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Pressure ulcers are areas of necrosis and ulceration where tissues are compressed between bony prominences and hard surfaces; they result from pressure alone or pressure in combination with friction, shearing forces, or both. Risk factors include old age, impaired circulation, immobilization, malnourishment, and incontinence. Severity ranges from nonblanchable skin erythema to full-thickness skin loss with extensive soft-tissue necrosis. Diagnosis is clinical. Treatment includes pressure reduction, avoidance of friction and shearing forces, local care, and sometimes skin grafts or myocutaneous flaps. Prognosis is excellent for early-stage ulcers; neglected and late-stage ulcers pose risk of serious infection and nutritional stress and are difficult to heal.

Etiology

An estimated 1.3 to 3 million patients in the US have pressure ulcers (PUs); incidence is highest in older patients, especially those who are hospitalized or in long-term care facilities. Aging increases risk, in part because of reduced subcutaneous fat and decreased capillary blood flow. Immobility and comorbidities increase risk further.

Patients who are cognitively impaired, immobile, or both are at increased risk. Immobility—because of decreased spontaneous movement (eg, due to stroke, sedation, or severe illness) or inability to change position frequently because of weakness—is the most important factor. Other risk factors include urinary and fecal incontinence; poor nutritional status, including dehydration; diabetes; and cardiovascular disease. Clinical assessment is sufficient to identify patients at risk; several scales (eg, Norton, Braden—see Fig. 1: Bites and Stings: Identifying pit vipers) are useful for predicting risk. The National Pressure Ulcer Advisory Panel has also issued guidelines for the prediction and prevention of PUs (see Table 1: Pressure Ulcers: Pressure Ulcer Staging.) (See also the Agency for Healthcare Policy and Research guidelines for prediction and prevention of pressure ulcers in adults.)

The Norton Scale for Predicting Pressure Sore 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 2:24, 1989.

Fig. 1
Braden scale for predicting risk for pressure ulcers. The patient is evaluated in 6 categories: sensory perception, moisture, activity, mobility, nutrition, and friction and shear. Pressure sore risk increases as the score decreases: 15–16 = mild risk; 12–14 = moderate risk; < 12 = serious risk. Adapted from Braden B, Bergstrom N: Pressure ulcers in adults: Prediction and prevention. Clinical Practice Guideline, no. 3, pp 14–17, May 1992. US Department of Health and Human Services.

Table 1
Pressure Ulcer Staging Stage Characteristics I Pressure-related changes of intact skin compared with the adjacent or opposite areas: Color (nonblanchable redness in lightly pigmented skin; red, blue, or purple hues in darkly pigmented skin) There may also be changes in Temperature (increased warmth or coolness) Consistency (firm or boggy feel) Sensation (pain) II Partial-thickness skin loss into but not deeper than the dermis, including abrasions, intact or ruptured blisters, and other shallow defects No exposure of subcutis or deeper structures III Full-thickness skin loss down to subcutaneous fat or, in areas without underlying fat (eg, nose, malleolus), to fascia, perichondrium, or periosteum No exposure of muscle, tendon, cartilage or bone Sometimes devitalized tissue, undermining, or tunneling but that does not hide deeper injury IV Full-thickness skin loss with exposure of muscle, tendon, bone, or adjacent structures (eg, joint spaces) Potentially extensive destruction and increased risk of osteomyelitis Adapted from the National Pressure Ulcer Advisory Panel (2007). Available at www.npuap.org.

Pathophysiology

PUs develop when soft tissues are compressed between bony prominences and contact surfaces or when friction (eg, rubbing against clothing or bedding) or shearing forces (which develop when skin clings to surfaces) cause erosion, tissue ischemia, and infarction. PUs most frequently develop over the sacrum, ischial tuberosities, trochanters, malleoli, and heels, but they can develop elsewhere, including behind the ears when nasal cannulae are used for prolonged periods. Also, poorly fitting prosthetic devices can cause PUs to develop over bony prominences. Increased force and duration of pressure directly influence risk and severity, but PUs can develop in as little as 3 to 4 h in some settings (eg, trauma patients who are immobilized on rigid spine-immobilization boards). Ulcers worsen when skin is overly moist and macerated (eg, from perspiration or incontinence).

Other causes of skin ulcers: Chronic arterial and venous insufficiency can result in skin ulcers, particularly on the lower extremities. Although the underlying mechanism is vascular, the same forces that cause PUs can worsen these ulcers, and principles of treatment are similar.

Symptoms and Signs

Several staging systems exist; the most common classifies ulcers according to the depth of soft-tissue damage (see Table 1: Pressure Ulcers: Pressure Ulcer Staging). PUs do not always present as Stage I and then progress to higher stages. Sometimes the first sign of a PU is a deep, necrotic stage III or IV ulcer. In a rapidly developing PU, subcutaneous tissue can become necrotic before the epidermis erodes. A small ulcer might, like an iceberg, be quite large under the surface.

Stage I PUs manifest as 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. This stage is a misnomer in the sense that 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 II PUs involve loss of epidermis with or without erosion (defect of epidermis) or true ulceration (partial-thickness loss of dermis); subcutaneous tissue is not exposed. The ulcers are shallow with a reddish base. Intact or partially ruptured blisters due to pressure are also stage II PUs. (Note: Non–pressure-related causes of erosion, ulceration, or blistering–eg, skin tears, tape burns, perineal dermatitis, maceration, excoriation–are excluded from stage II description.)

Stage III and IV PUs have deeper involvement of underlying tissue with more extensive destruction.

Ulcers covered with debris or eschar are by definition unstageable. However, stable, nonfluctuant heel lesions with dry eschar should not be debrided for the sake of staging. Bruising of an apparent stage II ulcer should raise the suspicion of a deeper-stage PU. PUs at any stage may be painful or pruritic but may not be noticed by patients with blunted awareness or sensation. Tenderness, erythema of surrounding skin, exudate, or foul odor suggests infection. Fever should raise suspicion of bacteremia or underlying osteomyelitis.

Complications

Nonhealing ulcers may be due to inadequate treatment but should raise suspicion of osteomyelitis or, rarely, squamous cell carcinoma within the ulcer (Marjolin's ulcer). Other complications of nonhealing PUs include sinus tracts, which can be superficial or connect the ulcer to deep adjacent structures (eg, to the bowel in sacral ulcers), and tissue calcification. In addition, PUs are a reservoir for hospital-acquired antibiotic-resistant organisms, which can slow healing and cause bacteremia and sepsis.

Diagnosis

• Clinical evaluation with continuous assessment
• Sometimes bone scan or MRI

Diagnosis is usually apparent clinically, but depth and extent can be difficult to determine. PUs are always colonized by bacteria, so wound surface cultures are uninterpretable. Underlying osteomyelitis is diagnosed with radionuclide bone scanning or gadolinium-enhanced MRI, but both have poor sensitivity and specificity. Diagnosis may require bone biopsy and culture.

Continuous assessment is mandatory for effective management. Serial photographs can also document healing.

Prognosis

Prognosis for early-stage PUs is excellent with timely, appropriate treatment, but healing typically requires weeks. PUs often develop in patients with suboptimal care; if care cannot be improved, long-term outcome is poor, even if short-term wound healing is accomplished.

Treatment

• Pressure reduction
• Direct ulcer care
• Management of pain, infection, and undernutrition
• Sometimes adjunctive therapy or surgery

Treatment requires multiple simultaneous elements.

Reducing pressure: Reducing tissue pressure is accomplished through careful positioning of the patient, protective devices, and variation 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. Bedbound patients should be turned a minimum of q 2 h, should be placed at a 30° angle to the mattress when on their side (ie, lateral decubitus) to avoid direct trochanteric pressure, and should be elevated as minimally as possible to avoid the shear forces on tissues that result from sliding down the bed. For repositioning patients, lifting devices (eg, a Stryker frame) or bed linen should be used instead of dragging the patient (which causes friction and shear forces). Patients placed in chairs should be repositioned every hour, and they should be encouraged to change position on their own q 15 min.

Protective padding includes pillows or foam wedges placed between knees, ankles, and heels when patients are on their side and pillows, foam, or heel protectors when patients are supine. 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. Donut-shaped devices and sheepskins should be avoided as a treatment for PUs.

Support surfaces under bedbound patients can be changed to reduce pressure. A change from standard mattresses is indicated when patients are unable to reposition themselves and periodic repositioning care is unavailable. (See also Cochrane review of support surfaces for pressure ulcer prevention)

Support surfaces are static or dynamic.

Static surfaces, which do not require electricity, include air, foam, gel, and water overlays and mattresses. Old-fashioned “egg crate” mattresses offer no advantage. In general, static surfaces increase surface support areas and decrease pressures and shear forces; they are indicated for high-risk patients without PUs and for patients with stage I PUs.

Dynamic surfaces require electricity. 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 I ulcers who develop hyperemia on static surfaces and for patients with stage III or IV ulcers. Air-fluidized or high-air-loss mattresses contain silicone-coated beads that liquefy when air is pumped through the bed. Advantages include reduction of moisture on surfaces and cooling. They are indicated for patients with nonhealing stage III and IV ulcers or numerous truncal ulcers (see Table 2: Pressure Ulcers: Options for Support Surfaces). Although specialized mattresses are designed to shift pressure and reduce forces that lead to PUs, they are best thought of as an adjunct to comprehensive care.

Table 2
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.

Ulcer care: Appropriate ulcer care involves cleaning, debridement, and dressings.

Cleaning should be done initially and with each dressing change; ordinary soap and water (not hot) is usually best. Cleaning often involves irrigation with saline solution at pressures sufficient to remove bacteria without traumatizing tissue; commercial syringes, squeeze bottles, or electrically pressurized systems can be used. 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 (eg, iodine, hydrogen peroxide) and antiseptic washes interfere with tissue healing and should be avoided. Rubbing of skin should be minimized, and moisturizer should be applied gently after each cleansing.

Debridement is necessary to remove dead tissue. Methods include

• Autolytic debridement: Synthetic occlusive dressings are used to facilitate digestion of dead tissues by enzymes normally present in wound fluids. Autolytic debridement may be used for small wounds with simple accumulation of tissue proteins and wounds that need to be sealed off anyway (eg, for protection from feces or urine). DuoDERM or Contreet (which is impregnated with silver and thus offers antimicrobial effects) are commonly applied. Infected wounds, however, should not be occluded.
• Mechanical debridement: Hydrotherapy (whirlpool baths), ultrasound, medical maggots, wound irrigation, or dextranomers (small carbohydrate-based beads that help absorb exudate and liquid debris) should be used to remove thick exudate or loose necrotic tissue. A scalpel or scissors can be used to remove eschar (except in heel ulcers, in which dry eschar in the absence of edema, erythema, fluctuance, or drainage can be safely left alone) or extensive areas of dead tissue. Modest amounts of eschar or tissue can be debrided at the patient's bedside, but extensive or deep areas should be debrided in the operating room. Urgent debridement is indicated in advancing cellulitis or sepsis. Debridement with wet-to-dry dressings should be done only for wounds with very loose exudate and only with great care because it is often painful and it may remove healthy tissue or overdry the wound.
• Enzymatic debridement (using collagenase, papain, fibrinolysin, or streptokinase Some Trade Names
  STREPTASE
  
  /streptodornase): This method can 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. Collagenase is especially effective as collagen comprises 75% of the dry weight of skin.

Dressings should be used for stage I ulcers that are subject to friction or incontinence and for all other ulcers (see Table 3: Pressure Ulcers: Options for Pressure Ulcer Dressings). Objectives are to keep the ulcer bed moist to retain tissue growth factors while allowing some evaporation and inflow of oxygen, to keep surrounding skin dry, to facilitate autolytic debridement, and to establish a barrier to infection. Transparent films (eg, OpSite, Tegaderm, Bioclusive) are sufficient for ulcers with limited exudate; they should not be used over cavities and must be changed every 3 to 7 days. Some experts recommend a small amount of triple antibiotic ointment under the dressing. Hydrogels (ClearSite, Vigilon, FlexiGel), which are cross-linked polymer dressings that come in sheets or gels, are indicated for very shallow wounds, such as re-epithelializing wounds with minimal exudate.

Table 3
Options for Pressure Ulcer Dressings Ulcer Type* Description Objective Use Options Shallow (stage II) 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-large exudate Absorb exudate Facilitate autolysis Maintain moisture Protect from infection Hydrocolloid or foam dressings Cover with: Alginates, hydrocolloid (with or without paste or powder), or polyurethane foam Wrap with: Gauze dressing or absorptive contact layer Deep (stages III–IV) Dry with minimal exudate Fill cavities Create or maintain moisture Protect from infection Hydrocolloids, alginates, 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-large 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 I ulcers.

Hydrocolloids (eg, RepliCare, DuoDERM, Restore, Tegasorb), which combine gelatin, pectin, and carboxymethylcellulose in the form of wafers, powders, and pastes, are indicated for light-to-moderate exudate; some have adhesive backings and others are typically covered with transparent films to ensure adherence to the ulcer and must be changed q 3 days. Alginates (polysaccharide seaweed derivatives containing alginic acid), which come as pads, ropes, and ribbons (AlgiSite, Sorbsan, Curasorb), are indicated for absorbing extensive exudate and for controlling bleeding after surgical debridement. Foam dressings (Allevyn, LYOfoam, Hydrasorb, Mepilex, Curafoam, Contreet) are useful as they can handle a variety of levels of exudate and provide a moist environment for wound healing. Waterproof versions protect the skin from incontinence. Those with adhesive backings stay in place longer and need less frequent changing.

Pain management: Primary treatment of pain is treatment of the PU itself, but NSAIDs or acetaminophen Some Trade Names
GENAPAP
TYLENOL
VALORIN
Click for Drug Monograph
is used for mild-to-moderate pain. Opioids should be avoided if possible because sedation promotes immobility. Opioids may be necessary during dressing changes and debridement. In cognitively impaired patients, changes in vital signs can be used as an indication of pain.

Infection management: PUs should be continually reassessed for bacterial infection using clinical signs of erythema, warmth, increased drainage, fever, and elevated WBC. Options for topical treatment include silver sulfadiazine Some Trade Names
SILVADENE
Click for Drug Monograph
, triple antibiotic, and metronidazole Some Trade Names
FLAGYL
Click for Drug Monograph
(the latter for anaerobic bacteria, which are often foul-smelling). Systemic antibiotics should be administered for cellulitis, bacteremia, or osteomyelitis guided by tissue culture or clinical suspicion and not by surface culture.

Nutrition: Undernutrition is common among patients with PUs and is a risk factor for nonhealing. Markers of undernutrition include albumin < 3.5 mg/dL or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day, sometimes requiring oral or parenteral supplementation (see Nutritional Support: Introduction), is desirable for optimal healing. Zinc supplementation supports wound healing, and replacement at a dose of 50 mg tid may be useful. Supplemental vitamin C 1 g/day may be provided. Providing a drink of water to patients at each repositioning may be useful to aid hydration. (See also Cochrane review of nutritional interventions for preventing and treating pressure ulcers.)

Adjuncts: Multiple adjunctive treatments have been tried or are under investigation. Negative pressure therapy (for clean wounds) and the use of various topical recombinant growth factors (eg, nerve growth factor, platelet-derived growth factor-BB) and skin equivalents are showing promise in wound management; however, they do not ameliorate mechanical forces and tissue ischemia. Electrical stimulation, heat therapy, massage therapy, and hyperbaric O₂ therapy have not proven effective.

Surgery: Surgical debridement is necessary for any ulcer with devitalized tissue, except for stable, dry, nonfluctuant heel ulcers. 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 (eg, sacrum, ischia, trochanters).

Ischemic and venous ulcers: Wound care treatments also are useful for ischemic ulcers, but the underlying pathophysiology must be addressed (eg, better control of the inflammatory process in a rheumatoid ulcer or surgical stenting or bypass surgery to improve circulation in atherosclerosis). Pentoxifylline Some Trade Names
TRENTAL
Click for Drug Monograph
has been tried with minimal success. Some evidence supports the use of dalteparin Some Trade Names
FRAGMIN
Click for Drug Monograph
for diabetic foot ulcers (5000 units sc once/day until healed); however, this finding has not been corroborated. Ischemic ulcers can become infected, often with anaerobic organisms, and the infection may spread, causing septicemia or osteomyelitis.

Venous ulcers are typically sterile at first but tend to lead to cellulitis. The same local care as for PUs can be used. In addition, treatment includes measures to reduce venous hypertension, such as using compression stockings or Unna boot bandages (applied at a pressure of 35 to 40 mm Hg) and elevating the leg above the heart. Pentoxifylline Some Trade Names
TRENTAL
Click for Drug Monograph
800 mg po tid for up to 24 wk may be useful.

Prevention

Prevention requires

• Identification of high-risk patients
• Repositioning
• Conscientious skin care and hygiene
• Avoidance of oversedation

The mainstay of prevention is frequent repositioning. Pressure should not continue over any bony surface for > 2 h. Patients who cannot move themselves must be repositioned using pillows. Even on low-pressure mattresses, patients must be turned. Pressure points should be checked for erythema or trauma at least once/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. (See also Table 1: Pressure Ulcers: Pressure Ulcer Staging the Agency for Healthcare Policy and Research guidelines for prediction and prevention of pressure ulcers and treatment of pressure ulcers in adults.)

Daily attention to hygiene and dryness is necessary to prevent maceration and secondary infection. Although sheepskin should not be used to redistribute pressure after ulceration has occurred, lying on a sheepskin as a preventive measure helps keep the skin in good condition. Protective padding, pillows, or a sheepskin can be used to separate body surfaces. Bedding and clothing should be changed frequently; sheets should be soft, clean, and free from wrinkles and particulate matter. In hot weather, the skin should be sponge-bathed and thoroughly dried afterward. 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 (eg, Skin-Prep). 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.

Oversedation should be avoided, and activity should be encouraged. Adequate nutrition is important.

Last full review/revision October 2008 by Daniel W. Collison, MD

Content last modified October 2008