Neuropathic (Charcots) joints

Neuropathic joints,Diabetes,Total Contact cast

1. Neuropathic Arthropathy
Dr.Subodh Pathak

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

7. Tabes Dorsalis
Spinal cord injury
Myelomeningocele
Intra-articular steroid injections
Congenital insensitivity to pain
CMTD
Familial interstial Polyneuropathy
Amyloidosis
Pernicious Anemia

8. Vitamin B12 Deficiency
Phenylbutazone ,Indomethacin
Ethyl Alcohol.

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.

11. Pathophysiology
 Major theories
–Neurotraumatic theory
–Neurovascular theory
–Most probably both

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.

22. Acute Charcot neuropathy

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

24. Diagnosis
Xrays.
Indium-111 WBC scan.
Gallium scan.
USG
MRI
Radionuclide scans

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.
LaterRadiographic 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

28. Atrophic Stage:
Rapid joint destruction
Loose bodies
Subchondral bone erosions
Subluxation
Pathological#

29. Hypertrophic Stage
Reduced jt space.
Subchondral bone sclerosis
Pathological # healing with callus
Multiple osteophyte formation with exoxtosis
formation.
Dislocations of joints

30. Radiographic features
6D’s Yochum and Rowe
Dense bones (subchondral sclerosis)
Degeneration
Destruction of articular cartilage
Deformity (pencil-point deformity of
metatarsal heads)
Debris (loose bodies)
Dislocation

32. Commonly Affected Joints
Foot Involvment
Knee involvement
Hip involvement
Shoulder
Elbow

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
of calcaneus, 2%

34. Classification ( Brodsky and
Rouse)

Type 1 Midfoot
Type 2 Hindfoot
Type 3a Ankle
3b Calcis tubercle
Type4 Combination
Type 5 Forefoot

36. Neuropathic JointsEv9uSkP9eh.d
PSd
-SPt5.khsud
Hypertophic
or
Productive
MIXED
Atrophic
or
Resorptive

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

38. Radiographic Staging
(Eichenholtz, 1966)
I Developmental (acute) stage
II Coalescence (quiescent) stage
III Consolidation (resolution) stage

39. Modified Eichenholtz Classification for the
Progression of Charcot Neuroarthropathy

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

42. Radiographs
Stage I

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

44. Radiographs
Stage II

45. Radiographs
Stage II

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

47. Radiographs
Stage III

49. Charcot Arthropathy

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.

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 ???

57. Shoulder

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.

62. Early stage
Total Contact cast.

65. CROW boots

66. Surgical options
Arthrodesis
Exostosectomy of bony prominences
Osteotomies
Reconstructive Surgeries
Autologous bone Grafting
Amputations

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.

68. Internal or External Fixation??

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

77. Complication
Ulcers
Osteomyelitis
Gross Deformity of the foot
Gangrene.

78. T
H
A
N
K


Y
O
U

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.