01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Native-joint septic arthritis most often follows haematogenous seeding of a vascular synovium. Direct inoculation and contiguous osteomyelitis or soft-tissue infection are other important routes.
Staphylococcus aureus is the dominant organism, with streptococci, Gram-negative bacilli and gonococcus relevant in specific hosts. A positive blood culture may identify the organism even when joint culture is sterile after antibiotics.
Diagnosis integrates joint aspiration, blood cultures and clinical probability. No single synovial white-cell threshold, serum CRP, Gram stain or crystal result excludes infection in a high-risk presentation.
Management has two inseparable components: systemic organism-active antibiotics and rapid removal of purulent inflammatory fluid. Persistent effusion or fever requires reassessment for inadequate drainage, adjacent bone infection or another metastatic focus.
Key points
- Septic arthritis is infection within a native synovial joint and can destroy cartilage within days; treat the acutely hot restricted joint as infection until adequately assessed.
- First diagnostic priority in a stable patient is urgent synovial aspiration before antibiotics for cell count, Gram stain, culture and crystal analysis.
- Do not delay antibiotics for aspiration in sepsis or haemodynamic instability; take blood cultures and treat immediately.
- Crystals do not exclude infection, and a negative Gram stain or modest synovial white-cell count cannot safely rule it out.
- Use ultrasound to identify and guide aspiration of an effusion; deep joints may require radiology or operative sampling.
- Drainage is definitive source control through serial aspiration or arthroscopic or open washout according to joint, response and surgical assessment.
- Empirical antibiotics follow local native-joint guidance, allergy, renal function, MRSA risk and likely source; narrow promptly to blood and synovial cultures.
- Search for endocarditis, osteomyelitis, skin infection, recent procedure and disseminated gonococcal infection when history or organism suggests them.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Haematogenous seeding
Transient or sustained bacteraemia deposits organisms in vascular synovium, making skin infection, endocarditis and intravascular access important sources.
Direct inoculation
Joint injection, arthroscopy, trauma, bite and penetrating injury introduce organisms directly into synovium and change the expected infecting flora.
Contiguous spread
Adjacent osteomyelitis, bursitis, cellulitis or a deep periarticular abscess can breach the joint capsule and infect synovial tissue.
Host susceptibility
Older age, rheumatoid disease, diabetes, immune suppression, damaged joints and injection drug use increase invasion and adverse-outcome risk.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Synovial bacterial growth
The highly vascular synovium lacks a limiting basement membrane, allowing bloodstream organisms to enter and multiply rapidly in joint fluid.
- 2Neutrophilic cartilage injury
Activated neutrophils release proteases and oxidants while cytokines stimulate chondrocyte damage, causing rapid irreversible cartilage loss.
- 3Pressure-related ischaemia
A tense purulent effusion raises intra-articular pressure, impairs synovial and epiphyseal perfusion and intensifies pain with movement.
- 4Bacteraemic dissemination
An infected joint may sustain bloodstream infection or represent one metastatic focus among endocarditis, vertebral and soft-tissue sites.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Rapid onset of severe pain, swelling, warmth and markedly restricted active and passive movement is the classic native-joint presentation.
Hip infection may present with groin pain and inability to weight bear, while shoulder or sternoclavicular disease can cause chest or proximal limb pain.
Fever, rigors, delirium, hypotension and malaise support invasive infection but may be absent in older or immunosuppressed patients.
Recent skin infection, intravascular access, injection drug use, endocarditis features or a distant infection suggests haematogenous seeding.
Young sexually active adults may have migratory arthralgia, tenosynovitis and sparse pustules before one or more joints become purulent.
Recent injection, arthroscopy or operation changes organism probability and requires exact procedural and antimicrobial history.
05InvestigationsWhat to request, why it matters and how to interpret it.
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
Urgent synovial aspirationFirst step - Why
- Obtain the most direct pre-treatment evidence of joint infection and alternative crystal disease.
- Interpretation and limitations
- Send sufficient fluid for Gram stain, aerobic and anaerobic culture, white-cell count with differential and crystals; low volume prioritises microbiology.
- 02
Synovial white-cell count and differential - Why
- Quantify intra-articular inflammation and support probability assessment.
- Interpretation and limitations
- A high neutrophil count increases suspicion, but no universal cutoff rules infection in or out, especially after antibiotics or during immune suppression.
- 03
Blood cultures - Why
- Detect bacteraemia and organism identity before antimicrobial exposure.
- Interpretation and limitations
- Take at least two sets in fever or suspected sepsis; concordant growth supports haematogenous infection and should prompt metastatic-source assessment.
- 04
Ultrasound-guided assessment - Why
- Confirm an effusion and guide aspiration in hip, shoulder or small difficult joints.
- Interpretation and limitations
- Ultrasound cannot distinguish sterile from infected fluid; its value is anatomical localisation and safe sampling.
- 05
Plain radiography - Why
- Provide a baseline and identify fracture, foreign body, chronic destruction or adjacent bone abnormality.
- Interpretation and limitations
- Early septic arthritis films may be normal apart from swelling; normal radiography does not exclude cartilage infection.
- 06
MRI or CT - Why
- Evaluate deep-joint infection, periarticular abscess, sacroiliac disease and associated osteomyelitis.
- Interpretation and limitations
- Use when anatomy or delayed response makes the result actionable; imaging must not postpone aspiration and sepsis treatment.
- 07
Sexual-health sampling - Why
- Detect gonorrhoea and chlamydia when exposure, rash, tenosynovitis or disseminated infection is plausible.
- Interpretation and limitations
- Obtain NAAT from all exposed sites and gonococcal cultures before antibiotics when feasible because joint culture sensitivity may be low.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Crystal arthritis
Gout and calcium pyrophosphate disease cause acute inflammatory monoarthritis, but crystal identification does not exclude simultaneous bacterial infection.
Inflammatory flare
Rheumatoid, psoriatic and reactive arthritis can produce a hot effusion and elevated inflammatory markers without positive microbiology.
Haemarthrosis or trauma
Anticoagulation, bleeding disorder and internal joint injury cause painful swelling, sometimes with blood in the aspirate.
Cellulitis and bursitis
Superficial erythema or a localised bursal collection may preserve passive joint movement better than intra-articular infection.
Osteomyelitis
Bone infection near a joint produces pain and inflammation and may coexist with or seed the synovial space.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ASPIRATESample the joint urgentlyFirst stepA new hot, swollen or severely restricted native joint has no better established diagnosis.+
- 1Assess ABCDE and sepsis, document every involved joint, skin source, procedure, immune status, sexual exposure and endocarditis risk.
- 2Take blood cultures and aspirate the joint before antibiotics when the patient is stable and aspiration can occur immediately.
- 3Send Gram stain, aerobic and anaerobic culture, cell count and crystals and inoculate appropriate culture bottles according to laboratory protocol.
- 4In sepsis, do not wait for aspiration: give empirical intravenous therapy after blood cultures and arrange drainage at the earliest safe opportunity.
02DRAINRemove infected synovial fluidPurulent aspirate or the combined clinical and laboratory picture makes septic arthritis likely.+
- 1Involve orthopaedics at once and choose serial closed aspiration, arthroscopic washout or open drainage according to joint, burden and response.
- 2Obtain multiple operative fluid and synovial tissue samples if surgery occurs and inspect cartilage, adjacent bone and periarticular tissue.
- 3Reassess pain, effusion, range of movement, fever and cultures after drainage and repeat washout when source control remains inadequate.
- 4Protect the joint during acute pain, then begin physiotherapy-guided movement to limit stiffness once infection and stability permit.
03TREATUse culture-directed systemic therapySeptic arthritis is suspected strongly or confirmed by joint, blood or operative findings.+
- 1Start the local native-joint empirical regimen based on sepsis, age, allergy, renal function, MRSA risk, Gram stain and exposure after cultures when feasible.
- 2Narrow promptly to the organism and susceptibility and review for intravenous-to-oral switch when drainage, physiology, absorption and an active oral option are secure.
- 3Set total duration with infection and orthopaedic specialists using organism, joint, bacteraemia, bone involvement and adequacy of washout.
- 4For Staphylococcus aureus bacteraemia, obtain clearance cultures and evaluate endocarditis and metastatic foci rather than treating the joint in isolation.
04REASSESSExplain persistent inflammationPain, fever, effusion or inflammatory markers fail to improve after drainage and active treatment.+
- 1Repeat joint examination and ultrasound and ask whether purulent material remains or another compartment was not drained.
- 2Review microbiology, tissue penetration, dosing, renal function, adherence and whether resistant or unusual organisms require new sampling.
- 3Arrange MRI for adjacent osteomyelitis, abscess or deep anatomy and search for endocarditis or another bacteraemic focus.
- 4Repeat operative washout or aspiration when source control is inadequate instead of responding only by lengthening or broadening antibiotics.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Empirical native-joint intravenous regimen
Give the exact local age-, allergy-, renal- and MRSA-risk-adjusted intravenous native-joint combination immediately after blood and synovial cultures when feasible.Local regimens differ because resistance and exposure differ; obtain microbiology advice for sepsis, immune compromise, injection exposure, bite, gonococcal risk or previous resistant isolates.
Flucloxacillin for susceptible staphylococci
Give 2 g intravenously every four to six hours when directed for methicillin-susceptible Staphylococcus aureus, with exact interval selected by the local severe-infection protocol.Clarify immediate penicillin allergy, review hepatic and renal function and sodium load, and investigate persistent bacteraemia, endocarditis and undrained infection rather than merely increasing duration.
Vancomycin for resistant Gram-positive risk
Use the current local intravenous loading and maintenance protocol based on actual body weight, renal function and measured serum exposure.Document dosing weight and target, monitor concentrations and kidney injury, check interacting nephrotoxins and switch to a narrower beta-lactam promptly when methicillin susceptibility permits.
Ceftriaxone for disseminated gonococcal infection
Give ceftriaxone 1 g intravenously or intramuscularly every 24 hours under sexual-health or infection-specialist guidance, tailoring duration and chlamydia treatment to cultures and current guidance.Obtain gonococcal culture before therapy when possible, assess severe beta-lactam allergy, test other STI sites and manage partners and test of cure through sexual-health services.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Permanent cartilage destruction
Delayed drainage permits irreversible proteolytic cartilage damage, joint-space loss, stiffness and chronic pain that may require later reconstructive surgery.
Osteomyelitis
Infection can extend across subchondral bone or arise from adjacent bone, increasing source-control complexity and treatment duration.
Bacteraemia and septic shock
Invasive joint organisms can spread systemically and cause endocarditis, metastatic abscesses, multiorgan dysfunction, septic shock and death.
Avascular necrosis
Raised pressure and vascular injury, particularly in the hip, can impair bone perfusion and collapse the articular surface.
Functional decline
Pain, immobilisation and surgery cause muscle loss, venous thrombosis risk and prolonged dependence without early rehabilitation.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Record observations, pain, effusion, passive and active range of motion and ability to weight bear at least daily during acute care.
- Review blood, synovial and operative cultures every day and document antimicrobial narrowing, route, dose and intended duration.
- Repeat blood cultures until clearance in Staphylococcus aureus or persistent bacteraemia and pursue echocardiography when indicated.
- Trend renal and liver function and drug concentrations during nephrotoxic or high-dose intravenous therapy.
- Assess the wound and drain output after washout and return to theatre promptly for recurrent effusion, fever or physiological decline.
- Arrange physiotherapy, joint-function review and specialist follow-up, including imaging or bone assessment when recovery is incomplete.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Crystals can coexist
Urate or calcium pyrophosphate crystals do not sterilise a joint; culture is still required when infection remains clinically plausible.
Gram stain lacks sensitivity
A negative synovial Gram stain cannot exclude infection and should not delay drainage in a high-probability presentation.
Cell count is contextual
Antibiotics, immune suppression and early sampling can lower synovial leukocytes, while inflammatory arthritis can raise them substantially.
Drainage protects cartilage
Purulent fluid contains bacteria, proteases and inflammatory cells that rapidly injure cartilage even after bloodstream antibiotics begin.
S aureus demands a wider search
Staphylococcus aureus in blood or joint should trigger clearance cultures and assessment for endocarditis and other metastatic infection.
Deep joints hide signs
Hip, sacroiliac and sternoclavicular infection may lack an obvious superficial effusion and need image-guided sampling or operative access.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not diagnose crystal arthritis and discard synovial culture merely because crystals are seen.
- 02
Do not delay antibiotics for aspiration when the patient has sepsis or haemodynamic instability.
- 03
Do not use a negative Gram stain, normal radiograph or modest CRP as a rule-out test.
- 04
Do not manage a purulent large-joint infection with antibiotics alone when drainage is feasible.
- 05
Do not apply a native-joint pathway unchanged to a prosthetic joint because sampling and surgery strategy differ.
- 06
Do not accept persistent Staphylococcus aureus bacteraemia without searching for endocarditis, bone infection and other metastatic foci.