Jan S. Ulbrecht

Assessment and Management of Foot Disease in Patients with Diabetes

Limb- or life-threatening complications in patients with diabetes can be prevented with an integrated, multidisciplinary approach. Most patients seen in clinical practice are in the early stages of the disease process. Glycemic control retards the progression of neuropathy, which is the most important risk factor for ulceration. Early detection of the loss of protective sensation and implementation of strategies to prevent ulceration will reduce the rates of limb-threatening complications. Clinicians should routinely examine the feet of diabetic patients. Education in foot care, proper footwear, and close follow-up are required to prevent or promptly detect neuropathic injury. If ulceration occurs, removal of pressure from the site of the ulcer and careful management of the wound will allow healing in most cases. The failure to heal despite these measures should prompt a search for associated arterial insufficiency. If infection is present, appropriate antimicrobial therapy combined with immediate surgical intervention, including revascularization when necessary, will increase the chances of saving the limb. With this comprehensive approach, it is possible to achieve the goal of a 40 percent decrease in amputation rates among diabetic patients by the year 2000.

Postural Instability in Patients with Diabetic Sensory Neuropathy

OBJECTIVE Recent survey evidence suggests that sensory ataxia due to diabetic neuropathy may be a more frequent and serious problem than is commonly recognized. This view is further supported by research that confirms the major contribution of the somatosensory system to the control of posture. We therefore sought to determine the effects of significant diabetic distal symmetrical polyneuropathy on the control of posture. RESEARCH DESIGN AND METHODS Fifty-one subjects, divided into three groups, participated in this study. Seventeen had diabetes and significant sensory neuropathy, 17 had diabetes and no neuropathy, and 17 had neither diabetes nor neuropathy. The subjects were matched across groups, and stringent exclusion criteria were applied. Postural stability during quiet standing was measured using a force platform. In addition to electrophysiological and quantitative sensory tests of neuropathy, a number of physical and functional characteristics were measured for all subjects. RESULTS Postural instability was found to be significantly associated with sensory neuropathy, but not with diabetes per se. Patients with sensory neuropathy demonstrated between 66 and 117% more instability than did control subjects (depending on the testing condition). Based on multiple linear regression analyses, the most significant correlates of instability were the quantitative sensory measures of neuropathy and age. CONCLUSIONS The loss of sensory perception secondary to diabetic distal symmetrical sensory neuropathy has a markedly detrimental effect on postural stability. The deficit is greatest when visual or vestibular cues are absent or degraded. Patients with neuropathy need to be informed of the postural consequences of this condition to limit the potential morbidity caused by falls.

Problems with gait and posture in neuropathic patients with insulin-dependent diabetes mellitus

Peripheral neuropathy secondary to diabetes mellitus is believed to cause postural instability and uncoordinated gait, although this is not well documented. Two groups of patients from the Pittsburgh Epidemiology of Diabetes Complications Study, matched for age and duration of Type 1 diabetes, but with significantly different vibratory sensation thresholds as determined by Vibratron II testing, were therefore surveyed. The mean ages were 32.9 and 31.9 years and durations of diabetes were 22.0 and 18.8 years for the neuropathic and control groups, respectively. Patients provided details of fall injuries, and perception of safety during standing and walking. Multiple linear and logistic regression models were used to account for potentially associated variables such as gender, retinopathy, and duration of diabetes. The neuropathic group had adjusted odds ratios for reported injuries during gait of 15.0 relative to the control group (95% confidence intervals 1.04–216.59). The neuropathic group also reported significantly lower scores (less safe, p = 0.004) than the control group on perceived safety in unusual conditions. It is concluded that peripheral neuropathy has an effect on gait and posture which is clinically significant and that this effect merits further biomechanical study in neuropathic patients.

Ulceration, unsteadiness, and uncertainty : the biomechanical consequences of diabetes mellitus

Diabetes mellitus, which results from a failure of the endocrine system to control blood glucose levels within normal limits, affects approximately 15% of the population over the age of 65 in developed countries. Between 20-50% of people with diabetes for more than 10 years will experience symmetrical distal sensory neuropathy resulting in a progressive, distal to proximal, loss of sensation in the lower extremities. The most common consequence is plantar ulceration that too often results in partial or total amputation of the foot. While neuropathy is a major permissive factor, plantar ulcers occur at locations of high plantar pressures. The measurement of pressure using tools developed and refined in the field of biomechanics has been shown to be a valuable asset to the management of the foot at risk for ulceration. In particular, the use of in-shoe measuring techniques has the potential to revolutionize the prescription of therapeutic footwear. Biomechanical techniques have also helped to evaluate other consequences of diabetic neuropathy on the foot such as callus formation, foot deformity, limited joint mobility and bony abnormalities. The reduction of afferent information from the lower extremities implies a lack of active feedback thought to be necessary for the control of human movements such as posture and gait. Our results show that diabetic neuropathy results in a significant increase in sway during standing that is not compensated for by other sensory systems. The study of the sagittal plane movements of the same individuals walking on a treadmill showed little effect on the kinematic control of gait when compared to age matched nonneuropathic control groups. This may indicate the dominance of efferent input over afferent feedback during gait. We believe that the study of the biomechanical consequences of diabetes can act as a model for many other diseases that have yet to come under the scrutiny of a multidisciplinary team.

The effect of insoles in therapeutic footwear—A finite element approach

Current practice in the prevention of recurrence of neuropathic foot ulcers is to prescribe accommodative in-shoe orthoses or insoles which reduce plantar pressure levels at locations of bony prominences, particularly under the metatarsal heads. To date, design of these orthoses has largely been a trial and error process. There is little quantitative information available regarding the effects of thickness and the influence of soft tissue characteristics on the cushioning effect of such interventions. The current paper investigated alterations in pressure under the second metatarsal head as a function of insole thickness and tissue thickness. Both experimental and quasi-static plane strain finite element approaches were employed. The orthoses chosen reduced plantar pressure by a maximum of approximately 30% and were more effective (on a percentage basis) in the setting of reduced sub-metatarsal tissue thickness. Peak normal stresses predicted by the FE models were, on average, within 5.9% of experimentally measured values for the normal tissue case and 8.1% for the reduced tissue case. The techniques presented represent a promising approach to understanding plantar cushioning and the principles involved in the design of therapeutic footwear for insensate feet.

Glucose-induced Alterations in Nerve Metabolism: Current Perspective on the Pathogenesis of Diabetic Neuropathy and Future Directions for Research and Therapy

Recent animal and in vitro studies have identified several interrelated metabolic abnormalities in diabetic nerve that are attributable to elevated ambient glucose concentrations. In combination, these metabolic changes may induce a variety of biochemical and biophysical alterations in peripheral nerve that are highly relevant to the pathogenesis of diabetic neuropathy. This article reviews the current status of several of these metabolic defects and describes ways in which their interaction could lead to pathogenetically important changes in nerve metabolism, function, and structure. Areas of related future research are also discussed.

Role of somatosensory input in the control of human posture

Abstract In this study we investigated the effects of somatosensory deficits on the control of balance during quiet stance using subjects with demonstrated loss of sensation to touch, joint movement perception, proprioception, and other somatosensory stimuli secondary to diabetic neuropathy. The results indicate that somatosensory deficits resulting from diabetic neuropathy lead to a marked decrease in the ability to maintain a stable stance position. Furthermore, this study clearly demonstrates that somatosensory function is at least as important as vision in the control of posture during quiet stance, and that the visual and vestibular systems cannot fully compensate for diminished somatosensory input.

New developments in the biomechanics of the diabetic foot

Biomechanical issues are now widely recognized as being important in the treatment of diabetic foot disease. The purpose of the present review is to identify advances that have occurred since the previous International Conference on the Diabetic Foot in 1995 in the understanding of foot biomechanics in relation to diabetes. Attention continues to be focused on the identification of a threshold plantar pressure that leads to tissue damage. Recent studies have suggested that peak barefoot pressure may be only 65% specific for the development of ulceration. The association between foot deformity and plantar pressure has been the subject of several quantitative studies, but new questions have been raised about the etiology of claw toes. The measurement of shear stress continues to be an elusive goal although several small studies have presented possibly feasible technical approaches. The importance of callus as a precursor to ulceration has been confirmed experimentally and quantitative measures of motor neuropathy have been presented. Although a number of new devices have been introduced as alternatives to the Total Contact Cast, few clinical studies of their efficacy are available yet. New information on the properties of insole materials has been published including data on changes with repeated cycling. Complications of prophylactic surgery have been shown to include a high rate of Charcot fractures. Two new series describing the fixation of such fractures have also been reported. Biomechanical issues have also been addressed in two sets of guidelines for treatment that have recently been published. These many studies confirm the central role of mechanical stress and its relief in the treatment of neuropathic foot problems in diabetes. Copyright

Single stage correction with external fixation of the ulcerated foot in individuals with Charcot neuroarthropathy.

The ulcerated foot in individuals with Charcot neuroarthropathy presents a complex problem when correction of the deformity is necessary but the presence of infection precludes the use of internal fixation. We reviewed 11 patients with midfoot Charcot neuroarthropathy, collapse, and ulceration who were at risk for amputation. These patients underwent operative debridement, corrective osteotomy, external skeletal fixation and culture-directed antibiotic therapy as a limb salvage procedure. Patients were transitioned from the external fixator (average 57 days) to total contact casting (average 131 days) and all subsequently progressed to therapeutic footwear in 12 to 49 months of follow-up (average 24 months), except one patient whose medical decline resulted in bedrest. We believe that when performed in properly selected patients, this procedure presents an alternative to amputation and, via corrective osteotomy, results in a shoe-able, functional foot that is potentially less prone to ulceration.

The Mechanism of Plantar Unloading in Total Contact Casts: Implications for Design and Clinical Use

Although the total contact cast (TCC) has been shown to be an extremely effective treatment for the healing of plantar ulcers in diabetic patients, little is known about the biomechanics of its action. In this study, plantar pressure and ground reaction force measurements were obtained from over 750 foot contacts as five subjects with known elevated plantar forefoot pressures walked barefoot, in a padded cast shoe, and a TCC. Peak plantar pressures in the forefoot were markedly reduced in the cast compared with both barefoot and shoe walking (reductions of 75% and 86% respectively, P < 0.05). Peak plantar pressures in the heel were not, however, significantly different between the shoe and the TCC, and the longer duration of heel loading resulted in an impulse that was more than twice as great in the cast compared with the shoe (P < 0.05). An analysis of load distribution indicated that the mechanisms by which the TCC achieves forefoot unloading are (1) transfer of approximately 30% of the load from the leg directly to the cast wall, (2) greater proportionate load sharing by the heel, and (3) removal of a load-bearing surface from the metatarsal heads because of the “cavity” created by the soft foam covering the forefoot. These results point out some of the “essential design features” of the TCC (which are different from what had been previously supposed), support the use of the TCC for healing plantar ulcers in the forefoot, but raise questions about its utility in the healing of plantar ulcers on the heel.