Recent studies showed that COVID-19 could be a risk factor of causing thromboembolism. What is the pathophysiology of it ? You may share your thoughts and opinions.
There is evidence of direct invasion of endothelial cells by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, potentially leading to cell injury. Other sources of endothelial injury include intravascular catheters and mediators of the acute systemic inflammatory response such as cytokines (eg, interleukin [IL]-6) and other acute phase reactants . A number of changes in circulating prothrombotic factors have been reported or proposed in patients with severe COVID-19 :
We know Covid 19 as a respiratory illness, but as more reports come in about the varied presentations of disease, we know that it is an inflammatory state where disseminated intravascular coagulopathy (DIC) different from that seen in sepsis leads to high mortality. The most typical haematological findings seen in patients with COVID-19 and coagulopathy are an increased D-dimer concentration, modest decrease in platelet counts, and prolonged prothrombin time.
In COVID-19, a systemic and pulmonary hypercoagulable state has been proposed independent of hypoxia, ARDS, and sepsis-
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