Stroke

The Management of Acute
Stroke: Selected Topics

STROKE DEFINITION
• THE SUDDEN ONSET OF FOCAL NEUROLOGIC
DYSFUNCTION
• SPEECH ISSUES APHASIA OR DYSARTHRIA
• HEMIPARESIS
• HEMI SENSORY ISSUES
• VISUAL LOSS
• ATAXIA
Types of Stroke
85% 15 %
Ischemic Primary Bleeds
Ischemia with Bleeding 10-15%
Amyloid Angiopathy
• LOBAR
Hypertensive Bleed
BASAL GANGLIA, PONS, CEREBELLUM
In addition to thrombotic occlusion at the site of cerebral artery
atherosclerosis, ischemic infarction can be produced by emboli
arising from proximally situated atheromatus lesions to vessels
located more distal in the arterial tree.
10
Ischemic Strokes
• Large Vessel Occlusion of the Major Vessels of the Neck
Outside the Cranial Vault i.e. Carotid or Vertebral Occlusion
• Large or Medium Sized Vessels in the Cranial Vault i.e.
Middle Cerebral or Basilar occlusion
• Embolic material breaking away from the heart and
occluding a vessel down stream so called cardiogenic
embolus
• Embolic material breaking away from carotid or basilar
atheromatous disease in the neck or within the cranium
and blocking a vessel down stream so called artery to
artery embolus
• Small Vessel Occlusions of penetrating vessels which take
off at right angles so called “Lacunar Strokes”
Many Causes of Stroke
16
Lacunar Strokes
• Small Penentrating Blood Vessels
• Pure Motor Stroke
• Pure Sensory Stroke
• Ataxia-Hemiparesis
• Clumsy Hand Dysarthria
• Excellent prognosis for recovery
Stroke Mimics
• Hypoglycemia
• Hyperglycemia
• Seizure
• Subdural
Hematoma
Stroke Differential Diagnosis
Ancillary Diagnostic Tests
• In selected patients
– Duplex / Doppler ultrasound
– MRA or CTA
– Diffusion and perfusion MR or perfusion CT
– Echocardiography, Chest X-ray
– Pulse oximetry and arterial blood gas analysis
– Lumbar puncture
– EEG
– Toxicology screen
Guidelines Ischaemic Stroke 2008

DWI Images
• Acute
STROKE
MRI
T2
DWI
ADC
Perfusion MRI Weighted Image
Perfusion Diffusion Mismatch The
HOLY GRAIL
Acute
Emergency Diagnostic Tests
• Mismatch Concept
– Mismatch between tissue abnormal on DWI and
tissue with reduced perfusion may reflect tissue at
risk of further ischaemic damage1
– There is disagreement on how to best identify
irreversible ischaemic brain injury and to define
critically impaired blood flow2
– There is no clear evidence that patients with
particular perfusion patterns are more or less likely
to benefit from thrombolysis3
1: Jansen O et al. Lancet (1999) 353:2036-2037
2: Kane I et al. Stroke (2007) 38:3158-3164
3: Albers GW et al. Ann Neurol (2006) Guidelines
60:508-517Ischaemic Stroke 2008
TPA 3-4.5 Hours
• ECASS 3 CRUCIAL EFFICACY NOT CLEAR: SAFETY IS
• Excludes anyone on Coumadin even if INR is
normal
• Excludes anyone over 80
• Excludes NIH Stroke Scale Score over 25
• Excludes patients with HTN and DM
• Does not compare to other therapies i.e. mixed
IV/IA or IA TPA
Blood Pressure Management
• Do NOT Treat BP in Ischemic Stroke unless it is
over 220/120 or the patient is having an MI,
Dissection or Acute Glomerulonephritis
• Stop ALL HOME BP Meds, Trandelenberg,
Raise BP???
• The key is the shift of the auto-regulatory
curve to the right in hypertensives and the
need to maintain perfusion
• Small Changes IN Local Perfusion NOT
represented by lowering of BP may cause
deterioration or fluctuation
PFO: A LONG STORY
• Percutaneous Device Closure of Patent Foramen Ovale for
Secondary Stroke Prevention
• A Call for Completion of Randomized Clinical Trials A Science
Advisory From the American Heart Association/American
Stroke Association and the American College of Cardiology
Foundation The American Academy of Neurology affirms the
value of this science advisory
• AJC ARTICLE
• Size
• ASD
• ASA
• ???Anti-Platelets vs Anti-Coagulation
Stroke as an Emergency
• Background
– Stroke is the most important cause of morbidity
and long term disability in Europe1
– Demographic changes are likely to result in an
increase in both incidence and prevalence
– 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
1: Lopez AD et al. Lancet (2006) 367:1747-1757

2: Rothwell PM et al. Lancet (2005) 366:1773-1783
Guidelines
3: O'Brien JT et al. Lancet Neurol (2003) 2:89-98 Ischaemic Stroke 2008
• 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

• Emergency care in acute stroke depends on a
four-step chain:
– Rapid recognition of, and reaction to, stroke signs
and symptoms
– Immediate EMS contact and priority EMS dispatch
– 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.
• Delays during acute stroke management have
been identified at three different levels1
– 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

1:Kwan J et al. Age Ageing (2004) 33:116-121
Education
Recommendations
 Educational programmes to increase awareness of stroke at
the population level are recommended (Class II,
Level B)
 Educational programmes to increase stroke awareness among
professionals (paramedics, emergency physicians) are
recommended (Class II, Level B)

Referral
Recommendations (1/2)
 Immediate EMS contact and priority EMS dispatch are
recommended (Class II, Level B)
 Priority transport with advance notification of the receiving
hospital is recommended (Class III, Level B)
 Suspected stroke victims should be transported without delay
to the nearest medical centre with a stroke unit that can
provide ultra-early treatment (Class III, Level B)
 Patients with suspected TIA should be referred without delay
to a TIA clinic or a stroke unit (Class III, Level B)

Referral
 Dispatchers and ambulance personnel should be trained to
recognise stroke using simple instruments such as the Face-
Arm-Speech-Test (Class IV, GCP)
 Immediate emergency room triage, clinical, laboratory and
imaging evaluation, accurate diagnosis, therapeutic decision
and administration of appropriate treatments are
recommended (Class III, Level B)
 In remote or rural areas helicopter transfer and telemedicine
should be considered to improve access to treatment (Class III,
Level C)

Emergency Management
• The time window for treatment of patients
with acute stroke is narrow
– Acute emergency management of stroke requires
parallel processes operating at different levels of
patient management
– Acute assessment of neurological and vital
functions parallels the treatment of acutely life-
threatening conditions
• Time is the most important factor

• The initial examination should include
– Observation of breathing and pulmonary function
and concomitant heart disease
– Assessment of blood pressure and heart rate
– 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

Recommendations
 Organization of pre-hospital and in-hospital pathways and
systems for acute stroke patients is recommended (Class III,
Level C)
 All patients should receive brain imaging, ECG, and laboratory
tests. Additional diagnostic examinations are necessary in
selected patients (Class IV, GCP)

Stroke Services and Stroke Units
Recommendations
 All stroke patients should be treated in a stroke unit
(Class I, Level A)
 Healthcare systems must ensure that acute stroke patients can
access high technology medical and surgical stroke care when
required (Class III, Level B)
 The development of clinical networks, including telemedicine,
is recommended to expand the access to high technology
specialist stroke care (Class II, Level B)

• Differentiate between different types of stroke
– Assess the underlying cause of brain ischaemia
– Assess prognosis
• Provide a basis for physiological monitoring of
the stroke patient
• Identify concurrent diseases or complications
associated with stroke
• Rule out other brain diseases

• 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 onset1
– Helps to identify other neurological diseases (e.g.
neoplasms)
– Most cost-effective strategy for imaging acute
stroke patients2
1: von Kummer R et al. Radiology (2001) 219:95-100

2: Wardlaw J et al. Stroke (2004) 35:2477-2483
DWI Images
• Acute
• 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 stroke1
– 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

1: Ay H et al. Cerebrovasc Dis (2002) 14:177-186
• Mismatch Concept
– Mismatch between tissue abnormal on DWI and
tissue with reduced perfusion may reflect tissue at
risk of further ischaemic damage1
– There is disagreement on how to best identify
irreversible ischaemic brain injury and to define
critically impaired blood flow2
– There is no clear evidence that patients with
particular perfusion patterns are more or less likely
to benefit from thrombolysis3
1: Jansen O et al. Lancet (1999) 353:2036-2037
2: Kane I et al. Stroke (2007) 38:3158-3164
3: Albers GW et al. Ann Neurol (2006) Guidelines
60:508-517Ischaemic Stroke 2008
• Ultrasound studies
– Cerebrovascular ultrasound is fast and non-invasive
and can be administered using portable machines.
– It is therefore applicable to patients unable to co-
operate with MRA or CTA1
– Combinations of ultrasound imaging techniques
and MRA can produce excellent results that are
equal to Digital subtraction angiography (DSA)2
1: Allendörfer J et al. Lancet Neurology (2005) 5:835-840

2: Nederkoorn P et al. Stroke (2003) 34:1324-1332
• Imaging in TIA-patients
– Up to 10% recurrence risk in the first 48 hours1
– Simple clinical scoring systems can be used to
identify patients at particularly high risk1
– Up to 50% of patients with TIAs have acute
ischaemic lesions on DWI. These patients are at
increased risk of early recurrent disabling stroke2
– There is currently no evidence that DWI provides
better stroke prediction than clinical risk scores3
1: Rothwell P et al. Lancet Neurol (2005) 5:323-331

2: Coutts S et al. Ann Neurol (2005) 57:848-854
3: Redgrave J et al. Stroke (2007) 38:1482-1488
• Electrocardiogram (ECG)
– Cardiac abnormalities are common in acute stroke
patients1
– Arrhythmias may induce stroke, stroke may cause
arrhythmias
– Holter monitoring is superior to routine ECG for the
detection of atrial fibrillation (AF)2
– It is unclear whether continuous ECG recording at
the bedside is equivalent to Holter monitoring for
the detection of AF
1: Christensen H et al. Neurol Sci (2005) 234:99 –103

2: Gunalp M et al. Adv Ther (2006) 23:854-60
• Echocardiography (TTE / TOE)
– Echocardiography can detect many potential causes of
stroke1
– 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 (TOE) might be
superior to transthoracic echocardiography (TTE) for
the detection of potential cardiac sources of embolism2
1: Lerakis S et al. Am J Med Sci (2005) 329:310-6

2: de Bruijn SF et al. Stroke (2006) 37:2531-4
• Laboratory tests
– Haematology (RBC, WBC, platelet count)
– Basic clotting parameters
– Electrolytes
– Renal and hepatic chemistry
– Blood Glucose
– CRP, sedimentation rate
– RPR, ANA, Rheumatoid factor
– Fasting Lipids
– Homocysteine

Hpercoag Work-Up
• Antiphospholipid Antibodies (Anti-Cardioppin
Antibodies and Lupus Anti-Coagulant-PTT
proxy)
• Factor V Leiden
• Anti Thrombin Three Activity
• Protein C
• Protein S
• Prothrombin Gene Mutation
Diagnostic Imaging
Recommendations
 In patients with suspected TIA or stroke, urgent cranial CT
(Class I), or alternatively MRI (Class II), is recommended (Level
A)
 If MRI is used, the inclusion of diffusion weighted imaging
(DWI) and T2*-weighted gradient echo sequences is
recommended (Class II, 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
 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
 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)

Primary Prevention
• Content
– Management of vascular risk factors
– Antithrombotic therapy
– Carotid surgery and angioplasty

Vascular Risk Factors
• Conditions and lifestyle characteristics identified
as a risk factors for stroke
High blood pressure High Cholesterol
Atrial fibrillation Hyper-homocysteinaemia
Diabetes mellitus Smoking
Carotid artery disease Heavy alcohol use
Myocardial infarction Physical inactivity
Obesity

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 BP1
– No class of antihypertensive is clearly superior
• LIFE: lorsatan is superior to atenolol2
• ALLHAT: chlorthalidone is more effective than amlodipine and
lisinopril3
1: Neal B et al. Lancet (2000) 356:1955-64

2: Dahlof B et al. Lancet (2002) 359:995-1003.
3: Mancia G et al. Eur Heart J (2007) 28:1462-536
Diabetes mellitus
• Background
– Independent risk factor for ischaemic stroke
– Improving glucose control may not reduce stroke1
– BP in patients with diabetes should be <130/80mmHg2
– Statin treatment reduces the risk of major vascular
events, including stroke3
– Elevated blood glucose in the early phase of stroke is
associated with death and poor recovery
1: Turner RC et al. JAMA (1999) 281:2005-12

2: Mancia GJ: Hypertens Suppl (2007) 25:S7-12
Guidelines
3: Sever PS et al. Diabetes Care (2005) Ischaemic Stroke 2008
28:1151-7
High Cholesterol
• Background
– Statin treatment reduces the incidence of stroke
from 3.4% to 2.7%1
– No significant effect for prevention of fatal stroke1
– Heart Protection Study found an excess of
myopathy of one per 10,000 patients per annum2
– No data support statin treatment in patients with
LDL-cholesterol <150 mg/dl (3.9 mmol/l)
1: Amarenco P et al.: Stroke (2004) 35:2902-2909

2: HPS Group: Lancet (2002) 360:7-22. Guidelines Ischaemic Stroke 2008
Cigarette Smoking
• Background
– Independent risk factor for ischaemic stroke in men
and women
– 2-3 fold increased risk compared to non-smokers1
– Spousal cigarette smoking may be associated with an
increased stroke risk2
– 50% risk reduction by 2 years after stopping smoking3
1: Shinton R et al.: BMJ (1989) 298:789-94.

2: Qureshi A et al.: Stroke (2005) 36:74-76
Guidelines
3: Colditz GA et al.: N Engl J Med (1988) Ischaemic Stroke 2008
318:937-41.
Alcohol Consumption
• Background
– Increased risk for both ischaemic (RR 1.69) and
haemorrhagic stroke (RR 2.18) with heavy alcohol
consumption (>60g/day)1
– BP elevation might be a reasonable explanation3
– Light alcohol consumption (<12g/day) associated
with reduced ischaemic (RR 0.80) and
haemorrhagic stroke1
– Red wine consumption carries the lowest risk2
1: Reynolds K et al.: JAMA (2003) 289:579-88
2: Mukamal K et al.: Ann Intern Med (2005) 142:11-19
3: Bazzano LA et al.: Ann Neurol (2007)
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)1
– This is mediated, in part, through beneficial effects on
body weight, blood pressure, serum cholesterol, and
glucose tolerance2
1: Lee C et al.: Stroke (2003) 34:2475-2481

Guidelines
2: Deplanque D et al.: Neurology (2006) Ischaemic Stroke 2008
67:1403-1410)
Body Weight, Diet, Nutrition
• Background
– High body mass index (BMI ≥25) increases risk of stroke
in men and women1
– Abdominal adiposity is a risk factor for stroke in men
but not women2
– A randomized trial in women found no effect of dietary
interventions to reduce the incidence of stroke3
– 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)
1: Kurth T et al.: Circulation (2005) 111:1992-1998
2: Hu G et al.: Arch Intern Med (2007) 167:1420-1427
3: Howard B et al.: JAMA (2006) 295:655-666
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
stroke1
Guidelines
1: Gabriel S et al.: Cochrane Review (2005) Ischaemic Stroke 2008
CD002229
Risk Factor Management
 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)

 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)

 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)

 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)

Antithrombotic Therapy
• Background
– In low risk persons low dose aspirin reduced
coronary events, but not stroke1
– In women over 45 years aspirin reduces the risk of
ischaemic stroke (OR 0.76; 95%CI 0.63-0.93) 2
– Aspirin reduces MI in patients with asymptomatic
carotid artery disease3
1: Bartolucci A et al.: Am J Cardiol (2006) 98:746-750

2: Berger J et al.: JAMA (2006) 295:306-313
Guidelines
3: Hobson R, 2nd et al.: J Vasc Surg (1993) Ischaemic Stroke 2008
17:257-263
Atrial fibrillation (AF)
• Background
– Average stroke rate of 5% per year
– Aspirin reduces stroke (RR 0.78) in patients with non-
valvular AF1
– 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 rate2
1: Hart RG et al.: Ann Intern Med (2007) 146:857-867

2: Connolly S et al.: Lancet (2006) 367:1903-1912
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
individuals1, 2
1: Rash A et al.: Age Ageing (2007) 36:151-156

2: Mant J et al.: Lancet (2007) 370:493-503
 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)

 Unless contraindicated, an oral anticoagulant (INR 2.0–3.0) 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)

 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 2–3 (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
• Background1,2
– 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%
1: ACAS: JAMA (1995) 273:1421-8.

2: ACST: Lancet (2004) 363:1491-1502Guidelines Ischaemic Stroke 2008
Asymptomatic carotid artery
(ICA) stenosis
• Specific issues
– No prospective trials tested the benefit of antiplatelet
drugs in patients with asymptomatic carotid stenosis1
– The ipsilateral stroke risk increases with the degree of
the stenosis2
– Patients with an occlusion of the contralateral ICA do
not benefit from endarterectomy3
– Women have lower benefit from CEA than men3
– Aspirin reduces stroke risk during and after CEA4
1: Chambers BR et al.: Cochrane Review (2005)
2: ECST Group: Lancet (1995) 345:209-12
3: Baker WH et al.: Stroke (2000) 31:2330-4
4: Engelter S et al.: Cochrane ReviewsGuidelines
(2003) Ischaemic Stroke 2008
Carotid Surgery and Angioplasty
Recommendations
 Carotid surgery is not recommended for asymptomatic
individuals with significant carotid stenosis (NASCET 60-99%),
except in those at high risk of stroke (Class I, Level C)
 Carotid angioplasty, with or without stenting, is not
recommended for patients with asymptomatic carotid stenosis
(Class IV, GCP)
 Patients should take aspirin before and after CEA (Class I, Level
A)

Secondary Prevention
• Content
– Management of vascular risk factors
– Antithrombotic therapy
– Surgery and angioplasty

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 stroke2
1: Rashid P et al.: Stroke (2003) 34:2741-8

2: PROGRESS group: Lancet (2001) 358:1033-41
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
– In addition there is a trend to reduce the combined
end point of death and major vascular events (HR
0.78; 95%CI 0.60-1.02; P=0.067)1

1: Wilcox R et al.: Stroke (2007) 38:865-73
High Cholesterol
• Background
– Atorvastatin (80mg) reduces stroke recurrence by
16%1
– Simvastatin (40mg) reduces risk of vascular events
in patients with prior stroke, and of stroke in
patients with other vascular disease (RR 0.76)2
– ARR for statin treatment is low (NNT 112-143 for 1
year)1
– Statin withdrawal at the acute stage of stroke may
be harmful3
1: Amarenco P et al.: N Engl J Med (2006) 355:549-559
2: Heart Protection Study: Lancet (2002) 360:7-22
3: Blanco M et al.: Neurology (2007) 69:904-10
Vitamins
• Background
– Beta carotene increased the risk (RR 1.10) of
cardiovascular death1
– Antioxidant supplements may increase mortality2
– Folate, B12, B6 vitamins given to lower
homocysteine levels may not reduce stroke
recurrence and may increase vascular events3
1: Vivekananthan D et al.: Lancet (2003) 361:2017-2023

2: Bjelakovic G et al.: JAMA (2007) 297:842-857
3: Bonaa K et al.: N Engl J Med (2006)Guidelines Ischaemic Stroke 2008
354:1578-1588
Hormone Replacement Therapy
• Background
– Oestrogen therapy is not effective in secondary
prevention after TIA or stroke and may increase
stroke severity1
Guidelines
1: Viscoli CM et al.: N Engl J Med (2001) Ischaemic Stroke 2008
345:1243-9.
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 mortality1
– Continuous positive airway pressure is the
treatment of choice for OSA.

1: Bassetti CL: Semin Neurol (2005) 25:19-32
 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)

 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)

 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)

• Background: Aspirin
– 13% relative risk reduction for stroke after TIA or
stroke1
– 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
Guidelines
1: Antithrombotic Trialists' Collaboration: Ischaemic
BMJ (2002) Stroke 2008
324:71-86
• 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 gradually3
1: Diener HC et al.: J Neurol Sci (1996) 143:1-13

2: Halkes P et al.: Lancet (2006) 367:1665-1673
Guidelines
3: Chang YJ et al.: Cerebrovasc Dis (2006) Ischaemic Stroke 2008
22:258-62
• Dipyridamole plus aspirin versus aspirin: Meta-analysis1
– Reduced vascular endpoint (vascular death, stroke, myocardial
infarction) with dipyridamole plus aspirin

1: Halkes P et al.: Lancet (2006) 367:1665-1673
• 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 PAD1
1: CAPRIE Steering Committee: Lancet Guidelines Ischaemic Stroke 2008

• 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-hospitalisation1
– 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
increased1,2
1: Diener H et al.: Lancet (2004) 364:331-337

2: Bhatt D et al.: N Engl J Med (2006) Guidelines Ischaemic Stroke 2008
354:1706-1717
 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)

 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 AF1
– 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 stroke2
1: EAFT Study Group: Lancet (1993) 342:1255-1262

2: Mohr JP et al.: N Engl J Med (2001)Guidelines Ischaemic Stroke 2008
345:1444-1451
Anticoagulation
• Specific issues
– In patients with AF and stable coronary disease, aspirin
should not be added to oral anticoagulation1
– Some retrospective studies suggest that anticoagu-
lation may be beneficial in aortic atheroma2, fusiform
basilar artery aneurysms3, or arterial dissection4
– It is unclear if patients with patent foramen ovale (PFO)
benefit from oral anticoagulation5
1: Flaker GC et al.: Am Heart J (2006) 152:967-73

2: Dressler FA et al.: J Am Coll Cardiol (1998) 31:134-8
3: Echiverri HC et al.: Stroke (1989) 20:1741-7
4: Engelter ST et al.: Stroke (2007) 38:2605-11
5: Mas JL et al.: N Engl J Med (2001) 345:1740-6
 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)

 Oral anticoagulation (INR 2.0–3.0) 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)

Carotid Endarterectomy (CEA)
• Background1,2
– CEA reduces the risk by 48% of recurrent disabling
stroke or death in patients with 70-99%NASCET ipsilateral
carotid artery stenosis
– If perioperative complications exceed 6%, the benefit
of CEA will diminish; if it approaches 10%, the benefit
will vanish entirely
– 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%
1: NASCET Collaborators: NEJM (1991) 325:445-453

2: Warlow C: Lancet (1991) 337:1235-1243
Carotid Endarterectomy
• Specific issues
– CEA should be performed as soon as possible (ideally
within 2 weeks) after the last cerebrovascular event1,2
– Elderly patients (>75 years) without organ failure or
serious cardiac dysfunction benefit from CEA1
– Women with symptomatic stenosis >70% should
undergo CEA. Women with moderate stenosis should
be treated medically2
1: Rothwell PM et al.: Lancet (2004) 363:915-924

2: Rothwell PM et al.: Stroke (2004) 35:2855-61
Effect of time from last
symptomatic event to
randomisation on the 5-
year relative risk (RR) of
ipsilateral ischaemic stroke
and any operative stroke or
death with CEA (pooled
data from ECST and
NASCET1)

1: Rothwell PM et al.: Stroke (2004) 35:2855-61
• Specific issues
– The benefit from CEA is lower with lacunar stroke
– Patients with leuko-araiosis should be made aware
of the increased operative risk
– Occlusion of the contralateral ICA carries a higher
perioperative risk
– Continuation of aspirin is required until surgery,
but heparin may be used in very severe stenosis
– All grading of stenoses should be according to
NASCET-criteria

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 CAS2
1: Ringleb PA et al.: Lancet (2006) 368:1239-1247

2: Mas JL et al.: NEJM (2006) 355:1660-1671
Carotid Artery Stenting
Metaanalysis CAS vs. CEA
Endpoint: any periprocedural stroke or death
Guidelines
1: Kastrup A et al.: Acta Chir Belg (2007) Ischaemic Stroke 2008
107:119-28
CREST STUDY
• Landmark NIH Clinical Trial Comparing Two
Stroke Prevention Procedures Shows Surgery
and Stenting Equally Safe and Effective
• Opportunities Exist to Target the Treatment to
the Patient
Intracranial Occlusive Disease
• Background
– Extracranial-Intracranial bypass is not beneficial in
preventing stroke in patients with MCA or ICA stenosis
or occlusion1
– No randomized controlled trials have evaluated
angioplasty, stenting, or both for intracranial stenosis
– Several non-randomized trials have shown feasibility
and acceptable safety of intracranial stenting, but the
risk of re-stenosis remains high2,3
1: The EC/IC Bypass Grp: N Engl J Med (1985) 313:1191-200

2: Bose A et al.: Stroke (2007) 38:1531-7
3: SSYLVIA Study investigators: StrokeGuidelines
35:1388-92
Surgery and Angioplasty
 CEA is recommended for patients with 70–99% stenosis
(NASCET criteria) (Class I, Level A). CEA should only be
performed in centres with a perioperative complication rate
(all strokes and death) of less than 6% (Class I, Level A)
 CEA should be performed as soon as possible after the last
ischaemic event, ideally within 2 weeks (Class II, Level B)

 CEA may be indicated for certain patients with stenosis of 50–
69% (NASCET criteria); males with very recent hemispheric
symptoms are most likely to benefit (Class III, Level C). CEA for
stenosis of 50–69% (NASCET criteria) should only be performed
in centres with a perioperative complication rate (all stroke and
death) of less than 3% (Class I, Level A)
 CEA is not recommended for patients with stenosis of less than
50% (NASCET criteria) (Class I, Level A)

 Patients should remain on antiplatelet therapy both before and
after surgery (Class I, Level A)
 Carotid percutaneous transluminal angioplasty and/or stenting
(CAS) is only recommended in selected patients (Class I, Level
A). It should be restricted to the following subgroups of
patients with severe symptomatic carotid artery stenosis:
those with contra-indications to CEA, stenosis at a surgically
inaccessible site, re-stenosis after earlier CEA, and post-
radiation stenosis (Class IV, GCP)

 Patients should receive a combination of clopidogrel and
aspirin immediately before and for at least 1 months after
stenting (Class IV, GCP)
 Endovascular treatment may be considered in patients with
symptomatic intracranial stenosis (Class IV, GPC)

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)
1: Gray CS et al.: Lancet Neurol (2007) 6:397-406

Guidelines
2: Langhorne P et al.: Age Ageing (2002) Ischaemic Stroke 2008
31:365-71.
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 37.5°C

 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)

 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)

 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)

 Severe hypoglycaemia (<50 mg/dl [<2.8 mmol/l]) should be
treated with intravenous dextrose or infusion of 10–20%
glucose (Class IV, GCP points)
 The presence of pyrexia (temperature >37.5°C) should prompt
a search for concurrent infection (Class IV, GCP)
 Treatment of pyrexia (>37.5°C) with paracetamol and fanning is
recommended (Class III, Level C)
 Antibiotic prophylaxis is not recommended in
immunocompetent patients (Class II, Level B)

Specific Stroke Treatment
• Content
– Thrombolytic therapy
– Early antithrombotic treatment
– Treatment of elevated intracranial pressure
– Prevention and management of complications

Thrombolytic Therapy (i.v. rtPA)
• Background (NINDS1, ECASS I2 + II3, ATLANTIS4)
– 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
1: NINDS rt-PA Grp: New Engl J Med (1995) 333:1581-1587

2: Hacke W et al.: JAMA (1995) 274:1017-1025
3: Hacke W et al.: Lancet (1998) 352:1245-1251
4: Clark WM et al.: Jama (1999) 282:2019-26.
• Specific issues
– A pooled analysis of the 6 i.v. rtPA trials confirms
that i.v. thrombolysis may work up to 4.5 hours1
– 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 study2
1: Hacke W et al.: Lancet (2004) 363:768-74

2: Wahlgren N et al.: Lancet (2007) 369:275-82
• Specific issues
– Factors associated with increased bleeding risk1
• elevated serum glucose
• history of diabetes
• baseline symptom severity
• advanced age
• increased time to treatment
• previous aspirin use
• history of congestive heart failure
• NINDS protocol violations
– None of these reversed the overall benefit of rtPA

1: Lansberg MG et al.: Stroke (2007) 38:2275-8
Risk and outcome from 6,483 patients of the SITS-Most treated
with iv-rtPA within a 3 hour time window1

1: Wahlgren N et al.: Lancet (2007) 369:275-82
• Mismatch based therapy
– The use of multimodal imaging criteria may be useful
for patient selection1,2
– Available data on mismatch, as defined by multimodal
MRI or CT, are too limited to guide thrombolysis in
routine practice3
– Data regarding the use of intravenous desmoteplase
administered 3 to 9 hours after acute ischaemic stroke
in patients selected on the basis of perfusion/diffusion
mismatch are conflicting
1: Köhrmann M et al.: Lancet Neurol (2006) 5:661-7
2: Chalela J et al.: Lancet (2007) 369:293-298
3: Kane I et al.: JNNP (2007) 78:485-490
Thrombolytic Therapy (i.a.)
• Background: the use of i.a. rtPA, i.a. urokinase
– Only cases and some prospective uncontrolled case
series
• Facts: about use of i.a. pro-urokinase
– Efficacy demonstrated in small RCT, 6h window1
– Not approved and substance not available

1: Furlan A et al.: JAMA (1999) 282:2003-11
Specific Treatment
 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
 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
 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)

Antiplatelet therapy
• Background
– Aspirin was tested in large RCTs in acute (<48 h)
stroke1,2
– Significant reduction was seen in death and
dependency (NNT 70) and recurrence of stroke
(NNT 140)
– A phase 3 trial for the glycoprotein-IIb-IIIa
antagonist abciximab was stopped prematurely
because of an increased rate of bleeding3
1: International-Stroke-Trial: Lancet (1997) 349:1569-1581
2: CAST-Collaborative-Group: Lancet (1997) 349:1641-1649
3: Adams HP, Jr. et al.: Stroke (2007) Guidelines Ischaemic Stroke 2008
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 ICH1
• Low molecular weight heparin
– No benefit on stroke outcome for low molecular
heparin (nadroparin, certoparin, tinzaparin, dalteparin)
• Heparinoid (orgaran)
– TOAST trial neutral2
1: International-Stroke-Trial: Lancet (1997) 349:1569-1581

2: TOAST Investigators: JAMA (1998) Guidelines Ischaemic Stroke 2008
279:1265-72.
Neuroprotection
• No adequately sized trial has yet shown
significant effect in predefined endpoints for
any neuroprotective substance
• A meta-analysis has suggested a mild benefit
for citocoline1

1: Davalos A et al.: Stroke (2002) 33:2850-7
Specific Treatment
 Aspirin (160–325 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
 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)

Elevated Intracranial Pressure
• Basic management
– Head elevation up to 30°
– Pain relief and sedation
– Osmotic agents (glycerol, mannitol, hypertonic saline)
– Ventilatory support
– Barbiturates, hyperventilation, or THAM-buffer
– Achieve normothermia
• Hypothermia may reduce mortality1
Guidelines2):S61-8.
1: Steiner T et al.: Neurology (2001) 57(Suppl Ischaemic Stroke 2008
• Malignant MCA/hemispheric infarction
– Pooled analysis of three European RCTs (N=93)1,2:
• Significantly decreases mortality after 30 days
• Significantly more patients with mRS <4 or mRS <3 in the
decompressive surgery group after one year
• No increase of patients surviving with mRS=5
– Surgery should be done within 48 hours1,2
– Side of infarction did affect outcome1,2
– Age >50 years is a predictor for poor outcome3
1: Vahedi K et al.: Lancet Neurol (2007) 6:215-22

2: Jüttler E et al.: Stroke (2007) 38:2518-25
3: Gupta R et al.: Stroke (2004) 35:539-43
Absolute risk reduction (ARR) and odds ratio (OR) for unfavourable outcome at 12
months: combined analysis of decompression trials1
1: Vahedi K et al.: Lancet Neurol (2007) 6:215-22 Guidelines Ischaemic Stroke 2008
 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)

 No recommendation can be given regarding hypothermic
therapy in patients with space-occupying infarctions (Class IV,
GCP)
 Ventriculostomy or surgical decompression can be considered
for treatment of large cerebellar infarctions that compress the
brainstem (Class III, Level C)

Management of Complications
• Aspiration and pneumonia
– Bacterial pneumonia is one of the most important
complications in stroke patients1
– 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 patient’s position in bed and pulmonary
physical therapy
– Prophylactic administration of levofloxacin is not
superior to optimal care2
1: Weimar C et al.: Eur Neurol (2002) 48:133-40

2: Chamorro A et al.: Stroke (2005) 36:1495-500
• Urinary tract infections
– Most hospital-acquired urinary tract infections are
associated with the use of indwelling catheters1
– Intermittent catheterization does not reduce the risk of
infection
– If urinary infection is diagnosed, appropriate antibiotics
should be chosen following basic medical principles
Guidelines
1: Gerberding JL: Ann Intern Med (2002) Ischaemic Stroke 2008
137:665-70c
• 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)1,2
1: Diener HC et al.: Stroke (2006) 37:139-44

2: Sherman DG et al.: Lancet (2007) 369:1347-55
• Pressure ulcer
– Use of support surfaces, frequent repositioning,
optimizing nutritional status, and moisturizing sacral
skin are appropriate preventive strategies1
• Seizures
– Prophylactic anticonvulsive treatment is not beneficial
• Agitation
– Causal treatment must precede any type of sedation or
antipsychotic treatment

1: Reddy M et al.: JAMA (2006) 296:974-84
• Falls
– Are common in every stage of stroke treatment
– Risk factors include cognitive impairment, depression,
polypharmacy and sensory impairment1
– A multidisciplinary package focusing on personal and
environmental factors might be preventive2
– Exercise, calcium supplements and bisphosphonates
improve bone strength and decrease fracture rates in
stroke patients3,4
1: Aizen E et al.: Arch Gerontol Geriatr (2007) 44:1-12
2: Oliver D et al.: BMJ (2007) 334:82
3: Pang MY et al.: Clin Rehabil (2006) 20:97-111
4: Sato Y et al.: Cerebrovasc Dis (2005) 20:187-92
• Dysphagia and feeding
– Dysphagia occurs in up to 50% of patients with
unilateral hemiplegic stroke and is an independent
risk-factor for poor outcome1
– For patients with continuing dysphagia, options for
enteral nutrition include NG or PEG feeding
– PEG does not provide better nutritional status or
improved clinical outcome, compared to NG2,3
1: Martino R et al.: Stroke (2005) 36:2756-63

2: Dennis MS et al.: Lancet (2005) 365:764-72
3: Callahan CM et al.: J Am Geriatr SocGuidelines
48:1048-54
 Infections after stroke should be treated with appropriate
antibiotics (Class IV, GCP)
 Prophylactic administration of antibiotics is not recommended,
and levofloxacin can be detrimental in acute stroke patients
(Class II, Level B)
 Early rehydration and graded compression stockings are
recommended to reduce the incidence of venous
thromboembolism (Class IV, GCP)
 Early mobilization is recommended to prevent compli-cations
such as aspiration pneumonia, DVT and pressure ulcers (Class
IV, GCP)
 Low-dose s.c. heparin or low molecular weight heparins should
be considered for patients at high risk of DVT or pulmonary
embolism (Class I, Level A)
 Administration of anticonvulsants is recommended to prevent
recurrent seizures (Class I, Level A)
 Prophylactic administration of anticonvulsants to patients with
recent stroke who have not had seizures is not recommended
(Class IV, GCP)
 An assessment of falls risk is recommended for every stroke
patient (Class IV, GCP)

 Calcium/vitamin-D supplements are recommended in stroke
patients at risk of falls (Class II, Level B)
 Bisphosphonates (alendronate, etidronate and risedronate) are
recommended in women with previous fractures (Class II,
Level B)
 In stroke patients with urinary incontinence, specialist
assessment and management is recommended (Class III, Level
C)
 Swallowing assessment is recommended but there are
insufficient data to recommend a specific approach for
treatment (Class III, GCP)
 Oral dietary supplements are only recommended for non-
dysphagic stroke patients who are malnourished (Class II, Level
B)
 Early commencement of nasogastric (NG) feeding (within 48
hours) is recommended in stroke patients with impaired
swallowing (Class II, Level B)
 Percutaneous enteral gastrostomy (PEG) feeding should not be
considered in stroke patients in the first 2 weeks (Class II, Level
B)

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

Rehabilitation
• Multidisciplinary stroke team for rehabilitation
– Stroke physician
– Nurses experienced in stroke management
– Physiotherapist trained in stroke rehabilitation
– Occupational therapist skilled in stroke
– Speech therapist familiar with speech problems in
stroke patients
– Neuropsychologist accustomed to stroke rehabilitation
– Social worker familiar with the problems of stroke
patients
Setting of Rehabilitation
 Admission to a stroke unit is recommended for acute stroke
patients to receive coordinated multidisciplinary rehabilitation
(Class I, Level A)
 Early discharge from stroke unit care is possible in medically
stable patients with mild or moderate impairment providing
that rehabilitation is delivered in the community by a
multidisciplinary team with stroke expertise (Class I, Level A)

Setting of Rehabilitation
 Rehabilitation should be continued after discharge during the
first year after stroke (Class II, Level A)
 Early initiation of rehabilitation is recommended (Class III,
Level C)
 It is recommended that the duration and intensity of
rehabilitation is increased (Class II, Level B)

Elements of Rehabilitation
 Physiotherapy is recommended, but the optimal mode of
delivery is unclear (Class I, Level A)
 Occupational therapy is recommended, but the optimal mode
of delivery is unclear (Class I, Level A)
 While assessment for communication deficits is recommended,
there are insufficient data to recommend specific treatments
(Class III, GCP)
 Information should be provided to patient and carers but
evidence does not support use of a dedicated stroke liaison
service for all patients (Class II, Level B)

 Rehabilitation must be considered for all stroke patients, but
there is limited evidence to guide appropriate treatment for
the most severely disabled (Class II, Level B)
 While assessment for cognitive deficits appears desirable,
there are insufficient data to recommend specific treatments
(Class I, Level A)
 Patients should be monitored for depression during hospital
stay and throughout follow up (Class IV, Level B)

 Drug therapy and non-drug interventions are recommended to
improve mood (Class I, Level A)
 Drug therapy should be considered to treat post stroke
emotionalism (Class II, Level B)
 Tricyclic or anticonvulsant therapy are recommended to treat
post-stroke neuropathic pain in selected patients (Class III,
Level B)
 Botulinum toxin should be considered to treat post-stroke
spasticity, but functional benefits are uncertain (Class III, Level
B)

Stroke

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Stroke

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The Management of Acute

Stroke: Selected Topics

Guidelines Ischaemic Stroke 2008

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Guidelines Ischaemic Stroke 2008

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