PIs have been a part of human history since ancient times. The earliest known historical reference comes from paleopathologists who identified extensive PI on the ischial bones and scapulas of a mummy belonging to an elderly priestess of Amun from the 21st Dynasty of ancient Egypt (1070 to 945 BC).7 The first written record of PI corresponds to Hippocrates (460‒370 BC), who described the appearance of such lesions in a paralyzed patient with bladder and bowel dysfunctions.8

During the Renaissance, Ambroise Paré (1510‒1590), considered the father of modern surgery, made the first documented description of a PI, focusing on addressing its cause to facilitate healing.7

Effective measures in the prevention and treatment of PI were already being implemented in the early 19th century. For example, in 1806, J.E. Aronssen from Berlin emphasized the importance of the bed in patient care and presented plans for a new and improved invalid chair of his invention.9

The term “bedsore” was documented by nurse Florence Nightingale in 1859.10 This term maintains its association with the bed, despite the understanding at the time that PI can occur whenever soft tissues are in contact with support surfaces, and the significant role played by shear forces and shear deformation. The addition of “sore, implied a raw” or painful place on the body.1

From the second half of the last century, awareness of PI increased alongside advances in healthcare, prompting various authors to study their etiology. Reichel in 195811 and Kosiak in 195912 with studies on ischemic injuries contributed significantly to the understanding of etiopathogenesis. The search for Norton et al. in 196213 resulted in the first risk assessment scale for PI. The term “pressure ulcer” started to gain popularity in the 1970s and 1980s, replacing terms like “bedsores” or “decubitus ulcers” and “pressure sores”. The formation of groups such as the National Pressure Ulcer Advisory Panel (NPUAP) in the United States in the 1970s, along with national groups such as the National Group for the Study and Advisory of Pressure Ulcers and Chronic Wounds in Spain (GNEAUPP) in 1994, and the European Pressure Ulcer Advisory Panel (EPUAP) in 1996, propelled the advancement of knowledge about PI during that time.7

Significant contributions to the understanding and prevention of PI include the conceptual model by Bergstrom et al. in 198714 who developed the Braden Scale, and Coleman et al. who presented direct and indirect causal factors,15 and the work of García Fernández et al. in 2014,16 who introduced the term “pressure injuries related to dependency”. This work modified the existing classification that GNEAUPP had already adopted and paved the way for reconsidering the term “pressure injuries” instead of “pressure ulcers”. This term was later adopted by the Pan Pacific Pressure Injury Alliance in 2014 and recently, albeit controversially, by the American NPUAP, generating intense debate due to the English connotations of the concept of “injury”.17 Thus, the NPUAP incorporated the “injury” (National Pressure Injury Advisory Panel ‒ NPIAP),1 however, in Europe, the EPUAP term pressure ulcer remains without this modification.1

In ICUs, patients are considered at high risk for developing PI due to clinical condition-related risk factors, such as immobility, inadequate nutrition, and support therapies like mechanical ventilation and hemodialysis.19,24 The cumulative incidence and prevalence were 10.0% to 25.9% and 16.9% to 23.8%, respectively in a global systematic review encompassing all diagnostic restrictions and types of ICU.24

The prevalence and incidence of PI in pediatric populations can vary considerably depending on the clinical context. Few studies focus on this population, but Razmus and Bergquist-Beringer conducted a study covering 678 pediatric acute care units with 39,984 patients in the United States.25 They reported that the rate of PI acquired in all facilities ranged from 0.57% to 3.7% in the pediatric ICU and 4.6% in rehabilitation settings.25

A study in Brazilian hospitals, tracking 314 children, found an average prevalence of 7.1% and an average incidence of 21.8%, with 22 children having 31 cases of PIs. According to the types of wards, the average prevalence was 1.8% in clinical pediatrics, 4.0% in surgical pediatrics, and 32.8% in pediatric ICUs.26 In another Brazilian study assessing 83 children in a tertiary hospital ICU in the interior of São Paulo, the incidence of PI was 21.6%.27

In neonates, injuries from medical devices are more common, especially in the ICU.28 A study that assessed the incidence of PI in both children and neonates identified a 50% higher risk of PI, primarily due to medical devices, with injuries to the septum from enteral tubes and the use of tracheostomies.29 Another study evaluated 625 children and neonates, among which those under eight years old developed one or more injuries from medical devices, with an incidence of 7%.30

A recent systematic review found the overall pediatric prevalence ranging from 0.47% to 31.2%. The combined prevalence among neonates was 27.0%, among children under 1-year old was 19.2%, and among children over 1-year old was 12.3%. The cumulative incidence of hospital-acquired PI in neonates was 9.8%.31

An increasingly frequent scenario is the institutionalization of older people. Due to the natural characteristics of the aging process and the clinical issues that limit mobility, PI is considered a concern for the safety of elderly individuals living in these institutions.32

A systematic review with meta-analysis showed that the prevalence, incidence, and occurrence of PI acquired in elderly care homes were 8.5%, 11.6% and 14.3%, respectively. The most common stages were Stages 1 and 2. The calcaneal and sacral regions were the most frequently affected sites. Additionally, it was observed that the amount of PI among the older people in these institutions is like that found in hospitalized patients.32

In patients with COVID-19, particularly those during the pandemic admitted to the ICU, the rates of PIs were significantly high. A study in Brazil demonstrated that out of 80 patients admitted to the ICU due to COVID-19, 44 (55%) developed PI during hospitalization.33 Another Brazilian study, among the 393 medical records analyzed, identified a prevalence of PI at 167 cases (42.5%), with patients having up to four PI.34

In terms of the location of the PI, a difference was noted during the pandemic related to the prone position, in which patients remained for 16 to 24 consecutive hours daily. PI frequently occurred on the bony prominences subjected to this position such as frontal, nasal, pectoral, breast and knee.35,36 The incidence of PI ranges from 25.7% to 48.5% in the prone position.37

A concern about PI related to the use of personal protective equipment by healthcare professionals has also been reported during the pandemic. A systematic review found a high incidence of these injuries, ranging from 30% to 92.8%, predominantly stage 1 PI38 and 58.8% in another study of the same stage.39 This is supported by a Brazilian study of ICU professionals, where 91.8% had some form of injury/erythema, primarily in the nasal region (74.1%) and the zygomatic region (45.9%).40

The change in terminology from “pressure ulcer” to “pressure injury” encompasses both intact skin and ulcerated lesions.17 Thus, PI describes Stage 1 lesions and deep tissue injuries without ulcerated skin. The staging and examples of anatomical involvement are described in Table 1.1

PI is not limited to the skin; it can also occur on mucous membranes, including the respiratory, gastrointestinal, and genitourinary tracts. Mucosal PI is primarily associated with medical devices, typically caused by tubes and/or their stabilization equipment exerting sustained compressive and shear forces on vulnerable mucous membranes and underlying tissues.1

The representation of the affected skin layers and images of representative pressure injuries according to each classification are in Figs. 4–10.

Figure 4.

(A) Stage 1 pressure injury. Source with permission of the National Pressure Injury Advisory Panel. (B) Patient with non-blanchable erythema in the sacral region. Source: Authors' own.

Figure 5.

(A) Stage 2 pressure injury. Source with permission of the National Pressure Injury Advisory Panel. (B) Patient with partial-thickness skin loss and an intact blister in the gluteal region. Source: Authors' own.

Figure 6.

(A) Stage 3 pressure injury. Source with permission of the National Pressure Injury Advisory Panel. (B) Patient with full-thickness dermal loss in the gluteal region and the presence of slough. Source: Authors' own.

Figure 7.

(A) Stage 4 pressure injury. Source with permission of the National Pressure Injury Advisory Panel. (B) Patient with full-thickness skin loss in the sacral region and exposure bone. Source: Authors' own.

Figure 8.

(A) Deep tissue pressure injury. Source with permission of the National Pressure Injury Advisory Panel. (B) Patient with extensive purpuric lesion in the gluteal region. Source: Authors' own.

Figure 9.

(A) Unstageable pressure injury. Source with permission of the National Pressure Injury Advisory Panel. (B) Patient with liquefactive necrosis and an area of coagulative necrosis in the sacral region, making it impossible to assess the depth of the pressure injury. Source: Authors' own.

Figure 10.

(A) Medical device-related pressure injury in a patient with a pressure injury on the inner surface of the right thigh caused by pressure from an indwelling urinary catheter. (B) Urethral mucosal pressure injury in a patient with an indwelling urinary catheter. Source: Authors' own.

Evidence-based recommendations for additional assessment techniques, such as skin temperature evaluation, subepidermal moisture measurement, and skin tone color charts, should be used when assessing skin and tissues and classifying PI, particularly in darker skin tones.1 Assessment of the skin using subepidermal moisture measurement scanners has gained international attention as it can detect the onset of PI approximately five days before becomes visually apparent,55 making it a promising advancement in the clinical practice of PI prevention.56

Some tools guide the assessment and documentation of PIs, such as the widely used PUSH (Pressure Ulcer Scale for Healing), which provides a guide for evaluating exudate, size, and tissue type, serving as a support for clinical progression.57,58 Another more current and comprehensive tool that supports professionals is the Bates-Jensen Wound Assessment Tool (BWAT)59 – adapted for Brazil in 201560 and its reliability was internationally validated in 2019.61 The BWAT consists of 13 wound characteristics: size, visible depth, wound edges, undermining and tunneling, type and amount of necrotic tissue, type and amount of exudate, surrounding skin discoloration, peripheral tissue edema, peripheral tissue induration, granulation tissue, and epithelialization.60,61

Laboratory tests help assess conditions that can hinder or delay PI healing, such as infection, anemia, poor nutritional status, and diabetes mellitus. It is recommended that a comprehensive metabolic panel, a complete blood count with differential, albumin and prealbumin (to evaluate nutritional status), and hemoglobin A1C be performed.62

Although swabs to assess for infection remain the most common method for wound sample collection due to their simplicity and low cost,63 wound cultures from superficial swabs may not be clinically valuable. They often reflect colonization rather than infection, leading to false-positive results.64–66

Tissue biopsy is considered the gold standard due to its precision, although it is more invasive, costly, and requires specialized skills for its performance.63 Additionally, biopsy has greater sensitivity for wounds infected with multidrug-resistant bacteria.65

Lesions caused by excessive moisture (sweat, exudate, and bodily fluids) compromise the epidermal barrier and can cause skin damage that may be confused with PI.1 Incontinence-Associated Dermatitis (IAD) is an irritant contact dermatitis and is the most common form of moisture-associated skin damage, as chronic exposure of the skin to urine and feces chemically injures the skin.1

The IAD is characterized as an inflammatory dermatosis with erythema, exudation, and excoriation.67 It also presents with persistent pigmentation changes, edema, maceration, vesicles, or blisters.68 It affects the perineum, the lower folds of the buttocks, the scrotal region, the thighs, and sometimes even the abdomen (Fig. 11A).

Figure 11.

Differential diagnosis of pressure injury. (A) Incontinence-associated dermatitis in a patient with urinary and fecal incontinence who developed intense erythema in the regions intergluteal, perianal and scrotum. (B) Kennedy’s terminal ulcer in a patient with multiple organ failure who rapidly developed (within 24 hours) a purpuric plaque in the sacral region.

Source: Authors' own.

End-of-life injuries are those that appear hours or weeks before a patient's death.69 Many synonyms describe the same type of injury, with the most well-known term being the eponym “Kennedy Terminal Ulcer” (KTU). KTU was first reported by Karen Lou Kennedy70 describing a discolored skin patch (purple, red, blue or black) usually located in the sacral or coccyx region, although it can affect other body parts, with a butterfly, pear, or horseshoe shape (Fig. 11B). Its progression is very rapid, with full-thickness ulcers evolving over the course of hours or a few days, indicating the imminence of death.1

There is debate as to whether KTU is a particular type of PI. However, there is a difference in the pathophysiology between them.71 PI is caused by unrelieved pressure, often accompanied by shear and friction, resulting in local ischemia and tissue damage. On the other hand, KTU is caused by hypoperfusion and multiorgan failure, and the hypoperfusion of the skin results in visible signs of tissue death. In this scenario, the ischemia associated with multiorgan failure, rather than the damaging effects of unrelieved pressure or shear, results in an unavoidable skin ulcer.69

Due to similar purple or brown discoloration and location, it can be challenging to differentiate it from deep tissue PI.72

This article aimed to support healthcare professionals and dermatologists in identifying risk factors and mechanisms of PI based on the most current concepts available in the scientific literature. The primary focus was providing resources to help them holistically assess, prescribe, and monitor patients. Additionally, it aimed to assist in evaluating each risk classification and distinguishing other skin conditions like PI.

Some key points of this review include: 1) The prevalence of PI remains high in the global population, with emphasis on patients in ICUs, institutionalized older adults, individuals with hip fractures, trauma or prolonged surgeries, spinal cord injuries, and chronic neurological conditions; 2) Children and neonates are also at risk of PI; 3) PI is not limited to the skin; it can also occur on mucous membranes primarily associated with medical devices; 4) Temperature assessment, subepidermal moisture measurement, and skin tone color charts can be used when assessing skin and tissue and grading PI, particularly in darker skin tones; 5) In cases of PI with suspected infection, wound cultures from superficial swabs are not indicated. A biopsy for microbiological analysis has greater sensitivity in detecting wounds infected with multidrug-resistant bacteria.

The authors invite you to read the subsequent article, which addresses the main complications inherent to PI, practical preventive measures, conventional treatments, and advanced technologies currently in use. Additionally, the next article provides a practical guide focusing on combating biofilm and updating debridement techniques.