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Deep tissue injury (DTI), a type of pressure ulcer, arises in the muscle layers adjacent to bony prominences due to sustained mechanical loading. DTI presents a serious problem in the clinic, as it is often not visible until reaching an advanced stage. One of the causes can be direct mechanical deformation of the muscle tissue and cell. The mechanism of cell death induced by mechanical compression was studied using bio-artificial skeletal muscle tissues. Compression was applied by placing weights on top of the constructs. The morphological changes of the cytoskeleton and the phosphorylation of mitogen-activated protein kinases (MAPK) under compression were investigated. Moreover, inhibitors for each of the three major MAPK groups, p38, ERK, and JNK, were applied separately to look at their roles in the compression caused apoptosis and necrosis. The present study for the first time showed that direct mechanical compression activates MAPK phosphorylation. Compression also leads to a gradual destruction of the cytoskeleton. The percentage apoptosis is strongly reduced by p38 and JNK inhibitors down to the level of the unloaded group. This phenomenon could be observed up to 24. h after initiation of compression. Therefore, cell death in bio-artificial muscle tissue caused by mechanical compression is primarily caused by a physiological mechanism, rather than through a physical mechanism which kills the cell directly. These findings reveal insight of muscle cell death under mechanical compression. Moreover, the result indicates a potential clinical solution to prevent DTI by pre-treating with p38 or/and JNK inhibitors.

For pressure ulcer prevention an ambitious goal would be the establishment of a mechanical threshold for tissue damage. In the past, several researchers have sought to establish such a threshold often involving the loading time. However, they have not resulted in a unique reliable value that could be used in practice. This limitation is probably due to the focus on interface pressure. The objective of this paper is to clarify to an audience with no conventional background in mechanics, why interface pressure is not the appropriate parameter to define a damage threshold, whereas internal local deformations (strains) may prove more suitable. The paper reveals that it may be possible to identify a damage threshold for healthy skeletal muscle tissue based on local internal deformations.

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, 150kDa) 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 degrees C. Compared to the D in the uncompressed model system, values in the compressed state were significantly reduced by 47+/-22% (p0.02). A 3 degrees C temperature decrease further reduced D in the compressed specimens by 10+/-6% (p0.05). 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.

Med Eng Phys 2001 Apr;23(3):195-200 Related Articles, Books, LinkOut Quantification and localisation of damage in rat muscles after controlled loading; a new approach to study the aetiology of pressure sores.Bosboom EM, Bouten CV, Oomens CW, van Straaten HW, Baaijens FP, Kuipers H.Department of Materials Technology, Eindhoven University of Technology, P.O. Box 513, 5600 MB, Eindhoven, The Netherlands. e.m.h.bosboom@tue.nlTo obtain more insight in the aetiology of deep pressure sores, an animal model was developed to relate controlled external loading to local muscle damage. The tibialis anterior muscle (TA) and overlying skin of a rat were compressed between indentor and tibia. Loads of 10, 70 and 250kPa at skin surface were applied for 2 or 6h. During half of the 10 and 250kPa experiments interstitial fluid pressure (IFP) in the TA was measured. The TAs were excised 24h after load application. Both amount and location of damage were assessed by histological examination using a semi-automated image-processing program. In six of eleven loaded muscles damage was found. The damage was located from superficial to deep muscle tissue in a zone never exceeding the diameter of the indentor. The IFP measurements interfered with the occurrence of damage; application of 10 and 70kPa loads only caused damage when combined with IFP measurements, whereas IFP measurements increased damage at 250kPa loads. The results showed that the developed animal model can be used to provoke local damage by applying a controlled load and that the amount and location of damage can be assessed using the newly developed techniques.

Skin can be considered to be a mixture of a solid and a fluid. A general theory for the description of the behaviour of mixtures is presented and applied to a mixture of a solid and a fluid. A numerical procedure is presented to solve the non-linear field equations describing such a mixture. The abilities of the procedure are demonstrated by means of a confined compression test.

In vitro compression studies have been performed on layers of porcine skin and fat. The tissue layers have been loaded by means of various indentors. Indentor displacements and interstitial fluid pressures have been measured. The results have been compared to finite element calculations with mixture elements. A qualitative agreement between calculations and measurements is found. The results support the hypothesis that skin and fat behave like solid/fluid mixtures.

A general model describing the wrinkling of thin membranes is given. The model is able to describe the wrinkling of anisotropic membranes in geometrically non-linear analysis. Wrinkling is accounted for by replacing a given deformation tensor, which by using the constitutive equation would give negative Cauchy stresses, by a modified deformation tensor.