Subacute osteomyelitis develops if the host response or incomplete antibiotic therapy partially suppresses the infection or if the pathogen is indolent. Presentation is more insidious, with symptoms present for 2 weeks or longer [6]. Instead of the exuberant inflammatory process often encountered in acute osteomyelitis, the infection is more localized, usually confined to the metaphysis, and shows little periosteal thickening. The lower extremity is almost invariably involved, with over 90 % of lesions in the femur or tibia. Over 60 % are metaphyseal, and most occur at the distal tibia. Subacute osteomyelitis may occur in the epiphysis. Most common in adolescents and males, subacute osteomyelitis has not been described in patients younger than 6 years of age.

Subacute osteomyelitis may manifest as a Brodie abscess, which develops in the cortex or medulla and is usually eccentric. It usually drains to the physis and may extend to the epiphysis. Eburnated bone along with fibrous and granulation tissue encloses a central area of osseous necrosis. Staphylococcus is the usual pathogen [7].

Chronic osteomyelitis has been present for at least 6 weeks and is more common in developing nations. Periosteal thickening has typically progressed, thickened, and ossified, forming an involucrum (from the Latin, involvere, envelop) that isolates the more central infection. Meanwhile, increasing pressure causes cortical bone infarction and necrosis, forming a sequestrum, which may then serve as a nidus of infection. The central infection may break through the cortex or penetrate to the physis, forming a (from the Latin, cloaca, sewer), which then permits the inflammatory debris to drain to the skin via a sinus tract [7]. Formation of an involucrum and sequestrum is unusual if antibiotics are administered at an early stage.

Erythrocyte sedimentation rate and white blood cell count can be normal and also nonspecific. Blood cultures are positive in up to 60 % of cases, whereas cultures of aspirated material yield an organism in as many as 85 % [7].

Brodie abscess, characteristic of subacute osteomyelitis, is composed of a central lucent focus in the metaphysis surrounded by sclerosis and accompanied by a tortuous channel that may drain to the physis (Figs. 19.6, 19.7, 19.8, and 19.9); identification of this channel confirms the diagnosis of subacute osteomyelitis [7]. Single or laminated periosteal new bone formation is typical, with little surrounding inflammation [6]. Epiphyseal subacute osteomyelitis usually appears as a lytic, cystic, intra-epiphyseal lesion.

Chronic osteomyelitis manifests with thick periosteum and cortex, forming the involucrum that encases the sclerotic sequestrum (Figs. 19.10 and 19.11). The prominent cortical thickening is termed “Garré sclerosing osteomyelitis.”

A triple-phase bone scan should be performed. Osteomyelitis has increased uptake in all three phases (Fig. 19.13). However, the delayed images are most definitive, and excluding unusual locations such as the pelvis (see Fig. 19.18 below) normal delayed images usually exclude the diagnosis of osteomyelitis. Pinhole images are helpful. Single photo emission computed tomography (SPECT) improves spatial resolution but can be difficult to perform in children [13].

Bone scans may not show disease that abuts the physis, and ischemia or a weak inflammatory response can result in a false-negative examination. Increased pressure or marrow ischemia can lead to decreased blood flow resulting in “cold” osteomyelitis and necrosis due to vascular thrombosis; both are more common with MRSA and might not be recognized at bone scan [14]. Findings of infection, tumor, and trauma can overlap. Gallium improves specificity to 80 % [6] and may delineate soft tissue abscesses, but it is less desirable than MRI, in part due to high radiation dose.

Because scintigraphy cannot delineate abscesses, it is generally less useful in the spine and pelvis, where abscesses are especially common (again, gallium may be employed). In the spine, delineation of intraspinous abscesses and possible cord compression is essential. Abscesses are less often associated with osteomyelitis of the long bones. Scintigraphy may be sufficient in these cases, provided that if there is a poor response to antibiotic therapy, then MRI is performed [10].

Spatial resolution has improved with fludeoxyglucose photon emission tomography (FDG-PET) and SPECT, allowing better differentiation of osteomyelitis from septic arthritis and cellulitis; specificity of combined SPECT/CT exceeds 80 % [11, 15]. If complementary white blood cell scanning is performed, then sensitivity and specificity exceed 90 %, as the white blood cell (WBC) scan is positive in marrow that is cold on SPECT because the normal marrow has been replaced with an infectious process. However, the application of WBC scintigraphy to pediatric imaging is limited, as it usually requires at least 15 mL of blood [13]. PET/CT may be useful in follow-up of acute osteomyelitis, as it can differentiate between reparative activity and acute infection [16]. It may also allow identification of a focus of active infection within chronic osteomyelitis.

The protocol includes T1, T2 with fat suppression, and short-tau inversion recovery (STIR) in orthogonal planes. Obtaining both pre- and postcontrast T1-weighted (T1-W) images facilitates correct interpretation of findings, but administration of gadolinium is somewhat controversial. Diffusion-weighted imaging is useful, increasing conspicuity.

Marrow signal alters 1–2 days after onset of symptoms. However, signal changes are more subtle in children than in adults due to the higher water content in their bone marrow, and fluid-sensitive sequences can be misleading as both normal and abnormal marrow can be hyperintense. T1-W sequences better delineate marrow morphology [12], and a wide zone of transition is usually apparent. Edema, inflammatory cells, and exudate appear as ill-defined low T1 signal and as high-intensity signal on fluid-sensitive sequences (T2 and STIR) (Figs. 19.3, 19.4, 19.5, and 19.6). MRI may overestimate the extent of bony involvement, as reactive inflammation has a similar appearance [4]. Cortical bone may lose its normal low signal, and high T2 signal may be seen around the cortex, due to layering periosteal fluid. Epiphyseal and physeal involvement is readily seen on sagittal and coronal scans. If subperiosteal abscesses form, high T2/low T1 lentiform fluid collections are evident. Cortical thickening is not present in acute infection [7].

There has been considerable debate about whether gadolinium should be administered to assess osteomyelitis; many authors conclude that gadolinium is unnecessary if T1- and T2-weighted (T2-W) sequences are normal. However, if edema is present, the addition of contrast helps delineate epiphyseal involvement and also the presence of intraosseous, subperiosteal, and soft tissue abscesses. This both improves diagnostic confidence and affects management, as the presence of abscesses mandates surgical drainage [21, 22]. Devascularized bone due to septic thrombosis of nutrient channels also fails to enhance but does not demonstrate the typical rim enhancement of an abscess. Distribution of antibiotics mirrors that of gadolinium, with important implications for treatment [21]. MRI is especially useful in Staphylococcus aureus osteomyelitis, which tends to be more severe and is accompanied with a higher incidence of soft tissue complications [14].

Fat globules, larger than lipocytes, are seen in 70 % of cases of acute osteomyelitis, perhaps due to coalescence of lipid from lipocytes that have undergone necrosis. However, this is not pathognomonic for osteomyelitis, as fat globules can also be seen in sarcomas after treatment, in infarcts, and in Gaucher disease [23]. An extraosseous fat-fluid level may be pathognomonic for osteomyelitis [24]. Extraosseous fat is more common during and after puberty [25].

Although follow-up MRI is generally not necessary, it is useful in patients whose C-reactive protein does not fall within 14 days or in those with an otherwise worsening clinical course who may require repeat surgical drainage [26].

Subacute osteomyelitis bears some resemblance to tumor, having a more geographic appearance than does acute osteomyelitis at T1-W imaging. Several MRI characteristics help differentiate subacute osteomyelitis: the presence of multiple distinct layers and the so-called penumbra, where a central low T1/high T2 signal abscess cavity is surrounded by a two-layered rim (Figs. 19.6 and 19.8). The inner rim of granulation tissue is isointense to muscle on T1-W imaging and hyperintense on T2, whereas the outer fibrous rim is hypointense on all sequences. A halo of T1-hypointense edema surrounds the hypointense rim [27]. The penumbra consists of a thin layer of granulation tissue that surrounds the abscess. On unenhanced T1-W sequences, it is slightly hyperintense, perhaps due to its relatively low water content compared to the more central abscess or the surrounding edema; it enhances intensely [28]. The penumbra is 75 % sensitive and specific for subacute osteomyelitis and can be useful for differentiation from tumor. Fat globules are not encountered in subacute osteomyelitis [23, 29].

Differential considerations include osteoid osteoma, stress fracture, and—less likely—Ewing sarcoma, lymphoma, or metastatic neuroblastoma. Epiphyseal subacute osteomyelitis may be mistaken for chondroblastoma.

Bone sclerosis and cortical thickening in chronic osteomyelitis are hypointense on all sequences. The sequestrum and involucrum do not enhance but are surrounded by enhancing granulation tissue (Fig. 19.11). Sinus tracts are hypointense on T1 and hyperintense on T2, and their margins demonstrate enhancement. Marrow edema is present, with a sharp, well-defined margin between normal and abnormal marrow (in acute osteomyelitis, the zone of transition is ill-defined) [7]. Fat signal—if present—is due to the restoration of normal marrow [23]. Primary differential considerations are osteosarcoma and Ewing sarcoma.

Long-term sequelae include restricted or angular growth secondary to physeal damage and resultant early growth plate fusion. Alternatively, limb overgrowth can occur, as a result of hyperemia. Epiphyseal avascular necrosis or destruction decreases growth and produces severe deformity (Fig. 19.15). MRI or CT can be useful to analyze physeal damage as well as to assess the condition of the epiphysis. Long-term follow-up radiographs assess the impact on growth and angular deformity (Fig. 19.16).

Involvement of the epiphyseal ossification center is common in infants, secondary to extension from the metaphysis. There is also an uncommon subacute primary form that occurs in early childhood; this follows direct hematogenous seeding of the epiphysis [30]. Pain and limp are often recurrent. The knee is affected almost exclusively, with distal femoral epiphyseal involvement more likely than proximal tibia. Staphylococcus aureus is the most common pathogen.

A well-circumscribed epiphyseal lucency is seen (Fig. 19.17), usually without any other bone involvement, and nuclear scintigraphy is positive. MRI demonstrates typical findings of osteomyelitis [30]. Differential diagnoses are limited and include chondroblastoma, epiphyseal osteoid osteoma, and normal developmental epiphyseal lucencies [31].

Pelvic osteomyelitis accounts for 10 % of cases of acute osteomyelitis and tends to occur in older males (average age 7–14 years) [32]. There is often a history of trauma [33]. Signs and symptoms vary, and as many as 50 % are afebrile; diagnosis is often delayed, with symptoms initially attributed to septic arthritis, slipped capital femoral epiphysis, Legg-Perthes disease, appendicitis, or tubo-ovarian abscess [32, 34]. Abscesses are especially common in pelvic osteomyelitis, perhaps because of the typical delay (average 12 days) in diagnosis [35]. An ESR of more than 55 may help predict the presence of an abscess [32].

Osteomyelitis in the pelvis occurs in metaphyseal equivalents that border cartilage, where—as in the metaphyses of long bones—sluggish blood flow in venous sinusoids favors bacterial deposition and proliferation. Prior to skeletal maturation, the bony margins of the triradiate cartilage and ischiopubic synchondroses are common sites of pelvic osteomyelitis, followed by the sacroiliac joint, pubic symphysis, ischium, and iliac apophysis [32–34].