HHE Rheumatology 2019 | Page 14

RHEUMATOLOGY Diagnosis and management of prosthetic joint infections in rheumatoid arthritis This article reviews the epidemiology, pathogenesis, investigation and management of prosthetic joint infections in patients with rheumatoid arthritis Georgina Beckley MBBS MRCP FRCPath Elizabeth Darley MBChB MRCP FRCPath MD North Bristol NHS Trust, Bristol, UK Infection following prosthetic joint infection (PJI) is a recognised surgical complication. However, it has serious consequences requiring both surgical and antimicrobial management. Patients with rheumatoid arthritis (RA) are both more likely to have joint replacement due to abnormal anatomy and be immunosuppressed due to the underlying disease and immunomodulatory therapies. These factors make them more at risk as a population for post- operative infection. Epidemiology Due to progressive joint destruction, patients with RA commonly have to undergo joint replacement. It is estimated that 24% of patients with RA will eventually require their first major joint replacement at 16–20 years after diagnosis. 1 Of those who have a total hip or knee replacement 5–7% have RA compared to 1% in the general population. 2 There is an increased risk of PJI due to the underlying RA which can be 2.5-times that of a person with osteoarthritis. 2 Pathogenesis In the general population, infection in PJI can occur from direct seeding peri- or post-operatively or haematogenous spread or recurrence of existing infection from previous prosthesis. The prosthetic material allows the bacteria to form a protective glycocalyx layer or biofilm. This means the bacterial colonies deep within this are protected from host defences and antimicrobials. There may also be poor wound healing and poor host defences due to the underlying inflammatory arthritis in patients with RA. This, coupled with immunomodulatory therapy, makes a favourable environment for infection. Investigation According to the International consensus meeting in 2013 on peri-prosthetic joint infections, the diagnostic criteria for PJI is as follows. 3 Major • Two positive peri-prosthetic cultures with phenotypically identical organisms • Sinus tract communicating with the joint. Minor • Raised C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) • Raised synovial fluid white blood count on leucocyte esterase test strip 14 HHE 2019 | hospitalhealthcare.com • Raised synovial fluid polymorphonuclear neutrophil percentage • Positive histological analysis of peri-prosthetic tissue • A single positive culture. A patient is required to have one major or three minors to be diagnosed. However, in a patient with RA, there are limitations to these criteria. Initial investigation of prosthetic joint infection in patients with RA is similar to other patients. A careful history and examination should be taken to ellicit: A) Local features of infection joint swelling, pain, wound breakdown and sinus tract B) Past medical and surgical history, including previous revisions, microbiology and previous antimicrobial treatment, previous limb cellulitis and other prosthetic material C) Medication and drug allergy. There should also be clear documentation on the use of immunosuppressants, acute prescriptions of corticosteroids and infusion therapy that may not be listed on patients’ regular medications as this can affect the immune system up to 12 months after administration. Full blood count, urea and electrolytes, CRP, ESR and liver function tests should also be part of the standard work up. However, in patients who have RA it might be difficult to differentiate between raised inflammatory markers due to infection or underlying inflammatory arthritis flare. CRP may also be falsely low due to use of immunomodulatory therapies. White blood cells can be elevated due to corticosteroid use. Other biomarkers specific for bacterial infection, for example, procalcitonin, interleukin-6 (IL-6) and tumour necrosis factor, are in development. A prospective study looking at the sensitivity and specificity of these in prosthetic joint infection identified a combination of IL-6 and CRP as the most useful and that procalcitonin was the most specific. 4 There has also been increasing interest in using joint fluid biomarkers to aid in the diagnosis of PJI (for example, CRP, adenosine deaminase (ADA), alpha-2-macroglobulin) which show some promise increasing the positive predictive value in diagnosing PJI vs aseptic loosening. 5 Leucoesterase dip stix are easy to use and commercially available but again could also be positive due to underlying RA rather than infection. However none of these biomarkers