6.8 Tendon disorders

Congenital anomalies of the tendons and tendon sheaths of the hand and wrist are common but rarely cause symptoms of pain or functional impairment. Asymptomatic anomalies are important as they may cause confusion in the interpretation of the physical examination.

Palmaris longus is absent in about 15% of hands and anomalous in 9%. It is implicated in the pathogenesis of carpal tunnel syndrome as it is absent in only 3% of patients with this condition. Its clinical significance is its use as a tendon transfer or free tendon graft.

The Linburg–Comstock anomaly consists of a tendinous slip or tenosynovial adhesion connecting the flexor pollicis longus tendon to the flexor digitorum profundus tendon of the index finger. It is found in 25% of cadavers and can cause pain by restricting independent movement of the index and thumb. The pathognomonic sign is obligatory flexion of the index finger when the thumb is flexed actively. There is pain in the wrist if flexion of the index is blocked as the thumb is flexed. The anomaly is usually only problematic in musicians. Surgical division of the connection is usually curative.

The flexor digitorum superficialis tendons of the index, middle, and ring fingers generally have individual muscle bellies and can act independently. Only 60% of little fingers have an independent flexor digitorum superficialis tendon. About 20% have no discernable function of the tendon though it may be present. This can lead to uncertainty when interpreting physical signs after lacerations of the little finger. In the remaining 20% the little finger superficialis tendon is linked to that of the ring finger. This can be demonstrated by the standard and modified flexor digitorum superficialis tests: the little finger cannot be flexed actively at the proximal interphalangeal joint whilst the other digits are held extended. When the ring finger is released, the ring and little finger proximal interphalangeal joints can be flexed together, but independently of the other digits.

Abductor pollicis longus is subject to considerable variation in the number of tendon slips and their insertion. Slips may attach to the abductor or extensor pollicis brevis tendons, the trapezium, joint capsule, or thumb metacarpal.

The extensor pollicis brevis tendon is also rather variable. Its anomalies include absence, connection with abductor pollicis longus, and insertion into the distal phalanx or extensor hood in place of (or in addition to) the proximal phalanx. In 30–60% of wrists, the extensor pollicis brevis tendon runs in a subcompartment of the first extensor compartment. Symptoms of de Quervain’s syndrome may persist if a subcompartment is overlooked at the time of release.

Anatomical variations in the contribution of the extensor digitorum communis tendon to the little finger account for the variable deficit that results from rupture or laceration of the extensor digiti minimi. Rupture of extensor digitorum minimi, which may herald rupture of extensor digitorum communis in rheumatoid arthritis, may pass unnoticed unless independent extension of the little finger is tested.

The terminology of tendon disorders is unsatisfactory. The terms tendinitis and tenosynovitis mean inflammation of the tendon and tenosynovium respectively. These conditions have recognizable and reproducible physical signs (swelling, tenderness, and crepitus along the line of the tendon), as well as characteristic pathological changes on histology (e.g. rheumatoid arthritis). In the absence of these features, and especially in the context of pain in the workplace, it is inappropriate to assign these diagnoses. The term tendinosis, which makes no aetiological or pathological assumptions, is preferable, but its use is not widespread. In many cases, a recognized tendon disorder can be diagnosed (e.g. de Quervain’s syndrome). If the clinical picture does not conform to a recognized disorder, but is clearly attributable to the action of a tendon, then a neutral term such as flexor carpi ulnaris tendon pain is appropriate. Terms such as forearm pain or non-specific arm pain can be used when the symptoms and signs are poorly localized.

Tenosynovitis is inflammation of the tenosynovium. Tenosynovitis is ultimately a pathological diagnosis, but a clinical diagnosis may be made in the presence of the characteristic features of tenderness, swelling, and crepitus along the line of the tendon sheath, along with restricted tendon excursion. Not all the signs are necessarily present simultaneously, but it would be difficult to justify the diagnosis of tenosynovitis in the absence of localized tenderness.

Tenosynovitis may be acute or chronic. Pyogenic tenosynovitis (see Chapter 6.14) is the commonest cause of acute tenosynovitis but rarely acute gout, calcium pyrophosphate deposition, and repetitive trauma may be responsible. Rheumatoid disease (see Chapter 6.5), mycobacterial infection, fungal infection, foreign body, sarcoidosis, gout, and amyloid may cause subacute or chronic tenosynovitis. Chronic flexor tenosynovitis can lead to median nerve compression.

Infection with atypical mycobacteria such as Mycobacterium kansasii and Mycobacterium marinum is now more common than tuberculous tenosynovitis (see Chapter 6.14). Mycobacterial infection should be considered whenever chronic tenosynovitis is not clearly associated with inflammatory arthritis and appropriate specimens sent for histology and mycobacterial culture.

The management is tenosynovectomy, which is both diagnostic and therapeutic, followed by appropriate antimycobacterial chemotherapy.

Foreign material within the tendon sheath may incite an inflammatory response in the absence of infection. The thorns of the blackthorn tree (Prunus spinosa) and Pyrocantha species are particularly liable to cause a subacute aseptic inflammation of joint or tendon sheath. The flexor tendon sheath of the finger is the most common site. Small foreign bodies may be identified by ultrasound examination. Tenosynovitis generally resolves once the foreign material is removed.

There are several conditions, including de Quervain’s syndrome and trigger finger, which have previously been attributed to inflammation of the tendon, sheath, or synovial lining, and which have been called ‘tenosynovitis’. The clinical features of tenosynovitis may indeed be seen when the tendon sheath is affected by an inflammatory disorder such as rheumatoid arthritis. However, histological studies of the common idiopathic forms of these dis-orders seldom show inflammation of the tendon, tendon sheath, or tenosynovium.

The pathological changes of de Quervain’s syndrome and trigger finger, which are the only conditions to have been studied in detail, are similar. The changes comprise an increase in extracellular matrix, thickening of the collagen fibrils, and areas of fibrocartilage metaplasia in the tendon sheath. Fibrillation or delamination of the tendon surface may be seen. Evidence of inflammation is notably absent. In the absence of clinical or pathological evidence of inflammation, it is illogical to refer to ‘tendinitis’ or ‘tenosynovitis’.

The cause of these common disorders is unclear. The symptoms may be initiated by a single injury such as a direct blow or sudden strain. While damage by overuse is an intuitively plausible theory, the evidence that these disorders are initiated by excessive activity is scant, except in the case of intersection syndrome (peritendinitis crepitans) affecting the second extensor compartment. However, the symptoms that these conditions produce are often aggravated by activity.

Rest, avoidance of aggravating activities, splintage, and analgesic medication constitute the first line of management. Injection of the tendon sheath with corticosteroid, which can be dramatically effective, is the second line of treatment. Complications of steroid injection are uncommon. Infection is very rare but potentially disastrous. Tendon rupture is also very rare and is probably due to underlying pathology in the tendon or its surroundings (e.g. rheumatoid arthritis) rather than to the injection itself. Atrophy of dermis or subcutaneous fat results from inadvertent injection into the subcutaneous tissues, which should be avoided. Surgical decompression of the affected tendon may be needed in cases that fail to respond to non-operative treatment.

The first dorsal compartment of the wrist, containing the tendons of abductor pollicis longus and extensor pollicis brevis, is the site of this painful disorder (Figure 6.8.1). The cause is unknown. It occurs spontaneously, more often in females than males, and may arise during or just after pregnancy. The chief symptom is pain during use of the thumb. Loss of ulnar deviation of the wrist and triggering of the abductor pollicis longus tendon are seen occasionally in severe cases. The physical signs are pain on resisted active extension of the thumb, swelling and tenderness over the compartment, and a positive Finkelstein’s test. The test described by Finkelstein is reproduction of pain by ‘grasping the patient’s thumb and quickly abducting the hand ulnarward’. Another test, originally described by Eichhoff but often attributed erroneously to Finkelstein, deviates the wrist ulnarward while the thumb is held in the palm beneath the flexed fingers. The differential diagnosis includes the intersection syndrome and arthritis of the trapeziometacarpal, scaphotrapezial, or radioscaphoid joints.

Management comprises rest, analgesics, thumb splintage, and steroid injection. Injections are effective in the long term in at least 80% of cases but injection into the extensor pollicis brevis tenosynovium resulted in 100% success in one series. Care should be taken to avoid subcutaneous extravasation of long-acting steroid, which can produce an unsightly patch of atrophic skin and subcutaneous tissue.

Operative release is indicated if pain persists or recurs after injection. It requires a longitudinal division of the roof of the first dorsal compartment and of any subcompartments (30–60% of first dorsal compartments have a septum that separates the abductor pollicis longus tendon from the extensor pollicis brevis). A transverse skin incision gives good exposure and a better scar than a longitudinal incision. It is crucial to protect the superficial radial nerve; a neuroma can be very troublesome. Release of the retinaculum toward the dorsal edge of the compartment leaves a palmar ridge of retinacular tissue that may help to prevent the uncommon complication of palmar subluxation of the abductor pollicis longus tendon on wrist flexion.

This condition is probably the only tendon disorder for which a consistent association with overuse has been demonstrated. Repetitive gripping activities, such as weightlifting and rowing, are often implicated. It is characterized by pain, tenderness, swelling, and, in severe cases, crepitus where the abductor pollicis longus and extensor pollicis brevis muscle bellies run obliquely across the second dorsal compartment. This point lies about 5cm proximal to the radial styloid and is well above the site affected in de Quervain’s syndrome. The pathology was previously thought to be due to friction between the first and second compartments causing tendinitis. However, Grundberg and Reagan (1985) found tenosynovitis in the second extensor compartment in each of 13 cases; in every case the symptoms were relieved by decompressing only the second compartment.

Conservative treatment of rest, splintage, and steroid injection is usually effective. Operative release of the second extensor compartment is rarely required.

The flexor carpi radialis tendon passes over the wrist joint in a fibro-osseous tunnel lined with synovium, running past the ulnar side of the tubercle of the scaphoid and along a groove in the medial face of the trapezium before inserting onto the base of the second metacarpal.

Pain related to the flexor carpi radialis tendon may arise spontaneously, typically in females of late middle age (in whom it may be associated with scaphotrapezial osteoarthritis), but may occasionally be associated with activities requiring strenuous flexion of the wrist.

The patient complains of pain localized to the tendon at the wrist. There is tenderness and swelling of the tendon sheath. Pain is aggravated by resisted flexion of the wrist. The differential diagnosis includes de Quervain’s syndrome, palmar wrist ganglion, and scaphotrapezial osteoarthritis. Treatment is by rest, splintage, analgesics, and steroid injection of the sheath. Operative release of the sheath is occasionally required.

Pain syndromes may be associated with several other tendons, including extensor pollicis longus, extensor indicis proprius, flexor carpi ulnaris, and extensor carpi ulnaris. The diagnosis is made from the findings of pain, swelling, local tenderness, and pain on active resisted tendon action. The management follows the lines described previously.

Trigger digit in adults is caused by a nodular thickening of the flexor tendon that is accompanied by stenosis of the first annular (A1) pulley of the tendon sheath at the level of the metacarpophalangeal joint. It occurs most often in middle-aged females. The ring finger, middle finger, and thumb are the most frequently affected digits.

Trigger digit presents with clicking or locking of the finger during flexion and extension. The digit may lock in flexion, typically with the finger flexed into the palm (Figure 6.8.2). Locking is often most troublesome on waking, requiring forcible extension using the opposite hand. Although locking appears to affect the interphalangeal joints of the fingers or the interphalangeal joint of the thumb, pain and tenderness are felt over the tendon sheath at the level of the metacarpophalangeal joint. The thumb occasionally locks in extension. Persistent locking of the finger may lead to a fixed flexion contracture at the proximal interphalangeal joint, especially in diabetic patients. Triggering at the A3 pulley is a rare variant described in bowlers that affects the flexor digitorum profundus and therefore the distal interphalangeal joint only.

Most cases arise spontaneously in otherwise normal individuals. There is no relationship to occupation but repetitive gripping activities may cause acute transient triggering. Triggering may be due to intratendinous nodules or tenosynovitis in rheumatoid disease, or to a tendon flap caused by a partial tendon division. Trigger digit is common in diabetes and in association with amyloidosis and mucopolysaccharidoses. Several digits may be affected in these groups of patients.

Triggering may resolve spontaneously. Mild triggering may need no treatment apart from reassurance. Splintage of the interphalangeal joints in extension at night improves locking on waking and may suffice in mild cases. Taping of the proximal interphalangeal joint by day may prevent flexion to the point of locking. Steroid injection of the tendon sheath cures about 70% of cases but is less effective in diabetic patients.

In the non-rheumatoid patient, surgical release of the A1 pulley is indicated for persistent or severe triggering with almost 100% success for open release. Percutaneous release with a needle shortens recovery while being equally effective and safe. In longstanding cases with persistent proximal interphalangeal joint contracture and tendon thickening, division of the proximal part of the A2 pulley or resection of the ulnar slip of flexor digitorum superficialis may be required.

Release of the A1 pulley is contraindicated in rheumatoid as it may exacerbate a tendency to ulnar drift. Synovectomy and resection of the ulnar slip of flexor digitorum superficialis is preferred.

Trigger thumb is the most common hand condition requiring operative treatment in children. A young child, usually between the ages of 6 months and 3 years, presents with a painless fixed flexion contracture of the interphalangeal joint of the thumb. On rare occasions, there is a history of triggering. Thickening of the flexor tendon and its sheath is palpable at the level of the metacarpophalangeal joint. It is often termed ‘congenital’ although this seems inappropriate, as no cases were found during examination of 4719 newborn infants and children rarely present before the age of 6 months. The cause is unknown. The differential diagnosis is congenital clasped thumb, which is caused by absence or hypoplasia of the thumb extensors. Trigger thumb may resolve spontaneously; almost half of 53 patients recovered after observation for a mean of 7 months. Spontaneous improvement after age 3 is uncommon. If the thumb is reducible, splinting is more effective than observation alone in improving triggering. For persistent triggering, operative treatment involves division of the proximal pulley with care to avoid the digital nerves, which are close to the midline and lie immediately beneath the skin.

Trigger finger is rare in children, accounting for about 14% of trigger digits. Unlike the thumb, locked trigger finger is uncommon. The middle finger is most commonly affected, followed by the ring and little fingers. Spontaneous recovery is common and splinting for trigger finger in children has had mixed success. Unlike adult trigger finger, release of the A1 pulley alone results in 44% recurrence In some cases, there is nodular thickening of the tendon and A1 pulley release alone suffices, while in others, there appears to be an abnormal relationship between the deep and superficial flexor tendons. In these patients, partial division of the A2 pulley or resection of one of the slips of flexor digitorum superficialis is effective.

Rarely, thickening of the tendon or synovium or may impede gliding at the wrist. This may cause triggering of the wrist (true trigger wrist) or fingers as well as median nerve compression. The cause is usually flexor tendon tenosynovitis for which tenosynovectomy and carpal tunnel release is usually curative. It is occasionally due to a discrete mass or extensor tendon pathology.

Tendon rupture is an important condition in the hand, not only because it impairs function but also because in some cases it can be prevented by timely intervention. The pathology of tendon rupture involves mechanical factors that increase tendon stress and pathological processes that weaken the tendon. Mechanical factors include abrasion on sharp surfaces (fractures, implants), change in direction, tendon anomalies (abnormal interconnections), and acute or chronic overloading. The tendon may be weakened by inflammation (rheumatoid disease, systemic lupus erythematosus, crystal deposition, osteoarthritis), ischaemia, or metabolic causes (chronic renal failure, systemic or local steroids).

Rupture of the extensor pollicis longus or flexor carpi radialis tendons is almost always an isolated lesion with a very low likelihood of other ruptures. Rupture of the finger extensors and of the tendons passing through the carpal tunnel is often sequential, so that detection of the first rupture and prompt intervention are crucial in preventing further loss of function.

The classical lesion of attrition rupture of extensor tendons was described by Vaughan-Jackson in two cases of osteoarthritis of the distal radioulnar joint (Figure 6.8.3A). The roughened ulnar head erodes through the dorsal capsule and then lies in contact with tendons in the fifth and fourth compartments. Rupture is generally painless and sequential, beginning with the extensor digiti minimi tendon. Since extension of the little finger can, in many cases, be activated by a tendon slip from the extensor digitorum communis of the ring finger, rupture of extensor digitorum minimi may pass unnoticed until the ring and little finger drop together. Loss of independent extension of the little finger (Figure 6.8.3B) signifies rupture of extensor digitorum minimi and the need for appropriate surgery of the distal radioulnar joint.

Osteoarthritis of the radiocarpal, scaphotrapezial, and distal radioulnar joints can lead to tendon ruptures within the carpal tunnel. Osteoarthritis of the scaphotrapezial joint may cause rupture of the flexor carpi radialis tendon (Figure 6.8.4), the proximal stump of which may form a painful fusiform swelling in the distal forearm.

The most common tendon rupture is of extensor pollicis longus, occurring a few weeks after fracture of the distal radius. The incidence is approximately 1% of all distal radial fractures. The rupture occurs typically in undisplaced fractures. The pathogenesis is uncertain but ischaemia probably plays a role. The tendon may be vulnerable to narrowing or irregularity of its sheath as it passes around the dorsal tubercle of the radius. At this point, it is subject to bending forces, has a poorly vascularized segment and lacks mesotenon. Nutrition at this point is from diffusion from the synovial fluid which may be hindered by haematoma contained in the intact sheath. The intact retinaculum also holds the tendon down against the sharp fracture edge.

Pain and crepitus over the third compartment with thumb movement is an indication for release of the retinaculum. Generally, however, the rupture occurs without warning.

There may be an extension lag at the interphalangeal joint (Figure 6.8.5), but a more reliable sign is loss of retroposition wherein the patient cannot lift the thumb off the table when the hand is placed flat—a movement that only extensor pollicis longus can achieve. Reconstruction by tendon transfer (using extensor indicis proprius or a slip of abductor pollicis longus) is straightforward and effective.

With the increasing use of plate fixation of the distal radius, iatrogenic tendon rupture is encountered. The distal edge of a dorsal plate can abrade the long finger extensors; excessive length of screws securing a volar plate may do the same. Dorsally angulated malunion of the distal radius may also cause rupture of flexor tendons in the distal forearm. Volar locking plates can cause flexor or extensor tendon ruptures.

Less common causes of tendon rupture include long-standing Kienböck’s disease, scaphoid non-union, and scapholunate dissociation. The flexor digitorum profundus tendon of the little finger is particularly prone to rupture; this can be due to non-union of the hook of the hamate, calcium pyrophosphate deposition in the triangular fibrocartilage, pisiform–triquetral instability, and osteoarthritis.

When no definite cause can be found, the rupture is termed spontaneous. In flexor tendons these are rarer than avulsion from the distal phalanx. Typically they occur in zone III of the flexor digitorum profundus to the little finger. Although the aetiology is unclear, the likely predisposing factors include tendon anomalies, repetitive microtrauma, vascular alterations, and genetic influences.