Plastic surgery





There are multiple overlapping clinical syndromes of inflammatory arthritis, all of which are generically lumped under the diagnosis of “rheumatoid arthritis.” However, these must be distinguished from each other as treatment and prognosis vary. Characteristic clinical features include1,2:

1.  Rheumatoid Arthritis. This is the most common and the most likely to be seen by the hand surgeon. Most cases have an insidious onset with initial symptoms of fatigue, malaise, diffuse musculoskeletal pain, and morning stiffness. Others present with acute onset. Symmetrical involvement is common. For example, if a swan-neck problem occurs in one finger, it is likely to develop in the same finger of the opposite hand. Reasons for this symmetry remain a mystery. Migratory arthritis is uncommon.

By far the most commonly involved joints are the metacarpophalangeal (MP), proximal interphalangeal (PIP), and wrist. Larger joints generally become symptomatic after the small joints. Subcutaneous nodules may occur especially on the extensor aspects of the elbows (Figure 91.1).

2.  Juvenile Rheumatoid Arthritis (JRA) (Figure 91.2). Three types occur—polyarticular, oligoarticular, and systemic illness with fever, rash, and lymphadenopathy (Still’s disease). The polyarthritic type affects primarily the large, rapidly growing joints (knees, wrists, elbows, and ankles). Small joints of the hand and feet are less commonly affected. Temporomandibular joint involvement is common, leading to limitation of bite and micrognathia. The oligoarthritic type most frequently involves isolated knee, ankle, or wrist.

FIGURE 91.1. Rheumatoid arthritis patient with (A) subcutaneous rheumatoid nodules and (B) olecranon bursitis.

3.  Psoriatic arthritis.1 Distal interphalangeal (DIP) joints are predominantly involved. Occasionally, arthritis mutilans occurs with dissolution of bone and radiographic “pencil in cup” joint changes. This gives the telescoping deformity of the fingers (“opera glass hands”) that can only be treated by arthrodeses to restore stability3,4 (Figure 91.3). Some cases may be clinically indistinguishable from rheumatoid arthritis. Ankylosing spondylitis may occasionally occur. Subcutaneous nodules do not occur. There is frequently a circumscribed shiny, exfoliative rash on the extensor aspects of the extremities and pitting of nails.

4.  Systemic lupus erythematosus (SLE).2 Joint involvement is the most common manifestation although systemic involvement is also frequent. Most common joints involved are PIP, MP, wrist, and knee. Deforming erosive arthritis does not occur, and articular surface preservation is commonly seen on radiographs. However, swan-neck deformities and finger ulnar deviation occur and have the clinical appearance of rheumatoid arthritis. Deformities are due to involvement of tendons and ligaments. Vasospastic Raynaud’s phenomenon may occur (Chapter 87). Systemic involvement includes malar rash, sun sensitivity, nail deformities, renal, gastrointestinal, central nervous problems, and lymphadenopathy.

5.  Scleroderma (systemic sclerosis). A small percentage of patients have symmetrical polyarthritis suggestive of rheumatoid arthritis, but are usually seronegative, with nonerosive changes, and without subcutaneous nodules. More commonly there is tight dorsal skin of the fingers and hands with PIP flexion contractures, MP extension contractures, distal bone resorption, with fingertip ulcers. Systemic cardiovascular, pulmonary, renal, and central nervous problems may occur. CREST syndrome (subcutaneous calcinosis, Raynaud’s phenomenon, esophageal hypomotility and strictures,sclerodactyly, telangiectasias) tends to be more indolent and slowly progressive (Figure 91.4).

FIGURE 91.2. Juvenile rheumatoid arthritis. Characteristic radiographic changes of patient with juvenile rheumatoid arthritis. The MP joints are relatively unaffected, but the wrists have become stiff and deformed and undergone autofusion.

FIGURE 91.3. Arthritis mutilans. A. Radiographic phalangeal bone resorption and (B) “telescoping” or “opera glass” deformity of the digits.

6.  Reiter’s disease. There is an association with arthritis, urethritis, eye problems (conjunctivitis and uveitis), and mouth ulcers. Ligament problems lead to Achilles tendonitis, plantar fasciitis, and back pain.

7.  Enteropathic arthritis. Peripheral arthritis may occur with ulcerative colitis and Crohn’s disease. Ankylosing spondylitis may occur.

8.  Ankylosing spondylitis. Peripheral arthritis does not occur, but psoriatic arthritis, Reiter’s syndrome, and enteropathic arthritis may be present. There is an association with HLA–B27 histocompatibility antigen. Low back pain and sacroiliitis are the hallmark. Paraspinal ossification occurs.

FIGURE 91.4. Scleroderma (CREST). Characteristic changes include: A. Subcutaneous calcifications; B. Tight dorsal skin and ulceration over little finger MP joint; C and D. Telangiectasias on hands and in oral cavity.

9.  Mixed connective tissue disease (MCTD). Nearly all patients with MCTD have joint pains and morning stiffness, and 60% develop peripheral arthritis. It is generally not as destructive as rheumatoid arthritis but the appearance of swan-neck deformity and ulnar deviation of fingers is often severe. Unlike SLE, classic joint erosions do occur and some may develop “arthritis mutilans” with severe osteolysis. Systemic pulmonary and gastrointestinal problems occur.

10.  Crystal-induced arthropathy. These include gout (uric acid crystals) and pseudogout (calcium pyrophosphate crystals). The former crystals are needle-like in shape and are negatively birefringent under the polarizing microscope, and the latter are rhomboid in shape and are positively birefringent. Although not pathognomonic for pseudogout, chondrocalcinosis of the triangular fibrocartilage and of the knee meniscus may occur as well as linear calcifications of hyaline cartilage. These conditions may present as acute arthritis or tenosynovitis, but chronic varieties occur with progressive degeneration of multiple joints. The surgeon may be called upon to operate on late-stage tophaceous gout that involves the wrist or fingers. Of importance to the hand surgeon is that these conditions may mimic acute or chronic infections, and even perhaps a tumor (secondary to bone and joint destruction). Gout is often called the “great imitator.”


Synovitis results in distention of the joint. Ligamentous restraints are destroyed and tendon orientation around affected joints is deranged. This results in changed force vectors. Irregular joint articular surface destruction then leads to further joint imbalance. Tendon ruptures may add to the instability. Finally, secondary zigzag deformities occur at the next distal joint:

1.  Finger deformity

a. Swan-neck deformity

Precise tendon balance exists volar and dorsal to PIP and DIP joints (Figure 91.5). The extensor central slip and flexor digitorum superficialis (FDS) insertion together with the volar plate form opposing dorsal and volar force vectors at the PIP joint. The extensor and flexor digitorum profundus (FDP) insertions likewise form opposing vectors at the DIP joint. Additionally, the intrinsic muscles and extensor hood mechanism are in fine balance with the intrinsics acting volar to the fulcrum of flexion of the MP joint and dorsal to the fulcrum of the PIP and DIP joints.

Swan-neck deformity results from disturbances of the volar/dorsal vector balance or from intrinsic muscle imbalance. Correct diagnosis of the specific cause of swan-neck deformity is important to institute correct treatment. Joint distention and stretch of the volar plate or FDS rupture may lead to PIP joint hyperextension. Chronic mallet deformity can also lead to swan-neck problems. Simple placement of an external splint across the DIP joint may be used diagnostically to correct the swan-neck problem in the clinic. If successful, DIP joint fusion may offer a simple solution.

MP joint volar subluxation (a common deformity in rheumatoid arthritis) may also result in swan-neck deformity (Figure 91.6). By clinical examination, one may be able to relocate the MP joint which, in turn, may resolve the swan-neck deformity. In this case, treating the MP joint problem resolves the swan-neck deformity.

FIGURE 91.5. (A, B) Tendon balance. The illustration depicts the balance provided by intrinsic and extrinsic muscle function. A. Intrinsic muscles pass volar to the center of rotation of the MP joint and dorsal to that for the PIP and DIP joints. Thus, they flex the MP joint and extend the IP joints (intrinsic plus). B. If the long extrinsic flexor and extensor tendons are not balanced by the dorsal central slip attachment and the FDS distal insertion at the middle phalanx, or by the intrinsic muscles, then the finger “collapses” at the interphalangeal joints into either a swan-neck or a boutonniere deformity.

FIGURE 91.6. Classic rheumatoid hand deformities showing A. Volar subluxation of MP joints with ulnar deviation. B. Swan-neck deformities. C. Radiographic changes. D. Postoperative radiography after silicone MP joint implant arthroplasties.

Finally, intrinsic tightness is a characteristic problem with rheumatoid arthritis (perhaps secondary to myofibrosis). This can be assessed by the intrinsic tightness test of Bunnell (Figure 91.7). Intrinsic release will resolve the problem (Figure 91.8A). Thus, potential causes of swan-neck deformity are5:

•  Mallet deformity

•  MP joint volar subluxation

•  FDS rupture

•  Intrinsic tightness

•  Volar plate laxity

Sometimes, there may be a combination of factors. Hence, at the time of MP joint surgery, one may simultaneously perform ulnar intrinsic release.

Corrective surgery for the swan-neck deformity is performed for functional reasons. Due to hyperextension at the PIP joint and dorsal “centralization” of the lateral bands, there is difficulty initiating PIP joint flexion. This will be complicated by an uncomfortable or painful snap as one attempts active PIP flexion, eventually leading to a fixed swan-neck deformity. The degree of PIP joint mobility and radiographic appearance of the affected PIP joint serve as the basis of the Nalebuff classification of swan-neck deformities and their treatment6-8:

Type I.  (Full PIP joint flexibility without intrinsic tightness)—Treatment may be nonoperative, using a Silver ring splint. Operative treatment may involve DIP fusion (if the prime pathology is a mallet finger) or flexor tenodesis at the PIP joint. The latter may be accomplished by using a distally based slip of FDS and suturing it around the leading edge of the A1 pulley or securing it into bone at the base of the proximal phalanx (Figure 91.8B and C). One can recreate the tenodesis of the oblique retinacular ligament of Landsmeer. Littler described releasing the ulnar lateral band proximally and rerouting it volar to the PIP joint axis of rotation (using Cleland’s ligament as a fulcrum). In rheumatoid arthritis, this fulcrum tends to stretch with time. A free tendon graft attached distally to the dorsum of the distal phalanx and routed spirally volar to the PIP joint and anchored to the proximal phalanx is a more reliable technique to correct swan-neck deformity9 (Figure 91.8D).

Type II.  (PIP joint flexibility, but with MP joint volar subluxation, and associated intrinsic tightness)—It is insufficient to prevent PIP hyperextension alone. Distal intrinsic release is also required, and possibly also MP joint realignment or even MP implant arthroplasty.

FIGURE 91.7. Intrinsic tightness test of Bunnell. With the MP joint passively extended, stretch is placed on the already tight intrinsic muscles and so passive PIP joint flexion is difficult (top). When the MP joint is passively flexed, PIP joint flexion is easier (bottom).

FIGURE 91.8. Surgical treatment for swan-neck deformity. A. Distal intrinsic release for intrinsic tightness accomplished by excision of the “wing tendons” with the lateral bands. BC. Distally based slip of FDS sewn to A1 pulley or proximal phalanx. D. Tenodesis of oblique retinacular ligament recreated by a spiral oblique retinacular ligament (SORL) reconstruction with free tendon graft.

Type III.  Motion of PIP joint limited by the extensor mechanism, but with radiographic preservation of joint surfaces)—Lateral band releases are necessary so that they can slide volar to the condyles. Lateral bands are sharply released from the central slip by two parallel longitudinal incisions. Occasionally, central slip release or lengthening may be required. PIP joint dorsal capsulotomy may also be required.

Type IV.  (Stiff PIP joint with intra-articular joint destruction).

—A salvage procedure is necessary—either fusion or arthroplasty, with the former being preferred.

b.  Boutonniere deformity

There is unopposed flexion of the PIP joint and secondary hyperextension at the MP and DIP joints occurs. The central slip and triangular ligament undergo stretch attenuation from PIP joint synovitis. The latter results in lateral band migration volar to the PIP joint axis of rotation, so that they become flexors of the PIP joint and extensors of the DIP joint (Figure 91.9). Nalebuff described a three-stage progressive classification of this deformity8,10:

FIGURE 91.9. Pathomechanical changes occurring in boutonniere deformity.

FIGURE 91.10. Surgical treatment of boutonniere deformity. A. Distal extensor tenotomy at triangular ligament. B. Release of transverse retinacular ligaments allows lateral band relocation dorsally.

Stage I.  (Mild PIP extension lag that is passively correctable with some DIP flexion limitation.) Treatment may include PIP extension splinting, allowing DIP flexion; or an open distal extensor tenotomy (Figure 91.10A) may be performed at the distal triangular ligament to improve DIP joint flexion.11

Stage II.  (Moderate PIP flexion deformity greater than 40° that may or may not be passively correctable.) Surgery aims at restoring extensor power to the PIP joint. The first step is longitudinal release of the transverse retinacular ligaments on each side, which allows dorsal migration of the lateral bands (Figure 91.10B). The attenuated central slip is reefed and the lateral bands are relocated dorsally by suturing to each other starting at the distal triangular ligament. Appropriate tension of repair can best be judged by performing the surgery under local anesthesia so that the patient can actively participate intraoperatively with gentle active finger flexion and extension. The terminal tendon is then assessed for residual tightness and released by tenotomy if necessary. The PIP joint is stabilized in extension with a Kirschner wire postoperatively but free active DIP joint range of motion is allowed. After three weeks, PIP joint range of motion is begun with intermittent extension splinting. If there is mild fixed flexion contracture, preliminary serial casting may be required before surgical correction or the volar plate may require release at the time of operative correction.

Stage III.  (Fixed PIP flexion deformity with joint destruction.) PIP joint fusion is generally favored.

2.  Thumb deformities

These deformities less commonly involve a side-to-side instability at either the MP or interphalangeal (IP) joints—generally on the ulnar side, resulting from lateral stresses with thumb pinch (Figure 91.11). These may necessitate ulnar collateral ligament reconstruction with a tendon graft, adductor release of the first web space, and sometimes even fusion. This is often associated with an MP joint flexion deformity as well.

More commonly, boutonniere or swan-neck deformities occur. There may be swan-neck deformity with MP joint hyperextension, but the most common thumb deformity is MP joint flexion and reciprocal IP joint hyperextension (boutonniere deformity). The latter begins with MP joint synovitis that attenuates the dorsal extensor mechanism causing the extensor pollicis longus (EPL) to subluxate ulnarly and, together with the intrinsics, to migrate volar to the joint axis of flexion.12 This deformity is perpetuated with thumb pinch activities. With time the MP flexion becomes fixed.

FIGURE 91.11. Lateral thumb instability.

When MP and IP joints are flexible, and the flexion deformity is mild, Nalebuff described releasing the EPL distally to the MP joint and rerouting it through the distally attached dorsal MP joint capsule flap and back on its self, providing extra MP joint extension force12 (Figure 91.12). The two sides of the extensor mechanism must then be sutured back to each other to restore IP joint active extension. This author prefers to anchor the rerouted EPL distally to the dorsal base of the proximal phalanx with a bone anchor, perhaps reducing the reputation that this procedure has for relapse when relying only on the soft tissues of the dorsal MP joint capsule.

FIGURE 91.12. Collapsing thumb boutonniere deformity. A. Preoperative appearance. B. EPL rerouted through distally based MP capsule flap for improved MP extension. C. Follow-up functional result.

In later stages, MP joint (and sometimes also IP joint) fusion is required—which is tolerated because the carpometacarpal joint in rheumatoid arthritis (unlike the case in lupus arthritis) is generally stable and motion is preserved.

3.  Finger MP joint deformity

The deformity at the MP joint results in:

•  Palmar subluxation.

•  Ulnar deviation.

These deformities result from a multitude of causes.5 Normal MP joint kinematics allow for slight finger ulnar deviation, but in rheumatoid arthritis, balanced support around the joint is lost and there is overpull of flexor tendons and intrinsic muscles, resulting in the classic flexion and ulnar deviation (Figures 91.13A and B). Additionally, as the wrist collapses and translates ulnarward, the metacarpals deviate radially, accentuating the ulnar pull of both the flexor and extensor tendons. Thus, any wrist deformity must always be corrected before the MP joint.13

As synovitis progresses, the radial sagittal bands weaken, allowing further ulnar migration of extensor tendons between the metacarpal heads. There is also synovial stretch of the flexor tendon sheath, resulting in volar and ulnar bowstringing of the flexor tendons. All of these unbalanced vectors result in an ulnar sweep of the fingers and an inability to “open” the hand around grasped objects, sometimes, for example, requiring two hands to pick up a cup or glass. The deforming forces at the MP joint are thus summarized as5:

•  Radial deviation and ulnar translation of carpus/metacarpals.

•  Ulnar and volar change in the flexor vectors.

•  Ulnar migration of the extensor tendons.

•  Ulnar intrinsic tightness.

Surgery at the MP joints is aimed at stabilizing the joint, decreasing pain, improving appearance, and increasing function. Even when the range of motion is not increased, the flexion arc is changed, bringing that arc into a more functional extended range.

If the articular surfaces are not destroyed and if the flexed deformity is not excessive (and especially if it can be passively corrected), then soft tissue rebalancing alone is performed. This may involve volar plate release, but most especially requires joint synovectomy, extensor tendon centralization, and radial sagittal band imbrication, with ulnar intrinsic release and so-called crossed intrinsic transfer (in which the released ulnar intrinsic is transferred across to the radial side of the next adjacent ulnar digit—generally now attached directly into the bone at the base of the proximal phalanx with a bone anchor) (Figure 91.14).

For advanced MP joint disease (and generally also for the instability that occurs with lupus arthritis in spite of articular preservation),16 silicone interposition arthroplasty is the treatment of choice17(Figure 91.15A). The amount of bone resection, to a degree, governs the flexibility achieved at the MP joint. Simultaneous rebalancing of extensor tendons, together with volar plate and ulnar intrinsic release, is usually required. Postoperative positioning and dynamic splinting with great attention to prolonged and meticulous therapy is needed (Figure 91.15B).

A flexible but strong capsule forms around the silicone implant and adds to its stability. Implant pistoning during flexion enhances joint motion.18 There is significant improvement in pain, appearance, and function at 1 year.19,20 However, results tend to deteriorate over time.17 Nonetheless, secondary replacement implant arthroplasty can be expected to meet with similar good outcomes to the primary surgery.

FIGURE 91.13. Classic flexion and ulnar drift of digits at MP joints. A. Clinical appearance. B. Loss of soft tissue support results in subluxation of flexor tendons ulnarly.

Pyrolytic carbon arthroplasty has recently been promoted, but cannot be used for dislocated joints or when there is significant cortical bone loss.

If there is also a problem at the PIP joint, one may be compelled to fuse that joint, especially if it has a fixed deformity.13

4.  Wrist deformities

a.  Radiocarpal joint and progressive carpal arthritis.

The caput ulnae syndrome is a frequent clinical appearance in rheumatoid arthritis. There are carpal supination and volar/ulnar translation of the carpus that result in the appearance of a more prominent dorsal distal ulna head. Actually, the ulna keeps its anatomic position and the carpus dislocates away from the ulna.5

A sequence of events in the ligaments of the wrist is initiated as they become attenuated by the synovial swelling. The radioscapholunate and scapholunate ligaments weaken with radiocarpal inflammation, leading to scaphoid rotatory subluxation and scapholunate dissociation. Further loss of integrity of the radioscaphocapitate and radiolunate ligaments results in loss of carpal height together with volar and ulnar translation of the wrist. Finally, carpal supination results from laxity of the ulnocapitate and ulnolunate ligaments (Figure 91.16). Adding to this instability, the extensor carpi ulnaris (ECU), which is a natural stabilizer of the distal ulna, subluxates in an ulnar and volar direction and becomes an ulnocarpal flexor. Thus, the main wrist deformities are5,21:

•  ECU translation.

•  Scaphoid rotatory dissociation and scapholunate instability.

•  Carpal height collapse.

•  Ulnar and volar translation of the carpus.

•  Carpal supination.

•  Dorsal distal ulnar prominence.

If the disease is located chiefly in the radiocarpal joint with midcarpal sparing, then a limited radioscapholunate fusion can be done22 (Figure 91.17). This helps with pain relief, prevents carpal ulnar translation, and maintains some wrist flexion and extension at the midcarpal joint. Interestingly, it has been noted in the natural course of rheumatoid arthritis that if spontaneous radiolunate fusion occurs, then midcarpal arthritis progression is spared.

Unfortunately, by the time most rheumatoid patients present to the hand surgeon, pan-arthritis has occurred with pain on wrist flexion and extension, carpal collapse, and ulnocarpal impaction.The “gold standard” for treatment of these patients has been a total wrist fusion, with distal ulnar resection and ligamentous stabilization of the distal ulna23 (Figure 91.18). This gives consistent pain relief and provides a stable base for power grip. An intramedullary pin was described for use in wrist fusion in rheumatoid patients, especially where bone stock and thin skin would prevent use of the older types of more high-profile plates.24 This, however, fuses the wrist in a neutral position, which is a somewhat disadvantaged functional position for power grip. Newer, lower profile, specifically designed, and angled wrist fusion plates facilitate wrist fusion in these patients.21,23 The ulna head (excised during the simultaneous Darrach procedure) provides the source for bone graft for the fusion.

FIGURE 91.14. Soft tissue correction of finger ulnar deviation. Ulnar intrinsic release followed by transfer to radial side of adjacent digit (crossed intrinsic transfer) together with centralization of the extensor mechanism.

FIGURE 91.15. MP joint silicone interposition arthroplasty. A. Intraoperative image. B. Postoperative dynamic splinting.

FIGURE 91.16. Rheumatoid arthritis changes at the wrist. Volar and ulnar translation of the wrist with progressive supination occurs as the restraining ligaments are successively disrupted.

FIGURE 91.17. Radioscapholunate fusion with preservation of midcarpal joint.

FIGURE 91.18. Total wrist arthrodesis with plate fixation and distal ulna resection.

Even patients who require bilateral wrist fusion do well provided that they have good elbow and shoulder function.25 Distal ulna resection frequently improves forearm pronation and supination. Wrist fusion also enables simultaneous prophylactic surgical measures to prevent spontaneous extensor tendon ruptures such as extensor synovectomy, correcting the caput ulnae, reducing the prominent radial Lister tubercle, and transposing the extensor retinaculum deep to the extensor tendons.26

Total wrist arthroplasty has undergone major technological advancements recently, and while it spares wrist motion, complication and revision rates remain high.21

b.  Distal radioulnar joint (DRUJ)

The DRUJ is affected early in the natural history of rheumatoid arthritis because of the synovial-rich prestyloid recess. Volar and dorsal radioulnar ligaments and the triangular fibrocartilage complex become attenuated. The ECU subluxates. All of these lead to ulnocarpal instability.27,28

Distal ulna instability alone can be treated with ulna head resection (Darrach procedure) and is favored for the elderly and lower demand wrist. Ulna head resection must be performed right at the sigmoid notch. This helps maintain stability of the resected ulna because the attachments of pronator quadratus are spared. A distally based strip of ECU can further stabilize the distal ulna.29Darrach procedure (without at least a simultaneous partial wrist arthrodesis) should be avoided if there is any evidence of carpal ulnar translation. The Darrach procedure provides predictable pain relief, with few complications (such as radioulnar impingement).27,28

The Sauve-Kapandji procedure creates a distal radioulnar fusion, and a more proximal ulna pseudoarthrosis for maintenance of forearm pronation and supination by resecting a segment of the ulna. This procedure is generally preferred over the Darrach resection in younger, more active patients because it maintains the buttressing effect of the ulna head, perhaps retaining better hand strength. It does not, however, totally prevent progressive further carpal volar and ulnar translation.

Some favorable results with prosthetic distal ulna head replacement in the rheumatoid patient have been reported, though less frequently performed than in the osteoarthritis patient because of the loss of adequate ligamentous and soft tissue structures around the distal ulna.28


Spontaneous tendon ruptures may occur from:

•  Attrition on sharp bony angular prominences.

•  Direct proliferative synovial invasion.

•  Weakening of tendons from high-dose systemic corticosteroids or direct steroid injection.

Most commonly, direct synovial tendon invasion and rupture occurs where there is a rich synovial environment such as in the extensor tendons at the wrist and in the flexor tendons in the digital flexor tendon sheath or the carpal tunnel. Flexor tendon ruptures can be mistaken for anterior interosseous nerve palsy and extensor tendon ruptures for posterior interosseous nerve palsy (both of which may occur in rheumatoid patients secondary to synovial cyst pressure on these nerves at the elbow and proximal forearm).30 Tendon ruptures are distinguished from nerve palsy because patients with tendon ruptures do not demonstrate reciprocal tenodesis of the fingers when the wrist is passively flexed or extended.

The most common attrition rupture occurs at the distal ulnar prominence and starts with the little finger and progresses radialward if untreated. This is the caput ulnae (or Vaughan-Jackson) syndrome31(Figure 91.19A). The distal ulna must be resected or stabilized, extensor synovectomy performed, and the retinaculum transposed. A single tendon rupture can be repaired by suturing to the adjacent finger extensor (Figure 91.19B). If extensor tendons to the three ulnar digits have ruptured, then EIP can be transferred to the ring and little fingers and the middle finger EDC sutured to that of the index. However, if all EDC tendons are ruptured, then a formal tendon transfer (such as flexor carpi radialis transfer) is required because the EIP alone is not sufficient to power all four fingers.26

Another confusing clinical picture for an extensor tendon rupture may occur if there is sagittal band attenuation, causing the extensor tendon to subluxate ulnarly at the MP joint. A clue that this is the case is that one can still see and palpate subcutaneous tension in the extensor tendon when attempting to actively extend the digit. More particularly, if the digit is passively positioned in extension, the patient can then actively maintain that position, but once the MP is flexed, then active extension cannot be initiated.

The EPL may rupture around the sharp fulcrum edge of Lister tubercle on the distal dorsal radius (Figure 91.20). There is generally not only loss of active thumb IP joint extension, but also of the MP joint. There is inevitably a tendon gap due to the frayed tendon ends. Although an interposition tendon graft may be performed, EIP tendon transfer to thumb extension is generally the preferred surgical treatment.

FIGURE 91.19. Caput ulnae syndrome. A. Extensor tendon ruptures. B. Extensor tendon side-to-side transfer with distal ulna resection and stabilization, extensor synovectomy, and retinacular transposition.

FIGURE 91.20. EPL rupture due to prominence of Lister’s tubercle.

Finally, flexor tendon rupture may occur on an exposed scaphoid tubercle deep in the carpal tunnel (Mannerfelt syndrome).32 First, there is inability to flex the thumb IP joint, followed sequentially by ruptures of the FDP tendons from radial to ulnar if not treated promptly (Figure 91.21). Carpal tunnel exploration must be performed to remove the sharp bony prominence and to cover that bone surface with a volar wrist capsular flap. FPL tendon rupture can be treated by tendon graft or transfer or even by IP joint fusion if that joint is already damaged by arthritis. FDP rupture is simply repaired by suturing to the adjacent uninjured FDP tendon.


Careful preoperative evaluation and necessary consultations may be required prior to surgery:

•  Assessment of cervical spine stability both clinically and radiographically. Use of a pharyngeal airway may be preferred to avoid potential neck hyperextension during placement of an endotracheal tube. Sometimes, fiberoptic intubation may be necessary.

•  Temporomandibular joint involvement and micrognathia (especially in JRA) may necessitate plans for nasotracheal or fiberoptic intubation.

•  Other associated illnesses such as pulmonary fibrosis and pulmonary hypertension and splenomegaly with neutropenia (Felty syndrome) may coexist.

•  Though a variety of newer disease-modifying medications are now more successful at treating rheumatoid arthritis, they may also interfere with postoperative wound healing and increase the possibility of surgical site infection. Methotrexate, although potentially harmful for large joint surgery, can be safely used perioperatively for hand surgery without the need to skip any doses.33 Anti-TNF (tumor necrosis factor) medications should be withheld (the dose preceding and possibly the dose following surgery) or the surgery is performed just before the regularly scheduled dose and then omitting that specific dose. All such treatment decisions are made in consultation with the rheumatologist.

FIGURE 91.21. Mannerfelt syndrome. A. FDP and FPL tendon ruptures showing inability to flex thumb and index finger. B. Sharp exposed scaphoid tubercle which resulted in tendon attrition ruptures.

•  Be aware of carpal tunnel syndrome (median nerve compression from hypertrophic synovium), which may require carpal tunnel release (with or without flexor synovectomy) either prior to or in conjunction with other hand surgical procedures.

In prior years, medical treatment of rheumatoid arthritis began with the least toxic medications, such as nonsteroidal anti-inflammatories, and then disease-modifying medications such as gold, methotrexate, cyclophosphamide, and glucocorticoids were added in the more recalcitrant cases. However, there has been a paradigm shift, especially with the development of newer biological response-modifying medications.34 Current teaching is that soon after the diagnosis is made, one starts with disease-modifying medications such as methotrexate alone or in combination with infliximab (Remicade), adalimumab (Humira), etanercept (Enbrel) (all anti-TNF-α medications), or anakinra (Kineret) (interleukin-1 receptor agent). Once remission is noted, doses can be tapered. Glucocorticoids may be used during flares. Early initiation of this therapy leads to improved long-term outcome and decreased joint destruction.


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4.  Rose JH, Belsky MR. Psoriatic arthritis in the hand. Hand Clin. 1989;5:137-144.

5.  Flatt AE. The Care of the Arthritic Hand. 5th ed. St. Louis, MO: Quality Medical Publishing, Inc.; 1995.

6.  Nalebuff EA. The rheumatoid swan-neck deformity. Hand Clin. 1989;5: 203-214.

7.  Nalebuff EA, Millender LH. Surgical treatment of the swan-neck deformity in rheumatoid arthritis. Orthop Clin North Am. 1975;6:733-752.

8.  Boyer MI, Gelberman RH. Operative correction of swan-neck and boutonniere deformities in the rheumatoid hand. J Am Acad Orthop Surg. 1999;7:92-100.

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