How To Manage Heel Ulcers In Patients With Diabetes

Author(s): 
By Jonathan Moore, DPM, and Pamela Jensen, DPM

   Diabetic heel ulcers constitute one of the most frustrating problems for podiatric physicians. Pressure ulcers affect nearly 2 million people each year and account for annual healthcare costs that range between $2.2 billion and $3.6 billion. The heel is the second leading site for development of pressure ulcers after the sacrum.1 While patients with diabetes are living longer than in the past, the incidence of hospital-acquired heel ulcers increased from 19 percent in 1989 to 30 percent in 1993.2    Costs for heel ulcers are nearly double that of the costs associated with forefoot ulceration.2 Given the higher incidence of osteomyelitis in the calcaneus along with the presence of vascular disease, patients with diabetic heel ulcers present a significant challenge for limb salvage. It is vital to have a thorough understanding of the associated comorbidities that complicate diabetic wounds in order to manage these patients successfully and prevent potential limb loss. Accordingly, a multidisciplinary approach is essential. Initiating appropriate consults and dialogue with vascular surgery, endocrinology and internal medicine is crucial to successful treatment.

Assessing Possible Etiologies

   As part of the preliminary evaluation, one should determine the etiology of the ulcer. The most common contributing factors to the development of diabetic heel ulcers include diabetic neuropathy, immobility, structural deformity, peripheral vascular disease, trauma and age. Additional factors may include shearing/friction, temperature, age, edema and anemia.3    Diabetic neuropathy is the most critical component in the development of the diabetic ulcer. Whether precipitated by repetitive stress from poor weight distribution or from dyshidrosis and fissuring from autonomic neuropathy, one must assess the presence and extent of neuropathy in order to prevent these types of ulcers effectively.    A lack of mobility can generate excessive levels of pressure to the skin among older patients and those with deformity or illness. Poor mobility in the presence of edema and/or vascular disease can be a major factor in the development of an ulceration.    Heel ulcers represent localized areas of cellular necrosis that result from prolonged circulatory interference from pressure or shearing forces. Although pressure is a critical factor involved with skin breakdown, researchers have shown that shearing forces (stretching of blood vessels) compound the ischemic changes produced by external pressure and lead to an increased rate of tissue breakdown.4    If the heel is subjected to prolonged periods of pressure that exceed capillary pressure, ulceration will result.    In addition to pressure and friction, the shock absorption in the heel declines with age. The decreased shock absorption contributes to tissue breakdown and increased morbidity. Atrophy of muscle and fat tissues in patients with diabetes has been proposed as one of the possible factors that increases the risk of ulceration. Researchers have determined that heel thickness in non-ulcerated patients with diabetes is 2 mm less than the heel thickness in non-diabetic patients.5 Diabetic patients with a history of ulceration have heel thicknesses 3 to 4 mm less than non-diabetic patients.5

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