Diabetes-associated neuropathic Charcot foot osteoarthropathy is a destructive disease process that frequently leads to severe deformity and disability. This diabetes-specific disease process consumes a disproportionate amount of health care resources for multiple surgical procedures, often leading to lower extremity amputation and premature death. There is growing interest among orthopaedic foot and ankle surgeons in addressing surgical correction of the acquired deformities with the goal of improving walking independence, which appears to reverse the impaired quality of life of affected individuals.

Reconstructive surgery in this patient population is fraught with a substantial potential for unique complications, as many of the patients are morbidly obese, have large wounds overlying substantial bony deformity, have impaired immunity due to their diabetes, and have underlying chronic osteomyelitis with poor bone quality. This review is focused on the use of circular external fixation following correction of deformity. This application is best reserved for those patients who are at the highest risk for complications or failure with standard orthopaedic methods of internal fixation.

Diabetes and Charcot Foot

French neurologist Jean-Martin Charcot first described a destructive neuropathic osteoarthropathy (Charcot foot) in patients with tertiary syphilis in 1868. [1,2] Although penicillin has virtually eliminated tertiary syphilis, this neuropathic arthropathy has not been eliminated, but is now more commonly associated with diabetes. The diabetes-specific neuropathic disorder was first described in the 1930s.

The American Diabetes Association estimates that the number of people with diabetes is rapidly rising, with a current estimate approaching 26 million children and adults affected in the United States alone. It is unclear whether the incidence of diabetes has increased or whether greater awareness has led to diagnosis in previously undiagnosed individuals. A combination of insulin and modern longitudinal management of diabetes and its associated cardiovascular and renal organ system morbidity has allowed people with diabetes to live longer and lead more active, productive lives.

A greater number of those who are newly diagnosed with diabetes are morbidly obese. [3] As with diabetes, it is difficult to determine whether the actual incidence of Charcot foot is growing or whether physicians are simply more aware. [4] Morbid obesity may be one of the key risk factors associated with Charcot foot. [5,6]: The incidence of morbid obesity in the population overall is increasing, which may be at least partially responsible for the growth in the number of people with diabetes. The growing number of patients with diabetes who develop Charcot foot has stimulated many orthopaedic foot and ankle surgeons to attempt creative methods of deformity correction and stabilization, thus avoiding the need for cumbersome and expensive custom-fabricated orthotic devices.

Charcot foot was commonly accepted as a relatively obscure manifestation of diabetes-related peripheral neuropathy. Many experts felt this process was responsible for some temporary disability, but only occasionally created deformity that would negatively impact quality of life and expose affected individuals to the risk of amputation or premature death. [5,7-9] There has been a growing recognition over the past decade, however, that patients with diabetes who develop Charcot foot arthropathy often experience a severe downturn in their quality of life. [10-13] In many affected individuals, this destructive process leads to severe structural deformity of the foot and ankle. The resultant deformity, combined with the historically used cumbersome protective therapeutic accommodative bracing and the frequently associated co-morbidity of morbid obesity, severely limits the independent ambulation of affected patients. [10,13,14] The acquired deformities of Charcoat arthropathy are further complicated by large wounds overlying the bony deformity and underlying contiguous osteomyelitis. Once patients develop associated foot ulcers and chronic osteomyelitis, their risk for lower extremity amputation and premature death is significantly greater than similar non-affected diabetic individuals. [7,13,15]

The typical person with diabetes who develops Charcot foot has had diabetes for more than 10 years, is morbidly obese, and has many of the organ system co-morbidities associated with longstanding diabetes. [5,8,16] Trauma very likely plays an integral role in the initiation of the process. The inciting trauma may be an acute traumatic fracture or dislocation, or it might initiate the pathologic process by the application of sub-fracture producing loads in subjects with impaired protective sensation. Experimental models support theories that the process may be an abnormal pathologic over-reaction to normally applied stress, or may be an insufficiency phenomena producing bony failure secondary to normally applied stresses during walking. Both mechanisms can accept mechanical acceleration of the pathologic process in patients with morbid obesity.

The common endpoint of the applied stress is the release of specific cytokines which upregulate osteoclasts to resorb bone. [17] The now weakened bone, often in morbidly obese subjects, then deforms under the applied loads of weight bearing. This theory would help to explain the radiographic appearance of Charcot foot, which often resembles the deformity of hypertrophic fracture nonunion. [18]

Historical Treatments

Treatment for Charcot foot has traditionally involved non-weight bearing immobilization of the involved limbs in plaster casts. [11] While two recent studies have supported weight bearing during the active phase of the disease process, most physicians advise non-weight bearing during the active destructive phase. [19,20] The avoidance of weight bearing greatly restricts independence in a generally obese patient population, often confining these individuals to a wheelchair, and to the first story of their homes. The ultimate mobility of these individuals is greatly restricted due to the cumbersome and expensive combination of custom fabricated braces and shoes. [21] Even when necessary, the cost of these devices may be prohibitive as many insurance plans only reimburse for a portion of the actual cost of the devices. Even when the braces are successful in accommodating the deformity, the cumbersome and bulky nature of the devices often leads to patient non-compliance.

Surgical treatment has been limited to resection of infected bone, or simple resection of bony prominences that do not allow for the use of the cumbersome accommodative devices. [11] Patients have been treated with these accommodative methods until infection or severe deformity necessitated amputation. They rarely become successful with prosthetic limb fitting due to their large size and the autonomic neuropathic swelling that precludes prosthetic limb fitting. Even when successful, the metabolic cost of walking with a prosthesis, or the associated encumbrance associated with the prosthetic device, often restricts the patient to minimal independent walking.

Surgical correction of the deformities associated with Charcot foot are challenging, due to the large size of the patients, the immune compromise that makes wound failure or infection common, and the severe osteoporosis and vitamin D deficiency that often leads to mechanical failure of the surgical construct. The multiple organ system, diabetes-associated co-morbidities create an increased risk for perioperative medical complications. [6,10,14,22,23,24]

There is a high incidence of postoperative wound infection in patients with diabetes due to impairments in both humeral and cellular immunity. [24] The use of standard orthopaedic metallic foreign body implants is further precluded in over half of patients due to the presence of wounds overlying the deformity that are, at best, contaminated, or, more likely, complicated by underlying osteomyelitis at the time of presentation. [25,26] Extensive surgical dissection leads to wound failure and/or wound infection. The mechanically poor-quality bone leads to late failure of the surgical construct. [18] Several innovative reconstructive surgeons are currently partnering with device manufacturers in the attempt to create innovative implant designs that address these restrictive realities. [27]

New Treatment Options

Understanding that historical accommodative methods of treatment have not always been successful in improving quality of life has convinced many orthopaedic foot and ankle surgeons to attempt surgical correction of these significant deformities. [10,13] This appreciation has evolved during a period when we have learned to partner with our medical colleagues to co-manage these complex patients and decrease the risk for the associated peri-operative medical complications. [28]

Sohn used the large United States Veterans Administration database to determine that patients with Charcot arthropathy are unlikely to undergo lower-extremity amputation unless they develop foot ulcers or infection. [15] Bevan and Tomlinson determined that patients who are radiographically plantigrade at the time of clinical presentation are unlikely to develop foot ulcers or foot infection. They studied weight bearing radiographs of patients followed longitudinally in an orthopaedic diabetic foot clinic. They observed that when a line drawn through the axis of the talus (representing the axis of the hindfoot) was reasonably colinear with a line drawn through the axis of the first metatarsal (representing the axis of the forefoot), patients were unlikely to develop foot ulcers or foot infection (Figure 1a,b). [29]


Figure 1a (top) and 1b. Anterior-posterior weight-bearing radiographs. Figure 1a shows a patient who is clinically plantigrade. Note that a line drawn through the axis of the hindfoot (talus) and the axis of the forefoot (1st metatarsal) are colinear. Figure 1b shows a patient who is both clinically and radiographically non-plantigrade. Note that there is a large angle of deformity (valgus) between the hindfoot and forefoot.

We observed similarly favorable outcomes when patients were determined to be both clinically and radiographically plantigrade at the time of presentation. Clinically plantigrade patients apply weight bearing loads through the uniquely adapted plantar skin of the foot. Clinically non-plantigrade patients are and more likely to develop foot ulcers overlying bony deformity. [30] Multiple surgical techniques have been described which utilize standard methods of orthopaedic internal fixation to maintain correction of the deformity. [31-35] A description of these techniques is beyond the scope of this discussion. It must be remembered that these surgical techniques should not be employed in the presence of large ulcers with exposed bone and chronic osteomyelitis to avoid the likelihood for the development of persistent bony infection. Several new orthopaedic implants are in the process of being developed to address the unique issues associated with osteopenic mechanically poor quality bone. [6,18,27]

Preoperative Planning

Many of the confounding variables associated with diabetes have led several surgeons to employ a modification of the method of Ilizarov to obtain and maintain correction of the acquired foot deformities with a minimal risk of the previously described complications. [25,36-38] This technique uses the Ilizarov concept of limited surgical dissection combined with external fixation achieved with thin tensioned wires.


Patients are operated on in the supine position on a standard operating table. Access for intraoperative fluoroscopy is beneficial.


The surgical approach is made at the apex of the deformity.


Step 1: Lengthening of the gastrocnemius-soleus muscle unit

This is accomplished by either percutaneous lengthening of the tendon or fractional lengthening of the musculotendinous junction. [25,26] The purpose is to establish a muscle balance between the ankle plantarflexors and dorsiflexors. The diabetes-associated peripheral neuropathy universally present in this patient population affects the smaller muscles and nerves of the anterior leg. The resultant motor imbalance creates an equinus bending moment at the junction between the hindfoot and the forefoot during mid-stance of gait. This bending moment may well be responsible for the location of the acquired deformity at the midfoot level in over 85% of patients. [5]

Step 2: Excision of all infected bone associated with the open wounds

Surgically obtained bone cultures are used to direct culture-specific parenteral antibiotic therapy. Patients with chronic open wounds and “negative” cultures, are also treated with a course of parenteral therapy with an antibiotic most likely appropriate to the clinical scenario. The surgery is performed in one stage.

Step 3: Correction of the deformity to create both a clinically and radiographically plantigrade foot

This is generally accomplished by excising a wedge of bone from the apex of the acquired deformity. Sometimes a standard corrective modified triple arthrodesis is used to correct the acquired deformity. Resecting bone at the apex of the deformity often allows loose wound closure. Once the correction of the deformity has been achieved, the surgical wounds can generally be loosely closed without tension. Negative pressure wound therapy or plastic surgery soft tissue surgery can also be used at the time of surgery or following removal of the fixator.

Step 4: Maintenance of the correction with a pre-constructed circular external fixator [25,26]

The method of Ilizarov is used to create a stable clinical construct with the use of fine tensioned wires and no implants at the site of the corrective surgery or previous infection. Thus, the surgery employs limited surgical dissection and leaves no metallic foreign bodies at the site of surgery. The tensioned thin wire external fixator fixation provides an extremely stable surgical construct during the healing phase without the use of bulky, encumbering casts. The known complications associated with gradual deformity correction are minimized since there is no stretching of the bone or soft tissues during the period of treatment.

Case Examples

Case 1: 55-year-old accountant with nonplantigrade deformity

Patient with a nonplantigrade deformity.

Weight-bearing radiograph demonstrating radiographic nonplantigrade deformity.

An incision is made over the apex of the deformity.

Model of the patient’s deformity.

A wedge of bone larger medially and plantar, is removed to correct the deformity.

A pre-constructed, three-level, static circular fixator is available. Note that the proximal ring can be upsized to accommodate a large calf.

The heel is centered in the foot ring. Olive wires are placed at a thirty degree angle to each other, parallel to the weight bearing surface of the foot. The wires are then tensioned and attached to the foot ring.

The forefoot is reduced to the hindfoot. This can be held in place provisionally with percutaneously drilled K-wires. Olive wires are drilled through the metatarsals, again, at a thirty degree angle to each other, parallel to the weight bearing surface of the foot.

Compression of the forefoot to the hindfoot is achieved by “arch wire” technique. This is accomplished by attaching the forefoot wires to the foot ring through holes one hole proximal to the position where the wire is straight.

With the tibia centered in the proximal ring, wires are placed to complete the application.

Case 2: 79-year-old morbidly obese woman

This 79 year old morbidly obese female has been treated with a non weight bearing total contact cast for 9+ months without any evidence of healing.

Non-weight-bearing radiographs reveal that not only is there a lateral dislocation of the talo-navicular joint, but the calcaneus is also dislocated from under the talus. Surgical correction was made with an incision through the open wound. Sufficient bone was removed to reduce the calcaneus under the talus and the forefoot to the reconstructed hindfoot. Provisional fixation was accomplished with percutaneous K-wires. A static frame was applied as described above.

Clinical and radiographic results at two years. The patient now walks with commercially available depth inlay shoes and custom fabricated accommodative foot orthoses.

Pearls and Pitfalls

Avoiding neurovascular injury from wire placement is achieved in two ways. The obvious method is to take care in pin placement. The exit point in the bone should be in “safe zones” that avoid vascular or nerve injury. Two fingers are used to place the wire in position to pierce the skin and hit the bone. The wire is drilled through two cortices with power, and then the drill is removed and the wire is tapped with a mallet through the soft tissues. This slow passing of wires is generally effective in avoiding injury.

Postoperative Care

Pin tract infection is to be expected, occurring in approximately 3% of wires placed. If the skin is tight around a wire, it should be relieved with a small scalpel blade. Patients are treated with oral cephlexin, 500 mg four times daily, until the pin-surrounding cellulitis subsides. Antibiotic therapy is continued at a twice-daily dose until the fixator is removed. Rarely, a persistent pin tract infection will require wire removal and bony debridement.

Patients should be non-weight bearing for 8 to 12 weeks. CT scans are used in difficult patients to determine bony union. Some patients will progress to fibrous union, which may be sufficiently stable to achieve a successful outcome.

The fixator is removed in the surgicenter, using sedation. A weight-bearing total contact cast is then applied for 4 to 6 weeks. Patients then are transitioned to a diabetic walking boot/fracture boot until the volume of the limb is sufficiently stable to allow fabrication of custom foot orthoses and fit the patient for commercially available therapeutic (inlay-depth) footwear.


Treatment of the Charcot foot, surgical or accommodative, has historically been described based on the metrics of wound healing, resolution of infection, or limb salvage. Modern functional outcomes should take these criteria into account, but must also address quality of life issues. A more reasonable description of a favorable outcome is a foot that is ulcer- and infection-free in a patient who is able to ambulate in the community using commercially available therapeutic footwear.


Wound infections are unusual, due to the limited dissection. Pin tract infections are discussed above.

In summary, there is increased interest in the surgical correction of Charcot foot arthropathy as a tool for improving health-related quality of life. Many surgeons have created specific surgical implants to assist in achieving this goal. The use of the Ilizarov circular external fixator has been demonstrated to achieve a high potential for enhanced clinical outcomes with a minimal risk for treatment-associated morbidity.


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