Ischemic Stroke¶
Chapter 438 | Part 13: Neurologic Disorders
KEY CLINICAL POINTS¶
- Ischemic stroke results from cerebral artery occlusion, leading to brain tissue infarction. Early revascularization is critical to salvage the ischemic penumbra.
- Thrombolysis with IV rtPA (within 4.5 hours) or endovascular thrombectomy (within 24 hours) is recommended for eligible patients.
- Antiplatelet agents (aspirin, clopidogrel, ticagrelor) and anticoagulants (warfarin, DOACs) are used for secondary prevention, depending on etiology.
- The ABCD2 score predicts stroke risk after TIA, guiding urgent evaluation and treatment.
- Carotid endarterectomy is indicated for symptomatic stenosis ≥ 70% or asymptomatic stenosis ≥ 80% with high surgical risk.
1. DEFINITION & OVERVIEW¶
Ischemic stroke occurs due to cerebral artery occlusion, leading to brain tissue infarction. The ischemic penumbra (reversible tissue) can be salvaged with revascularization. Early intervention is critical to prevent infarction.
Table 438-1: IV rtPA/Tenecteplase Administration Criteria¶
| INDICATION | CONTRAINDICATION |
|---|---|
| Clinical diagnosis of stroke | Sustained BP >185/11,1 mmHg despite treatment |
| Onset of symptoms to drug administration £4.5 h | Bleeding diathesis |
| CT scan showing no hemorrhage | Recent head injury or intracerebral hemorrhage |
| Age ‡18 years | Major surgery in preceding 14 days |
| No edema >1/3 of MCA territory | Gastrointestinal bleeding in preceding 21 days |
1.1 Pathophysiology¶
Acute occlusion of intracranial vessels reduces cerebral blood flow. Collateral circulation and systemic BP influence infarct size. Ischemia leads to ATP depletion, ion pump failure, glutamate release, and excitotoxicity. Reperfusion injury involves oxidative stress, inflammation, and blood-brain barrier disruption.
1.2 Ischemic Penumbra¶
The ischemic penumbra is the reversible tissue surrounding the infarct core. Perfusion imaging (CTP, MRI) identifies the mismatch between core and penumbra. Early revascularization aims to salvage penumbral tissue.
2. EPIDEMIOLOGY¶
Ischemic stroke is the most common stroke type (87% of cases). Risk factors include hypertension (68% relative risk reduction with antihypertensives), diabetes, atrial fibrillation, smoking, and hyperlipidemia. Incidence peaks in 65–85 years, with higher prevalence in males.
Table 438-4: Stroke Risk Factors¶
| RISK FACTOR | RELATIVE RISK | RELATIVE RISK REDUCTION WITH TREATMENT | NUMBER NEEDED TO TREAT |
|---|---|---|---|
| Hypertension | 2–5 | 38% | 100–300 |
| Atrial fibrillation | 1.8–2.9 | 68% (warfarin), 21% (aspirin) | 20–83 |
| Diabetes | 1.8–6 | No proven effect | |
| Smoking | 1.8 | 50% at 1 year | 560 |
| Hyperlipidemia | 1.8–2.6 | 16–30% | 230 |
| Symptomatic carotid stenosis (70–99%) | 65% at 2 years | N/A | 12 |
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Ischemic stroke arises from thrombosis, embolism, or hypoperfusion. Common causes include atherosclerosis, cardiac embolism (e.g., AF), and small-vessel disease. Pathogenesis involves endothelial dysfunction, platelet activation, and inflammatory responses.
Table 438-2: Causes of Ischemic Stroke¶
| COMMON CAUSES | UNCOMMON CAUSES |
|---|---|
| Thrombosis | Hypercoagulable disorders |
| Lacunar stroke (small vessel) | Protein C/S deficiency |
| Large-vessel thrombosis | Antiphospholipid syndrome |
| Embolic occlusion | Factor V Leiden mutation |
| Carotid bifurcation | Prothrombin G20210A mutation |
| Aortic arch | Systemic malignancy |
| Arterial dissection | Sickle cell anemia |
| Cardioembolic | b-Thalassemia |
3.1 Embolic Sources¶
Cardiac sources (AF, MI, valvular vegetations) and extracranial sources (carotid atherosclerosis, dissection) contribute to embolic strokes. Paradoxical embolism via PFO is a risk in patients with venous thrombosis.
3.2 Small-Vessel Disease¶
Lacunar infarcts result from small-vessel occlusion (e.g., lipohyalinosis). Clinical syndromes include pure motor hemiparesis, sensory stroke, and ataxic hemiparesis. Risk factors include hypertension and aging.
4. CLINICAL FEATURES¶
Symptoms include sudden focal neurological deficits (hemiparesis, aphasia, visual field loss). TIAs present with transient deficits resolving within 24 hours. Complications include cerebral edema, herniation, and secondary hemorrhage.
4.1 TIA Presentation¶
Transient ischemic attacks (TIAs) mimic stroke but resolve completely. Common symptoms include monocular blindness (retinal artery occlusion), hemiparesis, or dysarthria. TIAs predict future stroke risk.
4.2 Complications¶
Cerebral edema peaks 2–3 days post-stroke, risking herniation. Reperfusion injury may cause hemorrhagic transformation. Fever and hyperglycemia worsen outcomes.
5. DIFFERENTIAL DIAGNOSIS¶
Differentiate ischemic stroke from hemorrhagic stroke, TIA, migraine, and other neurological disorders. CT or MRI is essential to confirm infarction vs. hemorrhage.
6. INVESTIGATIONS & DIAGNOSIS¶
Noncontrast CT is first-line for stroke triage. CTA/CTP identifies penumbra and occlusion. MRI (DWI/FLAIR) detects acute infarction. ABCD2 score predicts stroke risk after TIA.
Table 438-5: ABCD2 Score for TIA Risk¶
| CLINICAL FACTOR | SCORE |
|---|---|
| Age ‡60 years | 1 |
| SBP >140 mmHg or DBP >90 mmHg | 1 |
| Unilateral weakness | 2 |
| Speech disturbance without weakness | 1 |
| Duration >60 min | 2 |
| Diabetes | 1 |
6.1 Imaging Criteria¶
CT: Hyperdensity in MCA territory suggests acute occlusion. MRI: DWI hyperintensity with restricted diffusion. CTP: Mismatch between core and penumbra guides thrombectomy eligibility.
6.2 Diagnostic Algorithms¶
For suspected stroke: CT to rule out hemorrhage. If negative, administer IV rtPA within 4.5 hours or consider endovascular therapy. Use ABCD2 score for TIA risk stratification.
7. MANAGEMENT & TREATMENT¶
Immediate revascularization (thrombolysis or thrombectomy) is critical. Antiplatelet agents (aspirin, clopidogrel) and anticoagulants (DOACs) prevent recurrence. Rehabilitation and secondary prevention are essential.
Table 438-3: Antithrombotic Recommendations¶
| CONDITION | RECOMMENDATION |
|---|---|
| Nonvalvular AF | CHADS-VASc score ‡2: OAC; score 0–1: Aspirin |
| Symptomatic carotid stenosis ‡70% | Carotid endarterectomy or stenting |
| Asymptomatic carotid stenosis ‡80% | Medical therapy or surgery based on risk |
| Post-stroke | Aspirin + clopidogrel for 21–30 days, then aspirin alone |
7.1 Thrombolysis¶
IV rtPA (0.9 mg/kg, max 90 mg) within 4.5 hours. Tenecteplase (0.25 mg/kg IV) is an alternative. Contraindications include recent bleeding or INR >1.7.
7.2 Endovascular Therapy¶
Mechanical thrombectomy for large-vessel occlusions (M1/M2, basilar artery) within 24 hours. CTA/CTP identifies target lesions. Benefits include improved outcomes in selected patients.
7.3 Antiplatelet/ Anticoagulation¶
Aspirin (81–325 mg/d) for primary/secondary prevention. Clopidogrel or ticagrelor for TIA/stroke within 21–30 days. DOACs (apixaban, rivaroxaban) preferred over VKAs for NVAF.
8. PROGNOSIS & COMPLICATIONS¶
Early revascularization improves outcomes. Recurrent stroke risk is 10–15% within 3 months. Complications include cerebral edema, hemorrhagic transformation, and long-term disability.
8.1 Prognostic Factors¶
Time to treatment, infarct location, and baseline neurological status predict outcomes. Patients with large infarcts or poor functional status have worse prognoses.
8.2 Long-Term Risks¶
Secondary stroke risk is 2–3% annually with optimal medical therapy. Cognitive decline and dementia may occur in patients with leukoaraiosis or CADASIL.
9. SPECIAL CONSIDERATIONS¶
Management in pregnancy, elderly, and pediatric populations requires tailored approaches. Anticoagulation in AF is critical for stroke prevention, while carotid stenosis management depends on symptom status and surgical risk.
9.1 Pregnancy¶
Avoid anticoagulants in first trimester. Low-dose aspirin and heparin are preferred. Monitor for placental abruption and fetal distress.
9.2 Carotid Surgery¶
Carotid endarterectomy is indicated for symptomatic stenosis ≥ 70% or asymptomatic ≥ 80% with high surgical risk. Benefits are greatest within 2 weeks of symptom onset.
10. KEY POINTS & CLINICAL PEARLS¶
- Administer IV rtPA within 4.5 hours of stroke onset for eligible patients. 2. Use ABCD2 score to assess TIA stroke risk. 3. Antiplatelet agents are first-line for secondary prevention. 4. Endovascular therapy is effective for large-vessel occlusions. 5. Monitor for rebleeding and hemorrhagic transformation after thrombolysis.