Skip Navigation LinksHome > August 2011 - Volume 24 - Issue 8 > Heel Pressure Ulcers: Purple Heel and Deep Tissue Injury
Advances in Skin & Wound Care:
doi: 10.1097/01.ASW.0000403250.85131.b9
Features: Clinical Management Extra

Heel Pressure Ulcers: Purple Heel and Deep Tissue Injury

Salcido, Richard MD; Lee, Augustine MD; Ahn, Chulhyun MD, MS

Free Access
Continued Education
Article Outline
Collapse Box

Author Information

Richard Salcido, MD • Editor-in-Chief of Advances in Skin & Wound Care and the Course Director for the Annual Clinical Symposium on Advances in Skin & Wound Care • William Erdman Professor, Department of Rehabilitation Medicine • Senior Fellow, Institute on Aging; and Associate, Institute of Medicine and Bioengineering • University of Pennsylvania Health System, Philadelphia, Pennsylvania

Augustine Lee, MD • Research Fellow • Hospital of the University of Pennsylvania • Philadelphia, Pennsylvania

Chulhyun Ahn, MD, MS • Resident Physician • Department of Physical Medicine and Rehabilitation • Hospital of the University of Pennsylvania • Philadelphia, Pennsylvania

All authors and staff in a position to control the content of this CME activity and their spouses/life partners (if any) have disclosed that they have no financial relationships with, or financial interests in, any commercial organizations pertaining to this educational activity.

To earn CME credit, you must read the CME article and complete the quiz and evaluation on the enclosed answer form, answering at least 13 of the 18 questions correctly.

This continuing educational activity will expire for physicians on August 31, 2012.

Collapse Box

Abstract

PURPOSE: To enhance the learner's competence with information about heel pressure ulcers.

TARGET AUDIENCE: This continuing education activity is intended for physicians and nurses with an interest in skin and wound care.

OBJECTIVES: After participating in this educational activity, the participant should be better able to:

1. Interpret factors contributing to potential pressure ulcers (PrUs).

2. Apply knowledge gained on risk factors, prevention and treatment of heel PrUs, suspected deep tissue injuries, and "purple heel" to patient care scenarios.

ABSTRACT: The heel is a frequent site of pressure ulcer formation, in particular, the development of suspected deep tissue injury. This article reviews the epidemiology, pathophysiology and prevention of heel pressure ulcers. Also, the related concept of purple heel, a not-well-recognized entity, is introduced.

Back to Top | Article Outline

INTRODUCTION

The heel of the foot is of primary importance in human biomechanics. It bears a significant portion of human body weight in the standing position and allows for human locomotion through the transmittal of ground forces to the skeletal system while absorbing shock, pressure, and shear. The heel also is the initial shock absorber during the gait cycle in the "heel strike" and early phase of the stance stage of the gait cycle in human locomotion. The anatomical nomenclature for the heel is calcaneus, which literally means "hard rock." The biomechanical and kinesiologic determinants of the heel are compromised during prolonged bed rest, especially if multiple comorbidities exist, which impedes the intrinsic neurovascular protective mechanisms. Most articles and discussions about the heel in the context of wounds simply classify the pathophysiologic and etiologic lesions as pressure ulcers (PrUs), and more recently, the clinical literature is focusing on the purple heel, that is, a sentinel of deep tissue injury (DTI).

A PrU, as defined by the National Pressure Ulcer Advisory Panel, is localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction.1 A number of contributing or confounding factors are also associated with PrUs; the significance of these factors is yet to be elucidated with scientific exactitude. Deep tissue injury is defined as a medical condition of a pressure-related injury to subcutaneous tissues under intact skin, as a result of prolonged compression of bony prominences on underlying soft tissues, particularly muscles.2 Pressure ulcers have imposed a concerning challenge to society, affecting both the quality of individual health and the economic resources of healthcare infrastructures.3 Underscoring their significance, PrUs were selected by the Centers for Medicare & Medicaid Services (CMS) as a condition subject to the Deficit Reduction Act provision requiring hospitals to report the secondary diagnoses that are present on admission of patients. This inclusion placed the responsibility of the cost of care for PrUs on the treatment facility unless the PrUs were present on admission.4 The CMS selected conditions that would become subject to this provision based on 3 criteria: (1) high cost or high volume or both, (2) a condition assigned to a higher diagnosis-related group when present as a secondary diagnosis, and, (3) a condition is reasonably preventable through application of evidence-based guidelines. This ruling emphasized the importance of identifying preexisting PrUs including suspected deep tissue injuries (sDTIs) with appropriate documentation, which allows for facilities to maintain treatment reimbursement for PrUs. The final common pathway for these initiatives is rooted in accountable care and, of course, better outcomes for patients.

By reading this article, clinicians will be better able to interpret the factors contributing to potential PrUs, design PrU prevention strategies, and differentiate between sDTIs and purple heel.

Back to Top | Article Outline

EPIDEMIOLOGY

Epidemiologic data suggest that heels are the second most common sites for PrUs after sacrum. Results of 9 international PrU prevalence surveys found that the prevalence of heel PrUs accounts for 23.7% of that of ulcers in acute care facilities, 22.5% of that in long-term acute-care facilities, and 22.9% of that in long-term-care facilities.5 The incidence of heel ulcers was 26.1% of that of PrUs in acute-care facilities, 23.6% of that in long-term acute-care facilities, and 24.5% of that in long-term-care facilities.

In the cases of suspected DTIs, the heel is the most common site of DTI development; DTIs found in the heels account for 41% of all DTIs, followed by those in the sacrum (19%) and buttocks (13%).6

In a recent study reporting the overall prevalence data and demographics of subjects with sDTIs from the International Pressure Ulcer Prevalence survey 2006-2009, the prevalence of sDTIs at the sacrum and coccyx, the buttocks, ischial tuberosities, and ankle and foot was found to be less than expected when compared with the prevalence of severe PrUs (Stages III and IV and unstageable) at the same anatomical distribution. However, the prevalence of sDTIs at the heel and elbow was conversely found to be greater than expected.6

Back to Top | Article Outline

PREVENTION

As a clinical axiom, skin color over the heel usually reflects the degree and extent of DTI. Red color heralds hyperemia and ischemia, purple color suggests infarction, and black color indicates tissue necrosis. In individuals with lightly pigmented skin, it is easy to observe the progression of skin color change; even in people with darkly pigmented skin, the plantar surface of the heel is comparatively devoid of melanin molecules, which enables monitoring of skin color change (Figures 1A and 1B).

Figure 1A
Figure 1A
Image Tools
Figure 1B
Figure 1B
Image Tools

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.

Back to Top | Article Outline

ANATOMY

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.

Figure 2
Figure 2
Image Tools

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.

Back to Top | Article Outline

PATHOPHYSIOLOGY

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:

Equation (Uncited)
Equation (Uncited)
Image Tools

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

Back to Top | Article Outline

PURPLE HEEL

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

Back to Top | Article Outline

SUMMARY

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.

Back to Top | Article Outline

Acknowledgment:

PRACTICE PEARLS...
PRACTICE PEARLS...
Image Tools

The authors express sincere gratitude to William Falone, MSN, RN, CWON, Wound and Ostomy Nurse Specialist, who provided the photographs in Figure 1.

Back to Top | Article Outline

REFERENCES

1. National Pressure Ulcer Advisory Panel. http://www.npuap.org/.

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.

30. Ruan C, Escobedo E, Harrison S, Goldstein B. Magnetic resonance imaging of nonhealing pressure ulcers and myocutaneous flaps. Arch Phys Med Rehabil 1998;79:1080-7.

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.

32. Heggers J, Haydon S, Ko F, Hayward P, Carp S, Robson M. Pseudomonas aeruginosa 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.

37. Plisko A, Gilchrest BA. Growth factor responsiveness of cultured human fibroblasts declines with age. J Gerontol 1983;38:513-8.

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.

39. Ryan TJ, Thoolen M, Yang YH. The effect of mechanical forces (vibration or external compression) on the dermal water content of the upper dermis and epidermis, assessed by high frequency ultrasound. J Tissue Viability 2001;11:97-101.

40. Salcido R. What is the "purple heel"? Adv Skin Wound Care 2006;19(1):11.

For more than 61 additional continuing education articles related to Skin and Wound Care topics, go to NursingCenter.com/CE.

Back to Top | Article Outline
CONTINUING MEDICAL EDUCATION INFORMATION FOR PHYSICIANS

Lippincott Continuing Medical Education Institute, Inc. is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Lippincott Continuing Medical Education Institute, Inc. designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Back to Top | Article Outline
PROVIDER ACCREDITATION INFORMATION FOR NURSES

Lippincott Williams & Wilkins, publisher of the Advances in Skin & Wound Care journal, will award 2.8 contact hours for this continuing nursing education activity.

LWW is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.

This activity is also provider approved by the California Board of Registered Nursing, Provider Number CEP 11749 for 2.8 contact hours. Lippincott Williams & Wilkins is also an approved provider of continuing nursing education by the District of Columbia and Florida #FBN2454.

Your certificate is valid in all states.

The ANCC's accreditation status of Lippincott Williams & Wilkins Department of Continuing Education refers only to its continuing nursing education activities and does not imply Commission on Accreditation approval or endorsement of any commercial product.

Back to Top | Article Outline
CONTINUING EDUCATION INSTRUCTIONS

* Read the article beginning on page 374.

* Take the test, recording your answers in the test answers section (Section B) of the CME enrollment form. Each question has only one correct answer.

* Complete registration information (Section A) and course evaluation (Section C).

* Mail completed test with registration fee to: Lippincott Williams & Wilkins, CE Group, 333 7th Avenue, 19th Floor, New York, NY 10001.

* Within 3 to 4 weeks after your CME enrollment form is received, you will be notified of your test results.

* If you pass, you will receive a certificate of earned contact hours and an answer key. Nurses who fail have the option of taking the test again at no additional cost. Only the first entry sent by physicians will be accepted for credit.

* A passing score for this test is 13 correct answers.

* Nurses: Need CE STAT? Visit http://www.nursingcenter.com for immediate results, other CME activities, and your personalized CME planner tool. No Internet access? Call 1-800-787-8985 for other rush service options.

* Questions? Contact Lippincott Williams & Wilkins: 1-800-787-8985.

Registration Deadline: August 31, 2013 (nurses); August 31, 2012 (physicians)

Back to Top | Article Outline
PAYMENT AND DISCOUNTS

* The registration fee for this test is $24.95 for nurses; $22 for physicians.

* Nurses: If you take two or more tests in any nursing journal published by LWW and send in your CE enrollment forms together by mail, you may deduct $0.95 from the price of each test. We offer special discounts for as few as six tests and institutional bulk discounts for multiple tests. Call 1-800-787-8985 for more information.

Keywords:

heel; pressure ulcer; purple heel; deep tissue injury

© 2011 Lippincott Williams & Wilkins, Inc.

Login

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.