MOJ ISSN: 2374-6939MOJOR

Orthopedics & Rheumatology
Review Article
Volume 6 Issue 2 - 2016
Charcot Ankle Neuroarthropathy Pathology, Diagnosis and Management: A Review of Literature
Ahmed E Galhoum1,2* and Mohammed Mokhtar Abd-Ella3
1Orthopaedic surgery specialist, Nasser institute for research and treatment, Egypt
2Foot and ankle surgery fellow, Schmerzklinik Basel, Switzerland
3Lecturer of Orthopaedic surgery, Ain Shams University, Egypt
Received: October 01, 2016 | Published: November 03, 2016
*Corresponding author: Ahmed E Galhoum, Orthopedic Department, Schmirzklinik, Basel, 11-15 Hirschgasslein, 4010 Basel, Switzerland, Email:
Citation: Galhoum AE, Abd-Ella MM (2016) Charcot Ankle Neuroarthropathy Pathology, Diagnosis and Management: A Review of Literature. MOJ Orthop Rheumatol 6(2): 00218. DOI: 10.15406/mojor.2016.06.00218

Keywords: Ankle charcot Arthropathy; Ankle arthrodesis; Ankle external fxation arthrodesis; Total contact cast; Ankle neuroarthropathy

Key Points

Charcot ankle neuroarthropathy is a common hard to treat condition, early diagnosis and proper management is the key point of treatment. Non- surgical options are feasible in certain stages, but surgical intervention is required in advanced disease.


Charcot neuroarthropathy can be described as a non-infective, destructive process activated by an isolated or accumulative neuro-traumatic stimulus that manifests as dislocation, peri-articular fracture or both in patients rendered insensate by peripheral neuropathy [1].

The ankle has swelling, warmth, and erythema, and the syndrome may initially be difficult to distinguish from infection. The bones and joints develop fractures, ligamentous laxity, dislocations, cartilage damage, bone erosions, and hypertrophic repair [2]. The resulting bone and joint deformities may be associated with instability and may compromise the fitting of shoes or braces. Furthermore, ulceration may result from instability or bony prominence and may cause chronic or recurrent soft tissue infection and osteomyelitis. Amputation may be required for management of infection or instability [2].

Almost all affected individuals have a dense sensory peripheral neuropathy. The neuropathy is most commonly associated with diabetes, but may also be associated with leprosy, alcoholism, tabes dorsalis (Syphilis), syringomyelia, peripheral nerve injuries, or congenital absence of pain sensation [2]. Usually the larger joints of the lower extremity are involved in syphilis, and the larger joints of the upper extremity are involved in syringomyelia [2]. In contrast, diabetes related Charcot arthropathy primarily affects the foot and ankle [3].

Risk Factors

The presence of sensory peripheral neuropathy is essential for Charcot arthropathy to develop [4] (Table 1).

Neuropathy (sensory, autonomic, motor)



Physical activity


Peripheral vascular disease


Plantar pressure


Achilles tendon / gastro soleus contracture

Table 1: Risk factors for the development of Charcot Arthropathy [5].

The amount of bone and joint damage in the Charcot ankle is determined by severity of sensory loss, mechanical stress on joints, and physical activity of the patient [2].
Vibration sensation and cardiovascular autonomic function are similar in patients with Charcot neuroarthropathy and diabetic patients with ulcers [5]. Obesity is present in at least two-thirds of patients with Charcot neuroarthropathy [6].

Trauma or surgery may initiate Charcot arthropathy [7-11] The trauma may be apparently minor, such as ligament sprain, twisting injury, or stress fracture [7,12,13]. A history of trauma is present in 22% to 53% of patients with Charcot Arthropathy [6,14,15].


Modified eichenholtz stages

Shibata T et al. [16] modified the Eichenholtz system to include an earlier stage prior to “development. “ Several authors have proposed that this early inflammatory phase following injury be called “Charcot in situ,” “pre-stage 1,” or “stage 0 Charcot” [17-20]. This classification is currently being applied by the majority of foot-and-ankle physicians to Charcot arthropathy patients in the staging of the disease (Table 2).




Differential Diagnosis

Stage 0: Charcot (Inflammatory) Arthropathy

Localized swelling

Diagnosis of this stage with MRI or technetium bone scan

Frequently, stage 0 patients are misdiagnosed as cellulitis, gout, or deep vein thrombosis

Stage I: Development-Fragmentation

Marked swelling
Increase warmth

Bone debris at joints
Fragmentation of subchondral bone

Stage II: Coalescence

Decrease erythema
Decrease swelling
Decrease warmth

Absorption of fine debris
New bone formation
Coalescence of large fragments
Sclerosis of bone ends

Stage III: Reconstruction-Consolidation

Resolution of edema
Residual deformity

Remodling, rounding of bone
Decrease sclerosis

Table 2: Modified Eichenholtz Stages [19,20].

Brodsky (anatomical) classification

The most widely used anatomic classification by orthopaedic foot and ankle surgeons is that based on the four most common anatomic regions affected [21] (Table3).

Type 1 

Tarsometatarsal (Lisfranc's)

Type 2 

Chopart’s/ subtalar

Type 3A


Type 3B


Type 4

Multiple regions :

Type 5


Table 3: Charcot arthropathy of the foot and ankle: Brodsky anatomical classification [21].

The ankle comprises 9% of Charcot joints of the foot and ankle (Type 3A) (Figure 1). [3] Although less common than midfoot or hindfoot Charcot joints, Charcot ankles may be complicated by ulceration at the malleoli and severen uncontrollable deformity and hypermobility that may preclude fitting of a brace.

Figure 1: Brodsky anatomical classification (22).

The diagnosis of Charcot arthropathy is primarily reliant on clinical presentation, but a physician’s high index of suspicion should not be underappreciated [7]. A thorough patient history is essential to any assessment; however, a neuropathic patient’s history can be unintentionally misleading. It is therefore up to the clinician to know what questions to ask and what information is important when making an assessment.

Special attention must be given to the patient especially if history of any trauma, history of neuropathy, recent swelling, redness in the limb. Counter intuitively, the history may include pain sensations in an insensate limb but no recollection of any sustained trauma. In a study of 55 patients with Charcot arthropathy, more than 75% complained of pain in the foot and ankle upon presentation even though all subjects had a clinical loss of protective sensation to the 10-g Semmes-Weinstein mono-filament wire [22].

Repetitive trauma to the foot and ankle may be entirely absent from verbal history even though clinical symptoms prove otherwise. The study found that only 22% of patients were able to recall some specific traumatic event prior to the onset of Charcot arthropathy. The loss of protective sensation may leave the patient unaware of any particular event or reoccurring minor events [23].

It is important to investigate any previous history of infection or ulcers to role out a recurring acute or chronic infection. The usual presentation of Charcot arthropathy involves, a warm, swollen, erythematous foot or ankle in an insensate patient and, because of its similarity to an acute soft-tissue infection, heightened awareness is needed when dealing with the diabetic neuropathy patient population [22]. Most infection in the diabetic foot and ankle involve a direct source of inoculation through an opening in the skin, usually caused by neuropathic ulcers [24,25].

When this initial stage is suspected but not proven, the patient should be prevented from incurring any additional injury to the suspected limb. With immobilization and offloading, the patient is protected while awaiting the results of further investigation.

Radiographs of the foot and ankle that are taken in the non-weight-bearing position can have obvious variability in image quality and may not show subtle instability compared to radiographs in the weight-bearing position. It is recommended that all foot-and-ankle radiographic examinations be obtained in a weight-bearing position if possible.

MRI examination are increasingly being used and recommended for diagnosing Charcot arthropathy, especially at the earliest stage [26-28].

In diagnosing Charcot arthropathy, one review described findings of abnormal values of bone-specific alkaline phosphatase, type 1 collagen carboxyterminal telopeptide, and urinary desoxypiridinoline cross-links, indicating increased osteoclastic/osteoblastic activities throughout Eichenholtz stages 1 and 2 [29].
Baumhauer et al. [30] found that Charcot arthropathy-reactive bone had osteoclasts disproportionately increased compared to osteoblasts, and the osteoclasts demonstrated immune reactivity for IL-1, IL-6 and TNFα. Although these laboratory findings may assist the clinicians’ assessment, it is impractical to obtain histological samples from patients presenting with the initial symptoms. It is recommended that biopsies be collected only when there is a non healing wound or suspected bone infection [26,31].

Modalities of treatment

  1. Non-Operative Treatment including
    1. Total Contact Cast (TCC) [26].
    2. Prefabricated Pneumatic Walking Brace (PPWB)
    3. Charcot Restraint Orthotic Walker (CROW)
    4. Antiresorptive Drugs
    5. Electrical Bone Stimulators
    6. Ultrasound
  2. Operative Treatment including
    1. Debridement of Ulcer.
    2. Ostectomy.
    3. Arthrodesis with Internal Fixation.
    4. Arthrodesis with External Fixation.
    5. Amputation: with uncontrolled infection and             
    6. Uncontrolled deformity.

Non operative therapies and medical management

The goals for every patients undergoing treatment for an acute or quiescent Charcot process should be to maintain or achieve structural stability of the foot and ankle, to prevent ulceration, and to preserve a plantigrade foot [15].

Total contact cast

Most cases of acute Charcot ankle especially stage 0 or stage 1 Eichenholtz Charcot neuroarthropathy can be treated non-surgically with pressure-relieving methods such as total contact casting (TCC), which is believed to be the gold standard of treatment [32].

TCC was developed in the 1950s. Most of the cast padding is eliminated for exact conformity to the lower extremity, with the goal of evenly distributing forces across the plantar surface of the foot. A tubular stockinette with low-density foam or one quarter inch felt is applied over the tibial crest and malleoli, and around the metatarsal heads with one layer of synthetic padding. A three layer inner plaster shell is followed by a fiberglass outer shell.

The total time of non-weight-bearing TCC and the immobilization period in weight-bearing TCC may last up to 4-6 months [33]. Once there is bony consolidation, custom inserts or extra-deep shoes can be worn, followed by proper physician visits to ensure no uneven distribution of plantar pressures. Although the TCC is an effective treatment for the ACA process, there have been complications associated with this treatment, usually related to weight- bearing allowance [34].

Prefabricated pneumatic walking brace

An alternative to TCC is a prefabricated pneumatic walking brace (PPWB). Use of the PPWB is limited in patients who have severe foot deformity or who are noncompliant.

Charcot restraint orthotic walker

After swelling and erythema resolve and radiographic stability has been achieved, the TCC is changed to either a CROW or an ankle foot orthosis or a patellar tendon-bearing brace, depending on residual anterior edema.

Antiresorptive drugs

Bisphosphonates are popular as antiresorptive drugs against osteoporosis, Paget’s disease, and other diseases with increased bone turnover [35], and there have been reports on the possibility of pharmacologic therapy for Acute Charcot Arthorpathy [36].

Electrical bone stimulators

Other adjunct therapies have also been offered to help manage ACA. Electric bone growth (EBG) stimulators [37] have been experimentally applied and clinically tested to promote healing of fractures in the acute phase.


A series of case reports has described the use of adjunct low-intensity ultrasound for Charcot arthropathy treatment. There are no subsequent studies to validate this method [38].

Surgical treatment (goals and Indications)

Goals of surgery in the charcot ankle include

  1. Restoration of stability and alignment.
  2. Prevention of deformity, to facilitate functional ambulation.
  3. Ulcer prevention with prescription footwear and braces [39].

Surgery for Charcot deformity does not eliminate the necessity for use one of non-operative methods [39]. An unstable ankle may be more difficult to control with an orthosis and may be more susceptible to ulceration and secondary deep infection. Therefore, surgery in the Charcot ankle may prevent ulceration and amputation. Limb salvage may be important, in part, because the contralateral foot may be at risk for Charcot neuroarthropathy; if an amputation is done and the other side becomes involved, the patient might end up with bilateral amputation [39,40].

Indications for surgery in the Charcot ankle include

  1. Acute dislocation [12]
  2. Recurrent ulceration,
  3. Secondary to either instability or bony prominence, that cannot be managed successfully non-surgically [39].

Severe or uncontrolled deformity or instability that may cause ulceration or that may make it impossible to fit a custom brace or footwear [41].

Timing of surgery

The demineralization, soft bone, and swelling in stage I may increase technical difficulty and surgical complications such as infection and loss of fixation [20,39]. Surgery may be considered after decrease in warmth, erythema, and swelling [2,41].

Arthrodesis with internal fixation

Arthrodesis with plate and screws: Arthrodesis using internal fixation has been a viable option for many surgeons. Banks & McGlamry [42] treated the Charcot foot and ankle by stabilizing the foot and ankle with internal fixation arthrodesis. Stabilization of the joints prevented the further progression of ulcerations and joint breakdown. These patients were immobilized with a cast postoperatively. Casting and immobilization can arrest the degenerative progression of Charcot disease but there is the potential for demineralization with cast disease. Because of the progressive nature of this pathology with Charcot hyperemia and bone demineralization caused by cast disease and non weight bearing, the internal fixation could fail. The importance of avoiding immobilization is that partial to full weight bearing helps to maintain bone stock if the foot and ankle are adequately stabilized [43].

Internal fixation used in arthrodesis for Charcot ankle neuroarthropathy may include 6.5-, 7.0-, or 7.3-mm cancellous bone screws, Locked plates, and staples. Screw fixation with smaller screws may be useful in midfoot arthrodesis, but multiple screws may be required because of the risk of hardware failure [44].

Arthrodesis with nail

Intramedullary fixation for arthrodesis of the ankle was first described by Adams in 1948 [45], but nowadays there are several specific ankle fusion nail:

  1. The TRIGEN™ Hindfoot Fusion Nail (HFN): Offers unique locking configurations allowing the surgeon to target the best bone possible within the hindfoot to maximize purchase and position.
  2. The ZIMMER Hindfoot Fusion Nail.

 In several published series, an intramedullary retrograde nail was used for advanced degenerative or post-traumatic arthrosis. Few studies have provided any indications for the use of this technique in Charcot neuroarthropathy [12].

The goal of treatment with intramedullary fixation is to obtain alignment of the ankle -foot system, reducing significantly the risk of ulceration. The percentages of success in the treatment of this complication are variable, with documentary evidence varying between 50% and 90 % [46,12]. The causes of failure are uncontrolled infection, hardware failure, and malunion. Recently, another study reported 90% limb salvage using intramedullary nail technique [47].

Arthrodesis with external fixation

External fixation is a viable alternative that allows micromotion to occur through fracture and joint dislocation areas. This can facilitate arthrodesis by compressing fragments or joint areas with osteoarthropathy through this protected micromotion [47]. External fixation allows rigid immobilization postoperatively. It has the ability to adjust compression and distraction at the breakdown level and allows for ambulation. Early weight-bearing provides biomechanical stress and compression to the bone to prevent osteopenic changes and cast disease.

This stresses the bone and will increase the chance for arthrodesis by compression and fracture healing. [48] Because of the hyperemic phase of the Charcot foot, this response will promote osseous bridging in fractures and dislocations.

External fixation should be strongly considered as the best choice of fixation when addressing the multiple degenerative areas of Charcot disease. Of the multiple uses of external fixation, Charcot reconstruction is ideal for helping the podiatric surgeon stop the progressive disease of joint breakdown and degeneration [49].

The goals of Charcot reconstruction with external fixator are three fold [50]:

  1. First, correct the patient’s equinus and reestablish the calcaneal inclination angle;
  2. Second, maintain the rear foot to leg relationship; and,
  3. Finally, correct and stabilize the degenerative joints.

This can usually be performed percutaneously and without hemostasis. It is very important to allow patients to weight-bear within 1 week postoperatively. This is possible with a unique combination of innovative external fixation techniques. Though this strategy is foreign and contrary to traditional thoughts and approaches to surgical intervention, external fixation allows for safe and percutaneous Charcot reconstruction. The use of uniplane and multiplane fixators in a percutaneous manner is an important facet of addressing Charcot pathology [50].

Complications of external fixation

The most common complications with external fixation in the Charcot ankle including pin tract infections that has been found to range from 0.92% to 60% [31]. Erythema and drainage around pin sites is usually due to micromotion or unstable pins and can be dissipated by tightening or retensioning pins, or by meticulous pin care. At times, short doses of oral antibiotics can also help alleviate these symptoms. The progressive pin tract infection, with resultant loosening of the frame, occurred in a small number of patients. This complication is treated with a frame revision in the operating room with removal of the infected, unstable pins and replacing them with additional fixation. Half pin fixation usually is replaced with 2 to 3 additional wires to improve fixation and reduce the risk of fractures through the larger pin sites.

Contraindications to Arthrodesis Include

  1. Stage 1 Charcot disease,
  2. Poor nutrition or diabetic control,
  3. Severe peripheral vascular disease,
  4. Active soft tissue or bone infection,
  5. Noncompliant patient, and
  6. Poor bone stock for fixation.


The Charcot arthropathy process can take up to 2 years to run its course. Primary care physicians must consider the diagnosis of Charcot arthropathy in any neuropathic patient presented with erythema, edema and warmth regardless of local or systemic signs of infection.


  1. Brodsky JW (1999) The diabetic foot. In: Coughlin MJ & Mann RA, (Eds.), Surgery of the Foot and Ankle, (7th edn), St Louis, Mosby, USA, pp. 895-969.
  2. Johnson JTH (1967) Neuropathic fractures and joint injuries. J Bone Joint Surg 49A: 1-30.
  3. Sinha S, Munichoodappa CS, Kozak GP (1972) Neuro-arthropathy (Charcot joints) in diabetes mellitus (clinical study of 101 cases). Medicine (Baltimore) 51(3): 191-210.
  4. Clouse ME, Gramm HF, Legg M, Flood T (1974) Diabetic osteoarthropathy: clinical and roentgenographic observations in 90 cases. Am J Roentgenol 121(1): 22 -34.
  5. Stevens MJ, Edmonds ME, Foster AVM, Watkins PJ (1992) Selective neuropathy and preserved vascular responses in the diabetic Charcot foot. Diabetologia 35(2): 148 -154.
  6. Pinzur MS, Sage R, Stuck R, Kaminsky S, Zmuda A (1993) A treatment algorithm for neuropathic (Charcot) midfoot deformity. Foot Ankle 14(4): 189 -197.
  7. Armstrong DG, Peter EJ (2002) Charcot’s arthropathy of the foot. Journal of the American Podiatric Medical Association 92(7): 390-394.
  8.  Connolly JF, Csencsitz TA (1998) Limb threatening neuropathic complications from ankle fractures in patients with diabetes Clin. Orthop 348: 212 -219.
  9. Kristiansen B (1980) Ankle and foot fractures in diabetics provoking neuropathic joint changes. Acta Orthop Scand 51(6): 975 -979.
  10.  Newman JH (1981) Non-infective disease of the diabetic foot. J Bone Joint Surg 63B: 593 -596.
  11. Thompson RC, Clohisy DR (1993) Deformity following fracture in diabetic neuropathic osteoarthropathy: operative management of adults who have type-I diabetes. J Bone Joint Surg 75(12): 1765 -1773.
  12. Lesko P, Maurer RC (1989) Talonavicular dislocations and midfoot arthropathy in neuropathic diabetic feet. Clin Orthop 240: 226-231.
  13.  Slowman-Kovacs SD, Braunstein EM, Brandt KD (1990) Rapidly progressive Charcot arthropathy following minor joint trauma in patients with diabetic neuropathy. Arthritis Rheum 33(3): 412 -417.
  14. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR (1997) The natural history of acute Charcot’s arthropathy in a diabetic foot specialty clinic. Diab Med 14: 357 -363.
  15.  Schon LC, Easley ME, Weinfeld SB (1998) Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res 349: 116 -131.
  16.  Shibata T, Tada K, Hashizume C (1990) The results of arthrodesis of the ankle for leprotic neuroarthropathy. J Bone Joint Surg Am 72(5): 749-756.
  17.  Schon LC, Marks RM (1995) The management of neuroarthropathic fracture-Dislocations in the diabetic patient. Orthop Clin North Am 26(2): 375-392.
  18.  Sella EJ, Barrette C (1999) Staging of Charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg 38(1): 34-40.
  19.  Paul B, Frobin W, Leivseth G (2002) The Ankle Joint. MusculSkeletal Biomechanics, (2nd edn), Verlag Stuttgart, Germany, p. 61-80.
  20.  Eichenholtz SN (1996) Charcot joints. CC Thomas, Springfield IL, USA, pp. 227.
  21.  Brodsky JW (1999) The diabetic foot. In: MJ Coughlin & RA Mann (Eds.), Surgery of the Foot and Ankle, (7th edn), St Louis, Mosby, USA, pp. 895-969.
  22. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR (1997) The natural history of acute Charcot’s arthropathy in a diabetic foot specialty clinic. J Am Podiatr Med Assoc 87(6): 272-278.
  23. Chantelau E, Richter A, Schmidt-Grigoriadis P, Scherbaum WA (2006) The diabetic Charcot foot: MRI discloses bone stress injury as trigger mechanism of neuroarthropathy. Exp Clin Endocrinol Diabetes 114(3): 118-123.
  24.  Sanders LJ (1994) Diabetes mellitus. Prevention of amputation. J Am Podiatr Med Assoc 84: 322-328.
  25. Singh N, Armstrong DG, Lipsky BA (2005) Preventing foot ulcers in persons with diabetes. JAMA 293(2): 217-228.
  26. Sanders L, Frykberg R (2007) The Charcot foot (pied de Charcot). In: Bowker JH & Pfeifer MA (Eds.), Levin and O’Neals the diabetic foot. (7th edn), Mosby Elsevier, Philadelphia, USA, pp. 257-283.
  27.  Lipsky BA (1997) Osteomyelitis of the foot in diabetic patients. Clin Infect Dis 25(6): 1321.
  28.  Chantelau E, Poll LW (2006) Evaluation of the diabetic Charcot foot by MR imaging or plain radiography- An observational study. Exp Clin Endocrinol Diabetes 114(8): 428-431.
  29.  Chantelau E, Onvlee GJ (2006) Charcot foot in diabetes: Farewell to the neurotrophic theory. Horm Metab Res 38(6): 361-367.
  30.  Baumhauer JF, Wervey R, McWilliams J, Harris GF, Shereff MJ (1997) A comparison study of plantar foot pressure in a standardized shoe, total contact cast, and prefabricated pneumatic walking brace. Foot Ankle Int 18(1): 26-33.
  31.  De Bastiani G, Apley AG, Goldberg A (2000) Orthofix external fixation in trauma and orthopedics. Springer-Verlag, New York, USA.
  32. Leo J de Souza (2008) Charcot Arthropathy and Immobilization in a Weight-Bearing Total Contact Cast. J Bone Joint Surg Am B90(4): 754-759.
  33. Frykberg RG, Zgonis T, Armstrong DG, Driver VR, Giurini JM, et al. (2006) Diabetic foot disorders: A clinical practice guideline (2006 revision). J Foot Ankle Surg 45: S1-S66.
  34. Guyton GP (2005) An analysis of iatrogenic complications from the total contact cast. Foot Ankle Int 26(11): 903-907.
  35. Rogers MJ (2003) New insights into the molecular mechanisms of action of bisphosphonates. Curr Pharm Des 9(32): 2643-2658.
  36.  Anderson JJ, Woelffer KE, Holtzman JJ, Jacobs AM (2004) Bisphosphonates for the treatment of Charcot neuroarthropathy. J Foot Ankle Surg 43(5): 285-289.
  37.  Grady JF, O’Connor KJ, Axe TM, Zager EJ, Dennis LM, et al. (2000) Use of electrostimulation in the treatment of diabetic neuroarthropathy. J Am Podiatr Med Assoc 90(6): 287-294.
  38. Strauss E, Gonya G (1998) Adjunct low intensity ultrasound in Charcot neuroarthropathy. Clin Orthop Relat Res 349: 132-138..
  39.  Johnson JE (1998) Operative treatment of neuropathic arthropathy of the foot and ankle. J Bone Joint Surg 80A: 1700 -1709.
  40.  Waters RL, Perry J, Antonelli D, Hislop H (1976) Energy cost of walking of amputees: the influence of level of amputation. J. Bone Joint Surg 58(1): 42 -46.
  41. Jacobs RL (1991) Charcot foot. In: MH Jahss (ed), Disorders of the Foot & Ankle, WB Saunders, Philadelphia, USA, pp. 2156-2169.
  42. Banks AS, McGlamry ED (1989) Charcot foot. Journal of the American Podiatric Medical Association 79: 213-235.
  43. Abdo RV, Wasilewski SA (1992) Ankle arthrodesis: a longterm study. Foot Ankle 13(6): 307-312.
  44. Verity S, Sochocki M, Embil JM, Trepman E (2008) Treatment of Charcot foot and ankle with a prefabricated removable walker brace and custom insole. Foot Ankle Surg 14(1): 26-31.
  45. Adams JC (1948) Arthrodesis of the ankle joint: Experiences with the transfibular approach. J Bone Joint Surg 30(3): 506-511.
  46.  Kile TA, Donnelly PA, Gehrke JC, Werner ME, Johnson KA (1994) Tibiotalo-calcaneal arthrodesis with an intramedullary device. Foot Ankle Int 15(12): 669-673.
  47. Patrick R, Burns DPM, Facfasdane K, Wukich MD (2008) Surgical Reconstruction of the Charcot Rearfoot and Ankle. Clin Podiatr Med Surg 25(1): 95-120.
  48. Chao EY, Aro HT, Lewallen DG, Kelly PJ (1989) The effect of fracture healing in external fixation. Clin Orthop Relat Res 241: 24- 35.
  49. Kuiper JE, Richardson JB, Ashton BA (2000) The effect of fracture site movement on callus formation and stiffness restoration: a computer simulation. Third Riva Congress, Riva Del Garda, Italy, p. 10- 14.
  50. Sticha RS, Frascone ST, Wertheimer SJ (1996) Major arthodesis in patients with neuropathic arthropathy. J Foot Ankle Surg 35(6): 560- 566.
© 2014-2018 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy