Septic Arthritis

Septic arthritis is a bacterial infection of a joint and a true orthopaedic emergency. Bacterial toxins and the host's own inflammatory mediators act together to destroy articular cartilage rapidly, and understanding how they do it is what makes the urgency of treatment obvious.

The clock. Glycosaminoglycan loss begins within hours of bacterial invasion; collagen loss, the irreversible step, comes later. Surgical drainage is required within 24 hours to prevent permanent joint damage.

Haematogenous spread. The most common route, 80% of cases, and the usual one in native joints. A transient bacteraemia seeds the synovium, which is highly vascular and has no basement membrane, so bacteria penetrate easily into the joint space. Intravenous drug use, immunosuppression and diabetes are risk factors.

Direct inoculation. The cause is iatrogenic (joint injection, arthroscopy, arthroplasty) or traumatic (penetrating injury, open fracture). The initial bacterial load is typically lower, and symptoms may be delayed.

Contiguous spread. Infection spreads from adjacent osteomyelitis or soft tissue infection, osteomyelitis especially in children. The hip, shoulder and elbow have an intra-articular metaphysis, so metaphyseal infection ruptures into the joint, and neonatal osteomyelitis commonly causes septic arthritis. In adults, vertebral osteomyelitis can seed the disc.

View larger

View larger

The host response. The host paradoxically contributes to the destruction. Infiltrating neutrophils release proteolytic enzymes, elastase, cathepsin G, collagenase and matrix metalloproteinases, that degrade the cartilage matrix, and a cytokine cascade of IL-1 and TNF-alpha drives continued inflammation. Bacterial toxins damage chondrocytes directly.

Pressure. Synovial inflammation raises intra-articular pressure, which compromises cartilage nutrition.

Biofilm. Bacteria can form biofilms on cartilage and synovial surfaces. The glycocalyx matrix protects them from antibiotics and host immune cells, and quorum sensing lets them communicate and coordinate toxin production. Persistent infection develops if a biofilm establishes on damaged cartilage.

The sequence. In the experimental model proteoglycan is lost first and collagen weeks later.

View larger

What drainage does. Washing out the joint removes the bacterial load and the proteolytic enzymes, reduces intra-articular pressure, prevents a biofilm establishing on the cartilage, and lets the surgeon see and debride the joint directly.

Why antibiotics alone fail. Antibiotics cannot penetrate an established biofilm, do not remove the enzymes already released, and cannot reduce the mechanical effect of raised pressure. The delay while they are given alone allows irreversible cartilage damage.

Staphylococcus aureus is the most common organism, causing 50-70% of septic arthritis overall and 60-70% of adult cases. Streptococcal species account for 15-20%. Gram-negative organisms (E. coli, Pseudomonas) are more common in the elderly and immunocompromised. Mycobacterial infection has an atypical presentation and a chronic course.

The organism follows the patient's age and risk factors.

Four predictors, and the probability of septic arthritis rises with each one present. The probabilities below, including 99.6% with all four, are from the original derivation cohort.

1. A history of fever, conventionally over 38.5°C (101.3°F). A measured temperature did not survive Kocher's multivariate model. Fever may be absent in the immunocompromised, low-grade fever is less predictive, and documented fever is the most reliable.
2. Non-weight bearing, refusal to bear weight on the affected limb. It is the most specific clinical sign but is also present in transient synovitis, and inability to bear weight is worse than a limp.
3. ESR of at least 40 mm/hr; exactly 40 counts. ESR is less specific than CRP and slower to rise and normalise, and a CRP over 20 mg/L is an alternative cut-off.
4. Serum WCC over 12,000 per microlitre. It may be normal in early infection and is less reliable than the synovial fluid WCC.

Septic arthritis is described by its route (above), the joint, the host, the pathogen (see Microbiology) and, at arthroscopy, the Gächter stage.

Native or prosthetic joint. Native joints have higher cure rates with appropriate treatment. Prosthetic joint infection is more complex and often requires removal of the implant.

The host. Immunocompetent patients have a better prognosis and are treated to standard protocols. The immunocompromised get atypical organisms and need prolonged treatment, and intravenous drug users present in unusual joints (see below).

Child or adult. In children the hip is more often involved, progression is rapid and there is a risk of avascular necrosis. In adults the knee is most common and the cartilage tolerates infection better.

Gächter stage. The arthroscopic appearance guides treatment. Stages I-II respond well to arthroscopic lavage; stages III-IV often require open surgery and carry a worse prognosis because of the cartilage damage.

The aspirate is the most important test. A synovial WCC over 50,000/μL is highly suggestive, and one over 25,000/μL is already suspicious. The Gram stain is immediate, but culture may take 48-72 hours.

Blood tests. The serum WCC is often raised but may be normal in the immunocompromised. CRP is raised and is useful for monitoring response; ESR is raised too but slower to change. Blood cultures are positive in 30-50% and are always taken if the patient is febrile.

Special investigations include:

• PCR for fastidious organisms (Kingella, mycobacteria)
• Procalcitonin, with higher sensitivity and specificity than CRP
• Lactate, raised in septic compared with inflammatory arthritis

Plain radiographs are the first-line image. Acutely they show joint space widening from the effusion, soft tissue swelling and loss of the fat planes, and they exclude a fracture or foreign body; chronic infection brings joint space narrowing and erosions. A radiograph cannot rule out sepsis.

Ultrasound detects an effusion, including the hip effusion in a child, guides aspiration and differentiates effusion from synovitis. It is operator-dependent and cannot distinguish septic from aseptic fluid.

View larger

Septic arthritis is usually monoarticular. Roughly 10-20% is polyarticular, involving two or more joints, and that is the presentation most likely to kill the patient.

Why it kills. Polyarticular sepsis reflects overwhelming bacteraemia, so mortality is much higher: quoted around 30-50% in some series, against roughly 10% for monoarticular disease.

The host and the organism. It is almost always haematogenous and usually S. aureus, sometimes streptococci, pneumococcus or gonococcus. It is strongly associated with pre-existing joint disease, rheumatoid arthritis being the classic host, and with immunosuppression (diabetes, steroids, malignancy).

Find the source. Two or more septic joints means blood-borne seeding, so hunt for the focus of the bacteraemia, and treat every affected joint as well as the systemic source.

• Infective endocarditis above all: echocardiography, repeated blood cultures, a new murmur, peripheral stigmata
• Skin
• Intravascular lines
• Urinary tract
• Spine

Sepsis of the sternoclavicular, sacroiliac, symphysis pubis and spinal joints is characteristic of intravenous 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 drug users. These joints get missed because they are deep, hard to examine and aspirate, and present insidiously.

Keep a high index of suspicion in these patients and use cross-sectional imaging early. The sternoclavicular joint's capacity for retrosternal and mediastinal spread is what raises the threshold from a simple washout toward joint resection.

Arthroscopic lavage is preferred for most joints. Through the standard portals for the joint, inspect it and document the state of the cartilage, irrigate copiously with a minimum of 9-12 litres of saline, debride fibrinous debris and synovitis, and take multiple tissue samples for culture.

The knee. Use the standard anteromedial and anterolateral portals, lavage every compartment including the suprapatellar pouch, and debride loculations and fibrinous adhesions. A posterolateral portal may be needed for complete access. Consider a synovial drain postoperatively.

Open arthrotomy is required for the hip and for some arthroscopic failures: a complete capsulotomy for drainage, copious irrigation and debridement, and closure in layers. Leaving a drain is controversial; most surgeons avoid one because of the risk of retrograde infection.

Small joints. Serial daily aspirations may be adequate for fingers and toes, but they must show a falling WCC and sterile cultures. Convert to surgical drainage if the joint is not improving.

When to go back. Repeat surgery is indicated by:

• Persistent fever beyond 48-72 hours after drainage
• A rising or plateaued CRP
• Ongoing joint swelling, effusion or erythema
• New positive cultures

Cartilage destruction. Enzymatic degradation by bacterial toxins and host proteases destroys the cartilage; once established it is irreversible and leads to arthritis. Early diagnosis and aggressive treatment are the prevention.

Systemic. Sepsis and septic shock occur in 5-10%, with multi-organ dysfunction, and metastatic infection can reach other joints or cause endocarditis.

By joint. In the child's hip the risk is avascular necrosis of the femoral head; in the knee, stiffness and secondary osteoarthritis; in the shoulder, rotator cuff damage and stiffness.

Antibiotics. Continue IV antibiotics for a minimum of 2 weeks and switch to oral when the patient is clinically improving and the CRP is falling, with culture-directed therapy once sensitivities are available. The total course is 2-6 weeks, depending on the joint and the response:

• Small joints (fingers, toes): 2 weeks
• Large joints (knee, elbow): 4 weeks
• Hip and spine: 6 weeks minimum
• Prosthetic joints: 12 weeks (DAIR) or staged revision

Monitoring. Assess the patient daily (pain, swelling, range of motion) and chart the temperature. Check the CRP every 2-3 days at first, then weekly; it should fall by 50% at 2 weeks. A CRP that fails to fall suggests inadequate drainage, a resistant organism or the wrong diagnosis, so consider repeat imaging and aspiration.

Rehabilitation. Start gentle passive range of motion as soon as it is tolerated, protect weight-bearing until the infection is controlled, and progress to strengthening once it has resolved. Full weight-bearing follows when the joint is pain-free and the infection controlled, sport and heavy activity 3-6 months after resolution, with long-term follow-up for secondary arthritis.

Native joints. With appropriate treatment the cure rate is 85-95%, and with early aggressive treatment 50-60% make a full recovery. Mortality in adults is 5-15%, higher in the elderly and those with comorbidities, and 10-20% need a joint replacement in the long term.

Prosthetic joints. Two-stage revision succeeds in 85-95%. Amputation is needed in 1-3%, after failed treatment or with comorbidities.

The paediatric hip. The risk of avascular necrosis is higher with delay. Coxa magna is a common sequela, and 30-40% develop arthritis in the long term.

What predicts the result. Delayed treatment beyond 24 hours significantly worsens outcomes, and each 24-hour delay increases the risk of cartilage destruction and a poor functional outcome.

Global Epidemiology

Native-joint septic arthritis affects approximately 4-10 per 100,000 person-years in high-income populations, rising to 30-70 per 100,000 in those with rheumatoid arthritis or a prosthetic joint. Incidence is increasing worldwide, driven by an ageing population, more joint replacement surgery, immunosuppression, diabetes and injecting drug use. Staphylococcus aureus is the leading pathogen globally, but the proportion of MRSA varies markedly by region (low in much of Scandinavia and the Netherlands, substantially higher in parts of the USA and Asia), which directly affects empirical antibiotic choice. In sexually active young adults, Neisseria gonorrhoeae remains an important cause where prevalence is high. Reported mortality is 7-15% and long-term joint dysfunction occurs in roughly a third of survivors despite treatment.

Side-by-Side Guidance