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  • Empiric evidence to guide the treatment of pressure injuries is limited. This requires clinicians to focus on critical components of management, including wound examination, documentation, and diagnosis, as well as understanding and implementing basic principles of wound care.

  • Pressure injuries are only one type of chronic wound seen in older adults. However, because of their association with the perception of quality, pressure injuries have become an important concern in regulatory, reimbursement, and risk-management arenas.

  • Pressure injuries have severe consequences, including increased length of stay, increased chance of readmission within 30 days of hospital discharge, prolonged rehabilitation, pain, disfigurement, infection, loss of limb, and death.

  • Risk assessment and risk factor intervention are key to pressure injury prevention. It is now accepted that nonmodifiable risk factors in many patients can lead to pressure injuries even when appropriate interventions are implemented.Many wounds have reduced or no chance of healing. For these wounds, palliative care principles may curtail suffering, improve quality of life, and decrease health care costs. When wounds are considered palliative, caregivers must reconsider expensive advanced wound care modalities and surgical procedures such as sharp debridements.

Pressure injuries are a common chronic wound in the geriatric population. Care of pressure injuries is interdisciplinary and involves nursing, nutrition, rehabilitation, and surgical subspecialties. Pressure injuries cause pain and are associated with a decreased quality of life, longer hospital stay, increased chance of readmission within 30 days after hospital discharge, increased chance of admission to a long-term care facility, and increased risk of death. Infectious complications include cellulitis, abscess, sepsis, pyarthrosis, and osteomyelitis. Pressure injuries often require surgical procedures ranging from sharp debridements to myocutaneous flaps, amputations, and ostomies for fecal diversion. According to the Agency for Healthcare Research and Quality, pressure injuries cost $9.1 to $11.6 billion per year, with the cost of individual patient care ranging from $20,900 to $151,700 per pressure ulcer. A vexing variety of treatments is available with few studies to prove efficacy of one over the other. The standard of care for pressure injuries is evolving, and all primary care providers need to be aware of prevention strategies, documentation standards, and treatment choices. These choices include a palliative care approach, which can avoid unnecessary and futile procedures, improve quality of life, and curtail health care costs.

Pressure injuries affect from 1.3 to 3 million adults in the United States, and their incidence and prevalence vary greatly depending on stage, setting, and how data are collected. In acute care, one study showed incidence ranging from 7% to 9% per year. Higher rates are consistently reported in older populations. Hospital prevalence rates range from 11.9% to 15.8%. In long-term care, prevalence ranges from 8.5% to 32.2%. In one study, up to 54.7% of terminally ill nursing-home residents had pressure injuries. The increase in pressure injury prevalence that occurred in the 20th century was largely a result of modern public health measures and advances in medical technology that resulted in longer life expectancy and greater numbers of people living with multiple chronic illnesses.

Pressure injuries are a designated quality measure in hospitals, long-term care, and home-care settings. As a result of their association with quality of care, pressure injuries have become a major risk management issue, and, according to the Agency for Healthcare Research and Quality, >17,000 lawsuits related to pressure injuries are filed annually. Pressure injury data for skilled-nursing facilities is currently published by CMS on the Nursing Home Compare Web site, but as yet there is no federal mandate for publication of pressure injury statistics for hospitals and home care. In addition, pressure injuries have been spotlighted in value-based purchasing and pay-for-performance initiatives. For example, in 2008 the CMS introduced a policy to decline payment to hospitals for certain hospital-acquired conditions that include stage 3 or 4 pressure injuries. These factors have resulted in an evolving standard of care that designates physicians as key players. Many hospitals and long-term care facilities require orders for wound care products, dressings, and devices to obtain Medicare reimbursement. Because pressure injuries are an identified geriatric syndrome, geriatrics providers with proper training can play a pivotal role in improving quality of care for this condition.

It has become increasingly recognized that many pressure injuries are unavoidable. Patients at severe risk with immobility and multiple chronic conditions, and patients who are dying, can develop pressure injuries even when standards of care for prevention are met. A pressure injury is therefore not necessarily indicative of poor quality care but rather may be a marker for disease severity or impending death. An expert panel (SCALE Panel 2009) assembled consensus statements about skin changes at life’s end that support the concept of unavoidable pressure injuries in patients who are actively dying. An extensive literature review and consensus study summarizing factors that lead to unavoidable pressure injuries was published. A key concept for understanding unavoidable pressure injuries is the nonmodifiable risk factor for which effective interventions cannot be implemented. The National Pressure Ulcer Advisory Panel (NPUAP) defines an unavoidable pressure injury as one that develops despite the provider having 1) evaluated the individual’s clinical condition and pressure injury risk factors; 2) defined and implemented interventions consistent with individual needs, goals, and recognized standards of practice; and 3) monitored and evaluated the impact of the interventions, revising the approaches as appropriate.

The skin is the largest organ of the body, and the concept of “skin failure” has been advanced to account for unavoidable pressure injuries in patients who are dying and other situations such as multiple organ system failure. Unlike other organ systems such as kidney, liver, and lung, there is currently no laboratory marker identifying skin failure. Although the concept of skin failure makes sense, universal agreement on its definition or clinical application has not yet been achieved.


Normal wound healing is a complex but orderly sequence of biologic events that includes hemostasis, inflammation, proliferation, and remodeling. Neutrophils are involved in the inflammatory phase, phagocytizing debris and microorganisms and providing a first line of defense. Macrophages play an important role in phagocytosis, debriding damaged tissue with proteases, creating granulation tissue, laying down extracellular matrix, and secreting chemotactic and growth factors. Granulation tissue consists of new blood vessels, fibroblasts, endothelial cells, myofibroblasts, and extracellular matrix. Fibroblasts produce collagen that increases the strength of the wound, plus other critical substances such as elastin, fibronectin, glycosaminoglycans, and proteases. Myofibroblasts, descended from fibroblasts, assist in contraction. Keratinocytes are the main cells responsible for epithelialization, the process of migrating across a bed of granulation tissue. Because of the disruption in normal anatomy and disorganization of new collagen, the tensile strength of a healed wound is only 50%–80% of that of undamaged skin.

Pressure injuries are one of a diverse group of lesions classified as chronic wounds. Chronic wounds share in common prolonged healing time and interference with normal wound healing that renders them stalled in the inflammatory and proliferative phases. The surface of a chronic wound often harbors an “antihealing environment” with elements that include biofilm, exudate that contains pro-inflammatory cytokines such as matrix metalloproteases and tumor necrosis factor alpha (TNF-α), and lack of pro-regenerative agents such as transforming growth factor (TGF-β), platelet-derived growth factor, and vascular endothelial growth factor.

Conditions leading to chronic wounds include repetitive trauma, decreased vascular perfusion, poor nutrition, poor oxygenation from anemia, diabetes or pulmonary disease, edema that interferes with nutrient delivery, pharmacologic barriers such as corticosteroids and immunosuppressants, incontinence, and biofilms. A biofilm is a community of microorganisms that secretes a mucilaginous extracellular coating that protects them from antibiotics and inhibits healing. These factors have greater impact on older adults, because they add to the processes of aging that include reduced fibroblasts, macrophages, and mast cells; loss of extracellular matrix components such as collagen and glycosaminoglycans; decreased amount and morphology of elastin; altered surface pH; reduced sebum secretion with decreased pilosebaceous units; and flattening of the dermal-epidermal junction.


A pressure injury is defined as localized damage to the skin and/or underlying tissue, usually over a bony prominence that results from pressure, or pressure in combination with shear. The current staging system defined by NPUAP is used only for pressure injuries (see Table 1). Staging of pressure injuries is determined by visible depth. If the base of the wound cannot be seen, the wound is determined as “unstageable.” A wound is designated a deep tissue pressure injury (DTPI) when the skin is intact and a purple bruise-like area is present in an area subjected to pressure. A DTPI can dissipate leaving intact skin, or it can evolve into a wound of varying severity. Stage 1 and DTPI can be difficult to assess in persons with dark skin, and examinations should be performed with adequate lighting and include palpation for detection of induration or warmth.

Table 1—National Pressure Ulcer Advisory Board Staging Criteria for Pressure Ulcers
Stage 1
Nonblanchable erythema
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, or warmer or cooler than adjacent tissue. May be difficult to detect in those with dark skin tones. May indicate “at risk” patients.
Stage 2
Partial thickness
Partial-thickness loss of skin presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured blister filled with serum or serosanguineous fluid. Presents as a shiny or dry shallow ulcer without slough or bruising (the latter indicates deep-tissue injury). This category should not be used to describe skin tears, tape burns, incontinence-associated dermatitis, maceration, or excoriation.
Stage 3
Full-thickness tissue loss
Full-thickness tissue loss; subcutaneous fat is visible, but bone, tendon, or muscle are not exposed/visible or directly palpable. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a Stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue, and Stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Stage 3 pressure ulcers.
Stage 4
Full-thickness tissue loss
Full-thickness tissue loss with exposed/visible bone, tendon, or muscle that is directly palpable. Slough or eschar may be present. Often includes undermining and tunneling. The depth of a Stage 4 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have (adipose) subcutaneous tissue, and these ulcers can be shallow. Stage 4 ulcers can extend into muscle and/or supporting structures (eg, fascia, tendon or joint capsule) making osteomyelitis or osteitis likely to develop.
Full-thickness skin or tissue loss, depth unknown
Full-thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and/or eschar are removed to expose the base of the wound, the true depth cannot be determined; but it will be either a Stage 3 or 4. 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.
Deep tissue pressure injury, depth unknown Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. May be preceded by tissue that is painful, firm, mushy, boggy, and warmer or cooler than adjacent tissue. May be difficult to detect in those 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.
© National Pressure Ulcer Advisory Panel, 2016

SOURCE: Adapted with permission of the National Pressure Ulcer Advisory Panel, 2018. The permission granted through this process cannot be transferred to others or used for other purposes than expressed above and approved by the NPUAP. ©NPUAP

The heel, the second most common site for pressure injuries after the sacrum, has unique anatomic features that warrant special consideration when evaluating an ulcer. These include thick skin, very little subcutaneous tissue and muscle, and vascular perfusion delivered around the large calcaneus bone that underlies the rear portion of the foot. The foot is also susceptible to circulatory impairment because of atheromatous disease of the leg, microvascular disease from diabetes mellitus, and decreased sensation from peripheral neuropathy of any etiology. Pressure injuries of the heels often present as blisters. A clear blister over a bony prominence is considered a stage 2 pressure injury, whereas a blood-filled blister is considered a DTPI.

Definitions and nomenclature for pressure injuries was recently modified by the NPUAP. The recommendation to change the term “pressure ulcer” to “pressure injury” has garnered controversy. Concerns include potential unintended consequences upon increased litigation risk as well as the burden of modifying CPT codes. For practical purposes, “pressure ulcer” and “pressure injury” are synonymous.


Pressure injuries must be detected early, because these wounds can usually heal quickly if discovered in early stages and treated properly. Alternatively, wounds can deteriorate quickly, particularly in patients with severe immobility in conjunction with multisystemic disease. As a result, timely examination and documentation is an important component of management. Consistent and complete documentation is required for coding and reimbursement, public reporting, risk management, and accurate transmittal of information as patients traverse the health care continuum. Providers should take the time to perform the examination rather than rely on others for the information. Proper wound evaluation can be time consuming, particularly in patients with multiple wounds. It often involves obtaining assistance with lifting or turning an immobile patient who may be in pain, and removing and replacing dressings. However, timely and thorough examination is mandatory for all patients with pressure injuries and will bring dividends in accurate documentation and improved decision making.

Wound documentation includes diagnosis, stage, location, length, width, depth, presence of odor and/or drainage, presence of undermining and tunneling, as well as characteristics of the wound bed, margin, and surrounding skin. Supplemental information can include warmth, capillary refill, and presence of pulses, edema, anasarca, and lymphedema. Measurement is an important component of wound assessment, particularly for determining the effectiveness of clinical interventions. Measurement involves head-to-toe length, width, and depth and should be both consistent and accurate. The simplest method uses a centimeter ruler to measure length and width, and a cotton-tipped swab to measure depth, tunneling, and undermining. Wound clinics and skilled-nursing facilities usually have structured documentation sheets with entry points for diagnosis, length, width, and depth, along with diagrams to designate location and undermining, as well as treatment in progress and response to treatment. If such structured documents are unavailable, it is advisable to describe the wound with as much detail as possible in narrative form.

Documentation of wound progression is an important component of management and should be ongoing, systematic, and consistent. Wounds should be formally assessed at least weekly, with descriptors that include measurements, nature of the wound bed and periwound area, pressure redistribution modalities, treatments in progress, and response to healing. Some authorities recommend a validated healing scale such as the Pressure Sore Status Tool or the Pressure Ulcer Scale for Healing. No single standard exists that mandates the type and extent of information to include in a wound assessment, but the more descriptors the better. Patients with pressure injuries frequently undergo transitions between locations within the health care continuum, and wounds should be thoroughly documented on both admission and discharge from hospitals and long-term care facilities. Similarly, initial home care visits should include thorough skin inspection. Reverse staging is not a recognized standard, because it does not accurately characterize the anatomic and physiologic process that occurs during healing.

Photographs can be valuable adjuncts to wound documentation; however, their implementation in a medical record must be consistent and within a formal policy and procedure guideline. Photographs must be of reasonable quality and accompanied by a label within the visual field that contains a patient identifier (name, initials, or medical record number), location of the wound, and date. Haphazard use of photographs or poor photographic technique can create discontinuities in documentation with risk-management implications. Providers who use personal cell phones to take photographs are committing potential HIPAA violations.


The standard of care for pressure injury prevention includes risk assessment followed by appropriate pressure redistribution interventions if the patient is deemed at risk.

Risk Assessment

There are many recognized risk factors for pressure injuries, and several validated instruments that quantify risk are available. The most widely used tool is the Braden Scale (www.in.gov/isdh/files/Braden_Scale.pdf), which combines sensory perception, moisture, activity, mobility, and friction and shear. This scale has been validated in home, skilled-nursing facilities, and hospital settings but not in ICUs. However, other studies have noted that risk assessment tools can be weak predictors of which patients are more likely to develop pressure injuries (SOE=B). Current scales also do not contain information related to organ system failure or physiologic factors such as hypoxia and hypotension, which may also engender increased pressure injury risk. Therefore, clinical judgment should be relied on to determine “at risk” status in addition to the formalized risk assessment scale.

Risk factors for pressure injuries can be classified as either extrinsic, intrinsic, or both. Immobility is a major risk factor that results from causes that are both external and internal to the patient. Nutritional compromise is a known risk factor for pressure injuries, and patients >75 years old with malnutrition and weight loss are 3.8 times more likely to develop pressure injuries.

Medical devices are increasingly recognized as causes of pressure ulceration. These include external devices such as tubing and orthopedic splints, casts, limb immobilizers, abdominal binders, and CPAP masks. Care plans for patients with external orthopedic devices should always include periodic skin assessment. Pressure injuries can develop over internally placed medical devices such as implantable neurostimulators and pain-control pumps that create new pressure points under the skin.

Skin assessment is an important component of prevention and should be done at least once per day for patients considered at risk in any setting. Areas of skin exposed to chronic moisture, over bony prominences, or under medical devices require special attention to detect early signs of impairment. Inspection of skin over bony prominences and under medical devices should be a routine part of the physician assessment, particularly on admission to the hospital or nursing home. Routine nursing care should include skin assessment, and skin should be cleansed with efforts to minimize both dryness and excessive moisture.

Moisture-associated skin damage (MASD) that occurs from perspiration, urine, diarrhea, fistulas, or wound exudate increases susceptibility to pressure injuries, and is a common occurrence in patients with constant loose stools from tube feeding or Clostridium difficile colitis. MASD involves more than simple maceration of skin, and contributors include mechanical factors such as friction, chemical irritants, and microbes, including bacteria and fungi. Strategies to avoid or treat MASD include moisture barrier creams, absorbable undergarments, continence care, and fecal and urinary diversion devices. Fungal infections require early diagnosis, because they can lead to impaired skin integrity if untreated. The diagnosis of fungal infection is sometimes missed because of the similarity in appearance to MASD, but close inspection of the border of redness and inflammation can reveal telltale satellite lesions characteristic of Candida albicans.

Prevention Strategies

There are many strategies for minimizing pressure, friction, and shear. Positioning devices such as pillows and foam wedges can help keep pressure off bony prominences, and lifting devices and draw sheets can minimize friction. Shear is a mechanical force that occurs when skin is pulled parallel to the body and is commonly caused by sitting up in bed. Backrest elevation of 30–45 degrees is associated with reduced risk of ventilator-associated pneumonia and aspiration related to tube feeding; however, sustained backrest elevation of >30 degrees is associated with increased pressure and shear to the lower back and buttocks. There is no current consensus as to how to balance the risks of pressure ulceration with minimizing the risks of ventilator-associated pneumonia and aspiration.

The industry standard for turning and positioning is every 2 hours, but there is minimal research to support this schedule (SOE=C). In addition, this standard was developed before the advent of advanced mattress and continence care technology. Research challenges the need for every-2-hour repositioning for patients using high-density foam mattresses (SOE=B). Patients who sit for long periods of time in chairs should be assessed for proper posture and alignment and provided with pressure relief schedules and cushioning. Strategies for preventing heel wounds include local skin care, cushioning, and lifting the heels off the mattress by placing a pillow under the legs when supine, also called “floating the heels” (SOE=B).

NPUAP defines “support surface” as a specialized device designed for management of tissue loads, microclimate, and/or other therapeutic needs. There are a large variety of support surface technologies and features. Mattress overlays go between the mattress and the patient and are more commonly used in rehabilitation facilities and home environments. A mattress replacement is a device placed in the bed frame that generally uses the low air-loss (LAL) technology; such a support surface provides a flow of air for managing skin microclimate, including heat and humidity.

Surfaces designed to prevent pressure injuries are defined by “immersion” and “envelopment.” Immersion refers to the depth that a mechanical load sinks, and envelopment is the characteristic that takes the shape of the applied load. The combination of immersion and envelopment gives the protective effect against pressure injuries. An alternating pressure air mattress does not use these characteristics, but rather “force redistribution” by taking a load from one place to another and allowing reperfusion of the previously loaded area, thereby preventing pressure injuries. Other advanced features of the specialized bed include pulsations for pulmonary toilet, multizoned surfaces, and lateral rotation. The evidence to guide surface choices is conflicting regarding efficacy at preventing pressure injuries, and efforts are underway by the NPUAP to standardize testing and measure outcomes objectively.


A holistic, patient-centered approach to pressure injury treatment involves assessing the overall health status of the patient, addressing psychosocial needs, treating underlying comorbidities, assessing and correcting causes of tissue damage, and assessing and monitoring the wound. It is essential to understand the patient’s functional and cognitive status, home environment, family support, and other factors such as the presence of depression. Wound assessment entails examination and description as discussed above, along with proper documentation. If the wound is an alteration in skin or tissue integrity over a bony prominence, it is most likely a pressure injury and staged in accordance with NPUAP criteria. Local malignancy must be considered in any chronic wound with consideration of biopsy, and all wounds should be assessed for infection (discussed below). Elements of pressure injury treatment involve offloading and pressure redistribution strategies, removing debris and necrotic tissue, and addressing moisture balance. Finally, the clinician must address pain, acknowledge advance directives, and be able to recognize wounds appropriate for a palliative approach and alter the plan accordingly.

Laboratory tests provide important information regarding the patient’s health and ability to heal. Anemia contributes to decreased oxygen delivery to vulnerable or healing tissue. Nutritional status as reflected in serum albumin and prealbumin levels can impair wound healing, but these laboratory tests are unreliable in the presence of inflammation and are losing their status as nutritional indicators. Increases in WBC count, erythrocyte sedimentation rate, or C-reactive protein may indicate ongoing infection or inflammation. The clinician must be aware of endocrinopathies such as hypothyroidism and poorly controlled diabetes mellitus. For wounds of the lower extremity, tests such as ankle-brachial index (ABI), pulse volume recording, and Doppler ultrasound can assist in evaluating arterial supply. ABI loses diagnostic value when arteries are noncompressible because of advanced atherosclerotic disease.

Numerous wound products are available, and the lack of controlled clinical trials and reliable measures of efficacy can make choosing an appropriate treatment bewildering. The lack of research is partially attributable to the FDA classification of most wound care products as medical devices (as opposed to pharmaceuticals), which exempts manufacturers from the requirement to demonstrate efficacy. As for all chronic wounds, correction of underlying factors leading to the chronic ulcer formation is more important than choice of topical dressing. With little evidence-based support for individual treatments, choices are often made based on product availability, insurance coverage, personal preference, cost considerations, expert opinion, and intrinsic rationale for product type. Table 2 presents some commonly used treatment modalities along with rationale for each (SOE=C).

Table 2—Common Wound Treatment Modalities

Best Use
Cotton, polyester, or other fabrics
Versatile, can be absorptive or protective, primary or secondary dressing
Secondary dressing, wet to moist, or wet to dry, or as a protective to the wound and surrounding skin. Note: wet to dry is not recommended.
Adhesive pad with moisture-activated, gel-forming material; gelatin and pectin
Moisture retention
Superficial, clean pressure ulcers with no necrosis or infection
Semipermeable films
Transparent polymer with acrylic adhesive
Moisture retention
Superficial, clean pressure ulcers with no necrosis or infection
Water in a delivery vehicle such as glycerin or cross-linked polymer sheets
Promote moist wound healing and autolytic debridement
Dry wounds; wounds with some necrosis
Polyurethane with or without adhesive borders
Absorb exudate, cushioning, secondary dressing
Control of exudate, protect the wound
Seaweed derivative; can be in different forms, including sheet or rope, and combined with other materials such as silver or charcoal
Absorptive dressing
Control of exudate
Animal-derived collagen formulated into gel, powder, paste, or sheet
Deactivates matrix metalloproteases that inhibit wound healing
Partial- or full-thickness wounds with minimal necrosis
Silver-containing dressings
Silver can be impregnated into multiple types of dressings
Silver has broad-spectrum antimicrobial activity
Wounds requiring control of bacterial balance
Enzymatic debriding agent
Enzyme in a petrolatum vehicle
Selected degradation of denatured collagen
Wounds with necrosis and slough
Cadexomer iodine dressing
Iodophor in a polysaccharide polymer
Absorbent, antimicrobial
Wounds with slough, infected wounds
Silicone dressings
Inert silicone polymer; sometimes has pores that allow passage of exudate
Contact layer that can be removed without causing trauma to wound or surrounding skin
When a nonadherent dressing is required, protects the wound and surrounding skin
Activated charcoal
Combined with silver or other vehicles
Control odor
Palliative wounds with odor
Medicinal grade honey can be used as a gel or impregnated into other dressing types
Antimicrobial properties, anti-inflammatory
Autolytic debriding agent on noninfected wounds
Topical antiseptics
Includes hydrogen peroxide, Dakin solution (hypochlorite), povidone-iodine
Reduce bacterial burden of wounds
Can be cytotoxic to healing wounds; for limited use in heavily contaminated or nonhealable wounds
Petrolatum-impregnated gauze
Woven mesh; medical petrolatum and 3% bismuth tribromophenate
Bacteriostatic, nonadherent, retains moisture
Use with larger wounds with minimal necrosis and slough

Wound bed preparation has emerged as a useful tool to conceptually organize the array of wound products in a manner that achieves maximal benefit for chronic wounds such as pressure injuries. Wound bed preparation focuses on critical components of management, including moisture and exudate, bacterial balance, and debridement. The foundation of this concept is an orderly approach to accelerate endogenous healing and facilitate the effectiveness of therapeutic measures. The goal is to reestablish the balance of growth factors, cytokines, proteases, and their natural inhibitors as found in acute wounds, thereby stimulating the healing process.

Moisture balance is an important component of wound healing, because a moist environment promotes autolytic debridement and encourages matrix formation. Alternatively, excess moisture inhibits wound healing through maceration that impairs both the wound bed and periwound area. Several products promote moist wound healing such as hydrocolloids, hydrogels, and other bio-occlusives. The exudate of chronic wounds contains heightened proteolytic activity, matrix metalloproteases, and macromolecules that inhibit growth factors, and products such as foams, hydrofibers, and alginates provide absorptive capabilities. Collagen-containing products inactivate harmful cytokines and factors that inhibit healing.

Bacterial balance in the wound bed is facilitated by cleansing, topical antibiotics, disinfectants, and debridement. Debridement removes necrotic tissue and bacteria, providing a clean surface that promotes healing. Debridement can be achieved by several ways, and selection should be individualized in accordance with goals of care and degree of necrosis. Autolytic debridement uses moisture-retentive topical dressings to take advantage of endogenous enzymes present in the wound, whereas enzymatic debridement uses a commercially produced enzyme to digest debris and dead tissue. Mechanical debridement methods include hydrotherapy (whirlpool), irrigation (pulsed lavage), and scraping the wound base and periwound area with a blunt instrument. Wet-to-dry or wet-to-moist gauze dressings are discouraged because of their nonselective nature in removing both debris and healthy granulation tissue.

Management of eschar depends on whether the tissue is stable or unstable. The term stable eschar is used to describe leathery or dry tissue, whereas unstable describes tissue that is undergoing a softening process caused by bacteria or developing infection. Sharp or excisional debridement includes the use of a scalpel, curette, or scissors, and requires written informed consent regardless of the location of care delivery. Other methods of debridement are available using ultrasonic or laser technology. Sharp debridement is best handled by an experienced clinician. Options for sharp debridement include scoring of the eschar with application of topical enzymatic debriding agents and use of a curette, scalpel, or scissors to remove eschar. Depending on the extent of the eschar, considerations include local or general anesthesia. Timing of debridement is a matter of clinical judgment as to whether the eschar is stable or unstable, and serial debridements are often needed. Pain management and control of bleeding are important components of mechanical and sharp debridement. Some clinicians advocate maggot debridement therapy, also called biological or larval therapy, which involves application of sterilized larvae of the Lucilia sericata fly directly in the wound. The fly larvae digest bacteria, secrete proteinases that degrade necrotic tissue, and stimulate granulation.

NPWT is the application of suction to a wound bed to facilitate healing. The wound is packed with foam and sealed with adhesive membrane, and a vacuum device delivers controlled negative pressure while collecting exudate and debris into a collection chamber or absorptive pad. Since its introduction in the 1980s, NPWT has become a multimillion dollar industry despite limited evidence in controlled clinical trials for efficacy. NPWT has been used in treatment of all types of wounds, including open abdominal incisions, dehisced surgical wounds, burns, preparation for skin grafts, traumatic wounds, venous stasis ulcers, diabetic foot ulcers, and pressure injuries.

The mechanism by which NPWT promotes healing is not known but may include removal of excess fluid, improved circulation, reduced bacterial load, and the mechanical effect of negative pressure. The FDA has issued a safety communication regarding complications of NPWT, including pain, retention of foreign bodies from the dressing, bleeding, infection, death, and complications stemming from power outages. NPWT should not be used over necrotic or infected wounds and is not a substitute for good nursing care to keep a wound clean. Patients should be carefully selected for NPWT and educated regarding its use and risks. NPWT initiation should be cautiously considered for a wound that is not expected to heal; if no observable improvement is seen after 2 weeks, NPWT should be discontinued.

Most experts agree that nutrition is an important component of pressure injury management. Carbohydrates and fats supply energy to cells, and protein is used in anabolic repair, whereas many vitamins and trace elements are essential for healing. Nutritional recommendations should be individualized in response to clinical conditions and goals of care. In general, the caloric requirement for wound healing is 30–35 Kcal/kg/day (SOE=B). Protein is required for wound healing, but the exact amount is not established. The current recommendation for protein is 1–1.5 g/kg/day, but more may be required depending on clinical condition. When determining nutritional needs, it is important to consider other factors such as preexisting protein-calorie nutrition and comorbidities. There is some evidence that 8 weeks of supplementation with an oral nutritional formula enriched with arginine, zinc, and antioxidants improves pressure ulcer healing (SOE=B).

Caution is advised when delegating wound care decisions to consultants, particularly with regard to procedures and ancillary treatment such as NPWT. Long-term care facilities that outsource wound care must ensure that treatment decisions remain part of the interdisciplinary team approach. Many types of providers practice wound care, including general surgeons; plastic and vascular surgeons; emergency physicians; dermatologists; physicians from nonsurgical specialties; podiatrists; advanced practice nurses; wound, ostomy, and continence nurses; physician assistants; and physical therapists. Wound care practitioners may not have had training in geriatrics or palliative care and may lack knowledge or skill with decision making in light of advance directives and end-of-life issues. The wound care consultant should be integrated into an overall and reasonable plan, particularly for patients in whom palliative principles apply. Wound care takes teamwork and communication, and weaknesses in the system have adverse consequences in terms of unnecessary procedures, pain, increased health care costs, risk-management, and quality of patient-centered care.


Localized infection or cellulitis occurs when microorganisms replicate and produce large enough numbers to elicit host response and cause injury. Local infectious complications of pressure injuries include cellulitis, abscess, osteomyelitis, and pyarthrosis. Pressure injuries can be the starting point for necrotizing fasciitis, a rapidly progressive infection that spreads along fascial planes within subcutaneous tissue. Systemic infections resulting from pressure injuries include sepsis and hematogenous seeding of distant structures, causing further problems such as endocarditis, infected prosthetic joints, and bacterial meningitis.

Identification and treatment of infection are critical to healing a pressure ulcer; however, there is little consensus on definition of wound infection in a chronic wound. Signs and symptoms include fever, increased drainage, pain, warmth, edema, erythema, slough, odor, cessation of healing, or worsening of the wound. Many of these may not be present in older patients, people with diabetes, or patients with malnutrition or immunocompromise. Diagnosis is based on clinical evaluation of local and systemic symptoms in concert with laboratory studies. Increased WBC count may be found when the infection is acute but is an unreliable indicator of chronic infection.

Because all wound surfaces are contaminated, swab cultures are best reserved for wounds with purulent drainage in the setting of high suspicion for infection. One reliable technique involves rotating a swab over a 1-cm2 area with enough pressure to express fluid from the wound (SOE=B). Tissue biopsy culture method includes removing a piece of the wound with a scalpel or curette, but this is painful and unavailable in many settings.

Treatment of infected wounds involves managing underlying conditions, including diabetes, anemia, poor nutritional status, cardiopulmonary disease, and any cause of edema. All wounds should be protected from contamination with urine and feces. Wound cleansers include water, saline, commercial cleansers, and irrigation devices, but these do not remove deeper bacteria. Bioburden can be managed by removing devitalized tissue with debridement, which can be autolytic, enzymatic, mechanical, or surgical. Antiseptics such as povidone-iodine, betadine, peroxide, and Dakin solution are generally discouraged because they harm living tissue, but they can be useful in heavily contaminated wounds when used in limited fashion.

Wound infections can be treated locally, systemically, or both, depending on the clinical situation. Local treatments include dressings containing antimicrobial compounds such as gentian violet, methylene blue, silver, and cadexomer iodine. Topical antibiotics include mupiricin, neomycin, polymixin B, and bacitracin. Multiple topical antifungals are available, including the imidazole, triazole, and thiazole compounds. Systemic treatment depends on the suspected organisms and clinical setting, and bone infection requires 6 weeks of intravenous therapy. Aggressive treatment and hospitalization should be guided by goals of care and advance directives in conjunction with education of the patient and family.


Ulcers of the foot and leg generally result from multiple etiologies. The most common causes of lower extremity ulcers are venous insufficiency, arterial insufficiency, neuropathic disease, and pressure injury. The most common cause is chronic venous insufficiency. These wounds are generally not painful and are seen most often above the medial or lateral malleolus and occur in beds of chronic venous insufficiency evidenced by edema and hemosiderin staining of the lower extremities.

Arterial wounds are painful and are seen in distal portions of the foot, generally in the presence of chronic atherosclerotic disease evidenced by pale, shiny, and cool skin; loss of skin appendages such as hair and sweat glands; decreased pedal pulses; and poor capillary refill. The presence of peripheral arterial disease (PAD) increases the risk of pressure injury. The ABI is unreliable in the geriatric population for assessment of arterial wounds, because hardening of the arteries falsely increases the result. Other noninvasive tests are recommended such as pulse-volume recordings, toe pressure, and Doppler ultrasound. Suspected PAD requires assessment by a vascular surgeon, and endovascular procedures can increase circulation and assist in healing.

Diabetic foot ulcers usually occur in the setting of longstanding diabetes mellitus and peripheral neuropathy. They result from various factors, including mechanical changes in the bony architecture of the foot, atherosclerotic PAD, loss of sensation, and disease of the microcirculation. Infected diabetic wounds often present atypically, and all diabetic foot ulcers require evaluation by a vascular surgeon and/or podiatrist.

Miscellaneous causes of leg ulceration in older adults include trauma, malignancy such as basal or squamous cell carcinoma, pyoderma gangrenosum, and vasculitis.


Skin integrity compromise impacts up to one-fourth of patients at life’s end. Fifty percent of these cases are pressure injuries, 20% are ischemic wounds related to PAD, and the remainder are related to malignancy, venous insufficiency, lymphedema, diabetes, skin tears, surgery, radiotherapy, and other causes. A palliative approach can reduce suffering, improve quality of life, and decrease health care costs by eliminating expensive and/or painful procedures and treatments. Palliative care for chronic wounds should be considered when it becomes clear that there is little or no realistic chance of healing within the patient’s lifetime and when the burdens of operative procedures or advanced treatment options outweigh the benefits. The decision to designate a wound as palliative arises when the wound is unresponsive to therapy and the process of achieving healing is inconsistent with overall goals of care. Some wounds that are designated as palliative can show signs of healing, but this should not alter the palliative plan. Because of the difficulty of studying this population, evidence-based guidelines are limited and the strength of evidence for existing guidelines is generally level C. For a mnemonic that summarizes the palliative care approach to wounds, see Table 3.

Table 3—Palliative Care of Wounds: the Mnemonic “SPECIAL”

S = Stabilize the wound

P = Prevent new wounds

E = Eliminate odor

C = Control pain

I = Infection prophylaxis

A = Absorbent wound dressings

L = Lessen or reduce dressing changes

SOURCE: Alvarez OM, Kalinski C, Nusbaum J, et al. Incorporating wound healing strategies to improve palliation (symptom management) in patients with chronic wounds. J Pall Med. 2007;10(5):1161–1189e.

Factors leading to designating a wound as palliative include unmodifiable risk factors or medical conditions such as poor nutrition, inadequate perfusion, multisystem organ failure, immunocompromise, irreversible anasarca, a terminal prognosis that prevents the normal healing process, and the presence of artificial life support. NPWT, hyperbaric oxygen, and other ancillary treatments are generally used when the goal is healing. The decision to consider a palliative approach is made in consultation with the patient, family, and wound specialist with honest and open dialogue regarding prognosis for healing and the burdens, benefits, adverse effects, and potential complications of more aggressive cure-oriented procedures.

A palliative approach to wounds involves providing counseling and emotional support for the patient and family, preventing further skin deterioration and infection, promoting comfort, and optimizing pain management and other symptoms such as odor and bleeding. The timing of dressings and repositioning can be modified to decrease pain associated with physical manipulation of the patient and the wound. Topical pain treatments include viscous lidocaine gel and dressings that deliver locally applied ibuprofen and opiates. An FDA advisory warns that topical skin-numbing products may have cardiopulmonary adverse effects when absorbed into the bloodstream, so caution is advised. Wound odor can be minimized with charcoal- or chlorophyll-containing dressings, or metronidazole gelOL. Dressings such as alginates and absorptive foam can manage excess drainage and protect the periwound areas from MASD.


Edsberg LE, Black JM, Goldberg M, et al. Revised National Pressure Ulcer Advisory Panel pressure injury staging system. J Wound Ostomy Continence Nurs. 2016;43(6):585‒597.

National Pressure Ulcer Advisory Panel. Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline. Washington, DC: NPUAP; 2014.

Westby M, Dumville JC, Soares MO, et al. Dressings and topical agents for treating pressure ulcers. Cochrane Database Syst Rev. 2017 Jun 22;6:CD011947.

Woo KY, Krasner DL, Kennedy B, et al. Palliative wound care management strategies for palliative patients and their circles of care. Adv Skin Wound Care. 2015;28(3):130–140.