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Pressure Ulcers

(Bedsores; Pressure Injuries; Decubitus Ulcers; Decubiti; Pressure Sores)

By

Ayman Grada

, MD, MS, Department of Dermatology, Boston University School of Medicine;


Tania J. Phillips

, MD, Boston University School of Medicine

Last full review/revision Sep 2019| Content last modified Sep 2019
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Topic Resources

Pressure ulcers are areas of necrosis and ulceration where soft tissues are compressed between bony prominences and external hard surfaces. They are caused by unrelieved mechanical pressure in combination with friction, shearing forces, and moisture. Risk factors include age > 65, impaired circulation and tissue perfusion, immobilization, undernutrition, decreased sensation, and incontinence. Severity ranges from nonblanchable skin erythema to full-thickness skin loss with extensive soft-tissue necrosis. Diagnosis is clinical. Prognosis is excellent for early-stage ulcers; neglected and late-stage ulcers pose risk of serious infection and are difficult to heal. Treatment includes pressure reduction, avoidance of friction and shearing forces, and diligent wound care. Sometimes, skin grafts or myocutaneous flaps are needed to facilitate healing.

Between 1993 and 2006, the number of hospitalized patients with pressure ulcers increased by > 75%, a rate over 5 times the increase of hospital admissions overall. The rate increased most in patients who developed pressure ulcers during hospitalization. An estimated 2.5 million cases of pressure ulcers are treated each year in acute care settings in the US, resulting in a significant financial burden to patients and health care institutions.

Pressure injury is terminology recommended by the National Pressure Ulcer Advisory Panel (NPUAP) instead of pressure ulcer to describe these chronic wounds because lesser degrees of skin damage due to pressure may not be associated with skin ulceration.

Etiology

Risk factors for pressure ulcers include the following:

Several scales (see table The Norton Scale for Predicting Pressure Ulcer Risk and the Braden Scale) have been developed to predict risk. Although use of these scales is considered standard care, they have not been shown to result in fewer pressure ulcers than skilled clinical assessment alone. Nevertheless, use of a risk assessment scale along with skilled clinical assessment is recommended.

Table
icon

The Norton Scale for Predicting Pressure Ulcer Risk*

Criterion

Score

Physical condition

4 = Good

3 = Fair

2 = Poor

1 = Very bad

Mental condition

4 = Alert

3 = Apathetic

2 = Confused

1 = Stupor

Activity

4 = Ambulant

3 = Walk with help

2 = Chair bound

1 = Bed bound

Mobility

4 = Full

3 = Slightly impaired

2 = Very limited

1 = Immobile

Incontinent

4 = Not

3 = Occasionally

2 = Usually/Urine

1 = Doubly

* Calculated as the sum of the scores in all 5 areas. A score < 14 indicates a high risk of pressure ulcer development.

Adapted from Norton, D: Calculating the risk: Reflections on the Norton scale. Decubitus 2(3):24–31, 1989.

Pathophysiology

The main factors contributing to pressure injuries are

  • Pressure: When soft tissues are compressed for prolonged periods between bony prominences and external surfaces, microvascular occlusion with tissue ischemia and hypoxia occurs. Pressures exceeding normal capillary pressure (range is 12 to 32 mm Hg) result in reduced oxygenation and compromise the microcirculation of the affected tissue. If compression is not relieved, a pressure ulcer can develop in 3 to 4 hours. This most commonly occurs over the sacrum, ischial tuberosities, trochanters, malleoli, and heels, but pressure ulcers can develop anywhere.

  • Friction: Friction (rubbing against clothing or bedding) can help trigger skin ulceration by causing local erosion and breaks in the epidermis and superficial dermis.

  • Shearing forces: Shearing forces (eg, when a patient is placed on an inclined surface) stress and damage supporting tissues by causing forces of muscles and subcutaneous tissues that are drawn down by gravity to oppose the more superficial tissues that remain in contact with external surfaces. Shearing forces contribute to pressure injury but are not direct causes.

  • Moisture: Moisture (eg, perspiration, incontinence) leads to tissue breakdown and maceration, which can initiate or worsen pressure ulcers.

Because muscle is more susceptible to ischemia with compression than skin, muscle ischemia and necrosis may underlie pressure injuries resulting from prolonged compression.

Symptoms and Signs

Pressure injuries at any stage may be painful or pruritic but may not be noticed by patients with blunted awareness or sensation.

Staging systems

Several staging systems exist. The most widely used system is from the National Pressure Ulcer Advisory Panel (NPUAP), which classifies pressure injuries into four stages (1 to 4) according to the extent of soft-tissue damage. However, the numerical staging does not imply linear progression of pressure injuries. That is, pressure injuries do not always manifest as stage 1 and then progress to higher stages. Sometimes, the first sign is a deep, necrotic stage 3 or 4 ulcer. In a rapidly developing pressure ulcer, subcutaneous tissue can become necrotic before the epidermis erodes. Thus, a small ulcer may in fact represent extensive subcutaneous necrosis and damage. Similarly, the scale does not imply that healing progresses from stage 4 through stage 1. The updated NPUAP staging system also includes definitions for unstageable, deep-tissue, medical device-related, and mucosal membrane pressure injuries (1).

Stage 1 pressure injuries manifest as intact skin with nonblanchable erythema, usually over a bony prominence. Color changes may not be as visible in darkly pigmented skin. The lesion may also be warmer, cooler, firmer, softer, or more tender than adjacent or contralateral tissue. An actual ulcer (a defect of skin into the dermis) is not yet present. However, ulceration will occur if the course is not arrested and reversed.

Stage 2 pressure ulcers are characterized by partial-thickness skin, with loss of epidermis (erosion or blister) with or without true ulceration (defect beyond the level of the epidermis); subcutaneous tissue is not exposed. The ulcer is shallow with a pink to red base. No slough or necrotic tissue is present in the base. Stage 2 also includes intact or partially ruptured blisters secondary to pressure. (NOTE: Non–pressure-related causes of erosion, ulceration, or blistering, such as skin tears, tape burns, maceration, and excoriation, are excluded from stage 2.)

Stage 3 pressure ulcers manifest as full-thickness skin loss with damage to subcutaneous tissue extending down to (but not including) the underlying fascia. The ulcers are crater-like without underlying muscle or bone exposure.

Stage 4 pressure ulcers manifest as full-thickness skin loss with extensive destruction, tissue necrosis, and damage to the underlying muscle, tendon, bone, or other exposed supporting structures.

When estimating the depth of pressure injuries for purposes of staging, it is important to take into account the anatomical location, especially in the case of stage 3 ulcers. For example, the bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue and, consequently, pressure ulcers in those locations will be very shallow. However, they are still graded as stage 3 because they are as significant as deeper stage 3 ulcers over locations with significant subcutaneous tissue (eg, the sacral region).

Unstageable pressure ulcers are characterized by full-thickness skin and tissue loss in which the extent of tissue damage cannot be determined because it is obscured by debris, slough, or eschar. If the slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed. However, stable, nonfluctuant lesions with dry eschar should never be debrided for the sake of staging.

Deep-tissue pressure injury is characterized by intact or nonintact skin with a localized area of damage to underlying tissue due to pressure and/or shearing forces. Findings include persistent, nonblanchable, purple to maroon discoloration of intact skin, and blood-filled vesicles or bullae. The area may feel firmer, boggier, warmer, or cooler compared with surrounding tissue. In this context, the term deep-tissue pressure injury should not be used to describe underlying vascular, traumatic, neuropathic, or dermatologic conditions.

Medical device-related pressure injury results from the use of devices designed and applied for therapeutic purposes (eg, casts, splints). Injury typically conforms to the pattern or shape of the device. The injury should be staged using the staging system.

Mucosal membrane pressure injury appears on mucous membranes where medical devices have been in use (eg, misfitting dentures, endotracheal tubes). Because of the anatomy of the tissue, these injuries cannot be staged.

Manifestations of Pressure Injury and Ulcer Stages 1 to 4

Pearls & Pitfalls

  • Suspect deeper tissue damage than is clinically evident in patients who have pressure ulcers.

Staging definition reference

  • 1. Editors of Nursing2017: Pressure ulcers get new terminology and staging definitions. Nursing 47(3):68–69, 2017. doi: 10.1097/01.NURSE.0000512498.50808.2b.

Complications

Pressure ulcers are a reservoir for hospital-acquired antibiotic-resistant organisms. High bacteria counts within the wound can hinder tissue healing. If wound healing is delayed despite proper treatment, underlying osteomyelitis (present in up to 32% of patients) or rarely squamous cell carcinoma within the ulcer (Marjolin ulcer) should be considered.

Other local complications of nonhealing pressure ulcers include sinus tracts, which can be superficial or connect the ulcer to deep adjacent structures (eg, sinus tracts from a sacral ulcer to the bowel), cellulitis, and tissue calcification. Systemic or metastatic infectious complications can include bacteremia, meningitis, and endocarditis.

Diagnosis

  • Clinical evaluation

  • Nutritional assessment

Diagnosis of pressure injury is based on clinical evaluation. A pressure injury is typically identified by its characteristic appearance and by its location over a bony prominence. The sacrum is the most common location, followed by the heels. Ulcers caused by arterial and venous insufficiency or diabetic neuropathy may mimic pressure ulcers, particularly on the lower extremities, and can also be worsened by the same forces that cause or worsen pressure ulcers.

Depth and extent of pressure ulcers can be difficult to determine. Serial staging and photography of wounds is essential for monitoring ulcer progression or healing. Many healing scales are available. The Pressure Ulcer Scale for Healing (PUSH), designed as a companion to the NPUAP staging scale, has been adopted by many institutions.

Routine wound culture is not recommended because all pressure ulcers are heavily colonized by bacteria.

A nutritional assessment is recommended in patients with pressure injury, particularly those with stage 3 or 4 pressure ulcers. Recommended tests include hematocrit, transferrin, prealbumin, albumin, and total and CD4+ lymphocyte counts. Undernutrition requires further evaluation and treatment.

Nonhealing ulcers may be due to inadequate treatment but should raise suspicion of a complication. Tenderness, erythema of surrounding skin, exudate, or foul odor suggests an underlying infection. Fever and leukocytosis should raise suspicion of cellulitis, bacteremia, or underlying osteomyelitis. If osteomyelitis is suspected, CBC, blood cultures, and ESR or C-reactive protein is recommended. Osteomyelitis is confirmed ideally by bone biopsy and culture, but this is not always feasible. Imaging tests lack the combination of high sensitivity and specificity. MRI is sensitive but not specific and can help define the extent of pressure ulcer spread. MRI with gadolinium can help identify draining or communicating sinus tracts.

Prognosis

Prognosis for early-stage pressure injuries is excellent with timely, appropriate treatment, but healing typically requires weeks. After 6 months of treatment, > 70% of stage 2 pressure ulcers, 50% of stage 3 ulcers, and 30% of stage 4 ulcers resolve. Pressure ulcers often develop in patients who are receiving suboptimal care and/or have significant disorders that impair wound healing (eg, diabetes, undernutrition, peripheral arterial disease). If care of the ulcer and management of concurrent disorders cannot be improved, long-term outcome is poor, even if short-term wound healing is accomplished.

Treatment

  • Pressure reduction

  • Direct wound care

  • Management of pain

  • Control of infection

  • Assessment of nutritional needs

  • Adjunctive therapy or surgery

(See also the American College of Physicians' guidelines for preventing and treating pressure ulcers.)

Pressure reduction

Reducing tissue pressure is accomplished through careful positioning of the patient, protective devices, and use of support surfaces.

Frequent repositioning (and selection of the proper position) is most important. A written schedule should be used to direct and document repositioning. Patients confined to a bed should be turned a minimum of every 2 hours and should be placed at a 30° angle to the mattress when on their side (lateral decubitus) to avoid direct trochanteric pressure. Elevation of the head of the bed should be minimal to avoid the effects of shearing forces. When repositioning patients, lifting devices (eg, a Stryker frame) or bed linen should be used instead of dragging patients to avoid unnecessary friction. Patients placed in chairs should be repositioned every hour and encouraged to change position on their own every 15 minutes.

Protective padding such as pillows, foam wedges, and heel protectors can be placed between the knees, ankles, and heels when patients are supine or on their side. Windows should be cut out of plaster casts at pressure sites in patients immobilized by fractures. Soft seat cushions should be provided for patients able to sit in a chair.

Support surfaces under patients confined to a bed can be changed to reduce pressure. They are often combined with other measures when treating pressure injuries.

Support surfaces are classified based on whether they require electricity to operate. Static surfaces do not require electricity, whereas dynamic surfaces do. Although dynamic surfaces are usually recommended for more severe pressure injuries, no conclusive evidence favors dynamic over static surfaces.

Static surfaces include air, foam, gel, and water overlays and mattresses. Egg-crate mattresses offer no advantage. In general, static surfaces increase surface support area and decrease pressure and shearing forces. Static surfaces have traditionally been used for pressure injury prevention or stage 1 pressure injuries.

Dynamic surfaces include alternating-air mattresses, low-air-loss mattresses, and air-fluidized mattresses. Alternating-air mattresses have air cells that are alternately inflated and deflated by a pump, thus shifting supportive pressure from site to site. Low-air-loss mattresses are giant air-permeable pillows that are continuously inflated with air; the air flow has a drying effect on tissues. These specialized mattresses are indicated for patients with stage 1 pressure injuries who develop hyperemia on static surfaces and for patients with stage 3 or 4 pressure ulcers. Air-fluidized (high-air-loss) mattresses contain silicone-coated beads that liquefy when air is pumped through the bed. Advantages include reduction of moisture and cooling. These mattresses are indicated for patients with nonhealing stages 3 and 4 pressure ulcers or numerous truncal ulcers (see Table: Options for Support Surfaces).

Table
icon

Options for Support Surfaces

Static

Dynamic

Standard Hospital Mattress

Foam

Static Flotation (Air or Water)

Alternating Air

Low Air Loss

Air Fluidized (High Air Loss)

Support area increase

No

Yes

Yes

Yes

Yes

Yes

Pressure reduction

No

Yes

Yes

Yes

Yes

Yes

Shear reduction

No

No

Yes

Yes

Unknown

Yes

Heat reduction

No

No

No

No

Yes

Yes

Low moisture retention

No

No

No

No

Yes

Yes

Cost

Low

Low

Low

Moderate

High

High

Adapted from Bergstrom N et al: US Agency for Health Care Policy and Research. Pressure Ulcer Treatment (Quick Reference Guideline Number 15). AHCPR Publication No. 95-0653, December 1994.

Direct wound care

Appropriate wound care involves cleaning, debridement, and dressings.

Cleaning should be done initially and with each dressing change. Normal saline is usually the best choice. Cleaning often involves irrigation at pressures sufficient to remove bacteria without traumatizing tissue; commercial syringes, squeeze bottles, or electrically pressurized systems can be used. Irrigation may also help remove necrotic tissue (debridement). Alternatively, a 35-mL syringe and an 18-gauge IV catheter can be used. Irrigation should continue until no further debris can be loosened. Antiseptics (iodine, hydrogen peroxide) and antiseptic washes can destroy healthy granulation tissue and thus should be avoided.

Debridement is necessary to remove necrotic tissue. Necrotic tissue serves as a medium for bacterial growth and blocks normal wound healing. Methods include

  • Mechanical debridement: This method includes hydrotherapy (whirlpool baths) and most commonly wet-to-dry dressings. Cleaning wounds by irrigation at sufficient pressures can also accomplish mechanical debridement. Mechanical debridement removes necrotic debris on the wound’s surface and should only be done on wounds with very loose exudate. In wet-to-dry dressings, exudate and necrotic tissue adhere to a gauze dressing as it dries so that removal of the gauze thus debrides the wound; this method must be used cautiously because dressing changes are painful and may remove underlying healthy granulation tissue.

  • Sharp (surgical) debridement: This method involves using a sterile scalpel or scissors to remove eschar and thick necrosis. Modest amounts of eschar or tissue can be debrided at the patient’s bedside, but extensive or deep areas (eg, if underlying bone, tendon, or joints are exposed) should be debrided in the operating room. Sharp debridement should be done urgently for advancing cellulitis or lesions suspected of causing sepsis.

  • Autolytic debridement: Synthetic occlusive (hydrocolloids/hydrogels) dressings or semi-occlusive (transparent film) dressings are used to facilitate the digestion of dead tissues by the enzymes already normally present in the wound. Autolytic debridement may be used for smaller wounds with little exudate. This method should not be used if a wound infection is suspected.

  • Enzymatic debridement: This technique (using collagenase, papain, fibrinolysin, deoxyribonuclease, or streptokinase/streptodornase) can be used for patients with mild fibrotic or necrotic tissue within the ulcer. It can also be used for patients whose caretakers are not trained to do mechanical debridement or for patients unable to tolerate surgery. It is most effective after careful and judicious cross-hatching of the wound with a scalpel to improve penetration.

  • Biosurgery: Medical maggot therapy is useful for selectively removing dead necrotic tissue; maggots (fly larvae) eat only dead tissue. This method is most helpful in patients who have exposed bone, tendons, and joints in the wound where sharp debridement is contraindicated.

Dressings are helpful for protecting the wound and facilitating the healing process (see Table: Options for Pressure Ulcer Dressings).

Dressings should be used for stage 1 pressure injuries that are subject to friction or incontinence and for all other pressure injuries (see Table: Options for Pressure Ulcer Dressings).

In stage 1 pressure injuries subject to increased friction, transparent films are sufficient. For injuries with minimal exudate, transparent films or hydrogels, which are cross-linked polymer dressings that come in sheets or gels, are used to protect the wound from infection and create a moist environment. Transparent films or hydrogels should be changed every 3 to 7 days.

Hydrocolloids, which combine gelatin, pectin, and carboxymethylcellulose in the form of wafers and powders, are indicated for pressure ulcers with light-to-moderate exudate and must be changed every 3 days.

Alginates (polysaccharide seaweed derivatives containing alginic acid), which come as pads, ropes, and ribbons, are indicated for absorbing extensive exudate and for controlling bleeding after surgical debridement. Alginates can be placed for up to 7 days but must be changed earlier if they become saturated.

Foam dressings can be used in wounds with various levels of exudate and provide a moist environment for wound healing. Foam dressings must be changed every 3 to 4 days. Waterproof versions protect the skin from incontinence.

Table
icon

Options for Pressure Ulcer Dressings

Ulcer Type*

Description

Objective

Use

Options

Shallow (stage 2)

Dry with minimal exudate

Create or retain moisture

Protect from infection

Transparent films or hydrogels

Cover with: Transparent film, thin hydrocolloid, or thin polyurethane foam

Wrap with:Nonadherent gauze dressing

Wet with moderate-to-extensive exudate

Absorb exudate

Facilitate autolysis

Maintain moisture

Protect from infection

Hydrocolloid (if light-to-moderate exudate) or foam dressings

Cover with: Alginates (if extensive exudate), hydrocolloids (with or without paste or powder), or polyurethane foam

Wrap with: Nonadherent gauze dressing or absorptive contact layer

Deep (stages 3 and 4)

Dry with minimal exudate

Fill cavities

Create or maintain moisture

Protect from infection

Hydrocolloids, hydrogels, or foam dressings

Fill with: Copolymer starch, hydrogel, or damp gauze

Cover with: Transparent thin film, polyurethane foam, or gauze pad

Wet with moderate-to-extensive exudate

Fill cavities

Absorb exudate

Maintain moisture

Protect from infection

Alginates or foam dressings

Fill with: Copolymer starch, dextranomer beads, calcium alginates, hydrofibers, or hydrocellular gauze or foam

Cover with: Transparent thin film or polyurethane foam

* Dressings are not usually needed for stage 1 pressure injuries unless subject to friction or incontinence.

Management of pain

Pressure injuries can cause significant pain. Pain should be monitored regularly using a pain scale. Primary treatment of pain is treatment of the injury itself, but a nonsteroidal anti-inflammatory drug or acetaminophen is useful for mild-to-moderate pain. Opioids should be avoided, if possible, because sedation promotes immobility. However, opioids or topical nonopioid preparations such as mixtures of local anesthetics may be necessary during dressing changes and debridement. In cognitively impaired patients, changes in vital signs can be used as indicators of pain.

Control of infection

Pressure injuries should be continually assessed for signs of bacterial infection such as increased erythema, foul odor, warmth, drainage, fever, and elevated white blood cell count. Impaired wound healing should also raise concern of infection. These abnormal findings indicate a wound culture should be done. However, because all pressure ulcers are colonized, results should be interpreted with caution; bacterial count rather than bacterial presence should guide treatment.

Local wound infection can be treated topically with agents such as silver sulfadiazine, mupirocin, polymyxin B, and metronidazole. Silver sulfadiazine and similar opaque topical agents should be used cautiously because they can impair visualization of the underlying wound and can be difficult to remove. A 2-week trial of topical antibiotics for all clean pressure injuries that do not heal despite 2 to 4 weeks of proper treatment is recommended. Systemic antibiotics should be given for cellulitis, bacteremia, or osteomyelitis; usage should be guided by tissue culture, blood culture, or both or clinical suspicion and not by surface culture.

Assessment of nutritional needs

Undernutrition is common among patients with pressure injuries and is a risk factor for delayed healing. Markers of undernutrition include albumin < 3.5 g/dL (< 35 g/L) or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day, sometimes requiring oral, nasogastric, or parenteral supplementation, is desirable for optimal healing. Current evidence does not support supplementing vitamins or calories in patients who have no signs of nutritional deficiency.

Adjunctive therapy

Multiple adjunctive therapies are being tried to promote healing:

  • Negative-pressure therapy: Negative-pressure therapy (vacuum-assisted closure, or VAC) applies suction to the wound. It can be applied to clean wounds. High-quality evidence of efficacy does not yet exist, but negative-pressure therapy has shown some promise in small studies.

  • Topical recombinant growth factors: Some evidence suggests that topical recombinant growth factors (eg, nerve growth factor, platelet-derived growth factor) and skin equivalents facilitate wound healing.

  • Electrical stimulation therapy: Electrical stimulation therapy combined with standard wound therapy can increase wound healing.

  • Therapeutic ultrasonography: Ultrasonography is sometimes used, but there is no good evidence of benefit or harm.

  • Electrical magnetic, phototherapy (laser) heat, massage, and hyperbaric oxygen therapies: No evidence supports efficacy of these treatments.

Surgery

Large defects, especially with exposure of musculoskeletal structures, require surgical closure. Skin grafts are useful for large, shallow defects. However, because grafts do not add to blood supply, measures must be taken to prevent pressure from developing to the point of ischemia and further breakdown. Myocutaneous flaps, because of their pressure-sharing bulk and rich vasculature, are the closures of choice over large bony prominences (usually the sacrum, ischia, and trochanters). Surgery may rapidly improve the quality of life in patients with pressure injuries. Surgical outcomes are best if preceded by optimal treatment of undernutrition and comorbid disorders.

Prevention

Prevention requires

  • Identification of high-risk patients

  • Repositioning

  • Conscientious skin care and hygiene

  • Avoidance of immobilization

Patient risk should be estimated based on the assessment of skilled clinicians and use of risk assessment scales (see Table: The Norton Scale for Predicting Pressure Ulcer Risk* and the Braden Scale).

Treatment and prevention overlap considerably. The mainstay of prevention is frequent repositioning. Pressure should not continue over any bony surface for > 2 hours. Patients who cannot move themselves must be repositioned and cushioned with pillows. Patients must be turned even when they are lying on low-pressure mattresses. Pressure points should be checked for erythema or trauma at least once per day under adequate lighting. Patients and family members must be taught a routine of daily visual inspection and palpation of sites for potential ulcer formation.

Daily attention to hygiene and dryness is necessary to prevent maceration and secondary infection. Protective padding, pillows, or sheepskin can be used to separate body surfaces. Bedding and clothing should be changed frequently. In incontinent patients, ulcers should be protected from contamination; synthetic dressings can help. Skin breakdown can be prevented with careful cleansing and drying (patting and not rubbing the skin) and using anticandidal creams and moisture barrier creams or skin-protective wipes. Use of adhesive tape should be minimized, because it can irritate and even tear fragile skin. Areas subject to friction may be powdered with plain talc. Use of cornstarch is discouraged because it may allow microbial growth.

Most importantly, immobilization should be avoided. Sedatives should be minimized, and patients should be mobilized as quickly and safely as possible.

Key Points

  • Pressure injuries can develop secondary to immobilization and hospitalization, particularly in patients who are elderly, incontinent, or undernourished.

  • Base the risk of pressure injury on standardized scaling systems as well as on the assessment of skilled clinicians.

  • Pressure ulcers are staged according to ulcer depth, but tissue damage may be deeper and more severe than is evident from the physical examination.

  • Assess patients with pressure injuries for local wound infection (sometimes manifesting as failure to heal), sinus tracts, cellulitis, bacteremic spread (eg, with endocarditis or meningitis), osteomyelitis, and undernutrition.

  • Treat and help prevent pressure injuries by reducing skin pressure, repositioning frequently, and using protective padding and support surfaces that can be dynamic (powered electrically) or static (not powered electrically).

  • Clean and dress wounds frequently to reduce bacterial counts and facilitate healing.

  • Apply transparent films or hydrogels (if exudate is minimal), hydrocolloids (if exudate is light to moderate), alginates (if exudate is extensive), or foam dressings (for various amounts of exudate).

  • Treat pain with analgesics, local wound infection with topical antibiotics, and cellulitis or systemic infections with systemic antibiotics.

  • Surgically close large defects, especially those with exposed musculoskeletal structures.

  • Optimize nutritional status and treatment of comorbid disorders before surgery.

  • Help prevent pressure injuries in at-risk patients with meticulous wound care, pressure reduction, and avoiding any unnecessary immobilization.

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SANTYL
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