AJR 2000; 174:165-169
© American Roentgen Ray Society
Sonography of Diabetic Muscle Infarction with MR Imaging, CT, and Pathologic Correlation
Lydia O. Delaney-Sathy1,
David P. Fessell1,
Jon A. Jacobson1 and
Curtis W. Hayes1
1
Department of Radiology, University of Michigan Health System, 1500 E. Medical
Center Dr., TC 2910, Ann Arbor, MI 48109-0326.
Received April 19, 1999;
accepted after revision June 29, 1999.
Address correspondence to D. P. Fessell.
Abstract
OBJECTIVE. The purpose of this article is to describe the
sonographic findings of muscle infarction in patients with diabetes with MR
imaging, CT, and pathologic correlation.
CONCLUSION. Sonographic findings of diabetic muscle infarction
include internal linear echogenic structures coursing through the lesion; an
absence of internal motion or swirling of fluid with transducer pressure; and
a lack of a predominately anechoic area. We believe that these sonographic
characteristics may help differentiate diabetic muscle infarction from abscess
or necrotic tumor. Additional study involving direct sonographic comparison of
these entities is needed to establish the role of sonography in diagnosis of
diabetic muscle infarction.
Introduction
Diabetic muscle infarction is a relatively rare entity. The
diagnosis is often difficult and can be confused with abscess, tumor, and
myositis. In the literature, investigators have proposed MR imaging as the
imaging study of choice to diagnose diabetic muscle infarction
[1,
2]. However, the MR imaging
findings of high signal intensity on T2-weighted images and ring enhancement
after administration of IV contrast material are not specific; an abscess or
necrotic tumor may have similar MR findings
[3,
4]. We have used sonography to
evaluate diabetic muscle infarction, and we present sonographic findings with
MR imaging, CT, and pathologic correlation.
Materials and Methods
Clinical data, laboratory results, images, and histopathologic results from
three cases of pathologically proven diabetic muscle infarction were
retrospectively reviewed. The institutional internal review board approved the
study. Sonography (n = 3), MR imaging (n = 2), and CT
(n = 2) were performed before percutaneous muscle biopsy (n
= 2) or surgical excisional biopsy (n = 1). Sonography was performed
with a curvilinear or linear 4- to 7-MHz transducer (HDI 3000, Advanced
Technology Laboratories, Bothell, WA; or Model 128, Acuson, Mountain View,
CA). CT scans were obtained using a HiSpeed Advantage scanner (General
Electric Medical Systems, Milwaukee, WI). One of the two patients who
underwent CT received IV contrast material. MR imaging was performed using a
1.5-T scanner with surface body coils (Signa; General Electric Medical
Systems) using a 256 x 192 or 256 x 256 matrix, a field of view of
between 14 x 14 and 48 x 48 cm, 2-4 excitations, and a 5- to 8-mm
thickness with a 1- to 2-mm intersection gap. The two patients who underwent
MR imaging were given IV gadopentetate dimeglumine (0.1 mmol/kg body weight).
MR imaging included axial T1-weighted spin-echo sequences with fat saturation
(TR range/TE, 500-566/14), sagittal and axial T2-weighted fast spin-echo
sequences (TR range/TE range, 3916-5966/78-84), coronal short inversion time
inversion recovery (STIR) images (TR/TE, 4000/22), and axial fast spinecho
proton density-weighted sequences with fat saturation (4000/14). Two patients
underwent CT-guided biopsy, during which 14- to 18-gauge core biopsy specimens
were obtained. The third patient underwent surgical excisional biopsy, during
which a 25 x 7 x 4.5 cm specimen was removed.
Results
The patient population consisted of one man and two women who ranged in age
from 26 to 42 years. Two patients had long-standing insulin-dependent diabetes
with end-organ damage (hypertension and renal failure). The third patient had
long-standing non-insulin-dependent diabetes with recent conversion to insulin
dependence and development of peripheral neuropathy. The affected area was the
thigh in all three patients. The vastus medialis and vastus intermedius
muscles were affected in one patient; the vastus intermedius muscle was
affected in the second patient; and the adductor magnus muscle was affected in
the third patient. All three patients had involvement of one muscle
compartment, and all patients presented with the acute onset of pain in the
afflicted thigh. One patient had a previous episode of presumed (but not
pathologically proven) diabetic muscle infarction in the contralateral thigh 3
months before the biopsy-proven episode. A second patient developed signs and
symptoms compatible with diabetic muscle infarction in the contralateral calf
5 months after biopsy and also had a prior episode of presumed diabetic muscle
infarction in the contralateral thigh 2 years earlier.
In addition to undergoing sonographic examination, the 26-year-old woman
underwent MR imaging, the 42-year-old woman underwent MR imaging and
unenhanced CT, and the 26-year-old man underwent contrastenhanced CT.
Sonography in all three patients showed a well-defined, predominately
hypoechoic lesion with mixed echogenicity
(Figs. 1A,
2A,
3A). Linear structures,
compatible with muscle fibers, were visualized within the lesions in all
patients. A predominately anechoic region was not present. Neither swirling of
fluid nor motion within the lesion with transducer pressure was seen. There
was subtle posterior acoustic enhancement in two of the three patients.
Posterior acoustic enhancement could not be adequately assessed in one patient
because the femur was directly beneath the lesion. Sonographic examination was
completed in 15 min or less for each patient.
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Fig. 1. —26-year-old woman with diabetes mellitus and acute onset of pain in
left thigh.
A, Transverse sonogram reveals hypoechoic area, which is limited to
vastus intermedius and vastus lateralis muscles (arrowheads), with
multiple internal echogenic lines (open arrows), compatible with
muscle fibers. Also, note outer cortex of femur (curved arrow) and
rectus femoris muscle (solid straight arrows). Note that posterior
acoustic enhancement cannot be adequately assessed because femur is directly
beneath lesion.
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Fig. 2. —42-year-old woman with diabetes and acute pain in left thigh.
A, Axial sonogram reveals well-defined, hypoechoic lesion involving
adductor magnus muscle (black arrows and cursors). Note
presence of posterior acoustic enhancement. Also, note echogenic structures
(white arrows), which appeared linear at real time, coursing through
lesion.
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Fig. 3. —26-year-old diabetic man with acute onset of pain in left thigh.
A, Axial sonogram shows well-defined hypoechoic area (straight
black arrows) with apparent increased through-transmission involving
vastus medialis muscle. Echogenic linear structures (white arrows)
course through lesion. Note outer cortex (curved arrows) of
femur.
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MR examinations (Figs. 1B,
Figs. 1C,
Figs. 1D and
Figs. 2B,
Figs. 2C,
Figs. 2D) revealed well-defined
regions with iso- to low signal intensity (relative to muscle) on T1-weighted
images and predominately high signal intensity on T2-weighted STIR or proton
density-weighted with fatsaturation images. The abnormal signal intensity was
limited to discrete muscle groups in both patients (vastus intermedius and
vastus lateralis muscles in one patient and the adductor magnus muscle in one
patient) and was demarcated by fascial planes. In both patients, prominent
ring enhancement was seen after the administration of IV contrast material.
Subfascial fluid was present in both patients. Additionally, subcutaneous
edema was present in both patients and was also noted distant from the
affected muscle groups.
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Fig. 1. —26-year-old woman with diabetes mellitus and acute onset of pain in
left thigh.
B, Corresponding axial T1-weighted MR image of left thigh shows no
significant signal intensity abnormality of vasti muscles and adductor magnus
muscle (arrows).
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Fig. 1. —26-year-old woman with diabetes mellitus and acute onset of pain in
left thigh.
C, Axial T2-weighted MR image with fat saturation shows diffusely
increased signal intensity involving discrete muscle groups: vastus medialis,
vastus lateralis, vastus intermedius, and adductor magnus muscles
(arrows). Note increased linear signal intensity in subcutaneous fat
and fascia (arrowheads), indicating subcutaneous edema and subfascial
fluid.
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Fig. 1. —26-year-old woman with diabetes mellitus and acute onset of pain in
left thigh.
D, Axial contrast-enhanced T1-weighted MR image with fat saturation
reveals diffuse enhancement of vastus muscles (black arrows): ring
enhancement of vastus intermedius and vastus lateralis muscles (white
arrows) and mild enhancement of adductor magnus muscle.
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Fig. 2. —42-year-old woman with diabetes and acute pain in left thigh.
B, Corresponding axial T1-weighted MR image shows mild heterogeneous
signal intensity in adductor magnus muscle (arrows) and linear low
signal intensity in subcutaneous fat (arrowheads), indicating
subcutaneous edema.
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Fig. 2. —42-year-old woman with diabetes and acute pain in left thigh.
C, Axial T2-weighted MR image with fat saturation shows diffusely
increased signal intensity involving adductor magnus muscle (arrows).
Note linear increased signal intensity in subcutaneous fat and fascial planes
(arrowheads), indicating subcutaneous edema and subfascial fluid.
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Fig. 2. —42-year-old woman with diabetes and acute pain in left thigh.
D, Axial contrast-enhanced T1-weighted MR image with fat saturation
shows marked ring enhancement (black arrows) with some internal
enhancement (white arrows) involving adductor magnus muscle.
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Contrast-enhanced CT (Fig.
3B) revealed a low-attenuation lesion with ring-enhancing margins
localized to the vastus intermedius and vastus lateralis muscles. Unenhanced
CT (performed for biopsy guidance) in one patient revealed low attenuation of
the adductor magnus muscle (Fig.
2E)
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Fig. 3. —26-year-old diabetic man with acute onset of pain in left thigh.
B, Corresponding axial contrast-enhanced CT image of left thigh
shows well-defined ring enhancement (arrows) surrounding
low-attenuation areas in vastus intermedius and vastus medialis muscles. Note
linear fluid attenuation in subcutaneous tissues, compatible with subcutaneous
edema.
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Fig. 2. —42-year-old woman with diabetes and acute pain in left thigh.
E, Axial unenhanced CT image of both thighs shows diffuse
enlargement of symptomatic left thigh. Note low attenuation throughout
adductor magnus muscle (arrows), which is enlarged to a greater
degree than other thigh muscles. Also, note extensive subcutaneous edema.
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Histopathologic evaluation was performed after CT-guided core biopsy with a
14- to 18- gauge needle in two patients; surgical excisional biopsy was
performed in one patient. Myonecrosis without significant inflammatory
infiltrate was observed in all patients
(Fig. 1E). In one patient,
fibrinoid necrosis and thrombi in small vessels were seen. No complications
related to the biopsies occurred.
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Fig. 1. —26-year-old woman with diabetes mellitus and acute onset of pain in
left thigh.
E, Photomicrograph shows myonecrosis (short straight
arrows), variable fiber size, abundant fibrous stroma (curved
arrows), multinucleated muscle fibers (long straight arrows),
and lack of inflammatory cells. (H and E, x100)
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Discussion
Diabetic muscle infarction is a rare complication of diabetes, with its
exact incidence unknown. To our knowledge, only 32 reports about this entity
have been published [2,
5]. The pathogenesis of
diabetic muscle infarction is not well understood. Proposed causes include
vascular occlusive disease caused by arteriosclerosis obliterans
[6] and embolized
atherosclerotic plaque [6].
The typical clinical presentation of a patient with diabetic muscle
infarction is that of a long-standing diabetic patient with peripheral
end-organ damage who presents with the abrupt onset of severe pain and
associated development of a palpable mass in an extremity (usually the thigh
or calf). The affected extremity is typically enlarged
(Fig. 2E). Pain occurs at rest
and is exacerbated by movement. No systemic signs of infection are seen.
Creatine kinase level is usually not elevated, and the erythrocyte
sedimentation rate may or may not be elevated. Recurrences in the same or
opposite limb have been shown to occur in approximately half the patients
[7] and was found in two of our
three patients.
Clinical differential diagnosis usually includes thrombophlebitis, abscess,
pyomyositis, neoplasm, spontaneous hematoma, ruptured Baker's cyst, fasciitis,
exertional muscle rupture, and diabetic lumbosacral plexopathy. Most of these
entities can be differentiated from diabetic muscle infarction by clinical
findings and laboratory examinations. However, the systemic features of
abscess may be absent in the diabetic population, and the differential
diagnosis frequently includes diabetic muscle infarction and abscess.
In the literature, investigators have proposed that MR imaging, especially
with administration of IV gadolinium, is the study of choice to diagnose
diabetic muscle infarction [1,
2]. However, MR imaging, even
using gadolinium, often does not enable clinicians to distinguish diabetic
muscle infarction from an abscess or necrotic tumor. To our knowledge, 32
reports have been published about diabetic muscle infarction, yielding 45
cases evaluated on MR imaging, 34 of which were pathologically proven
[1,
2,
5,
7,
8]. In each of these reports,
increased signal intensity on T2-weighted images was described. In 14 of the
patients with a pathologically proven diagnosis, MR imaging was performed with
IV gadolinium. In nine of these 14 patients, images were described as having
ring-enhancing patterns after administration of contrast material
[1,
4,
5,
8]. One group of researchers
reported minimal to modest enhancement (no pattern given)
[9], and another group of
researchers reported a "large area of increased signal"
[10]. Subfascial fluid and
subcutaneous edema was often present
[5,
9]. Because MR findings often
are not enough to differentiate diabetic muscle infarction from abscess or
tumor, biopsy is often considered. However, the role of biopsy is
controversial. Groups of researchers have reported adverse affects after
biopsy including bleeding into the lesion and an extended recovery period
[6,
9,
11]. Other researchers have
reported no deleterious affects after biopsy
[4,
7,
8,
10]. Although none of the
three patients we present had complications after biopsy, a reliable
noninvasive diagnostic technique would clearly be advantageous.
The sonographic features of diabetic muscle infarction have been only
briefly addressed in the literature. To our knowledge, three limited reports
of using sonography to reveal three cases of pathologically proven diabetic
muscle infarction have been published
[4,
9,
10]. In these cases,
sonographic appearance was inconsistent: diabetic muscle infarction was
described as hyperechoic in two cases
[4,
10] and as masslike region
with heterogeneous decreased echogenicity in the third case
[9]. In prior reports,
investigators have not addressed additional sonographic features that may be
useful in differentiating diabetic muscle infarction from other entities.
Diabetic muscle infarction appears as a well-marginated, hypoechoic,
intramuscular lesion with the following additional sonographic features:
internal linear structures that are compatible with muscle fibers coursing
through the lesion; a lack of a predominately anechoic region; and an absence
of motion or swirling of fluid with transducer pressure. The presence of these
three sonographic findings helps exclude a necrotic mass or abscess. Although
soft-tissue abscesses may have a variable sonographic appearance, they are
typically anechoic or hypoechoic and well defined, showing posterior acoustic
enhancing and possible intrinsic motion of fluid with transducer pressure
[12]. Two of the three cases
showed degrees of posterior acoustic enhancement. However, the posterior
enhancement was subtler and difficult to appreciate, likely due to the close
proximity of the lesions to the femur. The lesion in the third patient was
nearly apposed to the femur, and we were unable to adequately assess for
posterior acoustic enhancement. The significance of posterior acoustic
enhancement in our cases is therefore uncertain. Sonography of all patients
was performed while patients were experiencing pain in the affected extremity,
during the acute phase of diabetic muscle infarction. Because we performed
only one sonographic examination of each patient, we do not know whether and
how the sonographic appearance of diabetic muscle infarction changes over
time. Color or power Doppler technique was not used in this study, and
currently its role in enabling diagnosis of diabetic muscle infarction is
undefined.
Pathologic evaluation of diabetic muscle infarction reveals various stages
of muscle infarction and regeneration including focal areas of necrosis,
marginal infiltration of polymorphonuclear cells, hemorrhage, edema, and
interstitial fibrosis. Additionally, small-vessel walls are often hyalinized
and thickened. Some small vessels may be occluded with fibrin or calcium
fragments [11].
A limitation to this study includes the small number of cases. However,
only pathologically proven cases were included because we believe these cases
represent the ideal gold standard. Additionally, this study does not include
direct sonographic comparison of diabetic muscle infarction with tumor or
abscess. A blinded study directly comparing the sonographic features of
diabetic muscle infarction with those of abscess and necrotic tumor is needed
to reveal the true effectiveness of sonography in distinguishing among these
entities.
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Abstract
Introduction
