charcot mark

Charcot Foot and Treatment

Kentucky Podiatric Residency ProgramPodiatric Externship Program

Jonathan O’Quinn, Drew Pearson, Mark WittOctober 2001

Charcot Neuroarthropathy

Charcot Neuroarthropathy Background

originally described in 1868 by Jean Martin Charcot

patients with tabes dorsalis massive joint destruction,

subluxation and dislocation was seen


Charcot - Background Predisposing conditions:

diabetes mellitus alcoholism syringomyelia spinal cord lesions and others

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


Charcot Foot Radiographic

hallmarks: Bony destruction,

fragmentation Bony remodeling Joint destruction,

subluxation and dislocation


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


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


Pathogenesis Two theories…

neurotraumatic (German)

neurovascular (French)


PathogenesisNeurotraumatic 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


PathogenesisNeurotraumatic Theory

absence of protective sensation allows continued loading of fractured extremity

heightened healing response seen


Pathogenesis- Neurovascular 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


Pathogeneis- Neurovascular Theory

autonomic dysfunction causes arteriovenous shunting and vasodilitation

increases rate of blood flow to extremity

correlated with increased osteoclastic activity


Pathogenesis- Neurovascular Theory

marked demineralization of bone increases susceptibility to

subluxation, fracture and collapse


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


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%


Radiographic Staging (Eichenholtz, 1966)

I Developmental (acute) stage

II Coalescence (quiescent) stage

III Consolidation (resolution) stage


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


Radiographs Stage I


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


Radiographs Stage II


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


Radiographs Stage II


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


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


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


Clinical Presentation Acute

presentation


Clinical Presentation Rocker bottom

foot


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


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.


Total Contact Cast Permits

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


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.


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


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.


Treatment Very patient dependent Ostectomy, arthrodesis, midtarsus

closing wedge osteotomy, external fixation

TAL


Treatment Bone mineral density alterations

have been documented in Charcot patients Example: localized osteopenic

changes Increasing interest in the use of

bisphosphonates


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


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


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


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


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


Clinical Use Skin temp differences decreased from

3.4 0.7 C to 1.0 0.5 C 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


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


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


Clinical Use Jude et al, 2000 Double-blind, randomized,

placebo-controlled study Pts given either a single infusion of

90 mg pamidronate or a saline placebo

Results


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


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


Thank You


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.


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.


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

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