* This is the Professional Version. *
- Symptoms and Signs
- Key Points
- Resources In This Article
- Drugs Mentioned In This Article
(Pressure Sores; Bedsores; Decubitus Ulcers; Decubiti)
Pressure ulcers (PUs) are areas of necrosis and ulceration where tissues are compressed between bony prominences and hard surfaces. They are caused by pressure in combination with friction, shearing forces, and moisture. Risk factors include age > 65, impaired circulation, immobilization, undernutrition, and incontinence. Severity ranges from nonblanchable skin erythema to full-thickness skin loss with extensive soft-tissue necrosis. Diagnosis is clinical. Prognosis is excellent for early-stage ulcers; neglected and late-stage ulcers pose risk of serious infection and are difficult to heal. Treatment includes pressure reduction, avoidance of friction and shearing forces, and diligent wound care. Sometimes, skin grafts or myocutaneous flaps are needed to facilitate healing.
Between 1993 and 2006, the number of hospitalized patients with PUs increased by > 75%, a rate over 5 times the increase of hospital admissions overall. The rate increased most in patients who developed PUs during hospitalization. Today, an estimated 1.3 to 3 million patients in the US have PUs, resulting in a significant financial burden to patients and health care institutions.
Risk factors for PUs include the following:
Age > 65 (possibly due to reduced subcutaneous fat and capillary blood flow)
Decreased mobility (eg, due to prolonged hospital stay, bed rest, spinal cord injury, sedation, weakness that decreases spontaneous movement, and/or cognitive impairment)
Exposure to skin irritants (eg, due to incontinence)
Impaired capacity for wound healing (eg, due to undernutrition, diabetes, peripheral arterial disease, and/or venous insufficiency)
Several scales (see Braden scale for predicting risk for pressure ulcers.and see The Norton Scale for Predicting Pressure Ulcer Risk*) have been developed to predict risk. Although use of these scales is considered standard care, they have not been shown to result in fewer PUs than skilled clinical assessment alone. Therefore, use of a risk assessment scale along with skilled clinical assessment is recommended.
Braden scale for predicting risk for pressure ulcers.
The Norton Scale for Predicting Pressure Ulcer Risk*
The main factors contributing to PUs are
Pressure: When soft tissues are compressed between bony prominences and contact surfaces, microvascular occlusion with tissue ischemia and hypoxia occurs; if compression is not relieved, a PU can develop in 3 to 4 h. This most commonly occurs over the sacrum, ischial tuberosities, trochanters, malleoli, and heels, but PUs can develop anywhere.
Friction: Friction (rubbing against clothing or bedding) can help trigger skin ulceration by causing local erosion and breaks in the epidermis and superficial dermis.
Shearing forces: Shearing forces (eg, when a patient is placed on an incline) stress and damage supporting tissues by causing forces of muscles and subcutaneous tissues that are drawn down by gravity to oppose the more superficial tissues that remain in contact with external surfaces. Shearing forces contribute to PUs but are not direct causes.
Moisture: Moisture (eg, perspiration, incontinence) leads to tissue breakdown and maceration, which can initiate or worsen PUs.
Because muscle is more susceptible to ischemia with compression than skin, muscle ischemia and necrosis may underlie PUs resulting from prolonged compression.
PUs at any stage may be painful or pruritic but may not be noticed by patients with blunted awareness or sensation.
Several staging systems exist. The most widely used system, developed by the National Pressure Ulcer Advisory Panel (NPUAP), classifies ulcers according to the depth of soft-tissue damage.
Stage I PUs manifest as nonblanchable erythema, usually over a bony prominence. Color changes may not be as visible in darkly pigmented skin. The lesion may also be warmer, cooler, firmer, softer, or more tender than adjacent or contralateral tissue. This stage is a misnomer in the sense that an actual ulcer (a defect of skin into the dermis) is not yet present. However, ulceration will occur if the course is not arrested and reversed.
Stage II PUs manifest as a loss of epidermis (erosion) with or without true ulceration (defect beyond the level of the epidermis); subcutaneous tissue is not exposed. The ulcer is shallow with a pink to red base. Stage II also includes intact or partially ruptured blisters secondary to pressure. (Note: Non–pressure-related causes of erosion, ulceration, or blistering, such as skin tears, tape burns, maceration, and excoriation, are excluded from stage II.)
Stage III PUs manifest as full-thickness loss without underlying muscle or bone exposure.
Stage IV PUs manifest as full-thickness loss with exposure of underlying bone, tendon, or muscle.
Unstageable PUs are those covered with debris or eschar, which does not allow assessment of depth. Stable, nonfluctuant heel lesions with dry eschar should never be debrided for the sake of staging.
Suspected deep tissue injury is a newer category of findings that suggest damage to underlying tissue. Findings include purple to maroon areas of intact skin, and blood-filled vesicles or bullae. The area may feel firmer, boggier, warmer, or cooler compared with surrounding tissue.
PUs do not always present as stage I and then progress to higher stages. Sometimes, the first sign of a PU is a deep, necrotic stage III or IV ulcer. In a rapidly developing PU, subcutaneous tissue can become necrotic before the epidermis erodes. Thus, a small ulcer may in fact represent extensive subcutaneous necrosis and damage.
PUs are a reservoir for hospital-acquired antibiotic-resistant organisms. High bacteria counts within the wound can hinder tissue healing. If wound healing is delayed despite proper treatment, underlying osteomyelitis (present in up to 32% of patients) or rarely squamous cell carcinoma within the ulcer (Marjolin ulcer) should be considered. Other local complications of nonhealing PUs include sinus tracts, which can be superficial or connect the ulcer to deep adjacent structures (eg, sinus tracts from a sacral ulcer to the bowel), cellulitis, and tissue calcification. Systemic or metastatic infectious complications can include bacteremia, meningitis, and endocarditis.
Diagnosis is based on clinical evaluation. Ulcers caused by arterial and venous insufficiency or diabetic neuropathy may mimic PUs, particularly on the lower extremities, and can also be worsened by the same forces that cause or worsen PUs.
Depth and extent of PUs can be difficult to determine. Serial staging and photography of wounds is essential for monitoring ulcer progression or healing. Many healing scales are available. The PUSH scale, designed as a companion to the NPUAP staging scale, has been adopted by many institutions. (See Pressure Ulcer Scale for Healing (PUSH) .)
Routine wound culture is not recommended because all PUs are heavily colonized by bacteria.
A nutritional assessment is recommended in patients with PUs, particularly those with stage III or IV PUs. Recommended tests include Hct, transferrin, prealbumin, albumin, and total and CD4+ lymphocyte counts. Undernutrition requires further evaluation and treatment (see Undernutrition).
Nonhealing ulcers may be due to inadequate treatment but should raise suspicion of a complication. Tenderness, erythema of surrounding skin, exudate, or foul odor suggests an underlying infection. Fever and leukocytosis should raise suspicion of cellulitis, bacteremia, or underlying osteomyelitis. If osteomyelitis is suspected, CBC, blood cultures, and ESR or C-reactive protein is recommended. Osteomyelitis is confirmed ideally by bone biopsy and culture, but this is not always feasible. Imaging tests lack the combination of high sensitivity and specificity. MRI is sensitive but not specific and can help define the extent of PU spread. MRI with gadolinium can help identify draining or communicating sinus tracts.
Prognosis for early-stage PUs is excellent with timely, appropriate treatment, but healing typically requires weeks. After 6 mo of treatment, > 70% of stage II PUs, 50% of stage III PUs, and 30% of stage IV PUs resolve. PUs often develop in patients who are receiving suboptimal care. If care cannot be improved, long-term outcome is poor, even if short-term wound healing is accomplished.
Reducing tissue pressure is accomplished through careful positioning of the patient, protective devices, and use of support surfaces.
Frequent repositioning (and selection of the proper position) is most important. A written schedule should be used to direct and document repositioning. Bedbound patients should be turned a minimum of every 2 h and should be placed at a 30° angle to the mattress when on their side (lateral decubitus) to avoid direct trochanteric pressure. Elevation of the head of the bed should be minimal to avoid the effects of shearing forces. When repositioning patients, lifting devices (eg, a Stryker frame) or bed linen should be used instead of dragging patients to avoid unnecessary friction. Patients placed in chairs should be repositioned every hour and encouraged to change position on their own every 15 min.
Protective padding such as pillows, foam wedges, and heel protectors can be placed between the knees, ankles, and heels when patients are supine or on their side. 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. They are often combined with other measures when treating PUs.
Support surfaces are classified based on whether they require electricity to operate. Static surfaces do not require electricity, whereas dynamic surfaces do. Although dynamic surfaces are usually recommended for more severe PUs, no conclusive evidence favors dynamic over static surfaces.
Static surfaces include air, foam, gel, and water overlays and mattresses. Egg-crate mattresses offer no advantage. In general, static surfaces increase surface support area and decrease pressure and shearing forces. Static surfaces have traditionally been used for PU prevention or stage I PUs.
Dynamic surfaces include alternating-air mattresses, low-air-loss mattresses, and air-fluidized mattresses. 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 I PUs who develop hyperemia on static surfaces and for patients with stage III or IV PUs. Air-fluidized (high-air-loss) mattresses contain silicone-coated beads that liquefy when air is pumped through the bed. Advantages include reduction of moisture and cooling. These mattresses are indicated for patients with nonhealing stages III and IV PUs or numerous truncal ulcers (see Options for Support Surfaces).
Options for Support Surfaces
Appropriate ulcer care involves cleaning, debridement, and dressings.
Cleaning should be done initially and with each dressing change. Normal saline is usually the best choice. Cleaning often involves irrigation at pressures sufficient to remove bacteria without traumatizing tissue; commercial syringes, squeeze bottles, or electrically pressurized systems can be used. Irrigation may also help remove necrotic tissue (debridement). Alternatively, a 35-mL syringe and an 18-gauge IV catheter can be used. Irrigation should continue until no further debris can be loosened. Antiseptics (iodine, hydrogen peroxide) and antiseptic washes can destroy healthy granulation tissue and thus should be avoided.
Debridement is necessary to remove necrotic tissue. Necrotic tissue serves as a medium for bacterial growth and blocks normal wound healing. Methods include
Mechanical debridement: This method includes hydrotherapy (whirlpool baths) and most commonly wet-to-dry dressings. Cleaning wounds by irrigation at sufficient pressures can also accomplish mechanical debridement. Mechanical debridement removes necrotic debris on the wound’s surface and should only be done on wounds with very loose exudate. Wet-to-dry dressings must be used cautiously because changing them is often painful and may remove underlying healthy granulation tissue.
Sharp (surgical) debridement: This method involves using a sterile scalpel or scissors to remove eschar and thick necrosis. Modest amounts of eschar or tissue can be debrided at the patient’s bedside, but extensive or deep areas (eg, if underlying bone, tendon, or joints are exposed) should be debrided in the operating room. Sharp debridement should be done urgently for advancing cellulitis or lesions suspected of causing sepsis.
Autolytic debridement: Synthetic occlusive (hydrocolloids/hydrogels) or semi-occlusive (transparent film) dressings are used to facilitate the digestion of dead tissues by the enzymes already normally present in the wound. Autolytic debridement may be used for smaller wounds with little exudate. This method should not be used if a wound infection is suspected.
Enzymatic debridement: This technique (using collagenase, papain, fibrinolysin, deoxyribonuclease, or streptokinase/streptodornase) can be used for patients with mild fibrotic or necrotic tissue within the ulcer. It can also be used for patients whose caretakers are not trained to do mechanical debridement or for patients unable to tolerate surgery. It is most effective after careful and judicious cross-hatching of the wound with a scalpel to improve penetration.
Biosurgery: Medical maggot therapy is useful for selectively removing dead necrotic tissue. This method is most helpful in patients who have exposed bone, tendons, and joints in the wound where sharp debridement is contraindicated.
Dressings are helpful for protecting the wound and facilitating the healing process (see Options for Pressure Ulcer Dressings).
Dressings should be used for stage I PUs that are subject to friction or incontinence and for all other PUs (see Options for Pressure Ulcer Dressings). In stage I PUs subject to increased friction, transparent films are sufficient. For PUs with minimal exudate, transparent films or hydrogels, which are cross-linked polymer dressings that come in sheets or gels, are used to protect the wound from infection and create a moist environment. Transparent films or hydrogels should be changed every 3 to 7 days. Hydrocolloids, which combine gelatin, pectin, and carboxymethylcellulose in the form of wafers and powders, are indicated for PUs with light-to-moderate exudate and must be changed every 3 days. Alginates (polysaccharide seaweed derivatives containing alginic acid), which come as pads, ropes, and ribbons, are indicated for absorbing extensive exudate and for controlling bleeding after surgical debridement. Alginates can be placed for up to 7 days but must be changed earlier if they become saturated. Foam dressings can be used in wounds with various levels of exudate and provide a moist environment for wound healing. Foam dressings must be changed every 3 to 4 days. Waterproof versions protect the skin from incontinence.
Options for Pressure Ulcer Dressings
PUs can cause significant pain. Pain should be monitored regularly using a pain scale. Primary treatment of pain is treatment of the PU itself, but an NSAID or acetaminophen is useful for mild-to-moderate pain. Opioids should be avoided, if possible, because sedation promotes immobility. However, opioids or topical nonopioid preparations such as mixtures of local anesthetics may be necessary during dressing changes and debridement. In cognitively impaired patients, changes in vital signs can be used as indicators of pain.
PUs should be continually assessed for signs of bacterial infection such as increased erythema, foul odor, warmth, drainage, fever, and elevated WBC count. Impaired wound healing should also raise concern of infection. These abnormal findings indicate a wound culture should be done. However, because all PUs are colonized, results should be interpreted with caution; bacterial count rather than bacterial presence should guide treatment.
Local wound infection can be treated topically with agents such as silver sulfadiazine, mupirocin, polymyxin B, and metronidazole. Silver sulfadiazine and similar opaque topical agents should be used cautiously because they can impair visualization of the underlying wound and can be difficult to remove. A 2-wk trial of topical antibiotics for all clean PUs that do not heal despite 2 to 4 wk of proper PU treatment is recommended. Systemic antibiotics should be given for cellulitis, bacteremia, or osteomyelitis; usage should be guided by tissue culture, blood culture, or both or clinical suspicion and not by surface culture.
Undernutrition is common among patients with PUs and is a risk factor for delayed healing. Markers of undernutrition include albumin < 3.5 mg/dL or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day, sometimes requiring oral, nasogastric, or parenteral supplementation, is desirable for optimal healing. Current evidence does not support supplementing vitamins or calories in patients who have no signs of nutritional deficiency.
Multiple adjunctive therapies are being tried to promote PU healing:
Negative-pressure therapy: Negative-pressure therapy (vacuum-assisted closure, or VAC) applies suction to the wound. It can be applied to clean wounds. High-quality evidence of efficacy does not yet exist, but negative-pressure therapy has shown some promise in small studies.
Topical recombinant growth factors: Some evidence suggests that topical recombinant growth factors (eg, nerve growth factor, platelet-derived growth factor) and skin equivalents facilitate wound healing.
Electrical stimulation therapy: Electrical stimulation therapy combined with standard wound therapy can increase wound healing.
Therapeutic ultrasonography: Ultrasonography is sometimes used, but there is no good evidence of benefit or harm.
Electrical magnetic, heat, massage, and hyperbaric O2 therapies: No evidence supports efficacy of these treatments.
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 (usually the sacrum, ischia, and trochanters). Surgery may rapidly improve the quality of life in patients with PUs. Surgical outcomes are best if preceded by optimal treatment of undernutrition and comorbid disorders.
Patient risk should be estimated based on the assessment of skilled clinicians and use of risk assessment scales (see Braden scale for predicting risk for pressure ulcers.and see The Norton Scale for Predicting Pressure Ulcer Risk*).
Treatment and prevention overlap considerably. The mainstay of prevention is frequent repositioning. Pressure should not continue over any bony surface for > 2 h. Patients who cannot move themselves must be repositioned and cushioned with pillows. Patients must be turned even when they are laying on low-pressure mattresses. Pressure points should be checked for erythema or trauma at least once per day under adequate lighting. Patients and family members must be taught a routine of daily visual inspection and palpation of sites for potential ulcer formation.
Daily attention to hygiene and dryness is necessary to prevent maceration and secondary infection. Protective padding, pillows, or sheepskin can be used to separate body surfaces. Bedding and clothing should be changed frequently. In incontinent patients, ulcers should be protected from contamination; synthetic dressings can help. 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. Use of adhesive tape should be minimized, because it can irritate and even tear fragile skin. Areas subject to friction may be powdered with plain talc. Use of cornstarch is discouraged because it may allow microbial growth.
Most importantly, immobilization should be avoided. Sedatives should be minimized, and patients should be mobilized as quickly and safely as possible.
PUs can develop secondary to immobilization and hospitalization, particularly in patients who are elderly, incontinent, or undernourished.
Base risk of PUs on standardized scales as well as the assessment of skilled clinicians.
PUs are staged according to ulcer depth, but tissue damage may be deeper and more severe than is evident from the physical examination.
Assess patients with PUs for local wound infection (sometimes manifesting as failure to heal), sinus tracts, cellulitis, bacteremic spread (eg, with endocarditis or meningitis), osteomyelitis, and undernutrition.
Treat and help prevent PUs by reducing skin pressure, repositioning frequently, and using protective padding and support surfaces that can be dynamic (powered electrically) or static (not powered electrically).
Clean and dress PUs frequently to reduce bacterial counts and facilitate wound healing.
Apply transparent films or hydrogels (if exudate is minimal), hydrocolloids (if exudate is light to moderate), alginates (if exudate is extensive), or foam dressings (for various amounts of exudate).
Treat pain with analgesics, local wound infection with topical antibiotics, and cellulitis or systemic infections with systemic antibiotics.
Surgically close large defects, especially those with exposed musculoskeletal structures.
Optimize nutritional status and treatment of comorbid disorders before surgery.
Help prevent PUs in patients at risk with meticulous wound care, pressure reduction, and avoiding any unnecessary immobilization.
Drug NameSelect Trade
sulfadiazineNo US brand name
* This is the Professional Version. *