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Clinical staging and management of pressure-induced injury
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Clinical staging and management of pressure-induced injury
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2016. | This topic last updated: Apr 15, 2015.

INTRODUCTION — A pressure ulcer, also referred to as a pressure injury [1], is a localized area of damage to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear (eg, sacrum, calcaneus, ischium) (figure 1). The superficial skin is less susceptible to pressure-induced damage than deeper tissues, and thus, the external appearance may underestimate the extent of damage [2]. Pressure ulcers are typically related to immobility (ie, bed-bound or chair-bound individual), but can also result from poorly fitting casts or other medical equipment or devices.

The clinical staging that guides treatment of pressure ulcers is reviewed here. The pathogenesis, risk assessment, and preventive strategies are discussed elsewhere. (See "Epidemiology, pathogenesis and risk assessment of pressure ulcers" and "Prevention of pressure ulcers".)

CLINICAL FEATURES AND STAGING — The management of pressure ulcers begins with a comprehensive assessment of the patient's general medical condition to identify reversible conditions, and clinical assessment of the wound. Risk factors are reviewed separately. (See "Epidemiology, pathogenesis and risk assessment of pressure ulcers", section on 'Risk factors'.)

A pressure ulcer (ie, pressure injury [1]) is an area of localized damage to the skin and/or underlying tissue, usually over a bony prominence (figure 1), as a result of pressure, or pressure in combination with shear (eg, sacrum, calcaneus, ischium). These are usually clinically apparent on examination by the appearance of the skin and location. Superficial moisture-induced lesions, located over a bony prominence, should not be labeled as pressure ulcers, and neither should skin tears, tape burns, perineal dermatitis, or excoriation.

Identified areas of skin damage should be evaluated for length, width, and depth, presence of sinus tracts, necrotic tissue, or exudate, and evidence for healing such as the presence of granulation. Photographs of all wounds are helpful. Based upon this information, the pressure ulcer can be staged. (See 'NPUAP staging' below.)

Infections impair wound healing. The possibility of infection should be considered even if systemic signs, such as fever and leukocytosis, are absent [3]. Infection of pressure ulcers can present with local signs of soft tissue involvement, such as warmth, erythema, local tenderness, purulent discharge, and the presence of a foul odor. However, the manifestations of infection in pressure ulcers can be variable, with delayed wound healing being the only sign of infection. (See 'Treat infection' below.)

Pressure ulcers can serve as a reservoir for resistant organisms such as methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and multiply-resistant gram negative bacilli, and colonized or infected ulcers pose a potential risk to other hospitalized patients [4,5]. Precautions should be used when examining and treating ulcers. (See "General principles of infection control", section on 'Standard precautions'.)

Other complications associated with pressure ulcers are uncommon, but may include:

Sinus tracts that communicate with the deep viscera, including the bowel or bladder.

Occasional heterotrophic calcification.

Systemic amyloidosis due to the chronic inflammatory state arising from the ulcer.

Squamous cell carcinoma. This can develop in a chronic pressure ulcer and should always be considered in those with a nonhealing wound.

Staging — A number of staging systems have been developed to describe the extent of pressure-induced injury to the skin [6-8]. The most commonly used system is from the National Pressure Ulcer Advisory Panel (NPUAP) (table 1 and figure 2) [6]. NPUAP suggests using the terminology "pressure injury" to describe these wounds, given that lesser degrees of skin damage due to pressure may not be associated with skin ulceration. The European Pressure Ulcer Advisory Panel (EPUAP) recommends similar stages, except for the presence of suspected deep tissue injury and unstageable ulcers. The wound should be staged according to its deepest extent. As an example, although the majority of a wound may be stage 2, any portion that extends deeper classifies the ulcer as a higher stage.

NPUAP staging — The National Pressure Ulcer Advisory Panel (NPUAP) staging system is described below (table 1 and figure 2) [6]. The NPUAP stage is used to describe the initial appearance of an area of skin damage. The practice of changing the stage as healing occurs, known as reverse staging, is not recommended [9].

Stage 1 — Stage 1 is characterized by intact skin with a localized area of nonblanchable erythema (picture 1), which may appear differently in darkly pigmented skin. The presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury.

Stage 2 — Stage 2 is characterized by partial-thickness loss of skin with exposed dermis (picture 1). The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough, and eschar are not present.

These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. This stage should not be used to describe moisture-associated skin damage (MASD) including incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury (MARSI), or traumatic wounds (skin tears, burns, abrasions).

Stage 3 — Stage 3 is characterized by full-thickness loss of skin, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present (picture 1). Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage, and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss, this is an unstageable pressure injury.

The depth of a stage 3 pressure ulcer varies by anatomic location. Stage 3 ulcers can be shallow in areas without subcutaneous tissue, which include the bridge of the nose, ear, occiput, and the malleolus. By contrast, the gluteal region can develop very deep ulcers (stage 3, stage 4).

Stage 4 — Stage 4 is characterized by full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer. Slough and/or eschar may be visible (picture 1). Epibole (rolled edges), undermining, and/or tunneling often occur. Depth varies by anatomical location. If slough or eschar obscure the extent of tissue loss, this is an unstageable pressure injury  

The extent of stage 4 ulcers is often underestimated due to undermining and fistula formation; a relatively small superficial skin defect may mask extensive deep tissue necrosis. The depth of a stage 4 pressure ulcer also varies by anatomic location. As with stage 3 ulcers, the bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and stage 4 ulcers in these locations can be shallow. Stage 4 ulcers that extend into supporting structures, including fascia, tendon, or joint capsule, may be associated with osteomyelitis.

Unstageable — Pressure-induced skin damage is considered unstageable when there is full-thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed. Stable eschar (ie, dry, adherent, intact without erythema or fluctuance) on an ischemic limb or the heel(s) should not be removed.

Suspected deep tissue pressure injury — The “suspected deep tissue pressure injury” stage captures the lingering debate on how best to identify lesions with intact overlying skin [10-12]. Deep tissue pressure injury should be suspected whenever there is a localized area of skin (intact or non-intact) with persistent nonblanchable deep red, maroon, or purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This level of skin injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury, or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a full-thickness pressure injury (unstageable, stage 3 or stage 4). Do not use deep tissue pressure injury to describe vascular, traumatic, neuropathic, or dermatologic conditions.

Deep tissue pressure injury may be difficult to detect in individuals with dark skin tones. The area may be painful, firm or spongy, boggy, warm or cool compared with the surrounding tissue. (See "Epidemiology, pathogenesis and risk assessment of pressure ulcers".)

DIFFERENTIAL DIAGNOSIS — It is important to distinguish pressure ulcers from ulcers related to diabetes, arterial insufficiency, or venous insufficiency [13]. However, these also predispose to the development of a pressure ulcer, and many wounds, particularly in the lower extremity, have a multifactorial etiology. (See "Clinical assessment of wounds", section on 'Differentiation of chronic ulcers'.)

Pressure ulcers may also be confused with other conditions that cause skin erythema, such as cellulitis. (See "Cellulitis and erysipelas" and "Cellulitis and erysipelas", section on 'Clinical manifestations'.)

GENERAL CARE — The general approach to management of a patient with a pressure-induced skin injury should include the following [14]:

Reduce or eliminate underlying contributing factors by providing pressure redistribution with proper positioning and support surfaces.

Provide appropriate local wound care, which may include debridement for patients with necrotic tissue, based on the ulcer's characteristics.

Consider adjunctive therapies, such as negative pressure wound therapy.

Monitor and document the patient's progress.

Provide appropriate psychosocial support.

The extent and magnitude of psychosocial complications have not been well defined, and psychosocial support is often not considered. However, patients with pressure ulcers suffer pain and a loss of control over their lives. Wound care disrupts normal activities of daily life, and patients often feel stigmatized. This results in lifestyle changes leading to social isolation, depression, and decrements in overall health-related quality of life [15].

Control pain — Adequate pain relief should be provided as pressure ulcers can be quite painful [16]. Local factors that may be contributing to pain such as ischemia, infection, or breakdown of the surrounding skin should be addressed.

Initial and on-going pain assessment should be documented using a pain scale. Assessment is aimed at identifying the type and extent of pain present so that appropriate therapy may be provided. Pain may be classified as intermittent, which occurs at the time of wound debridement, or cyclic, which occurs at the time of a dressing change, or as persistent pain occurring all the time and related to the pressure ulcer.  

Oral non-opioid pain medications can be used for mild pain. Opioid analgesics may be needed for moderate to severe pain. (See "Overview of the treatment of chronic non-cancer pain".)

Topical local anesthetics (eg, lidocaine), which have shown some benefit in small randomized trials [17-19], can provide numbness for a short period of time and can be useful for a specific procedure, but should not be used as the only method of pain relief. Ibuprofen-releasing foam dressings can be used, if available [20]. However, many patients with deep ulcers will require systemic therapy for pressure ulcer pain.

Wound cleansing and dressing techniques may need to be reconsidered if they are causing severe pain. In particular, adequate pain control should be provided prior to dressing changes and debridement. Extensive debridement should be performed in the operating room as patients may require conscious sedation or general anesthesia for these invasive procedures.

Treat infection — All pressure ulcers are colonized with bacteria, but only clinically evident infections should be addressed with culture and antibiotic treatment [21,22]. Patients with deep ulcers should be evaluated for the presence of osteomyelitis. Treatment of infectious complications of pressure ulcers is discussed separately. (See "Infectious complications of pressure ulcers".)

Optimize nutrition — Patients with pressure ulcers are in a chronic catabolic state. Optimizing both protein and total caloric intake is important, particularly for patients with stage 3 and 4 ulcers [2].

Nutritional intake should be assessed by a nutritionist. This assessment may include protein and caloric intake, hydration status, serum albumin and/or prealbumin, and total lymphocyte count [23]. Nutritional deficiencies should be corrected. (See "Nutrition support in critically ill patients: An overview".)

If oral intake is not adequate to ensure sufficient calories, protein, vitamins, and minerals, nutritional supplementation with enteral or parenteral nutrition (according to the capabilities of the care facility) is recommended to correct deficiencies although clinical trial evidence supporting this approach is limited [24-28]. A retrospective cohort study of 882 patients with pressure ulcers at 95 long-term care facilities demonstrated that total caloric intake of at least 30 kcal/kg promoted healing and decreased the size of stage 3 and 4 pressure ulcers [29]. Increased dietary protein intake also promotes the healing of pressure ulcers [30,31]. The protein target is usually 1.5 g/kg/day, although some authors advocate higher protein intake [22].

Data do not support nutritional supplementation for patients who do not have nutritional deficiencies [32]. Vitamin C and zinc supplementation are commonly employed to promote healing, but their efficacy has not been conclusively demonstrated [26]. A number of randomized trials identified in systematic reviews have evaluated the role of nutritional supplements, but methodological flaws and study size have precluded confirmation of clinically significant results [14,26]. A later, larger trial randomly assigned 200 malnourished adult patients with pressure ulcers to a high calorie, protein-rich nutritional formula supplemented with arginine, zinc, and antioxidants, or to a control receiving a nutritional formula without supplements for eight weeks [33]. This study found a greater reduction in pressure ulcer area for the supplemented compared with control formula (mean reduction, 61 versus 45 percent). No difference was noted, though, in the secondary outcome of complete healing of the pressure ulcer. Because previous studies of the individual nutrients failed to show benefit, the authors postulated a synergistic effect among the nutrients.

Anabolic steroids are sometimes recommended in patients with weight loss and protein depletion. A clinical trial of 212 spinal cord injury patients with chronic pressure ulcers demonstrated no benefit from oxandrolone therapy [34].

Redistribute pressure — Proper positioning and support to minimize tissue pressure should be provided for all patients, particularly those with pressure ulcers. The development of any new areas of skin damage should prompt review of the method and intensity of preventive measures. The use of these measures to prevent the development of pressure ulcers is reviewed separately. (See "Prevention of pressure ulcers".)

To date, there are no randomized trials available to identify whether repositioning makes a difference in the healing rates or what should be the optimal repositioning regimen [35,36]. Nevertheless, in the absence of data, as a practice with good face value, patients should be positioned to minimize or avoid all pressure on the wound. Pressure-relieving support surfaces are also helpful in reducing tissue pressure. These support devices, as defined by the National Pressure Ulcer Advisory Panel Support Surface Standards Initiative, are described separately [37].

(See "Prevention of pressure ulcers", section on 'Support surfaces'.)

The effectiveness of support surfaces in promoting healing of pressure ulcers has been studied in a number of randomized clinical trials with inconsistent results [14]:

A randomized trial of 158 hospitalized patients found no difference in wound healing between 85 patients on nonpowered support devices and 83 on powered support devices [38].

In a study of 65 hospitalized patients with pressure-induced tissue damage, 31 patients were given an air-fluidized bed and repositioned every four hours, while 34 patients received conventional therapy with an air mattress covered by a foam pad and repositioning every two hours [30]. The latter group also used elbow or heel pads as needed. Pressure ulcers showed a median decrease in total surface area on the air-fluidized beds, while increasing in size with conventional therapy (-1.2 versus +0.5 cm2). The difference was even greater in patients with large ulcers at baseline.

In another report of 84 nursing home residents, subjects treated with a low-air-loss bed were 2.5 times more likely to heal their ulcer compared with those using a foam mattress [39].

Given limited data, it is uncertain if powered mattresses are superior to nonpowered mattresses [14]. The costs associated with powered beds become particularly significant when considering that treatment for at least two months is typically required [40]. However, specialized support surfaces appear to be of benefit and should be used rather than a standard mattress.

It should again be emphasized that support surfaces alone do not address the underlying issues that lead to pressure-induced skin injury. (See "Epidemiology, pathogenesis and risk assessment of pressure ulcers", section on 'Pathogenesis' and "Epidemiology, pathogenesis and risk assessment of pressure ulcers", section on 'Risk factors'.)

WOUND MANAGEMENT — Wound management is according to general principles of wound care, which includes debridement of necrotic tissue, and appropriate dressings or wound packing to promote healing of the wound bed, and wound coverage, when indicated. The important elements of wound care as they pertain to pressure ulcers are reviewed below. (See "Basic principles of wound management".)

Summary of treatment by stage — Specific treatment is guided by the stage of skin injury. The National Pressure Ulcer Advisory Panel (NPUAP) staging is presented above. (See 'Staging' above.)

Stage 1 skin injuries can be covered with transparent film for protection. The development of a stage 1 ulcer should be taken as an indication that the patient is at high risk for more serious ulcer development and intensive preventive measures should be taken. (See "Prevention of pressure ulcers".)

Stage 2 ulcers require a dressing that maintains a moist wound environment [41]. These wounds generally require little debridement and thus we avoid wet-to-dry dressings. Rather, we use a semiocclusive (transparent film) or occlusive dressings (hydrocolloids or hydrogels) so that any necrotic tissue that is present is digested by enzymes normally present in the wound base. It should not be used in the presence of infection [16,42,43]. (See 'Wound dressings' below.)

Stage 3 and 4 ulcers generally require debridement of necrotic tissue and coverage with appropriate dressings, and possibly treatment of infection.

Debridement — Necrotic tissue promotes bacterial growth and impairs wound healing. Debridement (mechanical, surgical, enzymatic) is a standard component of basic wound management. (See "Basic principles of wound management", section on 'Wound debridement'.)

Surgical debridement is often necessary to remove areas of extensive tissue necrosis or thick eschar. However, sharp debridement is generally not recommended for thick eschar overlying the heel (in the absence of signs of infection), particularly in the setting of reduced perfusion, due to the proximity of the bone [22].

For minor tissue slough and exudate at the base of a wound, it is not clear whether any particular form of nonsurgical debridement (eg, mechanical, enzymatic, biologic) offers any clear advantage [44].

Debridement should be discontinued once necrotic tissue has been removed and granulation tissue is present. Care should be taken with respect to debridement of the ischial spine, as this will potentially affect weightbearing and can lead to breakdown of the ischium on the opposite side. Removal of both ischial spines will increase the risk of perineal problems [2].

Wound dressings — Dressings serve to protect the wound from contamination, and facilitate healing by absorbing exudate and protecting healing surfaces. Excess fluid causes wound maceration, while desiccation will slow epithelial cell migration. Many different types of dressings are available (table 2). Although varying circumstances may favor choosing one dressing over another, no dressing has been shown to be consistently superior to another in clinical trials [14,45-47]. A systematic review identified six trials comparing topical treatments with and without antimicrobial activity [48]. Where differences in wound healing were found, these sometimes favored the comparator treatment without antimicrobial properties.(See "Basic principles of wound management", section on 'Wound dressings' and "Basic principles of wound management", section on 'Wound packing'.)

An absorptive dressing should be used to avoid build-up of chronic wound fluid that can macerate the wound and inhibit cell proliferation and wound healing [42]. Dressings with absorptive qualities include foams and alginates.

Desiccated ulcers lack wound fluids, which provide tissue growth factors to facilitate reepithelialization. Pressure ulcer healing is promoted by dressings that maintain a moist wound environment while keeping the surrounding intact skin dry [29,41,49]. Choices for a dry wound include saline moistened gauze, transparent films, hydrocolloids, and hydrogels.

Adjunctive therapies — A variety of adjunctive therapies such as electrical stimulation, negative pressure wound therapy, therapeutic ultrasound, hyperbaric oxygen, topical oxygen, and application of growth factors to the wound have been investigated for the treatment of pressure ulcers, but the indications for their use remain uncertain. Some of these adjunctive therapies are discussed below.

Negative pressure wound therapy enhances wound healing by increasing blood flow, decreasing edema, and increasing the formation of granulation tissue [36,50]. Randomized trials using NPWT as an adjunctive therapy for the management of pressure ulcers had not identified any statistically significant differences with respect to quantitative wound healing measures (eg, wound surface area reduction) [50-54]. However, NPWT improved patient comfort and was less labor intensive [55]. Negative pressure wound therapy is discussed in detail elsewhere. (See "Negative pressure wound therapy".)

Hyperbaric oxygen therapy (HBOT) has been advocated, but there have been no studies specifically looking at the treatment of pressure ulcers with HBOT. Systematic reviews of studies of HBOT for treating wounds concluded that while HBOT may be of benefit for some types of wounds, there is insufficient evidence of sustained benefit. The underlying study quality was poor; some serious adverse events were associated with HBOT, including seizures and pneumothorax [56,57]. (See "Basic principles of wound management", section on 'Hyperbaric oxygen therapy'.)

Ultrasound is sometimes used as therapy for pressure ulcers. A systematic review of three randomized trials found that methodologic limitations and small trial size made it impossible to rule out benefit or harm with ultrasound therapy [58].

Electrical stimulation, in which a direct current is applied to the wound, has also resulted in enhanced healing in several small studies [59,60] and a meta-analysis [61]. The electric current is provided twice daily through a wound overlay and is believed to promote the migration and proliferation of fibroblasts. A systematic review of randomized trials of electromagnetic therapy, a distinct form of electrotherapy, found no evidence of benefit [62]. Similarly, pulsed radiofrequency energy therapy and electromagnetic therapy have been proposed but evidence of benefit is limited [62,63].

MONITORING — Appropriate therapeutic goals should be set that consider discharge potential, quality of life, treatment preferences, and prognosis [22,64].

With appropriate care, most pressure ulcers should heal within an expected timeframe. Two studies from nursing home facilities that collectively followed over 1000 pressure ulcer patients found that more than 70 percent of patients with a stage 2 pressure ulcer, 50 percent with a stage 3 ulcer, and 30 percent with a stage 4 ulcer were ulcer-free at six months with standard wound care [65,66]. Among those followed over two years, 77 percent of stage 4 ulcers had healed.

Patients with persistent, nonhealing wounds should be reevaluated to identify infection, or the presence of reversible causes of ischemia. (See 'Clinical features and staging' above and 'Differential diagnosis' above.)

The following parameters of care should be monitored daily and documented [13]:

Evaluation of the ulcer (see 'Healing Scales' below)

Status of the dressing, if present

Status of the area surrounding the ulcer

Presence of pain, and adequacy of pain control

Presence of possible complications, such as infection

Healing Scales — The progress in healing is best described by scales that capture changes in surface area, extent of necrotic tissue and exudate, and the presence of granulation tissue. As noted above, reverse staging, which changes the initial NPUAP stage as the ulcer heals, is not recommended [9].

A number of scales are available for use in monitoring and documentation of the healing of pressure ulcers [13,67-70], including the Pressure Sore Status Tool (PSST) (table 3), the Sessing Scale, the Wound Healing Scale, and the Pressure Ulcer Scale for Healing (PUSH) tool (table 4) [67-70]. The PUSH tool, designed to be used in conjunction with the NPUAP Staging System (table 1 and figure 2), is the most readily applied tool [71]. This scale has been validated, is easy to use, and has been shown to be helpful in pressure ulcer management.

Given differences among available staging systems, the healing scale used should be explicitly described to facilitate effective communication among clinicians responsible for patients with a pressure ulcer. Training in the use of these scales is also required to ensure that ulcers are staged in a consistent manner.

WOUND COVERAGE — Most pressure-induced injuries are successfully managed using the basic principles of wound care and dressings described above. Operative management covers the wound, but ulcer recurrence occurs in 13 to 61 percent [72-74].  

Nevertheless, surgical wound coverage may benefit some patients, particularly good risk surgical candidates whose quality of life would be markedly improved by rapid wound closure. Whether to proceed with surgery ultimately depends upon patient preference, treatment goals, risk of recurrence, and quality-of-life considerations.  

A variety of operative procedures are available, the selection of which depends upon patient characteristics, ulcer site, and available surgical expertise [2]. Direct wound closure is usually not possible; thus, wound coverage entails using a skin graft, skin flap, or myocutaneous flap, often as a staged procedure. Prior to graft or flap placement, the ulcer should be free of devitalized tissue and infection, and patient factors predisposing to pressure ulcer development should be corrected, where possible. Nutrition should be optimized and smokers should be encouraged to stop since continued smoking impairs wound healing and may result in higher rates of recurrence [72]. (See "Principles of grafts and flaps for reconstructive surgery".)

Colostomy, which diverts the stool, is another option if the site of the ulcer is prone to fecal contamination. However, this procedure may be associated with a high complication rate in frail elderly patients and is of questionable efficacy [75]. (See "Overview of surgical ostomy for fecal diversion".)

MORBIDITY AND MORTALITY — Patients with pressure-induced injuries or those who develop a new ulcer are approximately two to three times more likely to die than patients without an ulcer [76-78]. However, these patients tend to have many other comorbid conditions; after adjusting for these other factors, pressure ulcers are at best a weak predictor of mortality.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Basics topic (see "Patient education: Pressure sores (The Basics)")


The treatment of pressure-induced injuries begins with a comprehensive assessment of the patient's general medical condition and evaluation of the wound. The development of an ulcer should underscore the need to review and intensify preventive measures. (See 'Clinical features and staging' above.)

A standardized system should be used to document the initial presentation, plan appropriate treatment, and follow the healing progress of the wound. (See 'Staging' above and 'Healing Scales' above.)

Close daily monitoring of the pressure ulcer, the dressing, the surrounding skin, any possible complications, and pain control should be documented. Documentation may be facilitated by using one of the scales for healing ulcers. (See 'Healing Scales' above.)

Adequate pain control should be provided for patients with pressure ulcers. Particular attention should be paid to pain management during wound dressing and debridement. (See 'Control pain' above.)

Nutritional status should be assessed in patients with pressure ulcers and any identified deficiencies should be corrected. For patients who do not have a documented nutritional deficiency, we suggest not giving nutritional supplementation (Grade 2B). (See 'Optimize nutrition' above.)

Patients should be positioned and repositioned at least every two hours to relieve tissue pressure. We suggest use of nonpowered support surfaces (eg, foam mattresses or overlays) for most patients with pressure ulcers (Grade 2C). When cost is not a limiting factor, powered surfaces (eg air-fluidized beds) may be appropriate for selected patients with large or multiple ulcers that preclude appropriate positioning. (See 'Redistribute pressure' above.)

For stage 1 skin injuries, treatment should focus on preventive measures and wound protection with transparent film. For stage 2 ulcers, dressings are required to maintain a moist wound environment. For stage 3 and 4 ulcers, treatment consists of treatment of wound infection if present, debridement of necrotic tissue, and appropriate dressings. Surgery is necessary for some full-thickness pressure ulcers. (See 'Wound management' above.)

Dressings are selected based on wound characteristics, including the presence of heavy exudate, desiccation, or necrotic tissue. (See 'Wound dressings' above.)

Necrotic tissue promotes bacterial growth and impairs wound healing. Wound debridement approaches include: irrigation, surgical debridement, enzymatic debridement, and biologic debridement. (See 'Debridement' above.)

Most patients are successfully managed without surgery; procedures such as direct closure, skin grafts, musculocutaneous flaps, and free flaps may be appropriate in patients whose quality of life would be markedly improved by rapid wound coverage. (See 'Wound coverage' above.)

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  1. http://www.npuap.org/national-pressure-ulcer-advisory-panel-npuap-announces-a-change-in-terminology-from-pressure-ulcer-to-pressure-injury-and-updates-the-stages-of-pressure-injury/ (Accessed on May 26, 2016).
  2. Bauer J, Phillips LG. MOC-PSSM CME article: Pressure sores. Plast Reconstr Surg 2008; 121:1.
  3. Livesley NJ, Chow AW. Infected pressure ulcers in elderly individuals. Clin Infect Dis 2002; 35:1390.
  4. Murphy S, Denman S, Bennett RG, et al. Methicillin-resistant Staphylococcus aureus colonization in a long-term-care facility. J Am Geriatr Soc 1992; 40:213.
  5. Gaynes RP, Weinstein RA, Chamberlin W, Kabins SA. Antibiotic-resistant flora in nursing home patients admitted to the hospital. Arch Intern Med 1985; 145:1804.
  6. National Pressure Ulcer Advisory Panel. Updated staging system. www.npuap.org (Accessed on December 02, 2008).
  7. Shea JD. Pressure sores: classification and management. Clin Orthop Relat Res 1975; :89.
  8. Yarkony GM, Kirk PM, Carlson C, et al. Classification of pressure ulcers. Arch Dermatol 1990; 126:1218.
  9. National Pressure Ulcer Advisory Panel. NPUAP position on reverse staging of pressure ulcers. Adv Wound Care 1998; 8:32.
  10. Black JM, National Pressure Ulcer Advisory Panel. Moving toward consensus on deep tissue injury and pressure ulcer staging. Adv Skin Wound Care 2005; 18:415.
  11. Sibbald RG, Krasner DL, Woo KY. Pressure ulcer staging revisited: superficial skin changes & Deep Pressure Ulcer Framework©. Adv Skin Wound Care 2011; 24:571.
  12. Smart H. Deep tissue injury: what is it really? Adv Skin Wound Care 2013; 26:56.
  13. Thomas DR. The new F-tag 314: prevention and management of pressure ulcers. J Am Med Dir Assoc 2006; 7:523.
  14. Reddy M, Gill SS, Kalkar SR, et al. Treatment of pressure ulcers: a systematic review. JAMA 2008; 300:2647.
  15. Gorecki C, Brown JM, Nelson EA, et al. Impact of pressure ulcers on quality of life in older patients: a systematic review. J Am Geriatr Soc 2009; 57:1175.
  16. Lyder, CH, Ayello, EA. Chapter 12. Pressure ulcers: a patient safety issue. www.ahrq.gov/qual/nurseshdbk/docs/LyderC_PUPSI.pdf (Accessed on April 01, 2013).
  17. Flock P. Pilot study to determine the effectiveness of diamorphine gel to control pressure ulcer pain. J Pain Symptom Manage 2003; 25:547.
  18. Zeppetella G, Paul J, Ribeiro MD. Analgesic efficacy of morphine applied topically to painful ulcers. J Pain Symptom Manage 2003; 25:555.
  19. Zeppetella G, Ribeiro MD. Morphine in intrasite gel applied topically to painful ulcers. J Pain Symptom Manage 2005; 29:118.
  20. Arapoglou V, Katsenis K, Syrigos KN, et al. Analgesic efficacy of an ibuprofen-releasing foam dressing compared with local best practice for painful exuding wounds. J Wound Care 2011; 20:319.
  21. Grey JE, Harding KG, Enoch S. Pressure ulcers. BMJ 2006; 332:472.
  22. Advisory Panel, European Pressure Ulcer Advisory Panel. Pressure ulcer treatment recommendations. In: Prevention and treatment of pressure ulcers: clinical practice guideline, National Pressure Ulcer Advisory Panel, Washington, DC 2009.
  23. Stechmiller JK, Cowan L, Whitney JD, et al. Guidelines for the prevention of pressure ulcers. Wound Repair Regen 2008; 16:151.
  24. Koretz RL, Avenell A, Lipman TO, et al. Does enteral nutrition affect clinical outcome? A systematic review of the randomized trials. Am J Gastroenterol 2007; 102:412.
  25. ter Riet G, Kessels AG, Knipschild PG. Randomized clinical trial of ascorbic acid in the treatment of pressure ulcers. J Clin Epidemiol 1995; 48:1453.
  26. Langer G, Fink A. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database Syst Rev 2014; :CD003216.
  27. Smith ME, Totten A, Hickam DH, et al. Pressure ulcer treatment strategies: a systematic comparative effectiveness review. Ann Intern Med 2013; 159:39.
  28. Teno JM, Gozalo P, Mitchell SL, et al. Feeding tubes and the prevention or healing of pressure ulcers. Arch Intern Med 2012; 172:697.
  29. Bergstrom N, Horn SD, Smout RJ, et al. The National Pressure Ulcer Long-Term Care Study: outcomes of pressure ulcer treatments in long-term care. J Am Geriatr Soc 2005; 53:1721.
  30. Allman RM, Walker JM, Hart MK, et al. Air-fluidized beds or conventional therapy for pressure sores. A randomized trial. Ann Intern Med 1987; 107:641.
  31. Breslow RA, Hallfrisch J, Guy DG, et al. The importance of dietary protein in healing pressure ulcers. J Am Geriatr Soc 1993; 41:357.
  32. Lyder CH. Pressure ulcer prevention and management. JAMA 2003; 289:223.
  33. Cereda E, Klersy C, Serioli M, et al. A nutritional formula enriched with arginine, zinc, and antioxidants for the healing of pressure ulcers: a randomized trial. Ann Intern Med 2015; 162:167.
  34. Bauman WA, Spungen AM, Collins JF, et al. The effect of oxandrolone on the healing of chronic pressure ulcers in persons with spinal cord injury: a randomized trial. Ann Intern Med 2013; 158:718.
  35. Moore ZE, Cowman S. Repositioning for treating pressure ulcers. Cochrane Database Syst Rev 2012; :CD006898.
  36. Levine SM, Sinno S, Levine JP, Saadeh PB. Current thoughts for the prevention and treatment of pressure ulcers: using the evidence to determine fact or fiction. Ann Surg 2013; 257:603.
  37. National Pressure Ulcer Advisory Panel Support Surface Standards Initiative. Terms and definitions related to support surfaces. www.npuap.org/NPUAP_S3I_TD.pdf (Accessed on April 07, 2013).
  38. Russell L, Reynolds TM, Towns A, et al. Randomized comparison trial of the RIK and the Nimbus 3 mattresses. Br J Nurs 2003; 12:254, 256.
  39. Ferrell BA, Osterweil D, Christenson P. A randomized trial of low-air-loss beds for treatment of pressure ulcers. JAMA 1993; 269:494.
  40. Bennett RG, Bellantoni MF, Ouslander JG. Air-fluidized bed treatment of nursing home patients with pressure sores. J Am Geriatr Soc 1989; 37:235.
  41. Sebern MD. Pressure ulcer management in home health care: efficacy and cost effectiveness of moisture vapor permeable dressing. Arch Phys Med Rehabil 1986; 67:726.
  42. 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.
  43. Brown-Etris M, Milne C, Orsted H, et al. A prospective, randomized, multisite clinical evaluation of a transparent absorbent acrylic dressing and a hydrocolloid dressing in the management of Stage II and shallow Stage III pressure ulcers. Adv Skin Wound Care 2008; 21:169.
  44. Dryburgh N, Smith F, Donaldson J, Mitchell M. Debridement for surgical wounds. Cochrane Database Syst Rev 2008; :CD006214.
  45. Dumville JC, Keogh SJ, Liu Z, et al. Alginate dressings for treating pressure ulcers. Cochrane Database Syst Rev 2015; :CD011277.
  46. Graumlich JF, Blough LS, McLaughlin RG, et al. Healing pressure ulcers with collagen or hydrocolloid: a randomized, controlled trial. J Am Geriatr Soc 2003; 51:147.
  47. Bluestein D, Javaheri A. Pressure ulcers: prevention, evaluation, and management. Am Fam Physician 2008; 78:1186.
  48. Norman G, Dumville JC, Moore ZE, et al. Antibiotics and antiseptics for pressure ulcers. Cochrane Database Syst Rev 2016; 4:CD011586.
  49. Gorse GJ, Messner RL. Improved pressure sore healing with hydrocolloid dressings. Arch Dermatol 1987; 123:766.
  50. Ubbink DT, Westerbos SJ, Evans D, et al. Topical negative pressure for treating chronic wounds. Cochrane Database Syst Rev 2008; :CD001898.
  51. Dumville JC, Webster J, Evans D, Land L. Negative pressure wound therapy for treating pressure ulcers. Cochrane Database Syst Rev 2015; :CD011334.
  52. Mandal A. Role of topical negative pressure in pressure ulcer management. J Wound Care 2007; 16:33.
  53. Ashby RL, Dumville JC, Soares MO, et al. A pilot randomised controlled trial of negative pressure wound therapy to treat grade III/IV pressure ulcers [ISRCTN69032034]. Trials 2012; 13:119.
  54. Ford CN, Reinhard ER, Yeh D, et al. Interim analysis of a prospective, randomized trial of vacuum-assisted closure versus the healthpoint system in the management of pressure ulcers. Ann Plast Surg 2002; 49:55.
  55. Wanner MB, Schwarzl F, Strub B, et al. Vacuum-assisted wound closure for cheaper and more comfortable healing of pressure sores: a prospective study. Scand J Plast Reconstr Surg Hand Surg 2003; 37:28.
  56. Wang C, Schwaitzberg S, Berliner E, et al. Hyperbaric oxygen for treating wounds: a systematic review of the literature. Arch Surg 2003; 138:272.
  57. Kranke P, Bennett MH, Martyn-St James M, et al. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev 2012; :CD004123.
  58. Flemming K, Cullum N. Therapeutic ultrasound for pressure sores. Cochrane Database Syst Rev 2000; :CD001275.
  59. Griffin JW, Tooms RE, Mendius RA, et al. Efficacy of high voltage pulsed current for healing of pressure ulcers in patients with spinal cord injury. Phys Ther 1991; 71:433.
  60. Feedar JA, Kloth LC, Gentzkow GD. Chronic dermal ulcer healing enhanced with monophasic pulsed electrical stimulation. Phys Ther 1991; 71:639.
  61. Gardner SE, Frantz RA, Schmidt FL. Effect of electrical stimulation on chronic wound healing: a meta-analysis. Wound Repair Regen 1999; 7:495.
  62. Flemming K, Cullum N. Electromagnetic therapy for the treatment of pressure sores. Cochrane Database Syst Rev 2001; :CD002930.
  63. Conner-Kerr T, Isenberg RA. Retrospective analysis of pulsed radiofrequency energy therapy use in the treatment of chronic pressure ulcers. Adv Skin Wound Care 2012; 25:253.
  64. Moss RJ, La Puma J. The ethics of pressure sore prevention and treatment in the elderly: a practical approach. J Am Geriatr Soc 1991; 39:905.
  65. Brandeis GH, Morris JN, Nash DJ, Lipsitz LA. The epidemiology and natural history of pressure ulcers in elderly nursing home residents. JAMA 1990; 264:2905.
  66. Berlowitz DR, Brandeis GH, Anderson J, Brand HK. Predictors of pressure ulcer healing among long-term care residents. J Am Geriatr Soc 1997; 45:30.
  67. Bates-Jensen BM. The Pressure Sore Status Tool a few thousand assessments later. Adv Wound Care 1997; 10:65.
  68. Thomas DR, Rodeheaver GT, Bartolucci AA, et al. Pressure ulcer scale for healing: derivation and validation of the PUSH tool. The PUSH Task Force. Adv Wound Care 1997; 10:96.
  69. Ferrell BA. The Sessing Scale for measurement of pressure ulcer healing. Adv Wound Care 1997; 10:78.
  70. Krasner D. Wound Healing Scale, version 1.0: a proposal. Adv Wound Care 1997; 10:82.
  71. www.npuap.org (Accessed on April 08, 2013).
  72. Niazi ZB, Salzberg CA, Byrne DW, Viehbeck M. Recurrence of initial pressure ulcer in persons with spinal cord injuries. Adv Wound Care 1997; 10:38.
  73. Disa JJ, Carlton JM, Goldberg NH. Efficacy of operative cure in pressure sore patients. Plast Reconstr Surg 1992; 89:272.
  74. Mandrekas AD, Mastorakos DP. The management of decubitus ulcers by musculocutaneous flaps: a five-year experience. Ann Plast Surg 1992; 28:167.
  75. Deshmukh GR, Barkel DC, Sevo D, Hergenroeder P. Use or misuse of colostomy to heal pressure ulcers. Dis Colon Rectum 1996; 39:737.
  76. Thomas DR, Goode PS, Tarquine PH, Allman RM. Hospital-acquired pressure ulcers and risk of death. J Am Geriatr Soc 1996; 44:1435.
  77. Berlowitz DR, Wilking SV. The short-term outcome of pressure sores. J Am Geriatr Soc 1990; 38:748.
  78. Berlowitz DR, Brandeis GH, Anderson J, et al. Effect of pressure ulcers on the survival of long-term care residents. J Gerontol A Biol Sci Med Sci 1997; 52:M106.
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