Chapter 36 Treatment of Boutonnière and Swan-Neck Deformities
The treatment of boutonnière and swan-neck deformities of the digits is guided by the etiology and staging of the condition, primarily differentiated as being the sequelae of trauma or as a part of the spectrum of rheumatoid disease. A thorough evaluation should include consideration for the current or potential pathology of adjacent joints, the active and passive motion of involved joints, subjective concerns for pain or instability, and radiographic assessment. Careful assessment of the deformity is critical to the decision on an appropriate and individualized treatment strategy. The primary goals of treatment of boutonnière and swan-neck deformities are to alleviate pain and to improve function. Treatment ranges from splinting and therapy to operative intervention. The surgical procedures include ligament repair or reconstruction and tenodesis or arthrodesis. Long-standing and severe deformities are difficult to correct and consequently full function of the digits may not be achieved. Patient selection is critical to achieving successful surgical outcomes.
The intricate and coordinated functions of the hand and digits rely extensively on the complex but balanced interactions between the extrinsic and intrinsic musculature of the hand. Alterations in the relationships between these extrinsic and intrinsic systems due to trauma or secondary to the effects of systemic disease may cause the development of functional deformities such as a boutonnière or swan-neck deformity. Such changes may be acute or chronic in nature. Treatment for these conditions should be guided by a comprehensive evaluation of the patient, a consideration for associated injuries or structural deficiencies, the timing of injury, and the severity of the deformity. Importantly, a functional assessment and recognition of the patient’s activity requirements and expectations are critical for creating a plan of care.
Post-traumatic boutonnière (or “buttonhole”) deformities, characterized by hyperextension of the metacarpophalangeal (MCP) joint, flexion of the proximal interphalangeal (PIP) joint, and hyperextension of the distal interphalangeal (DIP) joint, are caused by disruption of the central slip. Attenuation of the triangular ligament allows the lateral bands to migrate volar to the PIP joint axis of rotation, transforming the lateral bands into a flexion force at the PIP joint and extension force at the DIP joint (Figure 36-1).
Traumatic injuries to the central slip can be divided into two groups: (1) Closed injuries: Typically, avulsion of the central slip from its insertion occurs due to a hyperflexion injury or volar dislocation of the PIP joint. An associated avulsion fracture from the dorsal base of the middle phalanx may be present. (2) Open injuries: Lacerations to the dorsal digit can disrupt the central slip directly.
Often, patients present with complaints of “jamming” or spraining the affected digit and the clinician should be suspicious of a central slip injury particularly in the presence of localized swelling, ecchymosis, and/or tenderness to the dorsal PIP joint and a loss of full active PIP joint extension; a lack of motion should not be disregarded as a consequence of swelling or pain. Early diagnosis may be complicated by the delayed development of the deformity, often 2 to 3 weeks following initial injury.
Physical examination findings supportive of an acute central slip injury include: (1) A 15° to 20° extension lag at the PIP joint with the wrist and MCP joint held in full flexion.1 (2) Absence or weakness of resisted active extension of the PIP joint with the PIP joint starting in 90° of flexion.2,3 (3) Elson test: The patient attempts to extend actively the PIP joint of the involved finger against resistance from a 90° starting position over the edge of a table. The absence of extension force at the PIP joint accompanied by fixed extension of the DIP joint confirm disruption of the central slip as extension forces are being transferred to the DIP joint by the lateral bands.4,5 (4) Boyes test: A positive test may be found in progressive stages of boutonnière deformity but is not reliable for the diagnosis of acute central slip injuries.5 Loss of active flexion of the DIP joint with the PIP joint held in passive extension due to tension across the lateral bands following disruption of the central slip. Active flexion of the DIP is possible with the PIP joint flexed.
Post-traumatic swan-neck deformity is characterized by the inability of the terminal slip to extend the DIP joint combined with laxity of the PIP volar plate resulting in hyperextension of the PIP joint and flexion of the DIP joint. Attenuation of the transverse retinacular ligament coupled with hyperextension of the PIP joint leads to dorsal migration of the lateral bands in relation to the PIP joint axis of rotation, thereby exerting an extension force on the PIP joint and a flexion force on the DIP joint.
Laxity or incompetence of the volar plate can be caused by dorsal dislocation of the PIP joint. Recurrent injury may lead to chronic dorsal instability of the PIP joint. Conversely, terminal tendon avulsion from its insertion at the base of the distal phalanx may cause an imbalance in the extensor mechanism, resulting in hyperextension of the PIP joint.
Patients may present with a history of acute injury or recurrent dorsal PIP hyperextension injuries culminating in progressive subluxation or dislocations, often unrecognized. Patients presenting with a chronic “mallet” deformity should arouse suspicion for PIP hypermobility. On physical examination, the affected digit will exhibit PIP joint hyperextension and DIP joint flexion posturing, often with MCP joint flexion. For patients with flexible PIP and DIP joint deformities, active and passive motion of the PIP joint should be assessed and a Bunnell’s intrinsic tightness test should be performed.
Bunnell’s intrinsic tightness test: Increased resistance to passive PIP joint flexion with the MCP joint in extension compared with flexion indicates a relative shortening of the intrinsic muscle–tendon units.
Rheumatoid boutonnière deformities occur due to progressive erosion of the central slip, transverse retinacular ligaments, and the triangular ligament by the destructive synovitis characteristic of rheumatoid arthritis. As the restraints provided by triangular ligament are lost, the lateral bands migrate in a volar direction, transforming them into a flexion force at the PIP joint. The continued flexion deformity of the PIP joint results in contractures of the oblique retinacular ligament, the volar plate, and the collateral ligaments; progression from a flexible to a fixed deformity of the PIP joint occurs with time. The classic boutonnière deformity involves flexion of the PIP joint and hyperextension of the DIP and MCP joints and evolves through three stages.8 Stage I is considered a mild, involving PIP joint synovitis and a passively correctable flexion deformity of the PIP joint. Stage II, or a moderate deformity, involves a flexion contracture of the PIP joint and concomitant MCP joint hyperextension. Stage III involves a fixed contracture of the PIP joint and destruction of the articular surfaces.
Swan-neck deformities associated with rheumatoid disease are characterized by hyperextension of the PIP joint and concurrent MCP and DIP flexion deformities. A swan-neck deformity may be caused by primary pathology affecting the MCP, the PIP, or the DIP joint.7
MCP joint pathology: The characteristic rheumatoid digital deformity of flexion and ulnar drift leads to imbalance of the extensor mechanism. The PIP is hyperextended by the extension force exerted across the PIP by the dorsal shift of the lateral bands. The MCP joint component of a swan neck deformity is flexion, which can be secondary to chronic synovitis with degeneration of the sagittal bands, intrinsic tightness, and/or articular destruction resulting in volar subluxation of the MCP joint.
PIP joint pathology: The volar plate of the PIP joint, the collateral ligaments, and the insertion of the flexor digitorum superficialis (FDS) tendon can become attenuated in rheumatoid disease, resulting in PIP hyperextension. Also, progressive attenuation of the transverse retinacular ligaments results in a loss of the normal restraints to the dorsal migration of the lateral bands, leading to PIP joint hyperextension.
DIP joint pathology: Synovitis of the DIP joint may cause attenuation and eventual rupture of the terminal extensor tendon. Subsequently, the extensor forces are concentrated at the PIP joint, resulting in a hyperextension deformity of the PIP joint.
Thumb deformity associated with rheumatoid disease may be classified based on changes specific to the carpometacarpal (CMC), MCP, and interphalangeal (IP) joints, as outlined by a modified classification system of six types initially proposed by Nalebuff.9,10
The most common rheumatoid thumb deformity is the type I (boutonnière) deformity. This is characterized by IP joint hyperextension and MCP joint flexion without primary involvement of the CMC joint. Typically, the type I deformity begins with proliferative synovitis within the MCP joint, which leads to attenuation of the extensor pollicis brevis (EPB) tendon insertion and expansion of the extensor hood. Concurrently, the collateral ligaments become attenuated and the extensor pollicis longus (EPL) is displaced ulnar and volar to the MCP joint axis of rotation. Subsequently, the proximal phalanx becomes subluxed palmarly relative to the metacarpal head and the altered pull of the intrinsics and the EPL leads to IP joint hyperextension and MCP joint flexion. Radial abduction of the thumb metacarpal can occur in compensation for MCP joint flexion. Type I deformities are further divided into stages: (1) stage I, or mild: PIP joint synovitis and mild fully correctable extensor lag; (2) stage II, or moderate: marked flexion deformity of PIP joint, flexible or fixed; and (3) stage III, or severe: PIP articular destruction.
The second most common rheumatoid thumb deformity is the type III (swan-neck) deformity (Figure 36-2).9,11 CMC joint synovitis leads to erosion of the articular surface and capsular attenuation, which contributes to the dorsal and radial subluxation of the CMC joint. An adduction contracture of the metacarpal develops due to the alteration in forces across the CMC joint with daily activities such as pinch and grasp. Compensatory MCP joint hyperextension and IP joint flexion, characteristic of a type III swan-neck deformity, is potentiated as functional compensation for the progressive adduction contracture.12
Generally, non-surgical management is indicated for closed injuries within 8 to 12 weeks from the time of injury. This treatment is appropriate when the anatomical length relationship between the central slip and the lateral bands is restored after correction of the deformity. Nonoperative treatment can also be attempted in the cases with a volar dislocation or central slip avulsion fracture if the PIP joint is stable and acceptable joint and fracture reductions are achieved.
PIP joint extension splinting is applied when full passive extension and congruent reduction of the PIP joint is maintained. Supplemental transarticular Kirschner wire fixation can be considered. If a flexion contracture of the PIP joint is present, progressive static splinting or serial casting, or dynamic extension splinting is utilized in the attempt to restore a supple joint.
The splinting is maintained at all times for 6 to 8 weeks to completely immobilize the PIP joint. After this period, following reevaluation to confirm stable reduction, the patient is transitioned to buddy straps during the day and night-time extension splinting for an additional 4 to 6 weeks. Throughout the duration of the PIP joint splinting, the patient is instructed for active and passive DIP joint range of motion exercises.
Surgical intervention should be considered for patients who have failed 3 months of conservative treatment, such as extension splinting, and for open injuries or patients with fixed deformity and associated degenerative joint changes. Full passive extension of the PIP joint should be sought prior to surgical reconstruction. Burton and Melchior emphasized that boutonnière reconstructions are generally more successful in patients with flexible joints and that a first-stage joint contracture release, followed by an exercise and splinting program, can sometimes obviate the need for further procedures.13