Thromboembolic disease in COVID-19 patients: A brief narrative review
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REVIEW
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Thromboembolic disease in COVID-19 patients: A brief narrative review Samhati Mondal1 , Ashley L. Quintili2 , Kunal Karamchandani3
and Somnath Bose4*
Abstract Corona virus 2 (SARS-CoV2/ Severe Acute Respiratory Syndrome Corona Virus 2) infection has emerged as a global health crisis. Incidence of thromboembolic disease is reported to be high in SARS-CoV2 disease and is seen in a multitude of organ systems ranging from cutaneous thrombosis to pulmonary embolism, stroke or coronary thrombosis sometimes with catastrophic outcomes. Evidence points towards a key role of thromboembolism, hypercoagulability and over production of proinflammatory cytokines mimicking a “cytokine storm” which leads to multiorgan failure. This brief narrative review highlights the pathophysiology and risk factors of thromboembolic disease and provides a framework for management of anticoagulation based on the current evidence. Key words: COVID-19, thrombosis, thromboembolism, SARS-CoV2, management, coagulation
Introduction The current coronavirus pandemic caused by the SARSCoV2 has rapidly emerged as a global health crisis. To date, over four million people have been affected by coronavirus disease 2019 (COVID-19) worldwide in about 188 countries and the number continues to grow [1]. In the United States alone, confirmed cases and deaths continue to rise, with current estimates at more than 1.9 million positive patients and over 110,000 deaths [1]. Symptoms range from asymptomatic or mild constitutional symptoms to pneumonia, sepsis and sometimes severe acute respiratory distress syndrome (ARDS) necessitating hospitalization and intensive care unit (ICU) admission [2]. The pivotal role of thrombo-inflammation and endothelial injury in the pathogenesis of the disease is being increasingly recognized. Overproduction of proinflammatory cytokines, including tumor necrosis factor (TNF), Interleukin (IL) -6, IL-8, and IL-1β, is believed to be the cause of what is being termed, “cytokine release syndrome” or “cytokine storm”, a phenomenon which is * Correspondence: [email protected] 4 Department of Anesthesiology, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, One Deaconess Road, Rosenberg 470, Boston, MA 02215, USA Full list of author information is available at the end of the article
however not unique to this disease and has been noted in sepsis and sterile inflammation as well. This exaggerated cytokine response may lead to multiorgan failure and eventually death in some patients [3]. In addition to elevations in pro-inflammatory markers, hypercoagulability has been identified to be playing a key role determining prognosis in patients with COVID-19 [4]. In some observational series, thrombotic complications have been noted to be as high as 31% in patients requiring ICU admission and the risk persists even in patients on anticoagulation [5–8]. We searched for all published, readily accessible, peerreviewed, full articles written in English on PUBMED and EMBASE (betwee
