Abstract
Despite advances in intensive care and the widespread use of standardized care included in the Surviving Sepsis Campaign Guidelines, sepsis remains a leading cause of death, and the prevalence of sepsis increases concurrent with the aging process. The diagnosis of sepsis was originally based on the evidence of persistent bacteremia (septicemia) but was modified in 1992 to incorporate systemic inflammatory response syndrome (SIRS). Since then, SIRS has become the gold standard for the diagnosis of sepsis. In 2016, the Society of Critical Care Medicine and the European Society of Intensive Care Medicine published a new clinical definition of sepsis that is called Sepsis-3. In contrast to previous definitions, Sepsis-3 is based on organ dysfunctions and uses a sequential organ failure (SOFA) score as an index. Thus, patients diagnosed with respect to Sepsis-3 will inevitably represent a different population than those previously diagnosed. We assume that this drastic change in clinical definition will affect not only clinical practice but also the viewpoint and focus of basic research. This review intends to summarize the pathophysiology of sepsis and organ dysfunction and discusses potential directions for future research.
Highlights
Pro-inflammatory cytokines play major roles in inducing systemic inflammation and in the development of multiple organ dysfunction syndrome (MODS)
There have been significant advances in intensive care and the widespread use of standardized care in the Surviving Sepsis Campaign Guidelines
In accordance with the progress in our understanding of the pathophysiology of sepsis, the definition was greatly modified in 1992 to exclude bacteremia and to incorporate parameters related to systemic inflammation (Sepsis-1), Correspondence: fujishim@keio.jp Center for General Medicine Education, Keio University School of Medicine, Tokyo, Japan namely the systemic inflammatory response syndrome (SIRS) [2] (Fig. 1)
Summary
Pro-inflammatory cytokines play major roles in inducing systemic inflammation and in the development of MODS. Among the pro-inflammatory cytokines, tumor necrosis factor alpha (TNFα) and interleukin 1beta (IL-1β) are detected in the blood of patients with sepsis and are known to induce septic shock-like conditions when administered to animals in vivo, suggesting their key pathogenic roles in sepsis [8, 9].
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