Recent research revealed trigger finger as a multifactorial condition with diverse etiologies and affected sites beyond the A1 pulley.
In a comprehensive review, published in Advances in Rheumatology, investigators highlighted misconceptions about the trigger finger definition, pathophysiology, lesion sites, and etiology. They conducted an extensive literature review, analyzing original articles up to 2022 found through Google searches. They accessed close-access articles via the Egyptian Knowledge Bank.
The investigators found that trigger finger can occur at multiple anatomical locations, including A2 and A3 pulleys, Camper's chiasm, palmar aponeurosis, flexor retinaculum, and extensor tendons. Pathophysiology involves tendon-pulley diameter mismatch, but histological changes may vary based on underlying causes. Conditions associated with trigger finger may include diabetes mellitus, carpal tunnel syndrome, gout, amyloidosis, hypothyroidism, rheumatoid arthritis, acromegaly, and space-occupying lesions. Further, occupational factors may contribute to but are not the sole cause of trigger finger in most cases.
Although the A1 pulley is most common anatomical site implicated in trigger finger, the condition can also occur at:
- A2 or A3 pulleys
- Camper's chiasm (flexor digitorum superficialis decussation)
- Palmar aponeurosis (31% to 47% of cases in one study)
- Flexor retinaculum at the wrist
- Dorsal extensor retinaculum
- Lateral aspects of proximal interphalangeal joint.
Ultrasonography may reveal pulley thickening, hypervascularization, and cysts. Tendon changes include loss of fibrillar pattern and margin irregularity. Histopathology shows collagen irregularities, chondroid metaplasia, and ground substance increases
Etiology:
- Diabetes mellitus: About 1.5% to 20% of patients with diabetes may develop trigger finger through tendinopathy, AGE deposition, granulation tissues, and myxomatous degeneration. Risk factors may include female sex, age > 60 years, long disease duration, insulin dependency, high HbA1c, and other complications.
- Carpal tunnel syndrome: 43% of patients with the condition also had trigger finger in one study, with a 22% recurrence risk for subsequent trigger finger.
- Gout and pseudogout: Crystal deposition in various hand structures may lead to trigger finger.
- Amyloidosis: Multiple types may be implicated in the development of trigger finger, including dialysis-related, familial, and age-associated disease.
- Hypothyroidism: 2.9% of patients with thyroid disease may develop trigger finger.
- Rheumatoid arthritis: Nodular tenosynovitis and distal profundus entrapment could lead to trigger finger.
- Acromegaly: 25% of the patients with this condition developed trigger finger in one study.
- Space-occupying lesions: Exostosis, sesamoids, tumors, and hematomas could increase the risk of the condition.
- Dupuytren's contracture: External compression or unrelated tendon constriction may be implicated in the development of trigger finger.
- Raynaud's phenomenon: There may be a potential association between Raynaud's phenomenon and trigger finger; however, the mechanisms are still unclear.
- Medications: Fluoroquinolones, glucocorticoids, aromatase inhibitors, and statins have all been potentially linked to trigger finger.
Occupational factors such as highly repetitive finger movements may contribute to the development of trigger finger, but most cases develop for reasons other than occupation alone.
The investigators emphasized the importance of thorough patient evaluation to identify underlying causes and potential risk factors. Physicians should examine all possible affected sites beyond the A1 pulley for accurate diagnosis and treatment.
This comprehensive review challenges the traditional view of trigger finger as primarily an A1 pulley pathology, highlighting the complex interplay of anatomical, systemic, and environmental factors in its development.
The authors declared that they have no competing interests.