Background: Diabetic myonecrosis is a rare complication of diabetes mellitus with less than 200 cases reported in the literature since initial description in 19651. Diabetic myonecrosis most commonly affects the thigh and usually presents with acute muscle pain, edema, and erythema in the absence of trauma or fever1. The pathogenesis has yet to be elucidated—atherosclerosis, microangiopathy, vasculitis, and ischemia-reperfusion injury have been theorized. Laboratory findings are relatively nonspecific—of the findings reported in a systematic review, CRP was elevated in 90%, ESR elevated in 83.3%, WBC elevated in 42.5%, and CK elevated in 31.6%1. Definitive diagnosis can be made by muscle biopsy which demonstrates muscle necrosis and edema; however, it is not routinely recommended due to procedural complications. MRI is the diagnostic modality of choice for diabetic myonecrosis which is both sensitive and specific for the diagnosis2. Clinical Case: 76-year-old male with T2DM presented to regional hospital with severe right lower leg pain in the absence of fever, tachycardia, hypotension, or recent trauma. Physical exam demonstrated discrete erythema of distal 2/3 of posterior right lower leg extending to the ankle distally. Labs demonstrated normal CK, elevated ESR, HgbA1c 8.2%, and negative blood cultures. MRI of the right lower extremity demonstrated abnormal prolongation of T2 relaxation time involving posterior muscle compartment including soleus and gastrocnemius with associated perifacial and subcutaneous edema. These findings were consistent with diabetic myonecrosis without evidence of osteomyelitis or abscess. Rest, optimal glycemic control, and aspirin were recommended and patient improved gradually with complete clinical resolution on outpatient follow-up. Conclusions: Diabetic myonecrosis is a rare complication of diabetes and should be considered in patients presenting with acute muscle pain. Among cases described in literature, 5.7% have affected the soleus and 5% have affected the gastrocnemius respectively1. The diagnostic modality of choice is contrast enhanced MRI with typical findings including hyperintense signal on T2 weighted images with associated muscular, perifascial, and/or subcutaneous edema3. The optimal treatment is yet unknown, but reasonable strategies based on case series include rest, glycemic control, and NSAID therapy1. References: 1. Horton WB, Taylor JS, Ragland TJ, Subauste AR. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Res Care. 2015;3(1):e000082. doi:10.1136/bmjdrc-2015-000082 2. Morcuende JA, Dobbs MB, Crawford H, Buckwalter JA. Diabetic muscle infarction. Iowa Orthop J. 2000;20:65–74. 3. Goswami P, Baruah MP. The Role of MRI in Diagnosis of Diabetic Muscle Infarction : an Underdiagnosed Entity. Int J Endocrinol Metab. 2012;9(2):353–355. doi:10.5812/kowsar.1726913X.1886
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