Abstract
Background: The standard management for Eichenholtz Stage-I Charcot arthropathy has been with non-weight-bearing total contact casts. The purpose of this study was to evaluate the results of the use of weight-bearing total contact casts for similar patients.
Methods: Twenty-seven patients with Charcot arthropathy of the foot and ankle were studied prospectively over a period of eighteen years, from 1988 to 2006. The average duration of follow-up was 5.5 years. Of the twenty-seven patients, twenty-six had diabetes mellitus. Total contact casts were used to treat thirty-four feet with Eichenholtz Stage-I or early Stage-II Charcot arthropathy. These patients were allowed to bear weight as tolerated. Casts were changed at weekly intervals and were worn until resolution of the acute stage of the disease.
Results: No deleterious effect from weight-bearing, specifically with regard to skin ulceration or rapid deterioration of the osseous architecture, was observed in thirty-three of the thirty-four feet.
Conclusions: Immobilization in a weight-bearing total contact cast appears to be a safe method of treatment of acute Eichenholtz Stage-I Charcot arthropathy of the foot and ankle.
Level of Evidence: Therapeutic Level IV. See Instructions to Authors for a complete description of levels of evidence.
Charcot arthropathy occurs in patients with diabetic neuropathy, although it is occasionally encountered in patients who do not have diabetes mellitus. The disorder is important enough to have been placed second in the priority listing for the investigation of problematic foot conditions by the Research Council of the American Orthopaedic Foot and Ankle Society1. Neuroarthropathy was originally described by Jean Martin Charcot in 18682 and was mainly associated with tabes dorsalis resulting from syphilis. Jordan first noted its relationship to diabetes in 19363, and now most cases of Charcot arthropathy are associated with that condition. Charcot arthropathy is a chronic destructive arthropathy involving the foot and ankle. The exact mechanism remains unclear; however, there is increasing understanding of the pathophysiologic process. According to the neurotraumatic theory4,5, repetitive microtrauma gives rise to periarticular fracture and joint dislocation. The continued loading of the affected foot and ankle in the absence of protective sensation leads to a hypertrophic type of healing response—classically seen as hypertrophic osteoarthropathy in the later stages of the disease. According to the neurovascular theory4,5, the peripheral neuropathy brings about an impairment of autonomic function resulting in sympathetic overaction, hyperemia, and consequent bone loss. The resorption leads to weakening of bone and ligaments with consequent periarticular fracture or dislocation during normal loading. More recently, work with markers of osteoclast and osteoblast activity has suggested that, in the acute stage, there is excessive osteoclastic activity without a concomitant increase in osteoblastic function. This finding may be important in the pathogenesis of Charcot arthropathy6.
The incidence of Charcot arthropathy of the foot and ankle is not precisely known, but it has been stated that the disorder occurs in up to 7.5% of the diabetic population7. Type-II diabetes alone affects approximately 8% of adults in the United States8, and it is estimated that this figure will be much higher in the years to come. Charcot arthropathy usually appears after the first decade of the disease and is not related to the type or severity of the diabetes, to gender, or to insulin dependency.
Eichenholtz classified Charcot arthropathy into three stages on the basis of its natural history9. Stage I is the acute stage, or the stage of development. The patient presents with a swollen, erythematous, warm foot. The foot is acutely inflamed and hyperemic, and most patients report some pain in spite of the sensory peripheral neuropathy. At this stage, the radiographic findings classically consist of only periarticular soft-tissue swelling. Destructive changes consisting of periarticular fracture and joint subluxation develop at the end of this stage, as Stage II develops. Stage I lasts for two to six months. Stage II is termed the stage of coalescence. The swelling and warmth decrease, and the redness disappears. The inflammation settles but not without leading to structural weakness, to joint subluxation and dislocation, and to fracture. Often this results in deformity of the foot and ankle. The start of Stage III marks the end of inflammation. It is the time when consolidation and healing occur. There is no warmth or swelling; instead, the foot thickens as it settles into a deformed state. In combination, Stages II and III last from eighteen to twenty-four months.
Charcot arthropathy is also classified according to its site of involvement. In Brodsky's classification10, Type I involves the tarsometatarsal and naviculocuneiform joints. It is the most commonly encountered type and accounts for 65% to 70% of all cases. Type II involves the subtalar, talonavicular, and calcaneocuboid joints. This group accounts for 20% to 25% of the cases. Type IIIA involves the ankle joint, and Type IIIB involves only the tuberosity of the calcaneus.
Because of their location, these types are characterized by distinctive patterns of behavior and progression. Type-I arthropathy leads to the development of a rocker-bottom type of foot deformity with valgus at the midfoot. The osseous changes are essentially hypertrophic. In Type II, erosive changes are predominant, with a tendency for instability to develop, requiring longer periods of immobilization than are necessary for Type I. Furthermore, the resultant shift and enlargement of the hindfoot calls for appropriately modified footwear. Type IIIA, Charcot arthropathy of the ankle, usually ends up with shortening, with the foot drifting into varus or valgus. Problems of both instability and osseous prominences are noted in this type. In Type IIIB, the pathologic fracture involves the tuberosity of the calcaneus with proximal displacement of the often large fracture fragment.
The standard treatment for Charcot arthropathy is prolonged external immobilization, for as long as two years when all forms of immobilization are considered. The goal is to protect and rest the foot through the inflammatory and destructive stages until the foot stabilizes in a position of minimum deformity that can ultimately be accommodated in a shoe or an appropriate orthosis.
Classically, in Stage I and in the early part of Stage II, the disease is managed with use of total contact casts; after the active disease phase has subsided, the foot is immobilized in an accommodative orthosis or custom-made shoe7. The standard treatment for Stage-I Charcot arthropathy has been non-weight-bearing total contact casts, and the list of centers that recommend and stress the importance of non-weight-bearing is long11-21.
The indications for surgery are limited; they include marked instability, fixed deformity that cannot be treated with a brace, recurrent ulceration that is not controlled with cast immobilization, and infection. In an acute setting (Stage I), the indications for surgery may include severe dislocation without bone fragmentation resulting from ligamentous disruption22. Early arthrodesis has also been attempted23.
At the Hennepin County Medical Center, many diabetic patients with Charcot arthropathy tended to be noncompliant with our strong recommendation that they not put weight on the affected leg when it was immobilized in a cast; almost all of them bore weight on the leg. We observed that, during that early stage of the disease, weight-bearing against our advice did not cause the harm that we had expected. This initial observation led us to institute a formal prospective study in which patients with Charcot disease of the foot were allowed to bear weight on the limb while it was in a total contact cast. We thought that, if this approach turned out to not cause the harmful effects one associates with weight-bearing, it would be of tremendous benefit to these patients, and it would make the management of Charcot arthropathy much easier.
Of forty-seven patients with Charcot arthropathy of the foot and ankle who were seen over a period of eighteen years, from 1988 to 2006, twenty-seven were included in this prospective study. The remaining twenty were excluded because of irregular attendance, noncompliance, inadequate or lost radiographs, or inadequate follow-up. They were followed for an average of 5.5 years (range, one year to fourteen years).
Of the twenty-seven patients, twenty-one were female and six were male. Twenty-six had diabetes mellitus and one did not; of the twenty-six with diabetes, seventeen had Type-II disease and nine had Type-I disease. All patients had established neuropathy, twenty-two had retinopathy or another major visual problem, and twenty had nephropathy. Eleven of the patients with nephropathy had had a kidney transplant, and six were on dialysis (see Appendix).
Seven (26%) of the twenty-seven patients had bilateral involvement of the foot. This resulted in thirty-four individual feet affected by Charcot arthropathy. More than one Brodsky Charcot type was noted in eleven feet (see Appendix).
Total contact casts were used for all patients with Eichenholtz Stage-I or early Stage-II disease, and the patients were allowed to bear weight. Although various methods have been used to ascertain the end of Stage I and the beginning of Stage II, we relied on careful examination of the foot and ankle. The examiner identified diminished swelling by close observation and decreased warmth by meticulous palpation with the palm and the back of the hand and fingers. Water displacement methods, infrared thermometers, and skin thermistors were not used. Radiographs of the foot and ankle were routinely made at two-week intervals in the early phases of treatment. Later, they were repeated at less frequent intervals. As the disease progressed into the latter part of Stage II and into Stage III, a solid ankle patellar tendon bearing brace, a University of California at Berkeley Laboratory orthosis (UCBL), or a shoe with a deep and wide toe-box with a smooth vamp with no stitching was worn. More recently, we have used the CROW (Charcot Restraint Orthotic Walker)24 when indicated.
Total Contact Cast
No one method of applying a total contact cast has been universally accepted. In every variation that is employed, however, the essence has been to achieve an intimate fit of the cast around the foot and ankle through meticulous molding. At our institution, a regular stockinette is first placed around the foot, ankle, and leg, followed by the application of two layers of WEBRIL (Kendall, Mansfield, Massachusetts) padding. One-eighth inch (3.2 mm) of foam or felt is then placed over the medial and lateral malleoli and the tibial crest, and lamb's wool is placed between the toes. Three to four layers of Orthoflex (Johnson and Johnson, New Brunswick, New Jersey) plaster of Paris are then wrapped around the foot, ankle, and leg from 0.5 in (12.7 mm) distal to the tibial tubercle to just beyond the tips of the toes on the plantar aspect. The cast is painstakingly molded beneath the longitudinal arch and around the medial and lateral malleoli and the calf. The proximal and particularly the distal edges of the cast are checked for any irregularity or unevenness that might impinge on the skin. After the plaster of Paris has set, two or three layers of fiberglass bandage are wrapped around the plaster of Paris.
The ankle is maintained in a neutral position. Weight-bearing in a rocker-bottom cast boot is allowed after twenty-four hours to give enough time for the plaster of Paris to dry.
Should an ulcer be present, it is débrided if necessary. A piece of ADAPTIC gauze (Johnson and Johnson) is then placed over the ulcer, and it is covered by a sterile nonadhesive dressing and a 2 × 2-in (5 × 5-cm) gauze sponge. A piece of one-eighth-inch-thick felt is then placed around the ulcer to provide pressure relief. The cast is then applied as described above.
All patients were seen at weekly intervals, at which times the cast was changed and the foot and ankle were evaluated in detail with particular attention paid to swelling, redness, and warmth. The condition of the skin was checked for any evidence of localized pressure from the cast. The radiographs made at two-week intervals were reviewed to look for increased joint space or diastasis, subluxation or displacement, fragmentation, erosion or osseous destruction, angulation, settling, impaction or shortening, and hindfoot varus or valgus. These radiographic changes occur toward the latter part of Stage I as it progresses into Stage II.
Time was spent with the patients to explain the need for prolonged cast treatment, as they invariably found this discouraging. Those who were regular in their attendance were commended, and others who failed to keep their appointments or interfered with their casts were encouraged to comply with the treatment protocol.
The average period of immobilization in a total contact cast was fourteen weeks, with a range of four to twenty weeks (see Appendix). On the average, patients with a Brodsky Type-IIIA lesion had a longer period of cast treatment (sixteen weeks) than did those with Type I (nine weeks) or II (thirteen weeks).
Weight-Bearing and Its Effect on Osseous Stability
We paid meticulous attention to cast-application technique and to changing casts at regular weekly intervals, and we did not encounter any problems with the acute swelling characteristic of Stage I. The main reason advanced for the current practice of non-weight-bearing in Stage I is the prevention of a further shift in, or a separation of, the osseous architecture already rendered unstable by the process of capsular distension.
Of the thirty-four feet, seventeen had a Brodsky Type-I Charcot lesion; eight, Type-II; and seven, Type-IIIA. Only four feet (two with a Type-I and two with a Type-IIIA lesion) presented with normal anatomy at the time of application of the first cast. The remaining thirty feet had some anatomical change or disruption. The important finding was that, except for one (right) foot with Type-I involvement (Case 24; see Appendix), there was no further displacement of any importance in any foot once it had been immobilized in a weight-bearing total contact cast (Figs. 1-A and 1-B).
Of fifteen feet with a Type-I lesion (excluding the two with normal anatomy at the time of initial application of the cast), ten had erosions, fragmentation, or fracture with or without displacement in the tarsometatarsal region. Five had mild subluxations with or without these preceding changes. Of the eight feet with a Type-II lesion, two had erosions, fragmentation, or destruction in the talonavicular region, mainly involving the talar head. Six had mild subluxations with or without the preceding changes. Of the seven feet with a Type-IIIA lesion, two had normal anatomy at the initial presentation. Of the remaining five, three had Charcot changes that had occurred after open reduction and internal fixation of a fractured ankle, one had a fracture through the distal parts of the tibia and fibula involving the ankle with a resultant varus shift (Figs. 2-A and 2-B), and one had had a recurrent acute Charcot episode with incipient destruction after apparent healing of a Type-IIIA lesion.
Although some of the changes were substantive in terms of architectural disruption, they occurred before cast treatment was undertaken. The only important clinical deformity was the 5° of varus in the patient with the fracture through the distal parts of the tibia and fibula (Figs. 2-A and 2-B). The varus did not progress after the cast treatment was instituted.
Changes that were seen following weight-bearing in total contact casts in the acute stage were gradual in their progress and minimal in their extent except for those in Case 24 (see Appendix), a right foot with Type-I involvement that was seen to have deterioration of the osseous architecture after four weeks in a weight-bearing cast.
Weight-Bearing and the Development of Ulcers
Ulcers were noted in ten feet, but none of them occurred during the time that the feet were immobilized in a weight-bearing total contact cast. They all developed after the limb had been placed in an orthosis, when the arthropathy was in late Stage II or beyond (at an average of 6.5 weeks [range, six to 156 weeks] after fitting of the orthosis). The ulcers were located primarily in three areas: the malleoli, the plantar aspect of the foot, or the dorsum of the foot.
The literature is replete with recommendations that patients with diabetes mellitus and Stage-I Charcot arthropathy remain non-weight-bearing while the leg is in a total contact cast11-21. The main reason given is to prevent further progression of the deformity. In Stage I, the acute stage when the foot is acutely inflamed (swollen, red, and warm), the osseous structures fragment and ligaments are disrupted, resulting in subluxations, fractures, and fracture-dislocations. Most centers, therefore, still strongly recommend non-weight-bearing while the leg is in a total contact cast during Stage I of the disease. Laughlin et al.11 stated that, to prevent these complications: "Weight-bearing on the affected foot should not be allowed until the inflammation stage is over, which may take several weeks to several months." Miller20 explained it thus: "The initial treatment for uninfected Charcot foot should be to ‘cool down’ the foot or ankle because of the risk that the unstable bone will continue to fracture (either in large fragments or in microfractures) during ambulation causing more inflammation. The affected area should be immobilized and mechanical forces on the bone, such as those incurred during walking, should be minimized." Clohisy and Thompson12 went further by recommending prophylactic immobilization of the contralateral extremity in a protective cast or orthosis, in addition to non-weight-bearing cast treatment on the affected side.
While the literature enjoins strict adherence to non-weight-bearing when a total contact cast is used in Stage I of the disease, some physicians closely associated with the treatment of this problem are known to allow weight-bearing during this stage. With use of a questionnaire sent to selected members of the American Orthopaedic Foot and Ankle Society in a 2000 study of current practice patterns in the treatment of Charcot arthropathy, Pinzur et al.25 found that as many as 41% of the respondents allowed weight-bearing by patients with Eichenholtz Stage-I arthropathy even though 78% of them used total contact casts.
McDermott26 observed that these patients do, in fact, often bear weight for a variety of reasons, including reduced sensation from neuropathy, noncompliance, and the inability to use crutches or a walker because of problems with proprioception and balance. Brodsky10,14 is among the few to allow most of his patients with Stage-I Charcot arthropathy to bear weight with the leg in a total contact cast.
The initial impression at our center was that the patients who bore weight while wearing the total contact cast were merely noncompliant. A closer evaluation, however, revealed that these patients had deficiencies in many areas of health and function. Because of the neuropathy and reduced sensation, many could only gauge if they had a cast on from a feeling of increased weight; for the same reason, they were not sure if they were putting any weight on the leg in the cast, or not. Their often diminished eyesight added to their difficulties in following a straight path, and they were also encumbered by crutches. Also, they were not as strong as they once were. It was thus understandable why they had difficulties with the additionally imposed non-weight-bearing regimen.
When we realized early on that bearing weight on the leg while it was in the cast, against medical advice, was not causing much harm, a decision was made to let the patients continue to do this but at the same time to study the effects of weight-bearing in a formal and critical setting.
Except in one case, we did not observe a substantial shift or a progressive disorganization of the osseous architecture, nor did we see problems with the initial swelling on weight-bearing during the acute stage, as long as the casts were changed and the feet were carefully inspected each week. Furthermore, a skin ulcer or an infection did not develop in any of our patients during the time of weight-bearing cast treatment.
However, of the thirty-four feet treated, only four had normal anatomy at the time of the initial application of the cast. The remaining thirty feet had minor anatomical changes or disruption, which was the result of delay before their first visit to our clinic for treatment of the Charcot arthropathy. This was very likely the result of the associated neuropathy and the relative absence of pain as well as the lack of adequate information on the part of the referring physician. What was ultimately important was that no further change or deterioration occurred in all but one patient once the weight-bearing cast regimen was instituted.
Although we are convinced that weight-bearing causes no harm, it would have been ideal to have conducted a randomized study. However, because noncompliance by this type of patient arises not from choice primarily but from the debilitating nature of the illness, we believe that a randomized study comparing weight-bearing with non-weight-bearing total contact cast treatment would have been difficult, if not impossible, to conduct. Another limitation of the study was that it was difficult to know exactly when Eichenholtz Stage I ended and Stage II began. Therefore, we often extended the period of treatment with the weight-bearing total contact cast to include the earlier part of Stage II. The relative noncompliance of these patients with regard to attending clinic dates regularly and on time was another limitation, but we saw them often enough and long enough after Stage I had clearly ended to give us enough confidence about our decision to allow weight-bearing.
Notwithstanding these limitations, we believe that this study confirms that no harm ensues when a diabetic patient presenting with acute Eichenholtz Stage-I Charcot arthropathy bears weight with the leg in a total contact cast, and we are now firm in our confidence in that management protocol. The weight-bearing total contact cast would be changed every week until the arthropathy has clearly progressed to Stage II.
Tables showing the clinical data and periods of immobilization for each patient are available with the electronic versions of this article, on our web site at (go to the article citation and click on "Supplementary Material") and on our quarterly CD-ROM (call our subscription department, at 781-449-9780, to order the CD-ROM). 
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