COVID-19 and hypercoagulability

It has been observed that patients with COVID-19 infection may develop acute pulmonary embolism (APE), myocardial infarction, limb thrombosis, and venous / or arterial including central nervous system. Thrombosis formation in can be explained by the virchow triad. Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) directly attack vascular endothelial cells, causing excessive activation of immune system cytokine storm, thrombosis. Increased prothrombotic factors such as antiphospholipid antibodies, elevated factor VIII, high fibrinogen, circulating microparticles, neutrophil extracellular traps have reported infection. argued complement-mediated damage, increase pro-inflammatory cytokines interleukin (IL)-1, IL-6, IL-8 interferon-γ cause Autopsies revealed causes death were pneumonia embolism. When monitoring patients, platelet, prothrombin time (PT) activated partial thromboplastin (aPTT), fibrinogen D-dimer should initiated every 1-2 days, especially critically ill patients. High levels are associated mortality; indicate infection/sepsis, impending organ failure. Disseminated intravascular coagulation (DIC) seen but unlike DIC, is usually high. Clotting times platelet counts normal. Therefore, it appropriate to use sepsis-induced coagulopathy (SIC) criteria follow-up Infected areas related radiological appearance. Some enlarged subsegmental vessels. Treatment underlying disease most important treatment for all coagulopathies. Patients thromboembolism, inpatient medical, surgical, therapy receive anticoagulant unless there a contraindication anticoagulation (for example, active bleeding severe within previous 24 48 hours).