charcot foot and treatment
DESCRIPTION
Diabetic FootTRANSCRIPT
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 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
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
Charcot Neuroarthropathy
PathogenesisNeurotraumatic Theory
absence of protective sensation allows continued loading of fractured extremity
heightened healing response seen
Charcot Neuroarthropathy
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
Charcot Neuroarthropathy
Pathogeneis- Neurovascular Theory
autonomic dysfunction causes arteriovenous shunting and vasodilitation
increases rate of blood flow to extremity
correlated with increased osteoclastic activity
Charcot Neuroarthropathy
Pathogenesis- Neurovascular 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)
I 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
Selection of treatment plan Phase dependent, location, severity,
and the +/- of ulceration 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 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
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,
placebo-controlled 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