The classic presentation of AHO is a child with current or recent fever and progressive limp or extremity pain; however, focal bone tenderness (especially metaphyseal) may be the only finding at presentation. The ability to clinically discriminate the location of pain is diminished in nonverbal and young children. The presence of overlying warmth, redness, and swelling is variable, but range of motion is typically spared unless the adjacent joint is infected also. Most cases involve a single bone; however, multifocal bone disease with increased virulence has been noted in recent years, as have cases involving the adjacent joint and muscle.21,22 However, symmetric bone or primary diaphyseal disease is quite rare with AHO and should alert the clinician to noninfectious processes.
Most children with AHO will have a normal white blood count, about a third to half will have a positive BC and almost all have elevated inflammatory markers in the CA-MRSA era.21,22 Plain films of the involved bone are usually normal (80%) at presentation, but subtle signs of periosteal elevation of surrounding edema may exist.23
AHO may coincide with other musculoskeletal infections (especially myositis, and septic arthritis), but may present similarly to them as well. Children also may have a truly unrelated injury or bone disease (i.e., fracture, avascular necrosis) and a separate infection (viral or bacterial) that will confuse matters. Rheumatologic processes that may mimic AHO include oligoarticular juvenile idiopathic arthritis, rheumatic fever, chronic recurrent multifocal osteomyelitis, and the early stages of Hennoch–Schoenlein Purpura. Bone pain from ischemia in children with hemoglobinopathies can be very difficult to distinguish from AHO.
Guidelines developed by the Infectious Disease Society of America in collaboration with the American Academy of Pediatrics and Pediatric Infectious Disease Society provide recommendations for the management of pediatric bone and joint infections.24
Occasionally a child with AHO will present acutely ill with sepsis, but typically a child will be stable enough to allow clinicians to use a progressive evaluation and management strategy. Given the prolonged nature of antibiotic treatment required for AHO (typically 4–6 weeks for long bones), a focus on maximizing a microbiologic diagnosis has led to recommendations that a brief delay in antibiotics is reasonable while obtaining appropriate blood and tissue cultures and histology in stable children.
The preliminary evaluation of a child with possible AHO in the ED includes obtaining a CBC, ESR, CRP, and one or more BCs. Although typically normal in AHO, plain films of the involved bone (or entire extremity in younger children unable to localize pain) are recommended to rule out noninfectious causes or to confirm a subacute or chronic osteomyelitis. Early consultation of an orthopedic surgeon is helpful, especially in cases where joints may be involved and require aspiration or open drainage, or if a delay in beginning antibiotics cannot be justified secondary to clinical condition.
Increasingly, the confirmation of AHO is made by obtaining an MRI, which has very high sensitivity and specificity for the diagnosis.18,23,24 If the area of involvement is uncertain (e.g., a febrile toddler who will not walk), a bone scan may be helpful in localizing disease.23
In acutely ill or septic, appearing children, broad-spectrum parenteral antibiotics designed to cover the most common pathogens based on age and risk factors should begin as soon as BCs are obtained. Commonly, the administration of antibiotics can be delayed pending urgent obtaining of tissue cultures when feasible. Recent studies in younger children suggesting similar rates of osteoarticular infections caused by K. kingae as with S. aureus have led some experts to recommend adding a third generation cephalosporin to anti-staphylococcal coverage in this population. Antibiotics selected should be informed by local patterns of resistance, particularly when considering rates of MRSA versus MSSA, and clindamycin resistance among all S. aureus strains. Typically, vancomycin, clindamycin, or an anti-staphylococcal penicillin (nafcillin or oxacillin) is given. A third-generation cephalosporin may be added to cover gram-negative organisms in high risk patients (i.e., children with hemoglobinopathies or very young children are at risk for Kingella).
True recurrences of AHO are rare in children and likely are due instead to relapse (chronic osteomyelitis) within the same bone, or unrecognized (and often undrained) multifocal osteomyelitis.
Aside from new antibiotics, advances in management of AHO include a promising diagnostic tool for children with culture-negative osteomyelitis: polymerase chain reaction testing for species-specific ribosomal genes (16s rDNA) 3, 4, 18.25 In addition, progress toward a S. aureus vaccine continues, as more is understood about conserved antigens and normal host response to the bacterium.26
Although earlier literature hypothesized a traumatic or inflammatory etiology for discitis, most current opinion points to the cause as a low-grade infective spondylitis along the spectrum of vertebral osteomyelitis. Due to the mild presentation of clinical symptoms, there are likely many underdiagnosed cases. Case series reveal a peak in toddlers and early to mid-adolescence.27–30
Biopsy is not necessary to confirm the diagnosis and BCs are often negative. As such, most case series report no single pathogen as the primary cause. However, in studies where biopsies are performed, S.aureus is the predominant pathogenic organism found followed by K. kingae31. The likelihood of an identifying pathogen increases in patients with concomitant vertebral osteomyelitis. Several studies have proposed that the rich and anastomotic blood supply to the vertebral end plates of the young child allow them to limit the infection to the disc without allowing progression to the bone. This is further supported by the increased rate of bone destruction and osteomyelitis seen in adults.