Background: Injury to the finger's extensor mechanism is a common cause of swan neck deformity (SND). Progression of extensor and flexor tendon imbalance negatively affects laxity of the volar plate, resulting in the inhibition of proper finger motion. The complexity of finger anatomy, however, makes understanding the pathomechanics of these deformities challenging. Therefore, development of an SND model is imperative to understand its influence on finger biomechanics and to provide an in vitro model to evaluate the various treatment options.
Methods: The index, middle, and ring fingers from 8 cadaveric specimens were used in an in vitro active motion simulator to replicate finger flexion/extension. An SND model was developed through sectioning of the terminal extensor tendon at the distal insertion (creating a mallet finger) and transverse retinacular ligament (TRL). A strain gauge inserted under the volar plate measured laxity of the plate, and electromagnetic trackers recorded proximal interphalangeal joint (PIPJ) angles.
Results: Strain in the volar plate increased progressively with creation of the mallet and SND conditions (P = .015). Although not statistically significant, the mallet finger condition accounted for 26% of the increase, whereas sectioning of the TRL accounted for 74% (P = .031). As predicted, PIPJ hyperextension was not detectable by joint angle measurement; however, the PIPJ angle had a strong positive correlation with volar plate strain (R2 = 1.0, P < .001).
Conclusion: Volar plate strain measurement, in an in vitro model, can detect an induced SND. Moreover, as a surrogate for PIPJ hyperextension, volar plate strain may be useful to evaluate the time-zero effectiveness of various surgical interventions.
Keywords: laxity; strain; swan neck model; volar plate.