4th EDITION

the STROKE SOCIETY of the PHILIPPINES

Guidelines for the Prevention, Treatment and Rehabilitation of Brain Attack

A Project of the Stroke Society of the Philippines

 Front Panel Painting;
“LIFE”
By: William T. Chua, M.D
Director, Heart Institute
St. Luke’s Medical Center
Guidelines for the Prevention, Treatment and Rehabilitation
of Brain Attack
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.

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.
TABLE OF CONTENTS

I. Message from the Founding President

II. Message from the President
III. Guidelines for the Primary and Secondary Prevention of Stroke
a. Preface to the Guidelines for the Primary and Secondary
Prevention of Stroke
b. Hypertension
c. Transient Ischemic Attack
d. Diabetes Mellitus
e. Atrial Fibrillation
f. Acute Myocardial Infarction (With Left Ventricular Thrombus) and
Cardiomyopathy
g. Valvular Heart Disease
h. Carotid Stenosis
i. Intracranial Stenosis
j. Smoking
k. Excessive Alcohol
l. Peripheral Arterial Disease
m. Physical Inactivity
n. Obesity
o. Diet

IV. Guidelines for Acute Stroke Treatment

V. Special Section on Management of Aneurysmal Subarachnoid
Hemorrhage
VI. Guidelines on the Establishment and Operation of Stroke Units
VII. Guidelines for Stroke Rehabilitation
VIII. Guidelines for Nursing Management of Stroke Patients
IX. Strategy for Implementation of Guidelines
X. Working Committees
XI. List of Corporate Members
MESSAGE from the FOUNDING PRESIDENT

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
MESSAGE from the PRESIDENT

The three revisions and four editions of these Guidelines for the
Prevention, Treatment and Rehabilitation of Brain Attack since 1999 reflect the
dynamic evolution of the management of cerebrovascular diseases and its
outcomes in the last seven years. The latest data from the most recent trials
have been incorporated into the previous guidelines, resulting in these updated
Guidelines edition. Furthermore, there is a newly added section: The
Establishment and Operation of Stroke Units.

The working group of this fourth edition has strived hard to come out with
this new document, a project and testament of the SSP of its commitment to our
colleagues and to the fight against brain attack.

ABDIAS V. AQUINO, MD
President
Stroke Society of the Philippines
Guidelines for PRIMARY and SECONDARY PREVENTION of STROKE
 STROKE 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 knowledge on primary and secondary stroke
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. This knowledge would lead to proper
recommendations.
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
reviewer’s 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 recommendation 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 (Table 1).
Recommendations considered the cost-effective treatment of drugs with
established efficacy.
These guidelines concentrated on modifiable risk factors: hypertension,
diabetes, atrial fibrillation (AF) and other specific cardiac conditions,
dyslipidemia, carotid artery stenosis, peripheral arterial disease, obesity,
and lifestyle (exposure to cigarette smoke, excessive alcohol use, physical
inactivity and unhealthy diet).
Other less well-documented or potentially modifiable risk factors are
recognized. These include metabolic syndrome, drug abuse, oral
contraceptive use, sleep-disordered breathing, migraine headache,
hyperhomocysteinemia, hypercoagulability, inflammation and infection.
Future editions may highlight these topics.
 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
outcome 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.

Table 1. 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
Class II Conditions for which there is conflicting evidence and/or a
divergence 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
Class III Conditions for which there is evidence and/or general agreement
that 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

I. HYPERTENSION
Hypertension awareness, treatment and control remain low. Stroke mortality
rates are predicted by the prevalence of hypertension. Yet compelling data show
that first stroke can be prevented by blood pressure (BP) control, among others. 1

A. Epidemiology: Hypertension is directly related to primary and secondary

stroke risk. The higher the BP, the greater is the risk. Hypertension has a local
prevalence of 17.4%2 and is the most important modifiable risk factor for stroke.
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
hypertensions are risk factors.
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 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

B1. Primary Stroke Prevention

There is strong evidence that the control of high BP contributes to the
prevention of stroke.5 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 (Table 2).5

Table 2.Classification and management of BP for adults*

BP SBP* DBP* Lifestyle Initial drug therapy
Classification mmHg mmHg Modification Without With
Compelling Compelling
Indication Indications
Normal <120 and Encourage No Drug(s)for
<80 antihypertensive compelling
Prehypertension 120- or 80- Yes drug indicated. indications.‡
139 89
Stage 1 140- or 90- Yes Thiazide-type Drug(s)for the
Hypertension 159 99 diuretics for compelling
most. May indications.‡
consider Other
ACEI, ARB, antihypertensive
BB, CCB, or drugs (diuretics,
combination. ACEI, ARB,
BB, CCB) as
needed.
Stage 2 ≥160 or Yes Two-drug
Hypertension ≥100 combination for
most† (usually
thiazide-type
diuretic and
ACEI or ARB
or BB or CCB).
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.

B2. Secondary Stroke 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 are largely lacking. A meta-analysis showed a
significant reduction in recurrent stroke with diuretics and combined diuretics and
angiotensin-converting enzyme (ACE) 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.
With regard to stroke risk reduction, there may be beneficial non-BP-
lowering properties of certain classes of BP-lowering agents, particularly from
ACEIs and angiotensin-receptor blockers (ARBs).10,11 Among hypertensive
diabetics, the use of ACEIs or ARBs reduces the risk of major vascular events
and stroke by 24%.

C. Recommendation:

C1. For primary 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, are recommended.

C2. For secondary prevention

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).12
Because this benefit extends to people with or without a history of hypertension,
this recommendation should be considered for all ischemic stroke and TIA
patients (Class IIa-B). The absolute target BP level and reduction are uncertain
and should be individualized, but benefit has been associated with an average
reduction of 10/5 mmHg, and normal BP levels have been defined as <120/80
mmHg by JNC 7 (Class IIa-B). 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.
Several lifestyle modifications have been associated with BP reductions
and should be included as part of a comprehensive antihypertensive therapy
(Class IIb-C).
The optimal drug regimen remains uncertain; however, the available data
support the use of diuretics and the combination of diuretics and an ACEI (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). The Stroke Society of the Philippines supports
the guidelines set forth by the Philippine Society of Hypertension and the JNC 7.

Bibliography
1. Chapman N, Neal B. Blood pressure lowering for the prevention of first stroke. In: Chalmers J, ed.
Clinician’s 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. Phil J Med 2003;4D:1-6.
3. Gorelick PB. An integrated approach to stroke prevention. In: Chalmers J, ed. Clinician’s 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.
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 published
reviews. Stroke 2004;35:776-785.
9. Rashid P, Leonardi-Bee J, Bath P. Blood pressure reduction and secondary prevention of stroke 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.
II. TRANSIENT ISCHEMIC ATTACK
Conventionally, a person is diagnosed with stroke if neurological symptoms
persist more than 24 hours; otherwise, a focal neurological deficit lasting <24
hours was defined as a TIA. However, with modern brain imaging, infarctions can
be detected even in patients with brief symptoms. The most updated definition of
stroke used by clinical trials is either symptoms lasting >24 hours or an acute
clinically relevant brain lesion on imaging in patients with rapidly vanishing
symptoms. The proposed new definition of TIA is a “brief episode of neurological
dysfunction caused by a focal disturbance of brain or retinal ischemia, with
clinical symptoms typically lasting less than 1 hour, and without evidence of
infarction.1

A. Epidemiology: Although TIA is most correctly considered a manifestation of

cerebrovascular disease and not a stroke risk factor, it is an important predictor
of future strokes. Reported 90-day stroke risk associated with TIA reaches
10.5%, and the highest risk is apparent in the first week.2 The risk is 4% to 8% in
the first month, 12% to 13% in the first year, and 24% to 29% in 5 years.2-4
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

B. Risk Modification: The distinction between TIA and ischemic stroke has
become less important in recent years because many preventive approaches are
applicable in both. As the risk factors for ischemic stroke and TIA are the same,
the evidences supporting that modification of a particular risk factor are found in
the corresponding sections in these guidelines. 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, ticlopidine, cilostazol and clopidogrel.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.

C. Recommendations: Efforts to increase public awareness and that of health

workers regarding TIA and its significance should be maximized.
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 stenosis and other modifiable risk factors should be treated, as
outlined in these guidelines.
The cost and benefit of a drug should be considered when choosing an
antiplatelet agent. Aspirin is the first choice unless contraindicated.
Patients who developed stroke recurrence while on aspirin, or those who
cannot tolerate or have contraindications to aspirin may be given clopidogrel,
combined aspirin and dipyridamole, cilostazol, or other antiplatelets with RCT
evidence of benefit. Aspirin is not recommended for primary stroke prevention, as
this has no evidence especially among men.
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.
Bibliography:
1. 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.
2. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department
diagnosis of TIA. JAMA 2000;284:2901-2906.
3. Dennis M, Bamford J, Sandercock P, et al. Prognosis of Transient Ischemic Attacks in the Oxfordshire
Community Stroke Project. Stroke 1990;21:848-853.
4. 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.
5. Streifler JY, Benavente OR, Harbison JW, et al. Prognostic implications of retinal versus hemispheric
TIA in patients with high grade stenosis: observations from NASCET. Stroke 1992;23:159. Abstract.
6. 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.
7. 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.
8. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet
therapy for prevention of death, myocardial infarction, and stroke in high-risk patients. BMJ
2002;324:71-86.

APPENDIX OF TIA MANAGEMENT FOR STROKE PREVENTION

Since the 3rd edition of these guidelines, there have been several important trials
related to antiplatelets and anticoagulants. The 2006 recommendations of the
American Heart Association and the American Stroke Association are outlined
below:

ASA/AHA Recommendations for Antithrombotic Therapy for

Noncardioembolic Stroke or TIA (Oral Anticoagulant and Antiplatelet
Therapies)
For patients with noncardioembolic ischemic stroke or TIA, antiplatelet
agents rather than oral anticoagulation are recommended to reduce the risk of
recurrent stroke and other cardiovascular events (Class I-A).
Aspirin (50 to 325 mg/day), the combination of aspirin and extended-
release dipyridamole, and clopidogrel are all acceptable options for initial therapy
(Class IIa- A).
Compared with aspirin alone, both the combination of aspirin and
extended-release dipyridamole and clopidogrel are safe.
The combination of aspirin and extended-release dipyridamole is
suggested over aspirin alone (Class IIa-A).
Clopidogrel may be considered over aspirin alone on the basis of direct-
comparison trials. Insufficient data are available to make evidence-based
recommendations with regard to choices between antiplatelet options other than
aspirin. Selection of an antiplatelet agent should be individualized based on
patient risk factor profiles, tolerance, and other clinical characteristics (Class IIb-
B).
Addition of aspirin to clopidogrel increases the risk of hemorrhage and is
not routinely recommended for ischemic stroke or TIA patients (Class III-A).
For patients allergic to aspirin, clopidogrel is reasonable (Class IIa-B).
For patients who have an ischemic cerebrovascular event while taking
aspirin, there is no evidence that increasing the dose of aspirin provides
additional benefit. Although alternative antiplatelet agents are often considered
for noncardioembolic patients, no single agent or combination has been well
studied in patients who have had an event while receiving aspirin.

Reference: 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.

III. DIABETES MELLITUS

A. Epidemiology: 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 >125 mg/dL) according to the 2003
National Nutrition Health Survey1 is 4.6% (4.1% in males, 5% in females) while
impaired fasting glucose is 3.2% (similar rates for males and females).

People with type 2 DM have both an increased risk of atherosclerosis and

increased prevalence of atherogenic risk factors (i.e., hypertension, obesity and
abnormal blood lipids). DM is a definite risk factor for stroke.2 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.3 DM is frequently encountered in stroke care, being present
in 15% to 33% of patients with ischemic stroke.4 The local RIFASAF case-control
study showed a 1.6-fold higher risk for stroke among those with DM.5 However,
data supporting DM as a risk factor for recurrent stroke are sparse.

B. Risk Modification

B1. 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, 6 but not
macrovascular complications.7 Systematic review of RCTs on intensive insulin
therapy (IIT) showed that IIT can decrease the occurrence of macrovascular
events by up to 42%,8 including stroke, myocardial infarction (MI), angina and
claudication, among patients with type 1 DM. Sub-studies on diabetic patients
included in drug trials show that the use of ACEIs9 and ARBs10 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. 11
The American Diabetes Association (ADA) now recommends that all patients
with diabetes and hypertension be treated with a regimen that includes either an
ACEI or ARB.
Hyperlipidemia is a common comorbidity 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.12 The use of statins among DM patients can reduce vascular events,
including stroke.13,14 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%.
Among high-risk patients with type 2 DM, the thiazolidinedione, pioglitazone,
seems to reduce the composite of all cause mortality, non-fatal stroke and MI, as
well as reduce the need for insulin treatment.15

B2. Secondary Stroke Prevention

Most 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.16 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.

C. Recommendation: A long-term, intensified DM control, which includes

behavioral and pharmacological modification to prevent microvascular and
macrovascular complications, is recommended.
Rigorous BP and lipid control should be considered in patients with
diabetes (Class IIa-B). 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. 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).
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).
Bibliography
1. Dans AL, Morales DD, Abola TB, Roxas J, 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. Abbott R, Donahue R, Macmahon S, et al. Diabetes and the Risk of Stroke. JAMA 1987;257:949-952.
3. 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.
4. Karapanayiotides T, Piechowski-Jozwiak B, van Melle G, Bogousslavsky J, Devuyst G. Stroke patterns,
etiology, and prognosis in patients with diabetes mellitus. Neurology 2004;62:1558-1562.
5. Roxas A; for the Philippine Neurological Association and Department of Health. Risk factors for stroke
among Filipinos. Phil J Neurol 2002;6:1-7.
6. Reichard P, Nilsson BY, Rosenqvist U. The effect of long-term intensified insulin treatment on the
development of microvascular complications of diabetes mellitus. N Engl J Med 1993;329:304-309.
7. 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.
8. United Kingdom Prospective Study (UKPDS) 33. Lancet 1998:352;837-853.
9. Effects of ramipril on cardiovascular and microvascular outcomes in people with diabetes mellitus:
results of the HOPE study and MICRO-HOPE substudy. Heart Outcomes Prevention Evaluation Study
Investigators. Lancet 2000;355:253-259.
10. 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.
11. 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.
12. 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.
13. 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.
14. 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.
15. Gaede P, Parving HH, Pedersen O. The PROactive Study. Lancet 2006;367:23-24.
16. 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

IV. ATRIAL FIBRILLATION

A. Epidemiology: Non-valvular atrial fibrillation (NVAF) alone is associated with

a three- to four-fold increase in stroke risk after adjustment for other vascular risk
factors as shown in the Table 3.1
Table 3: Epidemiology of NVAF by Age Group1-6
Age group Prevalence PAR RR Risk reduction with treatment
50-59 y 0.5% 1.5% 4.0 Adjusted-dose warfarin vs control:
60-69 y 1.8 % 2.8% 2.6 62% (CI 48%-72%); 6 trials,
70-79 y 4.8 % 9.9% 3.3 n=2,900.
80-89 y 8.8% 23.5% 4.5 Aspirin vs placebo: 22% (CI 2%-
38%); 6 trials, n=3,119.
Adjusted-dose warfarin vs aspirin:
45% (CI 29%-57%): 6 trials,
n=4,025.
PAR, population-attributable risk; RR, relative risk.

The prevalence of ischemic stroke for those with NVAF but without prior
TIA or stroke is 2% to 4% per year.3,4
Table 3 also shows that the prevalence of NVAF increases with age. The
mean age of NVAF patients is 75 years.1,5 Estimates of attributable risk reveal
that about one quarter of strokes in the very elderly (>80 years old) are due to
NVAF.1 NVAF is also associated with increased mortality after adjustment for
other vascular risk factors partly because resultant strokes are large and
disabling.7

B. Risk Modification
RCTs have established the value of antithrombotic therapies, particularly
warfarin and aspirin, in reducing stroke risk in patients with NVAF (Table 3).
Adjusted-dose warfarin reduces stroke by 45% compared with aspirin.4
The absolute risk reduction from warfarin (from 4.5% for control down to
1.4% with treatment) means the prevention of 31 ischemic strokes each year for
every 1,000 patients treated. Overall, warfarin is relatively safe, with a 1,3%
annual rate of major bleeding compared with 1% for placebo or aspirin. The
optimal international normalized ratio (INR) for stroke prevention in AF patients
appears to be 2.0 to 3.0.
The absolute risk of stroke varies 20-fold among AF patients, according to
age and associated vascular diseases. Several stroke risk-stratification schemes
have been developed and validated.8-10 The 2001 American College of
Cardiology (ACC)/AHA/European Society of Cardiology (ESC) guidelines
recommended anticoagulation for AF patients >60 years old and have a history
of hypertension, DM, coronary artery disease (CAD), impaired left ventricular
(LV) systolic function, heart failure or prior thromboembolism, and those >75
years old.11 This stratification scheme had not been prospectively validated even
though the individual factors are validated.
Since publication of the 2001 ACC/AHA/ESC guideline, the so-called
CHADS2 stratification scheme has been proposed and validated.8 CHADS2
stands for Congestive heart failure (CHF), Hypertension, Age >75 years, DM,
and prior Stroke or TIA. The CHADS2 score was derived from independent
predictors of stroke risk in patients with NVAF as shown on Table 4. The score
gives 1 point each for CHF, hypertension, age >75 years, and DM; and 2 points
for prior stroke or TIA. The score was validated in a large cohort study and in
clinical trials.3,8,9 In this scheme, stroke risk of NVAF patients was reliably
predicted as low (usually comprises half of patients), moderate (25% of patients)
or high (25%).3 The validation study shows that patients with prior stroke or TIA
and no other risk factors average 10.8 strokes per 100 patient-years, and that in
the Stroke Prevention in Atrial Fibrillation (SPAF),12 patients with prior stroke or
TIA without other risk factors had a stroke rate of 5.9%/year. Therefore, patients
with stroke or TIA in the setting of AF should be treated with warfarin unless
contraindicated.
LV dysfunction, left atrial size, mitral annular calcification (MAC),
spontaneous echo contrast, and left atrial thrombus by echocardiography also
predict increased thromboembolic risk.
Anticoagulation is particularly underused in elderly patients with NVAF. 13
Although the attributable risk of stroke associated with AF increases with age,2
elderly (>75 years old) AF patients have about twice the risk of serious bleeding
complications during anticoagulation compared with younger patients.
Nevertheless, anticoagulation is still warranted if their risk of ischemic stroke
without warfarin is greater than their risk of bleeding. In addition to age, poorly
controlled hypertension and concomitant aspirin or non-steroidal anti-
inflammatory drug use confer higher bleeding risk during anticoagulation.
Therefore, age alone is not a contraindication to anticoagulation of high-risk AF
patients.
No data are available to address the question of when to initiate oral
anticoagulation in an AF patient after a stroke or TIA. In general, initiation is
recommended within 2 weeks of an ischemic stroke or TIA; however, for patients
with large infarcts or uncontrolled hypertension, further delays may be
appropriate. For AF patients with ischemic stroke or TIA despite therapeutic
anticoagulation, no data indicate that either increasing the intensity of
anticoagulation or adding an antiplatelet agent provides additional protection
from future ischemic events.

Table 4: NVAF Risk Stratification and Treatment Recommendations: Risk

Stratification by CHADS2 Scheme
CHADS2 Risk Level Stroke Rate Treatment Recommendations
Score* (%/year)
0 Low 1.0 Aspirin (75-325 mg/day)

1 Low-moderate 1.5 Warfarin INR 2.0-3.0 or aspirin (75-325

mg/day)†
2 Moderate 2.5 Warfarin INR 2.0-3.0†

3 High 5.0 Warfarin INR 2–3‡

>4 Very high >7.0

CHF, hypertension, age >75 years, or diabetes=1 point. Stroke or TIA=2 points.
All NVAF patients with prior stroke or TIA should be considered high risk and
treated with anticoagulants; the CHADS2 scheme should be applied for primary
prevention.
†
Consider patient preferences, bleeding risk and access to good INR monitoring.
For those with score=1, the number needed to treat with warfarin to prevent one
stroke over 1 year is around 100. Excellent anticoagulation control is essential to
achieve this benefit.
‡
If patient is >75 years old, an INR target of 1.6 -2.5 is recommended by some
experts.

C. Recommendations: Antithrombotic therapy with warfarin or aspirin is

recommended to prevent stroke in NVAF patients according to assessment of
absolute stroke risk, estimated bleeding risk, patient preferences, and access to
high-quality anticoagulation monitoring. For risk stratification and treatment
recommendations, the CHADS2 scheme (Table 4) should be followed (Class I-A).
Warfarin (INR=2.0-3.0) is recommended for high-risk (>4% annual stroke
risk) AF patients provided there are no clinically significant contraindications to
oral anticoagulants (Class I-A).
For patients with ischemic stroke or TIA with persistent or paroxysmal
(intermittent) AF, anticoagulation with adjusted-dose warfarin (INR=2.5 [2.0-3.0]
is recommended (Class I-A). In patients unable to take oral anticoagulants,
aspirin 325 mg/day is recommended (Class I-A).

Bibliography
1. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke. The
Framingham Study. Stroke 1991;22:983-988.
2. ACC/AHA guidelines for the management of patients with valvular heart disease. A report of the
American College of Cardiology/American Heart Association. Task Force on Practice Guidelines (Committee
on Management of Patients with Valvular Heart Disease). J Am Coll Cardiol 1998;32:1486-1588.
3. Go AS, Hylek EM, Chang Y, et al. Anticoagulation therapy for stroke prevention in atrial fibrillation: how
well do randomized trials translate into clinical practice? JAMA 2003;290:2685-2692.
4. van Walraven C, Hart RG, Singer DE, et al. Oral anticoagulants vs aspirin in nonvalvular atrial
fibrillation: an individual patient meta-analysis. JAMA 2002;288:2441–2448.
5. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial fibrillation in adults: national
implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial
Fibrillation (ATRIA) Study. JAMA 2001;285:2370-2375.
6. Benjamin EJ, Wolf PA, D’Agostino RB, et al. Impact of atrial fibrillation on the risk of death: the
Framingham Heart Study. Circulation 1998;98:946-952.
7. Hart RG, Benavente O, McBride R, Pearce LA. Antithrombotic therapy to prevent stroke in patients with
atrial fibrillation: a meta-analysis. Ann Intern Med 1999;131:492-501.
8. Gage BF, Waterman AD, Shannon W, et al. Validation of clinical classification schemes for predicting
stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001;285:2864-2870.
9. Gage BF, van Walraven C, Pearce L, et al. Selecting patients with atrial fibrillation for anticoagulation:
stroke risk stratification in patients taking aspirin. Circulation 2004; 110:2287-2292.
10. Hart RG, Halperin JL, Pearce LA, et al.; Stroke Prevention in Atrial Fibrillation Investigators. Lessons
from the Stroke Prevention in Atrial Fibrillation trials. Ann Intern Med 2003;138:831-838.
11. Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA Task Force on Practice Guidelines; ESC Committee
for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of
Patients With Atrial Fibrillation); North American Society of Pacing and Electrophysiology. ACC/AHA/ESC
Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary. A report of the
ACC/AHA Task Force on Practice Guidelines and the ESC Committee for Practice Guidelines and Policy
Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation)
Developed in Collaboration With the North American Society of Pacing and Electrophysiology. Circulation
2001;104:2118-2150.
12. Hart RG, Pearce LA, McBride R, et al. Factors associated with ischemic stroke during aspirin therapy in
atrial fibrillation: analysis of 2012 participants in the SPAF I-III clinical trials. The Stroke Prevention in Atrial
Fibrillation (SPAF) Investigators. Stroke 1999;30:1223-1229.
13. Hart RG. Warfarin in atrial fibrillation: underused in the elderly, often inappropriately used in the young.
Heart 1999;82:539-540.

V. ACUTE MYOCARDIAL INFARCTION (WITH 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: 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 is not recommended to prevent a first
stroke after an MI.
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). 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 atherosclerosis and total cholesterol >190
mg/dL or LDL >100 mg/dL, statins are recommended. Furthermore, adherence to
the 2005 Clinical Practice Guidelines for the Management of Dyslipidemia in the
Philippines is recommended.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).

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 after
myocardial infarction. Anticoagulants in the Secondary Prevention of Events in Coronary
Thrombosis (ASPECT) Research Group. Lancet 1994;343:499-503.
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.

VI. VALVULAR HEART DISEASE and PROSTHETIC HEART VALVES

A. Epidemiology

Annual rates of systemic thromboembolism (TE) in different valvular diseases are

shown in Table 51-4:

Table 5: Incidence of systemic thromboembolism in valvular heart disease

Alone With AF
(No AF) (vs without AF)
1. Prosthetic valve 20% Increased
2. Rheumatic mitral regurgitation 7.7% 22%
3. Rheumatic mitral stenosis 1.5%-4.0% Increased by 7-18x
4. Mitral valve prolapse <2% Increased
5. Aortic valve Not increased Increased

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 with valvular heart disease. The rate of TE in
patients with mechanical heart valves is 4.4 per 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: For patients with rheumatic mitral valve disease or

prosthetic valve without prior stroke or TIA, oral anticoagulation with coumadin is
recommended unless contraindicated.
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).
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)

Mitral Valve Prolapse

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: For patients with ischemic stroke or TIA in whom MAC is

not documented to be calcific, antiplatelet therapy may be considered (Class IIb-
C).
For patients with MR due to MAC and without AF, antiplatelet or warfarin
therapy may be considered (Class IIb-C).

Aortic Valve Disease

a. Epidemiology: Clinically detectable systemic embolism in isolated aortic valve
disease is increasingly 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 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

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

c. 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
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 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 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

d. Recommendations: 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).
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).
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).

Table 6. Summary of Recommendations for Patients With Cardioembolic Stroke

or TIA
Risk Factor Recommendation Class/Level of
Evidence
AF For patients with ischemic stroke or TIA with Class I-A
persistent or paroxysmal (intermittent) AF,
anticoagulation with adjusted-dose warfarin (target
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.
Acute MI and LV For patients with ischemic stroke caused by acute Class IIa-B
thrombus MI with LV mural thrombus identified by
echocardiography or another form of cardiac
imaging, oral anticoagulation is reasonable
(INR=2.0-3.0 for at least 3 months up to 1 year).

Aspirin up to 160 mg/day (preferably enteric-coated) Class IIa-A

should be used concurrently for patients with
ischemic CAD during oral anticoagulant therapy.

Cardiomyopathy For patients with ischemic stroke or TIA who have Class IIb-C
dilated cardiomyopathy, either warfarin (INR=2.0-
3.0) or antiplatelet therapy may be considered to
prevent recurrent events.
MVP For patients with MVP who have ischemic stroke or Class IIa-C
TIA, long-term antiplatelet therapy is reasonable.
MAC For patients with ischemic stroke or TIA and MAC Class IIb-C
not documented to be calcific, antiplatelet therapy
may be considered.
Among patients with MR due to MAC, without AF, Class IIb-C
antiplatelet or warfarin therapy may be considered.

Aortic valve For patients with ischemic stroke or TIA and aortic Class IIa-C
disease valve disease who do not have AF, antiplatelet
therapy may be considered.
Prosthetic heart For patients with ischemic stroke or TIA who have Class I-B
valves modern mechanical prosthetic heart valves, oral
anticoagulants are recommended, with an INR target
of 3.0 (range; 2.5-3.5).
For patients with mechanical prosthetic heart valves Class IIa-B
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 maintained at INR of 3.0 (range; 2.5-
3.5) is reasonable.

For patients with ischemic stroke or TIA who have Class IIb-C
bioprosthetic heart valves with no other source of
TE, anticoagulation with warfarin (INR=2.0-3.0)
may be considered.

Bibliography
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Heart J 1994;127:400-411.
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RW, Hirsh J, Marder V, Salzman EW, eds. Hemostasis and Thrombosis: Basic Principles and
Clinical Practice, 3rd ed. Philadelphia, Pa: JB Lippincott; 1994:1452–1468.
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.
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and patients on anticoagulation in patients with atrial fibrillation: observational study. BMJ
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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;101:32–37.
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.
26. Sullivan JM, Harken DE, Gorlin R. Pharmacologic control of thromboembolic complications of
cardiac-valve replacement. N Engl J Med. 1971;284:1391–1394.
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.

VII. CHOLESTEROL

A. Epidemiology: Epidemiological and observational studies have not shown a

definite correlation between serum cholesterol levels and the incidence of
stroke.1,2 According to the Asia Pacific Cohort Studies Collaboration,3 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. However, this trend in hemorrhagic stroke was not seen in
the HPS and combined data from the Long-term Intervention with Pravastatin in
Ischaemic Disease study (LIPID) and the Cholesterol and Recurrent Event study.
Furthermore, low cholesterol is common in patients with weight loss, severe
handicap, or severe and chronic illness, which may be confounding factors for
the demonstrated trend between hemorrhagic stroke and low total cholesterol.

B. Risk Modification
B1. Primary Stroke Prevention
A meta-analysis of 13 lipid-lowering trials prior to statin use showed no
change in risk for total stroke.4 With the advent of statins, a meta-analysis of
CARE, LIPID, HPS, the Scandinavian Simvastatin Survival Study (4S), the
Prospective Study of Pravastatin in the Elderly at Risk study (PROSPER), the
Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial
(ALLHAT), the Kyushu Lipid Intervention Study (KLIS), the GREek Atorvastatin
and Coronary-heart-disease Evaluation (GREACE), and the Anglo-Scandinavian
Cardiac Outcomes Trial (ASCOT) showed that the overall relative risk reduction
is 21% (ARR=9%).5 The greater the LDL reduction, the greater the intima-media
thickness and stroke risk reduction.6
Statins conferred an important and large relative reduction in
cardiovascular events including stroke among hypertensive patients who are not
conventionally deemed dyslipidemic.7 Pretreatment with statins seem to reduce
clinical severity in patients with stroke, especially among diabetics.8,9

B2. Secondary Stroke Prevention

HPS showed a 19% reduction in major vascular events, but the decrease
was due to reduction in coronary events and not in stroke recurrence.10
The Stroke Prevention with Aggressive Reduction of Cholesterol Levels
(SPARCL), a large-scale statin RCT in patients with a history of stroke or TIA
without CAD, and have mildly elevated lipid levels (mean LDL=133 mg/dL). 11 The
trial showed that atorvastatin 80 mg/day significantly reduced stroke by 16% in
this patient subgroup.
 Statins are likely to reduce stroke risk by stabilizing and /or repressing
plaque. Statins also have pleiotropic (anti-inflammatory, antioxidant) effects that
further justify their use in the primary and secondary prevention of
cerebrovascular disease.12-14 Statins have a favorable safety profile and are not
associated with increased hemorrhagic stroke or cancer risk.5

C. Recommendations
C1. Primary Stroke Prevention
Therapeutic lifestyle changes are recommended as an essential modality
in clinical management.2 These include smoking cessation, weight management,
regular physical activity and adequate BP monitoring and control.15 For patients
at any level of cardiovascular risk, especially those with established
atherosclerosis, a low-fat, low-cholesterol diet is recommended for life.
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).16,17
Adults with diabetes, especially those with additional risk factors, should
receive statins to lower the risk of a first stroke (Class I-A).16
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).3,16

C2. Secondary Stroke Prevention

Statins are recommended in patients with coronary heart disease or
symptomatic atherosclerotic disease to lower cholesterol levels to LDL<100
mg/dL (<70 mg/dL for very high-risk persons) (Class I-A).16,18-20
Patients with ischemic stroke or TIA presumed to be due to
atherosclerosis but without preexisting indications for statins are reasonable
candidates for statin treatment to reduce the risk of vascular events (Class IIa-
B).16
Patients with ischemic stroke or TIA and low HDL may be considered for
treatment with niacin or fibrates (Class IIb-B).3,16

Lastly, adherence to the statements of the 2005 Clinical Practice

Guidelines for the Management of Dyslipidemia in the Philippines is
recommended. These are15:

1. To reduce the overall cardiovascular risk, all patients, regardless of their

present morbid condition or risk profile, should be advised on the need for the
following:
Smoking cessation;
Weight management;
Regular physical activity; and
Adequate blood pressure monitoring and control.
2. For patients at any level of cardiovascular risk, especially those with
established atherosclerosis, a low-fat, low-cholesterol diet is recommended for
life.

3. In poorly nourished and elderly patients, correction of nutritional deficiencies

can be achieved even with a low-fat, low-cholesterol diet.

4. For low-risk patients without evidence of atherosclerosis, drug therapy is not

recommended, regardless of lipid levels. Risk factors include hypertension,
familial hypercholesterolemia, left ventricular hypertrophy, smoking, family history
of premature CAD, male sex, age >55 years, proteinuria, microalbuminuria, BMI
≥25. Low risk patients have <3 risk factors. The presence of familiar
hypercholesterolemia warrants treatment even without other risk factors.

5. For patients without established atherosclerosis but with ≥3 risk factors and
total cholesterol ≥190 mg/dL or LDL ≥100 mg/dL, statins may be recommended.

6. For diabetic patients without evidence of atherosclerosis and with total

cholesterol ≥190 mg/dL or LDL ≥100 mg/dL, statins are recommended.

7. Fibrates may be recommended as an alternative to statins in diabetic patients

with HDL ≤35 mg/dL and LDL ≤90 mg/dL.

8. For patients with established atherosclerosis and total cholesterol ≥190 mg/dL
or LDL ≥100 mg/dL, statins are recommended.

9. Fibrates may be recommended as an alternative to statins if HDL ≤35 mg/dL

and LDL ≤90 mg/dL.

10. In patients without risk factors and history or symptoms of established

atherosclerosis, screening for lipid levels is not recommended.

11. In patients without established atherosclerosis but with ≥3 risk factors, lipid
profile may be recommended.

12. In patients with established atherosclerosis or diabetes, the use of lipid profile
for screening is recommended.

Bibliography
1. Di Napoli M. Benefits of statins in cerebrovascular disease. Curr Opin Investig Drugs 2004;5:295-
305.
2. 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.
3. Zhang X, Patel A, Horibe H, et al.; Asia Pacific Cohort Studies Collaboration. Cholesterol, coronary
heart disease, and stroke in the Asia Pacific region. Int J Epidemiol 2003;32:563-572.
4. 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 Med 1993;119:136-145.
5. Amarenco P, Lavallee PC, Labreuche J, et al. Stroke prevention, blood cholesterol and statins.
Acta Neurol Taiwan 2005;14:96-112.
 6. Amarenco P. Effect of statins in stroke prevention. Curr Opin Lipidol 2005;16:614-618.
7. 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-LLA): a multicentre randomised controlled trial. Lancet 2003;361:1149-1158.
8. 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.
9. 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.
10. 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.
11. The SPARCL Investigators. The Stroke Prevention by Aggressive Reduction in Cholesterol Levels
(SPARCL) study. Cerebrovasc Dis. 2006;21(suppl 4):1. Abstract 1.
12. Vaughan CJ. Prevention of stroke and dementia with statins: Effects beyond lipid lowering. Am J
Cardiol 2003;91:23B-29B.
13. Welch KMA. Statins for the prevention of cerebrovascular disease: the rationale for robust
intervention. Eur Heart J Suppl 2004;6 (Suppl C):C34-C42.
14. Martin-Ventura JL, Blanco-Colio 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.
15. The Clinical Practice Guidelines for the Management of Dyslipidemia in the Philippines 2005.
Manila: The Philippine Heart Association Inc., Philippine College of Cardiology; 2005.
16. 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.
17. 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.
18. 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.
19. Waters DD, Schwartz GG, Olsson AG, et al.; MIRACL 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 (MIRACL) substudy. Circulation
2002;106:1690-1695.
20. 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.

VIII. CAROTID STENOSIS

A. Epidemiology: Extracranial carotid artery disease accounts for 15% to 20%

of all ischemic strokes.1 Individuals with carotid stenosis often have more
widespread atherosclerotic disease with a high prevalence of coronary heart
disease and claudication.2,3
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 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

B1. Primary Stroke Prevention

The role of carotid endarterectomy (CEA) in asymptomatic cases requires
special consideration. 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 a 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

B2. 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
CEA was harmful for symptomatic patients with less than 30% stenosis. It
had had no effect among patients with 30% to 49% stenosis, and 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 were randomized within 2
weeks of a TIA or a non-disabling ischemic stroke.4,9-11
Meta-analysis of five completed or terminated RCTs comparing
endovascular treatment and CEA (Carotid and Vertebral Artery Transluminal
Angioplasty Study [CAVATAS], Kentucky, Leicester, Wallstent, Stenting and
Angioplasty with Protection in Patients at High Risk for Endarterectomy
[SAPPHIRE]) found no difference in the odds of death or any stroke at 30 days
and at one year between the two groups.12 As yet, there is no evidence on the
long-term efficacy of angioplasty and stenting available from any of the studies.
Several international trials such as the Carotid Revascularization Endarterectomy
versus Stenting Trial (CREST),13 International Carotid Stenting Study (ICSS),14
Stent-protected Percutaneous Angioplasty of the Carotid versus Endarterectomy
(SPACE)15 and Endarterectomy versus Angioplasty in patients with severe
Symptomatic Stenosis (EVA-3s)16 are awaiting completion.
C. Recommendations: Antiplatelets, statins and modification of stroke risk
factors for all patients with carotid artery disease (Class I-C).
At present, mass screening for high-grade asymptomatic carotid stenosis
is not cost-effective. However it is reasonable to do screening using 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. It is also reasonable to consider CEA for patients
with asymptomatic stenosis of >60% if 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).
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).
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
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
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 simultaneous with coronary-artery bypass grafting (CABG).
Unless results of ongoing studies are reported, carotid angioplasty and
stenting (CAS) remains to be a second option to CEA. The endovascular
approach is favored in certain cases (e.g., stenosis is difficult to access
surgically; restenosis after CEA or medical conditions exist 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

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 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. 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. Coward L, Featherstone R, Brown M. Safety and efficacy of endovascular treatment of carotid artery
stenosis compared with carotid endarterectomy. A Cochrane systematic review of the randomized
evidence. Stroke 2005;36:905-911.
13. Hobson RW. CREST (Carotid Revascularization Endarterectomy versus Stent Trial): background,
design and current status. Semin Vasc Surg 2000;14:139-143.
14. Featherstone RL, Brown MM, Coward LJ. International carotid stenting study: protocol for a randomized
clinical trial comparing carotid stenting with endarterectomy in symptomatic carotid artery stenosis.
Cerebrovasc Dis 2004;18:69-74.
15. Ringleb PA, Kunze A, Allenberg JR, et al. The Stent-Supported Percutaneous Angioplasty of the
Carotid Artery vs Endarterectomy Trial. Cerebrovasc Dis 2004;18:66-68.
16. EVA 3S Investigators. Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid
Stenosis (EVA 3S). Cerebrovasc Dis 2004;18:62-65.
17. 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.
18. 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.
19. Barnett HJM, Warlow CP. Carotid endarterectomy and the measurement of stenosis. Stroke
1993;24:1281-1284.

IX. INTRACRANIAL STENOSIS

A. Epidemiology: Atherosclerotic intracranial stenoses are responsible for

ischemic stroke in 5% to 10% of Caucasian patients, and in up to 33% of Asian,
Hispanic and African patients.1-6 Other risk factors for intracranial atherosclerosis
include age, hypertension, smoking, diabetes, lipid disorders and metabolic
syndrome.7-12
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).13-18 In contrast, asymptomatic
MCA stenosis appears to have a benign prognosis with a low risk of ipsilateral
stroke (1.4% annually) in medically treated Caucasian patients.19-20
B. Risk Modification: There is currently no data available.
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 that warfarin does not confer an advantage over aspirin
in terms of stroke reduction (2-year ischemic stroke rate of 19.7% for aspirin vs.
17.2% for warfarin).16
In the Trial of cilOstazol in Symptomatic intracranial arterial Stenosis
(TOSS), adding cilostazol to aspirin was superior to aspirin monotherapy in
preventing progression of intracranial arterial stenosis.21 Continued trials are
warranted to confirm the efficacy of cilostazol in preventing 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 a high degree of technical success.22 Acceptable
anatomical and clinical results of up to 6 months were obtained in small groups of
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 trials.23-24 Further studies are
needed in larger cohorts with longer follow-up periods to fully determine the
effectiveness of interventional catheter-based procedures for intracranial
stenosis.

C. Recommendation: Patients with intracranial stenosis should be counseled

regarding optimal medical therapy (antiplatelets, statins) and aggressive
management of stroke risk factors.22,25
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)

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19. 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.
20. 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.
21. Kwon S, Cho YJ, Koo JS et al. Cilostazol prevents the progression of symptomatic intracranial stenosis.
Stroke 2005;36:782-786.
22. 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.
23. SSLYVIA Study Investigators. Stenting of symptomatic atherosclerotic lesions in the vertebral or
intracranial arteries (SSYLVIA). Stroke 2004;35:1388-1392.
24. Henkes H, Miloslavski E, Lowens S, et al. Treatment of intracranial atherosclerotic stenosis with balloon
dilatation and self-expanding stent deployment (WingSpan). Neuroradiology 2005;47:222-228.
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.

X. SMOKING

A. Epidemiology

A1. Prevalence
Asian countries have the highest prevalence of smoking in the world: 72%
in Korean men, 63% in Chinese men and 58% in Japanese men.1 The 2003
NNHeS survey showed that the prevalence of smoking in Filipinos is 56.3% in
males and 12.1% in females.2 Two national surveys on Filipino adolescents
revealed that one in five adolescents current smoking, males having a higher rate
than females (37.3% vs. 6.3%).3,4

A2. Smoking as Stroke Risk Factor

 A meta-analysis of 32 studies estimated the relative risk for cerebral
infarct to be 1.9 for smokers versus nonsmokers.5 Case control and prospective
studies have shown that cigarette smoking is an independent predictor of stroke,
with a dose-response relationship affecting both men and women.6-8 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 increased with the number of cigarettes smoked. 9
The large cohort study of U.S. male physicians showed heavy smokers (>20
cigarettes/day) had a relative risk of 2.71 for total nonfatal stroke, and 1,46 for
fatal stroke.10
Studies also suggest a dose-response relationship between pack-years of
smoking and carotid-artery intima-media wall thickness.11 Smoking only one
cigarette increases heart rate, blood pressure and cardiac index, and decreases
arterial distensibility.12 In addition, both active and passive smoke are associated
with the development of atherosclerosis.13
Stroke also increases the risk of hemorrhagic stroke. In men, current
smokers of <20 cigarettes/day had relatives risks of 1.65 for total hemorrhagic
strokes, 1.60 for intracerebral hemorrhage (ICH), and 1.75 for subarachnoid
hemorrhage (SAH) compared to those who never smoked.14 Current smokers of
>20 cigarettes/day had relative risks of 2.36 for total hemorrhagic stroke, 2.06 for
ICH and 3.22 for SAH.
In women, current smokers of <15 cigarettes/day had a relative risks of
1.93 for total hemorrhagic stroke, 2.5 for ICH and 1.70 for SAH.15 Women who
smoked >15 cigarettes/day had relative risks of 3.29 for total hemorrhagic stroke,
2.67 for ICH and 4.02 for SAH.

A3. Smoking Potentiates Effects of Other Stroke Risk Factors

A synergistic effect on the risk of cerebral infarction exists between the
use of oral contraceptives (OC) and smoking. With nonsmoking women who do
not use OC as reference group, the odds for cerebral infarction were 1.3 times
greater for women who smoked but did not use OC, 2.1 times greater for
nonsmoking OC users, and 7.2 times greater for OC users who smoked.16
A similar impact on hemorrhagic stroke is observed. The odds for
hemorrhagic stroke were 1.6 times greater for women smoked but did not use
OC, 1.5 times greater for nonsmoking OC users, and 3.7 times greater for OC
users who smoked.17

A4. Environmental Tobacco Smoke and Passive Smoking

Like outdoor air pollution, the effects of second-hand smoke are large and
rapid. Several studies suggest that environmental tobacco smoke is a substantial
risk factor for stroke, with risk approaching the doubling found seen with active
smoking.18 Passive smoking may exert detrimental effects on vascular
homoeostasis. Cohort studies showed an elevated prevalence of stroke among
women nonsmokers living with husbands who smoked, and prevalence
increased with increasing intensity and duration of husbands’ smoking. 19
B. Risk Modification: Both the Framingham Heart Study and the Nurses Health
Study showed that 5 years after cessation of smoking, risk ratios normalized.9,20
However, another study 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.21 Switching to pipe or cigar smoking confers little
benefit, emphasizing the need for complete cessation of smoking.22 A
combination of nicotine replacement therapy, social support and skills training
seems to be the most effective approach to smoking cessation.23,24

C. Recommendations: Smoking cessation for all current smokers is

recommended (Class I-C).25 Nonsmokers are also advised not to start smoking.
Exposure to environmental tobacco smoke should be minimized (Class IIa-C).
Republic Act No. 9211 or The Tobacco Regulation Act of 2003 should be
implemented to protect the populace from hazardous products, promote the right
to health and instill health consciousness. Effective behavioral and
pharmacological treatments should be advised and encouraged for nicotine
dependence (Class IIa-B).

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;282:2149-2155.
2. Dans AL, Morales DD, Abola TB, Roxas J, 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.
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. Shinton R, Beevers G. Meta-analysis of relation between cigarette smoking and stroke. BMJ
1989;298:789-794.
6. Bonita R, Seragg R, Stewart A, et al. Cigarette smoking and risk of premature stroke in men and
women. BMJ 1987;293;6-8.
7. Abott RD, Yin Yin MA, Reed DM, et al. Risk of stroke in male cigarette smokers. N Engl J Med
1986;315:717-720.
8. Colditz GA, Bonita R, Stampfer MJ, et al. Cigarette smoking as a risk factor for stroke. Framingham
Study. JAMA 1988:318:937-941.
9. Wolf PA, D'Agostino RB, Kannel WB, et al. Cigarette smoking as a risk factor for stroke. The
Framingham Study. JAMA 1988;259:1025-1029.
10. Robbins AS, Manson JE, Lee I, et al. Cigarette smoking and stroke in a cohort of US male physicians.
Ann Intern Med 1994;120:458-462.
11. Howard G, Burke GL, Szklo M, et al. Active and passive smoking are associated with increased carotid
wall thickness. The atherosclerotic risk in community study. Arch Intern Med 1994;154:1277-1282.
12. Kool MJ, Hoeks AP, Struijker Boudier HA, et al. Short- and long-term effects of smoking on arterial wall
properties in habitual smokers. J Am Coll Cardiol 1993;22:1881-1886.
13. Howard G, Wageknecht LE, Burker GL, et al. Cigarette smoking and progression of atherosclerosis: the
Atherosclerosis Risk in Communities (ARIC) Study. JAMA 1998;279:119-124.
14. Kurth T, Kase C, Nerger K, et al. Smoking and risk of hemorrhagic stroke in men. Stroke 2003;34;1151-
1155.
15. Kurth T, Kase C, Berger K et al. Smoking and Risk of hemorrhagic stroke in women. Stroke
2003;34;2792-2795.
16. Ischemic stroke and combined oral contraceptives: results of an international, multicentre, case control
study. WHO Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception.
Lancet 1996;348:498-505.
17. World Health Organization. Hemorrhagic strokes, stroke risk and combined oral contraceptives: results
of an international, multicentre, case controlled study: WHO Collaborative Study of Cardiovascular
Disease and Steroid Hormone Contraception. Lancet1996;348:505-510.
18. Barnoya J, Glantz S. Cardiovascular effects of second hand smoke. Circulation 2005;11:2628-2698.
19. Zhang X, Shu XO, Yang G, et al. Association of passive smoking by husbands with prevalence of stroke
among Chinese women nonsmokers. Am J Epidemiol 2005;161:213-218.
20. Golditz GA, Stamfer B, Willer WC, et al. Cigarette smoking and risk of stroke in middle aged women. N
Engl J Med 1988;18:937-941.
21. Tell GS, Polak JF, Ward BJ, et al. Relation of smoking with carotid artery wall thickness and stenosis in
older adults. The Cardiovascular Health Study. The Cardiovascular Health Study (CHS) Collaborative
Research Group. Circulation 1994;90:2905-2908.
22. Wannamabee SG, Shaper MC, Smoking cessation and the risk of stroke in middle aged men. JAMA
1998;274:155-160.
23. 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;2000.
24. Fiore MC, Bailey WC, Cohen SJ, et al. Smoking cessation. Rockville, Md: US Department of Health and
Human Services, Public Health Service, Agency for Health Care Policy and Research AHCPR
Publication;1996.
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.

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 Most studies suggest a J-shaped
association between alcohol and ischemic stroke: a protective effect with light to
moderate drinking, and an elevated risk with heavy consumption.5-8 While the
protective effect of light consumption alcohol 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 multiethnic 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 two drinks per day was

protective against ischemic strokes in Caucasians, Blacks and Hispanics, but
consumption above five drinks per day increased the risk of ischemic stroke. 14

C. Recommendations: Moderate intake of alcohol in those who drink alcohol

and have no health contraindications to its use. Consumption of alcohol, up to 30
mL (or 28 grams) of ethanol per day, equivalent to 60 mL or two jiggers of 100-
proof whiskey, 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).
Patients with ischemic stroke or TIA who are heavy drinkers should
eliminate or reduce their consumption of alcohol (Class I-A).
Those who do not customarily drink alcohol should not be encouraged to
do so.

Bibliography
1. Donahue RP, Abbott 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;16:773-780.
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 consumption and risk of ischemic stroke. The
Framingham Study. Stroke 2002;33:907-912.
7. Berger K, Ajani CA, Kase CS, et al. Light-to-moderate alcohol consumption and risk of stroke among
US male physicians, N Engl J Med 1999;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
1989;20:611-1626.
10. Kono S, Ikeda M, Tokudome S, et al. Alcohol and mortality: a cohort study of male Japanese
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. 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

A. Epidemiology: The prevalence of PAD is highly age dependent. Using

objective testing with ankle-brachial index (ABI) in a U.S. population showed the
prevalence was 2.5% in people aged <60 years old, while among the 60- to 69-
year age group the prevalence is 8.3%, and is 18.8% in those >70 years old.3
There is a 20% to 60% increased risk for MI and a two- to six-fold
increased risk of death due to coronary 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.
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

B. Risk Modification: In lower-extremity PAD, adverse cardiovascular events

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

B1. 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

B2. 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) compared with
conventional treatment, but did not reduce the risk of death or stroke.15

B3. 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.

B4. 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.
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: Individuals with risk factors for PAD, regardless of

whether they are symptomatic and asymptomatic, should be identified and ABI
measured. Therapeutic interventions to diminish the increased risk of MI, stroke
and death may be given (Class I-B). Treatment used in the management of
atherosclerotic conditions, such as CAD and cerebrovascular disease, as
recommended in the other sections of these guidelines, may reduce the risk of
stroke.
Those with PAD who smoke should be advised to quit. Smoking cessation
interventions, including behavior modification therapy or nicotine replacement
therapy, should be offered (Class I-B).
Reducing HbA1c to <7% through tight glycemic control may reduce
microvascular complications and improve cardiovascular outcomes (Class IIa-C).
Statins are indicated for all patients with PAD (Class I-B), and treatment
should aim to reduce serum cholesterol to < 70mg/dL when at very high risk of
ischemic events (Class IIa-B). Treatment with fibric acid derivatives can be useful
for PAD patients with low HDL, normal LDL and elevated triglycerides (Class IIa-
C).
Antihypertensive treatment should aim to reduce BP to <140/90 mmHg, or
<130/80 mmHg for those with DM or chronic renal disease (Class I-A). Beta-
blockers are effective and are not contraindicated in PAD patients (Class I-A).
It is reasonable to use ACEIs for those with symptomatic PAD to reduce
cardiovascular risk (Class IIa-B). ACEIs may be considered for asymptomatic
PAD patients to reduce cardiovascular risk (Class IIb-C).
Antiplatelets are indicated to reduce risk of MI, stroke and vascular death
in PAD patients (ClassI-A). Daily aspirin 75 to 325 mg is considered safe and
effective in reducing the risk of MI, stroke or vascular death (ClassI-A).
Clopigrel 75 mg/day is recommended as an alternate to (Class I-B). Oral
anticoagulation therapy with warfarin is not indicated to reduce the risk of
adverse cardiovascular events in patients with PAD (ClassIII-C).

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. 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.
4. Smith GD, Shipley MJ, Rose G. Intermittent Claudication, heart disease risk factors, and mortality. The
Whitehall Study. Circulation 1990;82:1925-1931.
5. 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.
6. 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.
7. Vogt MT, Cauley JA, Newman AB, et al. Decreased ankle/arm blood pressure index and mortality in
elderly women. JAMA 1993;270:465-469.
8. ZhengZj, SharrettAR ,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.
9. Abola MT, DansA; for the Council of Stroke and Peripheral Vascular Diseases, Philippine Heart
Association (PHILPAD Study). Phil J Int Med 2003;41:71-74.
10. Dans AL, Morales DD, Abola TB, Roxas J, 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.
11. 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.
12. Lassila R, Lepantalo M. Cigarette smoking and the outcome after lower limb arterial surgery. Acta Chir
Scand 1988;154:635-640.
13. 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.
14. 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.
15. 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.
16. 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.
17. 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.
18. Calligaro KD, Musser DJ, Chen AY, et al. Duplex ultrasonography to diagnose failing arterial prosthetic.
Surgery 1996;120:455-459.

XIII. PHYSICAL INACTIVITY

A. Epidemiology: Physical inactivity is a growing public health problem that

may have a major impact on the prevalence of atherothrombotic cardiovascular
disease in the coming decades. The relative risk of cardiovascular disease
associated with physical inactivity ranges from 1.5 to 2.4, a risk increase similar
to those observed with high blood cholesterol, high BP or cigarette smoking. 1
Physical inactivity is a risk factor for stroke, DM, colon and breast cancer,
obesity, hypertension, osteoporosis and depression.2-6 Local data shows the
odds ratio for stroke associated with physical inactivity is 1.23.7

B. Risk modification
 B1. Primary Stroke Prevention
Physical activity is defined as any bodily movement produced by skeletal
muscles that result in energy expenditure beyond resting expenditure. Physical
activity reduces stroke risk in both genders and across all racial/ethnic and age
groups (OR; 0.37).8,9 The Framingham Heart Study, the Honolulu Heart Program,
and the Oslo Study have shown the protective effect of physical activity for
men.10-12 There seems to be a graded linear relation between the volume of
physical inactivity and total stroke.13 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).14 The Harvard Alumni Study showed a decrease
in total stroke risk in men who were highly physically active (RR; 0.82).15
For women, the Nurses’ Health Study and the Copenhagen City Heart
Study showed an inverse association between level of physical activity and
stroke incidence.16,17 Physical activity (in sports, leisure time or at work) also
reduced risk of ischemic strokes, in particular.9,18
The protective effect of physical activity may be partly mediated by BP
reduction, improvement of lipid profiles (reduces triglyceride, increases HDL, and
decreases LDL:HDL ratios), improvement of glucose homeostasis and insulin
sensitivity, and improvement in body composition and weight. 3,4,19 Other benefits
of physical activity include reduction in blood coagulability,20-22 improvement of
coronary blood flow,23 augmentation of cardiac function, 24 enhancement of
endothelial function,25-27 improvement of autonomic tone,28 and reduction of
systemic inflammation.29

B2. Secondary Stroke Prevention

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 to volitional fatigue.30,31 Furthermore, stroke survivors are often
deconditioned and 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. Thus, 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; (3) to increase aerobic fitness.
Stroke patients can increase their cardiovascular health and fitness with
regular aerobic exercise.32 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.33 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.34 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.35

C. Recommendations

C1. Primary Stroke Prevention

Increased physical activity is associated with a reduction in stroke risk,
and is recommended (Class I-B). It is important to recognize that physical
education in school may form the starting point for an active lifestyle later in life.
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
(Class IIa-B). 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.36

C2. Secondary Stroke Prevention

Exercise for stroke patients is recommended and should be tailored to
individual needs and limitations. In general, aerobic training at 40% to 70% of
peak oxygen consumption or heart rate reserve may be advised to stroke
survivors.37 Continuous or accumulated aerobic training for 20 to 60 minutes
daily, three to seven days a week, depending on the patient’s level of fitness, is
advised.
Persons with known or suspected cardiovascular, respiratory or
neurological disorders should consult a physician before beginning or
significantly increasing physical activity. Adaptive programs for post-stroke
patients depending on neurological deficits are recommended.38

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. Taylor RS, Brown A, Ebrahim S, et al. Exercise-based rehabilitation for patients with coronary heart
disease: systematic review and meta-analysis of randomized controlled trials. Am J Med 2004;116:682-
692.
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 health. Can
J Appl Physiol 2001;26:161-216.
5. Warburton DE, Gledhill N, Quinney A. Musculoskeletal fitness and health. Can J Appl Physiol
2001;26:217-237.
6. Shephard RJ. Absolute versus relative intensity of physical activity in a dose-response context.
(discussion S419-20). Med Sci Sports Exerc 2001;33:S400-S418.
7. Roxas A; for the Philippine Neurological Association and Department of Health. Risk factors for stroke
among Filipinos. Phil J Neur 2002;6:1-7.
8. Thom T, Haase N, Rosamond W, et al. Heart Disease and Stroke Statistics 2006 Update: A report from
the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation
2006;113:e85-e151.
9. Sacco, RL, Gan R, Boden-Albala B, et al. Leisure-time physical activity and ischemic stroke risk: the
Northern Manhattan Stroke Study. Stroke 1998;29:380-387.
10. Kiely, DK, Wolf PA, Cupples LA, Beiser AS, Kannel WB. Physical activity and stroke risk: the
Framingham Study. Am J Epidemiol 1994;140:608-620.
11. Abbott, RD, Rodriguez BL, Burchfiel CM, Curb JD. Physical activity in older middle-aged men and
reduced risk of stroke: the Honolulu Heart Program. Am J Epidemiol 994;139:881-893.
12. 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.
13. Hu FB, Stampfer MJ, Colditz GA, et al. Physical activity and risk of stroke in women. JAMA
2000;283:2961-2967.
14. Lee IM, Hennekens CH, Berger K, et al. Exercise and risk of stroke in male physicians. Stroke
1999;30:1-6.
15. Lee IM, Paffenbarger RS Jr. Physical activity and stroke incidence: the Harvard Alumni Health Study.
Stroke 1998;29:2049-2054.
16. 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.
17. Manson JE, Colditz GA, Stampfer MJ, et al. A prospective study of maturity-onset diabetes mellitus and
risk of coronary heart disease and stroke in women. Arch Intern Med 1991;151:1141-1147.
18. Evenson KR, Rosamond WD, Cai J, et al. Physical activity and ischemic stroke risk: the Atherosclerosis
Risk in Communities Study. Stroke 1999;30:1333-1339.
19. American College of Sports Medicine. Position Stand. Physical activity, physical fitness, and
hypertension. Med Sci Sports Exerc 1993;25:i-x.
20. Physical activity and cardiovascular health. NIH Consensus Development Panel on Physical Activity
and Cardiovascular Health. JAMA 1996;276:241-246.
21. Rauramaa R, Salonen JT, Seppanen K, et al. Inhibition of platelet aggregability by moderate-intensity
physical exercise: a randomized clinical trial in overweight men. Circulation 1986;74:939-944.
22. 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.
23. 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.
24. 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.
25. Gokce N, Vita JA, Bader DS, et al. Effect of exercise on upper and lower extremity endothelial function
in patients with coronary artery disease. Am J Cardiol 2002;90:124-127.
26. 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.
27. Hambrecht R, Gielen S, Linke A, et al. Effects of exercise training on left ventricular function and
peripheral resistance in patients with chronic heart failure: a randomized trial. JAMA 2000;283:3095-
3101.
28. Tiukinhoy S, Beohar N, Hsie M. Improvement in heart rate recovery after cardiac rehabilitation. J
Cardiopulm Rehabil 2003;23:84-87.
29. 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.
30. 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.
31. King ML, Guarracini M, Lenihan L, et al. Adaptive exercise testing for patients with hemiparesis. J
Cardiopulm Rehabil 1989;9:237-242.
32. 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.
33. Potempa K, Lopez M, Braun LT, et al. Physiological outcomes of aerobic exercise training in
hemiparetic stroke patients. Stroke 1995;26:101-105.
34. 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.
35. 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.
36. Pearson TA, Blair SN, Daniels SR, et al. AHA guidelines for primary prevention of cardiovascular
disease and stroke: 2002 Update. Circulation 2002;106:388-391.
37. Palmer-McLean K, Harbst KB. Stroke and brain injury. In: Durstine JL, Moore GE, eds. ACSM’s
Exercise Management for Persons With Chronic Diseases and Disabilities. 2nd ed. Champaign, Ill:
Human Kinetics; 2003:238–246.
38. Wolf P, Clagett GP, Easton D et al. Preventing ischemic stroke in patients with prior stroke and transient
ischemic attack. A statement for healthcare professionals from the Stroke Council of the American
Heart Association. Stroke 1999;30:1991-1994.
XIV. OBESITY
A. Epidemiology: The World Health Organization defined “overweight” as
having a body mass index (BMI) >25 kg/m2 and “obesity” with a BMI >30 kg/m2
for the general population.1 However, the National Institute for Health and Clinical
Excellence (NICE) recommends that overweight or obesity among Asian adults
should be set at 23 and 27.5kg/m2 respectively.2
Waist circumference (WC) is positively correlated with disease risk, and is
one of the most practical measurements for assessing abdominal fat mass
(central obesity). For Asians, the cutoff points are 90 cm (35 inches) for males
and 80 cm (32 inches) for females.2
Another measure of abdominal fat deposition is the waist-hip ratio (WHR),
defined as the waist circumference divided by the hip circumference. Elevated
WHR is defined as >0.95 in males and >0.85 in females.3
In the Philippines, the prevalence of obesity based on BMI has increased
from 4.6% to 5.0% between 1998 to 2003.4 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 on 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 hypertension, diabetes and
cholesterol.6 Among women, data are inconsistent, with some studies showing
association, while others, none.7,8
Several studies suggest that abdominal obesity, rather than general obesity,
is more related to stroke risk.9,10 In the Northern Manhattan Study, a significant
and independent association between abdominal obesity (elevated WHR) and
ischemic stroke was found in all racial/ethnic groups, whereas BMI did not show
any significant association with ischemic stroke.9 Furthermore, persons with
elevated BMI or WHR have increased carotid artery intima-media thickness and
cross-sectional intima-media area, which are two preclinical predictors of
atherosclerosis.11

B. Risk Factor Modification

B1. 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 BP (Class I-A) and may thereby reduce the risk
of stroke. Modest weight loss (e.g., 10% of the initial body weight over 6 months)
is realistic and attainable.12 It is better to maintain a moderate loss over the long
term than to achieve a greater weight loss that cannot be maintained.

B2. Secondary Stroke Prevention

 Although no study has demonstrated that weight reduction will reduce
stroke recurrence in patients who have suffered a previous stroke or TIA, losing
weight significantly improves BP, fasting glucose values, serum lipids and
physical endurance.13 Because obesity is a contributing factor to other risk
factors associated with recurrent stroke, promoting weight loss and maintenance
of a healthy weight is important. Exercise and a diet rich in fruits and vegetables
can help control weight and reduce the risk of stroke, MI and death.14,15

C. Recommendation: Weight reduction should be considered for all overweight

patients to maintain the following goals: BMI=18.5 to 22.9 kg/m 2; WHR<0.95 in
males and <0.85 in females; and WC<90 cm (35 inches) in males and <80 cm
(32 inches) in females.16
Gradual and moderate weight loss is encouraged for overweight and
obese patients. Clinicians should encourage weight management as early as
childhood through an appropriate balance of caloric intake, physical activity,
exercise and behavioral counseling.

Table 7. Weight classifications and associated comorbidities risk according to

BMI and waist circumference in adult Asians16
Classification BMI (kg/m2) Risk of comorbidities
Waist circumference
<90 cm (men) ≥90 cm (men)
<80 cm (women) ≥80 cm (women)
Underweight <18.5 Low* Average

Normal range 18.5-22.9 Average Increased

Overweight (at 23-24.9 Increased Moderate
risk)
Obese I 25-29.9 Moderate Severe
Obese II ≥30 Severe Very severe
* But increased risk of other clinical problems

Bibliography
1. World Health Organization. Obesity: Preventing and managing the global epidemic. Report of a WHO
Consultation. WHO Technical Report Series 894(3), i-253. Geneva: WHO; 2000.
2. National Institute for Health and Clinical Excellence. Obesity: The prevention, identification, assessment
and management of overweight and obesity in adults and children. NICE guideline: first draft for
consultation, March 2006. London: NICE; 2006.
3. Sproston K, Primatesta P, eds. Health Survey for England 2002: volume 1: the health of children and
young people, London: The Stationery Office;2003.
4. Dans AL, Morales DD, Abola TB, Roxas J, 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.
5. Grundy SM, Balady GJ, Criqui MH, et al. 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,et al. 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, et al; for the Northern Manhattan Stroke Study. Stroke
2003;34;1586-1592.
10. Dey DK, Rothenberg E, Sundh V, et al. 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, et al. Association of obesity and central fat distribution with carotid
artery wall thickening in middle-aged women. Stroke 2002;33:2293.
12. Singapore Ministry of Health (MOH). Obesity. Singapore Ministry of Health – National Government
Agency. 2004.
13. Anderson JW, Konz Ec. Obesity and disease management: effects of weight loss on comorbid
conditions. Obes Res 2001:9 (Suppl 4);326S-334S.
14. Renaud S, Lorgeril M., Delaye J, et al. Cretan Mediteranean diet for prevention of coronary heart
disease. Am J Clin Nutr 1995:61 (Suppl):1360S-1367S.
15. Singh RB, Dubnov G, Niaz MA, et al. Effect of an Indo-Mediterranean diet in progression of coronary
artery disease in high risk patients (Indo-Mediterranean Diet Heart Study: a randomized single-blind
trial). Lancet 2002:360:1455-1461.
16. Regional Office for the Western Pacific of the World Health Organization, the International
Association for the Study of Obesity and the International Obesity Task Force. The Asia-
Pacific perspective: Redefining obesity and its treatment. Health Communications Australia
Pty. Limited, February 2000.

XV. DIET

A. Epidemiology: 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 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 reduced stroke risk.
Fruits and vegetables may contribute to stroke prevention though antioxidant
mechanisms or elevation of potassium levels.7-10 Increase sodium intake is
associated with hypertension, and reduction in salt consumption may significantly
lower BP and reduce stroke mortality.

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: 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 ≤2.3 g/day (100 mmol/day), and
the recommended potassium intake is ≥ 4.7 g/day (120 mmol/day).
It seems prudent to limit excess saturated fat and to replace vitamins B6
and B12 and folate when such deficiencies are identified
A diet rich in fruits and vegetable is advised (Class IIb-C).

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 intakes. JAMA 1995;247:1049-
1057.
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.

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.

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.
2. Eat fish as main dish at least three times a week.
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 group Allowed Restricted/avoided
Fats and oils In prescribed amounts: Olive, canola, corn, Fats and oils from animal foods,
soybean, palm, sunflower and peanut oils. butter. Hydrogenated vegetable
Coconut oil. oils (e.g., margarine, lard,
shortening, spread)
Meat and chicken fat drippings
used for sauces, bacon fat,
“chicharon”
Meat, fish, Eat frequently*: Fish (fresh, frozen or canned in Fish roe, crabfat “aligui” shrimp
poultry, eggs, water, tomato or vinegar); chicken breast without head, oyster, clams.
milk, dry skin or fat. Dried beans, lentils, fresh or frozen
beans sweetpeas; “vege-meat”, tokwa, taho, tofu & Fatty meats: cold cuts, canned or
other bean products; frozen meats, sausages.; fatty
poultry with skin; internal organs
Eat occasionally**: Very lean, well-trimmed cuts
(liver, kidney, heart, tripe,
of beef, pork, veal, lamb; crabmeat, shrimp
sweetbreads)
without head; whole eggs up to 3 pieces per
week, eggwhite as desired, may be cooked in Whole milk/cow’s milk and cheese
allowed fat; Skimmed milk or low fat milk or made from whole milk
cheese
Vegetable All vegetables prepared without fat or with Buttered, creamed, fried vegetables
allowed fats only. in restricted fats or cooked with fatty
Eat frequently*: Green leafy and yellow meat and sauces.
vegetables (they are good sources of beta-
carotene, vitamin C, calcium, iron and dietary
fiber among others)
Fruit All fruits; adjust fat allowance when using Avocado in moderation (due to its
avocado. high fat content)
Eat frequently*: Vitamin C-rich fruits and deep
colored fruits
Rice, corn, All cereals, roots/tubers, certain noodles/pasta, Croissants, muffins, crackers,
rootcrops, wheat bread, “pan de sal” except those restricted biscuits, waffles, pancakes,
noodles, Eat frequently*: Oatmeal, cold cereals, corn and doughnut, rolls made with whole
bread and sweet potato egg, butter, margarine or fat of
cereals unknown composition
Fresh mami or miki noodles
Potato chips, french fries, popcorn
Desserts Fat-free/low-fat/light dessert. Fresh or canned
fruits in light syrup only. Plain cakes with no icing
(angel or sponge cakes), meringue, yogurt,
sherbet
Rich dessert especially those made
with cream, butter, solid shortening,
lard, whole egg, chocolate cookies
and pies made from cream fudge, ice
cream; pastillas from whole milk,
yema

Soups Fat-free broths made from meat or chicken Cream soups, fatty broth or stock
stock. Soups prepared with skimmed/low-fat
milk.
Beverage Coffee (not more than 3 cups black), Soda fountain beverages such as
decaffeinated coffee, tea, carbonated milk shake, malted milk and
beverages in moderation. chocolate drinks.
Alcoholic drinks in moderation.
Alcoholic drinks: not more than 1 jigger for
women and not more than 2 jiggers for men
Miscellaneous Nuts (peanuts, walnut, almond, cashew, pili, Sauces and gravies with restricted
etc.) preferably boiled, roasted/baked, fats or milk; regular mayonnaise
consume in moderation.
Butter-dipped foods.
Nondairy cream in moderation
Packed dinners or “instant foods”
Spices and seasonings in moderation. Sauce of unknown fat content.
made with allowed fats and skimmed milk,
vinegar, pickles, mustard, catsup, banana
sauce.
*Eat frequently – at least 4 to 5 times a week.
**Eat occasionally – at most, once a month.
 APPENDIX TO STROKE PREVENTION

Independent Risk Factors for Stroke Among Filipinos (RIFASAF data)

Variable Odds Ratio 95% Confidence P-Value
Interval
Hypertension 6.01 4.48-8.05 0.000
Diabetes 1.60 1.10-2.32 0.014
Atrial Fibrillation 1.91 0.51-7.19 0.337
Myocardial 4.67 1.18-18.52 0.029
Infarction
Rheumatic Heart 3.69 1.05-12.99 0.042
Disease
Smoking 1.36 1.00-1.86 0.053
Snoring 3.37 2.49-4.58 0.000
Stress 1.69 1.25-2.29 0.001
Frequent Alcohol 1.75 1.14-2.70 0.011
Intake
Statistical model derived using multiple regression analysis (Strata v. 5.0)
The odds ratio estimates the risk of a patient for stroke if the variable (risk factor) is resent
compare with a similar person without the risk factor.
Reference: Roxas A, for the Philippine Neurological Association and Department of Health. Risk
factors for stroke among Filipinos. Phil J Neurol 2002;6:1-7.

Philippine Prevalence for Atherosclerosis Risk Factors (>20 years old)

(2003 National Nutrition Health Survey)

Risk Factor Basis Prevalence (%)

Hypertension BP or history 17.4
Diabetes FBS >125 mg/dL or 4.6
history or 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 (M/F) 1.0 for men; 0.85 for 12.1 / 54.8
women
Angina Pectoris History or 12.1
questionnaire
Peripheral Arterial Disease Questionnaire or 8.9
ankle-brachial index
Reference: Dans AL, Morales DD, Abola TB, Roxas J, 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.
Guidelines for ACUTE STROKE TREATMENT
 ACUTE STROKE TREATMENT

Definition of “stroke”
Sudden onset of focal neurological deficit lasting more than 24 hours due to an
underlying vascular pathology

Table 8: Definition of stroke severity

TIA and MILD STROKE MODERATE STROKE SEVERE STROKE

TIA: Deficits resolve within Awake patient with Comatose patient with non-
24 hours but usually lasts significant motor and/or purposeful response,
less than 1 hour without sensory and/or language decorticate, or decerebrate
evidence of acute infarction and/or visual deficit posturing to painful stimuli
on neuroimaging
or or
or
Disoriented, drowsy or Comatose patient with no
Alert patients with any of stuporous patient, but with response to painful stimuli
the following: purposeful response to
Mild pure motor weakness painful stimuli
of one side of the body,
defined as: can raise
arm above shoulder,
has clumsy hand, or
can ambulate without
assistance
Pure sensory deficit
Slurred but intelligible
speech
Vertigo with
incoordination (e.g.,
gait disturbance,
unsteadiness or clumsy
hand)
Visual field defects alone
Combination of (a) and (b)

See Guidelines for TIA See Guidelines for See Guidelines for Severe
and Mild Stroke Moderate Stroke Stroke
 GUIDELINES FOR TIA AND MILD STROKE
Management Ascertain clinical diagnosis of stroke or TIA (history and physical exam are
Priorities very important)
Exclude common stroke mimickers (Appendix I)
Provide basic emergent supportive care (ABCs of resuscitation)
Monitor neuro-vital signs, BP, MAP, RR, temperature, pupils
Perform stroke scales (NIHSS, GCS) (Appendix II)
Monitor and manage BP; treat if SBP>220 or DBP>120 or MAP>130
(Appendix III).
Precautions:
Avoid precipitous drop in BP (BP not >20% of baseline MAP)
(Appendix III). Do not use rapid-acting sublingual agents; when
needed, use easily titratable IV or oral antihypertensive medication
Ensure appropriate hydration. If IVF is needed, use 0.9% NaCl

Emergent Complete blood count (CBC) PT/PTT

Diagnostics Blood sugar (CBG, HGT or Plain CT scan of the brain as
RBS) soon as possible; computation
Electrocardiogram (ECG) of hematoma volume
(Appendix IV)

Early Ischemic Hemorrhagic

Specific Non-cardioembolic Cardioembolic
Treatment (Thrombotic, Lacunar) (Appendix V)
 Aspirin 160-325 mg/day Consider Early neurology and/
start as early as anticoagulation with IV or neurosurgeon
possible and continue heparin or SQ low consult for all ICH is
for 14 days (for molecular-weight recommended
CT Scan secondary prevention, heparin (LMWH)
Confirmed see under “Delayed (Appendix VI) Monitor and maintain
(Appendix V) Management and BP: MAP 110-130
Treatment”) or mmHg (lower limit
preferred) (Appendix
Neuroprotection Aspirin 160-325 mg/day III)
(Appendix V-D) (if anticoagulation is not
possible or Neuroprotection
Early rehabilitation once contraindicated) (Appendix V-D)
stable within 72 hours
Neuroprotection Early rehabilitation
(Appendix V-D) once stable within 72
hours
Early rehabilitation once
stable within 72 hours Give anticonvulsants
only if with seizures
If infective endocarditis
is suspected, give Steroids are not
antibiotics and do not recommended
anticoagulate
TIA Monitor and correct
metabolic
Aspirin 160-325 mg/day parameters

If crescendo TIA (multiple events within hours, Correct coagulation /

increasing severity and duration of deficits), bleeding
consider anticoagulation with IV heparin or SQ abnormalities
LMWH
Follow
recommendations for
neurosurgical
intervention
(Appendix VII)

For aneurysmal
SAH, refer to next
chapter.
 No specific emergent drug treatment recommended
CT Scan Not Neuroprotection (Appendix V-D)
Available Consult a neurologist or neurosurgeon
Early supportive rehabilitation

Place of Admit to Hospital Urgent Outpatient Work-up

Treatment (Stroke Unit)
1. Stroke onset within 48 hours 1. Single TIA more than 2 weeks
2. Patients requiring any specific 2. Transient monocular
active intervention, such as: blindness alone
BP control, monitoring and 3. Stable mild strokes >48 hours
stabilization from ictus not requiring
Cardiac stabilization, including AF, specific active intervention
CHF, acute MI
Hydration Advise immediate re-consult or
Anticoagulation, if cardioembolic admission if there is worsening of
3. Rapidly worsening deficits deficit
4. Recurrent TIA within the past 2
weeks, especially those with
increasing severity and duration of
deficits, cardiac arrhythmia, or
carotid bruit

Delayed Ischemic Hemorrhagic

Management Thrombotic/Lacunar Cardioembolic
and Control of risk factors
Treatment
(Secondary Antiplatelets (aspirin,
Prevention) ticlopidine, dipyridamole,
extended-release
dipyridamole + aspirin
combination, clopidogrel,
cilostazol) (Appendix VIII)
Carotid ultrasound: If this
reveals >70% stenosis,
refer to
neurologist/neurosurgeon/
vascular surgeon for
decision-making regarding
CEA or stenting
Recommend transcranial
Doppler (TCD) to
document intracranial
stenosis
Echocardiography Long-term strict BP
and/or cardiology control and
consult monitoring
If age <75 and Consider angiogram
PT/INR available, if age <45 years,
anticoagulation with normotensive, no
coumadin clear cause of ICH,
(target INR: 2-3) and/or is a candidate
for surgery
If age >75, aspirin
80-325 mg/day or
coumadin (target
INR: 2.0 [1.6 – 2.5])
 GUIDELINES FOR MODERATE STROKE

Management Ascertain clinical diagnosis of stroke (history and physical exam are very
Priorities important)
Exclude common stroke mimickers (Appendix I)
Basic emergent supportive care (ABCs of resuscitation)
Neuro-vital signs, BP, MAP, RR, temperature, pupils
Perform stroke scales (NIHSS, GCS) (Appendix II)
Monitor and manage BP; treat if SBP>220 or DBP>120 or MAP>130
(Appendix III).
Precaution: Avoid precipitous drop in BP (not >20% of baseline MAP)
(Appendix III). Do not use rapid-acting sublingual agents; when
needed use easily titratable IV or oral antihypertensive medication.
Identify comorbidities (cardiac disease, diabetes, liver disease, gastric
ulcer, etc.)
Recognize and treat early signs and symptoms of increased ICP
(Appendix IX)
Ensure appropriate hydration. If IVF is needed, use 0.9% NaCl

Emergent CBC ECG

Diagnostics CBG, HGT or RBS Plain CT scan of brain as
PT/PTT soon as possible;
Serum Na+ and K+ computation of hematoma
volume (Appendix IV)

Early Ischemic Hemorrhagic

Specific Non-cardioembolic Cardioembolic
Treatment (Thrombotic, Lacunar) (Appendix V)
 If within 3 hours of If within 3 hours of Early neurology and/ or
CT scan stroke onset, consider stroke onset, consider neurosurgical consult
confirmed IV recombinant tissue IV rtPA and refer to for all ICH is
(Appendix V) plasminogen activator specialist recommended
(rtPA) and refer to
specialist If within 6 hours of Monitor and maintain
stroke onset and in BP: MAP 110-130
If within 6 hours of specialized centers, mmHg (lower limit
stroke onset and in consider IA preferred)
specialized centers, thrombolysis
consider intra-arterial Neuroprotection
(IA) thrombolysis Aspirin 160-325 (Appendix V-D)
mg/day, start as early
Aspirin 160-325 as possible Give anticonvulsants
mg/day, start as early only if with seizures
as possible If source of embolism
can be demonstrated, Steroids are not
Neuroprotection consider early recommended
(Appendix V-D) anticoagulation
Monitor and correct
Early supportive Neuroprotection metabolic parameters
rehabilitation (Appendix V-D)
Correct
Early supportive coagulation/bleeding
rehabilitation abnormalities

If infective endocarditis Follow

is suspected, give recommendations for
antibiotics and do not neurosurgical
anticoagulate intervention (Appendix
VII)

Early rehabilitation
once stable

For aneurysmal SAH,

refer to next chapter.
 Likely Ischemic Likely Hemorrhagic
CT scan not No specific emergent drug treatment Refer to
available recommended neurologist/neurosurgeon for
further diagnostic work-ups
Neuroprotection (Appendix V-D) and/or subsequent surgery

Refer to neurologist Neuroprotection (Appendix V-D)

Early supportive rehabilitation Early supportive rehabilitation

Place of Hospital – Intensive Care Unit or Stroke Unit

Treatment

Delayed Ischemic Hemorrhagic

Management Thrombotic/Lacunar Cardioembolic
and Control of risk factors Echocardiography Long-term strict BP
Treatment and/or cardiology control and
(Secondary Antiplatelets (aspirin, consult monitoring
Prevention) ticlopidine, dipyridamole,
extended-release INR 2.0 (1.6 – 2.5) Consider CT
dipyridamole + aspirin If age <75 and angiography, MRA,
combination, clopidogrel, PT/INR available, or 4-vessel
cilostazol) (Appendix VIII) anticoagulation with angiography in
coumadin suspected cases of
Carotid ultrasound: If this (target INR: 2-3) aneurysm, AV
reveals >70% stenosis, malformation or
refer to If age >75, aspirin vasculitis
neurologist/neurosurgeon/ 80-325 mg/day or
vascular surgeon for coumadin (target
decision-making regarding INR: 2.0 [1.6 – 2.5])
CEA or stenting

Recommend TCD to
document intracranial
stenosis
 GUIDELINES FOR SEVERE STROKE

Management Ascertain clinical diagnosis of stroke (history and physical exam are very
Priorities important)
Exclude common stroke mimickers (Appendix I)
Basic emergent supportive care (ABCs of resuscitation)
Neuro-vital signs, BP, MAP, RR, temperature, pupils
Perform stroke scales (NIHSS, GCS) (Appendix II)
Monitor and manage BP; treat if SBP>220 or DBP>120 or MAP>130
(Appendix III).
Precautions:
Avoid precipitous drop in BP (not >20% of baseline MAP) (Appendix
III). Do not use rapid-acting sublingual agents; when needed, use easily
titratable IV or oral antihypertensive medication (Appendix IIIB)

Identify comorbidities (cardiac disease, diabetes, liver disease, gastric

ulcer, etc.)
Recognize and treat early signs and symptoms of increased ICP
(Appendix IX)
Ensure appropriate hydration. If IVF is needed, use 0.9% NaCl

Emergent CBC Serum Na+ and K+

Diagnostics CBG, HGT or RBS ECG
PT/PTT Plain CT scan of brain;
computation of hematoma
volume (Appendix IV)

Early Ischemic Hemorrhagic

Specific
Treatment
 Non-cardioembolic Cardioembolic
(Thrombotic) (Appendix V)
May give aspirin 160- May give aspirin 160- Supportive treatment:
CT scan 325 mg/day 325 mg/day 1. Mannitol 20% 0.5 -
confirmed 1 g/kgBW q 4-6
(Appendix V) In posterior circulation In posterior circulation hours for 3-7 days
strokes within 6 hour strokes within 6 hours
of onset, consider IA of onset, consider IA 2. Neuroprotection
thrombolysis and refer thrombolysis and refer (Appendix V-D)
to specialist to specialist
Neurosurgery consult
Neuroprotection Neuroprotection if:
(Appendix V-D) (Appendix V-D ) Patient not herniated;
bleed located in
If cerebellar infarct, If cerebellar infarct, putamen, pallidum,
consult neurosurgeon consult neurosurgeon cerebellum; family
as soon as possible as soon as possible is willing to accept
consequences of
Early supportive Early supportive irreversible coma or
rehabilitation rehabilitation persistent
vegetative state and
goal is reduction of
mortality
(Appendix VII)
2. ICP monitoring is
contemplated and
salvage surgery is
considered

Early supportive
rehabilitation

No specific emergent drug treatment recommended

CT scan not Neuroprotection (appendix V-D)
available Refer to neurologist

Place of Intensive Care Unit

Treatment

Delayed Discuss prognosis with relatives of the patient in most compassionate

Management manner
and Ischemic Hemorrhagic
Treatment Thrombotic Cardioembolic
(Secondary Control of risk factors Echocardiography Long-term strict BP
Prevention) and/or cardiology control and monitoring
Antiplatelets (Aspirin, consult
ticlopidine, Consider CT
dipyridamole, If age <75 and PT/INR angiography, MRA, or
extended-release available, 4-vessel angiography
dipyridamole + aspirin anticoagulation with in suspected cases of
combination, coumadin (target aneurysm, AV
clopidogrel or INR=2.0-3.0) malformation or
cilostazol) vasculitis
(Appendix VIII) If age >75, aspirin 80-
325 mg/day or
coumadin with target
INR 2.0 (1.6-2.5)
 APPENDIX I

Differential Diagnoses of Stroke

A. The presence of any of the following should alert the physician to

consider conditions other than stroke:
- Gradual progressive course and insidious onset
- Pure hemifacial weakness including forehead (Bell’s palsy)
- Trauma
- Fever prior to onset of symptoms
- Recurrent seizures
- Weakness with atrophy
- Recurrent headaches (migraine, tension-type headache)

B. Conditions that mimic stroke in the emergency department (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

Bibliography
Hand P, Kwan J, Lindley R, et al. Distinguishing a stroke and mimic at the
bedside. Stroke 2006;37:769 – 775.

Libman RB, Wirkowski E, Alvir J, Rao H. Conditions that mimic stroke in the
emergency department. Arch Neurol 1995;52:1119-1122.

The Brain Matters Stroke Initiative. Acute Stroke Management Workshop

Syllabus. Basic Principles of Modern Management for Acute Stroke.
 APPENDIX II

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
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

Total score=15

II. National Institutes of Health (NIH) Stroke Scale

Items Scale Definition

Ia. Level of 0 = Alert, keenly responsive
Consciousness 1 = Not alert, but arousable by minor stimulation to
(LOC) obey, answer or respond
2 = Not alert, requires repeated stimulation to attend, or
is obtunded and requires strong or painful stimulation
to make movements (not stereotyped)
3 = Responds only with reflex motor or autonomic
effects or totally unresponsive, or totally unresponsive,
flaccid, areflexic
Ib. LOC 0 = Answers both questions correctly
Questions 1 = Answers one question correctly
2 = Answers neither question correctly
Ic. LOC 0 = Performs both tasks correctly
Commands 1 = Performs one task correctly
2 = Performs neither task correctly
2. Best gaze 0 = Normal
1= Partial gaze palsy. Gaze is abnormal in one or both
eyes but forced deviation or total gaze paresis is not
present
2 = Forced deviation, or total gaze paresis is not
overcome by oculocephalic maneuver
3. Visual 0 = No visual loss
1 = Partial hemianopia
2 = Complete hemianopia
3 = Bilateral hemianopia (blind, including cortical
blindness)
4. Facial palsy 0 = Normal symmetrical movement
1 = Minor paralysis (flattened nasolabial fold,
asymmetry on smiling)
5. Motor (Arm) 0 = No drift; limb holds 90 (or 45) degrees for full 10
5 a. Left arm seconds
5 b. Right 1 = Drifts; limb holds 90 (or 45) degrees but drifts down
arm before full 10 seconds; does not hit bed or other
support
2 = Some effort against gravity, limb cannot get up to or
maintain (if cued) 90 (or 45) degrees; drifts down to
bed, but has some effort against gravity
3 = No effort against gravity; limb falls
4 = No movement
9 = Amputation or joint fusion; explain
6. Motor (Leg) 0 = No drift; leg holds 30-degree position for full 5
6 a. Right leg seconds
6 b. Left leg 1 = Driftd; leg falls by the end of the 5-second period
but does not hit bed
2 = Some effort against gravity; leg falls to bed by 5
seconds but has some effort against gravity
3 = No effort against gravity; leg falls to bed
immediately
4 = No movement
9 = Amputation or joint fusion; explain
7. Limb ataxia 0 = absent
1 = Present in one limb
2 = Present in two limbs
9 = Amputation or joint fusion; explain
8. Sensory 0 = Normal; no sensory loss
1 = Mild to moderate sensory loss; patient feels
pinprick is less sharp or dull on the affected side; or
there is a loss of superficial 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
 9. Best 0 = No aphasia
Language 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
comprehension
10. Dysarthria 0 = Normal
1 = Mild to moderate; patient slurs at least some words
and at worst, can be understood with some difficulty
2 = Severe; patient’s 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 hemiattention or hemi-inattention to more
than one modality. Does not recognize own hand or
orients to only one side of space

Total score=42

III. Modified Rankin Scale

Score
No symptoms at all 0
No significant disability despite symptoms; able to 1
carry out all usual duties and activities
Slight disability; unable to carry out all previous 2
activities but able to look after own affairs without
assistance
Moderate disability; requiring some help but able to 3
walk without assistance
Moderately severe disability; unable to walk without 4
assistance and unable to attend to own bodily needs
without assistance
Severe disability; bedridden, incontinent and requiring 5
constant nursing care and attention
Bibliography
Brott T, Adams H. Olinger CP, et al. Measurements of acute cerebral infarction: a clinical examination scale.
Stroke 1989;20:864-870.

Goldstein LB, Bartels C. Davis JN. Interrater reliability of the NIH Stroke Scale. Arch Neurol 1989;46:660-
662.

Rankin J. Cerebral vascular accidents in patients over the age of 60. Scot Med J 1957;2:200-215.

Van Swieten JC, Koudstaal JP, Visser MC, et al. Interobserver agreement for the assessment of handicap in
stroke patients. Stroke 1988;19:604-607.

The Brain Matters Stroke Initiative. Acute Stroke Management Workshop Syllabus. Basic Principles of
Modern Management for Acute Stroke.
 APPENDIX III

Blood Pressure Management

A. BP management in Acute Ischemic Stroke

1. Use the following definitions:

Cerebral Perfusion Pressure (CPP) = MAP – ICP
MAP = 2 (diastolic) + systolic
3

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:
 Acute MI
 Congestive heart failure
 Aortic dissection
 Acute pulmonary edema
 Acute renal failure
 Hypertensive encephalopathy

4. Treat with small doses of IV antihypertensives patients who are potential

candidates for rtPA therapy who have persistent elevations in SBP >185 mmHg
or DBP >110 mmHg. Maintain BP just below these limits.

5. Use the following locally available intravenous anti-hypertensives in acute

stroke:

Drug Dose Onset of Duration Availability Stability Adverse Action

Action of /Dilution Reactions
Action
1-15 5-10 1-4 (10 mg/ 10 1 to 4 Tachycardia, Inhibits calcium
mg/hour mins hours ml amp ); hours headache, ion from
10 mg in flushing, entering slow
Nicardipine

90 ml dizziness, channel,
NSS/D5W somnolence, producing
nausea coronary,
vascular,
smooth muscle
relaxation &
vasodilatation
 IV push 10- 10-20 3-8 25 mg/mL 4 days Tachycardia, Direct
20 mg/dose mins hours amp; 25 flushing, vasodilatation
Hydralazine q 4-6 hours mg/tab headache, of arterioles &
as needed, vomiting, decreased
may increased systemic
increase to angina resistance
40 mg/dose

5 mg IV 2-5 2-4 5 mg/ml in 72 Orthostatic Alpha- & beta-

push over 2 mins hours 40 ml vial; hours hypotension, blocker. Beta-
mins, 250 mg in drowsiness, adrenergic
repeat with 250 mL dizziness, blocking activity
incremental NSS/D5W lightheadednes is 7x > than
dose of 10, s, dyspnea, alpha-
Labetalol

20, 40, 80 wheezing & adrenergic

mg until bronchospasm blockers.
desired BP Produces dose-
is achieved dependent in
or a total BP without
dose of 300 significant in
mg has been HR or cardiac
administered output
0.25-0.5 mg/ 2-10 10-30 100 mg/ 48 Hypotension, Short-acting
kg IV push mins mins 10 ml vial; hours bradycardia, beta-adrenergic
1-2 mins 2,500 mg AV block, blocking agent.
followed by in 250 mL agitation, At low doses,
infusion of D5W/NSS confusion, has little effect
0.05 wheezing / on beta2
mg/kg/min. bronchoconstric receptors of
tion, phlebitis bronchial &
If there is no vascular
Esmolol

response, smooth muscle

repeat 0.5
mg/kg bolus
dose &
infusion to
0.10
mg/kg/min.
Maximum
infusion
rate=0.30
mg/kg/min

B. Blood pressure management in Acute Hypertensive ICH

Maintain MAP<130, but not lower than 110 mmHg

Sustained hypertension may alter cerebral autoregulation, promote
progression of bleed and increase edema
Hypotension may result in cerebral hypoperfusion especially in the setting of
increased intracranial pressure (ICP)
Absence of penumbra allows for more aggressive BP management

Bibliography
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.
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.

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.
th
Guyton A and Hall J. Guyton and Hall’s Textbook of Medical Physiology, 11 ed. USA: WB Saunders; 2005.

Kidwell CS, Saver JL, Mattiello J, et al. Diffusion perfusion MR evaluation of perihematomal injury in
hyperacute intracebral hemorrhage. Neurology 2001;57:1611-1617.

Powers WJ, Zazulia AR, Videen TO, et al. Autoregulation of cerebral blood flow surrounding acute (6-
22hours) intracerebral hemorrhage. Neurology 2001;57:18-24.

Qureshi A, Wilson D, Hanley D, Traystman R. No evidence for an ischemic penumbra in massive

experimental intracerebral hemorrhage. Neurology 1999;52:266-272.

Schellinger P, Fiebach J, Hoffman K, et al. Stroke MRI in intracerebral hemorrhage: is there a

perihemorrhagic penumbra? Stroke 2003;34:1647-1680.

The Brain Matters Stroke Initiative. Acute Stroke Management Workshop Syllabus. Basic Principles of
Modern Management for Acute Stroke.
 APPENDIX IV

Neuroimaging (CT and MRI)

A. Hyperacute or Acute Ischemic Stroke

Plain CT scan of the head is the initial neuroimaging study of choice in

acute stroke. The main objective is to exclude hemorrhagic stroke and
stroke mimickers. A plain study obviates the need to wait for creatinine
result.
CT scan is 100% sensitive in documenting intracranial hemorrhage (ICH)
and 96% sensitive in documenting subarachnoid hemorrhage (SAH).
Cerebral infarcts are often not documented within 3 hours from stroke
onset. However, 60% have “early” infarct signs when viewed very closely:
1. Dense MCA sign
2. Obscuration of the lentiform nucleus
3. Loss of the gray-white interphase along the lateral insula
(Insular ribbon sign)
4. Effacement of the sulci
In cases of neurologic deterioration, large infarcts or suspected
hemorrhagic conversion, a follow-up plain CT of the head is
recommended.
MRI has the technical advantage of documenting small lesions or those
located in the brainstem or posterior fossa.
MRI can detect early infarction as early as 90 minutes using Diffusion
Weighted Imaging (DWI).
Despite the superior diagnostic yield of MRI over CT, MRI is not
recommended as routine evaluation of patients with acute ischemic
stroke. It is more expensive, time-consuming and less readily available.

B. Intracerebral Hemorrhage

CT can accurately document the exact location of the hemorrhage and the
presence of mass effect, ventricular extension and hydrocephalus.
In hypertensive ICH, a repeat plain CT scan after 24 hours of ictus is
recommended especially in cases showing clinical deterioration to
document hematoma enlargement and/or development of hydrocephalus.

Computation of Hematoma Volume (Kothari method)

Hematoma volume (in cc) = A x B x C

2
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)
 Count slice as 1 if size of hematoma is >75% of largest diameter
Count slice as 0.5 if size of hematoma is 25-75% of largest
diameter
Disregard slice if size of hematoma is <25% of largest diameter

In suspected cases of AV malformation, aneurysm or tumor bleed, a

contrast CT of the head may be warranted

C. Subarachnoid Hemorrhage

Plain CT of the head is strongly recommended as the initial procedure for

diagnosis.
The diagnostic yield of CT goes down from 92% within the first 24 hours
to 50% within 7 days of onset.

Bibliography
Brott T, Broderick J, Kothari R, et al. Early Hemorrhage growth in patients with intracerebral hemorrhage.
Stroke 1997;28:1-5.

Culebras A, Kase C, Masdeu J, et al. Practice guidelines for the use of imaging in transient ischemic attacks
and acute stroke. Stroke 1997;28:1480-1497.

Kothari RU, Brott T, Broderick JP, et al. The ABCs of measuring intracerebral hemorrhage volumes. Stroke
1996;27:1304-1309.
st
Osborne A. Diagnostic Neuroradiology, 1 edition. USA: Mosby; 1994.
 APPENDIX V

Early Specific Treatment For Ischemic Stroke

A. Thrombolytic therapy
- Patients treated with IV recombinant tissue plasminogen activator (rtPA)
within 3 hours of stroke onset are at least 30% more likely to have minimal or
no disability at 3 months.
- Streptokinase has no role in acute thrombolysis for ischemic stroke .

National Institute of Neurological Disorders and Stroke (NINDS) rTPA

guidelines

1. Dose of rtPA is 0.9 mg/kg (maximum 90 mg). Ten percent of total dose
is given as IV bolus, the rest as infusion over 60 minutes.
2. rtPA is recommended within 3 hours of onset of ischemic stroke. The
benefit of IV rtPA for acute ischemic stroke beyond 3 hours from onset
of symptoms is not established. IV rtPA is not recommended when the
time of onset of stroke cannot be ascertained reliably, including strokes
recognized upon awakening.
3. Thrombolytic therapy is not recommended unless the diagnosis is
established by a physician with expertise in diagnosing stroke and CT
of the brain is assessed by physicians with expertise in reading this
imaging study. If CT demonstrates early changes of a recent major
infarction such as sulcal effacement, mass effect, edema or possible
hemorrhage, thrombolytic therapy should be avoided.
4. Thrombolytic therapy cannot be recommended for patients with any of
the following (NINDS Study):
a. Current use of oral anticoagulants or PT>15 seconds (INR>1.7)
b. Use of heparin in the previous 48 hours or prolonged PTT>1.5x
normal
c. Platelet count <100,000 mm3
d. Another stroke or a serious head injury within the previous 3
months
e. Major surgery within the preceding 14 days
f. Sustained pretreatment SBP>185 mmHg or DBP>110 mmHg
(when aggressive treatment necessary to lower BP)
g. Rapidly improving neurological signs
h. Mild, isolated neurological deficits, such as ataxia alone,
sensory loss alone, dysarthria alone, or minimal weakness
i. Prior ICH
j. Blood glucose <50 mg/dL or > 400 mg/dL
k. Seizure at onset of stroke
l. Gastrointestinal or urinary bleeding within preceding 21 days
m. Recent myocardial infarction (within the previous 3 months)
 5. Thrombolytic therapy should not be given unless emergent ancillary
care and the facilities to handle bleeding complications are readily
available.
6. Caution is advised before giving rtPA to persons with severe stroke
(NIH Stroke Scale Score >22)
7. Because the use of thrombolytic drugs carries the real risk of major
bleeding, whenever possible the risks and potential benefits of rtPA
should be discussed with the patient and his or her family before
treatment is initiated.
8. Patients given rtPA should not receive antiplatelets or anticoagulants
within 24 hours of treatment.

B. Antithrombotic therapy

1. International Stroke Trial (IST)

- Multicenter randomized clinical trial of 19,435 patients
- Regimen: Aspirin 300-325 mg/day vs. no aspirin
Heparin SC vs. no heparin
5,000 units bid or 12,500 units bid
- Started within 48 hours of stroke onset for 14 days or until
discharge
- Results:
Aspirin
- Fewer recurrent stroke within 14 days
- Fewer deaths and dependency at 6 months
Heparin
- No benefit even at 6 months
- If used should not exceed 5,000 units bid

2. Chinese Acute Stroke Trial (CAST)

- 21,106 patients randomized
- Aspirin 160 mg/day vs. placebo
- Started within 48 hours of stroke onset
- Results:
Risk of recurrent stroke or vascular death:
Aspirin 5.3%
Placebo 5.9% (p=0.03)

3. Meta-analysis on low molecular-weight heparin (LMWH) and

heparinoids in acute ischemic stroke involving 2,855 patients has
shown that treatment was associated with significant reduction in
venous thromboembolism (DVT and pulmonary embolism). LMWH has
no significant effect on reducing death and disability at 6 months.
Symptomatic ICH was not significantly increased.
C. Neuroprotection

1. 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
Aggressive BP lowering is detrimental in acute stroke.
Manage hypertension as per recommendation (Appendix III)

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 increased.

Avoid hypoglycemia or hyperglycemia

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 tight glycemic control at 80-110 mg/dL
Avoid glucose-containing (D5) IV fluids. Use isotonic saline
(0.9% NaCl)

Avoid Hyperthermia
Fever in acute stroke is associated with poor outcome
possibly related to increased metabolic demand, increased
free radical production and enhanced neurotransmitter
release.
For every 1 C increase in body temperature, the relative risk
of death or disability increases by 2.2.
Search for the source of fever.
Treat fever with antipyretics and cooling blankets.
Maintain normothermia.

D. Neuroprotectants
 Neuroprotectants are drugs that:
o Protect against excitotoxins and prolong neuronal survival
o Block the release of glutamate, free radicals, inflammatory cytokines,
and the accumulation of intracellular calcium cations.

Several neuroprotective drugs have reached phase III clinical trials, but
most had negative or disappointing results except for citicoline. Data-pooling
analysis on four trials involving 1,652 patients with ischemic stroke show that
treatment with citicoline within the first 24 hours increases the probability of
global recovery (NIHSS, mRS, BI) by 30% at 3 months.
CDP–choline helps increase phosphatidylcholine synthesis and inhibition
of phospholipase A2 within the injured brain during ischemia
Several phase III clinical trials (e.g. SAINT II, FAST-MAG) are currently
underway

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of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the
American Stroke Association. Neurology 2002;59:13-22.

Davalos A, Castillo J, Alvarez-Sabin J, et al. Oral citicoline in acute ischemic stroke: an individual patient
data pooling analysis of clinical trials. Stroke 2002;33:2850-2857.

International Stroke Trial Collaborative Group. The International Stroke Trial: a randomised trial of aspirin,
subcutaneous heparin, both or neither among 19,435 patients with acute ischemic stroke. Lancet
1997;349:1569-1581.

Labiche LA, Grotta JC. Clinical trials for cytoprotection in stroke. NeuroRx 2004;1:46-70.
Lyden P, Wahlgren N. Mechanism of action of neuroprotectants in stroke. Journal of stroke and
cerebrovascular diseases.2000; 9(6): 9 – 14.

NINDS rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med
1995;333:1581-1587.

Practice advisory: Thrombolytic therapy for acute ischemic stroke-summary statement. Report of the Quality
standards Subcommittee of the American Academy of Neurology. Neurology 1996;47:835-839.
 APPENDIX VI

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 annular calcification
Prosthetic heart valves Patent foramen ovale (PFO)
Recent MI Atrial septal aneurysm
LV/LA thrombus Calcific aortic stenosis
Atrial myxoma Mitral valve strands
Infective Endocarditis
Dilated 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

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

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 need, 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 coumadin
has reached therapeutic levels or once antiplatelet medication is
started for secondary prevention.

To date, there has been no trial directly comparing 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
Adams H. Emergent use of anticoagulation for treatment of patients with ischemic stroke. Stroke
2002;33:856-861.

Hart R, Palacio S, Pearce L. Atrial fibrillation, stroke and acute antithrombotic therapy. Stroke 2002;33:2722-
2727.

Moonis, M, Fisher M. Considering the role of heparin and low-molecular weight heparin in acute ischemic
stroke. Stroke 2002;33:1927-1933.
 APPENDIX VI

Early Specific Treatment of Hypertensive Intracerebral Hemorrhage

A. Medical Treatment for all ICH:

The goals are to prevent complications and careful manage BP.
a. Maintain MAP <130, but not lower than 110 mmHg
b. Manage increased ICP accordingly (see Appendix IX)
c. Start anticonvulsants only if with seizures
The incidence of seizures is higher in ICH, especially in lobar
hematomas.
The role of prophylactic anticonvulsants in deep
hemorrhages is unclear. It is justified to withhold
anticonvulsants until clinically indicated.
d. Prevent and treat respiratory complications. Endotracheal
intubation is performed in patients to provide airway protection
and in those in coma or with respiratory failure.
e. Prevent and treat infections.
f. Maintain adequate nutrition.
g. Ensure proper fluid and electrolyte balance; maintain
normothermia and normoglycemia.
h. Rehabilitate early once stable.
i. Practice bedsore precautions.
j. Deep-vein thrombosis and pulmonary embolism prophylaxis
should be instituted (use antiembolic stockings or intermittent
pneumatic compression devices)

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 hematoma volume > 85 mL

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 young patients with moderate or large
lobar hemorrhage.
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 >4
Patients with supratentorial hematoma with volume >30 cc

Bibliography
Academy of Filipino Neurosurgeons Guidelines on the Management of Hypertensive ICH

Broderick JP, Brott TG, Tomsick T, et al. Ultra-early evaluation of intracerebral hemorrhage. J Neurosurg
1990;72:195-199.

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.

Brott T, Broderick J, Kothari R, et al. Early hemorrhage growth in patients with intracerebral hemorrhage.
Stroke 1997;28:1-5.

Fujii Y, Tanaka R, Takeuchi S, et al. Hematoma enlargement in spontaneous intracerebral hemorrhage. J

Neurosurg 1994;80:51-57.

Juvela S, Heiskanen O, Poranen A, et al. The treatment of spontaneous intracerebral hemorrhage. A

prospective randomized trial of surgical and conservative treatment. J Neurosurg 1989;70:755-758.

Kazui S, Naritomi H, Yamamoto H, et al. Enlargement of spontaneous intracerebral hemorrhage. Incidence

and time course. Stroke 1996;27:1783-1787.

Kothari RU, Brott T, Broderick JP, et al. The ABCs of measuring intracerebral hemorrhage volumes. Stroke
1996;27:1304-1309.
 APPENDIX VIII

Antiplatelets for Secondary Stroke Prevention

A. Aspirin
1. Antiplatelet Trialist’s Collaboration
 65 trials involving 60,196 patients with symptomatic atherosclerosis
(e.g., unstable angina, MI, TIA, stroke)
 Aspirin 50-1,500 mg/day vs control
 23% odds reduction on composite outcome of MI, stroke or vascular
death
 Highest RRR was seen in the low (75-150 mg) and medium dose (160-
325 mg) groups

2. Mini-meta-analysis on aspirin among patient with prior stroke or TIA

 10 trials involving 6,171 patients with prior TIA or non-disabling stroke
 Aspirin reduced the odds for the cluster of stroke, MI or vascular death
by 16%
 No difference in RRR for low (<100 mg), medium (300-325 mg) and
high doses (>900 mg) of aspirin

B. Ticlopidine
1. Canadian American Ticlopidine Study (CATS)
 1,072 patients with recent thromboembolic stroke
 Ticlopidine 250 mg bid vs placebo
 30.2% risk reduction on composite outcome of MI, stroke, vascular
death over placebo

2. Ticlopidine Aspirin Stroke Study (TASS)

 3,069 patients with recent TIA/cerebral infarction
 Ticlopidine 250 mg bid vs aspirin 1,300 mg od
 12% risk reduction vs aspirin for stroke or death at 3 years

C. Clopidogrel
1. Clopidogrel vs Aspirin in Patients at Risk of Ischemic Events (CAPRIE)
 19,185 patients with prior stroke, MI or PAD
 Clopidogrel 75 mg/day vs aspirin 325 mg/day
 8.7% RRR vs aspirin for combined endpoint of stroke, MI and vascular
death

2. Clopidogrel and Aspirin combination (Management of Atherothrombosis

with Clopidogrel in High-Risk Patients with TIA or Stroke [MATCH])
 7,599 patients with prior stroke or TIA and additional risk factors
 Clopidogrel-aspirin 75 mg/75 mg vs clopidogrel 75 mg
 No significant difference in composite outcome of ischemic stroke, MI,
vascular death or rehospitalization secondary to ischemic events
 3. Clopidogrel for High Atherothrobotic Risk and Ischemic Stabilization,
Management and Avoidance (CHARISMA)
 15,603 patients with either clinically evident cardiovascular disease or
multiple risk factors
 Clopidogrel 75 mg with low-dose aspirin (75-162 mg) vs low-dose
aspirin only
 Overall, clopidogrel/aspirin combination was not significantly more
effective than aspirin alone in reducing rate of MI, stroke or vascular
death
 Suggestion of benefit with combination treatment in patients with
symptomatic atherothrombosis

D. Cilostazol
Cilostazol Stroke Prevention Study (CSPS)
 1,095 patients with cerebral infarction in the past 6 months
 Cilostazol 100 mg bid vs placebo
 41.7% RRR for recurrent stroke

E. Dipyridamole and asprin combination

1. European Stroke Prevention Study (ESPS 2)
 6,602 patients with recent TIA or stroke randomized to placebo, aspirin
25 mg bid, extended-release dipyridamole 200 mg bid, or aspirin 25
mg + ER-dipyridamole 200 mg bid
 Aspirin better than placebo; dipyridamole better than placebo;
combination treatment better than either agent alone.
 37.8% risk reduction for stroke with combination therapy over placebo
 No increased risk of major bleeding with combination treatment

2. European/Australasian Stroke Prevention in Reversible Ischemia Trial

(ESPRIT Trial)
 2,739 patients with recent TIA or minor stroke of arterial origin
randomized to aspirin 30-325 mg/day or aspirin 30-325 mg od +
dipyridamole 200 mg bid
 20% risk reduction for composite outcome of stroke, MI, vascular death
with combination therapy
 No increased risk of major bleeding with combination treatment

Bibliography
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

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.

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.
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.

CAPRIE Steering Committee. A randomized, blinded trial of clopidogrel vs aspirin in patients at risk of
ischemic events. Lancet 1996:348:1329-1339.

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.

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.

Gent M, Blakely JA, Easton JD, et al. The Canadian American Ticlopidine Study (CATS) in Thromboembolic
Stroke. Lancet 1989;1:1215-1220.

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.

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.

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.
 APPENDIX IX

Management of Increased Intracranial Pressure

A. Signs and symptoms of increased ICP

1. Deteriorating level of sensorium
2. Cushing’s 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. Control fever. Avoid hyperthermia.
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. Status epilepticus should
be managed accordingly.
4. Strict glucose control between 80-110 mg/dL
5. No dextrose-containing IVF. Hyperglycemia may extend ischemic zone
(penumbra) and further cause cerebral edema
6. Use stool softeners to prevent straining.

Specific
1. Elevate the head at 30 to 45 degrees to assist venous drainage.
2. Give osmotic diuretics: Mannitol 20% loading dose at 1 g/kg, maintenance
dose at 0.5-0.75 mg/kg) to decrease intravascular volume and free water.
3. Lost fluids must be replaced. Hypertonic saline is an option and has the
advantage of maintaining an effective serum gradient for a prolonged
period with lower incidence of rebound intracranial hypertension. Aim for
serum osmolarity=310 mOsm/L. (Serum osmolarity = 2 (Na) + Glucose/18
+ BUN /2.8)
4. Hyperventilate only in impending herniation by adjusting tidal volume and
pCO2 between 25 to 30. This maneuver is usually effective only for
approximately 6 hours. Otherwise maintain normal pCO2 between 35 and
40.
5. Carefully intubate patients with GCS 8 or less, or those unable to protect
the airway.
6. Do CSF drainage in patients with intraventricular hemorrhage (IVH) or
hydrocephalus.
7. Use barbiturates if all other measures fail. Available locally is thiopental
(loading dose=10 mg/kg, maintenance dose titrated at 1-12 mg/kg/hour
continuous infusion to achieve burst suppression pattern in EEG)
 8. Consider surgical evacuation for mass lesions.
9. Consider decompressive hemicraniectomy in cases of malignant middle
cerebral artery infarcts

C. Sedatives and Narcotics Available Locally

Drugs Usual Onset of Duration Comments Availability/Dilution
Dose Action of Effect
Midazolam 0.025-0.35 1 to 5 min 2 hours Unpredictable sedation 15 mg/3 mL amp;
mg/kg 5 mg/5 mL amp;
50 mg in 100 mL
NSS/D5W
Diazepam 0.1-0.2 Immediate 20 to 30 Sedation can be reversed with 10 mg/2 mL amp;
mg/kg minutes flumazenil (0.2-1 mg at 0.2 50 mg in 250 mL
mg/min at 20 min interval, max NSS/D5W
dose 3 mg in one hour)
Propofol 5-50 <40 secs 10 to 15 Expensive (10 mg/mL) 100 mL
ug/kg/min min vial (premixed)
Ketorolac 50-100 mg 1 hour 6 to 8 NSAID 30 mg/mL amp
IV hours
Tramadol 50-100 mg 1 hour 9 hours Centrally acting synthetic 50 mg/ 2 mL amp;
IV analgesic compound not 100 mg/2 mL amp
chemically related to opiates
but thought to bind to opioid
receptors and inhibit reuptake
of NE and serotonin
Fentanyl 50-100 1-2 mins >60 min Can be easily reversed with 100 ug/2 mL;
ug/hour naloxone (0.4-2 mg IVP; 2,500 ug in 250 mL
repeat at 2-3 min intervals, NSS/D5W
max dose 10 mg)
* 110x more potent than
morphine
Morphine 2-5 5 mins >60 min Opioid 10 mg/mL gr 1/6;
mg/hour 16 mg/ mL gr 1/4

Bibliography
th
Ropper A, Daryl G, Diringer M et al. Neurological and Neurosurgical Intensive Care. 4 ed. USA: Lippincott
Williams & Wilkins; 2003.

Wijdicks EFN. The Clinical Practice of Critical Care Neurology. 2nd ed. USA: Oxford University Press; 2003.
 Special Section: Guidelines for the
MANAGEMENT OF ANEURYSMAL SUBARACHNOID HEMORRHAGE
 MANAGEMENT OF ANEURYSMAL SUBARACHNOID HEMORRHAGE

I. DIAGNOSIS OF SUBARACHNOID HEMORRHAGE (SAH)

Clinical – may present with sudden, severe headache (thunderclap
headache), loss of consciousness or adult-onset seizures.
Neurological examination – signs of meningeal irritation (i.e., neck rigidity),
altered or decreased level of consciousness, CN III or VI nerve palsy.
Patients may or may not have focal neurological deficits

Emergent referral to a neurologist/neurosurgeon and transfer to a facility with

capabilities of managing acute stroke are recommended.

II. 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 an underlying
aneurysm.

2. Lumbar tap with CSF analysis in the absence of focal neurological

signs is an option in the following cases:
Cranial CT scan is negative
Cranial CT scan is unavailable
Special circumstances (e.g., issues with CT scan cost)
Multiple specimens (at least 3 tubes) should be collected to rule out
traumatic tap. Opening pressures should be measured.
3. Cerebral angiogram is the gold standard in determining the cause of
SAH. Early angiography should be performed in all cases, whether
poor- or good-grade SAH. If the initial angiogram is negative, a repeat
angiogram should be performed after 2 weeks.
4. Good-quality CT angiogram and MR angiography are other options.

III. SAH GRADING

1. Hunt and Hess Classification is recommended for the clinical grading
of SAH.

Table 9: Hunt and Hess Classification

Grade Description
1 Asymptomatic, or mild headache, slight nuchal rigidity
2 Moderate to severe headache, nuchal rigidity, no neurologic
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. Fisher grading may be used as a guide in considering therapeutic options.

Table 10: Fisher Grading

Grade Description (Blood on CT)
1 No subarachnoid blood detected
2 Diffuse or vertical layers <1 mm thick*
3 Localized clot or vertical layer >1 mm thick*
4 Intracerebral or intraventricular clot with diffuse or no SAH
*“Vertical layer” refers to blood in the subarachnoid spaces including in the
interhemispheric fissure and cisterns

IV. GENERAL SYMPTOMATIC TREATMENT

1. Absolute bed rest in a quiet, comfortable environment
2. Cardiac monitoring and frequent assessment of neuro-vital signs
3. Soft diet for alert patients, nasogastric-tube (NGT) feedings if with
impaired consciousness
4. Analgesics, including opiates for headache. Avoid aspirin and other
NSAIDs
5. Paracetamol and cooling blankets, if febrile
6. Maintenance of euglycemia
7. Sedatives, if agitated
8. Antiemetics, as needed for nausea and vomiting
9. Stool softeners

V. EARLY SPECIFIC TREATMENT

1. Nimodipine: A systematic review showed a significant reduction in poor
outcomes with calcium antagonists for SAH. The evidence rests mainly on
one large trial with oral nimodipine. It is uncertain whether nimodipine acts
through neuroprotection or through reduction of the frequency of
vasospasm, or both. Nimodipine 60 mg every 4 hours by mouth or NGT
for 3 weeks is recommended.
2. Anticonvulsants: Short-term anticonvulsants are recommended for
patients with documented seizures in the acute phase of SAH. Although
no randomized trial has proven that prophylactic anticonvulsants in SAH is
effective, they can be considered in patients with significant cortical
damage, thick cisternal clot, parenchymal hemorrhage, or those in coma.
Phenytoin is the recommended anticonvulsant, given as a 15 mg/kg IV
loading dose followed by 3 to 5 mg/kg/day in divided doses.
3. Steroids: Corticosteroids have no proven role and are not recommended
for use in SAH.
 4. Antifibrinolytic agents are not recommended. Although they reduce the
risk of rebleeding, they are associated with a higher rate of cerebral
ischemia.
5. Manage increased ICP
6. BP management: Although the best antihypertensive agent and BP
remains unsettled, IV nicardipine to a target SBP<150 in the pre-operative
phase is reasonable.

VI. PREVENTION AND MANAGEMENT OF VASOSPASM

1. Monitoring: Serial transcranial Doppler (TCD) is recommended for the
diagnosis and monitoring of vasospasm.
2. Maintenance of euvolemia: Evidence on the use of blood volume
expansion alone or in combination with induced hypertension and
hemodilution (triple H therapy) in the prophylaxis and management of
secondary ischemia (vasospasm) following aneurysmal SAH is lacking.
3. Endovascular angioplasty (chemical +/- mechanical) is a effective way of
managing vasospasm. Intervention has to be early before clinical signs
suggesting irreversible infarction (i.e., hemiplegia) are present.
4. Treatment strategies undergoing current investigation include intravenous
magnesium sulfate and statins.

VII. TREATMENT OF SAH

Excluding the aneurysm from the circulation is the main goal of treatment.
Obliteration the aneurysm can be achieved through surgical clipping or
endovascular coiling.

VIII. TIMING OF SURGERY

1. Definitions:
Early surgery is surgery 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 I-III) aneurysmal SAH patients to minimize the
chance of a devastating rebleed.
b. For poor grade patients (Grade IV-V), early surgery is recommended in
the presence of:
Hematoma
Hydrocephalus

Surgery may be delayed in the presence of:

Ischemia or infarction
Severe angiographic vasospasm
 Casted ventricles
Diffuse SAH (Fisher Grade III) Complex aneurysm on angiography.

c. A maximum cut-off age for early surgical management (for the elderly)
is not recommended in the absence of organ failure.

IX. COILING
1. Can be performed early in both good- and poor-grade patients.
2. Reduces the rebleed rate for poor-grade patients who would otherwise be
treated conservatively.
3. Vasospasm is not a contraindication and can be dealt with endovascularly
during coiling
4. Can be performed under local anesthesia if needed.

X. WHERE TO ADMIT
SAH patients should be admitted at the 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.

XI. NURSING ISSUES:

SOLICITUDE, THOUGHTFULNESS, PROTECTIVENESS
1. Acute Phase
a. Care must be exercised to prevent further ICP increase
b. There should be close monitoring of fluid status and for possible
secondary cardiac, respiratory or metabolic insults.
c. Persistent headache, deteriorating level of consciousness, other
signs of increased ICP and development of focal neurological
deficits should be recognized for urgent referral to a neurologist or
neurosurgeon.

2. Convalescent Phase
a. Presence of sensory or perceptual alterations, motor deficits, and
impaired verbal communication and physical mobility should be
addressed in nursing care.
b. Feelings of depression should be monitored. Emotional support and
encouragement should be provided.
c. Upon discharge, patients and relatives should be educated on
continuity of care, medication intake and follow-up

XII. REHABILITATION
1. Supportive rehabilitation is done initially in the pre-operative phase.
 2. Early rehabilitation is recommended for all SAH patients in the post-
operative period.

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Guidelines for STROKE REHABILITATION
 STROKE REHABILITATION

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.

Obtain medical history and physical examination.

Determine nature and extent of rehabilitation needs and services based on
stroke severity, functional status and social support.

MILD MODERATE SEVERE

STROKE STROKE 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 emotional deficits, sensory deficits.
3. Psychosocial assessment and family or caregivers support
4. Assessment of function (e.g., functional independence measure or
FIM).
5. Financial support.
 II. INPATIENT REHABILITATION

Post-stroke patient in inpatient rehabilitation

Determine level of care based on medical status, cognitive and motor function,
social support, and access to care and services.

Discuss rehabilitation program with patient and family.

Determine and document treatment plan

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 community living?
acute 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, Continue inpatient Go to III.

caregiver about future plans rehabilitation.
and home therapy.
Discharge patient to the home
or community.
Go to IV.
A. 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 decision 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 YES

function?

NO

Reassess periodically. Go to IV.

A. 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

Does patient need community-based NO Arrange primary-

rehabilitation services? care follow-up.
Provide home
rehabilitation
YES program.

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

Reassess periodically. Discharge to the home or

community setting.
Arrange primary-care
follow-up.
Provide home rehabilitation
program.
A. 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
 Guidelines for the
NURSING MANAGEMENT of STROKE PATIENTS
 NURSING MANAGEMENT OF STROKE PATIENTS

I. PREVENTIVE CARE

General Specific Process Outcome

Objective Objectives
1. Nurses will Provide 1. A nurse will 1. People
provide information on implement a health understand risk
preventive care stroke, risk education program factors and
through health factors, lifestyle (HEP) approved or show interest in
education modification and published by a duly modifying
activities based regular medical accredited or lifestyle.
on identified check-ups. recognized health
learning needs. agency. 2. Incidence of
stroke
2. A nurse will decreases.
implement the HEP
appropriate for the 3. Awareness
people’s level of increased.
understanding.
4. Use of
3. A nurse will use published
appropriate, available materials
teaching material. increase
participation in
4. A nurse will actively stroke
participate in fora on prevention fora.
health education on
stroke prevention.
2. Nurses will Identify people 1. The nurse will 1. Early
actively identify who are at risk implement assessment detection,
patients with for developing based on established referral and
risk factors. stroke. guidelines on stroke risk management of
factors and will use a risk- identified at-risk
assessment nursing people.
framework.
2. Risk
2. The nurse will identification
appropriately refer implemented in
identified people high risk a standardized
for stroke. manner.

3. The nurse will report 3. Contribute

and document identified factual,
people high risk for accurate data
stroke. due to existing
 stroke data
banks.
3. Nurses will Identify, 1. The nurse will identify 1. Increased
be actively promote and agencies in the awareness of
involved in participate in community that have available
HEP regarding available programs for lifestyle facilities and
lifestyle programs modification for stroke programs
modification. regarding prevention. regarding
lifestyle lifestyle
modification. 2. The nurse will modification.
recommend available
programs for lifestyle 2. Increased
modifications. adherence to
lifestyle
3. The nurse will facilitate modification.
referral to appropriate
community or health care
agency regarding lifestyle
modification.

II. CURATIVE CARE

General Specific Process Outcome

Objective Objectives
1. Nurses will 1. Promptly 1. Nurses will assess 1.Early needs
promptly identify and patients comprehensively identification
identify prioritize using current and and
patient’s needs patient’s needs. acceptable neurological prioritization.
by performing assessment tools.
proper health 2. Use and 2. Immediate
assessment perform proper 2. Nurses will correlate initiation of
with emphasis neurological patient’s history with signs management.
on neurological assessment and symptoms.
assessment techniques. 3. Early
techniques. 3. Nurses will identify transfer and
priority patient needs admission to
based on assessment. hospital with
stroke or
4. Nurses will prioritize intensive care
and facilitate series of unit.
diagnostic examinations
according to stroke
guidelines and will have
nursing responsibilities
 before, during and after
the procedure, including
patient safety and
informed consent.
2. Nurses will Plan and 1. Nurses will implement 1. Early
provide quality manage nursing emergency nursing identification
nursing care care based on measures if needed. and
based on the patient’s assessment of
identified condition, needs 2. Nurses will closely disease
patient needs and priorities: monitor, document and progression
in collaboration report neuro-vital signs.
with other a. Physiologic 2. No incidence
member of the care 3. Nurses will provide of falls and
health team, safety measures, such as aspirations.
utilizing a b. Safe a. Aspiration precautions
holistic Measures b. Fall precautions 3. No
approach. c. Use of restraints bedsores,
c. Comfort d. Seizure precautions contractures
Measures and muscular
4. Nurses will provide atrophy.
d. Therapeutic comfort measures, such
environment as: 4. Healing
a. Linen changes environment
e. Prevention of b. Personal hygiene attained.
complications c. Turning
and infections d. Proper positioning 5.
e. Range of motion (ROM) Complications
f. Spiritual and and infections
psychosocial 5. Nurses will provide a prevented
care therapeutic environment
a. Proper ventilation and 6. Psycho-
lighting emotional and
b. Minimize noise spiritual
c. Proper orientation to upliftment
time, place and person
d. Provisions of window 7. No
murals in every room medication
errors;
6. Nurses will prevent medications
complications and adhere to.
possible infections by:
a. Establishing patent 8. Self
airway expression
b. Monitoring and using
maintaining BP alternative
c. Observing and means, if
 providing catheter and needed.
tube care
d. Monitoring input and 9. Patient’s
output independent
e. Monitoring and functions
prevention of increased maximized;
ICP disabilities
f. Nutrition and hydration correctly
addressed.
7. Nurses will provide
spiritual and psychosocial 10.
care: Cooperation
a. Alleviation of anxiety by and active
encouraging verbalization participation of
of feelings clients and
b. Guidance in identifying significant
positive coping others.
mechanisms
c. Respect of patient’s 11. Complete,
beliefs and culture accurate
d. Facilitation of patient’s records
spiritual needs
12. Early
8. Nurses will apply the medical
principles of Bioethics in intervention
the Practice of Nursing
Care. 13. Utilization
of other health
9. Nurses will administer and community
medications observing the resources.
10 R’s.

10. Nurses will establish

alternative means of
communication if
necessary.

11. Nurses will assess

patient’s capabilities in
performing ADLs and
assist in identifying
alternative means.

III. REHABILITATIVE AND PROMOTIVE CARE

 General Specific Process Outcome
Objective Objectives
1. Nurses will 1. Assist the 1. Nurses will initiate 1. Performance
focus on early patient towards rehabilitation upon of simple ROM
rehabilitation maximum admission. exercises and
and discharge functional ADLs by
planning. capacity. 2. Nurses will assist the patient with
patient in performing ADLs minimal or no
2. Discuss the in collaboration with other supervision.
care plan with health team members.
the patient and 2. Maintenance
significant 3. Nurses will educate of sexual
others. patient on alternative, function.
physiologically safe sexual
3. Involve the practice (as indicated). 3. Performance
patient’s family of simple
and significant 4. Nurse will include nursing
others in significant others in procedures by
decision making providing specific nursing significant
and the care care, such as provisions of others with
plan. hygiene, nutrition, turning, minimal or no
positioning, pulmonary supervision
toile, ROM exercises, and from nurses.
other care.
4. Compliance
5. Nurses will ensure good to treatment
compliance to medications regimen and
and provide options for adherence to
compliance to outpatient outpatient
follow-up follow-up

6. The nurse will 5. Active

collaborate with the family participation of
and significant others in patient and
the care plan. family in care
plan.
2. Nurses will 1. Provide 1. Nurses will provide a 1. Adherence
assist in guidelines for discharge care plan of patient and
sustaining and home care. containing the following: family to
maintaining a. Activity and exercise prescribed
patient’s 2. Guide patient b. Medication regimen discharge care
healthy, in lifestyle c. Symptoms needing plan.
productive modification referral
lifestyle. based on d. Prescribed diet 2. Compliance
identified risk e. Medical follow-up to alternative
factors. schedule lifestyle.
f. Special care to be
3. Assist patient provided 3. Motivation
in accepting and and stimulation
adapting to 2. Nurses will facilitate of patient’s
disability. referrals to community interest in self-
resources. enhancing
activities.
3. Nurses will identify
appropriate lifestyle 4. Maximal
modification suited to the patient
patient’s current status. potential.

4. Nurses will involve 5. Active

patient in diversion participation of
activities that will enhance family
self-esteem. members.

5. Nurses will involve

family member in the care
plan.
Guidelines for the ESTABLISHMENT and OPERATION of STROKE UNITS
 ESTABLISHMENT and OPERATION of STROKE UNITS

I. 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 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 physician¹s 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

A Stroke Unit is a hospital unit that cares for stroke patients exclusively or
almost exclusively, with specially trained staff and a multidisciplinary approach to
treatment and care.1

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

E1. 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 diagnoses. The units accept patients acutely. Some have a program
of care similar to acute stroke units while others have a program similar to
a combined unit.

E2. Delayed admission unit

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.

E. 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

II. 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)
4. Ultrasound (continuous-wave, TC Duplex, transthoracic echocardiogram;
transesophageal echocardiogram)
5. Monitoring (RR, Respiration, Holter, O2 saturation)
6. Emergency laboratory

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
d. Occupational therapists
e. Speech pathologist
f. Nutritionists
g. Social workers

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
III. HOSPITALS IN THE PHILIPPINES WITH ACUTE STROKE UNITS

Table 11.
Hospitals Stroke Unit Type Contact Number

Metro Manila
East Avenue Medical Center Mixed acute units 9280611 loc.503
Jose Reyes Memorial Medical ASU 7119491 loc 262
Center
Makati Medical Center ASU
Manila Adventist Medical Center Mixed acute units 5259191 loc 324
Manila Doctors Hospital ASU 5243011
Manila Central University Mixed acute units 3672031 loc 1127
Philippine General Hospital ASU 5218450 loc 2406
Philippine Heart Center Mixed acute units 9252401 loc 2483
San Juan de Dios Medical Center Mixed acute units 8319731 loc 1226
St. Luke’s Medical Center ASU 7230101 loc 7399
Sto. Tomas University Hospital ASU 7313001 loc 2368
The Medical City Mixed acute units 6356789 loc 6281

Luzon
Mt. Carmel Diocesan General Mixed acute units 042-7102576
Hospital, Lucena
Lorma Medical Center, San Mixed acute units 072-700-0000
Fernando, La Union
Lucena United Doctors Hospital ASU 042-3736161

Cebu
Cebu Doctors Hospital ASU 032-2555555
Chong Hua Hospital Mixed acute units 032-2541461
ASU, acute stroke unit.

IV. RECOMMENDATIONS
Stroke patients should be treated in stroke units (Level I). Admission to
stroke unit decreases death, dependency and institutionalization.
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.
 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 education
Health Officer Recognition of stroke
Acute treatment of TIA and mild
Optional: stroke
Nurse/Midwife Referral of moderate and severe
Barangay Health strokes to Levels II or III centers
Worker Referral to Levels II or III centers for
diagnostic tests
Facilities: Rehabilitation
Municipal Health Secondary prevention of stroke and
Clinic follow-up visits

II Basic: Stroke prevention and public

Neurologist (If not education
available, other Recognition of stroke
physicians with Acute treatment of TIA, mild,
special training in moderate, and severe strokes
stroke) Referral of complicated strokes to
Neurosurgeon Level III centers
Stroke nurse Referral to Level III centers for
Radiologist further diagnostic tests
Physiatrist Rehabilitation
Secondary prevention of stroke and
Facilities*: follow-up visits
CT scan
Electrocardiogram
Laboratory
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 and
Neurosonologist 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

LEVELS OF STROKE CARE

STROKE CENTER LEVEL

STROKE SEVERITY I II III

TIA or Mild Stroke √ √ √

Moderate Stroke √ √

Severe Stroke √ √
 WORKING COMMITTEES

Primary and Secondary Prevention of Stroke

Dr. Artemio Roxas, Jr Dr. Raquel Alvarez
Dr. Dante Morales Dr. Epifania Collantes
Dr. Alejandro Diaz Dr. Vince De Guzman
Dr. Romulo Esagunde Dr. Maria Cristina San Jose
Dr. Fatima Collado Dr. Cymbeline Perez-Santiago

Acute Stroke Management

Dr. Abdias Aquino Dr. Maria Cristina San Jose
Dr. Carlos Chua Dr. Lina Salud
Dr. Ester Bitanga Dr. Vincent De Guzman
Dr. Rhoderick Casis Dr. Gerardo Legaspi

Spontaneous Intracerebral Hemorrhage

Dr. Manuel Mariano
Dr. Maria Cristina San Jose
Dr. Rhoderick Casis

Aneurysmal Subarachnoid Hemorrhage

Dr. Manuel Mariano Dr. Rhoderick Casis
Dr. Maria Cristina San Jose Dr. Gerardo Legaspi
Dr. Peter Rivera

Establishment and Operation of Stroke Units

Dr. Jose Navarro
Dr. Epifania Collantes
Dr. Alejandro Baroque II

Stroke Rehabilitation
Dr. Betty Mancao Dr. Alvin Mojica
Dr. Sharon Ignacio Dr. Josephine Bundoc
Dr. Teresita Evangelista Dr. Cory Hidalgo
Dr. Faith Legaspi

Nursing Management of Patients with Stroke

Ma. Isabelita Rogado, RN Noli Pagdanganan. RN
Ferdinand Aganon, RN Veronica Honculada,RN
Ana Merly Migo, RN Marilou Reyes, RN
Lydia Bienes, RN Josefine Rivera, RN

Dr. Artemio Roxas, Jr.

2006 Edition Overall Chairperson
CORPORATE MEMBERS

Boehringer Ingelheim
LR Imperial
Otsuka Philippines
Patriot Pharma
Pfizer
Sanofi-Aventis
Servier Philippines
UCB Philippines
Therapharma
SSP Annual 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
 Stroke Society of the Philippines

BOARD OF TRUSTEES
OFFICERS

President: Abdias V. Aquino, MD

1st Vice-President: Ester S. Bitanga, MD
2nd Vice-President: Jose C. Navarro, MD
Secretary: Artemio A. Roxas Jr., MD
Treasurer: Betty D. Mancao, MD
P.R.O.: Carlos L. Chua, MD
Immediate Past President: Joven R. Cuanang, MD

MEMBERS

Alejandro C. Baroque, MD
Fatima R. Collado, MD
Ma. Epifania V. Collantes, MD
Danilo J. Lagamayo, MD
Manuel M. Mariano, MD
Dante D. Morales, MD
Peter P. Rivera, MD
Isabelita C. Rogado, RN
Ma. Cristina San Jose, MD