Tag Archives: Charcot

Peroneal tendinopathy in resolved Charcot foot – management with foot orthoses: A case report

by Joshua Young BSc.(Hons), MBAPO Orthotist1*

The Foot and Ankle Online Journal 12 (3): 3

This case report presents an occurrence of painful peroneal tendinopathy in a high risk diabetic foot following Charcot neuroarthropathy, managed using foot orthoses. Self-reported pain intensity was assessed using the 11-point numeric pain rating scale (NRS-11). Peak plantar pressures were assessed using the Pressure Guardian system for three conditions: 3.2mm poron inlay (control), custom foot orthosis, and custom foot orthosis with lateral wedge. Following addition of lateral wedging to the existing foot orthoses, pain reduced to a satisfactory level for the subject. Plantar pressure measurement showed that the addition of lateral wedging did not increase peak plantar pressures above 200kPa, a proposed dangerous level of pressure. Additionally, the foot orthoses still successfully reduced peak plantar pressures to below 200kPa, compared to walking without them. Peroneal tendinopathy should be considered as a possible cause of lateral ankle pain in neuropathic diabetic feet. Lateral wedging can be considered as one option to reduce pain in peroneal tendinopathy, and may not compromise the protective effect of foot orthoses in high risk feet.

Keywords: Charcot, foot, peroneal, tendinopathy, orthoses, insoles

ISSN 1941-6806
doi: 10.3827/faoj.2018.1203.0003

1 – Roehampton Rehabilitation Centre, Queen Mary’s Hospital. St George’s University Hospitals NHS Foundation Trust, London, UK.
* – Corresponding author: Joshua.Young1@nhs.net

Pain can be present even in a diabetic foot with neuropathy. Causes of pain in this group could include painful diabetic neuropathy [1–3]⁠ and Charcot neuroarthropathy (CN) or ‘Charcot foot’ [4]⁠. The cause of the pain should be determined to inform appropriate management.

Tendinopathy may also occur and cause pain in the neuropathic diabetic foot. There is a higher risk of tendinopathy in diabetes [5–7]⁠. Chronic ankle instability or ‘hind foot varus’ have been suggested as predisposing factors to developing peroneal tendinopathy [8]⁠. In theory the ground reaction force on an inverted heel deviates medially, causing an increased ankle inversion moment which must be opposed by the peroneal muscles. A more supinated foot may develop as a result of CN [9,10]⁠.

It has been proposed that the conservative management of peroneal tendinopathy may include protection, relative rest, ice, compression, elevation, medications, and rehabilitative exercise modalities (PRICEMM) in addition to foot orthoses and strengthening of ankle evertors [11]⁠. There is limited evidence on the role of foot orthoses in peroneal tendinopathy. Some work has shown that foot orthoses alter peroneal muscle activity in runners with overuse injury symptoms [12] and in adults with chronic ankle instability [13]. A foot orthosis with a 10 degree lateral wedge has been shown to increase pronation at the rearfoot and reduce the ground reaction force magnitude, suggesting increased shock attenuation by the foot and ankle[14]⁠. This case study presents a case of painful peroneal tendinopathy, which developed in a foot following CN and was subsequently managed using foot orthoses (FOs). The CARE guidelines for reporting of case studies was followed [15]. Written informed consent was obtained for the publication of the materials in this article.


The subject was a 60 year-old male with type 2 diabetes with a history of CN affecting both feet. The CN resolved 8 months previously. There was a history of superficial ulceration (Texas grade A1) [16]⁠ to the left plantar 1st metatarsal-phalangeal joint and 1st tarso-metatarsal joint, both resolved for 8 months with the use of custom foot orthoses at the time of presentation with a primary concern of right foot pain.

Clinical Findings

There was sensory neuropathy, with only 1 out of 10 sites tested with a 10g monofilament being detected (Plantar 1st and 3rd toes, plantar 1st, 3rd and 5th metatarsal-phalangeal joints bilaterally). Circulation was good with triphasic posterior tibial pulses. Passive joint ranges of motion at the foot and ankle was generally good bilaterally except reduction in midtarsal movement on the left, and reduced extension at the left 1st metatarsal-phalangeal joint (45 degrees) compared to the right (60 degrees). Foot posture was rated using the foot posture index (FPI-6)[17]⁠ as +9 on the left and +3 on the right, indicating a highly pronated foot on the left and a relatively less pronated foot on the right (Figures 1 and 2). The FPI-6 differential of 6 points exceeds both normal values for foot asymmetry and mean asymmetry reported in a CN group [10,18]. The patient presented reporting a 6 week history of right foot pain, indicating the lateral ankle. This developed despite an existing 6mm lateral flare/float addition to the right heel, intended to resist ankle inversion. Pain intensity was reported as 7/10 on the numeric rating scale (NRS-11). 

Diagnostic Assessment

Palpation of the peroneal tendons posteriorly to the lateral malleolus reproduced the pain experienced during walking. A portable ultrasound system was used by the author at this stage, indicating some fluid in the peroneal tendon sheath. 

Figure 1 Left and right feet (anterior and posterior view).

Figure 2 Lateral radiographs of left and right feet.

Figure 3 Cross sectional ultrasound image of peroneus longus showing fluid within the tendon sheath.

Figure 4 Cross sectional ultrasound image of peroneus longus and brevis using power Doppler to show hyper vascularity in the tendons.

Figure 5 Left and right foot orthoses, plantar view.

Figure 6 Right foot orthosis, posterior view.

Referral to radiology for a definitive evaluation was made, which confirmed the diagnosis of peroneal tendinopathy (Figures 3 and 4). The report identified fluid in the common peroneal tendon sheath, in keeping with tenosynovitis, and marked thickening of the peroneus brevis tendon at the insertion, in keeping with tendinosis.

Therapeutic Intervention – Orthotic Prescription

The existing FOs consisted of a 3mm thick base with 50 shore A Ethylene-vinyl acetate (EVA) at the proximal half and 30 shore A EVA at the distal half. There are ‘plugs’ under the right cuboid region, left 1st metatarsal-phalangeal joint and 1st tarso-metatarsal joint where the base material has been replaced with grey poron (Poron 4000, Algeos, Liverpool). 6mm grey poron is used as a top cover, giving a total 9mm base thickness (Figure 5).

Lateral heel wedging (3 degrees) was added to the existing foot orthoses, however the patient reported no immediate change. A further 5 degrees (8 degrees total) was added on the same day – the patient reported that the pain reduced to 1/10 immediately.


At review 8 weeks later, the patient reported that the pain had reduced to 0/10 24 hours following the addition of the lateral wedge. However, 72 hours after the addition of the lateral wedge the pain returned to 4/10. At this stage, the lateral heel wedge was increased to 12 degrees (Figure 6) and extended to the midfoot. The patient again reported an immediate reduction from 4/10 to 0/10.

To ensure that the aggressive wedging added was not causing high pressures in other areas of the foot, in-shoe pressure measurement was used. Comparisons were made with a 3mm poron inlay only, the custom foot orthosis only, and the custom foot orthosis with 12 degree wedge (Table 1). 

Sensor location Peak pressure (kPa) – 3mm poron inlay  Peak pressure (kPa) – custom foot orthosis Peak pressure (kPa) – custom foot orthosis with 12 degree lateral wedge
Lateral plantar heel 71 28 32
Medial plantar heel 69 18 8
Lateral plantar midfoot (Charcot deformity) 244* 94 133
Plantar 1st metatarsal-phalangeal joint 28 33 31

Table 1 Peak plantar pressures (*Indicates a peak pressure value exceeding the proposed dangerous level of 200kPa).

Considering 200kPa as a dangerous level of pressure [19], the custom FO reduced the lateral plantar midfoot (Charcot deformity) pressure to below this level. Following the addition of the lateral wedge, all plantar pressures tested remained below the 200kPa level. Some increase in pressure at the lateral midfoot was measured, reflecting the extension of the wedge to the midfoot. Slight increase in pressure was seen at the lateral heel, which seems to indicate that the centre of pressure was moved laterally by the lateral heel wedge.

At a second review appointment 6 weeks later, the pain had returned back to 4/10. The patient declined any other management and was happy to continue using the laterally wedged foot orthoses. At a third review 8 weeks later, the pain was slowly reducing and now rated as varying between 2/10 and 4/10.


This case study illustrates a relatively successful outcome in reducing pain associated with peroneal tendinopathy, using FOs only. The initial pain level of 7/10 was reduced by at least 3 points, which exceeds reported minimal clinically important difference (MCID) values [20]. Of interest is the fact that the patient reported marked immediate effects following the addition of lateral wedging to the existing FOs. This initial effectiveness tended to reduce over time, with pain levels increasing again. One possible explanation for this reduction in initial success may be some compression of the orthoses, which were not made with rigid plastic. The outcome may have been more successful if accompanied by other approaches such as physical therapy, however in this case due to patient preference only one approach was used.

Following initial use of a lateral wedge at the heel only, longer term reductions in pain were achieved by extending the wedge to the midfoot. The extension of the wedge to the midfoot has a logical anatomical basis, as the insertion of the peroneus brevis is distal to the heel, at the base of the 5th metatarsal. It is therefore logical to apply the opposing force in this area. The angle of the lateral wedge also needed to be increased to maintain pain reduction. A systematic effect of altering heel wedge geometry on external forces acting on the foot has been shown by Sweeney [21]⁠ although this relates to medially positioned wedging. The need for these small adjustments highlights the importance in this case not just of selecting an appropriate modification, but also the size and location of the modification. 

Applying relatively aggressive wedging to orthoses for feet at risk of ulceration may be controversial, as traditional approaches to designing FOs for high risk feet often focus on accommodation, rather than altering function of the foot. In this case, use of pressure measurement enabled verification that pressure levels were brought below 200kPa by the FOs, and that this reduction persisted despite the addition of a large lateral wedge. This indicates that aggressive FO designs may be safely used in high risk diabetic feet. However pressure measurement should ideally be used to assess the effectiveness and safety of any orthotic prescription in the context of a high risk foot.

The cause of the tendinopathy in this case is uncertain. The right foot and ankle may have become more prone to inversion as a result of changes to the bony architecture following CN. This may have in turn caused increased inversion moments at the rearfoot, and hence more stress on the peroneal tendons. Neuromuscular control may also be a factor, as the timing of muscle activation has been shown to be altered in diabetic patients [22]⁠⁠. 

This case report has illustrated that lateral wedging up to 12 degrees may be safe and not compromise the protective function of a FO in a high risk diabetic foot. Clinicians should consider peroneal tendinopathy as a possible cause of lateral ankle pain in neuropathic diabetic feet. Clinicians may consider orthosis wedging as one option to reduce pain in peroneal tendinopathy, in addition to other approaches.


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Trigger events for Charcot neuroarthropathy: A retrospective review

by Brent H. Bernstein DPM  FACFAS1, Payel Ghosh DPM2, Colleen Law DPM3, Danielle Seiler DPM4, Thuyhien Vu DPM5

The Foot and Ankle Online Journal 10 (2): 3

Charcot arthropathy is a rare, but devastating disease process that has significantly debilitating sequelae. While several theories have been discussed within the literature regarding the causative factors, there remains much debate to the exact pathogenesis. Nevertheless, recognition and timely treatment of this issue remains a paramount task for every healthcare provider. In order to accomplish this, we investigated specific trigger events that led to the onset of the Charcot, by subjectively interviewing patients.  Ultimately, we were able to identify acute trauma, surgical events, infections, and also overuse injuries all as inciting events to this disease process. The overall goal of this paper is to improve recognition of the possible triggers that leads to the Charcot disease process in order to better care for patients. 

Keywords: Charcot, diabetic foot, trigger event, neuropathy, neuroarthropathy

ISSN 1941-6806
doi: 10.3827/faoj.2017.1002.0003

1 – Attending, Research Coordinator, Podiatry Residency, St. Luke’s Hospital Allentown, PA
2 – Podiatric Resident, St. Luke’s Hospital Allentown, PA
3 – Podiatric Resident, St. Luke’s Hospital Allentown, PA
4 – Associate at Premier Foot & Ankle Associates Wyomissing, PA
5 – Teaching Staff, Mercy Medical Center, Cambodia
* – Corresponding author: ghosh.payel@gmail.com

Charcot neuroarthropathy is a progressive and destructive process that can lead to debilitating sequelae such as ulcerations, foot deformity, fracture, dislocations, and even amputation [1]. Charcot has been associated with a number of different conditions; however, today diabetes mellitus is found to be the primary cause [2]. The epidemiological data shows that the prevalence of Charcot arthropathy in diabetic patients ranges from 0.08% to 13% while the incidence varies between 0.10% and 29% [1]. This wide difference in incidence within the literature is linked to higher index of suspicion from tertiary providers, such as wound care specialists.

The exact pathogenesis of Charcot remains ill defined.  The neurotraumatic and neurovascular theories continue to be the fundamental teachings; however, it is likely that there are a combination of several mechanisms involved [3]. It is thought that autonomic neuropathy, creates a hyperemic response by means of arterio-venous shunting leading to bone resorption and osteopenia.  Furthermore, it is suggested that motor neuropathy causes muscle imbalances within the foot, which leads to repetitive microtrauma.  This alone, or in combination with a traumatic event begins the process of osseous destruction.  Sensory neuropathy prevents the patient from recognizing this microtrauma, thus propagating the Charcot process [4].   Newer relate the pathogenesis to the disruption in the Charcot patient’s ability to regulate inflammation.  This results in increased levels of proinflammatory cytokines, such as tumor necrosis factor alpha (TNFα) and interleukin-1β (IL-1β) and a decrease of anti-inflammatory factors interleukin-4 and interleukin-10.  Increased TNFα leads to a cytokine cascade that eventually results in the activation of NF-κB, which causes osteoclast precursor cells to become mature osteoclasts.  This process causes excessive bone turnover due to increased osteoclast activity, thus resulting in the Charcot process [5].

To our knowledge, there have been no published reports aimed specifically at the initial inciting event that triggers the acute Charcot cascade. The purpose of this study was to analyze the trigger events leading to the development of Charcot neuroarthropathy with the hope that this information will give rise to preventative measures for these at risk patients.   


Data were obtained from the medical records of patients being treated by the primary author (BHB) with a diagnosis of Charcot neuroarthropathy between 2003 and 2010.  The diagnosis of Charcot was based on clinical presentation and radiographic evidence, including advanced imaging studies.  Swelling, erythema, warmth, pain, and a temperature gradient of four degrees Fahrenheit or more between the affected and contralateral limb were pertinent to the clinical diagnosis.  The clinical diagnosis was then confirmed with MRI or triple phase bone scan.

A total of 211 feet from the records were identified with Charcot; however, only 179 had complete data available. The triggering event was identified through patient interview and clinical examination.  Questions regarding prior trauma, surgery, infection, or overuse were discussed in detail in order to help determine the inciting event.  In 70 of the feet, a trigger could not be identified, and thus were excluded from the data analysis.  The triggering event preceding the acute onset of Charcot was analyzed and classified into five major categories.  The first category was acute injury, which included any single, identifiable event such as fractures or sprains that resulted in the onset of the Charcot process.  Diabetic ankle fractures were placed in their own separate category from the acute injury category due to their higher morbidity rate and more unique surgical protocol vs. a non-ankle fracture.  The surgical category consisted of patients who developed Charcot following recent non-elective or elective foot surgery.   The patients who had a recent of history of infection as an inciting event, but did not undergo any surgical procedures was placed into the infection category.  Lastly, the overuse category was for individuals who had an identifiable continued repetitive trauma from a particular event over a period of time.  Each foot was then classified based on Sander’s anatomic classification system as follows: Type 1=forefoot, Type II = tarso-metatarsal joint, Type III = naviculocuneiform and midtarsal joints, Type IV = ankle joint, Type V = calcaneus [1].  

The frequency of each trigger category as well as each anatomic location was analyzed.  For exploratory purposes only, given the small subgroup sizes, a chi square test of general association was conducted to compare trigger types by anatomic site.  A p-value < .05 denotes statistical significance.


Complete data was available on 179 out of 211 feet.  A specific trigger event could not be identified in 70 feet and these were excluded from the data analysis; therefore, the final cohort included 109 feet.  Demographic information is summarized in Table 1.  The mean age was 55.97 years old ranging from 28 to 84.  There were 64 males and 45 females included in the study.  90% of our patient population was diabetic while the other 10% had neuropathy from other etiologies. Other etiologies did include, but were not limited to Alcoholic Neuropathy, Cauda Equina Syndrome, Agent Orange Syndrome, Idiopathic and Hypothyroidism. Of note, there were two cases of combined Diabetic and Syphilitic Neuropathy.



(mean + standard deviation)

Gender Diagnosis
55.97 + 11.72(range 28 – 84) 64 male (58.7%)45 female (41.3%) Type II IDDM: 48 (44%)Type II NIDDM: 26 (23.9%)

Type I DM: 13 (11.09%)

DM Type unspecified: 11 (10%)

Idiopathic neuropathy: 2 (1.8%)

Syphilis/Type I DM: 2 (1.8%)

Alcohol/ETOH: 2 (1.8%)

Agent Orange poisoning: 1 (.9%)

Cauda Equina Syndrome: 1 (.9%)

Hypothyroid: 1 (.9%)

Type II IDDM/Agent Orange: 1 (.9%)

Non-diabetic: 1 (.9%)

Table 1 Demographic Characteristics (N=109)

Overall, the two most common trigger types identified were acute injury and overuse at 44% (48/109) and 18.3% (20/109) respectively as seen in Table 2.  These were followed by diabetic ankle fracture and foot surgery (17/109) for the third most common trigger at 15.6% (17/109).  Infection was the trigger event in 6.4% of the total feet (7/109).


Trigger Type Frequency (%)
Acute injury 48 (44%)
Overuse 20 (18.3%)
DM Ankle Fx 17 (15.6%)
Sx 17 (15.6%)
Infection 7 (6.4%)

Table 2 Trigger Category Percentages

After categorizing the inciting event into a classification of a trigger type, the data was analyzed to compare each event to its associated anatomic location. Acute Trauma was distributed affecting the forefoot 4.2% (2/48), the tarsometatarsal joint 45.8% (22/48), the midtarsal 22.9% (11/48), the ankle 18.8% (9/48) and the Calcaneus 8.3%  (4/48). Diabetic ankle fractures accounted for 17 cases and led to a midtarsal arthropathy 5.9% (1/17) and an ankle arthropathy 94.1% (16/17) of the time. Surgical intervention resulted in 17.6% (3/17) forefoot arthropathy, 41.2% (7/17) tarsometatarsal arthropathy, 23.5% (4/17) midtarsal arthropathy and 7.6% (3/17) ankle arthropathy.  Infection, which accounted for 7 cases of arthropathy, was observed 71.4% (5/7) at the tarsometatarsal level and 28.6% (2/7) at the level of the ankle joint. Overuse injury was observed to lead to arthropathy in 20 patients with 50% of those observed at the tarsometatarsal level (10/20), 45% (9/20) at the midtarsal level and 5% (1/20) at the level of the ankle joint.

Based on a chi square test of general association, there is a statistically significant association between trigger category and anatomic classification (p < .0001) in terms of the difference in frequencies (Table 3).


Anatomic Classification
Trigger Category Acute Trauma Count 2 22 11 9 4
% within Trigger Category 4.2% 45.8% 22.9% 18.8% 8.3%
DM Ankle Fx Count 0 0 1 16 0
% within Trigger Category .0% .0% 5.9% 94.1% .0%
Sx Count 3 7 4 3 0
% within Trigger Category 17.6% 41.2% 23.5% 17.6% .0%
Infection Count 0 5 0 2 0
% within Trigger Category .0% 71.4% .0% 28.6% .0%
Overuse Count 0 10 9 1 0
% within Trigger Category .0% 50.0% 45.0% 5.0% .0%
Total Count 5 44 25 31 4
% within Trigger Category 4.6% 40.4% 22.9% 28.4% 3.7%

Table 3 Association Between Anatomic Site and Trigger Categories


This study examines patients with Charcot neuroarthropathy and investigates the individual trigger events leading to the development of the disease process to further our insight as healthcare providers. The different trigger categories, as well as the anatomic classifications for each event were evaluated.  Our results indicate that the two most common triggers for developing acute Charcot were acute trauma and overuse.  Also, 40% of the total cases involved, developed Sanders type II Charcot.  Anatomic site II arthropathy was the most common form of Charcot that developed in all of the trigger categories, with the exception of a diabetic ankle fracture, which was the second most common and generated mainly type IV arthropathy.  This supports the general teaching that tarso-metatarsal joint Charcot arthropathy is traditionally the most common anatomic type that is observed [6]. In the process of investigating individual trigger events, the authors encountered patterns of inciting events, while no statistical significance could be drawn from these anecdotal incidences. One mechanism that was most closely associated with a Sanders type II arthropathy was the action of stepping on a ladder. This becomes important as a significant number of our patients work in a more industrial environment and are likely prone to an overuse or acute type injury of the tarsometatarsal complex. A similar mechanism that was demonstrated in a handful of patients was the actions of stepping down to a lower level or onto a curb.  Through these mechanisms was both Sanders II and Sanders IV type injuries were associated. Ultimately, while the collection of these events was not statistically significant, they have provided enlightenment to the providers and have affected the questions asked during intake today.

The results of this study were compared to current literature available where other researchers have attempted to understand the causes of Charcot neuroarthropathy. When looking further into the data it is interesting to note that 39% of the original 179 feet could not recall any precipitating event to their acute Charcot.  These patients were ultimately eliminated from data analysis for the purpose of this study.  This is in contrast to Armstrong et al where 73% of the subjects could not identify a single trigger event; however, it is possible that there is overlap between the overuse category and these patients.7 Furthermore, Papanas et al reported patients recalling a traumatic event in 36% of their patient population with a 12% association with surgical intervention [6]. Regardless, it is important to remember a singular trigger event may not always be identifiable and Charcot arthropathy should not be ruled out of the differential diagnosis subsequently.

In order to perform a comprehensive assessment of the diabetic foot, it is important to incorporate other considerations. Foltz et al evaluated both vascular and neurological findings in patients with Charcot foot deformity in order to identify high risk factors for development of a protocol for early detection in the non-hospital setting [8].   Additionally, Armstrong and Lavery analyzed peak plantar pressures of Charcot and non-Charcot feet to examine if this was a risk factor for or associated with the development of Charcot [7].  In conclusion, the authors felt that measuring these plantar pressures may be an effective addition to the screening protocol for these types of patients [9]. Rajbhandari et al proposed that pathognomonic factors for Charcot neuroarthropathy, likely involve a synthesis of competing classic theories [10]. It was believed that a substantial number of cases were likely triggered by a traumatic event, which also instigated an abnormal vascular reflex resulting in hyperemia to osseous components [11].

The limitations of this study includes the fact that it was a retrospective analysis.  Additionally, the report of each trigger event was subjective and dependent upon the insight from each patient.

We believe that the information from this study could be used in order to better educate our diabetic neuropathic patients on the topic of Charcot neuroarthropathy to aid in preventing its onset or to expedite treatment modalities with earlier recognition. Another important point for both clinicians to remember and for patient teaching purposes, is that the repetitive and overuse activities should not be overlooked as these can lead to a significant amount of neuroarthropathy. It is extremely important that all diabetic patients with peripheral neuropathy are properly educated on Charcot. The repercussions of a missed diagnosis given the expansive list of complications secondary to Charcot neuroarthropathy must be impressed upon high-risk patients. The intention of this paper was to display the different trigger categories and their frequencies so that this information could be used for prevention and educational purposes.

Funding Declaration The authors have no financial interests to disclose. Neither this research, nor its publication was funded.

Conflict of Interest Declaration The authors have no interests to declare.


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