Pressure Ulcers

Published on 26/03/2015 by admin

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Last modified 22/04/2025

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204 Pressure Ulcers

image 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.

image Risk Factors

There are multiple risk factors for the development of pressure ulcers; they can be categorized as intrinsic and extrinsic. Intrinsic risk factors are those related to the patient’s preexisting medical condition(s). Extrinsic factors are those related to the patient’s environment. Intrinsic risk factors include neurologic disease, motor impairment, cognitive impairment, sensory deficits, malnutrition, and hypoperfusion due to peripheral vascular disease or congestive heart failure. Extrinsic risk factors include inadequate mobilization by care providers, trauma, sedation, application of physical restraints, improper positioning (especially among patients under general anesthesia), moisture, and shearing forces. Among these risk factors, failure to frequently change position is thought to be the biggest contributor to pressure ulcer formation. The combination of improper positioning and moisture at the skin surface are frequent causes of pressure ulcer formation in critically ill patients.

Because of the underlying pathophysiology of pressure ulcer formation, there are several high-risk areas for the development of pressure ulcers. Pressure ulcers are more prone to develop in bony or cartilaginous areas. These include any area of the body that has limited soft-tissue coverage such as the coccyx, spinous processes, heels, elbows, and ankles. In patients who are mostly positioned on their side, the iliac crest and trochanters are considered high-risk areas. Additionally, patients with malnutrition and subsequent cachexia have significant loss of soft tissue and are more prone to the development of pressure ulcers at any location.

image 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.

TABLE 204-1 Pressure Ulcer Staging

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

image Prevention

Prevention of pressure ulcer formation should be standard practice. This is of particular importance when caring for critically ill patients, because they often possess multiple risk factors for pressure ulcer formation.

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.

image Treatment

A variety of treatment options and products are available for the management of pressure ulcers. Very few of the currently available treatment options have been rigorously evaluated in randomized controlled trials. An in-depth discussion of all the currently available products is beyond the scope of this text, so general classes of treatment options will be discussed rather than specific products.

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.

Annotated References

Anders J, Heinemann A, Leffmann C, et al. Decubitus ulcers: pathophysiology and primary prevention. Dtsch Arztebl Int. 2010;107:371-381. quiz 382

General overview of the pathophysiology of pressure ulcer formation and the basic physiologic principles underlying pressure ulcer prevention measures. Also included are comparisons of the various scoring systems for pressure ulcers and brief explanations for the various preventive measures commonly utilized in clinical practice.

Reddy M, Gill SS, Rochon PA. Preventing pressure ulcers: a systematic review. JAMA. 2006;296:974-984.

Systematic review of the recent literature regarding various clinical practices for pressure ulcer prevention. This article critically evaluates current literature regarding support surfaces, patient positioning, topical therapy, and nutritional supplementation.

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.

Description of the development and validation of the Braden Scale for pressure ulcer risk assessment.

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.

Overview of a variety of enzymatic débridement solutions. This article includes comparisons of various commercially available products and the indications for their use.

References

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.