Eric W. C. Tam

Biomechanics of pressure ulcer in body tissues interacting with external forces during locomotion.

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, often presented as deep-tissue injuries around bony prominences or as surface damage on the skin. In this article, we review the literature that describes how the involved tissues respond to epidermal loading, taking into account both experimental and computational findings from in vivo and in vitro studies. In particular, we discuss related literature about internal tissue deformation and stresses, microcirculatory responses, and histological, cellular, and molecular observations.

Pelvic movement and interface pressure distribution during manual wheelchair propulsion.

OBJECTIVE To investigate the movement of the ischial tuberosities and the redistribution of interface pressure during manual wheelchair propulsion. DESIGN Measurement of ischial tuberosity positions and comparison with corresponding position of the zones of peak pressure by using independent samples t tests. Analysis of variance was used to compare peak and average pressures under static and dynamic conditions. SETTING Human locomotion laboratory. PARTICIPANTS Ten subjects with spinal cord injury (SCI) and 10 individuals with no disabilities. INTERVENTIONS Manual wheelchair propulsion on a stationary wheelchair ergometer at the subjects maximum propulsion speed. MAIN OUTCOME MEASURES Seat interface pressure and the 3-dimensional position of the pelvis were measured with a pressure mat and an optical motion analysis system. RESULTS During wheelchair sprinting, the ischia were located at 19.2+/-11.7 mm behind the corresponding peak pressure locations. The anteroposterior rocking of the pelvis was 11.2 degrees and 5.2 degrees for the normal and SCI group, respectively. The average interface pressure over the ischial tuberosity area was lower under dynamic conditions. It was also observed in the SCI group that there was a concentration of high-pressure gradients around the peak pressure areas of the buttock during dynamic propulsion. CONCLUSION Peak pressure locations did not concur exactly with the ischial tuberosities during propulsion. The movements of the ischial bone and the cyclic loading imposed on the tissue underneath the ischial tuberosities during dynamic conditions may have implications for the etiology of decubitus ulcers.

Muscle apoptosis is induced in pressure-induced deep tissue injury.

Pressure ulcer is a complex and significant health problem. Although the factors including pressure, shear, and ischemia have been identified in the etiology of pressure ulcer, the cellular and molecular mechanisms that contribute to the development of pressure ulcer are unclear. This study tested the hypothesis that the early-onset molecular regulation of pressure ulcer involves apoptosis in muscle tissue. Adult Sprague-Dawley rats were subjected to an in vivo protocol to mimic pressure-induced deep tissue injury. Static pressure was applied to the tibialis region of the right limb of the rats for 6 h each day on two consecutive days. The compression force was continuously monitored by a three-axial force transducer equipped in the compression indentor. The contralateral uncompressed limb served as intra-animal control. Tissues underneath the compressed region were collected for histological analysis, terminal dUTP nick-end labeling (TUNEL), cell death ELISA, immunocytochemical staining, and real-time RT-PCR gene expression analysis. The compressed muscle tissue generally demonstrated degenerative characteristics. TUNEL/dystrophin labeling showed a significant increase in the apoptotic muscle-related nuclei, and cell death ELISA demonstrated a threefold elevation of apoptotic DNA fragmentation in the compressed muscle tissue relative to control. Positive immunoreactivities of cleaved caspase-3, Bax, and Bcl-2 were evident in compressed muscle. The mRNA contents of Bax, caspase-3, caspase-8, and caspase-9 were found to be higher in the compressed muscle tissue than control. These results demonstrated that apoptosis is activated in muscle tissue following prolonged moderate compression. The data are consistent with the hypothesis that muscle apoptosis is involved in the underlying mechanism of pressure-induced deep tissue injury.

Effects of prolonged surface pressure on the skin blood flowmotions in anaesthetized rats--an assessment by spectral analysis of laser Doppler flowmetry signals.

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.

Protective effect of caspase inhibition on compression-induced muscle damage

Non‐technical summary  A pressure ulcer, also known as a pressure sore, bedsore or decubitus ulcer, results from localized ulcerated tissue breakdown caused by sustained, unrelieved mechanical pressure in the body–support interface such as with a bed, wheelchair and orthoses/prostheses. Pressure ulcers are common in the wheelchair bound or bedridden frail elderly patients with neuromuscular disorder and orthoses/prostheses clients. Pressure ulcers represent a significant health problem as they impose a heavy burden on sufferers, with negative psychological, physical, social and financial consequences. Most importantly, there are currently no effective therapies for preventing and treating pressure ulcers. In the present study, our data demonstrate that pharmacological inhibition of caspase is effective in alleviating muscle damage induced by prolonged moderate compression. These findings suggest that regimens targeting caspase/apoptosis inhibition might be of use to prevent or treat pressure ulcers.

Opposing responses of apoptosis and autophagy to moderate compression in skeletal muscle

Aim:  The molecular mechanism that contributes to the pathogenesis of deep pressure ulcer remains to be elucidated. This study tested the hypotheses that: (1) apoptosis and autophagy are activated in compression‐induced muscle pathology and (2) apoptotic and autophagic changes precede pathohistological changes in skeletal muscle in response to prolonged moderate compression.

A Survey of Augmentative and Alternative Communication Service Provision in Hong Kong

A survey was conducted to understand the service provisions for augmentative and alternative communication (AAC) in Hong Kong. The response rates of special pre-school training centers and special schools were 59% and 71%, respectively. The response rate of adult settings was 18%. Results indicated that a higher proportion of students identified as having complex communication needs had access to AAC service provision in schools for children with intellectual and physical disabilities than those in special pre-school training centres and other types of special schools. Generalization of AAC service beyond the classroom setting remains problematic. Seventy-two percent of the respondents were dissatisfied with the training in AAC that they received during their basic professional preparation. More advocacy work is needed to increase awareness and knowledge of AAC use in Hong Kong.

Deformation and reperfusion damages and their accumulation in subcutaneous tissues during loading and unloading: A theoretical modeling of deep tissue injuries

Deep tissue injuries (DTI) involve damages in the subcutaneous tissues under intact skin incurred by prolonged excessive epidermal loadings. This paper presents a new theoretical model for the development of DTI, broadly based on the experimental evidence in the literatures. The model covers the loading damages implicitly inclusive of both the direct mechanical and ischemic injuries, and the additional reperfusion damages and the competing healing processes during the unloading phase. Given the damage accumulated at the end of the loading period, the relative strength of the reperfusion and the healing capacity of the involved tissues system, the model provides a description of the subsequent damage evolution during unloading. The model is used to study parametrically the scenario when reperfusion damage dominates over healing upon unloading and the opposite scenario when the loading and subsequent reperfusion damages remain small relative to the healing capacity of the tissues system. The theoretical model provides an integrated understanding of how tissue damage may further build-up paradoxically even with unloading, how long it would take for the loading and reperfusion damages in the tissues to become fully recovered, and how such loading and reperfusion damages, if not given sufficient time for recovery, may accumulate over multiple loading and unloading cycles, leading to clinical deep tissues ulceration.

Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology

BackgroundThe molecular mechanism initiating deep pressure ulcer remains to be elucidated. The present study tested the hypothesis that the ubiquitin proteasome system is involved in the signalling mechanism in pressure-induced deep tissue injury.MethodsAdult Sprague Dawley rats were subjected to an experimental compression model to induce deep tissue injury. The tibialis region of the right hind limb was subjected to 100 mmHg of static pressure for six hours on each of two consecutive days. The compression pressure was continuously monitored by a three-axial force transducer within the compression indentor. The left hind limb served as the intra-animal control. Muscle tissues underneath the compressed region were collected and used for analyses.ResultsOur results demonstrated that the activity of 20S proteasome and the protein abundance of ubiquitin and MAFbx/atrogin-1 were elevated in conjunction with pathohistological changes in the compressed muscle, as compared to control muscle. The administration of the proteasome inhibitor MG132 was found to be effective in ameliorating the development of pathological histology in compressed muscle. Furthermore, 20S proteasome activity and protein content of ubiquitin and MAFbx/atrogin-1 showed no apparent increase in the MG132-treated muscle following compression.ConclusionOur data suggest that the ubiquitin proteasome system may play a role in the pathogenesis of pressure-induced deep tissue injury.

Timed 360° Turn Test for Assessing People With Chronic Stroke

OBJECTIVES To investigate (1) the intrarater, interrater, and test-retest reliability of the timed 360° turn test in subjects with stroke; (2) the concurrent validity of the timed 360° turn test by exploring its correlation with other measures of stroke-specific impairments; and (3) the cutoff times that best discriminate individuals with stroke from healthy older adults. DESIGN Cross-sectional study. SETTING University-based rehabilitation center. PARTICIPANTS Individuals with chronic stroke (n=72) and healthy individuals (n=35) of similar age (N=107). INTERVENTIONS Not applicable. MAIN OUTCOME MEASURES The timed 360° turn test was administered along with the Fugl-Meyer assessment of the lower extremity, measurement of muscle strength of ankle dorsiflexors and plantarflexors using a handheld dynamometer, Berg Balance Scale, limit of stability test, five times sit-to-stand (FTSTS) test, 10-m walk test, and timed Up and Go (TUG) test. RESULTS The 360° turn times showed excellent intrarater, interrater, and test-retest reliability in individuals with stroke. A minimal detectable change of .76 seconds was found for subjects turning toward the affected side and 1.22 seconds for subjects turning toward the unaffected side. The 360° turn times were found to correlate significantly with Fugl-Meyer assessment of the lower extremity scores, dosiflexor strength of the affected ankle, plantarflexor strength of both ankles, FTSTS test times, balance performance, gait speed, and TUG test times. The 360° turn times of 3.43 to 3.49 seconds were shown to discriminate reliably between individuals with stroke and healthy older adults. CONCLUSIONS The timed 360° turn test is a reliable and an easily administered clinical tool to assess the turning ability of subjects with chronic stroke.