DEFORMITIES OF THE HAND IN RHEUMATOID ARTHRITIS

• Rheumatoid arthritis (RA) is the most common cause of chronic inflammatory joint disease.

• Most typi- cal features are a symmetrical polyarthritis and tenosynovitis, morning stiffness, elevation of the ery- throcyte sedimentation rate (ESR) and the appearance of autoantibodies that target immunoglobulins (rheumatoid factors) in the serum

• Rheumatoid arthritis is a systemic disease but the most characteristic lesions are seen in the synovium or within rheumatoid nodules. The synovium is engorged with new blood vessels and packed full of inflammatory cells.

• Stage 1 – pre-clinical Well before RA becomes clini- cally apparent the immune pathology is already begin- ning. Raised ESR, C-reactive protein (CRP) and RF may be detectable years before the first diagnosis.

• Stage 2 – synovitis Early changes are vascular conges- tion with new blood vessel formation, proliferation of synoviocytes and infiltration of the subsynovial layers by polymorphs, lymphocytes and plasma cells. There is thickening of the capsular structures, villous forma- tion of the synovium and a cell-rich effusion into the joints and tendon sheaths. Although painful, swollen and tender, these structures are still intact and mobile, and the disorder is potentially reversible

• Stage 3 – destruction Persistent inflammation causes joint and tendon destruction. Articular cartilage is eroded, partly by proteolytic enzymes, partly by vascu- lar tissue in the folds of the synovial reflections, and partly due to direct invasion of the cartilage by a pan- nus of granulation tissue creeping over the articular surface. At the margins of the joint, bone is eroded by granulation tissue invasion and osteoclastic resorption

• Stage 4 – deformity The combination of articular destruction, capsular stretching and tendon rupture leads to progressive instability and deformity of the joints.

FINGER DEFORMITIES CAUSED BY RHEUMATOID ARTHRITIS

• Deformities of the finger can be caused by the normal forces applied to damaged joints by the extrinsic flexors and extensors, tightness of the intrinsic muscles, displacement of the lateral bands of the extensor hood, rupture of the central slip of the hood, or rupture of the long extensor or long flexor tendons.

• .

• Here abnormal forces also act on joints already weakened by the disease.

• In addition, flexor tenosynovitis may produce limitation of interphalangeal joint motion, so the range of active flexion of these joints is significantly less than passive flexion

1.INTRINSIC PLUS DEFORMITY2.SWAN NECK DEFORMITY3.BUTTON HOLE DEFORMITY4.ULNAR DEVIATION

1.Intrinsic Plus Deformity • The intrinsic plus deformity is caused by tightness

and contracture of the intrinsic muscles.• In hands with intrinsic plus deformity, the

proximal interphalangeal joint cannot be flexed while the metacarpophalangeal joint is fully extended.

• Often, the deformity develops in combination with volar subluxation of the metacarpophalangeal joints and ulnar deviation of the fingers

Bunnell test for intrinsic tightness

Metacarpophalangeal joint is passively held in extension, causing passive extension of the proximal interphalangeal joint and preventing passive flexion of the proximal interphalangeal joint (Fig. 70-11). When the metacarpophalangeal joint is passively flexed, the intrinsics are relaxed, and passive flexion of the proximal interphalangeal joint is increased. With ulnar drift of the fingers, this intrinsic tightness may be present only on the ulnar side.

• To test this accurately, axial alignment of the finger with the metacarpal should be maintained in checking intrinsic tightness.

• Any ulnar deviation at the metacarpophalangeal joint during the test slackens the intrinsics on the ulnar side of the finger and confuses the findings.

• A tight first volar interosseous muscle pulls the extended index finger ulnarward, but if the finger is held in line with the second metacarpal during the test, tightness of this muscle can be shown.

• The first volar interosseous is a flexor and an adductor of the second metacarpophalangeal joint, and usually the first dorsal interosseous is an abductor only.

Test for tightness of oblique retinacular ligament. Proximal interphalangeal joint held in maximal extension by examiner. Resistance to passive flexion of distal interphalangeal joint is

evaluated

CORRECTION

• Sx - release of intrinsic tightness + synovectomy +/- arthroplasty/bone resection

2.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.

Swan-neck deformity. 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

Fixed rheumatoid swan-neck deformity, with proximal interphalangeal joint hyperextension and distal interphalangeal joint flexion

• This deformity may begin as a mallet deformity associated with a disruption of the extensor tendon at the distal joint with secondary overpull of the central tendon, causing hyperextension of the lax proximal interphalangeal joint. The proximal interphalangeal joint may actively flex normally.

• This deformity also may begin at the proximal interphalangeal joint because synovitis causes herniation of the capsule, tightening of the lateral bands and central tendon, and eventual adherence of the lateral bands in a fixed dorsal position, so they can no longer slide over the condyles when the proximal interphalangeal joint is flexed

• This limits proximal interphalangeal flexion. The dorsally and centrally displaced lateral bands become relatively slack and may be ineffective in extending the distal interphalangeal joint, which may secondarily assume a mallet deformity without actual rupture of the central tendons. This mallet deformity usually is not as severe, however, as that produced by a rupture of the central tendons.

•

• A swan-neck deformity may require synovectomy of the proximal interphalangeal joint, mobilization of the lateral bands, and release of the skin distal to the proximal interphalangeal joint. Wrinkles and normal laxity of the skin are lost at the level of the proximal interphalangeal joint after several weeks

• Nalebuff, Feldon, and Millender categorized swan-neck deformities into four types and recommended appropriate treatment plans for each type

• Type I deformities are flexible and require dermodesis, flexor tenodesis of the proximal interphalangeal joint, fusion of the distal interphalangeal joint, and reconstruction of the retinacular ligament.

• Type II deformities are caused by intrinsic muscle tightness and require intrinsic release in addition to one or more of the aforementioned procedures.

• Type III deformities are stiff and do not allow satisfactory flexion, but do not have significant joint destruction radiographically. These deformities require joint manipulation, mobilization of the lateral bands, and dorsal skin release.

• Type IV deformities have radiographic evidence of destruction of the joint surface and stiff proximal interphalangeal joints, which usually can be best treated with arthrodesis of the proximal interphalangeal joint or, in the ring and small fingers, with Swanson implant arthroplasty of the proximal interphalangeal joint.

• Kiefhaber and Strickland found that dorsoproximal interphalangeal capsulotomy and lateral band mobilization improved interphalangeal flexion by changing the arc of motion of the proximal interphalangeal joint

NALEBUFF AND MILLENDER TECHNIQUE

• FOR CORRECTION OF SWAN NECK • DEFORMITY• Begin a slightly curved dorsal incision at the

midportion of the proximal phalanx, continue it distally from this point over the dorsolateral aspect of the proximal interphalangeal joint and over the middle of the middle phalanx, and traverse obliquely dorsally to form the tail of a J (Fig. 70-16A

Nalebuff and Millender technique for correction of swan-neck deformity. Skin incision is shown curved to permit release of contracted skin. Incision should not be completely sutured. Lateral

tendons are mobilized by two longitudinal releasing incisions, and joint is flexed

• Elevate the skin carefully, taking with it the veins• Make a longitudinal incision between each lateral

band and the central tendon, releasing them from their fixed dorsal position

• Passively flex the proximal interphalangeal joint to observe that the lateral bands now slip volarward, sliding over the condyles of the joint

• A synovectomy can now be done, and good passive motion usually is established unless there is a bulging synovitis of the flexors

• Suture the skin incision proximally. Distally suturing may not be possible; the distal incision, being placed obliquely across the middle phalanx, gapes open and accomplishes a skin release. If the distal portion of the skin incision is sutured routinely, it might contribute again to hyperextension of the joint. The open portion of the incision usually heals without a graft in about 2 weeks

• Ensure in the preoperative evaluation that active motion can be established by evaluating active flexion of the joint by the profundus and sublimis tendons. When active flexor function is not confirmed, check the tendons by making an incision in the palm and pulling on the tendons through the palm to see that they are not stuck and are not held by rheumatoid nodules.

• Pass a Kirschner wire across the proximal interphalangeal joint to maintain this joint in flexion postoperatively for approximately 3 weeks. During this time, the open portion of the skin wound should close.

• Beckenbaugh observed that flexor tenosynovitis results in ineffective support by the flexor digitorum superficialis tendon and may be an important factor in initiating the development of swan-neck deformity in the rheumatoid hand.

• Every patient in his series had tenosynovitis with adherence of the superficialis tendon, preventing the tendon from stabilizing the proximal interphalangeal joint against hyperextension.

•

• The overpull of the central tendon, combined with synovitis of the proximal interphalangeal joint, stretches the surrounding tissue, resulting in a swan-neck or hyperextended position

• If there is marked hyperextension at the proximal interphalangeal joint and a normal radiographic appearance with maintenance of a normal joint space, tenodesis with the flexor sublimis tendon can be combined with release of the lateral bands and the distal skin

Beckenbaugh technique for correcting hyperextension deformity of proximal interphalangeal joint

• If there is marked proximal interphalangeal joint extension associated with joint destruction on radiographs, arthrodesis may be best if there is a near-normal metacarpophalangeal joint, or if metacarpophalangeal joint resection arthroplasty is anticipated.

• Numerous fixation techniques have been described to obtain successful proximal interphalangeal joint arthrodesis in arthritic joints, including a single Kirschner wire, crossed Kirschner wires, intraosseous wiring, bone pegs, polypropylene pegs, miniplates, compression plates, tension bands, and Herbert screws

3.Buttonhole, or Boutonnière, Deformity

• buttonhole deformity has a flexed proximal interphalangeal joint, with a hyperextended distal interphalangeal joint.

• It is commonly seen in patients with rheumatoid arthritis, although this tendon imbalance is not unique to rheumatoid disease. In a patient with rheumatoid arthritis, 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.

• 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.

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.

Nalebuff and Millender categorized buttonhole deformities on the basis of the radiographic appearance of the joint surface and the amount of active and passive motion

Mild buttonhole deformities• there is a flexion deformity at the proximal

interphalangeal joint with lessened ability to flex the distal joint fully, but the joint is not fixed in hyperextension.

• The flexion deformity at the proximal interphalangeal joint is passively correctable from a position of approximately 15 degrees of flexion.

• In these deformities, treatment may consist of releasing the lateral tendons near their insertion into the distal phalanx

• Moderate buttonhole deformity• has an approximately 40-degree flexion

contracture of the proximal interphalangeal joint, most of which is passively correctable. The distal joint is hyperextended, and usually the metacarpophalangeal joint is correctable to full flexion passively. The lateral bands are fixed in their subluxated position volarward by virtue of the contracted transverse retinacular ligament.

• To correct this deformity, there must be functional restoration of the central slip and correction of the subluxation of the lateral bands. Radiographs of these joints should show no severe joint destruction.

• If the metacarpophalangeal joint is destroyed and fixed, but the interphalangeal joint is preserved, this deformity can be treated with metacarpophalangeal joint arthroplasty or fusion

Severe or fixed buttonhole deformity• usually has joint changes on radiographs and a

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.

• Kiefhaber and Strickland found central extensor tendon reconstruction for rheumatoid boutonnière deformities unpredictable and recommended arthrodesis for severe boutonnière deformities

• The mildest deformities, with satisfactory motion and normal-appearing radiographs, can be treated with repositioning of the lateral band portion of the extensor mechanism, proximal interphalangeal joint synovectomy, and extensor tenotomy over the middle phalanx (Dolphin-Fowler procedure).

• For moderate deformities with a passively correctable proximal interphalangeal joint, normal flexor tendon function, and satisfactory preservation of joint space radiographically, a soft-tissue procedure with central slip reconstruction using the lateral band or a tendon graft is an option.

For severe deformities with stiff joints, the long, ring, and little fingers can be treated with extensor reconstruction and Silastic implant arthroplasty; in the index finger, arthrodesis of the proximal interphalangeal joint may suffice

• Arthroplasty of the proximal interphalangeal joints of the ring and little fingers may be done when there are near-normal metacarpophalangeal joints proximally

• Swanson advised proximal interphalangeal joint resection arthroplasty and implant for the index finger when the deformity is singular and severe. If the proximal interphalangeal joints of the index and middle fingers are involved, arthrodesis of the joint of the index finger and resection arthroplasty of the joint of the middle finger may be indicated.

• This procedure gives a more stable index finger for pinch and permits flexion of the middle finger for grasp. Resection arthroplasty for the ring and little fingers also can be done when indicated. If the joint contracture is so tight that extensive bone resection is required for satisfactory placement of the implant, arthrodesis should be considered

Deformities of the Distal Joint

• The rheumatoid deformities at the distal joint include a mallet, hyperflexed distal interphalangeal joint (Fig. 70-22), which may occur in conjunction with a swan-neck deformity or as a result of attenuation of the terminal central slip of the extensor tendon, and a hyperextensible distal interphalangeal joint, which also may be related to attenuation of capsuloligamentous structures or to flexor tendon rupture.

• Usually either of these deformities can be treated with distal interphalangeal joint arthrodesis. In a patient who has had a proximal interphalangeal joint arthrodesis, the distal interphalangeal joint mallet deformity might be left untreated because the small amount of mobility remaining in the distal interphalangeal joint can contribute significantly to fingertip function

mallet finger in long finger

4.Ulnar Drift or Deviation of the Fingers

• The deformity of ulnar drift or deviation of the fingers (Fig. 70-23) is found in conditions other than rheumatoid arthritis.

• In the normal hand, factors are• (1) the ulnar deviation of the phalanges at the metacarpophalangeal

joints, especially of the index finger;• (2) the small and sloping ulnar condyle of asymmetrical metacarpal

heads, especially those of the index and middle fingers;• (3) the approach from the ulnar direction of the long flexor and extensor

tendons to the metacarpophalangeal joints; • (4) the greater ulnar deviation than radial deviation of the digits

permitted by the radial collateral ligaments when the metacarpophalangeal joints are flexed; and

• (5) the greater strength of the abductor digiti quinti and flexor digiti quinti than of the third volar interosseous

• Factors found in the rheumatoid hand are• (1) stretching of the collateral ligaments of the

metacarpophalangeal joints by the volarly directed forces of the flexor tendons, permitting volar displacement of the proximal phalanges;

• (2) stretching of the accessory collateral ligaments that permits ulnar displacement of the flexor tendons within their tunnels;

• (3) stretching of the flexor tunnels that permits even more ulnar displacement of the long flexor tendons;

• (4) ulnar displacement of the long flexor tendons caused by surgical release of their sheaths for multiple trigger fingers or for improving strength of grasp by changing their angle of approach to the fingers;

• 5) contracture of the interosseous muscles that causes (in addition to ulnar deviation of the digits) hyperextension of the proximal interphalangeal joints, flexion, and eventually subluxation of the metacarpophalangeal joints and eventually subluxation of these latter joints;

• (6) attenuated radial sagittal bands that allow ulnar displacement of the long extensor tendons, further increasing their deforming influence (this displacement is caused by ineffective radial sagittal bands);

• (7) rupture of long extensor tendons at the distal edge of the dorsal carpal ligament that increases the possibility of dislocation of the metacarpophalangeal joints.

Ulnar deviation of fingers in rhuematoid arthritis

Subluxation of metacarpophalangeal joints of fingers in severe rheumatoid arthritis. B, Subluxations have been treated by resecting metacarpal heads. Because at surgery

articular cartilage of joints was eroded, intrinsic release would have been insufficient treatment

Severe Ulnar Drift and Metacarpophalangeal Dislocation

• In severe ulnar drift, often one or more metacarpophalangeal joints have dislocated (Fig. 70-27); consequently, this type of drift and dislocation of these joints are discussed together.

• Here the dislocation of the metacarpophalangeal joint in effect has released the soft-tissue structures that cross the joint and by decreasing tension has protected, at least partially, the proximal interphalangeal joint

• .

• . Conversely, if the proximal interphalangeal joint dislocates first, the metacarpophalangeal joint is partially protected. Because of the deforming forces mentioned earlier in this section, the metacarpophalangeal joints would have deviated ulnarward more and more

• For this type of ulnar drift, surgery is done mainly on the metacarpal head and its surrounding ligaments and tendons

Metacarpophalangeal dislocation in rheumatoid arthritis

Extensor Tenosynovitis

• Although it usually is relatively painless, tenosynovitis of the extensors of the digits and wrist causes visible swelling over the dorsum of the wrist with an area of constriction at the extensor retinaculum. One or all extensor tendons may be affected by rheumatoid tenosynovitis, which weakens the tendon and may lead to tendon rupture.

• Nonoperative treatment with medication and corticosteroid injections may lead to resolution of the tenosynovitis. Because of the possibility of extensor tendon rupture, extensor tenosynovectomy usually is recommended if there has been no improvement in the tenosynovitis with 6 months of nonoperative treatment.

RHEUMATOID DEFORMITIES OF THE WRIST

Synovitis of the Wrist • Often, the dorsum of the wrist is the location of the

first painful swelling in rheumatoid arthritis. The tenosynovial swelling may contribute to de Quervain disease, trigger finger, or carpal tunnel syndrome, whereas rheumatoid arthritis as the underlying cause may not be suspected.

• The swelling may begin as a small soft mass at the distal end of the ulna; radiographs may reveal a small pit at the base of the ulnar styloid as the first radiographic evidence of the disease.

• The synovitis can spread and cause massive swelling in the shape of an hourglass, its middle being constricted by the dorsal carpal ligament. Eventually, destruction of joints may contribute to dorsal subluxation of the distal ulna, ulnar shifting of the carpal bones, radial angulation of the metacarpals, and ulnar deviation of the fingers. Finally, the wrist may subluxate volarly. Tendons, especially those of the three ulnar finger extensors, may rupture

• If the synovitis is only moderate, and if changes in the bones are absent, but pain is significant, dorsal synovectomy of the wrist seems to be of lasting benefit.

• Persistent swelling at the dorsum of the wrist that continues for 6 weeks or longer despite adequate medical treatment may be an indication for a dorsal synovectomy.

• This may be considered a prophylactic measure to avoid rupture of the extensor tendons. Rupture of these tendons is quite disabling, and function can never be restored completely

• Any tendons ruptured at the level of the wrist can be repaired at the time of synovectomy.

• Options include side-to-side anastomosis, free tendon graft, and tendon transfers to bridge a defect in a tendon.

• If synovitis involves the wrist and the metacarpophalangeal joints, synovectomy often can be done at both levels through carefully planned incisions during the same operation, usually only on one limb at a time

• On the volar aspect of the wrist, even slight hypertrophy of the synovium undetectable clinically can cause compression of the median nerve and symptoms of carpal tunnel syndrome.

• . Synovitis is considered one of the most frequent causes of the syndrome.

• Compression of the nerve in rheumatoid arthritis should be relieved surgically if conservative treatment with splinting and steroid injections has been unsuccessful.

• If hypertrophy of the tenosynovium on the volar aspect of the wrist is obvious clinically, with or without symptoms of compression of the median nerve, a palmar (flexor) tenosynovectomy may be useful in relieving pain and in preventing rupture of tendons

Reconstructive proceduresavailable for an arthritic wrist joint include arthrodesis and arthroplasty

Flexor surface, left hand and wrist with rheumatoid tenosynovium bulging to palmar and ulnar (medial) side of distal forearm. B, At flexor tenosynovectomy. Note extension of

incision distally into palm and proximally into forearm. Excised tenosynovial mass lies to medial side of hand

Radiograph of wrist affected by severe rheumatoid arthritis with carpal collapse and radiocarpal disease. B, Film obtained after replacement of

wrist joint with Swanson silicone implant and titanium grommets

Correctly implanted Meuli III wrist prosthesis in 55-year-old woman with rheumatoid arthritis. A, Radiographs before surgery. B, Radiographs 4.5 years after surgery. Note

reconstruction of carpal height and axial alignment. Prosthesis is firmly fixed in carpal bone stock with no palmar protrusion

Long-standing rheumatoid disease and symptomatic wrist arthritis. C and D, Two years after total wrist arthroplasty

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