neuropathic arthritis
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About The Author
Dr Manoj R. kandoi is the founder president of Institute of Arthritis Care & Prevention
an NGO involved in the field of patient education regarding arthritis. Besides providingliterature to patient & conducting symposiums, the institute is also engaged in creating
patients Self Help Group at every district level. The institute also conducts a certificate
course for healthcare professionals & provide fellowship to experts in the field ofarthritis.The author has many publications to his credit in various journals. He has also written a
book The Basics Of Arthritis for healthcare professionals.
The author can be contacted at:Dr manoj R. kandoi
C-202/203 Navare Arcade
Shiv Mandir Road, Opposite Dena Bank
Shiv mandir Road, Opposite Dena bankShivaji Chawk, Ambarnath(E) Dist: Thane Pin:421501
State: Maharashtra Ph: (0251)2602404 Country: India
Membership Application forms of the IACR for patients & healthcare professionalscan be obtained from.
Institute of Arthritis Care & Prevention
C/o Ashirwad HospitalAlmas mension, SVP Road, New Colony,
Ambarnath(W) Pin:421501 Dist: Thane
State: Maharashtra Country: IndiaPh: (0251) 2681457 Fax: (0251)2680020
Mobile ;9822031683
Email:drkandoi@yahoo.co.in
Preface:
Studies have shown that people who are well informed & participate actively in
their own care experience less pain & make fewer visits to the doctor than do otherpeople with arthritis. Unfortunately in India & many third world countries we do not
have patient education & arthritis self management programs as well as support groups.
This is an attempt to give a brief account of various arthritis, their prevention & selfmanagement methods which can serve as useful guide to the patients of arthritis.
It would be gratifying if the sufferers of the disease knew most of what is given in the
book.
Acknowledgement\
I am thankful to Dr (Mrs) Sangita Kandoi for her immense help in proofreading & for her
invaluable suggestions. The help rendered by Nisha Jaiswal is probably unrivalled.
Thanks also to vidya, sheetal and parvati for their continous support throughout themaking of the book. The author is grateful to his family for the constant inspiration they
offered. The author alone is responsible for the shortcoming in this piece of work. He
welcomes suggestions for improvement from the readers.
mailto:drkandoi@yahoo.co.inmailto:drkandoi@yahoo.co.inmailto:drkandoi@yahoo.co.inmailto:drkandoi@yahoo.co.in -
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Neuropathic Arthritis:
Introduction:
Arthritis caused by repeated minor injuries to the joint which is insensitive to painleading to its disorganisation is known as neuropathic arthritis. It is named after Jeon-
Martin Charcot (1825-1893) who first described it in association with tabes dorsalis.
Disorders associated with charcot's joint:- Diabetes mellitus - Syringomyelia
- Syphilic - Spine bifida- Chronic alcoholism - Meningomyelocele
- Hansens disease - Congenital insensitivity to pain
- Peripheral nerve injuries - Amyloid neuropathy
- Charcot -marie -tooth disease
Etiopathogenesis:
Reduction in joint sensibility
Protective function of pain is lost
Loss of protective muscle reflex
Harmful joint strain go unprevented
Cumulative strains leading to severe degenerative changes
Articular cartilage and subchondral bone worn away.
ligament laxity and joint instability.
Types of charcots joints:
1. Atrophic: "Pencil -in -cup" deformation, resorption of bone end, usually affects upperextremities.
2. Hypertrophic: Joint space narrowing, with bony sclerosis, new periosteal boneformation, articular
surface fragmentation and joint subluxation can be seen.
Stages in formation of charcots joint:Stage I: Joint subluxation, osteoporosis, cortical defects.
Stage II: Osteolysis, fracture, periosteal elevation or new subperiosteal boneformation.
Stage III: Healing stage, reconstructive, decrease swelling and bony ankylosis.
Clinical features:
Knee, ankle and subtalar joints are most commonly affected in the lower limb andelbow in upper limits.
Joints in the spine may also be affected.
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Symptoms: Common presenting complaint is painless swelling and instability of joint.Signs:
Irregular hypertrophy at the bone ends Moderate restriction of movements ~ Ligament laxity with excessive side to side movements Localized erythema, swelling and increased skin temperature can also be noted.
Associated findings in charcot's joints:In tabes dorsalis, the lower extremities and spine are commonly involved. Other signs
include ataxia, argyll robertson pupils, absent knee reflexes and, absent deep position,
vibration and pain sense.In Syringomyelia upper extremities are commonly involved. Clinically features of
sensory dissociation, loss of pain and temperature, and preservation of touch is noted.
Deep sensation is undisturbed. Progressive muscle atrophy in the arms and fibrillation
and trophic changes in the fingers may also be noted.
Radiographic changes:
Exaggerated changes of degenerative arthritis seen such as loss of cartilage space,absorption of bone ends, hypertrophy of bone at the joints margins etc.
Subluxation or dislocation may be noted.Treatment:
Protocol
Conservative Surgicals
- Supportive and protective - Surgical fusion in corrective
bracing position can be obtained.- Role of biphosphate pamidronate
under investigation.
Criteria for surgical intervenation:
Instability of the foot or ankle Deformity Chronic ulceration Progressive joint destruction (despite conservative care) Adequate circulation No active infection Systemic factor: Patient should be medically stable and compliant and have the
potential for returning to an active lifestyle
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Surgical methods used:
Timing of surgical reconstruction / management:
It should be done when stage of reconstruction begins i.e. when acute inflammatorycondition has subsided & there is radiographic evidence of healing.
Patterns of bone & joint involvement in neuropathic diabetes:1. Forefoot: Radiographic findings are often atrophic & destructive mimicking
osteomyelitis. Plantar ulceration is an associated findings.
2. Tarsometatarsal joints: Characterized by disruption of the TMT joints often withcollapse of the midfoot. Plantar ulceration frequently develops at the apex of thecollapsed cuneiform or cuboid.
3. Naviculocuneiform, talonavicular & calcaneocuboid joints: There is usuallydislocation of the navicular or disintigeration of naviculocuneiform joints.
4. Ankle joint: Infrequent but associated with severe deformity & instability. It mayalso be associated with involvement of subtalar joint.
5. Calcaneus: It is characterized by rare avulsion fracture of the posterior process ofthe calcaneus.
Factors responsible for noninfective bone & joint destruction in diabetic foot:
Peripheral neuropathy with loss of protective sensation
Autonomic neuropathy with increased peripheral blood flow Mechanical stress of weight bearing , Repititive trauma Nonenzymatic glycosylation of collagen Decrease cartilage growth activity Corticosteroid -induced osteoporosis
J oint involved Methods used
Knee - Straight caliper with an ischial fitting ring
- Surgical arthrodesis using charnleys
compression appartusAnkle - Ankle corset
- Arthrodesis
Foot - Special shoes with steel arch supports plus
a cane- Surgical arthrodesis is usually not practical
Hip - Subtrochantric shanz osteotomy with 30
of abduction.
Spine - Corset- Spine fusion
Elbow - Hinged elbow support providing lateral
stability
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Acute Charcots Osteomyelitis in
joint in diabetes diabetes
- Absent Deep Tendon reflex + -
- Decreased vibratory sense + -
- Loss of protection sensation + -- Fever - +
- WBC Count Normal Raised
- Shift in differential WBC Count - +
- ESR / Normal
- Indium-III Scans- MRI Differentiates between two
- Bone Biopsy
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