Forces acting on the body via various external surfaces during locomotion are needed to support the body under gravity, control posture, and overcome inertia. Examples include the forces acting on the body via the seating surfaces during wheelchair propulsion, the forces acting on the plantar foot tissues via the insole during gait, and the forces acting on the residual limb tissues via the prosthetic socket during various movement activities.Excessive exposure to unwarranted stresses at the body support interfaces could lead to tissue breakdowns commonly known as pressure ulcers, presented often as deep tissue injuries around bony prominences and/or surface damages on the skin. In this paper, we review the literatures on how the involved tissues respond to epidermal loadings, taking into account both experimental and computational findings from in-vivo and in-vitro studies. In particular, related literatures on internal tissue deformation and stresses, microcirculatory responses, as well as histological, cellular and molecular observations are discussed.

2 0 0 6 ) Journal of Clinical Nursing 15, 581-587 Does access to bed-chair pressure sensors reduce physical restraint use in the rehabilitative care setting? Background. The common use of physical restraints in older people in hospitals and nursing homes has been associated with injurious falls, decreased mobility and disorientation. By offering access to bed-chair pressure sensors in hospitalized patients with perceived fall risk, nurses may be less inclined to resort to physical restraints, thereby improving clinical outcomes. Aims and objectives. To investigate whether the access of bed-chair pressure sensors reduces physical restraint use in geriatric rehabilitation wards. Design. Randomized controlled trial. Methods. Consecutively, patients admitted to two geriatric wards specialized in stroke rehabilitation in a convalescent hospital in Hong Kong, and who were perceived by nurses to be at risk of falls were randomly assigned to intervention and control groups. For the intervention group subjects, nurses were given access to bedchair pressure sensors. These sensors were not available to control group subjects, as in usual practice. The trial continued until discharge. The primary outcomes were the proportion of subjects restrained by trunk restraint, bedrails or chair-board and the proportion of trial days in which each type of physical restraint was applied. The secondary outcomes were the proportions of those who improved in the mobility and transfer domains of modified Barthel index on discharge and of those who fell. Results. One hundred and eighty subjects were randomized. Fifty (55AE6%) out of the 90 intervention group subjects received the intervention. There was no significant difference between the intervention and control groups in the proportions and duration of having the three types of physical restraints. There was also no group difference in the chance of improving in mobility and transfer ability, and of having a fall. Ó 2006 Blackwell Publishing Ltd 581Conclusion. Access to bed-chair pressure sensor device neither reduced the use of physical restraints nor improved the clinical outcomes of older patients with perceived fall risk.Relevance to clinical practice. The provision of bed-chair pressure sensors may only be effective in reducing physical restraints when it is combined with an organized physical restraint reduction programme.

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The objective of this study is to assess the effect of prolonged surface compression on the skin blood flowmotion in rats using spectral analysis based on wavelets transform of the periodic oscillations of the cutaneous laser Doppler flowmetry (LDF) signal. An external pressure of 13.3 kPa (100 mmHg) was applied to the trochanter area and the distal lateral tibia of Sprague-Dawley rats via two specifically designed pneumatic indentors. The loading duration was 6 hours/day for 4 consecutive days. Five frequency intervals were identified (0.01-0.04 Hz, 0.04-0.15 Hz, 0.15-0.4 Hz, 0.4-2 Hz and 2-5 Hz) corresponding to endothelial related metabolic, neurogenic, myogenic, respiratory and cardiac origins. The absolute amplitude of oscillations of each particular frequency interval and the normalized amplitude were calculated for quantitative assessments. The results showed that (1) tissue compression following the above schedule induced significant decrease in the normalized amplitude in the frequency interval of 0.01-0.04 Hz both in the trochanter area (p < 0.001) and tibialis area (p = 0.023), (2) prolonged compression induced significant increase in the absolute amplitude (p = 0.004 for the trochanter area and p = 0.017 for the tibialis area) but significant decrease in the normalized amplitude (p = 0.023 for the trochanter area and p = 0.026 for the tibialis area) in the frequency interval of 0.15-0.4 Hz, and (3) at the tibialis area, the flowmotion amplitude (frequency interval 0.15-0.4 Hz) measured prior to the daily tissue compression schedule was found to be significantly higher on day 4 than the measurements obtained on day 1. However, this finding was not observed at the trochanter area. Our results suggested that prolonged compression might induce endothelial damage and affect the endothelial related metabolic activities.

The molecular mechanisms that contribute to the pathogenesis of pressure-induced deep tissue injury are largely unknown. This study tested the hypothesis that oxidative stress and DNA damage signalling mechanism in skeletal muscle are involved in deep tissue injury. Adult Sprague Dawley rats were subject to an experimental protocol to induce deep tissue injury. Two compression cycles with a static pressure of 100 mmHg was applied to an area of 1.5 cm(2) over the mid-tibialis region of right limb of the rats. The left uncompressed limb served as intra-animal control. Muscle tissues underneath compression region were collected for examination. Our analyses indicated that pathohistological characteristics including rounding contour of myofibres and extensive nuclei accumulation were apparently shown in compressed muscles. The elevation of 8OHdG immunopositively stained nuclei indicated the presence of oxidative DNA damage. Increase in oxidative stress was revealed by showing significant elevation of 4HNE and decreases in mRNA abundance of SOD1, catalase and GPx, and protein content of SOD2 in compressed muscles relative to control muscles. Increase in nitrosative stress was demonstrated by significant elevation of nitrotyrosine and NOS2 mRNA content. The activation of tumor suppressor p53 signalling was indicated by the remarkable increases in protein contents of total p53 and serine-15 phosphorylated p53. The transcript expression of the DNA-repairing enzyme, Rad23A, was significantly suppressed in compressed muscles. Our time-course study indicated that increased oxidative/nitrosative stress and proapoptotic signalling were maintained in muscles receiving increasing amount of compression cycles and post-compression time. Furthermore, resveratrol was found to attenuate the histological damage, oxidative/nitrosative stress and proapoptotic signalling in response to prolonged moderate compression. In conclusion, our findings are consistent with the hypothesis that oxidative stress and DNA damage signalling in skeletal muscle are involved in the underlying mechanisms responsible for the pathogenesis of pressure-induced deep tissue injury.