INTRODUCTION ,PATHOGENESIS , CLINICAL MANIFESTATIONS,CLASSIFICATION, DIAGNOSIS, DIFFERENTIAL DIAGNOSIS,COMPLICATIONS & MANAGEMENT OF RHEUMATOID ARTHRITIS

1. INTRODUCTION ,PATHOGENESIS , CLINICAL
MANIFESTATIONS,CLASSIFICATION, DIAGNOSIS,
DIFFERENTIAL DIAGNOSIS,
COMPLICATIONS & MANAGEMENT
OF RHEUMATOID ARTHRITIS
Dr .Y.Saipramod

2. INTRODUCTION
Definition-
• Chronic inflammatory systemic disease of adults
characterized by destructive and proliferative changes
in synovial membrane , periarticular structures,
skeletal muscle and perineural sheath .
• Eventually leads to joint destruction , deformity and
ankylosis

3. • Historical background-
• Recognised In 1800 by French physician
Dr.Augustine Jacob.
• RA coined by Dr.Alfred Barring
• RA Factor discovered by Billing ,
Cecil and Dawson.

4. Epidemiology
• Prevalence of - 0.8% to 2.1% of the population
• Gender predilection ratio – Women: Men – 3:1
• Prevalence increases with age (40-50yrs)
• About 40-60% have severe disease
• Median life expectancy is shortened by 3 to 7
years
• Onset mostly between ages of 35 – 60 years

5. Aetiology
• Exact etiology is not known
• Family studies indicates a genetic predisposition like
HLA DR4& HLA DR1
• In genetically susceptible host, it may be a
manifestation to an infectious agent like
Mycoplasma, EBV, Rubella virus, parvo virus, CMV.
• Other possible causes would be allergic (
eosinophilia) endocrine (in response to
adrenocortical steroids)
• smoking has been clearly identified risk for RA in
genetically susceptible individuals.

7. PATHOGENESIS
• Most widely accepted theory is immunogenic
resposnse which takes place in synovium.
• The pathogenesis of RA involves a continuous
interaction of many cells, molecules, and
processes.
• B cells have been postulated to play a number
of roles, including autoantibody formation, T-
cell activation, antigen presentation, and
cytokine production.
• In some circumstances, B cells can act as
highly efficient antigen-presenting cells.

8. • Activated T cells, in turn, activate B cells directly
and via proinflammatory mediators.
• Activated B cells differentiate into antibody-
producing plasma cells.
• Both rheumatoid factor (RF) and anticitrullinated
C peptide (anti-CCP) antibodies form immune
complexes that can activate, complement, and
attract other inflammatory cells to the synovium.
• Activated B cells produce a number of
proinflammatory mediators, including IL-6, TNF-
alpha, interferon gamma, and lymphotoxin.

9. • Proinflammatory mediators from T cells and B
cells activate macrophages.
• Macrophages produce IL-6, TNF-alpha, IL-1,
and interferon gamma.
• Dendritic cells produce TNF-alpha, IL-1, and IL-
6, attracting additional cells to the
inflammatory infiltrate in the synovium.
• Macrophages directly secrete matrix
metalloproteases and other proteolytic
enzymes that damage the synovial tissue

10. • Causing inflammation of
the synovium which forms
pannus, a granulomatous
mass( containing
lymphocytes and other
inflammatory substances)
• The pannus grows and
destroys cartilage ,
tendons and ligaments.
• Systemic manifestations of
RA may be due to release
of inflammatory mediators
like IL-1, TNF, & IL-6 from
synovium

12. STAGES OF RHEUMATOID ARTHRITIS
• SYNOVITIS
• PANNUS
• FIBROUS
ANKYLOSIS
• BONY
ANKYLOSIS

13. PATHOLOGY
• JOINTS-
• Synovial joints
• Infiltrated with lymphocytes, plasma cells, and
macrophages .
• Pannus formation
• This replaces the articular cartilage with
fibrous connective tissue.
• Fibrous ankylosis
• Undergoes metaplasia to form bony ankylosis.

14. • MUSCLES-
• Nodular Polymyositis
• Degeneration of individual muscle fibre and
replaced by fibrous tissue
• Causing deformities and restriction of
movements.

15. • SUBCUTANEOUS NODULES-
• It is a basic rheumatoid unit with a
central fibrionid necrosis consisting
of cellular debris, fragmented
collagen fibres, fibrinous exudate
surrounded by radially arranged
proliferationg mononuclear cells
• Outer dense connective tissues with
marked round cell infiltrate.
• These are found over pressure
points like elbow , tibia.
• Similar leisions can occur in lungs,
pleura, pericardium, sclera.

16. CLINICAL FEATURES
• Chronic polyarthritis with Insidious onset
• Main symptom include pain & morning stiffness
of > 1hr of peripheral joint.
• Constitutional symptoms include generalized
weakness, fatigue, anorexia, weight loss, rarely
fever.
• Symmetrical pattern of involvement of joints is
more typical of RA.
• Clinically synovial inflammation in affected joint
causes warmth, swelling, tenderness, and
limitation of motion

17. • The affected inflamed joint usually held in a
position of flexion in order to maximize the
joint volume and minimize the distention of
the capsule.
• Later , soft tissue contractures or fibrous or
bony ankylosis leads to fixed defromities.

18. CHARACTERISTIC DEFORMITIES
• Wrist & hand-
• Z-Deformity- radial deviation of wrist and
ulnar deviation of digits often with palmar
subluxation of proximal phalanges

19. • Swan neck deformity- hyperextension of
proximal interphalangeal joints with
compensatory flexion of distal interphalangeal
joints.
• Boutonnires deformity- flexion at proximal
interphalangeal joints and extension of distal
interphalangeal joint.
• Synovitis of wrist can lead to carpal tunnel
syndrome.

20. • Foot-
• Hallux valgus
• Widening of forefoot
• Hammer toes
• Callosity under PIP joint
• Achilles tendinities

21. • Elbow- leads to swelling , limitation of
movements ,flexion contractures.
• Knee joint- synovial hypertrophy , chronic
effusion , ligamentous laxity . Chronic effusion
leads to bakers cyst.
• Hip joint – may cause erosion and remodelling of
acetabulum leading to protrusio acetabulum.
• Neck- inflammation of synovial joints of upper
cervical spine leads to atlanto axial subluxation
and presents as pain in occiput

22. • Rheumatoid nodule-
occurs in 20-30% of
patients with RA .
Usually on periarticular
structures, extensor
surfaces, and areas of
mechanical pressure like
proximal ulna, olecranon
bursa, achillis tendon
and occiput.

23. • Rheumatoid vasculitis- it can cause
polyneuropathy, mononeuritis multiplex,
cutaneous ulceration, dermal necrosis. Digital
necrosis and visceral infarction.
• Pleuro pulmonay manifestations- interstitial
fibrosis, pleuro pulmonary nodules ,
pneumonitis and arteritis.
• Cardiac- pericarditis , MI and aortitis
• Musculo skeletal- muscle wasting,
Tenosynovitis, bursitis and osteoporosis.

25. • Haematological – anaemia,
thrombocytosis, eosinophilia
• GI- splenomegaly , mesentric
vasculitis
• Feltys syndrome- consists of
splenomegaly , neutropenia,
chronic rheumatiod arthritis
• Renal- proteinuria,
glamerulonephritis
• Ocular- Episcleritis, scleritis,
iridocyclitis
• Neurological- neuropathy, cervical
cord compression.

26. CLASSIFICATION
Progression of rheumatoid arthritis classified in
to 4 stages based on CLINICAL & RADIOLOGICAL
Findings.ACR
Stage 1 (early RA)
• No destructive changes +/- evidence of
osteoporosis
stage II (moderate progression)
• Limited Joint mobility with no joint deformities
• Adjacent muscle atrophy
• Extra-articular soft tissue lesions
• periarticular osteoporosis with or without
subchondral bone destruction.

27. Stage III (severe progression)
• Joint deformity (eg, subluxation, ulnar deviation,
hyperextension) without fibrous or bony ankylosis
• Extensive muscle atrophy
• Extra-articular soft tissue lesions (eg, nodules,
tenosynovitis)
• Radiographic evidence of cartilage and bone
destruction in addition to periarticular
osteoporosis
Stage IV (terminal progression)
• Fibrous or bony ankylosis

28. DIAGNOSIS
X-rays
Early on, x-rays show only the
features of synovitis: soft-tissue
swelling and peri-articular
osteoporosis.
The later stages are marked by
the appearance of marginal
bony erosions and narrowing of
the articular space, especially in
the proximal joints of the hands
and feet.
 However, most individuals have
evidence of erosions within 2
years.

29. • In advanced
disease,articular
destruction and joint
deformity are obvious.
• Flexion and extension
views of the cervical spine
often show subluxation at
the atlanto-axial or mid-
cervical levels

30. Blood investigations
• Normocytic, hypochromic anaemia.
• In active phases the ESR and CRP concentration are
usually raised.
Serological tests:
-Rheumatoid factor(Auto antibody against Fc portion
of IgG)positive in about 80 per cent of patients
-antinuclear factors are present in 30 per cent.
• Neither of these tests is specific and neither is required
for a diagnosis of rheumatoid arthritis.
• Tests such as those for anti-CCP antibodies have added
much greater specificity but at the expense of
sensitivity.

31. Synovial biopsy
• Synovial tissue may be obtained by needle biopsy,
via the arthroscope, or by open operation.
• Unfortunately, most of the histological features of
rheumatoid arthritis are non-specific.

32. The “OLD” American College of Rheumatology (ACR)
criteria for the diagnosis of Rheumatoid arthritis 7
1. Morning stiffness
2. Arthritis of 3 or more joint areas, observed by a physician.
3. Arthritis of hand and wrist joints
4. Symmetric arthritis
5. Rheumatoid nodule
6. Serum Rheumatoid Factor
7. Radiographic changes hand and wrist radiographs--erosions
or juxta-articular osteopenia
• 1-4 MUST BE PRESENT ATLEAST FOR 6 WKS

33. NEW ACR Eular Criteria for RA 4 Domains
• 1. Domain: Joint involvement – max 5points
• 2. Domain: Serology -max 3points
• 3. Domain: Duration of synovitis- max 1point
• 4. Domain: Acute phase reactants -max 1point
• YOU NEED 6 points for a DEFINITE RA DIAGNOSIS

34. Domain: Joint involvement
 – 1 medium-large joint (0 points)
 – 2-10 medium-large joints (1 point)
 – 1-3 small joints (2 points)
 – 4-10 small joints (3 points)
 – More than 10 small joints (5 points)
 Note: Patients receive the highest point level
they fulfill within each domain. For example, a
patient with five small joints involved and four
large joints involved scores 3 points.

35. Domain: Serology -max 3points
-No RF or anti-CCP (0 points)
• – One positive at low titer, < 3x normal
(2 points)
• – One positive at high titer, > 3x normal
(3 points)

36. Domain: Acute phase reactants
• Neither (CRP) nor (ESR) is abnormal (0 points)
• –Abnormal CRP or abnormal ESR (1 point)

37. Domain: Duration of synovitis- max 1point
• < 6 weeks (0 points)
• >6 weeks or longer (1 point)

38. Symmetric joint disease is not a feature of new criteria.
Classic radiographic changes such as marginal erosions
automatically qualify patients for RA classification if they have a
single swollen joint.
 Imaging evidence of synovitis, including ultrasound or MRI, can
be used to classify patients even in the absence of symptoms
if patients have high titers of RF or Anti citrulinated peptide
Antibody and elevated acute phase reactants
Joint fluid is straw-colored, is slightly cloudy, and contains many
flecks of fibrin and 5000 to 25,000 whiteblood cells/mm3; at least
50% of these are polymorphonuclear leukocytes.

39. Differential diagnosis
• Psoriatic arthritis
• nail changes and skin symptoms
• Reactive arthritis
asymmetrically involves heel, sacroiliac joints and large joints of the
leg. It is usually associated with urethritis, conjunctivitis, iritis,
painless buccal ulcers..
• Ankylosing spondylitis
• This mainly involves the spine
• Gout & Pseudo gout
• usually involves particular joints (knee, MTP1, heels) and can be
distinguished with an aspiration of joint fluid if in doubt. Redness,
asymmetric distribution of affected joints, pain occurs at night and
the starting pain is less than an hour with gout.

40. • Lyme disease
• causes erosive arthritis and may closely resemble
RA – it may be distinguished by blood test in
endemic areas
• Polyarticular osteoarthritis (OA).
• Distinguished with X-rays of the affected joints
and blood tests, older age, starting pain less than
an hour, asymmetric distribution of affected
joints and pain worsens when using joint for
longer periods
• Viral arthritis.

41. COMPLICATIONS
• Fixed deformities.
• Tendon ruptures.
• Muscle weakness.
• Spinal cord compression.
• Systemic vasculitis.
• Amyloidosis.

42. MANAGEMENT :-
AIMS :
1.Relief of inflammation and pain.
2.Correction and control of systemic
manifestations.
3.Prevention of deformity
4.Correction of existing deformity.
5.Improvement of functional capacity

43. Supportive measures :
-Patient education :
Provide basic information about disease ,treatment
and importance of follow up.
-Behavioural modification :
Importance of rest, Exercise, and Proper nutrition
-Splints – These have 3 main function.
Rest and relief of pain.
Prevention and correction of deformity.
Fixation of damaged joint in good functional positions
-Physio therapy : various forms of local heating and cooling
used to reduce muscle spasm .

44. Drug therapy:
1. Non steroidal anti inflammatory drugs (NSAID’S)
NSAIDS reduce the signs and symptoms of inflammation but do not
eliminate the underlying cause. Joint damage continues during
administration of NSAIDS .
Mechanism of action :
Effects related to primary action of drugs by inhibitions Arachidonate cyclo
oxygenase (COX). Thus, inhibits the production of prostaglandins and
thromboxanes which mediate inflammation and other effects.
Drugs are:-
• Aspirin, Indomethacin ,Piroxicam, Tolmetin, (cox-1)
• Ibuprofen, Neproxen, Diclofenac, ketoprofen,( non selective)
• Nimusulide, Etoricoxib, Meloxicab, Rofecoxib,etc (cox-2)
Adverse effects;
Nausea, vomiting, Gastric damage, ulceration, and perforation, Skin reaction, Analgesic
associated nephropathy, Liver disorders etc

45. 2. Systemic Glucocorticoids :
one of the most effective treatment in providing symptomatic relief
in rheumatoid arthritis.
Mechanism of action :- It inhibits the synthesis prostaglandins.
It also inhibits TNF- , IL –1 and other proinflammatory mediators.
Dose :- Low dose (<7.5mg/d) prednisolone has been advocated to
control symptoms.
Efficacy :
It provides only symptomatic relief.. They do
not arrest the rheumatoid process nor prevent bone
erosions

46. Intra articular injection of steroids :
Mechanism of action : is similar to that of systemic steroids .
It increases the viscosity and haluronate concentration of
synovial fluid.
Efficacy : Most patients benefit from intraarticular steroids but
the effect last for few days.
Hydrocortisone - Few days to a week
Prednisolone - two weeks or more
Triamcilone- for longer periods
If one or two injection prove ineffective then discontinue
the drug.

47. 3.DMARDS (Disease modifying anti rheumatoid
drugs);
These drugs are known to alter the disease activity in RA.
They exert minimal non specific anti-inflammatory effects,
therefore NSAIDS must be continued during their
administration.
Appearance of benefit from DMARD therapy is usually
delayed for weeks or months.
Decreases C-reactive protein, and ESR and retard the
development of bone erosions.
Recent trend is to start DMARD, especially methotrexate early
in the disease activity.

48. DMARD’s are
• 1.Gold
• 2 .D.pencillamine
• 3. Chloroquine and hydroxy chloroquine
• 4. Sulfa salazine
• 5.Immuno suppressants;
a).Methotraxate
b). Azathioprine
c). Cyclosporine
d).Cyclophosphamide
e). Chlorombucil
f). Leflunomide

49. Chloroquine and hydroxycholoquine : - Antimalarial
drugs, found to induce upto 50% remission.
-Acts by reducing monocyte interluken-1 consequntly
inhibiting ‘B’ lymphocytes, so antigen processing may be
interfered.
Dose – Hydroxy choloroquine,400mg/day for 4-6 weeks
followed by 200-400 mg/day for maintainance (Tab
HCQS)
Adverse effect : Retinal Damage, corneal opacity, Graying
of hair, Irritable bowel syndrome, Myopathy and
neuropathy.

50. Sulfa salazine : Has anti-inflammatory activity and primarily
used in ulcerative colitis,
Acts by suppressing the superoxide radicals and cytokines
0f inflammatory cells.
Used in mild/early case.
Dose 1-3 gm/day in 2-3 devided doses.
(sazo en-500mg)
Chlorambucil ;-
It is effective but at the cost of substantial toxicity.
Rarely used specially in cases with secondary
Amylodosis.
dose 2-6 mg/day(Tab Leukerin 2mg,5mg) .

51. Methotrexate :
First DMARD’s of choice, it is an anticancer drug employed for use in
rheumatoid arthritis.
Mechanism of action :
acts by, inhibiting amino imidazine carboxamide (AILAR)
transformylase and thimidalate syntatase with secondary effect on
polymorpho nuclear chemotaxis.
Some effects on dihydro folate reductase and this effects
lymphocyte and macrophage function.
It also inhibits interleukin-1 activity.
Dose and Drug administration :-
-Low dose methotrexate is used in rheumatoid arthritis.
-High dose methotrexate is used an anticancer therapy.
- In rheumatoid arthritis the initial dose of methotrexate is
7.5mg/week, but the dose may be increased upto 20 mg/week
provided there is no toxicity.
-(Tab Altrex,Folitrex,Biotrexate as 2.5mg,5mg,7.5mg )

52. Adverse effects : Diarrhea, alopecia, hematological
toxicity including leucopenia, thrombocytopenia ,
renal failure, acute and chronic pulmonary toxicity.
It causes hepatic fibrosis leading to-Elevation of liver
enzymes and decrease serum albumin.
Use of Folic acid(1mg/day) reduces the Methotrexate toxicity.
Azathioprine;-
It is purine anti metabolite,
- acts by suppressing the cell mediated immunity,
- Given along with steroids because it has steroid sparing effect
-Usually used in cases with systemic manifestation,
Dose 50-150 mg/day. (Tab Azimune, Azoprine,Zymurine 50mg)

53. Cyclo sporine;-
Inhibits IL-1 and IL-2 receptor production by regulating gene
transcription and secondarily inhibit macrophage T cell interaction
and T-cell responsiveness.
Effective in RA but its renal toxicity which is accentuated by
NSAID’s preclude it’s routine use. Usually employed in refractory
cases.
Dose 2.5-5 mg/kg/day
Cyclophsophomide;-
• Suppresses T-cell and B-cell function by 30-40%.
• Due to more toxic reserved for cases with severe systemic
manifestation like necrotising vasculitis Dose 50-100mg/day
(Tab cycloxin, Ledoxen,50mg)

54. Leflunomide :
was approved in 1948 for treatment RA. Is a synthetic isoxazole derivative
with immunosuppressive and antiproliferative properties.
Mechanism of action : It inhibits dihydro orate dehydrogenase – decreases
pyrimidine synthesis –decresaes lymphocyte proliferation.
Dose :
Loading dose of 100mg daily for three days precedes the maintenance dose
of 10-20mg/day.
(Tab Arava, Tab cleft,Tab Lefumide 10mg,20mg)
The response rate of leflunomide in RA is similar to methotrexate.
It is teratogenic and contraindicated in pregnancy.

55. DMARD combination therapy :
The use of combination of DMARDs when a single DMARD
fails adequately to control RA is now generally accepted by
rheumatologist,
1,Triple DMARD’ therapy with methotraxate, sulasalazine and
Hydroxy chloroquine was more effective than methotrexate
alone or sulfasalazine and hyddroxychloroquine combination.
2,The COBRA regimen with step down combination of high
dose prednisolone (60 mg/day tapering to 7.5 mg after
6weeks and 0mg after 35 weeks.) Methotraxate (7.5
mg/weeks for 46weeks), sulfasalazine (2gm/day) was more
effective.
3,Finnish RA combination therapy:(1993-95) used 4 drugs i.e
Methotrexate, Sulfasalazine, Hydroxychloroquine, and
Prednisolone. Found 37 percent remission.

56. Biologics (Cytokine Therapies Targeting TNF and IL-1)
These modify the biologic response as observed in patho physiologic
inflammation process of RA
Agents :
1.Etanarcept;- Is the 1st TNF  inhibitor to be approved for use in RA.
Dose :- 25mg subcuateneous inj twice weekly.(Inj Enbrel 25mg vial)
Efficacy : Most effective drug in RA i.e in refractory disease.
- Combination of etanarecept + methotrexate provide additional benefit.
2. Infliximab;-
-It is chimeric anti TNF monoclonal antibody.
-Combination with methotrexate 7.5mg/week seemed to enhance the clinical
response and improves functional status and quality of life.
Dose : single dose of 10mg/kg body weight at 0,2,,6,10,14 weeks.
.

57. 3 Adalimumab :
is a recombinant human immunoglobulin G1 monoclonal antibody that
it is specific for TNF 
Dose – 40mg/week subcutaneous
4 Interleukin –1 Receptor antagonist : (Anakira) ;-
Recombinant human IL-1 Ra has been utilized in several RA trials.
Dose : Clinical responses are dose dependent with greatest response in
highest dose group.
-Given daily doses of 30, 75 or 150mg .
OTHER NEWER DRUGS (UNDER TRIAL) ARE
1-cytotoxic T-lymphocytic antigen 4-immunoglobulin
2-B-lymphocyte depletion therapy with Rituximab
3 IL-6 inhibition with monoclonal antibody

58. OPERATIVE TREATMENT :
Indicated in failure of medical treatment, severe pain,
loss of function and progression of disease
1.Synovectomy-
• relieves pain, and improves function.
• Usually done in knee, elbow and small joints of fingers ,in
addition synovectomy of tendon sheaths i.e flexors and
extensors of fingers should undertaken as a prophylactic
measure.
Indications
• In patients with no or minimal radiological evidance of
erosion,
• In presence of persistent pain and swelling of about 6
months .

59. 2.Radical surgery
under taken to relieve pain, restore function, correct
deformity and provide stability.
FINGER DEFORMITIES
A.Intrinsic plus deformity :
• This is due to contracture of the intrinsic muscles
• flexon of the MCP joint and extension of the
interphalangeal joint.
• The deformity develops in combination with the ulnar
deviation of the fingers.
• Inrinsic tightness can be detected by putting the MCP joint
in hyperextension and passively try to flex the distal inter
phalangeal joint. Which is not possible (Bunnell test)

60. -LittlersTechnique :
• Extensor aponeurosis at level of metacarpophalangeal joint consists of long extensor
tendon,
•transverse fibers (which flex metacarpophalangeal joint), and
•oblique fibers (which extend interphalangeal joint).
•The oblique fibers of the EA is incised at its extensor tendon insertion.
•Transverse fibres are preserved to avoid hyperextension of MCP joint.

61. B. SWAN NECK DEFORMITY
- flexion of DIP joint and hyperextension of PIP
joint with flexion of MCP joint
•The commonest cause being rupture of terminal
extensor and tenosynovitis or rupture of flexors
(FDS) may contribute to PIP hyper extension.

62. NALEBUFF, FELDON AND MILLEDER classification
TYPE 1 :PIP joint flexible in all directions with no intrinsic
tightness
Treated - manipulation.
- Flexor tenodesis (FDS) of PIP joint.
- Fusion of DIP joint and
- reconstruction of retinacular ligament or spiral
oblique ligament
TYPE II : Deformities due to intrinsic muscle tightness.
Treated - intrinsic release + one/more of the above procedures.

63. TYPE III : limited active PIP motion in a finger which rests in the
swan-neck position. The lateral bands are adherent in the dorsal
position preventing flexion.
Treated -joint manipulation, -
mobilization of lateral bands and dorsal skin release.
TYPE IV : Destruction of joint surface and often ankylosis of PIP joint.
Treatment : Best treated with Arthrodesis of PIP joint or in ring and
small fingers with Swanson implant arthroplasty of PIP joints.

64. C. Button hole deformity
/Boutonniere Deformity : -
-characterized by flexion of PIP joint and
hyperextension of the DIP joint.
1.Mild Deformity – Flexion deformity at PIP
joint with lessened ability to fully flex the
distal joint. The deformity is passively
correctable indicating that the lateral bands
have subluxated anteriorly but not
adherent. Normal appearing roentgeogram.
Treatment ; -Specific exercises, -
repositioning of lateral bands.
--Proximal inter phalangeal joint
synovectomy
--Extensor tenotomy over middle phalanx .

65. ii. Moderate Deformity :
-Flexion contracture is about 40degree at the PIP joint and hyper extended
DIP joint.
-The deformity is not passively correctable. Indicating that the lateral bands
are adherent ,
-Roentgenogram shows mild joint destruction.
Treatment :--Central slip reconstruction using the lateral band/tendon graft.--
-MCP joint arthroplasty/fusion.
iii. Fixed deformity :-
-Fixed flexion deformity of the PIP joint as much as 90 degree.
-The capsular structures are contracted and the PIP joint may show
ankylosis. The DIP joint may be fixed in hyperextension
Roentegenogram shows destructive joint changes.
Treatment : Because of joint destruction. Arthroplasty or fusion must be
performed.

66. ULNAR DRIFT/DEVIATION OF FINGERS
As the synovium proliferates at the MCP joint, the radial sagittal fibers
of the extensor hood attenuate allowing finger extensors to subluxate in an
ulnar direction into the cleft between metacarpals.

67. Mild to Moderate ulnar Drift :
• The MCP joints are swollen, flexor and extensor tendons are displaced ulnar
wards.
• However there is absence of severely diseased articular surfaces of
dislocated joints.
Treatment :
a-Intrinsic release
b-Extensor tendon realignment and intrinsic rebalancing i.e transferring
tendons from ulnar side to radial side.
C-MCP joint synovectomy.
Severe ulnar drift and MCP dislocation;-
• severe variety often with dislocation of one or more MCP joint.
• The dislocation will be due to the pull of the long flexor tendons on the
finger in the ulnar direction.
Treatment :-
Function of MCP joint may be improved by arthroplasty.
( Swanson implant arthroplasty )

68. severe rheumatoid arthritis. Subluxations have been treated by resecting
metacarpal heads.

69. RHEUMATOID WRIST;
• dorsal swelling on the wrist within tendon sheaths of extensor
tendons is one of the earliest sign of disease.
typically extensor carpi ulnaris and extensor digitorum
communis sheaths are involved .
Surgical options are;--
• synovectomy i.e volar or dorsal synovectomy.
• wrist arthrodesis in advanced stage, in bilateral fusion some
prefer one in dorsiflexion other in palmar flexion.
• Wrist arthroplasty; two types
1. resection arthroplasty (palmarshelf arthroplasty)
2. implant arthroplasty.(swanson silicone)

70. replacement of wrist joint with Swanson silicone implant and titanium grommets.

71. Thank you
• References-
• TUREK text book of orthopaedics
• Kelly text book of Rheumatology
• Campbell operative orthopaedics
• Harrisons textbook of internal medicine
• Internet.