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  • A Zone III extensor tendon injury characterized by  
    • PIP flexion
    • DIP extension
  • Mechanism
    • caused by rupture of the central slip over PIP joint from
      • laceration
      • traumatic avulsion (jammed finger)
      • capsular distension in rheumatoid arthritis
  • Pathoanatomy
    • pathoanatomic sequence includes
      • rupture of central slip 
        • causes the extrinsic extension mechanism from the EDC to be lost
        • prevents extension at the PIP joint
      • attenuation of triangular ligament 
        • causes intrinsic muscles of the hand (lumbricals) to act as flexors at the PIP joint
        • lumbricals also extend the DIP joint without an opposing or balancing force
      • palmar migration of collateral bands and lateral bands
        • the lumbricals' pull becomes unopposed, pulling through the base of the distal phalanx and volar to the PIP
        • causes PIP flexion and DIP extension
    • bone deformity
      • injury involves all three phalanges
      • the middle phalanx flexes on the proximal phalanx at the PIP joint
      • the distal phalanx is hyperextended relative to the middle phalanx at the DIP joint
  • Associated conditions
    • rheumatoid arthritis
    • pseudo-boutonniere
      • refers to PIP joint flexion contracture in the absence of DIP extension
  • Muscle
    • lumbrical muscles
      • originate from the FDP and insert on the lateral bands
  • Ligament anatomy
    • extensor hood and central slip
      • the extrinsic extensor tendon joins the extensor hood at the MCP
      • the central portion of the extensor hood forms the central slip
      • the central slip inserts onto the middle phalanx and acts to extend the PIP joint
    • lateral bands
      • the lateral bands are formed from the deep head of the dorsal interossi combining with the volar interossi
      • the lateral bands insert onto the base of the distal phalanx to extend the DIP joint
    •  triangular ligament
      • spans the two lateral bands, preventing them from subluxing volarly
    • transverse retinacular ligament
      • prevents dorsal subluxation of the lateral bands
  • Blood supply
    • interosseous muscles
      • receive blood from vessels formed by a combination of the deep palmer arch and the ulnar artery
  • Physical exam 
    • deformity
      • characterized by PIP flexion DIP extension 
    • Elson test  
      • is the most reliable way to diagnose a central slip injury before the deformity is evident
      • bend PIP 90° over edge of a table and extend middle phalanx against resistance.
        • in presence of central slip injury there will be
          • weak PIP extension
          • the DIP will go rigid
        • in absence of central slip injury DIP remains floppy because the extension force is now placed entirely on maintaining extension of the PIP joint; the lateral bands are not activated
  • Radiographs
    • recommended view
      • radiographs are not required in evaluation and treatment of Boutonniere deformity
  • Nonoperative
    • splint PIP joint in full extension for 6 weeks
      • indications
        • acute closed injuries (< 4 weeks)
      • technique
        • encourage active DIP extension and flexion in splint to avoid contraction of oblique retinacular ligament
        • complete part-time splinting for an additional 4-6 weeks
  • Operative
    • primary central band repair
      • indications
        • acute displaced avulsion fx (proximal MP avulsion seen on x-ray)
        • open wound that needs I&D
    •  lateral band relocation vs. terminal tendon tenotomy vs. tendon reconstruction 
      • indications
        • in chronic injuries after FROM is obtained with therapy or surgical release
      • technique
        • terminal tendon tenotomy (modified Fowler or Dolphin tenotomy)(never central slip tenotomy)
        • secondary tendon reconstruction (tendon graft, Littler, Matev)
        • triangular ligament reconstruction
    • PIP arthrodesis
      • indications
        • rheumatoid patients
        • painful, stiff and arthritic PIP joint

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Questions (2)

(OBQ09.80) Chronic injury to what anatomic structure can lead to a boutonnière deformity of the finger? Review Topic


terminal extensor tendon




sagittal band




volar plate




flexor digitorum profundis tendon insertion




central slip of the extensor tendon



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Rupture of the central slip of the extensor tendon and subsequent subluxation of the lateral bands leads to a boutonnière deformity, which is characterized by PIP flexion and DIP extension. Central slip injuries can be caused by a laceration or traumatic avulsion. In the listed reference, Imatami et al treated a series of central slip injuries associated with attachment fractures successfully with ORIF. As stated by Tuttle et al, rupture of the terminal extensor tendon leads to a mallet finger. Sagittal band injury can lead to subluxation of the extensor tendon at the level of the MCP joint. Chronic volar plate injuries can lead to swan neck deformities. Avulsion of the FDP insertion leads to a jersey finger. Illustrations A and B are a clinical photograph and anatomic diagram of a boutonneire deformity.


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(OBQ04.71) A 54-year-old female presents with a hand deformity. A surgical procedure is being considered that relocates the lateral bands dorsally to counteract the pathophysiology of the deformity. Which of the following deformities does this patient most likely have? Review Topic


Boutonneire finger deformity




Lumbrical plus finger deformity




Mallet finger deformity




Jersey finger deformity




Swan neck finger defomity



Select Answer to see Preferred Response


Boutonniere deformity is characterized with the PIP in flexion and the DIP in hyperextension as shown in Illustration A. It is caused by central slip rupture or attenuation (secondary to capsular distention, e.g., rheumatoid arthritis), laceration, or traumatic disruption. Volar subluxation of the lateral bands due to incompetence or disruption of the triangular ligaments leads to increased deformity as the lateral bands become flexors of the PIP. Relocation of the lateral bands to their original dorsal position to counteract the pathophysiology of the deformity is an option for patients that have an approximately 40 degree active flexion contracture but full passive extension.


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