Venous Thrombosis Among Critically Ill Patients With Coronavirus Disease 2019 (COVID-19) | Critical Care Medicine | JAMA Network Open | JAMA Network
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    2 Comments for this article
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    May 30, 2020
    Coagulopathy in CoVID19 patients
    Camilo Colaco, PhD | ImmunoBiology Ltd
    The normal range for D-Dimer is 0.21 to 0.32mg/L on some assays. In your study, the D-dimer levels were 3.3mg/L in patients without DVT and 5.4mg/L in those with DVT. As clotting is a cascade, it should be expected that some patients with elevated D-dimer levels may progress to develop DVT. Have you looked if there is a difference in blood markers (including D-dimer) in the 15% who develop DVT compared to those that don't?
    Pragmatically, should we start treating with anticoagulant therapy before admission to ICU, as lung microthrombi could manifest as breathing difficulties?
    CONFLICT OF INTEREST: None Reported
    June 2, 2020
    Author reply to Dr. Colaco
    Tristan Morichau-Beauchant, MD | Centre Cardiologique du Nord
    Thank you for your interest in our article.
    Comparing biological markers and in particular D-Dimer levels in the group who develops DVT 48h after ICU admission and the group who does not develop DVT brings no significant difference, but the sample sizes are small.
    Current guidelines regarding anticoagulant prophylaxis for patients with COVID-19 pneumonia are heterogenous. Intermediate doses and full dose anticoagulant therapy have been recommended in some guidelines for more severe patients or patients with high levels of D-Dimers based on retrospective data. While waiting for more solid proof, it seems reasonable in my opinion to use at     least intermediate doses of anticoagulant therapy for patients with COVID-19 and high levels of inflammatory markers and D-Dimer.
    CONFLICT OF INTEREST: None Reported
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    Research Letter
    Critical Care Medicine
    May 29, 2020

    Venous Thrombosis Among Critically Ill Patients With Coronavirus Disease 2019 (COVID-19)

    Julien Nahum, MD1; Tristan Morichau-Beauchant, MD1; Fabrice Daviaud, MD1; et al Perrine Echegut, MD2; Jérôme Fichet, MD1; Jean-Michel Maillet, MD1; Stéphane Thierry, MD1
    Author Affiliations Article Information
    • 1Intensive Care Unit, Centre Cardiologique du Nord, Saint-Denis, France
    • 2Ultrasound and Vascular Lab, Centre Cardiologique du Nord, Saint-Denis, France
    JAMA Netw Open. 2020;3(5):e2010478. doi:10.1001/jamanetworkopen.2020.10478
    COVID-19 Resource Center
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    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) was identified as a new coronavirus causing pneumonia and acute respiratory distress syndrome. It has become a pandemic, spreading particularly quickly across Europe and the US. Most deaths are related to severe acute respiratory distress syndrome, but other organ failures, such as acute kidney failure and acute cardiac injury, seem also related to the disease.1 Inflammatory response is highly increased in coronavirus disease 2019 (COVID-19) infection, and inflammation is known to favor thrombosis. High dimerized plasmin fragment D (D-dimer) levels and procoagulant changes in coagulation pathways were reported among patients with severe COVID-19.2,3 An elevated rate of venous and arterial thrombotic events associated with COVID-19 infection has also been reported.4,5 This case series reports a systematic assessment of deep vein thrombosis among patients in an intensive care unit (ICU) in France with severe COVID-19.

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