Managing Ulcers On The Charcot Foot

By Pamela M. Jensen, DPM, and John S. Steinberg, DPM

Neuropathic osteoarthropathy, or Charcot arthropathy, is a condition associated with a loss of sensory nerve function and concurrent vascular dynamic changes. In the acute setting, Charcot can result in bone and joint deformation and fragmentation. If it is not treated early and aggressively, the collapse of involved joints will cause instability, deformity and subject bony prominences to ulceration and infection. The incidence in the United States and internationally of those with diabetes who have Charcot arthropathy ranges from 7.5 to 13 percent. Internationally, 10 to 20 percent of those with tabes dorsalis and 20 to 25 percent of patients with syringomyelia have some degree of Charcot arthropathy. The age of onset is usually between the fourth and fifth decade with a diagnosed duration of diabetes greater than 15 years. Presentation is usually unilateral but bilateral involvement has been noted at 5.9 to 39.3 percent. Ethnic groups are equally susceptible to having a Charcot arthropathic event. Understanding The Etiology Of Charcot Arthropathy Two independent theories, the “neurotraumatic” and the “neurovascular” theories, have been proposed as to the cause of this deformity. However, the consensus of current literature indicates a combination of factors from both theories is generally present in Charcot arthropathy. The neurotraumatic theory (German theory) proposes that an unperceived trauma to an insensate foot renders the patient unaware of osseous destruction that occurs during ambulation. The resulting trauma leads to progressive destruction and significant damage to bone and joints. The neurovascular theory (French theory) proposes that autonomic neuropathy, caused by the underlying nervous system impairment and degeneration, results in hyperemic demineralization that leads to osteopenia. The combination of these theories with initial abnormal bone formation due to autonomic deformity and the following microtrauma of the insensate foot, results in multiple fractures and joint subluxation. Shapiro, et. al., (1988) concluded blood flow in Charcot patients is intact and loss of blood flow in patients with diabetes is protective against Charcot. While this may be worthy of further investigation, our clinical experience has demonstrated significant limb ischemia in the face of chronic Charcot. While blood flow may have been intact at the time of the initial Charcot episode, it may be deficient several years later when treating the chronic Charcot foot deformity. This is of particular importance when evaluating the non-healing Charcot ulceration and also in considering surgical alternatives in the management of this patient population. Key Clinical Signs And Symptoms The clinical presentation of Charcot arthropathy generally begins with inflammation, localized warmth to extremity (3 to 7ºF when compared to the non-affected foot or otherwise normal skin temperature), diffuse erythema, joint effusion, intact skin without ulceration and loss of protective sensation. Up to 75 percent of acute Charcot arthropathy patients will present with some level of pain. However, many present with no pain or pain that is significantly less than expected when one considers the clinical and radiographic findings. These patients may have instability, deformity and loss of joint function. In extreme cases, the foot may present as a “loose bag of bones.” Approximately 40 percent of Charcot arthropathy patients have a concomitant ulceration, thereby complicating the diagnosis and raising concern for osteomyelitis.1 Eichenholtz described the staging of Charcot arthropathy, which is based on clinical and radiographic changes that progress from the acute phase through the healing phase (calescence) to the resolution phase. One should use radiographs to stage the disease and monitor its progression. In the acute or active stage, you will see persistent or progressive joint effusion, narrowing of the joint space, soft tissue calcification, minimal subluxation, preservation of bone density (unless infected) and fragmentation of eburnated subchondral bone. This is often followed by progressive destruction of articular surfaces, subchondral sclerosis, osteophytosis, intraarticular loose bodies, continued subluxation and fracture/dislocation of the bony architecture.

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