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Calcific Myonecrosis of the Upper Extremity: Case Report
SCIENTIFIC ARTICLE
Calcific Myonecrosis of the Upper Extremity: Case Report Sara D. Rynders, Yaw D. Boachie-Adjei, MD, Cree M. Gaskin, MD, A. Bobby Chhabra, MD Calcific myonecrosis is an uncommon late sequela of limb trauma that results in calcification and necrosis of damaged muscle. It almost exclusively occurs in the lower extremity. We present a second case of calcific myonecrosis in the upper extremity. (J Hand Surg 2012;37A:130–133. Copyright © 2012 by the American Society for Surgery of the Hand. All rights reserved.) Key words Calcific myonecrosis, calcific myonecrosis of the upper extremity, Volkmann’s ischemic contracture, compartment syndrome.
ALCIFIC MYONECROSIS IS a rare soft tissue condition in which severely traumatized muscle, typically from a compartment syndrome or neurovascular compromise, becomes an enlarging calcified mass, characterized by central liquefaction and tissue necrosis over a period of decades.1,2 This condition was described in 1960 by Gallie and Thomson.1 More than 50 cases of calcific myonecrosis have been reported, and all but one have occurred in the lower extremity.1–31 Larson and colleagues,3 in 2004, reported a case of calcific myonecrosis in the forearm. We report an additional case of calcific myonecrosis in the upper extremity.
C
CASE REPORT A 66-year-old, left-handed woman presented with mild right forearm pain and the sensation of a mass for 6 weeks. When she was approximately 9 years old, she experienced an elbow fracture that was treated with traction and casting. She subsequently developed a Volkmann contracture of the right hand and wrist, rendering her with little use of the right upper extremity. Twelve years before presentation, she had a wrist arthFrom the Departments of Radiology and Orthopaedic Surgery, University of Virginia, Charlottesville, VA. Received for publication August 17, 2010; accepted in revised form September 27, 2011. No benefits in any form have been received or will be received related directly or indirectly to the subject of this article. Corresponding author: A. Bobby Chhabra, MD, University of Virginia Hand Center, Department of Orthopaedic Hand Surgery, P.O. Box 800876, Charlottesville, VA 22908-0876; e-mail: [email protected]. 0363-5023/12/37A01-0023$36.00/0 doi:10.1016/j.jhsa.2011.09.035
130 䉬 © ASSH 䉬 Published by Elsevier, Inc. All rights reserved.
rodesis and ulnar head excision, and it is not known whether any masses were seen at that time on examination or imaging. She denied recent history of injury to the right forearm and described the pain as a mild, intermittent ache, centered over the middle third of the forearm. She noted a firmness to the tissue in this area. She denied paresthesias, constitutional symptoms, or history of malignancy. The patient had irritable bowel syndrome, hypertension, hyperlipidemia, osteopenia, and lumbar spine degenerative disease. There was no history of diabetes mellitus. Physical examination revealed a contracted and atrophied right forearm, wrist, and hand (Fig. 1). The elbow was non-tender, with 90° of motion and no supination or pronation. The forearm was non-tender and had a subtle prominence of the soft tissues in the dorsoradial central third. The wrist was fixed in flexion and ulnar deviation. The fingers had minimal motion, but the thumb and index finger could achieve lateral pinch. Capillary refill was less than 2 seconds, the fingers were warm, and there were 2⫹ pulses of the radial and ulnar arteries. Anteroposterior and lateral radiographs were slightly limited due to the patient’s inability to extend and supinate the forearm. (Figs. 2A, 2B). A 6.4-cm ⫻ 1.7-cm lobulated and densely calcified mass was identified on the volar mid-forearm, just ulnar and volar to the ulnar diaphysis. A smaller, flatter calcification was seen more proximally near the antecubital fossa and was 1.5 cm long. Although the radiographs were suggestive of the diagnosis of calcific myonecrosis, computed tomography (CT) and magnetic resonance imag-
CALCIFIC MYONECROSIS OF THE UPPER EXTREMITY
FIGURE 1: A 66-year-old woman with Volkmann ischemic contracture and subtle mass of the forearm flexor compartment.
ing (MRI) were also performed (Figs. 2C–2F) for prudence as this was a rare occurrence of calcific myonecrosis in the upper extremity. The lack of enhancement, the notably elongated form, and the lack of aggressive-appearing mineralized matrix made malignancy quite unlikely. Furthermore, despite the prominent mass, there was little volume gain to this atrophied site, again suggesting that neoplasm was unlikely. The apparent latent presentation of the mineralized mass and the lack of clear trabecular bone suggested that myositis ossificans was unlikely. The latent presentation of a fusiform mineralized mass, conforming to a severely atrophied muscular compartment with a remote history of severe injury, made calcific myonecrosis the likely diagnosis. Given the patient’s history, examination, and imaging characteristics, the patient was diagnosed with calcific myonecrosis of the forearm. Biopsy was considered to confirm diagnosis. However, given the known high rate of wound complications after biopsy, a period of observation was recommended.2,32 The patient returned to the clinic 4 months later. She reported no new symptoms, no noticeable increase in the size of the mass, and diminished pain. Repeat x-rays of the forearm revealed the mass to be stable with no interval growth. The patient was advised to continue full activity and to monitor the forearm for new symptoms or enlargement. Radiographs were obtained 2 years and 3 years after initial presentation and demonstrated no significant interval change (not shown). DISCUSSION Calcific myonecrosis is itself a rare condition, with 54 cases appearing in the literature (all but one in the lower extremity) since an initial description1–31 in1960. Larson and colleagues3 reported the only case of calcific myonecrosis in the upper extremity in 2004. Nearly all
131
reported cases of calcific myonecrosis have a similar history and presentation. Typically, the patient presents with a firm, enlarging, and sometimes painful or tender mass at the site of a previous injury or trauma. Occasionally, the mass will be asymptomatic.3,5–7 The initial injury is usually a crush, fracture, or blunt trauma that caused vascular compromise or an untreated compartment syndrome 10 to 64 years before the presentation of the mass (average, 51 y after injury).2,4 There is one report of calcific myonecrosis in a patient with a history of juvenile dermatomyositis and no history of trauma.8 It is thought that neurovascular compromise leads to muscle necrosis and subsequent liquefaction and calcification of muscle tissue. The reason for the greatly delayed calcification and enlargement is unclear. Pathology reports from biopsied specimens reveal a densely fibrotic, calcified mass with the outer portion composed of hypocellular fibrous tissue and focal hemosiderin-laden macrophages.3,9,32 The interior reveals necrotic tissue with amorphous debris composed of cholesterol crystals, fibrin, and organizing thrombus9 appearing grossly as a thick reddish-brown liquid or paste.2,3,5,6,32 Calcific myonecrosis can be confidently diagnosed on radiographic and MRI studies due to its unique imaging characteristics.4,7,9,32 Calcific myonecrosis is usually first identified on plain radiographs as a fusiform mass, with its long axis paralleling the extremity and containing plaque-like, linear, or amorphous calcifications within an atrophied muscular compartment. A CT can be used to evaluate these features in finer detail to confirm muscular atrophy and the lack of aggressiveappearing mineralized matrix. However, CT is not required in every case if the radiographs and clinical history are characteristic. An MRI can also be performed for further evaluation, as it can best evaluate for solid enhancement versus cystic areas and help distinguish calcific myonecrosis from tumor.3,9,32 The differential diagnosis of calcific myonecrosis includes synovial sarcoma, epithelioid sarcoma, softtissue and parosteal osteosarcoma, myositis ossificans, diabetic myonecrosis, polymyositis or dermatomyositis, tumoral calcinosis, and posttraumatic pseudoaneurysms.4,6,8 –10,33 Calcific myonecrosis is a benign entity, although it is associated with local tissue destruction, discomfort, and deformity. In the past, management has consisted mainly of incisional biopsy or complete surgical debridement to obtain a definitive diagnosis.2,7,9 However, the complication rate after incisional or excisional biopsy of a calcific myonecrotic lesion is around 30%, principally draining sinuses and infections.2,6,7,9,11,12,19
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FIGURE 2: Restricted motion limited conventional positioning of the arm for imaging. A Anteroposterior and B lateral plain radiographs show a fusiform, densely calcified mass in a severely atrophied forearm. C Oblique coronal CT reformat image shows the mass in greater detail. D Oblique sagittal T1-weighted image demonstrates an elongated, low signal mass partially replacing severely atrophied muscle. The elongated shape would be unusual for neoplasm. E Oblique, sagittal short T1 inversion recovery image reveals similar characteristics without high signal that is typical of most tumors. F Oblique, sagittal T1 post-contrast fatsaturated image demonstrates no noteworthy enhancement within or around the mass.
In the literature, these complications usually required repeat incisions and drainages, oral or intravenous antibiotics, repeat office visits and hospital admissions, and in one case, amputation.2,11 Yet biopsy has often been the preferred plan of management to obtain a definitive diagnosis and rule out a malignant lesion. O’Dwyer and colleagues proposed in 2006 that calcific myonecrosis be considered a “don’t touch” lesion for cases in which there is a consistent history, examination, and minimal physical complaints and in which imaging shows clear characteristics of calcific myone-
crosis.32 In 2009, Muramatsu et al proposed similar recommendations.5 Observation, therefore, is becoming the preferred method of treatment for asymptomatic calcific myonecrosis, given a better understanding of the natural history of the disease and improving imaging techniques that allow for better visualization and characterization of calcific lesions.3– 6,32 Surgery might be indicated when (1) there is an infection or draining sinus that requires incision and drainage, (2) the patient’s history and advanced imaging do not provide a clear diagnosis of calcific myone-
JHS 䉬 Vol A, January
CALCIFIC MYONECROSIS OF THE UPPER EXTREMITY
crosis and there is concern for malignancy, and (3) the lesion causes major functional impairment and the patient wants improvement. Due to the high rate of complications after intralesional biopsy, O’Keefe proposed that if a biopsy is deemed necessary, surgery should be performed only when complete surgical excision is an option.7,10,12 Still lacking in the literature are recommendations for observing calcific myonecrosis. Currently, there are no recommendations on the frequency and duration to image lesions, what imaging modality is considered best for monitoring, and when regular monitoring can cease. The paucity of upper extremity cases might make the recognition and clinical diagnosis of calcific myonecrosis difficult. Since there is no typical antecedent pathology, a patient’s history might not immediately raise the suspicion of this diagnosis. Furthermore, its presentation can mimic that of a tumor or other soft tissue mass or malformation, all of which are far more common. REFERENCES 1. Gallie WE, Thomson S. Volkmann’s ischemic contracture: two case reports with identical late sequelae. Can J Surg 1960;3:164 –166. 2. Wang JW, Chen WJ. Calcific myonecrosis of the leg. Clin Orthop Relat Res 2001;389:185–190. 3. Larson RC, Sierra RJ, Sundaram M, Inwards C, Scully SP. Calcific myonecrosis: a unique presentation in the upper extremity. Skeletal Radiol 2004;33:306 –309. 4. Dhillon M, Davies AM, Benham J, Evans N, Mangham DC, Grimer RJ. Calcific myonecrosis: a report of ten new cases with an emphasis on MR imaging. Eur Radiol 2004;14:1974 –1979. 5. Muramatsu K, Ihara K, Seki T, Imagama T, Taguchi T. Calcific myonecrosis of the lower leg: diagnosis and options of treatment. Arch Orthop Trauma Surg 2009;129:935–939. 6. Janzen DL, Connell DG, Vaisler BJ. Calcific myonecrosis of the calf manifesting as an enlarging soft-tissue mass: imaging features. Am J Roentgenol 1993;160:1072–1074. 7. Holobinko JN, Damron TA, Scerpella PR, Hojnowski L. Calcific myonecrosis: keys to early recognition. Skeletal Radiol 2003;32: 35– 40. 8. Batz R, Sofka CM, Adler RS, Mintz DN, DiCarlo E. Dermatomyositis and calcific myonecrosis in the leg: ultrasound as an aid in management. Skeletal Radiol 2006;35:113–116. 9. O’Keefe RJ, O’Connell JX, Temple HT, Scully SP, Kattapuram SV, Springfield DS, et al. Calcific myonecrosis. Clin Orthop Relat Res 1995;318:205–213. 10. Zohman GL, Pierce J, Chapman MW, Greenspan A, GandourEdwards R. Calcific myonecrosis mimicking an invasive soft tissue neoplasm. J Bone Joint Surg 1998;80A:1193–1197. 11. Viau MR, Pedersen HE, Salciccoioli GG, Manoli A, II. Ectopic calcification as a late sequela of compartment syndrome. Report of two cases. Clin Orthop Relat Res 1983;176:178 –180.
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12. Snyder BJ, Oliva A, Buncke HJ. Calcific myonecrosis following compartment syndrome: report of two cases, review of the literature. J Trauma 1995;39:792–795. 13. Jassal DS, Low M, Ross LL, Zeismann M, Embil JM. Calcific myonecrosis: case report and review. Ann Plast Surg 2001;46:17– 177. 14. Tuncay IC, Demirors H, Isiklar ZU, Agildere M, Demirhan B, Tandogan RN. Calcific myonecrosis. Int Orthop 1999;23:68 –70. 15. Ryu KN, Bae DK, Park YK, Lee JH. Calcific tenosynovitis associated with calcific myonecrosis of the leg. Skeletal Radiol 1996;25: 273–275. 16. Finlay K, Friedman L, Ainsworth K. Calcific myonecrosis and tenosynovitis: sonographic findings with correlative imaging. J Clin Ultrasound 2007;35:48 –51. 17. Renwick SE, Naraghi FF, Worrell RV, Spaeth J. Cystic degeneration and calcification of muscle: late sequelae of compartment syndrome. J Orthop Trauma 1994;8:440 – 444. 18. Early JS, Ricketts DS, Hansen ST. Treatment of compartmental liquefaction as a late sequela of a lower limb compartment syndrome. J Orthop Trauma 1994;8:445– 448. 19. Malisano LP, Hunter GA. Liquefication and calcification of a chronic compartment syndrome of the lower limb. J Orthop Truama 1992;6:245–247. 20. Broder MS, Worrell RF, Shafi NQ. Cystic degeneration and calcification following ischemic paralysis of leg. Clin Orthop Relat Res 1997;122:193–195. 21. Hyder N, Shaw SL, Bollen SR. Myositis ossificans: calcification of the entire tibialis anterior after ischaemic injury (compartment syndrome). J Bone Joint Surg 1996;78B:318 –319. 22. Flinn J, Beggs I. Case of the month: Calcified leg. Br J Radiol 1996;69:371–372. 23. Rajapakse BN, Kiddle G. Calcifying haematoma mimicking a soft tissue sarcoma and myositis ossificans. ANZ J Surg 2006;76:1027– 1029. 24. Constantine S, Brennan C. Calcific myonecrosis: case report and radiopathologic correlation. Australas Radiol 2007;51:B77– 81. 25. Ozbarlas S, Kalaci A, Ozkan C, Togrul E. A previously healthy 77-year-old man with a painful mass in the calf for two months. Ann Saudi Med 2007;27:49 –50. 26. Guven M, Cakar M, Bassorgun I, Kadioglu B, Kilincoglu V, Eren A. Calcific Myonecrosis. Acta Orthop Traumatol Turc 2008;42:70 –73. 27. Okada A, Hatori M, Hosaka M, Watanuki M, Itoi E. Calcific myonecrosis and the role of imaging in the diagnosis: A case report. Ups J Med Sci 2009;114:178 –183. 28. Schneider St, Duewell St, Graf H, Forster A. Painful swollen leg 52 years after bimalleolar fracture. Praxis (Bern 1994) 2009;98:1457– 1461. 29. Papanna MC, Monga P, Wilkes RA. Post-traumatic calcific myonecrosis of the Flexor Hallucis Longus A case report and literature review. Acta Orthop Belg 2010;76:137–141. 30. Chun YS, Shim HS. Calcific myonecrosis of the antetibial area. Clin Orthop Surg 2010;2:191–194. 31. Papanikolaou A, Chini M, Pavlakis D, Lioni A, Lazanas M, Maris J. Calcific myonecrosis of the leg: Report of three patients presenting with infection. Surg Infect 2011;12:247–250. 32. O’Dwyer HM, Al-Nakshabandi NA, Al-Muzahmi K, Ryan A, O’Connell JX, Munk PL. Calcific myonecrosis: keys to recognition and management. Am J Roentgenol 2006;187:W67–W76. 33. Mirra JM. Calcific myonecrosis. Clin Orthop Relat Res 1996;327: 308 –310.
JHS 䉬 Vol A, January
Calcific Myonecrosis of the Upper Extremity: Case Report Sara D. Rynders, Yaw D. Boachie-Adjei, MD, Cree M. Gaskin, MD, A. Bobby Chhabra, MD Calcific myonecrosis is an uncommon late sequela of limb trauma that results in calcification and necrosis of damaged muscle. It almost exclusively occurs in the lower extremity. We present a second case of calcific myonecrosis in the upper extremity. (J Hand Surg 2012;37A:130–133. Copyright © 2012 by the American Society for Surgery of the Hand. All rights reserved.) Key words Calcific myonecrosis, calcific myonecrosis of the upper extremity, Volkmann’s ischemic contracture, compartment syndrome.
ALCIFIC MYONECROSIS IS a rare soft tissue condition in which severely traumatized muscle, typically from a compartment syndrome or neurovascular compromise, becomes an enlarging calcified mass, characterized by central liquefaction and tissue necrosis over a period of decades.1,2 This condition was described in 1960 by Gallie and Thomson.1 More than 50 cases of calcific myonecrosis have been reported, and all but one have occurred in the lower extremity.1–31 Larson and colleagues,3 in 2004, reported a case of calcific myonecrosis in the forearm. We report an additional case of calcific myonecrosis in the upper extremity.
C
CASE REPORT A 66-year-old, left-handed woman presented with mild right forearm pain and the sensation of a mass for 6 weeks. When she was approximately 9 years old, she experienced an elbow fracture that was treated with traction and casting. She subsequently developed a Volkmann contracture of the right hand and wrist, rendering her with little use of the right upper extremity. Twelve years before presentation, she had a wrist arthFrom the Departments of Radiology and Orthopaedic Surgery, University of Virginia, Charlottesville, VA. Received for publication August 17, 2010; accepted in revised form September 27, 2011. No benefits in any form have been received or will be received related directly or indirectly to the subject of this article. Corresponding author: A. Bobby Chhabra, MD, University of Virginia Hand Center, Department of Orthopaedic Hand Surgery, P.O. Box 800876, Charlottesville, VA 22908-0876; e-mail: [email protected]. 0363-5023/12/37A01-0023$36.00/0 doi:10.1016/j.jhsa.2011.09.035
130 䉬 © ASSH 䉬 Published by Elsevier, Inc. All rights reserved.
rodesis and ulnar head excision, and it is not known whether any masses were seen at that time on examination or imaging. She denied recent history of injury to the right forearm and described the pain as a mild, intermittent ache, centered over the middle third of the forearm. She noted a firmness to the tissue in this area. She denied paresthesias, constitutional symptoms, or history of malignancy. The patient had irritable bowel syndrome, hypertension, hyperlipidemia, osteopenia, and lumbar spine degenerative disease. There was no history of diabetes mellitus. Physical examination revealed a contracted and atrophied right forearm, wrist, and hand (Fig. 1). The elbow was non-tender, with 90° of motion and no supination or pronation. The forearm was non-tender and had a subtle prominence of the soft tissues in the dorsoradial central third. The wrist was fixed in flexion and ulnar deviation. The fingers had minimal motion, but the thumb and index finger could achieve lateral pinch. Capillary refill was less than 2 seconds, the fingers were warm, and there were 2⫹ pulses of the radial and ulnar arteries. Anteroposterior and lateral radiographs were slightly limited due to the patient’s inability to extend and supinate the forearm. (Figs. 2A, 2B). A 6.4-cm ⫻ 1.7-cm lobulated and densely calcified mass was identified on the volar mid-forearm, just ulnar and volar to the ulnar diaphysis. A smaller, flatter calcification was seen more proximally near the antecubital fossa and was 1.5 cm long. Although the radiographs were suggestive of the diagnosis of calcific myonecrosis, computed tomography (CT) and magnetic resonance imag-
CALCIFIC MYONECROSIS OF THE UPPER EXTREMITY
FIGURE 1: A 66-year-old woman with Volkmann ischemic contracture and subtle mass of the forearm flexor compartment.
ing (MRI) were also performed (Figs. 2C–2F) for prudence as this was a rare occurrence of calcific myonecrosis in the upper extremity. The lack of enhancement, the notably elongated form, and the lack of aggressive-appearing mineralized matrix made malignancy quite unlikely. Furthermore, despite the prominent mass, there was little volume gain to this atrophied site, again suggesting that neoplasm was unlikely. The apparent latent presentation of the mineralized mass and the lack of clear trabecular bone suggested that myositis ossificans was unlikely. The latent presentation of a fusiform mineralized mass, conforming to a severely atrophied muscular compartment with a remote history of severe injury, made calcific myonecrosis the likely diagnosis. Given the patient’s history, examination, and imaging characteristics, the patient was diagnosed with calcific myonecrosis of the forearm. Biopsy was considered to confirm diagnosis. However, given the known high rate of wound complications after biopsy, a period of observation was recommended.2,32 The patient returned to the clinic 4 months later. She reported no new symptoms, no noticeable increase in the size of the mass, and diminished pain. Repeat x-rays of the forearm revealed the mass to be stable with no interval growth. The patient was advised to continue full activity and to monitor the forearm for new symptoms or enlargement. Radiographs were obtained 2 years and 3 years after initial presentation and demonstrated no significant interval change (not shown). DISCUSSION Calcific myonecrosis is itself a rare condition, with 54 cases appearing in the literature (all but one in the lower extremity) since an initial description1–31 in1960. Larson and colleagues3 reported the only case of calcific myonecrosis in the upper extremity in 2004. Nearly all
131
reported cases of calcific myonecrosis have a similar history and presentation. Typically, the patient presents with a firm, enlarging, and sometimes painful or tender mass at the site of a previous injury or trauma. Occasionally, the mass will be asymptomatic.3,5–7 The initial injury is usually a crush, fracture, or blunt trauma that caused vascular compromise or an untreated compartment syndrome 10 to 64 years before the presentation of the mass (average, 51 y after injury).2,4 There is one report of calcific myonecrosis in a patient with a history of juvenile dermatomyositis and no history of trauma.8 It is thought that neurovascular compromise leads to muscle necrosis and subsequent liquefaction and calcification of muscle tissue. The reason for the greatly delayed calcification and enlargement is unclear. Pathology reports from biopsied specimens reveal a densely fibrotic, calcified mass with the outer portion composed of hypocellular fibrous tissue and focal hemosiderin-laden macrophages.3,9,32 The interior reveals necrotic tissue with amorphous debris composed of cholesterol crystals, fibrin, and organizing thrombus9 appearing grossly as a thick reddish-brown liquid or paste.2,3,5,6,32 Calcific myonecrosis can be confidently diagnosed on radiographic and MRI studies due to its unique imaging characteristics.4,7,9,32 Calcific myonecrosis is usually first identified on plain radiographs as a fusiform mass, with its long axis paralleling the extremity and containing plaque-like, linear, or amorphous calcifications within an atrophied muscular compartment. A CT can be used to evaluate these features in finer detail to confirm muscular atrophy and the lack of aggressiveappearing mineralized matrix. However, CT is not required in every case if the radiographs and clinical history are characteristic. An MRI can also be performed for further evaluation, as it can best evaluate for solid enhancement versus cystic areas and help distinguish calcific myonecrosis from tumor.3,9,32 The differential diagnosis of calcific myonecrosis includes synovial sarcoma, epithelioid sarcoma, softtissue and parosteal osteosarcoma, myositis ossificans, diabetic myonecrosis, polymyositis or dermatomyositis, tumoral calcinosis, and posttraumatic pseudoaneurysms.4,6,8 –10,33 Calcific myonecrosis is a benign entity, although it is associated with local tissue destruction, discomfort, and deformity. In the past, management has consisted mainly of incisional biopsy or complete surgical debridement to obtain a definitive diagnosis.2,7,9 However, the complication rate after incisional or excisional biopsy of a calcific myonecrotic lesion is around 30%, principally draining sinuses and infections.2,6,7,9,11,12,19
JHS 䉬 Vol A, January
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CALCIFIC MYONECROSIS OF THE UPPER EXTREMITY
FIGURE 2: Restricted motion limited conventional positioning of the arm for imaging. A Anteroposterior and B lateral plain radiographs show a fusiform, densely calcified mass in a severely atrophied forearm. C Oblique coronal CT reformat image shows the mass in greater detail. D Oblique sagittal T1-weighted image demonstrates an elongated, low signal mass partially replacing severely atrophied muscle. The elongated shape would be unusual for neoplasm. E Oblique, sagittal short T1 inversion recovery image reveals similar characteristics without high signal that is typical of most tumors. F Oblique, sagittal T1 post-contrast fatsaturated image demonstrates no noteworthy enhancement within or around the mass.
In the literature, these complications usually required repeat incisions and drainages, oral or intravenous antibiotics, repeat office visits and hospital admissions, and in one case, amputation.2,11 Yet biopsy has often been the preferred plan of management to obtain a definitive diagnosis and rule out a malignant lesion. O’Dwyer and colleagues proposed in 2006 that calcific myonecrosis be considered a “don’t touch” lesion for cases in which there is a consistent history, examination, and minimal physical complaints and in which imaging shows clear characteristics of calcific myone-
crosis.32 In 2009, Muramatsu et al proposed similar recommendations.5 Observation, therefore, is becoming the preferred method of treatment for asymptomatic calcific myonecrosis, given a better understanding of the natural history of the disease and improving imaging techniques that allow for better visualization and characterization of calcific lesions.3– 6,32 Surgery might be indicated when (1) there is an infection or draining sinus that requires incision and drainage, (2) the patient’s history and advanced imaging do not provide a clear diagnosis of calcific myone-
JHS 䉬 Vol A, January
CALCIFIC MYONECROSIS OF THE UPPER EXTREMITY
crosis and there is concern for malignancy, and (3) the lesion causes major functional impairment and the patient wants improvement. Due to the high rate of complications after intralesional biopsy, O’Keefe proposed that if a biopsy is deemed necessary, surgery should be performed only when complete surgical excision is an option.7,10,12 Still lacking in the literature are recommendations for observing calcific myonecrosis. Currently, there are no recommendations on the frequency and duration to image lesions, what imaging modality is considered best for monitoring, and when regular monitoring can cease. The paucity of upper extremity cases might make the recognition and clinical diagnosis of calcific myonecrosis difficult. Since there is no typical antecedent pathology, a patient’s history might not immediately raise the suspicion of this diagnosis. Furthermore, its presentation can mimic that of a tumor or other soft tissue mass or malformation, all of which are far more common. REFERENCES 1. Gallie WE, Thomson S. Volkmann’s ischemic contracture: two case reports with identical late sequelae. Can J Surg 1960;3:164 –166. 2. Wang JW, Chen WJ. Calcific myonecrosis of the leg. Clin Orthop Relat Res 2001;389:185–190. 3. Larson RC, Sierra RJ, Sundaram M, Inwards C, Scully SP. Calcific myonecrosis: a unique presentation in the upper extremity. Skeletal Radiol 2004;33:306 –309. 4. Dhillon M, Davies AM, Benham J, Evans N, Mangham DC, Grimer RJ. Calcific myonecrosis: a report of ten new cases with an emphasis on MR imaging. Eur Radiol 2004;14:1974 –1979. 5. Muramatsu K, Ihara K, Seki T, Imagama T, Taguchi T. Calcific myonecrosis of the lower leg: diagnosis and options of treatment. Arch Orthop Trauma Surg 2009;129:935–939. 6. Janzen DL, Connell DG, Vaisler BJ. Calcific myonecrosis of the calf manifesting as an enlarging soft-tissue mass: imaging features. Am J Roentgenol 1993;160:1072–1074. 7. Holobinko JN, Damron TA, Scerpella PR, Hojnowski L. Calcific myonecrosis: keys to early recognition. Skeletal Radiol 2003;32: 35– 40. 8. Batz R, Sofka CM, Adler RS, Mintz DN, DiCarlo E. Dermatomyositis and calcific myonecrosis in the leg: ultrasound as an aid in management. Skeletal Radiol 2006;35:113–116. 9. O’Keefe RJ, O’Connell JX, Temple HT, Scully SP, Kattapuram SV, Springfield DS, et al. Calcific myonecrosis. Clin Orthop Relat Res 1995;318:205–213. 10. Zohman GL, Pierce J, Chapman MW, Greenspan A, GandourEdwards R. Calcific myonecrosis mimicking an invasive soft tissue neoplasm. J Bone Joint Surg 1998;80A:1193–1197. 11. Viau MR, Pedersen HE, Salciccoioli GG, Manoli A, II. Ectopic calcification as a late sequela of compartment syndrome. Report of two cases. Clin Orthop Relat Res 1983;176:178 –180.
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