HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Schmidt, A. H. Articles by Swiontkowski, M. F. Search for Related Content PubMed PubMed Citation Articles by Schmidt, A. H. Articles by Swiontkowski, M. F.

Pathophysiology of Infections After Internal Fixation of Fractures

Dr. Schmidt is Assistant Professor of Orthopaedic Surgery, University of Minnesota School of Medicine, Minneapolis. Dr. Swiontkowski is Professor and Chairman, Department of Orthopaedic Surgery, University of Minnesota School of Medicine, Minneapolis.

Reprint requests: Dr. Schmidt, Hennepin County Medical Center, 701 Park Avenue, Minneapolis, MN 55415.

Infection complicating internal fixation of fractures is a serious complication that is difficult to treat. Whenever metallic devices are implanted in vivo, successful biointegration requires that host cells colonize the highly reactive implant surface. Bacteria such as staphylococci can also become adherent to metallic or polymeric implants and will compete with host cells for colonization of the implant surface. Once adherent, these bacteria form a biofilm and undergo phenotypic changes that make them resistant to the normal host immune response as well as to antibiotics. Furthermore, metallic implants themselves cause specific deficits in the function of the local immune system that may render the host response to infection inadequate. Any associated soft-tissue injury causes even greater impairment of local immune function. Despite the potentially detrimental impact of internal fixation, fracture stability is of paramount importance in achieving fracture union and in preventing infection. It has been demonstrated in animal models that contaminated fractures without internal fixation develop clinical infection more commonly than similar fractures treated with internal fixation at the time of colonization. Because of the potential for infection whenever internal fixation is utilized, appropriate prophylactic antibiotic coverage for staphylococci and Gram-negative organisms should be provided. Open wounds and severely damaged soft tissues require aggressive management so that a viable soft-tissue envelope is maintained around the implant. Host factors such as smoking and malnourishment should be corrected. Early diagnosis and aggressive treatment of implant-related infection with antibiotics, debridement, and maintenance of stable internal fixation are essential to successful treatment.

This article has been cited by other articles:

				X. Chen, A. H. Schmidt, D. T. Tsukayama, C. A. Bourgeault, and W. D. Lew Recombinant Human Osteogenic Protein-1 Induces Bone Formation in a Chronically Infected, Internally Stabilized Segmental Defect in the Rat Femur J. Bone Joint Surg. Am., July 1, 2006; 88(7): 1510 - 1523. [Abstract] [Full Text] [PDF]

				M. J. Patzakis and C. G. Zalavras Chronic Posttraumatic Osteomyelitis and Infected Nonunion of the Tibia: Current Management Concepts J. Am. Acad. Ortho. Surg., October 1, 2005; 13(6): 417 - 427. [Abstract] [Full Text] [PDF]