Diabetic muscle infarction is an unusual complication of late-stage diabetes. The first case was reported in 1965 by Angervall and Stener (1). There have been <100 cases reported since then (4). Clinical presentation is an acute atraumatic painful swelling of the affected muscle and a palpable mass. Diabetic muscle infarction has predilection for the quadriceps and thigh muscles and is found in diabetic subjects with established nephropathy and retinopathy (2).
We report a case of spontaneous quadriceps necrosis in a type 2 diabetic patient on hemodialysis. A 59-year-old woman had a type 2 diabetes history of >20 years and unsatisfactory glycemic control despite insulin therapy. This condition was complicated by proliferative retinopathy, neuropathy, and nephropathy. In 2003, the patient progressed to end-stage renal disease and required hemodialysis. Her serum creatinine level was 5.7 mEq/l (normal value 0.5–1.3). Other medical problems included hypertension, heart failure with pulmonary hypertension, and moderate myocardial depression. Coronary vessels were normal by catheterism.
The patient was admitted for a painful swelling of her left anterior thigh for 7 days. There was no history of recent trauma or muscular injection. On physical examination, she showed a localized swelling and heating of the left thigh. Her body temperature was 37.3°C. Laboratory findings included a normal leukocyte count at 10,000 cells/mcl (normal value 5,000–10,000), with 84.6% (55–65) neutrophils; creatine kinase at 313.5 IU/l (32–162); alkaline phosphatase at 424 IU/l (40–190); fibrinogen at 468 mg/dl (150–350); lactate dehydrogenase at 327 IU/l (150–450); Na+ at 126.5 mEq/l (135–145); and K+ at 5.7 mEq/l (3.5–5.0).
A Doppler ultrasound of her left inferior limb excluded a deep venous thrombosis and revealed minimal atheromatosis. Magnetic resonance imaging demonstrated edema and pronounced swelling of the left rectus femoris in T2-weighted sequences that suggested a muscular necrosis. The contralateral thigh was normal.
The differential diagnoses, i.e., deep venous thrombosis, thromboflebitis, fracture, pyomiositis, necrotizant fascitis, myositis or dermatomyositis, and connective tissue tumor, were excluded by the clinical presentation, together with the ultrasound and magnetic resonance imaging. A diagnosis of diabetic muscle necrosis was made. Symptomatic treatment, bed rest, and analgesia were continued, and the pain improved in a period of 3–4 weeks.
According to the literature, diabetic muscle infarction is more frequent in long-standing diabetic women (∼15 years), with an average age at presentation of 43 years and multiple end-organ diabetes complications, retinopathy, neuropathy, nephropathy in peritonal dialysis or hemodialysis, and gastroenteropathy (3). It has predilection for the quadriceps (62%), hip adductors (13%), hamstrings (8%), and hip flexors (2%) (4). Myonecrosis, although typically involving the thigh, can extend to the calf (5). Curiously, muscle enzymes could be normal or marginally elevated.
The pathogenesis of this disease is unclear. Several hypotheses have been suggested. Muscle infarction could be caused by atherosclerosis and diabetic microangiopathy. Other hypotheses discuss an alteration in the coagulation-fibrinolisis system as the cause of diabetic muscle infarction, as described by Palmer and Greco (6) in two patients with this disease and antiphospholipid syndrome. Gargiulo et al. (7) indicated the role of antiphospholipid antibodies in the progession of diabetes complications.
In summary, diabetic myonecrosis should be suspected in diabetic patients who develop a painful swollen muscle.
