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:
, where weight is the skin-support surface force at the region of interest, R is the radius of curvature of bony prominence, and T is the thickness of tissue overlying the bony prominence.
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.
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7. Lyman V. Successful heel pressure ulcer
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8. Pancorbo-Hidalgo PL, Garcia-Fernandez FP, Lopez-Medina IM, Alvarez-Nieto C. Risk assessment scales for pressure ulcer
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9. Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA 2006;296:974-84.
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13. Black J. Preventing heel
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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
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Keywords:© 2011 Lippincott Williams & Wilkins, Inc.
heel; pressure ulcer; purple heel; deep tissue injury