1. Charcot foot, or neuropathic osteoarthropathy, is a progressive condition characterized by joint destruction and instability associated with peripheral neuropathy. 2. It results from repetitive microtrauma to joints from loss of sensation and proprioception, as well as autonomic dysfunction leading to hyperemia and bone resorption. 3. Treatment involves complete offloading with non-weightbearing and immobilization to induce quiescence, followed by gradual protected weightbearing with custom bracing and accommodative footwear.

1. CHARCOT JOINT ARTHROPATHY AND
REHAB MANAGEMENT
Dr. Harshaand Popalwar
MBBS, MD,DNB, MNAMS, PGDHM, FDFM
Specialist Grade Two
Department of Physical Medicine and Rehabilitation
Safdarjung Hospital, New Delhi

2. DEFINITION
 Charcot foot (i.e.neuropathic
osteoarthropathy) can be defined as a
noninfectious and progressive condition of
single or multiple joints characterized by joint
dislocation, pathologic fractures, and severe
destruction of the pedal architecture that is
closely associated with peripheral
neuropathy.

3. INTRODUCTION
 The description of Charcot joints dates back to
1703 when neuropathic osteoarthropathy was
first described by W. Musgrave.
Jean-Martin Charcot a French neurologist is
credited for his work in 1868 for describing gait
anomalies of patients with syphilis (tabes
dorsalis).
 Jordan, in 1936, was the first to describe a
relationship of diabetes to neuropathic
arthropathy

4. ETIOLOGY
 Any condition resulting in decreased peripheral sensation, proprioception,
and fine motor control:
 Diabetes mellitus neuropathy with Charcot joints in 1/600-700 diabetics.
Related to long-term poor glucose control.
 Alcoholic neuropathy
 Cerebral palsy
 Leprosy
 Syphilis (tabes dorsalis), caused by the organism Treponema pallidum
 Spinal cord injury
 Myelomeningocele
 Syringomyelia
 Intra-articular steroid injections
 Congenital insensitivity to pain
 Spina bifida
 Peripheral nerve injury
 Multiple sclerosis
 Poliomyelitis

5. UNDERLYING MECHANISMS
 Two primary theories have been advanced:
 Neurotrauma throry: Loss of peripheral
sensation and proprioception leads to
repetitive microtrauma to the joint in question; this
damage goes unnoticed by the neuropathic
patient, and the resultant inflammatory resorption
of traumatized bone renders that region weak
and susceptible to further trauma. Indeed, it is
a vicious cycle. In addition, poor fine motor
control generates unnatural pressure on certain
joints, leading to additional microtrauma.
 .

6.  This micrtrauma produces intracapsular
effusions,ligamentous laxity,and joint
instability. With continued use of injured
extrimity,further degeneration ensues, which
results in a charcot joint

7.  Neurovascular theory: Neuropathic patients
have dysregulated autonomic nervous
system reflexes, and de-sensitized joints receive
significantly greater blood flow. The
resulting hyperemia leads to increased
osteoclastic resorption of bone, and this, in
concert with mechanical stress, leads to bony
destruction.

8.  In reality, both of these mechanisms probably
play a role in the development of a Charcot
joint.

9.  The presence of sensory neuropathy renders the
patient unaware of the initial precipitating trauma and
often profound osseus destruction taking place during
ambulation.
 The concomitent autonomic neuropathy with its
associated osteopenia and relative weakness of bone
predisposes it to fracture.
 Capsular and ligamentous distension or rupture is
also a part of this process,leading to the typical joint
subluxations and loss of normal pedal architecture in
the classic rocker bottom charcot foot.

10. CLASSIFICATION OF CHARCOT ARTHROPATHY.
 In 1966 Eichenholz proposed a classification of
Charcot joints which is broken down into three
distinctive stages.
 Stage one, or the development stage, shows debris
surrounding the joints on x-ray. Stage one can
develop over a period of days to weeks and is merely
radiographic change that occurs in response to
unperceived trauma.
 Stage two is the coalescence stage. In stage two,
the bone begins to heal with absorption of debris and
healing of large fracture fragments.
 .

11.  Stage three, often called the reconstruction or
reconstitution stage, notes a reduction in bone
turn over and reformation of stable bone
structure.
 Stage 0 was added in 1999 by Sella and
Barrette to include patients who exhibit clinical
symptoms of Charcot arthropathy but have yet
to show radiographic changes
 In clinical practice,the initial developmental
stage is considered active or acute, whereas the
coalescent and reconstructive stages are
considered to be the quiescent or reparative.

12. RADIOGRAPHIC FINDINGS
 Radiologically, osteoarthropathy takes on the
appearance of severely destructive form of
degenerative arthritis.
 Sanders and frykberg describe typical
neuropathic osteoarthropathy patterns of joint
involvement based on joint location in diabetic
patients. these patterns may exist independently
or in combination with each other as determined
through clinical and radiographic findings.

13. PATTERN 1:FOREFOOT

14.  Pattern 1 encompasses atrophic changes or
osteolysis of the MTP and interphalangeal
joints with the characteristic sucked candy
appearance of the distal metatarsals.
 Ten to thirty percent of the neuropathic
osteoarthropathies have been categorised in
various reports as pattern 1.

16. PATTERN 2:TARSOMETATARSAL(LISFRANC’S)
JOINT

17.  Pattern 2 involves lisfranc’s joint,typically with
the earliest clue being a very subtle lateral
deviation of the base of the second metatarsal
at the cunieform joint.
 Once the stability of this ‘keystone’ is lost, the
loisfranc joint complex will often subluxate
dorsolaterally.
 Fracture of the second metatarsal base allows
for greater mobility in which subluxation of other
metatarsals occur.

18.  The rupture of the intermetatarsal and
tarsometatarsal ligaments plantarly will also
allows a collapse of the arch during normal
weight bearing,leading to the classic rocker
bottom deformity.
pattern 2 is the most common presentation in
clinical practice.

20. PATTERN 3:MIDTARSAL AND
NAVICULOCUNIEFORM JOINTS
 Pattern 3 incorporates changes within the
midtarsal joint with the frequent addition of
naviculocunieform joint.
 Spontaneous dislocation of the talonavicular
joint with or without fragmentation
characterize this pattern.

23. PATTERN 4:ANKLE AND SUBTALAR JOINT.
 It involves the ankle joint, including the subtalar
joint and body of the talus.
 Massive osteolysis is frequently observed in
this pattern with attendent ankle or subtalar
subluxation and angular deformity.
 Tibial or fibular malleolar fracture are frequently
seen in association with osteoarthropathy in
this location and most likely precipitate the
development of the joint dissolution.
 It is found in approximately 10 % of reported
cases.

26. PATTERN 5: CALCANEUS (CALCANEAL
INSUFICIENCY AVULSION FRACTURE)
 It is least common presentation and is
characterised by extraarticular fracture of the
calcaneus.
 This is more appropriately considered a
neuropathic fracture of body or,more
commonly,the posterior tuberosity of
calcaneus.

28. CLINICAL PRESENTATION
Clinical features of acute charcot joint-
1.vascular- a) bounding pulse
b) erythema
c) swelling
d) warmth
2.neuropathic- a) absent or diminished:
pain, proprioception, deep tendon reflexes.

30. 3) skeletal- a) rocker bottom deformity
 b) medial tarsal subluxation
 c) digital subluxation
 d) rearfoot equinovarus
 e) rearfoot subluxation
 f) hypermobility
 4) cutaneous- a) neuropathic ulcer
 b) hyperkeratosis
 c) infection

31. ROCKER BOTTOM FEET

32. CLINICAL DIAGNOSIS OF ACUTE CHARCOT
ARTHROPATHY
 Plain radiographs are invaluable for
ascertaining the presence of
osteoarthropathy in a warm, swollen,
insensate foot.
 With a concomitant wound, it may initially be
difficult to differentiate between acute charcot
arthropathy and osteomyelitis solely based
on plain radiographs.

33.  When ulcer probes to bone, a bone biopsy
is indicated and should be considered most
specific method of distinguishing between
osteomyelitis and charcot arthropathy.
 A biopsy consisting of multiple shards of
bone and soft tissue embeded in the deep
layers of synovium is pathognomic for
neuropathic osteoarthropathy.

34.  Tecnetium bone scan- expensive and
nonspecific to differentiate between
osteomyelitis and charcot arthropathy.
 Indium scanning still expensive,but has been
shown to be more specific.

35. CONSERVATIVE MANAGEMENT.
Immobilization and reduction of stress are
considered the mainstay of treatment for
acute charcot arthropathy.
Non weight bearing on the affected limb for 8-
12 weeks removes the continual trauma and
should promote conversion of the active
charcot joint to the quiescent phase.

36. OFF-LOADING OR IMMOBILIZATION DEVICES
USED IN THE MANAGEMENT OF CHARCOT FEET.
 -wheelchai
 -crutches
 -walker
 -Elastic bandage or jones dressing
 -unna’s boot
 -total contact cast
 -fixed ankle walking brace
 -Posterior splint
 -patellar tendon-bearing brace
 -charcot restraint orthotic walker (CROW)
 -surgical shoe with custom inlay

37.  Off loading with or without immobilization
should be anticipated for approximately 3-6
months, depending on the severity of joint
destruction.
 When the patient enters quiescence phase,
management is directed at a gradual
resumption of weight bearing with prolonged
or permenent bracing.

38.  Care must be taken to wean the patient
gradually from non-weight bearing to partial
to full weight bearing with the use of assistive
devices.
 Charcot restraint orthotic walker(CROW) or
other similar total contact prosthetic walkers
have gained acceptance as useful protective
modalities for the initial period of weight
bearing.

39.  Feet must be closely monitored during the
time of transition to permanent footware to
ensure that the acute inflammatory process
does not recure.
 Forefoot and midfoot deformities (patterns 1-
3) often do well with custom full length
inserts and comfort or extra depth shoes
once bracing is no longer required.

40.  Severe midfoot deformities will often require the
fabrication of custom shoes to accommodate
the misshapen foot.
 Rearefoot osteoarthropathy with minimal
deformity may require only a deep, well
cushioned shoe with a full-length orthotic
device.
 For mildly unstable ankles without severe
deformity or joint dissolution,high-top custom
shoes can sometime provides adequate stability
against transverse plane rotational forces.

41.  The moderately unstable ankle will benefit
from an ankle foot orthosis(AFO) and a high-
top therapeutic shoe.
 The severely unstable or maligned rearfoot
will require a patrllar tendon-bearing (PTB)
brace incorporated into a custom shoe.

42. TOTAL CONTACT CUSTOM ORTHOSIS WITH
ROCKER SOLE

43. CHARCOT RESTRAINT ORTHOTIC WALKER
(CROW)

44. CHARCOT RESTRAINT ORTHOTIC WALKER

45. MEDICAL MANAGEMENT
 Control of sugar in diabetic patient
 Management of infection with antibiotics
 In the setting of altered bone mineral density
(BMD) in patients with diabetes,
bisphosphonates can be use to prevent
further osteoporosis in charcot arthropathy.

46. SURGICAL THERAPY
 Neuropathic arthropathy should not be considered
primarily a surgical disorder.
 Surgery should be contemplated only when attempts
at conservative care have failed to provide a stable,
plantigrade foot.
 instability, gross deformity,and progressive
destruction despite immobilization are the primary
indications for surgical intervention.
 Procedures such as simple bone resections,
osteotomies, midfoot or major tarsal reconstraction,
and ankle arthrodesis might become necessary.

47.  Amputations should usually be regarded as a
procedure of last resort in neuropathic
patients and not as a normal consequence of
osteoarthropathy.

48.  Thank you