Neuropathic arthropathy, also known as Charcot arthropathy, is a condition characterized by progressive joint destruction and deformity caused by loss of sensation in the joints. It is most commonly seen in patients with diabetes or neurological disorders. The main theories for its pathophysiology are neurotrauma from repetitive micro-injuries without pain perception, and neurovascular changes that increase bone resorption. Treatment involves initial casting to immobilize the joint, followed by bracing, orthotics, and immobilization over the course of 1-2 years to allow healing. Surgical options like fusion or reconstruction may be used for advanced cases or deformity correction.

2. Neuropathic Arthropathy
Dr.ARAIB LAIGA

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. Etiology
 Any condition that causes sensory or
autonomic neuropathy
 Diabetes mellitus neuropathy
 Multiple Sclerosis
 Alcoholic Neuropathy
 Syringomyelia
 Cerebral palsy
 Leprosy

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

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

7. 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.

8. 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.

9.  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.

10. 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.

11. 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

12.  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.

13. Acute Charcot neuropathy

14. 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

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

16. Lab Studies
 Inflammatory markers
ESR and WBC
– elevated in both infection and Charcot arthropathy
 Serum albumin >3.0g/dL

17. 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.

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

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

20. 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

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

23. 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

24. Neuropathic Joints
Hypertophic
or
Productive
Hypertophic
or
Productive
MIXED
Atrophic
or
Resorptive

25. 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

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

27. Modified Eichenholtz Classification for the
Progression of Charcot Neuroarthropathy

28. Radiographs
 Stage I

29. Radiographs
 Stage II

30. Radiographs
 Stage II

31. Radiographs
 Stage III

33. Charcot Arthropathy

36. 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.

39. 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 ???

41. 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.

42. 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.

44. Early stage
 Total Contact cast.

45. Total contact cast

46. Air cast

47. CROW boots

48. Treatment
2. Pharmacological Treatment.
 Pilot study first using pamidronate,1994.
Other Bisphosphonates were used to
decrease disease activity and bone
turnover markers.
 Calcitonin were also used.
 Given for 12 weeks or till temp gradient is
less than 2 on 2 consecutive visits.

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

50. 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.

51. Internal or External Fixation??

56. 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.

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

58. THANK
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