Throwing Injuries of the Elbow - Part 2

by Heidi Tuthill MD & Michael B Zlatkin MD

LATERAL PATHOLOGY

Radiocapitellar Overload Syndrome

UCL deficiency increases the magnitude of lateral compressive force generated during the throw, allowing the radial head to abut the overlying capitellum and result in radiocapitellar overload syndrome.(1) Chronic repetitive compression at this articulation can lead to chondromalacia; osteoarthritic changes generally follow (Fig. 1). Continued radiocapitellar compression can progress to osteochondral fracture and loose body formation.(1)

POSTERIOR PATHOLOGY

Posterior Impingement

Repetitive shear forces at the posterior elbow can lead to posterior impingement. As the elbow rapidly extends during overhead throwing, the posteromedial olecranon compresses upon and slides over the adjacent olecranon fossa. The rapid and repetitive nature in which this occurs in the throwing athlete induces hypertrophic osteophyte formation at the olecranon articular surface; the adjacent synovium and soft tissues can also hypertrophy. UCL insufficiency is believed to be an etiologic factor,(2,3) as valgus laxity augments posterior contact pressures.(4) Once formed, olecranon tip osteophytes can erode the subjacent trochlear cartilage; intraarticular bodies can eventually result from either cartilaginous injury or osteophyte fracture. This spectrum of posterior changes induced by medial laxity, known as the valgus extension overload syndrome,(2) causes pain in terminal extension, when the misshapen olecranon abuts its humeral fossa.

MR imaging reveals the posteromedial osteophytes, increased signal on T2 weighted images, (reflecting stress reaction) of the underlying bone (Fig. 2), and chondral loss at the medial olecranon and posterior trochlea (Fig. 3).(2,5) Affected patients may be unable to fully extend their elbows during MR imaging, which can be appreciated on sagittal images.(5)

Surgical treatment involves either arthroscopic or open debridement of osteophytes, hypertrophied soft tissues, and loose bodies. Careful resection is essential, as a fine balance exists between the elbow’s adaptive hypertrophy of the posteromedial osseous constraints and a lax UCL; excessive resection can further destabilize the joint and expose an already compromised UCL to additional stress and failure.(4,6) In one series, up to 25% of baseball pitchers required UCL reconstruction following resection of posteromedial osteophytes.(7)

Olecranon Stress Fractures

Olecranon stress fractures are a less common cause of posterior elbow pain in the throwing athlete. The loads incurred by the posterior elbow inflict microtrauma to the bone trabeculae; routine repair of this microtrauma generally occurs, and in fact, the above mentioned hypertrophic osteophytes are a manifestation of the olecranon’s attempt to maintain itself. However, if the bone’s reparative abilities are overcome by repeated stresses, the damage begins to accumulate, and a continuum of stress injury ensues. Initial stress reaction can progress to stress fracture, and stress fracture can progress to nonunion if repetitive forces enable the imbalance between repair and damage to continue.

Three sites of fracture have been described in throwing athletes: the olecranon tip, the proximal posteromedial olecranon, and the mid-olecranon.(8) Slight initial pain at terminal extension gradually worsens with continued activity. Stress reaction first develops at the site of injury, which on MR appears as edema-like signal or periosteal fluid (Fig. 4); as the injury progresses, a hypointense fracture line develops within the region of signal alteration (Fig. 5).(8) Early recognition of these changes is essential to prevent progression to nonunion.

Treatment varies upon the degree of injury and location of fracture.(1,9) Symptomatic stress reaction and nondisplaced fractures at all sites are treated conservatively. Complete transverse olecranon fractures displaced by more than 2 mm are often managed surgically, as are nonunited fractures. Complete olecranon tip fractures are excised.

Spontaneous spiral fractures of the humerus have also been described in throwing athletes, perhaps also the endpoint of a continuum of stress injury.(8,10)

Triceps tendinosis

Triceps tendinosis can also afflict the throwing athlete; it preferentially affects males.(11) Changes in morphology and signal of an affected triceps tendon mimic those described above in flexor-pronator tendinosis, including thickening and increased signal intensity within the tendon (Fig. 6).(12,13) Tendinosis may be acute or chronic; x-rays revealing calcifications in the region of the triceps tendon, or traction spurs at the olecranon insertion indicate more long-standing disease.(14) Treatment is conservative, although the presence of traction spurs or tendon calcifications have been associated with higher failure rates of conservative treatment and may be an indication for tendon debridement and spur excision.(11)

STRESS PATTERNS ON MR IMAGING

Although each site of pathology was discussed separately above, it is important to remember that valgus instability is the inciting factor for many of these entities and they can therefore occur simultaneously. Additionally, a common stress pattern is seen in throwers’ elbows of edema-like signal in the medial epicondyle, coronoid process, sublime tubercle, and olecranon (Fig. 7).

THE JUVENILE THROWING ELBOW

Throwing injuries also frequently afflict the pediatric athlete. More than two million children participate in Little League baseball in the United States each year; 17-58% of them report elbow pain.(15) The same three abnormal forces about the adult throwing elbow also affect children; the pathology which results, however, is unique to the pediatric population. Physeal status - open or fused - determines what type of pathology results from these forces. Physes are inherently weaker than ligaments, so when open, the brunt of injury is often transferred to the physeal plate rather than the ligaments and tendons which attach to them. Such is the case at the medial elbow, where the tensile forces preferentially affect the medial epicondylar apophysis rather than the UCL in patients with open physes. The same lateral compressive forces act at the radiocapitellar articulation, resulting in forms of chondral injury unique to juvenile throwers. Posterior shear forces infrequently cause pathology in this population,(16) but can affect the olecranon epiphysis.

As in adult athletes, many injuries occur from chronic overuse, although acute injuries also occur. In fact, the most common fracture of the juvenile throwing athlete occurs at the elbow: medial epicondyle avulsion.(15,16) This Salter fracture results from acute, large-magnitude valgus stress and/or forceful contraction of the flexor-pronator muscles; although significant tension is also generated within the UCL, the ligament is typically spared from injury at the cost of apophyseal avulsion.

Radiographs are often sufficient to make the diagnosis, revealing physeal widening which can be confirmed with comparison views of the normal elbow when subtle. Fractures are classified according to patient age and fragment size:(16) Type I in patients less than 14 years old with a large fragment, typically the entire apophysis; Type II in patients 15 years and older with a large fragment; and Type III in patients 15 years and older with a small fragment. Fragment rotation or possible entrapment in the joint space should be noted, as should the degree of fragment displacement. Controversy remains regarding the amount of fragment displacement in athletes that warrants surgical repair, 2 mm versus 3-5 mm.(16) Fragments trapped within the joint space also require surgical reduction.(14)

Lower-magnitude, chronic, repetitive valgus stress affects the medial epicondylar apophysis in a different way; traction apophysitis commonly results, causing medial elbow pain which is insidious rather than acute. The initial description of "Little Leaguer's elbow" referred to this type of medial elbow pain resulting from medial epicondylar apophysitis.(17) Recently, however, the term has been used more loosely to describe all of the pathology resulting from the stresses about the throwing elbow, including medial epicondylar apophysitis/avulsion; flexor-pronator tendinopathy; chondral injuries at the capitellum, radial head, and trochlea; and olecranon apophysitis.(15,16,18)

X-ray findings of medial apophysitis include hypertrophy, separation, and fragmentation of the medial epicondyle ossification center.(5,19) However, similar findings can also be seen in aymptomatic young throwing athletes; Hang et al(20) evaluated over 300 young elite baseball players, and found that 94% of them showed hypertrophy, 57% showed separation, yet only 52% of these patients reported pain. Similar to the adult throwing elbow, altered morphology in asymptomatic patients supports the idea that chronic overuse induces a spectrum of joint changes which may initially be physiologic and eventually pathologic with continued repetitive stress. This also reiterates the importance of interpreting imaging findings in conjunction with clinical history. Although often not crucial to the diagnosis, MR findings of medial apophysitis include physeal widening, marrow edema within the apophysis, and surrounding soft tissue edema. Treatment of medial apophysitis includes rest, followed by gradual return to activity if the patient remains pain-free.(21) Prompt identification and treatment of both acute and chronic medial apophyseal injuries are essential for good long-term prognosis, as continued throwing despite symptomatology can result in medial epiphyseal nonunion, leading to permanent deformity and predisposition to valgus instability.

Once the medial ossification center fuses, usually around age 15 in males, the medial tensile forces are transferred back to the structures that attach to it, and injury patterns resemble those of adults.(16) MR imaging may not be necessary in young throwers with medial elbow pain, as both medial epicondyle avulsion and apophysitis can be diagnosed by x-ray findings. However, in adolescent throwers with nearly-fused medial ossification centers, the utility of MRI increases because these patients may display features of both pre-fusion (medial epicondyle avulsion/apophysitis) or post-fusion injury patterns (UCL injury and medial epicondylitis), as seen in Figure 8.

Before evaluating the young thrower for UCL injury it is important to recognize two major differences in the MR appearance of the normal pediatric UCL, described by Sugimoto and Oshawa.(19) One involves the distal ulnar insertion, and the second the proximal humeral enthesis; these normal findings change in appearance as the medial epicondylar apophysis closes. Before apophyseal fusion, the proximal ulnar periosteum is normally separated from the underlying cortical bone; these findings appear on MR imaging as a thick, linear, universally hypointense outer periosteum separated from the underlying cortical bone of the sublime tubercle by thin linear hyperintensity. The distal A-UCL fuses with the thick outer periosteum and is therefore not directly attached to the sublime tubercle. As the apophysis fuses, so does the periosteum to the cortical bone, and the distal attachment of the A-UCL thereafter resembles that of adults. The second difference in the pediatric UCL occurs proximally, at the attachment of the A-UCL to the medial epicondylar hyaline cartilage; a distinct region of moderately-hyperintense T2/intermediately-intense T1 signal is believed to represent the UCL enthesis. These authors suggest a high elastin content creates the unique signal at this site; this normal finding should not be mistaken for injury. The T2 increased signal at the enthesis remains following apophyseal closure; however, the T1 signal decreases, becoming inhomogeneously hypointense.

Posterior compartment pathology uncommonly afflicts the skeletally-immature throwing athlete, although injury patterns similar to medial apophysitis can also occur at the olecranon apophysis. Repeated contraction of the triceps employed during the rapid extension of the throwing elbow can cause olecranon apophysitis, generally seen in younger throwing athletes.(1,22) X-rays reveal olecranon physeal widening; MRI can additionally show marrow edema within and around the ossification center. These same stresses in older adolescent throwers typically result in avulsion or stress fractures; the degree of fracture displacement is important to assess for treatment planning. Displacement less than 2 mm is treated with immobilization; large fragments displaced more than 2-4 mm are surgically reattached.(21) Just as in medial apophyseal injury, if throwing is continued in the setting of injury, nonunion can ultimately result.(21,22)

Laterally, repetitive compression of the radial head against the capitellum creates chondral lesions which are unique to the pediatric population; males are more commonly affected than females.(18,23,24) Although the exact mechanism of injury is unknown, repetitive microtrauma and ischemia are believed to be prominent factors.(23,24,25,26) The name of the lesion which develops depends on the age of the patient and the physeal closure status: younger patients (typically 5 to 11 years old) with open physes have Panner's disease, while older patients with nearly-complete capitellar ossification develop osteochondritis dissecans (OCD). Despite their similar etiologies, a distinction is made between the two as their clinical presentation, radiographic findings, and prognosis are quite different.

Panner's disease is a self-limiting osteochondrosis that involves the entire capitellum. Radiographs in Panner’s disease reveal flattening, fissuring, fragmentation, or diminished size of the capitellum, possibly with subchondral lucency; effusions can also be seen.(18,26) MRI depicts these morphologic changes of the capitellum, as well as decreased T1 and increased T2 signal within; the overlying cartilage is normal.(16) Treatment is directed towards alleviation of symptoms, which often occurs after 3 to 4 weeks of rest.(18) Follow-up imaging shows gradual reversion of these findings; the abnormalities usually resolve completely, without residual deformity, within two years.(18)

In contrast, osteochondritis dissecans affects only a focal area of the capitellum, typically anteriorly and distally. Once formed, and if subjected to repetitive forces, these lesions become progressively unstable, and can ultimately break off into the joint space.(23) OCD can therefore result in permanent sequelae, including articular surface damage, decreased joint stability and motion, and premature osteoarthritis.(16,23) Less than half of these lesions (47%) are seen on x-rays; findings range from subtle capitellar flattening and subchondral lucency in early-stage lesions to focal articular surface defects and loose bodies in advanced disease.(24) MRI provides superior sensitivity for detection of these lesions, and more importantly can detect lesions in their early stages,(24,32,27) when elbow immobilization may halt the progression of disease and prevent long-term complications. The earliest MR findings of OCD include flattening and decreased T1 signal intensity at the capitellum; more advanced lesions show increased signal on T2 weighted images, either peripherally, or homogeneously within (Fig. 9).(16,23) Once a lesion is identified, several other features must be described. First, the integrity of the overlying cartilage and subchondral plate must be assessed for irregularity or fractures, the latter seen as linear high signal passing through these structures. Second, the stability of the lesion must be determined; large fragment size (>5mm), circumferential fluid-like signal, large/multiple cystic changes at the lesion-bone interface, or frank displacement of the osteochondral lesion indicate instability;28 lack of central enhancement within the lesion following intravenous gadolinium administration also suggests instability.(29,30) Lastly, the joint must be inspected for loose bodies.

Accurate description of imaging findings is important to guide treatment planning. Stable lesions are treated conservatively, with cessation of throwing and rest. Unstable lesions, articular cartilage fracture, and loose bodies are surgical indications.(18) Surgical treatment for advanced lesions includes debridement, subchondral curettage or drilling to encourage vascular ingrowth, or fragment fixation.(18,26,31) Limited data on autologous osteochondral mosaicplasty suggests favorable results for the treatment of advanced lesions (displaced or detached fragments), although the long-term efficacy of this relatively new procedure is unknown.(31)

Lateral compression can less commonly result in OCD of the radial head.(1,16,18) Fractures of the radial neck physis have also been described;(1) patients have point tenderness on exam, while x-rays show effusion, seen as a posterior fat pad sign, and physeal displacement (Fig. 10).

LOOSE BODIES

Many of the above-described pathologies can result in loose body formation within the throwing elbow, including osteophyte avulsion and chondral injury. Ossified loose bodies may be detectable with plain radiographs, although not reliably; in one series, sensitivity of radiographs was only 27% for identification of surgically-confirmed loose bodies.(7) Seen as round to oval-shaped regions of ossification, loose bodies are most often located in the olecranon and coronoid fossae.(30)

MR imaging better depicts intraarticular loose bodies (figure 11) 30, especially when there is also joint fluid, either due to an effusion or related to injected gadolinium/saline.(32) Ossified loose bodies’ internal signal ranges from T1 increased signal, compatible with fatty marrow, to T2 hyperintensity compatible with edema, the latter of which is especially seen when concurrent impingement is present.(30) Chondral loose bodies’ internal signal matches that of adjacent cartilaginous surfaces.

CONCLUSION

Elbow pain in the throwing athlete is a complex clinical problem, which is simplified by an understanding of throwing biomechanics. Medial tensile, lateral compressive, and posterior shear forces occur within the throwing elbow because of the valgus stress created during overhead throwing. The ulnar collateral ligament is the keystone of elbow valgus stability; in adults, its integrity must be confirmed before other etiologies of pain and dysfunction are considered. Once injured, altered biomechanics result, and valgus instability creates predictable injury patterns elsewhere in the joint, which can be assessed with MR imaging. The pediatric throwing elbow results in unique pathology, all of which is important to identify and treat early to prevent long-term sequelae. Throwing athletes of all ages can show altered morphology regardless of symptomatology, so clinical and imaging findings must be carefully correlated in order to create a successful treatment plan.

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