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Rheumatoid Hand
Rheumatoid Hand
Rheumatoid Hand
• Boutonniére deformity
• Joint destruction lead to loss of physical function, inability to carry out daily tasks of
living.
ETIOLOGY
• Infections : Mycoplasma, Epstein-Barr virus, cytomegalovirus, parvovirus and rubella virus
have all been suggested
• Genetic susceptibility : rate in monozygotic twins is high, class II loci, class III genes for
TNF-, heat shock protein 70 (HSP70) and complement C4
• In the early stages, edema, microvascular proliferation, and T-lymphocyte infiltration occur
in the sub synovial tissue, followed by synovial lining cell proliferation
• Fibroblasts migrate to the synovial surface, with granulation tissue development, entailing
further proliferation of fibroblasts, synovial lining cells, and enhanced vascular infiltration
• The metacarpophalangeal joints and the wrist are affected early in rheumatoid arthritis,
whereas the distal joints usually are affected later
• The distal interphalangeal joint is flexed and the proximal interphalangeal joint is
hyperextended
• Deformity develops due to an in-equilibrium of the factors that provide control over the
digit
1. Extrinsic extensor group: Extensor digitorum communis, extensor digiti minimi and
the extensor indicis.
They produce extension at the MCP joint and along with
intrinsic muscles, also extend the PIP and DIP joints
2. The extrinsic flexor group: Flexor digitorum profundus (FDP) and superficialis (FDS)
3. The intrinsic muscles : Include the four lumbricals and the volar and dorsal interossei
• Other structures that act in passively stabilizing the finger include:
1. Flexion of the MCP joints by insertion into the base of the proximal phalanx
2. Extension of the PIP and DIP joints as the tendons cross dorsally and join the
extensor apparatus over the PIP
PATHOMECHANICS OF DEVELOPMENT OF SND:
• Any hyperextension of the PIP will secondarily produce flexion of the DIP joint and
conversely DIP flexion deformity produces hyperextension at PIP due to alteration of
forces
• PIP hyperextension relaxes the normal tension on the lateral extensor bands causing it to
move centrally and dorsally
• In such a lax position the bands lose ability to extend the DIP, which hence drops into
flexion
• The FDP is pulled by hyperextension of the PIP causing prominent flexion of DIP by the
law of maintaining constant length
• Another factor producing PIP hyperextension is the stretching of the capsule secondary to
active synovitis or ruptured flexor digitorum superficialis (FDS) tendon
• In rheumatoid arthritis, the DIP joint synovitis results in rupture of the extensor tendon
attachment to the distal phalanx
• Distal interphalangeal joint flexion relaxes lateral bands, concentrating the power of the
long extensor on central slip that inserting into the middle phalanx
• Here the intrinsic muscles oppose the extrinsic flexor muscles producing PIP
hyperextension
Type I: PIP joints are flexible in all positions of hand and fingers
• When the MCP joints are extended or radially deviated, passive PIP joint flexion is limited
while higher flexion is possible with MCP in flexion or ulnar deviation
Type III: PIP joint flexion is limited in all positions due to contracture of the extensor
mechanism, collateral ligaments and skin
Type IV: PIP joints get stiff and show radiographic destruction
MANAGEMENT :
NALEBUFF TYPE I DEFORMITY:
Treatment focuses on correcting the PIP hyperextension and hence the DIP secondarily corrects
OPERATIVE:
Tenodesis is produced proximal to the A1 pulley by removing FDS from the sheath
creating a flexion deformity at the PIP
• Focused on relieving the intrinsic tightness that is produced due to malposition of the finger
at MCP joint
2. Lateral band mobilization: The lateral bands are freed from the central slip and PIP
mobilized to full flexion completing the release passively
NALEBUFF TYPE IV DEFORMITY:
• Only salvage is possible for this type of deformity in the form of:
ARTHRODESIS—of PIP joint is particularly useful for the index and middle fingers,
because these digits need lateral stability when opposed to the thumb during pinch
• Arthrodesis is also commonly done if concomitant MCP joint arthroplasty is being done
ARTHROPLASTY—is performed when the soft tissue and ligamentous support is adequate
especially for ring and small fingers, where mobility aids grasp
BOUTONNIÉRE DEFORMITY
• The deformity presents with the PIP joint flexed and the DIP and MP joints
hyperextended
• The abnormal finger posture in RA starts with PIP joint flexion that leads to the changes
in the other joints
• The joint goes into partial flexion due to effusion and synovitis (position of maximum
capsular volume)
• Over time the lateral bands are displaced volarly and the spinal oblique retinacular
ligament are shortened which causes DIP hyperextension
• The MP joint hyperextends to compensate for the increasing PIP joint flexion
CLINICAL FEATURE
ELSON TEST
• This test is the most sensitive physical examination test to detect acute central slip rupture
• In Boutonniere deformity, incompetent triangular ligaments due to central slip rupture
allow volar subluxation of lateral bands
• With PIP joint extension the lateral bands will produce an extension at the DIP joint
MANAGEMENT
MILD BOUTONNIÉRE DEFORMITY
• Reconstruction of the extensor mechanism to shorten the central slip and repositioning
the lateral band dorsally
• For success of soft tissue reconstruction good dorsal skin, smooth joint surfaces,
functional flexor tendons and flexible PIP joint should be present
• Wrist deformity should be corrected before addressing the PIP extensor mechanism
SEVERE BOUTONNIERE DEFORMITY
3. Functional position of PIP flexion increases from the index finger (25˚) to little finger (40°)
4. PIP joint arthroplasty is acceptable option if the extensor mechanism isgood enough to be
repaired
5. Arthroplasty is useful for boutonniere deformities of the small and ring fingers to improve grip
strength
METACARPOPHALANGEAL JOINT
1. Radial deviation of metacarpals
3. Development of typical arthritic changes like cyst formation and loss of bony
architecture
MANAGEMENT :
• Conservative management
• The most popular method of restoring alignment and flexibility of MCP joint
• The procedure is combined with ulnar extensor expansion release and tendon balancing
• The metacarpal head and the base of proximal phalanx are cut perpendicular to the long axis
• The ulnar side of the wrist is most commonly affected producing distal radial ulnar joint
(DRUJ) disruption and caput ulna syndrome
• In late cases carpal coalition develops and where the carpal bones lose distinctive
boundaries and appear as a mass
INDICATIONS OF TOTAL WRIST ARTHROPLASTY:
• The ultimate indication is when the contralateral wrist has already been fused
• It can correct deformity and address the degenerated parts of the joint
CONTRAINDICATIONS
1. Infection
2. Tendon ruptures
3. Poor soft tissue envelope
4. Poor bone stalk
5. Charcot arthropathy
6. Chronic subluxation
7. Need of weight-bearing through the joint (assisted walk using crutches/walker)
8. Involvement of contralateral wrist that also needs treatment (relative)
THUMB DEFORMITIES
• Day-to-day activities like buttoning, combing and holding objects are all compromised
• Synovitis beginning in the thumb
metacarpophalangeal joint leads to a boutonniere
deformity, with palmar subluxation of the proximal
phalanx and MCP joint flexion, and IP joint
hyperextension
• During pinch the MCP joint always goes into flexion with hyperextension of the IP joint
• Other pathogenic mechanism for this deformity is rupture of EPL at wrist with IP joint
hyperextension due to volar plate attenuation and flexor pollicis longus (FPL) rupture
TYPE 2
• Flexion at the MP joint and hyperextension at the IP joint but there is additional MC
adduction due to CMC joint involvement
• As the patient attempts to open the first web space to grasp an object, the extension forces
are transmitted to the MP joint, resulting in the secondary hyperextension deformity of
IP joint
TYPE 3
• Carpometacarpal (CMC) subluxation resulting in a Swan neck deformity
the MP joint
shortened
• The pull of the FPL draws the distal phalanx into flexion completing swan-
neck
TYPE 4
• This is due to volar plate laxity causing primary MCP hyperextension and secondary IP
joint flexion
TYPE 6
• Deformity involves bone erosion at isolated or multiple joints with subluxation and
dislocation of the joints
Type I deformity:
• It is managed by stabilizing the MCP joint and correcting the adduction contracture by
Z-plasty
• Ulnar collateral ligament reconstruction is done to stabilize the MCP joint but if not
possible then an arthrodesis is done
• Volar plate advancement is a good option or even arthroplasty is now being preferred
MANAGEMENT OF TYPE VI DEFORMITY :
• The type of deformity that specifically develops is dependent on the forces acted by
extrinsic and intrinsic tendons
• Specific management options are available for correction of swan neck and boutonniere
deformities depending on the stage of development of deformity and extent of involvement
• Advanced destruction of MCP joint usually needs arthroplasty but destruction of wrist joint
needs arthrodesis in view of the unavailable long-term results of arthroplasty of wrist joint
REFERENCES :