Osteomyelitis is an inflammatory condition of bones usually caused by bacterial, or more rarely, fungal infection. Acute hematogenous osteomyelitis (AHO) is the most common form of osteomyelitis in children.1 It occurs as a result of hematogenous deposition of bacteria within bone following symptomatic or asymptomatic bacteremia. The time from onset of symptoms to diagnosis is usually rapid, within 14 days, although certain sites of infection (particularly vertebral and calcaneal) may have a more insidious course and present subacutely.2 Chronic osteomyelitis presents with either chronic, persistent, low-grade symptoms or an exacerbation of symptoms after a period of relative disease quiescence.3 The reported duration of symptoms required to establish a diagnosis of chronic osteomyelitis is quite varied, ranging from 6 weeks to 6 months. The distinction between acute and chronic osteomyelitis is important as it helps define the necessary treatment modalities given that a longer duration of symptoms before treatment may allow for the development of necrotic bone and soft tissues. Nonhematogenous osteomyelitis occurs with direct contamination of bone from trauma, surgery, or spread of infection from an adjacent soft tissue infection.4 This may present as acute or chronic infection. The primary focus of this chapter will be AHO as it is the form of disease that will be seen most commonly in primary care.
The reported incidence of AHO has ranged from 0.1 per 1000 children younger than 12 years to 8.7 per 1000 children younger than 13 years.5–7 In regions where community-associated methicillin resistant Staphylococcus aureus (CA-MRSA) is common, the incidence may be increasing but there are no population-based studies.8 Approximately 50–60% of children with AHO are younger than 5 years with approximately half of those being younger than 2 years.1,5–10 Most studies have documented a male predominance of AHO of approximately 1.5–2:1.1,6,7,9–11
AHO results from the interplay of host and microbial factors.12 The vascular anatomy of bone in infants and children uniquely presdisposes to bacterial infection in the metaphyseal region of long bones or the “metaphyseal-equivalent” portions of irregular or flat bones (e.g., apophyseal growth plates, such as the tibial tubercle, or greater trochanter).13 Bacteria enter the bone through the nutrient artery and travel to the metaphyseal arterioles. These arterioles form sharp loops adjacent to the epiphyseal growth plate and empty into venous sinusoids in the metaphysis of long bones and metaphyseal-equivalent areas. Sluggish blood flow through these sinusoids and endothelial gaps in the tips of growing metaphyseal vessels are thought to predispose to bacterial deposition in these sites.14
Once infection is initiated, pus spreads through vascular canals leading to vascular compression and compromise, ischemia, and bone necrosis. Perforation of the cortex of bone results in periosteal elevation and subperiosteal abscess.12 Capillaries that cross the physis, present in children younger than 18 months, allow spread of metaphyseal infection into the epiphysis...