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Pathogenesis and Treatment Strategies of COVID-19-Related Hypercoagulant and Thrombotic Complications
1Department of Blood Transfusion Medicine, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, China.
Insights
Severe COVID-19 involves blood hypercoagulability and microthrombosis, leading to fatal complications. Anticoagulation and anti-inflammatory therapies are proposed as key treatments for severe cases.
Area of Science:
- Infectious Diseases
- Pathology
- Critical Care Medicine
Background:
- Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) causes COVID-19, a global health concern.
- COVID-19 presents with symptoms like fever, cough, and can lead to fatal complications such as acute kidney injury and acute respiratory distress syndrome.
- Cytokine storm in severe COVID-19 induces vascular endothelial injury, promoting hypercoagulability and disseminated intravascular coagulation.
Purpose of the Study:
- To summarize the mechanisms of hypercoagulability and thrombotic complications in severe COVID-19.
- To propose blood hypercoagulability and intravascular microthrombosis as critical development points in severe COVID-19.
- To highlight anticoagulation and anti-inflammatory therapy as potential treatment strategies.
Main Methods:
- Review of existing literature on COVID-19 pathophysiology.
- Analysis of autopsy findings in COVID-19 patients.
- Synthesis of evidence linking cytokine storm to hypercoagulability and thrombosis.
Main Results:
- Severe COVID-19 is characterized by systemic cytokine storm leading to vascular endothelial injury.
- This injury promotes a pro-thrombotic state, resulting in blood hypercoagulability and microthrombosis.
- Autopsy pathology confirms widespread intravascular coagulation in fatal COVID-19 cases.
Conclusions:
- Blood hypercoagulability and intravascular microthrombosis are key pathological events in severe COVID-19.
- Anticoagulation therapy may mitigate thrombotic complications.
- Anti-inflammatory treatments could address the underlying cytokine storm, offering a dual therapeutic approach.
Abstract:
The new type of pneumonia caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is endemic worldwide, and many countries cannot be spared, becoming a global health concern. The disease was named COVID-19 by the World Health Organization (WHO) on January 30, 2020, when the WHO declared the Chinese outbreak of COVID-19 to be a public health emergency of international concern. The clinical features of COVID-19 include dry cough, fever, diarrhea, vomiting, and myalgia. Similar to SARS-CoV and MERS-CoV, nearly 20% of patients experienced various fatal complications, including acute kidney injury and acute respiratory distress syndrome caused by cytokine storm. Furthermore, systemic cytokine storm induced vascular endothelial injury, which extensively mediates hypercoagulability in blood vessels and disseminated intravascular coagulation. The autopsy pathology of COVID-19 confirmed the above. This article briefly summarizes the mechanism of hypercoagulability and thrombotic complications of severe COVID-19 and proposes that blood hypercoagulability and intravascular microthrombosis are the development nodes of severe COVID-19. Therefore, anticoagulation and anti-inflammatory therapy can be used as important treatment strategies for severe COVID-19.
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