arthritis. 2prof sds arthritis types of arthritis 1. non-inflammatory 2. inflammatory 3. infectious...

ArthritiArthritiss

2PROF SDS

ARTHRITISARTHRITIS

TYPES OF ARTHRITISTYPES OF ARTHRITIS

1.1. Non-inflammatory Non-inflammatory

2.2. InflammatoryInflammatory

3.3. InfectiousInfectious

4.4. Hemorrhagic ( Hemophilia, Sickle cell, PVNS)Hemorrhagic ( Hemophilia, Sickle cell, PVNS)

3PROF SDS

ARTHRITISARTHRITIS

NON INFLAMMATORY ARTHRITISNON INFLAMMATORY ARTHRITIS

1.1. OsteoarthritisOsteoarthritis

2.2. Neuropathic (Charcot joint)Neuropathic (Charcot joint)

3.3. Acute Rheumatic FeverAcute Rheumatic Fever

4.4. Ochronosis etc.Ochronosis etc.

4PROF SDS

OSTEOARTHRITISOSTEOARTHRITIS

DEFINITION

Osteoarthritis (OA) is a non-inflammatory Osteoarthritis (OA) is a non-inflammatory degenerative joint disease characterised by degenerative joint disease characterised by progressive loss of articular cartilage with progressive loss of articular cartilage with associated new bone formation and capsular associated new bone formation and capsular fibrosis.fibrosis.

5PROF SDS


CLASSIFICATION

1. Primary or idiopathic 1. Primary or idiopathic 2. Secondary 2. Secondary Infection Infection Congenital -Dysplasia Congenital -Dysplasia - Perthes’ - Perthes’ - SUFE - SUFE Trauma Trauma AVNAVN

6PROF SDS

OSTEOARTHRITIS - HistologyOSTEOARTHRITIS - Histology

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7PROF SDS

OSTEOARTHRITIS - PathologyOSTEOARTHRITIS - Pathology

8PROF SDS


SYMPTOMS

1.1. Pain Pain 2.2. SwellingSwelling3.3. StiffnessStiffness4.4. DeformityDeformity5.5. Decreased range of motion, crepitusDecreased range of motion, crepitus6.6. InstabilityInstability7.7. Loss of functionLoss of function

9PROF SDS


10PROF SDS

OSTEOARTHRITIS : X-ray changesOSTEOARTHRITIS : X-ray changes

1.1. Joint space narrowingJoint space narrowing

2.2. Subchondral sclerosisSubchondral sclerosis

3.3. Osteophytes Osteophytes

4.4. CystsCysts

11PROF SDS

OSTEOARTHRITIS : X-ray changesOSTEOARTHRITIS : X-ray changes

1.1. Joint space narrowingJoint space narrowing

2.2. Subchondral sclerosisSubchondral sclerosis

3.3. Osteophytes Osteophytes

4.4. CystsCysts

12PROF SDS

OSTEOARTHRITIS OSTEOARTHRITIS

TREATMENT

1.1. Protection of affected joints from overloading Protection of affected joints from overloading Weight loss Weight loss Use of walking stick Use of walking stick

2.2. Exercise of supporting muscles around joints to avoid wasting. Exercise of supporting muscles around joints to avoid wasting. 3.3. Supportive measures such as pain relief by analgesics or Supportive measures such as pain relief by analgesics or

NSAIDs. NSAIDs. 4.4. Hyaluronic acid injections.Hyaluronic acid injections.5.5. Glucosamine & chondroitin Glucosamine & chondroitin 6.6. Surgical treatmentSurgical treatment

13PROF SDS

OSTEOARTHRITIS : Surgical treatmentOSTEOARTHRITIS : Surgical treatment

ArthroscopyArthroscopy OsteotomyOsteotomy ArthrodesisArthrodesis Excision arthroplastyExcision arthroplasty Replacement arthroplastyReplacement arthroplasty

14PROF SDS

ARTHRITISARTHRITIS


1.1. OsteoarthritisOsteoarthritis

2.2. Neuropathic (Charcot joint)Neuropathic (Charcot joint)

3.3. Acute Rheumatic FeverAcute Rheumatic Fever

4.4. Ochronosis etc.Ochronosis etc.

15PROF SDS

NON NON INFLAMMATORYINFLAMMATORY ARTHRITIS ARTHRITIS

2. NEUROPATHIC (Charcot joint) JOINT:2. NEUROPATHIC (Charcot joint) JOINT:Joint destruction secondary to loss of sensory Joint destruction secondary to loss of sensory innervation of the joint.innervation of the joint.

CAUSES:CAUSES:Diabetes Diabetes Tabes dorsalis Syringomyelia (shoulder & elbow) Syringomyelia (shoulder & elbow) Hansen's Disease / Leprosy Hansen's Disease / Leprosy Myelomeningocele Congenital insensitivity to pain Congenital insensitivity to pain ((Hereditory Sensory Neuropathy) )

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16PROF SDS


Clinical:Clinical: Painless, swollen joint Painless, swollen joint mimics infection mimics infection

Radiographs:Radiographs: Advanced destruction Advanced destruction Scattered 'chunks' of bone Scattered 'chunks' of bone Heterotopic ossification Heterotopic ossification

Treatment:Treatment: Bracing & casting for mobility & stability Bracing & casting for mobility & stability Charcot Joint is a contraindication for total joint Charcot Joint is a contraindication for total joint

arthroplasty.arthroplasty.

17PROF SDS


3. ACUTE RHEUMATIC FEVER:3. ACUTE RHEUMATIC FEVER:

• Formerly most common cause of childhood Formerly most common cause of childhood arthritis.arthritis.• Sometimes included in inflammatory arthritis.Sometimes included in inflammatory arthritis.• Arthritis and arthralgia following untreated group Arthritis and arthralgia following untreated group A- Beta hemolytic streptococcus infection.A- Beta hemolytic streptococcus infection.• Arthritis is migratory, involves multiple joints.Arthritis is migratory, involves multiple joints.• Diagnosis based on Jones criteria.Diagnosis based on Jones criteria.

18PROF SDS

ACUTE RHEUMATIC FEVERACUTE RHEUMATIC FEVER

Diagnosis based on Jones criteria.Diagnosis based on Jones criteria.Two major and two minor criteria.Two major and two minor criteria.

ASO titer elevated in 80% patients.ASO titer elevated in 80% patients.Treatment includes penicillin and salicylates.Treatment includes penicillin and salicylates.

MAJOR CRITERIAMAJOR CRITERIA

1.1. Carditis Carditis

2.2. Polyarthritis Polyarthritis

3.3. Erythema marginatum Erythema marginatum

4.4. Subcutaneous nodules on Subcutaneous nodules on the extensor surfaces the extensor surfaces

5.5. Chorea Chorea

MINOR CRITERIA1. Fever 2. Arthralgia 3. Prior RF 4. Incr. ESR 5. Prolonged PR on ECG

19PROF SDS


OCHRONOSIS:OCHRONOSIS:

Degenerative arthritis resulting from alkaptonuria (genetic defect of the Degenerative arthritis resulting from alkaptonuria (genetic defect of the homogentisic acid oxidase system) homogentisic acid oxidase system)

Excess homogentisic acid is deposited in the large joints & polymerises Excess homogentisic acid is deposited in the large joints & polymerises (turns black) (turns black)

Ochronotic spondylitis presents in the fourth decade Ochronotic spondylitis presents in the fourth decade Black urine Black urine Disc space narrowing & calcification Disc space narrowing & calcification Homogentisic acid is also deposited in other tissues. Homogentisic acid is also deposited in other tissues. The extra-articular manifestations are ocular & skin The extra-articular manifestations are ocular & skin

pigmentations, genito-urinary calculi & pigmentations, genito-urinary calculi & cardiovascular ochronosis, (especially the aortic cardiovascular ochronosis, (especially the aortic valve). valve).

20PROF SDS

INFLAMMATORY ARTHRITISINFLAMMATORY ARTHRITIS

1.1. Rheumatoid ArthritisRheumatoid Arthritis

2.2. SLESLE

3.3. JRAJRA

4.4. SpondyloartropathiesSpondyloartropathies

5.5. Crystal deposition diseaseCrystal deposition disease

6.6. Relapsing polychondritisRelapsing polychondritis

Ankylosing SpondilitisReiters syndromePsoriaticEnteropathic

GoutChondrocalcinosis(Pseudogout)

21PROF SDS

RHEUMATOID ARTHRITISRHEUMATOID ARTHRITIS

Common inflammatory arthritisCommon inflammatory arthritis

Affects 3% populationAffects 3% population

Female> male (3:1)Female> male (3:1)

Rheumatoid Factor +ve in 80%.Rheumatoid Factor +ve in 80%.

HLA DR4 (chr 6)HLA DR4 (chr 6)

Mononuclear cells are the cellular mediator of tissue Mononuclear cells are the cellular mediator of tissue destruction destruction

22PROF SDS

RHEUM. ARTHRITIS – Signs & RHEUM. ARTHRITIS – Signs & SymptomsSymptoms

EARLY FEATURESEARLY FEATURES

Myopathy, tiredness, weight loss, malaiseMyopathy, tiredness, weight loss, malaise Proximal finger jointsProximal finger joints Wrists, feet, knees, shouldersWrists, feet, knees, shoulders Start up painStart up pain Tendon crepitusTendon crepitus

23PROF SDS


EXTRAARTICULAREXTRAARTICULAR1.1. Nodules - in 20% of RA - skin, synovium, tendons, sclera, viscera Nodules - in 20% of RA - skin, synovium, tendons, sclera, viscera

2.2. Lymphadenopathy Lymphadenopathy

3.3. Splenomegaly Splenomegaly

4.4. Vasculitis Vasculitis

5.5. Myopathy Myopathy

6.6. Sensory changes - neuropathy, or direct compression from Sensory changes - neuropathy, or direct compression from synovitis synovitis

7.7. Visceral Visceral

1.1. pericarditis pericarditis

2.2. pulmonary fibrosis, nodules, pleurisy pulmonary fibrosis, nodules, pleurisy

24PROF SDS


ARA CriteriaARA Criteria (revised 2000): (revised 2000):Morning stiffnessMorning stiffness

Morning stiffness in and around the joints, lasting at least 1 hour. Morning stiffness in and around the joints, lasting at least 1 hour. 1.1. Arthritis of 3 or more joint areasArthritis of 3 or more joint areas

At least 3 joint areas simultaneously have had soft tissue swelling or fluid At least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony overgrowth alone) observed by a physician; the 14 possible (not bony overgrowth alone) observed by a physician; the 14 possible joint areas are right or left proximal interphalangeal (PIP) joints, joint areas are right or left proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP) joints, wrist, elbow, knee, ankle, and metacarpophalangeal (MCP) joints, wrist, elbow, knee, ankle, and metatarsophalangeal (MTP) joints.metatarsophalangeal (MTP) joints.

2.2. Arthritis of hand jointsArthritis of hand joints At least 1 area swollen in a wrist, MCP or PIP joint.At least 1 area swollen in a wrist, MCP or PIP joint.

3.3. Symmetric arthritisSymmetric arthritis Simultaneous involvement of the same joint areas (see 2 above) on both Simultaneous involvement of the same joint areas (see 2 above) on both

sides of the body (bilateral involvement of PIPs, MCPs, or MTPs is sides of the body (bilateral involvement of PIPs, MCPs, or MTPs is acceptable without absolute symmetry)..acceptable without absolute symmetry)..

4.4. Rheumatoid nodulesRheumatoid nodules Subcutaneous nodules, over bony prominences, or extensor surfaces, or Subcutaneous nodules, over bony prominences, or extensor surfaces, or

in juxta-articular regions, observed by a physician. in juxta-articular regions, observed by a physician. 5.5. Serum rheumatoid factorSerum rheumatoid factor

Demonstration of abnormal amounts of serum rheumatoid factor by any Demonstration of abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in <5% of normal control method for which the result has been positive in <5% of normal control subjects. subjects.

6.6. Radiographic changesRadiographic changes Radiographic changes typical of RA on posteroanterior hand and wrist Radiographic changes typical of RA on posteroanterior hand and wrist

radiographs, which must include erosions or unequivocal bony radiographs, which must include erosions or unequivocal bony decalcification localized to or most marked adjacent to the involved joints decalcification localized to or most marked adjacent to the involved joints (osteoarthritis changes alone do not qualify) (osteoarthritis changes alone do not qualify)

25PROF SDS


Diagnosis:Diagnosis:

ARA Criteria (revised 2000):ARA Criteria (revised 2000):

Patient is said to have RA if he or she has satisfied at least Patient is said to have RA if he or she has satisfied at least 4 of 4 of the following 7 criteriathe following 7 criteria. .

Criteria 1 through 4 must have been present for at least 6 Criteria 1 through 4 must have been present for at least 6 weeks. weeks.

Patients with 2 clinical diagnoses are not excluded. Patients with 2 clinical diagnoses are not excluded. Designation as classic, definite, or probable RA is not to be Designation as classic, definite, or probable RA is not to be

made.made.

26PROF SDS

RHEUM. ARTHRITIS - RHEUM. ARTHRITIS - PATHOLOGYPATHOLOGY

SynovitisSynovitis

Chronic inflammation, synovial hypertrophy, effusionChronic inflammation, synovial hypertrophy, effusion

DestructionDestruction

Proteolytic enzymes, pannusProteolytic enzymes, pannus

DeformityDeformity

Articular destruction, capsular stretching, tendon ruptureArticular destruction, capsular stretching, tendon rupture

27PROF SDS

RHEUM. ARTHRITIS - RHEUM. ARTHRITIS - PATHOLOGYPATHOLOGY

Syndromes:Syndromes: Felty's Syndrome - splenomegaly + leukopaenia Felty's Syndrome - splenomegaly + leukopaenia Still's Disease - fever, rash + splenomegaly Still's Disease - fever, rash + splenomegaly Sjorgen Syndrome - decreased salivary & lacrimal gland Sjorgen Syndrome - decreased salivary & lacrimal gland

secretion & lymphoid proliferation secretion & lymphoid proliferation

Laboratory Findings:Laboratory Findings: Incr. ESR Incr. ESR Incr. CRP Incr. CRP RF +ve in 80% RF +ve in 80%

28PROF SDS

RHEUM. ARTHRITIS - Late RHEUM. ARTHRITIS - Late changeschanges

ADVANCED JOINT CHANGES:ADVANCED JOINT CHANGES:

Joint destructionJoint destruction PainPain DeformityDeformity InstabilityInstability

29PROF SDS

RHEUM. ARTHRITIS - X-ray RHEUM. ARTHRITIS - X-ray findingsfindings

Joint space narrowingJoint space narrowing Peri-articular osteopeniaPeri-articular osteopenia ErosionsErosions

30PROF SDS

RHEUM. ARTHRITISRHEUM. ARTHRITIS

31PROF SDS

RHEUM. ARTHRITISRHEUM. ARTHRITIS

32PROF SDS

Stop the Synovitis Stop the Synovitis Rest Rest Drugs - Pyramid Approach = NSAIDs - antimalarials - disease Drugs - Pyramid Approach = NSAIDs - antimalarials - disease

modifying agents (MTX, sulphasalazine, gold, penicillamine) - modifying agents (MTX, sulphasalazine, gold, penicillamine) - steroids - cytotoxic drugs - experimental drugs. steroids - cytotoxic drugs - experimental drugs.

Synovectomy - chemical, irradiation, surgical Synovectomy - chemical, irradiation, surgical

Prevent Deformity Prevent Deformity Splintage, Physiotherapy, Tendon repairs & joint stabilisation Splintage, Physiotherapy, Tendon repairs & joint stabilisation

Reconstruct Reconstruct Arthroplasty, Arthrodesis, Osteotomy Arthroplasty, Arthrodesis, Osteotomy

Rehabilitate Rehabilitate Occupational therapists - aids, support, Physiotherapy Occupational therapists - aids, support, Physiotherapy

RHEUM. ARTHRITIS - RHEUM. ARTHRITIS - TREATMENTTREATMENT

33PROF SDS

SYSTEMIC LUPUS SYSTEMIC LUPUS ERYTHEMATOSUSERYTHEMATOSUS

Chronic inflammatory autoimmune vasculitis disease.Chronic inflammatory autoimmune vasculitis disease. Women more affected ( african americans).Women more affected ( african americans). SLE not destructive as RA.SLE not destructive as RA.

Clinical:Clinical: Joint involvement is the most common feature (75%) Joint involvement is the most common feature (75%)

PIP, MCP, Carpus, knees etc.PIP, MCP, Carpus, knees etc. Fever, anorexia, weight loss, malaise Fever, anorexia, weight loss, malaise Skin rashes (butterfly malar rash) Skin rashes (butterfly malar rash) Raynaud's phenomenon Raynaud's phenomenon Splenomegaly Splenomegaly Nephritis, pericarditis, pleurisy Nephritis, pericarditis, pleurisy

34PROF SDS


35PROF SDS


Laboratory:Laboratory: Anaemia, Leucopenia Anaemia, Leucopenia ESR elevatedESR elevated ANA positive (RF & HLA-DR3 may be +ve) ANA positive (RF & HLA-DR3 may be +ve)

Treatment:Treatment: NSAID, Hydroxychloroquine, CyclphosphomideNSAID, Hydroxychloroquine, Cyclphosphomide Corticosteroids for severe disease Corticosteroids for severe disease Sunblock creams for malar rash.Sunblock creams for malar rash.Complications:Complications: AVN hip (? from steroids) AVN hip (? from steroids)

36PROF SDS

JUVENILE RHEUM. ARTHRITISJUVENILE RHEUM. ARTHRITIS

Persistent noninfectious arthritis lasting 6 weeks to 3 Persistent noninfectious arthritis lasting 6 weeks to 3 months after other causes have been ruled out.months after other causes have been ruled out.

Juvenile chronic arthritis (JCA) is gradually being used.Juvenile chronic arthritis (JCA) is gradually being used.

Diagnostic CriteriaDiagnostic Criteria Age under 16 at onset Age under 16 at onset Rash, RFRash, RF Iridocyclitis Iridocyclitis CSpine involvement CSpine involvement Pericarditis, Tenosynovitis Pericarditis, Tenosynovitis Fever, Morning stiffnessFever, Morning stiffness

37PROF SDS


Classification by onset (Schaller)Classification by onset (Schaller)

1. Systemic onset (Still's disease)1. Systemic onset (Still's disease) 2. Polyarticular onset2. Polyarticular onset

3. Pauciarticular (most common)3. Pauciarticular (most common)

Type 1 : ANA positiveType 2 : HLA-B 27 positive

Rh negativeRh positive

38PROF SDS

1.Systemic onset (Still's disease)1.Systemic onset (Still's disease)Age: usually under 5years but can be any age, Sex: <5yr female = male; Age: usually under 5years but can be any age, Sex: <5yr female = male; >5yr female > male >5yr female > male Fever (high with spikes up to 40°C daily) plus one of the followingFever (high with spikes up to 40°C daily) plus one of the followingMaculopapular rash, Iridocyclitis, Maculopapular rash, Iridocyclitis, RhF +ve, RhF +ve, Cervical spine involvement Cervical spine involvement Pericarditis, Generalised lymphadenopathy, Hepatomegaly, Pericarditis, Generalised lymphadenopathy, Hepatomegaly, Splenomegaly Splenomegaly Sites: knees, wrists, ankle, feetSites: knees, wrists, ankle, feet

2. Polyarticular onset2. Polyarticular onsetSeronegative (RhFactor -ve), Seronegative (RhFactor -ve), Age: any, even before age 1year!, Sex: Age: any, even before age 1year!, Sex: female > male female > male 5 or more joints involved in the first 3 months , Sites: knees (60%), 5 or more joints involved in the first 3 months , Sites: knees (60%), wrists, handswrists, handsRhFactor +ve, RhFactor +ve, Older children (9-10 years) with persistent activity and Older children (9-10 years) with persistent activity and rapid joint destruction affecting mainly the hands and feet.rapid joint destruction affecting mainly the hands and feet.

3. Pauciarticular (most common)3. Pauciarticular (most common)4 or less joints involved in the first 3 months 4 or less joints involved in the first 3 months Type I, Type I,

Younger onset <6yr, with females mainly affected. ANA +ve. Younger onset <6yr, with females mainly affected. ANA +ve. Danger because Danger because of development of iridocyclitis. Presence of ANA of development of iridocyclitis. Presence of ANA related to eye involvement.related to eye involvement.Type IIType II

Older onset 9yr+, with males mainly affected. Association with Older onset 9yr+, with males mainly affected. Association with HLA-B27.HLA-B27.

39PROF SDS


Medical Management

Aim: to suppress activity and therefore prevent joint deformity Multidisciplinary approach . PT to help prevent joint contractures. Hydrotherapy affective. OT for splints and orthoses

Surgical Management when necessary

40PROF SDS

Poor prognostic factorsPoor prognostic factors Onset < 1year Onset < 1year IgM (RhF) +ve IgM (RhF) +ve Eye involvement Eye involvement Hip involvement leads to a greater functional deficitHip involvement leads to a greater functional deficit

Medical ManagementMedical Management Aim: to suppress activity and therefore prevent joint deformity Aim: to suppress activity and therefore prevent joint deformity Multidisciplinary approach with rheumatologist, PT, OT, child Multidisciplinary approach with rheumatologist, PT, OT, child

psychologist, Opthalmologist etc psychologist, Opthalmologist etc PT to help prevent joint contractures and keep healthy muscles PT to help prevent joint contractures and keep healthy muscles

working. Hydrotherapy affective. working. Hydrotherapy affective. OT for splints and orthosesOT for splints and orthoses Surgical Management when necessarySurgical Management when necessary

41PROF SDS

SPONDYLOARTROPATHIESSPONDYLOARTROPATHIES

SPONDYLOARTROPATHIESSPONDYLOARTROPATHIES

1. Ankylosing Spondylitis2. Reiters syndrome3. Psoriatic4. Enteropathic

42PROF SDS

ANKYLOSING SPONDYLITISANKYLOSING SPONDYLITIS

0.2% of population0.2% of population Mainly affects spine and SI jointsMainly affects spine and SI joints Male > femaleMale > female HLA B27 in 90%HLA B27 in 90% SynovitisSynovitis Third and fourth decadeThird and fourth decade EnthesopathyEnthesopathy

43PROF SDS

Rome criteriaRome criteria

A - bilateral SI B - stiff lumbar spineA - bilateral SI B - stiff lumbar spine - stiff thoracic spine- stiff thoracic spine A+ 1xB - decreased chest A+ 1xB - decreased chest or 4xB expansion (<7cm)or 4xB expansion (<7cm) - >3/12 LBP- >3/12 LBP - iritis- iritis

44PROF SDS


Pathology:Pathology:

Inflammation & erosive destruction of: Inflammation & erosive destruction of: Diathrodial joints = sacroiliac, vertebral facet, Diathrodial joints = sacroiliac, vertebral facet,

costovertebralcostovertebral Fibro-osseous junctions - intervertebral discs, sacroiliac Fibro-osseous junctions - intervertebral discs, sacroiliac

ligaments, symphysis pubis ligaments, symphysis pubis 3 Stages: 3 Stages:

InflammationInflammation - round cell infiltration, granulation tissue, - round cell infiltration, granulation tissue, joint erosion joint erosion

FibrosisFibrosis - replacement of granulation tissue with fibrous - replacement of granulation tissue with fibrous tissue tissue

OssificationOssification - of fibrous tissue (e.g. syndesmophytes) - of fibrous tissue (e.g. syndesmophytes)

45PROF SDS

ANKYLOSING SPONDYLITISANKYLOSING SPONDYLITISClinical:Clinical: Spinal stiffness (progressive spinal flexion deformity) Spinal stiffness (progressive spinal flexion deformity) Wall Test - patient asked to stand with back against wall; should normally Wall Test - patient asked to stand with back against wall; should normally

be able to touch occiput, scapulae, buttocks & heels to wall. be able to touch occiput, scapulae, buttocks & heels to wall. Chest expansion < 7cm Chest expansion < 7cm Hip involvement with FFD Hip involvement with FFD Achilles tendon insertion pain Achilles tendon insertion pain Difficult cervical spine fractures with epidural haemorhage Difficult cervical spine fractures with epidural haemorhage

Extraskeletal:Extraskeletal: Prostatitis Prostatitis Conjunctivitis & uveitis in 20% Conjunctivitis & uveitis in 20% Carditis, aortic valve disease Carditis, aortic valve disease Pulmonary fibrosis Pulmonary fibrosis

46PROF SDS


Radiology:Radiology:

Squaring of vertebral bodies Squaring of vertebral bodies Syndesmophytes Syndesmophytes Bamboo spine Bamboo spine Erosive arthritis with progressive ankylosis Erosive arthritis with progressive ankylosis

47PROF SDS


Laboratory:Laboratory: High ESR High ESR HLA-B27 in 90% HLA-B27 in 90% RF negative RF negative

Management:Management: Postural management Postural management NSAIDs NSAIDs Operations to correct deformity & restore mobility Operations to correct deformity & restore mobility

Lumbar / cervical spine osteotomies Lumbar / cervical spine osteotomies THR THR

48PROF SDS

REITER’S SYNDROMEREITER’S SYNDROME

Hans Reiter, 1916 Hans Reiter, 1916

Triad = Urethritis + Arthritis + Conjunctivitis Triad = Urethritis + Arthritis + Conjunctivitis Causative organisms: Causative organisms:

Chlamydia trachomatis, shigella, salmonella, Chlamydia trachomatis, shigella, salmonella, campylobacter, Yersinia campylobacter, Yersinia

Lymphogranuloma venereum Lymphogranuloma venereum

49PROF SDS

REITER’S SYNDROMEREITER’S SYNDROME

Radiology: erosive arthropathy similar to AS

Laboratory: HLA-B27 in 80% ESR high in acute phase organism may be isolated from urethral fluids or faeces

Treatment: Supportive Tetracycline for persistent urethral infection

50PROF SDS

CRYSTAL DEPOSITION DISEASECRYSTAL DEPOSITION DISEASE

GOUTGOUT

Disorder of purine metabolism characterised by Disorder of purine metabolism characterised by hyperuricaemia & recurrent attacks of acute synovitishyperuricaemia & recurrent attacks of acute synovitis

M:F = 20:1 M:F = 20:1

2 Types: 2 Types: Primary (95%): inherited disorder with overproduction or Primary (95%): inherited disorder with overproduction or

under excretion of uric acid under excretion of uric acid Secondary (5%): myeloproliferative disorders, renal Secondary (5%): myeloproliferative disorders, renal

disease disease Only a small number of people with hyperuricaemia develop Only a small number of people with hyperuricaemia develop

gout. gout.

51PROF SDS

CDD - GOUTCDD - GOUTPathology:Pathology:

Humans lack the enzyme uricase which is involved in elimination of Humans lack the enzyme uricase which is involved in elimination of excess nucleic acid purines & nitrogenous waste products thru production excess nucleic acid purines & nitrogenous waste products thru production and excretion of alantoic acid; hence in humans, uric acid is end product of and excretion of alantoic acid; hence in humans, uric acid is end product of purines degradation purines degradation

Deposition of MSU (monosodium urate) crystals in synovial & Deposition of MSU (monosodium urate) crystals in synovial & periarticular tissueperiarticular tissue

History:History: Galen (129-199 AD), an ex-gladiatorial surgeon in the Galen (129-199 AD), an ex-gladiatorial surgeon in the

Pergamon arena in Asia Minor who moved to Rome, Pergamon arena in Asia Minor who moved to Rome, described gout as a discharge of the four humors of the described gout as a discharge of the four humors of the body in unbalanced amounts into the joints (hence body in unbalanced amounts into the joints (hence gout = gout = gutta, a dropgutta, a drop). The first radiological description of gout ). The first radiological description of gout was made by Huber in 1896, a few months after Röentgen was made by Huber in 1896, a few months after Röentgen described the x-ray. described the x-ray.

52PROF SDS

CDD - GOUTCDD - GOUTClinical:Clinical:The joints most commonly affected by gout are:The joints most commonly affected by gout are: Forefoot Forefoot

podagarapodagara: - classic presentation of acute attack of first MTP joint : - classic presentation of acute attack of first MTP joint Elbows and hands Elbows and hands

unlike RA hand and wrist joints will have preserved joint spaces and unlike RA hand and wrist joints will have preserved joint spaces and normal mineralization normal mineralization

The large joints (hips, knees, ankles and shoulders) are infrequently The large joints (hips, knees, ankles and shoulders) are infrequently involved involved

Spine very rarely affected. Spine very rarely affected.

NephrolithiasisNephrolithiasis is major extraarticular manifestation; - only is major extraarticular manifestation; - only small % of pts w/ gout get tophi, but many get renal small % of pts w/ gout get tophi, but many get renal stones; - pure uric acid stones are found in 80%, & uric stones; - pure uric acid stones are found in 80%, & uric acid is probably nidus for Ca-Phos & oxalate calculi in acid is probably nidus for Ca-Phos & oxalate calculi in remainder; - in 1/2, sx from renal stones actually precede remainder; - in 1/2, sx from renal stones actually precede arthritisarthritis

53PROF SDS

CDD - GOUTCDD - GOUT

Laboratory:

Hyperuricemia biochemical hallmark of gout, but not by itself diagnostic

for gout Leukocytosis Increased ESR Synovial Fluid

leukocyte counts = septic arthritis viscosity is < septic or inflammatory arthritis

MSU needle - like intracellular & extracellular crystals Negatively birefringent crystals under

polarized light microscopy

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54PROF SDS

CDD - GOUTCDD - GOUT

Treatment:

Acute Attacks: Indomethacin 75mg stat. then 25mg BD Colchicine intravenous - 0.6 mg 2 hours until pain decreases

Chronic: Allopurinol for hyperuricaemia & tophi Colchicine for prophylaxis

55PROF SDS

PSEUDOGOUTPSEUDOGOUT

CHONDROCALCINOSISCHONDROCALCINOSIS Acute arthritis caused by Calcium pyrophosphate dihydrate Acute arthritis caused by Calcium pyrophosphate dihydrate

(CPPD) crystal-induced inflammation (CPPD) crystal-induced inflammation May perfectly mimic gout during acute flare May perfectly mimic gout during acute flare Attacks occurring before age 50 are uncommon Attacks occurring before age 50 are uncommon

Clinical:Clinical: Most often affects the knee and the wrists Most often affects the knee and the wrists

Radiology:Radiology: CCalcificationalcification densities in hyaline or fibrocartilage, which are densities in hyaline or fibrocartilage, which are

found in knee menisci, acetabular labrum, & TFCCfound in knee menisci, acetabular labrum, & TFCC

56PROF SDS

PSEUDOGOUTPSEUDOGOUT

Laboratory:Laboratory:

Fluid analysis: Fluid analysis: CPPD crystals are visualized under compensated polarized light microscopy CPPD crystals are visualized under compensated polarized light microscopy crystals may be more difficult to detect than MSU crystals because of their crystals may be more difficult to detect than MSU crystals because of their

smaller size, more intralysosomal location, & less brilliant colors smaller size, more intralysosomal location, & less brilliant colors CPPD crystals show weak positive birefringency and have squared or CPPD crystals show weak positive birefringency and have squared or

rhomboidal shaped ends rhomboidal shaped ends alizarin red stain, can confirm that these clumps are masses of calcium crystalsalizarin red stain, can confirm that these clumps are masses of calcium crystals

Treatment:Treatment: aspiration of the involved joint and steroid injection, once diagnosis of aspiration of the involved joint and steroid injection, once diagnosis of

infection has been excluded, will usually control symptoms infection has been excluded, will usually control symptoms