Lateral: Extensor Carpi Radialis Brevis Tendon Injury

History

Lateral epicondylitis was first described in 1873 in German literature by . In 1883, Morris ( ) suggested an association of symptoms with the game of lawn tennis, which led to the common term tennis elbow . Historically, it was believed that an inflammatory process was the cause of lateral epicondylitis, proposing a partial tearing of the ECRB tendon alone, with separation of the periosteum from the lateral epicondyle to elicit this inflammatory response, resulting in symptoms. Currently, several neighboring structures to the ECRB tendon have been identified as contributing to lateral elbow pain, including the annular ligament, radial nerve, lateral capsule, and several different bands of the extensor digitorum communis. In addition, microscopic studies of excised tissue demonstrate a failure of reparative response in the ECRB tendon rather than an inflammatory response within the tissue. Nirschl is credited with redefining the pathology of damage to the ECRB as angiofibrotic dysplasia, or tendinosis, rather than tendonitis.

The clinical presentation of a patient with lateral epicondylitis is an adult individual in their fourth or fifth decade of life. There are no differences in diagnosis between men and women. It is more common in the dominant arm. Recent studies have identified several risk factors for lateral epicondylitis, including a history of manual labor with heavy tools and significant strain while performing repetitive tasks ( ). Roughly 80% of patients with newly diagnosed lateral epicondylitis improve over time, and most report symptomatic relief at one year. Most experience some residual symptoms, and only 4% to 11% of those seeking medical attention require surgical intervention ( ). Poor prognostic factors for successful nonsurgical treatment include participation in manual labor, dominant arm involvement, long duration of symptoms with high baseline pain levels, and poor coping mechanism ( ).

Pathoanatomy and Histology

and outlined the most commonly accepted theory of the pathogenesis of this disease. Nirschl built on the previous findings of , and , highlighting the fundamental underlying lesion was within the origin of the ECRB tendon. Overuse and repetitive motions lead to microtears in the ECRB origin. As described earlier, most microscopic studies of excised tissue demonstrate a failure of reparative response in the ECRB tendon. The normal ECRB tendon tissue is invaded by immature fibroblasts and nonfunctional vascular buds, and adjacent tissue is often disorganized and hypercellular ( ). coined the term angiofibroblastic tendinosis because of this microscopic appearance; here there is no evidence of acute inflammation. As a result of their research, tennis elbow is now thought to be a dysvascular degenerative-type process termed tendinosis rather than tendonitis . Nirschl and colleagues have noted that 35% to 50% of patients also have degenerative changes in the EDC. These changes, as seen within the ECRB tendon, are responsible for the pain that is associated with this condition.

Physical Examination and Workup

The typical presentation of a patient with lateral epicondylitis consists of pain at the lateral elbow worsened by active wrist extension or passive wrist flexion with the elbow extended. Patients may describe an inability to hold objects in their hand because of lateral elbow pain. Physical examination typically reveals a point of maximal tenderness 1 to 3 mm anterior and distal to the tip of the lateral epicondyle, which is reproducible by resisted wrist and finger extension. This location corresponds to the origin of the EDC and ECRB tendon. Infrequently, this pain is accompanied by warmth, swelling, or erythema. The tennis elbow stress test is performed when the examiner asks the patient to resist wrist extension from neutral while the elbow is flexed and extended, with pain isolated to the ECRB origin indicating a positive test. ( Box 29.1 and Table 29.1 ).

Imaging

Lateral epicondylitis is predominantly a clinical diagnosis, but several imaging modalities have been used to provide supplementary information. Plain films can occasionally show calcinosis within the mobile wad origin or intraarticular pathology ( ). Nirschl noted the findings of calcifications forecast persistent and refractory disease and were present in up to 20% of patients who required surgery ( ).

Magnetic resonance imaging (MRI) can be useful during the workup of lateral elbow pain. It is an excellent tool that can evaluate for intraarticular involvement, radial collateral ligament competency, and definition of the degree of tearing of the extensor origin. In 90% of symptomatic patients, MRI scans may show thickening and edema of the extensor tendon origin ( ). High-resolution and fine-cut scanning shows that the ECRB origin can be classified as the following: full tear of the tendon, partial tear of the tendon, thinning of the ligament, or separation away from the ulnar collateral ligament complex. However, there are some limitations when using MRI while assessing response to treatment for lateral epicondylitis. T2 signaling may persist for weeks after symptoms resolve following treatment ( ). One must correlate the findings of MRI with a clinical examination because 14% to 51% of asymptomatic elbows have edema in the common extensor origin ( ) ( Fig. 29.1 ).

Ultrasonography has a sensitivity of 64% to 88% when used to examine for pathology in the ECRB tendon, but specificity is variable, ranging from 36% to 100% ( ). It can identify peritendinous fluid, thickening of the common extensor origin, intrasubstance tears, and focal hypoechoic areas. This image modality is user dependent.