Charcot neuroarthropathic foot deformity is inherently difficult to treat. For the neuroarthropathic patient, dislocation through the midfoot can progress to a rigid, irreducible deformity, or alternately, the foot may develop gross instability at the level of the dislocation which is unbraceable and difficult to manage. Either sequela may lead to chronic ulceration, infection, osteomyelitis, and eventual amputation. Historically, management of the Charcot foot has included extended periods of casting and nonweight bearing until the foot “consolidates,” then treating residual deformity with a functional brace. In the past, surgery was limited to excision of bony prominences in the area of ulceration. More recently, attention has shifted toward surgical restoration of a plantigrade foot by reduction of the dislocation and arthrodesis of the midfoot joints at the level of dislocation. We described the technique of surgical reconstruction with long axial intramedullary screws which span the level of dislocation.^{1, 2} The screws can be applied percutaneously either proximally or distally. Applying fixation in this manner can facilitate reduction of the deformity and diminishes the required surgical exposure compared to plate, or more standard crossed screw techniques.

The initial treatment of neuropathic foot dislocations in most cases is nonoperative. However, some cases warrant initial treatment using operative means. Published classification systems may aid in deciding which patients warrant initial surgical therapy. Neuropathic midfoot dislocation has been classified by Sammarco and Conti and by Schon et al. based on the anatomic pattern of the involved joints and osseous structures.^{3, 4} Schon et al. classified the degree of deformity with either type alpha or beta designation. A beta stage indicates more severe deformity and is assigned if one or more of the following criteria are met: (1) a dislocation is present, (2) the lateral first metatarsal angle is ≥30 degrees, (3) the lateral calcaneal-fifth metatarsal angle is ≥0 degrees, or (4) the AP talar-first metatarsal angle is ≥35 degrees. In cases where the patient continues to have ulceration despite appropriate brace management, surgery is indicated. We believe that patients who either present with, or develop Schon-type beta deformity are best served by deformity correction with arthrodesis (Fig. 13-1). Some patients who have progressive deformity may warrant surgical intervention earlier, particularly if the foot is grossly unstable through the midfoot on physical examination. Patients with acute dislocation often represent an indication for reduction and arthrodesis. Assal and Stern⁵ presented a similar technique for the treatment of intractable ulceration in patients with midfoot dislocation.

Preoperative medical optimization cannot be overemphasized. Poorly controlled medical comorbidities will impede healing at the surgical site and can lead to wound breakdown and infection which in turn can lead to amputation. Vascular assessment is critical, as dysvascular limbs will not heal and are prone to rapid deterioration. It is important to resolve infection prior to surgery and this may require staged procedures including a formal incisional debridement, usually combined with a provisional reduction and use of an external fixator. It is our opinion that open ulceration with gross infection or underlying osteomyelitis is a contraindication to implanting permanent hardware, and that every effort should be made to resolve ulceration prior to surgery.

As this technique involves passing large screws through the articular surfaces of normal joints, it is only appropriate in patients with an insensate foot, as is typically found in diabetic or other forms of neuropathy.