Managing Pressure Ulcers: Practical Guidelines
Course AuthorsDavid Thomas, M.D. Professor of Medicine (Geriatrics), Saint Louis University School of Medicine. Dr. Thomas reports no commercial conflict of interest. Estimated course time: 1 hour(s). Albert Einstein College of Medicine – Montefiore Medical Center designates this enduring material activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. In support of improving patient care, this activity has been planned and implemented by Albert Einstein College of Medicine-Montefiore Medical Center and InterMDnet. Albert Einstein College of Medicine – Montefiore Medical Center is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.  
Learning Objectives
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Managing pressure ulcers is often frustrating for clinicians. First, there has been a lack of consensus about the best treatment options. For example, among 85 specific recommendations published by the Agency for Healthcare Policy & Research, only four level A recommendations (two or more randomized controlled clinical trials) and ten level B recommendations (two or more controlled trials in humans or animals) were made.(1) Second, pressure ulcers are difficult to heal. As few as 13% of pressure ulcers heal by two weeks in acute hospital settings.(2),(3) Healing rates at six months for Stage III pressure ulcers may be as high as 59%, but other patients require treatment for up to one year. Only one-third of Stage IV pressure ulcers heal after six months of therapy.(4) Given the clinical challenges of managing pressure ulcers, a careful treatment approach is necessary and it depends on a stepwise clinical plan. AssessmentCo-morbidityThe first step in ulcer management begins with an evaluation of the general status of the patient. The presence of co-morbid conditions, such as diabetes, peripheral vascular disease, congestive heart failure or limitations to mobility, require adjustments to the treatment plan. Risk for development of pressure ulcers can be predicted by co-morbidity or by using a formal instrument, such as the Braden or Norton scale. Nutritional AssessmentMalnutrition is not good for anyone. Dietary protein appears to be especially important in healing pressure ulcers. Pressure ulcers have shown a greater rate of healing with an enteral feeding containing 24% protein compared to 14% protein. However, changes in body weight or in biochemical parameters of nutritional status did not occur between groups.(5) In twelve enterally-fed patients receiving a formula containing either 17% or 25% of calories as protein, the group that were given higher protein had greater improvement. Those receiving 1.8 g/kg of protein had a 73% improvement in pressure ulcer surface area compared to a 42% improvement in surface area in the group given 1.2 g/kg of protein.(6) Optimum dietary protein intake in patients with pressure ulcers is unknown but may be much higher than current adult recommendations of 0.8 g/kg/day. A reasonable protein requirement is, therefore, between 1.25-1.50 g/kg/day. The deficiency of several vitamins has significant effects on wound healing but it is difficult to demonstrate a relationship between vitamin malnutrition and clinical outcome. In patients at risk for development of pressure ulcers, the calculated intake of vitamins C and A, zinc or iron did not predict ulcer development.(7) High doses of vitamin C have not been shown to accelerate wound healing.(8) Zinc supplementation has not been shown to accelerate healing except in zinc deficient patients.(9) High serum zinc levels interfere with healing and supplementation above 150 mg/day may interfere with copper metabolism.(10),(11) When documented or suspected vitamin and mineral deficiencies exist, supplementation may be indicated. Pain AssessmentExcept in neurologically impaired patients, chronic ulcers are painful. Each patient should be assessed for pain control and oral or parenteral pain medications should be used to control symptoms. Wound AssessmentThe location, size, presence of necrosis or exudate and the degree of granulation tissue and epithelization affect treatment decisions. A clinical staging protocol should be used. The most common staging protocol, recommended by the National Pressure Ulcer Advisory Panel and used in OBRA nursing home guidelines, derives from a modification of the Shea Scale.(12) Under this schematic, pressure ulcers are divided into four clinical stages. Four-Part Clinical StagingA Stage I pressure ulcer is defined by non-blanchable erythema of intact skin. The first response of the epidermis to pressure is hyperemia. Blanchable erythema occurs when capillary re-filling occurs after gentle pressure is applied to the area. Non-blanchable erythema exists when pressure of a finger in the reddened area does not produce blanching or capillary re-filling. Non-blanchable erythema is believed to indicate extravasation of blood from the capillaries. Diagnosing Stage I pressure ulcers in darkly pigmented skin is problematic. In persons with darker skin, discoloration, warmth, edema, or induration may indicate a Stage I pressure ulcer. Stage II ulcers involve the epidermis or dermis. The ulcer is superficial and presents clinically as an abrasion, blister, or shallow crater. Stage III pressure ulcers show full thickness skin loss involving damage or necroses of subcutaneous tissue that may extend down to, but not through, underlying fascia. Stage IV pressure ulcers are full-thickness wounds with extensive destruction, tissue necrosis or damage to muscle, bone or supporting structures. Undermining and sinus tracts may be associated with Stage IV pressure ulcers. No ulcer covered by eschar can be accurately staged until the eschar is removed. Healing of pressure ulcers occurs by contraction and scar tissue formation. The original architecture of the skin is not replaced as the pressure ulcer heals. Thus, the modified Shea scale cannot be used to describe improvement deterioration of pressure ulcers. A validated instrument to measure change in ulcer status over time, the Pressure Ulcer Scale for Healing, has been developed to aid in assessment.(13) Managing Tissue LoadsPositioningPressure relief is critical in the management of pressure ulcers. When the head of the bed is elevated, sacral pressure increases dramatically. Elevation of the head of the bed completely negates all pressure reducing devices and should be minimized. Heels and trochanters are particularly susceptible to pressure but removing pressure from the heel and trochanteric areas is difficult. Support SurfacesPressure-relieving devices have a therapeutic role in treating pressure ulcers. Support surfaces and mattress overlays can be divided into static or dynamic types. When the patient can re-position without assistance, a static surface can be effective. If the patient is unable to spontaneously re-position, a dynamic surface is required. No significant difference in pressure ulcer outcome has been shown among available static support surfaces. The choice is based on ease of use, durability or caregiver preference. Dynamic support surfaces use inflatable compartments to alternate pressure reduction. Two special dynamic devices include low-air loss beds and air-fluidized beds. Studies have shown that these devices are effective but expense often limits their use. Low-air-loss beds produced substantial improvement in ulcer size (9.0 v. 2.5 mm(2) per day) compared to a 10 cm convoluted foam mattress in nursing home patients.(14) In 95 nursing home patients with severe pressure ulcers treated on air-fluidized beds, 14% of pressure ulcers healed in a mean of 79 days. Forty-four percent of patients had greater than 50% reduction in surface area of the index ulcer. Very few patients had a reduction in ulcer surface area after one month of treatment on the specialized bed. The median length of time-to-healing was 119 days. The additional cost for the bed was $50-$100 per day.(15) Definition of a low-air loss bed or device varies among vendors, ranging from simple air pumps to provide flow around a patient to large-fan blowers that suspend the patient on cushions of air. When patients with pressure ulcers in an acute hospital setting were randomized to air-fluidized therapy or a vinyl alternating-air mattress, patients treated on air-fluidized beds had a greater decrease in ulcer size over a mean of 15 days. However, there was no difference in the number of ulcers showing a size reduction of at least 50%. The cost was estimated at an additional $80 per day.(15) SittingPatients who have pressure ulcers on sitting interfaces should not sit. All patients who sit for extended periods should have a pressure-reducing cushion. Even in the presence of a cushion, patients should be re-positioned hourly to relieve tissue loads. Managing the UlcerDebridementNecrotic debris increases the possibility of bacterial infection and delays wound healing.(16) The preferred method of debriding the wound remains controversial. Options include mechanical debridement with gauze dressings, sharp surgical debridement, autolytic debridement with occlusive dressings or application of exogenous enzymes. Unless clinically infected, heel ulcers occur in poorly vascularized tissues and are better left undebrided. Surgical sharp debridement produces the most rapid removal of necrotic debris and is required in the presence of infection. Mechanical debridement also can be accomplished by allowing saline gauze to dry before removal. Re-moistening of gauze dressings in an attempt to reduce pain at dressing changes can defeat the debridement effect. Thin portions of eschar can be removed by occlusion under a semi-permeable dressing. Thicker eschar can be loosened under occlusion for several days before surgical debridement. Both autolytic and enzymatic debridement require periods of several days to several weeks to achieve results. Penetration of enzymatic agents is limited in eschar and requires either softening by autolysis or cross-hatching by sharp incision prior to application. Enzymes evaluated in pressure ulcer trials include streptokinase/streptodornase (SK/SD) combination, collagenase, papain and trypsin. Collagenase reduced necrosis, pus and odor, compared to inactivated control ointment,(17) and produced debridement in 82% of pressure ulcers at four weeks compared to petrolatum.(18) Papain produced measurable debridement in four days compared to the control vehicle ointment.(19) Trypsin in balsam of Peru and castor oil was not better than mechanical gauze debridement.(20) Wound CleansingAlthough the guidelines recommend cleansing with each dressing change, cleansing the wound results in mechanical and chemical trauma. When and how to clean the wound remains controversial. Normal saline without preservative is the best agent for wound cleaning. Any chemical cleansing agent will delay epithelization but some are worse than others. Antiseptic agents are toxic to fibroblasts, including BetadineTM, HibiclensTM, pHisoHexTM, benzalkonium chloride, GranulexTM, acetic acid, and Dakien's solution.(4) Other commercial cleansing agents containing preservatives may be cytotoxic. All mechanical or chemical cleaning agents should be discontinued when the wound is clean. Wound DressingsA moist wound environment is essential to promote cellular migration and tissue repair. Moist wound healing allows experimentally-induced wounds to resurface up to 40% faster than air-exposed wounds.(21) Any therapy that dehydrates the wound, such as dry gauze, heat lamps, air exposure, or liquid antacids, is detrimental to chronic wound healing.(22),(23),(24),(25) The rapid development of topical wound dressings in the last 20 years has left the physician with a confusing number of choices. Saline-moistened gauze that is not allowed to dry is an effective wound dressing. When moist saline gauze has been compared to occlusive-type dressings, healing of pressure ulcers has been similar with both dressings.(26),(27),(28) The use of occlusive-type dressings has been shown to be more cost effective than traditional dressings, primarily due to a decrease in nursing time for dressing changes.(29) Occlusive dressings can be divided into broad categories of polymer films, polymer foams, hydrogels, hydrocolloids, alginates and biomembranes. Each has several advantages and disadvantages. No single agent is perfect. Comparative qualities among available agents are shown in Table 1.(30),(31) All of the occlusive dressings offer pain relief. Only absorbing granules or polymers fail to reduce pain. Polymer films are impermeable to liquid but permeable to gas and moisture vapor. Because of low permeability to water vapor, these dressings are not dehydrating to the wound. Non-permeable polymers, such as polyvinylidine and polyethylene, can be macerating to normal skin. Most films have an adhesive backing that may remove epithelial cells when the dressing is changed. Polymer films do not eliminate deadspace and do not absorb exudate. Hydrogels are hydrophilic polymers that are insoluble in water but absorb aqueous solutions. They are poor bacterial barriers and are non-adherent to the wound. Because of their high specific heat, these dressings are cooling to the skin, aiding in pain control and reducing inflammation. Most of these dressings require a secondary dressing to secure them to the wound. Hydrocolloid dressings are complex dressing similar to ostomy barrier products. They are impermeable to moisture vapor and gases and are highly adherent to the skin. Their adhesiveness to surrounding skin is higher than some surgical tapes but they are non-adherent to wound tissue and do not impair epithelization of the wound. The adhesive barrier is frequently overcome in highly exudative wounds. Hydrocolloid dressings cannot be used over tendons or on wounds with eschar formation. Several of these dressings include a foam padding layer that may reduce pressure to the wound. Only the hydrocolloid and biomembranes offer bacterial resistance. The biomembranes are very expensive and not readily available. Alginates are complex polysaccharide dressings that are highly absorbent in exudative wounds. This high absorbency is particularly suited to exudative wounds. Alginates are non-adherent to the wound but if the wound is allowed to dry, damage to the epithelial or granulation tissue may occur with removal. Dressings differ in the ease of application. This difference is important in pressure ulcers in difficult locations, such as bony contours, or when considering for home care. Hydrocolloid dressings should be left in place until wound fluid is leaking from the sides, a period of days to three weeks. Adjunctive TherapiesElectrotherapy has been used for Stage III and IV pressure ulcers unresponsive to conventional therapy. Several clinical trials suggest that this therapy is likely to be effective. Hyperbaric oxygen, vacuum therapy, warmth, infrared, ultraviolet and low-energy laser irradiation and ultrasound have insufficient data to recommend their use currently. No data supports the use of systemic vasodilator, hemorrheologics, serotonin inhibitors or fibrolytic agents in the treatment of pressure ulcers. Topical agents, such as zinc, phenytoin, aluminum hydroxide, honey, sugar, yeast, aloe vera gel or gold, have not been demonstrated to be effective in clinical trials. Growth factors have shown promising results in diabetic ulcers but are not recommended presently for use in pressure ulcers. SummaryPressure ulcers remain recalcitrant wounds in debilitated patients. Preventive strategies, detailed in the AHCPR prevention of pressure ulcers guideline,(32) are the most effective interventions. Much controversy remains. A number of clinically important questions lack definitive research for resolution. A stepwise approach can help promote an understanding of these complex wounds. |