Year 2021, Volume 7 , Issue 2, Pages 209 - 217 2021-03-04

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

Orcid: 0000-0003-4153-9953
Author: Hasan ÖLMEZ
Institution: Department of Pulmonary Diseases, Erzincan Binali Yıldırım University School of Medicine, Erzincan, Turkey
Country: Turkey


Orcid: 0000-0003-4153-9953
Author: Mustafa TOSUN
Institution: Department of Pulmonary Diseases, Erzincan Binali Yıldırım University School of Medicine, Erzincan, Turkey
Country: Turkey


Orcid: 0000-0002-0322-8102
Author: Edhem ÜNVER
Institution: Department of Pulmonary Diseases, Erzincan Binali Yıldırım University School of Medicine, Erzincan, Turkey
Country: Turkey


Orcid: 0000-0002-0722-6615
Author: Mehmet DOĞAN
Institution: Department of Pulmonary Diseases, Erzincan Binali Yıldırım University School of Medicine, Erzincan, Turkey
Country: Turkey


Orcid: 0000-0002-5192-6263
Author: Nurten ARSLAN IŞIK (Primary Author)
Institution: Department of Child Development, Erzincan Binali Yıldırım University Faculty of Health Sciences, Erzincan, Turkey
Country: Turkey


Dates

Application Date : November 26, 2020
Acceptance Date : February 5, 2021
Publication Date : March 4, 2021

EndNote %0 The European Research Journal COVID-19 and hypercoagulability %A Hasan Ölmez , Mustafa Tosun , Edhem Ünver , Mehmet Doğan , Nurten Arslan Işık %T COVID-19 and hypercoagulability %D 2021 %J The European Research Journal %P -2149-3189 %V 7 %N 2 %R doi: 10.18621/eurj.830973 %U 10.18621/eurj.830973