The Prevalence and Epidemiology of A0 Trigger Finger: A Novel Characterization

Purpose: Though trigger finger is traditionally associated with A1 pulley constriction, the A0 pulley, customarily known as the palmar aponeurosis, has been observed clinically to be responsible for trigger finger pathology. Previous cadaver studies have biomechanically implicated the A0 pulley in trigger finger, if not more so than the A1 pulley. This study attempts to outline the clinical prevalence and patient factors related to A0 pulley trigger finger in surgical patients.

 

Methods: This was a prospective IRB approved randomized clinical trial. Patient demographics, medical history, and trigger finger history (i.e. not triggering, triggering, locked in flexion, incomplete flexion) were documented prior to trigger finger release. Intra-operatively, a coin toss was used to randomize initial release of either the A0 or A1 pulley. Following release, the patient was asked to flex and extend the fingers under careful examination and documentation by the surgeon. The remaining pulley was then released and clinical trigger status was recorded. The A0 pulley was deemed responsible if the initial release of A1 failed, but subsequent release of A0 successfully resolved triggering. The A0 pulley was deemed at least partially involved if the initial A0 release completely or incompletely resolved the trigger status of the patient. Statistic analysis was performed with Chi square and multivariate regressions.

 

Results: To date, twenty-two fingers belonging to fourteen patients (11 (79%) right handed, 3 (21%) left handed; average age 56 yrs; 9 male (64%) and 5 female (36%)) have been released. Of the 22 fingers, 2 (9%) resolved after subsequent A0 release following a failed initial A1 release. Nine (41 %) showed resolution of symptoms following the initial release of A0, and 1 (5%) showed incomplete resolution following initial A1 release and complete resolution following the subsequent A0 release. Neither initial A1 or A0 release was significantly associated with complete release, incomplete release, or complete release failure. Multivariate regression revealed that diabetes status(p<0.001), occupation requiring manual labor(p=0.002), presence of past hand procedures(p=0.003), increased pain level at baseline(p=0.020), and absence of a palpable nodule(p=0.009) predicted incomplete resolution at first release. Incomplete release was independent of A1 or A0 release, age, sex, finger, smoking status, or steroid injections. We aim to recruit up to 50 fingers by study completion.

 

Conclusions: Our preliminary data suggest that 9% of trigger fingers may be primarily caused by the A0 pulley. Furthermore, the data suggest that up to 55% of trigger fingers have at least some involvement of the A0 pulley system. While literature documented factors such as diabetes status and past hand pathology appropriately predicted poor results from initial release, the actual pulley released did not. This implicates both pulleys in trigger finger and suggests that release of both the A1 and A0 may be necessary for comprehensive treatment. As our sample size increases, our results will become more generalizable, and patient factors potentially correlated with A0 pulley involvement will be clarified.