Occurrence of trigger finger following carpal tunnel release

Surgical treatment of carpal tunnel syndrome (CTS) was recently started in our department, and we noticed that the development of trigger finger (TF), with which neurosurgeons are generally unfamiliar, is not rare after such treatment. We summarized the clinical and pathogenetic aspects of TF and retrospectively analyzed the medical records of all 39 patients who underwent CTR in our department to investigate the occurrence of TF. In 39 patients with CTS, 46 surgical interventions were performed in our department. All surgical procedures were carried out by open release of the transverse carpal ligament under local anesthesia infiltration, but the distal forearm fascia was not released. The mean postoperative follow-up period was 21.1 ± 16.8 months. TF after CTR occurred in nine hands of eight patients (9 of 46 hands, 19.6%). The mean interval between CTR and TF onset was 5.3 ± 2.8 months. TF after surgical treatment of CTS is not rare; therefore, surgeons who treat CTS should understand the clinical features of TF and carefully assess affected patients, particulary at presentation and within 6 months postoperatively.

Key-words:

Carpal tunnel syndrome - surgery - trigger finger

Introduction

Carpal tunnel syndrome (CTS) is estimated to occur in 1%–4% of the general population and accounts for about 90% of all nerve compression syndromes.[[1]],[[2]],[[3]] Surgical treatment of CTS was recently started in our department, and to date, 46 surgical interventions have been performed in 39 patients with CTS.[[3]] Our clinical experience with these cases has shown that the development of trigger finger (TF), also termed stenosing flexor tenosynovitis, is not rare after surgical treatment of CTS, indicating that surgeons who treat CTS should increase their awareness of TF. Both CTS and TF are common diseases that may occur in the same patient, and some authors have reported the concurrence rate between these two conditions; however, the clinical implications of this association have not been fully established.[[4]],[[5]],[[6]] In the present manuscript, we (1) summarize the clinical and pathogenetic aspects of TF because neurosurgeons are generally considered unfamiliar with this disease, (2) retrospectively analyze our surgical cases, and (3) present a literature review of the occurrence of TF after surgical treatment of CTS.

Summary of Clinical and Pathogenetic Aspects of Trigger Finger

Anatomy related to trigger finger

Finger flexion is finely coordinated by the flexor tendon, which is guided by a tendon sheath and complex pulley system. This pulley system is composed of five annular pulleys (A1 through A5) and three cruciate pulleys (C1 through C3) [[Figure 1]]. These structures maintain the position of the flexor tendon relative to the bones, and the power of flexion is increased by preventing bowstringing of the flexor tendon. The flexor tendon passes through the tendon sheath, allowing it to glide smoothly when the finger bends and straightens. The tendon passes through the pulleys as the finger moves. The pulley at the base of the finger is called the A1 pulley, which is most often involved in TF. In patients with TF, the A1 pulley is inflamed or thickened, making it difficult for the flexor tendon to glide smoothly as the finger bends.[[7]],[[8]],[[9]].

Figure 1: Anatomy of flexor tendon showing the intricate pulley system that guides finger flexion. The pulley most often affected in trigger finger and subsequently released during open release for trigger finger is the A1 pulley. A - Annular pulley; C - Cruciate pulley

Clinical symptoms of trigger finger

Patients with TF typically present with stiffness, swelling (mainly in the morning), pain, clicking, catching, and loss of motion of the affected finger. Progression of clinical symptoms is usually divided into Stages 1–4. In the pretrigger phase (Stage 1), patients usually present with a slow onset of pain that occurs more frequently over time. The pain is aggravated by labor-intensive use of the hand. In the active phase (Stage 2), clicking of the symptomatic finger is recognized, although the patient is able to actively extend the finger. In the passive stage (Stage 3), mismatch between the tendon and flexor sheath diameter proceeds; as a result, the patient cannot extend (Stage 3a) or flex (Stage 3b) the finger without forcing it to straighten using the asymptomatic hand. In Stage 4, the finger remains in rigid flexion [[Table 1]]a.[[10]].

Table 1a: Classification of severity of trigger finger 29

Epidemiology of and risk factors for trigger finger

TF most commonly occurs in the fifth-to-sixth decades of life, and the frequency is six times higher in women than men. The lifetime risk of onset of TF is 2%–3%, but it increases to 10% in patients with diabetes.[[7]],[[11]] Other risk factors for TF include hypothyroidism, osteoarthritis, rheumatoid arthritis, tuberculosis,[[7]],[[12]] and repetitive activities that can strain the hand, such as playing a musical instrument.[[7]] The most commonly affected finger is the ring finger, followed by the thumb; however, TF can occur in the other figer as well.[[7]],[[8]],[[13]]

Treatment options for trigger finger

Initial management of TF usually involves nonsurgical treatments such as immobilization of the affected finger, nonsteroidal anti-inflammatory medication, and corticosteroid injections into the area of the inflamed tendon.[[7]],[[8]],[[9]],[[10]] Surgical treatment is indicated when nonoperative treatment fails.

Occurrence of Trigger Finger After Carpal Tunnel Release in Our Department

Surgical treatment of CTS was recently started in our department, and to date, 46 surgical interventions have been performed in 39 patients with CTS. The diagnosis was based on a standard history and physical examination and was confirmed by nerve conduction tests.[[3]] CTR was carried out under local anesthesia, and a pneumatic tourniquet on the upper arm was used. A longitudinal palmar skin incision about 4 cm was made distal from the wrist crease. This provides a view of the transverse carpal ligament (TCL). The TCL was divided along the ulnar aspect of the median nerve to protect the median motor branches. Internal neurolysis or tenosynovectomy were not performed. When the median nerve was confirmed to be fully decompressed, the tourniquet was deflated and hemostasis was achieved. The skin incision was closed with monofilament nonabsorbable sutures. The medical records of all 39 patients who underwent CTR were examined to investigate the occurrence of TF.

Data are expressed as mean ± standard deviation. The Chi-square test or Fisher's exact test was used for two-group comparisons of categorical variables. Student's t-test was used to compare the mean ages of two groups. Variables were considered statistically significant at P < 0.05.

Of the 39 patients who underwent CTR, 19 were male and 20 were female. The affected side was the right in 16 (41%) patients, the left in 16 (41%), and bilateral in 7 (18%). The mean age of the patients was 70.2 ± 11.8 years. CTS was categorized into three stages based on the clinical symptoms [[Table 1]]b. Stage 1 comprised 12 hands, Stage 2 comprised 32 hands, and Stage 3 comprised 4 hands. The mean postoperative follow-up period was 21.1 ± 16.8 months.

Table 1b: Clinical stages of carpal tunnel syndrome 20

Cases of TF were defined by the clinical history and/or presence of catching, clicking, or locking and tenderness over the A1 pulley. We found that TF after CTR occurred in nine hands of eight patients (9 of 46 hands, 19.6%). The mean age of the patients who developed TF was 66.7 ± 13.0 years. The mean interval between CTR and TF onset was 5.3 ± 2.8 months [[Table 2]].

Table 2: Summary of nine hands in eight patients who developed trigger finger after carpal tunnel release

The risk factors for TF after CTR were analyzed [[Table 3]]. However, we found no significant difference in the mean age of the patients with and without TF (66.7 ± 13.0 vs. 70.2 ± 11.8 years, respectively, P = 0.36). We also compared four age groups: >80 years, 79–70 years, 69–60 years, and <59 years. This comparison also showed no significant differences. A categorical comparison was performed by sex, laterality, clinical stage of CTS, and hemoglobin A1c (HbA1c) concentration (≥6.5% or <6.5%). These analyses showed that female patients were significantly more likely to develop TF than male patients (odds ratio, 10.0; 95% confidence interval, 1.15–486). In addition, no significant differences were detected in the clinical stage of CTS, laterality, or HbA1c concentration.

Table 3: Univariate analysis of the predictors of trigger finger occurrence

Reports of Concomitant Occurrence of Trigger Finger and Carpal Tunnel Release

CTS and TF are both common diseases and may occur in the same patient.[[4]],[[5]],[[6]] Several studies have investigated the concurrence rate between CTS and TF. In 2001, Garti et al.[[5]] evaluated 62 consecutive patients with TF but no signs or symptoms of CTS. Nerve conduction studies of the median nerve in 39, of these 62 (63%) patients showed increased distal motor latency. In 2009, Rottgers et al.[[6]] evaluated 108 consecutive patients presenting with CTS and/or TF. Of these 108 patients, 66 (61%) had evidence of concomitant CTS and TF. In 2009, Kumar and Chakrabarti [[4]] reported that 43% of patients presenting with TF also had CTS.

As mentioned above, both conditions exist concomitantly at the time of presentation with a certain probability. Hands with either CTS or TF are conceivably affected by a pathologic condition of the connective tissues that results in the other pathologic condition. However, different histopathologic abnormalities of the connective tissues have been reported between CTS and TF. The main pathology in CTS is noninflammatory fibrosis with vascular hypertrophy and proliferation with wall thickening and obstruction in the subsynovial connective tissue.[[14]] However, the main pathology in TF is irregular connective tissue with small collagen fibers and an abundant extracellular matrix containing chondroid matrix in the deep surface of the pulley.[[15]] Therefore, CTS and TF are not the result of the same pathologic condition of the connective tissue, and other factors should also be considered to be involved in the mechanism of concomitance of these two conditions.

A limitation of our case analysis is that we did not sufficiently confirm whether TF existed before surgical treatment of CTS. The presence of TF should be carefully assessed at presentation or before surgical treatment of CTS because TF is highly likely to be missed when the symptoms of TF are mild.

Reports of Trigger Finger Occurrence After Carpal Tunnel Release

The development of TF in patients undergoing surgical treatment of CTS has been analyzed by various authors [[Table 4]].[[16]],[[17]],[[18]],[[19]],[[20]],[[21]],[[22]],[[23]],[[24]],[[25]],[[26]],[[27]],[[28]] The reported incidence of TF after CTR is about 10%–20%, which is almost identical to the results of our study, and CTR has been attributed to acceleration of the development of TF in various studies.

Table 4: Reports that analyzed the occurrence of trigger finger after carpal tunnel release

Table 4: Contd...

The exact pathogenesis of TF after CTR is unknown. Some possible explanations include an edematous environment after surgery and an inflammatory process in the flexor tendons.[[22]] In addition, the flexor tendons at the wrist are displaced anteriorly, which alters the tendon biomechanics at the A1 pulley. Karalezli et al.[[27]] investigated the effect of TCL release on the entrance angle of the flexor tendons to the A1 pulleys in a cadaver study. They concluded that release of both the TCL and distal forearm fascia (FF) may be a predisposing factor for the development of TF by changing the entrance angle to the A1 pulley and consequently increasing the friction in this anatomic area, predisposing to triggering of the digit.[[27]] Acar et al.[[16]] demonstrated that patients undergoing TCL release and distal FF release had a higher risk of TF than those undergoing TCL release only. As mentioned above, we released the TCL but not the FF in all patients who underwent CTR. From the viewpoint of TF prevention, care should be taken to avoid releasing more FF than necessary.

Several independent risk factors for new-onset TF after CTR have been reported. In the present study, TF tended to be frequent in patients with diabetes mellitus, but this finding did not reach statistical significance. Although diabetes mellitus has been cited as a key predisposing condition for development of CTS and TF,[[28]] controversy exists regarding whether diabetes is a risk factor for the occurrence of TF after CSR.[[17]],[[18]],[[19]] Seven of the eight patients with TF in our study were female. This result is convincing considering that a male:female ratio of about 1:6 has been reported among patients with TF both associated and unassociated with CTS. With respect to the clinical stage of our patients with CTS, patients with Stage 1 tended to more frequently develop TF, although this finding also did not reach statistical significance. El-Hadidi [[17]] reported that surgery may exacerbate the onset of TF, especially when CTS is mild to moderate. He concluded that in severe cases of CTS, other factors such as hypertrophy of the flexor tenosynovium may mask the effect of surgery. Although all surgical procedures in our series were carried out by open release of the TCL, endoscopic procedures have been found to be a risk factor.[[17]] The traumatic effect of the endoscopic procedure and hematomas in the carpal tunnel on the surrounding soft tissue may cause inflammation and swelling, consequently increasing the occurrence of TF.

In contrast, the authors of several reports have insisted that CTR does not accelerate the development of TF. In 2005, Harada et al.[[20]] retrospectively analyzed 101 patients who required trigger digit release. They reported that trigger digit release was performed most often after CTR, especially within 3 months; however, the next most common was at the same time as CTR. Moreover, Zhang et al.[[26]] recently demonstrated that although new-onset TF is frequent in the operative hand after CTR, the frequency is even higher before surgery. They concluded that although CTR has some effect on postoperative TF, it does not increase the risk of newly developing TF in the operative hand.

The presence of TF should be carefully assessed at presentation or before surgical treatment of CTS, and patients should be informed that the symptoms of TF might appear or worsen after surgery, especially within 6 months.

Conclusion

Neurosurgeons are generally considered less familiar with TF. However, an understanding of the clinical features of TF is necessary for successful management of CTS. TF should be carefully assessed at presentation and within 6 months after surgical treatment of CTS.

Conflict of Interest

There are no conflicts of interest.

Financial support and sponsorship

Nil.

• References

• 1 Ghasemi-Rad M, Nosair E, Vegh A, Mohammadi A, Akkad A, Lesha E, et al. A handy review of carpal tunnel syndrome: From anatomy to diagnosis and treatment. World J Radiol 2014;6:284-300.
• 2 Ibrahim I, Khan WS, Goddard N, Smitham P. Carpal tunnel syndrome: A review of the recent literature. Open Orthop J 2012;6:69-76.
• 3 Yunoki M, Kanda T, Suzuki K, Uneda A, Hirashita K, Yoshino K, et al. Importance of recognizing carpal tunnel syndrome for neurosurgeons: A review. Neurol Med Chir (Tokyo) 2017;57:172-83.
• 4 Kumar P, Chakrabarti I. Idiopathic carpal tunnel syndrome and trigger finger: Is there an association? J Hand Surg Eur Vol 2009;34:58-9.
• 5 Garti A, Velan GJ, Moshe W, Hendel D. Increased median nerve latency at the carpal tunnel of patients with “trigger finger”: Comparison of 62 patients and 13 controls. Acta Orthop Scand 2001;72:279-81.
• 6 Rottgers SA, Lewis D, Wollstein RA. Concomitant presentation of carpal tunnel syndrome and trigger finger. J Brachial Plex Peripher Nerve Inj 2009;4:13.
• 7 Makkouk AH, Oetgen ME, Swigart CR, Dodds SD. Trigger finger: Etiology, evaluation, and treatment. Curr Rev Musculoskelet Med 2008;1:92-6.
• 8 Moore JS. Flexor tendon entrapment of the digits (trigger finger and trigger thumb). J Occup Environ Med 2000;42:526-45.
• 9 Saldana MJ. Trigger digits: Diagnosis and treatment. J Am Acad Orthop Surg 2001;9:246-52.
• 10 Dardas AZ, VandenBerg J, Shen T, Gelberman RH, Calfee RP. Long-term effectiveness of repeat corticosteroid injections for trigger finger. J Hand Surg Am 2017;42:227-35.
• 11 Stahl S, Kanter Y, Karnielli E. Outcome of trigger finger treatment in diabetes. J Diabetes Complications 1997;11:287-90.
• 12 Uotani K, Kawata A, Nagao M, Mizutani T, Hayashi H. Trigger finger as an initial manifestation of familial amyloid polyneuropathy in a patient with ile107Val TTR. Intern Med 2007;46:501-4.
• 13 Burman M. Stenosing tendovaginitis of the dorsal and volar compartments of the wrist. AMA Arch Surg 1952;65:752-62.
• 14 Ettema AM, Amadio PC, Zhao C, Wold LE, O'Byrne MM, Moran SL, et al. Changes in the functional structure of the tenosynovium in idiopathic carpal tunnel syndrome: A scanning electron microscope study. Plast Reconstr Surg 2006;118:1413-22.
• 15 Sampson SP, Badalamente MA, Hurst LC, Seidman J. Pathobiology of the human A1 pulley in trigger finger. J Hand Surg Am 1991;16:714-21.
• 16 Acar MA, Kütahya H, Güleç A, Elmadaǧ M, Karalezli N, Ogun TC, et al. Triggering of the digits after carpal tunnel surgery. Ann Plast Surg 2015;75:393-7.
• 17 El-Hadidi S. Is there a relation between carpal tunnel syndrome and trigger finger? BMC Proc 2015;9 Suppl 3:A65.
• 18 Goshtasby PH, Wheeler DR, Moy OJ. Risk factors for trigger finger occurrence after carpal tunnel release. Hand Surg 2010;15:81-7.
• 19 Grandizio LC, Beck JD, Rutter MR, Graham J, Klena JC. The incidence of trigger digit after carpal tunnel release in diabetic and nondiabetic patients. J Hand Surg Am 2014;39:280-5.
• 20 Harada K, Nakashima H, Teramoto K, Nagai T, Hoshino S, Yonemitsu H, et al. Trigger digits-associated carpal tunnel syndrome: Relationship between carpal tunnel release and trigger digits. Hand Surg 2005;10:205-8.
• 21 Hayashi M, Uchiyama S, Toriumi H, Nakagawa H, Kamimura M, Miyasaka T, et al. Carpal tunnel syndrome and development of trigger digit. J Clin Neurosci 2005;12:39-41.
• 22 Hombal JW, Owen R. Carpal tunnel decompression and trigger digits. Hand 1970;2:192-6.
• 23 Kim JH, Gong HS, Lee HJ, Lee YH, Rhee SH, Baek GH. Pre- and post-operative comorbidities in idiopathic carpal tunnel syndrome: Cervical arthritis, basal joint arthritis of the thumb, and trigger digit. J Hand Surg Eur Vol 2013;38:50-6.
• 24 King BA, Stern PJ, Kiefhaber TR. The incidence of trigger finger or de Quervain's tendinitis after carpal tunnel release. J Hand Surg Eur Vol 2013;38:82-3.
• 25 Lin FY, Wu CI, Cheng HT. Coincidence or complication? A systematic review of trigger digit after carpal tunnel release. J Plast Surg Hand Surg 2018;52:67-73.
• 26 Zhang D, Collins J, Earp BE, Blazar P. Relationship of carpal tunnel release and new onset trigger finger. J Hand Surg Am 2019;44:28-34.
• 27 Karalezli N, Kütahya H, Güleç A, Toker S, Karabörk H, Ogun TC, et al. Transverse carpal ligament and forearm fascia release for the treatment of carpal tunnel syndrome change the entrance angle of flexor tendons to the A1 pulley: The relationship between carpal tunnel surgery and trigger finger occurrence. ScientificWorldJournal 2013;2013:630617.
• 28 Chammas M, Bousquet P, Renard E, Poirier JL, Jaffiol C, Allieu Y, et al. Dupuytren's disease, carpal tunnel syndrome, trigger finger, and diabetes mellitus. J Hand Surg Am 1995;20:109-14.

Publication History

Article published online:
09 September 2022