Mark Wilczynski, Martin I. Boyer, and Fraser J. Leversedge
DEFINITION
Rheumatoid arthritis is a poorly understood systemic disease affecting the synovium of joints and tendon sheaths. The synovial tissue in rheumatoid arthritis is characterized by a proliferation of synovial lining cells, angiogenesis, and relative lymphocytosis.14
A combination of cartilage degeneration, synovial expansion and periarticular erosion, and ligamentous laxity creates an imbalance within the extrinsic and intrinsic tendon systems of the digit to cause progressive deformity.
A boutonnière (“buttonhole”) deformity involves disruption of the central slip. It results in a characteristic deformity involving hyperextension at the metacarpophalangeal (MCP) joint, flexion at the proximal interphalangeal (PIP) joint, and hyperextension at the distal interphalangeal (DIP) joint.
Swan-neck deformity is characterized by hyperextension of the PIP joint and flexion of the DIP joint. MCP joint flexion may also be present.
In the posttraumatic setting, it results from laxity of the PIP joint volar plate and inability of the terminal slip to extend the DIP joint.
Chronic deformity may be associated with progressive digital contracture.
Classification
Rheumatoid thumb deformity26,33
Type I: Boutonnière deformity: MCP joint flexion and interphalangeal joint hyperextension. Carpometacarpal (CMC) joint is not primarily involved.
Type II: Rare; a combination of types I and III involving MCP joint flexion and interphalangeal joint hyperextension and associated CMC joint subluxation or dislocation
Type III: Swan-neck deformity: MCP joint hyperextension, interphalangeal joint flexion, and thumb metacarpal adduction, resulting from progressive CMC joint pathology
Type IV: Gamekeeper's deformity. Attenuation of the ulnar collateral ligament of the thumb MCP joint results in radial deviation through the MCP joint and secondary metacarpal adduction deformity or contracture.
Type V: Results from attenuation of the MCP volar plate with progressive MCP joint hyperextension and secondary interphalangeal joint flexion. There is no metacarpal adduction deformity.
Boutonnière deformity
Stage I—mild: PIP joint synovitis and a mild, fully correctable extension lag
Stage II—moderate: Marked flexion deformity of the PIP joint, either flexible or fixed
Stage III—severe: PIP joint articular destruction
Swan-neck deformity
Type I: PIP joint is fully mobile and flexible.
Type II: Active and passive motions of the PIP joint are limited, with the MCP joint held in extension due to intrinsic tightness.
Type III: Decreased PIP joint motion in all positions of MCP joint flexion and extension
Type IV: Fixed PIP joint hyperextension with advanced destruction of the PIP joint articular surfaces
ANATOMY
Bone and Joint
The MCP joint is a condyloid joint with average range of motion from 15 degrees hyperextension to 90 degrees flexion.
A cam effect for collateral ligaments is due to the shape of the metacarpal head; collateral ligaments are taut with MCP joint flexion and lax with MCP joint extension.
The PIP joint (FIG 1A) is a hinge joint with greater inherent osseous stability than the MCP joint due to the configuration of the two condyles of the head of the proximal phalanx, which articulates with the median ridge at the base of the middle phalanx.
The collateral ligaments are taut throughout the joint arc of motion.
The volar plate is a thick, fibrocartilage structure that serves to resist PIP joint hyperextension; the volar plate originates within the A2 pulley on the proximal phalanx and inserts into the “rough area” at the base of the middle phalanx.
The DIP joint is stabilized by the collateral ligaments, the terminal extensor tendon insertion, the flexor digitorum profundus insertion, and the volar plate.
FIG 1 • A. Proximal interphalangeal (PIP) joint relationships. The flexor tendons (flexor digitorum superficialis [FDS] and profundus [FDP]) have been removed from the proximal digital flexor sheath at the A2 pulley. The FDP and FDS tendon orientation is demonstrated before they re-enter the flexor sheath at the A4 pulley. The PIP joint collateral ligament (cl) and the insertion of the central slip (cs) at the dorsal base of the middle phalanx have been reflected distally to highlight the volar plate (vp) and its proximity within the flexor sheath. P1, proximal phalanx; P2, middle phalanx. (continued)
FIG 1 • B. (continued) The dorsal digital extensor apparatus is derived from contributions of the extrinsic extensor tendons and the intrinsic musculature of the hand. The extrinsic extensor tendon (Ext) is identified at the level of the distal hand and splits into two lateral slips (LS) and the central tendon slip (CS). At the dorsal metacarpophalangeal (MCP) joint the extensor tendon is stabilized by the vertically orientated fibers of the sagittal band (sb), which originate from the radial and ulnar sides of the volar plate of the MCP joint and the volar base of the proximal phalanx. The MCP joint is extended via a sling-like mechanism of the sagittal band as there is no direct fiber insertion from the extrinsic extensor tendon at the proximal phalanx. The deep head of the interosseous muscle (IOM) courses superficial to the sagittal band (sb) at the level of the MCP joint and runs parallel and distal to the sagittal band over the proximal phalanx to form the transverse fibers (T) of the extensor apparatus. The lumbrical muscle (L) on the radial aspect of the digit forms the oblique fibers (O) of the extensor apparatus, which join with the lateral slip of the extrinsic extensor tendon to form the conjoined lateral band. C. The extrinsic extensor tendon divides into a central slip (CS) and two lateral slips. The central slip inserts at the dorsal base of the middle phalanx to extend the PIP joint, and the two lateral slips receive contributory fibers from the lumbricals via oblique fibers of the extensor hood to form the conjoined lateral bands (clb). These conjoined lateral bands coalesce to form the terminal tendon (TT), which inserts at the dorsal base of the distal phalanx to extend the distal interphalangeal joint. The triangular ligament (TL) stabilizes the conjoined lateral bands from volar subluxation. D. Lateral view of the digit demonstrating the coalescing fibers of the lateral slip (LS) and oblique fibers of the extensor apparatus (O), which combine to form the conjoined lateral band (clb). The two conjoined lateral bands combine to form the terminal tendon (TT), which inserts into the dorsal base of the distal phalanx. The transverse retinacular ligament (TRL) prevents dorsal subluxation of the lateral bands. The oblique retinacular ligament (ORL) passively links the proximal and distal interphalangeal joints as it travels from volar to dorsal from the fibro-osseous gutter (middle third of the proximal phalanx and A2 pulley) to the proximal aspect of the distal phalanx through the extensor tendon. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
Dorsal Restraining Structures of the Digit (FIG 1B–D)
The sagittal bands originate on both sides of the MCP joint, from the volar plate and the base of the proximal phalanx, and insert into the lateral margins of the extensor tendon over the dorsal MCP joint.
They stabilize the extrinsic extensor tendon over the MCP joint to prevent lateral subluxation.
They contribute indirectly to MCP joint extension and prevent extensor bowstringing.
The triangular ligament stabilizes the two conjoined lateral bands over the dorsal aspect of the middle phalanx and prevents volar subluxation of the conjoined lateral bands.
The transverse retinacular ligament is composed of fibers oriented in a volar–dorsal direction at the level of the PIP joint. It prevents dorsal subluxation of the conjoined lateral bands.
The oblique retinacular ligament (ORL) is a static restraining ligament, linking the PIP and DIP joints. It runs from the fibro-osseous gutter at the A2 flexor pulley and the middle third of the proximal phalanx to insert into the terminal extensor tendon and couples PIP joint and DIP joint extension.
Flexor Tendon: Digit
At the level of the A1 pulley, the flexor digitorum superficialis (FDS) tendon flattens and bifurcates to allow the more dorsal flexor digitorum profundus (FDP) tendon to pass distally within the flexor sheath to insert at the volar base of the distal phalanx.
The FDS tendon slips rotate laterally and dorsally around the FDP and then divide again into medial and lateral slips. The medial slips rejoin dorsal to the FDP tendon and insert into the distal aspect of the proximal phalanx. The lateral slips continue distally to insert into the base of the middle phalanx.
Extensor Tendon: Digit
At the base of the proximal phalanx, the extrinsic extensor tendon trifurcates with the central portion inserting into the dorsal base of the middle phalanx as the central slip.
The lateral slips are joined by the oblique fibers of the lumbrical tendons to form the conjoined lateral band. The conjoined lateral bands converge over the middle phalanx to form the terminal tendon, which inserts at the dorsal base of the distal phalanx, where it functions to extend the DIP joint.
The interosseous muscles contribute to the dorsal extensor apparatus through their deep muscle belly, which travels superficial to the sagittal band as the lateral tendon, becoming the transverse fibers of the extensor hood (MCP joint flexion).
PATHOGENESIS
Posttraumatic Boutonnière Deformity
Disruption of the central slip is the inciting pathology in the development of the boutonnière deformity.
Injury patterns can be grouped into two broad categories, closed and open.
Closed injuries: Forceful hyperflexion of the PIP joint may result in a detachment of the central slip from its insertion. An associated avulsion fracture involving the insertion of the central slip may be identified from the dorsal base of the middle phalanx.
Volar dislocations of the PIP joint or digital crush injuries may disrupt the central slip.
Open injuries: Dorsal laceration or deep abrasions over the PIP joint may disrupt the integrity of the central slip.
Disruption of the central slip and attenuation of the triangular ligament allows for the migration of the lateral bands volar to the PIP joint axis of rotation. This results in flexion at the PIP joint and extension at the DIP joint through the action of the displaced lateral bands.
The displaced lateral band becomes a flexor of the PIP joint and an extensor of the DIP joint.
Posttraumatic Swan-Neck Deformity
Unrecognized volar plate injury at the PIP joint may result in volar plate insufficiency. This leaves the action of the central slip unchecked by the volar plate, resulting in a progressive PIP joint hyperextension deformity.
Recurrent dorsal dislocation of the PIP joint is an example of an injury pattern that may result in volar plate incompetence.
Avulsion of the terminal tendon from its insertion at the base of the dorsal distal phalanx results in an imbalance in the extensor mechanism. Extension forces are concentrated at the central slip, producing a progressive hyperextension deformity of the PIP joint.
Patients predisposed to volar plate laxity (such as from generalized ligamentous laxity, inflammatory conditions, and collagen vascular disorders) are particularly susceptible to the development of deformity.
An extension malunion of the middle phalanx or peritendinous adhesions secondary to previous digital fracture or injury may contribute to the development of a swan-neck deformity.
Hyperextension of the PIP joint and attenuation of the transverse retinacular ligament permits dorsal migration of the lateral bands relative to the PIP joint axis of rotation. The displaced lateral bands act to extend the PIP joint and to flex the DIP joint.
Rheumatoid Boutonnière Deformity Fingers
Boutonnière (“buttonhole”) deformity results from pathologic synovitis of the PIP joint that causes progressive attenuation of the central slip, transverse retinacular ligaments, and triangular ligament. The PIP joint essentially “buttonholes” through the extensor mechanism.30 Characteristic flexion of the PIP joint and hyperextension deformities of the MCP and DIP joint prevail due to the extensor imbalance21(FIG 2A).
Subluxation of the lateral bands, volar to the axis of PIP joint rotation, occurs due to the loss of these restraints. The lateral bands become flexors of the PIP joint rather than extensors.
It is important to differentiate this pathologic involvement of the extensor mechanism from a flexion contracture of the PIP joint.
Due to persisting PIP joint flexion, the volar plate, collateral ligaments, and oblique retinacular ligaments become increasingly contracted, resulting in a stiff and subsequently fixed boutonnière deformity.
Thumb
Type I boutonnière deformity is the most common rheumatoid deformity of the thumb.29,37 It is characterized by MCP joint flexion and interphalangeal joint hyperextension (FIG 2B).
The pathologic changes affecting the thumb typically involve synovitis of the MCP joint with resulting attenuation of the extensor mechanism (dorsal joint capsule, extensor pollicis brevis tendon insertion, extensor hood). This relative extensor imbalance results in MCP joint flexion and possible joint subluxation.
Attenuation of the sagittal band permits ulnar and volar subluxation of the extensor pollicis longus (EPL) tendon, which accentuates MCP joint flexion and interphalangeal joint hyperextension as it translates volar to the axis of MCP joint rotation.
The destructive influence of prolific MCP joint synovitis can cause progressive articular erosion and altered joint surface mechanics, resulting in progressive joint instability and deformity.
FIG 2 • A. Boutonnière deformity of the finger. Note the flexion posture of the proximal interphalangeal joint and hyperextension of the distal interphalangeal joint. B. Lateral radiograph of the thumb demonstrating a boutonnière deformity. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
As the MCP joint flexion posturing increases in severity, compensatory radial abduction deviation of the thumb metacarpal ensues.
Rupture of the EPL tendon at the wrist can result in a similar “extrinsic-minus” deformity of the thumb.20,25
Boutonnière deformity can result, also, from a hyperextension deformity of the thumb interphalangeal joint secondary to joint synovitis with attenuation of the volar plate or to rupture of the flexor pollicis longus tendon.19
Generally, these primary interphalangeal joint etiologies present with less dramatic MCP joint flexion deformity.33
Rheumatoid Swan-Neck Deformity Fingers
Swan-neck deformity may result from pathologic rheumatoid synovitis of the MCP, PIP, or DIP joints and is characterized by PIP joint hyperextension and MCP and DIP flexion deformities.
Progressive attenuation of the volar plate, collateral ligaments, and insertion of the FDS tendon results in the development of a PIP hyperextension deformity.
Attenuation of the transverse retinacular ligaments may occur from synovitis, thereby resulting in a loss of the normal restraints to dorsal translocation of the lateral bands. As the lateral bands subluxate dorsal to the axis of PIP joint rotation, they become a constant hyperextension force on the PIP joint.
The DIP joint may be the primary cause of swan-neck deformity where synovitis results in the attenuation and possible rupture of the terminal extensor tendon. This leads to a concentration of the extensor forces at the PIP joint and a resultant hyperextension deformity.
Pathologic alterations in MCP joint mechanics may initiate the development of a swan-neck deformity. Progressive flexion deformity and ulnar drift of the digit results in an imbalance of the extensor mechanism whereby the lateral bands are drawn dorsally, concentrating an extension–hyperextension force at the PIP joint. Flexion deformity at the MCP joint may be secondary to several causes (FIG 3A,B):
Chronic synovitis and associated attenuation of the sagittal bands
Articular destruction with associated joint deformity and volar joint subluxation
The influence of intrinsic tightness or contracture
Persisting PIP hyperextension results in contracture of the extensor apparatus, particularly the triangular ligament, as well as the skin. These progressive changes result in a stiff and subsequently fixed PIP joint hyperextension contracture.
Digital flexor tenosynovitis may contribute to poor initiation of digital flexion and an increased extension imbalance at the PIP joint.
Chronic synovitis of the PIP joint, combined with altered joint mechanics, may result in progressive articular destruction that leads to greater joint deformity, a progressively fixed contracture, and, potentially, painful dysfunction of the digit.
Thumb
Type III rheumatoid thumb deformity is the second most common thumb deformity after boutonnière deformity.25,29
The deformity occurs as the result of CMC joint synovitis and associated alterations in thumb mechanics.
Progressive dorsal and radial subluxation of the thumb CMC joint occurs with the deleterious effects of chronic synovitis, including capsular attenuation and articular erosions.
The force vectors associated with pinch and grasp activities accentuate the CMC deformity and accentuate a progressive thumb metacarpal adduction contracture due to a loss of thumb abduction.
As the adduction contracture worsens, hyperextension of the MCP joint (permitted by volar plate laxity) and interphalangeal joint flexion becomes a functional compensation (FIG 3C,D).
FIG 3 • A,B. AP and lateral radiographs demonstrating the volar dislocation and ulnar drift of the metacarpophalangeal joints of the fingers. C. Swan-neck deformity of the thumb. D. Lateral radiograph of the thumb demonstrating a swan-neck deformity involving carpometacarpal joint subluxation, metacarpal adduction contracture, hyperextension of the metacarpophalangeal joint, and thumb interphalangeal joint flexion. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
NATURAL HISTORY
Traumatic Injury
Early diagnosis is critical for achieving satisfactory outcomes. Reconstructive options become limited as the deformity becomes rigid.
Boutonnière Deformity
Deformity may not be evident immediately after injury but may develop over 2 to 3 weeks.
The pathologic finger posture develops through five stages7 :
Disruption of the central slip results in resting flexion of the PIP joint and weak extension of the middle phalanx via the lateral bands.
Attenuation of the triangular ligament and contracture of the transverse retinacular ligaments results in the volar migration of the lateral bands. Active PIP joint extension is absent.
Extension forces are transmitted through the lateral bands, causing hyperextension at the DIP joint.
Progressive contracture of the PIP joint volar plate and the oblique retinacular ligament results in fixed flexion contracture at the PIP joint.
Progressive articular degeneration occurs after prolonged and untreated pathology.
Swan-Neck Deformity
The deformity may be subclassified into four groups that describe the natural history24 :
Presence of full passive range of motion at the PIP joint
Prolonged hyperextension of the PIP joint results in intrinsic tightness. The PIP joint exhibits full range of motion when the MCP joint is flexed. However, with the MCP joint extended, PIP flexion becomes limited.
As the transverse retinacular ligament attenuates and the triangular ligament contracts, the subluxated lateral bands become fixed dorsal to the PIP joint axis of rotation. Hyperextension of the PIP joint becomes fixed regardless of MCP joint position.
Progressive PIP joint articular degeneration occurs with chronic, fixed deformity.
Rheumatoid Deformity
The rate of progressive rheumatoid arthritis-related upper extremity deformity appears to be slowing due to improved medical management of this systemic disease process.
The incidence of uncorrectable boutonnière and swan-neck deformities during the first 2 years after the onset of systemic disease is about 16% and 8%, respectively.7
The prevalence of finger deformities in patients with established rheumatoid arthritis is about 36% for boutonnière and 14% for swan-neck deformities.7
The wrist, MCP, and PIP joints are the most commonly affected joints of the upper extremity, and pathologic proliferation of the flexor and extensor tenosynovium may influence digital function and deformity.
PATIENT HISTORY AND PHYSICAL FINDINGS
Posttraumatic Injury Boutonnière Deformity
A history of blunt trauma to the digit with swelling and tenderness over the PIP joint should arouse suspicion as to the condition. Often, patients report “jamming” or spraining the digit. History of a dorsal digital laceration is similarly concerning.
Deformity may not develop until 10 to 21 days after the injury, making early diagnosis challenging and diligent followup imperative. Laceration, ecchymosis, or tenderness over the dorsum of the PIP joint may be diagnostic when a PIP joint extension lag is present.
If the examination is limited due to pain, a digital block should be considered to facilitate a comfortable examination.
The following physical findings are supportive in confirming an early diagnosis:
15-to 20-degree PIP joint extension lag with the wrist and MCP joint fully flexed5
Weak extension of the middle phalanx against resistance18
Elson test: Effort to extend the PIP joint accompanied by rigidity of the DIP joint suggests that the central slip is ruptured and forces are being transferred by the lateral bands.
The Elson test is most reliable in diagnosing early boutonnière deformities.31
Boyes test: When the central slip is disrupted, passive extension of the PIP joint causes tension across the lateral bands, resulting in loss of active flexion at the DIP joint. When flexion at the PIP joint is restored, motion at the DIP joint returns.
Swan-Neck Deformity
A history of unrecognized or undertreated trauma or multiple dorsal PIP joint dislocations is common. A patient who presents with a longstanding “mallet” deformity should arouse suspicion, particularly if there is associated hypermobility in the PIP joint of unaffected digits.
Physical examination begins with inspection of the involved digit.
Typically, the PIP joint is hyperextended and the DIP joint is flexed. MCP joint flexion may be present also.
Active and passive range of motion of the PIP joint should be assessed.
In the presence of a flexible deformity, a Bunnell test for intrinsic tightness should be performed.
This test assists the examiner in determining the relative contribution of intrinsic tightness to the deformity.
Increased resistance to passive PIP flexion with the MCP joint in extension compared with flexion indicates a relative shortening of the intrinsic muscle–tendon units.
Rheumatoid Deformity
Diagnostic criteria for rheumatoid arthritis are based on the American College of Rheumatology's 1988 recommendations.2
Current medications and medical comorbidities may influence decision making for treatment and the timing for surgical intervention.
The evaluation of digital deformities associated with rheumatoid arthritis requires careful global assessment, including neurologic assessment (cervical spine, peripheral compressive neuropathy); appreciation for shoulder, elbow, and wrist involvement; and the awareness of lower extremity deformities that will need reconstructive surgery for which the use of ambulatory aids might be necessary.
As progressive deformity of the wrist occurs, its pathologic influence on digital function and deformity should be recognized.
The carpus typically collapses into supination, with concomitant volar translation and ulnar translocation.3
FIG 4 • Preoperative assessment of the digits should include evaluation of the wrist and metacarpophalangeal joints due to their influence on digital function. Wrist stabilization with total wrist arthrodesis and concomitant distal ulnar resection may include soft tissue reconstruction such as tendon repair or tenodesis; such reconstruction should occur before digital reconstructions due to its influence on the outcomes of swan-neck or boutonnière reconstructions. Reconstruction of the metacarpophalangeal joints should occur before or simultaneously with digital swan-neck or boutonnière reconstructions. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
Relative dorsal prominence of the distal ulna may involve a loss of distal radioulnar joint (DRUJ) congruity and may be associated with ruptures of the extensor carpi ulnaris tendon and extensor tendons to the small and ring fingers (caput ulnae syndrome). Inspection of the extrinsic digital extensors, including the EPL,20 should be done, particularly in the presence of active synovitis of the radiocarpal joint and DRUJ (FIG 4).
The MCP joint should be assessed for active synovitis and for characteristic volar subluxation and ulnar drift.
Just as pathologic changes to both the wrist and MCP joints may influence the development of swan-neck and boutonnière deformities of the digits, these changes may adversely affect the outcomes of digital reconstruction if they are not addressed.
Evaluation of the digits should be performed individually with inspection of the resting posture of each digit, assessment of the active and passive motion of each digital joint, and inspection for joint synovitis or tenosynovitis. Skin integrity is assessed for attenuation and for its contribution to joint contracture.
Flexor tenosynovitis may be identified by a palpable fullness in the distal volar forearm or along the digital flexor sheath. Swelling, palpable crepitus along the digital flexor sheath, and a discrepancy between active and passive digital motion are hallmarks of flexor tenosynovitis of the digit.
Flexor tendon rupture may be present, often secondary to attenuation at the volar carpus,19 and should be addressed in the presence of a loss of active digital joint flexion.
Extensor tenosynovitis at the wrist may be determined by palpable tenosynovial hypertrophy, or fullness, and crepitus along the dorsal extensor compartments, proximal and distal to the extensor retinaculum.
Tendon ruptures may be identified by a lack of active digital extension despite active muscular contraction, by palpable tendon deficit, and by a lack of digital extension through tenodesis with passive wrist flexion.
The adhesion of a ruptured tendon to the surrounding tissues and the influence of the junctura tendinea may limit the accuracy of these evaluations.
As described above, the Bunnell intrinsic tightness test should be performed for all fingers of patients with rheumatoid arthritis, particularly for patients with swan-neck deformity of the digits. This test assists the examiner in determining the relative contribution of intrinsic tightness to the development of the deformity.
Tightness of the oblique retinacular ligament, often appreciated in digits with early boutonnière deformity, is evaluated by assessing the relative degree of resistance to passive DIP joint flexion with the PIP joint held by the examiner in maximum extension.
IMAGING AND OTHER DIAGNOSTIC STUDIES
Plain radiographs (three views) are the mainstay of hand and wrist evaluation in the patient with either a traumatic or rheumatoid cause for deformity.
Staging of arthritis-related joint pathology and identification of joint subluxation or dislocation, important for diagnostic and management considerations, is performed using plain radiographs (FIG 5A).
Avulsion fractures from the dorsal base of the middle phalanx, volar subluxation of the PIP joint, or both suggest a central slip injury (FIG 5B).
FIG 5 • A. Radiographic appearance of periarticular (proximal interphalangeal [PIP] joint) soft tissue swelling and synovitis and moderate articular erosions involving the PIP joint. B. Lateral radiograph of the finger demonstrating a central slip avulsion injury involving an avulsion fracture from the dorsal base of the middle phalanx. There is no volar subluxation of the PIP joint in this example. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
In the presence of a fixed PIP joint flexion deformity, concomitant avulsion fracture of the volar plate suggests pseudoboutonnière pathology.
Fluoroscopic imaging or stress views may be helpful in differentiating collateral ligament injury from disruption of the central slip.
Avulsion fractures from the dorsal base of the distal phalanx suggest terminal tendon injury.
The presence of volar plate avulsion fractures in the setting of PIP joint hyperextension suggests volar plate incompetence.
MRI may be useful in assessing for soft tissue pathology such as tenosynovitis and tendon rupture, especially in rheumatoid patients.
DIFFERENTIAL DIAGNOSIS
Posttraumatic Injury
Pseudo-boutonnière deformity
Collateral ligament injury
Mallet finger
Volar plate avulsion fracture
Rheumatoid Deformity
Osteoarthritis
Psoriatic arthritis
Similar deformities as seen in rheumatoid arthritis, but skin lesions are common and DIP joint “pencil-in-cup” deformities may be present
Connective tissue disorders (scleroderma, systemic lupus erythematosus)
Systemic lupus erythematosus primarily affects soft tissue structures (ligamentous laxity, tendon subluxation) rather than joint destruction. Radiographs typically demonstrate joint deformities with well-preserved joint spaces. The thumb may be the first digit affected; lateral subluxation of the interphalangeal joint and flexion deformity of the MCP joint (secondary to extensor tendon subluxation) are common.
Patients with scleroderma often develop PIP joint flexion contractures and compensatory hyperextension posturing of the MCP joints.
Crystal-induced arthropathy (gout, calcium pyrophosphate deposition disease)
Hemochromatosis
Remitting symmetric seronegative synovitis
NONOPERATIVE MANAGEMENT
Posttraumatic Injury Boutonnière Deformity
Nonoperative management is indicated if correction of the deformity restores the anatomic length relationship between the central slip and the lateral bands. It is most appropriate in those with closed injuries who present within 8 to 12 weeks of injury. It may be attempted in those with central slip avulsion fractures or volar dislocation if satisfactory reduction and PIP joint stability can be obtained.
For patients with full passive extension of the PIP joint, PIP joint extension splinting is the treatment of choice.
A transarticular Kirschner wire maintaining the PIP joint in full extension is an alternative or adjunct to external splinting.
For patients with a PIP joint flexion contracture without secondary joint degenerative changes, progressive static or dynamic extension splinting should be pursued.
Full passive extension of the PIP joint should be sought before surgical intervention is considered.
Active and passive DIP joint range of motion should be emphasized while the PIP joint is being treated. Restoration of active DIP joint flexion while the PIP joint is extended suggests successful treatment. Restoration of full active extension at the PIP joint is the goal.
For most injuries, PIP joint extension splinting should be maintained for 6 to 8 weeks at all times, transitioning to protective buddy straps for daily activity and nighttime extension splinting for an additional 4 to 6 weeks.
Swan-Neck Deformity
Once the deformity has developed, nonoperative treatment is rarely effective.
Some patients with flexible deformities are capable of initiating PIP joint flexion with little impairment. They may complain of “snapping” or “cogwheeling” as the lateral bands relocate volarly during PIP joint flexion. These patients may benefit from a digital splint, such as a figure 8 ring splint, to prevent continued PIP joint hyperextension and to maintain the lateral bands in their anatomic position (FIG 6).
Rheumatoid Deformity Boutonnière Deformity
Nonoperative management of an early boutonnière deformity includes low-profile PIP joint extension splinting.
Oral anti-inflammatory medications, intra-articular corticosteroid injection of the PIP joint, or both are used to minimize joint synovitis.
Type I Swan-Neck Deformity
The goals of treatment for the flexible swan-neck deformity are prevention of PIP joint hyperextension and improvement in PIP joint flexion.
In the presence of minimal PIP joint synovitis, use of digital splints, such as a figure 8 ring splint, is advocated to prevent PIP joint hyperextension (Fig 6).
SURGICAL MANAGEMENT
Posttraumatic Injury Boutonnière Deformity
Surgical intervention is indicated for patients who fail to respond to at least 3 months of extension splinting, patients with open injuries, and patients with fixed deformity with associated degenerative joint changes.
FIG 6 • A figure 8 ring splint (Silver Ring Splint; Charlottesville, VA) used to prevent proximal interphalangeal joint hyperextension in a mild, flexible swan-neck deformity. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
Surgical decision making should be tempered by the observations of Burton and Melchior4 :
Boutonnière reconstructions are most successful on supple joints. If necessary, joint contracture release can be performed as a first stage. If the release is followed by an intensive exercise and splinting program, the second stage may be avoided.
An arthritic joint usually precludes soft tissue reconstruction. The surgeon should consider either a PIP joint fusion or arthroplasty with extensor reconstruction.
Boutonnière deformities rarely compromise PIP joint flexion and grip strength. The surgeon should not trade extension at the PIP joint for a stiff finger and a weak hand.
Swan-Neck Deformity
Surgery is indicated for patients with a flexible deformity who cannot actively initiate PIP joint flexion and in those with fixed deformities.
Patients with flexible deformities benefit from volar mobilization of the lateral bands and tenodesis to prevent PIP joint hyperextension.
Patients with fixed deformities have difficulty grasping objects. Often, functional contact is limited to the volar surface of the hyperextended PIP joint.
If the articular surfaces are well preserved, PIP joint release with concomitant procedures to restore flexion may be beneficial.
If the articular surfaces are damaged, PIP arthrodesis is a practical option.
Rheumatoid Deformity
Principles of surgical correction of rheumatoid deformities in the hand should be guided by the relief of pain and the improvement of function.28
Boutonnière Finger Deformity
Stage I—mild
For progressive boutonnière deformity associated with persistent PIP joint synovitis unresponsive to oral medication and intra-articular corticosteroid injection, PIP joint synovectomy may be considered. Concomitant central slip reconstruction and lateral band repositioning may be indicated due to soft tissue attenuation over the dorsal PIP joint.
Functional limitation due to DIP joint hyperextension may be treated by sectioning the terminal extensor tendon over the dorsal middle phalanx.
Stage II—moderate
For patients with moderate boutonnière deformity and preservation of the articular cartilage of the PIP joint, central slip reconstruction and terminal extensor tendon release may be indicated.12,44
Stage III—severe
If articular destruction is evident or if a severe fixed flexion contracture of the PIP joint is present, even without articular changes, then arthrodesis of the PIP joint is a reliable option for reducing pain and for improving function.
Implant arthroplasty of the PIP joint and concomitant terminal extensor tendon release is a less reliable option, particularly when there is attenuation of the dorsal extensor apparatus.
Swan-Neck Finger Deformity
Type I
The primary cause of the flexible swan-neck deformity must be determined before proceeding with surgical intervention. Although PIP synovitis and a resulting weakness of the volar PIP joint restraining structures are the most common findings, DIP joint synovitis may be a source of progressive deformity secondary to the transfer of extension forces to the PIP joint.
The potential influence of MCP joint pathology must be assessed. Extensor tendon subluxation at the level of the MCP joint or flexion contracture of the MCP joint should be addressed before, or concurrently with, surgical correction of the swan-neck deformity.
In a primary rheumatoid mallet finger where full PIP joint flexibility is preserved, DIP joint arthrodesis is a reasonable option. Postoperatively, the PIP joint is not immobilized, although the DIP joint is protected in a mallet-finger splint.
Frequently, patients with a flexible swan-neck deformity cannot initiate active PIP joint flexion from a resting, hyperextension position. Soft tissue reconstructive procedures that provide a check-rein to prevent PIP joint hyperextension may be considered, including volar skin dermodesis, oblique retinacular ligament reconstruction, lateral band tenodesis,13,45 and PIP joint flexor tenodesis.8
Type II
In type II swan-neck deformities, active and passive PIP joint motion is limited, with the MCP joint held in extension secondary to intrinsic tightness. MCP joint arthritis may be present. Therefore, MCP joint implant arthroplasty, intrinsic release, or both should be considered in planning for this swan-neck reconstruction.
Intrinsic release is accomplished via a dorsal approach to the MCP joint with exposure of the lateral band and extensor hood. A 1-cm segment of lateral band with attached sagittal band fibers is excised as described by Nalebuff.24,27 Release of the ulnar intrinsic tendon, with or without tendon transfer, may reduce the deforming force on the digit and reduce ulnar drift at the MCP joint.
If intrinsic release or MCP joint arthroplasty is performed, concomitant flexor tenodesis of the PIP joint may be required.
Type III
Type III swan-neck deformity is characterized by decreased active and passive PIP joint flexion irrespective of MCP joint positioning. The lateral bands are adherent dorsal to the PIP joint axis of rotation and a PIP joint soft tissue contracture is often present. Reconstruction involves lateral band release and volar translocation, combined with dorsal PIP joint capsulectomy, collateral ligament release, and extensor tenolysis.3,15,34
Type IV
There is a fixed hyperextension deformity of the PIP joint as well as destructive changes to the articular cartilage of the PIP joint.
Soft tissue procedures will not reliably relieve pain nor restore joint motion or function, and definitive treatment is limited to arthrodesis or implant arthroplasty.3
Rheumatoid Thumb
Type I: Boutonnière deformity
Mild: Passively correctable MCP and interphalangeal joints
Soft tissue reconstruction is indicated, as this may improve function despite a high incidence of deformity recurrence.38
Synovectomy of the MCP joint combined with EPL tendon rerouting will increase the extensor moment at the MCP joint through EPL attachment to the dorsal MCP joint capsule.26
Moderate: Fixed MCP joint deformity
The condition of the adjacent CMC and interphalangeal joints must be considered to determine whether to proceed with MCP arthrodesis or arthroplasty. Often, treatment at this stage of disease reduces the progression of thumb deformity.
If the extent of interphalangeal joint involvement warrants intervention, treatment of the interphalangeal joint is limited to arthrodesis. Therefore, preservation of motion at the MCP joint may be optimal through MCP implant arthroplasty, although function after MCP and interphalangeal arthrodesis is generally good.
Arthroplasty of the thumb MCP joint involves resection of the involved joint surfaces and prosthetic placement, most commonly with a flexible silicone implant. Extensor reconstruction, including EPL rerouting, is considered to augment extensor forces acting at the MCP joint. Postoperatively, the thumb MCP joint is splinted in extension for 4 to 6 weeks, allowing for controlled CMC and interphalangeal joint exercises. Good functional results with minimal progression of CMC or interphalangeal joint arthritis have been reported.11
Arthrodesis of the MCP joint is accomplished by one of several methods, including tension band wire fixation, crossing Kirschner wires, a headless compression screw, or plate and screw fixation. The joint is typically placed in 15 degrees of flexion and the arthrodesis site may be augmented with bone graft as needed to maximize bone surface contact area. The arthrodesis site is protected in a splint until radiographic union is confirmed. Early interphalangeal joint range of motion is encouraged to minimize extensor adhesions and stiffness.
Severe: Fixed deformities of MCP and interphalangeal joints
In this advanced stage, the treatment rationale is similar to that for moderate deformity, except that interphalangeal joint contracture or joint deterioration requires intervention. Rarely, interphalangeal joint capsular release may be indicated to improve motion, in the absence of articular deterioration. For cases involving interphalangeal joint instability or progressive arthritis, interphalangeal arthrodesis is indicated.
Carpometacarpal joint involvement
As rheumatoid arthritis has the potential to involve greater numbers of joints, motion-sparing procedures of the CMC joint are preferred compared to arthrodesis.
While total trapezial implant arthroplasty is relatively contraindicated in the rheumatoid patient due to the higher risk for implant failure or dislocation, resection or hemiresection arthroplasty with ligament reconstruction and soft tissue interposition arthroplasty should be considered.33
Type III: Swan-neck deformity
Mild: Isolated CMC joint involvement
In the absence of symptomatic relief from conservative treatment, CMC hemi-trapeziectomy or trapeziectomy and ligament reconstruction with soft tissue interposition arthroplasty is indicated.
Moderate: CMC joint pathology with mild MCP joint involvement (flexible deformity)
For CMC joint pathology with progressive MCP joint hyperextension deformity, CMC hemi-trapeziectomy or trapeziectomy and ligament reconstruction with soft tissue interposition arthroplasty and simultaneous MCP joint volar plate capsulodesis, sesamoidesis, or volar tenodesis are considered. Temporary transarticular pin stabilization of the MCP joint in 20 degrees of flexion for 3 to 4 weeks postoperatively permits early motion of the interphalangeal joint.
Severe: CMC joint dislocation with metacarpal adduction contracture and fixed MCP joint hyperextension deformity
Treatment for this advanced stage requires:
CMC joint reconstruction with resection arthroplasty and ligament reconstruction or tendon interposition arthroplasty
Correction of the metacarpal adduction contracture
MCP arthrodesis
Often, adduction contracture of the thumb metacarpal may be adequately treated with resection of the thumb metacarpal base and release of the restraining ligaments of the CMC joint during resection arthroplasty. If the adduction contracture persists, then fasciotomy of the first dorsal interosseous and adductor muscles may be completed.33 Web space reconstruction with Z-plasties is rarely indicated.
Preoperative Planning
The surgeon must plan ahead. Extended procedures associated with multiple digital reconstructions or the combined treatment of multiple joints should warrant careful and efficient use of tourniquet time.
Regional anesthesia (axillary block, IV regional) may be preferred for the reconstruction of digital deformities. This form of anesthesia may provide a greater duration of postoperative pain control and may minimize the systemic effects of general anesthesia.
Avoidance of general anesthesia may minimize the potential risks of cervical spine positioning in patients with cervical instability secondary to rheumatoid arthritis.
Procedures that may require the use of bone grafting should involve preoperative discussion with the patient to explain the potential need for bone grafting and to identify potential sources for the graft (ie, iliac crest, olecranon, distal radius, allograft or synthetic bone substitutes).
Posttraumatic Injury
A detailed history and physical examination should be performed.
Active and passive PIP joint range of motion should be assessed. Chronic, rigid deformities may require staged procedures with surgical release of the PIP joint before subsequent reconstructive procedures.
Radiographs should be reviewed for fractures, joint subluxation or dislocation, and degenerative joint changes.
Adjacent joint injuries and pre-existing degenerative changes should be considered during surgical planning.
Rheumatoid Deformity
Before surgical reconstruction of rheumatoid swan-neck or boutonnière deformities of the digits, a global assessment is completed to characterize the systemic involvement of rheumatoid disease.
Coordination of medical clearance and perioperative care may be pertinent for patients with medical comorbidities and for patients taking perioperative medications such as corticosteroids.
Preoperative cervical spine evaluation may be indicated to confirm stability of the spine for safe anesthesia administration.
Timing of rheumatoid swan-neck or boutonnière reconstruction should account for other musculoskeletal pathology as reviewed above. Postoperative protocols and anticipated prognosis for recovery should be reviewed carefully with patients to minimize potential conflicts with other medical or surgical management.
Positioning
Surgical reconstruction of the hand is performed typically in a supine position with the upper limb placed on a well-padded hand table.
A brachial tourniquet is used.
Preoperative shoulder and elbow assessment will minimize potential difficulties with surgical positioning, particularly for patients with severe limitations to joint mobility or joint instability.
Approach
Careful soft tissue handling is observed to minimize the risk of wound or soft tissue complications. Full-thickness skin flaps are raised during operative exposure.
Dorsal Approach
A longitudinal midline or curvilinear incision from the proximal phalanx to the DIP joint provides excellent visualization of the extensor mechanism.
Sharp dissection through the subcutaneous tissue and careful elevation of full-thickness flaps are performed to expose the central slip and lateral bands.
Exposure of volar structures is limited with this approach but can be enhanced by extending the incision proximally and distally.
Volarly, the Cleland ligament is divided, taking care to protect the neurovascular bundle, which is volar to the plane of dissection. The underlying PIP joint collateral ligament, PIP joint volar plate, and flexor sheath are exposed.
A small window can be made in the membranous flexor sheath between the A2 and A4 pulleys to improve exposure of the volar plate.
Volar Approach
Access to volar structures may be necessary to release the PIP joint. This can be accomplished via a midlateral or a Brunner incision centered at the PIP joint.
Dissection is carried down to the flexor sheath, elevating full-thickness flaps and preserving the digital neurovascular bundles.
Between the A2 and A4 pulleys, the membranous portion of the flexor sheath can be elevated to expose the flexor tendons and the underlying volar plate of the PIP joint.
Arthrodesis and arthroplasty techniques are detailed in separate chapters.
TECHNIQUS
BOUTONNIÈRE RECONSTRUCTION
Primary Central Slip Repair
Primary repair is accomplished through a dorsal approach.
After isolating the central slip, assess the redundant tissue with the PIP joint held in full extension.
Excise a chevron-shaped segment of redundant fibrous tissue, permitting repair of the free tendon edges with 4-0 braided suture using a multistrand, grasping or locking repair method.
V-Y advancement may be necessary to facilitate repair.
In the case of an avulsion fracture, identify and carefully elevate the fragment, preserving the attachment of the central slip.
For smaller fragments inappropriate for Kirschner wire or screw fixation, the fragment may be excised and the central slip repaired directly into the dorsal base of the middle phalanx using a pullout suture or suture anchor method.
If the fracture fragment is larger, reduce the fragment anatomically and stabilize it using appropriate fixation such as small screws or two small Kirschner wires.
The lateral bands must be restored to their anatomic location, dorsal to the axis of rotation of the PIP joint. Mobilize them by excising the triangular ligament and incising both transverse retinacular ligaments as necessary.
Approximate the lateral bands distal and dorsal to the PIP joint and suture them together using 4-0 nonabsorbable, braided suture.
The repair is protected and the PIP joint is held fully extended, usually using a transarticular Kirschner wire, for 6 weeks.
Central Slip Reconstruction Using Local Tissue
Central slip reconstruction using local tissue may be considered for patients with a flexible deformity and insufficient central slip for direct primary repair. Several methods have been described using a dorsal approach to the extensor apparatus.
Snow's Technique 32
Identify the proximal stump of central slip and dissect it free of the surrounding tissues.
Elevate a distally based flap of extensor tendon sharply, preserving sufficient length to span the tendinous defect.
Turn the flap down on itself and suture it to any distal tissue as well as the lateral bands using 4-0 braided, nonabsorbable suture.
After repair, passive PIP joint flexion of no less than 60 degrees must be possible without excessive tension across the repair site.
Aiche's Technique 1
Isolate the radial and ulnar lateral bands and divide them longitudinally from the trifurcation of the extrinsic tendon to the triangular ligament.
Mobilize the dorsal half of each lateral band dorsally and suture them together using 5-0 nonabsorbable, braided suture.
Lateral band relocation is recommended when the lateral bands are fixed volar to the PIP joint axis of rotation.
Littler and Eatron's Technique 17
Carefully isolate the radial and ulnar lateral bands.
Incise the lateral bands over the middle phalanx. Preserve at least one ORL; otherwise, DIP joint extension will be compromised.
Mobilize the incised lateral bands dorsally and suture them into the insertion of the central slip.
If excessive attenuation of the central slip precludes suture stabilization, this repair method is contraindicated.
Matev's Technique 22
After isolating the lateral bands from the surrounding soft tissue, incise the ulnar lateral band at the level of the DIP joint and incise the radial lateral band at the midpoint of the middle phalanx.
Suture the proximal stump of the ulnar lateral band to the distal stump of the radial lateral band over the dorsal digit, thereby lengthening the terminal slip (TECH FIG 1).
Weave the proximal stump of the radial lateral band into the remnants of the central slip and suture it to the base of the middle phalanx to restore PIP joint extension.
Postoperatively, the PIP joint is held in full extension for 6 weeks. A temporary transarticular Kirschner wire may be placed to protect the repair.
TECH FIG 1 • Boutonnière reconstruction using Matev's technique of lengthening the terminal tendon and reconstructing the central slip using the lateral bands. The ulnar lateral band is incised slightly proximal to the distal interphalangeal joint and the radial lateral band is incised more proximally, at the level of the mid-aspect of the middle phalanx. The proximal stump of the ulnar lateral band is then sutured into the distal stump of the radial lateral band as shown here. The free proximal stump of the radial lateral band (rlb) is then repaired into the dorsal base of the middle phalanx. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
TECH FIG 2 • Boutonnière reconstruction using a tendon graft. The tendon graft is passed through a transverse osseous tunnel in the dorsal base of the middle phalanx (P2) and the limbs of the graft are woven into the lateral bands (lb). (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
Expose the extensor mechanism via a dorsal, curvilinear incision. Identify the proximal stump of the central slip and isolate it from the surrounding tissues.
Harvest an autologous tendon graft, preferably the ipsilateral palmaris longus tendon (if present).
Create a transverse bone tunnel through the dorsal base of the middle phalanx.
Pass the palmaris longus tendon through the bone tunnel and weave the two limbs into the lateral bands with the digit held in neutral (TECH FIG 2).
The repair is protected for 6 weeks by maintaining PIP joint extension with a transarticular Kirschner wire.
Central Slip Reconstruction Using Tendon Graft
When a flexible deformity is present but there is insufficient local tissue for use in central slip reconstruction, a tendon graft reconstruction may be considered.
Extensor Tenotomy
Hyperextension deformity of the DIP joint may be addressed with extensor tenotomy.23
Tenotomy is indicated in the presence of mild, flexible deformities and for patients who have failed prior surgery directed at the PIP joint.
Extensor tenotomy may be considered as an adjunct to PIP joint arthrodesis performed for chronic boutonnière deformity with associated PIP joint arthritis.
Make a dorsal incision over the distal two thirds of the middle phalanx.
Identify the terminal tendon and elevate it proximally over a distance of 1.5 cm from the underlying phalanx and DIP joint.
Incise the terminal tendon distal to the triangular ligament.
Preserve the radial ORL so that DIP joint extension is not compromised.
Passively extend the PIP joint and passively flex the DIP joint to separate the incised tendon ends.
SWAN-NECK RECONSTRUCTION
Oblique Retinacular Ligament Reconstruction 16,39
Reconstruction of the ORL is indicated when a flexible swan-neck deformity develops secondary to an untreated mallet finger. This procedure is suited for patients with a well-preserved DIP joint.
Make an incision from the ulnar margin of the MCP joint flexion crease and continue it volarly and distally along the radial midaxial line before curving it dorsally to end over the DIP joint.
Isolate the radial neurovascular bundle from the surrounding tissue. Proximally, identify the A2 pulley. Distally, identify the terminal slip.
TECH FIG 3 • A. Oblique retinacular ligament reconstruction. The scissors illustrate the anatomic plane of dissection for the passage of a tendon graft for reconstruction. The plane extends from the A2 pulley volarly to the dorsal surface of the terminal extensor tendon. B. The palmaris tendon graft has been inserted, coursing from volar to the Cleland ligament to be secured to the dorsal aspect of the terminal extensor tendon insertion. The neurovascular bundle is carefully protected. (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
Harvest the ipsilateral palmaris longus tendon using a tendon stripper through a 1-cm transverse incision proximal to the wrist crease.
Alternatively, make a second transverse incision proximally, overlying the musculotendinous junction. Confirm the inserting muscular fibers at the musculotendinous junction before tendon harvest. If the palmaris longus is not present, obtain another suitable autologous tendon graft.
The DIP joint is held in full extension and the PIP joint is held in 25 degrees of flexion with transarticular Kirschner wires.
Suture the tendon graft to the terminal slip using nonabsorbable, braided suture.
Pass the graft deep to the radial neurovascular bundle and bring it to the volar surface of the digit. Suture it to the distal edge of the A2 pulley after tensioning the graft appropriately (TECH FIG 3).
Proximal Interphalangeal Joint Flexor Tenodesis
Creation of a check-rein to PIP joint hyperextension can be accomplished by PIP joint flexor tenodesis or by lateral band tenodesis (described below).
Via a Brunner or midaxial incision, elevate full-thickness skin flaps to expose the digital flexor sheath, protecting the digital neurovascular bundles.
Raise as a flap the membranous portion of the flexor sheath, from the distal aspect of the A2 pulley to the proximal edge of the A4 pulley, to expose the underlying flexor tendons.
Identify one slip of the FDS tendon and divide it proximally at the level of the decussation, leaving its insertion into the base of the middle phalanx intact (TECH FIG 4A,B).
Pass the divided tendon end from dorsal to volar through a transverse incision in the A2 pulley, about 3 mm from the pulley's distal margin, and suture it back onto itself with the PIP joint held in about 20 degrees of flexion (TECH FIG 4C,D).
TECH FIG 4 • A. Proximal interphalangeal (PIP) joint flexor tenodesis with exposure of the flexor tendons between the A2 pulley and the A4 pulley. One slip of the flexor digitorum superficialis (FDS) tendon is divided at the level of the decussation, leaving its insertion intact. B. The harvested FDS tendon (****) is brought through an opening created in the distal aspect of the A2 pulley to be repaired to itself with the PIP joint held in 20 degrees of flexion. C, D. Lateral band tenodesis to provide a check-rein to PIP joint hyperextension. The lateral band (**) has been detached distally (C) and has been rerouted within the flexor sheath (fs) before repair distally (D). (Photographs © Copyright of Fraser J. Leversedge, Charles A. Goldfarb, and Martin Boyer.)
Postoperative immobilization with a dorsal block splint maintains the joint in more than 20 degrees of flexion for 6 weeks. Flexion exercises for the PIP and DIP joints are started at 3 weeks postoperatively.
Lateral Band Tenodesis 42,45
The lateral band is rerouted so that it lies volar to the PIP joint axis of rotation and forms a restraint to PIP hyperextension.
Approach the extensor apparatus via a dorsal curvilinear incision. Expose the Cleland ligament and divide it to access the flexor sheath with preservation of the digital neurovascular bundles.
Leaving its proximal and distal attachments intact, dissect the dorsally subluxated lateral band free from the central slip and from its distal attachment to the triangular ligament overlying the base of the middle phalanx. Translocate the lateral band volar to the PIP joint axis of rotation, assisted by flexion of the PIP joint.
At the level of the PIP joint, elevate a dorsally based flap of the flexor sheath 0.5 to 1 cm wide and place the mobilized lateral band volar to the flap. Repair the flap to its anatomic position, restraining the lateral band as an effective pulley.
Alternatively, the lateral band may be detached from its insertion into the terminal tendon slip and rerouted within a roughly 0.5-to 1-cm segment of the flexor sheath at the A2 pulley before repairing it to the terminal tendon distally (Tech Fig 4A,B).
Confirm unimpeded gliding of the lateral band beneath the flexor sheath by gentle proximal and distal traction on the translocated lateral band.45
Postoperatively, a dorsal block splint maintains the joint in more than 30 degrees of flexion. Digital flexion exercises are encouraged early in the postoperative period. Full active PIP joint extension is not allowed for 6 weeks.
Type III Swan-Neck Reconstruction
Reconstruction of a type III swan-neck deformity must address the fixed translocation of the lateral bands dorsal to the PIP joint rotation axis and the associated PIP joint soft tissue contracture.
Management of these pathologic changes includes lateral band release from the central tendon and from the triangular ligament; translocation of the lateral bands to a position volar to the PIP joint rotation axis; dorsal PIP joint contracture release, with dorsal capsulectomy and collateral ligament release; extensor tenolysis of the digit; and possible limited flexor tenolysis, as indicated, for flexor tenosynovitis.
Via a dorsal curvilinear incision, raise full-thickness skin flaps to expose the underlying extensor apparatus.
Release the lateral bands along their dorsal attachment to the central tendon, from the proximal phalanx to their confluence over the dorsal aspect of the middle phalanx.
Complete a dorsal PIP joint capsulectomy and gradually release the radial and ulnar collateral ligaments, from dorsal to volar, until the PIP joint can be passively flexed to 90 degrees.
Because the mobile lateral bands will passively translate volar to the PIP joint axis of rotation with passive joint flexion, the lateral bands do not require stabilization.
After soft tissue releases, the PIP joint is stabilized in 20 degrees of flexion with a temporary transarticular Kirschner wire. The digital reconstructions are protected in a forearm-based splint, removed to permit MCP and DIP joint motion. The wire is removed 2 to 3 weeks postoperatively.
OUTCOMES
Traumatic Deformity Reconstruction
Surgery for established boutonnière and swan-neck deformities is technically challenging.
A variety of surgical options exist; there is little consensus regarding a preferred technique.
There are relatively few studies evaluating the long-term results after surgery for posttraumatic boutonnière and swanneck deformities. Direct comparisons may be difficult due to the variations in clinical stage at the time of presentation.
Boutonnière Deformity
Towfigh and Gruber43 reported on the results of surgical treatment of 114 flexible posttraumatic boutonnière deformities. The central slip was repaired directly, with local tissue, or reconstructed with a tendon graft. Follow-up averaged 40 months. Seventy-eight patients report good or excellent results. Satisfactory results were observed in 22 patients and poor results in 14 patients.
Meadows et al23 reported on the results of extensor tenotomy performed on 14 fingers with posttraumatic boutonnière deformity. The average preoperative PIP joint flexion contracture was 36 degrees. All the digits had DIP joint extension contractures with an average arc of motion from 6.5 degrees of hyperextension to 4.2 degrees of flexion. Postoperatively, DIP flexion improved to 44 degrees. Ten of the digits had an extension lag averaging 13 degrees. Seven digits had improved extension at the PIP joint by an average of 27 degrees.
Swan-Neck Deformity
Tonkin et al42 reported outcomes of lateral band tenodesis for swan-neck deformity. Thirty digits with swan-neck deformity of various causes were included. Preoperative PIP joint deformity averaged 16 degrees of hyperextension; this was improved to 11 degrees of flexion postoperatively.
Reconstruction of the oblique retinacular ligament was first described by Thompson et al.39 They reported improvement in PIP joint hyperextension and DIP joint flexion with this technique. Kleinman and Peterson16 described similar results with reliable correction of DIP joint flexion and secondary PIP joint hyperextension.
Rheumatoid Deformity Reconstruction
There is a relative lack of clinical outcomes studies evaluating the long-term results of surgical management for swanneck and boutonnière deformities in patients with rheumatoid arthritis.
Kiefhaber and Strickland15 reported on the results of surgical treatment for type III swan-neck and stage II boutonnière deformities. In 92 patients undergoing lateral band release, extensor tenolysis, and PIP joint dorsal capsulectomy for type III swanneck deformity, the authors reported an initial increase of 55 degrees flexion at the PIP joint; however, of 15 fingers assessed at 3 and 12 months postoperatively, there was a 17-degree loss of the early postoperative motion gains. Despite this deterioration of postoperative results, the arc of PIP motion shifted toward flexion, improving functional grasp.
In 19 patients undergoing central slip reconstruction for stage II boutonnière deformity, the authors found unpredictable results and reported that the deterioration of postoperative correction was greater with time. Four of 19 patients were able to extend the PIP joint beyond 20 degrees of flexion and 11 of 19 patients had a PIP joint extension deficit of greater than 45 degrees.
Tonkin et al published two separate studies assessing the outcomes of treatment for swan-neck deformities with lateral band translocation42 and with synovectomy and lateral band release and translocation.41While these studies are limited in their conclusions because of the varying stages of disease and their small patient populations, the trend toward positioning the arc of motion into flexion was observed, similar to the study results of Keifhaber and Strickland.15
Several long-term clinical outcomes studies of PIP and MCP joint implant arthroplasties have demonstrated poor correction of preoperative swan-neck or boutonnière deformities and in general have reported poorer results with respect to pain relief and range-of-motion recovery as compared to arthroplasties done for conditions of osteoarthritis or posttraumatic arthritis.6,35,36
A review of surgical treatment of varying stages of thumb boutonnière deformity by Terrono et al38 concluded that MCP joint synovectomy and EPL rerouting for early, correctable boutonnière deformity had a high rate of deformity recurrence (64%). The authors recommend MCP joint arthrodesis for cases of moderate severity with isolated joint involvement, but in severe cases, MCP joint arthroplasty and interphalangeal arthrodesis is considered.
COMPLICATIONS
Perioperative complications in the treatment of posttraumatic boutonnière and swan-neck deformities can be avoided by careful patient selection, appropriate intervention, and adherence to proper surgical technique.
Thorough perioperative patient counseling and education is imperative to avoid unrealistic patient expectations and unanticipated outcomes.
A successful operative result and the avoidance of perioperative complications in the treatment of a boutonnière or swanneck deformity in the rheumatoid hand is largely dependent on a thorough preoperative evaluation, correct staging of the pathologic condition, and appropriate timing of operative intervention. While the goals of reducing pain and improving function are primary, patient education is critical for avoiding unrealistic expectations and unanticipated results.
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