Cath Lab Digest

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Index: Ostomy Wound Manage. 2007;53(11):40-48.

  Higher rates of lower extremity amputation, coupled with an increased incidence and severity of coronary artery disease and higher cardiovascular mortality rates, are well recognized in persons with diabetes.¹ Foot and leg ulcer healing often is poor in patients with arterial insufficiency²; in people with diabetes, compromised healing is substantially increased and the atherosclerotic process accelerated.³ Although both macro- and microvascular disease are implicated in complications in this patient group, diagnosis and treatment strategies remain controversial. For example, the concept diabetic small vessel disease has long been refuted yet still appears in the literature and often results in less aggressive treatments that inappropriately lead to amputation as a primary endpoint.¹ The purpose of this paper is to provide an indepth examination of the mechanisms leading to peripheral vascular disease (PVD), as well as the role of hyperglycemia in persons with diabetes, to help elucidate potential diagnostic options, flaws in related research, and therapies that may prevent devastating sequellea.

Anatomy and Physiology

  The circulatory tree encompasses two distinct but connected vascular systems: macrovascular and microvascular. A reduction in macrovascular flow may predispose to flow reductions in the microvascular system. However, large and smaller vessel diseases in persons with diabetes do not progress at the same rate; small vessels in the toes may exhibit ischemia in the presence of palpable dorsalis pedis and posterior pulses.⁴ After reviewing the literature, Ennis and Meneses⁵ concluded that the importance of blood flow and oxygen delivery to a wound bed cannot be overstated. Despite heroic efforts by wound care specialists, ulcerations will not heal in the presence of pronounced PVD.

  Macrovascular disease. Strandness⁶ demonstrated that the prevalence of arterial disease in the limbs of persons with diabetes was approximately 20 times higher than in a comparable age- and sex-matched persons without diabetes. In a prospective study, Beach et al⁷ compared 252 volunteers between the ages of 50 and 70 years with type 2 (non-insulin-dependent) diabetes to 158 control subjects. The authors determined that in type 2 diabetes, new arterial disease developed in 14% of patients over a 2-year period with an 87% incidence of disease progression within the same time frame. More startling, the mortality rates for patients with occlusive disease reached 22% versus 4% in patients free of arterial disease.

  A review of the literature⁸ confirms that although arteriosclerosis (ASO) in persons with type 2 diabetes is physiologically similar to ASO in persons who do not have diabetes, its distribution appears more diffuse with a predilection for arteries distal to the knee and femoropopliteal segments (distal arteries in the foot and ankle usually are spared) in persons with diabetes. However, in persons with diabetes, medial calcification (Monckeberg’s medial sclerosis) may develop in the tibial and peroneal arteries.