Diabetic Muscle Infarction

Myocardial infarct equivalent

  1. Kai Ming Chow, MRCP1,
  2. Cheuk Chun Szeto, MRCP, MD1,
  3. Teresa Yuk-hwa Wong, MRCP1,
  4. Franky Kay-tai Leung, MRCP2,
  5. Au Cheuk, MRCP3 and
  6. Philip Kam-tao Li, FRCP, FACP1
  1. 1Department of Medicine & Therapeutics, Prince of Wales Hospital, the Chinese University of Hong Kong, Shatin, Hong Kong, SAR, China
  2. 2Department of Medicine & Geriatrics, Tuen Mun Hospital, Tuen Mun, Hong Kong, SAR, China
  3. 3Department of Medicine & Geriatrics, Princess Margaret Hospital, Hong Kong, SAR, China

    Diabetic muscle infarction (DMI) is a serious complication seen in patients with long-standing diabetes. Evidence is accumulating since the first description of this entity in 1965 (1). Increasing awareness has led to prompt recognition of this previously underdiagnosed condition. Typically, acute presentation with atraumatic painful swelling, notably of the quadriceps or thigh muscles, is found in diabetic subjects with established vasculopathy including retinopathy and nephropathy. Laboratory investigations generally show high erythrocyte sedimentation rate, normal white cell count, and normal or mild elevation of creatine phosphokinase. Magnetic resonance imaging (MRI) findings are invariably characterized by increased signal intensity of the diffusely enlarged muscle groups on T2-weighted sequences, inversion-recovery, and gadolinium-enhanced images (24). The disease is generally believed to be self-limiting, although recurrence can occur in half of the cases (4,5).

    We have previously reported two cases of diabetic muscle infarction in our dialysis population (6). Over the last 2 years, we encountered six patients who had confirmed diabetic muscle infarction. Half of them were males. The vast majority of subjects were in their forties, with a mean age of 43.5 ± 6.5 years. All cases had established complications of diabetic nephropathy and retinopathy. Of the six patients, five had reached end-stage renal disease, with average duration of dialysis for 17 months. Only one had angiographic evidence or symptoms suggestive of coronary artery disease. When we examined the survival outcome in temporal relationship to the onset of diabetic muscle infarct, there appeared to be an early hazard of death of all causes related to this particular complication. Of the original six patients, three had succumbed after a median follow-up of 10 months (range 2–20 months). No fatality was directly related to diabetic muscle infarct. One death was related to cardiac ischemia and the other two were attributed to infection. The estimated 1-year survival for the cohort was 55%, as compared with 58% in patients with ischemic heart disease and 75% for those without history of coronary heart disease or diabetic muscle infarct among our dialyzed diabetic populations. The low survival figure of the muscle infarct group is surprisingly comparable to the overall mortality of 59% at 1 year after acute myocardial infarction among (diabetic and nondiabetic) patients on long-term dialysis (7).

    Interestingly, our findings coincide with another series of six patients with diabetic muscle infarct, in which five subjects died after being followed-up for at least 4 years (8). The abysmal prognosis or survival outcomes of patients with diabetic muscle complications were also similar to that of the diabetic population after an acute myocardial infarction episode. In general, the chance of diabetic patients being alive 1 year after myocardial infarct was 47% (9).

    In other words, skeletal muscle infarction in a diabetic population has similar prognosis as compared with myocardial infarct. It should be pointed out that, although the two conditions have similar prognosis, they are probably mediated by different vascular events. The former is related to major coronary arterial occlusive disease while diabetic skeletal muscle infarction is believed to involve microvasculature and ischemia reperfusion injury (5,6,8). Nevertheless, both disease processes signify considerable vascular disease and systemic inflammation. Elevation of erythrocyte sedimentation rate in many cases of diabetic muscle infarction does support the presence of an inflammatory reaction (4), although it remains unclear whether this is a primary event or a consequence of muscle infarction and necrosis.

    From our preliminary findings and others (8), we have shown that DMI is a catastrophic event associated with dismal long-term survival. Current data support a link with inflammation, but the association between DMI and poor long-term survival has yet to be elucidated. Alternatively, DMI indicates a very late stage of terminal diabetic complication. This may represent a new paradigm for prognostic stratification of diabetic patients based on the presence of microangiopathy. It remains unknown whether therapeutic measures that are effective in improving the prognosis of patients after acute myocardial infarction, aspirin for example, would be equally useful in diabetic muscle infarction.

    Footnotes

    • Address correspondence to Dr. C.C. Szeto, Department of Medicine and Therapeutics, the Chinese University of Hong, Kong, Prince of Wales Hospital, Shatin, Hong Kong. E-mail: ccszeto{at}cuhk.edu.hk.

    References

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