Pressure Ulcers

(Bedsores; Pressure Sores; Decubitus Ulcers)

Pressure ulcers (PUs) are areas of necrosis and ulceration that usually develop 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, undernourishment, and incontinence. Severity ranges from skin erythema to full-thickness skin loss with extensive soft-tissue necrosis. Diagnosis is by examination. Treatment includes pressure reduction, avoidance of friction and shearing forces, local care, and sometimes nutritional supplementation and skin grafts or myocutaneous flaps. Prognosis is excellent for early-stage PUs; neglected and late-stage PUs pose risk of serious infection and are difficult to heal.

Geriatric Essentials

• The elderly are at greatest risk of developing pressure ulcers because of age-related changes in soft tissues and decreases in skin perfusion and subcutaneous fat.
• Patients who are immobilized because of injury or neurologic disease and those with undernutrition or incontinence are at highest risk.
• Complications, symptoms, signs, staging, diagnosis, treatment, and prevention are similar for younger patients who share risk factors.

An estimated 1.3 to 3 million patients in the US have pressure ulcers (PUs); estimated prevalence among patients in acute care hospitals ranges from 3 to 15%, but prevalence is higher among patients who need chronic care (41%) or are quadriplegic (60%) and among elderly patients recovering from a hip fracture (66%).

Etiology

The major factors contributing to PU development include pressure, friction, and shearing forces and moisture. Pressure is considered the most important etiologic factor and occurs when soft tissues are compressed between bony prominences and contact surfaces for prolonged periods. Friction is the force that resists relative motion between 2 surfaces that are in contact with each other. Shearing forces result from forces that tend to cause 2 opposing surfaces to slide and displace against each other. Unlike pressure, which is a perpendicular force, shearing forces act parallel to the tissue surface. Shearing forces occur when the skin is fixed; the consequent sliding pressure is transmitted to deeper tissues with angulation, often causing thrombosis of blood vessels. An example of this is when the upper body of a supine patient is raised to an angle >= 30° and is in contact with the mattress or other firm surface.

PUs most often develop over the sacrum, ischial tuberosities, trochanters, femoral condyles, malleoli, and heels (see Figure 124-1), but they can develop anywhere, including behind the ears when nasal cannulas are used for prolonged periods and in the corners of the mouth in patients needing nasogastric or endotracheal tubes.

Duration of pressure and degree of friction and shearing forces and maceration directly influence PU risk and severity; PUs can develop in <= 2 h in some settings. Immobilization or inability to change position frequently--caused by conditions such as dementia, stroke, oversedation, fractures, peripheral neuropathy, lower limb abnormalities, frailty, and activity intolerance (eg, from heart and lung disease)--increases duration of pressure and likelihood of friction and shearing forces on soft tissues and is therefore a primary risk factor. Fecal or urinary incontinence is a primary cause of soft-tissue maceration. Other risk factors include soft-tissue edema; undernutrition; dehydration; atherosclerosis and atherosclerosis risk factors (eg, hypertension, diabetes, dyslipidemia, smoking); and corticosteroid use, all of which impair soft-tissue repair and healing. Elderly people are at risk even without comorbidities because they have less subcutaneous fat and muscle to dissipate surface pressure and less robust soft-tissue repair responses to injury (eg, less cell proliferation, collagen deposition, development of wound tensile strength, wound contraction). Age-related decreases in ascorbic acid levels may also increase blood vessel and connective tissue fragility, whereas age-related decreases in the number of dermal blood vessels may predispose to ischemic injury from pressure and shearing forces.

PUs can become reservoirs for hospital-acquired resistant pathogens, which can slow healing and cause cellulitis, osteomyelitis, bacteremia, sepsis, and death. PUs may also develop sinus tracts that can be extensive, connecting the PU to deep structures (eg, to the bowel in sacral PUs).

Symptoms and Signs

Symptoms and signs vary by stage; several staging systems exist. The most common classifies PUs based on the depth of soft-tissue damage (see Table 124-1). Stage 1 PUs manifest with hyperemia, warmth, and induration (see Photo 124-1). This stage is a misnomer in the sense that an ulcer (an area of skin necrosis and ulceration) is not present. However, ulceration will develop if the changes are not arrested and reversed. Stage 2 PUs involve epidermal erosion or true ulceration without exposure of subcutaneous tissue (see Photo 124-2). Stages 3 and 4 PUs extend through the full skin thickness and cause more extensive destruction (see Photos 124-3 and 124-4). PUs often do not progress from lower to higher stages; when PUs develop quickly, subcutaneous tissue can become necrotic before the epidermis erodes, and the initial manifestation may be a stage 3 or 4 PU. Any small PU should be thought of as a possible tip of an iceberg, with a potentially deep base.

PUs at any stage may be painful or pruritic but may not be noticed by patients whose awareness is blunted. Tenderness, erythema of surrounding skin, exudate, or foul odor suggests infection. Fever should raise suspicion of osteomyelitis or bacteremia. Patients with PUs, especially those with a stage 3 or 4 PU, may feel stigmatized and experience social isolation.

Diagnosis

Patients at risk of developing PUs can be identified clinically with risk scales (eg, Braden and Norton; see Figure 124-2 and Table 124-2).

Diagnosis of PUs is usually obvious, but depth, extent, and presence of infection can be difficult to determine. PUs are always colonized by bacteria, so wound surface cultures are uninterpretable. A wound culture and sensitivity test, done with tissue obtained via needle aspiration or biopsy, is indicated if bacteremia or systemic infection (eg, elevated temperature, inflamed wound margins, foul-smelling exudate) is suspected or if the PU is not healing. Bacterial counts >= 100,000/g of tissue suggest that the PU will not heal without systemic antibiotics. Underlying osteomyelitis is diagnosed by radionuclide bone scanning or gadolinium-enhanced MRI, but both have poor sensitivity and specificity, and diagnosis may require bone biopsy and culture or assessment of the response to empiric treatment.

Treatment and Prevention

Treatment and prevention require many of the same, simultaneous elements. Prompt treatment is essential, because an untreated PU may deepen and promote cellulitis, osteomyelitis, nonhealing, bacteremia, and sepsis. Even uncomplicated PUs may cause suffering and disability. PU care involves appropriate cleaning, debridement, and dressings.

Reducing pressure, friction, and shearing forces: Reducing tissue pressure is a critical component of both treatment and prevention and is accomplished with repositioning, using protective devices, and modifying support surfaces.

Repositioning of immobilized patients should occur on a schedule, with frequency based on patient risk of developing additional PUs and tissue response to pressure. A written repositioning schedule is most effective, although some patients can be taught to shift their position regularly.

Usually, immobilized, bedbound patients must be turned at least every 2 h to the right or left 30° oblique position to relieve pressure on major pressure points; patients should not be placed on their sides (90° lateral position) because this position puts intense pressure on the greater trochanter and lateral malleolus. Patients who already have skin breakdown should not be positioned on the PU unless there is no alternative.

The head of the bed should not be elevated > 30° (except when patients are eating), and a pull sheet should be used to move patients, both to minimize shearing forces.

Patients at risk of PUs who are seated in a chair must be repositioned at least every hour and should not be left > 2 h, because sitting creates intense pressure on the ischial tuberosities. A chair that does not allow the patient to slide down prevents friction and shearing forces.

Protective devices include pillows or foam wedges placed between knees, ankles, and heels when a patient is in a lateral or decubitus position; pillows, foam, or sheepskin heel protectors when supine; and high-density foam, plastic cushions, or silicone gel pads when seated. Rubber rings (donuts) should not be placed on chairs because they may exacerbate soft-tissue compression and decrease blood flow to tissues near the center of the donut ring. A bed trapeze may help patients with upper motor strength to shift their weight or otherwise reposition themselves while in bed.

Support surfaces: Support surfaces on top or in place of standard mattresses diffuse pressure to a large support area. They are indicated when patients cannot reposition themselves or when periodic repositioning care is unavailable. When choosing a support surface (see Table 124-3), cost, ease of use, site of use (hospital vs home), required maintenance, and patient preference should be considered. Support surfaces may be static or dynamic.

Static surfaces include foam, gel, air, and water overlays and mattresses. In general, static surfaces are indicated for high-risk patients with no PUs, for patients with stage 1 PUs, and for patients who can change their position in bed without weight bearing on the PU.

Dynamic surfaces require electricity and cyclically change their support characteristics. Alternating-air mattresses have air cells that are cyclically 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 and provides cooling. These specialized mattresses are particularly indicated for patients who are at high risk of developing PUs or who already have stage 3 or 4 PUs. Air-fluidized or high-air-loss mattresses contain silicone-coated beads that, when air is pumped through the bed, diffuse pressure like a liquid. Advantages include moisture reduction on surfaces and cooling. They are indicated for patients with nonhealing stages 3 and 4 PUs or numerous truncal PUs (see Table 124-3).

Moisture reduction: Moisture reduction requires gentle washing and drying. Powders (eg, baby powder) are not very effective, but may be comforting. Incontinence must be managed, usually using diapers or pads, and assessed frequently; occasionally, bladder catheterization or rectal tubes may be temporarily helpful.

Nutritional support: Patients with or at risk of developing PUs should be screened for nutritional deficiencies. Markers include albumin < 3.5 mg/dL, BMI < 18 in patients with a triceps skinfold thickness or mid-arm muscle circumference < the 5th percentile, and unintentional weight loss > 15% of baseline.

Caloric intake of at least 30 cal/kg/day and protein intake of 1.25 to 1.5 g/kg/day are desirable for optimal healing; oral or parenteral supplementation may be needed.

In the absence of deficiency, there is little evidence that vitamin or mineral supplementation promotes healing of PUs, and one meta-analysis found no benefit in routine vitamin supplementation. Functional disabilities that affect nutritional intake (eg, poor dentition, ill-fitting dentures, secondary vision loss) should be addressed whenever possible.

Cleaning: Cleaning should be done initially and with each dressing change. Ordinary soap and water is usually best. Antiseptics such as povidone iodine and hydrogen peroxide and even antiseptic washes interfere with tissue healing and should be avoided. The PU should be irrigated 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: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 is indicated 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). Hydrocolloid or foam dressings (some of which are impregnated with silver and thus offer 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) is indicated when the wound has thick exudate or loose necrotic tissue. A scalpel or scissors should be used to remove eschar (except in heel PUs, 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 an operating room. Surgical debridement increases the risk of bleeding, infection, and wound enlargement and usually is more painful than other kinds of mechanical debridement. However, it is the best choice when the need is urgent (eg, to avoid worsening cellulitis, sepsis). After any type of mechanical debridement, a moist environment should be maintained with a dressing (eg, moist normal saline, hydrogel, alginate) to facilitate granulation and wound healing.

Enzymatic debridement (using exogenous collagenase, papain, fibrinolysin, or streptokinase/streptodornase) is an option for patients whose caretakers cannot perform mechanical debridement or for patients unable to tolerate surgery. It is most effective after cross-hatching the wound with a scalpel to improve penetration. Collagenase is often considered especially effective because collagen comprises 75% of skin's dry weight; however, there is no conclusive evidence to support its effectiveness.

Dressings: Dressings should be used for all stage 2 to 4 PUs and for stage 1 PUs that are subject to friction or incontinence (see Table 124-4). Dressings help keep the PU bed moist to retain tissue growth factors while allowing some evaporation and inflow of O₂, keep surrounding skin dry, facilitate autolytic debridement, facilitate epithelial cell migration, and establish a barrier to infection. The frequency of dressing change, regardless of type, varies from once daily (in wounds with the most exudate) to every 7 days (in wounds with the least exudate). There are several kinds of dressings.

Transparent films are nonabsorbent polymer-based dressings that are permeable to gases and vapors but not fluids. They facilitate moisture retention and are indicated for PUs with limited exudate. They should loosely cover about a 2.5-cm margin around the wound and should not be used over cavities.

Hydrogels are cross-linked polymer dressings that come in sheets or gels. They are indicated for stage 1 or 2 PUs, such as reepithelializing PUs with minimal exudate.

Hydrocolloids are combinations of gelatin, pectin, and carboxymethylcellulose (copolymer starch) in the form of wafers, powders, and pastes. Some have adhesive backings whereas others are covered with transparent films. Most are indicated for wounds with light to moderate exudates, and they facilitate autolytic debridement. Hydrocolloid pastes can be used for wounds with moderate to heavy exudates.

Alginates are polysaccharide seaweed derivatives containing alginic acid that come in the form of pads, ropes, and ribbons. They are highly absorptive and therefore are indicated for wounds with extensive exudate and for control of bleeding after surgical debridement. Hydrofibers are also highly absorptive dressings made of carboxymethyl cellulose spun into fibers.

Foam dressings are foam polymers (eg, polyurethane) that are indicated for all PU stages because they are highly absorptive, protect bony prominences, and provide a moist environment for autolytic debridement and wound healing. Waterproof versions protect the skin from incontinence.

Pain management: Daily pain assessment is a neglected part of PU management; changes in vital signs with examination or debridement can be used to assess pain in cognitively impaired patients. Primary treatment is treatment of the PU itself, but acetaminophen may be helpful for mild to moderate pain. NSAIDs can also be effective but involve usual risks (eg, GI bleeding). Opioids should be avoided if possible because sedation promotes immobility, but short-acting opioids may be necessary before dressing changes and debridement.

Infection management: PUs should be continually reassessed for bacterial infection by looking for clinical signs of erythema, warmth, tenderness, increased drainage, and fever; elevated WBC count offers further evidence of infection. Systemic antibiotics should be given for cellulitis, bacteremia, or osteomyelitis, guided by tissue culture results or clinical suspicion and not by surface culture results. Topical antibiotics or antiseptics are indicated for heavily contaminated PUs containing multiple pathogens; options include silver sulfadiazine and metronidazole (the latter for anaerobic bacteria, which often cause foul-smelling PUs).

Topical antibiotics that are common allergens (eg, bacitracin, neomycin) or antibiotics that are used systemically (eg, gentamicin, tobramycin) should be avoided. Many topical antiseptics (eg, chlorhydroxide, hydrogen peroxide, povidone iodine) promote cellular toxicity and can injure granulation tissue. Antimicrobial agents such as nanocrystalline silver have been combined with dressings and are effective against a broad range of aerobic, anaerobic, and gram-negative and gram-positive bacteria. Cadexomer iodine dressings release low concentrations of iodine into the wound, have broad-spectrum antibacterial activity, and are nontoxic to granulation tissue.

Monitoring: Continuously evaluating existing PUs for signs of healing is mandatory for effective management. The PU scale for healing (PUSH) measures healing by evaluating changes in PU size, amount of exudate, and types of tissue in the wound; serial photographs can also document healing. The PUSH, developed by the National Pressure Ulcer Advisory Panel (NPUAP), is available from NPUAP. Inability to heal may be due to inadequate treatment but should also raise suspicion of underlying osteomyelitis or, rarely, squamous cell carcinoma within the PU (Marjolin's ulcer).

Adjuncts: 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: Large wounds, especially those with exposed muscles and bones, may require surgical closure. Skin grafts are useful for large, shallow wounds. However, because skin grafts do not add to blood supply, measures must be taken to prevent pressure from causing ischemia and further breakdown. Myocutaneous flaps are the closures of choice for large bony prominences (eg, sacrum, ischia, trochanters) because of their pressure-sharing bulk and rich blood supply and because they are reliable barriers to infection. Extensive stage 4 PUs may require multiple procedures to establish closure.

Postoperative care includes monitoring the patient for infection and keeping pressure off the flap site. Patients who have undergone flap procedures should be placed on an air-fluidized or low-air-loss mattress (see Table 124-3) for 2 wk and gradually increase periods of time sitting or lying on the flap to increase its tolerance to pressure. Recurrence rates for PUs after surgical repair are an estimated 13 to 56%, so daily monitoring with attention to PU risk factors and prevention strategies is crucial.

Patient and Caregiver Issues

Providers should educate elderly high-risk patients and their caregivers about PUs and teach skills to prevent and manage skin breakdown. Both patients and caregivers should learn to examine high-risk sites daily, note any areas of redness over bony prominences, use assistive devices effectively, and know how to clean and dress wounds. Caregivers should also learn how to turn and position bedbound patients every 2 h by following a written turning schedule or kitchen timer.

This topic was last updated April 2006.