mail me for this ppt , drsushilvijay@rediffmail.com.

1. RHEUMATOID HAND
DR.SUSHIL VIJAY
PG STUDENT- D ORTH
SANTOSH MEDICAL COLLEGE &
HOSPITAL

2. Rheumatism
• Rheumatism is any painful disorder affecting
the loco-motor system including
joints, muscles, connective tissues, soft tissues
around the joints, and bones. This also
includes rheumatic fever affecting heart
valves.

3. Origin
• The term ''rheumatology'' originates from the
Greek word ''rheuma'', meaning “ something
that which flows as a river or stream," and the
suffix ''-ology'', meaning "the study of."

4. • Rheumatoid arthritis is a
chronic, systemic, inflammatory
disease, most often involving the small joints
of the hands and feet, although any synovial
joint can be affected

5. Rheumatoid arthritis : overview
• It is most common* type of chronic
inflammatory rheumatic disorder.
• The term inflammatory rheumatic disorder
covers a group of disorder that causes
pain, stiffness, and swelling around joints and
tendons.

6. Rheumatoid arthritis
• Basically , it is a systemic disease of young and
middle aged adults characterised by
proliferative and destructive changes in
synovial membrane, periarticular
structures, skeletal muscles and perineural
sheaths.
• Eventually, joints are destroyed , fibrosed or
ankylosed. It is a widespread vasculitis of the
small arterioles.

7. Etiology
• Still incompletely worked out.
• Important factors in evolution are
– Genetic susceptibility
– An immunological reaction
– An inflammatory reaction
– The appearance of Rh factor in blood and synovium
– Articular cartilage destruction

8. Genetic susceptibility
• More common in first degree relatives
• HLA DR4 +ve in 70% of people with RA.

9. Inflammatory reaction
• In joints and tendon sheath.
• As the APC/T cell interaction is initiated, various local
factors comes into play and leads to a progressive
enhancement of immune response.
• There is a marked proliferation of cells in the
synovium, with the appearances of new blood vessel
formation.
• Cytokines activate inflammatory cells like macrophage
and B cells.
• Some cytokines-chemokines attract other
inflammatory cells to area.
• Importanat cytokines are :- TNF, IL-1 and IL-6.
• The resulting synovitis, both in joints and tendon
sheath lining , is the hallmark of early RA.

10. Chronic synovitis and joint destruction
• Immune complexes are deposited in synovium and on
the articular cartilage, where they appear to augment
the inflammatory process.
• This leads to depletion of cartilage matrix and
eventually damage to cartilage and underlying bone.
Vascular proliferation and osteolytic activity most
marked at the edges of the articular surface, may
contribute further to the cartilage destruction and peri
articular bone erosion.

11. Rheumatoid factor
• B cell activation in RA leads to the production
of anti – IgG autoantibodies which are
detected in the blood as ‘rheumatoid factor’
• High levels are likely inflammatory in origin.
Low levels may normally be present in
individuals.
• Other autoantibodies idenified are anti-CCP
antibodies. Its presence is very specific for RA.

12. Pathology- Joints & tendons
• 4 stages:-
• Stage 1- Pre-clinical-
(Only raised ESR, CRP and RF)
• Stage-II- Synovitis
• Stage III- Destruction
• Stage IV- Deformity

13. Pathology
• Due to synthesis of autoantibodies, against
unknown antigenic antigens in the
synovium, primary synovitis sets in.
• Primary synovitis Pannus formation forms
villus.
• Villus migrates towards the joint causing its
destruction and ankylosis, fibrous in early stage
and bony in late stages.
• Pannus- medical term for an abnormal layer of fibrovascular tissue or granulation tissue
• Villus- any of the small, slender, vascular projections that increase the surface area of a membrane.

14. Rheumatoid arthritis
= synovitis+vasculitis+granuloma
SYNOVITIS
GRANULOMA VASCULITIS
FORMATION

15. Pathological process Tissue involved Results in Deformities
Vasculitis Joint structures Synovitis-effusion, Swelling, stiffness,
Necrosis articular cartilage instability ,
Fibrosis destruction, subluxation or
Pericapsulitis, dislocation
Ligamentous
instability
Arthritis Intrinsic plus
deformity
Plasma cell Tendon Tenosynovitis, rupture Ulnar deviation of
proliferation fingers, concertina
collapse of fingers.
Granulation tissue and Muscle Wasting, atrophy, Contracture, ankylosis
pannus formation fibrosis
Synovial hypertrophy : Bone Osteoporosis-thin
in joint, in tendon cortex loss of
trabeculae, cyst
formation-
subchondral erosions,
destruction

17. RA:- Clinical features
• Insideous onset
• Ocassionally acute
• Early stages:- polysynovitis, soft tissue swelling
and stiffness.
• Female predominance
• Swelling and loss of mobility in PIP of fingers.
• Other joints involved-wrists, feet, knees and
shoulders in order of frequency.

18. RA:-Clinical features
• Another classic feature generalised stiffness after period of
inactivity and especially after rising from bed in the early
morning, usually lasts longer than 30 minutes.
• Physical signs may be minimal, but usually there is
symmetrically distributed swelling and tenderness of the
MCP joints, the PIP and the wrists.
• Tenosynovitis is common in the extensor compartments of
the wrist and flexor sheath of the fingers, diagnosed by
feeling thickness , tenderness and crepitations over back of
the wrist or the palm while passively moving the fingers.

19. RA:- Clinical features
• If larger joints are involved, local warmth, synovial
hypertrophy and intraarticular effusion may be obvious.
• In late stages:- joint deformity increases and the acute pain
of synovitis is replaced by the more constant ache of
progressive joint destruction.
• The combination of the joint instability and the tendon
rupture produces the typical ‘rheumatoid
deformities, ulnar deviation of the fingers, radial, and volar
displacement of the wrists, valgus knees, valgus feet and
clawed toes.

20. RA:- Clinical features
• Joint movements are restricted and often very
painful.
• Cervical spine may be involved
• Daily activities hampered.

21. Extra articular manifestation

22. Extra articular manisfestations
• mercer

24. Investigations
• 1. CBC- Hb low, normochromic hypochromic
anemia. WBC’s or normal, lymphocytes
and ESR .
• 2. Serological tests :-
• Rheumatoid factor:- this in presence of
gamma globulins agglutinates certain strains
of streptococci sensitized by sheep cells and
latex prticles.

25. • Latex fixation test:- Unknown serum + 7-
globulin latex suspension.
agglutination
+ve when If –ve , do more sensitive
serum has test as there is less RA
abundant RAF factor in the serum

26. • Inhibition test :- This test uses the characterstics
of Euglobulin from unknown serum. Euglobulin
from normal serum neutralise the rheumatoid
factor thereby inhibiting agglutination.
• Euglobulin from rheumatoid serum has no effect
on the rheumatoid factor and agglutination
occurs.
• This is most sensitive test , positive even with
minute amounts of RA factor.

27. RA serum of known high agglutination activity
+
Unknown euglobulin
+
Standard 7-globulin latex suspension
Agglutination occurs
Unknown serum  -ve latex test
 +ve inhibition test
RA SLE (Le cell phenomenon)

28. Others
• C reactive proteins (inc.)
• Alkaline phosphatase (Inc)
• Platelets( Inc)
• Serum albumin (Dec)
• Anti CCP
• ANA may be +nt.

29. • Synovial fluid – not for diagnosis but to rule
out other causes of infection.
• Fluid in RA is typically yellow, turbid and
watery due to high WBC and low sugar
content.
• MRI :- Info about extent of soft tissue
involvement and damage

30. Classification criteria
• Different classification systems have evolved
for the diagnosis of rheumatoid arthritis with
time.

31. 1987 criteria

34. Treatment
• 1. General measures
• 2. Splints
• 3. Drugs
• 4. Surgical intervention

35. 1. General measures
• Aims to improve G.C of the patient and to keep
joints properly splinted in functional position to
guard against the ensuing ankylosis.
• Rest in bed
• Good diet, rich in proteins and minerals
• Correct anemia- hematinics or transfusion
• Hormones to improve bone stock
• Removal of any infective foci.

36. 2. Splints
• Splinting in functional position helps avoid
ankylosis.
• Removed daily
• Hot packs given or Hubbard tanks used and
joints are put into full range of motion
• With splints , muscle setting exercises
advocated and after removal of splints
resistance exercises begun.

37. Hubbard tanks

38. 3. Drugs
• Three classes used:-
• 1. Analgesics
• 2. Anti inflammatory
• 3. Disease modifying drugs

39. • No treatment is ideal and it is important to
assess the patient's response so that the most
effective regimen is adopted.
• Commonly used methods of assessment
include; duration of early morning
stiffness, number of tender swollen joints.
Functional assessment ESR, radiographs, etc.

40. • First Line of Drugs: NSAIDs
• These are
aspirin/ibuprofen/ketoprofen/diclofenac
sodium/ naproxen/piroxicam, etc.

41. Second Line of Drugs
• Second line of drugs are used only if an
adequate trial of first line drugs have failed to
relieve symptoms satisfactorily or if there is
radiological evidence of progressive disease.
Second line drugs are alternatively known as
disease-modifying antirheumatic drugs
(DMARD) and are slow acting drugs. When
second line therapy is introduced, sympto-
matic NSAIDs need to be continued in parallel

42. Commonly prescribed drugs include:
• • Injectable gold and oral gold (sodium aurothiomalate).
This is no longer preferred.
• Penicillamine
• Sulphasalazine
• Antimalarial drugs (e.g. chloroquine) • Dapsone and levamisole.
• The choice of the drug to be given first will
depend on the experience of the doctor and on the
facilities available for monitoring. There is little
evidence to suggest which drug should be prescribed first.
Methotrexate has now emerged as the drug of choice due to its
higher efficacy. Early institution and escalation of MTX to its
maximum tolerable dose is the latest mantra.

43. Antimalarial Drugs
• They do not require intensive blood monitoring
and if these facilities are limited, chloroquine or
hydroxy chloroquine can be particularly used.
• Other agents known to have second line drug
effect include levamisole and dapsone.
Levamisole is not freely available in some
countries and its toxicity seems to be greater
than that of gold and penicillamine. Dapsone has
a high toxicity

44. Quick facts of second line drugs
• Used only if first line fails. •
• Known as DMARD.
• To be continued for at least 6 months.
• Parallel NSAID is to be used.
• Choice of drugs is based on clinicians' experience.
• Antimalarial drugs are used if proper blood
monitoring is not available.
• All drugs are toxic.

45. Third Line of Drugs
• Azathioprim, cyclophosphamide and
chlorambucil can exert a second line effect
inpatients with rheumatoid arthritis

46. • Corticosteroids: Cyclosporine has been tried in
patients with rheumatoid arthritis. The fact
that it does not affect WBC is a theoretical
advantage in patients with Felty's syndrome.

47. Newer Drugs for Rheumatoid Arthritis
• Tumor Necrosis Factor (INF u-blockers) For example:
a. Etanarcept (25 mg/subcutaneous, twice a week)
b. Infliximab (2 mg/kg at 0, 6, 8 and weekly. IV infusions
combined with oral methotrexate).
c. Interleukin- 1 receptor antagonist (IL-IRA) Dose-100
mg/day by subcutaneous injection.
Indications
• Failure of at least two standard DMARD drugs one of which
is always methotrexate despite adequate trials (i .e. 6
months).
• Leflunomide (Immunomodulatory drug) Indicated dose is
100 mg/day for 3 days then 20 mg/ day.

48. 4. Surgical intervention: Goals
• Goals of surgery are to relieve pain, restore
function, correct or prevent deformity, and
inhibit disease progression

49. • A consideration in surgical intevention of
rheumatoid arthritis is the risk of anesthesia.
Most hand and wrist procedures can be
performed under regional anesthesia which
are generally safer, allow a quicker recovery
and provide better post op pain relief than
gen anesthesia. If a GA is considered than
lateral flexion and extension radiograph of
cervical spine must be obtained to rule out
C1-C2 instability.

50. Treatment
• Procedures usually considered for patients
with rheumatoid arthritis include
• tenosynovectomy,
• tendon repair or realignment,
• synovectomy,
• arthroplasty, and
• arthrodesis.

51. Modus operandi of surgical
procedures in rheumatoid arthritis
• Synovectomy
- Failed chemotherapy
- Joint destruction should be minimal
- Useful in knee/ankle
• Osteotomy
- Less than 60 years of age
- When joint is partially damaged
- Commonly done at hip (Intertrochanteric osteotomy and abduction
osteotomy)
• Arthrodesis
- Long-term relief
-Reserved for peripheral joints where arthroplasty results in pain
-Causes secondary osteoarthritis in bigger joints
• Arthroplasty
-Advanced stages in hip and knee

52. Rheumatoid Hand

53. Rheumatoid Wrist
• After MCP joints , most common site for RA.

54. Pathology
• Early stage:- Synovitis of joint and tendon
sheath.
• If disease persist:- DRUJ, R-C joints and
intercarpal joints eroded attenuation of
ligaments and tendons unstable wrist &
hand.

55. • The ulnar side of carpus goes into flexion and ulnar
subluxation, causing head of ulna to jut out prominently on
dorsum of wrist.
• Proximal carpal row slides ulnarwards & the metacarpal
bone deviate radialwardsreciprocal ulnar deviation of
fingers cardinal feature of rheumatoid hand.
• Scaphoid falls into flexion d/t erosion of interosseus lig and
loss of carpal height.
• This combination of instability and erosive tenosynovitis
eventually leads to tendon rupture-typically one or more of
extensors tendons.`

56. Clinical features
• Early-Pain, swelling and stiffness of wrist.
• Swelling initially localised to common extensor
tendon sheath or extensor carpi ulnaris, but as
time progresses the joint becomes thickened
and tender.
• Swelling of synovium in carpal tunnel may
cause median nerve compression.
• Articular surface erode + ligament
attenuated unstable wrist.
• Early infiltration of tendons may lead to
weakness of wrist extension and flexion.

57. • Piano key sign- Instability of DRUJ aggravates dorsal
protrusion of the ulnar head, which can be often
jogged up and down by pressing upon it with thumb.
• Tendon lesions in late stage.
• First to rupture EDM EC of little and ring finger.
• EPL is vulnerable.
• Flexor tendons may also rupture in digital sheaths or in
carpal tunnel.

58. X rays
• Peri articular osteoporosis + erosion of ulnar
styloid and the radio carpal and IP joints

59. Treatment
• Early stage :- Objective is to relieve pain and
counteract synovitis.
• Systemic treatment + intermittent splintage +
intrasynovial injections of corticosteroids.

60. Established disease:-
After joint erosion starts focus should be on joint stability
and prevention of deformity.
Extensor tenosynevectomy and soft tissue stabilization of
the wrist may forestall further deterioration.
Through a dorsal longitudinal incision the extensor
retinaculum is expose and carefully dissected but left
attached at the radial side. The thickened synovium around
the extensor tendons, as well as any bony protrusions on
the back of the wrist, are removed. The preserved extensor
retinaculum is then placed beneath the tendons to further
reduce the risk of later tendon rupture.

61. • If the radio-ulnar joint is involved,
svnovectomv can be combined with excision
of the ulnar head and trans position of the
extensor carpi radialis longus to the ulnar side
of the wrist (to counteract the tendency to
radial deviation).
• Fusion of the Iunate to the radius (chamay
procedure) prevents ulnar slide of the carpus.

62. • Flexor tenosynovitis is not as obvious as
extensor tendon involvement.
• May present as carpal tunnel
syndrome (median nerve compression by
swollen tendons in the carpal tunnel) which
requires open release of the flexor
retinaculum and tenosynovectomv.

63. • Obvious bony protrusions in the floor of the
carpal tunnel (due to carpal collapse) should be
removed and the raw area covered with a soft-tissue
flap.
• Median nerve symptoms in
patients with rheumatoid arthritis may be caused by
pathology in the proximal part of the limb or the
cervical spine, so these patients should always undergo
nerve conduction studies and electromyography
before the carpal tunnel decompression.

64. LATE DISEASE
• Tendon ruptures at the wrist, joint
destruction, instability and deformity may
require reconstructive surgery
• Ruptured extensor tendons can seldom be
repaired; side-to-side suture of a distal tendon
stump to an adjacent tendon, tendon grafting
or tendon transfer gives a satisfactory if not
perfect result.

65. • Rupture of the flexor pollicis longus tendon in
the carpal tunnel may be caused by scuffing of
the tendon against the distal pole of the
scaphoid or the edge of the trapezium - the
so-called `Mannerfelt lesion'.

66. • Painful joint destruction, instability and deformity
can be dealt with by either joint replacement or
arthrodesis.
• Arthroplasty using a silicone `spacer' has a high
failure rate; silicone synovitis and the difficulty of
revision have led to it being abandoned.
• Total wrist replacement with a metal-
polyethylene device is becoming more
reliable, but is only suitable for those with well-
preserved bone stock.

67. • Arthrodesis is widely considered to be
the best option for dealing with painful
instability in the radio-carpal joint.
• If the wrist is already 'fusing' itself
spontaneously, simple stabilization
with a Steinman pin passed between
the second and third metacarpals,
across the carpus and into the distal
radius is all that is needed.

68. • Bone grafts are not necessarily added but can
be taken from the ulnar head if it is excised.
For patients with better bone stock, pin
fixation is inadequate; formal arthrodesis with
a wrist fusion plate is preferable. In this
group, ulnar head replacement rather than
ulnar head excision should be considered.

69. • As a general rule, wrist deformities should be
corrected before hand deformities.
• Furthermore the dominant wrist should, if
possible, be fused in slight extension to
provide reliable power grip, while the non-
dominant wrist is fused in some flexion (or
replaced) so as to provide the posture needed
for perineal care.

70. Wrist arthroplasty
Two types
• 1. Resection arthroplasty with or without soft
tissue interposition and
• 2. Implant arthroplasty
• Palmar shelf arthoplasty* a type of resection
arthroplasty.

71. Palmar shelf arthroplasty
• In this the distal radius is resected so that it is perpendicular to the
longitudinal axis of radius in AP and lateral planes.
• Shallow socket is then created in the distal radius with a small volar
lip to keep the carpus from subluxating anteriorly.
• The carpus is reduced into socket and held with k wires temporarily.
• The volar capsule is detached proximally and sutured to the dorsal
rim of the radius which creates a soft tissue interposition that
discourages volar carpal dislocation.
• The dorsal capsule is repaired , any necessary extensor tendon
procedures are performed and the skin is closed over a drain.

72. CAPUT ULNAE SYNDROME
• Involvement of DRUJ. (blackdahl, 1963)
• Characterised by prominent appearing distal
ulna.
• Develops as the supporting ligaments around the
distal ulna deteriorate and the extensor carpi
ulnaris subluxates anteriorly causing flexion and
supination of the carpus.
• Infact the prominence of distal ulna is in part
secondary to the combined anterior subluxation
and supination of the carpus.

73. Cont:-
• C/o pain over ulnar border of wrist Aggravated
by pronation and supination.
• O/e swelling & tenderness over ulnar head.
• Combination of prominence of distal ulna &
tenosynovitis leads to rupture of EDQ and the
EDC tendons to ring and small fingers.

74. • Surgical Tt. Depends on degree of involvement.
• Synevctomy, reconstruction of supporting ligaments and ECQ
translocation alone rarely. (if no evidence of articular cartilage
destruction.)
• Usually head impossible to save .
• Thus distal ulna resected with ligament reconstruction & ECU
translocation.
• After resection ulnar translocation, volar sublux & supination of
carpus.

75. RA -HAND

76. RA-Hand
• The hand – most common site.
• The early stage is characterized by synovitis of
the joints and tendon sheaths.
• As disease progresses joint and tendon
erosions mechanical derangement.
• In late stage joint destruction, attenuation
of the ligaments and tendon
rupturesinstability and progressive
deformity.

77. Clinical features
• Stiffness and swelling of the fingers are early
symptoms.
• Sometimes the first symptoms are typical of
carpal tunnel compression, caused by flexor
tenosynovitis at the wrist

78. On examination
• Swelling of the MCP and PIP joints, giving the fingers a spindle
shape.
• Usually bilaterally similar.
• Swelling of tendon sheaths is usually seen on the dorsum of the
wrist and along the ulnar border (extensor carpi ulnaris).
• Thickened flexor tendons may also felt on the volar aspect of the
proximal phalanges.
• Joints are tender and crepitus may be felt on moving the tendons.
Joint mobility and grip strength diminished.

79. • As the disease progresses:-
• slight radial deviation of the wrist and ulnar
deviation of the fingers,
• correctable swan neck deformities of some
fingers.
• an isolated boutonniere or the sudden
appearance of a drop-finger or mallet thumb
(from extensor tendon rupture).

80. • In late stage, after inflammation subsides, established
deformities are the rule.
• the carpus settles into radial tilt and volar subluxation.
• there is marked ulnar drift of the fingers and volar
dislocation of the MCP joints, often associated with
multi swan-neck and boutonniere deformities.
• These rheumatoid deformities' are so characteristic
that they allow the diagnosis to be made at first glans.
When the abnormalities become fixed, functional loss
may be so severe that patients can no longer dress and
feed themselves.

81. General features
• 1. Weakness:- Rheumatoid hands are weak
because of combination of generalized
muscular weakness, pain inhibition, tendon
malalignment or rupture, joint stiffness and
nerve compression.
• 2. Rheumatoid nodules:- These arc
associated with aggresive disease in
seropositive patients. They tend occur at
pressure areas (e.g. the pulps of the fingers
and the radial side of the index finger).

82. • 3. Z-collapse :- If one of two adjacent joints
changes direction, then the overlying long
tendons will pull the other joint into the
opposite direction.

83. • 4. Deformities
– Intrinsic plus deformity
– Swan neck deformity
– Boutonniere’s deformity

84. Intrinsic plus deformity
• caused by tightness and contracture of the
intrinsic muscles
• the proximal interphalangeal joint cannot be
flexed while the metacarpophalangeal joint is
fully extended
• volar subluxation of the metacarpophalangeal
joints and ulnar deviation of the fingers may
be associated.

85. • Bunnell test for intrinsic tightness is done.

86. Swan-Neck Deformity
• Swan-neck deformity is described as a flexion posture
of the distal interphalangeal joint and hyperextension
posture of the proximal interphalangeal joint, at times
with flexion of the metacarpophalangeal joint.
• It is caused by muscle imbalance and may be passively
correctable, depending on the fixation of the original
and secondary deformities. Although usually
associated with rheumatoid arthritis, swan-neck
deformity may occur in patients with lax joints and in
patients with conditions such as Ehlers-Danlos
syndrome.

89. A, Terminal tendon rupture may be associated with synovitis of distal interphalangeal
joint, leading to distal interphalangeal joint flexion and subsequent proximal interphalangeal
joint hyperextension. Rupture of flexor digitorum superficialis tendon can be caused by
infiltrative synovitis, which can lead to decreased volar support of proximal interphalangeal
joint and subsequent hyperextension deformity.
B, Lateral-band subluxation dorsal to axis of rotation of proximal interphalangeal joint.
Contraction of triangular ligament and attenuation of transverse retinacular ligament are
depicted.

90. Types of swan neck deformities in RA
• Type I :- PIP joint flexible, independent of MCP
position (i.e. Bunnell's test negative).
Due to palmar plate
failure at PIP joint ± failure of
FDS
• Type II :- PIP joint flexibility dependent on MCP
position. Intrinsic muscle tightness.
Bunnell's test: with MCP joint passively
extended, passive PIP joint flexion
limited
• Type III:- PIP joint stiff regardless of MCP position.
Due to contracture of joint
• Type IV :- Destruction of PIP joint -

91. Tt. Swan neck deformity
• Type I require dermodesis, flexor tenodesis of the proximal interphalangeal
joint, fusion of the distal interphalangeal joint, and reconstruction of the
retinacular ligament.
• Type II require intrinsic release in addition to one or more of the aforementioned
procedures.
• Type III require joint manipulation, mobilization of the lateral bands, and dorsal
skin release.
• Type IV arthrodesis of the proximal interphalangeal joint or, in the ring and small
fingers, with Swanson implant arthroplasty of the proximal interphalangeal joint.

92. Buttonhole, or
Boutonnière, Deformity
• flexed proximal interphalangeal joint, with a
hyperextended distal interphalangeal joint
• it is thought to be caused by synovitis of the
proximal interphalangeal joint with a
stretching out of the central slip, forcing the
lateral bands to begin subluxating volarward.

94. • As the deformity progresses, the lateral bands are forced farther
over the condyles of the proximal interphalangeal joint and become
tightened by their new course and by pressure from the underlying
swollen joint.
• They finally become fixed in a subluxated position volar to the
transverse axis of the joint and act as flexors of the proximal
interphalangeal joint.
• This tightening causes a secondary hyperextension deformity of the
distal interphalangeal joint. The flexion deformity of the proximal
interphalangeal joint is compensated for by an extension of the
metacarpophalangeal joint. The metacarpophalangeal joint
deformity does not become fixed, as do the distal two joints.

95. Clinically
• In mild buttonhole deformities,The flexion deformity at the proximal
interphalangeal joint is passively correctable from a position of approximately 15
degrees of flexion. (normal-appearing radiographs)
In these deformities, treatment may consist of releasing the lateral tendons near
their insertion into the distal phalanx.
• A moderate buttonhole deformity has an approximately 40-degree flexion
contracture of the proximal interphalangeal joint, most of which is passively
correctable.. (satisfactory preservation of joint space radiographcally)
To correct this deformity, there must be functional restoration of the central slip
and correction of the subluxation of the lateral bands.
• A fixed buttonhole deformity  passively uncorrectable flexion contracture of the
proximal interphalangeal joint.
Combined procedures on both joints, usually metacarpophalangeal joint
arthroplasty or fusion with interphalangeal joint release or fusion, are necessary.

96. • Boutonnière deformity. A, Primary synovitis of proximal interphalangeal (PIP) joint can lead to
attenuation of overlying central slip and dorsal capsule and increased flexion at PIP joint. Lateral band
subluxation volar to axis of rotation of PIP joint can lead in time to hyperextension. Contraction of
oblique retinacular ligament, which originates from flexor sheath and inserts into dorsal base of distal
phalanx, can lead to extension contracture of distal interphalangeal joint.
• B, Clinical photograph illustrates flexion posture of PIP joint and hyperextension posture of distal
interphalangeal joint in boutonnière deformity.

97. Swanson technique
• A, Swan-neck deformity of fingers. B, Central tendon is separated from lateral tendons by
dividing connecting fibers. Central tendon is step-cut transversely and dissected
proximally, lengthening it. C, Lateral tendons relocate palmarward. After insertion of
implant, cut ends of central tendon are approximated with interrupted sutures. Knots are
buried.

98. • A, Buttonhole deformity of index finger with swan-neck deformity of other fingers.
B and C, Lengthened central tendon is advanced, and lateral tendons are released
and relocated dorsally by suturing their connecting fibers

99. X-rays
• Early stage :- soft-tissue swelling and
osteoporosis around the joints.
• Later :- Joint space narrowing and small peri-
articular erosions; these are commonest at the
MCP joints and in the styloid process of the ulna.
• In advanced cases, articular destruction may be
marked, affecting the MCP, PIP and wrist joints
almost equally.

100. Treatment
• EARLY STAGE DISEASE :- is directed essentially at
controlling the systemic disease and the local svnovitis.
• In addition to general measures, static splints may reduce
pain and swelling.
• These splints are not corrective but are designed to rest
inflamed joints and tendons; in mild cases they are worn
only at night, in more active cases during the day as well.
• Persistent synovitis of a few joints or tendon sheaths may
benefit from local injections of corticosteroid with local
anaesthetic

101. Established disease
• If disease progressesprevent deformity.
• Uncontrolled synovitis of joints or tendons
requires operative svnovectomy followed by
physiotherapy.

102. • Excision of the distal end of the ulna, synovectomy of the common ex-
tensor sheath and the wrist, and reconstruction of the soft tissues on the ulnar
side of the wrist may arrest joint destruction and progressive deformity.
• Early instability and ulnar drift at the MCP joints can be corrected by excising
the inflamed synovium, tightening the capsular structures and releasing
the ulnar pull of the intrinsic tendons.
• Mobile boutonniere and swan-neck deformities can be treated with
splints; if they progress or are fixed, then surgery may be needed. Isolated
tendon ruptures are repaired or bypassed by appropriate tendon
transfers. These procedures are followed by splin tage and hand therapy.
• Destruction of the MCP joints without ulnar drift can be treated with
surface replacement (chromepolyethylene or pyrocarbon)

103. Late disease
There is Deformity + articular destruction so soft-tissue
correction alone will not suffice.
For the MCP and IP joints of the thumb
arthrodesis gives predictable pain relief, stability
functional improvement.
The MCP joints of thefinger can be excised and replaced
with Silastic spacerswhich improve stability and correct
deformity
Replacement of IP joints gives less predictable results
if deformity is very disabling (e.g. a fixed swan-neck
it may be better to settle for arthrodesis in a in
functional position.

104. • At the wrist, painless stability be regained by
fusion of the radio-carpal, midcarpal and CMC
joints.
• Wrist replacement with Silastic metal-plastic
implants may fail; due to the loss of bone
stock that accompanies failure means that
salvage can be very difficult.

105. • Souter recommended starting with a
procedure that is likely to succeed, beginning
with the least involved hand. He grouped
hand procedures from the most effective
(group I) to the least effective (group V). In
addition, Souter advocated correcting
significant disease and deformity in the elbow
and shoulder before correcting hand
deformities.

107. The thumb in rheumatoid arthritis
• The combination of soft-tissue failure and joint erosion leads to
characteristic deformities of the thumb:
– rupture of flexor pollicis longus tendon,
– a boutonniere lesion at the MCP joint,
– CMC instability swan- neck deformity
– Ulnar collateral ligament instability.
• Depending on the deformity, the patient's demands
and the condition of the rest of the hand, treatment
may involve various combinations of splintage, tendon repair, joint
fusion, excision arthroplasty and joint replacement.

108. RH THUMB
• Pain free thumb with stability and mobility is very
imp.
• All three trapezio-metacarpal, MCP and IP joints
may be involved.
• Deformity of wrist affects more distal part, so if
Tr-Mc joint deformity compensatory deformity
at MCP and IP joints and MCP disease leads to IP
deformity.
• Thus most proximal affected joint must be
addressed first.

109. • synovitis beginning in the thumb MCP joint
frequently leads to a boutonnière deformity of
the thumb, with palmar subluxation and flexion
of the proximal phalanx with hyperextension of
the interphalangeal joint.
• When synovitis begins in the thumb
carpometacarpal joint, the deformity includes
dorsal subluxation of the metacarpal base and
hyperextension of the metacarpophalangeal joint
(swan-neck deformity).

110. • Another thumb deformity caused by synovitic destruction
of the capsuloligamentous supports on the ulnar side of the
metacarpophalangeal joint is the gamekeeper thumb,
which results from laxity of the ulnar collateral ligament of
the thumb at the metacarpophalangeal joint.
• Involvement of the metacarpophalangeal joint also can
result in laxity of the capsuloligamentous structures in the
volar plate, leading to hyperextension of the
metacarpophalangeal joint and interphalangeal
hyperflexion, but with a stable carpometacarpal joint.
Other, more severe deformities of the fingers and thumb
can be caused by an erosive rheumatoid disease, leading to
the “main en lorgnette” (opera glass hand).

113. Rh thumbs-types
• By Nalebuff into 5 types
• Type I- MCP flexion def with sec
compensatory IP hyperextension (due to
synovitis at MCP joints which causes
attenuation of the EPB tenson and extensor
hood , leading to extensor lag at MCP joints.
The EPL tendon subluxates in an ulnar and
volar direction functioning as an MCP flexor
and IP extesnor.

114. • Type II- Primary TMJ d’s with Sec. IP joint
hyperextension and instability.
Tt- TMJ must be reconstructed followed by IP
arthrodesis.

115. • Type III- Second most common deformity.
• Primary TMJ instability followed by compensatory
hyperextension deformity at MCP joints.
• Synovitis of the TMJ leads to laxity of the palmar
oblique ligament with dorsoradial suluxation of
the metacarpal base.
• Combined forces of APL and Adductor pollicis
lead to adduction of first metacarpal and
narrowing of first web space.

116. • Hyperextension deformity at the MCP joint
develops due to the first metacarpal
adduction contracture.
• As patient attempt to extend the thumb and
grasp objects, extension force is transmitted
to MCP joint instead of the metacarpal which
is fixed. Progressive volar plate laxity
develops, leading to a MCP hyperextension
deformity.

117. • Treatment :-
• Aimed primarily at TMJ
• Arthroplasty+ ligament stabilization
procedures like ligament reconstruction
combined with a silicone , fascial or tendon
interposition arthroplasty.
• Adduction contracture bone resection +/-
web space z plasty for abduction.

118. • Indication for MCP fusion at the time of TMJ
arthroplasty include either 20 degree of
passive hyperextension or 30 degree of valgus
instability.
• If the MCP joint is only mildly unstable, volar
tenodesis or capsuplasty instead of fusion.

119. • Type IV- Same as type III, except that the MCP
joint develops valgus instability.
• Type V- not original, added later
• Volar plate laxity at MCP joint and IP joint
flexion deformity. Primary pathology at MCP
joint
• Tt- Mcp joint capsulodesis or fusion.

120. • Thumb IP arthrodesis- 0-10 deg flex, neutral
abd-add, 5 deg pronation.
• MCP- 15 deg flex, 15 deg abd, and 15 deg of
pronation.

121. Management of thumb deformities
• 1. Ruptured FPL
– If painless: leave alone
– If painful: tendon graft, flexor digitorum sublimus transfer or IP fusion
• 2. Simple boutonniere deformity
– If passively correctible: cortisone injection to MCP joint and splintage
– MCP joint synovectomy and extensor realignment unreliable
– If MCP joint fixed but IP joint passively correctible and CMC joint
mobile: fuse MCP joint
– If MCP joint and IP joint fixed: fuse IP joint and either fuse or replace
MCP joint
• 3. Boutonniere with CMC joint failure
– Trapeziectomy and CMC joint stabilization, with MCP joint and IP joint
treated as above

122. 4. Swan-neck deformity
- CMC joint failure causes adduction contracture of thumb base and
MCP joint hyperextension
- If deformity severe: trapeziectomy with soft-tissue reconstruction or
fusion of MCP joint
5. Failure of ulnar collateral ligament (like 'gamekeeper's thumb)
Synovitis attenuates ulnar collateral ligament. Pinch grip causes
increasing deformity
Ligament reconstruction (if bone and soft-tissue quality allow) or
MCP joint fusion
6. Swan-neck with MCP joint and CMC joint preserved
Synovitis of MCP joint causes hyperextension v, secondary passive
flexion of IP joint
– Treat by palmar plate advancement or, if soft tissues tenuous, MCP
fusion
7. Arthritis mutilans
– Arthrodesis with interposition bone graft

123. RA-MCP JOINTS

124. Metacarpo-phalangeal deformities
• Chronic synovitis of the MCP joints results in
failure of the palmar plate and the collateral
ligaments.
• The powerful flexor tendons drag the proximal
phalanx palmarwards, causing subluxation of
the joint.
• The deformity may be aggravated by primary
or secondary intrinsic muscle tightness

125. • Most obvious deformity :- ulnar deviation of the
MCP joints.
• Reasons for this:
palmar grip and thumb pressure naturally tend to
push the index finger ulnarwards; weakening of
the collateral ligaments and the first dorsal
interosseous muscle reduces the normal
resistance to this force; the wrist is usually
involved and, as it collapses into radial
deviation, the MCP joints automatically veer in
the opposite direction (the ,so-called zig zag
mechanism).

126. Treatment RA-MCP
• Early stage before joint destruction and soft-tissue
instabilitysynovectomy
• When ulnar drift has started splintage
• With marked deformity but little joint damage a soft-tissue
reconstruction (reefing of the radial sagittal bands, tightening of the
radial collateral ligament with intrinsic muscle release and transfer)
• If marked damage to the joint surface, replacement with a Silastic
spacer, along with the soft-tissue reconstruction, is recommended.
• There is no point in correcting the MCP joints unless any wrist
deformity is also corrected; the tendency to zig-zag deformity will
otherwise lead to recurrence of the ulnar drift.

127. Tenosynovitis and tendon rupture
• Extensor tendons :- Extensor tendon rupture
is a common complication of chronic svnovitis.
• Tenosynovitis presents with mass over dorsum
of the hand with pain and limited motion.
• Extensor digiti minimi is usually the first to go
and predicts rupture of the other tendons.

128. • The extrinsic extensor tendons are the
primary extensors of the MCP joints, whereas
the intrinsics are the primary extensors of the
interphalangeal joints.
• As a result, extrinsic extensor tendon ruptures
only lead to a lag at the MCP joint level.

129. • The extensor pollicis tendon is a common tendon rupture
in the rheumatoid patient because of tension and friction
as the tendon passes around Lister's tubercle.
• Rupture of the EPL does not lead to a complete lack of
extension at the IP joint because of the attachments of the
APB and adductor pollicis (ADD) tendons to the dorsal
expansion.
• Instead, EPL rupture is best diagnosed by the inability of
the patient to extend the thumb while the hand is held flat
on a table, palm side down.

130. • Rupture of a single EDC tendon is treated by side-to-side repair to
an adjacent EDC tendon.
• Similarly, isolated EDQ rupture is treated by side-
to-side repair to EDC.
• Rupture of both EDQ and
EDC to small is best treated by EIP transfer to both
tendon stumps.
• Rupture of EDC to ring and small
is usually treated by side-to-side transfer of EDC
long to EDC ring and transfer of EIP to EDC
small.
• Rupture of EDC of long, ring, and small can be treated by side-to-
side transfer of EDC long to EDC index, and EIP to EDC ring and EDC
small.

131. • It can also be treated by EIP to EDC long and FDS ring to EDC ring
and small.
• Rupture of all of the extrinsic finger extensors (II-V) is usually
repaired using FDS tendons. FDS long is transferred to EDC index
and FDS ring is transferred to EDC long, ring, and small.
• The tension of the tendon transfers is critical for
optimal function. The tendon transfer for finger
extension is set with the wrist in maximal extension
and the fingers in full flexion. This ensures that the
transfer will not be too tight and thereby limit finger

132. • In those with a wrist fusion, the tendon
transfer is set with the interphalangeal joints
in full extension and the MCP joints flexed 25-
30°.

133. Flexor tendons
• Flexor tendons :- Flexor tenosvnovitis one of the earliest
features.
• FPL and profundus to small finger is commonest to rupture
• The restriction of finger movement is easily mistaken for
arthritis; however, careful palpation of the palm and the
nearby joints will quickly show where the swelling and
tenderness are located.
• Secondary problems include carpal tunnel
syndrome, triggering of one or more fingers and tendon
rupture Synovitis of the flexor digitorum superficialis also
con-
tributes to the swan-neck deformity

134. • If carpal tunnel release is needed, the operation should
include a flexor tenosvnovectomy.
• If the flexor tendons are bulky (best felt over the
proximal phalanges) and joint movement is
limited, then flexor tenosynovectomv should improve
movement and, just as important, should prevent
tendon rupture.
• Triggering, likewise, should be treated by
tenosynovectomy rather than simple splitting of the
sheath.

135. • Rupture of flexor digitorum profundus is best
treated by distal IP joint fusion.
• Rupture of flexor pollicis longus (due to
attrition against the underside of distal radius
or flexor svnovitis) can be treated eitherby
tendon grafting or by fusion of the thumb IP
joint.

136. • Surgical synectomy only after 6 months- if
conservative management fails.
• Primary repair is generally not possible for flexor
tendon injuries in these patients. Instead if
rupture occurs at level of the palm, it is repaired
side to side fashion to an intact flexor tendon.
• If the rupture occurs at a digital level , then the
superficialis tendon from another finger is used
as a transfer.

137. To Summarize…..
• General principles of orthopaedic care in RA are:-
• 1. Maintaining position and function of all joints by
physiotherapy and splintage.
• 2. Treating the soft tissue and joint processes as they
develop by injections, by principles of rest and, where
necessary by early surgery.
• 3. Correcting established deformity and attempting to
restore function- but this does not mean the severely
deformed ‘burned out’ rheumatoid hand in which there is
little motor power left.

141. RA Vs. OA
Rheumatoid arthritis Osteoarthritis
• It is an autoimmune disease and often strikes • It is an age-related disease due to wear and
in the prime of life. tear of the cartilage.
• It is usually seen between the ages of 25 and • It usually affects people after 40 years of age.
50 years of age
but can also occur in children and infancy.
• It affects joints on both sides of the body and • It usually affects isolated joints, or joints on
has a only one side of the body at first.
bilateral presentation.
• It causes redness, warmth and swelling of • It usually does not cause redness and
the joints. warmth of the joints.
• It affects many joints usually small joints of • It most commonly affects weightbearing
the hands joints or joints that are overused (e.g. knees
and feet, and may affect the elbow, shoulders, and hip).
wrist,
hip, knee and ankles.
• It can affect the entire system, with general • Discomfort is usually related to the affected
feeling of joint.
sickness and fatigue, as well as
weight loss.
• There is history of prolonged morning • Brief morning stiffness.
stiffness.

143. • Rheumatoid arthritis (RA)
• Features
• Mnemonic: RHEUMATISM
• R Rheumatoid factor (RF) +ve in 80%/Radial deviation of wrist
• H HLA-DR1 and DR-4
• E ESR/Extra-articular features (restrictive lung disease, subcutaneous
nodules)
• U Ulnar deviation of fingers
• M Morning stiffness/MCP+PIP joint swelling
• A Ankylosis/Atlanto–axial joint subluxation/Autoimmune/ANA +ve in
30%T T-cells (CD4)/TNF
• I Inflammatory synovial tissue (pannus)/IL-1
• S Swan-neck deformity, Boutonniere deformity, Z-deformity of thumb
• M Muscle wastage of small muscles of hand

144. • Management
• DMARDs (Disease-Modifying Anti-Rheumatic Drugs)
• Mnemonic: Most Sufferers Can Get Appropriate Pain
Control
• M Methotrexate
• S Sulfasalazine
• C Ciclosporin
• G Gold
• A Azathioprine
• P Penicillamine
• C HydroxyChloroquine