What Are The Best Modalities For Charcot's Foot?

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Essential Tips On Minimizing Limb Loss Caused By Charcot

In diagnosing Charcot’s foot and minimizing subsequent risk of amputation, Caputo, et. al., addressed six important points that every physician treating diabetic patients should know.7

1. Be aware that Charcot’s foot can mimic cellulitis or deep venous thrombosis. While you should certainly consider cellulitis in a patient who is diabetic and presents with a warm, edematous and erythematous foot, misdiagnosing Charcot’s arthropathy in the acute phase of the disease can be disastrous for the patient. Failure to initiate proper treatment not only exacerbates the problem but also can lead to inappropriate treatment with antibiotics, a futile attempt of incision and drainage and needless complications.

If there is any doubt about the presence of infection, you can initiate antimicrobial therapy but you must offload the extremity if the diagnosis of Charcot’s foot remains likely. In our practice, we have a high clinical suspicion of acute Charcot’s foot for all patients who present with diabetes and unilateral swelling of the lower extremity.

2. Do not allow the existence of little or no pain to mislead you or the patient. A finding of minimal pain or no pain can lead patients and physicians to ignore this debilitating disease.

3. Keep in mind that radiographic findings are often normal in the early developmental phase of the disease. X-ray findings often present later during the process of Charcot’s foot, making the diagnosis difficult. If you suspect acute Charcot’s arthropathy during the initial clinical presentation, institute a proper treatment regimen and take serial radiographs.

4. Strict immobilization and protection of the foot, preferably in a total contact cast, is the standard of care to managing the acute Charcot process.

5. A careful program of detailed patient education, protective footwear and a multidisciplinary team approach is required to prevent future complications. Reactivation of the Charcot process can occur and a foot with significant deformity remains at risk for ulceration, infection and osteomyelitis. Meticulous management for these patients, from a podiatric standpoint, is an integral aspect of a lifelong program of foot protection and prevention of skin breakdown.

6. Reconstructive surgery is often reserved for patients who are refractive to conservative measures despite compliance and aggressive treatment.

Here is a clinical view of Charcot’s arthropathy of the left lower extremity.
Total contact casting is the gold standard for offweighting the insensate foot and plantar ulcerations, according to the authors. When employing these casts in Charcot patients with associated ulcerations, the authors recommend weekly cast changes, depend
You can see one patient’s wound that was caused by the Charcot process.
Showing the effects of total contact casting, you can see the healed wound approximately two months after the above photo was taken.
Here is a view of an external fixator ring frame the authors used for a tibial-calcaneal arthrodesis, which they may perform after resecting an osteomyelitic talus secondary to a Charcot deformity.
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Author(s): 
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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