Abstract
Aim: To identify the microbiology of infected knee arthroplasty, emerging patterns of resistance over the last decade, and suggest appropriate empirical treatment.
Methods: A retrospective analysis was conducted of 121 patients with microbiologically proven infection, who underwent revision TKA between 1994–2008. The causative organism was identified from microbiological samples and the corresponding sensitivities recorded. The data was then collated to determine the most common causative organisms, changing patterns of antibiotic resistance over the time frame, and the antibiotics currently most effective at treating deep infection. A theoretical model combining gentamicin with other antibiotics was used to determine the most effective antibiotics for use as empirical treatments.
Results: Coagulase negative Staphylococcus (CNS) was the most common causative organism (49%). Staphylococcus aureus (SA) accounted for 13% of cases. The prevalence of CNS appears to be increasing, while that of SA and other organisms is decreasing. Vancomycin and teicoplanin were the most effective antibiotics with overall sensitivity rates of 100% and 96% respectively. Levels of resistance were significantly higher among the antibiotics commonly used in the community. Antimicrobial resistance was higher when the causative organism was CNS, suggesting that MRSE is becoming a problem in knee arthroplasty. Our theoretical model showed that gentamicin combined with vancomycin would be the most effective empirical treatment.
Conclusion: Understanding the microbiology of deep infection of the knee allows surgeons to treat this complication as effectively as possible. Vancomycin and tei-coplanin appear to be the most effective antimicrobials, with relative invulnerability to the development of resistance. Given the effectiveness of these antibiotics, the use of vancomycin in gentamicin bone cement, combined with IV teicoplanin potentially allows for infected knee arthoplasties to be treated with a one-stage procedure. The rational use of antibiotics may help limit the amount of antibiotic resistance which develops in the future.
The abstracts were prepared by Mr Matt Costa and Mr Ben Ollivere. Correspondence should be addressed to Mr Costa at Clinical Sciences Research Institute, University of Warwick, Clifford Bridge Road, Coventry CV2 2DX, UK.
