Septic arthritis is characterized by invasion of synovium and synovial fluid by microorganisms, most commonly bacterial. The diagnosis should be considered in the patient who presents with acute monoarthritis, particularly when associated with fever or laboratory signs of acute inflammation.
Septic arthritis is a rheumatologic emergency, associated with significant morbidity and mortality if the diagnosis and appropriate management is delayed. When septic arthritis is considered, prompt arthrocentesis is critical. Empiric treatment, including both antimicrobial management and drainage, is recommended when synovial fluid cell counts exceed 50,000 cells/mm3; however, lower cell counts do not exclude the diagnosis, particularly in the immunocompromised host.
Treatment is multimodal and includes antimicrobial therapy and effective drainage and debridement. Surgical drainage is most commonly employed (arthroscopically or via an open synovectomy) though serial percutaneous drainage may be considered in some circumstances. Antimicrobial therapy directed to the infecting organism for durations of between 2 and 6 weeks is generally advised.
Septic arthritis occurs when microorganisms invade the synovium and replicate within the synovium and synovial fluid. While septic arthritis remains rare (7.8 cases per 100,000 person-years from a recent population-based report from the United Kingdom), the incidence of this devastating infection has been increasing (Rutherford et al, 2016). The rise in incidence of septic arthritis likely relates to an increasing prevalence of underlying risk factors, including an aging population, a greater prevalence of immunocompromising conditions, a rise in injection drug use, and greater use of vascular catheters. Changing virulence of organisms over time (including an increasing prevalence of virulent strains of methicillin-resistant Staphylococcus aureus [MRSA]) may also contribute to the rise in septic arthritis.
Septic arthritis occurs through two primary mechanisms: hematogenous and contiguous spread of organisms. Hematogenous infection is more common, accounting for approximately 75% of cases of septic arthritis. In hematogenous infection, organisms travel to the synovium through the bloodstream. The synovium itself does not have a basement membrane; therefore, when organisms land in synovial capillaries, they are more easily able to seed the joint space. Once within the joint space, bacterial adhesion factors attach to host extracellular matrix proteins; low shear conditions further allow the organisms to take hold. Supported by nutrients within the joint fluid, the bacteria then proliferate and establish infection. Joint damage ensues, mediated by bacterial toxins and enzymes, the host inflammatory response, and tissue ischemia related to tamponade.
Often in hematogenous infection, the bacteremia itself may be transient and unrecognized and only become manifest at the onset of joint pain. In other cases, the bacteremia may be overt, associated with fever or other signs of sepsis. Hematogenous septic arthritis may occur without other comorbid infection, or it may be associated with endocarditis or other nidus of infection. The bacterial portal of entry itself is not always recognized and may be remote from the site of ...