Chapter 200. Osteomyelitis and Septic Arthritis

Osteomyelitis

1. How does bone become infected?

2. What tests and aspects of the history and physical exam are most helpful in diagnosis?

3. What treatment options should be considered?

4. How can response to treatment be monitored?

Septic Arthritis

1. What are the components of an evaluation for possible acute bacterial (septic) arthritis?

2. When should empiric antibiotics be used to treat suspected septic arthritis, and which antibiotics?

3. What are the key elements to treatment of septic arthritis?

Osteomyelitis is bone infection with accompanying inflammation and bone destruction. Bone resists infection under normal circumstances. Factors that influence the establishment and progression of osteomyelitis include the virulence of the pathogen, inoculum size, characteristics of the involved bone, presence of foreign objects, host immune system, and duration of infection. Bone may be infected by direct contamination during trauma or surgery, spread of infection from adjacent soft tissue, or hematogenous seeding of microbes. The diagnostic and therapeutic approach varies depending on the mode of infection. However, as treatment for osteomyelitis is long, complex, expensive, and not always successful even when management is optimal, proper diagnosis and pathogen identification is of great importance in all cases.

Bacteria infect bone through trauma or surgery, spread from adjacent soft tissue, or bacteremic seeding. They then attach to host cells and extracellular matrix components, as well as implanted biomaterials, if present. Bacterial strategies to evade the host immune response include elaboration of biofilm, a hydrated matrix that establishes a physical barrier against both host defenses and antibiotics. Bacteria embedded in biofilm are also less metabolically active, making them less susceptible to antibiotics. Inflammation associated with bacterial toxins and the host immune response leads to bone lysis. Over time, as infection becomes chronic, suppuration leads to vascular congestion, raised intraosseous pressure, and ischemia of infected bone. The necrotic bone separates from healthy bone to form a sequestrum, a diagnostic finding of chronic osteomyelitis. If the dead bone cannot be resorbed, new bone may form from the surrounding healthy bone tissue, encasing the sequestrum in an involucrum. The walled-off sequestrum may become functionally similar to an abscess, with bacterial growth continuing in a pocket of necrotic tissue inaccessible to immune surveillance or antibiotics. As pressure in the sequestrum builds, infection may erupt through the involucrum, leading to subperiosteal or soft tissue abscesses, or a sinus tract through overlying soft tissue.