Abstract
The most common complication of tunneled‐cuffed hemodialysis catheters is catheter‐related bacteremia (CRB), which contributes to patient morbidity and loss of vascular access. Gram positive microorganisms are the most common etiologic agents; coagulase negative staphylococcus and corynebacterium species are the two most prevalent strains in our center. These are the common inhabitants of skin flora, suggesting that infection of catheters occur through the exit site. The Biopatch is a chlorhexidine impregnated dressing designed to keep the exit site from colonization with skin flora. This may decrease the incidence of CRB due to organisms from the skin. Objective: To investigate whether the application of the biopatch at the exit site has any effect on the incidence and the etiology of CRB. Methods: Chart review of 63 pediatric chronic hemodialysis patients who were dialysed between January 1999 and December 2003 was performed. The mean age at start of hemodialysis was 13.9 ± 4.6 years. The pre‐Biopatch era started in January 1999 till the end of June 2001, and the Biopatch era started in July 2001 to December 2003. Biopatch was applied at the beginning of every dialysis week after Betadine cleansing of the exit site, which was then covered with a transparent dressing. In the pre‐Biopatch era, the exit site was cleansed with Betadine at every dialysis session and then covered with a transparent dressing. Results: The use of the Biopatch at the exit site caused a significant decrease in the exit site infections. However, contrary to what was expected, there was no decrease in the incidence of CRB. Pre‐Biopatch Era Biopatch Era p value Gram positive infections % 76% 76% NS Gram negative infections % 10% 14% NS Polymicrobial infections % 14% 10% NS Total number of infections 108 (19 patients) 143 (29 patients) NS Exit site infections‐number 20 (9 patients) 5 (3 patients) p < 0.05 Conclusion: The use of the Biopatch decreases exit site infections. However, it fails to decrease the incidence of CRB. It has no effect on the etiologic agent of the bacterial infection.
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