Osteomyelitis

Overview

Osteomyelitis refers to an infection of bone. Staphylococcus aureus is the most common organism although a variety of other bacteria, including mycobacteria, and fungi are possible culprits. Organisms can seed bone either via a hematogenous route, direct extension from a nearby soft-tissue infection, or directly from the environment if bone is exposed to the outside world. Once infected, an acute inflammatory response develops that can precipitate significant bone ischemia. If the acute response does not resolve the infection, a chronic healing response aimed at isolating the infected focus develops. The clinical consequences of osteomyelitis are those of both systemic and local inflammation; however, the signs and symptoms are typically subtle and become more so as the disease evolves into a chronic phase.

Etiology

By far, the most common cause of osteomyelitis is S. aureus. Other gram positive species, such as streptococci and Coagulase-negative staphylococci, are less common. The enterobacteriaceae are possible culprits, especially E. coli and pseudomonas. Fungal bone infections are possible but are relatively rare compared to bacterial etiologies.
In specialized populations certain organisms are more frequent. For example, in those with sickle cell disease who have undergone auto-splenectomy, salmonella is often encountered. Patients with diabetes mellitus or those with bone trauma will often develop polymicrobial infections that may include anaerobes. In developing countries with poor access to health care, mycobacterial osteomyelitis can be encountered.

Pathogenesis and Morphology

Microorganisms can inoculate bone via hematogenous spread or by direct seeding. Once infected, an acute inflammatory phase develops that can result in significant compromise of bone perfusion due to bone's rigid nature and precarious blood supply. Over time, the inflammatory infiltrate evolves into a chronic picture with an attendant healing response aimed at isolating the infected focus.

There are two basic routes by which microorganisms may seed the bone: Direct or Hematogenous inoculation. Direct inoculation may occur as a result of direct extension of an adjacent focus of soft tissue infection or simply by seeding from the external environment following trauma or an orthopedic surgery. In diabetic patients both mechanisms are likely involved as the soft tissues in diabetic extremities can harbor extensive polymicrobial infections while concurrent diabetic ulcers frequently erode to the bone. Predictably, hematogenous seeding is seen in patients harboring bacteremia; however, organisms in the blood may be undetectable and a hematogenous route may be inferred solely by the presence of a distant site bacterial infection. While any bone may become infected, children typically develop osteomyelitis in the metaphyses of their long bones whereas adults do so in the vertebrae. In general, infections from a direct route of inoculation are polymicrobial whereas those due to hematogenous spread consist of a single organism.

Bone destruction at sites of osteomyelitis are both the result of toxins produced by infecting microorganisms as well as the intense neutrophilic inflammation that occurs in response. Inflammation as well as the accompanying edema can result in significantly elevated intramedullary pressures, reducing blood supply, and in turn leading to ischemic necrosis of the involved bone. The pressurized focus of infection can also force its way to the bone cortex and ultimately under the periosteum which can separate from its underlying bone and in doing so compromise the bone's vascular supply, exacerbating ischemia and further contributing to bone ischemic necrosis. Particularly in children where bone and periosteum are loosely adhered, the infection can generate sub-periosteal abscesses or spread along sub-periosteal planes into adjacent joints. In adults, the infection can dissect through the periosteum and generate sinus tracts to the skin.

Over time a chronic inflammatory infiltrate replaces the neutrophilic infiltrate of the acute phase. Pieces of dead necrotic bone, termed "sequestra" can be observed with shells of reactive bone forming around them, termed "involucra", representing a healing response aimed at isolating foci of infection from surrounding healthy bone. An involucrum can harbor viable organisms for years and also tends to render the affected bone structurally weaker, leading to a propensity for fracture. Chronically draining sinus tracts through the skin to the surface of the body are a common feature of chronic osteomyelitis and the tract's epithelium has a tendency to develop skin squamous cell carcinoma.

Clinical Consequences

Acute Osteomyelitis is typically accompanied by both systemic and local signs of acute inflammation. Patients will display constitutional symptoms, especially fever, as well as pain, erythema, and edema at the site of infection. In general, clinical signs and symptoms may be subtle and thus a high clinical suspicion should be entertained in at-risk patients, especially those who have recently undergone orthopedic surgery. In diabetic patients, the capacity to probe to the bone from an ulcer is virtually diagnostic. In some cases, acute osteomyelitis may by associated with adjacent septic arthritis, as the two diseases can cause one another.

As osteomyelitis evolves into its chronic phase, clinical signs and symptoms typically attenuate, rendering diagnosis even more challenging. The presence of a chronically draining sinus tract should raise clinical suspicion and also trigger an evaluation for a possible skin squamous cell carcinoma within the sinus tract epithelium. In some cases, chronic osteomyelitis may come to light only after a pathological fracture in a structurally weakened bone.

Osteomyelitis requires long treatment courses with antibiotics. Antibiotic selection should be guided by direct biopsy and culture of the affected bone.

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