In susceptible individuals, the combination of immobility and extended periods of pressure or friction over bony prominences leads to reduction in capillary blood flow, tissue hypoxia, and ischemic tissue injury. This in turn evokes an inflammatory response that further impairs perfusion and augments soft tissue and skin injury. Current understanding favors a "bottom-up" model of tissue damage beginning deep in the muscle layer [10]. Muscle is more sensitive to pressure injury than skin because it is the more metabolically active layer and thus more susceptible to ischemic injury.

For a given patient, immobility that leads to unrelieved pressure to the skin over a boney prominence is the most important factor in the development of pressure injuries [5,10]. Individual risk factors for pressure injuries may be categorized as extrinsic or intrinsic. Extrinsic factors are external conditions in the immediate environment that place a vulnerable individual at risk (e.g., moisture, compression from an applied device). Intrinsic factors are conditions and comorbidities peculiar to the individual that confer risk (e.g., advanced age, poor nutrition, smoking history).

Poor nutrition, intravascular volume depletion, and peripheral vascular disease can each lead to unhealthy skin and impaired wound healing, which in turn increases the risk of developing pressure injuries. Low body weight is also a concern. Weight less than 119 pounds or a body mass index (BMI) less than 20 indicates increased risk for pressure injury development [19].

Recent weight loss, decreased nutritional intake, inadequate dietary protein, and impaired ability to feed oneself have been identified as risk factors for pressure injury development. An estimated 50% of elderly patients admitted to hospitals have suboptimal protein nutrition [19]. When there is a sustained deficit of protein as an energy source, skin and soft tissues become more vulnerable to injury. In managing patients with pressure injury, or those at risk, the amount of protein in the diet appears to influence prognosis for recovery and prevention. In one study, patients who received a 24% increase in protein intake had significant improvements in pressure injury healing and prevention of new skin injury compared to those who received a 14% increase [20]. The potential role of nutritional supplementation on pressure injury management and prevention is an area of ongoing research [21,22].

The National Pressure Ulcer Advisory Panel (NPUAP), in conjunction with a consensus conference format involving 400 health professionals, redefined the definition of pressure injuries in 2016 and provided an illustrated staging scheme that classifies pressure injuries by the depth and extent of tissue injury into six stages [29,30]. The NPUAP announced that it was changing its preferred terminology from pressure ulcer to pressure injury on the grounds that the latter term better described this injury process in both intact and ulcerated skin [31]. The term "pressure injury" will be used throughout this course as appropriate.

Deep tissue injury is described as a purple or maroon localized area of discolored, intact or non-intact skin or a blood-filled blister caused by damage of underlying soft tissue from pressure and/or shear (Image 1). The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue.

Unstageable pressure injuries are defined as full-thickness skin and tissue loss in which the base of the injury is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black), obscuring the wound bed (Image 6). Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined.

The standard signs and symptoms of inflammation are erythema, swelling, increased temperature, and pain. In normal healing, these signs are only minimally noticeable, and during the inflammatory phase of wound healing, they are considered a normal response [35]. In general, this phase occurs in the first 0 to 3 days after injury development but may last longer if healing is impaired.

Blood tests may be ordered to assess nutritional status and overall health status. No laboratory study of nutritional status can absolutely predict pressure injuries; however, monitoring a patient's protein status is of value. There are many serologic markers used to assess a patient's nutritional status; prealbumin level is one of the most sensitive. Prealbumin is a protein with a much shorter half-life than the other serologic markers; therefore, its level gives a more accurate picture of current conditions.

If infection is suspected, culture of the pressure injury is important to determine the pathogen. In some cases, a wound biopsy is performed to rule out vasculitis and skin cancers. An x-ray is done if bone infection is suspected and to rule out osteomyelitis. A bone scan is carried out when x-ray findings are equivocal.

The primary objectives for prevention and arrest of progression are:

The provision of an optimal diet (e.g., 30–35 kcalories/kg body weight for adults who are at risk for malnutrition), including the addition of supplemental protein, amino acids, zinc, and vitamins, has been shown to reduce risk of pressure-induced skin injury and to speed wound healing. The recommended daily protein intake for healthy adults (0.8 g/kg of body weight) may not be adequate in the frail elderly or under conditions of chronic inflammation and loss of lean body mass. For dietetic management of adults at high risk of pressure injury or delayed wound healing, the recommended intake is 1.25–1.5 g protein/kg body weight daily [29,42].

Generally, normal saline is used for cleansing pressure injuries. In injuries with necrotic tissue, debris, or confirmed or suspected infection, antimicrobials or surfactants should be considered. For infected wounds, diluted povidone-iodine may be used as the irrigation fluid. However, it should not be used during the granulation phase of healing. Acetic acid (0.5%) is highly effective in fungating lesions, especially against Pseudomonas aeruginosa. There are various cleansing agents available in the market, but normal saline is usually the best option [31,45]. Normal saline also should be used as a rinse after other solutions are used to irrigate the wound and minimize fluid shifts within newly forming tissue. Normal saline solution can reduce the drying effects that some irrigants may have on tissue [31].

The method of debridement used depends on the amount of necrotic tissue present, the location of the wound, and the patient's overall condition [35]. Patients with stage 3 or 4 pressure injuries who have undermining and/or tunneling or extensive necrotic tissue should have a surgical evaluation for possible surgical debridement of the wound, if this is consistent with their condition and goals of care [29]. Infected wounds may require systemic antibiotic treatment and immediate surgical debridement [15]. Maintenance debridement should be continued until there is a covering of granulation tissue in the wound bed and the wound is free of necrotic tissue [29]. Debridement is contraindicated if there is inadequate blood supply to support wound healing.

Autolytic debridement uses the body's own enzymes and moisture to heal the injury. To be successful, there must be sufficient white blood cells available to the wound and a moist environment [13]. A layer of wound exudate should be kept in contact with the surface of the wound, usually using a moisture-retaining dressing [10,15,35]. This allows fluid to accumulate in the wound, rehydrating necrotic tissue and making it possible for enzymes in the wound to digest the dead tissue [35]. For a wound covered with dry eschar, it is appropriate to crosshatch the eschar, as this allows a faster build-up of moisture in the wound [35]. In their clinical practice guidelines for pressure injury treatment, the Agency for Healthcare Research and Quality recommends autolytic and enzymatic debridement as the preferred approach for patients in long-term care or home care and for patients who cannot tolerate other methods of debridement [35,46]. In general, this type of debridement is ideal for patients with stage 3 or 4 injuries with light-to-moderate exudates.

Enzymatic debridement is a selective method of debridement in which concentrated enzymes (e.g., collagenase, papain, becaplermin, trypsin) attack collagen and liquefy necrotic wound debris without damaging viable tissue. Enzymatic debridement is used either alone or in combination with other techniques to remove necrotic tissue and promote wound healing [53,54]. For instance, collagenase and moisture retentive dressings can work in synergy, thereby enhancing debridement [47].

Silver-impregnated dressings are a treatment option for infected or heavily colonized wounds or wounds that are at increased risk for infection [29]. Silver has an antimicrobial effect on a broad spectrum of organisms and has been shown to reduce the bacterial count in wounds [13]. Sustained-release sliver dressings are toxic to bacteria and fungi but do not adversely affect healthy wound tissue [10]. However, silver-resistant organisms do exist, and the judicious use of silver is advised, similar to the approach adopted with antibiotics [13]. It is recommended that the use of silver dressings be limited to a two- to four-week period [13]. As stated, silver-based products should not be used for enzymatic debridement [47].

For mild-to-moderate pain, nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen may be used. Opioids should be avoided as much as possible, as the sedative effects boost immobility; however, they may be necessary during dressing changes and/or debridement.

This therapy consists of the placement of a high-voltage, pulsed electrical current onto the wound bed (direct) or near the wound (induced), usually once daily for several weeks. The electrical settings (e.g., the polarity, amplitude and voltage, amperage) are established according to wound and patient characteristics. The Institute for Clinical Systems Improvement 2012 guideline recommends considering the use of direct contact electrical stimulation in the management of recalcitrant stage 2 as well as stage 3 and 4 pressure injuries to facilitate wound healing [61]. Although electrical stimulation is used for the treatment of pressure ulcers, a 2020 Cochrane review found that available evidence is insufficient to support its widespread use apart from its use in research [66].

Reverse staging of pressure injuries is not an acceptable approach to gauging the level of wound healing. Healed pressure injuries do not replace lost muscle, subcutaneous fat, or dermis [29]. Tools that appropriately measure degrees of healing include the Bates-Jensen Wound Assessment Tool and the Pressure Ulcer Scale for Healing (PUSH) tool [15,86]. The Bates-Jensen Wound Assessment Tool has thirteen variables that provide a composite picture of the status of the wound [15]. The PUSH tool uses scores in three domains (i.e., size, exudate amount, and tissue type) to indicate improvement or deterioration of the injury (Table 6) [87]. When using this tool, surface area is calculated by multiplying the greatest length (head to toe) by the greatest width (side to side) in centimeters. After removal of the dressing and before applying any topical agent to the injury, the amount of exudate is estimated as none, light, moderate, or heavy. Finally, the type(s) of tissue present in the wound bed is evaluated (i.e., necrotic, slough, granulation, epithelial, or closed). A score of 0 on the PUSH tool indicates the wound has healed, whereas the highest score of 17 indicates wound degeneration [15]. Results of the assessment should be recorded; a decrease in score over time indicates improvement.

The condition of the surrounding skin surface up to 4 cm from the edge of the wound circumferentially must also be assessed and documented. Its characteristics should be noted, particularly color and integrity [10]. Maceration from excessive drainage may indicate that the dressing used is not appropriate and a different product is needed. Circumferential erythema and/or induration up to 2 cm from the wound are indicative of cellulitis.

Working from a model derived from a large inpatient data base, the sepsis task force was able to identify, and validate, a simple "bedside" clinical measure that can be used to identify which patients with suspected infection are at risk for developing sepsis. Designated the qSOFA (for quick SOFA), this measure consists of three elements [93,96]:

The first sign of Marjolin ulcer is a change in the character of the wound. Drainage increases, and the odor of the drainage becomes putrid. In some cases, there is frank bleeding. Diagnosis is made after histologic examination of a specimen removed from the injury, usually at the time of a flap closure. Confirmation of the diagnosis requires a preoperative tissue biopsy; wedge biopsy is the method of choice.

As noted, despite best patient care and treatment, not all pressure injuries are avoidable [139]. In long-term care, the NPIAP defines an unavoidable injury as one that occurs even though "the facility had evaluated the individual's clinical condition and pressure injury risk factors; defined and implemented interventions that are consistent with individual needs, goals, and recognized standards of practice; monitored and evaluated the impact of the interventions; and revised the approaches as appropriate" [140]. In addition to establishing the definition for long-term care facilities, in 2014 the NPIAP sought to establish consensus (80% agreement among conference delegates) on whether pressure injury development may be unavoidable in some individuals and whether there is a difference between pressure injuries and end-of-life skin changes. Unanimous consensus was reached for the following statements [141]: