Boutonniere Deformity


Definition

It is a deformity of the fingers or toes in which the proximal interphalangeal joint is flexed and the distal interphalangeal joint is hyperextended.

Mechanism/Pathophysiology

Mechanism

If the central slip of the digital expansion is ruptured, minimal deformity results as long as the transverse fibers of the expansion remain in tact. If they are also torn, a deformity is produced at the PIP joint.In this case, all extensor force will be transmitted to the distal phalanx by intact lateral bands, producing hyperextension of the DIP joint. The PIP joint buckles into flexion and protrudes through the breech in the extensor hood. The two lateral bands will now run on the palmar aspect of the PIP joint and will exaggerate flexion.[1]

The deformity is the result of a rupture of the central tendinous slip of the extensor hood and is most common after trauma or in rheumatoid arthritis.[2]

Pathophysiology

A boutonniere deformity (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.

Signs and Symptoms

Signs of boutonnière deformity can develop immediately following an injury to the finger or may develop a week to 3 weeks later.

  • The finger at the middle joint cannot be straightened and the fingertip cannot be bent.
  • Swelling and pain occur and continue on the top of the middle joint of the finger.[3]

Etiology

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. [5]

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.[6]

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.[7],[8]

Case reports have described congenital BDs. [9],[10] 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.

Treatment

Treatment options include prolonged splinting or surgery for patients who present for evaluation with a chronic injury.

Non-surgical

Treatment for acute injury is uninterrupted splinting of the PIP in full extension for 6 weeks. After 6 weeks of immobilization, exercises are begun.The exercise involves two sequential maneuvers. The first is active assisted PIP joint extension. This will stretch the tight volar structures, will cause the lateral bands to ride dorsal to the PIP joint axis, and will put longitudinal tension on the lateral bands and oblique retinacular ligaments.The second maneuver is maximal active forced flexion of the DIP joint while the PIP joint is held at 0°or as close to that position as the PIP will allow. This will gradually stretch the lateral bands and oblique retinacular ligaments to their physiologic length. Continue splinting 2 to 4 weeks when not exercising.When full PIP joint extension can be maintained throughout the day, then night splinting only is appropriate. Length of treatment and splinting may be several weeks.[1]

Surgical

While nonsurgical treatment of boutonnière deformity is preferred, surgery is an option in certain cases, such as when:

  • The deformity results from rheumatoid arthritis.
  • The tendon is severed.
  • A large bone fragment is displaced from its normal position.
  • The condition does not improve with splinting.

Surgery can reduce pain and improve functioning, but it may not be able to fully correct the condition and make the finger look normal. If the boutonniere deformity remains untreated for more than 3 weeks, it becomes much more difficult to treat.[3]

References

  1. 1.0 1.1 Darlene Hertling and Randolph M. Kessler,Management of common musculoskeletal disorders.4th ed,1983.
  2. David J Magee,Orthopedic Physical Assesment.1987.
  3. 3.0 3.1 https://orthoinfo.aaos.org/en/diseases--conditions/boutonniere-deformity/
  4. 4.0 4.1 Kim JP, Go JH, Hwang CH, Shin WJ. Restoration of the central slip in congenital form of boutonniere deformity: case report. J Hand Surg Am. 2014 Oct. 39 (10):1978-81. [Medline]
  5. Feldon P, Terrono AL, Nalebuff EA, Millender LH. Rheumatoid arthritis and other connective tissue diseases. Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH, eds. Green’s Operative Hand Surgery. 6th ed. Philadelphia: Elsevier; 2011. 2: 2052-6
  6. Muir IFK, Barclay TL. Burns and Their Treatment. London: Lloyd-Luke; 1962. 109
  7. Grishkevich VM. Surgical treatment of postburn boutonniere deformity. Plast Reconstr Surg. 1996 Jan. 97 (1):126-32. [Medline].
  8. Tsuge K. Congenital aplasia or hypoplasia of the finger extensors. Hand. 1975 Feb. 7 (1):15-21. [Medline]
  9. Carneiro RS. Congenital attenuation of the extensor tendon central slip. J Hand Surg Am. 1993 Nov. 18 (6):1004-7. [Medline].
  10. Elson RA. Rupture of the central slip of the extensor hood of the finger. A test for early diagnosis. J Bone Joint Surg Br. 1986 Mar. 68 (2):229-31. [Medline].
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