204 Pressure Ulcers
Epidemiology
A pressure ulcer is any wound that develops in the upper, outer layers of the skin as a result of sustained, external pressure.1 Pressure ulcers are serious complications among hospitalized patients. They increase healthcare costs, decrease patient quality of life, and often result in prolonged hospital stays. Current estimates of the prevalence of pressure ulcers among hospital patients vary. A recent analysis of acute care hospitals in the United States estimated a prevalence of 14% to 17% among hospitalized patients.2 Another recent Canadian study estimated that one out of four patients will develop a pressure ulcer during the course of their hospital stay.3 The prevalence of pressure ulcers is even higher among residents of long-term geriatric facilities, occurring in up to 30% of patients. Whereas the majority of the ulcers (50%) in hospitalized patients are stage 1, the prevalence of stage 3 and 4 ulcers is estimated to be as high as 4% in patients who reside in long-term care facilities.
Classification
All pressure ulcers begin in the outer layers of the skin. With ongoing pressure, the ischemia progressively extends to deeper layers of the skin. Therefore, the classification of pressure ulcers is based upon the depth of skin involvement. Pressure ulcers are classified as stage I through IV, with stage I being the most superficial, and stage IV being the deepest. The classification of pressure ulcers is listed in Table 204-1. Having a uniform, well-defined classification system for pressure ulcers is critical. It not only allows for standardization of wounds for research purposes but also allows for accurate communication of wound staging among healthcare providers. Once a pressure ulcer develops, it is important to classify the wound and monitor the progress of the wound bed. Having a standard grading system allows for continuity of care and objective monitoring of the progression of the wound.
National Pressure Ulcer Staging System | |
Stage I | Nonblanching erythema of intact skin |
Stage II | Partial-thickness skin loss involving the epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater. |
Stage III | Full-thickness skin loss with damage and/or necrosis of the subcutaneous tissue. The wound extends down to but not through the underlying fascia. |
Stage IV | Full-thickness skin loss with extensive destruction and necrosis of overlying structures including muscles, bone, or tendon |
Prevention
Risk Assessment
Prevention programs should include an initial risk assessment of the individual patient. This assessment should include questioning about previous or preexisting pressure ulcers, a thorough skin inspection, evaluating the patient’s mobility/activity level, continence, nutritional status, and a review of comorbid conditions that may contribute to the development of pressure ulcers. Assessment of these risk factors should be standardized and documented on all patients. Several tools have been developed for pressure ulcer risk assessment. The Braden Scale assesses external pressure forces and skin-related factors in a standardized fashion.4 The Norton Scale assesses patient-specific risk factors (age, cognitive impairment, mobility, incontinence) for pressure ulcer development.5 The Waterlow Scale assesses both intrinsic and extrinsic risk factors and was initially developed for use in the pediatric population.6
Prevention Plan
Once the individual patient risk assessment has been addressed, a plan for pressure ulcer prevention should be implemented. Regardless of the plan utilized, a frequent assessment of its efficacy must be performed and any necessary adjustments made. The key elements of prevention include patient mobilization, patient positioning to prevent/remove pressure, and the use of positioning aides to redistribute pressure. Among critically ill patients, this requires vigilance and team effort, particularly among those patients who are sedated for prolonged periods of time. Prevention also includes avoidance of skin damage by shearing forces and avoidance of maceration of the skin due to moisture from incontinence and heat accumulation. There are a variety of support services available to help decrease the risk of pressure ulcer formation. These pressure-reducing surfaces include static support surfaces (mattresses, mattress overlays) and dynamic support surfaces that mechanically alter the amount of pressure applied to the patient’s skin. Examples of dynamic support surfaces include low-air-loss beds, air-fluidized mattresses, and alternating pressure mattresses. The use of foam mattress overlays can reduce the risk of pressure ulcer development in high-risk populations.7 Although associated with higher costs, dynamic mattresses have not consistently been shown to be superior to static support surfaces. However, dynamic mattresses are better than standard hospital mattresses in preventing pressure ulcer formation.
Treatment
Wound Débridement
Débridement of the wound bed is a critical step in the healing process of pressure ulcers. The purpose of débridement is to remove foreign material and devitalized tissue from the wound. After débridement, a wound bed of healthy tissue should be visible. Débridement of the wound bed reduces the production of inflammatory mediators that inhibit wound healing. There are a variety of techniques utilized for wound débridement. These include surgical débridement, hydrotherapy, larval therapy, and application of topical enzymatic débridement solutions. The choice of débridement techniques utilized depends on multiple factors including the size of the wound, comorbid conditions, and the presence of infection. Surgical débridement is most often required in large-volume wounds when extensive tissue débridement is needed. However, surgical débridement requires the patient be a suitable candidate for general anesthesia. The risk of subjecting a critically ill patient to general anesthesia and a trip to the operating room must be weighed against the benefits of sharp surgical débridement of a pressure ulcer. Hydrotherapy, while commonly practiced, has not been rigorously evaluated in the setting of a large randomized controlled trial. However, some small studies of patients with stage III or IV pressure ulcers have demonstrated faster wound healing among patients receiving hydrotherapy as compared to those who did not receive hydrotherapy.8,9
Larval therapy, also referred to as biosurgery, has been used for débridement of pressure ulcers. The basic concept of larval therapy is that application of larvae to wounds results in rapid débridement of necrotic tissues, with avoidance of the potential complications of surgical débridement such as pain and bleeding. Currently, there is evidence that compared to topical enzymatics, larval therapy significantly reduces the time to débridement of necrotic tissue. However, the use of larval therapy did not appear to have any effect on time to wound healing.10
A variety of topical enzymatic débridement products are commercially available. These can be used alone or in conjunction with other débridement techniques. These agents are applied directly to the wound bed once or twice a day. Multiple randomized controlled trials have validated the efficacy of topical enzymatic débridement products for the removal of necrotic tissue from the wound bed.11 Prior to applying these agents, the wound bed should be cleansed with normal saline. The presence of any topical wound products containing metal will diminish the efficacy of topical enzymatics, and removing these agents from the wound bed is critical for the success of the enzymatics. In the event an eschar is overlying the wound bed, it is recommended that the eschar be cross-hatched with a surgical blade to allow for penetration of the topical enzymatic agent. Once applied, the wound bed should be covered with gauze. These agents are a viable and valuable therapy, particularly in those patients who are not candidates for alternative débridement methods.
Hydrocolloids
Hydrocolloid dressings are widely used in the management of pressure ulcers; their purpose is to absorb wound exudates. Typical hydrocolloid dressings contain some type of gel-forming agent placed in contact with the wound bed, and this is covered with a membrane that protects the wound against external contamination but allows for water evaporation.12 Hydrocolloid dressings are typically applied every 3 to 5 days, depending upon the amount of exudates being produced by the wound. When compared to standard gauze dressings, hydrocolloids have been shown to be more absorptive and less painful.12
Negative Pressure Therapy
The use of negative pressure therapy for wound healing has become increasingly common in the past decade. The basic concept behind this therapy is that applying negative pressure to the wound bed both removes edema fluid and increases blood flow to the area. Increased blood flow results in delivery of oxygen and nutrients which promote wound healing. In addition, the application of negative pressure to the wound results in wound contracture. Compared to standard wet-to-dry dressings, another benefit to patients of negative pressure therapy is decreased frequency of dressing changes. The use of negative pressure therapy for pressure ulcers has been associated with improved wound healing and decreased length of hospital stay.13 Traditionally, negative pressure therapy has been applied to clean wounds that had very little slough or necrotic tissue. However, there is some evidence that the application of negative pressure therapy to wounds that are covered with soft necrotic tissue is a viable option.14
Nutritional Support
The presence of malnutrition has a significant impact on wound healing. In fact, its mere presence results in weakening of the skin and increases the risk of pressure ulcer development. Unfortunately, nutritional assessment is often neglected, particularly in chronically institutionalized patients. Establishing nutritional assessment protocols as well as treating malnutrition are essential in preventing and healing pressure ulcers. This is best accomplished by a multidisciplinary team that includes physicians, dieticians, and nursing staff.15
Anders J, Heinemann A, Leffmann C, et al. Decubitus ulcers: pathophysiology and primary prevention. Dtsch Arztebl Int. 2010;107:371-381. quiz 382
Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA. 2006;296:974-984.
Bergstrom N, Demuth PJ, Braden BJ. A clinical trial of the Braden Scale for Predicting Pressure Sore Risk. Nurs Clin North Am. 1987;22:417-428.
Heyneman A, Beele H, Vanderwee K, Defloor T. A systematic review of the use of hydrocolloids in the treatment of pressure ulcers. J Clin Nurs. 2008;17:1164-1173.
Systematic review of commonly used hydrocolloids.
Ramundo J, Gray M. Enzymatic wound debridement. J Wound Ostomy Continence Nurs. 2008;35:273-280.
1 Anders J, Heinemann A, Leffmann C, et al. Decubitus ulcers: pathophysiology and primary prevention. Dtsch Arztebl Int. 2010;107(21):371-381. quiz 382
2 Whittington KT, Briones R. National Prevalence and Incidence Study: 6-year sequential acute care data. Adv Skin Wound Care. 2004;17(9):490-494.
3 Woodbury MG, Houghton PE. Prevalence of pressure ulcers in Canadian healthcare settings. Ostomy Wound Manage. 2004;50(10):22-24. 26, 28, 30, 32, 34, 36-38
4 Bergstrom N, Demuth PJ, Braden BJ. A clinical trial of the Braden Scale for Predicting Pressure Sore Risk. Nurs Clin North Am. 1987;22(2):417-428.
5 Norton D. Norton scale for decubitus prevention. Krankenpflege (Frankf). 1980;34(1):16.
6 Waterlow JA. Pressure sore risk assessment in children. Paediatr Nurs. 1997;9(6):21-24.
7 Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA. 2006;296(8):974-984.
8 Moore Z, Cowman S. A systematic review of wound cleansing for pressure ulcers. J Clin Nurs. 2008;17(15):1963-1972.
9 Burke DT, Ho CH, Saucier MA, Stewart G. Effects of hydrotherapy on pressure ulcer healing. Am J Phys Med Rehabil. 1998;77(5):394-398.
10 Dumville JC, Worthy G, Soares MO, et al. VenUS II: a randomised controlled trial of larval therapy in the management of leg ulcers. Health Technol Assess. 2009;13(55):1-182. iii-iv
11 Ramundo J, Gray M. Enzymatic wound debridement. J Wound Ostomy Continence Nurs. 2008;35(3):273-280.
12 Heyneman A, Beele H, Vanderwee K, Defloor T. A systematic review of the use of hydrocolloids in the treatment of pressure ulcers. J Clin Nurs. 2008;17(9):1164-1173.
13 Baharestani MM, Houliston-Otto DB, Barnes S. Early versus late initiation of negative pressure wound therapy: examining the impact on home care length of stay. Ostomy Wound Manage. 2008;54(11):48-53.
14 Nakayama M. Applying negative pressure therapy to deep pressure ulcers covered by soft necrotic tissue. Int Wound J. 2010. Available at: http://www.ncbi.nlm.nih.gov/pubmed/20455957 Accessed June 25, 2010
15 Barrett R, Tuttle V, Whalen E, Gatchell C, Dawe A. Pressure ulcers and nutritional support: a partnership to improve patient outcomes. J Nurs Care Qual. 2010;25(2):145-150.