Abstract
Background: Until 2016, the condition Sepsis was widely understood to be the systemic immune response syndrome in the presence or suspicion of an infectious source. Systemic immune response syndrome, an adaptive response, has been repeatedly demonstrated to lack specificity for sepsis. The current definition of sepsis describes a dysregulated host response to infection, yet the dysregulated nature of the response has yet to be defined. Successful recognition and management of sepsis are critically dependent on understanding and operationalizing the definition of sepsis.
Objective: The authors sought to review the current literature on sepsis and its relationship to oxygen downregulation within the mitochondria along the electron transport chain.
Methods: Articles retrieved from databases PubMed and CINAHL, pertaining to human cells, post 2001, in English, original experimental, quasi-experimental, or cohort design. Articles were selected and retrieved by the first author and synthesized by both authors.
Results: The 10 articles included in the review were all bench science cellular studies. They demonstrated consistent, statistically significant differences when investigating mitochondrial oxygen downregulation in sepsis versus control, offering strong, statistically significant support for the hypothesis of mitochondrial dysregulation in the septic host.
Conclusions: The evidence makes a compelling case for mitochondrial dysregulation to inform the current definition of sepsis as a dysregulated host response. As the evidence points to a linear, progressive time/exposure-dependent disruption in oxygen downregulation in sepsis at the cellular level, it lends credence to the recommendations for early intervention and its relationship with survivability. Time is not on the side of the individual with sepsis.