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
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
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
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
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.
