Case Presentation: 56-year-old woman with past medical history of hypertension, cerebrovascular accident, coronary artery disease, atrial fibrillation on apixaban presented with worsening left arm weakness. Patient was on full dose anticoagulation with apixaban 5 milligram(mg) every 12 hours and antiplatelet therapy with aspirin 81 mg. On physical examination patient had ischemic left upper extremity. Computed Tomography Angiography of chest, abdomen, and pelvis showed thrombus in the aortic arch extending into the left subclavian artery resulting in near occlusion. Also, intraluminal thrombus was seen in the infrarenal aorta and another thrombus just above the aortic bifurcation. On admission, D-dimer was 4.49 microgram/ml, C-reactive protein 32.1 mg/liter, platelet count 621,000/microliter and ferritin 539 nanogram/milliliter. Coronavirus disease 2019(COVID-19) polymerase chain reaction was positive. Patient was emergently taken to the operating room for left brachial artery exploration, left upper extremity angiogram, left brachial artery thrombectomy and repair and left subclavian artery bypass. Post operatively, patient was started on heparin IV drip for anticoagulation. There was concern for antiphospholipid antibody syndrome(APLA) because of miscarriage and multiples stroke in the past. But anti-cardiolipin Immunoglobulin(Ig)M, IgG, beta2-glycoprotein, lupus anticoagulant were unremarkable. So APLA was ruled out. Regarding anticoagulation, patient was eventually transitioned to warfarin on discharge. Initially patient required oxygen supplement via nasal cannula secondary to COVID-19. Patient was started on Dexamethasone, and was later able to wean off oxygen.

Discussion: COVID-19 is associated with hypercoagulable state. Venous thromboembolism(VTE) is more common than arterial thrombosis(AT). Angelo et al in their meta-analysis reported 26 % incidence of VTE in COVID-19 patient. When compared with VTE incidence, one study from France showed AT event rate of 5.6%. We report a case of massive arterial thrombosis which happened while patient was on full dose anticoagulation with apixaban. Thrombosis is commonly seen in patients with COVID-19, but massive arterial thrombosis while on full dose anticoagulation is extremely rare. Virchow’s triad that predisposes a person to development of thrombosis include hypercoagulability, stasis and endothelial injury. Prothrombotic factors in patients with COVID-19 include elevated factor VIII, elevated fibrinogen, hyperviscosity and circulating prothrombotic microparticles. Immobilization can cause stasis of blood flow. There is evidence of direct invasion of endothelial cell by COVID-19 virus, which can potentially lead to endothelial injury. Other mechanism of endothelial injury could include microvascular inflammation, endothelitis, and complement-medicated endothelial injury. Arterial thrombotic events in COVID-19 consists of myocardial infarction, stroke, limb ischemia, massive aortic thrombosis, renal artery thrombosis and splenic infarction. D-dimer level was strongly associated with arterial thrombotic events in COVID-19 patients.

Conclusions: AT is less common when compared to VTE in COVID-19 patient. Our case is yet another demonstration of hypercoagulable state in COVID-19. Thrombosis while on anticoagulation is extremely rare and more challenging in COVID-19 patients. In our patient, we changed anticoagulation from apixaban to warfarin, and patient is doing well on this regimen.