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. Treatment includes pressure reduction, avoidance of friction and shearing forces, and diligent wound care. Advanced treatments, including negative-pressure wound therapy, cellular and tissue-based products, and surgical intervention, are sometimes needed. Prognosis is excellent for early-stage injuries; neglected and late-stage injuries pose risk of serious infection and are difficult to heal.
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 older adults in particular were affected. The rate increased most in patients who developed pressure ulcers during hospitalization.
Pressure injuries affect up to 3 million adults in the United States annually, with a prevalence among hospitalized patients of 5% to 15%, with the percentage considerably higher in some long-term care environments and intensive care units (1).
"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.
Reference
1. Mervis JS, Phillips TJ. Pressure ulcers: Pathophysiology, epidemiology, risk factors, and presentation. J Am Acad Dermatol 81(4):881-890, 2019. doi: 10.1016/j.jaad.2018.12.069
Etiology of Pressure Injuries
Risk factors for pressure injury include the following:
Age > 65 (possibly due to reduced subcutaneous fat, reduced capillary blood flow, and other age-related degenerative changes in skin) (1)
Decreased mobility (eg, due to prolonged hospital stay, bed rest, coma, spinal cord injury, sedation, weakness that decreases spontaneous movement, and/or cognitive impairment)
Exposure to skin irritants (eg, due to urinary incontinence and/or fecal incontinence)
Impaired capacity for wound healing (eg, due to undernutrition; diabetes; impaired tissue perfusion due to peripheral arterial disease; immobility; venous insufficiency)
Impaired sensation
Pressure injury has also been reported in children with severe neurologic impairments such as spina bifida, cerebral palsy, and spinal cord injury.
Several scales (eg, The Norton Scale for Predicting Pressure Ulcer Risk, the Braden Scale) have been developed to predict risk. The Norton Scale is used to determine whether a patient is at high risk of pressure ulcer development based on the sum of the scores of five criteria: physical condition, mental condition, activity, mobility, and incontinence. The Braden scale is used to assess risk based on the sum of the scores of six categories: sensory perception, moisture, activity, mobility, nutrition, and friction/shear (2). Although use of these scales is considered standard care, they have not been shown to result in fewer pressure injuries than skilled clinical assessment alone. Nevertheless, use of a risk assessment scale along with skilled clinical assessment is recommended.
Etiology references
1. Farage MA, Miller KW, Elsner P, Maibach HI: Characteristics of the aging skin. Adv Wound Care (New Rochelle) 2(1):5–10, 2013. doi: 10.1089/wound.2011.0356
2. Bergstrom N, Braden BJ, Laguzza A, Holman V: The Braden scale for predicting pressure sore risk. Nurs Res 36(4):205–210, 1987.
Pathophysiology of Pressure Injuries
The main factors contributing to pressure injuries are
Pressure: When soft tissues are compressed for prolonged periods between bony prominences and external surfaces, microvascular occlusion with tissue ischemia and hypoxia occurs. Pressures exceeding normal capillary pressure (range is 12 to 32 mm Hg) result in reduced oxygenation and compromise the microcirculation of the affected tissue. If compression is not relieved, a pressure injury can develop in 3 to 4 hours. This most commonly occurs over the sacrum, ischial tuberosities, trochanters, malleoli, and heels, but pressure injuries 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 inclined surface) 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 pressure injury but are not direct causes.
Moisture: Moisture (eg, perspiration, incontinence) leads to tissue breakdown and maceration, which can initiate or worsen pressure injuries.
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 Signs of Pressure Injuries
Pressure injuries at any stage may be painful or pruritic but may not be noticed by patients with blunted awareness or sensation.
Staging systems
Several 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 (1).
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 loss, 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 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 have minimal subcutaneous tissue and, consequently, pressure injuries in those locations are 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 is 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, oxygen tubing, and other devices that are used to prevent or manage respiratory conditions such as COPD or COVID-19. 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.
Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.
BOILERSHOT PHOTO/SCIENCE PHOTO LIBRARY
Roberto A. Penne-Casanova/SCIENCE PHOTO LIBRARY
DR BARRY SLAVEN/SCIENCE PHOTO LIBRARY
Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.
Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.
BOILERSHOT PHOTO/SCIENCE PHOTO LIBRARY
Roberto A. Penne-Casanova/SCIENCE PHOTO LIBRARY
DR BARRY SLAVEN/SCIENCE PHOTO LIBRARY
Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.
Pearls & Pitfalls
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Staging definition reference
1. Editors of Nursing2017: Pressure ulcers get new terminology and staging definitions. Nursing 47(3):68–69, 2017. doi: 10.1097/01.NURSE.0000512498.50808.2b
Complications of Pressure Injuries
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, abscess, infectious bursitis, infectious arthritis, and necrotizing fasciitis. 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 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 infectious complications can include bacteremia, meningitis, and endocarditis.
Diagnosis of Pressure Injuries
Clinical evaluation
Nutritional assessment
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 system, has been adopted by many institutions.
Routine wound culture is not recommended because all pressure injuries are heavily colonized by bacteria.
1). Undernutrition requires further evaluation and treatment.
Nonhealing wounds 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.
Diagnosis reference
1. Bharadwaj S, Ginoya S, Tandon P, et al: Malnutrition: Laboratory markers vs nutritional assessment. Gastroenterol Rep (Oxf) 4(4):272–280, 2016. doi: 10.1093/gastro/gow013
Treatment of Pressure Injuries
Pressure reduction
Direct wound care
Management of pain
Control of infection
Assessment of nutritional needs
Adjunctive therapy or surgery
Pressure reduction
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 and/or under 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).
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.
Direct wound care
Appropriate wound care involves cleaning, debridement, and dressings.
Cleaning
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 (eg, whirlpool baths, pulsatile lavage) 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. In wet-to-dry dressings, exudate and necrotic tissue adhere to a gauze dressing as it dries so that removal of the gauze thus debrides the wound; this method must be used cautiously because dressing changes are 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.
Autolytic debridement: Synthetic occlusive (hydrocolloids/hydrogels) dressings 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:
Biosurgery: Medical maggot therapy is useful for selectively removing dead necrotic tissue; maggots (fly larvae) eat only dead 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. They should be used for stage 1 pressure injuries that are subject to friction or incontinence and for all other pressure injuries (see table Options for Pressure Injury Dressings).
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 exudate and can be left in place for up to 1 week depending on the amount of drainage.
Alginates (polysaccharide seaweed derivatives containing alginic acid), which come as pads, ropes, ribbons, and hydrofiber dressings 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.
Management of pain
Pressure injuries can cause significant pain. Pain should be monitored regularly using a pain scale.
In cognitively impaired patients, changes in vital signs can be used as indicators of pain.
Control of infection
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.
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.
Assessment of nutritional needs
Current evidence does not support supplementing vitamins or calories in patients who have no signs of nutritional deficiency.
Adjunctive therapy
Multiple adjunctive therapies are being tried to promote healing:
Negative-pressure wound therapy (vacuum-assisted closure, or VAC): This therapy is used to apply suction to the wound. It can be applied to clean wounds. High-quality evidence of efficacy does not yet exist, but negative-pressure wound 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) facilitate wound healing.
Cellular and tissue-based products: Cellular and acellular matrices (ie, skin substitutes) have been used to treat a variety of chronic wounds and have been reported to show benefit in advanced pressure injuries, but evidence is preliminary and controlled trials are lacking.
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, phototherapy (laser) heat, massage, and hyperbaric oxygen therapies: No evidence supports efficacy of these treatments.
Surgery
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.
Skin flaps, including myocutaneous, fasciocutaneous, and perforator-based flaps, are preferred and are the closures of choice over large bony prominences (usually the sacrum, ischia, and trochanters) (1).
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.
Surgery reference
1. Sameem M, Au M, Wood T, et al: A systematic review of complication and recurrence rates of musculocutaneous, fasciocutaneous, and perforator-based flaps for treatment of pressure sores. Plast Reconstr Surg 130(1):67e–77e, 2012. doi: 10.1097/PRS.0b013e318254b19f
Prognosis for Pressure Injuries
Prognosis for early-stage pressure injuries is excellent with timely, appropriate treatment, but healing typically requires weeks. After 6 months of treatment, most stage 2 pressure injuries, about half of stage 3 injuries, and some 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.
Prevention of Pressure Injuries
Prevention requires
Identification of high-risk patients
Repositioning
Conscientious skin care and hygiene
Avoidance of immobilization
Patient risk should be estimated based on the assessment of skilled clinicians and use of risk assessment scales (eg, The Norton Scale for Predicting Pressure Ulcer Risk, the Braden Scale).
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.
Most importantly, immobilization should be avoided. Sedatives should be minimized, and patients should be mobilized as quickly and safely as possible.
Key Points
Pressure injuries can develop secondary to immobilization and hospitalization, particularly in patients who are elderly, incontinent, or undernourished.
Base the risk of pressure injury on a standardized scaling system as well as on the assessment of skilled clinicians.
Pressure injuries are staged according to depth, but tissue damage may be deeper and more severe than is evident from the physical examination.
Assess patients with pressure injuries 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 pressure injuries 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 wounds frequently to reduce bacterial counts and facilitate healing.
Apply transparent films or hydrogels (if exudate is minimal), hydrocolloids (if exudate is light to moderate), alginates or hydrofibers (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 narrow-spectrum systemic antibiotics.
Surgically close large defects, especially those with exposed musculoskeletal structures.
Optimize nutritional status and treatment of comorbid disorders before surgery.
Help prevent pressure injuries in at-risk patients with meticulous wound care, pressure reduction, and avoiding any unnecessary immobilization.
More Information
The following English-language resources may be useful. Please note that THE MANUAL is not responsible for the content of these resources.
American College of Physicians: Guidelines for risk assessment and prevention of pressure ulcers and treatment of pressure ulcers (2015)
Journal of the American Academy of Dermatology: Pressure ulcers: Prevention and management (2019)
National Pressure Injury Advisory Panel: Pressure Ulcer Scale for Healing (PUSH)
