Stress Analyses Coupled With Damage Laws to Determine Biomechanical Risk Factors for Deep Tissue Injury During Sitting

2008 ◽  
Vol 131 (1) ◽  
Author(s):  
Eran Linder-Ganz ◽  
Amit Gefen

Deep tissue injury (DTI) is a potentially life-threatening form of pressure ulcer that onsets in muscle tissue overlying bony prominences and progresses unnoticeably to more superficial tissues. To minimize DTI, the efficacy of wheelchair cushions should be evaluated not only based on their performance in redistributing interface pressures but also according to their effects on stress concentrations in deep tissues, particularly muscles. However, a standard bioengineering approach for such analyses is missing in literature. The goals of this study were to develop an algorithm to couple finite element (FE) modeling of the buttocks with an injury threshold for skeletal muscle and with a damage-stiffening law for injured muscle tissue, from previous animal experiments, to predict DTI onset and progression for different patient anatomies and wheelchair cushions. The algorithm was also employed for identifying intrinsic (anatomical) biomechanical risk factors for DTI onset. A set of three-dimensional FE models of seated human buttocks was developed, representing different severities of pathoanatomical changes observed in chronically sitting patients: muscle atrophy and “flattening” of the ischial tuberosity (IT). These models were then tested with cushions of different stiffnesses representing products available on the market and semirigid supports. Outcome measures were the percentage of damaged muscle tissue volumes after 90min and 110min of simulated continuous immobilized sitting as well as muscle injury rates post-60min, -90min, and -110min of continuous sitting. Damaged muscle volumes grew exponentially with the level of muscle atrophy. For example, simulation of a subject with 70% muscle atrophy sitting on a soft cushion showed damage to 33% of the muscle volume after 90min of immobilized sitting, whereas a comparable simulation with a nonatrophied muscle yielded only 0.4% damaged tissue volume. The rates of DTI progression also increased substantially with increasing severities of muscle atrophy, e.g., 70% atrophy resulted in 8.9, 2.7, and 1.6 times greater injury rates compared with the “reference” muscle thickness cases, after 60min, 90min, and 110min of sitting, respectively. Across all simulation cases, muscle injury rate was higher when a “flatter” IT was simulated. Stiffer cushions increased both the extent and rate of DTI at times shorter than 90min of continuous sitting, but after 110min, volumes and rates of tissue damage converged to approximately similar values across the different cushion materials. The present methodology is a practical tool for evaluating the performances of cushions in reducing the risk for DTI in a manner that goes far beyond the commonly accepted measurements of sitting pressures.

2010 ◽  
Vol 43 (3) ◽  
pp. 570-575 ◽  
Author(s):  
Bastiaan J. van Nierop ◽  
Anke Stekelenburg ◽  
Sandra Loerakker ◽  
Cees W. Oomens ◽  
Dan Bader ◽  
...  

2009 ◽  
Vol 107 (4) ◽  
pp. 1266-1275 ◽  
Author(s):  
Parco M. Siu ◽  
Eric W. Tam ◽  
Bee T. Teng ◽  
Xiao M. Pei ◽  
Joann W. Ng ◽  
...  

Pressure ulcer is a complex and significant health problem. Although the factors including pressure, shear, and ischemia have been identified in the etiology of pressure ulcer, the cellular and molecular mechanisms that contribute to the development of pressure ulcer are unclear. This study tested the hypothesis that the early-onset molecular regulation of pressure ulcer involves apoptosis in muscle tissue. Adult Sprague-Dawley rats were subjected to an in vivo protocol to mimic pressure-induced deep tissue injury. Static pressure was applied to the tibialis region of the right limb of the rats for 6 h each day on two consecutive days. The compression force was continuously monitored by a three-axial force transducer equipped in the compression indentor. The contralateral uncompressed limb served as intra-animal control. Tissues underneath the compressed region were collected for histological analysis, terminal dUTP nick-end labeling (TUNEL), cell death ELISA, immunocytochemical staining, and real-time RT-PCR gene expression analysis. The compressed muscle tissue generally demonstrated degenerative characteristics. TUNEL/dystrophin labeling showed a significant increase in the apoptotic muscle-related nuclei, and cell death ELISA demonstrated a threefold elevation of apoptotic DNA fragmentation in the compressed muscle tissue relative to control. Positive immunoreactivities of cleaved caspase-3, Bax, and Bcl-2 were evident in compressed muscle. The mRNA contents of Bax, caspase-3, caspase-8, and caspase-9 were found to be higher in the compressed muscle tissue than control. These results demonstrated that apoptosis is activated in muscle tissue following prolonged moderate compression. The data are consistent with the hypothesis that muscle apoptosis is involved in the underlying mechanism of pressure-induced deep tissue injury.


Author(s):  
Eran Linder-Ganz ◽  
Amit Gefen

Deep tissue injury (DTI) is a serious and potentially deadly type of pressure ulcers, which initiate in deep muscle tissue under bony prominences of immobilized patients, and progress outwards towards the skin with no clear visual indications of the injury at the surface of the body. It had been suggested that DTI appear in muscle tissue first, due to the dense capillary vasculature in skeletal muscles which is susceptible to obstruction and occlusion by mechanical forces [1–3]. Though mechanical forces may cause capillaries to collapse and thus induce ischemic conditions in adjacent muscle cells [2], some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and so, other mechanisms, particularly excessive cellular deformations must be involved [1]. We hypothesize that physiological levels of stresses and strains in muscle tissue under bony prominences — even when muscles are highly loaded as during sitting — do not cause complete closure of muscle capillaries, and therefore, do not cause an acute ischemia in muscles. If this is indeed the case, then ischemia cannot be the only factor contributing to DTI onset. In order to test our hypothesis, we developed a finite element (FE) model of the microstructure of skeletal muscle, at the level of muscle fascicles, and employed the model to determine the stress and strain levels required for causing partial and complete closure of capillaries.


2016 ◽  
Vol 4 ◽  
pp. 1-10 ◽  
Author(s):  
Hongxue Shi ◽  
Haohuang Xie ◽  
Yan Zhao ◽  
Cai Lin ◽  
Feifei Cui ◽  
...  

Abstract Background Pressure ulcers (PUs) are a major clinical problem that constitutes a tremendous economic burden on healthcare systems. Deep tissue injury (DTI) is a unique serious type of pressure ulcer that arises in skeletal muscle tissue. DTI arises in part because skeletal muscle tissues are more susceptible than skin to external compression. Unfortunately, few effective therapies are currently available for muscle injury. Basic fibroblast growth factor (bFGF), a potent mitogen and survival factor for various cells, plays a crucial role in the regulation of muscle development and homeostasis. The main purpose of this study was to test whether local administration of bFGF could accelerate muscle regeneration in a rat DTI model. Methods Male Sprague Dawley (SD) rats (age 12 weeks) were individually housed in plastic cages and a DTI PU model was induced according to methods described before. Animals were randomly divided into three groups: a normal group, a PU group treated with saline, and a PU group treated with bFGF (10 μg/0.1 ml) subcutaneously near the wound. Results We found that application of bFGF accelerated the rate of wound closure and promoted cell proliferation and tissue angiogenesis. In addition, compared to saline administration, bFGF treatment prevented collagen deposition, a measure of fibrosis, and up-regulated the myogenic marker proteins MyHC and myogenin, suggesting bFGF promoted injured muscle regeneration. Moreover, bFGF treatment increased levels of myogenesis-related proteins p-Akt and p-mTOR. Conclusions Our findings show that bFGF accelerated injured skeletal muscle regeneration through activation of the PI3K/Akt/mTOR signaling pathway and suggest that administration of bFGF is a potential therapeutic strategy for the treatment of skeletal muscle injury in PUs.


2007 ◽  
Vol 103 (2) ◽  
pp. 464-473 ◽  
Author(s):  
Debby Gawlitta ◽  
Cees W. J. Oomens ◽  
Dan L. Bader ◽  
Frank P. T. Baaijens ◽  
Carlijn V. C. Bouten

Prolonged periods of tissue compression may lead to the development of pressure ulcers, some of which may originate in, for example, skeletal muscle tissue and progress underneath intact skin, representing deep tissue injury. Their etiology is multifactorial and the interaction between individual causal factors and their relative importance remain unknown. The present study addressed the relative contributions of deformation and ischemic factors to altered metabolism and viability. Engineered muscle tissue was prepared as previously detailed ( 14 ) and subjected to a combination of factors including 0% oxygen, lactic acid concentrations resulting in pH from 5.3 to 7.4, 34% compression, and low glucose levels. Deformation had an immediate effect on tissue viability {[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) assay}, which increased with time. By contrast, hypoxia evoked metabolic responses (glucose and lactate levels) within 24 h, but viability was only reduced after 48 h. In addition, lactic acidification downregulated tissue metabolism up to an acid concentration (∼23 mM) where metabolism was arrested and cell death enhanced. A similar tissue response was observed during glucose deprivation, which, at negligible concentration, resulted in both a cessation of metabolic activity and a reduction in cell viability. The combination of results suggests that in a short-term (<24 h) deformation, extreme acidification and glucose deprivation increased the level of cell death. By contrast, nonextreme acidification and hypoxia influenced tissue metabolism, but not the development of cell death. These data provide more insight into how compression-induced factors can lead to the onset of deep tissue injury.


Author(s):  
Eran Linder-Ganz ◽  
Noga Shabshin ◽  
Yacov Itzchak ◽  
Itzhak Siev-Ner ◽  
Amit Gefen

Deep tissue injury (DTI) is a severe type of pressure ulcers affecting the viability of muscle tissue under bony prominences first [1]. Most researchers agree that prolonged elevated muscle tissue strains and stresses cause the onset of DTI. We recently showed that internal strain and stress distributions in muscle tissue of individuals can be evaluated by integrating Open-MRI examinations with subject-specific finite element (FE) analyses [2]. However, sub-dermal soft tissue strain and stress data from paraplegic wheelchair users are missing in the literature. Our present goals were therefore (i) to determine the strain and stress distributions in the gluteus muscles and enveloping fat under the ischial tuberosities (IT) of paraplegic wheelchair users during sitting and lying in an Open-MRI, (ii) to compare the paraplegic data to those obtained previously from normal subjects [2], and (iii) to compare between results obtained from paraplegics in the sitting and lying postures, in order to quantify the effect of posture on sub-dermal tissue mechanical conditions, particularly intramuscular shear stress.


2016 ◽  
Vol 29 (4) ◽  
pp. 178-190 ◽  
Author(s):  
Hyochol Ahn ◽  
Linda Cowan ◽  
Cynthia Garvan ◽  
Debra Lyon ◽  
Joyce Stechmiller

2020 ◽  
Author(s):  
Marisa Graser(Former Corresponding Author) ◽  
Sarah Day ◽  
Arjan Buis(New Corresponding Author)

Abstract Background: The soft tissue of the residual limb in transtibial prosthetic users encounters unique biomechanical challenges. Although not intended to tolerate high loads and deformation, it becomes a weight-bearing structure within the residuum-prosthesis-complex. Consequently, deep soft tissue layers may be damaged, resulting in Deep Tissue Injury (DTI). Whilst considerable effort has gone into DTI research on immobilised individuals, only little is known about the aetiology and population-specific risk factors in amputees. This scoping review maps out and critically appraises existing research on DTI in lower-limb prosthetic users according to (1) the population-specific aetiology, (2) risk factors, and (3) methodologies to investigate both. Results: A systematic search within the databases Pubmed, Ovid Excerpta Medica, and Scopus identified 16 English-language studies. The results indicate that prosthetic users may be at risk for DTI during various loading scenarios. This is influenced by individual surgical, morphological, and physiological determinants, as well as the choice of prosthetic componentry. However, methodological limitations, high inter-patient variability, and small sample sizes complicate the interpretation of outcome measures. Additionally, fundamental research on cell and tissue reactions to dynamic loading and on prosthesis-induced alterations of the vascular and lymphatic supply is missing. Conclusion: We therefore recommend increased interdisciplinary research endeavours with a focus on prosthesis-related experimental design to widen our understanding of DTI. The results have the potential to initiate much-needed clinical advances in surgical and prosthetic practice and inform future pressure ulcer classifications and guidelines.


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