Pressure Ulcers, Part Two: Management Strategies
The goal of this article is to facilitate the successful resolution of pressure ulcers. The nurse practitioner (NP) is an ideal health care professionalto manage pressue ulcer care. This article reviews the basic principles related to wound care. The healing trajectory is discussed to assist an NP to determine appropriate therapy. Current, research-based management strategies are provided.
Pressure ulcers cost society not only money, but also human lives. The annual cost for pressure ulcer care ranges from $5,000 to $40,000,and approximately 60,000 people a year die from pressure ulcers (Maklebust, 1987; Pinchocofsky-Devin & Kaminski, 1986). Pressure ulcers are a serious health concern to which nursing can make a positive contribution. Pressure ulcers were first documented by the Egyptians in the year 2000 B.C. (Shenaq & Dinh, 1990). However, they have not been Seriously studied until this century. During the past decade, a research revolution has occurred regarding pressure ulcer prevention and management. Yet, old, outdated practices are still frequently used. This article focuses on current treatment strategies for pressure ulcers that the nurse practitioner (NP) can use to manage care and to help educate other nurses.
THE ROLE OF THE NURSE PRACTITIONER The NP is an ideal health care professional to provide medical management for pressure ulcers. The NP can influence the healing process by prescribing appropriate therapy and implementing other measures to prevent extension of the wound. In addition, the NP can provide written management protocols that will enable nurses Address correspondence to Susan L. Sanders, MSN, GNP, RN, C, 2-H Durban Court, Baltimore, MD 21236.
VOLUME 4, NUMBER 3, JULY-SEPTEMBER, 1992
to act immediately on discovery of an ulcer. To generate a commitment for the prescribed management strategies and to ensure proper technique, the NP can provide education regarding appropriate treatment of pressure ulcers, including the logic behind techniques and protocols. All these servicescan be included in a pressure ulcer prevention and management program that is marketed by the NP. The NP could also serve as a consultant to physicians for clients who have pressure ulcers, particularly slowly resolving ulcers, and should make his or her availability known. Nursing staff will recommend an NP who has had success with pressure ulcer management to physicians and family members. Experienced enterostomal therapists (ETs) are considered the experts for pressure ulcer management; thus, the NP may want to consult an E T for ulcers that are difficult to heal or for current management techniques or both. In addition, a collaborative relationship could be developed with an ET where mutual referrals are given, information is shared, and research is conducted jointly. The NP should also seek out product representatives to learn about wound care products and to participate in clinical research of new products. An ET can assist the NP in locating area representatives. If an NP is going to manage pressure ulcers, professional journals that include current information and research studies related to prevention and management should be read, such as Ostomyl Wound Management, Journal of Enterostomal Therafiy, and Decubitus.
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PHYSIOLOGY OF WOUND HEALING
During the second or proliferative phase (24 hours to 22 days), three significant events occur: epithelialization, neovascularization, and collagen synthesis (Cooper, 1990; Wysocki, 1989). Epithelialization seals and protects the wound from insults. Neovascularization, also known as granulation, is the formation of new capillaries, which explains its beefy red color. Through neovascularization, oxygen and nutrients are provided to the wound. Collagen synthesis creates tensile strength and is the support matrix for the recovering wound (Bruno & Craven, 1982; Sieggreen, 1987; Wysocki, 1989). Thus, the function of this phase is to rebuild the wounded tissue. Epithelialization, which seals the wound from bacteria and fluid loss, begins within 24 hours (Sieggreen, 1987; Wysocki, 1989). Epithelial tissue is extremely fragile and, therefore, can easily be wiped or washed away. A moist environment fosters epithelialization, whereas crust or dryness slows the process (Carrico et al., 1984; Sieggreen, 1987). This microscopic epithelial layer is vital because i t enables the wound healing process to proceed in a “safe” environment; therefore, great efforts should be taken to protect this fragile tissue and to foster its growth. Fibroblasts, which are stimulated by AGF and the growth factor secreted by platelets, are necessary for collagen production (Cooper, 1990; Sieggreen, 1987). Collagen synthesis is also dependent on ascorbic acid (vitamin C), zinc, magnesium, and other amino acids (Bruno & Craven, 1982; Cooper, 1990; Sieggreen, 1987; Wysocki, 1989). Oxygen and iron are also necessary for collagen synthesis. In fact, the occurrence of infection is more frequent in ischemic wounds (Carrico et al., 1984; Sieggreen, 1987). The final, or maturation phase, also known as the differentiation or remodeling phase, usually begins after 21 days and can take as long as 2 years. Collagen deposits continue, which make the wound thicker and more compact, with the end result of increased tensile strength (Cooper, 1990; Wysocki, 1989; Sieggreen, 1987). However, the maximum tensile strength will only be 80%of the preinjury capacity (Cooper, 1990).The wound will also have a dark, scarlet-red color, eventually fading to a silvery white color (Sieggreen, 1987). Fifty percent of the original tensile strength is restored usually within 6 weeks (Wysocki, 1989).
A basic understanding of the scientific principles of healing are necessary to appropriately manage wound care. Fortunately, the pressure ulcer research revolution has created scientific data to support wound care decisions. An overview of the wound-healing process follows. There are three major phases of wound healing: inflammatory, proliferative, and maturation. The inflammatory phase (4-5 days) is characterized by redness, heat, pain, and swelling, which in turn initiates the healing process (Sieggreen, 1987; Wysocki, 1989). The function of the inflammatory phase is to prevent further injury and blood loss. This is accomplished through coagulation and mobilization of the immune system (Cooper, 1990; Sieggreen, 1987; Wysocki, 1989). Initially, platelets line the vessel walls and release a growth factor that fosters tissue regeneration. Bradykinin and histamine, which cause vasodilation, are released from the traumatized tissue, leading to leakage of fluid and protein into extracellular space. This response creates the red, edematous appearance (erythema) indicating that the inflammation process has begun (Sieggreen, 1987). The immune response is activated through the complement system (C3a and C5a) resulting in vasodilation and chemoattraction for neutrophils and monocytes (Cooper, 1990). This hemostasis and phagocytosis stabilizes the wound and attempts to clear away dead cells and bacteria (Cooper, 1990; Sieggreen, 1987; Wysocki, 1989). Phagocytosis is a critical component of the inflammatory phase and for overall wound healing. Polymorphonuclear neutrophils, the initial phagocytic cell, are effective in controlling bacteria. Approximately 24 hours after injury, macrophages appear, remove dead tissue, and secrete angiogenesis factor (AGF). Angiogenesis factor is significant because it stimulates the formation of endothelial buds, thus leading to granulation, which is the beefy-red tissue that fills-in the wound (Bruno & Craven, 1982; Cooper, 1990; Sieggreen, 1987). Thus, the macrophage is essential to healing, especially for tissue synthesis (Carrico, Mehrhof, & Cohen, 1984; Cooper, 1990). Without a strong inflammatory response, successful wound healing can be greatly delayed. Consequently, medications (such as steroids), decreased tissue oxygenation, poor nutritional status, and aging (with delayed immune responses) can impair the wound MANAGEMENT STRATEGIES FOR healing process by reducing the inflammatory response PRESSURE ULCERS (Bruno & Craven, 1982; Carrico et al., Cooper, 1990; The first step of successful pressure ulcer management Sieggreen, 1987). In fact, the first few hours of the inflammatory process can determine the quality of is to thoroughly assess the wound. Document the dimensions and location of the pressure ulcer. Describe wound healing (Cooper, 1990). 102
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or i t may extend and more may develop. If preventive measures are beinn - used, a thorouah analvsis of the strategies and their method of implementation should Stage I Intact skin with delayed capillary refill time or be examined. Should the turning schedule be altered? nonblanchingtissue. Hallmarkof this stage is when Is the patient being positioned correctly? Should a erythema does not resolve after 30 minutes. pressure-relieving device be used? Is the patient being Stage II Break in skin that may involve a partial loss of kept clean and dry? dermis, erythma, or blistering; may be painful. Adequate nutrition, which provides protein, carbohSerous drainage may be present, but no necrotic ydrates, fats, minerals (zinc, magnesium, cooper), tissue. Stage Ill Skin ulceration that extends to subcutaneous vitamins (ascorbic acid), and water, is essential for tissue; necrotic tissue, undermining, exudate, or wound healing (Bobel, 1987; Carrico, et al., 1984; sinus tract may be present. Usually not painful. Ruberg, 1984; Wysocki, 1989; Stotts & Whitney, 1990). Deep full-thickness ulcer extending to fascia, Stage IV Protein is necessary for angiogenesis (granulation), muscle and/or bone; may involve necrotic tissue, collagen formation, and tensile strength. Carbohydrates purulent drainage, sinus tract, or undermining. provide energy for cellular growth. Fats assist in meeting Usually not painful increased caloric needs and are essential elements for Note. From Doughty (1988), Gosnell (1987), and Stotts (1990). cellular growth (Bobel, 1987; Ruberg, 1984; Stotts & Whitney, 1990). Another major nutritional component is adequate the wound and surrounding tissue, in terms of depth, degree of undermining (separation of tissue under hydration, which entails water consumption of at least epidermis creating a horizontal tunnel; measure with 2000-2500 cc/day (Burnside, 1988). Dehydration can a cotton tip applicator), presence of a sinus tract (vertical decrease tissue oxygenation and perfusion (Wysocki, tunnel), drainage, odor or necrotic tissue, and degree 1989).Therefore, adequate food and fluid intake should of pain or tenderness. Include the wound’s color and be maintained and monitored for patients with a amount of granulation (Allman, 1989; Braden & Bryant, pressure ulcer, particularly those who may be nutri1990; Cuzzell & Stotts, 1990; Doughty, 1988; Trelease, tionally compromised. In addition, weight should be 1988). An example of a pressure ulcer description is assessed at least monthly. A baseline serum albumin, the following: 4 cm X 6 cm X 3 cm (depth)sacral wound, cholesterol, and complete blood count (to assess for with 4 cm undermining in left upper quadrant; visible anemia and calculate total lymphocyte count) should muscle tissue; and pale pink color with no surrounding be obtained and repeated as indicated. To determine nutritional needs, the NP should conduct nutritional erythema, pain, odor, or purulent drainage. The assessment enables the NP to accurately stage assessments as previously described (Sanders, 1992). Ascorbic acid (vitamin C) plays a major role in wound a pressure ulcer (Table 1).Because muscle tissue is visible in the above wound description, it would be classified healing and can impair or alter the healing trajectory as Stage IV. The wound assessment should be on-going (Allman, 1990; Bobel, 1987; Ruberg, 1984; Sieggreen, and supported with documentation. In acute situations 1987; Stotts & Whitney, 1990). One research study and for medicare reimbursement, documentation should revealed that ascorbic acid had a dramatic influence on be daily; however, in long-term care settings, documen- wound healing. The group of patients ( N = 10) who tation can be once a week as long as there is not a received 500 mg of vitamin C by mouth twice daily had an 84% reduction in pressure ulcer size compared change in the wound’s status (Doughty, 1988). Three basic principles can guide the NP’s decisions with the control group ( N = lo), which had only a 43% reduction in ulcer surface area (Allman, 1990; regarding appropriate pressure ulcer management: 1. Eliminate or minimize precipitating factors such Taylor, Rimmer, Butcher, & Dymock, 1974). Ascorbic acid is essential for fibroblast production and collagen as pressure, friction and shearing, moisture, etc. 2. Provide nutritional support and monitor nutri- synthesis (Ruberg, 1984; Sieggreen, 1987; Stotts & Whitney, 1990). Therefore, the NP should consider tional status. 3. Create and maintain a wound environment that prescribing 500 mg of vitamic C by mouth twice daily fosters the healing process, e.g., keep the wound moist if the patient’s nutritional status is poor or if the pressure and clean, promote adequate circulation and oxygena- ulcer is healing slowly or both (Allman, 1990). Vitamin A, which is stored in the liver and adipose tion, and decrease bacteria count to at least 100,000 (which is evidenced by no purulent drainage and red, tissue, promotes epithelialization and granulation (Ruberg, 1984; Stotts & Whitney, 1990). Supplementahealthy-looking tissue). If not already in progress, prevention strategies must tion of this vitamin is often not necessary because it be implemented as soon as a pressure ulcer is discovered, takes several months to deplete the large stores of vitamin TABLE 1. STAGING CRITERIA FOR PRESSURE ULCERS
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A (Bobel, 1987; Stotts & Whitney, 1990).However, 25,000 units/day of vitamin A is recommended for patients who are on steroid therapy (Carricoet al., 1984).Vitamin A can counteract the anti-inflammatory effects that steroids create (Carrico, et al., 1984; Ruberg, 1984, Sieggreen, 1987). Zinc deficiency retards epithelialization and collagen synthesis, and reduces tensile strength (Ruberg, 1984; Sieggreen, 1987; Stotts & Whitney, 1990). Replacement therapy, 220 mg of zinc sulfate by mouth three times a day (Allman, 1990),is only indicated when a deficiency exists (Bobel, 1987). The zinc serum level should be re-evaluated 2 weeks after supplementation has been started and discontinued when normal. The question regarding zinc supplementation for accelerated healing remains controversial (Allman, 1990; Ruberg, 1984; Stotts & Whitney, 1990). To assist injured skin’s recovery, an environment conducive to healing must be created. Basic wound care consists of cleansing and debriding the wound, eradicating infection, and selecting a dressing that provides a clean, moist environment-without disturbance of fragile epithelial cells. A major treatment goal is to promote and maintain epithelialization, which is the capillary bed that is necessary for tissue growth and consequently healing. Therefore, antiseptic solutions (povidone-iodine, acetic acid, sodium hypochlorite, hydrogen peroxide)and enzymatic agents should be used cautiously and for a brief period because they are cytotoxic (destructive to tissue cells). A wound can be debrided surgically, chemically, or mechanically. If the wound has a thick, rubbery eschar, surgical debridement is recommended because chemical or mechanical debridement will take much longer to remove the dead tissue. The main principle to keep in mind when surgically debriding a wound is to stop removing tissue when bleeding occurs, which indicates viable tissue has been reached. Piece-by-piece surgical debridement, which often can be done at the bedside using aseptic technique, is more economical than chemical debridement with an enzymatic agent that may cost $50.00/tube or more, and take longer. Chemical debridement, though costly and time consuming, is effective for small, necrotic areas that are not dry or crusty (Seiler and Stahelin, 1989). The chemical debridement must stop once necrotic tissue has been removed because the enzyme will also destroy healthy tissue. The NP should educate the nursing staff about where to apply the enzymatic agent (only on the necrotic area) and that the agent should be stored in the refrigerator. Mechanical debridement (wet-to-dry dressings) takes time and also destroys the fragile epithelial cells protecting the wound. This method can be used with 104
exudating wounds or with wounds difficult to debride, i.e., deep, narrow sacral ulcer. Hydrocolloid dressings can also be used to soften and remove eschar on wounds that are not obviously infected (odor, purulent drainage, or cellulitic in appearance). The moistened environment and “soup” that is created from the hydrocolloid dressing facilitates the debridement process. There are also numerous products available for exudating wounds that are reported to be less caustic. By using the principles of healing, the NP can select the appropriate wound care products. Consideration of expense and time should also be included in the decision-making process. Whirlpool therapy also mechanically debrides wounds, yet can dry surrounding tissue, destroy fragile epithelial tissue, and require more staff time and energy (Braden & Bryant, 1990; Doughty, 1988). Therefore, it is recommended that whirlpool management be reserved for large wounds (Braden & Bryant, 1990). Whirlpool treatments, either once or twice a day, can be effective for large, exudating wounds. The therapy should be stopped once granulation has occurred over the wound bed so that the healthy tissue will not be disturbed (Doughty, 1988). T h e body’s own proteolytic enzymes provide additional debriding and cleansing (Alvarez, Rozint, & Wiseman, 1989; Doughty, 1988; Cuzzell & Stotts, 1990; Seiler & Stahelin, 1985). Autolysis usually begins in 72 to 96 hours, and occlusive dressings, such as hydrocolloid or polyurethane film, facilitate this process because they create a warm, moist environment. Note that the ulcer may get larger before healing occurs because of the autolytic process (Alvarez et al., 1989). Collagenase, which is an enzyme secreted by neutrophils and macrophages, is responsible for this mechanism and is designed to restore skin integrity (Wysocki, 1989). The fluid generated from autolysis is brownish-yellow that may have some pus because dead cells are being removed. Unless there is clinical evidence of infection (erythema, pain, heat, swelling), the NP should not be alarmed (Alvarez et al., 1989; Wysocki, 1989). After debridement has been done, the wound should be kept clean and moist so optimal epithelialization and granulation can occur. This can be done with either normal saline or lactated Ringer’s solution (contains sodium, calcium, potassium, chloride, and bicarbonate). These solutions are not cytotoxic and create an environment advantageous to granulation. Ringer’s solution fosters fibroblast survival, and thus is theoretically the preferred solution (Seiler & Stahelin, 1985; Seiler & Stahelin, 1989).Another advantage to these solutions is that they are less expensive in comparison with many wound care products. There are some very effective wound care products such as hydrocolloid or film dressings that provide moisture, serve as a barrier,
JOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS
and save nursing-care time since a dressing change is needed only every 3 to 5 days. The NP may want to investigate the cost effectiveness and efficacy of various wound care products. A local bacterial infection of a pressure ulcer must be resolved before healing can take place. The goal is to decrease bacterial count to less than lOO,OOO/g, eliminate anaerobic bacteria (Pseudomonas, aeruginosa, Klebsiella, and Providencia species), and produce a clean, beefy-red ulcer surface (Seiler & Stahelin, 1985; Seiler & Stahelin, 1989; Shenaq & Dinh, 1990; Wysocki, 1989).Because of cost and obtaining misleading cultures (Staphylococcus aureus, Pseudomonas, and other bacteria normally grow on skin surface),wounds should not be cultured unless there is obvious need and evidence of infection such as erythema, pain, odor, and purulent drainage. Systemic antibiotics should only be prescribed when there is evidence of cellulitis or sepsis, or when there is a risk of osteomyelitis(Allman, 1989; Thomason, 1988). Topical antibiotics, such as silver sulfadiazine, gentamicin, bacitracin zinc, and neosporin, may be effective and are not very cytotoxic (Allman, 1989; Alvarez et al., 1989). There is controversy related to the use of disinfectant agents, i.e., sodium hypochlorite, acetic acid, povidoneiodine, because they are caustic to healthy tissue with some (sodium hypochlorite) affecting clotting abilities. The key to successful management of antiseptic agents is to stop using them when purulent drainage or odor has ceased and growth is occurring. Dakin’s solution, which is sodium hypochlorite, is less destructive to the fragile cells of a healing wound when rinsed with normal saline and stopped when red, healthy tissue is visible. The solution should not be placed on the surrounding skin because it can burn healthy skin. After gently irrigating the wound with sodium hypochlorite, a saline wet-to-dry dressing should be applied. Povidone-iodine wet-to-drydressings should be used for infected wounds or when bone is exposed (because risk of osteomyelitis is greater), but preferably not for more than a week because it is cytotoxic. Acetic acid wetto-dry dressings can be used when there is an odor or evidence of infection, and discontinued when odor dissipates or when healthy tissue is present. Acetic acid is the preferred solution when Pseudomonas is the suspected bacteria (based on the presence of a foul, greenish discharge) (Thomason, 1988).The practitioner who chooses to use these agents should know about the antiseptic and also know that it is cytotoxic with risks of delaying healing or inducing bleeding, or both, in the case of sodium hypochlorite. The NP should teach the nursing staff about its use and when it should be stopped (when odor, drainage, and cellulitis ceases, or granulation tissue is present, or both), or the healing VOLUME 4, NUMBER 3, JULY-SEPTEMBER, 1992
will be slowed because of the cytotoxic effects of the an tiseptic. The wound can be protected from mechanical and bacterial insults, and a moist environment can be maintained by covering it with a dressing. The dressing choice should be based on the wound’s condition and location, patient’s responsiveness and sensation, nursing staff‘s abilities and time, and available funds. Hydrocolloid dressings and polyurethane films keep the wound moist, provide a protective barrier, reduce wound pain, and promote autolysis. They should not be used on infected wounds because a prime environment for bacterial growth would be created. Recently, DuoDermB was approved for use in clean Stage I11 or IV pressure ulcers, excluding third-degree burns (ConvaTec, 1991). These dressings should be changed every 3 to 5 days (Alvarez et al., 1989; Sieggreen, 1987; Wysocki, 1989). If the practitioner would like to monitor the wound closely for infection, polyurethane films would be the better choice, but the nursing staff should be educated about autolysis, which produces a brown, puslike fluid. Hydrocolloid and polyurethane film dressings can also serve as a protective barrier for Stage I and I1 ulcers. Gauze dressings are primarily used for wounds that need to be debrided or for exudating wounds (Alvarez et al., 1989; Seiler 8c Stahelin, 1989; Wysocki, 1989).Some practitioners use damp 4 X 4 dressings as a protective barrier that also create a moist environment. There is the risk, though, that healing will be delayed because the gauze can destroy the fragile epithelial cells (Alvarez et al. 1989; Bryant & Braden, 1990; Doughty, 1988; Wysocki, 1989). The key is to only dampen the 4 X 4 dressing. If saturated, the ulcer border could soften and become hypertrophic (B. Braden, personal communication, November 2, 1990). This author recommends that gauze dressings saturated with normal saline or Ringer’s solution be changed every shift to keep the wound moist and also to keep the nursing personnel involved in the care. If the dressing is not changed frequently, the risks of infection and delayed healing are greater. The NP should decide if the staff is capable of meeting the time demand for this strategy; if not a hydrocolloid dressing or some other appropriate dressing that requires fewer changes should be used.
SUMMARY The NP can improve the healing rate of pressure ulcers by using current pressure ulcer management strategies. The NP is also the most appropriate health care member to coordinate the treatment of pressure ulcers, especially in long-term care where this role is becoming more accepted and used. By understanding 105
the physiologic process of wound healing, the NP can should involve the client and family in wound care by make appropriate, successful management decisions so explaining management strategies and describing the that epithelialization and ultimately healing can occur. progress of healing. When possible, the N P should In addition, these principles can guide the NP in encourage the client or family or both to do wound care selecting wound care products that are effective and cost after teaching the appropriate technique; however, the ulcer should still be monitored and described in progress efficient. A thorough assessment of the ulcer should be done notes by nursing staff. This approach is especially helpful and followed with frequent reevaluation after interven- if the client or family will be doing dressing care at home. Successful pressure ulcer management uses the tion has begun. The assessment should include the dimensions and location of the pressure ulcer with the principles of wound healing as a guide for treatment. description, including the tissue color, depth, degree Frequent review of the healing trajectory and the of undermining, odor, drainage, or amount of necrotic associated cellular physiology will facilitate the learning process, especially when reinforced with clinical tissue. The main management goal is to keep the ulcer clean examples. When a strategy does not foster healing after and moist so that epithelialization can occur; thus, a couple of weeks, the client's nutritional status should healing takes place. Adequate nutrition is necessary to be evaluated and another treatment should be consiprovide the essential nutrients for healing. Necrotic or dered. As a rule, when making changes, at the most nonviable tissue must be removed, either surgically, two, should be implemented so as not to confound the chemically, or mechanically. Systemic antibiotics are evaluation. At first, wounds may need to be monitored appropriate only when there is evidence of cellulitis more frequently until the staff and NP become or osteomyelitis. Most of all, preventive measures should comfortable and experienced with treatment strategies. be implemented so precipitating factors are removed Pressure ulcer management is a science and art that requires time and experience before one feels confident and intervention is not in vain. To promote self-care and foster independence, the NP and competent, as any successful clinician will validate.
References Allman, R. M. Pressure ulcer among the elderly. New England Journal of Medicine, 320, 850-853. Allman. R. M. (1990). Pressure ulcers. In Hazard, W. R., Andres, R., Bierman, E. L. & Blass,J. P. (Eds.), Principles of Geriatric Medicine and Gerontology (2nd ed.) (pp. 1204-1211). New York: McGrawHill. Alvarez, 0.. Rozint, J., Wiseman, D. (1989). Moist environment for healing: Matching the dressing to the wound. Wounds: A Compendium of Clinical Research and Practice, 1 , 35-51. Bobel, L. M. (1987). Nutritional implications in the patient with pressure sores. Nursing Clinics of North America, 22, 379-389. Braden, B., & Bryant, B. (1990). Innovations to prevent and treat pressure ulcers. Geriatric Nursing, 1 1 , 182-186. Bruno, P., & Craven, R. F. (1987). A conceptual schema for the study of the etiology of pressure sores. Rehabilitation Nursing, 12, 812, 16. Burnside, I. M. (1988). Nursing and the Aged. New York: McGrawHill. Carrico, T. J., Mehrhof, A. I., & Cohen, I. K. (1984). Biology of wound healing. Surgical Clinics of North America, 64, 721 -733. ConvaTec, News Release. Bristol-Myers Squibb Company, Princeton, NJ. Cooper, D. M.(1990). Optimizing wound healing. Nursing Clinics of North America, 25, 165-1 79. Cuuell, J. Z., & Stotts, N. A. (1990). Trial & error yields to knowledge. American Journal of Nursing, 90, 53-60. Doughty, D. (1988). Management of pressure sores. Journal of €nterostomal Therapy, 15, 39-44. Gosnell, D. J. (1987). Assessment and evaluation of pressure sores. Nursing Clinics of North America, 22, 399-41 5. Maklebust, J. (1987). Pressure ulcers: Etiology and prevention. Nursing Clinics of North America, 22, 359-377.
Pinchocofsky-Devin, G. D.,& Kaminski, M. V. (1986). Correlation of pressure sores and nutritional status. Journal of Geriatrics Society, 35,435-440. Ruberg. R. L. (1984). Role of nutrition in wound healing. Surgical Clinics of North America, 64, 705-71 4. Sanders, S. L. (1992). Pressure ulcers, part one: Prevention strategies. Journal of the American Academy of Nurse Practitioners, 4, 6370. Seiler. W. 0. & Stahelin, M. B. (1985). Decubitus ulcers: Treatment through five therapeutic principles. Geriatrics, 40, 30-42. Seiler, W. O., & Stahelin, M. 8. (1989). Decubitus ulceration in the elderly. In Katz, P. R., & Calkins, E. (Eds.), Principles and Practice of Nursing Home Care (pp. 328-348). New York: Springer. Shenaq, S., & Dinh, T. A. (1990). Decubitus ulcers. Postgraduate Medicine, 87, 91-95. Sieggreen, M. Y. (1987). Healing of physical wounds. Nursing Clinics of North America, 22,439-447. Stotts, N. A. (1990). Seeing red and yellow and black-The threecolor concept of wound care. Nursing '90, 20, 59-61, Stotts, N. A., & Whitney, J. D. (1990). Nutritional intake and status of clients in the home with open surgical wounds. Journal of Community Health Nursing, 7, 77-86. Taylor, T., Rimmer, S.Butcher, J., & Dymock, I. (1974). Ascorbic acid supplementation in the treatment of pressure-sores. Lancet, 544, 544-546. Thomason, S. S. (1988). Pressure ulcers: Considerationsof intervention strategies. Ostomyl Wound Management, 27, 48-55. Trelease, C. (1988). Developing standards for wound care. Ostomy/ Wound Management, 28,47-56. Wysocki, A. B. (1989). Surgical wound healing. AORN Journal, 49, 502-51 8.
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The goal of this article is to facilitate the successful resolution of pressure ulcers. The nurse practitioner (NP) is an ideal health care professionalto manage pressue ulcer care. This article reviews the basic principles related to wound care. The healing trajectory is discussed to assist an NP to determine appropriate therapy. Current, research-based management strategies are provided.
Pressure ulcers cost society not only money, but also human lives. The annual cost for pressure ulcer care ranges from $5,000 to $40,000,and approximately 60,000 people a year die from pressure ulcers (Maklebust, 1987; Pinchocofsky-Devin & Kaminski, 1986). Pressure ulcers are a serious health concern to which nursing can make a positive contribution. Pressure ulcers were first documented by the Egyptians in the year 2000 B.C. (Shenaq & Dinh, 1990). However, they have not been Seriously studied until this century. During the past decade, a research revolution has occurred regarding pressure ulcer prevention and management. Yet, old, outdated practices are still frequently used. This article focuses on current treatment strategies for pressure ulcers that the nurse practitioner (NP) can use to manage care and to help educate other nurses.
THE ROLE OF THE NURSE PRACTITIONER The NP is an ideal health care professional to provide medical management for pressure ulcers. The NP can influence the healing process by prescribing appropriate therapy and implementing other measures to prevent extension of the wound. In addition, the NP can provide written management protocols that will enable nurses Address correspondence to Susan L. Sanders, MSN, GNP, RN, C, 2-H Durban Court, Baltimore, MD 21236.
VOLUME 4, NUMBER 3, JULY-SEPTEMBER, 1992
to act immediately on discovery of an ulcer. To generate a commitment for the prescribed management strategies and to ensure proper technique, the NP can provide education regarding appropriate treatment of pressure ulcers, including the logic behind techniques and protocols. All these servicescan be included in a pressure ulcer prevention and management program that is marketed by the NP. The NP could also serve as a consultant to physicians for clients who have pressure ulcers, particularly slowly resolving ulcers, and should make his or her availability known. Nursing staff will recommend an NP who has had success with pressure ulcer management to physicians and family members. Experienced enterostomal therapists (ETs) are considered the experts for pressure ulcer management; thus, the NP may want to consult an E T for ulcers that are difficult to heal or for current management techniques or both. In addition, a collaborative relationship could be developed with an ET where mutual referrals are given, information is shared, and research is conducted jointly. The NP should also seek out product representatives to learn about wound care products and to participate in clinical research of new products. An ET can assist the NP in locating area representatives. If an NP is going to manage pressure ulcers, professional journals that include current information and research studies related to prevention and management should be read, such as Ostomyl Wound Management, Journal of Enterostomal Therafiy, and Decubitus.
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PHYSIOLOGY OF WOUND HEALING
During the second or proliferative phase (24 hours to 22 days), three significant events occur: epithelialization, neovascularization, and collagen synthesis (Cooper, 1990; Wysocki, 1989). Epithelialization seals and protects the wound from insults. Neovascularization, also known as granulation, is the formation of new capillaries, which explains its beefy red color. Through neovascularization, oxygen and nutrients are provided to the wound. Collagen synthesis creates tensile strength and is the support matrix for the recovering wound (Bruno & Craven, 1982; Sieggreen, 1987; Wysocki, 1989). Thus, the function of this phase is to rebuild the wounded tissue. Epithelialization, which seals the wound from bacteria and fluid loss, begins within 24 hours (Sieggreen, 1987; Wysocki, 1989). Epithelial tissue is extremely fragile and, therefore, can easily be wiped or washed away. A moist environment fosters epithelialization, whereas crust or dryness slows the process (Carrico et al., 1984; Sieggreen, 1987). This microscopic epithelial layer is vital because i t enables the wound healing process to proceed in a “safe” environment; therefore, great efforts should be taken to protect this fragile tissue and to foster its growth. Fibroblasts, which are stimulated by AGF and the growth factor secreted by platelets, are necessary for collagen production (Cooper, 1990; Sieggreen, 1987). Collagen synthesis is also dependent on ascorbic acid (vitamin C), zinc, magnesium, and other amino acids (Bruno & Craven, 1982; Cooper, 1990; Sieggreen, 1987; Wysocki, 1989). Oxygen and iron are also necessary for collagen synthesis. In fact, the occurrence of infection is more frequent in ischemic wounds (Carrico et al., 1984; Sieggreen, 1987). The final, or maturation phase, also known as the differentiation or remodeling phase, usually begins after 21 days and can take as long as 2 years. Collagen deposits continue, which make the wound thicker and more compact, with the end result of increased tensile strength (Cooper, 1990; Wysocki, 1989; Sieggreen, 1987). However, the maximum tensile strength will only be 80%of the preinjury capacity (Cooper, 1990).The wound will also have a dark, scarlet-red color, eventually fading to a silvery white color (Sieggreen, 1987). Fifty percent of the original tensile strength is restored usually within 6 weeks (Wysocki, 1989).
A basic understanding of the scientific principles of healing are necessary to appropriately manage wound care. Fortunately, the pressure ulcer research revolution has created scientific data to support wound care decisions. An overview of the wound-healing process follows. There are three major phases of wound healing: inflammatory, proliferative, and maturation. The inflammatory phase (4-5 days) is characterized by redness, heat, pain, and swelling, which in turn initiates the healing process (Sieggreen, 1987; Wysocki, 1989). The function of the inflammatory phase is to prevent further injury and blood loss. This is accomplished through coagulation and mobilization of the immune system (Cooper, 1990; Sieggreen, 1987; Wysocki, 1989). Initially, platelets line the vessel walls and release a growth factor that fosters tissue regeneration. Bradykinin and histamine, which cause vasodilation, are released from the traumatized tissue, leading to leakage of fluid and protein into extracellular space. This response creates the red, edematous appearance (erythema) indicating that the inflammation process has begun (Sieggreen, 1987). The immune response is activated through the complement system (C3a and C5a) resulting in vasodilation and chemoattraction for neutrophils and monocytes (Cooper, 1990). This hemostasis and phagocytosis stabilizes the wound and attempts to clear away dead cells and bacteria (Cooper, 1990; Sieggreen, 1987; Wysocki, 1989). Phagocytosis is a critical component of the inflammatory phase and for overall wound healing. Polymorphonuclear neutrophils, the initial phagocytic cell, are effective in controlling bacteria. Approximately 24 hours after injury, macrophages appear, remove dead tissue, and secrete angiogenesis factor (AGF). Angiogenesis factor is significant because it stimulates the formation of endothelial buds, thus leading to granulation, which is the beefy-red tissue that fills-in the wound (Bruno & Craven, 1982; Cooper, 1990; Sieggreen, 1987). Thus, the macrophage is essential to healing, especially for tissue synthesis (Carrico, Mehrhof, & Cohen, 1984; Cooper, 1990). Without a strong inflammatory response, successful wound healing can be greatly delayed. Consequently, medications (such as steroids), decreased tissue oxygenation, poor nutritional status, and aging (with delayed immune responses) can impair the wound MANAGEMENT STRATEGIES FOR healing process by reducing the inflammatory response PRESSURE ULCERS (Bruno & Craven, 1982; Carrico et al., Cooper, 1990; The first step of successful pressure ulcer management Sieggreen, 1987). In fact, the first few hours of the inflammatory process can determine the quality of is to thoroughly assess the wound. Document the dimensions and location of the pressure ulcer. Describe wound healing (Cooper, 1990). 102
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or i t may extend and more may develop. If preventive measures are beinn - used, a thorouah analvsis of the strategies and their method of implementation should Stage I Intact skin with delayed capillary refill time or be examined. Should the turning schedule be altered? nonblanchingtissue. Hallmarkof this stage is when Is the patient being positioned correctly? Should a erythema does not resolve after 30 minutes. pressure-relieving device be used? Is the patient being Stage II Break in skin that may involve a partial loss of kept clean and dry? dermis, erythma, or blistering; may be painful. Adequate nutrition, which provides protein, carbohSerous drainage may be present, but no necrotic ydrates, fats, minerals (zinc, magnesium, cooper), tissue. Stage Ill Skin ulceration that extends to subcutaneous vitamins (ascorbic acid), and water, is essential for tissue; necrotic tissue, undermining, exudate, or wound healing (Bobel, 1987; Carrico, et al., 1984; sinus tract may be present. Usually not painful. Ruberg, 1984; Wysocki, 1989; Stotts & Whitney, 1990). Deep full-thickness ulcer extending to fascia, Stage IV Protein is necessary for angiogenesis (granulation), muscle and/or bone; may involve necrotic tissue, collagen formation, and tensile strength. Carbohydrates purulent drainage, sinus tract, or undermining. provide energy for cellular growth. Fats assist in meeting Usually not painful increased caloric needs and are essential elements for Note. From Doughty (1988), Gosnell (1987), and Stotts (1990). cellular growth (Bobel, 1987; Ruberg, 1984; Stotts & Whitney, 1990). Another major nutritional component is adequate the wound and surrounding tissue, in terms of depth, degree of undermining (separation of tissue under hydration, which entails water consumption of at least epidermis creating a horizontal tunnel; measure with 2000-2500 cc/day (Burnside, 1988). Dehydration can a cotton tip applicator), presence of a sinus tract (vertical decrease tissue oxygenation and perfusion (Wysocki, tunnel), drainage, odor or necrotic tissue, and degree 1989).Therefore, adequate food and fluid intake should of pain or tenderness. Include the wound’s color and be maintained and monitored for patients with a amount of granulation (Allman, 1989; Braden & Bryant, pressure ulcer, particularly those who may be nutri1990; Cuzzell & Stotts, 1990; Doughty, 1988; Trelease, tionally compromised. In addition, weight should be 1988). An example of a pressure ulcer description is assessed at least monthly. A baseline serum albumin, the following: 4 cm X 6 cm X 3 cm (depth)sacral wound, cholesterol, and complete blood count (to assess for with 4 cm undermining in left upper quadrant; visible anemia and calculate total lymphocyte count) should muscle tissue; and pale pink color with no surrounding be obtained and repeated as indicated. To determine nutritional needs, the NP should conduct nutritional erythema, pain, odor, or purulent drainage. The assessment enables the NP to accurately stage assessments as previously described (Sanders, 1992). Ascorbic acid (vitamin C) plays a major role in wound a pressure ulcer (Table 1).Because muscle tissue is visible in the above wound description, it would be classified healing and can impair or alter the healing trajectory as Stage IV. The wound assessment should be on-going (Allman, 1990; Bobel, 1987; Ruberg, 1984; Sieggreen, and supported with documentation. In acute situations 1987; Stotts & Whitney, 1990). One research study and for medicare reimbursement, documentation should revealed that ascorbic acid had a dramatic influence on be daily; however, in long-term care settings, documen- wound healing. The group of patients ( N = 10) who tation can be once a week as long as there is not a received 500 mg of vitamin C by mouth twice daily had an 84% reduction in pressure ulcer size compared change in the wound’s status (Doughty, 1988). Three basic principles can guide the NP’s decisions with the control group ( N = lo), which had only a 43% reduction in ulcer surface area (Allman, 1990; regarding appropriate pressure ulcer management: 1. Eliminate or minimize precipitating factors such Taylor, Rimmer, Butcher, & Dymock, 1974). Ascorbic acid is essential for fibroblast production and collagen as pressure, friction and shearing, moisture, etc. 2. Provide nutritional support and monitor nutri- synthesis (Ruberg, 1984; Sieggreen, 1987; Stotts & Whitney, 1990). Therefore, the NP should consider tional status. 3. Create and maintain a wound environment that prescribing 500 mg of vitamic C by mouth twice daily fosters the healing process, e.g., keep the wound moist if the patient’s nutritional status is poor or if the pressure and clean, promote adequate circulation and oxygena- ulcer is healing slowly or both (Allman, 1990). Vitamin A, which is stored in the liver and adipose tion, and decrease bacteria count to at least 100,000 (which is evidenced by no purulent drainage and red, tissue, promotes epithelialization and granulation (Ruberg, 1984; Stotts & Whitney, 1990). Supplementahealthy-looking tissue). If not already in progress, prevention strategies must tion of this vitamin is often not necessary because it be implemented as soon as a pressure ulcer is discovered, takes several months to deplete the large stores of vitamin TABLE 1. STAGING CRITERIA FOR PRESSURE ULCERS
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A (Bobel, 1987; Stotts & Whitney, 1990).However, 25,000 units/day of vitamin A is recommended for patients who are on steroid therapy (Carricoet al., 1984).Vitamin A can counteract the anti-inflammatory effects that steroids create (Carrico, et al., 1984; Ruberg, 1984, Sieggreen, 1987). Zinc deficiency retards epithelialization and collagen synthesis, and reduces tensile strength (Ruberg, 1984; Sieggreen, 1987; Stotts & Whitney, 1990). Replacement therapy, 220 mg of zinc sulfate by mouth three times a day (Allman, 1990),is only indicated when a deficiency exists (Bobel, 1987). The zinc serum level should be re-evaluated 2 weeks after supplementation has been started and discontinued when normal. The question regarding zinc supplementation for accelerated healing remains controversial (Allman, 1990; Ruberg, 1984; Stotts & Whitney, 1990). To assist injured skin’s recovery, an environment conducive to healing must be created. Basic wound care consists of cleansing and debriding the wound, eradicating infection, and selecting a dressing that provides a clean, moist environment-without disturbance of fragile epithelial cells. A major treatment goal is to promote and maintain epithelialization, which is the capillary bed that is necessary for tissue growth and consequently healing. Therefore, antiseptic solutions (povidone-iodine, acetic acid, sodium hypochlorite, hydrogen peroxide)and enzymatic agents should be used cautiously and for a brief period because they are cytotoxic (destructive to tissue cells). A wound can be debrided surgically, chemically, or mechanically. If the wound has a thick, rubbery eschar, surgical debridement is recommended because chemical or mechanical debridement will take much longer to remove the dead tissue. The main principle to keep in mind when surgically debriding a wound is to stop removing tissue when bleeding occurs, which indicates viable tissue has been reached. Piece-by-piece surgical debridement, which often can be done at the bedside using aseptic technique, is more economical than chemical debridement with an enzymatic agent that may cost $50.00/tube or more, and take longer. Chemical debridement, though costly and time consuming, is effective for small, necrotic areas that are not dry or crusty (Seiler and Stahelin, 1989). The chemical debridement must stop once necrotic tissue has been removed because the enzyme will also destroy healthy tissue. The NP should educate the nursing staff about where to apply the enzymatic agent (only on the necrotic area) and that the agent should be stored in the refrigerator. Mechanical debridement (wet-to-dry dressings) takes time and also destroys the fragile epithelial cells protecting the wound. This method can be used with 104
exudating wounds or with wounds difficult to debride, i.e., deep, narrow sacral ulcer. Hydrocolloid dressings can also be used to soften and remove eschar on wounds that are not obviously infected (odor, purulent drainage, or cellulitic in appearance). The moistened environment and “soup” that is created from the hydrocolloid dressing facilitates the debridement process. There are also numerous products available for exudating wounds that are reported to be less caustic. By using the principles of healing, the NP can select the appropriate wound care products. Consideration of expense and time should also be included in the decision-making process. Whirlpool therapy also mechanically debrides wounds, yet can dry surrounding tissue, destroy fragile epithelial tissue, and require more staff time and energy (Braden & Bryant, 1990; Doughty, 1988). Therefore, it is recommended that whirlpool management be reserved for large wounds (Braden & Bryant, 1990). Whirlpool treatments, either once or twice a day, can be effective for large, exudating wounds. The therapy should be stopped once granulation has occurred over the wound bed so that the healthy tissue will not be disturbed (Doughty, 1988). T h e body’s own proteolytic enzymes provide additional debriding and cleansing (Alvarez, Rozint, & Wiseman, 1989; Doughty, 1988; Cuzzell & Stotts, 1990; Seiler & Stahelin, 1985). Autolysis usually begins in 72 to 96 hours, and occlusive dressings, such as hydrocolloid or polyurethane film, facilitate this process because they create a warm, moist environment. Note that the ulcer may get larger before healing occurs because of the autolytic process (Alvarez et al., 1989). Collagenase, which is an enzyme secreted by neutrophils and macrophages, is responsible for this mechanism and is designed to restore skin integrity (Wysocki, 1989). The fluid generated from autolysis is brownish-yellow that may have some pus because dead cells are being removed. Unless there is clinical evidence of infection (erythema, pain, heat, swelling), the NP should not be alarmed (Alvarez et al., 1989; Wysocki, 1989). After debridement has been done, the wound should be kept clean and moist so optimal epithelialization and granulation can occur. This can be done with either normal saline or lactated Ringer’s solution (contains sodium, calcium, potassium, chloride, and bicarbonate). These solutions are not cytotoxic and create an environment advantageous to granulation. Ringer’s solution fosters fibroblast survival, and thus is theoretically the preferred solution (Seiler & Stahelin, 1985; Seiler & Stahelin, 1989).Another advantage to these solutions is that they are less expensive in comparison with many wound care products. There are some very effective wound care products such as hydrocolloid or film dressings that provide moisture, serve as a barrier,
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and save nursing-care time since a dressing change is needed only every 3 to 5 days. The NP may want to investigate the cost effectiveness and efficacy of various wound care products. A local bacterial infection of a pressure ulcer must be resolved before healing can take place. The goal is to decrease bacterial count to less than lOO,OOO/g, eliminate anaerobic bacteria (Pseudomonas, aeruginosa, Klebsiella, and Providencia species), and produce a clean, beefy-red ulcer surface (Seiler & Stahelin, 1985; Seiler & Stahelin, 1989; Shenaq & Dinh, 1990; Wysocki, 1989).Because of cost and obtaining misleading cultures (Staphylococcus aureus, Pseudomonas, and other bacteria normally grow on skin surface),wounds should not be cultured unless there is obvious need and evidence of infection such as erythema, pain, odor, and purulent drainage. Systemic antibiotics should only be prescribed when there is evidence of cellulitis or sepsis, or when there is a risk of osteomyelitis(Allman, 1989; Thomason, 1988). Topical antibiotics, such as silver sulfadiazine, gentamicin, bacitracin zinc, and neosporin, may be effective and are not very cytotoxic (Allman, 1989; Alvarez et al., 1989). There is controversy related to the use of disinfectant agents, i.e., sodium hypochlorite, acetic acid, povidoneiodine, because they are caustic to healthy tissue with some (sodium hypochlorite) affecting clotting abilities. The key to successful management of antiseptic agents is to stop using them when purulent drainage or odor has ceased and growth is occurring. Dakin’s solution, which is sodium hypochlorite, is less destructive to the fragile cells of a healing wound when rinsed with normal saline and stopped when red, healthy tissue is visible. The solution should not be placed on the surrounding skin because it can burn healthy skin. After gently irrigating the wound with sodium hypochlorite, a saline wet-to-dry dressing should be applied. Povidone-iodine wet-to-drydressings should be used for infected wounds or when bone is exposed (because risk of osteomyelitis is greater), but preferably not for more than a week because it is cytotoxic. Acetic acid wetto-dry dressings can be used when there is an odor or evidence of infection, and discontinued when odor dissipates or when healthy tissue is present. Acetic acid is the preferred solution when Pseudomonas is the suspected bacteria (based on the presence of a foul, greenish discharge) (Thomason, 1988).The practitioner who chooses to use these agents should know about the antiseptic and also know that it is cytotoxic with risks of delaying healing or inducing bleeding, or both, in the case of sodium hypochlorite. The NP should teach the nursing staff about its use and when it should be stopped (when odor, drainage, and cellulitis ceases, or granulation tissue is present, or both), or the healing VOLUME 4, NUMBER 3, JULY-SEPTEMBER, 1992
will be slowed because of the cytotoxic effects of the an tiseptic. The wound can be protected from mechanical and bacterial insults, and a moist environment can be maintained by covering it with a dressing. The dressing choice should be based on the wound’s condition and location, patient’s responsiveness and sensation, nursing staff‘s abilities and time, and available funds. Hydrocolloid dressings and polyurethane films keep the wound moist, provide a protective barrier, reduce wound pain, and promote autolysis. They should not be used on infected wounds because a prime environment for bacterial growth would be created. Recently, DuoDermB was approved for use in clean Stage I11 or IV pressure ulcers, excluding third-degree burns (ConvaTec, 1991). These dressings should be changed every 3 to 5 days (Alvarez et al., 1989; Sieggreen, 1987; Wysocki, 1989). If the practitioner would like to monitor the wound closely for infection, polyurethane films would be the better choice, but the nursing staff should be educated about autolysis, which produces a brown, puslike fluid. Hydrocolloid and polyurethane film dressings can also serve as a protective barrier for Stage I and I1 ulcers. Gauze dressings are primarily used for wounds that need to be debrided or for exudating wounds (Alvarez et al., 1989; Seiler 8c Stahelin, 1989; Wysocki, 1989).Some practitioners use damp 4 X 4 dressings as a protective barrier that also create a moist environment. There is the risk, though, that healing will be delayed because the gauze can destroy the fragile epithelial cells (Alvarez et al. 1989; Bryant & Braden, 1990; Doughty, 1988; Wysocki, 1989). The key is to only dampen the 4 X 4 dressing. If saturated, the ulcer border could soften and become hypertrophic (B. Braden, personal communication, November 2, 1990). This author recommends that gauze dressings saturated with normal saline or Ringer’s solution be changed every shift to keep the wound moist and also to keep the nursing personnel involved in the care. If the dressing is not changed frequently, the risks of infection and delayed healing are greater. The NP should decide if the staff is capable of meeting the time demand for this strategy; if not a hydrocolloid dressing or some other appropriate dressing that requires fewer changes should be used.
SUMMARY The NP can improve the healing rate of pressure ulcers by using current pressure ulcer management strategies. The NP is also the most appropriate health care member to coordinate the treatment of pressure ulcers, especially in long-term care where this role is becoming more accepted and used. By understanding 105
the physiologic process of wound healing, the NP can should involve the client and family in wound care by make appropriate, successful management decisions so explaining management strategies and describing the that epithelialization and ultimately healing can occur. progress of healing. When possible, the N P should In addition, these principles can guide the NP in encourage the client or family or both to do wound care selecting wound care products that are effective and cost after teaching the appropriate technique; however, the ulcer should still be monitored and described in progress efficient. A thorough assessment of the ulcer should be done notes by nursing staff. This approach is especially helpful and followed with frequent reevaluation after interven- if the client or family will be doing dressing care at home. Successful pressure ulcer management uses the tion has begun. The assessment should include the dimensions and location of the pressure ulcer with the principles of wound healing as a guide for treatment. description, including the tissue color, depth, degree Frequent review of the healing trajectory and the of undermining, odor, drainage, or amount of necrotic associated cellular physiology will facilitate the learning process, especially when reinforced with clinical tissue. The main management goal is to keep the ulcer clean examples. When a strategy does not foster healing after and moist so that epithelialization can occur; thus, a couple of weeks, the client's nutritional status should healing takes place. Adequate nutrition is necessary to be evaluated and another treatment should be consiprovide the essential nutrients for healing. Necrotic or dered. As a rule, when making changes, at the most nonviable tissue must be removed, either surgically, two, should be implemented so as not to confound the chemically, or mechanically. Systemic antibiotics are evaluation. At first, wounds may need to be monitored appropriate only when there is evidence of cellulitis more frequently until the staff and NP become or osteomyelitis. Most of all, preventive measures should comfortable and experienced with treatment strategies. be implemented so precipitating factors are removed Pressure ulcer management is a science and art that requires time and experience before one feels confident and intervention is not in vain. To promote self-care and foster independence, the NP and competent, as any successful clinician will validate.
References Allman, R. M. Pressure ulcer among the elderly. New England Journal of Medicine, 320, 850-853. Allman. R. M. (1990). Pressure ulcers. In Hazard, W. R., Andres, R., Bierman, E. L. & Blass,J. P. (Eds.), Principles of Geriatric Medicine and Gerontology (2nd ed.) (pp. 1204-1211). New York: McGrawHill. Alvarez, 0.. Rozint, J., Wiseman, D. (1989). Moist environment for healing: Matching the dressing to the wound. Wounds: A Compendium of Clinical Research and Practice, 1 , 35-51. Bobel, L. M. (1987). Nutritional implications in the patient with pressure sores. Nursing Clinics of North America, 22, 379-389. Braden, B., & Bryant, B. (1990). Innovations to prevent and treat pressure ulcers. Geriatric Nursing, 1 1 , 182-186. Bruno, P., & Craven, R. F. (1987). A conceptual schema for the study of the etiology of pressure sores. Rehabilitation Nursing, 12, 812, 16. Burnside, I. M. (1988). Nursing and the Aged. New York: McGrawHill. Carrico, T. J., Mehrhof, A. I., & Cohen, I. K. (1984). Biology of wound healing. Surgical Clinics of North America, 64, 721 -733. ConvaTec, News Release. Bristol-Myers Squibb Company, Princeton, NJ. Cooper, D. M.(1990). Optimizing wound healing. Nursing Clinics of North America, 25, 165-1 79. Cuuell, J. Z., & Stotts, N. A. (1990). Trial & error yields to knowledge. American Journal of Nursing, 90, 53-60. Doughty, D. (1988). Management of pressure sores. Journal of €nterostomal Therapy, 15, 39-44. Gosnell, D. J. (1987). Assessment and evaluation of pressure sores. Nursing Clinics of North America, 22, 399-41 5. Maklebust, J. (1987). Pressure ulcers: Etiology and prevention. Nursing Clinics of North America, 22, 359-377.
Pinchocofsky-Devin, G. D.,& Kaminski, M. V. (1986). Correlation of pressure sores and nutritional status. Journal of Geriatrics Society, 35,435-440. Ruberg. R. L. (1984). Role of nutrition in wound healing. Surgical Clinics of North America, 64, 705-71 4. Sanders, S. L. (1992). Pressure ulcers, part one: Prevention strategies. Journal of the American Academy of Nurse Practitioners, 4, 6370. Seiler. W. 0. & Stahelin, M. B. (1985). Decubitus ulcers: Treatment through five therapeutic principles. Geriatrics, 40, 30-42. Seiler, W. O., & Stahelin, M. 8. (1989). Decubitus ulceration in the elderly. In Katz, P. R., & Calkins, E. (Eds.), Principles and Practice of Nursing Home Care (pp. 328-348). New York: Springer. Shenaq, S., & Dinh, T. A. (1990). Decubitus ulcers. Postgraduate Medicine, 87, 91-95. Sieggreen, M. Y. (1987). Healing of physical wounds. Nursing Clinics of North America, 22,439-447. Stotts, N. A. (1990). Seeing red and yellow and black-The threecolor concept of wound care. Nursing '90, 20, 59-61, Stotts, N. A., & Whitney, J. D. (1990). Nutritional intake and status of clients in the home with open surgical wounds. Journal of Community Health Nursing, 7, 77-86. Taylor, T., Rimmer, S.Butcher, J., & Dymock, I. (1974). Ascorbic acid supplementation in the treatment of pressure-sores. Lancet, 544, 544-546. Thomason, S. S. (1988). Pressure ulcers: Considerationsof intervention strategies. Ostomyl Wound Management, 27, 48-55. Trelease, C. (1988). Developing standards for wound care. Ostomy/ Wound Management, 28,47-56. Wysocki, A. B. (1989). Surgical wound healing. AORN Journal, 49, 502-51 8.
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