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Abstract

Erosion of endothelial surface, disruption of endothelial glycocalyx and hyperinduction of inflammasome complexes are some of the main events taking place in early stages of COVID. Shedding of endothelial glycocalyx is also an important pathophysiologic finding in burn injury. It has also been shown that NLRP3 inflammosome is pivotal in activation of proinflammatory cascades triggered by burn injury which results in propagation to burn Systemic Inflammatory Response Syndrome (SIRS). Disruption of physiologic antithrombotic state of intravascular compartment is a hallmark of COVID. Complement activation especially mannose binding lectin pathway seems to have pivotal role in complement triggered inflammation and thrombotic state. This pathway is also implicated in burn injury triggered Systemic Inflammatory Response Syndrome (SIRS) as part of an innate immunity. Many pathophysiologic aspects of burn SIRS and sepsis share some important characteristics with those of COVID. Therefore, several dimensions of burn management should be implicated and investigated in the treatment of COVID.

Keywords: Systemic inflammatory response syndrome; COVID; Cytokines; Ventilation; Circulation