Sepsis and multiple organ failure.
OBJECTIVE
Sepsis and multiple organ failure are complex processes that result from dysregulation of the immune response and its associated hematological, hemodynamic and metabolic disturbances.


METHODS
Review of the pathophysiological basis for sepsis and a review of the literature on its mechanisms of expression.


RESULTS
Sepsis is the host response to an injury, often infectious in origin, that creates both pro- and anti-inflammatory immune responses. The level and duration of this response roughly correlates with outcome. Subcellular injury characterized by increased oxidative stress defines the central mitochondrial component of this process. Treatments which minimize the amplification of this response are usually more effective at reducing tissue injury than are measures aimed at suppressing the inflammatory response.


CONCLUSIONS
Sepsis is a complex process whose expression and treatment are just now being defined. Treatments that minimize the overall host response still represent the most effective strategies.
Pinsky
Michael R
MR
Department of Critical Care Medicine, Bioengineering and Anesthesiology, University of Pittsburgh, Pittsburgh, PA 15261, USA. pinskymr@upmc.edu
D016207:Cytokines / Q000502:physiology; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D007155:Immunologic Factors / Q000502:physiology; D018836:Inflammation Mediators / Q000502:physiology; D008928:Mitochondria / Q000502:physiology; D009102:Multiple Organ Failure / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology*; D016328:NF-kappa B / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D018805:Sepsis / Q000150:complications* / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy
D016207:Cytokines; D006360:Heat-Shock Proteins; D007155:Immunologic Factors; D018836:Inflammation Mediators; D016328:NF-kappa B