title: Lack of correlation between failure of gut barrier function and septic complications after major upper gastrointestinal surgery.
abstract: OBJECTIVE
  To determine the influence of abnormal gut barrier function on the risk of septic complications in patients undergoing major resectional surgery for upper gastrointestinal cancer.
  
  
  BACKGROUND
  A failure of the gut mucosal barrier to exclude bacteria and endotoxin from the portal and systemic circulation is incriminated in the development of sepsis and multiple organ failure. Although the experimental data is compelling, corroborative evidence from studies in humans is sparse. This study attempted to correlate both preoperative gut barrier dysfunction and the pattern of change after surgery with septic outcome.
  
  
  METHODS
  Sixty-eight patients undergoing curative resectional surgery for upper gastrointestinal cancer were monitored for 30-day septic morbidity (intraabdominal abscesses/empyema and pneumonia). Intestinal permeability, serum IgM and IgG anti-endotoxin antibodies (EndoCAb), and serum C-reactive protein were measured before surgery and on postoperative days 1 and 7.
  
  
  RESULTS
  Increased intestinal permeability before surgery did not predict septic outcome. Major surgery was associated with increased intestinal permeability and evidence of endotoxin exposure. Comparing sepsis and nonsepsis groups, however, there was no significant difference in intestinal permeability, endotoxin exposure, and the acute phase response after surgery.
  
  
  CONCLUSIONS
  This study demonstrates that gut barrier dysfunction occurs after surgery, but the magnitude of change does not differentiate patients in whom sepsis develops and those in whom it does not. Preoperative increased intestinal permeability had no predictive value for sepsis. This study failed to support the thesis that gut barrier dysfunction is directly linked to sepsis.
authors.affiliation: Academic Department of Surgery, St. James's University Hospital, Leeds, England.
authors.forename: S
authors.initials: S
authors.lastname: Kanwar
authors.forename: A C
authors.initials: AC
authors.lastname: Windsor
authors.forename: F
authors.initials: F
authors.lastname: Welsh
authors.forename: G R
authors.initials: GR
authors.lastname: Barclay
authors.forename: P J
authors.initials: PJ
authors.lastname: Guillou
authors.forename: J V
authors.initials: JV
authors.lastname: Reynolds
mesh_terms: D000210:Acute-Phase Reaction / Q000503:physiopathology; D000368:Aged; D018988:Bacterial Translocation / Q000502:physiology; D002463:Cell Membrane Permeability / Q000502:physiology; D004731:Endotoxins / Q000097:blood; D004938:Esophageal Neoplasms / Q000503:physiopathology / Q000601:surgery*; D005260:Female; D006801:Humans; D007413:Intestinal Mucosa / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000503:physiopathology / Q000601:surgery*; D011183:Postoperative Complications / Q000503:physiopathology*; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000503:physiopathology / Q000601:surgery*; D018746:Systemic Inflammatory Response Syndrome / Q000503:physiopathology*; D016896:Treatment Outcome
chemical_list: D004731:Endotoxins