The goal of this experiment was to investigate changes in the thickness of the soft tissue overlying the ischial tuberosity (IT) due to changes in hip flexion angle and the addition of a sitting load. Eleven healthy subjects were tested. An apparatus constructed from foam blocks and an air bladder was used to position the subjects in different postures within an MRI tube. MRI images of the buttocks and thigh were obtained for four postures: Supine, 45° Hip Flexion, Non-Weight-Bearing 90° Hip-Flexion, and Weight-Bearing 90° Hip-Flexion. The thickness of muscle, adipose tissue, and skin was measured between the IT tip and skin surface, perpendicular to the cushion placed beneath the thighs. The tissue overlying the IT was found to be significantly (P < 0.001) thinner in 90° Hip-Flexion (73.8 ± 9.0 mm) than in the supine position (135.9 ± 8.1 mm). Muscle thickness decreased significantly from Supine to Non-Weight-Bearing 90° Hip-Flexion (59.1 ± 8.5%, P < 0.001), and further decreased from Non-Weight-Bearing to Weight-Bearing 90° Hip-Flexion (46.2 ± 7.9%, P < 0.001). Under Weight-Bearing 90° Hip-Flexion, the muscle tissue deformed significantly (P < 0.001) more than the adipose tissue and skin. We concluded that the tissue thickness covering the IT significantly decreased with hip flexion, and further decreased by nearly half during loading caused by sitting. In addition, the muscle tissue experienced the largest deformation during sitting. The results of this study may improve our understanding of risk factors for pressure ulcer development due to changes in tissue padding over the IT in different postures.
Many rat/mouse pressure ulcer (PU) models have been developed to test different hypotheses to gain deeper understanding of various causative risk factors, the progress of PUs, and assessing effectiveness of potential treatment modalities. The recently emphasized deep tissue injury (DTI) mechanisms for PU formation has received increased attention and several studies reported findings on newly developed DTI animal models. However, concerns exist for the clinical relevance and validity of these models, especially when the majority of the reported rat PU/DTI models were not built upon SCI animals and many of the DTI research did not simulate well the clinical observation. In this study, we propose a rat PU and DTI model which is more clinically relevant by including chronic SCI condition into the rat PU model and to simulate the role of bony prominence in DTI formation by using an implant on the bone-tissue interface. Histological data and imaging findings confirmed that the condition of chronic SCI had significant effect on pressure-induced tissue injury in a rat PU model and the including a simulated bony prominence in rat DTI model resulted in significantly greater injury in deep muscle tissue. Further integration of the SCI condition and the simulated bony prominence would result a rat PU/DTI model which can simulate even more accurately the clinical phenomenon and yield research more clinically relevant findings.
Current animal models examining deep tissue injury (DTI) development as a mechanism for pressure ulcer (PU) formation are limited, as the created animal wounds do not usually reflect clinically observed tissue necrosis. This study aimed to establish a more clinically relevant rat PU model by including a SCI condition in the model and by examining the role of a simulated bony prominence in DTI formation. Tissue injury percentage of compressed tibialis anterior (TA) muscle from eight SCI (T9) rats was compared against eight neurologically intact control rats to examine PU development over the flat surface of the tibia. To examine DTI formation, five other rats were implanted with a hemispheric polypropylene bone mimic beneath the TA muscle and were allowed to heal prior to compression. The rats in the DTI model were then separated into three groups and were administered different levels of compression to determine the best experimental conditions for the model. Both MRI and light microscopy were used to analyze tissue necrosis due to compression, and histological data was processed and quantified using a custom Matlab code. Postoperative ultrasound images of the implant two weeks after surgery showed the implant was correctly oriented on the surface of the bone. Results from this experiment and subsequent histological analysis and MRI observation confirmed these models are successful in simulating a clinically relevant pressure‐induced deep tissue injury.
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