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10.1097/CCM.0000000000004458

http://scihub22266oqcxt.onion/10.1097/CCM.0000000000004458
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32467443!7255402!32467443
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suck abstract from ncbi

pmid32467443
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  • Coagulopathy of Coronavirus Disease 2019 #MMPMID32467443
  • Iba T; Levy JH; Levi M; Connors JM; Thachil J
  • Crit Care Med 2020[Sep]; 48 (9): 1358-1364 PMID32467443show ga
  • OBJECTIVES: Recent studies have reported a high prevalence of thrombotic events in coronavirus disease 2019. However, the significance of thromboembolic complications has not been widely appreciated. The purpose of this review is to provide current knowledge of this serious problem. DESIGN: Narrative review. DATA SOURCES: Online search of published medical literature through PubMed using the term "COVID-19," "SARS," "acute respiratory distress syndrome," "coronavirus," "coagulopathy," "thrombus," and "anticoagulants." STUDY SELECTION AND DATA EXTRACTION: Articles were chosen for inclusion based on their relevance to coagulopathy and thrombosis in coronavirus disease 2019, and anticoagulant therapy. Reference lists were reviewed to identify additional relevant articles. DATA SYNTHESIS: Coronavirus disease 2019 is associated with a strikingly high prevalence of coagulopathy and venous thromboembolism that may contribute to respiratory deterioration. Monitoring coagulation variables is important, as abnormal coagulation tests are related to adverse outcomes and may necessitate adjuvant antithrombotic interventions. In the initial phase of the infection, D-dimer and fibrinogen levels are increased, while activated partial prothrombin time, prothrombin time, and platelet counts are often relatively normal. Increased D-dimer levels three times the upper limit of normal may trigger screening for venous thromboembolism. In all hospitalized patients, thromboprophylaxis using low-molecular-weight heparin is currently recommended. The etiology of the procoagulant responses is complex and thought to be a result of specific interactions between host defense mechanisms and the coagulation system. Although the coagulopathy is reminiscent of disseminated intravascular coagulation and thrombotic microangiopathy, it has features that are markedly distinct from these entities. CONCLUSIONS: Severe acute respiratory syndrome coronavirus 2/coronavirus disease 2019 frequently induces hypercoagulability with both microangiopathy and local thrombus formation, and a systemic coagulation defect that leads to large vessel thrombosis and major thromboembolic complications, including pulmonary embolism in critically ill hospitalized patients. D-dimers and fibrinogen levels should be monitored, and all hospitalized patients should undergo thromboembolism prophylaxis with an increase in therapeutic anticoagulation in certain clinical situations.
  • |*Betacoronavirus[MESH]
  • |Anticoagulants/*therapeutic use[MESH]
  • |Blood Coagulation Disorders/epidemiology/*etiology/prevention & control[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/*complications/physiopathology[MESH]
  • |Disseminated Intravascular Coagulation/etiology[MESH]
  • |Female[MESH]
  • |Humans[MESH]
  • |Male[MESH]
  • |Pandemics[MESH]
  • |Platelet Aggregation Inhibitors/therapeutic use[MESH]
  • |Pneumonia, Viral/*complications/physiopathology[MESH]
  • |Pregnancy[MESH]
  • |Prevalence[MESH]
  • |SARS-CoV-2[MESH]
  • |Thromboembolism/etiology[MESH]
  • |Thrombophilia/etiology[MESH]


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  • suck abstract from ncbi

    1358 9.48 2020