Perc. Pantalar Fusion

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 - 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: Localized

osteoporosis 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 blood sugar 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 Loss of neuro-protection causing

repetitive microtrauma.

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

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 resulting in bone resorption and fragmentation.


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 localized osteoporosis, bone hyperemia, joint instability and sensorimotor deficits predisposes to changes seen with charcot


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%)


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:


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, localized osteopenia, subluxation, frank dislocation, fine periarticular fragmentation, debris formation


Radiographs Stage I


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


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 III


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


Clinical Presentation Rocker bottom

foot

Clinical Presentation


Clinical Presentation



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 (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.


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

Surgical Treatment of Charco’s AnkleWhat you do not want to see


Surgical Treatment of Charcot’s AnkleWhat you do not want to see



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.


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


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


Arthrodesis with multiple cannulated screws




















Medical 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, 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


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



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

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Perc. Pantalar Fusion