Sonographic Examination of Lateral Epicondylitis

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1 David Connell 1 Frank Burke Peter Coombes Stephen McNealy Donna Freeman David Pryde Greg Hoy Received July 11, 2000; accepted after revision September 18, All authors: Department of Radiology, Victoria House Private Hospital, 316 Malvern Rd., Prahran 3181, Melbourne, Victoria, Australia. Address correspondence to D. Connell. AJR 2001;176: X/01/ American Roentgen Ray Society Sonographic Examination of Lateral Epicondylitis OBJECTIVE. The purpose of this study was to describe the sonographic appearance of the common extensor origin in cadavers and asymptomatic volunteers, and to relate this appearance to the findings in patients with lateral epicondylitis. SUBJECTS AND METHODS. Seventy-two elbows in 71 patients with lateral epicondylitis were examined on sonography. Most of the patients (60/71) gave a history of repetitive microtrauma. The injuries were evaluated with respect to location and severity. Focal areas of degeneration, discrete cleavage tears, and involvement of the lateral collateral ligament were identified. Calcification and bony changes were noted. The appearance of the normal common extensor tendon was described, and cadaveric specimens were dissected. Twenty-one patients subsequently underwent surgery. RESULTS. The normal common extensor origin is composed of longitudinal fibrils bound closely with the extensor carpi radialis brevis constituting most of the deep fibers, with the extensor digitorum making up the superficial part. The lateral collateral ligament can be identified as a discrete and separate band. The most common appearance of lateral epicondylitis is a focal hypoechoic area in the deep part of the tendon (46/72). These focal areas were identified at surgery and corresponded histologically to collagen degeneration with fibroblastic proliferation. Often discrete cleavage planes traversing the tendon were manifest as partial (18/72) and complete (2/72) tears. The lateral collateral ligament was involved in eight of 72 elbows. CONCLUSION. Sonography of the common extensor origin can be used to confirm lateral epicondylitis in patients with lateral elbow pain and provide information about the severity of the disease. L ateral epicondylitis, colloquially known as tennis elbow, is generally a self-limiting condition often seen in tennis players, throwing athletes, and tradesmen [1]. The diagnosis is usually clinical and requires no imaging; most patients respond to conservative treatment including rest, physical therapy, antiinflammatory drugs, and steroid injections [2]. However in refractory cases, before considering surgery, the clinician should exclude other causes of lateral elbow pain [3, 4]. Imaging of lateral epicondylitis not only confirms the clinical suspicion but also allows assessment of the severity and location of the injury. Sonography is an operator-dependent test that is relatively inexpensive, accessible, and radiation-free. The advent of high-frequency probes has resulted in improved resolution, allowing application to extraarticular soft tissues for which sonography is increasingly used as an alternative to MR imaging. Our study shows the usefulness of sonography of the lateral epicondylitis. Specifically, the purpose was to describe the sonographic anatomy of the asymptomatic common extensor origin in cadavers and volunteers and the findings in patients with clinical evidence of lateral epicondylitis. We attempted to characterize the location and degree of injury, identify the portion of the common extensor tendon affected, and show involvement of the lateral collateral ligament. To our knowledge, this study is the first to examine sonographic findings in a relatively large series of patients. Subjects and Methods From February 1997 to October 1999, orthopedic surgeons, rheumatologists, and sports medicine physicians referred 76 consecutive patients with lateral elbow pain. There were 51 men and 25 women with a mean age of 45.6 years (age range, years). All 75 patients underwent sonography. Four patients had a normal-appearing common extensor AJR:176, March

2 Connell et al. origin on sonography. One of the four patients had posterior interosseous nerve entrapment. The remaining three of the four patients also underwent MR imaging; one of these three patients had degenerative change of the radiocapitellar joint. In the other two patients with the same types of symptoms, no abnormality was seen on either sonography or MR imaging. Hence, 71 patients and 72 elbows made up the study cohort, and of these, 21 patients went to surgery. One of the patients had bilateral disease. In addition, we studied 10 asymptomatic volunteers (six men; four women; mean age, 36.4 years) and dissected three cadavers to confirm the normal sonographic appearances of the common extensor origin and the complex relationship with the lateral collateral ligament. Sixty patients provided a history of repetitive injury from tennis (n = 30), lifting (n = 15), using a tool (n = 8), typing (n = 4), or other sports (n = 3). Two patients were professional tennis players. Eleven patients could not state any obvious cause of their injury. The initial diagnosis was made on the basis of history and clinical findings and confirmed on sonography. The interval from injury to sonography ranged from 1 day to 9 years (mean, 7.1 months). Patients were examined with a 10-MHz hockey-stick probe (HDI 3000; ATL, Bothell, WA). They were positioned comfortably in a chair with the elbow placed on the examination table in a flexed position; the common extensor origin was examined in both the longitudinal and transverse planes with respect to morphology and echotexture. The examination included comprehensive imaging of the four muscles that make up the common extensor origin, the radial collateral ligament, and the posterior interosseous nerve. The examination time was approximately 15 min. Correlation was made with the opposite elbow in all patients. The size of the tendon was examined relative to the normal elbow. The size was assessed as either normal, enlarged, or attenuated. A tendon was enlarged or attenuated if there was a 10% difference compared with the normal elbow. Tendon echotexture was normal if a uniform fibrillar pattern could be followed from the muscle to the attachment to the lateral epicondyle. Tendinopathy, graded mild (<30% of fibers affected), moderate (30 70%), and severe (>70%), was present if there was loss of this normal fibrillar pattern by focal areas of hypoechogenicity. A partial tear was defined as a focal anechoic area with no fibers intact or an echogenic irregular band that could run either horizontally or longitudinally in the common extensor origin. A complete tear was defined as a distinct complete interval traversing or extending through the full width of the common extensor origin. Confirmation of abnormality was performed in at least two planes of imaging. A confidence level was not assigned for partial versus complete tears because distinction between these two entities was unequivocal in all patients. Focal areas of calcification and echogenicity were recorded, and bony changes at the lateral epicondyle were noted. The size of the abnormality was measured in millimeters. The site of the abnormality was examined in two planes and assigned as predominantly affecting the superficial, mid, or deep fibers and the anterior, mid, or posterior fibers. The normal lateral collateral ligament can be identified as an echogenic continuous band distinct from the common extensor origin. The lateral collateral ligament was considered abnormal if it was thickened, irregular, or discontinuous. Evaluation of bony changes was recorded as no change, bony surface irregularity, or spur formation. An assessment of the posterior interosseous nerve was made in all patients. Sonography was performed by a trained musculoskeletal sonographer and a musculoskeletal radiologist with an information-collection sheet filled out in collaboration. Their interpretation represented the original sonography report. Twentyone patients subsequently underwent surgical examination with débridement or release of the tendon, or both. The surgeon knew the original sonographic findings at the time of surgery. Fiftyone patients were treated conservatively, including an injection of steroid, and were followed up clinically. Eight of these patients have undergone repeated sonography to show resolution of the common extensor origin tendinopathy. Exclusion criteria for this study were acute trauma and previous surgical intervention. Some patients had a blind injection of steroid but not within 21 days before imaging. We excluded seven patients who had received a steroid injection in the 3 weeks before sonography. Results On sonography, the normal common extensor origin is composed of longitudinal bands of tendon fibrils running in close parallel without disruption (Fig. 1). In the forearm, the extensor carpi radialis brevis, extensor digitorum, extensor digiti minimi, and extensor carpi ulnaris can be clearly defined as separate muscle groups. As each muscle group is followed proximally from its musculotendinous junction, the fibers that contribute to the common extensor origin can be traced. The fibrils are closely intertwined to form the common extensor origin and cannot be separated into discrete components. However, the fibers of the extensor carpi radialis brevis make up most of the articular side of the common extensor origin, whereas the extensor digitorum makes up most of the superficial portion. The extensor digiti minimi and extensor carpi ulnaris make only minor contributions. The lateral collateral ligament lies immediately deep in relation to the extensor carpi radialis brevis component of the common extensor origin and can be shown as a distinct and closely knitted fibrillated structure on sonography. The fibers of the lateral collateral ligament run in a slightly different direction to the common extensor origin and become more distinguishable when injured. At dissection, the lateral collateral ligament is also identifiable as a discrete structure although its fibers are intimately related and not necessarily separate from the overlying extensor carpi radialis brevis. Of the 72 elbows with sonographic confirmation of lateral epicondylitis, 43 (59.7%) of 72 elbows had a normal-sized tendon, whereas 25 (34.7%) of 72 elbows had an enlarged tendon and 4 (5.5%) of 72 elbows had a torn attenuated tendon. Of the latter four elbows, two had complete tears and two had high-grade partial tears. The most common sonographic appearance was a focal hypoechoic area on either a normal background (Fig. 2) or one characterized by a diffuse decrease in echotexture with loss of the normal fibrillar pattern. The size of the focal hypoechoic areas ranged from 3 to 15 mm (mean, 8.7 mm). This finding occurred in 46 of 72 elbows and was believed to represent focal areas of fibroblastic degeneration in a normal tendon or in one with underlying diffuse tendinopathy. Anechoic foci with no fibers intact Fig year-old healthy male volunteer. Longitudinal sonogram shows normal common extensor origin (arrow), characterized by uniform band of tendon fibrils running closely in parallel toward lateral epicondyle (asterisk). 778 AJR:176, March 2001

3 Sonography of Lateral Epicondylitis Fig year-old male professional tennis player who presented with acute onset of right lateral elbow pain. Longitudinal sonogram shows small hypoechoic focus (arrow) in deep fibers of otherwise normal-appearing tendon. Deep fibers are predominantly composed of extensor carpi radialis brevis that can be followed from forearm. Hypoechoic focus was thought to represent area of collagen degeneration and fibroblastic proliferation that was subsequently confirmed at surgery. Fig year-old male tennis player who presented with left elbow pain. Longitudinal sonogram reveals linear fissures extending obliquely through tendon (small arrows) from deep surface characteristic of partial tearing of common extensor origin (large arrow). Fig year-old woman with 6-month history of right lateral elbow pain. Longitudinal sonogram reveals large anechoic focus (between asterisks) with no normal fibers intact in mid and deep fibers of common extensor origin where fibers arise from bone. Focus occupied more than 70% of tendon depth and was thought to represent partial tear. Findings were confirmed at surgery. Fig year-old female chef with 2-year history of chronic lateral elbow pain. Longitudinal sonogram shows linear split (arrows) running in substance of common extensor origin compatible with high-grade partial tear. Tendon is thin and attenuated; however, some fibers were shown to continue to epicondyle. Partial tear was confirmed at surgery. were thought to represent partial tears (Fig. 3). Discrete cleavage planes on a background of decreased echotexture and loss of fibrillar pattern were thought to represent partial (18/72) (Figs. 4 and 5) and complete tears (2/72) (Fig. 6) on a background of more diffuse tendinopathy. Six elbows in six patients showed a discrete lack of echotexture and fibrillar pattern alone, characteristic of diffuse tendinopathy (Fig. 7). Thus, there was a broad spectrum of change ranging from mild to severe tendinopathy, with focal areas of fibroblastic degeneration, to the formation of discrete cleavage planes representing partial (18/72) and complete tears (2/72). Other findings included calcification in eight elbows (Fig. 8) and focal areas of echogenicity in four elbows. Histologic analysis identified foci of calcification and fibrocartilage formation in patients with lateral epicondylitis [5]. Injury to the deep fibers of the common extensor origin (53/66; the extensor carpi radialis brevis component) was more common than injury to the mid (5/66) or superficial fibers (8/66) (Fig. 9). Similarly when viewing the tendon in the anteroposterior plane, we found that injury more commonly affected the anterior (35/66) or mid fibers (23/66) than the posterior (8/66) fibers. Most patients (50/72) showed no sonographic evidence of bony abnormality. Sixteen patients had cortical irregularity, and six showed spur formation (Fig. 8). Spurring was present at all levels of the disease. The radial and posterior interosseous nerves were identified in all patients and shown to have normal AJR:176, March

4 Connell et al. morphology. The lateral collateral ligament was abnormal in eight of 72 elbows (Fig. 6B). Color and power Doppler sonography was used routinely but failed to show any neovascularization although Doppler mode was helpful in identifying calcification by producing a comet-tail artifact in and behind the foci. Twenty-one of the 72 elbows underwent surgery, and the sonographic findings were confirmed in all patients. At surgery, the common extensor origin was split in the line of its fibers from the tip of the epicondyle distally. This split revealed the deep portion of the origin. Surgical findings of lateral epicondylitis included a macroscopically amorphous gray tissue, a partially shredded tendon containing a space that was not separated or retracted, and a fluid-filled defect with smooth edges that was contiguous with joint fluid. These findings corresponded to tendinopathy, partial tears, and complete tears, respectively. The abnormality A Fig year-old male golfer with 6-month history of left lateral elbow pain. A, Longitudinal sonogram shows large linear hypoechoic cleft (straight arrows) extending from deep surface through torn attenuated common extensor origin, indicating complete tear. Note tear of lateral collateral ligament (curved arrow) and humerus (asterisk). B, Longitudinal sonogram of lateral collateral ligament shows complete disruption (arrow) of radial attachment. Complete tear of common extensor origin and lateral collateral ligament was confirmed at surgery. Note radial head (asterisk). Fig year-old male carpenter with lateral epicondylitis. Longitudinal sonogram shows diffuse thickened hypoechoic tendon (between asterisks) with loss of normal fibrillar pattern compatible with diffuse tendinopathy. determined the extent of resection. The extensor carpi radialis brevis was commonly released, the abnormal tendon was resected and repaired, and the epicondyle was débrided. Eight samples were sent for histologic analysis. Findings included collagen disorganization and degeneration with rupture of fibers, fibrofatty change, fibroblastic proliferation, and lymphocyte infiltration. Discussion In a patient presenting with lateral elbow pain, the differential diagnosis includes entrapment of the posterior interosseous nerve, chondromalacia or osteochondritis dissecans of the radiocapitellar joint, an intraarticular body, and posterolateral rotatory instability [3, 4, 6, 7]. Although lateral epicondylitis remains a clinical entity, sonography can confirm the diagnosis and reveal the extent and severity of the disease. In the absence of any significant findings, sonography can exclude posterior interosseous nerve entrapment and reveal lesions of the lateral collateral ligament. The diagnosis of partial or complete tear may encourage the clinician to refer the patient directly to surgery because these injuries are less likely to respond to conservative treatment. Other researchers have speculated about the cause of lateral epicondylitis [8 10]; however, the cause is generally considered the result of repetitive microtrauma sustained during supination of the forearm and dorsiflexion of the wrist. Repetitive microtrauma results in tendon degeneration with rupture of individual collagen fibers that stimulates a reparative response. Histologically, there is collagen fibrillar degeneration, angiofibroblastic proliferation, tissue necrosis with myxoid and hyaline degeneration, and fibrosis [5]. A chronic cycle of tendon degeneration and repair ensues with weakening of the common extensor origin and with potential for rupture [3]. In lateral epicondylitis, there is no histologic evidence of either acute or chronic inflammation [11]. The primary abnormality of lateral epicondylitis involves the origin of the extensor carpi radialis brevis and less commonly the anterior aspect of the extensor digitorum tendon [3]. The extensor carpi radialis brevis has a complex origin, receiving contribution from the common extensor tendon, the lateral collateral ligament, the annular ligament, the overlying fascia, and intramuscular septum. These contributions are intertwined and are not always B 780 AJR:176, March 2001

5 Sonography of Lateral Epicondylitis Fig year-old male weight lifter with bilateral elbow pain. A, Longitudinal sonogram shows large hypoechoic focus (arrow) in deep fibers of right common extensor origin characteristic of severe tendinopathy. B, Sonogram taken obliquely through focus of tendinopathy of same elbow as A shows two foci of calcification (arrows). C, Longitudinal sonogram of left common extensor origin shows mild diffuse tendinopathy and cortical bone spur (arrow). A A B C B Fig year-old female volleyball player with 5-week history of left elbow pain. A, Longitudinal sonogram shows hypoechoic focus (arrow, between asterisks) in most superficial fibers of common extensor origin where it abuts bony interface. This part of tendon consists predominantly of extensor digitorum. Deep fibers are preserved. B, Transverse sonogram shows anechoic focus (between asterisks) affecting mid fibers of superficial part of tendon. Imaging in two planes confirms finding and helps to exclude artifact due to anisotropy. AJR:176, March

6 Connell et al. separable on either sonography or MR imaging or at surgery. The most common finding in a patient with lateral epicondylitis is focal areas of low echogenicity with a background of intrinsic tendinopathy. The most common sites are the deep and anterior fibers of the extensor carpi radialis brevis component of the common extensor origin. The tendon is not usually enlarged, and foci of calcification (4/ 72 in our study) are uncommon. The amount of calcification is less than that found in other studies that have shown calcium in up to 25% of patients on radiography [3]. Our study showed cortical irregularity and spur formation, but no periostitis. Bony change did not correlate with disease severity. Focal hypoechoic areas confined to the common extensor origin correspond histologically to areas of collagen degeneration and intrasubstance fiber rupture, which may fill in with reparative granulation tissue. If these areas enlarge and extend to the surface, then partial or even complete tears ensue. Fluid may undermine the edges of the tear. Discrimination between focal areas of tendinopathy and partial tears can be difficult. In our study, we designated tendinopathy as focal hypoechoic areas with some preservation of tendon fibers, whereas well-defined anechoic foci with no fibers intact or discrete cleavage planes represented partial tears. The histologic changes observed in the common extensor tendon are similar to those observed in other tendons prone to degeneration such as supraspinatus [12] and patellar tendons [13]. Sonographic findings are also similar to those of the rotator cuff and the patellar tendon. The lateral collateral ligament lies immediately deep in relation to the common extensor origin and can be reliably seen on sonography. It should be routinely assessed because the cause of therapy failure could be injury to this structure that was subjected to repetitive microtrauma. The lateral collateral ligament is more likely to be thickened, partially torn, or completely torn with more severe grades of lateral epicondylitis [14] although in our population group, injury was not common. MR imaging has high contrast resolution and is, thus, a sensitive test for detecting lateral epicondylitis. The advantage in MR imaging lies in its ability to concomitantly examine associated injuries including attritional tears of the lateral collateral ligament and chondral injury [11]. One of the shortfalls of sonography is its inability to identify an intraarticular cause for the patient s symptoms. Sonography offers superior spatial resolution and is, therefore, sensitive in depicting focal areas of degeneration, macroscopic partial thickness tears, foci of calcification, and bony irregularities. Sonography remains an operator-dependent test requiring experience and surgical feedback for reliable reporting and disease definition. Martin and Schweitzer [15] have described abnormal tendon T1 signal intensity on MR imaging in asymptomatic individuals. This signal intensity could be caused by magic angle phenomena due to the orientation of collagen fibers fanning out from the lateral epicondyle. In our study, all healthy volunteers showed a normal fibrillar pattern without focal areas of degeneration. When performing sonography of the elbow, radiologists should consider certain technical aspects such as the use of a highresolution 10- to 15-MHz probe and positioning of the patient. Correlation with the opposite elbow is useful, particularly when the operator has limited experience. A common artifact is the drop out of echoes (anisotropy) where the extensor carpi radialis brevis component arises from the epicondyle, particularly in the transverse plane. Increasing gain, repositioning the probe, and confirmation of abnormality in at least two planes help prevent misinterpretation of anisotropy from a focus of tendinopathy. Limitations of this study are the surgeon s access to the sonographic reports at the time of surgery and the lack of surgical correlation in cases of low- to moderate-grade tendinopathy. These injuries are usually treated conservatively with satisfactory outcomes in 82 95% of patients [2, 3, 16]. Refractory cases may require surgery. Surgical options for the treatment of tennis elbow include excision of the degenerated tissue, release of the common extensor tendon, and débridement of the origin with release of the annular ligament. However, confirmation of the disease and exclusion of other causes may be wise before subjecting the patient to surgery. In conclusion, sonography of the common extensor origin can confirm the clinical suspicion of lateral epicondylitis and exclude other causes of lateral elbow pain. Sonography can provide useful information about the location, extent, and severity of lateral epicondylitis before surgery. References 1. Osgood RB. Radiohumeral bursitis, epicondylitis, epicondylalyia (tennis elbow). Arch Surg 1922;4: Coonrad RW, Hooper WR. Tennis elbow: its course, natural history, conservative and surgical management. J Bone Joint Surg Am 1973;55-A: Nirschl RP, Perrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg Am 1979;61-A: Plancher KD, Halbrecht J, Lourie GM. Medial and lateral epicondylitis in the athlete. Clin Sports Med 1996;15: Chard MD, Cawston TE, Riley GP, Gresham GA, Hazleman BL. Rotator cuff degeneration and lateral epicondylitis: a comparative histological study. Ann Rheum Dis 1994;53: Moore M Jr. Radiohumeral synovitis. Arch Surg 1952;64: Rose N, Maudsley RH. Radial tunnel syndrome: resistant tennis elbow as a nerve entrapment. J Bone Joint Surg Br 1972;54-B: Bosworth DM. The role of the orbicular ligament in tennis elbow. J Bone Joint Surg Br 1955;37-B: Trethowan WH. Tennis elbow. (letter) BMJ 1929; 2: Garden RS. Tennis elbow. J Bone Joint Surg Br 1961;43-B: Regan W, Wold LE, Coonrad R, Morrey BF. Microscopic histopathology of chronic refractory lateral epicondylitis. Am J Sports Med 1992;20: Potter HG, Hannafin JA, Morwessel RM, DiCarlo EF, O Brien SJ, Altchek DW. Lateral epicondylitis: correlation of MR imaging, surgical and histopathological findings. Radiology 1995;196: Bodne D, Quinn SF, Murray WT, et al. Magnetic resonance images of chronic patellar tendinitis. Skeletal Radiol 1988;17: Bredella MA, Tirman PF, Fritz RC, Feller JF, Wischer TK, Genant HK. MR imaging findings of lateral ulnar collateral ligament abnormalities in patients with lateral epicondylitis. AJR 1999;173: Martin CE, Schweitzer ME. MR imaging of epicondylitis. Skeletal Radiol 1998;37: Price R, Sinclair H, Heinrich I. Local injection treatment of tennis elbow: hydrocortisone, triamcinolone and lidocaine, compared. Br J Rheumatol 1991;30: AJR:176, March 2001

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