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Swan Neck Deformity (SND)

The deformity

Hyperextension at PIPJ

Flexion at DIPJ

Flexion at MCPJ


Possible causes of swan-neck deformity may involve any of the joints.

Site wise cause –


Synovitis of joint à leading to attenuation of volar plates and TRL (Transverse retinacular ligament) à allowing dorsal translocation of lateral bands & Destruction of FDS insertion àLeading to hyperextension of PIPJ

Hyperextension at PIPJ leads to tightening of FDP tendon and loss of tension in lateral bands à leading to DIPJ flexion

Over time adhesions develops leading to fixed deformity


Synovitis of MCPJ à causes weakening of insertion of long extension on proximal phalanx à causing force to be transmitted to base of proximal phalanx à leading to PIPJ hyperextension

Synovitis also leads to weakening of volar plates à cause subluxation of MCPJ – leading to adhesion and later shortening of intrinsic muscles – further contributing to PIPJ hyperextension.


Rupture of extensor tendon (due to trauma or synovitis) – leads to proximal migration and relaxation of lateral bands.

Extensor power is then concentrated on central slip à resulting in PIPJ hyperextension and SND

Wrist –

Synovitis causes – carpal collapse, carpal supination & ulnar tranlocation

Carpal collapse – leads to relative lengthening of long flexors and extensors à allowing intrinsics to overpower their action à leading to hyperextension at PIPJ and then to SND

Causes –

DIPJMallet finger (rupture of extensor tendon)
PIPJVolar plate laxity
Dorsal migration of TRL
FDS rupture
MCPJMP joint volar subluxation
Intrinsic muscle tightness
Weakening of insertion of long extensors on proximal phalanx
Wrist jointCarpal collapse

Classification –

Feldon et al

Type I – PIPJ – flexible in all position

Type II – PIPJ – flexion limited in certain position

Type III – limited flexion in all positions

Type IV – stiff joint with poor radiographic appearance

Nalebuff classification –

Type I – full PIPJ flexibility without intrinsic tightness

Type II – PIPJ flexible but with P joint volar subluxation and associated intrinsic tightness

Type III – motion of PIPJ limited by extensor mechanism but with radiographic preservation of joint surface

Type IV – stiff PIP joint with intrarticular joint destruction

Treatment –

Type I –

Can be managed non-operatively – by Splinting with Silver ring

Operative management –

If primary pathology at DIPJ – Mallet finger – DIPJ arthrodesis

If pathology at PIPJ level –

Flexor tenodesis @ PIPJ


Distally based slip of FDS

Littler’s ORL reconstruction

Free tendon graft (Spiral ORL reconstruction)

Type II –

In addition to above also require –

Intrinsic release

MCPJ reconstruction or MP implant arthroplasty

Type III –

In addition to above – PIPJ manipulation is required

Lateral band release

Central slip release or lengthening

PIPJ dorsal capsulotomy

Type IV –

PIPJ fusion or arthroplasty

Summary of treatment options for SND

TypeSite wise treatment required
I Dermodesis FDS sling (flexor tenodesis) Littler’s ORL reconstructionFusion
IIIntrinsic releaseAs for type IFusion
IIIAs for type I Plus MCPJ reconstruction as neededAs for type I Plus PIPJ manipulation(dorsal capsulotomy) Skin release Lateral band release Central slip release or lengthening Check flexor tendonsFusion
IVAs for type IIIAs for type III Plus Arthroplasty or fusionFusion

ORL (Oblique Retinacular ligament) –

ORL was described by Landsmeer hence a/k/a Landsmeer ligament

Originates – from flexor sheath at volar aspect of PIP joint and

Inserts – dorsally into terminal tendon

ORL thus connects flexor mechanism to extensor mechanism.

It tightens during PIPJ extension and results in DIPJ extension

ORL reconstruction –

Littler’s ORL reconstruction –

Ulnar lateral band is divided proximally and

Re-routed palmar to axis of PIPJ rotation using Cleland ligament as fulcrum and

Secured to flexor tendon sheath

Lateral band now act as ORL

Thompson’s Spiral ORL reconstruction –

Free tendon graft is used.

Tendon graft is placed through gauzed hole in distal phalanx and directed in spiral fashion over middle phalanx, deep to neurovascular bundle, over the flexor sheath and transversely through base of proximal phalanx

Graft tension is adjusted with PIPJ and DIPJ in neutral extension.

Proximal end is secured with button or hemoclips or both.

Active motion is allowed 3 weeks post-op.

Kleimen modification of Spiral ORL reconstruction –

Axial K-wire used to keep DIP in neutral and

Oblique K-wire to keep PIPJ in 10-15° of flexion.

Proximal pin removed at 3 weeks

DIP pin removed at 4.5 weeks

Followed by splinting of DIP for 1.5 weeks in extension

Secured the tendon graft to dorsal distal phalanx with 4-0 Bunnell steel pull-out wire

Proximal juncture was attached to palmar flexor sheath with non-absorbable suture.

FDS sling –

Distally based slip of FDS can be sutured to leading edge of A1 pulley or can be secured to bone at the base of proximal phalanx.

Lateral band release –

Lateral band release done through two parallel incision and released from central slip and now are slide volar to the condyle.

Central slip tenotomy or lengthening –

Relies on mature terminal tendon

Procedure is done usually 6-12 months after the injury.

The procedure results in proximal migration of extensor mechanism and thus correct “the slack” induced by elongation at the terminal tendon.

Finger is exposed by midlateral incision centered over PIPJ

Transverse retinacular ligament is incised

Freer elevator is inserted under the extensor mechanism proximal to the central slip and underneath the lateral bands distal to central slip.

The insertion of central slip is visualized under the extensor mechanism, the insertion is divided by sliding a scalpel from proximal to distal underneath the extensor mechanism and active extension of DIP joint attempted.

A dorsal view of extensor mechanism will not reveal any discontinuity.

This technique can correct extension lag of DIPJ up to 35°.

Triangular ligament is not damaged and hence boutonneire deformity will not occur.


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