Throwing Injuries of the Elbow - Part 1

by Heidi Tuthill MD & Michael B Zlatkin MD

INTRODUCTION
The elbow is injured in a predictable fashion in the overhead throwing athlete. Understanding throwing biomechanics of the elbow aids in the evaluation of the injured throwing elbow. Sports which put the elbow at greatest risk include baseball, American football, windmill softball, and javelin, as well as serving in tennis and the spike in volleyball.(1,2,3,4,5) The prevalence of elbow injuries amongst throwing athletes is increasing,(6) likely from the ever-increasing performance expectations that demand strenuous and longer training from earlier ages. Imaging is key to the diagnosis of both the acute and chronic injuries that result.

This article will first discuss the functional anatomy of the throwing elbow, followed by a brief review of biomechancis of throwing including the three forces which act upon the elbow during the overhead throw: medial tension, lateral compression, and posterior shear. Valgus overload is the foundation for these three forces, and generates distinct injury patterns which are then discussed by location: the medial soft tissue and osseous structures, the radiocapitellar joint, and the posterior humeroulnar articulation. The juvenile throwing elbow is discussed separately, as unique pathology afflicts the skeletally-immature throwing athlete.

ANATOMY & PATHOPHYSIOLOGY OF THE THROWING ELBOW

The elbow joint has a range of motion from 0 to roughly 140°;(7). Stability of the elbow joint throughout this range of motion results from the interaction of both soft tissue and osseous structures which play roles of varying importance which depend upon the degree of flexion. Ligaments and bones are static stabilizers, and the muscles about the elbow joint are dynamic stabilizers, compressing the asymmetrical but congruent joint surfaces against each other during motion.(8)

The soft tissue stabilizers include the anterior and posterior joint capsule, and the medial and lateral collateral ligaments. These soft tissue structures are the primary stabilizers of the elbow joint from 20 to 120° of flexion, which also happens to be the arc of motion where overhead throwing occurs.(1) The medial soft tissue stabilizers are of particular interest in the throwing athlete; of these, the ulnar collateral ligament (UCL) is paramount. The UCL is always composed of at least two bundles: the anterior oblique ligament (A-UCL) and the posterior oblique ligament (P-UCL). A third bundle, the transverse bundle, is variably present.(8) The A-UCL is the largest and most important of the bundles, as it is the primary restraint against valgus forces acting on the elbow joint,(1,8,9,10,11,12,13) incurring up to 55% of the valgus load stability.(9,13) The A-UCL originates from the anteroinferior medial humeral epicondyle, and inserts on the medial aspect of the ulnar coronoid process, a site known as the sublime tubercle; the A-UCL is best seen on coronal images as a distinct linear band, separate from the joint capsule, deep to the common flexor tendon, which, like all normal ligaments is homogeneously hypointense on all magnetic resonance (MR) sequences. The insertion site can either be directly onto the sublime tubercle, or alternatively up to 4 mm distal to this point.(14) A normal potential space, the ulnar collateral recess, can be seen deep to the humeral origin of this ligament, which on MR appears as linear hyperintensity (fluid) between the most proximal aspect of the ligament and the underlying medial trochlea;(15,16,17). Similarly, if the distal insertion is slightly past the sublime tubercle, normal intervening fluid can be seen distally.(14) The P-UCL is fan-shaped and often blends with the adjacent joint capsule, seen as focal capsular thickening rather than a discrete ligament; it arises from the same point as the A-UCL on the medial epicondyle but courses posteriorly to insert onto the medial margin of the ulnar semilunar notch.(17) The transverse ligament connects the distal insertions of the A-UCL and P-UCL. The function of the transverse ligament is not certain,(8) and the P-UCL does not play a major role in valgus stability;10 as both structures are also not routinely visualized on MR images(15,16) they will not be discussed further.

The flexor-pronator muscle mass acts as a dynamic medial soft tissue stabilizer, and consists of the pronator teres, flexor carpi radialis, flexor digitorum superficialis, and flexor carpi ulnaris; the latter two are the most important dynamic stabilizers.(18) These four muscles share a common flexor tendon which originates from the medial epicondyle, superficial to the ulnar collateral ligament. These muscles assist the UCL in resisting the valgus stress across the elbow during overhead throwing and flex the wrist during object release.(1,18)

At the extremes of extension, the osseous structures are primarily responsible for maintaining the elbow's stability when the olecranon process locks into its humeral fossa, limiting varus or valgus motion.(1,9) The radial head also assists in joint stability, acting as a secondary stabilizer against valgus force by engaging with the overlying capitellum; this role becomes more important as the integrity of the medial soft tissue stabilizers diminishes.(19)

BIOMECHANICS OF THROWING

The arm is cocked in preparation for a throw by abduction and external rotation of the shoulder, at the end of which the elbow is externally-rotated and flexed 90°. To decelerate the backwards rotation of the forearm and subsequently accelerate it forward, a large varus torque is generated on the forearm about the elbow joint.(3) Half of this forearm torque is generated from tension in the UCL; compression of the radial head against the capitellum generates nearly the entire other half, coupled with shoulder internal rotation.(3) Valgus strain results from the generation of this varus torque, the peak of which occurs during the transition from the late cocking to early acceleration phase. The elbow also extends during the acceleration phase at a rate of 3000°/sec,(20) and is fully-extended shortly after the point of ball release, rapidly bringing the olecranon into its fossa. Thus, three separate forces act upon the throwing elbow: tension within the medial structures (including the UCL, flexor-pronator muscle mass, medial epicondyle, and ulnar nerve), compression at the radiocapitellar articulation, and shear of the posteromedial olecranon against the adjacent olecranon fossa (Fig. 1).(3,21,22,23) Each of these three vectors results in predictable pathology, which will now be detailed below.

MEDIAL PATHOLOGY

UCL Injury

The A-UCL is particularly vulnerable to injury in throwing athletes, as it is the primary stabilizer against valgus stress; tremendous tension occurs within this ligament during throwing. Cadaveric UCL's have been shown to withstand an average maximum force of up to 33 N-m before failing; kinetic studies suggest a force within the UCL during pitching of up to 34 N-m.(24) Near-failure magnitude forces inflict microtrauma to the ligament; over time, as throwing continues, this damage accumulates.

Consequently, a throwing elbow differs from a nonthrowing elbow. Baseline changes have been shown in 87% of asymptomatic professional baseball players including UCL thickening, edema, and partial-thickness insertional tears, as well as osteophyte formation at the sublime tubercle.(25) Muscle hypertrophy also occurs; this hypertrophy combined with UCL changes are possible etiologies for both increased valgus carrying angles (greater than 15°) and slight flexion contractures observed in a large percentage of professional throwers' elbows.(1,26,27) Some of these findings may represent adaptations to the unnatural stresses incurred throughout years of play; alternatively, these changes could represent subclinical degrees of injury. Certainly superimposed injuries occur in these high-demand athletes. Cumulative microtrauma leads to chronic overuse injury causing insidious elbow pain. Acute injuries also occur; up to two-thirds of injured athletes can recall an exact throw during which they incurred an elbow injury.(12) MR findings in this population must therefore be carefully interpreted in conjunction with the athlete’s history and physical exam findings.

UCL injury initially presents clinically as decreased velocity and control during throwing, usually closely associated with pain during the late cocking/early acceleration phases of throwing. Injuries can be difficult to detect clinically, as medial elbow tenderness is nonspecific, and the valgus laxity allowed by the damaged UCL may not be evident on physical exam.(16) Arthroscopy also provides limited visualization of the A-UCL, the most important component to evaluate in symptomatic throwing athletes.(9,12,28,29) MR imaging allows visualization of the entire A-UCL, and therefore is crucial in the evaluation of patients with suspected injury.

MR imaging of chronic overuse injury to the UCL shows ligamentous thickening, contour irregularities, laxity, increased intraligamentous signal, or a combination of these findings.(17) Torn ligaments show similar findings and disruption of ligament fibers, ligament attachments, or both. Tears may be partial or complete; partial tears most commonly involve the deep fibers at the ulnar insertion, and are diagnosed when fluid-intensity tracks between the sublime tubercle and the A-UCL undersurface (Fig. 2), known as the “T-sign.”(16) Edema-like signal within the medial epicondyle or sublime tubercle is often present, which can reflect either acute injury or chronic stress reaction. Increased T1 and T2 periligamentous signal may occur, indicating hemorrhage and edema in the setting of injury,17 although isolated periligamentous T2 hyperintensity can also reflect scarring (Fig. 3).(30) Additional signs of chronic injury include sublime tubercle osteophytes/enthesophytes (Fig. 4) and heterotopic ossification along the A-UCL.(31) The presence of these associated findings combined with clinical history can aid in distinguishing distal partial tears from the A-UCL distal insertional variant described in the anatomy section above.(14) Complete tears are usually seen in association with acute valgus stress or traumatic elbow dislocation (Fig. 5).(32) Alternatively, the ligament may remain intact but avulse its attachment sites at the medial epicondyle or sublime tubercle.(33,34,35) Any of these functionally complete tears may also show tendon retraction.(17)

We do not routinely perform MRI arthrography in our practice, however in the literature, MR arthrography has been shown to improve sensitivity for detection of both partial and complete tears (16,30,36,37) by better delineating articular–sided UCL abnormalities or separation of the distal attachment (Fig. 6); frank contrast extravasation may be seen in the setting of complete UCL tear.(30)

Surgery is reserved for elite throwing athletes who wish to return to competitive play despite injuries which persist after conservative therapy. Surgical treatment most commonly consists of reconstruction using tendon grafts. The integrity of both the graft and its attachments should be evaluated; other markers of chronic medial valgus instability may be present (Fig. 7).

If surgery is not performed, and UCL-deficient athletes continue to throw, chronic medial valgus instability may result in the development of other pathologic lesions including flexor-pronator injury, ulnar neuritis, radiocapitellar arthritis, and posterior impingment.

Medial Epicondylitis

Because of their medial location, the flexor-pronator muscles are also subject to tensile forces generated from throwing. When the A-UCL is compromised, the flexor-pronator muscles are especially vulnerable to injury; the medial elbow stabilizers function synergistically, so when one is injured, pathology often ensues in the other. Increased strain on the flexor-pronator muscle group results in hypertrophy, acute musculotendinous tears, or tendinosis.(8,9,38) Common flexor tendinosis, or medial epicondylitis, results from imperfect healing following either microscopic or macroscopic avulsion of the tendon from the medial epicondyle.(38)

Radiographs may show hypertrophic spur formation at the medial epicondyle;(38) 20-25% of patients also form calcifications of the adjacent soft tissues.(27) On MRI, the common flexor tendon is best evaluated on coronal sequences; normally, the tendon is homogeneously hypointense, seen firmly attaching to the medial epicondyle. Findings in medial epicondylitis include increased T1 and T2 signal within a thickened common flexor tendon, as well as peritendinous soft tissue edema; the most specific of these findings is intermediate to high T2 signal within both the common flexor tendon and the surrounding soft tissues.38 Edema within the medial epicondyle can also be seen (Fig. 8).(38) Edema within the flexor-pronator muscle bellies indicates muscle strain; fluid-like signal disrupting muscle fibers indicates more advanced stages of muscle injury. It is imperative to also assess the integrity of the UCL in patients with findings of medial epicondylitis, as this may be the true underlying pathologic lesion.

Surgical treatment is reserved for patients who fail conservative management, although in elite throwing athletes, surgery may be performed sooner if tendon disruption is evident by physical exam or imaging; repair involves excision of damaged portions of the tendon and reattachment of any elevated portions back onto the medial epicondyle. (27)

Neuropathies

The ulnar nerve runs along the medial head of the triceps in the distal arm, posterior to the medial intermuscular septum; once it reaches the elbow, it enters the cubital tunnel. The borders of the cubital tunnel are formed by the medial epicondyle anteriorly; the medial edge of the trochlea, olecranon, and UCL laterally; and the arcuate ligament superficially. As it exits the cubital tunnel into the forearm, the ulnar nerve passes between the humeral and ulnar heads of the flexor carpi ulnaris muscle. The ulnar nerve provides motor innervation of this muscle, as well as the ulnar portion of the flexor digitorum profundus muscle, and also provides sensory innervation to the skin of the ulnar forearm, ulnar half of the fourth, and entire fifth digit.

Ulnar neuropathy in the throwing elbow may be caused by stretching, compression, friction, or a combination of these mechanical factors. Medial tension during throwing can result in stretch injury to the nerve; UCL deficiency augments these forces by allowing the medial joint to open during valgus strain and stretch the nerve even more.

Many factors may contribute to compression neuropathy in the throwing elbow. The cubital tunnel normally narrows 55% during flexion;(26) the degree of narrowing increases with UCL deficiency and resultant valgus instability.(39) Osteophyte formation at the osseous boundaries of the cubital tunnel, adjacent synovitis, or loose bodies can further decrease the tunnel’s dimensions. Compression can also occur outside the tunnel at multiple sites: between the two heads of flexor carpi ulnaris, along the medial head of the triceps in the distal arm, or at the arcade of Struthers, a fibrous tunnel present in 70% of individuals which connects the medial intermuscular septum of the arm to the tendon of the medial head of the triceps. Adaptive changes of the throwing elbow such as muscle hypertrophy and increased valgus carrying angles may predispose to compression neuropathy, as can the presence of an accessory muscle at the cubital tunnel, the anconeus epitrochlearis (Fig. 9).(4,39,40)

Friction can also contribute to ulnar neuropathy. Asymptomatic subluxation or dislocation from the epicondylar groove occurs in 10-16% of individuals during elbow flexion;(41) however, in throwing athletes who repeatedly flex and extend their elbows, this congenital excursion might be more likely to result in friction neuropathy. Pain associated with ulnar nerve excursion is known as snapping elbow syndrome; if the medial head of the triceps also dislocates over the medial epicondyle, rubbing and compressing the intervening ulnar nerve, it is called snapping triceps syndrome.(26,39) Nerves that do not dislocate might also be subject to friction in the throwing athlete, as recent cadaveric studies have documented motion of the ulnar nerve within the cubital tunnel during simulated throwing of up to 12.4 mm.(42)

In throwing athletes, the first symptoms of ulnar neuropathy can be fatigue after repetitive throwing, as well as loss of throwing velocity or control; pain or paresthesias during the late cocking or early acceleration phases of throwing also suggest ulnar neuropathy.(43)

Median nerve problems should be considered in the thrower with anterior elbow pain, although this nerve is much less commonly problematic in the throwing elbow. Volar forearm pain which radiates distally with paresthesias in the first three fingers are typical symptoms, evoked during the deceleration or follow through stages of throwing when the anterior structures are maximally strectched.(43) The most vulnerable site of injury is the area of the nerve’s passage beneath the pronator teres muscle, where repetitive elbow extension and supination during throwing can irritate the nerve; hypertrophy of this muscle can contribute to median neuropathy.(43) Other potential sites of compression include the flexor digitorum superficialis, the lacertus fibrosis, and the supracondylar process, a structure present in 1-3% of the population which projects from the anteromedial humerus 5 cm proximal to the medial epicondyle (Fig. 10).(39,43) The ligament of Struthers connects this bony process to the medial epicondyle, creating a tunnel that the median nerve must traverse in its course to the elbow; entrapment within this tunnel results in supracondylar process syndrome.(39)

MR imaging can aid in the evaluation of these neuropathies. Relative to muscle, normal nerves are isointense on T1 weighted images and iso- to slightly hyperintense on T2 weighted images.(39) Injured nerves show increased signal intensity on T2 weighted images, and may be associated with a mottled appearance and fascicular distortion.39 In cases of compression, fusiform or focal thickening of the nerve may be seen at or proximal to the site of compression (Fig. 11).(15,39)

Owing to the superficial location and abundant surrounding fat, MR provides excellent evaluation of the ulnar nerve at the elbow, especially on axial images.(39) The flexor carpi ulnaris and flexor digitorum profundus muscles should be assessed for signs of denervation; increased signal on T2 weighted images within the muscles can indicate acute denervation, while fatty atrophy implies chronic denervation injury.

The median nerve is often poorly visualized at the elbow where it courses between the pronator teres and brachialis muscles, due to a paucity of surrounding fat; the nerve is better visualized as it courses distally into the forearm, between the superficial and deep heads of the pronator teres muscle and then adjacent to the lacertus fibrosis; again, axial images are most useful.(39) The MR imaging evaluation of patients with median neuropathy localized to the elbow should span from the distal one third of the arm to the flexor digitorum superficialis muscle in the proximal forearm; radiographs should also be performed to exclude a supracondylar process.

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