Traumatic hyperextension instability of the finger PIP joint is managed in the acute or subacute setting with protective dorsal extension block splinting of the PIP joint [17
]. Bowers proposed that hyperextension deformity is more likely to occur in the absence of bone injury due to the poor vascularity of the distal volar plate [4
]. If extension block splinting, or later use of a PIP joint figure-of-eight ring splint and/or buddy taping, does not prevent recurrent PIP joint hyperextension deformity, the patient may experience difficulty initiating finger flexion and painful snapping as the lateral bands slide over the condyles of the proximal phalanx [17
]. A swan-neck deformity of the finger can develop, and the PIP joint surfaces may degenerate over time, complicating treatment.
Articular-based procedures to address traumatic, refractory hyperextension instability of the PIP joint include direct repair of the volar plate [4
], superficialis tenodesis [6
], fascial or tendon graft bridging of the joint [1
], and collateral ligament advancement [3
]. The joint must be supple and the articulating surfaces in reasonably good condition for a soft-tissue rebalancing operation; otherwise, PIP joint arthroplasty or fusion may be indicated. Direct repair of the volar plate is generally preferred [6
], whereas tenodesis using one or both slips of the FDS tendon is considered when the volar plate is found to be retracted or attenuated [6
]. Fascial and tendon graft bridging of the PIP joint and collateral ligament advancement are procedures largely of historical interest.
Stability of the PIP joint is restored with either direct volar plate repair or FDS tenodesis; however, flexion contractures of the PIP joint have been reported with both techniques [6
]. In addition, sacrificing one or both slips of the FDS tendon may lead to decreased finger flexion and diminished hand strength. Each procedure will necessitate a window in the flexor retinaculum, retraction of the flexor tendons, and manipulation the PIP joint capsule with a conceivable potential for scar, tendon adhesions, and tendon bowstringing. To our knowledge, there are no published studies that have specifically assessed the competency of the flexor tendon sheath and/or excursion of the flexor tendons following volar plate repair or FDS tenodesis.
] was the first to report an extra-articular technique to correct PIP joint hyperextension. He sectioned the ulnar lateral band at the musculotendinous junction in a rheumatoid patient with swan-neck deformities, leaving the distal insertion intact, and attached the free end to the flexor tendon sheath volar to the axis of rotation of the PIP joint on the ipsilateral side of the finger. The function of the oblique retinacular ligament was replicated: active extension of the PIP joint leads to passive tenodesis of the DIP joint into extension. Zancolli [28
] adapted the lateral band transfer concept in the treatment of PIP joint hyperextension instability in association with cerebral palsy by mobilizing one lateral band, without disrupting the proximal or distal attachments, and stabilizing the band in a sling created by approximating a slip of the FDS tendon to the volar plate.
There have been several reports of single lateral band transfers to treat PIP joint hyperextension and swan-neck finger deformities in association with rheumatoid arthritis and cerebral palsy [7
]. Further variations in technique include use of the radial lateral band, attachment of the lateral band to the bony proximal phalanx, use of a bone anchor [10
], rerouting the lateral band across the volar aspect of the PIP joint to the contralateral side of the digit, and use of a free tendon graft (the so-called spiral oblique retinacular ligament reconstruction) [23
]. The results have been generally favorable in the short term, but recurrent finger deformities with longer follow up have been reported [7
]. Progressive pannus formation in rheumatoid arthritis will lead to attenuation of soft tissues and joint deformity with a potential for relapsing instability [18
]. Failures in cerebral palsy have been postulated to result from suboptimal surgical technique, muscle imbalance, and postoperative rehabilitation measures [7
There are relatively few reports of single lateral band transfer for treatment of traumatic PIP joint hyperextension instability [2
]. Foucher et al. [8
] reported 16 patients with a traumatic PIP joint hyperextension deformity who were seen at a minimum of 6 months after unilateral lateral band transfer. There were no cases of recurrent PIP joint hyperextension instability; however, eight patients exhibited a PIP joint flexion contracture of greater than 20°. Tonkin et al. [24
] reported 1 patient with a 15° hyperextension deformity of the PIP joint who exhibited a 10° flexion of the joint 10 weeks following unilateral lateral band transfer. Ahmed and Goldie [8
] described one case of single lateral band transfer to treat concomitant hyperextension and lateral instability of the PIP joint. The joint was effectively stabilized and normal interphalangeal joint motion was recorded after 5 years.
We modified the lateral band transfer concept by re-routing slips of both lateral bands proximal and volar to the PIP joint axis of rotation and securing the tendon slips to the flexor retinaculum through small transverse slits. The gross integrity of the sheath was preserved. Given the absence of preoperative DIP joint deformity in our two patients, sections of each lateral band dorsally were retained in an effort to uphold normal tension across the terminal extensor tendon. Our premise was that a double, rather than a single, lateral band tenodesis would provide for a more durable and balanced restraint to PIP joint hyperextension over time.
A flexible PIP joint flexion deformity developed postoperatively in both of our cases, and a passively correctable extensor lag of the DIP joint developed in patient 2. At the final evaluation, a functional 30° passively correctable PIP joint flexion deformity persisted in patient 2. There was no recurrence of PIP joint hyperextension instability in either case. We suspect that the temporary DIP joint extensor lag in patient 2 resulted from diminution of excursion of the distal extensor apparatus, possibly related to scar tissue, whereas the persistent PIP joint extensor lag was the sequela of an overly tensioned transfer. A stiff extension deformity of the DIP joint from taught lateral band slips was not observed.
We propose a dual-slip lateral band transfer procedure as a viable option for treating chronic, post-traumatic hypextension instability of the PIP joint when the articulating surfaces and joint architecture are reasonably well-preserved. An extensor lag of the PIP joint may develop; however, the gross integrity of the flexor tendon sheath is preserved, and the flexor tendons and PIP joint capsuloligamentous complex are left undisturbed. Recognized limitations of our study include the case report format, the lack of preoperative DASH scores, and the absence of a direct comparison to other surgical procedures. Clinical and biomechanical studies are necessary to further assess the efficacy of this approach.