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Recon > Charcot Neuropathic Arthropathy > Flashcards

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
Q

What is Stage III of the Eichenholtz Classification

A

Remodeling/Reconstruction
- rounding of bone ends
- residual deformity
- increased bone density
- exuberant ossfication
- reduced sclerosis secondary to revascularization

26
Q

Does the Eichenholtz classify Charcot clinically?

A

No. Only radiographically

27
Q

What is Stage 0 of the Shibata Classification

A

Inflammatory
- localized warmth, swelling, redness.
- Minimal to no radiographic changes
- MRI may show nondisplaced, pathological fracture and increased marrow edema

28
Q

What is Stage I of Shibata Classification

A

Development
- localized warmth, swelling redness
- Radiographic presence of bony debris, fragmentation of subchondral bone, periarticualr fracture, subluxation/dislocation

29
Q

What is Stage II of the Shibata Classification

A

Coalescence
- continued but decreased warmth, swelling, redness
- new bone formation ,coalescence of fragments, ankylosis, scelrosis of bone ends

30
Q

What is Stage III of the Shibata Classification

A

Remodeling
- marked decrease in warmth, swelling, redness
- radiographic appearance of remodeled and new bone formation, decreased sclerosis, with residual gross deformity

31
Q

What is the purpose of the Sanders and Frykberg Classification for Charcot

A

Describes the anatomic location

32
Q

What is the Sanders & Frykberg Classification

A

I - Forefoot 15%
II - TMTJ 40%
III - Naviculocuneiform, TNJ, CCJ 30%
IV - Ankle and/or STJ 10%
V - Calcaneus 5%

33
Q

What is the Brodsky Classification

A

I - Midfoot 60%
II - Hindfoot (STJ, TNJ, CCJ) 30-35%
IIIA - Ankle (tibiotalar) 9%
IIIB - Posterior Calcaneus/Tuberosity <2%

34
Q

What is the Schon classification

A

Type I - Lisfranc’s
Type II - Naviculocuneiform
Type III - Perinavicular
Type IV - Transverse tarsal; chopart joint

35
Q

What are some non-operative treatment for Charcot

A

-Compression dressing
- Immobilization - TCC, SLC, bivalves TCC

36
Q

What are some benefits of Total Contact Casting

A
  • cast evenly to evenly distribute forces across plantar surface
  • decreases shear and edema
  • faster ulcer healing
  • voluntary reduction in activity level
37
Q

What is the ulceration complication rate with total contact casts

A

Up to 30%

38
Q

Non operative treatment for Charcot in the absence of edema

A
  • patellar tendon bracing
  • Custom Molded Ankle and Foot Orthotic (MAFO)
  • Rocker Bottom with stiff walking sole
  • Charcot Restraint Orthotic Walker (CROW)
39
Q

What is the benefit of patellar tendon bracing as a non op treatment for Charcot

A
  • 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
Q

What are the indications for surgical treatment for Charcot

A
  • failure of conservative therapy
  • recurrent ulceration
  • gross and unstable deformity (ankle)
41
Q

What are abnormal radiographic findings of Charcot patients

A
  • 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
Q

What are the components of surgical treatment for Charcot

A
  • 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
Q

What’s an adjunctive surgical procedure for Charcot patients

A

Exostectomy

44
Q

What are the possible surgeries involved in the posterior muscle group lengthening as part of the surgical treatment for Charcot

A
  • Gastroc recession
  • TendoAchilles Lengthening
45
Q

What do you have to be aware of with a TAL in Charcot patients

A
  • loss of 1 muscle grade (may be closer to 30%)
  • overcorrection
46
Q

When is the plantarflexory wedge osteotomy used in surgical treatment of Charcot patients

A
  • coalesced pathology
  • osteotomy types
  • realignment
47
Q

What is involved in the surgical treatment of Charcot patients

A
  • Posterior muscle group lengthening
  • Plantarflexory Wedge Osteotomy
  • Arthrodesis of affected joint - Glissane’s principles q
48
Q

What are the advantages of internal fixation in the surgical treatment for Charcot

A

Success rate of 87%
Psychologically appealing to the patient

49
Q

Disadvantages of internal fixation in the surgical treatment of Charcot patient

A
  • 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
Q

Like bone, cement is strong under _____ but weak under ______

A

Compression
Tension

51
Q

Beams are

A

Cannulated/weaker (7.0)

52
Q

Bolts are

A

Strong (5.0 and 6.5)

53
Q

What is Charcot superconsturcts

A
  • 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
Q

What are the advantages of external fixation in Charcot reconstruction

A
  • percutaneous
  • preserves soft tissue
  • allows for gradual anatomic reduction
  • potential for immediate WB
55
Q

What the disadvantages of external fixation in Charcot reconstruction

A
  • 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
Q

In Charcot patients with varus deformities of 40 degrees, how would you surgically manage

A

Staged procedures, gradual correction of remaining deformity with ex fix (3 weeks)

57
Q

In Charcot patient with varus deformities of less than 15 degrees what kind of correction

A

Acute correction
Be careful of deformities greater than 15 degrees b/c you can vasospasm

58
Q

What are adjunctive treatments for Charcot

A
  • bisphosphonates - bind to hydroxyapatite to prevent osteoclastic degeneration
  • bone stimulators
  • Prolia (Denosumab) Rank L antibody
59
Q

Convalescence for Charcot

A
  • close follow up- at least a year
  • NWB for 3-4 months
  • protected WB for 6-12 months
  • protect contralateral limb - 80% unilateral

Recon (10 decks)

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