The Critical Role of Comprehensive Prevention Strategies in Pressure Injury Management

Abstract

Pressure injuries (PIs), also known as pressure ulcers or bedsores, represent a significant healthcare challenge, leading to considerable patient morbidity, extended hospital stays, and increased healthcare costs. This article synthesizes contemporary understanding of pressure injury etiology and evidence-based prevention strategies, drawing upon the latest International Guideline from the National Pressure Injury Advisory Panel (NPIAP), European Pressure Ulcer Advisory Panel (EPUAP), and Pan Pacific Pressure Injury Alliance (PPPIA). Four primary pathophysiological pathways contribute to PI development: localized ischemia, reperfusion injury, direct cell deformation, and impaired lymphatic function. Effective prevention hinges on minimizing mechanical loads, particularly pressure and shear, on vulnerable tissues. Key preventive interventions include individualized repositioning regimens, optimal full body and seating support surfaces, and comprehensive nutritional support. Special emphasis is placed on the importance of frequent repositioning and the strategic use of 30-degree to 40-degree lateral positioning to maximize pressure redistribution and prevent injury. This paper underscores the necessity of a multifaceted, patient-centered approach to pressure injury prevention in clinical practice.

Keywords: Pressure injury, pressure ulcer, prevention, etiology, repositioning, support surfaces, nutrition, 30-degree to 40-degree lateral positioning, frequent turning.

1. Introduction

Pressure injuries (PIs) are defined as localized damage to the skin and/or underlying tissue, typically occurring over bony prominences or in relation to medical devices, resulting from sustained pressure or pressure combined with shear. This condition is also commonly referred to as bedsores, decubitus ulcers, or pressure sores. The International Clinical Practice Guideline (CPG) currently favors the term “pressure injury” (PI) in line with prevailing preferences in English-speaking populations such as Australia and the United States of America, while the World Health Organization (WHO) ICD-11 uses “EH90 Pressure ulceration”. PIs pose a substantial burden on healthcare systems globally, necessitating a robust focus on prevention. The International Guideline, a collaborative effort by the National Pressure Injury Advisory Panel (NPIAP), European Pressure Ulcer Advisory Panel (EPUAP), and Pan Pacific Pressure Injury Alliance (PPPIA), provides comprehensive, evidence-based recommendations for both the prevention and treatment of these injuries. The Fourth Edition of this guideline, launched online in February 2025, is developed as a “living guideline,” allowing for ongoing updates based on the latest research. This article will delve into the mechanistic understanding of PI development and outline the key prevention strategies, with a particular focus on repositioning techniques that are crucial for mitigating risk.

2. Etiology of Pressure Injuries: Understanding Tissue Compromise

The development of pressure injuries is a complex interplay of mechanical forces and physiological responses at the cellular and tissue levels. Prolonged mechanical loads exerted on the skin and underlying soft tissues initiate a cascade of events that can lead to tissue damage. These loads cause tissue deformation, which in turn can indirectly result in injury by occluding blood and lymph vessels, ultimately leading to necrotic and apoptotic cell death. Alternatively, tissue deformation can directly impair essential cellular functions, contributing to injury. The relationship between the magnitude of externally applied pressure, the duration of exposure, and the likelihood of tissue compromise has been well-established, represented by a sigmoid curve. It is critical to recognize that this relationship can be modified by various intrinsic factors, including age, nutritional status, skin integrity (e.g., history of wounds), and other comorbidities.

Damaging mechanical loads typically occur in body areas where skin, blood vessels, subcutaneous fat, or muscle tissue are compressed and sheared between stiff internal structures, such as bones or tendons, and adjacent external surfaces like mattresses, cushions, or medical devices. While research into the etiology and pathogenesis of PIs spans many decades, a modern, more nuanced understanding has emerged over the last two decades through extensive animal and cell model studies. Although the precise mechanisms by which mechanical loading conditions are transferred to local stresses and strains within deformed soft tissues, and how this ultimately leads to cell death, are not entirely clear or predictable, four main pathophysiological theories have been proposed and widely accepted:

2.1. Localized Ischemia The theory of localized ischemia posits that sustained tissue loading significantly reduces blood flow and tissue perfusion, leading to an insufficient supply of oxygen and vital nutrients. This deficiency results in the accumulation of metabolic waste products, including carbon dioxide, and localized acidosis, which eventually precipitates cell death. The susceptibility to ischemia varies considerably between tissue types; for instance, muscle tissue is far more vulnerable to reduced perfusion compared to skin, which exhibits greater resistance. It is also theorized that even under very high deformation, some vessels may remain patent, and the extent of ischemia can depend on anatomical location and the frequency of cyclical loading. The exact duration of ischemia required to induce tissue damage is not fully understood, though animal models suggest that more than 90 minutes may be necessary to observe cellular changes.

2.2. Reperfusion Injury Reperfusion injury occurs when tissues, after a period of mechanical loading and ischemia, are relieved, leading to a physiological reactive hyperemic response aimed at restoring oxygen and carbon dioxide levels. While this restoration of blood flow is essential, the reperfusion injury theory suggests that it can also trigger an immediate release of accumulated waste products, including reactive oxygen species, which subsequently cause inflammation and further tissue damage. This phenomenon is recognized in other medical conditions, such as myocardial infarction; however, direct extrapolation to PI development is challenging because PIs are not solely caused by complete occlusion of all blood vessels within compressed tissues. Evidence indicates that tissue injury may intensify with a greater number of ischemia-reperfusion cycles, increased duration of ischemia, and higher frequency of these cycles. Nevertheless, ischemia and reperfusion injury alone do not fully account for the rapid onset of deep ulceration that often undermines intact skin. Local tissue temperature can also influence the reactive hyperemic response, with cooling potentially reducing the speed and magnitude of local blood flow restoration.

2.3. Direct Cell Deformation Emerging evidence suggests that sustained mechanical deformation of cells can directly lead to cellular damage and death, independent of vascular occlusion. Proposed mechanisms include alterations to the cytoskeleton and an increase in the permeability of cell membranes, exceeding the threshold required for normal cell homeostasis. Under conditions of high tissue deformation, when the individual damage threshold is surpassed, this process is believed to occur rapidly, potentially within minutes. These observations have been predominantly made in muscle and subcutaneous fat tissue, with less direct evidence in the skin. Furthermore, research has indicated that cellular damage can propagate beyond the directly loaded regions in compression, suggesting a subject-specific tolerance to mechanical loading that cannot be solely explained by tissue deformation.

2.4. Impaired Lymphatic Function The theory of impaired lymphatic function posits that prolonged mechanical loading can impede lymph flow, thereby reducing the clearance of waste products and inflammatory mediators from soft tissues. Similar to theories related to tissue perfusion, empirical findings are primarily based on skin layers and demonstrate substantial interindividual variability. Evidence suggests that the level of tissue deformation required to occlude lymphatic vessels is lower than that for blood vessels, owing to their distinct anatomical and physiological characteristics. Lymphatic drainage plays a crucial role in clearing local edema and by-products of tissue compromise, such as metabolic waste and inflammatory cytokines, although its relative importance in the overall etiology of PIs is still an area of ongoing research.

2.5. Clinical Implications Animal and human studies, laboratory research, and computer simulations collectively indicate that all four pathophysiological pathways likely contribute to pressure injury development, often in combination. The precise critical threshold and active period of these pathways vary significantly among individuals, making it challenging to disentangle them in clinical research and practice. This is because, in loaded tissues, all processes operate simultaneously and at different structural and functional hierarchical levels, encompassing vessels, tissues, and cells. For example, while direct cell damage due to loading is well-described in muscle tissues and can be a fast process leading to deep tissue injuries, ischemia-related damage may take considerably longer to induce pathological tissue changes. These diverse pathways may explain the clinical differences observed between the rapid development of deep pressure injuries and more superficial PIs that are potentially linked to friction and shear. Comprehensive evidence suggests that signs of PI development can be detected across all involved tissues, including skin, subcutaneous fat, and muscle. Factors such as anatomical location, morphology (e.g., bone geometry, tissue thickness), properties of soft and stiff tissues, degree of tissue deformation, skin microclimate, individual tolerance, and intrinsic repair capacity collectively determine whether damage thresholds are exceeded, leading to either deeper or more superficial PIs. In summary, the likelihood of PI development increases with the magnitude and duration of soft tissue loading. Both direct deformation damage and perfusion-related damage pathways interact, and due to inherent complexity and substantial intra- and inter-individual variability, exact damage thresholds cannot be precisely predicted. Therefore, minimizing the magnitude and duration of load on vulnerable tissue sites and implementing a personalized prevention approach are paramount, aligning strongly with current understanding of pressure injury etiology.

3. Results: Key Prevention Recommendations

Effective pressure injury prevention relies on a comprehensive, multi-faceted approach addressing the various risk factors and etiological pathways. The International Guideline provides several key recommendations and good practice statements to guide clinical practice.

3.1. Repositioning for Pressure Injury Prevention Repositioning is a cornerstone of pressure injury prevention, universally recommended regardless of the type of pressure redistribution full body support surface in use. No support surface, regardless of its advanced capabilities, can entirely replace the need for regular repositioning. The goal of repositioning is to achieve optimal offloading of pressure points and maximum redistribution of pressure across the body.

3.1.1. Importance of Frequent Repositioning for Prevention The frequency of repositioning is a critical determinant in preventing pressure injuries. The International Guideline suggests that for most individuals at risk of pressure injuries, if they are also on an appropriate pressure redistribution full body support surface, repositioning at two-hourly or three-hourly intervals could be implemented. This recommendation is conditional and supported by very low certainty evidence from Tiers 1, 2, and 3A studies. A clarifier emphasizes the need to individualize the frequency of repositioning based on a comprehensive clinical assessment. This assessment should consider various factors of the individual, including their level of activity and mobility, ability to independently reposition, skin and tissue tolerance, clinical condition, comfort, sleep patterns, goals of care, and the specific support surface in use.

For critically ill individuals or those experiencing systemic hypoperfusion or shock states, more frequent, incremental repositioning may be required. This should be supplemented with assisted small shifts in body position. Conversely, for individuals receiving palliative or end-of-life care, repositioning frequency intervals should be tailored to their goals of care and comfort needs, with full knowledge of the pressure injury risk incurred with less frequent repositioning.

The guideline strongly suggests not routinely extending repositioning intervals to four, five, or six hourly for individuals at risk of pressure injuries. This is a conditional recommendation based on very low certainty evidence. However, progressive extension of repositioning intervals may be appropriate for some individuals based on a decreasing pressure injury risk, increased capacity for effective self-repositioning, and maintenance of normal skin and tissue status.

For critically ill individuals who are too unstable to maintain a regular repositioning regimen, or as a supplement to regular repositioning, it is good practice to initiate frequent, small and incremental shifts (micromovements) in body position. This is supported by indirect evidence and clinical expertise. Effective repositioning also necessitates the use of specialized equipment designed to reduce friction and shear. If manual handling is necessary, techniques that minimize friction and shear should always be applied. Education of both the individual and their informal carers on the rationale, significance, and safe strategies for regular repositioning is also deemed good practice. Implementing repositioning reminder strategies further promotes adherence to prescribed regimens. Emerging technologies, such as sensor systems that monitor individual movement, could also assist in evaluating repositioning needs when resources permit. Finally, implementing an early mobilization program, based on the individual’s activity tolerance, is suggested for individuals at risk of pressure injuries.

3.1.2. The Importance of 30-Degree to 40-Degree Turnings for Prevention Specific turning angles are crucial for effective pressure redistribution and, consequently, for preventing pressure injuries. The International Guideline suggests using 30-degree lateral positioning to prevent pressure injury occurrence in individuals at risk. This is a conditional recommendation based on very low certainty evidence from Tiers 1, 2, and 3A studies.

A vital clarifier to this recommendation emphasizes the need to individualize turning angles to ensure maximum offloading of both the sacrum and the trochanter. It is recognized that 30-degree lateral positioning may not be maintainable or adequately offload the sacrum in individuals with a higher body mass index (BMI). In such cases, modifying to a 40-degree lateral position might be necessary to achieve effective offloading. For pre-adolescent children, a 30-degree turn is considered equivalent to a full body turn due due to their smaller body width. This demonstrates that the specific angle is not a rigid rule but a guideline that requires clinical judgment and adaptation to individual patient characteristics to effectively prevent pressure injuries. It is crucial to reiterate that these recommendations for 30-degree and 40-degree lateral positioning are explicitly for preventing pressure injuries, and the provided sources do not offer information on their role in healing existing pressure injuries.

Beyond lateral positioning, it is suggested that head-of-bed elevation be maintained at 30-degrees or lower to prevent pressure injury occurrence, although higher elevation may be required in some clinical situations, such as for individuals at higher risk for aspiration. When an individual’s medical condition requires it, a prone position may be selected, but it should be ceased as soon as clinically appropriate.

3.2. Full Body Support Surfaces for Prevention Support surfaces play a complementary role to repositioning in pressure injury prevention. It is good practice for organizations to maintain an inventory of, or access to, a range of full body support surfaces appropriate to the clinical context, ensuring they are used and maintained according to manufacturer recommendations. The selection of a support surface should accommodate the individual’s weight, height, size, and body mass distribution.

The guideline strongly recommends using a pressure redistribution foam (reactive) full body support surface for individuals at risk of pressure injuries. Factors to consider when selecting or changing a mattress, overlay, or integrated bed support surface include the individual’s overall risk of pressure injuries, skin and tissue response, independence, mobility, activity needs, posture, sleeping position, need for microclimate management and shear reduction features, and their preferences and care goals.

Other suggestions for support surfaces include:

• Using either air (reactive) or pressure redistribution foam (reactive) full body support surfaces for individuals at risk.

• Using either alternating pressure air (active) or pressure redistribution foam (reactive) full body support surfaces for individuals at risk.

• Using either alternating pressure (active) air or air (reactive) full body support surfaces for individuals at risk.

• A medical-grade sheepskin could be used where geographically available, but its potential impact on the primary full body support surface must be considered. It is not recommended when a full body support surface with pressure redistribution properties is available, and only medical-grade sheepskins should be used, ensuring they do not interfere with the support surface’s properties.

• A fiber support surface is not suggested if a pressure redistribution foam (reactive) full body support surface is available.

• An air fluidized full body support surface is not routinely used for prevention, though it might be considered for individuals at very high risk (e.g., those immobilized with extensive burns) or who have previously experienced full thickness pressure injuries on different support surfaces. It may also be used for individuals with existing full thickness pressure injuries or following surgical reconstruction with flaps/grafts.

• A low air loss (reactive) full body support surface could be used, especially when moisture and heat at the skin-surface interface are contributing factors.

• A full body support surface with pressure redistribution features should be used for medical procedures and for individuals at risk during transit. Additionally, individuals should be transferred off spinal hard boards/backboards as soon as medically feasible.

3.3. Preventing Pressure Injuries in Seated Individuals Prevention strategies extend to seated individuals, who are also at significant risk. When selecting a seat or wheelchair, it is good practice to consider factors like the individual’s overall risk of pressure injuries, independence, mobility, activity needs, body size, shape and weight distribution, posture, deformity, asymmetry, need for enhanced features (e.g., dynamic weight shifting), and preferences and care goals.

A seating support surface with pressure redistribution properties is recommended for individuals at risk of pressure injuries when in a seated position. For those who cannot reposition themselves while seated, it is suggested that the duration of sitting out of bed should be limited as much as possible. Frequent repositioning is crucial for seated individuals at risk. Independent chair/wheelchair users should be taught and encouraged to perform pressure redistribution maneuvers and weight shifts as often as possible. Proper positioning in a seated position involves selecting a chair or wheelchair that provides support and maintains stability, selecting a reclined seated position with elevated and supported legs (heels free from the surface), or ensuring feet are well-supported, and utilizing dynamic weight shifting (tilt and recline).

3.4. Preventing Heel Pressure Injuries Heels are particularly vulnerable to pressure injury development. It is good practice to elevate the heels of individuals at risk so they are not in contact with the support surface. A heel offloading device appropriate to the individual’s mobility and activity level is suggested. If such a device is unavailable or inappropriate, standard pillows or cushions of sufficient height can be used to ensure the heels are off the support surface. The guideline makes no recommendation on the use of leave-on topical products for heel pressure injury prevention due to extremely low confidence in effect estimates and unclear mechanisms of action. However, a preventive dressing could be used as an adjunct to heel elevation and regular repositioning, where resources permit. If used, a soft silicone adhesive multilayered foam dressing is suggested.

4. Conclusion

Pressure injuries represent a preventable harm, and a robust understanding of their etiology is foundational to effective prevention. The complex interplay of localized ischemia, reperfusion injury, direct cell deformation, and impaired lymphatic function underscores the multifaceted nature of tissue compromise under sustained mechanical loads. The International Guideline provides critical evidence-based recommendations that emphasize minimizing the magnitude and duration of load on vulnerable tissue sites through individualized, comprehensive prevention approaches.

Central to these strategies is repositioning, which must be frequent and tailored to the individual’s specific needs and clinical status. The guideline advocates for two-hourly or three-hourly repositioning intervals for most at-risk individuals on appropriate support surfaces, with clarifiers for critically ill or palliative patients who may require different frequencies. Crucially, the guideline advises against routinely extending repositioning intervals to four, five, or six hourly. The use of specific angles, such as 30-degree lateral positioning, is a key strategy for preventing pressure injuries, particularly in offloading the sacrum and trochanters. For individuals with a higher body mass index, modifying to a 40-degree lateral position might be necessary to ensure maximum offloading, highlighting the need for individualized care even within standardized recommendations. These turning angles, as presented in the provided sources, are strictly for prevention and not for healing existing pressure injuries.

Beyond repositioning, the strategic use of appropriate full body and seating support surfaces, tailored to individual characteristics and risk profiles, further augments prevention efforts. Additionally, meticulous heel care and comprehensive nutritional assessment and intervention are integral components of a holistic prevention program. As the International Guideline continues to evolve as a “living guideline”, ongoing adherence to its recommendations and continuous education for healthcare professionals and caregivers will be paramount in reducing the incidence and burden of pressure injuries globally.

References

National Pressure Injury Advisory Panel, European Pressure Ulcer Advisory Panel and Pan Pacific Pressure Injury Alliance. (2025) Pressure Ulcers/Injuries: Definition and Etiology. In: Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline. The International Guideline: Fourth Edition. Available at: https://internationalguideline.com (Accessed: download date). [Cited as 1-10]

National Pressure Injury Advisory Panel, European Pressure Ulcer Advisory Panel and Pan Pacific Pressure Injury Alliance. (2025) Prevention and Treatment of Pressure Ulcers/Injuries: Quick Reference Guide Prevention Recommendations. The International Guideline: Fourth Edition. Available at: https://internationalguideline.com (Accessed: download date). [Cited as 51-88]