Prosthetic joint infection

Did You Know?

• The bacteria secrete adhesion proteins to attach to each other and the joint surface, then secrete autoinducer proteins that facilitate formation of an extracellular matrix biofilm.
• Biofilms take about four weeks to fully mature and greatly decrease antibiotic penetrance.
• Granulocytes have decreased phagocytic activity when encountering the biofilm, allowing bacteria to persist.

Cause

Prosthetic joint infections can arise at any time after joint replacement. Early infections, occurring within four weeks of surgery, are usually caused by Staphylococcus aureus, streptococci, or enterococci. Late infections, appearing three months or later, are typically due to coagulase-negative staphylococci or Cutibacterium. The highest risk period is the immediate postoperative phase, when bacteria may be directly inoculated into the joint during surgery, with risk remaining elevated for up to two years. Hematogenous spread from a bloodstream infection can occur at any time, with a risk as high as 34% in Staphylococcus aureus bacteremia. Direct spread from nearby skin, soft tissue, or bone infections, as well as distant infections such as respiratory, gastrointestinal, or urinary tract infections, may also cause PJI. Dental procedures can produce transient bacteremia leading to PJI, with Streptococcus viridans being the most common causative organism. Aerobic gram-positive bacteria account for over 50% of hip and knee PJIs, with Staphylococcus aureus comprising 38% of acute infections and aerobic gram-negative bacilli making up 24%. About 70% of PJIs are monomicrobial, 25% are polymicrobial, and 3% are fungal. Propionibacterium acnes is the most common cause of shoulder PJIs. Risk factors include diabetes, immunosuppression, smoking, obesity, chronic kidney disease, soft tissue infection, infection elsewhere in the body, increased fat tissue around the joint, wound dehiscence, and hematoma formation. The presence of multiple artificial joints, MRSA PJI, rheumatoid arthritis, or bacteremia increases the risk of multiple PJIs.

Diagnosis

A prosthetic joint infection is confirmed when one of the major diagnostic criteria is met: a sinus tract connecting the joint to the skin, purulence around the prosthesis, more than 2000 leukocytes per microliter or over 70% granulocytes in joint fluid, more than 23 granulocytes per 10 high-powered fields on joint fluid analysis, or microbial growth in culture of joint fluid, at least two tissue biopsies (or one if the organism is highly virulent), or over 50 colony-forming units per milliliter on culture of sonification fluid from the artificial joint. Sonification, which involves removing the prosthesis, placing it in liquid, and applying ultrasound to dislodge adherent microorganisms, has superior sensitivity to joint fluid culture. Polymerase chain reaction testing of joint fluid or sonification fluid may aid diagnosis. Skin swabs, sinus tract swabs, and swabbing of the artificial joint surface during surgery are not recommended due to high contamination risk and low diagnostic yield. Blood cultures are positive in about 25% of PJI cases, especially acute ones, but the organism isolated does not always match that from joint fluid, so blood cultures are not diagnostic. Routine blood tests such as white blood cell count, erythrocyte sedimentation rate, C-reactive protein, or procalcitonin are neither sensitive nor specific for PJI. Plain radiography has low sensitivity and specificity but may show radiolucent lines, bone breakdown, loosening, or migration of the prosthesis. Functional imaging like white blood cell scintigraphy or PET scan can identify hypermetabolic areas consistent with infection. Magnetic resonance imaging with metal artifact reduction sequence is useful for detecting soft tissue infections.

Treatment

Antibiotic treatment alone, without surgical debridement, usually fails. Acute infections, where the biofilm is immature, are often managed with the DAIR technique: debridement, systemic and local antibiotics, and implant retention, though mobile components are frequently replaced. DAIR is contraindicated if a sinus tract is present, the prosthesis is loose, or the wound cannot be closed. Microbial cure rates for DAIR are 74% in early, 49% in sub-acute, and 44% in late infections. Antibiotic-loaded polymethylmethacrylate beads can be placed in the joint, but these non-resorbable beads may themselves become colonized; bio-absorbable carriers such as calcium sulfate beads or resorbable gentamicin sponges are preferred. Bone grafting impregnated with antibiotics can achieve local concentrations well above the minimum inhibitory concentration. Chronic PJIs may be treated with one-stage revision, where the prosthesis is replaced in a single surgery, or two-stage revision, where an antibiotic spacer is placed before a second surgery to insert a new joint. Two-stage revision is associated with greater morbidity, longer hospital stays, longer immobilization, worse functional outcomes, and higher costs. For intact bone and soft tissue without prior revision, one-stage exchange is the treatment of choice. In hip PJIs, both approaches are equally effective, but one-stage surgery allows faster recovery. Negative pressure wound therapy is not recommended because the sponges are often colonized by biofilm or new organisms.

Prevention

Antibiotic prophylaxis, typically with second-generation cephalosporins given less than 60 minutes before joint replacement surgery, is believed to reduce the risk of acute PJI. Screening for and eradication of MRSA carriage, along with chlorhexidine wipes or soap-and-water skin cleansing before surgery, may possibly decrease PJI risk. The American Dental Association generally does not recommend prophylactic antibiotics before routine dental procedures for patients with prosthetic joints, though higher-risk circumstances may warrant such prophylaxis as determined by the dentist or physician.