04/20/2012    Tip Sullivan, DPM

Charcot Foot

I would like to get some comments on an
interesting case from a practical and medical/
legal standpoint. The main question that I think
this case brings up is when do we say “enough is
enough” and avoid the major expense on our
system that is incurred due to defensive
medicine??

42 y/o male, married, employed as a machine shop
foreman

PMH: NIDDM x 15 years—well controlled (FBS 110,
A1C 7.1), peripheral neuropathy not officially
diagnosed, but noticed by patient several years:
no other medical problems

NKDA

HPI: 2 week history of sudden swelling In Left
foot and ankle, no history of trauma, no fever
or chills, no pain in groin, foot stays swollen
and red ambulating or not, no dramatic change in
FBS or glucose management, has felt “OK”
generally except for occasional pain in foot.

PE: mid-aged male, 5’11”, 242#, A&Ox3, NAD,
normal affect

Bp: 140/83 R:78 Resp:16

Vasc: Doppler biphasic peaks DP and PT larger on
L than R, CFT immediate B/L, pulses palpable and
bounding B/L

Derm: L foot with increased temperature locally
up to the ankle, edema ¾ in L foot and lower 1/3
leg, erythema locally at dorsal L foot and
inferior to medial malleolus, no proximal
cellulitis or lymphangitis, no inguinal
lyophadenopathy, no break in integument/L,
R foot unremarkable

Neurological: gross epicritic sensation is
intact b/l, decreased vibratory sensation b/l =
up to knee, protective threshold (SW 5.07)
absent on plantar foot, DTR at AJ 2/4 b/l =

MSK: plantigrade feet b/l, normal angle and base
of gait, no limp in gait, Digits with mild/mod
reducible HT b/l, L foot ROM of midfoot and STJ
limited due to edema-no actual crepitus
appreciated, AJ ROM limited due to edema – no
crepitus appreciated(0-5 degrees max DF b/l),

Pertinent labs: All other labs WNL

Glu-97 nml

A1C-7.1 elevated

WBC- 10.6 elevated

Red cell count-4.32 low

Hgb-11.8 low

Hct-36 low

MCHC- 32.8 low

% neutro—70 nml

%lymph—20 nml

%monocytes –9 elevated

Absolute neutrophil—7.42 elevated

Absolute monocyte-0.95 elevated

Sed rate—57 elevated

MRI: radiology report “ 1) Charcot joint with
osteonecrosis suspected @ navicular &
cuneiforms 2) subacute navicular & 3rd MTJ
fracture”

With the data strongly pointing towards a
typical Charcot foot without infection, am I
obligated to biopsy to r/o infection, tumor,
etc. and confirm Charcot?

This gentleman is currently on my OR schedule—my
thoughts are—It only takes one of these that
goes bad to ruin your life — not to mention the
life of your patient. Addendum: These fractures
are stable when evaluated with “C” arm and I am
not planning on any sort of percut fixation—I
would consider pinning in an active charcot if
it were unstable at this time.

Tip Sullivan, DPM, Jackson, MS,
tsdefeet@MSfootcenter.net

Other messages in this thread:

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03/13/2010    Douglas Pacaccio, DPM, H. David Gottlieb, DPM,

$1,475,000 Settlement for MD's Failure to Diagnose Charcot Foot (Tip Sullivan, DPM

In regard to Dr. Jacobs’ comments, I went back
and was unable to find any thread in PM News
where any responder suggested that, “all or most
Charcot’s joint deformities require surgical
intervention.”

I admit that I do operate on Charcot, when
appropriate as stated. I do not operate to fix
the Charcot. I typically reconstruct the Charcot
when it is the underlying cause of a
recalcitrant ulcer, typically in patients with a
history of at least one, often more episodes of
abscess, osteomyelitis and/or sepsis. These
patients are very often given the option of
amputation to reduce the need to be in and out
of doctor’s offices for ulcers and infections.

The study in Diabetes Care from Loyola shows
that the Charcot is not the risk factor for
amputation. However, compared to Charcot alone,
patients with ulcers and NO Charcot have a 7
times more likely chance of amputation. Add a
diagnosis of Charcot with the ulcer and you see
a 12 times more likely chance for amputation.
Most of the time we operate on Charcot to treat
an unremitting ulcer putting the limb at risk.

I would also point out that Loyola is a world
class limb salvage institution and would caution
against concluding that similar outcomes would
hold true in a local community environment.
After seeing the “multispecialty team” approach
in training at Georgetown’s limb center and then
graduating to community practice, I would argue
good reasons for outcomes to be different
outside these settings.

Also as I stated in my previous comments, I
would like to see if PM news could post the
facts of the case to better understand whether
this was legitimate or as Dr. Jacobs’ put
it, “understandable.”

I think the original concern for those who wrote
in was and still is, “Is 2.27 million dollars
reduced to 1.475mil a reasonable award (even
with the most egregious of diagnostic mistakes)
for a patient who did not suffer an amputation?
We do know that the patient allegedly has
Charcot, ulcers, and infections, rendering him
unable to walk and possibly needing amputation.
So according to Dr. Jacobs, and I agree,
statistically this individual has a great chance
of being a community ambulator. When is enough,
enough with the large awards of money?

Douglas Pacaccio, DPM, Yorkville, IL,
douglaspacaccio@yahoo.com

The issue with Charcot foot, ulcers and
amputations is obviously a complex one. NIH held
an international symposium on this issue 2 years
ago, of which I was a participant. The consensus
of the meeting was that amputation is rarely
medically necessary and there are many
aggressively conservative non-surgical options
used for this condition by those who are well
educated in it's diagnosis and treatment.
Statistically this is supposed to be a rare
diabetic complication.

I believe that the most significant concern is
that due to the relative rarity of Charcot
joints it gets misdiagnosed. The amputations
that occur are in patients diagnosed with
osteomyelitis and the statistics reflect this
diagnostic skewing. Patients [and their family]
get tired of frequent visits, read press reports
and decide they and their insurance are being
bilked, and go to an orthopedist who looks at
the x-ray, screams 'This is infected and has to
be cut off' and consent to an amputation. That
is the 'gold standard' for treating
osteomyelitis. There's an x-ray that shows boney
destruction and there's an open lesion close to
bone. There is no need for confirmatory tests.
Once amputated there is no need for bone
cultures.

There's no way to prove this, but I believe that
a lot of the legs/feet that are amputated for
osteomyelitis are really misdiagnosed Charcot
and could have been managed more conservatively.

The bottom line? If you are going to treat
Charcot patients you must CYA: get sed rate
panels, CRP's, serial x-rays on a regular basis
to monitor treatment. Percutaneous bone biopsy
when uncertain. Educate, educate, educate your
patient and their family. Then do it again. Know
how to answer them when they go for a 2nd
opinion.

Or refer them to a colleague to treat their
Charcot. That colleague should then refer them
back to you for all other foot care besides
Charcot [i.e., the dental model of practice].
But that is a whole other topic.

H. David Gottlieb, DPM, Baltimore, MD,
hdavidgottliebdpm@gmail.com

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03/09/2010    Douglas J. Pacaccio, DPM

$1,475,000 Settlement for MD's Failure to Diagnose Charcot Foot

I would really like to know more about this case
because it severely concerns me that a jury
awarded a man, “2.27 million” dollars in
damages. How was this number reached? How much
does his lawyer get? I’d love to think that all
that money will go to support his family because
he was gainfully employed and can no longer work
because of his disability. But, we all have
patients with diabetes who have their Charcot
disease diagnosed correctly and still end up
with ulcers, deformity and face amputation. Is
this opening the door for any patient with
Charcot disease to sue the second they get an
ulcer and “cannot walk and MAY need an
amputation”?

All too often, I see patients who either did not
have their Charcot diagnosed correctly or even
worse, their primary doctor knows they have foot
deformity WITH an ulcer, but it is “just a foot”
and clearly their hypertension and kidney
function are the only issues worth any
attention. These patients get cycled from one
wound care center to the next for years
accepting that ulcers, infections and “wet to
dry dressings” performed by an RN are a fact of
life.

Lucky for me, there some really good primary
doctors in my area that “get it” and refer right
away. They also understand my methods are not
too aggressive as I routinely reconstruct these,
when appropriate. However, I tell all of these
patients that the indications for amputation are
already present, and many of them have been
offered amputation by our orthopedic
colleagues.

Anyone who does these will tell you that some of
them simply cannot be saved. The problem is
that I do not know which ones until I try. I’ve
had ones I thought would surely heal; fail and
others I thought would surely fail; heal. My
main point here is that it disappoints me that a
jury feels a Charcot with ulcers is worth 2.27
million dollars and I wonder who the plaintiff’s
witness was and what the lawyer’s argument for
it was.

Again, anyone who does these knows that they are
not financially rewarding. I do them because I
was trained to do them, I’m comfortable doing
them and the non-financial rewards are
gratifying when you win. I’m not defending
misdiagnosis of Charcot.

Quite the contrary, it completely aggravates me
when someone else hangs on to these (by
misdiagnosis or apathy) and finally refers it
after they have been paid for all their “wound
care”, only to turf an antibiotic resistant
(because of all the broad spectrum antibiotics
used to treat the –“osteo”) multi-bacterial,
deformed dysfunctional mess for someone else to
deal with. However, are we setting the stage
for every Charcot patient to be targeted by a
trial lawyer looking for someone, other than the
disease and often times the patient also, to
blame to the tune of millions.

This is why tort reform is needed in healthcare
reform. Ignoring the cost of lawsuits; we know
that limb salvage is a worthy endeavor not only
from a mortality perspective, but from a “cost
to the system” perspective as well; as our
colleague Dr. Lee Rogers has talked about many
times over. This type of behavior from our legal
system will not encourage doctors to take these
types of cases. It is the $2.27 million that
staggers me, despite the actual facts of the
case; “patient’s comparative negligence.”

Douglas J. Pacaccio, DPM, Yorkville, IL,
douglaspacaccio@yahoo.com

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12/03/2005    Paul Kesselman, DPM

Fosamax and Charcot Foot (David Armstrong, DPM)

RE: Fosamax and Charcot Foot (David Armstrong,
DPM)
From: Paul Kesselman, DPM

I have used Aredia(palmidronate) IV once or
twice a month to arrest the
acute Charcot foot followed by daily Miacalcin
nasal spray or weekly Fosomax.
I haven't had any experience with Boniva.

Aredia should not be administered in your
office, but should either be
given in a hospital outpatient dept, surgi-
center, or an oncologist’s office. These
facilities have the support staff and equipment
to monitor the patient's cardiac status with EKG
and serum calcium levels. Novartis has several
papers on the use of Aredia for Charcot as well
as a newer drug Zometa.

Note the following warning: The U.S. Food and
Drug Administration (FDA) and Novartis
Pharmaceuticals Corp. have notified dental
healthcare professionals by letter of
recommendations that cancer patients considering
intravenous (IV)
therapy with the bisphosphonates pamidronate
disodium (Aredia) or zoledronic
acid (Zometa) have a dental examination prior to
initiation of therapy and
avoid invasive dental procedures while receiving
IV bisphosphonate treatment. The recommendation
comes in light of potential risk of
osteonecrosis of the jaw (ONJ) associated with
use of IV bisphosphonates, according to an
alert sent yesterday from MedWatch, the FDA's
safety information and adverse event reporting
system.

Paul Kesselman, DPM, Woodside, NY,
pkesselman@pol.net

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12/01/2005    Donald A. Rhodes, DPM

Fosamax and Charcot Foot (David Armstrong, DPM)

RE: Fosamax and Charcot Foot (David Armstrong,
DPM)
From: Donald A. Rhodes, DPM

Dr. Armstrong refers to "Anomalies in OPG-RANK-L
balance seem to explain not only bony breakdown
in Charcot but also (paradoxically) vascular
calcification in persons with advanced
neuropathy."

I will be speaking at the Diabetic Foot Update
in San Antonio on Sunday, December 4th. I will
present the results of a small pilot study which
indicate that the bone mineral density loss
associated with diabetes and, in particular,
with Charcot joints is preventable and
reversible. This is based upon the production
of neuropeptides by the electronic stimulation
of specific nerves and acupuncture points. This
study was performed in cooperation with a number
of other physicians in our community. This
treatment is designed to create various
neuropeptides including VIP (vasoactive
intestinal polypeptide) which down-regulates
RANK and RANKL and, in addition, down-regulates
VEGF (vascular endothelial growth factor) which
is involved with the vascular calcification.

In our next diabetic study we will be joined by
a cardiologist who is an expert in endothelial
dysfunction. He has specialized equipment which
will be able to verify if we are normalizing
endothelial dysfunction.

References:
Rosa-Ranal M, de la Cruz DA, Lorena-Rubio Y,
Larrea F. New paradigms in the regulation of
bone metabolism. Rev Invest Clin. 2001 Jul-
Aug;53(4):362-9.
Mukohyama H, Ransjo M, Taniguchi H, Ohyama T,
Lerner UH. The inhibitory effects of vasoactive
intestinal peptide and pituitary adenylate
cyclase-activating polypeptide on osteoclast
formation are associated with upregulation of
osteoprotegerin and downregulation of RANKL and
RANK. Biochem Biophys Res Commun. 2000 Apr
29;271(1):158-63.

Donald A. Rhodes, DPM, Corpus Christi, TX,
DrRhodes2@aol.com

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11/29/2005    Howard Bonenberger, DPM

Charcot Foot (Elliot Udell, DPM)

RE: Charcot Foot (Elliot Udell, DPM)
From: Howard Bonenberger, DPM

In the past I have occasionally used patellar
tendon bearing braces (PTBs) with good success.
This allows you to visualize the foot (unlike a
cast) while offloading the area but still
maintaining weight on the limb which reduces
atrophy. I've not read anything about this but
in a diabetic I would imagine that allowing use
of the thigh and pelvic girdle muscles with a
PTB device would also help lower blood sugars
(versus a non-weight-bearing status) due to
muscle energy requirements (assuming proper
insulin management). If anyone has comments on
this I'd be interested.

Howard Bonenberger, DPM, Nashua, NH ,
howardbon@aol.com

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11/28/2005    Multiple Respondents

Fosamax and Charcot Foot (Elliot Udell, DPM)

RE: Fosamax and Charcot Foot (Elliot Udell, DPM)
From: Multiple Respondents

Bisphosphonates have been relatively widely used
for the last 10-15 years as an experimental
treatment for Charcot. An early case series
(Selby, et al., Diabetic Med, 1994) and
subsequent randomized controlled trial using the
Paget's dose of IV pamidronate by Ed Jude and
coworkers seemed to suggest that it might have
some marginal effect on disease progression
(Diabetologia. 2001 Nov;44(11):2032-7). While
others have also claimed some anecdotal degrees
of success, I'm not sure how they're measuring
that success. Our results have been somewhat
lackluster (translation: I'm not sure if popping
alendronate pills helps all that much). However,
much more recent work may suggest that a
different mechanism-- one modulating levels of
osteoprotegerin (OPG) and RANK-L, may prove more
therapeutically fruitful. To that end, we and
others have followed the (as yet theoretical)
work of our colleague William Jeffcoate
(Diabetologia. 2004 Sep;47(9):1488-92) and
attacked this very different pathway.

Anomalies in OPG-RANK-L balance seem to explain
not only bony breakdown in Charcot but also
(paradoxically) vascular calcification in
persons with advanced neuropathy. At least one
randomized trial, recently presented by a former
Czech fellow of ours, Robert Bem, at the
European Assn for the Study of Diabetes Meeting
in Athens, seems to suggest that intranasal
delivery of calcitonin may be very effective in
limiting progression of Charcot. Much more work
needs to be done here. That said, though, I
think that the work done by William Jeffcoate
may be the most important theoretical work
regarding Charcot in a very, very long time. If
it proves useful, I think it will stand up with
the excellent historical work by our
profession's own Lee Sanders as a second bookend
to a fascinating disease process.

David G. Armstrong, DPM, PhD, Professor of
Surgery, Chair of Research and Assistant Dean
Dr. William M. Scholl College of Podiatric
Medicine at Rosalind Franklin University of
Medicine and Science
armstrong@usa.net

The bisphosphonates, of which Fosamax
(alendronate) is one, have shown efficacy for
ACUTE Charcot foot. However, Fosamax itself has
not been used in any of the reported studies to
my knowledge. The studies looking at the
bisphosphonates for acute Charcot foot have all
used Aredia (pamidronate). Aredia is a potent
bisphosphonate and only available for
intravenous administration. The studies looking
at the use of Aredia advocate a one time dose of
90mg IV given over no less than 2-4 hours.
Realize that the use of the bisphosphonates for
Charcot foot is an off-label use of these
medications. For more information, see the
following papers:

Jude EB, Selby PL, Burgess, J, et al.:
Bisphosphonates in the treatment of Charcot
neuroarthropathy: a double-blind randomised
controlled trial. Diabetologia 44:2032-2037,
2001.

Anderson JJ, Woelffer KE, Holtzman JJ, Jacobs
AM: Bisphosphonates for the treatment of Charcot
neuroarthropathy. J Foot Ankle Surg 43:285-289,
2004.

Michael S. Downey, D.P.M., Philadelphia, PA
(Dowpod@aol.com)

Treating Charcot with a bisphosphate is not a
bad idea, although from the literature I have
read uses IV pamidronate or others of that
nature, what I have learned is that the kidney's
must me functioning properly and works well with
a one time dose. Although you would either have
to put them in the hospital for the IV or send
them to an infusion center which can be costly
either way.

Ronnie Bateh, DPM, Northeast Florida Endocrine
and Diabetes Association, Jacksonville, FL,
JBateh@aol.com

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11/26/2005    Elliot Udell, DPM

Fosamax and Charcot Foot

Query: Fosamax and Charcot Foot

I am part of the team that is caring for a man
who suffers with neuropathy (of unknown origin)
and is now developing "stress" fractures of his
rear foot. We are concerned that he might be at
the early stages of Charcot foot. We are trying
anything to delay or prevent this from
happening. To date we are using an EBI
stimulator and some immobilization. One of his
doctors asked if Fosamax would be helpful in
preventing the progression of Charcot foot. To
date there is scant literature to support this.
Does anyone reading this have any experience
with the use of Fosamax or similar
pharmaceuticals for the prevention or treatment
of early Charcot foot?

Elliot Udell, DPM, Hicksville, NY,
Elliotu@aol.com

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10/22/2003    Sylvia Trotter, DPM

Charcot Foot

Query: Charcot Foot

A middle age male patient, diabetic for many
years, neuropathic, presented several months ago
with a warm, swollen, red foot and mild achy
pain. He'd worked outside mending fences a week
prior in old boots. My first thought was early
Charcot. X-ray showed no changes from views
taken 2 or 3 months prior. With decreased
activity the swelling immediately reduced. I
sent him back to work as a deputy sheriff in
small town Wyoming a week or so later. Within 2
weeks it started up again. This time I ordered a
bone scan- which was read as RSD. We off-loaded
and continued off work for a short time, not
believing the RSD diagnosis, and again it
resolved. This has now been going off and on for
several months. Labs have been drawn- no
infection, mildly elevated ESR. MRI last week
finally verified my suspicion- Charcot. However,
there continues to be no degeneration of the
joints or fracture.

My question is, how long do I keep him off
work and immobilized? The symptoms resolve
quickly only to flare up just as quickly upon
weightbearing and usual activity. He can't
perform the duties of his job while in a walking
cast. What prognosis can I offer him? What can
be done to speed the process- keeping in mind
there are currently no fractures to heal.

Sylvia Trotter, DPM
Riverton, WY

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05/26/2003    Doug Milch, DPM

Bilateral Charcot Foot

Query: Bilateral Charcot Foot

Does anyone know how often diabetic Charcot
foot occurs bilaterally and at the same time?
Any references would be appreciated.

Doug Milch, DPM
Asheville, NC
ldmilch@cs.com