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Charcot Neuropathic Arthropathy Flashcards

1
Q

What is the incidence of Charcot in patients wit diabetes

A

7.5-13%

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2
Q

What is the incidence of Charcot in patients with diabetes and neuropathy

A

29%

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3
Q

What is the neurotrophic theory etiology of Charcot

A

CND degeneration from damage to “trophic centers” in anterior horn cells leading to neurogenic deficit in bone nutrition causing ataxic neuropathy (Trophic centers now speculated as autonomic nerves) … vascular disregulation

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4
Q

What is the neurovascular etiology of Charcot

A

Central sympathetic failure causing hyperemia (increased blood flow) causing increased osteocalstic activity leading to bone demineralization and mechanical weakening

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5
Q

What is neurotraumatic etiology of Charcot

A

Repetitive microtrauma to the insensate limb —> joint swelling, inflammation and effusion —> osteolysis and joint laity

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6
Q

What is the current etiology for Charcot

A
  • role of proinflammatory cytokines
  • RANK-L/OPG signaling pathway
  • “OPG inactivates RANK-L a disturbance of this balance may trigger excessive osteolysis, this cycle is fully realized in the insensate limb of a patient who continues to bear weight
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7
Q

What is the osteoclast-osteoblast imbalance etiology pathway in Charcot patients

A
  • inflammation secondary to unchecked/uninterrupted microtrauma to the insensate foot
  • pro-inflammatory cytokines (interleukin-1) triggers exaggerated inflammatory response to microtrauma.
  • increase osteoclastic activity
  • osteolysis, fracture
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8
Q

Describe the influence of RANK-L on monocytes in diabetic Charcot patients

A

Baseline increase in osteoclastic activity in Charcot patients compared to diabetic and healthy controls
- significant increase in osteoclastic activity with addition of RANK-L

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9
Q

What is the incidence of Charcot being unilateral

A

80%

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10
Q

What are the risk factors of Charcot

A
  • pain insensitivity **
  • load bearing intensity (obesity)
  • long standing DM (12-15 years)
  • history of trauma
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11
Q

Wha does the VASCULAR clinical picture of Charcot looks like

A
  • edema (AV shunting)
  • bounding pulses - concomitant PVD
  • erythema
  • warm (4 degrees vs. contralateral limb
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12
Q

What does the MUSCULOSKELTAL and NEUROLOGIC clinical picture of Charcot look like

A
  • equinus (non enzymatic glucosylation of fibrils)
  • apropulsive
  • rocker bottom foot (long standing, progressed deformity)
  • diminished/absent deep tendon reflexes
  • diminished/absent protective vibratory sensation
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13
Q

What does the dermatological clinical picture of Charcot looks like

A
  • ulceration
  • anhidrotic, waxy taut skin (non enzymatic glycosylation of keratinocytes)
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14
Q

What are some differentials of Charcot

A
  • Cellulitis
  • Osteomyelitis
  • Thrombophlebitis
  • VTE/DVT/PE
  • Gout, RA, etc
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15
Q

What are the signal intensity differences you see on MRI for osteo vs Charcot

A
  • osteo = high signal intensity of marrow space on T2
  • Charcot = low signal intensity of marrow space on both T1 and T2
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16
Q

On MRI, does describe the difference between forefoot and midfoot involvement for osteo vs charcot

A
  • osteo is typically forefoot
  • charcot is typically midfoot
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17
Q

Describe the difference in joint dislocation seen on MRI for osteo vs Charcot

A
  • osteo - joint dislocation not typical
  • Charcot - typically have joint dislocation
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18
Q

Describe the cystic changes seen on MRI for osteo vs. Charcot

A
  • Charcot has cystic changes
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19
Q

Does Charcot or osteo typically affecting multiple bones on MRI

A

Osteo usually confined to single bones
Charcot usually affects multiple bones

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20
Q

Does osteo or Charcot have visible soft tissue tracts on MRI

A

Osteo

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21
Q

Is the ghost phenomenon seen with osteo or charcot

A

Osteo

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22
Q

What’s one clinical test to differentiate between cellulitis and Charcot

A

Elevate legs for 10 mins:
- reduction in edema = Charcot
- no reduction in edema = cellulitis

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23
Q

What is Stage I of the Eichenholtz Calssification

A
  • Developmental/acute
  • capsular distention - increased mobility
  • fragmentation of subchondral bone
  • resorption
  • joint effusion
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24
Q

What is Stage II of the Eichenholtz Classification

A
  • Coalescence
  • Absorption of fine debris
  • healing of fractures
  • Fusion of large fragments
25
What is Stage III of the Eichenholtz Classification
Remodeling/Reconstruction - rounding of bone ends - residual deformity - increased bone density - exuberant ossfication - reduced sclerosis secondary to revascularization
26
Does the Eichenholtz classify Charcot clinically?
No. Only radiographically
27
What is Stage 0 of the Shibata Classification
Inflammatory - localized warmth, swelling, redness. - Minimal to no radiographic changes - MRI may show nondisplaced, pathological fracture and increased marrow edema
28
What is Stage I of Shibata Classification
Development - localized warmth, swelling redness - Radiographic presence of bony debris, fragmentation of subchondral bone, periarticualr fracture, subluxation/dislocation
29
What is Stage II of the Shibata Classification
Coalescence - continued but decreased warmth, swelling, redness - new bone formation ,coalescence of fragments, ankylosis, scelrosis of bone ends
30
What is Stage III of the Shibata Classification
Remodeling - marked decrease in warmth, swelling, redness - radiographic appearance of remodeled and new bone formation, decreased sclerosis, with residual gross deformity
31
What is the purpose of the Sanders and Frykberg Classification for Charcot
Describes the anatomic location
32
What is the Sanders & Frykberg Classification
I - Forefoot 15% II - TMTJ 40% III - Naviculocuneiform, TNJ, CCJ 30% IV - Ankle and/or STJ 10% V - Calcaneus 5%
33
What is the Brodsky Classification
I - Midfoot 60% II - Hindfoot (STJ, TNJ, CCJ) 30-35% IIIA - Ankle (tibiotalar) 9% IIIB - Posterior Calcaneus/Tuberosity <2%
34
What is the Schon classification
Type I - Lisfranc’s Type II - Naviculocuneiform Type III - Perinavicular Type IV - Transverse tarsal; chopart joint
35
What are some non-operative treatment for Charcot
-Compression dressing - Immobilization - TCC, SLC, bivalves TCC
36
What are some benefits of Total Contact Casting
- cast evenly to evenly distribute forces across plantar surface - decreases shear and edema - faster ulcer healing - voluntary reduction in activity level
37
What is the ulceration complication rate with total contact casts
Up to 30%
38
Non operative treatment for Charcot in the absence of edema
- patellar tendon bracing - Custom Molded Ankle and Foot Orthotic (MAFO) - Rocker Bottom with stiff walking sole - Charcot Restraint Orthotic Walker (CROW)
39
What is the benefit of patellar tendon bracing as a non op treatment for Charcot
- reduces plantar pressures by up to 32% - 65 N/cm^2 associated with ulcer risk development - 100 N/cm^2 average plantar pressures in Charcot patients
40
What are the indications for surgical treatment for Charcot
- failure of conservative therapy - recurrent ulceration - gross and unstable deformity (ankle)
41
What are abnormal radiographic findings of Charcot patients
- meary’s angle >27 Normally 0 - abnormal cuboid height Cuboid is normally much height than line drawn from the plantar surface of 5th MT head to calc
42
What are the components of surgical treatment for Charcot
- posterior muscle group - rocker bottom - rigid stabilization of rearfoot-to-leg relationship - control of forefoot-to-rearfoot relationship in frontal and transverse plane —> supinatus
43
What’s an adjunctive surgical procedure for Charcot patients
Exostectomy
44
What are the possible surgeries involved in the posterior muscle group lengthening as part of the surgical treatment for Charcot
- Gastroc recession - TendoAchilles Lengthening
45
What do you have to be aware of with a TAL in Charcot patients
- loss of 1 muscle grade (may be closer to 30%) - overcorrection
46
When is the plantarflexory wedge osteotomy used in surgical treatment of Charcot patients
- coalesced pathology - osteotomy types - realignment
47
What is involved in the surgical treatment of Charcot patients
- Posterior muscle group lengthening - Plantarflexory Wedge Osteotomy - Arthrodesis of affected joint - Glissane’s principles q
48
What are the advantages of internal fixation in the surgical treatment for Charcot
Success rate of 87% Psychologically appealing to the patient
49
Disadvantages of internal fixation in the surgical treatment of Charcot patient
- major tissue dissection - static correction: doesn’t account for the potentially progressive nature of the disease - screw failure: osteopenic bone - further osteopenia secondary to protracted NWB - vascular spasm and ischemia with aggressive deformity (varus) correction
50
Like bone, cement is strong under _____ but weak under ______
Compression Tension
51
Beams are
Cannulated/weaker (7.0)
52
Bolts are
Strong (5.0 and 6.5)
53
What is Charcot superconsturcts
- arthrodesis extending far beyond the zone of injury in order to take advantage of fixation in good and uninvolved bone - bone resection to shorten the underlying osseous architecture to facilitate reconstruction without increasing soft-tissue tension - fixation devices placed in biomechanically optimal locations - utilization of the strongest fixation device that will be tolerated by he soft tissues (bolts)
54
What are the advantages of external fixation in Charcot reconstruction
- percutaneous - preserves soft tissue - allows for gradual anatomic reduction - potential for immediate WB
55
What the disadvantages of external fixation in Charcot reconstruction
- fracture through pin tract - dressing changes - pin loosening - patient psychology and compliance - meticulous pin care (pin tract infection) - learning curve - delayed union and nonunion
56
In Charcot patients with varus deformities of 40 degrees, how would you surgically manage
Staged procedures, gradual correction of remaining deformity with ex fix (3 weeks)
57
In Charcot patient with varus deformities of less than 15 degrees what kind of correction
Acute correction Be careful of deformities greater than 15 degrees b/c you can vasospasm
58
What are adjunctive treatments for Charcot
- bisphosphonates - bind to hydroxyapatite to prevent osteoclastic degeneration - bone stimulators - Prolia (Denosumab) Rank L antibody
59
Convalescence for Charcot
- close follow up- at least a year - NWB for 3-4 months - protected WB for 6-12 months - protect contralateral limb - 80% unilateral

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