Rheumatoid Hand

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RHEUMATOID HAND

MODERATOR : DR PRABHU E SIR


PRESENTER : DR ARYADEV
SPECIFIC LEARNING OBJECTIVES
At the end of the class all participants should know about :

• Etiology and pathology of rheumatoid arthritis

• Swan neck deformity

• Boutonniére deformity

• Metacarpophalangeal joint deformities

• Wrist deformities seen in rheumatoid hand


INTRODUCTION
• Rheumatoid arthritis is a chronic, inflammatory, autoimmune disease that may involve
multiple organ systems but mainly targets the synovial joints

• It is more common in women than men

• Peak incidence somewhere between 35–50 years

• Diagnosed in individuals with symmetrical inflammatory polyarthritis affecting the small


joints of the hands, feet and wrists persisting for more than 6 weeks with characteristic
laboratory abnormalities
• Rheumatoid arthritis is the most common idiopathic inflammatory arthritis, affecting
approximately 0.8% of the population

• 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

• Environmental factors : Smoking, alcohol, socioeconomic status, oral contraceptive, red


meat, oral contraceptives
PATHOGENESIS

• In the early stages, edema, microvascular proliferation, and T-lymphocyte infiltration occur
in the sub synovial tissue, followed by synovial lining cell proliferation

• Increased cellularity includes synovial infiltration by B-cells, macrophages, and fibroblasts

• Fibroblasts migrate to the synovial surface, with granulation tissue development, entailing
further proliferation of fibroblasts, synovial lining cells, and enhanced vascular infiltration

• Soluble pro-inflammatory substances produced by activated lymphocytes, monocytes, and


macrophages are generated in the joint
RHEUMATOID HAND
• Rheumatoid hand deformities are usually bilateral and symmetric

• The metacarpophalangeal joints and the wrist are affected early in rheumatoid arthritis,
whereas the distal joints usually are affected later

• The metacarpophalangeal joint is the most important in affecting finger function

• Ulnar deviation of metacarpophalangeal joint, radial deviation of metacarpals and ulnar


deviation of wrist typifies the classical rheumatoid hand deformity
• Deformities usually occur due to ligamentous, osteochondral, intra-articular damage and
the forces applied through the intrinsic and extrinsic muscles
STAGES OF RHEUMATOID JOINT INVOLVEMENT

STAGE 1 : Synovitis without deformity

STAGE 2 : Synovitis with a passively


correctable deformity

STAGE 3 : Fixed deformity without joint


changes

STAGE 4 : Articular destruction


SWAN NECK DEFORMITY
• It is the most common finger deformity

• 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

• DIP FLEXED + PIP HYPEREXTENDED


Three sets of muscles and tendons provide digital equilibrium and control:

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. Fibrous joint capsule

2. The collateral ligaments

3. The volar plate

4. Retinacular system including the ligament of Landsmeer


• The intrinsic muscles act as a functional unit with two major effects :

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

• Gradually, the DIP joint gets fixed in flexion, resembling a mallet

• Distal interphalangeal joint flexion relaxes lateral bands, concentrating the power of the
long extensor on central slip that inserting into the middle phalanx

• This produces PIP joint hyperextension(secondary)


The pathogenic mechanisms in RA that produce a primary hyperextension at the PIP
followed by DIP flexion

1. Intrinsic type: Due to overactivity of intrinsic muscles

• Here the intrinsic muscles oppose the extrinsic flexor muscles producing PIP
hyperextension

2. Articular type: Secondary to weakening or destruction of normal stabilizing mechanisms


of the PIP that prevent hyperextension
CLASSIFICATION OF SWAN-NECK DEFORMITY
Four main types by NALEBUFF

Type I: PIP joints are flexible in all positions of hand and fingers

Type II: PIP joint flexion is limited in certain positions

• 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

NONOPERATIVE: Using silver rings (permit active PIP flexion and

limit hyperextension of the PIP joint)

or thermoplastic figure of 8 splints


NALEBUFF TYPE I DEFORMITY:

OPERATIVE:

• Distal interphalangeal joint FUSION along with PIP FLEXOR TENODESIS

Tenodesis is produced proximal to the A1 pulley by removing FDS from the sheath
creating a flexion deformity at the PIP

• Spiral oblique retinacular ligament reconstruction ± Dermodesis (removing elliptical


skin wedge from volar aspect of the PIP and resuturing under tension)
NALEBUFF TYPE II DEFORMITY:

• Focused on relieving the intrinsic tightness that is produced due to malposition of the finger
at MCP joint

• SURGICAL RESECTION OF THE LATERAL BANDS

• ULNAR EXTENSOR APONEUROSIS RELEASE is also done to prevent ulnar


subluxation of the tendons and reduce extensor tightness

• SILICONE ARTHROPLASTY is done in cases of severe involvement of the MCP joint


NALEBUFF TYPE III DEFORMITY:

• Focuses on restoration of passive motion to the PIP joint

• The following measures help in achieving the goals:

1. Proximal interphalangeal joint manipulation: By doing a dorsal skin release distal to


PIP joint and leaving the scar to heal over 2–3 weeks

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

• DIP HYPEREXTENDED + PIP FLEXED


PATHOMECHANICS

• Synovial proliferation in the PIP joint, weakens the extensor mechanism

• 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

• Bend PIP joint to 90° over a table top

• Block middle phalanx and ask patient to extend finger

• DIP should remain flaccid

• If DIP extends, this indicates a central slip rupture


• When the central slip is injured or incompetent, it is possible to generate extensor force
at the DIP joint with maximal passive PIP joint flexion, which is the basis of the Elson
test for detecting acute central slip rupture

• 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

1. Minimal distortion of the joint positions and functional loss

2. Slight extensor lag (10–15°) at the PIP joint

3. Slight hyperextension at the DIP joint

4. No involvement of the MP joint

• Mild deformity is usually corrected by EXTENSOR TENOTOMY to increase DIP joint


flexion
MODERATE BOUTONNIÉRE DEFORMITY

1. Flexion deformity at the PIP joint increases to 30–40°

2. The MCP joint begins to hyperextend (compensatory mechanism)

• 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

• The PIP joint can no longer be passively extended

• This stage is treated by :

1. Fusion of the joint or arthroplasty

2. Fusion of the PIP joint is performed in a flexed position

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

2. In late stages the joint is eroded

3. Development of typical arthritic changes like cyst formation and loss of bony
architecture
MANAGEMENT :
• Conservative management

• Medications (DMARDs or biologics) hardly improves established deformities but is the


most important aspect in prevention of deformities
OPERATIVE MANAGEMENT
SYNOVECTOMY:

• Typically done for joint swellings not remitted by


more than 6 months of medical therapy

• Joint erosions should be absent


EXTENSOR TENDON RELOCATION:

• This is usually combined with synovectomy for


patients who also demonstrate ulnar subluxation of
the tendon and early ulnar drift

• The extensor expansion is released from the ulnar


aspect (tight side) while radial imbrication or
tightening is done

• Overtightening should be avoided to avoid loss of


MCP flexion
INTRINSIC BALANCING:
• Intrinsic reconstructive procedures are tendon transfers or tenodesis
procedures that improve intrinsic balance in the fingers, thumb, or
both

• This is done by release of intrinsic muscles that relaxes the dorsal


digital expansion

• Crossed intrinsic transfer from ulnar side to radial side is another


option
METACARPOPHALANGEAL JOINT REPLACEMENT

• 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

• Shafts are reamed and the prosthesis is seated


RHEUMATOID ARTHRITIS OF WRIST JOINT

• The ulnar side of the wrist is most commonly affected producing distal radial ulnar joint
(DRUJ) disruption and caput ulna syndrome

• On the radial side destructive process involves radio-scapho-capitate ligament with


subluxation of the scaphoid and ulnar translocation of the carpal bones

• In late cases carpal coalition develops and where the carpal bones lose distinctive
boundaries and appear as a mass
INDICATIONS OF TOTAL WRIST ARTHROPLASTY:

• Painful radiocarpal arthritis that is significantly impacting on function

• 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

• Most of the patients with RA develop thumb deformities

• Synovial hypertrophy is a common pathway in development of deformities and joint


destruction

• 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

• When synovitis begins in the carpometacarpal


joint of thumb, the deformity includes dorsal
subluxation of the metacarpal base and
hyperextension of the MCP joint
TYPE 1
• Synovitis with dorsal hood disruption (due to stretching)

• The extensor pollicis longus (EPL) tendon subluxes


ulnarly

• Poor extension force at MCP joint produces volar


subluxation of proximal phalanx base

• Hyperextension of IP joint develops secondarily due to


altered pull of intrinsics and EPL
• There is loss of active MCP extension

• During pinch the MCP joint always goes into flexion with hyperextension of the IP joint

• This is the most common deformity of thumb in RA

• 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

• CMC joint is often subluxed (flexion and adducted)

• 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

• CMC joint synovitis initiates the dorso-radial subluxation and dislocation of


the first metacarpal base

• The first metacarpal is adducted

• Adduction combined with volar plate laxity results in hyperextension of

the MP joint

• Due to hyperextension at the MCP joint lateral bands are relatively

shortened

• The pull of the FPL draws the distal phalanx into flexion completing swan-

neck
TYPE 4

• Deformity is analogous to gamekeeper thumb

• The MP joint synovitis causes laxity and


inefficiency of the ulnar collateral ligament

• This often causes secondary adduction of the first


metacarpal
TYPE 5
• Deformity is identical to the type 3 deformity but without adduction of the first
metacarpal

• 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

• The thumb is also shortened


TREATMENT OF THUMB
DEFORMITIES
• The treatment of specific deformities depends on the
severity of disease in each involved joint and the type of
deformity

• In general, fixed joint deformities with bony destruction


are usually more suitable fusion than arthroplasty

Type I deformity:

• Metacarpophalangeal joint SYNOVECTOMY + EPL


REROUTING in early cases

• In late cases it is better to fuse the MP joint or do an


arthroplasty
MANAGEMENT OF TYPE III (AND TYPE II):

• Metacarpal adduction correction is the focus of treatment of type III deformity

• Block arthrodesis to restore abduction of metacarpal (± CMC arthrodesis)

• MCP hyperextension is corrected by capsulodesis, sesamoidesis, or arthrodesis (if fixed


deformity or minimal active flexion is present) in a slightly flexed position
MANAGEMENT OF TYPE IV 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

• Thumb abduction can be efficiently done by the thenar muscles then


MANAGEMENT OF TYPE V DEFORMITY:

• Best corrected by stabilization of the MP joint by a capsulodesis, sesamoidesis or fusion


in a slightly flexed position

• Volar plate advancement is a good option or even arthroplasty is now being preferred
MANAGEMENT OF TYPE VI DEFORMITY :

• Deformity is treated by fusion of the involved joints in functional position

• Arthroplasty has no role at all

• The IP joint should be fused at 0–20˚ of flexion


CONCLUSION
• Rheumatoid arthritis commonly involves the small joint of hand and wrist

• Destruction produced by synovitis causes deformities

• 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 :

• Campbell’s Operative Orthopaedics

• Kelley’s Textbook of Rheumatology

• Greens Operative Hand Surgery


THANK YOU

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