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.
- Deteriorating level of consciousness and pupillary asymmetry (indicates edema and brain herniation).
- Sudden worsening of neurological deficits with headache (indicates hemorrhagic transformation).
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.
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)
- Hypertension: The most important modifiable risk factor, doubling the stroke risk.
- Atrial Fibrillation: Increases stroke risk 5-fold by causing stasis of blood in the left atrial appendage, forming clots.
- Diabetes Mellitus: Accelerates large artery atherosclerosis and microvascular disease.
- Prior TIA: A Transient Ischemic Attack is a major warning sign; ~10% have a stroke within 90 days.
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.
Characteristic Clinical Presentation
- Sudden unilateral weakness: Hemiparesis of the face, arm, and/or leg, typical of Middle Cerebral Artery (MCA) strokes.
- Speech disturbance: Aphasia (expressive or receptive) if the dominant hemisphere is involved, or dysarthria.
- Visual field cuts: Homonymous hemianopsia or sudden painless monocular vision loss (amaurosis fugax).
- Ataxia and vertigo: Sudden unsteadiness or severe dizziness, typical of posterior circulation (cerebellar/brainstem) strokes.
Physical Examination Signs
- Facial droop (loss of nasolabial fold on affected side)
- Pronator drift (arm drops and pronates when held out)
- Aphasia (Broca's or Wernicke's) assessed via naming and repetition tests
- Gaze deviation (eyes look toward the side of the cortical lesion)
- Hemorrhagic Transformation: Reperfusion injury causing bleeding into the fragile, infarcted brain tissue, worsening deficits.
- Malignant Cerebral Edema: Massive swelling of a large MCA infarct, causing midline shift and fatal brain herniation.
- Aspiration Pneumonia: Due to dysphagia (swallowing impairment), a leading cause of post-stroke mortality.
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.
Differential Diagnosis
- Hemorrhagic Stroke (Intracerebral/Subarachnoid Hemorrhage)
- Todd's Paralysis (post-seizure focal deficit)
- Hypoglycemia (can perfectly mimic focal stroke)
- Complex Migraine with aura
Laboratory Tests & Biomarkers
- Point-of-care Blood Glucose: Must be checked immediately to rule out hypoglycemia.
- Coagulation panel (PT/INR, aPTT): To detect underlying coagulopathy or evaluate eligibility for thrombolytics (INR > 1.7 is a contraindication for tPA).
Imaging Modalities & Findings
- Non-contrast Head CT: Used immediately to rule out intracranial hemorrhage. Early ischemic signs: loss of insular ribbon, hyperdense MCA sign, sulcal effacement.
- CT Angiography (CTA) of Head/Neck: Identifies Large Vessel Occlusion (LVO), such as distal ICA or proximal MCA (M1) occlusion, guiding thrombectomy.
- MRI Brain (Diffusion-Weighted Imaging - DWI): Gold standard for identifying acute ischemia; shows bright restricted diffusion within minutes of symptom onset.
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Hyperacute
0 to 24 hours. Window for emergent reperfusion therapy (tPA up to 4.5h, thrombectomy up to 24h).
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Acute
1 to 7 days. High risk for cerebral edema, hemorrhagic transformation, and secondary complications (DVT, pneumonia).
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Subacute/Chronic
>7 days. Focus shifts completely to physical rehabilitation and secondary prevention.
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.
Recommended Lifestyle Changes
- Participate in daily intensive physical, occupational, and speech therapy.
- Adopt the Mediterranean diet.
- Perform swallow evaluation before oral intake to prevent aspiration.
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.
Frequently Asked Questions
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