Heel Ulcerations in the Diabetic Patient

Introduction 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. Materials and Methods During a five-year period (1995-2000), 53 patients with diabetes mellitus and a hospital-acquired heel ulcer were the basis for this study. All patients received either oral hypoglycemic medication, insulin, or both (Tables 1 and 2). Patients with vasculitis were excluded. Of 53 patients, 20 (38%) with heel ulcers lost their ipsilateral leg--15 below the knee (BK) and 5 above the knee (AK). Two of the five AK amputations were revisions of BK amputations. The time to healing for the remaining 33 patients was 31 to 301 days, with a mean of 142 days. Twelve of the 33 patients developed heel ulcers within one year of "healing" the first time, a recurrence rate of 35 percent. Four of these patients lost their lower extremity below the knee. Results Of those diabetic patients with limb loss and heel ulcers, the dominant features were ipsilateral stroke, smoking, inadequate circulation, and neuropathy (Table 2). Factors not statistically significant to diabetic lower-limb loss included race, gender, and age in patients with heel ulcers (Table 2). None of the treatments, except for the antibiotics used, differed from patient to patient in the amputation group. The treatments were overlapping and could not be comparatively assessed (Table 3). All wounds cultured multiple organisms. No attempt was made in the patient's chart to differentiate surface cultures from deep cultures. Discussion Heel ulcers more often result in limb loss than forefoot amputation. In a previous publication by this author, the authors state that transmetatarsal amputations are functional; heel amputations are not.6 The significant predictors of healing of heel ulcers include adequate circulation to the heel area, particularly the posterior tibial artery. A number of topical treatments were undertaken in this study; none proved more successful than any other. Multiple overlap existed among treatments; a further detailed assessment will be undertaken. Heel ulceration in the diabetic patient may have untoward outcomes. The combination of vascular insufficiency, neuropathy, and renal dysfunction superimposed on diabetes all contribute to a significant degree to heel ulceration. The ischemia contributes to the origin of the heel ulcer and deters the healing process. Although one can entertain the need/value for vascular reconstruction, this procedure was only applicable in 7 of the 53 (13%) patients. Local or regional flap reconstruction was not considered in any of these patients. Additionally, amputation was required frequently (in 20 of 53 [38%] patients).2,4,7 After a heel ulcer heals, recurrence rates may be as high as 70 percent at three years. The mechanical goal of treatment after heel ulcer healing should be to reduce pressures so the cumulative load is below that at which tissue damage occurs.8 A multi-institutional review was undertaken at four university-affiliated hospitals of all patients with wounds of the heel and arterial insufficiency; the latter was defined as absent pedal pulses or a decreased ankle-brachial index (ABI).4 Ninety-one patients (57 men, 34 women) were treated for heel wounds that did not heal for 1 to 12 months. The mean preoperative ABI was 0.51, and 31 percent of these wounds were infected. Of these patients, 55 percent had impaired renal function (creatinine > 1.5), with 24 percent undergoing dialysis; 70 percent had diabetes, and 64 percent smoked cigarettes. In this review, treatment was topical for all patients and operative in 50 percent. Infrainguinal bypass was performed for 81 of the 91 patients studied; three had a primary BK amputation. Postoperatively, 85 percent of the patients had flow to the foot with a single patent vessel, and the ABI improved by 0.4 to 0.91. All wounds in patients with occluded grafts failed to heal. Those variables determined to be statistically significant in predicting healing included normal renal function, a palpable pedal pulse, and a number of patent tibial arteries after bypass to the ankle.4 Complete wound healing of ischemic heel ulcers or gangrene may require up to six months; therefore, short-term graft patency is of minimal benefit. Patients with heel ulceration most often suffer from chronic, debilitating diseases, such as end-stage renal disease, and are subject to high rates of major amputation.7 Six guidelines for prevention of foot ulcers include 1) podiatric care, which allows for early detection and aggressive treatment of new lesions; 2) pulse examination; 3) protective shoes; 4) pressure reduction, which may include cushion insoles, custom orthoses, and padded hosiery; 5) prophylactic surgery; and 6) preventative education, which includes daily inspection and early intervention (and for the physician, the importance of foot lesions and a regular foot examination with a focus on the patient with diabetes).5,9 Patients with heel ulcers are often treated with primary amputation. The combination of distal neuropathy, repeated local trauma, and prolonged periods of pressure and peripheral arterial disease make these lesions particularly problematic in the diabetic population.2 Although many reconstructive options are available for treatment of heel ulcers, the cornerstone to their management is restoration of adequate arterial blood flow to the affected region. Although direct revascularization of the hindfoot by means of the posterior tibial artery is often an attractive option, its use is limited frequently in the diabetic population by tibial atherosclerosis.4,7 The clinical presentation of ischemic healing extends over a wide spectrum of pathologies, ranging from localized skin fissures extending into the dermis to extensive necrosis of subcutaneous tissues and Achilles tendon with underlying calcaneal osteomyelitis. Operative debridement or reconstruction is often required in a small number of patients. The argument evolves around whether an intact ischemic heel lesion should be left to resolve because of limited blood supply, or whether an aggressive debridement approach will result in extensive tissue loss and possible limb loss. Before one undertakes treatment, prompt drainage of the deep-space infection with aggressive wound care is necessary. Assessment by noninvasive means should always be undertaken to determine whether revascularization in these patients is necessary. After granulation tissue has been obtained, whether a split-thickness skin graft in the heel area is sufficient remains controversial. The aggressive approach of partial calcanectomy with an attempted primary closure often results in limited success.5 Problems of the heel ulcer are the threesome of neuropathy, diabetes, and ischemia. Ischemia not only has a role in the etiology of the heel ulcer, but after the ulcer has formed, the blood supply required to heal it is several times more than is necessary for the previously intact skin.3 Forefoot surgery usually leads to rehabilitation, while heel surgery more often leads to limb loss and functional disability.6,8 A transmetatarsal amputation is useable and functional and preserves the heel. Although multiple studies have documented that preventative diabetic care reduces complications and costs, it is the efforts of a multidisciplinary, diabetes-care team that result in fewer foot complications.9 The multidisciplinary care referral and therapeutic shoes for diabetic patients with heel ulcers may total two million to three million dollars for a cohort of 10,000 diabetic patients.3,8 The strategy of yearly comprehensive foot examinations and education, with appropriate interventions and risk reduction, can be a cost-effective means of improving both the quality and duration of life in those patients with diabetes.1,9 Acknowledgments The author thanks Gae O. Decker-Garrad for her editorial assistance and Mr. Donald Passidomo for his assistance in research.