Ischemic Stroke Or Cerebrovascular accident (CVA)

Introduction

Stroke or (CVA) is the sudden onset of a focal neurologic deficit(s) resulting from either infarction or hemorrhage within the brain.

Stroke is a medical emergency that requires rapid diagnosis and treatment.

It's the second leading cause of death worldwide & It's the leading cause of neurologic disability worldwide.

Chronic hypertension is the strongest risk factor for stroke and is present in most stroke patients

Risk of stroke increases after 45 years of age and is highest during the 7th and 8th decades, is approximately 15% in adults older than 80 years. Male > female at younger age but higher incidence in women with age ≥ 75 years.

Strokes can be hemorrhagic or ischemic: The overwhelming majority of strokes (about 85%) are ischemic, the remainder being hemorrhagic.

Ischemic stroke causes injury due to insufficient oxygen and nutrient delivery to brain tissue
Hemorrhagic stroke causes injury due to mechanical compression of brain tissue and local toxicity from blood breakdown products.

The nature and severity of neurologic deficits can vary according to the distribution and size of the stroke.

Hemorrhagic stroke tends to be more variable in presentation because the area of injury often crosses multiple vascular territories

Time of stroke onset is defined as the time patient’s symptoms began or time patient was last seen as normal. A patient who awakens with stroke has the onset defined as when they went to bed.

Hyperacute MRI may be used to estimate the time of onset for patients with strokes of unknown onset time to make decisions regarding thrombolysis.

The prognosis of stroke depends largely on the type of stroke and the size and territory of infarction.

Hemorrhagic stroke is associated with higher morbidity and mortality in the acute poststroke period compared with ischemic stroke with a 30-day mortality rate approaching 50% (5 times greater than ischemic stroke)

Ischemic strokes

Ischemic strokes it defined as a Focal neurologic deficit lasting more than 24 hours because of loss of blood flow to a portion of the brain that results in irreversible cell death.

Ischemic stroke can occur as a result of in situ occlusion, embolism, or watershed infarction.

Emboli are a common cause of TIA/CVA. Cardioembolic strokes account for about 20% of all ischemic strokes. In contrast to thrombotic strokes, which typically present in a single vascular territory, embolic strokes can involve multiple cerebral vascular territories, as well as noncerebral vascular territories (eg, kidney).
Atherosclerosis is the most common etiology of thrombus formation in large vessels.
Lipohyalinosis, usually because of hypertension, is the most common etiology of small-vessel disease. Small vessel strokes tend to develop more quickly than large vessel strokes, but not as suddenly as embolic strokes.
Hypoperfusion occurs because of general circulatory problems and often results in bilateral symptoms. Infarction commonly occurs in border zones between large vessels, resulting in watershed infarcts.

In all types of ischemic stroke, brain infarction occurs as a result of decreased cerebral perfusion, with associated decreased delivery of oxygen and nutrients.

An infarction will occur if blood supply is critically reduced (< 16 mL/100 g of brain tissue/min.)
A fall in cerebral blood flow to zero causes death of brain tissue within 4 to 10 minutes.
There is a higher CBF threshold for loss of electrical excitability than that for cell death—this has led to the concept of the ischemic penumbra—nonfunctioning cells that are still viable.

Ischemic penumbra

Ischemic penumbra: It's the tissue surrounding the core region of infarction is ischemic but reversibly dysfunctional and is called as the ischemic penumbra.
In ischemic penumbra, cellular death occurs by apoptosis days to weeks later.

The discrepancy between the region of poor perfusion and diffusion deficit is called diffusion perfusion mismatch and is a measure of ischemic penumbra.
Saving the ischemic penumbra is the goal of revascularization therapies.
The ischemic penumbra will eventually infarct if no change in flow occurs.

What is Causes of Stroke?

Emboli are a common cause of TIA/CVA. Cardioembolic strokes account for about 20% of all ischemic strokes.
Atherosclerotic: It's the most common cause of CVA in middle aged or elderly (85%)
Trauma being the most common cause of strokes (22%) in patients under 45 yrs.
Sickle cell anemia (SS disease) is a common cause of stroke in children.
Cervical artery dissection (ie, carotid or vertebral artery dissection) causes around 20% of ischemic strokes in young and middle-aged patients. Carotid dissection is more common than vertebral dissection.
Cocaine is one of the main causes of stroke in young patients. ICH, ischemic stroke, and SAH are all associated with cocaine use.
Blood disorders account for up to 5% of all strokes.

Embolic (hemorrhagic) stroke

Embolic stroke occurs when debris travels from a remote source and lodges within a cerebral artery.
Onset of embolic stroke—very acute or stormy (develops quickly in seconds) and deficits are maximal initially. Some patients with chronic significant cerebral atherosclerotic disease develop robust collateral circulation, mitigating the effects of an acute embolic event.
Embolic stroke can produces a hemorrhagic infarction: Vessel reperfusion after lysis of embolic material causes hemorrhage.
Nonrheumatic atrial fibrillation is the most common cause of cerebral embolism.

Atherosclerotic Strokes

Atherosclerotic strokes: it's an ischemic type of stroke caused by a platelet thrombosis that develops over a disrupted atherosclerotic plaque
Atherosclerotic strokes it's the most common cause of CVA in middle aged or elderly (85%)
Onset is insidious with stepwise progression. Commonly occurs during sleep or soon after waking. Classically the patient awakens from sleep with the neurologic deficits

Most atherosclerotic strokes are preceded by transient ischemic attacks

Watershed Stroke

Watershed stroke occurs when a systemic process results in cerebral hypoperfusion that affects the most vulnerable regions of the brain, which are typically the zones between neighboring vascular territories.
Watershed infarctions account for approximately 10% of all strokes. The incidences of anterior and posterior watershed infarctions are similar.
Systemic hypotension is associated with both types of watershed infarctions but most often results in subcortical watershed stroke.
Diffuse atherosclerosis of the cerebral arteries: The ICA, being the most proximal cerebral artery, is most likely to cause watershed stroke when there is severe atherosclerotic disease.

Watershed areas:

The cortical (external) watershed zones include: the anterior region within the frontal and parietal parasagittal cortex (MCA/ACA territory) and the posterior region within the parieto-temporo-occipital cortex (MCA/PCA).
The subcortical (internal) watershed zones include: the corona radiata (deep/superficial perforators of the MCA) and the centrum semiovale (superficial perforators of the ACA/MCA)

Clinical features & Types of Ischemic stroke

Classes of ischemic stroke

Transient ischemic attack (TIA): It is sudden neurological dysfunction due to cerebral ischemia lasting less than 24 hours (usually lasts less than 30 minutes) and the patient recovers completely within 24 hours.
Reversible ischemic neurological deficit (RIND): Neurodeficit persists for more than 24 hours, but recovers totally within 3 weeks
Evolving stroke: is a stroke that is worsening—the symptoms worsen gradually or in a step wise pattern over hours or days and the neurological deficit persists for more than 24 hours
Completed stroke: Clinical signs of neurological deficit are persistent
Partial non-progressive stroke (PNS): Neurodeficit persists for more than 3 weeks, but is either partial or ends up with minimal residual deficit.

Clinical features of Acute stroke

Weakness: Unilateral weakness is the classical presentation of stroke.
Speech disturbance: Dysphasia and dysarthria are the usual speech manifestations in stroke
Visual deficit: Monocular blindness in stroke can be caused by reduced blood flow in the internal carotid or ophthalmic arteries. If transient, this is called amaurosis fugax. Ischaemic damage to the occipital cortex or optic tracts causes contralateral hemianopia
Visuo-spatial dysfunction: Damage to the non-dominant cortex often results in contralateral sensory or visual neglect and apraxia.
Ataxia: Stroke causing damage to the cerebellum and its connections can present as acute ataxia, sometimes with brainstem features, e.g. diplopia and vertigo.
Headache: Sudden severe headache is the cardinal symptom of subarachnoid haemorrhage but also occurs in intracerebral haemorrhage.
Seizure: Seizure is unusual in acute stroke but may occur in cerebral venous disease.
Coma: Coma is an uncommon feature of stroke, though it may occur with a brainstem event. - In the first 24 hrs, coma usually indicates a subarachnoid or intracerebral haemorrhage.
Hemorrhagic conversion of an ischemic stroke is more likely in patients who are receiving anticoagulation or in patients with large strokes, particularly those with embolic ischemic infarcts.

How to recognize a Ischemic strokes on CT scan?

Ischemic strokes appear as dark areas on the CT scan (hemorrhagic strokes appear white).
The area in the brain is the same in both atherosclerotic and embolic strokes; however, the former is most likely a pale infarction (no reperfusion), whereas the latter is a hemorrhagic infarction (reperfusion).
Cerebral infarction infarct may not be seen reliably for 24 to 48 hours. Also, CT may fail to show small ischemic strokes in posterior fossa and small infarcts on cortical surface.
MRI is associated with a significantly higher sensitivity for ischemic stroke compared with CT imaging particularly for lesions in the posterior fossa and within the first hours after the event.

Signs of Hyperacute Infarct on NCCT

Hyperdense MCA sign: Hyperdense sign indicates the clot within the vessel and it’s one of the earliest signs.
Cortical ribbon “Insular ribbon sign” is caused by edema within insular cortex and basal ganglia and is an earliest indicator of cerebral infarction in MCA territory.
Ill-marginated lentiform nuclei
Sulcal effacement due to edema.

Cerebral edema occurs within 1 to 2 days and can cause mass effects for up to 10 days. Hyperventilation and mannitol may be needed to lower intracranial pressure (ICP).

Management & Early Treatment

Early recognition of the cause of stroke is unreliable, and early treatment is critical.

Blood glucose is the only essential lab to get immediately since it affects eligibility for IV tPA
Noncontrast head CT scan: image the brain in ≤ 20minutes of arrival in the E/R in ≥50% of eligible patients.
In unconscious patients Investigation of choice for stroke → NCCT Head as it rules out acute bleed or hemorrhagic infarct (which is a contraindication for thrombolysis)
ECG should be done to look for atrial fibrillation or ischemic changes.
All patients should have frequent blood pressure monitoring.
Overcorrection of blood pressure may lead to a worse outcome. Because collateral blood flow within the ischemic brain is blood pressure dependent, blood pressure should not be lowered acutely.
Oral administration of aspirin within 24 to 48 hours after stroke (but not within 24 hours of fibrinolytic therapy if it is given) is recommended. Aspirin 325 mg/day within 48 hours or 24 to 48 hours after thrombolytic therapy
CEA for asymptomatic high-grade carotid stenosis (≥60%) reduces the 5year risk of ipsilateral stroke in men, provided that the operator ’s surgical/angiography complication rate is <3%.
Statin use should be continued without interruption following acute stroke, trial showed benefit in secondary stroke reduction for patients with recent stroke or TIA who were prescribed atorvastatin, 80 mg/day.
Corticosteroids not recommended for cerebral edema and/or increased ICP complicating stroke.Avoid diuretics unless volume overloaded.
Oral contraceptives or hormonal therapies may need to be discontinued in women with stroke. Low dose estrogen containing oral contraceptive pills do not increase the risk of stroke in healthy women, but can cause stroke if associated with other risk factors.

Treatment options for stroke (medications, surgery, rehabilitation)

Acute—Supportive treatment (airway protection, oxygen, IV fluids) is initiated.

Oxygenation: Provide supplemental O2 to maintain O2 saturation >94%; Supplemental O2 is not recommended in nonhypoxic patients (no benefit)
Glucose: Avoid hyperglycemia in the 1st 24 hours after acute ischemic stroke (worse outome) - Goal: blood sugar 140– 180mg/dL

BP control—Monitor BP closely in the first 24 hours.

In acute ischemic stroke, BP should be lowered if there is malignant hypertension, concomitant myocardial ischemia or if BP is >185/110 mm Hg or if thrombolytic therapy is anticipated.
Goal is to lower BP ~15% in the first 24 hours if treatment is undertaken.
If thrombolytic therapy is planned, BP must be <185/110 mm Hg prior to administration of thrombolytics.
If there is suspicion of elevated ICP, reduce BP to a target cerebral perfusion pressure of between 61 mm Hg and 80 mm Hg.
Restart antihypertensive medications 24 hours after stroke onset for patients with a history of hypertension who are neurologically stable.

Antiplatelet drugs

Aspirin should be given as early as possible (unless t-PA is used), and ideally within 48 hours of stroke onset.
Alteplase (Activase®, Actilyse®) is the primary agent used clinically. It is FDA approved for the IV treatment of acute ischemic stroke
Ticagrelor is not recommended over ASA in the acute treatment of minor stroke (no benefit)
Patients with minor stroke: dual antiplatelet therapy (ASA+ clopidogrel) for 21 days starting ≤24 hrs can reduce secondary stroke for up to 90 days.

Anticoagulation

Heparin, low molecular weight heparin (LMWH), and warfarin anticoagulation are not recommended routinely for acute ischemic stroke.
Anticoagulation with a DOAC or warfarin is indicated to prevent recurrent embolic strokes because of atrial fibrillation. Target INR for warfarin therapy is 2–3.
Deep vein thrombosis (DVT) prophylaxis for immobilized patients: Anticoagulation with heparin/LMWH followed by warfarin is indicated for venous sinus thrombosis both with and without hemorrhagic infarcts.

Thrombolytic therapy (t-PA)

Eligibility: Candidates should be older than 18 years and have clinical evidence of an ischemic stroke, and the onset of symptoms must have occurred within the last 3 hours.
Dosage: In eligible patients, tissue plasminogen activator is given at a dose of 0.9 mg/kg intravenously, up to a total dose of 90 mg.
If t-PA is given, there is risk of intracranial hemorrhage. Therefore, do not give aspirin for the first 24 hours, perform frequent neurologic checks (every hour), and carefully monitor BP (Keep BP <185/110 mm Hg.)
If administered within 4.5 hours of the onset of an acute ischemic stroke, improved clinical outcome is seen at 3 months.
Do not give t-PA if the time of stroke is unknown, if more than 4.5 hours have passed, or if the patient has any of the following: uncontrolled HTN, bleeding disorder, is taking anticoagulants or has a history of recent trauma or surgery.

Endovascular thrombectomy

A noninvasive intracranial vascular study (usually a CTA) is obtained in potential candidates for endovascular therapy (EVT).
CT angiography and CT perfusion scans may be used to select patients who will benefit from thrombectomy up to 24 hours after the time they were last known well.
In eligible patients with large artery occlusion who present within 6 hours, endovascular thrombectomy.
New studies are supporting that the window for therapy could be extended from 6 hours up to 16 or 24 hours from the time patient was last known to be well.

TIA & Lacunar infarction

Transient ischemic attack (TIA)

Definition: It is a transient episode of neurologic dysfunction due to focal ischemia without permanent infarction on imaging, Typically the neurologic signs and symptoms of a TIA last for 5 to 15 minutes but, by definition, must last for <24 hours.
Stroke may be indistinguishable from a TIA at the time of presentation: duration of symptoms is the distinguishing feature.
Features: The blockage in blood flow does not last long enough to cause permanent infarction. Even in absence of neurologic signs & symptoms, infarcts of brain occur in 15 - 50% of TIAs.
TIAs can Involve either the carotid or the vertebrobasilar system
Causes: TIA is usually embolic, However, transient hypotension in the presence of severe carotid stenosis (>75% occlusion) can lead to a TIA.
Symptoms are transient with a TIA because reperfusion occurs, either because of collateral circulation or because of the breaking up of an embolus.
ABCD Scoring system for TIA includes: age, blood pressure (SBP & DBP), clinical symptoms (unilateral weakness, speech disturbance without weakness), duration and diabetes.
Diagnosis: Ist investigation for TIA → USG Doppler of carotid vessels-best modality to visualize small atherosclerotic plaque.
Treatment of TIA: Antithrombotic therapy as soon as intracranial hemorrhage has been ruled out, Antiplatelet therapy (aspirin, clopidogrel, or ticlopidine), Possible carotid endarectomy/stenting

Risk of stroke after TIA is ~10 - 15% in first 3 months, with most events occurring in first 2 days (50%)

Amaurosis fugax or a transient ischemic attack of the retina

Amaurosis fugax usually results from an embolus stuck in a retinal arteriole.
Emboli causing amaurosis fugax are composed of cholesterol (Hollenhorst plaque), calcium, or platelet-fibrin debris. Most common source is atherosclerotic plaque in carotid artery or aorta.
Complete occlusion of the central retinal artery produces arrest of blood flow and a milky retina with a cherry-red fovea.
Amaurosis fugax occurs in only one eye (painless monocular loss of vision). It can be a part of high-altitude neurologic events.
Hollenhorst plaque as a cholesterol embolus that originated from an atheromatous plaque in a more proximal vessel, usually internal carotid artery. It is a sign of severe atherosclerosis & is seen in a blood vessel of retina on ophthalmoscopy as a bright, glistening, refractile plaque at bifurcation of a retinal arteriole.

Four types of Amaurosis fugax

Type I: embolic “like a black curtain coming down” in one eye. Complete loss of vision, usually lasts 1–2 minutes
Type II: flow related. Retinal hypoperfusion → desaturation of color, usually described as a graying of vision
Type III: Vasospastic, May occur with migraines
Type IV: miscellaneous, May occur with anticardiolipin antibodies

Lacunar Strokes

Lacunar infarction refers to infarction following atherothrombotic or lipohyalinotic occlusion of a small artery (30 to 300 µm) in brain. It's s causes approximately 20% of all strokes.

Lacunar infarction is caused by narrowing of the arterial lumen is due to thickening of vessel wall (not by thrombosis).
Hyaline arteriolosclerosis, secondary to either hypertension or diabetes mellitus it's the most common cause of Lacunar infarction
Hypertension and age are the principal risk factors for lacunar infarcts. A history of HTN is present in 80% to 90% of lacunar infarctions.

Features of Lacunar infarction

Site of infarction: Lacunar infarction usually affects subcortical structures (basal ganglia, thalamus, internal capsule, brainstem) and not the cerebral cortex. The arteries affected include small branches of the MCA, the arteries that make up the circle of Willis, and the basilar and vertebral arteries.
Size of infarcts ranges from 3–20mm.
Unlike occlusions of large arteries, involvement of the smaller arteries cannot be visualized on angiography.
Diagnosis is based on the clinical syndrome and the presence of characteristic noncortical infarctions on head imaging, which are more likely to be found on MRI than CT.

Clinical features of Lacunar infarction

Pure sensory stroke or TIA (the most common lacunar manifestation)—if lesion involves the thalamus.
Pure motor hemiparesis (PMH)—(2nd most common lacunar manifestation)—if lesion involves the internal capsule.
Ataxic hemiparesis—incoordination ipsilaterally.
Clumsy hand dysarthria.

The quality and severity of deficits associated with lacunar infarctions are dependent on location.

Occlusion of a lenticulostriate vessel of MCA produces lacunar stroke within the internal capsule producing pure motor stroke or sensory-motor stroke contralateral to the lesion.
Lacunar infarction affecting the globus pallidus and putamen often produce few clinical signs, but parkinsonism and hemiballismus occur.
Lacunar syndrome dysarthria and a clumsy hand or arm due to infarction in the ventral pons or in the genu of the internal capsule.
Multiple lacunes deep in both hemispheres can result in gait disorders and dementia.
In virtually all forms of lacunar infarction, there is an absence of cortical deficits (eg, seizure, aphasia, amnesia, agnosia, apraxia, dysgraphia, alexia), which can be a clue to the diagnosis

Dr Lectures

Ischemic Stroke Or Cerebrovascular accident (CVA)