Diagnosis
Calcific myonecrosis.
Discussion
Calcific myonecrosis is a rare, late, sequela of trauma. It occurs almost exclusively in the anterior compartment of the lower leg. Recently, two other sites have been reported (foot and upper extremity). To date, approximately 37 cases (including this case) have been reported in the English literature. Several of these patients developed infections after biopsy, manifested by a chronic discharging sinus. However, de novo infection has been reported in only three cases [1]. Our case is unusual because of spontaneous drainage with extrusion of calcification.
It is postulated that these lesions result from post-traumatic ischaemia and cystic degeneration. Compartment syndrome and peroneal nerve injury are commonly associated.
Calcific myonecrosis is characterized by muscle replacement by a fusiform soft tissue mass containing peripheral calcifications and central liquefaction [2]. Radiographically, these calcifications are characteristically plaque-like and/or linear in shape, parallel to the long axis of the compartment, and without obvious bony matrix (see Fig. 1a in the presentation).
Dhillon et al. explained the increasing size of the mass by postulating a process of repeated intra-lesional haemorrhage [2]. The components with high signal intensity (SI) on the T1-weighted image (T1-WI) in our case (Fig. 2) are, indeed, suggestive of methaemoglobin. An increased volume of liquefactive necrosis may have resulted in mobility of the calcific plaques. A horizontally angulated plaque probably caused the visible cone-shaped deformity of the skin (see Fig. 1b in the presentation) and led to central necrosis of the skin (see Figs. 3 and 4 in the presentation).
Dhillon et al. reported a mean time between injury and diagnosis of 37 years (range 10-64 years) [2]. Because of this long delay between the primary injury and the clinical presentation of the mass, the history of significant trauma is often overlooked [3], causing confusion with other calcified soft tissue masses.
Differentiation from myositis ossificans (MO) can be made by a combination of clinical, radiographic and MR characteristics. In MO, there is a short interval (weeks to months) between the primary injury and development of the lesion. Lesions of myositis generally do not enlarge over time. Radiographically, MO typically shows zonation, with peripheral formation of trabeculated and lamellar osseous tissue, followed by progressive centripetal ossification. The plaque-like peripheral calcifications in calcifying myonecrosis do not ossify. On T2-weighted MR images peri-lesional muscle oedema can be visualized in the acute phase of MO. The chronic phase is characterized by marrow fat between mature bone trabeculae that presents with high signal intensity on T1-weighted images. On the other hand, calcific myonecrosis is of heterogeneous signal intensity, the calcified parts having low SI on both pulse sequences, the liquid centre having variable SI because of variable protein content. Peripheral rim enhancement is seen in only infected lesions.
Calcified soft-tissue neoplasms, such as osteosarcoma, appear more aggressive, have central calcifications and are enhanced markedly after administration of contrast medium.
Dystrophic calcifications may also occur as a result of haematoma or abscess, and may be seen in diabetic myonecrosis. Nevertheless, involvement of one single entire muscle or compartment, as often seen in calcific myonecrosis, is unusual.
References
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