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Prosthetic joint infections (PJIs)

Authoring team

Prosthetic joint infections (PJIs)

  • the annual PJI incidence rate in the United States, expressed as a percentage of the total number of arthroplasties performed, increased from 1.99 to 2.18% for hip arthroplasties and from 2.05 to 2.18% for knee arthroplasties from 2001 to 2009 (1)
    • hip and knee arthroplasties comprise the largest numbers of PJIs

  • factors that increase the risk of infection include co-morbid disease (e.g. diabetes mellitus, rheumatoid arthritis, immunosuppressive medications, malignancy), longer duration of surgery, previous arthroplasty involving the same joint
    • obesity has been associated with an increased risk of infection in many studies (1)
    • incidence of infection following arthroplasty revision surgery is higher than that following primary implantation
      • possible causes for this include prolonged operating time during the revision surgery or unrecognized infection at the time of revision, with subsequent recrudescence
      • abnormal soft tissue envelope may also be a contributing factor

  • following joint replacement, the organisms responsible for infection are often bacteria with low virulence in the absence of implanted material e.g. coagulase-negative staphylococci. Also infection with Staphylococcal aureus is common, including an increasing number of infections with meticillin-resistant Staphylococcus aureus (MRSA) (2)
    • majority of PJIs occurring within 1 year of surgery are initiated through the introduction of microorganisms at the time of surgery (1)
      • a significant factor in this process is the low inoculum of microorganisms needed to establish infection in the presence of the prosthetic material.

A review states (3):

  • prosthetic joint infections (PJIs) can occur at any time following surgery, with variable symptoms and signs
  • a high index of suspicion for PJI is necessary for patients presenting with unexplained pain in their joint
  • serum biochemistry tests cannot be used in isolation to confirm or exclude a PJI
  • empirical antibiotics should not be started in the community or emergency department unless red flags for sepsis are evident

Clinical manifestations of PJI

  • vary depending upon
    • the virulence of the organism
    • mode of initiation of infection
    • host immune response
    • oft tissue structure surrounding the joint
    • joint involved
  • commonly reported signs or symptoms of PJI include pain, joint swelling or effusion, erythema or warmth around the joint, fever, drainage, or the presence of a sinus tract communicating with the arthroplasty
    • presence of a sinus tract is considered by many to be definitive evidence of PJI (1)
    • presence of a sinus tract within the boundaries of the original incision is pathognomonic for a prosthetic joint infection and needs urgent referral to secondary care; however, well defined sinus tracts are uncommon and absence does not exclude a PJI (3)

Early infections (0-3 months postoperative) (3)

  • accounts for approximately 30% of PJIs
  • common organisms
    • virulent* organisms
      • Staphylococcus aureus
        • is one of the common causes of serious invasive infections, including nosocomial and health care-associated bloodstream infections, which can subsequently lead to PJI (1)
      • Streptococci
  • typically present with local signs of a joint infection:
    • pain,
    • erythema,
    • warmth, effusion,
    • discharge from the wound site
  • very early infections pose a diagnostic challenge as the normal postoperative joint can be painful, swollen, and warm to touch, which mimics some infective signs
  • systemic symptoms, particularly fever, severe pain, spreading cellulitis, purulent discharge, and a decline from initial postoperative function, are clues in differentiating an early infection from the body’s normal response to surgery (3)

* virulence can be defined as a pathogen's ability to cause damage to a host

  • with virulent organisms being much more capable of causing infection as opposed to slow growing (indolent) organisms.

Delayed infections (3-24 months postoperative) (3)

  • accounts for approximately 40% of PJIs
  • common organisms
    • indolent* organisms
      • Coagulase negative staphylococci
        • a number of species comprise the group of microorganisms referred to as the coagulase-negative staphylococci (1)
          • many are ubiquitous members of the human microbiome found on the skin
          • Staphylococcus epidermidis is the most frequently identified member of this group
          • coagulase-negative Staphylococcus species can cause PJI at any time after an arthroplasty has been placed
      • Cutibacterium sp
  • can present acutely with features of an acute infection (pain, erythema, warmth, effusion,discharge from the wound site) - however, a typical presentation is more insidious, with vague signs and symptoms and often unremarkable clinical examinations
  • may present with persistent pain and/or deterioration in joint function over weeks to months, often without overt signs of infection
  • patient may described that the joint has "never been right" or that their preoperative pain did not improve

* virulence can be defined as a pathogen's ability to cause damage to a host

  • with virulent organisms being much more capable of causing infection as opposed to slow growing (indolent) organisms

Late infections (>24 months postoperative) (3)

  • accounts for approximately 30% of PJIs
  • common organisms
    • virulent organisms
      • S aureus
      • Escherichia coli
      • Klebsiella
      • Enterobacter
  • have a range of presentations, therefore a high index of suspicion is necessary in all patients
    • may present acutely (pain, erythema, warmth, effusion) or can be insidious, with general malaise or sepsis of unknown origin
  • are often secondary to a different focus of infection, most commonly gastrointestinal or genitourinary, that results in haematogenous seeding to the prosthesis

* virulence can be defined as a pathogen's ability to cause damage to a host

  • with virulent organisms being much more capable of causing infection as opposed to slow growing (indolent) organisms

Diagnosis of PJI

  • based upon a combination of:
    • clinical findings
    • laboratory results from peripheral blood and synovial fluid
      • investigation of a suspected PJI (including if the only symptom is pain) includes
        • a full blood count, C reactive protein (CRP), D-dimer, and erythrocyte sedimentation rate (ESR)
          • .CRP is elevated during the first few weeks postoperatively, usually reaching a peak at day 3 and with a gradual and variable return to normal within 28 days
        • if the patient has no signs of sepsis or shows no overt signs of infection, investigative tests can be done in a community setting (3)
      • aspiration of a suspected PJI is an essential investigation that should be performed only in a sterile environment by the orthopaedic team
    • microbiological data
    • histological evaluation of periprosthetic tissue
    • intraoperative inspection
    • in some cases, radiographic results
      • imaging may support the diagnosis of PJI in certain circumstances but rarely has a definitive role in PJI diagnosis
        • plain radiographs are typically obtained in patients undergoing evaluation for possible PJI
      • radiography has 14% sensitivity and 70% specificity in detecting implant associated infections, and is more useful to exclude confounding diagnoses such as dislocation, fractures surrounding the implants, loosening of the prosthesis, and rare causes such as concurrent bone malignancy (3)

Management of a PJIs

  • requires a specialist multidisciplinary team comprising orthopaedic surgeons and microbiologist
  • empirical antibiotic therapy after diagnosis needs to be based on local policies due to different trends of antibiotic resistance
    • require a long course of antibiotics which is given intravenously initially, however this can often be done as an outpatient in parenteral antibiotic therapy clinics
      • there is often switch to oral antibiotics once their inflammatory markers are within the normal limits
      • a usual minimum course is six weeks of antibiotics
  • surgical management is required in most cases
    • antimicrobial therapy alone is sometimes attempted with a curative intent (1)
      • often results in a delay in appropriate surgical management and confusion regarding the microbiological diagnosis
        • nonsurgical management is not recommended

Reference:


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