Diabetic muscle infarction

A 55-year-old woman with type 2 diabetes of 8 years' duration experienced, over 2–3 days, the onset of pain, tenderness and swelling of the medial aspect of her right thigh.

She had recently commenced insulin therapy and was displaying good glycaemic control (HbA1c level of 6.4%). She had diabetic complications of autonomic and peripheral neuropathy, but no retinopathy. Other medical problems included chronic renal impairment, hypertension, polyarticular gout and hydralazine-induced lupus. A renal biopsy had not been performed, but her renal insufficiency was believed to be a result of diabetic nephropathy and hypertension. She was taking twice-daily mixed insulin (16 units in the morning and 10 units at night), felodipine (10 mg/day), paroxetine (10 mg/day), allopurinol (75 mg/day) and prednisolone (7.5 mg/day). Her serum creatinine level had peaked at 0.31 mmol/L, but stabilised at 0.21 mmol/L after cessation of an angiotensin-converting enzyme inhibitor. A 24-hour urine collection showed a creatinine clearance rate of 0.12 mL/s (normal range [NR], 1.5–2.5 mL/s) and a protein excretion rate of 4.6 g/day. Renal duplex ultrasound showed that her kidney size was well preserved, but there was a suggestion of renal artery stenosis on the right side.

There was no history of recent injury or injection to her thigh. She had not experienced any rigors and was afebrile. The area of the localised, tender swelling on the medial aspect of her right thigh was not erythematous and no local lymphadenopathy was noted. Apart from the thigh swelling, there was generalised wasting and weakness of the lower limbs, loss of ankle reflexes, and loss of sensation in a stocking distribution, consistent with a diagnosis of peripheral neuropathy. Examination of her left foot revealed two small gangrenous areas. Foot pulses were present and the gangrenous areas were thought to be caused by inappropriate footwear.

Figure 1: Computed tomography image of the thigh, showing marked oedema and thickening of the adductor muscle group (A), extensive subcutaneous oedema (B), and sparing of the hamstring muscle (C).

Investigations showed an elevated white cell count of 16 x 109/L (NR, 4.0–11.0 x 109/L), a platelet count of 432 x 109/L (NR, 150–400 x 109/L), an erythrocyte sedimentation rate of 110 mm/h (NR, 7–18 mm/h) and a C-reactive protein level of 119.3 mg/L (NR, 1.6–8.7 mg/L). Creatine kinase (174 U/L; NR, < 215 U/L) and lactate (0.6 mmol/L; NR, 0.5–2.0 mmol/L) levels were normal. Separate to the swelling on the medial aspect of the thigh, a presumed thrombus was palpable in the lateral accessory long saphenous vein. A subsequent ultrasound detected this thrombus extending from the mid thigh to the lateral aspect of the knee, but no deep venous thrombosis was found. She was treated with cephalexin and aspirin.

Over the next two weeks, the thigh swelling evolved into a tender, palpable mass measuring 6 x 20 cm. A computed tomography (CT) scan revealed marked swelling of the entire adductor muscle group, but no discrete mass (Figure 1). In the absence of a clear diagnosis, an exploratory operation of her right thigh was performed. This showed no haemorrhage or abscess, but evidence of extensive oedema and necrosis of the adductor muscles. Samples taken for microbiological analysis were sterile. Histological examination of a biopsy specimen showed necrotic muscle, an inflammatory cell infiltrate, fibrosis and evidence of muscle fibre regeneration. The occasional small blood vessel containing fibrin thrombus was also seen, but no features of vasculitis were identified (Figures 2 and 3). A diagnosis of diabetic muscle infarction was made.

Photomicrographs (original magnification x 250) of a biopsy specimen of the adductor group of muscles. Figure 2: Longitudinal section, showing necrotic muscle fibres (A) and granulomatous tissue (B). Figure 3: Cross-section showing necrotic muscle (A), an inflammatory cell infiltrate (B) and a blood vessel containing a thrombus (C). No evidence of vasculitis was seen.