What Is the Best Treatment for a Charcot Foot and Ankle?

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Chapter 74 What Is the Best Treatment for a Charcot Foot and Ankle?

Charcot, or neuropathic arthropathy, of the lower extremity is a destructive disease in which patients present with swelling, erythema, and progressive deformity of their feet. Despite diabetes becoming the most common causative agent, the incidence of Charcot neuropathy is quite low in the diabetic population. In a radiographic study,¹ the incidence was noted to be less than 1%, with similar incidence in retrospective clinical studies.² Other studies have reported the presence of Charcot radiographic bony changes in almost 16% of patients with diabetes.³ This large variability may be attributed to difference in definition, alternate diagnosis, and lack of clinical signs despite radiographic changes.

The cause of Charcot disease is related to presence of peripheral neuropathy. Two theories currently exist regarding the pathophysiology of the disease. One theory considers neurotraumatic destruction of the joint, in which multiple trauma to the insensate joint results in microfractures, which over time result in macrofractures and progressive deformity. This concept also includes major fractures that progress to clinical deformity and is similar to the pathway by which arthritic joints in neuropathic patients become Charcot joints with advanced bony changes. The second theory relies on neurosympathetic destruction in which vascular and absorptive changes occur secondary to abnormal neural function, leading to autonomic sympathectomy and vascular alterations, which eventually progresses to gross deformity.⁴ It is thought that a combination of both pathologies contributes to the disease process. A common finding that is not as frequently evaluated is that peripheral perfusion is maintained in this group of patients.

Biologically, the progressive bone resorption seen in Charcot joints is associated with a large number of osteoclasts lining resorptive bone lacunae. The osteoclasts outnumber osteoblasts and demonstrate immunoreactivity to cytokines: interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α). One study concludes that alteration in the synthesis, secretion, or activity of these regulatory molecules may alter bone remodeling and lead to healing without collapse or malalignment.⁵

CLASSIFICATION

The disease process has been divided into stages as described by Eichenholtz.⁶ Stage I is characterized by significant inflammatory response with hyperemia, erythema, swelling, and warmth. Radiographically, this is associated with bony fragmentation. Stage II, known as coalescence, involves decreasing inflammation and edema, with bony coalescence noted radiographically. In Stage III, the bones are consolidated with an absence of inflammatory signs leading to the presence of fixed deformity.⁴ A prodromal stage 0 (“pre-stage I”) category has been described in patients with neuropathy with an acute sprain or fracture that places them at risk for the development of full-blown Charcot arthropathy.⁷ Other classification systems have been developed since then that are based on anatomic location and type of deformity.^8,⁹ The only classification system tested to be reliable and reproducible involved the midtarsus.^9,¹⁰ In this radiographic classification, Charcot anatomic variants of midtarsus deformities are identified by Roman numerals (I-IV) beginning from the Lisfranc joints (I) and extending proximally to the transverse tarsal joints (IV). A severity stage (α [low risk] or β [high risk]) is assigned depending on radiographic features. If one of the following criteria is met, the foot is considered at high risk (β):

1. A dislocation is present

2. The lateral talar-first metatarsal angle is ≥ 30 degrees

3. The lateral calcaneal-fifth metatarsal angle ≥ 0 degrees

4. The anteroposterior talar-first metatarsal angle is ≥ 35 degrees

An α stage can be assigned when all four features are absent. By testing the system on 75 orthopedic surgeons, reliability and reproducibility were found to be high. It was believed to be useful as a tool for diagnosis, planning treatment, and assessing the prognosis.¹⁰

MANAGEMENT

Goals of treatment include the creation and maintenance of a stable plantigrade foot, wound and bone healing, elimination of infection, and prevention of deformity. Current treatment recommendations are based on the stage of disease presentation. Pinzur ¹¹ had reported that reviewing current orthopaedic textbooks reveals almost universal agreement that acute Charcot foot arthropathy, Stage I Eichenholtz, should be treated conservatively, and surgery has only been advised when accommodative treatment has failed.^12,¹³ Despite this general consensus, significant lack of evidence-based studies exist to support this recommendation, with a majority of current data from Level III and IV studies.¹¹ Therefore, a grade C recommendation exists regarding the use of total contact cast (TCC) for the initial management of Charcot arthropathy.

The American Orthopaedic Foot and Ankle Society (AOFAS) has taken an initiative to develop objective data for basing diagnostic and therapeutic guidelines for this disease. A two-part survey was done. Whereas the first part surveyed treatment patterns for 94 patients, the second part consisted of a questionnaire of the clinical preferences completed by 37 AOFAS members with special interest in the disease process.¹⁴ The AOFAS notes from their results that management of the Charcot foot in the community is inconsistent, and significant variability occurs from the current guidelines by both physicians in the community and the specialists.¹⁴

Adjuvant Medical Treatment

In addition to better diabetic control, a number of studies have looked at adjuvant medications during the acute phase to relieve the symptoms.¹⁵ A Level I, randomized, controlled, therapeutic trial of 39 patients with active Charcot neuroarthropathy randomly assigned patients to treatment with 90 mg pamidronate or placebo.¹⁶ The authors report the treatment group had statistically significant reduction of symptoms and warmth; there was also significant reduction in bone turnover markers, bone-specific alkaline phosphate and dehydroxypyridinoline, from 4 to 24 weeks. The authors conclude that pamidronate had a substantial effect on reducing symptoms and bone turnover markers in patients with active Charcot arthropathy.¹⁶ They also suggest that further studies may be necessary to evaluate dosing regimen and frequency of pamidronate administration. Therefore, a grade B recommendation exists for the use of pamidronate in reducing symptoms of active Charcot arthropathy.

Nonsurgical Management

Traditionally, acute Charcot arthropathy, or Eichenholtz Stage I, has been treated with non–weight bearing and TCC. In healthy subjects, plantar peak pressure was shown to be significantly less, and contact duration greater, under the metatarsal heads and heel during gait in a TCC than in a standard shoe.¹⁷ A general belief exists that the healing time for diabetic Charcot fractures may be twice as long as nondiabetic fractures^15,¹⁸; nevertheless, Boddenberg’s¹⁹ literature review found no conclusive evidence to support that assumption.¹⁹ His experience with 28 patients with diabetes compared with 17 patients in a control group found a healing rate of 3.5 versus 3 months in the control group.¹⁹ Another study noted differences in healing based on the location of pathology at an average of 86 ± 45 days, with hindfoot and midfoot Charcot taking longer than forefoot disease to complete healing.²⁰ Thus, grade B level of recommendation exists that the length of treatment of fractures in patients with Charcot arthropathy is similar or only slightly larger in nondiabetic fractures.

In a study of 55 patients with acute Charcot arthropathy who were treated with serial TCC for an average of 18.5 ± 10.6 weeks, all patients returned to permanent footwear over a period of 28.3 ± 14.5 weeks after casting.²¹ The authors note that the casting time to return to footwear was independent of anatomic site of involvement.²¹ However, patients with bilateral involvement required a longer duration of TCC treatment (28 ± 15 weeks) and a longer subsequent period for return to permanent footwear (48 ± 18 weeks; P < 0.02).²¹ A retrospective review of 237 patients showed successful nonoperative management with non–weight-bearing TTC in 115 (48.5%) patients. The cast was changed weekly and discontinued after dissipation of swelling and warmth.¹³ Another study involving 147 patients noted that 87 patients (59.2%) were successfully managed conservatively.¹¹ An additional retrospective study of 221 neuropathic fractures or Charcot joints identified 136 that were managed without surgical reconstruction.²²

However, compliance with non–weight-bearing status is variable and can be limited by physical or medical conditions, or both.¹⁵ Pinzur and colleagues^15,²³ managed 9 patients treated with TTC who were allowed to bear full weight on their casts. At 5 months, all patients progressed to consolidation without any complications or wound problems. In another case series, the authors used a well-padded bivalved cast (moldable, removable to check skin and padding) in 25 (51%) acute Charcot feet with good success.²⁴ Another study by Conti and coauthors^25,²⁶ compared plantar pressure measurements between short leg casts (SLCs) and TTC in 10 healthy subjects. They identified no significant difference between SLC and TTC, although there were marginal decreased hindfoot pressures in TTC.²⁵

In subacute (stage II) midfoot Charcot arthropathy, Myerson and coauthors ²⁷ note that TTC was successful in 70% of patients. As the stages evolved, weight bearing was advanced to full weight bearing, and patients were then placed in protective bracing to decrease the risk for flare-up or displacement.^15,²⁷

From these studies, one may summarize a grade B recommendation exists to support the concept “short leg cast is equivalent to TCC in dissipating pressure and grade C recommendations exist that ‘weightbearing is permissible in cast, in allowing significant proportional of Charcot patients to successfully follow a nonoperative protocol.’”