ABSTRACT
INTRODUCTION Diabetic foot ulcers pose a great burden to both the patient and the health care system. These ulcers have a poor tendency to heal and can result in infection and gangrene, leading to long-term in-hospital treatment and/or amputation (1). Foot ulcers have major negative effects on the quality of life due to morbidity, loss of work, loss of mobility, and reduction of social activities (2). As summarized by Boulton (3), the commonest component causes in the pathway to ulceration include diabetic neuropathy, foot deformity, external trauma, peripheral vascular disease, and peripheral edema. The vast majority of patients with a diabetic foot ulcer will have signs of sensory loss in their feet, although sensation can be present in some patients with pure ischemic foot ulcers (4). Because of the loss of protective sensation, acute trauma or chronic repetitive biomechanical stress caused by elevated foot pressures and/or ill-fitting shoes are perceived less well, and finally an ulcer develops (3,5). In addition, in most patients, foot ulceration is a sign of multiple and extensive changes that occur in the lower extremity as a consequence of diabetes. These changes include loss of normal anatomic integrity, loss of function, impaired tissue perfusion, and enhanced susceptibility to tissue damage and infection (6). In many patients, these processes develop with signs or symptoms that are not easily recognized by the patient and the health care workers involved. Moreover, many of the underlying pathologies are not limited to the foot but are a sign of widespread disease. In this chapter, current views on the clinical presentation, epidemiology, pathogenesis of diabetic neuropathy, and its consequences for the lower extremity have been summarized .
