Nonsurgical Management of Chronic Wounds in Patients With Diabetes

Diabetes mellitus increases the risk for disorders that result in more frequent hospitalizations, longer in-patient stays, and increased morbidity and mortality. The incidence and severity of coronary artery disease, cerebrovascular disease, and peripheral artery macrovascular and microvascular diseases are greater in diabetics than in nondiabetics. Diabetic foot wounds are the single greatest cause of nontraumatic amputations. Unfortunately, in both inpatient and outpatient settings, diabetes management is often a secondary consideration when compared with the presenting condition or problem.1 It is well known that diabetics are more susceptible to infection than are nondiabetics2 secondary to hyperglycemia-induced phagocyte dysfunction. These defects include impairment of phagocyte adherence, chemotaxis, phagocytosis, and bacterial killing.2–18 The defects are at least partially reversible once blood glucose levels are controlled.12,15 In vitro studies suggest that blood glucose levels greater than 200 mg/dl are sufficient to cause leukocyte dysfunction.13,14,16 Clearly, hyperglycemia causes immunosuppression. Reduction of serum glucose restores immune functions. Hyperglycemia is also causally linked to a variety of vascular problems, including hypertension19–21 and thrombosis.22–26 However, the hyperglycemic impairment of microvascular blood flow and microvascular responses to injury are large contributors to the development of chronic ulcers in patients with diabetes and to overall resistance to healing of even noninfected wounds. Diabetic microangiopathy and foot ulcer development are the result of a spectrum of factors that include continuous trauma, neuropathy, immunosuppression, arterial occlusive disease, and capillary perfusion and permeability dysfunction.27–33 Diabetic microangiopathy is a type of high perfusion angiopathy that can mimic chronic venous insufficiency27–35 and is associated with the development of stasis-related increases in capillary pressure.29–44 Furthermore, diabetes disrupts the autonomic pathways of regulation of skin perfusion, even before development of the regional sensory loss, or neuropathy, that is common in patients with diabetes.45 Diabetic sensory neuropathy also affects the neurally mediated vasodilatory response normally associated with increased local cutaneous pressure.46–49 In patients with diabetes, cutaneous blood flow is decreased in proportion to the increased local pressure. Skin temperature and microcirculatory flow are closely related,50 and it is likely that the aberrant, pressure-induced decrease in skin blood flow is exacerbated by the typically low skin temperature in patients with diabetes. The inability of skin microcirculation in diabetics to respond appropriately to injury is an important factor leading to chronic wounds and diabetic ulcer development. The similarly abnormal responses of skin capillary beds in diabetics to warm water immersion and cold water immersion challenges suggest enhanced arteriovenous anastomotic blood flow resulting in reduced nutritional blood flow.51