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STROKE Prof. Univ. Dr. Jianu Dragoș Cătălin Timișoara

Strokeneuro-vascular-dementia.eu/.../masa1/pdf/04.stroke.pdf · 2019-05-14 · Patients suspected of TIA should undergo neuroimaging: noncontrast MRI (DWI, Flair) or CT within 24

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STROKEProf. Univ. Dr. Jianu Dragoș Cătălin

Timișoara

Definition

➢ It is characterized by the sudden onset of a focal neurologic

impairment that can be ascribed to a specific location in the

brain, retina or spinal cord

➢ Can be subdivided into ischemic and hemorrhagic stroke

Hemorrhagic stroke

- Subarachnoid hemorrhage (SAH) –

caused by rupture of an intracranial

aneurysm

- Nontraumatic intracerebral

hemorrhage (ICH)

Ischemic stroke

- Lacunar

- Large arteryatherosclerotic

- Cardioembolic

- Cryptogenic

Diagnosis of Ischemic Stroke

➢ A complete neurologic examination – to localize the deficit to thecentral nervous system and inform prognosis

➢ In acute stroke – validated scales for measuring neurologicimpairment

➢ A noncontrast CT scan of the head will readily identify ICH andSAH – the initial test of choice

➢ Any patient suspected of SAH with normal CT lumbarpuncture

➢ MRI – the presence of cerebral infarction CT scan is notinformative; it can provide additional information about previousstroke or other intracranial pathology

Diagnosis of Ischemic Stroke

➢ MRI is rarely the initial imaging technique of choice

➢ CT with contrast is rarely helpful in the evaluation of brain

parenchyma

➢ Neurologic examination can provide specific neuroanatomic

localization of the stroke

➢ The examination is not sufficiently sensitive or specific to

identify the subtype of ischemic stroke vessel imaging

and cardiac evaluation are required

Diagnosis of Ischemic Stroke

■ Neurosonology

Transient Ischemic Attack (TIA)

➢ Transient focal neurologic symptoms from brain, retinal or spinalcord ischemia, was initially defined as lasting < 24 hours

➢ The absence of infarction on CT, independent of symptom duration

➢ Symptoms: are short lasting, usually 5 min to one hour

sudden-onset hemiparesis

hemisensory loss

change in speech function

loss of vision

inability to walk

TIA

➢ Patients suspected of TIA should undergo neuroimaging:noncontrast MRI (DWI, Flair) or CT within 24 hours

➢ Is considered a neurologic emergency

➢ A noncontrast CT is required to rule out hemorrhagic stroke

➢ All patients with suspected TIA expedited evaluation within48 hours, both cerebrovascular imaging and cardiac examination

➢ Patients who had a transient ischemic attack, the risk of strokeincreases as the ABCD2 score increases

➢ Hospital admission is recommended for an ABCD2 ≥ 3 or greater

Cardioembolic Stroke

➢ The most common cause is atrial fibrillation

➢ Other potential cardioembolic sources:

➢ reduced left ventricular ejection fraction

➢ severe mitral stenosis

➢ ventricular thrombus

➢ apical aneurysm

➢ congenital abnormalities

➢ Several findings on neuroimaging suggest a cardioembolic cause,such as involvement of the cortical surface in the absence ofcerebral artery atherosclerosis

➢ Cardiac evaluation: electrocardiography, in-hospital telemetry,transthoracic echocardiography, transesophageal echocardiography

Large Artery Atherosclerosis

➢ Commonly occurs after local thrombus formation in the area of

plaque rupture with subsequent distal embolization

➢ Common causes – extracranial internal carotid artery

atherosclerosis has the highest risk of recurrent stroke in the

first 2 weeks

➢ The risk is highest when the stenosis > 70%; stenosis in the 50%

to 70% range has a moderate risk of recurrence

➢ Prompt vascular imaging is recommended for patients with TIA or

a carotid territory infarction seen on neuroimaging

➢ Imaging modalities: ultrasonography, magnetic resonance

angiography (MR-A), CT-A or catheter digital subtraction

angiography

➢ Carotid ultrasonography is useful because of its high sensitivity forhemodynamically significant stenosis

➢ The anatomic location should be confirmed with either CT angiographyor MRA without contrast

➢ Unless carotid artery angioplasty with stenting is planned, catheterangiography is not routinely necessary

➢ Stoke arising from atherosclerosis of the intracranial arteries occurswith stenosis > 70% in the vertebro-basilar, intracranial internal carotidand middle cerebral arteries

➢ Intracranial atherosclerosis is associated with a high long-term risk ofrecurrent stroke

Small Subcortical Infarcts (Lacunes)

➢ Are commonly < 1.5 cm in size and arise from occlusion of

small perforating arteries emanating from the large

intracranial vessels

➢ Presents only motor or sensory findings on examination

➢ Cortical hemispheric symptoms (visual field cuts, aphasia,

hemispatial neglect are lacking)

➢ The main risk factor: hypertension associated

pathologic changes at the origin of perforating arteries

➢ Vascular imaging is required in affected patients

Cryptogenic and Rare Causes of Stroke

➢ Sizeable proportion of patients will have a cerebral infarction

with no definitive cause identified on cardiac or vascular

diagnostic testing

➢ Prolonged cardiac rhythm monitoring or interrogation of a

pacemaker may reveal undiagnosed paroxysmal atrial

fibrillation

➢ Headache preceding stroke in younger patients without

cardiovascular disease risk factors (particularly those with

recent head/neck trauma) suggests extra/endocranial

arterial dissection

➢ Testing for autoimmune and hypercoagulable disorders

➢ Echocardiography may reveal a PFO – present in up to 25% of the

general population

➢ In younger people, a PFO is likely to be causally related to stroke

(generally are at a low risk of subsequent stroke in the absence of

hypercoagulable disorder)

Acute Stroke Therapy

Ischemic Stroke Treatment

Thrombolysis

➢ The initial goal is to establish eligibility for intravenous thrombolysis

➢ The primary determinant of eligibility is the time since stroke onset – determined

by either self report or the time when the patient was last witnessed at a

prestroke baseline

➢ Thrombolysis aims to restore cerebral blood flow to the ischemic penumbra

➢ Intravenous thrombolysis is indicated

within 4,5 hours of onset in patients

with measurable deficit who do not

meet any of the exclusion criteria and

is most effective the earlier it is

administered

Thrombolysis

➢ A focused history, physical examination and a fingerstick

measurement of blood glucose level can determine any of the

exclusion criteria

➢ Rapid imaging with

noncontrast CT is required

to exclude ICH

➢ Laboratory testing: complete blood count, coagulation profile and

basic metabolic profile – suspicion of coagulopathy or

thrombocytopenia

➢ The optimal time to initiate the treatment with thrombolysis is 60

minutes or less from onset – marker of high-quality care

The guidelines state that patients should receive endovascular therapy

with a stent retriever if they meet all the following criteria (class I; level

of evidence A):

• Prestroke modified Rankin Scale (mRS) score 0 to 1;

• Acute ischemic stroke with receipt of intravenous recombinant tPA

within 4.5 hours of onset;

• Causative occlusion of the internal carotid artery or proximal (M1)

middle cerebral artery (MCA);

• Age 18 years or older;

• National Institutes of Health Stroke Scale (NIHSS) score of 6 or greater;

• ASPECTS score of 6 or greater; and

• Treatment that can be initiated (groin puncture) within 6 hours of

symptom onset.

Criteria for Eligibility for

Thrombectomy

➢ Main risk factors: protocol violations, notably treatment beyond the

time window and blood pressure above recommended targets

➢ Blood pressure <180/110 mmHg before thrombolysis – achieved

with intravenous labetalol or nicardipine

➢ After the initiation of intravenous thrombolysis using recombinant

tissue plasminogen activator, adherence to strict monitoring

protocols – blood pressure < 180/105 mmHg and to detect signs

of symptomatic ICH

➢ Other precautions – withholding all antithrombotic agents until a

repeat had CT or MRI performed within 24 hours after the

procedure excludes ICH and monitoring for angioedema

Antiplatelet, Anticoagulant and Other Agents

➢ Aspirin is appropriate – only after a dysphagia evaluation

documenting the ability to safely swallow; if unable to swallow –

rectal formulation of aspirin

➢ Aspirin taken within 48 hours of ischemic stroke onset modestly

reduces the risk of recurrent ischemic stroke at 2 weeks without

significantly increasing the risk of intracerebral hemorrhage

➢ In patients with a high-risk TIA (ABCD2 score ≥ 4) or minor

ischemic stroke (National Institute of Health Stroke Scale ≤ 3), a

21-day course of aspirin+clopidogrel or clopidogrel monotherapy

for 90 days, decrease the risk of subsequent stroke –

administrated within 24 hours of onset, compared with aspirin

monotherapy

➢ Heparinoids do not reduce the risk of recurrent stroke in the

acute setting for either cardioembolic or noncardioembolic

stroke

➢ Acute intravenous heparin occasionally is used in patients

with rare cause of stroke (dissection or a hypercoagulable

state), or in patients with mechanical valves – risk of

hemorrhage into the infarct is low

Antithrombotic Therapy After Ischemic Stroke

➢ In patients with infarcts without petechial hemorrhage and with

involvment < one third of the middle cerebral artery distribution +

atrial fibrillation, anticoagulation can be started before hospital

discharge (between 2-14 days).

➢ Warfarin is not recommended for patients with symptomatic

intracranial atherosclerosis unless another high-risk condition; is

associated with increased mortality.

➢ In noncardioembolic ischemic strokes, warfarin and antiplatelet

agents are equivalent in terms of efficacy; antiplatelet agents – are

considered first-line agents because of ease of use.

➢ For noncardioembolic stroke, low-dose (81mg/d) aspirin

monotherapy – often first-line therapy for patients not

previously taking antiplatelet agents

➢ Clopidogrel or aspirin + dipyridamole – patients who have a

recurrent ischemic stroke, despite adequate control of other

stroke risk factors, while taking aspirin monotherapy

Revascularization

either endarterectomy or stenting– in patients with > 70% stenosis and low

cardiovascular risk, as long as the operative complication rate is < 3%

➢ Symptomatic extracranial internal carotidartery stenosis is cause of stroke withhigh risk of recurrence

➢ 26% recurrent stroke at 2 years and 1%per day increase of risk of recurrent strokein the first 2 weeks

➢ Carotid revascularization within 14 days –indicated for nondisabling strokes or TIAsin patients with symptomatic extracranialinternal carotid artery stenosis

➢ The choice of one surgical approach –dictated by the risk of perioperative complications or anatomic complications

Endarterectomy

➢ Angioplasty-stenting – performed in patients at high risk for

periprocedural cardiopulmonary complications, restenosis

and previous radiation therapy

➢ Using angioplasty-stenting – not recommended for patients

with symptomatic intracranial artery stenosis because of the

high risk of periprocedural stroke and the high efficacy of

optimal medical therapy

Angioplasty -

Stenting

Lifestyle and Medical Management

➢ Treatment of modifiable vascular disease risk factors lead to asignificant decrease in the risk of recurrent stroke.

➢ Antihypertensive therapy for stable patients with a sustainedblood pressure ≥ 140/90 mmHg, including those older > 60years with preexisting cardiovascular disease

➢ Patients with recent lacunar infarct => systolic blood pressure≤ 130 mmHg

Lifestyle and Medical Management

➢ All patients with stroke require comprehensive lifestyle changes

(improving physical activity, diet, tobacco use)

➢ Statins are recommended for patients with plasma LDL

cholesterol level ≥ 100 mg/dL (2.59 mmol/L)

➢ Statins have been associated with high risk of hemorrhagic

stroke and may be contraindicated in patients with lobar ICH –

amyloid angiopathy

➢ Statins are indicated for patients at high risk for ischemic

events

Prognosis and Recovery

Neurologic Complications

Neurologic Complications

➢ Patients with a middle cerebral artery

infarction involving > 50% of the arterial

territory – high risk for malignant cerebral

infarction with associated edema and

cerebral herniation

➢ Hemicraniectomy –associated with

significant reduction in mortality and

severe disability compared with the best

medical therapy - considered early in

patients with malignant cerebral

infarction (exhibit impaired alertness,

least one pupil reactive to light)

➢ Aspiration pneumonia can be prevented by maintaining the head

of bed at 30 degrees and instituting oral hygiene protocols

➢ DVT prevention – required for all hospitalized stroke patients

unless they are fully ambulatory

➢ Subcutaneous unfractionated or low-molecular-weight heparin –

started in al patients with impaired mobility by hospital day 1 for

ischemic stroke and by hospital day 4 (if no active bleeding is

documented) in hemorrhagic stroke