eMedicine Specialties > Orthopedic Surgery > Hand & Upper Extremity

Swan-Neck Deformity: Treatment

Author: Roberto Sandoval, MD, Consulting Staff, Department of Emergency Medicine, Anaheim Memorial Medical Center, La Palma Intercommunity Hospital
Coauthor(s): John A Kare, MD, Assistant Professor of Emergency Medicine, Charles R Drew University of Medicine and Science/UCLA, Director of Research, Department of Emergency Medicine, Martin Luther King Jr/Charles R Drew Medical Center; Eleby R Washington III, MD, FACS, Associate Professor, Department of Surgery, Division of Orthopedics, Charles R Drew University of Medicine and Science; Roman V Voytsekhovskiy, MD, Fellow in Hand Surgery, Department of Orthopedic Surgery, Rush University Medical Center; Robert R Schenck, MD, Associate Professor, Departments of Plastic and Orthopedic Surgery, Rush Medical College; Director, Section of Hand Surgery, Department of Plastic and Orthopedic Surgery, Rush University Medical Center
Contributor Information and Disclosures

Updated: Nov 2, 2007

Treatment

Medical Therapy

See Surgical Therapy.

Surgical Therapy

Type I deformity

Swan-neck deformity can arise at the PIP or DIP joint; in either case, it can lead to the classic appearance of PIP joint hyperextension with DIP joint flexion. Patients with type I deformity maintain the ability to actively flex the PIP joint. When the deformity originates at the PIP joint, it is caused by stretching of the capsule secondary to active synovitis or rupture of the flexor digitorum superficialis tendon, removing the restraint to PIP joint hyperextension. If the synovitis involves the DIP joint, the deformity begins with stretching or rupture of the terminal tendon attachment of the extensor mechanism to the distal phalanx, resulting in a mallet deformity. (See also the eMedicine article Mallet Finger.) This subsequently causes extensor mechanism imbalance, with relative  overpull of the central slip; these problems, together with laxity of the PIP joint's volar plate, resultinPIP joint hyperextension.

The treatment of type I deformity is focused on correcting PIP joint hyperextension and restoring DIP joint extension. Conservative treatment can be used, with Silver Ring splints (Silver Ring Splint Co., Charlottesville, Va) being employed to permit active PIP flexion and limit hyperextension of the PIP joint. Alternatively, an inexpensive figure-8 thermoplastic splint can be fashioned by a hand therapist. These splints can be useful in the early stages of the disease.

If splints are not tolerated, several procedures can be considered, including DIP joint fusion (soft-tissue procedures at the DIP joint are unsuccessful) and PIP joint flexor tenodesis, in which a volar zigzag incision is made over the PIP joint to expose the flexor tendon sheath; the sheath is opened proximally to the A1 pulley, and the flexor digitorum superficialis is separated from the sheath, creating a slight flexion contracture of the PIP joint. Another option is retinacular ligament reconstruction and dermodesis, in which an elliptic wedge of skin is removed from the volar aspect of the PIP joint, and the skin defect is closed with the digit in flexion. However, this procedure is usually only of temporary value, because the skin stretches out with time.

Type II deformity

A type II deformity has an appearance similar to that of the type I deformity; however, PIP joint flexion is influenced by the position of the MP joints. When the MP joints are extended or radially deviated, passive PIP joint flexion is limited; when the MP joints are flexed or ulnarly deviated, a greater degree of PIP joint flexion is possible. As the patient's RA continues to progress, radial deviation of the metacarpals and volar subluxation of the MP joints increase secondary to increased tightness of the intrinsic muscles. Consequently, a swan-neck deformity develops.

The treatment of a type II deformity centers on the relief of intrinsic tightness, which is accomplished using intrinsic release. In this procedure, a dorsal longitudinal incision is made over the proximal phalanx, exposing the extensor mechanism. A rhomboid portion of the ulnar extensor aponeurosis is then resected (radial as well, if the tightness is severe). The surgeon resects the lateral band(s) through which the abnormally tight intrinsics have produced MP flexion and PIP hyperextension. In patients with severe involvement of the MP joints, silicone-implant arthroplasty is performed, combined with the rebalancing of the intrinsics and the long extensor tendons.³

Type III deformity

A type III deformity is characterized by a significant reduction of PIP joint motion, as well as by well-preserved joint spaces, as depicted on radiographs. The stiffness is caused by contracture of the extensor mechanism, collateral ligaments, and skin. The initial goal of the surgical reconstruction of a type III deformity is the restoration of passive motion to the PIP joint. This may be accomplished by using 1 or more procedures, including the following:

• PIP joint manipulation - This procedure involves dorsal skin release distal to the PIP joint to allow the skin edges to spread and scar contraction to occur in 2-3 weeks (leading to a linear scar).
• Lateral band mobilization - In this procedure, the lateral bands are freed from the central slip mechanism and the joint is gently manipulated into full flexion without releasing the collateral ligaments or lengthening the central slip.
• Flexor tenosynovectomy or tenolysis - This procedure involves exposing and applying traction to the flexor tendons of the distal palm. (See also the eMedicine article Hand, Tendon Lacerations: Flexors.)

Once passive motion has been restored, the deformity may be corrected with the previously mentioned procedures. Postoperative splinting and exercises are implemented by a hand therapist, under the supervision of the surgeon, to maintain the gains that were achieved surgically.

Type IV deformity

Patients with a type IV deformity have stiff PIP joints and associated radiographic changes consistent with advanced intra-articular disease. These deformities require a salvage-type procedure—namely, arthrodesis or arthroplasty. In deciding which of these procedures to perform, it is important to consider the status of adjacent joints, flexor tendons, and ligaments. It is also important to assess the function of the adjacent fingers. Fusion is particularly useful for the index and middle fingers, because these digits need lateral stability when opposed to the thumb during pinch. Arthroplasty is recommended for the ring and small fingers, where mobility aids grasp. If the MP joints require arthroplasty, PIP joint fusion is recommended, although it has been suggested that arthroplasty can be performed.

Proximal joint fusion involves a curved dorsal skin incision. A longitudinal incision is made through the tendon over the joint, resecting the collateral ligaments. Two Kirschner wires (K-wires) are then passed obliquely across the joint to provide stable fixation, usually at 25° of flexion for the index finger and slightly more for the third digit. Postoperative care consists of cast immobilization for 6-8 weeks.

Arthroplasty can be performed if the surrounding soft tissues are adequate. A dorsal incision is made to expose the extensor mechanism and is split longitudinally. The articular surfaces of the opposing proximal and middle phalanges are removed, and the medullary canals are prepared for the insertion of the implant. The skin is closed with the joint in slight flexion. A palmar incision is then made to release any flexor tendon adhesions. Postoperative care includes splinting the PIP joints in 10° or 20° of flexion and instituting passive and active exercises with a dynamic extension/flexion splint.

Follow-up

See Surgical Therapy.

Complications

The complications following swan-neck reconstruction include stiffness, infection, and a recurrence of the deformity. If prostheses are used, there may be early or late prosthetic dislocation, breakage, or both. On average, there is less functional improvement in swan-neck deformities caused by RA than in those resulting from trauma.

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