Is Rocker Bottom Reconstruction A Viable Option For Limb Preservation?

Author(s): 
By Scott Neville, DPM, Peter Blume, DPM, and Jonathan Key, DPM

   Although Charcot neuroarthropathy occurs in a small percentage (5 percent) of the diabetic population, the natural disease course is associated with severe morbidity including chronic ulcerations, infections and amputations.1 The medical necessity of limb preservation is well known to all podiatrists. However, the recent advent of rocker bottom reconstruction provides the podiatric surgeon with another tool in the fight for limb preservation.

   Those with ulcerations secondary to Charcot foot deformity are part of a complex subset of patients who require a multidisciplinary approach. The physician who intends to treat Charcot ulcerations successfully must have knowledge of podiatric surgery, plastic surgery and infectious disease, not to mention endocrinology, neurology, cardiology and vascular surgery just to name a few. Over the past decade, the focus of treatment has shifted away from prolonged conservative wound care toward surgical reconstruction with plastic surgery closure of ulcerations.

   A plethora of plastic surgery techniques have been described in the literature. A partial list includes rotational, advancement, pedicle and free flaps. Although these plastic techniques may initially accomplish wound closure, when they are used in isolation, they fail to address the underlying etiology of the ulceration. The root cause of the Charcot ulceration is increased pressure secondary to osseous deformity and concomitant biomechanical flaws. If one does not address this underlying etiology, a flawlessly executed plastic surgery closure or conservative wound care is doomed to fail. This logic has led to the advent of both osseous and soft tissue Charcot reconstruction.

Key Treatment Considerations

   The profound neuropathy coupled with hyperemia, which is idiopathic in the Charcot patient, plays havoc on the osseous structures of the foot. As the hyperemia washes out the bone, the profound neuropathy allows the patient to ambulate free of pain while the osseous structure of the foot is destroyed.

   Eichenholtz described a radiological staging system whereby patients with Charcot could be classified into three stages. The hallmark of the first stage is hyperemia with rapid fragmentation of joints and multiple fractures. The second stage is marked by coalescence of the fragmented osseous structures. In Stage II, the healing process begins and the inflammation starts to subside. Stage III is marked by resolution of inflammation with mature fracture healing. This healing process may result in significant deformity of the affected limb. If this natural disease course can be interrupted, one may minimize catastrophic osseous destruction if not prevent it entirely.2

   The most common deformity resulting from Charcot related osseous destruction is a midfoot collapse, which may result in a rocker bottom deformity.3,4 The midfoot ulcerations that occur secondary to the rocker bottom foot are especially difficult to treat. When conservative care fails to provide closure, the foot is at significant risk for infection and subsequent amputation.

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