neuropathic joint as diabetic complication

1. By Rafi Mahandaru 212
CHARCOT FOOT

2. By Rafi Mahandaru 212
CHARCOT FOOT

3. Jean-Marie Charcot
• 29 November 1825 – 16
August 1893
• The father of neurology
• Charcot triad-1  MS
• Charcot triad-2  AC
• Charcot joint, known as
Charcot neuroarthropathy
(CNA)/charcot
osteoarthropathy (COA) /
charcot foot/ neuropathic
joint

4. DEFINITION

5. Charcot foot
Charcot foot can be defined as
a relatively painless, progressive and degenerative
arthropathy of single or multiple joints caused by an
underlying neurological deficit.
It was a limbthreatening condition, wich can lead to amputation

6. ETIOLOGY

7. Firstly describes 1868
Tabes Dorsalis  late manifestation of shypilis
Bilateral degeneration of axons in BOTH
dorsal columns
• Pain, parestethic, sensory loss
• Muscle stretch reflex also messed up
because the sensory input to those
reflexes have been lesioned
• usually occurs at lumbar levels

8. Recent common cause
• Complication of diabetes melitus
• is estimated to affect
between 1-2.5% of people with
diabetes (2003)
• It is estimated to affect 0.8%-8% of
diabetic populations (2011)
•At least 10 years suffer

9. Another rare cause

10. PATHOPHYSIOLOGY

11. French Theory
• Charcot 1868  neurovascular theory
• “…the arthropathy of ataxic patients seems to
always start after the sclerotic changes have
taken place in the spinal cord.”
• Spinal cord lesion  autonomic neuropathy 
arterious venous shunting  increase blood flow
 increase osteoclast activity  bone resorption
and mechanical weakening  fractures and
deformity
• Increase blood flow  warmth foot and dilated
veins

12. German theory (1946)
• Volkman and Virchow  neurotraumatic theory
• “ peripheral neuropathy leading to loss of
protective sensation may render the foot
susceptible to injury from either repeated or
acute trauma “
• Insensitive joint
• Allow mechanical trauma  normaly prevented
by pain
• Spontaneous fracture, subluxation and
dislocation

13. Other Contributed Factor
• Bone pathology
• Atypical neuropathy
• Non-enzymatic collagen glycation
• Increased plantar pressures
• Excessive local inflammation

14. Acute Charcot Foot

15. Acute Charcot Foot
• H : Hminor trauma
• L : Swollen, erythem,
deform
• F : Warmth – hot
• M : Crepitation
• Discomfort 
considerably less than
might be expected
from the pathology
seen

16. Chronic Charcot foot

17. Chronic Charcot foot
• L : pemanent deform,
no erythem, reducing
swollen
• F : warmth or hot
temp., subside
• M : no crepitation, gait
tabes dorsalis,
• Sometimes with
unoticed ulcer

18. Clinical Course
• People risk for Charcot foot  stage 0
• Acute Charcot foot  stage I  Dev-fragmentation
– Swollen, hyperemia, bone fragmentation, join dislocation
and destruction
– Radiological still looks normal, bone debris, joint
subluxation and dislocation subsequently develop
• Chronic Charcot foot  stage II  coalescence
– Decreasing erythem, hot, swelling
– X-Ray :absorption of fine debris,formation of new bone,
coalescence of larger fragments and sclerosis of bone
ends
– Decrease joint mobility

19. Clinical Course
• Stage III  reconstruction - consolidation
– edema, erythema and warmth are not present,
– unless fractures have not healed
– Ulcers may develop at
– sites of residual deformity, while X-rays reveal
bony remodeling,
– rounding of bone ends and decreased sclerosis

20. Diagnose

21. Clinically
• Have been describe above
• Investigation should be make on early stage
and to differentiate between another disease
like Osteomyelitis, Gout, Arthritis
– History
– Predisposising factor
– Physical Examination
– Complication

22. X - Ray
• Atrophic changes :
“pencil pointing or
sucked candy “

23. X-Ray
• Hypertropic
changes :
– Bone proliferation
– Bone destruction
– Subcondral sclerosis
and
– Osteophtes may be
seen

25. Treatment

26. Conservative
 Immobilization and off loading
• Reducing swelling and mechanical stress 
elevation, bed rest, whell chair
• TCC  Total Contact Cast

27. Conservative
• Biphosphonat  inhibit Osteoclastic activity
– N-Containing
• Sodium alendronat (fosamax)
• Riserdonat (actonel)
– Non N-Containing
• Etidronat (didronel)
• Tiludronic (skelid)
INTRANASAL
CALCITONIN

28. Surgery
• Acute Charcot Foot  Contraindicated
• Chronic Ulcerated and fixed deformity 
indication of surgery  remove bony
prominent and correct the deformity
– Exostectomy
– Arthrodesis
– Tendon Lengthening

29. THANX … !