Our understanding of pressure injury etiology and development has grown in recent years through research, clinical expertise, and global interdisciplinary expert collaboration. Therefore, the National Pressure Ulcer Advisory Panel (NPUAP) has revised the definition and stages of pressure injury. The revision was undertaken to incorporate the current understanding of the etiology of pressure injuries, as well as to clarify the anatomical features present or absent in each stage of injury. An NPUAP-appointed Task Force reviewed the literature and created drafts of definitions, which were then reviewed by stakeholders and the public, including clinicians, educators, and researchers around the world. Using a consensus-building methodology, these revised definitions were the focus of a multidisciplinary consensus conference held in April 2016. As a result of stakeholder and public input, along with the consensus conference, important changes were made and incorporated into the new staging definitions. The revised staging system uses the term injury instead of ulcer and denotes stages using Arabic numerals rather than Roman numerals. The revised definition of a pressure injury now describes the injuries as usually occurring over a bony prominence or under a medical or other device. The revised definition of a Stage 2 pressure injury seeks to clarify the difference between moisture-associated skin damage and injury caused by pressure and/or shear. The term suspected has been removed from the Deep Tissue Pressure Injury diagnostic label. Each definition now describes the extent of tissue loss present and the anatomical features that may or may not be present in the stage of injury. These important revisions reflect the methodical and collaborative approach used to examine the available evidence and incorporate current interdisciplinary clinical expertise into better defining the important phenomenon of pressure injury etiology and development.

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PURPOSE: The purpose of this study was to determine overall pressure injury (PI) prevalence and hospital-acquired pressure injury (HAPI) prevalence in US acute care hospitals. Additionally, analysis of patient characteristics associated with HAPIs will be presented. DESIGN: Observational, cross-sectional cohort study. SUBJECTS AND SETTING: An in-depth analysis of data was performed from the International Pressure Ulcer Prevalence™ (IPUP) Survey database for years 2018-2019 that included 296,014 patients. There were 914 participating US acute care facilities in 2018 and 887 in 2019. Overall PI prevalence and HAPI prevalence over time were also examined for 2006-2019 acute care data from 2703 unique facilities (1,179,108 patients). METHODS: Overall PI prevalence and HAPI prevalence were analyzed from the 2006-2019 IPUP survey database. Recent data for 2018-2019 PI prevalence are reported separately for medical-surgical, step-down, and critical care unit types. PI stages, anatomic locations, Braden score associated with HAPIs, and body mass index were analyzed. RESULTS: Overall PI prevalence and HAPI prevalence data declined between 2006 and 2019; however, the prevalence plateaued in the years 2015-2019. Data from 2018 to 2019 (N = 296,014) showed that 26,562 patients (8.97%) had at least one PI and 7631 (2.58%) had at least one HAPI. Patients cared for in medical-surgical inpatient care units had the lowest overall PI prevalence (7.78%) and HAPI prevalence (1.87%), while critical care patients had the highest overall PI prevalence (14.32%) and HAPI prevalence (5.85%). Critical care patients developed more severe PIs (stage 3,4, unstageable, and deep-tissue pressure injuries [DTPIs]), which were proportionally higher than those in the step-down or medical-surgical units. The sacrum/coccyx anatomic location had the highest overall PI prevalence and HAPI prevalence, except for DTPIs, which most common occurred on the heel. CONCLUSIONS: Overall and HAPI prevalence has plateaued 2015-2019. Prevalence of HAPIs, especially in critical care units, remain high. While medical advancements have improved survival rates among critically ill patients, survival may come with unintended consequences, including PI development.

In the vast majority of cases, appropriate identification and mitigation of risk factors can prevent or minimize pressure ulcer (PU) formation. However, some PUs are unavoidable. Based on the importance of this topic and the lack of literature focused on PU unavoidability, the National Pressure Ulcer Advisory Panel hosted a multidisciplinary conference in 2014 to explore the issue of PU unavoidability within an organ system framework, which considered the complexities of nonmodifiable intrinsic and extrinsic risk factors. Prior to the conference, an extensive literature review was conducted to analyze and summarize the state of the science in the area of unavoidable PU development and items were developed. An interactive process was used to gain consensus based on these items among stakeholders of various organizations and audience members. Consensus was reached when 80% agreement was obtained. The group reached consensus that unavoidable PUs do occur. Consensus was also obtained in areas related to cardiopulmonary status, hemodynamic stability, impact of head-of-bed elevation, septic shock, body edema, burns, immobility, medical devices, spinal cord injury, terminal illness, and nutrition.

Analysis of the proteomic profile of pressure ulcers over time is a critical step in the identification of biomarkers of healing or nonhealing in pressure ulcers. The wound fluid from 32 subjects with 42 pressure ulcers was evaluated over 6 weeks at 15 time points. Samples specific to both the interior and the periphery of the wound bed were collected. Antibody screening arrays, isobaric tags for relative and absolute quantitation with mass spectrometry and multiplexed microarrays were used to characterize wound fluid and results were correlated with clinical outcome. Twenty-one proteins were found to distinguish between healed and chronic wounds and 19 proteins were differentially expressed between the interior and periphery of wounds. Four proteins, pyruvate kinase isozymes M1/M2, profilin-1, Ig lambda-1 chain C regions, and Ig gamma-1 chain C region, were present in lower levels for periphery samples when compared to interior samples and six proteins, keratin, type II cytoskeletal 6A (KRT6A), keratin, type I cytoskeletal 14, S100 calcium binding proteins A7, alpha-1-antitrypsin precursor, hemoglobin subunit alpha, and hemoglobin subunit beta, were present in higher levels in periphery samples when compared with interior samples. S100 calcium binding protein A6, S100 calcium binding protein A7, and soluble receptor for advanced glycation end-products had higher levels in the periphery of chronic wounds vs. the interior in planar arrays. A significant temporal trend was noted for monokine induced by gamma interferon (MIG), synonomous with chemokine (C-X-C motif) ligand 9 (CXCL9), which increased as wounds healed and remained nearly constant for ulcers that were not approaching closure.

Acute and chronic osteomyelitis can be difficult to treat by conventional means. Current methods of treatment involve the use of systemic antibiotics, the local implantation of non-degradable drug carriers, and surgical débridement. Each method has specific drawbacks. We report on the use of a new controlled release system utilizing gentamicin and bioerodible, biocompatible polymers (polyanhydrides) designed for drug delivery applications for the treatment of clinical osteomyelitis. We compared this system's ability to reduce bacterial levels in infected bone with that of conventional non-degradable delivery systems based on polymethylmethacrylate (PMMA) and gentamicin. Polyanhydride copolymers of bis-carboxyphenoxypropane and sebacic acid P loaded with gentamicin sulfate and PMMA/gentamicin matrices were implanted in the long bones of Sprague-Dawley rats infected with a strain of Staphylococcus aureus. After 3 weeks of implantation, the polymeric delivery devices were removed and quantitative cultures were used to determine bacterial levels in bone. The polyanhydride/gentamicin matrices demonstrated significant degradation over the 3 week implantation period. Levels of bacteria, measured in colony forming units, were significantly lower in bone implanted with the polyanhydride/gentamicin release system than in long bones of control animals without an implant (p < 0.01), of animals with a polyanhydride polymer implant alone (p < 0.01), and of animals with a PMMA/gentamicin implant (p = 0.03). Bioerodible polyanhydrides show promise as a new treatment modality for infections in bone.

PURPOSE:The purpose of this secondary analysis was to examine pressure injury (PI) prevalence, PI risk factors, and prevention practices among adult critically ill patients in critical care units in the United States using the International Pressure Ulcer Prevalence™ (IPUP) Survey database from 2018 to 2019. DESIGN: Observational, cohort study with cross-sectional data collection and retrospective data analysis. SUBJECTS AND SETTING:The sample comprised 41,866 critical care patients drawn from a sample of 296,014 patients in US acute care facilities who participated in the 2018 and/or 2019 IPUP surveys. The mean age among critical care patients was 63.5 years (16.3) and 55% were male. All geographic regions of the United States were represented in this sample, with the greatest percentages from the Southeast (47.5%) and Midwest (17.5%) regions. METHODS: Overall critical care PI prevalence and hospital-acquired PI (HAPI) rates were obtained and analyzed using the 2018/2019 IPUP survey database. Critical care PI risk factors included in the database were analyzed using frequency distributions. Prevention practices among critically ill patients were analyzed to evaluate differences in practices between patients with no PIs, superfi cial PIs (stage 1, stage 2), and severe PIs (stage 3, stage 4, unstageable, deep tissue pressure injury). RESULTS:The overall PI prevalence for critical care patients was 14.3% (n = 5995) and the overall HAPI prevalence was 5.85% (n = 2451). In patients with severe HAPIs, the most common risk factors were diabetes mellitus (29.5%), mechanical ventilation (27.6%), and vasopressor agents (18.9%). Signifi cant differences between patients with no PIs as compared to those with superfi cial or severe HAPIs ( P = .000) for all prevention practices were found. CONCLUSIONS: Study fi ndings support the gaps elucidated in previous critical care studies on PI development in this population. The 2 most persistent gaps currently challenging critical care practitioners are (1) accurate risk quantifi cation in this population and (2) the potential for unavoidability in PI development among critically ill patients.

The incidence rate of pressure ulcers in the USA ranges from 0.4% to 38% in acute care settings and from 2.2% to 23.9% in long-term care settings, and their treatment costs are in the billions of dollars yearly. The proteome of wound fluid may contain early indicators or biomarkers associated with healing in pressure ulcers that would enable treatment regimes to be optimised for each individual. Wound fluid was collected from the interior and periphery of 19 chronic pressure ulcers at 15 time points during 42 days for an analysis of protein expression. Proteins were fractionated using two-dimensional polyacrylamide gel electrophoresis. A comparison of the spot distributions indicates a biochemical difference between the interior and the periphery of wounds. Pressure ulcers that healed show a greater number of spots for interior and peripheral locations combined over time when compared with wounds that did not heal. Using this technique, protein S100A9 was identified as a potential biomarker of wound healing. The identification of differences within the proteome of healing versus non healing pressure ulcers could have great significance in the use of current treatments, as well as the development of new therapeutic interventions.