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 that increases the risk of foot injuries . When the foot is repeatedly injured, the joints that support weight begin to break.
The bones are weakened and can break or the joints can dislocate in 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 deformity of the foot 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 very important bone deformities, as a result of neuropathy, where the supply of nerves to bones and joints is not normal.
Mild trauma or prolonged walking can cause small areas of stress in the bone or joint that lead to a normal or stress fracture.
This is the same type of stress fracture that athletes develop.
But, due to the fact that the patient with diabetes can not perceive the pain of the stress injury, it continues to walk.
The stress crack in the bone begins to get worse and becomes a fracture. The fracture also gets worse as the walking progresses in the injured foot or ankle.
Charcot neuroarthropathy is a relatively infrequent but serious 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 largest cause of Charcot’s foot at present.
Eighty percent of patients who develop Charcot neuroarthropathy have a known diabetes with a duration of more than 10 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 this increases osteoclastic activity, which results in bone destruction, fragmentation and remodeling.
The initiating event of Charcot neuroarthropathy is often an apparently trivial lesion, which can result in a minor periarticular fracture or in a larger fracture despite the patient’s inability to remember the injury in many cases.
The patient may notice a change in the shape of the foot 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 increase in temperature in the foot and often, a pain or discomfort.
It is these processes that, 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 phase of development through a coalescence phase, in which the bone fragments are reabsorbed, the edema decreases and the foot cools.
In the reconstruction stage, when the final repair and regenerative modeling of the bone is 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 a subsequent amputation.
This abnormality of the foot, which is characterized by pain, redness, swelling and increased temperature of the foot, is a degenerative condition in which the joints of the arch collapse due to the alteration of pain sensitivity.
Often, there is only a minor trauma to start the sequence of events, so it is extremely important that diabetics 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 to the washing of the bone mineral.
Bone reabsorption compromises the area and produces larger fractures and joint damage.
Motor neuropathy and altered nerves for muscle control cause mechanical deformities and imbalances, and later result in the decomposition of the intrinsic musculature that acts as foot 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
For these reasons, this condition can often be confused with osteoarthritis , which is a much slower progressive deformity.
It is important to consult the specialist if these symptoms are noticed, especially if the patient suffers from diabetes.
Other signs and symptoms include the following:
- Pains, which may diminish or disappear for periods of time due to the neuropathic component of the deformity.
- Massive swelling of the foot joints.
- Bone destruction, which occurs in several places in the hindfoot and midfoot areas.
Charcot’s foot disease can be diagnosed with a physical examination as well as 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, and any fractures suffered by the patient must be treated in time.
Computed tomography and magnetic resonance imaging are the best tools to perform the differential diagnosis of Charcot’s foot.
The aim of the treatment is to prevent the appearance of severe deformities of the foot and that the patient can use a shoe without difficulty, any 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 a very important joint destruction and bone deformities.
Plaster for immobilization should last at least 18 weeks, once they are removed from the cast, patients need careful monitoring to ensure that no relapse occurs.
Skin temperature differences between the active and unaffected foot are still the best marker of Charcot’s foot activity and are the most commonly used tool to control the resolution of the process.
The treatment will depend on the severity and the deformity that is present in the bone.
Some cases require surgery immediately and others can be treated with only immobilization.
The use of a boot or plaster is important and you should not put weight on the foot until healing occurs.
Surgical intervention is usually complex and involves arthrodesis (fusion) procedures and the use of 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 the ankle is unstable and particularly 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 in a patient at risk is very important.
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 micro cellular rubber to absorb the blows. Extra depth shoes are also a good option.
- You should not go barefoot.
- You must use 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 often required.
- Immobilization and participation in activities without weight is 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 in the various grades of the condition.
- Immobilization usually requires three to four months. The return to activity should be gradual with the use of shoes molded with depth and with additional materials such as the impact absorption template.