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The Journal of Bone and Joint Surgery (American) 80:262-7 (1998)
© 1998 The Journal of Bone and Joint Surgery, Inc.

Idiopathic Necrosis of Skeletal Muscle in Patients Who Have Diabetes. Report of Four Cases and Review of the Literature*

TIMOTHY A. DAMRON, M.D.{dagger}, E. MARK LEVINSOHN, M.D.{ddagger}, THOMAS M. MCQUAIL, M.D.{dagger}, HAL COHEN, M.D.{dagger}, MICHAEL STADNICK, M.D.{dagger} and MICHELE ROONEY, M.D.{dagger}, SYRACUSE, NEW YORK

Investigation performed at the Departments of Orthopedic Surgery, Radiology, and Pathology, State University of New York at Syracuse, and the Department of Radiology, Crouse Hospital, Syracuse

Infarction of skeletal muscle in patients who have diabetes is an infrequently recognized clinicopathological entity1-17. Most of the reports on this condition have appeared in journals and textbooks on internal medicine and radiology. Radiographically, the lesion may be misinterpreted as a soft-tissue sarcoma or infection, in which case the patient may be referred to an orthopaedic surgeon. The mean age of the four patients reported on here was forty-two years (range, twenty-eight to fifty-nine years). The patients had sought medical attention because of an exquisitely tender swelling of the anterior aspect of the thigh, which had been present for ten days to four weeks before the initial evaluation. Two patients had a history of insulin-dependent diabetes, one had a history of non-insulin-dependent diabetes, and one was diagnosed with diabetes at the time of the initial evaluation. Three patients had no evidence of recurrence after a mean duration of follow-up of thirty-one months (range, twenty-four to forty-two months). The fourth patient had recurrence of the muscular necrosis and died six months later as a result of diabetic complications.
    Case Reports
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 Case Reports
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 References
 
CASE 1. A fifty-nine-year-old white man who had insulin-dependent diabetes mellitus was seen because of a three-week history of swelling of the distal two-thirds of the right thigh. The swelling had decreased during the week before the evaluation, leaving an exquisitely tender palpable mass. The patient had a twelve-year history of diabetes mellitus and had used thirty-five units of neutral protamine Hagedorn insulin each day for ten years. He had diabetic retinopathy and neuropathy but no evidence of nephropathy. He also had hypertension and coronary artery disease. Physical examination revealed an extremely tender mass, eight by five centimeters, in the anteromedial aspect of the distal part of the right thigh. Mild swelling was observed in the region of the vastus medialis muscle. The mass was not adherent to the skin, and the skin was neither warm nor erythematous. There was no evidence of adenopathy. The circumference of the right thigh was 1.5 centimeters greater than that of the left thigh. The ranges of motion of the hip and knee were within normal limits and were painless. The results of the neurological examination were normal, and peripheral pulses were symmetrically palpable. The erythrocyte sedimentation rate was elevated (sixty-nine millimeters per hour; normal, zero to twenty millimeters per hour), and the partial thromboplastin time was prolonged (46.2 seconds; normal, 21.7 to 33.4 seconds). The total white blood-cell count and differential; the levels of potassium, creatine kinase, creatinine, and blood urea nitrogen; the prothrombin time; the bleeding time; and the levels of fibrin split products and D-dimer were all normal. Urinalysis showed 3+ protein and 1+ hemoglobin. Plain radiographs of the thigh revealed normal findings. Magnetic resonance images, made before and after the intravenous administration of gadolinium, showed increased signal intensity within the vastus medialis muscle and portions of the vastus lateralis muscle (Figs. 1-A, 1-B, and 1-C). T1-weighted images demonstrated diffuse enlargement of the distal half of the vastus medialis muscle as well as a small area of intermediate signal intensity, which was suggestive of loculated fluid. Because of the possibility that the mass was a soft-tissue sarcoma, a complete staging evaluation was performed. A bone scan showed increased activity in the soft tissues of the right thigh but demonstrated no osseous abnormalities. Plain radiographs and computerized tomography scans of the chest revealed normal findings. An open incisional biopsy was performed. The surface of the vastus medialis muscle appeared cloudy and edematous, and the muscle fibers consisted of gray, poorly vascularized tissue. A small collection of serosanguineous fluid was found to be enclosed within the muscle fibers. Histopathological evaluation showed extensive necrosis of the muscle with signs of early organization and focal prominence of inflammatory cells (Fig. 1-D). The biopsy site healed with no complications. The patient initially had severe pain. He walked with crutches and was allowed to bear weight as tolerated. He stopped using the crutches within a few weeks and continued to improve slowly over the ensuing months. Physical therapy, range-of-motion and strengthening exercises, lifting, squatting, and yard work were not allowed during the first six months. He gradually returned to his former activities. The swelling resolved after six months, and there was no residual palpable soft-tissue mass. By twenty-eight months, the patient had had no recurrence of symptoms but still had subjective weakness of the lower extremity during daily activities, particularly when he attempted to stand from a seated position. At that time, the strength of the quadriceps was graded as 4 of 5 on manual muscle-testing. CASE 2. A twenty-eight-year-old black woman who had insulin-dependent diabetes was evaluated in September 1976 because of a two-month history of painful swelling of the left thigh. (This case was briefly discussed, without mention of follow-up, in a previous report10.) The results of a venogram were normal, and no organisms grew on culture of blood and aspirate from the ipsilateral knee. The swelling resolved spontaneously over the next two months. Eighteen months later, in March 1978, the patient was admitted to our hospital because of a ten-day history of recurrent painful swelling of the left thigh. The swelling was accompanied by malaise, nausea, vomiting, anasarca, and bilateral pleural effusion. The knee was held in a flexed position, and attempts to extend it were painful; the patient could tolerate an arc of motion of only 15 degrees. The thigh was warm, firm, and extremely tender over the distal part of the quadriceps muscle. The circumference of the left thigh, measured at a point ten centimeters proximal to the superior pole of the patella, was five centimeters greater than that of the right thigh. Although there was effusion in both knees, the finding was more pronounced on the left. The Homans sign was negative, and light-touch sensation was symmetrically diminished over the distal third of each leg. On admission, the erythrocyte sedimentation rate was 104 millimeters per hour (normal, zero to twenty millimeters per hour) and the white blood-cell count was 8.9 x 109per liter (normal, 4.0 to 10.0 x 109per liter) with 42 per cent bands (normal, 0 to 7 per cent bands) and 30 per cent neutrophils (normal, 33 to 73 per cent neutrophils). The patient had low levels of hemoglobin (seventy-three grams per liter; normal, 115 to 155 grams per liter) and albumin (twenty-nine grams per liter; normal, forty to fifty-two grams per liter), a low hematocrit (23 per cent; normal, 36 to 45 per cent), and elevated levels of creatine kinase (240 units per liter; normal, thirty to 160 units per liter), glucose (17.2 millimoles per liter; normal, 3.9 to 6.7 millimoles per liter), creatinine (230 micromoles per liter; normal, fifty-three to 106 micromoles per liter), blood urea nitrogen (16.8 millimoles per liter; normal, 2.1 to 7.1 millimoles per liter), and potassium (5.4 millimoles per liter; normal, 3.5 to 5.0 millimoles per liter). Tests for rheumatoid factor and antinuclear antibody were negative. Urinalysis showed 4+ glucose and 4+ protein. Two separate aspirations of the effusion in the left knee, performed during the first week of hospitalization, revealed straw-colored clear fluid. Laboratory evaluation of this fluid demonstrated no cells or organisms on gram-staining, no growth on culture, and no crystals. The patient was evaluated extensively by internists and nephrologists because of the nephrotic syndrome and associated anasarca. She was managed with diuretics, restriction of fluids, and repeated pleurocentesis. The swelling in the thigh was evaluated by consultants from the departments of rheumatology, orthopaedic surgery, general surgery, and neurology. The differential diagnoses included soft-tissue sarcoma, abscess, cellulitis, deep venous thrombosis, osteomyelitis, phlebitis, tuberculosis, gout, collagen vascular disease, and myositis. Plain radiographs showed a non-specific soft-tissue swelling. A venogram revealed normal findings. A bone scan showed increased nuclide activity in both knees, which was suggestive of osteoarthrosis, as well as non-specific nuclide activity in the distal portion of the left thigh, which was consistent with soft-tissue inflammation. Once the fluid overload was under reasonable control, the swelling became circumscribed to a ten-centimeter area over the anterior aspect of the distal portion of the left thigh. Ultrasonography showed swelling within the quadriceps muscle and no evidence of a discrete mass or a collection of fluid. Computerized tomography demonstrated edema of the quadriceps and biceps femoris muscles. The level of creatine kinase was 422 units per liter, with 100 per cent type-MM creatine kinase when fractionation was performed. On the basis of these findings, the presumptive diagnosis was myositis; a biopsy was not performed because the swelling and pain had decreased. The pain in the left thigh increased during the fourth week of hospitalization, and an open incisional biopsy was performed. The tissues could not be analyzed because they had been crushed. Six weeks after admission, shortly after physical therapy had been started in order to increase the range of motion and the strength of the knee and to enhance the ability to walk, the pain and swelling in the anteromedial portion of the thigh worsened. A second open incisional biopsy of the vastus medialis muscle, performed during the eighth week of hospitalization, revealed necrosis of skeletal muscle with areas of intense infiltration by polymorphonuclear leukocytes and other areas of reparative granulation tissue, which were suggestive of an old injury. Physical therapy was continued, as tolerated, from the sixth through the tenth week of hospitalization, with efforts being increasingly focused on walking rather than on range of motion and strengthening. At the time of discharge, in May 1978, the patient was able to walk with the support of a Swedish knee cage (a metal and leather orthosis that allows flexion but prevents hyperextension of the knee). Physical therapy was continued until medical complications made it impossible. The patient died as a result of diabetic complications in September 1978. CASE 3. A thirty-one-year-old white man was seen in 1993 because of a three-week history of swelling of the right thigh. The patient had pain in the medial aspect of the thigh when walking and was unable to flex the knee completely without increased pain. He recalled no traumatic episode and had continued to work despite the discomfort. The symptoms had not responded to the use of ice, non-steroidal anti-inflammatory medication, elevation of the extremity, or chiropractic manipulation. He had no history of medical illness, but he reported the recent onset of fatigue, malaise, polydipsia, and polyuria. Physical examination revealed a soft-tissue swelling of the anteromedial aspect of the distal portion of the right thigh; the swelling began approximately ten centimeters proximal to the medial femoral condyle and extended distally to the level of that structure. The mass was moderately firm, elliptical, and exquisitely tender; it was located deeply and was wrapped around the anteromedial portion of the thigh. There was no localized or generalized adenopathy, fluctuance, venous distension, erythema, or warmth. The patient had an antalgic gait, and flexion of the knee beyond 120 degrees was painful. Plain radiographs of the thigh demonstrated a soft-tissue mass. Venous Doppler ultrasonography was negative for deep venous thrombosis. Ultrasonography of the thigh showed diffuse soft-tissue swelling with decreased echogenicity in the medial portion of the quadriceps muscle. Magnetic resonance images showed increased signal intensity within the vastus medialis and sartorius muscles, and a provisional diagnosis of spontaneous infarction of skeletal muscle was considered. The level of fasting blood glucose was elevated (22.9 millimoles per liter; normal, 3.6 to 6.1 millimoles per liter), and urinalysis showed evidence of glucosuria and ketonuria. Blood-gas analysis indicated metabolic acidosis with a compensatory respiratory alkalosis. A diagnosis of diabetes was made, and insulin therapy was initiated. A biopsy was not performed, as the findings on imaging studies suggested muscular necrosis. No improvement was observed during the first four weeks. Over the subsequent two weeks, the swelling and pain resolved and the patient was allowed to walk, to perform range-of-motion exercises, and to participate in his regular daily activities. Formal physical therapy was intentionally withheld in order to minimize the likelihood of exacerbating the symptoms. The swelling and pain had resolved completely by three months. The patient had noticed tingling, and had diminished sensation to pinprick, in the toes of both feet. There was no evidence of recurrence three years and six months after the diagnosis had been made. CASE 4. A forty-eight-year-old black man was seen because of a four-week history of a tender mass in the anteromedial aspect of the right thigh, with pain and tightness that were localized to the region of the mass without proximal or distal radiation or extension. The tightness and the size of the mass had decreased within the previous week. The patient recalled no precipitating injury and reported that no similar episodes had occurred previously. Rest and heat had not alleviated the symptoms. A diagnosis of non-insulin-dependent diabetes mellitus had been made fifteen years earlier; at the time of presentation to us, the patient had diabetic retinopathy, neuropathy, nephropathy, and nephrotic syndrome. He also was being managed for hypertension. On physical examination, the blood pressure was 160/102 millimeters of mercury (21.33/13.60 kilopascals), the heart rate was regular, and the respirations were non-labored. A firm, tender mass, four by five centimeters, was found in the region of the vastus medialis muscle; the mass extended proximally from the superomedial corner of the proximal pole of the patella. The skin overlying the mass was taut, making it difficult to determine if the mass involved the subcutaneous or deeper tissues. There was no overlying erythema or warmth. The ranges of motion of the hip and knee were full and painless. There was no evidence of effusion in the knee or of joint-line tenderness. The calf was supple to palpation and free of swelling and tenderness. Neurological examination showed bilateral symmetrically diminished sensation to light touch in a stocking distribution. Manual muscle-testing revealed no motor weakness. Distal pulses were symmetrically palpable. The patient walked with a noticeable limp. The white blood-cell count, the level of hemoglobin, the hematocrit, and the level of potassium were normal. The levels of blood glucose (17.2 millimoles per liter), blood urea nitrogen (33.9 millimoles per liter), and creatinine (460 micromoles per liter) were elevated. Plain radiographs showed mild osteoarthrosis of the knee with no other osseous changes. T2-weighted magnetic resonance images demonstrated a homogeneous increase in signal intensity in the vastus medialis muscle, extending proximally for a distance of approximately fifteen centimeters from the attachment of the medial patellar retinaculum. On T1-weighted images, this region demonstrated slightly greater signal intensity than did the adjacent muscles. In addition, T2-weighted images demonstrated a small region of increased signal intensity within the posterior aspect of the vastus lateralis muscle, extending five centimeters proximally from the superior pole of the patella. A similar area of increased signal intensity was seen in the adjacent biceps femoris muscle. A mild joint effusion was identified, and no abnormality of the marrow was evident. T2-weighted images also demonstrated increased signal intensity in the subcutaneous fat about the distal portion of the thigh; this finding was consistent with edema. A biopsy was not performed because the symptoms had subsided, the size of the mass had decreased, and the findings on magnetic resonance imaging were suggestive of muscular necrosis. The patient was instructed to take time off from work in order to avoid the prolonged standing inherent in his job. He was managed at home with rest, the avoidance of strenuous activities, and the application of warm, moist compresses to the distal part of the thigh. Physical therapy was not ordered because the condition of the patient was improving. Three weeks after the initial evaluation and seven weeks after the onset of symptoms, the patient returned to work and was asymptomatic. Physical examination at that time showed the mass to be non-tender and to be further decreased in size. The limp had resolved. The patient was allowed to return to his previous activities as tolerated. Two years after the onset of symptoms, there was no evidence of recurrence.
    Discussion
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 Case Reports
 Discussion
 References
 
Necrosis of skeletal muscle in patients who have diabetes has been called tumoriform focal muscular degeneration and idiopathic diabetic muscle infarction1-17. Patients usually are seen because of swelling of the lower extremity with exquisite tenderness and pain that have been present for a short time (one month or less). The differential diagnosis includes soft-tissue neoplasm, abscess, intramuscular hematoma, deep venous thrombosis, and myositis. Necrosis of skeletal muscle must be considered during the evaluation of a patient who has diabetes mellitus and a mass involving skeletal muscle. The blood-cell count, the coagulation profile, and the levels of electrolytes and creatine kinase usually are normal1-17. Plain radiographs are rarely helpful except for the exclusion of a primary osseous process. Radionuclide scanning may show mild, non-specific uptake in the soft tissues in the region of the mass. Computerized tomography and magnetic resonance imaging are frequently useful for defining the extent of the process and for excluding neoplasm, abscess, and hematoma. The appearance of diabetic necrosis of skeletal muscle on magnetic resonance imaging is characterized by the absence of a discrete mass and the involvement of at least one major muscle group by a signal pattern that is indicative of intramuscular edema associated with an underlying inflammatory reaction (Fig. 1-B). This pattern consists of markedly increased signal intensity on T2-weighted images and slightly increased signal intensity on T1-weighted and proton-density-weighted images (Fig. 1-C). The histological findings consist of hemorrhagic necrosis of skeletal muscle and microangiopathy. The simultaneous presence of various stages of necrosis, degeneration, and regeneration of muscle is not uncommon (Fig. 1-D). Arteriosclerotic changes in the larger vessels have also been observed1-17. Banker and Chester proposed two theories regarding the etiology of diabetic necrosis of skeletal muscle. In their initial report2, those authors hypothesized that embolization from atherosclerotic plaques led to the necrosis. This hypothesis was supported by the postmortem finding of ulcerated plaques in the abdominal aorta of one of their two patients. In a later study, however, those authors were unable to find evidence of a potential embolic source in four other patients7. They postulated that atherosclerotic obliteration was the cause of muscular necrosis because these four patients had evidence of extensive arterial occlusive disease in the skeletal muscles, kidneys, and heart. Those authors believed that inadequate perfusion and resultant anoxia led to a mild compartment syndrome with worsening ischemia. Other authors have not found concomitant systemic arteriosclerotic disease9. There is no widely accepted treatment for diabetic necrosis of skeletal muscle as the symptoms usually resolve without intervention2,4,7,9,12,14,16,17. Initially, Banker and Chester2,7recommended an exercise program and walking within a few days after the biopsy. However, two of their patients had recurrent hemorrhage after excision of the entire abnormal muscle, and both patients needed a transfusion. In addition, the recovery period was prolonged because of repeated episodes of swelling. The iatrogenic complications that have been reported in the literature appear to have occurred only when attempts were made to excise the involved muscles and physical therapy was begun early in the postoperative period2,7. A number of authors have reported on patients in whom necrosis of skeletal muscle developed in the contralateral extremity2,4,12,17. We reviewed the reports of twenty-five patients who had diabetic necrosis of skeletal muscle1-17. Angervall and Stener apparently were the first to describe this entity, in 1965. Those authors reported on two patients and called the lesion tumoriform focal muscular degeneration. Chester and Banker2,7reported on six patients who were seen over a period of twenty years; to our knowledge, that has been the largest series to date. The mean age of the twenty-five patients described in the literature was thirty-seven years (range, twenty-five to fifty-seven years). Eleven patients were female, and thirteen patients were male; the gender of one patient was not recorded. The patients had had diabetes for a mean of sixteen years (range, two to twenty-seven years) and had taken insulin for a mean of fourteen years (range, zero to twenty-one years). The mean duration of symptoms before the initial examination was four weeks (range, two days to more than twelve weeks); twenty-three patients had had symptoms for four weeks or less. Although information regarding diabetic complications was not provided for every patient, a review of the available data revealed that twenty of twenty-two patients had nephropathy, seventeen of twenty had retinopathy, and twelve of fourteen had neuropathy. The swelling characteristically involved the large muscles of the thigh: the quadriceps was affected in sixteen patients, the hip abductors were affected in four6,8,14, and the hamstrings were affected in four3,6,9. In addition, the gastrocnemius-soleus was affected in four patients5,7,16,17. The largest dimension of the mass was a mean of seven centimeters (range, three to twelve centimeters). The authors of two of the earliest reports documented several complications after excisional biopsy2,7. However, no complications were found after incisional biopsy in twelve patients who were described in other studies8,13. Treatment usually has been directed toward alleviation of the symptoms and has included analgesics, rest, and immobilization2,7,8,15,17. Two of the twenty-five patients described in the literature needed additional insulin to control the diabetes while the mass was present1. Non-steroidal anti-inflammatory medications and nerve blocks were used for some patients4,8. The symptoms were reported to resolve slowly over six weeks to six or seven months after the initiation of treatment2,7,9,12,14,16,17. When physical therapy was begun within the first few weeks after the diagnosis had been made, however, the symptoms were exacerbated2,7,17. Eight patients had necrosis of skeletal muscle in the contralateral extremity within two years after the initial episode2,4,12,17. Seven of the twenty-five patients died of renal failure, between one and four years after the diagnosis had been made1-3,7. The features of the four patients in the current series were similar to those of the patients described in the literature. Three of the four patients had long-standing diabetes and associated complications. Incisional biopsy did not lead to complications in either of the two patients for whom that procedure was done. A biopsy was not performed for the other two patients because the findings on the imaging studies and the clinical appearance were fairly characteristic of necrosis of skeletal muscle and because the symptoms and swelling progressively resolved under close clinical observation. All patients were managed symptomatically, and the symptoms resolved within six months after the diagnosis. Early physical therapy led to an exacerbation of symptoms in the only patient for whom it was used. Necrosis of skeletal muscle developed in the contralateral extremity of one patient. One patient died as a result of medical complications within six months after the diagnosis. We believe that one of our patients (Case 1), who was fifty-nine years old at the time of diagnosis, is one of the oldest such patients reported on to date; that one (Case 3) is the first such patient to have had muscular infarction as the earliest manifestation of diabetes; and that one (Case 4) is the second of only two such patients to have had non-insulin-dependent diabetes mellitus. The apparent rarity of diabetic necrosis of skeletal muscle may make it difficult for clinicians and radiologists to become familiar with this entity. The clinical features that are highly suggestive of the diagnosis include involvement of more than one muscle group, diffuse swelling within involved muscles rather than displacement of normal structures by a mass, a short duration of symptoms (one month or less), exquisite tenderness, and a history of long-standing diabetes. We recommend that the evaluation of a painful swelling in the extremity of a patient who has diabetes should include plain radiography and magnetic resonance imaging. Magnetic resonance scans are preferable to computerized tomography scans for the evaluation of a soft-tissue lesion as they can help to determine the area and path of the biopsy, confirm the diagnosis, and corroborate the histopathological findings. The appearance of this entity on magnetic resonance scans is fairly characteristic. We believe that the potential risks of delaying the diagnosis of a soft-tissue sarcoma far outweigh the risk associated with a biopsy. NOTE: The authors thank Raymond J. Meeks, M.D., Hamilton, New York, and Anna Marie Ward, M.D., Norwich, New York, for providing clinical information on one of the patients described here (Case 3).


Figure 01
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Figs. 1-A through 1-D: Case 1. Fig. 1-A: T1-weighted axial magnetic resonance image made through the middle third of both thighs after the intravenous administration of gadolinium. There is increased signal intensity within the right vastus medialis muscle (Vm) and part of the vastus lateralis muscle, with diffuse swelling of the vastus medialis muscle and of the overlying subcutaneous fat. The remaining muscles and the neurovascular structures are normal. There is a small region of intermediate signal intensity (arrow) medially, which was found at the time of the biopsy to be an intramuscular collection of fluid. The cortical bone and the marrow space appear normal. The left thigh is normal.

 

Figure 02
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Fig. 1-B T2-weighted axial magnetic resonance image, made through the middle portion of the right thigh, showing increased signal intensity within the entire vastus medialis muscle (Vm); this finding was indicative of generalized edema. Areas of increased signal intensity also are seen in the vastus lateralis muscle. The thigh is otherwise normal.

 

Figure 03
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Fig. 1-C Proton-density-weighted coronal magnetic resonance image, made through both thighs, showing generalized swelling with diffusely increased signal intensity in the right vastus medialis muscle (Vm). The cortical bone and the marrow appear normal. The left thigh is normal. F = femur. (Reprinted, with permission, from: Damron, T. A., and Sim, F. H.: Soft-tissue tumors about the knee. J. Am. Acad. Orthop. Surg., 5: 146, 1997.)

 

Figure 04
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Fig. 1-D Photomicrograph revealing acute necrosis of skeletal muscle and associated soft tissues. The arrows indicate degenerating muscle fibers (hematoxylin and eosin, x100).

 
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

{dagger}Departments of Orthopedic Surgery (T. A. D. and T. M. McQ.), Radiology (H. C. and M. S.), and Pathology (M. R.), State University of New York at Syracuse, 550 Harrison Center, Syracuse, New York 13202. E-mail address for Dr. Damron: damront@vax.cs.hscsyr.edu.

{ddagger}Crouse Hospital, 736 Irving Avenue, Syracuse, New York 13210.


    References
 Top
 Case Reports
 Discussion
 References
 

  1. Angervall, L., Stener, B. Tumoriform focal muscular degeneration in two diabetic patients. Diabetologia, 1: 39-42. 1965;
  2. Banker, B. Q., Chester, C. S. Infarction of thigh muscle in the diabetic patient. Neurology, 23: 667-677. 1973;[Free Full Text]
  3. Barohn, R. J., Kissel, J. T. Case-of-the-month: painful thigh mass in a young woman: diabetic muscle infarction. Muscle and Nerve, 15: 850-855. 1992;[Medline]
  4. Barton, K. L., Palmer, B. F. Bilateral infarction of the vastus lateralis muscle in a diabetic patient: a case report and review of the literature. J. Diabetes and Complicat., 7: 221-223. 1993;
  5. Boluda, B., Mesa, J., Obiols, G., Simo, R. Focal muscle infarction in a diabetic. Diabete Metabol., 15: 269-270. 1989;
  6. Chason, D. P., Fleckenstein, J. L., Burns, D. K., Rojas, G. Diabetic muscle infarction: radiologic evaluation. Skel. Radiol., 25: 127-132. 1996;[Medline]
  7. Chester, C. S., Banker, B. Q. Focal infarction of muscle in diabetics. Diabetes Care, 9: 623-630. 1986;[Abstract]
  8. Hinton, A., Heinrich, S. D., Craver, R. Idiopathic diabetic muscular infarction: the role of ultrasound, CT, MRI, and biopsy. Orthopedics, 16: 623-625. 1993;[Medline]
  9. Lauro, G. R., Kissel, J. T., Simon, S. R. Idiopathic muscular infarction in a diabetic patient. Report of a case. J. Bone and Joint Surg., 73-A: 301-304. Feb. 1991;[Free Full Text]
  10. Levinsohn, E. M., Bryan, P. J. Computed tomography in unilateral extremity swelling of unusual cause. J. Comput. Assist. Tomog., 3: 67-70. 1979;[Medline]
  11. Mirra, J. M. Letter to the editor. Clin. Orthop., 327: 308-310. 1996;
  12. Nunez-Hoyo, M., Gardner, C. L., Motta, A. O., Ashmead, J. W. Skeletal muscle infarction in diabetes: MR findings. J. Comput. Assist. Tomog., 18: 986-988. 1993;
  13. Ratliff, J. L., Matthews, J., Blalock, J. C., Kasin, J. V. Infarction of the quadriceps muscle: a complication of diabetic vasculopathy. Southern Med. J., 79: 1595. 1986;[Medline]
  14. Reich, S., Wiener, S. N., Chester, S., Ruff, R. Clinical and radiologic features of spontaneous muscle infarction in the diabetic. Clin. Nucl. Med., 10: 876-879. 1985;[Medline]
  15. Rocca, P. V., Alloway, J. A., Nashel, D. J. Diabetic muscular infarction. Sem. Arthrit. and Rheumat., 22: 280-287. 1993;
  16. Vande Berg, B., Malghem, J., Putteman, T., Vandeleene, B., Lagneau, G., Meldague, B. Idiopathic muscular infarction in a diabetic patient. Skel. Radiol., 25: 183-185. 1996;[Medline]
  17. Van Slyke, M. A., Ostrov, B. E. MRI evaluation of diabetic muscle infarction. Magnet. Reson. Imag., 13: 325-329. 1995;

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