(Radiology. 1999;211:241-247.)
© RSNA, 1999
Muscle Infarction in Patients with Diabetes Mellitus: MR Imaging Findings1
James S. Jelinek, MD,
Mark D. Murphey, MD,
Albert J. Aboulafia, MD,
Robert G. Dussault, MD,
Phoebe A. Kaplan, MD and
William N. Snearly, MD 1
1 From the Depts of Radiology and Orthopedic Oncology, Washington Hospital Center, 110 Irving St, NW, Washington, DC 20010 (J.S.J.); Dept of Radiologic Pathology, Armed Forces Institute of Pathology, Washington, DC (J.S.J., M.D.M.); Dept of Radiology, University of Maryland School of Medicine, Baltimore (M.D.M.); Depts of Radiology and Nuclear Medicine, Uniformed Services University of the Health Sciences, Bethesda, Md (M.D.M.); Section of Orthopedics, Emory University School of Medicine, Atlanta, Ga (A.J.A.); and Dept of Radiology, University of Virginia, Health Sciences Center, Charlottesville (R.G.D., P.A.K., W.N.S.). From the 1997 RSNA scientific assembly. Received Nov 18, 1997; revision requested Feb 5, 1998; final revision received Aug 20; accepted Nov 6. Address reprint requests to J.S.J.
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Abstract
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PURPOSE: To describe the magnetic resonance (MR) imaging findings in diabetic patients with muscle infarction and to describe commonly associated clinical features.
MATERIALS AND METHODS: The MR imaging studies of 21 patients with diabetic muscle infarction were reviewed retrospectively. Of the 21 patients, 12 were women, and nine were men; the mean age was 48 years (range, 30–77 years).
RESULTS: Eight patients had bilateral lower-extremity involvement; six had involvement confined to the right lower extremity and seven to the left. The thigh was involved in 17 patients (81%). One or more of the musculi vastus, the most frequently affected muscle group, were affected in 16 patients (76%). Four patients (19%) had isolated calf involvement. MR imaging studies showed diffuse enlargement of involved muscle groups and partial loss of normal fatty intermuscular septa. MR imaging also allowed identification of areas of subfascial fluid in 16 patients (76%) and subcutaneous edema in 19 patients (90%). MR imaging showed involved muscle groups best with T2-weighted, inversion-recovery, and gadolinium-enhanced sequences, where the infarcted muscles appeared diffusely hyperintense compared with adjacent muscles. Comparison of T2-weighted and gadolinium-enhanced MR images of nine patients showed enlarged, enhancing muscles in all patients and small, focal, rim-enhancing fluid collections in six of nine patients (66%).
CONCLUSION: Diabetic muscle infarction is suggested in diabetic patients with sudden onset of severe pain in the thigh or calf muscles who have MR imaging findings of diffuse edema and swelling of multiple thigh and calf muscles (often in more than one compartment).
Index terms: Diabetes mellitus, complications, 44.44, 44.833, 45.44, 45.833 • Muscles, infarction, 44.44, 44.833, 45.44, 45.833 • Muscles, MR, 44.1214, 44.121411, 44.121413, 44.12143, 45.1214, 45.121411, 45.121413, 45.12143
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Introduction
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Muscle infarction in diabetic patients was described by Angervall and Stener in 1965 (1). Since that report, several authors have published case reports describing clinical findings associated with this condition (2–12). Case reports of diabetic muscle infarction that include findings from both computed tomographic (CT) and magnetic resonance (MR) imaging have appeared in the radiology literature (13–19). To our knowledge, the largest clinical series involved only six patients (3), and the largest radiologic description included only four patients (17).
Although the number of cases reported in the literature is small, we have personally been involved with 21 patients with diabetic muscle infarction over 4 years. This experience leads us to believe that the condition is more common than previously thought and may be unrecognized or misdiagnosed. The purpose of this study was to determine the clinical and MR imaging findings in patients with diabetic muscle infarction. In addition, we reviewed information in the literature to determine the typical MR imaging features that may be helpful in confirming the diagnosis.
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MATERIALS AND METHODS
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The MR imaging studies of 21 diabetic patients who presented with acute pain and swelling of the lower extremity that was subsequently diagnosed as diabetic muscle infarction during 4 years were reviewed retrospectively. Clinical data, including age, sex, presence of diabetes, insulin requirements, and the presence of diabetic nephropathy, diabetic neuropathy, or diabetic retinopathy were recorded.
All 21 patients presented with acute pain and swelling of the lower extremity, with a duration of symptoms ranging between 3 days and 3 weeks (mean, 10 days) before MR imaging. All 21 patients had a diagnosis of diabetic muscle infarction on the basis of a combination of clinical presentation and outcome, as well as MR imaging findings; in 17 patients, histopathologic confirmation was available. The four patients who had not undergone biopsy had a clinical diagnosis of diabetic muscle infarction on the basis of a classic clinical manifestation and outcome.
Clinical criteria for the diagnosis of diabetic muscle infarction included diabetes mellitus with an acute onset of severe tenderness and swelling, with or without a focal mass, that resolved gradually without the administration of antibiotics. In each patient, the diagnoses of deep venous thrombosis, trauma, soft-tissue abscess, and neoplasm had been excluded.
The 17 patients who underwent biopsy had histopathologic findings of various stages of muscle infarction, including zonal necrosis and hemorrhage. Small arterial vessels showed evidence of diabetic microangiopathy and arteriosclerosis. Only the muscles shown to be involved at MR imaging were examined with biopsy. No biopsies of uninvolved muscles were performed. The decision to defer biopsy in four patients was based on a strong clinical suspicion of diabetic muscle infarction, and conservative supportive therapy was followed until complete resolution of symptoms.
T1-weighted and T2-weighted MR images were obtained in all 21 patients with 0.5–1.5-T MR imagers. Typical spin-echo pulse sequences included T1-weighted sequences (300–800/10–30 [repetition time msec/echo time msec]) and T2-weighted sequences (1,800–4,500/60–120). Fast multiplanar inversion-recovery (3,000–6,000/30–120/100–150 [repetition time msec/echo time msec/inversion time msec]) sequences were used in four patients. Nine patients received intravenously administered contrast material (gadopentetate dimeglumine; Magnevist, Berlex Laboratories, Wayne, NJ).
The MR studies were reviewed by two musculoskeletal radiologists (J.S.J., M.D.M.) with consensus. Data recorded from MR studies included the site and extent of muscular involvement and the presence of subfascial fluid and subcutaneous edema. The muscle groups affected, signal intensity, muscle appearance, and contrast enhancement patterns were also reviewed. Dynamic enhanced MR imaging was not performed. The sizes of the muscle groups were compared with those of the contralateral side or those of adjacent unaffected muscles. The signal intensity of affected muscles was compared with that of skeletal muscle and subcutaneous fat on T1-weighted, T2-weighted, gadolinium-enhanced, and inversion-recovery images.
Gadolinium-enhanced T1-weighted images were compared with the nonenhanced T1-weighted and T2-weighted images. The enhancement pattern was assessed for uniformity and identification of rim-enhancing foci or for the absence of enhancement and also was compared with that on T2-weighted images.
Twelve women and nine men were in the study group. The mean age at presentation was 48 years, with a range of 30–77 years. Nine patients initially were seen for evaluation of a palpable, painful soft-tissue mass.
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RESULTS
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Patient data are shown in Table 1. The thigh was the most common site of involvement; of the 21 patients, 17 (81%) had involvement in this area (Figs 1–3). Eight patients (38%) had bilateral lower-extremity involvement. Four patients (19%) had calf involvement alone. Two patients had thigh and calf involvement (Fig 3). In addition to thigh involvement, three patients had involvement of the musculi gluteus and musculi gemellus, and two patients had involvement of the musculi psoas (Fig 2).
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Figure 1a. MR images from a 33-year-old woman with bilateral diabetic muscle infarction, showing the most common pattern of involvement of the musculi vastus. (a) Axial T1-weighted image (700/18) demonstrates bilateral subcutaneous edema (arrows), greater on the right than on the left. There is a suggestion of enlargement of the musculi vastus lateralis (*); however, the T1-weighted image does not show the specific muscles involved. (b) Axial fat-suppressed gadolinium-enhanced T1-weighted image (700/18) demonstrates areas of diffuse enhancement of the musculi vastus lateralis (*) and musculi rectus femoris (open arrows). Other areas in the left musculus rectus femoris and left musculus vastus lateralis show focal rim enhancement with a low–signal-intensity center (curved arrows). Presumably, these areas represent focal necrosis or fluid within the muscle. (c) Axial fat-suppressed T2-weighted image (3,817/90) shows extensively affected muscles to better advantage, particularly involvement of both musculi vastus lateralis (*) and left musculus rectus femoris (open arrow) and minimal involvement of both musculi vastus intermedius (arrowheads). Note the subcutaneous edema and the very minimal subfascial fluid (solid arrow). (d) Coronal inversion-recovery image (3,216/30/150) shows the extensive involvement of the vastus lateralis (*), with relative sparing of the right musculus rectus femoris (black arrow) and left musculus vastus medialis (white arrow).
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Figure 1b. MR images from a 33-year-old woman with bilateral diabetic muscle infarction, showing the most common pattern of involvement of the musculi vastus. (a) Axial T1-weighted image (700/18) demonstrates bilateral subcutaneous edema (arrows), greater on the right than on the left. There is a suggestion of enlargement of the musculi vastus lateralis (*); however, the T1-weighted image does not show the specific muscles involved. (b) Axial fat-suppressed gadolinium-enhanced T1-weighted image (700/18) demonstrates areas of diffuse enhancement of the musculi vastus lateralis (*) and musculi rectus femoris (open arrows). Other areas in the left musculus rectus femoris and left musculus vastus lateralis show focal rim enhancement with a low–signal-intensity center (curved arrows). Presumably, these areas represent focal necrosis or fluid within the muscle. (c) Axial fat-suppressed T2-weighted image (3,817/90) shows extensively affected muscles to better advantage, particularly involvement of both musculi vastus lateralis (*) and left musculus rectus femoris (open arrow) and minimal involvement of both musculi vastus intermedius (arrowheads). Note the subcutaneous edema and the very minimal subfascial fluid (solid arrow). (d) Coronal inversion-recovery image (3,216/30/150) shows the extensive involvement of the vastus lateralis (*), with relative sparing of the right musculus rectus femoris (black arrow) and left musculus vastus medialis (white arrow).
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Figure 1c. MR images from a 33-year-old woman with bilateral diabetic muscle infarction, showing the most common pattern of involvement of the musculi vastus. (a) Axial T1-weighted image (700/18) demonstrates bilateral subcutaneous edema (arrows), greater on the right than on the left. There is a suggestion of enlargement of the musculi vastus lateralis (*); however, the T1-weighted image does not show the specific muscles involved. (b) Axial fat-suppressed gadolinium-enhanced T1-weighted image (700/18) demonstrates areas of diffuse enhancement of the musculi vastus lateralis (*) and musculi rectus femoris (open arrows). Other areas in the left musculus rectus femoris and left musculus vastus lateralis show focal rim enhancement with a low–signal-intensity center (curved arrows). Presumably, these areas represent focal necrosis or fluid within the muscle. (c) Axial fat-suppressed T2-weighted image (3,817/90) shows extensively affected muscles to better advantage, particularly involvement of both musculi vastus lateralis (*) and left musculus rectus femoris (open arrow) and minimal involvement of both musculi vastus intermedius (arrowheads). Note the subcutaneous edema and the very minimal subfascial fluid (solid arrow). (d) Coronal inversion-recovery image (3,216/30/150) shows the extensive involvement of the vastus lateralis (*), with relative sparing of the right musculus rectus femoris (black arrow) and left musculus vastus medialis (white arrow).
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Figure 1d. MR images from a 33-year-old woman with bilateral diabetic muscle infarction, showing the most common pattern of involvement of the musculi vastus. (a) Axial T1-weighted image (700/18) demonstrates bilateral subcutaneous edema (arrows), greater on the right than on the left. There is a suggestion of enlargement of the musculi vastus lateralis (*); however, the T1-weighted image does not show the specific muscles involved. (b) Axial fat-suppressed gadolinium-enhanced T1-weighted image (700/18) demonstrates areas of diffuse enhancement of the musculi vastus lateralis (*) and musculi rectus femoris (open arrows). Other areas in the left musculus rectus femoris and left musculus vastus lateralis show focal rim enhancement with a low–signal-intensity center (curved arrows). Presumably, these areas represent focal necrosis or fluid within the muscle. (c) Axial fat-suppressed T2-weighted image (3,817/90) shows extensively affected muscles to better advantage, particularly involvement of both musculi vastus lateralis (*) and left musculus rectus femoris (open arrow) and minimal involvement of both musculi vastus intermedius (arrowheads). Note the subcutaneous edema and the very minimal subfascial fluid (solid arrow). (d) Coronal inversion-recovery image (3,216/30/150) shows the extensive involvement of the vastus lateralis (*), with relative sparing of the right musculus rectus femoris (black arrow) and left musculus vastus medialis (white arrow).
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Figure 2a. Images from a 65-year-old woman with diabetic muscle infarction of the left leg. (a) Axial T1-weighted MR image (500/15) shows only diffuse subcutaneous edema and evidence of inflammation between the intermuscular septa (arrows). The specific sites of muscle involvement are not clear from this image. (b) Axial T2-weighted MR image (4,000/105) shows extensive involvement of the thigh. On this transaxial image, there is extensive involvement of the musculus semimembranosus (short thick black arrow), musculus gracilis (long thin black arrow), musculus sartorius (arrowhead), musculus adductor (open arrow), and musculus vastus medialis (*). Note the striking sparing of the musculus biceps femoris (double curved white arrows) and musculus vastus lateralis (single curved white arrow). Subfascial fluid (medium black arrow) abuts the musculus vastus lateralis. This subfascial fluid is in an area that appears uninvolved with muscle infarction. (c) Axial CT scan at the same level as b shows marked swelling of the left leg compared with the right, with enlargement of the musculi adductor and musculi semitendinosus. Extensive subcutaneous edema is also identified; however, other than partial loss of intramuscular septa, it is difficult to be certain which specific muscles are involved. (d) Axial T2-weighted MR image (4,000/105) at a higher level than c shows not only extensive involvement of the musculus adductor (open arrow) but also involvement of the musculus obturatorius externus (*) and musculus iliopsoas (curved arrow). (e) Photomicrograph of biopsy specimen shows ischemic skeletal muscle fibers (arrows), with abundant fibrin deposition and early reparative changes with fibrosis. (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 2b. Images from a 65-year-old woman with diabetic muscle infarction of the left leg. (a) Axial T1-weighted MR image (500/15) shows only diffuse subcutaneous edema and evidence of inflammation between the intermuscular septa (arrows). The specific sites of muscle involvement are not clear from this image. (b) Axial T2-weighted MR image (4,000/105) shows extensive involvement of the thigh. On this transaxial image, there is extensive involvement of the musculus semimembranosus (short thick black arrow), musculus gracilis (long thin black arrow), musculus sartorius (arrowhead), musculus adductor (open arrow), and musculus vastus medialis (*). Note the striking sparing of the musculus biceps femoris (double curved white arrows) and musculus vastus lateralis (single curved white arrow). Subfascial fluid (medium black arrow) abuts the musculus vastus lateralis. This subfascial fluid is in an area that appears uninvolved with muscle infarction. (c) Axial CT scan at the same level as b shows marked swelling of the left leg compared with the right, with enlargement of the musculi adductor and musculi semitendinosus. Extensive subcutaneous edema is also identified; however, other than partial loss of intramuscular septa, it is difficult to be certain which specific muscles are involved. (d) Axial T2-weighted MR image (4,000/105) at a higher level than c shows not only extensive involvement of the musculus adductor (open arrow) but also involvement of the musculus obturatorius externus (*) and musculus iliopsoas (curved arrow). (e) Photomicrograph of biopsy specimen shows ischemic skeletal muscle fibers (arrows), with abundant fibrin deposition and early reparative changes with fibrosis. (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 2c. Images from a 65-year-old woman with diabetic muscle infarction of the left leg. (a) Axial T1-weighted MR image (500/15) shows only diffuse subcutaneous edema and evidence of inflammation between the intermuscular septa (arrows). The specific sites of muscle involvement are not clear from this image. (b) Axial T2-weighted MR image (4,000/105) shows extensive involvement of the thigh. On this transaxial image, there is extensive involvement of the musculus semimembranosus (short thick black arrow), musculus gracilis (long thin black arrow), musculus sartorius (arrowhead), musculus adductor (open arrow), and musculus vastus medialis (*). Note the striking sparing of the musculus biceps femoris (double curved white arrows) and musculus vastus lateralis (single curved white arrow). Subfascial fluid (medium black arrow) abuts the musculus vastus lateralis. This subfascial fluid is in an area that appears uninvolved with muscle infarction. (c) Axial CT scan at the same level as b shows marked swelling of the left leg compared with the right, with enlargement of the musculi adductor and musculi semitendinosus. Extensive subcutaneous edema is also identified; however, other than partial loss of intramuscular septa, it is difficult to be certain which specific muscles are involved. (d) Axial T2-weighted MR image (4,000/105) at a higher level than c shows not only extensive involvement of the musculus adductor (open arrow) but also involvement of the musculus obturatorius externus (*) and musculus iliopsoas (curved arrow). (e) Photomicrograph of biopsy specimen shows ischemic skeletal muscle fibers (arrows), with abundant fibrin deposition and early reparative changes with fibrosis. (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 2d. Images from a 65-year-old woman with diabetic muscle infarction of the left leg. (a) Axial T1-weighted MR image (500/15) shows only diffuse subcutaneous edema and evidence of inflammation between the intermuscular septa (arrows). The specific sites of muscle involvement are not clear from this image. (b) Axial T2-weighted MR image (4,000/105) shows extensive involvement of the thigh. On this transaxial image, there is extensive involvement of the musculus semimembranosus (short thick black arrow), musculus gracilis (long thin black arrow), musculus sartorius (arrowhead), musculus adductor (open arrow), and musculus vastus medialis (*). Note the striking sparing of the musculus biceps femoris (double curved white arrows) and musculus vastus lateralis (single curved white arrow). Subfascial fluid (medium black arrow) abuts the musculus vastus lateralis. This subfascial fluid is in an area that appears uninvolved with muscle infarction. (c) Axial CT scan at the same level as b shows marked swelling of the left leg compared with the right, with enlargement of the musculi adductor and musculi semitendinosus. Extensive subcutaneous edema is also identified; however, other than partial loss of intramuscular septa, it is difficult to be certain which specific muscles are involved. (d) Axial T2-weighted MR image (4,000/105) at a higher level than c shows not only extensive involvement of the musculus adductor (open arrow) but also involvement of the musculus obturatorius externus (*) and musculus iliopsoas (curved arrow). (e) Photomicrograph of biopsy specimen shows ischemic skeletal muscle fibers (arrows), with abundant fibrin deposition and early reparative changes with fibrosis. (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 2e. Images from a 65-year-old woman with diabetic muscle infarction of the left leg. (a) Axial T1-weighted MR image (500/15) shows only diffuse subcutaneous edema and evidence of inflammation between the intermuscular septa (arrows). The specific sites of muscle involvement are not clear from this image. (b) Axial T2-weighted MR image (4,000/105) shows extensive involvement of the thigh. On this transaxial image, there is extensive involvement of the musculus semimembranosus (short thick black arrow), musculus gracilis (long thin black arrow), musculus sartorius (arrowhead), musculus adductor (open arrow), and musculus vastus medialis (*). Note the striking sparing of the musculus biceps femoris (double curved white arrows) and musculus vastus lateralis (single curved white arrow). Subfascial fluid (medium black arrow) abuts the musculus vastus lateralis. This subfascial fluid is in an area that appears uninvolved with muscle infarction. (c) Axial CT scan at the same level as b shows marked swelling of the left leg compared with the right, with enlargement of the musculi adductor and musculi semitendinosus. Extensive subcutaneous edema is also identified; however, other than partial loss of intramuscular septa, it is difficult to be certain which specific muscles are involved. (d) Axial T2-weighted MR image (4,000/105) at a higher level than c shows not only extensive involvement of the musculus adductor (open arrow) but also involvement of the musculus obturatorius externus (*) and musculus iliopsoas (curved arrow). (e) Photomicrograph of biopsy specimen shows ischemic skeletal muscle fibers (arrows), with abundant fibrin deposition and early reparative changes with fibrosis. (Hematoxylin-eosin stain; original magnification, x100.)
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Figure 3a. MR images from a 51-year-old woman with left leg involvement including both the anterior portion of the thigh and the calf. (a) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) through the midthigh shows diffuse enhancement of the musculus vastus lateralis (arrow). No rim enhancement or necrosis is seen. (b) Axial fat-suppressed T2-weighted image (3,000/100) shows similar, although less striking, hyperintensity exclusively involving the musculus vastus lateralis (arrow). (c) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) at the level of the midcalf shows both enhancement and necrosis of muscle involving the medial aspect of the musculus gastrocnemius (*). Note subtle involvement of the musculus extensor hallucis longus (arrow). (d) Axial T2-weighted image (4,000/75) at the same level as c shows hyperintensity of the medial portion of the musculus gastrocnemius (*). The very subtle degree of hyperintensity of the musculus extensor hallucis longus (arrow) is less obvious than that seen in c.
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Figure 3b. MR images from a 51-year-old woman with left leg involvement including both the anterior portion of the thigh and the calf. (a) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) through the midthigh shows diffuse enhancement of the musculus vastus lateralis (arrow). No rim enhancement or necrosis is seen. (b) Axial fat-suppressed T2-weighted image (3,000/100) shows similar, although less striking, hyperintensity exclusively involving the musculus vastus lateralis (arrow). (c) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) at the level of the midcalf shows both enhancement and necrosis of muscle involving the medial aspect of the musculus gastrocnemius (*). Note subtle involvement of the musculus extensor hallucis longus (arrow). (d) Axial T2-weighted image (4,000/75) at the same level as c shows hyperintensity of the medial portion of the musculus gastrocnemius (*). The very subtle degree of hyperintensity of the musculus extensor hallucis longus (arrow) is less obvious than that seen in c.
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Figure 3c. MR images from a 51-year-old woman with left leg involvement including both the anterior portion of the thigh and the calf. (a) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) through the midthigh shows diffuse enhancement of the musculus vastus lateralis (arrow). No rim enhancement or necrosis is seen. (b) Axial fat-suppressed T2-weighted image (3,000/100) shows similar, although less striking, hyperintensity exclusively involving the musculus vastus lateralis (arrow). (c) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) at the level of the midcalf shows both enhancement and necrosis of muscle involving the medial aspect of the musculus gastrocnemius (*). Note subtle involvement of the musculus extensor hallucis longus (arrow). (d) Axial T2-weighted image (4,000/75) at the same level as c shows hyperintensity of the medial portion of the musculus gastrocnemius (*). The very subtle degree of hyperintensity of the musculus extensor hallucis longus (arrow) is less obvious than that seen in c.
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Figure 3d. MR images from a 51-year-old woman with left leg involvement including both the anterior portion of the thigh and the calf. (a) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) through the midthigh shows diffuse enhancement of the musculus vastus lateralis (arrow). No rim enhancement or necrosis is seen. (b) Axial fat-suppressed T2-weighted image (3,000/100) shows similar, although less striking, hyperintensity exclusively involving the musculus vastus lateralis (arrow). (c) Gadolinium-enhanced axial fat-suppressed T1-weighted image (500/25) at the level of the midcalf shows both enhancement and necrosis of muscle involving the medial aspect of the musculus gastrocnemius (*). Note subtle involvement of the musculus extensor hallucis longus (arrow). (d) Axial T2-weighted image (4,000/75) at the same level as c shows hyperintensity of the medial portion of the musculus gastrocnemius (*). The very subtle degree of hyperintensity of the musculus extensor hallucis longus (arrow) is less obvious than that seen in c.
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A total of 47 muscle compartments were involved, which included 107 muscles (mean, two compartments and five muscles per patient). The most commonly involved muscles were the musculus vastus intermedius (n = 16), musculus vastus medialis (n = 15), musculus vastus lateralis (n = 15), musculus rectus femoris (n = 6), musculus biceps femoris (n = 5), musculus sartorius (n = 5), musculi adductor (n = 4), and musculi peroneus (n = 4) (Table 2).
MR imaging demonstrated enlargement of the affected muscle groups with all pulse sequences. Loss of the normal fatty intramuscular septa was present in all cases and was identified most easily on T1-weighted images. Subcutaneous edema (n = 19 [90%]) and subfascial fluid (n = 18 [86%]) were commonly seen on the T2-weighted and inversion-recovery images. Subcutaneous edema was seen in areas not contiguous to the site of muscle involvement in 10 patients (48%) (Fig 2).
In all patients, affected muscles were isointense to unaffected muscle on T1-weighted images. Compared with the other imaging sequences, however, the degree of involvement of specific muscles was less conspicuous than that with the other sequences.
On T2-weighted and inversion-recovery images, the involved muscles were hyperintense compared with unaffected muscles and fat. Three patients (14%) also had tiny foci of hyperintense signal on both T1-weighted and T2-weighted images in the areas of muscle infarction; these hyperintense foci were consistent with foci of hemorrhage.
Nine patients received intravenously administered gadopentetate dimeglumine. The areas of MR contrast enhancement had higher signal intensity than unaffected skeletal muscle. The overall pattern and signal intensity were similar to those of the T2-weighted and inversion-recovery sequences, with the relative degrees of conspicuity approximately equal.
Areas of diabetic muscle infarction were very slightly more conspicuous on the gadolinium-enhanced images in five patients and very slightly more conspicuous on T2-weighted and inversion-recovery images in four patients. In addition, six of the nine patients (66%) evaluated with gadolinium-enhanced MR imaging also had small focal areas of rim enhancement that corresponded to areas of high signal intensity on T2-weighted images, representing infarction or necrosis within the areas of ischemic muscle.
Histopathologic findings in all patients revealed areas of muscle infarction with microangiopathy and atherosclerosis. Patchy areas of hemorrhagic necrosis were occasionally present. The predominant histopathologic areas were not characterized by marked polymorphonuclear or lymphocytic infiltration.
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DISCUSSION
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To our knowledge, only small series of patients with diabetic muscle infarction have been described in the clinical and radiology literature. Of the 19 articles that we found in the literature, 16 are case reports of one or two patients (1–19). Despite the lack of reports of large series of patients, we have been involved with 21 patients over 4 years, which suggests that this entity is more common than is recognized. The cause of diabetic muscle infarction is believed to be extensive thrombosis of medium and small arterioles; embolic thrombosis is believed to be a less likely cause (1–5).
Patients with diabetic muscle infarction present with sudden onset of severe pain and tenderness, with or without a palpable mass. Diabetic muscle infarction is frequently bilateral, as seen in 38% of our patients and 43% (13 patients) of the 30 patients identified in articles that we found in the literature. As shown in our series and in the literature (1–19), the thigh is the most common site of involvement. The thigh was involved in 17 of our patients (81%) and in 26 of the 30 patients (87%) in the literature (Tables 1, 2).
The second most commonly affected site was the calf. Four (19%) of our patients and four patients (13%) in the articles that we found in the literature had diabetic muscle infarction at this location. One of the patients cited in the literature had initial involvement of the calf, with subsequent involvement of the thigh, as occurred in two of our patients. Although any of the muscles of the thigh may be involved, the musculi vastus were the most frequently affected, both in our series (16 of 21 patients [76%]) and in the literature (27 of 30 patients [90%]). Involvement of the muscles about the hip (musculi gemellus, musculi psoas, musculus tensor fasciae latae, and musculi gluteus) is less frequent (n = 5 [24%] in our series).
Diabetic muscle infarction may be seen at histopathologic examination as varying areas of muscle infarction with zonal necrosis, foci of hemorrhage, and fatty infiltration. Small arterioles show hyalinosis and thickening of the lumen (2,3,12). Small areas of hemorrhagic necrosis are surrounded by muscle fibers in various stages of degeneration and regeneration. Atherosclerotic calcifications may be seen within the medium-sized arteries. Pathologic findings may show more severe atrophy of muscle fibers and more prominent infiltration of fat and interstitial fibrosis (1–5).
Because all of our patients underwent imaging while they were in the acute phase of diabetic muscle infarction, we can describe the later MR imaging findings only in two patients who subsequently underwent follow-up MR studies. The now asymptomatic areas of diabetic muscle infarction in these two patients no longer showed hyperintense signal on the T2-weighted MR images, and there were atrophic changes of the muscles, with more prominent fatty infiltration of these regions. Because of the small number of patients, the follow-up studies were not included in this study.
Diabetic muscle infarction represents a sequela of poorly controlled diabetes and often coexists with other complications of insulin-dependent diabetes mellitus. In addition to diabetic nephropathy, which was found in 62% (13 patients) of our 21 patients and in 73% (22 of 30 patients) of those in the literature, diabetic neuropathy was found in 57% (12 patients) and diabetic retinopathy in 33% (seven patients) of our 21 patients. The literature also describes the frequent association of neuropathy and diabetic retinopathy (2–5).
Fourteen percent (n = 3) of our patients died during the study period, as did 20% (six patients) of the 30 patients in the literature. The three patients in our study died of myocardial infarction, of diabetic ketoacidosis, and as a result of inadequate renal dialysis from progressive long-term complications of vascular access.
Areas of muscle infarction are seen on MR images as marked muscle swelling that is isointense on T1-weighted images and hyperintense compared with skeletal muscle on T2-weighted, inversion-recovery, and gadolinium-enhanced MR images; this reflects the acute edema and inflammatory changes. The pattern of enhancement on gadolinium-enhanced T1-weighted images was diffuse in all cases, and six patients also had small foci showing rim enhancement. This suggests that the entity may be more correctly described as diabetic muscle ischemia and that the areas of rim enhancement with low signal intensity centrally and high signal intensity on corresponding T2-weighted MR images represent areas of actual muscle infarction and necrosis.
Other than showing central areas of infarction or necrosis, the high signal intensity on the gadolinium-enhanced T1-weighted images was similar to that on the T2-weighted images. Conspicuity was not markedly different between gadolinium-enhanced T1-weighted and T2-weighted images; no areas that were markedly hyperintense on one set of images were not identified with the other sequence.
The radiologic differential diagnosis of diabetic muscle infarction includes soft-tissue abscess, pyomyositis, necrotizing fasciitis, and other causes of myositis (dermatomyositis, focal myositis, nodular myositis, and proliferative myositis) (20–26). The diagnosis of diabetic muscle infarction remains a clinical and radiographic diagnosis and, at times, may require a histopathologic diagnosis. Focal myositis, proliferative myositis, and nodular myositis are not individually distinguishable with clinical examination or MR imaging, and muscle biopsy is necessary to identify characteristic histologic features.
Of these three types of myositis, focal myositis is the most likely to be seen initially as a localized mass but is typically not painful. On histopathologic examination, focal myositis shows a predominant pattern of lymphocytic infiltration (21,22,24). Proliferative myositis is a similar condition that is characterized by infiltration with basophilic giant cells and proliferative fibroblasts (25,26). Nodular myositis is characterized histologically by an intense pleomorphic infiltration of muscle, with scattered foci of muscle fiber destruction and regeneration. This entity is most likely to be painful and likely to evolve into a diffuse myopathy (25).
Necrotizing fasciitis is a major differential consideration that may not be distinguishable from diabetic muscle infarction on the basis of only MR imaging findings (20). Patients with necrotizing fasciitis are more likely to have fever, cellulitis, and an elevated peripheral white blood cell count. Severe pain is very characteristic of diabetic muscle infarction and may not be seen with necrotizing fasciitis or pyomyositis (1–4,8–10,12,13,26,27). In addition, when diabetic muscle infarction is bilateral or occurs in multiple separate locations in a patient without sepsis, this entity is more easily differentiated from necrotizing fasciitis. Because necrotizing fasciitis is a surgical emergency, any patient in whom necrotizing fasciitis is a serious consideration should undergo immediate surgical intervention.
Another rare diagnostic consideration based on MR imaging studies alone is that of primary lymphoma of muscle (28–30). This entity may appear similar to diabetic muscle infarction and may affect single or multiple muscle groups, with or without bone marrow involvement (28–30). Primary lymphoma of muscle may extend beyond a single compartment and may show areas of subcutaneous stranding and involvement of subcutaneous tissue similar to diabetic muscle infarction.
However, most patients with primary lymphoma do not present with sudden and severe lower-extremity muscle pain. In addition, patients with primary lymphoma do not have bilateral disease or simultaneous yet completely discontinuous sites of disease, such as involvement of both the thigh and the calf. Most patients with primary lymphoma do not have insulin-dependent diabetes mellitus or its associated sequelae of nephropathy, retinopathy, or neuropathy. Patients with lymphoma also do not undergo spontaneous remission of symptoms, as is typically seen with diabetic muscle infarction (1–13). If primary lymphoma is a diagnostic consideration, again, biopsy is required.
In our opinion, correlation of the characteristic clinical manifestation and MR imaging findings in a patient with insulin-dependent diabetes mellitus may obviate biopsy in some cases. However, percutaneous core needle biopsy is fast and minimally invasive and can be used to confirm the diagnosis in patients in whom a diagnostic dilemma remains. Open biopsy and excision have been associated with complications such as hematoma, infection, and poor wound healing (3,4,6). MR imaging may be useful in the prebiopsy planning because it clearly identifies the location and site of muscle involvement. Clinical treatment is predominantly symptomatic and conservative (3,7,8,10,12), although some have suggested a role for anticoagulation therapy (12). The symptoms of diabetic muscle infarction resolve over several weeks (1–5).
In conclusion, diabetic muscle infarction characteristically involves patients with poorly controlled insulin-dependent diabetes mellitus, often in conjunction with other complications of diabetes, including neuropathy, nephropathy, and retinopathy. The entity is bilateral in more than one-third of the cases. Diabetic muscle infarction is suggested in a diabetic patient with sudden onset of severe pain in the thigh or calf and with MR imaging findings of diffuse edema and swelling of multiple thigh or calf muscles, often in more than one compartment. These clinical and MR imaging features may obviate biopsy in some patients. In patients in whom other diagnoses, such as necrotizing fasciitis or a primary myositis, remain a serious consideration, biopsy can be used for confirmation.
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Acknowledgments
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We acknowledge the wonderful help and dedication provided by Nancy S. Carnes in preparing the manuscript.
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Footnotes
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2 Current address: Dept of Radiology, Wilford Hall Medical Center, San Antonio, Tex. 
The opinions expressed herein are not to be construed as those of the Departments of Defense, Army, or Navy.
Author contributions: Guarantors of integrity of entire study, J.S.J., M.D.M.; study concepts, all authors; study design, J.S.J., M.D.M., A.J.A.; definition of intellectual content, J.S.J., M.D.M.; literature research, J.S.J., A.J.A.; clinical studies, all authors; data acquisition, all authors; data analysis, J.S.J., M.D.M.; statistical analysis, J.S.J.; manuscript preparation, editing, and review, J.S.J., M.D.M., A.J.A., P.A.K.
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Abstract
Introduction
