Me

Fig. 5.47 a,b

Cubital tunnel syndrome.a Short-axis US image of the cubital tunnel demonstrates the ulnar nerve (curvedarrow) which appears increasingly swollen and hypoechoic with absent fascicular pattern. Note the irregular appearance of the bony outlines of the medial epicondyle (ME) and the olecranon process (0) and the elevated floor of the tunnel due to bulging of synovial pannus (*) from the trochlea-ulna joint (whitearrow).b Schematic drawing over the short-axis of the cubital tunnel illustrates the mechanism of nerve compression

Ulnar neuropathy may also result from chronic synovitis, such as in hemophilic arthropathy. In late stage rheumatoid arthritis, some degree of elbow instability related to the inflammatory derangement of joint structures and disruption of the medial collateral ligament or following total elbow arthro-plasty may contribute to entrapment of the ulnar nerve in this area [81].At a more distal location, the ulnar nerve may be occasionally compressed by large effusions arising from the distal radioulnar joint and synovitis around the piso-triquetal joint and the hook of the hamate (Fig. 5.48).

In the lower limb, possible sites of nerve compression include the hip area for the femoral nerve, the popliteal fossa for the peroneal nerve and the tarsal tunnel for the tibial nerve. In the anterior hip, the iliopsoas bursa is a large synovial-lined communicating bursa which lies between the posterior aspect of the iliopsoas muscle and tendon and the anterior capsule of the hip joint [82]. The iliopsoas bursa primarily acts as a reservoir in cases of abundant joint effusions to limit the damage to the intra-articular structures related to a high intra-articular pressure (Fig. 5.49 a). When the bursa is filled with synovial pannus, such as in long-standing rheumatoid arthritis, it appears as a para-articular mass with internal hyperechoic solid components and expand to a large size because of the slow progression of the disease process [83].With severe joint synovitis the bursa can expand toward the pelvis superficial to the iliopsoas muscle or in between the iliac bone and the iliacus muscle, possibly causing compression of the femoral nerve that courses under the fascia of the iliacus (Fig. 5.49 b, c) [83,84].

Somewhat similar to the iliopsoas bursa, the abnormal distension of the semimembranosus-gastrocnemius bursa (Baker cyst) in patients with long-standing rheumatoid arthritis has been reported as a cause of peroneal nerve compression at the posterior knee [85]. At the medial ankle, the tibial nerve and its divisional branches (plantar nerves) travel in the tarsal tunnel between the flexor hallucis longus and the flexor digitorum longus tendons covered by the flexor retinaculum [77]. Because the synovial sheath of the flexor hallucis longus tendon often communicates with the ankle joint, an effusion surrounding this tendon more likely reflects the joint disease rather than a tendon abnormality, especially when considerable ankle joint involvement is present. In these cases, the nerve may be stretched and entrapped by the distended sheath in the retromalleolar region. Marked distension of the medial recesses of the subtalar joint by synovial pannus and effusion may also cause extrinsic compression and disturbances of tibial nerve function (Fig. 5.50).

Diabetes mellitus is one of systemic disorders associated with neuropathy. In this disorder, nerves are more vulnerable as they traverse osteofibrous tunnels. In diabetic patients with tarsal tunnel syndrome, the cross-sectional area of the tibial nerve is significantly larger compared with normal subjects and asymptomatic diabetics [86].

Ulnar neuropathy secondary to marked synovitis of the distal radioulnar joint and mild symptoms of ulnar neuropathy.a Photograph demonstrates considerable soft-tissue swelling (arrows) over the dorsoulnar aspect of the patient's wrist.bTransverse US image over the ventral aspect of the wrist reveals prominent synovitis (*) leading to displacement of the ulnar nerve (arrow) against the flexor carpi ulnaris (FCU).c Schematic drawing correlation.Arrowhead = ulnar artery

Ulnar neuropathy secondary to marked synovitis of the distal radioulnar joint and mild symptoms of ulnar neuropathy.a Photograph demonstrates considerable soft-tissue swelling (arrows) over the dorsoulnar aspect of the patient's wrist.bTransverse US image over the ventral aspect of the wrist reveals prominent synovitis (*) leading to displacement of the ulnar nerve (arrow) against the flexor carpi ulnaris (FCU).c Schematic drawing correlation.Arrowhead = ulnar artery

Femoral neuropathy related to hip joint synovitis.a Iliopsoas bursitis.Schematic drawing of a transverse view through the hip illustrates the mechanism of compression of the femoral nerve (large arrow) by an effusion located within the iliopsoas synovial bursa (*).The joint cavity communicates with the bursa through a thin pedicle (curved arrow).Note the anterior recess filled with fluid,the iliopsoas muscle (IPs) and tendon (white arrow). Empty arrow=anterosuperior labrum; a = femoral artery; b = femoral vein. b Transverse US image with (c) GRE T2* MR imaging correlation over the anterior inferior iliac spine reveals proximal migration of the synovitis (*) leading to an indirect compression of the femoral nerve (empty arrow) which courses under the fascia of the iliacus muscle

Fig. 5.50 a-c

Tarsal tunnel syndrome.a Schematic drawing of a sagittal view through the ankle illustrates the relationships of the tibial nerve (dashed lines) with the anterior (1) and posterior (2) recesses of the ankle joint,the posterior recess of the subtalar joint (3) and the flexor hallucis longus (FHL). Note the communication between the posterior recess of the ankle joint and the sheath of the flexor hallucis longus. b Tibial neuropathy in a patient with rheumatoid arthritis and remarkable distension of the sheath (*) of the FHL tendon by synovial pannus.The tibial nerve (arrow) and the posterior tibial artery (a) appear displaced by the synovial process. c Tibial neuropathy in a patient with rheumatoid arthritis and marked subtalar joint synovitis. Note the synovial tissue (arrowheads) as it projects within the tarsal tunnel between the flexor digitorum longus (FDL) and the FHL tendons leading to a displacement of the tibial nerve (arrow) and the posterior tibial artery (a) and vein (v). tp = tibialis posterior; MM = medial malleolus

5.12 Sport and rheumatology

The musculoskeletal system of athletes is submitted to continuous stress, both during training and when competing, so that it is exposed to the risk of trauma. A post-traumatic injury occurs when the athletic exercise involves a movement that overcomes the resistance limit of a musculo-tendinous structure, ligament, bone or joint. Exceeding resistance threshold of a specific anatomical structure may be caused both by acute (macrotraumas) pathogenetic mechanisms and chronic (repeated microtraumas). In the first case, the injury is the result of a repeated highly energetic movement carried out by the athlete, that eventually produces functional overload (overuse syndrome). The repetitive performance of an incorrect athletic movement promotes the occurrence of the lesion, especially in inexperienced and poorly trained athletes, or in athletes presenting with pre-existing musculoskeletal conditions which reduce the resistance threshold to mechanical load.

Acute lesions, instead, occur in a precise mechanical moment (falls or direct impacts) that produces immediate and painful lesions that necessitate interruption of the sport activity.

Lesions can therefore be divided into two types:

• Chronic lesions due to repeated functional overload (overuse syndromes).

• Acute lesions caused by macrotraumas (falls or direct impacts).

Functional overload pathology

Functional overload pathologies, or overuse syndromes, correspond to a range of musculoskeletal system conditions caused by a single pathogenet-ic mechanism represented by a continual micro-traumatic event occurring repeatedly on the same anatomical region. Repeated and highly intense athletic movement alters the delicate balance between the necessary working load for training and the capability of biological and mechanical functional recovery. Therefore, the continual repetition of some athletic movements can lead to a specific musculoskeletal condition, characterized by the overlap of several repeated microlesions. The lesions caused by microtraumas can accumulate because they are asymptomatic in early phas es and it is only later that they present with pain and sometimes with functional limitation. A micro-traumatic event occurs when the load applied to an anatomical structure overcomes its resistance limit. If energy remains the same, the severity of the lesion is inversely proportional to the resistance limit of the structure. Obviously an anatomical structure already damaged by previous microtraumas is more easily exposed to the risk of new lesions. Similarly, systemic metabolic and rheumatic conditions, together with ageing, may weaken some body regions and make them easy targets for micro- or macrotraumas [87]. In such cases, while evaluating a pathologic finding, the sonog-rapher should always consider a differential diagnosis of simple functional overload cause, pre-existing rheumatologic cause or both.

The functional overload may involve a bone segment, a joint or, more frequently, a musculo-tendinous functional unit.

The most frequent pathological findings in sport-related overuse syndromes are represented by tendon degenerative and inflammatory diseases, enthesopathies and bursitis. US is the imaging technique of first choice for the evaluation of an athlete's musculo-tendinous pathology. In tendinopathy the US appearance has a non-specific pattern and cannot be distinguished from analogous tendinopathies. Specific features in athletes include the lesion location, the performed athletic movement and the type of sport activity. The application of power and color Doppler techniques is useful because it adds important "functional" information on tendon perfusion and allows the evaluation of therapy response. The "functional" information is derived from the intensity of signal found.

Insertional tendinopathy of adolescent athletes has more specific characteristics. During growth the weakest anatomical region is found at the cartilage growth plate, where functional overload can causes damage to the growing cartilage (apophysi-tis) rather than tendinopathy. The typical alteration associated with apophysitis is represented by chon-dritis and consequent alteration of the growing enchondral ossification center, which appears typically fragmented.

A stress fracture may occur when athletic movements are performed repeatedly over a long period of time and at increased working loads.

Bone is a biologically active tissue with slow metabolism, and repairs lesions over a longer time than muscles and other tissues with faster metabolism. Even physiological load in sport, when repeated over a long period of time and in the presence of intrinsic (for example, size of a bone segment) and extrinsic (type of shoes, ground, etc.) factors, can be responsible for lesions involving the musculoskeletal system and particularly bone. When an excessive load is applied to a bone segment and the requested adaptation overcomes normal physiology resorption activity may outweigh the formation of new bone until a fracture occurs. A stress fracture is diagnosed when a fracture line is detected on a plain radiograph. Stress fractures alone represent 10% of all sport injuries. Considering this high incidence, the role of radiology is very important in detecting stress fractures because there are several conditions to be considered as differential diagnosis (tendino-pathies, reactive periostitis, muscular lesions, tumors). The distribution of lesions changes according to the type of activity and the specific athletic movement. The tarsal scaphoid is often injured in track and field specialties that involve hurdles and jumping; metatarsal and pelvic bones in running, mainly long distance; tibia and fibula in sprints, middle distance and hurdling.

Osteo-cartilagineous lesions or associated canalicular syndromes may be caused by excessive and repeated articular impact; similarly repeated friction may involve a nearby nervous structure.

Particularly in early phases, a conventional radiograph may show no fracture line; in this case it is necessary to perform further investigations such as scintigraphy, CT and particularly MR imaging. US has very limited usefulness because it can only rarely confirm fracture with the typical irregular cortical focus surrounded by a hypoechoic paraosteal edema and sometimes, a defined periosteal reaction thickening (Fig. 5.51).

Stress fracture of the diaphisis of 2nd metatarsal bone. a The plain film shows the periostal reaction (arrow) at the site of frac-ture.The fracture line cannot be seen. b Standard US examination shows a hypoechoic halo (calipers) that wraps the 2nd and part of the 3rd metatarsal bone.This is related to soft tissue edema. c The color Doppler scan shows a color spot inside the paraosteal edema.The MR scan T1 W,pre- and post-gadolinium) shows the metatarsal periostosis at the site of fracture and the paraosteal edema (*). It appears hypointense before gadolinium (d) and hyperintense after gadolinium (e) (courtesy of Dott. Antonio Barile)

Stress fracture of the diaphisis of 2nd metatarsal bone. a The plain film shows the periostal reaction (arrow) at the site of frac-ture.The fracture line cannot be seen. b Standard US examination shows a hypoechoic halo (calipers) that wraps the 2nd and part of the 3rd metatarsal bone.This is related to soft tissue edema. c The color Doppler scan shows a color spot inside the paraosteal edema.The MR scan T1 W,pre- and post-gadolinium) shows the metatarsal periostosis at the site of fracture and the paraosteal edema (*). It appears hypointense before gadolinium (d) and hyperintense after gadolinium (e) (courtesy of Dott. Antonio Barile)

Pathologic conditions

Lower limb

In runners, overuse syndromes exclusively affect the lower limb. Overload lesions consist almost exclusively of insertional tendinopathies and US is the investigation of choice. The following tendon insertions may develop overuse syndromes: the rectus femoris muscle insertion on the anteroinferior iliac crest (Fig. 5.52), the adductor muscles (responsible for pubalgia) and the flexor muscles of the knee (the socalled hamstring muscles). All of these cases have a US pattern consisting of typical insertional tendinopathy, in which the inser-tional tract appears thickened, inhomogeneous and hypoechoic and may show intratendinous pre-insertional calcification at a late stage [88]. MR imaging is necessary in therapy-resistant cases, to detect possible inflammatory involve ment of the bone at the tendon insertion (stress response) [89].

A very common tendinopathy in competitive athletes as well as amateurs, is Achilles tendinopathy [90]. There can be several conditions that involve the Achilles tendon, such as tendinitis, tendi-nosis, mixed forms (peritendinitis occurring on tendinosis), tendon ruptures and enthesopathies, but they can vary from patient to patient, depending on the evolutional phase of the pathology [91]. US is able to correctly identify tendon structure alteration and possible associated deep infracal-caneal bursitis and/or a superficial retrocalcaneal bursitis [92]. The power Doppler technique complements the standard US examination and can detect the degree of inflammatory hyperemia (and its change at follow-up), together with identyfing the peritendinitis and differentiate it from the mixed form of peritendinitis occurring on tendi-

Insertional tendinopathy of rectus femoris on the antero-inferior iliac crest. a The longitudinal US scan shows complete disarray of the tendon echotexture with rough calcification (arrow). b The power Doppler scan,complementing the information obtained with grayscale US shows some vascular spots, related to inflammatory hyperemia. c The plain film shows the insertional calcific metaplasia of the tendon (arrow) on the antero-inferior iliac crest nosis (Fig.5.53) [93-95]. In addition, the US diagnosis of Achilles overuse syndrome is of great importance, because it represents a severe risk factor for the spontaneous rupture of the tendon itself. Factors predicting rupture are the presence of focal hypoechoic zones and sagittal tendon thickness greater than 10 mm.

Such a US pattern may suggest that the rheuma-tologist includes metabolic causes of tendinosis in the differential diagnosis, such as gout and hyper-cholesterolemia. Both conditions cause thickening of the Achilles tendon due to the accumulation of deposits of uric acid and cholesterol, respectively (tendon xanthomatosis).

With the advent of US the role of conventional radiology for the study of achillodynia and thallo-dynia has diminished and has been exclusively directed to the study of bone for the detection of postero-superior calcaneal tuberosity hypertrophies (Haglund disease). This anatomical variant promotes the onset of insertional Achilles tendi-nopathy, which is often associated with bursitis and edema of the calcaneal spongy bone at the insertion site (Fig.4.40).

It should be kept in mind that an Achilles enthe-sopathy may be the sign of a systemic entheso-arthritis, such as psoriatic arthritis and Reiter dis ease, whose onset may be the consequence of mechanical impact; this hypothesis should be particularly considered in case of bilateral achillody-nia and of past arthralgia and enthesalgia, even if just transitory and in other sites (Fig. 5.54).

In these cases, the role of ultrasound is to detect the presence of an enthesitis in early phases, showing reduced echoes and a clear increase of the thickness at the insertional tract compared to the mid-distal tract. The comparison of the two sides usually does not add information since the condition may be symmetrical and bilateral [96]. The plain radiograph can be instead very useful to detect cal-caneal spurs in more advanced phases.

Ilio-tibial band inflammation, also known as "marathon runner's knee",is a syndrome represented by the friction of these structures on the lateral femoral epicondyle, caused by repeated flexion/extension of the knee during running. This syndrome is characterized by pain along the lateral aspect of the knee, so that a condition affecting the lateral meniscus should be considered in the differential diagnosis. The inflammation may first involve only the ilio-tibial band and afterwards spread around the nearby soft tissues and the synovial bursae.

The ilio-tibial band appears at ultrasound as a hyperechoic lamellar structure adjacent to the lat

Fusiform thickening of the Achilles tendon with disarray of the fibrillar echotexture typical of tendi-nosis (a).The power Doppler scan (b) shows several color spots depending on the peritendinous inflammatory hyperemia

Fusiform thickening of the Achilles tendon with disarray of the fibrillar echotexture typical of tendi-nosis (a).The power Doppler scan (b) shows several color spots depending on the peritendinous inflammatory hyperemia

Enthesopathy of the Achilles tendon. a The longitudinal scan shows inhomogeneous echotexture and thickening of the pre-insertional portion of the tendon,on a degenerative basis, with a rough calcaneal spur.Chronic inflammation of the superficial retrocalcaneal bursa with soft tissue thickening is also shown. b The color Doppler scan confirms inflammation of the retrocal-caneal bursa and shows many vascular spots in the tendon eral femoral condyle but, when it is involved in a inflammatory process, it appears thickened and hypoechoic, and often associated with a synovial reaction found between the band and the femoral condyle [97].

In jumpers, overload related musculo-tendi-nous injuries mainly affect the extensor tendons of the knee, producing the so-called jumper's knee. The clinical findings often consist of well localised pain, usually at the lower extremity of the patella, exacerbated by physical activity. The most common site of disease is in fact the proximal insertion of the patellar tendon (about 65% of cases), followed by the superior patellar extremity (25%) and the tibial tuberosity (10%). An accurate history together with clinical data, are often sufficient to derive a diagnosis. The role of diagnostic imaging is still of great importance to exclude the presence of other pathologic conditions presenting with anterior knee pain, often coexisting in these patients, such as bursitis, meniscal pathologies, chondromalacia or pathologies, chondromalacia or Hoffa's fat pad pathology. US is the technique of choice to define the degree of the tendon lesion [98]. Two different conditions can be detected by US: an insertional tendinopathy or a tendinosis, either singularly or co-existant.

Insertional tendinopathy is responsible for pain and it is also the most frequent (about 92% of cases). At US the tendon is inhomogeneous and hypoechoic at its insertional tract, where it appears thickened and widened with a fan-like shape (Fig. 1.13). Hypoechoic foci can be observed at the osteo-tendinous junction, reported to be focal microtears (Fig. 5.56).

In tendinosis, a condition that promotes tendon rupture, the patellar tendon is extensively tick-ened and inhomogeneously hypoechoic, sometimes showing pre-insertional intratendinous calcification [99].

Longitudinal scan of the sole of the foot showing inflammatory thickening (arrows) of the plantar fascia at its calcaneal insertion

Fig. 5.56 a,b a This longitudinal scan of the proximal third of the patellar tendon (T) shows diffuse disarray of the fibrillar echotexture with a small, well-defined, hypoechoic area (arrowheads), related to a partial tear. b The MR scan of the same patient (T2 W turbo spin echo (TSE)) confirms the diagnosis (hyperintense area, arrowhead)

Fig. 5.56 a,b a This longitudinal scan of the proximal third of the patellar tendon (T) shows diffuse disarray of the fibrillar echotexture with a small, well-defined, hypoechoic area (arrowheads), related to a partial tear. b The MR scan of the same patient (T2 W turbo spin echo (TSE)) confirms the diagnosis (hyperintense area, arrowhead)

Fig. 5.57 a,b

Osgood-Schlatter's disease.a Ultrasound allows assessment of the morphostructural alterations of the distal insertion of patellar ten-don,the inflammatory distension of the deep pretibial bursa and the unevenness of anterior tibial apophysis. Power Doppler scan shows a mild hyperemia on the bursal wall and at the tendon insertion.b Plain film of the same patient

In the enthesis of pediatric patients, the apophy-seal cartilage growth plate is a less resistant site in the muscle-tendon-bone functional/ anatomical unit. The mechanical overload occurring in athletes during growth is concentrated almost exclusively on the growth plate, sparing other anatomical sites. For this reason, tendon and ligament injuries are extremely rare in children and adolescents, while overuse syndromes are more frequent and show up with apophysitis. At the knee this may involve the anterior tibial tuberosity (Osgood-Schlatter's disease) or the inferior patellar extremity (Sinding-Larsen-Johansson's syndrome). Both syndromes are characterized by chondritis at the tendon insertion close to the apophyseal ossification center; the growing cartilage shows increased thickness and strong chondro-tendinous junction hyperemia is observed at power Doppler. An adja cent bursitis can be associated. The inflammatory hyperemia together with incorrect repeated movements may cause altered enchondral ossification, and the calcified center may appear bulky and fragmented (Fig. 5.57).

Upper limb

The painful shoulder syndrome in sport is usually a condition secondary to chronic microtrauma acting on the rotator cuff and on the long head of biceps. This condition affects mainly competitive athletes in overhead disciplines, in which the repeated athletic task carried out by the arm has to overcome the acromion-clavicular plane (volleyball, handball, throwing, water polo, swimming, tennis, gymnastics, weightlifting) [100].

Repeated and powerful athletic task, consistent with throwing specialties, produces continual trac tion overload on the rotator cuff tendons, particularly supraspinatus. The final pathological outcome consists of functional loss of supraspinatus that no longer acts to actively stabilize the shoulder and keep the humeral head in position. Consequently, the humeral head tends to go up with friction and impact against the acromial vault. The resulting coraco-acromial impingement syndrome causes a further worsening of the rotator cuff tendinopathy. This pathological condition evolves from a simple insertional tendinopathy of the supraspinatus to a tendinosis followed by rupture. The long head of biceps (tenosynovitis - tendi-nosis) and the subdeltoid bursa (acute bursitis -chronic bursitis) can also be involved [101]. In some sports, such as water polo, which involve maximum external rotation and abduction movements, other types of impingements, such as the postero-superior impingement; and coraco-humer-al impingement (also know as antero-internal impingement) can occur [102].

Another pathological condition caused by shoulder overuse is the long head of biceps tendon or dislocation (Fig. 4.49). This condition is often associated with other lesions involving adjacent structures, such as a complete or partial rupture of the subscapular tendon or, more rarely, an isolated rupture of the cora-cohumeral ligament [103].

In shoulder pain the diagnostic path is chosen mainly depends according to the patient's age and clinical presentation. Initial investigations include conventional radiology and US looking for calcium deposits in peri-articular soft tissues, and the site and the severity of the main injury affecting tendons and/or bursa respectively (Fig.5.58).A stable, non-surgical, painful shoulder, therefore, can be monitored with conservative therapy by means of US, complemented by power Doppler [104].

In case of a young competitive athlete presenting with unstable painful shoulder, the gold standard examination is arthroMRI, which is the only investigation able to point out a possible injury to bones, glenoid labrum, intracapsular tendons and ligaments.

A well-known example of tendinopathy affecting the upper limb is "tennis elbow", consisting of edema and swelling of the common epicondylar insertion of the extensor-supinator muscles and particularly of the extensor carpi radialis brevis. The epitrochleitis, also known as "golfer's elbow", is the most common cause of pain reported at the medial aspect of the elbow with involvement of the common epitrochlear insertion of the flexor/pronator muscles.A correct diagnosis of epitrochleitis is usually made with an accurate history together with an attentive clinical examination. Diagnostic imaging, including conventional radiograms, US and MRI, can be used as a complement to the clinical findings or in therapy-resistant cases. Plain film may show insertional calcifications and bone erosions.

Rough calcification of the supraspinatus tendon at its insertion.a US and (b) plain film

Rough calcification of the supraspinatus tendon at its insertion.a US and (b) plain film

US is able to detect insertional tendon thickening and corresponding degenerative alteration, appearing as hypoechoic spots often associated with an irregular appearance of the cortical bone and with intratendinous micro and macrocalcifications [105]. The use of Doppler techniques can add further information regarding the inflammatory hyperemia (Fig.5.59).

It is important to keep in mind that when facing therapy-resistant cases (4-10% of all cases), the physician should verify that the epicondylar pain is not due to a ligament injury in an unstable elbow; in such cases an MR examination should be performed. US is also able to confirm the hypothesis of bursal inflammation and identify contents (plain fluid in reactive and post-traumatic collections, corpuscular fluid in bacterial collections, complicated by synechiae and synovial hyperplasia in rheumatic conditions). Power Doppler analysis of the synovial proliferation allows further information on the presence and amplitude of inflammatory hypertermia.

In athletes performing repeated throwing inser-tional wrist tendinopathy is observed in some cases, particularly affecting the flexor carpi ulnaris, an anchor tendon inserting onto the pisiform. US may show focal thickening of the tendon at its insertion on the pisiform and disrray of the typical fibrillar pattern [107].

De Quervain's disease is a tenosynovitis of the

1st compartment of extensors, or rather of the abductor longus and extensor pollicis brevis tendons, as they run along the radial styloid. The pathogenesis relates to overuse of the thumb or wrist, caused by continual friction against the corresponding retinaculum. This often follows repeated and abrupt movements of abduction of the thumb and of ulnar deviation of the wrist (such as skiing and other sports involving the use of poles) [108]. The US pattern of De Quervain's disease is strictly related to its clinical stage. The early US finding consists of non-specific exudative tenosynovitis, mildly hyperemic on power Doppler analysis. In advanced, chronic stages, the main pattern is that of tendinosis, while the inflammatory component appears hypertrophic rather than exudative and, typically, the retinac-ulum gets thicker thereby worsening the impingement with tunderlying tendons (chronic stenosing tenosynovitis) (Fig.5.60).

About 4-6 cm proximal to the radial styloid, the 1st compartment extensor tendons intersect the 2nd compartment tendons (extensor carpi radialis bre-vis and longus), forming a critical anatomical area for the possible onset of intersection syndrome.This syndrome consists of a tenosynovitis affecting patients that carry out a continual flexion and extension of the wrist, such as weightlifters or rowers, and it is clinically characterized by local pain and swelling. The US pattern is characterized by

Lateral epicondylitis (tennis elbow).a The common extensor tendon appears thickened and inhomogeneous,on a degenerative basis.b Power Doppler shows vascular spots at the common extensor tendon insertion

Lateral epicondylitis (tennis elbow).a The common extensor tendon appears thickened and inhomogeneous,on a degenerative basis.b Power Doppler shows vascular spots at the common extensor tendon insertion

The longitudinal extended field of view (EFOV) US scan obtained at the wrist shows a tenosynovitis of the first compartment of the extensors.The sheath (*) is thickened while the tendon structures are intact (T)
The longitudinal US scan of flexor tendons obtained at the finger shows separation of the tendon from the underlying bone (arrows), following a rupture of a pulley.Note the fluid (*)

typical tenosynovial exudative inflammation of the corresponding tendons.

Tenosynovitis of the wrist flexor tendons may result in carpal tunnel syndrome. Even if this is one of the less common causes of carpal tunnel syndrome related to sports, it is still important to evaluate. Trigger finger (or Notta-Nelaton's disease) is a very common disorder consisting of painful clicking that occurs when trying to flex or extend a finger. The pathology of trigger finger is related to a chronic stenosing tenosynovitis affecting the flexor digitorum tendons at the first flexor pulley level. In these cases, a dynamic US examination is very useful to highlight the pseudo-nodular thickening of the tendon sheath.

In rock-climbing, the hand and wrist can be affected by several overuse injuries, the detection of which is essential to correct therapy and to prevent possible severe functional impairment.

The most common overuse syndrome is the flexor tenosynovitis, in which the patient cannot actively flex his/her finger (passive flexion is usually preserved). US is able to demonstrate tendon sheath involvement with assessment of the condition of the tendons and pulleys (whether or not ruptures and/or avulsions have occurred) allows either conservative or surgical therapy to be correctly chosen (Fig. 5.61).

Acute traumatic pathology

Traumatic pathology in sport is an important and extremely interesting subject for the rheumatolo-gist. Athletes are always running the risk of trauma, often occurring by accident, but sometimes due to poor training or to a lack of correct pre-exercise warm-up. Therefore, non-competitive athletes are also exposed to the risk of musculo-skeletal traumas and it is important that rheumatologists, while deriving a diagnosis, keep in mind "sport trauma".

When assessing an acute injury, plain films and US are the imaging techniques of first choice, the latter allows an accurate evaluation of soft tissues, tendons, muscles and ligaments.

Trauma can be classified as follows:

• direct trauma (contusions and impacts);

• indirect trauma (caused by incorrect distribution of mechanical forces: falls, sprains, abrupt or incorrect movements).

Sport-related trauma can produce:

• muscular injuries;

• tendinous injuries;

• ligamentous injuries;

• joint dislocation;

We should keep in mind that all the listed conditions may coexist. In addition, an acute injury can occur within a pre-existing chronic condition.

Acute traumatic pathologies and overuse syndromes should not then be considered different clinical conditions, but two entities that can coexist in the same clinical situation.

Muscular lesions

Acute muscular injuries are the most common lesions occurring in sport-related trauma, with an incidence varying from 10% to 30% of all sport traumas. They are often observed in sports involving running, jumping, abrupt changes of direction and physical contact with other athletes.

Adequate athletic training and pre-exercise warm-up are very important to prevent the occurrence of muscular injuries. There are several factors affecting the occurrence of a trauma, such as a high ratio between muscular belly volume and tendon length, past injury and degenerative disease. Extrinsic factors such as the sport ground hardness, the type of shoes, the temperature and many others should be considered.

A muscular injury can be produced in two ways:

• contusion or direct trauma: occurs when an object strongly hits the muscle (the more contracted the muscle at the impact, the more severe the lesion);

• sprain or indirect trauma: is more common and depends on an abnormal distribution of the mechanical forces on the muscular fibers.

The difference between contusion-derived and sprain-derived muscular ruptures is not limited to the pathogenetic mechanism, but is also based on the clinical findings and on the evolution (more favorable in sprain-derived ruptures).

Muscle ruptures, in both cases, can be classified into three degrees of severity of the injury that has occurred, directly proportional to the clinical presentation [109].

A strain rupture occurs when a sudden pull of the muscular fibers, over their resistance limit, causes tears in the critical weak areas. The most commonly exposed muscles are pennate bi-articular muscles and those muscles with a high white fiber density, whose critical areas consist of the central myo-aponeurotic junction, the myofascial junction, the myotendinous junction and the osteo-muscular junction.

In a 1st degree strain injury only a few fibers are torn within one or some fascicles. Blood extravasation may not be observed (distention) or it may be very minor (minor distraction).

A 2nd degree strain injury (Fig. 5.62) corresponds to laceration of one or more fascicles, involving less than three quarters of the anatomical section of the muscle at the injured level. As a rule, between the lesional edges a hematoma is found, which appears isoechoic during the first 24 hours and becomes hypo-anechoic 24-48 hours after the traumatic event. Follow-up examinations show a hyperechoic wall, growing thicker and thicker until it fills the cavity.

A 3rd degree strain injury corresponds to a lesion involving more than three quarters of the anatomical section of the muscle at the injured level (severe strain), including complete rupture with retraction of the stumps (Fig. 5.63). Blood collection is usually considerable and fills the rupture cavity. The covering fascia may be preserved, although in most cases the hematoma extends by passing through a laceration.

Muscle contusions may present with different US patterns, usually according to the degree of the injury. A 2nd and 3rd degree contusion rupture correspond to severe muscular injury showing irregular muscular fiber tears, inhomogeneously thickened by blood infarction, with a large hematoma occupying the intervening space. At the site of impact increased thickness of the skin and of the subcutaneous tissue can be observed. The muscular fascia (usually seen as a hypere-choic line) shows an irregular pattern. In acute

0 0

Post a comment