Current Concepts In Treating Acute Charcot's Arthropathy
Charcot’s arthropathy is a devastating complication of diabetes mellitus that frequently leads to permanent disability, ulceration and amputation. It is a rapidly progressive and severe form of arthritis. Researchers have equated the acute Charcot foot to a medical emergency since therapies are available that may alter its natural history.1 Unfortunately, the pathophysiology and development are poorly understood. This is frequently complicated by a delay in diagnosis until bony destruction is visible on plain radiographs. This delay often leads to worse outcomes.2 One study found the diagnostic delay averaged 29 weeks.3 Other inflammatory arthridities have treatments that are targeted at the pathophysiologic pathway. For example, there are disease modifying anti-rheumatic drugs (DMARDS) for rheumatoid arthritis (RA). In fact, the standard of care has changed for RA to the point that one should attempt using a DMARD for all patients with RA and not continue endless palliation with only anti-inflammatory medications.4 Perhaps we should approach the treatment of Charcot’s arthropathy, which behaves like an accelerated inflammatory arthritis, in a similar manner to that of RA. Though the exact pathophysiologic mechanisms of this disease process are yet undiscovered, it is generally accepted that trauma (macrotrauma or repetitive moderate trauma) leads to an inflammatory process, which increases blood flow in the extremity. Surprisingly, patients with Charcot have preserved vascular responsiveness in comparison to ulcerated neuropathic patients without Charcot.5 This intact reactivity helps to explain the intense warmth of the affected extremity, which is often 9 to 11ºF higher than the same point on the contralateral limb.6 The hyperemia and inflammation lead to focal osteopenia, allowing joint fragmentation and subluxation. In studies utilizing bone densiometry, researchers have shown the osteopenia.7,8 Researchers showed focalization of the bone loss to the foot in one study which compared the bone mineral density (BMD) of the foot with that of the lumbar spine in those with acute Charcot versus a set of age- and sex-matched controls. The Charcot foot had a T-score three standard deviations below normal (which denotes osteoporosis) in comparison to controls. Yet there was no difference in the stiffness of the lumbar spine between the two groups.7 Other authors have recently discovered the role that the receptor activator of nuclear factor kappa B ligand (RANK-L) plays with osteoporosis and the calcification of vascular smooth muscle cells. They theorize that there is a common thread between the decrease in bone mineral density and the concomitant Mönkeburg’s arteriosclerosis that occurs in patients with Charcot’s arthropathy.9 From what little information that already exists about the disease process, we know that when it comes to treating acute Charcot, we can target our current and future therapies to: • reduce or eliminate trauma; • reduce joint inflammation; and • increase the bone mineral density.