What Are The Best Modalities For Charcot's Foot?

By Guy R. Pupp, DPM, David T. Savage, DPM, MS, and Mark B. Hellmann, DPM, MS

Neuropathic osteoarthropathy is a debilitating condition that affects diabetic patients with peripheral neuropathy. This distinct pathologic entity, commonly known as Charcot’s arthropathy or Charcot’s joint disease, is characterized by pathologic fractures, joint dislocation and deformity, resulting in a foot at high risk for ulceration and amputation in severe cases.
Armstrong, et. al., found the prevalence of Charcot’s arthropathy ranges between 0.16 percent in the general diabetic population of patients to 13 percent of patients presenting to a high-risk diabetic foot clinic.1 Although several theories of this joint destructive process have emerged, the etiology is largely unknown and is probably multifactorial.
Neuropathy and trauma are believed to be the two primary components in the development of Charcot’s joint disease. Nerve dysfunction may be autonomic in nature as well, thus exhibiting abnormal vasomotor regulation. Autonomic neuropathy is central to the development of the Charcot’s foot, leading to hyperemia, increased bone resorption and osteopenia.
Increased blood flow promotes resorption of debris with a concomitant resorption and weakening of healthy bone. Increased lower limb blood flow in diabetes, likely a result of sympathetic denervation, is also associated with arteriovenous shunting. This increased blood flow in neuropathic limbs has been proven by studies such as plethysmography and venous pO2. Often, you may notice that the veins on the dorsum of the Charcot foot are mildly distended with increased skin temperatures as opposed to the contralateral non-affected side. Pedal pulses in patients with neuropathic osteoarthropathy are usually palpable.

What The Literature Suggests
One study involving over 100 patients with Charcot’s disease and quoted by Jeffcoate, et. al., showed the ankle/brachial index was greater than 1.0 in every case.2 Neuropathic patients also have a loss of pain perception, sympathetic functioning and proprioceptive function. With these sensory losses, joints are subjected to stresses that would otherwise not take place with intact protective mechanisms.

Continued ambulation results in capsular and ligamentous attenuation and joint laxity, which then lead to distension and subluxation of joints. The process then continues with cartilage fibrillation, osteochondral fragmentation and pathologic fractures. Further joint destruction precedes a natural hyperemic response to injury, causing additional resorption and destruction of the joints.3 Although there’s been much discussion on causative factors, the etiology still lies somewhere between neurovascular and neurotraumatic theories.
An article from The Journal of Bone and Joint Surgery revealed elevated peak plantar pressure in patients who have Charcot’s foot.4 This increased pressure, when combined with a tight Achilles tendon secondary to glycosylation, creates significant strain in the midtarsal joint region, which leads to collapse. The most common anatomical location of Charcot’s joint disease is at Lisfranc’s (tarsometatarsal) and Chopart’s (talonavicular/calcaneocuboid) joints in more than 80 percent of foot and ankle occurrences.1,4

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