At the center of our daily life activities, the hand is frequently exposed to both direct and indirect trauma and overuse injuries(1). Therefore, the detection and detailed evaluation of hand injuries are common referral indications for ultrasound (US) examinations. Most injuries to the hand are open injuries. These injuries occur more commonly to the extensor tendons rather than the flexor tendons(2). This review covers the most common injury patterns of pulleys, flexor and extensor tendons in the wrist and lesser fingers for a reader with a comprehensive knowledge of normal hand and wrist anatomy (for a detailed review of normal anatomy, please read the article by De Maeseneer
Extensor tendon tears may be the result of open injuries or closed ruptures. The classification of extensor tendon injuries into anatomical zones (by Kleinert and Verdan, Fig. 1) and the evaluation of injury characteristics by imaging are essential tools for the selection of the appropriate treatment(4). In every case of a tendon tear, the radiologist should report the following details for the referring surgeon(5):
exact location of the tear;
tear type: complete or partial-thickness;
in partial-thickness tears: the percentage of the tendon involved;
in cases of a complete tendon tear: the degree of tendon retraction and associated avulsion injury, including the degree of displacement of the avulsed bone fragment.
Full-thickness tears present on US as an absolute disruption of the tendon continuity (Fig. 2)(6,7). In acute indirect injury, tendon stumps are typically thickened and appear hypoechoic with inhomogeneities and loss of the normal fibrillar echotexture. After direct injury, the stumps typically appear even. Both static and dynamic US scanning should be used to assess the gap between the tendon stumps in order to inform the surgeon`s incision planning.
Partial-thickness tears typically present on US as an incomplete interruption in tendon continuity or focal disturbance of the parallel fiber lining. A hypoechoic or anechoic tendon defect is commonly observed, along with fusiform tendon swelling(6,7). Furthermore, a hematoma in the synovial tendon sheath is often seen in acute settings. In chronic lesions, hypoechoic areas with fibrosis and adhesions typically surround the ruptured tendon. Bony fragments in cases with associated fractures may present as hyperechoic areas with posterior shadowing on US imaging(5,7). An US finding of an uninterrupted, hypomobile tendon is often reported in healed finger injuries due to tendon elongation. In such cases, the examiner can use passive flexion and extension movements of the finger (and its comparison to other fingers or the contralateral side) in order to detect any mild gliding abnormalities.
The term “mallet finger” or “baseball finger” refers to a deformity of the finger due to injury of the extensor tendon at its insertion point along the base of the distal phalanx(5,7,8) (zone #1 injury; Fig. 3 and Fig. 4). The terminal portion of the tendon may rupture directly, or it may be torn from the insertion point with a small piece of bone, i.e., a so-called “bony avulsion injury” (Fig. 4). The typical injury mechanism is a sudden, forceful hyperflexion of an extended DIP joint, such as when a flying ball strikes the fingertip(8). If left untreated, a mallet finger may progress to a DIP joint flexion deformity and eventually result in a swan neck deformity.
Typical US findings in mallet fingers include a defect at the insertion point observed as a space during DIP flexion that closes during DIP extension, a swollen tendon over the distal middle phalanx, and a hypomobile deep flexor tendon(9).
If bone is not involved, mallet finger injuries are stabilized in a splint for several weeks. Surgery is recommended for cases with complex injury patterns, such as fractures involving more than 30–50% of the joint surface or posttraumatic malalignment of the DIP joint, in order to prevent development of a swan neck deformity or a prolonged extension deficit(8).
Less common sports injuries are closed disruptions of the central slip (Fig. 3) at the base of the middle phalanx. They may occur with or without bony fragment avulsion(5,10,11) (zone #3 injury, Fig. 1 and Fig. 5). In the acute phase, detection of central slip lesions may be difficult by clinical examination alone. The PIP joint may still extend due to the intact lateral slips. If a central slip lesion is overlooked, the patient often returns after 2–3 weeks with a so-called “boutonnière deformity” (Fig. 5). This term refers to a flexion deformity of the PIP joint and hyperextension of the DIP joint(12) and is caused by an increased triangular ligament tension resulting in palmar migration of the lateral slip. The boutonnière deformity often remains permanent since the tendon will heal with splinting, but in a lengthened position. Therefore, the key to a good outcome after central slip rupture is an early diagnosis and initiation of a full-time splinting(12).
For diagnosis, the US probe should be placed over the dorsal PIP joint in longitudinal alignment with the central slip. A pre-insertional extensor mechanism defect and impaired central slip gliding in finger flexion and extension are the primary diagnostic factors. Unfortunately, the anomalous location of the displaced lateral slip is more difficult to detect with US.
Sagittal bands are the most important component of the dorsal extensor hood at the metacarpophalangeal (MCP) joint (Fig. 3). The superficial and deep layers of the sagittal bands attach to the palmar plate volarly and to the extensor tendon dorsally(3). The extensor digitorum communis (EDC) tendon is stabilized at the MCP joint and protected from subluxation during digital movement by the sagittal bands. The radial band is thinner and weaker than the ulnar band. Closed disruption of an EDC tendon sagittal band (zone #5 injury; Fig. 6) is a common injury after direct trauma to the proximal phalanx or the dorsal aspect of the MCP joint. Most often the third digit(10,13) is affected.
Injuries to the sagittal band are classified into three types(5):
local contusion (type-1);
subluxation (type-2);
dislocation (type-3) of the EDC tendon to the volar aspect of the MCP joint.
Consequently, the EDC tendon may dislocate to the radial or ulnar side, such that the finger cannot actively extend at the MCP joint(14). Radial-sided ruptures of the sagittal band in particular frequently result in tendon instability. In dynamic US, sporadic snapping of the EDC tendon to one side (subluxation) or dislocation of the tendon between the metacarpal heads can be observed when the fist is clenched(13).
Acute injuries are treated with immobilization (splint in joint extension), whereas chronic lesions require surgical reconstruction of the injured sagittal band.
The term “tenosynovitis” is defined as any inflammation and swelling of the synovial sheath. Inflammatory processes, trauma, and overuse injuries lead to damage of the extrinsic extensor tendons and the surrounding tendon sheaths(15). In chronic tenosynovitis, one will find tears and ruptures of the tendons, as well as neighboring bony changes such as erosions or periosteal reactions.
Tenosynovitis may affect each extensor compartment (Fig. 7) at the level of the wrist(16).
Tenosynovitis occurs most commonly in the first compartment as “De Quervain`s syndrome” (Fig. 8). This chronic injury stems from the overuse and repetitive movement of the extensor pollicis brevis (EPB) and the abductor pollicis longus (APL) tendons under the retinaculum at the level of the distal radius(17). Initially, this manifests as tendon edema, ensuing constriction of the tendon against the retinaculum, and thickening of the retinaculum, caused by microinjuries and impaired healing.
Dynamic US scanning, preferably in the long-axis view, may detect real-time gliding of the obstructed tendon under the retinaculum(17). The normal oval shape of the EPB and APL tendons on short-axis view typically changes to a rounder appearance in chronic settings. Thickened tendons also lead to partial tears of the retinaculum. In the acute stage, increased vascularization is observed in both the tendons and the retinaculum, whereas in chronic conditions, thickening and fibrotic lesions are observed. Sometimes a vertical septum is observed as having divided the first compartment into two discrete tunnels and increasing the risk of tenosynovitis. In such cases, only the EPB is typically involved, while the APL tendon remains unaffected (Fig. 9). Common causes of De Quervain’s syndrome include sporting activities that require repetitive flexion or extension of the wrist in combination with thumb abduction against resistance. This syndrome develops frequently during new motherhood (“baby wrist”) due to hormonal changes and an incorrect wrist position while lifting the baby(18).
Proximal intersection syndrome (also called crossover syndrome, peritendinitis crepitans or oarsmen’s wrist) is a type of overuse injury presenting clinically with pain and swelling at the distal forearm, some centimeter proximal to Lister’s tubercle. Here lies the intersection point of the first (APL and EPB) and the second extensor compartment (extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB) tendons)(19). US may detect edematous changes in the APL and EPB (typically at the myotendinous junctions) and the loss of a hyperechoic plane deviding the two different compartments(5,20). Other findings include sheath effusion and swelling, typically of the tendons in the second extensor compartment. Sometimes even ganglion cysts may be seen.
Distal intersection syndrome occurs at the level of Lister’s tubercle, where the extensor pollicis longus (EPL) tendon, (i.e., third extensor compartment) crosses over the second extensor compartment tendons(16). The syndrome is often caused by mechanical rubbing between the tendons due to repeated flexion and extension movements of the wrist. Sheath effusion is typically observed around the EPL tendon proximal and distal to the intersection(21) (Fig. 10). During US examination, the carpal bones and joints should also be checked carefully along the full length of the tendon course, for impingement of tendons by underlying spurs or osteophytes. This syndrome can also be seen secondary to scaphoid fractures, or in patients with a scaphoid lunate advanced collapse (SLAC) wrist.
Non-displaced Colles fractures may cause EPL tendon rupture, whereas the stabilizing screw tips in a stabilized Colles fracture may protrude dorsally, with possible impingement of the EPL tendon(22).
Patients with inflammatory or infectious disorders often present with EDC tenosynovitis (Fig. 11)(16,23). US with Doppler imaging helps to assess the activity level of inflammatory diseases and to monitor treatment effects. Tendon impingement with signs of tenosynovitis may be seen in the postoperative setting, such as following treatment of distal radius fractures with screw tip impingement (Fig. 12). Furthermore, an anomalous extensor indicis proprius muscle passing with the EDC tendon in the fourth compartment may also cause tenosynovitis, known as “extensor indicis proprius syndrome”(24).
The extensor digiti minimi (EDM) tendon is known for frequent anatomic variations with a bifurcated tendon (proximal, distal, or at level of the retinaculum), often with a concomitant synovial septum. Some studies suggested that a distally bifurcated tendon might impinge on the synovial septum during full finger flexion, inducing tenosynovitis(25). The EDM lies close to the distal radioulnar joint (DRUJ). Therefore, EDM tenosynovitis frequently occurs in patients with arthritis of the distal radioulnar joint (DRUJ). In severe tenosynovitis, synovial pannus may infiltrate the DRUJ capsule, leading to rupture of the adjacent retinaculum, ulnar head dorsal subluxation, and tendinopathy(26). Dynamic US in varying degrees of pronation and supination might be helpful in order to assess the tendon position in relation to the distal radioulnar joint.
A retinaculum-like structure known as the “subsheath” holds the extensor carpi ulnaris (ECU) tendon within a groove in the ulnar head(5,16). Chronic repetitive stress may lead to stenosing tenosynovitis of the subsheath. Typical ultrasound findings include fibrosis, reactive tenosynovial effusion, and thickening of the extensor retinaculum. A weak or torn subsheath may cause ECU tendon instability or dislocation out of the ulnar groove (Fig. 13).
Typical causes of subsheath tears include recurrent stress injuries (e.g., in racket sports), an abrupt twisting(27), and severe DRUJ arthritis. Note: In healthy subjects the ECU tendon “dislocates” partially with supination of the forearm (up to 50% of the groove’s width) and relocates with pronation. This can be nicely seen with dynamic ultrasound.
High resolution US provides reliable evaluation of the flexor tendons of the finger (for anatomy, see Fig. 14 and Fig. 15) and distinction of tenosynovitis, partial-thickness tendon tears, and complete tears(28).
Using the anatomical classification system developed by Kleinert and Verdan(4), flexor tendon injuries are classified into 5 zones (Fig. 16). Flexor tendon injuries of the third, fourth and fifth digits are frequently open, caused by laceration, and often involve the mid-substance, but not the tendon insertion point(11). These injuries involve the flexor digitorum superficialis (FDS) tendon, the flexor digitorum profundus (FDP) tendon, or both. Injuries in Zones II to V injuries that involve the neurovascular bundle require urgent surgical repair (i.e., within 24 hours), particularly in Zone II(11)C. US permits measurement of cross-sectional flexor tendon thickness (i.e., when a tendon strain is suspected) and easy comparison with the contralateral finger(29).
The term “jersey finger” refers to a closed avulsion injury of the distal FDP tendon(27) (Fig. 17) that occurs when a DIP joint in active flexion is forcefully hyperextended. For example, in rugby or football games, a player snatches another player’s jersey with the fingertips as that player moves away(11). The fourth digit is frequently affected. FDP tendon avulsion injuries are assessed based on the extended Leddy and Packer classification(30) and largely require operative treatment. Type I injuries (i.e., FDP tendon retraction to the palm) often have compromised vascular flow and require urgent operative treatment within 7 to 10 days. Treatment options for chronic avulsion injuries older than 6 weeks depend on the function level of the digit(30).
Common causes of flexor tenosynovitis include overuse, local trauma, inflammatory arthritis, and infection(31).
Acute flexor tenosynovitis is characterized on US by hypoechoic or anechoic effusion in the synovial sheath, increased vascularization and distention of the tenosynovium. Furthermore, the echotexture in the involved tendon lacks the typical fibrillar pattern and the tendon appears thickened. Peritendinous edema is evident in some cases(28). Increased vascularization due to neo-vessels can be visualized with US color or power doppler in the tendon and the surrounding soft tissues(28).
In subacute and chronic cases of flexor tenosynovitis, the synovial sheath is thickened on US, and the flexor tendon is blurred(16). In infectious tenosynovitis and wound injuries, foreign bodies may be observed. In comparison, rice bodies may be found within the synovial sheath effusion in inflammatory arthritis, visualized as numerous, well-defined, floating echoic masses. US may be used for guided treatment with steroid injections, or for assessment of therapeutic treatments, with a successful response demonstrating decreased inflammatory activity.
In the fingers, the flexor tendons run through osseo-fibrous tunnels formed by the annular and cruciform pulleys and covered by the flexor retinaculum. In a “trigger-finger”, mechanical overuse causes thickening of the annular pulley, narrowing of the osseofibrous tunnel, and stenosing tenosynovitis of the adjacent flexor tendons(28)(Fig. 18).
Most injuries of the annular pulleys (for anatomy, see Fig. 19A) happen in rock climbers. The A2 pulley of the third and fourth digits is most commonly affected(27). Typically, excessive stress with flexor tendon contraction against the pulley system causes pulley injury. A common risk factor for pulley injuries is the “crimp position”, with 90° or more flexion of the PIP joint and slight DIP joint hyperextension. Using high-resolution US probes, a normal annular pulley is identified as a very thin (0.3–0.5 mm) band surrounding the flexor tendons on their volar side (Fig. 19B)(5). Pulley ligaments are best visualized on transverse scanning planes: the normal US appearance of an annular pulley is hyperechoic on the volar side and hypoechoic on the lateral side (the latter due to anisotropy). The thickness of the annular pulleys is often increased (1.5-fold) in asymptomatic climbers, when compared to non-climbers(32) (Fig. 20). This structural adaptation simplifies US visualization of the pulley bands. Annular pulley injuries include pulley strains and partial or complete ruptures, involve one or multiple pulleys, and often result in variable bowstringing of the flexor tendons. Clinically, bowstringing is typically only visible when multiple injuries have occured in the A2, A3, and A4 pulleys(33). With imaging (US and MRI) the detection of minor degrees of bowstringing is more sensitive(34). The tendon–to-bone distance (TBD) increases in cases with bowstringing. US with forced flexion is used to determine the site of maximal volar bowstringing (MVB) and to diagnose which pulley has ruptured. In an A2 pulley rupture, MVB occurs over the proximal phalanx. In an A3 pulley rupture, MVB occurs at the distal proximal phalanx at level of the volar plate. In an A4 pulley rupture, MVB occurs over the middle part of the middle phalanx. US should be performed along the finger’s long axis to detect tendon bowstringing and measure TBD (Fig. 21). The transverse scanning plane is best for assessment of the site of pulley detachment and visualization of any small osseous avulsion fragments.
Dynamic US is used to evaluate any instability of the flexor system associated with pulley injuries. Volar tendon displacement relative to the bone is measured at rest and in forced flexion. The normal TBD at the level of the A2 pulley ligament is <2 mm(31) (Fig. 19). In a complete, isolated A2 pulley tear, the TBD at the level of the proximal phalanx is >2 mm at rest and >4 mm during forced flexion(31). In combined A2, A3, and A4 pulley tears, the TBD is >2 mm at rest and >5.5 mm during forced flexion (Fig. 21). US during forced flexion is particularly helpful for differentiation of isolated A2 pulley tears and combined A2 and A3 pulley tears(5,34). Diagnosis of partial pulley ruptures is more challenging because they produce little to no tendon displacement. In such cases, the affected pulley is hypoechoic and swollen. Abnormal vascularization can be detected in both the tendons and pulleys in acute conditions using Doppler examination. A classification system adapted from Schöffl and Schöffl (grade I-IV) for grade I to IV flexor pulley injuries is used to guide treatment decision making(35). While grade I to III injuries (i.e., strain, partial rupture, and complete rupture of a single pulley) can be managed conservatively without operation, Grade IV injuries (i.e., multiple pulley ruptures or a single rupture of A2 or A3 with concomitant trauma (ligaments/lumbrical muscles)) require surgery.