Current Insights On Classifying Charcot Arthropathy
- Volume 22 - Issue 4 - April 2009
- 23220 reads
- 0 comments
Before the advent of insulin, death from diabetes occurred early in the disease process. Now people with diabetes are living longer and long-term complications of the disease are more common. One such complication is Charcot arthropathy and since the early report by Jordan linking it to diabetes, the number of case reports has steadily increased.1
Although the etiology of Charcot arthropathy is largely unknown, it is well recognized that this condition can occur in conjunction with any peripheral neuropathy. Researchers have found that Charcot arthropathy is associated with tabes dorsalis, syringomyelia, congenital insensitivity to pain, alcohol abuse, sarcoma of the spine, leprosy and recently, HIV-associated neuropathy.2-10 Today, diabetes is the most common cause of Charcot arthropathy.
Charcot arthropathy is a rapidly progressive and debilitating process, and the natural progression is well documented. J.M. Charcot, through detailed clinical observation, described the bone and joint changes associated with this condition. Acute Charcot arthropathy of the foot is characterized by inflammation. Clinical signs and symptoms of inflammation include profound unilateral edema, localized skin temperature increase and erythema. The affected foot may be as much as 9 to 11º F warmer than the same point on the contralateral limb.
These initial clinical signs and symptoms of inflammation precede bone and joint involvement. In acute Charcot, radiographs may appear normal. After the initial inflammatory phase, further trauma leads to progressive bone and joint destruction that becomes easily visible on radiographs (see “What You Should Know About Imaging And Charcot” on page 26).
A Guide To The Eichenholtz Classification
Attempts to define the natural course of Charcot arthropathy have produced a number of classification systems. In 1966, Eichenholtz classified the sequence of changes in “Charcot joints,” which he observed via serial radiographs.13 He divided these changes into three stages.
The predictable sequence of changes began with Stage 1 (stage of development), which is distinguished by clinical signs and symptoms of inflammation (warmth, erythema and edema) and the visibility of radiographic changes. Common radiographic findings include bone debris formation at the articular margins, fragmentation of the subchondral bone, subluxation, dislocation and capsular distention.
Eichenholtz stage 2 (stage of coalescence) is marked by decreased warmth, erythema and edema. Radiographs show absorption of fine debris and fusion of large fragments to adjacent bones. The bone ends become sclerotic. At this point, the deformity ceases to progress and transitions to the reconstructive or remodeling stage.
Stage 3 (stage of reconstruction or remodeling) is characterized by rounding of the bone ends with a decrease in sclerosis, leading to consolidation. A structural bone deformity may be present and this resultant deformity may lead to skin breakdown and potential infection followed by amputation.