Etiology Of Deep Tissue Injury Research Articles

The aetiology of deep tissue injury: a literature review.

Deep tissue injury affects patients of all ages in a variety of healthcare settings. It is therefore essential that nurses are aware of the underlying pathogenesis, in order to accurately assess the pressure ulcer risk of vulnerable patients, and to subsequently reduce patient harm. The majority of pressure ulcers are avoidable, however, a variety of intrinsic and extrinsic factors can contribute towards the development of deep tissue injury. Understanding the body's internal responses to external pressure will enable nurses to recognise that a visual assessment alone may not necessarily identify patients at risk of deep tissue damage. This article reviews the evidence for the internal causative mechanisms of deep tissue injury, while linking to clinical practice and pressure ulcer prevention.

Changes in permeability of the plasma membrane of myoblasts to fluorescent dyes with different molecular masses under sustained uniaxial stretching

Deep tissue injury (DTI) is a serious pressure ulcer which onsets in skeletal muscle tissues adjacent to weight-bearing bony prominences. Recent literature points at sustained large deformations in muscle tissue, which translate to static stretching of the plasma membrane (PM) at the cell-scale, as the primary cause of accumulated cell death in DTI. It has been specifically suggested that prolonged exposure to large tensional PM strains interferes with normal cellular homeostasis, primarily by affecting transport through the PM which could become more permeable when stretched. In this context, using confocal imaging and fluorescence-activated cell sorter (FACS), we visualized and quantified here the uptake of fluorescent Dextran dye by myoblasts that were statically stretched uniaxially, up to physiological strains of 3%, 6% and 9%, using two different molecular masses for the Dextran (4kDa and 20kDa). The confocal and FACS studies provided consistent evidence that the permeability of the PM increased at large static deformations. Furthermore, the FACS data indicated that the kinetics of the PM permeability very likely depends on the size of the biomolecular marker. Both results were consistent with reports published in the neurotrauma literature on the kinetics of uptake of fluorescent biomolecules by dynamically stretched neurons; hence there are some analogues in the biomechanical pathways of cellular-level injury between DTI and impact insults. The present work provides additional empirical support to the theory of cell-scale deformation-diffusion damage in the etiology of DTI, and may lead to better understanding of time courses for onset of cellular damage in DTI, by exploring mass transport processes across the PM of the involved cells.

How does muscle stiffness affect the internal deformations within the soft tissue layers of the buttocks under constant loading?

Mechanical loading of soft tissues covering bony prominences can cause skeletal muscle damage, ultimately resulting in a severe pressure ulcer termed deep tissue injury (DTI). Deformation plays an important role in the aetiology of DTI. Therefore, it is essential to minimise internal muscle deformations in subjects at risk of DTI. As an example, spinal cord-injured (SCI) individuals exhibit structural changes leading to a decrease in muscle thickness and stiffness, which subsequently increase the tissue deformations. In the present study, an animal-specific finite element model, where the geometry and boundary conditions were derived from magnetic resonance images, was developed. It was used to investigate the internal deformations in the muscle, fat and skin layers of the porcine buttocks during loading. The model indicated the presence of large deformations in both the muscle and the fat layers, with maximum shear strains up to 0.65 in muscle tissue and 0.63 in fat. Furthermore, a sensitivity analysis showed that the tissue deformations depend considerably on the relative stiffness values of the different tissues. For example, a change in muscle stiffness had a large effect on the muscle deformations. A 50% decrease in stiffness caused an increase in maximum shear strain from 0.65 to 0.99, whereas a 50% increase in stiffness resulted in a decrease in maximum shear strain from 0.65 to 0.49. These results indicate the importance of restoring tissue properties after SCI, with the use of, for example, electrical stimulation, to prevent the development of DTI.

A simple stochastic model to explain the sigmoid nature of the strain-time cellular tolerance curve

Using animal and tissue-engineered experimental models, we previously found that a decreasing sigmoidal function is adequate for describing the diminishing tolerance of skeletal muscle tissue/cells for static mechanical strains delivered over time. Compressive loads at the tissue scale, which are associated with weight-bearing, appear to stretch the plasma membrane (PM) of cells at the mesoscopic–microscopic scales. The permeability of such stretched PMs may then increase, which could alter the control mechanisms and consequently the homeostasis of the deformed cells. The present paper is aimed at demonstrating this suggested deformation–diffusion damage pathway – which is particularly relevant to the aetiology of deep tissue injury – at the level of a single cell, using simple stochastic computer modeling which is supported by experimental confocal microscopy imaging data. The modeling and confocal studies better explain the strain-time injury threshold previously proposed by our group, and in particular, they provide an explanation for the nature of the rapid decrease of the threshold curve. The simulations revealed that there was a clear trend of nearly inverse relationship between the level of stretch applied to the PM and the time for accumulation of cytotoxic contents of a diffusing biomolecule. Taken together with the confocal data, which correspondingly demonstrated increased permeability of the PM of statically stretched cells to a fluorescent dye, the present results point to cell-level deformation–diffusion damage as a factor that should be looked at more closely in aetiological research of pressure ulcers.

Diffusion of water in skeletal muscle tissue is not influenced by compression in a rat model of deep tissue injury

Sustained mechanical loading of skeletal muscle may result in the development of a severe type of pressure ulcer, referred to as deep tissue injury. Recently it was shown that the diffusion of large molecules (10–150 kDa) is impaired during deformation of tissue-engineered skeletal muscle, suggesting a role for impaired diffusion in the aetiology of deep tissue injury. However, the influence of deformation on diffusion of smaller molecules on its aetiology is less clear. This motivated the present study designed to investigate the influence of deformation of skeletal muscle on the diffusion of water, which can be measured with diffusion tensor magnetic resonance imaging (MRI). It could be predicted that this approach will provide valuable information on the diffusion of small molecules. Additionally the relationship between muscle temperature and diffusion was investigated. During deformation of the tibialis anterior a decrease of the apparent diffusion coefficient (ADC) was observed (7.2±3.9%). The use of a finite element model showed that no correlation existed between the maximum shear strain and the decrease of the ADC. The ADC in the uncompressed gastrocnemius muscle decreased with 5.9±3.7%. In an additional experiment a clear correlation was obtained between the decrease of the ADC and the relative temperature change of skeletal muscle tissue as measured by MRI. Taken together, it was concluded that (1) the decreased diffusion of water was not a direct effect of tissue deformation and (2) that it is likely that the observed decreased ADC during deformation was a result of a decreased muscle temperature. The present study therefore provides evidence that diffusion of small molecules, particularly oxygen and carbon dioxide, is not impaired during deformation of skeletal muscle tissue.

Reswick and Rogers pressure-time curve for pressure ulcer risk. Part 1

Pressure ulcers are one of the most potentially devastating complications in individuals confined to a bed or a wheelchair for an extended period. Severe pressure ulcers may form in deep tissues overlying bony prominences, and only at a later stage become visible, or may even induce a full-thickness breakdown of the soft tissues at the affected site. A new type of pressure ulcer known as'deep tissue injury' has therefore been defined internationally. To understand the aetiology of deep tissue injury, health professionals should be able to predict whether or not a certain state of internal mechanical loads in deep tissues, such as tissue deformations and forces per unit area of tissue, would lead to localised irreversible cell damage. Part one of this article explains the concepts of injury thresholds as related to deep tissue injury. Some serious flaws in the classical, commonly used Reswick and Rogers pressure-time curve are analysed, and an alternative contemporary tissue injury threshold, the sigmoid threshold, is suggested. Part two of this article describes recent and ongoing work aimed at defining injury thresholds that are specific for deep tissue injury, standardised and therefore suitable for use with different patients. Clinical implications of current injury thresholds are also discussed, in relation to obese patients and patients with muscle atrophy.

Compression-induced damage and internal tissue strains are related

Prolonged mechanical loading of soft tissues adjacent to bony prominences can lead to degeneration of muscle tissue, resulting in a condition termed pressure-related deep tissue injury. This type of deep pressure ulcers can develop into a severe wound, associated with problematic healing and a variable prognosis. Limited knowledge of the underlying damage pathways impedes effective preventive strategies and early detection. Traditionally, pressure-induced ischaemia has been thought to be the main aetiological factor for initiating damage. Recent research, however, proposes tissue deformation per se as another candidate for initiating pressure-induced deep tissue injury. In this study, different strain parameters were evaluated on their suitability as a generic predictive indicator for deep tissue injury. With a combined animal-experimental numerical approach, we show that there is a reproducible monotonic increase in damage with increasing maximum shear strain once a strain threshold has been exceeded. This relationship between maximum shear strain and damage seems to reflect an intrinsic muscle property, as it applied across a considerable number of the experiments. This finding confirms that tissue deformation per se is important in the aetiology of deep tissue injury. Using dedicated finite element modeling, a considerable reduction in the inherent biological variation was obtained, leading to the proposal that muscle deformation can prove a generic predictive indicator of damage.

The free diffusion of macromolecules in tissue-engineered skeletal muscle subjected to large compression strains

Pressure-related deep tissue injury (DTI) represents a severe pressure ulcer, which initiates in compressed muscle tissue overlying a bony prominence and progresses to more superficial tissues until penetrating the skin. Individual subjects with impaired motor and/or sensory capacities are at high risk of developing DTI. Impaired diffusion of critical metabolites in compressed muscle tissue may contribute to DTI, and impaired diffusion of tissue damage biomarkers may further impose a problem in developing early detection blood tests. We hypothesize that compression of muscle tissue between a bony prominence and a supporting surface locally influences the diffusion capacity of muscle. The objective of this study was therefore, to determine the effects of large compression strains on free diffusion in a tissue-engineered skeletal muscle model. Diffusion was measured with a range of fluorescently labeled dextran molecules (10, 20, 150 kDa) whose sizes were representative of both hormones and damage biomarkers. We used fluorescence recovery after photobleaching (FRAP) to compare diffusion coefficients ( D) of the different dextrans between the uncompressed and compressed (48–60% strain) states. In a separate experiment, we simulated the effects of local partial muscle ischemia in vivo, by reducing the temperature of compressed specimens from 37 to 34 °C. Compared to the D in the uncompressed model system, values in the compressed state were significantly reduced by 47±22% ( p<0.02). A 3 °C temperature decrease further reduced D in the compressed specimens by 10±6% ( p<0.05). In vivo, the effects of large strains and ischemia are likely to be summative, and hence, the present findings suggest an important role of impaired diffusion in the etiology of DTI, and should also be considered when developing biochemical screening methods for early detection of DTI.