A Guide To Early Intervention For The Charcot Foot

By Lee C. Rogers, DPM, and Robert G. Frykberg, DPM, MPH

     The Charcot syndrome is a devastating condition that can affect the feet or ankles of those with diabetes and peripheral neuropathy. The reports on the incidence and prevalence of Charcot foot vary widely, and range between 0.1 to 29 percent among people with diabetes. These studies indicate a trend for a higher frequency in those with peripheral neuropathy and in specialty clinics.1 The specialty clinic providers may have a higher clinical suspicion and may accordingly arrive at a diagnosis more rapidly and definitively.      The risk of amputation increases as the Charcot foot becomes more complicated. Therefore, early intervention is paramount to prevent deformity and ulceration. Effective management of the Charcot foot centers on early diagnosis, medical therapies and surgical interventions.      The timeliness of diagnosis is one of the most vital “interventions” that one can perform. The diagnostic delay averaged 29 weeks in one Charcot foot study.2 If one misses the Charcot syndrome diagnosis, joint subluxations and deformity can occur. Joint deformity is a risk factor for ulceration.3 The natural history of the Charcot foot is one of inflammation, deformity, ulceration and amputation.4      The “early” diagnosis is primarily clinical. It requires a heightened suspicion for the syndrome.5 The clinical signs and symptoms include a warm, edematous foot. The temperature difference is often near 10º F between feet while 4º is considered significant for diagnosis.6 One can measure the temperature with a non-contact infrared thermometer or a digital dermal thermometer (TempTouch, Diabetica Solutions).      Approximately half of the time, the patient will recall a minor, rather innocuous trauma that sparked the event.7 There must be some level of peripheral neuropathy although some patients report a deep pain with their Charcot foot. One may detect autonomic neuropathy during the clinical exam by using the Neuropad (Miro Verbandstoffe) or by checking for a lack of heart rate variability to deep breathing.      When it comes to more advanced presentations with rocker bottom deformity or ulceration, the diagnosis of Charcot foot might be more evident but differentiating it from osteomyelitis (or a concomitant presentation) can be difficult.8 In these cases, it can be useful to have an algorithm to determine if osteomyelitis is present.

Key Insights On Diagnostic Imaging

     The decision process begins with clinical suspicion and subsequent evaluation of plain radiographs. If there is no bone destruction on plain radiography, a standard three-phase technetium-99 bone scan can help to uncover increased bone turnover near the suspected joint.      If there is bone destruction on X-ray, the three-phase bone scan might not be of much use as it would likely be positive. In this case and with the presence of an ulcer, obtaining a white blood cell-labeled scan can help to confirm osteomyelitis. If this scan is negative, the diagnosis is likely Charcot foot. If it is positive, it is either osteomyelitis or Charcot joint disease with osteomyelitis.      There is some controversy about using magnetic resonance imaging (MRI) to differentiate Charcot syndrome from osteomyelitis as both appear similar with this method of imaging. While the white blood cell-labeled scan is extremely sensitive, it is of benefit to observe “secondary signs” on the MRI.9 Accordingly, physicians should keep the following points in mind with osteomyelitis.      • Osteomyelitis generally affects a single bone.      • Osteomyelitis generally has an extending tract.      • Osteomyelitis rarely results in joint deformity.      Additionally, C-reactive protein seems to be elevated in acute infection and not in the Charcot foot. This may aid in the differentiation of the two disease processes.9 More recently, researchers have proven that positron emission tomography (PET) scans are useful in differentiating Charcot foot from osteomyelitis, capitalizing on the metabolic rate differences of the two diseases.10

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