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Evaluation and Treatment of Diabetic Foot Ulcers
Author(s) -
Ingrid Kruse,
Steven V. Edelman
Publication year - 2006
Publication title -
clinical diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.931
H-Index - 37
eISSN - 1945-4953
pISSN - 0891-8929
DOI - 10.2337/diaclin.24.2.91
Subject(s) - medicine , diabetic foot , foot (prosody) , diabetes mellitus , intensive care medicine , endocrinology , philosophy , linguistics
D iabetic foot problems, such as ulcerations, infections, and gangrene, are the most common cause of hospitalization among diabetic patients. Routine ulcer care, treatment of infections, amputations, and hospitalizations cost billions of dollars every year and place a tremendous burden on the health care system.The average cost of healing a single ulcer is $8,000, that of an infected ulcer is $17,000, and that of a major amputation is $45,000. More than 80,000 amputations are performed each year on diabetic patients in the United States, and ∼ 50% of the people with amputations will develop ulcerations and infections in the contralateral limb within 18 months. An alarming 58% will have a contralateral amputation 3-5 years after the first amputation. In addition, the 3-year mortality after a first amputation has been estimated as high as 20-50%, and these numbers have not changed much in the past 30 years, despite huge advances in the medical and surgical treatment of patients with diabetes.“The majority of foot ulcers appear to result from minor trauma in the presence of sensory neuropathy.” This famous but simple quote from McNeely et al.1 best describes the critical triad most commonly seen in patients with diabetic foot ulcers: peripheral sensory neuropathy, deformity, and trauma. All three of these risk factors are present in 65% of diabetic foot ulcers. Calluses, edema, and peripheral vascular disease have also been identified as etiological factors in the development of diabetic foot ulcers.Although the pathogenesis of peripheral sensory neuropathy is still poorly understood, there seem to be multiple mechanisms involved, including the formation of advanced glycosylated end products and diacylglycerol, oxidative stress, and activation of protein kinase Cβ. Furthermore, the Diabetes Control and Complications Trial2 and other prospective studies have confirmed the pivotal role of hyperglycemia in the onset and …

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