Pan-talar Arthrodesis for Charcot's Arthropathy of the ankle with Localized osteoporosis

Ahmed Kholeif MD

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

Pathogenesis Neurotraumatic Theory

Loss of neuro-protection causing repetitive microtrauma. This trauma can lead to intracapsular effusions, ligamentous laxity and joint instability

Charcot Neuroarthropathy

Pathogenesis Neurotraumatic Theory

absence of protective sensation allows continued loading of fractured extremity heightened healing response seen

Charcot Neuroarthropathy

PathogenesisNeurovascular 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

PathogeneisNeurovascular 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

PathogenesisNeurovascular 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)

Charcot Neuroarthropathy

Type 1: Tarsometatarsal Joints:

Type 2: Choparts (Transverse Tarsal) and Subtalar Joints:

Type 3A: Ankle:

Type 3B: Posterior Calcaneus:

Type 4: Multiple Regions:

Type 5: Forefoot:

Radiographic Staging
(Eichenholtz,

1966)

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

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

Selection of treatment plan

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
Charcot Neuroarthropathy

Surgical Treatment of Charcos Ankle What you do not want to see

Charcot Neuroarthropathy

Surgical Treatment of Charcots Ankle What you do not want to see

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

Charcot Neuroarthropathy

Indications for surgery in the Charcot ankle:

1.

Acute dislocation
Recurrent ulceration Secondary to either instability or bony prominence

2.

3.

4.

Severe or uncontrolled deformity

Surgical procedures for Charcot Ankle

1.

Debridement of Ulcer. Ostectomy.

2.

3.

Arthrodesis with Internal Fixation.

Arthrodesis with External Fixation. Amputation.

4.

5.

Methods of fixation (arthrodesis):

1. 2.

3.

Arthrodesis with Internal Fixation: Arthrodesis with Plate and Screws. Arthrodesis with Nail. 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, Debridement to bleeding subchondral bone, Meticulous contact, fashioning of bone surfaces for

2.

3.

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 ulceration. risk of

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

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: Pagets 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

Charcot Neuroarthropathy

Intranasal Calcitonin
Intranasal Calcitonin in the Treatment of Acute Charcot Neuroosteoarthropathy A randomized controlled trial
Robert Bem, MD1, Alexandra Jirkovsk, MD, PHD1, Vladimra Fejfarov, MD1, Jelena Skibov1 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

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