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Biomechanics of Diabetic foot
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Biomechanics of the diabetic foot. Most evident consequences of progressive attacks of Diabetes mellitus to lower extremities are represented by the successive steps of the ulceration process, i.e. ulceration, infection and, unfortunately often, the consequent amputation. However, complications in the foot and the foot-ankle complex are wider and more destructive than expected, and may compromise structure and function of several human systems: vascular, nervous, somatosensory, musculoskeletal. Thus, a deeper comprehension of the alteration of gait and foot biomechanics in the Diabetic foot is of great interest, and may play a role in the design and onset of preventive as well as therapeutic actions . This section is thus dedicated to a summary of the main findings of the research in the field of the biomechanics of the Diabetic foot, and to the description of a functional model of the foot-ankle complex which well explain the overall effect of Diabetes in the performance of such crucial daily actions like walking and standing. Effect of Diabetes on the main structures of the foot-ankle complex Briefly, we can summarise the effect of Diabetes on the main structures of the foot-ankle complex as: * effects on skin: skin - and the soft tissues immediately underneath the skin - undergoes to greater compressive and shear loading than usual, thus explaining from a mechanically point of view the onset of tissue damages so deeply correlated to traumatic ulceration processes. Besides this, skin of the Diabetic foot suffers from loss of autonomic control and a consequent reduced hydration, which renders it less elastic and thus more vulnerable to the action of increased mechanical stress; * effects on tendons and ligaments: protein glycosilation and the consequent collagen abnormalities entail greater transversal section - i.e. thickening - of tendons and ligaments, and, reasonably, greater coefficient of elasticity. Particularly interested by this process are Plantar Fascia and Achilles Tendon. Both causes lead to an increased stiffness of those structures ; * effects on cartilage: similar to what happens to tendons and ligaments, cartilage changes its composition mainly due to the modification of collagen fibers; this increases its stiffness and represents an obstacle in the performance of physiological range of motion of each and every foot and ankle joint; * effects on muscles: Diabetes mellitus entails a severe damage to nerve conduction, thus causing a worsening in the management of the related muscle fibers; as a consequence, both intrinsic and extrinsic muscles of the foot-ankle complex are damaged as for structure (reduction of muscle volume) and function (reduction of muscle strength); * effects on peripheral sensory system: nerve conduction degeneration has a dramatic effect on the peripheral sensory system, since it leads to loss of protective sensation under the sole of the foot. This exposes the Diabetic foot to thermal or mechanical trauma, and to the late detection of infection processes or tissue breakdown; * effects on foot morphology (deformities): due to most of the above alterations, a significant inbalance of peripheral musculature and soft tissue does have place in the foot which seriously alters its morphology and determines the onset of foot deformities; most common deformities of the Diabetic foot are represented by a high longitudinal arch (rigid cavus foot), hammer toes and hallux valgus. A completely different morphologic degeneration is represented by the Charcot foot, whose analysis is not part of this discussion. Effect of Diabetes on the biomechanics of the foot-ankle complex - A short overview of the International research scenario Foot and ankle biomechanics has been widely investigated since the early 1800, and gait mechanisms have been widely described both through experimental research and modelling . First studies on the biomechanics of the Diabetic foot mainly focussed on the investigation of plantar pressure measurements and foot loading, since the development of abnormal pressures had been observed and correlated to the sites of plantar ulceration . Even though foot pressure analysis remains the most commonly investigated biomechanical aspect of the Diabetic foot - both for diagnosis and theraphy, both with floor-based instruments and in-shoe devices, several high-quality studies have been performed which investigated several other aspects of the foot biomechanics during gait. The main results of these studies are briefly summarised in the following. Alteration of ground reaction force (GRF) === GRF vertical component showed a significant increase in the peak value at the metatarsal area in patients with peripheral neuropathy. Concurrently, a progressive reduction of the peak value of this component was observed at the hallux and heel areas. The reduced vertical component beneath these two sub-areas could be related to peripheral neuropathy. The reduced load at the hallux area could be explained by severe deformities of the toes (claw toe) typical of the most advanced stages of diabetic motor neuropathy . The anterior-posterior component of GRF is mainly expressed during the strike and the push-off phases of gait. Under the heel and hallux areas the peak value of this component was found to be significantly reduced in patients with diabetic neuropathy. With regard to the medio-lateral GRF component, patients with previous ulceration usually show a significant increase in this component at the metatarsal area, maybe as a consequence of the peripheral neuropathy which is usually more severe in ulcerated than not ulcerated patients. On the other hand, the increased tangential stress could be a consequence of the previous ulceration, given that healed soft tissue presents different biomechanical characteristics, such as increased hardness, that can impair elasticity. In any case, the existence seems reasonable of a relationship between tangential forces recorded at the metatarsals area and the occurrence of neuropathic ulcers just under the metatarsal heads, justifying the increased risk of recurrence observed in patients with previous ulceration . Alteration of plantar pressures So many studies investigated the alteration of plantar pressures experienced by Diabetic foot during gait that it is difficult indeed to summarise them here . To be rigorous, evidence of the straight correlation between higher pressures and ulceration, as well as of a precise threshold level to be considered as a risk level for ulceration has been scarcely demonstrated, especially due to the difficulties in comparing data retrieved in the different studies. However, high pressures and, even more dangerous, abnormal pressure-time integrals in the area of the metatarsals heads has been frequently found in Diabetic patients with compromised foot function, and the main action addressed by orthotic therapy - in terms of noth shoes and insoles - is the reduction of overloading of the forefoot structures . Alteration of center of pressure (COP) pattern The accurate quantification of spatial and temporal evolution of COP pattern has been proved to be effective in describing the way in which the foot manages the floor during gait. Usually, healthy subjects show a COP progression which starts from the heel, passes through the metatarsals, reaches the anterior and medial part of the foot and stops on the hallux . Diabetic patients with severe neuropathy, instead, approach the floor with the most anterior part of the heel and perform their push-off phase at the metatarsals level, as it is proven by the reduction of the COP progression along the longitudinal axis. Mueller observed reduced ankle mobility and decreased plantar flexor strength in diabetic patients and suggested that changes in foot loading during gait may be the cause of the diminished ability of the plantar flexor muscles to push off and to generate plantar flexor moments or power during the last phase of the stance. In agreement with this hypothesis, the gait pattern of Diabetic neuropathic patients usually appears as a flat-footed gait, characterized by a stance-phase that involves the whole foot, with a minimal heel strike (as expressed by a reduction of the vertical and anterior-posterior component of GRF in the heel area) and a minimal push-off phase, and thus a minimal involvement of the hallux in the final phase of the stance of all the three GRF components in this area. Neuropathic gait is also characterised by a significant reduction of the COP trajectory along the medio-lateral axis and a concurrent shift of the loading pattern from the lateral towards the medial part of the foot. Alteration of joint mobility The assessment of the functionality of the ankle articular complex in diabetic patients, with and without peripheral neuropathy, showed a general trend towards the reduction of the range of motion in all planes of the anatomic reference system, and in both directions . The more severe the neuropathy, the greater the impairment, but, surprisingly enough, limitations were also evident in diabetic patients with NDS and/or VPT below the common neuropathic thresholds. Limitation of joint mobility seems greater in the sagittal plane than in the other two planes, and in dorsal flexion more than in plantar flexion. Diabetic neuropathic patients show joint mobility reduction in all planes and all directions of movement. The mobility of the 1st metatarso-phalangeal joint was also found to be impaired, the possible causes and effects of this finding being likely directly related to the alterations in the foot soft structures. Alteration of muscle performance during gait Hunt discussed eventual links between muscles and abnormal foot function; more specifically, he stated that between heel contact and 10% of stance, dorsiflexors act eccentrically and evertors concentrically. As the above muscle groups, especially tibialis anterior, are weak in neuropathic patients , they lack foot control in the heel strike phase, which entails a flat-footed approach and poor foot eversion. This in turn explains the poor lateral shift of the load also during foot flat phase, heel rise and push off, when the increased unbalance between plantar and dorsal flexors, and between invertors and evertors, greatly impairs the rise of the forefoot both in the sagittal and frontal planes. The investigation of muscle strength under isometric controlled and unloaded conditions showed a decreasing trend of the muscular functionality of the foot-ankle complex . A major reduction was measured in correspondence with moments due to the action of ankle dorsal flexors in the sagittal plane. The reduction was greater for neuropathic patients, but it was already present in Diabetic patients without neuropathy. Lower plantarflexion moments were also found in case of severe neuropathy. Neuropathic plantar flexors might indeed be weaker than those of healthy subjects, but other factors could influence the measured value of torque, first and foremost the modified thickness and elasticity of tendons, which in turn changes the stiffness of the whole muscle-tendon system. The study by Salsich reports an increased percentage of passive torque in diabetic neuropathic patients, who actually experience a reduction of active force in plantar flexors, but compensate it with the simultaneous increase of stiffness. Alteration of loading time As for the loading time, a significant increase in absolute values was found in patients with peripheral neuropathy . More specifically, the highest increase was recorded at the heel and metatarsal area, while loading time was significantly reduced at the hallux area. These results indicate that the increase in contact time is not homogeneous for the total foot during the stance phase. It is thus reasonable to infer that it could result not only from the loss of proprioception, but also from the hypothesised compartmental muscle weaknesses which, in the presence of neuropathy, affect ankle dorsal flexors more than other muscle compartments . Functional model of the diabetic foot All the above findings related to the analysis of foot-floor interaction show that diabetic neuropathic patients develop a “functional flat foot”. During stance, the shift of the instantaneous point of application of GRF from the rearfoot to the forefoot is faster than normal. Moreover, a wider plantar surface is instantaneously in contact with the ground, thus specific foot subareas, including metatarsal heads, remain loaded for longer percentages of stance phase. This simple functional model explains the increased pressure-time integrals under the metatarsal heads. It agrees with most experimental data, but it is unable to explain the increased vertical and medio-lateral GRF components under the same subareas, or the concurrent reduction of COP excursion along the medio-lateral axis of the foot. The model must then be improved by adding a second functional block accounting for joint mobility and muscular activity of the ankle articular complex. In a healthy human being, helicoidal movements of the foot-ankle complex take place to transform rotational movements of the leg around the vertical axis into prono-supination movements of the foot. This, in turn, allows the best management of forces, moments and energy during landing, stance and propulsion. Limited joint mobility in all the planes of the anatomical reference system reasonably entails impairments in the performance of physiological foot-floor interaction. Greater stiffness of the ankle complex, and the consequent poor accomplishment of the requested forefoot inversion-eversion, also explain why friction increases during propulsion, in terms of the medio-lateral GRF component under the metatarsal heads. It also explains why the COP pattern remains closer to the longitudinal axis of the foot during both transfer of load from rearfoot to forefoot and propulsion. It also allows the correct interpretation of the increased vertical force under the metatarsals and the consequent high pressures, as described by Fernando in a study that associates limited joint mobility with abnormal foot pressures and diabetic foot ulceration. The plantar soft tissue under the metatarsal region, in fact, experiences a greater vertical and medio-lateral stress for a longer time than normal. The final result is a greater thinning of the fat pad for the whole phase of propulsion, up to toe-off. The reduction of medio-lateral shift of COP pattern further unbalance the loading distribution under the forefoot: therefore those small regions undergoing dangerous peak pressures are the same small areas over which the load insists from midstance up to toe-off. It is reasonable to hypothesise then that all the changes in forefoot loading described here so far, together with the daily cumulative plantar tissue stress studied by Maluf , do contribute to the ulceration process. Muscular deficit of ankle dorsal flexors must be considered a further cause behind the overall change in walking strategy. The responsibility for landing control and shock absorption during the heel contact falls mostly on dorsal flexors. The altered functionality of ankle plantar flexors may worsen the muscular control in this phase, and produces abnormalities in the performance of propulsion. This model leads to a complementary definition of diabetic neuropathic foot as a foot that has “the function of a flat foot but the structure of a rigid pes cavus”. Besides limited joint mobility, limited muscular control and functional flat foot, important changes originate from the thickening of Achilles tendon and plantar fascia. These changes can be summarised as the onset of an early windlass mechanism , lasting from the very beginning of heel contact up to the end of propulsion. In a healthy foot, the windlass mechanism allows the stabilisation of the longitudinal arch of the foot during propulsion through the locking of the midtarsal joints. During heel contact and early stance phase, instead, foot joints need to be unlocked, so that the foot may absorb the forces that, applied to the talus, are exchanged between the floor and the overlying segments of the body. In the diabetic neuropathic foot this adaptation is lost: impairments in the tibia external rotation and in the corresponding internal rotation of the calcaneus concur in maintaining the midtarsal joints locked, metatarsal heads are abnormally loaded, little energy is stored during heel contact and insufficient energy is delivered to correctly perform propulsion. Limited joint mobility of the metatarso-phalangeal joints also increase tension in plantar fascia. Moreover, as well explained by Siegel through the use of accurate 3D simulation , the physiological dorsiflexion of the toes pulls forward the plantar fat pad under the metatarsal heads, the metatarsals move backwards and downwards, and compressive forces through the plantar fat pads increase. This means that the longer and more sustained the dorsiflexion - as in the neuropathic foot -, the longer and the higher the compression under the metatarsal heads. A further phenomenon, the development of hallux valgus, is frequently observed in neuropathic patients. When impaired, the hallux scarcely contributes to loading transmission or to the lengthening of the lever arm during the latest phase of propulsion. The functional changes observed and described in this long discussion give rise to an overall shift of the walking strategy from an ankle strategy to a hip strategy, which calls for a smaller medio-lateral shift of COP pattern, circumscribing the progression movement to the sagittal plane (2D pendulum model). Several studies have been conducted on this change of strategy, which should be contemporarily regarded as cause and effect of the functional impairments due to diabetes and diabetic neuropathy. In fact, it seems that this strategy is naturally chosen by neuropathic patients as the most safe, pain-relieving way of walking, and some researchers demonstrated that it contributes to reducing forefoot peak pressure . But, on the other hand, the unusual pattern of muscle activation and joint movement might entail further stiffness of ankle plantar flexors , thickening of Achilles tendon, and weakness of ankle dorsal flexors . This consequences deserve to be accurately assessed, since they might have a critical role in the development of dangerous plantar pressures and in the pathogenesis/recurrence of plantar ulcers. Highlights Particularly relevant for a deeper understanding of the current research in the management of abnormal loading of the Diabetic foot are the following references See Also
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