Orthotic Management of Diabetic
Neuropathic Arthropathy
John W. Michael, MEd, CPO
Max A. Isbell, PA-C
John M. Harrelson, MD
Overview
Progressive destruction of the insensate joint
was first described by Mitchell in 1831, but it
was most clearly delineated by Charcot in
1868 and hence is sometimes referred to as
"Charcot's changes" (1,2). During this pre-X-ray era, the classic clinical description was
the feeling of a "bag of bones" (3). Both
Mitchell and Charcot postulated this condition was the result of damage to that portion
of the nervous system believed to control
nutrition of the bones and joints. The famous German surgeon Volkmann challenged
this view almost immediately and argued
that progressive microtrauma to the unfeeling joint was the cause (4). This latter view
became known as the German Theory and
was widely taught as recently as 10 years ago.
Increasing evidence suggests the possibility of a neurovascular etiology: that bone resorption from hypervascularity secondary to
autonomic neuropathy is a likely cause (5).
This theory would explain several common
clinical observations:
- initial presentation of a hot, red swollen
foot (see Figure 1
)
- variable but often rapid destruction of
the bony architecture, sometimes within a
few weeks (see Figure 2
)
- documented progression of bony destruction despite complete bed rest or total
paralysis (3,6)
We have seen rapid bony loss in the neuropathic joint of one hospitalized patient on
strict bed rest and under close observation,
suggesting simple unweighting alone is not
always sufficient to prevent bony destruction. Orthotic intervention at the proper
time, however, can be very effective in reducing the secondary deformities that otherwise follow this acute stage of the disease.
Until the twentieth century, neuropathic
joints were a relatively rare problem primarily associated with tabes dorsalis infection
(7). The first case in a patient with diabetes
alone was not reported until 1936, but the
reported incidence has steadily risen since
then (8). In 1947 Bailey and Root placed the
incidence of diabetic arthropathy at 1 in
1,100; in 1972, Sinha reported an incidence
of 1 in 680 (9,10). The incidence in our Insensitive Foot Clinic for 1990 was 1 in 6. Nine
of 55 new patients with diabetes had neuropathic arthropathy! Like the etiology, the
actual incidence remains unknown but will
likely increase as diabetics live longer and
this pathology is more widely recognized.
It is important for the orthotist to understand this condition for several reasons:
- It can have a devastating effect on the
patient's mobility and quality of life.
- It is frequently misdiagnosed since early
symptoms may suggest a mild infection, minor fracture, tendon rupture or similar benign problem (11) (seeFigure 3a
,and Figure 3b
).
- Poorly conceived orthotic treatment
may result in substantial malpractice lawsuits should the deformity or resultant ulceration progress despite treatment (12).
- With comprehensive management,
most devastating deformity can be avoided
(13).
Classification of Diabetic Foot
Problems
Diabetic foot problems can be conveniently
divided into three major categories: Ischemia is similar to non-diabetic atherosclerosis. Lesions often begin as a small, seemingly
harmless "blood blister" that rapidly progresses into a painful ulcer, often over bony
prominences (5) (see Figure 4
). Typical
treatment is local debridement, antibiotic
therapy and pedorthic/orthotic management. Because protective sensation is present, foot orthoses or shoe modifications to
reduce local pressures are usually safe and
effective.
Neuropathic ulcerations are characteristically painless and typically rimmed with a
thick band of callous (5,13) (see Figure 5
).
They may result from injury, bony deformity
or other causes. Mild to moderate lesions are
successfully managed conservatively with
wet-to-dry dressings and unloading via
crutches, casts or pedorthic/orthotic modifications (see Figure 6a
, and Figure 6b
). Severe lesions may
require surgical excision or correction of the
underlying bony protrusion (13). Once
healed, these feet can often be maintained
ulcer-free with meticulous orthotic and pedorthic intervention plus regular follow-up.
It has been estimated that some degree of
neuropathy is present in up to 60 percent of
all diabetic feet, particularly if diabetes has
been present more than 20 years or is not
well-controlled (14). Although orthotic
treatment can be effective for this group,
routine follow-up is mandatory since it is im
possible for the patient to feel when the
problem areas are insufficiently relieved.
Since these feet usually don't hurt, they are
always at risk for a recurrence.
Neuropathic arthropathy is often mistaken
for gout, tumor, thrombophlebitis or infection since the initial clinical symptom is usually a reddened, swollen area with mild discomfort. It appears most commonly in the
mid-tarsal region, leading quickly to midfoot
collapse or forefoot valgus deformity. Neuropathic arthropathy also can develop in the
forefoot or hindfoot, and sometimes results
in pathologic fibular fracture (13). Once the
active disease process fully resolves, a fixed
deformity remains. The classic rigid, rockerbottom foot that results is always difficult
and sometimes impossible to manage with
orthoses, partly due to the characteristic denial that often accompanies painless lesions
(see Figure 7
).
It is currently impossible to halt progression of the disease, but it is quite feasible to
prevent the devastating secondary deformities with optimal management. The key factor is a high index of suspicion that patients
with peripheral neuropathy will develop
spontaneous, rapid progression of bony destruction. The clinical symptoms of swelling,
redness or excess warmth are not always present but should be considered warning signals. The earliest bony changes are readily
apparent on plain X-rays, and include:
- osteopenia
- periarticular fragmentation
- subluxation
- fracture (7) (see Figure 8
)
Orthotic Management
As soon as the active stage of the disease is
recognized, the patient must be immediately
and aggressively protected from excess
weightbearing (5,13). In severe cases, particularly with bilateral involvement, bed rest is
recommended. More agile diabetics with
unilateral involvement have done well with
crutch-walking on the contralateral foot. As
a general rule, forefoot lesions receive less
body weight and hence require less protection. Non-displaced forefoot fractures may
respond to a rocker-soled shoe or sandal
without full unweighting. Hindfoot lesions,
on the other hand, need absolute nonweightbearing during the resorptive phase to
avoid gross deformity (13) (see Figure 9a
, and Figure 9b
). It
may be useful to imagine the resolving Charcot foot as analogous to Legg-Calve'-Perthes disease of the hip: so long as the affected
joints are held in proper alignment and
weightbearing stresses are controlled,
marked skeletal deformities will not occur.
At Duke, we maintain our Charcot patients
under a protected weightbearing regime until the X-rays demonstrate sufficient healing
for bony stability. This typically requires
three to six months but has varied from six
weeks to nearly two years (13).
After this time, the active stage of the disease has passed. However, patients are still
at risk for pathologic fractures due to the
marginal bone density resulting from the disease. In essence, they are now osteoporotic,
and the typical lumbering "lead-foot" gait of
the insensate limb increases the likelihood of
stress fractures.
We routinely fit all recovering Charcot
feet with a double upright PTB orthosis with
double adjustable ankles attached to an extra-depth shoe with accommodative inlay,
steel shank and roller sole (seeFigure 10a
, and Figure 10b
).
Significantly deformed feet require custom-made shoes. All recovering Charcot patients
wear the orthosis for at least one year. until
radiographs clearly demonstrate resolution
of the osteopenia and reconstitution of normal-density bone (13).
We are not as interested in vertical unweighting (except in the obese individual) so
much as in transferring the floor reaction
forces to the tibia and proximal musculature
(15) (see Figure 11a
, Figure 11b
, Figure 11c
, Figure 11d
, Figure 11e
, and Figure 11f
). Particularly in the presence of midfoot or forefoot lesions, an anterior stop just prior to the patient's dorsiflexion endpoint significantly reduces plantar
stresses during ambulation (16) (see Figure
12a
Figure
12b
).
Because many of these patients already
have trouble walking, we prefer not to lock
the ankle against plantarflexion unless hindfoot problems exist. A spring dorsiflexion
assist is sometimes useful to reduce footslap
or aid toe clearance. The rocker sole is individualized since these feet are generally ulcer-free due to the weightbearing restrictions. A marked rocker has been shown to
significantly reduce forefoot pressures by
Brandt and others, but our patients complain it disrupts their balance (17) (see Figure 13
). Most have a tenuous sense of proprioception due to the progressive neuropathy and do not tolerate radical alterations to
their gait mechanics.
Because this is a long-term orthosis, and
because many diabetics also have volume
fluctuations secondary to edema, we find the
metal/plastic hybrid brace attached externally to the shoe is most often required. This
brace also allows independent adjustment of
the foot orthosis, shoes, weightbearing shell
or ankle control as the patient's condition
gradually changes. Pressure-gradient stockings (either custom-fitted or custom-made)
are used as necessary. We generally laminate
the tibial shell as described by Titus in 1975
(18). Patients weighing less than 300 lbs. may
be fitted with a thermoplastic equivalent
with comparable results (19, 20) (see Figure
14a
, and Figure
14b
, Figure 14c
, and Figure 14d
).
Once the X-rays suggest bone density has
returned to normal, the PTB superstructure
is removed, and the accommodative foot
orthosis and modified shoe provide continuing protection (13) (see Figure 15
). By using
this protocol in more than 50 cases since
1984, we have successfully avoided the development of marked deformities despite
the bony destruction documented on the radiographs. Well over 90 percent of our cases
with Charcot's arthropathy, managed as reported above, have avoided amputation and
continue to ambulate independently; many
have been able to discard the PTB orthosis
and wear only an accommodative foot orthosis and rocker sole.
Conclusion
Although not thoroughly understood, neuropathic arthropathy is expected to increase
in frequency due to the continuing increase
in the lifespan of the diabetic. We believe
that careful orthotic management, when
provided as part of a comprehensive multidisciplinary treatment plan, can significantly
improve the ambulatory potential and quality of life for patients who would otherwise
experience rapid bony destruction, recurrent
ulceration and eventual infection leading to
amputation of their feet.
John W. Michael, MEd, CPO, is an assistant clinical professor and director of the Department of
Prosthetics and Orthotics, Box 3885, Duke University Medical Center, Durham, NC 27710.
Max A. Isbell, PA-C, is a physician's associate
in orthopedics at Duke University Medical Center, Durham, NC 27710.
John M. Harrelson, MD, is associate professor
of orthopedic surgery and assistant professor of
pathology; director, Musculoskeletal Oncology
Division; and director, Diabetic Foot Clinic at
Duke University Medical Center, Durham. NC
27710.
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