Pathophysiology of thromboembolism in patients with COVID-19

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dc.contributor.authorVityala, Yethindra
dc.contributor.authorKrishna, Abhijit
dc.contributor.authorPandla, Dinesh
dc.contributor.authorPriya Kanteti, Krishna
dc.contributor.authorSadhu, Jahnavi
dc.contributor.authorBoddeti, Harsha Vardhan
dc.contributor.authorKintali, Tejesh
dc.contributor.authorKhalid, Mohammad Shaour
dc.date.accessioned2022-07-04T08:32:47Z
dc.date.available2022-07-04T08:32:47Z
dc.date.issued2022
dc.description.abstractIntroduction and aim. A small number of critically ill patients with coronavirus disease (COVID-19) develop thromboembolism (arterial or venous), both micro- and macrovascular complications such as deep vein thrombosis, pulmonary embolism, and pulmonary arterial thrombosis. The objective of the study is to describe the pathophysiology of venous thromboembolism in patients with COVID-19. Material and methods. In this article a narrative review regarding pathophysiology of thromboembolism in patients with COVID-19. Analysis of the literature. The development of coagulopathy is a consequence of the intense inflammatory response associated with hypercoagulability, platelet activation, and endothelial dysfunction. The pathophysiology that relates pulmonary thromboembolism (PTE) with COVID-19 is associated with a hypercoagulable state. PTE is suspected in hospitalized patients presenting dyspnea, decreased oxygen requirement, hemodynamic instability, and dissociation between hemodynamic and respiratory changes. In COVID-19-associated coagulopathy, initially, patients present with elevated levels of fibrinogen and D-dimer, with minimal changes in prothrombin time and platelet count. The main risk factor for the development of pulmonary embolism is the increase in D-dimer that is associated with the development of PTE. The administration of iodine-based contrast agent to patients with COVID-19 would affect P-creatinine and renal function, where Ultrasound is viewed as cost-effective and highly portable, can be performed at the bedside. Conclusion. Acute respiratory distress syndrome severity in patients with COVID-19 can explain PTE as a consequence of an exaggerated immune response.pl_PL.UTF-8
dc.identifier.citationEuropean Journal of Clinical and Experimental Medicine T. 20, z. 2 (2022), s. 212–216pl_PL.UTF-8
dc.identifier.doi10.15584/ejcem.2022.2.10
dc.identifier.eissn2544-1361
dc.identifier.urihttp://repozytorium.ur.edu.pl/handle/item/8079
dc.language.isoengpl_PL.UTF-8
dc.publisherWydawnictwo Uniwersytetu Rzeszowskiegopl_PL.UTF-8
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Międzynarodowe*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectacute respiratory distress syndromepl_PL.UTF-8
dc.subjectCOVID-19pl_PL.UTF-8
dc.subjectpathophysiologypl_PL.UTF-8
dc.subjectpulmonary embolismpl_PL.UTF-8
dc.subjectthromboembolismpl_PL.UTF-8
dc.titlePathophysiology of thromboembolism in patients with COVID-19pl_PL.UTF-8
dc.typereviewpl_PL.UTF-8
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European Journal of Clinical and Experimental Medicine T.20, z. 2 (2022)