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.
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
Charcot first described neuropathic osteoarthropathy, also
called neuroarthopathy or "Charcot Joint," in 1868.
Jordon noted the association of diabetes with neuropathic
osteoarthropathy in 1936.
Leprosy, spinal cord defects, alcoholism, multiple sclerosis,
poliomyelitis, syringomyelia, and intra-articular and
systemic steroid injections are other commonly recognized
antecedents of neuropathic osteoarthropathy.
Neuropathic osteoarthropathy is characterized by "rapid
onset of painless and severe joint destruction"
with associated neurosensory deficit.
Acute clinical presentation may include erythema, swelling,
and painless deformity of the affected extremity, and may be
readily confused with cellulitis, osteomyelitis, or gout.
The neurotraumatic theory of neuropathic osteoarthropathy
posits that repetitive mechanical trauma coupled with absent
protective sensation results in progressive joint
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.
Altered collagen cross-linking is thought to effect
structural changes in ligaments, with continued mechanical
injury producing joint instability.
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
An atrophic pattern is associated with syringomyelia and
peripheral nerve lesions, and is seen more commonly in
Imaging of atrophic disease demonstrates osseous absorption,
which resembles surgical amputation.
Goals of treatment are to create and maintain a stable,
mechanically sound foot, control swelling, provide skeletal
stability, and protect soft tissues.
Surgical repair of fractures, prolonged immobilization,
avoidance of weight bearing, cessation of tobacco, and
aggressive management of co-morbid illness are the mainstays
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.