You are in: eMedicine Specialties > Orthopedic Surgery > FOOT AND ANKLE Charcot ArthropathyArticle Last Updated: Aug 29, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Mrugeshkumar Shah, MD, MPH, Staff Physician, Physical Medicine and Rehabilitation, Massachusetts General Hospital/Spaulding Rehabilitation Hospital Mrugeshkumar Shah is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation Coauthor(s): Walter Panis, MD, Clinical Instructor, Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School Editors: James K DeOrio, MD, Director of Foot and Ankle Fellowship Program, Assistant Professor of Orthopedic Surgery, Orthopedic Surgery, St. Lukes Hospital, Jacksonville, Florida; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Shepard R Hurwitz, MD, Director of Clinical Services, Department of Orthopedic Surgery, University of Virginia School of Medicine; Director, Division of Foot and Ankle Surgery, Department of Orthopedic Surgery, University of Virginia Health System; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Jason H Calhoun, MD, FAAOS, Chairman, J Vernon Luck Distinguished Professor, Department of Orthopedic Surgery, University of Missouri Author and Editor Disclosure Synonyms and related keywords: Charcot joint, neuropathic osteoarthropathy, diabetic osteoarthropathy, diabetic neuroarthropathy, Charcot foot, Charcot neuroarthropathy, neuropathic arthropathy, neuropathic joint, Schon classification, Brodsky and Rouse system, Saunders and Mrdjencovich system INTRODUCTIONSection 2 of 11
  In 1703, William Musgrave first described a neuropathic joint as an arthralgia caused by venereal disease.1 In 1868, Jean-Martin Charcot gave the first detailed description of the neuropathic aspect of this disease; hence, the condition is named after him.2 Charcot noted this disease process as a complication of syphilis. Syphilis was believed to be the most common cause of Charcot arthropathy until 1936, when Jordan linked it to diabetes. Diabetes is now considered to be the most common etiology of Charcot arthropathy. ProblemAlso called Charcot joint or neuropathic joint, Charcot arthropathy is a progressive condition of the musculoskeletal system that is characterized by joint dislocations, pathologic fractures, and debilitating deformities. This disorder results in progressive destruction of bone and soft tissues at weight-bearing joints; in its most severe form, it may cause significant disruption of the bony architecture. Charcot arthropathy can occur at any joint; however, it occurs most commonly in the lower extremity, at the foot and ankle. FrequencyThe prevalence of Charcot arthropathy ranges from 0.1% to as high as 13% in specialized foot clinics. In patients with diabetes, the incidence of acute Charcot arthropathy of the foot and ankle ranges from 0.15-2.5%. Epidemiologic studies do not distinguish between acute and postacute disease. Bilateral disease occurs in less than 10% of patients. Recurrence of disease occurs in less than 5% of patients. Some studies indicate that men and women are equally affected, while others report a 3:1 predilection for males. EtiologyAny condition that causes sensory or autonomic neuropathy can lead to a Charcot joint. Charcot arthropathy occurs as a complication of diabetes, syphilis, chronic alcoholism, leprosy, meningomyelocele, spinal cord injury, syringomyelia, renal dialysis, and congenital insensitivity to pain. Diabetes is considered to be the most common cause of Charcot arthropathy. PathophysiologyThe exact nature of Charcot arthropathy remains unknown, but the following major theories exist regarding the pathophysiology of this condition:
Charcot arthropathy most likely results from a combination of the processes described in the above theories. The autonomic neuropathy leads to abnormal bone formation, and the sensory neuropathy leads to an insensate joint that is susceptible to trauma. The development of abnormal bone with no ability to protect the joint results in gradual bone fracture and in the subluxation of the joint. ClinicalThe clinical presentation of Charcot arthropathy can vary widely depending on the stage of the disease. Thus, symptoms can range from mild swelling and no deformity to moderate deformity with significant swelling. Acute Charcot arthropathy almost always presents with signs of inflammation. Profound unilateral swelling, an increase in local skin temperature (generally, an increase of 3-7º above the nonaffected foot's skin temperature), erythema, joint effusion, and bone resorption in an insensate foot are present. These characteristics, in the presence of intact skin and a loss of protective sensation, are often pathognomonic of acute Charcot arthropathy. Pain can occur in more than 75% of patients; however, the pain's severity is significantly less than would be expected based on the severity of the clinical and/or radiographic findings. Instability and loss of joint function also may be present. Passive movement of the joint may reveal a "loose bag of bones." Approximately 40% of patients with acute Charcot arthropathy have concomitant ulceration, which complicates the diagnosis and raises concerns that osteomyelitis is present. INDICATIONSSection 3 of 11
Surgery is warranted in less than 25% of cases and generally is used as a preventive measure. Surgery is performed when a deformity places the extremity at risk of ulceration and when the extremity cannot be safely protected in accommodative footwear. The goal of reconstruction is to create a stable, plantigrade foot that can be appropriately protected in accommodative footwear and that can support ambulation. Surgery is indicated for malaligned, unstable, or nonreducible fractures or dislocations, as well as for cases in which nonsurgical means fail. RELEVANT ANATOMYSection 4 of 11
Numerous classification systems based on clinical, radiographic, and anatomic pathology describe Charcot arthropathy. Anatomic classification systems are the most commonly used and have the added benefit of predicting outcome and prognosis. The most commonly used anatomic system is described by Saunders and Mrdjencovich.3 Based on the location of the arthropathy, their system classifies Charcot arthropathy into 5 different patterns, as follows:
Studies have shown that patterns 2 and 3 are the most common, with approximately 45% of cases involving pattern 2 and 35% involving pattern 3. Another commonly used classification system is the Brodsky and Rouse system. This system describes 3 anatomic Charcot joints (types 1, 2, and 3a and 3b):
The multilevel Schön classification system is also used; it comprises 4 types and characterizes Charcot joints on the basis of sites and degree of involvement.4 All 4 types have 3 subsets (eg, type IA, IB, IC), which are based on the severity of involvement. The 4 types are as follows:
The Schön classification system allows the prediction of outcomes and the estimation of treatment duration. CONTRAINDICATIONSSection 5 of 11
The major contraindication to surgery is active inflammation. Studies have shown less favorable outcomes when surgery is performed on an acute joint. WORKUPSection 6 of 11
Lab Studies
Imaging Studies
Diagnostic Procedures
StagingSee Relevant Anatomy. TREATMENTSection 7 of 11
Medical TherapyTreatment 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. 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. 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 TherapySurgical 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, reconstructive surgery, fusion with Achilles tendon lengthening, autologous bone grafting, and amputation. Patients treated with surgery have longer healing times. Surgical methods can be based on Schön's classification system. Open reduction and internal fixation 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. Follow-upFor excellent patient education resources, visit eMedicine's Diabetes Center, Sexually Transmitted Diseases Center, and Foot, Ankle, Knee, and Hip Center. Also, see eMedicine's patient education articles Diabetic Foot Care and Syphilis. COMPLICATIONSSection 8 of 11
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. Another 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. Other 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 PROGNOSISSection 9 of 11
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. Average healing times are as follows:
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 CONTROVERSIESSection 10 of 11
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.5, 6 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.7 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. REFERENCESSection 11 of 11
Article Last Updated: Aug 29, 2007 |
