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CASE STUDY

A case of diabetic Charcot arthropathy of the foot and ankle


John M. Embil and Elly Trepman
Background. A 61-year-old man with type 2 diabetes mellitus presented to a diabetic foot clinic 1 year after he injured his left foot in a slip injury. Examination showed collapse of the longitudinal arch with a rocker bottom deformity and a plantar ulcer under the plantar midfoot bony prominence. Investigations. Radiographs of the foot. Diagnosis. Diabetic Charcot arthropathy with rocker bottom deformity and plantar midfoot ulcer. Management. The ulcer was initially treated by debridement and immobilization. Subsequently, the patient underwent surgery that consisted of plantar midfoot ostectomy to remove the bony prominence that had caused the ulcer, and midfoot osteotomy with realignment arthrodesis to reconstruct the longitudinal arch.
Embil, J. M. & Trepman, E. Nat. Rev. Endocrinol. 5, 577581 (2009); doi:10.1038/nrendo.2009.174

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Learning objectives
Upon completion of this activity, participants should be able to: 1 Diagnose Charcots arthropathy of the foot and ankle effectively. 2 List effective nonoperative treatments for Charcots arthropathy. 3 Describe surgical therapy for Charcots arthropathy.

The case

A 61-year-old obese man with a 6-year history of type 2 diabetes mellitus was referred to a diabetic foot clinic for evaluation of left foot problems. 1 year before referral, he had slipped and felt a pulling pain on the plantar aspect of his left foot followed by swelling of the foot. Radiographs performed 9 months before the patients referral did not reveal fractures or dislocations. He
Competing interests The authors, the Journal Editor V. Heath and the CME questions author C. P. Vega declare no competing interests.

developed a prominence on the plantar left midfoot 3 months before referral. 1 week before referral, the patient had developed a blister on the plantar aspect of the foot and had been placed on antibiotics by his primary care physician. Examination of the patients left foot and ankle showed increased warmth, erythema, and swelling compared with that of the contralateral foot, and pulses were intact. A rocker bottom deformity with collapse of the longitudinal arch of the foot was noted (Figure 1), along with a callus on the plantar midfoot rocker bottom surface associated with a large blister. The blister was unroofed and the callus was excised, which revealed an ulcer (1 cm in diameter) under the plantar midfoot bony prominence (Figure 1). Neither cellulitis nor drainage from the ulcer were present. Radiographs of the foot showed a midfoot fracture dislocation with collapse of the midfoot arch, plantar displacement of the cuneiform and navicular bones, and fractures of the navicular, cuboid, and cuneiform bones, and in the bases of the lesser metatarsals with early callus formation (Figure 2). The diagnosis was diabetic Charcot midfoot arthropathy with a rocker bottom deformity that had caused a plantar midfoot ulcer. Initial management included debridement of the plantar callus and blister. The foot and ankle were immobilized in a non-weight-bearing manner by use of a bivalved cast, and a moist dressing was applied and changed once daily. The plantar ulcer healed within 2 weeks. Subsequently, the patient had surgery that consisted of plantar midfoot ostectomy to remove the bony prominence that had caused the ulcer, midfoot osteotomy with excision of a wedge of bone, and realignment arthrodesis to reconstruct the longitudinal arch (Figure 3).

Department of Medicine, Section of Infectious Diseases and Department of Medical Microbiology (J. M. Embil), Department of Medical Microbiology (E. Trepman), University of Manitoba, Winnipeg, MB, Canada. Correspondence: J. M. Embil, Infection Prevention and Control Unit, Health Sciences Centre, MS 673820 Sherbrook Street, Winnipeg, MB R3A 1R9, Canada jembil@hsc.mb.ca

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After surgery, the limb was maintained in a nonweight-bearing manner for the first 3 months. Postoperative follow-up examination was performed weekly for the first month and then every 3 weeks until 3 months after surgery. Partial weight bearing (12 kg) was recommended for an additional 3 months, after which the foot alignment remained stable (Figures 4 and 5) and progressive bony consolidation of the arthrodesis occurred (Figure 5). Subsequently, the patient was lost to follow-up.

Discussion of diagnosis

Figure 1 | The Charcot midfoot fracturedislocation of the patients left foot. The forefoot is in dorsiflexion and abduction relative to the hindfoot, with collapse of the arch and rocker bottom midfoot deformity. The plantar blister and callus were debrided to expose an ulcer under the rocker bottom bony prominence.

Figure 2 | Radiographs of the affected foot demonstrate plantar displacement of the navicular and cuneiform bones, with fragmentation of the midfoot bones and early callus formation.

Charcot arthropathy of the neuropathic foot and ankle is characterized by bone and joint destruction and deformities.13 The neuropathy is most commonly a result of diabetes, leprosy, tabes dorsalis, poliomyelitis, chronic alcoholism, or syringomyelia. The foot presents with swelling, warmth, and erythema. The syndrome can initially be difficult to distinguish from infection and patients with the syndrome may be mistakenly treated with antibiotics, as occurred in the case described before referral. The bones and joints develop fractures, ligamentous laxity, dislocations, cartilage damage, bone erosions, and hypertrophic repair. The resulting bone and joint deformities may be associated with bony prominences or hypermobility that compromise the fitting of shoes or braces and cause ulcers; the process eventually leads to chronic or recurrent soft tissue infection and osteomyelitis. Amputation may be required for management of infection or instability. However, early diagnosis and treatment may prevent progressive deformity and secondary ulceration that may lead to abscess, osteomyelitis and amputation. The reported prevalence of Charcot arthropathy is low, as it affects only 0.150.7% of all patients with diabetes.1 A primary care physician probably only rarely sees a patient with Charcot arthropathy, which might explain the delay in diagnosis in many cases. Patients may be incorrectly diagnosed as having more common conditions such as gout, rheumatoid arthritis, vasculitis, cellulitis, or nonspecific asymmetric venous swelling. The Charcot process in the patient described probably began between several months and 1 year before referral. The pathogenesis of Charcot arthropathy might be explained by neurotraumatic and neurovascular mechanisms. Repetitive microtrauma or an acute episode of trauma may initiate the process. The patient with sensory neuropathy who lacks normal protective sensation might continue walking when he or she has a minor foot injury, which results in further injury that exceeds the rate of healing. Furthermore, vasomotor neuropathy may cause arteriovenous shunting, and may lead to bone resorption, weakening, fracture, and deformation with continued walking. In addition, inflammation associated with trauma, ulcer, infection, or surgery may be associated with cytokine activation and associated osteopenia and osteolysis, which contributes to the

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CASE STUDY
development or progression of Charcot arthropathy.4 Diabetic Charcot arthropathy most frequently involves tarsometatarsal (Lisfranc) joints (type 1), followed by hindfoot joints (type 2), the ankle joint (type 3A), the posterior calcaneus (type 3B), multiple regions (type 4), or forefoot joints (type 5).1 The patient described had type 4 Charcot arthropathy. Charcot arthropathy progresses from onset to healing through three stages (Table 1).2,3 The time course of progression through the stages can vary from several weeks or months to many years, and reactivation of the Charcot process may occur. Complications, including bony displacement and ulcers, might occur during any of the stages.2,3 The key to early diagnosis of Charcot arthropathy is a high index of clinical suspicion in the patient with dia betes mellitus and peripheral neuropathy who presents with new-onset swelling, erythema, and increased warmth of the foot and ankle (Box 1). In addition, sensory neuropathy is present. 5 The patient may not recall any history of trauma or may report seemingly minor trauma, and initial radiographs may not show bony changes. Pain is frequently absent, and when present is usually not commensurate with the degree of destruction noted on physical examination and radiographs. Bilateral involvement may occur in approximately one-third of adult patients.2 Clinical distinction between Charcot arthropathy and infection can be difficult. Furthermore, both conditions may be present concurrently. Infection, when present, usually occurs as a result of direct invasion of bacteria from local erosions, breaks in the skin, or nail infection.2 The presence of an ulcer may make the possibility of infection even more difficult to exclude when signs of Charcot arthropathy are present. Systemic signs of inflammation (fever, leukocytosis, elevated erythrocyte sedimentation rate) may not help to distinguish Charcot arthropathy from infection. A useful clinical sign is that reduction of erythema may be observed upon elevation of the Charcot foot, whereas a cellulitic foot may remain erythematous upon elevation.1 Patients with an abscess or infection might feel and look systemically ill and notice a deterioration of glycemic control, but patients with Charcot arthropathy might feel well except for local foot swelling and pain and have no observed change in glucose control. The presence of a foot ulcer associated with Charcot arthropathy may necessitate the patients further evaluation and treatment, including hospital admission, nonweight-bearing of the affected limb, empiric antibiotic therapy, diagnostic imaging, and bone biopsy. Threephase 99mTc bone scintigraphy and 111In-labeled leukocyte scintigraphy are sensitive but unreliable techniques with which to distinguish between Charcot arthropathy and osteomyelitis.6 MRI may help distinguish Charcot arthropathy from osteomyelitis in some cases,7 but the potential utility of gadolinium-enhancement of MRI for this diagnostic process is undetermined.

Figure 3 | Surgical reconstruction of the rocker bottom deformity. The bony prominence was excised from the plantar aspect of the rocker bottom deformity. Then, Kirschner wires were placed perpendicular to the longitudinal axis of the hindfoot and forefoot, and osteotomes were driven parallel to the Kirschner wires to excise a medial-based bone wedge from the midfoot. The Kirschner wires were brought together to reduce the forefoot to the hindfoot, and the osteotomy was fixed with plates and screws.

Treatment and management

The goals of treatment include control of foot alignment and shape to achieve consolidation in a stable and plantigrade position. The functional goals include ambulation with available footwear and orthoses and avoidance of bony prominences that may result in ulcers. Prognosis for optimal function is best when deformity, ulcers, and contralateral involvement are avoided. Management of a patient with Charcot arthropathy may be facilitated at a multidisciplinary, comprehensive diabetic foot clinic with specially trained staff for education of patients, emergency response, social services, wound care, infection control, casting, orthoses and surgery. In the acute stage, off-loading may minimize mechanical stresses and enable progressive consolidation with minimal displacement or deformity. Off-loading is

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Figure 4 | Improvement in the condition of the foot 5 months after surgical reconstruction. Correction of the preoperative deformity is noted. The forefoot is neutrally aligned relative to the hindfoot and the midfoot arch of the foot has been restored. The foot is free of ulcers.

Figure 5 | Radiographs of the foot 5 months after surgical reconstruction show consolidation of the midfoot in neutral alignment.

achieved by non-weight-bearing or limited weightbearing with a plaster cast, bivalved cast (as used in the current case), prefabricated removable walker boot with a rigid rocker sole and custom insole,8 or total-contact cast.5 Frequent cast changes, especially in the acute stage, enable inspection of skin and adjustment of cast fit as swelling decreases. Specialized, custom-molded orthoses may be helpful to accommodate the morphologic changes and protect the foot from additional trauma. 9 After swelling has decreased and consolidation is achieved, therapeutic footwear and orthoses may protect the foot against ulceration at bony prominences. Contralateral fracture develops in a greater proportion of patients who are treated by weight-bearing methods than those treated by non-weight-bearing methods, which suggests that protection of the uninvolved contralateral extremity is advised during treatment of an acute neuropathic fracture. However, maintenance of strict non-weight-bearing status is usually a major practical difficulty; therefore, protected weight-bearing in a cast can be a practical alternative to non-weight-bearing methods if the patient is monitored closely and does not develop progressive deformity.

Surgery may be indicated to maintain or restore stability and alignment, prevent deformity and ulcer, and facilitate functional ambulation. 10 An unstable foot and ankle may be more difficult to control with an orthosis and may have increased susceptibility to ulceration and secondary deep infection. Surgery in the Charcot foot might, therefore, prevent ulceration and amputation. Indications for surgery in the Charcot foot include acute dislocation;11 recurrent ulceration, secondary to either instability or bony prominence that cannot be managed successfully nonsurgically;10,12 and, as in the case described, severe or uncontrolled deformity or instability that may cause ulceration or make it impossible to fit a custom brace or shoe.10,12 Surgical options include debridement of ulcers to remove necrotic and infected tissue;9 excision of bony prominences (ostectomy) that may cause an ulcer;9,10,13 and reconstruction with osteotomy and arthrodesis for correction of fixed deformity or severe instability to enable successful brace treatment. 12 Prolonged postoperative immobilization may be required after arthrodesis because of the potential for failure of fixation or hardware before adequate bony consolidation is achieved. Insufficient data support the use of other medical therapies such as bisphosphonates in routine treatment of Charcot arthropathy.1 Complications of Charcot arthropathy include recurrence, deformity and ulcers that may result in deep

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Table 1 | Stages of progression of Charcot arthropathy of the foot Stage
I: Development fragmentation

Acuity
Acute

Clinical manifestations
Warmth, erythema, and swelling

Radiographic findings
Early radiographs may be normal except for soft tissue swelling. Subsequent findings include bony debris at articular margins, fragmentation of subchondral bone, periarticular fracture, subluxation and dislocation Early bony healing, with absorption of fine debris, new bone formation and coalescence of bone fragments Fracture union or nonunion with remodeling of fractured and deformed bone

II: Coalescence III: Reconstruction consolidation

Subacute Chronic

Warmth, erythema, and swelling are decreased Warmth, erythema, and swelling are resolved. Residual deformity with bony prominence results in increased pressure and ulceration

infection, instability, and amputation. In a meta-analysis of 15 studies, mortality was 4% (11 deaths in 301 patients) within 2.5 years after treatment for Charcot arthropathy.14 In the same study, 20 (7%) of the 301 patients underwent partial or complete foot amputation in the follow-up period.14 In addition, 83 (28%) of 301 patients required an anklefoot orthosis, permanent bracing, or assistive devices.14 Quality of life may be negatively influenced by Charcot arthropathy, especially because of associated physical impairment.15

Box 1 | Diagnosis of Charcot arthropathy History and physical examination Peripheral neuropathy (diabetes, alcoholism, other) Sensory neuropathy: numbness, paresthesias, neuropathic pain, history of ulcer Motor neuropathy: contractures, claw toes Autonomic neuropathy: dry, scaly skin
New-onset swelling Erythema (may be reduced by elevation of foot) Increased warmth Pain (present or absent; may be mild despite presence of acute bone and joint destruction) Trauma (none, minor, or major; patient may not recall trauma) Bilateral involvement (approximately one-third of patients)

Conclusions

This case illustrates that diabetic midfoot Charcot arthropathy may be associated with deformity and forma tion of potentially limb-threatening ulcers. Diagnosis is frequently delayed but may be facilitated by a high index of clinical suspicion in patients with diabetes mellitus and neuropathy. Surgical excision of bone and realignment arthrodesis may result in successful salvage of a foot that might otherwise need to be amputated.
1. Trepman, E., Nihal, A. & Pinzur, M. S. Current topics review: Charcot neuroarthropathy of the foot and ankle. Foot Ankle Int. 26, 4663 (2005). Brodsky, J. W. The diabetic foot. In Surgery of the Foot and Ankle, 7th edn (eds Coughlin, M. J. & Mann, R. A.) 895969 (Mosby, St Louis, 1999). Eichenholtz, S. N. Charcot Joints (Charles C. Thomas, Springfield, Illinois, 1966). Jeffcoate, W. F. Charcot neuro-osteoarthropathy. Diabetes Metab. Res. Rev. 24 (Suppl. 1), S62S65 (2008). Armstrong, D. G., Todd, W. F., Lavery, L. A., Harkless, L. B. & Bushman, T. R. The natural history of acute Charcots arthropathy in a diabetic foot specialty clinic. Diabet. Med. 14, 357363 (1997). Palestro, C. J. et al. Marrow versus infection in the Charcot joint: indium111 leukocyte and technetium99m sulfur colloid scintigraphy. J. Nucl. Med. 39, 346350 (1998). 7.

Diagnostic studies Radiography: initially may reveal soft tissue swelling with no bone or joint changes; subsequent changes include bone and joint fragmentation, subluxation, and dislocation
Scintigraphy: sensitive but not specific Magnetic resonance imaging may be helpful

2.

3. 4.

5.

6.

Beltran, J., Campanini, D. S., Knight, C. & McCalla, M. The diabetic foot: magnetic resonance imaging evaluation. Skeletal Radiol. 19, 3741 (1990). 8. Verity, S., Sochocki, M., Embil, J. M. & Trepman, E. Treatment of Charcot foot and ankle with a prefabricated removable walker brace and custom insole. Foot Ankle Surg. 14, 2631 (2008). 9. Pinzur, M. S., Sage, R., Stuck, R., Kaminsky, S. & Zmuda, A. A treatment algorithm for neuropathic (Charcot) midfoot deformity. Foot Ankle 14, 189197 (1993). 10. Johnson, J. E. Instructional course lectures of the American Academy of Orthopaedic Surgeons: operative treatment of neuropathic arthropathy of the foot and ankle. J. Bone Joint Surg. 80A, 17001709 (1998). 11. Trepman, E. In Advanced Reconstruction: Foot and Ankle (eds Nunley, J. A. et al ) 405410 (American Academy of Orthopaedic Surgeons, Rosemont, 2004).

12. Schon, L. C., Easley, M. E. & Weinfeld, S. B. Charcot neuroarthropathy of the foot and ankle. Clin. Orthop. Rel. Res. 349, 116131 (1998). 13. Brodsky, J. W. & Rouse, A. M. Exostectomy for symptomatic bony prominences in diabetic Charcot feet. Clin. Orthop. Rel. Res. 296, 2126 (1993). 14. Sinacore, D. R. & Withrington, N. C. Recognition and management of acute neuropathic (Charcot) arthropathies of the foot and ankle. J. Orthop. Sports Phys. Ther. 29, 736746 (1999). 15. Sochocki, M. P . et al. Health related quality of life in patients with Charcot arthropathy of the foot and ankle. Foot Ankle Surg. 14, 1115 (2008). Acknowledgments Charles P. Vega, University of California, Irvine, CA is the author of and is solely responsible for the content of the learning objectives, questions and answers of the MedscapeCME-accredited continuing medical education activity associated with this article.

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