Heel Ulcerations in the Diabetic Patient

Morris D. Kerstein, MD


Wounds. 2002;14(6) 

In This Article

Abstract and Introduction

Of 53 diabetic patients with hospital-acquired heel ulcers, 20 (38%) lost their ipsilateral leg -- 15 below the knee, 5 above the knee. Time to healing of the remaining 33 patients with heel ulcers was 31 to 301 (mean 142) days. Of the 33 patients, 12 (36%) had a recurrence of their heel ulcers. Dominant features among the patients were ipsilateral stroke, smoking, and inadequate circulation. Race, gender, and age were not statistically significant.

Heel ulcers result in a break in the dermal barrier with subsequent erosion of the underlying subcutaneous tissue. As severity increases, the defect extends to muscle and bone, representing one of the most costly, in terms of dollars as well as disability, complications in the elderly. This complication escalates the length of hospital stay and cost of care. The heel is the second leading site for development of pressure ulcers after the sacrum.[1]

Hospital-acquired heel pressure ulcers represent a significant morbidity and often result in limb loss. Diabetic foot ulceration, including heel ulceration, is a major complication of diabetes mellitus, with a lifetime incidence of three percent a year and 15 percent in a lifetime. During the last five years, the incidence of hospital-acquired heel ulcers has increased from 19 percent to 30 percent.[2,3]

The lack of perfusion decreases tissue resistance, leads to rapid tissue death, and impedes wound healing. Ischemia due to vascular insufficiency impedes wound healing by reducing the supply of oxygen,[4] nutrients, and the mediators of the repair process. Although peripheral arterial disease alone infrequently precipitates ulceration, it has a dominant role in delayed wound healing and gangrene.

Neuropathy is a major contributing risk factor for foot ulcers and can involve both somatic and autonomic fibers. The myelinated type A sensory fibers are associated with proprioception, sensation of light touch, pressure, and vibration, and motor innervation of the muscle spindles. Neuropathy of the A fiber is ataxic gait and intrinsic weakness of the foot muscles. Neuropathy of the C sensory fibers is the loss of protective sensation; it results in the loss of pain threshold with prolonged and increased shear forces and associated repeated trauma. Loss of protective sensation due to peripheral neuropathy is the most common cause of ulceration.

Altered foot biomechanics, limited joint mobility, and bony deformities have been associated with an increased risk of ulceration and amputation. Abnormalities in foot biomechanics result in a dysfunctional gait, which leads to more damaging structural changes in the foot. Abnormal pressure points result in increased friction. Bony deformities of the metatarsal heads and forefoot result in areas of increased focal pressure.[1,5]

The risk of heel ulceration is proportional to the number of risk factors. The risk is increased by 1.7 in persons with isolated peripheral neuropathy, by 12 in those with peripheral neuropathy and foot deformity, and by 36 in those with peripheral neuropathy, deformity, and previous amputation as compared with persons without risk factors.

The focus of this manuscript is on those persons with heel ulcers and diabetes. These patients have mixed ischemic and neuropathic components. In fact, atherosclerosis occurs at a younger age in the diabetic patient, and neuropathy is present in 42 percent of diabetic patients after 20 years. Diabetic neuropathy is usually a distal symmetric sensorimotor polyneuropathy. The diabetic patient is prone to development of a neuro-osteoarthropathy, the Charcot foot; large and small vessel disease; autonomic neural dysfunction; tissue breakdown; and ulceration.

The purpose of this manuscript is to identify those risk factors that contribute to lower-extremity limb loss in a diabetic patient when the original problem is a heel ulcer. This study does not address moisture, friction, and shear.


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