neuropathic (charcots) joints
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Neuropathic joints,Diabetes,Total Contact castTRANSCRIPT
Neuropathic Arthropathy
Dr.Subodh Pathak
Jean-Martin Charcot
Jean-Martin Charcot 29 November 1825 – 16 August 1893) was a French neurologist and professor of anatomical pathology. He is known as "the founder of modern neurology"
Definition
Neuropathic arthropathy , neuropathic osteoarthropathy, Charcot joint refers to progressive condition of the musculoskeletal system that is characterized by joint dislocations, pathologic fractures, and debilitating deformities.
Charcot Arthropathy :James K DeOrio, MD Associate Professor of Orthopedic Surgery, Duke University School of Medicine .
Walter Panis, MD Clinical Instructor, Department of Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School
History
The first description of neuropathic arthropathy was by Musgrave in 1703, in his book De Arthritide Symptomatica.He described a neuropathic joint as an athralgia.
1868 Jean-Martin Charcot gave the first detailed description of this disease.
In 1892, Sokoloff --upper extremity with syringomyelia.
In 1927 Leriche stated that a lesion of sympathetic led to Hyperaemia and bone resorption. In 1936, Jordan -diabetes mellitus ---neuropathic changes in the foot and ankle.Associated with intra-articular corticosteroid injections by Chandler and Wright in 1958.A.C Brower—Neurovascular theory
Etiology
Any condition that causes sensory or autonomic neuropathy
Diabetes mellitus neuropathy Multiple Sclerosis Alcoholic Neuropathy Syringomyelia Cerebral palsy Leprosy
Tabes Dorsalis Spinal cord injury Myelomeningocele Intra-articular steroid injections Congenital insensitivity to pain CMTD Familial interstial Polyneuropathy Amyloidosis Pernicious Anemia
Vitamin B12 Deficiency Phenylbutazone ,Indomethacin Ethyl Alcohol.
Diabetes mellitus is currently the most common cause of neuropathic arthropathy.
Neuropathic joint destruction develops in approximately 0.1% of patients with diabetes and 5% of those with peripheral neuropathy
Neuroarthropathy among all pts with tabes dorsalis ranges b/w 5 to 10%
75% of this 5-10% involve lower extremities and 25% upper extremities.
Pathophysiology
Major theories
– Neurotraumatic theory
– Neurovascular theory
– Most probably both
Neurotraumatic Theory
Loss of peripheral sensation and proprioception leads to repetitive micro trauma to the joint in question
This damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma.
Poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma.
Neurovascular theory
A.C.Brower theory Postulates that neurologic changes produced by
an underlying medical disorder create a hypervascular region in the subchondral bone that is characterized by increased osteoclastic resorption and osteoporosis.
More recent theories implicate the role of inflammatory cytokines such as TNF-α and IL-1 in the pathogenesis of Charcot neuroarthropathy.
On the molecular level, these factors lead to increased expression of nuclear transcription factor-κB, which in turn stimulates osteoclast formation.
Joint destruction in the neuropathic joint is probably brought on by a combination of factors that include damage to the nociceptors of the joint and the periarticular tissues.
The activity of peptides such as substance P, calcium gene related peptide, and vasoactive intestinal peptide (VIP) could result in increased vascularity and inflammation, contributing to further joint destruction.
Substance P can enhance the cellular synthesis of collagenase and prostaglandin-E; activate T lymphocytes, monocytes, and neutrophils; and take an active part in inflammation
The initial pathologic changes occur in the underlying bone and cartilage. Recurrent effusions occur due to hyperplasia of the synovium.
The articular cartilage is slowly destroyed by a pannus, which helps distinguish Charcot's joints from other forms of osteoarthritis.
Gough et al concluded that…..
The serum carboxyterminal telopeptide of type 1 collagen, a marker of osteoclastic bone resorption, had significantly increased levels in the acute Charcot foot.
The lack of an associated increase in osteoblastic activity supports the idea that excess osteoclast activity is a feature of the early stages of Charcot's neuroarthropathy
Clinical History
A careful history may reveal an unrecognized traumatic event.
Charcot neuroarthropathy most frequently presents in the fifth decade, after an average duration of diabetes of 20 to 24 years; in those with type 2 diabetes.
Presentation
DEPENDS OF DURATION OF DISEASE Mild swelling w/o deformity-Moderate
deformity with extreme swelling. Signs of inflammation. Profound unilateral swelling. WBC and
ESR may be normal
Increase in localized temp Erythema, Joint effusion. 75% pt. have pain. The deep tendon reflexes
at the knee are absent in a majority of patients.
Acute Charcot neuropathy
On Examination
Marked Irregularities identified as bony projections.
Bone formation in soft tissues.
Bag of Bones:
Joint can be passively and painlessly moved in all Directions
Diagnosis
Xrays. Indium-111 WBC scan. Gallium scan. USG MRI Radionuclide scans
Lab Studies
Inflammatory markersESR and WBC– elevated in both infection and Charcot arthropathy
Serum albumin >3.0g/dL
IMAGING Early Changes similar to OA Nontraumatic dislocations may be an early
sign. LaterRadiographic evidence of joint
distention caused by fluid, hypertrophic synovitis, osteophytes, and subluxation.
The normal architecture of the joint is lost, with dislocation, fragmentation, attempted repair by osteophytes, and sclerosis
Atrophic Stage:
Rapid joint destruction Loose bodies Subchondral bone erosions Subluxation Pathological#
Hypertrophic Stage
Reduced jt space. Subchondral bone sclerosis Pathological # healing with callus Multiple osteophyte formation with exoxtosis
formation. Dislocations of joints
Radiographic features6D’s Yochum and Rowe
Dense bones (subchondral sclerosis) Degeneration Destruction of articular cartilage Deformity (pencil-point deformity of
metatarsal heads) Debris (loose bodies) Dislocation
Commonly Affected Joints
Foot Involvment Knee involvement Hip involvement Shoulder Elbow
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%
Classification ( Brodsky and Rouse)
Type 1 Midfoot
Type 2 Hindfoot
Type 3a Ankle
3b Calcis tubercleType4 Combination
Type 5 Forefoot
Neuropathic Joints
Hypertophic or
Productive
Hypertophic or
Productive
MIXED
Atrophic or
Resorptive
Brailsford
Stage of Hydrasthrosis:Distension of joint by serosanguinous effusion
Stage of atrophy:Destruction of affected articular cartilage and then the bone
Stage of hypertrophy:Massive hyperrophy of bone at periphery of articular cartilage
Radiographic Staging (Eichenholtz, 1966)
I Developmental (acute) stage
II Coalescence (quiescent) stage
III Consolidation (resolution) stage
Modified Eichenholtz Classification for the Progression of Charcot Neuroarthropathy
Stage 0(Shibata and Schon)
Swelling and erythema
No Radiographic Changes
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
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
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
Charcot Arthropathy
HIP
Charcot neuroarthropathy in the hip is rare. Painless and Functional: no treatment Try conservative management 50% of fractures of the femoral neck in
diabetics developed Charcot's joints.
KNEE
Most Commonly secondary to Syphilis. Results in Gross Instability If only one knee is involved and destruction
is severe, fusion is indicated.
Total knee arthroplasty ???
Shoulder
Treatment
Primarily nonoperative. Consists of Acute and Postacute phases.
– Acute– Casting along with crutches and walkers.
– Postacute– Include bracing, ankle-foot orthotics(AFO),
specialized shoes.
Treatment
Casting- changed every 1-2weeks, if ulcerations are present changed every week for wound care, duration from 3-6 months.
Shoes, bracing, and orthotics- duration from 6-24 months.
Typical total healing time 1-2 years.
Early stage
Total Contact cast.
CROW boots
Surgical options
Arthrodesis Exostosectomy of bony prominences Osteotomies Reconstructive Surgeries Autologous bone Grafting Amputations
Surgical treatmentAnkle:
Arthrodesis of ankle to place the foot Plantigrade.
IM nail/Charnley/Ilizarov External Fixators
Average time for Fusion:20 months(IM nail).
Talus -- fragmented and avascular--talectomy and tibiocalcaneal arthrodesis.
Internal or External Fixation??
Hindfoot neuroarthropathy
Mainstay of Treatment is NONSURGICAL.
Arthrodesis indicated for… Hindfoot valgus with subluxation of the
subtalar joint or midtarsals to prevent ulceration and infection.
Principles outlined by Papa et al.
Careful removal of cartilage and debris.Thorough removal of sclerotic bone.Adequate fashioning of congruent bone surfaces for apposition.Rigid fixation of the arthrodesis site.Complete resection of fibrotic capsular tissue and synovium
Complication
Ulcers Osteomyelitis Gross Deformity of the foot Gangrene.
TH
AN
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With the Lisfranc pattern, breakdown initially occurs along the medial column, with late changes progressing to the lateral column. The arch abducts and prominences develop, leading to deformity, fullness, and ulceration. The naviculocuneiform pattern leads to collapse at the naviculocuneiform joint, with development of a lateral rocker-bottom deformity. The perinavicular pattern is caused by osteonecrosis or fracture of the navicular. The lateral arch height decreases, leading to a lateral rocker and shortening of the medial column. Eventually this breakdown progresses to the central aspect of the foot, with severe plantar flexion of the talus and eventual ulceration. The transverse tarsal pattern is caused by lateral subluxation of the navicular on the talus and abduction of the foot with a valgus calcaneus. Calcaneal pitch eventually decreases, and a central rocker develops at the calcaneocuboid joint. In late stages, the talus is completely dislocated from the navicular, and ulceration develops at the calcaneocuboid interval. All four patterns eventually progress to a rocker-bottom deformity and chronic ulceration.