ETIOLOGY OF EXOGENOUS OSTEOMYELITIS

Exogenous (nonhematogenous) osteomyelitis results from the direct contamination of the bone by the infecting organism. The skin, subcutaneous tissue, and periosteum provide a protective barrier to contaminants; and as long as the skin and periosteum remain intact, the bone cannot be contaminated directly. These barriers can be violated by trauma (e.g., bullet wound, open fracture, direct blow) or by surgery, or they can be stripped away during displacement of fracture fragments (see Plate 8-5). When the protective skin is penetrated and the bone exposed, bacteria may invade the area, creating a focus of infection. Bone may also be contaminated during total joint replacement, application of traction-fixation devices, and implantation of fracture fixation devices. Even when careful surgical dissection is combined with thorough debridement and prophylactic administration of antibiotics, infection occurs in about 1% of major surgical interventions.

During the implantation of artificial joints and fixation devices, the blood supply is often stripped from the bone, creating areas of dead bone. The dead bone acts as a sequestrum, allowing a bacterial infection to persist. Osteomyelitis may become chronic, persisting until the necrotic sequestrum is completely removed and the foreign body, whether a fracture fixation device or total joint prosthesis, is removed.

Certain soft tissue infections may spread to adjacent bones (see Plate 8-6). For example, large soft tissue abscesses may erode the periosteum to infect the underlying bone. An infection of the pulp of the fingertip, called a felon, frequently extends to and infects the distal phalanx, to which the fibrous septa of the pulp of the finger are firmly attached. Retropharyngeal abscesses tend to involve the cervical vertebrae, and periapical infections of the tooth frequently spread to the adjacent mandible or maxilla. Infection in the paranasal sinuses may extend to the adjacent bones of the skull.