I would like to thank Dr. Avrum Froimson for his superb and comprehensive chapter “Tenosynovitis” that appeared in several previous editions of this book and constituted the framework from which this chapter was written.
Tendinopathy is a term used to encompass painful conditions affecting the tendons of the wrist and hand and is perhaps the most common reason for a visit to a hand surgeon. Tendinopathy includes conditions such as tendon entrapment and stenosis (e.g., trigger finger, de Quervain disease), as well as inflammatory conditions ( tenosynovitis ). Strictly defined, tenosynovitis refers to inflammation of the synovial lining of a tendon sheath and is abundantly demonstrated by the diffuse, invasive synovitis associated with rheumatoid arthritis (RA) or other inflammatory arthropathies. Such proliferative tenosynovitis is relatively uncommon, is erosive, is not restricted to the retinacular thickenings of the tendon sheath, and may lead to tendon rupture. Other causes of inflammatory or proliferative tenosynovitis include deposition diseases such as amyloidosis, crystalline tendinopathy (e.g., calcific tenosynovitis or gout), and septic tenosynovitis, including bacterial, mycobacterial, and viral agents.
A far more common condition than proliferative tenosynovitis is tendon entrapment or stenosing tendovaginitis , caused by narrowing or stenosis of a tendon’s retinacular sheath. The two most common conditions are trigger finger and de Quervain disease. Because there is a paucity of inflammatory tissue associated with tendon entrapment, the term tenosynovitis , when used to describe these conditions, is misleading and inaccurate from an etiologic perspective. Tendon entrapment occurs about the narrow fibroosseous canals that provide fulcrums for acute angulation of the digital and wrist tendons. Repeated motion of a tendon through such a narrow passageway can cause hypertrophy and fibrosis of the retinacular sheath that results in an impediment to gliding, edema, and, ultimately, catching or locking of the tendon on either side of the sheath. Rarely, these conditions may be initiated by direct trauma. Tendon entrapment is initially characterized by local pain, swelling, and crepitus. Over time, the affected retinacular sheath responds by thickening (up to three times its normal diameter) and undergoes fibrocartilaginous metaplasia. Pathologic examination rarely demonstrates hypertrophied synovium but rather thickening, nodularity, and attritional changes within the tendon, accompanied by gross thickening of the overlying sheath. These conditions as a group respond well in the early phase to conservative measures such as ice, splinting, and rest. Recalcitrant cases respond well to one or more corticosteroid injections. Surgical release of the retinacular sheath is definitive treatment because recurrence is rare.
It has been estimated that tenosynovitis of the hand and wrist will develop in 64 to 95% of patients with RA. The process may begin within the synovial lining of the tendon sheath, or it may invade the tendon from involvement of a contiguous joint. Rheumatoid tenosynovitis produces relatively painless bulky swelling along the entire extent of the synovial sheath and is most noticeable at the retinacular boundaries. Because of the thin, expansile dorsal skin of the hand, the disease may be quite prominent dorsally and produce noticeable swelling from the distal retinaculum to the metacarpal bases. The process can easily be differentiated from common wrist tumors such as ganglia or lipomas by the mobility of the mass with the extensor tendons and the tendency of the mass to bunch (the characteristic tuck sign ) at the retinacular edge with active digital extension. Tenosynovitis of RA is most common on the ulnar border of the wrist over the distal radioulnar joint and most frequently involves the fourth, fifth, and sixth dorsal compartments.
On the flexor surface, the earliest signs of considerable flexor tenosynovitis may be painful paresthesias caused by median nerve entrapment beneath the unyielding transverse carpal ligament. With time, palmar nodularity along the flexor tendons, crepitus, and frank triggering will develop in more than a third of patients with RA. Fusiform swelling of one or more digital flexor sheaths may cause a substantial impediment to flexion, pain, and stiffness mimicking rheumatoid arthropathy of the interphalangeal (IP) joints. Rarely, a finger may trigger in RA from entrapment of the profundus tendon by synovitis at the superficialis decussation (Camper chiasm). Helal described the cardinal sign of this syndrome as an inability to flex the distal interphalangeal (DIP) joint when the proximal interphalangeal (PIP) joint was held passively by the examiner in full flexion.
For a more detailed discussion of rheumatoid tenosynovitis and the medical and surgical treatment options, the reader is referred to Chapter 55 .
Precipitation of crystalline material within the confines of an enclosed space (joint or tenosynovial space) incites an acute, fulminant inflammatory reaction marked by intense swelling, erythema, and pain. Gout is a disorder of urate metabolism in which the overproduction of uric acid causes hyperuricemia and hyperuricosuria.
Gout affects over 6 million individuals in the United States and the incidence is reported to be rising. The low solubility of monosodium urate is responsible for its crystallization and deposition in peripheral sites, including subcutaneous, intraarticular, and tenosynovial locations. Attempted phagocytosis by peripheral leukocytes releases lysosomal enzymes that produce an intense inflammatory synovitis. If left unchecked, the disease results in the formation of gouty tophi , which are large, lobulated subcutaneous deposits of monosodium urate crystals commonly seen in the pinna of the ear and the great toe. Deposition in the hand occurs relatively late in the disease and is uncommon with good medical management. Radiographic manifestations of gouty arthritis may precede symptoms in up to 25% of patients and precedes deposition of gouty tophi in up to 42%. Gouty arthritis is manifested by acute and rapidly escalating joint pain over the first 24 hours, followed by spontaneous resolution over the next week to 10 days. Medical control of the disease is the mainstay of treatment. Gouty tenosynovitis in the hand can be present without visible tophi or previous involvement of the upper extremity. Often called “the great imitator,” gout may masquerade as septic arthritis, RA, or neoplasm, and the diagnosis is often delayed by weeks or months. Initial signs of flexor tendon involvement include marked pain, erythema, acute swelling, and warmth suggestive of acute suppurative tenosynovitis. Gouty flexor tenosynovitis within the carpal tunnel can compromise the median nerve and result in acute carpal tunnel syndrome. In unsuspected cases, an intense exudative inflammatory reaction can occur after carpal tunnel release that mimics infection but responds well to antiinflammatory medications and uricosuric agents. Gout can rarely coexist with RA, but it is perhaps more frequently misdiagnosed as RA because of its proliferative synovitis and because 10% to 20% of patients with RA have elevated uric acid levels.
Because hyperuricemia can be found in 5 to 7% of adult men, a diagnosis of gout should not be based on laboratory values alone. The combination of joint or tenosynovial aspiration, gram-stained smear results, and examination under polarized light is 85% sensitive for the diagnosis of gout and may be helpful in differentiating acute gouty tenosynovitis from RA or infection. Suspected pathologic material must be transported to the laboratory in ethanol rather than formalin to prevent degradation of the monosodium urate crystals. Compensated polarized light microscopy will demonstrate negatively birefringent (urate) crystals within the granuloma and histologic features otherwise typical of RA.
Other sites of gouty tenosynovial involvement in the hand include the extensor tendons at the dorsal retinaculum, a localized painful mass in the midpalm, and tophi over the dorsal aspect of the IP or metacarpophalangeal (MP) joints. Neglected cases can proceed to intratendinous infiltration, flexion contractures, tendon rupture, and skin ulceration in extreme cases. Acute attacks are generally well handled by the administration of colchicine and antiinflammatory agents. Prophylactic perioperative treatment is recommended to reduce the chance of a postoperative flare-up.
Indications for operative management include synovectomy for restoration of mobility, tendon transfers for tendon rupture, decompression for median nerve compression, and removal of painful or disfiguring tophi to prevent skin breakdown and infection ( Figure 56.1 ). When excising gouty tophi, care should be taken not to devascularize involved or compromised skin. Skin grafts are rarely necessary for coverage. Curettage is useful for bony involvement, and extensive stripping of periosteum is avoided. No attempt should be made to completely eradicate a tophus if excision would damage vital neurovascular structures or impair function. Bulky compression dressings are recommended to reduce dead space. Recurrence is rare after subtotal excision of gouty tophi and ample medical management.
An acute, intensely painful synovitis can accompany the release of calcium salts into the intrasynovial space in joints or tenosynovial sheaths and can resemble an infectious process. The disease is not unlike the deposition of calcium about major joints in the body, as exemplified by calcific bursitis of the hip, knee, shoulder, and elbow. Hypercalcemia is neither necessary nor sufficient to produce ectopic calcifications, and elevated laboratory values and systemic signs are characteristically lacking.
The cause of calcific tendinitis of the hand and wrist is unknown. Neither trauma nor repetitive use can be implicated, and the disorder occurs more commonly in men (40 to 60 years of age) than women (5 : 1) and rarely in children. The most common site is the flexor carpi ulnaris (FCU), although any of the flexors or extensors of the wrist may be afflicted. Histologic studies of crystalline material collected at surgery may demonstrate hydroxyapatite, which may induce the acute inflammatory reaction. As in other types of inflammatory synovitis, carpal tunnel syndrome has been reported to result from acute calcific tenosynovitis about the flexor tendons.
The patient may present for treatment of a “septic” tendon or joint but demonstrates a striking lack of systemic findings. The patient seldom has a history of penetrating trauma or previous infection. Although erythema is present, the pattern differs from that seen in cellulitis in that it seldom streaks proximally. The area of acute inflammation is typically more confined and localized. Radiographs should be carefully scrutinized for “fluffy” calcification in the area of symptoms or small soft tissue calcium deposits ( Figure 56.2, A and B ). Patients may recall similar events in the past. The diagnosis is frequently delayed, presumably because of confusion with infection.
Treatment with oral nonsteroidal antiinflammatory agents for 5 to 7 days is usually successful. Symptoms often subside within 24 hours. For patients who may not take these agents, a prepackaged tapered methylprednisolone oral dose pack (Medrol Dosepak) can be used. Splinting the afflicted joint may also lessen the pain. Although direct aspiration and injection of corticosteroids with lidocaine can be performed, this is seldom needed. Follow-up radiographs will generally show complete disappearance of small deposits in 2 to 4 weeks. Resistant or chronic cases with large calcific deposits may require surgical excision, but this is an exception. Incision of the affected tendon will allow extrusion of the material, which resembles “toothpaste.”
Other Crystalline Tendinopathies
Rarely, calcium pyrophosphate dihydrate (CPPD, or pseudogout) can precipitate within the carpal tunnel and cause an acute fulminant inflammatory tenosynovitis with resultant carpal tunnel syndrome. Radiographs may reveal fluffy soft tissue calcifications within the carpal tunnel and often show calcifications within the triangular fibrocartilage complex (TFCC). Pathologic examination reveals rhomboid-shaped crystals with faintly positive birefringence under polarized light.
Deposition of hydroxyapatite has also been reported to cause an acute carpal tunnel syndrome that is recalcitrant to antiinflammatory agents and rest. Both conditions are best treated by early decompression and excision of the crystalline material.
Amyloidosis is a condition resulting from the deposition of a low-molecular-weight serum protein, β 2 -microglobulin, in the bones and soft tissues. Excess protein accumulation can result from a rare primary enzymatic defect (Meretoja syndrome) but more commonly occurs in patients with renal failure who are undergoing peritoneal dialysis or hemodialysis. The protein is not filtered by standard dialysis membranes, and the severity of the disease is proportional to the age at initiation of hemodialysis and the duration of treatment.
Hand involvement in amyloidosis is usually characterized by cystic lesions in the carpal bones and destructive arthropathy involving the wrist and IP joints. Thick, plaquelike accumulations along the flexor tendons can cause trigger fingers, carpal tunnel syndrome, flexion contractures, and tendon rupture, usually without signs of inflammation. In a patient undergoing renal dialysis, paresthesias in the median nerve distribution and diminished active motion are strongly suggestive of amyloid deposition within the carpal canal. Surgical decompression along with débridement and complete removal of amyloid “tenosynovium” is effective in relieving symptoms, which usually do not recur ( Figure 56.3 ). Trigger fingers should be approached through standard incisions in the midpalm, and complete tenosynovectomy and division of the A1 pulley should be performed. Digital tenosynovitis may be excised through Bruner incisions, with retention of all other annular pulleys.
Alkaptonuria is an extremely rare autosomal recessive defect of tryptophan metabolism caused by a deficiency in the enzyme homogentisic acid oxidase. As a result, unmetabolized homogentisic acid is excreted in urine and deposited in the joints and soft tissues (ochronosis). The protein deposits have a characteristic dark pigmentation that causes darkened urine and deep staining of collagenous tissue. Joint deposition or accumulation in the intervertebral disk can lead to severe destructive arthropathy. The protein may be deposited within tendons and has been demonstrated to cause stenosing tenosynovitis. Seradge reported a case involving multiple digits of both hands that was unresponsive to corticosteroid injection. Surgical release of the A1 pulley was successful at eliminating the symptoms.
Acute suppurative flexor tenosynovitis is covered in Chapter 3 .
Certain indolent infections can be manifested as subacute tenosynovitis and must be included in the differential diagnosis. Such infections include tuberculosis, atypical Mycobacterium infection, gonococcal tenosynovitis, and fungal infections. These chronic infections are discussed in detail in Chapter 3 .
On occasion, sarcoidosis can be manifested as digital flexor tenosynovitis and must be included in the differential diagnosis of isolated, inflammatory tenosynovitis. Sarcoidosis is a systemic, immune-mediated granulomatous disease that primarily affects the lungs, spleen, and lymph nodes but may be manifested as bone, joint, or tenosynovial involvement in approximately 25% of patients. Radiographs of affected hands typically reveal well-defined cystic granulomatous lesions in the phalanges. The causative agent that triggers sarcoidosis has not been identified. Its progression is variable, with spontaneous regression in some but progression to a chronic fibrotic state in others. The disease is more common in women than men and affects blacks 10 times more frequently than whites in the United States. Sarcoidosis may precipitate secondary gout because of an overproduction of purines in the proliferative granulomas. Treatment includes surgical tenosynovectomy and systemic corticosteroids. Histopathologic examination of the excised material demonstrates noncaseating granulomas, as well as epithelioid and multinucleated giant cells.
Tendon entrapment (formerly known as stenosing tenosynovitis ) refers to mechanical impingement of a tendon in the hand or wrist caused by narrowing of its retinacular sheath. Unfortunately, tenosynovitis is generally very broadly defined and has been used to describe a heterogeneous collection of vague aching conditions of the upper extremity. Tendovaginitis (Latin for “tendon sheath” and Greek for “inflammation”) may be a more precise term than tenosynovitis to describe the thickened retinacular sheath that characterizes these conditions. In 1952, Burman tried to clarify the definition as follows: “Tendovaginitis is not tenosynovitis. Before there is stenosing tendovaginitis, there must be nonstenosing tendovaginitis. It takes time to make a sheath stenotic. The latter is reversible, the former is not.” As the term tendovaginitis is considered archaic, this group of conditions is best simply described as tendon entrapment .
The most common types of tendon entrapments are de Quervain disease and trigger digits, although the process has been reported to affect each of the tendons of the hand and wrist. Inflammation has been cited as the common denominator of a number of affectations of the upper extremity, including de Quervain disease, trigger digits, and carpal tunnel syndrome. In patients without a known history of inflammatory disease, several studies have failed to detect acute or chronic inflammatory cells in tenosynovial biopsy samples taken from patients undergoing carpal tunnel release. Similarly, in Fahey and Bollinger’s pathologic analysis of synovium from adults and children who underwent trigger release, synovial proliferation was uncommon (one case), and pathologic findings of degeneration, vascular proliferation, and cartilage formation were limited to the retinacular sheath. Similar histologic analysis of tissue removed during tenolysis for de Quervain disease or stenosis of the flexor carpi radialis (FCR) tendon documented perisynovial fibrous tissue and endothelial proliferation with a paucity of inflammatory tissue. The lack of pronounced inflammatory findings within the tenosynovium and the demonstration of fibrotic thickening in the retinacular ligament prompted Garsten in 1951 to coin the term peritendinitis stenosans and to suggest that the conditions may be related more to intrinsic anatomic and degenerative changes than to occupational factors.
Although the cause of tendon entrapment is disputed, certain epidemiologic factors are apparent. These conditions tend to cluster in certain patients, with coexistence of carpal tunnel syndrome, trigger digits, de Quervain disease, epicondylitis, and subacromial bursitis implicating a more systemic yet undefined predisposition. A recent study demonstrated a three-fold incidence of carpal tunnel syndrome in patients with multiple trigger digits. Each condition is far more common in women than men, and the peak incidence of trigger digits averaged 55 to 60 years of age in several series. The age distribution of trigger digits has not changed appreciably in more recent series despite an increase in the use of computer keyboards, personal digital assistants, and other “repetitive” tools and tasks in younger individuals. Bunnell proposed anatomic factors to explain the pronounced difference in prevalence among men and women. Degenerative factors may have an etiologic role in the development of flexor tendon entrapment of the digits, as evidenced by the increased incidence of these disorders in the dominant hand. Several studies point to a relationship between activities that require exertion of pressure in the palm while performing forceful grip or repetitive digital flexion, such as arc welding, use of heavy shears, or constant handheld tool work. Forceful use is unlikely to be the sole etiologic factor, however, as evidenced by the strikingly low incidence in males and athletes and an age distribution that peaks in the sixth decade. Trezies and colleagues demonstrated no significant difference between the occupational distribution of patients with trigger digits and that of the general population. A recent systematic review of 179 studies could find no causal link between de Quervain disease and occupational risk factors. Other anatomic and intrinsic factors undoubtedly contribute to a predisposition for the development of tendon entrapment in the hand and wrist.
Tendon entrapment of the fingers and thumb is one of the most common causes of hand pain and disability. The condition causes painful catching or popping of the involved flexor tendon as the patient flexes and extends the digits. On occasion, the digit will lock in flexion and require passive manipulation of the digit into extension. Rarely, a digit may be locked in extension. Over time, guarding and reluctance on the part of patients to fully range the digit can lead to secondary flexion contractures at the PIP joint.
Twenty-two extrinsic tendons cross the wrist and provide a unique combination of power and dexterity in the hand. Each tendon passes through a series of tight fibroosseous canals designed to optimize the balance between motion and production of force by maintaining the tendon in close apposition to the joint or joints that it controls. Division, attenuation, or rupture of a critical retinacular ligament, or pulley , will allow the tendon to drift away from the joint’s center of rotation and consequently increase its moment arm for production of force and lead to tendon imbalance and flexion contracture. Pulley disruption also effectively lengthens the tendon and limits its excursion.
The phenomenon of trigger finger is due to mechanical impingement of the digital flexor tendons as they pass through a narrowed retinacular pulley at the level of the metacarpal head. Proximal phalangeal flexion, particularly with power grip, causes high angular loads at the distal edge of the first annular (A1) pulley. Hueston and Wilson suggested that “bunching” of the interwoven tendon fibers occurs, akin to the effect of pulling a multifilament strand through the eye of a needle ; this may be responsible for the reactive intratendinous swelling sometimes noted at surgery. The most remarkable pathologic changes are seen in the pulley itself, which demonstrates gross hypertrophy, described by Bunnell as a “whitish, cicatricial collar-like thickening.” Microscopic examination demonstrates degeneration, cyst formation, fiber splitting, and lymphocytic or plasma cell infiltration. Ultrastructural studies comparing normal and trigger A1 pulleys have demonstrated the presence of chondrocytes in the normal innermost, or friction , layer of normal A1 pulleys and chondrocyte proliferation and the presence of type III collagen in pathologic pulleys. It is thought that the A1 pulley and the corresponding surface of the flexor tendon undergo fibrocartilaginous metaplasia under the influence of repetitive, compressive loads. A recent study by Miyamoto and colleagues in which a specialized ultrasonographic compression technique was used documented increases in both stiffness and thickness of the A1 pulley in patients with symptomatic triggering; notably, corticosteroid injection reversed these changes within 3 weeks of injection.
The most common form of trigger finger is the primary type, which is found predominantly in otherwise healthy middle-aged women with a frequency of two to six times that seen in men. Involvement of several fingers is not unusual; in patients with multiple trigger digits, the most commonly affected digit is the thumb, followed by the ring, long, little, and index fingers. Secondary trigger finger can be seen in patients with diabetes, gout, renal disease, RA, and other rheumatic diseases and is associated with a worse prognosis after conservative or surgical management. The lifetime incidence of trigger digits has been reported to be 2.2% in nondiabetic adults older than 30 years and up to 10% in patients with insulin-dependent diabetes mellitus.
Although the flexor tendon sheath is constricted at the MP joint, the patient or examining physician often localizes the phenomenon incorrectly to the PIP joint. A locked trigger digit can lead to an incorrect diagnosis of dislocation, Dupuytren disease, and even focal dystonia or hysteria. A locked trigger digit can be confused with so-called true locking of the MP joint (see Chapter 8 ). Except for rare instances of locking caused by a tumor of the tendon or sheath, a loose body in the MP joint, anomalies of the sesamoids, or entrapment of an intrinsic tendon on an irregularity of the metacarpal head, the diagnosis should be straightforward and can be confirmed with a simple lidocaine injection into the flexor sheath to unlock the digit. On occasion, de Quervain disease and tendon entrapment of the extensor pollicis longus (EPL) have been demonstrated to cause triggering of the thumb and may lead to an error in diagnosis. Rarely, localized enlargement of the flexor digitorum profundus can trigger at a stenotic A3 pulley and lead to persistence of symptoms after routine surgical incision of the A1 pulley. Up to a quarter of trigger digits in patients with RA may be due to profundus entrapment by synovitis at the superficialis decussation.
Attempts have been made to classify triggering, but in one such report by Newport and colleagues, no correlation was found between their grading scheme and outcome after injection therapy. I believe that some type of simple classification is useful if for no other purpose than to provide the clinician with a way to record notes in the patient’s chart for retrospective review. Several authors have used a scheme such as the following, originally proposed by Quinnell and modified by David Green (Green DP, personal communication, 1997):
Grade 1 (pretriggering)—Pain; history of catching, but not demonstrable on physical examination; tenderness over the A1 pulley
Grade II (active)—Demonstrable catching, but the patient can actively extend the digit
Grade III (passive)—Demonstrable catching requiring passive extension (grade IIIA) or inability to actively flex (grade IIIB)
Grade IV (contracture)—Demonstrable catching with a fixed flexion contracture of the PIP joint
Most primary trigger digits in adults can be successfully treated nonsurgically with corticosteroid injection or splinting. Early series recommended surgical treatment as straightforward and highly effective and regarded prolonged conservative treatment as “unreliable and expensive.” Subsequent follow-up series documented poor results in 7 to 9% of patients after surgical treatment, with complications including reflex sympathetic dystrophy, infection, persistent triggering, stiffness, and nerve injury. More recent reports continue to document infrequent but serious complications, including nerve transection, infection, incisional pain, flexion deformity, pulley rupture, flexor tendon bowstringing, and recurrence. The small but finite risk for complications from open trigger release warrants an initial attempt at splinting or corticosteroid injection, or both.
The popularity of corticosteroid injection has waxed and waned over the years. In primary trigger finger and thumb, corticosteroid injection has a highly satisfactory rate of success, particularly in nondiabetic patients with involvement of a single digit, a discrete palpable nodule, and a short duration of symptoms ( Table 56.1 ). Although several authors have demonstrated that improvement after injection is less likely in diabetic patients than in nondiabetic patients, the treatment is not ineffective in diabetic patients, and it is associated with a low complication rate. Rarely, tendon ruptures have been reported after corticosteroid injection, and the cause is difficult to discern. In one case, the flexor pollicis longus (FPL) ruptured in a 62-year-old patient who was opening a file drawer 4 years after two corticosteroid injections for trigger thumb. In a second case, both the superficialis and profundus tendons ruptured in a 77-year-old patient approximately a year after two steroid injections with triamcinolone acetonide (40 mg/mL). In a recently reported case, Gyuricza and colleagues described rupture of multiple flexor tendon pulleys and severe bowstringing after a series of corticosteroid injections for trigger finger. Even though a causative link between a particular corticosteroid preparation and tendon or pulley rupture cannot be made, all authors recommend that intratendinous injection be avoided given the known attritional effects of corticosteroids on collagen. No other serious complications of this technique have been reported. A transient rise in blood and urine glucose levels is common in diabetics, and these patients should be advised that this is likely to occur. Because of the theoretical chance of inhibition of wound healing, it is prudent to wait at least 6 weeks after corticosteroid injection before consideration of open surgical release.
|Author||Year||Cortisone Preparation||Findings||Number of Digits||Notes|
|Kolind-Sorensen||1970||Hydrocortisone||67% success overall; 78% for “primary” trigger digits||106||Only 50% success rate with trigger digits secondary to rheumatoid arthritis, diabetes|
|Lapidus and Guidotti||1972||Methylprednisolone||“Uniformly good results”||41||Follow-up unspecified|
|Rhoades et al||1984||Methylprednisolone||72% resolution overall; 93% resolution if <4 months||53||Favorable prognosis: single digit, short duration|
|Freiberg et al||1989||Triamcinolone acetonide||79% resolution overall: 93% for “nodular,” 48% for “diffuse”||101||Improved prognosis: nodular vs. diffuse type, shorter duration of symptoms|
|Marks and Gunther||1989||Triamcinolone acetonide||Single injection: 84% |
Two injections: 91%
|108||Average 44-month follow-up; better outcomes in female patients|
|Newport et al||1990||Betamethasone sodium phosphate||One to three injections: 77%||338||Favorable prognosis: single digit, <6 months’ duration; trigger grade had no effect on outcome|
|Griggs et al||1995||Betamethasone sodium phosphate||50% success in diabetics: 72% for NIDDM, 44% for IDDM||121||Incidence of multiple trigger digits and failure of injection statistically increased in IDDM population|
|Murphy et al||1995||Betamethasone sodium phosphate||64% resolution in steroid group, 20% placebo response||24||Sheath distention alone unsuccessful|
|Stahl et al||1997||Methylprednisolone||Diabetics: 49%||60||Diabetics: higher incidence of diffuse type, multiple digits; 7% complication rate in diabetics|
|Ring et al||2008||Triamcinolone vs. dexamethasone||6 weeks: 63%, 3 months 66% |
6 weeks: 38%, 3 months: 71%
|Significant improved satisfaction in triamcinolone group at 6 weeks, not sustained at 3 months.|
In a novel evidence-based study of cost-effectiveness, Kerrigan and Stanwix investigated five strategies of treatment ranging from one or two corticosteroid injections, followed by surgical release, to immediate open or percutaneous release. They concluded that the strategy of two corticosteroid injections followed by surgery in nonresponders was the least costly algorithm and was 250 to 340% less expensive than immediate surgical release.
Technique of Corticosteroid Injection.
There are many different techniques for injection of trigger fingers, but the following is my preferred method. A 3-mL syringe is loaded with 0.9 mL of plain lidocaine (no epinephrine) and 0.1 mL of sodium bicarbonate. Sodium bicarbonate, in a 1 : 10 mixture, neutralizes the acidity of lidocaine and effectively reduces the pain of injection. (Bupivacaine [Marcaine] should not be used when mixing with bicarbonate because precipitation may occur.) One milliliter of soluble corticosteroid solution is added to the mixture; I prefer betamethasone sodium phosphate or acetate, but other preparations such as dexamethasone or triamcinolone hexacetonide are equally satisfactory. A short 25- or 27-gauge needle is applied to the syringe. The hand is prepared with a povidone-iodine or alcohol solution and the digits slightly hyperextended. The metacarpal head is palpated, and the skin sprayed with ethyl chloride solution for a few seconds as a local refrigerant/anesthetic. The needle is introduced through the frosted skin and directly into the flexor tendon over the metacarpal head ( Figure 56.4 ). Needle placement can be confirmed if necessary by disengaging the syringe from the needle and asking the patient to bend the digit gently; however, injection studies have demonstrated similar outcomes in patients with extrasynovial injection of corticosteroid. Light pressure is applied to the plunger while simultaneously withdrawing the needle slowly. When the needle tip emerges from the tendon substance, dramatic relief of resistance is felt, and a fluid wave may be palpated throughout the tendon sheath proximal and distal to the injection site. Generally, no more than 1 to 2 mL of the solution can be injected. The needle is withdrawn and slight digital pressure applied. As an alternative to midline injection, Carlson and Curtis prefer a midaxial injection site at the level of the midproximal phalanx.
For those who decline injection, some consideration should be given to splinting the involved digit. To test the efficacy of simple splinting for trigger digits, Patel and Bassini compared the outcomes of splinting the MP joint in 15 degrees of flexion with a single injection of betamethasone. At a 1-year follow-up, 66% of all digits splinted were symptom free versus 84% of the injected digits. The authors concluded that splinting is an efficacious alternative for patients who are reluctant to consider corticosteroid injection. Rodgers and associates demonstrated 55% resolution of early trigger digits in 31 workers after splinting the DIP joint in full extension for 6 weeks. They proposed that limitation of profundus gliding, decreased differential gliding of the flexor tendons within the sheath, decreased overall use of the digit, or a combination of these factors were responsible for resolution of the symptoms in this manual laborer population.
The flexor digitorum profundus and superficialis tendons enter a narrow fibroosseous tunnel formed by a groove in the palmar surface of the metacarpal neck and the annular ligament. Doyle and Blythe demonstrated that the flexor sheath in the finger is a double-walled, hollow, synovial-lined, connective tissue tube that encloses the flexor tendons. These authors identified four annular and three cruciform pulleys ( Figure 56.5 ). The annular pulleys are thick and rigid. The second pulley (A2), attached to the proximal phalanx, and the fourth pulley (A4) are the most important functionally. It has been shown experimentally that section of only the first annular pulley (A1), as done for surgical release of trigger finger or thumb, produces no loss of flexor function. However, division of both the A1 and A2 pulleys causes substantial postoperative bowstringing and limitation of full active flexion to the distal palmar crease.
The FPL passes through a narrow tunnel formed by the grooved palmar surface of the first metacarpal neck and the transverse fibers of the annular ligament of the flexor sheath ( Figure 56.6 ). The thumb is enclosed in a similar double-layered synovial sheath, and its pulley system consists of one oblique and two annular pulleys. The first annular pulley is 7 to 9 mm wide and located palmar to the MP joint. Embedded on either side of the capsule of the MP joint is a sesamoid bone into which a tendon of one head of the flexor pollicis brevis inserts. This locale is the narrowest point in the FPL sheath and the point at which the constriction develops. Overlying the proximal phalanx is a second pulley that has variably been described as oblique or transverse but is critically important to prevent bowstringing of the FPL. The pulley is 9 to 11 mm wide and is continuous with a slip of the tendon of insertion of the adductor pollicis and courses in an ulnar-proximal to radial-distal direction. The oblique pulley must be preserved during trigger thumb release. Bayat and colleagues have called our attention to considerable variability of the thumb pulley system, with three distinct types of “Av” pulleys located between the oblique and first annular pulleys. The exact significance of the Av pulley and consequences of sectioning have not been elucidated; consequently, it is recommended that these fibers are left intact. The second annular pulley overlies the volar plate of the IP joint, just proximal to the insertion of the FPL on the distal phalanx.
Topographic Anatomy and Skin Incisions.
The proximal edge of the first annular pulley roughly coincides with the distal palmar crease in the fourth and fifth rays and the proximal palmar crease in the index finger and is halfway between the two creases in the middle finger ( Figure 56.7 ). An anatomic study of 256 cadaveric digits demonstrated that the palmar-digital skin crease lies midway between the proximal edge of the A1 pulley and the PIP flexion crease, thus allowing the examiner to precisely identify the A1 pulley’s leading edge. This study has practical surgical implications; with surprising accuracy, the surgeon can topographically identify the leading edge of the A1 pulley by first measuring the distance between the PIP flexion crease and the palmar-digital crease and then measuring the same distance proximally from the palmar-digital crease. The proximal edge of the FPL sheath annulus is directly deep to the MP flexion crease of the thumb and lies directly over the volar plate.
Short transverse incisions placed adjacent to the proximal or distal palmar crease—or for the middle finger, halfway between the two creases—thus provide excellent exposure of the A1 pulley to be divided. This site also positions the healed incision away from the underlying bony prominence of the metacarpal head, thereby lessening direct pressure on the scar in grasping spherical or cylindrical objects. Longitudinal incisions are favored by several authors because this extensile approach allows rapid and safe visualization of a longer segment of the flexor tendon and the leading edge of the A2 pulley. It is important to avoid crossing the palmar or digital creases with a longitudinal incision to prevent a painful scar contracture. In either approach, the location of the digital nerves and arteries that closely parallel each flexor sheath in the fingers must be understood and the bundles protected. In particular, the radial digital nerve of the thumb is vulnerable because it lies quite close to the deep layer of dermis at the flexion crease and will be lacerated if the initial incision is carried too deeply. The same nerve can also be injured by blind scissors dissection more proximally where it crosses the thumb flexor sheath diagonally ( Figure 56.8 ).
Operative Technique of Open Trigger Digit Release.
A padded pneumatic forearm tourniquet is applied to the awake patient, and 3 to 5 mL of 1% lidocaine (neutralized with sodium bicarbonate in a 10 : 1 lidocaine : bicarbonate solution) anesthetic is used to infiltrate the skin overlying the A1 pulley. It is not generally necessary to fill the flexor tendon sheath with anesthetic. The distance between the palmar-digital crease and the PIP crease is measured, and the leading edge of the A1 pulley is identified by the technique of Wilhelmi and associates, as described above. A 1- to 1.5-cm transverse, oblique, or longitudinal incision is made directly over the involved A1 pulley as dictated by local skin creases. In the thumb, the flexor pollicis tendon is approached through a 1.5-cm transverse incision in the MP flexion crease. Immediately after the skin has been incised, blunt dissection is used to spread the subcutaneous tissues and the palmar fascia to expose the flexor sheath. The digital nerves and vessels are retracted with small right-angled retractors and are not subjected to extensive dissection. The proximal edge of the thickened flexor sheath (proximal side of the A1 pulley) is identified, and a scalpel blade is used to divide the entire A1 pulley under direct vision ( Figure 56.9 ). Anatomic studies have demonstrated apparent continuity between the first and second annular pulleys in up to 40 to 60% of digits. Care is taken to avoid division of the A2 pulley and consequent bowstringing, although it has been demonstrated that up to 25% of either end of the A2 pulley can be divided without any detrimental mechanical effect on digital flexion. In the thumb, care is taken to preserve the oblique pulley in its entirety to prevent bowstringing. After release, the patient is asked to actively move the digit to confirm complete relief of the triggering. Meticulous hemostasis is obtained via electrocautery, and the wound is closed with one or two monofilament sutures.
A small hand dressing is applied, with all digits left free, and motion is encouraged on the day of surgery. The patient is counseled to use the hand for light activities, and supervised hand therapy is usually necessary only for patients with preoperative fixed flexion contractures. Sutures may be removed 7 to 10 days postoperatively. Most patients can resume full hand use within 3 to 4 weeks of surgery.
For the index through small digits, measure the distance between the palmar digital and PIP flexion creases, and measure this distance again proximal to the palmar-digital crease to identify the leading edge of the A1 pulley.
Make a transverse, oblique, or longitudinal incision directly over the A1 pulley.
Do not cross flexion creases with a longitudinal incision.
Spread down to the flexor sheath; retract the neurovascular bundles.
Sharply divide the A1 pulley fibers to expose the flexor tendons.
Preserve the A2 pulley in the fingers; preserve the oblique fibers in the thumb.
Confirm complete release by active flexion.
Use a small conforming bandage and advise immediate motion. Perform early therapy for fixed flexion contractures.
Percutaneous Trigger Finger Release ( ).
Open surgical release of trigger digits is not without complication; in fact, some authors report a dissatisfaction rate as high as 26%. Percutaneous trigger release has been reported by several authors to be a safe alternative to traditional open methods using a variety of instruments ( Table 56.2 ). Reported results have been encouraging, with success rates of 74 to 94% at medium-term follow-up and few reported complications. Incomplete relief of triggering has been reported in a higher percentage of patients with grade 4 trigger digits and fixed flexion contractures and in those undergoing hemodialysis. All authors agree that practice on cadaveric hands is recommended before attempting the procedure in patients.
|Author||Year||Number of Digits||FINDINGS||Follow-up (months)||Notes|
|Lorthioir||1958||52||Custom “tenotome”||100%||Longitudinal tendon scoring well tolerated|
|Tanaka et al||1990||210||4-mm scalpel blade||74%||24||29% poor results in fingers; best results in thumbs|
|Eastwood et al||1992||35||21-gauge needle||94%||13||1 repeat release; discouraged for thumbs|
|Lyu||1992||63||Custom hook device||88%||11||11% conversion to open release; no complications|
|Stothard and Kumar||1994||18||18-gauge needle||94%||One recurrence; several patients with temporary flexion contractures; superficial tendon scoring|
|Pope and Wolfe||1995||25 (cadaveric)||19-gauge needle||90%||N/A||Superficial scoring of tendon; not recommended for the thumb or index finger because of the proximity of digital nerves|
|1995||13||19-gauge needle||100%||N/A||5 of 13 pulleys incompletely divided distally; active trigger necessary to confirm release|
|Bain et al||1995 (cadaveric)||14-gauge angiocatheter||68% for digits, 58% for thumb||N/A||Five missed releases; not recommended for the thumb or little finger|
|Nagoshi et al||1997||67||18-gauge needle||78% idiopathic, 62% hemodialysis||9||Active triggering necessary at the time of release; higher grades and digits locked in extension do less well with the percutaneous method|
|Cihantimur et al||1998||34||16-gauge angiocatheter||100%||12||No complications|
|Bain and Wallwork||1999||31||14-gauge angiocatheter||97%||2||Active triggering at the time of release; not recommended for locked digits, tenosynovitis|
|Dunn and Pess||1999||52 (cadaveric)||Custom push knife||98%||N/A||No nerve or vessel injury; complete release|
|26||19-gauge needle||38%||Superficial scoring of tendons|
|Ha et al||2001||185||Custom hooked blade||94%||12||No complications; effective for locked digits|
|Guler et al||2013||87||18-gauge needle||98% open |
|23||5.7% digital nerve injury in percutaneous group|
This procedure is done in the office. The palm and affected digit are prepared with antiseptic solution and the digit exposed with a fenestrated drape. The MP joints are hyperextended over a rolled towel to displace the neurovascular structures dorsally. The A1 pulley is palpated directly over the metacarpal head. Ethyl chloride is sprayed by an assistant as a topical anesthetic, and the skin and flexor tendon sheath are infiltrated with 1 to 2 mL of neutralized 1% lidocaine solution using a 27-gauge needle. A 19-gauge needle is placed percutaneously through the annular pulley, and placement within the flexor tendon is confirmed by asking the patient to slightly flex the digit ( Figure 56.10 ). The needle is withdrawn slowly and rotated to align the bevel of the needle along the longitudinal axis of the tendon. A sweeping motion is used to score and section the A1 pulley proximal and distal to the site. Disappearance of a grating sensation indicates complete sectioning of the annulus. The needle is withdrawn and the patient is asked to flex and extend the digit several times. On occasion, a second needle stick is necessary to complete the release. An adhesive bandage is applied, and the patient is instructed to use the hand for activities as tolerated. Patients should be advised to expect a mild to moderate degree of discomfort for several days; ice and antiinflammatory agents are helpful in the immediate 48 to 72 hours postoperatively.