Pediatric Sports Medicine: Issues in Contemporary Sports Participation

Pathoanatomy

Little League shoulder (LLS), also termed proximal humeral epiphysiolysis, osteochondrosis, apophysitis, epiphysitis, stress fracture, or Salter Harris I injury of proximal humerus, is an overuse injury that affects the proximal humeral physis in skeletally immature athletes, caused by repetitive stress. It is most commonly seen in the throwing arm of young baseball pitchers, but can be seen in other baseball positions, and in other overhead sports, including tennis, gymnastics, swimming, and volleyball. Case series looking at patients diagnosed with LLS showed that the majority of the patients were baseball players (97%): 86% pitchers, 8% catchers, 7% other positions, and found a small group of tennis players (3%).

LLS is thought to be a caused as a result of repetitive micro traction and torque forces placed on the unossified cartilage of the proximal humeral physis in the skeletally immature arm, most commonly caused by the throwing motion. ^, Studies have suggested that the high torque forces generated during the late cocking phase in the pitching motion are strong enough to weaken the proximal humeral epiphysis, leading to humeral retroversion or proximal humeral epiphysiolysis.

Pediatric overhead athletes typically present with LLS between the ages of 11 and 16 years of age with peak incidence occurring at around 13 to 14 years of age, corresponding to the age in which total shoulder range of motion was found to be significantly decreased in adolescent baseball players. It has been alluded that this decrease in rotational motion may cause increased stress at the proximal humeral physis during the throwing motion.

A high volume of pitches and maximum effort throws, poor throwing mechanics, inadequate rest between pitches, and pitching while fatigued are risk factors which have been associated to contributing stress over the proximal humeral physis. ^,

History and Physical Exam Features

Patients commonly present with a history of progressive worsening upper arm pain with throwing motion. They often report pain exacerbating with harder and more frequent throws. As it progresses, it may even cause diffuse shoulder pain with activities of daily living and at rest. The throwing athlete may also complain of decreased pitching velocity and strength with throwing. It is not uncommon for the patient to present with progressive shoulder pain that has been ongoing for months prior to presenting to the physician’s office for evaluation.

A thorough history including number of weekly games and pitches, types of pitches thrown, and number of rest days between pitches should be obtained. Full-speed pitches thrown during practice, including those thrown in the bullpen and at home, should be included in weekly pitch count. It can also be helpful to ask patient which phase of the throwing motion elicits their symptoms.

On physical exam, the most common finding is bony tenderness to palpation along the proximal humeral physis. Pain may be elicited at terminal ends with shoulder range of motion testing. Patients may also present with decreased range of motion with limited external or internal rotation.

Imaging

LLS is a clinical diagnosis; however, common radiographic findings may include physeal widening, irregularity, and increased sclerosis compared to contralateral nonaffected shoulder ( Fig. 40.4 ). Lateral fragmentation, calcification, and cystic changes may also be noted. Anteroposterior (AP) Grashey view in external rotation views allows for physis evaluation and contralateral radiographs for comparison can be helpful with diagnosis. Conventional radiographs of the shoulder include AP Grashey, scapular Y, and axillary views. Magnetic resonance imaging (MRI) may be helpful in detecting occult physeal injuries when conventional radiographs are normal and the clinical exam is equivocal.

Nonoperative Treatment and Therapy

LLS is almost always treated with conservative management consisting of rest from activity that causes pain and cessation of throwing for approximately 3 months. Wasserlauf and Paletta recommend cessation of throwing for a minimum of 6 weeks after diagnosis, and an additional 6 weeks of no throwing during the strengthening phase of rehabilitation, for a total of minimum 3 months’ rest from throwing. ^, Physical therapy may begin when pain has subsided and should focus on strengthening of the rotator cuff, periscapular and core musculature, stretching and flexibility of the shoulder capsule, and scapular stabilization. ^, Proper form and pitching mechanics should be implemented.

Return to Play

Prior to returning to play, the athlete should have pain-free throwing motion and demonstrate full range of motion and strength. If the treating healthcare provider sees fit, they may return the athlete to play earlier in positions in which stresses to the arm are less, such as batting or first or second base. Third base should be avoided due to the long throwing distance to first base. The athlete should not return to full pitching or play that requires hard throwing until they have completed a gradual interval throwing program and are able to throw pain-free and exhibit no pain over the proximal humeral physis on exam. If significant widening of the proximal humeral physis was noted on radiographs, follow-up radiographs are recommended prior to return to full play. Numerous studies have reported an increased risk for shoulder and elbow injuries (upper extremity injuries) in young baseball pitchers based on poor biomechanics, high volume of pitches thrown per game and during season ( Table 40.4 ), and throwing with a fatigued arm more than the type of pitch thrown. ^{, ,} Diversification in positions (playing other positions besides just pitching) may protect against ulnar collateral ligament reconstructions (UCLRs) and other shoulder elbow injures. A preseason strengthening program focusing on core and rotator cuff strengthening and scapular stabilization is recommended. Patient education on discouraging participation in multiple leagues in the same season, focusing on preseason conditioning, with emphasis on proper form, throwing mechanics, pitch count, and pitch types (avoid throwing curveballs at a young age) are felt to be crucial in the prevention of shoulder injuries in young throwing athletes. Maintaining a healthy shoulder through appropriate stretching and strengthening program regularly both in season and preseason is recommended.

Complications

Premature physeal closure and physeal fracture extending into metaphysis have been reported in association with LLS, but is rare. ^,

Pathoanatomy/Mechanism

Glenohumeral internal rotation deficit (GIRD) is defined as side-to-side total motion arc difference of more than 25 degrees. GIRD can be a source of shoulder dysfunction and pain in the young throwing athlete, and more recent studies are starting to allude that GIRD may be more common among younger overhead athletes than previously thought. One case series looking at patients ages 8 to 16 years diagnosed with Little League shoulder that showed that one-third of patients with LLS demonstrated GIRD and those with GIRD in their group had approximately three times higher probability of recurrence of LLS compared to those without GIRD. Overhead athletes frequently gain external rotation adaptively due to repeated microtrauma to the anterior capsule during the cocking phase of throwing, thought to be advantageous for achieving maximal external rotation for cocking phase of throwing, allowing the athlete to increase throwing velocity. As external rotation increases, internal rotation tends to decrease. Decrease in internal rotation is caused by tightness and contracture of the posterior inferior capsule, which can lead to altered shoulder mechanics and possible injury, such as superior labrum anterior and posterior (SLAP) tears or posterior shoulder impingement. ^,

History and Physical Exam Features

Patients will complain of shoulder pain with throwing motions and may report decreased performance. They may also report difficulty reaching behind their back or reaching across their body. On exam, external and internal rotation are documented with the patient in supine position to help stabilize the scapula and with the arm in 90 degrees of abduction. GIRD can also be visualized with the patient in seated position ( Fig. 40.5 ).

Imaging

GIRD is a clinic diagnosis. An MRI can be obtained if an associated shoulder injury or pathology is suspected and can reveal associated pathology such as SLAP lesions or rotator cuff pathology if present.

Nonoperative Treatment/Therapy

Physical therapy focusing on stretching of the posterior capsule and rotator cuff is recommended ( Fig. 40.6 ). As a primary component of GIRD may be soft tissue contracture, treatment should involve the soft tissues as well. The sleeper stretch is the most commonly used exercise to increase internal rotation and is preferred in a side-lying position to stabilize the scapula. To place strain on various parts of the posterior capsule and muscles, the arm is placed at 60, 90, and 120 degrees abduction and a rotational stretch is applied. The motion is held at the point of tightness. Various other internal rotation stretching and mobilization of the posterior capsule has been shown to decrease posterior capsule tightness and improve GIRD, with numerous studies showing good results. ^, Anecdotal and clinical experience suggests that the vast majority (>90%) do improve with rehab programs focusing on various types of stretching and mobilization techniques. Posterior capsule stretching should be part a young throwing athlete’s conditioning program. Several studies have shown that those overhead athletes who maintain a regular posterior capsule stretching regimen were less likely to have shoulder problems and injury. These suggest GIRD prevention may play an important role in preventing shoulder injuries in overhead athletes and GIRD should be screened for during preseason and while in season.

Operative Treatment

Athletes who do not respond to stretching and do not regain internal rotation with therapy may be candidates for posterior-inferior capsule release. In those athletes who undergo capsular release, the posterior inferior capsule may be found to be thickened and scarred down, off the glenoid rim. Releasing the thickened scar tissue can improve internal rotation. This procedure is not indicated as a solo procedure, but should be done in conjunction as part of repair of the superior labral tear or treatment of internal impingement, as those with persistent pain despite internal rotation improvement may have a SLAP lesion that may need to be addressed operatively.

Pathoanatomy/Mechanism

The shoulder joint is the most unstable joint in the human body. It is important for those who care for pediatric athletes are familiar with the different types of shoulder instability and treatment options available. Shoulder instability in the pediatric skeletally immature athlete can be traumatic or atraumatic in etiology. Patients with traumatic shoulder instability typically have a single traumatic event—either subluxation or dislocation with spontaneous reduction or requiring manual reduction. Traumatic dislocations often are associated with structural damage either at the bony or soft tissue level of the GH joint. They are also related with a high risk of recurrent dislocation in young, active patients. ^,

Atraumatic instability is often due to multidirectional instability in the young patient. Atraumatic instability can be congenital (i.e., patients with generalized ligamentous laxity) or acquired (i.e., young overhead throwing athletes whose shoulders are stressed repeatedly in hyperextension, abduction).

The three anatomic GH instability patterns are: anterior, posterior, and multidirectional. Anterior instability is the most common instability pattern in young athletes, comprising 85% to 95% of all instability cases. The main cause of anterior instability is the result of traumatic, acute injury. It is less commonly due to repetitive overuse injury in overhead throwing athletes, such as pitchers.

Posterior instability comprises only 2% to 10% of all patients with shoulder instability. They are frequently associated with seizures, electrocution injuries, and severe trauma.

Multidirectional instability (MDI) is subluxation, dislocation, or instability of the shoulder joint that occurs in more than one direction. It is typically atraumatic in the pediatric population and can present as unilateral or bilateral GH instability. It accounts for less than 5% of all shoulder instability cases. There is varying pathophysiology for MDI, which continues to evolve in literature. It is more common in athletes who perform repetitive overhead activities such as swimmers, throwers, gymnasts, and tennis players.

Pediatric patients can also develop secondary shoulder subacromial impingement syndrome due to MDI. This secondary impingement syndrome is thought to be the result of the humeral head not being centered in the glenoid fossa and its tendency for upward migration into the subacromial space due to ligamentous laxity and weakness of rotator cuff muscles.

History and Physical Exam

The history and physical exam often lead to the diagnosis of shoulder instability. The clinician should take into consideration the mechanism of injury, position of arm at the time of trauma, sports participation, and goals. In traumatic anterior shoulder dislocation, they will report of a shoulder in abduction and external rotation and receiving a hit to the arm, with the arm in full outstretched motion. In a posterior traumatic dislocation, the patient may report a direct blow with the arm in forward elevation, adduction, and internal rotation. A common position is linemen in football.

Frank dislocations often present to the emergency department either before or after reduction of dislocation. Spontaneous reductions can occur, but are more common in chronic, recurrent, anterior instability or with multidirectional instability of the shoulder. The young patient will often report a history of his or her shoulder “coming out” or “slipping out,” then popping back in. This may indicate a possible recurrent shoulder subluxation or instability. Patients may also complain of anterolateral and anterior shoulder pain with overhead activities and motion.

Inspect for any shoulder deformity or muscle atrophy. A thorough neurovascular exam, including assessment of the axillary nerve (the most commonly injured nerve in up to 42% of traumatic anterior shoulder dislocations), should be performed. Physical examination should include a comprehensive shoulder exam.

Certain tests are helpful for evaluating GH shoulder instability. Apprehension and relocation tests assess anterior GH instability. The patient should be lying in supine position on examination table with their arm abducted to 90 degrees and externally rotated. If the patient feels a slipping sensation or fear of a impending dislocation of their shoulder with this motion that is improved with applying a posterior force to the GH joint, it is a positive relocation test. This means that the posterior force applied to GH joint relocated the humeral head in place. The sulcus sign is performed at 0 degrees of abduction ( Fig. 40.7 ). Downward traction is applied on the humerus. Dimpling or a “gap” formed in the GH joint is a positive sign, indicating laxity of the superior GH ligament. ^, The load and shift test is used to evaluate anterior and posterior GH laxity and is performed while the patient is in a seated or supine position with the humeral head centered in the glenoid fossa and performed. Grade 0 means normal translation. Grade 1: translation to rim and back, less than 1 cm. Grade 2: translation over the rim followed by spontaneous reduction, 1 to 2 cm. Grade 3: translation over the rim without spontaneous reduction, greater than 2 cm. Generalized joint laxity should also be assessed using the Beighton score (0–9 point scale). ^,

Subacromial impingement secondary to MDI may pre-sent as tenderness to palpation over the supraspinatus tendon insertion site on the greater tubercle. Patients may have scapular winging and pain with impingement maneuvers such as the Hawkins and Neer tests. A positive Neer test is when pain over the subacromial joint space is elicited with forcing the arm into position of maximal forward elevation. A positive Hawkins test is when pain is elicited with the arm in internal rotation with the arm forward elevated to 90 degrees and producing pain as the supraspinatus tendon impinges on the coracoacromial ligament or anterior acromion. Strength testing typically also reveals weak external rotators and supraspinatus.

Imaging

Radiographic evaluation should include: AP Grashey, Y-scapular lateral views, and axillary lateral view to evaluate the relationship of the humeral head to glenoid and possible posterior humeral head compression fracture (Hill-Sachs lesion) or fracture of the glenoid rim (a bony Bankart lesion). High rates of glenoid bone loss are noted in adolescents with a traumatic shoulder dislocation and are often not seen on conventional x-rays. If further shoulder capsule or labral tissue injury is suspected, an MRI can be helpful. An MR arthrogram is the gold standard for imaging traumatic capsular or labral pathology. SLAP (superior labral anterior to posterior) tears have been found to be commonly associated with shoulder instability patterns in adolescents. If a bony Bankart or large Hill Sachs lesion is noted on radiograph, a CT can be helpful in evaluating and quantifying bone loss. Large bony defects may change surgical management and may require additional or alternative procedures rather than just a capsulorrhaphy, labral repair, or capsulolabral reconstruction.

Nonoperative Treatment

The first line of treatment for anterior GH instability in the young athlete with a traumatic anterior GH dislocation is controversial. High rates of recurrent instability have been reported after first-time dislocation in patients less than 20 years of age. Patients with traumatic anterior shoulder subluxation events may have associated labral injuries as well. The mainstay treatment for young patients with multidirectional instability is typically conservative. Nonsurgical management has shown overall good results. Physical therapy should focus on periscapular and rotator cuff strengthening to optimize dynamic stabilizers, as static ligamentous stabilizers are deficient in these patients. Good to excellent results in 80% of the patients with atraumatic shoulder subluxations treated conservatively with an exercise program focusing on strengthening dynamic stabilizers of the shoulder—including scapular stabilizers, trapezius, rhomboids, serratus anterior—have been shown.

Operative Treatment

Initial GH dislocation management is discussed in Chapter 29 . In the pediatric population, traumatic anterior shoulder dislocation accounts for greater than 90% of shoulder dislocation. ^, The first line of treatment for traumatic anterior GH shoulder dislocations is controversial. The rate of recurrent dislocation/instability following a traumatic shoulder dislocation in patients less than 20 years of age is found to be very high (75%–90%) in those treated nonoperatively. ^{, ,} Traumatic anterior shoulder dislocations in skeletally immature patients have also been shown to be associated with a humeral avulsion of the glenohumeral ligament (HAGL) injury. The causes of re-dislocation are likely multifactorial, including ligamentous laxity and participation in collision sports/high-demand activities.

A prospective series looking at 252 patients (15–35 years old) showed 56% of the patients had recurrent instability episodes at a mean follow-up of 13 months after being treated nonsurgically.

Hence, the idea of early surgical intervention with a stabilization procedure in these patients following a traumatic dislocation is often considered. Recurrent dislocations are not only painful, but may lead to cartilage damage, and limit activities of daily living and sports participation in these young patients. Several factors should be taken into consideration following traumatic shoulder dislocation and should include: the sport the patient is involved in (contact, throwing, upper extremity weight bearing sport), patient’s goals of continuing athletic participation at a high level, and possible career aspirations long term.

Surgical treatment for primary traumatic GH anterior dislocation can be arthroscopic or open. Instability recurrence rates after arthroscopic repair with suture anchors are now equal to classic open Bankart procedure, due to improved technology and advances in equipment, implants, and methods. Currently, there are few studies of arthroscopic repair of adolescent shoulder instability in literature. A retrospective study of 32 patients (11–18 years of age) showed 5 re-dislocations (16%) at 2 years after arthroscopic repair. Eleven patients returned to sports. Another retrospective study reported that although not statistically significant, post-surgical patients who underwent an open Latarjet technique showed better signs of shoulder stability and higher return to same level of sport (92%) compared to the nonsurgically treated group (52%).

Presently, there is no widely accepted guideline for surgical management for patients with MDI laxity of shoulder joint. However operative treatment can be considered for those patients with debilitating symptoms or limit activity after at least a six-month trial of dedicated rehabilitation. Excessive external rotation (>130 degrees) on clinical exam may be an indication for anterior capsular plication. Open and arthroscopic procedures are both options for those patients who fail nonoperative treatment. Both open and arthroscopic procedures have a similar reported success rate of 88% to 100%, with good to excellent results, and a recurrence rate up to 10%. ^{, ,} Open capsulorrhaphy or arthroscopic procedure should focus on the direction of instability. Thermal-assisted capsular shrinkage has been used to treat shoulder instability, but its utility has been questioned. There have been reported complications of capsular ablation, chondrolysis, and axillary nerve palsies. ^,

Injuries to the skeletally immature patients are unique and oftentimes may be sport specific. Many respond well to conservative and nonsurgical management, but surgical intervention may be necessary for certain circumstances. There is still a paucity of studies focusing on surgical intervention and outcomes in the young pediatric patient. In the meantime, injury prevention is key to helping keep our young patients active yet healthy.

Anatomy

The ossification center of the medial epicondyle of the humerus appears between 5 and 7 years of age and unites with the humeral diaphysis between 18 and 20 years of age. The common tendon of the flexor muscles of the forearm and ulnar collateral ligament of the elbow insert on the medial epicondyle. The ulnar collateral ligament is the primary soft tissue stabilizer to valgus stress and originates from the distal aspect of the medial epicondylar apophysis. The ulnar nerve runs in a groove in the posterior aspect of this epicondyle. The medial epicondyle is an apophysis and does not contribute to longitudinal growth of the humerus.

Pathoanatomy/Mechanism

The mechanism of repetitive stress or acute injury is a valgus stress producing traction on the medial epicondylar apophysis through the flexor muscles. In sports, this may occur traumatically with a fall in an upper extremity weight-bearing athlete such as gymnast, or in repetitive or an acute or chronic avulsive fashion as in a baseball player engaged in valgus mechanics during throwing. ^,

Medial Epicondyle Apophysitis

Medial Epicondyle Avulsion

Information specific to upper extremity athletes will be covered here. For more detailed information, please refer to the upper extremity trauma section.

Operative Treatment

Displaced Fractures

While acceptable results for function in the nonoperative extremity athlete may be commonly reported following nonoperative treatment of displaced fractures, we advocate an operative treatment for any displacement beyond 2 mm in the upper extremity athlete. ^{, ,}

For operative management, the patient may be positioned either supine or prone. We have found the prone approach to be most useful for ease of reduction and intraoperative management. In this position the avulsion bed is more easily identified and the tension of the medial flexor musculature is decreased. Open reduction is performed through a medial longitudinal skin incision. The ulnar nerve is identified and retracted posteriorly. The fractured medial epicondyle is identified and is anatomically repositioned with a towel clip. We favor fixation with a partially threaded screw (most often 4.0 mm with or without a washer), often using a cannulated system to achieve temporary fixation ( Fig. 40.8 ). Care must be taken in young patients to prevent comminution of the predominantly cartilaginous distal fragment during fixation. After open reduction we immobilize the elbow in 90° flexion for 1 to 2 weeks, after which active range-of-motion exercises are initiated. We occasionally splint the wrist for an additional 3 to 4 weeks after cast removal to prevent active contraction of the flexor muscle mass, which might displace the distal fragment.

With advanced imaging following an elbow dislocation, or a known significant medial elbow valgus overload in an upper extremity athlete, a partial apophyseal avulsion or periosteal sleeve avulsion of the distal aspect of the medial epicondyle may be identified. This fragment may often have the majority of the origin of the ulnar collateral ligament attached. When displacement of this osteocartilaginous avulsion is felt to be significant and at risk for nonunion or malunion of the origin of the ulnar collateral ligament, open reduction and fixation may be employed. In these select cases, small 2 to 3 mm suture anchors may be placed in the distal aspect of the remaining intact epicondyle and suture fixation of the small partial or periosteal sleeve avulsion may be employed. In such cases, a similar postoperative and return to play protocol is followed as above.

Pathoanatomy/Mechanism

The anterior bundle of the medial ulnar collateral ligament (UCL) is the primary static stabilizer of valgus stress at the elbow. It originates on the distal osteocartilaginous portion of the medial epicondyle apophysis with an origin center point approximately 3 mm from the lateral edge of the bony apophysis. The ligament inserts on the medial aspect of the proximal ulna at and just distal to the sublime tubercle.

History and Physical Exam Features

A history of repetitive overuse with throwing as described above is most often present in baseball players with a finding of ulnar collateral ligament injury of the elbow. High repetition of in-season throwing, play on multiple teams, positions of pitcher and catcher, and continued play through medial elbow pain may be significant correlations. ^{, ,} The ulnar collateral ligament may also be injured acutely with a valgus weight-bearing event during upper extremity gymnastic weight bearing or with an elbow dislocation.

Similar to medial elbow flexor tendinitis and apophysitis, the patient with an ulnar collateral ligament injury may present with local tenderness to palpation and loss of elbow extension. Additionally, pain with valgus stress tests and local pain focally and distal to the ulnar collateral ligament origin and extending to the sublime tubercle region is common.

Imaging

Plain radiographs may often show chronic changes of valgus stress in the ulnar collateral ligament injured elbow. In the case of a partial or osteocartilaginous sleeve avulsion, this radiodense fragment or fleck may be identified on radiographs.

Ultrasound or MRI may be employed to investigate the soft tissue portion of the ulnar collateral ligament. ^{, ,} MRI with joint arthrogram is most commonly used. A low-grade (I or II) partial injury may be difficult to definitively assess. Complete mid-substance or origin, insertional injuries (III) may be more clear. ^a

a References , , , , , .

Nonoperative Treatment

Definitive complete injury of the ulnar collateral ligament requires correlation of history, physical exam, imaging, and often failure of return to sport. Particularly in the adolescent population, nonoperative modalities should often be employed prior to consideration of operative treatment. Prolonged rest from throwing, stretches to address internal rotation deficit of the shoulder, periscapular and glenohumeral strengthening, arm strengthening, and a graduated return to throwing program is required. This may require several months of rest from desired throwing. Adolescent patients may also be counseled regarding transition to a less demanding position that will allow them to play and avoid surgery in some cases. ^,

Operative Treatment

A detailed description of perioperative care and surgical technique for reconstruction of the ulnar collateral ligament of the elbow is beyond the scope of this age-specific text. Operative treatment should be reserved for select athletes who have failed all nonoperative measures and following shared decision making regarding the significant time in rehabilitation commitment required following this procedure to return to high-level upper extremity sport. Excellent outcomes can be achieved in the adolescent population with ligament reconstruction, with or without augmented internal bracing. In addition to meticulous surgical technique, supervised physical therapy and graduated return to sport over 9 to 18 months is required for successful outcomes. ^b

b References , , , , , .

Pathoanatomy/Mechanism

The exact processes leading to capitellar and repetitive radial head lesions are unclear. Osteochondrosis may occur without any distinguishing history. Capitellar OCD and radial head stress fractures occur most often in valgus-mechanics throwing or upper extremity weight bearing. It is postulated that repetitive compression and sheer stress on the incompletely ossified capitellum and proximal radial epiphysis may play a role in the development of these lesions.

Osteochondroses of the Elbow (Panner Syndrome)

Panner first described a lesion in the epiphysis of the capitellum similar to Legg-Calvé-Perthes disease in 1927. In 1964, Smith reviewed the literature and proposed that Panner disease was a self-limiting condition that was nontraumatic in origin. Histologic studies of Panner disease have documented focal areas of avascular necrosis, with repair and revascularization.

History and Physical Exam Features

The entity described by Panner and subsequently referred to as Panner disease affects children younger than 10 years and is associated with pain and stiffness in the elbow. These patients do not have constitutional symptoms and rarely have a history of trauma. There may be a flexion contracture and diffuse synovitis.

Imaging

Radiographically, the capitellum will show irregular areas of radiolucency with areas of sclerosis. An effusion may be noted. An MRI will demonstrate areas of edema surrounding poorly vascularized epiphyseal bone. These lesions may also be evaluated by ultrasound. The articular cartilage has been noted to be normal.

Nonoperative Treatment

Treatment usually consists of reassurance, activity restrictions, and NSAIDs. Occasionally extremely symptomatic patients benefit from a period of immobilization in a splint or cast if the symptoms fail to resolve with conservative measures. Panner syndrome that does not follow this course should be re-evaluated critically for signs of capitellar OCD.

Pathoanatomy/Mechanism

Schenck and colleagues have proposed a repetitive microtrauma mechanism for the development of OCD of the capitellum. In a cadaver study, they noted that the central section of the radial head was significantly stiffer than the lateral capitellum. Presumably, the disparity in the mechanical properties of the central radial head and lateral capitellum would increase strain in the lateral capitellum. During activities associated with high valgus stress, such as throwing, this increased strain may be a factor in the development of OCD of the elbow. ^{, ,}

History and Physical Exam Features

OCD of the capitellum is distinguished from Panner disease in that it occurs in older children, is generally associated with overhead athletes (usually baseball players and gymnasts), and is more likely to require surgical treatment. As with Panner disease, the initial symptoms are typically pain, loss of extension, and occasionally mechanical symptoms.

Imaging

Radiographically, OCD of the capitellum may be similar to Panner disease ( Fig. 40.9 ). MRI, CT, and ultrasound may be used to further delineate the stability of the lesion. Lesion stability, and subsequently consideration of nonoperative and operative treatment, is primarily dictated by the status of the articular surface. If there is a breach in the cartilage and subchondral bone indicating in situ instability, the lesion is unlikely to heal with nonoperative treatment. These advanced imaging modalities have all been shown to be useful but not entirely specific in detection of instability, and CT and MRI may be employed without intra-articular contrast to aid in detection of surface anatomy. ^c

c References , , , , , , .

Nonoperative Treatment

Initial treatment of OCD is dictated by the stability of the lesion and integrity of the cartilage surface. Small lesions (less than 8 mm in diameter), with no signs of instability, in young patients with short symptom duration may have the best opportunity to heal with complete forced rest from upper extremity sport. ^{, , ,} Hinged range of motion bracing may be employed to augment activity restrictions. We employ shoulder and arm strengthening and ensure full wrist and elbow range of motion prior to graduated return to activity.

Operative Treatment

Patients in whom conservative treatment fails can be treated with arthroscopy for the assessment of articular cartilage, followed by treatment dictated by the stability of the lesion. For stable lesions, transarticular fine wire (.045 or.062 K-Wire) drilling is employed. Drilling at 2- to 3-mm intervals throughout the lesion using arthroscopic visualization and lavage is advocated. Treatment by injection of the subchondral bone with blood or marrow elements, or introduction of bone graft, has little current support in the literature. For unstable lesions, fragment excision and marrow stimulation using multiple drilling techniques has been advocated with reasonable results. Attention to débridement of all necrotic bone, restriction to use in smaller more central lesions, and use in nonupper extremity athletes may yield improved results ( Video 40.1 ). ^, Osteochondral grafting has been extensively studied and advocated for larger lesions in higher demand patients. Both auto and allograft osteochondral techniques have been described. ^{, , , ,} Single plug fixation of 8- and 10-mm diameters may often be utilized. Mosaic-plasty of the larger lesions with 6-, 8-, and 10-mm grafts may be employed to reconstitute the curvature of the articular surface.

Physical Therapy and Return to Play

Early range of motion is employed following treatment. As in marrow stimulation techniques and other parts of the body, continuous passive motion may be employed for defects treated with marrow stimulation in the elbow; however the utility of this has not been well studied.

A 6- to 9-month healing and rehabilitation is recommended prior to attempt to return to sport. ^, Periscapular, glenohumeral, arm, and wrist strengthening are employed. A graduated return to activity is recommended.

Outcomes

Results after surgical treatment may be favorable following either excision and marrow stimulation, or grafting, although some have reported an inability to return to high-level competition. ^{, ,} Larger and more lateral (particularly those uncontained by the capitellar lateral margin) lesions may have residual symptoms and decreased return to play. ^{, , , ,} Return to activity levels and outcomes are available in the early and intermediate terms only. Further study will be required for longer-term outcomes of capitellar OCD treatment.

Complications

Despite good short-term results, permanent deformity and disability can develop. A number of studies have documented permanent changes in the radial head, presumably the result of growth stimulation because of hypervascularity. The radial head has also been noted to dislocate over time. Two long-term studies (17- and 23-year follow-up) reported pain and decreased motion in 50% of patients with OCD as adolescents. ^,