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 ~  Abstract
 ~ Introduction
 ~  Complications of...
 ~  Prosthetic Joint...
 ~ Incidence
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 ~ Risk Factors
 ~  Pathogenesis of ...
 ~ Microbiology
 ~  Diagnosis of Pro...
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 ~  Peripheral Blood...
 ~  Periprosthetic T...
 ~  Molecular Diagno...
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 ~  Antimicrobial Tr...
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 ~ Conclusion
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  Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 36  |  Issue : 4  |  Page : 475-487
 

Prosthetic joint infection: A major threat to successful total joint arthroplasty


1 Department of Microbiology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Orthopaedics, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication18-Mar-2019

Correspondence Address:
Dr. Benu Dhawan
Department of Microbiology, All India Institute of Medical Sciences, New Delhi - 110 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmm.IJMM_19_11

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 ~ Abstract 

Total joint arthroplasty (TJA) is one of the most common and reliable orthopaedic procedures that has significantly improved the quality of life of patients with degenerative joint diseases. Following the increase in the ageing population, availability of trained orthopaedic surgeons and advances in implantation procedures, demand for TJA both globally and in India is significantly increasing. Though TJA is one of the most cost-successful orthopaedic procedures, prosthetic joint infection (PJI) is one of the major complications of joint arthroplasty. Accurate diagnosis of PJI is challenging. Since total hip and knee arthroplasties comprises the majority of TJAs, this review focuses on the current understanding of incidence, risk factors, pathogenesis, causative microorganisms, diagnosis, treatment and prevention of PJI related to these two procedures.


Keywords: Biofilm, revision arthroplasty, sonication, total joint arthroplasty


How to cite this article:
Sebastian S, Malhotra R, Dhawan B. Prosthetic joint infection: A major threat to successful total joint arthroplasty. Indian J Med Microbiol 2018;36:475-87

How to cite this URL:
Sebastian S, Malhotra R, Dhawan B. Prosthetic joint infection: A major threat to successful total joint arthroplasty. Indian J Med Microbiol [serial online] 2018 [cited 2019 Oct 21];36:475-87. Available from: http://www.ijmm.org/text.asp?2018/36/4/475/254407



 ~ Introduction Top


Total joint arthroplasty (TJA) is commonly indicated for patients having degenerative joint diseases.[1] Though it is possible to replace any extra-axial joint with a prosthetic joint, hip and knee joints are most commonly repaired.[2] Osteoarthritis, rheumatoid arthritis, trauma and avascular necrosis are some of the most common indications for total knee arthroplasty (TKA) and total hip arthroplasty (THA) in developed countries.[3] In India, avascular necrosis (49%) and osteoarthritis (97%) are the most common indications for THA and TKA, respectively.[4]

Following the global ageing population and advances in implantation procedures, demand for TJA is greater than ever before. On account of the number of times a given joint is replaced, arthroplasty surgeries are denoted to as either primary or revision arthroplasty.[2] As per the study by Kurtz et al., a total of 284,000 primary THAs, 45,000 revision THAs, 619,000 primary TKA's and 59,500 revision TKAs were performed in the USA in 2009.[5] By 2030, the demand for primary TJA of the hip in the US will grow by 174% and of the knee by 673%.[6] In 2005, 745,000 THAs and 430,000 TKAs were performed in Europe. By 2012, the numbers increased to 820,000 THA's and 560,000 TKA's.[7]

With an increase in the ageing population, availability of trained orthopaedic surgeons, sedentary lifestyle, booming economy, improvement in the hospital infrastructure, and medical tourism demand for TJA in India is significantly increasing. Also, the recent price capping of medical devices by the central government has made TKA more affordable for the common man. In a study by Pachore et al., between October 2006 and April 2012, a total of 3,604 primary THAs, 261 revision THAs, 34,478 primary TKAs and 281 revision TKAs were performed in India by 40 surgeons.[4] As per the latest report published by Indian Society of Hip and Knee Surgeries Registry, a total of 10,407 hip replacements and 129,371 knee replacements were reported from October 2006 to March 2017 by 150 surgeons.[8]


 ~ Complications of Total Joint Arthroplasty Top


Though TJA is one of the most cost-successful orthopaedic procedures, <10% of the patients develop complications during their lifetime.[9] The major complications following TJA include instability, PJI, periprosthetic fracture/dislocation, wound complication, malalignment, stiffness, bearing surface wear, osteolysis, implant loosening, reoperation, revision, readmission, and death.[1],[10] Also, the number of high-risk patients (e.g., aged patients, diabetic patients) undergoing these procedures further increase the probability of postoperative complications.


 ~ Prosthetic Joint Infection Top


PJI is one of the major complications of joint arthroplasty and has a significant impact on both health care resources and the quality of life of patients.[1] PJI is defined as 'infection involving the joint prosthesis and adjacent tissue'.[11] PJI was the third most common cause for all hip revisions and the second most common indication for all knee revision surgeries and will become the dominant failure mode by 2030.[12]


 ~ Incidence Top


A number of studies, majority from the USA and Europe have reported the incidence of PJI.[13],[14] The incidence of PJI in primary hip and knee arthroplasties reported from single Institutional studies ranged from 0.03% to 2.7% [Table 1].[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24] In registry-based studies, the cumulative PJI incidence varied from 0.4% to 2.18% [Table 1].[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36] A single institutional PJI study from Northern India reported a cumulative incidence of 1.1% (THA: 1.53% and TKA: 0.89%).[24]
Table 1: Reported single-institutional and registry-based incidence of prosthetic joint infections in the literature

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 ~ Classification of Prosthetic Joint Infection Top


In order to guide the medical and surgical decisions in patients with PJI, a number of classification systems have been proposed for PJI.[37],[38] However, there is no international consensus on PJI classification.

The Zimmerli classification, which is one of the most commonly used, classifies PJI as early, delayed and late-onset infections based on the time to infection.[37] Early-onset infection occurs <3 months after arthroplasty, delayed-onset occurs after 3 months and before 12 months and late-onset after 12 months.

Another classification is the Tsukayama classification, which divides PJI into four categories (early postoperative, late chronic, acute haematogenous and positive intraoperative cultures in patients undergoing revision arthroplasty for presumed aseptic failure) based partly on time since the surgery and also on the presumed mode of PJI.[38] Both Zimmerli and Tsukayama classifications are the most commonly used and help to determine the best medical and surgical management for PJIs.


 ~ Risk Factors Top


Various studies have described a number of risk factors for the development of a PJI.[39],[40],[41],[42] However, the interpretation of the potential risk factors mentioned in these studies should be made cautiously due to the differences in the study methods, the definition of PJI/scoring system used and anatomical site studied.[41] Pre-existing patient co-morbidities such as diabetes mellitus, obesity, rheumatoid arthritis, malignancy, malnutrition, psoriasis, biologic disease-modifying antirheumatic drugs, corticosteroid use, smoking are associated with increased PJI risk.[16],[40],[41],[42] A history of prior arthroplasty and ongoing urinary tract infection also increases the risk of PJI.[40] Other factors that have been associated with an increased risk of PJI include male gender and antecedent bacteremia (during the previous year).[9],[40] Procedure-related risk factors associated with PJI include higher American Society of Anaesthesiologists and National Nosocomial Infections Surveillance scores, revision arthroplasty and prolonged duration of operation (>2.5 h).[40],[41],[42] In addition, postoperative wound healing complications, such as prolonged wound drainage, wound dehiscence, wound hematoma, or lack of resolution of joint pain after primary surgery should also be considered as risk for acquiring PJI.[16],[41],[42]


 ~ Pathogenesis of Prosthetic Joint Infection Top


Initiation of infection

Acquisition of PJI can occur by different mechanisms. Generally, it happens by direct seeding of microorganisms during surgery.[11],[43] After the initial contact (either direct or aerosolised contamination of the prosthesis or periprosthetic tissue), microorganisms colonise the surface of the implant. Various studies have shown that the bacterial concentration needed to induce an infection is significantly reduced in the presence of the prosthetic material.[44] Also, the presence of prosthesis can lessen the neutrophil activity thereby increasing the infection susceptibility.[45] Another mechanism of infection initiation is by the contiguous spread of infection from an adjacent site or by hematogenous seeding.[46]

Role of biofilm

The infection initiates with bacterial adhesion to the host tissues or prosthesis. In order to enhance the adhesion, bacteria express many structures like proteinaceous cell-wall-associated adhesins and capsular polysaccharide adhesins. These adherent microorganisms usually produce an extracellular matrix consisting of complex communities of microorganisms known as biofilms.[47] Organisms within these biofilms are protected from antibiotics and host defence mechanisms. This biofilm can decrease the effectiveness of host defence mechanisms and render the microorganisms extremely resistant to antimicrobial treatment. Formation of biofilms is one of the most critical steps in the pathogenesis of PJI's.[47] Biofilms may be monomicrobial or polymicrobial.

Prosthetic joint infection: Clinical manifestations

Pain, joint swelling or effusion, erythema, fever, drainage, or a discharging sinus are some of the most common clinical signs and symptoms of PJI.[48] Sinus tract communicating with the prosthesis is considered as definitive evidence for PJI.[49],[50],[51],[52]


 ~ Microbiology Top


Microbial profile of prosthetic joint infection

For appropriate empirical antimicrobial therapy, knowledge of the pathogen spectrum of PJI is necessary. The microbial pathogens involved in the PJI vary depending on the time of infection and joint involved.[11] In early-onset infections, Staphylococcus aureus and aerobic Gram-negative bacilli (GNB) are more frequently implicated. The increased virulence of these organisms may explain the early onset of infection within 3 months of surgery. In delayed-onset PJI's, coagulase-negative staphylococci (CoNS) and enterococci are more common.

Based on published reports, more than half (50%–60%) of all PJI's are caused by staphylococci (S. aureus and CoNS).[15],[53],[54] Staphylococcus epidermidis is the most commonly identified member of CoNS.[46],[54] In previous studies, aerobic GNB represented <10% of PJI cases.[11] However, recent studies have reported a higher frequency of Gram-negative PJI's.[55],[56],[57] Anaerobes including Cutibacterium acnes accounted for 0%–9%.[24],[54] Fungi and Mycobacterium spp. are less commonly involved in PJI's.[46] Most of the fungal PJI's were caused by Candida species and among them Candida albicans is the commonest.[46],[58] In endemic areas, tuberculosis can affect the joint in 1%–5% of cases.[59] The microbial aetiology of PJI reported from India and other International studies are given in [Table 2]. In contrast to the published reports, a high proportion of GNB was noted in the Indian study.[24]
Table 2: Organisms commonly cause prosthetic joint infections

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Polymicrobial infections are reported in <20% of cases.[11],[46],[57] Aerobic GNB, Enterococcus spp. and S. aureus, are the most frequently isolated bacteria in polymicrobial PJI's.[46],[57] Fungal and bacterial co-infections occur in 15%–20% of cases.[11]

Culture-negative infection

In culture-negative PJI (CN-PJI), the patient will have a negative microbiological result, but clinical evidence of infection and elevated inflammatory markers will be present. Prior antibiotic use, previously unrecognised causes of PJI, the method of sample collection and transportation to the laboratory, lack of availability of standard diagnostic methods or improper use of the available microbiological methods could result in CN-PJI.[60],[61] The incidence of CN-PJI varies from 5% to 42% and a pooled overall incidence rate of 11% was reported in a recent meta-analysis.[62],[63]


 ~ Diagnosis of Prosthetic Joint Infection Top


Accurate diagnosis of PJI is challenging and requires clinical suspicion and proper use of the available diagnostic methods. Lack of reference standard, bacteria present in the biofilm and difficulty in differentiating the pathogens from contaminants are some of the factors that make the diagnosis of PJI a difficult task. Since the treatment strategy between septic and aseptic failure is different, a misdiagnosis could lead to an unfavourable outcome. The current diagnostic algorithm for PJI includes a combination of clinical and laboratory findings, culture of periprosthetic tissue, and histological examination of intraoperative specimens [Figure 1].[49],[50],[51],[52] However, none of these clinical or laboratory findings are 100% accurate for PJI diagnosis.
Figure 1: Proposed diagnostic algorithm for diagnosis of prosthetic joint infection

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 ~ Diagnostic Criteria Top


Before 2011, there was a lack of standardised PJI diagnostic criteria in the literature. Thereafter many groups, including Musculoskeletal Infection Society (MSIS), Infectious Diseases Society of America (IDSA) and International Consensus Meeting on PJI by various organisations from around the world have published definitions of PJI.[49],[50],[51],[52] Though minor variations exists between these criteria's, all of them have noted that PJI may be present even in the absence of all of the criteria. The detailed definitions of the reported diagnostic criteria are shown in [Table 3].
Table 3: Definitions of prosthetic joint infection

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 ~ Clinical Presentation Top


In clinical diagnosis of PJI, pain is the most common symptom present in 79%–100% of patients.[30],[64] Fever is reported in 4%–43% of patients.[65],[66] Purulent discharge, erythema and swelling of the joint are common in acute or early infections.[67],[68],[69] Sudden onset of pain in a previously asymptomatic joint is seen in acute hematogeneous infections.[67],[68],[69] Typical symptoms are absent in late chronic infections and slowly increasing pain is the predominant feature.[69] A discharging sinus is a characteristic feature of chronic, indolent infections.[37],[38],[69]


 ~ Peripheral Blood Tests Top


Traditional serum biomarkers

Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are the most commonly used inflammatory markers for PJI.[11] For the diagnosis of PJI, both tests are ordered together and a threshold of >30 mm/h and >10 mg/L of ESR and CRP, respectively, used.[50] However, for the diagnosis of PJI during the acute postoperative period, a threshold of >100 mg/L was recommended for CRP.[51]

Other serum biomarkers

Other laboratory markers include white blood cell (WBC) count, interleukin-6, procalcitonin, and tumor necrosis factor-alpha.[70],[71],[72],[73] The test characteristics and reported sensitivities and specificities of these biomarkers are shown in [Table 4].
Table 4: Test characteristics and reported sensitivities and specificities of various pre- and intra-operative tests for diagnosis of prosthetic joint infection

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Imaging

Plain radiographs

Even though plain radiographs help in identifying periprosthetic fracture, arthroplasty material fracture or dislocation and also assist the surgeon with preoperative planning, they are neither sensitive nor specific to diagnose PJI.[74]

Advanced imaging studies

Studies have evaluated the potential of advanced imaging studies like CT, three-phase bone Scintigraphy and 18fluorodeoxyglucose-positron emission tomography in the diagnosis of PJI [Table 4].[74],[75],[76] But the cost and added benefit of their findings do not warrant the routine use of advanced imaging modalities and should be used only in exceptional situations.[76]

Synovial fluid analysis

Preoperatively or intraoperatively aspirated synovial fluid and its characteristics are routinely used for the PJI diagnosis.[49],[50],[51],[52] Arthrocentesis should be undertaken in patients with clinical suspicion of infection and increased inflammatory markers (i.e., CRP and ESR).[77] The aspirated synovial fluid is used for leucocyte count and neutrophil percentages, and bacterial cultures.

Synovial fluid leucocyte count and neutrophil percentage

Leucocyte count and neutrophil percentages of aspirated synovial fluid have high sensitivity and specificity for PJI.[78] Based on the results of previous studies, the revised MSIS diagnostic criteria have made synovial leucocyte count of 10,000 cells/μL and 3000 cells/μL, and PMN percentage of 90% and 80% as the cutoff in acute and chronic infections respectively.[51]

Synovial fluid leucocyte esterase

Leucocyte esterase is an enzyme released by activated WBC's and often found in infected body fluids. Leucocyte esterase reagent strips is a colourimetric strip traditionally used as a point-of-care test to detect urinary tract infections, peritonitis and chorioamnionitis. This has been recently used as a rapid and accurate method for the diagnosis of PJI.[79],[80]

Synovial fluid alpha-defensin

Alpha-defensin is an antimicrobial peptide part of the innate immune response and is released by PMN's in response to synovial fluid pathogens. Several published reports have shown promising results of alpha-defensin for the diagnosis of PJI.[79],[81] Alpha-defensin levels are neither affected by antimicrobial therapy nor influenced by systemic inflammation.[81]

Synovial fluid culture

Microbial culture of preoperatively aspirated synovial fluid is valuable for the early diagnosis of PJI. Knowing the bacteria and its antimicrobial susceptibility profile preoperatively could assist the surgeon to choose the best perioperative antimicrobials and antibiotics that can be used for the preparation of antimicrobial-loaded cement spacers. However, for an optimal culture result, all antimicrobial treatments should be stopped minimum two weeks before arthrocentesis.[11]

In a meta-analysis by Qu et al., the sensitivity and specificity of synovial fluid culture were 72% and 95% respectively.[82] Results of the published reports of synovial fluid culture demonstrates it as a test to 'confirm' or 'rule in' PJI rather than to 'rule out' PJI.[83],[84],[85],[86] By combining the results of synovial fluid analysis with those of culture, serum ESR, and CRP, sensitivity of detecting PJI can improve markedly to almost 99.7%.[87]

Studies have shown that synovial fluid culture in blood culture bottles (both aerobic and anaerobic) increases the sensitivity along with decreasing the risk of contamination.[61],[88],[89],[90]


 ~ Periprosthetic Tissue Top


Periprosthetic tissue culture

Periprosthetic tissue culture (PTC) is one of the most valuable diagnostic tools for PJI. In addition, conventional culture findings of periprosthetic tissue are used as a major criterion in all the currently used diagnostic criteria for PJI.[49],[50],[51],[52] Previous studies that have evaluated PTC for the diagnosis of PJI showed a wide range of sensitivity, from 32% to 99% and specificity values ranging from 82% to 100%.[24],[91],[92],[93]

For an accurate diagnosis of PJI, culture of multiple periprosthetic tissue specimens is recommended.[49],[50],[51],[52],[93] Recent studies recommend four periprosthetic tissue samples for PJI diagnosis.[94],[95] Both MSIS and IDSA guidelines recommended minimum of three and optimally five or six periprosthetic tissue samples for aerobic and anaerobic cultures.[49],[50] Due to low sensitivity and the difficulty in results interpretation, collection of a single tissue specimen is not recommended.[93],[94] Each set of tissue samples should be collected with a separate set of sterile instruments.[50] The retrieved periprosthetic tissues should be transported to the microbiology laboratory within 2 h. After homogenisation of tissue samples with brain-heart infusion broth or normal saline or sterile glass beads, aliquots of resulting suspension should be inoculated onto aerobic and anaerobic culture media.[94],[95],[96],[97] Since different microorganisms have different growth times, some authors recommended the extended incubation (up to 14 days) of microbial cultures to improve the sensitivity.[98]

Isolation of the same microorganism from a minimum of two periprosthetic tissue specimens is considered definitive evidence of PJI.[49],[50],[51],[52] However, a single positive culture by virulent organisms like S. aureus or aerobic GNB may also represent PJI.[50],[51],[52]

Histological analysis of periprosthetic tissue: Histopathological examination of frozen or fixed section of periprosthetic tissue for acute inflammation is used as an adjunctive test for the diagnosis of PJI.[99],[100],[101],[102] A neutrophil count of five per high-power field, in at least five separate microscopic fields, is commonly used to define an acute inflammation in PJI.[50]

Sonication of explanted implants and cement spacers

Biofilm-dislodging techniques like sonication can significantly improve the diagnosis of PJI.[103] In this technique, low-frequency ultrasound waves (40–50 kHz) pass through the liquid (PBS or normal saline) surrounding the explanted prosthesis, creating areas of high and low pressure [Figure 2]. As a result, microscopically small bubbles are formed in the fluid during the low-pressure stage and collapse during the high-pressure stage, releasing energy and generate local micro currents ultimately leading to the liberation of bacteria from the surface of the implant.[104] The fluid obtained is then cultured, and the colony forming units are quantified. Sonication helps to confirm the PJI using a single sample, unlike PTC where multiple samples are required.[103]
Figure 2: Sonication of extracted implants

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The optimal colony-forming units (CFU) cutoff values to determine the significant bacterial growth varied in sonication studies.[103],[105] Most studies that have used a concentration step reported a cutoff of 200 CFU per ml.[61],[103] Mayo Clinic guidelines recommends 20 CFU grown per plate (0.1 mL inoculum equals 10 mL of original sonicated sample) as cutoff value for positive sonicate fluid culture (SFC).[106] Though the reported threshold values in sonication studies without a centrifugation step varied from 1 to 50 CFU per ml, majority of the studies used a cutoff between 1 and 10 CFU per ml.[105],[107]

Several studies have proven the advantage of SFC of implants over PTC for pathogen detection.[103],[105],[106],[107],[108],[109],[110] Compared with PTC, SFC was even more sensitive in patients with history of antimicrobial therapy before surgery.[103],[107] Also, previous studies have reported the superiority of SFC over PTC for detecting polymicrobial PJI.[103],[105]

Studies have also demonstrated that sonication culture of antibiotic-loaded cement spacers is superior to PTC for the detection of persisting infection at the time of staged exchange procedures.[111],[112] However, before this can be used routinely in all staged implantation surgeries further, large studies are required.


 ~ Molecular Diagnosis of Prosthetic Joint Infection Top


PCR-based techniques such as broad-range 16S rRNA gene PCR, genus or group-specific PCR, PCR-electrospray ionisation mass spectrometry have been applied to PJI to increase the diagnostic yield [Table 4].[83],[84],[91],[92],[113],[114],[115]

Most studies have used the 16S rRNA gene target.[83],[92] The strength of 16S rRNA gene PCR assay followed by sequencing is its ability to detect slow-growing and uncultivable organisms.[60] It can also help detect rarely described human pathogens.[116] Also, PCR has been useful in diagnosing PJI in patients with history of recent antibiotic use.[91] Another potential benefit of 16S gene PCR followed by sequencing is the identification of all bacteria involved in polymicrobial infections.[117] However some studies have reported difficulty of detecting mixed infections by 16S gene PCR.[83],[92] The high variability in the ratio of different template DNA in polymicrobial infections might have resulted in the amplification of the dominant or single species in the sample.

A significant limitation of 16S PCR is its lack of specificity due to the presence of bacterial DNA in the glassware, plastic ware, and reagents used for testing.[118] The inability to detect fungi is another drawback of the 16S rRNA gene-targeted PCR approach.[58],[92] Utilisation of PCR methods using universal 18S rRNA fungal ribosomal DNA will be helpful for delineating fungal PJI's.

In a recent study, Kawamura et al. evaluated the diagnostic utility of a new multiplex real-time PCR assay for PJI diagnosis.[91] In this series, the sensitivity and specificity of the PCR assay were 92% and 99% respectively, and the PCR assay was found to be useful for the diagnosis of CN-PJI. Tarabichi et al. in 2018 evaluated the potential of next-generation sequencing (NGS) in PJI diagnosis and CN-PJI in particular and concluded that NGS might be a useful adjunct in the identification of causative organism(s) in CN-PJI.[114]

Molecular studies of explanted implants and cement spacers

PCR-based techniques performed on sonicate fluid has been reported in the literature.[61],[92],[109],[119],[120] Sonicate fluid PCR have the theoretical advantage of combining the high sensitivity of sonication and PCR. However, most of the studies reported almost comparable sensitivity and specificity for both sonicate fluid PCR and SFC.[61],[92]

In the literature, only a few studies have tested the diagnostic potential of extracted cement spacer for sonication culture and molecular analysis.[121],[122] In a recent study, Mariaux et al. found that culture and PCR analysis of sonicate fluid did not improve the persisting bacterial detection in two-stage exchange arthroplasty.[122]


 ~ Treatment Top


The goals of PJI treatment involve the eradication of infection and restoration of the pain-free function of the infected joint. However, it may not be possible to achieve all these goals in every patient with PJI.

Both surgical intervention and antimicrobial therapy are usually required for optimal management of PJI. The various surgical strategies used for the management of PJI include debridement with retention of the prosthesis, resection of the prosthesis without reimplantation, resection arthroplasty by one-stage or two-stage exchange procedures, arthrodesis, amputation, or antibiotic suppression without surgery.[11]

Debridement and retention of the prosthesis are commonly known as debridement, antibiotics, and implant retention procedure. This surgical strategy is preferred when the age of the implant is <30 days (early postoperative infections), or duration of the symptoms is <3 weeks, or no sinus tract is present.[49] Here, aggressive irrigation, removal of all infected or necrotic soft tissue and hematomas, removal and replacement of exchangeable components are done.

One-stage arthroplasty exchange or direct exchange procedure includes aggressive debridement and complete removal of prosthesis followed by reimplantation of a new prosthesis during the same procedure. One-stage arthroplasty exchange is usually done in: patients with PJI in THA; good bone stock; good surrounding soft tissue; the organism is identified preoperatively and is susceptible to antimicrobials available orally and in bone cement used for implant fixation.[49]

Two-stage arthroplasty exchange or staged exchange is a standard treatment for chronic or delayed PJI.[123] During the first stage surgery, all infected tissues are aggressively debrided, and prosthesis and its components are removed. Antibiotic-impregnated polymethyl methacrylate cement spacers are implanted into the joint space to maintain the limb length and local delivery of antimicrobials. Vancomycin in combination with an aminoglycoside is the most commonly used antibiotics for antibiotic-loaded cement spacer preparation.[124] Pathogen-specific antimicrobial agents are given for 4–6 weeks following first stage surgery, and this is followed by 2–6 weeks antibiotic-free period. Patient's inflammatory markers are carefully monitored, and synovial fluid aspiration is done to rule out persisting infection. After normalisation of the inflammatory markers and complete wound healing, the second stage procedure is done by cement spacer removal and reimplantation of the new prosthesis.

Resection arthroplasty without reimplantation and arthrodesis are reserved for patients with high risk of reinfection, severe loss of bone stock or no functional improvement after surgery is expected.[49]

When all other treatment modalities become unsuccessful, amputation is the final choice for PJI treatment. Amputation is usually done in cases where a severe bone loss or prior failed attempt for resection arthroplasty or arthrodesis is reported, or no medical therapy was available.[49] However, the functional outcome of amputation is poor.


 ~ Antimicrobial Treatment Top


Antimicrobial treatment alone: As optimal results are difficult to obtain, antimicrobial treatment without surgical intervention is not routinely recommended for management of PJI. However, antibiotic suppression alone is reserved for patients with multiple co-morbidities and not eligible for any surgical interventions, or for those patients who are unwilling for any surgery, and causative organisms are susceptible to oral antibiotics.[11] Antibiotic treatment alone may be more successful in patients with early infections. However, there is a lack of a consensus for the optimal antimicrobial treatment programme with a nonsurgical strategy.

Antimicrobial treatment of selected pathogens: The antimicrobial therapy for PJI should be based on the causative bacteria and its antimicrobial susceptibility testing results. A detailed list of suggested antimicrobial agents and their dosing for specific pathogens are available in IDSA PJI management guidelines.[49] Close haematological monitoring of should be done in all patients who are getting intravenous antimicrobials on an outpatient basis or when the patient is on prolonged oral antimicrobial therapy.


 ~ Prevention Top


The growing demands for TJA's emphasise the importance of implementing strategies to minimise the risk of infection. In the preoperative period, it is important to identify and optimise any modifiable risk factors known to predispose patients to PJI. Blood glucose control, smoking cessation, and assessment to exclude other sites of infection (e.g., urinary tract infection, dental, or skin and soft tissue infections) should be done before any elective orthopaedic procedure. By identifying and decolonizing patients colonised with S. aureus, studies have reported a reduction in deep surgical site infections.[125] However, its effectiveness in infection reduction is not clear and therefore this strategy is not routinely implemented in TJA.

Perioperative antimicrobial prophylaxis strategy is routinely used in TJA to reduce the risk of subsequent deep infections.[126] In TJA, the preferred antimicrobials for perioperative antimicrobial prophylaxis include cefazolin or cefuroxime.[127] However, recent studies have reported high resistance of organisms infecting patients with joint replacements to recommended prophylactic antibiotic agents.[56],[128] This raises the concern about the appropriateness of the currently recommended antimicrobial prophylactic regimens for TJA. During the postoperative period, particular attention should be given to infection control practices.


 ~ Conclusion Top


PJI is one of the most common causes of implant failure. With an increase in the number of primary TJA's being performed each year, the total number of PJI cases will greatly increase, significantly impacting health care system and patients. Despite the developments of various techniques and diagnostic criteria's, early and accurate diagnosis of PJI is still challenging. Since the pathogens are concentrated in the implant surfaces within the biofilm, diagnosis of PJI using conventional culture techniques which detect mainly planktonic bacteria are inadequate. Although no 'gold standard' test is available for PJI diagnosis, a combination of all the available methods including the biofilm breaking sonication technique should be used for all suspected cases of PJI. A wide range of microorganisms can cause PJI's. Knowledge of the local microbiological spectrum of infection and antibiogram of pathogens causing PJI's are essential for choosing appropriate perioperative antimicrobial agents and empirical antimicrobial therapy. Both surgical intervention and antimicrobial therapy are usually required for optimal management of PJI.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
 ~ References Top

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    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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2004 - Indian Journal of Medical Microbiology
Published by Wolters Kluwer - Medknow

Online since April 2001, new site since 1st August '04