Immunology · Year 2 · from Immunology
Case 8: Acute Ischemic Stroke in a Young Patient with COVID-19
Clinical Image
Source: Wikipedia - Ischemic stroke - Public Domain
Case Presentation
A 38-year-old male with no significant past medical history is brought to the emergency department by ambulance after his wife witnessed sudden onset of right-sided weakness, facial droop, and inability to speak at 07:15. EMS reports symptom onset was approximately 90 minutes prior to arrival. He had tested positive for SARS-CoV-2 5 days ago with mild fever and myalgias. He is a non-smoker, takes no medications, and has no family history of stroke or coagulopathy. On examination, BP is 156/92 mmHg, HR 102 bpm, SpO2 94% on room air, and temperature 38.1C. Neurological assessment reveals global aphasia, right hemianopia, right hemiplegia with forced left gaze deviation, and a National Institutes of Health Stroke Scale (NIHSS) score of 19. Non-contrast CT head shows no hemorrhage with an ASPECTS score of 8. CT angiography demonstrates complete occlusion of the left middle cerebral artery (MCA) at the M1 segment with good collateral circulation. CT perfusion reveals a large penumbral mismatch (ischemic core 18 mL, penumbra 124 mL). IV alteplase 0.9 mg/kg is administered (10% bolus, 90% over 60 minutes) within the 4.5-hour window. He undergoes emergent mechanical thrombectomy with successful recanalization (TICI 2b/3) at 3 hours post-onset. Retrieved thrombus histopathology reveals a platelet-rich thrombus with abundant NET-laden neutrophils, consistent with immunothrombosis. Post-procedure workup reveals D-dimer 8.4 mcg/mL FEU, fibrinogen 580 mg/dL, anticardiolipin IgM positive (transient), and lupus anticoagulant positive. He is started on therapeutic enoxaparin 1 mg/kg subcutaneously every 12 hours. At discharge on day 8, his NIHSS has improved to 4, and repeat antiphospholipid antibody testing at 12 weeks is negative, consistent with transient infection-associated antiphospholipid antibodies.
Key Learning Points
- COVID-19 increases the risk of acute ischemic stroke 3- to 8-fold, even in young patients without traditional cardiovascular risk factors; mechanisms include endotheliitis from direct viral invasion of endothelial cells, hypercoagulability with elevated von Willebrand factor and factor VIII, NET-mediated immunothrombosis, and cardioembolism from COVID-associated myocarditis or atrial fibrillation
- Large vessel occlusion (LVO) strokes in COVID-19 patients disproportionately affect younger patients and often involve multiple vascular territories simultaneously; thrombus histopathology characteristically shows NET-rich, platelet-rich composition distinct from typical atherothrombotic clots
- Transient antiphospholipid antibodies (anticardiolipin, anti-beta2-glycoprotein I, lupus anticoagulant) are found in 30-50% of hospitalized COVID-19 patients and contribute to thrombotic risk through complement activation and endothelial cell activation; persistent positivity at 12 weeks is required to diagnose true antiphospholipid syndrome
- Acute stroke management in COVID-19 follows standard guidelines (IV thrombolysis within 4.5 hours, mechanical thrombectomy for LVO within 24 hours with favorable perfusion imaging), but post-stroke anticoagulation decisions must weigh the transient hypercoagulable state against hemorrhagic transformation risk