Abstract

Abstract Diabetic myonecrosis is the term used for spontaneous ischemic necrosis of skeletal muscle, unrelated to atheroembolism or occlusion of major arteries. This is an uncommon manifestation of long-standing and poorly controlled diabetes mellitus. A 65-year-old Hispanic female presented to the Hospital with one-week history of worsening right thigh pain. She denied associated fever, trauma, history of blood clots, past surgery, recent travel, ect. Patient has history of uncontrolled diabetes type 2, diabetic neuropathy and End-Stage Kidney Disease on hemodialysis for the last 3 years. Home medications include gabapentin 300 mg daily and insulin 70/30 20 units twice a day. On physical exam, vital signs appeared within normal limits. There was right medial and anterior thigh fullness, warmth and tenderness without erythema or fluctuance. Laboratory studies are pertinent for HbA1C 8.8% (n <6.5%), C-reactive protein (CRP) 12.97 (n <0.5 mg/dL), Erythrocyte sedimentary rate (ESR) >130 (n 0–30 mm/hr), Creatinine: 6.2 (n 0.57–1.11 mg/dL), BUN 77 (n 6–20 mg/dL), CO2 19 (n 22–29 mEq/L) and albumin 2.7(n 3.5–5.0 gm/dL). Other labs including CPK, glucose, ANA panel and CBC are within normal limits. Patient was admitted with initial diagnosis of cellulitis without improvement in clinical status after 3 days of antibiotics. MRI of the right thigh showed proximal thigh muscle, cutaneous and subcutaneous edema. Right thigh muscle biopsy showed marked myonecrosis with surrounding endomysial edema, foci of histiocytes, fibroblasts, and regenerating muscle fibers. Histologic features, together with localized muscle pain, normal CPK, negative microbiologic studies and uncontrolled diabetes are consistent with diabetic myonecrosis. Insulin was adjusted for tight glucose control and patient was started on low dose aspirin with outpatient follow-up. Diabetic myonecrosis presents with acute onset of painful swelling that evolves over days or weeks. The most common affected areas are the front and back of the thigh and calf. The pathophysiology is not well understood but appears related to thromboembolic events secondary to microvascular endothelial damage leading to tissue ischemia, which triggers an inflammatory cascade causing local tissue damage and ischemic necrosis. Common laboratory findings include elevated ESR, CRP and HbA1C level. Treatment involves symptomatic management, rest, glycemic control, analgesia and low-dose aspirin. The optimal approach is uncertain and current treatment is based upon published case reports and case series; there have been no randomized trials to compare approaches or specific agents. Close patient follow-up and tight glycemic control are key elements to prevent progression of this condition.

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