Elbow Tendinopathies and Tendon Ruptures

History

In 1873, Runge described a condition associated with lateral humeral condylar tenderness and difficulty writing; Morris referred to it in 1882 as “lawn tennis arm.” Eventually, this entity became known as tennis elbow or lateral epicondylitis.

Multiple treatments have been proposed for epicondylitis affecting the elbow, ranging from benign neglect to physiotherapy, bracing modalities, injection of various substances, and surgery; the optimal treatment remains controversial. Boyer and Hastings suggested that “there is much witchcraft and pseudoscience involved in the treatment of patients with lateral tennis elbow.” In 1936, Cyriax suggested “that the condition usually clears up in eight to twelve months without any treatment except perhaps avoidance of the painful movements for a time,” although cases “lasting much longer…are encountered.” Few conditions elicit as much frustration and controversy regarding cause, treatment, and outcomes among patients and physicians.

Etiology, Associations, and Pathophysiology

Boyer and Hastings reported that “lateral tennis elbow is most commonly an idiopathic or a work-related condition. A distinct pathoetiology has not been definitively identified.” Lateral epicondylitis likely represents a multifactorial condition with elements of repetitive microtrauma in a physiologically susceptible individual. The imaging and clinical history and findings associated with lateral epicondylitis are associated with increasing age; it has been suggested to be a “benign, self-limited condition of middle age.”

The pathology associated with lateral epicondylitis is believed to involve the attachment of the extensor carpi radialis brevis (ECRB) at the lateral humeral epicondyle. It is suggested that the extensor digitorum communis (EDC) is involved in approximately one-third of cases, and rarely the extensor carpi radialis longus (ECRL) or extensor carpi ulnaris (ECU) is involved. ^, The ECRB and EDC origins are indistinguishable at the level of the lateral epicondyle. They only visibly become separate muscle-tendon units several centimeters distal to the elbow.

Lateral epicondylitis has been associated with forceful repetitive activities and smoking. ^{, ,} The peak prevalence is at age 45 years, with most patients 35 to 54 years old ^, and the dominant arm usually affected. There is an equal distribution between the genders. Of patients followed for 18 months after initial presentation to a general practitioner with the diagnosis of lateral epicondylitis, more than half exhibited a recurrence of symptoms.

It is now recognized that lateral epicondylitis is a degenerative tendinopathy or tendinosis, rather than an inflammatory tendinitis. ^{, ,} Nirschl described the histologic findings as an angiofibroblastic tendinosis, with a gross appearance of a gray friable edematous tendon structure. ^{, ,} The first three stages of epicondylitis include an inflammatory stage that is restricted to the early course of the disease, followed by angiofibroblastic degeneration in stage II and structural failure in stage III. The fourth stage has a hallmark of fibrosis or calcification in the setting of components of stage II or III. ^,

Repetitive contraction of the extensors is believed to cause microtrauma to the tendons, eventually resulting in lateral epicondylitis. ^, Other authors have suggested that impingement of the ECRB tendon against the lateral edge of the capitellum causes abrasion and wear of the tendon during elbow motion, which eventually results in the condition.

In the diseased state, the normally avascular tendon attempts to repair itself with fibroblastic elaboration of collagen and fibrovascular proliferation. ^{, , ,} Continued mechanical trauma in the setting of an inadequate healing response leads to tendinosis.

Histopathologic findings include fibrocartilaginous formation ^{, ,} or mucoid or hyaline degeneration, ^{, , ,} fibrovascular proliferation, ^{, ,} and focal calcifications. ^{, , , ,} Milz and colleagues investigated the gross and histologic and molecular features of the common flexor and extensor origins in cadaveric specimens to attempt to describe the ranges of normal and pathologic findings at these locations. The tendon insertions medially and laterally showed confluence with the underlying collateral ligaments, resulting in a complex integrated structure. Fibrocartilage, which had previously been thought to represent a pathologic condition, was found frequently in all age groups, suggesting that it may be present under normal conditions. In addition, degeneration of tendon structure at the epicondylar insertions was present in elderly specimens, indicating that the presence of degenerative changes at the epicondyle may be associated with age.

Although most of the evidence suggests the changes in tendon are pathologic and represent the cause of pain, some suggest that the pain generator is intraarticular, related to the capsule and/or synovial region at the lateral aspect of the elbow.

Presentation

In lateral epicondylitis, patients typically complain of pain localized to the lateral epicondyle and at the ECRB origin, just slightly distal and anterior to the lateral epicondyle; the pain is exacerbated by wrist extension. On clinical examination, pain is elicited with resisted wrist extension with the forearm pronated and elbow fully extended. Additionally, resisted supination with the wrist flexed can precipitate the pain of lateral epicondylitis. The “chair test,” in which the patient is asked to lift a chair with the arm in forearm pronation and wrist flexion, typically causes pain. There is an overlap with radial tunnel syndrome in patient complaints and physical findings with use of provocative tests. Pain occurs with resisted finger extension and resisted forearm supination in both processes, so these are not definitive tests for either diagnosis.

If the history is vague and pain is poorly localized or unrelated to activity, other conditions should be considered. This is especially true if the physical examination fails to localize the area of tenderness as described previously. Chondromalacia, arthritis, periarticular tumors, loose bodies, radiocapitellar plica, osteochondral defects, cervical radiculopathy, or ligamentous instability should be considered. Radial tunnel syndrome (supinator syndrome) may be concomitantly present (with an estimated incidence of 5%). ^,

Diagnosis

The diagnosis of lateral epicondylitis is based on the clinical history and examination findings of pain centered over the origin of the common extensor mechanism, particularly the area of the ECRB and EDC. Radiographic evaluation of the elbow is typically not helpful in lateral epicondylitis but is helpful to exclude other disease entities. There might occasionally be some ossification of the soft tissues, but whether this is a result of treatment from multiple injections or is a natural process of the disease is uncertain.

Frequently, magnetic resonance imaging (MRI) studies are obtained in patients with elbow pain, often ordered by the referring physician or requested by the patient. MRI findings consistent with lateral epicondylitis include increased signal on T1 and T2 sequences. ^, MRI can show frank tearing and separation of muscle from the bone, ^, and it has been suggested that there is good correlation between MRI findings and intraoperative findings.

Frequently, asymptomatic patients have false-positive findings with signal enhancement. ^, In addition, enhancement may persist in symptomatic individuals even after the clinical resolution of symptoms.

In practice, just about every patient with mild pain over the lateral aspect of the elbow seems to have signal changes on MRI, particularly if the patient has had a series of injections. MRI is not significantly helpful in making the diagnosis or dictating treatment but can be used as an adjunct to look for other causes of potential pain around the elbow.

Ultrasonography is increasingly being used in the evaluation of musculoskeletal pain and may be obtained in order to evaluate lateral elbow discomfort. Findings typically seen in the setting of lateral epicondylitis include thickening of the common extensor tendon, the presence of calcifications, hypoechogenicity of the common extensor origin, neovascularity, and bone cortical irregularity. However, ultrasonographic findings must be interpreted with caution; patients with pain frequently have similar findings to those without lateral epicondylar pain, as expected changes occur with age. Further, as with MRI, ultrasonographic findings that might be suggestive of epicondylitis are known to persist even following resolution of pain. ^{, , ,}

Presentation

Medial epicondylitis is much less common than lateral epicondylitis, with a prevalence of 0.4% compared with 1.3% in one study. Other studies have found an estimated prevalence of 3.2% to 8.2% in patients employed in repetitive labor tasks. ^{, ,} Medial epicondylitis is suggested to constitute 10% to 20% of all epicondylitis cases.

Risk factors are similar to those in lateral epicondylitis and seem to include obesity, physical loads, and smoking; some studies suggest a female preponderance, whereas others do not. ^{, , , ,}

There seems to be an association of medial epicondylitis with other work-related or overuse musculoskeletal disorders. ^, As in lateral epicondylitis, patients are typically middle-aged (fourth to fifth decades) and the dominant arm is usually involved. ^, An exception is young throwing athletes who may experience medial-sided elbow pain.

The history typically involves the insidious onset of pain at the medial aspect of the elbow. Tenderness exists at the medial epicondyle and distally over the pronator teres (PT) and flexor carpi radialis (FCR). Pain is worsened with resisted pronation and resisted wrist flexion.

Etiology and Pathogenesis

It has been suggested that the cause of epicondylitis is related to overuse or repetitive motions leading to microtrauma to the muscular origins at the medial epicondyle; most commonly, to the PT and FCR, but also occasionally to the palmaris longus, flexor digitorum superficialis, and flexor carpi ulnaris origins. ^{, , , , , ,} As implied by the layperson’s term golfer’s elbow, repetitive use and microtrauma can precipitate the condition, and it has been associated with repetitive valgus loads in golf, racquet sports, football, baseball, weight lifting, and archery, in addition to occupational exposures requiring repetitive motions of the hand, wrist, elbow, or forearm. ^{, , ,} One of the oldest references is that of Morris, who described a condition in rowers occurring after “long and vigorous sculling,” with pain at the “inner part of the elbow,” which resolved with rest and avoidance of pronosupination. Although usually associated with a chronic overuse type of phenomenon, occasionally a single sudden traumatic episode can cause avulsion of the flexor pronator origin and lead to this condition.

As in lateral epicondylitis, pathologic findings include a degenerative tendinosis rather than an inflammatory tendinitis, and it has been suggested that this is due to the repetitive microtears in the setting of an inadequate healing response and, eventually, altered biomechanics of the elbow joint. In pitchers, the stresses are conferred to the medial structures of the elbow, including the flexor pronator muscles and medial collateral ligament (MCL).

Acceleration and valgus forces may exceed the tensile strength of the medial constraints of the elbow, leading to tears with a spectrum of pathologic findings ranging from epicondylitis to MCL insufficiency. ^,

The pathologic change found in medial epicondylitis is indistinguishable from that found in lateral epicondylitis with angiofibroblastic tendinosis.

In 23% to 60% of patients, ulnar neuritis is present. ^{, , , ,} The pathophysiologic mechanism has been suggested to be a combination of traction injury with entrapment and compression.

Diagnosis

The differential diagnosis of epicondylitis includes neurologic conditions (ulnar nerve neuritis, cervical radiculopathy, pronator syndrome); intraarticular pathologic conditions such as elbow synovitis, arthritis, or osteochondral defects; and ligamentous deficiency (MCL insufficiency). Typically, the diagnosis is made on clinical grounds. Radiographs may reveal calcification adjacent to the medial epicondyle or traction spurs or calcifications, particularly in throwing athletes. ^, As in lateral epicondylitis, radiographs are not typically necessary for the diagnosis, but they may exclude alternative causes of elbow pain. Some authors have investigated use of other imaging modalities, and ultrasonography has been noted to be highly specific and sensitive. Typically, a focal hypoechogenic or anechogenic area is shown, although ultrasound is usually not necessary to make the diagnosis.

MRI may be useful to rule out other conditions, such as MCL insufficiency or intraarticular pathologic conditions such as osteochondral defects. In the setting of medial epicondylitis, MRI may show increased signal intensity on T1 and T2 series, but it is again typically not required to make the diagnosis and it is not specific because signal changes can be seen in asymptomatic individuals. It has been suggested that these signal changes in asymptomatic patients may represent senescent changes or prior epicondylitis that has become quiescent.

Because of a high rate of concomitant ulnar neuritis, the clinical examination should include evaluation of the ulnar nerve, including provocative maneuvers such as a cubital tunnel Tinel sign, a cubital tunnel compression test, and an elbow flexion test. ^, Electrodiagnostic testing is of limited utility because it is normal in 90% of patients with ulnar nerve symptoms.

The status of the MCL should be assessed to rule out ligamentous insufficiency. Valgus stress should be applied to the elbow in a position of 30 degrees short of full extension. Potential compensatory action of the flexor pronator group can be eliminated by placing the pronated forearm in a position of wrist flexion and 30 degrees of elbow extension before stress is applied. The milking maneuver, in which the examiner pulls on the patient’s thumb, generating a valgus stress when the forearm is supinated in a position of elbow flexion, also tests for MCL insufficiency. In both tests, pain and instability are typically absent in pure medial epicondylitis, and their presence may represent MCL injury. ^,