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

Author(s):  
Sandra Loerakker ◽  
Gustav J. Strijkers ◽  
Klaas Nicolay ◽  
Frank P. T. Baaijens ◽  
Dan L. Bader ◽  
...  

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.

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

Author(s):  
Sandra Loerakker ◽  
Emmy Manders ◽  
Gustav J. Strijkers ◽  
Frank P. T. Baaijens ◽  
Dan L. Bader ◽  
...  

Sustained mechanical loading of soft tissues covering bony prominences, as experienced by bedridden and wheelchair-bound individuals, may cause skeletal muscle damage. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Damage pathways leading to DTI can involve ischemia, ischemia/reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2h loading period [1,2]. However, ischemia and reperfusion may play a more important role in the damage process during prolonged loading periods.


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.


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.


2019 ◽  
Vol 32 (6) ◽  
pp. e4087 ◽  
Author(s):  
Jules L. Nelissen ◽  
Ralph Sinkus ◽  
Klaas Nicolay ◽  
Aart J. Nederveen ◽  
Cees W.J. Oomens ◽  
...  

2007 ◽  
Vol 63 (4) ◽  
pp. 788-797 ◽  
Author(s):  
Matthias Schoen ◽  
Robert Rotter ◽  
Philipp Gierer ◽  
Georg Gradl ◽  
Ulf Strauss ◽  
...  

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.


Author(s):  
Sandra Loerakker ◽  
Anke Stekelenburg ◽  
Gustav J. Strijkers ◽  
Klaas Nicolay ◽  
Dan L. Bader ◽  
...  

Prolonged mechanical loading of soft tissues, as present when individuals are bedridden or wheelchair-bound, can lead to degeneration of skeletal muscle tissue. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, e.g. skeletal muscle, near bony prominences and progresses towards the skin. Complications associated with DTI include sepsis, renal failure, and myocardial infarction. Damage pathways leading to DTI involve ischemia, ischemia-reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, the role of tissue deformation in the onset of skeletal muscle damage was established by combining animal experiments with finite element (FE) modeling [1]. After 2 hours of continuous loading, a clear correlation between maximum shear strain and damage was found.


2010 ◽  
Vol 19 (2) ◽  
pp. 67-76 ◽  
Author(s):  
Fang Lin ◽  
Atek Pandya ◽  
Andrew Cichowski ◽  
Mauli Modi ◽  
Briana Reprogle ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document