==== Front Ann Saudi MedAnn Saudi MedAnnals of Saudi Medicine0256-49470975-4466King Faisal Specialist Hospital and Research Centre 10.5144/0256-4947.2007.55asm-1-55What's Your Diagnosis?DIAGNOSIS: Calcific myonecrosis of the calf Correspondence and reprint requests: Aydıner Kalacı, MD Department of Orthopaedics and Traumatology Mustafa Kemal University Faculty of Medicine Hatay 31100, Turkey, T: +90-326-214 8661, F: +90-326-214 4977, kalaci@mku.edu.tr* Department of Orthopaedics and Traumatology, Çukurova University Faculty of Medicine † Department of Orthopaedics and Traumatology, Mustafa Kemal University Faculty of Medicine Jan-Feb 2007 27 1 55 59 01 8 2006 Copyright © 2007, Annals of Saudi Medicine2007This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. ==== Body Plain radiographs (Figure 1) showed a fusiform, sharply defined calcified mass anterolateral to the right tibia. MRI (Figure 2) of the calf showed a fusiform, sharply defined non-homogeneous mass with peripheral calcification replacing the tibialis anterior, extensor hallucis longus, and extensor digitorum longus muscles. No bony erosion or destruction and radiological findings of previous trauma were present. The radiological diagnosis was reported as a low-grade periosteal osteosarcoma. The pathological evaluation revealed that the major resection specimen consisted of abundant amorphous necrotic tissue, skeletal muscle, and fragments of bone; the specimen measured 15.5×6×4 cm and occupied the entire anterior compartment of calf. The specimen included multiple yellow-brown pasty materials. Histological examination showed massive deposition of amorphous calcification and necrotic soft tissue. No viable, malignant cell was observed. The wall of the cyst was composed of hypocellular fibrous tissue. Cultures for bacteria, fungi, mycobacterium, and parasites were negative. The histological diagnosis was necrotic tissue, and dystrophic calcification. DISCUSSION Calcific myonecrosis is a rare complication of leg trauma. Approximately 28 cases have been reported in the English literature (Table 1).1–18 The history of trauma consisted of twelve tibia, six femur, one ipsilateral femur and tibia, one ankle, two fibula fractures, two gun-shot injuries, two knee ligamentous injuries, one blunt trauma of the leg, and one crush injury in the upper extremity.1–18 Common complications included compartment syndrome, vascular problems, and neurologic injuries. However, no complication of previous trauma was present in our case. We observed that complications may not always be present when calcific myonecrosis develops. Development of a tumor mass after trauma is time-dependent. Most patients define a long duration of an enlarging mass of the leg. The reported interval from injury to clinical presentation has ranged from 10 to 64 years (average, 38.4 years). The history of trauma dated back to 5 years ago in the case reported here. This is the shortest interval among the cases in the literature.1–18 The typical radiographic finding of this lesion was a large fusiform soft tissue mass with peripheral plaque-like calcifications and a liquid center in the anterior compartment of the leg.1,5–7,12–14 Some authors say that this may be a consequence of pathologic processes including post-traumatic cysts of soft tissue, chronic expanding hematoma and calcific myonecrosis.19,20 Adjacent erosion and periosteal reaction of bone were noted in some cases.6,7,13,14 Because of the invasive radiographic appearance of the lesion, calcifying soft tissue sarcomas, such as synovial sarcoma, epithelioid sarcoma, soft tissue osteosarcoma and chondrosarcoma, were considered initially by some orthopaedic surgeons.5,7,13,14 The radiological features of calcific myonecrosis allow differentiation from other causes of enlarging soft-tissue masses, including neoplasm, abscess, diabetic myonecrosis, and dystrophic calcification associated with chronic hematoma or abscess, polymyositis, and dermatomyositis.5 Differential diagnosis of the calcific myonecrosis requires a combination of radiological and pathological findings. MRI of the calcific myonecrosis showed a mass with heterogeneous signal on T2-weighted imaging and a homogeneous intermediate signal throughout the central fluid region on T1-weighted images.5,11,15 T2-weighted images showed bright areas consistent with fluid while the other areas of the lesion demonstrated intermediate signal.7,15 The gross pathology characteristic of calcific myonecrosis is a yellow-brown amorphous material with dystrophic calcifications and necrotic areas. Calcified muscle or calcified intermuscular septa may also be present. Histologic evaluation may also show a fibrous cyst wall with the dystrophic calcifications interspersed.7,15 Different treatment options have been proposed in the literature. Some authors recommended incision and drainage,6 repeated aspiration of the mass,6,8,12 observation of the intact compartments if otherwise stable4,5,13 or debridement of all affected tissue with ablation of the resulting dead space with muscle flaps.2,10,15,16 A few patients reported in the literature had chronic drainage after an open biopsy.2,5,6,10,12 The surgeon must be cautious in the treatment of calcific myonecrosis. Incomplete excision and packing of the wound with dressings were associated with infection, chronic draining sinus, and amputation.5,6,12,13 O’Keefe et al7 reported a case experiencing hypotension, and cardiac arrest at the end of excision of a large extensive calcific myonecrosis of the leg with the wound packed open because of massive postoperative bleeding. The patient died of a gastrointestinal complication 2 months later. Seven of 28 lesions (25%) reported in the English literature have had associated infections. Zohman et al14 reported a successful result of surgical treatment of this lesion by total excision, closing the wound over a suction drain, followed by application of a bulky compression dressing. However, with extensive debridement, closing the wound over a suction drain, and application of a compression dressing, followed by appropriate antibiotic therapy, the wound healed gradually without residual infection or recurrence of the lesion.13 We would recommend this method. Muscle transfers may be helpful to fill the dead space but are not always necessary. As the affected persons have adapted to the impaired function of the limb, reconstructive procedures for the improvement of function are not often required. In conclusion, a prerequisite for the development of calcific myonecrosis usually involves trauma with resultant ischemia or neurological injury. Both ischemia and compartment syndrome are suggested as the primary etiology of this calcific entity but these findings may not always be present. The interval between initial trauma and presentation of the disease may be as recent as five years as in the case of the current report. The typical radiological findings of a well-defined calcified mass replacing the calf musculature allow differentiation from other causes of an enlarging soft-tissue mass. Observation of clinically stable lesions appears prudent because complications may be considerable. If an operation is performed, should a more aggressive approach be necessary, the surgeon should debride all affected tissue, close the wound over a suction drain, and apply a compression dressing. Figure 1 X-ray of the legs of the 77-year-old-man with calcific myonecrosis anterolateral to the right tibia. Anteroposterior (A) and lateral (B) radiographs show a fusiform, calcified, diffuse soft tissue mass in the anterior compartment of the calf. Figure 2a Frontal spin-echo T1-weighted MRI of the calf showing a fusiform mass with peripheral calcification. Figure 2b Axial T1- and T2-weighted MRI scan showing a three-lobular mass replacing the tibialis anterior, extensor hallucis longus, and extensor digitorum longus muscle (proximal section). Figure 2c Axial T1- and T2-weighted MRI scans showing the well-marginated soft tissue mass replacing the previous anterior compartment musculature with a peripheral rim of low signal surrounding a heterogeneous mass (distal section). Table 1 Cases of calcific myonecrosis reported in the literature. Authors Year Cases Antecedent trauma Complications of injury Interval from injury to diagnosis (years) Age at time of surgery (years) Complications Gallie and Thomson3 1960 1 Femoral fracture Volkmann’s necrosis 37 40 None 2 Femoral fracture Volkmann’s necrosis 27 34 None Broder et al1 1977 3 Femoral fracture Compartment syndrome 32 52 None Viau et al12 1983 4 Femoral fracture Compartment syndrome 64 80 Infection and amputation 5 Tibial fracture Compartment syndrome 38 54 Chronic draining sinus Malisano and Hunter6 1992 6 Gunshot wound Volkmann’s necrosis 40 64 Chronic infection Janzen et al5 1993 7 Fibular neck fracture Common peroneal nerve injury 52 77 Chronic draining sinus 8 Femoral fracture None NS 67 NS 9 Tibial fracture None NS 56 NS Renwick et al8 1994 10 Tibial fracture Compartment syndrome 37 68 None Early et al2 1994 11 Knee dislocation Volkmann’s necrosis 10 37 None 12 Tibial fracture Peroneal nerve injury 40 52 None O’Keefe et al7 1995 13 Tibial fracture Compartment syndrome 34 72 Cardiac arrest 14 Tibial fracture Compartment syndrome 51 62 None 15 Tibial fracture None 34 51 None Snyder et al10 1995 16 Blunt trauma Compartment syndrome 31 56 None 17 Femoral fracture Compartment syndrome 35 50 None Hyder et al4 1996 18 Femoral and tibial fracture Popliteal artery injury 14 31 No treatment Flinn and Beggs18 1996 19 Tibial fracture Compartment syndrome 50 74 No treatment Ryu at al9 1996 20 Fibular neck fracture None 47 70 NS Zohman et al14 1998 21 Knee ligamentous injury Compartment syndrome 30 49 None Tuncay at al11 1999 22 Shot-gun injury Compartment syndrome 42 64 None Jassal et al16 2001 23 Ankle fracture Compartment syndrome 57 66 None Wang and Chen13 2001 24 Tibial fracture Compartment syndrome 30 49 Infection Holobinko et al15 2003 25 Tibial fracture Compartment syndrome 40 57 None 26 Tibial fracture Compartment syndrome 51 67 Infection 27 Tibial fracture Compartment syndrome 21 37 Infection Larson et al17 2004 28 Crush injury upper extremity Compartment syndrome 55 60 None Current authors 29 Blunt trauma None 5 77 None ==== Refs REFERENCES 1 Broder MS Worrell RV Shafi NO Cystic degeneration and calcification following ischemic paralysis of the leg Clin Orthop 1977 122 193 195 2 Early JS Ricketts DS Hansen ST Treatment of compartmental liquefaction as a late sequelae of a lower limb compartment syndrome J Orthop Trauma 1994 8 5 445 448 7996332 3 Gallıe WE Thomson S Volkmann’s ischaemic contracture: two case reports with identical late sequelae Can J Surg 1960 3 164 166 13826150 4 Hyder N Shaw DL Bollen SR Myositis ossificans: calcification of the entire tibialis anterior after ischaemic injury (compartment syndrome) J Bone Joint Surg Br 1996 78 2 318 319 8666650 5 Janzen DL Connell DG Vaisler BJ Calcific myonecrosis of the calf manifesting as an enlarging soft-tissue mass: imaging features AJR Am J Roentgenol 1993 160 5 1072 1074 8470578 6 Malisano LP Hunter GA Liquefaction and calcification of a chronic compartment syndrome of the lower limb J Orthop Trauma 1992 6 2 245 247 1602347 7 O’Keefe RJ O’Connell JX Temple HT Calcific myonecrosis. 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