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General Medicine

Acute Ischemic Stroke

An acute ischemic stroke is a 'brain attack' where a blood clot blocks blood flow to a part of the brain, causing sudden weakness, speech difficulty, or vision loss.

Source: WHO / CDC / NIH Evidence Guidelines
Updated: Aug 09, 2026
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Red Flag Warning & Emergency Situations

Emergency Management: Patient presenting within 4.5 hours of symptom onset constitutes an absolute code emergency requiring rapid triage, immediate CT scan within 20 minutes, and administration of 'clot-busting' drugs (tPA) within 45 minutes of hospital arrival.

Core Definition:

An episode of neurological dysfunction caused by focal brain, spinal cord, or retinal infarction due to a sudden interruption of arterial blood supply. The core pathology is ischemia leading to irreversible cellular necrosis in the core region and a surrounding potentially salvageable area called the ischemic penumbra.

Detailed Overview

Ischemic stroke accounts for ~85% of all strokes. The brain cannot store glucose or oxygen; thus, blood flow cessation leads to rapid neuronal ATP depletion and cell death within minutes. Depending on the blocked vessel (e.g., Middle Cerebral Artery), predictable focal deficits occur, such as hemiparesis, aphasia, or hemianopsia. The primary therapeutic goal is rapid recanalization via thrombolysis or mechanical thrombectomy to salvage the penumbra and minimize permanent disability.

Epidemiology & Demographics

Incidence: ~795,000 strokes occur annually in the US. It is a leading cause of long-term disability. Risk doubles every decade after age 55. Higher incidence in Black populations compared to White populations.

Etiological Mechanism

Classified by the TOAST criteria: 1) Large-artery atherosclerosis (e.g., carotid stenosis), 2) Cardioembolism (e.g., atrial fibrillation), 3) Small-vessel occlusion (lacunar stroke due to lipohyalinosis), 4) Stroke of other determined etiology (e.g., arterial dissection), 5) Cryptogenic (unknown).

Primary Causes

Atrial Fibrillation (cardiac embolus)

Carotid artery atherosclerotic plaque rupture

Hypertension-induced small vessel disease (Lacunar)

Cervical artery dissection (trauma in young adults)

Occlusion of a cerebral artery drops cerebral blood flow below 10-15 mL/100g/min in the infarct core, causing failure of the Na+/K+ ATPase pump. This leads to anoxic depolarization, massive influx of intracellular calcium, release of excitotoxic glutamate, generation of free radicals, and immediate neuronal necrosis. Surrounding the core is the penumbra (flow 15-20 mL/100g/min), where cells are electrically silent but structurally intact. Without rapid reperfusion, the penumbra inevitably undergoes apoptosis and merges into the infarct core. Breakdown of the blood-brain barrier occurs over 24-48 hours, causing cytotoxic and vasogenic edema.

Diagnostic Criteria & Guidelines

Sudden onset of focal neurological deficits matching a vascular territory, combined with neuroimaging (CT or MRI) demonstrating an ischemic infarct or ruling out hemorrhage.

First-Line Treatment:

IV Thrombolysis (Alteplase 0.9 mg/kg or Tenecteplase 0.25 mg/kg) if patient presents within 4.5 hours of last known normal and has no contraindications. Mechanical Thrombectomy if LVO is present, up to 24 hours from onset based on perfusion imaging.

Second-Line & Adjunctive Therapy

If outside thrombolysis window: Antiplatelet therapy (Aspirin 162-325 mg PO within 24-48 hours). Permissive hypertension (allow BP up to 220/120 mmHg) to maintain collateral perfusion if not receiving tPA.

Surgical & Procedural Management

Decompressive hemicraniectomy for malignant MCA syndrome (large space-occupying edema) to prevent fatal uncal herniation.

Patient Counseling & Advice

Educate the patient and family on the acronym F.A.S.T (Face, Arms, Speech, Time to call 911) for recognizing future strokes. Emphasize that functional recovery continues for 6 to 12 months, requiring intense dedication to rehab.

Follow-Up & Monitoring Schedule

Outpatient echocardiogram and Holter monitor to evaluate for paroxysmal Atrial Fibrillation. Carotid ultrasound to check for stenosis. Continuous monitoring of BP, ensuring goal < 130/80 mmHg long-term.

Preventive Strategies

Cardioembolic: Lifelong anticoagulation (Apixaban 5 mg BID). Atherosclerotic: High-intensity statin (Atorvastatin 80mg) + Antiplatelet (Clopidogrel 75mg). Carotid endarterectomy if >70% symptomatic stenosis.

Highly variable based on infarct size and location (measured by NIHSS score). Around 10% are fatal within 30 days. Approximately 30-40% of survivors have moderate to severe long-term disability.

Authoritative Sources & Evidence References
World Health Organization (WHO) & CDC Guidelines: Information compiled from current international clinical practice guidelines.

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