This 22-year old female with a history of type 1 diabetes and other conditions presented with swelling, redness, and warmth in her left foot and ankle over 3 days without pain or trauma. Physical exam found erythema and swelling in the right foot and ankle with diminished sensation. X-ray revealed acute charcot arthropathy. She was diagnosed with acute charcot arthropathy and treated with splinting, casting, and eventually a ankle foot orthosis to allow full weight bearing over several months.

1. Charcot Case Study and
Review Questions

2. History of
Present
Illness
22 yr old female patient comes to the office
seeking treatment for a three day history of
left foot and ankle swelling, redness and
warmth. Pt does not complain of pain and
denies trauma or recent illness.

3. Past Medical
History
• Type I diabetes x 12 years with
associated neuropathy
• Anorexia nervosa
• Chronic diarrhea
• Osteoporosis due to anorexia,
• Chronic diarrhea and prolonged
amenorrhea
• Hospitalization: several times for tx of
DKA and exacerbation of her
psychiatric problems

4. Physical
Exam
• Vitals: Ht 160 Cm; Wt 52 Kg; VSS, Afebrile
• Derm: Right Foot And Ankle Is
Erythematous, Warm, Swollen; No Open
Lesions
• Vasc: Palpable Pedal Pulses
• Neuro: Diminished Perception Of Light
Touch In A Stocking Distribution
• M/S: Normal Muscle Strength; No Pain On
Palpation

5. Labs
• ESR: 130mm/hr
• WBC: 8.7 with normal differential
• Hgb: 8.6
• Hct: 29%
• Platelet count: 700,000/mm3

6. X-ray
X-ray:
Diagnosis: Acute charcot arthropathy

7. Diagnosis
and
Treatment
Diagnosis: Acute Charcot Arthropathy
Treatment:
• Posterior splint with compressive dressing x 3
days
• TCC applied once swelling subsided x 6 weeks
• Increased WB in short leg cast x 4 – 6 months
• Eventually went on to full WB in an AFO

8. Review Questions

9. 1. What are
some
differentials
for this case
study?
• Acute Charcot
• Osteomyelitis
• Cellulitis
• DJD
• Gout
• Acute septic arthritis
• Avascular necrosis
• Pigmented Villonodular Synovitis
• Psoriatic arthritis
• Rheumatoid arthritis

10. 2. What are
the four
factors
necessary for
charcot to
develop?
• Peripheral neuropathy
• Hypervascularization
• Repetitive microtrauma
• Unrecognized injury

11. 3.
Eichenholtz’s
three stages
of Charcot
are....
• I – Acute, Developmental, Destructive,
Dissolution – foot is inflamed, edematous and
erythematous; radiographs demonstrate bone
fragmentation (subchondral bone and articular
cartilage) and debris formation; joint
dislocation/subluxation may be present;
typically lasts 6 – 8 weeks
• II – Coalescence – healing begins and
inflammation subsides; radiographs show
coalescence and resorption of bony fragments;
larger fragments begin to fuse
• III – Remodeling, Resolution, Reconstructive,
Quiescence – inflammation is resolved; return
to normal radiographic density; reformation of
the joint architecture.

12. 4. What are
the
treatments
associated
with each
stage?
• Stage I – Resolution of edema with compression,
elevation and rest; total immobilization of the limb
by total contact casting, regular casting or pre-
fabricated cast boot
• Stage II – Progressive weight bearing in regular or
total contact cast; as the disease progresses move
from a cast to bracing such as a Charcot restraint
orthotic walker (CROW), double upright metal AFO
or other AFO with progressive weight bearing
• Stage III – Long term AFO bracing; extra depth shoes
or other types of accommodative foot wear.
• ***Remember that you must use clinical judgment
to decide when to progress to the next stage of
treatment***

13. 5. What are
the 6Ds of
Charcot?
• Distension of joints
• Dislocation
• Disorganization
• Density increases
• Debris production
• Destruction

14. 6. What
disorder has
the highest
percentage
of Charcot
joints?
• Syringomyelia; up to 25% will have charcot
joints
• Diabetes Type 2 is the most common cause!

15. 7. What
percentage of
diabetic
patients will
develop
charcot joints?
• 1 in 680
• From .13% to 25%
• This number depends on who is reporting it.

16. 8. What are
some
disorders
associated
with
Charcot?
- Diabetes
- Tabes dorsalis (syphilis)
- Syringomyelia
- Chronic alcoholism
- Hansen’s disease (leprosy)
- Spina bifida
- Meningomyelocele
- Congenital insensitivity to pain - CMT
- Multiple sclerosis

17. 9. Describe the
two theories
associated
with the
development
of Charcot
joints.
• Neurovascular (French) Theory damage to
the trophic nervous centers with an
alteration in the sympathetic control of
blood flow to bones and joints leads to
persistent hyperemia and active bone
resorption
• Neurotraumatic (German) Theory An
extreme progression of degenerative joint
disease following loss of proprioception and
protective pain sensation

18. 10. How do
you tell the
difference
between
Charcot and
osteomyelitis?
- Use of the MRI is becoming popular
- Definitive way: bone biopsy with
microbiological diagnosis
- Use of the WBC labeled bone scan
- Osteomyelitis will be hot, Charcot will not be
hot
- Plain radiographs:

19. PLAIN RADIOGRAPHS

20. 11. What are the patterns of bone and joint involvement?
Sanders & Frykberg. The Charcot foot, 1991.

21. Brodsky J et al. Patterns of breakdown in the Charcot tarsus of
diabetes and relation to treatment. Foot Ankle 5(12):353, 1986.reported
Brodsky J et al. Patterns of breakdown in the Charcot tarsus of diabetes and relation to
treatment. Foot Ankle 5(12):353, 1986.
Type 1 (Midfoot) Metatarsocuneiform
&
naviculocuneiform
Most common ~ 60%
Type 2 (Hindfoot) STJ, CC and TN jt Less common 30 – 35%
Type 3A (Ankle) Ankle joint Serious long lasting
changes
Associated with
discrete trauma
Type 3B
(Calcaneus)
Tubercle of the
calcaneus
Least common
Secondary
deformity and
collapse of the distal
portion of the foot
Associated with
discrete trauma

22. Schon LC et al. Charcot Neuroarthropathy of the foot and ankle.
Clinical orthopedics and related research. 349, 1998.
• Type I: Lis franc pattern
• Type II: Naviculocuneiform pattern
• Type III: Perinavicular pattern
• Type IV: Transverse tarsal pattern
Subtypes A, B and C with increasing severity from A to C

23. 12. During
what stage(s)
should
surgical
intervention
be attempted?
Well, like everything else in medicine recently,
it depends on who you read.

24. 12. During
what stage(s)
should
surgical
intervention
be attempted?
• Eichenholtz: early stage I or late stage III
Charcot joints pp 7 – 8. Springfield, IL 1996
• Mann: early stage I (before development of
osteopenia from local hyperemia) or late stage II
when new bone formation is occurring
Foot and Ankle Surgery, 1999.
• Johnson: operative treatment is usually carried
out in Stage III after conservative care has been
exhausted. An acute charcot fracture can be
treated with ORIF in stage I if performed early
before bone stock become insufficient for
fracture.
Johnson JE. Operative treatment of neuropathic
arthropathy of the foot and ankle. JBJS 80A Nov
1998.

25. 12. During
what stage(s)
should
surgical
intervention
be attempted?
• Myerson: surgery is necessary in the acute
phase of skin necrosis resulting from the
pressure of a dislocated bone is imminent or
other skin problems are likely to occur as a
result of casting.
• Surgery is also indicated at this time for marked
dislocation of the foot that is likely to cause
problems with shoewear at a later date. Surgery
can only be performed if bone stock is
adequate, therefore, he rarely operates if more
than 6 weeks after the beginning of the acute
phase.
• In the setting of acute neuroarthropathy
associated with infection and surgery is
indicated, Myserson uses an external fixator to
stabilize the foot. Surgery should probably be
reserved until Stage II or III. Foot and Ankle
Disorders, 1999.

26. 12. During
what stage(s)
should
surgical
intervention
be attempted?
• Simon: First paper to demonstrate successful
results in operative treatment in stage I Charcot.
Authors operated on 14 patients in the acute
phase of the disease with good anatomical
reduction and good results. All patients had
anatomic reduction, clinical union and stability
without an increased risk of adverse outcome.
Given this outcome along with decreased cost
when compared to ulcer care, authors believe
that early arthrodesis should be considered in
patients with early stage I charcot.
• Simon SR et al. Arthrodesis as an early
alternative to non-operative management of
charcot arthropathy of the diabetic foot. JBJS
82A July 2000.

27. 13. What is
the natural
history of
Charcot
arthropathy?
1. The foot goes numb
2. The bones become soft
3. The patient walks on the numb foot with soft bones
4. The soft bones fracture
5. The fractures heal with malposition of the fragments and
deposition of fracture fragments in the adjacent joint
capsule
6. The process repeats
7. The foot becomes shorter and wider and develops angular
bony prominences
8. The foot becomes ulcerated and infected as the patient
walks on the angular prominences.
9. All hell breaks loose

28. 14. What is
the primary
deforming
force in
many cases
of Charcot?
• Ankle joint equinus

29. 17. What is
the ‘gold
standard’ for
diagnosis?
• Bone biopsy: will histologically differentiate
between osteo and charcot.

30. 18 . What is
a plan for the
management
of Acute
Charcot?
• - Immobilization
• - Reduction of stress
• - Armstrong advocates the TCC (surprise,
surprise) The reduced stride length and
walking cadence will decrease the possibility
of causing charcot in the other limb

31. 19. What are
the
radiographic
signs of
Stage III
Charcot ?
• Trabecular bridging on serial radiographs

32. 15. What is
the history of
Charcot in
the
literature?
• Musgrave 1703 – first to report neuropathic
osteoarthropathy as an arthralgia secondary
to venereal disease.
• Jean Marie Charcot 1868 – French
neurologist. Concisely describe the
neuropathic component of the disease.
Linked the condition to syphilis which was
very common at the time.
• Jordan 1936 – Linked this condition to
diabetes mellitus.
• Etiology of the Condition:
Charcot 1868 – Deficient trophic centers in
the spine

33. 15. What is
the history of
Charcot in
the
literature?
• Volkman, Virchow and the “German School” –
neurotraumatic in nature. The neuropathic foot
would fracture with exuberant bone formation.
Eloesser (1917) – sectioned posterior nerve
roots in cats and noted neurotrophic changes in
71% of the animals
• Finsterbush & Friedman (1975) – repeated
Eloesser’s experiment in rabbits but casted the
rabbits hind legs. Different response noted in
denervated and sensate rabbits. Concluded that
trauma important but not primary factor.
• Edmonds et al (1985) – Increased blood flow
was partially responsible for the osteopenia and
‘washing out of bone’ seen in Charcot.
Neurovascular theory.

34. 16. What are
the relevant
lab tests that
can help lead
to a diagnosis
of charcot?
• WBC will be elevated with a left shift on the
differential acute osteomyelitis
• ESR is non-specific may not be helpful
• Tech 99 bone scans may or may not be helpful
• Indium 111 bone scans much more specific.
• If (+) do bone biopsy to confirm osteomyelitis
and r/o Charcot
• If (-) dx is charcot until proven otherwise
Certec scan labeled white blood cells. May also
be helpful
• Probe to bone
If (+) proceed to bone biopsy If - continue with
other tests