Septic Arthritis: Diagnosis and Management

Introduction

Septic arthritis is infection within a joint space, almost always bacterial. It is an orthopaedic emergency because purulent synovial fluid, together with the host inflammatory response it provokes, destroys articular cartilage rapidly - a joint can be irreversibly damaged within days of infection taking hold.¹ Delay in diagnosis is the single biggest determinant of a poor outcome, which is why the condition is examined so heavily.

It is typically monoarticular: a single joint becomes hot, swollen and exquisitely painful, most often the knee in adults, followed by the hip, shoulder, ankle and wrist. Polyarticular involvement is less common but should be considered in rheumatoid arthritis, in the immunosuppressed, and in disseminated gonococcal infection, where a migratory pattern is characteristic.

The exam mantra is worth learning as written: a hot, swollen, acutely tender joint with a restricted range of movement is septic arthritis until proven otherwise. The clinical task is not to be clever about ruling it out, but to aspirate promptly and treat empirically while awaiting confirmation.

Pathophysiology

Bacteria reach a joint by one of three routes.

Haematogenous spread

This is by far the commonest route in adults. Transient or sustained bacteraemia - from skin, respiratory, dental or urinary sources, or from an intravascular line - seeds the synovium, which is richly vascular and lacks a limiting basement membrane. A joint already damaged by disease, particularly rheumatoid arthritis, is far more susceptible to this seeding, and the inflamed synovium of an RA joint can also mask the usual signs of infection.²

Direct inoculation

Bacteria are introduced straight into the joint by penetrating trauma, an intra-articular corticosteroid injection, arthroscopy or other joint surgery. Risk rises with the number of injections a joint has had and with any breach of aseptic technique.

Contiguous spread

Infection tracks in from an adjacent focus - osteomyelitis or an overlying soft tissue or skin infection. This is especially relevant in young children, where the metaphysis of certain bones (notably the proximal femur) lies within the joint capsule, so metaphyseal osteomyelitis can rupture directly into the hip.

Once bacteria are established, the process that destroys the joint is driven as much by the host response as by the organism itself. Neutrophils flooding the synovial fluid release proteolytic enzymes and cytokines that break down cartilage matrix, while rising intra-articular pressure compromises the blood supply to synovium and cartilage. This combination can produce irreversible chondral loss within 24-48 hours of untreated infection, which is the basis for treating this as a time-critical emergency.

Risk factors

• Pre-existing joint disease, especially rheumatoid arthritis - both more susceptible to seeding and more likely to have symptoms masked by the underlying disease
• Prosthetic joints
• Diabetes mellitus
• Immunosuppression, including long-term corticosteroids and biologic agents such as anti-TNF therapy
• Intravenous drug use
• Increasing age
• Chronic renal or liver disease
• Recent joint surgery or intra-articular injection
• Overlying skin or soft tissue infection

Causative organisms

Staphylococcus aureus is the commonest cause of septic arthritis overall in adults, including MRSA in those with relevant risk factors. Streptococcal species, including group A and group B strep, are the next most frequent. The likely organism shifts predictably with age, sexual history and immune status, which is worth knowing both for the exam and for choosing empirical antibiotics.

Clinical features

The onset is typically acute, over hours to a couple of days. The affected joint is hot, red, swollen and exquisitely painful, and the patient instinctively holds it in the position that maximises capsular volume and minimises pressure - for example slightly flexed at the knee or hip. Both active and passive range of movement are severely and globally restricted; this is an important discriminator from bursitis or cellulitis overlying a joint, where movement of the joint itself is relatively preserved even though the surrounding tissue is inflamed.

• Rapid onset of a hot, swollen, erythematous joint
• Severe pain at rest, worsened further by any attempt at movement
• Joint held in a fixed, flexed position of comfort
• Global restriction of active and passive range of movement
• A joint effusion, often tense
• Fever and systemic upset - rigors, tachycardia, malaise
• Signs of the primary source in haematogenous spread, e.g. a skin lesion, or a recent injection or procedure

Presentation can be considerably more subtle in the elderly, in the immunosuppressed and in those on long-term corticosteroids, where fever may be low-grade or absent and the joint less dramatically inflamed. A high index of suspicion is needed in these groups precisely because the textbook picture is blunted.

Septic arthritis in children

In a limping or non-weight-bearing child, the key differential is between septic arthritis and transient synovitis, a self-limiting reactive synovitis that is far more common but does not require treatment. Kocher's clinical prediction algorithm uses four variables to estimate the probability of septic arthritis of the hip.³

Differential diagnosis

• Gout and pseudogout (crystal arthropathy) - can mimic septic arthritis closely and can coexist with it, so a positive crystal result on aspiration does not exclude infection and does not stop you sending for culture
• Reactive arthritis - typically follows a gastrointestinal or genitourinary infection by 1-4 weeks, and may include conjunctivitis and urethritis⁹
• Haemarthrosis - trauma, anticoagulation or a bleeding diathesis; the fluid is bloodstained on aspiration
• Acute flare of an inflammatory arthritis, e.g. rheumatoid arthritis - often more insidious and may be polyarticular, but can be very difficult to distinguish from superimposed infection⁵
• Transient synovitis in children - the key differential in the limping child, distinguished using the Kocher criteria and, where uncertain, aspiration
• Cellulitis or bursitis overlying a joint - the skin or bursa is inflamed but the joint itself typically retains a reasonable range of movement
• Osteomyelitis of the adjacent bone, which may coexist with or mimic septic arthritis, particularly in children

Investigations

Synovial fluid should be sent for Gram stain, microscopy and culture with sensitivities, and for crystal analysis under polarised light to look for gout or pseudogout. Turbid or frankly purulent fluid with a very high white cell count (typically well over 50,000/mm3, predominantly neutrophils) is strongly suggestive of infection, but a normal-looking aspirate does not exclude it, especially if antibiotics have already been given.

• FBC - raised white cell count, though this can be normal, particularly in the immunosuppressed
• CRP and ESR - both are usually elevated and useful for tracking response to treatment, but are non-specific
• Blood cultures - positive in a significant proportion of cases and should always be taken before antibiotics
• Plain X-ray - often normal in early disease; useful as a baseline, to look for a pre-existing joint abnormality, prosthesis, or joint space narrowing, and to help identify a contiguous osteomyelitis
• Ultrasound - useful to confirm and guide aspiration of a deep joint that is difficult to access clinically, particularly the hip
• MRI - the investigation of choice when adjacent osteomyelitis is suspected, as it detects bone marrow oedema and abscess formation with high sensitivity

No single blood test or imaging result confirms or excludes septic arthritis on its own. The diagnosis rests on clinical suspicion combined with synovial fluid analysis, and the decision to treat empirically should never wait for every result to return.

Management

Suspected septic arthritis warrants urgent orthopaedic referral and same-day joint aspiration. Empirical intravenous antibiotics are started as soon as the aspirate has been obtained (or immediately, with cultures sent, if the patient is too unwell to wait), chosen according to local microbiology policy.¹

• A first-line agent active against Staphylococcus aureus is used, commonly flucloxacillin⁷
• Vancomycin or teicoplanin is substituted or added where MRSA is a risk
• A penicillin allergy prompts a switch to, for example, clindamycin or a macrolide, per local policy
• Suspected gonococcal or Gram-negative infection is covered with a third-generation cephalosporin such as ceftriaxone pending culture results
• Antibiotics are rationalised once culture and sensitivity results are available, narrowing the spectrum wherever possible

Treatment typically continues for several weeks in total (commonly around 4-6 weeks, though duration is guided by clinical response and specialist advice), with a switch from intravenous to oral therapy once the patient is clinically improving, inflammatory markers are falling, and cultures allow a targeted, well-absorbed oral agent to be chosen.

Surgical washout - arthroscopic or open lavage and debridement of the joint - is required for confirmed septic arthritis, particularly of the hip (which is difficult to decompress adequately by aspiration alone) or a prosthetic joint. Washout may need to be repeated if the joint does not settle clinically or the inflammatory response fails to improve. The joint is rested acutely, with early, graded mobilisation and physiotherapy introduced once the infection is controlled, to limit stiffness and preserve function.

Complications

• Irreversible joint destruction, leading to secondary osteoarthritis and chronic pain or stiffness
• Osteomyelitis of the adjacent bone
• Sepsis and death, particularly if diagnosis and treatment are delayed
• Growth plate damage in children, especially with hip involvement, which can cause limb length discrepancy or deformity
• Loss of function requiring long-term rehabilitation, or joint replacement where cartilage destruction is severe

Red flags