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Pressure ulcer management includes debridement of necrotic tissue, management of infection and biofilms, adequate wound cleansing, and application of appropriate topical therapy. Wound debridement is necessary to reduce the necrotic tissue burden, decrease risk for infection, and promote granulation tissue formation. Benefits of debridement also may include removal of senescent fibroblasts and nonmigratory hyperproliferative epithelium, and stimulation of blood-borne growth factor production. Debridement is not indicated for dry eschar presenting on the heel or when the pressure ulcer presents on an ischemic limb.
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Five methods of debridement (eg, surgical or sharp, mechanical, autolytic, enzymatic, biosurgical) are available. Choice of debridement method is based on clinician preference and availability rather than specific evidence. Clinical practice guidelines on pressure ulcer treatment recommend wound debridement with surgical or sharp debridement for extensive necrosis or when obtaining a clean wound bed quickly is important and more conservative methods (autolytic and enzymatic) for those in long-term care or home care environments. Adequate wound debridement is essential to wound bed preparation and healing. Initial debridement with additional debridement at intervals is often necessary to maintain a biofilm-free wound bed and support healing.
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Sharp debridement involves use of a scalpel, scissors, or other sharp instruments to remove nonviable tissue. It is the most rapid form of debridement, and it is indicated over other methods for removing thick, adherent, and/or large amounts of nonviable tissue and when advancing cellulitis or signs of sepsis are present. Health care professionals who use sharp debridement must demonstrate their competency in sharp wound debridement skills and meet licensing requirements. One multicenter, randomized, controlled trial comparing the effects of topical growth factor versus placebo on healing noted that independent of treatment effects, centers that used sharp debridement more frequently experienced better healing rates than those that used sharp debridement less frequently. Sharp debridement is rapid, but is also considered nonselective as viable tissues may be inadvertently removed along with necrotic tissue.
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Mechanical debridement involves the use of wet-to-dry dressings, whirlpool, lavage, or wound irrigation. Wet-to-dry gauze dressings continue to be used for debridement, despite the significant disadvantages of increased time/labor for application/removal of the dressings, removing viable tissue as well as nonviable tissue, and pain. This method of debridement should be used cautiously, as it can traumatize new granulation tissue and epithelial tissue, and adequate analgesia should be administered when this method is employed. It is not recommended in clinical practice guidelines.
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Enzymatic debridement involves applying a concentrated, commercially prepared enzyme to the surface of the necrotic tissue, in the expectation that it will aggressively degrade necrosis by digesting devitalized tissue. The main enzyme ointment available in the United States is collagenase. Some of the effects noticed with enzymatic agents have been attributed to autolysis. Enzymatic ointments have yielded consistently positive results for their efficacy in wound debridement. Debridement with enzymatic ointments is faster than with autolysis, and more conservative than sharp debridement.
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Autolytic debridement is the process of using the body’s own mechanisms to remove nonviable tissue. Maintaining a moist wound environment allows collection of fluid at the wound site, which allows enzymes within the wound fluid to digest necrotic tissue. Autolytic debridement typically involves adequate wound cleansing to wash out the partially degraded nonviable tissue. It is more effective than wet-to-dry gauze dressings, as it selectively removes only the necrotic tissue and therefore protects healthy tissues. Autolytic debridement may be slower to achieve a clean ulcer bed than other methods.
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Biosurgery is the fifth method of debridement. Biosurgery is the application of maggots (disinfected fly larvae, Phaenicia sericata) to the wound typically at a density of 5 to 8/cm2. Comparative controlled studies evaluating the use of maggot therapy for pressure ulcer debridement have shown a higher proportion of complete debridement in maggot-treated wounds versus standard debridement therapy (80% vs 48%, respectively). Biosurgery may not be acceptable to all patients, and may not be available in all areas.
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Pressure ulcers are the result of ischemia and as such, they are more susceptible to infection. Stage 3, 4, and unstageable pressure ulcers should be evaluated for infection. One difference in dealing with infection in chronic wounds such as pressure ulcers compared to acute wounds is the assessment and treatment of bacterial biofilms. Biofilms are the critical colonization of microorganisms on the wound bed that develop support structures that protect the bacteria. Biofilms cause chronic inflammation and have enhanced resistance to endogenous antibodies and phagocytic cells and exogenous antibiotics and antimicrobial solutions. Approximately 60% of chronic wounds contain bacterial biofilms, and this may be the underlying pathology preventing wounds like pressure ulcers from healing. Biofilm presence in pressure ulcers should be suspected when any of the following exist:
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Lack of signs of healing for 2 weeks with appropriate care
Friable granulation tissue
Odor
Increased pain, heat, exudate, or necrotic tissue
Change in exudate character
Pocketing or tunneling in the wound bed
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Bacterial burden of the pressure ulcer should be determined by tissue biopsy or quantitative swab technique (do not swab necrotic tissue or exudate, rotate end of swab over 1 cm2 area for 5 seconds with sufficient force to cause tissue fluid expression). Use of antiseptic solutions for a course of therapy may be beneficial in reducing and/or preventing bacterial biofilms and supporting granulation tissue development and wound healing.
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The best method of preventing biofilm development is adequate, timely, and complete debridement of necrotic tissue followed by appropriate topical therapy.
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Pressure ulcer cleansing at each dressing change is recommended in clinical practice guidelines on pressure ulcer treatment. However, there is evidence that antiseptic solutions such as 5% mafenide acetate (Sulfamylon solution), 10% povidone with 1% free iodine (Betadine), 0.25% sodium hypochlorite (“half strength” Dakin solution), 3% hydrogen peroxide, and 0.25% acetic acid have varying effects on wound healing parameters as well as antimicrobial management in an animal wound model yet, how this affects human wounds is unclear.
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Use of antiseptic and antimicrobial solutions for cleansing clean pressure ulcers is not indicated based on in vitro studies of the toxicity of topical wound cleansers. Findings from in vitro studies have not been confirmed in human wounds. Use of antiseptic and antimicrobial solutions for cleansing pressure ulcers with necrotic debris should be employed thoughtfully with attention to the solution chosen, the characteristics of the microorganisms present in the wound, and duration of use (eg, course of therapy for 2 weeks with evaluation for continuation at that time).
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In general, if an ulcer contains necrotic debris or is infected, then antimicrobial activity is more important than cellular toxicity. The chemical and mechanical trauma of wound cleansing should be balanced by the dirtiness of the wound. For wounds with large amounts of debris, more vigorous mechanical force and stronger solutions may be used, while for clean wounds, less force and physiologic solutions such as normal saline should be used.
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Topical therapy for pressure ulcers should be provided using moist wound healing dressings. Randomized controlled trials as well as several comparative studies provide compelling support for use of moist wound healing dressings instead of any form of dry gauze dressings (eg, wet-to-dry gauze, dry gauze dressing, or impregnated gauze dressing) for pressure ulcers. Moist wound healing allows wounds to re-epithelialize up to 40% faster than wounds left open to air. Controlled trials suggest that the use of semiocclusive dressings such as transparent films and hydrocolloid dressings improves healing of stage 2 pressure ulcers. These dressings are changed every 3 to 5 days, which allows wound fluid to gather underneath the dressing, facilitating epithelial migration. Moderate evidence exists to specifically support use of hydrocolloid dressings for pressure ulcer care in stage 3/4 pressure ulcers. One multicenter, randomized trial demonstrated faster healing in stage 3/4 pressure ulcers when treated sequentially with calcium alginate dressings followed by hydrocolloid dressings versus nonsequentially with hydrocolloid dressings. However, the relative merits of different categories of moisture retentive dressings versus another remain unclear. Table 52-2 presents general characteristics of moisture retentive dressing categories.
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Evidence supporting use of advanced wound therapy in pressure ulcers is unclear. There is some evidence supporting use of negative pressure wound therapy (NPWT) in large stage 3 and 4 nonhealing pressure ulcers with poor granulation tissue or excess exudate. Several clinical practice guidelines and panels have recommended use of NPWT with large stage 3 and 4 pressure ulcers that have failed to improve with standard care with moist wound healing. A case series of 10 patients with stage 4 pressure ulcers treated with NPWT showed greater than 50% average reduction in wound volume and depth (55% and 61%, respectively) over 4 weeks. Some have suggested that NPWT use should result in pressure ulcer improvement within a 2-week time period with further use questionable if improvement is not evident. Use of skin and tissue substitutes has not been examined specific to pressure ulcers but may be of benefit in certain populations with full-thickness ulcers.
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Surgical treatment of pressure ulcers includes primary closure, a variety of approaches to skin grafts and myocutaneous flaps, and removal of underlying bony prominences. In patients with large infected pressure ulcers, more aggressive procedures such as amputation and hemicorporectomy are sometimes required. Surgical complication rates (including dehiscence, infection, necrosis, and hematoma) for both younger paraplegic patients and nonparaplegic elders are as high as 50%, and pressure ulcer recurrence at the same site has been reported ranging from 30% to 70%. Thus, the long-term outcomes have not been ideal even though 70% to 80% of surgically treated pressure ulcers are healed upon discharge from the hospital. Further, while recurrence of pressure ulcers at the same site is lower for elders (40%) compared to younger paraplegic patients (more than 70%), 30% of elders develop new ulcer sites, and mortality in elders ranges from nearly 50% to 68%.
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Thus, the benefits of surgical closure for pressure ulcer are uncertain. In addition to questions about the efficacy of surgical intervention, geriatric patients present with multiple chronic diseases and conditions that may make them less than ideal surgical candidates or affect rehabilitation efforts after surgery.
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Pharmacologic interventions for pressure ulcers focus on antibiotics and pain management. Antibiotics may be systemic or local. Clinicians should institute systemic antibiotics for patients exhibiting signs and symptoms of systemic infection such as sepsis or cellulitis with associated fever and an elevated white blood cell count. Systemic antibiotics should be initiated for osteomyelitis or for the prevention of bacterial endocarditis in persons with valvular heart disease and who require debridement of a pressure ulcer. Because of the high mortality of sepsis associated with pressure ulcers despite appropriate antibiotics, broad-spectrum coverage for aerobic gram-negative rods, gram-positive cocci, and anaerobes is indicated pending culture results in patients with suspected bacteremia. Ampicillin-sulbactam, imipenem, meropenem, ticarcillin-clavulanate, piperacillin-tazobactam, and a combination of clindamycin or metronidazole with ciprofloxacin, levofloxacin, or an aminoglycoside are appropriate choices for initial antibiotic therapy. Vancomycin may be required for MRSA.
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Use of cadexomer iodine (not the same as povidone iodine) topical dressings has been shown to be effective for pressure ulcers colonized with MRSA. The most effective strategy for preventing infection and dealing with existing infection is adequate and full debridement of necrotic tissue followed by additional debridement to remove and prevent bacterial biofilm development. In patients with signs and symptoms of systemic infection and in those who are septic, the appropriate debridement method is surgical debridement.
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Topical antibiotics are most appropriate for stage 3 or 4 ulcers when there is evidence of local infection such as erythema surrounding a clean nonnecrotic wound, failure to improve with adequate treatment, or friable granulation tissue. A 2-week trial of a broad- spectrum topical antibiotic can be considered for clean pressure ulcers that are not healing after 2 to 4 weeks of optimal management. Use of cadexomer iodine dressing or cleansing with hypochlorous acid solution may also be appropriate in this situation. On the other hand, clinicians should not use povidone-iodine, iodophor, sodium hypochlorite, hydrogen peroxide, or acetic acid as topical therapies on clean pressure ulcers. These antiseptic agents have been shown to be toxic to fibroblasts and to impair wound healing in in vitro laboratory studies, and how these solutions affect human wounds is unclear. There is no evidence for using prolonged silver release dressings in routine management of healing pressure ulcers.
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There is limited evidence to guide clinicians on appropriate management of pressure ulcer–related pain. The pressure ulcer alone may not require routine pain medication, but medication prior to procedures is essential. Lower levels of pain may be manageable with appropriate wound dressing choice and topical wound analgesia. Nonpharmacologic techniques useful for noncyclic and cyclic wound pain associated with procedures (eg, debridement, dressing changes, repositioning) include use of distraction (eg, talking to the patient while performing the procedure), allowing the patient to call a “time-out” during the procedure, and allowing the patient to control and participate in the procedure.
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Pressure ulcer–related pain can be minimized by keeping the pressure ulcer wound bed moist and covered. Use of hydrogels, hydrocolloids, alginates, polymeric membrane foams, and soft silicone dressings allows for less frequent dressing changes, and less trauma and pain on removal as they are nonadherent to the wound bed.
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Pharmacologic strategies for wound pain include providing opioids and/or nonsteroidal anti-inflammatory drugs (NSAIDs) 30 minutes prior to the procedure and afterward, and administering topical anesthetics or topical opioids using hydrogels as a transport media. Two options have been successful for use in chronic wound pain, EMLA cream and diamorphine gel. EMLA cream (eutectic mixture of lidocaine 2.5% and prilocaine 2.5%) reduces debridement pain scores in chronic venous ulcers, and may have a vasoactive effect cutaneously. Use of EMLA cream in venous ulcers has been associated with a reduction in pain scores (measured on a 100-mm scale) of 20.6 mm. Low-dose topical morphine (diamorphine) has been used in several small, randomized, placebo-controlled studies to successfully control pressure ulcer–related pain.
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Multiple studies have demonstrated a relationship between different markers of malnutrition (eg, serum albumin level, dietary protein intake, inability to feed self, and weight loss) and pressure ulcer formation. Other studies have demonstrated that the severity of the pressure ulcer is associated with the severity of the malnutrition. Malnutrition and/or weight loss has been associated with fourfold higher risk of pressure ulcer development. Although it seems intuitive, it has proven difficult to define a specific causal relationship between malnutrition and pressure ulcer development. Modest evidence exists to support providing oral nutritional supplements to persons at risk for pressure ulcers with relative reduction in pressure ulcer incidence of 25%. Moderately strong evidence exists that use of high-protein nutritional supplements (24%–25% protein) improves pressure ulcer healing. Providing 30 to 35 kcal/kg and 1.25 to 1.5 g/kg of calories and protein daily has been shown to significantly improve pressure ulcer healing. However, provision of nutritional supplementation by tube-feeding to persons with pressure ulcers has not achieved positive results.
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No evidence exists for use of supplemental vitamins or minerals (eg, vitamin A, E, C, zinc) in persons with pressure ulcers with no coexisting specific vitamin/mineral deficiency to improve pressure ulcer healing. Moderate evidence exists to support use of high-calorie, high-protein nutritional supplements containing arginine to promote pressure ulcer healing in older adults in general (significant decrease in ulcer size at 8 weeks favoring supplement), older adults who do not have preexisting malnutrition (significant decrease in ulcer size and PUSH score over 8 weeks favoring supplement), and persons with SCI (10 vs 21 weeks to healing favoring supplement). Persons with pressure ulcers or at risk of developing pressure ulcers who also demonstrate malnutrition should have a standard nutritional assessment to identify deficits and nutrition support as indicated. A daily multivitamin and mineral supplement that provides recommended daily allowances of vitamins and minerals is recommended for persons with suspected nutritional deficiencies.