DEFINITION

Septic arthritis is infection, usually bacterial, in the joint cavity. Since septic arthritis can lead to rapid joint destruction, immediate accurate diagnosis is essential. The joint cavity is normally sterile, with synovial fluid and cellular matter, including a few white blood cells. The majority of patients with bacterial septic arthritis will present with acute monoarthritis.

PREVALENCE

The incidence of septic arthritis has been estimated at 2 to 10 cases per 100,000 in the general population and as high as 30 to 70 cases per 100,000 in patients with rheumatoid arthritis.^1,2 The most common mode of spread is hematogenous, with predisposing factors including intravenous drug use, presence of indwelling catheters, and underlying immunocompromised states. Other potential predisposing conditions include preexisting arthritis such as rheumatoid arthritis, gout, or osteoarthritis. The knee is the most commonly involved joint, accounting for about 50% of the cases.³

PATHOPHYSIOLOGY

The most common route of spread is hematogenous; other routes include trauma or inoculation, as during steroid injections. On entering the joint space, the bacteria initially deposit in the synovial membrane and produce an inflammatory reaction, usually with polymorphonuclear and synovial cells, which readily migrate into the synovial fluid. Synovial membrane hyperplasia develops in 5 to 7 days, and the release of cytokines leads to hydrolysis of proteoglycans and collagen, cartilage destruction, and eventually bone loss.⁴ Direct pressure necrosis due to large synovial effusion results in further cartilage damage. Antigen-specific and polyclonal B-cell activation are seen in Staphylococcus aureus experimental arthritis.

The presence of the cna gene in S. aureus causes a higher incidence of septic arthritis in mouse experiments. This suggests that the cna gene product, a collagen adhesion factor, plays an important role in the development of septic arthritis.⁵

Most septic arthritides are monomicrobial infections, but polymicrobial infections may be seen in patients with direct inoculation of the joint space. The most common bacterial isolates in native joints include gram-positive cocci, with S. aureus found in 40% to 50% of the cases. Other isolates include Neisseria gonorrhoeae, streptococci, and gram-negative cocci, each in about 10% to 20% of cases. Other organisms less commonly isolated include mycobacteria and fungi.^3,6 Gram-negative bacilli are often present in neonates, the elderly, and patients with immune deficiency disorders. N. gonorrhoeae is seen in sexually active young adults, usually with associated dermatitis and tenosynovitis. Mycobacterial infections should be suspected in patients from endemic areas, and fungal arthritides are seen in immunocompromised patients. Haemophilus influenzae was a common cause of bacterial arthritis in young children, but the incidence has decreased almost 70% to 80% since the widespread use of H. influenzae b vaccine.⁷

SIGNS AND SYMPTOMS

Patients with septic arthritis usually present with a single swollen joint with pain on active or passive movement. The knee is involved in about 50% of the cases, but wrists, ankles, and hips are also commonly affected. Septic arthritis manifests as polyarticular arthritis in about 10% to 19% of patients and is more common in patients with prior joint damage, as in rheumatoid arthritis, gout, and systemic connective tissue disorders.⁸

Pertinent history in any patient with suspected septic arthritis includes joint disease, immunosuppressive states, intravenous drug use, recent steroid injection, history of sexually transmitted disease, and any constitutional symptoms. Physical examination should include a careful assessment of the pattern of joint involvement and inflammation of the eyes, skin, or mucosa and other sites of potential infection. Figure 1 gives a suggested algorithm for the workup of a single inflamed joint.

Figure 1 Algorithm for evaluating a hot, swollen joint.

CT, computed tomography.

(Adapted from Ruddy S, Harris ED Jr, Sledge CB (eds): Kelley’s Textbook of Rheumatology, 6th ed. Philadelphia, WB Saunders, 2001, p 1472.)

A classic presentation for septic arthritis is a febrile patient who has rigors, an increased leukocyte count, and elevated sedimentation rate. However, none of these is highly sensitive or specific for septic arthritis. In one series, only 40% to 60% of patients with septic arthritis were febrile, only 25% to 60% had an elevated leukocyte count, and only 60% to 80% had a sedimentation rate greater than 50 mm/hr.^4,9

DIAGNOSIS

Synovial fluid analysis is of paramount importance in diagnosing and managing septic arthritis. It should include Gram stain, culture, leukocyte count with differential, and crystal examination under a polarized microscope. Controversy exists as to whether synovial fluid culture yield is increased by the inoculation of blood culture bottles at the bedside as compared with using conventional agar plate culture in the laboratory. A study has shown no difference in the rate of isolation of bacteria by either of these methods.¹⁰

A synovial fluid leukocyte count of greater than 50,000 with a polymorphonuclear leukocyte predominance is usually seen in septic arthritis. This can, however, also be seen in crystal arthropathies, which can complicate the clinical picture. A history of gout in the same joint or the presence of crystals in the synovial fluid can indicate an episode of gout or pseudogout rather than septic arthritis.

Gram stain is positive in 11% to 80% of cases, but an occasional false positive is seen due to precipitated mucin in the synovial fluid. Synovial fluid culture is positive in up to 90% of nongonococcal bacterial arthritides.⁴

Synovial fluid glucose, protein, and lactic acid concentration are not well standardized and hence are not useful in the diagnosis of septic arthritis. Synovial polymerase chain reaction (PCR) has been used to diagnose Yersinia species, Chlamydia species, Ureaplasma urealyticum, N. gonorrhoeae, and Borrelia burgdorferi.⁴ It may be useful in the diagnosis of a fastidious organism and assist in the diagnosis of partially treated cases. Counterimmunoelectrophoresis has not been well studied in diagnosing synovial fluid infection and is not used for diagnosis of septic arthritis.

DIFFERENTIAL DIAGNOSIS

IMAGING

Radiography should be the first imaging modality used for septic arthritis. The inflamed synovial tissue and accompanying fluid in the joint cause a symmetrical soft-tissue swelling around the involved joint, as manifested by a widened joint space or displacement of the fat pads around the joint. Marginal erosions or erosion of bone that sits uncovered by cartilage but within the capsular attachment can also be seen. The hallmark of septic arthritis is the loss of the white cortical line over a long contiguous segment, unlike the segmental disruption seen in inflammatory arthropathies. Bacterial infection of a joint usually causes rapid joint space loss, with aggressive erosive changes and preservation of mineralization. The tuberculous septic joint tends to preserve the joint and causes marginal erosions with extensive demineralization and little repair.¹²

Bone scintigraphy may be used if radiographs are normal. A three-phase scan using Tc 99m methylene diphosphonate shows increased uptake in the synovium of the septic joint and, in the third phase, increased uptake in the articular ends of the bone. Gallium-67 citrate can be used in conjunction for additional information. However, it still may be difficult to distinguish an inflamed joint from an infected joint.

Magnetic resonance imaging (MRI) is highly sensitive for the diagnosis of septic arthritis, although it still lacks specificity because it cannot reliably distinguish inflamed from infected joints. MRI has been considered the diagnostic modality of choice by some clinicians.¹²