Abstract
Trigger finger is the snapping, triggering, or locking of the finger that occurs due to thickening of the retinacular sheath most commonly at the level of the A1 pulley. Clinical presentation often includes local pain and functional limitation. When conservative care such as splinting, anti-inflammatory medications, and activity modification is not adequately effective, local corticosteroid injection is a mainstay of treatment. Surgical release of the A1 pulley is effective percutaneously or by open technique.
Definition
Trigger finger is the snapping, triggering, or locking of the finger as it is flexed and extended. Thickening and disproportionate narrowing of the retinacular sheath relative to its flexor tendons occur due to hypertrophy and fibrocartilaginous metaplasia at the tendon-pulley interface. While known as stenosing tenosynovitis, tenovaginitis is a more accurate term as the histopathologic changes localize to the retinacular sheath and peritendinous tissue rather than the tenosynovium. Normal tendon glide is most prominently affected at the A1 pulley where there is greater angulation of the tendon as it enters the pulley system. Trigger finger is thought to arise from high pressures at the proximal edge of the A1 pulley, the most common site of triggering, at the level of the metacarpal head ( Fig. 37.1 ). The thumb (33%) and the ring finger (27%) are most commonly affected in adults, but 90% of pediatric trigger fingers involve the thumbs, 25% of which are bilateral. Pediatric trigger thumb occurs more frequently as a result of focal enlargement of the flexor pollicis longus, but no definite ultrasound abnormality of the A1 pulley has been noted. Primary idiopathic trigger finger is more common while secondary trigger finger is associated with diabetes mellitus, rheumatoid arthritis, hypothyroidism, histiocytosis, amyloidosis, and gout. Incidence is generally thought to be 2% in the general population, more common in women and in patients with diabetes (7%) and rheumatoid arthritis. The relationship of trigger finger to repetitive trauma has been cited in the literature; however, the exact mechanism of this correlation is still open to debate. Rarely, it is due to acute trauma or space-occupying lesions.
Symptoms
Patients may initially note clicking or catching in the finger with some limitation in range of motion, or locking of the digit in flexion that is overcome with forceful voluntary effort or passive assistance. As the stenosis increases, complaints of pain typically develop in the proximal interphalangeal (PIP) joint of the finger, rather than in the true anatomic location of the problem—about the metacarpophalangeal (MCP) joint. Some individuals may report swelling or stiffness in the fingers, particularly in the morning. Involvement of multiple fingers can be seen in patients with rheumatoid arthritis or diabetes. In one study, patients complained of pain with motion with trigger thumb whereas with trigger finger, they complained primarily of triggering and loss of range of motion.
Physical Examination
The essential element in the physical examination is the localization of the disorder at the level of the MCP joint. There is palpable tenderness and sometimes a tender nodule or crepitus over the volar aspect of the metacarpal head. Swelling of the finger may also be noted. Opening and closing of the hand actively produces a painful clicking as the inflamed tendon passes through a constricted sheath. With chronic triggering, the patient may have interphalangeal joint flexion contractures. In the absence of comorbidities such as carpal tunnel syndrome or diabetic neuropathy, neurologic examination should be normal except in severe cases associated with disuse weakness or atrophy.
Trigger finger has been graded as mild crepitus in a non-triggering digit (type 0), uneven movement in a non-triggering digit (type I), actively correctable triggering (type II), passively correctable triggering (type III), and fixed deformity (type IV).
Functional Limitations
Functional limitations include difficulty with grasping and fine manipulation of objects due to pain, locking, or both. Fine motor problems may include difficulty with inserting a key into a lock, typing, or buttoning a shirt. Gross motor skills may include limitation in gripping a steering wheel or in grasping tools at home or at work. Joint contracture at the MCP joint as well as the proximal and distal interphalangeal joints are noted in the triggering digit. Patients note lower perceived quality of life and activity level, with reduced hand strength and dexterity.
Diagnostic Studies
This is a clinical diagnosis. Patients without a history of injury or inflammatory arthritis do not need routine radiographs. Magnetic resonance imaging can confirm tenosynovitis of the flexor sheath, but this offers minimal advantage over clinical diagnosis. Alternatively, a diagnostic ultrasound examination can show tendon nodules, tenosynovitis, and active triggering at the level of the A1 pulley.
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Dupuytren disease
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Ganglion of the tendon sheath (retinacular cyst)
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Tumor of the tendon sheath (giant cell tumor or space-occupying lesion, such as an amyloidosis)
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Rheumatoid arthritis or other diagnoses associated with secondary trigger finger
Treatment
Initial
The goal of treatment is to restore the normal gliding of the tendon through the pulley system. This can often be achieved with conservative treatment. Initial noninvasive care includes activity modification, adaptive equipment, anti-inflammatories and splinting. When clinically appropriate, nonsteroidal anti-inflammatory drugs can be administered orally or transdermally. Progression to a local steroid injection is often based on the severity of the patient’s symptoms (more severe symptoms generally respond better to injections), required or target activity level (e.g., someone who needs to return to work as quickly as possible), and the preference of the patient and clinician.
Many types of splints are advocated including MCP joint at 0 degrees or at 10 to 15 degrees of flexion with the PIP and distal interphalangeal joints free, for up to 6 weeks continuously. Alternatively, the DIP may be immobilized with MCP, PIP, or DIP splinting providing lasting clinical success in up to 87% of patients, although less so in the thumbs. Splinting can decrease loss of time from work. A novel splint with NSAID microneedle delivery has been developed. Padded gloves provides protection and can decrease inflammation by avoiding direct trauma.
Rehabilitation
Rehabilitation may include treatment with an occupational or physical therapist experienced in the treatment of hand problems. Supervised therapy may be useful in the following scenarios: when a patient has lost significant strength, range of motion, or function from not using the hand or from prolonged splinting; when modalities such as ultrasound and iontophoresis are recommended to reduce inflammation; and when a customized splint is deemed to be necessary. Therapy should focus on increasing function and decreasing inflammation and pain. This can be done by techniques such as ice massage, contrast baths, paraffin, ultrasound, and iontophoresis with local steroid use. A custom splint may fit better and permit better function at work than a prefabricated splint. Range of motion, strength, and function can be improved through supervised therapy before surgery and postoperatively.
Procedures
When symptoms persist or are more functionally limiting, a local corticosteroid injection combined with local anesthetic ( Fig. 37.2 ) is indicated. Post-procedure care frequently includes splinting and relative protection for 1 week. Single injection to the A1 pulley has demonstrated symptom resolution in 54% to 73% of patients at 1 year along with decrease in pulley thickness and tendon thickness. Repeat injection is safe and effective with incremental benefit, though longer duration symptoms required greater number of injections. Corticosteroid injection is less effective with involvement of multiple digits or when the condition has persisted longer than 4 months. Diminishing response to injection is suggested to be due to the inability of corticosteroids to reverse the established fibrocartilaginous metaplasia.
