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There is an individual tolerance to mechanical loading in compression induced deep tissue injury
Abstract
p>Background: deep tissue injury is a type of pressure ulcer which originates subcutaneously due to sustained mechanical loading. The relationship between mechanical compression and damage development has been extensively studied in 2D. However, recent studies have suggested that damage develops beyond the site of indentation. The objective of this study was to compare mechanical loading conditions to the associated damage in 3D.
Methods: an indentation test was performed on the tibialis anterior muscle of rats (n = 39). Changes in the form of oedema and structural damage were monitored with MRI in an extensive region. The internal deformations were evaluated using MRI based 3D finite element models.
Findings: damage propagates away from the loaded region. The 3D analysis indicates that there is a subject specific tolerance to compression induced deep tissue injury. Interpretation: Individual tolerance is an important factor when considering the mechanical loading conditions which induce damage.</p
... Notably, the majority of the tissue damage was located close to and opposite to the indentation site whilst the middle regions of the muscle seemed intact. This is congruent with the results from fluorescence imaging as well other studies that reported a damage propagation away from the loaded region 28,29 . ...
... The differentiation between "cell death" and "no damage" was based around damage distribution. In samples with high cell death counts, damaged cells were arranged in a centralised pattern, which was also observed by other researchers in similar experiments 18,28,29 . In comparison, samples with low dead cell counts were missing a distinctive pattern with dead cells scattered throughout the samples. ...
In many populations like wheelchair and prosthetic users, the soft tissue is subject to excessive or repetitive loading, making it prone to Deep Tissue Injury (DTI). To study the skeletal muscle response to physical stress, numerous in vitro and in vivo models exist. Yet, accuracy, variability, and ethical considerations pose significant trade-offs. Here, we present an ex vivo approach to address these limitations and offer additional quantitative information on cellular damage. In this study, skeletal muscle tissue from Sprague Dawley rats was isolated and transversely loaded. Histological analysis and fluorescence staining demonstrated that the setup was suitable to keep the tissue alive throughout the experimental procedure. Mechanically induced cell damage was readily distinguishable through morphological changes and uptake of a membrane impermeable dye. Our comparably simple experimental setup can be adapted to different loading conditions and tissues to assess the cell response to mechanical loading in future studies.
... Recently the 2 hour indenter protocol has been investigated using 3D FE modelling, observing that damage propagates away from the loaded region and instead of a distinct strain threshold for tissue damage a transition region of higher risk of damage was observed [173,174]. This may provide insights into the mechanisms behind subject-specific tolerance to damage, and indicates that tissue damage is not dictated by the loading alone [174]. ...
... Recently the 2 hour indenter protocol has been investigated using 3D FE modelling, observing that damage propagates away from the loaded region and instead of a distinct strain threshold for tissue damage a transition region of higher risk of damage was observed [173,174]. This may provide insights into the mechanisms behind subject-specific tolerance to damage, and indicates that tissue damage is not dictated by the loading alone [174]. ...
The residual limb tissues of an individual with below knee amputation form a critical loaded interface with the prosthetic limb. In the early stages of rehabilitation, residual limb tissues have not been conditioned to support loading and are vulnerable to damage. This impacts upon quality of life and can lead to rejection of the prosthesis. Bioengineers have established an array of measurements to understand the pathogenesis of soft tissue damage and assess multiple aspects of tissue tolerance during loading. However, to date, there is a scarcity of literature utilising these techniques to evaluate the residual limb-socket interface, resulting in a lack of evidence-based practice to prevent socket sores. A protocol for applying representative mechanical loading on lower limb tissues was developed with a cohort of volunteers without amputation. This involved incremental pressure application through a pneumatic cuff and an array of measurements before, during and after this loaded period to characterise the response of the underlying skin and soft tissues. The protocol was then applied to a cohort of participants with unilateral transtibial amputation. In order to evaluate intrinsic factors (soft tissue composition), Magnetic Resonance Imaging was used to visualise tissue composition and gross soft tissue deformation and a MyotonPROTM device was used to estimate tissue stiffness. Transcutaneous oxygen and carbon dioxide tensions were measured, and inflammatory biomarkers were collected at sites relevant to prosthetic load transfer, each of which reflected compromise to the skin tissues. MRI revealed increased adipose infiltrating muscle tissue in residual limbs (median 2.5 %, range 0.2 - 8.9 %) compared to intact limbs (median ≤ 1.7 %, range 0.1 - 5.1 %), indicating muscle atrophy post-amputation. This effect was reduced significantly in the contralateral limbs of those individuals with greater socket use (r = -0.88, p <0.01), indicative of adaptation post-activity. During prescribed loading, cuff pressure at the highest inflation of 60 mmHg resulted in mean interface pressures ranging from 66.2 - 83.6 mmHg. In the majority of cases, residual limbs displayed less compressive strain when loaded compared to intact limbs, the differences being statistically significant at a number of tested sites (median strains -6 to 2 % vs. 4 to 13 %, respectively). Cuff loading was observed to produce a transient compromise to tissue viability, reflected in a reduction in transcutaneous oxygen tension and an upregulation of inflammatory biomarkers, suggesting a degree of local ischaemia and inflammation, respectively. In most cases, reduced ischaemia and inflammatory biomarker upregulation was observed in residual limbs compared to intact limbs, suggesting enhanced tolerance to loading. Nonetheless there was considerable variation within the heterogeneous cohort of participants with amputation. These studies represent a first-of-kind evaluation of residual limb tissue tolerance to representative prosthetic loads involving tissue characterisation and physiological monitoring. This experimental approach could be implemented to identify individual susceptibility to tissue damage which, in turn, could help inform appropriate rehabilitation programmes to maintain health of tissue during prosthetic rehabilitation. Furthermore, development of these techniques into real-time portable measurements would support both prosthetic users and prosthetists to assess in-socket tissue health, leading to more informed management of residual limb tissues.
... 16 In addition, the morphology, mechanical properties, and tissue tolerance to the loading can all change over time because of ageing, lifestyle, chronic injury, or disease. [16][17][18] In general, externally applied forces, even of a uniform nature, will lead to highly irregular internal tissue strain/stress responses, that is, different loading intensities at different tissue locations, depending on the internal anatomy, body posture, and properties of tissues of the individual. [19][20][21][22] This can also be referred to as heterogeneous or nonhomogeneous tissue responses to the applied loads. ...
In 2019, the third and updated edition of the Clinical Practice Guideline (CPG) on Prevention and Treatment of Pressure Ulcers/Injuries has been published. In addition to this most up-to-date evidence-based guidance for clinicians, related topics such as pressure ulcers (PUs)/pressure injuries (PIs) aetiology, classification, and future research needs were considered by the teams of experts. To elaborate on these topics, this is the third paper of a series of the CPG articles, which summarises the latest understanding of the aetiology of PUs/PIs with a special focus on the effects of soft tissue deformation. Sustained deformations of soft tissues cause initial cell death and tissue damage that ultimately may result in the formation of PUs/PIs. High tissue deformations result in cell damage on a microscopic level within just a few minutes, although it may take hours of sustained loading for the damage to become clinically visible. Superficial skin damage seems to be primarily caused by excessive shear strain/stress exposures, deeper PUs/PIs predominantly result from high pressures in combination with shear at the surface over bony prominences, or under stiff medical devices. Therefore, primary PU/PI prevention should aim for minimising deformations by either reducing the peak strain/stress values in tissues or decreasing the exposure time.
... 13 However, a target value for shear force has not yet been determined. Furthermore, individual differences in tissue tolerance to mechanical loading exist, 14 possibly explaining why some patients still develop PIs despite the use of preventive interventions to measure external forces and redistribute pressure. Biochemical measurement of biomarkers, such as skin blotting 15 and Sebutape, 16 has been proposed to assess tissue status or viability due to mechanical loading. ...
Pressure injuries (PIs) are localised skin injuries that result from pressure with or without shear force. Shear force is more destructive than pressure in clinical settings. Therefore, determining the critical external forces is important for selecting the appropriate care to prevent PIs. To quantitatively distinguish pressure and shear loading with high specificity, we focused on microRNAs (miRs). This study aimed to identify the miRs that are distinguishable between pressure with and without shear loading in rat skin. Microarray analysis identified six candidate miRs from the comparisons among the pressure, shear, and unloaded groups. We analysed the expression levels of the candidate miRs in the process of PI development using real-time reverse transcriptase polymerase chain reaction. In the pressure and shear groups, miR-92b expressions at 6 hours after loading were 2.3 ± 1.3 and 2.9 ± 1.0, respectively, which were significantly higher than those in the control group (P = .014 and .004, respectively). miR-877 expression at 6 hours after loading was significantly increased only in the shear group (2.8 ± 0.9) compared with the control group (P = .016). These results indicate that miR-92b and miR-877 are promising biomarkers to determine for which external force healthcare professionals should intervene.
... This is corroborated by finite element analyses, which give typical mean strain estimates of 3-15% for both principal tension, compression, and maximal shear, and strain peaks of 30-75% [15,17,38]. The estimated strain distribution lies below estimated thresholds for skeletal muscle damage from engineered tissue and rat models [39,40]. Strain predictions were consistent with the design intent for TSB [4] and PTB [5,6] socket types, and provided a noteworthy illustration of how sub-surface shear strain gradients-a marker of deep tissue injury risk-may be generated near bony prominences in the absence of interface pressure near the anterior distal tip of the tibia. ...
Personalised prosthetic sockets are fabricated by expert clinicians in a skill- and experience-based process, with research providing tools to support evidence-based practice. We propose that digital volume correlation (DVC) may offer a deeper understanding of load transfer from prosthetic sockets into the residual limb, and tissue injury risk. This study’s aim was to develop a transtibial amputated limb analogue for volumetric strain estimation using DVC, evaluating its ability to distinguish between socket designs. A soft tissue analogue material was developed, comprising silicone elastomer and sand particles as fiducial markers for image correlation. The material was cast to form an analogue residual limb informed by an MRI scan of a person with transtibial amputation, for whom two polymer check sockets were produced by an expert prosthetist. The model was micro-CT scanned according to (i) an unloaded noise study protocol and (ii) a case study comparison between the two socket designs, loaded to represent two-legged stance. The scans were reconstructed to give 108 µm voxels. The DVC noise study indicated a 64 vx subvolume and 50% overlap, giving better than 0.32% strain sensitivity, and ~3.5 mm spatial resolution of strain. Strain fields induced by the loaded sockets indicated tensile, compressive and shear strain magnitudes in the order of 10%, with a high signal:noise ratio enabling distinction between the two socket designs. DVC may not be applicable for socket design in the clinical setting, but does offer critical 3D strain information from which existing in vitro and in silico tools can be compared and validated to support the design and manufacture of prosthetic sockets, and enhance the biomechanical understanding of the load transfer between the limb and the prosthesis.
... 8 Such research encompasses a hierarchical approach, involving cell models, tissue-engineered constructs, and evaluations of specific subpopulations at risk of developing PUs. 9 Several studies have assessed the effects of large strains in subdermal tissues involving muscle and fat, by evaluating the biomechanical and physiological response of the tissues employing imaging and biomarker analysis. 10,11 However, this approach does not account for the damage mechanisms associated with the majority of PUs involving small tissue strains in superficial dermal tissues. Indeed, in this case, researchers have used biophysical and imaging techniques to assess the response of superficial skin tissues under representative loads. ...
Pressure ulcers are caused by prolonged mechanical loads deforming the underlying soft tissues. However, the mechanical loads for microcirculatory occlusion are unknown. The present study was designed to characterise the simultaneous response of microvascular and lymphatic structures under repeated mechanical loading.
The effects of two distinct loading/unloading cycles involving i) incremental pressures 30, 60 and 90mmHg and ii) three repeated cycles of 30mmHg, were evaluated on a cohort of able‐bodied volunteers. Microvascular response involved the monitoring of transcutaneous gas tensions, while dermal lymphatic activity was estimated from Near Infrared Imaging. Responses were compared during each load and recovery cycle.
Changes in microvascular response were dependent on the load magnitudes, with 30mmHg resulting in a reduction in oxygen tension only, while 90mmHg affected both oxygen and carbon dioxide values in most cases (54%). By contrast, lymphatics revealed near total occlusion at 30mmHg. Although there were inter‐subject differences, temporal trends consistently revealed partial or full impairment under load, with recovery during off‐loading.
The pressure required to cause microcirculatory occlusion differed between individuals, with lymphatic impairment occurring at a lower pressure to that of microvascular vessels. This highlights the need for personalised care strategies and regular off‐loading of vulnerable tissues.
Pressure ulcer/injury (PU) risk assessment is widely considered an essential component in clinical practice. It is a complex and broad concept that includes different approaches, such as clinical judgement, using standardised risk assessment instruments, skin assessments, or using devices to measure skin or tissue properties. A distinction between PU risk assessment and early detection is important. PU risk measures the individual's susceptibility to developing a PU under a specific exposure (primary prevention), and early detection includes the assessment of early (sub)clinical signs and symptoms to prevent progression and to support healing (secondary prevention). PU risk is measured using prognostic/risk factors or prognostic models. Every risk estimate is a probability statement containing varying degrees of uncertainty. It therefore follows that every clinical decision based on risk estimates also contains uncertainty. PU risk assessment and prevention is a complex intervention, where delivery contains several interacting components. There is a huge body of evidence indicating that risk assessment and its outcomes, the selection of preventive interventions and PU incidence are not well connected. Methods for prognostic model development and testing in PU risk research must be improved and follow state-of-the-art methodological standards. Despite these challenges, we do have substantial knowledge about PU risk factors that helps us to make better clinical decisions. An important next step in the development of PU risk prediction might be the combination of clinical and other predictors for more individualised care. Any prognostic test or procedure must lead to better prevention at an acceptable cost.
OBJECTIVE: 2D Ultrasound (US) imaging has been recently investigated as a more accessible alternative to 3D Magnetic Resonance Imaging (MRI) for the estimation of soft issue motion under external mechanical loading. In the context of pressure ulcer prevention, the aim of this pilot MRI study was to design an experiment to characterize the sacral soft tissue motion under a controlled mechanical loading. Such an experiment targeted the estimation of the discrepancy between tissue motion assessed using a 2D imaging modality (echography) versus tissue motion assessed using a (reference) 3D imaging modality (MRI).METHODS: One healthy male volunteer participated in the study. An MRI-compatible custom-made setup was designed and used to load the top region of the sacrum with a 3D-printed copy of the US transducer. Five MR images were collected, one in the unloaded and four in the different loaded configurations (400-1200 [g]). Then, a 3D displacement field for each loading configuration was extracted based on the results of digital volume correlation. Tissue motion was separated into the X, Y, Z directions of the MRI coordinate system and the ratios between the out-of-plane and in-plane components were assessed for each voxel of the selected region of interest.RESULTS: Ratios between the out-of-plane and in-plane displacement components were higher than 0.6 for more than half of the voxels in the region of interest for all load cases and higher than 1 for at least quarter of the voxels when loads of 400-800 [g] were used.CONCLUSION: The out-of-ultrasound-plane tissue displacement was not negligible, therefore 2D US imaging should be used with caution for the evaluation of the tissue motion in the sacrum region. The 3D US modality should be further investigated for this application.
Objective
2D Ultrasound (US) imaging has been recently investigated as a more accessible alternative to 3D Magnetic Resonance Imaging (MRI) for the estimation of soft issue motion under external mechanical loading. In the context of pressure ulcer prevention, the aim of this pilot MRI study was to design an experiment to characterize the sacral soft tissue motion under a controlled mechanical loading. Such an experiment targeted the estimation of the discrepancy between tissue motion assessed using a 2D imaging modality (echography) versus tissue motion assessed using a (reference) 3D imaging modality (MRI).
Methods
One healthy male volunteer participated in the study. An MRI-compatible custom-made setup was designed and used to load the top region of the sacrum with a 3D-printed copy of the US transducer. Five MR images were collected, one in the unloaded and four in the different loaded configurations (400–1200 [g]). Then, a 3D displacement field for each loading configuration was extracted based on the results of digital volume correlation. Tissue motion was separated into the X, Y, Z directions of the MRI coordinate system and the ratios between the out-of-plane and in-plane components were assessed for each voxel of the selected region of interest.
Results
Ratios between the out-of-plane and in-plane displacement components were higher than 0.6 for more than half of the voxels in the region of interest for all load cases and higher than 1 for at least quarter of the voxels when loads of 400–800 [g] were used.
Conclusion
The out-of-ultrasound-plane tissue displacement was not negligible, therefore 2D US imaging should be used with caution for the evaluation of the tissue motion in the sacrum region. The 3D US modality should be further investigated for this application.
Background
Pressure-induced tissue strain is one major pathway for Pressure Ulcer development and, especially, Deep Tissue Injury. Biomechanical investigation of the time-dependent stress–strain mechanical behaviour of skeletal muscle tissue is therefore essential. In the literature, a viscoelastic formulation is generally assumed for the experimental characterization of skeletal muscles, with the limitation that the underlying physical mechanisms that give rise to the time dependent stress–strain behaviour are not known. The objective of this study is to explore the capability of poroelasticity to reproduce the apparent viscoelastic behaviour of passive muscle tissue under confined compression.
Methods
Experimental stress-relaxation response of 31 cylindrical porcine samples tested under fast and slow confined compression by Vaidya and collaborators were used. An axisymmetric Finite Element model was developed in ABAQUS and, for each sample a one-to-one inverse analysis was performed to calibrate the specimen-specific constitutive parameters, namely, the drained Young's modulus, the void ratio, hydraulic permeability, the Poisson's ratio, the solid grain's and fluid's bulk moduli.
Findings
The peak stress and consolidation were recovered for most of the samples (N = 25) by the poroelastic model (normalised root-mean-square error ≤0.03 for fast and slow confined compression conditions).
Interpretation
The strength of the proposed model is its fewer number of variables (N = 6 for the proposed poroelastic model versus N = 18 for the viscohyperelastic model proposed by Vaidya and collaborators). The incorporation of poroelasticity to clinical models of Pessure Ulcer formation could lead to more precise and mechanistic explorations of soft tissue injury risk factors.
Linked Article: Hahnel et al. Br J Dermatol 2020; 183:256–264.
Pressure ulcers occur due to sustained mechanical loading. Deep tissue injury is a severe type of pressure ulcer, which is believed to originate in subcutaneous tissues adjacent to bony prominences. In previous experimental-numerical studies the relationship between internal tissue state and damage development was investigated using a 2D analysis. However, recent studies suggest that a local analysis is not sufficient. In the present study we developed a method to create animal-specific 3D finite element models of an indentation test on the tibialis anterior muscle of rats based on MRI data. A detailed description on how the animal specific models are created is given. Furthermore, two indenter geometries are compared and the influence of errors in determining the indenter orientation on the resulting internal strain distribution in a defined volume of tissue was investigated. We conclude that with a spherically-shaped indenter errors in estimating the indenter orientation do not unduly influence the results of the simulation.
Deformation of skeletal muscle in the proximity of bony structures may lead to deep tissue injury category of pressure ulcers. Changes in mechanical properties have been proposed as a risk factor in the development of deep tissue injury and may be useful as a diagnostic tool for early detection. MRE allows for the estimation of mechanical properties of soft tissue through analysis of shear wave data. The shear waves originate from vibrations induced by an external actuator placed on the tissue surface. In this study a combined Magnetic Resonance (MR) compatible indentation and MR Elastography (MRE) setup is presented to study mechanical properties associated with deep tissue injury in rats. The proposed setup allows for MRE investigations combined with damage-inducing large strain indentation of the Tibialis Anterior muscle in the rat hind leg inside a small animal MR scanner. An alginate cast allowed proper fixation of the animal leg with anatomical perfect fit, provided boundary condition information for FEA and provided good susceptibility matching. MR Elastography data could be recorded for the Tibialis Anterior muscle prior to, during, and after indentation. A decaying shear wave with an average amplitude of approximately 2 μm propagated in the whole muscle. MRE elastograms representing local tissue shear storage modulus Gd showed significant increased mean values due to damage-inducing indentation (from 4.2 ± 0.1 kPa before to 5.1 ± 0.6 kPa after, p<0.05). The proposed setup enables controlled deformation under MRI-guidance, monitoring of the wound development by MRI, and quantification of tissue mechanical properties by MRE. We expect that improved knowledge of changes in soft tissue mechanical properties due to deep tissue injury, will provide new insights in the etiology of deep tissue injuries, skeletal muscle damage and other related muscle pathologies.
Study design:
This was a prospective cohort study.
Objectives:
The objective was to describe the incidence, prevalence, characteristics of pressure ulcers (PUs) and the association with specific patient characteristics in a consecutive sample of in-patients with a spinal cord injury (SCI).
Setting:
An acute care and rehabilitation clinic specialized in SCIs in Switzerland.
Methods:
The presence and characteristics of PUs for all adult patients with a SCI admitted to the clinic from 1 September 2009 to 28 February 2010 were recorded on a daily basis during their complete hospitalization. Risk factors were analyzed in univariate and multivariate logistic regression models.
Results:
A total of 185 patients were included in the study and observed for the entirety of their hospitalization. The prevalence of at least one PU was 49.2% in all patients, compared with 25.4% in the group of patients admitted without PUs. The incidence was 2.2 per person and year. In 91 patients, a total of 219 PUs were observed. PUs were most frequently located on the foot (36.1%), and the coccyx/sacrum (15.1%). The risk for occurrence of a PU increased with age (odds ratio (OR)=1.04) and post SCI (OR=1.03). In the multivariate analyses, the risk for PUs was lower for patients with the American Spinal Injury Association (ASIA) Impairment Scale (AIS) of C or D (ORC=0.25, ORD=0.28) compared with patients with an AIS of A.
Conclusion:
Using a daily documentation system, PUs were detected as a frequent complication of SCIs. Completeness of injury, age and time since injury were significant risk factors for PUs. The foot was a region at high risk for PUs.
Models of skeletal muscle can be classified as phenomenological or biophysical. Phenomenological models predict the muscle’s response to a specified input based on experimental measurements. Prominent phenomenological models are the Hill-type muscle models, which have been incorporated into rigid-body modeling frameworks, and three-dimensional continuum-mechanical models. Biophysically based models attempt to predict the muscle’s response as emerging from the underlying physiology of the system. In this contribution, the conventional biophysically based modeling methodology is extended to include several structural and functional characteristics of skeletal muscle. The result is a physiologically based, multi-scale skeletal muscle finite element model that is capable of representing detailed, geometrical descriptions of skeletal muscle fibers and their grouping. Together with a well-established model of motor-unit recruitment, the electro-physiological behavior of single muscle fibers within motor units is computed and linked to a continuum-mechanical constitutive law. The bridging between the cellular level and the organ level has been achieved via a multi-scale constitutive law and homogenization. The effect of homogenization has been investigated by varying the number of embedded skeletal muscle fibers and/or motor units and computing the resulting exerted muscle forces while applying the same excitatory input. All simulations were conducted using an anatomically realistic finite element model of the tibialis anterior muscle. Given the fact that the underlying electro-physiological cellular muscle model is capable of modeling metabolic fatigue effects such as potassium accumulation in the T-tubular space and inorganic phosphate build-up, the proposed framework provides a novel simulation-based way to investigate muscle behavior ranging from motor-unit recruitment to force generation and fatigue.
Deep tissue injury (DTI) is a severe form of pressure ulcer where tissue damage starts in deep tissues underneath intact skin. Tissue deformation may play an important role in the aetiology, which can be investigated using an experimental-numerical approach. Recently, an animal-specific finite element model has been developed to simulate experiments in which muscle tissue was compressed with an indenter. In this study, the material behaviour and boundary conditions were adapted to improve the agreement between model and experiment and to investigate the influence of these adaptations on the predicted strain distribution. The use of a highly nonlinear material law and including friction between the indenter and the muscle both improved the quality of the model and considerably influenced the estimated strain distribution. With the improved model, the required sample size to detect significant differences between loading conditions can be diminished, which is clearly relevant in experiments involving animals.
Mechanical loading of soft tissues covering bony prominences can cause skeletal muscle damage, ultimately resulting in a severe pressure ulcer termed deep tissue injury. Recently, by means of an experimental-numerical approach, it was shown that local tissue deformations cause tissue damage once a deformation threshold is exceeded. In the present study, the effects of load exposure time and intermittent load relief on the development of deformation-induced muscle damage were investigated. The data showed that a 2 h loading period caused more damage than 10 min loading. Intermittent load reliefs of 2 min during a 2 h loading period had minimal effect on the evolution of skeletal muscle damage. In addition, a local deformation threshold for damage was found, which was similar for each of the loading regimes applied in this study. For short loading periods, these results imply that local tissue deformations determine whether muscle damage will develop and the exposure time influences the amount of tissue damage. Temporary load reliefs were inefficient in reducing deformation-induced damage, but may still influence the development of ischemia-induced damage during longer loading periods.
To obtain insight into the etiology of deep pressure sores, understanding of the relationship between prolonged transverse loading and local muscle damage is required. To date, the amount and location of muscle damage have been determined by histological examination. In the present study, we determined whether T2-weighted high-resolution magnetic resonance imaging (MRI) can also be applied to evaluate muscle tissue after prolonged transverse loading. The tibialis anterior muscle and overlying skin in the right hindlimbs of five rats were compressed between an indenter and the tibia. The in vivo magnetic resonance images of the loaded and contralateral hindlimbs were obtained 24 h after load application. The tibialis anterior muscles were then processed for histological examination. In the magnetic resonance images of all five loaded hindlimbs, signal intensity appeared higher in the loaded regions of the muscle compared with the unloaded regions. The location of the higher signal intensity coincided with the location of damage assessed from histology. Also the amount of damage determined with MRI was in good agreement with the amount of damage assessed from histological examination. Because MRI is nondestructive, it is a promising alternative for histology in research on pressure sore etiology, especially in follow-up studies to evaluate the development of muscle damage in time and in clinical studies.
Pressure distributions at the interface between skin and supporting tissues are used in design of supporting surfaces like beds, wheel chairs, prostheses and in sales brochures to support commercial products. The reasoning behind this is, that equal pressure distributions in the absence of high pressure gradients is assumed to minimise the risk of developing pressure sores. Notwithstanding the difficulty in performing reproducible and accurate pressure measurements, the question arises if the interface pressure distribution is representative of the internal mechanical state of the soft tissues involved. The paper describes a study of the mechanical condition of a supported buttock contact, depending on cushion properties, relative properties of tissue layers and friction. Numerical, mechanical simulations of a buttock on a supporting cushion are described. The ischial tuberosity is modelled as a rigid body, whereas the overlying muscle, fat and skin layers are modelled as a non-linear Ogden material. Material parameters and thickness of the fat layer are varied. Coulomb friction between buttock and cushion is modelled with different values of the friction coefficient. Moreover, the thickness and properties of the cushion are varied. High shear strains are found in the muscle near the bony prominence and the fat layer near the symmetry line. The performed parameter variations lead to large differences in shear strain in the fat layer but relatively small variations in the skeletal muscle. Even with a soft cushion, leading to a high reduction of the interface pressure the deformation of the skeletal muscle near the bone is high enough to form a risk, which is a clear argument that interface pressures alone are not sufficient to evaluate supporting surfaces.
The aetiology of pressure ulcers is poorly understood. The complexity of the problem, involving mechanical, biochemical, and physiological factors demands the need for simpler model systems that can be used to investigate the relative contribution of these factors, while controlling others. Therefore, an in vitro model system of engineered skeletal muscle tissue constructs was developed. With this model system, the relationship between compressive tissue straining and cell damage initiation was investigated under well-defined environmental conditions. Compression of the engineered muscle tissue constructs revealed that cell death occurs within 1–2 h at clinically relevant straining percentages and that higher strains led to earlier damage initiation. In addition, the uniform distribution of dead cells throughout the constructs suggested that sustained deformation of the cells was the principle cause of cell death. Therefore, it is hypothetised that sustained cell deformation is an additional mechanism that plays a role in the development of pressure ulcers. © 2003 Biomedical Engineering Society.
PAC2003: 8719Rr, 8719Ff, 8718La, 8780Rb
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 ( approximately 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.
Early diagnosis of deep tissue injury remains problematic due to the complicated and multi-factorial nature of damage induction, and the many processes involved in damage development and recovery. In this paper we present a comprehensive assessment of deep tissue injury development and remodeling in a rat model by multi-parametric magnetic resonance imaging (MRI) and histopathology. The tibialis anterior muscle of rats was subjected to mechanical deformation for 2 h. Multi-parametric in vivo MRI, consisting of T2, T2∗, mean diffusivity (MD), and angiography measurements, was applied before, during, and directly after indentation, as well as at several time points during a 14 days follow-up. MRI readouts were linked to histological analyses of the damaged tissue. The results showed dynamic change in various MRI parameters, reflecting the histopathological status of the tissue during damage induction and repair. Increased T2corresponded with edema, muscle cell damage, and inflammation. T2∗ was related to tissue perfusion, hemorrhage, and inflammation. MD increase and decrease reported on the tissue's microstructural integrity and reflected muscle degeneration, edema, as well as fibrosis. Angiography provided information on blockage of blood flow during deformation. Our results indicate that the effects of a single damage causing event of only 2 h deformation were present up to 14 days. The initial tissue response to deformation, as observed by MRI, starts at the edge of the indentation. The quantitative MRI readouts provided distinct and complementary information on the extent, temporal evolution, and microstructural basis of deep tissue injury related muscle damage.
The aim of this study was to determine the predictive validity of the Braden, Norton, and Waterlow scales in 2 long-term care departments in the Czech Republic. Assessing the risk for developing pressure ulcers is the first step in their prevention. At present, many scales are used in clinical practice, but most of them have not been properly validated yet (for example, the Modified Norton Scale in the Czech Republic). In the Czech Republic, only the Braden Scale has been validated so far. This is a prospective comparative instrument testing study. A random sample of 123 patients was recruited. The predictive validity of the pressure ulcer risk assessment scales was evaluated based on sensitivity, specificity, positive and negative predictive values, and the area under the receiver operating characteristic curve. The data were collected from April to August 2014. In the present study, the best predictive validity values were observed for the Norton Scale, followed by the Braden Scale and the Waterlow Scale, in that order. We recommended that the above 3 pressure ulcer risk assessment scales continue to be evaluated in the Czech clinical setting.
Pressure ulcers are a type of local soft tissue injury due to sustained mechanical loading and remain a common issue in patient care. People with spinal cord injury (SCI) are especially at risk of pressure ulcers due to impaired mobility and sensory perception. The development of load improving support structures relies on realistic tissue load evaluation e.g. using finite element analysis (FEA). FEA requires realistic subject-specific mechanical properties and geometries. This study focuses on the effect of geometry. MRI is used for the creation of geometrically accurate models of the human buttock for three able-bodied volunteers and three volunteers with SCI. The effect of geometry on observed internal tissue deformations for each subject is studied by comparing FEA findings for equivalent loading conditions. The large variations found between subjects confirms the importance of subject-specific FEA.
Since this paper is a contribution to a symposium dealing with many aspects of tissue trauma, we propose to limit our discussion to experience only at Rancho Los Amigos Hospital in Downey, California. We do not wish to imply that our methods are superior to all others but we hope that some different and useful ideas may obtain from our limited experience.
The Tissue Trauma Group of the Rehabilitation Engineering Center has been actively involved in research, development and patient service for both the sitting and the recumbent (or prostrate) patient. The approaches to these two types of problem are fundamentally different for the following reasons:
(i)
The projected area of support of a prostrate human being, when divided into his body weight, yields an average pressure of around so mm Hg. This is below the 30-35 mm Hg usually accepted as necessary to cause ischaemia.
(ii)
The projected area of support, including the feet (but not the back) of a sitting person when divided into his body weight, yields an average pressure of about 50 mm Hg. This is above the 30-35 mm Hg ‘ischaemic pressure’.
The logic of reason (i) has led us to develop devices to attempt to distribute the support pressure of the recumbent patient as uniformly as possible, so that such patients may lie in any position in definitely (usually through the night) without being turned. This approach has resulted in the Rancho Flotation Bed (mud bed) and the Poly-Flotation Mattress to be described later.
The problems of the seated patient suggested in reason (ii) have led to an approach that involves the development of optimum seat cushions, coupled with clinical service which relies on special pressure measurement techniques and procedures for custom modification of seat cushions and sitting positions. These will be discussed in detail.
Research and development have focused on new instrumentation to indicate the potential for tissue damage, studies of various support material characteristics and the development of support systems, both passive (viscoelastic seat cushions with or without cutouts, and flotation systems) and active (devices requiring external power) systems.
Acute compartment syndrome (ACS) of the lower leg is a time-sensitive orthopedic emergency that relies heavily on precise clinical findings. Late findings of ACS can lead to limb amputation, contractures, paralysis, multiorgan failure, and death. Hallmark symptoms of ACS include the 6 P's: pain, poikilothermia, pallor, paresthesia, pulselessness, and paralysis. Suspicion of ACS is confirmed by measurement of intracompartmental pressure of the affected compartment. The definitive treatment of ACS is timely fasciotomy. We review the pathophysiology, common causes, diagnosis, and treatment of this potentially devastating condition.
Deep tissue injury (DTI) is a life-threatening type of pressure ulcer which initiates subdermally with muscle necrosis at weight-bearing anatomical locations, where localized elevated tissue strains exist. Though it has been suggested that excessive sustained soft tissue strains might compromise cell viability, which then initiates the DTI, there is no experimental evidence to describe how specifically such a process might take place. Here, we experimentally test the hypothesis that macroscopic tissue deformations translated to cell-level deformations and in particular, to localized tensile strains in the plasma membrane (PM) of cells, increase the permeability of the PM which could disrupt vital transport processes. In order to determine whether PM permeability changes can occur due to static stretching of cells we measured the uptake of fluorescein isothiocyanate (FITC)-labeled Dextran (molecular weight = 4 kDa) by deformed vs. undeformed myoblasts, using a fluorescence-activated cell sorting (FACS) method. These PM permeability changes were then correlated with tensile strains in the PM which correspond to the levels of substrate tensile strain (STS) that were applied in the experiments. The PM strains were evaluated by means of confocal-microscopy-based cell-specific finite element (FE) modeling. The FACS studies demonstrated a statistically significant rise in the uptake of the FITC-labeled Dextran with increasing STS levels in the STS ≤ 12% domain, which thereby indicates a rise in the permeability of the PM of the myoblasts with the extent of the applied cellular deformation. The cell-specific FE modeling simulating the experiments further demonstrated that applying average PM tensile strains which exceed 3%, or, applying peak PM tensile strains over 9%, substantially increases the permeability of the PM of myoblasts to the Dextran. Moreover, the permeability of the PM grew rapidly with any further increase in PM strains, though there were no significant changes in the uptake above average and peak PM tensile strain values of 9 and 26%, respectively. These results provide an experimental basis for studying the theory that cell-level deformation-diffusion relationships may be involved in determining the tolerance of soft tissues to sustained mechanical loading, as relevant to the etiology of DTI.
Pressure ulcers are one of the most underrated conditions in critically ill patients. Despite the introduction of clinical practice guidelines and advances in medical technology, the prevalence of pressure ulcers in hospitalized patients continues to escalate. Currently, consensus is lacking on the most important risk factors for pressure ulcers in critically ill patients, and no risk assessment scale exclusively for pressure ulcers in these patients is available.
To determine which risk factors are most predictive of pressure ulcers in adult critical care patients. Risk factors investigated included total score on the Braden Scale, mobility, activity, sensory perception, moisture, friction/shear, nutrition, age, blood pressure, length of stay in the intensive care unit, score on the Acute Physiology and Chronic Health Evaluation II, vasopressor administration, and comorbid conditions.
A retrospective, correlational design was used to examine 347 patients admitted to a medical-surgical intensive care unit from October 2008 through May 2009.
According to direct logistic regression analyses, age, length of stay, mobility, friction/shear, norepinephrine infusion, and cardiovascular disease explained a major part of the variance in pressure ulcers.
Current risk assessment scales for development of pressure ulcers may not include risk factors common in critically ill adults. Development of a risk assessment model for pressure ulcers in these patients is warranted and could be the foundation for development of a risk assessment tool.
Deep tissue injury (DTI) is a severe form of pressure ulcer where tissue damage starts in deep tissues underneath intact skin. In the present study, the contributions of deformation, ischemia, and reperfusion to skeletal muscle damage development were examined in a rat model during a 6-h period. Magnetic resonance imaging (MRI) was used to study perfusion (contrast-enhanced MRI) and tissue integrity (T2-weighted MRI). The levels of tissue deformation were estimated using finite element models. Complete ischemia caused a gradual homogeneous increase in T2 (∼20% during the 6-h period). The effect of reperfusion on T2 was highly variable, depending on the anatomical location. In experiments involving deformation, inevitably associated with partial ischemia, a variable T2 increase (17-66% during the 6-h period) was observed reflecting the significant variation in deformation (with two-dimensional strain energies of 0.60-1.51 J/mm) and ischemia (50.8-99.8% of the leg) between experiments. These results imply that deformation, ischemia, and reperfusion all contribute to the damage process during prolonged loading, although their importance varies with time. The critical deformation threshold and period of ischemia that cause muscle damage will certainly vary between individuals. These variations are related to intrinsic factors, such as pathological state, which partly explain the individual susceptibility to the development of DTI and highlight the need for regular assessments of individual subjects.
Background:
Use of pressure ulcer risk assessment tools or scales is a component of the assessment process used to identify individuals at risk of developing a pressure ulcer. Indeed, use of a risk assessment tool is recommended by many international pressure ulcer prevention guidelines, however it is not known whether using a risk assessment tool makes a difference to patient outcomes. We conducted a review to provide a summary of the evidence pertaining to pressure ulcer risk assessment in clinical practice.
Objectives:
To determine whether using structured, systematic pressure ulcer risk assessment tools, in any health care setting, reduces the incidence of pressure ulcers.
Search methods:
In December 2013, for this second update, we searched the Cochrane Wounds Group Specialised Register; The Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library); Ovid MEDLINE; Ovid EMBASE; and EBSCO CINAHL.
Selection criteria:
Randomised controlled trials (RCTs) comparing the use of structured, systematic, pressure ulcer risk assessment tools with no structured pressure ulcer risk assessment, or with unaided clinical judgement, or RCTs comparing the use of different structured pressure ulcer risk assessment tools.
Data collection and analysis:
Two review authors independently assessed titles and abstracts of the studies identified by the search strategy for eligibility, obtained full versions of potentially relevant studies and screened these against the inclusion criteria.
Main results:
We included two studies in this review. One small, cluster randomised study found no statistical difference in pressure ulcer incidence in patients who were assessed by nurses using the Braden risk assessment tool (n=74) compared with patients assessed by nurses who had receiving training and then used unstructured risk assessment (n=76) (RR 0.97, 95% CI 0.53 to 1.77) and those patients assessed by nurses using unstructured risk assessment alone (n=106) (RR 1.43, 95% CI 0.77 to 2.68). The second study was a large single blind randomised controlled study which compared the effect of risk assessment on pressure ulcer incidence using the Waterlow risk assessment tool (n=411), the Ramstadius risk screening tool (n=420) and no formal risk assessment (n=420). There was no statistical difference in pressure ulcer incidence between the three groups (Waterlow 7.5% (n=31); Ramstadius 5.4% (n=22); clinical judgement 6.8% (n=28) (RR 1.10, 95% CI 0.68 to 1.81; Waterlow vs no formal risk assessment), (RR 0.79, 95% CI 0.46 to 1.35; Ramstadius vs no formal risk assessment), (RR 1.44, 95% CI 0.85 to 2.44; Waterlow vs Ramstadius).
Authors' conclusions:
Two studies were identified which evaluated the effect of risk assessment on patient outcomes; In one study, there was no statistically significant difference in pressure ulcer incidence between people who were assessed using the Braden risk assessment tool compared with those receiving unstructured risk assessment. Methodological limitations of this study prevent firm conclusions being drawn. However, a further high quality RCT identified no statistical differences in pressure ulcer incidence when people were assessed using either the Waterlow risk assessment tool, the Ramstadius risk assessment tool, or using clinical judgement alone. There is no reliable evidence to suggest that the use of structured, systematic pressure ulcer risk assessment tools reduces the incidence of pressure ulcers.
Pressure ulcers are localized areas of soft tissue breakdown due to mechanical loading. Susceptible individuals are subjected to pressure relief strategies to prevent long loading periods. Therefore, ischemia-reperfusion injury may play an important role in the etiology of pressure ulcers. To investigate the inter-relation between postischemic perfusion and changes in skeletal muscle integrity, the hindlimbs of Brown Norway rats were subjected to 4-h ischemia followed by 2-h reperfusion. Dynamic contrast-enhanced MRI was used to examine perfusion, and changes in skeletal muscle integrity were monitored with T2-weighted MRI. The dynamic contrast-enhanced MRI data showed a heterogeneous postischemic profile in the hindlimb, consisting of areas with increased contrast enhancement (14-76% of the hindlimb) and regions with no-reflow (5-77%). For T2, a gradual increase in the complete leg was observed during the 4-h ischemic period (from 34 to 41 msec). During the reperfusion phase, a heterogeneous distribution of T2 was observed. Areas with increased contrast enhancement were associated with a decrease in T2 (to 38 msec) toward preischemic levels, whereas no-reflow areas exhibited a further increase in T2 (to 42 msec). These results show that reperfusion after prolonged ischemia may not be complete, thereby continuing the ischemic condition and aggravating tissue damage.
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.
Sustained tissue compression can lead to pressure ulcers, which can either start superficially or within deeper tissue layers. The latter type includes deep tissue injury, starting in skeletal muscle underneath an intact skin. Since the underlying damage mechanisms are poorly understood, prevention and early detection are difficult. Recent in vitro studies and in vivo animal studies have suggested that tissue deformation per se can lead to damage. In order to conclusively couple damage to deformation, experiments are required in which internal tissue deformation and damage are both known. Magnetic resonance (MR) tagging and T2-weighted MR imaging can be used to measure tissue deformation and damage, respectively, but they cannot be combined in a protocol for measuring damage after prolonged loading. Therefore, a dedicated finite element model was developed to calculate strains in damage experiments. In the present study, this model, which describes the compression of rat skeletal muscles, was validated with MR tagging. Displacements from both the tagging experiments and the model were interpolated on a grid and subsequently processed to obtain maximum shear strains. A correlation analysis revealed a linear correlation between experimental and numerical strains. It was further found that the accuracy of the numerical prediction decreased for increasing strains, but the positive predictive value remained reasonable. It was concluded that the model was suitable for calculating strains in skeletal muscle tissues in which damage is measured due to compression.
Prolonged mechanical loading of soft tissues adjacent to bony prominences can lead to degeneration of muscle tissue, resulting in a condition termed pressure-related deep tissue injury. This type of deep pressure ulcers can develop into a severe wound, associated with problematic healing and a variable prognosis. Limited knowledge of the underlying damage pathways impedes effective preventive strategies and early detection. Traditionally, pressure-induced ischaemia has been thought to be the main aetiological factor for initiating damage. Recent research, however, proposes tissue deformation per se as another candidate for initiating pressure-induced deep tissue injury. In this study, different strain parameters were evaluated on their suitability as a generic predictive indicator for deep tissue injury. With a combined animal-experimental numerical approach, we show that there is a reproducible monotonic increase in damage with increasing maximum shear strain once a strain threshold has been exceeded. This relationship between maximum shear strain and damage seems to reflect an intrinsic muscle property, as it applied across a considerable number of the experiments. This finding confirms that tissue deformation per se is important in the aetiology of deep tissue injury. Using dedicated finite element modeling, a considerable reduction in the inherent biological variation was obtained, leading to the proposal that muscle deformation can prove a generic predictive indicator of damage.
To 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.
To study the aetiology of pressure ulcers an MR-compatible loading device was developed. Magnetic resonance imaging provides the possibility of non-invasive evaluation of muscle tissue after compressive loading. Pressure was applied to the tibialis anterior region of rats by means of an indenter. The developed MR-compatible loading device allowed high quality consecutive MR measurements for up to 6h. Tissue was evaluated both during and after loading. Two loading protocols were used; a large indentation of 4.5mm (mean pressure 150 kPa) was applied for 2h and a small indentation of 2.9 mm (mean pressure 50 kPa) was applied for 4h. T2-weighted MR images after the large indentation showed an immediate increase in signal intensity, associated with damage, following load removal. After 20 h the signal intensity remained higher in the affected regions. Afterwards the tissue was perfusion fixated for histological examination. Histological evaluation revealed an inflammatory response and severe muscle necrosis. No signal increase was observed after small indentation. With this new set-up, the different factors that may play a role in the onset of muscle damage can be studied, what we believe will lead to a better understanding of the contributing factors to pressure ulcer development.
Deep pressure sores (DPS) are associated with inadequate soft tissue perfusion and excessive tissue deformation over critical time durations, as well as with ischemia-reperfusion cycles and deficiency of the lymphatic system. Muscle tissue shows the lowest tolerance to pressure injuries, compared with more superficial tissues. In this communication, we present new histopathology data for muscle tissue of albino (Sprague-Dawley) rats exposed to pressures for 15 or 30 min. These data are superimposed with an extensive literature review of all previous histopathology reported for albino rat skeletal muscles subjected to pressure. The pooled data enabled a new mathematical characterization of the pressure-time threshold for cell death in striated muscle of rats, in the form of a sigmoid pressure-time relation, which extends the previous pressure-time relation to the shorter exposure periods. We found that for pressure exposures shorter than 1 h, the magnitude of pressure is the important factor for causing cell death and the exposure time has little or no effect: even relatively short exposures (15 min - 1 h) to pressures greater than 32 kPa (240 mmHg) cause cell death in rat muscle tissue. For exposures of 2 h or over, again the magnitude of pressure is the important factor for causing cell death: pressures greater than 9 kPa (67 mmHg) applied for over 2 h consistently cause muscle cell death. For the intermediate exposures (between 1 and 2 h), the magnitude of cell-death-causing pressure strongly depends on the time of exposure, i.e., critical pressure levels drop from 32 to 9 kPa. The present sigmoidal pressure-time cell death threshold is useful for design of studies in albino rat models of DPS, and may also be helpful in numerical simulations of DPS development, where there is often a need to extrapolate from tissue pressures to biological damage.
The underlying mechanisms leading to deep tissue injury after sustained compressive loading are not well understood. It is hypothesized that initial damage to muscle fibers is induced mechanically by local excessive deformation. Therefore, in this study, an animal model was used to study early damage after compressive loading to elucidate on the damage mechanisms leading to deep pressure ulcers. The tibialis anterior of Brown-Norway rats was loaded for 2 h by means of an indenter. Experiments were performed in a magnetic resonance (MR)-compatible loading device. Muscle tissue was evaluated with transverse relaxation time (T2)-weighted MRI both during loading and up to 20 h after load removal. In addition, a detailed examination of the histopathology was performed at several time points (1, 4, and 20 h) after unloading. Results demonstrated that, immediately after unloading, T2-weighted MR images showed localized areas with increased signal intensity. Histological examination at 1 and 4 h after unloading showed large necrotic regions with complete disorganization of the internal structure of the muscle fibers. Hypercontraction zones were found bilateral to the necrotic zone. Twenty hours after unloading, an extensive inflammatory response was observed. The proposed relevance of large deformation was demonstrated by the location of damage indicated by T2-weighted MRI and the histological appearance of the compressed tissues. Differences in damage development distal and proximal to the indenter position suggested a contribution of perfusion status in the measured tissue changes that, however, appeared be to reversible.
A common but potentially severe malady afflicting permanent wheelchair users is pressure sores caused by elevated soft tissue strains and stresses over a critical prolonged period of time. Presently, there is paucity of information regarding deep soft tissue strains and stresses in the buttocks of humans during sitting. Strain and stress distributions in deep muscle and fat tissues were therefore calculated in six healthy subjects during sitting, in a double-donut Open-MR system, using a "reverse engineering" approach. Specifically, finite element (FE) models of the undeformed buttock were built for each subject using MR images taken at the coronal plane in a non-weight-bearing sitting posture. Using a second MR image taken from each subject during weight-bearing sitting we characterized the ischial tuberosity sagging toward the sitting surface in weight-bearing, and used these data as displacement boundary conditions for the FE models. These subject-specific FE analyses showed that maximal tissue strains and stresses occur in the gluteal muscles, not in fat or at the skin near the body-seat interface. Peak principal compressive strain and stress in the gluteus muscle were 74+/-7% and 32+/-9 kPa (mean+/-standard deviation), respectively. Peak principal compressive strain and stress in enveloping fat tissue were 46+/-7% and 18+/-4 kPa, respectively. Models were validated by comparing measured peak interface pressures under the ischial tuberosities (17+/-4 kPa) with those calculated by means of FE (18+/-3 kPa), for each subject. This is the first study to quantify sub-dermal tissue strain and stress distributions in sitting humans, in vivo. These data are essential for understanding the aetiology of pressure sores, particularly those that were recently termed "deep tissue injury" at the US National Pressure Ulcer Advisory Panel (NPUAP) 2005 Consensus Conference.
Deep pressure ulcers develop in tissues subjected to sustained mechanical loading. Though it has been hypothesized that this damage mechanism results from local tissue ischemia, it has recently been shown with a cell model that sustained compression can cause cell deformation, leading to tissue breakdown. The present study focuses on the assessment of cell viability during compression and ischemia in an in vitro muscle model to determine their relative contributions to damage development. A model system was developed consisting of engineered skeletal muscle produced from the culture of murine muscle cells in a collagen gel. The tissue was subjected to 0, 20, or 40% compression under hypoxic or normoxic conditions. Experiments were performed on the stage of a microscope and cell viability was monitored using fluorescent markers for apoptotic and necrotic cell death. Hypoxia did not lead to significant cell death over a 22 h period. By contrast, compression led to immediate cell death that increased with time. No additional effect of hypoxia on cell death was observed. These data show that contrary to existing theories, compression can cause development of muscle damage and that hypoxia does not contribute to cell death development within 22 h in engineered muscle.
A rat model was used to distinguish between the different factors that contribute to muscle tissue damage related to deep pressure ulcers that develop after compressive loading. The separate and combined effects of ischemia and deformation were studied. Loading was applied to the hindlimb of rats for 2 h. Muscle tissue was examined using MR imaging (MRI) and histology. An MR-compatible loading device allowed simultaneous loading and measurement of tissue status. Two separate loading protocols incorporated uniaxial loading, resulting in tissue compression and ischemic loading. Uniaxial loading was applied to the tibialis anterior by means of an indenter, and ischemic loading was accomplished with an inflatable tourniquet. Deformation of the muscle tissue during uniaxial loading was measured using MR tagging. Compression of the tissues for 2 h led to increased T2 values, which were correlated to necrotic regions in the tibialis anterior. Perfusion measurements, by means of contrast-enhanced MRI, indicated a large ischemic region during indentation. Pure ischemic loading for 2 h led to reversible tissue changes. From the MR-tagging experiments, local strain fields were calculated. A 4.5-mm deformation, corresponding to a surface pressure of 150 kPa, resulted in maximum shear strain up to 1.0. There was a good correlation between the location of damage and the location of high shear strain. It was concluded that the large deformations, in conjunction with ischemia, provided the main trigger for irreversible muscle damage.
Presently, commercial cushioning products for pressure ulcer prevention are being evaluated for their protective effect exclusively based on interfacial pressures between the cushion/mattress and the patient. However, interface pressures cannot predict elevated mechanical stresses in deep tissues adjacent to bony prominences. Such deep tissue stress concentrations are associated with local ischaemia and hypoxia, which over time result in deep tissue necrosis, particularly of muscle tissue. In order to demonstrate this phenomenon, a physical phantom of the mechanical interaction between the ischial tuberosities (IT) and gluteus muscles of the buttocks was built, incorporating geometric replica of the human IT and real (bovine) muscle tissue. Internal muscle stresses directly under the IT were five to 11-fold greater than stresses at more distal locations, and a Pearson correlation test showed that they could not have been predicted from the interface pressures in the phantom. Accordingly, though pressure ulcer prevention clinics which utilize routine sitting pressure measurements report effective outcomes, the present results highlight a problem in using body-support pressure measurements to predict the risk for pressure-related deep tissue injury.
A pressure-related deep tissue injury (DTI) is a severe pressure ulcer, which initiates in muscle tissue overlying a bony prominence (e.g. the ischial tuberosities, IT) and progresses outwards through fat and skin, unnoticed by the paralyzed patient. We recently showed that internal strains and stresses in muscle and fat of individuals at anatomical sites susceptible to DTI can be evaluated by integrating Open-MRI scans with subject-specific finite element (FE) analyzes (Linder-Ganz et al., Journal of Biomechanics, 2007); however, sub-dermal soft tissue strains/stresses from paraplegics are still missing in literature. We hypothesize that the pathoanatomy of the buttocks in paraplegia increases the internal soft tissue loads under the IT, making these patients inherently susceptible to DTI. We hence compared the strain and stress peaks in the gluteus muscle and fat tissues under the IT of six healthy and six paraplegic patients, using the coupled MRI-FE method. Peak principal compression, principal tension, von Mises and shear strains in the gluteus were 1.2-, 3.1-, 1.4- and 1.4-fold higher in paraplegics than in healthy, respectively (p<0.02). Likewise, peak principal compression, principal tension, von Mises and shear stresses in the gluteus were 1.9-, 2.5-, 2.1- and 1.7-fold higher for the paraplegics (p<0.05). Peak gluteal compression and shear stresses decreased by as much as 70% when the paraplegic patients moved from a sitting to a lying posture, indicating on the effectiveness of recommending such patients to lie down after prolonged periods of sitting. This is the first attempt to compare internal soft tissue loads between paraplegic and healthy subjects, using an objective standardized bioengineering method of analysis. The findings support our hypothesis that internal tissue loads are significantly higher in paraplegics, and that postural changes significantly affect these loads. The method of analysis is useful for quantifying the effectiveness of various interventions to alleviate sub-dermal tissue loads at sites susceptible to pressure ulcers and DTI, including cushions, mattresses, recommendations for posture and postural changes, etc.
Deep tissue injury (DTI) is a severe pressure ulcer that results from sustained deformation of muscle tissue overlying bony prominences. In order to understand the etiology of DTI, it is essential to determine the tolerance of muscle cells to large mechanical strains. In this study, a new experimental method of determining the time-dependent critical compressive strains for necrotic cell death (E(zz)(c)(t)) in a planar tissue-engineered construct under static loading was developed. A half-spherical indentor is used to induce a non-uniform, concentric distribution of strains in the construct, and E(zz)(c)(t) is calculated from the radius of the damage region in the construct versus time. The method was employed to obtain E(zz)(c)(t) for bio-artificial muscles (BAMs) cultured from C2C12 murine cells, as a model system for DTI. Specifically, propidium iodine was used to fluorescently stain the development of necrosis in BAMs subjected to strains up to 80%. Two groups of BAMs were tested at an extracellular pH of 7.4 (n=10) and pH 6.5 (n=5). The lowest strain levels causing cell death in the BAMs were determined every 15min, during 285-min-long trials, from confocal microscopy fluorescent images of the size of the damage regions. The experimental E(zz)(c)(t) data fitted a decreasing single-step sigmoid of the Boltzmann type. Analysis of the parameters of this sigmoid function indicated a 95% likelihood that cells could tolerate engineering strains below 65% for 1h, whereas the cells could endure strains below 40% over a 285min trial period. The decrease in endurance of the cells to compressive strains occurred between 1-3h post-loading. The method developed in this paper is generic and suitable for studying E(zz)(c)(t) in virtually any planar tissue-engineered construct. The specific E(zz)(c)(t) curve obtained herein is necessary for extrapolating biological damage from muscle-strain data in biomechanical studies of pressure ulcers and DTI.
Etiologic factors in pressure sores, an experimental model.
- Daniel R.K.
- Priest D.L.
- Wheatly D.C.
Etiologic factors in pressure sores, an experimental model
- Daniel