
signs of stroke.

Anyone should consider stroke if they experience any of these symptoms:

1. Sudden numbness or weakness of the face, arm or leg, especially on one side of the body.
2. Sudden confusion, trouble speaking or understanding.
3. Sudden trouble seeing in one or both eyes.
4. Sudden trouble walking, dizziness, loss of balance or coordination.
5. Sudden, severe headache with no known cause

Similarly, the public are made aware on how to perform the Cincinnati Prehospital Stroke Scale
which tests three signs that can indicate that the patient may be having a stroke. If any one of
the three tests shows an abnormal finding, the patient may be having a stroke and should be
transported to a hospital as soon as possible.

11
Overview

The Cincinnati Prehospital Stroke Scale5 using the acronym FAST

Have the person smile or show his or her teeth. If one side doesn't move
Facial Asymmetry
as well as the other or it seems to droop, that could be sign of a stroke.

Have the person close his or her eyes and hold his or her arms straight out
Arm Drift
in front for about 10 seconds. Look for weakness or drift
Have the person say, "You can't teach an old dog new tricks," or some
Slurred Speech other simple, familiar saying. If the person slurs the words, gets some
words wrong, or is unable to speak, that could be sign of stroke
If any of the above 3 is present, then patients are advised to seek
Time immediate hospital consultation.

A local version of FAST is KAMBIO6 Sambitin at Gawin Upang Stroke ay

Alamin
Itaas ang Kamay at obserbahan kung may panghihina o drift
KAmay
Ipakita ang ngipin o mag-Smile. Tingnan kung may kaibahan ang kaliwa sa
Mukha kanang mukha
BIgkas Bigkasin at ulitin Kumukutikutitap ang lampara. Obserbahan kung may
mali sa pananlita
Oras If any of the above 3 is present, then patients are advised to seek
immediate hospital consultation.

Another local version of UTAK SSP 2009 Lay Education Campaign winner
Bigkasin at ulitin Kumukutikutitap ang lampara.
Utal, bulol o di makapagsalita Obserbahan kung may mali sa pananlita
Tabingi ang mukha or lakas ng kanan o Ipakita ang ngipin o mag-Smile. Tingnan kung may
kaliwang bahagi ng katawan kaibahan ang kaliwa sa kanang mukha; Itaas ang
Kamay at obserbahan kung may panghihina o drift
Angal ng angal ng biglaang matinding sakit Pakinggan ang daing ng pasyente.
ng ulo, pamamanhid o panlalabo ng mata
Kumilos kaagad at Kumunsulta Huwag magpatumpiktumpik at humarurot sa ospital!

A local study on the reasons for delays in the care of acute stroke patients included failure to
recognize symptoms as serious and stroke-related. Longer delays arise from healthcare-related
factors such as delays in neurologist referral and neuroradiologic diagnosis. Initial consultation
with a non-neurologist was seen in 97% of cases. The median delay from presentation to
neurological evaluation was 7.5 hours while the median time from presentation to brain imaging
was significantly shorter for patients brought to CT-equipped facilities (2 hrs) than those
needing transfer to another institution with neuroimaging facilities (11.5 hours).7
Public education on the necessity of early neurologic evaluation by trained health provider and
patient transport to a CT-equipped hospital are recommended. Thus, it is not enough to seek
immediate consult at a hospital but to choose a hospital equipped and prepared to handle an
acute stroke preferably, a hospital with a stroke unit.

12
 Overview
III. THE ROLE OF PHYSICIANS IN ACUTE STROKE CARE
Having recognized the early signs of stroke and reacting appropriately by rushing to a hospital,
patients would expect that they be provided with proper and immediate care. Is the hospital and
its medical staff prepared and equipped to provide stroke care? The admitting medical
personnel usually the ER physician - has the major responsibility to provide acute efficient
stroke management as TIME IS BRAIN and early medical treatment can reduce the risk of
death or disability from stroke! When available, referral to a physician trained in stroke care and
admission to a stroke unit would be ideal.

The Role of Physicians in Acute Stroke Care:

1. Confirm that the diagnosis is STROKE and not mimickers; that stroke is ISCHEMIC and
not HEMORRHAGIC.
2. Determine if acute treatment with thrombolytic agent is advisable.
3. Do diagnostics to screen for acute medical or neurological complications of stroke.
4. Determine vascular distributions of the stroke and provide clues on likely pathophysiology
and etiology

The role of physicians is to make an accurate diagnosis of stroke, determine stroke type, provide
acute general medical care and provide neuroprotection as well as promote tissue reperfusion if
needed. The giving of thrombolytic agent is not a simple procedure and should be reserved for
medical centers equipped and prepared for this. In as much as the local experience with the use
of thrombolytics is limited, the SSP has been disseminating information through thrombolytic
workshops to promote its use to eligible acute ischemic stroke patients. A section has been
allotted for this topic. Finally, if a hospital cannot provide proper stroke care, knowing when to
transfer a patient to a facility that can handle stroke care is important.

IV. THE EVOLVING DEFINITION OF STROKE AND TIA

The first challenge is making a correct clinical diagnosis of stroke. Unlike myocardial infarction,
stroke is a heterogenous disease and its manifestations are highly variable due to the complex
anatomy of the central nervous system and its vasculature. Knowing the definition of stroke is
essential. Understanding the reasons for the changing definitions thru time is appropriate for
setting the stage for the management of the disease.

Stroke has been traditionally defined since the 1970s by the WHO as a "neurological deficit of
cerebrovascular cause that persists beyond 24 hours, or is interrupted by death within 24 hours".
This may be attributed to ischemic stroke, hemorrhagic stroke, or cerebrovascular anomalies
such as intracranial aneurysms and arteriovenous malformations (AVMs). This definition was
supposed to reflect the reversibility of tissue damage with the time frame of 24 hours being
chosen arbitrarily. Thus, a person is diagnosed with stroke if neurological symptoms persisted
for more than 24 hours. A focal neurological deficit lasting <24 hours was defined to be a
transient ischemic attack (TIA).

13
Overview

However, studies worldwide have demonstrated that this arbitrary time threshold was too broad
because in 30% to 50% of cases with this definition of TIA, brain injury was evident on
diffusion-weighted magnetic resonance imaging (MRI). With the emergence of approved
therapy for acute ischemic stroke that should be given within the golden time frame of three (3)
hours to reduce stroke severity and mortality, many prefer the alternative terms such as brain
attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute
coronary syndrome respectively), which reflects the urgency of stroke symptoms and the need
to act swiftly.

Since most TIAs resolve within 15-20 minutes, a combined time-based and tissue-based
definition for TIA was proposed in 2002. The proposed definition was a brief episode of
neurological dysfunction caused by focal brain or retinal ischemia, with clinical
symptoms typically lasting less than one hour, and without evidence of acute infarction.
The availability of more studies showed that using time in the definition does not accurately
distinguish patients with or without acute cerebral infarction. It would be impossible to define a
specific time cut-off that can distinguish whether a symptomatic ischemic event will result in
brain injury with high sensitivity and specificity. In modern medicine, seeking the pathological
basis of disease and directing treatment at the underlying biological processes are central tenets.
Therefore, relying mainly on time-based definitions may unproductively focus diagnostic
attention on the temporal course rather than on the underlying pathophysiology.

Based on the above reasons, the American Heart Association has endorsed in 2009 a revised
definition for TIA as a transient episode of neurological dysfunction caused by focal
brain, spinal cord, or retinal ischemia, without acute infarction. Based on this definition
of TIA, an ischemic stroke is defined as an infarction of central nervous system tissue.
Similar to TIAs, this definition of ischemic stroke does not have an arbitrary requirement for
duration.

The Stroke Society of the Philippines and the Philippine Neurological Association
through its Stroke Council, convened on September 2010 to discuss the recent changes in
the definition of stroke and what definition of stroke/TIA to use particularly in this
handbook. Aware that the handbook will be used by local physicians practicing in places
with limited access to neuroimaging facilities and fully aware of the arguments for and
against the latest definitions, the working definitions for TIA and stroke agreed upon is as
follows:

?
Transient Ischemic Attack: a transient episode of neurological dysfunction caused
by focal brain or spinal or retinal ischemia, without evidence of acute infarction in which
clinical symptoms typically last less than an hour.
?
Stroke: sudden onset of focal (or global) neurologic deficit due to an underlying vascular
pathology.

14
 Overview
There are two major types of stroke namely ischemic stroke and hemorrhagic stroke.
Ischemic stroke is defined as an infarction of CNS tissue (it was agreed that no specific
time is included in the definition). The committee was unanimous on the importance of
underscoring that in acute ischemic stroke, there exists an area of penumbra around the
core of infarcted tissue that is potentially salvageable.

Unlike TIAs, ischemic strokes may be either symptomatic or silent. Symptomatic

ischemic strokes are manifested by clinical signs of focal or global brain, spinal, or retinal dysfunction
caused by infarction. On the other hand, silent infarct is a documented CNS infarction that was
asymptomatic.

The committee found no reason to review the definition for hemorrhagic stroke which is a
stroke that results from rupture of a blood vessel or an abnormal vascular structure directly into and around
the brain.

For patients with relatively brief symptom duration (e.g., symptoms that persist several hours
but less than a day) who do not receive a detailed diagnostic evaluation, it may be difficult to
determine whether stroke or TIA is the most appropriate diagnosis. For these patients, it would
be reasonable that a term such as acute neurovascular syndrome should be chosen, analogous to
the terminology used in cardiology. This term may also be appropriate for patients who have
just developed acute cerebrovascular symptoms in whom it is not yet known whether deficits
will rapidly resolve or persist and in whom neurodiagnostic testing has not yet been undertaken.

V. CLASSIFICATIONS OF STROKE
Strokes can be classified into two major categories: ischemic and hemorrhagic. About 80 % of
all strokes are ischemic and the remaining 20% are hemorrhagic. The proportion of
hemorrhagic strokes is relatively higher in Asia when compared to the West. Using the Saint
Lukes Medical Center (SLMC) stroke database and the PNA RIFASAF database, the
proportion of hemorrhagic stroke accounts for about 26-30%, which is relatively more in
comparison to western data (about 20%).

Being very heterogenous and highly variable, stroke classification schemes are helpful in the
practice of stroke medicine. There are many classifications available depending on what aspect
of stroke is being considered namely: timing, pathophysiology, initial clinical presentation and
severity of stroke.

The urgency and extent of treatment would be influenced by the timing or the phase of stroke
when patients are seen. Based on the ictus or time of onset of stroke, stroke can be arbitrarily
labeled as hyperacute (0 - 6 hrs), acute (6 to 72 hrs), subacute (3 days to <3 weeks) and chronic (3
or more weeks). The division of hyperacute from acute stroke is important as treatment may
vary depending on the number of hours from the ictus of stroke considering the existence of
the penumbra and the potential of salvaging threatened tissues.

15
Overview

Unique to this stroke handbook and acting on the dictum thinking globally and acting locally,
the Stroke Society of the Philippines classified stroke according to the severity of neurologic
deficits at onset, namely, mild, moderate and severe stroke. The SSP members have used this
classification and although no formal studies have been done to show its impact, it was found to
be useful, practical and cost-effective.

V.1. Classification of Stroke Based on Pathophysiology

Simply putting a diagnosis of ischemic stroke may not capture the diverse
pathophysiology as well as the extent of involvement of an affected blood vessel.
Management and prognosis may be different for the different types of ischemic
strokes. In drug trials, ischemic strokes are usually classified further into subtypes as
the results may differ depending on the different subtypes of ischemic strokes. Two
classifications of ischemic strokes that are often used are the TOAST Classification
and the Oxfordshire Classification of stroke.

The TOAST (Trial of ORG 10172 in Acute Stroke Treatment) classification is based
on the pathophysiology, clinical symptoms as well as results of further investigations
of an ischemic stroke.

TOAST Classification for Ischemic Stroke

1) Thrombosis or embolism due to a large artery atherosclerosis (LAA)
2) Embolism of cardiac origin (CE)
3) Occlusion of a small artery (SAO)
4) Other determined cause (OC)
5) Undetermined cause (UND).
For UND ischemic strokes, one of two explanations was needed: (a) no cause was found despite
extensive evaluation or (b) a most likely cause could not be determined because more than one
plausible cause was found. The TOAST investigators noted that stroke prognosis, risk of recurrence,
and choices for management were influenced by ischemic stroke subtype.

The Oxfordshire Community Stroke Project (OCSP) classification is a simple clinical

scheme to subdivide acute strokes and was originally devised for patients with first
ever in a lifetime stroke. The Oxfordshire Classification relies primarily on the initial
symptoms of stroke.

The Oxfordshire Classification of Stroke

1) Total anterior circulation (TAC_)
2) Partial anterior circulation (PAC_)
3) Lacunar (LAC_)
4) Posterior circulation (POC_)
A fourth code or letter is added to the above codes based on the etiology whether ischemic (TACI,
PACI, LACI, or POCI), hemorrhagic (TACH, PACH, LACH, or POCH) or syndromic if the
pathogenesis is indeterminate or prior to imaging (TACS, PACS, LACS, or POCS). These four
entities can predict the extent of the stroke, the area of the brain affected, the underlying cause, and
the prognosis.

16
 Overview
Lacunar syndromes (LACS) include pure motor stroke, pure sensory stroke,
sensorimotor stroke and ataxic hemiparesis. Patients with brain stem or cerebellar
signs, and/or isolated homonymous hemianopia are classified as posterior circulation
syndrome (POCS). Those with total anterior circulation syndromes (TACS), by
definition, present with the triad of hemiparesis (or hemisensory loss), dysphasia (or
other new higher cortical dysfunction) and homonymous hemianopia. Patients with
partial anterior circulation syndrome, by definition, present with only two of the
features of TACS, or isolated dysphasia or parietal lobe signs.

The Oxfordshire classification was used in a stroke sub-type study among ten Asian
countries which included the Philippines. The breakdown of stroke subtypes in this
study are as follows:

Stroke Sub-Types in 10 Asian Countries9

All Infarcts 895 (74%)

Partial Anterior Circulation Infarct (PACI) 274 (27%)
Total Anterior Circulation Infarct (TACI) 115 (12%)

Lacunar Infarct (LACI) 247 (25%)

Posterior Circulation Infarct (POCI) 99 (10%)
Parenchymal Intracerebral Hemorrhage 258 (26%)

V.2. Intracranial Versus Extracranial Stenosis

Ischemic strokes can be due to stenosis of blood vessels located inside the skull
(intracranial) or outside the skull (extracranial). Intracranial large artery occlusive
disease is significantly more frequent in Hispanics, Blacks, and Asians, while
extracranial carotid stenosis predominates among Whites. Studies among Chinese,
Taiwanese and Japanese have documented intracranial vascular lesions in 33-67% of
stroke/TIA patients, while extracranial carotid disease in 3-19%. Similar
observations were seen in the St Lukes stroke data bank where 33% had
atherosclerosis by transcranial duplex exam - 26 % of them with intracranial stenosis
alone, 3.7% had significant extracranial carotid disease alone while another 3.7% had
both intra and extracranial occlusive disease.9-10

Many prospective studies have confirmed that intracranial stenosis is an independent

predictor for poor outcomes such as recurrent vascular event and death despite the
use of antiplatelet agents. The annual event rate is approximately 15% per year.

17
Overview

VI. CLINICAL STROKE SYNDROME BASED ON BLOOD VESSEL INVOLVEMENT

Physicians seeing neurological cases are asked to answer several questions namely: Is there a lesion, Where is the
lesion and Can anything be done about the lesion?. A thorough history and goal directed physical
and neurological examination can often localize the region affected. This is particularly
important in TIA patients who have normal physical and neurological examinations.
As localization of lesion is a challenge, the table below on clinical stroke syndromes based on
blood vessel involvement can help one decide on what neuroimaging test to use and which area
to focus the study on.
Common Clinical Stroke Syndromes Based on Blood Vessel Involvement11-12
Blood Vessel
Signs and Symptoms Explanation
Involvement
- Contralateral weakness of the upper Involvement of more medial
and lower extremities, leg > face and structures which is supplied by
arm the ACA. Vascular variation
Anterior Cerebral - Bilateral lower extremity weakness may have both ACA arising
Artery - Incontinence from one cerebral stem
producing bilateral involvement
- Contralateral numbness of the upper
and lower extremities, leg > face and
arm
- Contralateral weakness of the upper Involvement of the somatic
and lower extremities, face and arm > motor area (face and arm)
leg supplied by the MCA in the
- Contralateral weakness of the lower frontal lobe
half of the face
- Preferential gaze looking away from Involvement of the frontal eye
the weakness fields in the prefrontal area.
Intact eye field forces the eye to
look the opposite side.
- Contralateral hemineglect Involvement of the parietal lobe
if the stroke is in the non-
Middle Cerebral dominant hemisphere
Artery - Contralateral hemisensory loss of the Involvement of the somatic
Proximal Segment upper and lower extremities sensory area (face and arm)
- Contralateral hemisensory loss of the supplied by the MCA in the
face to all modalities parietal lobe
- Receptive and Expressive Aphasia if Invovlement of areas for
with involvement of the dominant language. Expressive Aphasia
hemisphere (Brocas) is found in the fronto-
temporal area and Receptive
(Wernickes) is found in the
parieto-temporal area.
- Contralateral homonymous Involvement of the optic tracts
hemianopsia as it courses towards the
brainstem

18

Blood Vessel
Signs and Symptoms
Involvement
- Contralateral weakness of the
upper and lower extremities, face
and arm > leg
- Contralateral weakness of the
lower half of the face
Middle Cerebral
Artery - Contralateral hemisensory loss of
Superior Division the upper and lower extremities
- Contralateral hemisensory loss of
the face to all modalities
- Expressive aphasia
- Contralateral homonymous
hemianopsia
- Contralateral upper
quadrantanopsia
Middle Cerebral - Contralateral constructional
Artery apraxia
Inferior Division
- Receptive Aphasia
- Agraphia (inability to write)
Middle Cerebral - Acalculia (inability to calculate)
Artery - Right-Left confusion
(Gerstmann Syndrome) - Finger agnosia (inability to
recognize fingers)
Overview
Explanation
Involvement of the somatic motor
area (face and arm) supplied by the
MCA in the frontal lobe
Involvement of the somatic sensory
area (face and arm) supplied by the
MCA in the parietal lobe
Involvement of the Brocas area
found in the frontal suprasylvian
area
Involvement of the optic tracts as it
courses towards the brainstem
If with involvement of the non-
dominant parietal lobe
If with involvement of the
dominant temporal lobe,
infrasylvian including the angular
and supramarginal gyrus
(Wernickes)
Dominant inferior parietal lobe
(May occasionally include
ideomotor apraxia)

Posterior Cerebral
Involvement of the optic pathway
Artery - Homonymous hemianopsia
leading to the calcarine cortex
(Unilateral Occipital)

Damage to the primary visual

Posterior Cerebral cortex leads to blindness, with
- Bilateral visual loss
Artery involvement of the visual
- Unaware or denial of blindness
(Anton Syndrome) association areas, the patient is
unaware that they are unable to see

19
Overview

- Contralateral weakness of the Involvement of the yet

extremities uncrossed corticospinal tract
- Ipsilateral cranial nerve III palsy producing a contralateral
Posterior Cerebral Artery
with parasympathetic involvement weakness and the cranial nerve
(Weber Syndrome)
(dilated pupils) III producing ipsilateral third
nerve palsy at the midbrain

- Ipsilateral cerebellar ataxia Involvement of more lateral

Anterior Inferior - Contralateral weakness tracts of the pons.
Cerebellar Artery (Lateral - Contralateral numbness Contralateral numbness maybe
Pontine Syndrome/Marie-Foix variable
Syndrome)

- Ipsilateral facial numbness Involvement of the lateral

- Contralateral truncal and extremity tracts of the medulla.
numbness
Posterior Inferior
- Ipsilateral palatal, pharyngeal, and
Cerebellar Artery vocal cord paralysis producing
(Lateral Medullary dysphagia and dysarthria respectively
Syndrome/Wallenburg - Vertigo
Syndrome) - Ipsilateral ataxia
- Singultus (Hiccups)

- No affection of consciousness Commonly seen in ventral

- Quadriplegia pontine lesions
Basilar Artery - Unable to verbally communicate
(Locked in Syndrome) - ONLY Vertical Eye Movements
maybe intact

20
 Arterial Blood Supply of the Brain

Overview

Reference: Mumenthaler / Mattle, Fundamentals of Neurology 2006 Thieme.

21
Overview

VII. INCREASING THE YIELD FOR A CORRECT DIAGNOSIS OF STROKE

A good history is essential in arriving at a clinical diagnosis of stroke. Details in the history
particularly at the onset of the stroke are important to differentiate stroke from stroke
mimickers.

One should extract from patient or companions of patient the following:

? Exactly what time did the ictus (onset of stroke) occur?
?
What was the patient doing at the time of stroke?
?
What part or parts of the body was initially affected? Did it progress to involve
other parts?
?
Was the progression of neurologic deficit rapid or slow? Was the deficit maximal
at onset?
?
What are the accompanying signs and symptoms?
?
Did the event occur in the past?
?
If vital signs were taken, what was the blood pressure of the patient?
?
What were the interventions or medicines taken? What was the response of the
patient to the medicine?
?
What are the past and present illnesses of the patient e.g., hypertension, diabetes,
MI?

The presence of any of the following should alert the physician to consider conditions
other than stroke:

1. Gradual progressive course and insidious onset

2. Pure hemifacial weakness including forehead (Bells palsy)
3. Trauma
4. Fever prior to onset of symptoms
5. Recurrent seizures
6. Weakness with atrophy
7. Recurrent headaches (migraine, tension-type headache)
8. Isolated dizziness or vertigo
9. No vascular risk factor

There are other medical and neurologic conditions that can mimic a stroke. Hence, a list of stroke mimickers must
always be in the physicians head when providing care to a patient with suspected stroke.

22
 Overview
Conditions that can mimic stroke in the emergency department or clinics (according to
decreasing frequency):

1. Seizures
2. Systemic infection
3. Brain tumor
4. Toxic-metabolic
5. Positional vertigo
6. Cardiac
7. Syncope
8. Trauma
9. Subdural hematoma
10. Herpes encephalitis
11. Transient global amnesia
12. Dementia
13. Demyelinating disease
14. Cervical spine fracture
15. Myasthenia gravis
16. Parkinsonism
17. Hypertensive encephalopathy
18. Conversion disorder

VIII. CONFIRMATION OF THE DIAGNOSIS OF STROKE

Although the diagnosis of stroke is clinical, the differentiation between ischemic stroke and
hemorrhagic stroke would require neuroimaging. The SSP has been recommending on the
availability of at least a CT Scan in major municipalities in the country for use in documentation
and differentiation of types of stroke. Aware that there is a proven drug that can lyse the clot in a
blocked vessel and reduce disability makes the availability of CT scan a necessity. There are
scoring systems to help differentiate between the two types of stroke like Thailands Siriraj
scoring or the Philippines Diaz scoring.13 Unfortunately, the sensitivity and specificity of
scoring systems are not high enough to make a critical decision like giving thrombolytic agents in
a suspected ischemic stroke patient.

A thorough study of the CT Scan or MRI is important in testing eligibility for the thrombolytic
agent - Tissue Plasminogen Activator (r-TPA). The use of CT Scan and MRI for studying stroke
are discussed in the neuroimaging section of this handbook.

IX. RISK FACTORS FOR STROKE AND STROKE PREVENTION

The term CVA or Cerebro-Vascular Accident is still commonly used by many physicians. The
word accident is no longer acceptable as it is not surprising that a patient with known stroke
risk factors, especially if multiple and uncontrolled, eventually develops a stroke.

23
Overview

Strategies for preventing stroke and reducing stroke disability are many but can be divided into
primary (preventing a first stroke) or secondary (preventing stroke recurrence). Primordial
prevention is used to prevent the occurrence of risk factors for stroke.

Risk factors can be non-modifiable or modifiable. The non-modifiable risk factors consist of
older age, male sex, Non-White race, and positive family history for stroke or transient ischemic
attack.

The handbook provides recent evidences and corresponding guidelines for the more prevalent
modifiable risk factors for stroke. Locally, a nationwide case-control study showed the
following significant and independent risk factors for stroke among Filipinos.

The PNA-DOH RIFASAF Study14

(Risk Factors for Stroke Among Filipinos)

Variable Odds Ratio 95% Confidence Interval

Hypertension 6.01 4.48-8.05
Diabetes 1.60 1.10-2.32
Atrial Fibrillation 1.91 0.51-7.19
Myocardial Infarction 4.67 1.18-18.52
Rheumatic Heart Disease 3.69 1.05-12.99
Smoking 1.36 1.00-1.86
Snoring 3.37 2.49-4.58
Stress 1.69 1.25-2.29
Frequent Alcohol Intake 1.75 1.14-2.70
There are many emerging risk factors that may contribute to stroke which are not covered by this
handbook. Although the focus of this handbook is on individual risk factors, the appropriate
approach in preventing the first stroke or preventing stroke recurrence is evaluating the total risk
assessment for stroke and arriving at individualized or tailored risk management. Using risk
assessment tools such as the Framingham Score to predict the probability of developing stroke
has not been a practice of local physicians. We await the validation of the Framingham CVD
Risk Score and hopefully arrive at a recalibrated tool useful for Filipinos. Enabling a patient to
be aware of his risk of developing MI or stroke within 5 or 10 years time may encourage him to
address identified risks and initiate appropriate healthy lifestyle changes.

Atherothrombosis is the underlying condition that results in myocardial infarction, stroke and
vascular death. Awareness of the prevalence of these risk factors can help direct our efforts and
limited logistics to the more prevalent risk factors. The prevalence of risk factors for
atherosclerosis in the Philippines is shown below.

24
 Overview
Philippine Prevalence for Atherosclerosis Risk Factors15 (>20 years old)
(2003 National Nutrition Health Survey)

Risk Factor Basis Prevalence (%)

Hypertension BP or history 17.4
FBS >125 mg/dL or history or
Diabetes 4.6
use of anti-diabetes medication
Stroke History 1.4
Hypercholesterolemia TC =240 mg/dL 8.5
Current Smoking (M/F) History 56.3 / 12.1

Obesity: BMI BMI =30 4.8

Obesity: Waist Hip Ratio
1.0 for men; 0.85 for women 12.1 / 54.8
(M/F)
Angina Pectoris History or questionnaire 12.1
Questionnaire or ankle-brachial
Peripheral Arterial Disease 8.9
index

X. SSP CLINICAL PRACTICE GUIDELINES

Ten years since the release of the 1st edition of the SSP guidelines, there have been three
revisions of the SSP stroke guidelines reflecting the dynamic research interest and emergence
of new evidences in stroke management. Clinical practice guidelines are developed for the
purpose of reducing inappropriate care, controlling geographic variations in practice patterns,
and allowing effective use of health care resources. Despite the availability of numerous
guidelines on stroke, international stroke registries have shown that there is still underutilization
of evidence-proven treatments.

Among the barriers that could explain the variations is physician knowledge and attitude. The
SSP guidelines have been used by many including Filipino neurologists who handle primarily
stroke cases. A survey reported in 2009 among 176 of 217 locally practicing board-certified
Filipino adult neurologists revealed the following practice patterns in relation to the SSP
guidelines: underutilization of warfarin among patients with non-valvular atrial fibrillation,
preference to start pharmacologic control of BP below the recommended systolic levels
especially in ischemic stroke, extensive use of neuroprotective agents and limited experience
with thrombolytic use.16

Since its conception in 1995, the SSP has been engaging in various activities to pursue its mission
and vision. The annual conventions held in different parts of the country are designed to help
doctors, nurses, physical therapists, barangay health workers and emergency personnel to
perform well their different roles in stroke care delivery. SSP holds lay fora, conducts stroke

25
Overview

workshops and helps support stroke survivor groups. To provide the much needed data on
stroke, SSP encourages local stroke researches through its research contests and conducts its
own researches. Thru SSPs effort to promote awareness on stroke, proclamation no. 92 was
signed in 2001 by Pres. Gloria Arroyo declaring every third week of August as Brain Attack
Awareness Week. Having a multidisciplinary membership with nine chapters outside Manila,
SSP continues to align and collaborate with other societies to pursue its goal to limit the
incidence and the burden due to the second leading cause of mortality and the leading cause of
disability afflicting the Philippines - STROKE.

Bibliography

1. Dans AL, Morales DD, Abola TB, Roxas A , et al; for NNHeS 2003 Group. National Nutrition
and Health Survey (NNHeS): Atherosclerosis-related diseases and risk factors. Phil J Int Med
2005;43;103-115.
2. Navarro J. Prevalence of stroke: a community survey. Phil J Neuro 2005; 9:11-15.
3. Collantes, E. For SSP. The SSP SICAP (Stroke in Currimao Philippines) Study. Presented
during the 10th SSP Annual Convention - The Philippine Stroke Agenda. Holiday Inn, Clark
Field Pampanga, August 20-22, 2009
4. Roxas A. for SSP. The SSP SAGIP (Stroke Awareness Gap in the Philippines) Study. Presented
during the 10th SSP Annual Convention - The Philippine Stroke Agenda. Holiday Inn, Clark
Field Pampanga, August 20-22, 2009
5. Hurwitz AS, Brice JH, Overby BA, Evenson KR (2005). Directed use of the Cincinnati
Prehospital Stroke Scale by laypersons. Prehosp Emerg Care 9 (3): 2926.
6. The TMC Neurology Residents Stroke Education Program - stroke discharge pamphlet of The
Medical City
7. Yu R., San Jose C, Gan R. Et al. Sources and reasons for delays in the care of acute stroke
patients. Journal of Neurological Sciences 199; 49-54. 2002
8. Navarro J, Bitanga E, Suwanwela N, et al. Complication of acute stroke: A study in ten Asian
countries. Neurology Asia 2008; 13: 33-39
9. Leung TW, Kwon SU, Wong KS. Management of patients with symptomatic intracranial
atherosclerosis. Int J Stroke. 2006 Feb;1(1):20-5.
10. De Guzman V, Yu R and San Jose C. Risk factors and outcome among Filipino stroke patients
with intracranial stenosis - presented during the PNA annual convention
11. Brazis P., Masdeu J., Biller J., LOCALIZATION IN CLINICAL NEUROLOGY 5th ed.
Philadelphia:Lippincott Williams & Williams; 2007
12. Ropper A., Samuels M., ADAMS AND VICTORS PRINCIPLES OF NEUROLOGY 9th ed.
USA: McGraw Hill;2009
13. Diaz, A., A scoring system to differentiate cerebral hemorrhage from infarction. Santo Tomas
Journal of Medicine. Sept-Dec Vol 35 no. 3 1986; 168-174
14. Roxas A. for the PNA-DOH RIFASAF Collaborators. The RIFASAF Project: a case-control
study on risk factors for stroke among Filipinos. PJON June Vol 6 no.1 2002 1-7
15. Atherosclerosis Related diseases and risk factor. Antonio L. Dans MD, Dante D. Morales MD,
Teresa B. Abola MD, Artemio Roxas Jr. et al for NNHes 2003 Group. National Nutrition and
health Survey (NNHeS): Philippine Journal of Internal Medicine 2005 May- June 43; 103-115
16. Roxas A for the PNA Stroke Council. Management pattern of stroke by Filipino neurologists: a
nationwide cross-sectional survey of locally practicing board certified Philippine Neurological
Association fellows. PJON 2009

26
Primary & Secondary
Prevention
 PREFACE TO THE GUIDELINES ON
PRIMARY AND SECONDARY PREVENTION OF STROKE

?
These practice guidelines provide an overview of the epidemiology and evidences
associated with established and modifiable stroke risk factors, followed by
recommendations for reducing stroke risk. These revised guidelines reflect current
Primary & Secondary

knowledge on primary and secondary stroke prevention.

Prevention

?
The strategy in developing these guidelines was to utilize information from several existing
national consensus and evidence-based guidelines to highlight significant associations
between a risk factor and stroke and how modifying the risk factor through treatment or
lifestyle modification can improve outcome.
?
The Stroke Prevention Writing Group members are active members of the Stroke Society
of the Philippines and the Philippine Neurological Association invited by the committee
chairs on the basis of each reviewers interest, training and previous work in the relevant
topic areas. Members then updated the previous editions using recently published local
data. The updated working paper was submitted for initial comments by the society
members, and later to key opinion leaders and institutions.
?
Each major topic first discusses epidemiology (Section A) of a risk factor and its association
with stroke, then highlights clinical trials or interventions on the risk factor for preventing
stroke (Section B). When evidence is available, a separate subsection (Section B1) discusses
primary- and secondary-prevention trials. Section C states the recommendations based on
evidences.
?
When available, the strength of the recommendations are included and graded according to
the American Heart Association (AHA)/American Stroke Association methods of
classifying levels of certainty of the treatment effect and the class of evidence.

Classes and Levels of Evidence Used in AHA Recommendations

Class I Conditions for which there is evidence for and/or general agreement
that the procedure or treatment is useful and effective
Conditions for which there is conflicting evidence and/or a divergence
Class II of opinion about the usefulness/efficacy of a procedure or treatment
IIa Weight of evidence or opinion is in favor of the procedure or treatment
IIb Usefulness/efficacy is less well established by evidence or opinion
Conditions for which there is evidence and/or general agreement that
Class III the procedure or treatment is not useful/effective and in some cases may
be harmful
Level of Evidence A: Data derived from multiple randomized clinical trials
Level of Evidence B: Data derived from a single randomized trial or nonrandomized
studies
Level of Evidence C: Expert opinion or case studies
?
Recommendations considered the cost-effective treatment of drugs with established
efficacy.
?
These guidelines concentrated on modifiable risk factors: hypertension, diabetes, atrial

28
fibrillation (AF) and other specific cardiac conditions, dyslipidemia, carotid artery stenosis,
peripheral arterial disease, obesity, and lifestyle (exposure to cigarette smoke, excessive
alcohol use, and physical inactivity).
?
Other less well-documented or potentially modifiable risk factors are recognized. These
include metabolic syndrome, drug abuse, oral contraceptive use, sleep-disordered breathing,

Primary & Secondary

migraine headache, hyperhomocysteinemia, hypercoagulability, inflammation and infection.
Future editions may highlight these topics.

Prevention
?
Because most strokes are cerebral infarcts, these recommendations focus primarily on the
prevention of ischemic stroke or transient ischemic attack (TIA).
?
Although the primary outcome of interest is the prevention of stroke, many
recommendations reflect the evidence on the reduction of all vascular outcomes after
stroke, including stroke, myocardial infarction (MI) and vascular death.
?
For secondary stroke prevention, the aim is to provide comprehensive and timely evidence-
based recommendations on the prevention of ischemic stroke among survivors of ischemic
stroke or TIA.

I. HYPERTENSION

Stroke mortality rates are correlated with the prevalence of hypertension. Despite data showing
that the first and recurrent stroke can be prevented by blood pressure control, hypertension
awareness, treatment and control remain low.1

A. Epidemiology:

Hypertension is the most important modifiable risk factor for stroke. The higher the blood
pressure, the greater is the stroke risk. The prevalence of hypertension has increased to 25.3%
based on the 2008 NNHeS II survey. The population attributable risk (PAR) of hypertension
for stroke is high at around 25%.3 Hypertensive people are three to four times more likely to
have a stroke than non-hypertensive people. Furthermore, both systolic and diastolic
hypertension are risk factors. In the elderly, however, elevated systolic blood pressure is more
prevalent.

B. Risk Modification:

Treatment of hypertension substantially reduces the risk of stroke. All classes of

antihypertensive drugs are effective for BP control. A meta-analysis shows that BP lowering
confers a 30% to 40% stroke risk reduction. A 10 to 12 mmHg SBP reduction and a 5 to 6
mmHg DBP reduction confers relative reductions in stroke risk of 38%. The treatment of
isolated systolic hypertension in the elderly decreases the risk for stroke by 36%.4 Furthermore,
small BP reductions in a population may lead to substantial reductions in stroke risk. It is
estimated that a population strategy to reduce systolic BP (SBP) by 2 mmHg will reduce stroke
mortality by 6%.5 A 3 mmHg SBP reduction reduces risk by 8%. A 5 mmHg reduction reduces
risk by 14%. Similar to other cardiovascular disorders, stroke reduction is progressive as BP is
reduced to at least 115/75 mmHg.6

29
 Diet modification encouraging low salt and high potassium content (DASH diet) may help keep
the blood pressure of an individual within normal levels. Regular aerobic exercise and keeping
the body weight in normal range may also help the BP of an individual under control.

B.1. Primary Stroke Prevention

Primary & Secondary
Prevention

There is strong evidence that the control of high BP contributes to the prevention of
stroke.5 The benefit of treating the elevated blood pressure is seen even in the very
elderly. The choice of antihypertensive agents should be individualized. BP
reduction is generally more important than the specific agent used to achieve this
goal.

Hypertension remains undertreated in the community, and programs to improve

treatment compliance need to be developed and supported. The Seventh Report of
the Joint National Committee on Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure (JNC 7) provides a comprehensive, evidence based approach
to the classification and treatment of hypertension.5

Classification and Management of BP for Adults*

Initial drug therapy
BP SBP* DBP* Lifestyle Without
With Compelling
Classification mmHg mmHg Modification Compelling
Indications
Indication
Normal <120 and <80 Encourage No Drug(s) for
or Yes antihypertensive compelling
Prehypertension 120-139
80-89 drug indicated. indications.

Thiazide-type
diuretics for most.
Stage 1 140-159 or Yes May consider
Hypertension 90-99 ACEI, ARB, BB,
Drug(s) for the
CCB, or compelling
combination.
indications. Other
antihypertensive
Two-drug drugs (diuretics,
combination for ACEI, ARB, BB,
Stage 2 most (usually CCB) as needed.
=160 or =100 Yes thiazide-type
Hypertension
diuretics and
ACEI or ARB or
BB or CCB).

30
DBP, diastolic blood pressure; SBP, systolic blood pressure.
Drug abbreviations: ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin-receptor
blocker; BB, beta-blocker; CCB, calcium-channel blocker.
*Treatment determined by highest BP category.
Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension.
Treat patients with chronic kidney disease or diabetes to BP goal of <80 mmHg.

Primary & Secondary

B.2. Secondary Stroke Prevention

Prevention
The overall decrease in stroke is related to the degree of BP lowering achieved. Meta-
analyses of randomized controlled trials (RCTs) confirm an approximate 30% to
40% stroke reduction with BP lowering.7,8 Furthermore there is a continuous
association of both SBP and DBP with the risk of ischemic stroke.

The JNC 7 stresses the importance of lifestyle modifications in the overall

management of hypertension. SBP reductions have been associated with weight
loss; diet rich in fruits, vegetables and low-fat dairy products; regular aerobic physical
activity; and limited alcohol consumption.

Data on the relative benefits of specific antihypertensive regimens for secondary

stroke prevention continue to increase. A meta-analysis showed a significant
reduction in recurrent stroke with diuretics and combined diuretics and angiotensin-
converting enzyme inhibitors (ACEIs), but not with beta-blockers (BBs) or ACEIs
alone.9 Whether a particular class of antihypertensive drug or a particular drug
within a given class offers an advantage in patients after ischemic stroke remains
uncertain.

In addition, there are certain classes of BP-lowering agents, particularly ACEIs and
ARBs, that may have properties other than BP reduction that are beneficial with
regard to stroke risk reduction.10,11 Among hypertensive diabetics, the use of ACEIs
or ARBs reduces the risk of major vascular events and stroke by 24%.

There are data that show that early use of oral antihypertensives for secondary stroke
prevention, particulary ARBs, may be safe with no excess in adverse event. The
effect on functional outcome is apparently neutral.

C. Recommendations:

C.1. Primary Stroke Prevention

Regular screening for hypertension (at least every 2 years in most adults and more
frequently in minority populations and the elderly) and appropriate management
(Class I, Level A), including dietary changes, lifestyle modification and
pharmacological therapy as summarized in JNC 7 and ESH 2007, are recommended.

31
 C.2. Secondary Stroke Prevention

1) Antihypertensive treatment is recommended for both prevention of recurrent

stroke and of other vascular events in patients who have had an ischemic stroke or
TIA and are beyond the hyperacute period (Class I-A). Because this benefit
extends to people with or without a history of hypertension, this recommendation
Primary & Secondary

should be considered for all ischemic stroke and TIA patients (Class IIa-B).
Prevention

2) The absolute target BP level and reduction are uncertain and should be
individualized, but benefit has been associated with an average reduction of
10/5mmHg. BP levels of <140/90mmHg are acceptable targets. For diabetic
stroke patients, BP levels of <130/80mmHG are appropriate (Class IIa-B).

3) BP should be adequately controlled in patients with hypertension. Physicians

should check the BP of all patients at every visit. Patients with hypertension
should be advised to monitor their BP at home.

4) Several lifestyle modifications have been associated with BP reductions and should
be included as part of a comprehensive antihypertensive therapy (Class IIb-C).

5) The optimal drug regimen remains uncertain. However, available data support the
use of diuretics, CCBs, ACEIs, ARBs, or their combinations (Class I-A). The
choice of specific drugs and targets should be individualized on the basis of
reviewed data and consideration of specific patient characteristics (e.g.,
extracranial cerebrovascular occlusive disease, renal impairment, cardiac disease
or diabetes) (Class IIb-C).

6) The Stroke Society of the Philippines supports the guidelines set forth by the
Philippine Society of Hypertension.

Bibliography
1. Chapman N, Neal B. Blood pressure lowering for the prevention of first stroke. In: Chalmers J,
ed. Clinicians Manual on Blood Pressure and Stroke Prevention, 3rd ed. London: Science Press;
2002; p.21-31.
2. Sy RG, Dans AL, et al. Prevalence of dyslipidemia, diabetes, hypertension, stroke and angina
pectoris in the Philippines. NNHeS 2 2008
3. Gorelick PB. An integrated approach to stroke prevention. In: Chalmers J, ed. Clinicians
Manual on Blood Pressure and Stroke Prevention, 3rd ed. London: Science Press; 2002; p. 55-65.
4. SHEP Cooperative Research Group. Prevalence of stroke by antihypertensive drug treatment
in older persons with isolated systolic hypertension. Final result of the Systolic Hypertension in
the Elderly Program (SHEP). JAMA 1991;265:3255-3264
5. Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure; National High Blood Pressure Education Program Coordinating Committee. The
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-72.

32
 6. Lawes CMM, Bennett DA, Feigin VL, Rodgers A. Blood pressure and stroke. an overview
of published reviews. Stroke 2004;35:1024-1033.
7. Yusuf S, Sleight P, Pogue J, Bosch J, et al. Effects of an angiotensin-converting-enzyme
inhibitor, ramipril, on cardiovascular events in high-risk patients: the Heart Outcomes
Prevention Evaluation Study Investigators. N Engl J Med 2000;342:145-153.
8. Lawes CMM, Bennett DA, Feigin VL, Rodgers A. Blood pressure and stroke: an overview of

Primary & Secondary

published reviews. Stroke 2004;35:776-785.
9. Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke

Prevention
and other vascular events: a systematic review. Stroke 2003;34:2741-2748.
10. PROGRESS Collaborative Group. Randomized trial of a perindopril-based blood pressure
lowering regimen among 6105 individuals with previous stroke or transient ischemic attack.
Lancet 2001;358-1033-41.
11. Dahlof B. Deverux RB, Kjeldsen SE, et al. Cardiovascular morbidity and mortality in the
losartan intervention for endpoint reduction in hypertension study (LIFE) a randomized trial
against atenolol. Lancet 2002;359:995-1003.
12. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with
ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the
American Heart Association/American Stroke Association Council on Stroke [trunc]. Stroke
2006;37:577-617.
13. Morbidity and mortality after stroke. Epreosartan compared with nitrendipine for secondary
prevention: principal results of a prospective randomized controlled study.(MOSES) Stroke
2005 Jun 36(6);1218-26
14. Diener,HC,SaccoRL,Yusuf S et al. Effects of aspirin plus extended release dipyridamole versus
clopidogrel and telmisartan on disability and cognitive function after recurrent stroke in patients
with ischemic stroke in the Prevention Regimen for Effectively Avoiding Second Strokes
(PRoFESS) trial; a double blind, active and placebo controlled study. The
Lancet.com/neurology. published online August 30, 2008.
15. SchraderJ,Luders S,et al. The ACCESS Study. Evaluation of acute candesartan therapy in stroke
survivors. Stroke,2003;34;1699-1703
16. Treatment of hypertension in patients 80 years of age or older; The HYVET Study Group; N
Engl J Med 2008; 358:1887-1898

II. DIABETES MELLITUS

A. Epidemiology:

A.1. Epidemiology of Diabetes Mellitus in the Philippines

Diabetes mellitus (DM) is a serious public health problem in the Philippines. Estimated to
affect 8% of the adult population worldwide, the local prevalence of DM (fasting blood
sugar >125mg/dL) according to the 2003 National Nutrition Health Survey1 is 3.4%. The
2008 7th National Nutrition Survey of FNRI2 showed a further increase in the prevalence
of Filipinos with impaired FBS at 4.8% despite health campaigns.

A.2. Diabetes and Stroke

In adults with stroke, DM is often present as a co-morbid condition. The local RIFASAF
case-control study showed a 1.6-fold higher risk for stroke among those with DM

33
 compared to patients without stroke.3 Case-control studies of stroke patients and
prospective epidemiological studies have confirmed an independent effect of DM on
ischemic stroke, increasing risk by 1.8- to nearly 6-fold.4 DM is frequently encountered in
stroke care, being present in 15% to 33% of patients with ischemic stroke.5
Primary & Secondary

A.2.1. ICH
Prevention

Most case control studies examining the relationship between DM and ICH have not
concluded that DM is an independent risk factor for ICH. However, a cohort study
conducted on over 20,000 middle-aged male cigarette smokers found that the
presence of DM marginally increased the risk of ICH.6 A meta-analysis that
combined this cohort study with 9 case-control studies suggested that DM is a risk
factor for ICH (RR=1.30; 95% CI, 1.02 to 1.67).7 DM is not, however, as potent a
risk factor for ICH as chronic hypertension since epidemiologic studies have
consistently shown a stronger association between chronic hypertension and ICH.

Subarachnoid hemorrhage (SAH) is usually due to rupture of an intracranial

aneurysm. DM has not been found to be independently associated with aneurysmal
SAH in epidemiologic studies.

A.2.2. DM and Ischemic Stroke8

DM is a definite risk factor for stroke. The increased risk for stroke is primarily due to
the increased atherogenic risk within extracranial and intracranial arteries,
attributable to abnormal plasma lipid profiles, hypertension and hyperglycemia.
However, other pathological features associated with diabetes, such as insulin
resistance and hyperinsulinemia, also lead to atherosclerotic changes in these vessels
independently of glycemia, or other attendant cardiovascular risk factors. This is
particularly true within the smaller cerebral vessels increasing the incidence of both
overt and silent lacunar infarction.

A.3. Diabetes and Stroke Outcome

DM not only significantly increases the risk of stroke, but also is a predictor of reduced
survival following stroke. Diabetic patients have a worse prognosis, with a twofold
increase in the likelihood of subsequent strokes.9 The presence of diabetes is associated
with significantly greater permanent neurological and functional disability and longer
hospital stay. Death amongst survivors of the initial stroke is increased, with a doubling of
the rate within the first year and only a 20% 5-year survival rate. Diabetes also more than
triples the risk of stroke-related dementia.10

A.3.1. Increased Risk of ICH during RTPA

A study of 138 rtPA treated patients suggested that diabetes may be a predictor of
ICH in rtPA-treated patients.11 In this cohort of patients who were treated, DM was

34
associated with a 25% (8 of 32) symptomatic hemorrhage rate compared with a 5%
symptomatic hemorrhage rate (5 of 106) in non-diabetics. DM independently predicted ICH
(OR, 6.73; 95% CI 2.20 to 22.4).

A.3.2. Diabetes and Recurrent Stroke

Primary & Secondary

Diabetes is also one of the most consistent predictors of recurrent stroke or stroke

Prevention
after TIA.9, 1215 The increased risk of recurrent stroke due to diabetes ranges from
2.1 to 5.6 times that of nondiabetic patients9, 16 and is independent of glucose
control during the interstroke period.17 The significance of these findings is
underscored by the increased morbidity and mortality associated with recurrent
stroke.18

B. Risk Modification

B.1. Primary Stroke Prevention

DM has microvascular and macrovascular complications. Intensive DM therapy delays

the onset and slows down the progression of microvascular complications, such as
retinopathy, nephropathy and neuropathy,19 but its beneficial effect on macrovascular
complications such as stroke is uncertain.11 A systematic review of RCTs on intensive
insulin therapy (IIT) showed that IIT can decrease the occurrence of macrovascular events
by up to 42%, 20 including stroke, myocardial infarction (MI), angina and claudication,
among patients with type 1 DM.

In type 1 and type 2 diabetes, randomized controlled trials of intensive versus standard
glycemic control have not shown a significant reduction in CVD outcomes during the
randomized portion of the trials. Long-term follow-up of the DCCT and UK Prospective
Diabetes Study (UKPDS) cohorts suggests that treatment to A1C targets below or around
7% is associated with long-term reduction in risk of macrovascular disease.21

Studies on glucose lowering using oral antidiabetic agents are often confounded by other
factors such as duration of diabetes, age of patient and diabetes severity. In the UKPDS,
however, the use of metformin as first-line therapy in obese patients with type 2 diabetes
reduced stroke risk by 42% compared with the conventionally treated group.22
Sulphonylurea treatment over 10 years was found to reduce the development of
microvascular complications in subjects with diabetes, but the risk of stroke was raised.23

A recent meta-analysis of several controlled trials using pioglitazone demonstrated a

significant 18% (95% CI 628%; p = 0.005) reduction for MI, stroke or death as compared
with placebo.24 Further randomized, prospective trials (e.g. the ongoing National Institute
of Healths 4-year IRIS trial) will assess the efficacy of pioglitazone as a new approach to
preventing recurrent stroke and heart attack.

35
 Sub-studies on diabetic patients included in drug trials show that the use of ACEIs25 and
ARBs26 can reduce the combined outcome of MI, stroke and cardiovascular death by 21%
to 33%. Similarly, ACEIs and ARBs decrease new-onset diabetes. Primary stroke
prevention guidelines have emphasized more rigorous BP control (target BP < 130/80
mmHg) among both type 1 and type 2 diabetics.27 The American Diabetes Association
Primary & Secondary

(ADA) now recommends that all patients with diabetes and hypertension be treated with a
regimen that includes either an ACEI or ARB.
Prevention

The ideal goal for BP lowering among hypertensive coronary heart patients with diabetes
was studied in a substudy of the INVEST trial (International Verapamil SR-Trandolapril
Study) 28 where a calcium antagonist was compared against a beta-blocker, followed by
more drugs if needed to lower pressure to target level. Little difference was found between
the tight control (with systolic pressure maintained at below 130), and moderate control
groups (with pressures from 130 to under 140). Of the 6,400 studied: 12.7% who had tight
control, 12.6% of those with moderate control, and 19.8% of those with uncontrolled
blood pressure (with SBP above 140), died or had a heart attack or stroke. During the
extended follow-up period, the risk of death from any cause was actually higher in the tight
control group, compared to those in the moderate control group (22.85 versus 21.8%).28
This study suggests that moderate blood pressure control is a reasonable range to aim for
among patients with DM, hypertension and coronary heart disease.

Hyperlipidemia is a common co-morbidity of diabetes. For any given cholesterol level,

patients with diabetes have a greater frequency of cardiovascular events for which
aggressive therapy of diabetic dyslipidemia is indicated, aiming for LDL<100 mg/dL or
even up to 70 mg/dL among very high-risk groups.29 The use of statins among DM
patients can reduce vascular events, including stroke.30,31 Addition of a statin for DM
patients at high risk reduces stroke risk by 24%, and in those with one additional risk factor
by 48%.

B.2. Secondary Stroke Prevention

Patients with diabetes are even more vulnerable once they have suffered an initial stroke.
In such patients, the risk of a recurrent stroke is increased 12-fold and therefore more than
doubled as compared with non-diabetic patients with a history of stroke.32 Diabetic
patients with TIA have an increased stroke risk during the first week after a TIA.

Many of the available data on stroke prevention in DM patients pertain to primary

prevention. However, glycemic control is consistently recommended in multiple
guidelines of both primary and secondary prevention of stroke and cardiovascular disease.
Among patients with type 2 DM with or without vascular events, such as stroke,
multifactorial approaches involving intensive treatments to control hyperglycemia,
hypertension, dyslipidemia and microalbuminuria reduce the risk of cardiovascular
events.33 These approaches included behavioral measures and the use of a statin, ACEI,
ARB and antiplatelet drugs, as appropriate. The beneficial role of antiplatelets among
stroke patients with or without diabetes has been proven in many trials.

36
 Pioglitazone reduces the incidence of stroke among non-diabetic patients with a recent
history of TIA or ischemic stroke. In the PROACTIVE study, 34 patients with type 2
diabetes and macrovascular disease were randomized to either pioglitazone, or placebo, in
addition to existing glucose-lowering and cardiovascular agents. Stroke was frequent in
the placebo group with an event rate of 4.5%, even though over 80% of the patients were
taking an antiplatelet agent at baseline. In a sub-analysis of the patients with previous

Primary & Secondary

stroke in the PROACTIVE study, pioglitazone reduced the risk of recurrent stroke by 47%

Prevention
relative to placebo. A recent meta-analysis of several controlled trials using pioglitazone
demonstrated a significant 18% (95% CI 628%; p= 0.005) reduction for MI, stroke or
death as compared with placebo.27

Although the Heart Protection Study data revealed a 24% reduction of stroke incidence
for simvastatin compared with placebo in patients with diabetes, there was no documented
significant risk reduction for recurrent stroke.35 The SPARCL study showed that a higher
dose of 80 mg atorvastatin reduced the risk of recurrent stroke by 16% relative to placebo
even in patients with stroke or TIA without prior coronary heart disease.36 A recently
published meta-analysis of 14 randomized statin trials in 18,686 diabetic patients showed a
highly significant stroke risk reduction in diabetic patients (21%; 95% CI 733%) that was
more pronounced than in the non-diabetic group (16%; 95% CI 724%).37

C. Recommendation:

1) A long-term, intensified DM control, which includes behavioral and

pharmacological modification to prevent microvascular and macrovascular
complications, is recommended.
2) Lowering A1C to below or around 7% has been shown to reduce microvascular and
neuropathic complications of type 1 and type 2 diabetes. Therefore, for
microvascular disease prevention, the A1C goal for non-pregnant adults in general is
<7%.13 (Class I-A). The general goal of A1C of <7% appears reasonable for many
adults for macrovascular risk reduction which includes stroke prevention.13 (B)
3) Rigorous BP and lipid control should be considered in patients with diabetes (Class
IIa-B).
4) A target BP of <130/80 mmHg (Class I-A) is recommended as part of a
comprehensive risk-reduction program. An ACEI or ARB is preferred for DM
patients.
5) Among patients with DM, hypertension and coronary heart disease, aiming for
moderate control (BP <140/90) have similar effect than aiming for tight BP control
of <130/80.
6) Adults with DM, especially those with additional risk factors, should be treated with a
statin to lower the risk of a first stroke (Class I-A).
7) Among diabetic patients with TIA or stroke, glucose control is recommended to
near-normoglycemic levels to reduce microvascular complications (Class I-A) and
possibly macrovascular complications (Class IIb-B). The goal for hemoglobin A1c
should be <7% (Class IIa-B).
8) Use aspirin therapy (75162 mg/day) as a secondary prevention strategy in those
with diabetes with a history of CVD (A). However, there is no sufficient evidence to

37
 recommend aspirin for primary prevention in lower risk individuals with diabetes,
such as men <50 years of age or women <60 years of age without other major risk
factors. Among patients in these age-groups with multiple other risk factors, clinical
judgment is required .
Primary & Secondary

Bibliography
Prevention

1. Dans AL, Morales DD, Abola TB, Roxas A, et al; for NNHeS 2003 Group. National Nutrition
and Health Survey (NNHeS): Atherosclerosis-related diseases and risk factors. Phil J Int Med
2005;43;103-115.
2. http://www.fnri.dost.gov.ph
3. A Roxas. The RIFASAF project: A case control study on risk fctors fro stroke among Filipinos.
Phil J Neuro 2002 ; 6: 1-7
4. American Heart Association/American Council on Stroke. Guidelines for prevention of
stroke in patients with ischemic stroke or transient ischemic attack. Stroke 2006;37:577-617.
5. Kissela BM, Khoury J, Kleindorfer D et al. Epidemiology of ischemic stroke in patients with
diabetes: the Greater Cincinnati/Northern Kentucky Stroke Study. Diabetes Care 2005;
28:355-9.
6. Leppala JM, Virtamo J, Fogelholm R, Albanes D, Heinonen OP. Different risk factors for
different stroke subtypes: association of blood pressure, cholesterol, and antioxidants. Stroke
1999; 30:2535-2540.
7. Ariesen MJ, Claus, SP, Rinkel GJE, Algra A. Risk factors for intracerebral hemorrhage in the
general population. A systemic review. Stroke 2003; 34(8):2060-2065.
8. Abbott R, Donahue R, Macmahon S, et al. Diabetes and the risk of stroke. JAMA
1987;257:949-952.
9. Hankey GJ, Jamrozik K, Broadhurst RJ, Forbes S, Burvill PW, Anderson CS,Stewart-Wynne
EG: Long-term risk of first recurrent stroke in the Perth Community Stroke Study. Stroke
29:24912500, 1998
10. Luchsinger JA, Tang MX, Stern Y, Shea S, Mayeux R. Diabetes mellitus and risk of Alzheimers
disease and dementia with stroke in a multiethnic cohort. Am J Epidemiol 2001; 154:635-41.
11. Demchuk A, Morgenstern L, Krieger DW, Chi LT. Serum glucose level and diabetes predict
tissue plasminogen activator-related intracerebral hemorrhage in acute ischemic stroke. Stroke.
1999;30:34-39.
12. Johnston SC, Sidney S, Bernstein AL, Gress DR: A comparison of risk factors for recurrent
TIA and stroke in patients diagnosed with TIA. Neurology 60:280285, 2003
13. Staaf G, Lindgren A, Norrving B: Pure motor stroke from presumed lacunar infarct: long-term
prognosis for survival and risk of recurrent stroke. Stroke 32:25922596, 2001
14. Eriksson SE, Olsson JE: Survival and recurrent strokes in patients with different subtypes of
stroke: a fourteen-year follow- up study. Cerebrovasc Dis 12:171180, 2001
15. Petty GW, Brown RD Jr, Whisnant JP, Sicks JD, OFallon WM, Wiebers DO: Survival and
recurrence after first cerebral infarction: a population-based study in Rochester, Minnesota,
1975 through 1989. Neurology 50:208 216.
16. Petty GW, Brown RD Jr, Whisnant JP, Sicks JD, OFallon WM, Wiebers DO: Survival and
recurrence after first cerebral infarction: a population-based study in Rochester, Minnesota,
1975 through 1989. Neurology 50:208 216.
17. Alter M, Lai SM, Friday G, Singh V, Kumar VM, Sobel E: Stroke recurrence in diabetics: does
control of blood glucose reduce risk? Stroke 28:11531157, 1997
18. Jorgensen HS, Nakayama H, Reith J, Raaschou HO, Olsen TS: Stroke recurrence: predictors,
severity, and prognosis: the Copenhagen Stroke Study. Neurology 48:891 895, 1997

38
19. The Diabetes Control and Complications Trial (DCCT) Research Group. Effect of intensive
diabetes management on macrovascular events and risk factors in the diabetes control and
complications trial. Am J Cardiol 1995;75:894-903.
20. United Kingdom Prospective Study (UKPDS) 33. Lancet 1998:352;837-853.
21. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes
mellitus: results of the HOPE study and MICRO-HOPE substudy. Heart Outcomes

Primary & Secondary

Prevention Evaluation Study Investigators. Lancet 2000;355:253-259.
22. Executive Summary: Standards of Medical Care in Diabetes-2010. Diabetes Care, Volume 33,

Prevention
Supplement 1, January 2010.
23. Effect of intensive blood-glucose control with metformin on complications in overweight
patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group.
Lancet 1998; 352:854-65.
24. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional
treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK
Prospective Diabetes Study (UKPDS) Group. Lancet. 1998; 352:837-53.
25. Lincoff AM, Wolski K, Nicholls SJ, Nissen SE. Pioglitazone and risk of cardiovascular events in
patients with type 2 diabetes mellitus: a metaanalysis of randomized trials. JAMA 2007;
298:1180-8.
26. Lindholm LH, Ibsen H. Dahlof B, et al; LIFE Study Group. Cardiovascular morbidity and
mortality in patients with diabetes in the Losartan Intervention For Endpoint reduction in
hypertension Study (LIFE): a randomized trial against atenolol. Lancet 2002;359:1004-1010.
27. Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure; National High Blood Pressure Education Program Coordinating Committee. The
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-72.
28. Pepine CJ, Handberg EM, Cooper-DeHoff RM et al. A calcium antagonist vs a non-calcium
antagonist hypertension treatment strategy for patients with coronary artery disease. The
International Verapamil-Trandolapril Study (INVEST): a randomized controlled trial. JAMA.
2003 Dec 3;290(21):2805-16.
29. Executive Summary of the Third Report of the National Cholesterol Education Program
(NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in
Adults (Adult Treatment Panel III). JAMA 2001;285:2486-2497.
30. Cooper-DeHoff RM, Gong Y, Handberg EM, et al.. Tight blood pressure control and
cardiovascular outcomes among hypertensive patients with diabetes and coronary artery
disease. JAMA. 2010 Jul 7;304(1):61-8.
31. Collins R, Armitage J, Parish S, et al. For the Heart Protection Study Collaborative Group.
MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 5963 people
with diabetes: a randomized placebo-controlled trial. Lancet 2003;361:2005-2016.
32. Colhoun HM, Betteridge DJ, Durnington PN, et al; for CARDS investigators. Primary
prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative
Atorvastatin Diabetes Study (CARDS): multicenter randomized placebo-controlled trial.
Lancet 2004;364:685-696.
33. Gaede P, Vedel P, Larsen N, Jensen GV, et al. Multifactorial intervention and cardiovascular
disease in patients with type 2 Diabetes. N Engl J. Med. 2003; 348:383-393.
34. Dormandy JA, Charbonnel B, Eckland DJ et al. Secondary prevention of macrovascular events
in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial
In macroVascular Events): a randomised controlled trial. Lancet 2005; 366:1279-89.
35. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk
individuals: a randomised placebo-controlled trial. Lancet 2002; 360:7-22.

39
 36. Amarenco P, Bogousslavsky J, Callahan A 3rd et al. High-dose atorvastatin after stroke or
transient ischemic attack. N Engl J Med 2006; 355:549-59.
37. Collaborators CTTC, Kearney PM, Blackwell L et al. Efficacy of cholesterol-lowering
therapy in 18,686 people with diabetes in 14 randomised trials of statins: a meta-analysis.
Lancet 2008; 371:117-25
Primary & Secondary

III. ATRIAL FIBRILLATION

Prevention

This section has been moved to Chapter IV, under Guidelines for TIA and Atrial
Fibirillation.

IV. ACUTE MI, LEFT VENTRICULAR THROMBUS, and CARDIOMYOPATHY

ACUTE MI with LV THROMBUS

A. Epidemiology:

Stroke or systemic embolism are less common among uncomplicated MI patients but can occur
in up to 12% of patients with acute MI complicated by an LV thrombus. Acute MI is associated
with up to 5% risk of ischemic stroke within 2 weeks. The rate is higher in those with anterior
than inferior infarcts and may reach 20% in those with large anteroapical infarcts.1 The
incidence of embolism is highest during the period of active thrombus formation in the first 1 to
3 months, yet the embolic risk remains substantial even beyond the acute phase in patients with
persistent myocardial dysfunction, CHF or AF.

B. Risk Modification:

An overview of trials on anticoagulation after MI has shown that INR of 2.5 to 4.8 may increase
hemorrhagic stroke 10-fold, whereas INR below 2.0 may not be effective in preventing ischemic
stroke. An INR range of 2.0 to 3.0 with a target of 2.5 is recommended. Two studies of MI
patients (n= 4,618) found that warfarin (INR=2.8-4.8) reduced ischemic stroke risk by 55% and
40%, respectively, compared with placebo, over 37 months.2,3

Statins for secondary prevention in patients with established atherosclerosis (CAD, thrombotic
cerebral stroke, peripheral arterial disease or prior revascularization) significantly reduced
overall risk of stroke, total mortality, cardiovascular death, MI and revascularization when total
cholesterol is >190 mg/dL or LDL is >100 mg/dL. Stroke Prevention by Aggressive
Reduction in Cholesterol Levels study (SPARCL) showed that patients previously documented
to have stroke or TIA and no history of coronary heart disease benefited from atorvastatin 80
mg in reducing fatal stroke and TIA.4

C. Recommendations:

1) Oral anticoagulation for MI patients is recommended if they have one or more of the
following conditions: persistent AF, decreased LV function (e.g., ejection fraction
[EF] 28%) or when LV thrombi are detected within several months after MI.
Antiplatelets are not recommended to prevent a first stroke after an MI.

40
 2) For patients with ischemic stroke or TIA due to acute MI in whom LV mural
thrombus was identified by echocardiography or another form of cardiac imaging,
oral anticoagulation is reasonable, aiming for an INR of 2.0 to 3.0 for at least 3
months and up to 1 year (Class IIa-B).
3) Aspirin should be used concurrently for ischemic CAD during oral anticoagulant
therapy in doses up to 160 mg/d (Class IIa-A). For patients with established

Primary & Secondary

atherosclerosis and total cholesterol >190 mg/dL or LDL >100 mg/dL, statins are

Prevention
recommended.
4) Adherence to the 2005 Clinical Practice Guidelines for the Management of
Dyslipidemia in the Philippines is recommended.5
5) For patients with stroke or TIA but without coronary heart disease, statin therapy
should be administered to prevent recurrence of stroke and TIA.

CARDIOMYOPATHY

A. Epidemiology:

Two large studies found that the incidence of stroke is inversely proportional to EF.6,7 In the
Survival and Ventricular Enlargement (SAVE) study, patients with EF of 29% to 35%
(mean=32%) had a 0.8% stroke rate per year, whereas the yearly rate in those with EF <28%
(mean=23%) was 1.7%. There was an 18% incremental increase in stroke risk for every 5%
decline in EF. A retrospective analysis of data from the Studies of Left Ventricular Dysfunction
(SOLVD) trial, which excluded patients with AF, found a 58% increase in risk of
thromboembolic events for every 10% decrease in EF among women (p=0.01) but no
increased risk in men.8

In patients with non-ischemic dilated cardiomyopathy, the rate of stroke appears similar to that
associated with cardiomyopathy resulting from ischemic heart disease.

B. Risk Modification:

Warfarin is sometimes prescribed to prevent cardioembolic events in patients with

cardiomyopathy. However, no RCT has demonstrated the efficacy of anticoagulation.
Considerable controversy surrounds the use of warfarin in patients with cardiac failure or
reduced LVEF.9,10

Warfarin appears to reduce the risk of ischemic stroke in patients with non-ischemic
cardiomyopathy and in those with ischemic heart disease.11 Aspirin reduces the stroke rate by
around 20%.12 Potential antiplatelet therapies used to prevent recurrent stroke include aspirin
(50 to 325 mg/day), combined aspirin and extended-release dipyridamole (25mg/200 mg twice
daily), and clopidogrel (75 mg daily).

C. Recommendation:

For patients with ischemic stroke or TIA who have dilated cardiomyopathy, either warfarin
(INR=2.0-3.0) or antiplatelet therapy may be considered for prevention of recurrent events
(Class IIb-C).

41
 Bibliography

1. Visser CA, Kan G, Meltzer RS, et al. Long-term follow-up of left ventricular thrombus after
acute myocardial infarction: a two-dimensional echocardiographic study in 96 patients. Chest
1984;86:532-536.
2. Effect of long-term oral anticoagulant treatment on mortality and cardiovascular morbidity
Primary & Secondary

after myocardial infarction. Anticoagulants in the Secondary Prevention of Events in Coronary

Thrombosis (ASPECT) Research Group. Lancet 1994;343:499-503.
Prevention

3. Van Es RF, Jonker JJ, Verheugt FW, et al. Antithrombotics in the Secondary Prevention of
Events in Coronary Thrombosis-2 (ASPECT-2) Research Group. Aspirin and coumadin after
acute coronary syndromes (the ASPECT-2 study): a randomised controlled trial. Lancet
2002;360:109-113.
4. The SPARCL Investigators. The Stroke Prevention by Aggressive Reduction in Cholesterol
Levels (SPARCL) study. Cerebrovasc Dis. 2006;21(suppl 4):1. Abstract 1.
5. The Clinical Practice Guidelines for the Management of Dyslipidemia in the Philippines 2005.
Manila: The Philippine Heart Association Inc., Philippine College of Cardiology; 2005.
6. Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on mortality and morbidity in
patients with left ventricular dysfunction after myocardial infarction. Results of the survival and
ventricular enlargement trial. The SAVE Investigators. N Engl J Med 1992;327:669-677.
7. Loh E, Sutton MS, Wun CC, et al. Ventricular dysfunction and the risk of stroke after myocardial
infarction. N Engl J Med 1997;336:251-257.
8. Dries DL, Rosenberg YD, Waclawiw MA, Domanski MJ. Ejection fraction and risk of
thromboembolic events in patients with sinus rhythm: evidence of gender difference in the
studies of left ventricular dysfunction trial. J Am Coll Cardiol 1997;336:251-257.
9. Falk RH. A plea for clinical trial of anticoagulation in dilated cardiomyopathy. Am J Cardiol
1990;65:914-915.
10. Ezekowitz M. Antithrombotics for left ventricular impairment? Lancet 1998;351:1904.
11. Fuster V, Gersh BJ, Giuliani ER, et al. The natural history of idiopathic dilated cardiomyopathy.
Am J Cardiol 1981;47:525-531.
12. Hurlen M, Abdelnoor M, Smith P, et al. Warfarin, aspirin or both after myocardial infarction. N
Engl J Med 2002;347:969-974.

V. VALVULAR HEART DISEASE AND PROSTHETIC HEART VALVES

A. Epidemiology

Annual rates of systemic thromboembolism (TE) in different valvular diseases are shown in
the succeeding table.1-4

Incidence of systemic thromboembolism in valvular heart disease

A lo n e w ith A F
(No A F ) (vs w ith o u t AF )
1. Prosthetic valve 20% Increa se d
2. R heumatic mitral reg urgitatio n 7.7% 22%
3. R heumatic mitral s tenos is 1.5% -4.0% Increa se d by 7-18x
4. M itral valve prolapse <2% Increa se d
5. Ao rtic valve N ot increa sed Increa se d

42
Patients with paroxysmal or persistent AF and valvular heart diseases such as mitral stenosis
are at highest risk for future embolic events.

B. Risk Modification:

Antithrombotic therapy can reduce the likelihood of stroke and systemic embolism in patients

Primary & Secondary

with valvular heart disease. The rate of TE in patients with mechanical heart valves is 4.4 per

Prevention
100 patient-years without antithrombotic therapy; 2.2 per 100 patient-years with antiplatelet
drugs; and 1 per 100 patient-years with warfarin. With or without AF, all patients with
mechanical heart valves require anticoagulation with target anticoagulation levels varying
according to type and position of the valve, and the presence of other risk factors. The risk of
TE in patients with native valvular heart diseases or mechanical or biological heart-valve
prostheses must be balanced with the risk of bleeding. Nevertheless, because the frequency and
permanency of consequences of TE events are usually greater than the outcome of
hemorrhagic complications, anticoagulant therapy is generally recommended, particularly when
associated with AF.5

Rheumatic Mitral Valve Disease

A. Epidemiology:

The annual rate of TE in rheumatic mitral regurgitation (MR) and stenosis (MS) without AF are
7.7% and 1.5% to 4% respectively. The presence of AF increases TE by 22% in MR patients
and by seven- to 18-fold in MS patients.

Recurrent embolism occurs in 30% to 65% of patients with rheumatic mitral valve disease who
have a history of a previous embolic event.6-8 Between 60% to 65% of these recurrences
develop within the first year, most within 6 months.6,7

B. Risk Modification:

Although not evaluated in randomized trials, multiple observational studies have reported that
long-term anticoagulant therapy effectively reduces the risk of systemic embolism in patients
with rheumatic mitral valve disease.3,9 Long-term anticoagulant therapy in patients with MS
who had left atrial thrombus identified by transesophageal echocardiography can result in the
disappearance of the thrombus.10

C. Recommendations:

1) For patients with rheumatic mitral valve disease or prosthetic valve without prior
stroke or TIA, oral anticoagulation with coumadin is recommended unless
contraindicated.
2) For patients with ischemic stroke or TIA who have rheumatic mitral valve disease,
whether or not AF is present, long-term warfarin therapy is reasonable, with a target
INR of 2.5 (range; 2.0-3.0) (Class IIa-C).

43
 3) Antiplatelet agents should not routinely be added to warfarin to avoid the additional
bleeding risk (Class III-C). Aspirin 80 mg/day is suggested for patients with ischemic
stroke or TIA with rheumatic mitral valve disease, whether or not AF is present, who
have recurrent embolism while receiving warfarin (Class IIa-C).
Primary & Secondary

Mitral Valve Prolapse

Prevention

A. Epidemiology:

Mitral valve prolapse (MVP) is the most common form of valve disease in adults.11
Thromboembolic phenomena have been reported in patients with mitral valve prolapse in
whom no other source could be found.12-16 The annual rate of TE in those with MVP and no
AF is less than 2%. AF increases TE risk.

B. Risk Modification:

No randomized trials have addressed the efficacy of selected antithrombotic therapies for this
subgroup of stroke or TIA patients. The evidence on the efficacy of antiplatelet agents for
general stroke and TIA patients was used to reach these recommendations.

C. Recommendation:

For patients with MVP who had ischemic stroke or TIA, antiplatelet therapy is reasonable
(Class IIa-C).

Mitral Annular Calcification

A. Epidemiology:

Although the incidence of systemic and cerebral embolism is not clear, thrombus has been
found on heavily calcified annular tissue upon autopsy.17-22

B. Risk Modification:

From observations and in the absence of randomized trials, anticoagulant therapy may be
considered for patients with MAC and a history of TE.

C. Recommendations:

1) For patients with ischemic stroke or TIA in whom MAC is not documented to be
calcific, antiplatelet therapy may be considered (Class IIb-C).
2) For patients with MR due to MAC and without AF, antiplatelet or warfarin therapy
may be considered (Class IIb-C).

44
Aortic Valve Disease

A. Epidemiology:

Clinically detectable systemic embolism in isolated aortic valve disease is increasingly

Primary & Secondary

recognized because of microthrombi or calcific emboli.23 In an autopsy study of 165 patients
with calcific aortic stenosis, systemic embolism was found in 31 patients (19%). In the absence

Prevention
of associated mitral valve disease or AF, systemic embolism in patients with aortic valve disease
is uncommon. TE increases in patients with aortic valve disease.

B. Risk Modification:

No randomized trials on selected patients with stroke and aortic valve disease exist.

C. Recommendation:

For patients with ischemic stroke or TIA and aortic valve disease but no AF, antiplatelet therapy
may be considered (Class IIb-C).

Prosthetic Heart Valves

A. Epidemiology:

The annual percentage of occurrence of systemic TE in those with prosthetic heart valves is
20%. The risk increases with AF.

B. Risk Modification:

A variety of mechanical heart valve prostheses are available for clinical use, all of which require
antithrombotic prophylaxis.

The most convincing evidence that oral anticoagulants are effective in patients with prosthetic
heart valves comes from patients randomized to treatment for 6 months with either warfarin in
uncertain intensity or one of two aspirin-containing platelet-inhibitor regimens.24

In two randomized studies, concurrent treatment with dipyridamole and warfarin reduced the
incidence of systemic embolism,25,26 and the combination of dipyridamole (450 mg/day) and
aspirin (3.0 g/d) reduced the incidence of TE in patients with prosthetic heart valves.27

A randomized study of aspirin 1.0 g/day plus warfarin versus warfarin alone in 148 patients
with prosthetic heart valves found a significant reduction of embolism in the aspirin-treated
group.28 Another trial showed that the addition of aspirin 100 mg/day to warfarin (INR=3.0-
4.5) improved efficacy compared with warfarin alone.29

45
 The ESC guidelines recommend anticoagulant intensity in proportion to the TE risk associated
with specific types of prosthetic heart valves.30 For first-generation valves, an INR of 3.0 to 4.5
was recommended; an INR of 3.0 to 3.5 was recommended for second-generation valves in the
mitral position, whereas an INR of 2.5 to 3.0 was advised for second-generation valves in the
Primary & Secondary

aortic position. The 2004 American College of Chest Physicians recommended an INR of 2.5
to 3.5 for patients with mechanical prosthetic valves, and 2.0 to 3.0 for those with bioprosthetic
Prevention

valves and low-risk patients with bileaflet mechanical valves (such as the St. Jude Medical device)
in the aortic position.31 Similar guidelines have been promulgated conjointly by the ACC and
the AHA.11,32

C. Recommendations:

1) For patients who have modern mechanical prosthetic heart valves, with or without
ischemic stroke or TIA, oral anticoagulants should be administered to an INR target of
3.0 (range; 2.5-3.5) (Class I-B).
2) For patients with mechanical prosthetic heart valves who had an ischemic stroke or
systemic embolism despite adequate therapy with oral anticoagulants, aspirin 75 to 100
mg/day in addition to oral anticoagulants and maintenance of the INR at 3.0 (range;
2.5-3.5) are reasonable (Class IIa-B).
3) For patients with ischemic stroke or TIA who have bioprosthetic heart valves with no
other source of thromboembolism, anticoagulation with warfarin (INR=2.0-3.0) may
be considered (Class IIb-C).

Summary of Recommendations for Patients

with Cardioembolic Stroke or TIA

Class/Level of
Risk Factor Recommendation
Evidence
For patients with ischemic stroke or TIA with Class I-A
persistent or paroxysmal (intermittent) AF,
anticoagulation with adjusted-dose warfarin (target
AF INR=2.5 [2.0-3.0]) should be administered.
In patients unable to take oral anticoagulants, aspirin
Class I-A
325 mg/day is recommended.

46
 Class/ Leve l of
Risk Factor Recommendation
Evidence
Class IIa-B
For patients with ischemic stroke c aused by acute
MI with LV mural thromb us identified by

Primary & Secondary

echocardiograp hy or anoth er fo rm of cardiac
imaging, oral anticoagulation is reasonable

Prevention
A cute MI and LV (INR= 2.0-3.0 for at least 3 months up to 1 ye ar).
thrombus
Asp irin up to 160 mg/day (preferably enteric-
coated) should be used concurrently for patients
Class IIa-A
with ischemic CA D durin g oral anticoagulant
th erapy.
For patients with ischemic stroke o r TIA who have
dilated cardiomyopathy, either warfarin (INR=2.0-
Cardiomyopathy Class IIb-C
3.0) o r an tiplatelet therapy may be co nsidered to
prevent recurrent events.
For patients with MV P wh o have ischemic stroke or
MVP Class IIa-C
TIA, long-term antiplatelet therapy is reason ab le.
For patients with ischemic stroke o r TIA and MAC Class IIb-C
not documented to b e calcific, antiplatelet therapy
MAC may be co nsidered.
Amo ng patien ts with MR due to MAC, without AF,
Class IIb-C
antiplatelet or warfarin therapy may be c onsidered.
For patients with ischemic stroke o r TIA and aortic
Aortic valve
valve disease wh o do not have AF, antiplatelet Class IIa-C
disease
th erapy may be considered.
For patients with ischemic stroke o r TIA who have Class I-B
modern mechanical p rosth etic heart valves, oral
anticoagulants are recomm ended, with an IN R
target of 3.0 (range; 2.5-3.5).

For patients with mechanical prosthetic heart valve s

who had an ischemic stro ke or systemic embolism
Prosthetic heart despite adequate the rap y w ith oral anticoagulants,
aspirin 75 to 100 mg/day in addition to oral Class IIa-B
valves
anticoagulants maintain ed at INR of 3.0
(range; 2.5- 3.5) is reasonable.

For patients with ischemic stroke o r TIA who have

bioprosthetic heart valves with no other source of
Class IIb-C
TE, anticoagulatio n with warfarin (INR=2.0-3.0)
may be co nsidered.

47
 Bibliography

1. Israel DH, Sharma SK, Fuster V. Antithrombotic therapy in prosthetic heart valve replacement.
Am Heart J 1994;127:400-411.
2. Israel DH, Fuster V, Ip JH, et al. Intracardiac thrombosis and systemic embolization. In:
Colman RW, Hirsh J, Marder V, Salzman EW, eds. Hemostasis and Thrombosis: Basic Principles
Primary & Secondary

and Clinical Practice, 3rd ed. Philadelphia, Pa: JB Lippincott; 1994:14521468.

Prevention

3. Coulshed N, Epstein EJ, McKendrick CS, et al. Systemic embolism in mitral valve disease. Br
Heart J 1970;32:26-34.
4. Wood JC, Conn HL Jr. Prevention of systemic arterial embolism in chronic rheumatic heart
disease by means of protracted anticoagulant therapy. Circulation 1954;10:517-523.
5. Devereaux PJ, Anderson DR, Gardner MJ, et al. Differences between perspectives of
physicians and patients on anticoagulation in patients with atrial fibrillation: observational
study. BMJ 2001;323:1218-1222.
6. Carter AB. Prognosis of cerebral embolism. Lancet 1965;2:514-519.
7. Wood P. Diseases of the Heart and Circulation. Philadelphia, Pa: JB Lippincott; 1956.
8. Levine HJ. Which atrial fibrillation patients should be on chronic anticoagulation? J Cardiovasc
Med 1981;6:483-487.
9. Szekely P. Systemic embolization and anticoagulant prophylaxis in rheumatic heart disease. BMJ
1964;1:209-212.
10. Roy D, Marchand E, Gagne P, et al. Usefulness of anticoagulant therapy in the prevention of
embolic complications of atrial fibrillation. Am Heart J. 1986;112:1039-1043.
11. Bonow RO, Carabello B, De Leon AC, Jr., et al. ACC/AHA guidelines for the management of
patients with valvular heart disease. A report of the ACC/AHA Task Force on Practice
Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll
Cardiol 1998;32:1486-1588.
12. Jeresaty RM. Mitral Valve Prolapse. New York, NY: Raven Press; 1979.
13. Barnett HJ. Transient cerebral ischemia: pathogenesis, prognosis, and management. Ann R Coll
Phys Surg Can 1974;7:153-173.
14. Barnett HJ, Jones MW, Boughner DR, Kostuk WJ. Cerebral ischemic events associated with
prolapsing mitral valve. Arch Neurol 1976;33:777-782.
15. Hirsowitz GS, Saffer D. Hemiplegia and the billowing mitral leaflet syndrome. J Neurol
Neurosurg Psychiatry 1978;41:381-383.
16. Saffro R, Talano JV. Transient ischemic attack associated with mitral systolic clicks. Arch Intern
Med 1979;139:693-694.
17. Hanson MR, Hodgman JR, Conomy JP. A study of stroke associated with prolapsed mitral
valve. Neurology 1978;23:341.
18. Fulkerson PK, Beaver BM, Auseon JC, Graber HL. Calcification of the mitral annulus: etiology,
clinical associations, complications and therapy. Am J Med 1979;66:967-77.
19. Kalman P, Depace NL, Kotler MN, et al. Mitral annular calcifications and echogenic densities in
the left ventricular outflow tract in association with cerebral ischemic events. Cardiovasc
Ultrasonic 1982;1:155.
20. Nestico PF, Depace NL, Morganroth J, et al. Mitral annular calcification: clinical,
pathophysiology, and echocardiographic review. Am Heart J. 1984;107(pt 1):989-996.
21. Kirk RS, Russell JG. Subvalvular calcification of mitral valve. Br Heart J 1969;31:684-692.
22. Ridolfi RL, Hutchins GM. Spontaneous calcific emboli from calcific mitral annulus fibrosus.
Arch Pathol Lab Med 1976;100:117-120.
23. Brockmeier LB, Adolph RJ, Gustin BW, Holmes JC, Sacks JG. Calcium emboli to the retinal
artery in calcific aortic stenosis. Am Heart J. 1981;101:3237.

48
 24. Mok CK, Boey J, Wang R, et al. Warfarin versus dipyridamole-aspirin and pentoxifylline
aspirin for the prevention of prosthetic heart valve thromboembolism: a prospective
randomized clinical trial. Circulation 1985;72:1059-1063.
25. Chesebro JH, Fuster V, Elveback LR, et al. Trial of combined warfarin plus dipyridamole or
aspirin therapy in prosthetic heart valve replacement: danger of aspirin compared with
dipyridamole. Am J Cardiol 1983;51:1537-1541.

Primary & Secondary

26. Sullivan JM, Harken DE, Gorlin R. Pharmacologic control of thromboembolic
complications of cardiac-valve replacement. N Engl J Med. 1971;284:13911394.

Prevention
27. Taguchi K, Matsumura H, Washizu T, et al. Effect of athrombogenic therapy, especially high
dose therapy of dipyridamole, after prosthetic valve replacement. J Cardiovasc Surg (Torino)
1975;16:8-15.
28. Dale J, Myhre E, Storstein O,et al. Prevention of arterial thromboembolism with
acetylsalicylic acid: a controlled clinical study in patients with aortic ball valves. Am Heart J
1977;94:101-111.
29. Turpie AG, Gent M, Laupacis A, et al. Aspirin and warfarin after heart-valve replacement: a
comparison of aspirin with placebo in patients treated with warfarin after heart-valve
replacement. N Engl J Med 1993;329:524-529.
30. Gohlke-Barwolf C, Acar J, Oakley C, et al. Guidelines for prevention of thromboembolic
events in valvular heart disease. Study Group of the Working Group on Valvular Heart
Disease of the European Society of Cardiology. Eur Heart J 1995;16:1320-1330.
31. Proceedings of the Seventh ACCP Conference on antithrombotic and thrombolytic therapy:
evidence-based guidelines. Chest 2004;126 (3 Suppl):172S-696S.
32. Bonow RO, Carabello B, de Leon AC Jr. et al. Guidelines for the management of patients
with valvular heart disease: executive summary: a report of the ACC/AHA Task Force on
Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease).
Circulation. 1998;98:1949-1984.

VI. CHOLESTEROL

A. Epidemiology:

Stroke mortality rate is increasing due to higher incidence of ischemic stroke caused by both
extracranial and intracranial atherothromboembolism. This has been attributed to increase in
prevalence of hypercholesterolemia associated with increasing dietary intake of saturated fats,
physical inactivity, obesity and diabetes.1 Indeed, the populationattributable risk of ischemic
stroke due to non-optimal blood cholesterol concentration has been estimated to be as high as
45% in Asia Pacific countries.2 Intracranial atherosclerosis is the main stroke subtype in some
Asian countries for which hyperlipidemia, especially elevated LDL, is one of its implicated risk
factors.

For first or recurrent stroke, hypercholesterolemia and hyperlipidemia are not as well
established risk factors in stroke as that observed in cardiac diseases. Epidemiological and
observational studies have not shown a definite correlation between serum cholesterol levels
and the incidence of stroke.3,4 According to the Asia Pacific Cohort Studies Collaboration, the
relationship between cholesterol and stroke risk is more complex, with a stronger positive
association with ischemic stroke and a weaker negative association with hemorrhagic stroke.
Cholesterol, being an essential component of cell membranes, help maintain the integrity of
small cerebral vessels. Therefore low levels of cholesterol may potentially increase the risk of
hemorrhage.

49
 Furthermore, low cholesterol is common in patients with weight loss, severe handicap, high
alcohol consumption or severe and chronic illness, which maybe confounding factors for
demonstrated trend between hemorrhagic stroke and low cholesterol.

B. Risk Modification:
Primary & Secondary
Prevention

Statin, a HMG-CoA reductase inhibitor, is not only an accepted lipid-lowering agent, but it has a
variety of actions that affect the risks of stroke and stroke outcome. It can reduce
inflammation, has neuroprotective effect; upregulates endogenous tissue plasminogen activator
and experimentally promotes angiogenesis and neurogenesis.

Low HDL and elevated triglycerides may be risks factors for CVD. Other lipid lowering agents
include niacin, fibrates and cholesterol absorption inhibitors. Niacin is an effective drug for
increasing HDL levels and may also lower LDL and triglycerides. Fenofibrates reduced the rate
of unadjusted total strokes among men with coronary artery disease and those with low levels
of HDL-C5 because Fenobifrates can actually increase levels of HDL-C. Another class of
drugs, the cholesterol absorption inhibitors, lead to modest LDL-C reduction and these drugs
may be co-administered to an inhibitor of cholesterol synthesis or statins.

B.1. Primary Stroke Prevention

A meta-analysis of 13 lipid lowering trials prior to statin use showed no change in risk
for total stroke.6 With the advent of statins, a meta-analysis of 24 published
randomized trials showed that statin use was associated with a reduction of all stroke
types with RR of 0.85 (95% CI: 0.77 0.87). The greater the LDL reduction, the
greater the intima-media thickness and stroke risk reduction.7 Statins conferred an
important and large relative reduction in cardiovascular events including stroke
among hypertensive patients who are not conventionally deemed dyslipidemic.8
Pretreatment with statins seems to reduce clinical severity in patients with stroke,
especially among diabetics.9,10

A study conducted by the Michigan State University11 showed pretreatment with

statins was associated with better stroke outcomes in Whites but no beneficial effect
among Blacks. Likewise the ALL HAT-LLT showed pravastatin treatement was
associated with reduced stroke risk in non-Blacks but with increased stroke risk in
Blacks.

The MEGA Study or Management of Elevated Cholesterol the Primary Prevention

Group of Adult Japanese Study showed that Pravastatin produced a 35% relative risk
reduction in the incidence of cardiovascular disease, particularly cerebral infarction.

50
 B.2. Secondary Stroke Prevention

The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL)

study was conducted among patients with previous stroke or TIA and mildly elevated
LDL but without CHD. The trial showed significant reduction in recurrent stroke by

Primary & Secondary

16% with high dose atorvastatin 80 mg/day. A post hoc analysis showed an increase
in the number of hemorrhagic stroke but with no difference in the incidence of fatal

Prevention
hemorrhagic stroke. Several factors are associated with this increased risk of
hemorrhagic stroke namely advancing age, hypertension, cigarette smoking, use of
antithrombotic medication, and lower blood glucose and among patients with a
diagnosis of hemorrhagic stroke. Nevertheless, the overall benefit of atorvastatin
was significant because any possible excess of hemorrhagic stroke is greatly
outweighed by the positive effect against ischemic strokes. Likewise, SPARCL
showed statins reduced cerebro-cardiovascular events in patients with or without
carotid stenosis group with the latter having the greater benefit.

C. Recommendations:

C.1. Primary Stroke Prevention

1) Therapeutic lifestyle changes are recommended as an essential modality in

clinical management.4 These include smoking cessation, weight management,
regular physical activity and adequate BP monitoring and control.12
2) For patients at any level of cardiovascular risk, especially those with established
atherosclerosis, a low-fat cholesterol diet is recommended for life.
3) High-risk hypertensive patients and those with CAD should be treated with
lifestyle measures and a statin, even with normal LDL levels (Class I-A).13,14
4) Adults with diabetes, especially those with additional risks factors, should
receive statins to lower the risk of a first stroke (Class I-A).13
5) Patients with coronary artery disease and low HDL may be treated with weight
reduction, increased physical activity, smoking cessation, and possibly niacin or
fibrates (Class IIa-B).

C.2. Secondary Stroke Prevention

(Adapted from NCEP-ATP III)

1) Patients with ischemic stroke or TIA with elevated cholesterol, comorbid
coronary artery disease, or evidence of an atherosclerotic origin should be
managed according to NCEP III guidelines, which include lifestyle
modification, dietary guidelines, and medication recommendations (Class I-A).
Statin agents are recommended, and the target goal for cholesterol lowering for
those with CHD or symptomatic atherosclerotic disease is an LDL-C of <100
mg/dl and LDL-C of <70 mg/dL for very-high-risk individuals with multiple
risk factors (Class I- Level of evidence A).

51
 2) Patients with ischemic stroke or TIA presumed to be due to an atherosclerotic
origin but with no preexisting indications for statins (normal cholesterol levels,
no comorbid coronary artery disease, or no evidence of atherosclerosis) are
reasonable candidates for treatment with a statin agent to reduce the risk of
vascular events (Class IIa- Level of evidence B).
Primary & Secondary

3) Patients with ischemic stroke or TIA with low HDL cholesterol may be
considered for treatment with niacin or fenofibrate (Class IIb- Level of
Prevention

evidence B).

Bibliography

1. Graeme J. Hankey. Ka S, L. Wong et al. Management of cholesterol to reduce the burden of

stroke in Asia: consensus statement Int. J of Stroke 2010; 1-8
2. Grundy SM, Cleeman JI, Merz CN, et al.; National Heart, Lung, and Blood Institute; American
College of Cardiology Foundation; American Heart Association. Implications of recent clinical
trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines.
Circulation 2004,110:227-239.
3. Di Napoli M. Benefits of statins in cerebrovascular disease. Curr Opin Investig Drugs
2004;5:295-305.
4. Cheung BM, Lauder IJ, Lau CP, Kumana CR. Meta-analysis of large randomized controlled
trials to evaluate the impact of statins on cardiovascular outcomes. Br J Clin Pharmacol
2004;57:640-651.
5. Woodward M. Martiniuk A. Asia pacific Cohort Studies Collaboration. Et al. Elevated total
cholesterol; Its prevalence and population attributable fraction for mortality and coronary heart
disease and ischemic stroke in the Asia Pacific region . Eur J cardiovasc Prev Rehabil
2008;15;397-401.
6. Atkins D, Psaty BM, Koepsell TD, et al. Cholesterol reduction and the risk for stroke in men. A
meta-analysis of randomized, controlled trials. Ann Intern Mad 1993;119:136-145.
7. Amarenco P. Effect of statins in stroke prevention. Curr Opin Lipidol 2005;16:614-618.
8. Sever PS, Dahlof B, Poulter NR, et al., ASCOT investigators. Prevention of coronary and stroke
events with atorvastatin in hypertensive patients who have average or lower-than-average
cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial--Lipid
Lowering Arm (ASCOT-LEA): a multicentre randomised controlled trial. Lancet
2003;361:1149-1158.
9. Greisenegger S, Mullner M, Tentschert S, et al. Effect of pretreatment with statins on the
severity of acute ischemic cerebrovascular events. J Neurol Sci 2004,221:5-10.
10. Colhoun HM, Betteridge DJ, Durrington PN, et al., CARDS investigators. Primary prevention
of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin
Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet
2004,364:685-696.
11. Mathew J. Reeves, Julia Warner Gargano et al. Effect of pretreatment with statins on ischemic
stroke outcomes. Stroke AHA journals; 2008;39;1779-1785
12. The Clinical Practice Guidelines for the Management of Dyslipidemia in the Philippines 2005.
Manila: The Philippine Heart Association Inc., Philippine College of Cardiology; 2005.
13. Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with
ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the
American Heart Association/American Stroke Association Council on Stroke [truncl. Stroke
2006;37:577-617.

52
14. Corvol JC, Bouzamondo A, Sirol M, et al. Differential effects of lipid-lowering therapies on
stroke prevention: a meta-analysis of randomized trials. Arch Intern Med 2003;163:669-676.
15. Amarenco P, Lavallee PC, Labreuche J, et al. Stroke prevention, blood cholesterol and statins.
Acta Neurol Taiwan 2005;14:96-112. 1496-112.
16. Zhang X, Patel A, Horibe H, et al.; Asia Pacific Cohort Studies Collaboration. Cholesterol,

Primary & Secondary

coronary heart disease, and stroke in the Asia Pacific region. Int J Epidemic] 2003,32:563-572.

Prevention
17. Heart Protection Study Collaborative Group. Effect of cholesterol-lowering with simvastatin
on stroke and other major vascular events in 20536 people with cerebrovascular disease or other
high-risk conditions. Lancet 2004,363:757-767.
18. The SPARCL Investigators. The Stroke Prevention by Aggressive Reduction in Cholesterol
Levels (SPARCL) study. Cerebrovasc Dis. 2006,21 (suppi 4):1. Abstract 1.
19. Vaughan CJ. Prevention of stroke and dementia with statins: Effects beyond lipid lowering. Am
J Cardiol 2003;91,23B-29B.
20. Welch KMA. statins for the prevention of cerebrovascular disease: the rationale for robust
intervention. Eur Heart J Suppl 2004;6 (Suppl C):C34-C42.
21. 14, Martin-Ventura JL, Blanco-Colin LM, Gomez-Hernandez A, et al. Intensive treatment with
atorvastatin reduces inflammation in mononuclear cells and human atherosclerotic lesions in
one month. Stroke 2005;36:1796-1800.
22. LaRosa JC, Grundy SM, Waters DD, et al.; Treating to New Targets (TNT) Investigators.
Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med
2005,352:1425-1435.
23. Waters DD, Schwartz GG, Olsson AG, et al.; MIRAGE Study Investigators. Effects of
atorvastatin on stroke in patients with unstable angina or non-Q-wave myocardial infarction: a
Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRAGE) substudy.
Circulation 2002;106:1690-1695.
24. Wong LK. Global burden of intracranial atherosclerosis . Int. J Stroke 2006; 1;158-9
25. Amarenco P. Labeurche J Lipid management in the prevention of stroke; review and updated
meta-analysis of statins for stroke prevention. Lancet Neurol 2009; 8;453-63.
26. Goldstein, Pierre A et al. Statin Treatment and Stroke Trial Outcome in the Stroke Prevention
by Aggressive Reduction in Cholesterol Levels (SPARCL) Trial. Stroke AHA September 14,
2009.
27. Pierre Amarenco, Oscar Benavente et al. Results of the Stroke Prevention by Aggressive
Reduction in Cholesterol Levels (SPARCL) Trial by Stroke Subtypes; Stroke 2009;40;1405-1409
28. Goldstein LB, Amarenco P et al. Hemorrhagic stroke in the Stroke Prevention by Aggressive
Reduction in Cholesterol Levels (SPARCL) study; Neurology 2008;70:2364-2370.
29. AthyrosV., Tziomalos et al. Aggressive statin treatment, very low serum cholesterol levels and
hemorrhagic stroke: is there an association? Curr Opin Cardiol 25:000-000
30. Nambi V. Effect of Very High-intensity Statin Therapy on Regression of Coronary
Atherosclerosis: the ASTEROID Trial; Baylor College of Medicine, Houston, Texas
31. Sacco R, Adams R et al. Guidelines for prevention of stroke in patients with ischemic stroke or
transient ischemic attack. Stroke 2006;37:577-617

53
 VII. CAROTID STENOSIS

A. Epidemiology:
1
Extracranial carotid artery disease accounts for 15% to 20% of all ischemic strokes. Individuals
with carotid stenosis often have more widespread atherosclerotic disease with a high prevalence
Primary & Secondary

of coronary heart disease and claudication.2,3

Prevention

The stroke risk due to carotid artery stenosis is determined primarily by symptom status and is
related to lesion severity. Patients with symptomatic severe carotid stenosis defined as transient
or permanent focal neurological symptoms related to the ipsilateral hemisphere or retina have
an annual stroke risk of 13% to 15%, compared with 1% to 2% in those with no history of prior
stroke or TIA or those with asymptomatic lesions.4-6 In addition, echolucent or ulcerated
plaques, hypertension and progressive lesions are associated with increased risk of neurological
events.7

B. Risk Modification

B.1. Primary Stroke Prevention

The benefit of carotid endarterectomy in asymptomatic cases was modest based on 2

large RCT with reduction of stroke risk from 2% per year to 1%. Among patients
with asymptomatic carotid artery stenosis of 60% to 99% enrolled in the
Asymptomatic Carotid Artery Stenosis Study (ACAS), CEA combined with best
medical treatment reduced the 5-year ipsilateral-stroke risk from 11% to 5.1%
(RRR=53%).5 The Asymptomatic Carotid Surgery Trial (ACST) supports the
results of ACAS, showing a small but definite reduction in the risk of stroke with
surgery among patients with at least 60% stenosis (5-year stroke risk of 11.8% in the
medical arm compared with 6.4% in the combined CEA and medical treatment
arm).6 For asymptomatic patients to benefit from surgery, there should be an
exceptionally low perioperative complication rate (< 3%).5-7

Neither ACAS nor ACST showed increasing benefit from surgery with increasing
degree of asymptomatic stenosis within the 60%-to-99% range.5,6,8

B.2. Secondary Stroke Prevention

Among symptomatic patients with 70% stenosis or greater but without near
occlusion, combined CEA and medical treatment provide up to 16% absolute-risk
reduction or 61% relative-risk reduction in ipsilateral and perioperative stroke over
medical treatment alone (over 5 years).4,9-11

There was a trend toward benefit with surgery at 2 years (ARR=5.6 %) among
patients with near-total carotid occlusion, but this was seen only for in the short term
(-1.7% over 5 years).9

54
 CEA was of marginal benefit in patients with 50% to 69% stenosis. Greater benefit
was seen in men, those >75 years old, those with hemispheric symptoms (compared
with those with transient monocular blindness) and those who were randomized
within 2 weeks of a TIA or a non-disabling ischemic stroke.4,9-11

Primary & Secondary

CEA was harmful for symptomatic patients with less than 30% stenosis. It had effect
among patients with 30% to 49% stenosis.

Prevention
CEA in symptomatic patients is effective in preventing future ischemic events
provided that the peri-operative combined risk of stroke and death is not higher than
6%.

Pooled analysis of data from randomized controlled trials of CEA for symptomatic
stenosis has shown that benefit from surgery was greatest in patients who were
randomized within 2 weeks after their last ischemic event and fell rapidly with
increasing delay.12 In stable patients, there was no difference in operative risk
between early (first 3 weeks) vs late surgery (11 studies, OR 1.13; 95% CI 0.79 1.62;
p = 0.62).13

Several meta-analysis of completed or terminated RCTs comparing endovascular

treatment and CEA found no difference in the odds of death or any stroke at 2-3 year
follow up between the two groups. However, a consistent trend towards less
periprocedural stroke at 30 days (however more MI) was seen in the CEA group while
trend towards less periprocedural MI (however more strokes) was seen in the carotid
angioplasty/stenting group.14-18

The results of the recently published Carotid Revascularization Endarterectomy

versus Stenting Trial (CREST) has confirmed findings of the various meta-analysis
when it showed similar medium term results for both procedures (combined
endpoint of stroke/MI/death at 4 years of 6.8% and 7.1% with CEA and carotid
artery stenting, respectively). It has likewise demonstrated the significantly higher
30-day periprocedural risk of stroke associated with stenting and higher
periprocedural risk of MI with endarterectomy.19

An intriguing finding of CREST was the interaction of age and efficacy of therapy.
Carotid artery stenting tended to have greater efficacy in younger patients ( < 70
years) while endartectomy was slightly better in older patients.19

C. Recommendations:

1) At present, mass screening for high-grade asymptomatic carotid stenosis is not cost-
effective. However it is reasonable to do screening using readily available and reliable
non-invasive tests (e.g., carotid duplex) in patients at risk for significant carotid
disease, such as those who survived a stroke, or those who have carotid bruit,
peripheral vascular disease, and/or CAD.

55
 2) Aggressive management of vascular risk factors including antiplatelet therapy and
statins must be initiated for all patients with carotid artery disease (Class I-C). Patient
stratification into symptomatic or asymptomatic, high or low risk for operation and
degree of stenosis is essential when considering the role of carotid revascularization
procedures.
Primary & Secondary

3) It is reasonable to consider CEA for patients with asymptomatic stenosis of >60% if

Prevention

the patient has a life expectancy of at least 5 years and the perioperative risk can be
reliably documented to be <3% (Class I-A).
4) CEA combined with optimal medical management is recommended for patients
with recent TIA or stroke and ipsilateral severe carotid artery stenosis (70%-99%) if
perioperative risk of <6% can be attained (Class I-A).
5) For symptomatic patients with 50% to 69% stenosis, CEA is recommended
depending on patient-specific factors, such as age, gender, comorbidities and severity
of initial symptoms (Class I-A). When the degree of stenosis is <50%, there is no
indication for CEA (Class III-A).17,18
6) When CEA is indicated for patients with TIA or minor stroke with minimal imaging
evidence of infarction or mass effect, a stable deficit and normal level of
consciousness, surgery within 2 weeks is suggested rather than delaying surgery
(Class IIA level B).
7) Since benefit from CEA is dependent on the degree of stenosis, measurement must
be accurate and reliable. In deciding for surgical intervention, the North American
Symptomatic Carotid Endarterectomy Trial (NASCET) method of angiographically
defining the degree of stenosis is recommended (i.e., % stenosis = {1-[diameter of
stenosis/diameter of distal internal carotid artery]} x 100%).19
8) The endovascular approach is favored in patients at increased surgical risk for CEA
(e.g stenosis is difficult to access surgically; re-stenosis after CEA or medical co-
morbidities that greatly increase the risk of surgery) (Class IIb-B). CAS is reasonable
when performed by operators with established periprocedural morbidity and
mortality rates of <6% (Class IIb-B).18
9) While carotid endarterectomy remains the preferred treatment in most average
surgical risk patients, the lack of significant difference in medium term outcomes
between CEA and CAS, may support an individualized treatment approach.
Decision-making should incorporate availability of technology & expertise,
operators experience, consideration of risk-benefit ratio factoring in the difference
in perioperative/periprocedural outcomes between the two treatment options, cost
and patient preference (Class I- level B).
10) In patients with concomitant carotid and coronary artery disease, available data at
this time are insufficient to declare superiority of timing CEA either before or
simultaneously with coronary-artery bypass grafting (CABG).

56
Bibliography

1. Sacco RL, Ellenberg JA, Mohr JP, et al. Infarcts of undetermined cause: the NINDS Stroke
Data Bank. Ann Neuro 1989;25:382-390.
2. Hertzner, HR, Young JR, Beven EG, et al. Coronary angiography in 506 patients with

Primary & Secondary

extracranial cerebrovascular disease. Arch Intern Med 1985;145:849-852.
3. Caplan LR, Gorelick PB, Hier DB. Race, sex and occlusive cerebrovascular disease: a review.

Prevention
Stroke 1986;17:648-645.
4. Barnett HJ, Taylor DW, Eliasziw M, Fox AJ, Ferguson GG, Haynes RB, et al. Benefit of carotid
endarterectomy in patients with symptomatic moderate or severe stenosis. North American
Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1998;339:1415-1425.
5. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy
for asymptomatic carotid arterectomy stenosis. JAMA 1995;273:1421-1428.
6. MRC Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group. Prevention of
disabling and fatal strokes by successful carotid endarterectomy in patients without recent
neurological symptoms: randomized controlled trial. Lancet 2004;363:1491-1502.
7. Liapis C, Kakisis J and Kostakis, A. Carotid stenosis: Factors affecting symptomatology. Stroke
2001;32:2782-2786.
8. Rothwell PM and Goldstein LB. Carotid endarterectomy for asymptomatic carotid stenosis:
Asymptomatic carotid surgery trial. Stroke 2004;35:2425-2427.
9. Rothwell PM, Eliasziw M. Gutnikov SA for the Carotid Endarterectomy Trialists
Collaboration. Analysis of pooled data from the randomized controlled trials of
endarterectomy for symptomatic carotid stenosis. Lancet 2003;361:107-116.
10. Farrel B, Fraser A, Sandercock P, et al. Randomized trial of endarterectomy for recently
symptomatic carotid stenosis. Final results of the MRC European Carotid Surgery Trial
(ECST). Lancet 1998;351:1379-1387.
11. Mayberg MR, Wilson E, Yatsu F, et al. Carotid endarterectomy and prevention of cerebral
ischemia in symptomatic carotid stenosis. JAMA 1991;226:3289-3284.
12. Rothwel PM. Eliasziw M, Gutnikov SA for the Carotid Endarterectomy Trialists Collaboration.
Effect of endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and
to timing of surgery. Lancet 2004: 363; 915 - 924
13. Bond, R, Rerkasem K, Cuffe R et al. A systematic review of the risk of carotid endarterectomy
in relation to the clinical indication and the timing of surgery. Stroke 2003;34:2290 2301.
14. Murad MH, Flynn DN, Elamin MB, et al. Endarterectomy vs stenting for carotid artery stenosis:
A systematic review and meta-analysis. J Vasc Surg 2008; 48 (2): pp 487-493.
15. Brahmanandam S, Ding EL, Conte MS, et al. Clinical results of carotid artery stenting compared
with carotid endarterectomy. N Engl J Vasc Surg 2008; 47: pp 343-9
16. Ringleb PA, ChatellierG, Hacke W, et al. Safety of endovascular treatment of carotid artery
stenosis compared with surgical treatment: A meta-analysis. J Vasc Surg 2008;47: pp 350-5
17. Jeng JS, Liu HM, Tu YK. Carotid angioplasty with or without stenting versus carotid
endarterectomy for carotid artery stenosis: A meta-analysis. Journal of Neurological Sciences
270 (2008): pp 40-47
18. Ederle J, Feathersone, R and Brown, M. Randomized controlled trials comparing
endarterectomy and endovascular treatment for carotid artery stenosis: A Cochrane systematic
review. Stroke 2009; 40: 1373 1380.
19. Brott TG, Hobson RW II, Howard G et al. Stenting versus endarterectomy for treatment of
carotid-artery stenosis. N Engl J Med 2010

57
 20. Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy an evidence based review.
Report of the Therapeutics and Technology Assessment Subcommittee of the American
Academy of Neurology. Neurology 2005;65:794-801.
21. Sacco R, Adams R, Albers G, et al. Guidelines for the Prevention of Stroke in Patients with
Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals from
the American Heart Association/American Stroke Association Council on Stroke. Stroke
2006;37:577-617.
Primary & Secondary

22. Barnett HJM, Warlow CP. Carotid endarterectomy and the measurement of stenosis. Stroke
1993;24:1281-1284.
Prevention

VIII. INTRACRANIAL STENOSIS

A. Epidemiology:
Intracranial atherosclerotic disease (ICAD) is responsible for ischemic stroke in 5-10 % of
Caucasian patients, and in up to 15-17% Hispanic and African patients. ICAD related strokes
are more common and comprise 3337% of ischemic strokes among Chinese and Asian
population.1,2
Besides race and ethnicity, risk factors for intracranial atherosclerosis include age, hypertension,
smoking, diabetes, lipid disorders and metabolic syndrome.3-6
The annual risk of stroke among patients with symptomatic intracranial stenosis ranges from
3% to 15% (approximate annual values are: 7.6% for the carotid siphon, 7.8% for the middle
cerebral artery [MCA], 2%-7% for the vertebral artery and 11% in the basilar artery).7,8 The risk
of recurrent ipsilateral stroke is highest among patients with 70 - 99% intracranial stenosis
(annual risk of 19%) and those with recent symptoms (within 2 weeks of initial event).9
In contrast, asymptomatic ICAD appears to have a benign prognosis based on preliminary data.
The risk of ipsilateral stroke in asymptomatic MCA stenosis was 1.4% annually in medically
treated Caucasian patients.10,11 Among patients enrolled in WASID with coexistent
asymptomatic stenosis, the 1-year stroke rate in the territory of the asymptomatic stenosis was
3.5 %.8,12 Impaired vasoreactivity on CT or MR perfusion studies may have a role in predicting
future stroke risk in patients with asymptomatic intracranial stenosis.13-15
B. Risk Modification:
B.1. Primary Stroke Prevention:
There is currently no data available.
B.2. Secondary Stroke Prevention:
Among patients with stroke or TIA caused by a 50% to 99% stenosis of a major
intracranial artery, the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID)
study showed 1.) Aspirin was safer, and was as effective as warfarin for stroke
prevention (2-year ischemic stroke rate of 19.7% for aspirin vs. 17.2% for warfarin)
and 2.) The rate of ischemic events was high regardless of antiplatelet or
anticoagulant therapy.8

58
In the Trial of Cilostazol in Symptomatic intracranial arterial Stenosis (TOSS), adding cilostazol
100 mg BID to aspirin was superior to aspirin monotherapy in preventing progression of
intracranial arterial stenosis by MRA at 6 months.16 In TOSS 2 (Clinicaltrials.gov Identifier:
NCT00130039), a non-significant trend towards less ICAD progression was observed in
patients who received, in addition to standard Aspirin 75150 mg, Cilostazol 100 mg BID

Primary & Secondary

compared to Clopidogrel 75 mg OD (9.9 % vs 15.46%, respectively p = 0.49). Continued trials
are warranted to confirm the efficacy of cilostazol and other antiplatelets in preventing

Prevention
progression and further vascular events in patients with symptomatic intracranial arterial
stenosis.

The EC-IC Bypass Trial failed to show clinical benefit of revascularization procedure
(extracranial-intracranial anastomosis) in patients with atherosclerotic disease of the carotid
artery and MCA.17 Bypass-patency rate was 96%, but fatal and non-fatal stroke occurred more
frequently and earlier among those randomized to surgery.

Single-center experiences suggest that intracranial angioplasty and/or stenting can be

performed with high degree of technical success.18-20 Acceptable anatomical results were
obtained in medically refractory patients with strokes attributable to intracranial stenosis
enrolled in the Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial
Arteries (SSYLVIA) and Wingspan multi-center Phase I trials. Recurrent ischemic events at 30
days, 6 months and up to 1 year of follow-up were not worse than the natural history of lesions
treated with medical management alone.21-24

Whether interventional catheter-based procedures using the Wingspan system plus aggressive
medical management is superior to aggressive medical therapy alone in preventing recurrent
stroke in patients with > 70 % stenosis of a major intracranial artery is being evaluated in the
ongoing phase III Stenting and Aggressive Medical Management for the Prevention of
Recurrent Stroke in Intracranial Stenosis (SAMPRIS) trial (ClinicalTrials.gov. Identifier: NCT
00576693)

C. Recommendation:

1) In patients with ischemic stroke or TIA, screening for intracranial arterial stenosis by
vascular studies is recommended.
2) Non-invasive tests such as Transcranial Doppler (TCD), CT angiography (CTA) and
Magnetic resonance angiography (MRA) are important in evaluation for ICAD by
primary excluding the disease. Digital subtraction angiography is recommended for
accurate categorization of lesions detected on non-invasive testing and for
distinguishing atherosclerotic and non-atherosclerotic vasculopathies.
3) Best medical management must be targeted to antithrombotic treatment, plaque
regression and stabilization and global atherosclerotic risk management. Aspirin is
recommended in most patients to prevent recurrent ischemic events because it has a
better safety profile than anticoagulation. The combination of Cilostazol and
Aspirin is superior to Aspirin alone in preventing progression of intracranial stenosis.

59
 4) Management of cardiovascular risk factors such as hypertension, dyslipidemia,
diabetes mellitus based on secondary prevention guidelines is strongly advised
5) Further studies are warranted to evaluate short and long-term efficacy of angioplasty
and or stenting in patients with hemodynamically significant intracranial stenosis
(>50%) and symptoms despite medical therapy.25 (Class IIb-C)
Primary & Secondary

Bibliography
Prevention

1. Wong, KS, Huan L. Racial distribution of intracranial and extracranial atherosclerosis. J Clin
Neurosc 2003;10:30-34.
2. Wong KL. Global burden of intracranial atherosclerosis. Int J of Stroke 2006; 1: 158 159.
3. Arenillas JF, Molina CA, Chacon P, et al. High lipoprotein, diabetes and the extent of
symptomatic intracranial stenosis. Neurology 2004;63:27-32.
4. Bang Oy, Kim JW, Lee JH, et al. Association of the metabolic syndrome with intracranial
atherosclerotic stroke. Neurology 2005;65:296-298.
5. Bae, HJ, Lee J, Park JM, et al. Risk factors of intracranial stenosis among asymptomatics.
Cerebrovascular Dis 2007; 24: 355 360
6. Suwanwela NC, Chutinetr A. Risk factors for atherosclerosis of cervicocerebral arteries:
intracranial versus extracranial. Neuroepidemiology 2003; 22: 37 40.
7. Thijs VN, Albers GW. Symptomatic intracranial atherosclerosis: Outcome of patients who fail
antithrombotic therapy. Neurology 2000;55:490-497.
8. Chimowitz MI, Lynn MJ, Howlett-Smith H, et al. Warfarin-Aspirin Symptomatic Intracranial
Disease Trial Investigators. Comparison of warfarin and aspirin for symptomatic intracranial
arterial stenosis. N Engl J Med 2005;352:1305-1316.
9. Kasner, SE, Chimowitz MI, Lynn MJ, et al. Predictors of ischemic stroke in the territory of a
symptomatic intracranial arterial stenosis. Circulation 2006; 113: 555 563.
10. Kremer C, Schaettin T, Giorgiadis D, Baumgartner R. Prognosis of asymptomatic stenosis of
the middle cerebral artery. J Neurol Neurosurg Psychiatry 2004;75:1300-1303.
11. Kern R, Steinke W, Daffertshofer M, et al. Stroke recurrence in patients with symptomatic
versus asymptomatic middle cerebral artery disease. Neurology 2005;65:859-864.
12. Nahab, F. Cotsonis G, Lynn M. et al. Prevalence and prognosis of co-existent asymptomatic
intracranial stenosis. Stroke 2008; 39: 1039 1041.
13. Chen A, Shyr MH, Chen TY. et al. Dynamic CT perfusion imaging with acetazolamide challenge
for the evaluation of patient with unilateral cerebrovascular steno-occlusive disease, Am J
Neuroradiol 2006; 27: 1876 1881.
14. Ma J, Mehrkens JH., Holtmannspoetter M. et al. Perfusion MRI before and after acetazolamide
administration for assessment of cerebrovascular reserve capacity in patients with symptomatic
ICA occlusion: comparison with 99mTC-ECD SPECT. Neuroradiology 2007; 49: 317 326.
15. Grubb RL. Jr, Derdeyn CP, Fritsch SM et al. Importance of hemodynamic factors in the
prognosis of symptomatic carotid occlusion. JAMA 1998.; 280. 1055 1060.
16. Kwon S, Cho YJ, Koo JS et al. Cilostazol prevents the progression of symptomatic intracranial
stenosis. Stroke 2005;36:782-786.
17. The EC-IC Bypass Study Group. Failure of extracranial-intracranial arterial bypass to reduce
the risk of ischemic stroke. Results of an international randomized trial. N Eng J Med
1985;313:1191-1200.
18. Higashida R, Meyers PM, Connors J, et al. Intracranial angioplasty and stenting for cerebral
atherosclerosis: A Position Statement of the American Society of Interventional and
Therapeutic Neuroradiology, Society of Interventional Radiology, and the American Society of
Neuroradiology. J Vasc Interv Radiol 2005;16:1281-1285.
19. Jiang WJ, Xu XT, Jin M, et al. Apollo stent for symptomatic atherosclerotic intracranial stenosis
study results. Neuroradiology 2007; 28: 830 - 834

60
 20. Kurre W, Berkefeld J, Sitzer M et al. Treatment of symptomatic high grade intracranial stenosis
with the balloon-expandable Pharos stent. initial experience. Neuroradiology 2008; 50: 701 -
708
21. SSLYVIA Study Investigators. Stenting of symptomatic atherosclerotic lesions in the vertebral
or intracranial arteries (SSYLVIA). Stroke 2004;35:1388-1392.
22. Henkes H, Miloslavski E, Lowens S, et al. Treatment of intracranial atherosclerotic stenosis

Primary & Secondary

with balloon dilatation and self-expanding stent deployment (WingSpan). Neuroradiology
2005;47:222-228.

Prevention
23. Fiorella D, Levy EI, Turk AS et al. US multicenter experience with the wingspan stent system for
the treatment of intracranial atheromatous disease: periprocedural results. Stroke 2007; 38: 881
887
24. Zaidat OO, Klucznic R, Alexander MJ. et al. NIH Multicenter Wingspan Intracranial Stent
Registry Study Group. The NIH registry on the use of Wingspan stent for 70 99% intracranial
arterial stenosis. Neurology 2008; 70: 1518 1524.
25. Sacco R, Adams R, Albers G, et al. Guidelines for the Prevention of Stroke in Patients with
Ischemic Stroke or Transient Ischemic Attack: A Statement for Healthcare Professionals from
the American Heart Association/American Stroke Association Council on Stroke. Stroke 2006;
37:577-617.

IX. PERIPHERAL ARTERIAL DISEASE

Peripheral arterial disease (PAD) is characterized by arterial stenosis and occlusion of the
peripheral arterial bed. It can be symptomatic or asymptomatic. Symptomatic PAD ranges from
intermittent claudication (IC) to chronic limb ischemia. Regardless of symptomatology, PAD is
an indicator of diffuse systemic atherosclerosis. Risk factors include smoking, DM,
dyslipidemia, hypertension and hyperhomocysteinemia, which considerably and frequently
overlap and coexist with coronary and cerebrovascular disease. There are numerous reports on
the increased risk of MI, stroke and cardiovascular death in patients with PAD.1,2,26,27

A. Epidemiology:

The prevalence of PAD increases with age and with the presence of risk factors. Objective
testing using ankle-brachial index (ABI) in a U.S. based primary care population study
showed prevalence was up to 29% in people aged >70 yers old, and those 50 to 69-year age
group with diabetes.6

There is a 20% to 60% increased risk for MI and a two- to six-fold increased risk of death due to
cqoronary artery events in PAD patients.4-8 The risk of stroke is increased by approximately
40%. In the Atherosclerosis Risk in Communities (ARIC) study, men with PAD were four to
five times more at risk of stroke and TIA than those without PAD.8

In addition, all-cause mortality rate is 61.8% after 10 years in men with PAD compared with
16.9% in unaffected men.6 The corresponding mortality rates for women were 33.3% and
11.6%, respectively. The increase in total mortality was due to a sharp increase in cardiovascular
mortality, which persisted even after adjusting for pre-existing CAD and cerebrovascular
disease at baseline. The risk was proportional to the severity of PAD.

61
 Local studies reported that 2% of Filipinos aged 55 years and older have IC, and approximately
5% have PAD upon ABI confirmation. In a study on Filipino patients aged 40 years or older
and confined in the intensive care unit for heart attack, stroke or type 2 DM, 30% had silent
PAD.9 The 2003 NNHeS reported a PAD prevalence of 1.6% among Filipinos aged 20 years
and above.10
Primary & Secondary

The ABI, an objective and simple test for detecting the presence and severity of PAD has
Prevention

been found in several studies and by meta-analysis to have significant association with
increased rates of cardiovascular death, myocardial infarction and stroke in PAD
patients.3-5 Measurement and use of the ABI has been suggested by published guidelines
to improve cardiovascular risk assessment and prediction.1,24,25

B. Risk Modification:

In lower-extremity PAD, adverse cardiovascular events may be reduced with lifestyle

modification or elimination of risk factors, such as cigarette smoking, diabetes mellitus,
dyslipidemia and hypertension. Exercise and a non-atherogenic diet are strongly advised.

B.1. Smoking Cessation

No prospective RCTs have shown the effects of smoking cessation on cardiovascular

events. Only observational studies have shown that the risk of death, MI and limb
loss is greater in individuals who continue to smoke than those who stop smoking.11-13

B.2. Diabetes Mellitus

It is still unclear whether blood glucose control decreases the risk of adverse
cardiovascular events in those with lower-extremity PAD. Analysis of the Diabetes
Control and Complication Trial (DCCT) showed that the use of intensive insulin
therapy on type 1 DM patients only reduced risk of IC, peripheral revascularization
and amputation by 22%, which was not statistically significant.14 The 10-year United
Kingdom Prospective Study (UKPDS) showed that aggressive treatment (using
sulfonylureas or insulin) in type 2 DM patients reduced the risk of MI by 16%
(borderline significance), with a RRR in microvascular complications of 25%
compared with conventional treatment, but did not reduce the risk of death or
stroke.15

B.3. Dyslipidemia

Treatment of dyslipidemia in patients with systemic atherosclerosis can reduce

future adverse cardiovascular events.16 In the HPS, which included 6,748 PAD
patients, there was a 25% reduction of cardiovascular events in the simvastatin-
treated group.

62
 B.4. Hypertension

In PAD patients, antihypertensive treatment may diminish perfusion to the limb and
exacerbate symptoms of limb ischemia. However, most patients do not experience
any worsening of symptoms with appropriate antihypertensive therapy needed to
reduce risk of cardiovascular events.

Primary & Secondary

Prevention
The use of beta-blockers has been controversial in the treatment of PAD patients.
However, a meta-analysis of 11 placebo-controlled studies in patients with PAD
showed that beta-blockers did not adversely affect walking capacity.17

The Heart Outcomes Prevention Evaluation (HOPE), which included 4,051 PAD
patients randomized to ramipril or placebo, reported risk reduction for MI, stroke or
vascular death by 25%, similar to that achieved in the overall study population.18

C. Recommendations:

(Recommendations were adapted from the ACC/AHA 2005 Guidelines for PAD).
1) Individuals with PAD or risk factors for PAD, should undergo ABI measurement.
2) Therapeutic interventions to diminish the increased risk of MI, stroke and death as
mentioned in other sections of this guideline are recommended (Class I-B).

Bibliography

1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the
management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and
abdominal aortic) [trunc]. Circulation 2006;113:e463-e654.
2. Criqui MH,Denenberg JO, Langer RD, et al. The epidemiology of peripheral arterial disease:
importance of identifying the population at risk. Vasc Med 1997;2:221-226.
3. Resnick HE, Lindsay RS, McDermott MM; et al. Relationship of high and low ankle brachial
index to all-cause and cardiovascular disease mortality: the Strong Heart Study. Circulation.
2004;109(6):733-739.
4. OHare AM, Katz R, Shlipak MG, Cushman M, Newman AB. Mortality and cardiovascular risk
across the ankle-arm index spectrum: results from the Cardiovascular Health Study. Circulation.
2006
5. McDermott MM, Liu K, Criqui MH; et al. Ankle brachial index and subclinical cardiac and
carotid disease: the Multi-Ethnic Study of Atherosclerosis. Am J Epidemiol. 2005;162(1):33-
41006;113(3):388-393.
6. Hirsch AT, et al. JAMA 2001; 286:1317-1324.
7. Meijer WT, Hoes AW, Rutgers D, et al. Peripheral arterial disease in the elderly: The Rotterdam
Study. Arterioscler Thromb Vasc Biol 1998;18:185-192.
8. Smith GD, Shipley MJ, Rose G. Intermittent claudication, heart disease risk factors, and
mortality. The Whitehall Study. Circulation 1990;82:1925-1931.
9. Newman AB, Sutton-Tyrrel K, Vogt MT, et al. Morbidity and mortality in hypertensive adults
with low ankle/arm blood pressure index. JAMA 1993;270:487-489.
10. Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with
peripheral arterial disease. N Engl J Med 1992;326:381-386.

63
 11. Vogt MT, Cauley JA, Newman AB, et al. Decreased ankle/arm blood pressure index and
mortality in elderly women. JAMA 1993;270:465-469.
12. ZhengZj, Sharrett AR ,Chambless LE, et al. Associations of ankle/brachial index with clinical
coronary heart disease, stroke and preclinical carotid and popliteal Atherosclerosis Risk in
Communities (ARIC) Study. Atherosclerosis 1997;131:115-125.
13. Abola MT, Dans A; for the Council of Stroke and Peripheral Vascular Diseases, Philippine
Primary & Secondary

Heart Association (PHILPAD Study). Phil J Int Med 2003;41:71-74.

14. Dans AL, Morales DD, Abola TB, Roxas J, et al; for NNHeS 2003 Group. National Nutrition
Prevention

and Health Survey (NNHeS): Atherosclerosis-related diseases and risk factors. Phil J Int Med
2005;43;103-115.
15. Faulkner KW, House AK, Castleden WM. The effect of cessation of smoking on the
accumulative survival rates of patients with symptomatic peripheral vascular disease. Med J
Aust 1983;1;217-219.
16. Lassila R, Lepantalo M. Cigarette smoking and the outcome after lower limb arterial surgery.
Acta Chir Scand 1988;154:635-640.
17. Johnson T, Bergstrom R Cessation of smoking in patients with intermittent claudication: effect
on the risk of peripheral vascular complications: myocardial infarction and mortality. Acta Med
Scand 1987:221:253-260.
18. Effect of intensive diabetes management on macrovascular events and risk factors in the
Diabetes Control and Complications Trial. Am J Cardiol 1995;75:894-903.
19. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional
treatment and risk of complications in patient with type 2 diabetes (UKPDS 33) UK
Prospective Diabetes Study (UKPDS) Group, Lancet 1998;352:837-853.
20. Heart Study Collaboration Group. MRC/BHF Heart Protection Study of cholesterol lowering
with simvastatin in 20,536 high-risk individuals: a randomized placebo-controlled trial. Lancet
2002;360:7-22.
21. Radack K, Deck C. Beta adrenergic blocker therapy does not worsen intermittent claudication in
subjects with peripheral arterial disease: a meta-analysis of randomized controlled trials. Arch
Intern Med 1996;151:1769-1776.
22. Calligaro KD, Musser DJ, Chen AY, et al. Duplex ultrasonography to diagnose failing arterial
prosthetic. Surgery 1996;120:455-459.
23. Fowkes FG et al. ABI combined with Framingham Risk Study to predict cardiovascular events
and mortality a meta- analysis. JAMA 2008; 300(2): 197-208.
24. Norgren L, Hiatt WR, Dormandy JA; et al. Inter-society consensus for the management of
peripheral arterial disease (TASC II). Eur J Vasc Endovasc Surg. 2007;33(suppl 1):S1-S70.
25. Graham I, Atar D, Borch-Johnsen K; et al, European Socie ty of Cardiology (ESC); European
Association for Cardiovascular Prevention and Rehabilitation (EACPR); Council on
Cardiovascular Nursing; European Association for Study of Diabetes (EASD); International
Diabetes Federation Europe (IDF-Europe); European Stroke Initiative (EUSI); Society of
Behavioural Medicine (ISBM); European Society of Hypertension (ESH); WONCA Europe
(European Society of General Practice/Family Medicine); European Heart Network (EHN);
European Atherosclerosis Society (EAS). European guidelines on cardiovascular disease
prevention in clinical practice: full text: Fourth Joint Task Force of the European Society of
Cardiology and other societies on cardiovascular disease prevention in clinical practice
(constituted by representatives of nine societies and by invited experts). Eur J Cardiovasc Prev
Rehabil. 2007;14(suppl 2):S1-S113.
26. Steg G et al., for the REACH Registry Investigators. One-year cardiovascular event rates in
outpatients with atherothrombosis. JAMA. 2007;297:1197-1206

64
X. SMOKING

A. Epidemiology:

Asian countries have the highest prevalence of smoking in the world: 72% in Korean men, 63%

Primary & Secondary

in Chinese men and 58% in Japanese men.1 The NNHeS survey showed that among Filipinos,
the prevalence of smoking is 56.3% in males and 12.1% in females.2 Two national surveys of

Prevention
Filipino adolescents revealed that 1 out of 5 adolescents is currently smoking with a higher
percentage among males compared with females (37.3% vs. 6.3%).3,4

A.1. Cigarette Smoking and Risk of Stroke and its Subtypes

In a prospective study conducted by the Japan Public Health Center (JPHC), a total
of 19,782 men and 21,500 women aged 40 to 59 years, who were free of a prior
diagnosis of stroke, coronary heart disease, or cancer, and who reported their
smoking status, were followed from 1990-2001. The relative risks for current
smokers compared with never-smokers after adjustment for cardiovascular risk
factors were 1.27 (1.05 to 1.54) for total stroke, 0.72 (0.49 to 1.07) for
intraparenchymal hemorrhage, 3.60 (1.62 to 8.01) for subarachnoid hemorrhage, and
1.66 (1.25 to 2.20) for ischemic stroke. There was a dose-response relation between
the number of cigarettes smoked and the risk of ischemic stroke for men. A similar
positive association was observed between smoking and risks of lacunar infarction
and large-artery occlusive infarction, but not embolic infarction. Smoking raises the
risk of total stroke and subarachnoid hemorrhage for both men and women and the
risk for ischemic stroke, either lacunar or large-artery occlusive infarction, for men. 5

A meta-analysis of 22 studies indicates an approximate doubling of relative risk of

cerebral infarction among smokers versus nonsmokers.6 A prospective long term
study showed increased risk not only of cerebral infarction but of hemorrhagic
strokes with relative risk of 2.06 (95%CI 1.08 to 3.96) for ICH and 3.22 (95%CI 1.26
to 8.18) for SAH among smokers (>20 cigarettes/day).7 A strong positive
association was found between cigarette smoking and aneurysmal SAH in women,
which is virtually eliminated within a few years of smoking cessation.8
A.2. Dose Dependent Effect of Smoking

Case control9 and prospective studies have shown that cigarette smoking is an
independent predictor of stroke with a dose response relationship, affecting both
men10 and women.11 The Framingham Heart Study showed that the relative risk of
stroke in heavy smokers (<40 cigarettes/day) was twice that of light smokers (<10
cigarettes/day), and the risk of stroke increased with the number of cigarettes
smoked.12 The large cohort study of US male physicians showed that heavy smokers
(>20 cigarettes/day) had a relative risk of 2.7 for total nonfatal stroke and 1.46 for
fatal stroke.13

65
 Studies also suggest a dose response relationship between pack years of smoking and
carotid artery intima media wall thickness.14

A.3. Second Hand Smoke (SHS) and Risk of Stroke

Primary & Secondary

SHS may exert detrimental effects on vascular homeostasis. Cohort studies showed
an elevated prevalence of stroke among nonsmoking women living with husbands
Prevention

who smoked. The prevalence increased as the intensity and duration of husbands
smoking increased.15

A population-based cross-sectional study was done in Beijing, China among 1209

women who never smoked, 39.5% were exposed to SHS at home or in workplaces.
Those individuals who were exposed to SHS had a significantly higher risk of
coronary heart disease (adjusted odds ratio [OR], 1.69; 95% CI, 1.31 to 2.18) and
ischemic stroke (OR, 1.56; 95% CI, 1.03 to 2.35) than those never exposed to SHS
after adjustment for 13 potential risk factors.16

B. Risk Modification:

Both the Framingham Heart Study and Nurses Health Study showed a normalized risk ratio 5
12,17
years after cessation of smoking. Tell et al however, showed that the risk reduction was
dependent on the quantity of cigarettes smoked before stopping: light smokers (<20
cigarettes/day) reverted back to normal values but heavy smokers retained twice the incidence
of stroke as non smokers.18 Switching to pipe or cigar smoking confers little benefit,
emphasizing the need for complete cessation of smoking.19
B.1. Nicotine Dependence Treatment 20,21,22,23

Tobacco dependence is a chronic condition for which there are now effective
behavioral and pharmacotherapy treatments. A combination of nicotine
replacement therapy, social support, and skills training has been proven to be the
most effective approach for quitting.
1. Nicotine replacement patch, gum, lozenge, nasal spray, inhaler
2. Non-nicotine medications antidepressants, varenicline (Chantix), clonidine
3. Counseling, support groups, smoking cessation program

B.2. Smoke Free Initiatives24

Singapore has the most successful smoke free campaign. Singapore has the lowest
numbers of smokers (13%). In Singapore, smoking is banned in all public places.
Live it up without lighting up - the creative campaign which features gorgeous,
young, happy, confident people with unblemished skin in semi cartoon like
environments. This tells readers that Non smokers tend to look younger than
smokers of the same age and that Non smokers tend to be physically more fit than
smokers.

66
 Malaysia spent RM100 million (US$30 million) over 5 years on smoke free campaign
that was ineffective in bringing down the number of smokers in Malaysia.

In the UK, after extensive research of more than 8,500 smokers over a ten-year
period, the Institute for Social and Economic research found that the warnings on

Primary & Secondary

cigarette packets that smoking kills or maims are ineffective in reducing the number
of smokers. Likewise, chilling commercials or emotionally disturbing programs are

Prevention
also ineffective. The study also discovered that even when a close family member
becomes ill from the effects of smoking, the smoker takes no notice.

In fact, according to the study, smokers only reduced the number of cigarettes or
sometimes quit when their own personal health is at stake. And even failing health
may not persuade a smoker to reduce or even stop smoking because smoking is linked
to a lack of psychological well being and often failing health results in psychological
decline.

In the Philippines, the 2003 Tobacco Regulation Act (Law RA9211) was implemented
in 2004 to protect the populace from hazardous products and promote the right to
health and instill health consciousness among them.26

C. Recommendations:

1) Smoking cessation for all current smokers is recommended (Class II-B).

2) Smoking should be banned in public places since second hand smoke is associated
with increased risk of CVD (ClassII-B).
3) Effective behavioral and pharmacological treatments should be advised and
encouraged for nicotine dependence (ClassIIa-B).
4) Tobacco Regulation Act of 2003 should be implemented to protect the populace
from hazardous products, promote the right to health and instill health
consciousness.

Bibliography

1. Jee S, Suh I, Kim IS et al. Smoking and atherosclerotic cardiovascular disease in men with low
levels of serum cholesterol. The Korea Medical Insurance Corporation Study. JAMA 1999;
282:2149-55.
2. Antonio L. Dans, M.D., Dante D. Morales, M.D., Felicidad Velandria, Teresa B. Abola, M.D.,
Artemio Roxas Jr., M.D., Felix Eduardo R. Punzalan, M.D., Rosa Allyn G. Sy, M.D., Elizabeth
Paz Pacheco: National Nutrition and Health Survey (NNHeS): Atherosclerosis - related diseases
and risk factors: Phil. J of Intern Med May-June 2005,Vol.43.
3. UP Population Institute.YAFS 2 (Young Adult Fertility and Sexuality Study). 1994.
4. UP Population Institute.YAFS 3 (Young Adult Fertility and Sexuality Study). 2002.
5. Stroke. 2004;35:1248-1253

67
 6. Robbins AS, Manson JE. Lee I. Satterfield S. Hennekens GH. Cigarette smoking and stroke in a
cohort of US male physicians. Ann Intern Med 1994;120:458-62.
7. Howard G, Burke GL, Szklo M, Tell GS et al. Active and passive smoking are associated with
increased carotid wall thickness. The atherosclerotic risk in community study. Arch Intern Med
1994;154:1277-82.
Primary & Secondary

8. Shinton R. Beevers G. Meta-analysis of relation between cigarette smoking and stroke. Br Med J
1989; 298-789-794.
Prevention

9. Bonita R. Seragg R. Stewart A et al. Cigarette smoking and risk of premature stroke in men and
women. Br Med J 1987; 293;6-8
10. Abott RD, Yin Yin MA, Reed DM et al. Risk of stroke in male cigarette smokers. NEJM 1986;
315:717-720.
11. Colditz GA. Bonita R. Stampfer MJ et al. Cigarette smoking as a risk factor for stroke.
Framingham Study. JAMA 1988:318:937-041.
12. Wolf PA. D Agostino RB. Kannet WB. Bonita R. Belanger AJ. Cigarette smoking as a risk factor
for stroke. The Framingham Study. JAMA 1988;259:1025-9.
13. Kurth T, Kase C, Nerger K, Schaeffner E, Buring J, Gaziano J.Smoking and risk of hemorrhagic
stroke in men. Stroke 2003;34;1151-1155.
14. Anderson CS. Feigin V, Bennet D, Lin R, Hankey G, Jamrozik K for Australian Cooperative
Research on Subarachnoid Hemorrhage: an international population based case control study.
Stroke 2004;35;633-637.
15. Zhan X, Shu XO, Yang G, Li HL, Xiang YB, GaoYT, Li Q, Zeng W. Association of passive
smoking by husbands with prevalence of stroke among Chinese women nonsmokers. Am J
Epid 2005;161:213-218
16. Yao He, MD, PhD; Tai Hing Lam, MD. Passive smoking and risk of peripheral arterial disease
and ischemic stroke in chinese women who never smoked. Circulation. 2008;118:1535-1540.
17. Golditz GA, Stamfer B, Willer WC, Speizer R et al. Cigarette smoking and risk of stroke in
middle aged women. N Eng J Med. 1988;18:937-41
18. Tell GS, Polak JF, Ward BJ, Robbins J, Savage PJ. Relation of smoking with carotid artery wall
thickness and stenosis in older adults. The cardiovascular health study. Circulation 1994;902905-
9.
19. Wannamabee SG, Shaper MC, Smoking cessation and the risk of stroke in middle aged men.
JAMA 1998;274:155-60.
20. www.mayoclinic.com/nicotine-dependence
21. Fiore MC, Bailey WC, Cohen SJ, et al. Treating Tobacco Use and Dependence: Clinical Practice
Guideline. Rockville, Md: US Department of Health and Human Services, Public Health
Service;2000.
22. Hughes JR, Stead LF, Lancaster T. Antidepressants for smoking cessation. Cochrane Database
Syst Rev. 2003.
23. Silagy C, Lancaster T, Stead L, Mant D, Fowler G. Nicotine replacement therapy for smoking
cessation. Cochrane Database Syst Rev. 2004.
24. Bak S, Sindrup SH, Alslev T, Kristensen O, Christensen K, Gaist D. Cessation of smoking after
first-ever stroke: a follow-up study. Stroke2002;33:22632269
25. brandconsultantasia.wordpress.com/.../creative-campaign-not-the-solution-to-smoking-
issues-in-singapore/
26. www.doh.gov.ph/ra/ra9211.html

68
XI. EXCESSIVE ALCOHOL

A. Epidemiology

There is a direct, dose-dependent effect of the consumption of alcohol on the risk of

hemorrhagic stroke but the association with ischemic stroke varies with different studies.1-4

Primary & Secondary

Most studies suggest a J-shaped association between alcohol and ischemic stroke: a protective

Prevention
effect with light to moderate drinking, and an elevated risk with heavy consumption.5-8 While
the protective effect of light alcohol consumption is evident among Caucasians, this is not
evident among Asians.2, 4-6,9-11 Moderate alcohol consumption decreased risk of ischemic
stroke in a multi ethnic population.12 Heavy alcohol use, either daily or in binges, is related to
excess of stroke risk.13

B. Risk Modification

Alcohol consumption of up to 2 drinks per day was protective against ischemic strokes in
Caucasians, Blacks and Hispanics, but consumption above 5 drinks per day increased the risk of
ischemic stroke.14

C. Recommendations

1) Moderate intake of alcohol for those who drink alcohol and have no health
contraindications to its use. Consumption of alcohol, up to 30 mL (or 28grams) of
ethanol per day, equivalent to 60 mL or two jiggers of 100 proof whisky, one glass of
wine (240 mL) or two bottles of beer (720 mL), or two drinks per day for men and one
drink per day for non-pregnant women, may reduce the risk of ischemic stroke (Class
IIb-C).
2) Patients with ischemic stroke or TIA who are heavy drinkers should eliminate or
reduce their consumption of alcohol (Class I-A).
3) Those who do not customarily drink alcohol should not be encouraged to do so.

Bibliography
1. Donahue RP, Abbot RD, Reed DM, Yano K. Alcohol and hemorrhagic stroke. The Honolulu
Heart Program. JAMA 1986; 255: 2311-2314.
2. Tanaka H, Ueda Y, Hayashi M, et al. Risk factors for cerebral hemorrhage and cerebral
infarction in a Japanese rural community. Stroke 1982; 13: 62-73.
3. Tanaka H, Hayaski M, Date C, et al. Epidemiologic studies of stroke in Shibata, a Japanese
provincial city: preliminary report on risk factors for cerebral infarction. Stroke 1985; 16: 773-
380.
4. Iso H, Kitamara A, Shimamoto T, et al. Alcohol intake and the risk of cardiovascular disease in
middle-aged Japanese men. Stroke 1995; 26: 767-773.
5. Gill JS, Zezulka AV, Shipley MJ, et al. Stroke and alcohol consumption. N Engl J Med 1986; 315:
1041-1046.
6. Djousse L, Ellsion RC, Beiser A, et al. Alcohol consumptionand risk of ischemic stroke. The
Framingham Study. Stroke 2002; 33: 907-912.

69
 7. Berger K, Ajani CA, Kase CS, et al. Light to moderated alcohol consumption and risk of stroke
among US male physicians. N Engl J Med1999; 341: 1557-1564.
8. Stampfer MJ, Colditz GA, Willet WC, et al. A prospective study of moderate alcohol
consumption and the risk of coronary disease and stroke in women. N Engl J Med 1988; 319:
267-273.
9. Camargo CA, Moderate alcohol consumption and stroke. The epidemiologic evidence. Stroke
Primary & Secondary

1989; 20: 1611-1626.

10. Kono S, Ikeda M, Tokudome S, et al. Alcohol and mortality: a cohort study of male Japanese
Prevention

physicians. Int J Epidemiol 1986; 15: 527-532.

11. Kiyohara Y, Kato I, Iwamoto H, et al. The impact of alcohol and hypertension on stroke
incidence in a general Japanese population. The Hisayama Study. Stroke 1995; 26: 368-372.
12. Elkind MSV, Sciacca R, Boden-Albal B, et al. Moderate alcohol consumption reduces risk of
ischemic stroke. The Northern Manhattan Study. Stroke 2006; 37: 13-19.
13. Kozarerevic D, McGee D, Vojvodic N, et al. Frequency of alcohol consumption and morbidity
and mortality. The Yugoslavia Cardiovascular Disease Study. Lancet 1980; 1: 613-616.
14. Sacco RL, Elkind M, Boden B, et al. The protective effect of moderate alcohol consumption on
ischemic stroke. The Northern Manhattan Study. JAMA 1999; 281: 52-60

XII. PHYSICAL INACTIVITY

A. Epidemiology:

Physical inactivity is a growing public health concern that may have a major impact on the
prevalence of atherothrombotic cardiovascular disease in the coming decades. The relative risk
of cardiovascular disease (including stroke) associated with physical inactivity ranges from 1.5
to 2.4, a risk increase similar to that observed with high cholesterol, high blood BP or cigarette
smoking.1 In a meta-analysis of physical activity and stroke risk, moderate and high levels of
physical activity are associated with reduced risk of total ischemic and hemorrhagic strokes.2
Highly active individuals had a 27% lower incidence of stroke risk or mortality (RR=0.73) than
did low-active individuals in combined cohort and case-control studies. Physical inactivity is a
risk factor for stroke, DM, obesity, hypertension and depression.3,4 Local data shows the odds
ratio for stroke associated with physical inactivity is 1.23.5

B. Risk modification

B.1. Primary Stroke Prevention

Physical activity reduces stroke risk in both genders and across all racial/ethnic and
age groups (OR; 0.37).6,7 The Framingham Heart Study, the Honolulu Heart
Program, and the Oslo Study have shown the protective effect of physical activity for
men.8 There seems to be a graded linear relation between the volume of physical
inactivity and total stroke.9 The Physicians Health Study showed a lower total stroke
risk associated with vigorous exercise (five times a week or more) among men (RR;
0.86).10 The Harvard Alumni Study showed a decrease in total stroke risk in men
who were highly physically active (RR; 0.82).11

70
For women, the Nurses Health Study and the Copenhagen City Heart Study showed
an inverse association between level of physical activity and stroke incidence.12
Physical activity (in sports, leisure time or at work) also reduced risk of ischemic
strokes, in particular.7

Primary & Secondary

The protective effect of physical activity may be partly mediated by BP reduction,
improvement of lipid profiles (reduction in triglyceride, increase in HDL, and

Prevention
decrease in LDL:HDL ratios), improvement of glucose homeostasis and insulin
sensitivity, and improvement in body composition and weight. 3,4 Other benefits of
physical activity include reduction in blood coagulability,13 improvement of
coronary blood flow,14 augmentation of cardiac function,15 enhancement of
endothelial function,16 improvement of autonomic tone,17 and reduction of
systemic inflammation.18

B.2. Secondary Stroke Prevention

Among stroke survivors, approximately 14% achieve full recovery in physical

function, between 25-50% require at least some assistance with activities of daily
living, and half experience severe long-term effects such as partial paralysis. Activity
intolerance is hence, common among stroke survivors, especially in the elderly.19,20
Stroke survivors are also often deconditioned and thus are further predisposed to a
sedentary lifestyle that limits performance of activities of daily living, increases the
risk for falls, and may contribute to a heightened risk for recurrent stroke and
cardiovascular disease.

Cardiorespiratory Response to Acute Exercise in Stroke Survivors:

Many physiologic changes occur among stroke survivors, especially among those
with moderate to severe deficits. The cardiac response to acute exercise among
stroke survivors has been documented in some studies. Stroke patients achieve
significantly lower maximal workloads, heart rate and BP responses than control
subjects during progressive exercise testing.21 In general, oxygen uptake at a given
submaximal workload in stroke patients is greater than in healthy subjects, possibly
because of reduced mechanical efficiency, the effects of spasticity, or both. Another
physiologic change that occurs among stroke patients is reduction in peak oxygen
uptake. Ambulatory stroke survivors may be able to perform at reduced peak oxygen
consumption and reduced peak power output that can be achieved by age- and
gender-matched individuals without a history of stroke.19,20
Traditionally, the physical rehabilitation of stroke survivors typically ends within
several months after stroke because it was believed that most, if not all recovery of
motor function, occurred during this interval. Recent research studies have shown
that aggressive rehabilitation beyond this time period, including treadmill and aerobic
exercise, is beneficial especially in increasing strength, timing of muscle activations
and cardiorespiratory fitness or aerobic capacity 22 among stroke survivors.

71
 The major rehabilitation goals for the stroke patient are: (1) to prevent complications
of prolonged inactivity; (2) to decrease recurrent stroke and cardiovascular events;
and, more recently given emphasis, (3) to increase aerobic fitness. The first two goals
are well accepted tenets. For the last goal - the link between exercise training and
improved cardiovascular fitness and health among persons who are disabled by
Primary & Secondary

stroke remained unclear until recently.

Prevention

Stroke survivors can increase their cardiovascular health and fitness with regular
aerobic exercise 23 by a magnitude that is similar to that of healthy older adults who
engage in endurance training programs. In a RCT of 42 hemiparetic stroke
survivors, vigorous aerobic exercise training three times per week for 10 weeks
significantly improved peak oxygen consumption and workload, submaximal
exercise BP response, exercise time and sensorimotor function.24 In a study of 35
stroke patients with multiple comorbidities who underwent 12 weeks of a 1-
hour/day, 3-days/week exercise program of combined cardiovascular, strength and
flexibility training, the exercise group had significant gains in peak oxygen uptake,
strength and improvements in body composition compared with controls.25 In a
RCT involving 88 men with CAD and disability, two-thirds of whom were stroke
survivors, a 6-month home exercise training program significantly increased peak left
ventricular ejection fraction and HDL, and decreased resting heart rate and total
serum cholesterol.26

Having laid down the merits of physical fitness for stroke survivors, it is important to
mention that exercise is not without risks, and the recommendation that stroke
survivors participate in an exercise program is based on the premise that the benefits
outweigh these risks. The major potential health hazards of exercise for stroke
survivors include musculoskeletal injury and sudden cardiac death.

C. Recommendations

C.1. Primary Stroke Prevention

1) Increased physical activity is associated with a reduction in stroke risk, and is

strongly recommended. It is important to recognize that physical education in
school may form the starting point for an active lifestyle later in life.

2) At least 30 minutes of moderate-intensity aerobic exercise on most days of the

week (preferably all days) is recommended as part of a healthy lifestyle. Healthy
people should be advised to choose enjoyable activities that fit into their daily
routine, preferably for 30 to 45 minutes, four to five times weekly, at an intensity
to maintain 60% to 80% of the average maximum heart rate. Additional
benefits are gained from vigorous-intensity activity.27

72
 C.2. Secondary Stroke Prevention

1) It is recommended that all stroke survivors undergo a pre-exercise evaluation

that includes a complete medical history and a physical examination aimed at
identifying neurological complications and other medical conditions that
require special consideration or constitute a contraindication to exercise.28

Primary & Secondary

Persons with known or suspected cardiovascular, respiratory or neurological

Prevention
disorders should consult a physician before beginning or significantly increasing
physical activity. Adaptive programs for post-stroke patients depending on
neurological deficits are recommended.29

2) Exercise and aerobic fitness for stroke survivors is recommended and should be
tailored to individual needs and limitations. In general, aerobic training at 50-
80% of maximal heart rate may be advised to stroke survivors.30 Continuous or
accumulated aerobic training for 20 to 60 minutes daily, three to seven days a
week, depending on the patients level of fitness, is advised.

3) Adjunctive upper body and resistance training programs are also recommended
for clinically stable stroke patients. It may be prudent to prescribe 1-3 sets of
10-15 repetitions for 8-10 sets of exercises that involve the major muscle groups
(arms, shoulders, chest, abdomen, back, hips and legs), performed 2-3 days per
week.28 Adjunctive flexibility (stretching) and neuromuscular training
(coordination and balance activities) to increase range of motion of the
involved side, prevent contractures, and increase activities of daily living are also
recommended.29

APPENDIX I

DE FIN ITION of TER M S

Activity in which the body's large muscles move in a rhythm ic

m anne r for a sustained period of tim e. Aerobic activity, a lso
Aerobic physica l
ca lle d endurance ac tivity, im proves cardiorespiratory fitness.
activity
E xam ples include walking, ru nning, a nd swim ming, a nd
bicycling.

M axim al He art
Ra te Formula : Ma ximu m Heart Rate = 220 - age

On an absolute sca le, physica l activity th at is done at 3.0 to 5.9

Mode ra te
tim es the in te nsity of rest. On a sca le relative to an
intensity ae robic
individual's p ersonal c apacity, m oderate-intensity physica l
exercise
ac tivity is u sually a 5 or 6 o n a sca le of 0 to 10.

73
 DEFINITION of TERMS

The body's capacity to transport and use oxygen during a maximal exertion
Peak oxygen involving dynamic contractions of large muscle groups, such as during running
Primary & Secondary

consumption or
or cycling. Also known as maximal aerobic power and cardiorespiratory
uptake
Prevention

endurance capacity.

The ability to carry out daily tasks with vigor and alertness, without undue
fatigue, and with ample energy to enjoy leisure-time pursuits and respond to
Physical fitness emergencies. Physical fitness includes a number of components consisting of
cardiorespiratory endurance (aerobic power), skeletal muscle endurance, skeletal
muscle strength, skeletal muscle power, flexibility, balance, speed of movement,
reaction time, and body composition.

Resistance Physical activity, including exercise, that increases skeletal muscle strength,
training power, endurance, and mass.

Vigorous On an absolute scale, physical activity that is done at 6.0 or more times the
intensity physical intensity of rest. On a scale relative to an individual's personal capacity,
activity vigorous-intensity physical activity is usually a 7 or 8 on a scale of 0 to 10.

APPENDIX II

SUMMARY OF EXERCISE PROGRAMMING RECOMMENDATIONS FOR

STROKE SURVIVORS

Mode of Exercise Major Goals Intensity/Frequency/Duration

Aerobic
Increase
Large-muscle activities (eg, independence in 40%70% peak ox ygen uptake;
walking, treadmill, stationary ADLs 40%70% heart rate reserve; 50%
cycle, combined arm-leg
80% maximal heart rate; RPE 1114
ergometry, arm ergometry, Increase walking (620 scale)
seated stepper) speed/efficiency

74
 Mode of Exercise Major Goals Intensity/Frequency/Duration

Improve tolerance
for prolonged
physical activity 37 d/wk

Primary & Secondary

Reduce risk of
2060 min/session

Prevention
cardiovascular
disease (or multiple 10-min sessions)

Strength
Increase
Circuit training independen ce in 13 sets of 1015 repetition s of 810
AD Ls exercises involving the m ajor m uscle groups
Weight machines
Free weights 23 d/wk
Isometric exercise
Flexibility
Increase ROM of
involved extrem ities 23 d/wk (before or after ae ro bic or
Stretching Prevent strength train ing)
contractures
Hold each stre tch for 1030 seconds
Neuromuscular

Coordination an d Improve le vel of 23 d/wk (consider p erfo rm ing on same

balance activities safety durin g ADLs day as strength activities)

AD Ls in dicates activities of daily living; RPE, rating of perceived exertion; and ROM, range
of motion.
Re commende d inte nsity, frequency , and duration of exerc ise depe nd on each individual pa tients le vel of fitness.
Inte rmittent training se ssions may be indicated during the initial wee ks of rehabilitation.

Bibliography

1. Pate RR, Pratt M, Blair SN, et al. Physical activity and public health: a recommendation from the
Centers for Disease Control and Prevention and the American College of Sports Medicine.
JAMA 1995;273:402-407.
2. Lee, CD, Folsom AR, Blair SN. Physical activity and stroke risk. Stroke 2003;34:2475-2481.
3. Warburton DE, Nicol CW, Bredin SS. Health benefits of physical activity: the evidence. CMAJ
2006;174:801-809.
4. Warburton DE, Gledhill N, Quinney A. The effects of changes in musculoskeletal fitness on
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5. Roxas A; for the Philippine Neurological Association and Department of Health. Risk factors
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75
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the Northern Manhattan Stroke Study. Stroke 1998;29:380-387.
Primary & Secondary

8. Haheim, LL, Holme I, Hjermann I, Leren P. Risk factors of stroke incidence and mortality. A
12-year follow-up of the Oslo Study. Stroke 1993;24:1484-1489.
Prevention

9. Hu FB, Stampfer MJ, Colditz GA, et al. Physical activity and risk of stroke in women. JAMA
2000;283:2961-2967.
10. Lee IM, Hennekens CH, Berger K, et al. Exercise and risk of stroke in male physicians. Stroke
1999;30:1-6.
11. Lee IM, Paffenbarger RS Jr. Physical activity and stroke incidence: the Harvard Alumni Health
Study. Stroke 1998;29:2049-2054.
12. Lindenstrom E, Boysen G, Nyboe J. Lifestyle factors and risk of cerebrovascular disease in
women. The Copenhagen City Heart Study. Stroke 1993;24:1468-1472.
13. San Jose, C, Apaga N, Florento L, Gan R. Effects of aerobic exercise and training on
coagulation, platelet aggregation, and plasma lipids. Vasc Dis Prev 2005;2:1-5.
14. Hambrecht R, Wolf A, Gielen S, et al. Effect of exercise on coronary endothelial function in
patients with coronary artery disease. N Engl J Med 2000;342:454-60.
15. Warburton, DE, Haykowsky MJ, Quinney HA, et al. Blood volume expansion and
cardiorespiratory function: effects of training modality. Med Sci Sports Exerc 2004;36:991-
1000.
16. Kobayashi N, Tsuruya Y, Iwasawa T, et al. Exercise training in patients with chronic heart failure
improves endothelial function predominantly in the trained extremities. Circ J 2003;67:505-510.
17. Tiukinhoy S, Beohar N, Hsie M. Improvement in heart rate recovery after cardiac rehabilitation.
J Cardiopulm Rehabil 2003;23:84-87.
18. Adamopoulos S, Parissis J, Kroupis C, et al. Physical training reduces peripheral markers of
inflammation in patients with chronic heart failure. Eur Heart J 2001;22:791-797.
19. Roth EJ, Harvey RL. Rehabilitation of stroke syndromes. In: Braddom RL, ed. Physical
Medicine and Rehabilitation. 2nd ed. Philadelphia, Pa: WB Saunders; 2000: 11171163.
20. Gresham GE, Duncan PW, Stason WB, et al. Post-Stroke Rehabilitation. Clinical Practice
Guideline, No. 16. Rockville, Md: US Department of Health and Human Services, Public
Health Service, Agency for Health Care Policy and Research. AHCPR publication No. 95-0662;
May 1995.
21. Monga TN, Deforge DA, Williams J, et al. Cardiovascular responses to acute exercise in patients
with cerebrovascular accidents. Arch Phys Med Rehabil 1988;69:937-940.
22. Macko RF, Smith GV, Dobrovolny CL, et al. Treadmill training improves fitness reserve in
chronic stroke patients. Arch Phys Med Rehabil. 2001; 82: 879884.
23. Gordon, N., Gulanick M, Costa F, et al. Physical activity and exercise recommendations for
stroke survivors: an American Heart Association Scientific Statement from the Council on
Clinical Cardiology, Subcommittee on Exercise, Cardiac Rehabilitation, and Prevention; the
Council on Cardiovascular Nursing; the Council on Nutrition, Physical Activity, and
Metabolism; and the Stroke Council. Circulation 2004;109:2031-2041.
24. Potempa K, Lopez M, Braun LT, et al. Physiological outcomes of aerobic exercise training in
hemiparetic stroke patients. Stroke 1995;26:101-105.

76
 25. Rimmer JH, Riley B, Creviston T, et al. Exercise training in a predominantly African-American
group of stroke survivors. Med Sci Sports Exerc 2000;32:1990-1996.
26. Fletcher BJ, Dunbar SB, Felner JM, et al. Exercise testing and training in physically disabled men
with clinical evidence of coronary artery disease. Am J Cardiol 1994;73:170-174.
27. Pearson TA, Blair SN, Daniels SR, et al. AHA guidelines for primary prevention of

Primary & Secondary

cardiovascular disease and stroke: 2002 Update. Circulation 2002;106:388-391.
28. Pollock ML, Franklin BA, Balady GJ, et al. Resistance exercise in individuals with and without

Prevention
cardiovascular disease: benefits, rationale, safety, and prescription: an advisory from the
Committee on Exercise, Rehabilitation, and Prevention, Council on Clinical Cardiology,
American Heart Association. Circulation. 2000; 101: 828833.
29. Palmer-McLean K, Harbst KB. Stroke and brain injury. In: Durstine JL, Moore GE, eds.
ACSMs Exercise Management for Persons with Chronic Diseases and Disabilities. 2nd ed.
Champaign, Ill: Human Kinetics; 2003: 238246.

XIII. OBESITY

A. Epidemiology:

Obesity is defined by a body mass index (BMI) greater than 30 kg/m2, or waist-hip-ratio (WHR)
greater than 1.0 for men and 0.85 for women. Overweight has a cut off BMI of 25 kg/m2.1

In the Philippines, the prevalence of obesity based on BMI has increased from 4.6% to 5.0%
between 1998 to 2003.1 The 2003 National Nutrition and Health Survey (NNHeS) showed that
18 out of 100 females (18.3 percent) and 3 out of 100 (3.1 percent) males are considered to be
android obese based on waist circumference (WC) equal or greater than 40 inches in males and
35 inches in females. On the other hand, 55 out of 100 (54.8 percent) females and 12 out of 100
(12.1 percent) males are obese based on waist-hip-ratio (WHR) equal or above 1.0 for males and
0.85 for females. The NNHeS was conducted by the Food and Nutrition Research Institute of
the Department of Science and Technology (FNRI-DOST) in collaboration with the
Department of Health (DOH) and 14 medical specialty societies.2

The latest National Nutrition Survey (NNS) by the Food and Nutrition Research Institute of
the Department of Science and Technology (FNRI-DOST) revealed that from 2003 to 2008,
there was an increasing trend of overweight and obesity among adults aged 20 years and over. In
1998, there were about 20 out of 100 adults who were overweight. The number increased to 24
and 27 out of 100 in 2003 and 2008, respectively.3

Gender difference has become very evident in certain clinical threshold parameters that
predispose one to become overweight or obese. According to FNRI, first degree obesity (BMI
= 25 to more than 30) affects 18.9% of women compared to 14.9% of men. The FNRI survey
further reveals that second degree obesity (BMI = 30 to more than 40) prevails among 4.3% of
women and 2.1% of men. Higher waist circumference (WC) is evident among 10.7% of women
and only 2.7% of men.

77
 Android obesity, also called "apple-shaped" obesity due to excessive accumulation of fat from
the waist up, is significantly higher and more prevalent among women (39.5%) as compared to
men (7.9%), based on the waist-hip ratio criteria used in the FNRI survey. Upper body obesity,
another term for android obesity, is positive in women with WHR equal to or more than 0.85
and 1.0 in men. Obesity is a hallmark of affluence as seen in its high prevalence rate among
Primary & Secondary

industrialized countries. This trend is starting to change with recent survey results suggesting
obesity is becoming common among children and adults in developing countries like the
Prevention

Philippines.4

The changing meal pattern of Filipinos involves increasingly patronizing convenience and fast
foods that are heavy in fat, salt, food coloring, additives, preservatives, flavoring and other
artificial ingredients that are proven to be culprits in the development of diet related illnesses.
Modern lifestyle, where machines and computers have slowly invaded homes and the
workplace, makes jobs less strenuous and physical, allowing fat build-up in the body and
promoting sedentary lifestyle.

Obesity is increasingly being recognized as a modifiable risk factor for cardiovascular disease,
particularly ischemic heart disease.5 Primary prevention studies documenting the specific
impact of obesity to stroke have varied results. In men, findings from the Physicians Health
Study have shown that an increasing BMI is associated with a steady increase in ischemic stroke,
independent of the effects of hypertension, diabetes and cholesterol.6 Among women, data are
inconsistent, with some studies showing positive results7 and others with no association.8

Several studies have suggested that abdominal obesity, rather than general obesity, is more
related to stroke risk.9,10 In the Northern Manhattan Study6, a significant and independent
association between abdominal obesity (defined by elevated WHR) and ischemic stroke was
found in all racial/ethnic groups, whereas the use of BMI did not yield any significant
association with ischemic stroke. Furthermore, persons with elevated BMI or WHR have been
shown to have increased carotid artery intima-media thickness and cross sectional intima-media
area, which are 2 preclinical predictors of atherosclerosis.11

B. Risk Modification:

B.1. Primary Stroke Prevention

Epidemiological studies indicate that increased body weight and abdominal fat are
directly associated with stroke risk. Weight reduction is recommended because it
lowers blood pressure (Class I-A) and may thereby reduce the risk of stroke. Diet and
exercise are the mainstay treatment for weight reduction.

The use of appetite suppressants such as sibutramine has raised some safety concerns
due the reports of cardiovascular complications. Sibutramine reduces the reuptake
of serotonin, norepinephrine and dopamine which are necessary to enhance satiety.
A large randomized-controlled study with 10,742 patients (SCOUT) examined
whether or not sibutramine administered within a weight management program

78
 reduces the risk for cardiovascular complications in people at high risk for heart
disease and concluded that "six-week treatment with sibutramine appears to be
efficacious, tolerable and safe in this high-risk population for whom sibutramine is
usually contraindicated for sudden death, heart failure, renal failure and
gastrointestinal problems.12 However, the FDA is reviewing preliminary data from a

Primary & Secondary

recent study suggesting that patients using sibutramine have a higher number of
cardiovascular events (heart attack, stroke, resuscitated cardiac arrest, or death) than

Prevention
patients using a placebo. The preliminary data shows that cardiovascular events were
reported in 11.4% of patients using sibutramine compared to 10% of patients using
a placebo. This difference is higher than expected, suggesting that sibutramine is
associated with an increased cardiovascular risk in the study population. The analysis
of these data is ongoing and these findings highlight the importance of avoiding the
use of sibutramine in patients with a history of coronary artery disease (heart
disease), congestive heart failure (CHF), arrhythmias, or stroke, as recommended in
the current sibutramine labeling.13 On January 21, 2010, the European Medicines
Agency recommended suspension of marketing authorizations for Sibutramine
following a six-year study which showed an increased risk of non-fatal but serious
cardiovascular events in patients with a known or high risk for cardiovascular
disease.14 At the same time, the FDA also announced that sibutramine is
contraindicated in patients with history of cardiovascular disease.15

B.2. Secondary Stroke Prevention

Although no study has demonstrated that weight reduction will reduce stroke
recurrence in patients who had suffered a previous stroke or transient ischemic
attack, losing weight, however, significantly improves blood pressure, fasting glucose
values, serum lipids and physical endurance.16 Because obesity is a contributing
factor to other risk factors associated with recurrent stroke, promoting weight loss
and maintenance of a healthy weight should be given utmost importance. Exercise
as well as diets rich in fruits and vegetables can help with weight control and have
been shown to reduce the risk of stroke, myocardial infarction and death.17,18
.
C. Recommendations:

1) Weight reduction should be considered for all overweight patients to maintain the
following goals:
i. Body Mass Index of between 18.5 to 24.9 kg /m2
ii. Waist-Hip Ratio not greater than 1.0 in men, 0.85 in women
iii. Waist circumference not greater than 35 inches in men, 31 inches in women
2) Clinicians should encourage weight management through an appropriate balance of
caloric intake, physical activity and behavioral counseling.

79
 Bibliography

1. Antonio L. Dans MD, Dante D. Morales MD, Teresa B. Abola MD, Artemio Roxas Jr, MD, Felix
Eduardo Punzalan MD, Rosa Allyn G. Sy MD, Elizabeth Paz-Pacheco MD, Lourdes Amarillo,
Maria Vanessa Villaruz for NNHes 2003 Group.National Nutrition and health Survey
(NNHeS): Atherosclerosis related diseases and risk factor. Philippine Journal of Internal
Primary & Secondary

Medicine 2005 May- June 43; 103-115.

Prevention

2. Javier, C. Waist and hip ratio can predict risk to diabetes, heart disease. FNRI website. 2007 Sept.
3. Angeles-Agdeppa, I. More Overweight Filipinos at risk for heart disease, diabetes and
hypertension. FNRI website.
4. Solanzo, FG. Survey notes more obese Filipino women than men. FNRI website
5. Grundy SM, Balady GJ, Criqui MH, Fletcher G, Greenland P, Hiratzka LF, Houston- Miller N,
Kris-Etherton P,Krumholz HM, LaRosa J, Ockene IS, Pearson TA, Reed J, Washington R,
Smith SC Jr. Primary prevention of coronary heart disease: guidance from Framingham : a
statement for healthcare professionals from the AHA Task Force on Risk Reduction. American
Heart Association. Circulation 1998; 97:1876-1887.
6. Kurth T, Gaziano JM, Berger K, Kase CS,Rexrode KM, Cook NR,Buring JE. Body mass index
and the risk of stroke in men. Arch Intern Med. 2002; 162:2557-2562.
7. Rexrode KM, Hennekens CH, Willeu WC,Colditz GA, Stampfer MJ, Rich-Edwards JW, Speizer
FE, manson JE. A prospective study of body mass index, weight change, and risk of stroke in
women. JAMA. 1997:277; 1539-1545.
8. Lindenstorm E, Boysen G, Nyboe J. Lifestyle factors and risk of cerebrovascular disease in
women: Copenhagen City Heart Study. Stroke. 1993:24; 1468-1472.
9. Suk Sh, Sacco RL, Boden-Albala B, Cheun JF, Pitman JG, Elkind MS, Paik MC for the Northern
Manhattan Stroke Study. Stroke. 2003; 34; 1586-1592.
10. Dey DK, Rothenberg E, Sundh V. BosaeusI, Steep B. Waist circumference, body mass index,
and risk for stroke in older people: a 15 year longitudinal population study of 70-year olds. J Am
Geriatr Soc. 2002:50;1510-1518.
11. De Michelle M, Panico S, Iannuzzi A, Celentano E, Ciardullo AV, Galasso R,SAcchetti L, Zarrilli
F, Bond MG, Rubba P. Association of obesity and central fat distribution with carotid artery wall
thickening in middle-aged women. Stroke. 2002; 33: 2293.
12. Torp-Pedersen, C.; Caterson, I.; Coutinho, W.; Finer, N.; Van Gaal, L.; Maggioni, A.; Sharma, A.;
Brisco, W. et al. (2007). "Cardiovascular responses to weight management and sibutramine in
high-risk subjects: an analysis from the SCOUT trial". European heart journal 28 (23):
29152923.
13. Early Communication about an Ongoing Safety Review of Meridia (sibutramine
hydrochloride), [[U.S. Food and Drug Administration], November 20, 2009
14. Press Release, European Medicines Agency, January 21, 2010
15. Hitt, E. Sibutramine now contraindicated in patients with history of cardiovascular diease.
Medscape Today. 21 Jan 2010.
16. Anderson JW, Konz Ec. Obesity and disease management: effects of weight loss on comorbid
conditions. Obes Res.2001:9 suppl 4; 326S 334S.
17. Renaud S, Lorgeril M., Delaye J, Guidollet J, Jacquard F, Mamelle N, Martin JL, MonjaudJ, Salen
P, Toubol P. Cretan Mediteranean diet for prevention of coronary heart disease. Am J Clin Nutr.
1995: 61 (suppl): 1360S 1367S.
18. Singh RB,Dubnov G, Niaz MA, Ghosh S, Singh R, Rastogi SS, Mamor O, Pella D, Berry EM.
Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk
patients ( Indo-Mediterranean Diet Heart Study : a randomized single-blind trial. Lancet.
2002:360: 1455-1461.

80
 SPECIAL SECTION ON DIET FOR STROKE

A. Epidemiology:

Primary & Secondary

Although dietary factors may be risk factors for stroke, their role is poorly defined.
Homocysteine may be associated with stroke and is associated with deficiency of dietary intake

Prevention
of folate, vitamins B6 and B12 (observed in case-control studies but not clearly in prospective
studies).1 In ecological and some prospective studies, a higher level of sodium intake is
associated with an increased risk of stroke.2-5 Higher potassium intake is also associated with
reduced stroke risk in prospective studies.6,7 However, several methodological limitations,
particularly difficulties in estimating dietary electrolyte intake, hinder risk assessment and may
lead to false-negative results in observational studies.

B. Risk Modification:

Prospective studies show that increased fruit and vegetable consumption is associated with a
dose-related decrease in stroke risk. Fruits and vegetables may contribute to stroke prevention
through antioxidant mechanisms or elevation of potassium levels.7-10 Increased sodium intake
is associated with hypertension, and reduction in salt consumption may significantly lower BP
and reduce stroke mortality. Studies on the use of omega-3 fatty acids and fish oils, although
promising, is yet to show definitive risk reduction.12-16

The 2006 AHA Guidelines recommend a well-balanced diet containing = 5 servings of fruits
and vegetables per day to reduce stroke risk. The DASH diet, which emphasizes fruit,
vegetables and low-fat dairy products and is reduced in saturated and total fat, also lowers BP
and is recommended (Class I- A).11

C. Recommendations:

1) While awaiting more definitive data, reducing intake of sodium and increasing intake
of potassium to help lower BP is recommended (Class I-A). The recommended
sodium intake is ?
2.
4 g/day (100 mmol/ day),and the recommended potassium intake
is ?
4. day (
7 g/ 120 mmol/ day).17

2) It seems prudent to limit excess saturated fat and to replace vitamins B6,B12 and
folate when such deficiencies are identified.
3) A diet rich in fruits and vegetable is advised (
Class IIb-
C).

81
 Bibliography

1. Selhub J, Jacques PF, Bostom AG, et al. Association between plasma homocysteine
concentrations and extracranial carotid-artery stenosis. NEJM 1995;332:286-291.
2. Boushey CJ, Beresford SA, Omenn GS, et al. A quantitative assessment of plasma
homocysteine as a risk factor for vascular disease: probable benefits of increasing folic acid
Primary & Secondary

intakes. JAMA 1995;247:1049-1057.

Prevention

3. Perry IJ, Beevers DG. Salt intake and stroke: a possible direct effect. J Hum Hypertens
1992;6:23-25.
4. He J, Ogden LG, Vupputuri S, Bazzano LA, Loria C, Whelton PK. Dietary sodium intake and
subsequent risk of cardiovascular disease in overweight adults. JAMA 1999;282:2027-2034.
5. Nagata C, Takatsuka N, Shimizu N, Shimizu H. Sodium intake and risk of death from stroke in
Japanese men and women. Stroke 2004;35:1543-1547.
6. Joshipura KJ, Ascherio A, Manson JE, et al. Fruit and vegetable intake in relation to risk of
ischemic stroke. JAMA 1999;282:1233-1239.
7. Khaw KT, Barrett-Connor E. Dietary potassium and stroke-associated mortality. A 12-year
prospective population study. N Engl J Med 1987;316:235-240.
8. Ascherio A, Rimm EB, Hernan MA, et al. Intake of potassium, magnesium, calcium, and fiber
and risk of stroke among US men. Circulation 1998;98:1198-1204.
9. Gillman MW, Cupples LA, Gagnon D et al. Protective effect of fruits and vegetables on
development of stroke in men. JAMA 1995;273:1113-1117.
10. Khaw KT, Barret-Connor E. Dietary potassium and stroke associated mortality: A 12-year
prospective population study. NEJM 1987;316:235-240.
11. Goldstein LB, Adams R, Alberts MJ, et al. Primary prevention of ischemic stroke: a guideline
from the American Heart Association/American Stroke Association Stroke Council. Stroke
2006;37:1583-1633.
12. Din, JN, et al. Dietary intervention with oil rich fish reduces platelet-monocyte aggregation in
man. Atherosclerosis, Vol. 197, 2008, pp. 290-96
13. Bays, HE. Safety considerations with omega-3 fatty acid therapy. American Journal of
Cardiology, Vol. 99, No. 6A, March 19, 2007, pp. 35C-43C
14. Harris, WS. Omega-3 fatty acids and bleeding Cause for concern? American Journal of
Cardiology, Vol. 99, No. 6A, March 19, 2007, pp. 44C-46C
15. Iso, Hiroyasu, et al. Intake of fish and omega-3 fatty acids and risk of stroke in women. Journal
of the American Medical Association, Vol. 285, January 17, 2001, pp. 304-12 [40 references]
16. Anderson, Craig and Sally Poppitt. A randomized, placebo-controlled intervention trial of
Omega-3 PUFA, (fish oils), in people with ischaemic stroke. Stroke 2009 Nov;40(11):3485-92
17. The Seventh Report on the Joint National Committee on Detection, Prevention, Evaluation &
Treatment of High Blood Pressure (JNC 7)

APPENDIX OF DIET MODIFICATION FOR STROKE PREVENTION

The FNRI-DOST and the Nutritionists-Dietitians Association of the Philippines (NDAP)

provide a simple diet guide that clinicians can in advising patients on dietary fat modification.
However, patients requiring intensive dietary interventions for whatever reason or condition
should be referred to a nutritionist/dietitian for individualized counseling.

82
 Simple Dietary Plan for Fat Modification (2000)
The Biomedical Nutrition Research Division, FNRI-DOST, and NDAP

Some pointers to observe in planning meals:

1. Choose freely from fruits, vegetables, cereals, root crops, bread, dried beans and nuts.

Primary & Secondary

2. Eat fish as main dish at least three times a week.

Prevention
3. May eat chicken meat as a substitute to fish at least three to four times a week.
4. For other kinds of meat, use lean parts and prepare as boiled, baked, broiled, or
roasted. Trim off any visible fat.
5. Use evaporated filled milk or skimmed milk instead of whole milk and avoid whole
milk products such as cheese, butter, cream, etc. Use margarine made with allowed
vegetable oil.
6. Use unsaturated fats and oils such as corn oil, soybean oil, peanut butter, etc.
7. Limit eggs to only three per week.
8. Avoid rich desserts such as cakes, pastries, cookies, pies, ice cream and chocolates.
9. Always read the nutrition labels of packaged/processed foods.

FOOD SELECTION GUIDE

Food
Allowed
group
In prescribed amounts: Olive, canola, corn,
Fats and
soybean, palm, sunflower and peanut oils.
oils
Coconut oil.
Eat frequently*: Fish (fresh, frozen or
canned in water, tomato or vinegar);
chicken breast without skin or fat. Dried
beans, lentils, fresh or frozen sweetpeas;
Meat, fish, vege-meat, tokwa, taho, tofu & other
poultry, bean products;
eggs, milk,
Eat occasionally**: Very lean, well-trimmed
dry beans
cuts of beef, pork, veal, lamb; crabmeat,
shrimp without head; whole eggs up to 3
pieces per week, eggwhite as desired, may
be cooked in allowed fat; Skimmed milk
or low fat milk or cheese
Restricted/avoided
Fats and oils from animal
foods, butter. Hydrogenated
vegetable oils (e.g.,
margarine, lard, shortening,
spread)
Meat and chicken fat
drippings used for sauces,
bacon fat, chicharon
Fish roe, crabfat aligui
shrimp head, oyster, clams
Fatty meats: cold cuts,
canned or frozen meats,
sausages; fatty poultry with
skin; internal organs (liver,
kidney, heart, tripe,
sweetbreads)
Whole milk/cows milk and
cheese made from whole
milk

83
 Food
Allowed Restricted/avoided
group
Primary & Secondary

Vegetable All vegetables prepared without fat or with Buttered, creamed, fried
allowed fats only. vegetables in restricted fats or
Prevention

Eat frequently*: Green leafy and y ellow cooked with fatty meat and
vegetables (they are good sources of beta- sauces
carotene, vitamin C, calcium, iron and
dietary fiber among others)

Fruit All fruits; adjust fat allowance when using Avocado in mo deration (due to
avocado. its high fat content)
Eat frequently*: Vitamin C-rich fruits and
deep c olored fruits

Croissants, muffins,

crackers, biscuits, waffles,
Rice, corn, All cereals, roots/tubers, certain pancakes, doughnut, rolls
rootcrops, noodles/pasta, wheat bread, pan de sal made with w hole egg, butter,
noodles, except those restricted margarine or fat of unknown
bread and Eat frequently*: Oatmeal, cold cereals, corn composition
cereals and sweet po tato Fresh mami or miki noodles

Potato chips, french fries,

popcorn

Rich dessert especially those

Fat-free/low-fat/light dessert. Fresh o r
Desserts canne d fruits in light syrup only. Plain cakes
with no icing (angel or sponge cakes),
meringue, yogurt, sherbet
Fat-free broths made from meat or c hicken
Soups stock. Soups prepared with skimmed/low-
fat milk.
Coffee (not more than 3 cups black),
decaffeinated coffee, tea, carbonated
beverages in moderation.
Beverage
Alcoholic drinks: no t more than 1 jigger
for women and not more than 2 jiggers
for men
made with cream, butter, solid
shortening, lard, whole egg,
chocolate cookies and pies
made from cream fudge, ice
cream; pastillas from whole
milk, yema
Cream soups, fatty broth or
stock
Soda fountain beverages such
as milk shake, malted milk and
chocolate drinks
Alcoholic drinks in moderation

84
 Food group All owed Restricted/avoide d

Nuts (peanuts, waln ut, almo nd,

cashew, pili, etc.) preferably bo iled,
Sauces and gravies with

roasted/baked, consume in
restric ted fats or milk;
moderation .

Primary & Secondary

regular mayonnaise
Non-dairy cream in moderation

Miscellaneous Butter-dipped foods

Prevention
Sp ices and seaso nin gs in

Packed dinners or instant

moderation . Sauce made with
foods of unkn own fat
allowed fats and skimmed milk,
content
vinegar, pickle s, m ustard, catsup,
banana sauce.

*Eat frequently at least 4 to 5 times a week; **Eat occasionally at most, once a month

FOOD EXCHANGE LIST

I. VEGETABLES
A. Leafy vegetables - 1 serving = 1 cup raw or cup cooked
= 16 calories, 3 gm carbohydrate
B. Non-leafy vegetables - 1 serving = cup raw or cup cooked
= 16, calories, 3 gm carbohydrate
1. Fresh
2. Processed
Me asur em en t
G reen peas 1 ta bles po on
Bab y corn 2 p cs (8 cm lon g x 5 cm)
Mu shro om 1/ 3 cu p
To mat o juice cu p u nd iluted
II. FRUITS
1 serving = 40 calories, 10 gm carbohydrate

F ru it M easu rem en t
G u ava 2 pcs ( 4 cm d iameter )
M ang o g reen 1 slice (1 1 x 6 cm )
M ang o r ipe 1 slice ( 1 2 x 7 cm )
Pap aya rip e 1 slice (1 0 x5 x2 cm )
A p ple o f 8 cm diam eter
Ban ana 1 pc ( 9 x 3 cm )
G r apes 1 0 p cs (2 cm di am eter each)
Pin eapp le 1 slice (1 0 x 6 x 2 cm)

85
 III. MILK
M easurement Calories
Whole milk, fresh 1 cup 170 calories
Whole Milk, powdered 4 level tablespoons 170 calories
Primary & Secondary

Low fat Milk, Powdered 4 level tablespoons 125 calories

Skimmed (Non-Fat)
Prevention

Liquid 2/3 cup 80 cal ories

Powdered 4 level tablespoon 80 cal ories

IV. RICE
1 serving = 23 gm carbohydrate, 2 gm protein, 100 calories
Measurement
Rice cup
Lugaw 1 cup

Pan ameri cano 2 slices (9x8x1cm)

Pandesal 2 pieces (7x4 cm)

Wheat Bread 2 pcs (11 x 8 x 1 cm )

Noodles 1 cup

Potato 2 pcs (1/2 of 7 cm l ong x 4 cm diameter )

Oatmeal 1 cup, thick consistency

V. MEAT
A. Lean Meat = 1 serving = 41 calories, 8 gm protein, 1 gm fat

Measurement
Le an Meat ,beef 1 slice, matchbox size (5 x 3 x 1 cm)

Le an Meat, pork 1 slice, matchbox size (6 x 3 x 1 cm )

Fish 1 slice, (18 x 4 cm)

Chicken 1 small leg (13.5 c m X2 cm )

breast ( 6 c m long)
Shrimps 5 pcs ( 12 c m eac h )
Praw ns 2 pcs ( 13 c m )
Daing 1 pc medium
Squid 3 pcs ( 7 x 3 cm )
Mo nggo cup

86
 B. Medium Fat Meat = 86 calories, 8 gm protein, 6 gm fat

Measurement
Fish 1 slice

Primary & Secondary

Tofu cup

Prevention
Corned beef 3 tablespoon

Sardines, canned 1 pc ( 10 x 4 cm)

Chicken egg 1 pc

Beef (flank, brisket) 1 slice matchbox

Pork, pata 1 slice (4 cm diameter x 2 cm thick )

C. High Fat Meat = 122 calories, 8 gm protein, 10 gm fat

M easur em ent
P ork,tende rloin ,ste ak 1 pi ece ( 3 cm cube)
Bal ut 1 pi ece
H am burge r 1 pa tty
V ienn a Sausage 4 ( 5 x 2 x 2 cm )
C heese, filled 1 sli ce (6 x 3 x 2 1/3 cm )
H otdog 2 pc s (10x 4 cm )
L ong gani sa 1 pc ( 12x 2 cm )

VI. FAT
1 serving = 45 calories, 5 gm fat

M easurement
Ba con 1 strip ( 10 x 3 cm)
Butter , mar garine 1 tablesp oon
M ayonnaise 1 tablesp oon
Sitsaron 2 pc s ( 5 x 3 cm)
Oil , olive oil
( corn, soybean, can ola,sesame ) 1 teaspoon

Reference: St. Lukes Medical Center Food Exchange List for Meal Planning (Adapted from
FNRI-DOST Food Exchange List)

87
 Reviewed and Approved by the Philippine Society
of Parenteral and Enteral Nutrition (PHILSPEN)
Primary & Secondary
Prevention

Dr. Jesus Fernando B. Inciong

President

Dr. Luisito O. Llido

Immediate Past President

Dr. Maria Victoria G. Manuel

Board Member

Dr. Maria Divina Cristy Redondo

Assistant Secretary

Dr. Francoise Prairie

Nutrition Support Chief Fellow, SLMC

88
Acute Stroke
Treatment
 I. SSP CLASSIFICATION OF ACUTE STROKE BASED ON CLINICAL SEVERITY

Background and Rationale for Simplified Initial Classification of Acute Stroke Based
on CLINICAL Severity

There are various ways to classify stroke such as based on stroke type, localization, brain and
vascular territory involvement, patho-mechanism and time course. However utilization of
some of the standardized classification schemes may be difficult & time-consuming especially
for non-neuroscience specialists in an acute stroke setting.

The working committee of the first edition (1999) of the SSP Stroke Handbook has developed a
practical & locally relevant initial classification scheme which is based simply on observed
severity of patients neurological deficits, including level of sensorium and response to pain.
The present 2010 working committee still finds this format useful particularly in the acute
setting, reliable for both medical and paramedical personnel and advocates its continued use to
Acute Stroke

help direct crucial actions and decisions at the emergency room.

Treatment

After initial stabilization & management, additional work-ups are recommended for
determination and further classification of patients based on underlying stroke patho-
mechanism which is necessary for selection of appropriate secondary prevention strategies.

DEFINITION OF STROKE SEVERITY

MILD STROKE MODERATE STROKE SEVERE STROKE

Alert patients with any or a
combination of the following:
1. Mild pure motor weakness of
one side of the body, defined as:
can raise arm above shoulder, has
clumsy hand, or can ambulate
without assistance
2. Pure sensory deficit
Awake patient with significant
motor and/or sensory and/or
language and/or visual deficit
or
Disoriented, drowsy or light
stupor with purposeful
response to painful stimuli
Deep Stupor or comatose patient
with non-purposeful response,
decorticate, or decerebrate
posturing to painful stimuli
or
Comatose patient with no
response to painful stimuli

3. Slurred but intelligible speech

4. Vertigo with incoordination

(e.g., gait disturbance, unsteadiness
or clumsy hand)

5. Visual field defects alone

OR OR OR

NIHSS score = 0 5 NIHSS score = 6 21 NIHSS score > 22

See Guidelines for TIA See Guidelines for See Guidelines for Severe
and Mild Stroke Moderate Stroke Stroke

90
 II. GUIDELINES FOR TIA

(For detailed discussions on TIA, please see Chapter IV)

Ascertain clinical diagnosis of TIA (history and physical exam are very important)
Management Exclude common stroke mimickers
Priorities Provide basic emergent supportive care (ABCs of resuscitation)
Monitor neuro-vital signs, BP, MAP, RR, temperature, pupils
Perform stroke scales (NIHSS, GCS)
Perform risk stratification using the ABCD2 Scale
Monitor and manage BP; treat if MAP>130
Precautions:
Avoid precipitous drop in BP (not > 15% of baseline MAP). Do not use
rapid-acting sublingual agents; when needed, use easily titratable IV or short
acting oral antihypertensive medication.

Acute Stroke
Ensure appropriate hydration. Recommended IVF-0.9% NaCl if needed

Treatment

Emergent Complete blood count (CBC) Cranial MRI-DWI as soon as

Diagnostics Blood sugar (CBG or RBS) possible is preferred. May do Non-
Electrocardiogram (ECG) contrast Cranial CT scan if MRI is
PT/PTT not possible

Non cardioembolic Cardioembolic

Early Consider careful anticoagulation with IV heparin or
Aspirin 160-325 mg/day. Start
Specific as early as possible and SQ low molecular-weight heparin (LMWH) for
those at high risk for early recurrence (e.g. AF with
Treatment continue for 14 days.
thrombus, valvular heart disease or MI)
or
For secondary prevention, see
Aspirin 160-325 mg/day (if anticoagulation is not
under Delayed Management
possible or contraindicated)
and Treatment
Neuroprotection
Neuroprotection
If infective endocarditis is suspected, give antibiotics
and do not anticoagulate.

Admit to Hospital
Urgent Outpatient Work-up
(Stroke Unit)
Place of 1. TIA within 48 hours
Treatment 2. Crescendo TIAs (multiple & TIA > 2 weeks (but work-ups should
increasing symptoms) be done within 24 48hours)
3. TIA with known high risk cardiac
source of embolism, known
hypercoagulable state or symptomatic
ICA stenosis
4. Patient with ABCD2 score of > 3

91
 Non -cardioemb olic
(T hrom botic / Cardioemb olic O thers
L acu nar)

Delayed
Management Antiplatelets (aspirin,
clop idogrel, cilostazol,
and triflusal, dipyridam ole,
Specialized coagulation
Secondary tests such as screening for
extended-re lease Echocardiograp hy
Prevention dipyridamole + asp irin and/or cardiolo gy hyperc oagulab le states
(protein C, protein S,
combination consult
antithromb in III,
fibrinogen, hom ocystein e)
Control of risk factors If age < 75 and
and drug screening (e.g.,
PT /INR available,
metamphetamine, cocaine)
Recom mend vascular anticoagulation with
Acute Stroke

can be co nsidered for

studies such as carotid warfarin
Treatment

young patients with T IA

ultraso un d to docum ent
extracranial sten osis. If
this reve als >70%
stenosis, refer to
neurologist
/neurosurgeon/vascular
surgeon for decision-
making regarding CEA or
stenting
To document intracranial
stenosis, recom mend
eith er TCD or MRA or
CTA
(target INR: 2-3)
especially when no
vascular risk factors exist
If age > 75, warfarin
and no unde rlying cause is
(target INR: 2.0
identified
[1.6 2.5])
If vasculitis is suspected,
If antico agulation is
may do ESR, AN A, Lupus
contraindicated, give
antico agulan t te sting
antiplatelets (A SA
160mg325 mg)
Transesoph ageal
echoc ardiography (T EE)
to rule o ut PFO

GUIDELINES FOR MILD STROKE

Ascertain clinical diagnosis of stroke (history and physical exam are very important)
Management Exclude common stroke mimickers
Priorities Provide basic emergent supportive care (ABCs of resuscitation)
Monitor neuro-vital signs, BP, MAP, RR, temperature, pupils, O2 saturation
Perform and monitor stroke scales (NIHSS, GCS)
Provide O2 support to maintain O2 saturation > 95%
Monitor and manage BP; treat if MAP>130
Precautions:
Avoid precipitous drop in BP (not > 15% of baseline MAP). Do not use rapid-
acting sublingual agents; when needed, use easily titratable IV or oral
antihypertensive medication.
Ensure adequate hydration. Recommended IVF- 0.9% NaCl

92
 Emergent Complete blood count (CBC) Non-contrast CT scan of the brain or
Blood sugar (CBG or RBS) MRI-DWI as soon as possible
Diagnostics
Electrocardiogram (ECG) If ICH, compute for hematoma
PT/PTT volume

Ischemic Hemorrhagic
Early Specific Non-cardioembolic Cardioembolic
Treatment (Thrombotic, Lacunar)
Aspirin 160-325 Early neurology and/ or
Consider careful
mg/day start as early neurosurgeon consult
anticoagulation with IV
as possible and for all ICH is
continue for 14 days heparin or SQ low recommended
molecular-weight
CT-scan heparin (LMWH) for
For secondary Monitor and maintain
confirmed those high risk with

Acute Stroke
prevention, see under BP: Target MAP of 110

Treatment
early recurrence (e.g. AF
Delayed Management or SBP of 160
with thrombus, valvular
and Treatment
heart disease or MI)
Neuroprotection
Neuroprotection or
Early rehabilitation once
Aspirin 160-325 mg/day
Early rehabilitation (if anticoagulation is not stable within 72 hours
once stable within 72
possible or
hours contraindicated) Give anticonvulsants for
clinical seizures and
proven subclinical or
electrographic seizures.
Prophylactic AEDs are
generally not
recommended
Neuroprotection
Steroids are not
(Appendix V-D)
recommended
Early rehabilitation once Monitor and correct
stable within 72 hours
metabolic parameters
If infective endocarditis
Correct coagulation /
is suspected, give
bleeding abnormalities
antibiotics and do not
anticoagulate
Follow recommendations
for neurosurgical
intervention

For aneurysmal SAH,

refer to specific chapter
Place of
Admit to Hospital: Acute Stroke Unit / Regular Room
Treatment

93
 Is che mic Hemorrhagic
Delayed Non-cardi oembolic
Management (Thrombot ic, Lacu nar) Cardioe mbolic
and
Treatment Antiplatelets (aspirin,
(Secondary clopidogrel, cilostazol,
Prevention) triflus al, dipyridam ole, Echocardiography L ong-term strict BP
extended-release
and/or cardiology control and m onitoring
dipyridam ole + aspirin
consult
combination
Cons ider contrast CT
If age <7 5 and scan, 4 vess el cerebral
Control of risk factors
PT/IN R available, angiogram , MRA or
anticoagulation w ith CTA if patient is:
Acute Stroke

Recom mend vascular

Treatment

warfarin
studies such as carotid
(target IN R: 2-3) 1) < 45 years old,
ultras ound to docum ent
extracranial stenosis. If this 2) norm otensiv e
If age >7 5, warfarin 3) has lobar ICH
rev eals >70 % stenos is,
(target INR: 2 .0 4) uncertain cause of
refer to neurologist
[1.6 2.5 ]) ICH
/neurosurgeon/ vascular
5) suspected to hav e
surgeon for decision-
If anticoagulation is aneurysm , AV
m aking regarding CEA or
contraindicated, give malform ation or
stenting
antiplatelets (A SA vas culitis
160325 mg)
To document intracranial
stenosis, recom mend either
TCD or MRA or CTA

III. GUIDELINES FOR MODERATE STROKE

Management Ascertain c linical diagnosis of stroke (history and physical exam are very important)
Priorities Exclude commo n stroke mimicke rs
Basic eme rge nt supportive care (ABCs of resuscitation)
Neuro-vital signs, B P, MAP, RR, temp erature , pupils, oxygen saturation
Perform and monitor stroke sc ales (NIHSS, GCS)
Monitor and manage BP. Treat if MAP>130
Provide O 2 support to ma intain O 2 saturatio n > 95%
Precaution: Avoid precipitous drop in BP (not >15 % of baseline MAP). Do
not use rapid-ac ting sublingual agents; when nee ded use easily titratable IV or
oral antihy pertensive med ication.
Identify c omorbidities (cardiac disease, d iabetes, liver disease, gastric ulce r, etc.)
Recognize and treat early signs and symptoms of increased ICP
Ensure adequate hydratio n. Re comme nded IVF- 0.9% NaCl

94
 CBC with platelet count
Emergent CBG or RBS
Diagnostics PT/PTT
Serum Na+ and K +
Ischemic
Early Specific
Treatment Non-cardioembolic
(Thrombotic, Lacunar)
If within 3 hours of stroke
onset, consider IV
CT-scan recombinant tissue
confirmed
plasminogen activator (rt-PA)
and refer to neuro specialist
Selected patients within 3 - 4.5
hour time window may benefit
with IV recombinant tissue
plasminogen activator (see
section on thrombolytic
therapy)
Refer to neurologist for
evaluation & decision.
If within 6 hours of stroke
onset and in specialized
centers, consider intra-arterial
(IA) thrombolysis
Start ASA 160325mg 24 hours
after rtPA treatment.
If rtPA ineligible, start Aspirin
160-325 mg/day as soon as
possible
Neuroprotection
Early supportive rehabilitation
Consider early decompressive
Hemicraniectomy for large
malignant MCA infarction
Place of Hospital Intensive Care Unit or Stroke Unit
Treatment
ECG
Non-contrast CT scan of brain or
MRI-DWI as soon as possible.
If ICH, compute for hematoma volume
Hemorrhagic
Cardioembolic
Early neurology and/or
If within 3 hours of neurosurgical consult
stroke onset, consider for all ICH is
IV rt-PA and refer to recommended
neuro specialist
Acute Stroke
Monitor and maintain
Treatment
If within 6 hours of BP. Target
stroke onset and in MAP=110mmHg or
specialized centers, SBP=160mmHg
consider IA
thrombolysis Neuroprotection
If rt-PA ineligible or 24 Give anticonvulsants for
hours after rt-PA clinical seizures and
treatment, consider proven subclinical or
either careful electrographic seizures.
anticoagulation with Prophylactic AEDs are
generally not
recommended
IV heparin or SQ Steroids are not
LMWH for those at high recommended
risk for early recurrence
or ASA 160325 Monitor and correct
mg/day. metabolic parameters
Neuroprotection Correct coagulation/
bleeding abnormalities
Early supportive
rehabilitation Follow recommendations
for neurosurgical
If infective endocarditis intervention
is suspected, give
antibiotics and do not Early rehabilitation once
anticoagulate stable
For aneurysmal SAH,
refer to specific chapter
95
 Isc he m ic
Delayed No n-car di oem b o lic
Management
(Th rom b otic, La cun ar )
and
Treatment Anti platele ts (a spi rin,
(Secondary clopidog rel , c ilostazol ,
tr ifl usal, dip yrida mol e,
Prevention) extende d-rel ease
dipyri dam ole + aspi rin
comb ination
Control of ri sk f actors
Recom m end vascular
Acute Stroke
Hem or rh ag ic
Car di oem b o lic
L ong- te rm stri ct BP
contr ol and m oni to ring
E chocard iogr aphy
and/or card iolog y C onsi der contrast C T
consul t sc an, 4 ve ssel cere bral
angi ogr am, MR A or CTA
If ag e <7 5 and if patient is:
PT/IN R a vai lable,
anticoag ulation w ith 1) < 45 year s old,
war fari n 2) nor m ote nsi ve
(targ et IN R: 2-3) 3) has lobar IC H
4) unce rtain cause of ICH

studies such as caroti d If ag e >7 5, w arf arin 5) suspe cted to have

Treatment

ultr asound to doc umen t (ta rge t IN R: 2.0 aneury sm , AV

ex tracr anial stenosis. If
this r eveals > 70%
stenosis, r efer to
neur ologi st
/neur osur geon/ vasc ul ar
surge on f or d ecision-
m aking reg ardi ng CE A
or stenting
[1.6 2.5 ]) ma lform atio n or
va scul itis
If anti coagul ation is
contrai ndicated, g ive
antiplate lets (A SA
160325 m g)

To doc um ent intra crani al

stenosis, r ecom m end
ei ther TCD or M RA or
CT A

IV. GUIDELINES FOR SEVERE STROKE

Management Ascertain clinical diagnosis of stroke (history and physical exam are very important)
Exclud e common stroke mimickers
Priorities Basic emergent supportive care (ABCs of resuscitation)
Neuro-vital signs, BP, MAP, RR, temperature, pupils, oxygen saturation
Perform and monitor stroke scales (NIHSS, GCS)
Monitor and manage BP. Treat if MAP>130
Provide O2 support to maintain O2 saturation > 95%
Precaution: Avoid precipitous drop in BP (not >15 % of baseline MAP). Do not use
rapid-acting sublingual agents; when needed use easily titratable IV or oral
antihypertensive medication.
Id entify comorbidities (cardiac disease, diabetes, liver disease, gastric ulcer, etc.)
Recognize and treat early signs and symptoms of increased ICP
Ensure adequate hydration. Recommended IVF- 0.9% NaCl

CBC with platelet count ECG

Emergent
CBG or RBS Non-contrast CT scan of brain or MRI-DWI
Diagnostics as soon as possible.
PT/PTT
Serum Na+ and K+ If ICH, compute for hematoma volume

96
 Is che mic
No n-car di oem b o lic
Early
(T hrombot ic , Lacu nar)
Specific
Treatment
May give a sp irin 160-325
m g/d ay
Refer to n eu ro specia list
CT-scan
cases of po sterior
confirmed
circula tion strokes
with in 12 h ours o f on set
for ev aluat io n a nd
Hem or rh ag ic
Car di oem b o lic Su p po rt ive treatmen t:
1. Man n it ol 2 0%
Ma y give as pirin 0 .5-1g/kgB W
160-325 mg/ da y q 4-6 h ou rs for
3 -7 da ys
Refer to neuro
specialist cases o f 2. N eu ro p ro tect io n
po sterio r
circulat io n stro kes 3. G ive
a nt icon vu lsa nts
within 1 2 h o urs o f
on set fo r fo r clinical
eva lu atio n an d seizu res an d

Acute Stroke
d ecisio n rega rd in g
de cisio n regarding p rov en su b clin ical

Treatment
th rom bo lytic t hera py.
th ro mb o lytic o r electrograp h ic
th erap y. seizu res.
Neurop rot ectio n
P ro p hyla ctic
N eu ro pro tectio n A ED s a re
generally no t
recomm end ed

N eu ro surgery cons ult

if:
1. Pa tient no t
If cerebella r infarct ,
If cerebellar in fa rct,
con sult
con sult n eu ro surgeon as
neuro surgeon a s
so o n as p ossible
soo n a s po ssib le
Early sup p ortive
Ea rly su pp o rt ive
reha bilitat io n
reh ab ilit ation
h ern ia ted; L ob ar
b leed o r locat ed in
p ut am en,
p allid um,
cerebellum ;
Fa mily is willin g to
a ccept
co nsequ ences of
irreversible co ma
o r p ersistent
v egetat ive stat e
Go al is redu ct io n o f
m o rt ality

2. ICP m on ito rin g is

con tem p la ted an d
salvage surgery is
con sid ered

Ea rly su p po rt ive
reha bilitat io n
Place of Intensive Care Unit
Treatment

97
 D i s c u s s p ro g n o s is w it h re la t iv e s o f t h e p at ie n t in a m o s t
c o m p as s i o n at e m a n n e r
Isch em ic He mo rr ha gic
Delayed
Management Non -card io em bo lic
and (T hrombotic, Card io em b oli c
Lacu nar)
Treatment Long-term strict BP
Echocardiography
(Secondary control and
and/or cardiolog y
Prevention) con sult monitorin g

Antiplatelets (As pirin, If age <75 and Co nsider contrast C T

clopidogre l, PT/I NR available, s can, 4 vessel
cilostazol, triflusal, anticoagulation cereb ral ang io gram,
M R A or C TA if
Acute Stroke

dipyridamole, with warfarin

Treatment

ex tended-release (target I NR: 2-3) p atient is:

dipyridamole +
asp irin com bin ation
C ontrol o f vascular
risk factors
If age >75, warfarin
(targ et IN R: 2.0
[ 1.6 2.5] )
If anticoag ulation is
con traindicated,
g ive antip latelets
(ASA 160325 mg)
1) <45 years o ld,
2) normo tensive
3) has lobar IC H
4) uncertain cause of
I CH
5) susp ected to have
aneurys m, AV
m alform ation or
vasculitis

V. EARLY SPECIFIC TREATMENT FOR ISCHEMIC STROKE

A. ANTITHROMBOTIC THERAPY IN ACUTE STROKE
Drug Trial Design
International Stroke 19,435 patients with acute
Trial (IST, Lancet 1997; ischemic stroke were
349: 1569 1581) randomized within 48 hrs to
Aspirin 300 mg day,
subcutaneous heparin 5000
units BID or 12,500 units
BID, Aspirin plus heparin or
neither
Aspirin
Result
Aspirin treated patients had slightly
fewer deaths at 14 days, significantly
fewer recurrent ischemic strokes at
14 days and no excess of
hemorrhagic strokes.
For patients receiving heparin, there
were fewer deaths or recurrent

strokes ; however there were more

hemorrhagic strokes & serious
extracranial hemorrhage, mostly in
the higher dose heparin group,
resulting in no net benefit.

Chinese Acute Stroke 21,106 patients with acute Aspirin significantly reduced the risk
Trial (CAST, Lancet ischemic stroke within 48 of recurrent stroke or vascular death.
1997; 449: 1641 1649) hours were randomized to
Aspirin 160 mg OD or
placebo for up to 4 weeks

98
 Drug Trial Design Result
The trial was prematurely
terminated because of failure to
recruit patients at the pre-specified
392 patients with TIA or
recruitment rate because of increased
Fast Assessment of minor stroke within 24
Clopidogrel-ASA vs Aspirin

use of statins
Stroke and Transient hours were randomized to
Ischemic Attack to Clopidogrel (300 mg
Recurrent stroke at 90 days
Prevent Early loading dose then 75 mg
were : Clopidogrel-ASA
Recurrence, /day plus Aspirin 81 mg or
(7.1%), Aspirin alone (10.1%),
(FASTER, Lancet Aspirin 75 mg alone, with
absolute risk reduction of 3.8%
Neurology 2007; 6: 961- or without Simvastatin (in
p =0.19
969) factorial design) and
followed up for 90 days
Hemorrhagic events were

Acute Stroke
higher with the combination

Treatment
treatment
Meta-analysis of Ten trials involving The use of LMWH/heparinoids
randomized controlled 2885 patients with acute was associated with significant
LMWH

trials on low molecular ischemic stroke reduction in venous

weight heparins and thromboembolism (DVT and PE).
heparins in acute Low molecular weight However, it had no significant effect
ischemic stroke heparin or heparinoids on reducing death and disability at 6
(Stroke 2000; 31: 31: given within 7 days of months
1770-1778) stroke

B. NEUROPROTECTION AND NEUROPROTECTANT DRUGS

A. NEUROPROTECTIVE INTERVENTIONS:

The 5 H Principle
AVOID hypotension, hypoxemia, hyperglycemia or hypoglycemia and hyperthermia
(fever) during acute stroke in an effort to "salvage" the ischemic penumbra.

Avoid Hypotension and allow Permissive Hypertension during the 1st 7 days
Aggressive BP lowering is detrimental in acute stroke. Manage hypertension as
per recommendation.

Avoid Hypoxemia
Routine oxygenation in all stroke patients is not warranted
Maintain adequate tissue oxygenation (target O2 saturation >95%)
Do arterial blood gases (ABG) determination or monitor oxygenation via pulse
oximeter
Give supplemental oxygen if there is evidence of hypoxemia or desaturation
Provide ventilatory support if upper airway is threatened or sensorium is
impaired or ICP is increased.

99
 Avoid Hypoglycemia or Hyperglycemia
Background: Hyperglycemia can increase the severity of ischemic injury (causes lactic
acidosis, increases production of free radicals, worsens cerebral edema and weakens
blood vessels), whereas hypoglycemia can mimic a stroke.
Prompt determination of blood glucose should be done in all stroke patients
Ensure glycemic control at 110-180 mg/dL preferably within the first 6 hours
and maintain up to 3-5 days. May start intervention with insulin if
CBG>180mg/dL
Avoid glucose-containing (D5) IV fluids. Use isotonic saline (0.9% NaCl)

Avoid Hyperthermia
Backgound: Fever in acute stroke is associated with poor outcome possibly related to
increased metabolic demand, increased free radical production and enhanced
Acute Stroke

neurotransmitter release.
Treatment

Hyperthermia increases the relative risk of 1 year mortality by 3.4 times.

For every 1 C increase in body temperature, the relative risk of death or
disability increases by 2.2
Hypothermia can reduce infarct size by 44% in animal studies.
Search for the source of fever
Treat fever with antipyretics and cooling blankets
Maintain normothermia

B. NEUROPROTECTANT DRUGS:

Neuroprotectants are drugs with multi-modal action:

Protect against excitotoxins and help prolong neuronal survival
Block the release of glutamate and inflammatory cytokines, inhibit the
formation of free radicals and apoptosis

Over 50 neuroprotective agents such as glutamate, NMDA/AMPA antagonists, calcium

channel blockers, free radical scavengers have undergone phase III clinical trials but most have
failed. Several reasons have been raised to explain the apparent disappointments: animal
models were wrong, human trials were not done optimally (e.g., determination of time window,
patient heterogeneity, targeted neuroprotection which addresses single mechanism of
neuronal injury at a time, exclusion of concomitant treatment with thrombolytic agents).

Among the various pharmacologic agents investigated, CDP-choline (Citicoline) has shown
great promise as evidenced by numerous experimental studies showing consistent improved
functional outcome and reduced infarct size in animal models of stroke. Several trials in
ischemic and hemorrhagic strokes conducted worldwide have documented its excellent safety
profile. In individual patient data pooling analysis (4 trials, 1652 patients) oral citicoline given
within the first 24 hours of moderate to severe ischemic stroke significantly increased the
probability of global recovery by 30% at 3 months. Similar positive result in reduction in death
and disability from acute ischemic stroke was obtained in the latest meta-analysis in 2008.

100
CDPcholine has multimodal effects on the ischemic and reperfusion cascade. It helps increase
phosphatidylcholine synthesis for membrane stabilization and repair. It inhibits the activation
of phospholipase A2 and reduces oxygen free radicals and inflammatory cytokines within the
injured brain during ischemia.

A randomized double-blind placebo controlled trial on safety and efficacy of Citicoline 1 gm

twice a day in acute ischemic stroke within 24 hours for 6 weeks known as International
Citicoline Trial on Acute Stroke or ICTUS is currently underway to confirm results of the
pooled data analysis and metaanalysis.

The use of neuroprotectants in acute stroke remains a matter of preference by the

attending physician. The choice of Citicoline is a reasonable option.

Acute Stroke
Treatment
Two other pharmacologic agents with putative neuroprotective properties are currently
undergoing or recently completed phase III clinical trials.
An international, multicenter double blinded, placebo controlled randomized controlled trial
on Neuroaid known as Chinese Medicine Efficacy in Stroke Recovery or CHIMES) among
patients with acute ischemic stroke within 72 hours is currently ongoing in several countries in
Asia including Singapore, Philippines, Thailand, Korea, Sri Lanka.
A double-blind placebo controlled randomized clinical trial to evaluate the safety and efficacy of
Cerebrolysin in patients with Acute Ischemic Stroke in Asia in ASIA (CASTA) was recently
completed with results due this year.

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27 suppl 1: 148 155.
Acute Stroke

20. Secades J. and Lorenzo J. Citicoline: Pharmacological and clinical review 2006 update: Methods and
Treatment

findings in experimental and clinical pharmacology 2006: 26 (suppl B): 1 56.

21. Venketasubramanian N, CL Chen, R. Gan, et al. on behalf of the CHIMES Investigators, A double-
blind, placebo-controlled, randomized, multicenter study to investigate CHInese Medicine Neuroaid
Efficacy on Stroke recovery (CHIMES Study). International Journal of Stroke 2009; 4: 54-60

C. ANTICOAGULATION IN ACUTE CARDIOEMBOLIC STROKE

A. Cardioembolic Sources

High Risk Low or Uncertain Risk

AF (valvular or non-valvular) Mitral valve Prolapse
Rheumatic mitral stenosis Mitral annul ar calcification
Prosthetic heart valves Patent foramen ovale (PFO)
Recent MI Atrial septal aneurysm
LV/L A thrombus Cal cific aortic stenosis
Atrial myxoma Mitral valve strands
Infective Endocarditis
Di lated cardiomyopathy
Marantic endocarditis

B. Indications and Contraindications for Anticoagulation in Patients with

Cardioembolic Stroke
Probably Indicated Contraindicated
Intracardiac thrombus Bleeding diathesis
Mechanical prosthetic valve Non-petechial intracranial hemorrhage
Recent MI Recent major surgery or trauma
CHF Infective endocarditis
Bridging measure for long term
anticoagulation

102
C. When considering anticoagulation in acute cardioembolic stroke, the benefits of
anticoagulation in reducing early stroke recurrence should be weighed against the risk
of hemorrhagic transformation. The latter is higher in patients with large infarction,
severe strokes or neurological deficits and uncontrolled hypertension.

D. How to Anticoagulate

1. Requirements for IV anticoagulation of patients with cardiogenic source of

embolism:
a. Heparin sodium in D5W
b. Infusion pump, if available
c. Activated partial thromboplastin time (aPTT) or clotting time

Acute Stroke
Treatment
2. Procedure:
a. Start intravenous infusion at 800 units heparin/hour ideally using infusion
pump. IV heparin bolus is not recommended.
b. Perform aPTT as often as necessary, every 6 hours if needed, to keep aPTT at
1.5-2.5x the control. Risk for major hemorrhage, including intracranial bleed,
progressively increases as aPTT exceeds 80 seconds.
c. Infusion may be discontinued once oral anticoagulation with warfarin has
reached therapeutic levels or once antiplatelet medication is started for
secondary prevention.

To date, there has been no trial directly comparing the efficacy of unfractionated heparin vs
LMWH in patients with acute cardioembolic stroke. LMWH has the advantage of ease of
administration and does not require aPTT monitoring.

Bibliography

1. Adams H. Emergent use of anticoagulation for treatment of patients with ischemic stroke.
Stroke 2002;33:856-861.
2. Hart R, Palacio S, Pearce L. Atrial fibrillation, stroke and acute antithrombotic therapy. Stroke
2002;33:2722- 2727.
3. Moonis, M, Fisher M. Considering the role of heparin and low-molecular weight heparin in
acute ischemic stroke. Stroke 2002;33:1927-1933.
4. Paciaroni M, Agnelli G, Micheli S. et al. Efficacy and safety of anticoagulant treatment in acute
cardioembolic stroke: A meta-analysis of randomized controlled trials. Stroke 2007; 38:
423430.

103
 D. ADMINISTRATION of rt-PA to ACUTE ISCHEMIC STROKE PATIENTS
Randomized Trials on Intravenous rt-PA Therapy in Acute Ischemic Stroke
Trial
NINDS tPA trial: National Institute of
Neurological Disorders and Stroke tPA
trial (N Eng J Med 1995; 333:1581 -
1587)
Acute Stroke
Treatment
ECASS: European Australasian
Cooperative Acute Stroke Study
(JAMA 1995; 274: 1017 - 1025)
ECASS II: Second European
Australasian Cooperative Acute Stroke
Study (Lancet 1998; 352: 1245 1251)
ATLANTIS A: Alteplase Thrombolysis
for Acute Non-interventional Therapy
in Ischemic Stroke (Stroke 2000; 31:
811 816)
ATLANTIS B: Alteplase Thrombolysis
for Acute Non-interventional Therapy
in Ischemic Stroke (JAMA 1999; 282:
2019 2026)
EMS: Emergency Management of
Stroke Bridging Trial (Stroke 1999; 30:
2598 2605)
ECASS III: European Australasian
Cooperative Acute Stroke Study (N Eng
J Med 2008; 359: 1317 - 1329
104
Design
291 patients with acute
ischemic stroke < 3 hours
were randomized to tpa (0.9
mg / kg IV) or placebo and
assessed for 4-point
improvement in NIH stroke
scale or the resolution of
neurological deficit within 24
hours ; 333 patients received
IV rt-PA within 3 hours of
symptom onset and were
assessed for functional and
clinical outcome at 3 months
620 patients with acute
ischemic stroke < 6 hours
were randomized to tPA 1.1
mg / kg or placebo
800 patients with acute
ischemic stroke < 6 hours
were randomized to tPA 0.9
mg / kg or placebo
142 patients with acute
ischemic stroke < 6 hours
were randomized to tPA 0.9
mg / kg or placebo
613 patients with acute
ischemic stroke within 3 5
hours were randomized to
tPA or placebo
35 patients with acute
ischemic stroke < 3 hours
were randomized to IV plus
local intra-arterial (IA) tPA vs
intra-arterial tPA alone
821 patients with acute
ischemic stroke within 3 to
4.5 hours were randomized to
tPA 0.9 mg / kg or placebo
Results
No difference in neurologic
improvement at 24 hours, but patients
given IV rt-PA were 30% more likely
than controls to have minimal or no
disability at 3 months, despite more
symptomatic ICH (6.4% vs 0.6%).
Overall, there was no difference in
mortality at 3 months.
No difference in disability using
intention to treat analysis. However,
there were 109 major protocol
violations. Post hoc analysis excluding
these patients indicated better recovery
for tPA group at 90 days
No significant difference was seen in
the rate of favorable outcome at 3
months between rt-PA and placebo
treated group
No significant difference was seen on
any of the planned efficacy endpoints at
30 and 90 days between groups. The
risk of symptomatic ICH was increased
with rt-PA treatment particulary in
patients treated between 5 to 6 hours
No significant difference in functional
recovery at 90 days between groups.
Risk of symptomatic intracerebral
hemorrhage was increased in tPA
IV/IA treatment resulted in higher
recanalization rate but no difference in
outcome at 7 days or 3 months. The rate
of symptomatic intracerebral
hemorrhage was similar between groups
Significantly more patients in the rt-
PA treated group had favorable outcome
at 3 months (52.4% vs 45.2 %, p =
0.04). The incidence of intracranial
hemorrhage was higher with rt-PA but
mortality did not significantly differ
between the 2 groups.
Administration of rt-PA to Acute Ischemic Stroke Patients (0 3 hours)

1. Eligibility for IV treatment with rt-PA

Age 18 or older.
Clinical diagnosis of ischemic stroke causing a measurable neurological deficit.
Time of symptom onset well established to be less than 180 minutes before
treatment would begin.

2. Patient Selection: Contraindications and Warnings

Evidence of intracranial hemorrhage on pretreatment CT.
Only minor or rapidly improving stroke symptoms.
Clinical presentation suggestive of subarachnoid hemorrhage, even with normal
CT.

Acute Stroke
Active internal bleeding.

Treatment
Known bleeding diathesis, including but not limited to:
o Platelet count < 100,000/mm
o Patient has received heparin within 48 hours and has an elevated aPTT
(greater than upper limit of normal for laboratory)
o Current use of oral anticoagulants (e.g., warfarin sodium) or recent use with
an elevated prothrombin time > 15 seconds
Patient has had major surgery or serious trauma excluding head trauma in the
previous 14 days.
Within 3 months any intracranial surgery, serious head trauma, or previous stroke.
History of gastrointestinal or urinary tract hemorrhage within 21 days.
Recent arterial puncture at a non-compressible site.
Recent lumbar puncture.
On repeated measurements, systolic blood pressure greater than 185 mm Hg or
diastolic blood pressure greater than 110 mm Hg at the time treatment is to begin,
and patient requires aggressive treatment to reduce blood pressure to within these
limits.
History of intracranial hemorrhage.
Abnormal blood glucose (< 50 or > 400 mg/dL).
Post myocardial infarction pericarditis.
Patient was observed to have seizures at the same time the onset of stroke
symptoms were observed.
Known arteriovenous malformation, or aneurysm.

3. Treatment
0.9 mg/kg (maximum of 90 mg) infused over 60 minutes with 10% of the total
dose administered as an initial intravenous bolus over 1 minute.

4. Sequence of Events
Draw blood for tests while preparations are made to perform non-contrast CT
scan.
Start recording blood pressure.
Neurological examination.

105
 CT scan without contrast.
Determine if CT has evidence of hemorrhage.
If patient has severe head or neck pain, or is somnolent or stuporous, be sure
there is no evidence of subarachnoid hemorrhage.
If there is a significant abnormal lucency suggestive of infarction, reconsider the
patient's history, since the stroke may have occurred earlier.
Review required test results Hematocrit, Platelets, Blood glucose, PT or aPTT
(in patients with recent use of oral anticoagulants or heparin)
Review patient selection criteria.
Infuse rt-PA.
Give 0.9 mg/kg, 10% as a bolus, intravenously.
Do not use the cardiac dose.
Do not exceed the 90 mg maximum dose.
Acute Stroke

Do not give aspirin, heparin or warfarin for 24 hours.

Treatment

Monitor the patient carefully, especially the blood pressure. Follow the blood
pressure algorithm (see below and sample orders).
Monitor neurological status.

5. Adjunctive Therapy
No concomitant heparin, warfarin, or aspirin during the first 24 hours after
symptom onset. If heparin or any other anticoagulant is indicated after 24 hours,
consider performing a non-contrast CT scan or other sensitive diagnostic imaging
method to rule out any intracranial hemorrhage before starting an anticoagulant.

6. Blood Pressure Control

Pretreatment
Monitor blood pressure every 15 minutes. It should be below 185/110 mm Hg.
If over 185/110, BP may be treated with nitroglycerin paste and/or one or two
10-20mg doses of labetalol given IV push or Nicardipine infusion of 5 mg/hour
titrate up by 2.5 mg every 5 - 15 mins interval. If these measures do not reduce
BP below 185/110 and keep it down, the patient should not be treated with rt-PA.

During and after treatment.

Monitor blood pressure for the first 24 hours after starting treatment:
w Every 15 minutes for 2 hours after starting the infusion, then
w Every 30 minutes for 6 hours, then
w Every hour for 18 hours.
If systolic BP > 230 mm Hg and/or diastolic BP is 121-140 mm Hg, give labetalol
20 mg intravenously over 1 to 2 minutes. The dose may be repeated and/or
doubled every 10 minutes, up to 150 mg. Alternatively either an intravenous
infusion of 2 to 8 mg/min labetalol may be initiated after the first bolus of
labetalol or Nicardipine infusion 5 mg / hr infusion is started and titrated up by
2.5 mg / hr every 5 15 mins interval until the desired BP is reached.
If satisfactory response is not obtained, use sodium nitroprusside.

106
 If systolic BP is 180 to 230 mm Hg and/or diastolic BP is 105 to 120 mm Hg on two
readings 5 to 10 minutes apart, give labetalol 10 mg intravenously over 1 to 2 minutes.
The dose may be repeated or doubled every 10 to 20 minutes, up to 150 mg.
Alternatively, following the first bolus of labetalol, an intravenous infusion of 2 to 8
mg/min labetalol may be initiated and continued until the desired blood pressure is
reached.
Monitor blood pressure every 15 minutes during the antihypertensive therapy.
Observe for hypotension.
If, in the clinical judgment of the treating physician, an intracranial hemorrhage is
suspected, the administration of rt-PA should be discontinued and an emergency CT
scan or other diagnostic imaging method sensitive for the presence of intracranial
hemorrhage should be obtained.

Acute Stroke
Management of Intracranial Hemorrhage

Treatment
Suspect the occurrence of intracranial hemorrhage following the start of rt-PA
infusion if there is any acute neurological deterioration, new headache, acute
hypertension, or nausea and vomiting.
If hemorrhage is suspected then do the following:
w Discontinue rt-PA infusion unless other causes of neurological
deterioration are apparent.
w Immediate CT scan or other diagnostic imaging method sensitive for the
presence of hemorrhage.
w Draw blood for PT, aPTT, platelet count, fibrinogen, and type and cross
(may wait to do actual type and cross).
w Prepare for administration of 6 to 8 units of cryoprecipitate containing
factor VIII.
w Prepare for administration of 6 to 8 units of platelets.
If intracranial hemorrhage is present:
w Obtain fibrinogen results.
w Consider administering cryoprecipitate or platelets if needed.
w Consider alerting and consulting a hematologist or neurosurgeon.
w Consider decision regarding further medical and/or surgical therapy.
w Consider second CT to assess progression of intracranial hemorrhage.
w A plan for access to emergent neurosurgical consultation is highly
recommended.
This Protocol is Based on Research Supported by the National Institute of Neurological Disorders and Stroke (NINDS)
(N01-NS-02382, N01-NS-02374, N01-NS-02377, N01-NS-02381, N01-NS-02379, N01-NS-02373, N01-NS-02378,
N01-NS-02376, N01-NS-02380).

Expansion of IV rTPA Treatment Time Window up to 4.5 Hours

Eligibility for IV treatment follows the same criteria as treatment within the first 3 hours with the
following additional exclusion criteria:
Patients older than 80 years old
Patients on oral anticoagulants, regardless of INR level
Patients with NIHSS > 25
Patients with stroke and diabetes

107
 Ancillary care for patients receiving IV rTPA treatment at 3 - 4.5 hours after acute ischemic
stroke is similar to that listed above.

Bibliography
1. Adams H, del Zoppo G, Alberts M et al. Guidelines for the early management of patients with ischemic
stroke. 2007 Guidelines update, a scientific statement from the Stroke Council of the American Heart
Association. Stroke 2007;38:1655-1711.
2. Del Zoppo, G, Saver J, Juach E and Adams, H on behalf of the American Heart Association Stroke Council.
Expansion of the Time Window for Treatment of Acute Ischemic Stroke with Tissue Plasminogen
Activator, a science advisory from the American Heart Association / American Stroke Association. Stroke
2009; 40: 2945 2948.

The search for a thrombolytic agent that can be used beyond the 3 hours of acute ischemic
stroke is being addressed by the ongoing DIAS-3 study or Desmoteplase In Acute Stroke
Study. This double blind randomized trial will determine whether desmoteplase is
Acute Stroke
Treatment

effective and safe in the treatment of patients with acute ischaemic stroke when given
within 3-9 hours from onset of stroke symptoms. Patients should have an NIHSS Score
of 4-24 and a documented vessel occlusion or high-grade stenosis on MRI or CTA in
proximal cerebral arteries. The Philippines is participatory in this trial.

VI. BLOOD PRESSURE MANAGEMENT AFTER ACUTE STROKE

A. BP management in Acute Ischemic Stroke
1. Definition :

Mean Arterial Pressure (MAP) = 2 (Diastolic) + Systolic

3
Cerebral Perfusion Pressure (CPP) = MAP-ICP

Normal Values:
o ICP : 5-10 mm Hg
o CPP: 70-100 mm Hg
2. Check if patient is in any condition that may increase BP such as pain, stress, bladder
distention or constipation, which should be addressed accordingly.
3. Allow permissive hypertension during the first week to ensure adequate CPP but ascertain
cardiac and renal protection.
a. Treat if SBP>220 or DBP>120 or MAP>130
b. Defer emergency BP therapy if MAP is within 110-130 or SBP=185-220 mmHg or
DBP=105-120 mmHg, unless in the presence of
w Acute MI
w Congestive heart failure

108
 w
Aortic dissection
w
Acute pulmonary edema
w
Acute renal failure
w
Hypertensive encephalopathy
Rationale for Permissive Hypertension:

In acute ischemic stroke, autoregulation is paralyzed in the affected tissues

with CBF passively following MAP. Rapid BP lowering can lead to further
perfusion in the penumbra.

In acute ischemic stroke (AIS), autoregulation is paralyzed in the affected

tissues with Cerebral Blood Flow (CBF) passively following the MAP.

Acute Stroke
Rapid lowering can lead to further perfusion in the penumbra.

Treatment
HPN is typically present in acute stroke, with spontaneous decline in the
first 5-7 days.

ICP during the acute phase of large infarcts reduces the net CPP,

SBP dropped by 28% during the first day whether or not medications
were given (Oliviera-Filho et al)

Rapid and steep BP reductions may be harmful. SBP and DBP drops of
>20 mm Hg were associated with early neurological worsening, high rates
of poor outcome or death, larger volumes of infarctions (Castillo et al)

Based on a randomized trial, SCAST (Scandinavian Candesartan Acute

Stroke Trial) using an angiotension receptor blocker, there was no
indication that careful blood-pressure lowering treatment is beneficial in
patients with acute stroke and raised blood pressure. If anything, the
evidence suggested a harmful effect.

HPN is typically present in acute stroke, with spontaneous decline within

the first 5 - 7 days.

ICP during the acute phase of large infarcts reduces the net CPP.

Several reports have documented neurological deterioration & poor

outcome from rapid and aggressive pharmacologic lowering of BP.

109
 4. Use the following locally available intravenous anti-hypertensives in acute stroke to achieve
target MAP = 110130 mmHg:

Onset
Du rat io n Availability/ Adverse
Dru g Dose of o f Actio n Dilution Stabilit y Reaction s Action
Action
Inhibits calcium
Tachycard ia ,
Nicardipine

ion from entering

(10 mg/10 m l headache,
slow channel,
am p ); flushin g,
5-10 1 to 4 producing
1-15 mg/hour 1-4 hours 10 mg in 90 dizziness,
mins hours coron ary,
ml somn olence,
vasc ula r, smooth
NSS/D5W nausea
m uscle relaxation
& vasodilatation
Tachycard ia ,
IV push 10-20 D irect
Hydralazine
Acute Stroke

flushin g,
Treatment

mg/dose q 4-6 25 mg/m L vasodilatation of

headache,
hours as needed, 10-20 am p; 25 a rterioles &
3-8 hours 4 days vomiting,
may increase to mins mg/ta b decreased
increa sed
40 m g/dose sy stemic
an gina
resista nce
Alpha- & b eta-
blocker. Beta-
5 mg IV push a drenergic
over 2 mins, Orthostatic blocking activity
repea t with hypotension , is 7x > than
5 mg/ml in
incrementa l dose drowsiness,
Labetalol

40 ml vial; a lph a-a drenergic

of 10, 20, 40, 80 2-5 dizziness, blockers.
2-4 hours 250 m g in 72 hours
mg until desired mins ligh thea dedness Produces dose-
250 m L
BP is achieved or , dyspnea,
NSS/D5W dependent in
a total dose of wheezing &
BP witho ut
300 mg has been bronchospasm
adm inist ered significa nt in
HR or card ia c
output

0.25-0.5 mg/ kg
IV push 1-2 m in s
followed by
infusion of 0.05
Hypotensio n, Short-acting
mg/kg/min.
bradycardia, beta-adrenergic
100 m g/10
AV block, blocking agent.
If there is no ml vial;
Esmolol

agita tion, At low do ses, has

response, repeat 2-10 10-30 2,500 mg in
48 hours confusion, little effect on
0.5 m g/kg b olus mins mins 250 m L
wheezing / beta2 receptors
dose & D5W/NSS
broncho- of bronchial &
infusion to 0.10 constriction, vasc ula r smoo th
mg/kg/min.
phle bitis m uscle
maximum
infusion
rate=0.30
mg/kg/min

5. Treat patients who are potential candidates for rt-PA therapy who have persistent elevations
in SBP >185 mmHg or DBP >110 mmHg with small doses of IV antihypertensive agents.
Maintain BP just below these limits.

110
6. Arterial Hypotension in Acute Ischemic Stroke:

Rare in acute ischemic stroke

Baseline SBP <100 mm Hg or DBP < 70 mm Hg is associated with higher rates of

neurological worsening, poor neurological outcomes, or death

Cause of arterial hypotension in acute stroke should be sought: aortic dissection,

volume depletion, blood loss, and decreased cardiac output secondary to MI or
cardiac arrhythmias.

Correct hypovolemia with NSS, and treat arrhythmias to optimize cardiac output

Available vasopressors agents include dopamine, dobutamine, phenylephrine

Acute Stroke
Treatment
Bibliography
1. Adams H, Adams R, del Zoppo G, Goldstein L. Guidelines for the early management of
patients with ischemic stroke. 2005 Guidelines update, a scientific statement from the Stroke
Council of the American Heart Association. Stroke 2005;36:916-923.
2. Broderick JP, Adams HP, Barsan W, et al. Guidelines for the management of spontaneous
intracerebral hemorrhage: a statement for healthcare professionals from a special writing
group of the Stroke Council of the American Heart Association. Stroke 1999;30:905-915.
3. Fogelholm R, Avikainen S and Murros K. Prognostic value and determinants of first day
mean arterial pressure in spontaneous supratentorial intracerebral hemorrhage. Stroke
1997;28:1396-1400.
4. Guyton A and Hall J. Guyton and Halls Textbook of Medical Physiology, 11th ed. USA: WB
Saunders; 2005.
5. Kidwell CS, Saver JL, Mattiello J, et al. Diffusion perfusion MR evaluation of perihematomal
injury in hyperacute intracebral hemorrhage. Neurology 2001;57:1611-1617.
6. Powers WJ, Zazulia AR, Videen TO, et al. Autoregulation of cerebral blood flow
surrounding acute (6-22hours) intracerebral hemorrhage. Neurology 2001;57:18-24.
7. Qureshi A, Wilson D, Hanley D, Traystman R. No evidence for an ischemic penumbra in
massive experimental intracerebral hemorrhage. Neurology 1999;52:266-272.
8. Schellinger P, Fiebach J, Hoffman K, et al. Stroke MRI in intracerebral hemorrhage: is there
a perihemorrhagic penumbra? Stroke 2003;34:1647-1680.
9. The Brain Matters Stroke Initiative. Acute Stroke Management Workshop Syllabus. Basic
Principles of Modern Management for Acute Stroke.
10. Harold Adams Jr., Gregory del Zoppo, Mark J.Alberts, Deepak L. Bhatt, Lawrence Brass,
Anthony Furlan, Robert L. Grubb, Randall T. Higashida, Edward C. Jauch, Chelsea Kidwell,
Patrick D. Lyden, Lewis B. Morgenstern, Adnan I. Qureshi, Robert H. Rosenwasser, Phillip
A. Scott and Eelco F.M. Wijdicks, Guidelines for the Early Management of Adults with
Ischemic Stroke, STROKE 2007; 38; 1670-1674
11. . Oliveira-Filho J, Silva SC, Trabuco CC, Pedreira BB, Sousa EU, Bacellar A. Detrimental
effect of blood pressure reduction in the first 24 hours of acute stroke onset. Neurology.
2003;61:10471051.
12. . Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Davalos A. Blood pressure decrease
during the acute phase of ischemic stroke is associated with brain injury and poor stroke
outcome. Stroke. 2004;35:520 526.
13. Sandset EC, Bath PM, Boysen G et al. The angiotensin-receptor blocker candesartan for
treatment of acute stroke (SCAST): a randomised, placebo-controlled, double-blind trial.
Lancet. 2011 Feb 26;377(9767):741-50.)

111
 B. Blood pressure Management in Acute Hypertensive Intracerebral Hemorrhage
(ICH)

BP often markedly elevated in acute ICH, with elevations greater than that seen in
ischemic stroke.

Mechanisms:
o Stress activation of neuroendocrine system (sympathetic NS, renin-
angiotensin axis, glucocorticoid system)
o partly in response to increased ICP.

Absence of ischemic penumbra allows for more aggressive BP management

Acute Stroke

Hypertension could theoretically contribute to hydrostatic expansion of the

Treatment

hematoma, peri-hematoma edema, and rebleeding

Hypotension may result in cerebral hypoperfusion especially in the setting of

increased intracranial pressure (ICP)

Two recent phase II clinical trials on BP lowering namely ATACH and

INTERACT have shown that intensive BP lowering to SBP = 140 in acute ICH is
feasible and is probably safe. Phase III clinical studies are ongoing to determine
its clinical efficacy.

INTERACT (INTensive Blood Pressure Reduction in Acute Cerebral

Hemorrhage Trial): trend to less hematoma volume growth in 24 hours
with intensive BP lowering to goal of SBP 140 mm Hg, vs 180 mm Hg;
no excess of neurologic deterioration
ATACH (Antihypertensive Treatment in Acute Cerebral Hemorrhage)
trial: Early, rapid BP lowering in ICH (with IV Nicardipine) is clinically
feasible and probably safe.

Unlike SAH (subarachnoid hemorrhage), isolated ICH does not have the same
propensity to cause cerebral vasospasm, thus BP lowering can be somewhat more
aggressive.

Recommendations:
Treat if SBP > 180 mmHg or MAP > 130 mm Hg. Maintain MAP = 110 or SBP
= 160 mm Hg statement from AHA
For SBP 150-220, acute lowering of SBP to 140 is probably safe (Class IIa, Level
of Evidence B)
In patients with ICH and a history of hypertension, goal is MAP <130 mm Hg.

112
Bibliography
1. Lewis Morgenstern, J. Claude Hemphill III, Craig Anderson, Kyra Becker, Joseph P.
Broderick, E.Sander Connolly Jr, Steven Greenberg, James N. Huang, R. Loch Macdonald,
Steven R Messe, Pamela Mitchell, Magdy Selim, Rafael J. Tamargo, on behalf of AHA
Stroke Council and Council on cardiovascular Nursing, Guidelines for the Management of
Spontaneous ICH: A Guideline for Healthcare Professionals from the American Heart
Association/American Stroke Society, STROKE 2010; 41; 2115
2. Handbook of Stroke, 2nd edition 2006, David O Weibers, Valery L. Feigin, Robert
D.Brown, Jr., pp.203, 255

C. Subarachnoid Hemorrhage

Treat hypertension with modest reductions in BP to minimize vasospasm and

delayed cerebral ischemia (see section on Subarachnoid Hemorrhage)

Acute Stroke
Treatment
Goal MAP ? 130-140 mm Hg or SBP ? 180-200 mm Hg.

Use intermittent or continuous IV antihypertensive agents. (Handbook of Stroke,

2nd edition 2006, David O Weibers, Valery L. Feigin, Robert D.Brown, Jr., p.192,
434)

Preoperatively, for unsecured aneurysms the use of IV Nicardipine IV to a target

SBP <150 mm Hg is reasonable.

Bibliograph
1. Handbook of Stroke, 2nd edition 2006, David O Weibers, Valery L. Feigin, Robert
D.Brown, Jr., p.192, 434

VII. MANAGEMENT OF INCREASED INTRACRANIAL

PRESSURE
A. Signs and symptoms of increased ICP
1. Deteriorating level of sensorium
2. Cushings triad
i. Hypertension
ii. Bradycardia
iii. Irregular respiration
3. Anisocoria

B. Management options for increased ICP

General:
1. Control agitation and pain with short-acting medications, such as NSAIDS and
opioids.

2. Treat fever aggressively. Avoid hyperthermia.

113
 3. Control seizures if present. May treat with phenytoin with a loading dose of 18-
20 mg/kg IV then maintained at 3-5 mg/kg or Levetiracetam 500 mg/IV q 12.
Status epilepticus should be managed accordingly.

4. Strict glucose control between 110-180 mg/dL.

5. Maintain normal fluid and electrolyte balance.

a. Avoid excessive free water or any hypotonic fluids such as D5W.
Potential sources of free water including hypotonic tube feedings,
medications mixed in D5W, nasogastric tube flushes with water should
be minimized.
b. Maintain normal volume status (i.e. 3-3.5 liters per day in a 60 kg
patient).
Acute Stroke

c. Encourage hyperosmolar state with hypertonic saline and/or induce

Treatment

free water clearance with mannitol or diuretics.

6. Use stool softeners to prevent straining.

Specific:
1. Elevate the head at 30 to 45 degrees to assist venous drainage.

2. Do CSF drainage in the setting of hydrocephalus.

3. Administer osmotic therapy:

Give Mannitol 20%. Typical doses range from 0.5-1.5 g/kg every 3-6
hours. Doses up to 1.5 g/kg are appropriate when treating a
deteriorating patient because of mass effect.
Hypertonic Saline is an option. It has the advantage of maintaining an
effective serum gradient or rise in osmolality for sustained periods with
lower incidence of intracranial hypertension.
Always maintain serum osmolality at 300-320 mOsmol/kg
Serum osmolality = 2 (Na) + glucose/18 + BUN/2.8

4. Hyperventilate only in impending herniation by adjusting tidal volume to achieve

target PCO2 levels 3035 mm Hg. Hyperventilation is recommended only for a
short term as its effect on CBF and ICP is short lived (? 6hours). Prophylactic
hyperventilation without regard to the level of ICP and the clinical state should
not be done.

5. Carefully intubate patients with respiratory failure defined as SpO2 of less than
90% by pulse oximeter and PaO2 <60mmHg, and/or PaCO2 > 55mmHg by
arterial blood gas analysis.

6. Consider surgical evacuation or decompressive hemicraniectomy if indicated.

114
 7. ICP catheter insertion is useful for the diagnosis, monitoring and therapeutic
lowering of increased ICP. It is recommended in patients with a GCS8, those
with significant IVH or hydrocephalus. CPP should be maintained at 60-
70mmHg.
C. Sedatives and Narcotics available locally
Onset of Duration Comments
Drugs Usual Dose Availability/Dilution
Action of Effect

15 mg/3 mL amp;
0.025-0.35 1 to 5 Unpredictable 5 mg/5 mL amp;
Midazolam 2 hours
mg/kg min sedation 50 mg in 100 mL
NSS /D5W
Sedation can be
reversed with

Acute Stroke
flumazenil (0.2-1 10 mg/2 mL amp;

Treatment
0.1-0.2 20 to 30
Di azepam Immediate mg at 0.2 mg/min at 50 mg in 250 mL
mg/kg minutes
20 min interval, NSS /D5W
max dose 3 mg in
one hour)
(10 mg/mL) 100
5-50 10 to 15
P ropofol <40 secs Expensive mL vial
ug/kg/min min
(premixed)
50-100 mg 6 to 8
K etorolac 1 hour NSAID 30 mg/mL amp
IV hours
C entrally acting
synt hetic analgesic
compound not
chemically related
50-100 mg 50 mg/ 2 mL amp;
Tramadol 1 hour 9 hours to opiates but
IV 100 mg/2 mL amp
thought to bind to
opioid receptors and
inhibit reuptake of
NE and serotonin
C an be easily
reversed with
naloxone (0.4-2 mg
100 ug/2 mL;
50-100 1-2 IVP; repeat at 2-3
F entanyl >60 min 2,500 ug in 250
ug/hour mins min intervals, max
mL NSS/ D5W
dose 10 mg)
* 110x more potent
than morphine
10 mg/mL gr 1/6;
M orphine 2-5 mg/hour 5 mins >60 min Opioid 16 mg/ mL gr 1/ 4

1 mcg/kg/hr LD
for 10 mins then
maintenance
Dexmedetomidine
dosing at
30 60
3 5 mins
200 mcg / 2 ml
(Precedex)
0.4mcg/kg/hr
secs vial
(Dose range:
0.20.7 mcg/hr)

115
 VIII. HEMICRANIECTOMY FOR MALIGNANT MCA INFARCTION
Ten to fifteen percent of supratentorial infarcts will involve the entire MCA.1 Cerebral
ischemic infarcts are associated with cytotoxic, interstitial and vasogenic brain edema of
varying extents. Depending on the celerity and extent of edema formation, and on patients
compensatory mechanisms, ischemic brain edema in large MCA infarcts may lead to
transtentorial or transforaminal herniation, usually within 2-5 days from ictus. 2-3 Herniation
accounts for 78% of deaths during the first week.4 This subgroup of catastrophic infarcts
was first labeled as malignant MCA infarcts by Hacke et al in 1996. 3

Prognosis of patients with malignant edema formation after MCA infarct is poor despite
maximum conservative treatment, and in randomized or larger prospective observational
studies, mortality averages 5080% .5-10
Acute Stroke
Treatment

Figure 1: Natural Course of Malignant MCA Infarction

Because of the limitations of current medical therapies in preventing brain herniation and
improving patient outcome, varying surgical decompression techniques have been proposed
and used to achieve the following objectives: decrease mass effect or intracranial pressure
from malignant brain edema, prevent brain herniation, reduce or avert secondary injury to
the brain and reduce or avert further conversion of areas of ischemic penumbra to infarct.
This would ultimately translate to reduction in overall mortality rates and an improvement in
long term functional outcomes.

Criteria for Patient Selection

1. Patients who present clinically with a severe hemispheric stroke syndrome:

hemiplegia, forced eye deviation and head deviation to the side of the infarct, aphasia,
contralateral neglect and progressive decline in the level of consciousness usually
within the first 48 hours.

2. Imaging findings showing an infarct volume involving >50% MCA territory.

3. Age: 60 years and below. Mortality rate was 20.8% in patients = 60 yrs vs. 51.3% in
patients >60yrs. Poor outcome was seen in 33.1% of patients <= 60 yrs vs. 81.8% in
patients >60. 11 However, some authors have suggested that other factors might be
more important than age. This includes admission functional status, cognitive status,
social situation, extent of family support, psychosocial and financial burden of care.

116
 4. Dominance of hemisphere involved: Though some have expressed concern that
doing decompressive hemicraniectomy for malignant MCA infarcts involving the
dominant hemisphere will lead to a worse functional outcome, this has not been seen
in several studies, due to recovery of varying extents of communication skills or to
the equally negative impact of hemiplegia. 12

5. Exclusions: terminal illness, significant co morbid conditions like significant cardiac

disease, bleeding disorders.

6. Massachusetts General Hospital has proposed the STATE Criteria to determine

eligibility for hemicraniectomy and a treatment algorithm on this criteria.

STATE Criteria13

Acute Stroke
Treatment
STATE Criteria for IMMEDIATE NEUROSURGICAL
CONSULTATION for hemicraniectomy for malignant MCA
infarction
Factor Criteria

Score*,** NIHSS item 1a >=1 or GCS <= 8, and

NIHSS > 15 (non-dominant) or > 20
(dominant)
Time <=48 hr since last seen without neurological
deficits

Age <=60 years

Territory Infarct lesion volume >150 cm (use ABC/2

criteria for estimating lesion volume), or >50%
MCA territory infarction
Expectations Life expectancy 'reasonable' in the opinion of the
Neurology Attending or NeuroICU Fellow.
In addition, the health care proxy or family members
understand that while the procedure is proven to
reduce disability and mortality, the patient may still
survive with severe disability.

If all the above "STATE" criteria are met, proceed to hemicraniectomy

urgently (to OR within 4-6 hrs).
*for intubated/sedated patients, monitoring of the level of alertness can be
challenging and the clinical judgment of the Neurology Attending is
important in determining whether a patient meets this criterion. ** for
patients who meet all STATE criteria except the level of drowsiness, patients
should be triaged to the Neuro ICU for close neuromonitoring.

117
 Indications for EMERGENT HEMICRANIECTOMY: STATE
criteria met above, AND

Early Signs of Herniation Asymmetry in pupil size

Midline Shift >10mm at septum pellucidum, or >5mm

at pineal gland

Treatment Algorithm13

Assign the patient into one of 3 categories:

Acute Stroke

A.MOST LIKELY to benefit from early hemicraniectomy

Treatment

(meets all STATE criteria)

1. consult neurosurgery emergently
2. proceed for hemicraniectomy within the defined time frames
3. admit to the Neuro ICU before and after the procedure for close neurological
monitoring and medical treatment
4. For patients who meet all STATE criteria except for drowsiness, these patients
should be admitted the Neuro ICU and closely monitored. If they develop
drowsiness, they should be sent for hemicraniectomy.

B.UNCERTAIN to benefit from early hemicraniectomy

(age <75 yrs and meets many but not all STATE criteria)
1. hemicraniectomy is offered as a compassionate therapy if there is consensus
among the treating teams and family that the patient would want to proceed
recognizing that there is uncertainty as to the benefit.
2. regardless of the decision to proceed with hemicraniectomy, if full aggressive
treatment is requested by family and felt appropriate by treating team, then
admit the patient to an intensive care unit, preferably the Neuro ICU, for close
neurological monitoring and medical treatment.

Pre-surgical and Surgical Management13

A. If hemicraniectomy is offered, withhold anti-coagulation and anti-platelets until
deemed safe post-procedure with input from neurosurgery

B. For adequate external decompression, the size of the bone flap removed should
ideally be 12 cm (anterior-posterior) by 9 cm (superior-inferior), combined with
duraplasty

C. Temporal lobectomy may be considered during the procedure, at the neurosurgeon's

discretion. If performed, tissue should be submitted for neuropathological
examination.

118
 D. The bone flap should be placed in a subcutaneous abdominal pouch or stored in the
bone bank

Post-surgical Management13

A. Admit the patient to an intensive care unit, preferably the Neuro ICU. The
Neurocritical Care attending will be the attending of record.

B.Once appropriate, a protective helmet should be worn until the bone flap is replaced.

C. The bone flap should be replaced as soon as the patient can tolerate the surgery,
preferably within 12 weeks, unless the patient develops intercurrent infections or

Acute Stroke
other complications requiring delay.

Treatment
Adjunctive Therapy

Although not proven efficacious, medical strategies may reduce the risk of developing
fulminant brain edema. These strategies should be used in all patients with large MCA
stroke and as an adjunct to hemicraniectomy (if the patient is deemed eligible). They
should not used be to defer or delay hemicraniectomy if STATE criteria are met.

A. General management: patients with raised intracranial pressure require special

attention to pain relief, avoidance of noxious stimuli, proper head positioning,
adequate oxygenation, maintenance of normothermia, and prevention of DVT.
Avoid oral or gastric feedings if the patient is likely to go to surgery imminently.

B. Hyperventilation: a temporary measure to reduce ICP if signs of brain herniation

develop. Should be avoided unless other measures are exhausted and there is a plan
to proceed immediately to surgery.

C. Osmotic therapy

D. Invasive ICP monitoring (subarachnoid screw or bolt) is not required to determine

suitability for decompressive surgery. An external ventricular drain should be
considered if brain imaging shows evidence of acute hydrocephalus. It may be
useful to monitor the ICP post-operatively if there is concern that the
decompression was insufficient

Key Points in the Surgical Management of Malignant MCA Infarction

1. Anticoagulation and antiplatelet therapy should be withheld until deemed safe post
procedure.

119
 2. Optimal medical therapy including osmotic therapy should be instituted while
preparing patient for hemicraniectomy and postoperatively as indicated.

3. Timing of surgery: Better outcomes have shown if surgery is done early, within 24-48
hours from ictus 14,17, and before clinical signs of hernation like pupillary dilatation
and posturing 15. Surgical procedure consists of decompressive hemicraniectomy
with duraplasty. Removal of bone flap decreases intracranial pressure by 15% while
opening the dura reduces intracranial pressure by 70% 16,17. Dimensions of the
bone flap removed should be generous, with some institutions recommending a size
of 12 cm by 9 cm. Removal of a bone flap with a diameter 10 cm and less has been
associated with an increased incidence of shearing injury due to herniating brain
abutting against the edge of the craniectomy defect.17
Acute Stroke
Treatment

4. Strokektomy or the removal of infracted tissue should not be routinely done because
it is usually difficult to delineate between infracted versus ischemic tissue and
outcomes have not been shown to be significantly better.

5. The removed bone flap may be stored in a subcutaneous abdominal pocket or in the
bone bank if such is available.

6. Bone flap is replaced as soon as functional recovery has stabilized and patient
presents with no systemic contraindications.

Outcomes:

Results of different studies have shown that decompressive hemicraniectomy with

duraplasty has improved survival rates to 67-84% vs. 20-30% in patients managed
conservatively. Though the significant reduction in mortality brought about by surgery
is irrefutable, its impact on functional outcome is still the subject of some debate.
Different prospective studies and randomized clinical trials have shown that
decompressive hemicraniectomy has increased the numbers of survivors with
moderate or moderately severe disability. However, whether or not this translates to a
poorer quality of life is relative, with Kelly et al 18 showing that such an outcome is
acceptable when patients and or their families value prolongation of life much more
than the almost certain death with medical management alone. More recent trials have
likewise shown that decompressive surgery can improve long term functional outcome,
NNT of 2 to achieve a modified Rankin Scale score of <=4, and a NNT of 4 to achieve
a modified Rankin Scale score of <=3 at one year. The decision as to whether
decompressive surgery should be offered to a patient presenting with malignant MCA
infarction should therefore be individualized. 13

120
Table 1. Benefit of Hemicraniectomy 19

Study Name Year No. Time Primary Mortality (%) Good

of Inclusion Criteria to Tx Outcome Outcome
Pts (hrs) Measure
Surg Med Surg Med
DESTINY 2007 32 Age: 18-60 36 Death at 30 days, 17.6 53 47 27
MRS <4 at 6mos.
NIHSS: >18-20
DECIMAL 2007 38 Age18-55 24 MRS <4 at 6mos. 25 77.8 50 22.2
HAMLET 2009 64 Age 18-60 96 MRS <4 at 12mos. 22 59 25 25
HeADD NA 26 Acute unilat 96 Death, functional Results pending
FIRST MCA ischemia outcome, quality
of life, pt.

Acute Stroke
perceptions, acute

Treatment
health care use at
21,90, 100days
HEMMI NA NA Ischemic MCA 72 GCS, NIHSS,MRS, Results pending
stroke Barthel at 6 mos

DESTINY II NA NA Age>61, MCA 48 Recruiting patients

malignant infarct

For every 10 hemicraniectomies performed for MCA infarction, 5 patients will escape
death, and at one year, 1 of these patient will have mild disability, 1 patient will have
moderate disability and 3 will have severe disability.20

Bibliography
1. Berrouschot J, Sterker M, Bettin S, Koser J, Schneider D. Mortality of space-occupying
(malignant) middle cerebral artery infarction under conservative intensive care. Intensive Care
Med. 1998;24:620623
2 . Ropper AH, Shafran B. Brain edema after stroke. Clinical syndrome and intracranial
pressure. Arch Neurol 1984; 41:269.
3. Hacke W, Schwab S, Horn M, Spranger M, De Georgia M, von Kummer R. Malignant
middle cerebral artery infarction. Clinical course and prognostic signs. Arch Neurol 1996;
53:30915.
4. Heinsius T, Bogousslavsky J, Van Melle G. Large infarcts in the middle cerebral artery
territory. Etiology and outcome patterns. Neurology 1998; 59:34150.
4 . Silver SL, Norris JW, Lewis AJ, Hachinski VC. Early mortality following stroke: a prospective
review. Stroke 1984; 15:4926.
5. Kasner SE, Demchuk AM, Berrouschot J et al. Predictors of fatal brain edema in massive
hemispheric ischemic stroke. Stroke 2001; 32:211723.
6. Berrouschot J, Sterker M, Bettin S, Koster J, Schneider D. Mortality of space-occupying
(malignant) middle cerebral artery infarction under conservative intensive care. Intensive Care
Med 1998; 24:6203.
7. Vahedi K, Hofmeijer J, Juettler E et al. Early decompressive surgery in malignant middle
cerebral artery infarction: a pooled analysis of three randomised controlled trials. Lancet Neurol
2007; 6:21522.

121
 8. Vahedi K, Vicaut E, Mateo J et al. Sequential-design, multicenter, randomized, controlled
trial of early decompressive craniectomy in malignant middle cerebral artery infarction
(DECIMAL Trial). Stroke 2007; 38:250617.
9. Jttler E, Schwab S, Schmiedek P et al. Decompressive Surgery for the Treatment of
Malignant Infarction of the Middle Cerebral Artery (DESTINY): a randomized, controlled trial.
Stroke 2007; 38:251825.
10. Hofmeijer J, Kapelle LJ, Algra A et al. Surgical decompression for space-occupying cerebral
infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-
threatening Edema Trial (HAMLET)): a multicentre, open, randomised trial. Lancet Neurol 2009;
8:32633.
11. Ahmet Arac, Vanessa Blanchard, M.AMarco Lee, M.D, Gary K. Steinberg. Outcome of
decompressive craniectomy for malignant middle cerebral artery infarction in patients older
than 60: conclusions. www.ncbi.nlm.nih.gov/pubmed/19210913
12. Lanzino, D., & Lanzino, G. (2000). Decompressive craniectomy for spaceoccupying
Acute Stroke
Treatment

supratentorial infarction: Rationale, indications, and outcome. Neurosurgical Focus, 8, 17.

13. Victoria Marquevich MD, W. Taylor Kimberly, MD PhD, Christopher Ogilvy, MD, Lee
Schwamm, MD and Aneesh Singhal, MD.
www2.massgeneral.org/stopstroke/protocolHemicraniectomyGuidelines.aspx
14. Schwab, S., Steiner, T., Aschoff A., Schwarz, S., Steiner, H., Jansen, O., et al. (1998). Early
hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke, 29,
18881893.
15. Schwab, S., & Hacke,W. (2003). Surgical decompression of patients with large middle
cerebral artery infarcts is effective. Stroke, 34, 23042305.
16. Smith, E. R., Carter, B. S., & Ogilvy, C. S. (2002). Proposed use of prophylactic
decompressive craniectomy in poor-grade aneurismal subarachnoid hemorrhage patients
presenting with associated large sylvian hematomas. Neurosurgery, 51(1), 117124.
17. Tazbir J, Marthaler M, Moredich C, Keresztes P. Decompressive hemicraniectomy with
duraplasty - ischemic stroke: patient selection. www.medscape.com/viewarticle/512034
18. Kelly AG, Holloway RG. Health state preferences and decision-making after malignant
middle cerebral artery infarctions. Neurology 2010 E-pub 2010 Jul 14.
19. Arnaut O,Auon S, Batjer H, Bendok B. Neurosurgery focus.June 2011 ;30:1-5
20. Mayer S. Hemicraniectomy: A Second chance in life for patients with space occupying MCA
infarction. Stroke 2007; 38:2410-2412

122
 IX. STROKE SCALES

I. Glasgow Coma Scale

Category Score
Eye Opening
Spontaneous 4
To speech 3
To pain 2
None 1
Best Motor Response
Obeys 6
Localizes 5

Acute Stroke
Treatment
Withdraws 4
Abnormal flexion (decorticate) 3
Abnormal extension (decerebrate) 2
None 1
Best Verbal response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1

II. National Institutes of Health (NIH) Stroke Scale

It ems Scale Definition

0 = Alert, keenly responsive
1 = Not alert, but arousable by minor stimulation to obey,
answer or respond
2 = Not alert, requires repeated stimulation to attend, or is
Ia. Level of
obtunded and requires strong or painful stimulation to
Consciousness (LOC)
make movements (not stereotyped)
3 = Responds only with reflex motor or autonomic effects
or totally unresponsive, or totally unresponsive, flaccid,
areflexic
0 = Answers both questions correctly
Ib. LOC Questions 1 = Answers one question correctly
2 = Answers neither question correctly
0 = Performs both tasks correctly
Ic. LOC Commands 1 = Performs one task correctly
2 = Performs neither task correctly

123
 Items Scale Definition
0 = Normal
1= Partial gaze palsy. Gaze i s abnormal in one or both eyes but
2. Best gaze forced deviation or total gaze paresis is not present
2 = Forced deviation, or total gaze paresi s is not overcome by
oculocephalic maneuver
0 = No visual loss
1 = Partial hemi anopia
3. V isual
2 = Complete hemianopia
3 = Bilateral hemianopia (bl ind, including cortical blindness)
0 = Normal symmetrical movement
4. Facial palsy 1 = Minor paralysis (flattened nasolabial fold, asymmetry on
Acute Stroke
Treatment

smiling)
0 = No drift; limb holds 90 (or 45) degrees for full 10 seconds
1 = Drifts; limb holds 90 (or 45) degrees but drifts down before
full 10 seconds; does not hit bed or other support
5. Motor (Arm) 2 = Some effort against gravity, li mb cannot get up to or
5 a. L eft arm maintain (if cued) 90 (or 45) degrees; drifts down to bed, but
5 b. Right arm has some effort against gravity
3 = No effort against gravity; limb falls
4 = No movement
9 = Amputation or joint fusion; explain
0 = No drift; leg holds 30-degree position for full 5 seconds
1 = Drifts; leg fal ls by the end of the 5-second period but does
not hit bed
6. Motor (Leg)
2 = Some effort against gravity; leg falls to bed by 5 seconds
6 a. Right leg
but has some effort against gravity
6 b. L eft leg
3 = No effort against gravity; leg falls to bed immediately
4 = No movement
9 = Amputation or joint fusion; explain
0 = absent
1 = Present in one limb
7. L imb ataxi a
2 = Present in two l imbs
9 = Amputation or joint fusion; explain
0 = Normal; no sensory loss
1 = Mil d to moderate sensory loss; patient feels pi nprick is less
sharp or dull on the affected side; or there is a loss of superfici al
8. Sensory
pain with pinprick, but patient is aware he/she is being touched
2 = Severe or total sensory loss; patient is not aware of being
touched in the face, arm or leg

124
 9. Best Language 0 = No aphasia
(Fig. 1) 1 = Mild to moderate aphasia; some obvious loss of
fluency or facility of comprehension, without significant
limitation on ideas expressed or form of expression.
Reduction of speech and/or comprehension, however,
makes conversation on provided material difficult
2 = Severe aphasia; all communication is through
fragmentary expression; great need for inference,
questioning and guessing by the listener. Range of
information that can be exchanged is limited; listener
carries the burden of communication
3 = Mute, global aphasia; no usable speech or auditory

Acute Stroke
comprehension

Treatment
10. Dysarthria 0 = Normal
(Fig. 2) 1 = Mild to moderate; patient slurs at least some words
and at worst, can be understood with some difficulty
2 = Severe; patients speech is so slurred as to be
unintelligible in the absence of or out of proportion to
any dysphasia, or is mute/anarthric
9 = intubated or other physical barrier; explain
11. Extinction & 0 = No abnormality
Inattention 1 = Visual, tactile, auditory, spatial or personal
inattention or extinction to bilateral simultaneous
stimulation in one of the sensory modalities
2 = Profound hemi-attention or hemi-inattention to
more than one modality. Does not recognize own hand
or orients to only one side of space
*Total score=42

Fig. 1: Aphasia

Ask the patient to describe what is

happening on the picture and name items.

125
 Fig. 2: Dysarthria

Ask the patient to read or repeat words

from the list.

III. Modified Rankin Scale

Acute Stroke
Treatment

Score
No symptoms at all 0
No significant disability despite symptoms; able to carry out all
1
usual duties and activities
Slight disability; unable to carry out all previous activities but able
2
to look after own affairs without assistance
Moderate disability; requiring some help but able to walk without
3
assistance
Moderately severe disability; unable to walk without assistance
4
and unable to attend to own bodily needs without assistance
Severe disability; bedridden, incontinent and requiring constant
5
nursing care and attention
Death 6

Bibliography
1. Brott T, Adams H. Olinger CP, et al. Measurements of acute cerebral infarction: a clinical
examination scale. Stroke 1989;20:864-870.
2. Goldstein LB, Bartels C. Davis JN. Interrater reliability of the NIH Stroke Scale. Arch
Neurol 1989;46:660-662.
3. Rankin J. Cerebral vascular accidents in patients over the age of 60. Scot Med J 1957;2:200-
215.
4. Van Swieten JC, Koudstaal JP, Visser MC, et al. Interobserver agreement for the assessment
of handicap in stroke patients. Stroke 1988;19:604-607.
5. The Brain Matters Stroke Initiative. Acute Stroke Management Workshop Syllabus. Basic
Principles of Modern Management for Acute Stroke.

126
TIA and AF
 I. TRANSIENT ISCHEMIC ATTACK

Compared to previous editions of the SSP stroke guidelines, Transient Ischemic Attack (TIA) is
given a separate chapter because of the importance of diagnosing it correctly as it is a predictor
of future strokes. TIAs are often referred to as ministrokes, warning strokes, or transient
strokes because they resolve quickly. Health professionals and the public consider TIAs benign
but regard strokes as serious. These views are incorrect. Stroke and TIA are on a spectrum of
serious conditions involving brain ischemia. Both are markers of reduced cerebral blood flow
and an increased risk of disability and death. However, TIAs offer an opportunity to initiate
treatment that can forestall the onset of permanently disabling injury.1

A. Definition of TIA

The long-standing definition of TIA as focal neurologic deficit lasting < 24 hours has been
based on the assumption that TIAs are associated with complete resolution of brain ischemia
occurring rapidly enough to cause only transient symptoms and no permanent brain injury. In
contrast, ischemic stroke was thought to cause permanent injury to brain parenchyma.

The definition of TIA has been evolving with time as studies became clearer thru technological
advances particularly in neuroimaging. Relying solely on a time-based definition would not
TIA and AF

assure absence of infarcted CNS tissue among patients presenting with sudden neurologic
deficit of less than 24 hours. Studies worldwide have demonstrated that this arbitrary time
threshold was too broad because 30% to 50% of classically defined TIAs show brain injury on
diffusion-weighted magnetic resonance imaging.2

Evolving Definition of TIA

1960s (traditional definition - WHO) - sudden, focal neurologic deficit that lasts for
less than 24 hours, is presumed to be of vascular origin, and is confined to an area of the
brain or eye perfused by a specific artery. (timebased definition)

2002 (TIA working group - USA) - a brief episode of neurological dysfunction

caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than
one hour, and without evidence of acute infarction.2 (tissue-based with time based
definition)

2009 (American Heart Association - AHA) - a transient episode of neurological

dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute
infarction.3 (purely tissue-based definition)

128
The latest definition by the AHA will modestly alter stroke and TIA prevalence and incidence
rates but it will help ensure increasing accuracy of diagnosis. It is expected that a tissue-based
definition of TIA will harmonize cerebrovascular nosology with other ischemic conditions like
myocardial infarction. Most importantly, it will appropriately direct diagnostic attention to
identifying the cause of ischemia and whether brain injury has occurred. Currently, brain
imaging and probably serum diagnostic studies in the future will increase diagnostic certainty
regarding whether a particular episode of focal ischemic deficits was a TIA or a cerebral
infarction.

Aware that this handbook will be used by local physicians practicing in places with
limited access to neuroimaging facilities and fully aware of the arguments for and
against the latest definitions, the working definition for TIA agreed upon by the
Stroke Society of the Philippines and the Stroke Council of the Philippine
Neurological Associaton is as follows:

Transient Ischemic Attack - a transient episode of neurological dysfunction caused

by focal brain or spinal or retinal ischemia, without evidence of acute infarction in
which clinical symptoms typically last less than an hour (please see chapter on
overview of stroke evolving definition of stroke and TIA).

TIA and AF
B. Epidemiology

Precise estimates on the incidence and prevalence of TIAs are difficult to determine mainly
because of the varying criteria used in epidemiological studies to identify TIA. Reported 90-day
stroke risk associated with TIA reaches 10.5%, and the highest risk is apparent in the first week.
The risk is 4% to 8% in the first month, 12% to 13% in the first year, and 24% to 29% in 5 years.4-5

That TIA should be treated with urgency is due to the recognition that the risk for stroke is
particularly high in the first few days after TIA. Large cohort and population-based studies
reported in the last 5 years have demonstrated that 10 to 15% of patients have a stroke within 3
months, with one quarter to one half occurring within 48 hours.

Patients with hemispheric TIA and carotid stenosis of more than 70% have a particularly poor
prognosis, with a stroke rate of >40% in 2 years.4,5 In contrast, ischemic stroke appears to carry
a lower short-term risk of subsequent ischemic stroke than TIA, with reported 3-month risks
generally ranging from 4% to 8%.

C. Making a Diagnosis of TIA

Deciding whether a patient has TIA can be difficult because there are many TIA mimickers and
the signs have resolved before patient is evaluated. Often, patients have trouble describing their
symptoms and even among the neurologists, the inter-rater reliability is low.

129
 T IA Mi m icker s
Sim pl e an d co m ple x
pa rtia l s eizu re s R oo t /n erv e im pin ge m en t
Migra ine H y pe rgly c em ia / Hy p ogly c e m ia
Mu ltip le sc le ros is Sy n co p e
A cu t e co ron a ry Pa nic a t ta c k
sy nd rom e
Taking a detailed history and assessing the overall risk for stroke of a patient can help in arriving
at a diagnosis of TIA. Some important points in the history and symptoms may help.

Hi story not consistent w ith TI A:

Gradual build-up of symptoms (> 5 minutes)

Symptoms lasti ng <3 0 seconds
March of symptoms over several areas of the body
Evolution of symptoms from one type to another
Multiple recurrent spells over several months

Symptoms that should cast doubt for a di agnosis of TIA:

TIA and AF

Isolated v ertigo
Isolated diplopia
Isolated dysarthria
Lightheadedness or syncope
Binocular v isual loss (excluding hemianopia)
Generalized weakness
Incontinence
Sensory impairment
Amnesia
D. Assessment of Patients with Suspected TIA or Minor Stroke

The distinction between TIA and minor stroke has become less important in recent years
because many assessment and preventive approaches are applicable in both.

All patients with suspected TIA or minor stroke should have an immediate clinical evaluation
and additional investigations as required to establish the diagnosis to rule out stroke mimics and
develop a plan of care.

The use of a standardized risk stratification tool at the initial point of health care contact should
be used to guide the triage process. Because of the high risk of stroke after TIA, several risk
stratification tools have been proposed. The ABCD2 score applied at time of the TIA was
found useful in predicting risk for stroke. In combined validation cohorts, the 2-day risk of
stroke was 0% for scores of 0 or 1, 1.3% for 2 or 3, 4.1% for 4 or 5, and 8.1% for 6 or 7.7

130
 Actual Scoring System
ABCD2 Rule
Risk Factor Points
Age > 60 years 1
Blood pressure > 140/90 mm Hg 1
Clinical features
Unilateral weakness 2
Language disturbance without weakness 1
Diabetes 2
Durations > 60 min 2
Duration 10-59 min 1
Duration < 10 min 0

It is reasonable to hospitalize patients with TIA if they present within 72 hours and have an
ABCD2 score = 3, indicating high risk of early recurrence. The evaluation cannot be rapidly
completed in an outpatient basis. Close observation during hospitalization has the potential to

TIA and AF
allow more rapid and frequent administration of tissue plasminogen activator should a stroke
occur.8-9
Patients with suspected TIA or minor strokes should be referred to a physician with training in
stroke assessment and management or,if these options are not available,to an emergency
department that has access to neurovascular imaging facilities and stroke expertise.

Patients with suspected TIA or minor stroke require brain imaging with CT or magnetic
resonance imaging ( MRI). Emergent patients ( those patients classified at highest risk of
recurrent stroke)should have neurovascular imaging within 24 hours, and patients classified as
urgent should have neurovascular imaging within 7 days.

Patients who may be candidates for carotid revascularization should have computed
tomographic angiography, magnetic resonance angiography, or a carotid duplex ultrasound as
soon as possible (
within 24 hours for emergent patients,
and 7 days for urgent patients).
The following investigations should be undertaken routinely for patients with suspected
transient ischemic attack or minor stroke:complete blood count,electrolytes,renal function,
cholesterol level,
glucose level,
and electrocardiography.

D.Management of TIA

Many preventive approaches and treatments are similar for both TIA and ischemic strokes.The
risk factors for ischemic stroke and TIA are the same and the discussions on the evidences that
modification of a particular risk factor would lead to a reduction in vascular events are found in
the corresponding sections in these guidelines.

131
 Many clinical trials have demonstrated that antiplatelets reduce stroke risk after TIA or minor
stroke by 18% to 41%. RCTs on antiplatelet drugs that reduce stroke, either alone or as part of a
composite of vascular outcomes, include aspirin, dipyridamole, aspirin-dipyridamole
combination, clopidogrel, cilostazol and triflusal.6-8 Although some studies limited subjects to
those with minor strokes instead of TIA, it is reasonable to consider a similar prophylactic effect
in TIA patients.10,11 Based on cost-effective studies, aspirin remains the first option unless there
are contraindications. For guide on the choice of antiplatelets to use, please see the appendix
below on management for stroke prevention.

E. Recommendations:

Many of the recommendations given are adopted from current guidelines of the American
Heart Association and the Canadian best practice recommendations for stroke care which the
SSP deemed applicable to the local setting.3

1. Efforts to increase public awareness and that of health workers regarding TIA and its
significance should be maximized.
2. TIA should be treated with urgency due to increase risk for stroke. Patients with
suspected TIA should be evaluated as soon as possible after an event to establish the
diagnosis, rule out stroke mimics and develop a plan of care (AHA Class I, Level of
TIA and AF

Evidence B).
3. The use of standardized risk stratification tool at the initial point of health care
contact should be used to guide the triage process of how urgent workup should be
done (Evidence Level B).
4. Patients with TIA should preferably undergo neuroimaging evaluation within 24
hours of symptom onset. MRI, including DWI, is the preferred brain diagnostic
imaging modality. If MRI is not available, head CT should be performed (AHA,
Class I, Level of Evidence B).
5. Evaluation of TIA should be attempted to define cause and determine prognosis and
treatment. TIA patients should be expeditiously evaluated for vascular and cardiac
risk factors for stroke. Hypertension, hyperlipidemia, diabetes, carotid and
intracranial stenosis and other modifiable risk factors should be treated, as outlined in
these guidelines.
6. The following investigations should be undertaken routinely for patients with
suspected transient ischemic attack or minor stroke: complete blood count,
electrolytes, renal function, cholesterol level, glucose level, and electrocardiography
(Evidence Level C).
7. All risk factors for cerebrovascular disease must be aggressively managed, through
both pharmacologic and nonpharmacologic means, to achieve optimal control
(Evidence Level A). While evidence for the benefit of modifying individual risk
factors in the acute phase is lacking, there is evidence of benefit when adopting a
comprehensive approach, including antihypertensives and statin medication.
8. All patients with transient ischemic attack not on an antiplatelet agent at time of
presentation should be started on antiplatelet therapy immediately after brain
imaging has excluded intracranial hemorrhage (Evidence Level A).

132
 9. The cost and benefit of a drug should be considered when choosing an antiplatelet
agent. Aspirin is the first choice unless contraindicated. Those who cannot tolerate
or have contraindications to aspirin may be given cilostazol, clopidogrel, triflusal or
other antiplatelets.
10. While there is evidence of benefit of combined aspirin and clopidogrel in coronary
heart disease or post-revascularization patients, this combination is not
recommended for stroke prevention.
11. Patients with transient ischemic attack or minor stroke and >70% carotid stenosis on
the side implicated by their neurologic symptoms, who are otherwise candidates for
carotid revascularization, should have carotid endarterectomy performed as soon as
possible, within 2 weeks (Evidence Level A).
12. Patients with transient ischemic attack or minor stroke and atrial fibrillation should
consider anticoagulation using warfarin after brain imaging has excluded intracranial
hemorrhage, aiming for a target therapeutic international normalized ratio of 2 to 3.

Bibliography

1. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency
department diagnosis of TIA. JAMA 2000;284:2901-2906.

TIA and AF
2. Albers GW, Caplan LR, Easton JD, et al.; for the TIA Working Group. Transient ischemic attack:
proposal for a new definition. N Engl J Med 2002;347:1713-1716.
3. Easton JD, Saver JL, Albers GW et al. American Heart Association. American definition and
evaluation of transient ischemic attack: A Scientific Statement. Stroke 2009;40;2276-2293
4. Dennis M, Bamford J, Sandercock P, et al. Prognosis of transient ischemic attacks in the
Oxfordshire Community Stroke Project. Stroke 1990;21:848-853.
5. Whisnant JP, Wiebers DO. Clinical epidemiology of transient cerebral ischemic attacks (TIA) in
the anterior and posterior circulation. In: Sundt TM Jr, ed. Occlusive Cerebrovascular Disease:
Diagnosis and Surgical Management. Philadelphia, Pa: WB Saunders Co;1987:60-65.
6. Kleindorfer D, Panagos P, Pancioli A, Khoury J, Kissela B, Woo D, Schneider A, Alwell K, Jauch
E, Miller R, Moomaw C, Shukla R, Broderick JP. Incidence and short-term prognosis of
transient ischemic attack in a population-based study. Stroke. 2005;36:720 723.
7. Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, Sidney S.
Validation and refinement of scores to predict very early stroke risk after transient ischaemic
attack. Lancet. 2007;369: 283292.
8. Nguyen-Huynh MN, Johnston SC. Is hospitalization after TIA costeffective on the basis of
treatment with tPA? Neurology. 2005;65: 17991801.
9. Hacke W, Donnan G, Fieschi C, Kaste M et al. for the ATLANTIS Trials Investigators, ECASS
Trials Investigators, NINDS rt-PA Study Group Investigators. Association of outcome with
early stroke treatment: pooled analysis of ATLANTIS, ECASS, and NINDS rt-PA stroke trials.
10. Antiplatelet Trialists Collaboration. Collaborative overview of randomized trials of antiplatelet
therapy I: Prevention of death, MI, and stroke by prolonged antiplatelet therapy in various
categories of patients. BMJ 1994;308:81-106.
11. Antithrombotic Trialists Collaboration. Collaborative meta-analysis of randomized trials of
antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high-risk
patients. BMJ 2002;324:71-86.

133
 2010 ASA/AHA Recommendations for Antithrombotic Therapy
for Noncardioembolic Stroke or TIA
(Oral Anticoagulant and Antiplatelet Therapies)

1. For patients with noncardioembolic ischemic stroke or TIA, the use of

antiplatelet agents rather than oral anticoagulation is recommended to reduce
risk of recurrent stroke and other cardiovascular events ( Class I; Level A)

2. Aspirin (50 mg/d to 325 mg/d) monotherapy (Class I; Level A), the
combination of aspirin 25 mg and extended-release dipyridamole 200 mg twice
daily (Class I; Level B), and clopidogrel 75 mg monotherapy (Class IIa; Level B)
are all acceptable options for initial therapy. The selection of an antiplatelet
agent should be individualized on the basis of patient risk factor profiles, cost,
tolerance, and other clinical characteristics.

3. The addition of aspirin to clopidogrel increases risk of hemorrhage and is not

recommended for routine secondary prevention after ischemic stroke or TIA
(Class III; Level A)

4. For patients allergic to aspirin, clopidogrel is reasonable (Class IIa; Level C)

TIA and AF

5. For patients who have an ischemic stroke while taking aspirin, there is no
evidence that increasing the dose of aspirin provides additional benefit.
Although alternative antiplatelet agents are often considered, no single agent or
combination has been studied in patients who have had an event while
receiving aspirin (Class IIb; Level C)

Furie K, Scott E. Kasner SE, Adams RJ, et al. Guidelines for the Prevention of Stroke in Patients With
Stroke or Transient Ischemic Attack : A Guideline for Healthcare Professionals From the American Heart
Association/American Stroke Association ( Stroke. 2011;42:00-00 draft )

2008 European Stroke Organization Guidelines

in the Management of Ischemic Stroke

Secondary Stroke Prevention

It is recommended that patients receive antithrombotic therapy

It is recommended that patients not receiving anticoagulation should receive

antiplatelet therapy (Class I Level A). Where possible, combined ASA and
dipyridamole or clopidogrel alone should be given. Alternatively, Aspirin alone or
triflusal alone may be used (Class I Level A)

134
 The combination of Aspirin and clopidogrel is not recommended in patients with
recent ischemic stroke, except in patients with specific indications (unstable angina
or non-Q wave MI, or recent stenting) (Class I Level A)

It is recommended that patients who have a stroke on antiplatelet therapy be re-

evaluated for pathophysiology and risk factors

Oral anticoagulation (INR 2 3) is recommended after ischemic stroke associated

with atrial fibrillation (Class I Level A). Oral anticoagulation is not recommended
in patients with co-morbid conditions such as falls, poor compliance, uncontrolled
epilepsy, GI bleeding (Class III Level C). Increasing age alone is not a
contraindication to oral anticoagulation (Class I Level A)

It is recommended that patients with cardioembolic stroke unrelated to atrial

fibrillation should receive anticoagulants if the risk of recurrence is high (Class III
Level C)

Major Trials Using Antiplatelets for Secondary Stroke Prevention

TIA and AF
Drug Trial Design Result
23% odds reduction in the
65 trials involving composite outcome of MI,
Antiplatelet Trialist 60,196 patients with stroke or vascular death
Aspirin

Collaboration symptomatic
(ATC, BMJ 2002; atherosclerosis Highest relative risk reduction
324: 71 86) Aspirin dose 50 1500 was seen in the low (75-150
mg/day mg) and medium dose (160
325 mg) group
Canadian
1,072 patients with
American Ticlopidine reduced the risk of
recent thromboembolic
Ticlopidine Study composite outcome of MI,
stroke were randomized
(CATS, Lancet stroke and vascular death by
to Ticlopidine 250 mg
Ticlopidine

1989; 1: 1215 30 %
bid or placebo
1220)
3,069 patients with Ticlopidine reduced the risk of
Ticlopidine
recent TIA or recent stroke or death at 3 years by
Aspirin Stroke
cerebral infarction were 12% relative to aspirin
Study (TASS,
randomized to
N Eng J Med 1989;
ticlopidine 250 mg BID Neutropenia was more
501-507)
or Aspirin 1300 mg/day common with Ticlopidine

135
 Drug Trial Design Result
At 1.6 years, Clopidogrel
Clopidogrel vs 19,185 patients with reduced the combined
ASA at Risk of atherosclerotic disease endpoint of ischemic stroke,
Ischemic Events were randomized to MI or vascular death by 8.7%
(CAPRIE, Lancet Clopidogrel 75 relative to Aspirin
1996; 348: 1329 mg/day or Aspirin
1339) 325 mg/day Benefit was greatest in patients
with PAD
No significant difference
between groups in the
Management of 7,599 patients with
combined endpoint of
Atherothrombosis prior stroke or TIA
ischemi c stroke, MI, vascular
with Clopi dogrel and additional risk
death or re -hospitalization at
in High Risk factors were
18 months (Clopidog rel plus
Patients with TIA randomized to
ASA 15.7% vs Clopidogrel
Clopidogrel

or Stroke Clopidogrel 75 mg -
TIA and AF

16.7%, RRR 6.4% p > 0.05))

(MATCH, Lancet Aspirin 75 mg
2004; 364; 331 combination or
There was significant incr ease
337) Clopidogrel 75 mg
in major bleeding with
combination treatment
Overall, Clopidogrel plus
15, 603 pati ents with Aspirin was not significantly
either clinically more effective than Aspirin
Clopidogrel for
evident cardiovascular alone in reducing rate of MI,
High
disease (secondary stroke or vascular death
Atherothrombotic
prevention group) or
Risk and Ischemic
with multiple risk There was suggestion of
Stabilizati on,
factors (primary benefit of combination
Management and
prevention group) treatment among patients with
Avoidance
were randomized to symptomatic atheroscl erotic
(CHARISMA, N
Clopidogrel 75 mg disease
Eng J Med 2006;
with low dose Aspirin
354 : 1-12)
75 162 mg or low There was significant incr ease
dose Aspirin alone in major bleeding with
combination treatment

136
Drug Trial Design Result

Cilostazol Stroke 1,095 patients with

Prevention Study cerebral infarction in Active treatment with
(CSPS, J Stroke the past 6 months were Cilostazol reduced the risk of
Cerebrovasc Dis randomized to recurrent ischemic stroke by
2000; 9 : 147 Cilostazol 100 mg BID 41.7%
157) or placebo
135 patients with recent
ischemic stroke within 2
Trial of Cilostazol weeks due to Progression of symptomatic
in Symptomic symptomatic MCA or intracranial stenosis by MRA
Cilostazol

Intracranial Basilar artery stenosis was significantly lower with

Arterial Stenosis by MRI/MRA were Cilostazol and Aspirin
(TOSS I, Stroke randomized to compared with Aspirin alone
2005; 36: 782 Cilostazol 100mg BID

TIA and AF
786) plus Aspirin 100 mg or
Aspirin 100 mg a day
for 6 months
Yearly occurrence of stroke
(Infarction, ICH and
2757 patients with Subarachnoid hemorrhage)
cerebral infarction was 2.76 % in the Cilostazol
CSPS 2, Lancet, within the previous 26 group vs 3. 71% in the Aspirin
published online weeks were randomized group
Sept 11, 2010) to Cilostazol 100 mg
BID or Aspirin 81 mg a Hemorrhagic events occurred
day for 1 5 years less but headache, tachycardia,
diarrhea were more frequent in
the Cilostazol treated group

137
 Drug Trial Design Result
2,500 patients with
European Stroke strokes or TIAs were Active treatment with Aspirin
Prevention Study 1 randomized to Aspirin and Dipyridamole reduced the
(ESPS 1, Lancet 975 mg plus risk of stroke and death by
1987; 2: 325: 1261) Dipyridamole 225 33%
mg/day or placebo

Stroke reduction compared to

6,602 patients with
placebo were: Aspirin (18%),
recent TIA or stroke
European Stroke ER-DP (16%), Aspirin plus
were randomized to
Prevention Study 2 Dipyridamole (37.8%)
Dipyridamole

Aspirin 25 mg BID,
(ESPS 2, J Neuro
extended release
Sci 1996: 143:1 - There was no increased risk of
Dipyridamole 200 mg
13) major bleeding with
BID or both or
combination treatment
placebo X 2 years
TIA and AF

Composite outcome of stroke,

European / 2,739 patients with
MI and death were reduced by
Australasian recent TIA or minor
20% with ASA plus
Stroke Prevention stroke were
dipyridamole relative to aspirin
in Reversible randomized to Aspirin
alone
Ischemia Trial 30 325 mg/day plus
(ESPRIT, Lancet Dipyridamole 200 mg
There was no increased risk of
2006; 367:1665 BID or Aspirin 30
major bleeding with
1673) 325 mg alone
combination treatment

Prevention Similar rates of recurrent

ASA-Dipyridamole

20,332 patients with

Regimen for ischemic stroke at median ff
recent stroke within
Clopidogrel vs

Effectively up of 2.5 years between groups

past 120 days were
Avoiding Second (ASA-ER DP 9% and
randomized to aspirin
Strokes Clopidogrel 8.8 %)
25 mg plus ER-DP
(PROFESS, N
200 mg twice a day or
Eng J of Med There were more major
Clopidogrel 75
2008; 359: 1238 hemorrhagic events with ASA-
mg/day
1251) DP 4.1 % vs Clopidogrel 3.6%

138
 Drug Trial Design Result

Similar efficacy between

2,113 patients with groups in combined endpoint
recent TIA or of stroke, MI and vascular
Triflusal Aspirin
ischemic stroke within death (Aspirin 12.4% vs
Cerebral Infarction
the past 6 months Triflusal 13.1%)
Prevention
were randomized to
(TACIP, Stroke
Triflusal 600 mg/day Triflusal was associated with
2003; 34: 840
or Aspirin 325 significantly less risk of
848)
Triflusal

mg/day for median ff hemorrhagic complications

up of 30 months (any minor and any cerebral
or major hemorrhages)

No significant difference in
431 patients with
Triflusal vs Aspirin combined endpoint of stroke,
recent TIA or
in the Prevention MI vascular death & major
ischemic stroke within
of Infarction: A bleeding between groups
the past 6 months
Randomized (Aspirin 13.9 % vs Triflusal
were randomized to
Stroke Study 12.7%)

TIA and AF
Triflusal 600 mg/day
(TAPIRSS,
or Aspirin 325 mg
Neurology 2004: 62: Triflusal was associated with
/day for median ff up
1073 1080) significantly less overall risk of
of 28 months
hemorrhagic complications
2,206 patients with a
Warfarin-Aspirin
prior non-
Recurrent Stroke No difference between groups
cardioembolic stroke
Study in recurrent ischemic stroke or
Warfarin vs Aspirin

were randomized to
(WARSS, N Eng J death at 2 years (Warfarin
warfarin (INR 1.4
Med 2001: 345: 17.8% vs Aspirin 16%)
2.8) or Aspirin 325
1444 1451)
mg/day
Patients with stroke or
Warfarin-Aspirin
TIA caused by 50
in Symptomatic
99% stenosis of a No significant difference in 2
Intracranial
major intracranial year ischemic stroke rates
Disease (WASID-
artery were between groups (Warfarin 17.2
Prospective, N
randomized to dose % vs Aspirin 19.7%)
Eng J Med 2005;
adjusted warfarin or
65: 859 - 864)
Aspirin 1300 mg/day
Bibliography
1. Albers GW, Amarenco P, Easton JD, et al. Antithrombotic and thrombolytic therapy for
ischemic stroke. The Seventh ACCP Conference on Antithrombotic and Thrombolytic
Therapy. Chest 2004;126 (3 suppl):483S-512S
2. Algra A, van Gijn J. Aspirin at any dose above 30 mg offers only modest protection after
cerebral ischemia. J Neurol Neurosurg Psychiatry 1996;60:197-199.

139
 3. Antithrombotic Trialist Collaboration, Collaborative meta-analysis of randomized trials of
antiplatelet therapy for prevention of death, myocardial infarction and stroke in high-risk
patients. BMJ 2002;324:71-86.
4. Bhatt D, Fox K, Hacke W, et al; for the CHARISMA Investigators. Clopidogrel and aspirin alone
for the prevention of atherothrombotic events. N Eng J Med 2006;354:1-12.
5. CAPRIE Steering Committee. A randomized, blinded trial of clopidogrel vs aspirin in patients
at risk of ischemic events. Lancet 1996:348:1329-1339.
6. Diener HC, Cunha L, Forbes C, et al. European Stroke Prevention Study 2. Dipyridamole and
aspirin in the secondary prevention of stroke. J Neurol Sci 1996;143:1-13.
7. Diener HC, Bogousslavsky J, Brass LM, et al; for the MATCH Investigators. Aspirin and
clopidogrel compared with clopidogrel alone after recent ischemic stroke or TIA in high risk
patients (MATCH): a randomized, double- blind, placebo- controlled trial. Lancet
2004;364:331-337.
8. Gent M, Blakely JA, Easton JD, et al. The Canadian American Ticlopidine Study (CATS) in
thromboembolic stroke. Lancet 1989;1:1215-1220.
9. Gotoh F, Tohgi H, Hirai S, et al. Cilostazol Stroke Prevention Study: a placebo controlled trial
double-blind trial for secondary prevention of cerebral infarction. J Stroke Cerebrovasc Dis
2000;9:147-157.
10. Halkes PH, van Gijn J, Kappelle LJ, et al; for the ESPRIT Study Group. Aspirin plus
dipyridamole versus aspirin alone after cerebral ischemia of arterial origin. Lancet
2006;367:1665-1673.
11. Hass WK, Easton JD, Adams HP, et al. A randomized trial comparing ticlopidine hydrochloride
with aspirin for the prevention of stroke in high-risk patients. N Eng J Med 1989;321:501-507.
TIA and AF

II. ATRIAL FIBRILLATION

A. Epidemiology, Consequences and Risk Factors of Stroke in Patients with AF:

Without preventive treatment, approximately 1 in 20 patients or 5% with AF will have a stroke

each year. When transient ischemic attacks and clinically silent strokes are considered, the rate
of ischemic stroke associated with non-valvular AF exceeds 7% per year.1 AF is responsible for
15% of all strokes, and it is the leading cause of embolic stroke.2 Non-valvular atrial fibrillation
(NVAF) alone is associated with a 3- to 4-fold increase in risk of stroke after adjustment for
other vascular risk factors.3 AF in those with valvular heart disease especially rheumatic in
origin is discussed in the section on Valvular Heart Disease.

Stroke is a serious consequence and complication of AF. AF stroke is associated with increased
morbidity and mortality and is usually more severe than stroke due to other causes.4 The
mortality rate for patients with AF is double compared to those with normal heart rhythm.2

The risk of stroke varies widely from patient to patient as it depends on a range of factors.5 The
absolute risk of stroke varies 20-fold among AF patients according to age and associated
vascular disease.6 Several stroke riskstratification schemes have been developed but the only
one validated and most used has been the 2001 American College of Cardiology (ACC)/AHA/
European Society of Cardiology (ESC) guideline which recommended the so-called CHADS2
stratification scheme.6 CHADS2 is an acronym for congestive heart failure, hypertension, age

140
>75 years, diabetes mellitus, and prior stroke or TIA.5 These risk factors are shown on Table 1
with their individual relative risk for stroke in patients with non-valvular atrial fibrillation
(NVAF). The CHADS2 scores correspond to the number of risk factors present and these
scores in turn have the corresponding adjusted stroke risk as shown in Table 2.5,6,7 A
refinement to this is the CHA2DS2VASc8 shown in Table 3.

Table 1: CHADS2 Risk Factors, Estimated Relative Risk for Stroke

and CHADS2 Scoring

Re lativ e CHADS 2
ri sk for S coring
stroke
C onge stive hea rt failure (C ) 1.4 1
H ist ory of hyperte nsion(H) 1.6 1
Inc re asing a ge (A) 1.4 1
D iabet es (D) 1.7 1
Previous st ro ke or t ransient isch emic attac k( S2) 2.5 2

TIA and AF
Table 2: Stroke Risk Estimation using Total CHADS2 Scoring

Total Adjusted stroke risk

CHADS2 score in %/yr (95% CI) Risk Level NNT
0 1.9 (1.23.0) Low =100

1 2.8 (2.03.8) Low =100

2 4.0 (3.15.1) Intermediate

3 5.9 (4.67.3) Intermediate

4 8.5 (6.311.1) High =25

5 12.5 (8.217.5) High =25

6 18.2 (10.527.4) High =25

141
 Table 3: CHA2DS2VASC score and Stroke Rate

(a) Risk factors for stroke and thrombo-embolism in non-valvular AF

Major risk factor Clinically relevant non-major risk factors
Heart failure or moderate to
severe LV systolic dysfunction
Previous stroke, TIA, (e.g. LV EF < 40%)
or systemic embolism Hypertension - Diabetes mellitus
Age > 75 years Female sex - Age 6574 years
Vascular diseasea

(b) Risk factor-based approach expressed as a point based scoring system, with the acronym
CHA2DS2-VASc (Note: maximum score is 9 since age may contribute 0, 1, or 2 points)
Risk factor Score
Congestive heart failure/LV dysfunction 1
Hypertension 1
Age >75 2
Diabetes mellitus 1

Stroke/TIA/thrombo-embolism 2
1
TIA and AF

Vascular disease a

Age 6574 1
Sex category (i.e. female sex) 1
Maximum score 9
(c) Adjusted stroke rate according to CHA2 DS2-VASc score
CHA2 DS2 -VASc score Patients (N=7329) Adjusted stroke rate (%/year) b
0 1 0%
1 422 1.3%
2 1230 2.2%
3 1730 3.2%
4 1718 4.0%
5 1159 6.7%
6 679 9.8%
7 294 9.6%
8 82 6.7%
9 14 15.2%

a Prior myocardial infarction, peripheral artery disease, aortic plaque. Actual rates of stroke in
contemporary cohorts may vary from these estimates. b Based on Lip et al. AF = atrial
fibrillation; EF =ejection fraction (as documented by echocardiography, radionuclide
ventriculography, cardiac catheterization, cardiac magnetic resonance imaging, etc.); LV left
ventricular; TIA transient ischaemic attack.

142
B. Risk Modification: Its Safety and Limitations

In 2007, a meta-analysis of antithrombotic therapy for SPAF was conducted. Its objective was
to characterize the efficacy and safety of anticoagulants and antiplatelet agents for SPAF. All
published randomized trials of antithrombotic therapy for SPAF with a mean follow-up of 3
months were included and 29 trials were identified involving a total of 28,044 participants and
mean follow-up of 1.5 years. Treatment comparisons included: warfarin vs. placebo (6 trials;
N=2900), aspirin vs. placebo (7 trials; N=3990) and warfarin vs. aspirin (8 trials; N=3647).9

Table 4 shows the six key randomized controlled studies in the prevention of stroke in AF. They
pointed out that warfarin reduced the risk of stroke by 64% compared to placebo, that it was
better than aspirin in reducing thromboembolism and stroke by 38% and that aspirin (ASA) had
only limited efficacy of 19% reduction of stroke compared to placebo.9 Of these studies, all
were for primary prevention with only EAFT that showed secondary prevention with warfarin.
To achieve the beneficial effect of anticoagulation, the international normalized ratio (INR)
should be from 2 to 3 and at a higher intensity of anticoagulation of 2.5 to 3.5 for those with
mechanical prosthetic valve.10

TIA and AF
Table 4: Reductions in thromboembolic risk with warfarin compared with placebo11

Annual Rate
Primar y RRR
Study P-value
Outcome Warfarin Pl acebo (%)

Primary Prevention
AFASAK S, NSE, TIA, ICB 2.7 6.2 56 <0.05
SPAF S, NSE 2.3 7.1 67 0.01
BAATAF S 0.4 3.0 86 0.002
CAFA S, NSE, ICB, FB 3.4 4.6 26 0.25
SPINAF S 0.9 4.3 79 0.001

Seco ndary
Prevention
S, NSE, MI VD 8.5 16.5 47 0.001
EAFT

FB=fatal bleed; ICB=intracranial bleed; MI=myocardial infarction; NSE=non-CVS systemic

embolism; RRR=relative risk reduction; S=ischemic stroke; TIA=transient ischemic attack;
VD=vascular death

For better utilization of warfarin, table 5 details the guidelines in achieving therapeutic
range.12

143
 Table 5: Guidelines in achieving therapeutic range of warfarin

INR ACTION
<1.5 Increase weekly dose by 10-20 %
Consider giving one extra dose
Retest INR in 4-8 days or per I nvestigator discretion
1.5 to <2.0 Increase weekly dose by 5-10%
Retest INR in 7-14 days or per I nv es tigator discretion
2.0 to 3.0 No change
>3.0 to 3.5 Decrease weekly dose by 0-20%
Retest INR per Inv es tigator discreti on

>3.5 to 4.0 Withhold 0-1 doses and/or

Decrease weekly dose by 0-20%
Retest INR per Inv es tigator discreti on
>4.0 but <5.0 Withhold 1-2 doses and
Decrease weekly dose by 0-20% and
Retest INR in 3-7 days or per I nvestigator discretion
5.0 to <9.0 without Withhold 1-2 doses
significant bleeding Retest INR in 1-2 days or per I nvestigator discretion
TIA and AF

Res ume dosing once I NR <3 .0, but week ly dose

decreas ed by 5-20%
If the subject needs urgent surgery, then the subject
should receive Fresh Frozen Pl asma (FFP)
If necess ary, contact TIMI HOTLINE (US/Canada:
1-866 -480-173 4; other countries: +1 -6 17-278-0 900;
Emai l: timiengage@ partners.org) for cons ultation
>9.0 without Withhold study drug
significant bleeding Give Vitamin K(single 2.5-5mg oral dos e)
Repeat INR test daily until INR <5.0
If I NR remains too high, more Vitami n K dos es can be
considered
Res ume dosing once I NR <3 .0, but week ly dose
decreas ed by 10-20%
If the subject needs urgent surgery, then the subject
should receive Fresh Frozen Pl asma (FFP)
If necess ary, contact TIMI HOTLINE (US/Canada:
1-866 -480-173 4; other countries: +1 -6 17-278-0 900;
Emai l: timiengage@ partners.org) for cons ultation

The trade-off in the use of warfarin is bleeding. The risk factors for this are shown in table 6
with their corresponding individual scores.13 These in turn determine the risk level from low to
high. It is the balancing of the stroke prevention and bleeding that guides the physician in the
decision to anticoagulate. The risk factors for bleeding uses the acronym hemorrhages which
include hepatic or renal disease, ethanol use, malignancy, older age >75, reduced platelet count

144
or function, re-bleeding, uncontrolled hypertension, anemia, genetic factors, elevated risk of
fall and stroke. All these factors carry a score of 1 each except 2 for stroke. A total score of 0-1
has low risk level, 2-3 score was intermediate and >=4 total score was high risk. A newer risk
assessment for bleeding uses the acronym HAS BLED14 and shown in Table 7.

Table 6: HEMORR2HAGES Risk Criteria

Score
Hepatic or renal disease 1
Ethanol use 1
Malignancy 1
Older (age > 75) 1 Total score Risk lev el
Reduced platelet count or function 1 01 Low
Re-bleeding 2 23 I ntermediate
Hypertension, uncontrolled 1 4 High
Anemia 1
Genetic factors 1

TIA and AF
Elev ated ris k of fall 1
Stroke 1

Table 7: Clinical Characteristics Comprising the HAS BLED Bleeding Risk Score

Letter Clinical cha racteristic Points awarded

H Hypertension 1
A Abnormal renal and liv er function (1 point each) 1 or 2
S Stroke 1
B Bleeding 1
L Labile INRs 1
E Elderly (e.g. age >65 years) 1
D Drugs or alcohol (1 point each) 1 or 2
Maximum 9 points

Based on the prevention of stroke and attendant bleeding, for those with low risk of stroke at
2% per year, aspirin is recommended. Oral anticoagulation with vitamin K antagonist (VKA)
like warfarin is unlikely to be beneficial compared with aspirin. For those with intermediate risk
of stroke at 35% per year, opinion is divided as to whether VKAs should be used routinely or
selectively based on bleeding risk and patient preference. For those with high risk of stroke at
6% per year, warfarin is strongly favored over aspirin.

145
 Limitations of Warfarin and Alternatives

With the well-known benefits of warfarin however, it has a lot of limitations.15,16 Many patients
with AF do not receive effective prophylaxis against thromboembolism due to limitations of
currently available agents. Aspirin is convenient to use but provides insufficient protection for
stroke prevention in high-risk patients. Vitamin K antagonists (VKAs) like warfarin have
greater efficacy but the range of limitations make them challenging agents to use due to their
narrow therapeutic window, variable & unpredictable pharmacokinetics & pharmacodynamics,
wide variety of drugdrug and drugfood interactions, need for and cost of regular
anticoagulation monitoring and dose adjustments, and slow onset and offset of action.

As alternatives, three groups of antithrombotic agents have been considered, namely, direct
thrombin inhibitors, cyclo-oxygenase inhibitors and direct Factor Xa inhibitors. Of these, the
1st two have been studied in randomized controlled studies. Oral thrombin inhibitor-dabigatran
was studied in RE-LY in over 18,000 patients with NVAF and at risk for stroke. Results showed
that Dabigatran 150 mg twice a day was superior in reducing stroke compared to warfarin with
similar risk of major bleeding. On the other hand, dabigatran 110 mg twice a day had a similar
rate of stroke as warfarin but with significantly better reduction in major bleeding. Both doses
markedly reduced intra-cerebral, life-threatening and total bleeding. Dabigatran had no major
toxicity, but did increase dyspepsia and GI bleeding.17
TIA and AF

Cyclo-oxygenase inhibitor triflusal had several studies but only a few were randomized and
controlled and the treatment groups were small. In the study NASPEAF with a total population
of 1209 patients with NVAF and AF with mitral stenosis, the combined antiplatelet triflusal plus
moderate-intensity anticoagulation therapy had significantly better reduction in cardiovascular
events and stroke compared with anticoagulation alone. The combination was also proven to
be safe.18

Studies on factor Xa inhibitors like apixaban (ARISTOTLE, AVERROES), rivaroxaban

(ROCKET-AF), Edoxaban (ENGAGE-AF) and others are still ongoing and appear to be
promising.

C. Recommendations:

1) Estimating the risk of stroke for individual AF patients is important for the selection
of antithrombotic therapy. The validated CHADS2 scoring system can be used to
estimate the risk of stroke per year. A refinement to this is the CHA2DS2VASc.

Included are other less established indications.

For those with low risk of stroke at <2% per year like those with AF and with age less
than 65 years, no hypertension, diabetes, TIA, stroke or other clinical factors, oral
anticoagulation with vitamin K antagonists (VKA) like warfarin is unlikely to be
beneficial compared to aspirin. Thus aspirin may be used or none at all.

146
 For those with intermediate risk of stroke at 3-5% per year like those with AF with
age <65 with hypertension or diabetes mellitus or age of >65 years and not in the
high risk group, opinion is divided as to whether VKAs should be used routinely.
Here, one may use aspirin or warfarin selectively based on bleeding risk and patient
preference.

For patients with high risk for stroke at >6% per year like those with AF and with age
>65 with hypertension or diabetes, previous TIA or stroke, valvular heart disease,
heart failure, recent myocardial infarction, impaired left ventricular function on 2D-
Echo, thyroid disease and presence of left atrial thrombus, VKAs like warfarin are
strongly favored over aspirin.

2) Warfarin with INR of 2.0 to 3.0 is recommended for patients with atrial fibrillation
who have >4% annual risk of stroke (CHADS score of > 2) provided there is no
clinically significant contraindication to oral anticoagulants (Class IA).
3) For patients with high risk like in those with mechanical prosthetic valve, higher
intensity of anticoagulation achieved by adjusting warfarin dose is recommended to
be at INR of 2.5-3.5. (Class IA).
4) For patients unable to take oral anticoagulants, aspirin 325 mg/d is recommended
(Class IA). Although combined treatment with clopidogrel and ASA is superior to

TIA and AF
ASA alone in reducing rate of stroke, the problem with dual antiplatelet is greater
bleeding risk compared to ASA alone.19,20,21,22,23
5) For patients who prefer an anticoagulant least affected by food and medicines with
better pharmacokinetics, pharmacodynamics and half-life and in which prothrombin
time determination is not needed, an option can be the oral thrombin inhibitor
dabigatran, but it costs more. (Class IB)
6) Among patients with AF and high risk of thromboembolism, the addition of the
antiplatelet agent triflusal to reduced-intensity oral anticoagulation is a valid option.
(Class 1 B)

Bibliography

1. Atrial Fibrillation Investigators. Atrial fibrillation: warfarin reduces the risk of stroke and death.
Archives of Internal Medicine 1994;154:1449-57
2. Benjamin et al. Impact of atrial fibrillation on the risk of death: The Framingham Heart Study.
Circulation 1998;98:946-52
3. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke.
The Framingham Study. Stroke 1991:22;983-988
4. Savelieva I et al. Stroke in atrial fibrillation: Update on pathophysiology, new antithrombotic
therapies, and evolution of procedures and devices. Ann Med 2007;39:37191
5. AF Investigators. Risk factors for stroke and efficacy of antithrombotic therapy in atrial
fibrillation: Analysis of pooled data from five randomized controlled trials.Arch Intern Med
1994;154:1449-57
6. Gage BF et al. Validation of clinical classification schemes for predicting stroke. Results for
national registry of AF. JAMA 2001;285:286470

147
 7. Fuster V et al. ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial
fibrillation Circulation 2006;114:e257354
8. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijins HJ. Refining clinical risk stratification for
predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based
approach: The Euro Heart Survey on atrial fibrillation. Chest 2010;137:263-272
9. Hart RG et al. Antithrombotic therapy for atrial fibrillation stroke risk reduction. Ann Intern
Med 2007;146:85767
10. Hylek EM et al. Effect of intensity of oral anticoagulation on stroke severity and mortality in
atrial fibrillation. New England Journal of Medicine 349;13:2003
11. Albers GW et al. Antithrombotic therapy in atrial fibrillation;Chest 2001;119:194S-206S
12. Warfarin table
13. Gage BF et al. Clinical classification schemes for predicting hemorrhage: results from the
National Registry of atrial fibrillation (NRAF). Am Heart J 2006;151:7139
14. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijins HJ, Lip GY. A novel user-friendly score
(HAS-BLED) to assess one year risk of major bleeding in atrial fibrillation patients: The Euro
Heart Survey. Chest 2010; Mar 18 (Epub ahead of print)
15. Turpie AG. New oral anticoagulants in atrial fibrillation. Eur Heart J 2008;29:15565
16. Khoo CW et al. Novel oral anticoagulants. Int J Clin Pract 2009;63:63041
17. Connolly SJ, Yusuf Salim, Wallentin Lars et al and the Re-Ly Steering Committee and
Investigators. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med Sept
17 2009 vol 361 #12; 1139-1151
TIA and AF

18. Perez-Gomez, F, Mataix, L et al for the NASPEAF Investigators. Comparative effects of

antiplatelet, anticoagulant, or combined therapy in patients with valvular and nonvalvular atrial
fibrillation. JACC 2004;44:1557-66
19. Connolly SJ et al. Challenges of establishing new antithrombotic therapies in atrial fibrillation.
Am Heart J 2006;151:11871193
20. ACTIVE Investigators. Clopidogrel plus aspirin versus oral anticoagulation for atrial fibrillation
in the Atrial fibrillation Clopidogrel Trial with Irbesartan for prevention of Vascular Events
(ACTIVE W): A randomised controlled trial. Lancet 2006;151:190312
21. ACTIVE Investigators. Effect of clopidogrel added to aspirin in patients with atrial fibrillation.
N Engl J Med 2009;360:206678
22. ACTIVE W- 12, ACTIVE A- 13, Chinese ATAFS-ATAFS Group. Zhonghua Xin Xue Guan
Bing Za Zhi 2006;34:295-8
23. JAST- Sato et al. Japan Atrial Fibrillation Stroke Trial Group. Low-dose aspirin for prevention
of stroke. Stroke 2006;37:447-51

148
Hemorrhagic
Stroke
 INTRACRANIAL HEMORRHAGE

Intracranial hemorrhage results from the rupture of a vessel anywhere within the cranial cavity.
Intracranial hemorrhages are classified according to location (e.g., extradural, subdural,
subarachnoid, intracerebral, intraventricular), according to the nature of the ruptured vessel or
vessels (e.g., arterial, capillary, venous), or according to cause (e.g., primary, secondary).
Bleeding into subdural and epidural spaces is principally produced by trauma. SAHs are
produced by trauma and rupture of intracranial aneurysms or AV malformations.
Intraparenchymal and intraventricular hemorrhage are most often related to hypertension.
Trauma is often involved in the generation of extradural hematoma from laceration of the
middle meningeal artery or vein, and subdural hematomas from traumatic rupture of veins that
traverse the subdural space. This chapter will not be discussing trauma related intracranial
hemorrhages.

Intracerebral Hemorrhage

The worldwide incidence of ICH ranges from 10 20 cases per 100,000 population and
increases with age. ICH accounts for 20% of the stroke subtypes and the remaining 80% are
ischemic strokes. Recent studies involving the Asian population can account for as much as
30% of all strokes, particularly in Japanese and Koreans.

Intracerebral hemorrhage is characterized by bleeding into the substance of the brain, usually
originating from a small penetrating artery. Hypertension has been implicated as the cause of
weakening in the walls of arterioles and the formation of microaneurysms (Charcot-
Brouchard). Among elderly, nonhypertensive patients with recurrent lobar hemorrhages,
amyloid angiopathy has been implicated as an important cause. Other causes include
Hemorrhagic

arteriovenous malformations, aneurysms, moyamoya disease, bleeding disorders

Stroke

anticoagulation, trauma, tumors, cavernous angiomas, and illicit-drug abuse. In blood

dyscrasias (e.g., acute leukemia, aplastic anemia, polycythemia, thrombocytopenic purpura,
scurvy), the hemorrhages may be multiple and of varied size.

The arterial blood ruptures under pressure and destroys or displaces brain tissue. If the
hemorrhage is large, the ruptured vessel is often impossible to find at autopsy. The most
common sites for arterial hemorrhage are the putamen, caudate, pons, cerebellum, thalamus, or
deep white matter. Basal ganglia hemorrhages often extend to involve the internal capsule and
sometimes rupture into the lateral ventricle, spreading through the ventricular system into the
subarachnoid space.

Intraventricular extension increases the likelihood of a fatal outcome. Bleeding into one lobe of
the cerebral hemisphere or cerebellum usually remains confined within brain parenchyma. An
inferior cerebellar hemorrhage is a neurologic emergency that needs to be diagnosed promptly,
because early surgical evacuation of those hemorrhages of greater than 3 centimeters in
diameter may prevent tonsillar herniation and apnea.

150
If the patient survives an intracerebral hemorrhage, blood and necrotic brain tissue are removed
by phagocytes. The destroyed brain tissue is partially replaced by connective tissue, glia, and
newly formed blood vessels, thus leaving a shrunken fluid-filled cavity. Less frequently, the
blood clot is treated as a foreign body, calcifies, and is surrounded by a thick glial membrane.
Clinical Manifestations
The clinical picture is dictated by the location and size of the hematoma. It is usually
characterized by headache, vomiting, and the evolution of focal motor or sensory signs over a
period of minutes to hours. Among the moderate and large hematomas, consciousness is
sometimes impaired at the start, and often becomes a prominent feature in the first 24 to 48
hours. Patients with intracerebral hemorrhage are often younger than stereotypic stroke
patients, and in some series the condition was seen more frequently in men. The diagnosis and
localization are established easily with CT, which typically shows the high density of acute
blood.
Hypertensive intraparenchymal hemorrhage (hypertensive hemorrhage or hypertensive
intracerebral hemorrhage) usually results from spontaneous rupture of small penetrating
branches deep in the brain originating from the major cerebral arteries in the circle of Willis.
The most common sites are the basal ganglia, especially the putamen and adjacent internal
capsule 50%, thalamus 15%, cerebellar hemispheres 10%, pons 10% and lobar (central white
matter of the temporal, parietal or frontal lobes) 15%. Those in the putamen originates from
the ascending lenticulostriate branches of the MCA, those in the thalamus originates from the
ascending thalamogeniculate branches of the PCA, the pons in the paramedian branches of the
basilar artery and the cerebellum originates from the penetrating branches of the PICA, AICA
and SCA
When hemorrhages occur in other brain areas or in nonhypertensive patients, greater
consideration should be given to hemorrhagic disorders, neoplasms, vascular malformations,

Hemorrhagic
and other causes. The hemorrhage may be small or a large clot may form and compress adjacent
tissue, causing herniation and death. Blood may dissect into the ventricular space, which

Stroke
substantially increases morbidity and may cause hydrocephalus.
Most hypertensive intraparenchymal hemorrhages develop over 3090 min, whereas those
associated with anticoagulant therapy may evolve for as long as 2448 h. Within 48 h
macrophages begin to phagocytize the hemorrhage at its outer surface. After 16 months, the
hemorrhage is generally resolved to a slitlike orange cavity lined with glial scar and hemosiderin-
laden macrophages.
The major issues of therapy in patients with intracerebral hemorrhages are:
Enlargement of the hematoma within 24 48 hours.
Prevention of continued hemorrhage by early correction of coagulation and platelet
abnormalities.
Early control of elevated BP.
Identification and control of urgent surgical issues such as threatening mass effect,
intracranial hypertension.
Definitive diagnosis of the cause of the hemorrhage and definitive treatment of the
underlying cause.

151
 I. HYPERTENSIVE INTRACEREBRAL HEMORRHAGE

Early Specific Treatment of Hypertensive Intracerebral Hemorrhage

A. Medical Treatment for all ICH:

The goals are to prevent complications and careful management of BP.

a) Monitor and maintain MAP 110 mmHg or SBP 160. Recent studies have
shown that target lowering to SBP =140 is probably safe but clinical efficacy remains
to be determined.
b) Manage increased ICP accordingly (see section on ICP management)
c) Provide the appropriate treatment for bleeding abnormalities

1) Administer factor replacement (factor VII or platelet concentrates in patients

with severe coagulation factor deficiency or severe thrombocytopenia. (1c - new
recommendation)
2) For warfarin-related ICH, stop warfarin. Give IV Vit K and correct INR with
fresh frozen plasma (FFP).

d) Give anticonvulsants for clinical seizures and proven subclinical or electrographic

seizures. EEG monitoring should be considered in ICH patients with depressed
mental status out of proportion to the degree of brain injury.

The use of prophylactic AEDs is not recommended.

e) Prevent and treat respiratory complications. Endotracheal intubation & assisted

ventilation is performed in patients in coma to provide airway protection or those
with respiratory failure (defined as SPO2 of less than 90% by pulse oximeter and
Hemorrhagic

PaO2 <8kPa (60mmHg), and/or PaCO2 >7kPa (55mmHg) by arterial blood gas
Stroke

analysis).
f) Prevent and treat infections.
g) Maintain adequate nutrition.
h) Ensure proper fluid and electrolyte balance.
i) Manage fever aggressively to normal levels with antipyretics and other therapeutic
cooling devices such as cooling blankets.
j) Maintain normoglycemia (CBG 110 180 mg/dl). Hyperglycemia or
hypoglycemia should be avoided.
k) Rehabilitate early once stable.
l) Practice bedsore precautions.
m) Institute deep-vein thrombosis and pulmonary embolism prophylaxis using
intermittent pneumatic compression devices if available in addition to anti-
embolic stockings.

After documentation of cessation of bleeding by repeat imaging, low dose SQ LMWH or UH

maybe considered for prevention of venous thromboembolism in immobile patients after 1-4
days from onset of ICH. (Class IIB Level of Evidence C revised from previous guideline)

152
Patients with ICH who develop an acute proximal VT, particularly those with clinical or
subclinical pulmonary emboli, should be considered for acute placement of a vena cava
filter. (Class IIB Level of Evidence C)

B. Surgical Treatment:

Its role depends on the size, extent and location of the hematoma, and patient factors.

a. There is evidence of increase in hematoma size by 33% within 24 hours of

stroke onset in 38% of cases.
b. Considerations for surgical intervention:

Non-surgical candidates:
Patients with small hemorrhages (<10 mL) or minimal neurological
deficits
Patients with GCS<5 except those who have cerebellar hemorrhage and
brainstem compression
Patients with pontine or midbrain hemorrhage

Candidates for immediate surgery:

Patients with cerebellar hemorrhage >3 cm who are neurologically
deteriorating or have brainstem compression and hydrocephalus from
ventricular obstruction
Patients with bleed associated with a structural lesion such as an
aneurysm, AV malformation or cavernous angioma if there is a chance
for good outcome and the vascular lesion is surgically accessible
Clinically deteriorating patients especially young with moderate or large

Hemorrhagic
lobar hemorrhage

Stroke
Ventricular drainage for patients with intraventricular hemorrhage with
moderate to severe hydrocephalus

All other patients may benefit from surgery:

Patients with basal ganglia or thalamic hemorrhage
Patients with GCS 5 and above
Patients with supratentorial hematoma with volume >30 cc

Bibliography
1. Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, Mayberg M, Morgenstern L,
Ogilvy CS, Vespa P, Zuccarello M. Guidelines for the management of spontaneous intracerebral
hemorrhage in adults: 2007 update: a guideline from the American Heart
Association/American Stroke Association Stroke Council, High Blood Pressure Research
Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group.
Stroke. 2010;38:20012023.
2. Moon JS, Janjua N, Ahmed S, Kirmani JF, Harris-Lane P, Jacob M, Ezzeddine MA, Qureshi AI.
Prehospital neurologic deterioration in patients with intracerebral hemorrhage. Crit Care Med.
2008;36.

153
 3. Zubkov AY, Mandrekar JN, Claassen DO, Manno EM, Wijdicks EF, Rabinstein AA. Predictors
of outcome in warfarin-related intracerebral hemorrhage. Arch Neurol. 2008;65:1320 1325.
4. Cooper D, Jauch E, Flaherty ML. Critical pathways for the management of stroke and
intracerebral hemorrhage: a survey of US hospitals. Crit Pathw Cardiol. 2007;6:18 23.
5. Rdberg CT. Prognostic parameters in spontaneous intracerebral hematomas with special
reference to anticoagulant treatment. Stroke. 1991;22:571576.
6. Flaherty ML, Kissela B, Woo D, Kleindorfer D, Alwell K, Sekar P, Moomaw CJ, Haverbusch M,
Broderick JP. The increasing incidence of anticoagulant associated intracerebral hemorrhage.
Neurology. 2007;68: 116 121.
7. Ansell J, Hirsh J, Hylek E, Jacobson A, Crowther M, Palareti G; American College of Chest
Physicians. Pharmacology and management of the vitamin K antagonists: American College of
Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;
133(suppl):160S198S.
8. Hanley JP. Warfarin reversal. J Clin Pathol. 2004;57:11321139.
9. Hung A, Singh S, Tait RC. A prospective randomized study to determine the optimal dose of
intravenous vitamin K in reversal of over- warfarinization. Br J Haematol. 2000;109:537539.
10. Goldstein JN, Thomas SH, Frontiero V, Joseph A, Engel C, Snider R, Smith EE, Greenberg SM,
Rosand J. Timing of fresh frozen plasma administration and rapid correction of coagulopathy
in warfarin-related intracerebral hemorrhage. Stroke. 2006;37:151155.
11. Fredriksson K, Norrving B, Stro mblad LG. Emergency reversal of anticoagulation after
intracerebral hemorrhage. Stroke. 1992; 23:972977.
12. Gregory PC, Kuhlemeier KV. Prevalence of venous thromboembolism in acute hemorrhagic
and thromboembolic stroke. Am J Phys Med Rehabil. 2003;82:364 369.
13. Lacut K, Bressollette L, Le Gal G, Etienne E, De Tinteniac A, Renault A, Rouhart F, Besson G,
Garcia JF, Mottier D, Oger E; VICTORIAh (Venous Intermittent Compression and
Thrombosis Occurrence Related to Intra-cerebral Acute hemorrhage) Investigators.
Prevention of venous thrombosis in patients with acute intracerebral hemorrhage. Neurology.
2005;65:865 869.
14. Kothari RU, Brott T, Broderick JP, et al. The ABCs of measuring intracerebral hemorrhage
volumes. Stroke 1996;27:1304-1309.
15. Academy of Filipino Neurosurgeons Guidelines on the Management of Hypertensive ICH
Hemorrhagic

16. Kazui S, Naritomi H, Yamamoto H, et al. Enlargement of spontaneous intracerebral

Stroke

hemorrhage. Incidence and time course. Stroke 1996;27:1783-1787.

17. Kothari RU, Brott T, Broderick JP, et al. The ABCs of measuring intracerebral hemorrhage
volumes. Stroke 1996;27:1304-1309.

II. ANEURYSMAL SUBARACHNOID HEMORRHAGE

A. DIAGNOSIS OF SUBARACHNOID HEMORRHAGE (SAH)

Clinical: may present with sudden, severe headache best described as the worst headache of
my life in 80% of patients. The onset of headache may be associated with nausea and/or
vomiting, stiff neck, brief loss of consciousness and or focal neurologic deficits such as cranial
nerve palsies. Seizures may occur in up to 20% of patients after SAH, most commonly during
the 1st 24 hours.

Neurological Examination signs of meningeal irritation (i.e. neck rigidity, Kernigs and
Brudzinski signs), altered or decreased level of consciousness, CN III or VI nerve palsy.
Patients may or may not have focal neurological deficits.

154
Emergent referral to a neurologist/neurosurgeon and transfer to a facility with capabilities of
managing acute stroke are recommended.

B. NEURODIAGNOSTIC EXAMINATIONS

1. Non-contrast cranial CT scan should be done and interpreted immediately. Hyperdense blood
in the basal cisterns is usually diagnostic, but parenchymal clot in the temporal or basal frontal,
and intraventricular hemorrhage are also suggestive of a ruptured aneurysm.

Sensitivity of CT scan depends on the timing of imaging in relation to ictus from hemorrhage.

D uration of S AH CT s ca n se nsitiv ity

12 h o urs 98 to 100 %
24 h o urs 93 %
6 days 57 to 85 %

2. Lumbar tap with CSF analysis in the absence of focal neurological signs is
strongly recommend if Cranial CT scan is negative or is unavailable

a. The following are important considerations in the examination of CSF

Timing of LP in relation to SAH
RBC and WBC
Presence of xanthochromia

b. Multiple specimens (at least 3 tubes) should be collected to rule out traumatic
tap. Opening pressures should be measured.

Hemorrhagic
Stroke
3. Cerebral angiography is the gold standard in determining the cause of SAH.
Early catheter angiography should be performed in good and poor grade cases of
SAH.

If the initial angiogram is negative, a repeat cerebral angiogram should be

performed after 7-14 days.

4. Good quality CT angiography (CTA) or magnetic resonance angiography (MRA)

are acceptable options to catheter angiography in the ff. situations: (a.) poor
grade patients, (b.) when angiogram cannot be performed in a timely fashion or
(c.) as follow up when initial angiogram is negative.

C. SAH GRADING

Use the ff. grading scales to aid in making treatment decisions and prognostication.

155
 1. Hunt and Hess Classification
Grade Description
1 Asymptomatic or mild headache , slight nuchal rigidity
2 Moderate to severe headache, nuchal rigidity, no neurological
deficit other than cranial nerve palsy
3 Drowsiness, confusion or mild focal signs
4 Stupor, moderate to severe hemiparesis, possibly early
decerebrate signs
5 Deep coma, decerebrate rigidity, moribund appearance

2. World Federation of Neurological Surgery (WFNS) SCALE

Grade GCS Motor deficit

I 15 Absent
II 13-14 Absent
III 13-14 Present
IV 7-12 Present or absent
V 3-6 Present or absent
3. Fischers Grade
Grade Descriptio n (Bloo d on CT )
1 No subarachnoid blood detected
2 Diffuse or v ertical layers <1 mm thick*
3 Localized clot or vertical layer >1 mm thick *
Hemorrhagic

4 Intracerebral or intraventricular clot w ith diffu se or no S AH

Stroke

*Vertical layer refers to blood in the subarachnoid spaces including in the

interhemispheric fissure and cisterns

D. GENERAL SYMPTOMATIC TREATMENT

1. Absolute bed rest in a quiet, comfortable environment is recommended. Limit

visitors until aneurysm has been secured.
2. Monitor neurovital signs closely, including cardiac and pulmonary status.
3. Start soft diet for alert patients, nasogastric tube (NGT) feedings if with impaired
consciousness, but keep on nothing per orem (NPO), if there is planned immediate
intervention.
4. Give analgesics for headache. Avoid aspirin and other NSAIDS.
5. Give gastrointestinal prophylaxis for stress gastritis. Use Proton Pump Inhibitors or
H2 blockers.
6. Give anti-emetics if with nausea and vomiting.
7. Maintain euthermia. May give antipyretics and use cooling blankets, if febrile
8. Maintain euglycemia

156
 9. Give sedatives for restlessness or agitation.
10. Give stool softeners.
11. Start DVT prophylaxis using pneumatic compression devices, if available, or thigh
high anti-embolic stockings. Withhold SQ LMWH or unfractionated heparin until
aneurysm has been secured.

E. EARLY SPECIFIC TREATMENT

1. Calcium Channel Blockers:

Nimodipine 60mg every 4 hours by mouth or via NGT for 3 weeks is recommended.
It remains uncertain if Nimodipine acts through neuroprotection, through reduction
in the frequency of vasospasm, or both.

2. Anticonvulsants:
Prophylactic anticonvulsants may be considered in the immediate post-hemorrhagic
period.

Long term anticonvulsants are generally not recommended but may be considered in
patients at higher seizure risk such as: patients with prior seizures, parenchymal
hematoma, infarct, or middle cerebral artery aneurysms.

3. Anti-fibrinolytic agents are not recommended. Although they reduce the risk of
rebleeding, they are associated with higher rate of cerebral ischemia.

4. Managed increased ICP (see chapter). Ensure proper patient positioning with 30
degree head of bed position to facilitate adequate venous outflow.

Hemorrhagic
5. BP Management: Although the best antihypertensive agent and BP remains
unsettled, the use of IV Nicardipine to a target SBP of < 150 mmHg in the pre-

Stroke
operative phase (unsecured aneurysms) is reasonable.

6. Avoid using large amounts of hypotonic fluids. Maintain euvolemia.

7. Manage hyponatremia.

8. Steroids: Corticosteroids have no proven role and are not recommended for use in
SAH

F. PREVENTION AND MANAGEMENT OF VASOSPASM

1. Monitoring: Serial transcranial doppler (TCD) study is recommended for the

diagnosis and management of vasospasm.

Other newer modalities such as CT and MRI perfusion studies are helpful in the
detection and management of ischemia.

157
 2. Triple-H Therapy (e.g. volume expansion, induction of hypertension, and
hemodilution) is a reasonable approach for the management of symptomatic
vasospasm after aneurysm has been secured although a universal treatment protocol
is still lacking.

3. Acute treatment with intravenous magnesium sulfate and statins (simvastatin and
pravastatin) is safe and can help reduce cerebral vasospasm based on preliminary
studies. Trials are currently underway.

4. Endovascular angioplasty (chemical +/- mechanical) is an effective way of managing

vasospasm. Intervention has to be performed early before clinical signs suggesting
irreversible infarction (i.e. hemiplegia) are present.

G. TREATMENT OF SAH

Obliteration of the aneurysm as soon as possible from the circulation is the main goal of
treatment. This can be achieved through surgical clipping or endovascular coiling.

H. TIMING OF SURGERY

1. Definitions:
Early surgery is surgery ideally performed within 72 hours from ictus.
Late surgery is surgery performed more than 3 days from ictus.

2. Indications:
a. Early, immediate surgery is recommended for good to moderate grade
(Hunt and Hess or WFNS grades I-III) aneurysmal SAH patients to
minimize the chance of a devastating rebleed.
Hemorrhagic

b. For poor grade patients (Hunt and Hess or WFNS Grades IV-V), early
surgery is recommended in the presence of
Stroke

i. Hematoma
ii. Hydrocephalus

Surgery may be delayed in the presence of:

i. Ischemia or infarction
ii. Severe angiographic vasospasm

c. Advanced age (elderly) is not a contraindication for early surgical

management in the absence of organ failure.

I. COILING

1. Can be performed early in both good and poor grade patients.

2. Reduces the rate of rebleeding for poor grade patients who would otherwise be
treated conservatively.
3. Vasospasm is not a contraindication and can be dealt with endovascular coiling
4. Can be performed under local anesthesia if needed.

158
J. WHERE TO ADMIT

SAH patients should be admitted at the Acute Stroke Unit or Intensive Care Unit. In the
absence of an ASU/ICU, patients may be placed in a quiet, regular room with very close
monitoring.

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CT angiography in patients with suspected intracranial aneurysms. Am J Neuroradiol
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2. Andaluz N, Tomsick TA, Tew JM, et al. Indications for Endovascular therapy for refractory
vasospasm after aneurysmal subarachnoid hemorrhage. Surg Neurol 2002;58:131-138
3. Anderson GB, Steinke DE, Petruk KC et al. Computed tomographic angiography versus digital
subtraction angiography for the diagnosis and early treatment of ruptured intracranial
aneurysms. Neurosurg 1999;45:1315-1320.
4. Anzalone N, Triulzi F, Scotti G. Acute subarachnoid hemorrhage: 3D time of flight MR
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update. J Neuroimaging 2000;10:101-115.
6. Baker C, Prestigiacomo, et al. Short term perioperative anticonvulsant prophylaxis for the
surgical treatment of low-risk patients with intracranial aneurysms. Neurosurg 1995;37:863-
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7. Bederson J. Connoly ES, Bajjer H. Et al. Guidelines for the Management of Aneursymal
Subarachnoid Hemorrhage, A Statement for Healthcare Professionals from a Special Writing
Group of the Stroke Council, American Heart Association. Stroke 2009; 40: 994 1025.
8. Butzkueven H, Evans AH, Pittman A, et al. Onset seizures independently predict poor
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9. De Gans K, Nieuwkamp DJ, Rinkel G, Algra A. Timing of surgery in subarachnoid
hemorrhage: a systematic review of literature. Neurosurg 2002;50:336-342.

Hemorrhagic
10. Edlow JA. Diagnosis of subarachnoid hemorrhage. Neurocritic Care 2005; 2: 99 109.

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11. Greenberg, M. Handbook of Neurosurgery 2nd ed. FL: Greenberg Graphics; 1991.
12. Hillman J, Fridriksson J, Nillsson O et al. Immediate administration of tranexamic acid and
reduced incidence of early rebleeding after aneursymal subarachnoid hemorrhage: a
prospective randomized study. J Neurosurg 2002; 97 : 771 778.
13. Hope JK, Wilson JL, Thomson FJ. Three-dimensional CT angiography in the detection and
characterization of intracranial berry aneurysm. Am J Neuroradiol 1996;17:437-445.
14. ISAT Collaborative Group. International Subarachnoid Aneurysm Trial (ISAT) of
neurosurgical clipping versus endovascular coiling in 2143 patients with intracranial aneurysms:
a randomised trial. Lancet 2002;360:1267-1274.
15. Johansson M, Cesarini KG, Contant CF, et al. Changes in intervention and outcome in elderly
patients with subarachnoid hemorrhage. Stroke 2001;32:2845-2949.
16. Lennihan, Laura MD, Mayer, Stephan MD, Fink, Matthew MD et al. Effect of hypervolemic
therapy on cerebral blood flow after subarachnoid hemorrhage: a randomized controlled trial.
Stroke 2000; 31: 383-391.
17. Linn FH, Rinkel GJ, Algra A, van Gijn J. Headache characteristics in subarachnoid hemorrhage
and benign thunderclap headache. J Neurol Neurosurg Psychiatry 1998;65:791-793.
18. Lynch J, Wang J, McGirt M et al. Simvastatin reduces vasospasm after aneurysmal subarchnoid
hemorrhage: results of a pilot randomized clinical trial. Stroke 2005; 36: 2024 2026.

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in patients with vasospasm due to a ruptured cerebral aneurysm: A systematic review. Stroke
2001;32:2292-2298.
20. Molyneux AJ, Kerr Rs, Yu LM, et al. International Subarachnoid Aneurysm Trial (ISAT) of
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a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups
and aneurysm occlusion. Lancet 2005;366:809 -817.
21. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction
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hemorrhage (Review). The Cochrane Database of Systematic Reviews 2005. Issue 1. CD
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26. Roos Y; for the STAR Study Group. Antifibrinolytic treatment in subarachnoid hemorrhage a
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ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage.
Neurology 1989;39:1514-1518.
28. Sloan Mam Burch CM, Wozniak MA, et al. Transcranial doppler detection of vertebrobasilar
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30. Treggiari-Venzi M, Suter P, Romand JA. Review of medical prevention of vasospasm after
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31. Tseng M, Czosnyka M, Richards H et al. Effects of acute treatment with pravastatin on cerebral
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hemorrhage: a phase II randomized placebo-controlled trial. Stroke 2005; 36: 1627 - 1632
32. van Gijn J and Rinkel GJE. Subarachnoid hemorrhage: diagnosis, causes and management.
Brain 2001;124:249-279.
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tomograms. Neuroradiol 1982;23:153-156.
34. van der Wee N, Rinkel GJ, Hasan D, van Gijn J. Detection of subarachnoid hemorrhage on early
CT: is lumbar puncture still needed after a negative scan? J Neurol Neurosurg Psychiatry 1995;
58:357-359.
35. Velthius BK, Rinkel GJ, Ramos LM, et al. Subarachnoid hemorrhage: aneurysm detection and
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36. Velthius BK, Rinkel GJ, Ramos LM, et al. Computerized tomography angiography in patients
with subarachnoid hemorrhage: from aneurysm detection to treatment without conventional
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hemorrhage: a major update of a cochrane review. Stroke 2003;34:2308-2309.

160
III. CEREBRAL ARTERIO-VENOUS MALFORMATION

Arteriovenous malformations (AVMs) are congenital anomalies of the central nervous system
with poorly formed blood vessels that shunt blood directly or through a nidus from arterial
circulation to the venous system bypassing the capillary network. They are relatively uncommon
but are increasingly recognized lesions that can cause serious neurological symptoms and even
death. There are four types of Vascular Malformations described by McCormick in 1966 and
they are:
i. Arteriovenous Malformations (AVMs)
ii. Venous Angioma
iii. Cavernous Malformation
iv. Capillary Telangiectasia

Arteriovenous Malformations clinically are the most aggressive among the four types. They
tend to enlarge somewhat with age and often progress from a low flow to medium -to high flow
lesion in adults. The prevalence of AVM is probably slightly greater than the usually quoted
0.14% with a slight male preponderance. The clinical presentation most commonly occurs in
young adults with an age range of 20 to 40 years with an average age of 33 years. It carries a
morality rate of 10% and a morbidity rate of 30 to 50% (neurological deficit) from each bleed.
Brain hemorrhage is the most common presentation (50-61%), followed by seizures (20-25%).
The overall risk of intracranial hemorrhage in patients with known AVM is 2-4% per year with
an annual 1% mortality rate from AVM bleeding, though some series put it at 1% per year for
unruptured AVMs. Specific features of AVM that increase the risk of hemorrhage include:
young age, prior hemorrhage, small AVM size, deep venous drainage and high flow within the
nidus. Headache occurs in 10-50% of cases. The neurological deficits may be explained by the
mass effect of the enlarging AVM or venous hypertension in the draining veins. Occasionally
the deficit could occur due to the siphoning of blood flow away from adjacent brain tissue - so

Hemorrhagic
called steal phenomenon.

Stroke
DIAGNOSIS

Diagnosis usually includes high resolution imaging studies such as CT and MRI scans
supplemented by a digital subtraction angiography (DSA). AVMs appear as irregular or globoid
masses anywhere within the hemispheres or brain stem. They may be cortical, subcortical or in
deep gray or white matter. Cerebral catheter angiography or digital subtraction angiography
(DSA) is the gold standard for the definitive diagnosis of AVMs as this is necessary to assess
morphology and hemodynamic flows that are essential for planning treatment. Additionally,
important features such as feeding arteries, venous drainage pattern, and presence of arterial
and aneurysms can be provided by angiography.

MANAGEMENT

There are currently no level I or level II data available in the literature that define the treatment
of AVMs. Definitive treatment for AVMs aims to eliminate intracerebral hemorrhage risk and
preservation or maximize functional status of the patients. Once intervention is indicated, the

161
 benefits of treatment must be carefully weighed against the risks. The main goal is for a
complete nidal obliteration. Subtotal obliteration does not provide protection from future
hemorrhage. Over the last decade, there have been significant developments in the
management of AVMs. Evolution of microsurgical and endovascular and radiosurgical
techniques to treat these lesions have undergone tremendous advancement. Once the AVM is
identified, it is usually suited for one or more of the following treatment strategies: conservative
management or observation, microsurgical excision, stereotactic radiosurgery, endovascular
embolization or a combination of the different modalities.

-
TREATMENT GUIDELINES FOR CEREBRAL ARTERIO-VENOUS MALFORMATION

Patient diagnosed to have AVM

A B

Asymptomatic / Incidental findings Symptomatic

Elective Treatment Patien t presented with acute emergen t symptoms

Conservative Management vs (e.g. hemorrhage or seizures)
Surgery vs SRS vs Endovascular
depending on Patient and YES NO
AVM characteristics and
current thinking C D

Resolve Acute Condition
by medical or surgical
treatment
( e.g. evacuation
Hemorrhagic
Assess patient if candidate for treatment and assess
AVM characteristics
E F G

of hematoma
vs med ical management; S-M Grade S-M Grade S-M Grade
Stroke

seizure control) 1-2 3 4-5

Poor Patient NO
Offer Multi- Mainly
Status
Neurosurgical modality Conservative
YES AVM excision Approach and/or
Outcome may still be (Surgery, Palliative
poor even if definitive SRS, treatment.
Patient or endovascular Evaluate if
AVM treatm ent done.
Family refusal any
Discuss with relatives.
May or may not treatment is
NO better than
proceed with
YES conservative
def initive treatment
SRS and/or Neu rosurgical course of
endovascular AVM excision the patient
treatmen t

162
A
Observation may be the most appropriate for asymptomatic or large volume AVMs
(average 4-5 cm), especially when the AVM has not yet bled. The natural history of
hemorrhagic risk without treatment is 1-4% with an annual mortality rate of 1% from
AVM bleeding. The current recommended treatment, long term risk of hemorrhage, and the
outcomes from hemorrhage are controversial. A recent study of patients with AVMs without
history of hemorrhage published in Lancet Neurology 2008 found that there was no difference
in outcome between treated and untreated patients at the end of the third year of follow up.
This study recommended close monitoring as the most appropriate therapeutic option in
treating AVMs without a history of hemorrhage. The U.S. National Institute of Health is
currently supporting an Unruptured Brain AVMs (ARUBA) study, a randomized clinical trial of
patients with asymptomatic AVMs. This trial may provide critical information concerning the
optimal management of this group of asymptomatic patients. Each treatment option has
associated risks and benefits that have to be weighed individually.

B
For symptomatic patients, more than 50% of AVMs present with intracranial
hemorrhage. The next most common presentation is seizure occurring approximately
in 20-25% of the cases. Seizures may be focal or generalized. Other presentations
include headaches (15%), focal neurological deficit (5%) and pulsatile tinnitus (more common
for Dural Arteriovenous Fistula). AVMs are associated with 1-4% annual hemorrhage risk and a
17-90% lifetime risk of hemorrhage. The risk of recurrent hemorrhage increased to 6-18% in
the first year following the initial incident. The risk following the second bleed was 25% in the
first year.

C
Treatment of AVM especially surgical procedure is generally an elective procedure

Hemorrhagic
unless the patient presents with intracranial hematoma or a life threatening

Stroke
hydrocephalus secondary to hematoma. In such an emergency situation, excision of
the AVM should only be indicated for superficial AVMs, otherwise, hemorrhage or hematoma-
related complications must be resolved first, followed by a careful postoperative angiogram and
treatment plan. If the condition of the patient post-operatively remains to be poor, then any
treatment plan should be discussed with the relatives who may decide to be conservative or to
proceed with the least invasive treatment plan.

D
Accurate assessment of treatment planning especially of operative risk should be
discussed with the patient and/or family members. The Spetzler and Martin (SM)
grading scale is still the most widely used classification for AVMs and has been validated
both prospectively and retrospectively as a practical and reliable method for outcome prediction
and planning for AVMs. The SM grading scale approximates potential risks based upon AVM
size, location/eloquence, and venous drainage pattern. Outcome reports regarding the results
of surgical excision of brain AVMs are level V data. The majority of this information is
gathered in a retrospective fashion.

163
 SPETZLER-MARTIN AVM GRADING SYSTEM

Graded Feature Points * largest diameter of nidus on non-

magnified angiogram (is related to and
SIZE* therefore implicitly includes other factors
relating to difficulty of AVM excision, e.g.
Small (< 3 cm) 1 number of feeding arteries, degree of
steal, etc..)
Medium (3-6 cm) 2
+ eloquent brain: sensorimotor, language
Large (> 6 cm) 3 and visual cortex; hypothalamus and
thalamus; internal capsule; brain stem;
ELOQUENCE OF ADJACENT
cerebellar peduncles; deep cerebellar
BRAIN+
nuclei.
Non-eloquent 0
# considered superficial if all drainage is
through cor tical venous system;
Eloquent 1 considered deep if any or all is through
deep veins (e.g. internal cerebral vein, basal
PATTERN OF VENOUS
vein, or pre-central cerebellar vein)
DRAINAGE#
*Spetzler-Martin AVM Grade (IV) =
Superficial only 0
total number of points (size + eloquence
+ venous drainage).
Deep 1

E
For Grade I and II AVMs with a history of hemorrhage, microsurgery may be the best
Hemorrhagic

option with favorable outcomes observed in 92-100% and 94-95% of patients

Stroke

respectively. There is low morbidity and mortality due to surgery and an opportunity for
an immediate cure without a latency period. In patients who may have significant co-
morbidities or who refuse to have the surgery done, an alternative treatment option such as
stereotactic radiosurgery may be explored.

F
Grade III lesions are generally treated with microsurgery or stereotactic radiosurgery,
often with adjunctive endovascular therapy. Excellent or good outcomes using these
procedures in this grade range from 68-96%. SM grade III represents a heterogeneous
group of AVMs that are associated with increased technical difficulty and potential morbidity in
comparison to the lower grade lesions. The modified SM grading scale was created to address
discrepancies for this grade. It divided this group into two sub-groups: Grade IIIA (size >6 cm)
and Grade IIIB (venous drainage and/or eloquence). It was shown that for grade IIIA,
microsurgery with adjunctive endovascular therapy in the form of embolization, is the
preferred treatment, and for grade IIIB lesions radiosurgery, with or without embolization can
be done. Stereotactic radiosurgery (SRS) usually takes 1-3 years to work and during this latency

164
time there is a risk of bleeding. The actuarial hemorrhage rate from a patent AVM (before
complete obliteration during the latency interval) is 4.8% per year during the first two years after
SRS and 5% per year during the 3rd to the 5th year after SRS. The process is cumulative, with the
earliest obliterations noted within 2-3 months; 50% of the effect often seen within one year,
80% within two years and 90% within three years. If at the end of three years, residual AVM is
identified by imaging, repeat radiosurgery may be considered.

G
For Grade IV and V lesions, an individualized multi-modal approach is recommended
only if intervention is deemed beneficial and safe. Excellent or good outcome rate with
71-75% in grade IV and 50-70% in Grade V can sometimes be attainable in the hands
of competent cerebrovascular neurosurgeons. If patients will be handled conservatively, then
angiography is done every 5 years to look for the development of feeding vessel aneurysm or
outflow stenosis, both of which are risk factors for problems. Endovascular technique
(embolization) is very often inadequate by itself to permanently obliterate AVMs. There is also
no evidence that partial AVM embolization alters long-term hemorrhagic risk, and as such, it is
not recommended as a broad treatment strategy for AVMs. It has 3 potential goals when used
before radiosurgical intervention for AVMs: (1) to decrease target size to <3 cm in diameter,
because smaller volumes have a higher cure rate with less morbidity; (2) to eradicate
angiographic predictors of hemorrhage, such as intranidal aneurysms or venous aneurysms; and
(3) to attempt to reduce symptoms related to venous hypertension. Re-canalization has been
reported in 14-16% of cases.

Many factors may influence AVM treatment, simple AVM stratification systems, such as the
Spetzler-Martin grading scale and its modification provide a valuable framework for treatment
planning. Therefore the treatment of AVM consists of determining the treatment modality or
combination of modalities, with the greatest therapeutic effectiveness and safety according to
both patient characteristics and AVM architecture.

Hemorrhagic
Stroke
For a more complete discussion on the management of AVMs, the following articles are highly
recommended for review:

165
 Bibliography

1. Ogilvy CS, Stieg PE, Awad I, et al. AHA Scientific Statement: Recommendations for the
management of intracranial arteriovenous malformations: A statement for healthcare
professionals from a special writing group of the Stroke Council, American Stroke Association.
Stroke 2001; 32:1458-1471.
2. Starke RM, Komotar RJ, Hwang BY, Fischer LE, et al. Review article: Treatment guidelines for
cerebral arteriovenous malformation microsurgery. British Journal of Neurosurgery, 2009;
23:376-386.
3. Lunsford LD, Niranjan A, Kondziolka D, Sirin S, Flickinger JC. Arteriovenous malformation
radiosurgery: A twenty year perspective. Clinical Neurosurgery. 2008; Volume 55: 108-119.
4. Fleetwood IG, Steinberg GK. SeminarArteriovenous Malformations. Lancet. 2002; 359:863-
873.
5. Friedlander RM. Arteriovenous malformations of the brain. New England and Journal of
Medicine. 2007; 356:2704-2712.
6. The International Radiosurgery Association (IRSA) Radiosurgery Practice Guideline Initiative
Stereotactic radiosurgery for patients with intracranial arteriovenous malformations (AVM).
Radiosurgery Practice Guideline Report #2-03. March 2009. 1-22
Hemorrhagic
Stroke

166
NEUROIMAGING FOR STROKE

Neuroimaging
 NEUROIMAGING IN ACUTE STROKE

STROKE

Stroke is now a leading cause of mortality and morbidity worldwide. Diagnosis of acute stroke
is imperative for proper treatment especially with the current initiative to thrombolize those
patients whose onset of stroke coincides with the accepted temporal norm of patient selection,
i.e., onset of less than 3 hours, imaging becomes absolutely necessary.

Stroke may either be ischemic or hemorrhagic with the latter either being within the brain, that is
primary intracerebral hemorrhage or in the subarachnoid that result from ruptured aneurysm.

Fig. 1: Subacute Left Middle Cerebral Artery Infarct

Subacute left middle cerebral

artery infarct seen as
hypodense areas (white arrows)
in the fronto-parietal region,
the insula and the part of the
basal ganglia (A and B).

A B

Fig. 2: Acute Subarachoid Hemorrhage

Acute subarachnoid hemorrhage

seen as hyperdense areas brought
about by increased concentration of
protein due to clot retraction from
globin particles, in the basal cisterns,
Neuroimaging

Sylvian cistern and the cortical sulci

(dark arrows) (C and D).

C D
There are also different etiologic causes of stroke such as cardiogenic or embolic,
atherosclerotic, lacunar and watershed type of infarcts, among others. The discussion on these
etiologic factors is beyond the scope and purpose of this literature.

168
CT SCAN

CT scan and its many imaging variations, also known as multimodal CT Scan, and MRI also with
its own variations are the current imaging methods that are used to assess the presence of stoke.
Both imaging methods can determine the volume of the lesion in the case of ischemic stroke, to
determine if the infarcted brain volume has not exceeded one-third that of the middle cerebral
artery volume and to rule out hemorrhage which is a contraindication to thrombolytic
treatment.

Imaging is also necessary to rule out the possibility that the neurological deficit is not due to
stoke mimics. With thrombolytic therapy, patients are more likely to have good outcome if
treated within 3 hours form the onset of stroke. The risk increases as the time interval between
the stroke and treatment increase.

The recommended method of imaging in stroke is through the use of non-contrast Cranial CT
scan (NCCT) which has low sensitivity in the first 24-hours and particularly in the first 3 to 6
hours - the temporal window for thrombolytic treatment. This imaging method is applicable in
a wide variety of CT Scanners regardless of their vintage.

CT scan is preferred at this time due to its wide availability, ease and straightforward detection of
hemorrhage and its compatibility with monitoring equipments.

Early Findings in Stroke with the Use of Non-Contrast Cranial CT Scan

1. Hyperdense middle cerebral artery or dot sign

2. Obscure lentiform nucleus
3. Loss of gray-white matter differentiation
4. Insular ribbon sign
5. Sulcal effacement
Neuroimaging

Hyperdense middle cerebral artery represents the blood clot formed in a major intracranial
arterial trunk that will be seen as hyperdensity within the artery as a result of clot retraction
resulting to very high concentration of protein or globin component of blood (Fig. 3). Among
findings that had been previously enumerated, this is the least definite as a sign of hyperacute
stroke and has to be correlated with the clinical presentation of stroke. Likewise, if the
hyperdensity is noted in both middle cerebral arteries, its value as an early sign of stroke is no
longer as significant as when it is seen only at one side.

169
 Fig. 3: Hyperdense
Middle Cerebral Artery

Hyperdense left middle cerebral

artery sign (black arrow) seen at
the time of admission.
Completed infarct noted three
days after admission (white
arrow).

A B
Obscuration of the lentiform nucleus is the loss of the density of this structure against the
normally more hypodense internal and external capsules, due to unabated influx of water into
the cells as a result of the failure of ion pumps that is supposed to maintain homeostasis within
the cells resulting to cytotoxic edema (Fig. 4). Similar reason is also attributed to the loss of the
gray-white matter interface at the insular area (Fig. 5) and other parts of the cortex affected by
ischemia (Fig. 6) and the sulcal effacement resulting to swelling of the cortical region (Fig. 7).

Fig. 4: Obscuration
of the Lentiform Nucleus

The right lentiform nucleus is

obscured, an early sign of
hyperacute infarct (double black
arrows) with normal left lentiform
nucleus. Completed stroke 3 days
after initial imaging (white arrow).

A B
Fig. 5: Cortical Ribbon Sign
Neuroimaging

Cortical ribbon sign seen as loss of the

normal dense appearance of the insular
cortex at the hyperacute stage (black
arrow) compared to the normal cortical
ribbon (white arrow) (A). The same
patient exhibiting a completed infarct
after two days (white arrow head) at the
right insular cortical and subcortical
region that involves the external capsule
and lateral aspect of the right lentiform
nucleus (B).

A B

170
Fig. 6: Loss of Gray-White Matter Interface at the Right Temporal Region

Loss of gray-white matter interface at the

right temporal region, a feature of
hyperacute infarct resulting from
cytotoxic edema that swells the brain cells
rendering this part to be hypodense and
featureless (double arrow) compared to
the normal left side. Three days after, the
infarct is completed with more severe
hypodensity that is due to vasogenic
edema, an indicator of cell demise.

A B
Fig. 7: Sulcal Effacement

The insular cortex is flattened with

marked thinning of the right sylvian
cistern (double black arrow)
compared to the normal appearance
of the left side (black arrow). The
same area after two days with a
completed infarct (white arrow
head).

PERFUSION CT IMAGING

Due to the low sensitivity of CT scan in making a diagnosis of stroke and estimating the
ischemic core volume against that of the penumbra or the tissue at risk in the hyperacute phase
of stoke, an important CT scan evaluation of the brain, the perfusion CT imaging, is now added
to the acute stroke imaging protocol. This method will allow the determination of the infarct
core that may not be visible yet with the use of the conventional CT scan imaging to check if its
volume does not exceed one-third the size of the middle artery distribution, otherwise,
Neuroimaging
thrombolysis is no longer indicated due to the increased risk of complication such as
hemorrhagic conversion.

Perfusion CT imaging is performed by monitoring the first pass of iodinated contrast agent
bolus through the cerebral circulation. As the contrast agent passes through the brain
parenchyma, there will be transient hyperattenuation of the tissues that is directly proportional
to the amount of contrast material in the vessels and blood.

Through commercially available software, color coded perfusion maps showing cerebral blood
volume (CBV), mean transit time (MTT), and cerebral blood flow or CBF are created. The map
showing MTT will show the most prominent regional abnormality that can depict the ischemic

171
 area shown as an increase in MTT. CVB map depicts the infarct core similar to the area of
restricted diffusion in diffusion weighted MRI that is thought to be the brain tissue that is no
longer salvageable even with reperfusion, while the CBF depicts the altered area of the brain
that is at risk of infarction or the penumbra, that may eventually become infracted if blood
supply is not restored in time. Comparing the volume of the infarct core with the volume of the
tissue at risk is called the tissue mismatch (See Table 1).

The penumbra typically will show increased MTT with mildly decreased CBF and normal or
mildly increased CBV. The infarcted tissue on the other hand will demonstrate markedly
decreased CBF with an increased MTT with markedly decreased CVB.

CT ANGIOGRAPHY
Neuroimaging

CT angiography is another important addition to the imaging tools for diagnosis of stroke to
enhance its detection and improve prognosis. CT angiography can reveal the status of the large
cervical and intracranial arteries and show the site of occlusion. It can also demonstrate the
presence of arterial dissection and at the same time determine the degree of collateral blood
flow and diagnose atherosclerotic disease. This information shall serve as a good guide for
thrombolysis.

Intraarterial thrombolysis has a higher recanalization rate for occlusions of the internal carotid
artery, the middle cerebral artery stem and the basilar artery. CT angiography has the ability to
demonstrate occlusions of the vertebrobasilar system that supply the posterior circulation that
is very difficult to detect with non-enhanced CT scan examination.

172
The extent of arterial leptomeningeal collateral vessels beyond the occlusion in some patients
with better pial collateral formation appears to correlate with better prognosis. The use of these
parameters is now what is known as multimodal CT Scan examination in stroke. This is a fast
and accurate method in stroke diagnosis and considered straight forward although it will require
the use of multidetector CT Scanners which may not be available in smaller hospitals and
medical centers.

The core of the infarct can be identified in the CT angiogram source image (CTA SI), a post
contrast injection method that is seen as an area of hypointensity and is said to be synonymous
to DWI, an MRI stroke protocol. The lesion is seen as an area of hypodensity against the rest of
the brain parenchyma. DWI however is more sensitive in smaller infracts and those within the
brain stem and posterior fossa.

One difficulty in thrombolysis is the assessment of the volume of the infarct core, whether its
size is still within one-third the volume of the middle cerebral artery distribution. This process
is now aided with a more objective determination of the infarct core volume with the use of the
Alberta Stroke Program Early CT Score (ASPECTS) that is actually a simple scoring tool. Parts
of the brain are assigned points with the normal brain being a perfect 10 points. By deducting
the equivalent point/s for each area of the brain that is infarcted from the total perfect score of
10 points assigned to the normal brain, the volume of infarct core is estimated. A score below
ASPECTS 7 is equivalent to an infarct core of more than one-third the size of a middle cerebral
artery distribution and is considered ineligible for stroke thrombolysis.

MRI FOR STROKE

MRI is another imaging study that can be used in the diagnosis of stroke. This will provide a
tool that can allow stroke recognition and diagnosis within a short interval of thirty minutes
from the onset of the ischemic lesion. Non-contrast-enhanced MRI can readily show the
infarct core through diffusion weighted imaging (DWI) that is more sensitive than non-contrast
enhanced CT scan.

Fig. 8: Isotrophic Diffusion

Weighted Imaging (DWI)
Neuroimaging

Left image shows bright signal

indicative of hyperacute infarct
resulting from restricted diffusion of
water. The right image shows the
ADC map wherein the area of
restricted diffusion is seen as dark
signal to confirm the findings in
DWI from shine-through artifacts
which can also be bright but are not
real infarcts but T2 effects.

173
 MRI can demonstrate the penumbra or tissue at risk with the use of perfusion MR imaging or
(PWI). The volume of brain involvement in DWI and PWI can then be compared to determine
the mismatch between the two parameters. The tissue at risk or the penumbra can be
determined as the volume of brain with diminished perfusion beyond that of the infarct core,
this is the diffusion/perfusion mismatch.

Magnetic Resonance Imaging is a very powerful tool in differentiating between acute stroke
from other stroke mimics. It is able to demonstrate ischemic stroke with a very high accuracy
with the use of diffusion weighted imaging (DWI) when compared with non-enhanced CT scan
(NECT). However, DWI is also highly dependent on the type of magnet that is available in the
hospital.

The imaging protocols that are used for creating images of the human anatomy is called pulse
sequence and these pulse sequences show different levels of accuracy in imaging of ischemic
stroke and hemorrhage in the brain. High field gradients that is typically found in magnets that
is at least 1.5 Tesla to 3.0 Tesla is needed to create accurate diffusion weighted images which can
be aptly called echo planar imaging (EPI).

DWI is able to demonstrate stroke based on the demonstration of restriction of diffusion of

water molecules as a result of the movement of extracellular water into the intracellular
environment (cytotoxic edema) compared to the normal tissues wherein there is random
movement of water molecules (Brownian motion). The area of infarcted tissue then will be
demonstrated as bright signal in DWI. Since this pulse sequence is T2 based, artifactual bright
signal caused by shine through of high signal T2 abnormalities such as adjacent CSF or
vasogenic edema may be misinterpreted. Correlation of abnormal DWI bright signal findings
with the apparent diffusion coefficient map (ADC) that demonstrate restricted diffusion as low
intensity signal, greatly increases the specificity of this method. Abnormal DWI signal in acute
stroke with reduced ADC signal has been observed as early as 30 minutes after the onset of
ischemia. ADC map continues to decrease in intensity and reaches its peak in 3 to 5 days and
then it slowly increases again.

Other pulse sequences may also be able to detect stroke as bright signal, T2 weighted fluid
attenuated inversion recovery images (T2 FLAIR) or T2 weighted fast spin echo or T2 spin echo
images (T2TSE or T2 SE) may be able to demonstrate these but their findings can be seen late
Neuroimaging

that is beyond the cut off time for thrombolysis.

MRI is also a better tool in demonstrating infarction in the brain stem and the cerebellum in
contrast to CT Scan but a very important drawback is patient intolerance which includes
claustrophobia, a not too infrequent occurrence in MR stroke imaging, as well as medical
instability of the patient and patient motion during the scanning process.

Just like CT scan, MRI can be used to examine the vasculature of the brain and the neck with
time of flight imaging magnetic resonance angiography (MRA) that does not use intravenous
contrast material. Contrast enhanced MRA can also be performed for more accurate depiction

174
of vessel anomalies like aneurysms. The advantage of non-contrast study is that it can be
repeated even several times if necessary to produce images that are adequate for diagnosis
without the risks that is usually attributed to contrast material injection, using gadolinium in
both MRI and MRA.

NEUROIMAGING FOR HEMORRHAGIC STROKE

Intracerebral hemorrhage is very well detected by CT scan, even in the hyperacute phase. This
will be seen as a hyperdense area due to clot retraction which causes extravasated blood from
vessels to become a hyperconcentrated proteinaceous collection due to its globin particles.
This can be seen in the hyperacute to acute phase becoming isointense with the cortex towards
the subacute phase of hematoma. CT scan is the imaging method of choice, should the
historical data points to possible hemorrhage as the cause of stroke.

A very important consideration in prognosticating the outcome of intracerebral hemorrhage is

the volume of the hematoma, since the outcome of the patient is related to the hematoma
volume. The most accurate method of determining hematoma volume is through the pixel
method. In this method, the outline of the hematoma is marked and the volume is determined
by the computer system of the CT scan by determining the number of pixels that comprise the
area of the hematoma. Pixels are the small squares that make up the CT scan image. Since the
size of the pixels or picture elements are fixed and actually represents the volume elements or
voxels (the area of the pixel including the slice thickness of the CT Scan picture), the volume of
the hematoma can thus be determined at the CT scan work station or the control monitor and
this is through the effort of the radio technologist.

A more practical tool for volume measurement of intracerebral hemorrhage using the image of
the hematoma in the CT Scan film was devised by Khotari, et al., using a formula termed as:

Modified Khotari Method

Hematoma volume (in cc) = A x B x C

2
Neuroimaging

where: A= Largest diameter of hematoma (in cm)

B= Diameter perpendicular to A (in cm)
C= Number of slices on CT scan with hemorrhage X slice thickness (in cm)

A value of 1 cm thickness is given to the next CT slice if the hematoma volume of the
succeeding slices is about the same size as the original slice or it must not be less than 75%
of the largest hematoma volume. The CT scan thickness is considered to be of the slice
thickness of the succeeding hematoma volume if these are from 25% to 75% of the largest
volume. If the succeeding hematoma volume is less than 25% of the largest hematoma
volume, the slice is negated and no value is assigned to that CT Scan slice.

175
 The accumulated values for each of the measurements are added together that will represent
C or the height of the hematoma. The Khotari method of hematoma volume measurement
is fairly accurate when compared to hematoma volume determined through the use of the
formula for a sphere which is not the usual shape of hematomas.

Fig. 9A

Selected CT Scan images of a

patient who suffers from acute
intracerebral hemorrhage at the
right basal ganglia whose
volume has to be determined.

Fig. 9B

From the series of slices,

following the Kothari formula, the
equivalent thickness of this slice
will be one-half of its original
thickness (0.5 cm).
Neuroimaging

Fig. 9C

This slice has the picture of the

largest hematoma size and its
thickness will be equivalent to one
whole slice thickness (1.0 cm).

176
 Fig. 9D

This is the third slice and its size is

almost as large as slice (2) and is
assigned the full thickness (1.0cm).

Fig. 9E

This is the last slice in the series of

slices of an intracerebral
hematoma whose size is no longer
significant, its height is considered
non-contributory and is not
assigned any value.

Fig. 9F

This is the actual computation of

the hematoma size using Dr.
KhotariS volume computation
ABC/2.
Neuroimaging

CT scan demonstration of hematomas is straightforward and has a very short learning curve.
On the other hand, demonstration of hematoma in MRI is a bit more complicated, to say the
least, as the appearance of hematomas in T1 and T2 weighted images would depend on the age
of blood product within the lesion. Computation of hematoma volume using MRI is also
complicated as the margin of the hematoma may not be exact since the image bloom or
extends beyond the physical margin of the actual lesion.

177
 The detection of intracerebral hematoma using MRI is best achieved with the use of gradient
echo pulse sequence (GRE) or with T2*, depending on the imaging protocol that is available in
the magnet that is provided by the vendors. These pulse sequences are much more sensitive
than any of the spin echo or fast spin echo pulse sequences that approaches or may even exceed
the sensitivity of NECT in detecting intracerebral hematomas in some instances.

MRI provides an excellent presentation of the evolution of the different stages of blood
particularly when it is intracerebral. The basis for demonstration of hematomas is the
degradation of hemoglobin in the brain tissue from its intravascular state. Oxyhemoglobin that
is seen in the hyperacute phase of hematoma is typically isointense to slightly hypointense in T1
TSE and is slightly hyperintense in T2 TSE (Fig. 10). The blood products will degrade into
deoxyhemoglobin in the acute phase of the malady that is iso- to slightly hypointese in T1 TSE
and is markedly hypointse in T2 TSE (Fig. 11). A few more days thereafter, blood will further
degrade to methemoglobin but is still intracellular. Also called the early subacute phase, this will
be hyperintense in T1 TSE and is markedly hypointense in T1 TSE (Fig. 12). Then this will later
become extracellular methemoglobin with lysis of RBC in the late subacute phase that is
hyperintense in both T1 and in T2 TSE (Fig. 13). Blood products will finally become
hemosiderin and ferritin in the chronic phase that is hypointense in both T1 and in T2 TSE (Fig.
14).

In case of subarachnoid hemorrhage, the most sensitive pulse sequence is T2 FLAIR which will
show subarachnoid bleeding to be hyperintense in contrast to the normal hypointense
appearance of cerebro-spinal fluid as seen in this pulse sequence. While GRE pulse sequences
can show hemorrhage early in the brain, this may not hold true in detecting blood in the
subarachnoid space where T2 FLAIR excels. There is however the possibility of acquiring
artifactual bright signal due to fluid motion and pulsation that may mimic blood products and
will have to be correlated with other imaging protocols such as GRE.
Neuroimaging

T1TSE T2TSE GRE

Fig. 10: Hyperacute left lentiform nucleus hemorrhage, slightly hypointense in T1TSE (single arrow),
hyperintense in T2TSE (arrow head) and bright with blooming dark signal in GRE (double arrows).

178
 T1TSE T2TSE GRE

Fig. 11: Acute intracerebral hematoma with intraventricular extension, slightly hypointense to isointense in
T1TSE (arrow), dark in T2TSE (arrow head), dark blooming signal in (GRE) (double arrows).

Neuroimaging

Fig. 12: Early Subacute, Acute and Old Hematoma. Right subcortical hyperintense signal in T1TSE (single
black arrow) that is seen as hypointense signal lesion with surrounding hyperintense vasogenic edema that is
noted as blooming dark signal in T2FFE (GRE). Left subinsular isointense lesion in T1TSE (double dark
arrow) that is seen as dark signal in T2TSE that is also noted as blooming dark signal representing acute
hematoma. Left thalamic hypointense to hyperintense signal area in T1TSE (white arrow) that is dark in
T2TSE and seen as blooming dark signal in T2FFE (GRE) indicative of acute to early subacute hematoma.
Small dark signal lesion in the right thalamus with surrounding hemosiderin ring T1TSE (white arrow head)
that is bright in T2WI with surrounding dark signal hemosiderin that is also noted at blooming dark signal in
T2FFE (GRE).

179
 T1TSE T2TSE GRE

Fig. 13: Late subacute hematoma at the left posterior parietal region exhibiting hyperintense signal lesion in
T1TSE (black arrow), hyperintense signal lesion with dark signal hemosiderin rim in T2TSE (white
arrowhead) and hyperintense signal area with a dark signal rim in GRE (double arrow).

T1TSE T2TSE GRE

Neuroimaging

Fig. 14: Old or chronic hemorrhage in the right lentiform nucleus seen as elongated hypointense lesion in
T1TSE (arrow), markedly hypointense area with a central faint bright signal representing encephalomacia
(white arrow head), elongated blooming dark signal area in GRE (double arrow).

180
 Stroke Society of the Philippines NeuroImaging Guidelines in Acute Stroke:

A. Hyperacute or Acute Ischemic Stroke

Non contrast CT scan of the head is the initial neuroimaging study of choice in acute
stroke because of its cost, speed and availability. The main objective of immediate
imaging is to exclude hemorrhagic stroke. A non-contrast study obviates the need to
wait for creatinine result.

Cranial MRI DWI surpasses non contrast Cranial CT scan in detecting early
ischemic changes & in excluding some stroke mimics. MRI can be the initial imaging
of choice in patients who are rTPA candidates if it is available in the center and does
not result in undue delay of administration of thrombolytic agent.

A vascular study (CTA or MRA) to detect stenosis or occlusion is useful to further the
diagnosis of stroke, help triage patients to the best treatment and determine
prognosis. It is probably indicated in specialized centers together with the initial
imaging evaluation if it is available and does not unduly delay treatment with IV
thrombolysis.

Cerebral infarcts are often not documented by CT scan within 3 hours from stroke
onset. However early infarct signs maybe seen in 60% of cases:

In cases of early neurologic deterioration secondary to large infarcts, edema or

suspected hemorrhagic conversion, a follow-up non contrast CT of the head is
recommended.

MRI has the ff. technical advantage over non contrast Cranial CT scan :
Neuroimaging
1) DWI for documenting early ischemia/infarction
2) GRE for detecting microbleeds, hemorrhagic transformation and chronic
hemorrhages
3) T2W for small infarcts or lacunes or infarcts located in the brainstem or
posterior fossa.
4) Despite of its superior yield, it is however more expensive, time-
consuming and less readily available.

181
 B. Intracerebral Hemorrhage

CT scan and MRI T2 appear to have equal efficacy documenting acute intracranial
hemorrhage (ICH).

CT can accurately document the location of the hemorrhage and the presence of
mass effect, ventricular extension and hydrocephalus.

1) In hypertensive ICH, a repeat non contrast CT scan after 24 hours of ictus

is recommended especially in cases showing clinical deterioration to
document hematoma enlargement and/or development of
hydrocephalus.

2) Hematoma volume can be estimated by CT using planimetric method or at

the bedside using the Modified Khotari method

3) Computation of Hematoma Volume (Modified Khotari method) that is

fairly demonstrable

4) In suspected cases of AV malformation, aneurysm or tumor bleed, a

contrast CT and or CTA or MRI/MRA of the head may be warranted

C. Subarachnoid Hemorrhage

1) Non contrast CT of the head is strongly recommended as the initial

procedure for diagnosis.

2) The diagnostic yield of CT goes down from 92% within the first 24 hours
to 50% within 7 days of onset.
Neuroimaging

182
 Neuroimaging

I. Hypodense (dark/black on CT): a. Normal- CSF, fat, air in sinuses/mastoids

b. Abnormal - Infarction (arterial/venous), necrosis,encephalitis, resolving hematoma, abscess, air after surgery

II. Hyperdense (white on CT): a. Normal - bone, physiologic calcification of the pineal gland, choroid
plexus, basal ganglia and falx cerebri
b. Abnormal: blood, calcifications (from tumor, granuloma, AVM/aneurysm, hamartoma)
III. Mixed density (white and dark): Abnormal - hemorrhagic infarcts, tumors, abscess, AVM, contusion

Multiple lesions: tumors (metastases, lymphoma), abscesses, granulomas, multiple infarctions, trauma

Reference: Lindsay K. Neurology and Neurosurgery Illustrated. Churchill Livingstone 1997

183
 Bibliography

1. de Lucas EM, Sanchez E, Gutierrez A, Mandly, AG, Ruiz E, Florez AF, Izquierdo J, Arnaiz J,
Piedra T, Natalia V, Banales I, Quintana, F. CT Protocol for Acute Stroke: Tips and Tricks for
General Radiologists. Radiology 2008; 28:1673-1687.
2. Latchaw RE, Alberts MJ, Lev MH, Connors JJ, Harbaugh RE, Higashida RT, Hobson R,
Kidwell, CS, Koroshetz WJ, Mathews V, Villablanca P, Warach S, Walters M and on behalf of
the American Heart Association Council on Cardiovascular Radiology and Intervention, Stroke
council and the Interdisciplinary Council on Peripheral Vascular Disease. Stroke, 2009; 40, 3646-
3678.
3. Camargo ECS, Furie KL, Singhal AB, Roccatagliata L, Cunnanne ME.Halpern E, Harris GJ,
Smith WS, Gonzalez RG, Koroshetz WJ, Lev MH. Acute brain attack: Detection and
delinearion with CT angiographic source images versus nonenhanced CT scans. Radiology
2010; 244: 541- 548.
Neuroimaging

184
 Stroke Unit
Nurse-Rehab
 I. GUIDELINES ON THE ESTABLISHMENT
AND OPERATION OF STROKE UNITS

I.1. THE STROKE CENTER

A. Major Aspects of Acute Stroke Care in Stroke Center

1. Acute Stroke Teams: Hospital-based stroke teams should be available round-the-

clock, seven days a week in order to evaluate within 15 minutes any patient who
may have suffered a stroke.
2. Written Care Protocols: The availability of written protocols is key in reducing
time to treatment and treatment complications.
3. Emergency Medical Services: Emergency medical services (EMS) are vital in the
rapid transport and survival of stroke patients.
4. Emergency Department: The emergency department staff should be trained in
diagnosing and treating stroke and should have good lines of communication with
both EMS and the acute stroke team.
5. Stroke Unit: Where patients can receive specialized monitoring and care.
6. Neurosurgical Services: These should be provided to stroke patients within two
hours of when the services are deemed necessary.
7. Support of the Medical Organization: The facility and its staff, including
administration, should be committed to the Stroke Unit.
8. Neuroimaging: There must be capability to perform an imaging study within 25
minutes of the physicians order. A physician should evaluate the image within 20
minutes of completion.
9. Laboratory Services: Standard laboratory services should be available round-the-
clock, seven days per week at a Primary Stroke Center.
10. Outcomes/Quality Improvement: Primary Stroke Centers should have a database
or registry for tracking the type and number of stroke patients seen, their
treatments, timelines for treatments, and some measurements of patient outcome.
11. Educational Programs: The professional staff should receive at least eight hours
per year of continuing medical education credits. In addition to professional
education, the Stroke Center should plan and implement at least two annual
programs to educate the public about stroke prevention, diagnosis and availability
for emergency treatment.

B. Definition of a Stroke Unit

Nurse-Rehab

A Stroke Unit is a hospital unit that cares for stroke patients exclusively or almost
Stroke Unit

exclusively, with specially trained staff and a multidisciplinary approach to treatment

and care.1

186
C. Characteristics of a Stroke Unit

Organization
Coordinated multidisciplinary team care
Nursing integration with multidisciplinary care
Involvement of caregivers in rehabilitation process

Specialization
Medical and nursing interest
Expertise in stroke and rehabilitation

Education
Education and training program for staff, patients and caregivers

D. Goals of a Stroke Unit

1. Improve chances of survival

2. Reduce disability
3. Shorten length of hospital stay
4. Shorten length of rehabilitation

E. Types of Stroke Units

E.1. Acute Admission Units:

1. Intensive Care Units dedicated stroke unit with facilities such as ventilators
and intensive invasive and non-invasive monitoring equipment. The units focus
on the very acute care for a selected group of acute stroke patients and have little
or no focus on rehabilitation.
2. Acute stroke unit dedicated stroke units that accept patients acutely but
discharge them early (within 7 days) and have no or at best a modest focus on
rehabilitation. The units usually do not have intensive care facilities, but usually
have facilities for non-invasive monitoring of vital signs.
3. Combined acute/rehabilitation stroke unit dedicated stroke units which
accept stroke patients acutely for acute treatment combined with early
mobilization and rehabilitation for an average period of at least one to two
weeks.
4. Mixed acute units units that treat stroke patients and patients with other
Nurse-Rehab

diagnoses. The units accept patients acutely. Some have a program of care
Stroke Unit

similar to acute stroke units while others have a program similar to a combined
unit.

187
 E.2. Delayed Admission Units:

1. Rehabilitation stroke unit dedicated units that accept patients after a minimum
delay of seven days after stroke onset. The units focus on rehabilitation.

2. Mixed assessment/rehabilitation unit wards or units which have an interest

and expertise in the assessment and rehabilitation of disabling illness, but do
not exclusively manage stroke patients.

F. Effects of Stroke Unit Care on Recovery

Analysis on Cochrane Data Base involving 23 trials showed significant reduction of death
(OR; 0.88), death or dependency (OR; 0.75) and death or institutionalization (OR; 0.77)
when patients were treated in a stroke unit compared with those treated in general wards.2

Two trials evaluated the long-term effects of stroke unit care. On the 5-year follow-up,
admission in combined acute/rehabilitation stroke units reduced death (OR; 0.59,
NNT=9), death or dependency (OR; 0.36, NNT=6) and death or institutionalization (OR;
0.48, NNT=9). Ten-year follow-up of patients admitted in combined acute/rehabilitation
stroke units similarly showed a reduction in death (OR; 0.45), death or dependency (OR;
0.45) and death or institutionalization (OR;0.42).3-5

Patients admitted in a rehabilitation stroke unit even after a minimum delay of seven days
post-stroke resulted in reduced death (OR; 0.66, NNT=10) and death or dependency (OR;
0.83, NNT=90).6

The stroke unit benefits stroke patients of both sexes, all ages, and those with mild,
moderate or severe strokes.2, 7

Comparing the different stroke unit models, the unit with the strongest evidence of
benefit is the combined acute/rehabilitation stroke-unit model, and to some extent the
dedicated rehabilitation stroke unit.2

I.2. STROKE UNIT ORGANIZATION

A. The Stroke Unit:

Basic equipment:
1. 4 to 8 beds
2. Cranial computerized tomography (available 24 hours)
3. Angiography (available 24 hours)
Nurse-Rehab

4. Ultrasound (continuous-wave, TC Duplex, transthoracic echocardiogram;

Stroke Unit

transesophageal echocardiogram)
5. Monitoring (RR, Respiration, Holter, O2 saturation)
6. Emergency laboratory

188
 Monitoring:
1. Basic Holter, blood pressure, O2 saturation, respiration, temperature
2. Special transcranial doppler, embolus detection, electroencephalography,
central breathing patterns (sleep apnea)

B. Tasks
1. Admission within the unstable phase (in general, <24 hours)
2. Monitoring of vital and neurological parameters
3. Immediate diagnosis (etiology, pathogenesis)
4. Immediate treatment and secondary prevention
5. In general, length of stay not longer than seven days

C. Patient Selection
1. Indications for Admission to the Stroke Unit
a. Acute stroke (< 24 hours)
b. Awake, somnolent patient
c. Symptoms fluctuating or progressive
d. TIAs with high stroke risk (non-valvular AF, stenosis)
e. Vital parameters unstable
f. Thrombolysis; anticoagulation
g. New investigational treatment or procedure

2. Admission to Acute Stroke Unit Not Indicated

a. Patients with severe consciousness impairment (should be admitted to
intensive care unit instead)
b. Severely disabled patients by previous strokes
c. Very old patients or those with multiple comorbidities

3. Patients with the following should be admitted to the intensive care unit instead of
the acute stroke unit:
a. Stupor and coma
b. Central respiratory disorders requiring artificial ventilation
c. Space-occupying cerebral infarctions with risk of herniation
d. Severe cardiopulmonary insufficiency
e. Hypertensive-hypervolemic treatment

D. The Stroke Team

1. Personnel
a. Medical doctors
b. Nurses
c. Physiatrists
Nurse-Rehab

d. Occupational therapists
Stroke Unit

e. Speech pathologist
f. Nutritionists
g. Social workers

189
 2. Personnel with special interest in stroke are medical doctors or other paramedical
people who:
a. Have undergone continuing education on stroke and other related activities
or subspecialties on stroke
b. Have been attending at least one national or international meeting on stroke
in a year
c. Have undergone stroke fellowship or preceptorship training on stroke
d. Is a member or officer of a national or international organization devoted to
stroke

I.3. RECOMMENDATIONS

1) Stroke patients should be treated in stroke units (Level I). Admission to stroke
unit decreases death, dependency and institutionalization.
2) Stroke units should provide coordinated multidisciplinary care provided by
medical, nursing and therapy staff who specialize in stroke care (Level I).

Bibliography
1. Aboderin I, Venables G; for The Pan European Consensus Meeting on Stroke Management
(WHO). J Int Med 1996;240:173-180.
2. Stroke Unit Trialists Collaboration. A systematic review of organized inpatient (stroke unit)
care for stroke. Cochrane Library; Issue 4: 2002.
3. Indredavik B, Slordahl SA, Bakke F, et al. Stroke unit treatment long term effects. Stroke
1997;28:1861-1866.
4. Indredavik B, Slordahl SA, Bakke F, et al. Stroke unit treatment improves long term quality
of life: a randomized controlled trial. Stroke 1998;29:895-899.
5. Indredavik B, Slordahl SA, Bakke F, et al. Stroke unit treatment: 10 year follow-up. Stroke
1990;30:1524-1527.
6. Lincoln NB, Husbands S, Trescoli C, et al. Five year follow-up of a randomized controlled
trial of a stroke rehabilitation unit. BMJ 2000:320; 549.
7. Collaborative systematic review of the randomised trials of organised inpatient (stroke unit)
care after stroke. Stroke Unit Trialists' Collaboration. BMJ 1997;314:1151-1159.

II. GUIDELINES ON NURSING MANAGEMENT

OF PATIENTS WITH STROKE

The Guidelines on Nursing Management of Patients with Stroke was developed by reviewing
the guidelines, prevention, treatment, and rehabilitation of stroke from the Stroke Society of
the Philippines. A focus group discussion and consensus building was conducted with the
representatives of the nine (9) hospitals in Metro Manila who have Stroke Units.

The framework follows the nursing process and the dimensions of nursing care which include
the promotive, preventive, curative, and rehabilitative aspects respectively.
Nurse-Rehab
Stroke Unit

The structure comprises the objectives which state the general and specific objectives, the
processes which present the implementation of the standards, and the outcome standards
which quantify the measures of evaluation.

190
 PREVENTIVE ASPECT
GENERAL SPECI FIC
PROCESS STANDARDS
O BJECTIVES O BJECTIVE
1. Nurses will Pro vide A nurse must implem ent
provide p reventive inform ation a health education
care through hea lth campaign on th e progra m tha t is
education activities following: a pproved/ published by
based on t he a. Stroke duly accred ited hea lth
identified learning b. Risk factors a gencies (Stroke Society,
need of th e clients. c. Lifestyle D OH, etc.).
Modificatio A nurse must implem ent
n a nd health education
regular progra ms appropria te to
medical the clients level of
check-up understanding.
A nurse must be able to
use and promote the use
of the available teachin g
m aterials.
A nurse must take active
pa rticipation in forum
relevan t to health
educatio n on the
prevention of stroke.
2. Nurses will have a Identify who a re The nurse will im plement
role in a ctively at risk for a ssessm ent that is ba sed
identifying clients developing stroke on the established
with risk factors. guidelines on risk factors
(Screenin g) for stroke and shall utilize
a risk- assessm ent nursing
framework
The nurse will m ake
a pprop riate referra ls of
clients identified high-risk
for stroke
The nurse will report
a pprop riately an d
document identified
clients with high-risk for
stroke
3. Nurses will ta ke Identify, p rom ote The nurse identifies
active involvement an d participate in a gencies in the
in health education available community that has
program regarding progra ms progra ms fo r lifestyle
lifestyle regarding lifestyle m odification for the
modification. mo dification prevention of stroke
The nurse will be able to
recommend availa ble
progra ms to clients for
lifestyle modifications
The nurse facilitates
referral to ap propriate
community/ health care
a gency regarding lifestyle
m odification
A nurse must have the sufficient knowledge and skills in order to implement these standards.
OUTCO ME
STANTARDS
C lients express
un derstanding of
the risk factors and
interest to modify
lifestyle.
(Enumera te risk
factors, and
suggests wa ys of
m odifying lifestyles)
D ecrea se incidence
o f stroke
Increase people
a wareness
Increase utiliza tion
o f published
m aterials increa se
n umbers of forum
conducted
E arly detection ,
referral and
m anagement of
identified clients
R isk identification
will be implemented
in standardized
m eth od manner
C ontribute factual
a nd accura te da ta to
the existing data
b anks for stroke.
Increase a wareness
o f the clients on the
a va ila ble fa cilities
a nd programs
regarding lifestyle
m odifica tion
D ocument increa se
Nurse-Rehab
compliance/
Stroke Unit
a dherence to
lifestyle
m odifica tion
191
 CURATIVE ASPECT
GENERAL SPECIFIC
PROCESS STANDARDS OUTCOME STANTARDS
OBJECTIVES OBJECTIVE
1. Nurses will Promptly identify Nurses will assess patient Early identification and
promptly identify and and prioritize comprehensively with the prioritization of needs
prioritize patients patients needs use of current and Immediate initiation of
needs by utilizing and Utilize and acceptable neurologic management
performing proper perform proper assessment tools Early transfer/admission to
health assessment neurologic a. Glasgow Coma Scale hospital with stroke or
with emphasis on assessment b. Diaz Stroke Scale intensive care unit
neurological technique c. FIM/Barthel Index
assessment technique Scale
Nurses will correlate
patients history with
present signs and
symptoms
Nurses will identify priority
needs of patient based on
assessment
Nurses prioritize and
facilitate
series of diagnostic
examinations per stroke
guidelines
2. Nurses will provide Plan and manage Nurses will implement Early identification and
quality nursing care nursing care Emergency nursing assessment of disease
based on the according to measures if needed progression
identified patients patients Nurses will closely monitor
needs in collaboration condition, needs neurologic vital signs with
with other members and priorities proper documentation and
of the health team a. Physiological Care reporting of findings:
utilizing holistic b. Safe measures a. Every 15 mins. for the first
approach c. Comfort measures hour
d. Therapeutic b. Every 30 mins. For the
environment second hour then every
e. Prevention of hour for the next 4 hours
complications and until patient is stable
infection c. Continue reassessment of
f. Spiritual and the patients condition with
psychosocial care regards to the monitoring
To be able to of neurologic vital signs
provide specific d. Watch out for increased
nursing care in ICP, deterioration in No incidence of falls and
collaboration with sensorium and progression aspirations
other members of of motor deficits
the health team
Nurses will provide safety
measures accordingly such
as:
a. Aspiration precautions
b. Fall prevention No bedsores contractures
Nurse-Rehab

c. Use restraints based on and muscle atrophy

Stroke Unit

proper protocol
d. Seizure precautions

192
 GENERAL SPECIFIC
PROCESS STANDARDS OUTCOME STANTARDS
OBJECTIVES OBJECTIVE
Nurses will provide
comfort measures such as:
a. Li nen change everyday and
as necessary
b. Personal hygiene (oral care
and perineal care)
c. Turning patient every 2
hours during waking hours
and every 4 hours
thereafter as necessary and
depending on patients
condition
d. Proper positioning to semi-
fowlers position on 30
degrees angle
e. Passive range of motion Healing environment attained
exercises at least once a day
and as necessary
f. Use of Braden Scale in
relation to pressure sores

Nurses will provide

therapeutic environment
a. Proper ventilation and
lighting
b. Minimize noise Complications and infections
c. Proper orientation to time, prevented
place and person
d. Provisi on of
windows/murals for every
room

Nurses will prevent

complications and possibl e
infections by:
a. Establishing patent airway
through nebulization,
postural drainage, back
clapping and suctioning
b. Monitoring and
maintaini ng BP as
recommended by Stroke
Guidelines
c. Observing and provi ding
catheter and tube care.
Change per g uidelines and
as needed:
- IV every 72 hours
- FC every 7 days
- NGT every 7 days
- ET/Tracheostomy care
every shift
- Ventilator Tubes every 72
Nurse-Rehab

hours (follow
Stroke Unit

ICC/institution protocol)

193
 GENERAL SPECIFIC
PROCESS STANDARDS OUTCOME STANTARDS
OBJECTIVES OBJECTIVE
a. Monitoring of intake and
output Verbalizes psycho-emotional
b. Monitoring and prevention and spiritual upliftment
of increased ICP
c. Providing and monitoring
of adequate nutrition and
hydration in collaboration
with other health teams
and significant others

Nurses will provide

spiritual and psycho-social
care such as:
a. Alleviation of patients
anxiety by encouraging
verbalization of feelings No medication errors and
b. Guide the patient in adherence to prescribed
identifying positive coping medication regimen
mechanisms
c. Respect patients beliefs
and culture in the plan of
care
d. Facilitate the patients
spiritual needs

Nurses will administer Expresses self with the use of

medication observing the alternative means of
10 Rs communication
a. Neuroprotective agents Maximizes patients
b. Anti-HPN medications independent functions and
c. Laxatives correctly addresses other
d. Diuretics disabilities
e. Antiplatelets Demonstrates cooperation
f. Anticoagulants and active participation of
g. Steroids clients and significant others
h. Others as prescribed
Accurate and complete
Nurses will establish records
alternative means of
Early medical intervention
communication if
necessary Utilizes other health and
community resources
Nurses will assess patients
capabilities in per forming
ADL and assist in
identifying alternative
means
Nurses will provide health
education to patient and
significant others

Nurses will properly

document care and
prompt referral
Nurse-Rehab
Stroke Unit

Nurses will make referral

to social worker and other
support group if
applicable

194
 GENERAL SPECIFIC PROCESS OUTCO ME
OBJECTIVES O BJECTIVE STANDARDS STANTARDS
3. Nurses will Practice Nurses wil l reinforce
appl y the nursing care informed consent to
principles of Bio- using Bio- patient prior to
Ethics in the Ethical implementation of
practice of Standards any diagnostic and
nursing care medical Patient
interventions verbal izes
Nurses wil l ensure understanding
that the P atients Bill of their rights
of Rights is Bio-Ethi cally
observed acceptable
Nurses wil l nursing
collaborate with the practice
institutions Bio-
Ethical Committee
4. Nurses will Evaluate the Nurses wil l Individualized
evaluate effectiveness determine patients plan of care
care/intervention of nursing responses to specific
s provided care/ nursing
intervention interventions Enhanced
rendered Nurses wil l analyze, nursing care
interpret and
document patients
responses to care
Nurses wil l make
appropri ate referral
based on evaluation
Nurses wil l modify
plan of care
accordingly

In order to implement quality nursing care an adequate nurse-patient ratio must be considered.
Nurse-Rehab
Stroke Unit

195
 REHABILITATIVE ASPECT
GENERAL SPECIFIC
PROCESS STANDARDS OUTCOME STANTARDS
OBJECTIVES OBJECTIVE
1. Nurses will Assist the The nurses will Performance of
focus on early patient initiate rehabilitation simple ROM
rehabilitation and towards upon admission exercises and ADL
discharge maximum The nurses will assist by patient with
planning functional the patient in minimal or no
capacity performing daily supervision
Discuss with simple task of ADL
the patients in collaboration with
and other members of the
significant health team Maintains sexual
others the The nurses will function
plan of care educate patients on
Involve alternative and
patients physiologically safe Performance of
family and sexual practice (as simple nursing
significant indicated) procedures by
others in the The nurses will significant others to
patient care include significant patient with minimal
and decision- others in providing or no supervision
making specific nursing care from nurses
for patient with
stroke such as
provision of:
a. Hygiene
b. Nutrition
c. Turning and
Positioning
d. Pulmonary toilet
e. Range of motion Compliance to
exercises medication regimen
f. Other care as and adherence to
maybe deemed OPD follow-up
necessary
The nurses will ensure Active participation
good compliance to of patients family
medications and and significant
provide options for others
compliance to
outpatient follow-up
The nurses will
collaborate with
Nurse-Rehab
Stroke Unit

patients family and

significant others in
the plan of care

196
GENERAL SPECIFIC
PROCESS STANDARDS OUTCOME STANTARDS
OBJECTIVES OBJECTIVE
2. Nurses will assist The nurse will The nurse will provide Adherence of clients
in sustaining and provide a discharge care plan and family to
maintaining guidelines for contains the following prescribed discharge
patients healthy home care information: plan of care
and productive a. Activity and exercise
lifestyle b. Medication regimen
c. Symptoms to be referred
d. Diet prescribed
e. Medical follow-up
schedule
f. Special care to be
provided

The nurses will facilitate

referral to appropriate
Guide patient community resources Compliance to
in lifestyle alternative lifestyle
modification The nurses will identify
based on the appropriate lifestyle
risk factors modification, which suits
identified the patient current Motivation and
health status stimulation of patients
Assist patient interest in self
to accept and The nurses will involve enhancing activities
adapt with his patient in diversional Maximizes patients
disability activities that will potential
enhance self-esteem
such as:
a. Writing and sharing his
experiences regarding
stroke
b. Participating in forums/
trainings
c. Involvement in support Active participation of
group (if available) family members
d. Explore patients other
creative talents

Involves family
members in the
management of clients
plan of care
Nurse-Rehab
Stroke Unit

197
 COMPETENCY STATEMENTS FOR THE STROKE NURSE
IN VARIOUS PHASES AND ROLES IN STROKE CARE

The Competency Statements for the Stroke Nurse in Various Phases and Roles in Stroke Care
were developed by reviewing the guidelines, prevention, treatment, and rehabilitation of the
Stroke Society of the Philippines and evidence-based literatures.

The focus group discussion and consensus building was facilitated by the Critical Care Nurses
Association of the Philippines, Inc. through its President, Mrs. Ma. Isabelita C. Rogado. The
twelve (12) participants of the said guidelines formulation came from the different hospitals in
Metro Manila and the academe namely Amang Rodriguez Medical Center, Arellano University,
Asian Hospital and Medical Center, Capitol Medical Center, Cardinal Santos Medical Center,
Makati Medical Center, Manila Doctors Hospital, Our Lady of Lourdes Hospital, St. Lukes
Medical Center Quezon City & Global City, The Medical City, University of the Philippines
Philippine General Hospital, and University of Santo Tomas Hospital, Inc.

The phases of stroke care with levels and evidence and recommendations were adopted from
the Comprehensive Overview of Nursing and Interdisciplinary Care of the Acute Ischemic
Stroke Patient: A Scientific Statement from the American Heart Association (Summers et al
2009), Stroke, Journal of the American Heart Association.

Phase 1 of Stroke Care: The Emergency or Hyperacute Phase

A. From the Field to the ED: Stroke Patient Triage and Care
Class I
1) EDs should establish standard operating procedures and protocols to triage stroke
patients expeditiously (Class I, Level of Evidence B).
2) Standard procedures and protocols should be established for benchmarking time to
evaluate and treat eligible stroke patients with rTPA expeditiously (Class I, Level of
Evidence B).
3) Target treatment with rTPA should be within 1 hour of the patients arrival in the ED
(Class I, Level of Evidence A).
4) Eligible patients can be treated between the 3 to 4.5 hour window when evaluated
carefully for exclusions to treatment (Class I, Level of Evidence B).

B. Emergency Nursing Interventions in the Emergency/Hyperacute Phase of Stroke

Class I
1) Emergency personnel should be highly trained in stroke care (Class I, Level of
Evidence B).
2) Frequent neurological/stroke assessments should be done (Class I, Level of
Nurse-Rehab

Evidence C); these should be done more frequently for patients receiving rTPA.
Stroke Unit

3) Supplement oxygen should be given to patients with an oxygen saturation of 92%

and a decreased level of consciousness (Class I, Level of Evidence C). There is little
evidence that supplement oxygen should be provided routinely.

198
 4) The stroke patients head should be positioned in neutral alignment with the body,
and the head of the bed should be elevated 25 to 30 to help the patient handle oral
secretions, especially if dysphagia is present (Class I, Level of Evidence C).
5) Stroke patients in the ED should be kept NPO (not given anything orally) until ability
to swallow is assessed (Class I, Level of Evidence B).
6) Intravenous access should be obtained in at least 2 sites, with 1 site for administration
of rTPA and 1 site for delivery of intravenous fluids or other medications if the
patient is a candidate for rTPA (Class I, Level of Evidence C).
7) Only nondextrose, normotonic intravenous fluids such as normal saline should be
used in the AIS patient (Class I, Level of Evidence C).
8) Intravenous rTPA should be administered without delay and should not be excluded
in an eligible patient (Class I, Level of Evidence C)

Phase 2 of Stroke Care: The Acute Care

A. Nursing Care on Continued Stabilization of the Stroke Patient

Class I

1) Stroke neurological assessments should be performed every 4 hours after the

hyperacute phase of stroke, and then frequency should be based on the patients
stability and other comorbid conditions (Class I, Level of Evidence B).
2) Temperatures 99.6F should be managed aggressively (Class I, Level of Evidence C).
3) Continuous cardiac monitoring of the stroke patient should be provided for at least
24 to 48 hours after stroke to detect potential cardiac problems (Class I, Level of
Evidence B).
4) Careful, frequent monitoring and assessment for worsening of neurological deficits
or bleeding should be performed for up to 24 hours after thrombolytic therapy (Class
I, Level of Evidence B).
5) Oxygenation should be evaluated with an oxygen saturation monitor (Class I, Level
of Evidence C).
6) To prevent aspiration pneumonia, the patients lungs should be auscultated, and the
patient should be evaluated for signs of respiratory compromise and dysphagia
(Class I, Level of Evidence C). Nurses should report seizure activity, and treatment
should begin immediately (Class I, Level of Evidence B). Prophylactic treatment of
seizures should not be given.

B. Diagnostic Testing During the Acute Phase

Class I
Nurse-Rehab
Stroke Unit

All nurses should be familiar with the basic neuroimaging testing for stroke patients so that
they can educate and prepare patients and families (Class I, Level of Evidence C).

199
 C. General Supportive Care of Stroke

Class I
1) Infections, such as pneumonia and UTI, should be identified and treated immediately
with antibiotics (Class I, Level of Evidence B).
2) Early bowel and bladder care should be instituted to prevent complications such as
constipation and urinary retention or infection (Class I, Level of Evidence A). Use
of indwelling catheters should be avoided if possible because of the risk of UTI
(Class I, Level of Evidence A).
3) Early implementation of anticoagulant therapy or physical compression modalities
should be considered for all stroke patients who cannot ambulate at 2 days and who
are at risk for DVT or pulmonary embolus (Class I, Level of Evidence A). Early
mobility should always be attempted if safe for the patient (Class I, Level of Evidence
B).
4) Fall precautions should be initiated, and the stroke patient should be told not to
ambulate without assistance (Class I, Level of Evidence B).
5) Frequent turning should be instituted in bedridden patients to prevent skin
breakdown (Class I, Level of Evidence A). Use of Braden Scale in nursing practice
can assist in the prediction of stroke patients at high risk of developing pressure
ulcers (Class I, Level of Evidence A). Range-of-motion exercises should start in the
early phase of acute stroke care once risk has been assessed (Class I, Level of
Evidence C).
6) A swallow screen should be performed in the first 24 hours after stroke, preferably by
the speech language pathologist (Class I, Level of Evidence B). Nurses should be
familiar with bedside swallow assessment if a formal evaluation cannot be done
within the specified period. Stroke patients should be kept NPO until the screen has
been performed (Class I, Level of Evidence B). Further studies of dysphagia in the
setting of acute stroke should be performed.
7) Patients who cannot swallow should have a nasogastric tube placed, or if severity
warrants, a percutaneous endoscopic gastrostomy tube should be placed (Class I,
Level of Evidence B). Assessment of proper hydration is included in this
recommendation.

Class IIa
1) If an indwelling catheter is required, excellent pericare and prevention of infection
modalities should be instituted to prevent complications (Class IIa, Level of
Evidence C).
2) The stroke patient can be fed either by intravenous infusion or through nasogastric or
percutaneous endoscopic gastrostomy tubes (Class IIa, Level of Evidence B).

Class IIb
Nurse-Rehab
Stroke Unit

Nurses may provide passive range-of-motion (ROM) exercises between physical

therapy visits to help patients maintain joint mobility and prevent complications of
immobility (Class IIb, Level of Evidence C).

200
 COMPETENCY LEVELS OF STROKE NURSE

Requirements Level I Level II Level III

Nurse Clinician I Nurse Clinician II Nurse Specialist
Tenure in Stroke 1 year to 2 years 2 years to 3 years 3 years and above
Unit
PNA Certification Updated membership Updated membership Updated membership
SSP Certification Updated membership Updated membership Updated membership
ACLS Certification Updated membership Updated membership Updated membership
NIHSS Certification Updated membership Updated membership Updated membership
IV Therapy
Certification Updated membership Updated membership Updated membership
Knowledge in
Imaging Reading Can read basic Can read basic Can read basic
CT-Scan Imaging CT-Scan Imaging CT-Scan Imaging
with basic knowledge
in MRI Interpretation
Handled IV-rTPA Administered in IV- Administered in IV- Administered in IV-
rTPA Administration rTPA Administration rTPA Administration;
Supervised new staff
on IV-rTPA
administration
Rendered Stroke Rendered <10 stroke Rendered >11 stroke Rendered >21 stroke
Education education education education
Assisted Brain Attack Assisted <10 BAT calls Assisted >11 BAT calls Assisted >21 BAT
Team (BAT) Calls calls
Speakership Experienced in internal Experienced in external Experienced in
speakership speakership external speakership
Research Had joined research Had joined research Had produced stroke
team team research

Entry Requirement for Stroke Nurse

The following are recommendation for the minimum entry qualification and requirement for
a Stroke Nurse:

Must be a Registered Nurse in the Philippines

Must have a minimum of six months satisfactory working experience in a
Medical-Surgical area and have rendered nursing care to stroke survivors
Must have completed the Stroke Nursing Course
Must have satisfactorily passed the Stroke Care Skills Competency Check
Nurse-Rehab
Stroke Unit

Must have earned at least more than 20 credit units of Continuing Nursing
Education Programs related to Stroke or Neurological nursing topics

201
 APPENDIX ON PROPOSED STROKE NURSING COURSE

Course Objective:

This is a forty-hour program designed to provide nurses with the relevant information about
stroke, its diagnosis, treatment and management in the various phases. It will strengthen the
clinical thinking and practice of the nurses through the application of the principles and
concepts learned from the course and enable them to care for patients with acute and complex
event of stroke.

Specifically, the nurses will be able to:

1. Relate the normal anatomy and physiology of the brain with the event of an
ischemic or hemorrhagic stroke.
2. Describe the different types of stroke, its causes and risk factors, signs and
symptoms, and treatment options including medications, rehabilitative care,
nutrition, and exercise.
3. Describe the methods of assessment and diagnosis used for stroke and
management of the disease from a nursing perspective.
4. Develop clinical assessment utilizing various assessment tools.
5. Demonstrate nurses role through nursing management skills and specialized
stroke skills during the emergency, hyperacute and acute phase of stroke.
6. Formulate appropriate care plan for the different types of stroke.

Recommended Topics:

Review of the Anatomy and Physiology of the Human Brain

Pathophysiology of Ischemic and Hemorrhagic Stroke
Risk Factors
Stroke Mimic
o Stroke in the Young
o Transient Ischemic Attack (TIA)
Psychological Impact of Stroke
Complications After Stroke
Stroke Assessment Tools
Pre-hospital Tools
o Cincinnati Stroke Scale
o Los Angeles Prehospital Stroke Screen
Acute Assessment Tools
o Glasgow Coma Scale
o Hunt and Hess Scale
Nurse-Rehab
Stroke Unit

o National Institute of Health Stroke Scale

Functional Assessment
o Modified Rankin Scale

202
 Outcome Assessment Scale
o Barthel Index Scale
Pressure Sore Risk Assessment Tool
o Braden Scale
Nurses Role in the Emergency, Hyperacute and Acute Phase of Stroke
Diagnostic Procedures and Laboratory Studies
Treatment and Management
Pharmacological Management
Surgical Intervention
Rehabilitation
Nursing Management and Intervention Skills
Stroke Care Skills
Stroke Education
Dysphagia Screening
Imaging and Electroencephalography (EEG)
Basic interpretation of CAT scan and MRI (Bleed or Infarct)
o Special Equipment and Gadgets (ICP Monitors and Cerebral Oximeter)

ACKNOWLEDGEMENTS:
Special Thanks to the participants: Amang Rodriguez Medical Center, Arellano University,
Asian Hospital and Medical Center, Capitol Medical Center, Cardinal Santos Medical Center,
Makati Medical Center, Manila Doctors Hospital, Our Lady of Lourdes Hospital, St. Lukes
Medical Center Quezon City & Global City, The Medical City, University of the
Philippines Philippine General Hospital, University of Santo Tomas Hospital, Inc.

The Medical City - Acute Stroke Unit

Critical Care Nurses Association of the Philippines, Inc. (CCNAPI)

Mrs. Ma. Isabelita C. Rogado, RN,MAN

President, Critical Care Nurses Association of the Philippines, Inc.

Hon. Marco Santo Tomas

Member, Board of Nursing, Professional Regulation Commission
Nurse-Rehab
Stroke Unit

203
 III. GUIDELINES FOR STROKE REHABILITATION

METHODOLOGY

This guideline was developed through the formation of a consensus panel composed of a
chairperson and consultants from various hospitals in Metro Manila. Key issues with regards to
rehabilitation of stroke patients were identified. Existing clinical practice guidelines were
reviewed. Related literatures, with emphasis on systematic reviews and randomized controlled
trials were appraised.

BACKGROUND

The rehabilitation of a stroke patient is long and intensive. It is a lifelong commitment and an
important part of recovery. It facilitates relearning of basic skills such as eating, dressing and
walking. It could also improve strength, flexibility and endurance. The goal of rehabilitation is
to regain as much functional independence as possible. The conventional approach to
rehabilitation is a cyclical process and includes:

assessment: patients needs are identified and quantified

goal setting: goals are defined for improvement (long/medium/short term)
intervention: to assist in the achievement of the goals
re-assessment: progress is assessed against the agreed goals

Rehabilitation goals can be considered at several levels:

aims: often long term and referring to the situation after discharge
objectives: usually multi-professional at the level of disability
targets: short term time-limited goals

OBJECTIVES

The goal of this guideline is to assist individual clinicians and caregivers to optimize
management of stroke patients. The focus is on general rehabilitation, the prevention and
management of common complications and discharge planning.

INTENDED USERS

This guideline is intended for the use of any person who is interested in caring for patients who
had stroke such as primary physicians, paramedics and care givers. It provides basic standard
care for stroke patients although approach and management should be individualized as dictated
by patients condition.
Nurse-Rehab
Stroke Unit

204
MANAGING LIFE AT HOME AFTER STROKE

Suggested changes and approach to activities to make everyday living easier.

A. General Approach
If using wheelchair or assistive device (canes, walker), move extra furniture
out of the way to make room for a wheelchair or for walking with a walker
or cane.
Adjust lightning throughout home to decrease glare and help patient see
better in low-lit areas
Move electrical cords out of pathways
Install handrails for support in going up and down stairs
Remove loose carpets or floor rugs to minimize risk of slipping

B. Bathing and Toileting

Install sturdy hand rails and grab bars in the tub or shower
Place bathing supplies that are easy to reach and use
Consider use of squeeze bottles and pump bottles which may be easier to
use

C. Getting Dressed
Avoid tight fitting sleeves, armholes, pant legs and waistlines
Consider using clothes with front closures
Consider replacing buttons, zippers and laces with velcro fasteners

MANAGEMENT AND PREVENTION STRATEGIES

A. General Rehabilitation Principles

1. Early mobilization
Goal is to prevent complications of immobilization and deconditioning
(pneumonia, deep venous thrombosis, pressure ulcer)
Patient should be mobilized as early as possible (within 48 hours) after
stroke, if medically stable.
Patients and carers should have early active involvement in the
rehabilitation process.
Level of evidence: B
Patients and caregivers should have an early active involvement in the
rehabilitation process.
Stroke patients should be mobilized as early as possible after stroke.

2. Therapeutic positioning
Aim in positioning the patient is to try to promote optimal recovery by
Nurse-Rehab

modulating muscle tone, providing appropriate sensory information and

Stroke Unit

increasing spatial awareness and to prevent complications such as pressure

sores, contractures, pain and respiratory problems and to assist safer
eating.

205
 Five main positions recommended are lying on the unaffected side, lying
on the affected side, lying supine, sitting up in bed and sitting up in a chair.
In the upper limb, the affected shoulder should be in a position of
abduction and external rotation with the arm brought forward and the
fingers extended, to counteract the tendency for the shoulder to adduct
and rotate internally. While sitting, affected limb should be supported at
the arm to prevent shoulder subluxation.
The trunk should be straight. In the midline, avoid forward or side flexion
in both sitting and lying position.
For the lower limb, it should be in a neutral position with the ankle in 90
degrees of dorsiflexion (may provide foot board), with the knees bent to
90 degrees in sitting position.
In the first 48 hours after stroke, there is evidence to support reducing the
risk of hypoxia by sitting the patient in an upright position, if medically fit
to do so
Level of evidence: C
Patients should be placed in the upright sitting position, if medically fit to
do so.

3. Activities of daily living interventions

Occupational therapists use the process of activity analysis to grade
activities of daily living so that they are achievable, but challenging, in
order to promote recovery after stroke.
It includes supplying and training the patient in the use of adaptive
equipment to compensate for the loss of ability to perform ADLs.
Common activities of daily living that needs to be addressed include
bathing, dressing and grooming, eating and drinking, toileting and
transferring.
Level of evidence: A
Personal ADL training by an occupational therapist is recommended for
patients with stroke in the community.
Level of evidence: B
Personal ADL training by occupational therapists is recommended as part
of an inpatient stroke rehabilitation programme.

4. Plegia and paresis

Electrostimulation/functional electrical stimulation should be considered,
the goal of which is to prevent muscle atrophy and facilitate muscle
contraction.
Nurse-Rehab
Stroke Unit

Range of motion exercises should be done, the type of which depends on

muscle grade of the patient.

206
B. Gait, Balance and Mobility

1. Electrostimulation
May be effective for some patients with specific problems, when delivered
in a specific way such as in patients with drop-foot, where the aim of
treatment is the immediate improvement of walking speed and/or
efficiency.
Level of evidence: C
Functional electrical simulation may be considered as a treatment for
drop-foot, where the aim of treatment is the immediate improvement of
walking speed and/or efficiency.

2. Muscle strengthening
It is beneficial at improving muscle strength but insufficient evidence to
determine relationship between muscle strength and functional outcome.
Level of evidence: B
Muscle strength training is recommended when the specific aim of
treatment is to improve muscle strength.

3. Ankle foot orthosis

There is a positive impact of ankle foot orthosis on outcomes of walking
speed, efficiency and gait pattern and weight bearing during stance
Level of evidence: C
Where the aim of treatments is to have an immediate improvement on
walking speed, efficiency or gait pattern or weight bearing during stance,
patents should be as assessed efficiency.

4. Walking aids
Should be considered only after a full assessment of the potential benefits
and harms of the walking aid in relation to the individual patients stage of
recovery and presentation.
The use of a cane if indicated should be used on the unaffected side.

5. Treadmill training
It may be used to increase gait speed among people who are independent
in walking at the start of treatment.
Level of evidence: B
Nurse-Rehab
Stroke Unit

Treadmill training may be considered to improve gait speed in people who

are independent in walking at the start of treatment.

207
 6. Physical fitness training
Gait-oriented physical fitness training after stroke can improve gait speed
and endurance and may reduce the degree of dependence on other people
during walking.
Level of evidence: A
Gait-oriented physical fitness training should be offered to all patients
assessed as medically stable and functionally safe to participate, when the
goal of treatment is to improve functional ambulation.

7. Intensity of intervention
When safe, increasing the intensity of rehabilitation by doubling the
standard amount of therapy has beneficial effects on functional outcomes,
including gait.
Level of evidence: B
Where considered safe, every opportunity to increase the intensity of
therapy for improving gait should be pursued.

C. Upper limb function

1. Range of motion activities

Activities that promote range of motion of the affected limb (shoulder,
elbow, wrist) should be encouraged and should include fine motor
dexterity if applicable
.
2. Constraint induced movement therapy
It can produce a moderate improvement in upper limb function in stroke
patients.
Mainly in patients with at least 10 degrees of finger extension, limited
balance problems and intact cognition.
Level of evidence: B
Constraint induced movement therapy may be considered for carefully
selected individuals with at least 10 degrees of finger extension, intact
balance and cognition.

3. Repetitive task training

Not routinely recommended but can be done in patients whom there is a
clear functional goal.
Level of evidence: A
Repetitive task training is not routinely recommended for improving
upper limb function.

4. Imagery/mental practice
Nurse-Rehab
Stroke Unit

May be considered as an adjunct to normal practice to improve upper limb

function.

208
 Level of evidence: D
Mental practice may be considered as an adjunct to normal practice to
improve upper limb function after stroke.

5. Splinting
Splinting the wrist in either the neutral or extended wrist position to
prevent contractures in patients with moderate to severe spasticity.
Level of evidence:
Splinting of upper extremities (hands) in patients with moderate to severe
spasticity to facilitate positioning.

D. Communication

1. Aphasia
It is an acquired multimodal language disorder and can affect the persons
ability to talk, write and understand spoken and written language while
leaving other cognitive abilities relatively intact.
There is good evidence that people with aphasia benefit from speech and
language therapy.
Where patient is sufficiently well and motivated, a minimum of two hours
per week should be provided.
Where appropriate, treatments for aphasia may require a minimum period
of six months to be fully effective.
Level of evidence: B
Aphasic stroke patients should be referred for speech and language
therapy. Where the patient is sufficiently well and motivated, a minimum
of two hours per week should be provided.
Where appropriate, treatments for aphasia may require a minimum period
of six months to be fully effective.

2. Cognitive
Cognitive rehabilitation concerns efforts to help patients understand their
impairment and to restore function or to compensate for lost function
(e.g. by teaching strategies) in order to assist adaptation and facilitate
independence.

3. Dysarthria
It is a motor speech impairment of varying severity affecting clarity of
speech, voice, quality and volume and overall intelligibility.
Patients with dysarthria should be referred to speech and language therapy
service.
Nurse-Rehab
Stroke Unit

Level of evidence: B
Patients with dysarthria should be referred to an appropriate speech and
language therapy service for assessment and management.

209
 E. Dysphagia and Swallowing

All patients who are conscious and can follow command should be screened for
dysphagia before given food or drink. Water swallow test should be used as a part of
screening.

In the presence of abnormality during screening, modified barium swallow test

and fiber optic endoscopic evaluation of swallow are both valid methods for
assessing dysphagia.
Dietary modification and compensatory techniques should be taught to
patients who are assessed to be able to feed orally safely.
For patients who are at risk for aspiration and cannot feed adequately orally,
NGT and PEG insertion risks and benefits should be discussed with patient
PEG tube care:
Check your PEG tube often to see if it is loose or out of place.
You may use a PEG cleaning brush to help clean the inside of your
tube and flush the tube with warm water if it is clogged.
NGT care:
Verify proper placement of the nasogastric tube by auscultating a
rush of air over the stomach using the 60 mL Toomey syringe or by
aspirating gastric content.
Level of evidence: D
All patients who have dysphagia for more than one week should be assessed to
determine their suitability for a rehabilitative swallowing therapy program.
Consideration should be given to:
the nature of the underlying swallowing impairment
patient suitability in terms of motivation and cognitive status
Level of evidence: B
Patients with dysphagia should have an oropharyngeal swallowing
rehabilitation program that includes restorative exercises in addition to
compensatory techniques and diet modification.

F. Post-stroke spasticity

1. Stretching
Increase ROM by lengthening tendon and muscle beyond the available
range.
Include static stretching, static stretching with contraction of the
antagonist muscle (reciprocal inhibition), static stretching with
contraction of the agonist muscle, and ballistic stretching.

2. Cryotherapy
Nurse-Rehab
Stroke Unit

Decreased spasticity
Increased tissue viscosity with decreased tissue elasticity

210
3. Functional electrical stimulation
Although there was an increase in muscle force generated following FES,
there was no evidence of clinical benefit and no effect on muscle
spasticity.

4. Oral antispasticity agent

In patients whom it is considered to be used, oral agents should be
monitored regularly for efficacy and side effects and withdrawn when
ineffective following a therapeutic trial.
Level of evidence:
Where considered, oral agents should be monitored regularly for efficacy
and side effects and withdrawn where ineffective following a therapeutic
trial.

5. Clostridium botulinum toxin A

It can reduce spasticity (measured by modified ashworth scale or global
assessment scale) in the upper limb following stroke, with maximum
effects seen 4-6 weeks after injection, regardless of dose, and with return
to baseline within 10-16 weeks.
In the lower limb, it is more effective than phenol injection but with
inconsistent effects on walking speed and step length.
No significant effects on functional ability or quality of life measures seen
after treatment.
Compared to oral antispasticity agent tizanidine, it produced a greater
reduction in the modified ashworth scale in wrist flexor and finger flexor
tone.

6. Chemical neurolysis
May be an effective intervention for treatment of spasticity in both the
upper and lower extremities, however, one should consider the risk of
painful dysesthesia if used.

7. Surgery
Tibial nerve neurotomy may be effective in reducing spasticity in the lower
limb but further evaluation is required in RCTs before recommendation
for its use can be made.
Nurse-Rehab
Stroke Unit

211
 I. ACUTE POST-STROKE REHABILITATION

Patient with stroke during acute phase

Obtain medical history and physical examination.

Initial assessment of complications, impairment and rehabilitation needs including
NIHHS, GCS, MRS, FIMS/Barthel Index.

Initiate secondary prevention and prevention of complications.

Acute post-stroke patient assessed for rehabilitation services.

Determine nature and extent of rehabilitation needs and services based on stroke
severity, functional status and social support.

MILD MODERATE STROKE SEVERE STROKE

Go to II, III or IV Go to II Go to II

A. Initial brief assessment

Assessment for complications and prior and current impairment:
1. Risk factors for recurrent stroke and coronary heart disease
2. Medical comorbidities (DM, hypertension, increase ICP, re-bleed, re-stroke)
3. Consciousness and cognitive status
4. Brief swallowing assessment
5. Skin assessment and pressure ulcers
6. Mobility and need for assistance of movement
7. Deep-vein thrombosis (DVT) risk assessment
B. Assessment of rehabilitation needs
1. Prevention of complications: swallowing problems, skin breakdown, DVT,
bowel and bladder dysfunction, malnutrition, pain, contractures, SHS/CRP,
pulmonary
2. Assessment of impairments: communication impairments, motor
impairment, cognitive deficits, visual and spatial deficiency, psychological or
Nurse-Rehab

emotional deficits, sensory deficits

Stroke Unit

3. Psychosocial assessment and family or caregivers support

4. Assessment of function (e.g., functional independence measure or FIM)
5. Financial support

212
 II. INPATIENT REHABILITATION

Post-stroke patient in inpatient rehabilitation

Determine level of care based on medical status, cognitive and motor f unction, social support,
and access to care and services.

Discuss rehabilitation program with patient and family.

Initiate rehabilitation programs and interventions.

Reassess progress, future needs and risks with team .

Is patient progressing toward treatment goals?

NO YES

Address treatment adherence and barriers to Is patient ready for

improvement. If medically unstable, refer to acute community living?
services. If with other health factors, refer to other
health services.
NO YES

Severe stroke and/or maximum dependence, or poor

prognosis for functional recovery?

YES NO

Educate patient, family, caregiver Continue inpatient Go to III.

about future plans and home rehabilitation.
Nurse-Rehab

therapy.
Stroke Unit

Discharge patient to the home or

community.

213
 Reassessment of Rehabilitation Progress
1. General (medical status)
2. Functional status (FIM, etc.): Mobility, activities of daily living (ADL) and
instrumental ADLs, communication, nutrition, cognition,
mood/affect/motivation, sexual function
3. Family support: Resources, caretaker, transportation
4. Patient and family adjustment
5. Reassessment of goals
6. Risk for recurrent cerebrovascular events

III. OUTPATIENT REHABILITATION

Post-stroke patient ready for home

Does patient need outpatient rehabilitation NO Go to IV.

services?

YES

Reassess progress, rehabilitation interventions and optimal

environment for outpatient rehabilitation.

Discuss shared decisions regarding rehabilitation program and

treatment plan with patient and family.
Continue secondary prevention.

Continue rehabilitation intervention at nearby center or

hospital, or use home rehabilitation services.

Did patient plateau or achieve optimal function? YES

NO
Nurse-Rehab
Stroke Unit

Reassess periodically. Go to IV.

214
Assessment of Discharge Environment
1. Functional needs
2. Motivation and preferences
3. Intensity of tolerable treatment: Equipment, duration
4. Availability and eligibility
5. Transportation
6. Home assessment for safety

IV. COMMUNITY BASED REHABILITATION

Post-stroke patient ready for community living

Arrange
primary-care
Does patient need community-based NO follow-up.
rehabilitation services? Provide home
rehabilitation.
program.
YES

Determine optimal environment for community -based

rehabilitation.

Discuss shared decision regarding rehabilitation program and

treatment plan with patient and family.

Continue rehabilitation intervention with patient and

family/caregiver education.

Did patient plateau or achieve optimal function? YES

NO

Discharge to the home or

Reassess periodically.
community setting.
Nurse-Rehab

Arrange primary-care follow-up.

Stroke Unit

215
 Assessment of Discharge Environment
1. Functional needs
2. Motivation and preferences
3. Intensity of tolerable treatment: Equipment, duration
4. Availability and eligibility
5. Transportation
6. Home assessment for safety
7. Maximal patient functioning

Bibliography
1. Scottish Intercollegiate Guidelines Network (SIGN). Management of patients with stroke:
Rehabilitation, Prevention and Management of Complications and Discharge planning.
Edinburgh: SIGN; 2010. (SIGN publication no. 119). [cited 04 May 2010]. Available from
url: http://www.sign.ac.uk
2. Scottish Intercollegiate Guidelines Network (SIGN). Management of patients with stroke:
Identification and management of dysphagia. Edinburgh: SIGN; 2010. (SIGN publication
no. 119). [cited 04 May 2010]. Available from url: http://www.sign.ac.uk
3. National Institute for Health and Clinical Excellence (NICE). The assessment and
prevention of falls in older people. London: NICE; 2004. (NICE guideline CG21). [cited 03
May 2010]. Available from url: http://guidance.nice.org.uk/CG21
4. Duncan, P. W., Zorowitz, R., et al. Management of adult stroke rehabilitation care. A clinical
practice guideline. Journal of the American Heart Association 2005; 36: 100-143

IV. STRATEGY FOR IMPLEMENTATION OF GUIDELINES

To effectively implement the guidelines set forth in the previous sections, it is

recommended that Stroke Centers be established in every region. Stroke Centers shall be
designated according to levels as follows:
STROKE
REQUIREMENTS ACTIVITIES
CENTER LEVEL

I Basic: Stroke prevention and public

Physician/Municipal Health education
Officer Recognition of stroke
Acute treatment of TIA and mild
Optional: stroke
Nurse/Midwife Referral of moderate and severe
Barangay Health Worker strokes to Levels II or III centers
Referral to Levels II or III centers for
Facilities: diagnostic tests
Municipal Health Clinic Rehabilitation
Nurse-Rehab

Secondary prevention of stroke and

Stroke Unit

follow-up visits

216
STROKE
CENTER REQUIREMENTS ACTIVITIES
LEVEL

II Basic: Stroke prevention and public

Neurologist (If not available, other education
physicians with special training in Recognition of stroke
stroke) Acute treatment of TIA, mild,
Neurosurgeon moderate, and severe
Stroke nurse strokes
Radiologist Referral of complicated strokes
Physiatrist to Level III centers
Referral to Level III centers for
Facilities*: further diagnostic tests
CT scan Rehabilitation
Electrocardiogram Secondary prevention of stroke
Laboratory and follow-up visits
Stroke Team/Unit
Operating Room

III Basic: Stroke prevention and public

Neurologist education
Neurosurgeon Recognition of stroke
Stroke nurse Acute treatment of TIA, mild,
Neuroradiologist moderate, and severe strokes
Vascular surgeon Rehabilitation
Cardiologist Secondary prevention of stroke
Neurosonologist and follow-up visits
Physiatrist Training of stroke personnel
Research in stroke
Facilities:
CT scan, MRI
Cardiac diagnostic services (including
ECG, Doppler, echocardiogram)
Laboratory
Angiography
Stroke Unit
Rehabilitation Unit
Operating Room
Nurse-Rehab
Stroke Unit

217
 LEVELS OF STROKE CARE

STROKE CENTER LEVEL

STROKE SEVERITY I II III

TIA or Mild Stroke

Moderate Stroke

Severe Stroke

V. HOSPITALS IN THE PHILIPPINES WITH ACUTE STROKE UNITS

Stroke Number
Hospitals Chair Contact Number
Unit Type of Beds

Metro Manila
University of Santo Tomas
ASU 5 Dr. Jose C. Navarro 731-3001 local 2368
Hospital
Chinese General Hospital ASU 4 Dr. Johnny Lokin 711-4141 local 608
Mixed acute
East Avenue Medical Center 5 Dr. Ceferino Rivera 928-0611 local 503
units
Jose Reyes Mixed acute
10 Dr. Jose C. Navarro 711-9491 local 262
Memorial Medical Center units
Makati Medical Center ASU 2 Dr. Raquel Alvarez 888-8999

Mixed acute
Manila Central University 6 Dr. Rolando Perez 367-2031 local 2013
units
Mixed acute
Manila Doctors Hospital 10 Dr. Carlos Chua 524-3011 local 8118
units

Philippine Heart Center ASU 8 Dr. Jose C. Navarro 925-2401 local 2483

San Juan De Dios Mixed acute

2 Dr. Raquel Alvarez 831-9731 local 1226
Medical Center units
Nurse-Rehab
Stroke Unit

St. Luke's Medical Center

ASU 3 Dr. Cristina San Jose 723-0101 local 7399
Quezon City

218
 Stroke Number
Hospitals Chair Contact Number
Unit Type of Beds

Metro Manila
St. Lukes Medical Center Dr. Vincent de 789-7700 local 4104
ASU 4
Global City Guzman 4105
Mixed acute
The Medical City 8 Dr. Artemio Roxas Jr. 635-6789 local 6281
units

Luzon
Mixed acute
Baguio General Hospital 7 Dr. Socorro Sarfati 074-4424216
units
Dr. Dionisio Claridad
Baguio Medical Center 2 074-4423338
Dr. Socorro Sarfati
Lorma Medical Center, Mixed acute 072-700-0000 local
3 Dr. Raymond Espinosa
San Fernando, La Union units 144
Lucena United Doctors 042-3736161 local
ASU 4 Dr. Gerald Salazar
Hospital 210
Mt. Carmel Diocesan General
ASU 4 Dr. Glicerio Alincastre 042-7102576
Hospital, Lucena

Visayas
Mixed acute
Cebu Doctors Hospital 8 Dr. Emirito Calderon 032-2532972
units
Mixed acute 032-2558000 local
Chong Hua Hospital 2 Dr. Rogelio Chua
units 7201

Mindanao
Polymedic Medical Plaza,
Mized
National kauswagan, 2 Dr. Arturo F. Surdilla 0922 8242757
Type
Cagayan de Oro

*ASU, acute stroke unit.

Nurse-Rehab
Stroke Unit

219
 5th Edition SSP Handbook
WORKING COMMITTEES

Primary and Secondary Prevention of Stroke

Dr. Artemio Roxas, Jr
Dr. Maria Cristina San Jose
Dr. Raquel Alvarez
Dr. Cymbeline Perez-Santiago
Dr. Vincent De Guzman
Dr. Fatima Collado
Dr. Ester Bitanga
Dr. Dante Morales
Dr. Epifania Collantes
Dr. Alejandro Diaz
Dr. Romulo Esagunde
Dr. Victoria Manuel

Acute Stroke Management

Dr. Abdias Aquino Dr. Maria Cristina San Jose
Dr. Carlos Chua Dr. Lina Laxamana
Dr. Robert Gan

Definition of TIA and Stroke

Dr. Artemio Roxas, Jr Dr. Socorro Sarfati
Dr. Raymond Espinosa Dr. Maria Leticia Araullo

Hypertensive Intracerebral Hemorrhage

Dr. Manuel Mariano Dr. Maria Cristina San Jose
Dr. Rhoderick Casis Dr. Abdias Aquino
Dr. Carlos Chua Dr. Lina Laxamana

Aneurysmal Subarachnoid Hemorrhage

Dr. Rhoderick Casis Dr. Maria Cristina San Jose
Dr. Peter Rivera Dr. Ma. Cristina Macrohon

AV Malformation
Dr. Francis Santiago Dr. Eduardo Tan
Dr. Jose Navarro

Neuro-imaging in Stroke
Dr. Pedro Danilo Lagamayo Dr. Maria Cristina San Jose
Dr. Carlos Chua

220
 Establishment and Operation of Stroke Units
Dr. Jose Navarro Dr. Alejandro Baroque II
Dr. Epifania Collantes

Stroke Rehabilitation
Dr. Betty Mancao Dr. Arnel Malaya
Dr. Jose Alvin Mojica Dr. Reynaldo Rey-Matias
Dr. Sharon Ignacio Dr. Josephine Bundoc
Dr. Teresita Joy Ples Evangelista Dr. Jose Bonifacio Rafanan
Dr. Joycie Eulah Abiera Dr. Mayla Wahab-Tee

Nursing Management of Patients with Stroke

Hon. Marco Santo Tomas, RN
Noli Pagdanganan. RN
Veronica Honculada,RN
Marilou Reyes, RN
Josefine Rivera, RN
Ma. Isabelita Rogado, RN
Ferdinand Aganon, RN
Ana Merly Migo, RN
Lydia Bienes, RN

Support Staff
Ms. Marilou Olpindo Dr. Mark de Guzman
Ms. Catherine Mayordomo Dr. Antonio Piano
Ms. Desiree Mayordomo Dr. John Jerusalem Tiongson

Reviewers for the Revision of the 5th Edition ( 2011 )

Dr. Maria Cristina San Jose
Dr. Cristina Macrohon
Dr. Cymbeline Perez-Santiago
Dr. Romulo Esagunde
Dr. Ma. Leticia Araullo
Dr. Maria Cecilia Ocampo-Mallari
Dr. John Harold Hiyadan
Dr. Raquel Alvarez
Dr. Socorro Sarfati

Additional Chapter for 2011 printing:

Hemicraniectomy for Malignant MCA Infarction
Dr. Epifania Collantes Dr. Annabell Chua

Dr. Artemio A. Roxas, Jr.

Editor-in-Chief

221
 STROKE SOCIETY OF THE PHILIPPINES

Board Of Trustees Board Of Trustees

2008-2010 2010-2012

Officers Officers
DR. JOSE C. NAVARRO DR. CARLOS L. CHUA
President President
DR. CARLOS L. CHUA DR. ARTEMIO A. ROXAS JR.
1st Vice-President 1st Vice-President
DR. ARTEMIO A. ROXAS JR. DR. MARIA CRISTINA Z. SAN JOSE
2nd Vice-President 2nd Vice-President
DR. ALEJANDRO C. BAROQUE II DR. MA. EPIFANIA V. COLLANTES
Secretary Secretary
DR. BETTY D. MANCAO DR. BETTY D. MANCAO
Treasurer Treasurer
DR. MARIA CRISTINA Z. SAN JOSE DR. PEDRO DANILO J. LAGAMAYO
P.R.O. P.R.O.

Members Members
DR. MA. EPIFANIA V. COLLANTES Dr. RAQUEL M. ALVAREZ
DR. ROMULO U. ESAGUNDE Dr. ALEJANDRO C. BAROQUE II
DR. RAYMOND L. ESPINOSA Dr. ROMULO U. ESAGUNDE
DR. PEDRO DANILO J. LAGAMAYO Dr. JOHNNY K. LOKIN
DR. JOHNNY K. LOKIN Dr. MANUEL M. MARIANO
DR. MANUEL M. MARIANO Dr. DANTE D. MORALES
DR. DANTE D. MORALES Dr. ORLINO A. PACIOLES
DR. ORLINO A. PACIOLES Dr. PETER P. RIVERA
DR. PETER P. RIVERA Dr. MA. SOCORRO F. SARFATI

DR. ESTER S. BITANGA DR. ABDIAS V. AQUINO DR. JOVEN R. CUANANG

Immediate Past President, 2006-2008 Past President, 2004-2006 Founding President, 1995-2004

CHAPTER PRESIDENTS
PAMPANGA CHAPTER Dr. Ma. Leticia Araullo
BAGUIO-BENGUET CHAPTER Dr. Maria Socorro Sarfati
LA UNION CHAPTER Dr. Raymond Espinosa
CENTRAL LUZON CHAPTER Dr. Wilfredo Calma
ILO-ILO CHAPTER Dr. Joel Advincula
SOUTHERN MINDANAO CHAPTER Dr. Orlino Pacioles
PANGASINAN CHAPTER Dr. Philip Oliva
OLONGAPO CHAPTER Dr. Arturo Arkoncel
DUMAGUETE CHAPTER Dr. Brenda Diputado

222
 SSP CONVENTIONS

1st Philippine Congress on Brain on Brain Attack

Theme: Thinking Globally, Acting Locally
October 1-2, 1999
Manila Midtown Hotel
2nd Philippine Congress on Brain Attack
Theme: Organizing Stroke Services
Year 2001
3rd Philippine Congress on Brain Attack
Theme: Intracerebral Hemorrhage (ICH) and Subarachnoid Hemorrhage (SAH)
August 2002
4th SSP Biennial Convention
Theme: Ugaliing Tingnan, Ating Kalusugan, Upang Brain Attack ay Maiwasan
August 20-22, 2003
Bethel Guest House, Dumaguete City
5th SSP Annual Convention
Theme: Emerging Diagnostic Modalities & Therapeutic Interventions in Acute Brain Attack
August 19-21, 2004
Taal Vista Hotel, Tagaytay City
6th SSP Annual Convention
Theme: SSP Goes to the Community
August 18-20, 2005
Fort Ilocandia Hotel, Laoag City
7th SSP Annual Convention
Theme: SSP goes to Mindanao: Empowering the Community for Optimal Stroke Care
August 21-23, 2006
The Marco Polo Hotel, Davao City
8th Annual Convention
Theme: SSP goes to Central Luzon: Empowering the Community Against Stroke
August 16-18, 2007
El Centro Convention Center,Subic, Olongapo City
9th Annual Convention
Theme: Stop Stroke before it Stops You
August 22-24, 2008
Baguio Country Club, Baguio City
10th Annual Convention
Theme: The Philippine Stroke Agenda: Tackling Knowledge,Issues,Concerns and Awareness in Stroke
August 20-22, 2009
Holiday Inn, Clarkfield, Pampanga
11th Annual Convention
Theme: Harmonizing Strategies in Stroke: From Bench to Bedside to Backyard
August 18-20, 2010
Marco Polo Hotel, Davao City
12th Annual Convention
Theme: Strengthening the Weaker Links in Philippine Stroke Care
August 11-13, 2011
Sarabia Manor Hotel, Iloilo City

223
 SSP CORPORATE MEMBERS

United Laboratories Inc. (Therapharma)

Otsuka Philippines, Inc.
Natrapharm Pharmaceuticals
Sanofi Aventis
Servier Philippines Inc.
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