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Kentucky Podiatric Residency Program Podiatric Externship Program Jonathan O Quinn, Drew Pearson, Mark Witt October 2001
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:
Charcot Foot
Radiographic hallmarks:
Bony destruction, fragmentation Bony remodeling Joint destruction, subluxation and dislocation
Charcot Neuroarthropathy
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
Charcot Neuroarthropathy
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
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
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)
Charcot Neuroarthropathy
Eichenholtz Classification
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
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
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
Charcot Neuroarthropathy
Clinical Presentation
Charcot Neuroarthropathy
Treatment
Primary goals
Stability, plantigrade foot, and to keep the foot free of ulceration Phase dependent, location, severity, and the +/- of ulceration
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
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
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
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