Prosthetic-joint infection

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Microorganisms adhere to metal and polymer surfaces and form biofilm, where metabolic slowing and protective matrix reduce immune clearance and antimicrobial killing. Removal or radical debridement of colonised material is often required.

Acute postoperative infection presents with persistent wound drainage, erythema, pain or fever. Acute haematogenous infection presents suddenly in a previously functioning prosthesis, whereas chronic infection may cause only loosening and progressive pain.

Diagnostic confidence comes from the whole pattern: sinus tract, synovial analysis, multiple concordant tissue cultures, histology and implant findings. A single low-virulence isolate may be contamination or true biofilm disease and requires multidisciplinary interpretation.

Surgical strategy is selected before antibiotics when stability permits. Premature treatment can sterilise samples, obscure the organism and commit the patient to a poorly targeted prolonged course.

Key points

Prosthetic-joint infection is a biofilm infection involving an arthroplasty surface and surrounding tissue; it cannot be managed as simple cellulitis or native-joint sepsis.
Classify timing and symptom duration: early postoperative, acute haematogenous and chronic indolent presentations have different surgical opportunities.
In a stable patient, protect culture yield by withholding empirical antibiotics until aspiration or operative deep samples have been obtained.
Do not swab a sinus or superficial wound as the definitive culture; obtain multiple separately labelled deep tissue samples with clean instruments.
Plain radiographs assess loosening and fracture but cannot exclude infection; CRP and ESR support probability but may be normal in indolent disease.
Definitive management combines surgery with prolonged organism-directed therapy: DAIR, one- or two-stage exchange, resection or selected suppression.
DAIR is most successful with a stable implant, intact soft tissues, a susceptible organism and short symptom duration before mature biofilm establishes.
Rifampicin is used only in combination for selected susceptible staphylococcal retained-implant infections after adequate debridement; never prescribe it alone.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Perioperative inoculation

Skin or environmental organisms enter during arthroplasty and may present early or remain indolent within biofilm for months.

Haematogenous seeding

Bacteraemia from skin, dental, urinary, vascular or other sources can seed a previously functioning prosthesis abruptly.

Contiguous wound spread

Persistent wound drainage, dehiscence, soft-tissue necrosis or adjacent infection breaches the implant interface and establishes a mature microbial biofilm.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Surface adhesion
Staphylococci and other organisms attach to implant proteins and material using adhesins before producing a protective extracellular matrix.
2
Biofilm tolerance
Slow metabolic states, matrix diffusion barriers and altered gene expression reduce antimicrobial killing despite laboratory susceptibility.
3
Interface inflammation
Chronic innate immune activation causes progressive osteolysis, fibrous membrane formation, implant loosening and pain around infected prosthetic components.
4
Planktonic shedding
Biofilm intermittently releases organisms into joint fluid and blood, producing acute flares, sinus drainage or bacteraemia.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Early postoperative failureRed flag

Persistent drainage, wound breakdown, new erythema, effusion, escalating pain or fever soon after arthroplasty suggests early implant infection.

Acute haematogenous seedingRed flag

Sudden severe pain and loss of function in a previously well prosthesis during or after bacteraemia supports bloodstream implantation.

Chronic indolent infection

Progressive pain, stiffness, loosening, sinus or reduced function over months can occur without fever or marked inflammatory elevation.

Communicating sinusRed flag

A sinus tracking to the prosthesis is diagnostic of infection regardless of a superficial swab result.

Unstable constructRed flag

Dislocation, fracture, implant migration, gross loosening or neurovascular compromise requires urgent orthopaedic management alongside infection planning.

Host and soft-tissue constraint

Frailty, immune suppression, poor vascularity, previous revisions and deficient soft-tissue cover affect both surgical feasibility and chance of eradication.

Red flags requiring action

Hypotension, confusion, tachypnoea or rising lactate indicates prosthetic-joint infection with sepsis.
A draining sinus communicating with the prosthesis is definitive evidence of implant-associated infection.
Acute pain and effusion during Staphylococcus aureus bacteraemia suggests haematogenous prosthetic seeding.
Wound dehiscence, persistent drainage or exposed implant soon after surgery requires immediate arthroplasty-team review.
Progressive loosening, night pain or loss of function can represent indolent infection even without fever.
Neurovascular deficit, dislocation or periprosthetic fracture adds an orthopaedic emergency to the infection.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Plain joint radiographsFirst step
Why
Assess implant position, migration, radiolucency, osteolysis, fracture and baseline mechanical failure.
Interpretation and limitations
Loosening may be septic or aseptic and early infection may show no change; films guide mechanics but do not exclude infection.
02
CRP, ESR and blood profile
Why
Support infection probability and assess organ function before aspiration, surgery and antimicrobial therapy.
Interpretation and limitations
Raised markers are nonspecific and normal values do not exclude low-grade biofilm infection; trends are interpreted with symptoms and procedure timing.
03
Blood cultures
Why
Identify bacteraemia in fever, sepsis or acute haematogenous presentation.
Interpretation and limitations
Take before antibiotics; Staphylococcus aureus requires clearance cultures and endocarditis and metastatic-focus evaluation.
04
Image-guided synovial aspiration
Why
Obtain fluid for cell count, differential and prolonged aerobic and anaerobic culture before antibiotics.
Interpretation and limitations
Use joint- and timing-specific thresholds with the implant team. A dry tap or negative culture does not exclude indolent infection.
05
Multiple operative tissue cultures
Why
Provide definitive deep microbiology across the implant–tissue interface.
Interpretation and limitations
Take at least five separately labelled samples with separate clean instruments where local protocol specifies; repeated concordant growth is stronger than one isolate.
06
Periprosthetic histology
Why
Demonstrate acute inflammation and help distinguish infection from contamination or aseptic loosening.
Interpretation and limitations
Interpret neutrophil counts with sampling site, organism virulence and antibiotics; histology complements rather than replaces culture.
07
Ultrasound, CT or nuclear imaging
Why
Guide aspiration and define collection, sinus, component position or occult infection when standard tests remain uncertain.
Interpretation and limitations
Advanced imaging is selected by the revision team and cannot replace deep sampling or justify delaying source control in acute sepsis.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Aseptic loosening

Wear debris and mechanical failure cause pain and radiolucency without infection, but require pre-revision infection exclusion.

Dislocation or fracture

Abrupt pain and inability to bear weight can reflect mechanical implant catastrophe requiring urgent radiography and reduction or fixation.

Crystal or inflammatory arthritis

A prosthetic joint can develop acute crystal-associated inflammation, but identifying crystals does not exclude a concurrent implant-associated bacterial infection.

Superficial wound infection

Skin-limited erythema may not involve the prosthesis, yet persistent drainage and early postoperative anatomy demand specialist evaluation.

Referred pain

Spinal, tendon, bursal and neighbouring-joint disease can impair function without implant infection and should be examined systematically.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01STABLEPreserve diagnostic yieldFirst stepProsthetic-joint infection is suspected but the patient has no sepsis, wound catastrophe or neurovascular emergency.

1Contact the arthroplasty or implant surgeon early and document implant type, operation date, revisions, symptom duration, wound history and previous antibiotics.
2Obtain radiographs, CRP and ESR and arrange image-guided aspiration under the local prosthetic-joint protocol.
3Withhold empirical antibiotics until aspiration or operative tissue has been collected when this is clinically safe.
4Agree the likely surgical strategy and required number and handling of deep samples before the patient enters theatre.

02DAIRDebride and retain selectivelyInfection is acute, the implant is stable, soft tissues are salvageable and symptom duration and organism make retention plausible.

1Perform urgent open debridement, extensive synovectomy and exchange modular components where technically possible while retaining fixed stable components.
2Take multiple deep tissue samples before irrigation and antibiotics, using separate instruments and clear anatomical labels.
3Begin directed or empirical systemic therapy after sampling and add rifampicin combination therapy only when specialist criteria for susceptible staphylococcal retained-implant disease are met.
4Monitor wound closure, inflammatory and functional response closely and move to exchange strategy if infection control fails.

03EXCHANGERemove mature biofilmChronic infection, loose implant, difficult organism, deficient soft tissue or failed retention makes eradication with DAIR unlikely.

1Plan one-stage or two-stage exchange, component removal, debridement and reconstruction through an arthroplasty infection multidisciplinary team.
2Obtain multiple tissue and implant-interface samples and define bone loss, stability and plastic-surgery or vascular needs.
3Use organism-directed systemic treatment between and after procedures, avoiding a fixed schedule detached from cultures and operative findings.
4Confirm clinical and microbiological readiness for reimplantation according to the specialist pathway; no single CRP result proves eradication.

04NON-CURATIVEUse suppression only deliberatelyCurative revision carries disproportionate risk or is declined and infection cannot be eradicated surgically.

1Confirm the diagnosis and organism as reliably as possible and discuss prognosis, drainage, pain, function and sepsis risk with the patient.
2Use long-term oral suppressive therapy only after infection, microbiology and surgical agreement with a susceptible tolerable drug.
3Monitor toxicity, resistance, wound change and breakthrough bacteraemia and maintain rapid admission access for deterioration.
4Revisit goals and surgical feasibility when symptoms, organism or health status changes rather than allowing suppression to continue without review.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Provides broad early coverage after microbiological sampling while surgical findings and deep cultures define directed treatment.

Empirical prosthetic-joint intravenous regimen

Give the exact local implant-infection regimen after multiple deep samples, adjusted for timing, previous cultures, allergy, renal function and MRSA and Gram-negative risk.

Do not begin before sampling in a stable patient; obtain microbiology advice, use weight- and level-guided glycopeptide dosing when selected and narrow promptly.

Provides high-dose bactericidal treatment for susceptible staphylococcal implant infection after reliable deep cultures.

Flucloxacillin for methicillin-susceptible staphylococci

Give 2 g intravenously every four to six hours when directed, using the exact interval in the local bone-and-joint infection protocol.

Clarify immediate penicillin allergy, monitor hepatic and renal function and sodium exposure, and coordinate route and duration with implant retention or exchange surgery.

Adds biofilm-active activity against susceptible staphylococci when infected hardware is deliberately retained.

Rifampicin combination component

Give 300 to 450 mg orally twice daily only in combination with another active agent for selected susceptible staphylococcal retained-implant infection after adequate debridement.

Never use monotherapy; review major enzyme-inducing interactions, liver function and resistance risk, and avoid starting into uncontrolled bacteraemia or an undrained heavily infected wound.

Treats methicillin-resistant staphylococci or other susceptible resistant Gram-positive implant organisms when indicated.

Vancomycin for resistant Gram-positive infection

Use the local intravenous loading and maintenance protocol based on actual body weight, renal function and measured serum exposure.

Monitor concentrations and kidney injury, document target exposure, remove other nephrotoxins where possible and consider specialist alternatives for toxicity or difficult biofilm infection.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Chronic sinus and relapse

Retained implant biofilm sustains intermittent sinus drainage and recurrent deep infection after apparently successful courses of systemic antimicrobial therapy.

Bone loss and mechanical failure

Chronic inflammation and repeated revision procedures destroy available bone stock, loosen implant components and substantially complicate future reconstructive surgery.

Bacteraemia and metastatic infection

Organisms shed from the implant can cause sepsis, endocarditis and infection at other joints or vertebrae.

Amputation or resection

Uncontrolled infection, severe tissue loss or failed reconstruction may require excision arthroplasty, fusion or limb amputation.

Treatment morbidity

Multiple major operations, prolonged antimicrobials, immobility and medicine toxicity cause severe deconditioning, thromboembolism risk and substantial long-term psychological burden.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Inspect wound closure, drainage, erythema, effusion, pain and function after every operative stage and document any recurrent sinus.
Review all deep samples together, including number positive, organism identity, time to positivity and histology, before labelling contamination.
Repeat blood cultures to clearance in Staphylococcus aureus or persistent bacteraemia and assess endocarditis and other metastatic sites.
Monitor renal, hepatic and haematological toxicity, serum drug concentrations and rifampicin interactions throughout prolonged therapy.
Use CRP and ESR as contextual trends rather than pass–fail criteria for reimplantation or cure.
Track implant stability, rehabilitation, mobility aids, thromboprophylaxis, nutrition and soft-tissue healing through the multidisciplinary pathway.
After treatment provide direct access for new pain, wound drainage, fever or declining function because relapse can be subtle.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

A sinus is diagnostic

A tract communicating with the prosthesis establishes infection even if the surface culture is negative or grows a coloniser.

One culture needs context

A single low-virulence organism may represent contamination, while repeated concordant samples, histology and clinical features support true infection.

Symptom duration matters for DAIR

Mature biofilm becomes harder to eradicate while retaining components, so early referral preserves the opportunity for successful debridement.

Modular exchange improves debridement

Replacing accessible liners or heads removes biofilm-bearing material and permits wider synovectomy while stable fixed components remain.

Rifampicin resistance emerges quickly

Using rifampicin alone or in a high-burden undrained infection selects resistance and can remove a valuable biofilm-active option.

Mechanical failure can be infectious

Loosening and pain should not be labelled aseptic until infection has been assessed with an appropriate sampling strategy.

11Common pitfallsFrequent interpretation and management errors.

01
Do not start empirical antibiotics before aspiration or operative samples in a stable patient.
02
Do not use a superficial sinus swab as the organism definition for implant-directed treatment.
03
Do not apply native-joint aspiration thresholds or short cellulitis courses without prosthetic-joint specialist interpretation.
04
Do not choose DAIR without considering implant stability, soft-tissue condition, organism and symptom duration.
05
Do not prescribe rifampicin alone or begin it before adequate source control and an active companion drug.
06
Do not use a normal CRP as proof that indolent prosthetic-joint infection is absent.