Elbow

Osteochondritis Dissecans (Osteochondral Lesion) and Panner’s Disease ( Box 11.2 )

Although osteochondritis dissecans can occur in throwers and in nonthrowers, in dominant and in nondominant elbows, and in the capitellum and in the radial head, it tends to occur in the capitellum of the dominant arm in throwers. The exact cause is uncertain, but the leading hypothesis is that the lesion results from a combination of tenuous blood supply to the capitellum and repetitive trauma at the radiocapitellar joint, resulting in bone injury.

MRI demonstrates abnormal subchondral signal within the anterior capitellum, often with an associated subchondral fragment, and can help determine the stability of the osteochondral lesion. Unstable lesions are characterized by high signal fluid that encircles the osteochondral fragment on T2W images (or high signal gadolinium in the case of an MR arthogram) ( Fig. 11.1 ). Round, cystic lesions may be seen beneath the osteochondral fragment, and abnormal high signal may be seen on the T2W images within the fragment of bone (least specific sign). The overlying cartilage should be closely inspected for any chondral loss. Stable lesions are usually treated with rest and splinting. Unstable lesions are either pinned or excised.

Osteochondritis dissecans has been replaced in the literature by the term osteochondral lesion . This entity should be distinguished from Panner’s disease (an osteochondrosis of the capitellum), which coincidentally also occurs often in throwers as a result of repetitive trauma. The MRI appearance, patient’s age, and prognosis differ between these entities. An osteochondral lesion is seen in slightly older patients (12-16 years), whereas Panner’s disease occurs in younger patients (5-10 years old). Loose body formation usually is not seen with Panner’s disease, and the entire capitellum is generally involved with abnormal signal intensity (low signal on T1W images and high signal on T2W images) and may show irregular contour to the capitellum. Subsequent follow-up imaging in Panner’s disease reveals normalization of these changes with little to no residual deformity at the articular surface. An osteochondral lesion can lead to intra-articular loose bodies and significant residual deformity of the capitellum.

A pitfall in diagnosing an osteochondral lesion is the pseudodefect of the capitellum. This pseudodefect occurs because the most posterior, nonarticular portion of the capitellum has an abrupt slope. A coronal image through the posterior capitellum mimics a defect. Examination of this area in another plane and the lack of edema support the pseudodefect as the cause of the irregularity of the capitellum ( Fig. 11.2 ). Additionally, an osteochondral lesion generally begins on the anterior convex margin of the capitellum, whereas a pseudodefect is a finding in the posterior capitellum.

Unstable osteochondral lesions may fragment and migrate throughout the joint as loose bodies. Loose bodies can also occur from purely cartilaginous fragments breaking off in the joint from acute trauma or osteoarthrosis. Loose bodies can become large and cause mechanical symptoms, limiting mobility of the joint, or produce a synovitis that results in an effusion and stiff elbow ( Fig. 11.3 ). They are often identified in the posterior compartment in a throwing athlete and are easier to detect on MRI when joint fluid is present in the joint space; they appear as low to intermediate signal structures within high signal fluid. Loose bodies typically collect anteriorly or posteriorly in the joint because the capsule is not taut in those regions, as it is medially and laterally. Occasionally, a loose body can be ossified, demonstrating marrow within it. The signal characteristics follow that of fat: high in signal on T1W images. Axial and sagittal images aid in the diagnosis and location of loose bodies, and fragments containing bone may be more conspicuous on GRE images due to associated susceptibility (“blooming”) artifacts.

Fractures

MRI is useful in evaluating radiographically occult fractures when there is radiographic evidence of a joint effusion but a fracture is not visualized. Marrow-sensitive sequences (T1W imaging, [fast] short tau inversion recovery [STIR], and fat-suppressed FSE) are the most sensitive for assessing the fracture and edema associated with it ( Fig. 11.4 ). GRE is the least sensitive technique for evaluating the marrow. MRI is outstanding for evaluating stress fractures. An important stress fracture in the elbow involves the middle third of the olecranon ( Fig. 11.5 ). This type of fracture usually is seen in throwing athletes as a result of overload by the triceps mechanism. These fractures can displace and require surgical fixation. MRI is also an excellent tool for evaluating a skeletally immature patient because it can assess fractures extending through the physeal and epiphyseal cartilage.

Medial epicondyle fractures may occur in skeletally immature, overhead athletes. MRI aids in diagnosis as well as treatment planning because it can demonstrate a minimally or nondisplaced condylar fracture and assess the apophysis. The earlier the diagnosis is made, the earlier treatment can be initiated, improving the outcome for these patients.

Normal Radial Collateral Ligament Complex

The radial collateral ligament complex provides varus stability. This complex consists of the annular ligament, the radial collateral ligament, and the lateral ulnar collateral ligament ( Fig. 11.6 ). The annular ligament surrounds the radial head and originates and inserts onto the anterior and posterior margins of the lesser sigmoid notch of the ulna. It is the primary stabilizer of the proximal radioulnar joint and is best seen on axial images ( Fig. 11.7 ). The radial collateral ligament proper arises from the anterior margin of the lateral epicondyle and inserts onto the annular ligament and fascia of the supinator muscle ( Fig. 11.8 ). The lateral ulnar collateral ligament is more posterior and is absent in 10% of anatomic specimens; it is thought to provide the primary restraint to varus stress. It is a more superficial and posterior continuation of the radial collateral ligament, arising from the lateral epicondyle and extending along the lateral and posterior aspect of the proximal radius to insert on the ulna at the crista supinatoris ( Fig. 11.9 ).

The origin of the three ligaments is immediately adjacent and deep to the common extensor tendon. Functionally, the lateral ulnar collateral ligament is more important because it is the primary posterolateral elbow stabilizer and maintains the support of the radial head and radioulnar articulation. The radial collateral ligament proper and the lateral ulnar collateral ligament are well seen on coronal images, and both should be evaluated as discrete structures because of their difference in functional significance. The lateral ulnar collateral ligament is often identified on the same coronal image as the pseudodefect of the capitellum.

Abnormal Radial Collateral Ligaments

Disruption of the lateral collateral ligament complex is more unusual than that of the ulnar collateral ligament complex. Job-related or sports-related injuries usually result in chronic, repetitive microtrauma that produces varus stress. Injury to the radial collateral ligament complex commonly is associated with lateral epicondylar soft tissue degeneration and tearing of the common extensor tendon ( lateral epicondylosis or tennis elbow ). Acute varus injury or elbow dislocation also can be associated with radial collateral ligament complex injury. Insufficiency of the lateral ulnar collateral ligament may result in posterolateral rotatory instability (remember it supports the radial head), which allows transient rotatory subluxation of the joint. Rupture of this ligament occurs most commonly as a result of a posterior dislocation or varus stress, often in a patient who falls on an outstretched hand.

Posterior capitellar impaction injuries may result from posterolateral rotatory instability or elbow dislocation. These injuries typically result in a classic contusion pattern with edema-like signal intensity in the posterior capitellum and ventral aspect of the radial head (or radial head fracture). These injuries are typically associated with extensive ligamentous damage.

Insufficiency of the lateral ulnar collateral ligament also may occur after a lateral extensor release for tennis elbow (because of the close proximity of the origin of the ligaments and tendons) or with resection of the radial head. Laxity of the lateral ulnar collateral ligament after surgical lateral extensor release for tennis elbow has been described as a result of extensive subperiosteal elevation of the common extensor tendon and radial collateral ligament complex during surgery, and as a result of unrecognized lateral ulnar collateral ligament insufficiency preoperatively. Patients frequently complain of locking or snapping of the elbow. The physical examination may produce pain over the radial (lateral) aspect of the elbow, a subjective complaint of laxity or instability with varus stress, and a positive lateral pivot shift maneuver.

At surgery, laxity or disruption of the lateral ulnar collateral ligament and the posterolateral portion of the capsule and possible radial collateral ligament laxity can be identified. Reconstruction or reattachment of the lateral ulnar collateral ligament on the lateral epicondyle is performed. A sprain of the radial collateral ligament complex appears as a thickened or thinned ligament with high signal in and around it ( Fig. 11.10 ). A complete tear shows discontinuous fibers along the radial collateral ligament or lateral ulnar collateral ligament. Proximal detachment or avulsion of their common origin on the lateral epicondyle shows edema and hemorrhage extending into the defect and absence of the fibers of the radial collateral ligament complex ( Fig. 11.11 ). When the lesion is seen in association with lateral epicondylosis, bone marrow edema in the lateral epicondyle and high signal in the extensor tendon group can be identified. If surgical release of the common extensor tendon is being considered, the integrity of the radial and lateral ulnar collateral ligament must be assessed.

Normal Ulnar Collateral Ligament

The ulnar collateral ligament complex consists of three bundles: the anterior, posterior, and transverse bundles ( Fig. 11.12 ). The anterior bundle is a thick, discrete ligament with parallel fibers arising from the medial epicondyle and inserting onto the medial coronoid process at the “sublime” tubercle; it is the most important of the ligaments and is well seen on coronal and axial images. The MRI appearance is that of a low signal linear structure that is flared proximally and tapers distally ( Fig. 11.13 ). It is normal to see a slightly increased signal in the proximally flared portion of the anterior bundle. The anterior bundle of the ulnar collateral ligament provides the primary restraint to valgus stress and commonly is damaged secondary to overuse in throwers.

The fan-shaped posterior bundle of the ulnar collateral ligament is a thickening of the capsule that is best defined with the elbow flexed at 90 degrees. The transverse bundle of the ulnar collateral ligament is formed from horizontally oriented capsule fibers joining the inferior margins of the anterior and posterior bundles. It stretches between the tip of the olecranon and the coronoid and does not contribute to elbow stability because its origin and insertion are both on the ulna. The transverse and posterior bundles are located deep to the ulnar nerve and, in conjunction with the capsule, form the floor of the cubital tunnel. The posterior bundle is best seen on axial images, as it forms the floor of the cubital tunnel.

Abnormal Ulnar Collateral Ligament

Ulnar collateral ligament injury commonly occurs in throwing athletes and may accompany an injury to the overlying common flexor tendon. Injury to these medial stabilizing structures is typically caused by chronic microtrauma from repetitive valgus stress during the acceleration phase of throwing.

Complete rupture of the anterior bundle of the ulnar collateral ligament usually occurs suddenly. Patients with acute ulnar collateral ligament ruptures report sudden pain with or without a popping sensation that occurred with throwing, and they are unable to throw after the injury. These injuries are well seen on coronal MRI images. An abnormal signal is identified in the expected location of the linear, low signal structure of the ulnar collateral ligament ( Fig. 11.14 ). The torn fragments also can be identified.

In a large series of throwing athletes, midsubstance ruptures of the anterior bundle of the ulnar collateral ligament accounted for 87% of ulnar collateral ligament tears, whereas distal and proximal avulsions were found in 10% and 3%, respectively. Chronic degeneration of the ulnar collateral ligament is characterized by thickening of the ligament secondary to scarring, often accompanied by foci of calcification or heterotopic bone. The treatment of acute ulnar collateral ligament tears is evolving. Conservative treatment is recommended for nonelite athletes (mere mortals) because the flexor-pronator mass keeps the elbow functionally stable, although throwing is limited. Surgical reconstruction for competitive athletes has been recommended for many years.

Partial detachment of the deep undersurface fibers of the anterior bundle of the ulnar collateral ligament also may occur. These patients present with medial elbow pain. The diagnosis with routine MRI is difficult. This type of tear spares the superficial fibers of the anterior bundle and is invisible from an open surgical approach. These tears are more easily identified after the injection of intra-articular contrast material (MR arthrography). The capsular fibers of the anterior bundle, which normally insert on the medial margin of the coronoid process, show fluid beneath the distal extension of the anterior bundle, forming what is known as the “T” sign ( Fig. 11.15 ). This is often a very subtle finding but can cause functional debilitation in a throwing athlete. Partial tears are treated with repair or reconstruction in athletes.