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Covid-19 pandemic severely hits the world, and many countries need to adapt their health systems to handle a large influx of patients with pneumonia due to this new virus. This unique crisis is putting a strain on our hospitals, which have to respond to the influx of patients with Covid19. At the same time, physicians must provide care for patients suffering from other, and sometimes urgent, conditions. In this context, the management of patients requiring major oncological or cardiac surgery within adapted (often short) timeframes is a difficult preoccupation, especially since that some pathophysiological data on this virus leads us to believe that immunosuppressive changes due to surgery may increase susceptibility to the virus. In this article, we present areas for reflection regarding the management of these patients during the Covid-19 pandemic situation, based on the little-known pathophysiological data on this virus. COVID-19 is a virus of the b-coronavirus family and is responsible for the third human epidemic of coronavirus zoonosis after SARS-Cov (2002) and MERS-Cov (2012). It is more precisely named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-Cov-2) because of its high sequence homology with SARS-Cov, sharing 80% genetic similarities [1] and equivalence in physiophathological mechanisms. All continents are currently affected, and the World Health Organization estimates that 179,111 cases are currently confirmed and 7426 deaths have occurred as of 17 March 2020. These figures are most probably underestimated since 80% of cases may be pauci-symptomatic and 34% asymptomatic [2]. Severe forms with respiratory failure can constitute up to 15% of cases and would be more frequent in patients with cardiovascular comorbidities, diabetes or advanced age [2], which can evolve into an Acute Respiratory Distress Syndrome (ARDS) in a rapid manner. Pathological analysis of a deceased patient revealed the presence of typical ARDS lesions with tissue edema, epithelial desquamation and hyaline membrane formations, associated with lymphocyte infiltration [3]. Due to the high similarity with SARS-Cov (angiotensin-converting enzyme 2 as receptor to penetrate into pulmonary epithelial, leukocytes or endothelial cells), we can assume that cellular damages are equivalent, with rapid viral replication within the pulmonary epithelial cells responsible for capillary leakage, cell apoptosis and a local pro-inflammatory process responsible for lymphocyte influx. In addition, Covid-19 patients present a particular immune profile with lymphopenia, mainly to the detriment of CD4? and CD8? T lymphocytes, but also B and NK lymphocytes [2, 4] and hyperneutrophilia with an increase in the Neutrophil/Lymphocyte (N/L) ratio. At the same time, Covid-19 patients present an unbalanced cytokine profile with a predominantly proinflammatory response & Emmanuel Besnier emmanuel.besnier@chu-rouen.fr
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Besnier et al. (2020) studied this question.
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