CHRONIC WOUNDS: NONHEALABLE AND MAINTENANCE WOUND CATEGORIES
The holistic approach to healable wound management as outlined in Table 1 stresses an accurate diagnosis and successful treatment with a team approach. (See Enabler: Persons With Healable Chronic Wounds(s).) For patient wounds that do not have the ability to heal, the approach is different. (See Enabler: Persons With Nonhealable or Maintenance Wound(s).) These individuals with the inability to heal (nonhealable wound) may be due to inadequate blood supply and/or the inability to treat the cause or wound-exacerbating factors that cannot be corrected. The second category, a maintenance wound, is when the patient refuses the treatment of the cause (eg, will not wear compression) or a health system error or barrier (no plantar pressure redistribution is provided in the form of footwear or the patient cannot afford the device). These may change, and periodic re-evaluation may be indicated (see Enabler).
Chronic wounds are disabling and constitute a significant burden on patients' activities of daily living (ADLS) and the healthcare system. Of persons with diabetes, 2% to 3% develop a foot ulcer annually, whereas the lifetime risk of a person with diabetes developing a foot ulcer is as high as 25%.8 It is estimated that venous leg ulcers (VLUs) affect 1% of the adult population and 3.6% of people older than 65 years.9 As our society continues to age, the problem of pressure ulcers (PrUs) is growing. Each of these common types of chronic wound will require accurate and concise diagnosis and appropriate treatment as part of holistic care.
Local wound care may also be difficult to optimize. Chronic wounds are often recalcitrant to healing, and they may not follow the expected trajectory that estimates a wound should be 30% smaller (surface area) at week 4 to heal in 12 weeks.10,11 If all 5 components of WBP have been corrected (cause, patient-centered concerns, and the 3 components of local wound care) and a healable wound is stalled, re-evaluation of the current diagnosis and treatment plan is necessary to be sure each component has been idealized before considering active local advanced therapies (edge effect). This update will clarify the system outlined above, dividing chronic wounds into healable, maintenance, and nonhealable categories. The authors will develop the clinical parameters around critical colonization with any 3 or more of the 5 NERDS mnemonic criteria for topical therapy versus or any 3 or more of the 7 STONEES mnemonic criteria associated with the deep and surrounding skin infection for systemic antimicrobial agents.
The updated WBP 2011 quick reference guide is intended for all wound-healing practitioners from basic to intermediate or advanced levels ideally organized in transdisciplinary teams. To clarify the rationale for the evidence-informed practices, the authors discuss each item individually with reference to key supporting literature and enablers for practice where indicated.
IDENTIFY AND TREAT THE CAUSE(S) OF THE WOUND
- 1A: Determine if there is adequate blood supply to heal
This is often important, especially for ulcers on the leg or foot. It is important to inspect the foot and lower leg for signs of arterial compromise (dependent rubor, pallor on elevation, and loss of hair on the foot or toes), as well as palpating for a plantar pulse (dorsalis pedis or posterior tibial). Practitioners need to remember that a small percentage of patients may have an anomalous or anatomical variance resulting in absence of the dorsalis pedis artery. A palpable pulse indicates a foot arterial pressure of 80 mm Hg or higher. The authors record a pulse as present or absent. However, a palpable pulse may not always exclude an arterial etiology. Although a foot pulse might be palpable, the nonhealing wound might be situated in a different angiosome that has to be revascularized in order to induce healing (angiosome model).12 Doppler examination of the Ankle Brachial Pressure Index (ABPI) is indicated if the pulse is not palpable or to assess the appropriateness of high or modified compression bandaging for venous ulcers Table 2.
The audible Doppler signals may also be useful diagnostically: a triphasic normal sound, a biphasic sound indicative of arterial compromise, and the monophasic or absent signal with advanced ischemia. Complete segmental lower-leg arterial Doppler examinations are needed if there is a possibility of a proximal lesion or arterial restriction or blockage that is amendable through surgical bypass or endovascular dilatation. If blood supply is inadequate or cannot be immediately determined, dressing selection should be based on a maintenance wound program with moisture reduction and bacterial reduction until further assessments are performed.
Toe pressures are useful because about 80% of people with diabetes and 20% of the nondiabetic population have calcified large leg arterial vessels that are nonpliable and stiff, leading to falsely high ABPI levels often greater than 1.3.13 When ABPI levels are this high, no conclusions can be drawn about the quality of limb perfusion without further investigation. In Table 3, the arterial status is co-related to the vascular testing results.
- 1B: Identify the cause(s) as specifically as possible or make appropriate referrals
A comprehensive wound assessment is required to determine the cause of the wound. In order to achieve this, a holistic approach to the patient assessment is needed. An interprofessional team approach will facilitate a comprehensive review of the whole patient, the environmental factors, and the wound. In a recent community, comprehensive interprofessional assessment of leg and foot ulcer patients, more than 60% of diagnoses were changed or made more specific, leading to the implementation of best practices, thus facilitating the optimization of WBP and improving healing rates of chronic wounds.16
- 1C: Review cofactors/comorbidities (systemic disease, nutrition, medications) that may delay or inhibit healing
Wound healing can be delayed or interrupted in persons with a coexisting systemic disease and the multiple comorbidities associated with chronic wounds. In the case of diabetes, excess glycosylation of hemoglobin due to poor diabetic glucose control can result in prolonged inflammatory phase in addition to decreased neutrophil and macrophage phagocytosis of bacteria. Furthermore, diabetes affects the erythrocytes' ability to deliver oxygen to the wound, a fundamental step in collagen synthesis and tissue proliferation17 along with numerous other important factors in wound healing. An original investigation by Markuson et al18 demonstrated that individuals with lower hemoglobin A1c (HgbA1c)levels had improved and shorter healing time. This translated to a cost reduction because the closed wounds had decreased risk of infection compared with the ulcers that were still in the healing phase.
A detailed review and clinical analysis of patient cofactors and comorbidities that may influence healing should be carried out in a systems-based approach. Systemic diseases such as diabetes or autoimmune disease may interfere with the stages of wound healing and stall or prevent healing.
A low protein intake or relative deficiency can prevent the production of granulation tissue that will contribute to a stalled healing environment for the wound. A given albumin measurement in a patient implies nutritional status over a few months, and these levels are a gross indicator of long-term nutritional deficit. Albumin levels measure the large reservoir of amino acids that serve as the fundamental building block for wound healing. Several other patient stressors can influence albumin levels.19 Normal serum albumin levels are 3.4 to 5.4 g/dL,20 and levels 2.0 to 3.4 g/dL are associated with potential delayed healing and may need to be treated as a maintenance wound until they are corrected. Prealbumin (transthyretin) is a more sensitive indicator of protein deficiency, reflecting levels over 18 to 21 days. Transferrin is often thought of as an indirect measurement of nutrition; however, levels elevate in response to infection or inflammation; therefore, results can be misleading in persons with a chronic wound.21 Cost and access to transferrin level testing may be a challenge in some practice settings. Published literature attributes recumbent positioning of patients with a direct decrease in serum liver proteins such as albumin, prealbumin, and transferrin.22,23 Therefore, in utilizing the "whole patient" concept, we should optimize activity and mobilization.
Individualized patient medicine reconciliation should take place as part of any wound management protocol. Several medications that may alter the healing processes on the cellular level need to be identified. Some medications important to note in the assessment of a wound are high doses of systemic steroids, immunosuppressive drugs, and antimetabolite cancer chemotherapy. Vitamin E intake of more than the recommended 100 IU daily can impair healing24 because of its oxygen-scavenging property at the tissue level that is opposite to the oxygen-sparing property of vitamin C.
- 1D: Evaluate the person's ability to heal: healable, maintenance, nonhealable
Categorizing a wound according to its ability to heal (healability) assists the clinician in the determining an accurate diagnosis along with a realistic individualized treatment approach. Adequate tissue perfusion is necessary for a healable wound. As outlined above, decreased vasculature will increase the risk of infection and decrease healability. In order to be classified as a healable wound, the wound should have several attributes including an adequate blood supply; the cause of the wound must be corrected; existing cofactors, conditions, or medications that could potentially delay healing must be optimized or ideally corrected. A maintenance wound is a wound that may be healable but that either healthcare system factors or patient-related issues are preventing the wound from healing. A nonhealable wound is a wound that does not have adequate blood supply to support healing or the cause cannot be corrected. In nonhealable wounds, moist interactive healing is contraindicated and debridement should be on a conservative basis only (expert opinion for SCALE document).
Woo et al25 Table 4 assessed patients with lower-leg and foot ulcers. The healability percentages of consecutive consenting home care patients with leg and foot ulcers from Toronto and Mississauga (Ontario, Canada) districts have been tabulated in the final column of Table 2. The results indicated that most subjects had a demonstrated ability to correct the cause and achieve adequate circulation for healing (69.0%). Determining if a patient is healable, nonhealable (5.2%), or maintenance (24.9%) allows the clinician to identify and address specific individualized challenges, particularly for the nonhealable and maintenance wound patients. Along with the patient's input, the clinician is able to tailor the nonhealable or maintenance care plan, facilitating responsible use of available resources along with realistic treatment goals. In general, advanced active therapies are not indicated for maintenance or nonhealable wounds.
When a healable wound does not progress at the expected rate, a chronic and stalled wound results. These wounds are more prevalent in older adults and are attributed to the aged skin and comorbidities, such as neuropathy, coexisting arterial compromise, edema, unrelieved pressure, inadequate protein intake, coexisting malignancy, and some medications. Persistent inflammation may be the cause of a stalled wound and in some cases may not be correctable. The presence of multiple comorbidities in some older adult patients implies that healing is not a realistic end point.26 For nonhealable or maintenance wounds, pain and quality of life may be indicated as the primary goals of care. Palliative wound care often includes nonhealable wounds, but patients undergoing palliative care may have maintenance or even healable wounds.
Frequently, skin changes at life's end may be associated with individual risk factors and comorbidities. In 2009, an 18-member international expert panel explored the issues and research literature surrounding end-of-life skin and wound care, including the Kennedy Terminal Ulcer (case series evidence)27 and the concept of skin compromise.28 The panel developed a consensus document entitled "Skin Changes At Life's End" (SCALE). A modified Delphi process with 52 international distinguished reviewers was utilized to reach consensus on the document. The 10 final consensus statements have clarified the authors' views on skin and wound conditions at the end of life.
Of the 10 SCALE consensus statements, statement 1 is key: "Physiologic changes that occur as a result of the dying process may affect the skin and soft tissues and may manifest as observable (objective) changes in skin color, turgor, or integrity, or as subjective symptoms such as localized pain. These changes can be unavoidable and may occur with the application of appropriate interventions that meet or exceed the standard of care."29 The panel explored the work by Kennedy,27 where a descriptive study describes the phenomenon of PrUs that occur in the sacral area of dying patients was observed in a long-term-care facility. Kennedy's27 work was the first modern descriptive research to discuss this issue that was depicted in 1877 by Jean-Martin Charcot and termed the decubitus ominosus.
In an observational study that took place in a 10-bed large teaching hospital palliative care unit, the staff reported that 5% of the patients had skin changes of reddish-purple discoloration ranging from 2 hours to 6 days prior to death. These areas of intact skin rapidly became full-thickness PrUs.30 The staff turned patients hourly. Within minutes of the prior skin assessment, skin changes that were reddish purple and found over various areas of the body appeared shortly before death. This study provides observational data on some of the unavoidable skin changes at life's end.
- 2A: Develop an individualized plan of care
Following the wound assessment as described above, an individualized wound plan of care should be developed by the interprofessional team. The plan must be tailored to the individual, taking into consideration his/her unique biopsychosocial needs including
- risk factors
- quality-of-life issues
- support systems/circle of care
- access to care
- personal preferences
As discussed by Sackett et al,31 individualized patient preference must be honored and reflected in the wound care plan. Sackett et al31 recognized 3 dimensions of equal importance: best available scientific evidence, clinical expertise, and patient preference. This model of evidence-based medicine has been one of the most important healthcare trends in the past 20 years. Interprofessional, individualized patient-centered care must drive the care process.32
The wound care plan of care should be as follows:
- in writing and part of the permanent healthcare record
- routinely evaluated and updated
- updated with any significant change in the individual's health status.
- 2B: Treat the cause(s) related to specific wound etiology/diagnosis
Once an accurate type of wound is established, the treatment can be planned and implemented Table 5.
For example, in a person with a venous ulcer, compression therapy is contraindicated when ABPI is 0.5 or less, and a vascular consult is required for limb preservation.33 Under the care of an expert wound care team, modified compression therapy for patients with ABPI between 0.5 and 0.8 is beneficial and assists perfusion by increasing pulsatile flow,34 thereby decreasing venous pressure and facilitating the arterial-venous gradient.35
IMPORTANCE OF HOLISTIC INTERPROFESSIONAL COORDINATED AND COLLABORATIVE CARE
Accurate wound diagnosis and development of successful treatments plans can be a challenging undertaking, given the complexity of chronic wounds. A holistic interprofessional approach is required. Each member of the team possesses a unique professional skill set and knowledge base that should contribute to the individualized plan of care. Implemented treatment plans that do not yield wound-healing rates at the expected trajectory require a timely referral to an interprofessional team that can re-evaluate the diagnosis and causative factors. Redefining the treatment goals with the input from the patient, family, and healthcare provider is essential as well.
- 2C: Modify (if possible) systemic factors/other cofactors that may impair healing: medications, nutrition, hemoglobin, HgbA1c, blood pressure, creatinine, CHF, LFTs, and so on
A good example of systemic factors that affect wound healing is the hemoglobin level. Because hemoglobin carries the oxygen that is essential for new tissue building, hemoglobin levels should be optimized. Potential negative influences for adequate hemoglobin are common in patients living with other chronic illnesses such as renal disease, sickle cell, and other anemias, to name a few.
Persons with cardiopulmonary disease; cardiovascular disease, including congestive heart failure; and related conditions have diminished extremity tissue perfusion as a result of reduced ejection fractions. In particular, heart failure and associated decreased tissue perfusion to the periphery results in edema accumulation in the lower extremities, creating higher risk for lower-leg wound formation or delayed healing in existing wounds. In many cases, an internal medicine or subspecialty referral can optimize heart function and manage fluid balance and edema reduction. The offending cocontributors and cofactors that impede wound healing should be adjusted and corrected. By improving as many factors as possible may contribute to overall improvement of the patient's quality of life, reducing pain, improving mobility, and facilitating improved wound outcomes.
A patient with a chronic wound may require a thorough nutritional assessment by a registered dietitian, to address any underlying and correctable nutritional deficits. Proteins have a fundamental role throughout the wound-healing cycle influencing the function of leukocytes, phagocytes, monocytes, lymphocytes, and macrophages, all integral to a normal healing trajectory.36,37 A multinational European, prospective randomized controlled, double-blind trial has studied the effects of specific oral nutritional supplementation in nonmalnourished patients specific to PrU healing. The provision of a high-protein, micronutrient-enriched and arginine supplement resulted in improved healing rates and less wound care intensity for the care providers.38
Medications that may inhibit or delay wound healing should be reviewed, including the benefit, risk, and dose of each medication. Refer to section 1C for more detail.
ADDRESS AND TREAT INDIVIDUALIZED CONCERNS
- 3. Assess and support individualized concerns
- 3A: Pain
McCaffery39 has stated that pain is what the patient says it is.Every person experiences pain differently. Clinicians cannot treat pain that they do not know patients are experiencing. Pain measurement is subjective; however, the universally accepted measurement techniques are the utilization of visual analog scales (10-cm line with no pain at one end and worst possible pain at the other end, and the patient places an "x" at the appropriate point), Faces Pain Scale (various levels of happy and sad faces), or the numerical rating scale. The numerical rating scale asks if the patient has any pain on a 0- to 10-point scale with the anchors that 0 is no pain, 5 is the pain associated with a bee sting, and 10 would be the amount of pain experienced by slamming the car door on your thumb. Even in patients who cannot respond verbally, such as those with dementia, pain still needs to be assessed. There are pain scales for these patients that rely on nonverbal clues such as facial grimaces and pupil dilatation. (Assessment of pain for people with dementia can be found at www.hartfordign.org.) Pain levels should be recorded before dressing change, during dressing change, and after dressing reapplication.
Krasner has defined wound associated pain at dressing change (intermittent and recurrent) versus incident pain from debridement or the persistent pain between dressing changes. Woo carried the Krasner concept further and demonstrated that anxiety and other patient-related factors could intensify the pain experience. The Wound Associated Pain model of Woo and Sibbald Figure 1 defines pain from the cause of the wound as often being persistent or present between dressing changes and distinguishes this pain from the pain associated with local wound care components (dressing change, debridement, infection, lack of moisture balance). All of these factors can be modified by patient-centered concerns, including previous pain experience, anxiety, depression, mobility and awareness or lack of comfort with the setting, and the procedure or treatment plan. Pain is an underrecognized and undertreated component of chronic wound care that has been demonstrated to be more important to patients than healthcare professionals. Causes of pain at dressing change include the dressing material adhering to wound base, skin stripping from strong adhesives, and aggressive trauma from cleansing technique (eg, scrubbing with gauze).
Many patients also express chronic persistent pain between dressing changes even at rest. A systematized approach should examine other systemic and disease factors that may play a role in precipitating and sustaining persistent wound-related pain. Common systemic factors are bacterial damage from superficial critical colonization or deep and surrounding compartment infections, deep structural damage (eg, acute Charcot foot in patients with diabetes), abnormal inflammatory conditions (eg, vasculitis, pyoderma gangrenosum), or periwound contact irritant skin damage from enzyme-rich wound exudate.
The impact of chronic unrelenting pain can be devastating, eroding the individual's quality of life and constituting a significant amount of stress. Increased levels of stress have been demonstrated to lower pain threshold and decrease tolerance. The result is a vicious cycle of pain, stress/anxiety, anticipation of pain, and worsening of pain. Increased stress also activates the hypothalamus-pituitary-adrenal axis, producing hormones that modulate the immune system compromising normal wound healing. Medications including nonnarcotic for moderate pain and narcotic analgesics for moderate to severe pain are required to treat severe pain as outlined below. A consult from a pain and symptom management team may be considered. Comprehensive management should also include careful selection of atraumatic dressing, prevention of local trauma, treatment of infection, patient empowerment, stress reduction, and patient education.
The medical treatment of Wound Associated Pain and other components of pain management are outlined in the World Union of Wound Healing Societies documents.40,41 In general, wound-associated pain is both nociceptive and stimulus dependent (gnawing, aching tender, throbbing) versus neuropathic or non-stimulus-dependent or spontaneous pain (burning, stinging, shooting, stabbing). Nociceptive pain is treated with the WHO pain ladder medication starting with aspirin and nonsteroidal anti-inflammatory drugs and then progressing to weak and strong narcotics.42 Short-acting agents are often used to determine the dose of longer-acting agents, and then the short-acting agents may be used for breakthrough. The neuropathic pain often responds to tricyclic agents, particularly second-generation agents high in antinoradrenaline activity (nortriptyline and desipramine are often better than amitriptyline) and for nonresponders with alternate agents gabapentin and pregabalin or other antiepileptic agents. Neuropathic pain occurs even with the loss of protective sensation and can awaken persons with neuropathy at night with lightning-like flashes of pain.
- 3B: Activities of Daily Living
Living with a chronic leg ulcer and ADLs has the largest body of evidence, mainly using qualitative methodology, compared with other ulcer etiologies. Patients reported numerous negative influences on their ability to carry out ADLs including, pain, odor, mobility, finances, and aspects of living.43 Depression and anxiety were reported in as many as 68% of the subjects. Another recent study highlighted the dominant impact of social isolation in patients suffering from chronic leg ulcers.44 One study compared patients living with diabetic foot ulcers (DFUs) and those with amputation following foot ulcers and concluded that a higher quality of life was reported in those who underwent previous lower-limb amputations.45 Assessing the unique individual's concerns can be time-consuming but a necessary piece in addressing the patient's holistic needs. This highlights the emotional burden of living with a chronic wound.
- 3C: Psychosocial Well-being
Psychosocial well-being is the dimension of quality of life that most people equate with the quality piece.46 It includes the individual's psychological perspectives on his/her wound and overall life. It reflects the person's ability to socialize and interact with others.
There are many wound care interventions that can address and support a person's wound-related psychosocial issues. For example:
- If wound odor is an issue, charcoal or other odor-reducing dressings can be utilized.
- Dressing routines can be modified to accommodate individualized hygiene practices. For showers Mondays-Wednesdays-Fridays, dressing changes can be coordinated to Mondays-Wednesday-Fridays right after the shower.
Cigarette smoking is a leading preventable health problem causing damage to the endothelial function of arteries throughout the body,47 contributing to the development of vascular disease of both arterial and venous origin. The direct cutaneous effect of smoking is stated clearly by Rayner.48
"Cutaneous blood flow decreases as much as 40% to produce ischemia and impair healing.49 Smoking a single cigarette creates a vasoconstrictive effect for up to 90 minutes, while smoking a packet results in tissue hypoxia that lasts an entire day."50
Delayed wound healing for individuals who use tobacco is attributed to resultant tissue hypoxia.51 Smoking disrupts the normal healing process at many levels, decreasing cell proliferation and migration across the wound bed.52-54 Cigarettes contain more than 4000 substances, including carbon monoxide, nicotine, and cyanide derivatives,55 and each substance can potentially negatively influence wound healing. Useful patient smoking cessation strategies, including the pharmacological, behavioral, and effectiveness of these programs, are outlined by Ahn et al.55
Offering patients these strategies to quit smoking and improve tissue oxygenation may enhance healing.
- 3E: Access to care, financial limitations
Living with a wound can be a challenge for many patients who may have limited financial resources or access to care. Patients living with chronic illnesses compounded by a wound may have difficulties with transportation for medical appointments, and many are unemployed or on limited incomes. Depending on where the patient lives, there are differing resources available. Healthcare professionals should advocate for required patient resources. When a wound is determined to be maintenance or nonhealing, the healthcare team, along with the patient, can individualize the care plan to be most efficient for both the patient and the system.
- 4. Provide education and support to the person and his/her circle of care (including referral) to increase adherence (coherence) to the treatment plan
One strategy to provide support and education to a patient is by developing a therapeutic relationship.56 Trust implies sharing of information and communication, and open dialogue allows the patient and those in their circle of care to understand that each person involved has a meaningful contribution. Active participation by the patient in the development of an individualized plan of care provides reassurance to the patient that the team is working with them to achieve the best possible outcome. This helps to enhance adherence to the agreed upon treatment plan, as there is "trust." An additional concept in team dynamics is unit cohesion or the process of "sticking together" for the accomplishment of a mission or task. If the patient provides substantive input into the treatment plan, there is a greater chance that the patient will adhere (cohere) to a given plan. By way of example, patient participation, such as removing the dressing at dressing change, should be encouraged as clinically appropriate. People in the patient's circle of care such as family, caregivers, and healthcare professionals should also be part of the plan, including implementation and re-evaluation. Communication is paramount between healthcare sectors and professionals when managing chronic wounds. Once an expert team has determined that a wound is maintenance or nonhealable wound, it is important that this be communicated to prevent unnecessary investigations or interventions that may have already been unsuccessful. Healthcare professionals should review and educate the patient and family after determining their current knowledge gaps. Teaching the patient to report important signs that could indicate a deterioration of the wound is critical. Strategies to improve adherence have been reported in a comprehensive review by Osterberg and Blaschke.57
LOCAL WOUND CARE
- 5. Assess and monitor the wound history and physical examination
Documentation of a detailed patient and wound assessment is a legal requirement from both an organizational and professional standards perspective. Specific details about the wound history and physical will facilitate communication within the patient's circle of care. This includes the type of wound and history and the patient-centered plan of care and targeted patient-specific goals.58 The details of the wound assessment should be communicated to other professionals when referrals are made. If a wound is healable, nonhealable, or maintenance, an individualized care plan is made to identify specific interventions and outcomes that the patient and interprofessional team agree upon and modify based on a new holistic interprofessional assessment. One example is the mnemonic MEASURE,59 which describes the wound location plus MEASURE:
- Measure size-longest length with the widest width at right angles
- Exudate amount (none, scant, moderate, heavy) and characteristics (serous, sanguinous, pustular, or combinations)
- ppearance (base: necrotic [black], fibrin [firm yellow], slough [soft yellow], or granulation tissue [pink and healthy vs red and friable = easy bleeding, unhealthy])
- Suffering (pain)
- Undermining (measure in centimeters and use hands of clock to document: 12 o'clock, 6 o'clock, and so on)
- Edge (hyperkeratotic, macerated, normal)
Using a framework allows consistent documentation of a wound. When a framework is used to assess a wound over time, clinicians can identify if a wound is improving, stalled, or deteriorating.
There are several new electronic technologies available for wound assessment, but they may be costly for clinicians and healthcare systems. Novel camera systems accurately calculate length, width, depth, and surface of exposed wound areas. Limitations include undermined areas or sinuses that are not measureable using this technology requiring supplementation by visual clinical inspection and probing. Wound assessment devices markedly differ from computer-based documentation systems that capture multiple data points and assessments about wound parameters inputted by skilled clinicians.
- 6. Gently cleanse wounds with low-toxicity solutions: saline, water, and acetic acid (0.5%-1.0%). Do not irrigate wounds where you cannot see where the solution is going nor cannot retrieve (or aspirate) the irrigating solution.
The standard of care for wound cleansing is to use those solutions that are gentle and least cytotoxic to the wound as possible: saline, water, and acetic acid (0.5%-1.0%). Research has shown that certain solutions can be cytotoxic to healing cells, such as fibroblasts, in vitro.60
In the analysis of Cochrane Reviews prior to 2008, the authors' concluded "There is not strong evidence that cleansing wounds per se increases healing or reduces infection." The Cochrane Collaboration updated evidence reviews in 2011 on wound cleansing for PrUs and concluded there is "no good evidence to support use of any particular wound cleansing solution or technique for PrUs."61 A specific type of solution for wound cleansing in adults was an additional evidence review in 2010. The authors concluded that there is no evidence to indicate that using tap water to cleanse an acute wound increased infection rates. In addition, there is no strong evidence demonstrating that cleansing of wounds at all decreases healing infection or promotes healing.62 Expert opinion recommends that caution should be considered in the use of tap water for immunocompromised individuals, especially the use of nonpotable water, which may be a problem in developing countries.
Avoiding cytotoxic solutions, such as Dakin's and povidone-iodine, to cleanse healable wounds or using them for only limited periods is reasonably prudent practice. However, there is a place for these agents in the management of maintenance or nonhealable wounds to potentially control bioburden and odor. In these cases, the reduction in bioburden and moisture reduction outweighs the small potential for tissue toxicity.
Wound irrigation has also been the subject of controversy and disagreement between health professionals. In general, the authors recommend that clinicians should not irrigate wounds where they cannot see where the solution is being instilled into the dead space at the base of the wound, or if they cannot retrieve the irrigating solution. More research on wound cleansing is needed. (See Table 5 for antiseptic solutions and their utility for wound care.)
- 7. Debride: Healable wounds-sharp or conservative surgical, autolytic, mechanical, enzymatic, biological (medical maggots); nonhealable and maintenance-conservative surgical or other methods of removal of nonviable slough.
The wound bed is optimally prepared by aggressive and regular debridement of any firm eschar or soft slough if the wound is healable. A firm eschar serves as a proinflammatory stimulus inhibiting healing, whereas the slough acts as a culture media for bacterial proliferation and should be removed.63 Debridement may also promote healing by removing senescent cells that are deficient in cellular activities and biofilms that contain the bacterial colonies.64
Sharp debridement is the most expeditious method but may not always be feasible because of pain, bleeding potential, cost, professional/system regulations, and the lack of clinician expertise. Cardinal et al65 conducted a retrospective review on 366 persons with VLUs and 310 persons with DFUs over 12 weeks observing wound surface area changes and closure rates. Interestingly, VLUs had a significantly higher median wound surface area reduction with surgical debridement (when clinically indicated due to the presence of debris) versus no surgical debridement (34%, P = .019). Centers with more frequent debridement were associated with higher rates of wound closure (P = .007 VLUs, P = .015 DFUs). The debridement frequency did not statistically correlate to higher rates of wound closure. There was some minor evidence of a positive benefit of serial debridement in DFUs (odds ratio, 2.35; P = .069).
Alternatively, autolytic debridement is most accepted by keeping a moist wound environment to enhance the activities of phagocytic cells and endogenous enzymes on nonviable tissues. Mechanical debridement with saline wet-to-dry dressing contributes to local trauma and pain. In the United States, the Centers for Medicare & Medicaid Services, in its Tag F314 guidance, cautions that there should be limited use of wet-to-dry dressings. Emerging technology using ultrasonic devices has also been demonstrative WBP without the incumbent painful and traumatic scraping and cutting associated with sharp and mechanical debridement. When using enzymatic debridement, clinicians should ensure that the cleansing solutions and type of dressing used to cover the wound do not interfere with or cancel out the action of the enzyme.
Select the appropriate method of wound debridement considering the patient, the wound characteristics, and the skill and knowledge of the clinician, along with the available resources. In summary, the different methods of debridement have distinct features in terms of pain potential, cost, healthcare professional time and skill level required, resources used, and wound characteristics. (See the Enabler: Key Factors in Deciding Method of Debridement.)
- 8. Assess and treat the wound for superficial critical colonization/deep infection/abnormal persistent inflammation (mnemonic STONEES), or persistent inflammation: any 3 NERDS-treat topically: Non-healing, ↑Exudate, Red-friable tissue, Debris, Smell;any 3 STONEES-treat systemically: ↑Size, ↑Temperature, Os, New breakdown, ↑exudate, ↑Erythema/Edema (cellulitis), Smell; Persistent inflammation (non-infectious): Topical and/or systemic anti-iflammatories. (See Enabler: Sibbald Cube.)
Chronic wounds containing bacteria and/or the presence of bacteria obtained from a surface swab do not define or portend infection. In fact, the mean number of bacterial species per chronic ulcer has been found to range from 1.6 to 4.4.66 Critical to wound healing is the achieving of an appropriate bacterial balance and understanding the differences between contamination or colonization or frank bacterial damage with surface critical colonization or surrounding/deep infection. The risk of infection is determined by the number and nature of invading bacteria as well as host resistance as outlined in the following equation:
Infection = number of organisms × organism virulence
Host resistance is the most important factor, and it refers to the host immune response to resist bacterial invasion and prevent bacterial damage.67 In addition, adequate blood supply is needed for the wound to heal as a decreased or inadequate blood supply favors bacterial proliferation and damage that may prevent or delay healing. Infection is more prevalent in certain disease conditions. For example, individuals with diabetes have at least a 10-fold greater risk of being hospitalized for soft tissue and bone infections of the foot than nondiabetic individuals.68 Local factors inhibiting healing may include a large wound size, the presence of foreign bodies (prosthetic joints, a thread, or remnants of gauze or a retained suture), and an untreated deeper infection, such as osteomyelitis.69 External contamination of the wound bed by microorganisms can occur from the ambient environment, dressings, the patient's secretions and hands, along with the hands of healthcare providers (alcohol hand rinses are more effective in reducing hand bacteria than washing with soap and water).
By using this superficial and deep-surrounding tissue separation, the clinician can identify wounds with increased bacterial burden that may respond to topical antimicrobials and deep infection that usually requires the use of systemic antimicrobial agents. The mnemonics NERDS and STONEES represent the initials of the signs to categorize the 2 levels of bacterial damage or infection. This concept was introduced70 in 2007 and validated in 2009.71 Three or more of these signs should be sought for the diagnosis in each level. If increased exudate and odor are present, additional signs are needed to determine if the damage is superficial, deep, or both.
There are now at least 5 classes of antimicrobial dressings and some miscellaneous products for use in chronic wounds with critical colonization as defined by any 3 of the NERDS criteria.
- silver dressings combined with alginates, foams, hydrofibers, and hydrogels
- honey dressings in a calcium alginate wafer and hydrogel
- iodine in a cadexomer carbohydrate or polyethylene glycol slow release formulation (not available in the United States)
- PHMB (polyhexamethylene biguanidine) derivative of chlorhexidine in a foam or gauze packing)
- miscellaneous antimicrobial dressings often with a paucity of clinical studies to support their use
The treatment of critical colonization often takes 2 to 4 weeks in a healable wound where the cause has been corrected and patient-centered concerns have been addressed. There is some, but limited, evidence to show the benefit of these dressings.72 If the wound is in bacterial balance, antibacterial dressings are not needed for the re-epithelialization stage of wound healing, unless they also provide anti-inflammatory activity.72,73 They also are not efficacious in the treatment of deep and surrounding tissue infection that requires the use of systemic agents. Studies that do not select the proper subpopulation (eg, healable critically colonized wounds without deep infection) or measure complete wound healing have failed to demonstrate any benefit from these dressings.74
The use of antimicrobial dressings should be reviewed at frequent and regular intervals every 1 to 2 weeks and discontinued if critical colonization has been corrected or if they do not demonstrate a beneficial effect after 2 to 4 weeks. There is currently a great tendency to overuse antimicrobial dressings, creating a cost-inefficient use of these useful devices. The conflicting evidence and misuse of these dressings have led some European healthcare systems to completely delist silver products.
The effectiveness of silver-releasing dressings in the management of nonhealing (stalled) chronic wounds was reviewed by a meta-analysis.75 In comparison to alternative antimicrobials, silver dressings significantly:
- improved wound-healing rate (95% confidence interval [CI], 0.16-0.39, P < .001);
- reduced odor (95% CI, 0.24-0.52, P < .001) and pain-related symptoms (95% CI, 0.18-0.47, P < .001);
- decreased wound exudate (95% CI, 0.17-0.44, P < .001); and
- had a prolonged dressing wear time (95% CI, 0.19-0.48, P = .028) when compared with alternative wound management approaches.
Silver's broad spectrum of antimicrobial activity can be used in critically colonized chronic wounds that have the ability to heal. Silver must be ionized to exert an antimicrobial effect. Ionized silver requires an aqueous or water environment and should not be used in a maintenance or nonhealable wound where the desired outcome is the combination of moisture reduction and bacterial reduction. Silver should not be in close proximity to any oil-based products (eg, petrolatum, zinc oxide) where the oil molecules may interfere with the ionization of the silver. Products that produce a continuous supply of ionized silver are likely to be more efficacious, and higher levels of silver release are often necessary to treat micro-organisms such as pseudomonas in a complete environment, such as a wound. Pseudomonas require a higher silver level for silver to work than most other bacterial organisms. Silver resistance is uncommon because there are at least 3 antimicrobial mechanisms with silver targeting and combining with membranes, cytoplasmic organelles, and DNA.
The amount of silver released from these dressings is a fraction of the silver released from silver sulfadiazine (SSD) cream formulations. Serum silver levels even from high-release silver dressings are in the 1-5 micromolar range. Modern silver dressings seldom exceed normal range unless large surface areas are treated over prolonged time or the patient has a large skin surface area to total weight. Silver dressings can cause periwound temporary staining but not leave permanent silver deposits in the dermis (argyria or blue discoloration of the skin). The silver in the dressing should be combined with the appropriate moisture balance format matched to the wound to control exudate and prevent maceration, but facilitate the delivery of ionized silver to the wound surface.
HONEY, IODINE, AND PHMB
The Cochrane Collaboration conducted a systematic review of the honey literature and concluded that honey, as a topical treatment for superficial and partial-thickness burns, may improve healing times compared with some conventional dressings. Jull et al76 conducted a multicenter randomized controlled trial on VLUs with compression comparing honey to usual care. There were 187 patients in the honey group and 181 patients in the usual-care group with no difference between the 2 groups for total wound healing at 12 weeks.
In clinical practice, honey dressings may be useful for thick eschar that often continuously reforms when treated with other dressings. Some of this action may be due to the antibacterial and hyperosmolar characteristics of the honey. Scoring the wound with a blade to help break down the eschar may facilitate the process.
There are 10 trials with cadexomer iodine, and some of these trials are old, with venous ulcers treated topically without compression. In a randomized controlled trial study comparing cadexomer iodine with standard care with both groups receiving compression, the daily or weekly healing rates favored cadexomer iodine.77
In a pilot study of PHMB foam compared with foam alone, the PHMB dressing resulted in decreased pain and no change in wound size.78
EVALUATING EVIDENCE OF ANTIMICROBIALS IN VITRO AND ANIMAL MODELS: THE LITERATURE
Beware of in vitro testing of antimicrobial dressings because these results often do not correlate with clinical activity. Although the studies may demonstrate statistical significance, clinical significance is the parameter of interest; moreover, the strength of evidence for the majority of these in vitro studies is low. When evaluating topical antimicrobial agents for wound treatment, appropriate tests must be used. For instance, the in vitro evaluation of an antimicrobial agent such as silver can be performed with a multitude of tests, but of these, only the logarithmic reduction or decimal reduction time test conducted in serum has been shown to predict clinical outcomes.79,80 In vivo antimicrobial assays, such as the Walker Mason modified model (rodent) or the Wright model (porcine), can also be used with success to determine antimicrobial efficacy.81 Similarly, the evaluation of the efficacy of topical agents on wound healing can be evaluated in vitro (cellular culture or tissue explant models) or in vivo (rodent or porcine wound-healing models). However, the only model that predicts a clinical outcome is the porcine model of wound healing.82
A recent Cochrane Review explored antibiotic and antiseptic use for persons with VLUs. The authors concluded that there is no evidence for routine use of systemic antibiotics83 when treating the cause of VLUs.
- 9. Select a dressing to match the appropriate wound and individual person characteristics:
- Healable wounds: Autolytic debridement: alginates, hydrogels, hydrocolloids, acrylics
- Critical colonization: silver, iodides, PHMB, honey
- Persistent inflammation: anti-inflammatory dressings
- Moisture balance: foams, hydrofibers, alginates, hydrocolloids, films, acrylics
- Nonhealable, maintenance wounds: chlorhexidine, povidone-iodine
Whenever patients and healthcare professionals are developing a treatment plan for patients with wounds, dressing selection is an important primary focus. Once healable, nonhealable, or maintenance is determined, appropriate holistic interprofessional interventions that address cofactors can be optimized. The dressing selection should be the last part of the process because if the healability is not accurately assessed or other cofactors are unmanaged, then the wound will not heal. Dressing choice needs to consider unit costs and clinical effectiveness. Kerstein84 explored cost-effectiveness for venous and PrUs and concluded that the purchase price of the dressing should not be the only indicator. Normal saline gauze dressings (least expensive for product) were found to be the most expensive when nursing time and patient feedback were taken into account Table 6.
Chronic wounds may be stalled in the inflammatory stage. These wounds demonstrate markedly increased activity of inflammatory cells and associated mediators such as matrix metalloproteinases (MMPs) and elastase.85 Wound healing is stalled because degradation of extracellular matrix and growth factors occurs more rapidly than their synthesis, hindering the wound from progressing toward the proliferative phase and ultimately re-epithelialization. Harding et al86 reported that the longer a wound remains in the inflammatory phase, the more cellular defects are detected with potential delayed healing. Recently, there has been a renewal of interest in wound diagnostic testing that will result in tests for increased MMPs that will be available soon for bedside testing. There are wound dressings with oxidized reduced collagen and cellulose that can trap MMPs, and these dressings can be combined with antimicrobials such as silver. In the Sibbald cube (see Enabler), these specialized dressings can be combined antimicrobials, depending on the presence of the mnemonic NERDS (superficial antibacterial dressing criteria) or mnemonic STONEES (systemic antibiotic criteria) and where the presence of increased inflammation can also be treated topically or systemically.
Appropriate moisture is required to facilitate the action of growth factors, cytokines, and migration of cells including fibroblasts and keratinocytes. Moisture balance is a delicate process. Excessive moisture can potentially cause damage to the surrounding skin of a wound, leading to maceration and potential breakdown.87 Conversely, inadequate moisture in the wound environment can impede cellular activities and promote eschar formation, resulting in poor wound healing. A moisture-balanced wound environment is maintained primarily by modern dressings with occlusive, semiocclusive, absorptive, hydrating, and hemostatic characteristics, depending on the drainage and other wound bed properties.
- 10 . Evaluate expected rate of wound healing: Healable wounds should be 30% smaller by week 4 to heal by week 12. Wounds not healing at the expected rate should be reclassified or reassessed, and the plan of care revised
It is noted that a 20% to 40% reduction in 2 and 4 weeks is likely to be a reliable predictor of healing.88,89 Sheehan90 noted a 50% reduction at week 4 was a good predictor for persons with DFUs. One measure of healing is the clinical observation of the edge of the wound. If the wound edge is not migrating after appropriate WBP (debridement, bacterial balance, moisture balance) and healing is stalled, then advanced therapies should be considered. The first step prior to initiating the edge-effect therapies is a reassessment of the patient to rule out other causes and cofactors. Clinicians need to remember that 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.
- 11. Use active wound therapies (skin grafts, biological agents, adjunctive therapies, and so on) when other factors have been corrected and healing still does not progress (stalled wound)
A nonhealing wound may have a clifflike edge between the upper epithelium and the lower granulation in comparison to a healing wound with tapered edges like the shore of a sandy beach. Several edge-effect therapies support the addition of missing components: growth factors, fibroblasts, or epithelial cells or matrix components. If all the factors are corrected in a healable wound, active adjunctive therapies may be considered Table 7.
PROVIDE ORGANIZATION SUPPORT
- 12. For improved outcomes, education and evidence-informed practice must be tied to interprofessional teams and improved cost-effective patient care outcomes with the cooperation of healthcare systems
When a patient has a wound, it is important that the team provide education to the patient and his/her circle of care to involve everyone in the treatment plan. Healthcare professionals may assume that patients know more about their wounds than their current understanding. One study surveyed persons with DFUs and their self-foot-care behaviors. Healthcare providers conducted a detailed foot assessment and provided education on each visit. Results indicated that the knowledge base is often less than expected by the healthcare professional and leads to treatment gaps.109 Behavior of healthcare providers changed during the course of the study, resulting in an increased chance that the patient's socks were removed, leading to a thorough examination and patient education.
IMPORTANCE OF HOLISTIC INTERPROFESSIONAL COORDINATED AND COLLABORATE CARE
Accurate wound diagnosis and development of successful treatments plans can be a challenging undertaking, given the complexity of chronic wounds. A holistic interprofessional approach to care requires that each member of the team has a unique professional knowledge that contributes to the individualized plan of care. The management of patients with DFUs utilizing a team approach and primary healing outcomes can be associated with relatively low costs related to a visit with an interprofessional team, antibiotics, and plantar pressure downloading in the community setting.110 When healing occurs following an amputation, multiple hospital admissions and extended length of hospital stay are tabulated, with the cost for healing being significantly higher. Implemented treatment plans that do not yield wound-healing rates at the expected trajectory require a timely referral to an interprofessional team that can re-evaluate the diagnosis and causative factors. Redefining the treatment goals with the input from the patient, family, and healthcare provider is essential. Given the geographical and system differences, the ideal full complement of an interprofessional expert team may not always be accessible. Therefore, it is important to realize that only 2 disciplines working collaboratively with the patient and/or family may be successful.
Clinicians must distinguish between interdisciplinary networks with 2 members of the same profession (such as 2 nurses or assistants vs a nurse practitioner who may have a similar role to a physician on an interprofessional team), compared with the physician and nurse of an interprofessional team. For chronic wound care, the physician and nurse are best supplemented with a member of the allied healthcare team (eg, occupational therapist, physical therapist, foot care specialist, dietitian, social worker, and so on).
Many patients with chronic stalled wounds are complex, older adults who reside with multiple comorbidities, requiring lengthy assessment and coordination of the treatment interventions. This necessitates the healthcare system policy maker to support interprofessional clinician teams to provide the best possible evidence-informed practice.
In summary, the concept of WBP includes the treatment of the whole patient (treat the cause and patient-centered concerns). The approach to the local wound bed has 4 components starting with the mnemonic DIM: Debridement, Infection/prolonged Inflammation control, and Moisture balance, before the mnemonic DIME that includes the advanced Edge-effect therapies for wounds with the ability to heal.
In addition, this article has introduced the concept of healable, nonhealable, and maintenance wounds along with the integration of clinical criteria for superficial critical colonization (mnemonic NERDS) and topical antimicrobial dressings versus deep and surrounding tissue infections (mnemonic STONEES) requiring systemic agents. Bacterial damage needs to be distinguished from persistent inflammation with soon-to-be available bedside matrix metalloproteases (MMPs) testing. The ultimate treatment process should include the leadership of an interprofessional wound management team, and patient participation is paramount for the best achievable outcome.
After reading this article, clinicians can distinguish between healable, nonhealable, and maintenance wounds and design the appropriate management plans.
1. Sibbald RG, Williamson D, Orsted HL, et al. Preparing the wound bed: debridement, bacterial balance and moisture balance. Ostomy Wound Manage 2000;46(11):14-35.
2. Bowler PG, Davies BJ. The microbiology of acute and chronic wounds. Wounds 1999;11:72-99.
3. Sibbald RG, Orsted H, Schultz G, et al. Preparing the wound bed 2003: focus on infection and inflammation. Ostomy Wound Manage 2003;49(11):24-51.
4. Falanga V. Classifications for wound-bed preparation and stimulation of chronic wounds. Wound Repair Regen 2000;8:347-52.
5. 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.
6. Sibbald RG, Orsted HL, Coutts PM, et al. Best practice recommendations for preparing the wound bed: update 2006. Adv Skin Wound Care 2007;20:390-405.
7. Registered Nurses' Association of Ontario. Assessment and Management of Stage I to IV Pressure Ulcers (Revised). Toronto, ON, Canada: Registered Nurses' Association of Ontario; 2007.
8. Brem H, Sheehan P, Rosenberg H, et al. Evidence-based protocol for diabetic foot ulcers. J Plast Reconstr Surg 2006;117:193S-209S.
9. London NJ, Donnelly R. ABC of arterial and venous disease. Ulcerated lower limb. BMJ 2000;320:1589-91.
10. Falanga V, Sabolinski M. A bilayered living skin construct (APLIGRAF) accelerates complete closure of hard-to-heal venous ulcers. Wound Repair Regen 1999;7:201-7.
11. Margolis DJ, Allen-Taylor L, Hoffstad O, et al. The accuracy of venous leg ulcer prognostic models in a wound care system. Wound Rep Regen 2004;12:163-8.
12. Attinger CE, Evans KK, Bulan E, Blume P, Cooper P. Angiosomes of the foot and ankle and clinical implications for limb salvage: reconstruction, incisions and revascularization. Plast Reconstr Surg 2006;117(suppl):261S.
13. Sibbald RG, Alvi A, Norton L, et al. Compression therapies. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic Wound Care: A clinical source book for healthcare professionals. 4th ed. Malvern, PA: HMP Communications; 2007:481-8.
14. Browne AC, Sibbald RG. The diabetic neuropathic ulcer: An overview. Ostomy/Wound Manage 1999;45(suppl 1A):6S-20S.
15. Sibbald RG, Alavi A, Norton L, Browne AC, Coutts P. Compression therapies. In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Malvern, PA: HMP communications; 2007:481-8.
16. Woo K, Lo C, Alavi A, et al. An audit of leg and foot ulcer care in an Ontario community care access centre. Wound Care Canada 2007;5(suppl 1):S17-27.
17. Marston WA. Risk factors associated with healing chronic diabetic foot ulcers: the importance of hyperglycemia. Ostomy Wound Manage 2006;52(3):26-8, 30, 32.
18. Markuson M, Hanson D, Anderson J, et al. The relationship between hemoglobin A(1c) values and healing time for lower extremity ulcers in individuals with diabetes. Adv Skin Wound Care 2009;22:365-72.
19. Zagoren AJ, Johnson DR, Amick N. Nutritional Assessment and intervention in the adult with a chronic wound. In: Krasner DL, Rodever GT, Sibbald RG, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Malvern, PA: HMP Communications; 2007:127-36.
21. Hess CT. Clinical Guide to Wound Care. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005:34.
22. Lacy JA. Albumin overview: use as a nutritional marker and as a therapeutic intervention. Crit Care Nurse 1991;11:46-9.
23. Doweiko JP, Nompleggia DJ. Role of albumin in human physiology and pathophysiology. JPEN J Parenter Enteral Nutr 1991;15:207-11.
24. Stotts NA, Wipke-Telvis DD, Hopf HW. Cofactors in impaired wound healing. In: DL Rodeheaver GT, Sibbald RG, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Malvern, PA: HMP Communications; 2007:215-20.
25. Woo K, Alavi A, Botros M, et al. A transprofessional comprehensive assessment model for persons with lower extremity leg and foot ulcers. Wound Care Canada 2007;5(suppl 1):S35-47.
27. Kennedy KL. The prevalence of pressure ulcers in an intermediate care facility. Decubitus 1989;2:44-5.
28. Langemo DK, Brown G. Skin fails too: acute, chronic and end-stage skin failure. Adv Skin Wound Care 2006;19:206-11.
30. Brennan MR, Trombley K. Kennedy terminal ulcers: a palliative care unit's experience over a 12 month period of time. WCET 2010;30:20-2.
31. Sackett DL, Strauss SE, Richardson WS, et al. Evidence-Based Medicine: How to Practice and Teach EBM. 2nd ed. Edinburgh, Scotland: Churchill Livingstone; 2000.
32. Krasner DL, Rodeheaver GT, Sibbald RG. Interprofessional wound caring (chapter 1). In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Malvern, PA: HMP Communications; 2007:3-9.
33. Mosti G, Vattaliano V, Polignano R, et al. Compression therapy in the treatment of leg ulcers. Acta Vulnol 2009;7:1-12.
34. Mayrovitz HN. Compression-induced pulsatile blood-flow changes in human legs. Clin Physiol 1998;18:117-24.
35. Delis KT, Nicolaides AN. Effect of intermittent pneumatic compression of foot and calf on walking distance, hemodynamics and quality of life in patients with arterial claudication: a prospective randomized controlled study with 1-year follow-up. Ann Surg 2005;241:431-41.
36. Harris CL, Fraser C. Malnutrition in the institutionalized elderly: the effects on wound healing. Ostomy Wound Manage 2004;50(10):54-63.
37. Sussman C. Wound healing biology and chronic wound healing. In: Sussman C, Bates-Jensen B, eds. Wound care-a collaborative practice manual for physical therapists and nurses. Gaithersburg, MD: Aspen Publication; 1998:49-82.
38. Van Anholt RD, Sobotka L, Meijer EP, et al. Specific nutritional support accelerates pressure ulcer healing and reduces wound care intensity in non-malnourished patients. Nutrition 2010;26:867-72.
39. McCaffery M. Nursing practice theories related to cognition, bodily pain and main environment interactions. Los Angeles, CA: University of California Los Angeles; 1968.
40. Woo K, Sibbald G, Fogh K, et al. Assessment and management of persistent (chronic) and total wound pain. Int Wound J 2008;5:205-15.
43. Phillips T, Stanton B, Provan A, et al. A study of the impact of leg ulcers on quality of life: financial, social, and psychological implications. J Am Acad Dermatol 1994;31:49-53.
44. Persoon A, Heinen MM, van der Vleuten CJ, et al. Leg ulcers: a review of their impact on daily life. J Clin Nurs 2004;13:341-54.
45. Carrington AL, Mawdsley SK, Morley M, et al. Psychological status of diabetic people with or without lower limb disability. Diabetes Res Clin Pract 1996;32:19-25.
46. Price P. Health-related quality of life (chapter 10). In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Malvern, PA: HMP Communications; 2007:79-83.
47. Chalon S, Moreno H, Benowitz NL, et al. Nicotine impairs endothelium-dependent dilation in human veins in vivo. Clin Pharmacol Ther 2000;67:391-7.
48. Rayner R. Effects of cigarette smoking on cutaneous wound healing. Prim Intent 2006;14:100-2, 104.
49. Sorensen LT. Smoking and wound healing. Eur Wound Manage Assoc J 2003;3:13-15.
50. Smith JB, Smith SB. Cutaneous manifestations of smoking. eMedicine. 2004.
51. Ninikoski J. Oxygen and wound healing. Clin Plast Surg 1977;4:361-73.
52. Arrendondo J, Hall LL, Ndoye A, et al. Central role of fibroblast alpha3 nicotinic acetylcholine receptor in mediating cutaneous effects of nicotine. Lab Invest 2003;83:2007-225.
53. Snyder HB, Caughman G, Lewis J, Billman MA, Schuster G. Nicotine modulation of in vitro human gingival bibroblast beta1 integrin expression. J Periodontol 2002;73:505-10.
54. Wong LS, Green HM, Feugate JE, Yadav M, Nothnagel EA, martins-Green M. Effects of "second-hand" smoke on structure and function of fibroblasts, cells that are critical for tissue repair and remodelling. BMC Cell Biol 2004;5:13.
55. Ahn C, Mulligan P, Salcido RS. Smoking-the bane of wound healing: biomedical interventions and social influences. Adv Skin Wound Care 2008;21:227-36.
57. Osterberg L, Blaschke T. Adherence to Medication. N Engl J Med 2005;353:487-97.
58. Wild T, Rahbarnia A, Kellner M, et al. Basics of nutrition and wound healing. Nutrition 2010;26:862-6.
59. Keast DH, Bowering CK, Evans AW, et al. MEASURE: a proposed assessment framework for developing best practice recommendations for wound assessment. Wound Repair Regen 2004;12:S1-17.
60. Rodeheaver GT, Ratliff CR. Wound cleansing, wound irrigation, wound disinfection (chapter 34). In: Krasner DL, Rodeheaver GT, Sibbald RG, eds. Chronic Wound Care: A Clinical Source Book for Healthcare Professionals. 4th ed. Malvern, PA: HMP Communications; 2007:331-42.
61. Moore ZEH, Cowman S. Wound cleansing for pressure ulcers. Cochrane Database Syst Rev 2005;(4). Article CD004983. DOI: 10.1002/14651858.CD004983.pub2.
62. Fernandez R, Griffiths R. Water for wound cleansing. Cochrane Database Syst Rev 2008;(1). Article CD003861. DOI: 10.1002/14651858.CD003861.pub2.
64. Hurlow J, Bowler PG. Clinical experience with wound biofilm and management: a case series. Ostomy Wound Manage 2009;55(4):38-49.
65. Cardinal M, Eisenbud DE, Armstrong DG, et al. Serial surgical debridement: a retrospective study on clinical outcomes in chronic lower extremity wounds. Wound Repair Regen 2009;17:306-11.
66. Landis S, Ryan S, Wo K, Sibbald RG. Infections in chronic wounds. In: Chronic Wound Care: A Clinical Source Handbook for Healthcare Professionals. 4th ed. Malvern, PA: HMP Communications; 2007, 299-21.
67. Sibbald RG, Woo K, Ayello EA. Increased bacterial burden and infection: the story of the NERDS and STONES. Adv Skin Wound Care 2006;19:447-61.
68. Lavery LA, Armstrong DG, Wunderlich RP, et al. Risk factors for foot infections in individuals with diabetes. Diabetes Care 2006;29:1288-93.
69. 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.
70. Sibbald RG, Woo K, Ayello EA. Increased bacterial burden and infection: the story of the NERDS and STONES. Adv Skin Wound Care 2006;19:447-61.
71. Woo K, Sibbald RG. A cross-sectional validation study of using NERDS and STONEES to assess bacterial burden. Ostomy Wound Manage 2009;55(8):40-8.
72. Demling RH, DeSanti L. The rate of re-epitheliazation across meshed skin grafts is increased with exposure to silver. Burns 2002;28:264-6.
73. Nadworney PL, Wang JF, Tredget EE, Burrell RE. Anti-inflammatory activity of nanocyrstalline silver in a porcine contact dermatitis model. Nanomedicine: Nanotechnology, Biology and Medicine 2008;4:241-51.
74. Vermeulen H, van Hattem JM, Storm-Versloot MN, et al. Topical silver for treating infected wounds. Cochrane Database Syst Rev 2007;(1). Article CD005486. DOI: 10.1002/14651858.CD005486.pub2.
75. Lo SF, Chang CJ, Hu WY, et al. The effectiveness of silver-releasing dressings in the management of non-healing chronic wounds: a meta-analysis. J Clin Nurs 2009;18:716-28.
76. Jull A, Walker N, Rogers A, et al. Honey for leg ulcers-the HALT trial. Br J Surg 2008;95:175-82.
77. O'Meara S, Al-Kurdi D, Ologun Y, et al. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev 2010;(1). Article CD003557. DOI: 10.1002/14651858.CD003557.pub3.
78. Sibbald RG, Coutts P, Woo K. Reduction of bacterial burden and pain in chronic wounds using a new polyhexamethylene biguanide antimicrobial foam dressing-clinical trial results. Adv Skin Wound Care 2011;24:79-84.
79. Spacciapoli P, Buxton D, Rothstein D, et al. Antimicrobial activity of silver nitrate against periodontal pathogens. J Periodontal Res 2001;36:108-13.
80. Nadworny PL, Burrell RE. A review of assessment techniques for silver technology in wound care. Part 1: in vitro methods for assessing antimicrobial activity. J Wound Technol 2008;2:6-13.
81. Burrell RE, Heggers JP, Davis GJ, et al. Efficacy of silver-coated dressings as bacterial barriers in a rodent burn sepsis model. Wounds 1999;11(4):64-71.
82. Nadworny PL, Burrell RE. A review of assessment techniques for silver technology in wound care. Part II: tissue culture and in vivo methods for determining antimicrobial and anti-inflammatory activity. J Wound Technol 2008;2:14-22.
83. O'Meara S, Al-Kurdi D, Ologun Y, et al. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database Syst Rev 2010;(1). Article CD003557. DOI: 10.1002/14651858.CD003557.pub3.
84. Kerstein MD, Gemmen E, van Rijswijk L, et al. Cost and cost-effectiveness of venous and pressure ulcer protocols of care. Dis Manage Health Outcomes 2001;651-63.
85. Trengove NJ, Stacey MC, MacAuley S, et al. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Repair Regen 1999;7:422-52.
86. Harding KG, Moore K, Phillips TJ. Wound chronicity and fibroblast senescence-implications for treatment. Int Wound J 2005;2:364-8.
87. Basketter D, Gilpin G, Kuhn M, et al. Patch tests versus use tests in skin irritation risk assessment. Contact Dermatitis 1998;39:252-6.
88. Falanga V. Wound healing and its impairment in the diabetic foot. Lancet 2005;366:1736-43.
89. Margolis DJ, Allen-Taylor L, Hoffstad O, et al. The accuracy of venous leg ulcer prognostic models in a wound care system. Wound Repair Regen 2004;12:163-8.
90. Sheehan P, Jones P, Caselli A, et al. Percent change in wound area 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.
91. Niezgoda JA, Van Gils CC, Frykberg RG, et al. Randomized clinical trial comparing OASIS Wound Matrix to Regranex Gel for diabetic ulcers. Adv Skin Wound Care 2005;18:258-66.
92. Arévalo JM, Lorente JA. Skin coverage with Biobrane biomaterial for the treatment of patients with toxic epidermal necrolysis. J Burn Care Rehabil 1999;20:406-10.
93. Smiell JM, Wieman TJ, Steed DL, et al. Efficacy and safety of becaplermin (recombinant human platelet-derived growth factor-BB) in patients with nonhealing, lower extremity diabetic ulcers: a combined analysis of four randomized studies. Wound Repair Regen 1999;7:335-46.
94. Steed DL. Clinical evaluation of recombinant human platelet-derived growth factor for the treatment of lower extremity ulcers. Plast Reconstr Surg 2006;117:143S-51S.
95. Dinh TL, Veves A. The efficacy of Apligraf in the treatment of diabetic foot ulcers. Plast Reconstr Surg 2006;117:152S-59S.
96. Veves A, Falanga V, Armstrong DG, et al. Graftskin, a human skin equivalent, is effective in the management of noninfected neuropathic diabetic foot ulcers: a prospective randomized multicenter clinical trial. Diabetes Care 2001;24:290-5.
97. Redekop WK, Stolk EA, Kok E, et al. Diabetic foot ulcers and amputations: estimates of health utility for use in cost-effectiveness analyses of new treatments. Diabetes Metab 2004;30:549-56.
98. Falanga V, Margolis D, Alvarez O, et al. Rapid healing of venous ulcers and lack of clinical rejection with an allogeneic cultured human skin equivalent. Human Skin Equivalent Investigators Group. Arch Dermatol 1998;134:293-300.
99. Newton DJ, Khan F, Belch JJ, et al. Blood flow changes in diabetic foot ulcers treated with dermal replacement therapy. J Foot Ankle Surg 2002;41:233-7.
100. Hanft JR, Surperant MS. Healing of chronic foot ulcers in diabetic patients treated with a human fibroblast-derived dermis. J Foot Ankle Surg 2002;41:291-9.
101. Marston WA, Hanft J, Norwood P, et al. The efficacy and safety of Dermagraft in improving the healing of chronic diabetic foot ulcers: results of a prospective randomised trial. Diabetes Care 2003;26:1701-5.
102. Roeckl-Wiedmann I, Bennett M, Kranke P. Systematic review of hyperbaric oxygen in the management of chronic wounds. Br J Surg 2005;92:24-32.
103. Akai M, Kawashima N, Kimura T, et al. Electrical stimulation as an adjunct to spinal fusion: a meta-analysis of controlled clinical trials. Bioelectromagnetics 2002;23:496-4.
104. Flemming K, Cullum N. Therapeutic ultrasound for venous leg ulcers. Cochrane Database Syst Rev 2000;(4). Article CD00180.
105. Baba-Akbari SA, Flemming K, Cullum NA, et al. Therapeutic ultrasound for pressure ulcers. Cochrane Database Syst Rev 2006;(3). Article CD001275.
106. Armstrong DG, Lavery LA, Diabetic Foot Study Consortium. Negative pressure wound therapy after partial diabetic foot amputation: a multicentre, randomized controlled trial. Lancet 2005;366:1704-10.
107. Vin F, Teot L, Meaume S. The healing properties of Promogran in venous leg ulcers. J Wound Care 2002;11:335-41.
108. Wollina U, Schmidt WD, Kronert C, et al. Some effects of a topical collagen-based matrix on the microcirculation and wound healing in patients with chronic venous leg ulcers: preliminary observations. Int J Low Extrem Wounds 2005;4:214-24.
109. Litzelman DK, Slemenda CW, Langefeld CD, et al. Reduction of lower extremity clinical abnormalities in patients with non-insulin-dependent diabetes mellitus. A randomized, controlled trial. Ann Intern Med 1993;119:36-41.
110. Apelqvist J, Ragnarson-Tennvall G, Larsson J, Persson U. Diabetic foot ulcers in a multidisciplinary setting. An economic analysis of primary healing and healing with amputation. J Intern Med 1994;235:463-71.
For more than 65 additional continuing education articles related to Skin and Wound Care topics, go to NursingCenter.com/CE.
CONTINUING MEDICAL EDUCATION INFORMATION FOR PHYSICIANS
Lippincott Continuing Medical Education Institute, Inc. is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.
Lippincott Continuing Medical Education Institute, Inc. designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM. Physicians should only claim credit commensurate with the extent of their participation in the activity.
PROVIDER ACCREDITATION INFORMATION FOR NURSES
Lippincott Williams & Wilkins, publisher of the Advances in Skin & Wound Care journal, will award 4.3 contact hours for this continuing nursing education activity.
LWW is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.
This activity is also provider approved by the California Board of Registered Nursing, Provider Number CEP 11749 for 4.3 contact hours. Lippincott Williams & Wilkins is also an approved provider of continuing nursing education by the District of Columbia and Florida #FBN2454.
Your certificate is valid in all states.
The ANCC's accreditation status of Lippincott Williams & Wilkins Department of Continuing Education refers only to its continuing nursing education activities and does not imply Commission on Accreditation approval or endorsement of any commercial product.
CONTINUING EDUCATION INSTRUCTIONS
- Read the article beginning on page 415.
- Take the test, recording your answers in the test answers section (Section B) of the CE enrollment form. Each question has only one correct answer.
- Complete registration information (Section A) and course evaluation (Section C).
- Mail completed test with registration fee to: Lippincott Williams & Wilkins, CE Group, 333 7th Avenue, 19th Floor, New York, NY 10001.
- Within 3 to 4 weeks after your CME enrollment form is received, you will be notified of your test results.
- If you pass, you will receive a certificate of earned contact hours and an answer key. Nurses who fail have the option of taking the test again at no additional cost. Only the first entry sent by physicians will be accepted for credit.
- A passing score for this test is 13 correct answers.
- Nurses: Need CE STAT? Visit http://www.nursingcenter.com for immediate results, other CE activities, and your personalized CE planner tool. No Internet access? Call 1-800-787-8985 for other rush service options.
- Questions? Contact Lippincott Williams & Wilkins: 1-800-787-8985.
Registration Deadline: September 30, 2013 (nurses); September 30, 2012 (physicians)
PAYMENT AND DISCOUNTS
- The registration fee for this test is $32.95 for nurses; $22 for physicians.
- Nurses: If you take two or more tests in any nursing journal published by LWW and send in your CE enrollment forms together by mail, you may deduct $0.95 from the price of each test. We offer special discounts for as few as six tests and institutional bulk discounts for multiple tests. Call 1-800-787-8985 for more information.
Keywords:© 2011 Lippincott Williams & Wilkins, Inc.
wound bed preparation; stalled wound; chronic wound; holistic approach; leg and foot ulcers; healable and nonhealable wounds; maintenance wounds