Charcot neuropathic osteoarthropathy, also known as Charcot neuroarthropathy or Charcot foot, is a condition of localized inflammation leading to varying degrees and patterns of bone destruction, subluxation, dislocation, and deformity of the foot and ankle.1

It is named after Jean-Martin Charcot, a French neurologist who first described the condition in 1868 among patients with tertiary syphilis.

CN is a complication that can also be found in various conditions affected by peripheral neuropathy including HIV, leprosy, poliomyelitis, chronic alcoholism, tabes dorsalis, trauma, syringomyelia, Parkinson disease, sarcoidosis, rheumatoid disease, and psoriasis. However, diabetic neuropathy remains the most prevalent cause internationally.1

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CN is a rare complication of diabetes, and perhaps the least recognized. The prevalence of CN among patients with diabetes is between 0.08% to 0.40% and as high as 13% in some patients.2  

CN affects patient with both type 1 and type 2 DM. With 29.1 million people in the U.S. with diabetes, especially when one in 10 primary-care visits involve diabetes, the incidence of Charcot presenting at the primary care setting will inevitably increase.3

The diagnosis of CN is often delayed due to initially being mismanaged as cellulitis, osteomyelitis, acute gout, or deep vein thrombosis. The only universal predisposing factor of CN is peripheral neuropathy. Other inconclusive risk factors include osteopenia, localized trauma (often minor), history of ulceration or infection, recent foot surgery including successful revascularization.1

CN is a syndrome without definitive causation. The prevailing belief is that uncontrolled inflammation in the foot leads to osteolysis with consequent progressive fracture and dislocation. Another theory indicates that a neutrally mediated vascular reflex results in increased peripheral blood circulation and active bone reabsorption with consequent joint and bone destruction.1

Typical manifestations of Charcot foot are a markedly edematous, warm (three to six degrees Celsius higher), and often erythematous foot with mild-to-moderate discomfort or pain and bounding pedal pulses, except when concealed by edema.

Chronic CN presents with more obvious musculoskeletal deformity and lower extremity ischemia.1 X-rays are usually the initial imaging study of choice for diabetic foot disorders.

During the first three weeks of acute CN, there are usually no changes seen on foot x-rays. Radiographic evidence of dislocation and fracture appear at later stages.4  MRI is the study of choice in the timely diagnosis/confirmation of CN. In cases when MRI is contraindicated, nuclear medicine exams maybe used.1

The initial management of acute Charcot foot is offloading to arrest the progression or prevention of deformity. Immobilization with repeat application of a total contact case (TCC) is the preferred offloading method.

Another option is to use a prefabricated removable walking cast also known as “instant TCC” (this was initially prescribed to Mr. L). Once healed, as indicated by resolution of acute symptoms, the patient will require protective weight bearing in the form of specialized foot wear to minimize recurrence or ulceration secondary to boney deformities (recommended to Mr. L after postoperative healing).

There is no conclusive evidence in the use of antiresorptive medications such as bisphosphonates in active CN and limited support for use of external bone stimulators in the management of Charcot ankle.1

Surgical management is often reserved for patients not responding to offloading and immobilization or those with CN and chronic ulceration. There are three common surgical interventions for CN patients: exostectomy, Achilles tendon lengthening, and arthrodesis.1

Exostectomy involves shaving down bony prominences to alleviate bony pressure points which cause ulcerations.  Achilles tendon lengthening involves making small cuts into the Achilles tendon to stretch the tendon to reduce forefoot pressure.

Arthrodesis involves permanent fusion of affected joints with the use of instrumentation due to chronic joint nonunion and or instability. Hardware used to stabilize the fusion maybe placed internally (will not need to be removed, as in the case of patient Mr. L) or externally (requiring removal after three months).

Diabetes and cigarette smoking have been known to result in compromised surgical wound and bone healing. A study of patients who underwent subtalar arthrodesis reported a 3.8 times increase rate of nonunion in smokers compared to nonsmoker and that patients with diabetes were 18.7 times more likely to have a malunion.5  

Nicotine causes vasoconstriction, increases platelet adhesion, reduces proliferation of red blood cells, fibroblasts, and macrophages. Carbon monoxide decreases oxygen transport and metabolism. Hydrogen cyanide interferes with cellular oxidative metabolism and oxygen transport. 6

Over 100 physiologic factors have been implicated to cause poor wound healing in individuals with diabetes including decrease or impair growth factor production, angiogenic response, macrophage function, collagen accumulation, epidermal barrier function, and keratinocyte and fibroblast migration and proliferation.6

If a fusion procedure fails, the patient will likely require a limb amputation in the near future. For the above reasons, Mr. L was high risk for poor surgical outcome and was started preoperatively on cigarette cessation therapy.

CN also affects psychological well-being. It is a chronic mobility limiting condition, predisposing patients to the life-long consequences of limb amputations. Although it is well recognized that patients with diabetes are at higher risk for depression than the general population, having diabetes and CN (without active ulcerations or amputations) further increases the level of depression and anxiety compared with those who have only diabetes. Those of highest risks are within the CN-diabetes group are female, unemployed, and nonwhite.4

In conclusion, clinicians managing patients with diabetes should be aware of CN as a diagnostic differential in individuals presenting with peripheral neuropathy and foot inflammation.

CN is a rare, but potentially limb threatening condition. Prevention is the best way to minimize CN risk for patients with diabetes. Clinicians can increase awareness of lower extremity complications through self-management education regarding complications of diabetic neuropathy and lower extremity issues, the importance of maintaining good glycemic control, and encouraging daily foot self-examination with routine foot assessment at each clinical care visit for early detection.

Patients with diabetes should be referred to a diabetic foot center for an annual comprehensive foot examination as recommend by the American Diabetes Association to detect and manage diabetic neuropathy and other foot complications.7

Annie D. Lu, ANP-BC, ADM-BC, practices at the NYULMC-Hospital for Joint Diseases Diabetic Foot and Ankle Center.


  1. Rogers, LC et al. 2011; The Charcot Foot in Diabetes. Diabetes Care. 34: 2123-2129
  2. Armstrong, DG, Todd, WF, Lavery, LA, Bushman, TR. 1997; The Natural History of Acute Charcot Arthropathy in a Diabetic Foot Specialty Clinic. Diabetic Medicine. 14 (5): 357-3663
  3. Center for Disease Control and Prevention. 2014; National Diabetes Statistics Report: Estimates of Diabetes and Its Burden in the United States. US Department of Health and Human Services. Retrieved 10/9/14 from http://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes-report-web.pdf
  4. Chapman, Z, Shuttleworth, CMJ, Huber, JW. High Levels of Anxiety and Depression in Diabetic Patients with Charcot Foot. 2014; Journal of Foot and Ankle Research. 7-22
  5. Chahal, J et al. 2006; Factors Associated with Outcomes After Subtalar Arthrodesis. Journal of Orthopaedic Trauma. 20 (8): 555-561
  6. Brem, H, Tomic-Canic, M. 2007; Cellular and Molecular Basics of Wound Healing in Diabetes. The Journal of Clinical Investigation 117 (5): 1219-1222
  7. American Diabetes Association. 2014; Standards of Medical Care in Diabetes 2014. Diabetes Care. 37 (1): 514-577

All electronic resources accessed 12/18/2014.