Stroke is a disease that affects the arteries within the brain.
It is the 5th cause of death and a leading cause of disability in the United States.
A stroke occurs when a blood vessel that carries oxygen and nutrients to the brain is either blocked by a clot or bursts (or ruptures). When that happens, part of the brain cannot get the blood (and oxygen) it needs,and brain cells die.
4. Stroke is a disease that affects the arteries within the brain.
It is the 5th cause of death and a leading cause of disability in the
United States.
A stroke occurs when a blood vessel that carries oxygen and
nutrients to the brain is either blocked by a clot or bursts (or
ruptures). When that happens, part of the brain cannot get the
blood (and oxygen) it needs,and brain cells die.
4
5. Stroke involves abrupt onset of focal neurologic deficit that lasts
at least 24 hours and is presumed to be of vascular origin.
Stroke can be either ischemic or hemorrhagic.
Transient ischemic attacks (TIAs) are focal ischemic neurologic
deficits lasting less than 24 hours and usually less than 30 minutes.
5
7. 7
•The point prevalence of stroke in America is nearly 7 million Americans.
•Stroke is the fifth leading cause of death in the US.
•The incidence of stroke is around 800.000 people annually.
•The incidence of stroke has declined, but the morbidity has increased.
12. 12
ISCHEMIC STROKE
• Ischemic strokes (87% of all strokes) are due either to local thrombus formation or emboli
occluding a cerebral artery. Cerebral atherosclerosis is a cause in most cases, but 30% are of
unknown etiology. Emboli arise either from intra- or extracranial arteries. Twenty percent of
ischemic strokes arise from the heart.
• Carotid atherosclerotic plaques may rupture, resulting in collagen exposure, platelet
aggregation, and thrombus formation. The clot may cause local occlusion or dislodge
and travel distally, eventually occluding a cerebral vessel.
• In cardiogenic embolism, stasis of blood flow in the atria or ventricles leads to formation
of local clots that can dislodge and travel through the aorta to the cerebral circulation.
• Thrombus formation and embolism result in arterial occlusion, decreasing cerebral
blood flow and causing ischemia.
PATHOPHYSIOLOGY
14. 14
HEMORRHAGIC STROKE
Hemorrhagic strokes (13% of strokes) include subarachnoid hemorrhage (SAH),
intracerebral hemorrhage, and subdural hematomas.
SAH may result from trauma or rupture of an intracranial aneurysm or
arteriovenous malformation (AVM).
Intracerebral hemorrhage occurs when a ruptured blood vessel within the brain
causes a hematoma.
Subdural hematomas are usually caused by trauma.
Blood in the brain parenchyma damages surrounding tissue through a mass effect
and the neurotoxicity of blood components and their degradation products.
Hemorrhagic stroke can result in abrupt increased intracranial pressure leading to
herniation and death.
16. 16
Nonmodifiable risk factors or risk markers
Risk Factors
Age Gender Race
Family history
of stroke
Low birth
weight
17. 17
Hypertension—
single most
important risk
factor for ischemic
stroke
Atrial fibrillation—
most important
and treatable
cardiac cause of
stroke
Other cardiac
diseases
Diabetes—
independent risk
factor
Dyslipidemia Cigarette smoking Alcohol Sickle cell disease
Asymptomatic
carotid stenosis
Postmenopausal
hormone therapy
Lifestyle factors—
associated with
stroke risk
Obesity
Physical inactivity Diet
Modifiable, well documented
18. 18
Oral contraceptives Migraine Drug and alcohol abuse
Hemostatic and
inflammatory factors-
fibrinogen linked to
increased risk
Homocysteine Sleep-disordered breathing
Potentially modifiable, less well documented
20. 20
The patient may complain of weakness on one side of the body
Inability to speak
Loss of vision,
Vertigo, or falling.
Ischemic stroke is not usually painful, but patients may complain
of headache, and with hemorrhagic stroke, it can be very severe.
Symptoms
22. 22
• Patients usually have multiple signs of neurologic dysfunction, and the
specific deficits are determined by the area of the brain involved.
• Hemi- or monoparesis occurs commonly, as does a hemisensory deficit.
• Patients with vertigo and double vision are likely to have posterior
circulation involvement.
• Aphasia is seen commonly in patients with anterior circulation strokes.
• Patients may also suffer from dysarthria, visual field defects,and altered
levels of consciousness.
Signs
24. 24
DIAGNOSIS
• Laboratory tests for hypercoagulable states should be done only when the cause
cannot be determined based on presence of risk factors. Protein C, protein S, and
antithrombin III are best measured in steady state rather than in the acute stage.
• Computed tomography (CT) and magnetic resonance imaging (MRI) head scans can
reveal areas of hemorrhage and infarction.
• Carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram
(TTE), and transcranial Doppler (TCD) studies can each provide valuable diagnostic
information.
26. 26
TREATMENT
• Goals of Treatment: The goals are to
(1) reduce ongoing neurologic injury and decrease mortality and
long-term disability,
(2) prevent complications secondary to immobility and
neurologic dysfunction, and
(3) prevent stroke recurrence.
27. 27
NONPHARMACOLOGIC THERAPY
• Acute ischemic stroke: Surgical decompression is sometimes necessary to
reduce intracranial pressure. An interprofessional team approach that includes
early rehabilitation can reduce long-term disability. In secondary prevention,
carotid endarterectomy and stenting may be effective in reducing stroke incidence
and recurrence in appropriate patients.
• Hemorrhagic stroke: In SAH, surgical intervention to clip or ablate the vascular
abnormality reduces mortality from rebleeding. After primary intracerebral
hemorrhage, surgical evacuation may be beneficial in some situations. Insertion of
an external ventricular drain with monitoring of intracranial pressure is commonly
performed in these patients.
28. 28
PHARMACOLOGICAL THERAPY OF ISCHEMIC STROKE
• Evidence-based recommendations for pharmacotherapy of ischemic stroke are given in
Table –1.
• Alteplase (t-PA, tissue plasminogen activator) initiated within 4.5 hours of symptom
onset reduces disability from ischemic stroke. Adherence to a strict protocol is essential
to achieving positive outcomes:
(1) activate the stroke team
(2) treat as early as possible within 4.5 hours of onset
(3) obtain CT scan to rule out hemorrhage
(4) meet all inclusion and no exclusion criteria
(5) administer alteplase 0.9 mg/kg (maximum 90 mg) infused IV over 1 hour, with 10%
given as initial bolus over 1 minute
(6) avoid anticoagulant and antiplatelet therapy for 24 hours; and
(7) monitor the patient closely for elevated BP, response, and hemorrhage.
30. 30
• Aspirin 160 to 325 mg/day started between 24 and 48 hours after completion of
alteplase also reduces long-term death and disability.
• Secondary prevention of ischemic stroke:
✓ Use antiplatelet therapy in noncardioembolic stroke. Aspirin, clopidogrel, and
extended-release dipyridamole plus aspirin are all first-line agents .
Cilostazol is also a first-line agent, but its use has been limited by lack of data.
Limit the combination of clopidogrel and ASA to select patients with a recent MI
history or intracranial stenosis and only with ultra–low-dose ASA to minimize bleeding
risk.
✓ Oral anticoagulation is recommended for atrial fibrillation and a presumed cardiac
source of embolism. A vitamin K antagonist (warfarin) is first line, but other oral
anticoagulants (eg, dabigatran) may be recommended for some patients.
31. 31
• Treatment of elevated BP after ischemic stroke reduces risk of stroke recurrence.
Treatment guidelines recommend BP reduction in patients with stroke or TIA after
the acute period (first 7 days).
• Statins reduce risk of stroke by approximately 30% in patients with coronary artery
disease and elevated plasma lipids. Treat ischemic stroke patients, regardless of
baseline cholesterol, with high-intensity statin therapy to achieve a reduction of at
least 50% in LDL for secondary stroke prevention.
• Low-molecular-weight heparin or low-dose subcutaneous unfractionated heparin
(5000 units three times daily) is recommended for prevention of deep vein thrombosis
in hospitalized patients with decreased mobility due to stroke and should be used in all
but the most minor strokes.
32. 32
PHARMACOLOGICAL THERAPY OF HEMORRHAGIC STROKE
• There are no standard pharmacologic strategies for treating intracerebral
hemorrhage.
Follow medical guidelines for managing BP, increased intracranial pressure, and
other medical complications in acutely ill patients in neurointensive care units.
• SAH due to aneurysm rupture is often associated with delayed cerebral ischemia in
the 2 weeks after the bleeding episode. Vasospasm of the cerebral vasculature is
thought to be responsible for the delayed ischemia and occurs between 4 and 21
days after the bleed. The calcium channel blocker nimodipine 60 mg every 4 hours
for 21 days, along with maintenance of intravascular volume with pressor therapy, is
recommended to reduce the incidence and severity of neurologic deficits resulting
from delayed ischemia.
34. 34
EVALUATION OF THERAPEUTIC OUTCOMES
• Monitor patients with acute stroke intensely for development of neurologic
worsening (recurrence or extension), complications (thromboembolism, infection),
and adverse treatment effects.
• The most common reasons for clinical deterioration in stroke patients include:
(1) extension of the original lesion in the brain,
(2) development of cerebral edema and raised intracranial pressure,
(3) hypertensive emergency,
(4) infection (eg, urinary and respiratory tract),
(5) venous thromboembolism,
(6) electrolyte abnormalities and rhythm disturbances, and
(7) recurrent stroke. The approach to monitoring stroke patients is summarized in
Table –3.
