Key Considerations In Managing The Charcot Foot
Diabetic neuropathy is a major risk factor in patients with diabetes. However, a larger impending threat to patients with neuropathy is the risk of developing Charcot arthropathy and ultimately an ulcer that causes deformity or joint instability. In patients with diabetic neuropathy, Charcot arthropathy alone results in an increased risk of ulceration and/or amputation.1 The subsequent deformities one sees with Charcot, predominantly the rocker bottom deformity, are due to the loss of structural joint integrity.
The subsequent deformities one sees with Charcot, predominantly the rocker bottom deformity, are due to the loss of structural joint integrity. Therefore, one must take a very critical approach in addressing the Charcot joint. Clinicians often mistake neuroarthropathy for infection/cellulitis, gout or osteomyelitis. Early detection and diagnosis will afford the patient an attempt at aggressive offloading, medical management and the possibility of a less devastating deformity. However, in the face of the destructive manifestations of some Charcot joints, one must carefully weigh the surgical considerations and associated risks.
The pathogenesis of Charcot arthropathy has been discussed throughout the literature and researchers have proposed many theories. Various authors have adequately described and proven vascular, neurogenic and traumatic etiologies lending to the multifactorial processes involved in bone and joint destruction.2,3
This has given weight to many theories including: the repetitive microtrauma undetectable by diabetic patients with pain and sensory loss; blood flow response and vasomotion in neuropathic patients with Charcot; osteoclast versus osteoblast activity; and fatigue bone fractures in patients with diabetes. In light of such theories, the devastating effects of Charcot joints remain without debate.
Anatomic as well as pathologic classification systems have been described in attempts to define the breakdown process. Eichenholtz describes three stages dependent on radiographic findings: Stage I, the acute inflammatory process; Stage II, coalescence; and Stage III, the remodeling phase. Anatomic classification has demonstrated the predominance of midfoot arthropathy (Type I) involving the Lisfranc joint complex or the cuneonavicular joints.
Emphasizing Early Detection And Patient Education
Treatment for the neuroarthritic joint can be taxing on both the physician and the patient as a significant time commitment is required of both parties. Patient education plays a major role in reaching an appropriate treatment plan and the desired outcome. The physician must alert the patient of the time involvement in healing both conservative and surgical treatment methods. One must also address external factors with patients and incorporate them within the overall treatment regimen.
One cannot overemphasize the importance of early detection of Charcot arthropathy and appropriate offloading/immobilization. A thorough exam includes a detailed patient history. When evaluating patients with neuropathy, clinicians should pay particular attention to noting any pain and swelling in the absence of a portal for infection. Clinical evaluation should include a neurologic examination, vascular examination and dermal thermometry, all of which provide important diagnostic indicators in support of the diagnosis. In particular, thermometry enables the clinician to monitor healing and facilitate progressive treatment from immobilization to shoegear.