TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: The complications of coronavirus disease 2019 (COVID-19) involve the nervous system, including acute stroke, which is currently linked to the hypercoagulable state associated with COVID-19 [1]. CASE PRESENTATION: Our patient is a 70-year-old man with past medical history of hypertension and diabetes mellitus who presented to the emergency department with shortness of breath and fatigue for five days duration. Vitaly was stable, except for saturating 88% on the room air. He was alert and oriented on physical exam, lung exam was remarkable for bibasilar rales. He had no focal neurological deficits. Lab Work showed elevated COVID-19 markers. Chest x-ray showed left-sided infiltrates. He was admitted to the respiratory care unit and was started on dexamethasone, remdesevir, ceftriaxone, azithromycin, and enoxaparin prophylactic dose. His oxygen requirement continued to increase, and on the ninth day, he was placed on a nasal high-flow oxygen device with 60 liters FiO2 of 90%. On the eleventh day, the patient developed right facial droop, aphasia and right-sided weakness. The National Institutes of Health Stroke Scale was 16. Code stroke was called, and a brain computed tomography scan without contrast revealed cortical infarct in the high left parietal cerebral hemisphere without hemorrhage. Computed tomography angiography (CTA) of the head and neck showed mild narrowing within the middle cerebral artery. Magnetic resonance imaging, later on, showed left medial frontoparietal infarct in ACA territory. Cardiology workup confirmed no cardiac pathology. The neurology team decided not to start the tissue plasminogen activator (tPA) because he was out of the tPA window, and as no large vessel occlusion was found, a thrombectomy was not performed. DISCUSSION: COVID-19 infection is considered a highly coagulable status, especially the severe form of the disease. The pathophysiology behind this is not well understood yet. However, Severe COVID-19 is associated with cytokine activation, which activates endothelial cells and mononuclear cells with expression of tissue factor leading to coagulation cascade activation [2]. It has also been observed that COVID-19 can induce Antiphospholipid antibodies, which might play a role in thrombosis in those patients [3]. Our case confirms that COVID-19 induced acute stroke can occur in multiple territories despite the patient being well anticoagulated. CONCLUSIONS: Acute stroke should be suspected in COVID-19 patients with acute neurological changes even if the patient is on prophylactic anticoagulation. Frequent screening neurological examination can lead to early detection and treatment of acute stroke. REFERENCE #1: Verstrepen, K., Baisier, L. & De Cauwer, H. Neurological manifestations of COVID-19, SARS and MERS. Acta Neurol Belg 120, 1051–1060 (2020). https://doi.org/10.1007/s13760-020-01412-4 REFERENCE #2: Beyrouti R, Adams ME, Benjamin L, et alCharacteristics of ischaemic stroke associated with COVID-19Journal of Neurology, Neurosurgery & Psychiatry 2020;91:889-891. REFERENCE #3: Zhang Y, Xiao M, Zhang S, Xia P, Cao W, Jiang W, Chen H, Ding X, Zhao H, Zhang H, Wang C, Zhao J, Sun X, Tian R, Wu W, Wu D, Ma J, Chen Y, Zhang D, Xie J, Yan X, Zhou X, Liu Z, Wang J, Du B, Qin Y, Gao P, Qin X, Xu Y, Zhang W, Li T, Zhang F, Zhao Y, Li Y, Zhang S. Coagulopathy and Antiphospholipid Antibodies in Patients with Covid-19. N Engl J Med. 2020 Apr 23;382(17):e38. doi: 10.1056/NEJMc2007575. Epub 2020 Apr 8. PMID: 32268022;PMCID: PMC7161262. DISCLOSURES: No relevant relationships by Abdul Rahman Al Armashi, source=Web Response No relevant relationships by Ameed Bawwab, source=Web Response No relevant relationships by Arthur Boyd, source=Web Response No relevant relationships by Kanchi Patell, source=Web Response No relevant relationships by Keyvan Ravakhah, source=Web Response No relevant relationships by Francisco Somoza-Cano, source=Web Response
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