Charcot Foot and Treatment

Kentucky Podiatric Residency Program Podiatric Externship Program Jonathan O Quinn, Drew Pearson, Mark Witt October 2001

Charcot Neuroarthropathy Background



 

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

Charcot Neuroarthropathy

Charcot - Background


Predisposing conditions:
    

diabetes mellitus alcoholism syringomyelia spinal cord lesions and others

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

Charcot Neuroarthropathy

Charcot Foot


Radiographic hallmarks:


 

Bony destruction, fragmentation Bony remodeling Joint destruction, subluxation and dislocation

Charcot Neuroarthropathy

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
Charcot Neuroarthropathy

Pathogenesis
 

Has yet to be fully elucidated Sensory and autonomic neuropathy nearly universally present Arteriovenous shunting thought to play a role Normal blood supply and hyperglycemia also seen Repetitive microtrauma may be inciting factor
Charcot Neuroarthropathy

Pathogenesis


Two theories


neurotraumatic (German) neurovascular (French)

Charcot Neuroarthropathy

Pathogenesis Neurotraumatic Theory



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

Pathogenesis Neurotraumatic Theory



absence of protective sensation allows continued loading of fractured extremity heightened healing response seen

Charcot Neuroarthropathy

PathogenesisNeurovascular Theory


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

Charcot Neuroarthropathy

PathogeneisNeurovascular Theory


 

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

Charcot Neuroarthropathy

PathogenesisNeurovascular Theory
 

marked demineralization of bone increases susceptibility to subluxation, fracture and collapse

Charcot Neuroarthropathy

Pathogenesis


today, most agree that both theories play a role in charcot combination of osteopenia, bone hyperemia, joint instability and sensorimotor deficits predisposes to changes seen with charcot
Charcot Neuroarthropathy

Anatomic Classification
(Sanders and Frykberg,
  
1991)

 

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

Radiographic Staging
(Eichenholtz, 1966)


Developmental (acute) stage

II Coalescence (quiescent) stage III Consolidation (resolution) stage

Charcot Neuroarthropathy

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

Radiographs


Stage I

Charcot Neuroarthropathy

Radiographs


Stage I

Charcot Neuroarthropathy

Eichenholtz Classification


Stage II - Coalescence (quiescent)



  

Absorption of osseous debris, fusion of larger fragments Dramatic sclerosis Joints become less mobile and more stable Aka the hypertrophic , or subacute phase of Charcot
Charcot Neuroarthropathy

Radiographs


Stage II

Charcot Neuroarthropathy

Radiographs


Stage II

Charcot Neuroarthropathy

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
Charcot Neuroarthropathy

Radiographs


Stage II

Charcot Neuroarthropathy

Clinical Presentation
 

Red, hot, swollen foot Typically painless or only mildly painful unilateral swelling of extremity Can mimic cellulitis, gout, osteomyelitis and even DVT Plain films may appear normal initially

Charcot Neuroarthropathy

Clinical Presentation


Ortho exam may reveal joint hypermobility with crepitus +/cutaneous ulceration As disease progresses, longitudinal and transverse arches of foot may collapse, creating a rocker bottom foot

Charcot Neuroarthropathy

Clinical Presentation


Some degree of sensory deficit always present Deep tendon reflexes, vibratory sensation, and proprioception may be diminished or absent Due to autonomic sympathectomy, may see bounding pulses, calor, rubor, tumor and anhidrosis +/- xerosis
Charcot Neuroarthropathy

Clinical Presentation


Acute presentation

Charcot Neuroarthropathy

Clinical Presentation


Rocker bottom foot

Charcot Neuroarthropathy

Clinical Presentation


Rocker bottom foot

Charcot Neuroarthropathy

Treatment


Primary goals


Stability, plantigrade foot, and to keep the foot free of ulceration Phase dependent, location, severity, and the +/- of ulceration

Selection of treatment plan



Conservative vs. Surgical

Charcot Neuroarthropathy

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.
Charcot Neuroarthropathy

Total Contact Cast



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

Charcot Neuroarthropathy

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, AFO, etc.

Charcot Neuroarthropathy

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
Charcot Neuroarthropathy

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.
Charcot Neuroarthropathy

Treatment
 

Very patient dependent Ostectomy, arthrodesis, midtarsus closing wedge osteotomy, external fixation TAL

Charcot Neuroarthropathy

Treatment


Bone mineral density alterations have been documented in Charcot patients



Example: localized osteopenic changes

Increasing interest in the use of bisphosphonates

Charcot Neuroarthropathy

Bisphosphonates


Pyrophosphate analogs that inhibit osteoclastic bone resorption Used commonly in diseases characterized by abnormal bone turnover


Example: Paget s disease, osteoporosis, osteolytic bone metastasis, Gorham-Stout disease and others
Charcot Neuroarthropathy

Pamidronate


Most commonly used bisphosphonate is pamidronate (Aredia), a second generation bisphosphonate Acts by adsorbing onto hydroxyapatite crystals in newly synthesized bone matrix, blocking access of osteoclast precursors to this matrix and inhibiting bone resorption
Charcot Neuroarthropathy

Pamidronate


Benefit of inhibiting bone resorption while not significantly inhibiting bone remineralization in animal studies Shown to be 10 times and 100 times more potent at inhibiting bone resorption than clodronate and etidronate, respectively
Charcot Neuroarthropathy

Clinical Use
 

Guis et al, 1998 One case treated with IV infusions of 90 mg every four months for two years Clinical improvement in six months and cessation of bone destruction after two years

Charcot Neuroarthropathy

Clinical Use
 

Selby et al, 1994 Six cases treated adjunctively for 12 weeks each with IV infusions of 30 mg followed by five doses of 60 mg Skin temp differences between affected and non-affected extremities used as a marker of disease process Results
Charcot Neuroarthropathy

Clinical Use


Skin temp differences decreased from 3.4 s 0.7 rC to 1.0 s 0.5 rC after first infusion of 30 mg and remained within normal limits thereafter All six pts noted decreased pain and swelling and increased mobility Three pts maintained clinical improvement for more than one year after treatment

Charcot Neuroarthropathy

Clinical Use
 

Young, 1999 Two cases treated adjunctively with IV infusions Normalized skin temp differences and reduced edema within three months Decreased duration of active process and need for prolonged cast immobilization
Charcot Neuroarthropathy

Clinical Use
 

Young, 1999 (cont.) Infusions of 30 mg, 60 mg and 60 mg spaced two weeks apart Reported this is sufficient to resolve clinical signs in most cases

Charcot Neuroarthropathy

Clinical Use
 

Jude et al, 2000 Double-blind, randomized, placebocontrolled study Pts given either a single infusion of 90 mg pamidronate or a saline placebo Results

Charcot Neuroarthropathy

Clinical Use
 

39 pts Decreased ALP and skin temperature differences seen with pamidronate compared with placebo Concluded that a single dose of pamidronate produces a sustained reduction in bone turnover and disease activity
Charcot Neuroarthropathy

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
Charcot Neuroarthropathy

Thank You

Charcot Neuroarthropathy

References


1. Frykberg RG and Mendeszoon E: Management of the diabetic charcot foot. Diabetes Metab Res Rev 2000; Vol. 16, Supplement 1: 559-65. 2. Guis S et al: Healing of charcot s joint by pamidronate infusion. J Rheumatology 1999; Vol. 26, No. 8: 1843-45. 3. Caputo GM et al: The charcot foot in diabetes: six key points. Am Family Physician 1998; Vol. 57, No. 11: 2705-10. 4. Young MJ: The management of neurogenic arthropathy: a tale of two charcots. Diabetes Metab Res Rev 1999; Vol. 15: 59-64. 5. Reinherz RP et al: Identification and treatment of the diabetic neuropathic foot. J Foot Ankle Surg 1995; Vol. 34, No. 1: 74-8. 6. Pinzur MS et al: Current practice patterns in the treatment of charcot foot. Foot Ankle Intl 2000; Vol. 21, No. 11: 916-20.

Charcot Neuroarthropathy

References
 

7. Sella EJ and Barrette C: Staging of charcot neuroarthropathy along the medial column of the foot in the diabetic patient. J Foot Ankle Surg 1999; Vol. 38, No. 1: 34-40. 8. Fabrin J et al: Long-term follow-up in diabetic charcot feet with spontaneous onset. Diabetes Care 2000; Vol. 23, No. 6: 796-800. 9. Schon LC et al: Charcot neuroarthropathy of the foot and ankle. Clin Orthop Rel Res 1998; No. 349: 116-31. 10. Baker RE: Total contact casting. J Am Pod Med Assoc 1995; Vol. 85, No. 3: 172-76. 11. Mehta JA et al: Charcot restraint orthotic walker. Foot Ankle Intl 1998; Vol. 19, No. 9: 619-23. 12. Selby Pl et al: Bisphosphonates: a new treatment for diabetic charcot neuroarthropathy? Diabet Med 1994; Vol. 11, No. 1: 28-31.

Charcot Neuroarthropathy

References
 

    

13. Fitton A and McTavish D: Pamidronate: a review of its pharmacological properties and therapeutic efficacy in resorptive bone disease. Drugs 1991; Vol. 41, No. 2: 289-318. 14. Gough A et al: Measurement of markers of osteoclast and osteoblast activity in patients with acute and chronic diabetic charcot neuroarthropathy. Diabet Med 1997; Vol. 14: 527-31. 15. Young MJ et al: Osteopenia, neurological dysfunction, and the development of charcot neuroarthropathy. Diabetes Care 1995; Vol. 18, No. 1: 34-8. 16. Devlin RD et al: Interleukin-6: a potential mediator of the massive osteolysis in patients with gorham-stout disease. J Clin Endocrin Metab 1996; Vol. 81, No. 5: 1893-97. 17. www.sbu.ac.uk/~dirt/museum/pU-821.html 18. www.aafp.org/afp/980600ap/caputo.html 19. www.celos.psu.edu/DFC/module12b.html 20. www.gentili.net/diabeticfoot/charcot.htm 21. www.pulsus.com/Plastics/04_04/jain_ed.htm

Charcot Neuroarthropathy