ABSTRACT
The cytokine storm associated with coronavirus disease 2019 (COVID-19) triggers a hypercoagulable state leading to venous and arterial thromboembolism. Lab findings associated with this phenomenon are elevated D-dimer, fibrinogen, C-reactive protein (CRP), ferritin, and procalcitonin. We present the case of a 66-year-old male with dyslipidemia who was diagnosed with COVID-19 with worsening shortness of breath, myalgia, and loss of taste. Physical examination was remarkable for crackles with diminished lung sounds and use of his accessory muscles. Labs showed normal white blood cell count, D-dimer of 1.42 mg/L, ferritin of 961 ng/mL, lactate dehydrogenase (LDH) of 621 U/L, and CRP of 2.1 mg/dL. Chest X-ray showed atypical pneumonitis with patchy abnormalities. He required oxygen supplementation with fraction of inspired oxygen of 100% proning as tolerated. He received remdesivir, ceftriaxone, azithromycin, dexamethasone, prophylactic enoxaparin, and a unit of plasma therapy. His D-dimer had increased from 1.65 to 3.51 mg/L with worsening dyspnea. At this time, computed tomography angiogram (CTA) of the chest showed extensive ground-glass opacities and a 2.4 × 1.9 × 1.3 cm distal thoracic aortic intraluminal thrombus. He was started on a heparin drip. A follow-up CTA of the aorta showed thrombus or hypoattenuation within the splenic artery and wedge-shaped areas extending from the hilum with possible infarction and a 6 mm thrombus in the infrarenal abdominal aorta. He was transitioned to enoxaparin 1 mg/kg twice daily. He remained asymptomatic from his splenic infarction. This case adds more insight to splenic infarction associated with COVID-19 in addition to the 32 reported cases documented thus far. Management of thromboembolism includes a therapeutic dose of anticoagulation. To prevent thromboembolism, prophylactic anticoagulation is recommended for those hospitalized with COVID-19.