ETIOLOGY AND PREVALENCE OF HEMATOGENOUS OSTEOMYELITIS

In contrast to direct contamination of the bone from exogenous sources, hematogenous osteomyelitis results when the bone is seeded with bacteria from a distant site of infection in the body (see Plate 8-2). Common sources of infection are the throat, teeth, skin, urinary tract, gastrointestinal tract, and lungs. Infection in these locations can produce showers of bacteria in the bloodstream (bacteremia). Although the reticuloendothelial system clears most of these bacteria from the bloodstream, occasionally a few settle in the bone, creating a focus of infection. The areas of bone particularly vulnerable to hematogenous infection are the metaphyses of the long bones—especially the humerus, femur, and tibia. The organisms that cause hematogenous osteomyelitis are the same as those responsible for the primary infection; the most common pathogen is Staphylococcus aureus. Gram-negative infections are commonly the results of seeding from a primary infection in the urinary tract, usually secondary to medical instrumentation or catheterization.

Hematogenous osteomyelitis is usually seen in children but may develop in adults (particularly those who are immunocompromised); a second, fairly high peak in occurrence is seen in persons between 50 and 70 years of age.

PATHOGENESIS OF HEMATOGENOUS OSTEOMYELITIS

Hematogenous osteomyelitis is particularly common in growing children for several reasons. Children are especially susceptible to bacterial infections in general and, therefore, are likely to have frequent primary infectious foci and frequent episodes of bacteremia, which can lead to osteomyelitis. In addition, the peculiar anatomy of the growth plate may also play a substantial role in the development of hematogenous osteomyelitis in this age group. Virtually all cases of hematogenous osteomyelitis in children seem to originate in the metaphyseal bone, just beneath the growth plate. In this region, the terminal branches of the metaphyseal arteries form loops and enter afferent venous sinusoids, which are large and irregular (see Plate 8-3). The size of the vessels increases markedly from the metaphyseal artery to the venous sinusoids, and blood flow slows and becomes turbulent. The abrupt change in the dynamics of blood flow may allow bacteria to sludge and accumulate in this region, creating a focus of infection. Also, the cells in and around the venous sinusoids have little or no phagocytic activity, thus creating an ideal environment for bacterial growth.

After the bone is seeded with bacteria from the bloodstream, rapid bacterial duplication creates a localized abscess just beneath the growth plate. The developing abscess extends along the Volkmann canals to the subperiosteal region, where it elevates the thick periosteum. Elevation of the periosteum eventually stimulates the formation of new bone. Further extension of the abscess may cause it to rupture through the periosteum and extend to the subcutaneous tissue and then through the skin, creating a draining sinus. The infection may extend subperiosteally along the shaft of the bone; this extension strips a portion of the shaft of its blood supply and produces a dense, avascular piece of cortical bone called a sequestrum. The sequestrum, lacking a blood supply to deliver antibiotics or inflammatory cells to fight infection, acts as a nidus for the infection to persist.