Charcot's foot: what is it, causes, symptoms, treatment, prognosis

What is Charcot's foot?

Charcot's foot (or Charcot joint, neuropathic arthropathy, diabetic osteoarthropathy) Is a destructive joint disease caused by impaired pain or proprioceptive sensitivity as a result of various diseases, most often diabetes mellitus or stroke.

If the pathological process continues uncontrollably, Charcot's disease can lead to joint deformation, ulceration and / or superinfection, loss of function and, in the worst case, amputation or death. Early detection of joint changes is the best way to reduce morbidity.

Causes and risk factors

When certain nerves are damaged, patients lose their ability to feel pain. Damage to these nerves is possible in various diseases, for example, diabetes mellitus, diseases of the spinal cord (injuries and fluid-filled spinal cord cavities [syringomyelia]) and syphilis. The most common reasons are:

• diabetes;
• stroke.

Patients with nerve damage can injure the joint many times without noticing it. Injuries can occur several years before joint dysfunction. However, once the function of the joint is impaired, irreversible destruction of the joint can be observed in just a few months.

Symptoms and Signs

In the early stages, neuropathic arthropathy resembles osteoarthritis, as joints are characterized by stiffness and fluid buildup. Pain is a common early symptom. However, due to impaired perception of pain, pain is often abnormally low in severity when considering the extent of joint damage. Despite this, with the rapid progression of the disease, the appearance of extremely severe joint pain is possible. In such cases, the joint usually swells due to excess fluid and abnormal bone growth. The joint may look misshapen due to a fracture and a sprain, causing loose parts of bone and cartilage to protrude. Due to the protrusion of bone growths into the lumen of the joint, movement in the joint can be accompanied by a rough grinding. The joint can feel like a "bag of bones".

Different underlying diseases affect different joints. For example, complications with untreated syphilis lead to lesions of the knee and hip joint, and the result diabetes mellitus is the defeat of the foot and ankle. Syringomyelia usually affects the spine and joints of the upper extremities, especially the elbow and shoulder joints.

In rare cases, patients may develop secondary arthritiscaused by bacterial pathogens (see. infectious arthritis); there may or may not be a fever or general soreness (malaise) that is characteristic of infectious arthritis. Infectious (septic) arthritis is especially common in people with diabetes.

Overgrowth of bone tissue can compress structures such as blood vessels, nerves, or the spinal cord.

Epidemiology

Charcot's foot has been reported to affect between 0.1% and 0.9% of diabetic patients. An estimated 63% of patients with neuropathic arthropathy develop foot ulceration. A significant association was also found between elevated body mass index and Charcot neuropathic arthropathy..

Pathophysiology

To describe the pathogenesis of Charcot's foot, two generally accepted theories are used: neurotraumatic and neurovascular. The neurotraumatic theory suggests neuropathy, and repeated microtrauma causes joint destruction. The neurovascular theory suggests that increased peripheral blood flow leads to osteolysis and demineralization of the joints.

Key inflammatory markers have been identified pathophysiologically that contribute to the development of acute Charcot's foot. The calcitonin gene-linked peptide (CGRP) usually acts at a nerve ending to antagonistically synthesize nuclear factor ligand kB (RANKL), a cytokine involved in the inflammatory process. However, in the neuropathic foot, CGRP does not function and therefore RANKL is synthesized without inhibition. RANKL is a very important marker in the development of Charcot's foot as it is responsible for the spread of osteoclastogenesis. The osteoclastic ratios of RANKL are usually regulated by osteoprotegerin (OPG / OPG), acting as a decoy receptor for RANKL binding. In Charcot's foot, this link between RANKL and OPG is broken. The unregulated synthesis of RANKL explains the excessive turnover and accumulation of bone tissue seen in neuropathic arthropathy. In addition, CGRP may have an additional role in patients as it is involved in maintaining the integrity of the joint capsule. Therefore, it is assumed that its absence leads to destruction and dislocation of the joint, which is characteristic of Charcot's foot.

Diagnostics

- Clinical signs.

Clinical findings include erythema, edema, and fever in the affected joint. A plantar ulcer may be present in the neuropathic joints of the foot. Please note that it is often difficult to distinguish osteomyelitis from the Charcot joint, since it can have similar markings in the analysis of leukocytes and MRI (joint destruction, dislocation, edema). A bone or synovium biopsy may be required for a definitive diagnosis.

- X-ray signs.

First, it is important to understand that two types of deviations can be detected. One of them is called atrophic, in which there is osteolysis of the distal metatarsal bones of the forefoot. The most common form of destruction is joint hypertrophy, characterized by acute periarticular fracture and joint dislocation.

- Classification.

General classifications representing the stages of the Charcot foot include the Eichengoltz classification and the Sanders and Frickberg classification. The Eichengoltz classifications describe three stages of disease progression based on clinical and radiological data. The Sanders / Frickberg classification is used to describe and classify 5 common anatomical sites of disease.

Eichengoltz classification.

0 pre-Charcot stage / prodromal

• Clinically: red, warm, swollen feet. There is no deformation.
• X-ray: no changes are visible yet. The X-ray is normal.

Stage I development / destruction

• Clinically: erythema, edema of the foot, fever, no pain.
• X-ray: bone debris in the joints, fragmentation of the subchondral bone, joint subluxation and / or fracture-dislocation.

Stage II coalescence

• Clinically: reduced signs of inflammation.
• Radiographically: worsening stage 1. Absorption of bone debris to form new bone. Fusion of large fragments with sclerosis of the ends of the bones. Some increased stability

III stage of consolidation

• Clinically: resolution of inflammation. Changes in the general architecture of the foot due to major final bone remodeling, which can lead to new pressure points at risk of ulceration.
• X-ray: reconstruction of the affected bones and joints.

Sanders and Frickberg classification.

1. Metatarsophalangeal and interphalangeal joints: 15%
2. Tarsometatarsal joints: 40%
3. Scaphoid Cumulus, Scaphoid, Talonavicular and Calcaneal Cuboid: 30%
4. Ankle and subtalar joints: 10%
5. Calcaneus: 5%

Treatment

Shark's foot treatment is aimed at reducing the irreversible deformity of the foot and, ultimately, at ensuring the patient's stable movement. In the acute phase, it is necessary to immobilize the foot and limit the weight load to prevent irreversible deformation. Personal unloading bandage (IRP) and controlled movement of the ankle joint can provide a protected load. The individual unloading bandage redistributes and relieves pressure on the plantar foot, allowing movement.

There are also pharmacological therapies for controlling osteoclastic activity, including bisphosphonates and calcitonin supplements. Bisphosphonates can help in the acute phase of neuropathic arthropathy because they inhibit osteoclastic reabsorption. Calcitonin also acts as an antiresorptive agent. Alternative agents include pamidronate or zoledronic acid, which act on the new hydroxyapatite crystal to block osteoclast precursors in the newly formed bone matrix.

Surgery is also a treatment option, and it remains controversial whether to intervene in the acute or chronic phase of the disease. During the acute phase, there is a storm of inflammatory modulators and cytokines (tumor necrosis factor alpha, interleukin 1 and interleukin 6) that promote bone edema and resorption / fragmentation. The main argument in favor of Charcot joint reconstruction is surgical unloading to prevent ulceration and deformity. The surgeon can achieve this goal through several techniques, including exostectomy, tenotomy, isolated or multiple fusion with external and / or internal fixation. Because of the softer bone, surgeons typically "double" equipment to create a strong "superstructure" to prevent breakage. Based on the experience of the surgeon, minimally invasive intramedullary techniques are also used.

Medical optimization including smoking cessation, control of HbA1c levels below 7-8% and recognition microvascular or macrovascular disease, may reduce potential postoperative complications.

Forecast

It was found that the time for the resolution of acute Charcot's disease for the passage of all stages is about 8 months. In a study by Jansen et. others, 67% of patients with the disease developed complications such as ulcers. In addition, it was noted that non-adherence to treatment significantly worsened the prognosis.

Complications

• Foot deformities such as flat feet, hammer toes, ankle contracture.
• Bony bulges that can lead to ulceration, infection, and in some cases loss of a limb (amputation) or life.
• Recurrence of the Charcot joint
• From the first diagnosis of acute Charcot's disease, the 5-year mortality rate is 13%, which is similar to diabetes without Charcot's disease.