Consequences of Untreated Pediatric Trigger Thumb: Case Report

Abstract

Pediatric trigger thumbs present a conundrum for hand surgeons. Surgery for trigger thumbs has inherent risks, such as infection, nerve injury, and the risks of anesthesia, but will reliably solve the problem. But is surgical intervention necessary? Would these cases resolve spontaneously, eventually, without intervention? If not, what are the long-term consequences of the inability to fully extend the thumb interphalangeal joint? We present a pediatric trigger thumb that was symptomatic for 22 years, with complete resolution of symptoms after surgical intervention. This report illustrates at least some pediatric trigger thumbs will not resolve without surgical intervention, but treatment, even after 21 years, can result in normal thumb motion and function.

Introduction

Pediatric trigger thumb (PTT), or stenosing tendovaginitis of the flexor policis longus (FPL) tendon, occurs in 1 to 3 infants in 1000 live births. ¹ The exact etiology of PTT is unclear, possibly from trauma or chronic posturing, but it has been well established to be an acquired condition, often presenting at 2 years of age. ² Pediatric trigger thumb results from a size mismatch of the FPL tendon and A1 pulley, resulting in flexion deformity at the thumb interphalangeal (IP) joint and in severe cases hyperextension at the metacarpophalangeal (MCP) joint. ³ Nonsurgical management can be followed in children presenting at less than 2 years old, but surgical treatment with open A1 pulley release is often recommended in older patients. ⁴ The incidence and natural history of untreated, persistent PTT is unknown. In this report, the authors describe the pathologic findings and subsequent management of an adult patient with long-standing PTT whose treatment was delayed until age 23.

Case Report

The patient is a 23-year-old woman with a history of PTT first presenting at 2 years old. The patient presented to the office of the senior author (W.B.E.) with flexion deformity of her left thumb IP joint (Figure 1). The patient cited inability to voluntarily fully extend the thumb IP joint, but the joint flexed normally. On occasion, the thumb IP joint would “pop” painfully into full extension and would then be difficult to flex. Her parents sought for her medical attention regarding these complaints on several occasions over several years, but no surgery or treatment was offered, and the patient adapted to her condition.

Figure 1.

Preoperative clinical photo of a 38-year-old patient with a left thumb interphalangeal joint flexion deformity due to a chronic pediatric trigger finger. The image demonstrates loss of full extension secondary to stenosing tenosynovitis.

On examination, the left thumb IP joint had a 30° extension lag, with a firm end point, and full flexion. Notably, she also had a painful, palpable nodule at the A1 pulley, thought to be a ganglion cyst of the tendon sheath. She had no history of trauma or prior injury to the thumb or hand. Surgical treatment with open A1 pulley release was offered.

The patient underwent trigger finger release by the senior author at an outpatient surgery center. A 1-cm transverse incision was made through one of the flexion creases of the thumb metacarpophalangeal (MP) joint. The radial digital nerve was identified and protected. After full exposure of the tendon sheath, the author noted focal thickening of the A1 pulley with chondrometaplasia, a 3-mm nodule of mucinous infiltration of the FPL tendon with focal longitudinal delamination of the tendon and moderate fibrotic tenosynovium engulfing the tendon (Figures 2 and 3). The A1 pulley was released, the fibrotic tenosynovium was removed sharply, and the degenerated tendon was trimmed to a smooth surface. Postoperatively, the patient did well, with full painless range of motion at the thumb IP joint, no extension lag, and no further locking. The patient was allowed unrestricted thumb activities following uneventful healing of the skin incision.

Figure 2.

Intraoperative thumb A1 pulley prior to release and tendon debridement. At the center of the incision, there is a markedly thickened A1 pulley with chondrometaplasia, with blocking of full extension of the thumb interphalangeal joint.

Figure 3.

Intraoperative left thumb flexor policis longus tendon with focal, nodular mucinous infiltration.

Note. On the left image, asterisk marks fibrotic tenosynovium being peeled off the FPL tendon, and arrow marks the FPL tendon. On the right image, focal longitudinal delamination of the FPL tendon (asterisk) is debrided from FPL tendon. FPL = flexor policis longus.

Discussion

Patients presenting with PTT have been found to have 2 main outcomes if left untreated—spontaneous resolution and persistent flexion deformity. Published literature on the likelihood of each scenario has been conflicting. Baek and Lee ⁴ performed the first prospective study of observational management of PTT, reporting 66 of 87 thumbs (75.9%) resolved spontaneously in patients with a mean age of approximately 2 years old with a 5-year follow-up. On the contrary, in a recent prospective trial of 93 thumbs, Hutchinson et al ⁵ reported only 32% of patients resolved spontaneously at 5 years. The heterogeneous data presented on this topic serve to highlight the difficulty in studying this population. Specifically, there is a lack of consistency among patient cohorts, no treatment randomization, and trouble in reassuring parents to stick with continued observational management when their children have exhibited little improvement over the years.

It appears reasonable to offer observational management for patients with PTT even in the setting of unclear data on this subject. This treatment strategy is especially helpful in patients too young or small for surgery. More so, like any surgical intervention, even trigger finger release has inherent risks. Most hand surgeons employ some component of observation in their treatment algorithm and likely offer surgery if there exists a persistent deformity after a period of close monitoring. Patients who fail to resolve the locking on their own are thought to be at risk for irreversible, chronic flexion deformity of the thump IP joint, or even hyperextension with joint laxity of the thumb MP joint, leading to developmental or functional impairment. ⁶

The question of what happens to patients with persistent deformity who never receive treatment has not been described. When thinking about these patients and more importantly when discussing treatment options with parents, hand surgeons consider there may be long-term permanent sequelae for patients who defer surgical intervention of either loss of motion or impaired motor development/dexterity as the child matures. Based on the published series on this topic, in many cases the locking of the thumb can resolve, but nothing definitive can be said at any interval greater than 5 years. In this case report, we present the long-term effects of untreated PTT in an adult patient. Our patient had a 21-year history of a trigger thumb which never underwent spontaneous resolution, but instead resulted in a locked deformity providing a low level of ambient functional impairment and intermittent pain. Intraoperatively, the FPL tendon was found to have evidence of long-standing compression at the A1 pulley with secondary changes in the pulley (chondrometaplasia), minimal actual tendon damage, and full thumb IP joint motion once the pulley was released.

In other disease models where chronic compression is the insult, there are descriptions of tendinopathy occurring at the involved structures, resulting in mucinous or fatty infiltrative changes disrupting normal tendon cellular architecture. ⁷ Clinically, this may manifest as weakness and/or decreased grip strength if the tendon involved is painful. Kakel et al ⁸ found degenerative changes of the FPL tendons in the trigger thumbs of identical twins at 3.5 years old and without any abnormalities at the A1 pulley. In our patient, we saw mucinous and infiltrative changes at the FPL tendon, which we contend is a result of decades of compression at the A1 pulley leading to chronic ischemic injury.

Albeit present, chronic PTT seems to result in minor tendon damage without permanent consequence and no loss of motion in spite of the duration of symptoms. It remains unclear whether chronic PTT in some cases might lead to a fixed flexion contracture at the IP joint due to volar plate contracture, as this has not been reported in the literature. However, our patient maintained a passively correctable IP joint and some limited active motion on presentation, which likely protected her from developing this consequence.

Despite pathologic changes to the A1 pulley and the FPL tendon from the patient’s chronic trigger finger, surgical intervention provided complete resolution of her symptoms. Our findings in this case also suggest even patients with PTT who suffer a delayed presentation from either missed diagnosis or lack of access to care may still benefit from surgery. The benefit of a steroid injection in chronic PTT presenting in adulthood has not yet been studied. Immediate surgical intervention may be a better option for chronic PTT, as patients are likely to have some degree of A1 pulley thickening and inflammatory changes to the FPL tendon, as evidenced by our patient, which a steroid injection alone will be unlikely to correct. In these rare cases, the authors report A1 pulley release combined with debridement of the FPL tendon is effective in removing sufficient scar tissue at the compression site to restore normal tendon gliding. We were able to achieve this using a standard trigger finger incision, and these patients can then be managed as any other trigger finger release.

Conclusion

In summary, PTT is a clinical condition that results in flexion deformity at the IP joint. For patients with persistent contracture, treatment is advisable if the condition is painful or results in functional impairment. Our report suggests chronic intrinsic changes of the FPL tendon can occur in long-standing PTT when left untreated. Loss of motion is still reversible even after 21 years, and normal thumb function can still be obtained with a very late presentation. This case also indirectly supports the approach of surgical management of PTT at the time of original presentation, especially in the setting of severe flexion contracture, as the locking may not resolve even with a prolonged period of nonoperative treatment and early intervention would invariably shorten the duration of morbidity. Chronic PTT persisting to adulthood, despite tendon changes, can be focal at the site of A1 pulley compression and therefore may be effectively treated with simple pulley release.