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Published on: December 19, 2020
Incidental and Asymptomatic Splenic Infarction and Infrarenal Thrombus in a COVID-19 Patient
Jordan Childers1, Tuong Vi C Do2, Forest Smith1
1Internal Medicine, Appalachian Regional Healthcare, Harlan, USA.
Insights
Coronavirus disease 2019 (COVID-19) can cause a hypercoagulable state, leading to arterial and venous thromboembolism. This case highlights splenic infarction as a rare complication of COVID-19, emphasizing the need for anticoagulation therapy.
Area of Science:
- Cardiology
- Infectious Diseases
- Hematology
Background:
- Coronavirus disease 2019 (COVID-19) is associated with a hypercoagulable state, increasing the risk of thromboembolic events.
- Elevated inflammatory markers like D-dimer, C-reactive protein (CRP), and ferritin are common in severe COVID-19.
- Venous and arterial thromboembolism are recognized complications of COVID-19.
Observation:
- A 66-year-old male with COVID-19 presented with respiratory distress and elevated inflammatory markers.
- Initial imaging revealed atypical pneumonitis, but subsequent computed tomography angiogram (CTA) demonstrated extensive ground-glass opacities and an aortic intraluminal thrombus.
- Further CTA revealed splenic artery thrombus, possible splenic infarction, and infrarenal abdominal aortic thrombus.
Findings:
- The patient developed arterial thromboembolism, including aortic and splenic artery thrombi, in the context of COVID-19.
- Splenic infarction, a rare complication, was identified in this patient.
- Laboratory findings included elevated D-dimer, ferritin, lactate dehydrogenase (LDH), and CRP.
Implications:
- This case expands the understanding of splenic infarction as a potential complication of COVID-19, adding to the limited reported cases.
- Effective management of thromboembolism in COVID-19 patients involves therapeutic anticoagulation.
- Prophylactic anticoagulation is recommended for hospitalized COVID-19 patients to prevent thromboembolic events.
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.
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