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Primary care physicians involved in the management of patients with diabetes are likely to encounter the diagnostic and treatment challenges of pedal neuropathic joint disease, also known as Charcot foot. The acute Charcot foot is characterized by erythema, edema and elevated temperature of the foot that can clinically mimic cellulitis or gout. Plain film radiographic findings can be normal in the acute phase of Charcot foot. A diagnosis of Charcot syndrome should be considered in any neuropathic patient, even those with a minor increase of heat and swelling of the foot or ankle, especially after any injury. Early recognition of Charcot syndrome and immobilization (often with a total contact cast), even in the presence of normal radiographs, can minimize potential foot deformity, ulceration and loss of function. Orthopedic or podiatric foot and ankle specialists should be consulted when the disease process does not respond to treatment. (Am Fam Physician 2001;64:1591-8.)
Charcot neuropathy is a progressive deterioration of weight-bearing joints, usually in the foot or ankle. Historically, neuropathy of the knee was most frequently caused by syphilis, and neuropathy of the shoulder was usually caused by syringomyelia. Today, the Charcot foot occurs most often in patients with diabetic neuropathy; other predisposing conditions include alcoholic neuropathy, sensory loss caused by cerebral palsy or leprosy, and congenital insensitivity to pain. In 1868, Charcot identified neuropathic joints with an unusual pattern of bone destruction in patients with tabes dorsalis. The first description of neuroarthropathy occurring with diabetes mellitus was published in 1936.
Pathogenesis
Two theories (neurotraumatic and neurovascular) explain the pathogenesis of Charcot foot.' The neurotraumatic theory attributes bony destruction to the loss of pain sensation and proprioception combined with repetitive and mechanical trauma to the foot. The neurovascular theory suggests that joint destruction is secondary to an autonomically stimulated vascular reflex that causes hyperemia and periarticular osteopenia with contributory trauma. Intrinsic muscle imbalance with increased heel and plantar forces can produce eccentric loading of the foot, propagating microfractures, ligament laxity and progression to bony destruction.
As many as 50 percent of patients with Charcot foot remember a precipitating, minor traumatic event (such as an ankle sprain or previous foot procedure); however, multiple cases of spontaneous Charcot joint changes, including patients with foot infections, support hyperemia as...