The Role of Shear Stress and Shear Strain in Pressure Injury Development.

ABSTRACT: Although other patient safety indicators have seen a decline, pressure injury (PI) incidence has continued to rise. In this article, the authors discuss the role of shear stress and shear strain in PI development and describe how accurate assessment and management can reduce PI risk. They provide explanations of shear stress, shear strain, friction, and tissue deformation to support a better clinical understanding of how damaging these forces are for soft tissue. Clinicians must carefully assess each patient's risk factors regarding shear forces within the contexts of activity and mobility. The authors also provide a toolbox of mitigation strategies, including support surface selection, selection of materials that contact the individual, management of immobility using positioning techniques, and the use of safe patient handling techniques. With a clear understanding of how shear forces affect PI risk and mitigation strategies, clinicians will more accurately assess PI risk and improve PI prevention care plans, ultimately reducing PI incidence to become more aligned with other patient safety indicators.

Best-practices for preventing skin injury beneath personal protective equipment during the COVID-19 pandemic: A position paper from the National Pressure Injury Advisory Panel.

COVID-19 has infected millions of patients and impacted healthcare workers worldwide. Personal Protective Equipment (PPE) is a key component of protecting frontline clinicians against infection. The benefits of PPE far outweigh the risks, nonetheless, many clinicians are exhibiting skin injury caused by PPE worn incorrectly. These skin injuries, ranging from lesions to open wounds are concerning because they increase the susceptibility of viral infection and transmission to other individuals. Early into the COVID-19 pandemic (April 2020), the U. S. National Pressure Injury Advisory Panel (NPIAP) developed a series of position statements to improve wear-ability of PPE and protect healthcare professionals and their patients as safe from harm as possible under the circumstances. The NPIAP positions, which were formed by conducting a systematic review of what was known at the time, include: (a) Prepare skin before and after wearing PPE with skin sealants, barrier creams and moisturisers; (b) Frequent PPE offloading to relieve pressure and shear applied to skin; (c) treat visible skin injuries immediately caused by PPE to minimise future infection; (d) non-porous dressings may provide additional skin protection, but lack evidence; (e) health systems should take care to educate clinicians about placement and personal hygiene related to handling PPE. Throughout all of these practices, handwashing remains a top priority to handle PPE. These NPIAP positions provided early guidance to reduce the risk of skin injury caused by PPE based on available research regarding PPE injuries, a cautious application of evidence-based recommendations on prevention of device-related pressure injuries in patients and the expert opinion of the NPIAP Board of Directors. Clinicians who adhere to these recommendations reduce the prospects of skin damage and long-term effects (e.g. scarring). These simple steps to minimise the risk of skin injury and reduce the risk of coronavirus infection from PPE can help.

Our contemporary understanding of the aetiology of pressure ulcers/pressure injuries.

In 2019, the third and updated edition of the Clinical Practice Guideline (CPG) on Prevention and Treatment of Pressure Ulcers/Injuries has been published. In addition to this most up-to-date evidence-based guidance for clinicians, related topics such as pressure ulcers (PUs)/pressure injuries (PIs) aetiology, classification, and future research needs were considered by the teams of experts. To elaborate on these topics, this is the third paper of a series of the CPG articles, which summarises the latest understanding of the aetiology of PUs/PIs with a special focus on the effects of soft tissue deformation. Sustained deformations of soft tissues cause initial cell death and tissue damage that ultimately may result in the formation of PUs/PIs. High tissue deformations result in cell damage on a microscopic level within just a few minutes, although it may take hours of sustained loading for the damage to become clinically visible. Superficial skin damage seems to be primarily caused by excessive shear strain/stress exposures, deeper PUs/PIs predominantly result from high pressures in combination with shear at the surface over bony prominences, or under stiff medical devices. Therefore, primary PU/PI prevention should aim for minimising deformations by either reducing the peak strain/stress values in tissues or decreasing the exposure time.

Development of a Wheelchair Repair Registry.

OBJECTIVE: To describe the development of a wheelchair repair registry from large datasets to attain an understanding of wheelchair failures and service repairs. DESIGN: Guidelines for registry development were applied and anchored around Labor-Tracker, a web-based information management system for wheelchair suppliers to manage and track wheelchair repairs. The registry was designed using online analytical processing, allowing for rapid data queries from multiple dimensions that enable complex data analysis and discovery. SETTING: The Wheelchair Repair Registry (WRR) was developed through an industry and academic collaboration whereby repair data were collected in the field, entered into the Labor-Tracker system, deidentified, and then transferred to the registry and made available for analyses. PARTICIPANTS: Wheelchair supplier service technicians reported data from repair services provided to individuals who use power wheelchairs, manual wheelchairs, and scooters. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Wheelchair failure and repair data, including variables related to scheduling, equipment information (eg, manufacturer, model, serial number, purchase date), labor, parts, and reasons for repairs. RESULTS: The WRR was developed to analyze wheelchair repairs and failures from the Labor-Tracker system. Currently, the registry has more than 60,000 repairs conducted on more than 5000 wheelchair devices from 25 manufacturers. The devices include 60% power wheelchairs, 35% manual wheelchairs, and 5% scooters. CONCLUSIONS: The WWR creates opportunities to apply large-data analytical methodologies that will serve to inform quality standards, practice, equipment selection, preventative maintenance routines, product design, and policy.

A comparison of air-cell and gel surgical table pads and an evaluation of the influence of pressure distribution and other factors on pressure injury prevention.

Guidelines for pressure injury prevention consider the use of pressure-redistributing pads to prevent tissue deformation. However, limited research exists to assess the pressure distribution provided by the operating tables and the effectiveness of pressure-redistributing pads in preventing pressure injuries. In this study, we compared the pressure distribution properties of two surgical table pads and identified parameters influencing pressure injury outcomes after a lengthy surgical procedure. Twenty-seven patients undergoing left ventricular assist device implantation surgery participated in the study. Participants were randomly assigned to use either an air cell-based pad or a gel pad. Interface pressure was recorded during the surgery. We analyzed the effect of surgical table pad type, interface pressure distribution and pressure injury outcomes and analyzed what characteristics of the patients and the interface pressure are most influential for the development of pressure injuries. Comparing the interface pressure parameters between the air-cell group and the gel group, only the peak pressure index x time was significantly different (p < 0.05). We used univariate logistic regression analysis to identify significant predictors for the pressure injury outcome. The support surface was not significant. And, among patient characteristics, only age and BMI were significant (p ≤ 0.05). Among the interface pressure parameters, pressure density maxima, peak pressure index x time, and coefficient of variation were significant for pressure injury outcome (p ≤ 0.05). Peak pressure index, average pressure, and the surgery length were not statistically significant for pressure injury outcomes.

Sacral skin blood flow response to alternating pressure operating room overlay.

Pressure injuries resulting from long surgeries may be caused by prolonged ischemia. Operating table surfaces with alternating pressure (AP) features may reduce the risk of ischemia-induced pressure injuries by providing periodic relief of blood flow occlusions. Prior research investigated alternating loading applied with a single isolated rigid indenter and demonstrated increased perfusion. This study quantified effects of an overlay with AP on sacral skin perfusion for individuals lying supine for 60-min while blood flow was monitored. The mean normalized sacral skin blood flow was found to be greater with the AP overlay over an operating table pad compared to the operating pad alone (pad with AP mean SBF = 1.45 ±â€¯1.16, pad without AP mean SBF = 1.03 ±â€¯0.46, p = 0.10). Peak and average interface pressure at the sacrum was significantly lower during the deflation cycle of the AP surface compared to the operating pad alone (P < 0.001), suggesting this periodic reduction resulted in higher mean blood flow. Post-hoc regression analysis showed participant body mass index was a significant predictor of the effectiveness of the AP overlay (p = 0.012). The results suggest risk for pressure injuries due to prolonged ischemia might be mitigated by the addition of an alternating pressure feature on operating table pads for lower BMI patients.

Implementing local cooling to increase skin tolerance to ischemia during normal seating in people with spinal cord injury.

The purpose of this study was to investigate the effectiveness of local cooling in reducing reactive hyperemia after ischemia at the ischial tuberosities for people with spinal cord injury (SCI) during normal seating. The degree of the reactive hyperemic response is indicative of the extent of cellular stress caused by the ischemia. We hypothesized that reactive hyperemic skin blood flow (SBF) responses will be lower when local cooling is implemented by the wheelchair seat cushion. This study used a repeated measures design, and each subject underwent two conditions: normal seating with temperature control 'on' (cooling) and 'off' (non-cooling) for 30 min. Twenty-three participants with traumatic SCI were recruited. SBF and skin temperature were collected before, during and after seating. SBF signals were processed with short-time Fourier analyses to examine the underlying vascular control mechanisms, including the following (corresponding frequency bands): metabolic (0.0095-0.02 Hz), neurogenic (0.02-0.05 Hz), and myogenic (0.05-0.15 Hz) spectral densities. Our results showed that with cooling, skin temperature decreased (range -0.4 ~ -3.1 °C, p = 0.002), and reactive hyperemia parameters (normalized peak SBF and perfusion area) were reduced (p = 0.02, p = 0.033, respectively). In addition, changes in normalized peak SBF (non-cooling - cooling) was moderately correlated with changes in normalized metabolic and neurogenic spectral densities. Our findings suggested that local cooling has a positive effect on reducing the cellular stress caused by ischemia during normal seating. Metabolic and neurogenic SBF control mechanisms may play a minor role. Further exploration of the effect of temperature control on pressure injury prevention is warranted.

Detection and classification methodology for movements in the bed that supports continuous pressure injury risk assessment and repositioning compliance.

Pressure injuries are costly to the healthcare system and mostly preventable, yet incidence rates remain high. Recommendations for improved care and prevention of pressure injuries from the Joint Commission revolve around continuous monitoring of prevention protocols and prompts for the care team. The E-scale is a bed weight monitoring system with load cells placed under the legs of a bed. This study investigated the feasibility of the E-scale system for detecting and classifying movements in bed which are relevant for pressure injury risk assessment using a threshold-based detection algorithm and a K-nearest neighbor classification approach. The E-scale was able to detect and classify four types of movements (rolls, turns in place, extremity movements and assisted turns) with >94% accuracy. This analysis showed that the E-scale could be used to monitor movements in bed, which could be used to prompt the care team when interventions are needed and support research investigating the effectiveness of care plans.

Medical Rehabilitation: Guidelines to Advance the Field With High-Impact Clinical Trials.

The purpose of this Special Communication is to summarize guidelines and recommendations stemming from an expert panel convened by the National Institutes of Health, National Center for Medical Rehabilitation Research (NCMRR) for a workshop entitled The Future of Medical Rehabilitation Clinical Trials, held September 29-30, 2016, at the NCMRR offices in Bethesda, Maryland. The ultimate goal of both the workshop and this summary is to offer guidance on clinical trials design and operations to the medical rehabilitation research community, with the intent of maximizing the effect of future trials.

An MRI investigation of the effects of user anatomy and wheelchair cushion type on tissue deformation.

AIM OF THE STUDY: Tissue deformation is recognized as an important risk factor for pressure injuries. This study investigated the effects of anatomy and wheelchair cushion type on tissue deformation. MATERIALS AND METHODS: Direct 3-dimensional tissue deformation response was measured for six participants sitting on six different wheelchair cushions using MR imaging. Two participants had a traumatic spinal cord injury (SCI) within one year of the assessment, two sustained traumatic SCI at least 13 years prior, and two were without SCI. Tissue deformation was quantified using the difference in volume of tissue beneath the ischial tuberosity (IT) between unloaded and loaded (sitting) conditions. RESULTS: The participants with SCI tended to have less muscle tissue volume beneath their ITs while sitting compared to participants without SCI. Reductions in muscle and fat volumes in the loaded conditions varied depending on both cushion and participant. Higher interface pressures tended to be associated with lower unloaded tissue thicknesses. CONCLUSION: The study showed no single cushion type tested produced the lowest amount of tissue deformation across all participants. Individual anatomy and cushion type affect deformation response of tissue and related pressure injury risk.

Inflammatory Mediators Associated With Pressure Ulcer Development in Individuals With Pneumonia After Traumatic Spinal Cord Injury: A Pilot Study.

OBJECTIVE: To identify the inflammatory mediators around the time of pneumonia onset associated with concurrent or later onset of pressure ulcers (PUs). DESIGN: Retrospective. SETTING: Acute hospitalization and inpatient rehabilitation unit of a university medical center. PARTICIPANTS: Individuals (N=86) with traumatic spinal cord injury (SCI) were included in the initial analyses. Fifteen of the 86 developed pneumonia and had inflammatory mediator data available. Of these 15, 7 developed PUs and 8 did not. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Twenty-three inflammatory mediators in plasma and urine were assayed. The differences in concentrations of plasma and urine inflammatory mediators between the closest time point before and after the diagnosis of pneumonia were calculated. RESULTS: Initial chi-square analysis revealed a significant (P=.02) association between pneumonia and PUs. Individuals with SCI and diagnosed pneumonia had nearly double the risk for developing PUs compared with those with no pneumonia. In individuals with pneumonia, Mann-Whitney U exact tests suggested an association (P<.05) between the formation of a first PU and a slight increase in plasma concentrations of tumor necrosis factor-alpha (TNF-α), and a decrease in urine concentrations of TNF-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukin (IL)-15 after onset of pneumonia. CONCLUSIONS: These findings suggest that a relatively small increase in plasma TNF-α, and decreases in urine TNF-α, GM-CSF, and IL-15 from just before to just after the diagnosis of pneumonia could be markers for an increased risk of PUs in individuals with pneumonia after traumatic SCI.

How a diverse research ecosystem has generated new rehabilitation technologies: Review of NIDILRR's Rehabilitation Engineering Research Centers.

Over 50 million United States citizens (1 in 6 people in the US) have a developmental, acquired, or degenerative disability. The average US citizen can expect to live 20% of his or her life with a disability. Rehabilitation technologies play a major role in improving the quality of life for people with a disability, yet widespread and highly challenging needs remain. Within the US, a major effort aimed at the creation and evaluation of rehabilitation technology has been the Rehabilitation Engineering Research Centers (RERCs) sponsored by the National Institute on Disability, Independent Living, and Rehabilitation Research. As envisioned at their conception by a panel of the National Academy of Science in 1970, these centers were intended to take a "total approach to rehabilitation", combining medicine, engineering, and related science, to improve the quality of life of individuals with a disability. Here, we review the scope, achievements, and ongoing projects of an unbiased sample of 19 currently active or recently terminated RERCs. Specifically, for each center, we briefly explain the needs it targets, summarize key historical advances, identify emerging innovations, and consider future directions. Our assessment from this review is that the RERC program indeed involves a multidisciplinary approach, with 36 professional fields involved, although 70% of research and development staff are in engineering fields, 23% in clinical fields, and only 7% in basic science fields; significantly, 11% of the professional staff have a disability related to their research. We observe that the RERC program has substantially diversified the scope of its work since the 1970's, addressing more types of disabilities using more technologies, and, in particular, often now focusing on information technologies. RERC work also now often views users as integrated into an interdependent society through technologies that both people with and without disabilities co-use (such as the internet, wireless communication, and architecture). In addition, RERC research has evolved to view users as able at improving outcomes through learning, exercise, and plasticity (rather than being static), which can be optimally timed. We provide examples of rehabilitation technology innovation produced by the RERCs that illustrate this increasingly diversifying scope and evolving perspective. We conclude by discussing growth opportunities and possible future directions of the RERC program.

A Computational, Tissue-Realistic Model of Pressure Ulcer Formation in Individuals with Spinal Cord Injury.

People with spinal cord injury (SCI) are predisposed to pressure ulcers (PU). PU remain a significant burden in cost of care and quality of life despite improved mechanistic understanding and advanced interventions. An agent-based model (ABM) of ischemia/reperfusion-induced inflammation and PU (the PUABM) was created, calibrated to serial images of post-SCI PU, and used to investigate potential treatments in silico. Tissue-level features of the PUABM recapitulated visual patterns of ulcer formation in individuals with SCI. These morphological features, along with simulated cell counts and mediator concentrations, suggested that the influence of inflammatory dynamics caused simulations to be committed to "better" vs. "worse" outcomes by 4 days of simulated time and prior to ulcer formation. Sensitivity analysis of model parameters suggested that increasing oxygen availability would reduce PU incidence. Using the PUABM, in silico trials of anti-inflammatory treatments such as corticosteroids and a neutralizing antibody targeted at Damage-Associated Molecular Pattern molecules (DAMPs) suggested that, at best, early application at a sufficiently high dose could attenuate local inflammation and reduce pressure-associated tissue damage, but could not reduce PU incidence. The PUABM thus shows promise as an adjunct for mechanistic understanding, diagnosis, and design of therapies in the setting of PU.

Early Detection of Pressure Ulcer Development Following Traumatic Spinal Cord Injury Using Inflammatory Mediators.

OBJECTIVE: To identify changes in concentrations of inflammatory mediators in plasma and urine after traumatic spinal cord injury (SCI) and before the occurrence of a first pressure ulcer. DESIGN: Retrospective; secondary analysis of existing data. SETTING: Acute hospitalization and inpatient rehabilitation sites at a university medical center. PARTICIPANTS: Individuals with a pressure ulcer and plasma samples (n=17) and individuals with a pressure ulcer and urine samples (n=15) were matched by age and plasma/urine sample days to individuals with SCI and no pressure ulcer (N=35). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Plasma and urine samples were assayed in patients with SCI, capturing samples within 4 days after the SCI to a week before the formation of the first pressure ulcer. The Wilcoxon signed-rank test was performed to identify changes in the inflammatory mediators between the 2 time points. RESULTS: An increase in concentration of the chemokine interferon-γ-induced protein of 10kd/CXCL10 in plasma (P<.01) and a decrease in concentration of the cytokine interferon-α in urine (P=.01) were observed before occurrence of a first pressure ulcer (∼4d) compared with matched controls. CONCLUSIONS: Altered levels of inflammatory mediators in plasma and urine may be associated with pressure ulcer development after traumatic SCI. These inflammatory mediators should be explored as possible biomarkers for identifying individuals at risk for pressure ulcer formation.

Friction-induced skin injuries-are they pressure ulcers? An updated NPUAP white paper.

Friction injuries are often misdiagnosed as pressure ulcers. The reason for the misdiagnosis may be a misinterpretation of classic pressure ulcer literature that reported friction increased the susceptibility of the skin to pressure damage. This analysis assesses the classic literature that led to the inclusion of friction as a causative factor in the development of pressure ulcers in light of more recent research on the effects of shear. The analysis in this article suggests that friction can contribute to pressure ulcers by creating shear strain in deeper tissues, but friction does not appear to contribute to pressure ulcers in the superficial layers of the skin. Injuries to the superficial layers of the skin caused by friction are not pressure ulcers and should not be classified or treated as such.

Standardizing Support Surface Testing and Reporting: A National Pressure Ulcer Advisory Panel Executive Summary.

In 2001, the National Pressure Ulcer Advisory Panel's Research Committee identified the need to create uniform terminology, test methods, and reporting technical standards for support surfaces. As a result, the S3I Committee was formed and initial meetings of interested stakeholders who included clinicians, researchers, academics, manufacturers, providers, and regulators were held. The group's initial goal was to (1) establish common language to facilitate understanding by developing standardized terminology for describing and discussing support surfaces, (2) establish a suite of standardized tests of performance capable of repeatedly, reliably, and accurately reporting upon characteristics common to all support surfaces that are believed to be related to the extrinsic risk factors associated with skin breakdown, as indicated by the literature to date, and (3) identify and standardize methods to evaluate the effective life of a support surface. The purpose of this article was to summarize the current status of the effort of the Support Surface Standards Initiative (S3I) Committee to identify and standardize methods to evaluate the many characteristic factors that determine the effective life of a support surface.

Inducible protein-10, a potential driver of neurally controlled interleukin-10 and morbidity in human blunt trauma.

OBJECTIVE: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. DESIGN: Retrospective study. SETTINGS: Tertiary care institution. PATIENTS: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1ß, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1α and 1ß, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. CONCLUSION: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.

Hybrid equation/agent-based model of ischemia-induced hyperemia and pressure ulcer formation predicts greater propensity to ulcerate in subjects with spinal cord injury.

Pressure ulcers are costly and life-threatening complications for people with spinal cord injury (SCI). People with SCI also exhibit differential blood flow properties in non-ulcerated skin. We hypothesized that a computer simulation of the pressure ulcer formation process, informed by data regarding skin blood flow and reactive hyperemia in response to pressure, could provide insights into the pathogenesis and effective treatment of post-SCI pressure ulcers. Agent-Based Models (ABM) are useful in settings such as pressure ulcers, in which spatial realism is important. Ordinary Differential Equation-based (ODE) models are useful when modeling physiological phenomena such as reactive hyperemia. Accordingly, we constructed a hybrid model that combines ODEs related to blood flow along with an ABM of skin injury, inflammation, and ulcer formation. The relationship between pressure and the course of ulcer formation, as well as several other important characteristic patterns of pressure ulcer formation, was demonstrated in this model. The ODE portion of this model was calibrated to data related to blood flow following experimental pressure responses in non-injured human subjects or to data from people with SCI. This model predicted a higher propensity to form ulcers in response to pressure in people with SCI vs. non-injured control subjects, and thus may serve as novel diagnostic platform for post-SCI ulcer formation.