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Diabetic Myonecrosis Krista Fajman, MD January 29, 2010 Diabetic Myonecrosis 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 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 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 MRI – T2 weighted images show high intensity signal in affected muscles. T1 images show subcutaneous edema, subfascial fluid, loss of normal fatty intramuscular septa 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 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 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 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 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. www.Imaging.Consult.com