Current theories on the pathophysiology of multiple organ failure after trauma.
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.
Tsukamoto
Takeshi
T
Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA, USA. tsukamotot@upmc.edu
Chanthaphavong
R Savanh
RS
Pape
Hans-Christoph
HC
D003167:Complement Activation / Q000502:physiology; D003165:Complement System Proteins / Q000378:metabolism / Q000502:physiology*; D016207:Cytokines / Q000276:immunology* / Q000378:metabolism; D018450:Disease Progression; D024243:HMGB1 Protein / Q000009:adverse effects / Q000502:physiology; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D008297:Male; D009102:Multiple Organ Failure / Q000276:immunology / Q000503:physiopathology*; D009504:Neutrophils / Q000276:immunology; D017382:Reactive Oxygen Species / Q000009:adverse effects* / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*; D012128:Respiratory Distress Syndrome / Q000276:immunology; D018805:Sepsis / Q000276:immunology; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology; D014947:Wounds and Injuries / Q000150:complications*
D016207:Cytokines; D024243:HMGB1 Protein; D017382:Reactive Oxygen Species; D003165:Complement System Proteins