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Pan-talar Arthrodesis for Charcot's Arthropathy of the
ankle withLocalized osteoporosis
Ahmed Kholeif MD
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: Localized
osteoporosis 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 blood sugar 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 Loss of neuro-protection causing
repetitive microtrauma.
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
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 resulting in bone resorption and fragmentation.
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 localized osteoporosis, bone hyperemia, joint instability and sensorimotor deficits predisposes to changes seen with charcot
Charcot Neuroarthropathy
Anatomical Classification (Brodsky) Type 1: Tarso-metatarsal joint (70%). Type 2: Midtarsal & Subtalar joints
(20%). Type 3: (3 a) Ankle joint. (3 b) Avulsion of Tendo-achillis
(10%)
Charcot Neuroarthropathy
Anatomical Classification (Brodsky)
Type 1: Tarsometatarsal Joints:
Type 2: Chopart’s (Transverse Tarsal) and Subtalar Joints:
Type 3A: Ankle:
Type 3B: Posterior Calcaneus:
Type 4: Multiple Regions:
Type 5: Forefoot:
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, localized osteopenia, 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 III
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
Clinical Presentation
Charcot Neuroarthropathy
Clinical Presentation
Charcot Neuroarthropathy
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 (adds to risk of osteopenia)
Generally via total contact casting Some disagreement in the literature as
to whether or not to permit any weight bearing during this time
Others: 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
Surgical Treatment of Charco’s AnkleWhat you do not want to see
Charcot Neuroarthropathy
Surgical Treatment of Charcot’s AnkleWhat you do not want to see
Charcot Neuroarthropathy
Charcot Neuroarthropathy
Surgical 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 wear.
Charcot Neuroarthropathy
Surgical Treatment Very patient dependent Ostectomy, arthrodesis, midtarsus
closing wedge osteotomy, external fixation
Indications for surgery in the Charcot ankle:
1. Acute dislocation
2. Recurrent ulceration
3. Secondary to either instability or bony prominence
4. Severe or uncontrolled deformity
Surgical procedures for Charcot Ankle
1. Debridement of Ulcer.
2. Ostectomy.
3. Arthrodesis with Internal Fixation.
4. Arthrodesis with External Fixation.
5. Amputation.
Methods of fixation (arthrodesis):
Arthrodesis with Internal Fixation:
1. Arthrodesis with Plate and Screws.2. Arthrodesis with Nail.3. Arthrodesis with Steinmann pin.4. Arthrodesis with cannulated
screws
Arthrodesis with plate & screws
Charcot Neuroarthropathy
Important factors for success include:
1. Careful removal of all cartilage and debris,
2. Debridement to bleeding subchondral bone,
3. Meticulous fashioning of bone surfaces for contact,
4. Complete debridement of all synovial and
scarred capsule, stable internal fixation and
grafting.
2. Arthrodesis with nail:
Intramedullary fixation for arthrodesis of
the ankle was described by Adams in
1948.
The goal of treatment with intramedullary
fixation is to obtain alignment of the
ankle -foot system, reducing significantly
the risk of ulceration.
Method for estimating insertion site for retrograde intramedullary fixation :
Arthrodesis with nail:
3. Arthrodesis with A Steinmann pin:
Successful arthrodesis may be
achieved with a Steinmann pin from
the heel across the subtalar joint.
Arthrodesis with A Steinmann pin:
Arthrodesis with external fixation:
External fixation is a viable alternative that
allows micromotion to occur through
fracture.
External fixation should be strongly
considered as the best choice of fixation
when addressing the multiple degenerative
areas of Charcot disease.
Arthrodesis with Multiple Cannulated Screws
Minimally Invasive Lower incidence of infection Stable fixation specially in
resorbed talus Early rehabilitation with bracing
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Arthrodesis with multiple cannulated screws
Charcot Neuroarthropathy
Charcot Neuroarthropathy
Medical 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, 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
Bisphosphonates Benefit of inhibiting bone resorption while not
significantly inhibiting bone remineralization
Presently, only bisphosphonates have been demonstrated to have some benefit in patients with Charcot Neuroarthropathy
Bisphosphonates may have potential disadvantages in that they decrease bone remodeling and are contraindicated in patients with renal insufficiency
Intranasal Calcitonin Intranasal Calcitonin in the Treatment of
Acute Charcot Neuroosteoarthropathy
A randomized controlled trial Robert Bem, MD1, Alexandra Jirkovská, MD, PHD1, Vladimíra
Fejfarová, MD1, Jelena Skibová1 and Edward B. Jude, MD, FRCP2
Suggests that intranasal calcitonin treatment of acute CNO, including patients with renal insufficiency, could be an effective modality to prevent bone resorption and progression of this condition, although larger clinical trials are needed to assess the role of calcitonin in patients with acute CNO
Charcot Neuroarthropathy
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
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