Clinico-Radiological Characterisation for Remission of Acute Charcot-Neuroarthropathy of Foot

Charcot's neuro-arthropathy is a condition which is generally prevalent among the diabetic patient. It is a condition which primarily affects the bones and the joints. The presentation of charcot's neuro-arthropathy can be an acute or a chronic type depending upon the temperature difference between the two feet i.e. greater than 2 degree centigrade. Acute charcot's neuro-arthropathy presents with signs of redness, swelling and raised temperature of the involved area. The condition if not detected in the acute condition leads to chronic changes in the joints which leads to joint dislocation, fractures and development of rocker-bottom foot and also can lead to a state where amputation of the affected foot is needed. Acute charcot's neuro-arthropathy is characterized by signs of inflammation, hot, red swelling around the involved joint. This is often misdiagnosed as cellulitis, sprains or deep vein thrombosis. The diagnosis of this condition is mainly made clinically and aided by x-ray of foot, MRI of foot and sometimes by bone scan. The therapy that is accepted unanimously is putting on a total contact cast. The duration of this therapy depends on the regular temperature monitoring of both the feet. When the temperature difference between the two feet comes down to less than 2 degree centigrade, then it is defined as clinical remission and the offloading of the foot is stopped. Keeping in mind the effects of RANKL in the pathogenesis of acute Charcot neuro-arthropathy, Zoledronic acid was used as a treatment modality for acute charcot neuro-arthropathy. But it showed that it was inferior to the application of total contact cast. There have been trials were methylprednisolone combined with total contact cast have been used for treatment and the outcome has been compared with the use of zoledronate in patients on total contact cast. It had shown that zoledronate with total contact cast had an improvement of bone mineral density and on the other hand there was a decrease with steroids. Overall the effects of medical management of acute charcot's neuro-arthropathy was a mixed one with no definite recommendation regarding use of medical management in this condition. So total contact cast is the gold standard for the management of acute charcot's neuro-arthropathy. It has led to the healing of ulcers to the range of 75% in cases of acute charcot's neuro-arthropathy. If the patients are denied these treatment then there is progression of the disease process and can lead to the development of chronic changes in the form of fractures, dislocation, gangrene, foot ulcers and ultimately amputation.

The end point of the treatment with total contact cast is taken as the decrease in the temperature difference of less than 2 degree centigrade between the two feet. This point is regarded as the point of clinical remission in cases of acute charcot's neuro-arthropathy. But there has been instances where there have been 12-33% of recurrences when this clinical remission has been used as a criteria for discontinuation of offloading.

There has been advent of MRI and MRS of the foot for monitoring of acute charcot's neuro-arthropathy remission which is the most sensitive technique for the recognition of early bony changes in charcot neuro-arthropathy. PET scan has also been used including bone scan and FDG PET scan, for the evaluation of acute charcot's neuro-arthropathy remission. These modalities have been evaluated to test the actual remission of acute charcot's neuro-arthropathy. Even with these modalities the actual remission criteria that would decrease the complication of early offloading as done at the time of clinical remission, is still missing.

There is no quantitative method available to monitor the process of remission of acute charcot-neuroarthropathy and accurately label the remission.

The pathophysiology of acute charcot neuro-arthropathy has two main postulates. One is the neurovascular theory in which it is thought to have nerve damage and it leads to increased local vascularity which leads to activation of increased osteoclastic activity with development of secondary osteopenia, fractures and deformity. The other theory is the more accepted one and has attracted a lot of recent research around it. This involves the neuro-traumatic theory where due to the presence of neuropathy in these diabetic patients, they are not able to realize the microtrauma that they sustain. This leads to the development of a state of inflammation resulting in the raised levels of raised IL6 and TNFalpha. There is also activation of the RANKL and OPG pathways leading to bone destruction. This highlights the importance of RANKL in the pathogenesis of acute charcot neuro-arthropathy.