Abstract
Background:
The exact mechanism underlying flexor tendon sheath ganglion (FTSG) formation remains unclear. We hypothesized that steroid injections into the A1 pulley are a cause of FTSG. Therefore, this study aimed to evaluate the risk of FTSG after steroid injections in patients with stenosing flexor tenosynovitis.
Methods:
This prospective cohort study enrolled patients diagnosed with stenosing flexor tenosynovitis between August 2019 and May 2024. A total of 128 fingers in 114 patients with no history of injections within the past 6 months consented to participate in the study. An initial ultrasound of the A1 pulley was performed, and patients with preexisting FTSG were excluded. Based on patient preference, the injection group received a steroid injection (5 mg of triamcinolone + 0.5 ml of 1% lidocaine) into the flexor tendon sheath, followed by a follow-up ultrasound at 3 months. The control group underwent ultrasonography at the same time points without injections.
Results:
Three-month follow-up ultrasound evaluations were conducted on 53 fingers (43 patients) in the injection group and 22 fingers (21 patients) in the control group. The incidence of FTSG was significantly higher in the injection group, with 20 of 53 fingers (37.7%) developing FTSG compared with 1 of 22 fingers (4.5%) in the control group. The risk difference was 0.33 (95% confidence interval: 0.18-0.49; p < 0.01). Symptom improvement was observed in 93% of the injection group compared with 45% of the control group (p < 0.01), indicating more significant symptom relief in the injection group.
Conclusions:
This study concluded that small punctures caused by steroid injections for stenosing flexor tenosynovitis can lead to FTSG; however, further studies are required to fully elucidate the clinical significance of ganglion formation.
Level of Evidence:
Level II. See Instructions for Authors for a complete description of levels of evidence.
Introduction
The ganglion is a common palpable small cystic mass in the subcutaneous layer; however, it can sometimes cause pain and thus requires treatment. The most common locations of ganglion cysts are the dorsal and volar aspects of the wrist, followed by the digital flexor tendon sheath1. Among the ganglia distal to the wrist, 7% to 12% are flexor tendon sheath ganglia (FTSG)2. Ganglia in the fingers typically occur at the level of the metacarpophalangeal joints and proximal phalanges; 78% of finger FTSGs are located at the A1 and A2 tendon sheath areas, with the middle finger being the most common3. FTSGs in the A1 and A2 tendon sheath areas are characterized by symptoms of flexor tendon sheath inflammation. Tenderness is generally the common symptom. The exact mechanism of FTSG formation remains unclear, although several hypotheses have been proposed, including cystic tumors originating from the synovium, mucoid degeneration of the connective tissue, and herniation of the synovial fluid or synovium through small tissue defects caused by trauma4. Several studies have suggested that trauma plays a significant role in the development of FTSG. Al-Qawasmi et al. proposed a relationship between occupation, repetitive trauma, and FTSG etiology5. Similarly, in his report of 11 cases involving typists, Matthews noted that the middle finger was the most affected, with the ganglia located in the A1 pulley6. Abe hypothesized that repetitive finger use causes small defects and argued that increased synovial fluid inflow through these small defects likely leads to FTSG formation.
We observed some cases in which FTSG formed after steroid injections into the A1 pulley, leading us to hypothesize that steroid injections are a cause of FTSG. To date, no direct comparison has assessed whether steroid injection affects the incidence of FTSG in patients with stenosing flexor tenosynovitis.
Therefore, this prospective study aimed to evaluate the risk of FTSG after steroid injection in patients with stenosing flexor tenosynovitis.
Materials and Methods
This study was conducted with the approval of the Ethics Committee of our institute (reference number: 2,674) and in accordance with the principles of the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all participants.
Study Design
This was a prospective, cohort study. Patients diagnosed with stenosing flexor tenosynovitis in our hospital between August 2019 and May 2024 were enrolled if they had no history of injections within the past 6 months and provided consent to participate in the study. The diagnosis of stenosing flexor tenosynovitis was based on the presence of tenderness at the A1 pulley, triggering symptoms, pain on hyperextension of finger, and thickening of the tendon sheath, with the exclusion of other conditions such as pyogenic tenosynovitis. All diagnoses were made by a hand surgeon. The ultrasound appearance of FTSG was defined as a homogeneously hypoechoic region within or on the A1 pulley with clearly demarcated boundaries, no stalk, and no internal blood flow7. A total of 128 fingers in 114 patients consented to participate in the study, and ultrasonography of the A1 pulley was performed. Patients with FTSG during the initial ultrasound examination were excluded. Based on the patient's preference, the injection group received a steroid injection (5 mg of triamcinolone + 0.5 ml of 1% lidocaine) into the flexor tendon sheath. These patients underwent follow-up ultrasound 3 months later (Fig. 1). The control group consisted of patients who only underwent ultrasonography on the A1 pulley without injections, followed by an ultrasound 3 months later. Oral or topical pain relief was permitted in both groups. Patients in the control group who received steroid injections before the 6-month follow-up were excluded from the analysis.
Fig. 1.
Ultrasound findings of the tendon sheath before and after injection. Fig. 1-A Before injection: the tendon sheath is thickened, but no ganglion is present. Fig. 1-B After injection: an ultrasound conducted 3 months postinjection shows a hypoechoic image on the upper part of the tendon sheath (white arrow).
Data Collection
The study parameters included age, sex, dominant hand, presence of diabetes, duration of symptoms of stenosing flexor tenosynovitis, presence of diagnostic symptoms (tenderness of the A1 pulley, triggering finger, and pain during hyperextension of the affected finger), and Green classification.
Outcomes
The primary outcome was the existence of FTSG on ultrasound at the 3-month follow-up. Pain at rest and during use was measured using the visual analog scale (VAS), and changes in symptoms after 3 months were graded into 4 categories (complete disappearance of symptoms, partial disappearance of symptoms, no change, and worsening of symptoms).
Injection Method
The injection method varied depending on the surgeon who performed the procedure. The injection was administered into the tendon sheath either under ultrasound guidance or using the loss-of-injection method. For the latter, the needle was inserted through the sheath into the tendon and withdrawn until no resistance was felt before the injection. The ultrasound devices used were either Hi Vision Avius (Hitachi Medico) or Noblus (Hitachi Aloka Medical).
Statistical Analysis
Statistical differences in continuous variables between the 2 groups were examined using the Mann-Whitney U test, and categorical variables were examined using the χ2 test. Furthermore, the incidence of FTSG at 3 months and risk differences was calculated for each group. Statistical significance was set at p < 0.05. All analyses were performed using STATA14 (Stata Corp).
Results
Patients and Descriptive Data
A total of 102 fingers (84 patients) without FTSG on the initial ultrasound of the A1 pulley were included in the study. Eleven patients had 2 fingers with flexor tenosynovitis, 2 had 3 fingers, and 1 had 4 fingers. In total, there were 77 fingers (61 patients) in the injection group and 25 fingers (23 patients) in the control group. After 3 months, follow-up ultrasonography was conducted on 53 fingers (43 patients) in the injection group and 22 fingers (21 patients) in the control group (Fig. 2).
Fig. 2.
A total of 128 fingers (114 patients) were screened, with 26 fingers excluded because they had a ganglion at the first ultrasound. The 102 eligible fingers are divided into 2 groups: the injection group with a puncture procedure (n = 77) and a control group without any puncture (n = 25). Both groups were followed for 3 months. Of the 77 fingers in the injection group, 24 fingers (18 patients) dropped out, while 3 fingers dropped out from the 25 fingers in the control group. As a result, 53 fingers in the injection group and 22 fingers in the control group were included in the analysis.
There were no significant differences in sex, average age, affected finger on the dominant/nondominant hand, presence of diabetes, location of the affected finger, duration of illness, symptoms, Green classification, or pain VAS scores between the groups (Table I).
TABLE I.
Patient Characteristics at Baseline
| Variables | Category | Injection Group | Control Group | p |
|---|---|---|---|---|
| N | 53 | 22 | ||
| Sex—no | Female | 30 (57%) | 11 (50%) | 0.60 |
| Age (year)* | 70.0 ± 11.9 | 71.5 ± 13.5 | 0.49 | |
| Dominant hand—no | Yes | 43 (81%) | 17 (77%) | 0.70 |
| Diabetes mellitus—no | Yes | 9 (17%) | 4 (18%) | 0.90 |
| Location of diseased finger | Thumb | 17 (32%) | 4 (18%) | 0.58 |
| Index | 7 (13%) | 4 (18%) | ||
| Middle | 21 (40%) | 11 (50%) | ||
| Ring | 7 (13%) | 3 (14%) | ||
| Small | 1 (2%) | 0 (0%) | ||
| Duration of illness(month)* | 10.1 ± 13.8 | 10.6 ± 16.4 | 0.92 | |
| Symptoms | Tenderness in the A1 pulley | 48 (91%) | 19 (86%) | 0.59 |
| Triggering phenomenon | 44 (83%) | 18 (82%) | 0.90 | |
| Pain on hyperextension of finger | 46 (87%) | 15 (68%) | 0.06 | |
| Green classification | Grade 1 | 7 (13.2%) | 2 (9.1%) | 0.62 |
| Grade 2 | 30 (56.6%) | 16 (72.7%) | ||
| Grade 3 | 5 (9.4%) | 1 (4.6%) | ||
| Grade 4 | 11 (20.8%) | 3 (13.6%) | ||
| Pain VAS(mm)* | At rest | 15.3 ± 22.8† | 14.9 ± 21.4 | 0.96 |
| During use | 49.4 ± 29.2† | 49.1 ± 27.6 | 0.99 |
Plus-minus values are expressed as the mean ± SD.
Values were missing for 1 individual.
SD = standard deviation and VAS = Visual Analogue Scale.
Incidence of FTSG
FTSG was observed in 20 of 53 fingers (37.7%) in the injection group on ultrasonography conducted 3 months after the injection. By contrast, only 1 of the 22 fingers (4.5%) developed FTSG in the control group. The risk difference (incidence rate difference) was 0.33 (95% confidence interval: 0.18-0.49) with a p-value < 0.01, indicating a significantly higher risk of developing FTSG in the injection group (Table II).
TABLE II.
Ganglion Formation and Changes of Symptoms at Second Ultrasound Examination
| Variables | Category | Injection Group | Control Group | p |
|---|---|---|---|---|
| N | 53 | 22 | ||
| Ganglion formation | Yes | 20 (37.7%) | 1 (4.5%) | <0.01 |
| Changes of symptom at second ultrasound examination | 1. Complete disappearance of symptoms | 21 (39.6%) | 2 (9.1%) | <0.01 |
| 2. Partial disappearance of symptoms | 28 (52.8%) | 8 (36.4%) | ||
| 3. No change | 4 (7.5%) | 8 (36.4%) | ||
| 4. Worsening of symptoms | 0 (0.0%) | 4 (18.2%) |
Patient-Reported Outcome Measures
Regarding the effect of the injection on symptoms, 93% of the injection group showed an improvement in symptoms, whereas only 45% of the control group showed an improvement, clearly indicating that the injection group experienced more significant symptom improvement (p < 0.01) (Table II).
Comparison of Each Group of Patients with and without FTSG
Baseline characteristics and symptom progression at 3 months were compared between patients who developed FTSGs and those who did not, in both the injection and control groups. These comparisons are presented in Supplemental Tables S1 and S2 (see Supplemental Table S1 and Table S2).
No significant differences in baseline characteristics were observed between patients who developed FTSG after injection and those who did not. Furthermore, the presence or absence of FTSG at 3 months postinjection was not associated with clinical improvement (see Supplemental Table S1).
Histopathological Examination
One patient in the injection group who developed a FTSG and experienced a recurrence of stenosing flexor tenosynovitis underwent surgical tenosynovectomy. The tendon sheath, including the entire ganglion, was excised in 1 piece from the A1 pulley and examined in detail (Fig. 3-A). The specimen was sectioned sagittally, perpendicular to the transverse fibers, and multiple 5-μm thick slices were prepared for histological analysis. Hematoxylin and eosin (HE) staining was performed, and evaluation under an optical microscope revealed that the ganglion arose from the flexor sheath and consisted of fibrous tissue without an endothelial cell lining (Fig. 3-B). Notably, no synovial tissue was observed within the ganglion, and small defects or damage in the tendon sheath were also identified.
A FTSG excised during surgery for recurrent flexor tenosynovitis in a patient from the injection group.
Fig. 3-A.
Macroscopic examination of a tendon sheath. The ganglion cyst reveals an unilocular structure that contains yellow, gelatinous deposits.
Fig. 3-B.
Whole histological image of a FTSG with hematoxylin and eosin staining. In the longitudinal section, the outer layer of the flexor sheath, which contained fibrous tissue and vessels, had transitioned to the ganglion wall. The slit through which the ganglion communicated with the synovial surface was noted. The magnified image of the inner cavity is an enlarged view of the slit area. The principal lumen of the ganglion is surrounded by fibrous tissue and occasionally by flattened cells. There was no endothelial cell lining. FTSG = flexor tendon sheath ganglion.
Discussion
In this study, the incidence of FTSG after steroid injection was higher than the incidence of spontaneous FTSG over 3 months in patients with stenosing flexor tenosynovitis. The injection group exhibited a 33% higher risk than the control group. Our results support the new hypothesis that injections into the tendon sheath are involved in the development of FTSG. Our findings suggest that the small perforations created by the administration of steroid injections may have contributed to ganglion formation.
Although a priori power analysis was not conducted due to the observational design of this study, the statistically significant difference observed between the injection and control groups indicates that the sample size was sufficient to detect clinically meaningful differences.
At 3 months, 93% of patients in the injection group demonstrated symptomatic improvement, and the occurrence of FTSG did not seem to have a significant impact on the clinical outcome (see Supplemental Table S1). However, as the assessment period was limited to 3 months, it is presumed that the effects of steroid treatment were particularly pronounced during this timeframe. It is also possible that, in the natural course, the timing of ganglion formation and resolution may vary and that some ganglia may resolve after needling. Therefore, in future studies, it will be necessary to investigate the clinical significance of subsheath injections after tendon sheath puncture by examining the association between the presence of FTSG and the long-term patient outcomes, including symptom improvement, recurrence, and the need for surgical intervention.
FTSGs are generally a few millimeters in diameter, dome-shaped, and adhere closely to the tendon sheath at their base. Unlike ganglia at other locations, FTSGs are unilocular and do not show cystic branches from the main cyst. The walls are thin, and the contents vary from a viscous fluid to a jelly-like substance6. These findings are consistent with echo findings7. In cases in which stenosing flexor tenosynovitis recurred with ganglion development after injection, surgical procedures allowed direct macroscopic and histological examination to confirm the ganglion. The characteristic pathological feature of a ganglion is the absence of a cell-lining layer; similar findings were observed in our specimen8. These findings also correspond to the definition of a ganglion, supporting the reliability of the ultrasound diagnosis.
A prospective randomized study9 comparing steroid injections inside and outside the tendon sheath for stenosing flexor tenosynovitis reported no difference in symptom improvement 1 month after injection; however, the mean time to recurrence was shorter in the group that received steroid injections in the tendon sheath. Based on this report, direct injection into the tendon sheath may not be necessary.
In the actual pathological findings, a single narrow tear in the tendon sheath appeared to direct the tendon sheath fibers from the synovial surface toward the cavity of the mass, indicating a potential one-way inflow mechanism of the synovial fluid. An interesting study on ganglion formation involved the injection of a contrast agent into the joint area of patients. Although there was an inflow of contrast agent into the ganglion, there was no outflow from the ganglion to the joint, suggesting the presence of a valve mechanism during ganglion formation10. However, our results alone do not confirm the presence of a check-valve mechanism, which requires further investigation. Nevertheless, we believe that our study provides new insights and contributes to the understanding of the previously unknown mechanisms of FTSG formation.
This study had some limitations. (1) The diagnosis of a ganglion is exclusively reliant on ultrasonography; however, as previously noted, the utility of ultrasonography in this context is widely recognized, which may mitigate this limitation. (2) The control group had a limited sample size, which could affect the robustness of the comparative analysis. (3) The study lacked randomization; however, there were no statistically significant differences in the background or symptoms of flexor tenosynovitis among the participants in the injection and control groups at the first ultrasound. (4) Although the puncture techniques varied, the approach for penetrating the tendon sheath remained uniform, ensuring consistency in this methodology. (5) A uniform needle size should ideally have been used; however, in practice, injections were administered using needles of varying sizes at the discretion of the operator. (6) Twenty-four patients who demonstrated FTSG formation at the time of the initial ultrasound examination were excluded from the analysis, which may have bias in the estimation of the ganglion formation rate. (7) The dropout rate was higher in the injection group. Although this is presumed to be due to marked symptom improvement, we believe that the incidence of FTSG remains higher in the injected group even when taking into account the patients who dropped out. 8) Furthermore, this study did not include precise measurement of FTSG size; therefore, we were unable to examine the relationship between the size of the FTSG and clinical outcomes. Given that the size of a FTSG may potentially influence the recurrence of tenosynovitis or affect clinical outcomes, further longitudinal studies—including evaluation of ganglion size after injection for tenosynovitis—are warranted to clarify the long-term impact of FTSG on clinical outcomes.
Conclusion
In this study, the incidence of FTSG in the injection group was higher than that in the control group among patients with stenosing flexor tenosynovitis. Our results suggest that small punctures made by intrathecal injection may be one of the causes of FTSG formation.
Appendix
Supporting material provided by the authors is posted with the online version of this article as a data supplement at jbjs.org (http://links.lww.com/JBJSOA/A877). This content was not copyedited or verified by JBJS.
Footnotes
Investigation performed at The University of Tokyo Hospital, Tokyo, Japan
Disclosure: The Disclosure of Potential Conflicts of Interest forms are provided with the online version of the article (http://links.lww.com/JBJSOA/A876).
Contributor Information
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