Lateral Compression Injuries

The entities associated with lateral compression injuries are osteochondritis dissecans, osteochondrosis of the capitellum, and osteochondrosis or deformation of the radial head.

Osteochondritis Dissecans (OCD) of the Capitellum

The repetitive lateral compression forces placed on the elbow with throwing result in microfractures of the capitel-lar cartilage surface and subsequent edema of the underlying bone. This edema produces avascular necrosis because of the precarious circulation in the epiphyseal vessels of the developing capitellum. In advanced cases, this process can result in loose-body formation.

The patient is usually older than 13 years of age and presents with an insidious onset of poorly localized lateral elbow pain while throwing. The physical examination reveals radiocapitellar tenderness and possible joint effusion. In a series by Gill and Micheli, 79% of the cases revealed effusion and radiocapitellar tenderness.8 The patient's range of motion is diminished. There can be a progressive flexion contracture (>15°) and, sometimes, locking or catching from loose bodies.5,23

In these patients, radiographs show mottling at an early stage. Radiographic changes seen in later stages of the process are opacification, a focal area of involvement in the capitellum with well-defined sclerotic borders (Fig. 5.5), loose bodies, and an enlarged radial head in advanced cases. Tomograms are very sensitive for this con-dition.13 CT arthrography is useful for identifying loose bodies without calcification. Magnetic resonance imag-

FIGURE 5.5. Anteroposterior and lateral radiographs show osteochondritis dissecans of the capitellum. Arrow indicates area of lesion.

ing is not only helpful in confirming the diagnosis of OCD lesions, but in preoperative staging of the lesion and assessment of the status of overlying cartilage10,16 (Fig. 5.6).

The lesions are grouped into three stages based on the characteristics of the articular cartilage. This classification is used to direct treatment. In stage I, the articular surface is intact, and there is no subchondral displacement or fracture. Stage II lesions have articular surface fractures and fissuring. There may be partial detachment of a fragment. In stage III, the chondral or osteochondral fragments have become unstable and detached, producing intra-articular loose bodies.

The treatment for a stage I lesion is splinting for 4 weeks, followed by rest and range of motion for another

FIGURE 5.6. MRI shows osteochondritis dissecans of the capitellum. Arrow indicates area of lesion.

4 weeks. After 8 weeks, a follow-up radiograph is taken to assess evidence of revascularization and healing. If the patient is still symptomatic after 8 weeks, arthroscopic retrograde drilling is recommended.

The treatment for a stage II lesion is open drilling of the subchondral bed and stabilization of the partially detached lesion with one or more compression screws. Consideration should be given to the use of bioabsorbable screws. If the surgeon is unable to stabilize the lesion, it is treated as a stage III lesion. The stage III treatment involves arthroscopic or open removal of the loose bodies and microfracture or drilling of the lesion. Occasionally, the loose fragment is large enough and its quality is good enough to consider reduction and fixation. The use of osteochondral autografts or allografts is still experimental.

Immediately after surgery, the patient begins gentle passive range-of-motion exercises. The patient progresses to active-assisted range-of-motion exercises, as tolerated, during the first week. After the second week, emphasis is placed on improving strength and endurance. The preparation of the athlete to return to functional activities begins when he or she achieves full, nonpainful range of motion and strength, usually after the sixth week. The athlete starts a supervised interval-throwing program at approximately the eighth week and progresses to full activity, as tolerated.

The ability to return to throwing sports depends on the age of the patient (the likelihood of healing is better for younger patients), the stage of the lesion, and the presence or absence of symptoms.24,25 Although OCD is the leading cause of permanent elbow disability in throwing athletes, 85% of those treated with the excision and drilling return to throwing competitively in 6 to 12 months.26

A common complication of this condition and its treatment is an elbow flexion contracture. Flexion contracture is caused by the intimate congruency of the elbow complex, the tightness of its capsule, and a tendency of the anterior capsule to scar and form adhesions. Emphasis on early range of motion, elbow mobilization, and low-load, long-duration stretching is instituted in nonoperatively and operatively treated patients to avoid capsular restrictions. Radiological arthritic changes can occur in up to half of these patients regardless of treatment. Early detection and prevention are the best way to avoid these complications.

Osteochondrosis of the Capitellum (Panner's Disease)

Panner's disease is a condition of the growing elbow that is often compared with Legg-Calve-Perthes disease in the hip. It most often occurs in children between 7 and 12 years of age and is usually atraumatic and self-limiting (3-year period). The process begins with resorption followed by fragmentation, regeneration, and, finally, recalcification. The patient presents with a dull lateral ache,

FIGURE 5.7. Anteroposterior radiograph shows typical lesion of the capitellum (arrow) in a patient with Panner's disease.

a swollen elbow, and lack of extension. Radiographs show capitellar epiphyseal fragmentation and patchy rarefaction5,25,26 (Fig. 5.7). After ruling out OCD, treatment is always nonoperative and consists of rest until symptoms subside, followed by range-of-motion exercises and a supervised throwing program when the patient achieves pain-free motion and healing is evident on radiographs. The prognosis is favorable for relief of symptoms and return to play with excellent functional results.

Radial Head Osteochondrosis or Deformation

Injury to the radial head results from the lateral com-pressive forces, as well. These changes can occur in association with OCD lesions of the capitellum. The ossific nucleus of the radial head appears later than the ossific nucleus of the humeral capitellum.5 Moreover, the surface area of the capitellum is greater than that of the radial head.27 These factors concentrate lateral compression stresses on the epiphyseal plate of the radial head, leading to growth disturbances and angulation.11 The plasticity of the immature skeleton allows greater deformation of the articular surface when subjected to the chronic repetitive stress, which in turn results in more pronounced damage.11

The patient presents with diffuse dull pain and some joint stiffness. There is limitation of extension that increases with time and eventually interferes with sport participation. Some may show spontaneous locking and joint effusion.

When the radial head is ossified in a juvenile baseball player, radiographs show anterior angulation of the radial head.27 In these patients, OCD and even formation of loose bodies can occur later in life.

The treatment is nonoperative with rest until symptoms resolve, and an interval-throwing program is begun when the patient achieves a normal range of motion and strength. In patients in whom loose bodies or OCD lesions are present, the treatment is arthroscopic removal and drilling of the lesion.

Although this condition has excellent functional results after treatment, the patient might have loss of motion secondary to residual radial head spurring and anterior angulation.

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