Prosthetic joint infection (PJI), also known as peri-prosthetic joint infection, is an acute, sub-acute or chronic infection of a prosthetic joint. It may occur in the period after the joint replacement or many years later. It usually presents as joint pain, erythema (redness of the joint or adjacent area), joint swelling and sometimes formation of a sinus tract ( a tract connecting the joint space to the outer environment). PJI is estimated to occur in approximately 2% of hip and knee replacements, and up to 4% of revision hip or knee replacements. Other estimates indicate that 1.4-2.5% of all joint replacements worldwide are complicated by PJIs. The incidence is expected to rise significantly in the future as hip replacements and knee replacements become more common. It is usually caused by aerobic gram positive bacteria, such as Staph epidermidis or Staphylococcus aureus but enterococcus species, gram negative organisms and Cutibacterium are also known causes with fungal infections being a rare culprit. The definitive diagnosis is isolation of the causative organism from the synovial fluid (joint fluid), but signs of inflammation in the joint fluid and imaging may also aid in the diagnosis. The treatment is a combination of systemic antibiotics, debridement of infectious and necrotic tissue and local antibiotics applied to the joint space. The bacteria that usually cause prosthetic joint infections commonly form a biofilm, or a thick slime that is adherent to the artificial joint surface, thus making treatment challenging.
Signs and symptoms The most common symptom of periprosthetic joint infections is joint pain. Other local symptoms are also present, including erythema (redness of the joint), joint swelling, warmth of the joint, and loosening of the prosthetic joint. A sinus tract, or a tract connecting the joint space to the external environment, is more common in chronic PJI, and is definitively diagnostic of PJI. Fever may be present in PJI, but is uncommon.
Cause Prosthetic joint infections can occur any time after a joint replacement. Early infections (occurring within 4 weeks of a joint replacement) are usually due to Staph aureus, streptococci or enterococci. Whereas late infections (occurring 3 months or later after the joint replacement) are usually due to coagulase negative staphylococcus or cutibacterium. The highest risk of PJI is in the immediate post-operative period, when direct inoculation of bacteria into the joint space may occur during surgery. The risk of PJI is highest in this early period; within 2 years of the joint replacement. Hematogenous spread, or infection of a prosthetic joint via direct seeding from a bloodstream infection, may occur at any time after a joint replacement, with the risk being as high as 34% in staph aureus bacteremia. An additional possible cause of PJI is from direct spread to the joint from a nearby skin or soft tissue infection, a bone infection (osteomyelitis), or from more distal spread to the joint from a respiratory tract infection, gastroenteritis, or urinary tract infection. Dental procedures may cause a transient bacteremia which can lead to inoculation of the artificial joint and PJI, with strep viridans being the most common causative organism. The most common causes of PJIs are aerobic, gram positive bacteria, including staph aureus and coagulase negative staphylococcus (such as staph epidermidis), which make up greater than 50% of all causes of hip and knee PJIs. With regards to acute PJIs, the most common causative organism is staph aureus (comprising 38% of acute infections) followed by aerobic gram negative bacilli (making up 24% of acute infections). 70% of PJIs are monomicrobial (with a single causative organism identified), whereas 25% of cases are polymicrobial (with multiple causative organisms identified). 3% of PJIs are due to fungal organisms. Propionibacterium acnes is the most common cause of shoulder PJIs. Risk factors for PJI include diabetes, immunosuppression, smoking, obesity, chronic kidney disease, the presence of a soft tissue infection, or an infection in another part of the body or increased fat tissue around the replaced joint. Surgical factors that may lead to an increased risk of PJIs include wound dehiscence (unplanned opening of the surgical wound after the surgery) and hematoma (collection of blood) formation. The presence of multiple artificial joints, MRSA PJIs, rheumatoid arthritis or bacteremia place people at risk for multiple PJIs (either concurrent or subsequent infections). Prolonged operative times, in which the joint is left open to the external environment, determined as greater than 90 minutes in a single study, also increases the risk for PJIs.
Pathophysiology Prosthetic joint infections are generally difficult to treat as most causative organisms form a biofilm, or a thickly adherent membrane, against the artificial joint surface. The bacteria secrete adhesion proteins which help them attach to each other and to the joint surface. The bacteria then secrete autoinducer proteins that act as bacterial signals which facilitate the secretion of an intricate extracellular matrix, the biofilm. Biofilms greatly decrease antibiotic penetrance thereby shielding bacteria from the bacteriocidal effects of antibiotics. Biofilms usually take 4 weeks to fully mature. Granulocytes have decreased phagocytic activity encountering the biofilm, also allowing the bacteria to persist.
Diagnosis The presence of a PJI is confirmed when one of the proposed major diagnostic criteria are met:
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