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WHS guidelines update: Diabetic foot ulcer treatment guidelines

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

10.1111/wrr.12391

1524-475X

Lawrence A. Lavery, Kathryn E. Davis, Sandra Berriman, Liza R. Braun, Adam Nichols, Paul J. Kim, David J. Margolis, Edgar J.G. Peters, Chris Attinger,

Pressure Ulcer Prevention and Management

There are 22.3 million people in the United States with diabetes, of whom 15–25% are at risk for foot ulceration. Diabetic foot ulcers (DFUs) are a growing health problem. DFUs are a leading cause of infection, amputation, and hospitalization in patients with diabetes mellitus. Guidelines for the treatment of DFUs were published by the Wound Healing Society (WHS) in 2006. However, in the past few years new evidence has emerged that improves our understanding of previous recommendations. The objectives of the WHS DFU guidelines are to systematically evaluate the medical literature to assist clinicians in making health care decisions, identify areas that need additional research, and to clarify controversial diagnosis and treatment strategies. An advisory panel comprised of academicians, clinicians, researchers, and industry representatives was chosen to update the 2006 guidelines. In 2006, in an effort to develop guidelines that could provide clinicians with a reasonable approach to caring for patients, even in the absence of high quality human data, the WHS 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. Since the 2006 guidelines, we sought to capture the highest quality of literature available regarding DFU diagnosis and treatment using a key word search of PubMed, 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, 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 separate guidelines has undergone a Delphi consensus among the panel members. Not all panel members thought they had sufficient expertise to critique all of the separate sections of the guidelines. The first draft was of the guidelines was presented in 2014 for public comment and subsequent drafts revised based on those comments. Evidence Reference: Preamble: Ulcers of the lower extremity may be caused by a variety of conditions, including neuropathy, ischemia, venous hypertension, and pressure. Patients with diabetes develop wounds secondary to neuropathy with or without biomechanical abnormalities, peripheral vascular disease with ischemia, or both. There are over 20 million people in the United States with diabetes, of whom 15–25% are at risk for ulceration. It is imperative that the etiology be established to provide for proper therapy. Guideline #1.1: Clinically significant arterial disease should be ruled out by establishing that pedal pulses are clearly palpable or that the ankle:brachial index (ABI) is > 0.9. An ABI > 1.3 suggests noncompressible arteries. In elderly patients or patients with an ABI > 1.2, a normal Doppler-derived waveform, a toe:brachial index of > 0.7, or a transcutaneous oxygen pressure of > 40 mmHg and/or hyperspectral imaging analysis may help to suggest an adequate arterial flow. Color duplex ultrasound scanning provides anatomic and physiologic data confirming an ischemic etiology for the leg wound. (Level I) Principle: Diabetic ulcers can result from arterial insufficiency or neuropathy. Although clinical history and physical examination can be very suggestive of an ischemic etiology of the lower extremity diabetic ulcers, a definitive diagnosis must be established. When significant arterial disease is present, successful treatment requires that arterial insufficiency be addressed. Updated Evidence: Guideline #1.2: The presence of significant neuropathy can be determined by testing with a 10 g (5.07) Semmes–Weinstein monofilament. (Level II) Principle: Diabetic sensory neuropathy creates an environment in which repetitive trauma, injury and infection are unrecognized by the patient. Several simple clinical techniques can be used to identify sensory neuropathy with loss of protective sensation. The presence of sensory neuropathy can be determined by testing with a 10 g Semmes Weinstein monofilament, 128 Hz tuning fork, vibration perception threshold testing or a good neurological clinical examination for sensory loss. Updated Evidence: Preamble: Diabetic ulcerations on the sole of the foot are often associated with moderate to high pressures because of foot deformity, limited joint mobility, and neuropathy. Off-loading devices reduce pressure on the sole of the foot and often reduce the activity level of the patient. Off-loading the area of high pressure has been the mainstay to heal DFUs and prevent recurrence of foot ulcerations (Level I). Guideline #2.1: Protective footwear should be prescribed in any patient at risk for amputation (significant arterial insufficiency, significant neuropathy, previous amputation, previous ulcer formation, preulcerative callus, foot deformity, evidence of callus formation). (Level II) Protective footwear results in reduction in recurrent ulcerations in high-risk patients with a previous foot ulcer or amputation. (Level I). Principle: The etiology of many foot ulcers involves a biomechanical component. Most treatments do not eliminate the underlying biomechanical etiology of the foot ulcer. Abnormal pressure and shear stress is still present, so long-term off-loading is necessary. By reducing pressure and shear forces on the sole of the foot, repetitive injury to the foot is reduced, and existing wounds can heal or high-risk areas are protected from recurrent ulcers. Updated Evidence: Guideline #2.2: Acceptable methods of offloading include crutches, walkers, wheelchairs, custom shoes, depth shoes, shoe modifications, custom inserts, custom relief orthotic walkers, diabetic boots, forefoot and heel relief shoes, and total contact casts. (Level I) Principle: Relieving pressure on the diabetic wound is necessary to maximize healing potential. Updated Evidence: Preamble: Infection results when the bacteria: host defense equilibrium is upset in favor of the bacteria. Infection plays various roles in the etiology, healing, operative repair, and complications of diabetic ulcers. Guideline #3.1: Remove all necrotic or devitalized tissue by surgical, enzymatic, mechanical, biological, or autolytic debridement. (Level II; detailed discussion of debridement is in Wound Preparation Guidelines). Principle: Devitalized tissue provides a safe haven for bacterial proliferation, a barrier for antibiotics to reach bacterial pathogens. In addition, it limits the body's cellular defenses to fight infection. Removal of devitalized tissue reduces bacterial bioburden. Updated Evidence: Guideline #3.2: If there is suspected infection in a debrided ulcer, or if epithelialization from the margin is not progressing within two weeks of debridement and initiation of offloading therapy, determine the type and level of infection in a debrided diabetic ulcer by tissue biopsy or by a validated quantitative swab technique. (Level II) Principle: High levels of bacteria (≥106 CFU/g of tissue) impede wound healing and surgical wound closure. Reduction of the bacterial bioburden in the wound reduces the risk of clinical infection and improves wound healing. Cultures should be performed to isolate both aerobic and anaerobic bacteria. Updated Evidence: Guideline #3.3: For ulcers with levels of bacteria (>105 CFU/g of tissue) following adequate debridement, topical antimicrobial agent can decrease the bacterial levels. Once in bacterial balance, topical antimicrobial agent should be discontinued to minimize cytotoxic effects and emergence of bacterial resistance organisms. (Level I). Principle: Systemically administered antibiotics do not effectively decrease bacterial levels in granulating wounds, Topically applied antimicrobials can be effective to decrease bacterial levels in granulating wounds. Updated Evidence: Guidelines #3.4: Topical antimicrobial and antiseptic therapies are not effective to improve wound healing (Level I). Principle: New to the guidelines is evidence that topical antimicrobial and antiseptic therapies, while decreasing bioburden, do not improve wound healing. Updated Evidence: Guideline #3.5: For acute diabetic foot infections not confined to the granulating wound, systemic antibiotics are effective. (Level II) Principle: Systemic antibiotics have been demonstrated in most trials to be helpful in treating acute diabetic foot infections. Deep tissue cultures are most helpful in determining antibiotic usage. Updated Evidence: Guideline #3.6: Cellulitis (inflammation and infection of the skin and subcutaneous tissue most commonly due to streptococci or staphylococci) surrounding the ulcer should be treated with systemic Gram-positive bactericidal antibiotics. (Level II) Principle: Edema fluid (plasma) neutralizes the fatty acids of sebum and inactivates the normal bactericidal properties of skin. This renders the skin and subcutaneous tissue susceptible to infection by streptococci or staphylococci. Gram positive bacteria are the most common pathogens in cellulitis in DFUs. Updated Evidence: Guideline #3.7: If osteomyelitis is suspected, appropriate diagnostic measures include bone biopsy, probing the wound area to the bone with a sterile instrument, serial x-rays, MRI, CT and radionucleid scans. (Level II). PET leukocyte screening, and Tc99m WBC labeled-SPECT/CT. (Level II) Principle: Bone underlying a diabetic ulcer is often infected. Biopsy of the bone gives a definitive diagnosis, but less invasive techniques can be useful in establishing a diagnosis with a high degree of specificity and sensitivity. Updated Evidence: Guideline 3.8: If osteomyelitis is suspected, determine the type of bacterial pathogens by bone biopsy (Level II). Principle: Culture-directed antibiotic treatment seems to provide better clinical outcomes than empiric therapy. If diabetic foot osteomyelitis (DFO) is suspected, bone specimens should be obtained to identify the bacterial pathogens and to direct antibiotic therapy. Since the last publication of the WHS guidelines, data has emerged suggesting that culture-directed antibiotic treatment results in enhanced outcomes in osteomyelitis. Therefore, we have added this guideline to suggested treatment approaches to advance treatment of bioburden that results in osteomyelitis. Updated Evidence: Guideline #3.9: Osteomyelitis is best treated by removal of the infected bone, followed by 2–4 weeks of antibiotics. However, when this is not practical, osteomyelitis underlying a diabetic ulcer can be effectively treated with prolonged antibiotic therapy. (Level II) Principle: Osteomyelitis underlying a diabetic ulcer, like osteomyelitis elsewhere, is most effectively treated by debridement of the infected bone. When debridement has been adequate, a 2–4-week course of antibiotics is adequate. If the infected bone is not totally resected, a longer course (at least 6 weeks) is usually required. Updated Evidence: Guideline #3.10: Minimize the tissue level of bacteria, preferably to 105 CFU/g of tissue with no beta hemolytic Streptococci in the ulcer before attempting surgical closure by skin graft, skin equivalent, pedicled, or free flap. (Level II) Principle: A wound containing contaminated foci with greater than 105 organisms per gram of tissue cannot be readily closed, as the incidence of wound infection that follows is 50–100%. Updated Evidence: None. (Detailed discussions of infection control, dressings, and tissue engineering/growth factors are in infection control guidelines, dressings guidelines, and adjuvant agents [topical, device, and systemic] guidelines). Preamble: Wound bed preparation is defined as the management of the wound to accelerate endogenous healing or 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. This includes factors such as: (A) systemic diseases and medications, (B) nutrition, and (C) tissue perfusion and oxygenation. (Level I) Principle: (4.1.A) A general medical history, including a medication record, will help in identifying and correcting systemic causes of impaired healing. The presence of a major illness or systemic disease and drug therapies such as immunosuppressive drugs and systemic steroids will interfere with wound healing by alterations in immune functioning, metabolism, inflammation, nutrition, and tissue perfusion. Autoimmune diseases such as rheumatoid arthritis, uncontrolled vasculitis, or pyoderma gangrenosum can all delay healing and may require systemic steroids or immunosuppressive agents before local wound healing can occur. Patients undergoing major surgery have a diminished wound-healing capacity as do chronic smokers. Smoking is associated with impaired wound healing and increased risk of infection. Updated Evidence: Principle: (4.1.B) Nutrition must be adequate to provide sufficient protein to support the growth of granulation tissue. The patient's weight, prealbumin level (reflecting recent protein consumption), and serum albumin (reflecting long-term protein consumption) are useful in identifying patients who are outside the norms. Although most diabetic ulcer patients are ambulatory and not at the extremes of nutrition, nutritional support is required if an individual is undernourished. Updated Evidence: Principle: (4.1.C) 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 decrease tissue perfusion. Cigarette smoking decreases tissue oxygen by peripheral vasoconstriction. For optimal tissue perfusion, these factors must be eliminated or minimized. Updated Evidence: Guideline #4.2: 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 health care provider can choose from a number of debridement methods including surgical, enzymatic, mechanical, biological, or autolytic. More than one debridement method may be appropriate. (Sharp surgical debridement is preferred; Level I). Principle: Necrotic tissue, excessive bacterial burden, senescent cells, and cellular debris can all inhibit wound healing. The method of debridement chosen may depend on the status of the wound, the capability of the health provider, the overall condition of the patient, and professional licensing restrictions. Updated Evidence: Guideline #4.3: Wounds should be cleansed initially and at each dressing change using a neutral, nonirritating, nontoxic solution. Routine wound cleansing should be accomplished with a minimum of chemical and/or mechanical trauma. (Level III) Principle: Irrigating and cleansing the wound removes loose impediments to wound healing. Sterile saline or water is usually recommended. Tap water should only be used if the water source is reliably clean. Experimental data suggest that a nontoxic surfactant may be useful as may fluid delivered by increased intermittent pressure. Updated Evidence: Guideline #4.4: There should be an ongoing and consistent documentation of wound history, recurrence, and characteristics (location, size, base, exudates, condition of the surrounding skin, staging, and pain) to evaluate wound bed preparation. The rate of wound healing should be evaluated to determine whether treatment is optimal. (Level II) Principle: Ongoing evaluations of wound bed preparation are necessary; if the ulcer is not healing at the expected rate, interventions for wound bed preparation need to be reassessed. The longer the duration of the ulcer, the more difficult it is to heal. If an ulcer is recurrent, etiology, patient education, or issues of prevention and long-term maintenance need to be reassessed. Updated Evidence: Guideline #4.5: Patients who fail to show a reduction in ulcer size by 50% or more after 4 weeks of therapy should be reevaluated and other treatments should be considered. (Level II) Principle: Percent change in wound area of DFUs over four weeks of treatment is a good predictor of effectiveness of therapy and likelihood of healing. Updated Evidence: Guideline # 4.6: Optimizing glucose control improves wound healing. (Level II) Principle: Wound healing is more likely to be optimal in the setting of good diabetes management. Abnormal glucose levels also affect the nature of infection and cellular immunity Updated Evidence: Preamble: There are a large number of topical therapies available for DFUs. Most dressings are used in combination with off-loading, debridement, and infection control. It is thought that a moist wound environment physiologically favors cell migration and matrix formation. There are several criteria that should be considered when selecting a dressing including the cost, potential for iatrogenic injury, and wound exudate management. First, dressings should not damage the wound. If the wound and surrounding tissue have continuous contact with wound exudate, the local tissue can become macerated and impede healing. Likewise, dressings that are not secure can cause friction injuries to the surrounding skin or wound bed. The cost of health care provider time, healing rate, and the unit cost of dressings should be considered when determining cost efficacy. Randomized clinical studies have not yet identified that any dressing approach is more effective than others to facilitate wound healing. Guideline #5.1: Use a dressing that will maintain a moist wound-healing environment. (Level III) Principle: A moist wound environment physiologically favors cell migration and matrix formation while accelerating healing of wounds by promoting autolytic debridement. Updated Evidence: None Guideline #5.2: Use clinical judgment to select a moist wound dressing. (Level III) Principle: Wet-to-dry dressings are not considered continuously moist. Continuously moist saline gauze dressings are as effective as other types of moist wound healing in terms of healing rate. This guideline has not changed since the 2006 recommendations. However, additional information on adjuvant agents and dressings is available in Guideline 5.6. Updated Evidence: None. Guideline #5.3: Select a dressing that will manage the wound exudates and protect the peri-ulcer skin. (Level I) Principle: Peri-wound maceration and continuous contact with wound exudates can enlarge the wound and impede healing. Updated Evidence: None. Guideline #5.4: Select a dressing that stays in place, minimizes shear and friction, and does not cause additional tissue damage. (Level II) Principle: Wound location, peri-wound skin quality, and patient activity can all affect the choice of dressing. Updated Evidence: None. Guideline #5.5: Select a dressing that is cost effective. (Level I) Principle: Because of their low unit cost, moist saline gauze dressings are often viewed as the least expensive and, therefore, most cost-effective dressing. However, when determining cost efficacy, it is important to take into consideration health care provider time, ease of use, and healing rate, as well as the unit cost of the dressing. Updated Evidence: None. Guideline #5.6: Selectively use adjuvant agents (topical, device, and/or systemic) after evaluating a patient and their ulcer characteristics and when there is a lack of healing progress in response to more traditional therapies. (Level I) (Detailed discussions of these alternatives are in Adjuvant Agents [Topical, Device, Systemic] Guidelines) Principle: Emerging therapies through recombinant technologies and cell-based devices may offer benefit and increase healing in selected patients or difficult wounds. These therapies are quite diverse and are discussed in detail in the Adjuvant Agents Guidelines. Updated Evidence: Evidence references are detailed in the Adjuvant Agents (Topical, Device, Systemic Guidelines). Preamble: The mainstays of dressings and offloading are not successful in healing all diabetic ulcers. Over the years, multiple surgical procedures have been attempted to treat diabetic ulcers with varying degrees of success. True randomized clinical trials comparing operative techniques are difficult, but data are available supporting surgery in selected patients. Guideline #6.1: Achilles tendon lengthening improves healing of diabetic forefoot wounds. (Level II) Lengthening the Achilles tendon reduces pressure on forefoot plantar ulcers in patients with limited dorsiflexion of the ankle joint. Achilles tendon lengthening has been associated with a reduction in ulcer recurrence (Level I). Principle: A tight Achilles tendon contributes to increased forefoot pressures. Lengthening the Achilles tendon reduces pressure on forefoot plantar ulcers in patients with limited dorsiflexion and may be of benefit in healing certain DFUs. Updated Evidence: Guideline #6.2: Patients with ischemia should be considered for a revascularization procedure. Infrainguinal angioplasty and in situ bypass are associated with a significant improvement in ulcer healing. (Level ll) Principle: In patients with inadequate arterial inflow, improvement in blood supply is associated with an increase in oxygenation, nutrition, and wound healing. Updated Evidence: Preamble: Many agents have been suggested to be used as adjuvants to dressings and off-loading therapy in the treatment of diabetic ulcers. These adjuvant agents can be divided into topical agents to be applied to the ulcer, devices aimed at accelerating ulcer healing, and systemic drugs to treat the patient. Several of these agents have enough evidence to allow guidelines regarding their use. Guideline #7.1.1: Application of Platelet-derived growth factor (PDGF) reduces the time to heal and increases the proportion of ulcers that heal. (Level I) Principle: Cytokine growth factors are messengers/mediators in wound healing. Diabetic foot wounds are deficient in growth factors. Addition of growth factors to nonhealing wounds can therefore accelerate wound healing. Updated Evidence: Guideline #7.1.2: Cytokines and growth factors have demonstrated with improved DFW healing. (Level I) Principle: Cytokines and growth factors are messengers/mediators in wound healing. Updated Evidence: Guideline #7.1.3: Platelet-rich plasma (Level l) and epidermal growth factor (Level II) have not demonstrated an increase in the proportion of wounds that heal and the healing rate of DFUs. Principle: There is one systematic review and four RCTs with autologous and blood bank sourced platelet rich plasma that together suggest no improved wound healing effects. Updated Evidence: Guideline #7.2.1: Negative pressure wound therapy (NPWT) has been shown to increase the proportion of wounds that heal and the rate of wound healing compared with standard wound care in diabetic lower extremity wounds. (Level I) Principle: NPWT treatment may improve wound healing by reducing edema, removing bacterial products, and drawing together the edges of the wound, and should be considered when other treatments are not effective. Updated Evidence: Guideline #7.2.2: Cellular and Acellular skin equivalents improve DFU healing. (Level I) Principle: Healthy living skin cells assist in healing DFUs by releasing therapeutic amounts of growth factors, cytokines, and other proteins that stimulate the wound bed. Updated Evidence: Guideline #7.2.3: Electrical stimulation is recommended to accelerate wound closure. (Level I) Principle: Application of electric current to diabetic foot wounds increases local tissue perfusion and may affect protein synthesis, cell migration, and bacterial growth to improve wound healing. Updated Evidence: Guideline #7.2.4: Extracorporeal shock wave therapy accelerates diabetic ulcer healing (Level I). Principle: Extracorporeal shock wave therapy has been used in a variety of clinical application for fracture repair, tendon injuries and wound healing. Four RCTs evaluated shock wave therapy for patients with diabetic foot ulcers. Updated Evidence: Guideline #7.3: Hyperbaric oxygen therapy should be used to improve wound healing and reduce major amputation (Level I). Principle: Hyperbaric oxygen therapy may increase the amount of oxygen delivered to a wound in diabetic patients and thereby improve healing. Updated Evidence: Preamble: Diabetic ulcers of the lower extremity are a chronic problem. Recurrence rates are 8–59%. Therefore, longterm maintenance must be addressed even for healed ulcers. Guideline #8.1: Patients with healed diabetic ulcers should use protective footwear to prevent recurrence. (Level I) Principle: Most treatments do not eliminate the underlying increased pressure on the foot, so offloading is necessary long term. Updated Evidence: Guideline #8.2: Good foot care and daily inspection of the feet will not reduce the recurrence of diabetic ulceration. (Level I) Principle: There is contradictory data regarding the effectiveness of good foot care including proper bathing, nail trimming will reduce ulceration in diabetic feet. Self-care behaviors such as good foot care proper bathing and nail care should be included as part of a comprehensive care program that includes professional foot care, education and therapeutic shoes and insoles. Updated Evidence: Guideline #8.3: Home monitoring of foot temperatures with an infrared thermometer reduces re-ulceration (Level I). Principle: Local areas of increased temperature are a sign of inflammation and deep tissue injury that would precede the development of ulceration. By daily assessment of temperature changes, patients could identify early warning signs of tissue inflammation and reduce their activity to avert the development of an ulceration. Updated Evidence: