Essential Insights On Treating Diabetic Heel Ulcers

Diabetic heel ulcers are particularly challenging to treat as a wide range of factors can affect potential healing. With this in mind, this author discusses the challenges of wound bed preparation, key considerations with offloading and the possible impact of peripheral arterial disease.

   Despite a better understanding and the advent of preventive measures that have been developed to address heel ulcers, the problems we encounter due to complications of diabetes make treating this specific patient population more challenging.

   The problem of heel ulcers will increase in conjunction with our increasing diabetic and aging population. The prevalence of heel ulcers across settings is high and continues to increase. In hospitalized patients, it ranges between 10 to 18 percent. Heel ulcers continue to be prevalent after patients are discharged.1

   Researchers have shown that diabetic foot ulcers correlate with multiple co-morbidities and an increased mortality. They often serve as a barometer of a patient’s health in general and correlate with a decrease in mobility and independence. Heel ulcers are often the precursor to hospitalization, osteomyelitis, lower extremity amputation and death. Diabetic patients with foot ulcers have a higher rate of surgical intervention (97 percent versus 85 percent) and amputation (71 percent versus 63 percent) than non-diabetic patients with heel ulcers.2

   Although heel ulcers are less frequent than forefoot ulcers, higher expenses and higher morbidity rates are associated with heel ulcers. Researchers have estimated that heel ulcers are one and one-half times more expensive to treat and are two to three times less likely to heal in comparison to metatarsal ulcers.2

   Also keep in mind that heel ulcers are not strictly the result of a deep tissue injury resulting from pressure alone. Peripheral arterial disease (PAD), lymphedema, neuropathy, connective tissue disorders and malignancies are just some of the complicating factors and etiologies we encounter when it comes to managing heel ulcers that can be exacerbated by the underlying presence of diabetes.

   The frustration of discovering the onset of a new heel ulcer reflects the understanding that an extensive and often complicated course of intensive treatment awaits the unfortunate patient. From a medicolegal perspective, heel ulcers are a nightmare for hospitals, extended care facilities and providers as the formation of a heel ulcer carries an implication of negligence, abuse or overall poor quality of care. The addition of diabetes puts a patient at a greater risk for developing a heel ulcer. Once a heel ulcer is present in a patient with diabetes, it can be an event that ultimately leads to amputation or death.

   While prevention is critical and diligence in the utilization of preventative measures must be ongoing, heel ulcers are still an unfortunate but permanent reality in healthcare.

   A working knowledge of pressure (decubitus) ulcer classification is all well and good, but understanding how to manage the Stage l through the Stage lV ulcer is critical.

   What do you do when you have been consulted to manage a heel ulcer? What happens when a heel ulcer develops in a patient who is already under your care? What should you know in order to achieve optimal treatment results and successful outcomes in a scenario that typically is already suboptimal with the proverbial deck being “stacked against you?” What can you do to protect yourself in the course of managing a patient with a diabetic heel ulcer?

   Accordingly, let us take a closer look at the treatment of heel ulcers complicated by diabetes and its complications.

A Guide To Pertinent Anatomical Considerations

   The most obvious component required to heal any wound is oxygen. Without adequate perfusion, hypoxia occurs and tissue dies. The genesis of pressure ulcers lies in the hypoxic deep tissue injury that occurs from decreased perfusion, which is typically caused by an underlying bony prominence paired with an area of external focal pressure.

   Of the factors that make heel ulcers unique, the anatomical structures at this region of the foot contribute readily to the formation of heel ulcers and the complexity in their resolution.

   The posterior and plantar aspects of the calcaneus create inherent areas of focal pressure. While fat pads and bursa are protective in their function, they add an avascular dimension that complicates healing. Unlike many other areas of the body where proximity to underlying muscle ensures a relatively rich blood supply conducive to healing, once a skin injury occurs at the heel, the underlying tissue is primarily avascular.

   In addition to the lack of perfusion to the protective fat pad, patients with diabetes tend to have atrophy of the fat pad in the heel regions. Hsu and colleagues found that heel pad tissue properties are altered heterogeneously in people with diabetes.3 The combination of increased macrochambers and decreased microchamber stiffness may cause diminished cushioning capacities in diabetic heels.

   It has been my clinical experience that perfusion and repair often occur along the periphery of heel ulcers as opposed to originating from the base of the wound. Achieving granulation tissue in heel ulcers is often an arduous process as the underlying avascular tissue and the extent of the deep tissue injury play key roles in the overall diminished perfusion to the region.

Understanding The Potential Impact Of PAD

   Further complicating an already delicate situation is the presence of peripheral arterial disease. Many patients with diabetes suffer from PAD. Calcification of the posterior tibial artery and the calcaneal branch decreases perfusion as well as any chance at healing. If one suspects PAD, referrals to vascular specialists are appropriate. Physicians must strongly consider attempts to improve circulation pharmacologically and/or through surgical and endovascular intervention.

   In 1987, Taylor and Palmer introduced the concept of angiosomes, a vascular mapping of the body, analogous to neurological dermatomes.4 Their study shows anatomical regions between the skin and bone that are supplied by specific arteries and veins. An appreciation of angiosomes can help provide a better prediction of whether a region has the capacity to heal from a perfusion standpoint. This is especially helpful when you combine these findings with those from non-invasive diagnostic procedures such as microcirculatory assessment of skin via skin perfusion pressure and macrocirculatory assessment via pulse volume recording and segmental Doppler.

   Knowledge of angiosomes can also allow:

   • plastic surgeons to plan vascularly sound reconstruction;
   • foot and ankle surgeons to design safe exposures of the underlying skeleton; and
   • the vascular surgeon to choose the most effective revascularization for a given wound.5

Other Potential Obstacles To Healing

   While anatomical considerations are predictable in the sense that skin, bone, fat and vasculature are consistent in their location, there are a variety of other factors which could prove to be obstacles to managing heel ulcers.

   These factors may include infection, compromised nutritional status and less than optimal hydration, anemia of chronic disease, neuropathy, contracture of the lower extremity, ambulatory status, gait and the mental status of the patient. The healthcare setting, access to care and resources available to treat the ulcer are other variables that may further complicate the treatment plan.

   Each additional variable in the treatment equation makes diabetic heel ulcers exponentially more challenging than others when it comes to achieving a successful outcome.

What You Should Know About Eschar And Debridement

   In regard to a stepwise evidence-based approach to treating chronic wounds, physicians can apply some of these principles to treating diabetic heel ulcers. Extensive studies have shown that a relatively clean and slightly moist environment is optimal in enhancing tissue perfusion, promoting granulation and facilitating eventual epithelialization.6,7

   Algorithms provide sound clinical guidelines for managing a variety of ulcers. Without the use of an algorithm, a simplified approach to healing a diabetic heel ulcer can be broken down into two parts: cleaning up the wound and focusing on healing.

   Eschar is the black, often leathery, necrotic tissue that we typically see in decubitus heel ulcers. Physicians may also see this with ischemic ulcers of the heel as well as other locations throughout the foot and leg. Eschar represents an area of focal ischemic tissue death.

   While removing eschar and other devitalized necrotic tissue through debridement is essential, many providers struggle in determining how aggressive and extensive they should be when it comes to debriding heel ulcers.

   Assuming that blood glucose, nutritional status and vascular status in particular have been appropriately addressed, how should debridement of eschar proceed? Physicians should keep in mind the anatomical considerations of the heel. Complete excision of eschar, especially in an ulcer greater than 1.0 cm in diameter, may instantly create a wound with bone or tendon and fascia exposed.

   Eschar may serve as nature’s own protective dressing so one should base debridement on the degree of demarcation that is occurring between the wound and eschar. Serial debridement of eschar along the periphery of the ulcer over weeks or months may be advantageous in comparison to radical excision of eschar.

   In patients in whom there is significant demarcation of eschar or when one observes loose slough, drainage, foul odor, crepitus or fluctuance, complete removal of eschar would be appropriate. Physicians may complement sharp
surgical excision with the use of modalities such as hydrosurgery (Versajet, Smith & Nephew) or acoustic ultrasound debridement.

   When serial debridement is warranted, it is common to combine non-surgical and non-selective debridement methods to remove devitalized tissue. Types of non-surgical debridement include enzymatic agents, autolytic modalities (concurrent use of semi-occlusive dressing), physical modalities (high pressure irrigation) and biosurgical modalities (maggots of the green bottle fly Lucilia sericata). All of these debridement options have varying levels of evidence to support their use. It is up to the clinician to know where the use of each may be indicated.

Addressing Bacterial Burden And Infection

   Keeping bacterial burden under control is critical during the transition of the wound from deep tissue injury or eschar to granulation. Since slough and necrotic tissue harbor bacteria, regular cleaning of a heel ulcer should take place.

   Further management of bacterial burden should also be ongoing. Utilization of hyperbaric oxygen therapy (HBOT) can assist in the reduction of bacterial burden. Topical antimicrobial dressings (silver or iodine impregnated), Dakin’s solution and topical antibiotics such as gentamycin-clindamycin-polymyxin) are important adjunctive therapies in assisting these already immunocompromised patients. While physicians commonly use these modalities, one should consider resistance patterns of bacteria and periodically re-evaluate extended use of any one topical antimicrobial dressing.

   In patients in whom one has confirmed osteomyelitis within the calcaneus, consider the extent or degree of the infection. A partial calcanectomy of varying degree may be indicated in severe cases.

   When one has confirmed an infectious process or underlying osteomyelitis, intravenous antibiotic therapy is required and an infectious disease consult is highly recommended. Physicians must carefully monitor renal function in patients with diabetes as many are already afflicted with chronic kidney disease. Close monitoring, particularly of creatinine and blood urea nitrogen (BUN), during a course of any extended antibiotic regimen is critical to prevent the onset of acute renal failure. Additional assistance via a consultation with a nephrologist is also highly recommended in diabetic patients with previously established or new onset renal disease.

Keys To Ensuring Proper Offloading

   When adequate cleanup of the diabetic heel ulcer is underway, the immediate focus can shift to expediting the healing process. A diabetic heel ulcer need not be completely free of slough or necrotic tissue for granulation and epithelialization to occur in other sections of the wound, especially along the periphery.

   The promotion of granulation tissue, the precursor to epithelialization, can be an arduous process. Assuming once again that nutritional status has been addressed and any needed revascularization has taken place, one returns to considering the ulcer’s location on the heel. Offloading is critical whether the patient with diabetes is bedridden, wheelchair bound or ambulatory.

   For bedridden patients or those in wheelchairs, foam egg crate heel protectors work well at reducing pressure along the posterior aspect of the heel. Rigid or hard materials such as metal or plastic are used in a number of heel protection splint devices. Unfortunately, the hard components of these splints can create potential areas of pressure. This is especially the case when the patient’s leg may shift or come to rest along the ridge between the soft inner lining and the outer protective aspect of such a device.

   Foam egg crate heel protectors can also be effective in offloading the plantar heel ulcers in non-ambulatory patients with diabetes.

   The air loss mattress is another effective modality that helps to disperse focal pressure under bony prominences in bedridden patients. The treating physician should order this modality in hospitals or facilities. For homebound, bedridden patients, air mattresses may be covered through Medicare and other insurers.

   When treating a heel ulcer along the plantar surface of an ambulatory patient with diabetes, physicians may apply the same principles of offloading they would use for the forefoot or midfoot. The key here is “forced adherence” and keeping the ulcer at the weightbearing surface protected at all times. One may pursue aggressive offloading through modalities such as total contact casting, instant total contact casting and soft total contact casting. All of these modalities provide offloading while reducing the patient’s potential for a lack of adherence.

When Advanced Modalities Come Into Play

   Once the diabetic heel ulcer is “clean” (defined as removal of necrotic tissue with evidence of granulation tissue) and the physician has established appropriate offloading with adequate patient tolerance, consider the use of additional advanced modalities.

   Negative pressure wound therapy (NPWT) is an adjunctive advanced modality physicians can utilize to remove excessive serous drainage while stimulating angiogenesis in many wounds, including diabetic heel ulcers.

   Physicians can simultaneously use NPWT with other advanced modalities to achieve coverage of the ulcer. These modalities include split thickness skin grafting, skin substitutes, biological coverings or collagen containing dressings. Many products are available and various levels of efficacy have been established for each so the provider must ultimately determine which modality under the given circumstances will facilitate the most efficient course of healing.

In Conclusion

   Despite advances in wound management and revascularization in particular, the treatment of heel ulcers, especially in patients with diabetes, is difficult at best. Prevention still remains the key as it is always easier to prevent a wound than it is to treat a wound.

   Clinicians must ultimately recognize trends and subtleties during the course of treatment of any wound. Heel ulcers in patients with diabetes have the potential to deteriorate rapidly so frequent re-evaluation is critical.

   A team approach is highly recommended in the management of diabetic heel ulcers as this population of patients typically has comorbidities that make treatment a lengthy and complicated process. A healthy person does not typically develop a heel ulcer. A diabetic heel ulcer is symptomatic of a complex series of factors working against the patient.

   When one manages these factors passively, it will likely result in disaster. A proactive, aggressive approach to the management of diabetic heel ulcers can yield successful results despite statistics and odds indicating otherwise.

Dr. Bell is a board certified wound specialist of the American Academy of Wound Management, and a Fellow of the College of Certified Wound Specialists. He is the founder of the "Save a Leg, Save a Life" Foundation, a multi-disciplinary non-profit organization dedicated to the reduction in lower extremity amputations and improving wound healing outcomes through evidence based methodology and community outreach.

For related articles, see “How To Manage Heel Ulcers In Patients With Diabetes” in the March 2005 issue of Podiatry Today or “Mastering Difficult Heel Ulcers” in the November 2002 issue.

References:

1. Wong VK, Stotts NA. Physiology and prevention of heel ulcers: the state of the science. JWOCN 2003; 30(4):191-8. 2. Jacobs TS, Kerstein MD. Is there a difference in outcome of heel ulcers in diabetic patients and non-diabetic patients? Wounds 2000; 12(4):96-101. 3. Hsu CC, Tsai WC, et al. Diabetic effects on microchambers and macrochambers tissue properties in human heel pads. Clin Biomech 2009; 24(8):682-6. 4. Taylor GI, Pan WR. Angiosomes of the leg: anatomic study and clinical implications. Plast Reconstr Surg 1998; 102(3):599-616. 5. Attinger CE, Evans KK, Bulan E, Blume P, Cooper P. Angiosomes of the foot and ankle and clinical implications for limb salvage. Plast Reconstr Surg 2006 117(7Supp):295. 6. Hinnman CD, Maibach HI. Effect of air exposure and occlusion on experimental human skin wounds. Nature 1963; 200:377-8. 7. Ovington LG. Wound dressings: their evolution and use. In Falanga V (ed): Cutaneous wound healing. Martin Dunitz Ltd., London, 2001, pp.221-31. 8. Witkowski JE, Lemont H. Tumors. In Color atlas of cutaneous disorders of the lower extremities. Igaku-Shoin, New York-Tokyo, 1993, pp. 127.