A swollen knee: and the father of hysteria

Abstract

In July, 2006, a 69-year-old woman was in our foot clinic, when she mentioned that her right knee had been painful and swollen for 2 months. The swelling had gradually increased; the patient recalled no injury. Her type 2 diabetes was poorly controlled: we saw her regularly in the foot clinic for a neuropathic ulcer, which was healing slowly; she had had several laser treatments for bilateral diabetic maculopathy. The knee was hot and swollen; its range of movement was limited by pain. Her other joints were normal. Her knee and ankle refl exes were absent—as we had observed previously—and she had reduced sensation to pain, touch, vibration, and temperature in both feet: these fi ndings were consistent with neuropathy. We suspected osteoarthritis. However, blood tests showed a white-cell count of 13∙4×109 cells per L, and a C-reactive-protein concentration of 128 mg/L. Radiography showed destruction and lucent defects of the right tibial plateau, and reduction of the medial and lateral compartments of the tibiofemoral joint (fi gure). These fi ndings were consistent with erosive arthropathy or septic arthritis. Microscopy and culture of a knee aspirate showed no bacteria or crystals, so we ruled out sepsis, gout, and pseudogout as possible causes of the swelling. CT showed bone destruction in the proximal tibia. We diagnosed a Charcot knee. We gave the patient conservative treatment, immobilising the knee in a Genurange (Medi UK, Hereford, UK) cast. When the patient was last seen, in June, 2008, the swelling was reduced; she was still wearing the brace during the day, and was mobilising with a Zimmer frame. The Charcot joint is a relatively painless, progressive arthropathy caused by a neurological defi cit. In 1868, Jean-Martin Charcot, famous for his descriptions of hysteria, gave the fi rst detailed account of neuropathic joint damage caused by syphilis. His patient, who had tabes dorsalis, had increasing swelling and instability of the knees; the joints were severely deformed. In 1936, Jordan attributed Charcot joints to diabetes, which is now thought to be the most common cause. Nonetheless, Charcot arthropathy is found in only around 1% of people with diabetic neuropathy. The factors that predispose to its development are unknown. Most commonly, it aff ects the ankle joint and the forefoot: damage to the knee is rare. Acute infl ammation, characterised by hyperaemia, is self-limiting, and succeeded by re-ossifi cation. Initial fi ndings on radiography can be unremarkable, or resemble those in osteoarthritis. Further imaging with CT, MRI, or isotope bone scanning may be necessary. Charcot joints should be immobilised early, to prevent further joint destruction. Since the knee bears the weight of the body, and has little surrounding soft tissue for stabilisation, it is especially susceptible to progressive destruction and instability. The knee should be given protective bracing for 6–18 months, to provide stability and reduce shear stresses across the joint. Bisphosphonates have been used to reduce osteoclast activity. If bracing fails to provide stability, arthrodesis has been recommended (with reasonable success), rather than internal fi xation or joint replacement. The disease must be in a quiescent phase for successful union to occur. Total joint arthroplasty of the neuropathic knee is controversial, and should be reserved for (usually severely deformed) unstable joints or fractures, because the potential complications are many: risks include fracture, and dislocation of parts of the femoral or tibial prosthesis. Total joint arthroplasty has been done in a few cases, but only when conservative treatment has failed, and arthroplasty has been the only viable option.