Boutonniere (Buttonhole) Deformity

A BD manifests after injury to the extensor mechanism of the finger. To understand the pathoanatomy of a BD, it is necessary first to understand the complex normal anatomy of the extensor mechanism of the finger.[3]

Three muscles give rise to the extensor mechanism of the fingers: the extensor digitorum communis (EDC) muscle, the lumbrical muscle, and the dorsal interosseous muscle. The EDC trifurcates into a single central slip and two lateral slips as it passes dorsal to the proximal phalanx and proximal to the PIP joint (see the image below).

Lateral view of relevant finger anatomy.

The central slip traverses the PIP joint dorsally and inserts at the dorsal base of the middle phalanx, extending the PIP joint when the extensor mechanism is fired. Each lateral slip advances radially or ulnarly to insert on the radial or ulnar conjoint lateral band. It is important to note that the two lateral bands normally pass dorsal to the axis of rotation of the PIP joint and eventually fall dorsally to coalesce with each another and insert at the dorsal base of the distal phalanx, working to extend the DIP joint when the extensor mechanism is fired.

Both the lumbrical muscle and the dorsal interosseous muscle contribute to the conjoint lateral bands distally, further generating an extension force at the DIP joint.

A BD occurs as a consequence of disruption of the central slip of the extensor tendon and attenuation of the triangular ligament, which connects the lateral bands to the terminal tendon. This disruption permits each of the conjoint lateral bands of the digit to slide volarly. Once the lateral bands slide volar to the axis of rotation of the PIP joint, this joint is subjected to a pathologic flexion force and an extension lag; all tendons traversing the PIP joint in this setting elicit flexion of the joint. (See the images below.)

Normal lateral band location, dorsal to axis of rotation of proximal interphalangeal joint.

After central slip disruption, lateral bands migrate volar to axis of rotation of proximal interphalangeal joint.

Shortly after the disruption of the central slip, the dorsal interphalangeal joint may experience an extensor lag; however, under the pull of the lumbrical and interosseous muscles, the untethered conjoint lateral bands contract and eventually create a pathologic extension force across the DIP joint. This occurs as the triangular ligament becomes further attenuated and the transverse retinacular ligaments contract.

With the DIP joint in hyperextension, the oblique retinacular ligament, which is located at the dorsal DIP joint, will contract over time, contributing to the hyperextension deformity of this joint.

BDs may develop secondary to trauma (including a direct laceration to the extensor mechanism), secondary to rheumatoid arthritis (RA), and in the setting of burns. There are even reports of congenital BDs.[4] The pathogenesis of a BD varies according to its etiology.[3]

Patients who suffer a traumatic BD may have been subject to a direct injury to the central slip or a force that placed the central slip on stretch, leading to failure of the extensor mechanism. Direct injuries can occur when lacerations disrupt the central slip. Central slip injuries may also occur in the setting of passively forced flexion of an actively extended PIP joint. In another scenario, a volar PIP joint dislocation can avulse the dorsal lip of the middle phalanx base and create a central slip disruption.

BDs in the setting of RA develop and progress over time as the soft tissues of the digit are compromised. Specifically, synovial proliferation within the PIP joint results in stretching of the extensor mechanism. Consequently, a subtle extensor lag may develop as the central slip is unable to achieve full extension.

With the PIP joint in slight flexion, the lateral bands are subluxated volarly and become fixed volar to the axis of rotation. Furthermore, the oblique retinacular ligaments contract, resulting in hyperextension and restricted flexion at the DIP joint. Early in the progression of the deformity, the joints remain passively correctable; however, over time, capsular tissues contract and fibrosis occurs within and around the PIP joint. At this time, the BD becomes a fixed deformity.[5]

BDs secondary to burns may occur due to direct injury of the central slip, as in the case of a full-thickness burn. Alternatively, the central slip may be injured by the onset of an infection; in rare cases, the central slip may undergo ischemic necrosis resulting from the pressure of an overlying eschar.[6, 7]

Case reports have described congenital BDs.[8, 9] Such cases offer an interesting perspective into how altered anatomy may affect the forces across the metacarpophalangeal (MCP), PIP and DIP joints. In one such report, Kim et al described BDs of bilateral little fingers secondary to an extensor mechanism that failed to trifurcate into a central slip and two lateral bands and that consequently failed to insert at the dorsal base of the middle phalanx.[4] Presumably as a result, the triangular ligament also failed to develop.

Upon presentation, a careful patient history should be obtained to determine the etiology of the boutonnière (buttonhole) deformity (BD). If the deformity is of traumatic origin, it is important to determine when the causative incident occurred to provide insight into the timeline of the deformity’s progression. If the deformity is chronic, it is worthwhile to discuss the functional limitations the patient is experiencing. Such a discussion will be relevant in arriving at an appropriate management strategy.

In the evaluation of a patient with a potential BD (see the image below), a general extremity examination should be conducted. The examiner should take note of any deformity or muscle atrophy, assess the patient for tenderness, and conduct an adequate neurovascular examination to ensure that peripheral sensation and motor function are intact.

Boutonnière deformity. Image courtesy of David Bozentka, MD, University of Pennsylvania School of Medicine, published by Medscape (Late Reconstruction of Flexor and Extensor Tendon Injuries at http://www.medscape.com/viewarticle/717388).

In the context of a suspected BD, there are two special tests that help identify the presence of an injury to the extensor mechanism, as follows:

• Elson test
• Boyes test

The Elson test is conducted by fixing the proximal interphalangeal (PIP) joint at 90° of flexion and asking the patient to extend the affected digit. A patient with an intact central slip will demonstrate PIP extension strength, but, most notably, if the PIP joint is rigidly held at 90°, the patient will be unable to extend the distal interphalangeal (DIP) joint. Conversely, a patient with a central slip injury will exhibit an inability to extend at the PIP joint; however, this patient will exhibit additional extension force at the DIP joint.[10]

Alternatively, the Boyes test is conducted by extending the PIP joint and asking the patient to flex the DIP joint. If the extensor mechanism is intact, the patient will be able to flex the DIP joint. However, if an extensor mechanism injury has led to contracted lateral bands, as may be seen in a subacute or chronic BD, the patient will be unable to actively flex the DIP joint.[11]

It is important to distinguish a BD from a so-called pseudoboutonniere deformity.[12]

A boutonnière (buttonhole) deformity (BD) can be assessed by means of plain radiography (see the image below). The lateral radiograph of the affected digit can define the degree of hyperextension at the distal interphalangeal (DIP) joint. Furthermore, radiographs may identify any osseous abnormality.

Radiographic evidence of boutonnière deformities. Image courtesy of Radiopaedia.org; case by Dr Aditya Shetty (http://radiopaedia.org/cases/rheumatoid-arthritis-13).

In the setting of an acute injury to the central slip, conservative management should be employed in an attempt to permit tendon healing before the onset of a boutonnière (buttonhole) deformity (BD). Left untreated, an injury to the central slip can result in a BD within 2-3 weeks.

For an acute injury with a supple digit, management consists of either splinting or pinning of the proximal interphalangeal (PIP) joint in full extension for 4-6 weeks (see the image below). During this time, the distal interphalangeal (DIP) joint is not splinted; rather, this joint is taken through frequent flexion/extension exercises.

Bunnell safety-pin splint.

With the contralateral index finger stabilizing the PIP joint in full extension and the contralateral thumb placed on the volar aspect of the DIP joint, the patient actively flexes the DIP joint. This exercise protocol stabilizes the PIP joint and the central slip while stretching the lateral bands and the oblique retinacular ligaments, preventing contracture and the pathologic boutonnière posture. Thereafter, PIP joint flexion exercises are introduced; however, PIP joint extension splinting is continued at night for an additional 4-8 weeks.[13, 14]

In the case of a large avulsion of the dorsal lip of the middle phalanx, fixation with a Kirschner wire (K-wire) or screw fixation can be employed to reconstitute the extensor mechanism. If the fragment is small and nondisplaced, the injury can be managed nonoperatively with the splinting protocol as described above.

Open injuries should always be irrigated appropriately. The central slip should be repaired if it is completely lacerated. The proximal central slip tendon can be directly repaired to the residual central slip distally, or if there is insufficient tendon distally, the proximal end of the central slip can be anchored directly to the middle phalanx. In concert with nonoperative management, the PIP joint should be maintained in full extension to permit healing.

Classification

BDs can be categorized according to the Burton classification, as follows[15] :

• Burton stage I - BD with a supple and passively correctable joint
• Burton stage II - BD with a fixed contracture and contracted lateral bands; PIP joint spaces are maintained
• Burton stage III - BD with a fixed deformity, contractures of lateral bands, volar plate and collateral ligaments; the PIP joint suffers from intra-articular fibrosis
• Burton stage IV - BD with a fixed deformity, contractures of lateral bands, volar plate and collateral ligaments; the PIP joint suffers from intra-articular fibrosis and arthritis as evident on radiography

The Burton classification is based on the clinical examination and plain radiographs. Ultimately, surgical management is guided by the degree of deformity at the PIP joint, the suppleness or correctability of the joints, and the presence of arthritis at the PIP joint.[5, 16]

Management

For many patients, a BD does not impart excessive functional deficits; however, for those patients that suffer moderate-to-severe functional deficits, an operative approach may be indicated. In such instances, a detailed conversation with an orthopedic hand surgeon should be pursued to explore the options and to arrive at appropriate expectations.

In the setting of a mild deformity, in which the PIP joint can be corrected passively, patients may still suffer from an extensor lag at the PIP joint and from hyperextension at the DIP joint. Because the functional limitation is secondary to the lack of PIP joint extension and DIP joint flexion, management is aimed at correcting these deformities.

To relieve the hyperextension at the DIP joint and to permit increased flexion, an extensor tenotomy overlying the middle phalanx can be performed. The extensor tenotomy is performed through a midaxial longitudinal incision overlying the dorsum of the middle phalanx, lengthening the extensor mechanism and returning a degree of flexion to the DIP joint. Because the flexion deformity at the PIP joint is, by definition, passively correctable in a mild deformity, dynamic splinting is utilized to reduce the extension lag.[17, 18]

In patients with a moderate BD, the PIP joint flexion deformity may exceed 30-40°. Nonetheless, if the PIP joint is passively correctable, the BD is amenable to soft-tissue reconstruction.

Operative management entails reconstruction of the extensor mechanism through shortening of the central slip and reduction of the lateral bands dorsally.[19] It is vital to the functionality of the digit that PIP joint flexion be preserved; accordingly, such a reconstruction should not be performed in a patient with an incompetent flexor mechanism. This operation is often coupled with an extensor tenotomy to enable functional DIP flexion.

Severe BDs involve fixed contractures and may exhibit PIP joint arthrosis on radiographs. Fixed deformities are not amenable to the soft-tissue reconstruction techniques described above. In an attempt to achieve extension at the PIP joint, dynamic splinting or serial casting may be employed to achieve passive extension. This may be coupled with soft-tissue releases, including releases of the accessory collateral ligaments.

In the setting of PIP arthrosis, management consists of fusion or arthroplasty. In PIP fusion, the joint is fused in relative flexion to permit grasping of objects. Splinting is utilized to allow union to occur over a period of 4-6 weeks. PIP joint arthroplasty, on the other hand, entails a more extensive approach, in that the surgeon must recreate and maintain functional motion at the PIP joint. Consequently, soft-tissue reconstruction is once again necessary and includes shortening of the central slip and reduction of the lateral bands dorsally.

The full course of treatment of a BD should be discussed at the initiation of therapy. Patients will often wear a static splint maintaining full PIP extension after an operation to allow for healing. Thereafter, patients will proceed to intermittent splinting and undergo passive stretching exercises. Throughout the course of treatment, dedicated hand therapy is integral to the management and correction of a BD.

Correction of a BD is not without complexity. While there is an attempt at improvement in function, patients may experience any of the following:

• Continued debility
• Incomplete correction of the deformity
• Recurrence of the deformity
• Loss of mobility—specifically, flexion at the PIP joint or extension at the DIP joint
• Chronic pain
• Infection at the site of open injury or the surgical site
• Reoperation