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The COVID-19 Pandemic: Disproportionate Thrombotic Tendency and Management Recommendations
Sabina Karim1, Amin Islam2,3,4, Shafquat Rafiq5
1Department of Paediatric Haematology and Oncology, National Institute of Cancer Research and Hospital, Mohakhali, Dhaka 1212, Bangladesh.
Insights
COVID-19 infection increases thrombosis risk due to inflammation and coagulopathy. This review covers laboratory findings, thromboembolic events, and treatments for COVID-19 associated coagulopathy.
Area of Science:
- Infectious Diseases
- Hematology
- Critical Care Medicine
Background:
- COVID-19, caused by SARS-CoV-2, presents a significant risk of thrombosis.
- Pathological mechanisms include excessive inflammation, platelet activation, endothelial dysfunction, and circulatory stasis.
- Coagulopathy in COVID-19 patients elevates mortality risk.
Purpose of the Study:
- To review laboratory findings in COVID-19 associated coagulopathy.
- To summarize the prohemostatic state and incidence of thromboembolic events.
- To explore potential therapeutic interventions and the role of biomarkers.
Main Methods:
- Literature review focusing on laboratory findings, clinical outcomes, and therapeutic strategies.
- Exploration of biomarkers for thrombosis and inflammation in relation to COVID-19 severity.
- Analysis of challenges in managing antithrombotic therapy for patients with pre-existing conditions.
Main Results:
- COVID-19 patients exhibit a prothrombotic state with increased risk of thromboembolic events.
- Biomarkers of thrombosis and inflammation correlate with disease severity.
- Empirical anticoagulation in severe cases without thrombosis requires careful consideration against evidence-based trials.
Conclusions:
- COVID-19 associated coagulopathy is a complex condition requiring careful management.
- Antithrombotic therapy needs individualized adjustments, especially in patients with pre-existing thrombotic diseases.
- Further research and evidence-based guidelines are crucial for optimizing patient care.
Abstract:
COVID-19 is an infectious disease caused by the SARS COV-2 virus. Patients with COVID-19 are susceptible to thrombosis due to excessive inflammation, platelet activation, endothelial dysfunction, and circulatory stasis, resulting in an increased risk of death due to associated coagulopathies. In addition, many patients receiving antithrombotic therapy for pre-existing thrombotic diseases can develop COVID-19, which can further complicate dose adjustment, choice and laboratory monitoring of antithrombotic treatment. This review summarizes the laboratory findings, the prohemostatic state, incidence of thromboembolic events and some potential therapeutic interventions of COVID-19 associated coagulopathy. We explore the roles of biomarkers of thrombosis and inflammation according to the severity of COVID-19. While therapeutic anticoagulation has been used empirically in some patients with severe COVID-19 but without thrombosis, it may be preferable to provide supportive care based on evidence-based randomized clinical trials. The likely lifting of travel restrictions will accelerate the spread of COVID-19, increasing morbidity and mortality across nations. Many individuals will continue to receive anticoagulation therapy regardless of their location, requiring on-going treatment with low-molecular weight heparin, vitamin K antagonist or direct-acting anticoagulants.
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