The Charcot Foot: What You Need to Know

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

   The flowchart concentrates on nuclear imaging since magnetic resonance imaging (MRI) is unable to distinguish between Charcot and osteomyelitis without consideration of “secondary signs” or the full clinical picture, which is often unavailable to the reading radiologist.4 Newer modalities, such as the positron emission tomography (PET) scan, may be able to distinguish between the two conditions by a single test.5 The “gold standard” has long been the bone biopsy. However, contamination of the biopsy can lead to false positive osteomyelitis reports.

   Treatment goals are obtaining a stable, plantigrade foot without ulcers. There are various ways to achieve those goals, depending on the stage of presentation with and without surgery. In 2008, the authors proposed a unique two-axis classification for Charcot foot (see “Classifying Charcot Arthropathy” on page 60). This axis uses clinical signs and anatomic levels of involvement to determine the prognosis of the disease.6 As the condition becomes more proximal or more complicated, the risk of major amputation increases. Other more traditional classifications are the Eichenholtz system and the Sanders Frykberg classification.7,8

   One should ensure that the soft tissue is not infected and there is adequate circulation. Physicians commonly misdiagnose the Charcot foot as a diabetic foot infection since there is erythema and increased warmth. However, without a portal of entry such as an ulcer, an infection is unlikely.

   Even if there is an ulcer, physicians should conduct definitive testing to confirm the presence of osteomyelitis. When it comes to the acute Charcot foot, there are often bounding pulses and the foot is warm with an abundance of blood flow.

How To Address Acute Charcot

   There are different treatments for the acute and chronic phases of Charcot. In regard to acute Charcot foot, one should concentrate on eliminating the cycle of inflammation that leads to further bone destruction. There have been no randomized controlled trials with substantial patients in the treatment of Charcot foot.

   While there are currently no specific evidence-based recommendations about the treatment of acute Charcot foot, there are some therapies that have limited evidence. Non-weightbearing in a total contact cast or other device is an absolute necessity. With total contact casting alone, it can take an average of 18 weeks before the temperature of the feet normalizes.9

   Researchers have studied the ability of two bisphosphonates to arrest the Charcot process. These bisphosphonates are pamidronate (IV) (Areida, Novartis) and alendronate (PO) (Fosamax, Merck).10-12 Research has shown that both treatments reduce the temperature differences between feet and the lower urinary by-products of bone turnover. However, the IV therapy was able to achieve this in a matter of weeks versus the oral therapy in months. One trial used intranasal calcitonin to achieve a reduction in foot temperature and markers of bone turnover.13

   We have had some initial experience using self-contained ice water bladders (Cryocuff, Aircast) to reduce the temperature of the Charcot foot. This is based on a proof of concept trial looking at cooling of the diabetic foot and the duration of such cooling.14 However, one should exercise caution in order to avoid causing a cold injury with the neuropathic patient. We have prescribed cryotherapy 30 minutes twice daily and monitored temperatures weekly via thermal imaging.

A Closer Look At The Isolated Tendo-Achilles Lengthening And Exostectomy Procedures

   If medical therapy fails and there is severe deformity, an ulcer or an unstable foot, surgical treatment may be indicated. There are three categories of surgical treatments progressing from relatively simple to more complex.

   Isolated tendo-Achilles lengthening. The Achilles tendon is diseased in the diabetic with neuropathy and often a component to the midfoot dislocation that ensues from Charcot arthropathy.15 The reduction in tendon elasticity and even contracture of the tendon pulls proximally on its insertion on the calcaneus. This acts as a lever through the arch, which increases the deforming forces on the midfoot. One can lengthen the Achilles tendon or, in effect, weaken it. Doing so will reduce this deforming force and may prevent progression of the deformity.

   Physicians should take precautions to minimize complications that are typically associated with Achilles tendon lengthening. These complications include over-lengthening with subsequent calcaneal gait or frank rupture of the tendon.

   During the first three weeks postoperatively, we generally place patients in an instant total contact cast (iTCC), which is a removable cast walker rendered irremovable for 24 hours a day. The patient should not bear weight without the device or he or she may risk tendon rupture. Patients wear the iTCC at night as a splint to prevent the plantarflexion associated with sleeping supine, which can shorten the tendon. Gastrocnemius recession is an alternative to the tendo-Achilles lengthening that might avoid some of the aforementioned complications.

   Exostectomy. Surgeons may perform an exostectomy either alone or in combination with a tendo-Achilles lengthening. A midfoot collapse results in a prominence laterally under the cuboid or medially under the navicular. One can perform the exostectomy through the ulcer, if one exists, or through a separate incision. The surgeon must remove enough of the bone in order to flatten the rocker bottom deformity.

   In a study examining the recurrence rate of ulceration after exostectomy, researchers found that medial exostectomies had the most positive outcomes.16 The authors recommended reconstruction for the lateral cuboid deformities with ulceration. One can also lengthen the Achilles tendon during this procedure.

Essential Insights On Charcot Foot Reconstruction

   Total reconstruction. This category is the most extensive. This operation is physiologically stressful for the patient as it takes between three and six hours. Before considering this procedure, one should conduct a thorough medical review to ensure the patient can tolerate such an operation. Also, the postoperative period requires therapy, a possible stay at a skilled nursing care facility and nearly three months of non-weightbearing on the surgical side.

   In order to correct the deformity, we concentrate on restoring two angles, the lateral talo-first metatarsal angle and the calcaneal inclination angle.17 Occasionally, we consider the forefoot abductus angle if it is extreme. The surgeon may correct the calcaneal inclination angle with a tendo-Achilles lengthening or an Achilles tenotomy. One does not have to completely restore the angle but it should at least not be below 0 degrees.

   Temporarily fixate the calcaneus and talus with a Steinmann pin and complete the remainder of the surgery with the calcaneal inclination angle reduced. After this fixation, the forefoot appears dorsiflexed.

   Plan the other incisions based on the apex of the deformity. We generally perform a medial and lateral incision along the foot. We dissect the soft tissue away from the bone to create a channel in which one can pass a malleable retractor dorsal and plantar to the joint affected (midtarsal or tarsometatarsal).

   Perform an osteotomy with a plantar-based wedge. The size of the wedge depends on the amount of plantarflexion necessary to bring the forefoot to neutral. After removing the osseous wedge, temporarily fixate the forefoot with two Steinmann pins from the first metatarsal into the talus and from the fifth metatarsal into the calcaneus.

   Then the surgeon employs the hardware fixation of choice. It is recommended to use either locking plates for internal hardware or static circular fixation for external hardware in order to avoid fixation failure associated with this osteopenic bone. One can use either internal or external bone stimulation as an adjunct.

   The postoperative period requires strict adherence to the recommendations of non-weightbearing and close observation for postoperative complications, such as infection or fixation failure. Protection of the contralateral extremity is paramount as the incidence of bilateral Charcot foot is 30 to 40 percent. The increase in stress on the contralateral foot can spark a Charcot incident. Therefore, hopping with a walker is not recommended. A Roll-A-Bout (Roll-A-Bout Corp.) can be beneficial to keep the patient mobile and avoid undue stress on the contralateral extremity.

In Conclusion

   The Charcot foot is a complicated entity associated with peripheral neuropathy. Currently, it most commonly occurs with diabetes mellitus. Diagnosis of the Charcot foot is often delayed or missed, resulting in a worse prognosis. Amputation is a common but, in many cases, avoidable sequela of Charcot foot. The goals of therapy are to obtain a stable, plantigrade foot that remains ulcer free.

Dr. Bevilacqua is an Associate Medical Director of the Amputation Prevention Center at Valley Presbyterian Hospital in Los Angeles. He is a Fellow of the American College of Foot and Ankle Surgeons.

Dr. Rogers is an Associate Medical Director of the Amputation Prevention Center at Valley Presbyterian Hospital in Los Angeles. He is a Fellow of the American College of Foot and Ankle Orthopaedics and Medicine.

For related articles, see “Managing Ulcers On The Charcot Foot” in the July 2003 issue of Podiatry Today, “Point-Counterpoint: Active Charcot: Should You Proceed With Surgery?” in the March 2005 issue or “Current Insights On Classifying Charcot Arthropathy” in the April 2009 issue.

References:

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