You’re in the OR, knee exposedand the diagnosis is clear: periprosthetic joint infection (PJI) after total knee arthroplasty (TKA). The stakes are high, the clock is tickingand the pressure to get it right is immense. This isn’t just another revision case; it’s a battlefield where surgical precision meets microbiological complexity. The two-stage exchange remains the gold standard for chronic PJI, but the devil is in the details. How do we navigate this minefield efficiently, minimizing morbidity while maximizing eradication?
Traditionally, the two-stage exchange has been a rigid protocol: explant, place a static spacer, six weeks of antibiotics, then reimplant. This approach, while effective, often sacrifices function and prolongs disability. Emerging evidence challenges this dogma, pushing us toward articulating spacers, tailored antibiotic regimensand more nuanced timing for reimplantation. The “noise” of outdated protocols obscures the “signal” of patient-centered, evidence-driven refinements. It’s time to recalibrate our approach.
Step One: Explantation and Debridement
The first stage demands meticulous surgical technique. Complete removal of all prosthetic components and cement is non-negotiable. Retained material is a nidus for persistent infection. We must extend our debridement beyond the obvious: excise all devitalized tissue, synovectomyand irrigate copiously. The literature supports pulse lavage with saline, but the addition of antiseptic solutions remains controversial-our judgment must balance efficacy with tissue toxicity.
A critical nuance lies in the decision to use static versus articulating spacers. Static spacers offer simplicity but at the cost of joint stiffness and muscle atrophy. Articulating spacers, increasingly favored, preserve soft tissue planes and allow early range of motion. They demand surgical skill and careful patient selection but pay dividends in functional outcomes. Spacer design is no longer a trivial choice; it’s a strategic decision that shapes the entire treatment trajectory.
Step Two: Antibiotic Strategy
Systemic antibiotics are the backbone of infection control. Culture-directed therapy is ideal but not always feasible given culture-negative infections. Here, multidisciplinary collaboration with infectious disease specialists is paramount. We must tailor regimens based on organism sensitivity, biofilm penetrationand patient comorbidities. The timing of antibiotic cessation before reimplantation is another gray area. Emerging data suggest that a drug holiday may improve culture yield at reimplantation, but this must be balanced against the risk of infection flare.
Local antibiotic delivery via the spacer is a powerful adjunct. The choice and dosage of antibiotics mixed into the cement influence elution kinetics and mechanical properties. High-dose vancomycin and gentamicin remain staples, but we must avoid compromising spacer integrity. This interplay between pharmacology and biomechanics is a subtle art often overlooked in surgical training.
Step Three: Reimplantation Timing and Technique
Determining when to reimplant is as much art as science. Traditional protocols advocate a fixed interval, often six weeks, but recent studies argue for a more individualized approach based on clinical, serologicand synovial fluid markers. Normalization of inflammatory markers like CRP and ESR is helpful but not definitive. Synovial fluid analysis, including leukocyte count and differential, adds granularity but is imperfect. We must synthesize all data points and clinical judgment rather than rely on a single “test.”
At reimplantation, the surgical principles mirror primary TKA but with heightened vigilance. Scar tissue, bone lossand soft tissue compromise complicate exposure and implant fixation. We often need augments, stemsor constrained implants to restore stability. The risk of reinfection persists, so meticulous technique and thorough irrigation remain critical. Some advocate for intraoperative frozen sections or repeat cultures, but their utility is debated. Our focus should be on achieving stable, well-aligned reconstruction while minimizing additional trauma.
The Editor’s Take
The two-stage exchange for infected TKA is not a rote protocol but a dynamic process demanding surgical finesse, interdisciplinary collaborationand individualized patient care. We must move beyond the “one-size-fits-all” mindset and embrace the nuances that influence outcomes: spacer choice, antibiotic strategy, timing of reimplantationand reconstructive technique. These elements are interconnected; optimizing one without the others risks failure.
For the learner, the takeaway is clear: mastery of the two-stage exchange requires more than technical skill. It demands critical thinking, adaptabilityand a willingness to challenge entrenched dogma. We should view each infected TKA as a unique puzzle, where evidence guides but clinical acumen leads. By refining our approach, we not only eradicate infection but restore function and quality of life-our ultimate surgical mandate.
