Pressure ulcers are localised areas of soft tissue breakdown that develop over bony prominences as a result of sustained mechanical loading. They are particularly common in bedridden and wheelchair-bound individuals, and represent one of the most common secondary complications in spinal cord injured subjects. A specific form of pressure ulcers is termed deep tissue injury (DTI), which is defined as pressure-related injury to subcutaneous tissues such as skeletal muscle, initially under intact skin. DTI represents a severe problem, because tissue damage at the skin surface only becomes apparent at an advanced stage, and is associated with a variable prognosis. Therefore, early identification and subsequent treatment of DTI are critical to reduce comorbidities and the financial and manpower burdens associated with treatment. This requires a better understanding of its underlying aetiology, in order to develop appropriate risk assessment tools and early detection methods. Therefore, the main goal of the present thesis was to study the aetiology of DTI. In addition, some explorative studies were performed to examine potential methods for the early detection of DTI. The aetiological factors were investigated using a combination of experiments and numerical models. This involved an established rat model for DTI that has previously been used to study the effects of deformation due to 2 h continuous loading. In the present thesis, different loading regimens were applied to further investigate the role of deformation. In addition, a previously developed finite element model to estimate muscle deformations during loading, was substantially improved to enable a local comparison of deformation with damage. Furthermore, the duration of the experiments was extended to 6 h to investigate the effects of ischaemia and reperfusion. It was found that deformation is the primary trigger for muscle damage for loading periods up to 2 h when a specific deformation threshold is exceeded. Ischaemia started to cause changes in muscle tissue between 2-4 h loading. Therefore, the damage development in skeletal muscle during prolonged loading is determined by deformation, ischaemia, and reperfusion, each mechanism exhibiting a unique time profile. The developed methods were also applied to a porcine model for DTI to investigate the deformations of the different soft tissues of the buttocks during loading. In this study, it was shown that the relative mechanical properties of the different tissue layers have a large influence on the distribution of the internal deformations. The release of biochemical damage markers from injured muscle tissue into the circulation was studied to investigate the possibility of using these proteins for the early detection of DTI. Baseline variations of creatine kinase, myoglobin, heart-type fatty acid binding protein, and C-reactive protein were assessed in able-bodied and spinal cord injured human volunteers. These variations were small compared to the predicted increase in biomarker concentrations during DTI development, indicating that this combination of markers may prove appropriate for the early detection of DTI. Moreover, a considerable increase in myoglobin concentrations in blood and urine was observed in a rat model for DTI after 6 h mechanical loading. The present findings have implications for clinical practice. In particular, it is important to minimise the internal tissue deformations in subjects at risk of DTI, such as present in subjects with spinal cord injury and those positioned on hard surfaces, such as stretchers or operating tables, for prolonged periods. Furthermore, the period of loading should be limited to prevent the accumulation of ischaemic damage. The observation of increased myoglobin levels in blood and urine after mechanical loading demonstrates the potential of using biochemical markers of muscle damage for the early detection of DTI. Moreover, the increase of myoglobin levels in urine suggests that a noninvasive approach for this screening method may be satisfactory.
|Qualification||Doctor of Philosophy|
|Award date||20 Sep 2011|
|Place of Publication||Eindhoven|
|Publication status||Published - 2011|