Anatomy

The ulnar collateral ligament (UCL) is composed of an anterior bundle, a posterior bundle, and a variable transverse oblique bundle, sometimes referred to as the Cooper ligament. The anterior bundle arises from the inferior-most aspect of the medial epicondyle and inserts on the sublime tubercle of the coronoid process of the ulna. The anterior bundle is composed of an anterior and a posterior band, which provide restraint against valgus stress at different degrees of flexion.

The anterior bundle is the primary restraint to valgus stress of the elbow at 30° to 90° of flexion and is a coprimary restraint along with the posterior bundle at 120° of flexion. The anterior band provides restraint to valgus stress from 0° to 85° of flexion, whereas the posterior band provides the most restraint from 85° to 120°. Fifty percent of the valgus torque imparted on the elbow is transmitted to the UCL. The remainder of this stress is taken up by the strong flexor-pronator muscle mass on the medial side of the elbow.

Etiology

The valgus and extension forces across the elbow during throwing activities often exceed the failure strength of the UCL. Repetitive or excessive stress leads to microtrauma and potentially acute rupture of the ligament. There is a cumulative effect of this microtrauma, and athletes who do not take adequate time to heal are at increased risk for rupture.

UCL injuries are seen in tennis players, football players, wrestlers, javelin throwers, and most commonly, baseball players, especially pitchers. Risk factors for UCL injury in baseball players include high-pitch velocity, inadequate warm-ups, and inadequate rest time. Chronic attenuation of the UCL can lead to further injury in the elbow due to increased bony stress, including radiocapitellar arthritis and posteromedial olecranon arthritis.

History and physical

Acute injury is typically described with pain or a pop on one throwing motion. The athlete is unable to continue play and may describe a feeling of paresthesias within the ulnar nerve distribution. In contrast, patients with chronic injury to the UCL may report a loss of ball control, loss of velocity, or increased fatigability. Pain is often reported by patients to be associated with the acceleration phase of throwing. Patients in the later stages of chronic UCL injury may report pain with terminal extension of the elbow.

Physical examination should begin with assessment of both passive and active range of motion. Any joint effusion or flexion contracture should be documented. The carrying angle of the elbow, normally 11° in men and 13° in women, may be as large as 15° in throwers. This is thought to be the result of adaptive change secondary to the repetitive stress and laxity of the UCL.

The elbow should be palpated to determine sites of abnormal tenderness. Lateral pain with pronation and supination may indicate arthritic change due to overload of the lateral structures, whereas posterior discomfort in full extension suggests posteromedial olecranon arthritic change secondary to repetitive extension overload. Neurologic changes should be assessed, as laxity of the UCL can cause tension on the ulnar nerve, leading to complaints of weakness or paresthesias.

The “milking test” is used to assess for UCL laxity ( Fig. 1 ). The examiner stands behind the patient while the forearm is supinated and the elbow is flexed to 90°. The examiner applies a valgus force to the elbow by pulling on the patient’s thumb. Apprehension, pain on the medial side, or instability indicates laxity of the UCL.

Milking maneuver test: the examiner grasps onto the patient’s thumb, using his elbow as a fulcrum and applies a valgus directed force to the arm.

The “moving valgus stress test” has been shown to be 100% sensitive and 75% specific for UCL laxity ( Fig. 2 ). The test is performed by maximally flexing the elbow. The examiner applies a valgus torque to the elbow as it is quickly extended. Apprehension, pain, or instability, usually from 70° to 120° of flexion, signifies a positive result.

Moving valgus stress test. ( A ) Examiner places valgus stress with elbow at 90° of flexion. ( B ) Elbow is quickly extended to approximately 30° with continuous valgus stress.

UCL disruptions are commonly seen in conjunction with other injuries of the elbow. Ulnar neuritis, medial epicondyle apophysitis, and flexor-pronator mass tendonitis must remain in the clinician’s differential diagnosis. Posterior and lateral elbow pain may indicate posteromedial olecranon and radiocapitellar arthritis secondary to laxity of the medial ligaments. A thorough examination of the shoulder is also mandated, as overhead throwers may have concomitant rotator cuff and glenohumeral capsulolabral injuries.

Imaging

Anteroposterior (AP), lateral, internal oblique, external oblique, and axial radiographs should be obtained. The examiner should assess for osteophytes, loose bodies, or calcification of the ligaments. In cases in which the diagnosis of UCL injury is in doubt, valgus stress views of the affected elbow in 25° of flexion should be compared with the contralateral elbow. Gapping of greater than 3 mm compared with the contralateral side indicates laxity of the UCL.

Ultrasound is an inexpensive and noninvasive imaging study to assess the UCL. Sonogram of an injured UCL will exhibit heterogeneity, hypoechoic foci, thickening, and possibly calcifications. Dynamic stress ultrasonography can be a useful adjunct when static ultrasound fails to yield the diagnosis. As with other forms of ultrasound imaging, ability to detect pathology is dependent on the skills and technique of the technician.

Advanced imaging with magnetic resonance imaging (MRI) and computed tomography (CT) arthrogram may be necessary when the diagnosis of UCL injury is in doubt, as well as for preoperative planning. For partial tears, CT arthrogram is 86% sensitive and 91% specific, whereas MRI is less sensitive (57%) and more specific (100%). MR-arthrogram remains the test of choice, having the highest interobserver reliability and the greatest ability to identify complete tears, with 86% sensitivity for partial tears, 95% for complete tears, and 100% specificity for both ( Fig. 3 ).

MR arthrogram demonstrating a partial UCL tear.

Treatment

Initial treatment of a partial UCL injury is typically nonoperative. The player is removed from active throwing for at least 3 months and a course of passive and active range of motion is instituted. Ice and anti-inflammatory medications are helpful for symptomatic relief. Limited data suggest that 42% of players are able to return to play nearly 6 months after institution of therapy. Unfortunately, no data are available as to which findings in the history or physical examination predict successful nonoperative treatment.

Platelet-rich plasma (PRP) injections have shown some promise by increasing return to play rate following partial UCL tears. PRP injection for has been shown to improve Disabilities of the Arm, Shoulder, and Hand scores and decrease medial joint space gapping under stress while maintaining an 88% return to preinjury level of play. Average time for return to play is 12 weeks after PRP injection. Additional studies are required to validate these results.

Surgical indications in the throwing athlete include complete ruptures of the UCL and partial tears that have failed conservative therapy. Repair of the native ligament has traditionally yielded only 50% return to play, whereas early reports of reconstructive techniques showed 68% rate return to play, these techniques have evolved to produce a 92% success rate.

Jobe and colleagues performed the first recognized UCL reconstruction in 1974. An incision over the medial epicondyle is made with identification of the medial antebrachial cutaneous nerve. The origin of the flexor-pronator mass is reflected off of the medial epicondyle. A free tendon graft (typically palmaris longus) is tunneled in a figure-of-eight fashion through bone tunnels in the medial epicondyle and the ulna. At the conclusion of the case, the ulnar nerve is transposed submuscularly. Athletes typically had a 63% return to play at preinjury levels for at least 1 year ; however, there were significant morbidities associated with detachment of the flexor-pronator mass as well as ulnar nerve complications. Later modifications preserve the flexor-pronator mass with exposure of the medial epicondyle by reflecting the flexor carpi ulnaris anteriorly and without transposition of the ulnar nerve. This modified Jobe reconstruction yielded excellent results in 93% of high-level athletes who had not had a previous procedure.

The “docking technique” has produced the highest statistical return to play of 92%. The flexor carpi ulnaris is split to access the anterior bundle of the UCL, which is subsequently incised longitudinally to expose the joint. A single anterior humeral tunnel is created by connecting 2 smaller tunnels drilled from the posterior cortex. The graft tissue is passed through the ulna anteriorly and is “docked” to the humerus. The 2 limbs of the Krakow stitch in the graft are passed through their respective posterior tunnels and joined over a bony bridge on the dorsal aspect of the humerus. The docking procedure allows for easier placement of bone tunnels as well as greater ease of appropriate tensioning of the graft.

After reconstruction of the UCL, the arm is immobilized in a posterior splint. Range of motion exercises are prescribed for the wrist and hand. After 1 week of immobilization, the elbow is placed in a hinged elbow brace that allows for 30° to 100° of flexion. At week 3, the elbow is allowed 15° to 110° and is subsequently advanced 5° of extension and 10° of flexion each week thereafter. Strengthening begins at week 4 and continues through week 9 when plyometric exercises are started. At week 12, players can begin an interval throwing program. Players must be instructed that return to play can take up to a year if not longer.

Etiology

The ulnar nerve arises from the medial cord of the brachial plexus, receiving major contributions from C8 and T1 and a minor contribution from C7. As the nerve courses down the medial aspect of the arm and posterior to the elbow, it is subject to multiple sites of compression leading to ulnar nerve irritation.

The most proximal site of compression exists as a thick band of fibrous tissue located 8 to 9 cm proximal to the medial epicondyle. This has historically been referred to as the “Arcade of Struthers,” which in reality is neither an arcade nor did Sir John Struthers define it. Instead, the medial intermuscular septum and the internal brachial ligament converge to form this thick band of tissue at the point where the ulnar nerve transitions from the posterior to the anterior compartments of the arm. Surgically, this can become a major site of entrapment if not released during anterior transposition of the ulnar nerve.

More distally, the medial head of the triceps, the medial intermuscular septum, and osteophytes of the medial epicondyle all potentially impinge on the ulnar nerve. As the nerve travels posterior to the medial epicondyle, it enters the cubital tunnel, the floor of which is formed by the UCL. The roof of the cubital tunnel, known as the Osborne ligament, is formed by the attachment of the humeral and ulnar heads of the flexor carpi ulnaris. As the elbow flexes, the Osborne ligament becomes taut, trapping the ulnar nerve between itself and the medial collateral ligament. The pressure inside the cubital tunnel increases 7-fold to 20-fold, causing not only deformation of the nerve but also compromising its vascular supply. Osteophyte formation within the medial aspect of the elbow also may lead to narrowing of this anatomic tunnel.

The anconeus epitrochlearis is an anomalous muscle originating from the medial border of the olecranon and inserting onto the medial epicondyle. It is present in up to 34% of arms, making it the most common anomalous muscle in the upper extremity. This muscle overlies the ulnar nerve posteriorly and may cause compression of the nerve with elbow flexion. As the ulnar nerve enters the forearm, it is subject to compression at the aponeuroses of both the flexor carpi ulnaris and the flexor pronator mass.

Repetitive tensile force on the ulnar nerve has been implicated as a cause of ulnar neuritis. The throwing motion subjects the elbow to significant valgus stress, which in turn causes traction on the medial structures of the elbow, including the ulnar nerve. The early acceleration phase causes an average ulnar nerve strain of 5% to 13%. Additionally, the nerve has been noted to undergo axial translation of 12 mm as the elbow ranges from full flexion to full extension.

History and examination

The diagnosis of ulnar neuritis relies heavily on clinical examination. A thorough history may reveal pain and paresthesias in the ring and small fingers and intrinsic weakness in the hand. Throwing athletes may complain of loss of ball control or coordination.

The McGowan scale is useful for preoperative grading of ulnar nerve compression. Grade I consists of purely subjective complaints of paresthesias and hypesthesia in the ulnar nerve distribution. Weakness of the hand intrinsic musculature and sensory loss define Grade II. Grade III has the worst prognosis, with muscle atrophy, occasional clawing of the fingers, and severe sensory loss.

The repetitive flexion and extension motions caused by the throwing cycle may exacerbate an ulnar nerve already prone to subluxation. The throwing athlete with ulnar nerve subluxation may describe a popping or snapping sensation at the medial elbow. This may be accompanied by pain or paresthesias both at the elbow and within the ulnar nerve distribution distally.

Physical examination may demonstrate weakness of the intrinsic musculature of the hand, the flexor digitorum profundus to the ring or small finger, or the first dorsal interosseous. Note any positive Tinel sign over a potential point of compression of the nerve. However, a Tinel sign should be interpreted within the context of the patient’s complaints; 10% of the healthy population may have a positive Tinel sign at the cubital tunnel. However, the negative predictive value of a Tinel at the elbow is 98%.

The ulnar nerve should be palpated along its course to assess for enlargements along its course and for subluxation during flexion. The carrying angle of the elbow found to be of abnormal valgus angulation also may predispose to traction injury of the ulnar nerve. Grip strength should be recorded both as a diagnostic measure and as a tool for assessing rehabilitation.

The scratch-collapse test has an accuracy rate of 98% for compression of the ulnar nerve at the elbow ( Fig. 4 ). The test is performed with the elbow flexed to 90° in neutral rotation and the arm adducted. The examiner tests the patient’s ability to resist internal rotation at the shoulder. The internal rotation force is removed and the arm is returned to the adducted position. The examiner gently scratches the skin over the cubital tunnel and subsequently reexamines the patient’s ability to resist internal rotation. A positive result is demonstrated by significant loss of external rotation strength compared with the baseline test.

Scratch collapse test of the right arm for ulnar nerve impingement at the cubital tunnel. ( A ) Patient resists internal rotation with arm adducted at the side and the elbow flexed to 90°. ( B ) Examiner scratches over the ulnar nerve at the cubital tunnel. ( C ) Positive test is an inability to resist internal rotation.

Electrodiagnostic studies are useful in cases in which the diagnosis is in doubt or where suspicion exists of multiple compression sites. The clinician should obtain electromyography as well as motor and sensory conduction studies. Motor conduction sensitivity has been reported as low as 37% for cubital tunnel syndrome. Testing should be performed with the elbow in flexion, as the length of the ulnar nerve is often underestimated with the elbow extended. Standardization based on the performing site and skin temperature should be included.

Treatment

Treatment for ulnar neuritis generally begins with a period of activity modification, anti-inflammatory medications, and physical therapy. Corticosteroid injections may cause further damage to already injured ligamentous and cartilaginous structures and should be avoided. Nocturnal extension splinting in semi-extension or elbow pads can be considered. Generally 6 weeks of abstinence from throwing is recommended. Once symptoms begin to resolve, an interval throwing program is implemented.

The role of nonoperative treatment in high-level throwing athletes is limited and consideration may be given to early operative intervention. Patients refractory to nonoperative treatment also may require operative intervention. Options include in situ decompression or anterior transposition. Decompression of the cubital tunnel is a good option for stage I or II patients when the nerve does not subluxate anteriorly. However, this technique does not address intraneural tension, and may lead to anterior subluxation of the nerve.

Anterior transposition can be performed either subcutaneously or submuscularly. Whichever method is chosen, critical importance must be placed on protecting the medial antebrachial cutaneous nerve, avoiding creation of new compression proximally or distally, and early range of motion to prevent scar formation.

Subcutaneous transposition

Subcutaneous transposition is performed via a 6-cm to 8-cm incision that parallels the ulnar nerve posterior to the medial epicondyle. The incision must be long enough to allow access to the internal brachial ligament proximally and to the ulnar and humeral heads of the flexor carpi ulnaris distally. Blunt dissection is performed with protection of the medial antebrachial cutaneous nerve. Once the ulnar nerve is identified, it is mobilized while preserving the accompanying vascular structures.

All sites of compression of the nerve must be released, particularly proximally and distally. A finger is passed proximally to ensure the internal brachial ligament does not contribute to nerve compression of the nerve and should be released. The same technique distally evaluates the fascia of the flexor carpi ulnaris. The first motor branch of the ulnar nerve to the flexor carpi ulnaris may need to be mobilized to allow for untethered anterior transposition.

At the elbow, the surgeon must identify and release the anconeus epitrochlearis, if present, and the cubital retinacular ligament. A segment of the intermuscular septum is resected and a judicious pocket is created in the subcutaneous tissue into which the nerve is placed. The nerve is checked once more to ensure smooth gliding with flexion and extension of the elbow. The patient may be placed in a sling until the first postoperative visit when early range-of-motion exercises are begun.

Submuscular transposition

Submuscular transposition begins with a slightly larger incision than its subcutaneous counterpart. After the nerve is mobilized as described previously, a z-plasty incision is made in the tendon of the flexor-pronator origin. The musculofascial flaps are elevated, taking care not to disrupt the first motor branch to the flexor carpi ulnaris. The nerve is laid deep to the flexor-pronator mass next to the median nerve. The nerve is inspected throughout its course to ensure that no proximal or distal site of compression exists with elbow range of motion. The flexor-pronator origin is repaired in a slightly lengthened position with nonabsorbable suture. The wound is irrigated and closed and a posterior splint is applied with the elbow at 90° of flexion for 2 weeks. Passive range-of-motion exercises and formal therapy are begun at the first postoperative visit.

Medial epicondylar injury

Medial epicondyle apophysitis is the most common cause of little league elbow and probably exists on a spectrum with damage to the apophyseal plate or avulsion injury of the medial epicondyle in adolescent throwing athletes and young pitchers.

Adolescent throwing athletes with medial elbow pain will commonly describe an insidious onset of pain accompanied by a steady decrease in velocity and accuracy. An acute onset of pain, although rare, should prompt the examiner to look for signs of apophyseal avulsion injury. A thorough history will include any change in training schedule, pitch count, and innings pitched.

The patient will demonstrate point tenderness over the medial epicondyle as well as medial elbow pain with resisted wrist flexion and pronation. More advanced cases may exhibit decreased range of motion of the elbow. Medial epicondylar fractures will present with swelling, often accompanied by a flexion contracture.

AP, lateral, and axial radiographs of both elbows for comparison should be obtained. In the case of normal films, a stress view may be necessary to determine physeal versus ligamentous injury. Widening of the epiphyseal lines or hypertrophy of the medial epicondyle suggests chronic and advanced injury.

Medial epicondylar apophysitis is treated by complete cessation of throwing injuries. Ice, massage, and oral analgesia may be used as adjuncts. Splinting may be required for refractory cases or patients with pain at rest. Pediatric athletes with stable avulsion fractures of the medial epicondyle and minimal displacement can be treated in a long-arm cast for 3 to 4 weeks with excellent results. Open fractures and fractures with incarcerated fragments are absolute indications for surgery. Although the degree of fracture displacement has long been used as a threshold for surgical intervention, recent literature has shown that interobserver reliability on plain radiographs is poor. CT scan, although exposing the athlete to increased radiation, may help in determining the true fracture displacement and better guiding treatment. Although surgical indications based on fragment displacement vary from 5 to 15 mm, the ultimate decision for surgical intervention should be based on mechanism of injury, degree of elbow instability, and patient expectations. The surgeon should remain aware that avulsion fractures can occur in association with UCL injury and the medial ligaments may require treatment as well.

Prevention of medial epicondylar injury in pitchers through limiting pitch counts and innings pitched should be performed. Contrary to popular thought, pitch count is more important than type of pitch thrown. Additionally, consideration must be given for the child’s skeletal age, especially when playing in an age-determined league.

Flexor-pronator mass injury

The valgus forces across the elbow during late-cocking and early acceleration phases of throwing often exceed the failure strength of the UCL. The flexor-pronator muscles act as dynamic stabilizers of the elbow against valgus stress and help to prevent injury to the medial ligamentous complex. Laboratory studies suggest that the flexor carpi ulnaris and the flexor digitorum superficialis contribute to the greatest stability during throwing activities.

The tendinous origins of these medial-sided muscles are predisposed to injury because of their dynamic function. Repetitive throwing can cause a spectrum of injury from inflammation and tendinitis to acute tears. Athletes will complain of pain over the origin of the flexor-pronator mass. The location of tenderness elicited by palpation on examination should be carefully recorded; flexor-pronator mass injury will exhibit pain just distal to the medial epicondyle, whereas the location of pain in medial ligamentous injury is more distal and posterior, corresponding to the anterior band of the UCL location.

Flexor-pronator mass injuries respond well to conservative treatment. The athlete should cease throwing activities but can continue with active range-of-motion exercises accompanied by ice and anti-inflammatory agents. Once the patient’s pain has resolved, an interval throwing program is instituted with anticipated return to preinjury level of play. Athletes who fail initial conservative therapy may benefit from a well-placed corticosteroid injection. However, care must be taken to avoid introduction of steroid into the UCL complex.

Recalcitrant cases should prompt the clinician to investigate other causes of medial elbow pain, particularly UCL injury. In the absence of concomitant injury, the athlete may benefit from open debridement and repair of the flexor-pronator mass to the medial epicondyle. Passive range-of-motion therapy is instituted early in the postoperative period and full return to play can be expected within 10 to 12 weeks after regaining motion and strength.