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Pressure ulcers: A renewed awareness

BARANOSKI, SHARON RN, APN, CWOCN, MSN, FAAN

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All health care providers need to be involved in preventing and treating these problematic wounds. Here's what you need to know.

Wake up to what all nurses need to know about pressure ulcers. Read about evidence-based initiatives for preventing and managing these debilitating wounds to make sure you're meeting current patient-care standards.

Sharon Baranoski is director of acute care nursing at Provena St. Joseph Medical Center in Joliet, Ill.

The author has disclosed that she has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

PRESSURE ULCERS are costly to patients, their families, and health care facilities. Institutions can lose valuable staff time as well as their reputations. For patients, the toll of pain, infection and other complications, stress, delayed healing, and altered self-image is immeasurable.

Although pressure ulcers were once considered a nursing problem, all health care providers need to be responsible for preventing and treating them. This renewed awareness of the problem has led to several initiatives. The national health prevention program Healthy People 2010 has made one of its objectives to reduce pressure ulcers among nursing home residents. Evaluating patients for pressure ulcer risk on admission and regularly thereafter is among the practices endorsed by the private National Quality Forum to reduce adverse events. Facilities across the country, in collaboration with quality improvement agencies and the Centers for Medicare and Medicaid Services (CMS), are developing initiatives to address pressure ulcers. The National Pressure Ulcer Advisory Panel continues to research this growing concern.

In this article, I'll describe how pressure ulcers develop, how to assess and manage your patient, and steps you can take to help prevent pressure ulcers in high-risk patients.

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A decubitus by any other name…

A pressure ulcer—previously called a decubitus ulcer, pressure sore, or bedsore—is a wound caused by unrelieved pressure that damages underlying tissue. Low pressure sustained over long periods of time can be just as detrimental to tissue as high pressure for short periods. This pressure interferes with the tissue blood supply, leading to vascular compromise, tissue anoxia, and cell death. Body tissues differ in their ability to tolerate pressure, with muscle being more sensitive to pressure damage than skin.

Pressure ulcers usually are located over bony prominences, such as the sacrum, coccyx, hips, or heels. They can also develop in such often-overlooked areas as the occiput (especially in infants and toddlers), ears, and the great toe region. In acute care facilities, the most common site for pressure ulcers is the sacrum, with heels being second.

Many other factors are at play in the development of pressure ulcers. Extrinsic factors include moisture, friction, and irritants. Intrinsic factors include spinal cord injury, poor nutrition, and use of steroids, which affect collagen synthesis needed for wound healing. Intrinsic factors that affect tissue perfusion include low systemic blood pressure, low serum protein, smoking, low hemoglobin and hematocrit levels, vascular disease, diabetes, use of vasoactive drugs, and increased body temperature.

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How do pressure ulcers develop?

The etiology of pressure ulcers is still unclear. One well-accepted theory is that pressure ulcers begin from the bone and proceed outward. External pressure from the epidermis is transmitted inward toward the bone at the same time that counterpressure is produced from the bone, compressing the tissue and blood vessels in between. Deep tissue injury near the bone occurs first because muscle and subcutaneous fat have a low tolerance for decreased blood flow. Eventually damage reaches the outer layer of the skin (the epidermis); at this point, the skin shows evidence of injury. Destruction of tissue below the skin level isn't visible until surface damage is evident.

Another theory, known as the top-to-bottom model, postulates that skin destruction occurs first at the epidermis and proceeds downward to the deeper tissue layers.

Besides pressure, the mechanical forces of friction and shear contribute to pressure ulcer development. Shear and friction are separate phenomena that often work together to create tissue ischemia and damage to the epidermis and dermis. Tissue injury from these forces may look like a superficial skin insult.

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Pressure ulcer assessment

If your patient has a pressure ulcer, you'll need to clean it before you can assess it. Cleaning can remove devitalized tissue, letting you see the wound bed, and decreases the bacterial burden, which can delay healing. Use a cleaner that won't traumatize the ulcer; 0.9% sodium chloride solution is usually best because it won't damage healthy tissue.

Don't expect a pressure ulcer to heal unless you've effectively managed the underlying causes. Identify and treat diseases or health problems (such as urinary incontinence), nutritional deficits, psychological or emotional stress, and pain that may have placed the patient at risk for pressure ulcer development. Monitor for immobility and unrelieved pressure and intervene as appropriate. Using a pressure ulcer risk assessment tool such as the Braden scale can help you identify problems that need to be addressed. (The scale also suggests appropriate interventions based on the patient's score.)

Perform a comprehensive wound assessment. Document the ulcer's anatomic location and size (length, width, depth, and extent of any tunneling or undermining). Assess for drainage (type, amount, odor, color) and note the color of the ulcer and surrounding skin. Also document pressure-ulcer-related pain, using a pain-rating scale, and any previous treatments for the ulcer.

The next step is to stage the ulcer (see Staging pressure ulcers). You'll need to be able to see the wound bed to determine the stage. If the wound bed is covered with necrotic tissue, document it as “unstageable” if you're in acute care or a home health care setting, or as Stage IV if you're in long-term care. Document that you can't determine the ulcer depth.

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All about debridement

Necrotic tissue can promote pathogen growth and delay healing, so it should be removed. (An exception may be eschar or necrotic tissue on a heel ulcer because an open heel wound can easily become infected and lead to osteomyelitis.) Several debridement methods are available; the choice depends on the amount of necrotic tissue, absence or presence of infection, patient preferences, and economic considerations. Let's look at the five main debridement methods.

  • surgical (sharp) debridement, which involves cutting dead tissue away from the wound. Considered the fastest and most effective type of debridement, this method can be done at the bedside, in the surgical suite, or in the outpatient setting. Your state's nurse practice act may let you perform sharp debridement if you have special training. Surgical debridement should be considered when infection such as cellulitis or sepsis is suspected.
  • mechanical debridement, which uses force to remove necrotic tissue; for example with wet-to-dry gauze dressings, whirlpool treatments, or wound irrigation devices. Because this debridement method can damage healthy granulation tissue and delay healing, use it with caution.
  • autolytic debridement, which uses the body's own natural enzymes to digest necrotic tissue. To use this method, you'll cover the wound with a semiocclusive or occlusive moisture-retentive dressing. Enzymes in the wound liquefy the necrotic tissue, which is then digested by macrophages. Follow the dressing manufacturer's recommendations for when to change the dressing. Although relatively painless, this type of debridement takes longer than sharp debridement and isn't appropriate for infected wounds. Be sure to monitor the wound for signs and symptoms of infection.
  • enzymatic (chemical) debridement, which employs proteolytic enzymes to soften and loosen necrotic tissue from the wound bed. This form of debridement is slow but effective in many necrotic wounds and can be used with infected wounds. Check the manufacturer's guidelines before using enzymatic debridement; some enzymes are inactivated by certain wound cleaners or metallic compounds.
  • biologic debridement (maggot therapy), which places maggot larvae in the wound. Their proteolytic secretions break down necrotic tissue. The larvae ingest the microorganisms, destroying them. This therapy, popular in Europe, is gaining popularity in the United States.
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Managing pressure ulcers

Once your patient's pressure ulcer has been cleaned, debrided if necessary, staged, and documented, cover the ulcer with a moisture-retentive dressing that protects the ulcer and promotes healing. Hundreds of dressings in many types are available, so choose a dressing that matches wound bed characteristics. For example, use:

  • gauze for packing a wound
  • transparent films for uninfected wounds with little or no drainage
  • foams for deep wounds with moderate to heavy drainage
  • hydrocolloids for shallow wounds with moderate drainage
  • alginates for wounds with heavy drainage.

The next step is pressure redistribution. You can choose from among various support surfaces to redistribute or relieve pressure. Your goal is to keep existing pressure ulcers from worsening and prevent new ulcers from developing in high-risk patients.

The CMS divides support surfaces into these three categories for reimbursement purposes.

  • Group One devices don't require electricity. Besides redistributing pressure, they may decrease shearing and are relatively inexpensive. Examples include air, foam, gel, and water overlays or mattresses. A foam mattress or overlay should be more than 4 inches (10 cm) thick. These devices are ideal for a patient who's at low to moderate risk for pressure ulcers.
  • Group Two devices are dynamic powered devices, such as alternating air mattresses, and advanced nonpowered devices, such as low-air-loss mattresses. Alternating air mattresses may not reduce heat accumulation on the patient's body; low-air-loss mattresses reduce heat accumulation and moisture retention. These beds or mattresses are good for patients at moderate to high risk for pressure ulcers, those who have full-thickness or multiple pressure ulcers, and patients who've had flap or graft surgery.
  • Group Three consists only of air-fluidized beds, another dynamic device. Although these beds reduce heat accumulation and moisture retention, patients may have difficulty moving in them. They're used for patients at very high risk for pressure ulcers, those with nonhealing full-thickness pressure ulcers or numerous full-thickness truncal pressure ulcers, and those who've undergone flap or graft surgery.
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Fuel for healing

Often overlooked, nutrition is an important treatment element. Many patients with pressure ulcers are malnourished, and all patients need increased calories and protein stores to heal. Giving vitamin and mineral supplements, even to patients who don't have a deficiency, may also help pressure ulcer healing. If the patient can't meet his caloric needs through an oral diet, the clinician will consider enteral or parental nutrition. Consult with the dietitian and obtain a nutritional screening if needed.

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Controlling infection

All pressure ulcers become colonized with aerobic and anaerobic bacteria, so swab culturing the surface of a pressure ulcer isn't a reliable test for infection. Instead, express and culture fluid from the wound to identify microorganisms in the wound tissue. Signs and symptoms of infection in a pressure ulcer include fever, warmth, erythema, edema, pain, and purulent drainage. However, not all infected ulcers cause these signs and symptoms; some look like nonhealing ulcers.

Getting the infection under control is crucial to helping the ulcer heal. Generally, treatment consists of a week or two of oral antibiotic therapy (if a systemic infection is suspected) or therapy with topical agents such as silver sulfadiazine or silver antimicrobial dressings for a local infection. Some studies support cleaning an infected wound with 1% povidone-iodine solution to reduce the bacterial load and increase healing.

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Can I use reverse staging?

Using the staging system in reverse to monitor pressure ulcer healing isn't appropriate because it's inaccurate; the muscle and other tissue lost to a pressure ulcer isn't restored, but replaced by scar tissue. However, several instruments have been developed and validated to assess healing. The two most widely used tools are the Pressure Sore Status Tool (PSST, also called the Bates-Jensen Wound Assessment Tool) and the Pressure Ulcer Scale for Healing (PUSH).

The PSST comprises 13 variables, which provide a numeric indicator of ulcer status. The variables assessed include ulcer size and depth, type and amount of necrotic tissue, type and amount of exudate, color of periwound skin, and presence of granulation tissue and epithelization. This tool provides a comprehensive wound assessment and is being evaluated for use with other wound types.

The PUSH tool comprises three variables: surface area (length and width), exudate amount, and tissue appearance. The PUSH tool intentionally takes a minimalist approach, making it ideal for monitoring large groups of patients and for identifying patients whose wounds are deteriorating and who may need treatment changes. The tool doesn't provide a comprehensive wound assessment and hasn't been validated with other types of wounds.

Another way to measure wound healing is with high-frequency portable ultrasound, which can capture three-dimensional measurements and provide objective evidence of healing.

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Adjunctive therapies

The fastest growing area in pressure ulcer management involves adjunctive therapies, including the following treatments.

  • Electrical stimulation uses electrical current to stimulate cellular processes involved in wound healing. Use of this therapy is limited in clinical practice.
  • Hyperbaric oxygen therapy, in which oxygen is delivered at increased atmospheric pressure inside a special chamber, is believed to promote wound healing by stimulating fibroblasts, collagen synthesis, epithelization, and the body's inflammatory response to combat infection. This therapy also improves the blood's capacity to carry oxygen, thereby improving tissue oxygenation.
  • Cytokine or fibroblast growth factors and skin equivalents are emerging therapies for treating pressure ulcers, and their effectiveness is still being researched.
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P is for prevention

A good prevention program begins with assessing all patients for the risk of pressure ulcer development, followed by a complete body assessment. Once you have information on the patient's risk factors, you can develop a plan of care to address his specific needs. Here are some basic steps to take:

  • Assess the patient's skin daily in acute and long-term care settings or at each home health care visit. Document your findings. Teach him how to prevent skin injury during activities of daily living. For example, his bathing schedule should be individualized based on his age, skin texture, and whether his skin is dry or oily. He may not need a daily bath. He should use nondrying products to clean his skin, use tepid (not hot) water, and avoid excessive friction. After bathing, he should use a moisturizer that doesn't contain alcohol.
  • Protect the skin against irritation from incontinence by cleaning skin immediately after an episode of incontinence, then applying a moisture barrier or ointment. If the patient uses containment products, follow the correct methods of application. Determine the reason for incontinence and address the cause.
  • Protect bony prominences using dressings such as films, hydrocolloids, or foams. Don't massage red bony prominences; this can increase tissue damage. Keep the patient's heels off the bed. Use heel protection devices if appropriate. Pillows, wedges, and foot elevation devices can help you accomplish this. A folded bath blanket under the calves can “float the heels,” completely relieving heel pressure in a bedridden, immobile patient. For more information, see “Treating Heel Pressure Ulcers,” Wound andSkin Care, in the January issue of Nursing2005.
  • Be careful when repositioning or transferring your patient. Use appropriate devices such as a turn sheet or mechanical lifting device to prevent friction injuries to the patient's skin.
  • Watch for shear injuries. Unless contraindicated by the patient's condition, keep the head of the bed below 30 degrees to prevent shearing injuries; for example, from slipping down in bed.
  • Individualize the patient's repositioning schedule. Reposition chairbound patients every hour and encourage them to perform small shifts in weight every 15 minutes. Although turning and repositioning a bedridden patient every 2 hours is a standard of care, it may not be appropriate for all patients. For example, for some patients receiving palliative care, turning every 2 hours might cause more pain and discomfort than benefit. Conversely, some patients may need more frequent turning.
  • Make sure the patient's caloric, protein, and vitamin and mineral needs are met.
  • Consult physical and occupational therapists. They can help patients select appropriate-sized wheelchairs and evaluate their seating angles and postural alignment.
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Easing the burden

Awareness of the problems created by pressure ulcers has exploded across the country. A multidisciplinary approach to managing and preventing pressure ulcers can help health care providers and patients avoid the devastating consequences of these wounds.

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Staging pressure ulcers

Pressure ulcer staging is based on the depth and type of tissue damage. This system was developed by the National Pressure Ulcer Advisory Panel.

  • Stage I: Observable, pressure-related alteration of intact skin with one or more of the following local changes, compared with the adjacent or opposite area of the body: skin temperature (warmth or coolness), tissue consistency (firm or boggy feel), or sensation (pain or itching). The ulcer appears as a defined area, persistently red in light skin or red, blue, or purple in darker skin.
  • Stage II: Partial-thickness skin loss involving the epidermis, dermis, or both. The ulcer is superficial and looks like an abrasion, blister, or shallow crater.
  • Stage III: Full-thickness skin loss involving damage to or necrosis of subcutaneous tissue, which may extend down to, but not through, underlying fascia. The ulcer is a deep crater with or without undermining of adjacent tissue.
  • Stage IV: Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures (such as tendon or joint capsules). Undermining and sinus tracts may be present.
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SELECTED WEB SITES

Bates-Jensen Wound Assessment Tool

http://borun.medsch.ucla.edu/modules/Pressure_ulcer_prevention/puBWAT.pdf

National Pressure Ulcer Advisory Panel

http://www.npuap.org

Last accessed on July 3, 2006.

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SELECTED REFERENCES

Ayello EA, et al. TIME heals all wounds. Nursing2004. 34(4):36–42, April 2004.
    Cuddigan J, et al. (eds). National Pressure Ulcer Advisory Panel (NPUAP). Pressure Ulcers in America: Prevalence, Incidence and Implications for the Future. Reston, Va., NPUAP, 2001.
      Dyson M, Lyder C. Wound management—physical modalities. In Morison M (ed), The Prevention and Treatment of Pressure Ulcers. Edinburgh, United Kingdom, Harcourt Brace/Mosby International, 2001.
        Maklebust J, Sieggreen M. Pressure Ulcers: Guidelines forPrevention and Management, 3rd edition. Philadelphia, Pa., Lippincott Williams & Wilkins, 2001.

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