Etiology

Bacteria are the most common pathogens in acute skeletal infections. In osteomyelitis, Staphylococcus aureus (Chapter 174.1) is the most common infecting organism in all age groups, including newborns. Community-acquired methicillin-resistant S. aureus (CA-MRSA) isolates account for >50% of S. aureus isolates recovered from children with osteomyelitis in some reports. The USA300 clone of S. aureus is the most common among CA-MRSA isolates in the USA and is more likely to cause venous thrombosis in children with acute osteomyelitis than other S. aureus clones or other bacteria for reasons that are not known.

Group B streptococcus (Chapter 177) and gram-negative enteric bacilli (Escherichia coli, Chapter 192) are also prominent pathogens in neonates; group A streptococcus (Chapter 176) constitutes <10% of all cases. After 6 yr of age, most cases of osteomyelitis are caused by S. aureus, streptococcus, or Pseudomonas aeruginosa (Chapter 197). Cases of Pseudomonas infection are related almost exclusively to puncture wounds of the foot, with direct inoculation of P. aeruginosa from the foam padding of the shoe into bone or cartilage, which develops as osteochondritis. Salmonella species (Chapter 190) and S. aureus are the two most common causes of osteomyelitis in children with sickle cell anemia. S. pneumoniae (Chapter 175) most commonly causes osteomyelitis in children <24 mo of age or children with sickle cell anemia. Bartonella henselae (Chapter 201.2) can cause osteomyelitis of any bone but especially in pelvic and vertebral bones.

Kingella kingae may be the second most common cause of osteomyelitis in children <5 yr of age in some parts of the world. K. kingae is a slow-growing, gram-negative, β-hemolytic bacterium in pairs or short chains of short bacilli. The organism, once thought to be rare, is increasingly recognized as a cause of osteomyelitis, spondylodiskitis, septic arthritis and bacteremia, and, less commonly, in endocarditis. It has been identified as the causative agent in pneumonia and meningitis. Nearly 90% of identified K. kingae infections have been in young children.

Infection with atypical mycobacteria (Chapter 209), S. aureus, or Pseudomonas can occur after penetrating injuries. Fungal infections usually occur as part of multisystem disseminated disease; Candida (Chapter 226) osteomyelitis sometimes complicates fungemia in neonates with or without indwelling vascular catheters.

A microbial etiology is confirmed in ∼60% of cases of osteomyelitis. Blood cultures are positive in ∼50% of patients. Prior antibiotic therapy and the inhibitory effect of pus on microbial growth might explain the low bacterial yield.

Epidemiology

The median age of children with musculoskeletal infections is ∼6 yr. The incidence of osteomyelitis in children is estimated to be 1 : 5,000. Bone infections are more common in boys than girls; the behavior of boys might predispose them to traumatic events. Except for the increased incidence of skeletal infection in patients with sickle cell disease, there is no predilection for osteomyelitis based on race.

The majority of osteomyelitis cases in previously healthy children are hematogenous. Minor closed trauma is a common preceding event in cases of osteomyelitis, occurring in ∼30% of patients. Infection of bones can follow penetrating injuries or open fractures. Bone infection following orthopedic surgery is uncommon. Impaired host defenses also increase the risk of skeletal infection. Other risk factors are noted in Table 676-1.

Table 676-1 MICROORGANISMS ISOLATED FROM PATIENTS WITH OSTEOMYELITIS AND THEIR CLINICAL ASSOCIATIONS

Modified From Lew DP, Waldvogel FA: Osteomyelitis, Lancet 364:369–379, 2004.

Pathogenesis

The unique anatomy and circulation of the ends of long bones result in the predilection for localization of bloodborne bacteria. In the metaphysis, nutrient arteries branch into nonanastomosing capillaries under the physis, which make a sharp loop before entering venous sinusoids draining into the marrow. Blood flow in this area is thought to be “sluggish,” predisposing to bacterial invasion. Once a bacterial focus is established, phagocytes migrate to the site and produce an inflammatory exudate (metaphyseal abscess). The generation of proteolytic enzymes, toxic oxygen radicals, and cytokines results in decreased oxygen tension, decreased pH, osteolysis, and tissue destruction. As the inflammatory exudate progresses, pressure increases spread through the porous metaphyseal space via the haversian system and Volkmann canals into the subperiosteal space. Purulence beneath the periosteum may lift the periosteal membrane of the bony surface, further impairing blood supply to the cortex and metaphysis.

In newborns and young infants, transphyseal blood vessels connect the metaphysis and epiphysis, so it is common for pus from the metaphysis to enter the joint space. This extension through the physis has the potential to result in abnormal growth and bone or joint deformity. During the latter part of the 1st year of life, the physis forms, obliterating the transphyseal blood vessels. Joint involvement, once the physis forms, can occur in joints where the metaphysis is intra-articular (hip, ankle, shoulder, and elbow), and subperiosteal pus ruptures into the joint space.

In later childhood, the periosteum becomes more adherent, favoring pus to decompress through the periosteum. Once the growth plate closes in late adolescence, hematogenous osteomyelitis more often begins in the diaphysis and can spread to the entire intramedullary canal.

Clinical Manifestations

The earliest signs and symptoms of osteomyelitis, often subtle and nonspecific, are generally highly dependent on the age of the patient. Neonates might exhibit pseudoparalysis or pain with movement of the affected extremity (e.g., diaper changes). Half of neonates do not have fever and might not appear ill. Older infants and children are more likely to have fever, pain, and localizing signs such as edema, erythema, and warmth. With involvement of the lower extremities, limp or refusal to walk is seen in approximately half of patients.

Focal tenderness over a long bone can be an important finding. Local swelling and redness with osteomyelitis can mean that the infection has spread out of the metaphysis into the subperiosteal space, representing a secondary soft-tissue inflammatory response. Pelvic osteomyelitis can manifest with subtle findings such as hip, thigh, or abdominal pain. Back pain with or without tenderness to palpation overlying the vertebral processes is noted in vertebral osteomyelitis.

Long bones are principally involved in osteomyelitis (Table 676-2); the femur and tibia are equally affected and together constitute almost half of all cases. The bones of the upper extremities account for one fourth of all cases. Flat bones are less commonly affected.

Table 676-2 SITES OF OSTEOMYELITIS IN CHILDREN

Modified from Gafur OA, Copley LA, Hollmig ST, et al: The impact of the current epidemiology of pediatric musculoskeletal infection on evaluation and treatment guidelines, J Pediatr Orthop 28(7):777–785, 2008.