title: Poor outcome from peritonitis is caused by disease acuity and organ failure, not recurrent peritoneal infection.
abstract: OBJECTIVE
  The purpose of the study is to determine whether organ failure develops in patients despite control of peritoneal infection and whether the process is, in part, neutrophil (polymorphonuclear leukocyte [PMN]) mediated.
  
  
  BACKGROUND
  Peritonitis generally responds to prompt surgical intervention and systemic antibiotics; however, some patients continue a septic course and progress to organ failure and death.
  
  
  METHODS
  One hundred five consecutive patients with peritonitis between 1988 and 1996 who required operation and a postoperative hospital stay greater than 10 days were studied. Mice were injected with a monoclonal anti-PMN antibody 24 hours before cecal ligation and puncture (CLP) to deplete PMNs.
  
  
  RESULTS
  Thirty-eight patients died, and all but 1 had identified organ failure. Seventy-seven patients had either pulmonary failure alone (25 patients) or as a component of multisystem organ failure (52 patients). All but one of these patients showed resolution of their intraperitoneal infection as evident by clinical course, abdominal computed tomographic scan, second-look laparotomy, or autopsy. Recurrent intra-abdominal infection developed in 15 patients, but only 1 had organ failure, and 2 died. At 18 hours after CLP, lung injury, PMN content, interleukin-1 mRNA expression, and liver injury were significantly reduced by anti-PMN treatment, whereas serum endotoxin levels actually increased.
  
  
  CONCLUSIONS
  Disease acuity and organ failure, and not recurrent peritoneal infection, are the major causes of adverse outcome in patients with peritonitis. The authors' experimental data indicate that such organ injury is, in part, PMN mediated but not endotoxin mediated. Attraction of PMNs toward the site of primary infection, and thereby away from remote organs, is a logical future therapeutic approach in such patients who are critically ill with peritonitis.
authors.affiliation: Department of Surgery, University of Louisville School of Medicine, KY, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Wickel
authors.forename: W G
authors.initials: WG
authors.lastname: Cheadle
authors.forename: M A
authors.initials: MA
authors.lastname: Mercer-Jones
authors.forename: R N
authors.initials: RN
authors.lastname: Garrison
mesh_terms: D018806:APACHE; D000328:Adult; D000368:Aged; D000818:Animals; D000911:Antibodies, Monoclonal; D005260:Female; D006801:Humans; D007167:Immunotherapy; D007375:Interleukin-1 / Q000378:metabolism; D008168:Lung / Q000503:physiopathology; D008297:Male; D051379:Mice; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000209:etiology*; D009504:Neutrophils / Q000276:immunology*; D010538:Peritonitis / Q000150:complications* / Q000401:mortality / Q000503:physiopathology / Q000628:therapy; D009195:Peroxidase / Q000378:metabolism; D012008:Recurrence; D018805:Sepsis / Q000209:etiology; D000637:Transaminases / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D007375:Interleukin-1; D009195:Peroxidase; D000637:Transaminases