CONSENSUS STATEMENT ON THE

MANAGEMENT OF ISCHAEMIC STROKE

PREFACE.

Stroke is presently a major cause of mortality and morbidity in our country and it will assume
greater importance in the future. There is thus a need to provide some form of guidelines and
standards in stroke management to optimise outcome.

The focus of this statement is on acute stroke management, but for the purpose of
comprehensiveness, other relevant areas of stroke care are also mentioned in brief.

Extensive review of important published materials has been made and because of repetitions
of references in different sections, it was decided to list the reference in alphabetical order.

I hope the information in this booklet will be useful to clinicians and wish to thank all panel
members for their valuable contribution and support.

Thank you.

Yours sincerely,

Dato’ Dr Mohd Rani Jusoh

MEMBERS OF THE EXPERT PANEL:

1. Dato’ Dr. Mohd Rani Jusoh - Chairman

Senior Consultant Neurologist and
Head Department of Neurology
Hospital Kuala Lumpur

2. Professor Tan Chong Tin

Senior Consultant Neurologist and
Head of Division of Neurology
Department of Medicine
University of Malaya, Kuala Lumpur

3. Associate Professor M. Nyunt Win

Consultant Neurologist
International Medical University
Sesama Centre- Plaza Komanwel
Bukit Jalil, Sri Petaling
Kuala Lumpur

4. Professor Raymond Azman Ali

Consultant Neurologist and Head,
Department of Medicine
Hospital Universiti Kebangsaan Malaysia
Jalan Tenteram, Cheras,
Kuala Lumpur

5. Dr. Veronica Tan

Neurologist
Department of Medicine
Hospital Universiti Kebangsaan Malaysia
Jalan Tenteram, Cheras,
Kuala Lumpur

6. Dr. Md. Hanip Rafia

Consultant Neurologist
Hospital Sultanah Aminah,
Johor Bahru,
Johor Darul Takzim

7. Dr. Yong Fee Man

Consultant Neurologist
Sri Kota Medical Centre
Jalan Monet, Klang.

8. Dr. Shahnaz Merican

Neurologist
Department of Neurology
Hospital Kuala Lumpur

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1. Introduction and Overview of Stroke.

Stroke is a devastating illness and is the most common cause of severe disability in adult.
The average incidence of stroke is about 2:1,000 population, and the risk of stroke
increases with age such that after the fifth decade, the incidence doubles with every
decade of life.

Data from the Framingham study showed that the incidence of stroke rises exponentially
from 1 to 2 per 1,000 in the 45 to 54 years old age group to nearly 10 per 1,000 in the 65-
to 74 years old age group. For persons of 75 to 84 years old, the incidence rises to nearly
20 per 1,000. As the incidence increases with age, so too is the prevalence. Stroke
prevalence is about 6:1,000 population and prevalence of stroke disability is 4:1,000.

In developed countries, the incidence of stroke has been steadily decreasing since 1960’s
and the initial fall in incidence was largely attributed to better control of hypertension.
Subsequent fall in incidence was due to better control of other risk factors such as heart
disease, diabetes, smoking and obesity. However stroke remains a major cause of death
and consistently the third most common cause of death after heart disease and cancers.
The economic and psychosocial cost of stroke is tremendous.

In the USA it is estimated that there are 3 million stroke survivors, with nearly 0.5 million
new or recurrent strokes per year. The cost of treatment and rehabilitation is about US 40
billions per year.

In Australia, there are 40,000 stroke cases per year. Stroke accounts for 10% of all deaths
and 25% of chronic disability. The direct and indirect cost excluding cost from loss of
earning is AUS 1.7 billion annually.

There are no national figures on stroke but hospital records do show progressive increase
in stroke discharges and deaths at government hospitals. Every year about 2,500 deaths
and 12,000 stroke discharges are recorded in government hospitals. As the country
progress the importance of stroke will increase because of improved longevity and higher
proportion of elderly population. In 1997 the life expectancies of Malaysian males and
females were 69.58 and 74.47 years respectively, and the proportion of people above 60
years old was 6.1%. In future as longevity continues to improve, the proportion of senior
citizens will reach 15-20% or more as in developed countries now.

A study done in the University Hospital showed 400 stroke cases per year, of which 71%
were due to infarcts (31.8% large vessels, 39.2% small vessels) and 19% due to
haemorrhage.

In Kuala Lumpur Hospital (KLH) 1,000 stroke cases are seen per year with 30-35% acute
mortality. Cerebral infarcts formed 60.8% of cases (53% large vessels, 7.8% small
vessels) and 33% were due to haemorrhage. The higher percentage of haemorrhage seen
in KLH was probably due to the availability of neurosurgical service which was not
available in the University Hospital at the time of the study.

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2. Prognosis of Stroke.

The prognosis of stroke depends on the stroke type, size and location of stroke. Best
prognosis is seen in lacunar stroke with 85% chance of full recovery and the worst
prognosis is in cerebral haemorrhage with acute mortality rate of 60-80%. For larger
cerebral infarcts, the mortality rate is 20-30% depending on the size and location of the
infarct. Brain stem infarcts and large hemisphere infarcts carry a worse prognosis.

In developed countries, acute mortality of stroke has also been decreasing but in recent
years the rate of improvement is leveling off and the mortality figures are reaching
plateau. The initial improvements were attributed to better general care of stroke patients
and further improvement can be expected with better definitive or specific treatments
such as thrombolytic and neuroprotective therapies.

Overall, about 12% of stroke patients die within the first week, 20% at one month and
25% at one year. Mortality rate among survivors is in the range of 6-12% per year. The
Framingham study showed that at 10 years after stroke, 35% of the patients were still
alive. Survival was better in the group of patients without comorbidity factors. About
50% of the deaths were due to the stroke and recurrent strokes while 40% were due to
heart disease. A study in Germany showed a figure of 40% survival 5 years after stroke.

Of the survivors, about 10% can recover almost fully, 15-20% severely disabled and the
rest have mild to moderate disability. Overall about 15% can be expected to recover
sufficiently well to enable gainful employment. Up to 80% can have some degree of
independent activity, half of which may have difficulty coping outside the house.

In countries with comprehensive service for stroke care, about 60% of stroke survivors
are discharged home, 15-20% discharged to rehabilitation hospitals and 20-25%
discharged to institutions for long-term care.

In terms of morbidity and mortality among patients who survived longer than 6 months,
32% have depression, 48% hemiparetic, 22% cannot walk, 12-18% dysphasic and 24-
53% require partial or complete assistance for Activities of Daily Living (ADL).

In a study at KLH in 1995 among patients with first stroke, acute mortality (within 2
weeks) was 29%. At discharge, 47% were bedridden, 22% were wheelchair-bound, 86%
had feeding problems, 36% had speech problems and 32% had bladder problems.

3. Diagnosis.

The diagnosis of ischaemic stroke, like any other disease, is made by evaluating and
analyzing information derived from a good history, examination and the appropriate
laboratory investigations. Because of the nature of the illness and the dramatic manner the
neurological deficits occur, history is of utmost importance. Every effort must be made to
obtain the story of the illness from the patient, family members or friends.

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 The diagnosis should provide answers to the following questions:

3.1. What is the neurological deficit?

3.2 Where is the lesion?
3.3 What is the lesion?
3.3 What stage is the lesion? And
3.4 Why has the lesion occurred?

4. Key issues in the history.

In attempting to answer some of the above points, the following areas in the history need
to be enquired:

1. The nature of the complaint, e.g. monocular blindness, visual field defects,
hemiparesis, dysphasia, dysarthria, vertigo, ataxia and diplopia, will guide the
clinician toward the anatomical location of the stroke.
2. The onset of the complaint - a sudden or abrupt onset is characteristic of ischaemic
stroke. However, the onset may also be more gradual, over several hours (either
steadily or in a stepwise fashion), or overnight. If patients are able to recall what they
were doing at that time, the onset is almost certainly sudden. If the onset is over more
than just a few days, the diagnosis of stroke is unlikely.
3. Associated symptoms such as chest pain, palpitations, sudden blood loss (e.g.
massive haematemesis), may suggest an “extracranial” cause of stroke.
1. Past medical history of hypertension, diabetes mellitus, ischaemic heart disease,
hyperlipidaemia and previous transient ischaemic attacks (TIAs) is important and
relevant to the management and prevention of stroke.
1. The patient’s drug history is crucial as it may reveal, for instance, prolonged use of
oral contraceptives.
1. The patient’s social habits including cigarette smoking, alcohol consumption, diet and
physical activity provide further information regarding stroke risk factors.

A full neurological examination, including the patient’s conscious level and tests of higher
mental function (such as the mini-mental state examination) is mandatory. There are no
shortcuts in a neurological examination. Every positive finding must then be carefully
synthesized and constructed to a comprehensive neurological syndrome, which should
point to the site of the lesion in the brain or brain stem.

The physical examination must also include a general examination, paying particular
attention to the vital signs, cardiovascular system and stigmata of hyperlipidaemia. In the
cardiovascular examination, all the pulses must be palpated and assessed for rhythm,
vessel wall character and volume, the carotids auscultated for bruits, and the heart
examined for evidence of cardiomegaly, double apical impulse (left ventricular
aneurysm), murmurs and added heart sounds (valvular heart disease and myxomas). In
older patients, particularly those without evidence of risk factors for atherosclerosis, the
pupils should be examined (Argyll-Robertson pupils) and superficial temporal arteries
palpated (giant-cell arteritis).

A drowsy or comatose patient usually has either a large cerebral infarct, a brain stem
infarct affecting the reticular activating system, cerebral haemorrhage or an unrelated
systemic or metabolic condition that has compromised consciousness, such as hypoxia,
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hyponatraemia or hypoglycaemia. Certain key clinical features are helpful in pointing to
the site of the stroke. These can be divided into 2 broad groups: a) clinical features that
are caused by anterior circulation (carotid artery) stroke, and b) those caused by posterior
circulation (vertebrobasilar system) stroke (see table).

Table: Clinical features of stroke

Due to anterior circulation stroke Due to posterior circulation stroke

 Homonymous hemi- or  Homonymous hemianopia

quadrantonopia  Cortical blindness
 Dysphasia  Ataxia
 Hemiparesis / plegia  Dysarthria
 Hemisensory loss / disturbance  Diplopia
 Parietal lobe dysfunction, e.g.  Dysphagia
astereognosis, agraphaesthesia,  Horner’s syndrome
impaired two-point discrimination,  Hemiparesis or hemisensory loss
sensory and visual inattention, left- contralateral to the cranial nerves palsy
right dissociation and acalculia

Brain imaging is the ultimate diagnostic tool in stroke. There are essentially 2 imaging
modalities for stroke: computed tomography (CT) and magnetic resonance imaging
(MRI). Brain CT may be normal in the first 24 hours of an infarct, but will demonstrate
haemorrhages from the onset of stroke. Early signs of cerebral infarction on CT include
loss of normal grey-white matter differentiation, effacement of the sulci or outline of the
lentiform nuclei and loss of visualisation of the insular ribbon. Brain CT may also miss
very small infarcts beyond its resolution and infarcts in the brain stem, MRI is superior to
CT in this respect. The main purpose of brain imaging is to rule out other causes of an
acute neurological deficit (in particular, haemorrhage) because this will influence
management. Hence, in the vast majority of cases, brain CT, the cheaper and more readily
available technique, is adequate, and should be done on admission. Haemorrhagic stroke
cannot be reliably differentiated from ischaemic stroke based on the history and clinical
examination alone, including sophisticated clinical scoring methods. Clinical scoring
method such as the Allen and Sirriraj scores and the more recent one suggested by Besson
et. al. will be wrong in up to 10% of cases, and are, therefore, not recommended for
routine clinical practice. Brain imaging is also mandatory prior to thrombolytic therapy
for stroke. Diffusion-weighted (DWI) and more recently, perfusion MR imaging (PI) can
detect very early infarcts (as early as within 6 hours of the stroke), but these are currently
only of academic interest because, as mentioned earlier, the primary role of brain imaging
is to exclude haemorrhage. Thus, there is no point in delaying or repeating the brain CT in
the hope of demonstrating the infarct. If the lesion is suspected to lie in the brain stem or
cerebellum and the clinical diagnosis of stroke is in doubt, a brain MRI, should be
subsequently requested, instead of a repeat CT.

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 When evaluating the brain images, the following questions must be answered:

4.1 What is the nature of the lesion?

The characteristics of the lesion should be those of an infarct appropriate to the imaging
modality. Hence, it should be hypodense on CT, and hypointense on T1-weighted and
hyperintense on T2-weighted, MRI. The morphology of large hemispheral infarcts should
conform to a vascular territory, and thus should be wedge-shaped, or rounded if the
infarcts are smaller and deep. Lacunar infarcts (infarcts < 15 mm in diameter) are
rounded or oval, and are commonly located in the capsular regions, basal ganglia and
corona radiata.
4.2 In what arterial territory is the lesion?
This information may guide further management. Infarcts in the anterior circulation, for
instance, should be evaluated further with carotid duplex ultrasound.

4.3 How big is the lesion?

Prognosis is influenced by the size of the infarct. In general, the bigger the infarct, the
poorer the outcome and recovery.

4.4 Could it be anything else?

Where appropriate, differential diagnosis such as brain tumours, demyelination and
abscesses should be considered. Although large hemispheral infarcts may exhibit marked
perilesional oedema, exert pressure effects or cause midline shift, these features should
raise doubts about the diagnosis of stroke and signal the possibility of a brain tumour,
especially if the lesion lies in the deep white matter and spares the cortex. If in doubt, a
repeat CT with contrast, may reveal a cortical nodule corresponding to the tumour.

5. Initial Investigations.

The initial investigations for patients with ischaemic stroke must be aimed at:
1. Confirming the diagnosis and excluding treatable differential diagnosis
2. Confirming the nature and size of the stroke
3. Determining the size/extent of the stroke, and
4. Identifying new, and assessing pre-existing, risk factors for stroke, or factors which
may compromise its recovery.

Blood investigations

Full blood count.

Both anaemia and polycythaemia are relevant to ischaemic stroke. Polycythaemia may be
severe enough to cause arterial thrombosis on its own. Sudden torrential blood loss may
cause ischaemic stroke, and anemia of any cause may compromise the viability
of the ischaemic penumbra. Although rarer, platelet counts above 1000 x 10 9/L may
also lead to arterial thrombosis. Leukocytosis may occur in ischaemic stroke, but may
also reflect underlying infection in the lungs (aspiration pneumonia) or elsewhere (e.g.
urinary tract, because of catheterisation). In addition, in young patient thrombocytopaenia
may suggest the presence of the antiphospholipid antibody syndrome.

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Random blood glucose.
The random blood glucose level may reveal previously undiagnosed diabetes mellitus. In
patients already diagnosed with diabetes, blood glucose level monitoring is crucial in the
treatment and prognostication of stroke patients.

Blood urea and electrolytes.

Fluid and electrolyte balance is a crucial component in the management of stroke. Poor
oral intake of fluids may cause dehydration, which in turn, may lead to hypotension and
compromise the blood supply to ischaemic areas. Renal failure and disturbances in
sodium homeostasis are common complications of stroke.

Fasting serum lipid.

Both hypercholesterolaemia and hypertriglyceridaemia are recognised risk factors for
ischaemic stroke. If the serum cholesterol level is normal during admission, it must be
repeated three months later, because it usually falls during the acute phase of stroke.

Cardiac enzymes.
The serum creatine kinase, aspartate transaminase and lactate dehydrogenase levels
should be checked if acute/recent myocardial infarction is suspected from the ECG.

Arterial blood gas analysis.

It is mandatory to check the blood gases and acid-base balance in stroke patients who are
comatose or drowsy, or suspected of having pneumonia or a concomitant chronic lung
disease.

Erythrocyte sedimentation rate (ESR).

In younger patients (< 45 years of age), a raised ESR may indicate the presence of a
connective tissue disease, in particular, systemic lupus erythematosus, or atrial myxoma.
In older patients, a raised ESR may suggest giant cell arteritis or multiple myeloma
(causing hyperviscocity)

VDRL.
A positive VDRL in older patients will alter the management of stroke. In younger
patients, it raises the possibility of the antiphospholipid antibody syndrome.

Collagen screen.
Younger patients, regardless of the ESR, must have their serum complement, antinuclear
antibody and antiphospholipid antibody levels checked.

Thrombophilia screen.
Younger patients should also be screened for protein C, protein S and antithrombin III
deficiency and activated protein C resistance1.

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Imaging.

Computed Tomography (CT) of the brain.

If the facility is available, all stroke patients should have a brain scan, and a plain CT is
sufficient in the vast majority of cases. The main reason for doing a brain CT is to exclude
haemorrhage as the basis of stroke. Apart from a small brain stem haemorrhage, which
may be obscured by bony artifact at the base of the skull, all haemorrhages in the brain
are immediately visible on a brain CT. Another reason is to select patients for
thrombolytic therapy. It also helps the physician in advising about prognosis.

Magnetic Resonance Imaging (MRI).

Magnetic resonance imaging is only necessary if the brain CT is equivocal and further
management of the patient depends on it. Equivocal hypodense lesions in the brain stem
often require further evaluation with MRI. Cerebellar infarct requiring neurosurgical
intervention is an indication for MRI.

Carotid Doppler (Duplex) ultrasound.

All patients with an anterior circulation infarct should have a carotid Doppler ultrasound
to identify and evaluate potentially treatable stenotic lesions. This investigation can be
done on an outpatient basis.

Four-vessel angiography and arch aortogram.

It is mandatory for younger patients to undergo angiography to assess the arterial supply
of the brain and brain stem, and the aortic arch. Non-atherosclerotic vascular diseases
such as moyamoya disease and vasculitis (arteritis) can be diagnosed with angiography.
Magnetic resonance angiography (MRA) or computed tomographic angiography (CTA)
are non-invasive, and are currently being evaluated for their sensitivity, but conventional
angiography remains the goal standard. Patients who have more than 70% stenosis of the
carotid artery contralateral to the stroke on carotid Doppler ultrasound should also
proceed to angiography. These investigations need not be done during the initial
admission.

Two-dimensional echocardiography.
In younger patients, 2D-echocardiography should be done to exclude a cardiogenic source
of emboli, as an initial investigation. Atrial myxoma, rheumatic valvular disease,
cardiomyopathy and infective endocarditis are the usual cardiac lesions causing stroke.
Septal defects and persistent foramen ovale may require the injection of contrast (agitated
saline) for visualization. Transthoracic echocardiography (TTE) is adequate in the
majority of cases, but left atrial thrombi, atrial septal defects and vegetations on mitral or
aortic valves can only be demonstrated by transoesophageal echocardiography (TOE).
Echocardiography should also be done in older patients suspected or known to have
valvular heart disease, ischaemic heart disease and atrial fibrillation to (re-) evaluate the
lesion, size and function of the relevant cardiac chambers, and to determine the presence
of thrombi.

9
 Chest radiograph.
All patients must have a chest radiograph to assess the size of the heart (an independent
risk factor for stroke), look for intercurrent lung infection or aspiration pneumonia
(complicating the stroke) and exclude a primary cancer of the lung (brain metastases are
known to masquerade as stroke).

Other tests.

12-lead electrocardiogram.
A 12-lead ECG is mandatory in all patients, for it may reveal unsuspected myocardial
infarction or ischaemia, left ventricular hypertrophy, arrhythmias (e.g. atrial fibrillation)
and a propensity for arrhythmias (such as Wolf-Parkinson-White syndrome).

Ambulatory ECG.
All younger patients and patients with suspected of having paroxysmal tachyarrhythmias
or sinoatrial node disease should have longer ECG recordings (at least 24 hours). This
investigation can be done on an outpatient basis.

6. The Philosophy and Principles of Stroke Management.

The decade of the brain saw exciting advances in imaging techniques of brain disorders
including stroke. In tandem with these there are also advances that make stroke treatment
in similar modalities as for coronary heart disease a real possibility. Faced with new
treatments and technologies, clinicians are forced to make choices for their patients. The
principles in guiding the decision-making are familiar to doctors but are worth
reinforcing.

The Patient.
First and foremost as in other clinical situations, it is crucial to place the interest of the
patient as paramount. That the stroke is seen in the context of the whole patient. With so
much promising information on many fronts relating to stroke management, it may be
easy to lose focus and not put the patient in the forefront. There may be unconscious
temptations to see stroke in isolation as opposed to a patient with a stroke. That it is the
patient with a stroke we are treating, after which we hope to bring the patient back to his
family, community and if possible his vocation. In evaluating the whole patient, the
factors to be considered are numerous and include the age, concurrent medical problems
and quality of life expected. Some of these factors are already in-built to the guidelines
relating to the use of the specific modalities of treatment or technologies.

Scientific Evidence.
The primary considerations in evaluating new treatments and technologies are safety and
efficacy and likewise all stroke treatments must be assessed scientifically. Only those
treatments with scientific evidence of safety and efficacy should be used. Treatments of
unproven value or with inadequate data should not be routinely used to treat stroke. It is
unfortunate that sometimes adequate good data require time to accrue, but this is a
principle that cannot be compromised. In the interest of patient care and good clinical
practice it is necessary to delay recommending wide usage of any potentially useful
treatment until there are adequate evidence to its value.

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 Cost Benefit.
This is another consideration that will increasingly appear in the future. On the surface of
it, this factor is at variance with the patient - first principle, but it is a necessary
consideration given the fact that in many systems of health care, the cost is paid by
somebody else or through pooling of resources. The rapid pace of advances in medical
science and technology have enabled many possibilities to be done to patients at various
levels of stroke management that can far outstrip the capacity for payments. Yet the
resources are always limited and clinicians have important role to evaluate and decide as
what would be appropriate and cost effective.

Multidisciplinary Team.
Stroke management has several phases and each phase has several modalities involving
different professional groups. Very often neurologist are heavily involved in the acute
phase of the management and contact with patient may decrease with time as other
professional groups increase their presence. It is also important that each professional
group treat other professional colleagues with respect and that all these groups must be
able to interact positively for patient well-being. To ensure this happening, interactions
must occur early in the patient's illness and comprehensive treatment for the patient
planned right from the start.

7. General Management.

Stroke must be regarded and treated as a medical emergency. The general management of
stroke is of crucial importance, since a major reduction in stroke mortality is largely due
to continuing improvement of its general management. Ideally, all stroke cases should be
managed in an Intensive Care Unit (ICU), High Dependency Unit (HDU) or at least in an
acute bay where close monitoring is possible. The major areas of concern are:

7.1 Resuscitation.

This is the first step of stroke management. And this is especially crucial in the drowsy
and comatose patients. The general guideline of ABCs (airway, breathing and circulation)
applies. In certain situations oxygen supplement may be required.

7.2 Observation.

The head chart should be done at least 4 hourly which includes vital signs, conscious
state, pupillary size and reaction. Alternatively, Glasgow Coma Scale (GCS) chart can be
used. Whenever there is a clinical deterioration, the observation should be done more
closely.

7.3 Nursing.

An excellent nursing care is very important. Two hourly turning and early usage of high
quality ripple mattress could prevent pressure sores. Conscious patients should be nursed
in a prop-up position. Patient may require urinary catheter or condom drainage to monitor
intake and output accurately.

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7.4 Blood Pressure.

Most patients with acute stroke will have stress-related high blood pressure (BP) on
admission. In the majority of them, there is no urgency to treat moderate BP elevation as
it will normalise or return to baseline over a week although a third of them remain
hypertensive. A slightly higher systemic BP is required to maintain the cerebral perfusion
in the situations of increased ICP, partial thrombosis and disturbed cerebral
autoregulation. There is evidence that reductions in blood pressure carry a risk of
producing further ischaemic brain damage in patients with ischaemic stroke and
intracerebral haemorrhage. Current guidelines recommend that treatment of hypertension
should be delayed for several days or up to two weeks after a stroke unless there is
hypertensive encephalopathy, heart failure, cardiac ischaemia, aortic dissection, continued
intracerebral bleeding or severe hypertension (mean BP > 130 mmHg or systolic BP> 220
mmHg ). Persistent hypertension after 2 weeks should be treated since hypertension is the
single most important risk factor for stroke and recurrent stroke. In a known hypertensive
patient, the best policy is to continue the same medications that the patient is taking.
Usually, oral medications are adequate and only rarely is parenteral anti-hypertensive
drug required.

7.5 Blood glucose.

Both hyper and hypoglycaemia have significant effects on the infarcted brain tissues.
Transient stress-related hyperglycaemia occurs after stroke. Mildly elevated blood
glucose is usually not deleterious. There is general agreement to recommend control of
hypoglycaemia and hyperglycaemia after stroke. Hypoxia depletes high-energy
phosphates and glucose is then metabolised via the anaerobic pathway causing lactate
accumulation. Thus the need to control significant hyperglycaemia. In a known diabetic
patient, the best policy is to continue the current medications and avoid extreme
hypoglycaemia. A short course of insulin therapy may be necessary in the very ill and
difficult cases.

7.6 Hydration and Nutrition.

Patients with swallowing problems should initially be given intravenous fluids and
commenced on nasogastric tube feeding when neurologically stable. Fluid replacement of
2 litres daily is usually sufficient. Urine output (normally at least 500-1000 ml/day)
should be monitored closely and compared with intake.

When the patient is alert and able to shallow, oral feeding in the form of thickened liquids
or semi-solids diet can be started. This is followed gradually with the introduction of
mechanically soft, blended diet and then a regular one. A daily intake of 1300-1400
calories with vitamin supplements is recommended. A full liquid and soft diet is easier to
swallow without aspiration than clear fluid for patient with various degrees of dysphagia.

Short-term use of nasogastric tube feeding for 4-6 weeks is suggested if the patient still
has dysphagia. Percutaneous endoscopic gastrostomy (PEG) tube may be considered if
the patient has poor prognosis for regaining an adequate and safe swallowing mechanism.
Such a complication is usually associated with hemispheric and brain stem strokes.

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7.7 Haemodilution.

There are several clinical observations, which suggest that haemodilution, may be useful
in the acute management of strokes. Polycythaemia rubra vera (PRV) patients with a
raised haematocrit are prone to thromboembolic events including strokes. A stroke can
also be due to various haematological abnormalities that can increase plasma viscocity.

When local blood flow is interrupted, collateral blood supply may maintain some delivery
of oxygen and nutrients, albeit at a low level, and structural integrity of the neurons is
preserved. These border zones or ischaemic penumbra can be visualised by high
resolution regional blood flow measurements. Intentional haemodilution enhances the
blood flow to the penumbra but decrease its oxygen carrying capacity.

Meta-analysis of trials, which assess the effects of haemodilution in acute strokes using
plasma expanders with or without venesection, has shown no benefits. However the risk
of venous thromboembolism may be decreased by haemodilution. To date, there is still
insufficient evidence to recommend the general use of haemodilution.

7.8 Raised intracranial pressure (ICP):

This is a common cause of death in the first week of stroke. It is a complication of

occlusion of major intracranial arteries and large multilobar infarcts and may be fatal in
the first 24-48 hours. The peak incidence is 3-5 days post infarct.

All patients with large infarct should be managed with head end of the bed elevated to 20-
30 degrees. This is a simple measure to reduce venous pressure and thereby reduce
intracranial pressure. The stable patient who is awake and alert does not require any
treatment. Only 10%-20% of cerebral oedema warrants medical interventions. These
patients show signs of raised ICP such as deteriorating GCS (Glasgow Coma Scale),
clinical features of herniation e.g. pupil enlarging ipsilateral to the infarcted hemisphere
or pathological corticospinal signs contralateral or ipsilateral to the hemispheric lesion.

The goal of treatment is to reduce ICP, maintain adequate cerebral perfusion and avoid
brain herniation.

Factors exacerbating raised ICP which include fluid overload, hypoxia, hypercarbia and
hyperthermia should be avoided. Hypoosmolar fluid e.g. 5% dextrose may worsen the
cerebral oedema. Avoid acute elevation of serum osmolality of more than 20 mosm above
the patient’s usual level to prevent precipitating encephalopathy.

Hyperventilation reduces the blood carbon dioxide concentration by 5-10 mmHg and
results in lowering the ICP by 25-30%. This effect can be almost immediate.

Hyperosmolar agents e.g. glycerol or mannitol have been used to reduce the ICP.
Barbiturates and steroids have also been tried with disappointing results. It has been
shown that glycerol delays the time of death with temporary survival of patients suffering
serious physical and mental handicaps. The lack of statistically significant beneficial long
term effects does not support the wide use of glycerol.

13
 Mannitol is widely used to reduce significant or symptomatic ICP. It is postulated that
mannitol acts by reducing the overall water content, improves cerebral blood perfusion by
decreasing the blood viscosity and as a free radical scavenger. The regime usually
followed is 20% mannitol at a dose of 0.25 - 0.5 g/kg intravenously over 20 minutes and
then, if necessary, repeated every 6 hours with the maximum daily dose is 2 g/kg. The
complications include rebound cerebral oedema, renal failure, fluid and electrolyte
imbalance, cardiogenic pulmonary oedema and hypersensitivity.

7.9 Seizure:

Seizure in the first 2 weeks of stroke occurs in 4-8% of patients, being more common in
frontal lobe infarctions. The seizure are localization related and may remain partial
(nonconvulsive) or may progress to become generalise. Quick termination of seizure is
indicated using intravenous diazepam. Subsequently the patient requires a period of
therapy with anticonvulsant agents. Seizures occurring more than once should be treated
as stroke related epilepsy and managed with the appropriate anticonvulsant agents such as
carbamazepine, phenytoin, sodium valproate or other agents.

8. Specific Treatment.

8.1 Antiplatelet Agents.

The effectiveness of antiplatelet agents in the secondary prevention of stroke is well

established. Recent evidence from two large trials have shown, in addition, that early
antiplatelet therapy with aspirin in acute ischaemic stroke, is associated with a small but
definite nett benefit.

Aspirin
The role of platelet activation and aggregation in the pathogenesis of acute ischaemic
stroke is well recognised. Aspirin irreversibly inhibits platelet cyclooxygenase, thereby
inhibiting platelet aggregation.

The benefits: The results of the International Stroke Trial and the Chinese Acute Stroke
Trial taken together show that early treatment with aspirin reduces the rate of death or
recurrent ischaemic stroke at 14 days, and the rate of death and dependency at discharge
and for up to six months later.

The risks. Although there was a slight excess of haemorrhagic stroke in the patients
receiving aspirin in both trials, this was not sufficient to offset the overall benefit of early
aspirin treatment.

Contraindications: Contraindications include aspirin hypersensitivity, active peptic

ulceration or recent upper gastrointestinal bleeding. Pre-existing oral anticoagulation in
non-comatose patients is not an absolute contraindication, provided the patient is not
over-anticoagulated (APTT <2.0) (Chamoro et al 1995). However, the absolute
requirement for combined treatment should be carefully assessed for each individual
patient.

14
Dose. The doses used in the International Stroke trial and the Chinese Acute Stroke Trial
were 300mg and 160mg respectively. The benefit of either dose over the other has not
been conclusively proven and controversy remains over the most effective dose in stroke
prevention. A reasonable approach would be to commence the patient on 300mg on day
one, followed by 150mg daily subsequently. The rationale for this approach is that the
complete inhibition of platelet aggregation by low dose aspirin (75mg or less) is delayed
by 2-3 days after starting therapy, whereas 300mg is effective on the first day (Brown
1995). Low doses of aspirin are associated with a lower incidence of gastrointestinal side
effects and would therefore theoretically be preferable in long term usage.

Timing. Evidence from both trials suggests that aspirin should be started as soon as
possible after the onset of ischaemic stroke, preferably within 48 hours.
Size of infarct. Although these trials were not designed to answer the question as to
whether there is an increased rate of haemorrhagic transformation in large infarcts with
early aspirin treatment, the results of these trials (which did not exclude patients with
large infarcts) together with those of previous studies (Toni et al 1996) suggest that
aspirin should be started regardless of infarct size.

Pre-treatment imaging. Imaging in the form of a CT-scan or MRI of the brain is

recommended before aspirin is commenced for all cases of acute stroke. In stuporose or
comatose patients, or patients on anticoagulation at presentation, pre-treatment imaging
should be considered mandatory. However, if there is likely to be a significant delay in
obtaining the required scan, in non-comatose patients in whom the stroke is clinically
very likely to be ischaemic, aspirin may be started in the interim and its use reviewed
with the scan results (Baigent et al 1999).

Other Antiplatelet Drugs.

There is currently no available data from clinical trials on the efficacy of early
ticlopidine, clopidogrel or dipyridamole in the treatment of acute ischaemic stroke. These
drugs have established roles in the secondary prevention of ischaemic stroke.

Ticlopidine, an inhibitor on ADP-induced platelet aggregation, has been established as

superior to aspirin (12% relative risk reduction) in the secondary prevention of stroke but
requires regular haematological monitoring.

Clopidogrel, which similarly inhibits ADP-induced platelet aggregation, is also superior

to aspirin in secondary prevention (relative risk reduction 9.4%), and is as safe as aspirin.

The European Stroke Prevention Study 2 (ESPS-2) that examined the use of low dose of
aspirin (50 mg) and combination of aspirin and extended-release dipyridamole (400 mg)
showed that the combination is superior to aspirin alone in secondary prevention of stroke
(relative risk reduction 17%)
In the absence of specific contraindication, aspirin should now be started as soon as
possible in all patients presenting with acute stroke and should be continued long-term
wherever possible.

15
8.2 Anticoagulation.

Heparin has been used to treat ischaemic stroke for many years, well before the CT-scan
era. Even in those early years, there were suggestions that in the treated group deaths due
to pulmonary embolism were reduced, but there was no difference in stroke death per se.
In one of the earlier studies that used CT scan for patient selection, Duke showed that
heparin was not useful in cerebral thrombosis. There was no significant difference in
stroke progression, death at 7 days and functional status at 1 year. In a review by
Sandercock of 10 controlled trials done after CT scan era, there was no significant
difference in deaths from all causes, but there was significant reduction in incidence of
deep vein thrombosis (DVT) as detected by radio-iodine scanning and venography. There
was also reduction of pulmonary embolism in the treated group but it was not statistically
significant.

The International Stroke Trial that randomised 19,435 patients also did not show
immediate or long-term benefit with heparin.

With regard to low-molecular weight (LMW) heparin initial study indicated that LMW
heparin (Nadoprin) given in the dosage of 4100 IU twice daily subcutaneously within 48
hours from the onset of the acute ischaemic stroke for 10 days was effective in improving
outcomes (deaths and dependency) at six months. There was no significant difference
between the treated and placebo group in haemorrhagic transformation of the infarct or
other complications. However a later study using LMW heparinoid did not show benefit.

In patient with thromboembolic or cardioembolic strokes, oral anticoagulant (warfarin)

can be started one week from the stroke, since the chances of a recurrent stroke within a
week from these conditions are relatively low. The level of anticoagulation should be
aimed between INR 2 - 2.5 for those with atrial fibrillation and slightly higher for those
with prosthetic cardiac valves.

8.3 Thrombolytic therapy:

Intravenous administration of tissue plaminogen activator (rtPA) is believed to be

efficacious in the treatment of ischaemic stroke. However, due to the potential serious
complication i.e. haemorrhage, the following conditions must be met if thrombolytic
therapy is contemplated.

a. The presence of a physician with the expertise and experience in the

diagnosis and management of stroke.
b. 24-hour availability of high-resolution imaging facilities and of trained and
experienced personnel to interpret the results
c. Capability to handle potential complications of thrombolysis, particularly
intracranial haemorrhage

There are no data concerning the use of rtPA for the treatment of acute ischaemic stroke
in neonates, infants, or children. The use of rtPA in this group is not recommended.

16
A. Recommendations for initiating thrombolytic treatment.
1. Intravenous rtPA at a dose of 0.9 mg/kg with a maximum of 90 mg is the recommended
treatment for patient presenting within 3 hours of onset of ischaemic stroke. 10% of
the dose is given as a bolus, followed by an infusion lasting 60 minutes. Intravenous
rtPA for a person who has a stroke more than 3 hours is not recommended.
Intravenous rtPA is not recommended when the time of onset of stroke cannot be
ascertained reliably; this includes person whose stroke is recognised upon awakening.
2. Data on the efficacy or safety of any other intravenously administered thrombolytic
drugs are not available to provide a recommendation.
3. If a CT brain demonstrates early changes of a recent major infarction, oedema, or
possible haemorrhage, thrombolytic therapy should be avoided
4. The risk and potential benefits of rtPA should be discussed whenever possible with the
patient and family before treatment is initiated.
5. The patient need close observation, frequent neurological assessments and
cardiovascular monitoring.
6. An excessively high blood pressure might predispose the patients to bleeding, while
an excessive lowering blood pressure may worsen ischaemic symptoms. Monitor
blood pressure carefully during the first 24 hours after starting treatment.
 Every 15 minutes for 2 hours after starting the infusion, then
 Every 30 minutes for 6 hours, then
 Every 60 minutes until 24 hours after starting treatment.
7. Central venous access and arterial punctures are restricted during the first 24 hours.
8. Placement of an indwelling bladder catheter should be avoided during the period of
infusion and for at least 30 minutes following the end of the infusion.
9. Insertion of a nasogastric tube should be avoided if possible during the first 24 hours
after treatment

B. Contraindications for intravenous thrombolytic therapy.

1. Current use of oral anticoagulant or a prothrombin time (PT) > 15 seconds

(INR > 1.7)
2. Use of heparin in the previous 48 hours and a prolonged partial thromboplastin
time (PTT)
3. A platelet counts < 100,000/mm3
4. Another stroke or any serious head injury in the previous 3 months
5. Major surgery within the preceding 14 days
6. Arterial puncture at noncompressible site within the last 21days
7. Pre-treatment systolic blood pressure >185 mmHg or diastolic blood
pressure > 110 mmHg
8. Neurological signs that are improving rapidly
9. Isolated mild neurological deficits, such as ataxia alone, sensory loss alone,
dysarthria alone or minimal weakness
10. Prior intracranial haemorrhage
11. A blood glucose < 2.7 mmol/l or > 22.2 mmol/l
12 12. Seizure at the onset of stroke
13. Gastrointestinal or urinary bleeding within the preceding 24 days
13 14. Recent myocardial infarction

17
 Old age is not a contraindication but it is not wise to use it in patients above 75 years old.
Caution is advised before giving intravenous rtPA to persons with severe stroke

C. Management of bleeding complications.

Bleeding should be considered the cause of neurological worsening following use of a

thrombolytic drug and the treatment should be stopped immediately. A CT scan must be
arranged immediately. As a rule any life-threatening haemorrhagic complication,
including intracranial bleeding should lead to the following sequential steps:

1. Discontinue infusion of thrombolytic drug if still being given

2. Obtain blood samples for coagulation tests (PT, PTT or INR), fibrinogen, haematocrit
and haemoglobin level
3. Arrange for infusion of cryoprecipitate or fresh frozen plasma, platelets or pack red
blood cells.
3. Obtain neurosurgical consultation, as necessary.

D. Antithrombotic and antiplatelet aggregating drugs and use of thrombolytic drugs.

Persons who have taken aspirin are eligible for treatment with rtPA if they meet all other
criteria for therapy. The lack of information about the safety of rtPA in management of
acute ischaemic stroke in persons who have taken ticlopidine or other antiplatelet agents
does not permit any recommendation. Person given intravenous rtPA should not receive
aspirin, heparin, warfarin, ticlopidine, or other antithrombotic or antiplatelet aggregating
drugs within 24 hours of treatment. Additional research on the usefulness of such
adjunctive therapies is needed because they may affect time to lysis, degree of
reperfusion, occurrence of reocclusion, and/or clinical outcome.

The status of intra-arterial thrombolysis is still uncertain. Preliminary small studies

indicate that the rate of clot lysis and recanalization is higher via the intra-arterial route.
But as yet no general recommendation can be made. The difficulty of the procedure will
certainly limit its usage to centres with high expertise only.

8. 4 Neuroprotective agents:

Several classes of drugs reduce infarction size in animal models. These include calcium
channel antagonists, antioxidants, NMDA antagonists, nootropics and gangliosides. They
protect ischaemic cells from injury by various mechanisms and may be useful in man.
These agents however need to be given early to have any protective effect. Presently, the
data are insufficient for these agents to be recommended for therapy.

9. Primary Prevention.

Primary prevention is the key factor in any plan to reduce the incidence of stroke and this
should be targeted to the whole population as well as high risk groups by increasing
awareness, promoting healthy lifestyles to reduce risk factors for stroke. The strategies
should be integrated in the overall programme of health promotion for vascular diseases.

High risk groups must be identified and the risk factors modified or treated an the
results monitored.
18
 Of the modifiable risk factors, hypertension is the single most important risk factor to
both ischaemic and haemorrhagic stroke. The risk of stroke is related to the height of BP
and the risk increases with increase in BP. For every 7.5 mmHg rise in diastolic BP in the
range of 70-110 mmHg the risk of stroke doubles. Similar relationship also occurs in
isolated hypertension which occurs in 20% and 35% of men and women above 75 years
old respectively.

Reduction of diastolic pressure by 5-6 mmHg reduces the risk of stroke by 40%. For
isolated hypertension (systolic BP greater than 160 mmHg and diastolic less than 90
mmHg), reducing the systolic BP by 10 mmHg reduces the risk of stroke by 36%.

Other important modifiable risk factors are cardiac disease, diabetes, atrial fibrillation,
smoking, hypercholesterolaemia, asymptomatic carotid stenosis, lack of exercise, obesity
and history of arterial disease elsewhere in the body.

The public needs to be continuously educated about stroke, its symptoms, signs and the
risk factors that predispose to stroke. Motivation programmes and activities are also
required to ensure compliance with healthy lifestyle programme.

10. Secondary Stroke Prevention.

The ultimate goal is to reduce the incidence of recurrent stroke and from there all its
untoward sequalae such as disability, dependency and mortality

Recurrent strokes occur in 15-40% of survivors and according to the Copenhagen study
the rate of recurrence is 9% per year. For each individual patient, the key to prevention of
recurrence is the identification of modifiable risk factors and treating them.

Lifestyle changes are required such as eating habits, exercise, stress management,
smoking and alcohol abuse. The major risk factors such as hypertension, diabetes, heart
disease and hyperlipidaemia must be treated and monitored.

Among the strategies that have proven beneficial are the use of antiplatelet agents such as
aspirin, ticlopidine, dipyridamole, anticoagulants and carotid endarterectomy. Other
specific interventions would be determined by the specific risk factors that operate in the
particular patient.

Aspirin. Aspirin reduces the relative risk of stroke or death by about 20% per year after
transient ischaemic attack (TIA) or minor ischaemic stroke. This translates to an absolute
benefit of 12 strokes (12 patients) prevented per 1,000 patient treated for one year with an
associated risk of one cerebral haemorrhage.

Other antiplatelet agents. Ticlopidine, clopidogrel and dipyridamole in combination

with aspirin have all been shown to be more superior to aspirin for secondary prevention
of stroke. Neutropaenia occurs in up to 2.4% of patients with ticlopidine and severe
neutropaenia may occur in the first 90 days in up to 0.8% of patients. Regular blood count
is advised fortnightly in the initial period.

19
 Warfarin. This is used to prevent stroke due to atrial fibrillation, valvular heart disease
and if there is evidence of a thrombus in the left ventricle. In patients with TIA or minor
stroke not due to valvular heart disease, warfarin reduces the relative risk of recurrent
stroke by 70%. This translates into prevention of 80 strokes by treating 1,000 patients for
one year. The occurrence of major cerebral haemorrhage as consequence of treatment is
0.2%. Thus the use of warfarin is associated with serious complications, and its usage
requires careful patient selection and monitoring. The recommended INR level is 2-3

Carotid Endarterectomy. This is a procedure that requires a great amount of skill and
expertise. Beneficial results can only be expected to occur if the perioperative stroke or
death is less than 5.8%.

Both the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the
European Carotid Surgery Trial (ECST) showed benefit from operation in severe (>70%)
carotid stenosis. The relative risk reduction with surgery was 65% and with absolute
reduction of 17%. This translates to prevention of 1 stroke in 2 years by operating on 6
patients (NASCET) or 8 patients (ECST).

The benefit for moderate stenosis (50-69%) is less strong, with relative reduction of 36%
and absolute reduction of 5.3%. This translates to preventing 1 stroke by operating 19
patients.

For patients with less than 50% stenosis, there is no benefit from carotid endarterectomy.

Angioplasty and stenting are both being tried, but presently there is no conclusive data to
recommend their usage.

11. Rehabilitation.

Stroke rehabilitation is an important component in the overall care of stroke patients. This
is so because of the nature of stroke as an illness that causes a whole range of physical,
cognitive and psychological disturbances. Thus it is mandatory that every stroke patient
be assessed by a multidisciplinary team as soon as possible to plan and carry out
individualised rehabilitation programme. And this team should meet regularly to monitor
progress and make adjustments to the plan.

Stroke rehabilitation is an active process beginning during acute hospitalisation,

progressing for those with residual impairments to a systematic program of rehabilitation
services, and continuing after the individual returns to the community. It is an organised
effort to help stroke patients maximize all opportunities for returning to an active and
productive life.

The rehabilitation process involves six major areas:

1. Preventing, recognizing and managing co-morbid illness and medical complications

2. Training for maximum independence
3. Facilitating maximum psychological coping and adaptation by patient and family
20
 4. Preventing secondary disability by promoting community integration, including
resumption of home, family, recreational and vocational activities
5. Enhancing quality of life in view of residual disability
6. Preventing recurrent stroke and other vascular conditions such as myocardial
infarction that occur with increased frequency in patients with stroke
Clinical manifestations of stroke are multifaceted and as such stroke rehabilitation is best
implemented through coordinated efforts of a team of rehabilitation professionals.

Rehabilitation can be looked at in two aspects:

I. The process of rehabilitation
II. The aim or end-point of rehabilitation

I. The process of rehabilitation

Assessment - Identification and measurement of problems

Analyse the cause
Planning - Goal-setting
Identify aims, objectives and targets
Aims = set at level of handicap
Objectives = described in terms of changes in level of disability
Target = described in terms of specific abilities to be achieved

Intervention - Therapy to influence change [recovery]

Care to maintain status quo
Evaluation - Reassessment

II. The aim or end-point of rehabilitation

To maximise the patient’s role fulfillment and independence in his environment, all within
limitations imposed by the underlying pathology and impairments and by availability of
resources.

To help the person make the best adaptation possible

A well-conceived integrated rehabilitation management plan is the basis for all

rehabilitation. It is vital for team to modify the aims and expectations of the patients and
family. All members of the team should involved at discussions and agree upon decisions
together as a team.

FIRST STEP • Assessment

• Identify areas of difficulty
• Underlying causes [impairments, pathologies]
• Prognostic factors relating to natural history and
successful interventions
SECOND STEP • Match the patient with the appropriate rehabilitation
21
 services and setting
THIRD STEP • Identify aims and set goals
• Agree on time frame
• Realistic short-, intermediate- and long-term goals
FOURTH STEP • Continuous assessment and evaluation
• Have goals been achieved
• Have new problems appeared ?? Identify and act
• Why have the goals not been met ?? Identify and act
• Reset the aims and expectations of the patient and
family

Patient selection process:

Reasonable medical stability, significant functional disability and the ability to learn are
the primary criteria for rehabilitation. Patients with severe cognitive deficits resulting in
the inability to learn new strategies are unlikely to benefit from rehabilitation. A minimal
level of physical endurance is also essential.

Rehabilitation setting:
The choice of level or intensity of rehabilitation depends on the level of assistance needed
to perform daily activities, requirement of close medical supervision and ability to
tolerate intense therapy.

A patient requiring moderate assistance can tolerate several hours of intense physical
rehabilitation in a hospital or nursing facility. A patient who is unable to tolerate intense
treatment will require a lower level of therapy at a nursing facility or at home.

Multidisciplinary team meeting:

It is important to meet regularly, at least weekly in initial stages of rehabilitation. The
entire team can be introduced to new patients, and existing patients can be reviewed and a
change in their condition or new problem can be discussed. Review patient’s progress and
goal setting can be reset jointly and appropriate course of action or intervention to meet
these goals.

Important to involve patient and carer in separate meetings especially if certain problems
need to be addressed such as discharge from hospital, etc. Recording the work of the team
is an important aspect of management.

Therapeutic Intervention:
There is no evidence at present to support any specific therapeutic approach. A
pragmatic, functional and flexible approach is a good basis for rehabilitation.

Information for Patients and Carers:

Studies of the attitudes of patients and their carers to medical services in UK, in general,
and of stroke services in particular, have demonstrated that one of the greatest sources of
dissatisfaction is with communication. Patients and carers may receive very little
information about the nature of stroke, its cause, management and likely prognosis. Even
where information is provided it may be in a form which is difficult to understand or
retain. One area of concern is the transfer from hospital to community based services. The
King’s Fund Consensus Conference [1988] identified poor discharge planning as being a
major problem.
22
 Adequate information about stroke and rehabilitation should be given to family members
to avoid any misunderstandings and misconceptions. Participation of the family and
caregiver throughout rehabilitation and continuous education will help maintain a patient
and family focus.

Scientific basis for Stroke Rehabilitation

Rehabilitation is effective. At present, there is no easy method to differentiate between
the influence of specific interventions and the natural recovery process. Ottenbacher and
Jannel performed a meta-analysis of 3717 patients from 36 studies that examined the
outcome of rehabilitation for post-stroke patients. Each study compared two or more
treatments designed to improve functional performance in subjects with hemiparesis.
Both authors found that the average patient receiving a program of focused stroke
rehabilitation performed functional tasks better than approximately two thirds of those
patients in comparison groups. Improvement in performance appears to be related to early
initiation of treatment, but not to the duration of treatment. In another critical review by
Wagenaar and Meijer, the authors concluded that stroke patients with hemiplegia benefit
from expert care if it is offered early and intensively, but cautioned that retraining may be
more effective when it is task specific.

12. Conclusion.

Over the last decade, major advances have been made in acute management of ischaemic
stroke. These advances have occurred along with advances in imaging methods and
treatments for primary and secondary prevention. There are now more concrete data
available regarding the use of aspirin, heparin, low-molecular-weight heparin,
thrombolysis and endarterectomy. Some of the recommendations may be adopted for
general use while there are others that may only be used in controlled settings with highly
experienced and dedicated teams.

Further studies will better define the usage of these agents in terms of identifying the
subgroup of patients who are best suited for certain kinds of therapy.

The general care of stroke victims while in the ward still plays an important role in the
quest to achieve better outcome. Many complications can be avoided with better general
care and institution of certain prophylactic measures. Most parts of the country already
have the basic infrastructure for acute stroke care. Some reorganization and strengthening
of the various components are necessary to enable multidisciplinary inputs to avail early
for patient benefits.

The multidisciplinary team established while the patient is in hospital must continue to
monitor the patient after discharge. Thus there is an urgent need to strengthen all the
components of in-hospital and after-discharge care.

Research and audit are needed to be carried out to know the pattern of illness in our own
community, what happens to patients and what kinds of support are available outside the
hospital.

23
 There is also a need to forge linkage and enhance cooperation with non-governmental
organizations so that there is integrated approach to providing support once the patient
returns to the community.
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