Is External Fixation Overutilized In Managing Charcot In The Diabetic Foot?

By George Liu, DPM, FACFAS

External fixation may provide indirect stabilization of the skeletal defect spanning the area of bone resection or to protect bone graft through percutaneous methods that limit soft tissues exposure.
Inability to offload the affected limb. Overweight and obese patients are significantly associated with diabetes, cardiovascular disease, arthritis and general poor health status.11 The energy consumption required for five minutes of three-point crutch ambulation is markedly elevated as it reportedly increases the heart rate by 53 percent and oxygen uptake by 32 percent.12 Combined with limited cardiac reserve and obesity, most Charcot patients demonstrate difficulty or an inability to offload the affected limb safely despite physical therapy training. With unintentional weightbearing, the patients’ excessive weight may exceed the mechanical limits of internal fixation devices, compromising the purchase of these devices to bone or causing implant failure.
External fixation may provide stable reduction of the realignment arthrodesis, simultaneously allowing a shared loading of the fusion site without exceeding the mechanical limits of the fixator maintaining the correction.
Unstable or non-braceable limb deformities. Both acute and chronic Charcot neuroarthropathy may result in severe and unstable limb deformities that are not structurally stable for weightbearing. Additionally, one cannot reasonably offload these deformities with casting or bracing without exposing the limb to areas of focal high pressures, leading to ulceration. With joint fragmentation, bone resorption and severe deformity that one sees with acute Charcot, internal fixation may not adequately achieve direct stabilization to maintain alignment of open arthrodesis.
External fixation may span areas of demineralized bone and maintain the alignment in arthrodesis. In cases of correction of severe chronic Charcot, osseous correction may be limited by adapted soft tissue and neurovascular structures that may not tolerate acute, single stage correction without complications of soft tissue contracture, wound dehiscence or soft tissue necrosis. One may gradually correct deformities with circular spatial frame or hinge axis methods that allow concomitant soft tissue lengthening and relaxation to occur.

Conservative Management: Can It Have An Impact?
Plantigrade stable foot. Various authors consider a clinically stable, plantigrade, shoeable/braceable foot a successful and desirable outcome of treatment for Charcot neuroarthropathy.4,6,9,10,13-24 Despite significant radiographic patterns of breakdown that are common to see during the quiescent phase, there is little evidence to support elective prophylactic realignment procedures in these patients with clinically stable plantigrade feet that can be safely fit into extra-depth shoes or braces. Furthermore, complications associated with Charcot reconstruction with internal fixation, including limb loss, may not be considered reasonable risks in this lower risk patient group.
Stage 0 and 1. In regard to clinical manifestations of acute Charcot neuroarthropathy in the absence of radiographic signs of joint destruction or deformity, which surgeons refer to as Stage 0 or pre-Charcot, various authors suggest it is best to use compression therapy and subsequent nonweightbearing cast immobilization.22,23,26 This conservative method, including total contact casting, is also widely advocated as the gold standard for Eichenholtz stage I Charcot. In this stage, one may see radiographic signs of early joint fragmentation, destruction and debris formation without significant fracture displacement, joint dislocation or mechanical axis malalignments.
However, surgical intervention during these early stages of Charcot is controversial.

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