Abstract
Sepsis remains a major worldwide cause of morbidity and mortality and remains amongst the leading causes of death in medical Intensive Care Units (ICUs). Increasing injury severity associated with trauma is a significant independent risk factor for sepsis and many of these patients require intensive care unit resource utilization with increased rates of mortality. There are many postulated theories regarding the mechanism surrounding the correlation between trauma and shock. One such theory evaluated the deterioration of the immune system after trauma with the activation of Damage Associated Molecular Proteins (DAMPs) and the potential role of mitochondrial release into the bloodstream following physical injury leading to the onset of the Systemic Inflammatory Response Syndrome (SIRS). Despite these proposed theories, a breach of cellular integrity seems to unravel a multitude of immunologic responses that in essence account for the deleterious symptoms associated with sepsis. The association between traumatic injury and sepsis is very complex. This review explores the multifaceted immunoinflammatory response and gives an in depth immunologic explanation of the fundamental mediators in the initiation and continuation of the inflammatory response following the loss of cellular integrity.
Highlights
BackgroundPost-traumatic sepsis is a significant cause of mortality and there are many factors, both demographically including age and race and injury factors including the mechanism and severity of injury that predict post traumatic sepsis to a considerable extent (Osborn et al, 2004)
Sepsis, defined by the Systemic Inflammation Response Syndrome (SIRS) criteria, has many overlapping features of those seen in traumatic injury and is essentially indistinguishable from an immunological standpoint
The dual function alarmins HMGB-1, Interleukin-1 alpha (IL-1a) and interleukin 33 (IL-33) represent fundamental mediators in both the initiation and continuation of the inflammatory response following the loss of cellular integrity as outlined in this review
Summary
BackgroundPost-traumatic sepsis is a significant cause of mortality and there are many factors, both demographically including age and race and injury factors including the mechanism and severity of injury that predict post traumatic sepsis to a considerable extent (Osborn et al, 2004). How these mechanisms of hyperinflammation and immunosuppression develop are poorly understood there is developing evidence that damaged tissues which release endogenous danger signals play a developing role in the immune dysfunction seen in traumatic injury (Marshall, 1997). Nitric Oxide (NO) and Tumor Necrosis Factor Alpha (TNF-alpha), a pleiotropic inflammatory cytokine, are activated upon epithelial injury which stimulate pro-apototic signaling proteins of immune effector cells, which may contribute to sepsis-associated MODS after severe trauma (Lenz et al, 2007).
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