Etiology

Isolation of a bacterial source of osteomyelitis occurs in 50% to 80% of patients when both blood and bone are cultured. The bacteria responsible for osteomyelitis in children vary by age and underlying condition (see Figure 88-1). Staphylococcus aureus is the most common pathogen in any age group (70%-90% of cases), with community-acquired methicillin-resistant S. aureus (CA-MRSA) becoming more prevalent in recent years. In infants younger than 2 months of age, group B streptococci and gram-negative enteric bacteria are seen in addition to S. aureus. In children younger than 5 years of age, S. aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and Kingella kingae are leading causes of osteomyelitis. Children older than 5 years of age are most commonly infected by S. aureus or S. pyogenes. Neisseria gonorrhoeae may be the etiologic agent in sexually active adolescents.

Approximately 10% of cases of acute hematogenous osteomyelitis are caused by S. pyogenes, a pathogen that tends to cause higher fever and white blood cell (WBC) count than S. aureus. An upper respiratory tract infection often precedes osteomyelitis with K. kingae, and this organism has been associated with outbreaks at daycare centers. Joint involvement is more common with S. pneumoniae than with S. aureus and S. pyogenes, perhaps because children with osteomyelitis caused by S. pneumoniae tend to be younger.

After introduction of the Haemophilus influenzae type b (Hib) conjugate vaccine, the frequency of osteomyelitis caused by this organism has significantly decreased. Actinomyces spp. have been isolated in facial and cervical osteomyelitis. Mixed flora, including Pseudomonas spp., S. aureus, and anaerobes, are seen in osteomyelitis that occurs after a puncture wound to the foot through sneakers. Salmonella spp. are an important cause of osteomyelitis in patients with sickle cell disease. Mycobacterium tuberculosis causes skeletal lesions in 1% of children with tuberculosis, typically manifested by lower thoracic vertebral osteomyelitis (Pott’s disease).

Pathogenesis

The pathogenesis of acute hematogenous osteomyelitis is dictated by the anatomy of growing bone in young children. The rich vascular supply of the metaphysis and its sluggish flow allow deposition of bacteria that enter via the nutrient artery (Figure 88-2). An absence of macrophages in the metaphyseal capillary loops allows bacterial replication, inducing an inflammatory response that may lead to abscess formation, infarction of bone, and necrosis. Acute hematogenous osteomyelitis is preceded by minor trauma to the site of infection in one-third of cases; resultant small hematomas may make the underlying metaphysis more favorable for bacterial deposition.

Figure 88-2 Pathogenesis of hematogenous osteomyelitis.

Transphyseal vessels in children younger than 18 months of age can lead to spread of the infection from the metaphysis into the epiphysis and joint space, causing a secondary septic arthritis. The growth plate, after it has formed, serves as a barrier to extension of infection into the epiphysis and joint. The hip or shoulder joint can be involved at any age because the metaphyses of the proximal humeri and femurs are located within their respective joints.

Clinical Presentation

Patients with acute hematogenous osteomyelitis describe localized bone pain that worsens over a brief period of time; the majority of these patients present to medical attention within 2 weeks of symptom onset. Pain precludes use of an affected extremity (pseudoparalysis). Fever is often present. Less common associated signs include malaise, anorexia, and vomiting. On physical examination of a patient with acute hematogenous osteomyelitis, swelling, erythema, warmth, and point tenderness that is out of proportion to the soft tissue findings may be present over the affected bone.

Ten percent of hematogenous osteomyelitis is categorized as subacute based on a slower progression of mild to moderate pain over the site of infection and the absence of systemic symptoms. Chronic osteomyelitis is characterized by waxing and waning pain and swelling that does not respond to prolonged antibiotics.

The clinical presentation of pelvic osteomyelitis includes pain in the hip, buttock, groin, lower back, or abdomen; gait abnormality; and, in some cases, fever. There is point tenderness over the affected bone and pain with manipulation of the hip. Distinguishing pelvic osteomyelitis and septic arthritis of the hip can be difficult, although range of motion of the hip joint is typically preserved in pelvic osteomyelitis.

Vertebral osteomyelitis can present with back, abdominal, chest, or leg pain; low grade–fever; and tenderness over the affected vertebrae. Fewer than 25% of patients demonstrate neurologic abnormalities. Symptoms can be subtle and slowly progressive, making diagnosis difficult. Vertebral osteomyelitis can be similar in presentation to diskitis but tends to affect older children and adolescents.

Chronic recurrent multifocal osteomyelitis is a distinct autoinflammatory disorder that is characterized by episodes of pain, swelling, and low-grade fever that recur over several years, radiographic findings of multiple lesions that have the appearance of osteomyelitis, an inability to isolate an infectious etiology, and a lack of clinical response to antimicrobial therapy. Girls are more commonly affected than boys, with symptom onset around 10 years of age.

Diagnosis

The diagnosis of osteomyelitis is made by a high index of clinical suspicion in the setting of confirmatory laboratory and imaging studies. Blood and bone cultures should be obtained before initiation of antibiotic therapy, if possible. If a joint is involved, synovial fluid cultures may aid in the microbiologic diagnosis. The peripheral white blood cell count and platelets may be normal or elevated. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are elevated in the majority of cases. The CRP typically peaks 48 hours after treatment initiation and returns to normal in 1 week. The ESR typically peaks 3 to 5 days after treatment initiation and may take 3 weeks to return to normal.

Plain radiographs show soft tissue swelling within 3 days of symptom onset; osteolytic lesions and periosteal elevation are apparent after 10 to 20 days; and after 1 month of symptoms, sclerosis of bone can be seen. Technetium-99 bone scanning has a sensitivity of 80% to 100% for osteomyelitis and can be helpful early on when plain films are normal and can identify multiple sites of infection, when present. Because the radionuclide bone scan can be falsely negative in 5% to 20% of children in the first few days of illness, magnetic resonance imaging (MRI) may be performed. MRI has a sensitivity of 92% to 100% for osteomyelitis and is effective in distinguishing soft tissue infection (e.g., cellulitis) from osteomyelitis. Pelvic and vertebral osteomyelitis are best imaged by MRI. Additionally, chronic osteomyelitis may have a different appearance from acute osteomyelitis on MRI (Figure 88-3).

Figure 88-3 Magnetic resonance imaging findings in early and late acute osteomyelitis.