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Neuropathic Arthropathy
Dr.Subodh Pathak
Jean-Martin Charcot
Jean-Martin Charcot
29 November 1825 – 16
August 1893)
was a
French neurologist and
professor of anato...
Definition
 Neuropathic arthropathy , neuropathic
osteoarthropathy, Charcot joint refers to
progressive condition of the ...
History
 The first description of neuropathic arthropathy
was by Musgrave in 1703, in his book De
Arthritide Symptomatica...
In 1927 Leriche stated that a lesion of
sympathetic led to Hyperaemia and bone
resorption.
In 1936, Jordan -diabetes mel...
Etiology
 Any condition that causes sensory or
autonomic neuropathy
 Diabetes mellitus neuropathy
 Multiple Sclerosis
...
 Tabes Dorsalis
 Spinal cord injury
 Myelomeningocele
 Intra-articular steroid injections
 Congenital insensitivity t...
 Vitamin B12 Deficiency
 Phenylbutazone ,Indomethacin
 Ethyl Alcohol.
 Diabetes mellitus is currently the most
common cause of neuropathic arthropathy.
 Neuropathic joint destruction develop...
 Neuroarthropathy among all pts with tabes
dorsalis ranges b/w 5 to 10%
 75% of this 5-10% involve lower extremities
and...
Pathophysiology
 Major theories
– Neurotraumatic theory
– Neurovascular theory
– Most probably both
Neurotraumatic Theory
 Loss of peripheral sensation and proprioception
leads to repetitive micro trauma to the joint in
q...
Neurovascular theory
 A.C.Brower theory
 Postulates that neurologic changes produced by
an underlying medical disorder c...
 More recent theories implicate the role of
inflammatory cytokines such as TNF-α and
IL-1 in the pathogenesis of Charcot
...
 Joint destruction in the neuropathic joint is
probably brought on by a combination of
factors that include damage to the...
 The activity of peptides such as substance P,
calcium gene related peptide, and vasoactive
intestinal peptide (VIP) coul...
 The initial pathologic changes occur in the
underlying bone and cartilage. Recurrent
effusions occur due to hyperplasia ...
Gough et al concluded that…..
 The serum carboxyterminal telopeptide of
type 1 collagen, a marker of osteoclastic
bone re...
Clinical History
 A careful history may reveal an unrecognized
traumatic event.
 Charcot neuroarthropathy most frequentl...
Presentation
 DEPENDS OF DURATION OF DISEASE
 Mild swelling w/o deformity-Moderate
deformity with extreme swelling.
 Si...
 Increase in localized
temp
 Erythema,
 Joint effusion.
 75% pt. have pain.
 The deep tendon
reflexes at the knee are...
Acute Charcot neuropathy
On Examination
Marked Irregularities identified as bony
projections.
Bone formation in soft tissues.
Bag of Bones:
Joint c...
Diagnosis
 Xrays.
 Indium-111 WBC scan.
 Gallium scan.
 USG
 MRI
 Radionuclide scans
Lab Studies
 Inflammatory markers
ESR and WBC
– elevated in both infection and Charcot arthropathy
 Serum albumin >3.0g/...
IMAGING
 Early Changes similar to OA
 Nontraumatic dislocations may be an early
sign.
 LaterRadiographic evidence of j...
 The normal architecture of the joint is lost,
with dislocation, fragmentation, attempted
repair by osteophytes, and scle...
Atrophic Stage:
 Rapid joint destruction
 Loose bodies
 Subchondral bone erosions
 Subluxation
 Pathological#
Hypertrophic Stage
 Reduced jt space.
 Subchondral bone sclerosis
 Pathological # healing with callus
 Multiple osteop...
Radiographic features
6D’s Yochum and Rowe
 Dense bones (subchondral sclerosis)
 Degeneration
 Destruction of articular...
Commonly Affected Joints
 Foot Involvment
 Knee involvement
 Hip involvement
 Shoulder
 Elbow
Anatomic Classification
(Sanders and Frykberg, 1991)
 I - forefoot, 10-30%
 II - Lisfranc’s joint, most
common
 III - m...
Classification ( Brodsky and
Rouse)
Type 1 Midfoot
Type 2 Hindfoot
Type 3a Ankle
3b Calcis tubercle
Type4 Combination

Neuropathic Joints
Hypertophic
or
Productive
Hypertophic
or
Productive
MIXED
Atrophic
or
Resorptive
Brailsford
 Stage of Hydrasthrosis:Distension of joint by
serosanguinous effusion
 Stage of atrophy:Destruction of affec...
Radiographic Staging
(Eichenholtz, 1966)
 I Developmental (acute) stage
 II Coalescence (quiescent) stage
 III Consolid...
Modified Eichenholtz Classification for the
Progression of Charcot Neuroarthropathy
Stage 0(Shibata and Schon)
 Swelling and erythema
 No Radiographic Changes
Eichenholtz Classification
 Stage I - Developmental (acute)
– Hyperemia due to autonomic neuropathy weakens
bone and liga...
Radiographs
 Stage I
Charcot Neuroarthropathy
Eichenholtz Classification
 Stage II - Coalescence (quiescent)
– Absorption of osseous debris, f...
Radiographs
 Stage II
Radiographs
 Stage II
Eichenholtz Classification
 Stage III - Consolidation (resolution)
– Osseous remodeling
– for clinical purposes, stage I ...
Radiographs
 Stage III
Charcot Arthropathy
HIP
 Charcot neuroarthropathy in the hip is rare.
 Painless and Functional: no treatment
 Try conservative management
...
KNEE
 Most Commonly secondary to Syphilis.
 Results in Gross Instability
 If only one knee is involved and destruction
...
Shoulder
Treatment
 Primarily nonoperative.
 Consists of Acute and Postacute phases.
– Acute
– Casting along with crutches and wa...
Treatment
 Casting- changed every 1-2weeks, if
ulcerations are present changed every week
for wound care, duration from 3...
Early stage
 Total Contact cast.
CROW boots
Surgical options
 Arthrodesis
 Exostosectomy of bony prominences
 Osteotomies
 Reconstructive Surgeries
 Autologous b...
Surgical treatment
Ankle:
 Arthrodesis of ankle to place the foot
Plantigrade.
 IM nail/Charnley/Ilizarov External Fixat...
Internal or External Fixation??
Hindfoot neuroarthropathy
 Mainstay of Treatment is NONSURGICAL.
 Arthrodesis indicated for…
 Hindfoot valgus with subl...
Principles outlined by Papa et al.
Careful removal of cartilage and debris.
Thorough removal of sclerotic bone.
Adequat...
Complication
 Ulcers
 Osteomyelitis
 Gross Deformity of the foot
 Gangrene.
THANK
YOU
 With the Lisfranc pattern, breakdown initially occurs along the medial column,
with late changes progressing to the late...
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
Neuropathic (Charcots) joints
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Neuropathic (Charcots) joints

  1. 1. Neuropathic Arthropathy Dr.Subodh Pathak
  2. 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. 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. 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. 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. 6. Etiology  Any condition that causes sensory or autonomic neuropathy  Diabetes mellitus neuropathy  Multiple Sclerosis  Alcoholic Neuropathy  Syringomyelia  Cerebral palsy  Leprosy
  7. 7.  Tabes Dorsalis  Spinal cord injury  Myelomeningocele  Intra-articular steroid injections  Congenital insensitivity to pain  CMTD  Familial interstial Polyneuropathy  Amyloidosis  Pernicious Anemia
  8. 8.  Vitamin B12 Deficiency  Phenylbutazone ,Indomethacin  Ethyl Alcohol.
  9. 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. 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. 11. Pathophysiology  Major theories – Neurotraumatic theory – Neurovascular theory – Most probably both
  12. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 22. Acute Charcot neuropathy
  23. 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. 24. Diagnosis  Xrays.  Indium-111 WBC scan.  Gallium scan.  USG  MRI  Radionuclide scans
  25. 25. Lab Studies  Inflammatory markers ESR and WBC – elevated in both infection and Charcot arthropathy  Serum albumin >3.0g/dL
  26. 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. 27.  The normal architecture of the joint is lost, with dislocation, fragmentation, attempted repair by osteophytes, and sclerosis
  28. 28. Atrophic Stage:  Rapid joint destruction  Loose bodies  Subchondral bone erosions  Subluxation  Pathological#
  29. 29. Hypertrophic Stage  Reduced jt space.  Subchondral bone sclerosis  Pathological # healing with callus  Multiple osteophyte formation with exoxtosis formation.  Dislocations of joints
  30. 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
  31. 31. Commonly Affected Joints  Foot Involvment  Knee involvement  Hip involvement  Shoulder  Elbow
  32. 32. 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
  33. 33. Classification ( Brodsky and Rouse) Type 1 Midfoot Type 2 Hindfoot Type 3a Ankle 3b Calcis tubercle Type4 Combination 
  34. 34. Neuropathic Joints Hypertophic or Productive Hypertophic or Productive MIXED Atrophic or Resorptive
  35. 35. 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
  36. 36. Radiographic Staging (Eichenholtz, 1966)  I Developmental (acute) stage  II Coalescence (quiescent) stage  III Consolidation (resolution) stage
  37. 37. Modified Eichenholtz Classification for the Progression of Charcot Neuroarthropathy
  38. 38. Stage 0(Shibata and Schon)  Swelling and erythema  No Radiographic Changes
  39. 39. 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
  40. 40. Radiographs  Stage I
  41. 41. 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
  42. 42. Radiographs  Stage II
  43. 43. Radiographs  Stage II
  44. 44. 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
  45. 45. Radiographs  Stage III
  46. 46. Charcot Arthropathy
  47. 47. 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.
  48. 48. 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 ???
  49. 49. Shoulder
  50. 50. 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.
  51. 51. 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.
  52. 52. Early stage  Total Contact cast.
  53. 53. CROW boots
  54. 54. Surgical options  Arthrodesis  Exostosectomy of bony prominences  Osteotomies  Reconstructive Surgeries  Autologous bone Grafting  Amputations
  55. 55. 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.
  56. 56. Internal or External Fixation??
  57. 57. 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.
  58. 58. 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
  59. 59. Complication  Ulcers  Osteomyelitis  Gross Deformity of the foot  Gangrene.
  60. 60. THANK YOU
  61. 61.  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.
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Neuropathic joints,Diabetes,Total Contact cast

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