Wound Series Part 3: Pressure Ulcers - Risk Factors, Diagnosis, Staging, Management

To provide the most recent evidence based information on risk factors, diagnosis, staging and management of pressure ulcers.

• Discuss risk factors of pressure ulcers.
• Apply common pressure ulcer risk assessment tools
• Stage pressure ulcers
• Describe evidence-based interventions to prevent pressure ulcers.
• Discuss evidence-based interventions to consider in the management of pressure ulcers.

The National Pressure Ulcer Advisory Panel (NPUAP) defines a pressure ulcer as, "localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction (NPUAP, 2009)." Pressure ulcers (PUs) have been known as "bedsores" for hundreds of years. Historically, the term decubitus ulcer or decubiti has also been used to describe these wounds related to pressure and/or immobility.

PUs are chronic wounds occurring in approximately 3 to 23% of patients in long term care and rehabilitation facilities and approximately 30 to 60% of all persons with spinal cord injuries in their lifetime (Russo et al., 2006). About 60,000 persons in the US die each year as a direct result of pressure ulcers (AHRQ, 2011). PUs are painful, prone to infection, reduce quality of life, and create a world-wide economic dilemma (Maklebust, 2005; Fogerty et al., 2008). In addition, health care costs related to the management and treatment of chronic wounds in the U.S. exceeds $20 billion annually (AHRQ, 2011). While the quality of health care and medical technology has improved in the United States during the past 20 years, it seems this has not significantly affected overall national pressure ulcer prevalence or incidence (Thomas, 2001; VanGilder, MacFarlane & Meyer, 2008). Concurrent with this advancing technology, modern day patients live longer and are typically hospitalized with higher acuity levels than patients hospitalized years ago.

Historically, pressure ulcers have been described in medical literature since at least the 1500s when Fabricius Hildanus first documented his hypotheses of the causes and characteristics of bedsores. He highlighted the role of "internal supernatural" and "external natural" factors that interrupt the supply of blood and nutrients to tissue as causes of bedsores. Mechanical pressure and incontinence were first identified and key factors in the development of pressure ulcers by French surgeon de la Motte in 1722 (Defloor, 1999). Major risk factors identified for pressure ulcer development in the scientific literature since 1987 include increased age, impaired mobility, decreased physical activity, poor nutrition, urinary and/or fecal incontinence, and sensory impairment (Allman, 1997; Ayello & Lyder, 2001; Reddy, Gill, & Rochon, 2006). Other studies have identified additional risk factors including smoking status, diabetes mellitus (DM), coronary artery disease (CAD), intensive care unit (ICU) stay greater than 3 days, ventilator dependency, pneumonia, sepsis, obesity, surgery, female gender, and peripheral vascular disease (PVD) (Berlowitz et al., 2001; de Souza, & Santos, 2007; Cowan et al., 2012). Most pressure ulcers are considered to be avoidable, therefore, preventable (Jalali & Rezaie, 2005; Bryant & Nix, 2007; NPUAP, 2009). An "avoidable" pressure ulcer means that the patient developed a pressure ulcer and the facility or health care givers did not perform (or document) one or more of the following: evaluate the patient's / resident's clinical condition and pressure ulcer risk factors; define and implement interventions that are consistent with resident needs, resident goals, and recognized standards of practice; monitor and evaluate the impact of the interventions; or revise the interventions as appropriate. Thomas (2001) suggests there may be a few instances where pressure ulcers are unavoidable. "Unavoidable" means the patient / resident developed a pressure ulcer despite the fact that the facility and health care providers had evaluated (and documented) the resident's clinical condition and pressure ulcer risk factors; defined and implemented interventions that are consistent with resident needs, goals, and recognized standards of practice; monitored and evaluated the impact of the interventions; and revised the approaches as appropriate all within a timely manner. Kennedy ulcers (a specific type of pressure ulcer often seen at the end of life due to organ/system failure) are one example of "unavoidable" pressure ulcers.

Fogerty et al. (2008) conducted a very large retrospective case-control study reviewing admission and discharge data from over six million subjects in the Nationwide Inpatient Sample (NIS) to identify risk factors and demographic differences between those who developed pressure ulcers and those that did not. Some may describe their study as a nested case-control (Gordis, 2004) because they identified a cohort (inpatients in the NIS dataset), followed their records retrospectively from their hospital admission until hospital discharge (during 2003), and separated them into 2 groups: those who developed pressure ulcers (cases) and those that did not (controls). There were 94,758 incident pressure ulcers documented among a final discharge sample of 6,610,787 persons. Utilizing multivariate logistic regression analysis on 45 common diagnoses identified in persons with pressure ulcers, they reported odds ratios (estimate of relative risk) for the most significant risk factors associated with developing pressure ulcers. Analysis was also conducted stratifying the sample by age, race and gender. Age over 75 years was the strongest pressure ulcer risk factor identified with an Odds Ratio (OR) of 12.63 (meaning people over 75 years are almost 13 times more likely to develop pressure ulcers than younger age groups). Other strong risk factors identified (listed in descending order) include: diagnosis of gangrene (OR 10.94, 95% CI 10.43-11.48), septicemia (OR 9.78, 95% CI 9.33- 10.26), osteomyelitis (OR 9.38, 95% CI 8.81-9.99), nutritional deficiencies (OR9.18, 95% CI 8.81-9.99), pneumonitis (OR 8.70, 95% CI 8.33-9.09), urinary tract infection (OR 7.17, 95% CI 6.96-7.38), paralysis (OR 10.30, 95% CI 9.69-10.96), age 59 to 75 years (OR 5.99, no CI reported), and African American race (OR 5.71, 95% CI 5.35-6.10). Fogerty et al. also reported a statistically significant interaction between race and age, such that as African Americans age, their risk of developing pressure ulcers increases faster than the risk Caucasians experience as they age, indicating noteworthy racial disparities. Other significant findings identified in their study highlight some of the strongest risk factors are non-modifiable (age, paralysis, race) while others are potentially modifiable (infection, nutritional deficiencies). Therefore, exploration is needed to determine when interventions are most effective in those persons with non-modifiable risk factors (such as age > 75) or if interventions should be initiated in all persons over 75 years old. Investigations should also examine the most effective interventions to reduce or eliminate the identified modifiable risk factors (infection and nutritional deficiencies) and ways to accurately identify them in patients.

The purpose of identifying a risk factor is to intervene and lower the associated risk. Identifying the strongest pressure ulcer risk factors is important to be able to provide evidence-based interventions and thereby lower the likelihood of someone developing a pressure ulcer or halting the progression of the pressure ulcer. Pressure ulcer risk assessment tools provide a tangible way to quantify potential risk so that interventions may be reserved for those at highest risk and avoid unnecessary interventions and higher financial expenditures on those who may not need them (Defloor & Grypdonck, 2005).

Cowan et al. (2012) conducted a retrospective analysis in a Veteran population to identify the strongest pressure ulcer predictive model which demonstrated four medical factors (malnutrition, surgery, pneumonia, candidiasis) were more predictive of pressure ulcers than total Braden Scale for Predicting Pressure Ulcer scores. The finding of a diagnosis of candidiasis as a risk factor for pressure ulcers may be related to medical conditions where candidiasis is most common (could it be a proxy variable for impaired immune function?). More research is needed to explore these relationships. Nevertheless, this research provides valuable information that may enhance current risk factor assessments. Identification of factors affecting the development of pressure ulcers is imperative in the present day population in order to select patients for effective prevention interventions. Furthermore, evaluation of the efficacy of existing preventive interventions must be ongoing and new innovative interventions must be explored in order to significantly impact pressure ulcer incidence and prevalence (Fogerty et al, 2008; Armstrong et al., 2008).

One criticism of existing risk assessment tools is that "neither risk factors nor the weights attributed to them have been identified using adequate statistical techniques" (Schoonhoven et al., 2002). Risk factors are those factors or conditions that are noted to be most strongly associated with the outcome of interest. In order to provide evidence-based measures in the prevention of pressure ulcers, an effective means of identifying those at highest risk is imperative. Current risk assessment tools may require further development, improved statistical evaluation, and possibly modification in order to remain applicable to present day populations.

Thomas (2001) posits an explanation for an unchanging incidence of pressure ulcers as "a failure of known effective prevention treatment to be applied, or the failure of prevention strategies to be effective despite being applied" (p.298). Effective preventive measures may not be applied if individuals are not appropriately identified as being at risk. Risk-screening tools are useless if they are not applicable to the population being screened, if they are used inconsistently, or scored incorrectly (Thomas, 2001; Papanikolaou, Lyne, & Anthony, 2007).

Pressure ulcers or "bed sores" have been documented for thousands of years. Diagnosing pressure ulcers largely depends on assessing possible pressure, shear and moisture- related etiological factors as well as location of the tissue damage. The first question in your mental wound assessment "checklist" should be: "Is it over a boney prominence?" While pressure ulcers may develop over any boney prominence on the body, the sacrum, coccyx, buttocks, and heels of the feet are the most prevalent sites for pressure ulcers (Perneger, Heliot, Rae, Borst, & Gaspoz, 1998; Lyder, 2003; Vangilder, MacFarlane, & Meyer, 2008). Other common locations may include greater trochanters, ischial tuberosities, ankles, knees, elbows, scapulas, shoulders, and occiput. In addition, pressure related injury may also be related to devices such as oxygen tubing, drain tubes and foley catheters. Device related pressure ulcers may be seen over the ears, around the urethral opening of the genitals or other soft tissue location not associated with a bony prominence. Furthermore, this type of device related injury may cause full thickness tissue damage which is difficult to stage because, as in the case of the ears, there is no subcutaneous tissue evident - a very shallow wound may result in exposure of cartilage (full thickness wound) without the involvement of muscle, tendon or bone. Again, it is important to note that while the onset of pressure ulcers is associated with unrelieved pressure of course, it can also be caused by a combination of pressure, friction and shearing forces. Evaluating these potential forces (head of bed raised for long periods, patient sliding down in the bed, chair transfers, improper overhead sling positioning, etc.) is imperative when assessing your patient's skin integrity risks.

Pressure ulcer staging provides a way to communicate the degree of tissue damage in pressure ulcers. The staging system was defined by Shea in 1975 and provides a name to the amount of anatomical tissue loss. The original definitions were confusing to many clinicians and lead to inaccurate staging of ulcers associated or due to perineal dermatitis and those due to deep tissue injury (NPUAP 2007). The stages range from Stage I (less obvious and potentially reversible damage) to Stage IV (damage extending to muscle, tendon and/or bone) with 'Unstagable' and 'suspected Deep Tissue Injury' (sDTI) discoloration added as additional 'stages' or descriptors (Black, Baharestani, Cuddigan, Dorner, Edsberg, & Langema, et al., 2007). Pressure ulcers should never be "back-staged," meaning once a wound is identified as a Stage III pressure ulcer, it is never referred to as a Stage I or II. Rather, the stage III pressure ulcer which is healing would be referred to as a "healing Stage III pressure ulcer." In addition, only pressure ulcers are "staged." Diabetic foot ulcers may be "graded" (such as Wagner Grades) but no other wounds are "staged." 2009, the National Pressure Ulcer Advisory Panel (NPUAP) updated their Categories or Stages of Pressure Ulcers and published a National Guidelines document. These can be found on the NPUAP website and are listed below.

• Pressure Ulcer Stages/Categories from the National Pressure Ulcer Advisory Panel (NPUAP)
• Category/Stage I: Non-blanchable erythema: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Category I may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons.
• Category/Stage II: Partial thickness: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled or sero-sanginous filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising*. This category should not be used to describe skin tears, tape burns, incontinence associated dermatitis, maceration or excoriation. *Bruising indicates deep tissue injury.
• Category/Stage III: Full thickness skin loss: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a Category/Stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and Category/Stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Category/Stage III pressure ulcers. Bone/tendon is not visible or directly palpable.
• Category/Stage IV: Full thickness tissue loss: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present. Often includes undermining and tunneling. The depth of a Category/Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis or osteitis likely to occur. Exposed bone/muscle is visible or directly palpable.
• Additional Categories/Stages for the USA
• Unstagable/Unclassified: Full thickness skin or tissue loss depth unknown: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar are removed to expose the base of the wound, the true depth cannot be determined; but it will be either a Category/Stage III or IV. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as "the body's natural (biological) cover" and should not be removed.
• Suspected Deep Tissue Injury depth unknown: Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

Whittington & Briones (2004) estimate annual medical costs in the United States (US) associated with treating pressure ulcers exceed $5 billion dollars annually. Fogerty et al. (2008) estimates this cost to be higher at $10,845 per patient, exceeding a total $18.5 billion dollars annually. Furthermore, Jalali & Rezaie (2005) suggest it may cost as little as $500 to prevent a pressure ulcer, indicating prevention "is more cost-effective than treatment" (p.92). Individuals with pressure ulcers have higher mortality rates (Redelings et al., 2005) and up to five fold increased hospital length of stay (Graves, Birrell & Whitby, 2005). Interestingly, Barbara Braden gave a NPUAP lecture "Costs of Pressure Ulcer Prevention: Is it really cheaper than treatment? Given May 9, 2013, she discussed the fact that when pressure ulcer prevention interventions are put in place, patient falls are also noted to decrease.

There are few (if any) current randomized controlled trials (RCTs) where random vulnerable patients are assigned to receive an intervention suspected of "causing" full thickness pressure ulcers. Three important documents impact biomedical research around the world by helping to determine what is ethically right or wrong. These documents are: The Nuremberg Code (1947), the World Medical Association's Declaration of Helsinke (originally adopted in 1964), and the Belmont Report of the National Commission for the Protection of Human Subjects in the United States (Beauchamp & Childress, 2001). In a nutshell, these documents came about after tragic medical research practices were disclosed to the world. The Nuremberg Code was written in 1946-1947 after the horrific, criminal medical research on Jews and other prisoners in Nazi concentration camps came to light. The Code's purpose is described as providing ten directives for human experimentation, including informed consent and assurance within research protocols that "all unnecessary physical and mental suffering and injury" as a result of the experimentation process is avoided. The Declaration of Helsinki built on these directives in a document that has been revised by the World Medical Association at least six times (Portney & Watkins, 2000; Murphy, 2004). These documents and a report describing other unethical medical research practices discovered in the United States (The Belmont Report) led to the development of the US National Research Act in 1974 to ensure the protection of all human research subjects is a standard practice (Portney & Watkins, 2000). The ethical dilemma for pressure ulcer research arises when you want to do a RCT where the dependent variable of interest is a poor medical outcome like a stage III pressure ulcer. It would not be ethical to divide two elderly groups of people into experimental and control groups and apply some type of intervention to one group and not to others while you observed both groups to see who developed a stage III pressure ulcer. Ethically, researchers should desire to prevent harm (pressure ulcers) in all of the subjects and if something were to cause skin or tissue injury, you would want to intervene immediately. To merely record how bad things got in one group or the other would go against biomedical ethical principles of "not causing harm." However, RCTs can be conducted that investigate potentially positive outcomes. Several RCTs have been reported involving patients deemed at risk for pressure ulcers that introduce a theoretically preventative intervention (such as a new support surface) versus standard care (existing mattress) to see which is more effective at preventing pressure ulcer development.

Please see the AHRQ 2011 toolkit for preventing PU in hospitals online . The approach to managing pressure ulcers should always focus on PREVENTION. Prevent the ulcer in the first place! If the patient develops pressure related injury (despite preventive measures), then evidence-based practice related to wound healing should be administered but always with PREVENTION in the treatment plan. Prevent further breakdown. Prevent the pressure ulcer from deteriorating or worsening to a deeper stage. Evidence suggests that offloading and pressure reduction/redistribution should be a primary goal of treatment of pressure ulcers, along with eliminating shearing and friction forces. Addressing other key contributing or risk factors is also critical. Knowing what intrinsic and extrinsic factors contribute to skin breakdown is important. Intrinsic factors such as age, immune function, nutrition and disease states (co-morbid conditions) should be considered. Extrinsic factors such as dry skin, friction, transfer equipment, medications, and moisture should also be addressed.

Maintaining adequate nutrition and hydration should be an essential component of PU management plans. Nutritional assessments should include: current and usual weight, history of involuntary weight loss, nutrition intake (protein, calories, fluid), appetite, dental health, chewing, swallowing or feeding problems, medical or surgical history affecting intake or absorption, drug / nutrient interactions, psychosocial factors (mood, finances, cooking ability, culture, preferences) and appropriate laboratory values. Common laboratory analysis includes serum albumin (20 day half life indicates chronic disease state, values below 3.5g/dl indicates increased risk); serum pre-albumin has a 2 to 3 day half life, providing a more current reflection of protein stores (values below 15 mg/dl indicates increased risk); a total lymphocyte count is an indicator of protein-calorie malnutrition (values below 1,800 mm3 indicates risk); serum transferring is also a malnutrition indicator (values below 200 mg/dl indicates risk).

Managing excessive moisture (incontinence, sweat, spilled liquids) on the skin surface of patients at risk for PU is another critical preventive and management goal. Managing incontinence includes establishing a bowel and bladder program, cleansing the skin after soiling with pH balanced cleansers, and using incontinence skin barriers (creams, ointments, etc) to protect and maintain intact skin. Consider a pouching system or collection device to protect from effluence if fecal incontinence is an issue. Indwelling catheters may be indicated for short term use with severe incontinence related dermatitis and difficult to manage urinary incontinence. In addition, limit the use of diapers, but if briefs, diapers or underpads are used, make sure they are the type that wick moisture from skin.

Addressing impaired mobility includes patient and caregiver education and establishing a turning/repositioning schedule for patients confined to the bed or a chair. This should include repositioning the patient every 2-4 hours with the support of bony prominences. Keep the head of the bed at 30 degrees or less except for tube fed patients (but allow elevation for 1 hour after meals). Avoid "donuts" (rings meant for under coccyx areas), and pulling of the patient across the bed or a chair surface. Place pressure-redistribution surfaces on bed and chair surfaces.

Open pressure ulcers are wounds. Many become chronic wounds and stage III/IV pressure ulcers have been associated with a higher complication rate (especially infection and sepsis) and higher mortality rate that some other chronic wounds. Wound healing principles have been discussed in previous educational papers, but as a brief summary, we will review some helpful mnemonics to guide wound bed preparation and wound management of full thickness open wounds. The first mnemonic is T-I-M-E. Schultz et al. (2003), and Leaper et al. (2013) have written pivotal articles describing T-I-M-E as a way to guide clinicians in the management of full thickness wounds.

• T stands for tissue: address non-viable tissue in the wound bed. Removing dead and necrotic tissue from the wound bed promotes wound healing, inflammation and reduces bacterial breeding grounds.
• I stands for infection and inflammation: address potential sources of bacterial contamination. Use excellent technique when changing the dressings and providing wound care. Identify early signs of infection and address them. Culture the wound bed if warranted using appropriate methods (quantitative tissue cultures). Chronic wounds tend to be stuck in an inflammatory phase of wound healing. High levels of wound enzymes (MMPs or Matrix metalloproteinases) and inflammatory chemical messengers (cytokines) dominate the wound fluid of these wounds, making a very inhospitable environment for healing processes and cells. Consider wound dressings and topical therapies which address this and help minimize it.
• M stands for moisture. Maintaining adequate moisture in the wound is necessary for healing cells to migrate and microcellular processes to continue optimally. A dry wound bed may take almost 50% longer to heal than a moist wound environment (Winter, 1962). Too much moisture, on the other hand, perpetuates high levels of MMPs and cytokines, and may contribute to the chronic inflammatory state of a chronic wound.
• E stands for the edges of the wound (and surrounding tissue). Healthy wound edges have a "beachfront" look to them, as if the edges of the wound were the sand on the water's edge of the beach gently flowing down into the water. If the edge of the wound is rolled under, like a cliff instead of a beach, or if it is undermined as if a cave were hiding under the wound edge, then skin cells (keratinocytes/epithelial cells) cannot migrate easily and the wound will not contract (get smaller) normally. These problematic wound edges need to be addressed and smoothed out in order to facilitate or stimulate wound healing. In some cases rolled edges may be addressed by chemical cauterization with silver nitrate on a stick by a professional who is trained to do this within their scope of practice.

Dorothy Doughty, MSN, RN, CWOCN, FAAN (2012) gave the following mnemonic to illustrate similar principles for topical wound therapy:

• D - Debride any non-viable tissue (necrotic tissue is an impediment to wound healing)
• I - Identify and treat infection infection is a powerful impediment to wound healing (get a biopsy versus a swab culture)
• P - Pack dead space LIGHTLY the wound environment should be friendly to fibroblasts (the white cells that manufacture new granulation tissue in full thickness wounds). Packing a wound too tightly, reduces the fibroblast activity, impairs cellular migration and may actually cause some tissue ischemia in the wound bed if excessive pressure results from the packing.
• A - Absorb EXCESS exudate
• M - Maintain MOIST wound surface
• O - Open or excise closed wound edges
• P - Protect healing wound from trauma/infection
• I - Insulate (maintain body temp. at normal to reduce vasoconstriction and enhance cellular activity).

Stillman (2009) suggested this DIDN'T HEAL mnemonic device to help remember factors that adversely affect wound healing:

• D = Diabetes: The long-term effects of diabetes impair wound healing by diminishing sensation and arterial inflow. In addition, even acute loss of diabetic control can affect wound healing by causing diminished cardiac output, poor peripheral perfusion, and impaired polymorphonuclear leukocyte phagocytosis.
• I = Infection: Infection potentiates collagen lysis. Bacterial contamination is a necessary condition but is not sufficient for wound infection. A susceptible host and wound environment are also required. Foreign bodies (including sutures) potentiate wound infection.
• D = Drugs: Steroids and antimetabolites impede proliferation of fibroblasts and collagen synthesis.
• N = Nutritional problems: Protein-calorie malnutrition and deficiencies of vitamins A, C, and zinc impair normal wound-healing mechanisms.
• T = Tissue necrosis, resulting from local or systemic ischemia or radiation injury, impairs wound healing. Wounds in characteristically well-perfused areas, such the face and neck, may heal surprisingly well despite unfavorable circumstances. Conversely, even a minor wound involving the foot, which has a borderline blood supply, may mark the onset of a long-term nonhealing ulcer. Hypoxia and excessive tension on the wound edges also interfere with wound healing because of local oxygen deficits.
• H = Hypoxia: Inadequate tissue oxygenation due to local vasoconstriction resulting from sympathetic overactivity may occur because of blood volume deficit, unrelieved pain, or hypothermia, especially involving the distal extent of the extremities.
• E = Excessive tension on wound edges: This leads to local tissue ischemia and necrosis.
• A = Another wound: Competition between several healing areas for the substrates required for wound healing impairs wound healing at all sites.
• L = Low temperature: The relatively low tissue temperature in the distal aspects of the upper and lower extremities (a reduction of 1-1.5C [2-3F] from normal core body temperature) is responsible for slower healing of wounds at these sites.

Prevention is paramount! Off load!

Address healing impediments, especially nutrition, moisture, friction and shear.

Use appropriate mnemonics to help guide wound bed preparation and wound healing approaches.

Any topical wound therapy that you select should show expected improvement in 2 to 4 weeks. If not, then re-evaluate the wound and evaluate for possible infection (quantitative tissue analysis). Consider measures to address etiologic and systemic factors (nutrition, shear, diabetes or comorbid disease control). Change to another product. If the wound continues to worsen or does not improve after doing these things, consider malignancy (biopsy for histopathology) or autoimmune disease(s) as potential contributing factors such as Pyoderma Gangrenosum.

As stated before, many changes have occurred in health care over the past 20 years. Nursing care delivery, hospital organizational frameworks, quality improvement, financial coverage, not to mention technology (including electronic records), and perhaps the overall face of our present day patient population (Edelman, 1995; CDC, 1997; Vincent et al., 2006). Yet, even with multiple pressure ulcer prevention programs implemented nationwide, pressure ulcer incidence and prevalence has not changed significantly in many facilities. Researchers need to determine why and develop innovative approaches to solve this dilemma. The effectiveness of pressure ulcer prevention and treatment interventions must be determined. Guidelines must be based on current, high-quality scientific evidence, and impediments to guideline implementation must be addressed. There are significant gaps in the scientific literature regarding pressure ulcer risk assessment, particularly in regard to present day populations. New conceptual models of pressure ulcer development, risk assessment, and new interventions may need to be developed (Armstrong et al., 2008).

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