Tag Archives: Lisfranc’s dislocation

Outcome after early open reduction and Kirschner wire fixation of Lisfranc joint injuries

by Irfan Ahmad Latoo (MS)1, Reyaz Ahmad Dar (MS)1, Mubashir Maqbool Wani (MS)1, Iftikhar Hussain Wani (MS)1, Mohammad Shafi bhat1pdflrg

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

The study was a consecutive study conducted over a period of four years commencing in 2008 on Lisfranc joint injuries of feet. We studied the outcome of early open reduction and internal fixation of 20 cases of Lisfranc injuries using AOFAS-M score (American Orthopaedic Foot and Ankle Society-Midfoot score). Most patients were in the age group of 18-35 years. In our series the cause of injury was road traffic accidents in 50% cases followed by fall from height in 40% of cases. Most of Lisfranc fractures were of type B (60%) followed by type A. Most common associated injuries were metatarsal fracture (30% cases). The follow-up was 1-3 years with an average of 2 years. The mean AOFAS-M score was 78.36 with patients losing points to pain and decreased recreational function. Ours was not a comparative study but we strongly feel that early open reduction and Kirschner wire fixation of Lisfranc fracture dislocations within 24 hours of injury considerably improves functional outcome in these cases.

Key words: Lisfranc fracture, Kirschner wire

ISSN 1941-6806
doi: 10.3827/faoj.2014.0701.0001

Address correspondence to: Mubashir Maqbool Wani, Hospital for Bone and Joint Surgery Barzulla, India 190005.
Email: mubashirmaqboolwani@yahoo.co.in


The Lisfranc joint has been an eponym of tarsometatarsal joint injuries since Jacques Lisfranc, a field surgeon in Napoleon’s army described an amputation through the joint for gangrenous injuries of the forefoot [1]. Fracture dislocations of the Lisfranc (tarsometatarsal) joints of foot are uncommon but serious injuries with high potential for chronic disability. These injuries can easily be missed in the emergency department as radiographs may show only subtle incongruity of the joint [2].

In the treatment of fracture dislocation of tarsometatarsal joints, early accurate diagnosis combined with prompt anatomic reduction and stable internal fixation provides optimal results [3]. Closed reduction and percutaneous Kirschner wire fixation has been advocated by some [4,5], but the trend is towards open reduction and screw/Kirschner wire fixation [6,7].

The purpose of this study was to evaluate the functional outcome of patients with Lisfranc joint injuries treated with open reduction and internal fixation with Kirschner wires within 24 hours of injury.

Lisfrcfig1

Figure 1 X-ray right foot AP view showing C2 injury.

Materials and Methods

We performed a consecutive study of 20 patients with tarsometatarsal joint injuries at our hospital commencing in 2008 after approval by hospital ethics committee. An informed consent was taken from all the patients. Only those patients were included who presented < 24 hours of injury and were aged between 16 years and 65 years, the patients who were excluded from study were patients with open injuries, patients presenting > 24 hours of injury and polytrauma patients. The injuries were classified by Myerson’s modification of Hardcastle classification [8].

Lisfrcfig2

Figure 2 X-ray right foot oblique view of same patient as Figure 1.

Surgical Technique

A dorsal longitudinal incision was made between the first and second metatarsal. The extensor hallucis longus tendon, deep peroneal nerve and dorsalis pedis artery were identified and retracted as a unit.

Small irreducible fragments were debrided from the joint. The first tarsometatarsal joint was aligned by reducing the medial border of medial cuneiform to the medial border of the first metatarsal. The planter medial aspect of the joint was directly visualized to ensure that there was no planter gap. The second metatarsal was then reduced to the medial border of middle cuneiform. The joints were fixed with Kirschner wires. In some cases a second longitudinal incision was made centered over the fourth metatarsal and the third metatarsocuneiform joint was reduced. The fourth and fifth metatarsals usually reduced once the above three reductions were achieved and were held with one or two transarticular K-wires from the base of 5th metatarsal to the cuboid.

Lisfrcfig3

Figure 3 X-ray foot AP View of same patient 8 weeks after fixation.

Results

Most patients (70%, n=14) were in age group of 18-35 years with a mean 33.2 years. Males (80%, n=16) outnumbered females (20% n=4). Both right and left foot were equally involved. Cause of injury were road traffic accidents in 50% cases (n=10), fall from height in 40% (n=8) and other causes in 10% (n=2).

Metatarsal fracture was the most common associated injury (30%, n=6). The injuries were classified by Myerson,s modification of Hardcastle classification [8]. The majority of injuries (60%, n=12) were type B followed by type A (20%, n=4). All the operations were done within 24 hours of injury.

Lisfrcfig4

Figure 4 X-ray foot AP view of same patient 1.5 years after fixation.

Following surgery a posterior splint was applied and left in place for 10-14 days. During this period alternate wound dressings were done. Stitches were removed at around 14 days and short leg cast was given at the time of removal of stitches. K-wires were removed at 8 weeks. Full weight bearing was allowed at 10-12 weeks. Anatomical reduction was obtained in 19 patients (95%).

There was one case of loss of reduction in our study. There were two cases of superficial wound infection in our series both of them responded to antibiotics. Primary closure of skin was done in 90% cases (n=18) while in two patients delayed primary closure was done. There was no case of compartment syndrome of foot in our series. Good to fair results were seen in 90% cases (n=18).

Lisfrcfig5

Figure 5 X-ray foot Lateral view of the same patient after 1.5 years of fixation.

The mean AOFAS-M score in our study was 78.36 with most patients losing points to pain and decreased recreational function. Eighty percent of patients were able to return to their original occupation, including 10 household or office workers and six laborers.

Discussion

Lisfranc injuries result from high-energy injuries. In our study, motor vehicular accidents were the most common cause of injury, a finding consistent with the already available literature. Anatomic reduction and internal fixation has become standard principle governing treatment of tarsometatarsal fracture dislocations. Most authors agree stable anatomic reduction leads to optimal results [9]. The advantage of open reduction is that it allows direct visualization of the fracture dislocation for debridement of comminuted fracture fragments and osteochondral defects.

There is controversy about which method of fixation is best. There are proponents of k-wire fixation [10,11], while others rely on screw fixation [9,12]. In our study the age group ranged from 16-65 years with mean of 33.2 years.

In Goossens et al study [13], age groups ranged from 10-52 years with mean of 34 while as reported in Pereira et al [14], age group ranged from 17-50 years with mean of 31.53. The mean age group in our study was close to the study of Goossens et al [13]. Males outnumbered females in our study with ratio of 4:1 while as in Hesp et al [15], the male to female ratio was 2.3:1. The reason for higher male to female ratio in our study may be due to the fact that most of females in our setup are household sedentary workers. Both right and left feet were equally involved in our study.

The mode of injury was road traffic accidents (RTA) in majority of patients (50%) followed by fall from height which was consistent with Hardcastle et al [8], 40.3% RTA and Kuo et.al. [16], with RTA 42%. In our study most of the Lisfranc injuries (60%) were type Hardcastle type B followed by type A (20%). In Enríquez et al [17] series type B injuries were most common Lisfranc injuries (50%). While as in Pereira et al series [14], type B Lisfranc joint injuries constituted 80.94 percent of Lisfranc fracture dislocations. Metatarsal fracture were the most common associated injury in our study in 30% cases. In Goossens et al, series [13] metatarsal injuries were also the most common associated injuries (40%).

The mean duration of hospital stay in our series was three days. K-wire were removed at mean of 8 weeks in our study while as in Kuo et al [16] K-wires were removed at 6-8 weeks. There was no case of compartment syndrome in our study and primary closure was done in 90% cases. While two cases delayed primary closure was done. Complication in our study included loss of reduction in one case and two cases of superficial wound infection. Both cases occurred within one week of surgery and responded well to antibiotics and daily dressings. In Kuo et al series [16], there was no case of postoperative wound infection and one patient in their series required fasciotomy with split-thickness skin graft. There was one case of loss of reduction in our series.

The percentage of loss of reduction with K-wires was less in our series as we immobilized the foot for longer duration in short leg cast (mean 8 weeks). Molded arch support was given to patients after three months, which was discarded at 6 months in 70% cases while as 30% cases felt its need up to one year. In our study good to fair results were seen in 90% cases as per scale used by Pereira et al [14], with mean AOFAS score 78.23. Our mean AOFAS score was higher than Kuo et al [16], while as in Pereira et al [14] it was 77.36. Like this study most of our patients lost points to pain and decreased recreational function.

We believe that early open reduction and K-wire fixation considerably improves the functional outcome in these injuries. There is an added advantage that no second surgery for removal of hardware is required. The disadvantage is that this method needs longer period of immobilization in a cast. The limitation of our study is that there was no control group so that we could compare our results.

References

1. Cain PR, Seligson D. Lisfranc’s fracture-dislocation with intercuneiform dislocation: presentation of two cases an a plan for treatment. Foot Ankle. 1981;2 (3): 156-60. – [Pubmed]
2. Norfray JF, Geline RA, Steinberg RI et-al. Subtleties of Lisfranc fracture-dislocations. AJR Am J Roentgenol. 1981;137 (6): 1151-6. – [Pubmed]
3. Kuo RS, Tejwani NC, Digiovanni CW et-al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A (11): 1609-18. – [Pubmed]
4. Arntz CT, Veith RG, Hansen ST. Fractures and fracture-dislocations of the tarsometatarsal joint. J Bone Joint Surg Am. 1988;70 (2): 173-81. – [Pubmed]
5. Buzzard BM, Briggs PJ. Surgical management of acute tarsometatarsal fracture dislocation in the adult. Clin Orthop Relat Res. 1998;(353): 125-33. – [Pubmed]
6. Curtis MJ, Myerson M, Szura B. Tarsometatarsal joint injuries in the athlete. Am J Sports Med. 21 (4): 497-502. – [Pubmed]
7. Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orthop Clin North Am. 1989;20 (4): 655-64. – [Pubmed]
8. Myerson MS, Fisher RT, Burgess AR et-al. Fracture dislocations of the tarsometatarsal joints: end results correlated with pathology and treatment. Foot Ankle. 1986;6 (5): 225-42. – [Pubmed]
9. Rosenberg GA, Patterson BM. Tarsometatarsal (Lisfranc’s) fracture-dislocation. Am J Orthop. 1995;Suppl : 7-16. – [Pubmed]
10. Pérez blanco R, Rodríguez merchán C, Canosa sevillano R et-al. Tarsometatarsal fractures and dislocations. J Orthop Trauma. 1988;2 (3): 188-94. – [Pubmed]
11. Tan YH, Chin TW, Mitra AK et-al. Tarsometatarsal (Lisfranc’s) injuries–results of open reduction and internal fixation. Ann Acad Med Singap. 1995;24 (6): 816-9. – [Pubmed]
12. Jeffreys TE. Lisfranc’s fracture-dislocation: a clinical and experimental study of tarso-metatarsal dislocations and fracture-dislocations. J Bone Joint Surg Br. 1963;45 : 546-51. – [Pubmed]
13. Goossens M, De stoop N. Lisfranc’s fracture-dislocations: etiology, radiology, and results of treatment. A review of 20 cases. Clin Orthop Relat Res. 1983;(176): 154-62. – [Pubmed]
14. Pereira CdJ, Espinosa EG, Miranda I, Pereira MB, Canto RSdT. Evaluation of the surgical treatment of Lisfranc joint fracture-dislocation. Acta ortop bras. 2008;16(2) – [Webpage]
15. Hesp WL, Van der werken C, Goris RJ. Lisfranc dislocations: fractures and/or dislocations through the tarso-metatarsal joints. Injury. 1984;15 (4): 261-6. – [Pubmed]
16. Kuo RS, Tejwani NC, Digiovanni CW et-al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am. 2000;82-A (11): 1609-18. – [Pubmed]
17. Enríquez CJA, López VA, García HA, González TA, Ventura MA, Soto RV. Lisfranc’s fracture dislocation. Epidemiological study and results at the General Hospital in Mexico. Acta Ortop Mex 2005; 19 (s1). – [Webpage]

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.

Discussion

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.

References

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.
4. Brower AC, Allman RM: Pathogenesis of the neurotrophic
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