Charcot Foot: Causes, Symptoms, Diagnosis, Treatment and Prevention

It is a deformity that results from damage to the nerves (neuropathy) in the foot or ankle.

Damage to the nerve causes a loss of sensitivity, increasing the risk of foot injuries. When the foot is repeatedly injured, the joints that support weight break.

The bones are weakened and can break, or the joints can dislocate the foot or ankle. If it does not stop at its earliest stage, the joints in the foot collapse, and the foot eventually deforms.

A deformed foot can cause sores on the feet. An open wound with foot deformity can cause an infection and even reach amputation.

The first signs of Charcot’s foot include redness, swelling, and increased foot temperature.

Charcot’s disease can cause significant bone deformities due to neuropathy, where the supply of nerves to bones and joints is not regular.

Mild trauma or prolonged walking can cause small areas of stress in the bone or joint that lead to a typical stress fracture.


This is the same type of stress fracture that athletes develop.

But, because the patient with diabetes can not perceive the pain of the stress injury, he continues to walk.

The bone’s stress crack begins to worsen and becomes a fracture. The fracture also declines as the walking progresses in the injured foot or ankle.

Charcot neuroarthropathy is a relatively infrequent but severe complication of neuropathy.

It was recorded for the first time in a patient with diabetes in 1936, and since then, the population suffering from diabetes has grown to become the single most significant cause of Charcot’s foot.

Eighty percent of patients who develop Charcot neuroarthropathy have known diabetes for more than ten years.

The long duration of diabetes before the start of the Charcot process reflects the degree of neuropathy that is invariably present in these patients.

It is assumed that autonomic neuropathy has a role in the increase of bone vascularization and increasing osteoclastic activity, which results in bone destruction, fragmentation, and remodeling.

The initiating event of Charcot neuroarthropathy is often a trivial lesion, which can result in a minor periarticular fracture or a more extensive fracture despite the patient’s inability to remember the injury in many cases.

The patient may notice a change in the foot’s shape, and others describe the sensation, or sound, of the bones that creak as they walk.

After this, there is a rapid onset of swelling, an increased temperature in the foot, and often, pain or discomfort.

These processes, if left untreated, cause the characteristic patterns of deformity in Charcot’s foot, including the collapse of the longitudinal and transverse arches that produce the tilting foot.

They also produce the cuneiform metatarsal or the collapsed and distorted ankle joints, which is seen in Charcot neuroarthropathy.

Charcot neuroarthropathy goes into an acute development phase through a coalescence phase, in which the bone fragments are reabsorbed, the edema decreases, and the foot cools.

In the reconstruction stage, when the bone’s final repair and regenerative modeling are made, it is passed to a stable and chronic foot of Charcot.

The intervention must be performed at the earliest stage to prevent deformity, disability, ulceration, and subsequent amputation.


This abnormality of the foot, characterized by pain, redness, swelling, and increased foot temperature, is a degenerative condition in which the joints of the arch collapse due to the alteration of pain sensitivity.

Often, there is only minor trauma to start the sequence of events, so people with diabetes must pay more attention to their feet.

When these minor episodes are not treated, small fractures around the joint go unrecognized, eventually leading to active bone resorption or washing of the bone mineral.

Bone reabsorption compromises the area and produces more extensive fractures and joint damage.

Motor neuropathy and altered nerves for muscle control cause mechanical deformities and imbalances, resulting in the decomposition of the intrinsic musculature that acts as food stabilizers.

It can also affect larger and more proximal muscles, causing muscle imbalance and abnormalities in the feet.


Charcot neuroarthropathy is often overlooked as the cause of a swollen, hot leg in a neuropathic patient with diabetes. Symptoms of Charcot’s foot disease may include:

  • Presence of swelling.
  • Redness of the foot.
  • Feeling of heat in the foot.

This condition can often be confused with osteoarthritis, a much slower progressive deformity.

It is essential to consult the specialist if these symptoms are noticed, especially if the patient has diabetes.

Other signs and symptoms include the following:

  • Pains may diminish or disappear for periods due to the neuropathic component of the deformity.
  • Massive swelling of the foot joints.
  • Bone destruction occurs in several places in the hindfoot and midfoot areas.


Charcot’s foot disease can be diagnosed with physical examination, x-rays, and bone scans.

The diagnosis should be initiated with the history of injuries, even if a simple trip has occurred; X-rays are mandatory exams even if the other signs have not yet developed. Any fractures suffered by the patient must be treated in time.

Computed tomography and magnetic resonance imaging are the best tools for differential diagnosis of Charcot’s foot.


The treatment aims to prevent the appearance of severe deformities of the foot and that the patient can use a shoe without difficulty, and support of the weight on the foot should be limited.

Once the diagnosis has been made, immediate and total immobilization is the best way to reduce the deformity.

Continue walking with weight support can cause significant joint destruction and bone deformities.

Plaster for immobilization should last at least 18 weeks; once removed from the cast, patients need careful monitoring to ensure no relapse.

Skin temperature differences between the active and unaffected feet are still the best marker of Charcot’s foot activity. They are the most commonly used tool to control the resolution of the process.

The treatment will depend on the severity and deformity present in the bone.

Some cases require surgery immediately, and others can be treated with only immobilization.

A boot or plaster is essential, and you should not put weight on the foot until healing occurs.

Surgical intervention is usually complex and involves arthrodesis (fusion) procedures, bone grafts, and internal fixation devices to stabilize, restore position and function, and prevent further destruction.

The bone can take up to a year to heal, and you may have to use the boot during this healing phase.

Late surgery to correct the deformity of the middle foot can be considered as long as the foot is stable and not infected.

Once the ankle has become deformed or is unstable, mainly if there is ulceration, primary amputation may be the best way to provide the patient with a functional limb for walking since attempts at orthopedic surgical repair are often partially successful. Or they fail.


Prevention of a patient at risk is essential.

To help prevent the development of Charcot’s foot, the following should be taken into account:

  • Comfortable shoes should be worn, with a soft insole of microcellular rubber to absorb the blows. Extra-depth shoes are also a good option.
  • It would help if you did not go barefoot.
  • It would help if you used seamless socks that do not irritate sensitive or diabetic feet.
  • A high rate of alertness should be maintained, and the feet should be checked frequently for early signs of Charcot’s foot to prevent further bone destruction. It is necessary to carry out a daily inspection with the help of a mirror.
  • In addition, it must be taken into account that this condition often goes unnoticed by the best doctors or is left under treatment as if it were a condition, such as arthritis.
  • Rest is usually required.
  • Immobilization and participation in activities without weight are essential with any fracture, whether painless or not.
  • The use of compression dressings to reduce edema, special surgical footwear, splints, orthopedic appliances, casts, walkers or crutches, and wheelchairs will be necessary for the various grades of the condition.
  • Immobilization usually requires three to four months. The return to activity should be gradual with shoes molded with depth and additional materials such as the impact absorption template.