Etiology, Pathophysiology, and Clinical Presentation: Osteomyelitis may occur from direct or hematogenous inoculation; it may be iatrogenic, related to orthopedic implants; or it may be from secondary extension from primary septic arthritis or pyomyositis. Hematogenous osteomyelitis is preponderantly a disease of children; however, infantile and even neonatal cases are not uncommon. Bacteria are the most common inflammatory agents, but growing bones may also be invaded by other pathogens, including viruses, spirochetes, and fungi.

The incidence of pediatric osteomyelitis in the United States is 1 in 5150 and has increased 2.8-fold in 20 years.¹ This increased incidence is confounded, however, because of differences in access to health care and advances in imaging diagnosis. Staphylococcus aureus remains the most common causative organism of acute osteomyelitis in children. Unfortunately, community-acquired methicillin-resistant S. aureus (MRSA) strains are increasing in prevalence.² Haemophilus influenzae osteomyelitis and septic arthritis have become less common since the availability of effective vaccination (H. influenzae type B vaccine).³

In sickle cell disease, bone complications include osteonecrosis and osteomyelitis. Osteonecrosis is approximately 50 times more frequent than osteomyelitis.⁴ The proposed mechanism of osteomyelitis is hematogenous, with bacteria gaining entrance to blood vessels through ischemic bowel and finding suitable culture material in foci of infarcted bone marrow. Both S. aureus and Salmonella commonly occur in sickle cell patients.²

In chronic granulomatous disease of childhood, an X-linked recessive disorder of leukocyte function, repeated infections occur in solid organs, skin, and bone. Approximately one third of patients develop osteomyelitis. Phagocytes are unable to kill catalase-positive organisms such as Staphylococcus and Aspergillus.⁵

Hematogenous osteomyelitis usually involves the highly vascularized metaphysis of the fastest growing bones, such as the distal femur and radius and the proximal tibia and humerus. The most common location for hematogenous osteomyelitis is about the knee (distal femur, proximal tibia).² Pain, localized signs, fever, reduced range of motion, and reduced weightbearing are the most common initial clinical features. A history of trauma is seen in approximately 30% of cases,² and the male-to-female ratio is approximately 1.8 : 1.

Organisms lodge most frequently in the terminal capillary sinusoids of the metaphyses.⁶ Rarely, they may locate initially in the epiphyses related to the terminal capillary sinusoids of the metaphyseal equivalent region immediately next to the spherical growth plate (Fig. 138-1). A small abscess forms in the marrow of the metaphysis, followed by local decalcification and destruction of the adjacent bone. When focal abscesses are generated, multiple small foci of bone destruction develop and later coalesce. Inflammatory swelling increases the intraosseous pressure because of the rigid bony walls of the marrow cavity; this can force extension of the infected exudate into several sites, as indicated in Figure 138-2. The most common route is via the haversian canals of the cortex to the subperiosteal space, where a subperiosteal abscess is formed. Simultaneously, spread also occurs farther within the medullary cavity. Rupture of the periosteal abscess is responsible for extension of infection into the adjacent soft tissues. Inflammation and rapidly increased intraosseous pressure may cause thrombosis of the vascular channels.

The most common location for direct inoculation osteomyelitis is the foot. Plantar puncture wounds secondary to walking on broken glass, metal (nail), or vegetable matter (thorn, toothpick) may result in infectious cellulitis, plantar fasciitis, and osteomyelitis, whether the foreign body is removed or retained. The calcaneus is often involved, and Pseudomonas aeruginosa is often found related to direct inoculation, usually with a history of a puncture through a shoe.⁵

Imaging: Imaging guidelines for the evaluation of suspected osteomyelitis include radiographs first to exclude alternative etiologies, such as a fracture or neoplasm, as an explanation for symptoms. If radiographs are normal, ultrasound (US) is recommended if the symptoms are localized to an osteoarticular region. If US is negative, scintigraphy is the next study of choice, if symptoms are nonlocalizable.⁷ If symptoms can be localized, targeted magnetic resonance imaging (MRI) of the affected region should be performed both for diagnostic purposes and for planning surgical treatment.^8,9

Radiography: With acute osteomyelitis, the earliest change on radiographs is soft tissue swelling; osseous changes are seldom present until the second week of disease (Fig. 138-3).¹⁰ The earliest bone changes seen on conventional images are one or more small radiolucencies, usually in the metaphyseal region, where necrosis and destruction of bone has occurred (Fig. 138-4). On serial examinations, these areas of bone destruction enlarge and become confluent.

With continuing appropriate antibiotic therapy, periostitis is visible when the periosteum begins to produce new bone on its undersurface after the second or third week (Fig. 138-5). Osteogenic function by the periosteum suggests that infection has been at least partly locally controlled. Subsequent healing may involve remodeling of the cortical new bone and reconstitution of the underlying bone or, if damage has been extensive, it may involve an increase in the amount of periosteal reaction to form an involucrum (Fig. 138-6), a living bone sheath around the fragments of the old devitalized bone (sequestrum).

Scintigraphy: Early bone scans may demonstrate a “cold” metaphyseal lesion as a result of compression or occlusion of the metaphyseal vessels. In these cases, increased activity is observed toward the diaphysis, beyond the cold metaphyseal area, which subsequently becomes “hot” and merges with the adjacent increased activity. The multiphase bone scan is very sensitive and is usually positive 24 to 48 hours after the onset of symptoms.⁷ It can detect extension of metaphyseal osteomyelitis into the epiphysis through the growth plate (Fig. 138-7).

In the early detection of acute bone infection, radionuclide imaging is more sensitive than radiographs and can identify additional foci of disease not clinically apparent. Vascular phase images done within the first 5 minutes following injection, delayed images with pinhole collimators, and special attention to the affected area have proven of great value. Osteomyelitis appears as an area of increased tracer activity that reflects the hyperemia and bone turnover induced by the infectious process. In a study of 100 children with acute limb pain, the sensitivity and specificity of three-phase bone scans for acute osteomyelitis were 84% and 97%, respectively.¹¹ Errors arise from simulation of infection by fracture or sickle cell disease, obscuration of osteomyelitis by septic arthritis, prior antibiotic treatment, and “cold” defects that result from ischemia. It is difficult to detect infection close to the growth plate, because both the growing physis and the nearby area of infection show increased activity.

Computed Tomography: Computed tomography (CT) is of limited clinical value in acute osteomyelitis.¹² It is more useful in advanced or chronic disease to help determine the quality of bone stock, including determinations of cortical destruction, involucrum, and sequestra (see Fig. 138-6).

Magnetic Resonance Imaging: MRI is the optimal study to evaluate for infection and alternative etiologies for symptoms, particularly when radiographs are normal. MRI can identify early bone changes, and it delineates the anatomy and extent of marrow involvement; for this reason, it has become an important tool for imaging of suspected osseous infection. However, MRI does carry additional cost, and depending on the availability of scanner time and the need for sedation or anesthesia, delays in definitive diagnosis and treatment are possible. Imaging should aim at guiding or modifying treatment if necessary.

When precontrast MRI exams are entirely normal and show no evidence to suggest osteomyelitis, routine post-gadolinium images may not be necessary.13,14 When abnormal, MRI can reveal marrow alterations and extent of disease in bone, soft tissues, or adjacent joints (Fig. 138-8).¹⁵ Early MRI findings of osteomyelitis may have a tumefactive appearance and may be paradoxically hypointense on fluid-sensitive sequences (e-Fig. 138-9). Over time, the lesion may remain masslike and demonstrates the expected, more homogeneous hyperintense signal on fluid-sensitive sequences, indicative of its inflammatory nature (Fig. 138-10). Eventually, periostitis and adjacent soft tissue involvement may be seen in the early phase of osteomyelitis (e-Fig. 138-11). Subperiosteal abscess formation may be seen by sonography (Fig. 138-12) or MRI (Fig. 138-13), preceding radiographic bony changes. A salt-and-pepper appearance to the marrow may be seen in the late acute phase of osteomyelitis and is presumed to represent small areas of noncoalescent microabscess formation and early bone destruction (Fig. 138-14).

Treatment: Although the mortality and morbidity of bone infection have decreased significantly, permanent sequelae do occur, largely as a result of delay in diagnosis or inadequate treatment with complications related to generalized bacterial sepsis.²⁴ Complications of bone infection include pathologic fracture through regions of bone destruction,²⁵ venous thrombosis,²⁶ and adjacent infectious arthritis and destruction of joints (Fig. 138-18).

Identification of a bacterial pathogen for underlying osteomyelitis ranges from 9% to 22% by blood culture and 40% to 50% by bone or joint aspiration.²⁴