Surbhi Warrior, Elizabeth Behrens, Joshua Thomas, Sefer Gezer, Parameswaran Venugopal, Shivi Jain
{"title":"COVID-19患者血栓栓塞事件的预防","authors":"Surbhi Warrior, Elizabeth Behrens, Joshua Thomas, Sefer Gezer, Parameswaran Venugopal, Shivi Jain","doi":"10.1055/a-1576-6201","DOIUrl":null,"url":null,"abstract":"The novel coronavirus disease 2019 (COVID-19)-associated coagulopathy is a known cause of signi fi cant morbidity and mortality in patients affected by coronavirus. The proposed pathogenesis of hypercoagulability in COVID-19 patients is attributed to Virchow ’ s Triad, wherein hypoxia, severe in-fl ammation, and cytokine storm cause endothelial injury, activation of the coagulation cascade, and immobilization in critically ill patients, all contribute to increased risk of thrombosis. 1 Patients requiring intensive care unit (ICU) admission have increased risk of thrombosis despite standard dose of thromboprophylaxis. 2 – 4 COVID-19 treatment has focused on targeting the unregulated in fl ammatory state to decrease incidence of COVID-19-related complications, including thrombosis. Due to increased risk of thromboembolism, prophylactic anticoagulation is recommended in all hospitalized COVID-19 patients and intermediate to therapeutic dosing is sug-gested in patients with severe COVID-19, such as those requiring ICU admission. 5,6 In addition tohypercoagulability, COVID-19 patients are also at an increased risk for bleeding events due to variance in platelet production and destruc-tion, consumption of coagulation factors in the setting of severe in fl ammation, increased exposure to and dosing of anticoagulation","PeriodicalId":22238,"journal":{"name":"TH Open: Companion Journal to Thrombosis and Haemostasis","volume":"5 3","pages":"e415-e419"},"PeriodicalIF":0.0000,"publicationDate":"2021-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8463134/pdf/","citationCount":"0","resultStr":"{\"title\":\"Prevention of Thromboembolic Events in Patients with COVID-19.\",\"authors\":\"Surbhi Warrior, Elizabeth Behrens, Joshua Thomas, Sefer Gezer, Parameswaran Venugopal, Shivi Jain\",\"doi\":\"10.1055/a-1576-6201\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The novel coronavirus disease 2019 (COVID-19)-associated coagulopathy is a known cause of signi fi cant morbidity and mortality in patients affected by coronavirus. The proposed pathogenesis of hypercoagulability in COVID-19 patients is attributed to Virchow ’ s Triad, wherein hypoxia, severe in-fl ammation, and cytokine storm cause endothelial injury, activation of the coagulation cascade, and immobilization in critically ill patients, all contribute to increased risk of thrombosis. 1 Patients requiring intensive care unit (ICU) admission have increased risk of thrombosis despite standard dose of thromboprophylaxis. 2 – 4 COVID-19 treatment has focused on targeting the unregulated in fl ammatory state to decrease incidence of COVID-19-related complications, including thrombosis. Due to increased risk of thromboembolism, prophylactic anticoagulation is recommended in all hospitalized COVID-19 patients and intermediate to therapeutic dosing is sug-gested in patients with severe COVID-19, such as those requiring ICU admission. 5,6 In addition tohypercoagulability, COVID-19 patients are also at an increased risk for bleeding events due to variance in platelet production and destruc-tion, consumption of coagulation factors in the setting of severe in fl ammation, increased exposure to and dosing of anticoagulation\",\"PeriodicalId\":22238,\"journal\":{\"name\":\"TH Open: Companion Journal to Thrombosis and Haemostasis\",\"volume\":\"5 3\",\"pages\":\"e415-e419\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-08-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8463134/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"TH Open: Companion Journal to Thrombosis and Haemostasis\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1055/a-1576-6201\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/7/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"TH Open: Companion Journal to Thrombosis and Haemostasis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1055/a-1576-6201","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/7/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
Prevention of Thromboembolic Events in Patients with COVID-19.
The novel coronavirus disease 2019 (COVID-19)-associated coagulopathy is a known cause of signi fi cant morbidity and mortality in patients affected by coronavirus. The proposed pathogenesis of hypercoagulability in COVID-19 patients is attributed to Virchow ’ s Triad, wherein hypoxia, severe in-fl ammation, and cytokine storm cause endothelial injury, activation of the coagulation cascade, and immobilization in critically ill patients, all contribute to increased risk of thrombosis. 1 Patients requiring intensive care unit (ICU) admission have increased risk of thrombosis despite standard dose of thromboprophylaxis. 2 – 4 COVID-19 treatment has focused on targeting the unregulated in fl ammatory state to decrease incidence of COVID-19-related complications, including thrombosis. Due to increased risk of thromboembolism, prophylactic anticoagulation is recommended in all hospitalized COVID-19 patients and intermediate to therapeutic dosing is sug-gested in patients with severe COVID-19, such as those requiring ICU admission. 5,6 In addition tohypercoagulability, COVID-19 patients are also at an increased risk for bleeding events due to variance in platelet production and destruc-tion, consumption of coagulation factors in the setting of severe in fl ammation, increased exposure to and dosing of anticoagulation