Emerging Evidence On Treatment Of The Diabetic Charcot Foot
Given the challenges of managing the diabetic Charcot foot, the chairmen of a recent international Charcot foot task force review the task force’s recommendations on diagnosing this syndrome and also discuss consensus findings on medical and surgical management.
Charcot foot is a devastating bone and joint disease. While it most commonly occurs in those with diabetes and neuropathy, it has been known to occur with other non-diabetic neuropathies as well. Charcot foot commonly leads to disability and premature retirement. If one is unsuccessful in treating the Charcot foot, amputation is usually the endpoint.
In January 2011, the International Task Force on the Charcot Foot, an international panel of 18 Charcot foot experts, convened via the American Podiatric Medical Association and the American Diabetes Association. The task force met in Paris at the La Salpetriere Hospital, the location where Jean-Martin Charcot, MD, practiced and conducted his research. We were the chairmen of the panel. The goal was to achieve a consensus on the definition, pathophysiology, diagnosis and treatment of Charcot foot, which has not been achieved in the 130 years since the discovery of the condition. The recommendations of the task force were eventually published in the Journal of the American Podiatric Medical Association and Diabetes Care.1,2
Charcot foot is a syndrome consisting of a group of signs and symptoms. Recognizing the Charcot foot as a syndrome as opposed to a disease is an important distinction. The constellation of signs and symptoms in Charcot foot may not be the same in every patient. In fact, they rarely are the same. Most patients complain of a painful, swollen foot, which is notably warmer and erythematous.
Charcot arthropathy is frequently misdiagnosed as cellulitis, gout or deep venous thrombosis. Often, primary care providers are unaware of the condition and the diagnosis can be delayed by months. The rocker bottom deformity is a late finding with the Charcot foot and indicates that the physician previously missed the diagnosis at some point, the patient received inadequate treatment or the patient was non-adherent with recommendations. Foot ulcers can occur at the apex of the osseous deformity where there is maximal plantar pressure.
What You Should Know About Charcot Pathophysiology
While there is no singular cause for the development of Charcot foot syndrome, the prevailing thinking is that the pathophysiology is primarily related to a combination of neurogenic vascular dysregulation and repetitive trauma.1 The individual may be susceptible to Charcot foot, either by having neuropathy or by the presence of a recently discovered genetic polymorphism. The relationship between increased vascularity and bone resorption may lead to a reduced focal bone mineral density and predispose one to fractures. Dislocations can occur in those with normal bone mineral density.
Uncontrolled inflammation results from an inciting trauma in a patient with neuropathy. This phase causes the release of pro-inflammatory cytokines including tumor necrosis factor-alpha and interleukin-1 beta, which lead to an increased expression of the polypeptide receptor activator of nuclear factor kappa-beta ligand (RANKL). The RANKL stimulates the maturation of osteoclasts and the production of osteoprotegerin from osteoblasts. Osteoprotegerin is a decoy receptor that antagonizes RANKL. In the Charcot foot, there is an imbalance of RANKL and osteoprotegerin, leading to an increase in the ratio of osteoclasts to osteoblasts, causing bone resorption.