Clot in Transit and Pulmonary Embolism in COVID-19

Clot in Transit in COVID-19 Introduction: Thromboembolism is a known complication of COVID-19, frequently occurring in patients receiving deep venous thrombosis (DVT) prophylaxis. This case report describes a patient with COVID-19 on DVT prophylaxis who had no other risk factors and developed a pulmonary embolism (PE) and subsequently was found to have a clot in transit in the right ventricular outflow tract on echocardiography. Case Report: 53-year-old male with no previous history of tobacco use, venous thromboembolism, malignancy, or clotting disorder was admitted with acute hypoxemic respiratory failure due to COVID-19. On initial examination, the patient was found to be hypoxic and tachycardic, requiring high flow nasal cannula. Chest x-ray showed multifocal airspace opacities consistent with COVID-19 pneumonia. CT pulmonary angiography was performed due to hypoxia and tachycardia, which revealed no evidence of PE. Laboratory results showed elevated inflammatory markers and a D-dimer of 1,700. The patient was admitted and started on dexamethasone, remdesivir, and subcutaneous heparin for DVT prophylaxis. The patient improved and oxygen was weaned down. On day 6 of hospitalization the patient developed acute dyspnea, worsening hypoxia, and tachycardia. Repeat CT pulmonary angiogram revealed multiple PE and therapeutic enoxaparin was started. An echocardiogram was performed and revealed an enlarged right ventricle and a large multi-lobulated hyperechoic mass in the right ventricular outflow tract, consist with a clot in transit. Interventional Radiology successfully performed aspiration thrombectomy, and the patient quickly improved and was discharged home on Apixaban. Discussion: As COVID-19 patients often present with hypoxemic respiratory failure and elevated D-dimer, it can be challenging for physicians to determine who should be screened for the presence of PE. Our case demonstrates the severity of hypercoagulability in COVID-19 and the importance of maintaining high suspicion for thromboembolism in COVID-19, even in patients receiving appropriate DVT prophylaxis and without risk factors. SARS-CoV-2 has been shown to bind to ACE2 on platelets and enhance thrombosis, indicating that infection itself can lead to DVT or PE. Even patient under guideline directed DVT prophylaxis frequently develop venous thromboembolism. Further investigation into how to prevent and catch pulmonary embolism in COVID-19 patients is needed. Methods such as daily D-dimer level trending, may be helpful in identifying patients at higher risk of developing PE or DVT but more research is needed to identify ideal cutoffs and DVT prophylaxis in these patients.