Amit Gefen

Biomechanical analysis of the three-dimensional foot structure during gait: a basic tool for clinical applications

A novel three-dimensional numerical model of the foot, incorporating, for the first time in the literature, realistic geometric and material properties of both skeletal and soft tissue components of the foot, was developed for biomechanical analysis of its structural behavior during gait. A system of experimental methods, integrating the optical Contact Pressure Display (CPD) method for plantar pressure measurements and a Digital Radiographic Fluoroscopy (DRF) instrument for acquisition of skeletal motion during gait, was also developed in this study and subsequently used to build the foot model and validate its predictions. Using a Finite Element solver, the stress distribution within the foot structure was obtained and regions of elevated stresses for six subphases of the stance (initial-contact, heel-strike, midstance, forefoot-contact, push-off, and toe-off) were located. For each of these subphases, the model was adapted according to the corresponding fluoroscopic data, skeletal dynamics, and active muscle force loading. Validation of the stress state was achieved by comparing model predictions of contact stress distribution with respective CPD measurements. The presently developed measurement and numerical analysis tools open new approaches for clinical applications, from simulation of the development mechanisms of common foot disorders to pre- and post-interventional evaluation of their treatment.

Plantar soft tissue loading under the medial metatarsals in the standing diabetic foot

Diabetes mellitus (type 2) is the most frequent cause of non-traumatic lower-limb amputations. The major cause of impairment to the feet of diabetics is persistent hyperglycemia, potentially leading to peripheral neuropathy as well as to pathological changes in plantar soft tissue, which stiffen its structure and diminish its ability to effectively distribute foot-ground contact loads. In this study, a computational model of the foot structure in the standing position was utilized to evaluate stress distributions in plantar soft tissue under the medial metatarsal heads of simulated diabetic versus normal feet. The model comprises five anatomic planar cross-sections in the directions of the foot rays, which were solved for internal stresses under static ankle joint reaction (300 N) and triceps surae muscle forces (150 N) using the finite element method. Tissues were assumed to be homogenous, isotropic and elastic materials, with nonlinear stress-strain relations for the ligaments, fascia and plantar tissue. The model revealed significant tension stress concentrations (90-150 KPa) in the plantar pad of the simulated diabetic forefoot: they were four times the normal maximum stress under the first metatarsal head and almost eight times the normal maximum stress under the second metatarsal head. It was shown that with increased severity of stiffening of the plantar pad, as related to glucose-exposure, peak forefoot contact stresses may rise by 38 and 50% under the first and second metatarsal heads, respectively. The increase in averaged (von Mises) internal stresses within the plantar soft tissue is even more pronounced, and may rise by 82 and 307% for the tissue under the first and second metatarsal heads, respectively. These results, which conform to experimental data gathered over the last two decades, suggest that the process of injury in diabetic feet is very likely to initiate not on the skin surface, but in deeper tissue layers, and the tissues underlying the distal bony prominences of the medial metatarsals are the most vulnerable ones.

Analysis of muscular fatigue and foot stability during high-heeled gait

Plantar pressure measurements and surface electromyography (EMG) were used to determine the effects of muscular fatigue induced by high-heeled gait. The medio-lateral (M/L) stability of the foot was characterized by measuring the M/L deviations of the center of pressure (COP) and correlating these data with fatigue of lower-limb muscles seen on EMG. EMG measurements from habitual high-heeled shoe wearers demonstrated an imbalance of gastrocnemius lateralis versus gastrocnemius medialis activity in fatigue conditions, which correlated with abnormal lateral shifts in the foot-ground or shoe-ground COP of these women.

In Vivo Muscle Stiffening Under Bone Compression Promotes Deep Pressure Sores

Pressure sores (PS) in deep muscles are potentially fatal and are considered one of the most costly complications in spinal cord injury patients. We hypothesize that continuous compression of the longissimus and gluteus muscles by the sacral and ischial bones during wheelchair sitting increases muscle stiffness around the bone-muscle interface over time, thereby causing muscles to bear intensified stresses in relentlessly widening regions, in a positive-feedback injury spiral. In this study, we measured long-term shear moduli of muscle tissue in vivo in rats after applying compression (35 KPa or 70 KPa for 1/4-2 h, N = 32), and evaluated tissue viability in matched groups (using phosphotungstic acid hematoxylin histology, N = 10). We found significant (1.8-fold to 3.3-fold, p < 0.05) stiffening of muscle tissue in vivo in muscles subjected to 35 KPa for 30 min or over, and in muscles subjected to 70 KPa for 15 min or over. By incorporating this effect into a finite element (FE) model of the buttocks of a wheelchair user we identified a mechanical stress wave which spreads from the bone-muscle interface outward through longissimus muscle tissue. After 4 h of FE simulated motionlessness, 50%-60% of the cross section of the longissimus was exposed to compressive stresses of 35 KPa or over (shown to induce cell death in rat muscle within 15 min). During these 4 h, the mean compressive stress across the transverse cross section of the longissimus increased by 30%-40%. The identification of the stiffening-stress-cell-death injury spiral developing during the initial 30 min of motionless sitting provides new mechanistic insight into deep PS formation and calls for reevaluation of the 1 h repositioning cycle recommended by the U.S. Department of Health.

In vivo biomechanical behavior of the human heel pad during the stance phase of gait

A technique is introduced for simultaneous measurements of the heel pad tissue deformation and the heel-ground contact stresses developing during the stance phase of gait. Subjects walked upon a gait platform integrating the contact pressure display optical method for plantar pressure measurements and a digital radiographic fluoroscopy system for skeletal and soft tissue motion recording. Clear images of the posterior-plantar aspect of the calcaneus and enveloping soft tissues were obtained simultaneously with the pressure distribution under the heel region throughout the stance phase of gait. The heel pad was shown to undergo a rapid compression during initial contact and heel strike, reaching a strain of 0.39 +/- 0.05 in about 150 ms. The stress-strain relation of the heel pad was shown to be highly non-linear, with a compression modulus of 105 +/- 11 kPa initially and 306 +/- 16 kPa at 30% strain. The energy dissipation during heel strike was evaluated to be 17.8+/-0.8%. The present technique is useful for biomechanical as well as clinical evaluation of the stress-strain and energy absorption characteristics of the heel pad in vivo, during natural gait.

Stress analysis of the standing foot following surgical plantar fascia release

Plantar fascia release is a surgical alternative for patients who suffer chronic heel pain due to plantar fasciitis and are unaffected by conservative treatment. A computational (finite element) model for analysis of the structural behavior of the human foot during standing was utilized to investigate the biomechanical effects of releasing the plantar fascia. The model integrates a system of five planar structures in the directions of the foot rays. It was built according to accurate geometric data of MRI, and includes linear and non-linear elements that represent bony, cartilaginous, ligamentous and fatty tissues. The model was successfully validated by comparing its resultant ground reactions with foot-ground pressure measurements and its predicted displacements with those observed in radiological tests. Simulation of plantar fascia release (partial or total) was accomplished by gradually removing parts of the fascia in the model. The results showed that total fascia release causes extensive arch deformation during standing, which is greater than normal deformation by more than 2.5mm. Tension stresses carried by the long plantar ligaments increased significantly, and may exceed the normal average stress by more than 200%. Since the contribution of the plantar fascia to the foots load-bearing ability is of major importance, its release must be very carefully considered, and the present model may be used to help surgeons decide upon the desired degree of release.

Strain-time cell death threshold for skeletal muscle in a tissue-engineered model system for deep tissue injury

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.

Biomechanical analysis of the keratoconic cornea.

Keratoconus is a non-inflammatory disease characterized by irregular thinning and gradual bulging of the cornea, which results in distortion of the corneal surface that causes blurred vision. We conducted three-dimensional finite element (FE) simulations to analyze the biomechanical factors contributing to the distorted shape of a keratoconic cornea. We assumed orthotropic linear elastic tissue mechanical properties, and simulated localized tissue thinning (reduction from 0.5 mm to 0.35 or 0.2 mm). We analyzed tissue deformations, stresses and theoretical dioptric power maps predicted by the models, for intraocular pressure (IOP) of 10, 15 20 and 25 mmHg. The analyses revealed that three factors affect the shape distortion of keratoconic corneas: (i) localized thinning, and (ii) reduction in the tissues meridian elastic modulus or (iii) reduction in the shear modulus perpendicular to the corneal surface, whereas thinning showed the most predominant effect. Maximal stress levels occurred at the centers of the bulged regions, at the thinnest points. The IOP levels had little influence on dioptric power in the healthy cornea, but a substantial influence in keratoconic conditions. The present FE studies allowed characterization of the biomechanical interactions in keratoconus, toward understanding the aetiology of this poorly studied malady.

Is obesity a risk factor for deep tissue injury in patients with spinal cord injury

Deep tissue injury (DTI) is a severe form of pressure ulcers that occur in subcutaneous tissue under intact skin by the prolonged compression of soft tissues overlying bony prominences. Pressure ulcers and DTI in particular are common in patients with impaired motosensory capacities, such as those with a spinal cord injury (SCI). Obesity is also common among subjects with SCI, yet there are contradicting indications regarding its potential influence as a risk factor for DTI in conditions where these patients sit in a wheelchair without changing posture for prolonged times. It has been argued that high body mass may lead to a greater risk for DTI due to increase in compressive forces from the bones on overlying deep soft tissues, whereas conversely, it has been argued that the extra body fat associated with obesity may reduce the risk by providing enhanced subcutaneous cushioning that redistributes high interface pressures. No biomechanical evaluation of this situation has been reported to date. In order to elucidate whether obesity can be considered a risk factor for DTI, we developed computational finite element (FE) models of the seated buttocks with 4 degrees of obesity, quantified by body mass index (BMI) values of 25.5, 30, 35 and 40kg/m(2). We found that peak principal strains, strain energy densities (SED) and von Mises stresses in internal soft tissues (muscle, fat) overlying the ischial tuberosities (ITs) all increased with BMI. With a rise in BMI from 25.5 to 40kg/m(2), values of these parameters increased 1.5 times on average. Moreover, the FE simulations indicated that the bodyweight load transferred through the ITs has a greater effect in increasing internal tissue strains/stresses than the counteracting effect of thickening of the adipose layer which is concurrently associated with obesity. We saw that inducing some muscle atrophy (30% reduction in muscle volume, applied to the BMI=40kg/m(2) model) which is also characteristic of chronic SCI resulted in further substantial increase in all biomechanical measures reflecting geometrical distortion of muscle tissue, that is, SED, tensile stress, shear stress and von Mises stress. This result highlights that obesity and muscle atrophy, which are both typical of the chronic phase of SCI, contribute together to the state of elevated tissue loads, which consequently increases the likelihood of DTI in this population.

A new pressure ulcer conceptual framework.

Aim This paper discusses the critical determinants of pressure ulcer development and proposes a new pressure ulcer conceptual framework. Background Recent work to develop and validate a new evidence-based pressure ulcer risk assessment framework was undertaken. This formed part of a Pressure UlceR Programme Of reSEarch (RP-PG-0407-10056), funded by the National Institute for Health Research. The foundation for the risk assessment component incorporated a systematic review and a consensus study that highlighted the need to propose a new conceptual framework. Design Discussion Paper. Data Sources The new conceptual framework links evidence from biomechanical, physiological and epidemiological evidence, through use of data from a systematic review (search conducted March 2010), a consensus study (conducted December 2010–2011) and an international expert group meeting (conducted December 2011). Implications for Nursing A new pressure ulcer conceptual framework incorporating key physiological and biomechanical components and their impact on internal strains, stresses and damage thresholds is proposed. Direct and key indirect causal factors suggested in a theoretical causal pathway are mapped to the physiological and biomechanical components of the framework. The new proposed conceptual framework provides the basis for understanding the critical determinants of pressure ulcer development and has the potential to influence risk assessment guidance and practice. It could also be used to underpin future research to explore the role of individual risk factors conceptually and operationally. Conclusion By integrating existing knowledge from epidemiological, physiological and biomechanical evidence, a theoretical causal pathway and new conceptual framework are proposed with potential implications for practice and research.