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Diabetic Musculoskeletal Complications and Their Imaging Mimics Dr. Mohit Goel JR II, 28 th march 2014 RadioGraphics, http://pubs.rsna.org/doi/abs/10.1148/rg.327125054 Published in: Jonathan C. Baker; Jennifer L. Demertzis; Nicholas G. Rhodes; Daniel E. Wessell; David A. Rubin; RadioGraphics 2012, 32, 1959-1974. DOI: 10.1148/rg.327125054 © RSNA, 2012

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Diabetic Musculoskeletal Complications and Their Imaging Mimics

Dr. Mohit GoelJR II, 28th march 2014

RadioGraphics, http://pubs.rsna.org/doi/abs/10.1148/rg.327125054

Published in: Jonathan C. Baker; Jennifer L. Demertzis; Nicholas G. Rhodes; Daniel E. Wessell; David A. Rubin; RadioGraphics  2012, 32, 1959-1974.DOI: 10.1148/rg.327125054© RSNA, 2012

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Muscle Disorders in Diabetes

Pedal Disorders in Diabetes

Spinal Disorders in Diabetes

Diabetic Musculoskeletal Complications

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Muscle Disorders in Diabetes

1. Diabetic Muscle Ischemia

2. Infectious and Inflammatory Myositis

3. Muscle Denervation

4. Other Muscle Disorders

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Pedal Disorders in Diabetes

1. Osteomyelitis

2. Neuropathic Osteoarthropathy

3. Infected Neuropathic Osteoarthropathy

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Spinal Disorders in Diabetes

1. Dialysis-associated Spondyloarthropathy

2. Pyogenic Spondylodiskitis

3. Neuropathic Spine

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Muscle Disorders in Diabetes

Diabetic Muscle Ischemia

DMI, also referred to as diabetic muscle infarction or diabetic myonecrosis, characteristically occurs in patients with long-standing, poorly controlled diabetes.

Pathology: muscle fiber necrosis and edema are seen in association with fibrinous occlusion of arterioles and capillaries

The clinical onset of DMI is abrupt, with severe thigh or calf pain and swelling that evolve over days or weeks, in the absence of leukocytosis and fever.

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MR imaging features of DMI include muscle enlargement, muscle edema, and fascial.

Muscle enhancement is seen, often with central regions of hypoenhancement or nonenhancement.

The findings may be unilateral or bilateral and often are seen in noncontiguous muscles in the thighs and calves

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DMI in a 40-year-old man with poorly controlled diabetes who presented after several weeks of severe right thigh pain and swelling.

T1WI FATSAT

T2WIFATSAT

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Contrast enhanced T1-weighted fat-suppressed

Subtraction MR images

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Infectious Myositis

Because of underlying immune dysfunction, diabetic patients are vulnerable to infectious pyomyositis, a disease that results from the hematogenous spread of bacteria to muscle.

This entity is an important differential diagnostic consideration in patients in whom the presence of DMI is suspected.

Although the imaging appearances of the two entities may overlap, imaging features favoring the diagnosis of pyomyositis over that of DMI include the presence of smooth-walled intramuscular abscesses with rimlike enhancement.

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By contrast, areas of muscle ischemia or necrosis in DMI tend to appear heterogeneous, with linear streaks of enhancement crossing central nonenhancing regions surrounded by extensive regions of enhancing muscle.

Clinical features favoring the diagnosis of infectious pyomyositis over that of DMI include fever, leukocytosis with a left shift, elevated inflammatory markers, and bacteremia.

The distinction between DMI and pyomyositis is important, because the latter requires antibiotic therapy and abscess drainage.

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Infectious pyomyositis in a 58-year-old man with tense and reddened calves, leukocytosis, and an elevated ESR.

T2-weighted fat-suppressed MR image

Contrast-enhanced T1-weighted MR image

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Inflammatory Myositis

Unlike DMI, inflammatory myopathies such as dermatomyositis, polymyositis, and inclusion body myositis usually manifest with insidious, gradually progressive proximal muscle weakness.

MR imaging findings of bilateral symmetric edema in the proximal muscles, particularly those in the pelvis and thighs, are helpful for identifying inflammatory myopathy and determining its severity.

The diagnosis is based on clinical history, physical examination, muscle enzyme testing, and muscle biopsy with immunostaining.

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Polymyositis in a 55-year-old woman with weakness of the proximal thigh muscles. T1-weighted MR image

T2-weighted MR image

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Muscle Denervation

Muscle denervation has a multiple etiology, with diabetic peripheral neuropathy being one of the most common causes.

Subacute muscle denervation is characterized by T2 signal hyperintensity in the affected muscles, which maintain their normal signal intensity and architecture on T1-weighted images.

In contrast, muscles affected by chronic denervation have reduced bulk and show evidence of fatty infiltration, which is best depicted on T1-weighted images.

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Subacute or chronic denervation manifests early and prominently in diabetic patients, usually affecting the intrinsic musculature of the foot.

Involvement of muscles within a peripheral nerve distribution, lack of associated fascial edema, and presence of peripheral neuropathy at physical examination help distinguish denervation due to diabetic peripheral neuropathy from that caused by DMI.

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Subacute-on-chronic muscle denervation in a 58-year-old diabetic woman.

T1WI

T2WI

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Other Muscle Disorders

Unilateral or bilateral pain and swelling of the thighs and calves also may result from deep vein thrombosis.

Because the clinical symptoms of DVT are nonspecific, the condition is often detected incidentally at MR imaging of the lower extremity.

The MR imaging manifestations of DVT are similar to those of DMI and include edema of deep muscle and fascia on images obtained with fluid-sensitive sequences. However, the presence of branching, tubular structures with peripheral enhancement and the involvement of contiguous muscles within the distribution of a draining vein help identify deep vein thrombosis.

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Deep venous thrombosis mimicking DMI in a 47-year-old man with rapidly developing left calf pain and swelling.

T2 FATSAT

T1 FATSAT

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Pedal Disorders in Diabetes

Osteomyelitis

Diabetic pedal osteomyelitis almost invariably results from an ulcer or abscess in contiguous soft tissue. Ulcers tend to occur in the anatomic sites that are subjected to the highest contact pressures during ambulation.

The development of classic radiographic features of osteomyelitis, including periostitis and bone destruction, may lag behind the clinical manifestations by 10–20 days, and radiography is relatively insensitive to small amounts of bone destruction.

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For these reasons, if the findings at initial radiography are inconclusive and the clinical suspicion persists that diabetic pedal osteomyelitis is present, the Infectious Diseases Society of America recommends that radiography be repeated 2–4 weeks later.

The most important finding for a diagnosis of diabetic pedal osteomyelitis is bone marrow edema immediately adjacent to a soft-tissue infection or ulcer, with or without evidence of cortical destruction

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Calcaneal osteomyelitis with necrotic soft tissue in the right heel of a 75-year-old diabetic man.

T1WI FAT SAT

T2WI FAT SAT

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POST CONTRAST T1 FAST SAT

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Neuropathic Osteoarthropathy

Although its pathogenesis is not completely understood, it has been suggested that repetitive trauma to insensate joints and autonomic dysfunction of blood flow result in bone hyperemia, resorption, and weakening. Localized inflammation then leads to bone destruction, joint subluxation and dislocation, and foot deformity.

In the setting of acute neuropathic osteoarthropathy, MRI shows extensive soft-tissue edema occurring in the absence of infection or ulceration.

Multiple foci of marrow edema are seen on both T1WI and fluid-sensitive MR images in the affected bones.

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Prominent subchondral edema and enhancement may extend far into the medullary cavity, although superimposed fractures also can contribute to changes in marrow signal intensity.

Subchondral cyst formation, articular erosions, and joint effusions are common, with periarticular enhancement occurring after the administration of intravenous contrast material.

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Acute neuropathic osteoarthropathy initially misdiagnosed clinically as pedal osteomyelitis in a 46-year-old diabetic man.

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T1 FATSAT

Post contrast

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Chronic neuropathic osteoarthropathy has a less inflammatory appearance, with less visible swelling and less marked edema and enhancement at MR imaging.

The bones may appear sclerotic at radiography, and they have low marrow signal intensity at MR imaging regardless of the pulse sequence used.

Subchondral cysts are well defined, and proliferative bone may be seen with debris, intraarticular bodies, and ankylosis. Joint subluxation or dislocation is common due to subchondral collapse, with resultant articular instability in later stages of the disease process.

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Chronic neuropathic osteoarthropathy in a 49-year-old diabetic woman

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Spinal Disorders in DiabetesDialysis-associated Spondyloarthropathy

The disorder was attributed to amyloid (β2-microglobulin) deposition in synovium, intervertebral disks, and other connective tissues.

Amyloid deposition may occur in both appendicular and axial skeletal structures; in the axial skeleton, it develops predominantly in the lower cervical spine

Characteristics of dialysis-associated spondyloarthropathy include intervertebral disk space loss, extensive vertebral endplate erosion and cyst formation, and minimal formation of endplate spurs.

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Dialysis-associated spondyloarthropathy in a 55-year-old man.

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T1W FATSAT T2W FATSAT

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Infectious spondylodiskitis, ankylosing spondylitis, and degenerative disk disease are important differential diagnostic considerations.

Clinical features including the absence of a fever and the presence of a normal ESR and normal WBC count also favor the diagnosis of dialysis-associated spondyloarthropathy over that of infectious diskitis.

Although degenerative disk disease also results in disk space narrowing and changes in the signal intensity of subchondral bone marrow, the endplate erosions with minimal osteophytosis that are found in dialysis-associated spondyloarthropathy are not expected to be present in degenerative disk disease.

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Pyogenic Spondylodiskitis

Classic imaging findings include a narrowed disk space with destruction of the neighboring vertebral endplates.

Spine infection usually begins in the anterior aspect of the vertebral body because of its rich blood supply and subsequently extends through the disk to neighboring vertebral bodies.

MRI shows decreased T1 signal intensity and increased T2 signal intensity in the affected vertebral endplates and disk.

Post contrast images at an early stage of the disease process include enhancement of the disk and along the vertebral endplates; at a later stage, enhancement is accompanied by progressive destruction of the vertebral body.

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Pyogenic spondylodiskitis in a 54-year-old diabetic man.

T1W FATSAT T2W FATSAT

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Contrast-enhanced T1-weighted fat-suppressed

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MRI features favoring pyogenic spondylodiskitis over dialysis-associated spondyloarthropathy include the presence of intradiskal fluidlike signal intensity and enhancement, both of which are uncommon in the latter condition.

A finding of paraspinal or epidural abscess also supports a diagnosis of infectious spondylodiskitis.

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Similarly, MR imaging features can help distinguish spondylodiskitis from degenerative disk disease.

In degenerative disk disease with Modic type 1 endplate changes are seen; the disk and endplates may also demonstrate enhancement; however, fluidlike signal intensity is generally lacking from the disk in the setting of degenerative disease, and a paravertebral phlegmon or fluid collection would be an unusual finding.

The presence of gas in the disk space is also suggestive of a degenerative process.

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Neuropathic Spine

Diabetes mellitus is now the most common cause of neuropathic disease of the spine.

The neuropathic spine (Charcot spine) displays intervertebral space narrowing, vertebral osteolysis and osteosclerosis, subluxations, abrupt curvature, and large endplate spurs.

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Neuropathic spine in a 64-year-old man.

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T2W FATSAT Contrast-enhanced T1 FATSAT

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Several features help distinguish neuropathic spinal arthropathy from spinal infection:

Observations of the disk vacuum phenomenon and facet involvement favor the diagnosis of neuropathic arthropathy over that of infection.

Spondylolisthesis and bone fragmentation also are seen primarily in neuropathic spinal arthropathy and not infection.

Finally, rimlike enhancement of the disk and marrow signal intensity changes throughout the vertebral body favor the diagnosis of arthropathy, whereas diffuse enhancement of the disk with marrow signal abnormalities confined to the vertebral body endplates support the diagnosis of infection.

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