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ESSENTIALS OF DIAGNOSIS
A skin ulcer caused by ischemia due to prolonged pressure or pressure in combination with shear and/or friction.
Occur on weight bearing or bony prominences (eg, sacrum, hip, heel).
Differentiate from ulcers caused by venous or arterial insufficiency.
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Extrinsic and intrinsic factors cause pressure ulcers. Extrinsic factors are prolonged pressure, moisture, friction, and shear. Intrinsic causes are the susceptibility of aged skin (less thickness and elasticity), loss of sensation, circulatory compromise, immobility, weight loss, dehydration, malnutrition, and cognitive impairment including sedation.
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When admitting a patient to acute or long-term care, document the condition of the occiput, spinous processes, scapulae, elbows, sacrum, ischia, greater trochanters, malleoli, and heels. Extra vigilance is needed in cognitively or sensorially impaired elders who wear support stockings, casts, or other orthopedic devices. These should be removed for inspection when possible. The admitting nurse will also do a complete skin assessment; the physician should review, verify, and document concurrence with the findings. Table 41-2 summarizes the AHRQ (Agency for Healthcare Research and Quality) guidelines for pressure ulcer prevention. Screening scales such as Braden and Norton help quantify risk and tailor treatment plans. The downside to these scales is the misconception that low- and moderate-risk patients are not as vulnerable; it takes them 2 hours to develop a stage I ulcer, the same as the high-risk patient. Although never studied, patient repositioning every 2 hours remains a mainstay in clinical practice.
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Differential Diagnosis
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Among the differential diagnoses for pressure ulcers are vascular ulcers, diabetic ulcers, and cellulitis. Venous ulcers are the result of prolonged venous hypertension and are usually located over the medial malleolus. Arterial ulcers are predominantly caused by atherosclerotic vessels, and may be located between toes, over phalangeal heads, or around the lateral malleolus. Diabetic ulcers are produced by a variety of factors: micro- and macrovascular injury, peripheral neuropathy, and mechanical changes in the bony architecture of the foot. These are usually located on the plantar aspect of the foot, metatarsal heads, or under the heel. Cellulitis is an acute inflammation of the dermis and subcutaneous tissue and thus blanches with palpation.
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The National Pressure Ulcer Advisory Panel (NPUAP) Classification
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Stage I ulcers are characterized by intact skin with nonblanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones and may indicate “at risk” persons (a heralding sign of risk).
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Preventive efforts should be intensified. Transparent films like Op-site or Tegaderm can be used; they provide barrier, prevent contamination, and reduce friction. The wound should be pressure-free. Donut cushions and bunny boots worsen ulcers. Use foam or gel overlay for beds or chairs, and inflatable heel elevators to protect feet. Compared with standard hospital mattresses, these devices decrease the incidence of ulcers. For a stage I, use group 1 support surfaces. (A good description of support surfaces can be found at www.wocn.org/pdfs/WOCN_Library/Fact_Sheets/medicare_part_b.pdf.)
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Stage II is characterized by partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. It may also present as an intact or open/ruptured serum-filled blister, or as a shiny or dry shallow ulcer without slough or bruising. (Bruising indicates suspected deep-tissue injury.) This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation.
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Cleansing around the wound with cleanser rather than normal saline has been shown to promote healing in stage II–IV ulcers, with stage II gaining the greatest benefit in healing time. Normal saline is fine if cleanser is not available. Do not use old favorites such as hydrogen peroxide, povidone-iodine (Betadine), liquid detergent, acetic acid, or hypochlorite solutions. Even when diluted, they are potentially toxic to both fibroblasts and white blood cells. Occlusive or semipermeable dressing that will maintain a moist wound environment should be used after cleansing. Hydrogel alone (Intrasite, Solosite) or hydrogel sheets (eg, NuGel) or hydrogel-impregnated gauze (eg, Normlgel) are appropriate. Wet/dry dressing should be avoided, as these ulcers need little debridement. If the wound is exudating, then use a dressing that will absorb the exudate such as alginate (Sorbsan or Aquacel) or NaCl-impregnated gauze (Mesalt.). If multiple stage II ulcers develop while patient is on a group 1 surface for ≥1 month, consider a group II device. Seventy-five percent of stage II ulcers will heal in 8 weeks.
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Stage III is characterized by full-thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. This stage may include undermining and tunneling. The depth of a stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable.
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Use a sterile Q-tip while examining in order to document tunneling. Do not use this to culture the wound; it will not yield reliable results, as it is not a sterile culture. If necrotic tissue or slough is present, sharp debridement is the best management. Exceptions are heel ulcers, thrombocytopenia, or patient refusal. Other methods of debridement are pulse lavage, whirlpool, wet to dry dressings (NaCl-impregnated gauze several times daily), chemical debridement (Santyl), or autolytic debridement via an occlusive dressing (Duoderm). Occlusive dressings are good for eschar attached to intact skin; once separated, it is more easily debrided mechanically or chemically. Combinations are also effective: Santyl with pulse lavage is an example.
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Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. This stage often includes undermining and tunneling.
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As in stage III, the depth of a stage IV pressure ulcer varies by anatomical location. Stage IV ulcers can extend into muscle and/or supporting structures (eg, fascia, tendon, or joint capsule), which could result in osteomyelitis. Exposed bone/tendon is visible or directly palpable.
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These are bad wounds; only 62% ever heal, and only 52% heal within 1 year. They should be managed as in stage III. If after 14 days there is no sign of healing, consider infection; see appropriate management under the section on treatment, later.
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Two other stages are grouped with stage IV because of their similar severity levels.
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Ulcers characterized by full-thickness tissue loss, in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed, cannot be staged.
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Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed.
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F. Suspected Deep-Tissue Injury
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A purple or maroon localized area of discolored intact skin or a blood-filled blister may indicate damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. Deep-tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment.
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The most common complications are cellulitis, osteomyelitis, and sepsis. If local erythema of ≥1 cm occurs around the wound, topical antibiotics such as mupirocin should be used. If the erythema is rapidly expanding, with heat, edema, or induration, the patient should be treated for cellulitis with systemic antibiotics. Use local susceptibility patterns to guide therapy. If the patient exhibits systemic symptoms, such as fever, rigors, delirium, or leukocytosis, draw blood cultures and obtain a sterile wound culture by needle aspiration or punch biopsy. We recommend consulting infectious disease specialists if any infection is suspected. Update tetanus immunity.
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Osteomyelitis is another complication and should be suspected in painful and nonhealing ulcers and whenever bone is visible. The 99mTc bone scan and magnetic resonance imaging (MRI) have equal sensitivity. CT has good specificity, poor sensitivity. Needle biopsy of bone is the most useful single test, with a sensitivity of 73% and a specificity of 96%.
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Sepsis is a serious consequence of infected pressure ulcers and a frequent cause of death, with mortality rates as high as 48%.
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We recommend a team approach once a stage 1 ulcer is identified. The wound should be checked daily and documentation of healing performed weekly. A tool to document healing has been developed by the NPUAP. The pressure ulcer status for healing (PUSH) tool measures three components—size, exudate amount, and tissue type. This tool has been validated, has good inter-rater reliability, and is sensitive to change over time.
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Enlist the care of a wound team. A physical therapist will mobilize the patient. Unless contraindicated, no elder should be on bed rest. An occupational therapist can assist with positioning for safety and recommend devices to minimize pressure. A wound nurse will document and often photograph the wound, and will recommend appropriate dressings and support surfaces.
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Nutrition is essential to healing. A dietician will assist with protein, calorie, and water recommendations as well as nutritional deficiencies. A BMI of <19, with >5% weight loss in 30 days or >10% loss in 180 days, and a serum albumin of <3.5 g/dL suggest malnutrition. Daily administration of 30–40 kcal/kg body weight, 1.2–1.5 g protein/kg body weight, and minimum fluid intake of 30 mL/kg body weight is recommended for at-risk patients. Those with ulcers are in a catabolic state and will require a more intensive and tailored approach by a clinical dietician. While supplements of vitamin C and zinc are commonly recommended, there is no evidence that they enhance wound healing unless the patient is deficient. Zinc at 100 mg daily can cause nausea and vomiting. A speech therapist and oral surgeon/dentist should be involved as needed.
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Urinary and fecal incontinence must be managed on a case-by-case basis. The risk of Foley catheter urinary tract infection must be weighed against the projected benefit of a dry wound site. Fecal incontinence can cause skin breakdown and impair healing. Toilet ambulatory patients frequently, manage diarrhea, and use containment devices when necessary.
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Attend to pain management: both physical and psychic. Patient dignity should be valued and respected. While use of sedation is associated with significantly increased risk of ulcers, pain from them must be addressed. This is especially important before dressing changes. Topical narcotics may be effective and have the added advantage of minimal systemic absorption, sedation, and constipation.
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B. Alternative Therapies
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As of 2013 no benefits have been established for a number of therapies in the frail elderly, including platelet-derived growth factors, therapeutic ultrasound, electromagnetic therapy, nutritional supplements, hyperbaric oxygen, infrared, UV, low energy, laser irradiation, and most recently, honey.
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C. Cultural Considerations
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Some studies have shown higher incidence and severity of pressure ulcers in the African American and Native American populations. Postulated contributing factors are dark skin color and economic factors.
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Caring for a patient with pressure ulcers is demanding. It is likely that the patient who develops a pressure ulcer has significant comorbidities that necessitate palliative treatment and, in fact, may indicate imminent end of life. Direct caregivers to resources such as AAA, Home Health, and support groups.
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For chronically or terminally ill patients with longstanding or recurrent ulceration, aggressive treatment may not be beneficial. Under these circumstances, maintaining patient comfort should be the primary goal rather than instituting major invasive procedures.
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Berlowitz
D Prevention and treatment of pressure ulcers.
UpToDate (available at
www.uptodate.com; accessed April 14, 2010; last updated Feb.2013).