Cerebrovascular stroke

By
DR
Omar Elbahie
Prof of cardiology
&
Angiology
 Classification of CVS

CVS

A) Ischemic CVD (80%) B) Hemorrhagic CVD (20%)

I) Focal II) Diffuse

1) Transient 2) Permanent Intracerebral &

Syncope coma Subarachnoid
hemorrhage

1) Transient 2) Permanent
TIAs Ischemic strokes (cerebral infarction)
 Stroke vs. Transient ischemic
attacks (TIAs)
Stroke: focal neurological deficit lasting > 24hs, caused by CBF in a particular
cerebral artery. The usual pathological outcome is cerebral infarct.
* TIAs: a similar condition lasting < 24hs.
Complete VS. Incomplete stroke:
It is based on the severity of functional loss (e.g. hemiplegia vs. hemiparesis)
Stroke in evolution (progressive stroke):
It may involve one or more of the following factors:
* COP (CHF, AMI, Arrhythmia), hypertension and blood viscosity.
*Clot propagation. *Progression of cerebral edema *Bleeding into infarct
area.
 A) Ischemic strokes
I) Focal ischemic strokes
1) TIAs :( transient)
Etiology:
1. Thrombo-embolism: from plaques in heart or large arteries.
2. Congenital carotid kinking or stenosis.
3. Subclavian steel. 4. Cervical spondylosis. 5. Polycythemia.
6. Spasm of a cerebral artery. 7. Sudden change in BP.
Risk factors:
A) Unmodifiable:
Prior stroke. Older age. Family history of stroke. Male sex. *Race: black

B) Modifiable:
*HTn *ArrhythmiaAF *Atheroma of carotid artery
*Metabolic: DM, Dyslipidemia, fibrinogen, homocysteine, uric acid.
*Hypercoagulable states: antithrombin III, protein C
*Others: smoking, alcohol, obesity, sedentary life, Psychosocial stress (e.g. depression),
and drugs (e.g. cocaine, amphetamines)
Pathophysiology:
Spasm & disturbance of auto regulation transient ischemia complete resolution.
 Subclavian steal
The term subclavian steal has been used to describe retrograde blood flow in the
vertebral artery associated with proximal ipsilateral subclavian artery stenosis or
occlusion proximal to the origin of the vertebral artery.
 TIAs :
Clinical picture: sudden onset & gradual offset

I) Carotid system affection II) Vertebrobasilar system affection

Transient Unilateral: Transient Bilateral:

1. Ibsilateral blindness+ No macular sparing 1. Bilateral blindness + macular sparing
2. Contralateral hemiparesis (double blood supply)
3. Contralateral hemianaesthesia 2. Temporal lobeAmnesia
4. Aphasia or dysphasia Testing for 3. Ataxia
macular sparing: 4. Brain stem
by moving a red *3rd CNophthalmoplegia & diplopia
target form the *5th CNParasthesia of face
non-seeing field *8th CNvertigo & nystagmus
into the seeing *9th &10th CN dysphagia.
field. If the red *12th CN dysarthria
pin is noticed *Tractsquadriplegia, bilateral sensory loss.
before it crosses NB: to diagnose TIA due to vertebrobasilar
the mid-line, affection 2 or more of the following
macular sparing should be present:
is present. *Diplopia *Dysphagia *Dysarthria
*Vertigo *Ataxia
 TIAs :
Investigations:
I) Imaging: Brain CT, MRI, MRA N . Carotid Doppler?atheroma.
II) Lab tests: For risk factors (CBC, ESR, PT, Lipid profile, Homocysteine, protein-C).
III) ECG, Echocardiogram.

Treatment:
I) Treatment of risk factors:
*Stop smoking *control of DM, HTn *lifestyle modification

II) Treatment of TIAs:

1. Anti-plateletsAspirin + Clopidogril
2. Anti-coagulants:
*Heparin: 5000 IU Loading dose + 1000 IU / hr infusion (controlled by PTT1.5-2 of normal)
*Oral anti-coagulants: (controlled by INR2-3)
3. Vasodilators: Nimodipine (CCB) = Nimotop main use is in the prevention of cerebral vasospasm
and resultant ischemia, a complication of subarachnoid hemorrhage
4. Surgical correction of any treatable cause
*Carotid artery endarterectomy.
 2) Permanent Focal Ischemic Stroke
(cerebral infarction)
Causes:
1. Cerebral atherosclerosis (most common causeeither in situ occlusion or emboli of a
plaque)
2. Emboli of cardiac origin:
*Mural thrombi due to MI
*Valvular vegetations (RHD, Infective endocarditis, Prosthetic valve, MVP)
*Cardiac myxoma *Arrhythmia (AF) *Paradoxical emboli
3. Vasculitis
4. Hematological disorders:
*Hyperviscosity syndromes (multiple myeloma, polycythemia, macroglobulinemia)
*Hypercoagulable states (carcinoma).
*Protein-C or S deficiency.
*Antiphospholipid anti-bodies (Lupus anticoagulants, anticardiolipin antibodies).
5. Drugs: oral contraceptives, cocaine, heroin.
6. nonthrombotic occlusion of small, deep cerebral arteries (lacunar infarction)
 Clinical picture of acute
ischemic strokes:
* History of TIAs
*Onset: Sudden (in Embolism) Acute (in Thrombosis)
*Focal manifestations:
I) Typical presentation (infarction in **internal capsule + corticobulbar fibers to facial
nucleus): due to occlusion of Lenticulo-striate artery Of middle cerebral artery (most common
occluded artery) **Uncrossed hemiplegia i.e. Both hemiplegia+UMNL of facial on
opposite side + **No aphasia
II) If motor cortex is affected:
Monoplegia (wider cortical presentation) on opposite side + Aphasia (if infarction
affects the dominant side) + Cortical manifestations (Jacksonian Fits)

III) Brain stem affection (occlusion of posterior cerebral artery (PCA)

This is a branch of vertebrobasilar system.
**Crossed hemiplegia i.e. Ipsilateral LMNL of facial + contralateral hemiplegia

IV) Thalamic syndrome: the body becomes oversensitive to pain (Dysesthesia), as a

result of damage to a sensory relay station in thalamus. The pain in thalamic syndrome can be
made worse with hot and cold temperature, emotional distress.
 Astereognosis: inability to identify an object by active touch

Graphesthesia: inability to recognize writing on the skin

B) Hemorrhagic strokes

I) Intracerebral Hemorrhage

II) Subarachnoid Hemorrhage

I) Intracerebral hemorrhage

Causes:
1. Hypertension (commonest cause)
2. Other causes:
*Trauma *Cerebral aneurysm *Drugs (anti-coagulants)
* Blood disease *Hemorrhagic infarction *Vascular malformation
*Granulomatous Angitis *Cerebral amyloidosis

Pathology:
*Commonest artery: Lenticulo-striate artery (Branch of middle cerebral artery)
*Site of hemorrhage: 1. internal capsule 2. Thalamus 3. Pons
4. Cerebellum
*Hematoma compression of surrounding structures + replaced by scar
 Clinical manifestations of
intracranial hemorrhage
I)CP of ICP: 1.Projectile Vomiting. 2. Headache. 3. Blurring of Vision.
II) + signs of Meningeal Irritation:
III) Focal manifestations of intracerebral hemorrhage:
CP Int. capsule Thalamic Pontine Cerebellar

1.Unconscious Late Late Early** Late

2.Contralateral Yes+contralat Yes+contralat Quadriplegia+ipsilat Late+ipsilat

Hemiparesis Facial(UMNL) Facial(UMNL) Facial(LMNL) Facial(LMNL)
3.Contralateral yes Yes yes Late
hemi anesthesia
4.Hemianopia yes Yes No NO

5.Pupil N Small Small N

6.Gaze paresis *contralateral *contralateral *Ipsilateral *Ipsilateral

7.conjugate dev *Ipsilateral *Ipsilateral *contralateral *contralateral
8.down eye NO Yes (compress NO NO
deviation Midbrain)
9.Vomiting&gait NO, ---- NO, ---- Often, ---- Severe, ataxia
 Investigations of intracerebral
hemorrhage:
A) Lab. Investigation
1. Blood: CBC, PT, PTT, ESR
2. CSF exam.
B) EEG:generalized slowing
C) Imaging Studying
1. CT scan: acute hemorrhage
hyper dense signal intensity
Perihematomal edema and displacement
of tissue with herniation.
2. CT angiography permits screening
of large and medium-sized vessels for AVMs,
vasculitis, and other arteriopathies.
 Treatment of intracerebral
hemorrhage:
I) Medical therapy
1. Control of BP: Cautiously lower blood pressure but avoid excessive hypotension.
2. Treatment of increased ICP: *hyperventilation *Diuretics *IV infusion of manitol
3. Recombinant factor VIIa (rFVIIa) within 4 hours after the onset of intracerebral hemorrhage
limits the growth of the hematoma, reduces mortality, and improves functional outcomes at 90
days.
4. Correct any identifiable coagulopathy with fresh frozen plasma, vitamin K, protamine, or
platelet transfusions.
5. Initiate phenytoin or other anticonvulsant for seizure

II) General care of comatosed:

1. Perform endotracheal intubation. 2. Avoid hyperthermia

III) Surgical Care: evacuation of hematoma

Indications:
1. Progressive deterioration of consciousness
2. Signs of cerebellar hematoma. 3. Signs of pontine compression
4. Large hematoma>3cm. 5. Dilated ventricle
Nicardipine is a
dihydropyridine
calcium-channel
blocking agent
used for the
treatment of
vascular
disorders such
as chronic stable
angina,
hypertension,
and Raynaud's
phenomenon. It
is available in
oral and
intravenous
formulations
 II) Subarachnoid hemorrhage

Causes:
1. Primary SAH: from rupture of the following:
(The first 2 are most common)
*Saccular aneurysm
*AVM
*Mycotic aneurysmal rupture
*Angioma
*Bleeding inside a neoplasm
2. SAH may be also due to
a. bleeding from hypertension or neoplasm.
b. Post traumatic
c. Blood diseases and anti-coagulants
Types of cerebral aneurysms:
I) Saccular (Berrys A )
*Congenital defects in media of
arteries of circle of Willis.
*It may be familial as:
It is associated with poly cystic
kidney or hereditary CT diseases
as Marfan's syndrome or Ehlers-
Danlos syndrome
*It may rupture by sudden BP
II) Fusiform A
*Ectatic (i.e. dilated)
aneurysm
Due to atherosclerosis.
*In large cerebral arteries.
III) Mycotic A
* Septic degeneration of
media from septic emboli by
infective endocarditis.
*In distal sites of cerebral
vessels
 CP of Subarachnoid hemorrhage
I) Before rupture of A II) After rupture of A
A) Prodromal (warning) or sentinel 1. Sudden, severe headache radiating to shoulder & back.
Symptoms: headache (hours-months before rupture)
2. N, V, fever
by minor blood leakage without signs of
ICP nor meningeal irritation. 3. Neck stiffness (meningeal irritation)

B) Signs:
1. May be asymptomatic (discovered 1. Signs of meningeal irritation:
accidently by X-ray skull or CT angio.
*Neck rigidity *Lessegue,s sign (raise leg i.e. flex hip with extended
2. Signs according to site: knee)pain
*Visual field defect(ant. Communicating *Kernigs sign (Flex hip with flexion knee at 90)try to extend the kneepain.
a)
*Prodzniski,s sign: Passive flexion neckflexion of both Hip & knee.
*3rd CN palsy(IC artery)
*Passive flexion hip flexion of other Hip & knee.
*Aphasia, Facial weakness(MCA)
2. Vital signs
*Eye bruit, pulsating exophthalmos
*BP mild-to-moderate HT in of cases.
(Carotid- cavernous fistula)
*Fever common after the 4th day *Tachycardia present for several days

3. Convulsion, coma,hemiparesis

4.Compressionoptic&ocular CNs

5. Audible IC bruit. 6. Eye signs:*Papilledema *Retinal hemorrhage.

 Investigations of Subarachnoid
hemorrhage :
I) Lab Studies: 1. CBC , PT, APTT. 2. Serum electrolytes to detect later hyponatremia.

II) Imaging Studies:

1. CT scanning revealed subarachnoid hemorrhage in 100% of cases within 12 hours of onset.
2. CT also can detect intracerebral hemorrhage, mass effect, and hydrocephalus.
3. Cerebral angiography is performed once the SAH diagnosis is made
4. MRI mostly is used to identify possible AVMs that are not visible on angiography.
5. Multi-slice CT angiography has gained more popularity
comparable to cerebral angiography.

III) Lumbar puncture: (LP) is indicated if the patient has possible SAH and negative CT scan
findings Xanthochromia
 Complication of
Subarachnoid hemorrhage
1. Hydrocephalus may develop within the first 24 hours because of
obstruction of CSF outflow in the ventricular system by clotted blood.
2. Rebleeding of SAH occurs in 20% of patients in the first 2 weeks.
Peak incidence of rebleeding occurs the day after SAH. This may be from lysis
of the aneurysmal clot.
3. Vasospasm from arterial smooth muscle contraction is symptomatic in
36% of patients.
4. Neurologic deficits from cerebral ischemia peak at days 4-12.
5. Hypothalamic dysfunction causes excessive sympathetic
stimulation, which may lead to myocardial ischemia or labile detrimental BP.
6. Hyponatremia may result from cerebral salt wasting.
7. Aspiration pneumonia
8. Left ventricular systolic dysfunction: This may be explained by
excessive release of norepinephrine from myocardial sympathetic nerves,
which could damage both myocytes and nerve terminals.
 Treatment of Subarachnoid
hemorrhage
1. Absolute rest
2. Medical treatment:
*Analgesic (paracetamole but not aspirin) *Anti-epileptic
*Anti-fibrinolytic (Aminocaproic acid)
* Decrease elevated ICP when herniation is suspected:
Use osmotic agents, such as mannitol,
Loop diuretics, such as furosemide
IV steroid therapy

3. Surgical: Angioplasty surgery. to control brain edema is controversial and

debated.
Thank you
 Guidelines for Management of
Ischaemic Stroke 2008

The European Stroke Organization

- ESO -
 ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation

Guidelines Ischaemic Stroke 2008

 Background
Stroke is the most important cause of morbidity and long
term disability in Europe1
Stroke is also the second most common cause of dementia,
the most frequent cause of epilepsy in the elderly, and a
frequent cause of depression2,3
 Background
Stroke is a medical and occasionally a surgical emergency
The majority of ischaemic stroke patients do not reach the
hospital quickly enough
The delay between stroke onset and hospital admission is;
reduced if the Emergency Medical Systems (EMS) are
used
increased if doctors outside the hospital are consulted
first
 Stroke as an Emergency
Emergency care in acute stroke depends on a four-
step chain:
Rapid recognition of, and reaction to, stroke signs and
symptoms
Immediate EMS contact
Priority transport with notification of the receiving hospital
Immediate emergency room triage, clinical, laboratory and
imaging evaluation, accurate diagnosis, and administration
of appropriate treatments at the receiving hospital.
 Stroke as an Emergency
Delays during acute stroke management have been
identified at three different levels:
at the population level, due to failure to recognize the
symptoms of stroke and contact emergency services
at the level of the emergency services and emergency
physicians, due to a failure to prioritize transport of stroke
patients
at the hospital level, due to delays in neuroimaging and
inefficient in-hospital care
 ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation
 Stroke Unit
A stroke unit
Is a dedicated and geographically defined part of a hospital
that takes care of stroke patients
Has specialised staff with coordinated multidisciplinary
expert approach to treatment and care
Comprises core disciplines: medical, nursing, physiotherapy,
occupational therapy, speech and language therapy, social
work 1
Recommendations
All stroke patients should be treated in a stroke unit
(Class I, Level A)
 ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation
 Emergency Management

The time window for treatment of patients with acute

stroke is narrow
Time is the most important factor
 Emergency Management
The initial examination should include
Assessment of vital signs.
Determination of arterial oxygen saturation
Blood samples for clinical chemistry, coagulation and
haematology studies
Observation of early signs of dysphagia
Targeted neurological examination
Careful medical history focussing on risk factors for
arteriosclerosis and cardiac disease
 Ancillary Diagnostic Tests
In all patients
Brain Imaging: CT or MRI
ECG
Laboratory Tests
Complete blood count and platelet count,
prothrombin time or INR, PTT
Serum electrolytes, blood glucose
CRP or sedimentation rate
Hepatic and renal chemical analysis
 Ancillary Diagnostic Tests
In selected patients
Duplex / Doppler ultrasound
MRA or CTA
Echocardiography, Chest X-ray
Pulse oximetry and arterial blood gas analysis
Lumbar puncture
EEG
Toxicology screen
 Emergency Diagnostic Tests
Differentiate between different types of stroke
Assess the underlying cause of brain ischaemia
Assess prognosis
Identify concurrent diseases or complications
associated with stroke
Rule out other brain diseases
 Emergency Diagnostic Tests
Cranial Computed Tomography (CT)
Immediate plain CT scanning distinguishes reliably between
haemorrhagic and ischaemic stroke
Detects signs of ischaemia as early as 2 h after stroke onset
Helps to identify other neurological diseases (e.g.
neoplasms)
Most cost-effective strategy for imaging acute stroke
patients
 Emergency Diagnostic Tests
Magnetic Resonance Imaging (MRI)
Diffusion-weighted MRI (DWI) is more sensitive for
detection of early ischaemic changes than CT
DWI can be negative in patients with definite stroke
Identifies ischaemic lesions in the posterior fossa reliably
Detects even small intracerebral haemorrhages reliably on
T2* sequences
MRI is particularly important in acute stroke patients with
unusual presentations
 Emergency Diagnostic Tests
Electrocardiogram (ECG)
Cardiac abnormalities are common in acute stroke patients
Arrhythmias may induce stroke, stroke may cause
arrhythmias
Holter monitoring is superior to routine ECG for the
detection of atrial fibrillation (AF)
 Emergency Diagnostic Tests
Echocardiography (TTE / TOE)
It is particularly required in patients with history of cardiac
disease, ECG pathologies, suspected source of embolism,
suspected aortic disease, suspected paradoxical embolism

Transoesophageal echocardiography (TEE) might be

superior to transthoracic echocardiography (TTE) for the
detection of potential cardiac sources of embolism
 Emergency Diagnostic Tests
Laboratory tests
Haematology (RBC, WBC, platelet count)
Basic clotting parameters
Electrolytes
Renal and hepatic chemistry
Blood Glucose
CRP, sedimentation rate
 Diagnostic Imaging
Recommendations
In patients with suspected TIA or stroke, urgent cranial CT
(Class I), or alternatively MRI (Class II), is recommended (Level
A)

In patients with TIA, minor stroke, or early spontaneous

recovery immediate diagnostic work-up, including urgent
vascular imaging (ultrasound, CT-angiography, or MR
angiography) is recommended (Class I, Level A)
 Other Diagnostics
Recommendations (1/2)
In patients with acute stroke and TIA, early evaluation of
physiological parameters, routine blood tests, and
electrocardiography (ECG) is recommended (Class I, Level A)
All acute stroke and TIA patients should have a 12-channel
ECG. Continuous ECG recording is recommended for ischaemic
stroke and TIA patients (Class I, Level A)
 Other Diagnostics
Recommendations (2/2)
For stroke and TIA patients seen after the acute phase, 24-hour
Holter ECG monitoring should be performed when arrhythmias
are suspected and no other causes of stroke are found (Class I,
Level A)
For all stroke and TIA patients, a sequence of blood tests is
recommended
Echocardiography is recommended in selected patients (Class
III, Level B)
 ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation
 A) Primary Prevention

Content
Management of vascular risk factors
Antithrombotic therapy
Carotid surgery and angioplasty
 Primary Prevention
I) Vascular Risk Factors
Conditions and lifestyle characteristics identified as a
risk factors for stroke
High blood pressure
Atrial fibrillation
Diabetes mellitus
Carotid artery disease
Myocardial infarction
High Cholesterol
Hyper-homocysteinaemia
Smoking
Heavy alcohol use
Physical inactivity
Obesity
1) High blood pressure (BP)
Background
High blood pressure (>120/80mmHg) is the most important
and prevalent modifiable risk factor for stroke
Significant reduction of stroke incidence with a decrease in
BP
No class of antihypertensive is clearly superior
LIFE: lorsatan is superior to atenolol
ALLHAT: chlorthalidone is more effective than amlodipine and
lisinopril
2) Diabetes mellitus

Background
Independent risk factor for ischaemic stroke
Improving glucose control may not reduce stroke
BP in patients with diabetes should be <130/80mmHg
Statin treatment reduces the risk of major vascular events,
including stroke
Elevated blood glucose in the early phase of stroke is
associated with death and poor recovery
 3) High Cholesterol
Background
Statin treatment reduces the incidence of stroke from 3.4%
to 2.7%1
No significant effect for prevention of fatal stroke
No data support statin treatment in patients with LDL-
cholesterol <150 mg/dl (3.9 mmol/l)
 4) Cigarette Smoking

Background
Independent risk factor for ischaemic stroke in men and
women
2-3 fold increased risk compared to non-smokers
50% risk reduction by 2 years after stopping smoking
 5) Alcohol Consumption
Background
Increased risk for both ischaemic (RR 1.69) and
haemorrhagic stroke (RR 2.18) with heavy alcohol
consumption (>60g/day)
BP elevation might be a reasonable explanation
Light alcohol consumption (<12g/day) associated with
reduced ischaemic (RR 0.80) and haemorrhagic stroke
Red wine consumption carries the lowest risk
 6) Physical Activity

Background
Regular exercise (at least 3x30min/week) is associated with
a decreased risk of stroke
Physically active individuals have a lower risk of stroke or
death than those with low activity (RR 0.73)
This is mediated, in part, through beneficial effects on body
weight, blood pressure, serum cholesterol, and glucose
tolerance
 7) Body Weight, Diet, Nutrition
Background
High body mass index (BMI 25) increases risk of stroke in
men and women
Abdominal adiposity is a risk factor for stroke in men but
not women
A randomized trial in women found no effect of dietary
interventions to reduce the incidence of stroke
Tocopherol and beta carotene supplementation do not
reduce the risk of stroke. Vitamin E might increase mortality
when used at high-dose (400 IU/d)
8) Hormone Replacement Therapy

Background
Stroke rates rise rapidly in women after the menopause
Hormone replacement therapy in postmenopausal women
is associated with an 44% increased risk of stroke
 Risk Factor Management

Recommendations (1/4)
Blood pressure should be checked regularly. High blood
pressure should be managed with lifestyle modification and
individualized pharmacological therapy (Class I, Level A) aiming
at normal levels of 120/80 mmHg (Class IV, GCP)
 Risk Factor Management

Recommendations (2/4)
Blood glucose should be checked regularly. Diabetes should be
managed with lifestyle modification and individualized
pharmacological therapy (Class IV, Level C).
In diabetic patients, high blood pressure should be managed
intensively (Class I, Level A) aiming for levels below 130/80
mmHg (Class IV, Level C). Where possible, treatment should
include an angiotensin converting enzyme inhibitor or
angiotensin receptor antagonist (Class I, Level A)
 Risk Factor Management
Recommendations (3/4)
Blood cholesterol should be checked regularly. High blood
cholesterol (e.g. LDL>150mg/dl [3,9mMol/l]) should be
managed with lifestyle modification (Class IV, Level C) and a
statin (Class I, Level A)
Cigarette smoking should be discouraged (Class III, Level B)
Heavy use of alcohol should be discouraged (Class III, Level B)
Regular physical activity is recommended (Class III, Level B)
 Risk Factor Management
Recommendations (4/4)
A diet low in salt and saturated fat, high in fruit and vegetables
and rich in fibre is recommended (Class III, Level B)
Subjects with an elevated body mass index are recommended
to take a weight-reducing diet (Class III, Level B)
Antioxidant vitamin supplements are not recommended (Class
I, Level A)
Hormone replacement therapy is not recommended for the
primary prevention of stroke (Class I, Level A)
Primary prevention:
II) Antithrombotic Therapy
Background
In low risk persons low dose aspirin reduced coronary
events, but not stroke

In women over 45 years aspirin reduces the risk of

ischaemic stroke (OR 0.76; 95%CI 0.63-0.93)
 Atrial fibrillation (AF)
Background
Average stroke rate of 5% per year
Aspirin reduces stroke (RR 0.78) in patients with non-
valvular AF
Warfarin (INR 2.0-3.0) is more effective than aspirin at
reducing stroke (RR 0.36; 95%CI 0.26-0.51)1
Combination of aspirin and clopidogrel is less effective than
warfarin and has a similar bleeding rate.
 Atrial fibrillation (AF)
Background
Anticoagulation with an INR below 2.0 is not effective
Increased risk for bleeding complications with an INR > 3.5
Patients <65 years of age with lone AF (without other risk
factors) are at low risk,
whereas patients older than 65 years are at a higher risk for
embolic stroke
Anticoagulation can be safe and effective in older
individuals
 Antithrombotic Therapy
Recommendations (1/4)
Low-dose aspirin is recommended in women aged 45 years or
more who are not at increased risk for intracerebral
haemorrhage and who have good gastro-intestinal tolerance;
however, its effect is very small (Class I, Level A)
Low-dose aspirin may be considered in men for the primary
prevention of myocardial infarction; however, it does not
reduce the risk of ischaemic stroke (Class I, Level A)
 Antithrombotic Therapy
Recommendations (2/4)
Antiplatelet agents other than aspirin are not recommended
for primary stroke prevention (Class IV, GCP)
Aspirin may be recommended for patients with non-valvular
AF who are younger than 65 years and free of vascular risk
factors (Class I, Level A)
Unless contraindicated, either aspirin or an oral anticoagulant
(international normalized ratio [INR] 2.0-3.0) is recommended
for patients with non-valvular AF who are aged 65-75 years
and free of vascular risk factors (Class I, Level A)
 Antithrombotic Therapy

Recommendations (3/4)
Unless contraindicated, an oral anticoagulant (INR 2.03.0) is
recommended for patients with non-valvular AF who are aged
>75, or who are younger but have risk factors such as high
blood pressure, left ventricular dysfunction, or diabetes
mellitus (Class I, Level A)
 Antithrombotic Therapy
Recommendations (4/4)
Patients with AF who are unable to receive oral anticoagulants
should be offered aspirin (Class I, Level A)
Patients with AF who have mechanical prosthetic heart valves
should receive long-term anticoagulation with a target INR
based on the prosthesis type, but not less than INR 23 (Class
II, Level B)
Low dose aspirin is recommended for patients with
asymptomatic internal carotid artery (ICA) stenosis >50% to
reduce their risk of vascular events (Class II, Level B)
 Asymptomatic carotid artery (ICA)
stenosis
Background
Carotid endarterectomy (CEA) is still a matter of controversy
in asymptomatic individuals
RRR for stenosis >60%NASCET is 38-53%
ARR is 5.9-12.6%
NNT to avoid one stroke/year is 63-166
The combined surgical risk must not exceed 3%
 Asymptomatic carotid artery (ICA)
stenosis

Specific issues
No prospective trials tested the benefit of antiplatelet drugs
in patients with asymptomatic carotid stenosis
The ipsilateral stroke risk increases with the degree of the
stenosis
Women have lower benefit from CEA than men
Aspirin reduces stroke risk during and after CEA
 B) Secondary Prevention

Content
Management of vascular risk factors
Antithrombotic therapy
Surgery and angioplasty
 I) Management of risk factors:

1) Blood pressure control

Background
Antihypertensive drugs reduce stroke recurrence risk after
stroke or TIA (RR 0.76; 95%CI 0.63-0.92)1
Target BP level and reduction should be individualized
The reduction in stroke occurs regardless of baseline BP and
type of stroke
 2) Diabetes mellitus

Background
In people with type 2 diabetes with previous stroke
pioglitazone reduces fatal or nonfatal stroke (HR 0.53;
95%CI 0.34-0.85; P=0.0085)1
 3) High Cholesterol
Background
Atorvastatin (80mg) reduces stroke recurrence by 16%
Simvastatin (40mg) reduces risk of vascular events in
patients with prior stroke, and of stroke in patients with
other vascular disease (RR 0.76)
ARR for statin treatment is low (NNT 112-143 for 1 year)
Statin withdrawal at the acute stage of stroke may be
harmful
 4) Vitamins

Background
Beta carotene increased the risk (RR 1.10) of cardiovascular
death
Antioxidant supplements may increase mortality
Folate, B12, B6 vitamins given to lower homocysteine levels
may not reduce stroke recurrence and may increase
vascular events
 5) Hormone Replacement Therapy

Background
Oestrogen therapy is not effective in secondary prevention
after TIA or stroke and may increase stroke severity
 6) Sleep-disordered Breathing
Background
Sleep-disordered breathing (SDB) is both a risk factor and a
consequence of stroke
More than 50% of stroke patients have SDB, mostly in the
form of obstructive sleep apnoea (OSA).
SDB is linked with poorer long-term outcome and increased
long-term stroke mortality
Continuous positive airway pressure is the treatment of
choice for OSA.
 Risk Factor Management

Recommendations (1/3)
Blood pressure should be checked regularly. Blood pressure
lowering is recommended after the acute phase, including in
patients with normal blood pressure (Class I, Level A)
Blood glucose should be checked regularly. Diabetes should be
managed with lifestyle modification and individualized
pharmacological therapy (Class IV, GCP)
In patients with type 2 diabetes who do not need insulin,
treatment with pioglitazone is recommended after stroke
(Class III, Level B)
 Risk Factor Management

Recommendations (2/3)
Statin therapy is recommended (Class I, Level A)
Cigarette smoking should be stopped (Class III, Level C)
Heavy use of alcohol should be discouraged (Class IV, GCP)
Regular physical activity is recommended (Class IV, GCP)
A diet low in salt and saturated fat, high in fruit and vege-
tables, and rich in fibre is recommended (Class IV, GCP)
 Risk Factor Management
Recommendations (3/3)
Subjects with an elevated body mass index are recommended
to take a weight-reducing diet (Class IV, Level C)
Antioxidant vitamins supplements are not recommended
(Class I, Level A)
Hormone replacement therapy is not recommended for the
secondary prevention of stroke (Class I, Level A)
Sleep-disordered breathing such as obstructive sleep apnoea is
recommended to be treated with continuous positive airway
pressure breathing (Class III, Level GCP)
 II) Antithrombotic Therapy
Background: Aspirin
13% relative risk reduction for stroke after TIA or stroke
Most widely studied dosages of aspirin are 50-150mg
The incidence of GI-disturbances with aspirin is dose
dependent
No difference in effectiveness amongst low (< 160mg),
medium (160 325mg) or high (500 - 1500mg) dose aspirin
 Antithrombotic Therapy

Background: Dipyridamole plus aspirin

Relative risk reduction of vascular death, stroke or
myocardial infarction with the combination is significantly
greater (RR 0.82; 95%CI 0.71-0.91) than with aspirin alone1,2
ARR 1.0% per year (NNT 100)2
Incidence of dipyridamole induced headache may be
reduced by increasing the dose gradually
 Antithrombotic Therapy
Dipyridamole plus aspirin versus aspirin: Meta-analysis1
Reduced vascular endpoint (vascular death, stroke, myocardial
infarction) with dipyridamole plus aspirin
 Antithrombotic Therapy
Background: Clopidogrel:
Clopidogrel is slightly but significantly more effective than
medium-dose aspirin (RRR 8.7%, ARR 0,5%) in preventing
vascular events in patients with previous stroke, MI or PAD
Antithrombotic Therapy
Background: Clopidogrel plus aspirin
Compared with clopidogrel the combination of aspirin and
clopidogrel does not reduce the risk of ischaemic stroke,
myocardial infarction, vascular death, or re-hospitalisation
Compared with aspirin alone the combination does not
reduce the risk of myocardial infarction, stroke, or
cardiovascular death2
Risk of life-threatening or major bleeding is increased
 Antithrombotic Therapy

Recommendations (1/4)
Patients should receive antithrombotic therapy (Class I, Level
A)
Patients not requiring anticoagulation should receive
antiplatelet therapy (Class I, Level A). Where possible,
combined aspirin and dipyridamole, or clopidogrel alone,
should be given. Alternatively, aspirin alone, or triflusal alone,
may be used (Class I, Level A)
Antithrombotic Therapy
Recommendations (2/4)
The combination of aspirin and clopidogrel is not
recommended in patients with recent ischaemic stroke, except
in patients with specific indications (e.g. unstable angina or
non-Q-wave MI during the last 12 months, or recent stenting);
treatment should be given for up to 9 months after the event
(Class I, Level A)
Patients who have a stroke on antiplatelet therapy should be
re-evaluated for pathophysiology and risk factors (Class IV,
GCP)
 Anticoagulation
Background
Oral antiocoagulation (target INR 2.0 3.0) reduces the risk
of recurrent stroke in patients with AF
Oral anticoagulation is well established for other causes of
embolism such as mechanical prosthetic valve replacement,
rheumatic valvular heart disease, ventricular aneurysm and
cardiomyopathy
There is no indication for oral anticoagulation in patients
with non-cardiac cause of ischaemic stroke
Anticoagulation

Specific issues
In patients with AF and stable coronary disease, aspirin
should not be added to oral anticoagulation1
Some retrospective studies suggest that anticoagulation
may be beneficial in aortic atheroma, fusiform basilar
artery aneurysms3, or arterial dissection
It is unclear if patients with patent foramen ovale (PFO)
benefit from oral anticoagulation
 Antithrombotic Therapy
Recommendations (3/4)
Anticoagulation should not be used after non-cardio-embolic
ischaemic stroke, except in some specific situations, such as
aortic atheromas, fusiform aneurysms of the basilar artery,
cervical artery dissection, or patent foramen ovale in the
presence of proven deep vein thrombosis (DVT) or atrial septal
aneurysm (Class IV, GCP)
If oral anticoagulation is contraindicated, combined low dose
aspirin and dipyridamole should be given (Class IV, GCP)
 Antithrombotic Therapy
Recommendations (4/4)
Oral anticoagulation (INR 2.03.0) is recommended after
ischaemic stroke associated with AF (Class I, Level A). Oral
anticoagulation is not recommended in patients with co-
morbid conditions such as falls, poor compliance, uncontrolled
epilepsy, or gastrointestinal bleeding (Class III, Level C).
Increasing age alone is not a contraindication to oral
anticoagulation (Class I, Level A)
Patients with cardioembolic stroke unrelated to AF should
receive anticoagulants (INR 2.0-3.0) if the risk of recurrence is
high (Class III, Level C)
III) Carotid Endarterectomy (CEA)

Background
CEA reduces the risk by 48% of recurrent disabling stroke or
death in patients with 70-99%NASCET ipsilateral carotid artery
stenosis

There is also some risk reduction in male patients with 50 -

69% stenosis of the ipsilateral carotid artery, provided that
the complication rate is below 3%
 Carotid Endarterectomy

Specific issues
CEA should be performed as soon as possible (ideally within
2 weeks) after the last cerebrovascular event
Elderly patients (>75 years) without organ failure or serious
cardiac dysfunction benefit from CEA
Women with symptomatic stenosis >70% should undergo
CEA.
Women with moderate stenosis should be treated
medically
 Carotid Artery Stenting (CAS)

Background
No randomized trial has demonstrated equivalent
periprocedural risk for CAS compared to CEA in treatment
of symptomatic carotid artery stenosis
A European study only marginally failed to prove the non-
inferiority of CAS compared to CEA
A French study was stopped prematurely because of a 2.5
fold higher risk of any stroke or death after CAS
 ESO Guidelines 2008

Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment X X
Acute Treatment
Management of Complications
Rehabilitation
 General Stroke Treatment

Content
Monitoring
Pulmonary and airway care
Fluid balance
Blood pressure
Glucose metabolism
Body temperature
Monitoring
Continuous monitoring
Heart rate
Breathing rate
O2 saturation
Discontinuous monitoring
Blood pressure
Blood glucose
Vigilance (GCS), pupils
Neurological status (e.g. NIH stroke scale or Scandinavian
stroke scale)
 Pulmonary function
Background
Adequate oxygenation is important
Improve blood oxygenation by administration of > 2 l O2
Risk for aspiration in patients with side positioning
Hypoventilation may be caused by pathological respiration
pattern
Risk of airway obstruction (vomiting, oropharyngeal
muscular hypotonia): mechanical airway protection
 Blood pressure
Background
Elevated in most patients with acute stroke
BP drops spontaneously during the first days after stroke
Blood flow in the critical penumbra passively dependent on
the mean arterial pressure
There are no adequately sized randomised, controlled
studies guiding BP management
 Blood pressure
Specific issues
Elevated BP (e.g. up to 200mmHg systolic or 110mmHg
diastolic) may be tolerated in the acute phase of ischaemic
stroke without intervention
BP may be lowered if this is required by cardiac conditions
Upper level of systolic BP in patients undergoing
thrombolytic therapy is 180mmHg
Avoid and treat hypotension
Avoid drastic reduction in BP
 Glucose metabolism
Background
High glucose levels in acute stroke may increase the size of
the infarction and reduce functional outcome
Hypoglycemia can mimic acute ischaemic infarction
Routine use of glucose potassium insulin (GKI) infusion
regimes in patients with mild to moderate hyperglycaemia
did not improve outcome1
It is common practise to treat hyperglycemia with insulin when
blood glucose exceeds 180mg/dl2 (10mmol/l)
Body temperature
Background
Fever is associated with poorer neurological outcome after
stroke
Fever increases infarct size in experimental stroke
Many patients with acute stroke develop a febrile infection
There are no adequately sized trials guiding temperature
management after stroke
It is common practice treat fever (and its cause) when the
temperature reaches 37.5C
General Stroke Treatment
Recommendations (1/4)
Intermittent monitoring of neurological status, pulse, blood
pressure, temperature and oxygen saturation is recommended
for 72 hours in patients with significant persisting neurological
deficits (Class IV, GCP)
Oxygen should be administered if sPO2 falls below 95% (Class
IV, GCP)
Regular monitoring of fluid balance and electrolytes is
recommended in patients with severe stroke or swallowing
problems (Class IV, GCP)
General Stroke Treatment
Recommendations (2/4)
Normal saline (0.9%) is recommended for fluid replacement
during the first 24 hours after stroke (Class IV, GCP)
Routine blood pressure lowering is not recommended
following acute stroke (Class IV, GCP)
Cautious blood pressure lowering is recommended in patients
with any of the following; extremely high blood pressures
(>220/120 mmHg) on repeated measurements, or severe
cardiac failure, aortic dissection, or hyper-tensive
encephalopathy (Class IV, GCP)
 General Stroke Treatment
Recommendations (3/4)
Abrupt blood pressure lowering should be avoided (Class II,
Level C)
Low blood pressure secondary to hypovolaemia or associated
with neurological deterioration in acute stroke should be
treated with volume expanders (Class IV GCP)
Monitoring serum glucose levels is recommended (Class IV,
GCP)
Treatment of serum glucose levels >180mg/dl (>10mmol/l)
with insulin titration is recommended (Class IV, GCP)
 General Stroke Treatment
Recommendations (4/4)
Severe hypoglycaemia (<50 mg/dl [<2.8 mmol/l]) should be
treated with intravenous dextrose or infusion of 1020%
glucose (Class IV, GCP points)
The presence of pyrexia (temperature >37.5C) should prompt
a search for concurrent infection (Class IV, GCP)
Treatment of pyrexia (>37.5C) with paracetamol and fanning is
recommended (Class III, Level C)
Antibiotic prophylaxis is not recommended in
immunocompetent patients (Class II, Level B)
 ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation
 Specific Stroke Treatment

Content
Thrombolytic therapy
Early antithrombotic treatment
Treatment of elevated intracranial pressure
Prevention and management of complications
 I) Thrombolytic Therapy (i.v. rtPA)

Background (NINDS, ECASS I + II, ATLANTIS)

Intravenous rtPA (0.9mg/kg, max 90mg) given within 3
hours of stroke onset, significantly improves outcome in
patients with acute ischaemic stroke
Benefit from the use of i.v. rtPA beyond 3 hours is smaller,
but may be present up to at least 4.5 hours
Several contraindications
Thrombolytic Therapy (i.v. rtPA)
Specific issues
A pooled analysis of the 6 i.v. rtPA trials confirms that i.v.
thrombolysis may work up to 4.5 hours.

Caution is advised when considering i.v. rtPA in persons with

severe stroke (NIHSSS>25), or if the CT demonstrates
extended early infarcts signs

Thrombolytic therapy must be given by an experienced

stroke physician after the imaging of the brain is assessed
by physicians experienced in reading this imaging study
Thrombolytic Therapy (i.v. rtPA)
Specific issues
Factors associated with increased bleeding risk
elevated serum glucose
history of diabetes
advanced age
increased time to treatment
previous aspirin use
history of congestive heart failure
Specific Treatment
Recommendations (1/5)
Intravenous rtPA (0.9 mg/kg BW, maximum 90 mg), with 10%
of the dose given as a bolus followed by a 60-minute infusion,
is recommended within 3 hours of onset of ischaemic stroke
(Class I, Level A)
Intravenous rtPA may be of benefit also for acute ischaemic
stroke beyond 3 hours after onset (Class I, Level B) but is not
recommended for routine clinical practice. The use of
multimodal imaging criteria may be useful for patient selection
(Class III, Level C)
 Specific Treatment

Recommendations (2/5)
Blood pressures of 185/110 mmHg or higher must be lowered
before thrombolysis (Class IV, GCP)
Intravenous rtPA may be used in patients with seizures at
stroke onset, if the neurological deficit is related to acute
cerebral ischaemia (Class IV, GCP)
Intravenous rtPA may also be administered in selected patients
over 80 years of age, although this is outside the current
European labelling (Class III, Level C)
 Specific Treatment

Recommendations (3/5)
Intra-arterial treatment of acute MCA occlusion within a 6-
hour time window is recommended as an option (Class II, Level
B)
Intra-arterial thrombolysis is recommended for acute basilar
occlusion in selected patients (Class III, Level B) Intravenous
thrombolysis for basilar occlusion is an acceptable alternative
even after 3 hours (Class III, Level B)
II) Antiplatelet therapy
Background

Aspirin was tested in large RCTs in acute (<48 h) stroke

Significant reduction was seen in death, dependency and

recurrence of stroke.
 Anticoagulation
Unfractionated heparin
No formal trial available testing standard i.v. heparin
IST showed no net benefit for s.c. heparin treated patients
because of increased risk of ICH
Low molecular weight heparin
No benefit on stroke outcome for low molecular heparin
(nadroparin, certoparin, tinzaparin, dalteparin)
Heparinoid (orgaran)
TOAST trial neutral
 Specific Treatment
Recommendations (4/5)
Aspirin (160325 mg loading dose) should be given within 48
hours after ischaemic stroke (Class I, Level A)
If thrombolytic therapy is planned or given, aspirin or other
antithrombotic therapy should not be initiated within 24 hours
(Class IV, GCP)
The use of other antiplatelet agents (single or combined) is not
recommended in the setting of acute ischaemic stroke (Class
III, Level C)
The administration of glycoprotein-IIb-IIIa inhibitors is not
recommended (Class I, Level A)
 Specific Treatment

**** Recommendations (5/5)

Early administration of unfractionated heparin, low molecular
weight heparin or heparinoids is not recommended for the
treatment of patients with ischaemic stroke (Class I, Level A)

Currently, there is no recommendation to treat ischaemic

stroke patients with neuroprotective substances (Class I, Level
A)
IV) Elevated Intracranial Pressure
Basic management
Head elevation up to 30
Pain relief and sedation
Osmotic agents (glycerol, mannitol, hypertonic saline)
Ventilatory support
Barbiturates, hyperventilation,
Achieve normothermia

Hypothermia may reduce mortality

 Elevated Intracranial Pressure
Malignant MCA/hemispheric infarction

Surgery should be done within 48 hours

Side of infarction did affect outcome

Age >50 years is a predictor for poor outcome

Elevated Intracranial Pressure

Recommendations (1/2)
Surgical decompressive therapy within 48 hours after symptom
onset is recommended in patients up to 60 years of age with
evolving malignant MCA infarcts (Class I, Level A)
Osmotherapy can be used to treat elevated intracranial
pressure prior to surgery if this is considered (Class III, Level C)
 ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation
 Management of Complications
1) Aspiration and pneumonia
Bacterial pneumonia is one of the most important
complications in stroke patients
Preventive strategies
Withhold oral feeding until demonstration of intact swallowing,
preferable using a standardized test
Nasogastric (NG) or percutaneous enteral gastrostomy (PEG)
Frequent changes of the patients position in bed and pulmonary
physical therapy
Prophylactic administration of levofloxacin is not superior to
optimal care
Management of Complications

2) Urinary tract infections

Most hospital-acquired urinary tract infections are
associated with the use of indwelling catheters
Intermittent catheterization does not reduce the risk of
infection
If urinary infection is diagnosed, appropriate antibiotics
should be chosen following basic medical principles
 Management of Complications

3) Deep vein thrombosis and pulmonary embolism

Risk might be reduced by good hydration and early
mobilization
Low-dose LMWH reduces the incidence of both DVT (OR
0.34) and pulmonary embolism (OR 0.36), without a
significantly increased risk of intracerebral (OR 1.39) or
extracerebral haemorrhage (OR 1.44)
 Management of Complications
4) Pressure ulcer
Frequent repositioning, optimizing nutritional status, and
moisturizing sacral skin are appropriate preventive
strategies

5) Seizures
Prophylactic anticonvulsive treatment is not beneficial

6) Agitation
Causal treatment must precede any type of sedation or
antipsychotic treatment
Management of Complications

7) Dysphagia and feeding

Dysphagia occurs in up to 50% of patients with unilateral
hemiplegic stroke and is an independent risk-factor for poor
outcome

For patients with continuing dysphagia, options for enteral

nutrition include NG or PEG feeding
ESO Guidelines 2008
Content:
Education, Referral and Emergency room
Stroke Unit
Imaging and Diagnostics
Prevention
General Treatment
Acute Treatment
Management of Complications
Rehabilitation
Rehabilitation

Early rehabilitation
More than 40 % of stroke patients need active rehabilitation
Active rehabilitation should start early, providing the
patient is clinically stable
Passive rehabilitation should be given if the patient is
unconscious or paralysed
Rehabilitation should be continued as long as perceptable
recovery is taking place
Thank you