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In the Name of ALLAH, Ever Beneficent,
Infinitely Merciful
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Charcot Foot and Treatment
Dr. Asim Bin Zafar M.C.P.S., M.D Consultant
Physician Senior Registrar Baqai Institute of
Diabetology Endocrinology Baqai Medical
University Medical Unit IV Karachi.
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Charcot Neuroarthropathy Background

• originally described in 1868 by Jean Martin
  Charcot
• patients with tabes dorsalis
• massive joint destruction, subluxation and
  dislocation was seen

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Charcot - Background

• Cause
• Today, most common in diabetics, commonly in the
  lower extremity

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Charcot and Diabetes Mellitus

• Average disease history of 10-12 years or more
• Generally poor glycemic control
• Reported incidence varies widely in literature,
  from 0.08-0.5 up to 16 of diabetics

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Pathogenesis

• Three theories
• Neurotraumatic
• Neurovascular
• Inflammatory theory

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Pathogenesis Neuro traumatic Theory

• proposes that Charcot arthropathy results from
  repetitive mechanical trauma from weight bearing
  on insensate extremity
• this trauma can lead to intra capsular effusions,
  ligamentous laxity and joint instability

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Pathogenesis-Neurovascular Theory

• proposes that Charcot is a sequelae of increased
  peripheral blood flow resulting from autonomic
  sympathectomy
• autonomic sympathectomy produces a failure of the
  normal regulatory mechanisms that control blood
  flow

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Pathogenesis-Neurovascular Theory

• autonomic dysfunction causes arteriovenous
  shunting and vasodilitation
• increases rate of blood flow to extremity
• correlated with increased osteoclastic activity

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Pathogenesis-Inflammatory Theory

• It has been suggested that acute CN may be
  triggered in a susceptible individual by any
  event that leads to localized inflammation in the
  affected foot.
• William J. Jeffcoate 2 January 2008
• G. Mabilleau,1 N. L. Petrova,2 M. E. Edmonds, 2
  and A. SabokbarDiabetologia. 2008June 51(6)
  10351040 1

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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

Charcot Neuroarthropathy
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Clinical Presentation
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Acute presentation
Charcot Neuroarthropathy
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Chronic presentation
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Rocker bottom foot
Charcot Neuroarthropathy
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Rocker bottom foot
Charcot Neuroarthropathy
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Anatomic Classification (Sanders and Frykberg,
1991)

• I - forefoot, 10-30
• II - Lisfrancs joint, most common
• III - midtarsal joint, often including
  naviculocuneiform joint
• IV - ankle and subtalar joints, 8-10
• V - (posterior pillar) fractures of calcaneus,
  2

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Radiographic Staging (Eichenholtz, 1966)

• I Developmental (acute) stage
• II Coalescence (quiescent) stage
• III Consolidation (resolution) stage

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Bone Scan
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Radiographs

• Stage I

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Stage I
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Eichenholtz Classification

• Stage II - Coalescence (quiescent)
• Absorption of osseous debris, fusion of larger
  fragments
• Dramatic sclerosis
• Joints become less mobile and more stable
• the hypertrophic, or subacute phase of Charcot

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Stage II
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Stage II
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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

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Stage III
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Mimics

• Osteomyelitis
• DVT
• Acute Gout

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Treatment

• Primary goals
• Stability, plantigrade foot, and to keep the foot
  free of ulceration
• Selection of treatment plan
• Phase dependent, location, severity, and the /-
  of ulceration
• Conservative vs. Surgical

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Treatment

• Initially consists of immobilization during acute
  phase to prevent disease progression
• Generally via total contact casting
• Some disagreement in the literature as to whether
  or not to permit any weight bearing during this
  time
• Others Unna boot, Pneumatic Walker brace, etc.

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Total Contact Cast

• Permits ambulation while uniformly distributing
  weight bearing pressures over the entire foot
  surface

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Treatment

• After acute phase has passed, long-term or
  permanent bracing is often needed
• Gradual return to protected weight bearing
• Examples Charcot Restraint Orthotic Walker
  (CROW), patellar tendon-bearing braces,
  custom-molded shoes, etc.

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Patellar Tendon-Bearing Brace

• Used to transfer weight bearing forces from the
  orthosis through the patellar tendon, thereby
  decreasing weight bearing forces through the foot
  and ankle

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Treatment

• ONLY considered after all conservative measures
  exhausted
• Surgical intervention is necessary in some cases
  of continued ulceration, gross instability,
  presence of infection, limb shortening and
  difficulty in shoe gear.

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Treatment

• Rx is largely patient dependent
• Ostectomy, arthrodesis, mid tarsus closing wedge
  osteotomy, external fixation

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Treatment

• Bone mineral density alterations have been
  documented in Charcot patients
• Example localized osteopenic changes
• Increasing interest in the use of bisphosphonates

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Conclusions

• Charcot a potentially devastating sequela of
  diabetes mellitus
• Treatment requires careful initial management and
  long-term follow-up
• Conservative, surgical treatment options can be
  augmented with the pharmacologic use of
  bisphosphonates

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Thank You