Management of Thrombotic Complications in COVID-19: An Update
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REVIEW ARTICLE
Management of Thrombotic Complications in COVID‑19: An Update Adrija Hajra1 · Sheetal Vasundara Mathai1 · Somedeb Ball2 · Dhrubajyoti Bandyopadhyay3 · Maedeh Veyseh1 · Sandipan Chakraborty4 · Carl J. Lavie5 · Wilbert S. Aronow6
© Springer Nature Switzerland AG 2020
Abstract Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV‑2), is now a global pandemic. This virus primarily affects the respiratory tract and causes lung injury characterized by acute respiratory distress syndrome. Although the pathophysiology of COVID-19 is not yet clear, the most widely accepted mechanism is systemic inflammation. A clinically significant effect of the inflammation is coagulopathy. As a result of this effect, patients are found to have a high risk of venous thromboembolism. Studies have reported a high incidence of thrombotic complications in critically ill patients with COVID-19. In this review, we discuss the most updated evidence on the pathophysiology, diagnosis, and treatment of the coagulopathy of COVID-19. Prophylactic anticoagulation is recommended for all in-patients with COVID-19. Those with a higher risk of developing thromboembolic events or who have already developed venous thromboembolism should be treated with therapeutic anticoagulation. We also discuss post-discharge prophylaxis for highrisk patients and some newly proposed treatments for the hypercoagulability that could improve the outcomes of the affected patients.
1 Introduction The unrelenting storm of coronavirus disease 2019 (COVID19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to overwhelm the health systems worldwide. The infection has already resulted in 2 million cases and a death toll of greater than 100,000 in the USA alone [1]. The exact pathophysiology and management of this global pandemic are evolving. COVID-19 is an acute complex systemic disorder that, in its most severe state,
presents with interstitial pneumonia progressing to acute respiratory distress syndrome (ARDS), sepsis, and multi-organ failure [2, 3]. Current evidence points to a hypercoagulable state, a sequela of hyper-inflammation, to be an important pathogenic mechanism contributing to increased mortality in COVID-19 [4–6]. This theory is backed by the reports of elevated inflammatory and coagulation markers; and a correlation between elevated interleukin (IL)-6 and fibrinogen levels [7, 8]. It remains unknown whether the hypercoagulable state could be a direct consequence of SARS
* Adrija Hajra [email protected]
1
Jacobi Medical Center/Albert Einstein College of Medicine, 1400 Pelham Pkwy S, The Bronx, NY 10461, USA
Sheetal Vasundara Mathai [email protected]
2
Texas Tech University Health Sciences Center, Lubbock, TX, USA
Somedeb Ball [email protected]
3
Icahn School of Medicine at Mount Sinai/Mount Sinai St. Luke’s West Hospital, Manhattan, NY, USA
Dhrubajyoti Bandyopadhyay [email protected]
4
Miami Valley Hospital, Dayton, OH
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