Outline

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.

The boutonnière and swan-neck deformities of the digits are differentiated as being the sequelae of trauma, or as a part of the spectrum of rheumatoid disease.

Post-Traumatic Deformity

Post-Traumatic Boutonnière Deformity

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).

Figure 36-1 Lateral view of the digit demonstrating the volar subluxation of the lateral bands (clb) in a simulated boutonniere deformity (central slip [CS]).

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.

After a traumatic injury to the central slip, the boutonnière deformity generally progresses through five stages ⁶:

1 Disruption of the central slip results in resting flexion of the PIP joint and weak extension of the middle phalanx via the lateral bands

2 Absent active PIP joint extension combined with attenuation of the triangular ligament and contracture of the transverse retinacular ligaments results in the volar migration of the lateral bands

3 Extension forces are transmitted through the lateral bands, causing hyperextension at the DIP joint

4 Progressive contracture of the PIP joint volar plate and the oblique retinacular ligament causes fixed flexion contracture at the PIP joint

5 Progressive articular degeneration occurs after prolonged and untreated pathology

Post-Traumatic Swan-Neck Deformity

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.

The post-traumatic swan-neck deformity may progress through four characteristic stages ⁷:

1 Full passive PIP joint range of motion

2 Intrinsic tightness secondary to prolonged hyperextension of the PIP joint

3 Fixed hyperextension of the PIP joint regardless of MCP position due to attenuation and contraction of the transverse retinacular ligament and dorsal subluxation of the lateral bands

4 Articular degeneration and fixed hyperextension deformity of the PIP joint

Rheumatoid Deformity

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