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Charcot foot
This document discusses Charcot foot, which is a progressive and degenerative arthropathy of the foot caused by underlying neurological deficits such as diabetes. It begins by defining Charcot foot and describing its historical identification and causes. It then explains the pathophysiology, describing both the French and German theories. The document outlines the clinical stages of acute and chronic Charcot foot and how they present. It discusses the diagnosis process and treatments, including conservative options like casting and immobilization as well as surgical interventions.
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Charcot foot
- 1. By Rafi Mahandaru 212 CHARCOT FOOT
- 2. By Rafi Mahandaru 212 CHARCOT FOOT
- 3. Jean-Marie Charcot • 29November 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
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- 5. Charcot foot Charcot footcan 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
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- 7. Firstly describes 1868 TabesDorsalis 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
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- 11. French Theory • Charcot1868 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
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- 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
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- 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 • Peoplerisk 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 • StageIII 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
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- 21. Clinically • Have beendescribe 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
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- 26. Conservative Immobilization andoff 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 CharcotFoot Contraindicated • Chronic Ulcerated and fixed deformity indication of surgery remove bony prominent and correct the deformity – Exostectomy – Arthrodesis – Tendon Lengthening
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