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A 15-year-old boy presented with left-sided chest pain and a palpable chest wall mass. PA radiograph of the chest demonstrated osseous expansion and periosteal reaction in the left mid 8th rib and a large associated soft tissue mass (Fig. 91.1a). Axial contrast-enhanced CT of the chest demonstrated a heterogeneous soft tissue mass along the left chest wall. There was expansion, destruction, and periosteal reaction of the involved rib (Fig. 91.1b, c). An MRI of the abdomen, obtained to evaluate for metastases, was negative and also included the lower chest (Fig. 91.1d, e, f). This demonstrated a large heterogeneous T2 bright mass surrounding the left lower rib. The mass and marrow of the affected rib demonstrated restricted diffusion (bright signal on diffusion-weighted imaging [DWI] with dark signal on ADC map). Bone scan (not shown) did not demonstrate any metastases. Ewing’s sarcoma of the chest wall was suggested as the most likely diagnosis. Subsequent pathology defined the lesion as an undifferentiated sarcoma of the chest wall.
A one-month-old girl had a physical examination suggesting developmental dysplasia of the hip (DDH). A coronal sonographic image through the right hip in neutral position, performed at one month of age, demonstrated an abnormal alpha angle of 47 degrees and less than 50% coverage of the femoral head under the acetabular roof (Fig. 83.1a). Pelvic AP radiograph at three months of age demonstrated a steep right acetabular roof with asymmetrically delayed ossification of the right femoral head (Fig. 83.1b).
A three-year-old girl with a chromosomal deletion syndrome presented with bilateral hip pain and difficulty with abduction. Pelvic AP radiograph demonstrated dysplastic acetabulae with bilateral femoral head dislocation, pseudoacetabula formation, and valgus deformity (Fig. 83.2a). Frog leg view demonstrated that the hips did not relocate with abduction (Fig. 83.2b). This appearance is typical of secondary neurogenic hip dislocation related to muscle imbalance and overactive hip adductors.
AP and lateral radiographs of the right lower extremity in a young infant demonstrated diffuse exuberant periosteal reaction, diaphyseal sclerosis, and metaphyseal irregularity with horizontal metaphyseal lucent lines (Fig. 87.1a,b), suggestive of bony changes of congenital syphilis. AP radiograph of the bilateral lower extremities in a different infant with congenital syphilis demonstrated irregular, focal lucencies of the medial proximal metaphyses of the bilateral tibiae, the Wimberger sign (Fig. 87.2). AP radiographs of bilateral upper extremities in another infant demonstrated metaphyseal lucencies and diaphyseal sclerosis (Fig. 87.3).
Congenital syphilis is transferred through the placenta in the second or third trimester in mothers with untreated or recently treated primary or secondary syphilis. The pathogenesis of this disease is transplacental migration of Treponema pallidum bacteria. Bony changes are thought to result mostly from trophic effects rather than direct osteomyelitis. There is inhibition of osteogenesis and disturbance of active endochondral ossification. Symmetric involvement of the sites of endochondral ossification leads to bony changes at the epiphyseal-metaphyseal junctions, costochondral junctions, and endochondral ossification sites in the sternum and spine. A baby born to a mother with untreated syphilis in the primary or secondary stage has a nearly 100% chance of acquiring the infection. Radiographic changes occur approximately six to eight weeks after initial infection, so that they may not be present at birth but only manifest subsequently. Direct clinical examination, treponemal tests, VDRL (venereal disease research laboratory [test for syphilis]), and rapid plasma reagin are used to confirm the diagnosis. Results are considered conclusive when the infant’s titer is at least four times higher than that of the mother.
A 13-year-old male patient had a twisting injury of the right ankle. Radiographs of the right ankle (in temporary cast) demonstrated a fracture of the right medial malleolus with a medially displaced fracture fragment (Fig. 88.1a). The fracture was noted to have metaphyseal, physeal, and epiphyseal components consistent with a Salter–Harris type IV injury. In addition, there was mild separation of the distal tibia and fibula, suggesting an injury of the tibiofibular syndesmosis. The patient was referred to orthopedic surgery for surgical fixation. A postsurgical radiograph of the right ankle demonstrated anatomic alignment of tibia and fibula with stabilizing screws in the medial malleolus and through the distal tibiofibular syndesmosis (Fig. 88.1b).
In 1931, McFarland described a pediatric fracture of the medial malleolus of the distal tibia that extended across the physis and sometimes into the metaphysis. These fractures were therefore previously described as McFarland fractures. The Salter–Harris classification has since become more frequently used to characterize pediatric fractures (Fig. 88.2). Salter–Harris I fractures extend through the physis. Type II fractures pass through the physis and metaphysis. Type III fractures extend through the physis and epiphysis. Type IV fractures pass through the epiphysis, physis, and metaphysis. Salter–Harris type V injury is a compression or crush injury of the physeal plate, associated with growth disturbance at the physis (Fig. 88.2). An avulsion fracture of the medial malleolus of the distal tibia that extends through the physis and epiphysis is therefore characterized as a Salter–Harris III or IV fracture depending upon whether there is extension of the fracture line into the metaphysis. The medial collateral ligament (MCL) of the ankle, also called the deltoid ligament, can be involved. The MCL is a strong ligamentous complex that is an important stabilizer of the ankle. The MCL components include a deep layer which courses from the medial malleolus to the talus and a deltoid-shaped superficial layer that extends from the medial malleolus to the navicular, the spring ligament, and the calcaneus. The importance of this fracture is that it often occurs in children and any disruption or damage to the developing growth plate can result in growth arrest.
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