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Protected Weight Bearing During Treatment of Acute Charcot Neuroarthropathy: A case series

by Jeremy J. Cook, DPM,MPH,CPH, Emily A. Cook, DPM,MPH,CPH

The Foot and Ankle Online Journal 4 (7): 1

Standard of care in the treatment of acute Eichenholtz stage I Charcot neuroarthropathy includes complete non-weight bearing immobilized with total contact casting. This small case series of three patients focuses on patients with acute phase midfoot Charcot neuroarthropathy treated with non-casting immobilization therapy. All patients were male with a mean age of 48.7 (range 46-53) years. Patients were instructed to assume complete non-weight bearing during treatment. Due to financial restrictions, all patients reported fully weight bearing in the non-removable immobilization boot because of work related obligations. Immobilization therapy lasted a mean duration of 90.3 days (range 76 – 133 days) and was discontinued once there was clinical resolution of inflammation and osseous stability. Serial radiographs revealed absence of deformity progression and eventual consolidation in all cases. All patients remained ulcer and callus free during immobilization therapy, without progression of a rocker-bottom deformity, while fully weight bearing and maintaining full-time manual labor employment. This preliminary case series adds to the evidence base that it may be possible to allow protected weight bearing during acute phase Charcot neuroarthropathy with adequate immobilization of the foot at all times.

Key words: Diabetes, Charcot neuroarthropathy, Foot Deformity, Casting, Foot fractures, Diabetic Foot.

Accepted: June, 2011
Published: July, 2011

ISSN 1941-6806
doi: 10.3827/faoj.2011.0407.0001

Charcot neuroarthropathy is an increasingly common clinical entity encountered by foot and ankle professionals. In the early decades of the last century syphilis was the most commonly associated etiology. That has changed with the advent of insulin and the resulting extended survival of patients suffering from diabetes mellitus.

Delay in diagnosis and patient non-compliance can result in severe destruction of the foot and ankle with permanent disability from ulceration, infection, and eventual amputation. [1-14]

The standard of care for treatment of Eichenholtz stage 115 Charcot neuroarthropathy has been immobilization in a total contact cast and complete non-weight bearing. [16-20] The period of non-weight bearing immobilization should last until erythema, edema, and warmth subside and the foot becomes stable and consolidated enough to prevent anatomic destruction while ambulating. This process has been reported to last anywhere from a few months to over two years. [20-26]

Total contact casts (TCC) have been shown in numerous studies to be an effective immobilization device in the treatment of acute Charcot neuroarthropathy. [5,7-14,16-20]

It is recommended that TCCs be changed frequently in order to prevent cast irritation, ulceration and to maintain immobilization as edema subsides. Minor complications such as skin irritation are anticipated with TCC. The risk of major complications such as ulceration and infection can be minimized with proper application techniques, as well as frequent casts changes, which permit careful monitoring, and adequate patient education. [27] Many centers have specially-trained orthotists who apply TCCs on a routine basis. Most studies support changing TCCs for the treatment of Stage I Charcot neuroarthropathy every 1-2 weeks. [11,13,17,19,22,27-31] Some institutions have allowed weight bearing in the TCC due to its inherent stability with success in preliminary reports. [9,27-31]

Although weight bearing during stage I of Charcot neuroarthropathy is controversial, many patients tend to be non-compliant. This is because this period of prolonged non-weight bearing may be detrimental in quality of life and may pose to be an unacceptable disability. [32,33] While the alternative may be amputation, advances in immobilization technology may allow protected weight bearing during the early stages of Charcot without the development of severe deformity. [34,35] The purpose of this study was to report results of acute Stage 1 Charcot neuroarthropathy in individuals immobilized in a vacuum stabilization boot that maintained full weight bearing.

Case Series

Three consecutive patients presented with acute Stage I Charcot neuroarthropathy over a three month period (November 2009 to January 2010). All three patients had Brodsky type I deformity involving the tarsometatarsal and naviculocuneiform joints. [18] Patients were referred for examination and treated within two weeks of symptom onset. Clinical examination revealed erythema, warmth, and edema involving the midfoot with gross instability, crepitation with midfoot range of motion, and bounding pedal pulses. One patient had diabetic neuropathy while the other two were diagnosed with alcoholic neuropathy. Peripheral neuropathy was confirmed by the absence to detect the Semmes-Weinstein 10gm monofilament.

Two of the three patients reported a minor injury preceding the Charcot event. The third patient had had previous amputations of digits two and three for localized osteomyelitis secondary to contiguous digital ulcerations. All three patients were male with a mean age of 48.7 (range 46-53) years. All patients presented within two weeks of first symptoms and were ulcer free at the time of initial presentation with this being their first occurrence of Charcot neuroarthropathy. Radiographs were obtained with findings consistent with early signs of Charcot neuroarthropathy. (Fig. 1A and 1B) Magnetic resonance (MR) imaging further confirmed the diagnosis with diffuse bone marrow edema adjacent to the Lisfranc joint.


Figure 1A and 1B  Initial anterior posterior (AP) (A) and lateral (B) radiographs demonstrating soft tissue edema with early signs of osteolysis, cortical thickening, fragmentation, and osseous destruction within the tarsometatarsal and naviculocuneiform joints.

All three patients were treated with immobilization in a vacuum stabilization boot (VACOcast®, OPED Inc, Framingham, MA) with instructions to remain strictly non-weight bearing. (Fig. 2) Despite these recommendations, all three patients reported bearing weight on the affected limb in order to prevent loss of their job. All three patients were sole providers in their household with jobs that required extensive manual labor. The patients were compliant in wearing the boot at all times as this was verified through inspecting the undamaged compliance locks on the boot.

Figure 2   In this boot, by removing air from a vacuum cushion, small beads contour around the lower limb and create vacuum stabilization.

Serial monitoring was conducted by clinical examinations and plain radiographs. Patients were kept immobilized in the vacuum stabilization boot until resolution of edema, warmth (examined by palpation with back of hand and fingers and comparing to contra-lateral limb), and clinical stability was achieved. Successive radiographs were taken to ensure the absence of deformity progression every 3-4 weeks. (Fig. 3A, 3B and 3C) Throughout the treatment period each patient maintained normal full weight bearing in the conduct of their full-time jobs.


Figure 3A, 3B and 3C  Progression of acute phase of Charcot neuroarthropathy.  AP (A), Oblique (B) and lateral (C) views demonstrate increased osseous destruction and osteolysis.

Patients wore the vacuum stabilization boot for a mean of 90.3 days (range 76 – 133 days). One patient developed a superficial abrasion on the dorsal proximal interphalangeal joint of the second digit. This healed after two weeks of wound care and the additional of padding to the boot in this area. There were no other complications experienced. During the treatment of acute Stage I Charcot neuroarthropathy, all three patients remained ulcer and callus free while ambulating in the immobilization boot. Once the Charcot events had progressed to the consolidation phase, patients were transitioned to accommodative shoes or boots with supportive inserts.

Two of the three patients were compliant with accommodative shoes and molded insoles. After 16 months from the initial presentation, both patients have not developed ulcers, callus, or progression of deformity. (Fig. 4A, 4B and 4C) During the 12 weeks that the third patient was wearing the immobilization boot, the deformity did not progress and the patient remained ulcer and callus free.


Figure 4A, 4B and 4C  AP (A), Oblique (B) and lateral (C) views showing progression into chronic Charcot neuroarthropathy with maintenance of anatomic alignment with consolidation of osseous destruction.

However, the third patient did not obtain prescribed accommodative shoes or inserts citing financial limitations. He was subsequently lost to follow-up for five months after completing 12 weeks of immobilization therapy. His Charcot neuroarthropathy had developed a rocker bottom foot deformity and plantar midfoot ulcer after five months of interrupting care.


Management of Charcot neuroarthropathy is a complex process which requires flexibility and constant attention. This small case series demonstrates that despite the overt disregard for non-weight bearing management instructions, all patients were able to maintain employment and prevent progression of rocker bottom midfoot deformities during acute Eichenholtz stage I Charcot neuroarthropathy as there was continuous utilization of the vacuum immobilization boot.

Patients were continuously immobilized in a vacuum stabilizing below-knee boot with compliance confirmed by boot locks. There were minimal complications during the acute phase treatment with one patient developing a superficial digital abrasion from the boot. This was identified immediately and rectified by adjusting the boot. Despite fully weight-bearing, a rocker bottom deformity was prevented with adequate and constant immobilization.

Standard of care for acute Eichenholtz stage I traditionally includes total contact casting and complete non-weight bearing to prevent progression of deformity. This has been recently challenged by allowing weight bearing in the total contact cast in combination with frequent cast changes and close monitoring. Two prospective case series have reported successfully preventing deterioration of osseous alignment from acute phase Charcot deformity with weight-bearing total contact casts. [28,29]

The amount of non-restrained cumulative load forces across acute Charcot joints is also believed to increase the amount of deformity progression. By immobilizing the foot with a walking total-contact cast, the acute phase resolved and further progression towards a rocker bottom foot was prevented. [30]

The immobilization boot reported in this study was chosen for several reasons. Total contact casts require frequent changes and proper construction to prevent complications related to this casting technique. This immobilization boot had the advantage of clinical efficiency as no time was necessary beyond properly sizing and fitting the patient and providing instructions on its use. The vacuum boot can be adjusted to accommodate changes in edema. The removable sole allows patients to sleep with the boot without dirtying the linens. It also has a radiolucent frame that permits radiographic evaluation without removal. Finally, the compliance locking straps prevent unknown patient removal. Although none of the affected limbs had an open ulcer necessitating daily care, had local wound care been necessary by a visiting nurse an additional key would have been provided.

Limitations of this study include its retrospective nature. The initial treatment plan did not permit patients to weight bear during acute phase Charcot neuroarthropathy, however, weight bearing did not adversely impact the treatment outcome. Both mechanical and comparative studies are needed to further investigate the ability of nontraditional immobilization devices to effectively prevent osseous deformity in a disease which can cause permanent disability and eventual amputation. Future prospective studies with a larger sample size are needed to assess the long-term outcomes of this immobilization technique. Comparison studies of different immobilization techniques would also be very useful. Finally, the definition of adequate immobilization needs further investigation in order to achieve a balance of prevention of serious Charcot-related complications and quality of life.


Patients with acute Eichenholtz stage I midfoot Charcot neuroarthropathy were able to fully weight bear and maintain manual labor employment without development of a rocker bottom foot deformity while wearing a vacuum stabilization below-knee boot. Advances in immobilization therapy may allow improvement in the quality of life in acute phase Charcot neuroarthropathy.


1. Holewski, J, Moss KM, Stess RM, Graf PM, Grunfeld C. Prevalence of foot pathology and lower extremity complications in a diabetic outpatient clinic. J Rehab Res and Devel 1989 26: 35-44.
2. Sohn MW, Stuck RM, Pinzur M, Lee TA, Budiman-Mak E. Lower-extremity amputation risk after charcot arthropathy and diabetic foot ulcer. Diabetes Care 2010 33: 98-100.
3. van der Ven A, Chapman CB, Bowker JH. Charcot neuroarthropathy of the foot and ankle. J Am Acad Orthop Surg 2009 17: 562-571.
4. Sohn MW, Lee TA, Stuck RM, Frykberg RG, Budiman-Mak E. Mortality risk of Charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone. Diabetes Care 2009 32: 816-821.
5. Boulton AJ, Jeffcoate WJ, Jones TL, Ulbrecht JS. International collaborative research on Charcot’s disease. Lancet 2009 J373 (9658): 105-106.
6. Shibuya N, La Fontaine J, Frania SJ. Alcohol-induced neuroarthropathy in the foot: a case series and review of literature. J Foot Ankle Surg 2008 47: 118-124.
7. Nielson DL, Armstrong DG. The natural history of Charcot’s neuroarthropathy. Clin Podiatr Med Surg 2008 1: 53-62.
8. Frykberg RG, Belczyk R. Epidemiology of the Charcot foot. Clin Podiatr Med Surg 2008 1:17-28.
9. Pinzur MS. Current concepts review: Charcot arthropathy of the foot and ankle. Foot Ankle Int 2007 8: 952-959.
10. Sanders LJ. What lessons can history teach us about the Charcot foot? Clin Podiatr Med Surg 2008 1: 1-15.
11. Wukich DK, Sung W. Charcot arthropathy of the foot and ankle: modern concepts and management review. J Diabetes Complications 2009 23: 409-426.
12. Jeffcoate WJ. Charcot neuro-osteoarthropathy. Diabetes Metab Res Rev 2008 24 (Suppl 1): S62-65.
13. Petrova NL, Edmonds ME. Charcot neuro-osteoarthropathy-current standards. Diabetes Metab Res Rev 2008 24 (Suppl 1): S58-61.
14. Chantelau E. The perils of procrastination: effects of early vs. delayed and treatment of incipient Charcot fracture. Diabet Med 2005 22: 1707–1712.
15. Eichenholtz SN. Charcot Joints. Springfield, Illinois: Charles C. Thomas, 1966.
16. Shaw JE, His WL, Ulbrecht JS. The mechanism of plantar unloading in total contact casts: implications for design and clinical use. Foot Ankle Int 1997 18: 809-817.
17. Pinzur MS, Shields N, Trepman E, Dawson P, Evans A. Current practice patterns in the treatment of Charcot foot. Foot Ankle Int 2000 21: 916–920.
18. Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, editors. Surgery of the Foot and Ankle. Vol 2. 7th ed. St. Louis, Mosby. 1999, 895-969.
19. Pinzur MS, Shields N, Trepman E, Dawson P, Evans A. Current practice Patterns in the treatment of Charcot foot. Foot Ankle Int 2000 21: 916-920.
20. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot’s arthropathy in a diabetic foot specialty clinic. Diabetic Med 1997 14: 357-363.
21. Molines L, Darmon P, Raccah D. Charcot’s foot: newest findings on its pathophysiology, diagnosis and treatment. Diabetes Metab 2010 36: 251-255.
22. Pinzur, MS. Surgical vs. accommodative treatment for Charcot arthropathy of the midfoot. Foot Ankle Int 2005 25: 545-549.
23. Myerson MS, Henderson MR, Saxby T, Short KW. Management of midfoot diabetic neuroarthropathy. Foot Ankle Int. 1994 15: 233-241.
24. Alpert SW, Koval KJ, Zuckerman JD. Neuropathic arthropathy: review of current knowledge. J Am Acad Orthop Surg. 1996 4: 100-108.
25. Fabrin J, Larsen K, Holstein PE. Long-term follow-up in diabetic Charcot feet with spontaneous onset. Diabetes Care 2000 23: 796-800.
26. Schon LC, Easley ME, Weinfeld SB. Charcot neuropathy of the foot and ankle. Clin Orthop Relat Res 1998 349: 116-131.
27. Wukich DK, Motko J. Safety of total contact casting in high-risk patients with neuropathic foot ulcers. Foot Ankle Int 2004 25: 556-560.
28. Pinzur MS, Lio T, Posner M. Treatment of Eichenholtz stage I Charcot foot arthropathy with a weightbearing total contact cast. Foot Ankle Int 2006 27: 324-329.
29. de Souza LJ. Charcot arthropathy and immobilization in a weight-bearing total contact cast. JBJS 2008 90A:754-759.
30. Kimmerle R, Chantelau E. Weight-bearing intensity produces charcot deformity in injured neuropathic feet in diabetes. Exp Clin Endocrinol Diabetes 2007 115: 360-364.
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35. Stöckle U, König B, Tempka A, Südkamp NP. Cast immobilization or vacuum stabilizing system? Early functional results after osteosynthesis of ankle fractures. Unfallchirurg 2000 103: 215-219.

Address correspondence to: Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA.
Email: jeremycook@post.harvard.edu

1,2  Clinical Instructors in Surgery at Harvard Medical School, Division of Podiatric Surgery, Department of Surgery.
185 Pilgrim Road, PB Span 3, Beth Israel Deaconess Medical Center, Boston, MA. 617-632-7098

© The Foot and Ankle Online Journal, 2011

The Clinical Importance of the Os Peroneum: A Dissection of 156 Limbs Comparing the Incidence Rates in Cadavers versus Chronological Roentgenograms

by Brion Benninger, MD 1 , Jessica Kloenne 

The Foot and Ankle Online Journal 4 (2): 2

Introduction: The purpose of this study was to assess radiograph incidence versus cadaver incidence rates of the os perineum (OP) within the fibularis (peroneus) longus tendon (FLT) and to assess why broad variants have occurred in previous radiograph and cadaver studies. The OP or sesamoid bone in the FLT has a history of controversy regarding the terminology and frequency. Recent histological studies have proven sesamoid terminology. Cadaver studies have revealed high incidence rates (IR), yet virtually all texts and atlases exclude it. Clinicians recognize it in routine foot radiographs. No studies have compared IRs between cadavers and injured patients of the general population.
Methods: A literature search of texts, atlases, journals and websites was conducted identifying incidence of OP within the FLT. Dissection of 82 embalmed cadavers (M 52, F 30) identified the IR of the OP. Oblique foot radiographs from 1,025 individuals were examined.
Results: A literature review revealed OP in 20% of atlases, 7.69% in texts, and previous cadaver study results are 46%, 90%, and 14.9%. This study’s cadaver results reported an IR of 88.46% with an average age of 78.1 (45 – 89yrs). Radiographic results revealed 15.12% incidence with an average age 41.97 (10 – 89yrs). The average IR from 10 to 70 years was 13.32%. From 70 onwards it increased to 32.98%. The p value per decade from radiographic analysis was 0.0005.
Conclusion: This study suggests there is a high IR of an OP in cadavers (88.46%). This may be a result of the average age of cadavers 78.1 and the technique used to locate the OP. Radiographic results were significantly lower and may be explained by an age factor. Radiographs reviewed were from an emergency room where the majority of patients receiving foot radiographs were between the ages of 19 – 45. The clinical importance has been understated regarding the area of the os peroneum, which can be mistaken for styloid and Jones’ fractures.

Key words: Os peroneum, incidence, foot injury, sesamoid bone, Jones fracture, styloid process.

Accepted: January, 2011
Published: February, 2011

ISSN 1941-6806
doi: 10.3827/faoj.2011.0402.0002

The purpose of this study was to examine the important clinical relevance of the ‘os peroneum’ (OP) within the fibularis longus (FLT) by investigating the incidence of the OP between cadaveric specimens and radiological images.

The ‘os peroneum’ within the fibularis (peroneus) longus tendon has a history of controversy regarding its incidence in both individual and combined radiographic and cadaver studies. Radiographic and cadaveric studies have reported incidence rates of the OP within the FLT, however, a limited number of anatomical textbooks and atlases used by healthcare professionals and trainees mention or illustrate the OP.

Research to date reports a wide variation of incidence rates (IR), which are different in radiographic and cadaveric research. Previously Cilli, et al., in 2005 conducted a radiographic study on males only reporting 31.8% IR. A cadaveric study was conducted by Muehleman, et al., in 2009 which reported a 46% IR. Despite the various studies conducted thus far, no previous studies have conducted a comparison of incidence rates between radiographs and cadavers from separate populations. The objective of this research project was to assess radiograph incidence versus cadaver incidence rates of OP within the FLT and to assess why broad variants have occurred in previous radiograph and cadaver studies. (Fig. 1 and Fig. 2)

Figure 1 Os peroneum in the fibularis longus tendon. (Reproduced with kind permission from Lippincott Williams & Wilkins, Grant’s Anatomy, 12th edition.)

Figure 2 Location of os peroneum in the foot. (Reproduced with kind permission from Elsevier, Gray’s Anatomy, 40th edition.)


A literature search was conducted of anatomical texts and atlases, specialty texts, journals and websites regarding the presence or incidence of the OP within the FLT. Oblique foot radiographs from 1,025 individuals (range 10-89) were examined to identify OP within the FLT. (Fig. 3A and 3B) Dissection of 82 (156 sides) embalmed cadavers (52M, 30F) with a mean of 78.1 years (range 45- 89) was performed to identify the incidence rate of the OP within the FLT. A skin incision was made from the fifth toe to the styloid process distal to proximal along the lateral border of the foot. Then an oblique incision was made to the lateral malleolus to expose the FLT. (Fig. 4A)

Figure 3A and 3B Oblique radiographs of the OP in the FLT. (A and B)  (Thanks to the OHSU Radiology Department for radiograph.)

At the styloid process a horizontal incision was made along the surface of the foot to the opposite side, then exposing the FLT within the tunnel it traverses. The FLT was freed from its attachment point distally and reflected back. Palpation of the FLT was performed to identify the OP. A longitudinal incision was performed 2cm proximal and distal to the OP and then opened to reveal the ‘sesamoid bone’s’ existence or not. (Fig. 4B) A second examiner palpated and analyzed the longitudinal incision and reported their findings. A paired t-test was conducted on the radiographic data.

Figure 4A and 4B OP within the FLT in a cadaver.


The literature search revealed the OP within the FLT was discussed in anatomy texts (7.69%), contemporary atlases (20%) and specific imaging texts (16.6%). This study’s radiographic evaluation of OP within the FLT from 1,025 individuals with a mean age of 41.97 years had an incidence rate of 15.12% overall.

Incidence by ten-year increments revealed 12.16% for 10-19 years, 11.31% for 20-29 years, 13.87% for 30-39 years, 16.17% for 40-49 years, 15.15% for 50-59 years, 10% for 60-69 years, 41.38% for 70-79 years, and 19.44% for 80-89 years. The number of radiographs analyzed per ten-year increment was from approximately 100 individuals. (Graphs 1 and 2) The p value for the radiographic images was 0.0005. In this study, the incidence rate of the cadaver dissections was 88.46% with a mean age of 78.1.

Graph 1 Radiographic incidence of the OP within the FLT per ten-year increment.

Graph 2 Identification of the OP within the FLT in educational texts.


The OP is a sesamoid bone that is located within the FLT. [12] The shape of the OP can be round, oval, triangular, irregular and can also be found as bipartite or multipartite. [6,7]

The etiology of the OP is unknown; however, it has been thought that it arises from both mechanical and genetic factors. [7,11] A literature search of contemporary anatomical texts, atlases and specialty radiographic texts revealed incidence rates of 7.69%, 20% and 16.6%, respectively. This lack of recognition of the OP in commonly used texts and atlases contradicts radiographic and cadaver evidence from our study.

Our study’s incidence rate of identifying the OP within the FLT from radiographs (15.12%) was consistent with other radiographic studies. (Table 1). Radiographic studies report incidence rates of 31.8%, 4.7%, 14%, 14% and 9%. [3,4,1,11,13] The reason the incidence of the OP within the FLT in the images of our study was less than cadaveric results may be due to the average age of the individuals from the radiographs (41.97 years).

Table 1 Review of OP within the FLT in radiographic and cadaveric studies.

The radiographs reviewed were from an emergency room where on average the majority of patients receiving foot radiographs are between the ages of 19-61. [9] The incidence rate might have been higher if the average age of the individuals was higher. Another study had a mean age of 51 years. [11] Two other studies only provided the range of their subjects and none were greater than 72 years. [3,4] Two other radiographic studies did not provide any information on the mean age or range. [1,13] To collect comprehensive research on the radiographic incidence of the OP within the FLT, further data is required in the age range of 60 and up.

The IR of the OP within the FLT in the cadavers (88.46%) was consistent with one cadaveric study with an incidence rate of 90%.8 This consistency may be related to similar methods of identification of the OP within the FLT. Recent cadaveric studies have reported incidence rates of 46% and 14.9%. [7,10]

One study assessed radiographic imaging from the 33 cadavers dissected, but did not look at separate populations for radiographic and cadaveric data. [7] Furthermore, that study did not report the incidence rate of the OP within the FLT when solely palpating the FLT on cadavers; their incidence rate was reported after radiographic and histologic investigation. A combined radiographic (500 individuals) and cadaveric (20 cadavers) study showed 12.3% incidence rate; this study did not separate incidence rates for radiographic and cadaveric results. [5]

In our study, the average age of the cadavers (78.1 years) is much older than the average age of the individuals in the radiographs, which may contribute to the high incidence rate of the OP within the FLT in the cadavers. Other studies that researched incidence rate of the OP within the FLT in cadavers had mean ages that were consistent with our study (81.0, 75.2 and 77.7 years). [7,8,10] However, the age range (33-97 years) was only given for one of these studies. [8]

The method of identification may also contribute to the high incidence rate of the OP within the FLT because our study palpated and dissected open the OP, but did not use histology or radiology to confirm presence of OP from cadavers.

A conflict between cadaveric and radiographic results is the fact that cadaver incidence can be based on a partially ossified OP. Therefore a partially ossified OP could be recorded as positive. In contrast, an incomplete ossification may not be obvious or present on typical radiographs. A partially ossified OP can be cartilaginous and at times cartilage cannot be recognized on ordinary (not over or under penetrated images) radiographic images. [12]

A possible factor affecting the radiographic results of our study is that we used only those patients who presented to the emergency room with foot pain. It is not common for people over age 60 to present to the emergency room with sprained ankles or fractured 5th metatarsals. The over 60 age group population present acutely with hip fractures or with gout of the great toe. There may have been different results if we had randomly chosen from the general population for OP in the FLT.


The clinical importance has been understated regarding the area of the os peroneum, which can be mistaken for styloid and Jones’ fractures. The radiograph IR was always over 10% regardless the age group while the cadaveric incidence rate was 88.46%. This suggests that teaching the OP in the FLT is clinically relevant because lower limb injuries are common.


1. Burman MS, Lapidus PW. The functional disturbance caused by the inconstant bone and sesamoids of the foot. Arch Surg 1931 22: 936.
2. Carter DR, Orr TE, Fyhrie DP, Schurman DJ. Influences of mechanical stress on prenatal and postnatal skeletal development. Clin Orthop Relat Res 1987 219: 237-250.
3. Cilli F, Akcaoglu M. The incidence of accessory bones of the foot and their clinical significance. Acta Orthop Traumatol Turc 2005 39: 243-246.
4. Coskun N, Yuksel M, Cevener M, Arican RY, Ozdemir H, Bircan O, Sindel T, Ilgi S, Sindel M. Incidence of accessory ossicles and sesamoid bones in the feet: a radiographic study of Turkish subjects. Surg Radiol Anat 2009 31: 19-24.
5. Le Minor JM. Comparative anatomy and significance of the sesamoid bone of the peroneus longus muscle (os peroneum). J Anat 1987 151: 85-99.
6. Mellado JM, Ramos A, Salvadó E, Camins A, Danús M, Saurí A. Accessory ossicles and sesamoid bones of the ankle and foot: imaging findings, clinical significance and differential diagnosis. Eur Radiol 2003 13: L164-L177.
7. Muehleman C, Williams J, Bareither ML. A radiologic and histologic study of the os peroneum: prevalence, morphology, and relationship to degenerative joint disease of the foot and ankle in a cadaveric sample. Clin Anat 2009 22: 747-754.
8. Oydele O, Maseko C, Mkasi N, Mashanyana M. High incidence of the os peroneum in a cadaver sample in Johannesburg, South Africa: possible clinical implication? Clin Anat 2006 19: 605-610.
9. Reason for Visits to Emergency Room – National Hospital Ambulatory Medical Care Survey 1998-2006. U.S. Department of Health and Human Services; Centers for Disease Control and Prevention; National Center for Health Statistics.
10. Rühli FJ, Solomon LB, Henneberg M. High prevalence of tarsal coalitions and tarsal joint variants in recent cadavers sample and its possible significance. Clin Anat 2003 16: 411-415.
11. Sarin VK, Erickson GM, Giori NJ, Bergman AG, Carter DR. Coincident development of sesamoid bones and clues to their evolution. Anat Rec 1999 257: 174-180.
12. Stranding, S. Gray’s Anatomy: The Anatomical Basis of Clinical Practice, 40th ed. Philadelphia: Elsevier 2005, pg 1420.
13. Tsuruta T, Shiokawa Y, Kato A, Matsumoto T, Yamazoe Y, Oike T, Sugiyama T, Saito M. Radiological study of the accessory skeletal elements in the foot and ankle (abstract). J Jap Orthop Assoc 1981 55: 357-370.

Address correspondence to: Oregon Health & Science University
611 SW Campus Drive, Portland, OR 97239.

1 Department of Surgery, Department of Integrative Biosciences, Department of Orthopaedic Surgery & Rehabilitation, Department of Oral Maxillofacial Surgery, Oregon Health & Science University, Portland, OR.
2 Department of Integrative Biosciences, Oregon Health & Science University, Portland, OR.

© The Foot and Ankle Online Journal, 2011

Fracture of the Posterior Process of Talus with Pilon Fracture: A case report

by SS Suresh MS Orth, MCh Orth

The Foot and Ankle Online Journal 3 (12): 1

Fractures of the posterior process of the talus are extremely rare and more so when it is associated with a pilon fracture. Anatomical reduction and fixation of these injuries are important to prevent post traumatic ankle and subtalar arthritis and nonunion. The author presents a case of fracture of the posterior process of the talus with pilon fracture. In addition to these he also had ipsilateral, undisplaced extra articular fracture of the calcaneum, undisplaced fracture of the navicular and fracture of the first metatarsal.

Key words: Talus; Posterior process; Foot; Fracture.

Accepted: November, 2010
Published: December, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0312.0001

The posterior process of the talus has two tubercles, the medial and lateral, with the groove for the flexor hallucis longus tendon in between. The more prominent of these is the lateral tubercle. The posterior process is an intra articular component to the subtalar and ankle joints and any incongruity to the posterior process can lead to early degenerative arthritis of both joints.

Fracture of the entire posterior process of the talus is a very rare injury with only 13 cases reported to date. [1,2,3,4] Pilon fractures of the tibia account for 1-10% of lower limb fractures5, and is usually the result of high energy trauma in active people. Concomitant injuries reported with posterior process fracture include medial malleolus fracture [1], and subtalar dislocation6. Pilon fracture in association with fracture of entire posterior process of the talus is not reported so far. The patient in this study also had ipsilateral extra articular os calcis fracture, fracture of the navicular and fracture of the first metatarsal bone.

Case Report

A 29 year-old male expatriate worker was brought to the accident and emergency with history of a heavy sheet falling on his both lower legs. The right ankle and lower leg was grossly swollen. There was mild swelling of the left ankle with tenderness over the lateral malleolus. He didn’t have any co-morbid medical illness. He also had a puncture wound over the medial malleolus on the right. There was no distal neurovascular deficit.

X-rays performed in the emergency department showed comminuted fracture of the right distal tibia extending to the tibial plafond and the medial malleolus, with suprasyndesmotic fracture of the fibula. (Figs. 1 A and B, and 2) In addition, he so had undisplaced fracture of the right os calcis, navicular and first metatarsal bone. X-rays of the left ankle showed an undisplaced fracture of the lateral malleolus.

Figure 1 A and B Lateral (A) and anterior posterior (B) view x-rays of the ankle showing the extent of injury.

Figure 2 Lateral view of ankle showing posterior process fracture. (see arrow)

The puncture wound over the right medial malleolus was debrided in the emergency department operating room, and a back slab was given for comfort. Antibiotic prophylaxis was started with intravenous cephradine due to fear of infection on the medial side. Computed tomography (CT) scan of the right ankle showed minimally displaced fracture of the posterior process of the talus without significant comminution. (Fig. 3)

Figure 3A and 3B Computed tomography (CT) scan showing posterior process fracture. (A)  Fractured posterior talar process on axial CT. (B)

He was taken for surgery the very next day. Under epidural anaesthesia the fibular fracture was fixed first with a third tubular plate. The wound over the medial malleolus was debrided again and the pilon fracture was fixed through a minimally invasive approach, with stab incisions, and a spoon plate was used for stabilization. The fixation was checked with imaging intra operatively and the posterior process fracture was found minimally displaced. This was approached by extending the lateral incision and fixation was done with a 4 mm partially threaded cancellous screw. The peroneal tendons were displaced to visualize the fracture.

The soft tissue attachments to the fragment were not disturbed. The wound was closed in layers with a drain on the lateral side. Post operatively the leg was immobilized in a slab for 6 weeks. The patient remained in the hospital for 11 days due to necrosis of skin on the lateral side which eventually healed with dressings.

X-rays taken during the post operative period showed acceptable reduction of all fractures. (Figs. 4) The patient was followed up at 6 weeks where the immobilization was removed. The patient was also advised non weight bearing mobilization of the ankles. We were unable to follow up this patient as went to his home country and attempts to contact him failed. The patient was informed that data regarding his case would be used for publication and gave his written consent.

Figure 4A and 4B X-rays showing fixation of the fractures. (A)  X-rays Oblique view of ankle showing reduction of the posterior process fracture. (B)


Fractures of the posterior process of the talus are very rare injuries with only few published reports in the English literature. [1,3,7] Fracture of the posterior process of the talus involves both medial and lateral tubercles There are few reports of isolated fracture of the posterior process after the first report by Nasser and Manoli. [4,8,9] Subsequent to this reports of posterior process fracture with other ipsilateral injuries have been reported.

The posterior process of the talus has two tubercles, medial and lateral, with the groove for flexor hallucis longus in between. Lateral tubercle is the larger one and this projects more posterior than the medial tubercle. [4] The fractures of the posterior process cause damage to two joints; the posterior facet of the subtalar joint and the ankle joint. Forced plantar flexion of the foot compressing the posterior talus between the calcaneum and tibia is presumed to be the mechanism of injury. [2,3,8] Another mechanism documented is forceful inversion of the foot. [9]

Prompt diagnosis and appropriate reduction and internal fixation are needed to prevent complications of malunion; non union and post traumatic arthritis. [6] Management varies from conservative treatment [10] to immediate open reduction. [6]

Anatomical reduction is important to prevent avascular necrosis and also helps in early mobilization. Moreover presence of an os trigonum can add to the confusion. [4,11] Failure to diagnose undisplaced fracture can cause painful non-union and significant disability. [2,4,12] The commonest fracture in the posterior aspect of the talus is fracture of the lateral tubercle. Lateral tubercle fractures are often missed and misdiagnosed as ankle sprains. [12]

Posteromedial approach, [9] after mobilization of the neurovascular bundle is used by most of the authors. This fracture can be approached either through a posterolateral or posteromedial approach. [9] Nadim recommends open reduction if the displacement of the fragment is more than 3 mm. [1,9] Though conservative treatment is recommended for minimally displaced or undisplaced fractures the patients can have poor outcomes with persisting painful limitation of ankle movements and recurrent effusion. [12]

A CT scan can show the amount of displacement and the degree of comminution. [12] Reduction and stabilization of the fracture through a posteromedial incision is with risk of damage to the neurovascular structures. Flexor hallucis longus tendon may prevent accurate reduction by closed methods. [6] In the series by Bhanot, et al., one case was fixed through a separate postero lateral incision though the fracture was visualized and reduced through the medial approach. [1] In the case report by Naranja the fracture was approached through the posterolateral route. [6] The soft tissue attachments (insertions of the posterior talofibular ligament and the deltoid ligament) should be carefully preserved during surgery. [7]

Excision of the posterior part of the talus is suggested by Nyska in late diagnosed cases, though there are no published reports. [12] Concomitant fractures are not reported [6,7], and to the author’s knowledge the only report is that of medial malleolus and posterior process fracture by Bhanot, et al.,. [1] Naranja, et al., reported on a case of open medial subtalar dislocation in association with fracture of posterior process of the talus. [6]


High index of suspicion is needed to diagnose isolated posterior process fracture, but if associated with concomitant injuries the diagnosis becomes easy. A CT scan is useful to determine the amount of displacement. Early operative intervention and fixation prevents post traumatic arthritis.


1. Bhanot A, Kaushal R, Bhan R, Gupta PN, Gupta RK, Bahadur R. Fracture of the posterior process of talus. Injury 2004; 35: 1341-1344.
2. Ahmad R, Ahmad SMY. Fracture of the posterior process of the talus: An unusual injury. Emerg Med J 2007: 24: 867.
3. Prasad G, Mittal D, Harlekar V, Raut VV. Fracture of the posterior process of the talus: A case report. Eur J Orthop Surg Traumatol 2007; 17: 417-419.
4. Nakai T, Murao R, Temporin K, Kakiuchi M. Painful nonunion of fracture of the entire posterior process of the talus: a case report. Arch Orthop Trauma Surg 2005; 125(10) 721-724.
5. Sirkin M, Sanders R. The treatment of Pilon fractures. Orthop Clin North Am 2001; 32(1): 91-102.
6. Naranja RJ Jr, Monaghan BA, Okereke E, Williams GR Jr. Case report: Open medial subtalar dislocation associated with fracture of the posterior process of the talus. J Orthop Trauma 1996; 10(2): 142-144.
7. Chen YJ, Liang SC, Huang TJ. Fracture of entire posterior process as an obstacle to reduction of an anterior talar subluxation: Case report. J Trauma 1997; 42(2): 314-317.
8. Nasser S, Manoli A. Fracture of the entire posterior process of the talus: a case report. Foot Ankle 1990; 10(4): 235-238.
9. Nadim Y, Tosic A, Ebraheim N. Open reduction and internal fixation of fracture of the posterior process of the talus: A case report with review of the literature. Foot Ankle Int 1999; 20(1): 50-52.
10. Jimulia TR, Parekh AN. Fracture of the entire posterior process of the talus. J Postgrad Med 1995; 41: 54-55.
11. Kose O, Okan AN, Durakbase MO et al. Fracture of the os trigonum: a case report. J Orthop Surg 2006; 14(3): 354-356.
12. Nyska M, Howard CB, Matan Y, Cohen D , Peyser A, Garti A, Bar-Ziv J. Fracture of the posterior body of the talus-the hidden fracture. Arch Orthop Trauma Surg 1998; 117: 114-117.

Address correspondence to: SS Suresh MS Orth, MCh Orth, PO Box 396, Ibri 516, Oman email: dr.s.s.suresh@gmail.com

1 Head of Department of Orthopaedics, Department of Orthopaedics, Ibri Regional Referral Hospital, PO Box 46 Ibri 516, Sultanate of Oman.

© The Foot and Ankle Online Journal, 2010

Primary Modified Blair Arthrodesis for Group-III Hawkins Fracture-Dislocation: A Series of Five Cases

by Arunangsu Bhattacharyya, MS(Ortho)1 , Dibyendu Biswas, MS(Ortho)2 , Rajat Ghosh,M.B.B.S. 3

The Foot and Ankle Online Journal 3 (10): 1

Background: Fracture of the neck of the talus with dislocation of talo-tibial joint and subtalar joint might be one of the worst injuries that can happen around the ankle joint. Almost all cases are complicated with avascular necrosis of the body of the talus and takes years to be revascularized even after prolonged non weight bearing. Different types of arthrodesis has been advocated by several authors. In the reported series, Blair fusion is the opted procedure because of several merits.
Methods and Material: Five patients with Hawkins Group III were selected in this series. (4 male, 1 female) One patient had compound fracture-dislocation. They were treated with Blair arthrodesis and followed up for more than two years with serial radiographs and assessment of tibiopedal movement.
Results: Three patients (60%) recovered with excellent result with range of Tibiopedal movement was 15 to 20 degrees and it was painless and one had good result (20%) with occasional pain and range of movement was 10 to 15 degrees. One patient had pain on walking and the outcome was graded as poor (20%) and range of movement was less than 10 degrees. Heel shape and heel height were maintained after surgery.
Conclusions: Blair fusion may be recommended as it is a relatively easy way out of a complex problem around the ankle. Remained tibiopedal movement helps the patient to walk more physiologically

Key words: Fracture talar neck, Hawkins fracture-dislocation, Dislocation of body, Primary Modified Blair fusion, arthrodesis.

Accepted: September, 2010
Published: October, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0310.0001

Fracture of the neck and the body of the talus is one of the most devastating injuries around the ankle. Fractures are very often complicated with dislocation of talo-navicular or subtalar or talo-tibial joint.

Fractures that create difficulty in management are fractures of the talar neck with or without dislocation; dislocations of the body of the talus; and fractures with loss of a segment of the body of the talus because those are commonly complicated with avascular necrosis of the talus. There are different opinions on suitable treatment of this type of injury. Talar neck fracture and talar body dislocation can occur due to forced dorsiflexion of the talus against the anterior edge of the tibia. Non-displaced fracture of the body of the talus, subtalar or talonavicular subluxation or dislocation can be treated with closed manipulation and plastering.

In 1939, Miller and Baker recommended subtalar or pantalar fusion for the fractures with poor reductions. [1] Triple or subtalar arthrodesis as treatment of improperly reduced fracture dislocation of talus was suggested by Schrock, et al.,. [2]

In 1943, Blair described a type of tibiotalar fusion in which the body of the talus was excised and a sliding cortical bone graft was positioned between the anterior aspects of the tibia and the head of the talus. [3]

In 1969, Detenbeck and Kelley recommended talectomy and tibiocalcaneal compression arthrodesis as the primary treatment for fracture-dislocation of the talus. They reported no significant functional disability after this procedure, but it has the disadvantages of widening the hind part of the foot and shortening the foot, both of which make shoe fitting difficult. [4]

In 1970, Hawkins proposed a very useful classification of talar neck fractures. In Group I, the vertical fracture of the neck must be undisplaced. In Group II, the fracture is displaced and the subtalar joint is subluxated or dislocated, and the ankle joint normal. In Group III, the fracture fragments are displaced and the body of the talus is dislocated from both the ankle and subtalar joints. [5] Incidence of avascular necrosis of body of talus is different in each type.

Group I undisplaced fractures of talar neck are usually not complicated with avascular necrosis. [5,6,7] Fractures of the neck associated with subtalar subluxation or dislocation had an incidence of avascular necrosis of 36 per cent in Kenwright and Taylor’s series. [7] Hawkins series acknowledged avascular necrosis in 42 per cent of his Group-II fracture-dislocations, but union of the fracture took place in all. [5] Incidence of avascular necrosis in Group III fracture-dislocation ranges from 75 [7] to 100 [8] per cent. According to Watson-Jones avascular necrosis is almost inevitable in fractures of the talar neck with dislocation of the body. So avascular necrosis following fracture of the neck of the talus is a very common incidence, hence, it is a challenging subject for the orthopaedic or podiatric surgeon.

Harry D. Morris and associates, in1971, did modify Blair method of tibio-talar fusion and added a cortical screw through the graft up to posterior cortex of the distal end of the tibia and a Steinmann pin through calcaneus into the Tibia to stabilize the Ankle. [9] The present paper reports five almost such operations with follow-up of two years. In this series part of the body of talus was not excised. It was positioned in between calcaneus and tibia with cancellous bone graft taken from bed of sliding cortical graft with the idea that inter positioned cortical and cancellous bone would make sound ankylosis of ankle with maintenance of heel height.

This reported series has shown the results of the treatment of five cases of fracture of talar neck with dislocation of body after primary Blair’s method of fusion modified by Morris, et al,. Cases were followed up for more than two years.

Subjects and Methods

In our series, five cases with fracture of the neck of the talus with talar body dislocation were included. It was of Group III according to Hawkins classification. Study was conducted from the year 2006 to 2010. (i.e. for four years) Out of five patients, four were male and one was female. Median age was approximately thirty years. (range 24 – 40 years) Right ankle was injured in four cases. Median follow-up was up to 28.6 months. (range 24 – 35 months) In one case, the fracture was of compound type. Initially wound was debrided and sensitive intravenous antibiotic continued for two weeks before final surgery. (i.e. tibio-talar fusion)

Primary Blair fusion modified after Morris, et al., was the preferred option in the reported series. Ethical committee permission was taken for this study.

In all cases, surgery was delayed routinely to provide time for swelling to subside. Absence or reduction of swelling helped to do thorough, meticulous dissection along the tissue planes.

Figures 1-3 shows the first example of a case of a modified Blair fusion in a group III – Hawkins fracture dislocation. Here, the dislocated part of the body of the talus was excised. The gap between calcaneus and tibia was filled with cancellous bone taken from lower tibia, anterior surface from the bed of sliding cortical graft and ipsilateral iliac crest. Remaining steps of the surgical procedure were almost same like those of Morris modification of Blair fusion i.e. one cortical screw was used to fix the sliding graft and thick K-wire of 2.5mm diameter was used instead of Steinmann pin.

Figure 1 Example 1 – Case 1 (see table 1): Fracture of the neck of the talus with dislocation of the body (i.e. Group -3, Hawkins fracture with no neurovascular deficit.)

Figure 2  Example 1 – Case 1:  Radiograph shows that the talar body was excised and Ankle fused with a 2.5mm K-wire and a 4.5 mm cortical screw, passed through a sliding tibial graft and up to posterior cortex of tibia. (Modified Blair fusion)

Figure 3 Example 1 –  Case 1:  The patient now stands on the floor with both feet on the ground and shape of left foot is well maintained after Modified Blair fusion.

The operation was performed by exposing the ankle through `universal incision’ to foot and ankle (i.e. antero-lateral approach.) Incision was started at the upper end from eight to ten centimeters above the ankle joint and extended distally and end at the base of the fourth metatarsal. Incision was made over the fascia and the superior and inferior extensor retinacula down to the periosteum of the tibia and the capsule of the ankle joint. This dissection usually divides the anterolateral malleolar and lateral tarsal arteries.

Cutaneous nerves were identified and protected. Extensor digitorum brevis muscle was detached from its origin and reflected distally. Extensor tendons, the dorsalis pedis artery and the deep peroneal nerve were retracted medially and the capsule was incised to expose the ankle.

With the joint widely exposed, dislocated talar body was excised with an osteotome or nibbled out and the head and neck was left undisturbed. The talonavicular joint and anterior and medial portions of the talocalcaneal joint were untouched. A sliding graft 2.0 by 6.0 centimeters was sliced from the distal anterior portion of the tibia with the help of a thin power saw. This graft was placed into a notch of approximately two centimeters deep made into the neck of the talus. The ankle was held in roughly 10 to 15 degrees of plantarflexion while the graft was fit into the neck of the talus. The graft was fixed with a cortical screw of 4.5mm diameter with lower tibia and a thick K-wire of 2.5mm diameter was inserted through the plantar aspect of the heel traversing the calcaneus and extending into the medullary canal of the tibia for 10 – 12 centimeters.

Cancellous graft was packed around the fusion site. Graft was harvested from bed of the sliding graft or ipsilateral iliac crest. Subjects have given informed consent, and that the study has been approved by an institutional review board. A below knee plaster slab was applied after surgery for better soft tissue healing. Cast was substituted after stitch removal and K-wires were routinely taken out after four weeks of surgery. (Figures 4, 5A, 5B, 6A and 6B) Non –weight bearing crutch walking was continued up to almost 12 weeks after surgery. They were followed up at monthly interval for one year.

Figure 4 Example 2 – Case 4 (see table 1):  Post operative photograph shows the Steinmann pin introduced from plantar surface of heel which is removed prior to cast application.


Figure 5A and 5B Example 2 – Case 4 (see table 1):  Post operative radiographs show advanced fusion and nice graft incorporation lateral (A) and anteroposterior (B) views.


Figure 6A and 6B Example 2 –  Case 4 (see table 1):  Post operative Photographs shows healed Antero-Lateral incision, anterior view (A) and lateral view (B), started   8 to 10 cm above the ankle and extended downwards over the joint and in the line of fourth metatarsal bone more distally over foot.

From second year onwards patients were followed up at every six months in Outpatient Department. The operated ankle was assessed with serial roentgenograms to look for progress of fusion with proper bony alignment and measurement of tibiopedal movement. Tibiopedal motion is defined as the curve of motion between maximum dorsiflexion and maximum plantarflexion of ankle and the angles were subtended by the long axis of the tibia and that of the foot in the lateral projection. The range of tibiopedal motion was measured with use of a goniometer between the axis of the tibia and the foot in positions of maximum dorsiflexion and plantarflexion.

In our study, results were considered excellent if the patient had completely asymptomatic foot and ankle and comfortable in Activities of Daily Life (ADL) and if tibiopedal movement ranged from 15 to 20 degrees. If there was occasional discomfort which caused no restriction in ADL and tibiopedal movement ranged from 10 to 15 degrees, then results were considered good. Poor result was with less than 10 degree tibiopedal movement and painful ankle to limit ADL.


According to the above mentioned protocol all five patients were followed up and evaluated after surgery. Mean age of patients in this series was twenty nine years. Right sided ankles were more commonly affected here (4:1). Roughly 4 months was required for bony fusion to take place. (range 3 – 6months)
Three cases out of five were considered as with excellent outcome, two were with good outcome after follow up according to the mentioned criteria.

Tibiopedal movement was 15 to 20 degrees in three cases and 10 to 15 degrees in one case and lower than 10 degree in one case. Sound fusion took place in four cases. In one case fusion was not sound, so it was painful on walking. It was with poor outcome. Another case with good result had occasional discomfort in ankle though there was solid bony fusion. Patient who had compound Group- III fracture dislocation had poor outcome in follow up. It was possibly due to formation of fibrosis from infected tissues inside even after thorough primary wound clearance and formation of pseudoarthrosis at fusion site. But heel height and shape was maintained in all cases. Inversion and eversion was partially restricted in all patients.

Antero lateral incision easily and widely exposed the ankle without any neurovascular injury. It could be freely extended upwards or downwards to fulfill the requirement during surgery. In one case posterolateral exposure was also necessary for removal of posteriorly dislocated body of the talus in addition to standard anterolateral incision. Table 1 shows the details of all five cases of this series.

Table 1 This table compares basic descriptive information of five cases with a Hawkins Group III fracture–dislocation of neck of talus treated with Modified Blair arthrodesis. They were followed up for two to three years. Three out of five patients had an excellent result.


Fracture of the neck of the talus, treated with Blair fusion or with its different modifications, has been published in few journals in different times. But it has not been discussed and published at many places as it deserves .In the reported series five cases of Hawkins Group III were operated with modified Blair’s fusion.

In 1943, Blair used a distal tibial sliding cortical graft without fixation in two patients with acute fracture of the neck of the talus. At the time of follow-up (minimum, four months), both fractures had united in follow-up (minimum, four months).3 Morris et al., in 1971 modified the procedure .They used a cortical screw up to posterior cortex of tibia to fix the sliding graft and a Steinmann pin introduced through planter surface of heel traversing calcaneus into the tibia by 10 to 12 centimeters. Four of their ten patients had a talar fracture with avascular necrosis, and six had an acute fracture. Seven had an excellent result and three, a good result.9 Later, Morris reported a series of four patients with a minimum two months follow-up after modified Blair procedure for the treatment of a fracture and osteonecrosis.10 Result was excellent in those two cases.

MD Dennis and HS Tullos, in 1980 ,performed a retrospective clinical and roentgenographic study on seven patients who underwent Blair tibiotalar arthrodesis with the average follow-up was 3.9 years. Results were good in five patients, fair in one, and poor in one. In two patients, pseudoarthrosis developed: painful in one and asymptomatic in one. [11]

In 1982, Lionberger, et al., described arthrodesis of the distal aspect of the tibia to the talar neck with use of a pediatric hip-compression screw. Five patients were treated and followed up for a mean of one year, one developed a delayed union. [12] Canale and Kelly reported a series of seventy-one fractures through the neck of the talus. Blair procedure was used for two fractures but both had poor result. [13]

In the reported series five cases were included. All five cases were categorized as Hawkins Group- III. (i.e. fracture of neck of the talus with dislocation of talo-tibial joint and subtalar joint, full displacement of the body of the talus from ankle) Fractures were treated with primary modified Blair arthrodesis because there was 75 to 100 percent chance of development of avascular necrosis of the body of the talus after this type of fracture-dislocation according to several reports.

Morris and associates, in 1971 advocated immediate excision of the extruded body for patients with comminuted fractures of the talar body as well as those with closed Group- III fracture-dislocation of talar neck since avascular necrosis occurs in over 90 per cent of these injuries. In this reported series, the modification was also after those of Morris. (i.e. one cortical screw and one thick k-wire were used)
In contrary to the modification presented by Morris, the body of the talus was partially excised in this study group with the hope that remained cortical bone with added cancellous bone from lower tibia would make sound fusion with maintenance of height of the heel. K-wire inserted through calcaneus into the tibia enhanced the stabilization of ankle construct for first four weeks. That helped the fusion process to take place initially.

Most of our patients had a successful clinical result with high rate of union, in spite of the complex nature of their problems. Three cases out of five (60%) were considered as excellent, one was with good (20%) and one (20%) was with poor outcome after follow up of almost two years. Tibiopedal movement was 15 to 20 degrees in three cases and 10 to 15 degrees in one and less than 10 degrees in one case. Fusion took place in all cases. Two cases had occasional discomfort in ankle though there was solid bony fusion. Heel height and shape was maintained in all cases.

In essence, a modified Blair arthrodesis may be opted for patients who have Hawkin’s Group III fracture- dislocation. It has the advantage over tibiocalcaneal arthrodesis of giving a normal-appearing foot, producing no shortening, and allowing motion to remain at the talonavicular and anterior subtalar joints thus helping the patients to walk with comfort.


Modified Blair fusion may be recommended for fracture of the neck of the talus with dislocation of talar body, as it is a relatively easy way out of a complex problem around the ankle. As avascular necrosis of talar body after Group III fracture- dislocation takes place in almost all cases, primary osteosynthesis has practically no role in management. Postoperative tibiopedal movement also helps the patient to walk more physiologically. Above all, heel height and shape is maintained after Blair fusion, so patients usually enjoy well fitted shoe.


1. Miller 0L, Baker LD. Fracture and fracture-dislocation of the astragalus. Southern Med J 1939 32: 125-136.
2. Schrock RD, Johnson HE, Waters CH, Jr. Fractures and fracture-dislocations of astragalus (talus). JBJS 1942 24A: 560-573.
3. Blair HC. Comminuted fractures and fracture dislocations of the body of the astragalus. Operative treatment. Am J Surg1943. 59: 37-47.
4. Detenbeck LC, Kelly PJ. Total dislocation of the talus. JBJS 1969 51A: 283-288.
5. Hawkins LG. Fractures of the neck of the talus. JBJS 1970 52A: 991-1002.
6. Colart WD. “Aviator’s Astragalus”. JBJS 1952 34B: 545-566.
7. Kenwright J, Taylor R0. Major injuries of the talus. JBJS 1970 52B: 36-48.
8. Pennal GF. Fractures of the talus. Clin Orthop1963 30: 53-63.
9. Morris HD, Hand WL, Dunn AW. The modified Blair fusion for fractures of the talus. JBJS 1971 53A: 1289-1297.
10. Morris HD. Aseptic necrosis of the talus following injury. Orthop Clin North America 1974 5: 177-189.
11. Dennis MD, Tullos HS. Blair tibiotalar arthrodesis for injuries to the talus. JBJS 1980 62A: 103-107.
12. Lionberger DR, Bishop JO, Tullos HS. The modified Blair fusion. Foot and Ankle 1982. 3: 60-62.
13. Canale ST, Kelly, FB Jr. Fractures of the neck of the talus. Long-term evaluation of seventy-one cases. JBJS 1978 60A: 143-156.

Address correspondence to: Dr Arunangsu Bhattacharyya,MS(ORTHO)
A-8/4,Bidhan Abasan,Block-FB,Sector-3,Saltlake,Kolkata-700097.West
Bengal,India. Email: orthoarunangsu@yahoo.com

Assistant Professor. ,Dept. of Orthopaedics, Medical College,Kolkata.
Assistant Professor, Dept. Of Orthopaedics, North Bengal Medical College & Hospital,West Bengal.
Medical Officer. North Bengal Medical College & Hospital.

© The Foot and Ankle Online Journal, 2010

Congenital Fibular Sesamoid Aplasia: A case report

by Tugrul Alici, MD1, Semih Dedeoglu, MD2, Yunus Imren, MD3, Hakan Gundes, MD4

The Foot & Ankle Journal 2 (2): 1

Congenital absence of the lateral sesamoid bone is a relatively rare condition. Literature review reveals very few case presentations relevant to this condition. We present a case of lateral sesamoid aplasia that was incidentally detected upon roentgenograms of a patient presenting with a fracture to the base of the proximal phalanx.

Key words: Lateral sesamoid, fibular sesamoid, phalangeal fracture, aplasia, absent sesamoid

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: January, 2009
Published: February, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0202.0001

Case Report

A 31 year-old male hit his right foot during a rafting event. The patient presents with pain and swelling to the right foot. Previous treatment included cold compression and irregular use of analgesics for pain and swelling. The physical examination demonstrated edema around the first metatarsophalangeal joint, palpation-induced tenderness at the medial aspect of the joint, with complete and painful range of motion. Further examination with plane foot anteroposterior radiographs showed a medial, non-displaced fracture at the base of proximal phalanx. (Fig.1)

Figure 1  Radiograph showing medial, non-displaced, proximal phalangeal fracture.  Aplasia or an absent fibular sesamoid is also seen.

In addition, the lateral or fibular sesamoid appeared aplasic or absent in routinely-ordered foot axial sesamoid radiograph. (Fig.2)

Figure 2  Axial sesasmoid radiograph reveals absent fibular sesamoid with a slightly visable ossified region central to the aplastic sesasmoid.

The patient was questioned about any previous problems relating to his right foot. The patients other sport activity included basketball once or twice a week. He denies any injury to his right foot from this activity and has had no previous foot surgery. Physical examination of the right foot was considered as normal except of the signs associated with the proximal phalangeal fracture. It was decided that this variation had no bearing on functional loss or activity for the patient. He was placed in a short leg circular cast, non-weight bearing for 2 weeks. The cast was then removed and partial weight bearing was provided through soft shoes. Complete weight bearing was allowed at 4 weeks and sport activities was permitted at the end of 2 months. A 6-month follow-up of patient demonstrated that the lateral or fibular sesamoid aplasia, considering his younger age, did not adversely influence his attendance to sport activities before or after injury.


Sesamoid bones of the foot originate from a cartilage bud at the 12th gestational week. [1] Ossification usually occurs between 8 and 10 years of age. [5] Inferior contact surfaces of metatarsal heads become flattened with compression and form the intersesamoid ridge called crista. [2]

The reasons for development of sesamoid aplasia are not fully understood but it is thought to be congenital. Congenital absence or aplasia of one or two of the sesamoid bones of toe is reported to be rare. It is reported that lateral or fibular sesamoid aplasia is rarer than medial or tibial sesamoid aplasia. [6,7] It is known that sesamoid bone excision in hallux valgus surgery (i.e. McBride bunionectomy) may result in varus, valgus, and hallux extensus or cock-up hallux deformities by altering the biomechanics of the toe. [2,4]

Similar to the reviewed literature, findings of physical examination of this aplasia was assessed to be within normal limits without rendering loss of function. The hallucal sesamoids, although small and seemingly insignificant, play an important role in the function of the great toe by absorbing weight-bearing stress, reducing friction, and protecting tendons. [8,9] They are also known to exert biomechanical features similar to that of the patella by increasing the efficiency of flexor hallucis brevis muscle by elevating its lever arm. [4,5] Secondary causes of aplasia may include infection. A case of sesamoid bone resorption secondary to infection was reported by Conway, et al. [3] The reason for normal biomechanics of toe in congenital sesamoid aplasia may be the presence of a cartilaginous sesamoid, which is non-calcified, and hence not seen in direct roentgenogram. [7]


1. Brenner E, Gruber H, Fritsch H. Fetal Development of the first metatarsophalangeal joint complex with special reference to the intersesamoidal ridge. Ann Anat 184:481-487, 2002.
2. Brenner E. The intersesamoidal ridge of the first metatarsal bone: anatomical basics and clinical considerations. Surg Radiol Anat. May;25(2):127-131, 2003.
3. Conway WF, Hayes CW, Murphy WA. Total resorption of the lateral sesamoid secondary to Pseudomonas aeruginosa osteomyelitis. Skeletal Radiol 18:483-484,1989.
4. Coughlin MJ. Sesamoids and accessory bones of the foot. In Mann RA, Coughlin MJ (eds) Surgery of the Foot and Ankle, 7th Edition. Mosby, St Louis, vol. 1, pp.437-499, 1999.
5. Downey MS, Merritt SC, Sharrock-Maher CJ, Bernbach MR. Digital and Sesamoid Fractures. McGlamry’s Forefoot Surgery ,LWW, Philadelphia 559-573, 2004.
6. Goez J, De Lauro T. Congenital absence of the tibial sesamoid. J Am Podiatr Med Assoc 85:509-510,1995.
7. J.M. Le Minor. Congenital absence of the lateral metatarso-phalengeal sesamoid bone of the human hallux. Surg Radiol Anat. 21(3):225-227,1999.
8. Richardson EG: Hallucal sesamoid pain: causes and surgical treatment. J Am Acad Orthop Surg 7(4):270-278,1999.
9. Cardona,T., Kline, A. Surgical excision of painful fibular sesamoid. The Foot and Ankle Journal 1(8):2, 2008.

Address correspondence to:
Tugral Alici, MD
Department of Orthopedics and Traumatology
University of Maltepe, Istanbul, Turkey
Feyzullah Cad. No:39 34843

Email: tugrulalici71@hotmail.com

1Asistant Prof. , Department of Orthopaedics & Traumatology, Maltepe University, Istanbul.
2Department of Orthopaedics & Traumatology, Vakif Gureba Training and Research Hospital, Istanbul.
3Department of Orthopaedics & Traumatology, Vakif Gureba Training and Research Hospital, Istanbul.
4Prof., Department of Orthopaedics & Traumatology, Maltepe University, Istanbul.

© The Foot & Ankle Journal, 2009

Divergent Lisfranc’s Dislocation and Fracture in the Charcot Foot: A case report

by J. Terrence Jose Jerome, MBBS, DNB (Ortho), MNAMS (Ortho)1

The Foot & Ankle Journal 1 (6): 3

A case report discusses the presentation, diagnosis and treatment of a 45 year old diabetic man with a divergent, Lisfranc’s dislocation of the first metatarsal in a Charcot foot. The patient also presents with associated laterally subluxed lesser metatarsals and multiple fractures. Conservative treatments such as TTC or total contact casting, prefabricated pneumatic walking brace (PPWB), patellar-tendon brace and CROW custom orthosis are discussed.

Key words: Charcot foot, Lisfranc’s dislocation, fracture

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: May 2008
Published: June 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0106.0003

Charcot joint in the foot typically refers to painless fracture and dislocation of the foot in patients without normal sensation or feeling in their foot. Loss of sensation in the foot for any reason can be responsible for developing a Charcot fracture, although this is most commonly seen with neuropathy. Neuropathy of the nerves that affect the foot is most commonly seen with diabetes, but is associated with other diseases as well. Treatment depends on the severity of the condition and the amount of deformity that is present.

We present a 45 year old diabetic man with Lisfranc’s dislocations along with fracture of 2,3,4,5 metatarsals. These patients frequently present complaining of a deep, aching, non-descript pain in the ankle joint that worsens with activity.

Case Report

A 45 year old man came to our out patient department with complaints of swelling in the left foot for 20 days duration. There was no history of trauma, fever or constitutional symptoms. The patient is a non-insulin dependent diabetic on oral hypoglycemic drugs. The swelling was diffuse, red, warm, non tender on palpation. (Fig. 1)

Figure 1   Diffuse swelling is noted to the left foot in a typical, Charcot presentation.  The swelling is diffuse and non-painful.

There was no sinus or active discharge. Radiographs of the foot showed fractures at the neck of 2,3,4, and shaft of 5 metatarsal along with divergent type of Lisfranc’s dislocation, bony destruction, fragmentation, joint subluxation and bony remodeling. (Figs. 2,3)

Figure 2   Oblique views reveal a divergent, Lisfranc dislocation of the first metatarsal with associated lesser metatarsal fractures.

Figure 3   Dorsoplantar view reveals complete dislocation of the first metatarsal at the medial cuneiform articulation.  Typical TMT joint fracture, fragmentation, joint subluxation and bone remodeling is seen.

Random blood sugar was 201mg/dl. C-reactive protein was negative; Erythrocyte sedimentation rate was 12mm/hr. Other blood parameters were normal. The patient was treated with a total contact cast.

Casts were replaced approximately every 2 weeks. The foot was inspected, and cutaneous temperature measurements were done. Serial plain radiographs were taken approximately every month. Casting lasted for 3 months. We used a patellar tendon¬ bearing brace in addition to custom-molded footwear after the cast. The brace was eliminated from the regimen after six months. Thereafter, continued use of custom footwear to protect and support the foot was given.


Charcot neuropathy is a progressive deterioration of weight-bearing joints, usually in the foot or ankle. It is a condition of acute or gradual onset and, in its most severe form, causes significant disruption of the bony architecture of the foot. It often results in foot deformities and causes abnormal pressure distribution on the plantar surface, foot ulcers and, in some cases, requires amputation. The exact pathogenesis is unknown, but underlying sensory neuropathy is nearly universal. Arteriovenous shunting due to autonomic neuropathy is also thought to play a role. Repeated unrecognized microtrauma or an identifiable injury may be the inciting factors of Charcot foot. Approximately 50 percent of patients with Charcot foot will remember a precipitating event such as a slip or a trip, or they may have had unrelated surgery on the foot as an antecedent event. In approximately 25 percent of patients, a similar problem ultimately develops on the other foot. [1,2]

The process is characterized by pathologic fractures with an exuberant repair mechanism and is associated with mixed peripheral neuropathies. The common denominator in these various conditions is that motor function is not as severely affected as are sensory modalities in the patient. [3,4,5] The Charcot foot in the diabetic patient is a progressive condition that is not confined to bones but affects all of the tissues in the lower extremity. It is often confused with osteomyelitis and massive infection of the foot necessitating early identification and management to prevent amputation of the lower extremity. With the advent of advanced surgical techniques and a better understanding, the physician may be optimistic with the treatment of this condition. By thoroughly understanding the etiologic factors and deforming forces, treatment can be planned for each specific patient.

The etiology of Charcot joints has been argued by many authors. Two theories (neurotraumatic and neurovascular) explain the pathogenesis of Charcot foot. [4]
The neurotraumatic theory attributes bony destruction to the loss of pain sensation and proprioception combined with repetitive and mechanical trauma to the foot. The neurovascular theory suggests that joint destruction is secondary to an autonomically stimulated vascular reflex that causes hyperemia and periarticular osteopenia with contributory trauma. Intrinsic muscle imbalance with increased heel and plantar forces can produce eccentric loading of the foot, propagating microfractures, ligament laxity and progression to bony destruction. [6] Neuropathic arthropathy is prevalent in 0.8 to 7.5 percent of diabetic patients with neuropathy; 9 to 35 percent of these affected patients have bilateral involvement. [7,8] The higher prevalence is seen in referral-based practices. Most patients with neuropathic arthropathy have had poorly controlled diabetes mellitus for 15 to 20 years. Clinical findings in patients with an acute Charcot process include warmth, erythema and swelling. [13,14,15] Pain and tenderness are usually absent because of sensory neuropathy, which is universal and is probably a component of the basic pathogenesis of the Charcot foot. Cellulitis should be considered in any patient with diabetes. Missing the diagnosis of Charcot foot can be disastrous since failure to initiate proper treatment of the Charcot foot exacerbates the problem. We strongly recommend that the diagnosis of acute Charcot foot be considered in any patient with diabetes and unilateral swelling of the lower extremity and/or foot. The existence of little or no pain can often mislead the patient and the physician.

The tarsometatarsal (Lisfranc’s) joint is the most common site for arthropathy, with initial involvement usually occurring on the medial column of the foot. The distribution of neuropathic arthropathy is 70 percent at the midfoot and 15 percent at the forefoot or rearfoot; it is usually contained in one area.

Nearly 50 percent of patients with neuropathy had an associated plantar ulcer. [8,9]

Bony destruction, fragmentation, joint subluxation and bony remodeling are considered radiographic hallmarks of the disease. These radiographic changes take time to develop, however, and may be absent at the time of presentation. The initial radiographic findings can be normal, making the diagnosis difficult but, if a Charcot foot is strongly suspected from the clinical presentation, treatment should be initiated and serial radiographs should be taken. Biopsy is the definitive test for the diagnosis of Charcot joints. The specimen will demonstrate the presence of multiple shards of bone and cartilage embedded within the deeper layers of the synovium. If osteomyelitis is of concern then a bone biopsy is essential for proper and accurate diagnosis.

The proper treatment for a hot, swollen foot in a patient with sensory neuropathy is immobilization. We believe that the best form of immobilization is a total contact cast, when available. Strict immobilization and protection of the foot (most often in a total contact cast) is the recommended approach to managing the acute Charcot process. [11,12,13,14,15] We used the total contact cast for our patient which allowed some measure of ambulation for the patient and prevented the progression of deformity. (Fig. 4)

Figure 4   Total Contact Cast is used for immobilization and protection of the Charcot foot.  It is commonly used as initial conservative treatment in the acute Charcot episode.

Charcot fractures that are not treated progressively, typically lead to marked deformity and skin ulceration over the new bony prominence. Casts should be replaced approximately every one to two weeks. The foot should be inspected, and cutaneous temperature measurements should be made. Serial plain radiographs should be taken approximately every month during the acute phase. Casts should be kept on until the active phase of the Charcot process is complete, as evidenced by temperature normalization and radiographic stability. Casting usually lasts from three to six months. The initial post-cast phase usually includes the use of some sort of a brace to protect the foot.

We used a patellar tendon¬ bearing brace in addition to custom-molded footwear. The brace can sometimes be eliminated from the regimen after six to 24 months. Thereafter, continued use of custom footwear to protect and support the foot is essential.

An alternative to TCC is a prefabricated pneumatic walking brace (PPWB), which has been found to decrease forefoot and midfoot plantar pressure in the treatment of neuropathic plantar ulceration. [11,12,13,14,15] (Fig. 5)

Figure 5   The alternative to the total contact cast is the PPWB or prefabricated pneumatic walking brace.  (Courtesy Aircast Corp.®)

Benefits include easier wound surveillance, ease of application and the ability to use several types of dressings. Use of the PPWB is limited in patients who have severe foot deformity or who are noncompliant. After swelling and erythema resolve and radiographic stability has been achieved, the TCC can be changed to a CROW, an ankle foot orthosis or a patellar tendon-bearing brace, depending on residual anterior edema. If anterior edema persists, the CROW full-enclosure system is used. (Fig. 6) This device is used for six months to two years, until a stable foot is obtained.


Figure 6   The CROW or Charcot Restraint Orthotic Walker (A) and the patellar tendon-bearing brace (B).  The CROW is a custom molded device that when properly constructed can improve plantar off-loading up to 50 percent.  It can be used for 6 months to 2 years until the foot is stabilized.  The patellar tendon-bearing brace can reduce offloading pressures of up to 90 percent. [16]

Patients can then be fitted for extra-depth shoes with custom insoles or orthotics to accommodate any residual deformity. Return to conventional foot gear may not be possible in all cases.

Other treatments for the Charcot process have included electrical bone stimulation or low-intensity ultrasonography during the acute phase to enhance healing. [11,12] Another study found that use of a bisphosphonate (pamidronate) resulted in decreased erythema, decreased temperature and decreased Charcot activity. [12,13,14] Additional controlled studies are needed to further evaluate the effectiveness of these treatments.

While it is still unknown why some patients with diabetes develop a Charcot process and others do not and more interestingly why some patients only develop this condition in one of their feet, an introspective review is necessary.

The literature on Charcot foot is huge and refers, not specifically, to every joint and metatarsals. The fact that 2,3,4,5 metatarsal involvement has not been extensively described, does contribute a base for our observation.

In summary, the Charcot foot commonly goes unrecognized, particularly in the acute phase, until severe complications occur. Early recognition and diagnosis, immediate immobilization and a lifelong program of preventive care can minimize the morbidity associated with this potentially devastating complication of diabetic neuropathy. If unrecognized or improperly managed, the Charcot foot can have disastrous consequences, including amputation. A lifelong program of patient education, protective footwear and routine foot care is required to prevent complications such as foot ulceration.

With proper planning, timing and knowledge of all facets of diabetic neuropathy, many patients may retain their foot and benefit from its function.


1. Gregory M. Caputo, M.D, Jan Ulbrecht, M.D., Peter R. Cavanagh, Ph.D., and Paul Juliano, M.D., The Charcot Foot in Diabetes: Six Key Points American Academy of Family Physicians, Vol. 57/No. 11 (June, 1998)
2. Cavanagh PR, Young MJ, Adams JE, Vickers KL, Boulton AJ. Radiographic abnormalities in the feet of patients with diabetic neuropathy. Diabetes Care 17:201-9, 1994.
3. Johnson JTH: Neuropathic fractures and joint injuries J Bone Joint Surg 49A: 1, 1967.
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joint: neurotraumatic vs neurovascular. Radiology 139: 349, 1981.
5. Banks AS, McGlamry ED: Charcot Foot. J Am Pod Med Assoc. 79: 5, 1989.
6. Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop 349:116-31, 1998.
7. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The natural history of acute Charcot’s arthropathy in the diabetic foot specialty clinic. Diabet Med 14: 357-63, 1997.
8. Harrelson JM. The diabetic foot: Charcot arthropathy. Instr Course Lect 42:141-6, 1993.
9. Eichenholtz SN. Charcot joints. Springfield, Ill.: Thomas, 1966.
10. Kelikian AS. Operative treatment of the foot and ankle. Stamford, Conn.: Appleton & Lange, 153, 1999.
11. Caputo GM, Ulbrecht J, Cavanagh PR, Juliano P. The Charcot foot in diabetes: six key points. Am Fam Physician 57:2705-10, 1998.
12. Brodsky JW. The diabetic foot. In: Mann RA, Coughlin MJ, eds. Surgery of the foot and ankle. 6th ed. St. Louis: Mosby, 1993.
13. Giurini JM, Chrzan JS, Gibbons GW, Habershaw GM. Charcot’s disease in diabetic patients. Correct diagnosis can prevent progressive deformity. Postgrad Med 89(4):163-9, 1991.
14. Holmes GB Jr, Hill N. Fractures and dislocations of the foot and ankle in diabetics associated with Charcot joint changes. Foot Ankle Int 15:182-5, 1994.
15. Sinha J, Thomas EM, Foster A, Edmonds M. Fractures in the neuropathic diabetic foot. Foot 4:28-30, 1994.
16. Pupp, G., Wilusz, P.M. Reassessing The Impact of Diabetic Footwear. Podiatry Today, online article. ISSN: 1045-7860 – 17:3, March 2004.

Address correspondence to: Dr. J. Terrence Jose Jerome, MBBS.,DNB (Ortho), MNAMS (Ortho)
Registrar in Orthopedics, Dept. of Orthopedics
St. Stephen’s Hospital, Tiz Hazari, Delhi 54, India
E-mail: terrencejose@gmail.com

1Registrar in Orthopedics, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India.

© The Foot & Ankle Journal, 2008