CLINICAL HISTORY A 71-year-old woman with ankle pain.

FINDINGS (A) Axial proton density and (B) T2-weighted, fat-suppressed magnetic resonance images (MRI) of the ankle show a thickened and split posterior tibial tendon (PTT). There is increased T2-weighted signal within the tendon with surrounding fluid in the sheath.

DIFFERENTIAL DIAGNOSIS None.

DIAGNOSIS PTT longitudinal split tear.

DISCUSSION The PTT is the largest and thickest of the three medial flexor tendons. The tendon courses under the medial malleolus and attaches to the medial navicular bone, the three cuneiforms, and the bases of the first to fourth metatarsals. Most PTT tears occur at the level of the medial malleolus. This tendon is one of the primary arch supporters for the foot. Tears of this tendon can cause flatfoot deformity and significant chronic pain and osteoarthritis [1]. Sinus tarsi syndrome has been described in association with PTT tear [2].

CLINICAL HISTORY A 9-year-old girl with ankle injury.

FINDINGS Anteroposterior (AP) ankle radiograph shows an intra-articular fracture plane extending vertically through the medial aspect of the tibia, passing through the epiphysis, growth plate, and metaphysis, and separating the medial malleolus from the remainder of the tibia.

DIAGNOSIS Salter type IV fracture, medial malleolus.

DISCUSSION Salter type IV fractures pass through the metaphysis, growth plate, and epiphysis. In this case, a vertical fracture in the sagittal plane can be seen passing through these three structures. These fractures require accurate open reduction and internal fixation (ORIF), because misalignment of the principal fragments would allow a bone bridge to form across the growth plate [3]. Such a bone bridge would tether the growth plate on one side and result in a progressive varus deformity as the open, lateral portion of the growth plate continued to lengthen the bone. The potential for deformity is greater in young children, who have a longer remaining growth period. The risk of complications is high if the fracture has more than 2 mm of displacement. A Salter type I or type II fracture of the fibula may be associated with this injury.

CLINICAL HISTORY A 14-year-old boy with lacrosse injury.

FINDINGS (A, B) AP, lateral radiographs, (C) sagittal, (D) coronal reformatted, and (E) three-dimensional volume rendering computed tomography (CT) of the right ankle demonstrate a vertical fracture through the epiphysis that runs from anterior to posterior, and an oblique fracture through the posterior distal tibial metaphysis. The medial malleolus is intact, as is the lateral metaphysis. The central part of the distal tibial growth plate is closed, the most medial portion of the growth plate is open, and the lateral portion is abnormally widened.

DIFFERENTIAL DIAGNOSIS Salter type II fracture, Salter type III fracture, Salter type IV fracture, juvenile Tillaux fracture, triplane fracture.

DIAGNOSIS Triplane fracture.

DISCUSSION The radiographs and CT show fractures of the distal tibia that appear to involve the growth plate. One fracture component extends through the metaphysis in the oblique coronal plane, and one fracture extends through the epiphysis in the sagittal plane. Because the fracture through the growth plate that connects the metaphyseal and epiphyseal fractures is in the axial plane, the components of this fracture occur in three different planes, defining the diagnosis of a triplane fracture. The triplane fracture has elements of Salter type II and type III fractures, and because it crosses the epiphysis, growth plate, and metaphysis, it can also be considered a Salter type IV fracture. The juvenile Tillaux fracture, in comparison, is a fracture in which the anterolateral aspect of the tibia epiphysis is avulsed by tension from the anterior tibiofibular ligaments during external rotation of the foot; the juvenile Tillaux fracture can be classified as a Salter type III fracture.

Triplane fractures only occur when physeal closure of the distal tibia is incomplete [4,5]. The distal tibial growth plate begins to close centrally, then medially, and finally laterally. Plantar flexion and external rotation are believed to be the mechanisms of injury in the triplane fracture, in which the lateral fragment of tibia that includes a portion of the epiphysis and metaphysis is avulsed by tension on the tibiofibular ligaments. Fracture of the fibula may accompany these injuries. When the separated epiphysis has two fragments, one of which has a portion of posterior tibial metaphysis attached to it and the other comprises a fragment of the medial epiphysis, a three-part triplane fracture is produced. Three-part fractures are usually more severe than two-part fractures, since there is greater displacement of the epiphyseal fragments. ORIF is used more frequently for three-part injuries.

The mean age at the time of fracture is about 15 years in boys and 13 years in girls, with a range from about 12 to 17 years in boys and 10 to 15 years in girls. Triplane fractures comprise 15% and 7% of ankle fractures in boys and girls under the age of 18 years, respectively, but the proportion would be much higher in the age range in which these fractures occur. If an epiphyseal gap of 3 mm or greater remains after ORIF, there is a greater risk of premature physeal closure [6].

CLINICAL HISTORY A 4-year-old boy who refuses to walk. A-B, 2 weeks after presentation; C-F, 6 weeks after presentation.

CLINICAL HISTORY A 29-year-old man with lower leg swelling.

CLINICAL HISTORY A 33-year-old man with ankle pain.

CLINICAL HISTORY A 28-year-old woman with ankle sprain.

FINDINGS (A, B) Axial proton density and (C, D) T2-weighted fat-suppressed MRI demonstrates complete tear of anterior talofibular (ATF) ligament surrounded by fluid signal. The calcaneofibular (CF) ligament is also torn underneath the peroneus tendon sheath. The posterior talofibular (PTF) ligament shows increased signal intensity with preserved fibers consistent with sprain. Also, noted is bone marrow edema in the posterior talus and peroneal tubercle of calcaneus.

DIAGNOSIS Lateral ankle ligament tear.

DISCUSSION The lateral collateral ligament complex is made up of three ligaments: the ATF, CF, and PTF ligaments. Injuries to this complex are very common, especially in the young, active population. Of these ligaments, the ATF ligament is the weakest and most easily torn. As inversion stress increases, the CF ligament becomes torn. PTF ligament injury is uncommon, and is almost always associated with injury to both the ATF and CF ligaments. Acute grade I and II tears, stretching and partial tears, are often treated conservatively. The treatment of grade III tears, complete rupture of a ligament, is more controversial. Regardless of the treatment, the prognosis of most ankle sprains is quite good. Unfortunately, 10% to 20% of patients develop chronic instability [15]. MR arthrography of the ankle has been shown to be a highly sensitive modality for detecting and accurately staging lateral ankle ligament tears. MR arthrography allows the evaluation of the torn free ends of the ligaments to assess the feasibility of primary repair and the evaluation of adjacent structures, which may potentially be used in surgical reconstruction [16].

CLINICAL HISTORY A 34-year-old woman with foot pain.

CLINICAL HISTORY An 8-year-old boy with ankle pain.

CLINICAL HISTORY A 10-year-old boy with ankle pain.

FINDINGS (A, B) Lateral and mortise radiographs of the ankle show disordered mineralization in the distal tibial epiphysis. The epiphysis is ossifying from multiple centers. There is a dense horizontal line of sclerosis across the distal tibial metaphysis. The ossification patterns in the medial and lateral malleoli are also disordered.

DIFFERENTIAL DIAGNOSIS Osteonecrosis, epiphyseal dysplasia, trauma, osteomyelitis.

DIAGNOSIS Osteonecrosis in sickle cell disease.

DISCUSSION The appearance of the epiphysis with multiple centers of ossification is that of revascularized osteonecrosis. In this case, the patient was known to have sickle cell disease, and the clinical question was the cause of his ankle pain. Sickle cell disease is caused by an inherited structural defect in hemoglobin that leads to red cell dysfunction. The radiologic features of sickle cell disease in bone are the result of bone marrow hyperplasia, vascular occlusion, and osteomyelitis [21]. Hyperplasia of the bone marrow expands the marrow space. Vascular occlusion results in osteonecrosis. Any portion of any bone may be infarcted; frequent sites include the medullary space of long bones, growing epiphyses, and the hands. Involvement of growing epiphyses leads to growth disturbances. If the femoral head is involved, the pathophysiologic events and sequelae are indistinguishable from those of Legg-Calvé-Perthes disease. A growth disturbance in the vertebral body leads to development of H-shaped vertebrae. Localized infarctions of bone with repair or dystrophic calcification result in focal areas of bony sclerosis scattered about the skeleton.

Patients with sickle cell disease have a high incidence of osteomyelitis. Unlike hematogenous osteomyelitis in other situations, the infection in sickle cell disease is most frequent at the diaphysis of the long bones, where the oxygen tension is lowest. In approximately 50% of cases, Salmonella species or mixed flora are the causative organisms (their presence is exceedingly unusual under any other circumstance); the remaining cases are usually caused by Staphylococcus species. Chronicity and recurrence are common. Osteomyelitis may be difficult to differentiate from infarction on both clinical and radiologic grounds [22,23]; either one can be a complication of the other. The radiographic signs of osteomyelitis would superimpose on whatever preexisting bone changes existed from the sickle cell disease.

CLINICAL HISTORY A 63-year-old man with newly diagnosed prostate cancer.

CLINICAL HISTORY A 32-year-old woman with chronic swelling and ankle pain.

CLINICAL HISTORY A 26-year-old woman with skin problems.

FINDINGS Oblique ankle radiograph. There is amorphous dense soft tissue calcification, distributed in vertical sheets. No underlying osseous abnormality is identified. No joint disease is present.

DIFFERENTIAL DIAGNOSIS Dermatomyositis, systemic lupus erythematosus (SLE), scleroderma, hypervitaminosis D, hyperparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism, parasitic infection.

DIAGNOSIS Dermatomyositis.

DISCUSSION Extensive soft tissue calcification is present, some of which is subcutaneous, but some appears to be intramuscular and possibly intratendinous. The calcifications are amorphous in character, without defined internal structure. Numerous disorders can be associated with soft tissue calcifications, including dermatomyositis, SLE, scleroderma, hypervitaminosis D, hyperparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism, and parasitic infection.

Dermatomyositis is an idiopathic disorder with non-infectious inflammation of the skin and skeletal muscle. Polymyositis involves muscle alone. Multiple types of the disease have been described based on the clinical presentation, and a clinical form associated with underlying malignancy has been described. Regardless of subtype, nearly all patients experience muscle weakness, usually proximal. Skin rashes and arthralgias are common clinical findings and may be the presenting symptoms. Involvement of cardiac, pulmonary, renal, neurologic, and gastrointestinal tissues will alter the presentation. Laboratory tests reveal elevation of creatine kinase during active inflammation, and electromyographic alterations can be detected. Soft tissue findings tend to be more common and severe in children than adults. Soft tissue swelling may be appreciated by dedicated soft tissue films in areas of complaint, but soft tissue calcifications represent the most dramatic radiographic finding. Distinct patterns of soft tissue calcification have been described, the most common of which are linear, sheet-like calcification in the interfascial planes. Reticular and rounded calcifications may be seen in the subcutaneous tissues, and deep rounded calcifications are common. In childhood disease, spontaneous remission of soft tissue calcifications has been reported with the onset of puberty. Joint changes on radiographs are rare and usually limited to soft tissue swelling. Distal tuft resorption may be seen in association with soft tissue calcification, which may be confused with scleroderma.

MRI is a useful method for evaluating the extent and activity of disease. Actively involved muscle tends to demonstrate increased signal on T2-weighted images; inversion recovery or fat-suppressed, T2-weighted images are the most sensitive method for displaying these changes [29]. Antimyosin scintigraphy may be even more sensitive than MRI for detecting active disease [30]. Identification of active disease is useful for directing biopsy.

CLINICAL HISTORY A 73-year-old woman with persistent lateral foot pain after twisting her ankle.

FINDINGS (A, B) Sagittal T1-weighted and inversion recovery MRI of the hindfoot shows edema and resultant loss of the normal fat signal within the sinus tarsi region.

DIFFERENTIAL DIAGNOSIS None.

DIAGNOSIS Sinus tarsi syndrome.

DISCUSSION The sinus tarsi is the space between the talar neck and distal calcaneus. This space contains ligaments, neurovascular structures, and fat. In a severe ankle inversion injury, inflammation or hemorrhage in this region may produce chronic pain. The ligaments within the sinus tarsi may also be torn, producing a sensation of instability. MRI can demonstrate ligamentous tears within the sinus tarsi—usually the cervical ligament or interosseous talocalcaneal ligament [32,33]—as well as edema or fibrosis within the surrounding fat. Sinus tarsi syndrome may also occur due to flatfoot deformities and inflammatory arthropathies [34]. Treatment is usually conservative. An arthroscopic subtalar joint synovectomy is an effective treatment when conservative measures fail [35].

CLINICAL HISTORY A 20-year-old man with foot pain.

CLINICAL HISTORY A 47-year-old alcoholic with chronic ankle pain but no history of trauma.

FINDINGS (A-C) Lateral, AP, and mortise radiographs of the right ankle show subchondral lucency, subchondral sclerosis, and flattening of the talar dome.

DIFFERENTIAL DIAGNOSIS Osteochondral fracture, osteonecrosis, osteoarthritis, neuropathic osteoarthropathy.

DIAGNOSIS Osteonecrosis.

DISCUSSION The radiographic findings of linear subchondral lucency, subchondral sclerosis, and collapse of the articular surface are diagnostic of osteonecrosis (avascular necrosis) involving an articular surface. Note the preservation of joint space and normal appearance of the tibial plafond, indicating that the disease process is primary to the talus rather than the joint itself. The opposing joint surface is typically normal in osteonecrosis until late in the disease, when manifestations of secondary degenerative joint disease may be seen. Once revascularization of the necrotic bone has become reestablished, attempts at repair by creeping substitution result in sclerosis as new viable bone is apposed to necrotic bone. Sclerosis represents the earliest radiographic manifestation of osteonecrosis. Resorption of bone may result in a loss of mechanical strength, sometimes leading to subchondral fracture. Subchondral fracture may be evident as linear subchondral lucency—the crescent sign—and it is a highly specific sign of osteonecrosis. The subchondral fracture may even contain nitrogen gas formed in the joint during traction. Continued application of forces across the joint with associated attempts at repair leads to collapse of the articular surface, as in this case. The joint surface may then fragment, and resulting joint incongruity eventually leads to the development of osteoarthritis.

Atraumatic osteonecrosis of the talar dome has numerous causes, including alcoholism, SLE, sickle cell disease, excessive corticosteroids (endogenous or exogenous), pancreatitis, dysbarism, and marrow packing disorders such as Gaucher disease. Some cases have no apparent cause, but the majority of patients with atraumatic osteonecrosis of the talus have osteonecrosis elsewhere, especially the femoral head, and approximately half have bilateral involvement of the tali [36]. Atraumatic osteonecrosis is relatively uncommon, with most cases of osteonecrosis being related to fractures of the talar neck [37].

CLINICAL HISTORY A 26-year-old man in a motorcycle accident.

FINDINGS (A) Lateral radiograph of the foot. The talus remains within the ankle mortise, but the relationship of the posterior facets of the talus and calcaneus is abnormally widened and oriented. Easy to overlook, the head of the talus overlaps the navicular, rather than articulating with it. Oblique (B) and AP (C) radiographs of the ankle and foot. The entire midfoot has dislocated medially and inferiorly. Most obvious are the naked articular surfaces of the distal aspect of the talus and the proximal aspect of the navicular.

DIFFERENTIAL DIAGNOSIS None.

DIAGNOSIS Subtalar dislocation.

DISCUSSION Simultaneous dislocation of the talocalcaneal and talonavicular joints is referred to as subtalar dislocation. Of the ligamentous supports about the talus, the talonavicular and talocalcaneal ligaments and capsules are weaker than the calcaneonavicular ligaments and capsule and the ankle ligaments, so the entire midfoot and calcaneus may dislocate as a single unit [38]. Most of these injuries represent high-energy trauma, such as that sustained in motorcycle accidents or falls from a height, but relatively minor stumbling trauma may also cause this injury. Approximately 90% of subtalar dislocations are closed. In approximately 80% of cases, the foot dislocates medial to the talus. Severe open subtalar dislocations occur in major trauma [39], typically motorcycle accidents. Associated injuries include injuries of the tibial nerve, ruptures of the PTT, lacerations of the posterior tibial artery, and articular fractures of the subtalar joint, talonavicular joint, and talar dome. The outcome is often poor, and the risk of osteonecrosis of the talus is significant.

CLINICAL HISTORY A 18-year-old adolescent boy with painful flatfoot deformity.

CLINICAL HISTORY A 1-month-old male infant with foot deformity.