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dc.contributor.authorWang, Janice
dc.contributor.authorHajizadeh, Negin
dc.contributor.authorMoore, Ernest E.
dc.contributor.authorMcIntyre, Robert C.
dc.contributor.authorMoore, Peter K.
dc.contributor.authorVeress, Livia A.
dc.contributor.authorYaffe, Michael B.
dc.contributor.authorMoore, Hunter B.
dc.contributor.authorBarrett, Christopher D.
dc.date.accessioned2020-05-12T19:50:14Z
dc.date.available2020-05-12T19:50:14Z
dc.date.issued2020-04
dc.identifier.issn1538-7933
dc.identifier.issn1538-7836
dc.identifier.urihttps://hdl.handle.net/1721.1/125190
dc.description.abstractA hallmark of severe COVID-19 is coagulopathy, with 71.4% of patients who die of COVID-19 meeting ISTH criteria for disseminated intravascular coagulation (DIC) while only 0.6% of patients who survive meet these criteria (1). Additionally, it has become clear that this is not a bleeding diathesis but rather a predominantly pro-thrombotic DIC with high venous thromboembolism rates, elevated D-dimer levels, high fibrinogen levels in concert with low anti-thrombin levels, and pulmonary congestion with microvascular thrombosis and occlusion on pathology in addition to mounting experience with high rates of central line thrombosis and vascular occlusive events (e.g. ischemic limbs, strokes, etc.) observed by those who care for critically ill COVID-19 patients (1-7). There is evidence in both animals and humans that fibrinolytic therapy in Acute Lung Injury and ARDS improves survival, which also points to fibrin deposition in the pulmonary microvasculature as a contributory cause of ARDS and would be expected to be seen in patients with ARDS and concomitant diagnoses of DIC on their laboratory values such as what is observed in more than 70% of those who die of COVID-19 (8-10).en_US
dc.language.isoen
dc.publisherWileyen_US
dc.relation.isversionofhttp://dx.doi.org/10.1111/jth.14828en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alikeen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/en_US
dc.sourceWileyen_US
dc.titleTissue plasminogen activator (tPA) treatment for COVID‐19 associated acute respiratory distress syndrome (ARDS): A case seriesen_US
dc.typeArticleen_US
dc.identifier.citationWang, Janice et al. "Tissue plasminogen activator (tPA) treatment for COVID‐19 associated acute respiratory distress syndrome (ARDS): A case series." Journal of Thrombosis and Haemostasis (April 2020): 1-4 © 2020 International Society on Thrombosis and Haemostasisen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.relation.journalJournal of Thrombosis and Haemostasisen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2020-05-12T17:02:18Z
dspace.date.submission2020-05-12T17:02:20Z
mit.licenseOPEN_ACCESS_POLICY
mit.metadata.statusComplete


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