Diabetic Heel Ulcers: A Major Risk Factor for Lower Extremity Amputation

    The heel plays a vital role in weight transmission and in the dynamics of walking. When a person is standing, the weight of the body is transmitted from the femur and tibia through the heel bones (talus and calcaneus) to the ground and to the heads of the metatarsals. When a person is walking, the heel is the first part of the body to transmit the weight to the ground at the heel strike.¹

    The development of ulcers on this area is a serious problem, requiring lengthy hospital stays and periods of disability, and often leads to lower limb amputation. Heel ulceration, on average, costs 1.5 times more than metatarsal ulceration; limb salvage of the heel is two to three times less likely than metatarsal salvage.² The exact incidence of diabetic heel ulcers is not known, but the incidence of pressure heel ulcers in patients with and without diabetes ranges from 19% to 32%.^3,4 Heel ulcers develop from the pressure of the shoes or from shearing forces concentrated on a small area that directly overlies a bony prominence encountered during walking or standing that consequently progresses toward skin loss and ulceration (see Figure 1). The capacity of the heel pad for shock absorption declines with age, contributing to tissue breakdown and heel ulceration.⁵

    Progression of infection to heel bones or long tissue planes around the ankle joint is a major concern that results from failure of conservative treatment and leads to lower limb amputation. The objectives of heel ulcer treatment should include early intervention to 1) control infection, 2) promote healing of the ulcer, and 3) prevent recurrence after healing.

Pathogenesis of Diabetic Heel Ulcers

    The pathogenesis of foot ulcers in diabetes has many components. Several studies have shown that peripheral sensory neuropathy, trauma, and deformity are the major predisposing factors for foot ulceration.^6,7 Other factors involved in heel ulceration are ischemia, edema, limited joint mobility, and lower limb immobility (see Table 1). The repetitive trauma of walking may increase pressure on the heels; the combination of this trauma with the gradual thinning of the heel pad that occurs with aging and in patients with diabetes may result in loss of skin integrity and ulceration. These ulcers become prone to infection. Direct extension of infection to the calcaneus bone or along tissue planes proximal to the ankle joint is one of the major causes of lower extremity amputation.^6,8,9

    Diabetic neuropathy. Neuropathy is the major etiologic component of most diabetic ulcerations; it is reported in more than 80% of patients with diabetes who have foot wounds.^6,10,11 The lack of protective sensation, combined with improper weight distribution due to loss of joint sensation or the presence foot deformities, exposes patients with diabetes to repetitive stress that leads to skin breakdown and ulcer formation.¹¹ Autonomic neuropathy in the diabetic foot manifests in several ways. Denervation of dermal structures leads to decreased sweating, resulting in dry skin and fissure formation that provides a potential port of entry for micro-organisms; thus, predisposing the skin to infection. In patients with adequate blood supply, this "autosympathectomy" may lead to increased blood flow around the joints, implicated as one of the etiologic factors in the development of Charcot's joint deformity.¹²

    Peripheral arterial occlusive disease. The second highest risk factor, peripheral arterial disease (PAD), is four times more prevalent in patients with diabetes than those without the disease.¹³ In patients with diabetes, PAD typically involves the tibial and peroneal arteries but spares the dorsalis pedis artery. It develops at an early age and has an equal sex distribution. The presence of hyperlipidemia, hypertension, and smoking contributes to the increased prevalence of peripheral arterial occlusive disease in patients with diabetes.^10,14

    The heel region is sensitive to decreased arterial blood supply by virtue of its weight-bearing anatomical location. A combination of clinical signs and symptoms, plus abnormal noninvasive vascular tests such as the ankle-brachial index (ABI), toe systolic pressure, and transcutaneous oxygen measurement, suggest the presence of an ischemic heel ulcer.^10,15,16

    Limited joiunt mobility and lower limb immobility. Limited joint mobility contributes to foot ulceration in the susceptible foot. Ankle equinus deformity and reduced ankle dorsiflection have significantly higher peak plantar pressures in patients with diabetes than in normal people; thus, providing a higher risk for ulceration.^17,18 Lower limb immobility can lead to posterior heel ulceration as a direct result of gravity pressure. This occurs when the patient is positioned on a hard, unyielding surface - ie, a hard mattress - for too long. Lying supine in a hospital bed generates heel-to-bed pressure of 50 mm Hg to 94 mm Hg, which exceeds the normal capillary filling pressure of approximately 32 mm Hg and can cause local vascular occlusion sufficient to produce ischemia and subsequent necrosis of skin and subcutaneous tissues, leading to heel ulceration.¹⁹ The presence of lower limb edema, especially around the ankle region, also can predispose patients with diabetes to skin breakdown and heel ulceration.²⁰

    Past history of ulceration or amputation. Patients with former amputation or ulcers are at a higher risk for developing foot ulcers.^8,10 Changes in foot dynamics due to previous ulceration, joint deformity, or amputation can cause the abnormal distribution of plantar and heel pressures and may result in heel ulceration.²¹

Prevention of Heel Ulcers

    Close attention to foot care and proper management of minor foot injuries are key to preventing heel ulceration. Daily foot inspection by the patient is the cornerstone of proper foot care. Regular curetting of the hyperkeratotic tissues around the heel, in addition to gentle cleansing with soap and water followed by the application of topical moisturizers, helps maintain healthy skin that can better resist breakdown and injury.²² Athletic shoes and thick absorbent socks are adequate in most patients. Custom shoes, provided under the guidance of the orthotist and podiatrist, that offer stability but not much weight on the heel may be required in patients with foot deformities to decrease the risk of heel ulceration.

Evaluation of Heel Ulcers

    An adequate description of the ulcer characteristics - ie, size, depth, extent of bacterial invasion, and the healing phase - provides an idea about the magnitude of the problem, necessary for monitoring progress during treatment. Determining the underlying etiology of the ulcer and ascertaining whether the lesion is neuropathic, ischemic, or induced by adjacent foot deformity is important. An easy-to-use scoring system that provides a uniform description of an ulcer (including depth of the ulcer, extent of bacterial invasion, phase of healing, and associated etiology [DEPA]) has been shown to help plan treatment strategies and predict outcomes in terms of healing and lower-limb amputations.²³ According to this system, heel ulcers are classified into three grades: low, moderate, and high grade ulcers (see Table 2). The validity of this system is scheduled to be published in the Journal of Foot and Ankle Surgery in the July-August 2004 issue.

    The patient's inability to perceive the pressure of a 10-g monofilament is an indicator of sensory neuropathy (see Figure 2). A standard tuning fork (128 cycles/second) can be used to detect sensory neuropathy. Results reflect abnormality if the patient cannot sense the vibration when it is placed firmly on the distal interphalangeal joint.

    The depth of the heel ulcer can be determined using a blunt sterile probe. Gentle probing can detect dissection of the ulcer into tendon sheaths, joint capsule, or bone (see Figure 3). The presence of odor and exudate and the co-existence of cellulitis or fasciitis and ankle swelling must be recognized. The color of the ulcer and the presence or absence of granulation tissue also must be noted. Infection of the heel ulcer is diagnosed if a foul smell or purulent discharge is present with other local signs of infection (warmth, erythema, lymphangitis, lymphadenopathy, edema, pain). The presence of foot deformity always should be recorded. Charcot joint deformity of the ankle or ankle equinus deformity may lead to the development of heel ulcers.

    Vascular status must be assessed because the presence of ischemia is associated with poor prognosis. Signs and symptoms may include intermittent claudication, pain occurring in the heel region at rest or during the night, absence of popliteal or posterior tibial pulses, thinned or shiny skin, absence of hair on the lower leg and foot, thickened nails, redness of the heel area when the legs are dependent, and pallor when the foot is elevated.²⁴ Palpable pedal pulse is the most reliable indication of arterial perfusion to the foot. However, the absence of pedal pulses in the presence of a normal-colored warm foot is common in patients with diabetes and reflects adequate collateral circulation. Ischemic heel ulcers should be evaluated further with non-invasive vascular tests (eg, transcutaneous oxygen measurement and ABI) that can be easily performed in the office. For the ABI, a blood pressure cuff is placed on the upper arm and inflated until no brachial pulse is detected by the Doppler device. The cuff is then slowly deflated until a Doppler-detected pulse returns (the systolic pressure). The same maneuver is repeated on the leg, with the cuff wrapped around the distal calf and the Doppler device placed over the dorsalis pedis or posterior tibial artery. The ankle systolic pressure divided by the brachial systolic pressure gives the ABI. Arteriography is indicated if lower extremity ischemia is strongly suspected. Vascular surgery consultation and possible revascularization should be considered if clinical signs of ischemia are present in the lower extremity, if the patient has evidence of peripheral vascular disease suggested by the results of non-invasive vascular tests or imaging studies, or if non-infected ulcers do not progress toward healing despite full standard management^25,26 (see Figure 4).

Management of Heel Ulcerations

    Despite the best preventive measures, many patients with diabetes will develop heel ulcers. Frequently, the edge of these ulcers is covered by callus or fibrotic tissue; trimming the hyperkeratotic tissue is an important management step. Typically, heel ulcers are painless due to neuropathy. Even in the presence of severe infection, many patients have few subjective complaints and often are more concerned with the odor and soiled footwear and stockings than with the wound itself. Adequate blood sugar control with insulin is the first step in the management of most heel ulcers. The target would be Hb A1C of <7%. Scheduled debridement is mandatory to control infection and to convert the ulcer from chronic to acute. Piecemeal debridement using a bone rongeurs is a good way to maintain maximum tissue preservation and debridement at the same time. The necrotic tissue and surrounding callus are removed with the rongeurs until a healthy bleeding edge is revealed (see Figure 5). The ulcers are dressed with saline-moistened gauze to provide a moist environment. Extension of the ulcer to the calcaneus is a cautionary sign but it does not always signify osteomyelitis. Plain-film radiographs should be obtained to look for soft tissue gas and to evaluate the ulcer for bone infection.

    Grading. After debridement, ulcers should be graded according to standard classification systems (eg, Meggitt, Wagner, Pecoraro, University of Texas Classification System). Patients with low-grade heel ulcers require debridement of non-viable or infected tissue, local wound care, and broad spectrum antibiotics. Oral second-generation cephalosporins (ie, Cefuroxime) are a good choice for these cases. Complete healing of these ulcers is expected in a few weeks. Dry heel ulcers covered by eschar require simple protection until the eschar dries and separates. These are suggested guidelines of management of diabetic ulcers in general compiled from data from several relevant resources and modified in the authors' clinic to fit diabetic heel ulcers in particular (see Figure 6).

    Moderate-grade ulcers require a short period of in hospital stabilization (1 to 2 weeks), during which patients receive intravenous antibiotics (second- or third-generation cephalosporins (eg, Cefoxitin, Cefuroxime, Ceftazidine, Ceftriaxone) to control infection; insulin therapy to control hyperglycemia; and daily debridement of infected or gangrenous tissue. Once adequately stabilized, the patient can be discharged home to continue oral antibiotics, daily saline dressings, and offloading techniques such as the use of crutches, walkers, wheelchairs, and other devices. Agents that promote healing (ie, platelet-derived growth factors, phenytoin powder) are helpful in these ulcers once infection has been controlled.^27-31

    High-grade heel ulcers typically are infected ischemic ulcers and are associated with swelling of the foot and ankle region. For these ulcers, a trial of conservative therapy is recommended for 1 to 2 weeks, provided the patient is not in sepsis. During this period, daily debridement, insulin therapy, and strong antibiotics are tried. Once the ulcer shows some improvement, agents to promote healing are recommended. Ulcers that show no signs of improvement or that continue to deteriorate with appropriate local and systemic measures require vascular evaluation. Patients with no hope for vascular reconstruction or angioplasty or patients with severe necrotizing infection around the ankle or deep infection reaching the heel bones should be offered life-saving amputation (see Figure 6).

    Hyperbaric oxygen therapy. Frequently used in wound care, hyperbaric oxygen therapy seems to accelerate the rate of healing and reduce the need for amputation in non-ischemic diabetic foot ulcers.³² However, its role in the management of heel ulcers is unknown and, in theory, far from benign. Supra-therapeutic oxygen levels can cause vasoconstriction and can worsen heel ischemia because of the loss of the local vasodilatation caused by mild hypoxia. Furthermore, systemic application of hyperbaric oxygen can cause central nervous system problems.^32,33

    Vascular involvement. Vascular evaluation and reconstruction are necessary for nonhealing diabetic heel ulcers caused by the lack of perfusion. Autogenous vein grafts are used for long bypasses below the knee. According to Shah et al,³⁴ this graft can be extended to the distal tibial and pedal arteries, with limb salvage of 80% at 5 years. Short stenotic lesions in large vessels can be managed by balloon angioplasty, but this has limited value in patients with diabetes who have small vessel disease.^2,34

    Calcanectomy. Partial calcanectomy has been recommended for patients with large heel ulcerations. However, in several studies, not all patients treated with this method had diabetes. In one study, of the 22 patients receiving calcanectomy, only nine had diabetes, and in another study of 12 patients, seven had diabetes.^35,36 Progressive necrotizing soft tissue infections and blood sepsis are the major risk factors in patients with heel ulcers who eventually require lower extremity amputation. None of these can be controlled by limited amputation. Moreover, surgical amputation should proceed through tissue that is free from infection. In addition, performing limited amputation on patients with diabetes with heel ulceration prolongs hospital stay and puts their life at risk due to sepsis.

    Amputation. Life-saving amputation should be a consideration for patients with high-grade heel ulcers. Below- and above-the-knee amputations frequently are the only effective treatment for infection or gangrene around the heel region. The goal of amputation in these cases is either preservation of life or improving the quality of life by replacing a dysfunctional foot with a prosthesis. Amputation surgery in these sick patients may be the first step in rehabilitation because most of them are non-ambulatory and bedridden. The decision for amputation should not be delayed when indications support it. Below-the-knee amputation is an ideal level in such cases; the objective is direct reconstruction of the residual limb for an artificial prosthesis. The major value of below-the-knee amputation is the presence of a knee joint capable of tolerating the forces involved in walking; thus, reducing the energy requirement and improving walking ability in these patients.

Conclusion

    Diabetic heel ulcers are a significant healthcare problem resulting from a combination of several problems including neuropathy, inadequate blood supply, and abnormal pressure on the heal bones. Patient education regarding foot hygiene, skin care, and proper footwear is crucial in preventing heel ulceration. Aggressive treatment including appropriate antibiotics, blood sugar control, debridement, keeping the affected limb non-weight-bearing, using aggressive revascularization, and using healing-promoting agents may lower the rate of below-the-knee amputation. 

Acknowledgements

    The authors wish to acknowledge Sana Tamimi for the hand drawings and Saleh Mssad for taking the pictures.

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