01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Acute monoarthritis means new inflammation or dysfunction centred on one joint, usually evolving over hours to days. Establish exact onset, trauma, fever, recent infection, skin breach, injection, surgery, prosthesis, antimicrobial exposure, immunosuppression, anticoagulation and previous attacks. Ask about sexual exposure and disseminated infection when relevant without stereotyping. Examine physiology, skin, heart, other joints and the complete limb neurovascular status.
Septic arthritis and crystal arthritis overlap clinically. Fever may be absent; CRP may be normal early; and crystals may coexist with bacterial infection. The safest decision is therefore based on aspiration, culture, blood cultures and illness severity rather than a single score. Ultrasound can confirm a difficult effusion and guide aspiration, but it does not identify the organism or replace synovial analysis.
Management is simultaneous rather than sequential when infection is plausible: resuscitate, obtain cultures, arrange drainage and start locally recommended intravenous antibiotics after samples if the patient is stable enough. Native and prosthetic joints follow different surgical and microbiological pathways. Once culture results and clinical response are available, narrow treatment, ensure adequate source control and revisit crystal or inflammatory alternatives.
Key points
- Treat acute monoarthritis as septic arthritis until infection has been actively considered and, where feasible, synovial fluid has been obtained.
- Examine whether pain is truly intra-articular: severe restriction of both active and passive movement supports joint pathology; focal bursal or tendon pain may preserve passive range.
- Take blood cultures before antibiotics when systemic infection is suspected, but never postpone antimicrobials for sampling in a haemodynamically unstable patient.
- Aspirate using aseptic technique and send sufficient fluid for Gram stain, bacterial culture, cell count where locally available and compensated-polarised-light microscopy for crystals.
- Neither a low synovial white-cell count nor identified urate or CPP crystals reliably excludes concurrent infection; culture and clinical trajectory remain essential.
- Serum urate may fall during a gout flare and cannot diagnose the cause of an acutely swollen joint by itself.
- A painful prosthetic joint, joint after recent procedure, or hot joint in an immunosuppressed patient needs early orthopaedic and microbiology involvement.
- After immediate danger is controlled, determine whether the episode is the first manifestation of gout, inflammatory arthritis, haemarthrosis or structural injury and plan prevention.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Joint infection
Haematogenous bacterial seeding, direct inoculation or spread from adjacent tissue can infect native or prosthetic joints, with risk increased by immunosuppression and damaged joints.
Crystal inflammation
Monosodium urate or calcium pyrophosphate crystals activate intense innate inflammation, producing abrupt pain, swelling and erythema that can closely mimic infection.
Traumatic and inflammatory causes
Haemarthrosis, fracture, internal derangement, palindromic inflammation and early systemic arthritis may initially affect a single joint before the wider pattern emerges.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Synovial inflammatory surge
Bacteria, crystals or immune activation recruit neutrophils and inflammatory mediators into the synovial space, rapidly increasing pressure and pain.
- 2Cartilage vulnerability
Bacterial enzymes, neutrophil products and raised intra-articular pressure can damage cartilage within a short period, making source control urgent.
- 3Systemic dissemination
An infected joint can seed or arise from bloodstream infection, while inflammatory vasodilatation and cytokine release may progress to sepsis and organ dysfunction.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Acute severe pain, effusion and markedly painful passive movement with fever, rigors, skin infection or bacteraemia risk requires urgent aspiration and source-control planning.
New pain, swelling, wound change or systemic illness around a prosthesis may represent periprosthetic infection and needs urgent orthopaedic review before casual aspiration or oral antibiotics.
An explosive attack peaking within hours, podagra, tophi or previous self-limited episodes supports gout; acute knee or wrist disease in older people suggests calcium pyrophosphate arthritis.
Trauma, anticoagulation, bleeding disorder, rapid tense swelling or radiographic injury suggests blood in the joint and requires structural and haemostatic assessment.
Preserved passive range with focal superficial tenderness points toward bursitis, tendon disease or cellulitis, although adjacent infection can spread and still warrants close review.
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
Synovial-fluid aspirationFirst step - Why
- Obtain the decisive specimen for microbiology and crystal identification before treatment changes the yield.
- Interpretation and limitations
- Record appearance and volume; send Gram stain and culture even when crystals are seen. Cell counts overlap across infection and sterile inflammation, and inadequate volume should prioritise culture.
- 02
Blood cultures and sepsis blood panel - Why
- Detect bacteraemia, organ dysfunction and a systemic inflammatory response in suspected septic arthritis.
- Interpretation and limitations
- Take at least the locally specified culture sets before antibiotics when feasible. FBC, CRP, renal, liver and lactate results support severity assessment but cannot exclude a local infection.
- 03
Compensated polarised-light microscopy - Why
- Identify monosodium urate and calcium pyrophosphate crystals within synovial fluid.
- Interpretation and limitations
- Needle-shaped, strongly negatively birefringent urate and rhomboid, weakly positively birefringent CPP crystals support diagnoses; expertise and prompt specimen handling affect sensitivity.
- 04
Ultrasound and plain radiography - Why
- Locate an effusion, guide difficult aspiration and identify fracture, chondrocalcinosis, prosthesis or established structural disease.
- Interpretation and limitations
- Normal early radiographs do not exclude infection. Chondrocalcinosis supports CPP deposition but is neither required nor sufficient to explain the acute episode.
- 05
Targeted infection testing - Why
- Identify gonococcal, mycobacterial, fungal or adjacent sources when exposure, host factors or chronicity suggests them.
- Interpretation and limitations
- Discuss sample type and prolonged or molecular testing with microbiology before collection; a routine negative culture after antibiotics may require repeat or operative sampling.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Septic arthritis
Marked pain on passive movement, systemic illness, bacteraemia risk or a prosthesis raises concern, but mild fever or normal blood tests cannot exclude infection.
Gout or CPP crystal arthritis
Rapid onset, previous stereotyped attacks, tophi or chondrocalcinosis supports crystal disease; definitive identification requires correctly examined synovial fluid when uncertainty matters.
Trauma or haemarthrosis
Injury, anticoagulation, bleeding disorder or lipohaemarthrosis redirects assessment towards structural damage and bleeding while infection may still coexist.
Periarticular mimic
Bursitis, cellulitis and tendinopathy may appear joint-centred, but passive range and precise localisation can show that the synovial cavity is not the primary source.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Unwell hot jointResuscitate, culture and drainFirst stepAcute monoarthritis with sepsis, systemic toxicity, rapidly worsening pain or high-risk host features.+
- 1Perform ABCDE, obtain intravenous access, analgesia, blood cultures and organ-function tests, and contact orthopaedics and microbiology immediately.
- 2Aspirate the joint urgently unless this would delay life-saving treatment; start locally approved intravenous antibiotics after samples in a stable patient or immediately if unstable.
- 3Give orthopaedics explicit ownership of native-joint drainage and source control. Select repeated aspiration, arthroscopic washout or open drainage according to the joint, macroscopic or radiological damage, organism and response; review cultures and clinical progress with microbiology, then narrow treatment when results permit.
02Stable but uncertainLet fluid answer the central questionA new effusion without shock where infection, crystals and bleeding remain plausible.+
- 1Document risk factors and full examination, withhold unnecessary antibiotics until prompt synovial and blood samples are secured, and avoid injecting corticosteroid into an undiagnosed hot joint.
- 2EscalationRequest culture and crystal examination together, add imaging for trauma or a difficult deep joint, and provide analgesia while maintaining a clear escalation threshold.
- 3Review preliminary microscopy and the patient's trajectory the same day; do not discharge solely because crystals are present or inflammatory markers are modest.
03Crystal disease confirmedTreat the flare and prevent recurrenceA stable patient has a compatible phenotype and crystals with no current microbiological or clinical evidence of infection.+
- 1Choose an anti-inflammatory option using renal, gastrointestinal, cardiovascular, anticoagulant and interaction risks, and give written advice on expected response and urgent return features.
- 2AlternativeRecheck if improvement is not prompt because infection, fracture or an alternative inflammatory diagnosis may have been missed despite the initial result.
- 3Assess indications for long-term urate-lowering therapy after the flare and address medicines, kidney disease, alcohol and other modifiable contributors without blame.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Empirical intravenous antibacterial therapy for suspected native-joint septic arthritis
There is no single universal UK agent or dose. If the patient is stable, obtain synovial fluid and blood cultures first, then start the current local intravenous regimen; in sepsis or septic shock, take blood cultures promptly but do not delay time-critical intravenous antibiotics for joint aspiration. Microbiology must select and document the agent, dose and interval using Gram stain, likely source, prior cultures, allergy, renal and hepatic function, native versus prosthetic joint, and MRSA, resistant Gram-negative or gonococcal risk.Do not use a casual oral regimen before sampling in a stable undiagnosed hot joint. A prosthetic joint follows a separate implant-infection pathway. Review cultures, susceptibilities, renal function, toxicity and clinical response promptly; narrow, change route and set duration only with orthopaedic and microbiology oversight, reassessing source control if improvement is inadequate.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Rapid joint destruction
Untreated septic arthritis can erode cartilage and subchondral bone, leaving permanent pain, instability and severe functional loss despite later microbiological cure.
Sepsis and metastatic infection
Bacteraemia may cause shock, endocarditis, vertebral infection or other seeded sites, especially with Staphylococcus aureus or delayed source control.
Recurrent crystal disease
Repeated gout or calcium pyrophosphate attacks cause disability, and uncontrolled urate deposition can produce tophi, erosions and urate nephrolithiasis.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Record temperature, heart rate, blood pressure, consciousness, urine output and lactate trajectory when systemic infection is possible.
- Trend joint pain, passive range, swelling and ability to bear weight after aspiration or washout; persistent deterioration suggests inadequate source control.
- Review blood and synovial cultures until final, including after discharge, with a documented person responsible for acting on late growth.
- Monitor renal, hepatic and haematological parameters according to the antimicrobial or anti-inflammatory regimen and comorbid risk.
- After a crystal flare, review recurrence, serum urate at an appropriate stable interval and adherence or tolerance if urate-lowering therapy begins.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Crystals and bacteria can coexist
Finding urate or CPP crystals explains inflammation but does not sterilise the sample; maintain culture and clinical review when infection remains plausible.
Appearance is not enough
Cloudy or purulent fluid raises concern, yet bloody, inflammatory and partially treated samples overlap, so laboratory analysis and trajectory are indispensable.
Deep joints hide
Hip, shoulder and sacroiliac infection may lack an obvious superficial effusion; inability to move or bear weight can be the strongest clue.
Prostheses need a separate route
Sampling technique, antibiotic timing and surgical strategy affect later diagnosis and implant retention, so involve the responsible orthopaedic team early.
Serum urate is a longitudinal measure
It supports long-term gout assessment but can be normal during an acute flare and never substitutes for aspiration when sepsis is possible.
11Common pitfallsFrequent interpretation and management errors.
- 01
Starting oral antibiotics for a prosthetic-joint presentation before cultures and orthopaedic discussion in a stable patient.
- 02
Excluding septic arthritis because the patient has no fever, a normal radiograph or only a modest CRP rise.
- 03
Stopping microbiological investigation after crystals are reported in an immunosuppressed or systemically unwell patient.
- 04
Injecting corticosteroid into a hot joint before infection has been adequately excluded.
- 05
Allowing a difficult aspiration to end assessment rather than arranging image guidance or operative sampling.