Given the challenges of managing the diabetic Charcot foot, the chairmen of a recent international Charcot foot task force review the task force’s recommendations on diagnosing this syndrome and also discuss consensus findings on medical and surgical management.
Charcot foot is a devastating bone and joint disease. While it most commonly occurs in those with diabetes and neuropathy, it has been known to occur with other non-diabetic neuropathies as well. Charcot foot commonly leads to disability and premature retirement. If one is unsuccessful in treating the Charcot foot, amputation is usually the endpoint.
In January 2011, the International Task Force on the Charcot Foot, an international panel of 18 Charcot foot experts, convened via the American Podiatric Medical Association and the American Diabetes Association. The task force met in Paris at the La Salpetriere Hospital, the location where Jean-Martin Charcot, MD, practiced and conducted his research. We were the chairmen of the panel. The goal was to achieve a consensus on the definition, pathophysiology, diagnosis and treatment of Charcot foot, which has not been achieved in the 130 years since the discovery of the condition. The recommendations of the task force were eventually published in the Journal of the American Podiatric Medical Association and Diabetes Care.1,2
Charcot foot is a syndrome consisting of a group of signs and symptoms. Recognizing the Charcot foot as a syndrome as opposed to a disease is an important distinction. The constellation of signs and symptoms in Charcot foot may not be the same in every patient. In fact, they rarely are the same. Most patients complain of a painful, swollen foot, which is notably warmer and erythematous.
Charcot arthropathy is frequently misdiagnosed as cellulitis, gout or deep venous thrombosis. Often, primary care providers are unaware of the condition and the diagnosis can be delayed by months. The rocker bottom deformity is a late finding with the Charcot foot and indicates that the physician previously missed the diagnosis at some point, the patient received inadequate treatment or the patient was non-adherent with recommendations. Foot ulcers can occur at the apex of the osseous deformity where there is maximal plantar pressure.
What You Should Know About Charcot Pathophysiology
While there is no singular cause for the development of Charcot foot syndrome, the prevailing thinking is that the pathophysiology is primarily related to a combination of neurogenic vascular dysregulation and repetitive trauma.1 The individual may be susceptible to Charcot foot, either by having neuropathy or by the presence of a recently discovered genetic polymorphism. The relationship between increased vascularity and bone resorption may lead to a reduced focal bone mineral density and predispose one to fractures. Dislocations can occur in those with normal bone mineral density.
Uncontrolled inflammation results from an inciting trauma in a patient with neuropathy. This phase causes the release of pro-inflammatory cytokines including tumor necrosis factor-alpha and interleukin-1 beta, which lead to an increased expression of the polypeptide receptor activator of nuclear factor kappa-beta ligand (RANKL). The RANKL stimulates the maturation of osteoclasts and the production of osteoprotegerin from osteoblasts. Osteoprotegerin is a decoy receptor that antagonizes RANKL. In the Charcot foot, there is an imbalance of RANKL and osteoprotegerin, leading to an increase in the ratio of osteoclasts to osteoblasts, causing bone resorption.
Essential Diagnostic Insights
The diagnosis of Charcot foot syndrome is primarily a clinical one. A hot, red, swollen foot in a patient with neuropathy is Charcot foot until proven otherwise. Clinicians must have a high index of suspicion.3 One can sometimes elicit a personal history of antecedent trauma. The patient usually recalls the trauma to be trivial. There is usually a temperature differential between feet of between 4 and 10ºF.4 One can obtain temperature measurements by contact dermal thermometer, non-contact infrared thermometer or by infrared thermography. Obtaining temperature measurements is the single most important test in our practices for uncovering inflamed Charcot feet.
The task force reviewed all the existing classifications for Charcot foot. We determined that while all the classifications are descriptive, none are particularly helpful in providing a prognosis of the condition or determining treatment.1,2 Therefore, the task force recommended a simple clinical classification based upon inflammation. If there is inflammation present, the Charcot foot will be active. When there is no inflammation, the Charcot foot will be inactive. These are better descriptors than acute and chronic since the latter only describes time or duration of the condition. One can discern active and inactive Charcot foot clinically, and help determine what treatment is best.
In regard to the initial presentation, X-rays may be normal, but subtle changes in bone quality or subluxations can be visible. If the syndrome progresses unfettered, frank dislocation and fractures occur. Medial calcification of the arteries can be visible on X-ray as a secondary finding. Magnetic resonance imaging (MRI) allows for the detection of subtle changes in the marrow and can be positive when the X-rays are normal.
Magnetic resonance imaging is not good at differentiating Charcot foot from osteomyelitis as both conditions appear similar.5 Even experienced radiologists have difficulty discerning between the two conditions. Looking for secondary signs can help one differentiate between the two. In regard to secondary signs, osteomyelitis primarily affects one bone while Charcot foot affects several bones and joints. Deformity is rare with osteomyelitis but common with Charcot foot. Osteomyelitis usually occurs in the toes, forefoot and heel while Charcot foot usually occurs in the midfoot and ankle. Other tests like nuclear imaging, positron emission tomography (PET) scans or sulfur colloid marrow scans are helpful in some cases.
The task force offered the diagnostic recommendations.1,2
• The diagnosis of active Charcot foot is primarily based on history and clinical findings. One should confirm the diagnosis with imaging.
• Inflammation, the earliest finding in Charcot, plays a key role in the pathophysiology of the Charcot foot.
• The occurrence of acute foot or ankle fractures or dislocations in neuropathic individuals is considered active Charcot foot. This is due to the inflammatory process of bone healing, even in the absence of deformity.
• X-rays should be the initial imaging. One should look for subtle fractures or subluxations if no obvious pathology is visible.
• In the absence of radiographic findings, MRI or nuclear imaging can confirm clinical suspicions.
What The Literature Reveals About Medical Treatment
The most important immediate treatment for the active Charcot foot is offloading. The use of a total contact cast immobilizes and offloads the foot.6 In certain settings, a removable cast walker would be appropriate. In some cases, we recommend total non-weightbearing.
Patients can use rolling walkers and wheelchairs but should exercise caution with the use of crutches. Many people with diabetes and Charcot foot are obese and all have peripheral neuropathy, which impairs proprioception and can lead to falls. Many don’t have the cardiovascular reserves to use crutches effectively. Additionally, the use of walkers for more than balance is not advisable since hopping on the unaffected foot can be a traumatic event and can lead to a Charcot process. Nearly 30 percent of patients with Charcot have bilateral Charcot foot so one must be cautious to avoid trauma.1
There are some studies on pharmacologic therapies to arrest the active Charcot foot. Bisphosphonates such as pamidronate (Aredia, Novartis) and alendronate (Fosamax, Merck) have shown benefit in some small studies.7,8 Pamidronate is a single dose intravenous infusion. Alendronate is a once weekly oral therapy. A recent large population study from the United Kingdom showed no benefit for bisphosphonates.9
Intranasal calcitonin is another option. Patients spray calcitonin in the nostril once daily, alternating nostrils. Advocates have theorized it is a better treatment than bisphosphonates because it has direct action on the RANKL/osteoprotegerin pathway.10 Others have discussed the use of potent anti-inflammatories, such as TNF-alpha inhibitors typically used in inflammatory arthritides.11
In regard to medical treatment, the task force made the following recommendations.1,2
• Offloading the foot and immobilization are the most important treatment recommendations for active Charcot foot. These can prevent further destruction of the foot.
• There is little evidence to guide the utilization of available pharmacologic therapies to promote the healing of Charcot foot.
• Protected weightbearing is required after an active episode. This consists of prescription devices such as shoes, boots or braces.
What The Task Force Recommends On Surgical Treatment
The task force consisted mostly of Europeans of non-surgical specialties and Americans in surgical specialties. Naturally, there was division on the recommendations for surgery along those lines. The panelists agreed that one should reserve surgery for cases of severe instability, non-braceable deformity, infection or failed ulcer healing.1,2 Additionally, the panel agreed that surgery could be a primary treatment for Charcot arthropathy of the ankle since the outcomes with any medical treatments are poor.
The surgical approach is based primarily on expert opinion as there are only a few larger retrospective studies. The task force agreed that there will likely never be high-quality surgical studies in the Charcot foot due to the rarity and difficulty in performing surgical studies. The goals of surgery should be to create a more stable plantigrade foot that one can brace with a shoe or Charcot restraint orthotic walker (CROW), and heal any ulcers.
The approach differs based upon the joints affected, the severity of the condition and the surgeon’s experience or preference. Usually one would address the Achilles tendon surgically since equinus is known to be a deforming force at the midfoot, causing dislocation. Authors have described techniques using internal and external fixation.12 Surgical arthrodesis is generally effective and radiographic fusions are common, but fibrous pseudarthroses may produce the same positive outcome. Most experienced surgeons recommend more stable fixation, longer non-weightbearing time and longer follow-up times when correcting the Charcot foot. Complications are common and the surgeon should address them as they happen.13
The task force made the following recommendations about surgical management.1,2
• Surgical treatment is beneficial in Charcot foot or ankle cases refractory to offloading and immobilization. Surgery is also beneficial in the case of recalcitrant ulcers.
• The initial management of acute neuropathic fractures and dislocations should not differ from initial management techniques for other fractures.
• Exostectomy is useful in relieving any bony pressure that orthotics and prosthetics cannot accommodate.
• Lengthening of the Achilles tendon or gastrocnemius tendon reduces forefoot pressure. It also improves the alignment of the ankle and hindfoot to the midfoot and forefoot.
• Arthrodesis can be useful in patients with instability, pain or recurrent ulcerations who fail non-operative treatment, despite a higher rate of incomplete bony union.
• For severe Charcot arthropathy of the ankle, one could consider surgical management as a primary treatment.
The Charcot foot syndrome is a complex complication of diabetes and neuropathy, but physicians can prevent major deformity associated with this syndrome. We should have a high index of suspicion when examining a neuropathic patient with a hot, swollen foot. If one implements existing treatments early, they are effective at preventing ulceration and bony destruction.
Offloading is the most important initial treatment and given the risk benefit ratio, offloading should begin even during the diagnostic period. Other pharmacologic treatments have not shown conclusive benefits. Surgical treatments can be effective when experienced surgeons perform them. However, one should reserve surgical treatment for cases in which offloading and bracing fail, or in cases of severe instability.
Jean-Martin Charcot, MD, concluded his seminal paper on tabetic arthropathies, which now bear his name, with the statement “sera continue,” which means “to be continued.” More than 130 years later, his statement remains true. There is much we have to learn about the pathophysiology of this condition, which will generate future therapies.
Dr. Rogers is the Co-Director of the Amputation Prevention Center at the Valley Presbyterian Hospital in Los Angeles.
Dr. Frykberg is the Chief of the Podiatry Section and the Podiatric Residency Director at the Carl T. Hayden Veterans Affairs Medical Center in Phoenix.
1. Rogers LC, Frykberg RG, Armstrong DG, et al. The Charcot foot in diabetes. J Am Podiatr Med Assoc. 2011;101(5):437-446.
2. Rogers LC, Frykberg RG, Armstrong DG, et al. The Charcot foot in diabetes. Diabetes Care. 2011;34(9):2123-2129.
3. Rogers LC, Bevilacqua NJ. The diagnosis of Charcot foot. Clin Podiatr Med Surg. 2008;25(1):43-51.
4. Armstrong DG, Lavery LA. Monitoring healing of acute Charcot’s arthropathy with infrared dermal thermometry. J Rehabil Res Dev. 1997;34(3):317-321.
5. Rogers LC, Bevilacqua NJ. Imaging of the Charcot foot. Clin Podiatr Med Surg. 2008;25(2):263-274.
6. Frykberg RG, Mendeszoon E. Management of the diabetic Charcot foot. Diabetes Metab Res Rev. 2000;16(Suppl 1):S59-65.
7. Jude EB, Selby PL, Burgess J, et al. Bisphosphonates in the treatment of Charcot neuroarthropathy: a double-blind randomised controlled trial. Diabetologia. 2001;44(11):2032–2037.
8. Pitocco D, Ruotolo V, Caputo S, et al. Six-month treatment with alendronate in acute Charcot neuroarthropathy: a randomized controlled trial. Diabetes Care. 2005;28(5):1214–1215
9. Game FL, Catlow R, Jones GR, et al. Audit of acute Charcot’s disease in the UK: the CDUK study. Diabetologia. 2012;55(1):32-35.
10. Bem R, Jirkovska A, Fejfarova V, et al. Intranasal calcitonin in the treatment of acute Charcot neuroosteoarthropathy. Diabetes Care. 2006;29(6):1392-4.
11. Khanna D, Arnold EL, Pencharz JN, et al. Measuring process of arthritis care: the Arthritis Foundation’s quality indicator set for rheumatoid arthritis. Semin Arthritis Rheum. 2006;35(4):211-237.
12. Bevilacqua NJ, Rogers LC. Surgical management of Charcot midfoot deformities. Clin Podiatr Med Surg. 2008;25(1):81-94.
13. Rogers LC, Bevilacqua NJ, Frykberg RG, Armstrong DG. Predictors of postoperative complications of Ilizarov external ring fixators in the foot and ankle. J Foot Ankle Surg. 2007;46(5):372-375.