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Wickel DJ, Cheadle WG, Mercer-Jones MA, et al. Poor outcome from peritonitis is caused by disease acuity and organ failure, not recurrent peritoneal infection. Ann Surg. 1997;225(6):744-53; discussion 753-6doi: 10.1097/00000658-199706000-00012.
Wickel, D. J., Cheadle, W. G., Mercer-Jones, M. A., & Garrison, R. N. (1997). Poor outcome from peritonitis is caused by disease acuity and organ failure, not recurrent peritoneal infection. Annals of surgery, 225(6), 744-53; discussion 753-6. https://doi.org/10.1097/00000658-199706000-00012
Wickel, D J, et al. "Poor outcome from peritonitis is caused by disease acuity and organ failure, not recurrent peritoneal infection." Annals of surgery vol. 225,6 (1997): 744-53; discussion 753-6. doi: https://doi.org/10.1097/00000658-199706000-00012
Wickel DJ, Cheadle WG, Mercer-Jones MA, Garrison RN. Poor outcome from peritonitis is caused by disease acuity and organ failure, not recurrent peritoneal infection. Ann Surg. 1997 Jun;225(6):744-53; discussion 753-6. doi: 10.1097/00000658-199706000-00012. PMID: 9230815; PMCID: PMC1190882.
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Wolters Kluwer Free PMC Article

Ann Surg. 1997 Jun;225(6):744-53; discussion 753-6. doi: 10.1097/00000658-199706000-00012.

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

Annals of surgery

D J Wickel, W G Cheadle, M A Mercer-Jones, R N Garrison

Affiliations

  1. Department of Surgery, University of Louisville School of Medicine, KY, USA.

PMID: 9230815 PMCID: PMC1190882 DOI: 10.1097/00000658-199706000-00012
Free PMC Article

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.

SUMMARY BACKGROUND DATA: 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.

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