S.

Tentishev memorial Asian Medical Institute

Cerebrovascular diseases
Ischemic and Hemorrhagic stroke

lecturer: Alymidin kyzy Ayjarkyn

Kant 2024
Cerebrovascular diseases
include a variety of disorders that affect
the blood vessels of the brain and the cerebral
circulation.
In cerebrovascular disease an area of the
brain is temporarily or permanently affected
by ischemia or bleeding and one or more of
the cerebral blood vessels are involved in the
pathological process.
 Classification of CVD
TIA

Ischemic stroke
Acute disturbance
of cerebral
circulation
Hemorrhagic
Cerebrovascular stroke
diseases
Chronic
disturbance of
Vascular dementia
cerebral circulation
 What is a Stroke?
• Stroke is the acute onset of a focal neurologic
deficit resulting from decreased perfusion to
the brain, or bleeding to brain tisssue (SAH,
incracerebral) causing permanent tissue
damage (an infarction or hemorrhage).
• Strokes are usually the result of vascular
disease.
• The symptoms of a stroke depend on the part
of the brain involved.
• 85% are ischemic (interruption of blood)
• 15% are hemorrhagic (bleeding)
 An Updated Definition of Stroke for the 21st Century by AHA/ASA
(American Heart Association/American Stroke Association)

• Stroke is a neurological deficit attributed to an

acute focal injury of the central nervous
system by a vascular cause, including cerebral
infarction, intracerebral hemorrhage, and
subarachnoid hemorrhage, and is a major
cause of disability and death worldwide.
(Stroke Vol. 44, No. 7An Updated Definition of Stroke for the 21st Century)
Transient ischaemic attacks - TIAs
definition
Difference between TIAs and Stroke
NEW DEFINITION of TIAs
a TIA is a brief episode of neurologic dysfunction
caused by focal brain or retinal ischemia, with
clinical symptoms typically lasting less than one
hour, and without evidence of acute infarction.

The corollary is that persistent clinical signs or

characteristic imaging abnormalities define
infarction — that is, stroke
 Old TIA Definition
“Transient ischemic attacks” – are the episodes of focal
neurological symptoms due to inadequate blood
supply to the brain, witch resolves in 24 hours, that
improve without causing damage to the brain
(cerebral infarction).
• The old definition was improvement in 24 hours, BUT:
– Some patients have brain injury (cerebral infarcation) on
MRI after less than an hour, even if symptoms improve
– Some patients can have symptoms longer than 24 hours
without brain injury (cerebral infarction) on MRI
– Even brief TIAs predict increased risk of upcoming stroke
Significance, Types, and Risk
Factors of Stroke
 Significance of Stroke

• Stroke is second-leading cause of death

(11,6% of total deaths) and the third-leading
cause of death and disability combined (5,7%
of total DALYs) in 2019.

Source
https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(21)00252-0/fulltext
2021 Heart Disease & Stroke Statistical Update Fact Sheet Global Burden of Disease

2019:
In 2019:
• incident cases (new cases) of stroke were
12, 2 million.
• Global prevalence of stroke in 2019 was 101.5
million people in worldwide.
2021 Heart Disease & Stroke Statistical Update Fact Sheet Global Burden of Disease

• In 2019, there were 6.6 million deaths attributable to

cerebrovascular disease worldwide.

• Globally in 2019:
– 3.3 million individuals died of ischemic stroke,
– 2.9 million died of intracerebral hemorrhage,
– 0.4 million died of subarachnoid hemorrhage

Cerebrovascular disease accounts not only for 11,6 % of all deaths;

it is the leading cause of disability in patients surviving the insult.
 Global, regional, and national burden of stroke and its risk factors, 1990–2019: a
systematic analysis for the Global Burden of Disease Study 2019

• From 1990 to 2019:

– the absolute number of incident strokes increased by
70,0% (67,0–73,0),
– prevalent strokes increased by 85,0% (83,0–88,0),
– deaths from stroke increased by 43,0% (31,0–55,0),
– DALYs due to stroke increased by 32,0% (22,0–42,0).

Without urgent implementation of effective primary

prevention strategies, the stroke burden will probably
continue to grow across the world, particularly in low-
income countries!!!
 Types of Strokes
• There are two general types of stroke –
ischemic and hemorrhagic
• Ischemic stroke occurs when blood supply to
the brain is reduced or interrupted and
accounts for around 85% of all strokes
• Hemorrhagic stroke occurs when a blood
vessel in the brain ruptures
– Sometimes an ischemic stroke can “convert” to a
hemorrhagic stroke, since blood vessels are also
injured in an area of infarction
 Types of Stroke

Ischemic Stroke Hemorrhagic stroke

 Stroke Subtypes and Incidence
Hemorrhagic stroke
Rare causes of stroke
include things like Other
15%
coagulation disorders, 5%
drug abuse, etc.
Like heart disease:
atherosclerotic plaque
causes clot or debris to
There is lots we still Cryptogenic dislodge and occlude
30% Atherosclerotic brain arteries.
don’t understand about
cerebrovascular
stroke, and sometimes
disease
there are no clear
reasons for one.
20%
Cardiogenic Small vessel
embolism disease
20% “lacunes”
25%
Ischemic stroke
85%
Chronic injury causes
local injury to small
Clots from the heart
vessels directly in the
travel to the brain (e.g.
brain.
in atrial fibrillation).
Percentage of stroke types
 Risk Factors for Stroke
Non-modifiable risk factors Modifiable risk factors
• Older age • Hypertension
• Male gender • Diabetes mellitus
• Non-white genetic background • Atrial fibrillation
• Family history • Carotid artery disease
• Prior stroke or TIA • Dyslipidemia
• Cardiac disease
• Cigarette smoking
• Obesity
• Others…

Previous TIA or stroke is the most important

risk factor for stroke.
Hypertension is the most prevalent.
Risk factors for Stroke:
In 2019, the five leading risk factors for stroke were:

• high systolic blood pressure

• high body mass index
• high fasting plasma glucose
• ambient particulate matter pollution
• smoking

due to systematic analysis for the Global Burden of Disease Study 2019/
Global, regional, and national burden of stroke and its risk factors, 1990–2019

https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(21)00252-0/fulltext
 Risk Factors:
Modifiable Risks
• Risk factors such as lifestyle habits and disease
processes can be modified or controlled

– Hypertension – the higher the blood pressure the higher

the risk of stroke
– Cholesterol – high cholesterol increases the risk of stroke:
eat low fat diet
– LDH < 130mg/dl
– HDL > 45mg/dl
- high level of total cholesterol in the blood (240 mg/dL or higher) is a
major risk factor for heart disease, which raises the risk of stroke
– Diabetes – controlling blood sugar may reduce stroke risk
– Smoking – smokers have twice the risk of non-
smokers: STOP!
– Alcohol – excessive alcohol use increases the risk for
stroke: more than 2 drinks a day
– Sedentary lifestyle – low activity level increases the
chances of stroke: workout 30-60 min 3 X week
– Obesity and increased abdominal fat – (waist
circumference greater than 40” for man and 35” for
women) increases the risk for stroke
– Atrial fibrillation – this arrhythmia is associated with
3-4 times greater stroke risk

Medications and lifestyle changes can dramatically

reduce many of these risks
 Risk Factors:
Non-Modifiable Risks
• Age – stroke increases with age and doubles for each decade
after 55
• Gender – men have an increased risk of stroke but more
women die as a result of stroke
• Heredity and race - there is a greater risk of stroke if a parent,
grandparent, sister or brother has had a stroke. Blacks have a
much higher risk of death from a stroke than Caucasians do,
partly because they are more prone to having high blood
pressure, diabetes and obesity
• Prior stroke, TIAs, or heart attack: Those who have had a stroke
are at much higher risk of having another one. Those who have
had a heart attack are also at higher risk of having a stroke
 Risk of Stroke with TIA
• 10% of patients who present to ED and are
diagnosed with a TIA will have a stroke in the
next 30 days
• 50% of those patients have their stroke in the
next 48 hours
• Risk of major stroke is increased by about 15%
for 3 months after a mild stroke or TIA

 We must treat TIAs like actual strokes in order

to prevent a major stroke
 Etiology of ischaemic stroke:
1. Occlussion:
• Atheromatous/ trombotic
– Large vessel occlusion or
stenosis
– Branch vessel occlusion
or stenosis
– Perforating vessel
occlusion (lacunar
infarction)
• Non-atheromatous
deseases of vessel wall:
– Collagen diseases (SLE)
– Vasculitis ( polyarteris
nodosa, temporal
arteritis)
– Granulamatous vasculitis
– Syphilitic vasculitis
2. Embolisation:
• Atheromatous plague
from the carotid
bifurcation/ or from
aortic arch
• Cardio embolic: valvular
heard diseases,
arrhythmias, ischemic
heard disease, bacterial
endocarditis, atrial
myxoma, cardiomyopsthy,
• Another: fat emboli; air
emboli; tumor emboli
 Etiology of ischaemic stroke:

3. Hematologic disorders: 4. Decreased cerebral

- Coagulophaties or perfusion:
- haemaglobinophaties - Arterial Hypotension
(hypercoagulable from cardiac arrhythmia
disorders) or GI bleed can lead to
infarction in watershed
between arterial
territories
 Etiology of hemorrhagic stroke
• Hypertention
• Amyloid vasculaphaty
• Aneurysm
• Arterivenous malformation
• Neoplasm
• Coagulophaties (haemophilia)
• Vasculitis
Pathophysiology of ischemic stroke
 Pathophysiology of ischemic stroke:
• The reduction or cessation of blood flow in the brain may produce different
levels of damage depending on the time elapsed, cell resistance and
magnitude of the ischemia, and activates a very complex cascade of
interrelated cellular and molecular events with a temporal overlapping
profile that evolves over minutes, hours or days, inducing injury in all cell
types and damage that can range from transient to irreversible (e.g., cell
death). This event produces two different areas of damage: the ischemic core
and the penumbra. In the ischemic core, blood flow is abruptly reduced and
the cells are permanently injured and die rapidly by necrosis. The size of this
area will depend primarily on the duration and magnitude of the ischemia
and the location of the stroke. The penumbra is located around the ischemic
core. This zone is perfused by collateral blood vessels which allow cells that
are structurally intact but functionally weakened. These functionally impaired
cells can be slowly incorporated into the ischemic stroke or saved.
• The ischemic penumbra cells can survive in this state for about three hours.
• It is very important in etiological treatment of stroke - if antitrombolitic
therapy is started in first 3 hours after acute onset, we can save this idling
cells (cells of ischemic pemumbra), and neurological deficit will be not very
wild.
Pathophysiology of cerebral infarction: Ischaemic cascade
 Ischaemic cascade
• Ischemic cascade refers to several interrelated and
overlapped pathological mechanisms that are activated after
a few minutes of blood vessel occlusion and whose progress
occurred on a different time scale. The first event of the
ischemic cascade is the reduction of oxygen and glucose
which leads to a failure to produce high-energy molecules to
maintain the cellular homeostasis.
• This sets off several mechanisms that include ionic
imbalance, glutamate- excitotoxicity, calcium overload,
cytotoxic and vasogenic edema, peri-infarct depolarization,
oxidative and nitrosative stress, blood-brain barrier (BBB)
disruption, inflammation, and apoptosis.
• All these pathological mechanisms, at finally, leads to brain
cell death –cerebral infarction.
Ischemic cascade:
 Stages of ischemic stroke

• The classification of stroke stages used here is commonly utilized in

imaging studies:
– Acute period
• The acute stage starts immediately after injury and covers the first 24 hours. In the
ischemic core, the events progress rapidly, and within minutes or hours there is
depletion of cellular energy stores, ionic imbalance, release of excitatory
neurotransmitters and inhibition of their reuptake, peri-infarct depolarization, BBB
disruption, cellular edema, and excitotoxicity, causing irreversible injury and cell
death, mainly caused by excitotoxicity, ionic imbalance and oxidative and nitrosative
stress.
– Subacude period
• This stage includes the time period from 24 hours to 5 days after stroke onset. All
the events occur in the penumbra. Several pathological mechanisms present in the
acute phase are still active in this area as vasogenic edema, BBB disruption, oxidative
and nitrosative stress, inflammation and apoptosis.
– Chronic period
• This stage includes the period of time after 5 days to months following stroke onset
and all the events occur in the penumbra. Several processes are still active, such as
vasogenic edema, apoptosis, astrogliosis, and inflammation. On day 6 after injury, a
subset of reactive astrocyte, NG2 cells, and reactive microglia start the glial scar
formation, which is completed between 2 and 4 weeks after stroke onset, beginning
a chronic state that lasts many months
 Clinical manifestations of ischaemic stroke
The clinical manifestations of ischemic stroke
will depend to a large extent on the:
 location and size of the vessel occluded,
 duration of occlusion
 adequacy of collateral circulation. These will govern
the location and extent of tissue ischemia and
infarction.
Knowing the location of the lesion and its
vascular supply allows to begin to speculate on the
underlying pathophysiology as different stroke
mechanisms characteristically affect certain
cerebral vessels.
 Specialties of cerebral circulation

1. High cerebral metabolism – high demand for oxygen and glucose.

Cerebral metabolism is highly active and requires 20% of the body's
oxygen while representing only 2% of a person's total body weight. This
suggests that the brain is highly vulnerable to hypoxia and
hypoperfusion. There are no reserves of oxygen and glucose in the
brain, so oxygen and glucose must be supplied to it continuously with
blood. Ischemic changes and infarcts evolve within minutes of low
blood flow. The brain needs and uses approximately 500 ml of oxygen
and 100 mg of glucose each minute, hence the need for a rich supply of
oxygenated blood containing glucose. Cerebral blood flow comprises
nearly 18% of cardiac output to generate 50 mL/min/100 g of brain
tissue per minute. Flow of <28 ml/min/100mg results in the
development of the morphological changes of infarction. At nearly one-
fifth of the normal flow, membrane pumps fail and the typical
electrochemical gradient is lost, leading to neuronal and glial cell death.
2. Autoregulation of cerebral circulation:

Cerebral autoregulation is a homeostatic process that regulates and maintains cerebral

blood flow (CBF) constant across a range of blood pressures. It has upper and lower
limits. In healthy adults, the limits are between 50 and 150 mm Hg cerebral perfusion
pressure (CPP) or 60 and 160 mm Hg mean arterial pressure (MAP), where CPP = MAP –
intracranial pressure (ICP). This homeostatic mechanism ensures that as MAP or CPP
increases, resistance increases (vasoconstriction) in the small cerebral arteries.
Conversely, this process maintains constant CBF by decreasing cerebrovascular resistance
or vasodilation when MAP or CPP decreases. However, given that the lower limit of
cerebral autoregulation frequently influences clinical management, it should be noted that
this value has been challenged as being too low. The limits of autoregulation are shifted to
higher values in patients with chronic uncontrolled hypertension. At the lower limit of
autoregulation, further falls in perfusion pressure will lead to a reduction in CBF.
However, this may be tolerated without symptoms. By increasing oxygen extraction from
the blood, adequate compensation can be made even if blood flow is reduced to
approximately 20-25 ml/100 g per minute. As cerebral blood flow falls further, metabolic
paralysis, initially without cell disruption, ensues and this may be reversible. However if
prolonged, infarction is inevitable. When CBF falls below 20 ml/100 g per minute oxygen
extraction starts to fall and changes may be detected on electroencephalography. At levels
below 10 ml/100 g per minute cell membrane functions are severely disrupted and the
membrane cation pumps fail to maintain cell ionic integrity. Below 5 ml/100 g per minute
cell death is inevitable within a short time.
3. A large amount of collateral circulation, the main of them - Willis circle.
Autoregulation of cerebral circulation
Normal blood suply of brain
Circle of Willis
Anterior circulation
Anterior circulation
 Posterior Circulation

This includes:
• Vertebral arteries
• Posterior inferior
cerebellar artery (PICA)
• Anterior inferior
cerebellar artery (AICA)
• Basilar artery (BA)
• Pontine arteries
• Superior cerebellar artery
(SCA)
• Posterior cerebral artery
(PCA)
 Supply areas of the cerebral arteries.
A: axial slice; B: coronal slice. (1) Anterior cerebral artery, (2) middle cerebral artery,
(3) posterior cerebral artery, (4) anterior choroidal artery, (5) lenticulostriate arteries.
Clinical classification of stroke
 Clinical syndromes of Ischemic stroke
• LARGE VESSEL OCCLUSION
The pattern of infarction after large vessel occlusion
depends on the size of the vessel occluded and the
adequacy of collateral supply. Intracranial large
vessel occlusion, such as middle cerebral artery or
its cortical branches, is more likely to be caused by
thromboembolism from the heart, aortic
atherosclerosis or internal carotid artery stenosis,
than by local occlusive disease, in contrast to
lacunar infarction.
 Occlusion of the ICA

• •can result in ischemia in both MCA and ACA

territory simultaneously.
 Middle cerebral artery

• About two-thirds of all

ischemic stroke occurs in
the middle cerebral
artery territory.
• MCA stroke can involve
the frontal, temporal, and
parietal lobes
• MCA stroke can also
involve the basal ganglia
through the
lenticulostriate arteries
Large right middle cerebral artery region infarct visualized with MRI
Left: Axial view MRI with fluid-attenuated inversion recovery (FLAIR). Area of infarct is indicated by an
arrow.
Right: MRI with diffusion-weighted imaging (DWI), infarcted area has been outlined
MCA all cortical branches syndromes
Left hemisphere (ie, dominant) Right hemisphere (ie, nondominant)
•
•Left hemiparesis or hemiplegia
• •Right hemiparesis or paralises - Variable
involvement of face and upper and lower •
•Left-sided sensory loss –
extremity hemianaestethia
• •Right-sided sensory loss – hemianastesia
• •Left homonymous hemianopia -
• Usually involves all modalities, decreased Same pattern as on right
stereognosis, and agraphesthesia, left- • •Dysarthria
right confusion
•
• •Neglect of the left side of
•Right-sided homonymous hemianopia
•
environment
•Dysarthria
• •Aphasia, (dominant) • •Anosognosia – neglect syndrome
• •Alexia, Agraphia, Acalculia, Apraxia (neglecting of conralateral paralised
extremities)
The deep branches (perforating branches) of MCA may be source of
hemorrhage or small - lacunar infarcts.
 Anterior cerebral artery
• Normal MR Angiography of MCA, ACA
 ACA occlusion syndrome
• Contralateral leg paresis
> arm paresis
• •Or, bilateral leg
weakness if both ACAs
are involved
• •Abulia, disinhibition,
executive dysfunction
• •In some cases, akinetic
mutism if bilateral
caudate head infarction
 PCA stroke syndromes:
cortical branches occlusion perforating branches
occlusion
The most common syndromes
Thalamic syndrome:
involve the occipital lobe, the
medial temporal lobe or the - Chorea or hemiballismus with
thalamus.
• Occipital lobe: contralateral
• Contralateral homonymous
hemianopia with macular sparing
hemianaesthesia
(macular area also supplied by Midbrain syndromes:
MCA) - Weber syndrome (III CN
• Cortical blindness (bilateral lesions)
palsy with contralateral
• Medial temporal lobe:
hemiplegia)
• Deficits in long-term and short-
term memory
PCA perforating branches occlusion

Thalamic syndrome:
- Chorea or hemiballismus
with
contralateral
hemianaesthesia
–Executive dysfunction
–Decreased level of
consciousness
–Memory impairment
 Basilar artery occlusion syndromes
Basilar artery occlusion can lead to reducing of blood flow into
perforating vessels supplying the central brainstem structures or the
two upper cerebellar arteries.
In the medulla, lower cranial nerves may be affected, giving rise to a
lower motor neuron type bulbar palsy. Upper motor neuron
impairment of the same structure may cause a pseudobulbar palsy,
with brisk facial reflexes, jaw jerk and a spastic tongue. This is often
accompanied by spontaneous laughter or crying (emotional lability).
Above the medulla, pontine infarction may cause a sixth nerve palsy,
gaze paresis, internuclear ophthalmoplegia and pinpoint pupils.
Emboli may lodge at the top of the basilar causing midbrain infarction
with loss of vertical eye movement, pupillary abnormalities and
coma. All these syndromes will be accompanied by quadriplegia to
some degree, which may be very asymmetric.
Partial brainstem or midbrain syndromes may also be caused by localized
occlusion of one of the perforating arteries from small vessel disease.
Paramedian perforating vessel occlusion gevis a “locked-in syndrome”.
PICA occlusion – Wallenberg syndrome
PICA occlusion – lateral medullary syndrome (Wallenberg syndrome)
 Lacunar stroke (small vessel occlusion)
• Lacunar infarction is caused by occlusion of small penetrating vessels in the
subcortical deep white matter, internal capsule, basal ganglia or pons.
• The two pathological appearances underlying small vessel occlusion are
lipohyalinosis and microatheroma.

The clinical syndromes of lacunar stroke

- patients do not have cortical signs

- Pure motor hemiparesis

- Sensorimotor hemiparesis
- Pure sensory stroke
- Ataxic hemiparesis
- Dysarthria - clumsy hand syndrome
- Hemiballismus
 Clinical diagnosis of ischemic stroke

• 1. HISTORY AND PHYSICAL EXAMINATION

- History and physical examination remain the
pillars of diagnosing stroke.
most common historical feature –
acute onset;
the most common physical findings of ischemic stroke –
focal neurological deficits, that reflect involvement
of the territory of particular cerebral blood vessel.
 Time is Brain
• Physicians need to quickly assess persons with
suspected acute ischemic stroke because
acute therapies for stroke have a narrower
time window of effectivenessof
antitrombolitic thepary. Because the exact
time of onset of symptoms is critical for
determining eligibility for thrombolysis.
 Stroke diagnostic tools
• National Institute of Health Stroke Scale
(NIHSS);
• Cincinnati Prehospital Stroke Scale
• Face, Arm, Speech Test (FAST)
• Recognition Of Stroke In the Emergency Room
scale (ROSIER)
Cincinnati Prehospital Stroke Scale
 Differential Diagnosis
• Rule out other causes of weakness or altered
mental status:
– Hypoglycemia
– Trauma (recent head injury or fall)
– Tumor (slow onset)
– Seizure disorder (post seizure paralysis)
 Investigation of stroke and transient ischaemic attack

All infarction and haemorrhage Selected patients

• Neck ultrasound or MRA

• Brain CT or MRI
Autoantibody screen
• Full blood count
• Thrombophilia screen
• Platelet count
• Syphilis serology
• ESR
• Drug screen
• Urea and electrolytes
•
• Sickle-cell test
Blood sugar
• Cholesterol • Flomocysteine
• Chest X-ray • Screening for genetic causes of
• Electrocardiogram (ECG)
stroke
• All haemorrhage
• Echocardiography 24-hour ECG
• Clotting screen • Cerebral angiography
 Management of ischemic stroke
• Treatment aims:
– Recanalise blocced vessels
– Prevent progression of present event
– Prevent immedicate complication
– Prevent the development of subsequent events
– Rehabilitate the patient
 General measures (non-differenciated treatment of Strokes

• The area of penumbra can be protected ensuring of

adequate supply of glucose and oxygen.
• Factors maintaining protection of penumbra cells:
– Hydration
– Oxygenation (oxygene saturation - 95%)
– Blood pressure ( consider treatment if 185/110). Cerebral
autoregulation is lost after stroke and therefore lowering blood
pressure may reduce important perfusion to penumbral areas.
– Glucose (maintain between 4-11 mmol/l)
– Treat chest infection and chardiac failure/arrythmias)
– Higher temperatures and increasing tissue damage from the
ischemia equates to increased intracranial pressure.
 Specific measures:
1. Trombolysis:
– i/v recombinant tissue plasminogen activator t-PA
(alteplase) in first 3 hours.
t‐PA: Indications
• The indication for t‐PA is for the management
of Acute Ischemic Stroke (AIS). It is the only
pharmacological intervention FDA approved
for the treatment of AIS.
 t‐PA - Contraindications:

• Any active internal bleeding

• Suspicion OR confirmed bleed in the brain
• If heparin was administered within 48 hours of the onset of the stroke
• Uncontrolled hypertension (185/110) at time of the infusion of t‐PA
• A seizure witnessed at the time of the stroke
• Any history of intracranial or intraspinal surgery
• Any history of intracranial bleeding
• Bleeding disorders
• A current use of anticoagulants
• Additionally, t‐PA cannot be administered if :
• • Blood glucose is <50 mg/dl or > 400mg/dl
• • There was an arterial puncture at non‐compressible site in previous
seven days
• The CT Scan show multi‐lobular infarction
 t‐PA: Dosing
• t‐PA is weight based (maximum dose 90mg):
• 0.9mg/kg
• – 10% of dose IV bolus over 1‐2 minutes
• – 90% of dose IV infusion over 1 hour
• • The nurse will bolus the calculated amount followed
by an infusion administered via a dedicated IV line.
• • If invasive lines are required they should be placed
prior to t‐PA infusion.
• • Once t‐PA is initiated blood pressure must be kept
under 185/110 to decrease the
• chance of hemorrhaging.
 t‐PA: Complications
• There are risks involved with t‐PA which
should be discussed with the patient and their
family. The risks include bleeding in the brain,
internal bleeding (non‐brain), and an allergic
reaction to t‐PA itself. Because there is such a
high risk of bleeding internally and into the
brain, frequent neurologic and invasive line
insertion site checks must be completed and
documented.
• 2. if trombolysis is contraindicated:
– Aspirin 300 mg daily for 2 weeks or
– Clopidogrel
3. To transfer to stroke unit
4. Essesment of swallowing
5. Early mobilization
6. In special situations –
decompressive hemicraniectomy
 Neurosurgical intervention in ischaemic stroke

Hemicraniectomy is sometimes performed to

decompress the brain in patients with malignant
brain oedema after total middle cerebral artery
territory infarction in the non-dominant
hemisphere, and posterior fossa craniectomy
may be indicated for cerebellar infarction with
brainstem compression. This is obviously
lifesaving in some cases and may improve the
quality of life for survivors. However,
randomized clinical trial data to support this
treatment is lacking
Interventional Radiology

If a patient is outside of the three‐hour window of IV t‐PA administration there is another intervention
option.
Mechanical embolectomy is a procedure where the clot is mechanically removed from the artery. A
neuroradiology interventionalist must be present to perform this intervention.
Intervention
• 0‐3 hours-IV t‐PA
• 3‐4.5 hours-IV t‐PA (off‐label)
• 0‐6 hours-IV t‐PA (off‐label)
• 0‐8 hours-Mechanical Embolectomy
• > than 8 hours-Anticoagulants & Antiplatelet
 Standards of Care
1. Rapid recognition
2. Rapid transport to a Primary Stroke Center
3. tPA when indicated
4. DVT (deep venous trombosus) prophylaxis
5. Discharge with anti-thrombotic treatment (eg,
aspirin)
6. Anticoagulation for atrial fibrillation
7. Dysphagia screening
8. Stroke education (risk factors, prevention, etc.)
9. Smoking cessation
10. Plan for rehabilitation
Hemorrhagic Stroke
 Hemorrhagic Stroke
 As mentioned earlier, ~ 15% of all strokes are
hemorrhagic.
 A hemorrhagic stroke is defined as a bleeding
which occurs directly into the brain.
 The mortality of this type of stroke is higher
than an ischemic stroke.
 It carries with it a 30‐day mortality rate of 32‐
52% with half of these deaths dying within two
days
 Intracerebral hemorrhage
• may be divided into a number of categories
depending on location. These are:
• Deep (centered on basal ganglia structures)
• Lobar
• Pontine
• Cerebellar hemorrhage
Common symptoms of a subarachnoid hemorrhage include:

• Severe headache — the worst headache

• Loss of consciousness
• Double vision
• Nausea or vomiting (repeated vomiting)
• Trouble speaking
• Drooping eyelid
• Confusion and trouble concentrating
• Sensitivity to light
• Neck stiffness
• Seizures
 Diagnosis
 CT
 LP
 Angiography
 Laboratory testing for revealing coagulophaties

Complications of aneurysmal SAH:

- rebleeding
- vasospasm
 Hemorrhagic stroke
• should be suspected in any patient with severe headache, vomiting,
elevated systolic blood pressures or decreased level of consciousness.
• Rapid diagnosis is crucial for appropriate care and better functional
outcomes.
• Early deterioration in the first few hours after initial onset is common,
from haematoma expansion and from secondary injury.
• In addition to a prompt clinical history and neurological examination,
rapid neuroimaging with a non-contrast head CT is highly sensitive
and specific for ICH and is the key to early diagnosis.
• CT scan will reveal not only the location and size of the ICH but also
intraventricular extension, mass effect, hydrocephalus and early signs
of herniation.
• CT angiogram is very sensitive for identifying associated vascular
abnormalities
 Appearance of ischemic and hemorrhagic strokes on CT scan. An ischemic stroke
appears dark compared to the rest of the brain, while a hemorrhagic stroke appears
bright. In both cases above, the stroke appears on the left side of the brain.
Intraventricular hemorrhage MRI
Subarachnoid hemorrhage CT scan
 Management of Hemorrhagic Stroke
1. Maintaing BP
Labetalol or nicardipine infusion for aggressive BP control if SBP>200 mm Hg. If SBP >180 mm Hg,
target SBP <160 if no elevated ICP or <140 if elevated ICP

2. Hemostatic therapy
Reverse anticoagulation as quickly as possible. The efficacy and safety of platelet transfusions in the
setting of antiplatelet-associated ICH have not been established.

3. Maintaining of ICP for protecting from cerebral edema.

If elevated ICP, need medical stabilization followed by surgical evacuation of the hematoma.
Intubation and short-term hyperventilation followed by osmotherapy with either mannitol or
hypertonic saline.
4. Seizures prophylaxis
5. Surgical treatment:
Craniotomy
Haematoma expansion
Ventricular dranage
Minimally invasive surgery:
Endovascular therapy – e/v coil embolization, clipping, stend- assisted coiling
• 6. Glucose management. Hyperglycaemia on admission is associated with worse morbidity and mortality
independent of the presence of target glucose level at 100–150 mg/dL for patients with ICH.
• 7. Fever control
• Fever is common after ICH, particularly in patients with intraventricular extension. Sustained fever after
ICH is an independent prognostic factor for worse outcome.
• 8. deep vein thrombosis prophylaxis and treatment
Prevention of stroke