update on management of ischemic stroke 2

8/8/2019 Update on Management of Ischemic Stroke 2

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Update on

Management of Ischemic Stroke

Dr Muhammad Wazir Ali Khan

Assistant Professor of NeurologySheikh Zayed Medical College,Rahim Yar Khan


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Historical Background

During the 17th and 18th centuries, it wasrecognized that the dead brains containedhaemorrhages and softenings and that braindamage could result from either bleeding orocclusion of the vital blood supply.

During the 19th and early 20th centuries,correlating the neurological symptoms and signs

found in stroke patients during life with theanatomical region of damage in the brain foundafter death.


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During the 20th century, clinicopathologicalanalysis of stroke syndromes was done.

Clinical symptoms were attributed to definitecerebral anatomical areas.

Correlation between cardiac and cranial vasculardisease and stroke and TIA were identified.


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Explosive advances occurred in brainimaging

Computed tomography, CT Magnetic resonance imaging, MRI

Single-photon emission computed tomography, SPECT

Positron emission tomography, PET

Digital subtraction angiography, DSA

MR angiography, MRA CT angiography, CTA

Extracranial and transcranial ultrasonography.


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Pathophysiology

The brain is the most metabolically active organ inthe body.

It represents only 2% of the body's mass.

It requires 15-20% of the total resting cardiacoutput to provide the necessary glucose andoxygen for its metabolism.


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Pathophysiology

Ischemic strokes result from events that limit orstop blood flow, such as Embolism

Thrombosis in situ

Relative hypoperfusion.

As blood flow decreases, neurons ceasefunctioning.

Irreversible neuronal ischemia and injury begin atblood flow rates of less than 18 mL/100 mg/min.


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Ischemic cascade

Within seconds to minutes of the loss of glucoseand oxygen delivery to neurons, the cellularischemic cascade begins. There is cessation of the normal electrophysiologic function of the

cells.

The resultant neuronal and glial injury producesedema in the ensuing hours to days after stroke,

causing further injury to the surrounding tissues.


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Ischemic cascade

Brain regions without significant flow are referredto collectively as the core. Neuronal cells in these areas are presumed to die within minutes of

stroke onset.

Zones of decreased or marginal perfusion arecollectively called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours

because of marginal tissue perfusion. Pharmacologic interventions target this penumbra.


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Mechanisms of Stroke

Embolic strokes Emboli of cardiac or arterial origin.

Cardiac sources include:

Atrial fibrillationRecent myocardial

infarction

Prosthetic valves

Native valvular disease

Endocarditis

Mural thrombiDilated cardiomyopathy

Patent foramen ovale.

Arterial sources

include: Atherothrombolic

Cholesterol emboli thatdevelop in the arch of theaorta and in the

extracranial arteries.


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Thrombotic strokes Thrombotic strokes include large-vessel strokes and

small-vessel or lacunar strokes.

In situ occlusions on atherosclerotic lesions in thecarotid, vertebrobasilar, and cerebral arteries, typicallyproximal to major branches.

Thrombogenic factors may include:

Injury to and loss of endothelial cells exposing thesubendothelium

Platelet activation by the subendothelium

Activation of the clotting cascade, inhibition of fibrinolysis, andblood stasis.


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Lacunar Strokes 20% of all ischemic strokes.

They occur when the penetrating branches becomeoccluded.

Causes include microatheroma, lipohyalinosis, fibrinoidnecrosis secondary to hypertension or vasculitis, hyalinearteriosclerosis, and amyloid angiopathy.

Watershed Infarcts Develop from relative hypoperfusion in the most distal

arterial territories.


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Epidemiology of Stroke

United States 795,000 strokes occur each year.

625,000 are ischemic strokes.

By the year2025, the annual number of strokes is

expected to reach 1 million. Currently, more than 4.4 million people in the United

States are stroke survivors.

International Population older than 65 years will rise from 390 million

now to 800 million by 2025. The WHO estimates that 15 million people suffer a

stroke worldwide each year, resulting in 5 million deathsand 5 million people permanently disabled.


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Race Stroke has a higher incidence in the black population

than in the white population.

Blacks have an age-adjusted risk of death from strokethat is 1.49 times that of whites.

Hispanics have a lower overall incidence of stroke thanwhites and blacks but more frequent lacunar strokes and

stroke at an earlier age.


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Sex In patients younger than 60 years, the incidence of

stroke is greater in males (3:2 ratio).

Males have a stroke incidence slightly lower than

females and lower death rates than females.

Age Stroke can occur in patients of all ages, including

children.

Risk of stroke increases with age, especially in patientsolder than 64 years, in whom 75% of all strokes occur.


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Risk factors for ischemic stroke

Non-modifiable risk factors include: Age

Race

Sex

Ethnicity History of migraine headaches

Sickle cell disease

Fibromuscular dysplasia

H

eredity


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Risk factors for ischemic stroke

Modifiable risk factors include the following: Hypertension (the most important)

Diabetes mellitus

Cardiac disease - Atrial fibrillation, valvular disease,

mitral stenosis, Hypercholesterolemia

Transient ischemic attacks (TIAs)

Carotid stenosis

Hyperhomocystinemia

Lifestyle issues - Excessive alcohol intake, tobacco use,illicit drug use, obesity, physical inactivity

Oral contraceptive use.


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Stroke-Differential Diagnosis

Venous Infarction

Multiple Sclerosis - a Demyelinating Plaque

Mass Lesions:

Brain tumour Abscess

Subdural haematoma

Carotid or Vertebral Artery Dissection

Polycythaemia, Hyperviscosity Syndromes

Fat and Air Embolism

Rarities: Arteritis, Neurosyphilis, SLE,Mitochondrial Disease.


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Management of Ischemic Stroke

Pre-hospital/EMS management

Hospital care

Secondary prevention

Rehabilitation

Physical therapy Speech therapy

Occupational therapy


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NINDS and ACLS Recommended Stroke Evaluation Time

Benchmarks for Potential Thrombolysis Candidate

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 monitored bed 3 h


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General Management of Patients With Acute

Stroke

BloodGlucose

Treat hypoglycemia with D50Treat hyperglycemia with insulin if serum glucose >200 mg/dL

Seizures Occur in 2%focal or generalized. Use conventional AED.

Cardiacmonitoring

Continuous monitoring for ischemic changes or atrial fibrillation

Elevated ICP 1 g/kg stat, then 50 g every 2 or 3 h. Hyperventilate

Intravenousfluids

Avoid D5W and excessive fluid administrationIV isotonic sodium chloride solution at 50 mL/h unlessotherwise indicated

Oral Intake NPO initially; aspiration risk is great, Use NG/PEG tube feed

Oxygen Supplement if indicated (Sa02


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Blood Pressure Management in Patients With

Stroke*

Patients who are candidates for rtPA

Pre-treatment

SBP >185 or

DBP >110 mmH

g

Labetalol 10-20 mg IVP 1-2 doses orEnalapril 1.25 mg IVP

Post-treatment

DBP >140 mm Hg Sodium nitroprusside (0.5 mcg/kg/min)

SBP >230 mm Hg orDBP 121-140 mm Hg

Labetalol 10-20 mg IVP and consider labetalolinfusion at 1-2 mg/min or nicardipine 5 mg/h IVinfusion and titrate

SBP 180-230 mm Hg orDBP 105-120 mm Hg

Labetalol 10 mg IVP, may repeat and double every10 min up to maximum dose of 150 mg

*Adopted from 2005 Advanced Cardiac Life Support (ACLS) guidelines and 2007 American Stroke Association ScientificStatement


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Blood Pressure Management in Patients With

Stroke*

Patients Who are not Candidates for rtPA

DBP >140 mm HgSodium nitroprusside 0.5 mcg/kg/min; may reduceapproximately 10-20%

SBP >220 orDBP 121-140 mm Hg orMAP >130 mm Hg

Labetalol 10-20 mg IVP over 1-2 min; may repeatand double every 10 min up to maximum dose of150 mg or nicardipine 5 mg/h IV infusion and titrate

SBP


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Acute Therapy of Ischemic Stroke

Hemodynamic Considerations Cerebral perfusion depends on the mean systemic

arterial pressure (MAP).

Areas of brain distal to narrowed or occluded arteriesmay be supplied by collateral vessels.

When fully dilated flow in these vessels becomespassively dependent on the MAP.

Therefore, it is desirable to maintain MAP high in thesetting of acute stroke.


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Hemodynamic Considerations It is common for patients with acute stroke to have acute

BP elevations on presentation.

In general, this BP should not be lowered, unless BPlowering is necessary to fulfill criteria for safethrombolysis, or unless acute medical issues demand it:

Acute myocardial infarction

Aortic dissection

H

ypertensive crisis with end-organ involvement. Congestive heart failure (CHF)

Renal failure

Hypertensive encephalopathy


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Hemodynamic Considerations Consensus guidelines from the ASA suggest therapy if:

Diastolic BP above 120

Systolic BP above 220

Target BP for tissue plasminogen activator (TPA)therapy:

Systolic BP less than or equal to 185

Diastolic BP less than or equal to 110


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Surgical Care

Surgical evacuation in case of hemorrhage or hemorrhagictransformation following t-PA.

The management of life-threatening elevations of ICP.

Hemicraniectomy to treat life-threatening ICP: Shorter ICU stays

Lower mortality rate if surgery is performed before clinicaldeterioration.

These benefits are not confirmed by clinical trials.


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Investigations

The purpose of investigations in both stroke andTIA is to: Confirm clinical diagnosis.

Distinguish between haemorrhage and thrombo-embolicinfarction.

Look for underlying causes of disease and to directtherapy, either medical or surgical.


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CT Scan

CT is most important in the evaluation of patientswith acute stroke.

Noncontrast CT is very sensitive in detectingintracerebral and subarachnoid hemorrhage, aswell as subdural hematomas.

Infarctions are usually detectable at 1 week

although 50% are never detected on CT.


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CT Scan

CT may demonstrate other pathologies: Neoplasm Aneurysm/Arteriovenous malformation Abscess

H

ydrocephalus

CT angiography may demonstrate the location ofvascular occlusion.

CT perfusion studies together with CT angiographyare becoming more available and utilized in theacute evaluation of stroke patients.


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Brain Infarction-CT

Early Day 3


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Brain Infarction-CT


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MRI and MRA

MRI with magnetic resonance angiography (MRA)is a major advance in the neuroimaging of stroke.

MRI provides great detail in structural andmetabolic imaging.

Diffusion-weighted MRI (DW-MRI) can detectareas of ischemic brain injury earlier than standard

T1/T2-weighted MRI images or CT scan.


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MRI and MRA

Perfusion MRI (PW-MRI) uses injected contrastmaterial to demonstrate areas of decreasedperfusion.

These sequences combined with DW-MRI yieldareas of DW-MRI/PW-MRI mismatch, therebyidentifying potentially salvageable tissues.

MRA is a noninvasive technique whichdemonstrates vascular anatomy and occlusivedisease of the head and neck.


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MRI


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MCA Infarction DWI & MRA


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DWI & PWI-MRI


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Other studies

Digital subtraction angiography, DSA Gold standard for demonstrating vascular lesions:

Occlusions, stenoses, dissections, and aneurysms.

It also allows for intra-arterial therapies.

Intra-arterial thrombolytics. Investigational catheter devices.

Angiography requires special facilities and a skilledoperator and it carries a stroke risk of 1%.

MR spectroscopy is an experimental techniquedistinguishing areas of salvageable neurons.


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Other studies

Carotid duplex scanning Performed for carotid stenosis and to stratify patients

either for medical management or carotid intervention.

Transcranial Doppler ultrasonography (TCD) To assess the location and degree of arterial occlusions

in extracranial carotid and large intracranial vessels

It can also be used to detect restoration of flow afterthrombolytic therapy.

Single-photon emission computed tomography(SPECT) defines areas of altered regional bloodflow.


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Other studies

Echocardiography: For evaluation of possible cardiogenic sources of stroke. TEE can evaluate the aortic arch and thoracic aorta for

plaques or dissections.

Electrocardiography/ECG: ECG may demonstrate cardiac arrhythmias, such as

atrial fibrillation, or may indicate acute ischemia. All patients with stroke should have an ECG as part of

their initial evaluation.

Chest radiography should be performed whenclinically indicated.


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Other studies

Lumbar puncture: This is indicated only in unusual circumstances, such as

when blood syphilitic serology is positive.

Blood for: Polycythaemia Infection Vasculitis Thrombophilia

Syphilitic serology Clotting studies Autoantibodies Lipids


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Thrombolysis in acute ischemic stroke

0.9 mg/kg IV TPA IV under 3 hrs of onset Inclusion Criteria:

onset 15 SBP >186 or DBP >110, Hg

update on management of ischemic stroke 2

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