Monoarthritis

Septic Arthritis

The assessment of a patient with acute monoarthritis is focused on excluding a septic arthritis. Septic arthritis can cause rapid joint destruction, morbidity and mortality.

Pathogenesis and pathology

Non-gonococcal bacterial arthritis occurs when bacteria enter the synovial lining of a joint via the haematogenous route, local spread from nearby soft-tissue infections or following penetrating trauma or injury to a joint. Bacteria reach the synovium, cause swelling and destruction of articular cartilage, which may extend to subchondral bone, and produce irreversible damage within days. The commonest causative organisms are staphylococci and streptococci.

Epidemiology and risk factors

The prevalence of septic arthritis ranges between 4 and 10 per 100,000 patients per year and appears to be rising. It is also almost seven times more common in Indigenous Australians.

Risk factors for septic arthritis include inflammatory arthritis (especially rheumatoid arthritis), diabetes mellitus and systemic factors, such as age greater than 80 years, as well as local factors, such as recent joint surgery, joint prosthesis and overlying skin infection. These individual risk factors increase the risk of septic arthritis by two- to threefold. Skin infection overlying a prosthetic joint increases the risk of infection by 15-fold. Immunosuppressants heighten susceptibility to septic arthritis. The risk of septic arthritis depends on the potency of immunosuppression that is used.

Clinical features

Septic arthritis presents with joint pain and swelling in more than 80% of cases, which may be associated with systemic symptoms, such as sweats and rigors. The hip and knee joints are the most commonly involved joints.

The patient may be febrile and the affected joint is usually swollen, warm, erythematous and tender. Classically there is reduced ability to actively move the joint and marked pain on passive movement. Unfortunately, the symptoms and signs are not sensitive, and a patient with septic arthritis may present with only some of these features. Thus septic arthritis cannot be excluded with confidence on the history and examination alone, and so must be considered in any presentation of monoarthrtis.

Differential diagnosis

The differential diagnosis of acute monoarthritis is shown in Table 14.2.1 . Risk factors include a history of rheumatoid arthritis, connective tissue disease, gout or other inflammatory arthritis, as well as risk factors for infection, such as immunosuppression (which patients may neglect to mention), diabetes and corticosteroids. Recent trauma or history of a bleeding diathesis or anticoagulation are also relevant. Recent sexually transmitted infections, including gonococcal infection or non-specific urethritis, or any systemic features including uveitis and/or gastrointestinal infection, may point toward a reactive arthritis.

Clinical investigations

Imaging

X-ray may be normal in septic arthritis, as it takes at least 1 week for destructive changes to appear on plain x-ray. Magnetic Resonance Imaging (MRI) is helpful to determine if the pathology is in the joint or juxta-articular bone.

Criteria for diagnosis of septic arthritis

There is no ‘gold standard’ test for the diagnosis of septic arthritis. Synovial fluid Gram stain has a sensitivity of up to 50% only, while culture has a sensitivity up to 85%. Combined with an appropriate clinical presentation, the presence of microorganisms in synovial fluid on Gram stain and/or a positive synovial fluid culture with high synovial white cell count are diagnostic. New molecular techniques for diagnosis of infection in synovial fluid are promising but not yet readily available (e.g. 16S rRNA polymerase chain reaction [PCR]).

Treatment

Treatment of septic arthritis requires an urgent referral to orthopaedics for surgical drainage with admission to hospital. Antibiotic use should follow local guidelines and be discussed with the orthopaedic and infectious disease units. Empirical antibiotic therapy pending microbiology results should cover against Staphylococcus ; administer dicloxacillin or flucloxacillin 2 g IV 6 hourly or cephazolin 2 g IV 6 hourly if the patient is allergic to penicillin. The patient with suspected hip or prosthetic joint sepsis must be referred to orthopaedics urgently without attempting joint aspiration.

Gout

Gout is an intra-articular inflammatory response to monosodium urate crystal deposition usually related to hyperuricaemia. It is more common in males than females, but is extremely rare in the premenopausal female.

Aetiology and pathogenesis

Uric acid is derived from purine metabolism. Hyperuricaemia is the strongest predictor for gout and relates to either overproduction or under excretion of uric acid. Hyperuricaemia may also cause radiolucent renal calculi.

Overproduction of uric acid is due to dietary factors or endogenous factors associated with high cell turnover, such as a haematological malignancy. Reduced excretion is related to chronic kidney disease, hypovolaemia, metabolic acidosis and medications, such as diuretics, cyclosporin, pyrazinamide and ethambutol. There is also frequently a family history of gout.