The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles: Computational Studies

2007 ◽  
Author(s):  
Eran Linder-Ganz ◽  
Amit Gefen
Keyword(s):  
Muscle Tissue ◽  
Skeletal Muscles ◽  
Tissue Injury ◽  
The Body ◽  
Acute Ischemia ◽  
Fe Model ◽  
Mechanical Forces ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Complete Closure

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.

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

2010 ◽  
Vol 43 (3) ◽  
pp. 570-575 ◽  
Author(s):  
Bastiaan J. van Nierop ◽  
Anke Stekelenburg ◽  
Sandra Loerakker ◽  
Cees W. Oomens ◽  
Dan Bader ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Rat Model ◽  
Tissue Injury ◽  
Skeletal Muscle Tissue ◽  
Deep Tissue ◽  
Deep Tissue Injury

scholarly journals Muscle apoptosis is induced in pressure-induced deep tissue injury

2009 ◽  
Vol 107 (4) ◽  
pp. 1266-1275 ◽  
Author(s):  
Parco M. Siu ◽  
Eric W. Tam ◽  
Bee T. Teng ◽  
Xiao M. Pei ◽  
Joann W. Ng ◽  
...  
Keyword(s):  
Cell Death ◽  
Muscle Tissue ◽  
Pressure Ulcer ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Tissue Injury ◽  
Immunocytochemical Staining ◽  
Sprague Dawley ◽  
Deep Tissue ◽  
Deep Tissue Injury

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.

Temporal differences in the influence of ischemic factors and deformation on the metabolism of engineered skeletal muscle

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
Keyword(s):  
Skeletal Muscle ◽  
Cell Death ◽  
Muscle Tissue ◽  
Tissue Injury ◽  
Glucose Deprivation ◽  
Tissue Response ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Tissue Metabolism ◽  
Glucose Levels

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.

Peak Gluteal Muscle Strain and Stress Values During Sitting Are Greater in Paraplegics Than in Normals

2007 ◽  
Author(s):  
Eran Linder-Ganz ◽  
Noga Shabshin ◽  
Yacov Itzchak ◽  
Itzhak Siev-Ner ◽  
Amit Gefen
Keyword(s):  
Muscle Tissue ◽  
Tissue Injury ◽  
Normal Subjects ◽  
Stress Distributions ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Wheelchair Users ◽  
Open Mri ◽  
Ischial Tuberosities ◽  
Severe Type

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.

The Relative Contributions of Muscle Deformation and Ischemia to Pressure Ulcer Development

2012 ◽  
Author(s):  
Sandra Loerakker ◽  
Gustav J. Strijkers ◽  
Klaas Nicolay ◽  
Frank P. T. Baaijens ◽  
Dan L. Bader ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Tissue ◽  
Pressure Ulcer ◽  
Soft Tissues ◽  
Tissue Injury ◽  
Skeletal Muscle Tissue ◽  
Ischemia And Reperfusion ◽  
Deep Tissue ◽  
Deep Tissue Injury ◽  
Damage Process

Sustained mechanical loading of soft tissues covering bony prominences may lead to degeneration of skeletal muscle tissue. This can result in a condition termed deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Previously, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2 h loading period [1,2]. Recently, we also showed that ischemia and reperfusion may contribute to the damage process during prolonged loading [3]. In the present study, we investigated the relative effects of deformation, ischemia, and reperfusion on the temporal and spatial damage process of skeletal muscle tissue during a 6 h period using magnetic resonance imaging (MRI) techniques.

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
Keyword(s):  
Risk Factors ◽  
Muscle Atrophy ◽  
Muscle Tissue ◽  
Muscle Injury ◽  
Tissue Injury ◽  
Injury Rate ◽  
Stress Concentrations ◽  
Deep Tissue ◽  
Injury Rates ◽  
Deep Tissue Injury

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.

Healing effects of curcumin nanoparticles in deep tissue injury mouse model.

2020 ◽  
Vol 18 ◽  
Author(s):  
Zirui Zhang ◽  
Shangcong Han ◽  
Panpan Liu ◽  
Xu Yang ◽  
Jing Han ◽  
...  
Keyword(s):  
Wound Healing ◽  
Mrna Expression ◽  
Tissue Injury ◽  
Inflammatory Cells ◽  
Pcr Analysis ◽  
Protective Effects ◽  
Deep Tissue ◽  
Deep Tissue Injury

Background: Chronic inflammation and lack of angiogenesis are the important pathological mechanisms in deep tissue injury (DTI). Curcumin is a well-known anti-inflammatory and antioxidant agent. However, curcumin is unstable under acidic and alkaline conditions, and can be rapidly metabolized and excreted in the bile, which shortens its bioactivity and efficacy. Objective: This study aimed to prepare curcumin-loaded poly (lactic-co-glycolic acid) nanoparticles (CPNPs) and to elucidate the protective effects and underlying mechanisms of wound healing in DTI models. Methods: CPNPs were evaluated for particle size, biocompatibility, in vitro drug release and their effect on in vivo wound healing. Results : The results of in vivo wound closure analysis revealed that CPNP treatments significantly improved wound contraction rates (p<0.01) at a faster rate than other three treatment groups. H&E staining revealed that CPNP treatments resulted in complete epithelialization and thick granulation tissue formation, whereas control groups resulted in a lack of compact epithelialization and persistence of inflammatory cells within the wound sites. Quantitative real-time PCR analysis showed that treatment with CPNPs suppressed IL-6 and TNF-α mRNA expression, and up-regulated TGF-β, VEGF-A and IL-10 mRNA expression. Western blot analysis showed up-regulated protein expression of TGF-β, VEGF-A and phosphorylatedSTAT3. Conclusion: Our results showed that CPNPs enhanced wound healing in DTI models, through modulation of the JAK2/STAT3 signalling pathway and subsequent upregulation of pro-healing factors.

Evaluation of infrared technology to detect category I and suspected deep tissue injury in hospitalised patients

2019 ◽  
Vol 28 (Sup12) ◽  
pp. S9-S16
Author(s):  
Fazila Abu Bakar Aloweni ◽  
Shin Yuh Ang ◽  
Yee Yee Chang ◽  
Xin Ping Ng ◽  
Kai Yunn Teo ◽  
...  
Keyword(s):  
Skin Temperature ◽  
Infrared Thermography ◽  
Tissue Injury ◽  
Mean Difference ◽  
Deep Tissue ◽  
Thermal Images ◽  
Deep Tissue Injury ◽  
Hospitalised Patients ◽  
Significant Difference ◽  
The Mean

Objective: To evaluate the use of an infrared thermography device in assessing skin temperature among category I pressure ulcer (PU) and/or suspected deep tissue injuries (SDTI) with intact skin. Methods: An observational cross-sectional study design was used. Adult inpatients (cases) who had a category I PU or suspected deep tissue injury (skin intact) on the sacral or heel during the study period (March to April 2018) were recruited. Patients without a PU were also recruited to act as control. Thermal images of the patient's PU site and non-PU site were taken within 24 hours of PU occurrence. Thermal images of the control patients (no PU) were also taken. Each PU case was matched to three control patients in terms of age, gender, race and anatomical sites. All thermal images were taken using a portable CAT S60 Thermal Imaging Rugged Smartphone (Caterpillar Inc., US) that provided readings of the skin temperature in degrees Celsius. Results: A total of 17 cases and 51 controls were recruited. Among the cases, the mean difference in skin temperature between the PU site (mean: 31.14°C; standard deviation [SD]: 1.54) and control site within the cases (mean: 28.93°C; SD: 3.47) was significant (difference: 2.21±3.66°C; p=0·024). When comparing between all cases and controls, the mean temperature difference was non-significant. When comparing between the category I PU and suspected deep pressure injury cases, the mean difference was also non-significant. Conclusion: Using infrared thermography technology at the bedside to measure skin temperature will support the clinical diagnosis of patients with skin types I to III. However, there is a need for a more accurate and objective measurement to identify and diagnose early category I PU or suspected deep tissue injury in adult patients with darker skin types 4 and above, enabling early initiation of preventive measures in the hospital acute care setting.

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