Lucan · Conditions

Septic arthritis

Australian guidance: eTG Antibiotic — Septic Arthritis

1. Definition and epidemiology

Septic arthritis is a medical emergency defined as bacterial infection of a native joint space, causing rapid destruction of articular cartilage if not treated promptly. In Australia, the incidence is approximately 2 to 10 per 100,000 population per year, with higher rates in Indigenous Australians, older adults, and people who inject drugs. Risk factors include pre-existing joint disease (especially rheumatoid arthritis), diabetes mellitus, immunosuppression, recent intra-articular injection, skin breaches, and intravenous drug use.

2. Pathophysiology

Bacteria reach the joint space most commonly via haematogenous spread from a distant focus of infection, but may also arrive by direct inoculation (trauma, arthrocentesis) or contiguous spread from adjacent osteomyelitis. The synovial membrane lacks a basement membrane, making it highly susceptible to bacterial seeding during bacteraemia. Once bacteria establish within the synovial fluid, the innate immune response is rapidly activated: pattern recognition receptors on synoviocytes and infiltrating neutrophils detect pathogen-associated molecular patterns, triggering a cascade of interleukin-1 beta, interleukin-6, and tumour necrosis factor alpha release. The resulting purulent exudate raises intra-articular pressure, compromising synovial and subchondral vascular supply. Neutrophil proteases and bacterial toxins (staphylococcal exotoxins, streptococcal hyaluronidase) degrade proteoglycans and collagen directly. Within 24 to 48 hours, irreversible cartilage loss begins; without drainage and antibiotic therapy, subchondral bone erosion, fibrous ankylosis, and permanent loss of joint function follow. Staphylococcus aureus is the dominant pathogen overall (accounting for approximately 40 to 50% of native joint infections in adults), followed by streptococcal species; Neisseria gonorrhoeae is the leading cause in sexually active adults under 35 years (Robbins Ch 26).

3. Clinical presentation and diagnostic criteria

The classic presentation is an acutely hot, swollen, erythematous, exquisitely tender joint with a restricted and painful range of motion in all planes (distinguishing it from periarticular pathology). The knee is the most commonly affected joint (approximately 50%), followed by the hip, shoulder, wrist, and ankle. Systemic features including fever (present in approximately 60 to 80%), rigors, and malaise support the diagnosis. Polyarticular involvement occurs in 10 to 20% of cases and is more common with gonococcal infection and rheumatoid arthritis. In the immunocompromised or elderly, systemic signs may be absent despite advanced joint infection. No validated clinical diagnostic criteria exist; the combination of joint effusion, warmth, restricted movement, and fever in the right clinical context mandates urgent joint aspiration. A prior diagnosis of gout or pseudogout does not exclude concurrent septic arthritis.

4. Investigations and AU-specific cutoffs

Joint aspiration is mandatory and should not be delayed by imaging. Synovial fluid analysis is the cornerstone of diagnosis:

• Cell count: white cell count above 50,000 cells per microlitre with greater than 75% polymorphonuclear leucocytes is highly suggestive of septic arthritis; counts above 100,000 per microlitre are strongly associated with bacterial infection. Counts between 20,000 and 50,000 occur in crystal arthropathy and reactive arthritis.
• Gram stain: positive in only 30 to 50% of cases but guides empirical therapy when positive.
• Culture: synovial fluid culture is positive in 70 to 90% of non-gonococcal cases; blood cultures should always accompany joint aspiration and are positive in approximately 50% of cases. In suspected gonococcal arthritis, urogenital, pharyngeal, and rectal swabs should be taken in addition.
• Glucose and protein: synovial glucose below 50% of simultaneous serum glucose and elevated protein support infection but are non-specific.

Serum inflammatory markers including C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) are elevated in nearly all cases; white cell count is elevated in approximately 50%. Plain X-ray of the affected joint should be performed but is usually normal early; it may show soft tissue swelling, joint space widening from effusion, or pre-existing joint disease. Ultrasound and MRI confirm effusion and guide aspiration of deep joints (hip, shoulder). In children and when osteomyelitis is suspected, MRI is preferred. CT should not substitute for MRI in equivocal cases.

5. Management

Management requires simultaneous joint drainage and systemic antibiotic therapy; neither alone is sufficient.

Drainage: Daily needle aspiration to dryness is the preferred initial approach for accessible joints. If the joint reaccumulates rapidly, if the aspirate is too thick to drain, if there is inadequate clinical response after 5 to 7 days, or if the hip joint is involved (in adults and all ages in children), surgical arthroscopic or open drainage with washout is indicated. Hip septic arthritis in adults and all cases in children require urgent surgical drainage, as the blood supply to the femoral head is at risk from raised intra-articular pressure.

Antibiotic therapy: Therapy should commence after joint aspiration and blood cultures have been collected. Empirical therapy targets Gram-positive cocci, with modification on culture results:

• Non-penicillin-allergic adults without MRSA risk factors: flucloxacillin 2 g intravenously every 6 hours.
• If MRSA risk factors are present (healthcare exposure, prior MRSA, Indigenous Australian communities with known MRSA prevalence) or the patient has had a severe penicillin hypersensitivity reaction: vancomycin intravenously, dosed by weight and renal function per the Therapeutic Guidelines pharmacokinetic targets (trough 15 to 20 mg per litre, or AUC-guided dosing).
• Suspected gonococcal arthritis: ceftriaxone 1 g intravenously or intramuscularly daily until clinical improvement (at least 24 to 48 hours), then step-down to oral therapy guided by susceptibilities.
• Gram-negative cover should be added in neonates, elderly adults, immunocompromised patients, and those with gram-negative bacteraemia risk.

Intravenous therapy is continued until there is clear clinical improvement (typically 5 to 14 days for most pathogens), after which an early switch to high-bioavailability oral therapy is appropriate and supported by evidence from the OVIVA trial and eTG guidance. Total duration is typically 3 to 4 weeks for uncomplicated infection; longer courses are required for S. aureus bacteraemia or delayed clinical response.

6. Pharmacology and AU PBS notes

Flucloxacillin (Flopen, Staphylex): penicillinase-resistant penicillin; first-line for methicillin-susceptible S. aureus (MSSA). Adult dose 2 g IV 6-hourly. Oral step-down: 500 mg to 1 g orally 6-hourly. No specific PBS streamlined authority code for septic arthritis; prescribed as Section 85 general benefit.

Vancomycin: glycopeptide reserved for MRSA, penicillin allergy (severe), or culture-confirmed MRSA. Dosed by weight and renal function using AUC-guided or trough-guided monitoring; target AUC 24-hour 400 to 600 mg.h per litre per current Therapeutic Guidelines and ASHP-IDSA consensus. AU brand: Vancocin (Pfizer). Requires therapeutic drug monitoring in all patients.

Ceftriaxone (Rocephin): third-generation cephalosporin for gonococcal arthritis and Gram-negative cover. 1 g IV or IM daily. PBS authority not required for this indication.

Oral step-down options (once clinically improving, culture-directed): cefalexin 1 g orally 6-hourly (MSSA), amoxicillin-clavulanate (polymicrobial or Gram-negative), ciprofloxacin 750 mg orally 12-hourly (susceptible Gram-negatives). Ciprofloxacin is not appropriate for S. aureus empirically due to resistance risk.

7. Complications and monitoring

Joint destruction: irreversible cartilage loss can occur within days of untreated infection, leading to secondary osteoarthritis and chronic pain. Risk is highest for the hip in children (avascular necrosis of the femoral head) and in patients with pre-existing inflammatory arthropathy.

Osteomyelitis: contiguous spread to adjacent bone occurs in 10 to 20% of cases; MRI should be performed if clinical resolution is slower than expected.

Bacteraemia and metastatic infection: S. aureus bacteraemia carries a risk of endocarditis (particularly on prosthetic valves), vertebral osteomyelitis, and psoas abscess. Echocardiography and CT chest-abdomen-pelvis should be considered when S. aureus bacteraemia is confirmed.

Chronic or recurrent infection: failure to drain adequately, inadequate antibiotic duration, or unrecognised resistant organisms.

Monitoring schedule: - Daily joint aspiration until effusion resolves or surgical drainage is performed. - CRP and white cell count every 48 hours until normalising. - Repeat synovial fluid culture at 48 to 72 hours if no clinical improvement. - Vancomycin trough or AUC monitoring with every dose change and at least every 72 hours. - Renal function at baseline and every 48 to 72 hours with IV vancomycin. - Joint function assessment and physiotherapy referral once acute infection has resolved.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.