Sibbald, R. Gary BSc, MD, FRCPC (Med) (DERM), FAPWCA, MEd; Woo, Kevin RN, MSc, ACNP GNC(C); Ayello, Elizabeth A. PhD, RN, APRN,BC, CWOCN, FAPWCA, FAAN
The wound bed preparation paradigm allows the clinician to optimally evaluate a patient with a chronic wound to delineate an accurate diagnosis and initiate treatment. It requires a holistic, team approach to assessing the whole patient, treating the underlying cause(s), and addressing patient-centered concerns, all of which must be considered before examining the wound itself.1 Clinical documentation of the wound characteristics (debris or necrosis, increased bacterial burden or persistent inflammation, and the amount of exudate) serves as the benchmark for the selection of topical treatment.
This article focuses specifically on persistent inflammation and infection, and it is the first in a 4-part series that will address the local wound components of wound bed preparation (debridement, infection/inflammation, moisture balance, and the edge effect as a marker for active and advanced therapies). The debate about appropriate terms to describe infection and inflammation, as well as the use of clinical enablers for improved practice, will also be described.
EXAMINE THE EVIDENCE
Evidence-based medicine2 is fast becoming a requirement in wound care, with clinicians demanding evidence before the introduction of new products or a change in wound care practices.3 Sackett2 defined evidence-based wound management as "the integration of best research evidence with clinical expertise and patient values." Scientific evidence should be translated for current practice. For example, despite the findings in the 1960s that wounds treated according to moist wound healing principles will heal at a faster rate, toxic local antiseptic agents or saline wet-to-dry dressings that inhibit healing are still commonly prescribed.
The wound bed preparation concept was first described in 2000 by Sibbald et al4 and Falanga.5 The Sibbald et al4 model encourages the clinician to examine the whole patient, treating the cause and patient-centered concerns before focusing on the hole in the patient. Local wound care can be optimized using moist healing principles by addressing 3 components: debridement, bacterial balance or persistent inflammation, and moisture balance. The algorithm in Figure 1 combines the components necessary for obtaining maximal benefits from today's wound care products1,4 and applies the principles of evidence-based medicine.
The authors of the present article have used the wound bed preparation model to develop a practical clinical guide to the treatment of critical colonization and infection in chronic wounds.
BALANCE AND RESISTANCE
All chronic wounds contain bacteria. But whether the wound is in bacterial balance (contamination with organisms on the surface or colonization with organisms in the tissue arranged in micro colonies without causing damage) or bacterial imbalance (critical colonization and infection) is of primary importance to healing (Figure 2). A continuum of bacterial presence progressing from bacterial balance to bacterial damage in a chronic wound is illustrated in Figure 3. The diagnosis of infection should be made clinically based on signs and symptoms in and around the local wound bed, the deeper structures, and the surrounding skin.
The potential damage caused by invading wound bacteria is determined by the following equation: infection = number of organisms × organism virulence. The most important factor in this equation is host resistance, which is defined as the ability of the host to resist bacterial invasion and damage by mounting an immune response (increased bacterial burden or infection). Systemic and local factors can decrease host resistance. Systemically, an adequate blood supply is needed for wound healing. A decreased or inadequate blood supply favors bacterial proliferation and damage that may prevent or delay healing. Uncontrolled edema, smoking, poor nutrition, diabetes with a poorly controlled blood glucose level, excess alcohol intake, drugs that interfere with the immune system, or immunodeficiency diseases may all challenge wound healing. Local factors inhibiting healing may include a large wound size, local presence of foreign bodies (prosthetic joints, retained thread of gauze, or suture), and an untreated deeper infection, such as osteomyelitis.6
Most bacteria enter the wound bed through external contamination from the environment, dressings, the patient's body fluids, or the hands of the patient or health care provider. If the surface organisms attach to the tissue and multiply, colonization is established but a bacterial balance remains.
However, if bacteria continue to multiply, critical colonization or local infection (covert infection, increased bacterial burden) may develop. Wound-related bacteria can release metalloproteases and other mediators of inflammation that will lead to local tissue damage. The first sign of critical colonization or local infection may be a delay in the healing process so that there is no change in the wound size measured with a simple length × width measurement (longest length and the widest width at right angles). Exudate on the surface can increase at this stage as an inflammatory reaction to the surface tissue damage. The exudate may be clear or serous before it is frankly purulent or hemorrhagic.
Gram-positive organisms may be the first to invade a wound with decreased host resistance, followed by Gram-negative bacteria and then anaerobic species. A foul odor may accompany the exudate due to tissue breakdown caused by the presence of these Gram-negative and anaerobic organisms. Small areas of yellow to brown slough may be present on the surface of the wound as a result of a hostile local environment, leading to surface cell death and local tissue necrosis. The granulation tissue may bleed easily due to bacterial stimulation of vascular endothelial growth factor (VEGF), resulting in an excess formation of new blood vessels. Exuberant (beefy red) granulation builds up on the surface; bacterial interference results in a poor quality of collagen matrix that will not support reepithelialization and healing. These signs are localized in the superficial wound bed and are potentially treatable with topical agents, including antimicrobial dressings.7-9
Bacterial damage can extend beyond the local wound bed with a lower host resistance. More extensive bacterial damage results in a deeper and surrounding skin compartment infection that usually requires systemic antimicrobial treatment (Table 1).
The presence of surrounding skin pain, warmth, and swelling should alert the clinician to the possibility of a coexisting soft tissue cellulitis. If the deep portion of the ulcer probes to bone, osteomyelitis is a possibility, especially in persons with diabetes and neurotrophic foot ulcers.10 With infection of the surrounding or deeper structures, the wound often increases in size and satellite areas of breakdown may occur (Figure 4). At this stage, bacterial testing procedures may be useful. The gold standard for bacterial damage in a wound is the tissue biopsy for culture. More than 1.0 × 106 colony-forming organisms per gram of tissue is indicative of sufficient bacteria to usually cause infection in the deep compartment. A bacterial swab can be performed to give an accurate semiquantiative estimate of bacterial numbers. The swab should be taken after the wound has been adequately cleaned, and the Levine method should be utilized. The swab is placed on healthy granulation tissue and enough pressure is applied to extract fluid. The swab is then rotated 360 degrees and placed in the transport media. Surface slough and debris should be avoided. If the wound surface is dry, the swab can be premoistened in the transport media before swabbing the wound. A heavy growth or 4+ bacteria from the swab culture can often be equated to approximately 105 colony-forming units of bacteria per gram of tissue. Bacterial culture can help to determine antimicrobial sensitivities for selection of appropriate oral or parental antimicrobial treatment and to identify colonization with resistant organisms such as methicillin-resistant Staphylococcus aureus (MRSA). Clinicians often must make treatment decisions before the swab results are available and fine-tune the treatment if the patient does not respond or if an unsuspected organism is isolated. In general, wounds of less than 1 month's duration should be treated for Gram-positive organisms. If the wound has been present for more than 1 month or the patient is immunocompromised (including persons with diabetes), the patient will need to be protected against Gram-positive, Gram-negative, and anaerobic organisms.11
Clinicians can apply this new understanding of bacterial balance and imbalance by using the following recommendations or enablers of best practice for wound infection:
1. Identify and correct the cause and cofactors that may inhibit healing as well as address patient-centered concerns. It is important to make an accurate diagnosis of the underlying cause of the wound and correct the cause of impaired healing as a first step. For example:
* Venous disease without coexisting arterial disease should receive appropriate compression for edema control.
* A pressure ulcer requires not only pressure offloading but also nutritional assessment and treatment, correction of friction and shear, optimization of mobility and incontinence management.
* Assess the vascular supply of patients who have a foot ulcer and diabetes to ensure adequate circulation for wound healing.
* Evaluate for infection as classically defined by pain, erythema, edema, and warmth.
* In persons with neuropathy (diabetes and other causes) check for callus formation on the feet to determine if pressure offloading is needed. The presence of callus indicates excess local pressure. If a blister is present, consider friction and shear. An easy way to remember the approach to a person with neuropathy (usually due to diabetes) is to remember the mnemonic "VIPs," not meaning very important persons but, alternately representing Vascular supply, Infection control and Pressure downloading along with Sharp Surgical debridement.
Patients with acute ulcers and postsurgical wounds require the same holistic assessment to determine inhibitors to healing, including infections, coexisting diseases, and lifestyle choices.
In addition to treatment of the cause, a paradigm shift is needed in the plan of care to make the patient central to all treatment decisions. This patient-centered approach represents a paradigm shift moving away from compliance (to obey an order or command) to adherence (to follow through on a treatment plan from the patient's perspective) and, finally, to coherence (to have a negotiated treatment with both the patient and health care provider perspective). Ask patients what their expectations and goals are for their care.
Clinicians must also consider pain control and issues around the quality of life and activities of daily living that may be affected by the presence of a chronic wound. These aspects of care are often more important to the patient than to the clinician.
2. Differentiate the wound's ability to heal: classify as healable, maintenance, or nonhealable wound. The approach to a chronic wound depends on the ability of the wound to heal. A wound is considered healable if there is adequate blood supply, the cause is corrected, and patient-centered concerns have been addressed. A maintenance wound has enough blood supply to heal but the patient cannot adhere to treatment due to personal or system-related factors (eg, they cannot afford shoes and inserts or a removable cast walker for offloading).
A wound is nonhealable if the cause cannot be corrected. For leg and foot ulcers with a palpable pulse, the blood supply is usually adequate for healing (80 mm Hg and higher). If the pulse is not palpable, Doppler examination of the ankle-brachial pressure index (ABI) is necessary to determine if the wound is healable. The pressure in the dorsalis pedis artery should be at least 50% of the pressure in the brachial artery, or an ABI of 0.5. Some patients have calcified vessels in the leg producing a falsely high ankle brachial pressure ratio (20% of all patients and 80% of patients with diabetes).
A full arterial Doppler of the lower extremity with toe pressures is usually recommended when an ABI is more than 1.2. Toe systolic pressure provides an accurate vascular assessment because the artery in the large toe is of a small caliber without a fully developed adventitial layer to facilitate circumferential calcium deposits. For healability, a person with diabetes should have a toe pressure of more than 50 mm Hg. Healing may occur if the pressure is between 30 and 50 mm Hg and if all other factors are optimized.
Many hyperbaric oxygen centers also measure transcutaneous oxygen saturation. This test requires expensive equipment and is labor intensive. Values over 40 mm Hg are normal; values of 30 to 39 mm Hg indicate some oxygen impairment. Values of 20 to 29 mm Hg indicate moderate impairment, and a value below 20 mm Hg indicates severe ischemia; healing is unlikely.
3. Use topical antiseptics for nonhealable or maintenance wounds. Moist interactive healing is the gold standard for patients with adequate blood supply who can produce healthy granulation tissue, reepithialization, and mature healing.
In a wound that does not have the ability to heal (eg, inadequate vascular supply or gangrene), moisture balance and active debridement are contraindicated. Instead, clinicians should focus on the use of topical antimicrobial and antiseptics to decrease the local bacterial count and subsequent invasion of organisms into proximal viable tissue (Table 2
The lowest tissue toxicity in this group of agents occurs with chlorhexidine and povidone-iodine.9 Both of these agents have a low sensitization potential and a broad spectrum of antibacterial action. Povidone-iodine application may be associated with local stinging and should be used with caution on very large wounds and in persons with thyroid disease because of the potential for absorbed iodine to interfere with thyroid gland function. Both of these agents can be used long term with a low incidence of tissue toxicity. Acetic acid (0.5 to 1.0%) is toxic to granulation tissue but is very effective as a compress or soak (often for 5 to 10 minutes at the time of dressing change) for Pseudomonas with green discoloration and a distinctive sickeningly sweet odor on the wound surface. This agent may be used short term when bacterial burden is of more concern than tissue toxicity.
Aniline dyes, such as scarlet red, Proflavine, and crystal violet, will treat Gram-positive organisms but have high-tissue toxicity and may act as carcinogens. Use of these dyes is not recommended. Sodium hypochlorite solutions consist of bleach and are appropriate for decontaminating inanimate objects, but they are not ideal on wounds; they combine high-tissue toxicity with antibacterial action. Quaternary ammonia compounds have the highest tissue toxicity of all topical agents in this group.
4. Determine if the wound is in bacterial balance, if it has an increased bacterial burden in the superficial compartment or infection in the deep compartment, or both the superficial and deep compartments are affected. Early recognition of bacterial imbalance, including infection, is crucial to wound management. Criteria to identify subtle clinical signs of infection have been suggested by 2 independent teams of researchers.7,12 Both identify exudate and friable granulation tissue as indicators of infection.7,12
Interestingly, both sets of researchers found a change in wound pain to be a leading indicator of infection. Using a Delphi process, Cutting et al12 extended their research to determine a more precise wound-type identification of infected wounds. They determined the following clinical indicators of infection to be common to all wounds: cellulitis, malodor, pain, delayed healing, wound deterioration or breakdown, and increase in exudate volume (except for acute wounds healing by primary intention and full-thickness burns).12
Cutting et al12 noted crepitus for pressure ulcers, phlegmon for neuropathic/diabetic ulcers, increase in local skin temperature for venous ulcers, and dry necrosis that may turn moist and boggy at the edges of the necrotic tissue for arterial disease associated tissue breakdown.
Clinicians may find the mnemonics, or enablers, NERDS© and STONES© helpful in making wound infection assessments (Figures 4-5). For superficial infection, think of NERDS:
* Nonhealing wounds
* Exudative wounds
* Red and bleeding wound surface granulation tissue
* Debris (yellow or black necrotic tissue) on the wound surface
* Smell or unpleasant odor from the wound.
For deep infection, think of STONES:
* Size is bigger
* Temperature increased
* Os [probe to or exposed bone]
* New or satellite areas of breakdown
* Exudate, erythema, edema
By using this superficial and deep separation, clinicians can identify wounds with increased superficial bacterial burden that may respond to topical antimicrobials and deep infections that usually require the use of systemic antimicrobial agents. Also, remember that bacterial swabs can guide therapy or identify resistant organisms, but the diagnosis of increased superficial bacterial burden or deep infection is made clinically. The bacteria in NERDS can be thought of as misbehaving. Treat superficial increased bacterial burden topically. Clinicians often need to look for 2 or 3 of the signs and symptoms of NERDS before making a diagnosis of increased superficial bacterial burden.
When considering whether the patient has a deeper compartment infection, remember that STONES sink to the bottom, that is, the characteristics of STONES are found when bacteria are deep within the chronic wound tissue or have penetrated the surrounding skin. Early recognition of infection is crucial so that appropriate systemic treatment can be started and further damage can be prevented.
5. Obtain a bacterial swab in selected patients. The diagnosis of infection is made through clinical assessment; however, the clinician may find the information gathered through bacterial swab cultures helpful in making treatment-based decisions. The results of the swab culture may assist the clinician in selecting antibiotic therapy and in ruling out bacterial resistance. The use of the Levine method of rotating the swab over 1 cm2 of tissue while applying gentle pressure seems to be the best approach to obtaining a semiquantitative sample.11,13 After obtaining the swab, the clinician should follow the protocol for storage and delivery of the swab to the laboratory.
Diagnostically, the semiquantitative method for assessing burden is acceptable in most clinical settings.11,13 Systemic treatment plans need to be reviewed once the results of the swab culture are available.
6. Select the appropriate topical treatment for superficial increased bacterial burden and benchmark criteria for monitoring response to treatment. Because NERDS are misbehaving, clinicians need to employ STAR-performing topical agent to bring them in line. Choose topical agents that are:
* not used Systemically
* not high in Tissue toxicity
* not likely to induce Allergy,
* not likely to be associated with bacterial Resistance.
Commonly used systemic agents, which should be avoided topically, include gentamicin and tobramycin. These agents will induce resistant organisms, such as Pseudomonas, on the wound surface and are occasional allergens. A number of traditional antimicrobial agents are cytotoxic. They are not well suited to the wound bed preparation paradigm and do not facilitate autolytic debridement or moisture balance. These agents are discussed under recommendation number 3.
Other common topical agents such as neomycin and bacitracin are associated with strong allergic sensitivity. Agents that can be considered for occasional use include silver sulfadiazine (broad spectrum but cannot be used in patients with a sulfa allergy), metronidazole (this is the exception to the rule and can be successfully used topically and systemically for anaerobes; resistance is not a problem), gramicidin, and polymyxin creams (broad-spectrum combination antimicrobial action, but avoid ointment vehicles that contain bacitracin).
For the superficial compartment infection, effective topical antimicrobial agents should be combined with moist interactive dressings that may also provide autolytic debridement. This has been accomplished with moisture control dressings that contain ionized silver.
The introduction of silver-based dressing has led to an explosion of products available on the market. No one product is appropriate for all patients. Clinicians must be aware of the level of ionized silver released and the mechanism of moisture balance in the dressing to match appropriate characteristics with the clinical features of the wound bed (Table 3). In some cases, the selection is mandated by the availability of products in the health care system's formulary.
Silver-based dressing products should be chosen for their relative silver release and moisture absorptive and retentive properties. Combinations with calcium alginates, hydrogels, and hydrocolloids will facilitate autolytic debridement. The highest silver-releasing dressings are available in the Acticoat (Smith & Nephew, Largo, FL) group. These dressings do not cause argyria as reported with silver sulfadiazine creams, but can temporarily stain the surrounding skin. A moderate release of silver is provided by Contreet Foam (Coloplast Corp, Marietta, GA), and SILVERCEL (Johnson & Johnson, Somerville, NJ). Many of the other silver dressings have a low release of the active ionized silver into the wound are also available. One exception is Actisorb (Johnson & Johnson), which only binds the silver in the dressing.
Organisms such as Pseudomonas may require higher concentrations of silver ions for bacterial killing. If superficial increased bacterial burden is present, silver dressings are often a good choice. But if the wound does not respond in 2 to 4 weeks, or signs of deeper infection become evident, then systemic antibacterial agents should be used. All silver dressings have a low toxicity to wounds, but they should be reserved for wounds with increased bacterial burden and their use should be discontinued when bacterial balance is established.
Cadexomer iodine is another treatment option using a topical antimicrobial therapy combined with moisture balance properties. This preparation is a sustained release of low-level iodine combined with cadexomer, providing moisture balance and absorbing 5 to 7 times its weight in water. The resulting hydrogel also provides autolytic debridement. Several studies have shown the benefit of this preparation, but they predate current best practices and the introduction of the wound bed preparation paradigm.
Krasner14 suggests consideration of the following when selecting dressings:
* Consider dressings by generic categories and compare new products with older products from the same category.
* Select the safest, most effective, user-friendly, and cost-effective dressing possible.
* Change the dressing based on the patient, wound characteristics, and dressing performance assessment as a guide rather than setting standardized routines.
* As the wound moves through the phases of the wound healing process, adjust the dressing protocol to optimize wound healing.
* Clinical experience with dressing materials is required to optimize their performance parameters and related unique characteristics or tricks.
7. Use appropriate systemic agents for increased deep and surrounding skin compartment infection (STONES) and benchmark criteria for monitoring response to treatment. Deep tissue infection can penetrate to bone and produce osteomyelitis. Grayson et al10 have demonstrated that probing to bone or exposed bone in patients with diabetes and foot ulcers is usually a reliable and valid sign of osteomyelitis, especially in persons with neuropathy and foot ulcers. This sign may not be as reliable for pressure ulcers of the pelvic region or in the absence of neuropathy; radiographs and scanning procedures for those wounds (eg, magnetic resonance imaging and bone scans) may be more reliable.
Surrounding tissue infection is referred to as cellulitis and is associated with pain, increased temperature, edema, and erythema. Cellulitis greater than 2 cm on the leg or foot of a patient with diabetes can be associated with a limb-threatening infection.15 Otherwise, the mnemonic STONES can help to identify deep tissue infection.
Clinicians need to be aware that both increased exudate and odor can indicate superficial and deep involvement. The other clinical criteria need to be assessed to decide whether bacterial damage is in the superficial or deep compartments, or even both.
Systemic antimicrobial therapy depends on local practice. In general, chronic wounds are initially affected by Gram-positive bacteria in the first month and, after that time, Gram-negative bacteria and anaerobes invade the tissue as well. The diagnosis of infection is made clinically. Swab results are used to identify organisms and their sensitivities. The duration of therapy depends on the benchmarked clinical parameters.
8. Reassess the wound at 1 week, and again at 2 and 4 weeks. If the benchmarked criteria are not improving, reassess recommendations 1 through 7. In addition, Flanagan16,17 noted that a 20% to 40% reduction in 2 and 4 weeks, respectively, is likely to be a reliable predictor of healing. Sheehan et al18 noted that a 50% reduction at week 12 was a good predictor of healing for patients with diabetic foot ulcers. One measure of healing is the clinical observation of the edge of the wound. If the wound edge is not migrating after appropriate antimicrobial therapy and healing is stalled, then advanced therapies (eg, growth factors, matrix metalloprotease inhibitors) should be considered to improve the healing process. However, these advanced and often expensive therapies should be initiated only after reassessment of the patient, coexisting causes of the wound, and cofactors have been ruled out. Wound healing is not always the primary outcome. Consider other wound-related outcomes, such as reduced pain, reduced bacterial load, reduced dressing changes, or an improved quality of life.
9. Do not use topical or systemic antibacterial agents long term without weighing the benefits and the risks. Discontinue antibacterial agents after the wound is in bacterial balance, unless the patient is prone to reinfection due to local or systemic factors (ie, when the patient is immunocompromised). A combination of the following evidence-based wound management principles is required:
* the product is effective in idealized clinical setting (efficacy) and this can be translated to efficiency in everyday practice, with safety substantiated by clinical studies
* exudate management has been optimized
* effective amount of silver or other antimicrobial is released over the wear-time of the dressing.
* enhanced quality of life has been facilitated by minimizing pain and optimizing activities of daily living for the patient
* cost-effectiveness has been demonstrated to make the dressing acceptable for the health care system.
10. Empower patients through education about wound bed preparation, coherent treatment plans, and the ability to practice prevention. Treatment plans that are developed without patient involvement are set up for failure. Empowerment of patients requires an appropriate explanation of evidence-based educational initiatives. Treatment plans need to be tailored to meet individual needs and ability of the patient to adhere to the treatment. The clinician should be sensitive to socioeconomic, cultural, psychosocial, and other individual domains when planning all interventions with the patient.
The Keller et al model19 provides guidance for clinicians to enhance patient communication by including 4 "E's" with every patient visit: engage, empathize, educate, enlist. For example, try to know something about the patient other than the reason for his or her visit (engage). Demonstrate true concern for the patient's well-being (empathy). Make sure the patient fully comprehends his or her disease process and agrees with the treatment plan (educate). Finally, determine if the clinician and the patient have mutually decided on a treatment plan and follow-up outcome (enlist).
Assessing the wounds for clinical signs and symptoms of inflammation and infection is an important part of preparing the wound bed for healing. Clinicians need an interprofessional team to optimize care but also must include the patient as a central part of all decisions. In this article, the clinician has been equipped with easy-to-use clinical criteria for diagnosing increased superficial bacterial burden and deep tissue infection (NERDS and STONES) as well as an organized approach to the selection of appropriate topical and systemic treatment (Table 4).
1. Sibbald RG, Orsted H, Schultz G, Coutts P, Keast D; International Wound Bed Preparation Advisory Board; Canadian Chronic Wound Advisory Board. Preparing the wound bed 2003: focus on infection and inflammation. Ostomy Wound Manage 2003;49(11):24-51.
2. Sackett DL. The fall of "clinical research" and the rise of "clinical-practice research." Clin Invest Med 2000;23:379-81.
3. Ryan S, Perrier L, Sibbald RG. Searching for evidence-based medicine in wound care: an introduction. Ostomy Wound Manage 2003;49(11):67-75.
4. Sibbald RG, Williamson D, Orsted H, et al. Preparing the wound bed-debridement, bacterial balance, and moisture balance. Ostomy Wound Manage 2000;46(11):14-35.
5. Falanga V. Classifications for wound bed preparation and stimulation of chronic wounds. Wound Repair Regen 2000;8:347-52.
6. Dow G. Infection in chronic wounds. In: Krasner D, Rodeheaver GT, Sibbald G, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 3rd ed. Wayne, PA: HMP Communications; 2001:343-56.
7. Gardner SE, Frantz RA, Doebbeling BN. The validity of the clinical signs and symptoms used to identify localized chronic wound infection. Wound Repair Regen 2001;9:178-86.
8. Cutting KF, Harding KG. Criteria for identifying wound infection. J Wound Care 1994;3:198-201.
9. Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen 2003;11(Suppl 1):S1-28.
10. Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW. Probing to bone in infected pedal ulcers: a clinical sign of underlying osteomyelitis in diabetic patients. JAMA 1995;273:721-3.
11. Dow G, Browne A, Sibbald RG. Infection in chronic wounds: controversies in diagnosis and treatment. Ostomy Wound Manage 1199:45(8);23-40.
12. Cutting KF, White RJ, Mahoney P, Harding KG. Clinical identification of wound infection: a Delphi approach. In: EWMA Position Document-Identifying Criteria for Wound Infection. London: MEP Ltd; 2005:6-9.
13. Levine NS, Lindberg B, Mason AD Jr, Pruitt BA Jr. The quantitative swab culture and smear: a quick method for determining the number of viable aerobic bacteria on open wounds. J Trauma 1976;16:89-94.
14. Krasner D. Dressing decisions for the twenty-first century: on the cusp of a paradigm shift. In: Krasner D, Kane D, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 2nd ed. Wayne, PA: Health Management Publications, Inc, 1997:139-51.
15. Joshi N, Caputo GM, Weitekamp MR, Karchmer AW. Infections in patients with diabetes mellitus. N Engl J Med 1999;341:1906-12.
16. Flanagan M. Improving accuracy of wound measurement in clinical practice. Ostomy Wound Manage 2003;49(10):28-40.
17. Flanagan M. Wound measurement: can it help us to monitor progression to healing? J Wound Care 2003;12:189-94.
18. Sheehan P, Jones P, Caselli A, Giurini JM, Veves A. Percent change in wound are of diabetic foot ulcers over a 4-week period is a robust predictor of complete healing in a 12-week prospective trial. Diabetes Care 2003;26:1879-82.
19. Keller V, White MK, Carroll JG, Segal E. Physician-Patient Relationships Workbook. West Haven, CT: Bayer Institute for Health Care Communication; 1995.
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