AJR 2003; 181:1216
© American Roentgen Ray Society
Radiologic–Pathologic Conference of Wilford Hall Medical
Center |
Diabetic Muscle Infarction
Justin Q. Ly1,
Edward K. Yi2 and
Douglas P. Beall1
1 Department of Radiology, Wilford Hall Medical Center, Ste. 1, 2200 Bergquist
Dr., Lackland AFB, TX 78236-5300.
2 Hickam Primary Care Clinic, 755 Scott Cr., Hickam AFB, HI 96853.
Received December 19, 2002;
accepted after revision January 22, 2003.
The opinions and assertions contained herein are those of the authors and
should not be construed as official or as representing the opinions of the
Department of the Air Force or the Department of Defense.
Address correspondence to J. Q. Ly.
A55-year-old man with diabetes initially presented with a 3-week history of
a nonhealing wound at the anterolateral aspect of the distal left lower
extremity. Over the course of 10 days before presentation, he had noticed
progressive redness, pain, and swelling of his anterior left leg. Radiography
of the distal left lower extremity showed nonspecific swelling of the
anterolateral soft tissues (Fig.
1A). Two days after the patient's initial presentation and
admission, he acutely developed left foot drop. Further evaluation with MRI of
the distal lower extremity showed edema involving the anterior compartment
muscles and mild bulging of the fascial planes (Figs.
1B and
1C), which was compatible with
anterior compartment syndrome. Arteriography revealed a filling defect within
the popliteal artery consistent with an embolic phenomenon. Subsequent
débridement of the wound revealed histopathologic findings consistent
with necrotic muscle (Fig. 1D).
The final diagnosis was diabetic muscle infarction caused by microangiopathic
disease with thromboembolic phenomena.
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Fig. 1A. —55-year-old man with diabetic infarction of distal lower
extremity anterior compartment musculature. Radiograph of lateral distal lower
extremity shows moderate anterior soft-tissue edema (arrows).
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Fig. 1B. —55-year-old man with diabetic infarction of distal lower
extremity anterior compartment musculature. Axial T1-weighted image shows
subtle increased hypointensity of anterolateral compartment
(arrowheads) relative to nearby musculature.
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Fig. 1C. —55-year-old man with diabetic infarction of distal lower
extremity anterior compartment musculature. Axial fat-suppressed T2-weighted
image shows diffuse edema of tibialis anterior and extensor digitorum longus
muscles.
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Fig. 1D. —55-year-old man with diabetic infarction of distal lower
extremity anterior compartment musculature. Photomicrograph of biopsy specimen
reveals focal necrosis of skeletal muscle cells. (H and E, x200)
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Diabetic muscle infarction is a rare complication of diabetes and is often
associated with nontraumatic swelling of the affected extremity and gradual
or, less commonly, sudden onset of muscle pain. Biopsy of the affected muscle
usually shows histopathologic findings consistent with edematous and necrotic
tissue. Poorly controlled and long-standing diabetes and extensive end-organ
disease caused by microvascular disease are characteristic of patients with
this process. The disease can be bilateral in more than one third of cases
[1]. The thigh and calf are the
most commonly involved areas, and multiple muscle involvement is common.
A proposed mechanism begins with a thromboembolic event, leading to
compartment syndrome and resultant ischemic muscle injury. This process is
followed by inflammation, hyperemia, and reperfusion associated with reactive
oxygen species that cause further damage both directly and through worsening
of the compartment syndrome from edema
[2]. In effect, a vicious cycle
is initiated, with eventual muscle necrosis. Radiography may show diffuse
swelling. MRI reveals edematous muscle, which is a nonspecific but
characteristic finding. The differential diagnosis for diffuse muscle edema on
MRI includes posttraumatic muscle contusions, strains, delayed onset muscle
soreness, subacute denervation, radiation therapy, compartment syndrome,
polymyositis, infectious myositis, compartment syndrome, and rhabdomyolysis
[3]. Edema limited to the
muscles of a specific compartment, with enlargement of that same compartment,
is suggestive of compartment syndrome.
Of note, the chronic form of compartment syndrome is indicated if these
abnormal imaging changes fail to return to baseline after postexertional
(15–25 min) MRI [1]. MRI
after contrast administration revealing central areas of nonenhancement
surrounded by enhancing muscle is indicative of muscle infarction of the
nonenhancing areas [4]. In most
cases, correlation of imaging findings with clinical information is useful and
often essential for delineating the exact cause of muscle edema. MRI is also
useful in directing biopsy to the site with the highest diagnostic yield and
for differentiating between acute and potentially more treatable disease
versus chronic disease.
Treatment consists of analgesics and non– weight-bearing activity.
Physical therapy and rehabilitation may be useful after the acute phase has
passed. The recovery period is usually 4–6 weeks.
References
- Nguyen B, Brandser E, Rubin DA. Pains, strains, and fasciculations:
lower extremity muscle disorders. Magn Reson Imaging Clin N
Am 2000;8:391
–408[Medline]
- Silberstein L, Britton KE, Marsch FP, Raftery MJ, D'Cruz D. An
unexpected cause of muscle pain in diabetes. Ann Rheum
Dis 2001;60:310
–312[Abstract/Free Full Text]
- May DA, Disler DG, Jones EA, Balkissoon AA, Manaster BJ. Abnormal
signal intensity in skeletal muscle at MR imaging: patterns, pearls and
pitfalls. RadioGraphics2000; 20:S295
–S315[Abstract/Free Full Text]
- Jelinek JS, Murphey MD, Aboulafia AJ, et al. Muscle infarction in
patients with diabetes mellitus: MR imaging findings.
Radiology1999; 211:241
–247[Abstract/Free Full Text]
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