Poor outcome from peritonitis is caused by disease acuity and organ failure, not recurrent peritoneal infection

• Published in: Annals of surgery 1997-06, Vol.225 (6), p.744-756
• Main Authors: Wickel, D J, Cheadle, W G, Mercer-Jones, M A, Garrison, R N
• Format: Article
• Language: English
• Subjects: Adult; Aged; Animals; Antibodies, Monoclonal; APACHE; Female; Humans; Immunotherapy; Interleukin-1 - metabolism; Lung - physiopathology; Male; Mice; Middle Aged; Multiple Organ Failure - etiology; Neutrophils - immunology; Peritonitis - complications; Peritonitis - mortality; Peritonitis - physiopathology; Peritonitis - therapy; Peroxidase - metabolism; Recurrence; Sepsis - etiology; Transaminases - metabolism
• ISSN: 0003-4932; 1528-1140
• DOI: 10.1097/00000658-199706000-00012

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. Peritonitis generally responds to prompt surgical intervention and systemic antibiotics; however, some patients continue a septic course and progress to organ failure and death. 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. 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. 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.