Pressure injuries are areas of necrosis and often ulceration (also called pressure ulcers) where soft tissues are compressed between bony prominences and external hard surfaces. They are caused by unrelieved mechanical pressure in combination with friction, shearing forces, and moisture. Risk factors include age > 65, impaired circulation and tissue perfusion, immobilization, undernutrition, decreased sensation, 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 injuries; neglected and late-stage injuries 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. Show Between 1993 and 2006, the number of hospitalized patients with pressure ulcers increased by > 75%, a rate over 5 times the increase of hospital admissions overall, and particularly affects older people. The rate increased most in patients who developed pressure ulcers during hospitalization. An estimated 2.5 million cases of pressure ulcers are treated each year in acute care settings in the US, resulting in an annual cost estimated to be up to $17.8 billion in the US alone. Globally, pressure ulcers caused 24,400 deaths in 2019. Pressure injury is terminology recommended by the National Pressure Injury Advisory Panel (NPIAP) instead of "pressure ulcer" to describe these chronic wounds because lesser degrees of skin damage due to pressure may not be associated with skin ulceration. Risk factors for pressure injury include the following:
Pressure injury has also been reported in children with severe neurologic impairments such as spina bifida, cerebral palsy, and spinal cord injury. Several scales (see table The Norton Scale for Predicting Pressure Ulcer
Risk The Norton Scale for Predicting Pressure Ulcer Risk*  The main factors contributing to pressure injuries are
Because muscle is more susceptible to ischemia with compression than skin, muscle ischemia and necrosis may underlie pressure injuries resulting from prolonged compression. Symptoms and SignsPressure injuries at any stage may be painful or pruritic but may not be noticed by patients with blunted awareness or sensation. Staging systemsSeveral staging systems exist. The most widely used system is from the National
Pressure Injury Advisory Panel (NPIAP), which classifies pressure injuries into four stages (1 to 4) according to the extent of soft-tissue damage. However, the numerical staging does not imply linear progression of pressure injuries. That is, pressure injuries do not always manifest as stage 1 and then progress to higher stages. Sometimes, the first sign is a deep, necrotic stage 3 or 4 injury. In a rapidly developing pressure injury, subcutaneous tissue can become necrotic before the epidermis
erodes. Thus, a small injury may in fact represent extensive subcutaneous necrosis and damage. Similarly, the scale does not imply that healing progresses from stage 4 through stage 1. The updated NPIAP staging system also includes definitions for unstageable, deep-tissue, medical device-related, and mucosal membrane pressure injuries
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Staging definition reference Pressure injuries are areas of necrosis and often ulceration (also called pressure ulcers) where soft tissues are compressed between bony prominences and external hard surfaces. They are caused... read more Stage 1 pressure injuries manifest as intact skin with 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. 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 2 pressure injuries are characterized by partial-thickness skin, with loss of epidermis (erosion or blister) with or without true ulceration (defect beyond the level of the epidermis); subcutaneous tissue is not exposed. The injury is shallow with a pink to red base. No slough or necrotic tissue is present in the base. Stage 2 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 2.) Stage 3 pressure injuries manifest as full-thickness skin loss with damage to subcutaneous tissue extending down to (but not including) the underlying fascia. The ulcers are crater-like without underlying muscle or bone exposure. Stage 4 pressure injuries manifest as full-thickness skin loss with extensive destruction, tissue necrosis, and damage to the underlying muscle, tendon, bone, or other exposed supporting structures. When estimating the depth of pressure injuries for purposes of staging, it is important to take into account the anatomical location, especially in the case of stage 3 injuries. For example, the bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue and, consequently, pressure injuries in those locations will be very shallow. However, they are still graded as stage 3 because they are as significant as deeper stage 3 injuries over locations with significant subcutaneous tissue (eg, the sacral region). Unstageable pressure injuries are characterized by full-thickness skin and tissue loss in which the extent of tissue damage cannot be determined because it is obscured by debris, slough, or eschar. If the slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed. However, stable, nonfluctuant lesions with dry eschar should never be debrided for the sake of staging. Deep-tissue pressure injury is characterized by intact or nonintact skin with a localized area of damage to underlying tissue due to pressure and/or shearing forces. Findings include persistent, nonblanchable, purple to maroon discoloration of intact skin, and blood-filled vesicles or bullae. The area may feel firmer, boggier, warmer, or cooler compared with surrounding tissue. In this context, the term deep-tissue pressure injury should not be used to describe underlying vascular, traumatic, neuropathic, or dermatologic conditions. Medical device–related pressure injury results from the use of devices designed and applied for therapeutic purposes (eg, casts, splints). Prolonged use of poorly placed, ill-fitted medical devices can cause pressure injury to skin or mucosal membranes. Injury typically conforms to the pattern or shape of the device. The injury should be staged using the staging system. Medical device–related pressure injury has been extended to include injury caused by personal protective equipment (PPE), including face masks, continuous positive airway pressure (CPAP) masks, and other devices that are used to prevent or manage COVID-19 COVID-19 COVID-19 is an acute, sometimes severe, respiratory illness caused by the novel coronavirus SARS-CoV-2. Prevention is by vaccination, infection control precautions (eg, face masks, handwashing... read more . Examples of device-related pressure injury include moisture-associated skin damage (MASD) and skin tears. Mucosal membrane pressure injury appears on mucous membranes where medical devices have been in use (eg, misfitting dentures, endotracheal tubes). Because of the anatomy of the tissue, these injuries cannot be staged. Staging definition reference
Pressure injuries are a reservoir for hospital-acquired antibiotic-resistant microorganisms. High bacteria
counts within the wound can hinder tissue healing. Infections are the most common complications of pressure injury. Infections include cellulitis
Osteomyelitis Osteomyelitis is inflammation and destruction of bone caused by bacteria, mycobacteria, or fungi. Common symptoms are localized bone pain and tenderness with constitutional symptoms (in acute... read more
Other local complications of nonhealing pressure injury include sinus tracts, which can be superficial or connect a pressure ulcer to deep adjacent structures (eg, sinus tracts from a sacral ulcer to the bowel)
and tissue calcification. Systemic or metastatic infectious complications can include bacteremia
Bacteremia Bacteremia is the presence of bacteria in the bloodstream. It can occur spontaneously, during certain tissue infections, with use of indwelling genitourinary or IV catheters, or after dental... read more ,
meningitis Overview of Meningitis
Meningitis is inflammation of the meninges and subarachnoid space. It may result from infections, other disorders, or reactions to drugs. Severity and acuity vary. Findings typically include... read more , and
endocarditis
Infective Endocarditis Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci or staphylococci) or fungi. It may cause fever, heart murmurs, petechiae, anemia, embolic... read more
Diagnosis of pressure injury is based on clinical evaluation. A pressure injury is typically identified by its characteristic appearance and by its location over a bony prominence. The sacrum is the most common location, followed by the heels. Injuries caused by arterial and venous insufficiency or diabetic neuropathy may mimic pressure injuries, particularly on the lower extremities, and can also be worsened by the same forces that cause or worsen pressure injuries. Depth and extent of pressure injuries can be difficult to determine. Serial staging and photography of wounds is essential for monitoring injury progression or healing. Many healing scales are available. The Pressure Ulcer Scale for Healing (PUSH), designed as a companion to the NPIAP staging scale, has been adopted by many institutions. Routine wound culture is not recommended because all pressure injuries are heavily colonized by bacteria. Nonhealing injuries 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, complete blood count, blood cultures, and erythrocyte sedimentation rate 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 pressure injury spread. MRI with gadolinium can help identify draining or communicating sinus tracts. Prognosis for early-stage pressure injuries is excellent with timely, appropriate treatment, but healing typically requires weeks. After 6 months of treatment, > 70% of stage 2 pressure injuries, 50% of stage 3 injuries, and 30% of stage 4 injuries resolve. Pressure injuries often develop in patients who are receiving suboptimal care and/or have significant disorders that impair wound healing (eg, diabetes, undernutrition, peripheral arterial disease). If care of the injury and management of concurrent disorders cannot be improved, long-term outcome is poor, even if short-term wound healing is accomplished.
(See also the American College of Physicians' guidelines for preventing and treating pressure ulcers.) 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. Patients confined to a bed should be turned a minimum of every 2 hours 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 minutes. 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 patients confined to a bed can be changed to reduce pressure. They are often combined with other measures when treating pressure injuries. 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 pressure injuries, 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 pressure injury prevention or stage 1 pressure injuries. Dynamic surfaces include alternating-air mattresses, low-air-loss mattresses, and air-fluidized mattresses. In addition to reducing pressure, some mattresses increase the area of support, reduce heat and promote cooling, and decrease shear. 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 1 pressure injuries who develop hyperemia on static surfaces and for patients with stage 3 or 4 pressure injuries. 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 3 and 4 pressure injuries or numerous truncal injuries ( see Table: Options for Support
Surfaces Options for Support Surfaces Friction reduction using barrier protectants such as petroleum jelly has been shown to reduce the friction caused by personal protective equipment by 25% immediately after application. However, frequent reapplication (every hour) is necessary to maintain the protective effect. Appropriate wound 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
In stage 1 pressure injuries subject to increased friction, transparent films are sufficient. For injuries 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 pressure injuries 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 protective environment for wound healing. Foam dressings must be changed every 3 to 4 days. Waterproof versions protect the skin from incontinence. Pressure injuries can cause significant pain. Pain should be monitored regularly using a pain scale. Primary treatment of pain is treatment of the injury itself, but a nonsteroidal anti-inflammatory drug 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. Pressure injuries should be continually assessed for signs of bacterial infection such as increased erythema, foul odor, warmth, drainage, fever, and elevated white blood cell count. Impaired wound healing should also raise concern of infection. These abnormal findings indicate a wound culture should be done. However, because all pressure ulcers 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-week trial of topical antibiotics for all clean pressure injuries that do not heal despite 2 to 4 weeks of proper treatment is recommended. Narrow-spectrum 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. Limiting the use of broad-spectrum antibiotics is important to help prevent adverse effects and to help prevent inducing bacterial resistance and disrupting the skin and gut microflora. Undernutrition is common among patients with pressure injuries and is a risk factor for delayed healing. Markers of undernutrition include albumin < 3.5 g/dL (< 35 g/L) 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 healing:
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 pressure injuries. Surgical outcomes are best if preceded by optimal treatment of undernutrition and comorbid disorders. Prevention requires
Treatment and prevention overlap considerably. The mainstay of prevention is frequent repositioning. Pressure should not continue over any bony surface for > 2 hours. Patients who cannot move themselves must be repositioned and cushioned with pillows. Patients must be turned even when they are lying 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 injury 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, injuries 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.
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Click here for Patient Education What lab tests are done for pressure ulcers?Laboratory Studies. A complete blood count (CBC) with differential may show an elevated white blood cell (WBC) count indicative of inflammation or invasive infection. ... . Imaging Studies. A diagnosis of underlying osteomyelitis can be evaluated first with plain films. ... . Biopsy. ... . Histologic Findings.. What labs do you monitor for wounds?Important parameters to evaluate include protein levels, complete blood count, erythrocyte sedimentation rate, liver function tests, glucose and iron levels, total lymphocyte count, blood urea nitrogen and creatinine levels, lipoprotein levels, vitamin and mineral levels, and urinalysis.
What observation should be reported about a pressure ulcer?To identify a stage I pressure ulcer, compare the suspected area to an adjacent area or to the same region on the other side of the body. Indications of a stage I pressure ulcer include differences in skin temperature (warmth or coolness), tissue consistency (firm), and sensation (pain).
How is decubitus ulcer diagnosed?Diagnosis of a Decubitus Ulcer
Medical personnel may take samples of the pressure ulcer tissue and fluid to look for bacteria or cancer. They may also do blood cultures, bone scans or other tests depending on the seriousness of the ulcer.
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A patient has developed a decubitus ulcer. what laboratory data would be important to gather
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