0E010.1177/1753193413479506The Journal of Hand SurgeryLee et al. 2013
JHS(E)
Full length article
The relationship of trigger finger and flexor tendon volar migration after carpal tunnel release
The Journal of Hand Surgery (European Volume) 0E(0) 1–5 © The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1753193413479506 jhs.sagepub.com
S. K. Lee, K. W. Bae and W. S. Choy
Department of Orthopedic Surgery, Eulji University College of Medicine, Daejeon, South Korea
Abstract It has been suggested that the increased frequency of trigger finger (TF) after carpal tunnel release (CTR) may be caused by the volar migration of the flexor tendons at the wrist altering the tendon biomechanics at the A1 pulley. This hypothesis has not been validated. We performed pre- and post-operative ultrasonography (USG) on the affected wrists of 92 patients who underwent CTR. Pre-operative USG was performed in neutral with no tendon loading; post-operative USG was performed in neutral unloaded and in various positions of wrist flexion whilst loading the flexor tendons with gripping. The mean volar migration of the flexor tendons after CTR was 2.2 (SD 0.4) mm in the unloaded neutral position. It was 1.8 (SD 0.4) mm in patients who did not develop TF and 2.5 (SD 0.5) mm in those who did (p = 0.0067). In loaded wrist flexion, the mean volar migration of flexor tendons after CTR in patients who did not develop TF and those who did was 2.1 and 3.0 mm in 0° flexion; 3.2 and 3.9 mm in 15° flexion; 4.3 and 5.1 mm in 30° flexion; and 4.9 and 5.8 mm in 45° flexion, respectively. There were significant differences between patients with and without TF at each flexion angle. Our data indicate that patients with greater volar migration of the flexor tendons after CTR are more likely to develop TF. This conclusion supports the hypothesis that the occurrence of TF after CTR may be caused by the bowstringing effects of the flexor tendons. Keywords Carpal tunnel release, trigger finger, bowstringing effect Date received: 1st February 2012; revised 24th January 2013; accepted 28th January 2013
Introduction Carpal tunnel syndrome (CTS) and stenosing tenosynovitis or trigger finger (TF) are common. TF is associated with CTS (Ferree et al., 2012; Harada et al., 2005; Hayashi et al., 2005; Hombal and Owen, 1970; Kim et al., 2013; Kumar et al., 2009) and occurs more frequently after carpal tunnel release (CTR) (Harada et al., 2005; Hayashi et al., 2005; Hombal and Owen, 1970; King et al., 2013). Stahl et al. (1997) reported that the lifetime incidence of trigger finger was 2.2% in nondiabetic adults older than 30 years and up to 10% in patients with insulin-dependent diabetes mellitus. The incidence of TF associated with CTS has been reported to be 10.2% to 21% (Assmus, 2000; Hayashi et al., 2005; Kumar et al., 2009). The incidence of TF after CTR has been reported to be between 6.3% and 21.9% (Goshtasby et al., 2010; Harada et al., 2005; Hayashi et al., 2005; Hombal and Owen, 1970; Kim et al., 2013; King et al., 2013). Some studies have
investigated the significance of variable risk factors predisposing patients to developing TF after CTR (Goshtasby et al., 2010; Harada et al., 2005; Hayashi et al., 2005). Netscher et al. (1997) demonstrated on magnetic resonance imaging (MRI) scans that there was an increased volar migration of the median nerve and flexor tendons after CTR. This has led to suggestions that the increased incidence or exacerbation of TF following CTR can be explained by the volar migration of the flexor tendons following release of the flexor retinaculum; this may cause a greater friction between the FDS tendon and A1 pulley (Goshtasby Corresponding author: Professor Sang Ki Lee, M.D., Department of Orthopedic Surgery, Eulji University College of Medicine, 1306 Dunsan-dong, Seo-gu, Daejeon 302-799, South Korea Email:
[email protected]
2 et al., 2010; Harada et al., 2005; Hayashi et al., 2005). This suggestion has not been confirmed in clinical studies. The aim of this study was to investigate the volar migration of the flexor tendons at the wrist following CTR and assess whether the amount of volar migration correlated with the incidence of subsequent TF.
Methods Between September 2007 and January 2011, all 497 patients who underwent open CTR for idiopathic CTS were selected for this study. All the operations were performed by a single hand surgeon using a minimal incision open technique for CTR under local anaesthesia. Follow-up after CTR was scheduled for 1, 3, 6, 12, and 18 months post-operatively. The following exclusions were applied: any comorbidity that might result in TF, such as diabetes mellitus, rheumatoid arthritis, scleroderma and amyloidosis that cause systemic deposition of protein (Ryzewicz and Wolf, 2006); previous TF; hand injuries including flexor tendon injuries and fractures; interphalangeal and metacarpophalangeal (MP) joint contractures; and follow-up < 1 month.
Diagnosis of TF after CTR At follow-up, all patients (100%) were seen at 1 month; 340 (68%) at 3 months; 217 (44%) at 6 months; 73 (15%) at 12 months; and 52 (10%) at 18 months. During the follow-up period, the occurrence of TF was diagnosed by careful clinical assessment. A diagnosis of TF was made based on the presence of local tenderness, a palpable lump, and triggering of the flexor tendon at the A1 pulley. For patients diagnosed with TF, follow-up was performed every month from the diagnosis of TF.
The Journal of Hand Surgery (Eur) 0(0) The only flexor tendons included in the measurements were the flexor digitorum superficialis (FDS) tendons. We decided to exclude the flexor digitorum profundus (FDP) tendons from the measurements based on previous experience, which showed limited volar migration of the FDP tendons possibly related to the attachment of the lumbrical muscles. Moreover, the tendons that primarily lead to triggering are the FDS tendons. Post-operative USG was conducted unloaded in neutral as above and loaded in different positions of wrist flexion: 0°, 15°, 30°, and 45°. The positions of flexion of the wrist loading were controlled in a custom jig (Figure 1) with the MP joints in neutral and proximal and distal interphalangeal joints flexed holding a handle connected to a 2 kg weight (Figure 1). Because of difficulties in reproducing the position of the thumb, we excluded the flexor pollicis longus (FPL) tendons from measurement. We performed post-operative USG on 47 patients who subsequently developed TF after CTR and 45 patients as a control group. Control patients were those of similar age and gender randomly selected from the 319 patients who underwent preoperative USG. They were followed until last scheduled follow-up to confirm that they did not develop TF postoperatively. In the 47 patients who developed TF, USG was performed promptly when diagnosed at follow-up. However, in patients diagnosed with TF at 1 month of follow-up, USG was only performed at 3 months because we felt that 1 month was not enough to adequately resolve post-operative swelling. In the 45 control patients, post-operative USG scans were performed at 6 months post-operatively.
Imaging evaluation Ultrasonography (USG) was performed pre-operatively on the symptomatic wrists of 319 (64.2%) patients using a scanner with a 12/5-MHz linear-array transducer (Philips IU 22; Philips Medical Systems, Bothell, Washington, USA). Patients were examined supine with their hand palm up and resting alongside their body on the examination table, unloaded in a neutral position. We measured the cross-sectional area of the carpal tunnel, degree of compression of the median nerve, and distance from volar surface of the capitate to volar surface of the flexor tendons. Volar migration of flexor tendons was measured at the same level as the cross-section area.
Figure 1. The loaded wrist flexion position for USG. Wrist was flexed at each angle (0°, 15°, 30°, 45°). Proximal and distal interphalangeal joints are flexed in a position bearing a 2 kg weight.
3
Lee et al. USG measurements were performed by a single author. To reduce errors, measurements were performed in duplicate and mean values were calculated. Intraobserver reliability between the two sets of measurements was recorded according to the criteria of Winer et al. (1971).
Statistical analysis The data were normally distributed. The Student’s t-test was used to analyze differences in crosssectional area of the carpal tunnel, between patients with and without TF. Fisher’s exact test was used to analyze differences in dichotomous variables, such as sex, smoking history, hand dominance, and osteoarthritis. The Mann–Whitney U test was used to analyze the volar migration of flexor tendons at each flexion position. A p value of < 0.05 was considered significant. Our institutional review board approved this study.
Results Occurrence of TF There were 497 patients; 113 men and 384 women, with a mean age of 49 (range 21–79) years. TF occurred post-operatively in 72 fingers of 59 patients (11.9%); there were 11 men and 48 women, with a mean age of 56 (range 32–74) years. TF occurred in one finger in 46 patients and two fingers in 13 patients. Seven of 13 patients with two trigger digits had a trigger thumb. Triggering occurred in the thumb in 22 patients, index finger in eight, middle finger in 21, ring finger in 19, and little finger in two patients. Triggering was first noted in four fingers at 1 month after CTR, 31 more fingers at 3 months, 26 more fingers at 6 months, and 11 more fingers at 12 months. No further triggering was noted at 18 months. All trigger digits were treated conservatively with a single steroid injection combined with activity modification and nonsteroidal anti-inflammatory drugs for 3 months. The symptoms improved after conservative treatment in 21 fingers. In the other 51 fingers, in which symptoms did not improved, open surgical release of the A1 pulley was performed.
Imaging data Upon pre-operative USG performed on 319 patients, the mean cross-sectional area of the carpal tunnel in all patients was 2.46 cm2; 2.42 cm2 in the TF group (47 patients) and 2.46 cm2 in the non-TF group (272 patients). In men, the mean cross-sectional area was
2.50 cm2 with a mean of 2.49 cm2 in the TF group and 2.52 cm2 in the non-TF group. In women, it was 2.39 cm2 overall, 2.37 cm2 in the TF group, and 2.41 cm2 in the non-TF group. There was no significant difference between those who did and did not developed TF (p > 0.05). For measurement of the cross-section area, intraobserver reliability was 0.92 (classified as excellent: 0.9–1). Upon post-operative USG, mean volar migration of the flexor tendons after CTR was 2.2 (SD 0.4) mm in the unloaded neutral position; 2.5 (SD 0.5) mm in the TF group and 1.8 (SD 0.4) mm in the non-TF group, a significant difference (p = 0.0067). In postoperative loaded wrist flexion, mean volar migration of the flexor tendons was in neutral 3.0 (SD 0.3) mm in the TF group and 2.1 (SD 0.2) mm in non-TF group; at 15° flexion 3.9 (SD 0.4) mm and 3.2 (SD 0.4) mm, respectively; at 30° flexion 5.1 (SD 0.4) mm and 4.3 (SD 0.3) mm; and at 45° flexion 5.8 (SD 0.4) mm and 4.9 (SD 0.3) mm, respectively (Figure 2). There were significant differences between the TF and non-TF groups at each flexion angle. The intraobserver reliability for measurement of volar migration was also 0.92.
Significance of risk factors There were no significant differences with regard to mean age, sex, smoking history, or hand dominance between patients with and without TF. The only statistically significant difference was in osteoarthritis (p = 0.013).
Figure 2. Comparison of the degree of mean volar migration of the flexor tendons after CTR between TF and nonTF groups in each loaded wrist flexion angle. The TF group had a greater mean volar migration of the flexor tendons than non-TF group, and there were significant differences in each flexion angle. Values of the mean volar migration are given as mean (SD).
4
Discussion A few studies (Goshtasby et al., 2010; Harada et al., 2005; Hayashi et al., 2005; Hombal and Owen, 1970; Kim et al., 2013; King et al., 2013) have reported the incidence of TF after CTR. These studies reported the prevalence of TF after CTR to be between 6.3% and 21.9%. The overall prevalence in this study was 11.9%. We think it was somewhat lower than previous studies because patients with factors predisposing to TF were excluded in this study. Hombal and Owen (1970) carried out a retrospective study of 132 patients who underwent CTR. They noted the incidence of TF after CTR to be 21.9% and suggested that the bowstringing effects of the flexor tendons after CTR can give rise to increased frictional force and, thus, changes in the sheath or flexor tendon leading to the TF. These researchers conceded that experimental verification was needed before acceptance of this idea. Netscher et al. (1997) showed on MRI scans that there was volar migration of the flexor tendons after CTR. However, the study only investigated changes of volar migration of the flexor tendons as a result of various methods of transverse carpal ligament reconstruction after CTR and did not examine a correlation of the effect of volar migration with TF. In this study, mean volar migration of the flexor tendons after CTR was 2.2 (SD 0.4) mm in the unloaded neutral position. It was greater in the TF (2.5, SD 0.5) than non-TF group (1.8, SD 0.4); this difference was statistically significant. Netscher et al. (1997) recorded volar migration of the flexor tendons after CTR of 2.4 (SD 0.8) in neutral and 2.4 (SD 1.5) in 45° of wrist flexion. Our results are similar but smaller. However, it is difficult to make a simple comparison between the results of this and previous studies because of the different study designs, and individual and racial variation. Unlike the study of Netscher et al. (1997), we noted a significant increase in volar migration with wrist flexion and loading. In a biomechanical study, Kutsumi et al. (2005) reported that gliding resistance between the tendon and extensor retinaculum is higher when the wrist is flexed or extended; that is, friction between the tendon and extensor retinaculum increases as the angle between them increases. Higher friction may cause surface damage to the tendons and extensor retinaculum, resulting in secondary changes, such as tenosynovitis. In addition, inflammatory enzymes may destroy lubricating glycoproteins on the surface of the tendons and extensor retinaculum, resulting in a cycle of increased friction and damage (Kutsumi et al., 2005). Our results indicate that the incidence of TF increases as volar migration of the flexor tendons increases after CTR. The flexor tendons have to go
The Journal of Hand Surgery (Eur) 0(0) through a small bend as they enter the flexor sheath at the entrance to the A1 pulley. We postulate that this increases with increasing volar migration of the flexor tendons at the wrist causing increased friction leading to TF. Conservative treatment only resolved 29% of the cases of TF in this study compared with a success rate of 72% to 93% for primary TF (Freiberg et al., 1989; Newport et al., 1990; Rhoades et al., 1984). This may be because the mechanics are different, that we used only a single steroid injection, or due to other factors which contribute to CTS. A previous study reported a success rate of 84% to 92% with a single steroid injection and 91% to 97% with repeated steroid injections for primary TF (Marks and Gunther, 1989). Although there is a high success rate with steroid injections (and an even higher rate with repeated steroid injections) for primary TF, we believe that because of the mechanical change after CTR, steroid injections for TF after CTR would not give patients satisfactory results and repeated steroid injections would not significantly increase the success rate; therefore, we decided to use only a single steroid injection. The timing of surgery after the failure of corticosteroid injections is somewhat controversial. A previous study (Patel and Bassini, 1992) reported that patients with marked triggering, symptoms for more than 6 months, and multiple trigger digits had a higher rate of failure with conservative treatment. We performed conservative treatment for only 3 months, not 6 months. We also released the A1 pulley after 3 months if conservative treatment failed. The reported factors that increase the risk of TF after CTR include using an endoscopic technique, thyroid disease, osteoarthritis, and use of a soft postoperative dressing (Goshtasby et al., 2010). Goshtasby et al. (2010) have suggested that the blunt insertion of the endoscope at an endoscopic CTR can have a traumatic effect on the surrounding soft tissue, which may lead to increased inflammation and post-operative swelling, and consequently, an increased incidence of TF. Conversely, Isaac et al. (2010) reported that the use of a splint after carpal tunnel decompression does not improve outcome. The only risk factor found to significantly predispose patients to TF occurrence after CTR in our study was osteoarthritis. We were unable to investigate the relation between other variable potential risk factors and TF occurrence after CTR because of the small number of cases in our study. This study has some limitations. First, we did not perform pre-operative USG in loaded wrist flexion. Second, we did not use MRI (a more reliable tool to identify tendons than USG) due to its cost. Third, we
Lee et al. excluded the thumb when measuring the volar migration of the flexor tendons due to the difficulty of maintaining it in a constant position during USG and in selecting a reference point to measure the volar migration of the FPL. Fourth, we were unable to perform long-term follow-up on all patients who underwent CTR. This was partly because the patients who achieved symptom relief after CTR did not return to the outpatient clinic. Thus, the rate of TF after CTR may have been higher if long-term follow-up on all cases had been performed. In conclusion, we confirm that patients with greater volar migration of the flexor tendons after CTR are at a higher risk of developing TF. We have identified that osteoarthritis may be a significant risk factor contributing to TF occurrence after CTR. We believe early operative treatment is required because of the high failure rate of conservative treatment compared with the treatment of primary TF, although we have not tested or proven this. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors
Conflict of interests None declared.
Ethical approval Our institutional review board approved this study (Eulji University Hospital, protocol No: 11-113).
References Assmus H. Tendovaginitis stenosans: a frequent complication of carpal tunnel syndrome. Nervenarzt. 2000, 71: 474–6. Ferree S, Neuhaus V, Becker SJ, Jupiter JB, Mudgal CS, Ring DC. Risk factors for return with a second trigger digit. J Hand Surg Eur. 2012 (epub). DOI: 1753193412469129. Freiberg A, Mulholland RS, Levine R. Nonoperative treatment of trigger fingers and thumbs. J Hand Surg Am. 1989, 14: 553–8. Goshtasby PH, Wheeler DR, Moy OJ. Risk factors for trigger finger occurrence after carpal tunnel release. Hand Surg. 2010, 15: 81–7. Harada K, Nakashima H, Teramoto K, Nagai T, Hoshino S, Yonemitsu H. Trigger digits associated carpal tunnel syndrome: relationship between carpal tunnel release and trigger digits. Hand Surg. 2005, 10: 205–8.
5 Hayashi M, Uchiyama S, Toriumi H, Nakagawa H, Kamimura M, Miyasaka T. Carpal tunnel syndrome and development of trigger digit. J Clin Neurosci. 2005, 12: 39–41. Hombal JW, Owen R. Carpal tunnel decompression and trigger digits. Hand. 1970, 2: 192–6. Isaac SM, Okoro T, Danial I, Wildin C. Does wrist immobilization following open carpal tunnel release improve functional outcome? A literature review. Curr Rev Musculoskelet Med. 2010, 3: 11–7. Jacobs JH, Hess EV, Beswick IP. Rheumatoid arthritis presenting as tenosynovitis. J Bone Joint Surg Br. 1957, 39: 288–92.[AQ: 1] Kim JH, Gong HS, Lee HJ, Lee YH, Rhee SH, Baek GH. Preand post-operative comorbidities in idiopathic carpal tunnel syndrome: cervical arthritis, basal joint arthritis of the thumb, and trigger digit. J Hand Surg Eur. 2013, 38: 50–6. King BA, Stern PJ, Kiefhaber TR. The incidence of trigger finger or de Quervain’s tendinitis after carpal tunnel release. J Hand Surg Eur. 2013, 38: 82–3. Kumar P, Chakrabarti I. Idiopathic carpal tunnel syndrome and trigger finger: is there an association? J Hand Surg Eur. 2009, 34: 58–9. Kutsumi K, Amadio PC, Zhao C, Zobitz ME, An KN. Gliding resistance of the extensor pollicis brevis tendon and abductor pollicis longus tendon within the first dorsal compartment in fixed wrist positions. J Orthop Res. 2005, 23: 243–8. Marks MR, Gunther SF. Efficacy of cortisone injection in treatment of trigger fingers and thumbs. J Hand Surg Am. 1989, 14: 722–7. Netscher D, Mosharrafa A, Lee M, Polsen C, Choi H, Steadman AK, Thornby J. Transverse carpal ligament: its effect on flexor tendon excursion, morphologic changes of the carpal canal, and on pinch and grip strengths after open carpal tunnel release. Plast Reconstr Surg. 1997, 100: 636–42. Newport ML, Lane LB, Stuchin SA. Treatment of trigger finger by steroid injection. J Hand Surg Am. 1990, 15: 748–50. Patel MR, Bassini L. Trigger fingers and thumb: when to splint, inject, or operate. J Hand Surg Am. 1992, 17: 110–3. Rhoades CE, Gelberman RH, Manjarris JF. Stenosing tenosynovitis of the fingers and thumb. Results of a prospective trial of steroid injection and splinting. Clin Orthop Relat Res. 1984, 190: 236–8. Ryzewicz M, Wolf JM. Trigger digits: principles, management, and complications. J Hand Surg Am. 2006, 31: 135–46. Stahl S, Kanter Y, Karnielli E. Outcome of trigger finger treatment in diabetes. J Diabetes Complications. 1997, 11: 287–90. Winer BJ. Statistical principles in experimental design. 2nd ed. New York: McGraw Hill; 1971.
