In people with diabetes mellitus, the Charcot foot is a specific manifestation of peripheral neuropathy that may involve autonomic neuropathy with high blood flow to the foot, leading to increased bone resorption. It may also involve peripheral somatic polyneuropathy with loss of protective sensation and high risk of unrecognized acute or chronic minor trauma. In both cases, there is excess local inflammatory response to foot injury, resulting in local osteoporosis. In the Charcot foot, the acute and chronic phases have been described. The former is characterized by local erythema, edema, and marked temperature elevation, while pain is not a prominent symptom. In the latter, signs of inflammation gradually recede and deformities may develop, increasing the risk of foot ulceration. The most common anatomical classification describes five patterns, according to the localization of bone and joint pathology. This review article aims to provide a brief overview of the diabetic Charcot foot in terms of etiology, pathophysiology, and classification.
Charcot foot; classification; diabetes mellitus; diabetic foot; neuropathy; osteoarthropathy
Reduced traumatic and posttraumatic (nociceptive) pain is a key feature of diabetic neuropathy. Underlying condition is a gradual degeneration of endings of pain nerves (A-delta fibers and C-fibers), which operate as receivers of noxious stimuli (nociceptors). Hence, the absence of A-delta fiber mediated sharp pain (“first” pain), and of C-fiber mediated dull pain (“second” pain). However, patients with diabetic neuropathy and acute Charcot foot often experience deep dull aching in the Charcot foot while walking on it.
To create a unifying hypothesis on the kind of pain in an acute Charcot foot.
Absence of punctuate (pinprick) pain perception at the sole of a Charcot foot, as was shown recently, likely corresponds to vanished intraepidermal A-delta fiber endings. C-fiber nociceptors are reduced, according to histopathology studies. Both types of fibers contribute to posttraumatic hyperalgesia at the skin level, as studies show. Their deficiencies likely impact on posttraumatic hyperalgesia at the skin level and, probably, also at the skeletal level.
It is hypothesised that deep dull aching in an acute diabetic Charcot foot may represent faulty posttraumatic hyperalgesia involving cutaneous and skeletal tissues.
pain perception; diabetic neuropathy; Charcot neuroarthropathy
Patients with diabetes are often prescribed foot orthoses to help prevent foot ulcer formation. Orthotics are used to redistribute normal and shear stress. Shear stresses are not easily measurable and considered to be responsible for skin breakdown. Local elevation of skin temperature has been implicated as an early sign of impending ulceration especially in regions of high shear stress. The purpose of this study was to measure the effects of commonly prescribed insole materials on local changes in plantar foot temperature during normal gait.
Six commonly used foot orthosis materials were tested using the Thermo Trace™ infrared thermometer to measure foot temperature. Ten healthy adult volunteers without any history of diabetes or abnormal sensation participated in the study. During each trial the subject walked on a treadmill with the test material in the dominant foot's shoe, for six minutes at a speed of four miles per hour and rested for six minutes between trials. Four locations on the foot (hallux, first and fifth metatarsal heads, and heel) and the contralateral bicep temperatures were measured at 0, 1, 3, 5 minutes during the rest period. The order of material and skin location testing was randomized.
Significant differences were found between baseline temperatures and foot temperatures for all materials. However, no differences were found between materials for any location on the foot.
Previous studies have attempted to characterize materials based on laboratory and clinical testing, while other studies have attempted to characterize the effect of pressure on skin temperature. However, no study has previously attempted to characterize foot orthosis materials based on foot temperatures. This study compared foot temperatures of healthy adults based on the material tested. Although this study was unable to distinguish between materials based on foot temperatures, it was able to show a rise in foot temperature with any material used. This study demonstrates a need to a larger study on a population with diabetes.
To investigate the clinical efficacy of zoledronic acid in patients with diabetes and acute Charcot neuroarthropathy.
RESEARCH DESIGN AND METHODS
Thirty-nine consecutive patients were randomly assigned to placebo or three intravenous infusions of 4 mg zoledronic acid. The primary outcome was clinical resolution of acute Charcot neuroarthropathy determined by total immobilization time (casting plus orthosis).
At baseline, there was no significant difference between the randomly assigned groups with respect to Charcot disease activity or other baseline values. In the zoledronic acid group, the median time for total immobilization was 27 weeks (range 10–62), and in the placebo group it was 20 weeks (20–52) (P = 0.02).
Zoledronic acid had no beneficial effect on the clinical resolution of acute Charcot neuroarthropathy in terms of total immobilization time. It is possible that it may prolong the time to clinical resolution of Charcot neuroarthropathy.
Elevated plantar loading has been implicated in the etiology of plantar ulceration in individuals with diabetes mellitus and peripheral neuropathy. Total contact casts and cast walker boots are common off-loading strategies to facilitate ulcer healing and prevent re-ulceration. The purpose of this study was to compare off-loading capabilities of these strategies with respect to plantar loading during barefoot walking.
Twenty-three individuals with diabetes, peripheral neuropathy, and plantar ulceration were randomly assigned to total contact cast (N=11) or removable cast walker boot (N=12). Each subject underwent plantar loading assessment walking barefoot and wearing the off-loading device. Analysis of covariance was used to compare loading patterns in the off-loading devices for the whole foot, hindfoot, midfoot, and forefoot while accounting for walking speed and barefoot loading.
For the foot as a whole, there were no differences in off-loading between the two techniques. Subjects wearing cast walker boots had greater reductions in forefoot peak pressure, pressure-time integral, maximum force, and force-time integral with respect to barefoot walking. Healing times were similar between groups, but a greater proportion of ulcers healed in total contact casting compared to cast walker boots.
In subjects with diabetes, peripheral neuropathy, and plantar ulceration, cast walker boots provided greater load reduction in the forefoot, the most frequent site of diabetic ulceration, though a greater proportion of subjects wearing total contact casts experienced ulcer healing. Taken together, the less effective ulcer healing in cast walker boots despite superior forefoot off-loading suggests an important role for patient compliance in ulcer healing.
Diabetic neuroarthropathy was observed in four patients; these are the first cases of this nature reported in the Canadian medical literature. The criteria for this diagnosis included: (1) long-standing diabetes; (2) arthropathy, most frequently involving the foot, which shows deformity, shortening and ulceration without evidence of infection or peripheral circulatory failure; (3) abolition or diminution of pain on weight-bearing; (4) diabetic peripheral neuropathy with impaired sense of position or vibration and weak or absent deep tendon reflexes. Radiographic findings were similar to those in patients with Charcot's arthropathy from any cause.
Tabes dorsalis, leprosy, syringomyelia, myelodysplasia and the arthropathies of corticosteroid therapy were ruled out in these cases. In addition to conventional medical therapy the patients were treated by means of walking-casts for several months.
Diabetic neuroarthropathy is probably more common than the medical literature would indicate. Diminished sensation in the lower limbs in diabetics of long standing appears to be the major factor contributing to this disorder.
Charcot neuroarthropathy is a disabling complication of diabetes. Although its pathogenesis remains unknown, we suppose that genetics may play a relevant role.
RESEARCH DESIGN AND METHODS
We performed a case-control study with 59 subjects with diabetic Charcot neuroarthropathy (Ch group), 41 with diabetic neuropathy without Charcot neuroarthropathy (ND group), and 103 healthy control subjects (H group) to evaluate the impact of two single nucleotide polymorphisms (SNPs) of the osteoprotegerin gene (G1181C and T245G) on the risk of Charcot neuroarthropathy.
Regarding the SNPs of G1181C, we found a significant linkage between the G allele and Charcot neuroarthropathy (Ch vs. ND, odds ratio [OR] 2.32 [95% CI 1.3–4.1], P = 0.006; Ch vs. H, 2.10 [1.3–3.3], P = 0.002; and ND vs. H, 0.90 [0.7–1.9], P = 0.452); similarly, we found a linkage with the G allele of T245G (Ch vs. ND, 6.25 [2.2–19.7], P < 0.001; Ch vs. H, 3.56 [1.9–6.7], P = 0.001; and ND vs. H, 0.54 [0.6–5.7], P = 0.304), supporting a protective role for the allele C and T, respectively. For this reason we investigated the frequency of the protective double homozygosis CC + TT (7% in Ch) that was significantly lower in Ch compared with H (0.18 [0.06–0.5], P = 0.002) and with ND (0.17 [0.05–0.58], P = 0.006), whereas there was no difference between H and ND (1.05 [0.43–2.0], P = 0.468). In a multivariate logistic backward regression model, only weight and the lack of CC and TT genotypes were independently associated with the presence of Charcot neuroarthropathy.
This is the first study that shows an association between genetic regulation of bone remodeling and Charcot neuroarthropathy.
Diabetic neuropathy consists of multiple clinical manifestations of which loss of sensation is most prominent. High temperatures under the foot coupled with reduced or complete loss of sensation can predispose the patient to foot ulceration. The aim of this study was to look at the correlation between plantar foot temperature and diabetic neuropathy using a noninvasive infrared thermal imaging technique.
Infrared thermal imaging, a remote and noncontact experimental tool, was used to study the plantar foot temperatures of 112 subjects with type 2 diabetes selected from a tertiary diabetes centre in South India.
Patients with diabetic neuropathy (defined as vibration perception threshold (VPT) values on biothesiometry greater than 20 V) had a higher foot temperature (32–35 °C) compared to patients without neuropathy (27–30 °C). Diabetic subjects with neuropathy also had higher mean foot temperature (MFT) (p = .001) compared to non-neuropathic subjects. MFT also showed a positive correlation with right great toe (r = 0.301, p = .001) and left great toe VPT values (r = 0.292, p = .002). However, there was no correlation between glycated hemoglobin and MFT.
Infrared thermal imaging may be used as an additional tool for evaluation of high risk diabetic feet.
diabetic neuropathy; infrared thermal imaging; mean foot temperature; serum cholesterol; type 2 diabetes
Ground reaction forces from walking result in stress (pressure) and soft tissue strain at the plantar aspect of the foot. Excessive plantar pressure and tissue strain on the insensate foot may lead to ulceration. Our study investigated the effect of therapeutic footwear and custom-made orthotic inserts on pressure and tissue strain along the second ray of the plantar foot, and how these two variables are associated.
Twenty subjects (mean age 57.3 [SD 9.3], 12 male, 8 female, body mass index 32.5 [SD 7.4]) with diabetes mellitus, peripheral neuropathy, and a history of a plantar ulcer participated. Plantar pressure data were recorded during computed tomography scans for four conditions (barefoot, shoe, shoe+total contact insert, and shoe+total contact insert+metatarsal pad). For each condition tested, tissue strain and plantar pressure were determined at the second metatarsal head and at 15 other points along the second ray.
Differences were noted between the 4 conditions for pressure (p < 0.004) and soft tissue strain (p < 0.042) at the second metatarsal head. Correlation coefficients demonstrated an association between pressure and strain (Barefoot r = 0.81, Shoe r = 0.75, Shoe+total contact insert r = 0.73, and Shoe+total contact insert+metatarsal pad r = 0.44).
Footwear and orthotic devices tested in this study decreased pressure and soft tissue strain at the second ray of the foot, and these two variables were strongly related. A better understanding of the role tissue strain plays in distributing plantar forces may lead to improvements in the design of orthotic devices.
Plantar ulceration; Diabetes mellitus; Metatarsal pad; Total contact insert
Despite the high cumulative plantar stress associated with standing, previous physical activity reports of diabetic patients at risk of foot ulceration have not taken this activity into account. This study aimed to monitor spontaneous daily physical activity in diabetic peripheral neuropathy (DPN) patients and examine both walking and standing activities as important foot-loading conditions.
RESEARCH DESIGN AND METHODS
Thirteen DPN patients were asked to wear a body-worn sensor for 48 h. Body postures (sitting, standing, and lying) and locomotion (walking, number of steps, and postural transition) were extracted.
Patients daily spent twice as much time standing (13 ± 5%) as walking (6 ± 3%). They spent 37 ± 6% of time sitting and 44 ± 8% lying down. The average number of steps per day was 7,754 ± 4,087, and the number of walking episodes was 357 ± 167 with maximum duration of 3.9 ± 3.8 min.
The large portion of DPN patients' time spent standing with the feet loaded requires further consideration when treating and preventing foot ulcers.
To measure prospectively bone mineral density (BMD) of the Charcot and non-Charcot foot in 36 diabetic patients presenting with acute Charcot osteoarthropathy.
RESEARCH DESIGN AND METHODS
Calcaneal BMD was measured with quantitative ultrasound at presentation, at 3 months of casting, and at the time of the clinical resolution.
BMD of the Charcot foot was significantly reduced compared with BMD of the non-Charcot foot at presentation (P = 0.001), at 3 months of casting (P < 0.001), and at the time of clinical resolution (P < 0.001). Overall, from the time of presentation to the time of resolution there was a significant fall of BMD of the Charcot foot (P < 0.001) but not of the non-Charcot foot (P = 0.439).
Although the Charcot foot was treated with casting until clinical resolution, there was a significant fall of BMD only from presentation up until 3 months of casting.
Despite increased information on the importance of an inappropriate inflammatory response in the acute Charcot process, there has been no previous attempt to define the specific pathways that mediate its pathogenesis. Here, the role played by monocytes was analyzed.
RESEARCH DESIGN AND METHODS
The immune phenotype of peripheral monocytes was studied by fluorescence-activated cell sorter analysis comparing patients with acute Charcot (n = 10) in both the active and recovered phase, diabetic patients with neuropathy (with or without osteomyelitis), and normal control subjects.
When compared with diabetic control subjects and healthy subjects, monocytes from acute Charcot patients showed a proinflammatory immune phenotype characterized by increased production of proinflammatory cytokines, reduced secretion of anti-inflammatory cytokines, increased expression of surface costimulatory molecules, and increased resistance to serum withdrawal-induced apoptosis. In addition, the pattern of circulating cytokines confirmed activation of proinflammatory cytokines. No modulation of the monocyte phenotype was documented in diabetic control subjects and healthy subjects, thus indicating that the proinflammatory alterations of monocytes are specific and causative of acute Charcot.
Together, these data provide evidence for the role of proinflammatory changes in the immune phenotype of monocytes in the pathogenesis of acute Charcot. These alterations may explain the abnormally intense and prolonged inflammatory response that characterizes this disorder and may represent a potential therapeutic target for specific pharmacological interventions.
The author reports his experience on Refsum's disease and that gained after personally examining in detail 64 patients with Charcot-Marie-Tooth disease over the past ten years. The "cerebellar" inco-ordination in Charcot-Marie-Tooth disease (with or without distal wasting) and in Refsum's disease is analysed. Some variations in the motor and sensory neuropathy of Charcot-Marie-Tooth disease and Refsum's disease are discussed. The adequacy of motor conduction velocity in genetically distinguishing types of the above mentioned familial peripheral neuropathies is reviewed. Data on the neuropathy assessed by modern techniques of three original patients of Roussy and Levy (1926) are given. The possibility of extensor plantar responses in patients with Charcot-Marie-Tooth and Refsum's disease without structural lesion of the pyramidal tract is pointed out. The existence of the association between Friedreich's ataxia and Charcot-Marie-Tooth disease is criticised. It is emphasised that spinocerebellar degeneration (other than Friedreich's ataxia) presenting with distal limb weakness and wasting and sensory impairment may mimic Charcot-Marie-Tooth disease.
In people with diabetes and peripheral neuropathy (DM+PN), injury risk is not clearly known for weight bearing (WB) vs. non-weight bearing (NWB) exercise. In-shoe peak plantar pressures (PPP) often are used as a surrogate indicator of injury to the insensitive foot.
Compare PPPs in people with DM+PN during selected WB and NWB exercises.
15 subjects with DM+PN participated. PPPs were recorded for the forefoot, midfoot, and heel during level walking and compared to; WB exercises - treadmill walking, heel and toe raises, sit to stands, stair climbing, single leg standing; and NWB exercises - stationary bicycling, balance ball exercise and plantar flexion exercise.
Compared to level walking; mean forefoot PPP during treadmill walking was 13% higher, but this difference was eliminated when walking speed was used as a covariate. Mean PPPs were similar or substantially lower for other exercises, except for higher forefoot PPP with heel raise exercises.
Slow progression and regular monitoring of insensitive feet are recommended for all exercises, but especially for heel raises, and increases in walking speed. The remaining WB and NWB exercises pose no greater risk to the insensitive foot due to increases in PPP compared to level walking.
Diabetes; Peripheral Neuropathy; Plantar pressure; Exercise
Neuropathic deformities impair foot and ankle joint mobility, often leading to abnormal stresses and impact forces. The purpose of our study was to determine differences in radiographic measures of hind foot alignment and ankle joint and subtalar joint motion in participants with and without neuropathic midfoot deformities and to determine the relationships between radiographic measures of hind foot alignment to ankle and subtalar joint motion in participants with and without neuropathic midfoot deformities.
Sixty participants were studied in three groups. Forty participants had diabetes mellitus (DM) and peripheral neuropathy (PN) with 20 participants having neuropathic midfoot deformity due to Charcot neuroarthropathy (CN), while 20 participants did not have deformity. Participants with diabetes and neuropathy with and without deformity were compared to 20 young control participants without DM, PN or deformity. Talar declination and calcaneal inclination angles were assessed on lateral view weight bearing radiograph. Ankle dorsiflexion, plantar flexion and subtalar inversion and eversion were assessed by goniometry.
Talar declination angle averaged 34±9, 26±4 and 23±3 degrees in participants with deformity, without deformity and young control participants, respectively (p< 0.010). Calcaneal inclination angle averaged 11±10, 18±9 and 21±4 degrees, respectively (p< 0.010). Ankle plantar flexion motion averaged 23±11, 38±10 and 47±7 degrees (p<0.010). The association between talar declination and calcaneal inclination angles with ankle plantar flexion range of motion is strongest in participants with neuropathic midfoot deformity. Participants with talonavicular and calcaneocuboid dislocations result in the most severe restrictions in ankle joint plantar flexion and subtalar joint inversion motions.
An increasing talar declination angle and decreasing calcaneal inclination angle is associated with decreases in ankle joint plantar flexion motion in individuals with neuropathic midfoot deformity due to CN that may contribute to excessive stresses and ultimately plantar ulceration of the midfoot.
Foot alignment; Deformity; Ankle and foot joint goniometry; Limited joint mobility
The surgical management of ankle fractures among the diabetic population is associated with higher complication rates compared to the general population. Efforts toward development of better methods in prevention and treatment are continuously evolving for these injuries. The presence of peripheral neuropathy and the possible development of Charcot neuroarthropathy in this high risk patient population have stimulated much surgical interest to create more stable osseous constructs when open reduction of an ankle fracture/dislocation is required. The utilization of multiple syndesmotic screws (pro-syndesmotic screws) to further stabilize the ankle mortise has been reported by many foot and ankle surgeons. In addition, transarticular Steinmann pins have been described as an adjunct to traditional open reduction with internal fixation (ORIF) of the ankle to better stabilize the talus, thus minimizing risk of further displacement, malunion, and Charcot neuroarthropathy. The authors present a unique technique of ORIF with pro-syndesmotic screws and the application of a multi-plane circular external fixator for management of a neglected diabetic ankle fracture that prevented further deformity while allowing a weight-bearing status. This techniqu may be utilized for the management of complex diabetic ankle fractures that are prone to future complications and possible limb loss.
revisional foot and ankle surgery; diabetes; Charcot neuroarthropathy; trauma-external fixation; complications
The volume of sweat produced by axon reflex stimulation using acetylcholine was measured in one foot each of 35 control subjects and 52 feet of 37 diabetic patients (28 with neuropathic ulceration, 11 with Charcot arthropathy, nine with somatic neuropathy but no foot lesion and four with no evidence of somatic neuropathy). In controls, the volume of sweat was greater in males than females. A flare response was seen in 94% of control feet. In diabetics, the volume of sweat was within the control range in 17 feet, increased in one, reduced in seven, and absent in 27. Sweating was absent in 75% of feet with a neuropathic ulcer; a flare response was absent in 86% of them. Sweating was only absent in 36% of feet with Charcot arthropathy and was increased in one, whereas the flare response was absent in all. Autonomic cardiovascular reflexes were more frequently abnormal than the sweat test; sweating was absent in only one patient with normal cardiovascular reflexes.
Charcot's neuroarthropathy of ankle leads to instability, destruction of the joint with significant morbidity that may require an amputation. Aim of surgical treatment is to achieve painless stable plantigrade foot through arthrodesis. Achieving surgical arthrodesis in Charcot's neuroarthropathy has a high failure rate. This is a retrospective nonrandomized comparative study assessing the outcomes of tibio-talar arthrodesis for Charcot's neuroarthropathy treated by uniplanar external fixation assisted by external immobilization or retrograde intramedullary interlocked nailing.
Materials and Methods:
Records of the authors′ institution were reviewed to identify those patients who had undergone ankle fusion for diabetic neuroarthropathy from January 1998 to December 2008. A total of11 patients (six males and five females) with a mean age of 56 year and diabetes of a mean duration of 15.4 years with ankle tibio-talar arthrodesis using retrograde nailing or external fixator for Charcot's neuroarthropathy were enrolled for the analysis. Neuropathy was clinically diagnosed, documented and substantiated using the monofilament test. All procedures were performed in Eichenholz stage II/III.Six patients were treated with uniplanar external fixator, while the remaining five underwent retrograde intramedullary interlocking nail. The outcomes were measured for union radiologically, development of complications and clinical follow-up, according to digital archiving systems and old case notes.
All five (100%) patients treated by intramedullary nailing achieved radiological union on an average follow-up of 16 weeks. The external fixation group had significantly higher rate of complications with one amputation, four non unions (66.7%) and a delayed union which went on to full osseous union.
The retrograde intramedullary nailing for tibio-talar arthrodesis in Charcot's neuroarthropathy yielded significantly better outcomes as compared to the use of uniplanar external fixator.
Charcot's diabetic neuropathy; retrograde intramedullary nailing; tibio-talar arthrodesis; uniplanar external fixator
Our aims were to compare osteoclastic activity between patients with acute Charcot’s osteoarthropathy and diabetic and healthy controls, and to determine the effect of the receptor activator of nuclear factor-kappaB ligand (RANKL) and its decoy receptor osteoprotegerin (OPG).
Peripheral blood monocytes isolated from nine diabetic Charcot patients, eight diabetic control and eight healthy control participants were cultured in the presence of macrophage-colony stimulating factor (M-CSF) alone, M-CSF and RANKL, and also M-CSF and RANKL with excess concentrations of OPG. Osteoclast formation was assessed by expression of tartrate-resistant acid phosphatase on glass coverslips and resorption on dentine slices.
In cultures with M-CSF, there was a significant increase in osteoclast formation in Charcot patients compared with healthy and diabetic control participants (p = 0.008). A significant increase in bone resorption was also seen in the former, compared with healthy and diabetic control participants (p < 0.0001). The addition of RANKL to the cultures with M-CSF led to marked increase in osteoclastic resorption in Charcot (from 0.264 ± 0.06% to 41.6 ± 8.1%, p < 0.0001) and diabetic control (0.000 ± 0.00% to 14.2 ± 16.5%, p < 0.0001) patients, and also in healthy control participants (0.004 ± 0.01% to 10.5 ± 1.9%, p < 0.0001). Although the addition of OPG to cultures with M-CSF and RANKL led to a marked reduction of resorption in Charcot patients (41.6 ± 8.1% to 5.9 ± 2.4%, p = 0.001), this suppression was not as complete as in diabetic control patients (14.2 ± 16.5% to 0.45 ± 0.31%, p = 0.001) and in healthy control participants (from 10.5 ± 1.9% to 0.00 ± 0.00%, p < 0.0001).
These results indicate that RANKL-mediated osteoclastic resorption occurs in acute Charcot’s osteoarthropathy. However, the incomplete inhibition of RANKL after addition of OPG also suggests the existence of a RANKL-independent pathway.
Charcot’s osteoarthropathy; OPG; Osteoclasts; Osteolysis; RANKL; Resorption
Offloading plantar pressure is a key strategy for the prevention or healing of neuropathic plantar ulcers in diabetes. Non-removable walking casts, such as total contact casts, are currently considered the gold-standard for offloading this type of wound. However, alternative methods for offloading that are more cost effective and easier to use are continually being sought. The aim of this study was to evaluate the capacity of the DH Pressure Relief Shoe™ to offload high pressure areas under the neuropathic foot in diabetes.
A within-subjects, repeated measures design was used. Sixteen participants with diabetic peripheral neuropathy were recruited and three footwear conditions were evaluated in a randomised order: a canvas shoe (the control), the participants’ own standard shoe, and the DH Pressure Relief Shoe™. The primary outcome was peak plantar pressure, measured using the pedar-X® mobile in-shoe system between the three conditions.
Data analysis was conducted on 14 out of the 16 participants because two participants could not complete data collection. The mean peak pressure values in kPa (±SD) for each condition were: control shoe 315.9 (±140.7), participants’ standard shoe 273.0 (±127.1) and DH Pressure Relief Shoe™ 155.4 (±89.9). There was a statistically significant difference in peak plantar pressure between the DH Pressure Relief Shoe™ compared to both the control shoe (p = 0.002) and participants’ standard shoe (p = 0.001). The DH Pressure Relief Shoe™ decreased plantar pressures by 51% compared to the control shoe and by 43% compared to participants’ standard shoe. Importantly, for a couple of study participants, the DH Pressure Relief Shoe™ appeared unsuitable for day-to-day wearing.
The DH Pressure Relief Shoe™ reduced plantar pressures more than the other two shoe conditions. The DH Pressure Relief Shoe™ may be a useful alternative to current offloading modalities used in clinical management of diabetic foot ulceration. However, clinical trials are needed to test their effectiveness for ulcer healing and to ensure they are useable and safe for patients in everyday activities.
Diabetic foot disease is characterized by progressive foot deformities that lead to amputation and disabling morbidity. The purpose is to investigate the classification of two distinct phenotypes of mid foot structural polymorphism in individuals using plantar kinetic and pressure distribution and tarsal bone density assessments.
Twenty-two individuals (26 ft) with diabetes mellitus, peripheral neuropathy and at least one mid foot deformity were compared to 29 age-, gender- and race-matched healthy controls (58 ft). Eleven subjects with diabetes mellitus and peripheral neuropathy (11 ft) had lateral deformity; 11 subjects (15 ft) had medial deformity. Each subject had calcaneal bone mineral density and plantar force and pressure assessments walking barefoot over an EMED-ST P-2 platform.
Control subjects had lower mid foot vertical forces and pressures despite significantly higher preferred walking speed. In subjects with diabetes and neuropathy, maximum vertical force was 6-fold greater, force–time integral 9.5-fold greater, peak pressure 6.7-fold higher, pressure–time integral was 9.7-fold greater, contact area 2-fold greater and contact time 1.9-fold higher than controls. Pressure values were larger in involved vs uninvolved (P ≤ 0.05). During stance in the mid foot, subjects with medial column phenotype showed greater pressure in the medial mask; subjects with lateral column phenotype had greater pressures in the lateral mask (P < 0.05). Calcaneal bone density was lower for the deformity foot vs the non-deformity foot; bone mineral density was lower in medial column phenotype vs lateral column phenotype (P = 0.02).
Diabetic foot disease can be classified as stereotypical, structurally-distinct phenotypes of deformities of the medial and lateral columns of the mid foot. Assessments of pedal bone density and plantar mid foot force and pressure during barefoot walking can characterize the structural polymorphic phenotypes and may assist the foot care specialist in clinical decision making.
Mid foot deformity; Plantar pressure; Tarsal bone density
Conservative management of Charcot foot neuroarthropathy remains efficacious for certain clinical scenarios. Treatment of the patient should take into account the stage of the Charcot neuroarthopathy, site(s) of involvement, presence or absence of ulceration, presence or absence of infection, overall medical status, and level of compliance. The authors present an overview of evidence-based non-operative treatment for diabetic Charcot neuroarthropathy with an emphasis on the most recent developments in therapy.
diabetic foot; osteomyelitis; Charcot neuroarthropathy; ulcer; bone stimulation
Diabetic foot ulcers are known to have a biomechanical etiology. Among the mechanical factors that cause foot lesions, shear stresses have been either neglected or underestimated. The purpose of this study was to determine various plantar pressure and shear variables in the diabetic and control groups and compare them. Fifteen diabetic patients with neuropathy and twenty non-diabetic subjects without foot symptoms were recruited. Subjects walked on a custom built platform capable of measuring local normal and tangential forces simultaneously. Pressure-time integral quantities were increased by 54% (p=0.013) in the diabetic group. Peak AP and resultant shear magnitudes were found to be 32% larger (p<0.05) even though diabetic subjects walked at a slower velocity. Lower AP and ML stress range (peak-to-peak) values were observed in the control subjects (p<0.05). Shear-time integral values were increased in the diabetic group by 61% and 132% for AP and resultant shear cases, respectively (p<0.05). Plantar shear is known to be effective in callus formation which has previously been associated with higher ulcer incidence. During gait shear forces are induced with twice the frequency of pressure characteristically. Therefore, plantar shear should be investigated further from a broader perspective including the temporal specifics and fatigue failure characteristics of the affected plantar tissue.
Foot biomechanics; diabetes; diabetic ulcers; plantar stresses; plantar shear; diabetic neuropathy; diabetic foot lesions
Patients with diabetic polyneuropathy (DPN) are often confronted with ulceration of foot soles. Increased plantar pressure under the forefoot has been identified as a major risk factor for ulceration. This study sets out to test the hypothesis that changes in gait characteristics induced by DPN related muscle weakness are the origin of the elevated plantar pressures.
Three groups of subjects participated: people diagnosed with diabetes without polyneuropathy (DC), people diagnosed with diabetic polyneuropathy (DPN) and healthy, age-matched controls (HC). In all subjects isometric strength of plantar and dorsal flexors was assessed. Moreover, joint moments at ankle, knee and hip joints were determined while walking barefoot at a velocity of 1.4 m/s. Simultaneously plantar pressure patterns were measured.
Compared to HC-subjects, DPN-participants walked with a significantly increased internal plantar flexor moment at the first half of the stance phase. Also in DPN-subjects the maximal braking and propelling force applied to the floor was decreased. Moreover, in DPN-subjects the ratio of forefoot-to-rear foot plantar pressures was increased. Body-mass normalized strength of dorsal flexors showed a trend to be reduced in people with diabetes, both DC and DPN, compared to HC-subjects. Plantar flexors tended to be less weak in DC compared to HC and in DPN relative to DC.
The results of this study suggest that adverse plantar pressure patterns are associated with redistribution of joint moments, and a consequent reduced capacity to control forward velocity at heel strike.
The aim of this study was to assess and compare the response to two forms of treatment-immobilization with zoledronic acid injection and immobilization with oral weekly Alendronate, in patients with diabetes mellitus and acute Charcot arthropathy (CA) of foot in terms of clinical and radiological parameters.
Material and Methods:
Patients attending the endocrinology and podiatry clinic with history of diabetes mellitus and Acute CA were taken for study. The patients were randomized into two treatment groups. Group Z-zoledronic acid injection along with total contact cast (TCC). Group A-Tab. Alendronate 70 mg. once a week till the complete clinical resolution of acute CA along with TCC. Forty-five patients were randomized and 40 of them completed the study. The primary end point was complete clinical resolution of acute CA-defined as temperature difference between normal and affected foot <1°F.
Among the 40 patients, 30 (75%) had complete clinical resolution. The mean number of days taken for complete clinical resolution since the initiation of treatment (either Zoledronic acid or Alendronate) was approximately 122 days. There was no significant difference in a number of days required for complete clinical resolution, between the two forms of therapy. There was more than 50% reduction in the visual score between the baseline and the final scan. The target to non-target ratio in the skeletal phase also showed an average of 40% reduction from the baseline to the final skeletal scintigraphy.
Both Intravenous Zoledronic acid and oral alendronate had comparable efficacy with respect to the time taken for attaining complete clinical resolution of acute CA of foot. However, Alendronate therapy was cost effective among the two. 99mTc MDP bone scan can be used as an adjuvant to the clinical parameters in assessing the response to therapy.
Arthropathy; alendronate; Charcot; resolution; zoledronic acid