Osteochondritis Dissecans of the Elbow

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CHAPTER 6 Osteochondritis Dissecans of the Elbow

Guillem Gonzalez-Lomas, Christopher S. Ahmad, Tony Wanich, Neal S. ElAttrache

Sport-specific injuries more frequently affect young athletes with earlier and more rigorous participation in sports. The radiocapitellar compartment of the young athlete’s elbow is punished by significant stresses during repetitive throwing or during sports (e.g., gymnastics) that convert the elbow joint into a weight-bearing joint.¹ Lateral compartment compression can lead to Panner’s disease (i.e., osteochondrosis) in the 6- to 10-year old patient or to various stages of capitellar osteochondritis dissecans (OCD) in the adolescent or young adult.²^–⁵ This chapter describes Panner’s disease and OCD and outlines a treatment algorithm, including arthroscopic management using osteochondral grafting.

PANNER’S DISEASE

In 1927, Hans Jessen Panner published a description of osteochondrosis of the capitellum, likening it to Legg-Calvé-Perthes disease of the hip.⁶ Like other ostochondroses, it consists of non-inflammatory, disordered endochondral ossification. Its specific cause and relation to OCD remain debatable. It is known that abnormal radiocapitellar compressive forces during a period of vulnerability, typically while the physes are still open, predispose children to Panner’s disease.²^,⁵^,⁷ It may result from the combination of an avascular insult (likely related to the capitellum’s predominantly end-artery supply) and repetitive microtrauma.⁸

Epidemiology

Panner’s disease predominantly affects boys younger than age 10 years.⁹ Young boys may be predisposed to it for two reasons. First, compared with girls, they have a delayed appearance and maturation of their secondary growth centers. Second, boys traditionally are more prone to trauma during the more aggressive early childhood activities they select.⁷ This may change as more girls choose higher-risk athletic activities at younger ages. Although Panner’s disease can be confused with OCD, and the age of onset may overlap, it is distinguished by three epidemiologic characteristics. Panner’s disease does not share the strict association with repetitive throwing that OCD does, it is usually self-limited, and it resolves without any long-term sequelae.

Patient Evaluation

Panner’s disease initially manifests as pain and stiffness in the elbow, which is relieved by rest. On physical examination, patients have poorly localized tenderness over the lateral elbow. Radiographs initially show fissuring, lucencies, fragmentation, and irregularity of the capitellum (Fig. 6-1), particularly near or at the chondral surface. Subsequent x-ray films, taken at 3 to 5 months, demonstrate larger radiolucent areas followed by reossification of the bony epiphysis, with a corresponding resolution of symptoms. In 1 to 2 years, the epiphysis regains its contour, usually without flattening.⁴ As in Legg-Calvé-Perthes, radiographs often lag behind clinical symptoms. Magnetic resonance imaging (MRI) may be used effectively to document the extent of the lesion. Typically, edema is localized to the chondral surface and the bone adjacent to it, with less involvement of the deeper subchondral bone compared with the OCD (Fig. 6-2).

FIGURE 6-1 Panner’s disease. An anteroposterior radiograph of the left elbow demonstrates fragmentation and lucency of the capitellum (circle) near the chondral surface.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

FIGURE 6-2 T2-weighted magnetic resonance imaging shows the effects of Panner’s disease. A Panner’s lesion (circle) is demarcated by small arrows opposite the radial head (RH). Notice the more typical finding of edema adjacent to the capitellar chondral surface, rather than deeper in the subchondral bone, as in osteochondritis dissecans.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

Treatment

Treatment involves rest and cessation of the aggravating activity and administering therapeutic modalities such as ice and anti-inflammatory medication. The elbow occasionally may need to be immobilized for 3 to 4 weeks to control symptoms. We favor a hinged elbow brace set at the pain-free motion to protect the area while allowing some motion and decreasing the risk of stiffness.

Symptoms usually resolve within 6 to 8 weeks, although they occasionally persist for months. Activities should be reinstituted progressively and as tolerated. The condition has an excellent long-term prognosis, although some patients may have a slight residual flexion contracture.

OSTEOCHONDRITIS DISSECANS

OCD of the capitellum is a non-inflammatory degeneration of subchondral bone occurring in the context of repetitive trauma to the lateral compartment of the elbow. Panner’s disease and OCD may represent two different stages of the same disorder,⁴ but they do have different characteristics: age of onset, cause, and natural history. Although Panner’s disease affects children younger than 10 years, OCD victimizes older athletes, usually between the ages of 11 and 15 years.¹⁰ Unlike Panner’s disease, OCD is thought to be directly linked to repetitive trauma. OCD is not always a self-limited disease, and if left unaddressed, it results in profound destruction of the capitellum.¹⁰

Anatomy

The elbow’s osseous anatomy and the capitellum’s idiosyncratic blood supply may predispose young athletes to OCD. The elbow is a diarthrodial joint in which the distal humerus articulates with the proximal ulna and the radial head. Its unique bony configuration allows for −15 to 0 degrees° of extension to 150 degrees of flexion. Rotation of the radial head over the stationary ulna gives an arc of almost 180 degrees of forearm rotation.¹¹ The osseous and articular congruency of the humerus, ulna, and radial head accounts for the greater part of elbow stability, particularly at less than 20 degrees of extension or more than 120 degrees of elbow flexion.¹²

In young, skeletally immature athletes, the elbow possesses a greater degree of cartilaginous elasticity. Hyperextension, facilitated by this increased range of motion, can generate increased radiocapitellar compressive loads and tension of the medial capsule and ulnar collateral ligament (UCL). Overhead throwing athletes during the throwing motion and gymnasts during weight-bearing handstands in elbow hyperextension further exaggerate these stresses. Repetitive stress on this system can precipitate OCD. Medial-sided pathologies, such as medial apophysitis, UCL injury, and posteromedial impingement from the excess valgus stress, can occur concurrently.¹³

The tenuous end-artery vascular supply to the capitellum predisposes it to injury. In the young adult population, the capitellum is supplied by two end arteries coursing from posterior to anterior, which are branches of the radial recurrent and interosseous recurrent arteries (Fig. 6-3).¹⁴ As a result of the longitudinal blood supply to the capitellar epiphyseal plate and minimal collateral circulation in the area, blood flow to the capitellum may be disrupted by repetitive microtrauma resulting in an avascular state and by a single traumatic event leading to post-traumatic subchondral bone bruises.¹⁵^,¹⁶

FIGURE 6-3 Capitellar blood supply. In young adults (<20 years), the radial recurrent and interosseous recurrent arteries give off branches that course from posterior to anterior and supply the capitellum (circle). This end-artery blood supply makes the capitellum susceptible to an avascular insult.

(Modified from Mirzayan R, Itamura JM, Rockwood CA. Shoulder and Elbow Trauma. New York, NY: Thieme; 2004.)

Patient Evaluation

History

OCD arises from repetitive, excessive compressive forces generated by large valgus stresses on the elbow during throwing or racket swinging or by constant axial compressive loads on the elbow, such as those endured by gymnasts.¹⁰^,¹⁷^,¹⁸ Specific risk factors predispose to the condition. In the case of baseball players, throwing sliders and breaking pitches, throwing more than 600 pitches per season, and increased age of the athlete increase the risk of developing OCD.¹⁸ In female gymnasts, overtraining involving excessive handstand maneuvers has been linked to OCD.¹⁹^,²⁰ There also may be a genetic predisposition to OCD.

Patients with OCD initially complain of pain and stiffness in the elbow that is relieved by rest. The onset is usually insidious, and a history of specific trauma is often absent. If left unaddressed, the symptoms may progress to locking or catching due to intra-articular loose bodies or an inflamed plica. Throwing athletes may present with painful posterolateral clicking or catching caused by a radiocapitellar plica. These symptoms can overlap with those from the OCD lesion, and the plica itself may be responsible for chondral wear in the radiocapitellar compartment.

Physical Examination

Because throwing athletes may have injured medial and lateral and posterior elbow structures, a full elbow examination is essential. We test UCL integrity by performing a valgus stress test at 30 degrees, the milking maneuver, and the moving valgus stress test. We screen for posteromedial impingement by performing a bounce test. A positive test result elicits pain posteromedially when the elbow undergoes forced hyperextension.

In athletes with OCD, physical examination findings tend to be remarkable for poorly localized lateral elbow tenderness over the radiocapitellar joint. Loss of range of motion with a 15- to 20-degree flexion contracture is common. Loss of extension is more common than loss of flexion. An effusion is often apparent and can be palpated by flexing the elbow and feeling the lateral portal area, triangulated by the radial head, olecranon, and lateral epicondyle. The provocative maneuver for the radiocapitellar joint we prefer is the active radiocapitellar compression test (Fig. 6-4). A positive test result elicits pain in the lateral compartment of the elbow when the patient pronates and supinates the forearm with the arm in extension. In patients with an associated symptomatic radiocapitellar plica, snapping typically occurs at greater than 90 degrees of elbow flexion with the forearm in pronation.

FIGURE 6-4 In the radiocapitellar compression test, pain in the lateral elbow is elicited when the extended arm is pronated and supinated.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

Diagnostic Imaging

Anteroposterior radiographs in full extension, anteroposterior radiographs in 45 degrees of flexion, and lateral views of the elbow should be obtained. Radiographic findings may be negative early in the disease process. As the condition progresses, flattening and sclerosis of the capitellum, typically on its anterolateral aspect, will become apparent. Irregular areas of lucency and intra-articular loose bodies also appear. The capitellar lesions of OCD and medial-sided epicondylar fragmentation are best seen on an anteroposterior radiograph at 45 degrees of elbow flexion (Fig. 6-5).

FIGURE 6-5 An anteroposterior radiograph shows the osteochondritis dissecans lesion (circle) more clearly with elbow flexed to 45 degrees.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

MRI should be used to assess suspected OCD. It can detect bone edema early in the disease process.²¹ An MR arthrogram can further delineate the extent of the injury. Contrast can show separation of a detached or partially detached piece from subchondral bone (Fig. 6-6). This is important in determining whether to proceed with operative or nonoperative management. Peiss and colleagues²² thought that fragment enhancement (Fig. 6-7B) (as opposed to the perifragment enhancement seen in Fig. 6-6) denoted viability and might be a reasonable indication for nonoperative treatment. They also suggested that enhancement of the fragment and subchondral bone interface was caused by vascular granulation tissue, indicating instability and requiring operative intervention.

FIGURE 6-6 The MR arthrogram shows contrast surrounding an unstable osteochondritis dissecans fragment (arrow).

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

FIGURE 6-7 Progress of a stage 1 osteochondritis dissecans lesion is evaluated on magnetic resonance imaging (MRI). A stable, intact, nondisplaced fragment (circles) has abnormal signal intensity on coronal slices in T1-weighted (A) and T2-weighted (B) MRI sequences. After 6 months of conservative management, the T1-weighted (C) and T2-weighted (D) MRI sequences show reconstitution of subchondral bone in the area of the lesion. The patient was symptom free at the 6-month follow-up assessment.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

Pseudolesions, which appear on the posteroinferior junction of the articular and nonarticular portions of the capitellum, must be differentiated from OCD, which almost always manifests on the anterolateral aspect. The examiner also should observe whether the capitellar physis is open or closed.

Treatment

Indications, Contraindications, and Classification

Management of OCD lesions is based primarily on the status and stability of the overlying cartilage. The size and location of the lesion and the patency of the capitellar growth plate also influence decision making.²³^–²⁵

To guide treatment, detailed classification systems based on radiographic ²⁶^,²⁷ and arthroscopic²³ findings have been delineated.²⁸^,²⁹ We have simplified these algorithms into a three-stage classification that provides a template for management. Table 6-1 shows the classification.

TABLE 6-1 Classification and Treatment of Capitellar Osteochondritis Dissecans Lesions

Stage 1.

In stage 1, the osteochondral fragment is intact, stable, and not displaced. Radiographic findings are often negative. The MRI signal varies; it is typically abnormal on T1-weighted and normal on T2-weighted images, although the T2 signal may also be abnormal. Figure 6-7A and B shows a stage 1 lesion with coronal-slice signal that is abnormal on T1- and T2-weighted images. Arthroscopically, the articular cartilage is intact, with general preservation of subchondral stability.

This stage is best treated nonoperatively. All activity involving the affected arm should be stopped. The elbow should be rested in a hinged elbow brace for 3 to 6 weeks. Progressive physical therapy should ensue as symptoms abate. Return to sports usually can be expected at 3 to 6 months and should be governed by primarily by the patient’s clinical response, because radiographic changes often lag behind the clinical symptoms by several months or years. Nevertheless, follow-up radiographs and MRI scans should be obtained at 2- to 3-month intervals to track progress. Figure 6-7C and D shows the same patient as in Figure 6-7A and B at the 6-month follow-up assessment after conservative treatment, with clear reconstitution of the subchondral bone.

If symptoms return, additional rest is mandated. With persistently refractory symptoms, pitchers may have to change positions, and gymnasts may have to change sports. Lesions that progress to stage 2 should be treated accordingly.

Stage 2.

In stage 2, the osteochondral fragment is partially separated, as documented radiographically and arthroscopically. Radiographs demonstrate fissuring, lucencies, and fragmentation. On MRI, T1- and T2-weighted sequences show abnormal signal intensity and a margin around the fragment, denoting its instability (Fig. 6-8). Computed tomography (CT) may reveal the partially separated fragment. Arthroscopically, the cartilage is fractured, and the subchondral bone is unstable and partially displaced (Fig. 6-9).

FIGURE 6-8 A stage 2 osteochondritis dissecans lesion is assessed by magnetic resonance imaging (MRI). T1-weighted (A) and T2-weighted (B) MRI sequences show a margin around the fragment (circles), denoting its instability.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

FIGURE 6-9 A stage 2 osteochondritis dissecans lesion is assessed arthroscopically. A, The arrow points to the osteochondral fragment located at its donor site. B, The arrow points to the space between the osteochondral fragment and bone, denoting fractured cartilage and instability.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

When an unstable lesion is identified, conservative treatment should be bypassed. It warrants prompt surgical intervention to return the athlete to his or her sport or activities of daily living as soon as possible. In stage 2 lesions, the size and location of the lesion govern treatment. For smaller lesions, débridement is an option. Patients typically have immediate relief of symptoms, but the long-term natural history includes arthritis. Fragment fixation has been advocated by some for this stage, although questions linger concerning the long-term healing potential of fixed fragments and clinical results of the procedure.²⁶^,²⁷^,³⁰^,³¹ Osteochondral autografts or synthetic grafts can address large, radial head–engaging defects involving the lateral buttress of the capitellum. If the decision rests between fixation and osteochondral restoration, we prefer osteochondral or synthetic plug grafting, because it has generated more reliable results.

Size.

Takahara and coworkers ³² differentiated among small (<5% of the capitellum on an anteroposterior radiograph of the elbow, <60-degree angle formed by lines drawn along the borders of the lesion on a lateral radiograph), moderate (5% to 70%), and large (>70%, >90 degrees) lesions. They concluded that large lesions should be addressed operatively. Shimada and associates³³ suggested that smaller lesions (<1 cm²) could be treated with débridement, chondroplasty, and possibly microfracture or drilling as described by Bradley and Dandy.³⁴ Larger lesions (>1 cm²) should be treated with osteochondral autografts.

Location.

We think the location of the lesion may be more important in guiding treatment than some other factors. Extension of the lesion into the lateral margin of the capitellum, as described by Chappell and ElAttrache ³⁵ and by Ruch and colleagues,³⁶ is associated with a potentially poorer prognosis. The lateral column of the capitellum supports large compressive forces when the elbow is stressed in valgus or with axial loading. When the lateral column is intact, a defect treated with microfracture alone is relatively protected, and fibrocartilage healing may occur. Lesions that do not involve a significant portion of the lateral buttress of the capitellum and do not engage the radial head during arthroscopic observation (i.e., pronation and supination with the elbow in extension) have been successfully treated with microfracture or retrograde or antegrade subchondral drilling. Figure 6-10 shows an OCD lesion with a predominantly intact lateral column.

FIGURE 6-10 The osteochondritis dissecans lesion with an intact lateral column. A, The lesion (oval) is adjacent to a significant portion of the intact lateral column (arrow). B, The lateral column (arrow) supports the radial head and does not permit engagement with the defect.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

Lateral column involvement of more than about 6 to 7 mm cannot be dealt with acceptably by microfracture. The absence of a lateral buttress forestalls fibrocartilage healing by subjecting the defect to increased radiocapitellar forces. Engagement of the radial head in the defect also compromises healing and may lead to accelerated radiocapitellar arthrosis. For these larger, engaging defects or those that extend substantially into the lateral buttress (>6 to 7 mm) (Fig. 6-11), we recommend removal of the loose fragment and osteochondral restoration by means of mosaicplasty or osteochondral autograft transfer system (OATS).

FIGURE 6-11 The lesion extends into the lateral column. A, The osteochondritis dissecans lesion (circle) can be seen. B, The white dotted line denotes the ulnar margin of the lateral column. The lesion extends 7 mm into the lateral column (black dotted line) and allows the radial head (RH) to engage.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

For early, partially detached fragments, the detached portion (usually central) should be débrided from central to lateral aspects. After stable osteochondral borders have been obtained, the lesion is carefully evaluated arthroscopically to ascertain how much of the lateral column is involved and if the radial head engages with the defect. Chappell and ElAttrache ³⁵ reported that lesions larger than 1 cm² (average, 1.32 cm²) and no lateral column involvement were treated successfully with microfracture, whereas those involving the lateral column did well with osteochondral grafting. Fragment fixation also is an option, but we have had superior and more consistent results with grafting.

Stage 3.

In stage 3, the fragment is fully displaced and has become or is imminently becoming a loose body. Figure 6-12 shows an example of a stage 3 lesion seen on MRI and arthroscopically. Patients may present with mechanical symptoms related to loose bodies, such as locking.

FIGURE 6-12 A stage 3 osteochondritis dissecans lesion is assessed by magnetic resonance imaging (MRI) and arthroscopy. T1-weighted, coronal MRI (A) and T1-weighted, sagittal MRI (B) show an unroofed lesion. C, Arthroscopy shows the lesion (oval) with no overlying cartilage. Small arrows demarcate edge of lesion. D, The loose body osteochondral fragment (arrow) is found in the joint.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

In this stage, débridement, drilling, or osteochondral replacement is indicated. If the loose osteochondral piece is acutely displaced in a patient with previously documented OCD, the surgeon can attempt to fix it to its donor site. Results of fixation are, however, inconsistent. Chronically loose bodies (documented by serial radiographs or MRI) should be removed and the donor bed débrided in preparation for one of the aforementioned treatment options, following the same algorithm. These patients often are unable to return to sports, and the long-term prognosis usually includes radiocapitellar arthrosis.

Nonoperative treatment mandates complete cessation of elbow use, including activities such as throwing, gymnastics, arm wrestling, push-ups, and weightlifting. The arm may be immobilized but not for more than 3 weeks.²⁹ Gentle range of motion should be instituted immediately after this period of immobilization if this therapeutic route is chosen. The patient is followed clinically at regular intervals (every 4 to 6 weeks) with serial radiographs. Gentle exercises are performed for the first 3 to 4 months, advancing to strengthening at 4 to 5 months. At that point, an interval throwing program can be initiated based on satisfactory clinical and radiographic findings. Return to sports should be governed by the patient’s symptoms, because radiographic changes can persist for years.³⁸^,³⁹

Rest.

Takahara and associates ³²^,³⁸ observed that repetitive forces on existing OCD lesions led to an increase in lesion size. Cessation of repetitive stress on the elbow should be emphasized to the athlete’s parents, trainers, and coaches. They must be reminded that this is a potentially sport-ending injury, with degenerative arthritis as a possible outcome. The incidence of residual capitellar deformity in high-level pitchers is very low,⁴⁰ and this suggests that athletes who develop a degenerative elbow from failed OCD treatment do not go on to play high-level baseball. The athletes may be able to do active controlled rest by offloading with a brace and by continuing only those activities that are pain free.

Stage and Management.

Because early-stage OCD responds better to nonoperative treatment than advanced stage lesions, identifying the disease promptly can have a significant impact on prognosis. Matsuura and colleagues ⁴¹ found that 91% of early-stage OCD but only 53% of advanced-stage OCD improved after nonoperative treatment.

Stability.

Stability of the fragment also affects the final outcome. Mitsunaga and coworkers ⁴² showed that less than 50% of stable fragments went on to become unstable in the long term. However, Takahara and associates²⁶ demonstrated that fragments that did become unstable had a low rate of healing.

Patient Age and Growth Plate Status.

Age has not been correlated with the likelihood of healing.³⁷^,³⁸ However, Mihara and colleagues²⁵ found a significant correlation between open capitellar growth plates and healing. In their study, 94% of patients with early-stage lesions and with open growth plates healed, whereas the rate for those with closed growth plates was only 71%.

Operative Treatment

Failure of conservative treatment for early-stage, stable lesions (i.e., about 6 weeks of no improvement or 4 to 6 months of persistent symptoms) or diagnosis of an advanced-stage, unstable lesion is an indication for pursuing operative treatment. The ultimate goals of surgery are to eliminate mechanical symptoms and stimulate a healing response. Takahara and coworkers ²⁷ found that patients with unstable lesions that did well with surgery compared with elbow rest had the following common findings at presentation: a closed capitellar growth plate, radiographic fragmentation, and restriction of elbow motion of more than 20 degrees. Patients with closed capitellar physes did significantly better with surgery than with elbow rest. Larger lesions had better results with reconstruction of the articular surface than with simple fragment fixation.

Arthroscopic Positioning.

Elbow arthroscopy can proceed with the patient supine, prone, or in the lateral decubitus position. We use the supine position because it facilitates general anesthesia and enables an easy conversion to an open procedure if needed (Fig. 6-13). Structures also may lie in a more anatomic orientation in this position. In the supine position, the elbow is positioned at 90 degrees of elbow flexion and 90 degrees of shoulder abduction with the hand suspended from a pulley and using 5 pounds of traction. The lateral position gives improved posterior compartment access. The prone position also gives good posterior compartment access and does not require traction. General anesthesia provides complete muscle relaxation and obviates the need for a regional block that may prevent diagnosing a postoperative neurologic problem. A tourniquet can be used at the surgeon’s discretion.

FIGURE 6-13 The patient is positioned supine with the arm held at 90 degrees of shoulder abduction, 90 degrees of elbow flexion, and in neutral rotation by a pulley system (i.e., 5 pounds of traction).

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

Arthroscopic Technique.

Available instruments include 2.9- and 4.0-mm, 30-degree arthroscopes, burrs, and shavers. The elbow is distended with 30 to 50 mL of saline through the direct lateral portal. Standard arthroscopic portals are created. Diagnostic arthroscopy is performed to look for loose bodies, osteophytes, and chondral damage. The arthroscope usually is in the anteromedial portal, and working instrumentation is in the anterolateral portal. In throwers, a valgus stress test with the elbow flexed to 70 degrees can be performed during the diagnostic portion of the procedure. A 1- to 2-mm opening of the ulnohumeral joint denotes laxity of the UCL, although clinical correlation is mandatory.

After the initial arthroscopic examination is complete, a midlateral portal (i.e., lateral soft spot) is created in line with the lateral epicondylar ridge and entered with the arthroscope. The radial head, capitellum, trochlear notch, and trochlear ridge are best seen through this portal. Care should be taken to avoid the posterior antebrachial cutaneous nerve, which is at risk near this portal. A working portal is created adjacent to and slightly ulnar to the midlateral portal (Fig. 6-14). Carefully placed dual direct lateral portals do not damage lateral ligamentous structures and provide superior exposure to the capitellum.⁴³ Patients with OCD and lateral compartment symptoms occasionally also have a thickened radiocapitellar plica (Fig. 6-15). If found, the plica should be resected.

FIGURE 6-14 Dual, direct lateral portals are created. A midlateral portal (A) is created first by triangulating its location using the radial head (RH), lateral epicondyle (LE), and the lateral aspect of the olecranon (O). A working midlateral portal (B) is created adjacent and slightly lateral to the first portal.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

FIGURE 6-15 A, Arrows point to the radiocapitellar plica, which may cause abrasion of the radial head (RH) and capitellar (C) chondral surfaces. B, The circle demarcates the region formerly occupied by plica, which has been resected.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

The OCD lesion is evaluated and graded. If unstable and loose, the lesion is prepared by removing any loose fragments, shaving loose fragments of cartilage down to subchondral bone and establishing healthy cartilage borders (Fig. 6-16). The size of the lesions is determined by a calibrated probe. If osteochondral grafting is planned, the portals must allow access for the required 4- to 6-mm instruments. At this point, depending on the indication, one of the following procedures can be performed: abrasion chondroplasty, drilling, microfracture, fixation of large fragments, and osteochondral autograft transfer (i.e., OATS or mosaicplasty).

FIGURE 6-16 The osteochondritis dissecans lesion (A) is débrided with a shaver (arrow) to stable borders (B).

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

PEARLS& PITFALLS

PEARLS

• An accessory midlateral portal, placed adjacent and slightly ulnar to the standard midlateral portal, can facilitate access to the lesion.

• Resect a thickened radiocapitellar plica if present.

• Determine the size of the lesion after débriding damaged cartilage.

• Lesions involving more than 6 to 7 mm of the lateral column of the capitellum should be treated with osteochondral grafting.

• Microfracture can be used for smaller lesions or for a residual lesion after osteochondral grafting.

PITFALLS

• The size of 6 to 7 mm refers to the amount of lateral buttress involved, not the total diameter of the lesion.

• Any lesion that engages with the radial head in supination or pronation should be treated with osteochondral grafting. Microfracture alone will likely fail in these cases.

• Access to the lesion must be as perpendicular as possible for osteochondral grafting. Use a spinal needle to find the most direct angle.

• Articular step-off after grafting should be less than 1 mm.

Microfracture and Subchondral Drilling.

The indications for microfracture or subchondral drilling are similar: early-stage lesions with cartilage fibrillation and fissuring and small, stage 2 lesions with exposed bone that do not significantly involve the lateral column of the capitellum. The lesion bed is prepared as described earlier (see Fig. 6-16). Detached fragments or loose bodies are removed. With the arthroscope in the direct lateral portal, a 0.062-inch Kirschner wire is inserted through the accessory lateral portal and used to perforate the lesion (Fig. 6-17A). Multiple holes are made in the lesion (see Fig. 6-17B). Marrow elements released from the holes induce a fibrocartilage healing response.

FIGURE 6-17 A, Using the microfracture technique, A 0.062-inch Kirschner wire (arrow) is inserted through the accessory midlateral portal and used to perforate the lesion. B, Holes (arrow) in the lesion allow marrow elements to induce a fibrocartilage healing response.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

If microfracture is elected, a similar approach can be employed using microfracture awls instead of pins. Bojanic and as sociates ⁴⁴ reported symptom resolution in three adolescent (13- to 15-year-old) gymnasts 5 months after arthroscopic débridement and microfracture of lesions that were about stage 2. They remained symptom free 1 year postoperatively. Using microfracture in 11 athletes with an average age of 15 years, Chappell and ElAttrache³⁶ obtained excellent results at the 3-year follow-up, with a return to the previous level of activity by all 11. The size of the OCD lesions ranged from 7 × 6 mm to 17 × 15 mm.

Mosaicplasty.

Mosaicplasty has been applied in the context of elbow OCD lesions. In this procedure, small, cylindrical osteochondral grafts are obtained from the lateral periphery or trochlear edge of the femoral condyles and transplanted to prepared osteochondral defects.⁴⁵ Mosaicplasty is indicated when a large capitellar lesion engages the radial head, as observed while rotating the extended arm during arthroscopy, or when there is significant (>6 to 7 mm) lateral column involvement (Fig. 6-18A). Radial head degeneration and severe deformities of the capitellum are relative contraindications.

FIGURE 6-18 Osteochondral plug reconstruction is used for a capitellar osteochondritis dissecans defect that extends into the lateral column. A, The defect extends into the lateral column of the capitellum (circle). B, The arrow points to the donor site for an osteochondral plug (i.e., 6 mm in diameter and 1 cm deep), which is harvested from the medial trochlea of the knee on the lateral aspect of the medial femoral condyle (MFC). C, The arrow points to implantation of an osteochondral plug using an inserter. D, The circle demarcates the osteochondral plug after implantation.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

A midlateral working portal is used to establish healthy, stable cartilage borders. In the case of a partially detached fragment, the detached area is first evaluated. Often, the detached region is located centrally. In this situation, ElAttrache recommends débriding the partially detached portion by beginning centrally and proceeding laterally toward the lateral column. Débridement proceeds until an area of bony integrity, consisting of an osseous connection between the fragment and the subchondral bone, is encountered, if one is present. The extent of posterolateral column involvement is then determined (see Fig. 6-18A), and an arthroscopic evaluation (i.e., supination and pronation of the extended forearm) of radial head engagement in the defect is performed. If more than 6 to 7 mm of the lateral column is involved or the radial head engages in the defect, osteochondral grafting proceeds. The goal should be to restore a bony buttress to prevent radial head subluxation into the defect, not necessarily replace every millimeter of the lesion.

If osteochondral grafting is elected, the elbow is then flexed 90 to 100 degrees, and a spinal needle is introduced through the anconeus to gauge the feasibility of a perfectly perpendicular approach to the lesion (typically 3 to 4 cm distal to the midlateral portal).⁴⁶ The incision is widened to provide access for a 4- to 6-mm diameter plug, so that it is in line with the perpendicular path delineated by the needle. After bluntly spreading the soft tissue to avoid neurovascular structures, the recipient site is then drilled as perpendicular to the chondral surface as possible, creating a tunnel of the necessary diameter.

At this point, the knee, which has been prepared, undergoes an arthroscopic harvest of an identically sized chondral plug from the intercondylar notch. The arthroscope is placed into an anterolateral portal. Instrumentation is inserted through an anteromedial portal. Using the harvesting instrumentation, a 6-mm-diameter, 1-cm-deep plug is harvested from the trochlear edge off the medial femoral condyle (see Fig. 6-18B). Usually, one plug is sufficient because of the small size of the capitellar lesions.

The plug is introduced into the recipient site and impacted flush with the surrounding cartilage (see Fig. 6-18C and D). The goal is to reconstitute the lateral buttress (Fig. 6-19A and B) so that the radial head does not subluxate into the defect. The process of osteochondral grafting is repeated until the lateral column integrity is adequately restored. If some corners of the lesion cannot be fully replaced, they are treated with drilling or microfracture (see Fig. 6-19C and D). If autograft is unavailable, allograft or synthetic scaffolding can be used.

FIGURE 6-19 The lateral buttress of the capitellum is reconstructed with an osteochondral autograft. A, The osteochondritis dissecans lesion extends into the lateral column of the capitellum (circle). During the arthroscopic examination (i.e., pronation and supination in extension), the radial head (RH) engages the defect. B, The osteochondral plug (circle) is placed in the lateral aspect of the capitellum, reconstituting the lateral buttress. The radial head no longer engages. C, The circle surrounds the osteochondral plug, and the arrow points to the remaining lesion, which is addressed with microfracture using a 0.0062-inch Kirschner wire. D, After microfracture, holes (arrows) allow release of the marrow elements.

(Courtesy of Neal S. ElAttrache, MD, Kerlan-Jobe Orthopaedic Clinic, Los Angeles, CA.)

With this method, Iwasaki and associates ⁴⁵ obtained good or excellent results in 7 of 8 teenage baseball players with OCD. Yamamoto and colleagues⁴⁸ found that 6 of 9 adolescents with grade 3 and 8 of 9 with grade 4 OCD returned to competitive baseball after an OATS procedure. Chappell and ElAttrache³⁵ treated five baseball players with OCD using OATS. All five returned to competitive baseball and were still playing 5 years postoperatively. The investigators recommended the procedure, particularly when more than 6 to 7 mm of the lateral column is involved and when the radial head is seen to be engaging the lesion with a careful arthroscopic examination during supination and pronation and during flexion and extension of the forearm.

Fragment Fixation.

Fragment fixation has been performed in patients with unstable, partially open OCD lesions.³⁰ Kuwahata and coworkers³¹ described using cancellous bone grafts and a Herbert screw in an open technique. At 32 months of follow-up, they reported pain-free return to sports and an improvement in range of motion of 18 degrees in all seven patients who underwent the procedure. Takahara and colleagues²⁶^,²⁷ described using bone pegs harvested from the lateral olecranon to fix partially attached lesions. This was also done through an open approach. Newer bioabsorbable implants may allow fragment fixation to be performed routinely arthroscopically. Although these surgeons have reported encouraging results, data on fixation are still preliminary. Our recommendation remains excision and drilling or grafting for partially detached lesions.

Postoperative Rehabilitation

Postoperatively, all patients should be protected for 2 to 3 weeks with a long arm cast or hinged brace. Active motion should not be started until bony union is seen on radiographs. Gentle resistance exercises are initiated at 3 months, progressing to greater resistance at 4 months. For throwing athletes, a throwing program is started at 5 months. Full-effort return to sports is usually achieved 6 months after surgery. Athletes who have undergone simple débridement and drilling or microfracture can usually return 1 to 2 months sooner, depending on their rehabilitation progress.

Return to Sport.

Return to sports has varied. Historically, gymnasts have had inferior outcomes compared with throwers, perhaps related to significantly increased axial loads borne by their elbows. Jackson and associates ³ treated 10 female gymnasts with removal of loose bodies and drilling after failure of nonoperative treatment. Only one returned to sport. Although surgery for lesions refractory to conservative treatment may improve symptoms, the investigators concluded that a return to gymnastics is unlikely.

Newer technical advancements and lesion-specific management may be improving these outcomes. Bojanic and colleagues ⁴⁴ found that 3 of 3 female gymnasts successfully returned to their previous level after loose body removal and microfracture. Although Byrd and coworkers⁴⁷ suggested that arthroscopic surgery reliably improved symptoms but returned only 4 of 10 adolescent baseball players to competitive baseball, Yamamoto and associates⁴⁸ reported a return to competitive levels for 14 of 18 male baseball players with unstable fragments (in situ or displaced) after osteochondral autografting. Chappell and ElAttrache³⁶ had 8 of 8 male baseball players return to their sport and previous level at an average of 3 years of follow-up after microfracture or osteochondral autografting.