- Causes of Charcot Joint
- Pathophysiology of Charcot Joint
- Presentation of Charcot Joint
- Classification of Charcot Joint Disease
- Lab Studies
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Charcot joint or Charcot arthropathy is the name given to neuropathic joint disease is a condition that causes progressive destruction of bone and soft tissues of joints especially weight-bearing joints and may also cause disruption of the bony architecture. Charcot arthropathy can occur at any joint; however, it occurs most commonly in the lower extremity, at the foot and ankle.
Charcot’s joint is named after Jean-Martin Charcot. Syphilis was believed to be the most common cause of Charcot arthropathy until 1936, now it is diabetes.
The prevalence of Charcot arthropathy has been reported from 0.1% – 13% in different studies. The bilateral disease occurs in less than 10% of patients. Males and females are reported to be equally affected in some studies whereas others show male preponderance.
Causes of Charcot Joint
It is a neuropathic condition and any condition that causes sensory or autonomic neuropathy can lead to a Charcot’s joint. Charcot joint has been reported as a complication of following diseases.
- Diabetes [most common cause]
- Chronic alcoholism
- Spinal cord injury
- Renal dialysis
- Congenital insensitivity to pain.
Pathophysiology of Charcot Joint
The exact mechanism of Charcot joint disease is not known. Following theories suggest various mechanisms which may be responsible for this disease.
There is an injury to an insensate joint in presence of preexisting sensory neuropathy and bony destruction that occurs is not perceived. This continuous microtrauma leads to progressive destruction and damage to bone and joints.
Due to a preexisting condition, there is an increased blood flow in the limb. This results in an imbalance in destruction and synthesis. The autonomic neuropathy leads to an abnormal bone formation, and the sensory neuropathy leads to an insensate joint that is susceptible to trauma.
Presentation of Charcot Joint
The clinical presentation of Charcot joint may vary from mild swelling and no deformity to moderate deformity with significant swelling depending on the stage of the disease.
Acute Charcot arthropathy presents with swelling, an increase in local skin temperature, erythema, joint effusion, and bone destruction. These features, in the presence of intact skin and a loss of protective sensation often point towards Charcot joint disease.
Pain, when occurs, is significantly less than the severity of joint involvement. The patient may also have instability and loss of joint function. Passive movement of the joint may reveal a loose bag of bones. About 40% of patients with acute Charcot arthropathy have concomitant ulceration which might raise suspicion of osteomyelitis.
Classification of Charcot Joint Disease
Saunders and Mrdjencovich classification is the most commonly used system. Based on the location of the arthropathy, their system classifies Charcot arthropathy of foot and ankle into 5 different patterns, as follows
It involves the forefoot i.e. the interphalangeal joints, the phalanges, and the metatarsophalangeal joint
It involves the tarsometatarsal joint
Involves the cuneonavicular, talonavicular, and calcaneocuboid joints
Involves the ankle joint
Involves the posterior calcaneus
Patterns 2 and 3 are the most common.
A complete metabolic profile is done to identify the underlying cause. Elevated levels of creatine and of blood, urea, nitrogen could suggest renal disease. Increased glucose level suggests diabetes. The white blood cell count and ESR levels can be to rule out infection or osteomyelitis.
Depending on patient history and examination, other tests may be ordered like
- Glycosylated hemoglobin (HbA1C) to check hyperglycemic control in diabetes. Hyperglycemia can cause nonenzymatic collagen glycosylation, which can lead to laxity in ligaments and unstable joints.
- Levels of alkaline phosphatase, calcium, phosphorus, and parathyroid hormone can help the physician to identify bone diseases, such as Paget disease.
- Hypercalcemia may be indicative of cancer or metastases.
- Vitamin B12/folate deficiency could suggest peripheral neuropathy or chronic alcoholism.
- Liver function tests/coagulation studies may be done in chronic alcoholism.
- Rapid plasma reagin/fluorescent treponemal antibody – absorption tests aid in the diagnosis of syphilis.Diagnostic Procedures
Other diagnostic procedures like lumbar puncture [when rapid plasma reagin test is positive], bone probe, infrared dermal thermometry [for skin temperature assessment] and synovial biopsy may be done if required to reach at the diagnosis.
Xrays help to confirm and stage disease and tell whether the disease is active. Osteopenia, periarticular fragmentation of bone, subluxations, dislocations, and fractures are usual finding in x-ray of Charcot joint depending on the destruction of the joint.
A bone scan can assist in differentiating between Charcot arthropathy and osteomyelitis.
Magnetic resonance imaging allows for anatomic imaging of the area. It also may help to distinguish between osteomyelitis and Charcot arthropathy.
Doppler ultrasound is used to rule out deep venous thrombosis.
Treatment of Charcot arthropathy is primarily nonoperative.
Immobilization and reduction of stress is the mainstay of treatment. Immobilization usually is accomplished by cast application which is checked periodically for fit and effectiveness. Casting usually is necessary for 3-6 months. if casts are not suitable for any reason metal braces and orthoses may also be used.
Xrays are done approximately every month to evaluate progress. Immobilization is discontinued based on clinical, radiographic, and dermal thermometric signs of quiescence.
Patients are asked to reduce stress by remaining nonweight bearing or partial weight bearing with crutches or walker.
After the removal of the cast lifelong protection of the involved limb is desired. Patients should wear a brace to protect the foot. A rocker-bottom sole can be used in presence of an ulcer. Plastazote inserts can be used for insensate feet.
The total healing process typically takes 1-2 years. Patients should prevent further injury, note rise in temperature, examine the oints and limb daily, report trauma.
The major contraindication to surgery is active inflammation. Studies have shown less favorable outcomes when surgery is performed on an acute joint.
Nondisplaced fractures, destroyed joints, destroyed bones, deformities like rocker bottom foot or clubfoot may require surgical treatment which may include removal of bony prominence, osteotomy, arthrodesis, screw and plate fixation, open reduction and internal fixation, reconstructive surgery, fusion with Achilles tendon lengthening, autologous bone grafting, and amputation.
The choice of procedure is guided by the involvement of the joint and severity of destruction.