Transcript Diabetic Myonecrosis - University of North Carolina at

Diabetic Myonecrosis
Krista Fajman, MD
January 29, 2010
Diabetic Myonecrosis
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Also known as diabetic muscle infarction
Usually affects longstanding poorly controlled
type I diabetics
In literature reviews, ages ranged from 18-91
years. Average age at presentation is 44.
Equal distribution between males and females.
Not related to trauma.
Signs and Symptoms
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Acute or subacute onset of pain and swelling. Can be
mild or severe. May have palpable mass.
Occurs in the quadriceps > 80% of the time. Calf
muscles 20% of the time. Rare in upper extremities.
Bilateral involvement in 10-30% of cases, recurrence in
occurs in 50%.
May have fever or leukocytosis.
CK and ESR elevated in 50% of patients. Elevation
does not correlate with disease activity.
Rare if any reports of associated adenopathy,
compartment syndrome or gangrene.
Differential Diagnosis
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Pyomyositis (due to Staph aureus)
Spontaneous gangrenous myonecrosis (due to Strep pyogenes)
Ischemic muscle necrosis
Clostridial myonecrosis
Necrotizing fasciitis
DVT, superficial venous thrombosis
Intramuscular hematoma
Neoplasm (sarcoma or lymphoma)
Focal or systemic myositis
Localized abscess
Osteomyelitis
Cellulitis
Diagnostic Imaging
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MRI – T2 weighted images show high
intensity signal in affected muscles. T1
images show subcutaneous edema,
subfascial fluid, loss of normal fatty
intramuscular septa
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Gadolinium can help but caution in this
patient group – likely have some degree
of renal dysfunction.
X-rays usually unhelpful
Ultrasound may show hypoechoic, well
defined intramuscular lesion which may
help differentiate from a necrotic mass or
abscess but no studies comparing
modalities have occurred.
Needle electromyography - may show
fibrillation potentials, small motor unit
potentials and positive sharp waves, some
areas of muscle can by silent indicating
replacement of muscle by fibrous tissue.
Muscle Biopsy
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Grossly presents as nonhemorrhagic, pale, whitish
muscle
Light microscopy shows large areas of muscle necrosis
and edema, phagocytosis of necrotic muscle fibers,
granular tissue and collagen. May also see occlusion of
arterioles and capillaries by fibrin.
At later stages you have replacement of necrotic muscle
fibers by fibrous tissue, myofiber regeneration, and
mononuclear cell infiltration.
Pathogenesis
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Etiology unclear but thought that muscle infarction arises from
vascular disease including atherosclerosis and diabetic microangiopathy
Chester and Banker – initial ischemic event (?embolic) leads to
ischemia that causes tissue swelling which through mass effect and
swelling compromises blood flow.
Small thrombotic/emoblic event leads to ischemic muscle damage,
causes an inflammatory response, reperfusion with generation of
reactive oxygen species causes further muscle damage, muscle edema.
Long standing hyperglycemia may affect arterial vasculature, platelets,
thrombolytic factors
Some authors feel that abnormality in the coagulation-fibrinolysis
system leading to hypercoagulability leads to venous occlusion leading
to increased plasma levels of plasminogen activatory inhibitor and
thrombomodulin.
Treatment
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No ideal treatment plan.
Rest and analgesics – anti-inflammatory agents ideal but caution
with NSAIDS depending on renal function. May need narcotics.
Antiplatelet agents. Daily ASA.
Daily activity okay but may be painful. Physical therapy may be
harmful.
Glycemic control
Glucocorticoids
Pentoxyfilline
Surgical excision – not recommended, associated with
complications
Short term prognosis good. Usually resolves over weeks to
months but overall poor prognosis.
References
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Hordon, Lesley. UpToDate Online. “Diabetic Muscle Infarction”
Morcuende, J. et al. “Diabetic Muscle Infarcation” The Iowa Orthopaedic Journal.
2000; 20: 65-74.
Silberstein et al. “An unexpected cause of muscle pain in diabetes”. Annals of
Rheumatologic Disease. 2001; 60: 310-312.
Trujillo-Santos, A.J. “Diabetic Muscle Infarcation. An underdiagnosed complication
of long-standing diabetes.” Diabetes Care. January 2003. Vol 26. No 1. 211-215.
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