Heel ulcers pose unique challenges with respect to anatomy, blood flow, offloading and healing potential. Accordingly, the author discusses often overlooked aspects of determining effective treatment plans for these difficult cases.
Heel ulcers of any etiology represent a difficult group of lower extremity wounds to manage and treat successfully. There is inherent liability in managing patients with heel ulcers. Challenges are varied and can include the underlying health issues of the patient, the circumstances surrounding the development of the wound, anatomical considerations, patient mobility and the setting where care is provided among others.
Originally developed in 2002, the “never event” list, referring to serious adverse medical events or errors, is now comprised of 29 “serious reportable events” that are grouped into seven categories.1,2 Within the care management event category is the description of “any Stage 3 to 4, or unstageable pressure ulcers acquired after admission/presentation to a health care facility.”1,2
While prevention is always the most important principle in the management of any pressure-related injury or chronic wound, a greater understanding of pertinent principles in the treatment of heel ulcers can facilitate the greater likelihood of successful outcomes.
Understanding Deep Tissue Injury And Hypostasis
The earliest sign of the onset of a pressure ulcer is the presence of non-blanchable erythema, which is indicative of a deep tissue injury. This represents a disruption in the blood flow to the skin. Often direct pressure over a bony prominence is responsible for decreased perfusion to the specific area of soft tissue, which results in hypoxic injury and tissue death.
Specifically, the term for this phenomenon is “hypostasis” and the pathophysiology is the same as that observed within 45 minutes after the heart stops beating in a recently deceased person. Hypostasis is caused by disintegration of the capillary walls due to ischemia. The blood is released into the surrounding tissues where it floats freely and follows gravity. After 12 to 20 hours, the hypostasis becomes fixed. Pressing on the skin elicits a negative capillary refill or non-blanching.
When classifying pressure ulcers, a stage 1 ulcer involves the presence of non-blanchable erythema but no break in the skin. Stage 1 ulcers represent full-thickness underlying damage that may temporarily disappear but the lesion may reappear as a purple, deep tissue injury approximately seven days later.
The timeline is important. Two to three days after the appearance of a deep tissue injury, which is now nine to 11 days after the initial injury, the epidermis will blister and slough off, exposing red to purple underlying tissue. Somewhere around day 13 to 15, eschar will form. Additionally, skin temperature changes near the deep tissue injury site may reflect an inflammatory response, causing local heating and subsequently local cooling.
The key here is the seven days surrounding the injury. For the purposes of deep tissue injuries that present as a demarcated red or purple area, clinicians can count backward seven days to pinpoint when the actual pressure damage occurred. This is especially important when considering factors such as “where was the patient,” “what were the circumstances of the injury,” and when patients have been in facility settings, “on whose watch did this occur?”3,4 Documentation of heel ulcers becomes an extremely important medicolegal issue that can have significant ramifications if a “never event” scenario is suggested.
Considering Underlying Contributors To Heel Ulcers
Before the actual treatment process can proceed, a holistic approach is warranted. Holistic refers to the understanding that a chronic wound does not typically occur in a healthy individual. Therefore, identifying the underlying causes and obstacles to healing is essential.
Heel ulcers are not solely limited to an underlying etiology of pressure. Even when pressure and subsequent hypostasis have resulted in a tissue injury and ulcer, conditions such as diabetes, peripheral arterial disease, lymphedema, peripheral neuropathy, immobility (from any cause), connective tissue disorders, malignancies, lower extremity contracture, and other conditions may exacerbate the situation. The development or presence of infection or underlying osteomyelitis during the history of the ulcer are other challenges we often encounter.
As such, the treatment plan must reflect consideration of all factors, including the nutritional status of the patient. I will discuss the assessment of nutritional status as it pertains to wound healing later in this article. Addressing and attempting to reverse the underlying contributing factors of heel ulcers is the first step in the healing process. The body was designed to heal itself but when its ability has been compromised, knowing how to enhance reparative processes is essential.
Recognizing The Unique Anatomic Aspects And Challenges Of Heel Ulcers
The anatomy involved in heel ulcers contributes uniquely to both their formation and the complexity of their resolution. The posterior and plantar portions of the calcaneus create inherent areas of focal pressure. Fat pads and bursae are protective in their function, but add an avascular dimension that further complicates potential healing. Unlike other areas of the body where underlying muscle ensures a rich blood supply conducive to healing, once a skin injury occurs at the heel, much of the underlying tissue is avascular.
As a result, many heel ulcers do not heal in the often observed “from the bottom up” process, in which granulation tissue populates the wound base and inherent angiogenesis occurs, further leading to epithelialization. When a deep tissue injury or eschar is present, the process of healing can be arduous, requiring diligence and patience as the extent of the wound may not be apparent. Sharp excisional debridement of an entire stable eschar overlying injured or fatty tissue may create a structural deficit or entry point for bacteria.
Prior to debridement of any lower extremity wound, especially when involving the heel, a thorough arterial assessment is warranted. Additionally, one should consider the angiosome concept, which is a vascular mapping of the skin, analogous to neurological dermatomes.5 Angiosomes are regions of the skin that are supplied by specific arteries and veins. For example, the calcaneal branches of the peroneal and posterior tibial arteries supply the heel.
Knowledge of the angiosomes that supply the skin at the heel is an important concept and may provide insight as to potential arterial stenosis or occlusion in cases that involve peripheral arterial disease (PAD). It can also provide a better prediction of whether a region has the capacity to heal from a perfusion standpoint. Without optimal perfusion to the site, healing often occurs from the periphery and more superficially along the edges of the eschar or injured tissue.
Combining findings of non-invasive diagnostic testing such as skin perfusion pressure or TcPO2 (microcirculatory) and segmental doppler and pulse volume recordings (macrocirculation) can provide significant perspective. These initial tests can also assist in the decision as to whether to consult with a vascular or endovascular specialist.
In patients with diabetes, additional atrophy of the protective plantar fat pad may occur. Within the protective fat pad are chambers composed of fat and soft tissue fibers. These chambers help to keep fat localized in a focal area and to assist in the dispersion of force applied to the plantar surface during gait or when static pressure is applied.
Hsu and colleagues found that heel pad tissue properties are altered heterogeneously in people with diabetes.6 The combination of increased macrochambers and decreased microchamber stiffness may cause diminished cushioning capacities in diabetic heels. These factors can lead to greater trauma on overlying skin, whether during ambulation or in non-weightbearing settings. Pressure and shearing from the footboard of a bed, for example, can lead to skin injury in these more at-risk patients.
Essential Concepts In Heel Ulcer Treatment
At this time, the active treatment of heel ulcers may include but is not limited to: debridement (sharp, enzymatic, mechanical, biological, hydrosurgical or autolytic), offloading, revascularization, hyperbaric oxygen, negative pressure wound therapy and topical dressings, including cellular tissue products. Deciding when to implement any of these modalities should be based on reversing the issues that led to the formation of the ulcer. Additionally, knowing how and when to use modalities efficaciously and safely requires an appreciation of what the patient can tolerate.
Algorithms can assist in this decision-making process when considering the use of the aforementioned modalities.
Understanding The Impact Of Nutritional Status On Heel Ulcer Outcomes
Management of soft tissue infection, osteomyelitis, vascular status, blood glucose and other issues is essential. However, simple nutritional assessment is often overlooked and knowing how to manage this aspect of health and healing is essential.
One can almost assume inadequate nutrition in the elderly and diabetic patient populations when heel ulcers are present. Body mass index alone does not indicate the quality of nutritional status and subsequent ability to heal wounds. Monitoring the lab indices of my hospitalized patients over the years led to a realization that even well-fed appearing individuals are often undernourished when it comes to the quality of calories and nutrients.
When treating patients with chronic wounds, one should ensure adequate assessment of nutrition to ensure that adequate nutrients are present. Knowing which indices to evaluate, what supplements to consider and when to request a nutritional consult can expedite healing and prevent failure of other more advanced technologies.
In a 2011 article, Posthauer reviewed the roles of albumin and pre-albumin in assessing wound healing potential in patients with wounds.7
Albumin. Found in vascular and interstitial spaces, albumin functions as a carrier protein. When a patient experiences an inflammatory process, such as an ulcer, cytokines increase and the body produces increased acute phase proteins. The increase in cytokine production then pulls albumin away from the intravascular spaces until the inflammation resolves. Additionally, corticosteroids, insulin, thyroid hormone and dehydration increase albumin levels and one should consider this when evaluating lab values.
Prealbumin/transthyretin. Prealbumin is also a visceral protein. It is a transport protein for thyroxine and a carrier for retinal-binding protein. In general, prealbumin is considered a better indicator of nutritional repletion since it has a half-life of only two to three days. Similar to albumin, prealbumin is affected by inflammation, decreasing in the acute phase. Prealbumin increases with corticosteroids and in acute renal failure. It decreases with infection, hyperglycemia, dialysis, liver disease and surgery.7
Again, it is important to carefully review the individual patient’s circumstances in relation to his or her nutritional testing results. Studies have not proven a clear relationship between nutritional status and serum protein levels. However, low levels of albumin and prealbumin are indicators of morbidity and mortality. Therefore, improvement in these levels could indicate progressive improvement in wound healing potential.7
Total protein. Total protein is another commonly ordered lab test to assess nutritional status of an individual. Low levels may suggest underlying malnutrition and could be a valuable piece of data when compiling a nutritional profile on a patient with a heel ulcer.
Current And Emerging Insights On Offloading For Heel Ulcers
Heel wounds are often present in areas of increased pressure or weightbearing. This makes effective and safe offloading of these ulcers an ongoing challenge. One must consider a variety of factors when determining optimal offloading methods. Removable versus non-removable methods of offloading, the functional and living status of the patient, as well as the treatment setting are among the important concepts to evaluate. The heel ulcer of a bedbound patient with limited mobility is similar to that of an ambulatory patient in location and classification only. Therefore, one must customize the method of offloading to the patient.
Especially for bedridden patients and those in wheelchairs, a newer product known as the Heel Keeper (Ulcer Solutions) offers a promising design. This device was developed by a wound specialist physician, Christopher Finley, MD, FACEP, CWSP, who had witnessed and managed many heel ulcers in long-term and acute settings. Several heel protection devices have rigid or hard materials such as metal or plastic. Unfortunately, the hard components of these splints can create potential additional 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 materials. The Heel Keeper is made of soft, cradling foam with an optional wedge to prevent external leg rotation.
The low air loss mattress is another effective and commonly utilized modality that helps disperse focal pressure under bony prominences in bedridden and immobile patients. The treating physician should order this modality in hospitals or extended care facilities. For homebound, bedridden patients, air mattresses may be covered through Medicare and other insurers.
When treating a heel ulcer along the plantar surface in 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 with customized offloading. All these modalities provide offloading while reducing the patient’s potential for a lack of adherence as the patient cannot remove these devices.
“Never events” are only one scenario when heel ulcers can have a profound impact on patients. Their anatomic location, angiosomes and lack of surrounding muscle tissue make heel ulcers uniquely challenging in the wound care field. Careful evaluation, including a comprehensive chronologic history of injury, identification of the reason for deep tissue injury, and effective wound care are the first steps to healing the ulcer. During treatment, nutritional status and truly effective and adherent offloading are often overlooked. By integrating these concepts into the overall treatment plan, clinicians may experience enhanced outcomes and decreased complications in these often perplexing cases.
Dr. Bell is in private practice in Jacksonville, Fla., and is the Founder and President of the Save A Leg, Save A Life Foundation. He is a Certified Wound Specialist by the American Board of Wound Management and has served on its Board of Directors and the American Board of Wound Management Foundation. He is a Fellow of the Faculty of Podiatric Medicine with the Royal College of Physicians and Surgeons (Glasgow).
1. Agency for Healthcare Research and Quality. Never events. Available at: https://psnet.ahrq.gov/primers/primer/3/Never-Events. Updated January 2019. Accessed July 16, 2019.
2. National Quality Forum. Serious reportable events in healthcare - 2006 update. Available at: http://www.qualityforum.org/Publications/2007/03/Serious_Reportable_Events_in_Healthcare–2006_Update.aspx. Published March 2007. Accessed July 19, 2019.
3. Hettrick H. Lessons learned from the dead to help the living: applying forensic principles to wound pathophysiology. Lecture at SAWC Spring/WHS conference, April 28, 2018.
4. Gefen A. Deep tissue injury from a bioengineering point of view. OWM. 2009;53(4):1-7.
5. Bell D. Essential insights on treating diabetic heel ulcers. Podiatry Today. 2010; 23 (3):36-47.
6. Hsu CC, Tsai WC, Wang CL, et al. Microchambers and macrochambers in heel pads: are they functionally different? J Appl Physiol. 2007;102(6):2227-2231.
7. Posthauer ME. Albumin and pre-albumin: are they markers of nutritional status in wound management? Wound Source. Available at: https://www.woundsource.com/blog/albumin-and-pre-albumin-are-they-markers-nutritional-status-wound-management . Published June 24, 2011. Accessed July 16, 2019.