Ahmad CS

The supraphysiological demands imposed on the elbow of a throwing athlete result in predictable patterns of injury. This is especially true of baseball pitchers. Knowledge of elbow anatomy, as well as the biomechanics of throwing, assist in making diagnostic and therapeutic decisions and also influence surgical technique when surgery is required. During the late cocking and early acceleration phases of throwing, valgus torque can reach 65 Nm with angular velocities of the forearm reaching 5000°/sec, which is considered the fasted recorded human movment.¹ The valgus torque and rapid extension synergistically create 3 major forces placed on the elbow. The first is a tensile stress along the medial aspect of elbow affecting the ulnar collateral ligament (UCL), flexor pronator mass, and medial epicondyle. Secondly, compression forces affect the lateral aspect of the elbow at the radiocapitellar joint. Finally, a shearing stress occurs in the posterior compartment at the posterior medial tip of the olecranon and the olecranon fossa.

These forces generated on the elbow result in predictable pathology. The recurring tensile forces applied on the medial aspect on the elbow can compromise the integrity of the UCL. It is well known that injury to the UCL leads to valgus instability. Individuals with valgus instability who continue to throw may trigger and/or aggravate injury in the posterior and lateral components of the elbow. Lateral compression forces can often reach 500 N, resulting in radiocapitellar overload syndrome, which occurs in combination with medial ligament instability and valgus extension overload.² Radiocapitellar compression may cause chondral or osteochondral fracture with resulting intra-articular loose bodes. This compression also contributes to the etiology of osteochondritis dissecans (OCD) in skeletally immature athletes. In the posterior elbow, throwing forcefully and repeatedly pushes the olecranon into the olecranon fossa. Shear stress on the medial olecranon tip and fossa, due to combined valgus and extension forces, lead to the development of osteophytes. This collection of injuries in the medial, lateral, and posterior aspects of the elbow is known as “valgus extension overload syndrome” or VEO. Symptoms in VEO can be the result of chondral lesions, loose bodies, and marginal exostosis.³

The aim of this review is to provide understanding regarding both the relevant anatomy and pathomechanics of VEO, key aspects to clinical evaluation, and effective treatment options.

Functional Anatomy

A functional comprehension of elbow anatomy and biomechanics is essential to understanding the constellation of injuries in VEO. The osseous anatomy of the elbow permits a variety of movements. These include flexion-extension and pronation-supination, which are mediated by the ulnohumeral and radiocapitellar articulations. While in full extension, the elbow has a normal valgus carrying angle of 11° to 16°. It is important to know that 50% of the elbow’s stability is attributed to the configuration of the bones.^4-6 This is especially true in varus stress while the elbow is in full extension. The soft tissues, including muscle and ligaments such as the UCL, lateral UCL, and radial UCL complexes, provide the remaining elbow stability.^4-6

The UCL complex is composed of 3 main segments known as the anterior, posterior, and oblique bundles (transverse ligament). Collectively, these bundles are responsible for providing medial elbow stability. However, each of these bundles contributes to medial elbow stability in its own way. The first and arguably the most important bundle is the anterior bundle; its most important function is providing stability against valgus stress.^4,5,7 It is composed of parallel fibers inserting on the medial coronoid process.^4,5,7 Furthermore, its eccentric location with respect to the axis of elbow allows it to provide stability throughout the full range of elbow motion.⁶ The anterior bundle can be further divided into individual anterior and posterior bands that have reciprocal functionality.^5,8,9 The anterior band acts as the chief restraint to valgus stress up to 90° of flexion.⁹ Any flexion beyond 90° renders the anterior band’s role secondary in resisting valgus stress.⁹ The posterior band’s function in resisting valgus stress is most important between 60° and full flexion, while having a secondary role in lesser degrees of flexion.^8,9 Notably, the posterior band is isometric and is more important in the overhead-throwing athlete due to the fact its primary role in resisting valgus stress occurs at higher degrees of flexion.¹⁰

The remaining posterior and oblique bundles of the UCL complex have lesser roles in maintaining elbow stability. The posterior bundle of the UCL complex is fan-shaped, originates from the medial epicondyle, and inserts onto the medial margin the semi-lunar notch. It is more slender and frailer than the anterior bundle. This is reflected in its functionality, as it plays a secondary role in elbow stability during elbow flexion beyond 90°.^4,5,8 In contrast to the anterior and posterior bundles, the oblique bundle, also known as the transverse ligament, does not cross the elbow joint. It is a thickening of the caudal most aspect of the joint capsule, which extends from the medial olecranon to the inferior medial coronoid process and as a result functions in expanding the greater sigmoid notch.⁶

The musculotendinous components of the elbow are essential to providing dynamic functional resistance to valgus stress.¹¹ These components are flexor-pronator musculature that originate from the medial epicondyle. Listed proximally to distally, the flexor-pronator muscles include pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis, and the flexor carpi ulnaris (FCU).

Pathomechanics

Once familiarized with the relevant function anatomy, it is crucial to understand the mechanics of throwing in order to understand the pathomechanics of VEO. The action of overhead throwing has been divided into 6 phases.^6,12-16 Phase 4, acceleration, is the most relevant when discussing forces on elbow, since the majority of forces are generated during this state. Phase 4 represents a rapid acceleration of the upper extremity with a large forward-directed force on the arm generated by the shoulder muscles. Additionally, there is internal rotation and adduction of the humerus with rapid elbow extension terminating with ball release. The elbow accelerates up to 600,000°/sec² in a miniscule time frame of 40 to 50 milliseconds.^1,5 Immense valgus forces are exerted on the medial aspect of the elbow. The anterior bundle of the UCL bears the majority of the force, with the flexor pronator mass enabling the transmission.¹¹ The majority of injuries occur during stage 4 as a result of the stress load on the medial elbow structures like the UCL. The proceeding phases 5 (deceleration), and 6 (follow-through) involve eventual dissipation of excess kinetic energy as the elbow completely extends. The deceleration during phase 5 is rapid and powerful, occurring at about 500,000°/sec² in the short span of 50 milliseconds.^1,6,12-16 High-velocity throwing, such as baseball pitching, generates forces in the elbow that are opposed by the articular, ligamentous, and muscular portions of the arm. The ulnohumeral articulation stabilizes motion of the arm from 0° to 20° of flexion and beyond 120° of flexion. Static and dynamic soft tissues maintain stability during the remaining of 100° arc of motion.

During deceleration, the elbow undergoes terminal extension resulting in the posteromedial olecranon contacting the trochlea and the olecranon fossa with subsequent dissipation of the combined valgus force and angular moment (Figure 1). This dissipation of force creates pathologic shear and compressive forces in the posterior elbow. Poor muscular control and the traumatic abutment that occurs in the posterior compartment may further add to the pathologic forces. Reactive bone formation is induced by the repetitive compression and shear, resulting in osteophytes on the posteromedial tip of the olecranon (Figure 2). Consequent “kissing lesions” of chondromalacia may occur in the olecranon fossa and posteromedial trochlea. The subsequent development of loose bodies may also occur. The presence of osteophytes and/or loose bodies may result in posteromedial impingement (PMI).

The association between PMI of the olecranon and valgus instability has been elucidated in both clinical and biomechanical investigations.^17,18,19,20 Conway¹⁸ identified tip exostosis in 24% of lateral radiographs of 135 asymptomatic professional pitchers. Approximately one-fifth (21%) of these pitchers had >1.0 mm increased relative valgus laxity on stress radiographs. Roughly one-third (34%) of players with exostosis had >1.0 mm of increased relative valgus laxity, compared to 16% of players without exostosis formation. These results provide evidence for a probable association between PMI and valgus laxity. In biomechanical research, Ahmad and colleagues¹⁷ studied the effect of partial and full thickness UCL injuries on contact forces of the posterior elbow. Posteromedial compartments of cadaver specimens were subjected to physiologic valgus stresses while placed on pressure-senstive film. Contact area and pressure between posteromedial trochlea and olecranon were altered in the setting of UCL insufficiency, helping explain how posteromedial osteophyte formation occurs.

Additional biomechanical studies have also investigated the posteromedial olecranon’s role in functioning as a stabilizing buttress to medial tensile forces. Treating PMI with aggressive bone removal may increase valgus instability as well as strain on the UCL, leading to UCL injury following olecranon resection.^19,20 Kamineni and colleagues¹⁹ investigated strain on anterior bundle of UCL as a function of increasing applied torque and posteromedial resections of the olecranon. This investigation was done utilizing an electromagnetic tracking placed in cadaver elbows. A nonuniform change in strain was found at 3 mm of resection during flexion and valgus testing. This nonuniform change implied that removal of posteromedial olecranon beyond 3 mm made the UCL more vulnerable to injury. Follow-up investigations looked at kinematic effects of increasing valgus and varus torques and sequential posteromedial olecranon resections.²⁰ Valgus angulation of the elbow increased with all resection levels but no critical amount of olecranon resection was identified. The consensus in the literature indicates that posteromedial articulation of the elbow is a significant stabilizer to valgus stress.^17-22 Thus, normal bone should be preserved and only osteophytes should be removed during treatment.

In addition, VEO may lead to injury in the lateral compartment as well. After attenuation and insufficiency of the UCL due to repetitive stress, excessive force transmission to the lateral aspect of the elbow occurs. Compressive and rotatory forces escalate within the radiocapitellar joint, causing synovitis and osteochondral lesions.^3,23 These osteochondral lesions include osteochondritis dissecans and osteochondral fractures that may fragment and become loose bodies.

Evaluation of VEO

History

Patients will typically have a history of repetitive throwing or other repetitive overhead activity. VEO is most common in baseball pitchers but may also occur in other sports, such as tennis, football, lacrosse, gymnastics, and javelin throwing. In baseball pitchers, clinical presentation is often preceded by a decrease in pitch velocity, control, and early fatigability. It presents with elbow pain localized to the posteromedial aspect of olecranon after release of the ball, when the elbow reaches terminal extension. Patients also report limited extension, due to impinging posterior osteophytes. Also, locking and catching caused by loose bodies and chondromalacia may be present. VEO may also occur in combination with concomitant valgus instability, as well as in a patient with a prior history of valgus instability. Flexor pronator injury, ulnar neuritis, and subluxation may also be present in a patient with VEO.

Physical Examination

VEO may occur in an isolated fashion or with concomitant pathology. Therefore, a comprehensive physical examination includes evaluating the entire kinetic chain of throwing and a focused examination covering VEO and associated valgus instability. Patients may exhibit crepitus and tenderness over the posteromedial olecranon and a loss of extension with a firm end point. The extension impingement test should be performed where the elbow is snapped into terminal extension. This typically elicits pain in the posterior compartment in a patient with VEO. The arm bar test involves positioning the patient’s shoulder at 90° of forward flexion, full internal rotation, with the patient’s hand placed on the examiner’s shoulder.²⁴ The examiner pulls down on the olecranon, simulating forced extension; pain is indicative of a positive test. It is important to note if there are signs of ulnar neuritis or subluxing ulnar nerve, especially if planning to utilize medial portals during arthroscopic treatment.

Examination maneuvers for valgus instability should also be conducted during evaluation of VEO. The physical examination for valgus instability in the elbow is ideally performed with the patient seated. Secure the patient’s wrist between the examiner’s forearm and trunk, and flex the patient’s elbow between 20° and 30° to unlock the olecranon from its fossa. Proceed to apply valgus stress. This stresses the anterior band of the anterior bundle of the UCL.^6,25,26 Palpate the UCL from the medial epicondyle to the proximal ulna as valgus stress is applied. Occasionally, valgus laxity can be appreciated when compared to contralateral side. The milking maneuver is a helpful test to determine UCL injury. Pull on the patient’s thumb while the forearm is supinated, shoulder extended, and the elbow flexed beyond 90°.⁶ The milking maneuver exerts valgus stress on a flexed elbow. A patient with an injured UCL will experience the subjective feeling of apprehension and instability, with medial elbow pain.

The most sensitive test is the moving valgus stress test. This is performed with the patient in the upright position and the shoulder abducted 90°. Starting with the arm in full flexion, the examiner applies a constant valgus torque to the elbow and then rapidly extends the elbow. Reproduction of pain during range of motion from 120° to 70° represents UCL injury, while pain with extension beyond 70° represents chondral injury to the ulnohumeral joint. Be aware that the absence of increased pain with wrist flexion, along with pain localized slightly posterior to the common flexor origin, differentiates a UCL injury from flexor-pronator muscle injury.^6,26,27Examine range of motion in affected and unaffected elbows. Loss of terminal extension may be present, along with secondary to flexion contracture due to repeated attempts at healing and stabilization.²⁵

Imaging

Imaging is essential to the accurate diagnosis of VEO and related conditions. Anterior posterior (AP), lateral, and oblique radiographs of elbow (Figures 3A-3C) may show posteromedial olecranon osteophytes and/or loose bodies. Calcification of ligaments or other soft tissues may also be seen. An AP radiograph with 140° of external rotation may best visualize osteophytes on posteromedial olecranon.18 A computed tomography scan with 2-dimensional sagittal and coronal reconstruction and 3-dimensional surface rendering (Figures 4A, 4B) may best demonstrate morphological abnormalities, loose bodies, and osteophytes. Magnetic resonance imaging (MRI) is essential for assessment of soft tissues and chondral injuries. MRI may detect UCL compromise, synovial plicae, bone edema, olecranon, or stress fractures.

Treatment

Nonoperative Treatment

Treatment consists of both nonoperative and operative modalities. Nonoperative treatment methods are first line in treating VEO. Patients should modify their physical activity and rest from throwing activities. Nonsteroid anti-inflammatory drugs are appropriate to treat pain along with intra-articular corticosteroid injections of the elbow. A wide assessment of pitching mechanics should be performed in an attempt to correct errors in throwing technique and address muscular imbalances. After cessation of the resting period, the patient may initiate a progressive throwing program supervised by an experienced therapist and trainer. A plan for returning to competition should be made upon completion of the throwing program.

Operative Treatment

Surgical treatment is reserved for patients who fail nonoperative treatment. These patients have persistent symptoms of posteromedial impingement and desire to return to pre-injury level of performance. Posteromedial decompression is not recommended when provocative physical examination maneuvers are negative, regardless of presence of olecranon osteophytes on imaging. Osteophytes are an asymptomatic finding typically seen in professional baseball players and do not warrant surgical treatment.^18,28 UCL compromise is a relative contraindication to olecranon debridement as UCL injury could become symptomatic following surgery. Surgical options in the appropriate patient to decompress posterior compartment include arthroscopic olecranon debridement or limited incision arthrotomy. Excessive resection of posteromedial osteophytes must be avoided. Arthroscopy has limited morbidity and allows for complete diagnostic assessment. UCL reconstruction should also be considered in combination with posteromedial debridement when the UCL is torn. More challenging indications for UCL reconstruction occur when the UCL is partially torn or torn and asymptomatic. Isolated posteromedial decompression in this setting risks future development of UCL symptoms that would then need to be addressed.

Surgical Technique

As previously mentioned, elbow arthroscopy or limited excision arthrotomy are the preferred operative methods for decompression of the posterior compartment and thus treatment of VEO. Anesthesia and patient positioning should be selected based on the surgeon’s preference. The patient should be positioned supine, prone, or in lateral decubitis. When a UCL reconstruction is expected, supine position is advantageous to avoid repositioning after completing the arthroscopic portion of the procedure. However, arthroscopy can be performed in the lateral position with subsequent repositioning, repeat prepping, and draping for UCL reconstruction (Figures 5A, 5B).

Prepare for elbow arthroscopy by distending the elbow joint with normal saline to aid in protection of neurovascular structures and simplify the insertion of the scope trocar. Perform diagnostic anterior arthroscopy via the proximal anteromedial portal. Assess for presence of loose bodies and osteochondral lesions of the radiocapitellar joint, as well as osteophytes of the coronoid tip and fossa. Utilizing a spinal needle under direct visualization establish a proximal lateral portal with adequate view of the anterior compartment. Proceed to visualize the medial compartment and assess for UCL injury. Apply valgus stress while in 70° of flexion. Visualize the coronoid process and look for medial trochlea gapping of 3 mm or greater, which indicates UCL insufficiency.³⁰

Establish the posterolateral port for visualization of the posterior compartment. A posterior portal is established through the triceps tendon. Proceed to shave and ablate synovitis in order to create an adequate working space. Inspect the posteromedial olecranon, looking for any osteophytes or chondromalacia in the area (Figure 6). Examine the posterior radiocapitellar joint, looking specifically for loose bodies. The presence of loose bodies may require creating an extra mid lateral portal for removal. The ulnar nerve is located superficial to the elbow capsule and can be damaged by instruments utilized in the posteromedial gutter. As a precaution, be sure to remove suction attached to shaver. Place a curved articulating retractor in an accessory posterolateral portal to assist in protecting the ulnar nerve by retracting the capsule away from the surgical field (Figures 7A, 7B).

The osteophyte may be encased in soft tissue. Using a combination of ablation devices and shavers, the osteophyte can be exposed. The olecranon osteophyte can be removed with a small osteotome located at the border of the osteophyte and the normal olecranon. A motorized shaver or burr may also be introduced through the direct posterior portal or the posterolateral portal to complete the contouring of the olecranon (Figures 8A, 8B). Intraoperative lateral radiographs may be obtained for guidance in adequate bone removal and to ensure no bone debris is left in the soft tissues. It is critical that only pathologic osteophyte is removed and that normal olecranon is not compromised. This prevents an increase in UCL strain during valgus loading.¹⁹ However, in some non-throwing athletes, more aggressive debridement can be performed due to a smaller risk of UCL injury after posterior decompression.

Often, with the presence of osteophytes on the olecranon, there may be associated chondromalacia of the trochlea. These kissing lesions must be addressed after debridement of osteophytes. Loose flaps or frayed edges are carefully debrided and for any significant lesion the edges are contoured to a stable rim using shavers and curettes. Once altered to a well-shouldered lesion, microfracture is performed. Anterograde drilling of the lesion with perforations separated by 2 to 3 mm allow for the release of marrow elements and induction of a fibrocartilage healing response.

For an isolated posteromedial decompression, early rehabilitation begins with simple elbow flexion and extension exercises. It is important to restore flexor-pronator strength. Six weeks postoperatively, a progressive throwing program that includes plyometric exercises, neuromuscular training, and endurance exercises can be initiated. Patients can typically return to competition 3 to 4 months after surgery, if they have successfully regained preoperative range of motion, preoperative strength in the elbow, and there is no pain or tenderness on stress testing or palpation.

Outcomes

Safety and Advances in Arthroscopy

A clearer understanding of portal placement and proximity to neurovasculature in conjunction with advances in equipment have allowed for continual improvements in elbow arthroscopy techniques. There is plenty of literature indicating that arthroscopic posteromedial decompression is a safe, reliable, effective procedure, with a high rate of patient satisfaction.^22,30-34] Andrews and Carson³⁰ published one of the earliest investigations indicating the effectiveness of elbow arthroscopy utilizing objective and subjective outcome scores. They found that preoperative scores indicating patient satisfaction increased from 50% to 83%. Patients who underwent only loose body removal had the best outcomes. Andrews and Timmerman³¹ later evaluated the results of 72 professional baseball players who underwent either arthroscopic or open elbow surgery. They found that posteromedial olecranon osteophytes and intraarticular loose bodies were the most common diagnoses, present in 65% and 54% of players, respectively. In addition, a 41% reoperation rate was reported after posteromedial olecranon resection, along with 25% a rate of valgus instability necessitating UCL reconstruction. Andrews and Timmerman³¹ propose that the incidence of UCL injuries is underestimated and that UCL pathology must be treated prior to treating its secondary effects. Recently, Reddy and colleagues³² reviewed the results of 187 arthroscopic procedures. Posterior impingement, loose bodies, and osteoarthritis were the most common problems, occurring in 51%, 31%, and 22% of patients, respectively. Reported results were encouraging, with 87% good to excellent results and 85% of baseball players returning to preinjury levels.

Conclusion

An understanding of the relevant functional anatomy and the biomechanics of throwing is essential to understanding VEO. Potential concomitant valgus instability and UCL injury must be carefully assessed. Only symptomatic patients who have failed conservative treatment should undergo surgery. It is critical to avoid exacerbating and/or causing valgus instability by surgical excessively removing normal bone from the olecranon. Arthroscopy has been shown to be a safe and effective method to treat refractory cases of VEO.

The supraphysiological demands imposed on the elbow of a throwing athlete result in predictable patterns of injury. This is especially true of baseball pitchers. Knowledge of elbow anatomy, as well as the biomechanics of throwing, assist in making diagnostic and therapeutic decisions and also influence surgical technique when surgery is required. During the late cocking and early acceleration phases of throwing, valgus torque can reach 65 Nm with angular velocities of the forearm reaching 5000°/sec, which is considered the fasted recorded human movment.¹ The valgus torque and rapid extension synergistically create 3 major forces placed on the elbow. The first is a tensile stress along the medial aspect of elbow affecting the ulnar collateral ligament (UCL), flexor pronator mass, and medial epicondyle. Secondly, compression forces affect the lateral aspect of the elbow at the radiocapitellar joint. Finally, a shearing stress occurs in the posterior compartment at the posterior medial tip of the olecranon and the olecranon fossa.

These forces generated on the elbow result in predictable pathology. The recurring tensile forces applied on the medial aspect on the elbow can compromise the integrity of the UCL. It is well known that injury to the UCL leads to valgus instability. Individuals with valgus instability who continue to throw may trigger and/or aggravate injury in the posterior and lateral components of the elbow. Lateral compression forces can often reach 500 N, resulting in radiocapitellar overload syndrome, which occurs in combination with medial ligament instability and valgus extension overload.² Radiocapitellar compression may cause chondral or osteochondral fracture with resulting intra-articular loose bodes. This compression also contributes to the etiology of osteochondritis dissecans (OCD) in skeletally immature athletes. In the posterior elbow, throwing forcefully and repeatedly pushes the olecranon into the olecranon fossa. Shear stress on the medial olecranon tip and fossa, due to combined valgus and extension forces, lead to the development of osteophytes. This collection of injuries in the medial, lateral, and posterior aspects of the elbow is known as “valgus extension overload syndrome” or VEO. Symptoms in VEO can be the result of chondral lesions, loose bodies, and marginal exostosis.³

The aim of this review is to provide understanding regarding both the relevant anatomy and pathomechanics of VEO, key aspects to clinical evaluation, and effective treatment options.

Functional Anatomy

A functional comprehension of elbow anatomy and biomechanics is essential to understanding the constellation of injuries in VEO. The osseous anatomy of the elbow permits a variety of movements. These include flexion-extension and pronation-supination, which are mediated by the ulnohumeral and radiocapitellar articulations. While in full extension, the elbow has a normal valgus carrying angle of 11° to 16°. It is important to know that 50% of the elbow’s stability is attributed to the configuration of the bones.^4-6 This is especially true in varus stress while the elbow is in full extension. The soft tissues, including muscle and ligaments such as the UCL, lateral UCL, and radial UCL complexes, provide the remaining elbow stability.^4-6

The UCL complex is composed of 3 main segments known as the anterior, posterior, and oblique bundles (transverse ligament). Collectively, these bundles are responsible for providing medial elbow stability. However, each of these bundles contributes to medial elbow stability in its own way. The first and arguably the most important bundle is the anterior bundle; its most important function is providing stability against valgus stress.^4,5,7 It is composed of parallel fibers inserting on the medial coronoid process.^4,5,7 Furthermore, its eccentric location with respect to the axis of elbow allows it to provide stability throughout the full range of elbow motion.⁶ The anterior bundle can be further divided into individual anterior and posterior bands that have reciprocal functionality.^5,8,9 The anterior band acts as the chief restraint to valgus stress up to 90° of flexion.⁹ Any flexion beyond 90° renders the anterior band’s role secondary in resisting valgus stress.⁹ The posterior band’s function in resisting valgus stress is most important between 60° and full flexion, while having a secondary role in lesser degrees of flexion.^8,9 Notably, the posterior band is isometric and is more important in the overhead-throwing athlete due to the fact its primary role in resisting valgus stress occurs at higher degrees of flexion.¹⁰

The remaining posterior and oblique bundles of the UCL complex have lesser roles in maintaining elbow stability. The posterior bundle of the UCL complex is fan-shaped, originates from the medial epicondyle, and inserts onto the medial margin the semi-lunar notch. It is more slender and frailer than the anterior bundle. This is reflected in its functionality, as it plays a secondary role in elbow stability during elbow flexion beyond 90°.^4,5,8 In contrast to the anterior and posterior bundles, the oblique bundle, also known as the transverse ligament, does not cross the elbow joint. It is a thickening of the caudal most aspect of the joint capsule, which extends from the medial olecranon to the inferior medial coronoid process and as a result functions in expanding the greater sigmoid notch.⁶

The musculotendinous components of the elbow are essential to providing dynamic functional resistance to valgus stress.¹¹ These components are flexor-pronator musculature that originate from the medial epicondyle. Listed proximally to distally, the flexor-pronator muscles include pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis, and the flexor carpi ulnaris (FCU).

Pathomechanics

Once familiarized with the relevant function anatomy, it is crucial to understand the mechanics of throwing in order to understand the pathomechanics of VEO. The action of overhead throwing has been divided into 6 phases.^6,12-16 Phase 4, acceleration, is the most relevant when discussing forces on elbow, since the majority of forces are generated during this state. Phase 4 represents a rapid acceleration of the upper extremity with a large forward-directed force on the arm generated by the shoulder muscles. Additionally, there is internal rotation and adduction of the humerus with rapid elbow extension terminating with ball release. The elbow accelerates up to 600,000°/sec² in a miniscule time frame of 40 to 50 milliseconds.^1,5 Immense valgus forces are exerted on the medial aspect of the elbow. The anterior bundle of the UCL bears the majority of the force, with the flexor pronator mass enabling the transmission.¹¹ The majority of injuries occur during stage 4 as a result of the stress load on the medial elbow structures like the UCL. The proceeding phases 5 (deceleration), and 6 (follow-through) involve eventual dissipation of excess kinetic energy as the elbow completely extends. The deceleration during phase 5 is rapid and powerful, occurring at about 500,000°/sec² in the short span of 50 milliseconds.^1,6,12-16 High-velocity throwing, such as baseball pitching, generates forces in the elbow that are opposed by the articular, ligamentous, and muscular portions of the arm. The ulnohumeral articulation stabilizes motion of the arm from 0° to 20° of flexion and beyond 120° of flexion. Static and dynamic soft tissues maintain stability during the remaining of 100° arc of motion.

During deceleration, the elbow undergoes terminal extension resulting in the posteromedial olecranon contacting the trochlea and the olecranon fossa with subsequent dissipation of the combined valgus force and angular moment (Figure 1). This dissipation of force creates pathologic shear and compressive forces in the posterior elbow. Poor muscular control and the traumatic abutment that occurs in the posterior compartment may further add to the pathologic forces. Reactive bone formation is induced by the repetitive compression and shear, resulting in osteophytes on the posteromedial tip of the olecranon (Figure 2). Consequent “kissing lesions” of chondromalacia may occur in the olecranon fossa and posteromedial trochlea. The subsequent development of loose bodies may also occur. The presence of osteophytes and/or loose bodies may result in posteromedial impingement (PMI).

The association between PMI of the olecranon and valgus instability has been elucidated in both clinical and biomechanical investigations.^17,18,19,20 Conway¹⁸ identified tip exostosis in 24% of lateral radiographs of 135 asymptomatic professional pitchers. Approximately one-fifth (21%) of these pitchers had >1.0 mm increased relative valgus laxity on stress radiographs. Roughly one-third (34%) of players with exostosis had >1.0 mm of increased relative valgus laxity, compared to 16% of players without exostosis formation. These results provide evidence for a probable association between PMI and valgus laxity. In biomechanical research, Ahmad and colleagues¹⁷ studied the effect of partial and full thickness UCL injuries on contact forces of the posterior elbow. Posteromedial compartments of cadaver specimens were subjected to physiologic valgus stresses while placed on pressure-senstive film. Contact area and pressure between posteromedial trochlea and olecranon were altered in the setting of UCL insufficiency, helping explain how posteromedial osteophyte formation occurs.

Additional biomechanical studies have also investigated the posteromedial olecranon’s role in functioning as a stabilizing buttress to medial tensile forces. Treating PMI with aggressive bone removal may increase valgus instability as well as strain on the UCL, leading to UCL injury following olecranon resection.^19,20 Kamineni and colleagues¹⁹ investigated strain on anterior bundle of UCL as a function of increasing applied torque and posteromedial resections of the olecranon. This investigation was done utilizing an electromagnetic tracking placed in cadaver elbows. A nonuniform change in strain was found at 3 mm of resection during flexion and valgus testing. This nonuniform change implied that removal of posteromedial olecranon beyond 3 mm made the UCL more vulnerable to injury. Follow-up investigations looked at kinematic effects of increasing valgus and varus torques and sequential posteromedial olecranon resections.²⁰ Valgus angulation of the elbow increased with all resection levels but no critical amount of olecranon resection was identified. The consensus in the literature indicates that posteromedial articulation of the elbow is a significant stabilizer to valgus stress.^17-22 Thus, normal bone should be preserved and only osteophytes should be removed during treatment.

In addition, VEO may lead to injury in the lateral compartment as well. After attenuation and insufficiency of the UCL due to repetitive stress, excessive force transmission to the lateral aspect of the elbow occurs. Compressive and rotatory forces escalate within the radiocapitellar joint, causing synovitis and osteochondral lesions.^3,23 These osteochondral lesions include osteochondritis dissecans and osteochondral fractures that may fragment and become loose bodies.

Evaluation of VEO

History

Patients will typically have a history of repetitive throwing or other repetitive overhead activity. VEO is most common in baseball pitchers but may also occur in other sports, such as tennis, football, lacrosse, gymnastics, and javelin throwing. In baseball pitchers, clinical presentation is often preceded by a decrease in pitch velocity, control, and early fatigability. It presents with elbow pain localized to the posteromedial aspect of olecranon after release of the ball, when the elbow reaches terminal extension. Patients also report limited extension, due to impinging posterior osteophytes. Also, locking and catching caused by loose bodies and chondromalacia may be present. VEO may also occur in combination with concomitant valgus instability, as well as in a patient with a prior history of valgus instability. Flexor pronator injury, ulnar neuritis, and subluxation may also be present in a patient with VEO.

Physical Examination

VEO may occur in an isolated fashion or with concomitant pathology. Therefore, a comprehensive physical examination includes evaluating the entire kinetic chain of throwing and a focused examination covering VEO and associated valgus instability. Patients may exhibit crepitus and tenderness over the posteromedial olecranon and a loss of extension with a firm end point. The extension impingement test should be performed where the elbow is snapped into terminal extension. This typically elicits pain in the posterior compartment in a patient with VEO. The arm bar test involves positioning the patient’s shoulder at 90° of forward flexion, full internal rotation, with the patient’s hand placed on the examiner’s shoulder.²⁴ The examiner pulls down on the olecranon, simulating forced extension; pain is indicative of a positive test. It is important to note if there are signs of ulnar neuritis or subluxing ulnar nerve, especially if planning to utilize medial portals during arthroscopic treatment.

Examination maneuvers for valgus instability should also be conducted during evaluation of VEO. The physical examination for valgus instability in the elbow is ideally performed with the patient seated. Secure the patient’s wrist between the examiner’s forearm and trunk, and flex the patient’s elbow between 20° and 30° to unlock the olecranon from its fossa. Proceed to apply valgus stress. This stresses the anterior band of the anterior bundle of the UCL.^6,25,26 Palpate the UCL from the medial epicondyle to the proximal ulna as valgus stress is applied. Occasionally, valgus laxity can be appreciated when compared to contralateral side. The milking maneuver is a helpful test to determine UCL injury. Pull on the patient’s thumb while the forearm is supinated, shoulder extended, and the elbow flexed beyond 90°.⁶ The milking maneuver exerts valgus stress on a flexed elbow. A patient with an injured UCL will experience the subjective feeling of apprehension and instability, with medial elbow pain.

The most sensitive test is the moving valgus stress test. This is performed with the patient in the upright position and the shoulder abducted 90°. Starting with the arm in full flexion, the examiner applies a constant valgus torque to the elbow and then rapidly extends the elbow. Reproduction of pain during range of motion from 120° to 70° represents UCL injury, while pain with extension beyond 70° represents chondral injury to the ulnohumeral joint. Be aware that the absence of increased pain with wrist flexion, along with pain localized slightly posterior to the common flexor origin, differentiates a UCL injury from flexor-pronator muscle injury.^6,26,27Examine range of motion in affected and unaffected elbows. Loss of terminal extension may be present, along with secondary to flexion contracture due to repeated attempts at healing and stabilization.²⁵

Imaging

Imaging is essential to the accurate diagnosis of VEO and related conditions. Anterior posterior (AP), lateral, and oblique radiographs of elbow (Figures 3A-3C) may show posteromedial olecranon osteophytes and/or loose bodies. Calcification of ligaments or other soft tissues may also be seen. An AP radiograph with 140° of external rotation may best visualize osteophytes on posteromedial olecranon.18 A computed tomography scan with 2-dimensional sagittal and coronal reconstruction and 3-dimensional surface rendering (Figures 4A, 4B) may best demonstrate morphological abnormalities, loose bodies, and osteophytes. Magnetic resonance imaging (MRI) is essential for assessment of soft tissues and chondral injuries. MRI may detect UCL compromise, synovial plicae, bone edema, olecranon, or stress fractures.

Treatment

Nonoperative Treatment

Treatment consists of both nonoperative and operative modalities. Nonoperative treatment methods are first line in treating VEO. Patients should modify their physical activity and rest from throwing activities. Nonsteroid anti-inflammatory drugs are appropriate to treat pain along with intra-articular corticosteroid injections of the elbow. A wide assessment of pitching mechanics should be performed in an attempt to correct errors in throwing technique and address muscular imbalances. After cessation of the resting period, the patient may initiate a progressive throwing program supervised by an experienced therapist and trainer. A plan for returning to competition should be made upon completion of the throwing program.

Operative Treatment

Surgical treatment is reserved for patients who fail nonoperative treatment. These patients have persistent symptoms of posteromedial impingement and desire to return to pre-injury level of performance. Posteromedial decompression is not recommended when provocative physical examination maneuvers are negative, regardless of presence of olecranon osteophytes on imaging. Osteophytes are an asymptomatic finding typically seen in professional baseball players and do not warrant surgical treatment.^18,28 UCL compromise is a relative contraindication to olecranon debridement as UCL injury could become symptomatic following surgery. Surgical options in the appropriate patient to decompress posterior compartment include arthroscopic olecranon debridement or limited incision arthrotomy. Excessive resection of posteromedial osteophytes must be avoided. Arthroscopy has limited morbidity and allows for complete diagnostic assessment. UCL reconstruction should also be considered in combination with posteromedial debridement when the UCL is torn. More challenging indications for UCL reconstruction occur when the UCL is partially torn or torn and asymptomatic. Isolated posteromedial decompression in this setting risks future development of UCL symptoms that would then need to be addressed.

Surgical Technique

As previously mentioned, elbow arthroscopy or limited excision arthrotomy are the preferred operative methods for decompression of the posterior compartment and thus treatment of VEO. Anesthesia and patient positioning should be selected based on the surgeon’s preference. The patient should be positioned supine, prone, or in lateral decubitis. When a UCL reconstruction is expected, supine position is advantageous to avoid repositioning after completing the arthroscopic portion of the procedure. However, arthroscopy can be performed in the lateral position with subsequent repositioning, repeat prepping, and draping for UCL reconstruction (Figures 5A, 5B).

Prepare for elbow arthroscopy by distending the elbow joint with normal saline to aid in protection of neurovascular structures and simplify the insertion of the scope trocar. Perform diagnostic anterior arthroscopy via the proximal anteromedial portal. Assess for presence of loose bodies and osteochondral lesions of the radiocapitellar joint, as well as osteophytes of the coronoid tip and fossa. Utilizing a spinal needle under direct visualization establish a proximal lateral portal with adequate view of the anterior compartment. Proceed to visualize the medial compartment and assess for UCL injury. Apply valgus stress while in 70° of flexion. Visualize the coronoid process and look for medial trochlea gapping of 3 mm or greater, which indicates UCL insufficiency.³⁰

Establish the posterolateral port for visualization of the posterior compartment. A posterior portal is established through the triceps tendon. Proceed to shave and ablate synovitis in order to create an adequate working space. Inspect the posteromedial olecranon, looking for any osteophytes or chondromalacia in the area (Figure 6). Examine the posterior radiocapitellar joint, looking specifically for loose bodies. The presence of loose bodies may require creating an extra mid lateral portal for removal. The ulnar nerve is located superficial to the elbow capsule and can be damaged by instruments utilized in the posteromedial gutter. As a precaution, be sure to remove suction attached to shaver. Place a curved articulating retractor in an accessory posterolateral portal to assist in protecting the ulnar nerve by retracting the capsule away from the surgical field (Figures 7A, 7B).

The osteophyte may be encased in soft tissue. Using a combination of ablation devices and shavers, the osteophyte can be exposed. The olecranon osteophyte can be removed with a small osteotome located at the border of the osteophyte and the normal olecranon. A motorized shaver or burr may also be introduced through the direct posterior portal or the posterolateral portal to complete the contouring of the olecranon (Figures 8A, 8B). Intraoperative lateral radiographs may be obtained for guidance in adequate bone removal and to ensure no bone debris is left in the soft tissues. It is critical that only pathologic osteophyte is removed and that normal olecranon is not compromised. This prevents an increase in UCL strain during valgus loading.¹⁹ However, in some non-throwing athletes, more aggressive debridement can be performed due to a smaller risk of UCL injury after posterior decompression.

Often, with the presence of osteophytes on the olecranon, there may be associated chondromalacia of the trochlea. These kissing lesions must be addressed after debridement of osteophytes. Loose flaps or frayed edges are carefully debrided and for any significant lesion the edges are contoured to a stable rim using shavers and curettes. Once altered to a well-shouldered lesion, microfracture is performed. Anterograde drilling of the lesion with perforations separated by 2 to 3 mm allow for the release of marrow elements and induction of a fibrocartilage healing response.

For an isolated posteromedial decompression, early rehabilitation begins with simple elbow flexion and extension exercises. It is important to restore flexor-pronator strength. Six weeks postoperatively, a progressive throwing program that includes plyometric exercises, neuromuscular training, and endurance exercises can be initiated. Patients can typically return to competition 3 to 4 months after surgery, if they have successfully regained preoperative range of motion, preoperative strength in the elbow, and there is no pain or tenderness on stress testing or palpation.

Outcomes

Safety and Advances in Arthroscopy

A clearer understanding of portal placement and proximity to neurovasculature in conjunction with advances in equipment have allowed for continual improvements in elbow arthroscopy techniques. There is plenty of literature indicating that arthroscopic posteromedial decompression is a safe, reliable, effective procedure, with a high rate of patient satisfaction.^22,30-34] Andrews and Carson³⁰ published one of the earliest investigations indicating the effectiveness of elbow arthroscopy utilizing objective and subjective outcome scores. They found that preoperative scores indicating patient satisfaction increased from 50% to 83%. Patients who underwent only loose body removal had the best outcomes. Andrews and Timmerman³¹ later evaluated the results of 72 professional baseball players who underwent either arthroscopic or open elbow surgery. They found that posteromedial olecranon osteophytes and intraarticular loose bodies were the most common diagnoses, present in 65% and 54% of players, respectively. In addition, a 41% reoperation rate was reported after posteromedial olecranon resection, along with 25% a rate of valgus instability necessitating UCL reconstruction. Andrews and Timmerman³¹ propose that the incidence of UCL injuries is underestimated and that UCL pathology must be treated prior to treating its secondary effects. Recently, Reddy and colleagues³² reviewed the results of 187 arthroscopic procedures. Posterior impingement, loose bodies, and osteoarthritis were the most common problems, occurring in 51%, 31%, and 22% of patients, respectively. Reported results were encouraging, with 87% good to excellent results and 85% of baseball players returning to preinjury levels.

Conclusion

An understanding of the relevant functional anatomy and the biomechanics of throwing is essential to understanding VEO. Potential concomitant valgus instability and UCL injury must be carefully assessed. Only symptomatic patients who have failed conservative treatment should undergo surgery. It is critical to avoid exacerbating and/or causing valgus instability by surgical excessively removing normal bone from the olecranon. Arthroscopy has been shown to be a safe and effective method to treat refractory cases of VEO.

The supraphysiological demands imposed on the elbow of a throwing athlete result in predictable patterns of injury. This is especially true of baseball pitchers. Knowledge of elbow anatomy, as well as the biomechanics of throwing, assist in making diagnostic and therapeutic decisions and also influence surgical technique when surgery is required. During the late cocking and early acceleration phases of throwing, valgus torque can reach 65 Nm with angular velocities of the forearm reaching 5000°/sec, which is considered the fasted recorded human movment.¹ The valgus torque and rapid extension synergistically create 3 major forces placed on the elbow. The first is a tensile stress along the medial aspect of elbow affecting the ulnar collateral ligament (UCL), flexor pronator mass, and medial epicondyle. Secondly, compression forces affect the lateral aspect of the elbow at the radiocapitellar joint. Finally, a shearing stress occurs in the posterior compartment at the posterior medial tip of the olecranon and the olecranon fossa.

These forces generated on the elbow result in predictable pathology. The recurring tensile forces applied on the medial aspect on the elbow can compromise the integrity of the UCL. It is well known that injury to the UCL leads to valgus instability. Individuals with valgus instability who continue to throw may trigger and/or aggravate injury in the posterior and lateral components of the elbow. Lateral compression forces can often reach 500 N, resulting in radiocapitellar overload syndrome, which occurs in combination with medial ligament instability and valgus extension overload.² Radiocapitellar compression may cause chondral or osteochondral fracture with resulting intra-articular loose bodes. This compression also contributes to the etiology of osteochondritis dissecans (OCD) in skeletally immature athletes. In the posterior elbow, throwing forcefully and repeatedly pushes the olecranon into the olecranon fossa. Shear stress on the medial olecranon tip and fossa, due to combined valgus and extension forces, lead to the development of osteophytes. This collection of injuries in the medial, lateral, and posterior aspects of the elbow is known as “valgus extension overload syndrome” or VEO. Symptoms in VEO can be the result of chondral lesions, loose bodies, and marginal exostosis.³

The aim of this review is to provide understanding regarding both the relevant anatomy and pathomechanics of VEO, key aspects to clinical evaluation, and effective treatment options.

Functional Anatomy

A functional comprehension of elbow anatomy and biomechanics is essential to understanding the constellation of injuries in VEO. The osseous anatomy of the elbow permits a variety of movements. These include flexion-extension and pronation-supination, which are mediated by the ulnohumeral and radiocapitellar articulations. While in full extension, the elbow has a normal valgus carrying angle of 11° to 16°. It is important to know that 50% of the elbow’s stability is attributed to the configuration of the bones.^4-6 This is especially true in varus stress while the elbow is in full extension. The soft tissues, including muscle and ligaments such as the UCL, lateral UCL, and radial UCL complexes, provide the remaining elbow stability.^4-6

The UCL complex is composed of 3 main segments known as the anterior, posterior, and oblique bundles (transverse ligament). Collectively, these bundles are responsible for providing medial elbow stability. However, each of these bundles contributes to medial elbow stability in its own way. The first and arguably the most important bundle is the anterior bundle; its most important function is providing stability against valgus stress.^4,5,7 It is composed of parallel fibers inserting on the medial coronoid process.^4,5,7 Furthermore, its eccentric location with respect to the axis of elbow allows it to provide stability throughout the full range of elbow motion.⁶ The anterior bundle can be further divided into individual anterior and posterior bands that have reciprocal functionality.^5,8,9 The anterior band acts as the chief restraint to valgus stress up to 90° of flexion.⁹ Any flexion beyond 90° renders the anterior band’s role secondary in resisting valgus stress.⁹ The posterior band’s function in resisting valgus stress is most important between 60° and full flexion, while having a secondary role in lesser degrees of flexion.^8,9 Notably, the posterior band is isometric and is more important in the overhead-throwing athlete due to the fact its primary role in resisting valgus stress occurs at higher degrees of flexion.¹⁰

The remaining posterior and oblique bundles of the UCL complex have lesser roles in maintaining elbow stability. The posterior bundle of the UCL complex is fan-shaped, originates from the medial epicondyle, and inserts onto the medial margin the semi-lunar notch. It is more slender and frailer than the anterior bundle. This is reflected in its functionality, as it plays a secondary role in elbow stability during elbow flexion beyond 90°.^4,5,8 In contrast to the anterior and posterior bundles, the oblique bundle, also known as the transverse ligament, does not cross the elbow joint. It is a thickening of the caudal most aspect of the joint capsule, which extends from the medial olecranon to the inferior medial coronoid process and as a result functions in expanding the greater sigmoid notch.⁶

The musculotendinous components of the elbow are essential to providing dynamic functional resistance to valgus stress.¹¹ These components are flexor-pronator musculature that originate from the medial epicondyle. Listed proximally to distally, the flexor-pronator muscles include pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis, and the flexor carpi ulnaris (FCU).

Pathomechanics

Once familiarized with the relevant function anatomy, it is crucial to understand the mechanics of throwing in order to understand the pathomechanics of VEO. The action of overhead throwing has been divided into 6 phases.^6,12-16 Phase 4, acceleration, is the most relevant when discussing forces on elbow, since the majority of forces are generated during this state. Phase 4 represents a rapid acceleration of the upper extremity with a large forward-directed force on the arm generated by the shoulder muscles. Additionally, there is internal rotation and adduction of the humerus with rapid elbow extension terminating with ball release. The elbow accelerates up to 600,000°/sec² in a miniscule time frame of 40 to 50 milliseconds.^1,5 Immense valgus forces are exerted on the medial aspect of the elbow. The anterior bundle of the UCL bears the majority of the force, with the flexor pronator mass enabling the transmission.¹¹ The majority of injuries occur during stage 4 as a result of the stress load on the medial elbow structures like the UCL. The proceeding phases 5 (deceleration), and 6 (follow-through) involve eventual dissipation of excess kinetic energy as the elbow completely extends. The deceleration during phase 5 is rapid and powerful, occurring at about 500,000°/sec² in the short span of 50 milliseconds.^1,6,12-16 High-velocity throwing, such as baseball pitching, generates forces in the elbow that are opposed by the articular, ligamentous, and muscular portions of the arm. The ulnohumeral articulation stabilizes motion of the arm from 0° to 20° of flexion and beyond 120° of flexion. Static and dynamic soft tissues maintain stability during the remaining of 100° arc of motion.

During deceleration, the elbow undergoes terminal extension resulting in the posteromedial olecranon contacting the trochlea and the olecranon fossa with subsequent dissipation of the combined valgus force and angular moment (Figure 1). This dissipation of force creates pathologic shear and compressive forces in the posterior elbow. Poor muscular control and the traumatic abutment that occurs in the posterior compartment may further add to the pathologic forces. Reactive bone formation is induced by the repetitive compression and shear, resulting in osteophytes on the posteromedial tip of the olecranon (Figure 2). Consequent “kissing lesions” of chondromalacia may occur in the olecranon fossa and posteromedial trochlea. The subsequent development of loose bodies may also occur. The presence of osteophytes and/or loose bodies may result in posteromedial impingement (PMI).

The association between PMI of the olecranon and valgus instability has been elucidated in both clinical and biomechanical investigations.^17,18,19,20 Conway¹⁸ identified tip exostosis in 24% of lateral radiographs of 135 asymptomatic professional pitchers. Approximately one-fifth (21%) of these pitchers had >1.0 mm increased relative valgus laxity on stress radiographs. Roughly one-third (34%) of players with exostosis had >1.0 mm of increased relative valgus laxity, compared to 16% of players without exostosis formation. These results provide evidence for a probable association between PMI and valgus laxity. In biomechanical research, Ahmad and colleagues¹⁷ studied the effect of partial and full thickness UCL injuries on contact forces of the posterior elbow. Posteromedial compartments of cadaver specimens were subjected to physiologic valgus stresses while placed on pressure-senstive film. Contact area and pressure between posteromedial trochlea and olecranon were altered in the setting of UCL insufficiency, helping explain how posteromedial osteophyte formation occurs.

Additional biomechanical studies have also investigated the posteromedial olecranon’s role in functioning as a stabilizing buttress to medial tensile forces. Treating PMI with aggressive bone removal may increase valgus instability as well as strain on the UCL, leading to UCL injury following olecranon resection.^19,20 Kamineni and colleagues¹⁹ investigated strain on anterior bundle of UCL as a function of increasing applied torque and posteromedial resections of the olecranon. This investigation was done utilizing an electromagnetic tracking placed in cadaver elbows. A nonuniform change in strain was found at 3 mm of resection during flexion and valgus testing. This nonuniform change implied that removal of posteromedial olecranon beyond 3 mm made the UCL more vulnerable to injury. Follow-up investigations looked at kinematic effects of increasing valgus and varus torques and sequential posteromedial olecranon resections.²⁰ Valgus angulation of the elbow increased with all resection levels but no critical amount of olecranon resection was identified. The consensus in the literature indicates that posteromedial articulation of the elbow is a significant stabilizer to valgus stress.^17-22 Thus, normal bone should be preserved and only osteophytes should be removed during treatment.

In addition, VEO may lead to injury in the lateral compartment as well. After attenuation and insufficiency of the UCL due to repetitive stress, excessive force transmission to the lateral aspect of the elbow occurs. Compressive and rotatory forces escalate within the radiocapitellar joint, causing synovitis and osteochondral lesions.^3,23 These osteochondral lesions include osteochondritis dissecans and osteochondral fractures that may fragment and become loose bodies.

Evaluation of VEO

History

Patients will typically have a history of repetitive throwing or other repetitive overhead activity. VEO is most common in baseball pitchers but may also occur in other sports, such as tennis, football, lacrosse, gymnastics, and javelin throwing. In baseball pitchers, clinical presentation is often preceded by a decrease in pitch velocity, control, and early fatigability. It presents with elbow pain localized to the posteromedial aspect of olecranon after release of the ball, when the elbow reaches terminal extension. Patients also report limited extension, due to impinging posterior osteophytes. Also, locking and catching caused by loose bodies and chondromalacia may be present. VEO may also occur in combination with concomitant valgus instability, as well as in a patient with a prior history of valgus instability. Flexor pronator injury, ulnar neuritis, and subluxation may also be present in a patient with VEO.

Physical Examination

VEO may occur in an isolated fashion or with concomitant pathology. Therefore, a comprehensive physical examination includes evaluating the entire kinetic chain of throwing and a focused examination covering VEO and associated valgus instability. Patients may exhibit crepitus and tenderness over the posteromedial olecranon and a loss of extension with a firm end point. The extension impingement test should be performed where the elbow is snapped into terminal extension. This typically elicits pain in the posterior compartment in a patient with VEO. The arm bar test involves positioning the patient’s shoulder at 90° of forward flexion, full internal rotation, with the patient’s hand placed on the examiner’s shoulder.²⁴ The examiner pulls down on the olecranon, simulating forced extension; pain is indicative of a positive test. It is important to note if there are signs of ulnar neuritis or subluxing ulnar nerve, especially if planning to utilize medial portals during arthroscopic treatment.

Examination maneuvers for valgus instability should also be conducted during evaluation of VEO. The physical examination for valgus instability in the elbow is ideally performed with the patient seated. Secure the patient’s wrist between the examiner’s forearm and trunk, and flex the patient’s elbow between 20° and 30° to unlock the olecranon from its fossa. Proceed to apply valgus stress. This stresses the anterior band of the anterior bundle of the UCL.^6,25,26 Palpate the UCL from the medial epicondyle to the proximal ulna as valgus stress is applied. Occasionally, valgus laxity can be appreciated when compared to contralateral side. The milking maneuver is a helpful test to determine UCL injury. Pull on the patient’s thumb while the forearm is supinated, shoulder extended, and the elbow flexed beyond 90°.⁶ The milking maneuver exerts valgus stress on a flexed elbow. A patient with an injured UCL will experience the subjective feeling of apprehension and instability, with medial elbow pain.

The most sensitive test is the moving valgus stress test. This is performed with the patient in the upright position and the shoulder abducted 90°. Starting with the arm in full flexion, the examiner applies a constant valgus torque to the elbow and then rapidly extends the elbow. Reproduction of pain during range of motion from 120° to 70° represents UCL injury, while pain with extension beyond 70° represents chondral injury to the ulnohumeral joint. Be aware that the absence of increased pain with wrist flexion, along with pain localized slightly posterior to the common flexor origin, differentiates a UCL injury from flexor-pronator muscle injury.^6,26,27Examine range of motion in affected and unaffected elbows. Loss of terminal extension may be present, along with secondary to flexion contracture due to repeated attempts at healing and stabilization.²⁵

Imaging

Imaging is essential to the accurate diagnosis of VEO and related conditions. Anterior posterior (AP), lateral, and oblique radiographs of elbow (Figures 3A-3C) may show posteromedial olecranon osteophytes and/or loose bodies. Calcification of ligaments or other soft tissues may also be seen. An AP radiograph with 140° of external rotation may best visualize osteophytes on posteromedial olecranon.18 A computed tomography scan with 2-dimensional sagittal and coronal reconstruction and 3-dimensional surface rendering (Figures 4A, 4B) may best demonstrate morphological abnormalities, loose bodies, and osteophytes. Magnetic resonance imaging (MRI) is essential for assessment of soft tissues and chondral injuries. MRI may detect UCL compromise, synovial plicae, bone edema, olecranon, or stress fractures.

Treatment

Nonoperative Treatment

Treatment consists of both nonoperative and operative modalities. Nonoperative treatment methods are first line in treating VEO. Patients should modify their physical activity and rest from throwing activities. Nonsteroid anti-inflammatory drugs are appropriate to treat pain along with intra-articular corticosteroid injections of the elbow. A wide assessment of pitching mechanics should be performed in an attempt to correct errors in throwing technique and address muscular imbalances. After cessation of the resting period, the patient may initiate a progressive throwing program supervised by an experienced therapist and trainer. A plan for returning to competition should be made upon completion of the throwing program.

Operative Treatment

Surgical treatment is reserved for patients who fail nonoperative treatment. These patients have persistent symptoms of posteromedial impingement and desire to return to pre-injury level of performance. Posteromedial decompression is not recommended when provocative physical examination maneuvers are negative, regardless of presence of olecranon osteophytes on imaging. Osteophytes are an asymptomatic finding typically seen in professional baseball players and do not warrant surgical treatment.^18,28 UCL compromise is a relative contraindication to olecranon debridement as UCL injury could become symptomatic following surgery. Surgical options in the appropriate patient to decompress posterior compartment include arthroscopic olecranon debridement or limited incision arthrotomy. Excessive resection of posteromedial osteophytes must be avoided. Arthroscopy has limited morbidity and allows for complete diagnostic assessment. UCL reconstruction should also be considered in combination with posteromedial debridement when the UCL is torn. More challenging indications for UCL reconstruction occur when the UCL is partially torn or torn and asymptomatic. Isolated posteromedial decompression in this setting risks future development of UCL symptoms that would then need to be addressed.

Surgical Technique

As previously mentioned, elbow arthroscopy or limited excision arthrotomy are the preferred operative methods for decompression of the posterior compartment and thus treatment of VEO. Anesthesia and patient positioning should be selected based on the surgeon’s preference. The patient should be positioned supine, prone, or in lateral decubitis. When a UCL reconstruction is expected, supine position is advantageous to avoid repositioning after completing the arthroscopic portion of the procedure. However, arthroscopy can be performed in the lateral position with subsequent repositioning, repeat prepping, and draping for UCL reconstruction (Figures 5A, 5B).

Prepare for elbow arthroscopy by distending the elbow joint with normal saline to aid in protection of neurovascular structures and simplify the insertion of the scope trocar. Perform diagnostic anterior arthroscopy via the proximal anteromedial portal. Assess for presence of loose bodies and osteochondral lesions of the radiocapitellar joint, as well as osteophytes of the coronoid tip and fossa. Utilizing a spinal needle under direct visualization establish a proximal lateral portal with adequate view of the anterior compartment. Proceed to visualize the medial compartment and assess for UCL injury. Apply valgus stress while in 70° of flexion. Visualize the coronoid process and look for medial trochlea gapping of 3 mm or greater, which indicates UCL insufficiency.³⁰

Establish the posterolateral port for visualization of the posterior compartment. A posterior portal is established through the triceps tendon. Proceed to shave and ablate synovitis in order to create an adequate working space. Inspect the posteromedial olecranon, looking for any osteophytes or chondromalacia in the area (Figure 6). Examine the posterior radiocapitellar joint, looking specifically for loose bodies. The presence of loose bodies may require creating an extra mid lateral portal for removal. The ulnar nerve is located superficial to the elbow capsule and can be damaged by instruments utilized in the posteromedial gutter. As a precaution, be sure to remove suction attached to shaver. Place a curved articulating retractor in an accessory posterolateral portal to assist in protecting the ulnar nerve by retracting the capsule away from the surgical field (Figures 7A, 7B).

The osteophyte may be encased in soft tissue. Using a combination of ablation devices and shavers, the osteophyte can be exposed. The olecranon osteophyte can be removed with a small osteotome located at the border of the osteophyte and the normal olecranon. A motorized shaver or burr may also be introduced through the direct posterior portal or the posterolateral portal to complete the contouring of the olecranon (Figures 8A, 8B). Intraoperative lateral radiographs may be obtained for guidance in adequate bone removal and to ensure no bone debris is left in the soft tissues. It is critical that only pathologic osteophyte is removed and that normal olecranon is not compromised. This prevents an increase in UCL strain during valgus loading.¹⁹ However, in some non-throwing athletes, more aggressive debridement can be performed due to a smaller risk of UCL injury after posterior decompression.

Often, with the presence of osteophytes on the olecranon, there may be associated chondromalacia of the trochlea. These kissing lesions must be addressed after debridement of osteophytes. Loose flaps or frayed edges are carefully debrided and for any significant lesion the edges are contoured to a stable rim using shavers and curettes. Once altered to a well-shouldered lesion, microfracture is performed. Anterograde drilling of the lesion with perforations separated by 2 to 3 mm allow for the release of marrow elements and induction of a fibrocartilage healing response.

For an isolated posteromedial decompression, early rehabilitation begins with simple elbow flexion and extension exercises. It is important to restore flexor-pronator strength. Six weeks postoperatively, a progressive throwing program that includes plyometric exercises, neuromuscular training, and endurance exercises can be initiated. Patients can typically return to competition 3 to 4 months after surgery, if they have successfully regained preoperative range of motion, preoperative strength in the elbow, and there is no pain or tenderness on stress testing or palpation.

Outcomes

Safety and Advances in Arthroscopy

A clearer understanding of portal placement and proximity to neurovasculature in conjunction with advances in equipment have allowed for continual improvements in elbow arthroscopy techniques. There is plenty of literature indicating that arthroscopic posteromedial decompression is a safe, reliable, effective procedure, with a high rate of patient satisfaction.^22,30-34] Andrews and Carson³⁰ published one of the earliest investigations indicating the effectiveness of elbow arthroscopy utilizing objective and subjective outcome scores. They found that preoperative scores indicating patient satisfaction increased from 50% to 83%. Patients who underwent only loose body removal had the best outcomes. Andrews and Timmerman³¹ later evaluated the results of 72 professional baseball players who underwent either arthroscopic or open elbow surgery. They found that posteromedial olecranon osteophytes and intraarticular loose bodies were the most common diagnoses, present in 65% and 54% of players, respectively. In addition, a 41% reoperation rate was reported after posteromedial olecranon resection, along with 25% a rate of valgus instability necessitating UCL reconstruction. Andrews and Timmerman³¹ propose that the incidence of UCL injuries is underestimated and that UCL pathology must be treated prior to treating its secondary effects. Recently, Reddy and colleagues³² reviewed the results of 187 arthroscopic procedures. Posterior impingement, loose bodies, and osteoarthritis were the most common problems, occurring in 51%, 31%, and 22% of patients, respectively. Reported results were encouraging, with 87% good to excellent results and 85% of baseball players returning to preinjury levels.

Conclusion

An understanding of the relevant functional anatomy and the biomechanics of throwing is essential to understanding VEO. Potential concomitant valgus instability and UCL injury must be carefully assessed. Only symptomatic patients who have failed conservative treatment should undergo surgery. It is critical to avoid exacerbating and/or causing valgus instability by surgical excessively removing normal bone from the olecranon. Arthroscopy has been shown to be a safe and effective method to treat refractory cases of VEO.

Posterolateral rotatory instability (PLRI) of the elbow is well recognized¹ and is the most common type of chronic elbow instability. PLRI is often an end result of traumatic elbow dislocation.² The “essential lesion” in patients with PLRI of the elbow is injury to the lateral ulnar collateral ligament (LUCL).¹ However, more recent research has emphasized the importance of other ligaments in the lateral ligament complex (radial collateral and annular ligaments) in preventing PLRI.^3-5 Nevertheless, when conservative treatment fails, the most commonly used surgical treatment involves LUCL reconstruction.^1,6-11

Numerous techniques for LUCL reconstruction have been described.^1,7-9,11-13 The chosen technique ideally restores normal anatomy. Therefore, the isometric point of origin at the lateral epicondyle and insertion at the supinator tubercle are important landmarks for creating tunnels that reproduce isometry, function, and normal anatomy. Most often, 2 tunnels are created in the ulna to secure the graft. It has been our experience that ulnar tunnel creation can affect the length of the bony bridge and the orientation of the graft.

We conducted a study to identify the precise proximal ulna tunnel location—anterior to posterior, with the distal tunnel at the supinator tubercle on the crest—that allows for the largest bony bridge and most geometrically favorable construct. We hypothesized that a most posteriorly placed proximal tunnel would increase bony bridge size and allow for a more isosceles graft configuration. An isosceles configuration with the humerus tunnel at the isometric location would allow for anterior and posterior bands of the same length with theoretically equal force distribution.

Methods

After obtaining institutional review board approval, we retrospectively reviewed the cases of 17 adults with elbow computed tomography (CT) scans for inclusion in this study. The scans were previously performed for diagnostic workup of several pathologies, including valgus instability, olecranon stress fracture, and valgus extension overload. The scan protocol involved 0.5-mm axial cuts with inclusion of the distal humerus through the proximal radius and ulna in the DICOM (Digital Imaging and Communications in Medicine) format. Exclusion criteria included poor CT quality, inadequate visualization of the entire supinator crest, and age under 18 years. Fifteen patients with adequate CT scans met the inclusion criteria. MIMICS (Materialise’s Interactive Medical Image Control System) software was used to convert scans into patient-specific 3-dimensional (3-D) computer models. (Use of this software to produce anatomically accurate models has been verified in shoulder¹⁴ and elbow¹⁵ models.) These models were uploaded into Magics rapid prototyping software (Materialise) and manipulated for simulated tunnel drilling by precise bone subtraction methods. This software was used to define an ulnar Cartesian coordinate system with anatomical landmarks as reference points in order to standardize the position of each model (Figure 1).¹⁶ The y-axis was defined by the longitudinal axis of the ulna, and the x-axis was the transepicondylar axis, defined as the perpendicular line connecting the y-axis with the supinator crest. The z-axis was then established as the line perpendicular to the x- and y-axes—yielding a 3-D coordinate system that allowed us to manipulate the models in standardized fashion, maintaining the exact positions of the ulna while making measurements.

Surgical simulations were performed in the rapid prototyping software by creating a cylinder and placing it at the desired location of each tunnel. Cylinder diameter was 4 mm, matching the diameter of the drill we use to create each tunnel in our practice. The cylinder was inserted into the bone, perpendicular to the surface of the ulna at the point of insertion, so the cylinder’s deepest point entered the medullary canal of the ulna. Using a Boolean operation in the rapid prototyping software, we subtracted cylinder from bone to create a tunnel (Figure 2).¹⁵

In a previous study,¹⁷ we determined that the radial head junction is reproducibly about 15 mm proximal to the distinct supinator tubercle, which may be absent or not readily appreciated in up to 50% of cases. Therefore, proximal ulnar tunnels were placed 0, 5, and 10 mm posterior to the supinator crest at the radial head junction. Distal tunnels were placed 15 mm anterior to the radial head junction on the supinator crest (Figure 2). The bony bridges created by these tunnels were measured, as was the distance between the distal tunnel and the supinator tubercle.

Ideal graft configuration was described as an isosceles triangle with ulna tunnels perpendicular to the humeral tunnel (Figure 3).¹¹ Location of the humeral origin in the sagittal plane was determined by finding the isometric point of the lateral humerus using only bony landmarks. Similar techniques have been used to find the isometric point on the medial epicondyle for medial ulnar collateral ligament reconstruction.^15,18 With a circle fit into the trochlear notch of the ulna, the isometric point can be determined by the center of the circle. This point was then superimposed on the humerus to identify the starting point (Figure 4). In our simulation, we measured the isosceles configuration by drawing a line between the proximal and distal tunnels, and then another line connecting the bisecting point of the first line with the isometric point on the humerus from which the graft would originate. The angle between the 2 lines was measured; if isosceles, the angle was 90° (Figure 5). Length of the more proximal limb of the graft and the more distal limb of the graft was determined by measuring the distance from the isometric point to the proximal and distal tunnels, respectively (Figure 6).

One-way analysis of variance was used to compare all the tunnels’ bony bridge sizes, graft lengths, and angles to the isometric point. For all comparisons, statistical significance was set at P < .05. As no other studies have compared bony bridges by varying tunnel creation parameters, and as the present study is observational and not comparative, no power analysis was performed.

Results

Bony bridges were significantly longer, and angles more perpendicular, with increasing distance from the proximal tunnel to the supinator crest (Table 1, Figure 5, Figure 7). The bony bridge 0 mm posterior to the supinator crest yielded a mean (SE) bony bridge length of 11.0 (0.2) mm. This proximal tunnel also yielded the smallest mean (SE) perpendicular angle to the isometric point, 131.2° (1.9°). The tunnel most posterior to the supinator crest yielded the longest mean (SE) bony bridge, 13.7 (0.2) mm, and the largest mean (SE) degree of perpendicularity, 95.8° (1.4°). The differences between all tunnels’ bony bridges and isometric angles were statistically significant (P < .00001). The difference between the more distal limb and the more proximal limb of the graft was smallest in the more posteriorly placed proximal tunnel (Table 2, Figure 8). In fact, there was no statistical difference between the proximal and distal limbs of the graft when the proximal tunnel was placed 10 mm posterior to the supinator crest: Mean (SE) was 9.4 (0.5) mm at 0 mm (P < .00001) and 1.1 (0.6) mm at 10 mm (P = .24).

Discussion

PLRI of the elbow is best initially managed nonoperatively. However, when nonoperative management fails, the LUCL is often surgically reconstructed. Reconstruction methods vary by fixation method, graft choice, and bone tunnels.^1,7-9,11-13 In 1991, O’Driscoll and colleagues¹ described a “yoke” technique for LUCL reconstruction. Since then, the docking technique⁷ and other techniques have been developed. All these techniques emphasize maximizing anatomical precision and isometry with careful placement of tunnels or fixation devices. The humeral fixation site, at the anterior inferior aspect of the lateral epicondyle at the point of isometry, can be accessed relatively reproducibly. By contrast, the ulnar points of fixation are more variable, because of increased bone stock and overlying soft-tissue and bony anatomy.

Among the challenges in determining the points of ulnar fixation is the bony anatomy that is often used for landmarks. In the literature, the supinator crest or the supintor tubercle is the landmark for placing the distal tunnel.^1,7-9,11-13 This is a problem for 2 reasons. First, the supintor crest, a longitudinal structure on the lateral aspect of the ulna, originates from the radial head junction and extends tens of millimeters distally; further specification is needed to guide these ulnar tunnels. The second reason is that use of the supinator tubercle, a prominence on the supinator crest, adds specificity to the location of the ulnar tunnels. During surgery, however, the supinator tubercle may not be a reliable, independently prominent structure; instead, it may be indistinguishable from the supinator crest, on which it rests. One study determined that only about 50% of computer models of patient ulnas had a distinct prominence that could be classified as the supinator tubercle.¹⁷ The percentage presumably is lower during surgery, with limited exposure and overlying soft tissues.

In a study of patients with a prominent tubercle, mean (SE) distance from radial head junction to tubercle was 15 (2) mm.¹⁷ This finding led us to use the radial head junction as the primary bony landmark in determining the location of the proximal tunnel and placing the distal tunnel 15 mm distally—achieving the same fixation described in the literature but using more distinct landmarks. Our study thus provided a reliable, verified approach to locating the ulnar tunnels in the proximal-distal axis.

We also explored the anterior-posterior orientation of the proximal ulnar tunnel. The 2 primary considerations surrounding the varied proximal tunnel placements were the bony bridge formed between the proximal and distal tunnels and the perpendicularity of the triangle formed by the fixation points. Maximizing the bony bridge is obviously ideal in securing and preventing fixation blowout. Achieving an isoceles reconstruction has been reported in the literature on the various fixation techniques for LUCL reconstruction.¹¹ Although the biomechanical advantage of this fixation type is not fully clear, we assume the construct produces graft stands of equal length, tension, and stability. In addition, the larger footprint created by an isoceles reconstructed ligament increases the stability of the radial head.

Results of the present study showed that the more posterior the proximal ulnar tunnel, the longer the bony bridge and the more isoceles the reconstruction. The difference in bony bridge distance from the most anterior to the most posterior tunnel was about 2 mm, or 18%. For every 1 mm of posteriorization, the bony bridge was 0.2 mm longer. The line from the isometric point of humeral fixation bisecting the proximal and distal tunnels was also more perpendicular with the most posterior tunnel, by about 40°. The resulting proximal and distal limbs of the reconstruction were equal in length, as demonstrated by the smaller difference between the limbs. We assume this isoceles reconstruction more likely applies uniform restraint on the radial head. Thus, an effort should be made to posteriorize the proximal ulnar tunnel during reconstruction.

The study was limited by the number of patient-specific elbow models used. However, given the statistical consistency of measurements, sample size was sufficient. Another limitation, inherent to the model, was that only bony anatomy was incorporated. However, the overlying muscles, tendons, and ligaments can significantly alter tunnel placement, and this study provided other means and cues using more reliable landmarks to adequately place the tunnels. As this was a simulation study, we cannot confirm whether these results would make a difference clinically. The strengths of this study include development and verification of reliable landmarks that can be used to guide ulnar tunnel locations during LUCL reconstruction; these landmarks have been used for medial ulnar collateral ligament reconstruction.¹⁵ Other strengths include precise and accurate placement of tunnels and measurement of resulting bony bridges—accomplished independently and without compromising specimen quality.

Conclusion

We recommend drilling the proximal ulnar tunnel posterior to the supinator crest at the level of the radial head junction. A reasonable goal is 10 mm posterior to the crest, though the overlying soft tissue must be considered, and care should be taken to aim the drill anteriorly, toward the ulna’s intramedullary canal, to avoid posterior cortical breach. The distal ulnar tunnel should be drilled just posterior to the supinator crest, 15 mm distal to the radial head junction.

Posterolateral rotatory instability (PLRI) of the elbow is well recognized¹ and is the most common type of chronic elbow instability. PLRI is often an end result of traumatic elbow dislocation.² The “essential lesion” in patients with PLRI of the elbow is injury to the lateral ulnar collateral ligament (LUCL).¹ However, more recent research has emphasized the importance of other ligaments in the lateral ligament complex (radial collateral and annular ligaments) in preventing PLRI.^3-5 Nevertheless, when conservative treatment fails, the most commonly used surgical treatment involves LUCL reconstruction.^1,6-11

Numerous techniques for LUCL reconstruction have been described.^1,7-9,11-13 The chosen technique ideally restores normal anatomy. Therefore, the isometric point of origin at the lateral epicondyle and insertion at the supinator tubercle are important landmarks for creating tunnels that reproduce isometry, function, and normal anatomy. Most often, 2 tunnels are created in the ulna to secure the graft. It has been our experience that ulnar tunnel creation can affect the length of the bony bridge and the orientation of the graft.

We conducted a study to identify the precise proximal ulna tunnel location—anterior to posterior, with the distal tunnel at the supinator tubercle on the crest—that allows for the largest bony bridge and most geometrically favorable construct. We hypothesized that a most posteriorly placed proximal tunnel would increase bony bridge size and allow for a more isosceles graft configuration. An isosceles configuration with the humerus tunnel at the isometric location would allow for anterior and posterior bands of the same length with theoretically equal force distribution.

Methods

After obtaining institutional review board approval, we retrospectively reviewed the cases of 17 adults with elbow computed tomography (CT) scans for inclusion in this study. The scans were previously performed for diagnostic workup of several pathologies, including valgus instability, olecranon stress fracture, and valgus extension overload. The scan protocol involved 0.5-mm axial cuts with inclusion of the distal humerus through the proximal radius and ulna in the DICOM (Digital Imaging and Communications in Medicine) format. Exclusion criteria included poor CT quality, inadequate visualization of the entire supinator crest, and age under 18 years. Fifteen patients with adequate CT scans met the inclusion criteria. MIMICS (Materialise’s Interactive Medical Image Control System) software was used to convert scans into patient-specific 3-dimensional (3-D) computer models. (Use of this software to produce anatomically accurate models has been verified in shoulder¹⁴ and elbow¹⁵ models.) These models were uploaded into Magics rapid prototyping software (Materialise) and manipulated for simulated tunnel drilling by precise bone subtraction methods. This software was used to define an ulnar Cartesian coordinate system with anatomical landmarks as reference points in order to standardize the position of each model (Figure 1).¹⁶ The y-axis was defined by the longitudinal axis of the ulna, and the x-axis was the transepicondylar axis, defined as the perpendicular line connecting the y-axis with the supinator crest. The z-axis was then established as the line perpendicular to the x- and y-axes—yielding a 3-D coordinate system that allowed us to manipulate the models in standardized fashion, maintaining the exact positions of the ulna while making measurements.

Surgical simulations were performed in the rapid prototyping software by creating a cylinder and placing it at the desired location of each tunnel. Cylinder diameter was 4 mm, matching the diameter of the drill we use to create each tunnel in our practice. The cylinder was inserted into the bone, perpendicular to the surface of the ulna at the point of insertion, so the cylinder’s deepest point entered the medullary canal of the ulna. Using a Boolean operation in the rapid prototyping software, we subtracted cylinder from bone to create a tunnel (Figure 2).¹⁵

In a previous study,¹⁷ we determined that the radial head junction is reproducibly about 15 mm proximal to the distinct supinator tubercle, which may be absent or not readily appreciated in up to 50% of cases. Therefore, proximal ulnar tunnels were placed 0, 5, and 10 mm posterior to the supinator crest at the radial head junction. Distal tunnels were placed 15 mm anterior to the radial head junction on the supinator crest (Figure 2). The bony bridges created by these tunnels were measured, as was the distance between the distal tunnel and the supinator tubercle.

Ideal graft configuration was described as an isosceles triangle with ulna tunnels perpendicular to the humeral tunnel (Figure 3).¹¹ Location of the humeral origin in the sagittal plane was determined by finding the isometric point of the lateral humerus using only bony landmarks. Similar techniques have been used to find the isometric point on the medial epicondyle for medial ulnar collateral ligament reconstruction.^15,18 With a circle fit into the trochlear notch of the ulna, the isometric point can be determined by the center of the circle. This point was then superimposed on the humerus to identify the starting point (Figure 4). In our simulation, we measured the isosceles configuration by drawing a line between the proximal and distal tunnels, and then another line connecting the bisecting point of the first line with the isometric point on the humerus from which the graft would originate. The angle between the 2 lines was measured; if isosceles, the angle was 90° (Figure 5). Length of the more proximal limb of the graft and the more distal limb of the graft was determined by measuring the distance from the isometric point to the proximal and distal tunnels, respectively (Figure 6).

One-way analysis of variance was used to compare all the tunnels’ bony bridge sizes, graft lengths, and angles to the isometric point. For all comparisons, statistical significance was set at P < .05. As no other studies have compared bony bridges by varying tunnel creation parameters, and as the present study is observational and not comparative, no power analysis was performed.

Results

Bony bridges were significantly longer, and angles more perpendicular, with increasing distance from the proximal tunnel to the supinator crest (Table 1, Figure 5, Figure 7). The bony bridge 0 mm posterior to the supinator crest yielded a mean (SE) bony bridge length of 11.0 (0.2) mm. This proximal tunnel also yielded the smallest mean (SE) perpendicular angle to the isometric point, 131.2° (1.9°). The tunnel most posterior to the supinator crest yielded the longest mean (SE) bony bridge, 13.7 (0.2) mm, and the largest mean (SE) degree of perpendicularity, 95.8° (1.4°). The differences between all tunnels’ bony bridges and isometric angles were statistically significant (P < .00001). The difference between the more distal limb and the more proximal limb of the graft was smallest in the more posteriorly placed proximal tunnel (Table 2, Figure 8). In fact, there was no statistical difference between the proximal and distal limbs of the graft when the proximal tunnel was placed 10 mm posterior to the supinator crest: Mean (SE) was 9.4 (0.5) mm at 0 mm (P < .00001) and 1.1 (0.6) mm at 10 mm (P = .24).

Discussion

PLRI of the elbow is best initially managed nonoperatively. However, when nonoperative management fails, the LUCL is often surgically reconstructed. Reconstruction methods vary by fixation method, graft choice, and bone tunnels.^1,7-9,11-13 In 1991, O’Driscoll and colleagues¹ described a “yoke” technique for LUCL reconstruction. Since then, the docking technique⁷ and other techniques have been developed. All these techniques emphasize maximizing anatomical precision and isometry with careful placement of tunnels or fixation devices. The humeral fixation site, at the anterior inferior aspect of the lateral epicondyle at the point of isometry, can be accessed relatively reproducibly. By contrast, the ulnar points of fixation are more variable, because of increased bone stock and overlying soft-tissue and bony anatomy.

Among the challenges in determining the points of ulnar fixation is the bony anatomy that is often used for landmarks. In the literature, the supinator crest or the supintor tubercle is the landmark for placing the distal tunnel.^1,7-9,11-13 This is a problem for 2 reasons. First, the supintor crest, a longitudinal structure on the lateral aspect of the ulna, originates from the radial head junction and extends tens of millimeters distally; further specification is needed to guide these ulnar tunnels. The second reason is that use of the supinator tubercle, a prominence on the supinator crest, adds specificity to the location of the ulnar tunnels. During surgery, however, the supinator tubercle may not be a reliable, independently prominent structure; instead, it may be indistinguishable from the supinator crest, on which it rests. One study determined that only about 50% of computer models of patient ulnas had a distinct prominence that could be classified as the supinator tubercle.¹⁷ The percentage presumably is lower during surgery, with limited exposure and overlying soft tissues.

In a study of patients with a prominent tubercle, mean (SE) distance from radial head junction to tubercle was 15 (2) mm.¹⁷ This finding led us to use the radial head junction as the primary bony landmark in determining the location of the proximal tunnel and placing the distal tunnel 15 mm distally—achieving the same fixation described in the literature but using more distinct landmarks. Our study thus provided a reliable, verified approach to locating the ulnar tunnels in the proximal-distal axis.

We also explored the anterior-posterior orientation of the proximal ulnar tunnel. The 2 primary considerations surrounding the varied proximal tunnel placements were the bony bridge formed between the proximal and distal tunnels and the perpendicularity of the triangle formed by the fixation points. Maximizing the bony bridge is obviously ideal in securing and preventing fixation blowout. Achieving an isoceles reconstruction has been reported in the literature on the various fixation techniques for LUCL reconstruction.¹¹ Although the biomechanical advantage of this fixation type is not fully clear, we assume the construct produces graft stands of equal length, tension, and stability. In addition, the larger footprint created by an isoceles reconstructed ligament increases the stability of the radial head.

Results of the present study showed that the more posterior the proximal ulnar tunnel, the longer the bony bridge and the more isoceles the reconstruction. The difference in bony bridge distance from the most anterior to the most posterior tunnel was about 2 mm, or 18%. For every 1 mm of posteriorization, the bony bridge was 0.2 mm longer. The line from the isometric point of humeral fixation bisecting the proximal and distal tunnels was also more perpendicular with the most posterior tunnel, by about 40°. The resulting proximal and distal limbs of the reconstruction were equal in length, as demonstrated by the smaller difference between the limbs. We assume this isoceles reconstruction more likely applies uniform restraint on the radial head. Thus, an effort should be made to posteriorize the proximal ulnar tunnel during reconstruction.

The study was limited by the number of patient-specific elbow models used. However, given the statistical consistency of measurements, sample size was sufficient. Another limitation, inherent to the model, was that only bony anatomy was incorporated. However, the overlying muscles, tendons, and ligaments can significantly alter tunnel placement, and this study provided other means and cues using more reliable landmarks to adequately place the tunnels. As this was a simulation study, we cannot confirm whether these results would make a difference clinically. The strengths of this study include development and verification of reliable landmarks that can be used to guide ulnar tunnel locations during LUCL reconstruction; these landmarks have been used for medial ulnar collateral ligament reconstruction.¹⁵ Other strengths include precise and accurate placement of tunnels and measurement of resulting bony bridges—accomplished independently and without compromising specimen quality.

Conclusion

We recommend drilling the proximal ulnar tunnel posterior to the supinator crest at the level of the radial head junction. A reasonable goal is 10 mm posterior to the crest, though the overlying soft tissue must be considered, and care should be taken to aim the drill anteriorly, toward the ulna’s intramedullary canal, to avoid posterior cortical breach. The distal ulnar tunnel should be drilled just posterior to the supinator crest, 15 mm distal to the radial head junction.

Posterolateral rotatory instability (PLRI) of the elbow is well recognized¹ and is the most common type of chronic elbow instability. PLRI is often an end result of traumatic elbow dislocation.² The “essential lesion” in patients with PLRI of the elbow is injury to the lateral ulnar collateral ligament (LUCL).¹ However, more recent research has emphasized the importance of other ligaments in the lateral ligament complex (radial collateral and annular ligaments) in preventing PLRI.^3-5 Nevertheless, when conservative treatment fails, the most commonly used surgical treatment involves LUCL reconstruction.^1,6-11

Numerous techniques for LUCL reconstruction have been described.^1,7-9,11-13 The chosen technique ideally restores normal anatomy. Therefore, the isometric point of origin at the lateral epicondyle and insertion at the supinator tubercle are important landmarks for creating tunnels that reproduce isometry, function, and normal anatomy. Most often, 2 tunnels are created in the ulna to secure the graft. It has been our experience that ulnar tunnel creation can affect the length of the bony bridge and the orientation of the graft.

We conducted a study to identify the precise proximal ulna tunnel location—anterior to posterior, with the distal tunnel at the supinator tubercle on the crest—that allows for the largest bony bridge and most geometrically favorable construct. We hypothesized that a most posteriorly placed proximal tunnel would increase bony bridge size and allow for a more isosceles graft configuration. An isosceles configuration with the humerus tunnel at the isometric location would allow for anterior and posterior bands of the same length with theoretically equal force distribution.

Methods

After obtaining institutional review board approval, we retrospectively reviewed the cases of 17 adults with elbow computed tomography (CT) scans for inclusion in this study. The scans were previously performed for diagnostic workup of several pathologies, including valgus instability, olecranon stress fracture, and valgus extension overload. The scan protocol involved 0.5-mm axial cuts with inclusion of the distal humerus through the proximal radius and ulna in the DICOM (Digital Imaging and Communications in Medicine) format. Exclusion criteria included poor CT quality, inadequate visualization of the entire supinator crest, and age under 18 years. Fifteen patients with adequate CT scans met the inclusion criteria. MIMICS (Materialise’s Interactive Medical Image Control System) software was used to convert scans into patient-specific 3-dimensional (3-D) computer models. (Use of this software to produce anatomically accurate models has been verified in shoulder¹⁴ and elbow¹⁵ models.) These models were uploaded into Magics rapid prototyping software (Materialise) and manipulated for simulated tunnel drilling by precise bone subtraction methods. This software was used to define an ulnar Cartesian coordinate system with anatomical landmarks as reference points in order to standardize the position of each model (Figure 1).¹⁶ The y-axis was defined by the longitudinal axis of the ulna, and the x-axis was the transepicondylar axis, defined as the perpendicular line connecting the y-axis with the supinator crest. The z-axis was then established as the line perpendicular to the x- and y-axes—yielding a 3-D coordinate system that allowed us to manipulate the models in standardized fashion, maintaining the exact positions of the ulna while making measurements.

Surgical simulations were performed in the rapid prototyping software by creating a cylinder and placing it at the desired location of each tunnel. Cylinder diameter was 4 mm, matching the diameter of the drill we use to create each tunnel in our practice. The cylinder was inserted into the bone, perpendicular to the surface of the ulna at the point of insertion, so the cylinder’s deepest point entered the medullary canal of the ulna. Using a Boolean operation in the rapid prototyping software, we subtracted cylinder from bone to create a tunnel (Figure 2).¹⁵

In a previous study,¹⁷ we determined that the radial head junction is reproducibly about 15 mm proximal to the distinct supinator tubercle, which may be absent or not readily appreciated in up to 50% of cases. Therefore, proximal ulnar tunnels were placed 0, 5, and 10 mm posterior to the supinator crest at the radial head junction. Distal tunnels were placed 15 mm anterior to the radial head junction on the supinator crest (Figure 2). The bony bridges created by these tunnels were measured, as was the distance between the distal tunnel and the supinator tubercle.

Ideal graft configuration was described as an isosceles triangle with ulna tunnels perpendicular to the humeral tunnel (Figure 3).¹¹ Location of the humeral origin in the sagittal plane was determined by finding the isometric point of the lateral humerus using only bony landmarks. Similar techniques have been used to find the isometric point on the medial epicondyle for medial ulnar collateral ligament reconstruction.^15,18 With a circle fit into the trochlear notch of the ulna, the isometric point can be determined by the center of the circle. This point was then superimposed on the humerus to identify the starting point (Figure 4). In our simulation, we measured the isosceles configuration by drawing a line between the proximal and distal tunnels, and then another line connecting the bisecting point of the first line with the isometric point on the humerus from which the graft would originate. The angle between the 2 lines was measured; if isosceles, the angle was 90° (Figure 5). Length of the more proximal limb of the graft and the more distal limb of the graft was determined by measuring the distance from the isometric point to the proximal and distal tunnels, respectively (Figure 6).

One-way analysis of variance was used to compare all the tunnels’ bony bridge sizes, graft lengths, and angles to the isometric point. For all comparisons, statistical significance was set at P < .05. As no other studies have compared bony bridges by varying tunnel creation parameters, and as the present study is observational and not comparative, no power analysis was performed.

Results

Bony bridges were significantly longer, and angles more perpendicular, with increasing distance from the proximal tunnel to the supinator crest (Table 1, Figure 5, Figure 7). The bony bridge 0 mm posterior to the supinator crest yielded a mean (SE) bony bridge length of 11.0 (0.2) mm. This proximal tunnel also yielded the smallest mean (SE) perpendicular angle to the isometric point, 131.2° (1.9°). The tunnel most posterior to the supinator crest yielded the longest mean (SE) bony bridge, 13.7 (0.2) mm, and the largest mean (SE) degree of perpendicularity, 95.8° (1.4°). The differences between all tunnels’ bony bridges and isometric angles were statistically significant (P < .00001). The difference between the more distal limb and the more proximal limb of the graft was smallest in the more posteriorly placed proximal tunnel (Table 2, Figure 8). In fact, there was no statistical difference between the proximal and distal limbs of the graft when the proximal tunnel was placed 10 mm posterior to the supinator crest: Mean (SE) was 9.4 (0.5) mm at 0 mm (P < .00001) and 1.1 (0.6) mm at 10 mm (P = .24).

Discussion

PLRI of the elbow is best initially managed nonoperatively. However, when nonoperative management fails, the LUCL is often surgically reconstructed. Reconstruction methods vary by fixation method, graft choice, and bone tunnels.^1,7-9,11-13 In 1991, O’Driscoll and colleagues¹ described a “yoke” technique for LUCL reconstruction. Since then, the docking technique⁷ and other techniques have been developed. All these techniques emphasize maximizing anatomical precision and isometry with careful placement of tunnels or fixation devices. The humeral fixation site, at the anterior inferior aspect of the lateral epicondyle at the point of isometry, can be accessed relatively reproducibly. By contrast, the ulnar points of fixation are more variable, because of increased bone stock and overlying soft-tissue and bony anatomy.

Among the challenges in determining the points of ulnar fixation is the bony anatomy that is often used for landmarks. In the literature, the supinator crest or the supintor tubercle is the landmark for placing the distal tunnel.^1,7-9,11-13 This is a problem for 2 reasons. First, the supintor crest, a longitudinal structure on the lateral aspect of the ulna, originates from the radial head junction and extends tens of millimeters distally; further specification is needed to guide these ulnar tunnels. The second reason is that use of the supinator tubercle, a prominence on the supinator crest, adds specificity to the location of the ulnar tunnels. During surgery, however, the supinator tubercle may not be a reliable, independently prominent structure; instead, it may be indistinguishable from the supinator crest, on which it rests. One study determined that only about 50% of computer models of patient ulnas had a distinct prominence that could be classified as the supinator tubercle.¹⁷ The percentage presumably is lower during surgery, with limited exposure and overlying soft tissues.

In a study of patients with a prominent tubercle, mean (SE) distance from radial head junction to tubercle was 15 (2) mm.¹⁷ This finding led us to use the radial head junction as the primary bony landmark in determining the location of the proximal tunnel and placing the distal tunnel 15 mm distally—achieving the same fixation described in the literature but using more distinct landmarks. Our study thus provided a reliable, verified approach to locating the ulnar tunnels in the proximal-distal axis.

We also explored the anterior-posterior orientation of the proximal ulnar tunnel. The 2 primary considerations surrounding the varied proximal tunnel placements were the bony bridge formed between the proximal and distal tunnels and the perpendicularity of the triangle formed by the fixation points. Maximizing the bony bridge is obviously ideal in securing and preventing fixation blowout. Achieving an isoceles reconstruction has been reported in the literature on the various fixation techniques for LUCL reconstruction.¹¹ Although the biomechanical advantage of this fixation type is not fully clear, we assume the construct produces graft stands of equal length, tension, and stability. In addition, the larger footprint created by an isoceles reconstructed ligament increases the stability of the radial head.

Results of the present study showed that the more posterior the proximal ulnar tunnel, the longer the bony bridge and the more isoceles the reconstruction. The difference in bony bridge distance from the most anterior to the most posterior tunnel was about 2 mm, or 18%. For every 1 mm of posteriorization, the bony bridge was 0.2 mm longer. The line from the isometric point of humeral fixation bisecting the proximal and distal tunnels was also more perpendicular with the most posterior tunnel, by about 40°. The resulting proximal and distal limbs of the reconstruction were equal in length, as demonstrated by the smaller difference between the limbs. We assume this isoceles reconstruction more likely applies uniform restraint on the radial head. Thus, an effort should be made to posteriorize the proximal ulnar tunnel during reconstruction.

The study was limited by the number of patient-specific elbow models used. However, given the statistical consistency of measurements, sample size was sufficient. Another limitation, inherent to the model, was that only bony anatomy was incorporated. However, the overlying muscles, tendons, and ligaments can significantly alter tunnel placement, and this study provided other means and cues using more reliable landmarks to adequately place the tunnels. As this was a simulation study, we cannot confirm whether these results would make a difference clinically. The strengths of this study include development and verification of reliable landmarks that can be used to guide ulnar tunnel locations during LUCL reconstruction; these landmarks have been used for medial ulnar collateral ligament reconstruction.¹⁵ Other strengths include precise and accurate placement of tunnels and measurement of resulting bony bridges—accomplished independently and without compromising specimen quality.

Conclusion

We recommend drilling the proximal ulnar tunnel posterior to the supinator crest at the level of the radial head junction. A reasonable goal is 10 mm posterior to the crest, though the overlying soft tissue must be considered, and care should be taken to aim the drill anteriorly, toward the ulna’s intramedullary canal, to avoid posterior cortical breach. The distal ulnar tunnel should be drilled just posterior to the supinator crest, 15 mm distal to the radial head junction.

The responsibilities of team physicians have increased dramatically since the early 19th century, when these physicians first appeared on the sidelines during football games.¹ Although the primary role of the team physician is to care for the athlete, other responsibilities include administrative and legal duties, equipment- and environment-related duties, teaching, and communication with parents, coaches, and other physicians.^2-4 These responsibilities differ greatly by the level of the athlete and the team being covered. For example, compared with high school and collegiate sport physicians, physicians caring for professional athletes may have increased interaction with the media.⁵

Despite the increasing demands and responsibilities of team physicians, it is important that they continue to advance the field of sports medicine through teaching and research.^3,6 Team physicians have direct access to athletes at multiple levels of competition, from novice to professional, and therefore have a unique understanding of the injuries that commonly affect these athletes. Efforts to both teach and study the prevention, diagnosis, and treatment of these injuries have dramatically advanced the field of sports medicine. In fact, several advancements in sports medicine have come from team physicians, including advancements in anterior cruciate ligament reconstruction,^7,8 shoulder arthroscopy,⁹ and “Tommy John” surgery,¹⁰ to name a few.

Given the important role of team physicians (particularly orthopedic team physicians) in advancing sports medicine, it is important to understand the degree to which team physicians at all levels of sport contribute to teaching and research.

We conducted a study to determine the overall academic involvement of orthopedic team physicians at all levels of sport, including the degree to which these physicians are affiliated with academic medical centers (by level of sport and by professional sport) and the quantity and impact of these physicians’ scientific publications. We hypothesized that orthopedic physician academic involvement would be higher at the professional level of sport than at the collegiate or high school level and that the degree of physician academic involvement would differ between professional sporting leagues.

Materials and Methods

In August 2012, we performed a comprehensive telephone- and Internet-based search to identify a sample of team physicians caring for athletes at the high school, collegiate, and professional levels of sport. Data were collected on all team physicians, regardless of medical specialty. We defined a physician as any person listed as having either a doctor of medicine (MD) or a doctor of osteopathic medicine (DO) degree. A physician listed as a team physician at 2 different levels of competition (high school, college, professional) was included in both cohorts. A physician listed as a team physician in 2 different professional sports leagues was included independently for both leagues. All other medical personnel, including athletic trainers, therapists, and nursing staff, were excluded. Data on our sample population were collected as follows:

1. High school. Performing a comprehensive database search through the US Department of Education, we generated a list of all 20,989 US schools that include grades 9 to 12.¹¹ We then used a random number generator (random.org) to randomly select a sample of 120 high schools. These schools were contacted by telephone and asked to identify the team physician(s) for their sports teams. Twenty of these schools reported not having an athletic team, so we randomly generated a list of 20 additional high schools. High schools that had an athletic team but denied having a team physician were included in the analysis.

2. College. We used the National Collegiate Athletic Association (NCAA) website (ncaa.org) to generate a list of all colleges affiliated with the NCAA. Of these colleges, 347 were Division I, 316 were Division II, and 443 were Division III. The random.org random number generator was used to generate a list of 40 schools for each division, for a total of 120 schools. An Internet-based search was then performed to identify any and all team physicians caring for athletes at that particular school. In select cases, telephone calls were made to determine all the team physicians involved in the care of athletes at that institution.

3. Professional. Team physician data were collected for 4 of the most popular professional sporting leagues¹²: Major League Baseball (MLB), National Basketball Association (NBA), National Football League (NFL), and National Hockey League (NHL). Each team’s official website was identified through its league website (mlb.com, nba.com, nfl.com, nhl.com), and the roster or directory listing of all team physicians was recorded. In 2 cases, the team’s medical personnel listing could not be retrieved through the Internet, and a telephone call had to be made to identify all team physicians. Team physicians were identified for 122 professional teams: 30 MLB, 30 NBA, 32 NFL, and 30 NHL.

For this study, all physicians were classified as either orthopedic or nonorthopedic. Orthopedic surgeons—the focus of this study—were defined as those who completed residency training in orthopedic surgery. Median number of orthopedic and nonorthopedic surgeons per team was calculated at the high school, collegiate, and professional levels.

After identifying all orthopedic team physicians, we performed additional Internet searches to determine any affiliation between each physician and an applicable academic medical center. Physicians were placed in 1 of 3 different categories based on “level” of academic affiliation. Orthopedists with no identifiable connection to an academic medical center were listed under none. The first 100 search results were studied before this determination was made. Orthopedists with any academic affiliation below the level of full professorship were placed in the category associate/assistant/adjunct professor, which included any physician who was an associate professor, adjunct professor, clinical instructor, or volunteer instructor at an academic medical center. Last, orthopedists listed as full professors were placed in the professor category.

Number of publications written by each orthopedic team physician was then calculated using SciVerse Scopus (scopus.com), a comprehensive abstract and citation database of research literature that offers complete coverage of the Medline and Embase databases.¹³ Scopus offers a Scopus Author Identifier, which assigns each author in Scopus a unique identification number.¹⁴ This number is based on an “algorithm that matches author names based on their affiliation, address, subject area, source title, dates of publication citations, and co-authors.”¹⁴ Authors whose names did not appear in Scopus were assumed to have no publications, and this was reported after cross-referencing with Medline to ensure no documents were missed. This study included all publications: original research articles, reviews, letters, and commentaries. Any level of authorship (first, second, etc) was included. All publications were scanned, and duplicate listings were not included. Median number of publications per orthopedic team physician was calculated at the high school, college, and professional levels.

We also determined the h-index for each orthopedic team physician. The h-index is used to measure the impact of the published work of a scholar: “A scientist has index h if h of his/her papers have at least h citations each, and the other papers have no more than h citations each.”¹⁵ For example, an h-index of 12 means that, out of an author’s total number of publications, 12 have been cited at least 12 times, and all of his or her other publications have been cited fewer than 12 times. All authors in Scopus are automatically assigned h-indexes, and we collected these numbers.¹⁶ Of note, citations for articles published before 1996 are not included in the h-index calculation. Median h-index score per orthopedic team physician was calculated at the high school, college, and professional levels.

Analysis of variance was used to compare continuous data (eg, number of publications per surgeon) across different groups (eg, physicians from respective sports). Chi-square tests were used to detect whole-number differences between groups (eg, difference in number of physicians per team across the various professional sports leagues). Statistical significance was set at P < .05.

Results

We identified 1054 team physicians among the 362 total high schools, colleges, and professional sports teams included in this study. Of the 1054 physicians, 678 (64%) were orthopedic surgeons (Table 1). Seventy-two (60%) of the 120 high schools did not have a team physician, whereas all the colleges and professional teams did. Number of orthopedic surgeons per team was higher at the collegiate level (2.29; range, 0-11) and professional level (2.21; range, 1-9) than at the high school level (1.11; range, 0-24) (Table 1). Median number of nonorthopedic surgeons was highest in professional sports (1.88; range, 0-9) followed by college sports (1.06; range, 0-9) and high school sports (0.16; range, 0-2) (Table 1).

Of the 678 orthopedic team physicians, 298 (44%) were officially affiliated with an academic medical center, either as clinical instructor, associate/adjunct professor, or full professor. Percentage of orthopedists affiliated with an academic medical center was highest in professional sports (173/270, 64%) followed by collegiate sports (98/275, 36%) and high school sports (27/133, 20%) (P < .001, Table 2). Percentage of orthopedists identified as full professors was highest at the professional level (42/270, 16%) followed by the collegiate level (14/275, 5.1%) and the high school level (3/133, 2.3%) (P < .001, Table 2).

We found 12,036 publications written by the 678 orthopedic team physicians included in this study. Median number of publications per orthopedist was significantly higher in professional sports (30.6; range, 0-460) than in collegiate sports (10.7; range, 0-581) and high school sports (6.0; range, 0-220) (P < .001). Number of authors with more than 25 publications was highest at the professional level (82) followed by the collegiate level (27) and the high school level (7) (Table 3). Median number of publications per orthopedist was also higher at the professional level (12) than at the collegiate level (2) and high school level (1). Median h-index was higher among orthopedists in professional sports (7.1; range, 0-50) than at colleges (2.7; range, 0-63) and high schools (1.8; range, 0-32) (P < .001). Median h-index was also significantly higher at the professional level (5) than at the collegiate level (1) and high school level (0).

At the professional level of sports, we identified 499 team physicians (270 orthopedic, 54%; 229 nonorthopedic, 46%). Median number of orthopedic team physicians varied by sport, with MLB (2.8; range, 1-8) and the NFL (2.4; range, 1-4) having relatively more of these physicians than the NHL (2.0; range, 1-6) and the NBA (1.7; range, 1-9) (Table 4). Percentage of orthopedic team physicians affiliated with academic medical centers was highest in MLB (58/83, 69.9%) followed by the NFL (47/76, 61.8%), the NHL (37/60, 61.7%), and the NBA (31/51, 60.8%) (Table 5). Median number of publications by orthopedists also varied by sport, with the highest number in MLB (37.9; range, 0-225) followed by the NBA (32.0; range, 0-227) and the NFL (30.4; range, 0-460), with the lowest number in the NHL (20.7; range, 0-144) (Table 6). Median number of publications was the same (17.5) in MLB and the NFL and lower in the NBA (11) and the NHL (7.5). Median h-index was highest in the NFL (8.2; range, 0-50) and MLB (7.9; range, 0-32) followed by the NBA (6.6; range, 0-35) and the NHL (4.9; range, 0-20) (Table 7) Median h-index was the same (6) in MLB and the NFL and lower (3) in the NBA and the NHL.

Discussion

To our knowledge, this is the first study of academic involvement and the research activities of orthopedic team physicians at the high school, college, and professional levels of sport. We found that, on average, there were almost twice as many orthopedists at the collegiate and professional levels than at the high school level—likely because 72 of the 120 high schools randomly selected did not have a team physician, despite having sports teams. We can attribute this to the organizational structure of teams in a high school setting, where it is fairly common that no medically educated health care provider is readily available for the student athletes.⁵ Although the median number of orthopedists was similar at the collegiate and professional levels, the number of nonorthopedic team physicians was higher at the professional level than at the collegiate level. Although most collegiate and professional teams have an internist and an orthopedist on staff, medical staff at the professional level may also include several subspecialists from a variety of medical fields (eg, dental medicine, ophthalmology, neurology).¹⁷

We found that a significantly larger proportion of orthopedists at the professional level (64%) were affiliated with academic medical centers as associate/adjunct professors and full professors compared with orthopedists at the collegiate level (36%) and high school level (20%). The academic relationship with collegiate teams was much lower than expected. Regarding professional sports, however, this finding confirmed our hypothesis, and the explanation is likely multifactorial and historical. Moreover, the median number of publications was higher for orthopedists at the professional level (30.8) than at the collegiate level (10.7) and high school level (6). In the late 1940s and early 1950s, many orthopedic team physicians entered into contracts with major universities.⁴ For many physicians, this contractual relationship increased their prestige, and some orthopedic groups were alleged to have endorsed scholarships at those schools.⁴ Given the high level of publicity and scrutiny surrounding medical decisions at the professional level of sports, it is possible that professional sports teams specifically seek orthopedists who are well respected within academia. Moreover, contracts between universities/academic medical centers and professional teams may mandate that a faculty member from that organization provide the orthopedic/medical care for the team. This may also increase the likelihood of professional teams being paired with academic orthopedic physicians. However, such contractual agreements are made between professional teams and large private medical groups as well.

In addition to measuring quantity of publications, we used the h-index to measure their quality. Following the same pattern as the publication rate, median h-index per orthopedic team physician was significantly higher at the professional level (7.1) than at the collegiate level (2.7) and high school level (1.8). As with publication volume, this is not entirely surprising, as h-index has been shown to correlate with academic rank in other surgical specialties,¹⁸ and there was a higher percentage of academic physicians at the professional level than at the collegiate and high school levels.

At the professional level of sports, 56% of all team physicians were orthopedic surgeons. Orthopedists caring for MLB teams had the highest median number of publications (37.9), followed by the NBA (32.0), the NFL (30.4), and the NHL (20.7). One likely explanation is the higher percentage of MLB physicians affiliated with academic medical centers. Regarding the h-index, MLB and NFL physicians had the highest values (7.9 and 8.2, respectively).

Our study had several limitations. First, we may not have captured data on all the team physicians at the high school, college, and professional levels. By following a detailed protocol in identifying surgeons, however, we tried to minimize the impact of any such omissions. In addition, teams may have had many unofficial consultants acting as team physicians, whether orthopedic or nonorthopedic, and, if these physicians were not listed in an official capacity, they may have been omitted from this study. We further realize that a true measure of academic productivity should also include book chapters and books published, research grants awarded, and patents registered. By including only peer-reviewed articles, we omitted these other criteria.

To our knowledge, the data presented here represent the first attempt to quantify the academic involvement and research productivity of orthopedic team physicians at the high school, college, and professional levels of sport. These data help us understand how research productivity varies by orthopedic team physicians at different levels of sport and may be useful to those considering a career as a team physician, as they can better evaluate their own productivity in the context of team physicians across different levels of competition.

The responsibilities of team physicians have increased dramatically since the early 19th century, when these physicians first appeared on the sidelines during football games.¹ Although the primary role of the team physician is to care for the athlete, other responsibilities include administrative and legal duties, equipment- and environment-related duties, teaching, and communication with parents, coaches, and other physicians.^2-4 These responsibilities differ greatly by the level of the athlete and the team being covered. For example, compared with high school and collegiate sport physicians, physicians caring for professional athletes may have increased interaction with the media.⁵

Despite the increasing demands and responsibilities of team physicians, it is important that they continue to advance the field of sports medicine through teaching and research.^3,6 Team physicians have direct access to athletes at multiple levels of competition, from novice to professional, and therefore have a unique understanding of the injuries that commonly affect these athletes. Efforts to both teach and study the prevention, diagnosis, and treatment of these injuries have dramatically advanced the field of sports medicine. In fact, several advancements in sports medicine have come from team physicians, including advancements in anterior cruciate ligament reconstruction,^7,8 shoulder arthroscopy,⁹ and “Tommy John” surgery,¹⁰ to name a few.

Given the important role of team physicians (particularly orthopedic team physicians) in advancing sports medicine, it is important to understand the degree to which team physicians at all levels of sport contribute to teaching and research.

We conducted a study to determine the overall academic involvement of orthopedic team physicians at all levels of sport, including the degree to which these physicians are affiliated with academic medical centers (by level of sport and by professional sport) and the quantity and impact of these physicians’ scientific publications. We hypothesized that orthopedic physician academic involvement would be higher at the professional level of sport than at the collegiate or high school level and that the degree of physician academic involvement would differ between professional sporting leagues.

Materials and Methods

In August 2012, we performed a comprehensive telephone- and Internet-based search to identify a sample of team physicians caring for athletes at the high school, collegiate, and professional levels of sport. Data were collected on all team physicians, regardless of medical specialty. We defined a physician as any person listed as having either a doctor of medicine (MD) or a doctor of osteopathic medicine (DO) degree. A physician listed as a team physician at 2 different levels of competition (high school, college, professional) was included in both cohorts. A physician listed as a team physician in 2 different professional sports leagues was included independently for both leagues. All other medical personnel, including athletic trainers, therapists, and nursing staff, were excluded. Data on our sample population were collected as follows:

1. High school. Performing a comprehensive database search through the US Department of Education, we generated a list of all 20,989 US schools that include grades 9 to 12.¹¹ We then used a random number generator (random.org) to randomly select a sample of 120 high schools. These schools were contacted by telephone and asked to identify the team physician(s) for their sports teams. Twenty of these schools reported not having an athletic team, so we randomly generated a list of 20 additional high schools. High schools that had an athletic team but denied having a team physician were included in the analysis.

2. College. We used the National Collegiate Athletic Association (NCAA) website (ncaa.org) to generate a list of all colleges affiliated with the NCAA. Of these colleges, 347 were Division I, 316 were Division II, and 443 were Division III. The random.org random number generator was used to generate a list of 40 schools for each division, for a total of 120 schools. An Internet-based search was then performed to identify any and all team physicians caring for athletes at that particular school. In select cases, telephone calls were made to determine all the team physicians involved in the care of athletes at that institution.

3. Professional. Team physician data were collected for 4 of the most popular professional sporting leagues¹²: Major League Baseball (MLB), National Basketball Association (NBA), National Football League (NFL), and National Hockey League (NHL). Each team’s official website was identified through its league website (mlb.com, nba.com, nfl.com, nhl.com), and the roster or directory listing of all team physicians was recorded. In 2 cases, the team’s medical personnel listing could not be retrieved through the Internet, and a telephone call had to be made to identify all team physicians. Team physicians were identified for 122 professional teams: 30 MLB, 30 NBA, 32 NFL, and 30 NHL.

For this study, all physicians were classified as either orthopedic or nonorthopedic. Orthopedic surgeons—the focus of this study—were defined as those who completed residency training in orthopedic surgery. Median number of orthopedic and nonorthopedic surgeons per team was calculated at the high school, collegiate, and professional levels.

After identifying all orthopedic team physicians, we performed additional Internet searches to determine any affiliation between each physician and an applicable academic medical center. Physicians were placed in 1 of 3 different categories based on “level” of academic affiliation. Orthopedists with no identifiable connection to an academic medical center were listed under none. The first 100 search results were studied before this determination was made. Orthopedists with any academic affiliation below the level of full professorship were placed in the category associate/assistant/adjunct professor, which included any physician who was an associate professor, adjunct professor, clinical instructor, or volunteer instructor at an academic medical center. Last, orthopedists listed as full professors were placed in the professor category.

Number of publications written by each orthopedic team physician was then calculated using SciVerse Scopus (scopus.com), a comprehensive abstract and citation database of research literature that offers complete coverage of the Medline and Embase databases.¹³ Scopus offers a Scopus Author Identifier, which assigns each author in Scopus a unique identification number.¹⁴ This number is based on an “algorithm that matches author names based on their affiliation, address, subject area, source title, dates of publication citations, and co-authors.”¹⁴ Authors whose names did not appear in Scopus were assumed to have no publications, and this was reported after cross-referencing with Medline to ensure no documents were missed. This study included all publications: original research articles, reviews, letters, and commentaries. Any level of authorship (first, second, etc) was included. All publications were scanned, and duplicate listings were not included. Median number of publications per orthopedic team physician was calculated at the high school, college, and professional levels.

We also determined the h-index for each orthopedic team physician. The h-index is used to measure the impact of the published work of a scholar: “A scientist has index h if h of his/her papers have at least h citations each, and the other papers have no more than h citations each.”¹⁵ For example, an h-index of 12 means that, out of an author’s total number of publications, 12 have been cited at least 12 times, and all of his or her other publications have been cited fewer than 12 times. All authors in Scopus are automatically assigned h-indexes, and we collected these numbers.¹⁶ Of note, citations for articles published before 1996 are not included in the h-index calculation. Median h-index score per orthopedic team physician was calculated at the high school, college, and professional levels.

Analysis of variance was used to compare continuous data (eg, number of publications per surgeon) across different groups (eg, physicians from respective sports). Chi-square tests were used to detect whole-number differences between groups (eg, difference in number of physicians per team across the various professional sports leagues). Statistical significance was set at P < .05.

Results

We identified 1054 team physicians among the 362 total high schools, colleges, and professional sports teams included in this study. Of the 1054 physicians, 678 (64%) were orthopedic surgeons (Table 1). Seventy-two (60%) of the 120 high schools did not have a team physician, whereas all the colleges and professional teams did. Number of orthopedic surgeons per team was higher at the collegiate level (2.29; range, 0-11) and professional level (2.21; range, 1-9) than at the high school level (1.11; range, 0-24) (Table 1). Median number of nonorthopedic surgeons was highest in professional sports (1.88; range, 0-9) followed by college sports (1.06; range, 0-9) and high school sports (0.16; range, 0-2) (Table 1).

Of the 678 orthopedic team physicians, 298 (44%) were officially affiliated with an academic medical center, either as clinical instructor, associate/adjunct professor, or full professor. Percentage of orthopedists affiliated with an academic medical center was highest in professional sports (173/270, 64%) followed by collegiate sports (98/275, 36%) and high school sports (27/133, 20%) (P < .001, Table 2). Percentage of orthopedists identified as full professors was highest at the professional level (42/270, 16%) followed by the collegiate level (14/275, 5.1%) and the high school level (3/133, 2.3%) (P < .001, Table 2).

We found 12,036 publications written by the 678 orthopedic team physicians included in this study. Median number of publications per orthopedist was significantly higher in professional sports (30.6; range, 0-460) than in collegiate sports (10.7; range, 0-581) and high school sports (6.0; range, 0-220) (P < .001). Number of authors with more than 25 publications was highest at the professional level (82) followed by the collegiate level (27) and the high school level (7) (Table 3). Median number of publications per orthopedist was also higher at the professional level (12) than at the collegiate level (2) and high school level (1). Median h-index was higher among orthopedists in professional sports (7.1; range, 0-50) than at colleges (2.7; range, 0-63) and high schools (1.8; range, 0-32) (P < .001). Median h-index was also significantly higher at the professional level (5) than at the collegiate level (1) and high school level (0).

At the professional level of sports, we identified 499 team physicians (270 orthopedic, 54%; 229 nonorthopedic, 46%). Median number of orthopedic team physicians varied by sport, with MLB (2.8; range, 1-8) and the NFL (2.4; range, 1-4) having relatively more of these physicians than the NHL (2.0; range, 1-6) and the NBA (1.7; range, 1-9) (Table 4). Percentage of orthopedic team physicians affiliated with academic medical centers was highest in MLB (58/83, 69.9%) followed by the NFL (47/76, 61.8%), the NHL (37/60, 61.7%), and the NBA (31/51, 60.8%) (Table 5). Median number of publications by orthopedists also varied by sport, with the highest number in MLB (37.9; range, 0-225) followed by the NBA (32.0; range, 0-227) and the NFL (30.4; range, 0-460), with the lowest number in the NHL (20.7; range, 0-144) (Table 6). Median number of publications was the same (17.5) in MLB and the NFL and lower in the NBA (11) and the NHL (7.5). Median h-index was highest in the NFL (8.2; range, 0-50) and MLB (7.9; range, 0-32) followed by the NBA (6.6; range, 0-35) and the NHL (4.9; range, 0-20) (Table 7) Median h-index was the same (6) in MLB and the NFL and lower (3) in the NBA and the NHL.

Discussion

To our knowledge, this is the first study of academic involvement and the research activities of orthopedic team physicians at the high school, college, and professional levels of sport. We found that, on average, there were almost twice as many orthopedists at the collegiate and professional levels than at the high school level—likely because 72 of the 120 high schools randomly selected did not have a team physician, despite having sports teams. We can attribute this to the organizational structure of teams in a high school setting, where it is fairly common that no medically educated health care provider is readily available for the student athletes.⁵ Although the median number of orthopedists was similar at the collegiate and professional levels, the number of nonorthopedic team physicians was higher at the professional level than at the collegiate level. Although most collegiate and professional teams have an internist and an orthopedist on staff, medical staff at the professional level may also include several subspecialists from a variety of medical fields (eg, dental medicine, ophthalmology, neurology).¹⁷

We found that a significantly larger proportion of orthopedists at the professional level (64%) were affiliated with academic medical centers as associate/adjunct professors and full professors compared with orthopedists at the collegiate level (36%) and high school level (20%). The academic relationship with collegiate teams was much lower than expected. Regarding professional sports, however, this finding confirmed our hypothesis, and the explanation is likely multifactorial and historical. Moreover, the median number of publications was higher for orthopedists at the professional level (30.8) than at the collegiate level (10.7) and high school level (6). In the late 1940s and early 1950s, many orthopedic team physicians entered into contracts with major universities.⁴ For many physicians, this contractual relationship increased their prestige, and some orthopedic groups were alleged to have endorsed scholarships at those schools.⁴ Given the high level of publicity and scrutiny surrounding medical decisions at the professional level of sports, it is possible that professional sports teams specifically seek orthopedists who are well respected within academia. Moreover, contracts between universities/academic medical centers and professional teams may mandate that a faculty member from that organization provide the orthopedic/medical care for the team. This may also increase the likelihood of professional teams being paired with academic orthopedic physicians. However, such contractual agreements are made between professional teams and large private medical groups as well.

In addition to measuring quantity of publications, we used the h-index to measure their quality. Following the same pattern as the publication rate, median h-index per orthopedic team physician was significantly higher at the professional level (7.1) than at the collegiate level (2.7) and high school level (1.8). As with publication volume, this is not entirely surprising, as h-index has been shown to correlate with academic rank in other surgical specialties,¹⁸ and there was a higher percentage of academic physicians at the professional level than at the collegiate and high school levels.

At the professional level of sports, 56% of all team physicians were orthopedic surgeons. Orthopedists caring for MLB teams had the highest median number of publications (37.9), followed by the NBA (32.0), the NFL (30.4), and the NHL (20.7). One likely explanation is the higher percentage of MLB physicians affiliated with academic medical centers. Regarding the h-index, MLB and NFL physicians had the highest values (7.9 and 8.2, respectively).

Our study had several limitations. First, we may not have captured data on all the team physicians at the high school, college, and professional levels. By following a detailed protocol in identifying surgeons, however, we tried to minimize the impact of any such omissions. In addition, teams may have had many unofficial consultants acting as team physicians, whether orthopedic or nonorthopedic, and, if these physicians were not listed in an official capacity, they may have been omitted from this study. We further realize that a true measure of academic productivity should also include book chapters and books published, research grants awarded, and patents registered. By including only peer-reviewed articles, we omitted these other criteria.

To our knowledge, the data presented here represent the first attempt to quantify the academic involvement and research productivity of orthopedic team physicians at the high school, college, and professional levels of sport. These data help us understand how research productivity varies by orthopedic team physicians at different levels of sport and may be useful to those considering a career as a team physician, as they can better evaluate their own productivity in the context of team physicians across different levels of competition.

The responsibilities of team physicians have increased dramatically since the early 19th century, when these physicians first appeared on the sidelines during football games.¹ Although the primary role of the team physician is to care for the athlete, other responsibilities include administrative and legal duties, equipment- and environment-related duties, teaching, and communication with parents, coaches, and other physicians.^2-4 These responsibilities differ greatly by the level of the athlete and the team being covered. For example, compared with high school and collegiate sport physicians, physicians caring for professional athletes may have increased interaction with the media.⁵

Despite the increasing demands and responsibilities of team physicians, it is important that they continue to advance the field of sports medicine through teaching and research.^3,6 Team physicians have direct access to athletes at multiple levels of competition, from novice to professional, and therefore have a unique understanding of the injuries that commonly affect these athletes. Efforts to both teach and study the prevention, diagnosis, and treatment of these injuries have dramatically advanced the field of sports medicine. In fact, several advancements in sports medicine have come from team physicians, including advancements in anterior cruciate ligament reconstruction,^7,8 shoulder arthroscopy,⁹ and “Tommy John” surgery,¹⁰ to name a few.

Given the important role of team physicians (particularly orthopedic team physicians) in advancing sports medicine, it is important to understand the degree to which team physicians at all levels of sport contribute to teaching and research.

We conducted a study to determine the overall academic involvement of orthopedic team physicians at all levels of sport, including the degree to which these physicians are affiliated with academic medical centers (by level of sport and by professional sport) and the quantity and impact of these physicians’ scientific publications. We hypothesized that orthopedic physician academic involvement would be higher at the professional level of sport than at the collegiate or high school level and that the degree of physician academic involvement would differ between professional sporting leagues.

Materials and Methods

In August 2012, we performed a comprehensive telephone- and Internet-based search to identify a sample of team physicians caring for athletes at the high school, collegiate, and professional levels of sport. Data were collected on all team physicians, regardless of medical specialty. We defined a physician as any person listed as having either a doctor of medicine (MD) or a doctor of osteopathic medicine (DO) degree. A physician listed as a team physician at 2 different levels of competition (high school, college, professional) was included in both cohorts. A physician listed as a team physician in 2 different professional sports leagues was included independently for both leagues. All other medical personnel, including athletic trainers, therapists, and nursing staff, were excluded. Data on our sample population were collected as follows:

1. High school. Performing a comprehensive database search through the US Department of Education, we generated a list of all 20,989 US schools that include grades 9 to 12.¹¹ We then used a random number generator (random.org) to randomly select a sample of 120 high schools. These schools were contacted by telephone and asked to identify the team physician(s) for their sports teams. Twenty of these schools reported not having an athletic team, so we randomly generated a list of 20 additional high schools. High schools that had an athletic team but denied having a team physician were included in the analysis.

2. College. We used the National Collegiate Athletic Association (NCAA) website (ncaa.org) to generate a list of all colleges affiliated with the NCAA. Of these colleges, 347 were Division I, 316 were Division II, and 443 were Division III. The random.org random number generator was used to generate a list of 40 schools for each division, for a total of 120 schools. An Internet-based search was then performed to identify any and all team physicians caring for athletes at that particular school. In select cases, telephone calls were made to determine all the team physicians involved in the care of athletes at that institution.

3. Professional. Team physician data were collected for 4 of the most popular professional sporting leagues¹²: Major League Baseball (MLB), National Basketball Association (NBA), National Football League (NFL), and National Hockey League (NHL). Each team’s official website was identified through its league website (mlb.com, nba.com, nfl.com, nhl.com), and the roster or directory listing of all team physicians was recorded. In 2 cases, the team’s medical personnel listing could not be retrieved through the Internet, and a telephone call had to be made to identify all team physicians. Team physicians were identified for 122 professional teams: 30 MLB, 30 NBA, 32 NFL, and 30 NHL.

For this study, all physicians were classified as either orthopedic or nonorthopedic. Orthopedic surgeons—the focus of this study—were defined as those who completed residency training in orthopedic surgery. Median number of orthopedic and nonorthopedic surgeons per team was calculated at the high school, collegiate, and professional levels.

After identifying all orthopedic team physicians, we performed additional Internet searches to determine any affiliation between each physician and an applicable academic medical center. Physicians were placed in 1 of 3 different categories based on “level” of academic affiliation. Orthopedists with no identifiable connection to an academic medical center were listed under none. The first 100 search results were studied before this determination was made. Orthopedists with any academic affiliation below the level of full professorship were placed in the category associate/assistant/adjunct professor, which included any physician who was an associate professor, adjunct professor, clinical instructor, or volunteer instructor at an academic medical center. Last, orthopedists listed as full professors were placed in the professor category.

Number of publications written by each orthopedic team physician was then calculated using SciVerse Scopus (scopus.com), a comprehensive abstract and citation database of research literature that offers complete coverage of the Medline and Embase databases.¹³ Scopus offers a Scopus Author Identifier, which assigns each author in Scopus a unique identification number.¹⁴ This number is based on an “algorithm that matches author names based on their affiliation, address, subject area, source title, dates of publication citations, and co-authors.”¹⁴ Authors whose names did not appear in Scopus were assumed to have no publications, and this was reported after cross-referencing with Medline to ensure no documents were missed. This study included all publications: original research articles, reviews, letters, and commentaries. Any level of authorship (first, second, etc) was included. All publications were scanned, and duplicate listings were not included. Median number of publications per orthopedic team physician was calculated at the high school, college, and professional levels.

We also determined the h-index for each orthopedic team physician. The h-index is used to measure the impact of the published work of a scholar: “A scientist has index h if h of his/her papers have at least h citations each, and the other papers have no more than h citations each.”¹⁵ For example, an h-index of 12 means that, out of an author’s total number of publications, 12 have been cited at least 12 times, and all of his or her other publications have been cited fewer than 12 times. All authors in Scopus are automatically assigned h-indexes, and we collected these numbers.¹⁶ Of note, citations for articles published before 1996 are not included in the h-index calculation. Median h-index score per orthopedic team physician was calculated at the high school, college, and professional levels.

Analysis of variance was used to compare continuous data (eg, number of publications per surgeon) across different groups (eg, physicians from respective sports). Chi-square tests were used to detect whole-number differences between groups (eg, difference in number of physicians per team across the various professional sports leagues). Statistical significance was set at P < .05.

Results

We identified 1054 team physicians among the 362 total high schools, colleges, and professional sports teams included in this study. Of the 1054 physicians, 678 (64%) were orthopedic surgeons (Table 1). Seventy-two (60%) of the 120 high schools did not have a team physician, whereas all the colleges and professional teams did. Number of orthopedic surgeons per team was higher at the collegiate level (2.29; range, 0-11) and professional level (2.21; range, 1-9) than at the high school level (1.11; range, 0-24) (Table 1). Median number of nonorthopedic surgeons was highest in professional sports (1.88; range, 0-9) followed by college sports (1.06; range, 0-9) and high school sports (0.16; range, 0-2) (Table 1).

Of the 678 orthopedic team physicians, 298 (44%) were officially affiliated with an academic medical center, either as clinical instructor, associate/adjunct professor, or full professor. Percentage of orthopedists affiliated with an academic medical center was highest in professional sports (173/270, 64%) followed by collegiate sports (98/275, 36%) and high school sports (27/133, 20%) (P < .001, Table 2). Percentage of orthopedists identified as full professors was highest at the professional level (42/270, 16%) followed by the collegiate level (14/275, 5.1%) and the high school level (3/133, 2.3%) (P < .001, Table 2).

We found 12,036 publications written by the 678 orthopedic team physicians included in this study. Median number of publications per orthopedist was significantly higher in professional sports (30.6; range, 0-460) than in collegiate sports (10.7; range, 0-581) and high school sports (6.0; range, 0-220) (P < .001). Number of authors with more than 25 publications was highest at the professional level (82) followed by the collegiate level (27) and the high school level (7) (Table 3). Median number of publications per orthopedist was also higher at the professional level (12) than at the collegiate level (2) and high school level (1). Median h-index was higher among orthopedists in professional sports (7.1; range, 0-50) than at colleges (2.7; range, 0-63) and high schools (1.8; range, 0-32) (P < .001). Median h-index was also significantly higher at the professional level (5) than at the collegiate level (1) and high school level (0).

At the professional level of sports, we identified 499 team physicians (270 orthopedic, 54%; 229 nonorthopedic, 46%). Median number of orthopedic team physicians varied by sport, with MLB (2.8; range, 1-8) and the NFL (2.4; range, 1-4) having relatively more of these physicians than the NHL (2.0; range, 1-6) and the NBA (1.7; range, 1-9) (Table 4). Percentage of orthopedic team physicians affiliated with academic medical centers was highest in MLB (58/83, 69.9%) followed by the NFL (47/76, 61.8%), the NHL (37/60, 61.7%), and the NBA (31/51, 60.8%) (Table 5). Median number of publications by orthopedists also varied by sport, with the highest number in MLB (37.9; range, 0-225) followed by the NBA (32.0; range, 0-227) and the NFL (30.4; range, 0-460), with the lowest number in the NHL (20.7; range, 0-144) (Table 6). Median number of publications was the same (17.5) in MLB and the NFL and lower in the NBA (11) and the NHL (7.5). Median h-index was highest in the NFL (8.2; range, 0-50) and MLB (7.9; range, 0-32) followed by the NBA (6.6; range, 0-35) and the NHL (4.9; range, 0-20) (Table 7) Median h-index was the same (6) in MLB and the NFL and lower (3) in the NBA and the NHL.

Discussion

To our knowledge, this is the first study of academic involvement and the research activities of orthopedic team physicians at the high school, college, and professional levels of sport. We found that, on average, there were almost twice as many orthopedists at the collegiate and professional levels than at the high school level—likely because 72 of the 120 high schools randomly selected did not have a team physician, despite having sports teams. We can attribute this to the organizational structure of teams in a high school setting, where it is fairly common that no medically educated health care provider is readily available for the student athletes.⁵ Although the median number of orthopedists was similar at the collegiate and professional levels, the number of nonorthopedic team physicians was higher at the professional level than at the collegiate level. Although most collegiate and professional teams have an internist and an orthopedist on staff, medical staff at the professional level may also include several subspecialists from a variety of medical fields (eg, dental medicine, ophthalmology, neurology).¹⁷

We found that a significantly larger proportion of orthopedists at the professional level (64%) were affiliated with academic medical centers as associate/adjunct professors and full professors compared with orthopedists at the collegiate level (36%) and high school level (20%). The academic relationship with collegiate teams was much lower than expected. Regarding professional sports, however, this finding confirmed our hypothesis, and the explanation is likely multifactorial and historical. Moreover, the median number of publications was higher for orthopedists at the professional level (30.8) than at the collegiate level (10.7) and high school level (6). In the late 1940s and early 1950s, many orthopedic team physicians entered into contracts with major universities.⁴ For many physicians, this contractual relationship increased their prestige, and some orthopedic groups were alleged to have endorsed scholarships at those schools.⁴ Given the high level of publicity and scrutiny surrounding medical decisions at the professional level of sports, it is possible that professional sports teams specifically seek orthopedists who are well respected within academia. Moreover, contracts between universities/academic medical centers and professional teams may mandate that a faculty member from that organization provide the orthopedic/medical care for the team. This may also increase the likelihood of professional teams being paired with academic orthopedic physicians. However, such contractual agreements are made between professional teams and large private medical groups as well.

In addition to measuring quantity of publications, we used the h-index to measure their quality. Following the same pattern as the publication rate, median h-index per orthopedic team physician was significantly higher at the professional level (7.1) than at the collegiate level (2.7) and high school level (1.8). As with publication volume, this is not entirely surprising, as h-index has been shown to correlate with academic rank in other surgical specialties,¹⁸ and there was a higher percentage of academic physicians at the professional level than at the collegiate and high school levels.

At the professional level of sports, 56% of all team physicians were orthopedic surgeons. Orthopedists caring for MLB teams had the highest median number of publications (37.9), followed by the NBA (32.0), the NFL (30.4), and the NHL (20.7). One likely explanation is the higher percentage of MLB physicians affiliated with academic medical centers. Regarding the h-index, MLB and NFL physicians had the highest values (7.9 and 8.2, respectively).

Our study had several limitations. First, we may not have captured data on all the team physicians at the high school, college, and professional levels. By following a detailed protocol in identifying surgeons, however, we tried to minimize the impact of any such omissions. In addition, teams may have had many unofficial consultants acting as team physicians, whether orthopedic or nonorthopedic, and, if these physicians were not listed in an official capacity, they may have been omitted from this study. We further realize that a true measure of academic productivity should also include book chapters and books published, research grants awarded, and patents registered. By including only peer-reviewed articles, we omitted these other criteria.

To our knowledge, the data presented here represent the first attempt to quantify the academic involvement and research productivity of orthopedic team physicians at the high school, college, and professional levels of sport. These data help us understand how research productivity varies by orthopedic team physicians at different levels of sport and may be useful to those considering a career as a team physician, as they can better evaluate their own productivity in the context of team physicians across different levels of competition.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.

The overhead athlete’s shoulder is exposed to extremes of stress and range of motion (ROM), predisposing this joint to unique injury patterns. Prompt diagnosis and management begin with a comprehensive history and a physical examination, supplemented by imaging studies as needed. Furthermore, the throwing shoulder undergoes adaptive changes, such as partial undersurface rotator cuff tears and capsular laxity. Imaging studies typically demonstrate abnormalities in asymptomatic throwers. Therefore, clinicians must be skilled in history taking and physical examination in throwing athletes to accurately determine the cause of symptoms and provide optimal treatment. This primer provides orthopedic surgeons with the key points in performing a thorough physical examination of the shoulder in overhead athletes.

When working with overhead athletes, surgeons must elicit the precise nature of symptoms. For example, it is important to distinguish pain from fatigue, as well as complaints related purely to decline in performance. Often, collaboration with the player’s parent or coach may help clarify the chief complaint. In addition, surgeons must have an intricate knowledge of the various stages of the overhead motion, as symptoms in specific stages (late cocking/early acceleration) may raise suspicion for distinctive pathology (labral/biceps complex). Last, it is imperative to understand that the shoulder represents only one part of the kinetic chain in overhead athletes. Successful throwing relies on integrity of the entire kinetic chain, starting with the lower extremity and trunk, extending through the spine, scapula, and shoulder, and terminating with the hand and fingers. Pathology anywhere in the chain must be evaluated and addressed.

When examining the shoulder in overhead athletes, surgeons must address several anatomical structures, both bony and soft tissue. Proper examination begins with comprehensive assessment of the ROM and strength of the various muscles around the shoulder, along with visual inspection to identify any asymmetry of these structures. In addition, the scapulothoracic structures must be examined in detail to rule out underlying dyskinesis. The capsular and ligamentous components of the shoulder joint must be further assessed to note any capsular contracture causing glenohumeral internal rotation deficit (GIRD) or any pathology with the rotator cuff or labral/biceps complex. Last, a comprehensive neurovascular examination should be performed to rule out any compression or neuropathy affecting the shoulder and overhead motion. Findings from the physical examination may then require further imaging to correlate the history and physical examination findings.

1. Inspection, palpation, strength testing

Every examination of the shoulder must begin with visual inspection, along with assessment of basic ROM and strength. The patient must be positioned and exposed adequately to promote visualization of the entire shoulder and scapular girdle, from both anterior and posterior. Visual inspection focuses on identifying any areas of asymmetry, such as position of the bony prominences or bulk of the muscular fossae. Asymmetry of the bony architecture may indicate prior trauma, and atrophy of the muscular fossae may indicate nerve compression. For example, atrophy of the infraspinatus fossa may be caused by compression of the suprascapular nerve at the spinoglenoid notch (likely by a cyst, often associated with labral pathology, but infraspinatus atrophy can result even without the presence of a compressive cyst¹). Alternatively, atrophy of both the supraspinatus and infraspinatus fossae may indicate underlying compression of the suprascapular nerve at the suprascapular notch (either by a cyst or by the transverse scapular ligament). Static and dynamic observation of the posterior aspect of the shoulder may help identify gross pathology with scapular positioning or retraction, indicating underlying dyskinesis (discussed later). Deformity of the acromioclavicular joint may indicate prior trauma or separation. Last, all prior surgical scars should be noted.

Selective palpation may help identify pathology in the shoulder of the throwing athlete. Tenderness at the acromioclavicular joint may be especially common in patients who have had prior sprains of this joint or who have degenerative changes. Tenderness along the biceps tendon may be present in those with biceps tendinitis or partial tear. In addition, tenderness at the coracoid may be present in those with scapular dyskinesis. Posteriorly, palpation at the inferomedial aspect of the scapula (Figure 1), as with palpation along the medial border of the scapula, may elicit tenderness in those with scapulothoracic bursitis.

Strength testing in the shoulder is performed to elicit any deficiencies of the rotator cuff/musculature or surrounding structures. Weakness in forward elevation may indicate pathology in the supraspinatus, whereas weakness in external rotation may reflect deficiency in the infraspinatus or teres minor. Teres minor deficiency may be more isolated with weakness in a position of shoulder abduction to 90°. Last, weakness in internal rotation may indicate subscapularis deficiency. Lag signs and other provocative maneuvers are similarly elicited but typically are positive only in the event of large tears of the rotator cuff. These signs and maneuvers include the internal rotation lag sign or belly press test for subscapularis integrity, the drop-arm sign for supraspinatus function, the external rotation lag sign for infraspinatus function, and the hornblower sign for teres minor integrity. Supporting muscles of the shoulder may also be tested. Latissimus strength may be tested with resisted downward rotation of the arm with the shoulder in abduction and the elbow flexed to 90°.

2. ROM and GIRD assessment

After inspection and palpation, the shoulder should be ranged in all relevant planes of motion. Our standard examination includes forward elevation in the frontal and scapular planes, along with external rotation at the side and at 90° of abduction, as well as internal rotation behind the back with documentation of the highest spinal level that the patient can reach. This examination may be performed with the patient upright, but supine positioning can help stabilize the scapula and provide more accurate views of motion. Deficits of internal rotation may be a common finding in overhead athletes, and the degree of this deficit should be quantitatively noted.

Bony and soft-tissue remodeling of the shoulder (and associated structures) in the overhead athlete can lead to contracture of the posterior capsule. This contracture can cause excessive external rotation and subsequent decrease in internal rotation, leading to pain and anterior instability in the throwing shoulder.² For precise measurements of the internal and external rotation arc, the scapula must be stabilized. This can be done with the patient supine on the examining table or seated upright with manual stabilization of the scapula by the examiner. Once the scapula is stabilized, the arc of internal and external rotation (with the arm in about 90° of abduction) can be measured with a goniometer, with maximum values obtained as the scapula begins to move along the posterior chest wall.² The difference in internal rotation between the dominant and nondominant arms defines the extent of the athlete’s GIRD. Internal rotation can also be qualitatively assessed by having the athlete internally rotate each arm and reach up the spine while the examiner notes the difference in level achieved. However, this does not provide a quantitative assessment of the patient’s GIRD.

In general, the sum of the internal and external rotation arcs on the 2 sides should be symmetric. Consequently, in GIRD, excessive external rotation is balanced by decreased internal rotation. Symptomatic GIRD may be present when there is more than 25° of discrepancy in internal rotation between the athlete’s dominant and nondominant arms.² The goal is to reduce this discrepancy to less than 20°.

3. Internal impingement: rotator cuff and labrum

In overhead athletes, an intricate relationship involving rotator cuff, labrum, and biceps tendon allows for efficient, pain-free force delivery at the shoulder. However, because of the significant external rotation and abduction required in the overhead motion, there may be internal impingement of the posterosuperior rotator cuff (infraspinatus and posterior aspect of supraspinatus) between the posterior labrum and the greater tuberosity. Detailed examination of these structures must be performed in any assessment of an overhead athlete. Symptomatic patients may complain of pain during the throwing cycle, particularly in late cocking and early acceleration.

The modified relocation examination is a common maneuver to detect internal impingement.³ In this examination, the patient’s arm is brought into a position of maximal external rotation and abduction mimicking that found in late cocking or early acceleration. In this position, a patient with internal impingement complains of pain in the posterior shoulder. A posteriorly directed force on the humerus relieves this pain.

There are also many examinations for detecting labral pathology, specifically a SLAP (superior labrum, anterior to posterior) lesion, which is commonly found in patients with internal impingement. One commonly tested maneuver is the O’Brien active compression test (Figures 2A, 2B), which has excellent sensitivity and specificity in detecting type II SLAP lesions.⁴ In this examination, the patient holds the arm in about 15° of adduction and 90° of forward elevation. A downward force is applied with the forearm pronated and subsequently supinated. If pain is noted on the force applied to the pronated arm, and if this pain decreases in the supinated examination, the test is positive for labral pathology.

Anterior instability is routinely found in these patients. Translation is measured with the anterior load and shift test. Anterior translation is tested with the patient supine, with the arm in abduction and external rotation, and with the examiner placing an anteriorly directed force on the humeral head. Translation is compared with the contralateral side and graded on a 3-point scale (1+ is translation to glenoid rim, 2+ is translation over glenoid rim but reduces, 3+ is translation over glenoid and locking). We also use the anterior release test, in which the patient is supine, the arm is brought into abduction and external rotation, and the examiner places a posteriorly directed force on the humeral head. When the examiner removes this force, the patient notices symptoms of instability caused by subluxation (Figures 3A, 3B).

Biceps tendon testing should also be performed to help elicit signs of labral pathology. The Speed test is performed by placing a downward force on the patient’s arm, which is held in 90° forward elevation, and with elbows in extension and forearm in supination. Pain in the long head of the biceps tendon is considered a positive sign and suggestive of SLAP lesion. Although not commonly found in these athletes, external impingement should also be elicited through both the Neer test and the Hawkins test. In the Neer test, the patient’s arm is brought to maximal forward elevation with the forearm supinated and elbow extended, while the scapula is stabilized by the examiner. Pain in the shoulder indicates a positive examination. In the Hawkins test, the patient’s arm is brought into a position of forward elevation, internal rotation, and elbow flexion. The arm is then further internally rotated, and shoulder pain defines a positive examination.

Any of these findings can be concomitant with scapular dyskinesis. Moreover, symptoms related to internal impingement may be exacerbated by concomitant scapular pathology, and therefore proper assessment of scapulothoracic motion must also be performed.

4. Scapulothoracic examination

Motion coupled between the scapula and the rest of the arm (scapular rhythm) allows for efficient use of the shoulder girdle. The scapula helps transfer the force generated by the core so that the hand can efficiently deliver it. Therefore, scapular pathology (or dyskinesis) results in inefficient functioning of the arm, which can be especially debilitating in an overhead athlete.

Scapular assessment begins with visual inspection of the patient, typically from the posterior view, which allows for assessment of the resting position of the scapula. Evidence of prominence of the medial or inferomedial border, coracoid malposition (or pain on palpation), or general scapular malposition should be noted. On active ROM, as the patient forward-elevates the arm, any asymmetric prominence of the inferomedial border of the scapula should be noted. Such asymmetry may indicate underlying scapular dyskinesis. In another important test, the lateral scapular slide test (described by Kibler⁵), the distance from the inferomedial angle of the scapula to the thoracic spine should be measured for both sides and in 3 difference positions, noting any asymmetry between the affected and nonaffected sides. These 3 positions (Figures 4A–4C) are with arms at side, with hands on hips (internal rotation of humerus in 45° abduction), and in 90° of shoulder abduction. Last, medial and lateral scapular winging—caused by long thoracic nerve and spinal accessory nerve pathology, respectively—can be detected by asking the patient to do a “push-up” against the wall while the examiner views from posterior.

After assessment of scapular position at rest and through motion, a series of provocative maneuvers⁶ may aid in the diagnosis of scapular dyskinesis. The first maneuver is the scapular assistance test, in which the examiner provides a gentle force at the inferomedial angle of the scapula, promoting upward rotation and posterior tilt as the patient elevates the arm (Figures 5A, 5B). If the patient experiences a decrease or absence of symptoms through this arc, the test is considered positive. The second maneuver is the scapular retraction test, in which strength testing of the supraspinatus is performed before and after retraction stabilization of the scapula. In the baseline state, the strength of the supraspinatus is tested in standard fashion, with resisted elevation of the internally rotated and abducted arm. The strength is then tested with the scapula stabilized in retraction (the examiner medially stabilizes the scapula). With scapular stabilization, an increase in strength or a decrease in symptoms is considered a positive test.

5. Neurovascular examination

It is essential to perform a comprehensive neurovascular examination in all overhead athletes. This includes basic cervical spine testing for any motor or sensory deficits, along with assessment of scapular winging to detect long thoracic or spinal accessory nerve palsy for medial and lateral winging, respectively. Although neurovascular injury may be a rare finding in the overhead athlete, a detailed examination must still be performed to rule it out.

Thoracic outlet syndrome

Thoracic syndrome is a compressive neuropathy of nerves and vasculature exiting the thorax and entering the upper extremity. Common symptoms include pain and tingling (sometimes vague) in the neck and upper extremity. These symptoms may be positional as well.

Diagnosis of thoracic outlet syndrome begins with visual inspection of the involved upper extremity, noting atrophy or asymmetry. Weakness may also be present. Additional provocative maneuvers can be used to detect decrease or loss of pulses, along with reproduction of symptoms, during a provocative maneuver with subsequent return of pulses and resolution of symptoms after the maneuver is completed.

One examination that can be used to detect thoracic outlet syndrome is the Adson test.⁷ During this maneuver, the radial pulse is palpated with the arm at rest on the patient’s side. The patient then turns to the symptomatic side, hyperextends the arm, and holds inspiration. A positive test coincides with both decreased pulse and reproduction of symptoms, indicating compression within the scalene triangle. In the Wright test,⁷ the pulse is again palpated at rest with the arm at the side. The patient then holds inspiration and places the arm in a position of abduction and external rotation. If the pulses decrease with this maneuver, the test is considered positive, indicating compression in the sub–pectoralis minor region deep to the coracoid. In a third test, the costoclavicular test, again pulses are measured before and during the provocative maneuver, which is with the shoulders thrust backward and depressed downward. A positive test indicates compression between the clavicle and the first rib. In our practice, we use a modified Wright test in which the arm is held in abduction and external rotation while radial pulses are palpated. The fist is then opened and clenched rapidly, and diminution of radial pulses is considered a positive examination (Figures 6A, 6B).

Effort thrombosis

Overhead athletes are at increased risk for developing effort thrombosis⁸ (Paget-Schroetter syndrome). This thrombosis, which results from repetitive motion involving the upper extremity, is not limited to overhead sports; it may be caused by underlying compression of or microtrauma to the venous infrastructure. On physical examination, there may be swelling of the affected limb, along with diffuse pain and fatigue, as well as dermatologic changes. Positive findings warrant further testing, such as coagulation profile testing and advanced imaging or venography.

Arterial aneurysm

Although rare, arterial aneurysms, especially of the axillary artery, must be ruled out in the overhead athlete with vague upper extremity pain (especially distally) and without clear diagnosis.⁹ Aneurysm of the axillary artery can result from repetitive microtrauma related to repetitive overhead motion of the upper extremity. This condition may cause showering of emboli distally to the vasculature of the hand and fingers (Figure 7). Patients may complain of pain in the fingers, difficulty with grip, cyanosis, or cold sensation. On examination, the sufficiency of the radial and ulnar arteries should be assessed, as with detailed sensorimotor examination of the fingers. The fingernails should be examined for splinter hemorrhages.

Conclusion

Overhead athletes place extreme stress on the shoulder during the throwing motion and are at high risk for injury because of repetitive stress on the shoulder girdle. When examining overhead athletes with shoulder pain, surgeons must consider the entire kinetic chain, as inefficiencies anywhere along the chain can lead to altered mechanics and pathology in the shoulder.