To The Editor:
I read "Arthrodesis as an Early Alternative to Nonoperative
Management of Charcot Arthropathy of the Diabetic Foot" (82-A:
939-50, July 2000), by Simon et al., with interest. I offer
my congratulations to the authors, who have taken such care to produce
evidence, from their study of fourteen patients, that a carefully
and correctly performed arthrodesis of neuropathically damaged bone
should result in stable healed bone and satisfactory function, if
the foot is adequately immobilized. My hope is that their results
will inspire others to reconstruct deformed neuropathic feet.
In 1964, I performed my first arthrodesis to treat a totally
neuropathic foot, deformed because of continued unprotected weight-bearing
by bones decalcified due to chronic infection. There was microtrauma
that had led to impaction of the mid-tarsal joints and
collapse of the medial arch, and the foot was in danger of ulceration
of both the skin and deeper tissues. Radiographs made preoperatively
and both radiographs and photographs made at the twenty-year follow-up
showed that such treatment measures can be successful and long-lasting1. Since that first operation, I have
performed over a thousand arthrodeses to reduce the disability caused
by bone disintegration in patients with neuropathy from many causes
including diabetes, which is the principal cause in developed societies.
I have found that the required duration of immobilization depends
on the site of the lesion and on the amount of stress that the healed bone
must bear. The immobilization time required after both nonsurgical and
surgical treatment is similar, because it must allow for adequate recalcification
of the newly healed bone so that unprotected weight-bearing in a limb
with reduced pain perception will not result in further trauma.
I would like to challenge the statement made by Simon et al.
that they are the first to propose early orthopaedic surgery for
neuropathic feet. I had indicated a similar mode of management in my
article in the British edition of The Journal in
19712.
However, the recently published article is timely as I still
find that many clinicians believe that bone disintegration resulting
from neuropathic arthropathy cannot be healed, and, therefore, they do
not attempt to treat the problem. Diabetic patients with foot ulceration are
often referred to a vascular or a general surgeon for treatment.
I and my colleagues, like Simon et al., are of the opinion that
the structural deformity of the foot should be treated by orthopaedic
surgeons, and we have recently drawn attention to this fact3. Can we inspire clinicians with the realization
that, in the developed world, neuropathy due to diabetes is a very significant
problem? Neuropathy from any cause involves a high incidence of bone
lesions that are neglected because of attendant abnormalities in
pain perception. In spite of this, effective treatment can prevent
permanent deformity, disability, and ulceration.
Dr. Simon and colleagues stated that their operative procedures
were done for Eichenholtz stage-1 Charcot neuropathy, in
which patients have a degree of deformity without evidence of coalescence
or callus formation. We have found that, at this stage, there is
usually some hypermobility of the affected area (usually the midfoot)
and that it is usually possible to mold those feet into a functional
position, once the marked edema has been reduced by two to four days
of complete elevation and immobilization. If a strong, correctly
molded total-contact cast can be applied to maintain that functional
position, these feet will heal, often without significant deformity,
in the position held in the cast. If, after a few weeks or months, radiographs
show that the position is not satisfactory, then surgery can be performed
and the bones can be internally fixed. With or without internal fixation
there is no need for the patient to completely
avoid weight-bearing if the cast provides full support. We routinely
use walking total-contact casts, applied as soon as all acute inflammation
has settled, on patients with Charcot arthropathy treated either
nonsurgically or surgically for bone disintegration. This allows
patients to continue normal activities during treatment instead
of having to limit their activities of daily living, as described
by Simon et al. We found that walking actually improves the rate
of healing, which is two to three times as long as that for a similar fracture
in the sensate limb4.
S.R. Simon, S.G. Tejwani, D.L. Wilson, T.J. Santner,
and N.L. Denniston reply:
We wish to thank Dr. Warren for her kind remarks about our article.
It was most gratifying to note that she has performed over 1000
arthrodeses to treat bone disintegration in the neuropathic foot
and has found that, if correctly performed, a lasting, stable healed
bone with satisfactory function will result. This is truly a laudable
accomplishment, and her experience encompasses far more cases than
the fourteen that we reported in our article.
Our article discussed and cited only the literature related to
Charcot arthropathy of the foot that is caused by diabetes. When
Charcot arthropathy appears in patients with diabetes, the involvement of
that disease in other organ systems and their treatment complicates
the treatment of the neuropathic foot. Like others in the literature,
we identified Charcot arthropathy related to diabetes as a distinct
entity when considering the nature of the disease and the results
of treatment. Dr. Warren’s letter and her publications
suggest a priori that all neuropathic
foot deformities can be treated similarly and that the results are independent
of the etiology of the neuropathy.
This is potentially a very important point. If she is correct,
we apologize to Dr. Warren for suggesting that we were the first
to describe a study of early, successful orthopaedic surgical intervention
for the treatment of Charcot arthropathy of the foot in patients
with diabetes. Our statement was prompted by the absence in the
literature of any successful description of such surgery at the
earliest stage of this lesion in the diabetic patient. We were aware
of her 1971 article2, which described
the treatment of the neuropathic foot in individuals with leprosy.
In her Hunterian lecture delivered at the Royal College of Surgeons of
England in 19891, there is only
a brief mention that the same procedures performed in patients with
leprosy had been applied to treat patients with diabetes, congenital
neuropathies, spina bifida, and traumatic paraplegia. Unfortunately,
we could not have been aware of her two most recent publications3,4 as our paper had been submitted
prior to their availability. We are also aware that we are most
likely not the first to operate successfully on such subjects; we
are sure that some orthopaedic surgeons have operated successfully
on these patients and have not published their results. Identifying
who is the first to describe the treatment is less important than
the fact that it "works"; early surgical intervention
is a viable option, and treatment of this order should be viewed
similarly to that of a Lisfranc fracture-dislocation.
Most importantly, Dr. Warren’s letter infers that Charcot
arthropathy can be treated similarly regardless of the underlying
cause of the neuropathy. If this is true, anatomical alignment can and
should be the goal of treatment for this problem in the diabetic
patient; if it cannot be achieved through nonsurgical treatment,
then surgical treatment is a viable alternative. If, as she states, "it
is usually possible to mold those feet into a functional position,
once the marked edema has been reduced by two to four days of complete
elevation and immobilization [and] a strong, correctly molded
total-contact cast can be applied to maintain that functional position" and
it does, then surgery would not be needed. If, however, "after
a few weeks or months, radiographs show that the position is not
satisfactory, then surgery can be performed and the bones can be
internally fixed." We believe that our study and those
that we cited relative to the treatment of this disorder in the
diabetic patient come to the same conclusion. Dr. Warren routinely
uses a walking total-contact cast for patients with this disorder
whether treatment is nonsurgical or surgical. According to physiological
principles, such casts should improve the rate of healing if stability
is achieved, and healing should take two to three times longer than
it does for a similar fracture in a sensate limb. As our data agree
with the healing time that Dr. Warren suggests without early weight-bearing,
perhaps early weight-bearing should be tried as an alternative as
well.