COVID-19 update: Covid-19-associated coagulopathy
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COVID‑19 update: Covid‑19‑associated coagulopathy Richard C. Becker1
© Springer Science+Business Media, LLC, part of Springer Nature 2020
We are too much accustomed to attribute to a single cause that which is the product of several, and the majority of our controversies come from that. Marcus Aurelius
The Covid-19 pandemic has introduced an array of organspecific and systemic phenotypes- some previously observed in viral infections, including severe acute respiratory syndrome (SARS) and others that appear to be unique to SARScoronavirus (CoV)-2. Rapidly emerging information from clinical observations, autopsy-based findings, extrapolations from in vitro and ex vivo studies and dynamic modeling are informing management guidelines; however, many questions remain unanswered and clinical trials that are required to provide evidence have not been completed in most areas. Among the many questions that require careful thought, reflection and investigation are the mechanism(s) underlying the development of a systemic coagulopathy and acquired thrombophilia characterized in a majority of cases by a proclivity for venous, arterial and microvascular thrombosis. The following review summarizes emerging insights into the pathobiology, mechanism(s), diagnosis, management, foundations for research and either planned or ongoing clinical trials for Covid-19-associated coagulopathy.
Venous and arterial thrombosis in Covid‑19 infection Klok et al. [1] evaluated the occurrence of venous and arterial thrombotic events, including deep vein thrombosis (DVT), pulmonary embolism (PE), ischemic stroke, * Richard C. Becker [email protected] 1
Heart, Lung and Vascular Institute, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, USA
myocardial infarction and systemic arterial events in 184 patients with Covid-19 pneumonia admitted to the intensive care unit (ICU). All patients received standard thromboprophylaxis (Nadroparin 2850 to 5700 IU per day based on body weight). The composite incidence of thrombotic events was 31%. Venous thromboembolic events were the most common (27%) and a majority were PEs. Independent predictors of thrombotic events were increased age and evidence on screening blood tests for a coagulopathy (prothrombin time [PT] > 3 s above the upper limit of normal [ULN]), activated partial thromboplastin time [APTT] > 5 s above the ULN; adjusted hazard ratio 4.1, 95% CI 1.9–9.1). None of the patients experiencing thrombotic events met strict criteria for disseminated intravascular coagulation (DIC). Tang et al. reported on abnormal coagulation parameters and poor prognosis in 183 consecutive patients with Covid-19 pneumonia [2]. Those who did not survive their illness compared with survivors had higher D-dimer levels, fibrin(ogen) degradation products (FDP) and longer PT and APTT values. Abnormal coagulation parameters were evident early after hospitalization and in some patients, fibrinogen concentrations and antithrombin activity decreased over time. The same investigato
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