Cerebrovascular Accident

Cerebrovascular Accident
(Stroke)
Do You really Know it..!!
Usama Ragab Yousif (Msc.)
Internal Medicine Department

Learning Objectives
• To be able to differentiate
between stroke and other
conditions
• To discuss the latest stroke
treatment strategies (either
interventional or non
interventional)
• To be able to define stroke, its pathophysiology and risk
factors
• To emphasize the role of early evaluation and
management of stroke patients

Disease makes men more physical, it leaves
them nothing but body.
Thomas Mann

Epidemiology
• Globally, about 17
million strokes occur
every year and stroke is
the second leading
cause of death after
coronary heart disease,
and the third most
common cause of
disability.
1- Krishnamurthi RV: Lancet Glob Health. 2013;1(5):e259.
Figure: http://www.who.int/mediacentre/factsheets/fs310/en/

Epidemiology
• Globally, the incidence of stroke due to ischemia is 68
%, while the incidence of hemorrhagic stroke
(intracerebral hemorrhage and subarachnoid
hemorrhage combined) is 32 %.
• Men have a higher incidence of stroke than women at
younger but not older ages, with the incidence reversed
and higher for women by age 75 years and older.
Mikulik R: J Intern Med 2015; 278: 145–165.
Lozano R, et al: Lancet. 2012 Dec;380(9859):2095-128.

Brief History of Definitions of Stroke and TIA
• The word “stroke” was likely
first introduced into medicine in
1689 by William Cole.
Before Cole, the common term
used to describe very acute
nontraumatic brain injuries was
“apoplexy.” Apoplexy was used
by Hippocrates circa 400 BC.

• The World Health Organization definition of stroke
(in 1970) is “rapidly developing clinical signs of
focal (or global) disturbance of cerebral function,
lasting more than 24 hours or leading to death,
with no apparent cause other than that of vascular
origin (time frame of 24 hours being chosen arbitrarily).
• The term brain attack was introduced for use
according to the American Stroke Association,
who since 1990 have used the term.
2- Segen's Medical Dictionary. Farlex, Inc. 2010.
1- World Health Organisation (1978). Cerebrovascular Disorders (Offset Publications). Geneva

• In 2002 then in 2009, an expert
committee of the AHA/ASA published
proposed definition that was: a
transient episode of neurological
dysfunction caused by focal brain,
spinal cord, or retinal ischemia
without acute infarction (arbitrary
time point of < 24 hours was
suspended).
During the 1950s, physicians felt the need to also introduce a term
for temporary vascular-related episodes of brain dysfunction that
would not qualify as strokes, and “transient ischemic attack” came
into use.
Stroke. 2009 Jun;40(6):2276-93.

• The International Classification of Diseases (ICD) system
aims to standardize diagnostic classification for most
diseases. Recent iterations, including the 10th revision
along with its clinical modification (ICD-11-CM) published in
2010,11 classified cerebrovascular disorders chiefly as TIA,
cerebral ischemic stroke, ICH, or SAH.

The World Health Organization’s definition of stroke is
obsolete. Based on advances including modern brain imaging,
the 24-hour inclusion criterion for cerebral infarction is
inaccurate and misleading, because permanent injury can
occur much sooner.
Sacco R L: Stroke 44 (2013): 2064-2089.

The word “transient” indicates a lack of permanence. Modern
brain imaging has shown that many patients in whom
symptoms and signs of brain ischemia are clinically transient
have evidence of brain infarction. If the ischemia caused death
of the tissue, it is misleading to designate the ischemia as
transient. Sacco R L: Stroke 44 (2013): 2064-2089.

The updated definition of stroke incorporates clinical and
tissue criteria and can be incorporated into practice,
research, and assessments of the public health.
Sacco R L: Stroke 44 (2013): 2064-2089.

 Central nervous system infarction is defined as brain,
spinal cord, or retinal cell death attributable to ischemia,
based on neuropathological, neuroimaging, and/or
clinical evidence of permanent injury.
 Central nervous system infarction occurs over a clinical
spectrum: either overt or silent
 Stroke also broadly includes intracerebral hemorrhage
and subarachnoid hemorrhage.
Sacco R L: Stroke 44 (2013): 2064-2089.

It is still a matter of great debate

Lacunar Infarction
• Lacunar stroke or lacunar infarct (LACI) is a type
of stroke that results from occlusion of one of the
penetrating arteries that provides blood to the brain's deep
structures.
• The term was penned by Charles Miller Fisher, a
Canadian neurologist who described "lacunes" (Latin for
"empty space") within the brains of stroke victims post
mortem, he also connected them with 5 classic
syndromes.
• Lacunar infarcts are small (<20 mm) infarcts.
Neurology. 1997 May. 48(5):1204-11.

Lacunar Infarction (cont.)
It is marked by hemiparesis or hemiplegia that
typically affects the face, arm, or leg of the
contralateral side.
Pure motor
stroke/hemiparesis (most
common lacunar syndrome:
33-50%)
It displays a combination of cerebellar and motor
symptoms, including contralateral weakness and
clumsiness.
Ataxic hemiparesis (second
most frequent lacunar
syndrome)
The main symptoms are dysarthria and
clumsiness (i.e., weakness) of the hand, which
often are most prominent when the patient is
writing.
Dysarthria/clumsy
hand (sometimes considered
a variant of ataxic
hemiparesis)
Marked by persistent or transient numbness,
tingling, pain, burning, or another unpleasant
sensation on one side of the body.
Pure sensory stroke
This lacunar syndrome involves hemiparesis or
hemiplegia with contralateral sensory impairment
Mixed sensorimotor stroke
Bamford, J et al. (1987): Stroke 18 (3): 545–51.

Review of Anatomy
• Blood reaches the brain through 2 systems:
1. The carotid system (Anterior Circulation)
2. The vertebral system (Posterior Circulation)

Review of Anatomy
The circle of Willis is a part of
the cerebral circulation and is
composed of the following arteries:
•Anterior cerebral artery (left and right)
•Anterior communicating artery
•Internal carotid artery (left and right)
•Posterior cerebral artery (left and right)
•Posterior communicating artery (left and
right)
•Basilar artery
The middle cerebral arteries, supplying the
brain, are not considered part of the circle.

Hearing/association
& Smell & taste
Short term Memory
Voluntary
Motor
Sensations
Pain & Touch
Taste
Balance,
Coordination of each
muscle group
Arms
Head
Legs
Mom: Bowel/bladder
Reasoning/judgment
Long term memory
Vision &
visual
memory
CN 5,6,7,8
P,R, B/P CN 9,10,11,12
Tracks cross over
Coordinate
movement,
HR,B/P

Pathophysiology of Ischemic stroke
Normal cerebral blood flow (CBF): > 50
mL/100gm/min of brain tissues.1
18-50 mL/100gm/min of brain = oligemia.
Less than 18 mL/100gm/min of brain =
neurological deficit due to electrical failure
(transiant; TIA or permanent; infarction)
 < 8 mL = core infarction.
8-18 mL/100gm/min of brain = Penumbra
1- Cipolla MJ. The Cerebral Circulation. San Rafael (CA):
Morgan & Claypool Life Sciences; 2009.
Figure: P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248.
Print.

Penumbra is zone of reversible
ischemia around core of irreversible
infarction—salvageable in first few
hours after
ischemic stroke onset
Penumbra damaged by:
• Hypoperfusion
• Hyperglycemia
• Fever
• Seizure
http://www.strokecenter.org/professionals/brain-
anatomy/cellular-injury-during-ischemia/the-ischemic-
penumbra/ (HON code certified)

Sir Winston Churchill
Prime Minister of the United Kingdom from
1940 to 1945 and again from 1951 to 1955
Famous People Who Died of Stroke
http://www.ranker.com/list/famous-people-who-died-of-stroke/reference

ATHEROSCLEROSIS AND THROMBOSIS
Atherosclerosis: decades-long process; progression
favored by hypercholesterolemia, HTN, cigarette smoking
•Fatty streak: yellowish discoloration on intimal surface of
blood
•Focal plaques: eccentric thickening at bifurcations; addition
of massive extracellular lipids that displaced normal cells and
matrix
•Complicated fibrous plaques: central acellular area of lipid
covered by a cap of smooth muscle cells and collagen

Risk factors for stroke
POTENTIALLY Modifiable risk factorsFixed risk factors
Blood pressure
Cigarette smoking
Hyperlipidaemia
Heart disease
Atrial fibrillation
Congestive cardiac failure
Infective endocarditis
Diabetes mellitus
Excessive alcohol intake
Oestrogen-containing drugs
Polycythaemia
Age
Gender (male > female except at
extremes of age)
Race (Afro-Caribbean > Asian >
European)
Previous vascular event
 Myocardial infarction
 Stroke
Peripheral vascular disease
Heredity
High fibrinogen
P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248. Print.

Risk factors for stroke
• Ecology and risk factors:
 Age and gender: Most thrombotic and embolic strokes related to atherosclerosis
occur in older patients. In contrast, hemorrhages (both ICH and SAH) are
common in adolescents and young adults. Cardiac-origin embolism is also
common in young people who are known to have heart disease.
 Smoking — Smoking increases the likelihood of extracranial occlusive vascular
disease, more than doubling the risk of stroke. The risk of ischemic stroke
decreases over time after smoking cessation.
 Diabetes increases the likelihood of large and small artery occlusive disease and
ischemic stroke but has not been shown to predispose to hemorrhagic stroke.
However, data from the Nurses’ Health Study suggest that type 1 diabetes might
also be a risk factor for hemorrhagic stroke.
Diabetes Care. 2007 Jul;30(7):1730-5.

Risk factors for stroke (cont.)
Heart disease — Heart
disease, including atrial
fibrillation, valvular disease,
recent myocardial infarction,
and endocarditis, increases
the probability of a stroke
due to embolism. Of these,
atrial fibrillation is the most
prominent, causing nearly
half of all cardioembolic
strokes.
Wolf et al. 1991. Stroke. 1991; 22: 983-988

 Hypertension — Hypertension is an
important stroke risk factor, including
isolated systolic hypertension.
Epidemiologic studies show that
there is a gradually increasing
incidence of both coronary disease
and stroke as the blood pressure
rises above 110/75 mmHg. Both
prior blood pressure and current
blood pressure are important risk
factors (for both ischemic and
hemorrhagic stroke).
Data from Prospective Studies Collaboration, Lancet 2002; 360:1903.

Bishop T, Figueredo VM. Hypertensive therapy: attacking the renin-angiotensin system. Western Journal of Medicine. 2001;175(2):119-124.

Howard G. Bruenn, "Clinical Notes On The Illness and Death of President Franklin D. Roosevelt," Ann. of Int. Med. 72 (1970): 579–59.
Franklin Delano Roosevelt:
represents a unique and superb
example of the natural history of
untreated hypertension and the
complications that can arise if left
untreated.
Dr Bruenn reported the President's
last words: "I have a terrific
headache.“
Of notable FDR had suffered also
from severe anemia (Hb: 4.5 gm%),
proteinuria 4+ and cholelithiasis!!!

 Other risk factors — Other risk factors for stroke include the following:
 (Dyslipidemia): Elevated total cholesterol and decreased high density
lipoprotein (HDL) cholesterol have been associated with increased risk of
ischemic stroke and large artery stroke in some, but not all, studies.
 Elevated serum lipoprotein(a) has been associated with intracranial,
extracranial, and aortic large artery occlusive disease.
 Stroke during the puerperium has an increased likelihood of being related to
venous or arterial thrombosis.
 The presence of a known bleeding disorder or prescription of warfarin or
other anticoagulants predisposes to hemorrhage, into either the brain or the CSF.
 Vascular anomaly: Arteriovenous malformation, Cavernous haemangioma.

TIA is a risk factor for future stroke
SC Johnston et al: Validation and refinement of score to predict very early stroke risk after transient ischaemic attack.
Lancet 369:283, 2007.

Potential Genetic Risk Factors for Stroke
• Apolipoprotein E4
• Elevated homocysteine levels
• Factor V mutation

Joseph Stalin
The leader of the Soviet Union from the
mid-1920s until his death in 1953

Etiology
1- Ischemic Stroke
Prothrombotic statesEmbolism
Hemostatic regulatory protein
abnormalities
Antiphospholipid antibodies
 Atrial fibrillation
 Sinoatrial disorders
 Recent MI
 Endocarditis
 Cardiac tumors
 Valvular disorders
 Patent foramen ovale
 Carotid/basilar artery
stenosis
 Atherosclerotic lesions
 Vasculitis

Etiology
1- Ischemic Stroke (cont.)

Etiology
2- Hemorrhagic Stroke
 Chronic HTN
 Cerebral Amyloid Angiopathy
 Anticoagulation
 AVM
 Ruptured aneurysm (usually subarachnoid)
 Tumor
 Sympathomimetics
 Infection
 Trauma
 Transformation of ischemic stroke
 Physical exertion, Pregnancy
 Post-operative

Etiology
Aneurysm
• Localized dilation of arterial lumen
• Degenerative vascular disease
• Bifurcations of circle of Willis
– 85% anterior
– 15% posterior

• AVM
– Tangled mass of arteries and veins
– Seizure or ICH

So, in brief stroke is either:

Presentation
• Sudden onset
• Focal neurological deficit
• Progresses over minutes to hours
• Depends on location
• Symptoms include:
 SUDDEN numbness or weakness of face, arm or leg
 SUDDEN confusion, trouble speaking or understanding.
 SUDDEN trouble with vison.
 SUDDEN trouble walking, dizziness, loss of balance or coordination.
 SUDDEN severe headache.

Presentation (cont.)

Clinical Clue to diagnosis
Stroke type Clinical course Risk factors Other clues
Intracerebral
hemorrhage
Gradual progression during
minutes or hours
Hypertension, trauma, bleeding
diatheses, illicit drugs (eg,
amphetamines, cocaine),
vascular malformations. More
common in blacks and Asians
than in whites.
May be precipitated by sex or
other physical activity. Patient
may have reduced alertness.
Subarachnoid
hemorrhage
Abrupt onset of sudden, severe
headache. Focal brain
dysfunction less common than
with other types.
Smoking,
hypertension, moderate to
heavy alcohol use, genetic
susceptibility (eg, polycystic
kidney disease, family history of
subarachnoid hemorrhage) and
sympathomimetic drugs (eg,
cocaine)
May be precipitated by sex or
other physical activity. Patient
may have reduced alertness.
Ischemic
(thrombotic)
Stuttering progression with
periods of improvement.
Lacunes develop over hours or
at most a few days; large artery
ischemia may evolve over
longer periods.
Atherosclerotic risk factors (age,
smoking, diabetes mellitus,
etc.). Men affected more
commonly than women. May
have history of TIA.
May have neck bruit.
Ischemic (embolic)
Sudden onset with deficit
maximal at onset. Clinical
findings may improve quickly.
Atherosclerotic risk factors as
listed above. Men affected more
commonly than women. History
of heart disease (valvular, atrial
fibrillation, endocarditis).
Can be precipitated by getting
up at night to urinate, or sudden
coughing or sneezing.
Caplan, L. Overview of the evaluation of stroke. In: UpToDate, Kanser S (Ed), UpToDate, Waltham, MA. (Accessed on December 2015.)

Charles Dickens
English writer and social critic

Time is BRAIN
• The longer the time period that the person remains
unresponsive, the less likely it is that the person will
recover.
• It has calculated that in a typical large-vessel acute
ischaemic stroke, about 1.9 million neurons die every
minute during which stroke is untreated, 14 billion
synapses, and 12 km (7.5 miles) of myelinated fibers are
destroyed.1
• The first few days after onset is critical.
1- Saver, J. L. (2006). Time is brain—quantified. Stroke, 37(1), 263-266.

Assessment
Stroke Signs – Cincinnati Stroke Scale (Smile, Wave, Talk)
Interpretation: if any of these 3 signs is abnormal, the probability of a stroke is 72%

Assessment (cont.)
Teasdale G, Jennett B. (1974). "Assessment of coma
and impaired consciousness. A practical
scale.". Lancet 13 (2): 81–4.
Glasgow Coma Scale:
The Glasgow Coma Scale or GCS is
a neurological scale that aims to give a
reliable, objective way of recording the
conscious state of a person for initial as well as
subsequent assessment. A patient is assessed
against the criteria of the scale, and the
resulting points give a patient score between 3
(indicating deep unconsciousness) and either
14 (original scale) or 15 (the more widely used
modified or revised scale).

Assessment (cont.)
Score Description
0 No symptoms at all
1
No significant disability despite symptoms; able to carry out all usual
duties and activities
2
Slight disability; unable to carry out all previous activities, but able to
look after own affairs without assistance
3
Moderate disability; requiring some help, but able to walk without
assistance
4
Moderately severe disability; unable to walk without assistance and
unable to attend to own bodily needs without assistance
5
Severe disability; bedridden, incontinent, and requiring constant
nursing care and attention
6 Dead
Modified Rankin scale: a commonly used scale for measuring the degree of disability or dependence
in the daily activities of people who have suffered a stroke or other causes of neurological disability.
Van Swieten JC, Koudstaa PJ, Visser MC, et al. Interobserver agreement for the assessment of handicap in stroke patients.
Stroke 1988; 19:604.

• Maximum score described is 5 in which
% of mortality at 30 days is nearly 100%.
• Although an ICH Score of 6 is possible
with the scale, this is rarely observed and
is considered highly likely to be fatal.
ICH Score
JC Hemphill et al: Stroke 32:891, 2001; JC Hemphill et
al: Neurology 73:1088,2009.

Modified Hunt and Hess classification
For Subarachnoid Hemorrhage
Based upon initial neurologic examination; adapted from: Hunt W, Hess R, J Neurosurg 1968; 28:14.

World Federation of Neurosurgeon (WFNS)
For Subarachnoid Hemorrhage
Based upon data from: Report of World Federation of Neurological Surgeons Committee on a Universal
Subarachnoid Hemorrhage Grading Scale. J Neurosurg 1988; 68:985.

Differential Diagnosis
‘Functional’ stroke mimics‘Structural’ stroke mimics
Todd’s paresis (after epileptic
seizure)
Hypoglycaemia
Migrainous aura (with or without
headache)
Focal seizures
Ménière’s disease or other vestibular
disorder
Conversion disorder
Encephalitis
CO2 narcosis
Primary cerebral tumours
Metastatic cerebral tumours
Subdural haematoma
Cerebral abscess
Peripheral nerve lesions (vascular or
compressive)
Demyelination
P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014.
1231-248. Print.

By the year 2000 the commonest killers such
as coronary heart disease, stroke, respiratory,
diseases and many cancers will be wiped out.
Anonymous
Irish Times (24 Apr 1987)

Al Capone
American gangster

Investigations
Investigation of acute stroke aims to confirm the vascular
nature of the lesion, distinguish cerebral infarction from
haemorrhage and identify the underlying vascular disease
and risk factors

Investigations (cont.)
Diagnostic question
CT/MRIIs it a vascular lesion?
CT/MRIIs it ischaemic or haemorrhagic?
CT/lumbar punctureIs it a subarachnoid haemorrhage?
Electrocardiogram (ECG)
24-hour ECG
Echocardiogram
Is there any cardiac source of embolism?
Duplex ultrasound of carotids
Magnetic resonance
angiography (MRA)
CT angiography (CTA)
Contrast angiography
What is the underlying vascular disease?
Full blood count
Cholesterol
Blood glucose
What are the risk factors?
Erythrocyte sedimentation rate
Serum protein electrophoresis
Clotting/thrombophilia screen
Is there an unusual cause?

Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from
ICH (Class I; Level of Evidence A)
For diagnosing ischemic stroke in the emergency setting:
CT scans (without contrast enhancements):
sensitivity= 16%specificity= 96%
MRI scan:
For diagnosing hemorrhagic stroke in the emergency setting:
CT scans (without contrast enhancements):
MRI scan:
Contrast-enhanced CT scans add specificity by showing contrast enhancement of subacute
infarcts and allow visualization of venous structures. Coupled with multidetector scanners, CT
angiography (CTA) can be performed with administration of IV iodinated contrast allowing
visualization of the cervical and intracranial arteries, intracranial veins, aortic arch, and even
the coronary arteries in one imaging session.
Hemphill et al. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. Stroke. 2015;46:000-
000. DOI: 10.1161/STR.0000000000000069.

 CT imaging is also sensitive for detecting SAH (although by itself does not rule
it out), and CTA can readily identify intracranial aneurysms.
 Because of its speed and wide availability, noncontrast head CT is the imaging
modality of choice in patients with acute stroke, and CTA and CT perfusion
imaging may also be useful and convenient adjuncts.
MRI reliably documents the extent and location of infarction in all areas of the
brain, including the posterior fossa and cortical surface.
MRI scanners with magnets of higher field strength produce more reliable and
precise images. Diffusion-weighted imaging is more sensitive for early brain
infarction than standard MR sequences or CT, as is fluid-ttenuated
inversion recovery (FLAIR) imaging. Using IV administration of gadolinium
contrast, MR perfusion studies can be performed. Brain regions showing poor
perfusion but no abnormality on diffusion provide, compared to CT, an
equivalent measure of the ischemic penumbra.

Cerebral Angiography
 Conventional x-ray cerebral angiography is the gold standard for identifying
and quantifying atherosclerotic stenoses of the cerebral arteries and for
identifying and characterizing other pathologies, including aneurysms,
vasospasm, intraluminal thrombi, fibromuscular dysplasia, arteriovenous
fistulae, vasculitis, and collateral channels of blood flow.
 Conventional angiography carries risks of arterial damage, groin hemorrhage,
embolic stroke, and renal failure from contrast nephropathy, so it should be
reserved for situations where less invasive means are inadequate.

A. Computed tomography (CT)
perfusion mean-transit time
map showing delayed
perfusion of the left MCA
distribution (blue).
B. Predicted region of infarct
(red) and penumbra (green)
based on CT perfusion data.
C. Conventional angiogram
showing occlusion of the left
internal carotid–MCA
bifurcation (b4 & after
successful thrombectomy).
D. The clot rmoved by
thrombectomy device.
E. CT scan of the brain 2 days
later; note infarction in the
region predicted in B but
preservation of the
penumbral region by
successful revascularization.

A. MRI diffusion-weighted image
(DWI) of an 82-year-old woman 2.5 h
after onset of right-sided weakness and
aphasia reveals restricted diffusion
within the left basal ganglia and internal
capsule (colored regions).
B. Perfusion defect within the left hemisphere
(colored signal) imaged (gadolinium contrast). The discrepancy between
the region of poor perfusion shown in B and the diffusion deficit shown in
A is called diffusion-perfusion mismatch and provides an estimate of the
ischemic penumbra.
C. Fluid-attenuated inversion recovery image obtained 3 days later
showing a region of infarction (coded as white) that corresponds to the
initial DWI image in A, but not the entire area at risk shown in B,
suggesting that successful embolectomy

 Ultrasound Techniques
Stenosis at the origin of the internal carotid artery can be identified and
quantified reliably by ultrasonography that combines a B-mode ultrasound
image with a Doppler ultrasound assessment of flow velocity (“duplex”
ultrasound). Transcranial Doppler (TCD) assessment of MCA, ACA, and
PCA flow and of vertebrobasilar flow is also useful.
However, its sensitivity & specificity is expert
dependent…

Carotid Doppler US:
Stenosis more than 70% should raise our mind to possible intervention

Infarction appears as hypodense (more dark) area on CT
Hemorrhage appeare as hyperdesne (bright) area on CT

Modified Fisher scale on CT brain (predict risk of vasospasm):
Risk of vasospasmIVHSAH
24%-No or minimalGrade I
33%+MinimalGrade II
33%-Diffuse focal or thickGrade III
40%+Diffuse focal or thickGrade IV
Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified
Fisher Scale." Neurosurgery 59.1 (2006): 21-27.

Fisher, CM, Kistler, JP, Davis, JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by CT
scanning. Neurosurgery 1980; 6:1.
Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified
Fisher Scale." Neurosurgery 59.1 (2006): 21-27.

Louis Pasteur
French chemist and microbiologist

Treatment
The era of interventional therapy (Not Egypt)
NINDS* and ACLS** Recommended Stroke Evaluation Time Benchmarks for
Potential Thrombolysis Candidate
*National Institute of Neurological Disorders and Stroke
**Advanced Cardiac Life Support guidelines
Time Interval Time Target
Door to doctor 10 min
Access to neurologic
expertise
15 min
Door to CT scan completion 25 min
Door to CT scan interpretation 45 min
Door to treatment 60 min
Admission to stroke unit or
ICU
3 h

1- Primary Prevention
FACTORS RECOMMENDATION
Physical activity Physical activity is recommended because it is associated
with a reduction in the risk of stroke (Class I; Level of
Evidence B).
Diet Reduced intake of sodium and increased intake of potassium
as indicated in the US Dietary Guidelines for Americans are
recommended to lower BP (Class I; Level of Evidence A).
A DASH-style diet, which emphasizes fruits, vegetables, and
low-fat dairy products and reduced saturated fat, is
recommended to lower BP127,218 (Class I; Level of Evidence
A).
Hypertension Annual screening for high BP and health-promoting lifestyle
modification are recommended for patients with prehypertension
(SBP of 120 to 139 mmHg or DBP of 80 to 89 mmHg) (Class I;
Level of Evidence A).
Patients who have hypertension should be treated with
antihypertensive drugs to a target BP of <140/90 mm Hg (Class
I; Level of Evidence A).
Stroke. 2014;45:3754–3832.

1- Primary Prevention (cont.)
Dyslipidemia In addition to therapeutic lifestyle changes, treatment with an
HMG coenzyme-A reductase inhibitor (statin) medication is
recommended for the primary prevention of ischemic stroke in
patients estimated to have a high 10-year risk for cardiovascular
events as recommended (Class I; Level of Evidence A).
Obesity Among overweight (BMI=25 to 29 kg/m2) and obese (BMI >30
kg/m2) individuals, weight reduction is recommended for
lowering BP and reducing the risk of stroke (Class I; Level of
Evidence A).
Diabetes mellitus Control of BP in accordance with guidelines to a target of
<140/90 mm Hg is recommended in patients with type 1 or type
2 diabetes mellitus (Class I; Level of Evidence A).
Treatment of adults with diabetes mellitus with a statin,
especially those with additional risk factors, is recommended to
lower the risk of first stroke (Class I; Level of Evidence A).
Smoking Cessation of smoking.
Stroke. 2014;45:3754–3832.

1- Primary Prevention (cont.)
AF For patients with valvular AF at high risk for stroke, defined as a
CHA 2DS2-VASc score of ≥2 and acceptably low risk for
hemorrhagic complications, long-term oral anticoagulant therapy
with warfarin at a target INR of 2.0 to 3.0 is recommended (Class I;
For patients with nonvalvular AF, a CHA2DS2-VASc score of ≥2,
and acceptably low risk for hemorrhagic complications, oral
anticoagulants are recommended (Class I). Options include warfarin
(INR, 2.0 to 3.0) (Level of Evidence A), dabigatran (Level of
Evidence B), apixaban (Level of Evidence B), and rivaroxaban
(Level of Evidence B).
Alcohol Reduction or elimination of alcohol consumption in
heavy drinkers (Class I; Level of Evidence A).
Prophylactic
aspirin !
Aspirin is not useful for preventing a first stroke in lowrisk
individuals (Class III; Level of Evidence A).
 Aspirin is not useful for preventing a first stroke in people with
diabetes mellitus in the absence of other highrisk conditions (Class
III; Level of Evidence A).
Stroke. 2014;45:3754–3832.

Primary Prevention (cont.)
Jacobson et al. Journal of Clinical Lipidology (2014) 8, 473–488

SPRINT trial
The SPRINT Research Group N Engl J Med 2015; 373:2103-2116
9361 persons was randomly assigned were at least 50 years old with a
systolic blood pressure of 130 mm Hg or higher (180 mmHg) and an
increased cardiovascular risk, but without diabetes, to a systolic blood-
pressure target of less than 120 mm Hg (intensive treatment) or a target of
less than 140 mm Hg (standard treatment).

SPRINT trial (cont.)
All participants had at least 1 other significant cardiovascular
risk factor, including chronic kidney disease; age 75 years or
older; a previous cardiovascular event (except stroke); or an
elevated cardiovascular risk based on their Framingham risk
score.

The primary composite outcome was myocardial infarction,
other acute coronary syndromes, stroke, heart failure, or death
from cardiovascular causes. (Funded by the National Institutes
of Health; ClinicalTrials.gov

The mean baseline blood pressure among all
participants was 139.7/78.1 mm Hg.
Mean blood pressure values at 1 year into the
study were 121.4/68.7 mm Hg in the intensive
treatment group and 136.2/76.3 mm Hg in the
standard treatment group.
1- ClinicalTrials.gov. Systolic Blood Pressure Intervention Trial (SPRINT).
https://clinicaltrials.gov/ct2/show/NCT01206062?term=Systolic+Blood+Pressure+Intervention+Trial&rank=1. Accessed November 9,
2015.

The intervention was stopped early after a median
follow-up of 3.26 years in stead of December
2018 which was the Estimated Study Completion
Date1
1- ClinicalTrials.gov. Systolic Blood Pressure Intervention Trial (SPRINT).
https://clinicaltrials.gov/ct2/show/NCT01206062?term=Systolic+Blood+Pressure+Intervention+Trial&rank=1. Accessed November 9,
2015.

 The lower target group of less than 120 mm Hg systolic
blood pressure had a 25% lower relative risk for the primary
composite end point of myocardial infarction, acute coronary
syndrome, stroke, acute decompensated heart failure, and
cardiovascular death vs the group with a target of less than
140 mm Hg.

 In addition, the lower-target group had 27% lower risk for
all-cause mortality and 43% lower risk for cardiovascular
death. However, this group also had higher adverse events
such as hypotension, syncope, and acute kidney injury or
kidney failure.

Rates of serious adverse events of hypotension,
syncope, electrolyte abnormalities, and acute
kidney injury or failure, but not of injurious falls,
were higher in the intensive-treatment group than in
the standard-treatment group.

CONCLUSIONS
Among patients at high risk for cardiovascular events but
without diabetes, targeting a systolic blood pressure of less
than 120 mm Hg, as compared with less than 140 mm Hg,
resulted in lower rates of fatal and nonfatal major
cardiovascular events and death from any cause, although
significantly higher rates of some adverse events were
observed in the intensive-treatment group.

Dr Marc Pfeffer (Harvard Medical School, Boston, MA)
CAUTIONS AS REGARD STUDY
A lot of effort is required to hit this target, including initial combination therapy
and frequent office visits “marathon effort”.
Excluding diabetics is "a black hole" in the study and limits its applicability.
Only approximately half of adults achieve a blood pressure of 140 mm Hg or
less, as consistent with current recommendations.
“Physicians "shouldn't expect a 'thank you' from patients
when you add another pill to reduce their blood pressure.“1

Alfred Nobel
Swedish chemist, engineer, innovator, and
armaments manufacturer. He was the
inventor of dynamite.

2- Acute Treatment
1. supportive management-
airway, temperature, blood
pressure, blood glucose,
cardiac assessement
2. Specific treatment
according to type of stroke

Treatment (cont.)
I- General Management of Acute ischemic Stroke
Factors Recommendation
Airway &Breathing Supplemental oxygen should be provided to maintain
oxygen saturation >94% (Class I; Level of Evidence C).
Supplemental oxygen is not recommended in nonhypoxic
patients with acute ischemic stroke (Class III; Level of Evidence
B).
Mobilization Early mobilization of less severely affected patients and
measures to prevent subacute complications of stroke are
recommended (Class I; Level of Evidence C).
Blood Glucose Glucose should be monitored. Both hyperglycemia and
hypoglycemia should be avoided (Class I; Level of Evidence C).
Nutrition A formal screening procedure for dysphagia should be
performed in all patients before the initiation of oral intake to
reduce the risk of pneumonia (Class I; Level of Evidence B).
Insert a nasogastric tube if the patient fails the swallow test.
Consider PEG only if prolonged enteral feeding is required
(Class I; Level of Evidence B).Stroke. 2013;44:870-947.

Infection and
fever
Sources of hyperthermia (temperature >38°C) should be identified and
treated, and antipyretic medications should be administered to lower
temperature (Class I; Level of Evidence C).
Routine use of prophylactic antibiotics has not been shown to be
beneficial (Class III; Level of Evidence B).
Patients with suspected pneumonia or urinary tract infections should be
treated with appropriate antibiotics (Class I; Level of Evidence A).
Hypovolemia Hypovolemia should be corrected with intravenous normal saline, and
cardiac arrhythmias that might be reducing cardiac output should be
corrected (Class I; Level of Evidence C).
Seizures Clinical seizures should be treated with antiseizure drugs (Class I;
Prophylactic antiseizure medication is not recommended (Class III;
Level of Evidence B).
Prolonged
recumbency
Subcutaneous administration of anticoagulants is recommended for
treatment of immobilized patients with ischemic infarction to prevent deep
vein thrombosis (Class I; Level of Evidence A).
The use of aspirin is reasonable for treatment of patients who cannot
receive anticoagulants for prophylaxis of deep vein thrombosis (Class IIa;
Treatment (cont.)

Hypertension in acute stroke a
management dilemma
Ischemic stroke
The treatment of arterial hypertension immediately after stroke is problematic.
Observational studies have found that a rapid and steep reduction in BP during
the first 24 h after stroke onset might be harmful.1-2
Two important pathophysiologic processes should be considered during
management of acute stroke. These are:
1. Impaired cerebral autoregulation.
2. Increased intracranial pressure (ICP).
In patients with ischemic stroke, perfusion pressure distal to the obstructed vessel
is low, and the distal vessels are dilated. Thus, elevated BP is necessary to maintain
brain perfusion in borderline ischemic areas3
. Lowering of BP in patients with acute
ischemic stroke has been associated with clinical deterioration.
1- Stroke 2004; 35:520–527. 2- Neurology 2003; 61:1047–1051. 3- Stroke 2009; 40:2251–2256.

management dilemma (cont.)
Kaplan, NM. Management of hypertensive emergencies. Lancet 1994; 344:1335.

The guidelines:
In patients with markedly elevated blood pressure who do not receive fibrinolysis,
a reasonable goal is to lower blood pressure by 15% during the first 24 hours after
onset of stroke. The level of blood pressure that would mandate such treatment is
not known, but consensus exists that medications should be withheld unless the
systolic blood pressure is >220 mm Hg or the diastolic blood pressure is >120
mmHg. (Class I; Level of Evidence C)
If BP is not maintained at or below 185/110 mmHg, do not consider administering
recombinant tissue plasminogen activator (rtPA). During and after thrombolytic
therapy, BP should be maintained below 180/105 mmHg for at least 24 h (Class I;
Level of Evidence B)
Circulation 2010; 122 (Suppl 3): S818–S828.
Stroke. 2013;44:870-947.

The guidelines:
Evidence from one clinical trial indicates that initiation of antihypertensive therapy
within 24 hours of stroke is relatively safe. Restarting antihypertensive medications
is reasonable after the first 24 hours for patients who have preexisting hypertension
and are neurologically stable unless a specific contraindication to restarting
treatment is known (Class IIa; Level of Evidence B).
Stroke. 2013;44:870-947.

Treatment Recommendations
rTPA In selected patients presenting within 3 hours: IV rt-Pa (0.9mg/kg,
maximum 90mg ) with 10% given as a bolus followed by an infusion over
one hour.
Patients eligible for intravenous r-tPA should receive intravenous r-tPA
even if endovascular treatments are being considered (Class I; Level of
Evidence A).
In patients eligible for intravenous rtPA, benefit of therapy is time
dependent, and treatment should be initiated as quickly as possible. The
door-to-needle time (time of bolus administration) should be within 60
minutes from hospital arrival (Class I; Level of Evidence A).
Intravenous rtPA (0.9 mg/kg, maximum dose 90 mg) is recommended for
administration to eligible patients who can be treated in the time period of
3 to 4.5 hours after stroke onset (Class I; Level of Evidence B).
Intravenous rtPA is reasonable in patients whose blood pressure can be
lowered safely (to below 185/110 mm Hg) with antihypertensive agents,
with the physician assessing the stability of the blood pressure before
starting intravenous rtPA (Class I; Level of Evidence B).
Treatment (cont.)

American Heart Association/American Stroke Association. Stroke. 2013;44:870–947.
Inclusion criteria:
Diagnosis of ischemic stroke causing measurable neurological deficit
Onset of symptoms <3 hours before beginning treatment
Aged ≥18 years
Exclusion criteria:
χSignificant head trauma or prior stroke in previous 3 months
χSymptoms suggest subarachnoid hemorrhage
χArterial puncture at noncompressible site in previous 7 days
χHistory of previous intracranial hemorrhage
χIntracranial neoplasm, arteriovenous malformation, or aneurysm
χRecent intracranial or intraspinal surgery
χElevated blood pressure (systolic >185 mm Hg or diastolic >110 mm Hg)
χActive internal bleeding
The American Heart Association/American Stroke Association (AHA/ASA)
inclusion guidelines for the administration of rt-PA in under 3 hours are as
follows:

American Heart Association/American Stroke Association. Stroke. 2013;44:870–947.
Exclusion criteria (cont.):
χAcute bleeding diathesis
χPlatelet count <100 000/mm³
χHeparin received within 48 hours, resulting in abnormally elevated aPTT
greater than the upper limit of normal
χCurrent use of anticoagulant with INR >1.7 or PT >15 seconds
χCurrent use of direct thrombin inhibitors or direct factor Xa inhibitors with
elevated sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT;
TT; or appropriate factor Xa activity assays)
χBlood glucose concentration <50 mg/dL (2.7 mmol/L)
χCT demonstrates multilobar infarction (hypodensity >1/3 cerebral hemisphere)

Treatment Recommendations
Neuroprotective
Agents
The utility of induced hypothermia for the treatment of patients with
ischemic stroke is not well established, and further trials are recommended
(Class IIb; Level of Evidence B).
At present, no pharmacological agents with putative neuroprotective
actions have demonstrated efficacy in improving outcomes after ischemic
stroke, and therefore, other neuroprotective agents are not recommended
(Class III; Level of Evidence A).
Routine use of nutritional supplements has not been shown to be
Anticoagulant
s
Guidelines: Guidelines issued in 2013 by the American
Heart Association/American Stroke Association state that urgent
anticoagulation is not recommended for the treatment of patients with acute
ischemic stroke. Similarly, 2012 guidelines from the American College of
Chest Physicians (ACCP) recommend early aspirin therapy over
therapeutic parenteral anticoagulation for patients with acute ischemic
stroke or transient ischemic attack (TIA).
Treatment (cont.)
Stroke. 2013;44:870-947. Chest 2012; 141:e601S.

Anti Coagulation following Acute non
hemorrhagic Stroke
 While parenteral anticoagulation is not recommended during the first 48 hours
after acute ischemic stroke, oral anticoagulation is recommended for secondary
stroke prevention in patients with atrial fibrillation and other high-risk sources of
cardiogenic embolism (see later).
 The timing of its initiation for such patients is mainly dependent on the size of the
infarct, which is presumed to correlate with the risk of hemorrhagic
transformation. Thus, for medically stable patients with a small or moderate-
sized infarct, warfarin can be initiated soon (after 24 hours) after admission with
minimal risk of transformation to hemorrhagic stroke, while withholding
anticoagulation for two weeks is generally recommended for those with 1large
infarctions, 2symptomatic hemorrhagic transformation, or 3poorly controlled
hypertension.

A systematic review updated in 2015 examined the effect of anticoagulant therapy
vs. control in the early treatment of patients with acute ischemic stroke. This review
included 24 trials involving 23,748 subjects.
The anticoagulants tested were standard unfractionated heparin, low molecular
weight heparins, heparinoids, oral anticoagulants, and thrombin inhibitors. The
following were the major findings:
●Based upon 11 trials (22,776 patients), anticoagulant therapy did not reduce the
odds of death from all causes (odds ratio 1.05, 95% CI 0.98-1.12).
●Based upon eight trials (22,125 patients), anticoagulants did not reduce the odds
of being dead or dependent at the end of follow-up (odds ratio 0.99, 95% CI 0.93-
1.04).
●Although full anticoagulant therapy was associated with about 9 fewer recurrent
ischemic strokes per 1000 patients treated, it was also associated with a 9 per 1000
increase in symptomatic intracranial hemorrhages.
Sandercock PA, Counsell C, Kane EJ. Anticoagulants for acute ischaemic stroke. Cochrane Database Syst Rev 2015; 3:CD000024.
Anti Coagulation following Acute non
hemorrhagic Stroke (con.)

Atrial fibrillation and cardioembolic
stroke
A subject of intense debate is the role of immediate anticoagulation with heparin in
stroke patients with atrial fibrillation (AF).
A 2007 meta-analysis examined seven trials involving 4624 patients and compared
heparin or low molecular weight heparins started within 48 hours for acute
cardioembolic stroke with other treatments (aspirin or placebo). The following
observations were reported:
●Anticoagulants were associated with a statistically non significant reduction in
recurrent ischemic stroke within 7 to 14 days (3.0 vs. 4.9 %, odds ratio [OR] 0.68,
95% CI 0.44-1.06)
●Anticoagulants were associated with a statistically significant increase in
symptomatic intracranial hemorrhage (2.5 vs. 0.7 %, OR 2.89, 95% CI 1.19-7.01)
●Anticoagulants and other treatments had a similar rate of death or disability at final
follow-up (≈ 74%)
Thus, the results do not support early anticoagulant treatment of acute
cardioembolic stroke
Paciaroni M, et al. Stroke 38.2 (2007): 423-430.

Progressing stroke
(Stroke in evolution)
• Heparin was once widely used to treat patients who
continued to have neurologic deterioration in the first
hours or days after ischemic stroke.
• Urgent anticoagulation, with the goal of preventing early
recurrent stroke, halting neurological worsening, or
improving outcomes after acute ischemic stroke, is not
recommended for treatment of patients with acute
ischemic stroke (Class III; Level of Evidence A).
JAMA 1998; 279:1265.
Rödén-Jüllig A &Britton M. J Intern Med 2000; 248:287.

Anti Platelets following Acute Stroke
Recommendations
ASA/AHA, 20131 NICE, 20082
 Oral administration of aspirin (initial dose
is 325 mg) within 24 to 48 hours after
stroke onset is recommended for
treatment of most patients (Class I; Level
of Evidence A).
 The usefulness of clopidogrel for the
treatment of acute ischemic stroke is not
well established (Class IIb; Level of
Evidence C).
 The use of aspirin is reasonable for
treatment of patients who cannot receive
anticoagulants for prophylaxis of deep
vein thrombosis (Class IIa; Level of
Evidence A).
All people presenting with acute stroke
who have had a diagnosis of primary
intracerebral haemorrhage excluded by
brain imaging should, as soon as possible
but certainly within 24 hours, be given:
aspirin 300 mg orally if they are not
dysphagic or
aspirin 300 mg rectally or by enteral
tube if they are dysphagic.
People with disabling ischaemic stroke
who are in atrial fibrillation should be
treated with aspirin 300 mg for the first
2 weeks before considering anticoagulation
treatment.
1- Stroke. 2013;44:870-947.
2- National Institute for Health and Clinical Excellence (NICE) (2008):
Stroke: Diagnosis and initial management of acute stroke and transient
ischaemic attack (TIA)

Anti Platelets following Acute Stroke
Recommendations
ACCP, 2012
 In patients with acute ischemic stroke or transient ischemic attack (TIA), we recommend
early (within 48 h) aspirin therapy at a dose of 160 to 325 mg over no aspirin therapy
(Grade 1A).
 In patients with acute ischemic stroke or TIA, we recommend early (within 48 h) aspirin
therapy with an initial dose of 160 to 325 mg over therapeutic parenteral anticoagulation
(Grade 1A).
 In patients with a history of ischemic stroke or TIA and atrial fibrillation, including
paroxysmal AF, who are unsuitable for or choose not to take an oral anticoagulant (for
reasons other than concerns about major bleeding), we recommend combination
therapy with aspirin and clopidogrel over aspirin (Grade 1B).
Chest . 2012;141(2_suppl):e601S-e636S.

Single antiplatelet agents
Chinese Acute Stroke Trial (CAST)2International Stroke Trial (IST)1
21,100 patients19.435 patients with suspected acute
ischemic stroke
Patients allocated to aspirin (300 mg)
within 48 hours of symptom onset
60 mg of aspirin daily or placebo, also
within 48 hours of the onset of acute
ischemic stroke
Aspirin-allocated patients experienced
a 14 percent reduction in total
mortality at four weeks (3.3 versus 3.9
percent).
significant reductions in the 14-day
recurrence of ischemic stroke (2.8
versus 3.9 percent) and in the
combined outcome of nonfatal stroke
or death (11.3 versus 12.4 percent).
IST and CAST trials3
The combined data demonstrated a reduction of 13 per 1000 patients after
several weeks to six months of follow-up
1- Lancet 1997; 349:1569. 2- Lancet 1997; 349:1641. 3- Stroke 2000; 31:1240.

Dual antiplatelet agents
Circulation 2013; 128:1656.
 A 2013 meta-analysis of early dual antiplatelet therapy versus monotherapy for
patients with noncardioembolic acute ischemic stroke or TIA identified 14 trials
with over 9000 adults.
 Dual antiplatelet therapy significantly reduced risk of stroke recurrence (risk
ratio, 0.69; 95% confidence interval, 0.60-0.80; P<0.001) and the composite
outcome of stroke, TIA, acute coronary syndrome, and all death (risk ratio,
0.71; 95% confidence interval, 0.63-0.81; P<0.001) when compared with
monotherapy, and non significantly increased risk of major bleeding (risk ratio,
1.35; 95% confidence interval, 0.70-2.59, P=0.37).

Treatment (cont.)
II- General Management of Acute hemorrhagic Stroke
Factors Recommendation
Airway
&Breathing
Supplemental oxygen should be provided to maintain
oxygen saturation >94% (Class I; Level of Evidence C).
Supplemental oxygen is not recommended in nonhypoxic patients
with acute ischemic stroke (Class III; Level of Evidence B).
Mobilization Early mobilization of less severely affected patients and measures
to prevent subacute complications of stroke are recommended
(Class I; Level of Evidence C).
Blood Glucose Glucose should be monitored. Both hyperglycemia and
hypoglycemia should be avoided (Class I; Level of Evidence C).
Nutrition A formal screening procedure for dysphagia should be performed
in all patients before the initiation of oral intake to reduce the risk of
pneumonia (Class I; Level of Evidence B).
Insert a nasogastric tube if the patient fails the swallow test.
Consider PEG only if prolonged enteral feeding is required (Class
I; Level of Evidence B).
Stroke. 2015; 46: 3020-3035

Infection and
fever
Treatment of fever after ICH may be reasonable (Class IIb; Level of
Evidence C).
Sources of hyperthermia (temperature >38°C) should be identified and
treated, and antipyretic medications should be administered to lower
temperature in hyperthermic patients with stroke (Class I; Level of
Evidence C).
Routine use of prophylactic antibiotics has not been shown to be
Patients with suspected pneumonia or urinary tract infections should be
treated with appropriate antibiotics (Class I; Level of Evidence A).
Seizures Clinical seizures should be treated with antiseizure drugs (Class I;
Prophylactic antiseizure medication is not recommended (Class III;
Treatment (cont.)

Prolonged
recumbency
As regard ICH, After documentation of cessation of bleeding, lowdose
subcutaneous low-molecular-weight heparin or unfractionated heparin
may be considered for prevention of venous thromboembolism in
patients with lack of mobility after 1 to 4 days from onset (Class IIb;
Patients with ICH should have intermittent pneumatic compression for
prevention of venous thromboembolism beginning the day of hospital
admission (Class I; Level of Evidence A).
Hemostasis
and
Coagulopathy
Patients with a severe coagulation factor deficiency or severe
thrombocytopenia should receive appropriate factor replacement therapy
or platelets, respectively (Class I; Level of Evidence C).
Patients with ICH whose INR is elevated because of VKA should have
their VKA withheld, receive therapy to replace vitamin K–dependent
factors and correct the INR, and receive intravenous vitamin K (Class I;
Level of Evidence C).
Treatment (cont.)

Hemorrhagic stroke
The conflict1
:
(1) Severe elevations in BP may worsen ICH.
(2) Enlargement of the hematoma is associated with neurologic deterioration and
worse outcomes. These observations indicate that significant improvements in
patient outcome from ICH can be achieved by minimizing hematoma
enlargement.
1- Stroke 2007; 38:1072–1075.

The guidelines:
For ICH patients presenting with SBP between 150 and 220 mm Hg and without
contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe
(Class I; Level of Evidence A) and can be effective for improving functional
outcome (Class IIa; Level of Evidence B).
For ICH patients presenting with SBP >220 mmHg, it may be reasonable to
consider aggressive reduction of BP with a continuous intravenous infusion and
frequent BP monitoring (Class IIb; Level of Evidence C).
Stroke. 2015; 46: 3020-3035

Studies have been carried out in that respect:
(1) In a randomized controlled trial [INTensive Blood Pressure Reduction in Acute
Cerebral Hemorrhage trial (INTERACT1)]1 on 404 patients with acute
spontaneous ICH, intensive BP lowering treatment (target SBP 140 mmHg),
compared with traditional management (target SBP 180 mmHg), was associated
with a reduction in hematoma growth at 24 h (14 vs. 26%). The study showed
that SBP greater than 140–150 mmHg within 12 h of ICH is associated with more
than double the risk of subsequent death or dependency. Most recently, the main
phase [(INTERACT2)]2 trial has shown no increase in death or serious adverse
events from early intensive BP lowering in eligible patients with elevated SBP.1
(2) The Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial
further confirmed these findings.3
1- Stroke. 2012;43:2236–2238. 2- N Engl J Med. 2013;368:2355–2365. 3- Neurocrit Care 2007; 6:56–66.

3- Secondary Prevention
The major treatable atherosclerotic risk factors for stroke are the following:
●Hypertension
●Diabetes mellitus
●Smoking
●Dyslipidemia
Factors
Treatment
Recommendations
Hypertension
Initiation of BP therapy is indicated for previously untreated patients
with ischemic stroke or TIA who, after the first several days, have an
established BP ≥140 mm Hg systolic or ≥90 mm Hg diastolic (Class I;
Resumption of BP therapy is indicated for previously treated patients
with known hypertension for both prevention of recurrent stroke and
prevention of other vascular events in those who have had an ischemic
stroke or TIA and are beyond the first several days (Class I; Level of
Evidence A).
ASA/AHA. Stroke. 2014; 45: 2160-2236

3- Secondary Prevention (cont.)
Factors
Treatment
Recommendations
Hypertension
(cont.)
Goals for target BP level or reduction from pretreatment baseline
are uncertain and should be individualized, but it is reasonable to
achieve a systolic pressure <140 mm Hg and a diastolic pressure
<90 mm Hg (Class IIa; Level of Evidence B).
For patients with a recent lacunar stroke, it might be reasonable
to target a systolic BP of <130 mm Hg (Class IIb; Level of
Evidence B).
Glucose
disorders
After a TIA or ischemic stroke, all patients should probably be
screened for DM with testing of fasting plasma glucose, HbA1c, or
an oral glucose tolerance test. (Class IIa; Level of Evidence C).

Factors
Treatment
Recommendations
Dyslipidemia Statin therapy with intensive lipid-lowering effects is recommended to
reduce risk of stroke and cardiovascular events among patients with
ischemic stroke or TIA presumed to be of atherosclerotic origin and an
LDL-C level ≥100 mg/dL with or without evidence for other
ASCVD (Class I; Level of Evidence B).
Statin therapy with intensive lipid-lowering effects is recommended to
reduce risk of stroke and cardiovascular events among patients with
ischemic stroke or TIA presumed to be of atherosclerotic origin, an
LDL-C level <100 mg/dL, and no evidence for other clinical
ASCVD (Class I; Level of Evidence C).
Obesity All patients with TIA or stroke should be screened for obesity with
measurement of BMI (Class I; Level of Evidence C).

Factors
Treatment
Recommendations
Intracranial
atherosclero
sis
For patients with recent stroke or TIA (within 30 days) attributable to severe
stenosis (70%–99%) of a major intracranial artery, the addition of clopidogrel
75 mg/d to aspirin for 90 days might be reasonable(Class IIb; Level of
Evidence B).
For patients with a stroke or TIA attributable to 50% to 99% stenosis of a
major intracranial artery, maintenance of systolic BP below 140 mm Hg and
high-intensity statin therapy are recommended(Class I; Level of Evidence
B).
AF For patients who have experienced an acute ischemic stroke or TIA with no
other apparent cause, prolonged rhythm monitoring (≈30 days) for AF is
reasonable within 6 months of the index event (Class IIa; Level of Evidence
C).
VKA therapy (Class I; Level of Evidence A), apixaban (Class I; Level of
Evidence A), and dabigatran (Class I; Level of Evidence B) are all indicated
for the prevention of recurrent stroke in patients with nonvalvular AF, whether
paroxysmal or permanent.

Factors
Treatment
Recommendations
AF (cont.)
Rivaroxaban is reasonable for the prevention of recurrent stroke in
patients with nonvalvular AF (Class IIa; Level of Evidence B).
For patients with ischemic stroke or TIA and AF who are unable to take
oral anticoagulants, aspirin alone is recommended (Class I; Level of
Evidence A). The addition of clopidogrel to aspirin therapy, compared with
aspirin therapy alone, might be reasonable (Class IIb; Level of Evidence
B).
For most patients with a stroke or TIA in the setting of AF, it is
reasonable to initiate oral anticoagulation within 14 days after the onset of
neurological symptoms (Class IIa; Level of Evidence B).
In the presence of high risk for hemorrhagic conversion (ie, large infarct,
hemorrhagic transformation on initial imaging, uncontrolled hypertension,
or hemorrhage tendency), it is reasonable to delay initiation of oral
anticoagulation beyond 14 days (Class IIa; Level of Evidence B).

Factors
Treatment
Recommendations
Antiplatelet
For patients with noncardioembolic ischemic stroke or TIA, the use of
antiplatelet agents rather than oral anticoagulation is recommended to
reduce the risk of recurrent stroke and other cardiovascular events (Class
Aspirin (50–325 mg/d) monotherapy (Class I; Level of Evidence A) or
the combination of aspirin 25 mg and extended-release dipyridamole 200
mg twice daily (Class I; Level of Evidence B) is indicated as initial
therapy after TIA or ischemic stroke for prevention of future stroke.
Clopidogrel (75 mg) monotherapy is a reasonable option for secondary
prevention of stroke in place of aspirin or combination aspirin/dipyridamole
(Class IIa; Level of Evidence B).
The combination of aspirin and clopidogrel might be considered for
initiation within 24 hours of a minor ischemic stroke or TIA and for
continuation for 21 days (Class IIb; Level of Evidence B).

Treatment (cont.)
Embolectomy
The idea…..

Treatment (cont.)
The Merci Retrieval System
Removal of the clot may be attempted in
those where it occurs within a large blood
vessel and may be an option for those who
either are not eligible for or do not improve
with intravenous thrombolytics.

Treatment (cont.)
The Merci Retrieval System
The guidelines: Patients eligible for intravenous r-tPA should receive
intravenous r-tPA even if endovascular treatments are being considered
(Class I; Level of Evidence A).
As with intravenous r-tPA, reduced time from symptom onset to reperfusion
with endovascular therapies is highly associated with better clinical outcomes.
To ensure benefit, reperfusion should be achieved as early as possible and
within 6 hours of stroke onset (Class I; Level of Evidence B).
Use of stent retrievers is indicated in preference to the MERCI device. (Class
AHA/ASA Stroke. 2015; 46: 3020-3035

Treatment (cont.)
Known Factors That Cause Stroke Progression
• Hypotension
• Hyperglycemia
• Hyperthermia
• Infection
• Cerebral hypoperfusion
These factors affect penumbra………………

ACS vs. Stroke
The success of thrombolytic therapy in coronary occlusive syndromes
created high expectations for thrombolytic therapy in acute, ischemic stroke,
and these expectations prompted a massive effort to create “stroke centers”
in major hospitals, each with a “stroke team” to direct the management of
acute stroke. The following is an accounting of what this effort has
accomplished:
Number of strokes each year in the United States 700,0001
Number of ischemic strokes (88% ) 616,000
Number of stroke patients who receive lytic therapy (2%) 12,320
Number of patients who benefit from lytic therapy (1 in 9) 1,369
% of strokes that benefit from lytic therapy (1369/700,000) 0.2%
True Story….
1- Mozzafarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the
American Heart Association.Circulation. 2015:e29–322.

Overall Bottom Line
Remember
• “Time is brain”
• Stroke awareness: health care team, info for everyone
• Common mistakes may lead to fatal consequences
• “There is no Stroke Motel”: Patients will receive best care; if
length of stay shortened

Yasser Arafat
Palestinian leader
Died on 11 November 2004 at the age of 75 of
what French doctors called a massive
hemorrhagic cerebrovascular accident
(hemorrhagic stroke).

Cerebrovascular Accident

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