![]() ![]() Thromboembolism and hyper-coagulopathy are other components in the pathogenesis of severe COVID-19. The presence of viral cytopathic-like changes, infiltration of inflammatory cells (mononuclear cells and macrophages), and viral particles in histopathological samples are considered a consequence of both direct viral infection and immune hyperactivation. Results from autopsy series in COVID-19 patients have demonstrated a wide range of findings, including vascular involvement, congestion, consolidation, and hemorrhage as well as diffuse alveolar damage in lung tissue consistent with acute respiratory distress syndrome (ARDS). In addition to the lungs, the virus has been isolated from blood, urine, faeces, liver, and gallbladder. ![]() COVID-19 may involve multiple organ systems. ![]() Although the pathogenesis of COVID-19 has not been fully explained, the data obtained so far in hospitalized patients has revealed that serum cytokine and chemokine levels are high in severe COVID-19 patients, similar to those found with sepsis. As a consequence, the old definitions now require consideration of this new etiologic agent, namely SARS-CoV-2. From the outset of the pandemic, various reports have indicated that although there are some unique features pertinent to COVID-19, many of its acute manifestations are similar to sepsis caused by other pathogens. The COVID-19 pandemic has created a major alteration in the medical literature including the sepsis discussion. ![]()
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