Etiology/Pathology

Despite the uncertainty of its etiology, symptomatic OCD of the capitellum arises primarily from repetitive stress to the elbow ( ). Provoking compressive forces on the capitellum commonly occur in the dominant arm of overhead throwing athletes and from weight-bearing stress in gymnasts in the second decade of life. Overhead athletes place the medial elbow stabilizing complex under significant repetitive stress with consequent lateral elbow compression and shear forces. This occurs primarily during the late cocking phase of the throwing cycle as the radiocapitellar articulation, a prime secondary stabilizer to valgus stress, experiences as much as 60% of the axial compression force across the elbow ( Fig. 32.1 ). Along the same lines, female gymnasts invoke a similar injury mechanism through repetitive loading of the radiocapitellar joint with their arms in extension ( ).

Side view of a pitcher at the point of maximal shoulder and elbow stress. This point is defined as early acceleration with the shoulder near its point of maximal external rotation.

From Crotin RL. A collaborative approach to prevent medial elbow injuries in baseball pitchers. Strength & Conditioning Journal . 2011;33(5):1–24.

The pathophysiology of OCD resembles that of mechanical trauma to articular cartilage. Repetitive microtrauma in the susceptible elbow initiates fatigue fracture, resorption, and ultimately fragment separation from the underlying subchondral bone, as demonstrated by through rabbit models. With time, the overlying articular cartilage begins to break down and is increasingly vulnerable to shear stress because of inadequate subchondral osseous support, leading to separation, fragmentation, and loose body formation ( ). The Research in Osteochondritis of the Knee (ROCK) study group has come to define OCD as “a focal, idiopathic alteration of subchondral bone with risk of instability and disruption of adjacent articular cartilage that may result in premature osteoarthritis” ( ). This same phenomenon extends to OCD of the capitellum.

In concert with traumatic insult, the vascular anatomy of the distal humerus underscores ischemia as a likely contributor to OCD of the capitellum. The blood supply to the capitellum arises primarily from posterior perforating vessels that traverse the epiphyseal articular cartilage without metaphyseal collateral circulation ( ). Through a cadaveric ink-injection study of the skeletally mature elbow, determined that the main arterial contributors to the lateral elbow are the radial and middle collateral, radial recurrent, and interosseous recurrent arteries. Repetitive stress to and compression of this tenuous blood supply may cause ischemia of the subchondral bone within the capitellum and the characteristic osteonecrosis observed in OCD. Hence, this compromise of the subchondral support structure promotes articular cartilage fragmentation and loose body formation ( ).

History and Physical Examination

Patients who present with OCD of the capitellum are typically athletes between ages 11 and 21 years ( ). OCD of the capitellum is more commonly found in male adolescent athletes engaging in repetitive overhead activities and has been associated with baseball, gymnastics, tennis, weight lifting, wrestling, and cheerleading. The dominant arm is more commonly involved, although bilateral involvement has been reported ( ). Athletes with OCD of the capitellum often complain of diffuse, nonspecific pain with activity. The most common early symptom of a capitellar OCD lesion is a gradual, progressive onset of lateral elbow pain. Patients may also complain of accompanying elbow stiffness and loss of motion. Athletes rarely recall any specific trauma to the elbow. Rest and antiinflammatory medications are typically effective in relieving the pain, features that may contribute to the delayed presentation that often occurs with this pathology. In more severe cases, athletes may develop mechanical symptoms, such as catching, clicking, and locking, suggesting the presence of intraarticular loose bodies.

Physical examination reveals tenderness over the radiocapitellar joint in the posterolateral elbow in some cases. Crepitus at the elbow may be palpable with flexion and extension. The elbow should be examined for any evidence of effusion. With delayed presentation, patients may lack the terminal 15 to 30 degrees of elbow extension ( ). The radiocapitellar compression test is a useful physical examination maneuver for diagnosis. With this maneuver, passive forearm pronation and supination with the elbow in midrange flexion and extension during application of an axial load recreates pain at the radiocapitellar joint. An elbow ligamentous stability examination should be performed to assess for both ulnar collateral ligament insufficiency and posterolateral rotatory instability. Athletes often present to the physician’s office after a period of rest, lowering the diagnostic yield of physical examination. For this reason, the senior author (CWN) often exercises athletes in the office (i.e., throwing baseballs) to provoke their symptoms.

Panner’s disease must be considered in the differential diagnosis of a young athlete with elbow pain. This disorder is an idiopathic osteochondrosis of the entire immature capitellum. It occurs in a younger age group (4–12 years) than capitellar OCD and is predominantly found in boys. The involvement of the capitellum is more diffuse, with radiographs revealing loss of the normal contour of the capitellum ( ). Unlike OCD, Panner’s disease is a self-limiting process that normally resolves completely with activity modification and rest ( ).

Diagnostic Imaging

In the evaluation for suspected osteochondritis dissecans of the capitellum, standard elbow radiographs, including anteroposterior (AP), oblique radial head, and lateral views, should be obtained ( Fig. 32.2 ). Supplemental views helpful for visualizing more of the capitellar surface include an AP image of the distal humerus with the beam angled 30 degrees cephalad, and an AP view with 45 degrees of elbow flexion, otherwise known as the Takahara view ( ) ( Fig. 32.3 ). An axillary view of the bent elbow, taken in the style of a knee Merchant view, may also provide better visualization of the capitellum as well as the posteromedial aspect of the elbow, where loose bodies are often found ( ) ( Fig. 32.4 ). Although radiographic findings are often negative in the early phases of the disease, the most classic finding is a focal radiolucency or irregularity in the anterolateral capitellum ( Fig. 32.5 ). In later stages, the capitellar surface may flatten and the lesion is often surrounded by a rim of sclerotic bone ( ). Late findings include the presence of loose bodies, degenerative changes, and radial head enlargement. Although radiography is a crucial initial imaging study, its sensitivity for detection of capitellar OCD is as low as 66% according to one study ( ). Computed tomography (CT) may be used to better define the osseous anatomy and subchondral bone, and CT arthrography can more accurately assess for loose bodies ( ). A disadvantage to consider with CT is the radiation exposure imparted on the young athlete.

AP (A) , lateral (B) , and oblique AP (C) radiographs demonstrating the radiocapitellar joint from different angles.

Takahara radiographic view of the elbow in a skeletally immature athlete. The elbow is positioned in approximately 45 degrees of flexion with the beam aimed perpendicular to the forearm.

Axillary radiographic view of the elbow. Elbow is flexed 110 to 120 degrees, and the shoulder is slightly externally rotated.

Classic radiography finding of capitellar OCD with radiolucency of the anterolateral capitellum.

Magnetic resonance imaging (MRI) is a valuable tool for assessing OCD of the capitellum and is more sensitive than radiographs. In early-stage lesions, the T1-weighted MR image demonstrates uniform low-intensity changes in the superficial capitellum, although the T2-weighted imaging findings remain normal. Changes evolve on T2-weighted imaging as the lesion progresses ( ). The stability of OCD lesions has a significant impact on prognosis and treatment and can be predicted on MRI in some cases. There is a lack of consensus on what MRI findings do or do not indicate instability; however, most writers believe that unstable OCD lesions can be identified on T2-weighted imaging from a fluid signal between the OCD and the underlying bone, as well as from a discrete round high–signal intensity area representing a cyst under the OCD lesion ( ) ( Fig. 32.6 ). Investigators have found high sensitivity (89% to 100%) of MRI for detecting unstable lesions when all four of the following Kijowski criteria are present: (1) a rim of high signal on T2-weighted images, (2) surrounding cysts, (3) a fluid-filled osteochondral defect, and (4) a thin high-intensity fracture line on T2-weighted images ( ). Although intravenous gadolinium contrast enhancement of the lesion may suggest vascularity and thus viability of a fragment, MR arthrography has not been shown to provide any added benefit in assessing for the presence or stability of OCD lesions ( ).

( A and B ) MR images demonstrating fluid deep to the OCD lesions and ovoid bodies. Both are believed to be signs of OCD instability.

Ultrasonography is another potential diagnostic imaging tool for capitellar OCD. described a method to visualize the articular surface and subchondral bone by utilizing long-axis and short-axis views of the anterior and posterior capitellum. A capitellar OCD prevalence study used ultrasound as the screening examination and found that it had a 100% positive predictive value. On ultrasound, loss of the smooth articular surface served as an excellent indicator of an OCD . A major disadvantage of ultrasound is the high variability in its accuracy, which is based on the skill and experience of the operator ( ). Nonetheless the use of ultrasound as a simple and noninvasive tool has been advocated by several writers as a way to screen young, susceptible athletes for asymptomatic lesions as well as to access vascularity of the lesion ( ).

Classification

Many classification systems have been proposed to help guide the diagnosis and management of capitellar OCD lesions. Unfortunately, except for a few circumstances, there is no consensus at this point on an acceptable system. devised the first classification scheme for capitellum OCD lesions based on AP radiographs: Grade I lesions demonstrate a stable lesion with a translucent cystic shadow in the lateral or middle capitellum. Grade II lesions possess a clear zone between the lesion and the adjacent subchondral bone. Grade III lesions are associated with loose bodies.

MRI has proved useful for better characterizing OCD lesions and guiding treatment. proposed a classification scheme of capitellar OCD lesion stability based on T2-weighted MRI sequences. Stage I lesions appear as normally shaped capitellum with several spotted areas whose signal intensity is high but lower than that of cartilage. Stage II is marked by several spotted areas of higher intensity than cartilage. Stage III lesions show a discontinuous and noncircular capitellum chondral surface. Stage IV lesions are characterized by separation from the capitellum chondral surface by a high signal interface. Stage V is marked by displaced capitellar lesions or the presence of a capitellar defect.

An arthroscopic classification was developed by and later modified by the International Cartilage Repair Society. In this system, grade I lesions are stable with continuous but softened areas of intact cartilage. Grade II lesions are stable when probed but demonstrate partial discontinuity. Grade III lesions show complete discontinuity but have not dislocated. A grade IV lesion is either an empty defect, a defect with a dislocated fragment, or a loose fragment lying within the bed. This scheme has been well adopted because of its relative ease of use; however, it has not been shown to correlate well with treatment outcomes ( ).

devised a more simplified classification, assigning lesions as stable or unstable. Stable lesions are those that heal with rest and are characterized by an open capitellar growth plate, contained flattening or radiolucency of the subchondral bone, and decent range of motion. On the contrary, unstable lesions possess one of the following characteristics: a closed capitellar growth plate, lesion fragmentation, or restricted elbow motion ≥ 20 degrees.

Nonsurgical Management

Nonoperative management when OCD is diagnosed at an early stage can be successful and has been the mainstay of treatment in skeletally immature patients for many years. Unfortunately, the ability to prognosticate when conservative treatment will be successful is not well established, and the decision whether to initiate nonoperative versus operative management in capitellar OCD focuses on the extent of disease, the time from onset of symptoms, and the patient’s expectations and desires. As in the treatment of knee OCD lesions, results of nonoperative treatment are better in younger, prepubescent athletes with wide open physes ( ). We also believe that if the radiographs or MRI do not show separation of the fragment with fluid between the native and progeny bone, a period of rest has a decent chance to result in a full functional recovery in at least half of cases. However, once an athlete complains of clicking or locking, regardless of the timeliness of diagnosis and the patient’s age, the likelihood that conservative management will be successful decreases.

Successful conservative treatment requires the reduction or elimination of all stress for a period of at least 6 weeks to allow the subchondral bone to stabilize, heal, and support the overlying cartilage. Deciding when healing has occurred to an extent great enough to start a slow and planned progression back into daily functioning and, ultimately, athletic activities is difficult. Use of repeated imaging, although intuitively a good idea, is not established as a viable method to determine the appropriate timing of return to activities. Furthermore, patients’ lesions often heal their and patients return to full activities despite the lack of full radiographic healing. Many writers suggest that the timeline may be as long as 6 months to allow complete healing.

When rest is difficult to accomplish, bracing, use of a sling, or even a period of casting is used. However, we are very careful with this treatment arm of the algorithm because the elbow loses functional range of motion faster than most joints in the body when it is immobilized. Ultimately, a return to activities is appropriate only after there is complete resolution of symptoms and the athlete has regained full range of motion and strength not only about the elbow but also of the shoulder girdle ( ).