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Wound healing society 2015 update on guidelines for pressure ulcers

2015; Wiley; Volume: 24; Issue: 1 Linguagem: Inglês

10.1111/wrr.12396

1524-475X

Lisa J. Gould, Mike Stuntz, Michelle Giovannelli, Amier Ahmad, Rummana Aslam, Margaret Mullen‐Fortino, JoAnne D. Whitney, Jason H. Calhoun, Robert S. Kirsner, Gayle M. Gordillo,

Diabetic Foot Ulcer Assessment and Management

The Wound Healing Society guidelines for the treatment of pressure ulcers were originally published in 2006. These guidelines provided recommendations, along with their respective levels of evidence and strength on various categories. Over the last seven years, a great deal of literature regarding these aspects of pressure ulcer management has been published. An advisory panel comprised of academicians, clinicians, and researchers was chosen to update the 2006 guidelines. Members included vascular surgeons, internists, plastic surgeons, anesthesiologists, dermatologists, emergency medicine physicians, and registered nurses, all with expertise in wound healing. The goal of this article is to evaluate relevant new findings, upon which an updated version of the guidelines will be based. In 2006, in an effort to develop guidelines that were could provide clinicians with a reasonable approach to caring for patients, even in the absence of high quality human data, the Wound Healing Society developed guidelines using a different approach to evidence citations and past approaches to evidence-based guidelines. Most past approaches relied only on publications regarding clinical human studies. Laboratory or animal studies were not cited. We have used well-controlled animal studies that present proof of principle, especially when a clinical series corroborated the laboratory results. Because of this variation, a different system was used to grade the weight of evidence supporting a given guideline. The strength of evidence supporting a guideline is listed as Level I, Level II, or Level III. The guideline levels were: Level I: Meta-analysis of multiple RCTs or at least two RCTs supporting the intervention of the guideline. Another route would be multiple laboratory or animal experiments with at least two clinical series supporting the laboratory results. Level II: Less than Level I, but at least one RCT and at least two significant clinical series or expert opinion papers with literature reviews supporting the intervention. Experimental evidence that is quite convincing, but not yet supported by adequate human experience. Level III: Suggestive data of proof of principle, but lacking sufficient data such as meta-analysis, RCT, or multiple clinical series. Since the 2006 guidelines, we sought to capture the highest quality of literature available regarding pressure ulcer diagnosis and treatment using a key word search of Pubed, Embase, and Cochrane Library databases. Similarly, the citations of relevant articles were examined by hand. Key terms were generated from the existing guidelines. In this search as opposed to the previous data collection prior to 2006, we used human and disease specific data and limited to meta-analyses, systematic reviews, randomized controlled trials (RCTs), retrospective series reviews, clinical case series, and expert panel recommendations published between January 2006 and present. References prior to 2006 supporting the original guideline recommendations are not included. Therefore, in some cases no additional updated references were included and the support for the guideline recommendation is based on evidence presented in the 2006 guideline. Therefore, no updated references are presented. It was further limited to only English publications. Any relevant additional references found after the formal search were also included. The findings of these articles have been divided into one or more of the appropriate categories as performed in the original guideline. Each of the guidelines underwent a Delphi consensus among the panel members. Each set was critically evaluated by all panel members. There was a consensus of at least 10 panel members on each individual guideline. The first draft was of the guidelines was presented in 2014 for public comment and subsequent drafts revised based on those comments. The majority of the guidelines had unanimous concurrence. The resultant guidelines for the treatment of pressure ulcers are attached. These are guidelines for treatment. They are intended to guide wound caretakers in choosing the best available options. They are NOT meant to be standards of care. Evidence reference: Preamble: Pressure and compression to soft tissue plays a role in the etiology of pressure ulcers. Patient positioning and selection of support surfaces to reduce pressure-related tissue damage are recognized as important components of a comprehensive treatment strategy. While there are limited definitive studies, the best current evidence and expert opinion suggest the following guidelines: Guideline # 1.1: Establish a repositioning schedule and avoid positioning patients on pressure ulcers and bony prominences. (Level II—no change) Principle: Pressure ulcers are thought to result from hypoperfusion to soft tissues. Compression of soft tissues against a bony prominence may contribute to hypoperfusion. It is reasonable to assume that pressure on an ulcer may result in delayed healing. Patients should be repositioned to relieve pressure over bony prominences. The exact turning interval is not known and is derived empirically. Reductions in pressure ulcers have been achieved, but positioning is not universally effective. Updated Evidence: Guideline #1.2 (revised): Maintain the head of bed at the lowest degree of elevation consistent with medical conditions and other restrictions. Limit the amount of time the head of bed is elevated and elevate only when there is a compelling medical indication (e.g., 1–2 hours after tube feeding or with severe respiratory or cardiac compromise). When possible, the patients' knees should be raised before the head of the bed is raised to reduce shearing forces. (Level III) Principle: Elevation of the head of the bed produces shear and friction forces between the skin and the bed surface. Friction and shear may predispose to the development of pressure ulcers. Updated Evidence: Guideline #1.3 (revised): Assess all patients for their risk of developing a pressure ulcer. Use a pressure reducing surface in those patients at risk. Provide a support surface that is properly matched to the individual's need for pressure redistribution, shear reduction, and microclimate control. (Level I—no change) Principle: When compared with a standard hospital mattress, a meta-analysis looking at randomized controlled trials for higher specification foam support surfaces, found that they reduced the incidence of pressure ulcers by 60%. The goal of using a support surface is to reduce the forces of pressure and friction against the patient's body. Descriptive terms for support surfaces have changed from "static" or "dynamic" options to "reactive" or "active." This is per a joint effort of the National Pressure Ulcer Advisory Panel and the European Pressure Ulcer Advisory Panel in an attempt to clarify and standardize the terminology around support surfaces. Individual patient characteristics will influence the surface selection choice. If the patient "bottoms out," that is, if there is less than one inch of material between the bed and the pressure ulcer when feeling under the support surface with the palm of your hand, the device may be ineffective. Updated Evidence: Guideline #1.4 (revised): A reactive support surface may be appropriate for patients with a pressure ulcer who can assume a variety of positions without placing pressure on the ulcer or "bottoming out." (Level III—decreased) Principle: A reactive support is defined as a powered or nonpowered support surface with the capability to change its load distribution properties only in response to applied loads. Reactive surfaces include foam, air or gel filled devices, as well as low air-loss and air fluidized mattresses or cushions. Rigorous review of clinical data regarding the use of support surfaces for the treatment of pressure ulcers (guideline #1.3 addresses prevention) in the interval since the publication of the original guidelines have concluded that the quality of evidence is not sufficient to demonstrate a clear benefit for any specific type of support surface. The recommendations of Expert Panels are that support surfaces should be viewed as an important component of a comprehensive pressure ulcer treatment program. The strength of evidence has been changed to level III to reflect the current state of knowledge on support surfaces. Updated Evidence: Guideline #1.5 (revised): An active support surface may be appropriate for patients with multiple pressure ulcers, patients with a pressure ulcer who cannot assume a variety of positions in bed, patients who "bottom out" on a reactive surface, or those whose ulcer is failing to progress toward healing. (Level II—decreased) Principle: An active support surface is defined as a powered surface with the capability to change its load distribution properties, with or without applied load. Currently, alternating pressure mattresses are the only type of "active" surfaces available for clinical use. There is evidence from 1 RCT (see Malbain et al.) to support the use of active support surfaces in the treatment of pressure ulcers in patients who have limited mobility. Updated Evidence: Guideline #1.6 (DELETE): In patients with a large stage 3 or 4 pressure ulcer, or multiple pressure ulcers involving several turning surfaces, a low-air loss or air-fluidized bed may be indicated. (Level I—DELETE) Principle: Detailed review of the literature on these types of support surfaces, including all the references cited in the original guidelines, was performed by CMS in 2002 (see Ref. #4). Specifically they found that, "The available evidence is not of adequate quality to reliably conclude that air-fluidized beds are clinically superior to any of the Group 2 support surfaces for the treatment of Stage III or Stage IV pressure ulcers." While, this evidence is not new, it was included to make the updated guidelines consistent with the current state of knowledge Updated Evidence: Guideline #1.7: A patient at risk for a pressure ulcer should avoid prolonged sitting. Postural alignment, distribution of weight, balance, stability, and pressure redistribution should be considered in seated individuals. (Level III—no change) Principle: Tissue compression between the sitting surface and bony prominence should be relieved in at-risk patients. In patients with a pressure ulcer, sitting on the pressure ulcer should be avoided. Updated Evidence: Guideline #1.8: Use a seat cushion based on the needs of the individual who requires pressure redistribution in the sitting position. Avoid using doughnut-type devices. (Level III—no change) Principle: Several seat cushions reduce pressure in seated individuals. Examine seating cushions and devices for "bottoming out." There is insufficient evidence on the value of seat cushions in preventing pressure ulcers. Ring cushions (doughnut-type devices) increase venous congestion and edema. Updated Evidence: Guideline # 1.9 (new): Patients that use a wheelchair as their primary means of mobility should be provided with a wheeled mobility seating assessment and properly fitted wheelchair and seat cushion. (Level III) Principle: The goal of proper fitting is to reduce the forces of pressure and friction and against the patient's body. Postural alignment, distribution of weight, balance, stability, and pressure reduction should be considered in seated individuals. Updated Evidence: Preamble: Protein, carbohydrates, vitamins, minerals, and trace elements are required for wound healing. Nutrition is valued and considered in practice as a significant factor in the prevention and treatment of pressure ulcers. In addition adequate hydration is needed for normal intracellular processes including collagen synthesis. However, there are limited definitive studies documenting the efficacy of nutritional treatments for pressure ulcer healing. Guideline #2.1: Nutritional assessment should be performed on entry to a new healthcare setting and whenever there is a change in an individual's condition that may increase the risk of under-nutrition. (Level II—no change) Principle: Nutrition must be adequate to provide sufficient protein to support the growth of granulation tissue. The patient's weight documented at health care visits or on admission to a clinical setting is a good starting point. Assess body weight regularly and when there is a change in an individual's condition that may increase the risk of under-nutrition. Patients who are overweight or obese may be malnourished as evidenced by levels of nutritional biomarkers that are below normal. Assessment of pre–albumin level (reflecting recent protein consumption) and serum albumin level (reflecting long-term protein consumption) is useful to identify patients who are outside the norm at the time of initial assessment or when patient condition changes. Serum albumin and prealbumin are influenced by factors such as hydration, presence of infection, acute stress and may not reflect actual nutritional deficit, thus should be considered in addition to other assessment parameters. No individual clinical parameter identifies adult malnutrition. Presence of two or more of six parameters is recommended by the Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition for identification of malnutrition: insufficient energy intake, weight loss, loss of muscle mass, loss of subcutaneous fat, localized or generalized fluid accumulation that may mask weight loss, decreased functional status measured by hand grip. Other laboratory values associated with infection; e.g., C-reactive protein, white blood cell count, or blood glucose may be helpful in determining if malnutrition is related to starvation, chronic disease or acute disease/injury. Resting energy expenditure is increased in patients with pressure ulcers while at the same time energy intake may be inadequate. Standard clinical approaches to determine energy requirements may underestimate actual need. Therefore, calculation of intake (kcal/kg/day) to meet true energy demand may require adjustment (increase) to account for this in patients with pressure ulcers. Encourage nutritional support if an individual is undernourished. Under-nutrition is associated with poor clinical outcomes, including increased risk of mortality, so early identification of actual or potential nutritional need allows for timely intervention to mitigate nutritional decline. Updated Evidence: Guideline #2.2: Encourage dietary intake or oral nutrition supplement if an individual who is undernourished is at risk of developing a pressure ulcer. (Level III—no change) Principle: Nutrients are basic to cellular integrity and data suggest that a nutritional supplement may have a modest effect in preventing the development of pressure ulcers, largely in stage 1 ulcers. Dietary intake through meals and with any supplementation provided should be monitored to assess intake adequacy. Updated evidence: None. Guideline #2.3: Ensure adequate dietary intake to prevent under-nutrition to the extent that this is compatible with the individual's wishes. (Level I—increased) Principle: Adequate nutrition is essential for life and undernutrition is associated with the development of pressure ulcers. Providing nutrition supports pressure ulcer healing or improvement in ulcer status and is associated with preventing pressure ulcers. Nonetheless, the nutritional plan needs to be consistent with the individual's personal goals and medical condition. Updated Evidence: Guideline #2.4: If dietary intake continues to be inadequate, impractical, or impossible, nutritional support provided using other routes should be considered with the goal of achieving positive nitrogen balance (approximately 30–35 calories/kg/day and 1.25–1.50 g of protein/kg/day) according to the goals of care. (Level II—increased) Principle: Anabolism is facilitated with a positive nitrogen balance and when individuals are not able to meet nutritional needs through oral intake, alternative methods should be undertaken to optimize nutritional status. Updated Evidence: Guideline #2.5: Give vitamin and mineral supplements if deficiencies are confirmed or suspected. (Level I—increased) Principle: Supplements of vitamins and minerals that are needed for wound healing should be provided when intake is insufficient or when a deficit is identified. The unique contribution of specific vitamins, minerals or amino acids is uncertain. However, enhanced supplements consisting of various combinations of Vitamins A, C, E, zinc, fatty acids, and arginine are associated with pressure ulcer healing and/or prevention of ulcer formation. Amino acid supplements have been effective in the healing some non-pressure related wounds. Emerging evidence suggests that arginine may increase the rate of healing in patients with pressure ulcers. Updated Evidence: Preamble: Infection results when the microbe: host defense equilibrium is upset in favor of the microbes. Infection plays various roles in the etiology, healing, operative repair, and complications of pressure ulcers. Therefore, guidelines are necessary to address the treatment of infection in each of these circumstances. Guideline #3.1: Treat distant infections (e.g., urinary tract, cardiac valves, cranial sinuses) with appropriate antibiotics in pressure-ulcer-prone patients or patients with established ulcers. (Level II—no change) Principle: Bacteria entering the bloodstream or lymphatics can lodge in compressed tissue, denervated tissue, edematous tissue, or established wounds by the compromised tissue acting as a locus minoris resistentiae Updated Evidence: Guideline #3.2: Remove all necrotic or devitalized tissue by sharp, enzymatic, biological, mechanical, or autolytic debridement. Larval therapy provides both debridement and antibacterial activity. Although there are no recent randomized controlled trials of larval therapy for pressure ulcers, this biologic therapy has been shown to reduce the time to debridement but does not significantly increase the rate of healing in leg ulcers. (Level I—no change) Principle: Necrotic tissue is laden with bacteria while devitalized tissue impairs the body's ability to fight infection and serves as pabulum for bacterial growth. Updated Evidence: Guideline #3.3: If there is suspected infection in a debrided ulcer, or if contraction and epithelialization from the margin are not progressing within 2 weeks of debridement and relief of pressure, determine the type and level of infection in the debrided ulcer by tissue biopsy or by a validated quantitative swab technique. (Level I—increased) Principle: The reference standard for the diagnosis of infection of chronic wounds is a tissue biopsy for culture obtained after debridement to remove bacteria that are present as surface colonization. If quantitative cultures are obtained, microbial loads of greater than 105 of any organism per gram of wound tissue or the presence of any level of beta-hemolytic streptococcus is typically considered an indicator of infection of chronic wounds. Updated Evidence: Principle: Classic signs of inflammation (purulent exudate, erythema, heat) may be absent in the presence of a wound infection. These signs are often used to diagnose infection; however, their presence/absence is not specific for infection, particularly in chronic wounds. Updated Evidence: Guideline #3.5 (new): Little evidence exists supporting the use of one type of wound cleansing solution or technique for pressure ulcers. Systemic antibiotics have not been shown to lower bacterial bioburden in wounds. Topical antimicrobials (silver-containing cream, antimicrobial containing foam dressing, cadexomer iodine) have been shown to decrease the bacterial load in an ulcer. Avoid wound cleansing with antiseptic agents as granulation tissue will be destroyed. Furthermore, tap water is also appropriate to use to cleanse wounds. (Level I) Principle: Pressure ulcers contain an endogenous bacterial load, which should be managed to prevent the progression from colonization to infection. Updated Evidence: Guideline #3.6: Obtain bacterial balance (≤105 cfu/ gram of tissue and no beta hemolytic streptococci) in the pressure ulcer before attempting surgical closure by skin graft, direct wound approximation, pedicled, or free flap. (Level I—no change) Principle: A wound containing contaminated foci with >105cfu per gram of tissue cannot be readily closed, as the incidence of wound site complications including dehiscence and persistent infection is 50–100%. Updated Evidence: Guideline #3.7: Obtain bone biopsy for culture and histology in cases of suspected osteomyelitis associated with a pressure ulcer. (Level II—no change) Principle: The sensitivity and specificity of noninvasive tests for diagnosing osteomyelitis are not as high as direct bone biopsy and are not as useful in determining treatment. Updated Evidence: Guideline #3.8 (revised): Once confirmed, osteomyelitis underlying a pressure ulcer should be adequately debrided and, treated with culture guided antibiotics. Flap reconstruction with well vascularized tissue may facilitate healing of osteomyelitis in appropriately selected patients. (Level I—no change) Principle: Muscle, myocutaneous, and fasciocutaneous flaps effectively control bacterial levels under acute experimental conditions. However, acute osteomyelitis in pressure ulcers is associated with a high rate of recurrence unless eradicated by a combination of debridement of devitalized bone and antibiotic therapy. Not all patients are appropriate candidates for flap reconstruction. Culture-guided antibiotic therapy for osteomyelitis is recommended for 6 weeks. Eight weeks of antibiotic therapy is recommended for MRSA osteomyelitis. Updated Evidence: Guideline #3.9 (new): Heel ulcers do not need debridement if they lack signs of inflammation/infection (edema, erythema, drainage) and are stable with dry eschar. (Level III). Principle: The determination of whether to debride heel ulcers depends upon the clinical goals. In those patients with dry heel eschar who cannot be revascularized, have multiple comorbidities, and are immobile with no functional goals the heel eschar may be left intact. Heel ulcers with dry eschar should be monitored closely and debrided if they develop signs of infection. Updated Evidence: Guideline #3.10 (new): The establishment of bacterial biofilm contributes to the development of chronic non-healing wounds. A biofilm should be suspected with poorly healing chronic wounds, as well as wounds with a high multispecies bacterial burden and can be identified using molecular microbial identification. Sharp debridement significantly reduces the number of microorganisms in a wound bed, and is vital in biofilm control. (Level III) Principle: Bacterial biofilm is a significant barrier to wound healing. Biofilms are communities of microorganisms organized into microcolonies covered with a slime called extracellular polymeric substance. As a result, they are typically multispecies and metabolically inert. These characteristics make them resistant to current antimicrobial techniques. In animal models, biofilm formation in the wound is associated with continuous inflammation and delayed wound healing. Updated Evidence: Guideline #3.11 (new): Chronic wound fluid samples should be tested for proteolytic activity. High levels may be indicative of wound infection or may be due to host factors. Concurrent treatment of wound infection with a targeted protease modulator may facilitate wound closure. Wound fluid should be retested as needed until the levels of proteases are normal. (Level III) Principle: The remodeling and deposition of extracellular matrix in the wound bed is affected by proteolytic activity. The total protease activity is a combination of host and bacterial proteases which act synergistically to promote tissue breakdown in infected wounds. Bacterial proteases may upregulate host production of matrix metaloproteinases.The combination of bacterial and host proteases can lead to an imbalance resulting in tissue destruction, cytokine degradation and loss of cellular function. Modulation of protease levels may facilitate healing. Updated Evidence: Preamble: Wound bed preparation is defined as the management of the wound to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures. The aim of wound bed preparation is to convert the molecular and cellular environment of a chronic wound to that of an acute healing wound. Guideline #4.1: Examination of the patient as a whole is important to evaluate and correct causes of tissue damage. It is important to examine the patient's systemic diseases and medications. (Level I—no change). Principle: When integrating the necessary steps of the wound bed preparation process, it is paramount to first consider other contributing etiologies that might interfere with wound closure and to evaluate the individuals other indirect comorbidities. General medical history, including a medication record, will help in identifying and correcting systemic causes of impaired healing. Any major illness, systemic disease or drug therapies that cause alterations in immune functioning, metabolism, nutrition, and tissue perfusion will interfere with wound healing. Systemic disease, such as systemic sepsis, organ failure (hepatic, renal, respiratory, gut), major trauma/burns, diabetes, autoimmune diseases, and drug therapies such as immunosuppressive drugs and systemic steroids will delay wound healing. Updated Evidence: Guideline 4.2: Examination of the patient as a whole is important to evaluate and correct causes of tissue damage. It is important to examine the patient's nutritional status. (Level II—no change). Principle: Nutrition must be adequate to provide sufficient protein to support the growth of granulation tissue. Patients' barriers to achieving dietary sustenance should be kept in mind when prescribing supplementation. (See also the nutritional sections of this guideline). Updated Evidence: Guideline 4.3: Examination of the patient as a whole is important to evaluate and correct causes of tissue damage. It is important to examine the patient's tissue perfusion and oxygenation. (Level I—no change) Principle: Wounds will heal in an environment that is adequately oxygenated. Oxygen delivery to the wound will be impaired if tissue perfusion is inadequate. Dehydration and factors that increase sympathetic tone such as cold, stress, or pain will all decrease tissue perfusion. Cigarette smoking decreases tissue oxygen by peripheral vasoconstriction. Patients whose wounds are ischemic should be referred to a vascular surgeon before aggressively engaging in moist wound healing and wound debridement. Updated Evidence: Guideline #4.4: Initial debridement is required to remove the obvious necrotic tissue, excessive bacterial burden, and cellular burden of dead and senescent cells. Maintenance debridement is needed to maintain the appearance and readiness of the wound bed for healing. The healthcare provider can choose from a number of debridement methods including sharp, mechanical, enzymatic and autolytic. More than one debridement method may be appropriate. (Level I—no change) Principle: Once tissue perfusion is checked (see Guideline #4.3) and ischemia has been ruled out, initial and maintenance debridement of devitalized tissue in the wound bed should become routine with regards to wound care. Debridement will remove necrotic tissue, senescent cells, decrease bacterial bioburden and disrupt biofilms. The health care provider can choose from a number of debridement methods including sharp, mechanical, enzymatic and autolytic. More than one debridement method may be appropriate. Wounds covered with dry eschar that are not infected, but ischemic should not be debrided until patient's arterial flow is reestablished and/or unless symptoms of acute infection or wet gangrene ensue. Updated Evidence: A. Surgical or sharp debridement: involves use of instruments (scissors, scalpels, forceps) or laser to remove necrotic tissue from the wound. Debridement of large amounts of necrotic tissue should be done in the operating room. Surgical debridement is indicated when the goal is to achieve fast and effective removal of large amounts of necrotic tissue. Surgical debridement is contraindicated if there is lack of expertise in this method, inadequate vascular supply to the wound and absence of systemic antibacterial coverage in systemic sepsis. Relative contraindication is bleeding disorders or anticoagulation therapy. Updated Evidence: B. Mechanical debridement: physically removes necrotic tissue with wet-to-dry dressings, wound irrigation, and whirlpool techniques. Wet to dry dressing may induce mechanical separation of eschar but can be painful and if dry, may damage viable newly formed tissue. High or low-pressure streams or pulsed lavage may be quite effective in removing loose necrotic tissue, provided the pressure does not cause trauma to the wound bed. Effective ulcer irrigation pressures range from 4 to 15 psi of pressure. A 30 mL syringe filled with saline can be used to flush a wound through an 18 gauge catheter. Irrigation pressures below 4 psi may not be effective to cleanse the wound and pressures greater than 15 psi may cause trauma and drive the bacteria into the tissue. Whirlpool therapy is no longer recommended due to increased risk for bacterial contamination, circulatory compromise and tissue maceration. Updated Evidence: C. Enzymatic debridement: is achieved by topical application of exogenous enzymes to the wound surface to remove necrotic tissue. Updated Evidence: D. Autolytic debridement: is achieved when a moist wound environment is created over time by the use of an occlusive dressing. These dressings allow the natural wound fluid and its endogeno