Review Question - QID 970

The clinical presentation is consistent with neuropathic (Charcot) joint. Possible causes of neuropathic joint include diabetes mellitus, syringomyelia, leprosy, and neurosyphilis. Figure A and B shows an AP and lateral of the knee with characteristic finding of Charcot joint including fragmentation of both articular surfaces, joint subluxation, and surrounding soft tissue edema. Reiter's syndrome is not a known cause of neuropathic joint.

Neuropathic osteoarthropathy can be defined as bone and joint changes that occur secondary to loss of sensation and that accompany a variety of disorders. The pathophysiology of neuropathic arthropathy is debatable. The general consensus is that the loss of proprioception and deep sensation leads to recurrent trauma, which ultimately leads to progressive destruction, degeneration, and disorganization of the joint.

Kim et al reviewed 19 Charcot knees that underwent TKA and found at 5 year follow-up the average HSS Knee Score was double, but there was a 16% rate of loosening and 6 patients had to undergo a fusion.

Parvizi et al found that in 49 Charcot knees 75% required long-stem, constrained components secondary to ligamentous instability and 75% required bone augmentation in the form of allograft, autograft, or metal wedges. However, they found good functional outcomes at 8 years if attention was paid to the technical challenges found in this patient population.

Illustration A and B shows a severe case of Charcot neuroarthropathy of the knee.