Current theories on the pathophysiology of multiple organ failure after trauma

Injury. 2010 Jan;41(1):21-6. doi: 10.1016/j.injury.2009.07.010.

Abstract

Despite the enormous efforts to elucidate the mechanisms of the development of multiple organ failure (MOF) following trauma, MOF following trauma is still a leading cause of late post-injury death and morbidity. Now, it has been proven that excessive systemic inflammation following trauma participates in the development of MOF. Fundamentally, the inflammatory response is a host-defence response; however, on occasion, this response turns around to cause deterioration to host depending on exo- and endogenic factors. Through this review we aim to describe the pathophysiological approach for MOF after trauma studied so far and also introduce the prospects of this issue for the future.

Publication types

  • Review

MeSH terms

  • Complement Activation / physiology
  • Complement System Proteins / metabolism
  • Complement System Proteins / physiology*
  • Cytokines / immunology*
  • Cytokines / metabolism
  • Disease Progression
  • HMGB1 Protein / adverse effects
  • HMGB1 Protein / physiology
  • Humans
  • Intestinal Mucosa / metabolism
  • Male
  • Multiple Organ Failure / immunology
  • Multiple Organ Failure / physiopathology*
  • Neutrophils / immunology
  • Reactive Oxygen Species / adverse effects*
  • Reactive Oxygen Species / metabolism
  • Reperfusion Injury / physiopathology*
  • Respiratory Distress Syndrome / immunology
  • Sepsis / immunology
  • Systemic Inflammatory Response Syndrome / immunology
  • Wounds and Injuries / complications*

Substances

  • Cytokines
  • HMGB1 Protein
  • Reactive Oxygen Species
  • Complement System Proteins