ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Clinical staging and general management of pressure-induced skin and soft tissue injury

Clinical staging and general management of pressure-induced skin and soft tissue injury
Literature review current through: Jan 2024.
This topic last updated: Aug 16, 2023.

INTRODUCTION — Pressure-induced skin and soft tissue injuries are localized areas 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 [1]. Lesions are typically related to immobility but can also result from poorly fitting casts or other medical equipment or devices. Medical devices may also cause mucosal pressure injury.

The clinical staging that guides treatment of pressure-induced skin and soft tissue injuries and their management are reviewed here. The pathogenesis, risk assessment, and preventive strategies are discussed elsewhere. (See "Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury" and "Prevention of pressure-induced skin and soft tissue injury".)

DEFINITIONS AND TERMINOLOGY — Pressure-induced skin and soft tissue injuries are areas 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, even if located over a bony prominence, should not be labeled as pressure injuries, and neither should skin tears, tape burns, perineal dermatitis, or excoriation.

Changes were made to the National Pressure Injury Advisory Panel (NPIAP) system favoring the use of the term "pressure injury" instead of "pressure ulcer" to recognize the fact that lesser degrees of skin damage due to pressure may not be associated with skin ulceration (stage 1) and that deep tissue pressure injury can occur without overlying skin ulceration (table 1). (See 'NPIAP staging' below.)

However, the generalized term "pressure injury" does not address the many other types of injury that can result from pressure, such as rhabdomyolysis in an unconscious patient. Thus, we will use the following terminology:

"Pressure-induced skin and soft tissue injury" is used to encompass the broad range of ischemic damage that can be caused by prolonged pressure.

The terms "pressure-induced skin injury" or "pressure-induced soft tissue (or deep tissue) injury" are used where specifically applicable.

We use the terms "pressure injury" or "pressure-induced injury" when referring to the staging of a specific lesion as defined by the NPIAP classification (eg, unstageable pressure injury), to replace the term "pressure ulcer" in studies published prior to this classification change or that use "pressure ulcer" generically when the stage is not specified.

CLINICAL EVALUATION — The management of pressure-induced skin and soft tissue injuries begins with clinical assessment of the wound and a comprehensive assessment of the patient's general medical condition and risk factors to identify reversible conditions. Risk factors that promote pressure-induced skin and soft tissue injuries are reviewed separately. (See "Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury", section on 'Risk factors'.)

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 lesion can be staged. (See 'NPIAP staging' below.)

Pain is frequently associated with pressure-induced skin and soft tissue injuries, and pain may be an early manifestation of a developing wound. A comprehensive pain assessment should be performed in all individuals with pressure-induced skin and soft tissue injuries.

Infections impair wound healing. The possibility of infection should be considered even if systemic signs, such as fever and leukocytosis, are absent [2]. Infection of pressure injuries 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 can be variable, with delayed wound healing as the only sign of infection. (See 'Treat infection' below.)

Pressure-induced skin and soft tissue injuries 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 [3,4]. Precautions should be used when examining and treating ulcers. (See "Infection prevention: Precautions for preventing transmission of infection", section on 'Standard precautions'.)

Other complications may include:

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

Occasional heterotropic calcification.

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

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

Differential diagnosis — It is important to distinguish ulcers that are due to pressure from ulcers related to diabetes, arterial insufficiency, or venous insufficiency [5]. However, these also predispose to the development of pressure-induced injury, and many wounds, particularly in the lower extremity, have a multifactorial etiology. (See "Clinical assessment of chronic wounds", section on 'Differentiation of chronic ulcers'.)

Pressure-related skin and soft tissue injury may also be confused with other conditions that cause skin erythema, such as cellulitis. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Cellulitis and erysipelas' and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)

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 Injury Advisory Panel (NPIAP) (table 1 and figure 2) [6]. NPIAP 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. Our usage of these terms is described above. (See 'Definitions and terminology' above.)

NPIAP staging — The NPIAP staging system is described below (table 1 and figure 2) [6]. The NPIAP stage is used to describe the initial appearance of an area of skin damage. An unintended consequence of numerical staging is misinterpretation that a 'stage' implies progression or regression (forward or backward). The NPUAP staging does not imply a step-wise sequence (either direction). In addition, the practice of changing the stage as healing occurs, known as reverse staging, is not recommended [9].

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 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 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.

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 obscures the extent of tissue loss, this is an unstageable pressure injury.

Unstageable pressure injury is characterized by 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 the heel or ischemic limb should not be softened or removed. (See 'General wound management' below and "Local care of pressure-induced skin and soft tissue injury", section on 'Specific wound management'.)

Deep tissue pressure injury is characterized as intact or non-intact skin with a localized area of persistent non-blanchable deep red, maroon, 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 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.

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. 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). The depth of a stage 4 pressure injury 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. 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. Stage 4 ulcers that extend into supporting structures, including fascia, tendon, or joint capsule, may be associated with osteomyelitis. 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.

GENERAL CARE — The general approach to management of a patient with a pressure-induced skin and soft tissue injury should include the following [10]:

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. Patients with pressure-induced skin and soft tissue injuries do suffer from 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 reduced health-related quality of life [11].

Control pain — Adequate pain relief should be provided, as pressure-induced injuries can be quite painful [12]. Local factors that may be contributing to pain such as ischemia, infection, or breakdown of the surrounding skin should be addressed.

Initial and ongoing 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.

Oral nonopioid pain medications can be used for mild pain. Opioid analgesics may be needed for moderate-to-severe pain. (See "Pharmacologic management of chronic non-cancer pain in adults".)

Topical local anesthetics (eg, lidocaine) have been used and can provide pain relief for a short period of time, but there is little evidence of effectiveness from clinical trials. Topical opioids, such as a morphine gel, have shown some benefit in small trials [13-15]. Ibuprofen-releasing foam dressings can be used, if available [16]. However, many patients with deep ulcers will require systemic therapy for 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 open ulcers are colonized with bacteria, but only clinically evident infections should be addressed with culture and antibiotic treatment [17,18]. The presence of bacterial biofilm (thin layer of microorganisms adhering to the surface of a structure) may impair wound healing. Patients with deep wounds should be evaluated for the presence of osteomyelitis. Treatment of infectious complications is discussed separately. (See "Infectious complications of pressure-induced skin and soft tissue injury".)

Optimize nutrition — Patients with pressure-induced skin and soft tissue injuries often are in a chronic catabolic state. Optimizing both protein and total caloric intake is important, particularly for patients with stage 3 and 4 pressure injuries (table 1 and figure 2) [1].

Nutritional intake should be assessed by a nutritionist. Elements of this comprehensive assessment may include protein and caloric intake, hydration status, serum albumin and/or prealbumin, and total lymphocyte count [19]. Lab markers by themselves are not a sufficient marker of nutritional status. Nutritional deficiencies should be corrected. (See "Clinical assessment and monitoring of nutrition support in adult surgical patients".)

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 [20-24]. A retrospective cohort study of 882 patients with pressure injuries 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 wounds [25]. Increased dietary protein intake also promotes healing [26,27]. The protein target is usually 1.25 to 1.5 g/kg/day, although some authors advocate higher protein intake [18]. (See "Nutritional demands and enteral formulas for adult surgical patients" and "Postoperative parenteral nutrition in adults".)

Data do not support nutritional supplementation for patients who do not have nutritional deficiencies [28]. Vitamin C and zinc supplementation are commonly used to promote healing, but their efficacy has not been conclusively demonstrated [22]. 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 [10,22]. A later, larger trial randomly assigned 200 malnourished adult patients with pressure injuries 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 [29]. This study found a greater reduction in area of pressure injury 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-induced injury. Because previous studies of the individual nutrients failed to show benefit, the authors postulated a synergistic effect among the nutrients.

Redistribute pressure — Proper positioning and support to minimize tissue pressure should be provided for all patients, particularly those with open wounds. 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-induced injury is reviewed separately. (See "Prevention of pressure-induced skin and soft tissue injury".)

To date, there are no randomized trials available to identify whether repositioning makes a difference in the healing rates or the optimal repositioning regimen [30,31]. 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 Injury Advisory Panel Support Surface Standards Initiative, are described separately [32]. (See "Prevention of pressure-induced skin and soft tissue injury", section on 'Support surfaces'.)

The effectiveness of support surfaces in promoting healing has been studied in a number of randomized clinical trials with inconsistent results [10]:

A randomized trial of 158 hospitalized patients found no difference in wound healing between 85 patients on nonpowered fluid mattress and 83 on powered alternating pressure support devices [33].

In a study of 65 hospitalized patients with pressure-induced injury, 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 [26]. The latter group also used elbow or heel pads as needed. The total surface area of pressure-induced injury was decreased on the air-fluidized beds (-1.2 versus +0.5 cm2), while increasing in size with conventional therapy. 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 [34].

Given limited data, it is uncertain if powered mattresses are superior to nonpowered mattresses [10]. The costs associated with powered beds become particularly significant when considering that treatment for at least two months is typically required [35]. 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-induced skin and soft tissue injury", section on 'Pathogenesis' and "Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury", section on 'Risk factors'.)

Prevent contamination — Contamination of wounds from urinary or fecal soiling may impair wound healing. Urinary catheters or rectal tubes are often used to help promote healing, but there is little evidence for benefit. (See "Placement and management of urinary bladder catheters in adults", section on 'Indications for catheterization' and "Complications of urinary bladder catheters and preventive strategies".)

Colostomy, which diverts the stool, is another option if the site is prone to fecal contamination. Surgical colostomy may be considered; however, this procedure may be associated with a high complication rate in frail older adult patients and is of questionable efficacy [36,37]. Mortality following surgical colostomy may be especially high in people with hypoalbuminemia [38]. (See "Overview of surgical ostomy for fecal diversion".)

GENERAL 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. (See "Local care of pressure-induced skin and soft tissue injury".)

Specific treatment is guided by the stage of skin injury (table 1 and figure 2). The development of pressure injury should be taken as an indication that the patient is at high risk for other pressure-induced injury, and intensive preventive measures should be taken. (See "Prevention of pressure-induced skin and soft tissue injury".)

The National Pressure Injury Advisory Panel (NPIAP) staging is presented above. Specific regimens for local care of pressure-induced skin and soft tissue injury are summarized briefly below. (See 'Staging' above and "Local care of pressure-induced skin and soft tissue injury", section on 'Local care by stage'.)

Stage 1 skin injuries should be covered for protection.

Stage 2 pressure injuries generally need little debridement and require a dressing that maintains a moist wound environment [39].

Stage 3 and 4 pressure or deeper injuries generally require debridement of necrotic tissue and possibly treatment of infection. Following appropriate wound bed preparation, coverage may involve skin grafting or other tissue transfer procedures. (See "Surgical management of pressure-induced skin and soft tissue injuries".)

Uncertain benefit for adjunctive therapies — A variety of adjunctive therapies such as electrical stimulation, therapeutic ultrasound, hyperbaric oxygen, and topical oxygen have been investigated for the treatment of pressure-induced skin and soft tissue injuries, but the indications for their use remain uncertain. Some of these adjunctive therapies are discussed below.

Hyperbaric oxygen therapy (HBOT) has been advocated, but there have been no studies specifically looking at the treatment of pressure injuries 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. There is some evidence to support the use of hyperbaric oxygen therapy in chronic refractory osteomyelitis [40], which can be considered for patients with nonhealing ulcers who are not candidates for operative intervention [41]. The underlying study quality was poor; some serious adverse events were associated with HBOT, including seizures and pneumothorax [42,43]. (See "Basic principles of wound management", section on 'Hyperbaric oxygen therapy'.)

Ultrasound is sometimes used as a wound therapy. A systematic review of three trials found that methodologic limitations and small trial size made it impossible to rule out benefit or harm with ultrasound therapy [44]. However, two later studies using high frequency ultrasound (1 MHz), which penetrates to greater tissue depths, demonstrated greater reductions in wound surface area as compared with controls [45,46]. [45,47]

Electrical stimulation, in which a direct current is applied to the wound, has also resulted in enhanced healing in several small studies [48-51] and a meta-analysis [52]. Electrical stimulation has been shown to improve rates of wound healing in wounds demonstrating sufficient granulation tissue [50]. Electrical stimulation is applied to the periwound tissues. The duration and voltage have not been clearly defined. The electric current is provided once or 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 [53]. Similarly, pulsed radiofrequency energy therapy and electromagnetic therapy have been proposed, but evidence of benefit is limited [53,54].

MONITORING — Appropriate therapeutic goals should be set that consider discharge potential, quality of life, treatment preferences, and prognosis [18,55].

With appropriate care, most pressure-induced skin and soft tissue injuries should heal within an expected timeframe. Two studies from nursing home facilities that collectively followed over 1000 patients found that more than 70 percent of patients with stage 2 pressure injuries, 50 percent with stage 3 pressure injuries, and 30 percent with stage 4 pressure injuries were ulcer free at six months with standard wound care [56,57]. Among those followed over two years, 77 percent of stage 4 pressure injuries had healed.

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

The following parameters of care should be monitored daily and documented [5]:

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 NPIAP stage as the wound heals, is not recommended [9].

A number of scales are available for use in monitoring and documentation of the wound healing [5,58-61], including the Pressure Sore Status Tool (PSST) (table 2), the Sessing Scale, the Wound Healing Scale, and the Pressure Ulcer Scale for Healing (PUSH) tool (table 3) [58-61]. The PUSH tool, designed to be used in conjunction with the NPIAP Staging System (table 1 and figure 2), is the most readily applied tool [62]. This scale has been validated, is easy to use, and has been shown to be helpful.

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

MORBIDITY AND MORTALITY — Patients who develop pressure-induced skin and soft tissue injuries are approximately two to three times more likely to die compared with patients without this problem [63-65]. However, affected patients tend to have many other comorbid conditions; after adjusting for these other factors, the presence of pressure-induced injury is at best a weak predictor of mortality.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic wound management" and "Society guideline links: Pressure-induced skin and soft tissue injury".)

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)")

SUMMARY AND RECOMMENDATIONS

Patient assessment – The treatment of pressure-induced skin and soft tissue 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 evaluation' above.)

Documentation – 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.)

General care

Controlling pain – Adequate pain control should be provided. Particular attention should be paid to pain management during wound dressing and debridement. (See 'Control pain' above.)

Assessing and improving nutrition – Nutritional status should be assessed, 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.)

Repositioning – 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-induced skin and soft tissue injuries (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.)

Monitoring – Close daily monitoring of the pressure injury, 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.)

Wound management – Specific wound management is guided by the stage of skin injury with increasing needs for debridement, wound dressings, and coverage for higher stage wounds. Dressings are selected based on wound characteristics, including the presence of heavy exudate, desiccation, or necrotic tissue. Surgical debridement and flap coverage may be needed for some full-thickness wounds. (See 'General wound management' above and "Local care of pressure-induced skin and soft tissue injury", section on 'Specific wound management'.)

  1. Bauer J, Phillips LG. MOC-PSSM CME article: Pressure sores. Plast Reconstr Surg 2008; 121:1.
  2. Livesley NJ, Chow AW. Infected pressure ulcers in elderly individuals. Clin Infect Dis 2002; 35:1390.
  3. 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.
  4. 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.
  5. Thomas DR. The new F-tag 314: prevention and management of pressure ulcers. J Am Med Dir Assoc 2006; 7:523.
  6. https://cdn.ymaws.com/npuap.site-ym.com/resource/resmgr/npuap_pressure_injury_stages.pdf (Accessed on August 19, 2019).
  7. Shea JD. Pressure sores: classification and management. Clin Orthop Relat Res 1975; :89.
  8. Kottner J, Cuddigan J, Carville K, et al. Pressure ulcer/injury classification today: An international perspective. J Tissue Viability 2020; 29:197.
  9. National Pressure Ulcer Advisory Panel. NPUAP position on reverse staging of pressure ulcers. Adv Wound Care 1998; 8:32.
  10. Reddy M, Gill SS, Kalkar SR, et al. Treatment of pressure ulcers: a systematic review. JAMA 2008; 300:2647.
  11. 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.
  12. 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).
  13. Flock P. Pilot study to determine the effectiveness of diamorphine gel to control pressure ulcer pain. J Pain Symptom Manage 2003; 25:547.
  14. Zeppetella G, Paul J, Ribeiro MD. Analgesic efficacy of morphine applied topically to painful ulcers. J Pain Symptom Manage 2003; 25:555.
  15. Zeppetella G, Ribeiro MD. Morphine in intrasite gel applied topically to painful ulcers. J Pain Symptom Manage 2005; 29:118.
  16. 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.
  17. Grey JE, Harding KG, Enoch S. Pressure ulcers. BMJ 2006; 332:472.
  18. 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.
  19. Stechmiller JK, Cowan L, Whitney JD, et al. Guidelines for the prevention of pressure ulcers. Wound Repair Regen 2008; 16:151.
  20. 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.
  21. 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.
  22. Langer G, Fink A. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database Syst Rev 2014; :CD003216.
  23. Smith ME, Totten A, Hickam DH, et al. Pressure ulcer treatment strategies: a systematic comparative effectiveness review. Ann Intern Med 2013; 159:39.
  24. Teno JM, Gozalo P, Mitchell SL, et al. Feeding tubes and the prevention or healing of pressure ulcers. Arch Intern Med 2012; 172:697.
  25. 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.
  26. 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.
  27. Breslow RA, Hallfrisch J, Guy DG, et al. The importance of dietary protein in healing pressure ulcers. J Am Geriatr Soc 1993; 41:357.
  28. Lyder CH. Pressure ulcer prevention and management. JAMA 2003; 289:223.
  29. 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.
  30. Moore ZE, Cowman S. Repositioning for treating pressure ulcers. Cochrane Database Syst Rev 2012; :CD006898.
  31. 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.
  32. 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).
  33. 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.
  34. Ferrell BA, Osterweil D, Christenson P. A randomized trial of low-air-loss beds for treatment of pressure ulcers. JAMA 1993; 269:494.
  35. Bennett RG, Bellantoni MF, Ouslander JG. Air-fluidized bed treatment of nursing home patients with pressure sores. J Am Geriatr Soc 1989; 37:235.
  36. Pussin AM, Lichtenthäler LC, Aach M, et al. Fecal diversion does not support healing of anus-near pressure ulcers in patients with spinal cord injury-results of a retrospective cohort study. Spinal Cord 2022; 60:477.
  37. Deshmukh GR, Barkel DC, Sevo D, Hergenroeder P. Use or misuse of colostomy to heal pressure ulcers. Dis Colon Rectum 1996; 39:737.
  38. Rubio GA, Shogan BD, Umanskiy K, et al. Simple Diverting Colostomy for Sacral Pressure Ulcers: Not So Simple After All. J Gastrointest Surg 2023; 27:382.
  39. 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.
  40. Savvidou OD, Kaspiris A, Bolia IK, et al. Effectiveness of Hyperbaric Oxygen Therapy for the Management of Chronic Osteomyelitis: A Systematic Review of the Literature. Orthopedics 2018; 41:193.
  41. Kranke P, Bennett MH, Martyn-St James M, et al. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev 2015; 2015:Cd004123.
  42. Wang C, Schwaitzberg S, Berliner E, et al. Hyperbaric oxygen for treating wounds: a systematic review of the literature. Arch Surg 2003; 138:272.
  43. Kranke P, Bennett MH, Martyn-St James M, et al. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev 2012; :CD004123.
  44. Baba-Akbari Sari A, Flemming K, Cullum NA, Wollina U. Therapeutic ultrasound for pressure ulcers. Cochrane Database Syst Rev 2006; :CD001275.
  45. Polak A, Taradaj J, Nawrat-Szoltysik A, et al. Reduction of pressure ulcer size with high-voltage pulsed current and high-frequency ultrasound: a randomised trial. J Wound Care 2016; 25:742.
  46. Polak A, Franek A, Blaszczak E, et al. A prospective, randomized, controlled, clinical study to evaluate the efficacy of high-frequency ultrasound in the treatment of Stage II and Stage III pressure ulcers in geriatric patients. Ostomy Wound Manage 2014; 60:16.
  47. Polak A, Franek A, Blaszczak E, et al. A prospective, randomized, controlled, clinical study to evaluate the efficacy of high-frequency ultrasound in the treatment of Stage II and Stage III pressure ulcers in geriatric patients. Ostomy Wound Manage. 2014;60(8):16-28.
  48. 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.
  49. Feedar JA, Kloth LC, Gentzkow GD. Chronic dermal ulcer healing enhanced with monophasic pulsed electrical stimulation. Phys Ther 1991; 71:639.
  50. Polak A, Kloth LC, Blaszczak E, et al. The Efficacy of Pressure Ulcer Treatment With Cathodal and Cathodal-Anodal High-Voltage Monophasic Pulsed Current: A Prospective, Randomized, Controlled Clinical Trial. Phys Ther 2017; 97:777.
  51. Polak A, Kloth LC, Blaszczak E, et al. Evaluation of the Healing Progress of Pressure Ulcers Treated with Cathodal High-Voltage Monophasic Pulsed Current: Results of a Prospective, Double-blind, Randomized Clinical Trial. Adv Skin Wound Care 2016; 29:447.
  52. Gardner SE, Frantz RA, Schmidt FL. Effect of electrical stimulation on chronic wound healing: a meta-analysis. Wound Repair Regen 1999; 7:495.
  53. Flemming K, Cullum N. Electromagnetic therapy for the treatment of pressure sores. Cochrane Database Syst Rev 2001; :CD002930.
  54. 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.
  55. 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.
  56. 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.
  57. 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.
  58. Bates-Jensen BM. The Pressure Sore Status Tool a few thousand assessments later. Adv Wound Care 1997; 10:65.
  59. 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.
  60. Ferrell BA. The Sessing Scale for measurement of pressure ulcer healing. Adv Wound Care 1997; 10:78.
  61. Krasner D. Wound Healing Scale, version 1.0: a proposal. Adv Wound Care 1997; 10:82.
  62. www.npuap.org (Accessed on April 08, 2013).
  63. Thomas DR, Goode PS, Tarquine PH, Allman RM. Hospital-acquired pressure ulcers and risk of death. J Am Geriatr Soc 1996; 44:1435.
  64. Berlowitz DR, Wilking SV. The short-term outcome of pressure sores. J Am Geriatr Soc 1990; 38:748.
  65. 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.
Topic 2887 Version 42.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟