Septic Arthritis

Septic arthritis is a bacterial infection of a joint. It is an orthopaedic emergency because cartilage destruction occurs rapidly (within 24-48 hours).

Pathophysiology

Bacteria enter the joint via haematogenous spread (most common), direct inoculation (injection, surgery), or spread from adjacent osteomyelitis.

Inflammatory response and bacterial enzymes cause rapid cartilage destruction.

Risk Factors

• Rheumatoid arthritis
• Diabetes mellitus
• Immunosuppression
• Recent joint injection or surgery
• IV drug use
• Prosthetic joint

Routes of Infection

Bacteria reach the synovial space through three main routes:

1. Haematogenous spread (most common, 70-80%)

   • Bacteraemia from distant focus (skin, UTI, pneumonia)
   • Synovium is highly vascular with no basement membrane
   • Bacteria lodge and proliferate rapidly

2. Direct inoculation (15-20%)

   • Joint injection or aspiration
   • Arthroscopy or open surgery
   • Penetrating trauma

3. Contiguous spread (5-10%)

   • Adjacent osteomyelitis
   • Soft tissue infection spreading to joint

Pathological Cascade

Microbiology

Clinical Features

• Painful, swollen joint - acute onset over hours to days
• Unable to bear weight (if lower limb)
• Limited ROM (held in position of comfort - flexion for knee, abduction/ER for hip)
• Warmth and erythema over joint
• Fever (may be absent in elderly, immunocompromised)
• Usually monoarticular (knee most common, then hip, shoulder)

Joint Distribution

Differential Diagnosis

The acute hot, swollen joint has a wide differential. Crystals and infection can coexist, so identifying crystals NEVER excludes sepsis if the clinical picture fits.

The clinical section notes septic arthritis is "usually monoarticular", and the prognosis list flags "polyarticular involvement (often haematogenous)" as a poor sign — but the polyarticular form is never developed, and it is the presentation most likely to kill the patient.

• It is the minority but the more lethal form. Most septic arthritis is monoarticular; roughly 10-20% is polyarticular (two or more joints). Polyarticular disease reflects overwhelming bacteraemia, so its mortality is much higher — quoted around 30-50% in some series versus roughly 10% for monoarticular disease.
• The host and the organism are characteristic. It is almost always haematogenous, usually Staphylococcus aureus (sometimes streptococci, pneumococcus or gonococcus), and is strongly associated with pre-existing joint disease — rheumatoid arthritis is the classic host — and immunosuppression (diabetes, steroids, malignancy).
• It mandates a hunt for the source. Two or more septic joints means blood-borne seeding, so you must find the focus of bacteraemia — above all infective endocarditis (echocardiography, repeated blood cultures, examine for a new murmur and peripheral stigmata), plus skin, intravascular lines, the urinary tract and the spine. Treat each affected joint (aspiration or washout) and the systemic source.

The microbiology section flags that IV drug users present with sepsis in "unusual joints — sternoclavicular, SI joint", but these are never developed — and they are exactly the joints that get missed, because they are deep, hard to examine and present insidiously.

• Who and what. Septic arthritis of the sternoclavicular (SC) joint, sacroiliac (SI) joint, symphysis pubis and spine is characteristic of IV drug users (and the immunosuppressed). The organism is still most often S. aureus, but with a notably higher rate of Pseudomonas and other Gram-negatives in IVDU.

• The take-home. These axial joints are deep, hard to examine and aspirate and present insidiously, so they are under-recognised. Maintain a high index of suspicion in IVDU and the immunosuppressed, use cross-sectional imaging (CT/MRI) early, and remember the SC joint's capacity for retrosternal/mediastinal spread, which raises the threshold from a simple washout toward joint resection.

Joint Aspiration (Gold Standard)

Aspiration technique:

• Aseptic technique essential
• Mark anatomical landmarks
• Aspirate BEFORE antibiotics if possible (but do not delay treatment)

Synovial fluid analysis:

Important: WCC greater than 50,000 has 90% sensitivity but crystals do NOT exclude infection - can coexist.

Blood Tests

• WCC - elevated in 50-60%
• CRP - elevated in greater than 90% (most sensitive)
• ESR - elevated but slow to change
• Blood cultures - positive in 40-50%
• Procalcitonin - may help differentiate from crystal arthropathy

Imaging

Algorithm

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Guidelines, Registries & Global Practice

Global epidemiology:

• Annual incidence of native-joint septic arthritis is roughly 4-10 per 100,000 in the general population, rising to 30-70 per 100,000 in patients with rheumatoid arthritis or prosthetic joints.
• S. aureus dominates worldwide; the proportion that is MRSA varies widely by region (low in much of Scandinavia and the Netherlands, considerably higher in parts of the USA, South Asia and among community strains in remote and Indigenous populations).
• Gonococcal arthritis remains an important cause in young sexually active adults globally; tuberculous and fungal joint sepsis are disproportionately common in high-TB-burden and resource-limited settings and in the immunocompromised.

Side-by-side guidance:

Regional empirical regimens differ chiefly in how aggressively they cover MRSA — driven by local resistance data rather than true clinical disagreement. The universal principles (aspirate first, urgent drainage, source control, ID/microbiology involvement) are consistent across all bodies.

Registry and resource notes:

• Arthroplasty registries (NJR, AJRR, AOANJRR, the Swedish and Norwegian registers) track PJI as a leading cause of revision and inform implant- and fixation-specific infection risk; deep infection is among the top three reasons for revision knee arthroplasty in most registries.
• High-resource settings favour arthroscopic washout, antibiotic-loaded cement spacers and multidisciplinary bone-infection units. In limited-resource settings, open arthrotomy with serial saline lavage, longer empirical courses, and a lower threshold for considering tuberculous or fungal aetiology are appropriate adaptations.

• Antibiotic duration. The Gjika RCT (PMID 30992295) showed 2 weeks non-inferior to 4 weeks after surgical drainage, but the cohort was dominated by hand/wrist joints. How far this extends to large weight-bearing joints, S. aureus bacteraemia, or immunocompromised hosts remains unsettled, and most units still use 3-6 weeks for large-joint or staphylococcal disease.
• Needle aspiration vs surgical washout for native joints. Serial closed aspiration achieves source control in selected accessible joints (notably the knee) in some series, while many surgeons regard urgent arthroscopic or open washout as standard. No RCT settles this; decision rests on joint, organism, loculation and response.
• Arthroscopic vs open drainage. Meta-analytic data (PMID 33939020) favour arthroscopy for knee and shoulder, but the evidence is low-quality and retrospective; the hip is still generally opened.
• DAIR vs early revision in acute PJI. Success of DAIR depends heavily on a short symptom duration, well-fixed implant, susceptible organism and exchange of modular parts. The exact time threshold (often quoted as ~3 weeks) and the role of rifampicin combinations for staphylococci are debated.
• Diagnostic biomarkers. Synovial alpha-defensin, leucocyte esterase and serum/synovial procalcitonin add specificity but are imperfect; none replaces aspiration, culture and clinical judgement. The "WCC over 50,000" threshold is a guide, not an absolute cut-off (sensitivity is well under 100%).
• Crystals plus infection. Demonstrating gout or CPPD does not exclude concurrent sepsis; missed co-existent infection is a recognised pitfall.