DAIR, Double DAIR, and DAPRI Procedures: Where Are the Unseen Bacteria?

Editor’s note: The Final Cut is a recurring editorial series written by a member of the AAOS Now Editorial Board.

One of the most devasting complications after total knee replacement is periprosthetic joint infection (PJI). Treatment options for PJI include a variety of bone-preserving, single-stage irrigations and debridements (I&Ds) or washouts. At present, debridement, antibiotics, and implant retention (DAIR); double DAIR; and debridement, antibiotic pearls, and retention of the implant (DAPRI) procedures are attempted to treat PJI.

Failure of I&D for PJI likely has several technical causes. First, there is most likely incomplete removal of bacteria-laden biofilm in the PJI region or on the implant. It has been proposed that after PJI I&D, bacteria re-emerge from biofilm, causing infection recurrence. Biofilm is a slimy, sticky, and adherent complex of biopolymers formed by bacteria within hours after bacterial contamination of a total joint replacement site (i.e., material that is impossible to remove by irrigation alone). Surgeons who perform I&D for PJI face two challenges. First and foremost, biofilm is not visible to the naked eye. Second, we don’t know where exactly biofilm exists on infected implants. Biofilm could exist on any or all 3D areas of implant surfaces. In general, I&D surgeons do their best to thoroughly clean an infected site during an I&D, but they do not know which surface areas should be targeted for cleaning. The questions this Final Cut article proposes are: Where are the unseen bacteria in PJI, and how do we improve our PJI I&Ds?

The DAIR procedure has a reported success rate of 50 to 80 percent. This relatively limited success rate prompted Calanna et al to modify the DAIR procedure by adding antibiotic-eluting pearls (calcium sulfate beads) to the infected site before wound closure to hopefully improve infection-eradication rates. Thus, DAIR became DAPRI. The infection-eradication rates for DAIR and DAPRI procedures are better than the success rate for the traditional two-stage salvage of an infected total knee arthroplasty (60 to 84 percent) reported by Insall et al in the Journal of Bone and Joint Surgery in 1983.

There are two goals for improving infection prevention and treatment. First, improving patient care. Second, to avoid overburdening busy arthroplasty surgeons who could be doing other things for patients instead of time-consuming infection work. Therefore, the reported success rates for I&D (DAIR, DAPRI, etc.) and two-stage exchanges do not significantly accomplish either goal. Furthermore, because both methods—I&D and exchanges—have recurrences, workload for the arthroplasty surgeon is arguably overburdened due to PJIs. Clearly, successful single-stage PJI procedures have an enormous benefit of preserving bone stock, which lessens PJI morbidity and possibly mortality, while also reducing the workload on arthroplasty practices.

Moving toward fewer infections and improved treatment protocols begins with two separate studies that reported Staphylococcus aureus within host osteocytes and skin keratinocytes. In the osteocyte publication, the tissue samples studied were obtained from the tibial medullary canal. Therefore, if bacteria are residing in medullary osteocytes in osteomyelitis, could bacteria also be residing in osteocytes in the medullary canals adjacent to tibial and femoral components? Moreover, if implants are undisturbed and retained in single-stage PJI procedures (i.e., no canal I&D), are infectious bacteria being missed and left to cause infection recurrences? This concept is unproven and remains to be studied. Future studies may also report additional host cells that bacteria enter, such as myocytes and so forth.

Regarding the question of where the unseen bacteria are that may be causing infection recurrences, the first unseen source includes intracellular bacteria, followed closely by bacterial-laden biofilm. Furthermore, not only are bacteria unseen in biofilm, but the biofilm is largely unseen too. It is easy to identify hardware within a surgical site infection (SSI) or PJI, but where exactly is the biofilm in an SSI? This has not been studied extensively, and until then, the PJI I&D surgeon must assume that biofilm is everywhere within an SSI. In the author’s opinion, improving biofilm detection and removal during PJI I&D may come from application of a biofilm stain to visualize biofilm’s location. No biofilm stain has been approved for in vivo use. Staining biofilm would improve the visualization of unseen dormant bacteria, improve the thoroughness of I&D, and in turn improve the outcomes of PJI I&D procedures.

In summary, orthopaedic SSIs are difficult to treat. This difficulty in treating SSI/PJIs is multifactorial, and in the author’s opinion, the focus going forward to improve SSI treatment outcomes should be on visualizing all biofilm and intracellular bacteria within an SSI to improve debridement thoroughness. We have made great strides in bacteria identification with gene-sequencing techniques and other assays. However, it will be improved I&D methods and biofilm-formation prevention that will likely improve orthopaedic SSI treatments and prevention. Finally, although there is evidence supporting unseen (intracellular) bacteria within an SSI, data are lacking that these bacteria are the culprits in infection recurrences after I&D procedures. More research is required in this area.

Daniel R. Schlatterer, DO, MBA, FAAOS, is the former chair of the orthopaedic surgery residency program and former chief of orthopaedic trauma at Atlanta Medical Center, Atlanta, Georgia. He is a member of the AAOS Now Editorial Board.

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