Immobility is a primary risk factor for developing a heel PrU40; it is a present factor in up to 87% of cases.41 Some degree of immobility is seen in most hospitalized patients; however, those with a fractured leg,40,42-44 spinal cord injury (SCI),3 or stroke are at particularly high risk for skin breakdown on the heel. Following a hip fracture, the circulation and innervation to the extremity is impaired, and the patient does not move the fractured leg, increasing the risk for tissue breakdown. Stotts et al42 reported that patients with a fractured hip and open reduction with internal fixation have a 45.1% probability of developing a partial-thickness (Stage I-II) heel PrU, whereas Duncan and Mataya43 reported a heel PrU incidence of 53% in 30 hip fracture patients hospitalized for 5 days or longer. Many individuals who fall and fracture a hip may be immobile for hours to a day or more before being found by another person. With impaired innervation and circulation, and with being immobile, the fractured leg is not moved and becomes "dead weight" with very high tissue-interface pressures. It is not uncommon for health care personnel to discover a Stage IV, unstageable, or deep tissue injury (DTI) on these individuals, but often not for a few days or more after the fall. In addition, if Buck traction is initiated before surgery, this continues to compromise the mobility of the leg. Duncan and Mataya43 prospectively studied the effect of heel pressure relief and demonstrated a reduction in incidence to 0%.

COMORBID RISK FACTORS

It is reported that the risk is great in patients who are older, debilitated, incontinent, paralyzed, or unconscious, as well as those with metastatic cancer.44,45 Patients in the ICU are at risk,46 as well as patients on a vasopressor and/or a ventilator, those requiring elevation of the head of the bed, or those unable to reposition independently. Another high-risk group of patients is those with DM. Most have some degree of peripheral vascular disease (PVD), which compromises circulation, have neuropathy, and/or have a foot deformity.40 Krueger47 reported that 25% of heel PrUs are related to diabetic neuropathy and peripheral arterial occlusive disease. Heel ulcers in the person with diabetes are often associated with neuropathic and ischemic etiologies48 related to lower resting perfusion pressures and higher superficial and/or deep pressures when under load.15 An individual with DM has a heel ulcer occur 4 times more often than an individual without DM.49

Neuropathy (pathological changes in the peripheral nervous system) is poorly understood, but is seen frequently with age and DM. It occurs eventually in individuals with DM within 5 to 10 years of diagnosis, impairing sensation and increasing the vulnerability to break down primarily by interfering with one's awareness of the presence of pressure.50 Neuropathy of the foot consists of 3 simultaneous phases: (1) sensory, with loss of sensation and pressure; (2) motor, with loss of intrinsic muscles and ankle-jerk reflex; and (3) autonomic, resulting in the absence of sweat and oil production, leaving the skin dry and inelastic.51,52

Edema compromises capillary blood flow, along with impaired oxygen and nutrient transport and waste removal.53 The weight of the excess fluid can lead to higher resting tissue pressures, further impairing tissue tolerance to pressure.29 All these factors contribute to the fact that, on the heel, a PrU is frequently of full thickness when initially discovered.1

An individual with a cerebrovascular accident is at risk for a heel PrU related to his or her limited ability to move one or both legs, as well as from friction and shear, and/or impaired cognition.52 Patients who have had an SCI are at risk for neuropathy associated with impaired autonomic, motor, and sensory systems. Skin that is impaired neurologically undergoes metabolic changes that can take 3 to 5 years to stabilize after injury. These changes include increased collagen catabolism, defective collagen synthesis resulting in fragile skin, abnormal vascular skin reactions, and lessened elasticity of skin. Paralysis causes reduced muscle bulk, including that over bony prominences, exposing skin to injury.54 Some of these at-risk individuals propel themselves in their wheelchairs using their heels, increasing their PrU risk.38,39

A study of 242 patients in a 333-bed community hospital identified risk factors for a heel PrU to be type 2 diabetes mellitus PVD, low serum albumin, and low Braden Scale score.55 Patients with severe PVD, patients with a history of PrUs, and those with poor nutrition, leg spasms, contractures, or agitation are also at risk.5,40 A 2006 study47 reported that additional individual risk factors for heel PrUs include friction and reduced sensation (individual subscales on the Braden Scale), as well as compromised circulation, the presence of antiembolic stockings, fluid intake of less than 1500 mL/d, inadequate sensation of pain and temperature, smoking, surgical procedures longer than 60 minutes, the presence of a lower-extremity cast, and immobility, particularly with restraints. According to Drennan,5 any patient assessed on the Braden Scale with a score of 15 or less is at risk.

Patients who undergo epidural analgesia for surgery are at risk to develop a heel PrU. Epidural analgesia produces both a sensory and motor block, restricting a patient's movement and leading to prolonged pressure on the heels and the loss of the protective sensation to move the legs in response to the pressure. According to Koziak,27 "a constant pressure of 70 mm Hg for more than 2 hours produces tissue ischemia and irreversible tissue damage."

Although a PrU on the heel may appear within 24 hours of surgery, it often does not develop for several days.56 Individuals who undergo surgery for more than 3 hours or who are in the postanesthesia care unit for extended periods are among those at risk.41 Shah56 reported on 3 cases of fairly young individuals who developed a heel PrU following epidural anesthesia. Other reports have been made of the development of a heel PrU following epidural anesthesia for labor and delivery, as well as for hip replacement or urological surgery.57-60 Heel PrUs can also occur in children.61

DEEP TISSUE INJURY

Some heel PrUs may become a DTI. A (suspected) DTI was defined by the National Pressure Ulcer Advisory Panel62 in 2007 as "a purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. DTI may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment." In fact, many DTIs have quickly developed into large Stage IV ulcers.63 The etiology is felt to be related to high levels of pressure at the bone-tissue interface.64

The DTI can present as a deep red or purple area, have a bruised appearance, or appear as a fluid or blood-filled blister. A fluid-filled blister would be more indicative of a Stage II PrU, whereas a blood-filled blister is more indicative of a Stage III-IV PrU.65 This color is related to tissue necrosis and subsequent coagulation of the blood from stasis.65

Animal research has revealed that skin is the last tissue layer to lose viability and die under prolonged pressure and can be nonviable and still remain intact for up to 14 days.66,67 Farid65 observed, "The tensile strength of skin rivals that of connective tissue and ligaments, a phenomenon frequently noted in deep tissue pressure damage."

It is also known that an area of hyperemia can indicate damage from what is called a reperfusion injury. This is seen when ischemia occurs from arterial insufficiency and pressure, followed by pressure relief and reestablishment of circulation (eg, pressure is relieved), and the sudden reperfusion creates additional insult and injury to the tissue. The "tissue injury increases with each ischemia-reperfusion cycle, the duration of ischemia, and frequency of ischemia-reperfusion cycles."65

A hyperemic area can quickly become a DTI if offloading is inadequate or if offloading is adequate but the patient has an arterial embolus (eg, lower extremity).65

If clinicians wait to observe a nonblanchable lesion to call it a "true" Stage I PrU, they can miss the opportunity to prevent irreversible tissue damage.65 In other words, if the DTI or possible DTI diagnosis is missed on admission, it would appear as a nosocomial DTI normally 7 to 14 days later, when the DTI actually was present on admission. For this reason, capillary refill should be assessed at least twice (preferably every 8 hours) during the first 24 hours after admission,65 to distinguish between a Stage I PrU and a DTI, particularly for a patient with DM and PVD. The recommendation would be to photograph all reddened areas, as well as other obvious lesions, on admission or soon after admission. When the reddened area maintains capillary perfusion, recovery can occur in the following 72 hours.68-72 In a DTI that "presents as a demarcated red/purple area, clinicians can count back 7 days to pinpoint when the actual pressure damage occurred."65

Clinicians are cautioned that capillary refill may seem to be present in the first 24 hours after admission; however, this is a phenomenon known as hypostasis-a condition present in early tissue decomposition (death) that mimics capillary refill.73,74 It is actually "loose blood" accumulating from capillary collapse.65 Thus, a DTI can appear as a pale, whitish area with a waxy appearance in lighter-skinned individuals. In patients with darker skin pigment, the DTI can appear as a lighter patch of skin surrounded by an abnormally darker area that shows no color change when testing capillary refill.65 This is seen more commonly on the sacrum, but may also be seen on the heel.

It is important to pay attention not only to the total risk assessment score, but also to the subscale categories with low scores, such as mobility, sensation, and activity.40 In patients with DM and impaired mental capacity, it is critical to complete a thorough assessment every shift and, more frequently, even up to 3 times a day.75

APPEARANCE OF A HEEL PRESSURE ULCER

A Stage I PrU on the heel appears red, generally nonblanchable, and is often painful.76 This injury has the potential to recover if offloaded continuously.76 A Stage II heel PrU often appears as a blister or shallow skin tear, whereas a full-thickness (Stage III-IV) PrU appears open and deeper. A heel PrU caused by friction generally appears red and often is blistered from friction to tissue.47

A heel PrU can also be a DTI, which can occur very quickly with the minimal padding over the bony angular heel prominence. A DTI can have a bruised, purplish appearance or can appear as a blood-filled blister of intact skin. If pressure continues without relief, there can be tissue necrosis and eschar development.76Figure 1 defines PrU stage characteristics.

Figure 1. CHARACTERISTICS OF A HEEL PRESSURE ULCER BY NPUAP STAGE

HEEL PRESSURE ULCER PREVENTION AND TREATMENT RESEARCH

A 4-phase study of 242 patients was performed in a 333-bed community hospital. The experimental prospective component, trialing a heel PrU prevention protocol, documented a reduction in the incidence of heel PrU development.12 Bots and Apotheker77 studied prevention of heel ulcers using a self-adhesive hydropolymer foam dressing on 140 surgical patients in the ICU over 2 years. Risk was assessed using the Norton Scale, the duration of surgery was documented, and a foam dressing was applied postoperatively. Heels were inspected daily for up to 10 days. A 76.7% reduction in heel PrUs was documented with this method.

A similar study by Nakagami et al18 compared the shear forces exerted over the heel in a sample of 30 older adult patients in a Japanese hospital. One group used a PrU preventive hydrocolloid dressing, whereas the other used a thin film dressing. Mean interface pressures were not statistically different between the 2 dressings on a paired t test (70.7 +/- 16.5 and 70.2 +/- 15.2 mm Hg; P = .4198). However, there was a statistically significant difference in shear force between the 2 groups on a Wilcoxon signed rank test (2.2 +/- 1.4 and 11.7 +/- 5.8; P < .001). The specially designed PrU preventive dressing had a slippery surface that helped reduce friction, and the coefficient of kinetic energy was small enough to reduce the shear force. The authors did not evaluate the ability of the specially designed PrU dressing to prevent a PrU and stressed that a longitudinal study was needed to evaluate the dressing's effectiveness in prevention of a PrU.

Yet another study compared a standard preventive bandage on the heel with the Allevyn (Smith & Nephew, Largo, FL) heel hydrocellular dressing. Of the 111 patients who completed the study, significantly (P = .001) fewer heel PrUs developed in the Allevyn group (2 of 61 patients, or 3.3%) as compared with the protective dressing group (22 of 50 patients, or 44%).78

Products need to be evaluated on actual patients with actual risk for a particular morbidity. A good device to reduce pressure on the heel will separate and protect the ankles from one another, maintain heel suspension, and prevent foot drop.40 Pressure-redistributing/relieving devices should consistently reduce interface pressure below 32 mm Hg or pressure-reducing support (pressure less than standard support surfaces, but not below 32 mm Hg).75

The heel often requires additional protection beyond the use of topical dressings and specialty beds and overlays. An experimental study evaluated the effectiveness of hospital pillows versus a commercial, triangular-shaped heel elevation device in a sample of 52 patients from 27 to 90 years of age. The heel device was 4 times more likely not to suspend the heel off the bed than the pillow.79 A more recent randomized clinical trial of 338 adults compared 3 pressure-reduction devices (bunny boot, egg crate, and foot waffle) in the prevention of heel ulcers on moderate to high-risk patients: 12 PrUs developed, with 11 Stage I and 1 Stage II PrUs present; and the incidence was not significant (bunny boot = 3.9%, egg crate = 4.6%, and foot waffle = 6.6%).80 In a 41-patient prospective study comparing 4 pressure-reducing devices used over 12 days, foam splints and eggshell foam were found to be more effective than Duoderm (ConvaTec, Princeton, NJ) and heel protector boots; however, the researchers stressed that use of one of these only serves to enhance meticulous skin care.44

A study of 52 patients compared a control group (n = 30) who received "only high-level nursing care" with 22 patients who received the Heelift Suspension Boot (DM Systems, Evanston, IL). No PrUs occurred in the Heelift-treated group, whereas 17% of the control group developed a heel PrU (T.I. Bordner, personal communication, April 2003). Yet another prospective study of 30 hip-fracture patients hospitalized 5 days or longer and treated with heel pressure relief documented a reduction in heel PrU incidence from 53% to 0%.43

SPECIFIC PREVENTION AND TREATMENT INTERVENTIONS

As most of the interventions to prevent a heel PrU are the same as those used to treat PrUs, prevention and treatment interventions will be discussed together for the purposes of this article. First, the clinician needs to perform a heel PrU risk assessment.

Individuals need to be assessed for risk of heel PrU development, most particularly those who are mobility impaired, are unable to move on their own, have impaired sensation and/or circulation of the lower extremities, have DM, or have a foot deformity. A well-researched risk assessment scale should be used. Unfortunately, most commonly used risk assessment scales do not have a subscale or factor for nonmovement of the lower extremity. Consequently, a patient with a leg fracture may not be appropriately assessed and scored on the activity subscale. Should individuals with PVD and peripheral neuropathy be considered cognitively impaired related to the lack of cognitive awareness of their lower extremities? The authors recommend that most older adults with a hip/leg fracture should be placed in an at-risk category, and appropriate preventive interventions should be implemented, from the time of the fracture through the application of Buck traction, surgery, and postoperatively until mobility is regained. Figure 2 illustrates the Heel PrU Risk Assessment Tool.

Figure 2. HEEL PRESSURE ULCER RISK ASSESSMENT TOOL

Patients/residents with cognitive impairment are at increased risk for heel PrU development and need to have their heels assessed. Individuals who are wearing TEDs (Kendall, Mansfield, MA) need to have them removed at least once, and preferably twice, a day to assess the heels. Patients with contractures and foot deformities need careful assessment of the feet and heels and for properly fitting footwear. Individuals who use their heels to propel themselves in a wheelchair are at risk as well.38,39

All patients need to be assessed for risk upon admission, with a significant change in condition, and periodically thereafter, appropriate to the setting and in accordance with agency policies. In acute care, this should be done at least every 48 hours and whenever there is a significant change in condition,36,39 whereas the authors recommend at least daily assessment. In long-term care, assessments should be made weekly for the first month, then either monthly or quarterly, depending on agency protocol. In home care, assessments should be made during every visit by a licensed nurse. Each agency needs to define its own protocols and time frame for risk assessment based on scientific evidence and the patient/resident population.36,39

Blaszczyk et al81 developed a heel PrU risk stratification tool. A total score is calculated for each patient, with 1 point given to each risk factor present. Then the nurse would determine activity level and refer to the flow chart to determine the patient's risk level Figure 2. The authors recommended the following courses of action: daily reassessment of heels; float heels of all intubated or unresponsive patients until assessed for risk and further actions implemented; institute strict precautions if heels are red or skin appears damaged; and use heel protector/floats on all individuals at risk for heel breakdown.82 Further interventions are outlined in that article.

PROTOCOLS

The pivotal focus for preventing and treating a heel PrU is on the interaction between external pressure and the heel vasculature.3 Prevention strategies for heel ulcers need to be comprehensive and should include the following: identification of comorbidities, including nutrition; at least daily skin assessment; routine risk assessment using a tested scale; implementation of evidenced-based prospective interventions; early aggressive application of pressure-redistributing devices; immediate initiation of prevention and/or treatment interventions; and ongoing product evaluation with frequent documentation of heel integrity.12,83 Black et al63 recommended that an individual with both DM and PVD should have twice-daily heel assessments, and those in acute care with impaired mental capacity should be assessed 2 to 3 times a day. During an assessment, it is important to palpate peripheral pulses (popliteal, posterior tibial, and dorsalis pedis). Also, check for foot sensation in at-risk patients. Consider whether the risk assessment score indicates risk and whether the patient will be immobile for 4 or more hours.

Heels must be assessed frequently, and each setting or institution needs to define its own protocol. The Agency for Healthcare Research and Quality (formerly known as the Agency for Health Care Policy and Research) and Wound, Ostomy and Continence Nurses Society Guidelines36,39 recommend at least daily assessments. If a patient has difficulty moving, assessments can be performed using a mirror held under the heel, which provides a good visualization of the area, allowing the assessor to see if there is a purple or bruised look, or if there appears to be a "blood blister" present. These factors could be indicative of DTI. Capillary refill/blanching should be checked during assessment, and the heels must be felt for a boggy/mushy feeling and undue temperature changes. Keep in mind the importance of heel anatomy, as "anatomy can be destiny."84 Patients wearing compression stockings need to have them removed at least once and preferably twice a day to allow for both visual and palpatory assessments for changes. Pedal pulses need to be routinely assessed and documented. Figure 1 elaborates on the characteristics of heel PrUs by stage.

Turning or repositioning the patient frequently is a good way to help prevent the development of a heel PrU.85 Defloor et al86 compared 4 turning schemes (q2hr or q3hr on standard mattress, and turning q4hr or q6hr on a viscoelastic foam [VEF] mattress) on 838 nursing home patients and found that turning every 4 hours on a VEF mattress significantly reduced PrU development.

Complete elimination of heel pressure using a pressure-relief device is critical.40 At-risk patients should have a heel pressure-redistributing device in place to prevent breakdown and protect from the effects of pressure, friction, and shear forces to the heel tissue.39,40 Groups of patients for whom these boot-type devices are in order include those with DM, particularly those with PVD and/or peripheral neuropathy; those with poor or limited mobility; those with absent or poor foot pulses; those undergoing surgeries longer than 2 hours and/or those who will be immobile in the recovery room and bed afterward; those with severe PVD without DM; those with a history of a PrU; and those identified at risk on the risk assessment tool.5 A variety of boot-type devices are available for redistributing pressure to the heels.

According to Black,40 "the best heel-pressure-reducing products also separate and protect the ankles, maintain heel suspension, and prevent foot drop." Some mattresses on the market have built-in pressure-reducing areas for the heels. A static device that distributes pressure over a surface larger than the body area is often satisfactory for patients who are able to shift their weight. Examples of these devices are foam mattresses and devices filled with air, gel, or water.11 A dynamic device is best for patients who cannot shift their weight. This category of devices would include powered devices that alternately inflate and deflate to reduce pressure. Some beds on the market have built-in, heel-area pressure-redistribution properties (eg, Clinitron [Hill-Rom, Batesville, IN], ZoneAire [Hill-Rom], Plexus Auto Aire Select [Gaymar Industries, Orchard Park, NY] [not a complete list]), whereas other beds do not have built-in heel pressure relief. No device replaces repositioning, so frequent repositioning of the patient is essential. We do know that some effectiveness of these devices can be nullified when the head of the bed is elevated.

Although the literature varies, it is reported that these devices do not effectively reduce tissue-interface pressure below minimal capillary closing pressures.18,85 The devices provide some, albeit limited, protection against friction and shear to bony prominences, particularly when the patient is in a side-lying position.18 Foam boots work well, as the exterior surface helps reduce friction; however, the more rigid the foam boot, the more likely it is that pressure areas can develop on the lateral ankles or the heel plantar surface. Boot-type devices help lessen external and internal rotation, but unless they are more rigid, they do not prevent it. Air boots are lighter weight and help lessen external and internal rotation, but again, they do not prevent it. Feet can sweat in air boots unless air holes are present to facilitate circulation. Some boots have a surface that allows them to slip around more on the bed surface; thus, it is important to allow for more frequent positioning checks. Straps need to be applied so the boot will stay on, but straps should not be too tight as to cause pressure. Bootstraps can cause undue pressure on the lower leg and dorsum of the foot; thus, they need to be routinely removed, and the entire foot and leg assessed for signs of undue pressure. Clinicians must check to see that the patient is actually wearing the pressure-redistributing devices and that they are worn correctly.

Heels can also be "floated," and pressure can be removed with a folded towel or blanket, or a pillow, particularly when in Buck traction. It is helpful to use a pillow along the entire length of the lower extremity to protect the knee and not to place the elevating device under the Achilles tendon. One can verify if the heels are actually floating by slipping a sheet of paper between the heel and bed surface without it touching the heel or by slipping the clinician's hand between the heel and the bed surface. The bed knee gatch can be raised as long as the heel is floated and the Achilles tendon is protected. When the foot of the bed is elevated (eg, to reduce edema), remember to also elevate the patient's knee(s) to prevent suspending the leg by the heel.40 Ascertain that foot drop is not present, which could allow for heel cord contractures.5 When possible, get the patient moving and minimize bed rest time. When feet are elevated to reduce edema, it is very important to have the patient flex his or her knees to prevent hyperextension and reduce pressure on the heels.40

Preserving the integrity of the skin is critical in preventing a PrU on the heel or other foot bony prominences. This can be accomplished by removing the pressure, by using lubricants and/or moisturizers, and by using protective dressings (film, foam, or hydrocolloid) or protective padding.36,38,39 These dressings do not provide pressure relief. With a Stage I heel PrU, relieving the pressure is often all that is needed for the tissues to recover. If a blister is present on the heel, do not break it. Merely elevate the leg and heel. If the PrU has eroded the skin (Stage II-IV), a moldable dressing is appropriate to protect it, keep it clean, and maintain moist wound healing (eg, hydrocolloid, impregnated gauze, or foam). If infection is suspected, do not use an occlusive dressing that can hold bacteria in the wound and encourage spread.76 Twice-daily moist gauze dressings would be an alternative for this situation.76 Monitor the heel area for signs of deterioration, including erythema, odor, increasing drainage, color and type of drainage, fever, increasing pain, and/or exposed bone.40

See Figure 1 for further elaboration on this topic. Treatment of a Stage III or IV heel PrU remains controversial, and additional research is in order. The current consensus is to not remove stable eschar, allowing it to separate on its own.38,39 Heel vascularity underlying the eschar is essentially absent, with only a subcutaneous or fat tissue pad normally; thus, it is susceptible to infection with limited to no ability of the body to fight it. In the presence of eschar, wrap the heel in gauze and relieve the pressure.76 Also assess it at least twice a day for changes, such as bogginess, edema, redness, drainage, or overt signs of infection. The presence of infection necessitates a change in the treatment plan. As the eschar loosens from the underlying tissue, a qualified debridement clinician can trim the loosened eschar and nonviable tissue.76 When the eschar is open or cracked or infection is present, debridement of the tissue is in order.38 Containment of drainage is important.83

It is important to perform a nursing nutritional assessment, assessing both the nutritional and hydration status of the patient. If the patient is identified at nutritional risk or if the patient has a heel PrU, obtain a full nutritional evaluation and ensure adequate dietary intake to prevent malnutrition.38,39 As needed, the registered dietitian will recommend, and the physician will order, a nutritional supplementation if the patient has a PrU, has inadequate dietary intake (particularly protein), or is malnourished. Treatment should include a balanced diet with good sources of vitamins and adequate protein and calories as prescribed by the dietitian.38,87 Research has not yet documented that high doses of vitamin C will accelerate wound healing.88

CONCLUSION

The heel, although currently the second most frequent body site for a PrU, is fast on the path to becoming the most common PrU site. Heel PrU prevalence is increasing and is a real and present danger, particularly in individuals with cognitive or sensory impairment and/or limited mobility. It is critical that all health care team members integrate prevention and early intervention strategies into their practice to prevent heel ulcers. Risk identification, comprehensive histories, daily or more frequent foot inspections, and immediate preventive interventions are all vital. Patients and health care workers need to know the latest strategies on preventing heel ulcers, identifying them at an early stage, and implementing appropriate measures for healing. Each clinical setting needs to develop evidence-based protocols specific to its patient population. Heels of at-risk patients need to be assessed and floated. As the annual cost of treating nosocomial PrUs is estimated to be $2.2 to $3.6 billion per year89 and the cost to treat a Stage IV PrU can be upward from $70,000,90 spending $35 or more per heel protection boot would seem to be a wise and cost-effective preventive investment.

REFERENCES

1. Bennett L, Lee BY. Pressure vs. shear in pressure sore causation. Chronic ulcers of the skin. New York, NY: McGraw Hill; 1985. Chapter 3. [Context Link]

2. Hunter SM, Langemo DK, Olson B, et al. The effectiveness of skin care protocols for pressure ulcers. Rehabil Nurs 1995;20:250-5. [Context Link]

3. Wong VK, Stotts NA. Physiology and prevention of heel ulcers: the state of science. J Wound Ostomy Continence Nurs 2003;30:191-8. [Context Link]

4. Horn SD, Bender SA, Bergstrom N, et al. Description of the National Pressure Ulcer Long-Term Care Study. J Am Geriatr Soc 2002;50:1816-25. [Context Link]

5. Drennan DB. Heel pressure ulcers are preventable. Ext Care Product News 2003;87(3):4-5. [Context Link]

6. Younes NA, Albsoul AM, Awad H. Diabetic heel ulcers: a major risk factor for lower extremity amputation. Ostomy Wound Manage 2004;50(6):50-60. [Context Link]

7. Brandeis B, Morris JN, Nash DV, et al. The epidemiology and natural history of pressure ulcers in elderly nursing home residents. JAMA 1990;264:2905-9. [Context Link]

8. Barczak CA, Barnett RI, Childs EJ, et al. Fourth national pressure ulcer prevalence survey. Adv Wound Care 1997;10:18-26. [Context Link]

9. Amlung SR, Miller WL, Bosley LM. National prevalence pressure ulcer survey: a benchmarking approach. Adv Skin Wound Care 2001;14:297-301. [Context Link]

10. Ovington L. Prediction and prevention of heel pressure ulcers. Wound Care Newsl. November 1998. [Context Link]

11. National Pressure Ulcer Advisory Panel support surface standards initiative. Terms and definitions related to support surfaces. Version 01/29/07. Washington, DC: NPUAP S3I, 2007. Available at: http://www.npuap.org/NPUAP_S3I_TD.pdf . Last accessed April 7, 2008. [Context Link]

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. [Context Link]

13. Gray H. Gray's Anatomy: The Anatomical Basis of Medicine and Surgery. Philadelphia, PA: Elsevier; 2004. [Context Link]

14. Graff MK, Bryant K, Beinlich N. Preventing heel breakdown. Orthop Nurs 2000;19:63-9. [Context Link]

15. Mayrovitz HN. Effects of different cyclic pressurization-relief patterns on heel skin blood perfusion. Adv Skin Wound Care 2002;15:158-64. [Context Link]

16. Thompson P, Langemo D, Anderson J, et al. Skin care protocols for pressure ulcers and incontinence in long-term care: a quasi-experimental study. Adv Skin Wound Care 2005;18:422-9. [Context Link]

17. Bennett L, Kavner D, Lee BK, et al. Shear vs pressure as causative factors in skin blood flow occlusion. Arch Phys Med Rehabil 1979;60:309-14. [Context Link]

18. Nakagami G, Sanada H, Konya C, et al. Comparison of two pressure ulcer preventive dressings for reducing shear force on the heel. J Wound Ostomy Continence Nurs 2006;33:267-72. [Context Link]

19. Abu-Own A, Sommerville K, Scurr JH, et al. Effects of compression and type of bed surface on the microcirculation of the heel. Eur J Endovasc Surg 1995;9:327-34. [Context Link]

20. Counsell C, Seymour S, Guin P, et al. Interface skin pressure on four pressure-relieving devices. J Enteros Ther 1990;17:150-3. [Context Link]

21. Ek AC, Gustavsson G, Lewis DH. Skin blood flow in relation to external pressure and temperature in the supine position on a standard hospital mattress. Scand J Rehab Med 1987;19:121-6. [Context Link]

22. Allen V, Ryan DW, Murray A. Potential for bedsores due to high pressures: influence of body sites, body position, and mattress design. Br J Clin Pract 1993;47:195-7. [Context Link]

23. Allen V, Ryan DW, Murray A. Measurements of interface pressure between body sites and the surfaces of four specialized air mattresses. Br J Clin Pract 1994;48:125-9. [Context Link]

24. Mayrovitz HN, Smith J, Delgado M, et al. Heel blood perfusion responses to pressure loading and unloading in women. Ostomy Wound Manage 1997;43:16-20, 22, 24. [Context Link]

25. Mayrovitz HN, Smith J. Heel-skin microvascular perfusion responses to sustained pressure loading and unloading. Microcirculation 1998;5:227-33. [Context Link]

26. Mayrovitz HN, Sims N, Taylor MC, et al. Effects of support surface relief pressures on heel skin blood perfusion. Adv Skin Wound Care 2003;16:141-5. [Context Link]

27. Koziak M. Etiology of decubitus ulcers. Arch Phys Med Rehabil 1961;42:19-29. [Context Link]

28. Reswick JB, Rogers J. Experiences at Ranchos Los Amigos Hospital with devises and techniques to prevent pressure ulcers. In: Kenedi RM, Cowden JM, Scales JT, eds. Bedsore Biomechanics. London, England: Macmillan Press; 1976:301-13. [Context Link]

29. Scanlon E, Stubbs N. Pressure relieving devices for treating heel pressure ulcers (protocol). Cochrane Database Syst Rev 2003;4. [Context Link]

30. Kinoshita H, Francis PR, Murase T, et al. The mechanical properties of the heel pad in elderly adults. Eur J Appl Physiol 1996;73:404-9. [Context Link]

31. Vogt MT, Wolfson SK, Kuller LH. Lower extremity arterial disease and the aging process: a review. J Clin Epidemiol 1992;45:529-42. [Context Link]

32. Kannell WB, Shurtleff D. The Framingham Study. Cigarettes and the development of intermittent claudication. Geriatrics 1973;28:61-8. [Context Link]

33. Armstrong DG, Lavery LA. Diabetic foot ulcers: prevention, diagnosis and classification. Am Fam Physician 1998;57:1325-32, 1337-8. [Context Link]

34. LoGerfo FW, Coffman JD. Current concepts. Vascular and microvascular disease of the foot in diabetes. Implications for foot care. N Engl J Med 1984;311:1615-9. [Context Link]

35. De Laat E, Schoonhoven L, Pickkers P, Verbeek AL, Achterberg T. Implementation of a new policy results in a decrease of pressure ulcer frequency. Int J for Quality Health Care Advances 2006;18:107-11. [Context Link]

36. Agency for Health Care Policy and Research. Pressure ulcers in adults: prediction and prevention. Clinical practice guideline no. 3. AHCPR, Public Health Service, US Department of Health and Human Services. Rockville, MD: US Department of Health and Human Services; 1992. [Context Link]

37. Dinsdale SM. Decubitus ulcers: role of pressure and friction in causation. Arch Phys Med Rehabil 1974;55:147-52. [Context Link]

38. Agency for Health Care Policy and Research. Treatment of pressure ulcers. Clinical practice guideline no. 15. AHCPR, Public Health Service, US Department of Health and Human Services. Rockville, MD: US Department of Health and Human Services; 1994. [Context Link]

39. Wound, Ostomy and Continence Nurses Society. Guideline for prevention and management of pressure ulcers. Glenview, IL: WOCN; 2003. [Context Link]

40. Black J. Preventing heel pressure ulcers. Nursing 2004;34:17. [Context Link]

41. Beckrich K, Aronovitch SA. Hospital-acquired pressure ulcers: a comparison of costs in medical vs. surgical patients. Nurs Econ 1999;17:263-71. [Context Link]

42. Stotts NA, Deosaransingh K, Roll FJ, et al. Underutilization of pressure ulcer risk in hip fracture patients. Adv Wound Care 1998;11:32-8. [Context Link]

43. Duncan C, Mataya J. Prevention of heel ulcers among hip fracture patients. Poster presented at the Clinical Symposium on Skin & Wound Care; Denver, CO, September 30-October 4, 1999. [Context Link]

44. Reuler JB, Cooney TG. The pressure sore: pathophysiology and principles of management. Ann Intern Med 1981;94:661-6. [Context Link]

45. Waltman N, Bergstrom N, Armstrong N, et al. Nutritional status, pressure sores and mortality in elderly patients with cancer. Oncol Nurs Forum 1991;18:867-73. [Context Link]

46. Burdette-Taylor SR, Kass J. Heel ulcers in critical care units: a major pressure problem. Crit Care Nurse Q 2002;25:41-53. [Context Link]

47. Krueger RA. Pressure relieving support surfaces: A randomized evaluation. Poster presented at the 9th European Pressure Ulcer Advisory Panel Conference; August 31 to September 2, 2006; Berlin, Germany. [Context Link]

48. Mannari RJ, Wyatt PG, Ochs DE, et al. Successful treatment of recalcitrant diabetic heel ulcers with topical becaplermin gel. Wounds 2002;14:116-21. [Context Link]

49. Kannell WB, McGee DL. Diabetes and glucose tolerance as risk factors for cardiovascular disease: the Framingham study. Diabetes Care 1979;2:120-6. [Context Link]

50. McNeeley MJ, Boyko EJ, Ahroni JH, et al. The independent contributions of diabetic neuropathy and vasculopathy in foot ulceration. How great are the risks? Diabetes Care 1995;18:216-9. [Context Link]

51. Armstrong DG, Lavery LA, Harkless LB. Validation of a diabetic wound classification system: the contribution of depth, infection, and ischemia to risk of amputation. Diabetes Care 1998;21:855-9. [Context Link]

52. Sussman C, Bates-Jensen B. Wound Care: A Collaborative Practice Manual for Health Professionals. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007. [Context Link]

53. Ryan TJ. The epidermis and its blood supply in venous disorders of the leg. Trans St Johns Hosp Dermatol Soc 1969;55:51-63. [Context Link]

54. Garber SL, Biddle AK, Click CN, et al. Pressure ulcer prevention and treatment following spinal cord injury: a clinical practice guideline for health-care professionals. J Spinal Cord Med 2001;24:S40-101. [Context Link]

55. Walsh J, DeOcampo M, Waggoner D. Keeping heels intact: evaluation of a protocol for prevention of facility-acquired heel pressure ulcers. Poster presented at the Symposium for Advanced Wound Care; April 2006; San Antonio, TX. [Context Link]

56. Shah JL. Postoperative pressure sores after epidural anesthesia. BMJ 2000;321:941-2. [Context Link]

57. Alexander R. Pressure sore following low-dose epidural infusion. Anaesthesia 2000;55:709-10. [Context Link]

58. Smet IG, Vercauteren MP, DeJongh RF, et al. Pressure sores as a patient-controlled epidural analgesia after cesarean delivery. Reg Anesth 1996;21:338-41. [Context Link]

59. Pither CE, Hartrick CJ, Raj PP. Heel sores in association with prolonged epidural analgesia. Anesthesiology 1985;63:459. [Context Link]

60. Punt CD, van Neer PAFA, de Lange S. Pressure sores as a possible complication of epidural analgesia. Anesth Analg 1991;73:657-9. [Context Link]

61. Silverwood B. Prevention of sore heels: evidence and outcomes. Paediatr Nurs 2004;16:14-8. [Context Link]

62. NPUAP. Pressure Ulcer Definition and Stages. Washington, DC: NPUAP; 2007. [Context Link]

63. Black J, Black S. Deep tissue injury. Wounds 2003;15:380. [Context Link]

64. Black J, Baharestani M, Cuddigan J, et al. National Pressure Ulcer Advisory Panel's updated pressure ulcer staging system. Adv Skin Wound Care 2007;20:269-74. [Context Link]

65. Farid KJ. Applying observations from forensic science to understanding the development of pressure ulcers. Ostomy Wound Manage 2007;53(4):26-44. [Context Link]

66. 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;7:23-4, 26, 28. [Context Link]

67. Nola GT, Vistnes LM. Differential response of skin and muscle in the experimental production of pressure sores. Plast Reconstr Surg 1980;6:728-33. [Context Link]

68. Baumann DS, McGraw D, Rubin B. An institutional experience with arterial atheroembolism. Ann Vasc Surg 1994;8:258-65. [Context Link]

69. Blaisdell FW, Steele M, Allen RE. Management of acute lower extremity arterial ischemia due to embolism and thrombosis. Surgery 1978;84:822-34. [Context Link]

70. Chakrabarty A, Phillips TJ. What is the diagnosis? Critical leg ischemia. Wounds 2003;15:167-72. [Context Link]

71. Chauvapun JR, Dryjski M. Distal peripheral microembolism. Vascular 2005;13:50-7. [Context Link]

72. Mayo RR, Swartz RD. Redefining the incidence of clinically detectable atheroembolism. Am J Med 1996;100:524-9. [Context Link]

73. Henssge C, Knight B, Krompecher T, et al. The Estimation of the Time of Death in the Early Postmortem Period. Boston, MA: Edward Arnold; 1995:219. [Context Link]

74. Sauko P, Knight B. Knight's Forensic Pathology. 3rd ed. London: Arnold Press; 2004. [Context Link]

75. Preventing heel pressure ulcers in immobilized patients. Adv Skin Wound Care 2005;18:22. [Context Link]

76. Black J. Treating heel pressure ulcers. Nursing 2005;35:68. [Context Link]

77. Bots TC, Apotheker BF. The prevention of heel pressure ulcers using a hydropolymer dressing in surgical patients. J Wound Care October 2004;13:375-8. [Context Link]

78. Torra i Bou JE, Rueda Lopez J, Camanes G, et al. Heel pressure ulcers. Comparative study between heel protective bandage and hydrocellular dressing with special form for the heel. Rev Enferm 2002;25:50-6. [Context Link]

79. Tymec AC, Pieper B, Vollman K. A comparison of two pressure-relieving devices on the prevention of heel pressure ulcers. Adv Wound Care 1997;10:34-44. [Context Link]

80. Gilcreast DM, Warren JB, Yoder LH, et al. Research comparing three heel ulcer-prevention devices. J Wound Ostomy Continence Nurs 2005;32:112-20. [Context Link]

81. Blaszczyk J, Majewski M, Sato F. Make a difference: standardize your heel care practice. Ostomy Wound Manage 1998;44:32-40. [Context Link]

82. Brem H, Lyder C. Protocol for the successful treatment of pressure ulcers. Am J Surg 2004;188:9-17. [Context Link]

83. Ayello EA. Pressure ulcers on the heels. Presented at the Pressure Ulcer Best Practices; November 3, 2006; University of Nebraska Medical Center. [Context Link]

84. De Keyser G, Dejaeger E, De Meyst H, et al. Pressure-reducing effects of heel protectors. Adv Wound Care 1994;7:30-2. [Context Link]

85. Schoonhoven L, Verbeek AL, Deuth T, et al. Guideline implementation results in a decrease of pressure ulcer incidence in critically ill patients. Presented at the 9th EPUAP Open Meeting; August 31 to September 2, 2006; Berlin, Germany. [Context Link]

86. Defloor T, DeBacquer D, Grypdonck MH. The effect of various combinations of turning and pressure reducing devices on the incidence of pressure ulcers. Int J Nurs Stud 2005;42:37-46. [Context Link]

87. Posthauer ME. What is the role of vitamins in wound healing? Adv Wound Care 2007;20:260, 263-4. [Context Link]

88. ter Riet G, Kessels AG, Knipschild PG. Randomized clinical trial of ascorbic acid in the treatment of pressure ulcers. J Clin Epidemiol 1995;48:1453-60. [Context Link]

89. Whittington KT, Briones R. National prevalence and incidence study: 6-year sequential acute care data. Adv Skin Wound Care 2004;17:490-4. [Context Link]

90. Young ZF, Evans A, Davis J. Nosocomial pressure ulcer prevention: a successful project. J Nurs Admin 2003;33:380-3. [Context Link]