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Published on: December 19, 2020
Pulmonary Thrombosis and Thromboembolism in COVID-19
1Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Insights
COVID-19 increases pulmonary thrombosis risk, even with anticoagulation. This review covers COVID-19
Area of Science:
- Pulmonary Medicine
- Hematology
- Infectious Diseases
Background:
- COVID-19 (Coronavirus Disease 2019) is linked to a heightened risk of pulmonary thrombosis.
- This risk persists even in patients receiving prophylactic anticoagulation.
- Pulmonary thrombosis in COVID-19 may stem from hypercoagulability and direct vascular/endothelial injury.
Purpose of the Study:
- To review the epidemiology and pathophysiology of COVID-19-associated pulmonary thrombosis.
- To discuss diagnostic challenges and treatment strategies for pulmonary embolism (PE) in COVID-19 patients.
- To examine the rationale behind aggressive anticoagulation protocols in severe COVID-19.
Main Methods:
- Literature review of epidemiologic and pathophysiologic features.
- Analysis of diagnostic challenges in differentiating PE from COVID-19 pneumonia.
- Review of current treatment approaches, including aggressive anticoagulation.
Main Results:
- COVID-19 presents a complex thrombotic risk involving both large-vessel thromboembolism and microvascular thrombosis.
- Pulmonary thrombosis can explain disproportionate hypoxemia in some COVID-19 pneumonia cases.
- Diagnosing PE in COVID-19 is challenging due to overlapping symptoms.
Conclusions:
- Pulmonary thrombosis is a significant complication of COVID-19.
- Understanding the dual mechanisms of thrombosis is crucial for effective management.
- Aggressive anticoagulation strategies are being employed to mitigate COVID-19-related thrombotic events.
Abstract:
COVID-19, the disease responsible for the devastating pandemic that began at the end of 2019, has been associated with a significantly increased risk of pulmonary thrombosis, even in patients receiving prophylactic anticoagulation. The predilection for thrombosis in COVID-19 may be driven by at least two distinct, but interrelated, processes: a hypercoagulable state responsible for large-vessel thrombosis and thromboembolism and direct vascular and endothelial injury responsible for in situ microvascular thrombosis. The presence of pulmonary thrombosis may explain why hypoxemia is out of proportion to impairment in lung compliance in some patients with COVID-19 pneumonia. Because pulmonary embolism (PE) and COVID-19 pneumonia share many signs and symptoms, diagnosing PE in patients with COVID-19 can be challenging. Given the high mortality and morbidity associated with severe COVID-19 and the concern that aspects of the disease may be driven by thrombosis, many hospital systems have instituted aggressive anticoagulation protocols above standard VTE prophylaxis. In this review, the epidemiologic and pathophysiologic features, diagnosis, and treatment of COVID-19 pulmonary thrombosis and thromboembolism are discussed.
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