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Pressure ulcers are areas of necrosis and ulceration where tissues are compressed between bony prominences and hard surfaces; they may also develop from friction and shearing forces. Risk factors include old age, impaired circulation, immobilization, malnourishment, and incontinence. Severity ranges from 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 and Pathophysiology

An estimated 1.3 to 3 million patients in the US have pressure ulcers (PUs); incidence is highest in older patients, especially when 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.

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. In persons wearing prosthetic devices, they often occur over bony prominences due to ill-fitting prostheses. 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. Ulcers are worsened when skin is overly moist and macerated (eg, from perspiration or incontinence).

Patients with cognitive impairment, immobility, or both are at higher risk. Immobility is the most important factor, either from decreased spontaneous movement (such as from stroke, sedation, severe illness) and/or inability to change position frequently because of weakness. Others include urinary and fecal incontinence; poor nutritional status, including dehydration; diabetes; and heart disease. Clinical assessment is sufficient to identify patients at risk; several scales (eg, Norton, Braden) help predict risk (see Fig. 1: Pressure Ulcers: Braden scale for predicting risk for pressure ulcers.). (See also 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. Modified 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.

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 based on the depth of soft-tissue damage (see Table 1: Pressure Ulcers: Pressure Ulcer Staging). Stage 1 PUs manifest hyperemia, warmth, and induration. This stage is a misnomer in the sense that an ulcer (a defect of skin into the dermis) is not present. However, ulceration will form if the course is not arrested and reversed. Stage 2 PUs involve erosion (defect of epidermis) or true ulceration; however, subcutaneous tissue is not exposed. Stage 3 and 4 PUs have deeper involvement of underlying tissue with more extensive destruction. Patients do not always progress from lower to higher stages. Sometimes the first sign is a deep, necrotic Stage 3 or 4 ulcer. When PUs develop quickly, subcutaneous tissue can become necrotic before the epidermis erodes. Any small ulcer should be thought of as an iceberg, with a potentially deep base.

Table 1
Pressure Ulcer Staging Stage Characteristics 1 Observable pressure-related changes of intact skin compared to the adjacent or opposite areas, including differences in: Color (redness in lightly pigmented skin; red, blue, or purple hues in darkly pigmented skin) Temperature (increased warmth or coolness) Consistency (firm or boggy feel) Sensation (pain, itching) 2 Partial-thickness skin loss involving the epidermis and/or dermis Ulcer is superficial and manifests as an abrasion, blister, or shallow crater 3 Full-thickness skin loss involving damage or necrosis of subcutaneous tissue, which may extend down to, but not through, underlying fascia Ulcer is a deep crater with or without undermining of adjacent tissue 4 Full-thickness skin loss with extensive tissue destruction and/or necrosis, or damage to muscle, bone, or supporting structures (such as tendons or the joint capsule) Adapted from the National Pressure Ulcer Advisory Panel, Consensus Development Conference Statement.

PUs at any stage may be painful or pruritic but may not be noticed by patients with blunted awareness. Tenderness, erythema of surrounding skin, exudate, or foul odor suggests infection. Fever should raise suspicion of bacteremia or underlying osteomyelitis.

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 resistant organisms, which can slow healing and cause bacteremia and sepsis.

Diagnosis

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 and Treatment

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

Treatment requires multiple simultaneous elements.

Reducing pressure: Reducing tissue pressure is accomplished through positioning, protective devices, and modification of support surfaces. Frequent repositioning (and selection of the proper position) is most important. 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. A Stryker frame facilitates turning patients with spinal cord injuries. Patients who can sit should be encouraged or stimulated to change position q 15 to 60 min.

Protective padding includes pillows or foam wedges placed between knees, ankles, and heels when a patient is on his side and pillows, foam, or sheepskin heel protectors when 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.

Support surfaces under bedbound patients can be changed to reduce pressure. A change from standard mattress is indicated when the patient is unable to reposition himself 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 1 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 1 ulcers who develop hyperemia on static surfaces and for patients with Stage 3 or 4 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 3 and 4 ulcers or numerous truncal ulcers (see Table 2: Pressure Ulcers: Options for Support Surfaces).

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 cleaning, debridement, and dressings are needed.

Cleaning should be performed initially and with each dressing change; ordinary soap and water is usually best. Antiseptics such as iodine and hydrogen peroxide and even antiseptic washes interfere with tissue healing and should be avoided. Cleaning involves irrigation with saline solution at pressures sufficient to remove bacteria without traumatizing tissue; this can be done with commercial syringes, squeeze bottles, or electrically pressurized systems. Alternatively, a 35-mL syringe and a 19-gauge IV catheter can be used. Irrigation should continue until no further debris can be loosened.

Debridement is necessary to remove dead tissue. There are several methods. Autolytic debridement uses synthetic occlusive dressings 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 used. Infected wounds should not be occluded.

Mechanical debridement with wet-to-dry dressings, hydrotherapy (whirlpool baths), wound irrigation, or dextranomers (small carbohydrate-based beads that help absorb exudate and liquid debris) should be used for thick exudate or loose necrotic tissue. A scalpel or scissors can be used to remove eschar (except in heel ulcers, in which eschar in the absence of edema, erythema, fluctuance, or drainage can be safely left alone) or extensive areas of dead tissue. Modest 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.

Enzymatic debridement (using collagenase, papain, fibrinolysin, or streptokinase Some Trade Names
STREPTASE

/streptodornase) is an option for patients whose caretakers are not trained to perform mechanical debridement or for patients unable to tolerate surgery. It is most effective after 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 1 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 q 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 2) Dry with nominal 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-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 3–4) Dry with nominal 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-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, polyurethane foam *Dressings are not usually needed for Stage 1 ulcers.

Hydrocolloids (eg, RepliCare, DuoDERM, Restore, Tegasorb), which are combinations of 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 extensive exudate and for control of 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 and fever; elevated WBC offers further evidence. Options for topical treatment include silver sulfadiazine Some Trade Names
SILVADENE
Click for Drug Monograph
, triple antibiotic, and metronidazole Some Trade Names
FLAGYL
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(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: Malnutrition is common among patients with PUs and is a risk factor for nonhealing. Markers of malnutrition include albumin < 3.5 mg/dL and/or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day is desirable for optimal healing; oral or parenteral supplementation (see Nutritional Support) may be needed. 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. (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 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. 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
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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 followed by vigilant attention to skin care and hygiene. (See also Agency for Healthcare Policy and Research guidelines for prediction and prevention of pressure ulcers and treatment of pressure ulcers in adults.) Pressure points should be checked for erythema or trauma at least once/day under adequate lighting. Patients and families must be taught a routine of daily visual inspection and palpation of sites for potential ulcer formation.

The mainstay of prevention is frequent repositioning. Pressure should not be allowed to continue over any bony surface for > 2 h. Patients who cannot move by themselves must be repositioned using pillows. Even on low pressure mattresses, the patient must be turned.

Daily attention to hygiene and dryness is necessary to prevent maceration and secondary infection. Lying on a sheepskin 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. The skin should be sponged in hot weather and thoroughly dried afterward. For incontinent patients, ulcers should be protected from contamination; synthetic dressings are helpful for this. 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). Areas subject to friction may be powdered with plain talc. Cornstarch may allow fungal growth.

Oversedation should be avoided, and activity should be encouraged. Adequate nutrition is important. Adhesive tape can irritate and even tear fragile skin adjoining ulcers, and its use should be minimized.

Last full review/revision November 2005

Content last modified November 2005