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. 2014;34:74–77.

Magnetic Resonance Imaging of Diabetic Muscle Infarction: Report of Two Cases

Anugayathri Jawahar, Ravikanth Balaji
PMCID: PMC4127726  PMID: 25328463

Abstract

Diabetic muscle infarction (DMI) occurs as a rare complication of long standing or severe diabetes mellitus. The condition usually occurs spontaneously and patients usually present with acute pain and swelling of affected muscles which persists for weeks, and resolves spontaneously without intervention. Magnetic resonance (MR) imaging is the modality of choice in patients with suspected DMI based on appropriate clinical setting and plays a major role in the diagnosis, assessing the extent of involvement and differentiating DMI from other conditions. The DMI affected muscles are bulky and appear heterogeneous with hyperintense signals on T2-weighted and STIR sequences, hypo or isointense on T1-weighted images with loss of normal fatty intramuscular septae. Subcutaneous and perifascial edema can be present. On postgadolinium scans, there is diffuse heterogeneous enhancement with non-enhancing foci, which may represent areas of necrosis. Biopsy can be avoided as MR findings are highly sensitive and specific. Treatment is usually conservative. Surgical intervention is required only in patients who do not respond to conservative management. The common differential diagnosis includes cellulitis, abscess, necrotizing fasciitis and polymyositis. We present two cases below to highlight the clinical, MR imaging findings and differential diagnosis of DMI.

Introduction

Diabetic muscle infarction (DMI) was first described by Angervall and Stener in 1965 as Tumoriform muscular degeneration' in two patients with non-insulin dependent diabetes mellitus (NIDDM)1. DMI occurs as a rare complication of long-standing or severe diabetes mellitus. The condition usually occurs spontaneously, without concurrent or preceding infection or trauma. It is more frequent in diabetic women (61.53%) with mean age at presentation being 39 ±12 years2'3'4'5'6.

Patients who develop DMI present with acute pain and swelling of affected muscles which persist for weeks and resolve spontaneously without intervention. Rarely a mass can be palpated. Magnetic resonance imaging (MRI) is the modality of choice in patients with suspected DMI based on appropriate clinical setting, due to superior soft tissue contrast and multi-planar image acquisitions7. It also plays a major role in the diagnosis, assessing the extent of involvement and differentiating DMI from other conditions like cellulitis, abscesses and necrotizing fasciitis.

We present the report on two cases of DMI to highlight the importance of MRI findings in guiding non-invasive management of the condition.

Case report 1

A 44-year-old woman with history of insulin dependent diabetes mellitus (IDDM) for eight years presented with two weeks of pain and swelling in her right leg. There was no history of trauma and no clinical or biochemical evidence of infection. Clinical examination showed a non-erythematous tender swelling along the lateral aspect of right leg, extending from below knee to just above the ankle. Patient had no improvement of pain with analgesic medications and hence MRI was requested for further evaluation of the clinical condition.

Magnetic resonance imaging of the legs revealed involvement of muscles in the lateral compartment of leg including the peroneus longus, peroneus brevis and extensor digitorum longus. The muscles were bulky and appeared heterogeneous with hyperintensities on T2-weighted and STIR (Short Tau Inversion Recovery) sequences with loss of definition of intramuscular septae on T1-weighted sequence (Figure 1). Post-gadolinium scans revealed heterogeneous enhancement within the muscles with focal hypointense non-enhancing areas (Figures 2, Figure 3). The skin and subcutaneous fat over the leg was thickened and edematous. The clinical and MRI findings were highly suggestive of DMI and the patient was managed conservatively.

Figure 1. Axial T1-weighted image showing homogenous low signal intensity within the muscle with loss of fatty intramuscular septae (open arrow). Thickened skin and subcutaneous fat can be noted.

Figure 1

Figure 2, 3. Coronal and axial fat suppressed gadolinium-enhanced Tl-weighted images showing diffuse heterogeneous enhancement of the affected muscles with focal non-enhancing areas which may represent necrosis (white arrow).

Figure 2, 3

Case Report 2

A 39-year-old lady with history of IDDM for the past ten years presented with pain and swelling of her left leg of two months duration. There was no preceding history of trauma or infection. Clinical examination revealed tender swelling of her proximal left leg with tense, shiny and edematous skin. Hematological and biochemical parameters were normal. The patient was referred for MRI because of a clinical concern regarding a soft tissue sarcoma.

On MRI, the medial head of the gastrocnemius, soleus and flexor digitorum longus muscles were bulky. The muscles appeared hyperintense on T2-weighted and STIR sequences (Figures 4, Figure 5) while on T1-weighted sequence the muscles were uniformly hypointense with loss of normal fatty intramuscular septae. The skin and subcutaneous tissues along the anterior, medial and posterior aspects of the leg were thickened with replacement of subcutaneous fat. A diagnosis of diabetic muscle necrosis was offered and biopsy was deferred. The patient was managed with analgesics and bed rest. Follow-up in one week showed complete resolution of symptoms.

Figure 4, 5. Coronal STIR (Short Tau Inversion Recovery) and axial T2-weighted images demonstrating bulky gastrocnemius muscle with high signal intensity (asterisk). Thickened skin with replacement of subcutaneous fat can be noted.

Figure 4, 5

Discussion

Diabetic muscle infarction has also been described as aseptic or ischemic myonecrosis2. DMI can occur in both patients with IDDM and poorly controlled NIDDM on insulin therapy. Risk factors include long-standing diabetes mellitus (mean 15 years), poor glycemic control and diabetic vascular disease. Patients who develop DMI almost always have severe diabetic vascular disease at the time of presentation. According to Angervall and Stener, diabetic microangiopathy and arteriosclerosis can be of importance in the pathogenesis of DMI1,6,8,9. Vascular endothelial damage and a hypercoagulable state precipitate small and medium vessel thrombosis resulting in myonecrosis2,10,11. Histopathology shows areas of muscle necrosis, infarction, hemorrhage and focal fibrosis.

The thigh muscles are most commonly involved followed by the calf muscles5,12. The upper limb is rarely involved. Multiple muscles or muscle compartments can be involved and at times involvement can be bilat-eral2,11,13,14. Systemic signs of infection like fever, leukocytosis or elevated ESR may be absent15. Laboratory investigations are not helpful in diagnosis, though some authors have reported transient elevation of creatine kinase, white blood cell count and erythrocyte sedimentation rate2'4'10'14'15'16.

For DMI, MRI is the diagnostic modality of choice. Axial MR images are ideal for diagnosis, although coronal and sagittal images can help in documenting the extent of involvement3. STIR and T2-weighted images closely reflect the underlying pathological processes as both are fluid sensitive sequences. The affected muscles are usually bulky and appear heterogeneous with hyperintense signals on T2-weighted and STIR sequences. This is secondary to increased water content from edema and inflammatory changes that accompany the infarction and sometimes due to presence of hemorrhagic foci10,14,15. The affected muscles appear hypointense or isointense on T1-weighted images with loss of normal fatty intramuscular septae. Hyperintensity on T1-weighted images may likely represent hemorrhagic infarction4,17. Subcutaneous and perifascial edema can be present7,18,19. On post-gadolinium scans, there is diffuse heterogeneous enhancement with low signal, non-enhancing foci which may represent areas of necrosis. Rim enhancement can be seen around these areas of necrosis within the areas of ischemic muscle4,14. The bone and marrow changes can also be assessed simultaneously to rule out concurrent osteomyelitis. As MRI findings are highly sensitive and specific to some extent, biopsy can be avoided in these patients.

The common differential diagnosis includes infections (cellulitis, abscess, necrotizing fasciitis), inflammatory (thrombophlebitis, polymyositis), traumatic (muscle tear, intramuscular hematoma) and neoplastic causes (soft tissue sarcoma, lymphoma)2,8,12. In cellulitis, subcutaneous swelling is seen, but with no muscle involvement. Necrotizing fasciitis has MR findings including muscle swelling, edema and inflammatory changes similar to DMI. But when compared to DMI, necrotizing fasciitis has less pronounced muscle involvement and more extensive fascial involvement. Additionally, gas bubbles and fluid collection may be seen in the tissues. Also, clinically, they present with systemic signs of infection, including fever and elevated peripheral WBC count, in addition to cellulitis, and do not present with severe pain which is characteristic of DMI4,10,14. Soft tissue tumors usually present as masses within a single muscle or multiple muscle groups in a compartment. Multiple, discontinuous muscle involvement and/or bilateral involvement is extremely unlikely in primary tumors. These masses may be enhancing or non-enhancing depending on the tissue types and may have intratumoral necrosis. They usually do not present with sudden and severe muscle pain10.

Treatment includes bed rest, analgesics and careful metabolic control of diabetes to prevent possible recurrence. Surgical intervention is required only in patients who do not respond to conservative management. Short term prognosis is usually good with spontaneous resolution of symptoms in a few weeks. Long-term prognosis is generally poor, due to the fact that the patient already has widespread diabetic vascular disease by the time they present with DMI. Although self-limiting, recurrence is common, either in the same muscle or in another muscle2,3,11,12,16,19. Mean mortality rate within two years of DMI onset is 10%, with cause of death being diabetic macroangiopathy complications4,5,11,19.

In summary, presence of edematous and bulky muscles with high signal on T2-weighted and STIR sequences of MRI along with a clinical history of sudden onset, severe pain in the thigh or calf in a patient with long standing diabetes mellitus strongly favors a diagnosis of diabetes muscle infarction. With appropriate and adequate clinical history and typical MR findings, a confirmatory diagnosis of DMI can be made and biopsy or surgical intervention can be avoided.

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