Diabetic foot ulcers and infections: Current concepts

Advances in Skin & Wound Care, Jan/Feb 2002 by Calhoun, Jason H, Overgaard, Kristi A, Stevens, C Melinda, Dowling, James P E, Mader, Jon T

PURPOSE

To offer an educational experience that will help improve the participant's understanding of diabetic foot ulcers and infections.

TARGET AUDIENCE

This CME/CE activity is intended for physicians and nurses with an interest in the prevention and treatment of diabetic foot ulcers and infections.

LEARNING OBJECTIVES

1. Describe the factors that put a diabetic patient's foot at risk for ulceration.

2. Identify the components of optimal treatment of diabetic foot ulcers.

3. Explain the roles of vascular and orthopaedic surgery in the treatment of diabetic foot ulcers and infections.

ADV SKIN WOUND CARE 2002;15:31-45.

Submitted August 23,2000; accepted in revised form May 29,2001.

Diabetic foot ulcers and infections are complicated and difficult to treat.

They occur in individuals with a systemic illness that has compromising effects on multiple areas of the body, including the nervous, vascular, musculoskeletal, and immunologic systems. Each of these compromised systems plays a variably weighted role in the occurrence, chronic nature, and eventual recovery or loss of limb in this patient population. The pathogenesis of diabetic foot ulcers and subsequent infections is complex and involves 3 interactive processes: angiopathy, neuropathy, and immunopathy. An understanding of these processes is essential for the treatment and prevention of diabetic foot ulcers.

Standard wound care for diabetic foot ulcers consists of thorough debridement, application of adequate wound dressings, frequent dressing changes, and use of off-loading devices. Adjunctive therapy such as hyperbaric oxygen, should be considered for nonhealing diabetic foot ulcers. Newer technologies brought about by tissue engineering and growth factor research offer further treatment options for some difficult-to-heal wounds.

Infection complicates treatment of a diabetic foot wound, requiring the use of antibiotic therapy and a more aggressive wound care strategy. The systemic nature of diabetes requires a team approach to the care of diabetic foot ulcers and infections, with wound care provided at a specialized facility. Ultimately, prevention of ulcers is the best form of care for the diabetic foot.

Pathophysiology

A diabetic foot wound is the most common cause for hospitalization of patients with diabetes.1-4 Pecoraro et als showed that ischemia was singularly responsible for lower limb amputation. McNeely et alb found 3 tests to be significant and independent predictors of foot ulceration: absence of the Achilles' tendon reflex, a foot insensate to the 5.07 SemmesWeinstein monofilament7 (North Coast Medical, Inc, San Jose, CA), and a transcutaneous oxygen tension (TcPO2) of less than 30 mm Hg. Of these, impaired cutaneous oxygenation was found to be the strongest risk factor for foot ulceration. These characteristics indicate a significant alteration of the wound healing process in the diabetic patient. The pathogenesis is complex and involves the interactive processes of angiopathy, neuropathy, and immunopathy.

Angiopathy

Diabetic angiopathy is perhaps the most frequent cause of morbidity and mortality in a patient with diabetes.8 Angiopathy can be divided into 2 categories: macroangiopathy and microangiopathy.

Macroangiopathy in a diabetic patient presents as a more diffuse disease than in a nondiabetic patient, with more multisegmental involvement and compromised collateral circulation. It is more often seen bilaterally in the lower extremities; the infrapopliteal vessels are more frequently involved9 than in nondiabetic patients. Vascular impairment, evaluated by resting Doppler ankle pressure, was found to correlate with the development of diabetic foot ulcers.11 Large vessel disease predisposes a patient with diabetes to foot lesions secondary to ischemic skin changes that, in turn, lead to ulceration and possible infection.

The subject of microangiopathy is a debated topic, with some researchers showing that it is a factor in diabetic foot ulceration and others showing that it is not. Tooke and Brash" discussed the hemodynamic hypothesis of the pathogenesis of diabetic microangiopathy. This hypothesis states that in the early stages, vessel capillaries of diabetic patients have increased microvascular pressure and flow. The increased capillary pressure results in an injury response within the microvascular endothelium. Injury causes release of extravascular matrix proteins, resulting in microvascular sclerosis. Sclerosis is manifested in the arteriole as hyalinosis and in the capillary as basement membrane thickening,12,is the ultrastructural hallmark of diabetic microangiopathy. With increasing duration of diabetes, the sclerotic process results in limitation of vasodilatation with reduced maximal hyperemia and in loss of autoregulatory capacity. A key observation has been that nailfold capillary pressure is elevated in the early stages of type 1 diabetes. This has been positively correlated with glycemic control, judged by the glycosylated hemoglobin value at the time of pressure measurement. In addition, pressure appears to be particularly high in those individuals at high risk for microangiopathy, yet relatively normal in patients who have avoided the clinical complications of diabetes over many years.