CASE SUMMARY

A 75-year-old retired television repairman with diabetes, hypertension, and heart disease complained of foot pain and flat feet. He attributed his deformity and prior fractures to having "walked all over Europe and half the Pacific!" Physical examination of the right foot showed diminished sensation, pes planus, and a bony prominence of the medial midfoot with a 1-cm partial-thickness ulceration (figures 1 through 3). The rest of the physical examination was essentially normal. Laboratory data revealed normal complete blood count, serum glucose of 173, spot microalbumin:creatinine ratio of 379, and glycosylated hemoglobins of 6.7 and 7.0.

DIAGNOSIS

Neuropathic osteoarthropathy

IMAGING FINDINGS

Three view and weight-bearing films of the feet demonstrated a washed-out appearance of bone bilaterally, pencil wasting of the diaphysis of the third right metatarsal, and Lisfranc disruption of the right midfoot with lateral subluxation of the bases of all four metatarsals. An old healed fracture of the shaft of the second metatarsal and "rocker-bottom deformity" were also noted (figures 4 through 6).

DISCUSSION

Charcot first described neuropathic osteoarthropathy, also called neuroarthopathy or "Charcot Joint," in 1868. ¹ Jordon noted the association of diabetes with neuropathic osteoarthropathy in 1936. ¹ Leprosy, spinal cord defects, alcoholism, multiple sclerosis, poliomyelitis, syringomyelia, and intra-articular and systemic steroid injections are other commonly recognized antecedents of neuropathic osteoarthropathy. ^1,2

Neuropathic osteoarthropathy is characterized by "rapid onset of painless and severe joint destruction" ¹ with associated neurosensory deficit. ^1,2 Acute clinical presentation may include erythema, swelling, and painless deformity of the affected extremity, and may be readily confused with cellulitis, osteomyelitis, or gout. ^1,3

The neurotraumatic theory of neuropathic osteoarthropathy posits that repetitive mechanical trauma coupled with absent protective sensation results in progressive joint destruction. ^2,3 Proponents of neurovascular causation suggest that sympathetic denervation enables vasodilation and hyperemia of affected tissue, provoking a complex biochemical cascade ending in bone resorption and weakened subchondral bone. ^2,3 Altered collagen cross-linking is thought to effect structural changes in ligaments, with continued mechanical injury producing joint instability. ^1-3

Neuropathic osteoarthropathy manifests in two radiographic patterns. Hypertrophic disease, which is common in weight-bearing joints, is reflected in joint destruction and bone frag-mentation, osseous sclerosis, and osteophyte formation. ² An atrophic pattern is associated with syringomyelia and peripheral nerve lesions, and is seen more commonly in non-weight-bearing joints. ² Imaging of atrophic disease demonstrates osseous absorption, which resembles surgical amputation. ²

Goals of treatment are to create and maintain a stable, mechanically sound foot, control swelling, provide skeletal stability, and protect soft tissues. ¹ Surgical repair of fractures, prolonged immobilization, avoidance of weight bearing, cessation of tobacco, and aggressive management of co-morbid illness are the mainstays of therapy. ^1,3

ACKNOWLEDGMENT

The authors would like to thank two of their colleagues at the Ralph H. Johnson VA Medical Center, Charleston, SC: John Baroody, Medical Photographer, for his assistance with reproduction of images, and Peter Rosenthal, MD, Radiology Department, for clinical support.