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Osteomyelitis is an inflammatory condition of bones usually caused by bacterial and more rarely by fungal or mycobacterial infection. Acute hematogenous osteomyelitis (AHO) is the most common form of osteomyelitis in children.1 It results from 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 There is no consensus on the reported duration of symptoms required to establish a diagnosis of chronic osteomyelitis, with definitions ranging from 6 weeks to 6 months. The distinction between acute and chronic osteomyelitis is important as it helps define treatment because 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 condition may present as acute or chronic infection. The primary focus of this chapter will be AHO as it is the form of disease that is seen most commonly in primary care.

The reported incidence of AHO varies widely among regions and ranges from approximately 0.1 per 1000 children younger than 12 years to 8.7 per 1000 children younger than 13 years.5–7 In regions where methicillin-resistant Staphylococcus aureus (MRSA) emerged in the early 2000s, AHO incidence increased, but there is no evidence from population-based studies of changes in the incidence of this disease since then.8,9 Approximately 50–60% of children with AHO are younger than 5 years, and approximately half of those are younger than 2 years.1,5,8 Most studies have documented a male predominance of AHO of approximately 1.5–2 : 1.1,10 In some cases, there is a history of minor or blunt trauma preceding the development of AHO; however, the role of minor trauma in the pathogenesis of AHO is unknown.11


Acute hematogenous osteomyelitis results from the interplay of host and microbial factors.12 The vascular anatomy of bone in infants and children 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. In the metaphysis of the developing bone these arterioles form sharp loops adjacent to the epiphyseal growth plate and empty into venous sinusoids. 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


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