الفهرس 
? Introduction & Aim of the workOnly 14 pages are availabe for public view
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Abstract
Persons with diabetes who develop foot ulcers are at high risk for subsequent foot ulcers and amputations. The hospital discharge rate for foot ulcers has decreased in the United States in recent years; however methodological differences may be partially responsible. Specific evidence is available demonstrating the benefit of better blood glucose control, and self-care strategies learned through patient education to prevent lesions in high-risk patients. Although an occlusive disease of the microcirculation does not exist, functional impairment of the microcirculation in diabetes may contribute to secondary complications such as foot infections and ulcerations. Microcirculation to the diabetic foot suffers both structural and functional derangements. Nerve–axon-related microvascular reactivity is clearly impaired in the diabetic population and there is a growing belief that both the failure of the vessels to dilate and the impairment of the nerve-axon reflex are major causes for impaired wound healing in patients with diabetes. Foot ulcers in diabetes result from multiple pathophysiological mechanisms, including roles for neuropathy, peripheral vascular disease, foot deformity, higher foot pressures, and diabetes severity. Diabetic neuropathy and peripheral vascular disease are the main etiological factors which predispose to foot ulceration and may act alone, together, or in combination with other factors, such as microvascular disease, biomechanical Abnormalities, and an increased susceptibility to infection. Trauma is needed in addition to neuropathy and vascular disease to cause tissue breakdown.Trauma could be intrinsic, such as repetitive stress from high pressure and/or callus, or extrinsic such as from ill-fitting footwear rubbing on the skin or an object inside the shoe (e.g., drawing pin and pebble).