A Theoretical Analysis of Damage Evolution in Skeletal Muscle Tissue With Reference to Pressure Ulcer Development

[+] Author and Article Information
Roel G. M. Breuls, Carlijn V. C. Bouten, Cees W. J. Oomens, Frank P. T. Baaijens

Eindhoven University of Technology

Dan L. Bader

Queen Mary University of London

J Biomech Eng 125(6), 902-909 (Jan 09, 2004) (8 pages) doi:10.1115/1.1634287 History: Received April 14, 2003; Revised July 16, 2003; Online January 09, 2004

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, 1998, “Pressure Ulcers Prevalence, Cost and Risk Assessment: Consensus Development Conference Statements,” Decubitus, 2, 24–28.
Bliss,  M. R., 1993, “Aetiology of Pressure Sores,” Clinical Gerontology,3, 379–397.
Bosboom, E. M. H., Bouten, C. V. C., Oomens, C. W. J., Baaijens, F. P. T., and Nikolay, K., 2003, “High-Resolution MRI to Assess Skeletal Muscle Damage After Transverse Loading,” J. Appl. Physiol., in press.
Bosboom,  E. M. H., Bouten,  C. V. C., Oomens,  C. W. J., van Straaten,  H. W., Baaijens,  F. P. T., and Kuipers,  H., 2001, “Quantification and Localization of Damage in Rat Muscles After Controlled Loading; a New Approach to Study the Aetiology of Pressure Sores,” Meas. Control, 23(3), 195–200.
Bosboom,  E. M. H., Hesselink,  M. K. C., Oomens,  C. W. J., Bouten,  C. V. C., Drost,  M. R., and Baaijens,  F. P. T., 2001, “Passive Transverse Mechanical Properties of Skeletal Muscle,” J. Biomech., 34, 1365–1368.
Bours,  G. J. J. W., Halfens,  R. J. G., Abu-Saad,  H. H., and Grol,  R. T. P. M., 2002, “Prevalence, Prevention, and Treatment of Pressure Ulcers: Descriptive Study in 89 Institutions in the Netherlands,” Res. Nurs. Health, 25, 99–110.
Bouten, C. V. C., Bosboom, E. M. H., and Oomens, C. W. J., 1999, “The Aetiology of Pressure Sores: A Tissue and Cell Mechanics Approach,” in L. H. V. van de Woude, M. T. E. Hopman, and C. H. van Kemenade, editors, Biomedical Aspects of Manual Wheelchair Propulsion: The State of the Art II, pages 52–62, IOP Press Amsterdam, ISBN 90 5199 4427.
Bouten,  C. V. C., Knight,  M. M., Lee,  D. A., and Bader,  D. L., 2001, “Compressive Deformation and Damage of Muscle Cell Subpopulations in a Model System,” Ann. Biomed. Eng., 29(2), 153–163.
Breuls, R. G. M., Bouten, C. V. C., Oomens, C. W. J., Bader, D. L., and Baaijens, F. P. T., 2003, “Compression Induced Cell Damage in Engineered Skeletal Muscle Tissue: An In Vitro Model to Study Pressure Ulcer Aetiology,” Ann. Biomed. Eng., accepted.
Breuls,  R. G. M., Sengers,  B. G., Oomens,  C. W. J., Bouten,  C. V. C., and Baaijens,  F. P. T., 2002, “Predicting Local Cell Deformations in Engineered Tissue Constructs: A Multilevel Finite-Element Approach,” J. Biomech. Eng., 124, 198–207.
Caplan, A., Carlson, J., Faulkner, J. A., and Fischman, D., 1998, “Skeletal Muscle,” in J. L. Y. Woo and J. A. Buckwalter, editors, Injury and Repair of the Musculoskeletal Soft Tissues, pages 213–291, Park Ridge: American Academy of Orthopaedic Surgeons.
Chow,  C. C., and Odell,  E. I., 1978, “Deformations and Stresses in Soft Body Tissues of a Sitting Person,” J. Biomech. Eng., 100, 79–86.
Collinsworth,  A. M., Zhang,  S., Kraus,  W. E., and Truskey,  G. A., 2002, “Apparent Elastic Modulus and Hysteresis of Skeletal Muscle Cells Throughout Differentiation,” American Journal of Physiology—Cell Physiology,283(4), C1219–C1227.
Daniel,  R. K., Priest,  D. L., and Wheatley,  D. C., 1981, “Etiologic Factors in Pressure Sores: An Experimental Model,” Arch. Phys. Med. Rehabil., 62(10), 492–498.
Dinsdale,  S. M., 1974, “Decubitus Ulcers: Role of Pressure and Friction in Causation,” Arch. Phys. Med. Rehabil., 55, 147–152.
Geist, A., Beguelin, A., Dongarra, J., Jiang, W., Manchek, R., and Sunderam, V., 1994, “PVM: Parallel Virtual Machine, A Users Guide and Tutorial for Networked Parallel Computing,” MIT Press, Scientific and Engineering Computation, Janusz Kowalik, Editor, Massachusetts Institute of Technology.
Guilak,  F., and Mow,  V. C., 2000, “The Mechanical Environment of the Chondrocyte: A Biphasic Finite-Element Model of Cell-Matrix Interactions in Articular Cartilage,” J. Biomech., 33(12), 1663–1673.
Husain,  T., 1953, “An Experimental Study of Dome Pressure Effects on Tissues, With Reference to the Bedsore Problem,” J. Pathol. Bacteriol., 66, 347–358.
Jain,  M. K., Chernomorsky,  A., Silver,  R., and Berg,  R. A., 1988, “Material Properties of Living Soft Tissue Composites,” J. Appl. Biomater, 22(A3), 311–326.
Kosiak,  M., 1961, “Etiology of Decubitus Ulcers,” Arch. Phys. Med. Rehabil., 42, 19–29.
Kouznetsova,  V., Brekelmans,  W. A. M., and Baaijens,  F. P. T., 2001, “An Approach to Micro-Macro Modelling of Heterogeneous Materials,” Comput. Mech., 27(1), 37–48.
Mak,  A. F. T., Huang,  L., and Wang,  Q., 1994, “A Biphasic Poroelastic Analyses of the Flow-Dependent Subcutaneous Tissue Pressure and Compaction Due to Epidermal Loadings: Issues in Pressure Sore,” J. Biomech. Eng., 116, 421–429.
Nola,  G. T., and Vistnes,  L. M., 1980, “Differential Response of Skin and Muscle in the Experimental Production of Pressure Sores,” Journal of Plastic and Reconstructive Surgery,66(5), 728–733.
Oomens, C. W. J., Bressers, O. F. J. T., Bosboom, E. M. H., Bouten, C. V. C., and Bader, D. L., 2003, “Can Loaded Interface Characteristics Influence Strain Distributions in Muscle Adjacent to Bony Prominences?,” Computer Methods in Biomechanical and Biomedical Engineering, 6 (3), 171–180.
Oomens,  C. W. J., Van Campen,  D. H., and Grootenboer,  H., 1987, “In Vitro Compression of a Soft Tissue Layer on a Rigid Foundation,” J. Biomech., 20, 923–935.
Reswick, J., and Rogers, J., 1976, “Experience at Rancho Los Amigos Hospital With Devices and Techniques to Prevent Pressure Sores,” in R. M. Kennedy, J. M. Cowden, and J. J. Scales, editors, Bed Sore Mechanics, pages 301–310, MacMillan Press, London.
Sacks,  A. M., 1989, “Theoretical Prediction of a Time-at-Pressure Curve for Avoiding Pressure Sores,” J. Rehabil. Res. Dev., 26(3), 27–34.
Salcido,  R., Donofrio,  J. C., Fisher,  S. B., LeGrand,  E. K., Dickey,  K. D., Schosser,  R., and Liang,  R., 1994, “Histopathology of Pressure Ulcers as a Result of Sequential Computer-Controlled Pressure Sessions in a Fuzzy Rat Model,” Adv. Wound Care, 7(5), 23–40.
Smit,  R. J. M., Brekelmans,  W. A. M., and Meijer,  H. E. H., 1998, “Prediction of the Mechanical Behavior of Nonlinear Heterogeneous Systems by Multilevel Finite-Element Modeling,” Comput. Methods Appl. Mech. Eng., 155(1–2), 181–192.
Todd,  B. A., and Thacker,  J. G., 1994, “Three-Dimensional Computer Model of the Human Buttocks, In Vivo,” J. Rehabil. Res. Dev., 31(2), 111–119.
Wu,  J. Z., and Herzog,  W., 2000, “Finite-Element Simulation of Location and Time-Dependent Mechanical Behavior of Chondrocytes in Unconfined Compression Tests,” Ann. Biomed. Eng., 28, 318–330.
Zhang,  J. D., Mak,  A. F. T., and Huang,  L. D., 1997, “A Large Deformation Biomechanical Model for Pressure Ulcers,” J. Biomech. Eng., 119, 406–408.
Zhang, M., Turner-Smith, A. R., and Roberts, V. C., 1994, “The Reaction of Skin and Soft Tissue to Shear Forces Applied Externally to the Skin Surface,” Proceedings of the Institute of Mechanical Engineers, 208 :217–222.


Grahic Jump Location
Contour plot of macroscopic damage evolution in muscle tissue, with cell properties κ=18.7 kPa and G=1.9 kPa, and parameters α=6⋅10−3,Tcell=9⋅10−3.
Grahic Jump Location
Damage evolution in four selected microstructures at four different external pressures P(P=4 kPa, 4.4 kPa, 5 kPa and 6 kPa). The damage in the four microstructures, positioned at different locations in the macroscopic mesh, are represented by the four subplots. The vertical axis of each subplot is the external pressure P whereas the horizontal axis denotes the time of compression. The color bars represent the percentage damaged cells in the microstructures.
Grahic Jump Location
Damage evolution in a particular microstructure at four different external pressures P(P=4 kPa, 4.4 kPa, 5 kPa and 6 kPa). The vertical axis is the external pressure P whereas the horizontal axis denotes the time of compression. The color bar represents the percentage damaged cells in the microstructure.
Grahic Jump Location
(a) Macroscopic mesh representing a muscle and skin layer that are compressed against a bony prominence, by an external pressure P. The nine circles in one particular macroscopic element indicate the location of the macroscopic integration points to which the microstructural models are assigned, (b) Microstructural mesh representing a simplified geometry of randomly dispersed cells embedded in extracellular matrix material (ECM).
Grahic Jump Location
Cell damage evolution in engineered skeletal muscle tissue constructs, adopted from 9. The percentage of dead cells is shown as a function of time for two different gross compressive strain levels. Unstrained constructs were identified as “control.”
Grahic Jump Location
Plot of J versus damage initiation time for different values of a with Tcell=0.009 [s]. The three lines correspond to α=0.002, 0.006, 0.010[−].
Grahic Jump Location
Damage evolution in an RVE, subjected to gross compressive strains of 30% and 50% compression for 8 hours, which is simulated by 40 time increments. Each circle represents one time increment.
Grahic Jump Location
Contour plot of macroscopic damage evolution in muscle tissue, with cell properties κ=150 kPa and G=15.6 kPa and parameters α=6⋅10−3,Tcell=9⋅10−3. The gray scale bars represent the percentage damaged cells in a macroscopic point as determined from the underlying microstructure.
Grahic Jump Location
Contour plot of macroscopic damage evolution in muscle tissue, with lower cell stiffnesses κ=18.7 kPa and G=1.9 kPa, and parameters α=6⋅10−3,Tcell=9⋅10−3.



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