Cath Lab Digest

Given the potential complications of Charcot foot in the diabetic population, these authors review the pathophysiology of the disease, discuss key diagnostic considerations and offer their perspectives on possible surgical treatments.

   The Charcot foot poses quite a challenge in even the most organized centers. The outcomes are often poor and can lead to osteomyelitis, amputation and permanent disability. The diagnostic delay averages 29 weeks.¹ Even when appropriate diagnosis occurs early, there is no agreement on the best treatment approach.

   Charcot foot, also known as Charcot arthropathy, neuro-osteoarthropathy and Charcot’s arthropathy, is named after Jean Martin Charcot. Charcot was a French neurologist who first described this condition in 1868 as a consequence of syphilis and called it tabetic arthropathy.

   Charcot did make some connections between the appearance of tabetic neuropathy and diabetic neuropathy. However, it was not until 1936 that William Riely Jordan, MD, described arthropathy of the foot secondary to diabetes mellitus.² It can also occur in other neuropathy-producing diseases like HIV/AIDS, hereditary neuropathy and alcoholism.

   Since that time, diabetes has become the most common cause of Charcot foot in the world. The other comorbidities associated with diabetes cause the patient with Charcot foot to fare worse than those without diabetes. Namely, peripheral arterial disease and diabetic immunosuppression negatively affect the outcome.

   The neurovascular or the neurotraumatic model can describe the pathophysiology. The common day “unified theory” suggests it is a combination of both models. Neuropathy affects all three divisions of the peripheral nervous system: sensory, motor and autonomic.

   The sensory impairment leads to repetitive unfelt trauma. Motor impairment causes abnormal gait through contractures such as equinus deformity, leading to increased plantar pressure and midfoot dislocation forces. Autonomic dysfunction leads to flushing of the capillary beds, including increased diameter in the Haversian systems in the bone. This “washing out” of the mineral content of the bone causes focal osteopenia of the affected foot or joint. In combination, all of the above lead to joint subluxations and frank dislocation or fracturing.

Pertinent Insights On Diagnosing Charcot

   The diagnosis of Charcot foot begins at the bedside. The history may include some form of trauma, major or minor. Patients will generally have diabetes and neuropathy for a period between eight and 12 years. There will be swelling, redness and increased warmth of the foot. The affected foot may be 10ºF or more warmer than the unaffected foot. A dermal thermometer or infrared thermal imager can quantify the temperature difference between feet.

   Neuropathy will be present but many patients still experience some deeper pain. In the later stages of the process, the foot may already be deformed with a “rocker bottom” appearance, which can lead to an ulcer in the area of highest pressure.

   After entertaining a clinical suspicion, one must confirm the diagnosis by imaging and differentiate the Charcot from other bone and joint diseases such as osteomyelitis. Physicians can use a stepwise flowchart (see “When There Is Clinical Suspicion Of Charcot Foot” on page 58) to help determine if bone destruction is due to Charcot arthropathy, osteomyelitis or both.³