Experimental model of trigger finger through A1 pulley constriction in a human cadaveric hand: a pilot study

Although it can be reasonably assumed that trigger digits occur as the result of a size mismatch in the pulley-tendon system, it is unclear whether locking, histological changes, and nodule formation occur owing to an intrinsically too small pulley or an enlarged digital flexor tendon. Our purposes in this feasibility study were to (1) create a model of trigger digit by pulley constriction in nonpreserved human tissue, (2) measure the change in work of flexion as the force of pulley constriction increased, (3) compare the work of flexion between nontriggering and triggering conditions, and (4) determine whether triggering can occur at the A2, A3, and A4 pulleys under similar conditions.

Using a tensiometer, we studied the work of flexion in 4 fingers (thumb, index, middle, and ring) in a human cadaveric hand. The load of flexion was measured as the A1 to A4 pulleys were incrementally constricted in order to induce triggering. Work of flexion was analyzed for differences among trial conditions.

Triggering was successfully induced in all 4 digits through constriction of the A1 pulley. No triggering occurred in any of the A2, A3, or A4 pulley systems in this model.

We successfully created a trigger model in a human cadaveric hand. Our results demonstrate that the A1 pulley can cause triggering from manual constriction of the pulley alone.

A trigger model such as this may allow investigations of pathophysiology, and this may result in novel treatment strategies and modalities.