Chronic Wounds: Palliative Management for the Frail Population—PART II

Author(s): 
Oscar M. Alvarez, PhD;1 Marge Meehan, RN, MIM;2 William Ennis, DO;3 David R. Thomas, MD, FACP;4 Frank D. Ferris, MD;5 Karen Lou Kennedy, RN, CS, FNP;6 Roisin Rogers, RN, MSN, CWCN;7 Marianne Bradley, RN, MS, CWOCN;8 Judith J. Baker, PhD;9 Adolfo Fernandez-Obregon, MD;10 George Rodeheaver, PhD;11

Chronic Wounds in the Frail Population

This section will review specific wounds most often seen among frail elderly that may have gradually become recalcitrant and nonresponsive to treatment regimes.

Pressure ulcers. Definition. Of all the chronic wound categories included in this document, pressure ulcers have the least satisfactory definition, which may account for the broad application of this term to ulcers having different etiologic factors. The definition of a pressure ulcer, according to the Pressure Ulcers in Adults: Prediction and Prevention is “…any lesion caused by unrelieved pressure resulting in damage of underlying tissue.”21 These ulcers usually occur over bony prominences and are classified based on depth of penetration through soft tissue layers to bone. Pressure ulcers are virtually the only type of wound that are solely attributed to external forces: pressure, shear, friction, and maceration.

Assessment. The presence of a pressure ulcer on a frail elderly person demands a comprehensive assessment of the entire patient to determine what factors and underlying diseases may have contributed to that ulcer’s occurrence. Pressure ulcers, theoretically, should always be considered healable, since external forces can generally be controlled. However, pressure ulcers among the frail population present some unique challenges.

The relationship between frailty and pressure ulcers is linked by significant commonalities in the core definition of frailty and key etiologic influences for pressure ulcers. Impaired mobility and abnormal nutrition form the cornerstone that defines frailty. Not surprisingly, these same factors are associated with the development of pressure ulcers.

Physical appearance. Pressure ulcers have a wide range of shapes and depth but can generally be confined to breakdown observed over bony prominences that have been exposed to some degree of pressure and probably other physical forces. The wound’s edges and its shape provide clues as to the influencing factors that initiated the skin breakdown. An oblong wound with a pocket of undermined tissue is most likely caused by a combination of pressure and shearing forces. This type of pressure ulcer is found most commonly over the sacral and ischial prominences. Wounds that form from blisters, with immune system or chemical irritant etiologies ruled out, are most likely caused by pressure and friction forces. Pressure ulcers that present with only a small opening to the skin and may drain foul smelling exudates are referred to as closed ulcers. These ulcers are formed through exposure to excessive pressure that has damaged the deep soft tissue before the epidermal layer. Another common pressure ulcer is one that is completely covered with eschar, often found on the heel. It is important to rule out other etiologic influences, such as peripheral vascular disease, before making the determination a wound is solely caused by pressure.

The wound bed of a pressure ulcer is also subject to a wide range of appearances. Exposure to excessive amounts of moisture and chemical irritation, such urine and/or fecal matter, will cause a pressure ulcer’s wound bed to become heavily contaminated while also weakening the surrounding intact skin.

Comorbidities. The occurrence of pressure ulcers is often accompanied by underlying medical conditions that predispose a patient to this type of ulcer. Clinical conditions that are the primary risk factors for developing pressure ulcers include continuous urinary incontinence or chronic voiding dysfunction, chronic bowel incontinence, paraplegia, quadriplegia, sepsis, and the illnesses and conditions listed above under Nonhealing Chronic Wounds.

Disease management treatments that contribute to pressure ulcer risk include steroid therapy, radiation therapy, chemotherapy, renal dialysis, and head elevation the majority of the day.

References: 

References
1. American Association of Homes & Services for the Aging. http://www.aahsa.org/public/agingbkg.htm#graying. Accessed November 13, 2001.
2. Lazarus GS, Cooper DM, Knighton DR, et al. Definitions and guidelines for assessment of wounds and evaluation of healing. Arch Dermatol 1994;130:489–93.
3. Stadelmann, Wayne K, Diigenis J, et al. Impediment to wound healing. Am J Surg 1998;176;395–475.
4. Ferrell BA, Osterweil D, Christenson P. A randomized trial of low-air-loss beds for treatment of pressure ulcers. J Am Med Assoc 1993;269:494–7.
5. Colburn L. Prevention of chronic wounds. In: Krasner D, Kane D (eds). Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, Second Edition. Wayne, PA: Health Management Publications, Inc., 1997:9–15.
6. Panel for the Prediction and Prevention of Pressure Ulcers in Adults. Pressure Ulcers in Adults: Prediction and Prevention. Clinical Practice Guideline Number 3. AHCPR Publications No. 92-0047. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services, 1994;18.
7. San Marum RJ, Ooms ME, Ribbe MW, van Eijk JT. The Dutch pressure sore assessment score or the Norton scale for identifying at-risk nursing home patients? Age & Ageing 2000;29:63–8.
8. Hagisawa S, Barbenel J. The limits of pressure sore prevention. J Roy Soc Med 1999; 92:576–8.
9. Bergstrom NI. Strategies for preventing pressure ulcers. Clin Geriatr Med 1997;3:437–54.
10. Cullum N, Dickson R, Eastwood A. The prevention and treatment of pressure sores. Nursing Standard 1996;10:32–3.
11. Carlson EV, Kemp MG, Shott S. Predicting the risk of pressure ulcers in critically ill patients. Am J Crit Care 1999;8:262–9.
12. Gunningberg L, Lindholm C, Carlsson M, Sjoden PO. Implementation of risk assessment and classification of pressure ulcers as quality indicators for patients with hip fractures. J Clin Nurs 1999;8:396–406.
13. Al Qattan MM, Bowen R. Effect of pre-existing health conditions on the results of reconstructive microvascular surgery. Microsurgery 1993;14:152–7.
14. Goldberg NH. Outcomes in surgical intervention. Adv Wound Care 1995; 8:69–70.
15. Table: Life Expectancy for total population: United States, 1997. Centers for Disease Control & Prevention. National Center for Health Statistics. National Vital Statistics Report. 1997;47(28). December 13, 1999.
16. Walson J, Fried LP. Frailty and the older man. Med Clinic N Amer 1999;83:1173–94.
17. Chin A, Paw MJ, Dekker JM, Feskens EJ. How to select a frail elderly population: A comparison of three working definitions. J Clin Epidemiol 1999;52:1015–21.
18. Gealey SG. Quantification of the term frail as applied to the elderly client. J Am Acad Nurse Pract 1997;9:505–10.
19. Carlson JE, Zocchi KA, Bettencourt DM, et al. Measuring frailty in the hospitalized elderly: Concept of functional homeostasis. Am J Phys Med Rehab 1998;77:252–7.
20. Lynn J, Teno JM, Phillips RS, et al. Perception by family members of the dying experience in older and seriously ill patients (Modules 2, 4, 10). The Study to Understand Prognoses and Perferences for Outcomes and Risks for Treatment (SUPPORT). Ann Intern Med 1997;126:97–106
21. Agency of Health Care Policy Research. Treatment of Pressure Ulcers. Clinical Practice Guideline Number 15. AHCPR Publication No. 95-0652. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human ServicesDecember, 1994;12.
22. Browse NL, Burnand KG. The cause of venous ulceration. Lancet 1983;2;243–5.
23. Coleridge-Smith PD, Thomas P, et al. Causes of venous ulceration: A new hypothesis. Br Med J 1988;296;21726–8.
24. Lubisch K. Wound care: Management of peripheral vascular disease and pressure ulcers (course offering). Wild Iris Medical Education. Available at: www.nursingceu.com. Access date: October 1, 2002.
25. Burton CS. Management of chronic and problem lower extremity wounds. Derm Clin 1993;11(4):767–73.
26. Baker SR. Epidemiology of chronic venous ulcers. Br J Surg 199;78:864–7.
27. Gay J. On varicose diseases of the lower extremities. The Lettsomian Lectures of 1867. London: Churchill Livinstone, 1949.
28. Homans J. The etiology and treatment of vericose ulcer of the leg. Surg Gynecol Obstet 1917;24:300–11.
29. Bjordal R. Flow and pressure studies in venous insufficiency. Acta Chir Scand 1988;544(Suppl):30–3.
30. McEnroe CS.Correlation of clinical findings with venous hemodynamics in 386 patients with chronic venous insufficiency. Am J Surg 1988;156:148–52.
31. Summer DS. Applied physiology in venous problems. In: Bergan JJ (ed). Surgery of the Veins. Philadelphia, PA:Grune & Stratton,1985;3–23.
32. Phillips TJ, Dover JS. Leg ulcers. J Am Acad Derm 1991;25;965–87.
33. Falanga V. Venous ulceration. J Dermatol Surg Oncol 1993;19:764–71.
34. Rubano M, Kerstein M. Arterial insufficiency and vasculitides. J WOCN 1998;25:147–57.
35. TransAtlantic Inter-Society Consensus (TASC). Management of peripheral arterial disease. J Vasc Surg 2000; 31(1):1–96.
36. Altemose G, Weiner D. Control of risk factors in peripheral vascular disease: Management of hypertension. Surg Clin North Am 1998;78(3):69.
37. Cooke J, Ma A. Medical therapy of peripheral arterial occlusive disease. Surg Clin North Am 1995;75(4):569.
38. Holloway GA. Arterial ulcers: Assessment, classification and management. In: Krasner D, Kane D (eds). Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, Second Edition. Wayne, PA: Health Management Publications, Inc., 1997:158–64.
39. Vandenberghe NJ. Duplex scan assessment of arterial occlusive disease. J Vasc Technol 1994;18:287–93.
40. Burnham CB. Segmental pressures and doppler velocity waveforms in the evaluation of peripheral arterial occlusive disease. J Vasc Technol 1994;18:249–55.
41. Gathan V. The noninvasive vascular laboratory. Surg Clin North Am 1998;78:508–18.
42. Ligush J, Reavis SW, Preisser JS, Hansen KJ. Duplex ultrasound scanning defines operative strategies for patients with limb-threatening ischemia. J Vasc Surg 1998;28:482–91.
43. Rooke TW. The use of transcutaneous oximetry in the noninvasive vascular laboratory. Int Angiol 1992;11(1):36–40.
44. McMahon JH, Grigg MJ. Predicting healing of lower limb ulcers. Aust NZJ Surg 1995; 65(3):173–6.
45. Bunt TJ, Holloway GA. TcpO2 as an accurate predictor of therapy in limb salvage. Ann Vasc Surg 1996;10(3):224–7.
46. Zink M, Rousseau P, Holloway GA. Lower-extremity ulcers. In: Bryant R (ed). Acute and Chronic Wounds: Nursing Management. St. Louis, MO:Mosby-Year Book, 1992;164–204.
47. Holloway GA. Arterial ulcers: Assessment, classification and management. In: Krasner D, Kane D (eds). Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, Second Edition. Wayne, Pa: Health Management Publications, Inc., 1997:158–64.
48. Steed DL. Diabetic wounds: Assessments, classification, and management. In: Krasner D, Kane D (eds). Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, Second Edition. Wayne, Pa: Health Management Publications, Inc., 1997:171–8
49. Boulton AJM. The diabetic foot: Neuropathic in etiology? (Lawrence Lecture). Diabetic Med 1990;7:852–8.
50. Eagleton WH, Falanga V. Chronic wounds. Surg Clin North Am 1997;77(3):689–700.
51. Young MJ, Breddy J, Veves A, Boulton AJM. The prediction of diabetic neuropathic foot ulceration using vibration perception thresholds. Diab Care 1994;17:5557–60.
52. Cavanagh PR, Ulbrecht JS, Caputo GM. The non-healing diabetic foot wound fact or fiction? Ost/Wound Manag 1998; 44 (3 Suppl): 6S–12S.
53. Levin ME. Prevention and treatment of the diabetic foot. J WOCN 1998;25(3):129–46.
54. McCulloch JM. Management of ulceration caused by sensory loss. Wound Management: Methods and Products 1997;1:20–7.
55. Grunfeld C. Diabetic foot ulcers: Etiology, treatment and prevention. Adv Intern Med 1991;37:103–32.
56. Education for Physicians on End-of-Life Care (EPEC), Module 2. EPEC Project. Princeton, NJ: Robert Wood Johnson Foundation, 1999;2–7.
57. Levin ME. Preventing amputation in the patient with diabetes. Diabetes Care 1995;(18)10:1383–94
58. Steed DL. Foundations of good ulcer care. Am J Surg 1998;176 (suppl 2A):20S-25S.
59. O’Neal LW. Debridement and amputation. In: Levin ME, O’Neal LW (eds). The Diabetic Foot, Fourth Edition. St. Louis, MO:Mosby-Year Book, Inc., 1988.
60. Steed DL, Donohue D, Webster MW, et al. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. J Am Coll Surg 1996;183:61–4.
61. Rodeheaver G, Baharestani M, Brabec M, et al. Wound healing and management: focus on debridement. Adv Wound Care 1994;7(1):22–36.
62. Witkowski JA, Parish LE. Debridement of cutaneous ulcers: Medical and surgical aspects. Clin Derm 1992;9:585–91.
63. Robson MC, Stenberg BD, Heggers JP. Wound healing alternations caused by infection. Clin Plast Surg 1990;19:485–92.
64. Burden C. Venous ulceration. Clinical Materials 1991;8:203.
65. Friedman ST, Su WPD. Management of leg ulcers with hydrocolloid occlusive dressing. Arch Dermatol 1984;120:1329–36.
66. Hurley JP. Chronic venous insufficiency: Venous ulcers and other consequences. In: Krasner D (ed). Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. King of Prussia, PA: Health Management Publications, Inc., 1990:213-22.
67. Lawrence W. Thomas MD. Clinical Management of Nonhealing Wounds in Wound Healing: Pro Chemical and Clinical Aspects. Philadelphia, PA: W.B. Saunders Company, 1992;541–61.
68. Plewa MC. Altered host response and special infections in the elderly. Emerg Med Clin North Am 1990;8(2):193–206.
69. Rodeheaver G. Wound cleansing, wound irrigation, wound disinfection. In: Krasner D, Kane D (eds). Chronic Wound Care: A Clinical Source Book for Healthcare Professionals, Second Edition. Wayne, PA: Health Management Publications, Inc., 1997;209–18.
70. Robson MC. Wound Infection: A failure of wound healing caused by an imbalance or bacteria. Surg Clin North Am 1997;77(3):637–50.
71. Robson MC, Shenberg BD, Hegger J. Wound healing alterations caused by infection. Clin Plast Surg 1990;17(3):485–92.
72. Levine NS, Lindberg RB, Mason AD, Pruitt BA. The quantitative swab culture and smear: A quick simple method for determining the number of viable aerobic bacteria in open wounds. J Trauma 1976;16(2):89–94.
73. Miller M. The role of infection in wound healing. Nurse Prescrib 1996;4:33–5.
74. Cutting KF, Harding KG. Criteria for identifying wound infection. J Wound Care 1994;3(4):198–201.
75. Bowler PG, Davies BJ, Jones SA. Microbial involvement in chronic wound malodour. J Wound Care 1999;8(5):216–8.
76. Wilson APR, Weavill C, Burridge J, Kelsey MC. The use of the wound scoring method ASEPSIS in postoperative wound surveillance. J Hosp Inf 1990;16:297–309.
77. Lipsky BA, Pecoraro RE, Ahroni JH. Foot ulceration and infections in elderly diabetics. Clin Geriatr Med 1990;6(4):747–69.
78. Wheat LJ, Allen SD, Henry M. Diabetic foot infections: Bacteriologic analysis. Arch Intern Med 1990;146:1935–40.
79. Harding KG. Wound care: Putting theory into practice. Wounds 1990;2(1):21–32.
80. Edelson RL, Fink JM. The immunologic function of skin. Scientific Am 1985;252(6):46–53.
81. Horan MA, Ashcroft GS. Ageing, defense mechanisms, and the immune system. Age and Ageing 1997;26(S4):15–9.
82. Miles AA, Miles EM, Burke J. The value and duration of defense reactions of the skin to the primary lodgment of bacteria. Br J Exp Pathol 1957;38:79–96.
83. Thornton FJ, Schaffer MR, Barbul A. Wound healing in sepsis and trauma. Shock 1997;8(6):391–401.
84. Grayson ML, Gibbons GW, Balogh K, et al. Probing to bone in infected pedal ulcers: A clinical sign of underlying osteomyelitis in diabetic patients. J Am Med Assoc 1995;273:721–8.
85. Lewis VL, Bailey MH, Paulowski G, et al. The diagnosis of osteomyelitis in caontact with pressure sores. Plast Reconstr Surg 1988;81:229.
86. Lipsky BA. Evidence-based antibiotic therapy of diabetic foot infections. FEMS Immunol Med Microbiol 1999;26(3-4):267–76.
87. Alexander L, Spungen M, Liu M, et al. Resting metabolic rate in subjects with paraplagia: The effect of pressure sores. Arch Phys Med Rehab 1995;76:819–22.
88. Krasner D. The chronic wound pain experience: A conceptual model. Ost Wound Manag 1995;41:20–5.
89. Rook JL. Wound care pain management. Adv Wound Care 1997;22(3):122–35.
90. Stadelmann WK, Diigenis AG. Impediment to wound healing. Am J Surg 1998;176:395–475.
91. BoyntonPR, Jarworski D, Paustran C. Meeting the challenges of healing chronic wounds in older adults. Nurs Clin North Am 1999;34(4):921–32.
92. Palmer MH. Urinary Continence. Gaithersburg, MD: Aspen Publishers, 1996.
93. Chassagne P, Landrin I, Neveu C, et al. Fecal incontinence in the institutionalized elderly: Incidence, risk factors, and prognosis. Am J Med 1999;106(2):185–90.
94. Doughty DB (ed). Urinary and Fecal Incontinence. St. Louis, MO: Mosby Year Book, Inc., 1991;179.
95. Marks J, Hughes LE, Harding KG, et al. Prediction of healing time as an aid to the management of open granulating wounds. World J Surg 1983;7:641–5.
96. Kramer JD, Kearney M. Patient, wound, and treatment characteristics associated with healing in pressure ulcers. Adv Skin Wound Care 2000;13 (1):17–24.
97. Berlowitz DR, Wilking SVB. The short-term outcome of pressure sores. J Am Ger Soc 1990;38:748–52.
98. FDA Guidance for Industry. Chronic Cutaneous Ulcer and Burn Wounds: Developing Products for Treatment. U.S. Department of Health and Human Services. FDA Center for Biologics Evaluation and Research; Center for Devices and Radiologic Health; Center for Drug Evaluation and Research. June 2000. Section II Claims, A. General Considerations.



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