Control of Charcot arthropathy early in the disease process reduces the risk that patients will end up with deformities which may precipitate subsequent ulceration (Petrova 2001, Chantelau 2005)
Non-surgical management
- Metabolic control – Charcot arthropathy is often related to deteriorating control of blood glucose
- Prevention or minimisation of deformity by total contact casting or use of a diabetic walker boot (Armstrong et al 1997). Traditionally, patients were advised to avoid weightbearing, to avoid forces that might lead to displacement of fractures and dislocations. de Souza (2008) allowed 27 patients with Charcot arthropathy to bear weight as tolerated in a total contact cast, and displacement occured in only one patient.
- Jude (2000) reported a RCT showing that bisphosphonates can alter the metabolic markers of the acute Charcot process such as temperature, swelling, CRP and excretion of collagen degradation products. The trial did not show any effect of treatment on overall clinical outcome. Recent preliminary data from the UK National Charcot Registry suggest that treatment with bisphosponates slows bone healing. Further trials are probablyneeded.
Surgery
Surgery has been reported for severe instability in the early stages of the Charcot process, with progressive deformity, ulceration or infection. Although Charcot disease is commonest at the tarsometatarsal joints and the lesser tarsal bones (Brodsky 1), severe instability is commoner in peritalar (Brodsky 2) disease.
Surgical stabilisation requires internal fixation with as stable a construct as possible in poor quality bone. Plates, often multiple, may be required as well as standard lag screw constructs in the midfoot. Ankle disease can be stabilised with a retrograde nail.
Although this is extremely demanding surgery in patients with poor bone stock and oedematous soft tissues, good results can be achieved. Simon et al (2000) achieved stable fusion in all of 14 patients with good return to function and no late ulceration. Saltzmann (2005) reported a series of 115 Charcot patients, most of whom were treated with standard total contact casting. However, fourteen patients whose deformities could not be controlled in casts (and presumably had among the highest risk for poor outcome and amputation), had realignment fusions. In the 14 patients who had realignment fusions, none had amputations compared with 15 in the other 101 patients. A prospective trial would be useful, although it would need to include several centres to recruit enough patients.