Neuropathic arthropathy

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Neuropathic arthropathy (or neuropathic osteoarthropathy ), also known as Charcot joint (often " Charcot foot ") for progressive degeneration of the load bearing joint, a process characterized by bone damage, bone resorption, and ultimately deformity due to loss of sensation. Onset is usually dangerous.

If this pathological process continues to be out of control, it can lead to joint deformity, ulceration and/or superinfection, loss of function, and in the worst case scenario, amputation or death. Early identification of joint changes is the best way to limit morbidity.

Video Neuropathic arthropathy

Symptoms and signs

Clinical presentation varies depending on the stage of the disease from mild swelling to severe swelling and moderate deformity. Inflammation, erythema, pain and increased skin temperature (3-7 degrees Celsius) around the joint may be visible on examination. X-rays can reveal bone resorption and degenerative changes in joints. These findings in the presence of whole skin and loss of protective sensation are pathognomonic of acute Charcot artropathy.

Approximately 75% of patients experience pain, but less than expected based on the severity of clinical and radiographic findings.

Maps Neuropathic arthropathy

Pathogenesis

Any condition that causes decreased peripheral sensation, proprioception, and fine motor control:

Diabetes mellitus neuropathy (most common in the US today, resulting in foot and ankle joint damage), with the Charcot joints at 1/600-700 diabetics. Associated with poor long-term glucose control.
Alcoholic neuropathy
Cerebral palsy
Leprosy
Syphilis ( tabes dorsalis ), caused by the organism Treponema pallidum
spinal cord injury
Myelomeningocele
Syringomyelia
Intra-articular steroid injections
Congenital insensitivity to pain
Peroneal muscle atrophy

Underlying mechanism

Two main theories have been put forward:
- Neurotrauma : Loss of peripheral sensation and proprioception causes repeated microtrauma in questionable joints; this damage is not noticed by the neuropathic patient, and the inflammatory resorption resulting from the traumatized bone makes the region weak and vulnerable to further trauma. In addition, poor fine motor control produces unnatural pressure on certain joints, which causes additional microtrauma.
- Neurovascular : Neuropathic patients have irregular reflexes of the autonomic nervous system, and insensitive joints receive significantly greater blood flow. The resulting hyperemia leads to an increase in bone osteoclastic resorption, and this, along with mechanical stress, leads to bone destruction.

In fact, both of these mechanisms may play a role in the development of the Charcot joint.

Shared engagement

Diabetes is the main cause in America today for neuropathic joint disease, and the foot is the most affected area. In those with foot deformities, about 60% are in tarsometatarsal joints (medial joints affected more than laterally), 30% Metatarsophenangeal joints and 10% have ankle disease. More than half of diabetic patients with neuropathic joints can remember some types of trauma triggers, usually minor.

Patients with neurosyphilis tend to have knee involvement, and patients with syringomyelia from the spinal cord can show shoulder deformity.

Damage to the hip joint is also seen in neuropathic patients.

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Diagnosis

Clinical findings

Clinical findings include erythema, edema and increased temperature in affected joints. In a neuropathic foot joint, plant ulcers may be present. Note that it is often difficult to distinguish osteomyelitis from a Charcot joint, as they may have similar WBC and MRI scan features (joint destruction, dislocation, edema). A definite diagnosis may require a bone or synovial biopsy.

Radiological findings

First, it is important to recognize that two types of abnormalities can be detected. One is called atrophy, where there is osteolysis of the distal metatarsal on the forefoot. The more common form of damage is hypertrophic joint disease, characterized by acute peri-articular fractures and joint dislocations. According to Yochum and Rowe, the "6D" hypertrophy is:

Combine together
Increased density
Production of debris
Dislocation
Disorganized
Destruction

The natural history of the collective destruction process has its own classification scheme, offered by Eichenholtz several decades ago:

Stage 0: Clinically, there is joint edema, but the radiographs are negative. Note that bone scan may be positive before radiography, making it a sensitive but not very specific modality.

Stage 1: osseous fragmentation with joint dislocations seen on radiography ("acute Charcot").

Stage 2: Local edema decreases, with fragment blend and fine bone fragment absorption

Stage 3: No local edema, with consolidation and re-modeling (though defective) of fracture fragments. The legs are now stable.

Atrophy features:

"Lick candy stick" appearance, usually seen on the distal aspect of the metatarsal
diabetic osteolysis
Bone resorption

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Treatment

Once the process is known, it should be handled through VIP - vascular management, infection management and prevention, and pressure relief. Aggressively pursuing these three strategies will accelerate the trajectory of wound healing. Relief pressure (off-loading) and immobilization with total contact casting (TCC) are essential to help prevent further joint damage.

TCC involves wrapping the patient's complete legs, including the toes, and lower legs in specialist cast that redistribute weight and pressure in the lower legs and legs during daily movement. It redistributes the pressure from foot to foot, which is better able to hold the load, protect the wound, allow it to regenerate tissue and heal. TCC also keeps the ankle spinning during walking, which prevents the shearing and twisting forces that can further damage the wound. TCC helps maintain quality of life by helping patients stay mobile.

There are two scenarios in which the use of TCC is appropriate for managing neuropathic arthropathy (Charcot's feet), according to the American Orthopedic Foot and Ankle Society. First, during initial treatment, when the damage occurs, and the foot shows edema and erythema; the patient does not need to hold the load on the legs, and TCC can be used to control and support the foot. Secondly, when the foot has been deformed and ulceration has occurred; TCC can be used to stabilize and support the feet, and to help move the wound towards healing.

Braces running under control by pneumatics are also used. Surgical correction of the joints is rarely successful in the long term in these patients. However, off-loading alone does not mean optimal results without proper management of vascular disease and/or infection. Duration and aggressiveness (non-weight-bearing vs removable device) should be guided by clinical assessment of neuropathic artropathy based on edema, erythema, and skin temperature changes. It can take 6-9 months for edema and the affected joint erythema will recede.

eichenholtz classification | The Bone School

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Results

Results may vary depending on the location of the disease, the degree of damage to the joint, and whether surgical repair is necessary. The average healing time varies from 55-97 days depending on the location. Up to 1-2 years may be required for total healing.

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References

The Radiology Assistant : Diabetic foot - MRI examination

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Neuropathic arthropathy

Kamis, 07 Juni 2018