Posttraumatic boutonnière and swan neck deformities are complex clinical problems that are often poorly understood. A boutonnière deformity consists of flexion of the proximal interphalangeal (PIP) joint and hyperextension of the distal interphalangeal (DIP) joint. The anatomy and pathophysiology of this deformity was described by Hauck1 in 1923, and is discussed in detail here.
A swan neck deformity consists of hyperextension of the PIP joint and flexion of the DIP joint. Although swan neck deformity was first described in the setting of inflammatory arthritis, posttraumatic swan neck deformity has been recognized for nearly a century. Watson-Jones2 described a swan neck deformity that resulted from a chronic disruption of the terminal tendon insertion at the distal phalanx (ie, mallet finger). Portis3 described a swan neck deformity caused by a hyperextension injury of the PIP joint. Patients present to hand surgery clinics with a broad spectrum of acute, chronic, supple, and fixed boutonnière and swan neck deformities that require a range of treatment.
Anatomy
An understanding of the anatomy and mechanics of the extensor mechanism of the finger is crucial to management of boutonnière and swan neck deformities4-7 (Figure 1 and Table 1). The three muscles that contribute to the extensor mechanism of the finger are the extensor digitorum communis (EDC), the lumbrical, and the dorsal interosseous. The EDC is stabilized by the radial and ulnar sagittal bands as it crosses the metacarpophalangeal (MP) joint. The sagittal bands arise from the EDC tendon dorsally and travel transversely to insert on the volar plate of the MP joint and the volar periosteum of the proximal phalanx (P1). In addition to stabilizing the EDC tendon, the sagittal bands help to extend the MP joint through a lasso effect.
After crossing the MP joint, the EDC tendon trifurcates into a central slip and two lateral slips. The central slip inserts onto the dorsal base of the middle phalanx (P2) and extends the PIP joint. The two lateral slips travel radially and ulnarly to join their respective conjoint lateral bands.
The lumbrical muscle originates on the flexor digitorum profundus tendon and is located on the radial aspect of the finger only. The lumbrical tendon passes volar to the deep intermetacarpal ligament at the level of the MP joint. Distally, the lumbrical tendon gives off contributions to the oblique fibers overlying the distal aspect of the P1. The oblique fibers join the medial bands of the interosseous and, with the central slip, extend the PIP joint. The lumbrical tendon terminates in the conjoint lateral band.
The dorsal interosseous contribution to the extensor mechanism is arguably the most complex of the three muscles that contribute to the extensor mechanism.4-7 The anatomy of first dorsal interosseous muscle varies slightly from that of other interosseous muscles1 but, in general, the dorsal interosseous muscles are divided into two muscle bellies, the superficial and the deep heads.8 The superficial head gives rises to the medial tendon, which passes deep to the sagittal band and inserts on the base of the P1. The medial tendon abducts the digit. The deep head gives rise to the lateral tendon, which passes superficial to the sagittal band. Distally, the lateral tendon gives off contributions to the transverse fibers over the middle aspect of P1, which flex the MP joint. Distal to the transverse fibers, the lateral tendon gives off contributions to the oblique fibers and the medial band of the interosseous, which extend the PIP joint. The lateral tendon then joins with the lateral slip of the EDC and the lumbrical tendon to form the conjoint lateral band.
Distal to the PIP joint, the radial and ulnar conjoint lateral bands are anchored dorsally by the triangular ligament and volarly by the transverse retinacular ligament, preventing volar and dorsal subluxation of the conjoint lateral bands, respectively. Overlying the distal aspect of the P2, the radial and ulnar conjoint lateral bands come together to form the terminal tendon. The terminal tendon inserts into the base of the distal phalanx and extends the DIP joint.
The oblique retinacular ligament is a controversial structure, but most studies report that it attaches to the flexor sheath proximally and the terminal tendon distally.4-7 It passes dorsal to the axis of the DIP joint and volar to the axis of the PIP joint, linking the action of the DIP and PIP joints. As the PIP joint extends, the oblique retinacular ligament tightens and transmits force across the terminal tendon, resulting in DIP extension.
Boutonnière Deformity
Pathomechanics
As mentioned earlier, a boutonnière deformity is a flexion deformity at the PIP joint and a hyperextension deformity at the DIP joint (Figure 2). It is the result of a disruption of the central slip and triangular ligament on the dorsum of the finger. Common mechanisms of injury include blunt trauma, an open laceration, or a volar dislocation of the PIP joint.9,10
An injury to the central slip and triangular ligament allows the conjoint lateral bands to subluxate volarly with PIP flexion. Over time, a PIP joint extension lag develops. Without prompt treatment, the PIP extension lag becomes a fixed flexion deformity, causing the lateral bands to become permanently subluxated volarly. The injury to the central slip and triangular ligament also allows the lateral bands to migrate proximally because of the loss of the tethering effect of the central slip. As the lateral bands subluxate volarly, they migrate further proximally secondary to the pull of the lumbrical and interosseous muscles. This leads to increased tension on the terminal tendon and hyperextension at the DIP joint.
A true boutonnière deformity should not be confused with a pseudo deformity, in which a hyperextension injury to the PIP joint leads to a PIP flexion contracture.11-14 In a pseudo deformity, the central slip and triangular ligament remain competent, and the DIP joint retains full mobility. The flexion contracture is caused by scarring of the volar plate and joint capsule rather than by a derangement of the extensor mechanism. Although they both have a similar clinical presentation, distinguishing between these two entities by using clinical examination tests, including the Elson and Boyes tests, is important because the appropriate treatment options are different for a pseudo deformity. Treatment of a pseudo deformity involves early, aggressive motion, whereas treatment of a true boutonnière deformity involves a period of immobilization.
Clinical Evaluation and Classification
Several signs can lead the examiner to suspect an injury to the extensor mechanism in a patient with an injury to the PIP joint. The Elson test is the most reliable maneuver for diagnosis of an acute boutonnière injury.15,16 The examiner holds the PIP joint in 90° of flexion and instructs the patient to actively extend the DIP joint. With an intact extensor mechanism, holding the PIP joint in 90° of flexion causes slack in the lateral bands as they are held distally by their attachments to the central slip. The patient is unable to generate any extension power at the DIP joint. With a boutonnière injury, flexion of the PIP joint does not advance the lateral bands distally secondary to disruption of the central slip. Tension is generated in the terminal tendon because of the disrupted central slip. Therefore, the patient is able to generate an abnormal amount of active extension at the DIP joint with the PIP joint held in flexion (Figure 3). It may be necessary to perform a digital block before the Elson test is done to allow an accurate assessment.
Another useful clinical maneuver is the Boyes test, which is used to assess the patient’s ability to actively flex the DIP joint with the PIP joint held in extension. Patients with an intact extensor mechanism should be able to fully and actively flex the DIP joint. Patients with contracted lateral bands will have decreased active flexion at the DIP joint when the PIP joint is held in extension. This test may not be positive in an acute setting.17
Plain radiographs of the finger should be obtained in patients with an injury to the PIP joint. Radiography may demonstrate subtle DIP hyperextension that can be difficult to detect with a clinical examination alone. Central slip avulsions may involve a bony fragment, which can alter treatment. In general, advanced imaging modalities are not needed for diagnosis of boutonnière deformity.
Chronic boutonnière deformities are categorized using the Burton classification (Table 2).18 This classification system is based on clinical examination findings and the radiographic appearance of the PIP joint.
Nonsurgical Management
For patients who present with an acute, closed boutonnière injury (Burton stage I), nonsurgical management is generally recommended; this consists of splinting the PIP joint in extension for 4 to 8 weeks to allow the central slip to heal. Active DIP flexion exercises are performed multiple times daily to pull the lateral bands dorsally and to counteract the proximal migration of the lateral bands. After 4 to 8 weeks of full-time splinting, PIP flexion exercises are introduced, but the PIP extension splint is worn at night for an additional 4 to 6 weeks.10
Chronic, fixed boutonnière deformities (Burton stage II) are often amenable to nonsurgical management, as long as full passive PIP extension can be achieved with a therapy protocol. Full passive PIP extension is achieved with serial casting or dynamic splinting over a period of 6 to 12 weeks. Active DIP flexion exercises are a critical part of the therapy protocol in this situation, as well. Once full passive PIP extension is achieved, it is maintained with extension splinting for 6 to 12 weeks, followed by a protocol to gradually resume PIP flexion.
Surgical Management
Acute Boutonnière Deformity
Surgical intervention is occasionally necessary for boutonnière deformities. In patients with acute, closed injuries (Burton stage I) that are not amenable to full-time PIP extension splinting, pinning of the PIP joint may be beneficial. The PIP joint is extended, effectively reducing the lateral bands, and a 0.045-inch Kirschner wire is placed across the joint. The wire is left in place for 4 to 6 weeks and then removed, followed by initiation of PIP flexion exercises.10
Patients with acute, open boutonnière injuries often have joint involvement and may benefit from irrigation and débridement in the operating room. At the time of débridement, a primary repair of the central slip can be performed or the slip can be reattached to the base of the P2 with a bone anchor or through bone tunnels. After repair of the central slip, the PIP joint is pinned in extension for 6 weeks to protect the repair.
Bony avulsions of the central slip may also warrant surgical management in the acute setting. Although patients with small bony fragments may be managed nonsurgically as described earlier, larger bony fragments require fixation to the base of the P2 with Kirschner wires or screws. Other factors, such as chronicity, displacement, and patient compliance, should also be considered. The decision to treat a bony boutonnière injury surgically or nonsurgically is best left to an experienced hand surgeon.
Chronic Boutonnière Deformity
Surgical management of chronic boutonnière deformities should be approached with caution. Seven principles for management of a chronic boutonnière deformity described by Burton18 are outlined in Table 3. Patients with a boutonnière deformity generally retain full flexion and grip strength and have few functional limitations. Surgical intervention may lead to extension contractures of the PIP joint and poor functional outcomes. Prior to undertaking any surgical reconstruction, it is imperative to thoroughly discuss the risks and expected outcomes with the patient.
If a patient wishes to proceed with surgical correction of a chronic boutonnière deformity, the first step is to achieve full passive PIP joint extension with a preoperative therapy program that includes splinting or casting, a dynamic external fixator, or an open joint contracture release. Once full passive PIP joint extension has been achieved, several tendon rebalancing procedures can be used.
The simplest tendon rebalancing procedure is a terminal tendon tenotomy (ie, distal Fowler or Dolphin tenotomy).19,20 By dividing the terminal tendon, the hyperextension force on the DIP joint is removed. The extensor mechanism retracts, allowing for more force to be transmitted to the PIP joint and decreasing the PIP extensor lag. Postoperatively, a DIP extension splint is worn at all times for 6 to 8 weeks, except during range-of-motion (ROM) exercises.
The tendon rebalancing technique developed by Littler and Eaton21 can also be used. Through a dorsal incision, the lateral bands are sharply released from the lumbrical muscle contribution and the oblique retinacular ligament. The lateral bands are then mobilized dorsally and sutured together in the midline, distal to the PIP joint. This effectively diverts all active extension power (extrinsic and intrinsic) to the PIP joint, while maintaining DIP extension through the action of the preserved oblique retinacular ligament.
Curtis et al22 described a staged reconstruction performed with local anesthesia to allow accurate assessment of active motion intraoperatively. In the first stage, an extensor tenolysis is performed through a dorsal incision. If full active extension is present at this point, the procedure is complete. If an extensor lag remains, then the transverse retinacular ligaments are transected, allowing the lateral bands to swing dorsally. Active extension is reassessed. If full active extension is present, then the procedure is complete. If an extensor lag <20° remains, then a Fowler tenotomy is performed. If an extensor lag >20° remains after the transverse retinacular ligaments are transected, then the central tendon is dissected free and advanced 4 to 6 mm into a drill hole at the base of the P2.23 The slackened lateral bands can then be loosely sutured dorsally to the central tendon to augment the tendon advancement. Occasionally, the central slip is attenuated and a reconstructive procedure, such as a turndown procedure, is required.
Finally, for patients with arthritic change and pain at the PIP joint associated with a long-standing boutonnière deformity, an arthrodesis is the procedure of choice.
Swan Neck Deformity
Etiology
Unlike a boutonnière deformity, which is the result of an injury to the central slip and triangular ligament, a posttraumatic swan neck deformity can result from a variety of initial injuries.24-26 Zancolli26 classified these injuries into three categories: extrinsic, intrinsic, and articular (Table 4).
Extrinsic causes of swan neck deformities are the result of excessive extension force on the P2. In the setting of a flexible PIP joint, hyperextension develops over time, with chronic extension force. For example, disruption of the terminal tendon (eg, a mallet finger injury) allows the lateral bands to migrate proximally, increasing the extension force on the P2 (Figure 4). Posttraumatic wrist or MP joint flexion contractures also increase the tension on the EDC tendon, increasing the extensor force on the P2 and leading to deformity over time.
The intrinsic causes of swan neck deformities are related to tightness of the intrinsic muscles, or an intrinsic-plus finger. Chronic volar subluxation of the MP joint (either posttraumatic or the result of inflammatory arthritis) can lead to tightening of the intrinsic muscles over time. Other mechanisms include ischemic contractures that develop after compartment syndrome of the hand and intrinsic tendon adhesions.
Articular causes of swan neck deformity include injury to or degeneration of the volar structures of the PIP joint. This can be the result of a posttraumatic injury, inflammatory arthritis, or generalized hyperlaxity. Hyperextension injury to the PIP joint can lead to disruption of the volar plate and volar capsule, which can lead to chronic insufficiency of the volar structures if not appropriately treated. The flexor digitorum superficialis (FDS) tendon also serves as a palmar stabilizer of the PIP joint; therefore FDS disruptions can also lead to PIP hyperextension deformity over time.
Clinical Evaluation and Classification
A careful history and physical examination can help the clinician determine the etiology of the swan neck deformity. A history of prior injuries (eg, mallet injury, FDS tendon laceration, PIP joint hyperextension injury) makes determining the etiology straightforward. In the absence of a known injury, physical examination and imaging can aid in diagnosis. Some persons with ligamentous laxity are able to hold their fingers in a swan neck posture naturally, but they rarely have any functional limitations.
The physical examination should start by assessing the patient for signs of inflammatory arthritis, such as the involvement of multiple joints in the hands and wrists because the treatment recommendations for a posttraumatic swan neck deformity are significantly different than those for a swan neck deformity associated with autoimmune synovitis. If signs of inflammatory arthritis are present, a referral to a rheumatologist is indicated. The flexibility of the DIP, PIP, and MP joints should be assessed with active and passive motion. The integrity of the FDS tendon should be assessed, as well.
The Bunnell test can be used to assess the flexibility and tightness of the intrinsic muscles.27 Because the intrinsic tendons pass volar to the MP joint axis of rotation, they are relaxed and tensioned with MP joint flexion and extension, respectively. Conversely, because the intrinsic tendons pass dorsal to the PIP joint axis of rotation, they are relaxed with PIP joint extension and tensioned with PIP joint flexion. If the intrinsic muscles are excessively tight, holding the MP joint in extension will tighten the intrinsic tendons even further and increase the extension force across the PIP joint. Therefore, a patient with intrinsic muscle tightness will have a decrease in passive and active flexion of the PIP joint with the MP joint held in extension.
Radiography is an important part of the clinical assessment of swan neck deformity. The presence of fractures (eg, bony mallet, avulsion fracture of the PIP volar plate) may change the treatment plan, particularly if the fragment is large enough to undergo open reduction and internal fixation. The presence of arthritis will change the treatment recommendations, as well. Advanced imaging (eg, MRI, CT) is rarely indicated.
The classification of swan neck deformities is based on the ROM of the PIP joint and radiographic findings. This classification system can serve as the basis for treatment recommendations10 (Tables 5 and 6).
Nonsurgical Management
For patients with mild swan neck deformities and full active flexion of the PIP joint, nonsurgical management is often indicated. These patients often report difficulty initiating flexion from the hyperextended posture. They may also report snapping of the lateral bands, which occurs when the dorsally subluxated lateral bands reduce volarly as the finger moves from hyperextension to flexion. A silver ring splint or other functional splint that limits PIP hyperextension while allowing full flexion can limit these symptoms. These splints are low profile, easy to wear, and aesthetically pleasing28 (Figure 5).
Surgical Management
For patients with mild deformity who do not wish to wear a splint or those with more severe deformity, surgery is indicated. The choice of procedure is based on the severity of the deformity. For patients with type I deformities and full ROM of the PIP joint, soft-tissue procedures are indicated to limit hyperextension of the PIP joint. These procedures can be combined with an arthrodesis of the DIP joint if the flexion contracture of the DIP joint is severe.
Several soft-tissue procedures have been used to limit hyperextension of the PIP joint. The most widely used technique is the FDS tenodesis, or FDS sling technique.29 Through a volar zig-zag incision, a window is made in the flexor sheath on either side of the A3 pulley. One slip of FDS is incised approximately 1.5 cm from its insertion, leaving the distal attachment intact. The PIP joint is flexed 20° to 30°, and the detached FDS slip is fixed proximally to the bone with an anchor, or it is sutured to the distal edge of the A2 pulley, forming a static tether to PIP hyperextension. Postoperatively, the joint is splinted in 30° of flexion for 3 weeks. At 3 weeks, active flexion is initiated, but extension block splinting is continued to prevent hyperextension for at least an additional 3 weeks.
Oblique retinacular ligament reconstruction is another technique used to address hyperextension of the PIP joint.30-32 The ulnar lateral band is freed from the extensor mechanism and incised proximally, leaving the distal insertion intact. The lateral band is then transposed volar to the Cleland ligaments to bring it volar to the axis of rotation of the PIP joint. The lateral band is passed to the opposite side of the finger and sutured to the flexor tendon sheath, with the PIP joint held in 30° of flexion. In theory, this reconstruction should correct the PIP hyperextension by providing a static tether as well as increasing the extension force on the DIP joint to correct the DIP flexion deformity. In practice, however, the terminal tendon is often attenuated and incompetent, so the DIP joint deformity is rarely completely corrected with this method. Alternatively, the oblique retinacular ligament can be reconstructed using an autologous tendon graft.33
When a disruption of the volar plate was the initial injury that led to the swan neck deformity, a direct repair of the volar plate is indicated.34-36 Volar plate repair can be done through a volar incision, using bone anchors or drill holes in the base of the P2.
Lateral band translocation and dermadesis have also been used to manage mild swan neck deformities.26,37 These procedures can be done alone or in conjunction with one of the procedures described earlier.
For patients with a type II swan neck deformity with intrinsic tightness, an intrinsic release should be combined with one of the procedures described earlier to address PIP hyperextension. An intrinsic release is performed through a dorsoulnar longitudinal incision over the P1. The structures of the extensor mechanism are identified. The lateral band and oblique fibers are incised at the level of the distal half of the P1, with care taken to leave intact the central slip, the lateral slips of the extensor tendon, and the transverse fibers.38,39
For patients with a type III swan neck deformity, full passive ROM of the PIP joint must be restored before addressing the deformity. This can be done with a stepwise approach, starting with a closed gentle manipulation of the PIP joint, with the goal of achieving 80° to 90° of flexion. If motion is restored, but the dorsal skin is blanched and at risk of necrosis, a skin release can be done. The skin release is performed distal to the joint, with an oblique incision made over the P2. The skin is allowed to heal by secondary intention. If a closed manipulation does not restore adequate motion, an open release of the lateral bands is performed by making two parallel incisions on either side of the central slip, allowing the lateral bands to move volarly.24
After passive PIP flexion is restored with any of these methods, flexor tendon gliding should be assessed to ensure that no secondary adhesions of the flexor tendons are present. This can be done by assessing active motion if the surgery is performed under local anesthesia or by making an incision in the palm and pulling direct traction on the flexor tendons. Once adequate PIP joint motion has been achieved and smooth flexor tendon gliding has been ensured, any of the previously described procedures to address PIP hyperextension can be performed. Typically, an intrinsic release is necessary.
For patients with a type IV swan neck deformity, the PIP joint should be addressed with arthroplasty or arthrodesis. If arthroplasty is performed, it is necessary to address the soft-tissue balancing around the joint with a procedure to limit PIP hyperextension. The decision between arthroplasty and arthrodesis depends on many variables and should be made on a case-by-case basis for each patient.
Summary
Determining the appropriate course of treatment for each patient with a posttraumatic boutonnière or swan neck deformity requires the clinician to have a thorough understanding of the anatomy of the extensor mechanism, the etiology of the deformity, the available nonsurgical management modalities, and the techniques for surgical correction. The clinician should work with the patient to elucidate any functional limitations and to ensure that he or she maintains realistic expectations.
References
Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, reference 28 is a level II study. References 11, 13, 14, 16, 19, 20, 22, 23, 29-33, and 35-38 are level IV studies. References 3, 8, 12, 16, 21, 27, 30, and 34 are level V expert opinion.
References printed in bold type are those published within the past 5 years.
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