Boutonnière & Swan Neck

Boutonnière and swan neck deformities are paired reciprocal deformities of the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints of the fingers, resulting from imbalance of the extensor mechanism. Understanding the anatomy of the extensor apparatus — particularly the central slip, lateral bands, retinacular ligaments, and volar plate — is essential to understanding how these deformities develop and how they are corrected.

• Extensor mechanism anatomy at the PIP joint: the extensor tendon trifurcates into the central slip (inserts dorsal base of middle phalanx) and two lateral bands (converge distally to form the terminal tendon, inserting into the dorsal base of the distal phalanx); the lateral bands are held dorsal to the PIP joint axis by the triangular ligament (between the two lateral bands) and in correct position by the transverse retinacular ligaments; the oblique retinacular ligament (ORL — Landsmeer`s ligament) runs from the flexor sheath of the proximal phalanx to the terminal tendon, coupling PIP and DIP joint extension
• The volar plate at the PIP joint prevents hyperextension; it is the primary static restraint against PIP hyperextension; disruption leads to PIP hyperextension (swan neck)
• The central slip is the primary extensor of the PIP joint; disruption leads to PIP flexion with DIP hyperextension (boutonnière)

Boutonnière deformity is characterised by PIP flexion combined with DIP hyperextension. The name derives from the French word for "buttonhole" — the PIP joint protrudes through a buttonhole-like defect in the extensor mechanism.

• Mechanism: central slip disruption (from trauma, RA synovitis, or progressive attrition) → PIP cannot be extended → PIP goes into flexion → lateral bands displace volarly below the PIP joint axis (they lose dorsal restraint as the triangular ligament stretches) → once volar to the axis, the lateral bands flex the PIP further and extend the DIP → DIP hyperextension; the deformity is self-perpetuating once the lateral bands displace
• Causes: acute trauma (central slip rupture from volar dislocation of PIP or laceration); RA (PIP synovitis attenuates the central slip); burns; congenital (trigger digit producing central slip lengthening)
• Elson test for central slip integrity: PIP joint flexed to 90° over the edge of a table; patient asked to extend the finger against resistance at the middle phalanx; if the central slip is intact → force transmitted to middle phalanx, DIP joint remains flail (flexible); if central slip is ruptured → no force at middle phalanx, DIP joint becomes rigid (extension force transmitted through lateral bands to distal phalanx) — the Elson test is POSITIVE for central slip rupture when the DIP becomes RIGID

• Acute traumatic central slip rupture: splint the PIP in full extension for 6 weeks — the DIP must be free to flex (this actively pulls the lateral bands proximally and dorsally, helping to restore their position); failure to leave the DIP free perpetuates lateral band volar displacement; full-time day and night splinting required for 6 weeks
• Operative central slip repair: for lacerations with confirmed central slip rupture; reattach to dorsal base of middle phalanx using bone anchors or transosseous sutures; protect with K-wire across PIP for 4–6 weeks

Swan neck deformity is characterised by PIP hyperextension combined with DIP flexion. The posture resembles the S-shaped curve of a swan`s neck.

• Mechanism: multiple mechanisms can initiate swan neck deformity; the common final pathway is relative shortening of the central slip (or relative lengthening of the lateral bands), causing the lateral bands to migrate dorsally — this hyperextends the PIP and increases tension on the terminal tendon, flexing the DIP
• Causes: (1) Volar plate attenuation or rupture (from hyperextension injury, RA PIP synovitis) → PIP hyperextension; (2) Intrinsic tightness (RA interosseous contracture) → dorsal migration of lateral bands; (3) Mallet finger (loss of terminal tendon) → DIP flexion → retraction of lateral bands → PIP hyperextension; (4) FDS rupture → loss of PIP flexor → PIP hyperextension

• Nalebuff Stage II (intrinsic tightness test): PIP flexion is possible when the MCPJ is flexed but not when the MCPJ is extended — this is positive for intrinsic tightness; when the MCPJ is extended, the intrinsic muscles are stretched and cannot allow PIP flexion; confirms intrinsic muscle/tendon tightness as the driver
• FDS tenodesis for swan neck: a slip of FDS is sutured to the volar aspect of the A2 pulley or the PIP volar plate — prevents PIP hyperextension while preserving PIP flexion; most commonly used procedure for flexible Stage I–II swan neck
• Silver ring splint (Oval-8 splint): custom-made ring that blocks PIP hyperextension while allowing full flexion; non-operative management for chronic flexible swan neck; effective in Stage I

• Timing of boutonnière splinting: critical — if splinting begins within 3 weeks of injury, non-operative treatment is highly effective with approximately 80% success; delay beyond 3 weeks significantly reduces success rates as the lateral bands progressively contract in a volar position; all suspected central slip injuries should be splinted immediately while awaiting NCS or specialist review
• Mallet finger as initiator of swan neck deformity: loss of terminal tendon insertion (from DIP extensor rupture) causes DIP flexion → retraction of extensor mechanism proximally → relative tension increase in the central slip → PIP hyperextension; untreated mallet finger can therefore lead to progressive swan neck deformity over months to years; early mallet splinting (Stack splint, 8 weeks continuous) prevents this cascade
• Intrinsic tightness test in RA: Stage II swan neck is defined by PIP flexibility only in MCPJ flexion — confirming intrinsic tightness; the treatment principle is to release the intrinsic muscles proximal to the finger (lateral band release at the lateral band-central slip junction) to restore normal PIP motion; without this, the deformity recurs after volar plate repair
• Oblique retinacular ligament (ORL) reconstruction (Littler procedure): for correction of established swan neck without joint destruction; a graft or the lateral band is rerouted from the flexor sheath of the proximal phalanx volarly across the PIP joint to the lateral band distally; recreates the coupling between PIP extension and DIP extension; technically demanding; the ORL couples the two joints so that when the PIP extends, the DIP also extends, and when the PIP flexes, the DIP flexes

• Boutonnière: PIP flexion + DIP hyperextension; central slip disruption → lateral bands displace volarly; self-perpetuating once lateral bands are volar to PIP axis
• Elson test for central slip: PIP at 90° over table edge; resist extension at middle phalanx — RIGID DIP = positive = central slip ruptured (extension force diverted through lateral bands)
• Acute central slip rupture: PIP extension splint × 6 weeks; DIP MUST be free to flex actively — this pulls lateral bands dorsal and proximal; failure to free DIP = worse outcome
• Swan neck: PIP hyperextension + DIP flexion; causes include volar plate injury, intrinsic tightness, mallet finger, FDS rupture
• Nalebuff Stage II swan neck: flexible only in MCPJ flexion = intrinsic tightness; treatment = lateral band (intrinsic) release
• FDS tenodesis: slip of FDS to A2 pulley/volar plate; prevents PIP hyperextension; used for Stage I–II flexible swan neck
• Silver ring splint: blocks PIP hyperextension; allows full flexion; Stage I flexible swan neck non-operative management
• PIP arthrodesis position cascade: index 25–30° → middle 30–35° → ring 35–40° → small 40–45°
• Mallet finger → swan neck: untreated mallet causes retraction of extensor mechanism → PIP hyperextension → swan neck over time; Stack splint × 8 weeks prevents this
• ORL (Landsmeer ligament): couples PIP and DIP extension/flexion; reconstruction (Littler procedure) for swan neck without joint destruction