2. Jean-Martin Charcot
Jean-Martin Charcot
29 November 1825 – 16
August 1893)
was a
French neurologist and
professor of anatomical
pathology. He is known as
"the founder of modern
neurology"
3. Definition
Neuropathic arthropathy , neuropathic
osteoarthropathy, Charcot joint refers to
progressive condition of the musculoskeletal
system that is characterized by joint
dislocations, pathologic fractures, and
debilitating deformities.
Charcot Arthropathy :James K DeOrio, MD Associate Professor of Orthopedic
Surgery, Duke University School of Medicine .
Walter Panis, MD Clinical Instructor, Department of Physical Medicine and
Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School
4. History
The first description of neuropathic arthropathy
was by Musgrave in 1703, in his book De
Arthritide Symptomatica.He described a
neuropathic joint as an athralgia.
1868 Jean-Martin Charcot gave the first detailed
description of this disease.
In 1892, Sokoloff --upper extremity with
syringomyelia.
5. In 1927 Leriche stated that a lesion of
sympathetic led to Hyperaemia and bone
resorption.
In 1936, Jordan -diabetes mellitus ---neuropathic
changes in the foot and ankle.
Associated with intra-articular corticosteroid
injections by Chandler and Wright in 1958.
A.C Brower—Neurovascular theory
6. Etiology
Any condition that causes sensory or
autonomic neuropathy
Diabetes mellitus neuropathy
Multiple Sclerosis
Alcoholic Neuropathy
Syringomyelia
Cerebral palsy
Leprosy
9. Diabetes mellitus is currently the most
common cause of neuropathic arthropathy.
Neuropathic joint destruction develops in
approximately 0.1% of patients with diabetes
and 5% of those with peripheral neuropathy
10. Neuroarthropathy among all pts with tabes
dorsalis ranges b/w 5 to 10%
75% of this 5-10% involve lower extremities
and 25% upper extremities.
12. Neurotraumatic Theory
Loss of peripheral sensation and proprioception
leads to repetitive micro trauma 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.
Poor fine motor control generates unnatural
pressure on certain joints, leading to additional
microtrauma.
13. Neurovascular theory
A.C.Brower theory
Postulates that neurologic changes produced by
an underlying medical disorder create a
hypervascular region in the subchondral bone
that is characterized by increased osteoclastic
resorption and osteoporosis.
14. More recent theories implicate the role of
inflammatory cytokines such as TNF-α and
IL-1 in the pathogenesis of Charcot
neuroarthropathy.
On the molecular level, these factors lead to
increased expression of nuclear transcription
factor-κB, which in turn stimulates osteoclast
formation.
15. Joint destruction in the neuropathic joint is
probably brought on by a combination of
factors that include damage to the
nociceptors of the joint and the periarticular
tissues.
16. The activity of peptides such as substance P,
calcium gene related peptide, and vasoactive
intestinal peptide (VIP) could result in increased
vascularity and inflammation, contributing to
further joint destruction.
Substance P can enhance the cellular synthesis
of collagenase and prostaglandin-E; activate T
lymphocytes, monocytes, and neutrophils; and
take an active part in inflammation
17. The initial pathologic changes occur in the
underlying bone and cartilage. Recurrent
effusions occur due to hyperplasia of the
synovium.
The articular cartilage is slowly destroyed by
a pannus, which helps distinguish Charcot's
joints from other forms of osteoarthritis.
18. Gough et al concluded that…..
The serum carboxyterminal telopeptide of
type 1 collagen, a marker of osteoclastic
bone resorption, had significantly increased
levels in the acute Charcot foot.
The lack of an associated increase in
osteoblastic activity supports the idea that
excess osteoclast activity is a feature of the
early stages of Charcot's neuroarthropathy
19. Clinical History
A careful history may reveal an unrecognized
traumatic event.
Charcot neuroarthropathy most frequently
presents in the fifth decade, after an average
duration of diabetes of 20 to 24 years; in
those with type 2 diabetes.
20. Presentation
DEPENDS OF DURATION OF DISEASE
Mild swelling w/o deformity-Moderate
deformity with extreme swelling.
Signs of inflammation.
Profound unilateral swelling. WBC and
ESR may
be normal
21. Increase in localized
temp
Erythema,
Joint effusion.
75% pt. have pain.
The deep tendon
reflexes at the knee are
absent in a majority of
patients.
23. On Examination
Marked Irregularities identified as bony
projections.
Bone formation in soft tissues.
Bag of Bones:
Joint can be passively and painlessly moved in
all Directions
25. Lab Studies
Inflammatory markers
ESR and WBC
– elevated in both infection and Charcot arthropathy
Serum albumin >3.0g/dL
26. IMAGING
Early Changes similar to OA
Nontraumatic dislocations may be an early
sign.
LaterRadiographic evidence of joint
distention caused by fluid, hypertrophic
synovitis, osteophytes, and subluxation.
27. The normal architecture of the joint is lost,
with dislocation, fragmentation, attempted
repair by osteophytes, and sclerosis
33. Anatomic Classification
(Sanders and Frykberg, 1991)
I - forefoot, 10-30%
II - Lisfranc’s joint, most
common
III - midtarsal joint, often
including naviculocuneiform
joint
IV - ankle and subtalar joints,
8-10%
V - (“posterior pillar”) fractures
37. Brailsford
Stage of Hydrasthrosis:Distension of joint by
serosanguinous effusion
Stage of atrophy:Destruction of affected
articular cartilage and then the bone
Stage of hypertrophy:Massive hyperrophy of
bone at periphery of articular cartilage
40. Stage 0(Shibata and Schon)
Swelling and erythema
No Radiographic Changes
41. Eichenholtz Classification
Stage I - Developmental (acute)
– Hyperemia due to autonomic neuropathy weakens
bone and ligaments
– Diffuse swelling, joint laxity, subluxation, frank
dislocation, fine periarticular fragmentation, debris
formation
43. Charcot Neuroarthropathy
Eichenholtz Classification
Stage II - Coalescence (quiescent)
– Absorption of osseous debris, fusion of larger
fragments
– Dramatic sclerosis
– Joints become less mobile and more stable
– Aka the “hypertrophic”, or “subacute” phase of
Charcot
46. Eichenholtz Classification
Stage III - Consolidation (resolution)
– Osseous remodeling
– for clinical purposes, stage I is regarded as the
acute phase, while stages II and III are regarded
as the chronic or quiescent phase
52. HIP
Charcot neuroarthropathy in the hip is rare.
Painless and Functional: no treatment
Try conservative management
50% of fractures of the femoral neck in
diabetics developed Charcot's joints.
53.
54.
55. KNEE
Most Commonly secondary to Syphilis.
Results in Gross Instability
If only one knee is involved and destruction
is severe, fusion is indicated.
Total knee arthroplasty ???
59. Treatment
Primarily nonoperative.
Consists of Acute and Postacute phases.
– Acute
– Casting along with crutches and walkers.
– Postacute
– Include bracing, ankle-foot orthotics(AFO),
specialized shoes.
60. Treatment
Casting- changed every 1-2weeks, if
ulcerations are present changed every week
for wound care, duration from 3-6 months.
Shoes, bracing, and orthotics- duration
from 6-24 months.
Typical total healing time 1-2 years.
67. Surgical treatment
Ankle:
Arthrodesis of ankle to place the foot
Plantigrade.
IM nail/Charnley/Ilizarov External Fixators
Average time for Fusion:20 months(IM nail).
Talus -- fragmented and avascular--talectomy and
tibiocalcaneal arthrodesis.
75. Hindfoot neuroarthropathy
Mainstay of Treatment is NONSURGICAL.
Arthrodesis indicated for…
Hindfoot valgus with subluxation of the
subtalar joint or midtarsals to prevent
ulceration and infection.
76. Principles outlined by Papa et al.
Careful removal of cartilage and debris.
Thorough removal of sclerotic bone.
Adequate fashioning of congruent bone
surfaces for apposition.
Rigid fixation of the arthrodesis site.
Complete resection of fibrotic capsular tissue
and synovium
80. With the Lisfranc pattern, breakdown initially occurs along the medial column,
with late changes progressing to the lateral column. The arch abducts and
prominences develop, leading to deformity, fullness, and ulceration. The
naviculocuneiform pattern leads to collapse at the naviculocuneiform joint, with
development of a lateral rocker-bottom deformity. The perinavicular pattern is
caused by osteonecrosis or fracture of the navicular. The lateral arch height
decreases, leading to a lateral rocker and shortening of the medial column.
Eventually this breakdown progresses to the central aspect of the foot, with
severe plantar flexion of the talus and eventual ulceration. The transverse tarsal
pattern is caused by lateral subluxation of the navicular on the talus and
abduction of the foot with a valgus calcaneus. Calcaneal pitch eventually
decreases, and a central rocker develops at the calcaneocuboid joint. In late
stages, the talus is completely dislocated from the navicular, and ulceration
develops at the calcaneocuboid interval. All four patterns eventually progress to
a rocker-bottom deformity and chronic ulceration.