Focus on: Pressure ulcers
Adapted from PIER
Many situations can predispose a patient to develop a pressure ulcer that erupts a week after hospital admission. In-hospital care relies on recognizing even subtle signs, such as a small blister or discoloration that signals a deep tissue injury that suddenly becomes noticeable, said Eugenia L. Siegler, MD, a hospitalist and professor of clinical medicine at Weill Cornell Medical College in New York City.
"One phenomenon that we see is the incipient ulcer can be missed completely because the skin can look a little purplish or a little abnormal but there's no sign of anything going on underneath," she said. "Sometimes that little bit of blistering or change in color may seem benign, but it reflects a tremendous amount of inner injury to the connective tissue underneath, and a week later the whole area breaks down."
Teaching hospital staff to recognize these subtle signs relies on education and change through the facility. It's a matter not of neglect and blame, but of applying in-service training about preventive measures.
"If you have a ventilator-associated pneumonia, you know where to look," Dr. Siegler said. "If you have an early pressure ulcer, or deep tissue injury that's not easy to recognize, where do you begin? If we are really to reduce the incidence and severity of these wounds, you have to look everywhere from the moment the person gets sick."
Prevention and screening
Screen patients for pressure ulcers on admission to the hospital or nursing home and after a major change in condition (e.g., postoperatively or after a new stroke). Use a standard risk-assessment tool to stratify low- and high-risk patients, even though there is insufficient evidence for using one scale over another. Available scales include the Braden scale for Predicting Pressure Sore Risk and the Norton scale
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Pressure is highest over a bony prominence. Therefore, damage can occur in the deep tissues before it occurs in the more superficial layers. To relieve pressure over the bony prominences, such as the greater trochanter, sacrum, ischium and heel, turn and reposition bed-bound patients every two hours and patients in wheelchairs every hour. Leaning patients in wheelchairs forward with the chest toward the thighs affords greatest pressure relief over the ischial tuberosities. Significant pressure relief can also be achieved with a 65-degree backward tilt. No studies have rigorously documented how frequently high-risk patients need to be turned. After turning a patient or caring for incontinence, examine the trunk and heels. Pay special attention when examining darkly pigmented skin, which may obscure the color changes seen with early pressure damage.
Progression of a pressure ulcer. Illustration by Brian Evans/Photo Researchers Inc.
Subcutaneous pressure damage occurs when externally applied pressure exceeds capillary filling pressure (30 mm Hg) for more than two hours. Use pressure-relieving mattresses, mattress overlays or pads at all times for high-risk patients in hospitals and nursing homes unless contraindicated. Pressure-relieving mattresses and overlays disperse the pressure over bony prominences. Many mattresses and overlays have pressure profiles superior to those of standard hospital beds. Special padding, mattresses, cushions and beds may allow longer intervals in the turning schedule.
Use heel elevation to prevent heel and foot pressure ulcers in high-risk patients. Heel ulcers account for 10% to 20% of all ulcers in prospective incidence studies. Although there are some data to suggest that foam heel protectors actually increase pressure ulcer risk, use pressure-relieving mattresses for all high-risk patients. Reserve more expensive mechanical boot-like heel elevators for very high-risk patients, such as those with a leg cast or brace that is weighing down the leg.
Make sure that all staff involved in giving care in hospitals and nursing homes are trained frequently on the importance of preventive strategies for pressure ulcers. Identifying early tissue damage—bruising, hyperemia, erythema or minor ulcerations—facilitates early treatment. If a patient is cognizant, encourage him or her to remind the caregivers about timely turning and repositioning and the use of padding.
Although malnutrition may be a risk factor in the development of pressure ulcers, a recent Cochrane review concluded that it remains unclear whether nutritional interventions such as dietary supplements are effective in preventing or treating them.
Diagnosis
Use a standard staging method to describe pressure ulcers:
I—Nonblanchable erythema caused by extravasation of erythrocytes into the interstitium, without damage to deeper layers.
II—Ulceration that involves the epidermis and dermis; depth is no more than several millimeters; underlying tissue should appear normal.
III—Full-thickness ulcerations through the dermis; ulcerations can be extensive and deep and may involve subcutaneous fat; underlying tissue should appear normal.
IV—Ulcerations exposing muscle, tendon, or bone; stage IV heel ulcers can be only 4 to 5 mm deep; stage IV sacral ulcers in obese patients can be many centimeters deep.
Recent guidelines correctly highlight the difficulty of identifying stage I pressure ulcers in darkly pigmented persons (National Pressure Ulcer Advisory Panel [NPUAP], Stage I Assessment in Darkly Pigmented Skin, 1998). Unfortunately, these guidelines for stage I ulcers still allow for the inclusion of tissue consistency with a firm or boggy feel and ulcers that may appear with persistent red, blue or purple hues, which most likely represent deep tissue injury rather than superficial pressure damage. Thus, until new definitions are established based on an improved understanding of the natural history of pressure damage under intact skin, avoid assigning such lesions to stage I and simply describe them instead.
The stage of a pressure ulcer is associated with time needed for healing and with morbidity and mortality. Do not use existing staging systems if there are eschars, blisters or deep-tissue damage under intact skin. Eschars often are associated with full-thickness tissue damage, and debridement may reveal stage III or IV pressure ulcers.
Describe the lesion accordingly, and assign a stage only when the full extent of damage is apparent. Do not "reverse stage" by assigning lower stage numbers to stage III or IV pressure ulcers that are healing; NPUAP issued a Statement on Reverse Staging of Pressure Ulcers. Use validated tools instead to describe healing, such as the NPUAP 's Pressure Ulcer Scale for Healing (PUSH) and the Pressure Sore Status Tool.
Routine laboratory tests are limited in assessing the risk and prognosis associated with pressure ulcers. Do not do laboratory testing for patients with minor stage I or II pressure ulcers other than that related to any underlying illness.
Obtain blood cultures rather than a culture of the pressure ulcer to identify the cause of fever when bacteremia related to a pressure ulcer is suspected in an acutely ill patient. There are few indications for culturing a pressure ulcer; all pressure ulcers are colonized with bacteria and usually by multiple organisms. Cultures of pressure ulcers should be done only rarely as part of an infection-control surveillance program when screening for specific resistant organisms such as methicillin-resistant Staphylococcus aureus or vancomycin-resistant enterococci.
There are no rigorous studies on the use of nuclear medicine scans and radiographs to diagnose osteomyelitis, which occurs only rarely as a complication of stage IV pressure ulcers. False-positive nuclear bone scans are common because of inflammation of adjacent soft tissue. Pressure ulcers in which bone can be visualized usually heal without antibiotic treatment, but when osteomyelitis does occur, it requires months of antimicrobial therapy. Consider nuclear medicine scans and radiographs to identify osteomyelitis underlying pressure ulcers in the following situations:
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if fever or leukocytosis continues after the initial debridement and disinfection of necrotic stage IV ulcers,
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if healing ulcers exhibit ongoing purulent drainage, and/or
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if stage IV ulcers do not heal.
Differentiate between areas of pressure damage, such as heel ulcers or eschars, and other types of ulcers, such as arterial or venous insufficiency ulcers, which can occur in the same patient. Treatment must be directed at the underlying pathophysiology that caused the skin abnormality. Traumatic injuries, abscess cavities or dehisced surgical incisions are not related to pressure damage. An incorrect diagnosis may lead to inappropriate treatment.
Non-drug therapy
Eliminating pressure, maximizing treatment and offering nutritional support are common to the treatment of any ulcers.
Reducing the pressure between the body and support surface (interface pressure) below that of capillary perfusion pressure (30 mm Hg) decreases the incidence of new tissue damage and facilitates healing. Consider whether a patient requires a low-air-loss or air-fluidized bed, which minimizes pressure more effectively than conventional mattresses. A study in Annals of Internal Medicine showed that the estimated relative odds of showing improvement with air-fluidized beds were 5.6-fold (95% CI, 1.4-fold to 21.7-fold; P= 0.01) greater than with conventional therapy. A study in JAMA showed that low-air-loss beds were 2.5 times more likely to heal ulcers in a given length of time than were foam mattresses (combined cure probability ratio, 2.66 [95% CI, 1.34 to 5.17]; P< 0.004).
It remains unclear whether debridement hastens healing of pressure ulcers. However, most clinicians use enzymatic ointments to debride small amounts of necrotic material in the ulcer, reserving surgical debridement for more extensive necrosis. Necrosis retards wound healing and provides an environment that supports bacterial growth. Although there is insufficient evidence to promote the use of one debriding agent over another, wet-to-dry gauze dressings must be applied at least three times daily and cause more discomfort to the patient. Hydrogel significantly reduced necrotic wound area compared with dextranomer polysaccharide paste only in one study. Consider watchful waiting for dry, hard eschars on the heels if there are no signs of subcutaneous necrosis, but be prepared for urgent debridement if deeper necrosis or signs of infection develop.
Once the wound is adequately debrided, the goal is to maintain a clean moist wound bed to accelerate tissue repair. Use alginate, foams and other hydrophilic dressings for exudative wounds. If the wound is dry, use hydrogels or other wetting agents such as normal saline wet gauze dressings to maintain a moist wound bed. Hydrocolloid dressings can be used to moisten dry shallow ulcers and may be superior to other conventional moist dressings, which tend to dry out. Change to a protective-film dressing or petroleum gauze to reverse any hypergranulation. There are insufficient data to establish with certainty whether other types of advanced dressings have greater efficacy compared to conventional dressings.
Although it remains unclear whether oral protein and other types of nutritional supplements are effective in accelerating healing of pressure ulcers, tissue repair is a highly anabolic process, and most clinicians believe that it is important to maintain nutritional support in patients with underlying medical problems who remain at risk. Provide adequate calories to support metabolic demands, including increased calories for patients with large pressure ulcers. Use a multivitamin supplement in patients whose dietary intake is inadequate, but note that supratherapeutic doses of vitamins and minerals have not been shown to accelerate pressure ulcer healing.
Maximize functional status with restorative nursing and when appropriate initiate physical and occupational therapy, including walking programs and range-of-motion exercises, to maintain function and reduce the risk of contractures. Other treatments that might have efficacy for accelerating pressure ulcer healing are vacuum-assisted closure, electrical stimulation, hyperbaric oxygen, ultrasound and radiant heat. Biologic manipulation includes collagen dressings and growth factors. However, the evidence base supporting these strategies is scant.
Drug therapy
Base drug therapy on results of thorough patient assessment and on the status of the pressure ulcer.
Antiseptic dressings should be used cautiously and by experienced practitioners in patients with local symptoms and signs of pressure ulcer infection, low-grade fever and otherwise stable vital signs. Reexamine the pressure ulcer after 24 to 48 hours before continuing to use dressings. Avoid antiseptics that can retard granulation and inactivate enzymatic debriding ointments.
Antibiotic ointment or cream can be used under film or petroleum gauze dressings that protect superficial pressure ulcers undergoing epithelialization. Superficial dressings can prevent damage from friction, maintain a moist wound bed and prevent the dressing from sticking to the ulcer bed, while topical antibiotics may be useful in treating ulcers that are not making adequate progress toward healing. Expensive antibiotics are not more effective than less expensive alternatives.
Use intravenous antibiotics for patients with fever, hypotension or presumed bacteremia related to a pressure ulcer. Sepsis is probably most likely to occur in patients with closed abscesses associated with pressure ulcers, rather than in patients with large, open and even deep pressure ulcers. Broad-spectrum intravenous antibiotics are needed for polymicrobial sepsis caused by infected pressure ulcers.
Assess and treat pain in patients with pressure ulcers with mild analgesics (e.g., acetaminophen, acetaminophen with low doses of codeine), which usually provide adequate pain relief. Question cognizant patients about pain related to pressure ulcers. For patients with dementia or altered level of consciousness, question caregivers and be sensitive to nonverbal responses to treatment that might relate to pain.
Follow-up
Regularly evaluate and document the healing of each pressure ulcer:
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Evaluate pressure ulcers that are being debrided mechanically daily;
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Evaluate pressure ulcers that are being treated with astringent antiseptic dressings every 24 to 48 hours;
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Evaluate chronic ulcers at least weekly;
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Document objective assessments (e.g., location, dimensions, depth, and presence or absence of necrosis, granulation, epithelialization); and
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Document odor, purulence, drainage or erythema.
Confirm on an ongoing basis that the pressure ulcer treatment is appropriate to the stage of healing. Tailor treatment with a modality that addresses the therapeutic goal. Most of the hundreds of items that are marketed for pressure ulcer treatment can be categorized as debridants, antibacterials, protectants or substances that maintain a moist wound bed (e.g., hydrocolloids, hydrogels, alginates).
Give patients and family members a realistic prognosis about the length of time for pressure ulcer healing. Discuss the possibility of deterioration when deep tissue injuries are identified.
This information comes from the PIER module "Pressure Ulcers" (ACP membership required). The information included herein should never be used as a substitute for clinical judgment and does not represent an official position of ACP.
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