Current literature involving PrU prevention emphasizes the value of recognizing high-risk patients7 and typically doing so with the utilization of risk assessment scales. Evidence suggests that risk scale utilization results in an increase in the effectiveness of preventive measures for all PrUs.8 Some report that identifying high-risk patients is the first step in preventing heel PrUs, although no risk assessment scale currently exists that is specific for heel PrUs.
In a systematic review of PrU prevention, it was concluded that having optimal nutrition, treating dry skin with moisturizer, and utilizing sheepskin bed overlays to reduce heel pressure were the most promising approaches to reducing PrU incidence. Although no available bed surfaces were found that could provide complete pressure relief, specialized foam and sheepskin overlays were found superior to standard hospital mattresses in preventing PrUs.9
Various techniques of heel off-loading have been attempted, given the fact that a complete heel pressure relief bed surface does not exist. These techniques varied from simple hospital pillows to more complex boot-shaped air cushion devices or heel protectors made of siliconized hollow fibers. Comparison studies found that hospital pillows were more effective in reducing heel pressure than the heel protector made of siliconized hollow fibers.10 In addition, in an acute-care hospital setting, the air cushion device was less likely to suspend the heel off the bed than its pillow counterpart,11 and the patients tended to develop PrUs more rapidly than did pillow-using patients.
An evaluation of a protocol for prevention of facility-acquired heel PrUs concluded that a pressure-relieving device was more effective in reducing heel PrU incidence if it did not dislodge during patient movement. In addition, it was observed that the combination of a pressure-relieving device along with frequent, regular, and rigorous nursing staff heel skin assessments was more effective in reducing the risk of developing PrUs.12
Effective heel PrU prevention involves a multifaceted approach including risk identification, comorbidity assessment, and implementation of pressure redistribution devices early and aggressively. Ideal heel pressure-reducing products have been described as those that reduce pressure, friction, and shear; separate and protect the ankles; maintain heel suspension; and prevent footdrop.13 Specific interventions recommended for patients considered to be at higher risk based on low Braden Scale scores include heel elevation off the bed and avoidance of knee hyperextension. Clinical guidelines and algorithms have been developed for managing and identifying at-risk patients. One guideline, developed by Fowler et al,14 primarily involves heel off-loading interventions. Another, developed by Cuddigan et al,15 involves an algorithm that assesses patient stability and incorporates early use of heel elevation.
Adapted to the function of withstanding forces of great magnitude, the heel is composed of the calcaneus, the largest bone in the foot, and a tough heel pad. The skin overlying the heel has a mean thickness of about 3.8 mm, with a relatively thick epidermis of around 0.46 mm. Ramifications of fibrous septa connect and anchor the skin to the periosteum of calcaneus. The septae form the boundaries of fat compartments of diameter ranging from 1 to 5 mm.16 The heel has only a thin layer of muscle tissue, the panniculus carnosus, in the subcutaneous tissue. Pockets of fat, also known as loculi, which lie between the septae of the heel and are fluid in texture, play an important role absorbing shock at the heel (See Figure 2).16 Sweat glands, but no hair follicles or sebaceous glands, are present in the heel pad.
The plantar fascia, which lies deep to the fatty tissue, is a 2- to 4-mm-thick plane of connective tissue that originates at the calcaneus, courses along the plantar aspect of the foot, and attaches to the heads of the metatarsal bones.
The arterial supply of the heel is provided anteriorly by the lateral plantar artery and to a lesser extent by the medial plantar artery and posteriorly by the medial calcaneal branch of the posterior tibial artery. Two arterial plexuses formed by anastomosing vessels are found, one at the periosteum and the other subdermally supplying the panniculus carnosus muscle. By contrast, the fat compartments are virtually avascular. Medial and lateral calcaneal nerves provide the sensation of the heel.
The development of heel ulcers and chronic wounds in general appears to be associated with the following commonly identified factors: pathomechanics, chronic hypoxia/reperfusion injury, impaired nutrient supply, growth factor abnormalities, and chronic inflammation.3
Unrelieved pressure is the critical pathomechanical factor in the development of PrUs. The tissue cannot tolerate pressures above 32 mmHg-the critical interface pressure-for an indefinite period of time without sustaining irreversible damage.17 There is an inverse, hyperbolic relationship between pressure and the duration of pressure application necessary to cause ulcers.18 Unrelieved pressures 4 to 6 times systolic blood pressure cause necrosis in less than an hour. However, pressures less than the systolic blood pressure might require 12 hours to produce a similar lesion.
The surface pressure may not be a good measure of the true pressure in deep tissues, however.19 Deep muscle layers that cover bony prominences are often exposed to higher stresses than overlying skin surfaces. Prolonged compression increases muscle stiffness around the bone-muscle interface, which further stresses the muscles, making the muscle even more prone to ischemia and infarction.20
The fibrous septae forming the loculations of the subcutaneous fat inhibit dissipation of external pressure. In this situation, the fat compartments build pressure leading to edema and inflammation, which subsequently lead to more pressure and ischemia and reperfusion injury.16 A previous study that involved biopsies of PrUs in humans demonstrated early necrosis of subcutaneous fat.21
By lowering the ulceration threshold 6-fold, shear stresses exacerbate the tendency for ulceration caused by pressure.22 The classic example of shear stress generation is when a patient reclines in a hospital bed with the head of that bed elevated, which places the sacrum at increased risk for tissue breakdown. The heel is also a site of frequent shear stress exposure. Although the epidermis of heel skin is thick and relatively resistant to tissue damage, shear stresses especially in the presence of other complicating factors, such as excessive perspiration and urinary or fecal incontinence, can cause damage to the skin in the early phases of PrU development.16 Moreover, even without any overt shear stress present on the heel skin surface, pressures on the heel skin can generate shear stresses on bone-soft tissue interface.
The Compression Intensity Index (CII) is defined as follows:
The CII was proposed as an anatomical index for a quick assessment of the mechanical loading intensity in the soft tissue under the bony prominence of an individual and therefore of the relative biomechanical risk for that individual to develop DTI, based on the well-established association between the magnitude of mechanical loads and the extent of tissue damage.2
Analyses of sDTI prevalence data consistent with the CII model were reported in the International Pressure Ulcer Prevalence Survey, which found sDTIs to be disproportionately more prevalent than severe PrUs at the heel and elbow.2
According to this CII model, the heel is at greater risk for development of sDTIs because of the relatively small radii of curvature of the bony prominence and the relatively thin overlying soft tissue.2 Both factors contribute to a greater index of compression and greater mechanical loading intensity applied by the bony prominence to the overlying soft tissue. Because of its small surface area and high tissue-interface pressure, the heel is one of the most difficult anatomical areas to effectively off-load pressure.23
This model also offers an explanation for the relatively low incidence of proportional sDTIs in anatomic locations, such as the sacrum where the PrU prevalence is the highest. Unlike the heel, areas such as the sacrum or buttocks are typically made up of a greater overlying soft-tissue and a bony prominence of a relatively larger radius of curvature, thus creating a lesser index of compression and lesser mechanical loading intensity applied by the bony prominence to the overlying soft tissue.
Other than normal and shear stresses, decreased tissue perfusion provides an important contributory role in the pathophysiology of PrUs including sDTIs. In particular, once an open lesion is formed, chronic ischemia impairs granulation tissue deposition, proliferation of fibroblasts, mononuclear cell infiltration, and delayed epithelialization.24-26 A study found low ankle-brachial index (ABI) to be 1 of 3 significant risk factors, along with male sex and duration of time spent in bed, for lower-extremity PrUs in older adults.23 In this study, an ABI cutoff level of 0.8 provided high sensitivity and adequate specificity at predicting the development of lower extremity PrUs.
Muscle tissue is metabolically highly active and thus exquisitely vulnerable to ischemia. The thin panniculus carnosus muscle in the subcutaneous tissue of the heel is fed a moderately rich vascular supply. Thus, the panniculus carnosus muscle may be the primary site of injury in heel PrUs.16 Supportive evidence was demonstrated by a study that experimentally induced PrUs over the trochanteric region of the fuzzy rat, which subsequently developed early necrosis of the panniculus carnosus muscle.27 The loculated fat in the heel is another particularly vulnerable tissue supply to ischemia having the most marginal vascularity. In comparison with other tissues, the skin is quite resistant to ischemia and has been shown to withstand normothermic ischemia up to 12 hours without necrosis.28
Ischemia-reperfusion injury is another mechanism of PrU development on the heel. Tissue reperfusion followed by ischemia can cause reactive oxygen species that overwhelm endogenous antioxidants, resulting in a cascade of events including mast cell degranulation, recruitment of neutrophils to endothelial wall, arteriolar constriction, and increased vascular permeability that leads to inflammation and edema.29,30 Animal studies have reported that, in young animals, chemotaxis, oxidant release, and phagocytosis by neutrophils play key roles in tissue damage following reperfusion, whereas increased oxidative stress and mast cell density/action appear to have a more significant perturbation on the antioxidant defense in older animals.29,30 Individuals with diabetes mellitus are at increased risk of reperfusion injury secondary to decreased levels of microvessel nitric oxide, a potent vasodilator that protects the vascular endothelium from reperfusion injury.31
Although colonization with bacteria is normal and can even be helpful during the initial healing phase, critical colonization and local infection impede healing. Wounds that have greater than 105 organisms per gram of tissue tend not to heal and are "stuck" in the inflammatory stage.32
Patients with spinal cord injury (SCI) and associated comorbidity are at an increased risk for the formation of PrUs. These individuals are paralyzed below a certain level of the body, which limits their ability to relieve the pressure acting on the immobile portions of the body. Moreover, the sensory loss that results from SCI renders the patients unaware of the impending or existing injury caused by prolonged pressure. Also, the neural and metabolic regulatory mechanisms for the maintenance of adequate tissue blood flow are impaired in patients with SCI.33,34
Another population group at risk for pressure ulceration is older adults. Aging is associated with slower wound healing and subsequent functional wound closure. Reduced proliferation of fibroblasts, keratinocytes, and vascular endothelial cells; decreased collagen synthesis; and diminished fibroblast response to growth factors are associated with advanced ages.35-37 The heel pad skin becomes less resilient, and the shock-absorbing ability of the heel pad declines with age.38,39
By contrast to DTI, which is a distinct histopathological entity with mechanical stress being the essential etiologic factor, "purple heel" is not a well-recognized entity or syndrome.40 Nonetheless, clinicians know empirically that a change in color over the heel can mean impending, evolving, and significant pathology that is typical of DTI.40 However, it is not certain that purple heel is exclusively the consequence of relentless pressure and friction causing DTI. Purple heel shares several risk factors-atherosclerosis, diabetes, and arterial emboli/thrombi-with purple/blue toe syndrome that may occur bilaterally and is characterized by intense pain, purple/blue color, skin necrosis, and ischemic gangrene in the affected toes. In both purple heel and purple/blue toe syndrome, sudden changes in skin color are an ominous clue of imminent ulceration and the progression of ischemia and necrosis.40
PrUs affect both an individual's health and the economic resources of healthcare infrastructures. The heel is the second most frequent site of PrUs in general and the most common location for sDTIs. By instituting regular, frequent repositioning of the extremity; skin assessment; and introducing heel-protective devices, the prevalence of hospital-acquired heel PrUs can be significantly reduced.
The authors express sincere gratitude to William Falone, MSN, RN, CWON, Wound and Ostomy Nurse Specialist, who provided the photographs in Figure 1.
2. Gefen A. The Compression Intensity Index: a practical anatomical estimate of the biomechanical risk for a deep tissue injury. Technol Health Care 2008;16:141-9.
3. Salcido R, Ahn C, Wu SSH, Goldman RJ. Prevention and management of chronic wounds. In: Braddom RL, ed. Physical Medicine and Rehabilitation. Philadelphia, PA: Elsevier; 2011:683-712.
4. Bua EA, McKiernan SH, Wanagat J, McKenzie D, Aiken JM. Mitochondrial abnormalities are more frequent in muscles undergoing sarcopenia. J Appl Physiol 2002;92:2617-24.
5. Vangilder C, Macfarlane GD, a Meyer S. Results of nine international pressure ulcer prevalence surveys: 1989 to 2005. Ostomy Wound Manage 2008;54(2):40-54.
6. VanGilder C, MacFarlane GD, Harrison P, Lachenbruch C, Meyer S. The demographics of suspected deep tissue injury in the United States: an analysis of the International Pressure Ulcer Prevalence Survey 2006-2009. Adv Skin Wound Care 2010;23:254-61.
7. Lyman V. Successful heel pressure ulcer prevention program in a long-term care setting. J Wound Ostomy Continence Nurs 2009;36:616-21.
8. Pancorbo-Hidalgo PL, Garcia-Fernandez FP, Lopez-Medina IM, Alvarez-Nieto C. Risk assessment scales for pressure ulcer prevention: a systematic review. J Adv Nurs 2006;54:94-110.
9. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA 2006;296:974-84.
10. De Keyser G, Dejaeger E, De Meyst H, Eders GC. Pressure-reducing effects of heel protectors. Adv Wound Care 1994;7(4):30-2, 34.
11. Tymec AC, Pieper B, Vollman K. A comparison of two pressure-relieving devices on the prevention of heel pressure ulcers. Adv Wound Care 1997;10(1):39-44.
12. Walsh JS, Plonczynski DJ. Evaluation of a protocol for prevention of facility-acquired heel pressure ulcers. J Wound Ostomy Continence Nurs 2007;34:178-83.
13. Black J. Preventing heel pressure ulcers. Nursing 2004;34(11):17.
14. Fowler E, Scott-Williams S, McGuire JB. Practice recommendations for preventing heel pressure ulcers. Ostomy Wound Manage 2008;54(10):42-8, 50-2, 54-7.
15. Cuddigan J, Ayello EA, Black J. Saving heels in critically ill patients. WCET 2008;28(2):2-8.
16. Cichowitz A, Pan WR, Ashton M. The heel: anatomy, blood supply, and the pathophysiology of pressure ulcers. Ann Plast Surg 2009;62(4):423-9.
17. Salcido R, Carney J, Fisher S. A reliable animal model of pressure sore development: the role of free radicals. J Am Paraplegia Soc 1993;16:61.
18. Kosiak M. Etiology and pathology of ischemic ulcers. Arch Phys Med Rehabil 1959;40:62-9.
19. Bouten CV, Oomens CW, Baaijens FP, Bader DL. The etiology of pressure ulcers: skin deep or muscle bound? Arch Phys Med Rehabil 2003;84:616-9.
20. Gefen A, Gefen N, Linder-Ganz E, Margulies SS. In vivo muscle stiffening under bone compression promotes deep pressure sores. J Biomech Eng 2005;127:512-24.
21. Witkowski JA, Parish LC. Histopathology of the decubitus ulcer. J Am Acad Dermatol 1982;6:1014-21.
22. Dinsdale S. Decubitus ulcers: role of pressure and friction in causation. Arch Phys Med Rehabil 1974;55:147-52.
23. Okuwa M, Sanada H, Sugama J, et al. A prospective cohort study of lower-extremity pressure ulcer risk among bedfast older adults. Adv Skin Wound Care 2006;19(7):391-7.
24. Padberg F, Back T, Thompson P, Hobson R. Transcutaneous oxygen (TcPo2
) estimates probability of healing in the ischemic extremity. J Surg Res 1996;60:365-9.
25. Wu L, Xia YP, Roth SI, Gruskin E, Mustoe TA. Differential effects of platelet-derived growth factor BB in accelerating wound healing in aged versus young animals: the impact of tissue hypoxia. Plast Reconstr Surg 1997;99:815-22; discussion 823-4.
26. Wu L, Brucker M, Gruskin E, Roth SI, Mustoe TA. Transforming growth factor-beta1 fails to stimulate wound healing and impairs its signal transduction in an aged ischemic ulcer model: importance of oxygen and age. Am J Pathol 1999;154:301-9.
27. Salcido R, Donofrio JC, Fisher SB, et al. Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Adv Wound Care 1994;7(5):23-4, 26, 28.
28. Milton SH. Experimental studies on island flaps. II. Ischemia and delay. Plast Reconstr Surg 1972;49:444-7.
29. Gute DC, Ishida T, Yarimizu K, Korthuis RJ. Inflammatory responses to ischemia and reperfusion in skeletal muscle. Mol Cell Biochem 1998;179:169-87.
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31. van Marum RJ, Meijer J, Bertelsmann F, Ribbe M. Impaired blood flow response following pressure load in diabetic patients with cardiac autonomic neuropathy. Arch Phys Med Rehabil 1997;78:1003-6.
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exotoxin A: its role in retardation of wound healing. J Burn Care Rehabil 1992;13:512-8.
33. Li Z, Leung JY, Tam EW, Mak AF. Wavelet analysis of skin blood oscillations in persons with spinal cord injury and able-bodied subjects. Arch Phys Med Rehabil 2006;87:1207-12.
34. Rappl LM. Physiological changes in tissues denervated by spinal cord injury tissues and possible effects on wound healing. Int Wound J 2008;5:435-44.
35. Reed MJ, Ferara NS, Vernon RB. Impaired migration, integrin function, and actin cytoskeletal organization in dermal fibroblasts from a subset of aged human donors. Mech Ageing Dev 2001;122:1203-20.
36. Gosain A, DiPietro LA. Aging and wound healing. World J Surg 2004;28:321-6.
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38. Abu-Own A, Sommerville K, Scurr JH, Coleridge Smith PD. Effects of compression and type of bed surface on the microcirculation of the heel. Eur J Vasc Endovasc Surg 1995;9:327-34.
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Keywords:© 2011 Lippincott Williams & Wilkins, Inc.
heel; pressure ulcer; purple heel; deep tissue injury