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1 All authors: Department of Radiology, Victoria House Private Hospital, 316 Malvern Rd., Prahran 3181, Melbourne, Victoria, Australia.
Received July 11, 2000;
accepted after revision September 18, 2000.
Address correspondence to D. Connell.
Abstract
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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.
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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.
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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. Twenty-one 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. Fifty-one 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.
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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 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. 6A,6B) 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. 8A,8B,8C) and focal areas of echogenicity in four elbows. Histologic analysis identified foci of calcification and fibrocartilage formation in patients with lateral epicondylitis [5].
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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. 9A,9B). 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.
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Most patients (50/72) showed no sonographic evidence of bony abnormality. Sixteen patients had cortical irregularity, and six showed spur formation (Fig. 8A,8B,8C). 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 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 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.
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Other researchers have speculated about the cause of lateral epicondylitis [8,9,10]; 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 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 short-falls 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 high-resolution 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.
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