365 Day

365 The etiology of pedal ulceration among patients with diabetes mellitus is usually multifactorial. While the initiating element may be singular, there are usually coexisting factors that help to lower the threshold for pedal ulceration. Thus, the precipitating event produces tissue breakdown and ultimately ulceration. There have been numerous studies of the risk factors for amputation in the diabetic patient, factors that parallel those for ulceration. While several studies have shown the associated contribution of local physiologic and structural factors that lead to pedal ulceration, other systemic physiologic and relative socioeconomic elements have been shown to contribute to the risk of ulceration (Table 1). In 1992, Reiber et al1 proposed the causal pathway to amputation model consisting of component causes that, in and of themselves, do not typically produce ulceration and the sufficient cause, which is the accumulation of component causes that lead to amputation. That model showed that component factors such as neuropathy, vasculopathy, and impaired wound healing provided the underlying environment that facilitated progression to amputation in the lower extremity following some traumatic event. It is important to understand this model when considering the risk factors for ulceration in that these factors rarely occur alone.

[1]  A. Boulton,et al.  The Association Between Callus Formation, High Pressures and Neuropathy in Diabetic Foot Ulceration , 1996, Diabetic medicine : a journal of the British Diabetic Association.

[2]  N. Chaturvedi,et al.  The Relationship Between Socioeconomic Status and Diabetes Control and Complications in the EURODIAB IDDM Complications Study , 1996, Diabetes Care.

[3]  Juan C. Garbalosa,et al.  Foot Function in Diabetic Patients after Partial Amputation , 1996, Foot & ankle international.

[4]  L. Lavery,et al.  Increased Foot Pressures After Great Toe Amputation in Diabetes , 1995, Diabetes Care.

[5]  J E Tooke,et al.  Microvascular Function in Human Diabetes: A Physiological Perspective , 1995, Diabetes.

[6]  J. Tooke,et al.  Pathophysiology of microvascular disease in non-insulin-dependent diabetes. , 1995, Clinical science.

[7]  A. Shore,et al.  Capillary Pressure in Patients With NIDDM , 1994, Diabetes.

[8]  A. Veves,et al.  The Prediction of Diabetic Neuropathic Foot Ulceration Using Vibration Perception Thresholds: A prospective study , 1994, Diabetes Care.

[9]  A. Boulton,et al.  Role of Experimental Socks in the Care of the High-Risk Diabetic Foot: A multicenter patient evaluation study , 1993, Diabetes Care.

[10]  T. Koepsell,et al.  Risk Factors for Amputation in Patients with Diabetes Mellitus , 1992, Annals of Internal Medicine.

[11]  J. Tooke,et al.  Aetiology of Diabetic Foot Ulceration: A Role for the Microcirculation? , 1992, Diabetic medicine : a journal of the British Diabetic Association.

[12]  A. Veves,et al.  Relationship of Limited Joint Mobility to Abnormal Foot Pressures and Diabetic Foot Ulceration , 1991, Diabetes Care.

[13]  G. Reiber,et al.  Pathways to Diabetic Limb Amputation: Basis for Prevention , 1990, Diabetes Care.

[14]  Michael J. Mueller,et al.  Insensitivity, limited joint mobility, and plantar ulcers in patients with diabetes mellitus. , 1989, Physical therapy.

[15]  D. Yue,et al.  Limited Joint Mobility in the Diabetic Foot: Relationship to Neuropathic Ulceration , 1988, Diabetic medicine : a journal of the British Diabetic Association.

[16]  D. Sims,et al.  Plantar sensory threshold in the ulcerative foot. , 1986, Leprosy review.

[17]  J. Bowker,et al.  Impaired Vibratory Perception and Diabetic Foot Ulceration , 1986, Diabetic medicine : a journal of the British Diabetic Association.

[18]  R. Weg The Physiological Perspective , 1983 .

[19]  P. Brand Management of the insensitive limb. , 1979, Physical therapy.