Key Points
- Record last-known-well time and whether the presenting deficit is disabling.
- Check glucose immediately and obtain noncontrast head CT without delay.
- Add CTA when large-vessel occlusion is possible; advanced perfusion imaging is for selected patients and should not delay clearly indicated therapy.
- IV thrombolysis remains time dependent, with tenecteplase and alteplase used according to current protocol and patient eligibility.
- Mechanical thrombectomy eligibility has expanded and should be assessed urgently, including selected late-window, large-core, and basilar occlusions.
- Avoid hypotension, hypoxia, fever, and severe glucose derangement because each can worsen ischemic injury.
- Do not use intensive systolic BP lowering below 140 mm Hg after successful reperfusion solely to improve outcome.
- Perform dysphagia screening before oral intake and begin coordinated stroke-unit care early.
Algorithm
- Activate stroke alert; establish last-known-well time, baseline function, medication history, and focused contraindications.
- Assess ABCs, obtain NIHSS, check point-of-care glucose, place monitors and IV access.
- Obtain immediate noncontrast head CT and CTA when LVO is suspected; do not wait for routine laboratory results unless a specific abnormality is reasonably suspected.
- If eligible for IV thrombolysis, control blood pressure to the treatment threshold and administer tenecteplase or alteplase per institutional protocol.
- If an LVO is present, engage the neurointerventional team immediately and transfer rapidly when thrombectomy is not available on site.
- After reperfusion, monitor neurologic status and blood pressure closely and obtain emergent imaging for headache, vomiting, acute hypertension, or neurologic decline.
- Complete etiologic evaluation, swallow screening, telemetry, venous thromboembolism prevention, and secondary prevention once the patient is stabilized.
- Admit to a stroke unit or neuro-ICU and coordinate early rehabilitation planning.
Clinical Synopsis & Reasoning
Suspect acute ischemic stroke in any patient with sudden focal neurologic dysfunction, including unilateral weakness or numbness, aphasia, dysarthria, visual loss, neglect, gaze deviation, ataxia, or an unexplained acute change in consciousness. Establish the exact last-known-well time and determine whether symptoms are disabling, because treatment eligibility depends on both timing and clinical impact. Perform a rapid neurologic examination with the NIH Stroke Scale, but do not let scoring delay imaging or treatment. Check point-of-care glucose immediately because hypoglycemia can mimic stroke. Noncontrast head CT is the fastest standard test to exclude intracranial hemorrhage and major established infarction; CTA from arch to vertex should be obtained rapidly when large-vessel occlusion is possible. Advanced CT or MR perfusion imaging can identify selected patients with salvageable tissue beyond conventional windows, but should not delay treatment in patients who already meet criteria for reperfusion. The differential includes hemorrhage, seizure with postictal deficit, migraine aura, hypoglycemia, functional neurologic disorder, toxic-metabolic disease, CNS infection, and mass lesion. Review anticoagulant use, recent surgery or bleeding, platelet count when indicated, blood pressure, premorbid function, pregnancy status when relevant, and recent stroke or head trauma. Current AHA/ASA guidance recognizes broader eligibility for tenecteplase within 4.5 hours and expanded thrombectomy populations, including selected large-core and basilar artery occlusions. Every minute of untreated large-vessel ischemia can reduce the chance of functional independence, so parallel processing is essential.
Treatment Strategy & Disposition
Activate the institutional stroke pathway, stabilize airway and oxygenation, and avoid hypotension. Give supplemental oxygen only when needed to maintain adequate saturation. For eligible adults within 4.5 hours, IV thrombolysis should be offered promptly after hemorrhage is excluded and contraindications are reviewed. Tenecteplase is now an endorsed thrombolytic option in the 2026 AHA/ASA guideline and is particularly operationally attractive because it is given as a single bolus; alteplase remains an accepted therapy where used by protocol. Blood pressure must be reduced to the protocol threshold before IV thrombolysis, traditionally no higher than 185/110 mm Hg, and maintained below the post-treatment threshold. Evaluate suspected large-vessel occlusion urgently for endovascular thrombectomy. Selection now extends beyond older narrow criteria and may include appropriately selected patients with large ischemic cores, late presentation, and basilar artery occlusion. Do not delay transfer to a thrombectomy-capable center for completion of nonessential tests. Avoid aggressive glucose normalization; treat hypoglycemia and marked hyperglycemia while avoiding intensive targets that increase hypoglycemia. Treat fever and identify complications such as aspiration, cerebral edema, malignant hemispheric infarction, hemorrhagic transformation, and seizures. Withhold antiplatelet and anticoagulant therapy for the first 24 hours after IV thrombolysis and obtain follow-up brain imaging before starting antithrombotic treatment. Patients should be admitted to a dedicated stroke unit or neurocritical care setting based on severity, reperfusion therapy, airway status, blood pressure needs, and risk of edema.
Epidemiology / Risk Factors
- Ischemic stroke accounts for the majority of strokes and remains a leading cause of long-term adult disability.
- Major modifiable risks include hypertension, atrial fibrillation, diabetes, tobacco use, dyslipidemia, and carotid or intracranial atherosclerosis.
- Large-vessel occlusion causes a disproportionate share of severe disability and is the primary target for thrombectomy.
- Wake-up and unknown-onset strokes may still be treatable when advanced imaging demonstrates favorable tissue characteristics.
- Prehospital routing and rapid transfer systems materially affect access to reperfusion therapy.
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| Noncontrast CT head | Excludes intracranial hemorrhage and identifies major early ischemic change | May be normal early or show loss of gray-white differentiation | Required rapidly before thrombolysis in most pathways |
| CT angiography | Detects intracranial and extracranial large-vessel occlusion | Abrupt arterial cutoff or severe stenosis | Obtain rapidly when thrombectomy is possible |
| CT or MR perfusion | Estimates ischemic core and potentially salvageable tissue | Core-penumbra mismatch in selected patients | Useful for extended-window or uncertain-onset selection; should not delay otherwise indicated treatment |
| Point-of-care glucose | Identifies a common reversible stroke mimic | Hypoglycemia or marked hyperglycemia | Check immediately |
| CBC and coagulation testing | Identifies thrombocytopenia or coagulopathy when clinically relevant | Variable | Do not delay thrombolysis for routine results when abnormality is not suspected |
| ECG and telemetry | Detect atrial fibrillation, ischemia, or other arrhythmia | AF or other rhythm abnormality | Should not delay reperfusion |
| MRI brain | Confirms ischemia and defines small or posterior circulation lesions | Restricted diffusion | Useful when diagnosis remains uncertain or for selected wake-up stroke protocols |
IV Thrombolysis Quick Screen
| Item | Threshold or Rule |
|---|---|
| Brain imaging | No intracranial hemorrhage; no other imaging finding that clearly contraindicates thrombolysis |
| Time and tissue eligibility | Usually within 4.5 hours by clock time, with selected extended or unknown-onset treatment based on imaging and current protocol |
| Blood pressure before IV thrombolysis | Reduce to 185/110 mm Hg or lower before treatment under standard protocols |
| Recent anticoagulant exposure | Assess agent, timing, renal function, and relevant coagulation testing when required |
| Deficit severity | Treatment is based on whether symptoms are disabling, not NIHSS alone |
| LVO assessment | IV thrombolysis should not delay thrombectomy evaluation or transfer when a treatable occlusion is suspected |
Pharmacology
| Medication | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Tenecteplase | Fibrin-specific plasminogen activator | Minutes | IV thrombolysis in eligible acute ischemic stroke under current protocol | Intracranial and systemic bleeding; dose is weight based and indication specific |
| Alteplase | Recombinant tissue plasminogen activator | Minutes | Established IV thrombolytic alternative | Bleeding risk; requires bolus plus infusion and strict eligibility review |
| Aspirin | Irreversible platelet COX-1 inhibition | Hours | Early antiplatelet therapy when hemorrhage is excluded | Delay until follow-up imaging after IV thrombolysis; bleeding and allergy |
| Labetalol | Alpha and beta adrenergic blockade | Minutes | Short-acting BP control around reperfusion | Bradycardia, bronchospasm, hypotension |
| Nicardipine | Dihydropyridine calcium-channel blocker | Minutes | Titrated BP control before or after reperfusion | Hypotension and reflex tachycardia; infusion monitoring required |
Prognosis / Complications
- Functional outcome correlates strongly with time to reperfusion, baseline stroke severity, age, collateral circulation, infarct volume, and successful recanalization.
- Symptomatic intracranial hemorrhage is an important complication of thrombolysis but occurs in a minority of appropriately selected patients.
- Large hemispheric and cerebellar strokes can deteriorate from edema over subsequent days despite initially stable vital signs.
- Stroke-unit care improves outcomes through standardized prevention of aspiration, immobility complications, fever, and recurrent vascular events.
- Recovery may continue for months, and early multidisciplinary rehabilitation improves function and discharge planning.
Patient Education / Counseling
- Teach patients and families to call emergency services for any sudden focal neurologic symptom even if it improves, because transient symptoms may represent TIA or fluctuating stroke.
- Explain that treatment benefit is time dependent and that driving to the hospital can delay prehospital stroke activation.
- Before discharge, review the identified mechanism, antithrombotic plan, blood pressure goals, lipid therapy, diabetes care, smoking cessation, and rhythm monitoring when indicated.
- Discuss dysphagia, fall risk, communication deficits, depression, cognition, and caregiver needs as part of recovery planning.
- Provide clear instructions about urgent return for new neurologic symptoms, severe headache, repeated vomiting, or sudden decline.
Notes
The acute stroke workflow should be organized around parallel rather than sequential tasks. Imaging, medication reconciliation, blood pressure management, thrombolytic preparation, and thrombectomy communication can occur simultaneously. Current practice should follow the 2026 AHA/ASA guideline and local stroke-system protocols, particularly because thrombectomy eligibility has expanded and tenecteplase use has broadened. A patient who improves should not automatically be considered safe for discharge because fluctuating deficits can reflect persistent occlusion or high-risk TIA. Likewise, a low NIHSS does not mean a deficit is nondisabling. Aphasia, hemianopia, dominant-hand weakness, and gait-limiting ataxia may be profoundly disabling despite a modest score. After the reperfusion decision, attention turns to aspiration prevention, temperature, glucose, blood pressure, edema surveillance, antithrombotic timing, mechanism evaluation, and early rehabilitation.
References
- 2026 AHA/ASA Guideline for the Early Management of Patients With Acute Ischemic Stroke — Link
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