title: Epidemiology, pathophysiology and clinical presentation of gram-negative sepsis.
abstract: OBJECTIVE
  To review the epidemiology and pathophysiology of gram-negative sepsis and the new consensus terminology describing the clinical signs of sepsis.
  
  
  METHODS
  Review of the medical literature and compiled data from animal and clinical trials.
  
  
  METHODS
  Members of the Society of Critical Care Medicine, American College of Chest Physicians and American Association of Critical-Care Nurses with expertise on the subject of sepsis and its complications.
  
  
  RESULTS
  Preconference and general sessions were offered at the National Teaching Institutes of the American Association of Critical-Care Nurses, with the goal of clarifying the epidemiology, risk factors and pathophysiology of gram-negative sepsis. In addition, current terminology and new (1992) consensus terminology describing the clinical signs of sepsis were presented. Special emphasis was placed on the role of the healthcare provider in the prevention and recognition of sepsis and the role of the septic mediators in the septic cascade.
  
  
  CONCLUSIONS
  If the incidence of sepsis is to be reduced, the healthcare provider must be aware of the risk factors for sepsis and methods of reducing nosocomial infections. A thorough understanding of the role of mediators and consensus terminology used to describe sepsis, severe sepsis, septic shock and multiple organ dysfunction syndrome is necessary to recognize early or progressive signs of sepsis and to initiate state-of-the-art therapy.
authors.affiliation: Division of Trauma, Vanderbilt University Medical Center, Nashville, TN 37212.
authors.forename: M F
authors.initials: MF
authors.lastname: Hazinski
authors.forename: T J
authors.initials: TJ
authors.lastname: Iberti
authors.forename: N R
authors.initials: NR
authors.lastname: MacIntyre
authors.forename: M M
authors.initials: MM
authors.lastname: Parker
authors.forename: D
authors.initials: D
authors.lastname: Tribett
authors.forename: S
authors.initials: S
authors.lastname: Prion
authors.forename: H
authors.initials: H
authors.lastname: Chmel
mesh_terms: D000328:Adult; D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism / Q000502:physiology; D002423:Cause of Death; D002648:Child; D003167:Complement Activation / Q000502:physiology; D003422:Critical Care; D003428:Cross Infection / Q000175:diagnosis / Q000453:epidemiology* / Q000503:physiopathology* / Q000628:therapy; D003937:Diagnosis, Differential; D004731:Endotoxins / Q000502:physiology*; D016905:Gram-Negative Bacterial Infections / Q000175:diagnosis / Q000453:epidemiology* / Q000503:physiopathology* / Q000628:therapy; D006321:Heart / Q000503:physiopathology; D006801:Humans; D015994:Incidence; D007375:Interleukin-1 / Q000502:physiology; D009102:Multiple Organ Failure / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D009569:Nitric Oxide; D012307:Risk Factors; D012772:Shock, Septic / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D012955:Societies, Medical; D012956:Societies, Nursing; D009626:Terminology as Topic; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D014481:United States / Q000453:epidemiology
chemical_list: D004731:Endotoxins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D016718:Arachidonic Acid; D009569:Nitric Oxide