Despite advances in health care that extend life and improve functional status, pressure ulcers continue to be a frequent accompaniment of chronic illness in elderly individuals. Pressure ulcers are characterized as a localized area of tissue necrosis that develops when tissue that overlies bony prominences is compressed between the bone and an external surface for a prolonged period of time. Exposure of the tissues to prolonged pressure in excess of capillary pressure inhibits circulation and limits normal exchange of oxygen and other substrates as well as waste products. If an inadequate level of circulation persists, cellular metabolism is disrupted and tissue injury and destruction ultimately occurs.
In response to injured tissue, the body initiates the repair process characterized by three phases of healing: inflammation, proliferation, and matrix formation and remodeling. During the initial inflammatory phase, platelets aggregate in the injured tissue and promote hemostasis. Neutrophils and polymorphonuclear leukocytes are attracted to the tissue to phagocytize bacteria and debris. The proliferation and matrix formation phase overlaps with inflammation and serves to deposit connective tissue and collagen that fills the wound and gives it strength. During collagen production, capillaries form as budlike structures from nearby vessels, creating a granular appearance on the wound surface, termed granulation tissue.
The final component of the proliferative phase is re-epithelialization, characterized by the creation of a protective epithelial covering over the wound surface. In wounds with minimal tissue loss, involving only epidermis and dermis, epithelial migration occurs concurrendy with collagen synthesis. When tissue destruction extends below the level of the dermis, epthelialization is delayed until a bed of granulation tissue is established. After epithelial cells cover the wound bed, weeping of body fluid and electrolytes ceases and the wound is viewed, from a clinical perspective, as a closed wound. However, in those wounds where the tissue destruction extends below the dermis, the remodeling phase of healing will continue to degrade and resynthesize collagen in the scar. The scar will decrease in bulk and gain tensile strength, achieving a maximum of 80% of normal tissue strength.
Aging affects all phases of wound healing. Compromised cellular activity leads to a delayed or decreased inflammatory response, reduced collagen synthesis and reduced quality of collagen, and slower epithelialization (Ashcroft, Horan, & Ferguson, 1998; Van de Kerhof, Van Berg, Spruijt, & Kuiper, 1994). Because the older adult population is especially vulnerable to impaired healing of injured tissue such as pressure ulcers, it is essential that health care providers institute interventions to provide the optimal systemic and localized topical support to maximize healing and eliminate correctable impediments. This article provides an overview of an evidencebased protocol (EBP) on treatment of pressure ulcers (Folkedahl, Frantz, & Goode, 2002b). The full text of the EBP is available from the Research Dissemination Core Office.
The purpose of the EBP is to treat pressure ulcers among elderly patients. The goal is to enhance the healing of pressure ulcers through the use of evidence-based interventions.
Definition of Pressure Ulcers
A pressure ulcer is any injury caused by unrelieved pressure that damages the skin and underlying tissue, usually over a bony prominence. Pressure ulcers are also called decubitus ulcers, bedsores, or pressure sores, and their severity ranges from reddening of the skin to severe, deep craters formed into the muscle and bone.
Classification of Pressure Ulcers
The severity and depth of tissue involvement of pressure ulcers have been classified according to stages. When making decisions related to pressure ulcer treatment, one must consider the level of tissue injury according to these stages. There are four stages, as defined by the Panel for the Prediction and Prevention of Pressure Ulcers in Adults, U.S. Department of Health and Human Services, Agency for Health Care Policy and Research (1992) guidelines.
* Stage 1: Non-blanchable erythema of intact skin, the heralding lesion of skin ulceration. In individuals with darker skin, discoloration of skin, warmth, edema, induration, or hardness may also be indicators. This definition was further refined by the National Pressure Ulcer Advisory Panel (NPUAP) (1998) to
A Stage I pressure ulcer is an observable pressure related alteration of intact skin whose indicators as compared to the adjacent or opposite area on the body may include changes in one or more of the following: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel), and sensation (pain, itching). The ulcer appears as a defined area of persistent redness in lightly pigmented skin, whereas in darker skin tones, the ulcer may appear with persistent red, blue, or purple hues.
* Stage 2: Partial thickness skin loss involving epidermis, dermis, or both (e.g., abrasion, blister, shallow crater).
* Stage 3: Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia (deep crater with or without undermining). The ulcer presents clinically as a deep crater with or without undermining adjacent tissue.
* Stage 4: Full thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (e.g., tendon or joint capsule).
INDIVIDUALS AT RISK FOR PRESSURE ULCERS
Those individuals with existing pressure ulcers may be susceptible to the development of additional ulcers. Therefore, all individuals admitted to a health care facility (i.e., hospital, nursing home, home care agency) with a pressure ulcer should be assessed for risk of developing additional pressure ulcers. This can be accomplished with use of a standardized risk assessment tool, such as the Braden Scale for Predicting Pressure Sore Risk (Bergstrom, Braden, Laguzza, & Holman, 1987). Composed of six subscales (i.e., sensory perception, activity, mobility, moisture, friction/shear, nutrition), the scale provides information on the patient's overall risk, as well as an indication of areas in which to focus interventions to prevent additional pressure ulcer development. (Further information on risk assessment is available in the EBP: Prevention of Pressure Ulcers by Folkedahl, Frantz, and Goode, 2002a).
ASSESSMENT OF PRESSURE ULCERS
A comprehensive assessment of the overall health status of patients and their pressure ulcers forms the basis for treatment decisions. A complete history and physical examination, combined with a detailed assessment of the characteristics of the ulcer, provides the essential information needed to target treatment interventions specific to the status of the wound. Factors to be included in a thorough assessment of the ulcer include:
* Location and stage of the ulcer size (i.e., length, width, depth).
* Type of tissue in the ulcer.
* Presence of tunneling, tracts, or undermining.
* Exudate characteristics.
* Presence of odor.
* Condition of the peri-wound skin.
Table 1 provides a guide for use in pressure ulcer assessment.
DESCRIPTION OF THE INTERVENTION
Interventions for the treatment of pressure ulcers are directed toward supporting the normal events of wound healing and preventing further injury to the tissue. Nursing interventions focus on removal of necrotic tissue and debris, provision of a moist wound environment, control of bacterial levels in the wound, supply of essential substrates for tissue repair, and management of tissue loads.
The presence of devitalized tissue in the wound provides a culture medium for the growth of bacteria (Dhingra, Schauerhamer, & Wangensteen, 1976). High levels of bacteria in pressure ulcers have been shown to delay healing (Robson & Heggers, 1969). Removal of necrotic tissue by some form of debridement method (e.g., sharp, mechanical, autolytic, enzymatic) will reduce the bacterial burden of pressure ulcers and promote healing. Autolytic and enzymatic debridement methods generally are specific to necrotic tissue and do not harm healthy tissue. Mechanical debridement with wet to dry gauze dressings is nonspecific and can harm healthy tissue and be painful. All three approaches are slow to debride the devitalized tissue. Sharp debridement is the most expethent at removing devitalized tissue, but does require specially trained personnel to perform (Bale & Harding, 1990; Bryant, 2000).
PRESSURE ULCERS ASSESSMENT GUIDE
PROCESS EVALUATION MONITOR
The progression of wound healing can be slowed by the presence of nonadherent foreign material such as exudates and metabolic wastes. Interventions to cleanse the wound bed of inflammatory material will facilitate optimal healing. Pressure ulcers should be cleansed at each dressing change using a noncytotoxic solution, such as normal saline. In those instances where the ulcer is more heavily laden with surface debris, a commercial wound cleanser may be used (Bryant, 2000; Foresman, Payne, Becker, Lewis, & Rodeheaver, 1993).
Care should be taken to avoid use of anticeptics (e.g., povidone iodine, iodophor, Dakin's solution, hydrogen peroxide, acetic acid) for wound cleansing, because these agents have been shown to be toxic to cells in the wound tissue (Lineaweaver et al., 1985). Cleansing should be performed in a manner that minimizes trauma to the tissue. Safe and effective removal of debris from the wound surface can be accomplished with irrigation devices that deliver fluid stream pressures ranging from 4 to 15 pounds per square inch (Rodeheaver, Pettry, Thacker, Edgerton, & Edlich, 1975; Stevenson, Thacker, Rodeheaver, Bacchetta, & Edgerton, 1976).
It is well established that a moist wound environment promotes reepithelialization and healing. Allowing a wound surface to dry out and form a scab will slow the healing process because epidermal cells must tunnel under the scab to reach a moist layer of tissue and migrate across the wound bed (Winter & Scales, 1963). Applying a dressing to the ulcer that maintains a continuously moist environment will retard scab formation and support re-epithelialization of the wound. Numerous moist dressings are available, including hydrocolloids, hydrogels, transparent films, alginates, foams, and saline-moistened gauze. Randomized trials comparing one type of moist dressing with another consistently showed no differences in pressure ulcer healing outcomes (Aim et al., 1989; Colwell, Foreman, & Trotter, 1992; Neill, Conforti, Kedas, & Burris, 1989; Oleske, Smith, White, Pottage, & Donavan, 1986; Xakellis & Chrischilles, 1992).
For pressure ulcers to heal, bacterial levels must be reduced to low levels. Heavy bacterial overgrowth or compromised host defenses can produce colony counts that are not compatible with wound healing. It has been shown that pressure ulcers with greater than 1,000,000 organisms per gram of tissue fail to heal even with optimum local wound management and pressure relief (Robson & Heggers, 1969). To minimize bacterial growth in pressure ulcers, effective cleansing and debridement is essential to remove the debris that encourage organism growth. Systemic antibiotics are indicated for controlling bacterial levels only in the presence of bacteremia, sepsis, advancing cellulites, or osteomelitis and are not required for signs of local infection (Lewis et al., 1988). Topical antibiotics may be initiated as an intervention when the ulcer continues to produce exudates and fails to progress toward closure following sustained debridement and cleansing to remove nonviable tissue (Bendy et al., 1964; Kucan, Robson, Heggers, & Ko, 1981). Use of routine swab cultures to determine the presence of a wound infection should be avoided because they detect only surface contaminants and not the level of bacteria in the wound tissue.
PRESSURE ULCERS MANAGEMENT MONITOR
Substrates essential for healing pressure ulcers include protein, calories, vitamins (e.g., A, B complex, C), and minerals (e.g., zinc). Unfortunately, the specific requirements of each nutrient needed to promote healing are yet to be established. However, it is generally agreed that nutritional support sufficient to put the patient in a positive nitrogen balance (approximately 30 to 35 calories/kg per day and 1 .25 to 1.50 grams of protein/kg per day) is a reasonable initial level of intervention for wound healing (Chernoff, Milton, & Lipschitz, 1991).
Along with interventions to promote wound healing, support of the repair process necessitates that pressure on the ulcer be eliminated. If possible, the patient with a pressure ulcer should be positioned to avoid any external force on the ulcer. When the ulcer is located in the sacral area, the patient should refrain from sitting until the wound has healed. Further information on interventions to manage tissue loads can be found in the EBP: Prevention of Pressure Ulcers (Folkedahl, Frantz, & Goode, 2002a).
EVALUATION OF PATIENT PROCESS FACTORS AND OUTCOMES
To evaluate the aptitude of health care providers to use this protocol, both process and outcome factors should be evaluated. Process indicators are those factors related to the preparedness of health care providers to use the protocol. One process factor is the knowledge of staff about pressure ulcer treatment. Following proper education on pressure ulcer treatment, care providers should be given a test, such as the five-item Treatment of Pressure Ulcers Knowledge Assessment Test, contained in the EBP on treatment of pressure ulcers. Incorrect answers on the test can be used as a guide for further education. A second process factor is the perceived preparedness of the health care provider to use the pressure ulcer treatment protocol. After care providers have used the treatment protocol for approximately 1 month, they are given the Process Evaluation Monitor to complete (Table 2). Those with higher scores on this monitor are well-prepared to implement the protocol, and understand its use and purpose. On the other hand, those who have relatively low scores are in need of more education or support in the protocol.
Outcome indicators are those factors expected to change or improve from consistent implementation of the protocol. The major outcome indicators that should be monitored over time are improvement or deterioration in the ulcer and presence or absence of new ulcers (Table 3). The Pressure Ulcer Scale for Healing (PUSH) Tool (NPUAP, 1998; available at www.npuap.org/push3-0.htm) provides an evidence-based method of monitoring changes in pressure ulcers over time and accurately differentiates a healing from a non-healing ulcer (Stotts et al., 2001) These outcomes should be assessed and recorded on a weekly basis.
Those who provide direct care to older adults with pressure ulcers play a significant role in ensuring the environment is optimal for wound healing. Use of the evidence-based guideline "Treatment of Pressure Ulcers" (Folkedahl, Frantz & Goode, 2002b) can provide a template for implementation of interventions to maximize the repair process.
- Key: R = Research, (L) = Literature, (N) = National Guidelines
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- Ashcroft, G.S., Horan, M.A., & Ferguson, M.W. (1998). Aging alters the inflammatory and endothelial cell adhesion molecule profiles during human cutaneous wound healing. Laboratory Investigation, 78(11), 47-58. (R)
- Bale, S., & Harding, K.D. (1990). Using modern dressings to effect debridement. Professional Nurse, 5(5), 244, 246, 248. (L)
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- Bergstrom, N., Braden, B.J., Laguzza, A., & Holman, V. (1987). The Braden Scale for predicting pressure sore risk. Nursing Research, 36(4), 205-210. (R)
- Bryant, R.A. (2000). Acute and chronic wounds; Nursing management (2nd ed.). St. Louis, MO: Mosby. (L)
- Chernoff, R., Milton, K., & Lipschitz, D. (1991). The effect of a very high-protein liquid formula (Replete) on decubitus ulcer healing in long-term tube-fed institutionalized patients [Abstract]. Journal of the American Dietetic Association, 90(9), A-130. (R)
- Colwell, J.C., Foreman, M.D., & Trotter, J.R (1992). A comparison of the efficacy and cost-effectiveness of two methods of managing pressure ulcers. Decubitus, 6(4), 2836.(R)
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- Folkedahl, B.A., Frantz, RA., & Goode, C. (2002a). Prevention of pressure ulcers evidence-based protocol. In M. Titler (Señes Ed.), Series on evidence-based practice for older adults (pp. 1-20). Iowa City, IA: The University of Iowa Gerontological Nursing Interventions Research Center, Research Dissemination Core. (R)
- Folkedahl, B.A., Frantz, RA., & Goode, C. (2002b). Treatment of pressure ulcers evidence-based protocol. In M. Titler (Series Ed), Series on evidence-based practice for older adults (pp. 1-30). Iowa City, IA: The University of Iowa Gerontological Nursing Interventions Research Center, Research Dissemination Core. (R)
- Foresman, P.A., Payne, D.S., Becker, D., Lewis, D., & Rodeheaver, G.T. (1993). A relative toxicity index for wound cleansers. Wounds, 5(5), 226-231. (R)
- Kucan, J.O., Robson, M.C., Heggers, J.P., & Ko, F. (1981). Comparison of silver sulfadiazine, povidone-iodine and physiologic saline in the treatment of chronic pressure ulcers. Journal of the American Geriatria Society, 29(5), 232-235. (R)
- Lewis, V.L., Jr., Bailey, M.H., Pulawski, G., Kind, G., Bashioum, RW., & Hendrix, RW. (1988). The diagnosis of osteomyelitis in patients with pressure sores. Plastic and Reconstructive Surgery, 8(2), 229-232. (R)
- Lineaweaver, W, Howard, R, Soucy, D., McMorris, S., Freeman, J., Crain, C, Robertson, J., & Romley, T. (1985). Topical antimicrovial toxity. Archives of Surgery, 120(3), 267-270. (R)
- National Pressure Ulcer Advisory Panel. (1998, February). NPUAP statement on Stage I assessment in darkly pigmented skin. Retrieved March 26, 2004, from www.npuap.org/positn4.htm (N)
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- Oleske, D.M., Smith, X.R, White, P., Pottage, J., & Donavan, M.I. (1986). A randomized clinical trial of two dressing methods for the treatment of low-grade pressure ulcers. Journal of Enterostomal Therapy, 13(3), 9098.(R)
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PRESSURE ULCERS ASSESSMENT GUIDE
PROCESS EVALUATION MONITOR
PRESSURE ULCERS MANAGEMENT MONITOR