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The authors of this case series describe the use of tissue plasminogen activator (tPA) in COVID-19–associated coagulopathy. The authors note the high rate of severe coagulopathy seen in deceased patients with COVID-19 compared with survivors (71.4% vs 0.6%) and highlight that the coagulopathy is predominantly thrombotic disseminated intravascular coagulation. They report the outcomes of 3 patients with COVID-19–related ARDS and coagulopathy who had transient improvement in their pulmonary function with tPA administration, which may further improve with repeated or higher dosing. Such treatment of hypothesized pulmonary microthrombi contributing to COVID-19–associated ARDS needs further study.
In this limited case series, the use of tPA resulted in transient improvement in pulmonary function among patients with COVID-19–associated ARDS. Larger prospective investigations may be warranted to determine if therapeutic anticoagulation and/or thrombolytics are associated with improved clinical outcomes while leveraging the risk of associated major bleeding events.
– Curtis Lachowiez, MD
This abstract is available on the publisher's site.
A 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).