Current Concepts In Diagnosing Chronic Diabetic Foot Ulcerations

Author(s): 
Molly Judge, DPM, FACFAS

   Think about the last time a diabetic ulceration gave you a problem. Do you recall just how thick the skin was? Did it seem like the center of the ulcer was improving but that the edges of the wound became thick, keratotic and kept developing a macerated base? Have you ever noticed the center of an ulcer that seemed to fill in but the edges of the wound stayed so stiff that the margins never would epithelialize toward the center?

   What is missing in this scenario is the identification and treatment of an associated dermopathy. While the easiest way to a diagnosis is biopsy of the skin, in the case of diabetic dermopathy, a simple pinprick test can be revealing. There are a few types of dermopathy associated with the population of patients with diabetes and those entities can often thwart wound healing progress.

   Dermatopathology associated with ulcerations in patients with diabetes. Chronic skin conditions can be present as a primary etiology of ulceration or as a secondary complicating condition interfering with the wound healing process. Diabetic dermopathy, necrobiosis lipoidica diabeticorum and diabetic thick skin are categories of dermatopathology that physicians commonly encounter yet they often go undiagnosed.

   Diabetic dermopathy. One can suspect diabetic dermopathy when the history includes the development of darkening spots throughout the pretibial portion of the limb. The pattern of distribution is asymmetric and typically bilateral. These areas of skin appear atrophic and heal by way of scarring.22 Under the microscope, you will see edema of the papillary dermis, thickened superficial blood vessels, extravasation of erythrocytes and a mild lymphocytic infiltrate. Whenever red blood cells extravasate into layers of the skin, the iron in the hemosiderin essentially causes a tattooing of the skin and dark patches develop.23-25

   Necrobiosis lipoidica diabeticorum. This is a degenerative disease of collagen of the skin and subcutaneous tissue in which an atrophic epidermis and granulomatous dermis develop. If patients are exposed to trauma, trivial or otherwise, an ulceration can develop. In some patients, the lesions become vesicular and rupture the skin, often causing ulcerations in the most vulnerable portion of the lower extremity, the pretibial region. As many as one-third of these lesions may go on to ulcerate.26,27 What causes this condition? It is not perfectly understood but the theory is that microangiopathy causes degradation of dermal collagen. Some authors have suggested that it may be an immune modulated dysfunction that causes the condition.26,27

   Chronic inflammation of the lower extremity from exposure to cytokines may be responsible for the degradation of collagen.28,29 This condition reportedly affects 0.3 to 0.7 percent of patients with diabetes, and affects women more often. At their earliest onset, necrobiosis lipoidica diabeticorum lesions look well-circumscribed with erythematous plaques that have a concave and waxy telangiectatic centroid.26,30

   Early on, these areas appear vasculitic. Microscopic examination will confirm these areas of vasculitis to be the result of neutrophil infiltration. Over time, lesions progress from granulomatous to sclerotic and most often present in the pretibial regions. When this occurs in regions other than the lower extremity, there is less of an association with diabetes.23,31-32

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