Osteomyelitis is an infection of bone. This is a relatively common occurrence in the pediatric age group; the incidence of osteomyelitis in the United States is 1 in 5000 children per year and 1 in 1000 neonates per year.1 Osteomyelitis most often occurs due to hematogenous inoculation of the bone with bacteria. Organisms can also be introduced via a puncture wound or by way of spread from an adjacent structure (e.g., skin or paranasal sinuses). Organisms other than bacteria are occasionally involved, including viruses, fungi, and spirochetes. Classification schemes for osteomyelitis involve the nature of the infecting organism (e.g., pyogenic, fungal, tuberculous, or viral), the mechanism of bone inoculation (e.g., hematogenous or direct implantation), and the chronicity of the infection (i.e., acute, subacute, and chronic osteomyelitis).2–7
Acute bacterial osteomyelitis is the most common type of bone infection in children. This most frequently occurs by way of hematogenous spread from a remote source. The metaphyseal region is the most susceptible osseous site for hematogenous infection, due to the presence of slowly flowing blood within sinusoidal networks that lack active phagocytes. In at least 50% of instances of epiphyseal osteomyelitis, there is a contiguous focus of infection in the metaphysis. Transphyseal spread of infection from the metaphysis to the epiphysis is most common during the first year of life, when cartilaginous channels span the growth plate and serve as conduits for passage of microorganisms between these structures.
The typical pathophysiology of hematogenous osteomyelitis involves the transport of organisms into the bone via the nutrient arteries. The terminal arteriole branches of the nutrient arteries form loops (loop capillaries) along the metaphyseal margin of the growth plate. Blood then passes into the venous sinusoids in the intramedullary portion of the metaphysis. Slow turbulent flow of blood within these venous sinusoids facilitates implantation of the infecting organisms. Bacteria proliferate and cause an exudative process within the intramedullary portion of the involved metaphysis. The resultant edema causes elevation of intraosseous pressure, which thereby diminishes local perfusion. The sinusoids and adjacent arterioles and venules may thrombose, leading to bone necrosis.
The elevated interosseous pressure that occurs as part of a bone infection contributes to the dissemination of organisms through the interstices of endosteal bone. Longitudinal spread occurs through the medullary cavity of the metaphysis and, potentially, into the diaphysis. Lateral extension may result in penetration through the cortex and into the subperiosteal space, where an exudate may form. If penetration occurs through the periosteum, secondary infection of the adjacent deep soft tissue structures occurs. Because cortical penetration most often is at the level of the metaphysis, those joints with capsules that encompass the metaphysis are at greatest risk for secondary septic arthritis; the hip and the shoulder are the most important of these joints.
The physis serves as a barrier to the extension of a metaphyseal infection ...