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.

A Randomized Clinical Trial of Wheeled Mobility for Pressure Injury Prevention and Better Function.

OBJECTIVES: To evaluate the effectiveness of wheelchair assessment and configuration on pressure injury incidence, mobility, and functioning in a wheelchair. DESIGN: Randomized controlled trial with participants individually randomized into intervention and control groups. SETTING: Nursing home. PARTICIPANTS: Nursing home residents aged 60 and older who used wheelchairs and were at risk for pressure injuries (N=258). INTERVENTION: Treatment and evaluation, individually configured wheelchair and skin protection cushion; control and evaluation, facility-provided wheelchair and skin protection cushion. MEASUREMENTS: Pressure injury incidence, Nursing Home Life Space Diameter score, Functioning Every Day in a Wheelchair-Capacity (FEW-C) score, and Wheelchair Skills Test (WST) score. RESULTS: No differences in pressure injuries (p=.77) were found. Pelvic rotation (odds ratio (OR)=0.15, 95% confidence interval (CI)=0.03-0.70, p=.02) and Day 14 WST skill score (OR=0.74, 95% CI=0.60-0.91, p=.004) were significant predictors of pressure injuries. Significant differences were observed between groups in change in FEW-C independence scores between before randomization and endpoint (p=.03) and before randomization and 14 days (p=.04). CONCLUSION: Participants with individually configured wheelchairs improved more in the safe and effective use of their wheelchairs than residents with facility-provided wheelchairs. The outcomes indicated that nursing home residents functioned safely at a higher level in their wheelchairs if their devices were individually configured using a comprehensive wheelchair and seating assessment process. There was no difference in the incidence of pressure injuries between the two groups. TRIAL REGISTRATION: NCT01275313.

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.

Association between presence of pneumonia and pressure ulcer formation following traumatic spinal cord injury.

OBJECTIVE: To determine if the presence of pneumonia and pressure ulcers are associated in individuals with an acute spinal cord injury during acute care and rehabilitation hospitalizations. DESIGN: Retrospective, secondary analyses of data obtained from the Spinal Cord Injury Model Systems enrolled from 1993 until 2006 Setting: Acute care hospitalization and inpatient rehabilitation facilities Participants: A cohort of individuals hospitalized in acute care (n = 3,098) and inpatient rehabilitation (n = 1,768) was included in the analysis. Frequencies of pressure ulcer formation and episodes of pneumonia were noted in both settings. INTERVENTIONS: Not applicable. OUTCOME MEASURES: Pressure ulcer formation and diagnosis of pneumonia Results: The development of pressure ulcers, including stage I, was 20.3% acute care and 21.1% during in inpatient rehabilitation. Multivariate logistic regression analyses revealed a significant association of pneumonia with occurrence of pressure ulcers (P ≤ 0.001, OR = 2.3 and 2.2 respectively), the American Spinal Injury Association Impairment Scale grades (P < 0.001), and utilization of mechanical ventilation (P < 0.01) in both settings. CONCLUSION: A higher presence of pressure ulcers was found in individuals with pneumonia, after adjusting for injury severity, age, sex, and utilization of mechanical ventilation. Impaired inflammatory response and decreased mobility in individuals with pneumonia may predispose these individuals to develop pressure ulcers. Surveillance and preventive measures for pressure ulcers should be rigorous in individuals with SCI and pneumonia.

Feasibility of freehand ultrasound to measure anatomical features associated with deep tissue injury risk.

Deep tissue injuries (DTI) are severe forms of pressure ulcers that start internally and are difficult to diagnose. Magnetic resonance imaging (MRI) is the currently preferred imaging modality to measure anatomical features associated with DTI, but is not a clinically feasible risk assessment tool. B-mode ultrasound (US) is proposed as a practical, alternative technology suitable for bedside or outpatient clinic use. The goal of this research was to confirm US as an imaging modality for acquiring measurements of anatomical features associated with DTI. Tissue thickness measurements using US were reliable (ICC=.948) and highly correlated with MRI measurements (muscle r=.988, p ≤ .001; adipose r=.894, p ≤ .001; total r=.919; p ≤ .001). US measures of muscle tissue thickness were 5.4mm (34.1%) higher than MRI, adipose tissue thickness measures were 1.6mm (11.9%) lower, and total tissue thickness measures were 3.8mm (12.8%) higher. Given the reliability and ability to identify high-risk anatomies, as well as the cost effectiveness and availability, US measurements show promise for use in future development of a patient-specific, bedside, biomechanical risk assessment tool to guide clinicians in appropriate interventions to prevent DTI.

Predictive validity of the Spinal Cord Injury Pressure Ulcer Scale (SCIPUS) in acute care and inpatient rehabilitation in individuals with traumatic spinal cord injury.

OBJECTIVE: To evaluate the validity of the Spinal Cord Injury Pressure Ulcer Scale (SCIPUS) during acute care and inpatient rehabilitation following spinal cord injury (SCI) by determining critical cutoff points and assessing the ability to predict risk for pressure ulceration (PrU). DESIGN: Retrospective. METHODS: Sensitivity, specificity, and area under the curve (AUC) for the receiver operating characteristic were determined for the scale's ability to predict PrU 2-3 and 5-7 days after administrating the SCIPUS during acute care, and 5-7 and 14-21 days after administrating the SCIPUS during inpatient rehabilitation. RESULTS: During acute hospitalization, SCIPUS's ability to assess risk for PrUs within 2-3 days was determined at cutoff score of 15 with 100% sensitivity and 75% specificity, AUC = 0.85. The scale was unable to assess PrU risk at 5-7 days, AUC < 0.6 at cutoff score of 13. During inpatient rehabilitation, the scale was unable to assess PrU risk at 5-7 and 14-21 days, AUC < 0.6 at cutoff score of 9. CONCLUSIONS: The SCIPUS could predict PrU occurring within 2-3 days following administration during acute, but unable to predict over a longer term within acute or inpatient rehabilitation. Improved PrU risk assessment following SCI may be possible with modification to the SCIPUS.

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.

Relative contributions of interface pressure, shear stress, and temperature on ischemic-induced, skin-reactive hyperemia in healthy volunteers: a repeated measures laboratory study.

Although the primary risk factors for pressure ulcer development - pressure, shear, skin temperature, moisture, and friction - have been identified for decades, the relative contribution of each to this risk remains unclear. To confirm the results of and expand upon earlier research into the relative contributions of interface pressures, shear stress, and skin temperature among 4 healthy volunteers, a study involving 6 additional healthy 40- to 75-year-old volunteers was conducted and results of the 2 studies were pooled. All 3 variables (interface pressures, shear stress, and skin temperature) were systematically and randomly varied. In the prone position, volunteers each underwent 18 test conditions representing different combinations of temperature (28˚ C, 32˚ C, 36˚ C), pressure (8.0 and 13.3 kPa), and shear (0, 6.7, and 14.0 kPa) using a computer-controlled indenter applied to the sacrum for 20 minutes exerting weights of 100 g and 200 g to induce 0.98 N and 1.96 N of shear force, respectively. Each condition was tested twice, resulting in a total of 360 trials. Magnitude of postload reactive hyperemia as an index of ischemia was measured by laser Doppler flowmetry. Fixed effects regression models were used to predict 3 different indices of reactive hyperemic magnitude. Friedman tests were performed to compare the reactive hyperemia among 3 different skin temperatures or shear stresses under the same amount of localized pressure. In all regression models, pressure and temperature were highly significant predictors of the extent of reactive hyperemia (P <0.0001 and P <0.0001, respectively); the contributions of shear stress were not statistically significant (P = 0.149). With higher temperature, reactive hyperemia increased significantly, especially at greater localized pressure and shear stress, and the difference was more profound between 32˚ C and 36˚ C than between 28˚ C and 32˚ C. These results confirm that, in laboratory settings, temperature is an important factor in tissue ischemia. Additional studies examining the relative importance of pressure, shear, and temperature and potential effects of lowering temperature on tissue ischemia in healthy volunteers and patients at risk for pressure ulcer development are warranted. Because deformation at weight-bearing areas often results in blood flow occlusion, actively lowering the temperature may reduce the severity of ischemia and lower pressure ulcer risk. In this study, shear did not appear to contribute to ischemia in the dermal tissues when assessed using laser Doppler; further work is needed to examine its effect on deeper layers, particularly with regard to nonischemic mechanisms.

Effectiveness of local cooling for enhancing tissue ischemia tolerance in people with spinal cord injury.

OBJECTIVE: To investigate the effects of localized cooling and cooling rate on pressure-induced ischemia for people with and without neurological deficits. DESIGN: A 2 × 3 mixed factorial design with two groups: (1) people with spinal cord injury (SCI) and (2) people without neurological deficits (control), and three test conditions: (1) pressure only, (2) pressure with fast cooling (-4°C/min), and (3) pressure with slow cooling (-0.33°C/min). SETTING: University laboratory. PARTICIPANTS: Fourteen controls and 14 individuals with SCI. INTERVENTIONS: Pressure on the sacrum was 0.4 kPa for 5 minutes, then 8 kPa for 20 minutes, and finally 0.4 kPa for 15 minutes. Fast and slow cooling to 25°C applied during 8 kPa of pressure. OUTCOME MEASURES: Reactive hyperemia and its spectral densities in the metabolic, neurogenic, and myogenic frequency ranges. RESULTS: In controls, reactive hyperemia was greater in pressure only as compared with both cooling conditions. No change was noted in all spectral densities in both cooling conditions, and only neurogenic spectral density increased without cooling. In subjects with SCI, no difference was noted in reactive hyperemia among conditions. However, metabolic and myogenic spectral densities increased without cooling and all spectral densities increased with slow cooling. No change was noted in all spectral densities with fast cooling. CONCLUSION: Local cooling reduced the severity of ischemia in controls. This protective effect may be masked in subjects with SCI due to chronic microvascular changes; however, spectral analysis suggested local cooling may reduce metabolic vasodilation. These findings provide evidence towards the development of support surfaces with temperature control for weight-bearing soft tissues.

The relative contributions of interface pressure, shear stress, and temperature on tissue ischemia: a cross-sectional pilot study.

Tissue ischemia is thought to play a major role in the development of pressure ulcers. Pressure, shear, and temperature are acknowledged contributors, but the relative magnitude of each factor is largely unknown. A cross-sectional pilot study was conducted on the sacrums of four healthy volunteers to estimate the relative contributions of each variable by systematically varying and assessing the resulting level of ischemia in the skin tissue. Using a repeated measures design, 21 combinations of temperature (28˚C, 32˚C, and 36˚C); pressure (0 kPa, 8.0 kPa, and 13.3 kPa), corresponding to 0 mm Hg, 60 mm Hg, and 100 mm Hg; and shear stress (0 kPa, 6.7 kPa, and 14.0 kPa), corresponding to 0 mm Hg, 50 mm Hg, and 100 mm Hg (practical testing values), were tested twice, for a total of 168 trials. Using laser Doppler flowmetry, the magnitude of post-load reactive hyperemia was used as an index of ischemia. Fixed Effects and Ranks linear regression models were developed to predict three different indices of reactive hyperemic magnitude with pressure, shear stress, and temperature as the variables. Pressure and temperature were always highly significant predictors of the extent of reactive hyperemia (P <0.0001 for Perfusion Area, peak minus baseline blood flow, and Normalized Peak blood flow), and the contributions of shear stress were insignificant (P = 0.5351 for Perfusion Area, P = 0.6403 for Peak minus Baseline blood flow, and P = 0.8941 for Normalized Peak blood flow). Depending upon the model, comparison of coefficients suggested that an increase of 1.0˚C contributes as much to reactive hyperemia in the skin as 12 mm Hg to 15 mm Hg of interface pressure (coefficient ratios of temperature/pressure are 14.33 for Perfusion Area, 11.77 for Peak minus Baseline, and 12.97 for Normalized Peak, respectively). The findings also indicate that post-load metabolic repayment varied with temperature only at higher pressures, suggesting protective vasodilation was able to keep pace with mild compression. If confirmed in subsequent studies, the results suggest that managing both skin pressure and temperature may reduce the risk of ischemia.

Interface shear and pressure characteristics of wheelchair seat cushions.

Pressure ulcer incidence rates have remained constant despite advances in support surface technology. Interface shear stress is recognized as a risk factor for pressure ulcer development and is the focus of many shear reduction technologies incorporated into wheelchair cushions; however, shear reduction has not been quantified in the literature. We evaluated 21 commercial wheelchair seat cushions using a new methodology developed to quantify interface shear stress, interface pressure, and horizontal stiffness. Interface shear stress increased significantly with applied horizontal indenter displacement, while no significant difference was found for interface pressure. Material of construction resulted in significant differences in interface shear stress, interface pressure, and horizontal stiffness. This study shows that the existing International Organization for Standardization (ISO) 16840-2 horizontal stiffness measure provides similar information to the new horizontal stiffness measure. The lack of a relationship between interface shear stress and the overall horizontal stiffness measure, however, suggests that a pressure and shear force sensor should be used with the ISO 16840-2 horizontal stiffness measure to fully quantify a cushion's ability to reduce interface shear stress at the patient's bony prominences.

School bus transportation for students seated in wheelchairs.

For children with Individualized Education Plans (IEPs), transportation is considered a related service and a part of their education. This paper presents an overview of the current status of wheelchair transportation for students on school buses within the United States. The review includes the school transportation environment for wheelchair-seated students, applicable regulations and voluntary standards, primary safety issues for wheelchair-seated students, and key stakeholders roles in improving wheelchair transportation safety. Future actions to improve wheelchair transportation safety in school transportation are discussed, including the need to improve data collection, mandate payment for and use of RESNA WC19-compliant wheelchairs, improve training for bus operators and attendants, and require specialty certification for school bus operators who transport wheelchair-seated students.

Wheelchair transportation safety on school buses: stakeholder recommendations for priority issues and actions.

This paper presents results from and provides discussion of a state-of-the-science workshop in which highly informed stakeholders in wheelchair transportation safety for students on school buses were participants. The Nominal Group Technique was used to create a process in which the main issues preventing safe transportation of wheelchair-seated students and key strategies to overcome these issues were identified and ranked. These results, along with a synthesis of group discussion and recommendations for action, are presented along with consideration of current policies, regulations, and political realities. Critical safety shortcomings exist in this highly specialized enterprise that varies from state to state. Recommended strategies include implementing wheelchair requirements in federal transportation safety standards, creation of a clearinghouse for wheelchair transportation best practices and education, creation of national standards for training, practices, and monitoring, and increased "buy-in" to voluntary wheelchair standards by wheelchair manufacturers.

Effect of wheelchair headrest use on pediatric head and neck injury risk outcomes during rear impact.

Comparative risks or benefits to wheelchair-seated pediatric occupants in motor vehicles associated with wheelchair headrest use during rear impact were evaluated using pediatric head and neck injury outcome measures. A Hybrid III 6-year-old anthropomorphic test device (ATD), seated in identical WC19-compliant pediatric manual wheelchairs, was used to measure head and neck response during a 25 km/h (16 mph), 11 g rear impact. ATD responses were evaluated across two test scenarios: three sled tests conducted without headrests, and three with slightly modified commercial headrests. Head and neck injury outcomes measures included: linear head acceleration, head injury criteria (HIC) values, neck injury criteria (N(ij)) values, and combined rotational head velocity and acceleration. Neck and head injury outcome measures improved by 34-70% in sled tests conducted with headrests compared to tests without headrests. Headrest use reduced N(ij) values and the likelihood of concussion from values above established injury thresholds to values below injury thresholds. Injury measure outcome reductions suggest lower head and neck injury risks for wheelchair-seated children using wheelchair-mounted headrests as compared to non-headrest users in rear impact. Use of relative comparisons across two test scenarios served to minimize effects of ATD biofidelity limitations.