14 year old boy presented initially for a sprained right ankle. No abnormalities were found at that time. The patient returned to clinic after 15 months due to increased swelling and pain in the right ankle over a 6 month period.
Physical exam at follow-up visit revealed swelling, erythema, and tenderness to palpation at the medial ankle.
Figure 1: Initial anteroposterior (A-P) radiograph of the right distal tibia and fibula 15 months prior to the current presentation showed no evidence of fracture and mild soft tissue swelling around the lateral malleolus. Incidentally, a lucent lesion with a well defined cortical margin was found along the lateral distal tibia, consistent with a nonossifying fibroma.
Figure 2: Follow-up A-P radiograph of the right distal tibia and fibula 15 months after the initial injury shows a bilocular lytic lesion of the metaphysis and a unilocular lytic lesion of the epiphysis at the medial aspect of the tibia. The lesions are surrounded by a well defined sclerotic border with benign-appearing periosteal reaction and mild soft tissue swelling medially. The metaphyseal lesions extend across the physis into the epiphysis. There are no fracture lucencies and the joint spaces are maintained. The nonossifying fibroma of the lateral distal tibia is unchanged.
Figure 3: A Tc-99m HDP bone scan demonstrates increased radiotracer uptake at the distal tibial meta-epiphysis, most marked on the medial aspect of the epiphysis.
Figure 4: Axial T1-weighted MR image of right leg reveals multiple well defined low signal intensity masses surrounded by a thick medium intensity rim with a low signal intensity periphery. The tibial metaphyseal component measures 2.1cm longitudinal x 1.6cm transverse x 2.1cm AP. The epiphyseal component measures 2 cm longitudinal x 2.3cm transverse x 3cm AP. The inflammatory process extends posteromedially through the cortex of the tibial epiphysis to involve the adjacent soft tissues.
Figure 5: On axial T2-weighted fat saturated MR image of the right leg, masses become high-signal intensity surrounded by low-signal intensity rims. The high signal-intensity inflammation extends into the adjacent soft tissues. There is a low signal intensity thickening of the soft tissues medially which extends anteriorly to the anterior aspect of the anterior-tibial tendon and posteriorly to the lateral aspect of the tibial tendon, flexor digitorum longus tendon and hallucis longus tendon. There are non-enhancing foci within the soft tissue consistent with extensive inflammation.
Figure 6: Axial T1-weighted MR image after contrast demonstrates well defined masses with non-enhancing centers, enhancing thick rim, and non-enhancing periphery. The non-enhancing central lesions correspond to the low signal intensity centers seen on T1-weighted MR and high signal intensity centers seen on T2-weighted MR, which together is consistent with necrosis. The epiphyseal lesion expands through the anteromedial border of the tibia with extension of the abscess into the adjacent soft tissues. High-signal-intensity bone marrow edema extends 5.5cm proximally into the distal tibial diaphysis from the site of the lesions.
Dx: Brodieâ€™s abscess
Dx Confirmed by: Histology and cultures grew Staphylococcus aureus
Treatment for Brodieâ€™s abscess includes surgical debridement and antibiotic therapy.
Histopathologic evaluation showed granulation tissue, acute and chronic inflammation, dense fibroconnective tissue, and bone fragments.
Cultures grew Staphylococcus aureus.
In the 1830â€™s, Sir Benjamin Collins Brodie recognized a chronic inflammatory process in the tibia with no acute symptoms or known precipitating infection. This rare lesion, known today as a Brodieâ€™s abscess, is a localized type of subacute or chronic pyogenic osteomyelitis. Pathogenesis is due to an insidious bacteremia with septic emboli to a normal or minimally traumatized long bone, often from an infection with Staphylococcus aureus. The lesion is predominant in young males with unfused epiphyseal plates, typically presenting during the second decade of life. Brodieâ€™s abscess is described as a small, eccentric, localized, lytic lesion with surrounding reactive sclerosis. It is characteristically found in the metaphyseal region of long bones of the lower extremity, most commonly in the tibia. The usual presenting complaint is recurrent pain and localized swelling; systemic symptoms are typically absent.
Radiographs of a Brodieâ€™s abscess often demonstrate a localized area of radiolucency with surrounding sclerosis. The lucent region is commonly located in the metaphysis where it may extend to the growth plate by a tortuous channel. Detection of this focal metaphyseal abscess with involvement of the growth plate is diagnostic for osteomyelitis. Conventional radiographs should be the initial imaging study for evaluating osteomyelitis although, in early osteomyelitis they are usually normal or may show soft tissue swelling or benign periosteal reaction.
Bone scans are more sensitive than conventional x-rays for the early detection of osteomyelitis although not as sensitive as MR imaging. A focal area of radiopharmaceutical uptake at the site of suspected infection would suggest a Brodieâ€™s abscess. Both Brodieâ€™s abscesses and eosinophilic granulomas show radiopharmaceutical uptake and therefore this cannot be used as a distinguishing feature.
Magnetic resonance (MR) imaging provides a greater accuracy in delineating the extent of disease, a more rapid evaluation. Furthermore, MR imaging possesses a high sensitivity in the detection of bone infection. On T1-weighted MR images, subacute osteomyelitis with Brodieâ€™s abscess presents as a low-intensity signal mass with low-signal-intensity rim that becomes a high-intensity signal mass with a thick, low-intensity rim on T2 weighted MR images. The abscess may rarely extend into the cortex and into soft tissues. In addition, the infection may rarely traverse the open growth plate, to involve the epiphysis. Other findings of chronic osteomyelitis include cortical bone thickening, sequestra, sinus tracts to the adjacent soft tissues. Post-contrast MR images show a non-enhancing mass with enhancing periphery.
On the imaging studies, our patient showed findings consistent with a Brodieâ€™s abscess with additional more unusual findings of extension across the growth plate into the epiphysis and cortical invasion into adjacent soft tissues. Alternate diagnoses in the differential can be excluded by the absence of a lesion 15 months prior to detection in this skeletally immature youth. Histopathologic confirmation with and positive cultures for Staphylococcus aureus, however, provide definitive diagnosis of a Brodieâ€™s abscess.
Treatment for Brodieâ€™s abscess includes surgical debridement and antibiotic therapy. A sterile abscess may be treated without antibiotics only if there is symptomatic improvement and radiographic regression of the lesion. More aggressive treatment, such debridement followed by bone grafting, may be needed for abscesses that form slightly before or after bone maturation and do not resolve with surgical treatment.
Osteomyelitis may result from open injury to bone and surrounding soft tissue, from hematogenous and local spread from adjacent tissues and as a postoperative complication(1). The specific organism isolated in bacterial osteomyelitis is often associated with the age of the patient or a common clinical scenario (i. e., trauma or recent surgery). Staphylococcus aureus is implicated in most patients with acute hematogenous osteomyelitis. Staphylococcus epidermidis, S. aureus, Pseudomonas aeruginosa, Serratia marcescens and Escherichia coli are commonly isolated in patients with chronic osteomyelitis.
Treatment generally involves clinical evaluation, imaging evaluation for disease extent, laboratory determination of microbial etiology and susceptibilities, antimicrobial therapy and, if necessary, debridement, dead-space management and stabilization of bone. Localized bone pain, erythema and drainage around the affected area may be present. The cardinal signs of subacute and chronic osteomyelitis include draining sinus tracts, deformity, instability and local signs of impaired vascularity, range of motion and neurologic status.
When there is clinical suspicion for osteomyelitis after physical examination and history, baseline radiographs should be performed followed by magnetic resonance imaging when available to define the extent of osteomyelitis and cellulitis. When MRI is not available, bone scans are useful for determining the extent of the infection. Laboratory tests may show leukocytosis (especially in the acute presentation) and elevations in the erythrocyte sedimentation rate and C-reactive protein level may be noted. Blood cultures are positive in as high as one-half of children with acute osteomyelitis.
In acute osteomyelitis, the radiographs may be negative or may show only soft tissue swelling and periosteal reaction. Evidence of medullary destruction may not appear until approximately two weeks after the onset of infection. Positive radiographic findings, when present include osteolysis, periosteal reaction and sequestra (segments of necrotic bone separated from living bone by granulation tissue).
A bone abscess found during the subacute or chronic stage of hematogenous osteomyelitis is known as a Brodie's abscess. Magnetic resonance imaging (MRI) is the most sensitive test for evaluating osteomyelitis and the areas of osteomyelitis and cellulitis show high signal intensity on T2-weighted MR images enhancement on postcontrast T1-weighted MR images.
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