Correction of swan-neck deformity

The swan-neck deformity is characterized by proximal interphalangeal (PIP) joint hyperextension and distal interphalangeal (DIP) joint flexion.

Swan-neck posturing is a result of tendon imbalance; the root cause can be at the wrist or at the metacarpophalangeal (MCP), PIP, or DIP joints. Tendon imbalance may be caused by inflammatory arthritis, trauma, tendon rupture, or general ligamentous laxity.

Possible abnormalities in a swan-neck deformity include ( Fig. 39.1 ):

• Intrinsic muscle shortening

• Volar subluxation of the MCP joint

• Dorsal displacement of the lateral bands

• Laxity of the PIP joint volar plate

• Oblique retinacular ligament laxity

• Mallet deformity with terminal extensor tendon disruption

• Flexor tendon adhesions or lacerations

• Joint stiffness or arthritic joint destruction

• Skin tightness or loss

The Nalebuff classification system is used to describe the severity of a swan-neck deformity and is based on the degree of PIP joint stiffness:

• Type 1: PIP joint is flexible in all positions of the MCP joint.

• Type 2: PIP joint flexion is limited in certain positions of the MCP joint.

• Type 3: PIP joint flexion is limited in all positions of the MCP joint.

• Type 4: PIP joint is stiff and arthritic.

PIP hyperextension and stiffness impair a patient’s ability to make a fist. First-line treatment includes splinting with the DIP joint in extension and dorsal blocking of the PIP joint with 40 to 60 degrees of flexion for 8 weeks. Surgery is indicated for patients who do not respond to nonoperative management, have full passive range of motion (ROM), and are functionally limited.

There are multiple surgical techniques available to treat swan-neck deformities depending on the etiology of the problem. The key to a successful repair is to identify and treat each pathologic structure.

The goals of surgical repair include: (1) correcting PIP joint hyperextension, (2) improving PIP joint motion, (3) correcting DIP joint flexion deformity, (4) improving lateral band “snapping” on PIP joint flexion, and (5) improving extension at the MCP joint.

Active and passive ROM are assessed independently at the MCP, PIP, and DIP joints. Special attention is paid to PIP joint motion.

When passive motion is greater than active motion at the PIP joint, flexor tendon adhesions may be present.

In patients with limited PIP joint motion in all MCP positions, examine closely for adhesions that affect the central extensor and dorsal translocation of the conjoint lateral bands.

If ulnar drift is present at the MCP joint, PIP joint motion is assessed with the MCP joint extended with radial and ulnar inclination. This examines for isolated intrinsic muscle shortening of the radial or ulnar interosseous muscle.

The Bunnell test is used to examine for intrinsic tightness. The test is performed by holding the MCP extended and passively flexing the PIP joint. The MCP is then flexed. If PIP flexion increases, intrinsic muscle tightness is present. Normally, MCP extension does not restrict PIP motion and no change in motion is detected ( Fig. 39.2A–C ).

Standard three-view radiographs are used to evaluate the articular surfaces ( Fig. 39.3A–C ).

Patients with articular damage are best treated with arthrodesis or arthroplasty, rather than soft-tissue reconstruction. In rheumatoid arthritis (RA), the ligamentous support of the PIP joint is typically poor. PIP fusion is more reliable than silicone arthroplasty.

Detailed knowledge of the extensor mechanism is necessary for diagnosis and treatment of swan-neck deformities.

Three muscles contribute to the extensor mechanism of the finger – the extensor digitorum communis (EDC), the lumbrical, and the interossei. The EDC runs along the dorsum of each finger and is stabilized at the MCP joint by the sagittal bands. The sagittal bands wrap transversely around the metacarpal head and insert onto the volar plate and proximal phalanx.

Distal to the MCP joint, the EDC tendon trifurcates into a central slip and two lateral slips. The central slip inserts onto the base of the middle phalanx and extends the PIP joint. The lateral slips contribute to the conjoint lateral bands.

The lumbrical muscles originate from the flexor digitorum profundus tendons in the palm and pass volar to the intermetacarpal ligaments at the MCP level. Oblique fibers join the central slip over the proximal phalanx. Distally, the lumbrical inserts onto the radial conjoint lateral band.

The dorsal interossei arise from the metacarpals and have two muscle bellies: the superficial and deep head. The superficial head becomes the medial tendon, which runs deep to the sagittal band and inserts on the base of the proximal phalanx (it abducts the digit). The deep head gives rise to the lateral tendon, which passes superficial to the sagittal band and is more complex. The lateral tendon has transverse, oblique, and distal fibers. Transverse fibers insert on the midproximal phalanx and help flex the MCP joint. Oblique fibers help extend the PIP joint. Distal fibers of the lateral tendon insert onto the conjoint lateral band.

The conjoint lateral bands travel distally to form the terminal tendon, which insert onto the dorsal base of the distal phalanx and extend the DIP joint.

The triangular, transverse retinacular, and oblique retinacular ligaments stabilize the conjoint lateral bands and coordinate motion of the extensor mechanism ( Fig. 39.4A–B ).

Disruption of the terminal tendon at the DIP joint (mallet injury) causes the lateral bands to migrate proximally, increasing the extension force at the PIP joint.

Attenuation of the PIP joint volar plate from synovitis, posttraumatic arthritis, or generalized laxity can cause PIP hyperextension.

Chronic volar subluxation of the MCP joint from inflammatory arthritis or posttraumatic contracture increases tension on the EDC and leads to PIP joint hyperextension.

Carpal collapse at the wrist can cause relative lengthening of the extrinsic tendons. Intrinsic muscle forces may overpower the extrinsic forces, leading to PIP joint hyperextension.