Natural history of pediatric hematogenous osteomyelitis of the tibial metaphysis. (a) The infection begins in the metaphysis, forming an intraosseous abscess that (b) decompresses through the thin metaphyseal cortex to become a subperiosteal abscess. (c) The abscess elevates the periosteum, stripping the blood supply to the bone. (d) One or more areas of the bone become necrotic (sequestrae). The host periosteal response of new bone formation, involucrum, stabilizes the mechanical environment, partially or completely resorbs sequestrae, and reconstitutes bone loss
In hematogenous osteomyelitis, organisms typically lodge in the metaphyseal region because of sluggish blood flow in venous sinusoids adjacent to the physis. The organisms proliferate, and intramedullary pressure increases due to the host inflammatory response. The infected material breaks through the thin metaphyseal cortex, resulting in a subperiosteal abscess. This subperiosteal abscess can expand, elevate the periosteum, and deprive the cortical bone of its blood supply, resulting in bone necrosis and the development of a sequestrum or sequestrae (Fig. 29.2). The entire shaft may become sequestered. Sequestrae are less common in adults than in infants and children. The communication between the medullary canal and a subperiosteal abscess is called a “cloaca.” Eventually, the abscess can break through the skin, forming a sinus tract. The host response, as seen in the periosteum, is an attempt to reestablish stability by new bone formation—the involucrum (Fig. 29.3). The involucrum is typically less robust in adults than it is in children. Where the metaphysis is intracapsular (proximal femur, proximal radius, proximal humerus, distal fibula), there is a risk of coexisting septic arthritis. Organisms have a number of mechanisms to evade the hosts defenses, and antibiotics, such as forming a glycocalyx, slowing their metabolism, and migrating to an intracellular location. In some severe cases of infection the organisms essentially hijacks the host’s inflammatory response in order to form abscesses and to disseminate through the vascular system. The evolution from an acute to a chronic disease state depends on access to treatment and whether the treatment has been successful. With early diagnosis and treatment most cases of osteomyelitis can be eradicated.
Fig. 29.2
(a–d) Examples of sequestrae and involucra. (a, d) The involucra of the tibia and metatarsals are partial, weak, and poorly demarcated from the indistinct sequestrae. (b, c) The involucra are complete and robust around the well-demarcated sequestrae in the ulnar shaft and the proximal femur
Fig. 29.3
The involucrum varies considerably in appearance. It may appear as a (a, b) smooth periosteal density as seen here in the midshaft of the humerus and both sides of the tibia. (c, d) As a smooth and sclerotic reaction from the addition of multiple layers of new bone in this patient with clavicular osteomyelitis and a draining sinus over the medial clavicle. (d) A fluffy appearance to the new bone formation as seen on both sides of the tibia, and (e) as a thickened, densely sclerotic reaction
Subacute Osteomyelitis
Subacute osteomyelitis presents with intermittent bone pain, usually at night, which is often exacerbated by activity and with few or no systemic signs or symptoms. The symptoms of local discomfort to palpation or mild soft tissue swelling are often present for at least 2 weeks before the patient arrives in the clinic or OPD. This is due to the combination of an indolent organism and strong host defenses. Laboratory studies are usually normal, although inflammatory markers can be slightly elevated. Staphylococcal species are most often cultured.
The radiographic features vary from a well-circumscribed lytic metaphyseal lesion with a sclerotic rim (Brodie’s abscess) that can cross the physis, to a diaphyseal lesion with an aggressive periosteal reaction. The differential diagnosis includes benign or malignant bone tumors and tuberculous osteomyelitis. A biopsy is often required to establish the diagnosis. Empiric antibiotics can be considered when characteristic x-ray features are present, such as a sclerotic rim to the lucency, a lucency that crosses physis, has a serpentine shape or multiple cavities, is epiphyseal, and is not associated with changes in the surrounding bone, and the patient has no systemic symptoms.
Chronic Osteomyelitis
The evolution from acute osteomyelitis to chronic osteomyelitis is highlighted in previous sections outlining the development of sequestrae, and the host’s reaction in the form of involucra. This chronic disease state involves a persistence of dead bone and/or debris which has been incompletely resorbed and essentially represents a “standoff” between the immune system and the infectious focus or foci. Patients with chronic osteomyelitis present with a history of intermittent bone pain extending over months to years, localized tenderness, and usually a draining sinus. Foci of dead bone and/or devitalized tissue harbor microorganisms, causing intermittent episodes of infection. Some patients may have exposed bone. Other findings at presentation can include pathological fracture, limb length discrepancy, or angular deformity. Plain radiographs are sufficient for evaluation. Laboratory tests are usually normal unless active infection is present. Since neoplasia can mimic chronic infection (Fig. 29.4), a biopsy should be obtained in selected cases. The treatment involves removal of all infected material (similar to tumor surgery), followed by reconstruction of any bone loss and correction of any other sequelae such as angular deformity. Antibiotics are an adjunct (see Chap. 31).
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