Sonography of pathological changes in the hand

Abstract

Everyday medical practice shows that most common problems within the hand result from overload, injuries and degeneration. Dorsal side pathologies such as de Quervain's and Wartenberg's disease, intersection syndrome or degenerative lesions of carpometa-carpal joint of the thumb discussed in the paper can be accurately diagnosed and differentiated by means of ultrasound examination. Ultrasound is similarly powerful in detection and grading of traumatic lesions involving extensor tendons and their sagittal bands or the flexor tendons and their pulleys. In the case of carpal tunnel syndrome one can not only visualize the median nerve but also other structures of the tunnel that may cause compression. Similarly ulnar nerve compression within the Guyon's canal can be well evaluated. In cases of nerve trauma one can precisely define the level, and in cases of nerve discontinuity, the distance between stumps can be measured which is important in surgery planning. Often nerve trauma is a sequelae of tendon reconstruction. In such cases scars and nerve entrapment can be depicted. Tumors within a hand are usually benign, of which the most common are ganglia. On ultrasound examination a connection between a ganglion and its source (usually a joint or sheath) can frequently be defined. The relationship of tumors to nerves, tendon sheaths or vessels may suggest their nature. Ultrasound with dynamic tissue assessment is a very valuable adjunct to clinical examination.

Introduction

Most common hand conditions causing pain, numbness or malfunction are postraumatic, overload-derived or degenerative. Rheumatic diseases, despite their predilection to joints of the hand, are rare in everyday non-rheumatological practice ⁽¹⁾. Ultrasonography (US) is a superb method for diagnosing hand pathology and is useful for treatment planning and follow-up. US hand examinations should be performed using a high-end machine equipped with a broadband transducer of higher than 12 MHz frequency.

Dorsal side pathologies of the wrist

De Quervain's disease

De Quervain's disease results from overload and conflict between tendons of the first extensor compartment (abductor pollicis longus – APL, extensor pollicis brevis – EPB) and their pulley at the level of radial physis. It is more common in patients who have a septum between tendons ⁽²⁾. In such cases EPB is more often affected ⁽³⁾.

The initiating factor is first compartment tendon over-load (frequently in mothers carrying babies – baby wrist) which results in tissue irritation and further inflammatory process within the tendinous sheath – tendovaginitis. As a consequence of overuse an inflammatory-fibrous process is initiated within the pulley. Thickening and constriction of the pulley is a sequelae of that process. A cycle of microtears and repair results in pulley degeneration. Hypertrophy of the pulley restricts the tendon which may result in decreased tendon glide. Not every case of tendovaginitis of the first extensor compartment results in pulley thickening and constriction. The disease may occur in rheumatoid patients. Up to 0.5% working men and 1.3% working women are affected. In women, menopausal age, pregnancy and early motherhood are predisposing factors. The disease is unrelated to hand dominance ⁽⁴⁾ (fig. 1).

Fig. 1.

The painful zone in de Quervain's disease

Patients complain of pain at the level of the styloid process of the radius during pronation or supination, grip, clenching fist and compression. Pain is generated in the retinaculum, which is compressed or stretched. The tendons are thickened above and below the retinaculum. Patients may continue to function normally with chronic microtearing and repairing of the retinaculum. In normal conditions tendons glide stretching the pulley evenly. Hypertrophy and stiffening of the pulley constricts the tendons and results in stretching of the pulley producing microtears and pain. When the thickened part of the tendon passes through the pulley the patient may report a click. Recurrent microtrauma and a disorganized repair process results in tissue degeneration of both the retinaculum and tendons.

US is the method of choice in the diagnosis of de Quervain's disease. In longitudinal and transverse scans thickening of the pulley is observed. Usually there is no synovial effusion and synovial thickening. Pain may result in limitation of normal hand movements. US can determine if the whole retinaculum or only one compartment (in the case of a septum) is ill. On longitudinal scans stretching of pulley by narrowed and thickened ill tendon (tendons) can be observed in dynamic examination (fig. 2).

Fig. 2.

A thickened/hypertrophied pulley of the 1^st extensor compartment on transverse and longitudinal scan. Effusion, synovial thickening of the tendon sheath with edema/fibrosis of the APL tendon

Intersection syndrome

Intersection syndrome is less frequent than de Quervain's disease. It derives from impingement between tendons of the 1^st extensor compartment (APL and EPB) and tendons of the 2^nd extensors compartment (extensor carpi radialis longus – ECRL and brevis – ECRB) at the level of their crossing and that is approximately 3.5–4.8 cm proximal to the dorsal tuberculum of radius ⁽⁵⁾. Tendovaginitis of both compartments may originally be caused by tendovaginitis within only one compartment. It is typically encountered in rowers, heavy weight lifters, skiers, and persons who repeatedly flex and extend their wrists ⁽⁶⁾. Patients with intersection syndrome complain of mild edema and pain of the distal forearm in the radialdor-sal region and crepitations during flexion and extension of the wrist (fig. 3). With chronicity tendons and their sheaths undergo diffuse fibrosis and microtearing/partial tearing. US is very accurate in delineating this. It is important to define whether the tendon or tendons are partially torn or fibrosed. In partial tears steroid injections should be avoided as the reparative process is impaired by corticosteroids. Immobilization is the treatment of choice with torn tendons. Improper healing may lead to massive fibrosis or tendon rupture.

Fig. 3.

Scheme of the painful zone at the 1^st/2^nd extensor compartment crossing

On US the tendon sheaths of the intersecting tendons demonstrate fluid with thickening of the synovial membrane. With chronic intersection syndrome there are microtears with fibrosis resulting in scarring with alteration of the fibrillar tendon structure.

The presence of anechoic zones within the tendon without internal vascularity indicates mucoid degeneration and therefore increased risk of rupture. Degenerative scars removed from patients’ tendons histologically demonstrate the presence of low cellularity and glass-like degeneration with tissue decomposition. In severe cases necrosis may be seen. Increased vascularity on Doppler indicates the presence of rebuilding and hyperactive tissue, i.e. a healing process, rather than an inflammatory process. Corticosteroid injections may inhibit the healing process and create even more degeneration. So even if the patient experiences less pain after steroid injection it may be that the severity of disease has increased.

Wartenberg's disease

The disease results from the irritation of the superficial branch of the radial nerve. The problem may occur as a sequelae of radial vein inflammation at the level it pierces the fascia, i.e. 60 mm proximally of the radial styloid process tip, as well as a iatrogenic injury or postsurgical scarring or instrumentation after fracture stabilization.

Patients with Wartenberg's disease complain of pain, numbness and paresthesia of the distal radial-side of the forearm as well as wrist and thumb (fig. 4).

Fig. 4.

The innervation zone of the superficial radial branch

On high-resolution US examination the superficial branch of the radial nerve is very well defined along nearly all its course, down to the metacarpal level. In the distal 3^rd of the forearm, 80 mm proximal to tip of the radial styloid process, the nerve lies laterally and posteriorly of the radial artery. Under the brachioradialis tendon, and between the brachioradialis and ECRL the nerve pierces the fascia at the margin of the EPB. Further down it lies in the subcuta-neous fat on the surface of the APL and EPB near the radial vein. Distally the nerve divides into dorsal nerves of fingers.

The nerve should be assessed in longitudinal and transverse planes. Precise definition of the nerve lesion or the location of the stumps location is very important in the treatment planning process (fig. 5).

Fig. 5.

Superficial branch of the radial nerve entrapped by scar: A. distal to scar; B. proximal to scar

Osteoarthritis of the 1^st carpometacarpal joint

Osteoarthritis of the 1^st carpometacarpal joint occurs six times more often in women than in men, mostly in the postmenopausal age ⁽⁷⁾. Narrowing of the joint space, cartilage destruction, subchondral bone destruction and deformity of the thumb base may be observed.

It has been suggested that capsuloligamentous laxity in young and middle aged leads to joint subluxation and early osteoarthritis. Thumb trauma and rheumatoid arthritis (RA) may influence the course of the disease ⁽⁷⁾.

Patients complain of pain at the base of thumb radiating to metacarpophalangeal (MCP) joint, and weak grip during everyday activities such as holding large objects, twisting off caps and writing. Gradually the thumb grip weakens and thumb motion decreases.

US examination may detect synovial membrane inflammation (effusion, swelling, increased vascularity), erosions and cysts as well as proliferation of bone margins. US examination may allow differentiation between osteoarthritis and de Quervain's disease (fig. 6).

Fig. 6.

Degenerative changes in the 1^st carpometacarpal joint: A. X-ray; B, C. ultrasound osteophytes, cartilage destruction and joint space narrowing with thickening and synovial hypervascularity

Traumatic lesions in extensor tendons

Boutonniere deformity

Flexion deformation of the finger in the proximal interphalangeal joint (PIP) is the sequelae of a tear of the central band of the extensor digitorum/digiti minimi which attaches to the dorsal side of middle phalanx base. At the level of distal interphalangeal joint (DIP) the finger remains extended or hyperextended due to domination of the lateral bands of extensor anchoring to the base of a distal phalanx.

The boutonniere deformity is diagnosed mostly in RA patients with tears of the central band of the extensor tendon, caused by chronic friction against osteophytes. In other cases the central band may tear during a direct trauma of the dorsal side of finger.

Clinically, the patient cannot extend the PIP joint and flex the DIP joint. There may be some pain and edema at the dorsal side of PIP joint.

US examination can precisely show the extensor tendon and its attachments to both the middle and distal phalanx as well as the joints of the finger. In cases of avulsion fractures of the middle phalanx base (extensor central band attachment) the size of the bony fragment and its location relative to the fracture bed should be determined to aid treatment planning.

Swan neck deformity

In normal conditions flexion in the DIP joint occurs together with flexion in the PIP joint. In swan neck finger deformity the finger flexes in the DIP when all other finger joints remain extended. This type of deformation may be present in the course of RA, less frequently in cerebral palsy or early congenital joint laxity. The cause of deformation is rupture of lateral extensor bands which anchor at the dorsal side of distal phalanx. It is quite often to see avulsion fractures of distal phalanx base. In RA patients the tear results (as in the boutonniere deformity) from friction of tendons against osteophytes. Other cause may be a direct trauma against the tip of an extended finger (volleyball, basketball).

The patient presents a finger flexed in DIP joint and can not actively extend it. At the dorsal side of DIP joint there may be some pain and edema/thickening.

In US examination the structure of extensor tendon can be visualized. The site of a tear should be pointed out. If avulsion fracture is present the distance between bony fragment and its bed should be determined. All finger joints should be scanned to determine presence of erosions and osteophytes. Dynamic examination rarely shows retracting stump. More often an elongated scar. It is useful when a bony fragment is fractured from insertion. The exam in non-RA patients should be performed as soon after injury as possible to optimize the treatment with good chance to complete healing without operative intervention (fig. 7).

Fig. 7.

Extensor tendon tear at the level of the middle phalanx head. Normal extensor tendon on the right image

Sagittal band injuries (Boxer's knuckle)

The disease is a subluxation of the extensor digitorum/digiti minimi tendon at the MCP joint due to a tear of the sagittal band or bands. Sagittal bands connect the extensor tendons to collateral ligaments and to the volar plates of the MCP joints. Most common reason for sagittal band tear is a direct injury, usually to the radial band. Subluxation may also result from degenerative changes of the sagittal band, inflammatory changes in the course of RA, may be congenital.

Patients complain of pain and edema at the MCP joint as well as range of motion decrease

At US examination the extensor and sagittal band should be assessed in longitudinal and transverse scans. Torn sagittal band is thickened and hypoechogenic. Hyperperfusion may be seen within repairing tissues. As a result of the band thickening and diffused fibrosis of tissues the tendon's movement may be impaired (fig. 8). In cases of complete tear of the sagittal band the subluxation/luxation of extensor tendon is seen, especially during flexion of the MCP joint.

Fig. 8.

On the left a partial tear of the sagittal band and edema of the extensor tendon. On the right contralateral normal tendon and its sagittal band

Tumors and tumor-like lesions

Ganglia

Ganglia are most common tumor-like lesions of the hand. They are filled with fluid or jelly and localized near joints and tendons. It is suspected that they appear as sequelae of a trauma or overstretch of capsule-ligamentous structures, which induces mucine production breaking outside the joint or sheath. Ganglia are most common in women at the age of 20–40 ⁽⁸⁾.

In most cases ganglia are painless and well palpable. Some appear or grow bigger after an exercise and intensive hand use and disappear or become smaller during low activity periods. High-pressure ganglia are formed when a valve allows the fluid to get into a ganglion and prevents it from going back. Joint fluid entrapped in a ganglion is dehydrated in time and then it becomes dense, jelly-like.

Published data show that most ganglions are lobulated with irregular margins ⁽⁸⁾. In our practice simple ganglia are more common. The most common site for them to appear is dorsal side of the wrist. Some may be a result of dorsal scaphoid-lunate ligament or dorsal capsule of the wrist tear. Ganglia if supplied with fluid may expand between extensor compartments into the subcutaneous tissue (fig. 9). They may become large as the tissue pressure of the dorsal wrist is low. They may arise from flexor tendons sheaths.

Fig. 9.

Ganglion of the dorsal wrist arising from radioscaphoid joint, localized between the two wrist extensors (arrows)

US examination allows to visualize ganglia and in 25% of them their origin ⁽⁸⁾. Increased vascularity in the ganglion wall may be a result of a recent tear and indicates presence of repairing process, not inflammatory one. In differentiation a benign tendinous sheath tumor (giant cell) should be considered (see below).

Tumors

Majority of hand tumors are benign. Ganglia are the most common lesions. Other commonly encountered lesions are giant cell tumors of the tendinous sheath, lipomas, pseudoaneurysms, schwannomas, glomus tumors, vessel malformations and Dupuytren's contracture ⁽⁹⁾.

Malignant tumors are rare.

Patients usually present with a visible mass in the hand. Depending on the location tumors may compress surrounding structures and cause limitation of motion. Tumors near the nerves may cause neurological symptoms. Glomus tumors in the typical localization under the nail will produce exquisite pain when compressed or cooled.

US allows us to define the localization, echostructure and vascularity of the lesion as well as its relation to other structures.

Giant cell tumors usually originate from the tendon sheath. It is a well-defined solid mass close to the tendon or joint, which may show increased vascularity. It may appear like the less common fibroma. Connection of the tumor with the sheath is pathognomonic. Bony erosion and tendon subluxation may occur.

Lipomas usually appear on the volar side of the hand, most frequently around the thumb base and hypothenar eminence ⁽¹⁰⁾. They are compressible, and do not show increased vascularity (fig. 10).

Fig. 10.

Lipoma around the thumb base

Pseudoaneurysms may arise from trauma of arteries or veins. They may be filled with blood or clot.

Schwannomas and neurofibromas are benign tumors of the peripheral nervous system (figs. 11 and 12). Schwannomas grow as round or oval, hyperperfused hypoechoic lesions attached to the nerve. There is posterior acoustic enhancement. Traumatic neuromas are a result of microtearing of nerve fibers with subsequent fibrosis. They may be multifocal or diffuse. Glomus tumors arise from neuroarterial structures and typically grow in the nail bed. They usually occur in the 4^th–5^th decade of life ⁽¹⁰⁾ (fig. 13).

Fig. 11.

A. Schwannoma. B. Nerve at the edge of schwannoma

Fig. 12.

Hamartoma at the level of hand, volar side

Fig. 13.

Glomus tumor modeling distal phalanx

Dorsal side pathologies

Carpal tunnel syndrome

Carpal tunnel syndrome results from median nerve compression at the level of transverse carpal ligament.

In many cases it is difficult to define a reason for the compression. Median neuropathy at the carpal tunnel level may be due to repetitive microtrauma of the transverse carpal ligament leading to fibrosis and thickening and therefore narrowing of the tunnel. Tunnel narrowing may be congenital, posttraumatic, inflammatory or due to presence of abnormal structures within. Diabetics, alcoholics and patients with amyloidosis are also prone to develop carpal tunnel syndrome. It has been observed that fluid retention during menopause, pregnancy and in hormonal disorders may trigger symptoms from the median nerve.

Patients complain of paresthesia in digits I–III and radial side of IV, pain in the wrist radiating proximally and distally, weakening of the muscles and inability to hold objects. There may be night pain which may or may not disappear after shaking the hand.

US assessment focuses on median nerve structure and size around and within the carpal tunnel. Nerve edema is seen just proximal to the carpal transverse ligament. In cross-section the nerve becomes more rounded, with low echogenicity and loss of the fascicular structure of the nerve. In severe cases hypervascularity of the edematous part of the nerve is demonstrated (fig. 14). The threshold for pathological thickening of the nerve above the tunnel is not universally accepted. The range in published data is 10–15 mm². In our practice a value of 12 mm² after a manual delineation of the inner nerve (without the perineurium) seems a good criterion. Predefined ellipses should not be used for cross-sectional nerve assessment. Another good criterion of nerve thickening is a comparison of the cross-section at the pronator quadratus and proximal to the transverse ligament. The difference should not be greater than 2 mm² in a single bundle nerve, and 4 mm² in a double bundle. Narrowing of the nerve at the level of the transverse ligament is subjective and of less use than measuring nerve thickening. There are cases when the nerve is compressed in the distal part of tunnel (fig. 15). Hyperperfusion detected on Doppler examination of the nerve is not always present but pathognomonic for neuropathy. In normal conditions blood vessels are not present on Doppler. Information regarding anatomical variants are important to the surgeon. The presence of an artery along the nerve is not regarded as pathological. Thrombosis of the artery within the tunnel is a rare reason for presence of symptoms ⁽¹¹⁾.

Fig. 14.

Median nerve edematous proximally to the tunnel: transverse (1), longitudinal (2). Normal contralateral (3, 4)

Fig. 15.

Neurofibroma of the median nerve distally from the carpal transverse ligament

Trigger finger

Trigger finger is one of the most common conditions in hand surgery. It is diagnosed in up to 2.2% of population, usually in patients above 30 years old. It is seen in up to 10% of patients with type 1 diabetes⁽¹²⁾. Normal movement of digital flexor tendons is supported by fibrous pulleys of the tendons sheath. In digits II–V there are five annular pulleys (A1–A5), and in the thumb there are three (A1–A3) (fig. 16).

Fig. 16.

Diagram showing the location of DII–V finger annular pulleys

Trigger finger is a condition of the A1 pulley and is the finger equivalent of de Quervain's disease. In some cases of tendovaginitis induced by overload the A1 pulley undergoes diffuse fibrosis resulting in thickening and contracture on flexor tendon/tendons. Impingement between tendons and pulley cause pain ⁽¹³⁾. Like in de Quervain's disease the tendon stretches the pulley when the finger flexes or extends. Microtears with inadequate repair leads to degeneration of the tissues.

Patients complain of pain during motion. When the resistance during flexion is overcome there is a painful click. This corresponds to the moment that the thickened tendon outside the pulley passes under the thickened pulley. The tendon may become entrapped and may require manipulation to reduce.

On US examination pulley thickening is seen. Frequently the pulley is hypervascular (fig. 17). The affected tendon may be thickened and hypervascular, and in later stages becomes fibrotic. There may be inflammatory changes in the tendinous sheath. On dynamic examination a pulley stretched by the tendon can be observed.

Fig. 17.

Thickened DIV A1 pulley: longitudinal (A), transverse (B). The pulley is hyperperfused due to inflammatory-reparative process

Disease of the flexor carpi ulnaris (FCU)

The distal tendon of the FCU does not have a sheath and may suffer from tendinopathy ⁽¹⁴⁾. FCU tendinopathy appears in 1–2% population, more frequently in 4^th and 5^th decade of life ⁽¹⁵⁾. There is pain at the pisiform insertion of tendon. Structural changes appear as result of overuse with recurrent microtears. Tissues undergoing repair have an increased level of fibroblasts and vessels, referred to as angiofibroblastic hyperplasia.

On US examination varying amounts of scar tissue may be present. Frequently there is enthesopathic change with mineralization (fig. 18). On Doppler increased vascularity may be present. The ultrasound assessment of FCU tendinosis is more precise than on X-rays.

Fig. 18.

Mineralization at the pisiform enthesis of the FCU

Guyon's canal syndrome

Ulnar neuropathy may result from its compression at the level of Guyon's canal. Possible causes of the Guyon's canal syndrome are primary nerve tumors within the canal (ganglia, lipomas, giant cell tumors), anatomical variants/ anomalies (accessory abductor of the little finger, accessory palmaris longus muscle), aneurysms or thrombosis of the ulnar artery, and compression neuropathy resulting from sports or walking with a cane ⁽¹⁶⁾ (fig. 19).

Fig. 19.

Ulnar nerve pushed medially in the Guyon's canal by a ganglion arising from the triquetrum-pisiform joint

Clinically sensory or sensory-motor or motor symptoms depend on the level. In long-standing nerve damage muscle atrophy and grip-strength loss may occur.

US can delineate the structure of the ulnar nerve in and around Guyon's canal, the level of the division of the nerve, the hook of the hamate (deep branch of the nerve). Hamate hook fractures should be identified on X-ray ⁽¹⁷⁾. The ulnar artery should be assessed as well as walls of the Guyon's canal.

Nerve trauma

Nerve damage in the hand occurs most often due to direct trauma. Rarely the cause is iatrogenic – either by cutting or chronic compression.

Clinical symptoms depend on the degree of damage, ranging from sensory disturbance to serious neurological disorders distal from the damage zone.

It is important to report the level of the nerve damage, detailing the nerve integrity, and surrounding structures. In cases of nerve discontinuity the level of the stumps should be reported (fig. 20) ⁽¹⁸⁾. US has a very important role in treatment planning.

Fig. 20.

Total tear of the median nerve: proximal stump with a neurofibroma (1), distal stump (2), distance between stumps (3)

Conflict of interest

Authors do not report any financial or personal links with other persons or organizations, which might affect negatively the content of this publication and/or claim authorship rights to this publication.