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Charcot Arthropathy Treatment & Management

  • Author: Mrugeshkumar Shah, MD, MPH, MS; Chief Editor: Jason H Calhoun, MD, FACS  more...
Updated: Dec 18, 2014

Medical Therapy

Treatment of Charcot arthropathy is primarily nonoperative. Treatment consists of 2 phases: an acute phase and a postacute phase. Management of the acute phase includes immobilization and reduction of stress.[11]

Immobilization usually is accomplished by casting. Total contact casts have been shown to allow patients to ambulate while preventing the progression of deformity. Casts must be checked weekly to evaluate for proper fit, and they should be replaced every 1-2 weeks. Patients with concomitant ulceration must have their casts changed weekly for ulcer evaluation and debridement. Serial plain radiographs should be taken approximately every month during the acute phase to evaluate progress. Casting usually is necessary for 3-6 months and is discontinued based on clinical, radiographic, and dermal thermometric signs of quiescence. Other methods of immobilization include metal braces and ankle-foot orthoses (AFOs), but they may prolong healing times.

Reduction of stress is accomplished by decreasing the amount of weight bearing on the affected extremity. While total non-weight bearing (NWB) is ideal for treatment, patients are often not compliant with this treatment. Studies have shown that partial weight bearing (PWB) with assistive devices (eg, crutches, walkers) also is acceptable without compromising healing time. However, full weight bearing (FWB) in the acute phase tends to lengthen total time in the cast.

Healing time varies according to the location of the disease. Pattern 1, or forefoot pathology, heals in two thirds the time of pattern 3 or pattern 4. One study revealed that the mean time in a cast is 18.5 weeks, while another study showed that the acute phase lasts 12.5 weeks.

Management following the removal of the cast includes lifelong protection of the involved extremity. Patient education and professional foot care on a regular basis are integral aspects of lifelong foot protection. After cast removal, patients should wear a brace to protect the foot. Many types of braces may be used, including a patellar tendon-bearing brace, accommodative footwear with a modified AFO, a Charcot restraint orthotic walker (CROW), and a double metal upright AFO.[12]

Custom footwear includes extra-depth shoes with rigid soles and a plastic or metal shank. If ulcers are present, a rocker-bottom sole can be used. Also, Plastazote inserts can be used for insensate feet. This regimen may be eliminated after 6-24 months, based on clinical, radiographic, and dermal thermographic findings. Continued use of custom footwear in the postacute phase for foot protection and support is essential.

The total healing process typically takes 1-2 years. Preventing further injury, noting temperature changes, checking feet every day, reporting trauma, and receiving professional foot care also are important tenets of treatment.


Surgical Therapy

Surgical procedures and techniques vary based on the location of the disease and on surgeon preference and experience with Charcot arthropathy. Surgical procedures include exostosectomy of bony prominence, osteotomy, arthrodesis, screw and plate fixation, open reduction and internal fixation (ORIF), reconstructive surgery, fusion with Achilles tendon lengthening, autologous bone grafting, and amputation. Patients treated with surgery have longer healing times.[11]

Surgical methods can be based on Schön's classification system. The following recommendations may be made:

  • ORIF should be used for an ankle with displaced fractures
  • Ankle arthrodesis is necessary in patients with tibiotalar destruction
  • In cases in which the hindfoot has avascular necrosis of the talus, a talectomy with tibiocalcaneal fusion is necessary
  • Arthrodesis may be necessary for patients with hindfoot involvement
  • For a midfoot pattern, surgical correction of rocker-bottom deformity and osteotomies for bony prominences are used
  • If there is an associated hindfoot/ankle equinus contracture, then a posterior release/Achilles tendon lengthening procedure is required
  • For forefoot patterns, patients with bony prominences or recurrent ulcerations may need a resection arthroplasty or cheilectomy

One small study found minimally invasive arthrodesis plus gradual Charcot foot correction with the Taylor spatial frame to be an effective treatment. This technique may aid in the avoidance of incomplete deformity correction, fixation failure, infections, shortening of the foot, and the use of long-term casts or braces.[13]

Wirth et al reported on the use of the Ilizarov ring fixator for surgical treatment of Charcot arthropathy,[14] citing results from their own experience and from the literature. The concluded that the Ilizarov ring fixator is a viable method for preserving the affected foot in patients with Charcot neuro-osteopathy. They recommend that in assembling the apparatus, the principles of Ilizarov be followed to avoid failure and that a detailed preoperative analysis of corrective osseous and soft tissue interventions be undertaken.

Sohn et al performed a retrospective study to compare the risks of lower-extremity amputation in patients with Charcot arthropathy alone and those with diabetic foot ulcers.[3] They found that Charcot arthropathy by itself does not pose a serious amputation risk, but amputation risk is multiplied in the presence of ulcer complications. In patients younger than 65 years, amputation risk, was 7 times higher for patients with ulcer alone than for those with Charcot arthropathy alone, and 12 times higher for those with Charcot and ulcer.

Della Paola et al evaluated, as an alternative to amputation in patients with Charcot arthropathy, surgical treatment of osteomyelitis of the midfoot or the ankle and stabilization with external fixation.[4] Of the 45 patients studied, 39 healed when treated with emergency surgery to drain an acute infection with maintenance of fixation (average, 25.7 weeks); two were treated with intramedullary nails in follow-up surgery; and in four, infection could not be controlled and amputation was still necessary.[4]





Charcot fractures that are not identified and treated properly may progress to marked joint deformity and to skin ulceration over a bony prominence. The ulceration can result in a severe infection, which may lead to amputation of the extremity.

An additional complication of Charcot arthropathy is foot collapse leading to the formation of a clubfoot. Another commonly seen deformity is the rocker-bottom foot, in which collapse and inversion of the plantar arch occurs. Further complications include the ossification of ligamentous structures, the formation of intra-articular and extra-articular exostoses, the collapse of the plantar arch, and the development of osteomyelitis.


Outcome and Prognosis

Outcomes for Charcot arthropathy are based on immediate diagnosis and treatment. A more favorable outcome is elicited when joints are treated within 2 weeks of injury and when there is strict adherence to weight-bearing precautions.

Location of the disease also affects outcome. Forefoot arthropathies heal in less time than midfoot, hindfoot, or ankle arthropathies, as the following list illustrates:

  • Ankle - Mean healing time, 83 ± 22 days
  • Hindfoot - Mean healing time, 97 ± 16 days
  • Midfoot - Mean healing time, 96 ± 11 days
  • Forefoot - Mean healing time, 55 ± 17 days

Surgical treatment prolongs healing time. The extent of the injury also affects healing time. The more severe the injury, the longer it takes to heal and the greater the likelihood of permanent deformity. It generally takes 1-2 years to completely heal a Charcot joint, from the active phase to quiescence.


Future and Controversies

The current mainstay of therapy for patients with Charcot arthropathy is immobilization and NWB on the affected extremity. However, other treatment options are currently being tested. One option is the use of bisphosphonates, which are potent inhibitors of bone resorption that have minimal effect on bone formation.[15, 16] This action stops the osteoclastic activity of bone breakdown, promotes healing, and decreases local inflammation. However, only a few case reports have examined this treatment as an alternative.

Another therapy that is currently being researched is low-intensity ultrasound.[17] Pulsed low-intensity ultrasound has been shown to transmit micromechanical force and strains to the fracture site and to promote bone formation. Studies have demonstrated an acceleration in healing and an increase in strength at the callus site.

Finally, the use of electrical stimulation and of magnetic field therapy to stimulate bone formation has been discussed in a few case reports. These therapies have shown some benefit in accelerating healing times. However, no prospective studies indicate a positive effect.

Contributor Information and Disclosures

Mrugeshkumar Shah, MD, MPH, MS Staff Physician, Physical Medicine and Rehabilitation, Massachusetts General Hospital/Spaulding Rehabilitation Hospital

Mrugeshkumar Shah, MD, MPH, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.


Walter Panis, MD Clinical Instructor, Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School

Walter Panis, MD is a member of the following medical societies: American Academy of Neurology, American Society of Neurorehabilitation, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Jason H Calhoun, MD, FACS Department Chief, Musculoskeletal Sciences, Spectrum Health Medical Group

Jason H Calhoun, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Diabetes Association, American Medical Association, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Michigan State Medical Society, Missouri State Medical Association, Southern Medical Association, Southern Orthopaedic Association, Texas Medical Association, Texas Orthopaedic Association, Musculoskeletal Infection Society

Disclosure: Nothing to disclose.

Additional Contributors

James K DeOrio, MD Associate Professor of Orthopedic Surgery, Duke University School of Medicine

James K DeOrio, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Foot and Ankle Society

Disclosure: Received royalty from Merete for other; Received royalty from SBi for other; Received royalty from BioPro for other; Received honoraria from Acumed, LLC for speaking and teaching; Received honoraria from Wright Medical Technology, Inc for speaking and teaching; Received honoraria from SBI for speaking and teaching; Received honoraria from Integra for speaking and teaching; Received honoraria from Datatrace Publishing for speaking and teaching; Received honoraria from Exactech, Inc for speaking a.

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Neuropathic arthropathy (Charcot joint). Neuropathic arthropathy of the shoulder in a patient with syringomyelia. Note the destruction of the articular surface, dislocation, and debris, which are pathognomonic for a neuropathic joint.
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