Shoulder & Elbow

Throwing and batting each require repetitive motions that can result in injuries unique to baseball. Fortuantely, advances in operative and nonoperative treatments have allowed players to return to competition after sustaining what previously would have been considered a career-ending injury. Once a player has been deemed ready to return to throwing or hitting, a comprehensive, multiphased approach to rehabilitation is necessary to reintroduce the athlete back to baseball activities and avoid re-injury. This article reviews the biomechanics of both throwing and hitting, and outlines the phases of rehabilitation necessary to allow the athlete to return to competition.

Throwing

Biomechanical Overview

The overhead throwing motion is complex and involves full body coordination from the initial force generation through the follow-through phase of throwing. The “kinetic chain”—the concept that movements in the body are connected through segments culminating with the highest energy in the final segment—is paramount to achieving the force and energy needed for throwing.^1-8 The kinetic chain begins in the lower body and trunk and transmits the energy distally to the shoulder, elbow, and hand, ending with kinetic energy transfer to the ball.^3-5,7 The progression of motion through the kinetic chain during throwing includes stride, pelvis rotation, upper torso rotation, elbow extension, shoulder internal rotation, and wrist flexion. Disruptions in this chain due to muscle imbalance or weakness can lead to injury downstream, particularly in the upper extremity.^3,7,9

The importance of the kinetic chain can be highlighted in the 6 phases of throwing motion. These include wind-up, early arm cocking, late arm cocking, arm acceleration, arm deceleration, and follow-through (Figure 1).^1,2,9,10

The wind-up phase starts with initiation of motion and ends with maximal knee lift of the lead leg; its objective is to place the body in an optimal stance to throw.^3-5,7 There are minimal forces, torques, and muscle activity in the upper extremity during this phase, but up to 50% of throw speed is created through stride and trunk rotation.⁶ During the early cocking phase, the thrower keeps his stance foot planted and drives his lead leg towards the target, while bringing both arms into abduction. This is coupled with internal rotation of the stance hip, external rotation of the lead hip, and external rotation of the throwing shoulder. This creates linear velocity by maximizing the length of the elastic components of the body. Elbow, wrist, and finger extensors are also contracting during this phase to control elbow flexion and wrist hyperextension.³

The late cocking phase begins when the lead foot contacts the ground and ends with maximum shoulder external rotation.^3-5 Lead foot contact is followed by quadriceps contraction to decelerate and stabilize the lead leg. This is followed by rotation of the pelvis and upper torso. The result is energy transfer to the throwing arm with a shear force across the anterior shoulder of 400 N.⁴ The shoulder stays in 90° of abduction, 15° of horizontal adduction, and externally rotates to between 150° and 180°. This produces a maximum horizontal adduction moment of 100 N^.m and internal rotation torque of 70 N^.m.⁴ Simultaneously, the elbow generates maximum flexion and a 65 N^.m varus torque.⁷ Forces about the elbow are generated to resist the large angular velocity experienced (up to 3000°/second). This places an extreme amount of valgus stress along the medial elbow, particularly on the ulnar collateral ligament. The shoulder girdle and rotator cuff muscles simultaneously act to stabilize the scapula and glenohumeral joint.

The arm acceleration phase is from maximal shoulder external rotation until ball release.^3-5 In this phase, the thrower flexes his trunk from an extended position, returning to neutral by the time of ball release while the lead leg straightens. The shoulder stays abducted at 90° throughout while the rotator cuff internal rotators and scapular stabilizers contract to explosively internally rotate the shoulder, creating a maximal internal rotation velocity greater than 7000°/second by ball release.^1,4,7 The elbow also begins to extend, reaching maximum velocity during mid-acceleration phase from a combination of triceps contraction and torque generated from rotation at the shoulder and upper trunk.³ Finally, the wrist flexors contract to move the wrist to a neutral position from hyperextension as the ball is released.

During arm deceleration, the shoulder achieves maximum internal rotation until reaching a neutral position and horizontally adducts across the body. This is controlled by contraction of the shoulder girdle musculature; the teres minor has the highest activity.^3,4 The greatest forces produced during the throwing motion act at the shoulder and elbow during deceleration and can contribute to injury.² These include compressive forces of greater than 1000 N, posterior shear forces of 400 N, and inferior shear forces of 300 N.^4,7

The final phase, the follow-through phase, starts at shoulder maximum internal rotation and ends when the arm assumes a balanced position across the trunk. Lower extremity extension and trunk flexion help distribute forces throughout the body, taking stress away from the throwing arm. The posterior shoulder musculature and scapular protractors contribute to continued deceleration and muscle firing returns to resting levels. This complex motion of throwing fueled by the kinetic chain lasts less than 2 seconds and can result in ball release speeds as high as 100 miles per hour.^3,4

Return to Throwing: Principles

Nonoperative and postoperative rehabilitation programs allow restoration of motion, strength, static and dynamic stability, and neuromuscular control. The initiation of an interval throwing program (ITP) is based on the assumption that tissue healing is complete and a complete physical examination has been conducted to the treating physician’s approval.¹¹ An ITP progressively applies forces along the kinetic chain in a controlled manner through graduated throwing distances, while minimizing the risk of re-injury.

Reinold and colleagues¹² described guidelines that were used in the development of the ITP.¹² These factors include: (1) The act of throwing a baseball involves the transfer of energy from the feet up to the hand and therefore careful attention must be paid along the entire kinetic chain; (2) gradual progression of interval throwing decreases the chance for re-injury; (3) proper warm-up; and (4) proper throwing mechanics minimizes the chance of re-injury.

Variability. Unlike traditional rehabilitation programs that advance an athlete based on a specific timetable, the ITP requires that each level or phase to be completed pain-free or without complications prior to starting the next level. Therefore, an ITP can be used for overhead athletes of varying skill levels because progression will be different from one athlete to another. It is also important to have the athlete adhere strictly to the program, as over-eagerness to complete the ITP as quickly as possible can increase the chance of re-injury and thus slow the rehabilitation process.¹²

Warm-up. An adequate warm-up is recommended prior to initiating ITP. An athlete should jog or cycle to develop a light sweat and then progress to stretching and flexibility exercises. As emphasized before, throwing involves nearly all the muscles in the body. Therefore, all muscle groups should be stretched beginning with the legs and working distally along the kinetic chain.

Mechanics. Analysis, correction, and maintenance of proper throwing mechanics is essential throughout the early phases of rehabilitation and ITP. Improper pitching mechanics places increased stress on the throwing arm, potentially leading to re-injury. Therefore, it would be valuable to have a pitching coach available to emphasize proper mechanics throughout the rehabilitation process.

The Interval Throwing Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 1.

Phase 1. We have adopted the ITP as described by Reinold and colleagues.¹² Phase begins with the overhead athlete throwing on flat ground. He or she begins tossing from 45 feet and gradually progresses to 60, 90, 120, 150, and 180 feet.

As discussed earlier, it is critical to use proper mechanics throughout the ITP. The “crow hop” method simulates a throwing act and helps maintain proper pitching mechanics. Crow hop has 3 components: hop, skip, and throw. Using this technique, the pitcher begins warm-up throws at a comfortable distance (generally 30 feet) and then progresses to the distance as indicated on the ITP. The athlete will then need to perform each step 2 times, with 1 day of rest between steps, before advancing to the next step. The ball should be thrown with an arc and have only enough momentum to reach the desired distance.

For example, Step 1 calls for the athlete to perform 2 sets of 25 throws at 45 feet, with adequate rest (5 minutes) between sets. This step will be repeated following 1 day of rest. If the athlete demonstrates the ability to throw at the prescribed distance without pain, he or she can progress to Step 2, which calls for 3 sets of 25 throws at 45 feet. If pain is present at any step, the thrower returns to the previous asymptomatic step and can progress once he is pain-free.

Positional players are instructed to complete Phase 1 prior to starting position-specific drills. Pitchers, on the other hand, are instructed to stop once they reach and complete 120 feet. They will then progress to tossing at progressive distances of 60, 90, and 120 feet, followed by throwing at 60 feet 6 inches with normal pitching mechanics, initiating straight line throws with little to no arc.

Phase II (Throwing off the Mound). Once a pitcher completes Phase 1 without pain or complications, he is ready to begin throwing off the mound. The same principle remains in Phase 2: pitchers must complete each step pain-free before advancing to the next stage. Pitchers should first throw fastballs at 50% effort and progress to 75% and 100% effort. Because athletes often find it difficult to gauge their own effort, it is important to emphasize the importance of strictly adhering to the program. Fleisig and colleagues¹³ studied healthy pitchers’ ability to estimate their throwing effort. When targeting 50% effort, athletes generated ball speeds of 85% with forces and torque approaching 75% of maximum. A radar gun may be valuable in guiding effort control.

As the player advances through Phase 2, he will increase the volume of pitches as well as the effort in a gradual manner. The player may introduce breaking ball pitches once he demonstrates the ability to throw light batting practice. Phase 2 concludes with the pitcher throwing simulated games, progressing by 15 throws per workout.

Hitting

Biomechanics Overview

The mechanics of hitting a baseball can be broken down into 6 phases: the preparatory phase, stance phase, stride phase, drive phase, bat acceleration phase, and follow-through phase.¹⁴ While progressing through a return-to-play protocol, it is important to understand and teach the player proper swing mechanics during each phase in order to minimize the risk of re-injury (Figure 2).

The preparatory phase occurs as the player positions himself into the batter’s box. This phase is highly individualized, depending on each player’s personal preference. Though significant variability in approach exists, there are 3 basic stances a player can take in preparation to bat. In the closed stance, the batter’s front foot is positioned closer to the plate than the back foot. A more popular stance is the open stance, where the player’s back foot is placed closer to the plate than the front foot. The square batting stance is the most common stance. This stance is where both feet are in line with the pitcher and parallel with the edge of the batter’s box. Most authors agree that the square stance is the optimal position because it provides batters the best opportunity to hit pitches anywhere in the strike zone and limits compensatory or extra motion to their swing.¹⁵

Once the player begins the swing, he has entered the loading period, which is divided into the stance, stride, and drive phases. The loading period, also known as coiling or triggering, begins as the athlete eccentrically stretches agonist muscles and rotates the body away from the incoming ball. The elastic energy stored during this stretching is released during the concentric contraction of the same muscles and transferred through the entire kinetic chain as different segments of the body are rotated; it culminates in effort directed at hitting the baseball.¹⁶

In each phase of the loading period, certain critical motions should be monitored and corrected in order to return the player to his previous level of competition. Stride length has been shown to be critical in the timing of a batter’s swing. A short stride length can cause early initiation of the swing, while a longer stride can produce delayed activation of hip rotation. As the player enters the drive phase, he should have increased elbow flexion in the back elbow compared to the front elbow. The bat should be placed at a position approximately 45° in the frontal plane, and the bat should bisect the batter’s helmet. The back elbow should be down, both upper extremities should be positioned close to the hitter’s body, and the proximal interphalangeal joints of the hands should align on the handle of the bat. Athletic trainers and coaches should be aware that subtle compensations due to deficits during these movements could cause injury during the swing by disrupting the body’s natural motion.

The bat acceleration phase occurs from maximal bat loading through striking the ball. In this time, the linear force that has been exerted by the player must be transferred into rotational force through the trunk and upper extremities. When the lead leg contacts the ground, the player has created a closed kinetic chain, where the elastic energy gathered during the loading period is used to produce segmental rotation beginning in the hips and rising through the trunk and out to the arms and hands, finally producing contact with the baseball.¹⁶ To produce effective bat velocity, each segment must rotate in a sequential manner. If the upper extremities reach peak velocity before any lower segment, then the player has lost the ability to efficiently transfer kinetic energy up the kinetic chain.

Finally, the follow-through phase occurs after contact with the baseball and ends with complete deceleration, completing the swing. In order to achieve optimal effort, full hip rotation is needed, which is aided by rotation of the trail foot. Both hips and back laces should face the pitcher upon completion of the swing producing maximum power output.¹⁵

Return to Hitting: Principles

As with the initiation of the ITP, an interval hitting protocol (IHP) is designed to begin only after the player has been assessed on impairment measures, physical performance measures, and self-assessment.¹⁷ The player should have minimum to no pain, have no tenderness to palpation, and show adequate range of motion and strength to meet the demands of performing a full hitting cycle.¹² It is recommended that before beginning a return-to-play protocol, the involved extremity should be at least 80% as strong as the uninvolved extremity.¹⁸ Physical measures challenging an athlete’s ability to perform tasks specific to hitting a baseball must also be considered through standardized examinations of the involved area.¹⁹ Finally, the athlete’s self-perception of functional abilities must be taken into account. This gives a subjective account of what the hitter perceives they are able to perform, providing useful insight into whether they are mentally prepared to participate in the protocol.

Like the ITP, progression through the IHP is also based on the player’s level of pain and soreness rather than following a specific timetable (Table). The program features a 1 day on, 1 day off schedule during which the player completes 1 step per day. The athlete must remain pain-free to progress to the next step and monitor his level of soreness during their workout. If pain or soreness persists, the player should rest for 2 days and be reevaluated upon return.¹⁷

The same principles of proper warm-up and mechanics apply in the IHP. An athlete should jog or cycle for a minimum of 10 minutes and perform stretching exercises focused on both upper and lower extremity muscles, as batting involves whole body movement. As the athlete progresses through the IHP, having a hitting coach to analyze, correct and maintain proper swing mechanics is valuable in enhancing performance as well as decreasing risk of re-injury.

The Interval Hitting Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 2.

Phase 1 (Dry Swings). Only the most basic fundamentals are stressed during this phase. The player should focus on properly moving from one phase of the swing to the next, without the goal of hitting the baseball. Trainers should measure critical points in the swing and correct deficits early.

Phase 2 (Batting Off a Tee). In this phase, the player is reintroduced to batting at low intensity with a fixed position target. The initial steps have the batter swing in a position of greatest comfort and natural movement, while the final steps in this phase test the athlete’s range of motion and confidence in the previous, healed injury.

Phase 3 (Soft Toss). As the player progresses to this phase, a baseball with trajectory is used to simulate differences in placement of pitches used during a game. As the hitter is able to pick up differences in target position, his performance and confidence should both increase.²⁰ The coach should sit about 30 feet away, facing the hitter at an angle of 45°, and toss the ball in an underhand motion.

Phase 4 (Simulated Hitting). In this phase, the player and coach should focus on the timing of sequential body movements in order to elicit proper loading and force production. With the randomized pitch delivery and increased velocity, the hitter will practice against pitches similar to those delivered in competition.

Conclusion

Interval throwing and hitting programs are designed to allow the athlete to return to competition through a gradual, stepwise program. This permits the player to prepare his body for the unique stresses associated with throwing and hitting. The medical personnel should familiarize themselves with the philosophy of the interval throwing and hitting programs and individualize them to each athlete. Emphasis on proper warm-up, mechanics, and effort control is paramount in expediting return to play while preventing re-injury.

Throwing and batting each require repetitive motions that can result in injuries unique to baseball. Fortuantely, advances in operative and nonoperative treatments have allowed players to return to competition after sustaining what previously would have been considered a career-ending injury. Once a player has been deemed ready to return to throwing or hitting, a comprehensive, multiphased approach to rehabilitation is necessary to reintroduce the athlete back to baseball activities and avoid re-injury. This article reviews the biomechanics of both throwing and hitting, and outlines the phases of rehabilitation necessary to allow the athlete to return to competition.

Throwing

Biomechanical Overview

The overhead throwing motion is complex and involves full body coordination from the initial force generation through the follow-through phase of throwing. The “kinetic chain”—the concept that movements in the body are connected through segments culminating with the highest energy in the final segment—is paramount to achieving the force and energy needed for throwing.^1-8 The kinetic chain begins in the lower body and trunk and transmits the energy distally to the shoulder, elbow, and hand, ending with kinetic energy transfer to the ball.^3-5,7 The progression of motion through the kinetic chain during throwing includes stride, pelvis rotation, upper torso rotation, elbow extension, shoulder internal rotation, and wrist flexion. Disruptions in this chain due to muscle imbalance or weakness can lead to injury downstream, particularly in the upper extremity.^3,7,9

The importance of the kinetic chain can be highlighted in the 6 phases of throwing motion. These include wind-up, early arm cocking, late arm cocking, arm acceleration, arm deceleration, and follow-through (Figure 1).^1,2,9,10

The wind-up phase starts with initiation of motion and ends with maximal knee lift of the lead leg; its objective is to place the body in an optimal stance to throw.^3-5,7 There are minimal forces, torques, and muscle activity in the upper extremity during this phase, but up to 50% of throw speed is created through stride and trunk rotation.⁶ During the early cocking phase, the thrower keeps his stance foot planted and drives his lead leg towards the target, while bringing both arms into abduction. This is coupled with internal rotation of the stance hip, external rotation of the lead hip, and external rotation of the throwing shoulder. This creates linear velocity by maximizing the length of the elastic components of the body. Elbow, wrist, and finger extensors are also contracting during this phase to control elbow flexion and wrist hyperextension.³

The late cocking phase begins when the lead foot contacts the ground and ends with maximum shoulder external rotation.^3-5 Lead foot contact is followed by quadriceps contraction to decelerate and stabilize the lead leg. This is followed by rotation of the pelvis and upper torso. The result is energy transfer to the throwing arm with a shear force across the anterior shoulder of 400 N.⁴ The shoulder stays in 90° of abduction, 15° of horizontal adduction, and externally rotates to between 150° and 180°. This produces a maximum horizontal adduction moment of 100 N^.m and internal rotation torque of 70 N^.m.⁴ Simultaneously, the elbow generates maximum flexion and a 65 N^.m varus torque.⁷ Forces about the elbow are generated to resist the large angular velocity experienced (up to 3000°/second). This places an extreme amount of valgus stress along the medial elbow, particularly on the ulnar collateral ligament. The shoulder girdle and rotator cuff muscles simultaneously act to stabilize the scapula and glenohumeral joint.

The arm acceleration phase is from maximal shoulder external rotation until ball release.^3-5 In this phase, the thrower flexes his trunk from an extended position, returning to neutral by the time of ball release while the lead leg straightens. The shoulder stays abducted at 90° throughout while the rotator cuff internal rotators and scapular stabilizers contract to explosively internally rotate the shoulder, creating a maximal internal rotation velocity greater than 7000°/second by ball release.^1,4,7 The elbow also begins to extend, reaching maximum velocity during mid-acceleration phase from a combination of triceps contraction and torque generated from rotation at the shoulder and upper trunk.³ Finally, the wrist flexors contract to move the wrist to a neutral position from hyperextension as the ball is released.

During arm deceleration, the shoulder achieves maximum internal rotation until reaching a neutral position and horizontally adducts across the body. This is controlled by contraction of the shoulder girdle musculature; the teres minor has the highest activity.^3,4 The greatest forces produced during the throwing motion act at the shoulder and elbow during deceleration and can contribute to injury.² These include compressive forces of greater than 1000 N, posterior shear forces of 400 N, and inferior shear forces of 300 N.^4,7

The final phase, the follow-through phase, starts at shoulder maximum internal rotation and ends when the arm assumes a balanced position across the trunk. Lower extremity extension and trunk flexion help distribute forces throughout the body, taking stress away from the throwing arm. The posterior shoulder musculature and scapular protractors contribute to continued deceleration and muscle firing returns to resting levels. This complex motion of throwing fueled by the kinetic chain lasts less than 2 seconds and can result in ball release speeds as high as 100 miles per hour.^3,4

Return to Throwing: Principles

Nonoperative and postoperative rehabilitation programs allow restoration of motion, strength, static and dynamic stability, and neuromuscular control. The initiation of an interval throwing program (ITP) is based on the assumption that tissue healing is complete and a complete physical examination has been conducted to the treating physician’s approval.¹¹ An ITP progressively applies forces along the kinetic chain in a controlled manner through graduated throwing distances, while minimizing the risk of re-injury.

Reinold and colleagues¹² described guidelines that were used in the development of the ITP.¹² These factors include: (1) The act of throwing a baseball involves the transfer of energy from the feet up to the hand and therefore careful attention must be paid along the entire kinetic chain; (2) gradual progression of interval throwing decreases the chance for re-injury; (3) proper warm-up; and (4) proper throwing mechanics minimizes the chance of re-injury.

Variability. Unlike traditional rehabilitation programs that advance an athlete based on a specific timetable, the ITP requires that each level or phase to be completed pain-free or without complications prior to starting the next level. Therefore, an ITP can be used for overhead athletes of varying skill levels because progression will be different from one athlete to another. It is also important to have the athlete adhere strictly to the program, as over-eagerness to complete the ITP as quickly as possible can increase the chance of re-injury and thus slow the rehabilitation process.¹²

Warm-up. An adequate warm-up is recommended prior to initiating ITP. An athlete should jog or cycle to develop a light sweat and then progress to stretching and flexibility exercises. As emphasized before, throwing involves nearly all the muscles in the body. Therefore, all muscle groups should be stretched beginning with the legs and working distally along the kinetic chain.

Mechanics. Analysis, correction, and maintenance of proper throwing mechanics is essential throughout the early phases of rehabilitation and ITP. Improper pitching mechanics places increased stress on the throwing arm, potentially leading to re-injury. Therefore, it would be valuable to have a pitching coach available to emphasize proper mechanics throughout the rehabilitation process.

The Interval Throwing Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 1.

Phase 1. We have adopted the ITP as described by Reinold and colleagues.¹² Phase begins with the overhead athlete throwing on flat ground. He or she begins tossing from 45 feet and gradually progresses to 60, 90, 120, 150, and 180 feet.

As discussed earlier, it is critical to use proper mechanics throughout the ITP. The “crow hop” method simulates a throwing act and helps maintain proper pitching mechanics. Crow hop has 3 components: hop, skip, and throw. Using this technique, the pitcher begins warm-up throws at a comfortable distance (generally 30 feet) and then progresses to the distance as indicated on the ITP. The athlete will then need to perform each step 2 times, with 1 day of rest between steps, before advancing to the next step. The ball should be thrown with an arc and have only enough momentum to reach the desired distance.

For example, Step 1 calls for the athlete to perform 2 sets of 25 throws at 45 feet, with adequate rest (5 minutes) between sets. This step will be repeated following 1 day of rest. If the athlete demonstrates the ability to throw at the prescribed distance without pain, he or she can progress to Step 2, which calls for 3 sets of 25 throws at 45 feet. If pain is present at any step, the thrower returns to the previous asymptomatic step and can progress once he is pain-free.

Positional players are instructed to complete Phase 1 prior to starting position-specific drills. Pitchers, on the other hand, are instructed to stop once they reach and complete 120 feet. They will then progress to tossing at progressive distances of 60, 90, and 120 feet, followed by throwing at 60 feet 6 inches with normal pitching mechanics, initiating straight line throws with little to no arc.

Phase II (Throwing off the Mound). Once a pitcher completes Phase 1 without pain or complications, he is ready to begin throwing off the mound. The same principle remains in Phase 2: pitchers must complete each step pain-free before advancing to the next stage. Pitchers should first throw fastballs at 50% effort and progress to 75% and 100% effort. Because athletes often find it difficult to gauge their own effort, it is important to emphasize the importance of strictly adhering to the program. Fleisig and colleagues¹³ studied healthy pitchers’ ability to estimate their throwing effort. When targeting 50% effort, athletes generated ball speeds of 85% with forces and torque approaching 75% of maximum. A radar gun may be valuable in guiding effort control.

As the player advances through Phase 2, he will increase the volume of pitches as well as the effort in a gradual manner. The player may introduce breaking ball pitches once he demonstrates the ability to throw light batting practice. Phase 2 concludes with the pitcher throwing simulated games, progressing by 15 throws per workout.

Hitting

Biomechanics Overview

The mechanics of hitting a baseball can be broken down into 6 phases: the preparatory phase, stance phase, stride phase, drive phase, bat acceleration phase, and follow-through phase.¹⁴ While progressing through a return-to-play protocol, it is important to understand and teach the player proper swing mechanics during each phase in order to minimize the risk of re-injury (Figure 2).

The preparatory phase occurs as the player positions himself into the batter’s box. This phase is highly individualized, depending on each player’s personal preference. Though significant variability in approach exists, there are 3 basic stances a player can take in preparation to bat. In the closed stance, the batter’s front foot is positioned closer to the plate than the back foot. A more popular stance is the open stance, where the player’s back foot is placed closer to the plate than the front foot. The square batting stance is the most common stance. This stance is where both feet are in line with the pitcher and parallel with the edge of the batter’s box. Most authors agree that the square stance is the optimal position because it provides batters the best opportunity to hit pitches anywhere in the strike zone and limits compensatory or extra motion to their swing.¹⁵

Once the player begins the swing, he has entered the loading period, which is divided into the stance, stride, and drive phases. The loading period, also known as coiling or triggering, begins as the athlete eccentrically stretches agonist muscles and rotates the body away from the incoming ball. The elastic energy stored during this stretching is released during the concentric contraction of the same muscles and transferred through the entire kinetic chain as different segments of the body are rotated; it culminates in effort directed at hitting the baseball.¹⁶

In each phase of the loading period, certain critical motions should be monitored and corrected in order to return the player to his previous level of competition. Stride length has been shown to be critical in the timing of a batter’s swing. A short stride length can cause early initiation of the swing, while a longer stride can produce delayed activation of hip rotation. As the player enters the drive phase, he should have increased elbow flexion in the back elbow compared to the front elbow. The bat should be placed at a position approximately 45° in the frontal plane, and the bat should bisect the batter’s helmet. The back elbow should be down, both upper extremities should be positioned close to the hitter’s body, and the proximal interphalangeal joints of the hands should align on the handle of the bat. Athletic trainers and coaches should be aware that subtle compensations due to deficits during these movements could cause injury during the swing by disrupting the body’s natural motion.

The bat acceleration phase occurs from maximal bat loading through striking the ball. In this time, the linear force that has been exerted by the player must be transferred into rotational force through the trunk and upper extremities. When the lead leg contacts the ground, the player has created a closed kinetic chain, where the elastic energy gathered during the loading period is used to produce segmental rotation beginning in the hips and rising through the trunk and out to the arms and hands, finally producing contact with the baseball.¹⁶ To produce effective bat velocity, each segment must rotate in a sequential manner. If the upper extremities reach peak velocity before any lower segment, then the player has lost the ability to efficiently transfer kinetic energy up the kinetic chain.

Finally, the follow-through phase occurs after contact with the baseball and ends with complete deceleration, completing the swing. In order to achieve optimal effort, full hip rotation is needed, which is aided by rotation of the trail foot. Both hips and back laces should face the pitcher upon completion of the swing producing maximum power output.¹⁵

Return to Hitting: Principles

As with the initiation of the ITP, an interval hitting protocol (IHP) is designed to begin only after the player has been assessed on impairment measures, physical performance measures, and self-assessment.¹⁷ The player should have minimum to no pain, have no tenderness to palpation, and show adequate range of motion and strength to meet the demands of performing a full hitting cycle.¹² It is recommended that before beginning a return-to-play protocol, the involved extremity should be at least 80% as strong as the uninvolved extremity.¹⁸ Physical measures challenging an athlete’s ability to perform tasks specific to hitting a baseball must also be considered through standardized examinations of the involved area.¹⁹ Finally, the athlete’s self-perception of functional abilities must be taken into account. This gives a subjective account of what the hitter perceives they are able to perform, providing useful insight into whether they are mentally prepared to participate in the protocol.

Like the ITP, progression through the IHP is also based on the player’s level of pain and soreness rather than following a specific timetable (Table). The program features a 1 day on, 1 day off schedule during which the player completes 1 step per day. The athlete must remain pain-free to progress to the next step and monitor his level of soreness during their workout. If pain or soreness persists, the player should rest for 2 days and be reevaluated upon return.¹⁷

The same principles of proper warm-up and mechanics apply in the IHP. An athlete should jog or cycle for a minimum of 10 minutes and perform stretching exercises focused on both upper and lower extremity muscles, as batting involves whole body movement. As the athlete progresses through the IHP, having a hitting coach to analyze, correct and maintain proper swing mechanics is valuable in enhancing performance as well as decreasing risk of re-injury.

The Interval Hitting Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 2.

Phase 1 (Dry Swings). Only the most basic fundamentals are stressed during this phase. The player should focus on properly moving from one phase of the swing to the next, without the goal of hitting the baseball. Trainers should measure critical points in the swing and correct deficits early.

Phase 2 (Batting Off a Tee). In this phase, the player is reintroduced to batting at low intensity with a fixed position target. The initial steps have the batter swing in a position of greatest comfort and natural movement, while the final steps in this phase test the athlete’s range of motion and confidence in the previous, healed injury.

Phase 3 (Soft Toss). As the player progresses to this phase, a baseball with trajectory is used to simulate differences in placement of pitches used during a game. As the hitter is able to pick up differences in target position, his performance and confidence should both increase.²⁰ The coach should sit about 30 feet away, facing the hitter at an angle of 45°, and toss the ball in an underhand motion.

Phase 4 (Simulated Hitting). In this phase, the player and coach should focus on the timing of sequential body movements in order to elicit proper loading and force production. With the randomized pitch delivery and increased velocity, the hitter will practice against pitches similar to those delivered in competition.

Conclusion

Interval throwing and hitting programs are designed to allow the athlete to return to competition through a gradual, stepwise program. This permits the player to prepare his body for the unique stresses associated with throwing and hitting. The medical personnel should familiarize themselves with the philosophy of the interval throwing and hitting programs and individualize them to each athlete. Emphasis on proper warm-up, mechanics, and effort control is paramount in expediting return to play while preventing re-injury.

Throwing and batting each require repetitive motions that can result in injuries unique to baseball. Fortuantely, advances in operative and nonoperative treatments have allowed players to return to competition after sustaining what previously would have been considered a career-ending injury. Once a player has been deemed ready to return to throwing or hitting, a comprehensive, multiphased approach to rehabilitation is necessary to reintroduce the athlete back to baseball activities and avoid re-injury. This article reviews the biomechanics of both throwing and hitting, and outlines the phases of rehabilitation necessary to allow the athlete to return to competition.

Throwing

Biomechanical Overview

The overhead throwing motion is complex and involves full body coordination from the initial force generation through the follow-through phase of throwing. The “kinetic chain”—the concept that movements in the body are connected through segments culminating with the highest energy in the final segment—is paramount to achieving the force and energy needed for throwing.^1-8 The kinetic chain begins in the lower body and trunk and transmits the energy distally to the shoulder, elbow, and hand, ending with kinetic energy transfer to the ball.^3-5,7 The progression of motion through the kinetic chain during throwing includes stride, pelvis rotation, upper torso rotation, elbow extension, shoulder internal rotation, and wrist flexion. Disruptions in this chain due to muscle imbalance or weakness can lead to injury downstream, particularly in the upper extremity.^3,7,9

The importance of the kinetic chain can be highlighted in the 6 phases of throwing motion. These include wind-up, early arm cocking, late arm cocking, arm acceleration, arm deceleration, and follow-through (Figure 1).^1,2,9,10

The wind-up phase starts with initiation of motion and ends with maximal knee lift of the lead leg; its objective is to place the body in an optimal stance to throw.^3-5,7 There are minimal forces, torques, and muscle activity in the upper extremity during this phase, but up to 50% of throw speed is created through stride and trunk rotation.⁶ During the early cocking phase, the thrower keeps his stance foot planted and drives his lead leg towards the target, while bringing both arms into abduction. This is coupled with internal rotation of the stance hip, external rotation of the lead hip, and external rotation of the throwing shoulder. This creates linear velocity by maximizing the length of the elastic components of the body. Elbow, wrist, and finger extensors are also contracting during this phase to control elbow flexion and wrist hyperextension.³

The late cocking phase begins when the lead foot contacts the ground and ends with maximum shoulder external rotation.^3-5 Lead foot contact is followed by quadriceps contraction to decelerate and stabilize the lead leg. This is followed by rotation of the pelvis and upper torso. The result is energy transfer to the throwing arm with a shear force across the anterior shoulder of 400 N.⁴ The shoulder stays in 90° of abduction, 15° of horizontal adduction, and externally rotates to between 150° and 180°. This produces a maximum horizontal adduction moment of 100 N^.m and internal rotation torque of 70 N^.m.⁴ Simultaneously, the elbow generates maximum flexion and a 65 N^.m varus torque.⁷ Forces about the elbow are generated to resist the large angular velocity experienced (up to 3000°/second). This places an extreme amount of valgus stress along the medial elbow, particularly on the ulnar collateral ligament. The shoulder girdle and rotator cuff muscles simultaneously act to stabilize the scapula and glenohumeral joint.

The arm acceleration phase is from maximal shoulder external rotation until ball release.^3-5 In this phase, the thrower flexes his trunk from an extended position, returning to neutral by the time of ball release while the lead leg straightens. The shoulder stays abducted at 90° throughout while the rotator cuff internal rotators and scapular stabilizers contract to explosively internally rotate the shoulder, creating a maximal internal rotation velocity greater than 7000°/second by ball release.^1,4,7 The elbow also begins to extend, reaching maximum velocity during mid-acceleration phase from a combination of triceps contraction and torque generated from rotation at the shoulder and upper trunk.³ Finally, the wrist flexors contract to move the wrist to a neutral position from hyperextension as the ball is released.

During arm deceleration, the shoulder achieves maximum internal rotation until reaching a neutral position and horizontally adducts across the body. This is controlled by contraction of the shoulder girdle musculature; the teres minor has the highest activity.^3,4 The greatest forces produced during the throwing motion act at the shoulder and elbow during deceleration and can contribute to injury.² These include compressive forces of greater than 1000 N, posterior shear forces of 400 N, and inferior shear forces of 300 N.^4,7

The final phase, the follow-through phase, starts at shoulder maximum internal rotation and ends when the arm assumes a balanced position across the trunk. Lower extremity extension and trunk flexion help distribute forces throughout the body, taking stress away from the throwing arm. The posterior shoulder musculature and scapular protractors contribute to continued deceleration and muscle firing returns to resting levels. This complex motion of throwing fueled by the kinetic chain lasts less than 2 seconds and can result in ball release speeds as high as 100 miles per hour.^3,4

Return to Throwing: Principles

Nonoperative and postoperative rehabilitation programs allow restoration of motion, strength, static and dynamic stability, and neuromuscular control. The initiation of an interval throwing program (ITP) is based on the assumption that tissue healing is complete and a complete physical examination has been conducted to the treating physician’s approval.¹¹ An ITP progressively applies forces along the kinetic chain in a controlled manner through graduated throwing distances, while minimizing the risk of re-injury.

Reinold and colleagues¹² described guidelines that were used in the development of the ITP.¹² These factors include: (1) The act of throwing a baseball involves the transfer of energy from the feet up to the hand and therefore careful attention must be paid along the entire kinetic chain; (2) gradual progression of interval throwing decreases the chance for re-injury; (3) proper warm-up; and (4) proper throwing mechanics minimizes the chance of re-injury.

Variability. Unlike traditional rehabilitation programs that advance an athlete based on a specific timetable, the ITP requires that each level or phase to be completed pain-free or without complications prior to starting the next level. Therefore, an ITP can be used for overhead athletes of varying skill levels because progression will be different from one athlete to another. It is also important to have the athlete adhere strictly to the program, as over-eagerness to complete the ITP as quickly as possible can increase the chance of re-injury and thus slow the rehabilitation process.¹²

Warm-up. An adequate warm-up is recommended prior to initiating ITP. An athlete should jog or cycle to develop a light sweat and then progress to stretching and flexibility exercises. As emphasized before, throwing involves nearly all the muscles in the body. Therefore, all muscle groups should be stretched beginning with the legs and working distally along the kinetic chain.

Mechanics. Analysis, correction, and maintenance of proper throwing mechanics is essential throughout the early phases of rehabilitation and ITP. Improper pitching mechanics places increased stress on the throwing arm, potentially leading to re-injury. Therefore, it would be valuable to have a pitching coach available to emphasize proper mechanics throughout the rehabilitation process.

The Interval Throwing Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 1.

Phase 1. We have adopted the ITP as described by Reinold and colleagues.¹² Phase begins with the overhead athlete throwing on flat ground. He or she begins tossing from 45 feet and gradually progresses to 60, 90, 120, 150, and 180 feet.

As discussed earlier, it is critical to use proper mechanics throughout the ITP. The “crow hop” method simulates a throwing act and helps maintain proper pitching mechanics. Crow hop has 3 components: hop, skip, and throw. Using this technique, the pitcher begins warm-up throws at a comfortable distance (generally 30 feet) and then progresses to the distance as indicated on the ITP. The athlete will then need to perform each step 2 times, with 1 day of rest between steps, before advancing to the next step. The ball should be thrown with an arc and have only enough momentum to reach the desired distance.

For example, Step 1 calls for the athlete to perform 2 sets of 25 throws at 45 feet, with adequate rest (5 minutes) between sets. This step will be repeated following 1 day of rest. If the athlete demonstrates the ability to throw at the prescribed distance without pain, he or she can progress to Step 2, which calls for 3 sets of 25 throws at 45 feet. If pain is present at any step, the thrower returns to the previous asymptomatic step and can progress once he is pain-free.

Positional players are instructed to complete Phase 1 prior to starting position-specific drills. Pitchers, on the other hand, are instructed to stop once they reach and complete 120 feet. They will then progress to tossing at progressive distances of 60, 90, and 120 feet, followed by throwing at 60 feet 6 inches with normal pitching mechanics, initiating straight line throws with little to no arc.

Phase II (Throwing off the Mound). Once a pitcher completes Phase 1 without pain or complications, he is ready to begin throwing off the mound. The same principle remains in Phase 2: pitchers must complete each step pain-free before advancing to the next stage. Pitchers should first throw fastballs at 50% effort and progress to 75% and 100% effort. Because athletes often find it difficult to gauge their own effort, it is important to emphasize the importance of strictly adhering to the program. Fleisig and colleagues¹³ studied healthy pitchers’ ability to estimate their throwing effort. When targeting 50% effort, athletes generated ball speeds of 85% with forces and torque approaching 75% of maximum. A radar gun may be valuable in guiding effort control.

As the player advances through Phase 2, he will increase the volume of pitches as well as the effort in a gradual manner. The player may introduce breaking ball pitches once he demonstrates the ability to throw light batting practice. Phase 2 concludes with the pitcher throwing simulated games, progressing by 15 throws per workout.

Hitting

Biomechanics Overview

The mechanics of hitting a baseball can be broken down into 6 phases: the preparatory phase, stance phase, stride phase, drive phase, bat acceleration phase, and follow-through phase.¹⁴ While progressing through a return-to-play protocol, it is important to understand and teach the player proper swing mechanics during each phase in order to minimize the risk of re-injury (Figure 2).

The preparatory phase occurs as the player positions himself into the batter’s box. This phase is highly individualized, depending on each player’s personal preference. Though significant variability in approach exists, there are 3 basic stances a player can take in preparation to bat. In the closed stance, the batter’s front foot is positioned closer to the plate than the back foot. A more popular stance is the open stance, where the player’s back foot is placed closer to the plate than the front foot. The square batting stance is the most common stance. This stance is where both feet are in line with the pitcher and parallel with the edge of the batter’s box. Most authors agree that the square stance is the optimal position because it provides batters the best opportunity to hit pitches anywhere in the strike zone and limits compensatory or extra motion to their swing.¹⁵

Once the player begins the swing, he has entered the loading period, which is divided into the stance, stride, and drive phases. The loading period, also known as coiling or triggering, begins as the athlete eccentrically stretches agonist muscles and rotates the body away from the incoming ball. The elastic energy stored during this stretching is released during the concentric contraction of the same muscles and transferred through the entire kinetic chain as different segments of the body are rotated; it culminates in effort directed at hitting the baseball.¹⁶

In each phase of the loading period, certain critical motions should be monitored and corrected in order to return the player to his previous level of competition. Stride length has been shown to be critical in the timing of a batter’s swing. A short stride length can cause early initiation of the swing, while a longer stride can produce delayed activation of hip rotation. As the player enters the drive phase, he should have increased elbow flexion in the back elbow compared to the front elbow. The bat should be placed at a position approximately 45° in the frontal plane, and the bat should bisect the batter’s helmet. The back elbow should be down, both upper extremities should be positioned close to the hitter’s body, and the proximal interphalangeal joints of the hands should align on the handle of the bat. Athletic trainers and coaches should be aware that subtle compensations due to deficits during these movements could cause injury during the swing by disrupting the body’s natural motion.

The bat acceleration phase occurs from maximal bat loading through striking the ball. In this time, the linear force that has been exerted by the player must be transferred into rotational force through the trunk and upper extremities. When the lead leg contacts the ground, the player has created a closed kinetic chain, where the elastic energy gathered during the loading period is used to produce segmental rotation beginning in the hips and rising through the trunk and out to the arms and hands, finally producing contact with the baseball.¹⁶ To produce effective bat velocity, each segment must rotate in a sequential manner. If the upper extremities reach peak velocity before any lower segment, then the player has lost the ability to efficiently transfer kinetic energy up the kinetic chain.

Finally, the follow-through phase occurs after contact with the baseball and ends with complete deceleration, completing the swing. In order to achieve optimal effort, full hip rotation is needed, which is aided by rotation of the trail foot. Both hips and back laces should face the pitcher upon completion of the swing producing maximum power output.¹⁵

Return to Hitting: Principles

As with the initiation of the ITP, an interval hitting protocol (IHP) is designed to begin only after the player has been assessed on impairment measures, physical performance measures, and self-assessment.¹⁷ The player should have minimum to no pain, have no tenderness to palpation, and show adequate range of motion and strength to meet the demands of performing a full hitting cycle.¹² It is recommended that before beginning a return-to-play protocol, the involved extremity should be at least 80% as strong as the uninvolved extremity.¹⁸ Physical measures challenging an athlete’s ability to perform tasks specific to hitting a baseball must also be considered through standardized examinations of the involved area.¹⁹ Finally, the athlete’s self-perception of functional abilities must be taken into account. This gives a subjective account of what the hitter perceives they are able to perform, providing useful insight into whether they are mentally prepared to participate in the protocol.

Like the ITP, progression through the IHP is also based on the player’s level of pain and soreness rather than following a specific timetable (Table). The program features a 1 day on, 1 day off schedule during which the player completes 1 step per day. The athlete must remain pain-free to progress to the next step and monitor his level of soreness during their workout. If pain or soreness persists, the player should rest for 2 days and be reevaluated upon return.¹⁷

The same principles of proper warm-up and mechanics apply in the IHP. An athlete should jog or cycle for a minimum of 10 minutes and perform stretching exercises focused on both upper and lower extremity muscles, as batting involves whole body movement. As the athlete progresses through the IHP, having a hitting coach to analyze, correct and maintain proper swing mechanics is valuable in enhancing performance as well as decreasing risk of re-injury.

The Interval Hitting Program

For a PDF patient handout that summarizes the phases of this program, see Appendix 2.

Phase 1 (Dry Swings). Only the most basic fundamentals are stressed during this phase. The player should focus on properly moving from one phase of the swing to the next, without the goal of hitting the baseball. Trainers should measure critical points in the swing and correct deficits early.

Phase 2 (Batting Off a Tee). In this phase, the player is reintroduced to batting at low intensity with a fixed position target. The initial steps have the batter swing in a position of greatest comfort and natural movement, while the final steps in this phase test the athlete’s range of motion and confidence in the previous, healed injury.

Phase 3 (Soft Toss). As the player progresses to this phase, a baseball with trajectory is used to simulate differences in placement of pitches used during a game. As the hitter is able to pick up differences in target position, his performance and confidence should both increase.²⁰ The coach should sit about 30 feet away, facing the hitter at an angle of 45°, and toss the ball in an underhand motion.

Phase 4 (Simulated Hitting). In this phase, the player and coach should focus on the timing of sequential body movements in order to elicit proper loading and force production. With the randomized pitch delivery and increased velocity, the hitter will practice against pitches similar to those delivered in competition.

Conclusion

Interval throwing and hitting programs are designed to allow the athlete to return to competition through a gradual, stepwise program. This permits the player to prepare his body for the unique stresses associated with throwing and hitting. The medical personnel should familiarize themselves with the philosophy of the interval throwing and hitting programs and individualize them to each athlete. Emphasis on proper warm-up, mechanics, and effort control is paramount in expediting return to play while preventing re-injury.

Major league baseball (MLB) is one of the most popular sports in the United States, with an average annual viewership of 11 million for the All-Star game and almost 14 million for the World Series.¹ MLB has an average annual revenue of almost $10 billion, while the net worth of all 30 MLB teams combined is estimated at $36 billion; an increase of 48% from 1 year ago.² As the sport continues to grow in popularity and receives more social media coverage, several issues, specifically injuries to its players, have come to the forefront of the news. Injuries to MLB players, specifically pitchers, have become a significant concern in recent years. The active and extended rosters in MLB include 750 and 1200 athletes, respectively, with approximately 360 active spots taken up by pitchers.³ Hence, MLB employs a large number of elite athletes within its organization. It is important to understand not only what injuries are occurring in these athletes, but also how these injuries may be prevented.

Epidemiology

Injuries to MLB players, specifically pitchers, have increased over the past several years.⁴ Between 2005 and 2008, there was an overall increase of 37% in total number of injuries, with more injuries occurring in pitchers than any other position.⁵ While position players are more likely to sustain an injury to the lower extremity, pitchers are more likely to sustain an injury to the upper extremity.⁵ The month with the most injuries to MLB players was April, while the fewest number of injuries occurred in September.⁵ One injury that has been in the spotlight due to its dramatically increasing incidence is tear of the ulnar collateral ligament (UCL). Several studies have shown that the number of pitchers undergoing ulnar collateral ligament reconstruction (UCLR), commonly known as Tommy John surgery, has significantly increased over the past 20 years (Figure 1).^4,6 Between 25% to 33% of all MLB pitchers have undergone UCLR.

While the number of primary UCLR in MLB pitchers has become a significant concern, an even more pressing concern is the number of pitchers undergoing revision UCLR, as this number has increased over the past several years.⁷ Currently, there is some debate as to how to best address the UCL during primary UCLR (graft type, exposure, treatment of the ulnar nerve, and graft fixation methods) because no study has shown one fixation method or graft type to be superior to others. Similarly, no study has definitively proven how to best manage the ulnar nerve (transpose in all patients, only transpose if preoperative symptoms of numbness/tingling, subluxation, etc. exist). Unfortunately, the results following revision UCLR are inferior to those following primary UCLR.^4,7,8 Hence, given this information, it is imperative to both determine and implement strategies aimed at minimizing the need for revision.

Risk Factors for Injury

Although MLB has received more media attention than lower levels of baseball competition, there is relatively sparse evidence surrounding injury risk factors among MLB players. The majority of studies performed have evaluated risk factors for injury in younger baseball athletes (adolescent, high school, and college). The number of athletes at these lower levels sustaining injuries has increased over the past several years as well.⁹ Several large prospective studies have evaluated risk factors for shoulder and elbow injuries in adolescent baseball players. The risk factors include pitching year-round, pitching more than 100 innings per year, high pitch counts, pitching for multiple teams, geography, pitching on consecutive days, pitching while fatigued, breaking pitches, higher elbow valgus torque, pitching with higher velocity, pitching with supraspinatus weakness, and pitching with a glenohumeral internal rotation deficit (GIRD).^10-17 The large majority of these risk factors are essentially part of a pitcher’s cumulative work, which consists of number of games pitched, total pitches thrown, total innings pitched, innings pitched per game, and pitches thrown per game. One prior study has evaluated cumulative work as a predictor for injury in MLB pitchers.¹⁸ While there were several issues with the study methodology, the authors found no correlation between a MLB pitcher’s cumulative work and risk for injury.

Given our current understanding of repetitive microtrauma as the pathophysiology behind these injuries, it remains unclear why cumulative work would be predictive of injury in youth pitchers but not in MLB pitchers.¹⁶ Several potential reasons exist as to why cumulative work may relate to risk of injury in youth pitchers and not MLB pitchers. Achieving MLB status may infer the element of natural selection based on technique and talent that supersedes the effect of “cumulative trauma” in many players. In MLB pitchers, cumulative work is closely monitored. In addition, these players are only playing for a single team and are not pitching competitively year-round, while many youth players play for multiple teams and may pitch year-round. To combat youth injuries, MLB Pitch Smart has developed recommendations on pitch counts and days of rest for pitchers of all age groups (Table).¹⁹ While data do not yet exist to clearly demonstrate the effectiveness of these guidelines, given the risk factors previously mentioned, it seems that these recommendations will show some reduction in youth injuries in years to come.

Some studies have evaluated anatomic variation among pitchers as a risk factor for injury. Polster and colleagues²⁰ performed computed tomography (CT) scans with 3-dimensional reconstructions on the humeri of both the throwing and non-throwing arms of 25 MLB pitchers to determine if humeral torsion was related to the incidence and severity of upper extremity injuries in these athletes. The authors defined a severe injury as those which kept the player out for >30 days. Overall, 11 pitchers were injured during the 2-year study period. There was a strong inverse relationship between torsion and injury severity such that lower degrees of dominant humeral torsion correlated with higher injury severity (P = .005). However, neither throwing arm humeral torsion nor the difference in torsion between throwing and non-throwing humeri were predictive of overall injury incidence. While this is a nonmodifiable risk factor, it is important to understand how the pitcher’s anatomy plays a role in risk of injury.²⁰ Understanding nonmodifiable risk factors may be helpful in the future to risk stratify, prognosticate, and modulate modifiable risk factors such as cumulative work.

Elbow

Injuries to the elbow have become more common in recent years amongst MLB players, although the literature regarding risk factors for elbow injuries is sparse.^4,6 Wilk and colleagues²¹ performed a prospective study to determine if deficits in glenohumeral passive range of motion (ROM) increased the risk of elbow injury in MLB pitchers. Between 2005-2012, the authors measured passive shoulder ROM of both the throwing and non-throwing shoulder of 296 major and minor league pitchers and followed them for a median of 53.4 months. In total, 38 players suffered 49 elbow injuries and required 8 surgeries, accounting for a total of 2551 days spent on the disabled list (DL). GIRD and external rotation insufficiency were not correlated with elbow injuries. However, pitchers with deficits of >5° in total rotation between the throwing and non-throwing shoulders had a 2.6 times greater risk for injury (P = .007) and pitchers with deficits of ≥5° in flexion of the throwing shoulder compared to the non-throwing shoulder had a 2.8 times greater risk for injury (P = .008).²¹ Prior studies have demonstrated trends towards increased elbow injury in professional baseball pitchers with an increase in both elbow valgus torque as well as shoulder external rotation torque; maximum pitch velocity was also shown to be an independent risk factor for elbow injury in professional baseball pitchers.^10,11 These injuries typically occur during the late cocking/early acceleration phase of the pitching cycle, when the shoulder and elbow experience the most significant force of any point in time during a pitch (Figure 2).¹⁷ At our institution, there are several ongoing studies to determine the relative contributions of pitch velocity, number, and type to elbow injury rates. Prospective studies are also ongoing at other institutions.

Shoulder

Shoulder injuries are one of the most common injuries seen in MLB players, specifically pitchers. Similar to the prior study, Wilk and colleagues²² recently performed a prospective study to determine if passive ROM of the glenohumeral joint in MLB pitchers was predictive of shoulder injury or shoulder surgery. As in the previous study, the authors’ measured passive shoulder ROM of the throwing and non-throwing shoulder of 296 major and minor league pitchers during spring training between 2005-2012 and obtained an average follow-up of 48.4 months. The authors found a total of 75 shoulder injuries and 20 surgeries among 51 pitchers (17%) that resulted in 5570 days on the DL. While total rotation deficit, GIRD, and flexion deficit had no relation to shoulder injury or surgery, pitchers with <5° greater external rotation in the throwing shoulder compared to the non-throwing shoulder were more than 2 times more likely to be placed on the DL for a shoulder injury (P = .014) and were 4 times more likely to require shoulder surgery (P = .009).²² The authors concluded that an insufficient side-to-side difference in external rotation of the throwing shoulder increased a pitcher’s likelihood of shoulder injury as well as surgery.

Other

One area that has not received as much attention as repetitive use injuries of the shoulder and elbow is acute collision injuries. Collision injuries include concussions, hyperextension injuries to the knees, shoulder dislocations, fractures of the foot and ankle, and others.²³ Catchers and base runners during scoring plays are at a high risk for collision injury. Recent evidence has shown that catchers average approximately 2.75 collision injuries per 1000 athletic exposures (AE), accounting for an average of 39.1 days on the DL per collision injury.²³ However, despite these collision injuries, catchers spend more time on the DL from non-collision injuries (specifically shoulder injuries requiring surgical intervention), as studies have shown 19 different non-collision injuries that accounted for >100 days on the DL for catchers compared to no collision injuries that caused a catcher to be on the DL for >100 days.²³ The position of catcher is not an independent risk factor for sustaining an injury in MLB players.⁵

Preventative Measures

Given that recent evidence has identified certain modifiable risk factors, largely regarding shoulder ROM, for injuries to MLB pitchers, it stands to reason that by modifying these risk factors, the number of injuries to MLB pitchers can be decreased.^21,22 However, to the authors’ knowledge, there have been no studies in the current literature that have clearly demonstrated the ability to prevent injuries in MLB players. Based on the prior studies, it seems logical that lowering peak pitch velocity and ensuring proper shoulder ROM would help prevent injuries in MLB players, but this remains speculative. Stretching techniques that have been shown to increase posterior shoulder soft tissue flexibility, including sleeper stretches and modified cross-body stretches, as well as closely monitoring ROM may be helpful in modifying these risk factors.^24-26

Although the number of collision injuries is significantly lower than non-collision repetitive use injuries, MLB has implemented rule changes in recent years to prevent injuries to catchers and base runners alike.^23,27 The rule change, which went into effect in 2014, prohibits catchers from blocking home plate unless they are actively fielding the ball or are in possession of the ball. Similarly, base runners are not allowed to deviate from their path to collide with the catcher while attempting to score.²⁷ However, no study has analyzed whether this rule change has decreased the number of collision injuries sustained by MLB catchers, so it is unclear if this rule change has accomplished its goal.

Outcomes Following Injuries

One of the driving forces behind injury prevention in MLB players is to allow players to reach and maintain their full potential while minimizing time missed because of injury. Furthermore, as with any sport, the clinical outcomes and return to sport (RTS) rates for MLB players following injuries, especially injuries requiring surgical intervention, can be improved.^4,28,29 Several studies have evaluated MLB pitchers following UCLR and have shown that over 80% of pitchers are able to RTS following surgery.^4,30 When critically evaluated in multiple statistical parameters upon RTS, these players perform better in some areas and worse in others.^4,30 However, the results following revision UCLR are not as encouraging as those following primary UCLR in MLB pitchers.⁷ Following revision UCLR, only 65% of pitchers were able to RTS, and those who were able to RTS pitched, on average, almost 1 year less than matched controls.⁷ Unfortunately, results following surgeries about the shoulder in MLB players have been worse than those about the elbow. Cohen and colleagues28 reported on 22 MLB players who underwent labral repair of the shoulder and found that only 32% were able to return to the same or higher level following surgery, while over 45% retired from baseball following surgery. Hence, it is imperative these injuries are prevented, as the RTS rate following treatment is less than ideal.

Future Directions

Although a concerted effort has been made over the past several years to mitigate the number of injuries sustained by MLB players, there is still significant room for improvement. New products are in development/early stages of use that attempt to determine when a pitcher begins to show signs of fatigue to allow the coach to remove him from the game. The mTHROW sleeve (Motus Global), currently used by several MLB teams, is an elastic sleeve that is worn by pitchers on their dominant arm. The sleeve approximates torque, velocity, and workload based upon an accelerometer positioned at the medial elbow and sends this information to a smart phone in real time. This technology theoretically allows players to be intensively monitored and thus may prevent injuries to the UCL by preventing pitchers from throwing while fatigued. However, elbow kinematic parameters may not change significantly as pitchers fatigue, which suggests that this strategy may be suboptimal. Trunk mechanics do change as pitchers become fatigued, opening up the possibility for shoulder and elbow injury.^17,31,32 Further products that track hip-to-shoulder separation and trunk fatigue may be necessary to truly lower injury rates. However, no study has proven modifying either parameter leads to a decrease in injury rates.

Conclusion

Injuries to MLB pitchers and position players have become a significant concern over the past several years. Several risk factors for injury have been identified, including loss of shoulder ROM and pitch velocity. Further studies are necessary to determine the effectiveness of modifying these parameters on injury prevention.

Major league baseball (MLB) is one of the most popular sports in the United States, with an average annual viewership of 11 million for the All-Star game and almost 14 million for the World Series.¹ MLB has an average annual revenue of almost $10 billion, while the net worth of all 30 MLB teams combined is estimated at $36 billion; an increase of 48% from 1 year ago.² As the sport continues to grow in popularity and receives more social media coverage, several issues, specifically injuries to its players, have come to the forefront of the news. Injuries to MLB players, specifically pitchers, have become a significant concern in recent years. The active and extended rosters in MLB include 750 and 1200 athletes, respectively, with approximately 360 active spots taken up by pitchers.³ Hence, MLB employs a large number of elite athletes within its organization. It is important to understand not only what injuries are occurring in these athletes, but also how these injuries may be prevented.

Epidemiology

Injuries to MLB players, specifically pitchers, have increased over the past several years.⁴ Between 2005 and 2008, there was an overall increase of 37% in total number of injuries, with more injuries occurring in pitchers than any other position.⁵ While position players are more likely to sustain an injury to the lower extremity, pitchers are more likely to sustain an injury to the upper extremity.⁵ The month with the most injuries to MLB players was April, while the fewest number of injuries occurred in September.⁵ One injury that has been in the spotlight due to its dramatically increasing incidence is tear of the ulnar collateral ligament (UCL). Several studies have shown that the number of pitchers undergoing ulnar collateral ligament reconstruction (UCLR), commonly known as Tommy John surgery, has significantly increased over the past 20 years (Figure 1).^4,6 Between 25% to 33% of all MLB pitchers have undergone UCLR.

While the number of primary UCLR in MLB pitchers has become a significant concern, an even more pressing concern is the number of pitchers undergoing revision UCLR, as this number has increased over the past several years.⁷ Currently, there is some debate as to how to best address the UCL during primary UCLR (graft type, exposure, treatment of the ulnar nerve, and graft fixation methods) because no study has shown one fixation method or graft type to be superior to others. Similarly, no study has definitively proven how to best manage the ulnar nerve (transpose in all patients, only transpose if preoperative symptoms of numbness/tingling, subluxation, etc. exist). Unfortunately, the results following revision UCLR are inferior to those following primary UCLR.^4,7,8 Hence, given this information, it is imperative to both determine and implement strategies aimed at minimizing the need for revision.

Risk Factors for Injury

Although MLB has received more media attention than lower levels of baseball competition, there is relatively sparse evidence surrounding injury risk factors among MLB players. The majority of studies performed have evaluated risk factors for injury in younger baseball athletes (adolescent, high school, and college). The number of athletes at these lower levels sustaining injuries has increased over the past several years as well.⁹ Several large prospective studies have evaluated risk factors for shoulder and elbow injuries in adolescent baseball players. The risk factors include pitching year-round, pitching more than 100 innings per year, high pitch counts, pitching for multiple teams, geography, pitching on consecutive days, pitching while fatigued, breaking pitches, higher elbow valgus torque, pitching with higher velocity, pitching with supraspinatus weakness, and pitching with a glenohumeral internal rotation deficit (GIRD).^10-17 The large majority of these risk factors are essentially part of a pitcher’s cumulative work, which consists of number of games pitched, total pitches thrown, total innings pitched, innings pitched per game, and pitches thrown per game. One prior study has evaluated cumulative work as a predictor for injury in MLB pitchers.¹⁸ While there were several issues with the study methodology, the authors found no correlation between a MLB pitcher’s cumulative work and risk for injury.

Given our current understanding of repetitive microtrauma as the pathophysiology behind these injuries, it remains unclear why cumulative work would be predictive of injury in youth pitchers but not in MLB pitchers.¹⁶ Several potential reasons exist as to why cumulative work may relate to risk of injury in youth pitchers and not MLB pitchers. Achieving MLB status may infer the element of natural selection based on technique and talent that supersedes the effect of “cumulative trauma” in many players. In MLB pitchers, cumulative work is closely monitored. In addition, these players are only playing for a single team and are not pitching competitively year-round, while many youth players play for multiple teams and may pitch year-round. To combat youth injuries, MLB Pitch Smart has developed recommendations on pitch counts and days of rest for pitchers of all age groups (Table).¹⁹ While data do not yet exist to clearly demonstrate the effectiveness of these guidelines, given the risk factors previously mentioned, it seems that these recommendations will show some reduction in youth injuries in years to come.

Some studies have evaluated anatomic variation among pitchers as a risk factor for injury. Polster and colleagues²⁰ performed computed tomography (CT) scans with 3-dimensional reconstructions on the humeri of both the throwing and non-throwing arms of 25 MLB pitchers to determine if humeral torsion was related to the incidence and severity of upper extremity injuries in these athletes. The authors defined a severe injury as those which kept the player out for >30 days. Overall, 11 pitchers were injured during the 2-year study period. There was a strong inverse relationship between torsion and injury severity such that lower degrees of dominant humeral torsion correlated with higher injury severity (P = .005). However, neither throwing arm humeral torsion nor the difference in torsion between throwing and non-throwing humeri were predictive of overall injury incidence. While this is a nonmodifiable risk factor, it is important to understand how the pitcher’s anatomy plays a role in risk of injury.²⁰ Understanding nonmodifiable risk factors may be helpful in the future to risk stratify, prognosticate, and modulate modifiable risk factors such as cumulative work.

Elbow

Injuries to the elbow have become more common in recent years amongst MLB players, although the literature regarding risk factors for elbow injuries is sparse.^4,6 Wilk and colleagues²¹ performed a prospective study to determine if deficits in glenohumeral passive range of motion (ROM) increased the risk of elbow injury in MLB pitchers. Between 2005-2012, the authors measured passive shoulder ROM of both the throwing and non-throwing shoulder of 296 major and minor league pitchers and followed them for a median of 53.4 months. In total, 38 players suffered 49 elbow injuries and required 8 surgeries, accounting for a total of 2551 days spent on the disabled list (DL). GIRD and external rotation insufficiency were not correlated with elbow injuries. However, pitchers with deficits of >5° in total rotation between the throwing and non-throwing shoulders had a 2.6 times greater risk for injury (P = .007) and pitchers with deficits of ≥5° in flexion of the throwing shoulder compared to the non-throwing shoulder had a 2.8 times greater risk for injury (P = .008).²¹ Prior studies have demonstrated trends towards increased elbow injury in professional baseball pitchers with an increase in both elbow valgus torque as well as shoulder external rotation torque; maximum pitch velocity was also shown to be an independent risk factor for elbow injury in professional baseball pitchers.^10,11 These injuries typically occur during the late cocking/early acceleration phase of the pitching cycle, when the shoulder and elbow experience the most significant force of any point in time during a pitch (Figure 2).¹⁷ At our institution, there are several ongoing studies to determine the relative contributions of pitch velocity, number, and type to elbow injury rates. Prospective studies are also ongoing at other institutions.

Shoulder

Shoulder injuries are one of the most common injuries seen in MLB players, specifically pitchers. Similar to the prior study, Wilk and colleagues²² recently performed a prospective study to determine if passive ROM of the glenohumeral joint in MLB pitchers was predictive of shoulder injury or shoulder surgery. As in the previous study, the authors’ measured passive shoulder ROM of the throwing and non-throwing shoulder of 296 major and minor league pitchers during spring training between 2005-2012 and obtained an average follow-up of 48.4 months. The authors found a total of 75 shoulder injuries and 20 surgeries among 51 pitchers (17%) that resulted in 5570 days on the DL. While total rotation deficit, GIRD, and flexion deficit had no relation to shoulder injury or surgery, pitchers with <5° greater external rotation in the throwing shoulder compared to the non-throwing shoulder were more than 2 times more likely to be placed on the DL for a shoulder injury (P = .014) and were 4 times more likely to require shoulder surgery (P = .009).²² The authors concluded that an insufficient side-to-side difference in external rotation of the throwing shoulder increased a pitcher’s likelihood of shoulder injury as well as surgery.

Other

One area that has not received as much attention as repetitive use injuries of the shoulder and elbow is acute collision injuries. Collision injuries include concussions, hyperextension injuries to the knees, shoulder dislocations, fractures of the foot and ankle, and others.²³ Catchers and base runners during scoring plays are at a high risk for collision injury. Recent evidence has shown that catchers average approximately 2.75 collision injuries per 1000 athletic exposures (AE), accounting for an average of 39.1 days on the DL per collision injury.²³ However, despite these collision injuries, catchers spend more time on the DL from non-collision injuries (specifically shoulder injuries requiring surgical intervention), as studies have shown 19 different non-collision injuries that accounted for >100 days on the DL for catchers compared to no collision injuries that caused a catcher to be on the DL for >100 days.²³ The position of catcher is not an independent risk factor for sustaining an injury in MLB players.⁵

Preventative Measures

Given that recent evidence has identified certain modifiable risk factors, largely regarding shoulder ROM, for injuries to MLB pitchers, it stands to reason that by modifying these risk factors, the number of injuries to MLB pitchers can be decreased.^21,22 However, to the authors’ knowledge, there have been no studies in the current literature that have clearly demonstrated the ability to prevent injuries in MLB players. Based on the prior studies, it seems logical that lowering peak pitch velocity and ensuring proper shoulder ROM would help prevent injuries in MLB players, but this remains speculative. Stretching techniques that have been shown to increase posterior shoulder soft tissue flexibility, including sleeper stretches and modified cross-body stretches, as well as closely monitoring ROM may be helpful in modifying these risk factors.^24-26

Although the number of collision injuries is significantly lower than non-collision repetitive use injuries, MLB has implemented rule changes in recent years to prevent injuries to catchers and base runners alike.^23,27 The rule change, which went into effect in 2014, prohibits catchers from blocking home plate unless they are actively fielding the ball or are in possession of the ball. Similarly, base runners are not allowed to deviate from their path to collide with the catcher while attempting to score.²⁷ However, no study has analyzed whether this rule change has decreased the number of collision injuries sustained by MLB catchers, so it is unclear if this rule change has accomplished its goal.

Outcomes Following Injuries

One of the driving forces behind injury prevention in MLB players is to allow players to reach and maintain their full potential while minimizing time missed because of injury. Furthermore, as with any sport, the clinical outcomes and return to sport (RTS) rates for MLB players following injuries, especially injuries requiring surgical intervention, can be improved.^4,28,29 Several studies have evaluated MLB pitchers following UCLR and have shown that over 80% of pitchers are able to RTS following surgery.^4,30 When critically evaluated in multiple statistical parameters upon RTS, these players perform better in some areas and worse in others.^4,30 However, the results following revision UCLR are not as encouraging as those following primary UCLR in MLB pitchers.⁷ Following revision UCLR, only 65% of pitchers were able to RTS, and those who were able to RTS pitched, on average, almost 1 year less than matched controls.⁷ Unfortunately, results following surgeries about the shoulder in MLB players have been worse than those about the elbow. Cohen and colleagues28 reported on 22 MLB players who underwent labral repair of the shoulder and found that only 32% were able to return to the same or higher level following surgery, while over 45% retired from baseball following surgery. Hence, it is imperative these injuries are prevented, as the RTS rate following treatment is less than ideal.

Future Directions

Although a concerted effort has been made over the past several years to mitigate the number of injuries sustained by MLB players, there is still significant room for improvement. New products are in development/early stages of use that attempt to determine when a pitcher begins to show signs of fatigue to allow the coach to remove him from the game. The mTHROW sleeve (Motus Global), currently used by several MLB teams, is an elastic sleeve that is worn by pitchers on their dominant arm. The sleeve approximates torque, velocity, and workload based upon an accelerometer positioned at the medial elbow and sends this information to a smart phone in real time. This technology theoretically allows players to be intensively monitored and thus may prevent injuries to the UCL by preventing pitchers from throwing while fatigued. However, elbow kinematic parameters may not change significantly as pitchers fatigue, which suggests that this strategy may be suboptimal. Trunk mechanics do change as pitchers become fatigued, opening up the possibility for shoulder and elbow injury.^17,31,32 Further products that track hip-to-shoulder separation and trunk fatigue may be necessary to truly lower injury rates. However, no study has proven modifying either parameter leads to a decrease in injury rates.

Conclusion

Injuries to MLB pitchers and position players have become a significant concern over the past several years. Several risk factors for injury have been identified, including loss of shoulder ROM and pitch velocity. Further studies are necessary to determine the effectiveness of modifying these parameters on injury prevention.

Major league baseball (MLB) is one of the most popular sports in the United States, with an average annual viewership of 11 million for the All-Star game and almost 14 million for the World Series.¹ MLB has an average annual revenue of almost $10 billion, while the net worth of all 30 MLB teams combined is estimated at $36 billion; an increase of 48% from 1 year ago.² As the sport continues to grow in popularity and receives more social media coverage, several issues, specifically injuries to its players, have come to the forefront of the news. Injuries to MLB players, specifically pitchers, have become a significant concern in recent years. The active and extended rosters in MLB include 750 and 1200 athletes, respectively, with approximately 360 active spots taken up by pitchers.³ Hence, MLB employs a large number of elite athletes within its organization. It is important to understand not only what injuries are occurring in these athletes, but also how these injuries may be prevented.

Epidemiology

Injuries to MLB players, specifically pitchers, have increased over the past several years.⁴ Between 2005 and 2008, there was an overall increase of 37% in total number of injuries, with more injuries occurring in pitchers than any other position.⁵ While position players are more likely to sustain an injury to the lower extremity, pitchers are more likely to sustain an injury to the upper extremity.⁵ The month with the most injuries to MLB players was April, while the fewest number of injuries occurred in September.⁵ One injury that has been in the spotlight due to its dramatically increasing incidence is tear of the ulnar collateral ligament (UCL). Several studies have shown that the number of pitchers undergoing ulnar collateral ligament reconstruction (UCLR), commonly known as Tommy John surgery, has significantly increased over the past 20 years (Figure 1).^4,6 Between 25% to 33% of all MLB pitchers have undergone UCLR.

While the number of primary UCLR in MLB pitchers has become a significant concern, an even more pressing concern is the number of pitchers undergoing revision UCLR, as this number has increased over the past several years.⁷ Currently, there is some debate as to how to best address the UCL during primary UCLR (graft type, exposure, treatment of the ulnar nerve, and graft fixation methods) because no study has shown one fixation method or graft type to be superior to others. Similarly, no study has definitively proven how to best manage the ulnar nerve (transpose in all patients, only transpose if preoperative symptoms of numbness/tingling, subluxation, etc. exist). Unfortunately, the results following revision UCLR are inferior to those following primary UCLR.^4,7,8 Hence, given this information, it is imperative to both determine and implement strategies aimed at minimizing the need for revision.

Risk Factors for Injury

Although MLB has received more media attention than lower levels of baseball competition, there is relatively sparse evidence surrounding injury risk factors among MLB players. The majority of studies performed have evaluated risk factors for injury in younger baseball athletes (adolescent, high school, and college). The number of athletes at these lower levels sustaining injuries has increased over the past several years as well.⁹ Several large prospective studies have evaluated risk factors for shoulder and elbow injuries in adolescent baseball players. The risk factors include pitching year-round, pitching more than 100 innings per year, high pitch counts, pitching for multiple teams, geography, pitching on consecutive days, pitching while fatigued, breaking pitches, higher elbow valgus torque, pitching with higher velocity, pitching with supraspinatus weakness, and pitching with a glenohumeral internal rotation deficit (GIRD).^10-17 The large majority of these risk factors are essentially part of a pitcher’s cumulative work, which consists of number of games pitched, total pitches thrown, total innings pitched, innings pitched per game, and pitches thrown per game. One prior study has evaluated cumulative work as a predictor for injury in MLB pitchers.¹⁸ While there were several issues with the study methodology, the authors found no correlation between a MLB pitcher’s cumulative work and risk for injury.

Given our current understanding of repetitive microtrauma as the pathophysiology behind these injuries, it remains unclear why cumulative work would be predictive of injury in youth pitchers but not in MLB pitchers.¹⁶ Several potential reasons exist as to why cumulative work may relate to risk of injury in youth pitchers and not MLB pitchers. Achieving MLB status may infer the element of natural selection based on technique and talent that supersedes the effect of “cumulative trauma” in many players. In MLB pitchers, cumulative work is closely monitored. In addition, these players are only playing for a single team and are not pitching competitively year-round, while many youth players play for multiple teams and may pitch year-round. To combat youth injuries, MLB Pitch Smart has developed recommendations on pitch counts and days of rest for pitchers of all age groups (Table).¹⁹ While data do not yet exist to clearly demonstrate the effectiveness of these guidelines, given the risk factors previously mentioned, it seems that these recommendations will show some reduction in youth injuries in years to come.

Some studies have evaluated anatomic variation among pitchers as a risk factor for injury. Polster and colleagues²⁰ performed computed tomography (CT) scans with 3-dimensional reconstructions on the humeri of both the throwing and non-throwing arms of 25 MLB pitchers to determine if humeral torsion was related to the incidence and severity of upper extremity injuries in these athletes. The authors defined a severe injury as those which kept the player out for >30 days. Overall, 11 pitchers were injured during the 2-year study period. There was a strong inverse relationship between torsion and injury severity such that lower degrees of dominant humeral torsion correlated with higher injury severity (P = .005). However, neither throwing arm humeral torsion nor the difference in torsion between throwing and non-throwing humeri were predictive of overall injury incidence. While this is a nonmodifiable risk factor, it is important to understand how the pitcher’s anatomy plays a role in risk of injury.²⁰ Understanding nonmodifiable risk factors may be helpful in the future to risk stratify, prognosticate, and modulate modifiable risk factors such as cumulative work.

Elbow

Injuries to the elbow have become more common in recent years amongst MLB players, although the literature regarding risk factors for elbow injuries is sparse.^4,6 Wilk and colleagues²¹ performed a prospective study to determine if deficits in glenohumeral passive range of motion (ROM) increased the risk of elbow injury in MLB pitchers. Between 2005-2012, the authors measured passive shoulder ROM of both the throwing and non-throwing shoulder of 296 major and minor league pitchers and followed them for a median of 53.4 months. In total, 38 players suffered 49 elbow injuries and required 8 surgeries, accounting for a total of 2551 days spent on the disabled list (DL). GIRD and external rotation insufficiency were not correlated with elbow injuries. However, pitchers with deficits of >5° in total rotation between the throwing and non-throwing shoulders had a 2.6 times greater risk for injury (P = .007) and pitchers with deficits of ≥5° in flexion of the throwing shoulder compared to the non-throwing shoulder had a 2.8 times greater risk for injury (P = .008).²¹ Prior studies have demonstrated trends towards increased elbow injury in professional baseball pitchers with an increase in both elbow valgus torque as well as shoulder external rotation torque; maximum pitch velocity was also shown to be an independent risk factor for elbow injury in professional baseball pitchers.^10,11 These injuries typically occur during the late cocking/early acceleration phase of the pitching cycle, when the shoulder and elbow experience the most significant force of any point in time during a pitch (Figure 2).¹⁷ At our institution, there are several ongoing studies to determine the relative contributions of pitch velocity, number, and type to elbow injury rates. Prospective studies are also ongoing at other institutions.

Shoulder

Shoulder injuries are one of the most common injuries seen in MLB players, specifically pitchers. Similar to the prior study, Wilk and colleagues²² recently performed a prospective study to determine if passive ROM of the glenohumeral joint in MLB pitchers was predictive of shoulder injury or shoulder surgery. As in the previous study, the authors’ measured passive shoulder ROM of the throwing and non-throwing shoulder of 296 major and minor league pitchers during spring training between 2005-2012 and obtained an average follow-up of 48.4 months. The authors found a total of 75 shoulder injuries and 20 surgeries among 51 pitchers (17%) that resulted in 5570 days on the DL. While total rotation deficit, GIRD, and flexion deficit had no relation to shoulder injury or surgery, pitchers with <5° greater external rotation in the throwing shoulder compared to the non-throwing shoulder were more than 2 times more likely to be placed on the DL for a shoulder injury (P = .014) and were 4 times more likely to require shoulder surgery (P = .009).²² The authors concluded that an insufficient side-to-side difference in external rotation of the throwing shoulder increased a pitcher’s likelihood of shoulder injury as well as surgery.

Other

One area that has not received as much attention as repetitive use injuries of the shoulder and elbow is acute collision injuries. Collision injuries include concussions, hyperextension injuries to the knees, shoulder dislocations, fractures of the foot and ankle, and others.²³ Catchers and base runners during scoring plays are at a high risk for collision injury. Recent evidence has shown that catchers average approximately 2.75 collision injuries per 1000 athletic exposures (AE), accounting for an average of 39.1 days on the DL per collision injury.²³ However, despite these collision injuries, catchers spend more time on the DL from non-collision injuries (specifically shoulder injuries requiring surgical intervention), as studies have shown 19 different non-collision injuries that accounted for >100 days on the DL for catchers compared to no collision injuries that caused a catcher to be on the DL for >100 days.²³ The position of catcher is not an independent risk factor for sustaining an injury in MLB players.⁵

Preventative Measures

Given that recent evidence has identified certain modifiable risk factors, largely regarding shoulder ROM, for injuries to MLB pitchers, it stands to reason that by modifying these risk factors, the number of injuries to MLB pitchers can be decreased.^21,22 However, to the authors’ knowledge, there have been no studies in the current literature that have clearly demonstrated the ability to prevent injuries in MLB players. Based on the prior studies, it seems logical that lowering peak pitch velocity and ensuring proper shoulder ROM would help prevent injuries in MLB players, but this remains speculative. Stretching techniques that have been shown to increase posterior shoulder soft tissue flexibility, including sleeper stretches and modified cross-body stretches, as well as closely monitoring ROM may be helpful in modifying these risk factors.^24-26

Although the number of collision injuries is significantly lower than non-collision repetitive use injuries, MLB has implemented rule changes in recent years to prevent injuries to catchers and base runners alike.^23,27 The rule change, which went into effect in 2014, prohibits catchers from blocking home plate unless they are actively fielding the ball or are in possession of the ball. Similarly, base runners are not allowed to deviate from their path to collide with the catcher while attempting to score.²⁷ However, no study has analyzed whether this rule change has decreased the number of collision injuries sustained by MLB catchers, so it is unclear if this rule change has accomplished its goal.

Outcomes Following Injuries

One of the driving forces behind injury prevention in MLB players is to allow players to reach and maintain their full potential while minimizing time missed because of injury. Furthermore, as with any sport, the clinical outcomes and return to sport (RTS) rates for MLB players following injuries, especially injuries requiring surgical intervention, can be improved.^4,28,29 Several studies have evaluated MLB pitchers following UCLR and have shown that over 80% of pitchers are able to RTS following surgery.^4,30 When critically evaluated in multiple statistical parameters upon RTS, these players perform better in some areas and worse in others.^4,30 However, the results following revision UCLR are not as encouraging as those following primary UCLR in MLB pitchers.⁷ Following revision UCLR, only 65% of pitchers were able to RTS, and those who were able to RTS pitched, on average, almost 1 year less than matched controls.⁷ Unfortunately, results following surgeries about the shoulder in MLB players have been worse than those about the elbow. Cohen and colleagues28 reported on 22 MLB players who underwent labral repair of the shoulder and found that only 32% were able to return to the same or higher level following surgery, while over 45% retired from baseball following surgery. Hence, it is imperative these injuries are prevented, as the RTS rate following treatment is less than ideal.

Future Directions

Although a concerted effort has been made over the past several years to mitigate the number of injuries sustained by MLB players, there is still significant room for improvement. New products are in development/early stages of use that attempt to determine when a pitcher begins to show signs of fatigue to allow the coach to remove him from the game. The mTHROW sleeve (Motus Global), currently used by several MLB teams, is an elastic sleeve that is worn by pitchers on their dominant arm. The sleeve approximates torque, velocity, and workload based upon an accelerometer positioned at the medial elbow and sends this information to a smart phone in real time. This technology theoretically allows players to be intensively monitored and thus may prevent injuries to the UCL by preventing pitchers from throwing while fatigued. However, elbow kinematic parameters may not change significantly as pitchers fatigue, which suggests that this strategy may be suboptimal. Trunk mechanics do change as pitchers become fatigued, opening up the possibility for shoulder and elbow injury.^17,31,32 Further products that track hip-to-shoulder separation and trunk fatigue may be necessary to truly lower injury rates. However, no study has proven modifying either parameter leads to a decrease in injury rates.

Conclusion

Injuries to MLB pitchers and position players have become a significant concern over the past several years. Several risk factors for injury have been identified, including loss of shoulder ROM and pitch velocity. Further studies are necessary to determine the effectiveness of modifying these parameters on injury prevention.

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.

Charles Darwin once said that apes “...are quite unable, as I have myself seen, to throw a stone with precision”.¹ Yet humans can throw with precision and speed, a skill that likely had significant advantages: throwing can affect change at a distance—something few species can do. Throwing can provide protection against predators and can allow for predation for food resources. Throwing would be important in contesting other hominids for scarce resources. As such, throwing has been critically important in human evolution and likely is a skill that has been promoted through natural selection.^2-5

In the orthopedic literature, most published work on throwing will ask proximate questions: “how, what, who, when, and where?” Evolutionary biologists are concerned with ultimate questions^6,7: “why?” Asking ultimate questions provides insight into how a behavior might offer advantages under natural selection, which can then improve our understanding of the proximate questions for that behavior.

With regard to the shoulder, a number of mysteries exist that, to date, proximate studies have not been able to solve. This article argues that the human shoulder has evolved for throwing and by using this frame of reference, many of the mysteries surrounding the anatomy of the shoulder can be understood.

Pitching Kinematics

The mechanics of pitching have been analyzed extensively. Fleisig and colleagues⁸ performed kinematic and electromyographic analyses of pitchers to identify the critical moments of pitching (defined as where the forces are highest and injury is most likely going to occur). They found 2 moments where the forces about the shoulder are highest during pitching: the late cocking phase (defined by the point where the humerus reaches maximal external rotation); and the early deceleration phase (defined by the point when the ball is released). If throwing is important in natural selection of humans, then the shoulder anatomy should be optimized to withstand the forces generated in these positions.

Late Cocking Phase of Throwing

The early phases of throwing are attempting to maximize external rotation of the abducted arm as the velocity of the pitched ball correlates to the amount of external rotation achieved.^9-11 In this position, kinetic energy in external rotation is stored and converted into kinetic energy in internal rotation.¹² The position of the shoulder during late cocking is 94 ± 21° of thoracohumeral abduction, 11 ± 11° of horizontal adduction, and a remarkable 165 ± 11° of thoracohumeral external rotation (Figure 1).⁸

Fleisig and colleagues⁸ estimated the torque and forces about the shoulder, which are quite high for joint compression (480 ± 130 N). They also analyzed the shear forces and while trying to describe the origin of superior labrum anterior to posterior (SLAP) lesions and anterior labral tears, broke down the major shear vector into an anterior force vector (310 ± 100 N) and a superior force (250 ± 80 N).⁸ Note that the resulting shear vector is in an anterosuperior direction and is approximately 400 N.

Early Deceleration Phase of Throwing

Interestingly, the position of the humerus during this critical moment of throwing is not much different than the position during the late cocking phase of throwing, with 93 ± 10° of thoracohumeral abduction, 6 ± 8° of horizontal adduction.⁸ The major difference in the position of the arm is found in the amount of thoracohumeral rotation, which is now 64 ± 35° of external rotation (Figure 2).⁸

The forces in early deceleration are tremendous, with an estimated 1090 ± 110 N joint compression force, and an anteroinferior shear force of approximately 130 N.⁸

Clearly, if throwing is an important skill in human evolution, adaptations must exist in the shoulder to withstand the high forces in these 2 critical moments of throwing.

Solving Mysteries of Shoulder Anatomy in the Context of Throwing

There are many anatomic features of the shoulder that remain poorly understood. These include the alignment of the glenohumeral joint, the function of the glenohumeral ligaments, the function of the coracoacromial ligament, the depression of the human greater tuberosity, and the nature and function of the very tendinous subscapularis and long head of the biceps. These mysteries of the human shoulder can be solved if one considers the hypothesis that the shoulder has evolved to throw.

Glenohumeral Joint Alignment

The cartilage of the humeral head is thickest at its center, and thinnest at the periphery (Figure 3A).^13,14 Conversely, the cartilage of the glenoid is thinnest at the fovea and thickest in the periphery (Figure 3B).¹⁴ It seems obvious that in order to maximally distribute high loads across this joint, the center of the humeral head should rest in the center of the glenoid. Interestingly, this does not occur during most positions of the shoulder. When upright, the center of the humeral head is directed above the glenoid in the coronal plane (Figure 3C). In order to align the glenohumeral joint optimally for the distribution of loads across the joint, the humerus must be abducted approximately 60° relative to the scapula. Assuming a 2:1 glenohumeral to scapulothoracic abduction for arm abduction relative to the thorax,¹⁵ this equates to approximately 90° of thoracohumeral abduction—the exact kinematic position of the shoulder during both critical moments of throwing (Figure 3D).

Function of the Glenohumeral Ligaments

The glenohumeral joint capsule has thickenings that help to stabilize the joint. The function of these glenohumeral ligaments has been evaluated biomechanically for their role in preventing translation and instability by a number of authors. The inferior glenohumeral ligament has classically been described as resisting anterior translation of the abducted arm.¹⁶ The coracohumeral ligament has been described as important to prevent inferior translation of the adducted arm.¹⁷

Interestingly, these ligaments are also the most important ligaments in resisting external rotation of the adducted arm.¹⁸ The dominant arm of throwing athletes has been shown to have increased inferior translation¹⁹ and increase external rotation.^19-22 While the external rotation is partly related to bony adaptation,^23,24 the ligamentous restraints to external rotation are likely under tremendous load, which may explain why Dr. Frank Jobe revolutionized the surgical treatment of the throwing athlete by performing an “instability” operation,^25,26 as he believed these athletes had “subtle instability” that produced pain, but not symptoms of looseness.²⁷

While these ligaments may exist in part to prevent translation and instability, current thinking suggests that “over-rotation” may lead to internal impingement and may be responsible for symptoms in the thrower’s shoulder,²⁸ as SLAP lesions seem to occur easier with external rotation.²⁹ Again, the importance of maximizing external rotation in throwing and the finding that this position is a critical moment with very high forces suggests that these ligaments may represent an adaptation to restrain external rotation while throwing.

Coracoacromial Ligament

The coracoacromial ligament is unique in that it connects 2 pieces of the same bone, and is only seen in hominids—not other primates.³⁰ Its function has been debated for decades. This ligament is generally thought to limit superior translation of the humeral head,^31,32 an effect that is critically important in patients with rotator cuff tears ^33,34 Its importance is demonstrated by the fact that it seems to regenerate after it has been resected.^35,36 Yet release or resection of this ligament has been a standard treatment for shoulder pain for decades.

Its function becomes clear if one examines the coracoacromial ligament with respect to the kinematics of throwing. As mentioned above, in the late cocking phase of throwing, tremendous shear forces exist in the shoulder. Fleisig and colleagues8 estimated a superior force of 250 ± 80 N, and an anterior shear force of 310 ± 100 N. While Fleisig and colleagues8 analyzed these shear forces with respect to the development of superior and anterior labral tears, it is important to note that these shear forces are vectors that should be combined. When one does this, it becomes apparent that in the late cocking phase of throwing there is shear force in an anterosuperior direction of approximately 400 N (Figure 1). The coracoacromial ligament is positioned to restrain this tremendous force. If throwing is an important adaptation in the evolution of humans, then the function of this ligament and its importance becomes clear.

Depressed Greater Tuberosity and the Pear-Shaped Glenoid

Compared to other primates, the greater tuberosity in humans sits significantly lower (Figure 4). This depression effectively decreases the moment arm of the muscle tendon unit, making the supraspinatus less powerful for raising the arm.³⁷ In addition, by tenting the supraspinatus tendon over the humeral head, a watershed zone is created with decreased vascularity, which is thought to contribute to rotator cuff disease.³⁸ What would be the advantage of the depressed tuberosity?

In primates, a lower tuberosity allows for more motion, particularly for arboreal travel.³⁷ In order to throw with velocity, the humerus must achieve extremes of external rotation. A large tuberosity would limit external rotation of the abducted arm. Similarly, the pear-shaped glenoid cavity allows for the depressed tuberosity to achieve maximal external rotation. It is conceivable that a depressed greater tuberosity that allows for throwing would be an adaptation that could be favorable despite its proclivity toward rotator cuff disease in senescence.

Nature of the Subscapularis and the Role of the Long Head of the Biceps

The subscapularis is unique among rotator cuff muscles in that the upper two-thirds of the muscle is surprisingly tendinous.³⁹ Why should this rotator cuff muscle have so much tendon material? Why is the tendon missing from the inferior one-third of the muscle? This situation is not optimal to prevent anterior glenohumeral instability, where inferior tendon material would be preferred.⁴⁰

The function of the tendon of the long head of the biceps has long been debated and remains unclear.^41-43 Cadaver experiments suggest the long head of the biceps provides glenohumeral joint stability in a variety of directions and positions, yet in vivo studies may not show this effect. Electromyography studies show little activity of the long head of the biceps with shoulder motion when the elbow is immobilized, leading some to suggest it is important as a passive restraint.⁴³ This lack of understanding has led some to believe the biceps is not important and can be sacrificed without much concern.^42,43

Again, these questions can be answered if one considers them in the context of throwing. At the point of maximal external rotation, the shoulder quickly moves from external rotation to internal rotation. This occurs by converting kinetic energy of external rotation into stored potential energy in the tissues. This energy is then converted into internal rotation. This elastic energy storage is critical for developing the necessary velocities to launch a projectile. While many structures are responsible for storing this energy,¹² the subscapularis and long head of the biceps are particularly important. In fact, these 2 structures are important restraints to external rotation of the abducted arm–and become increasingly important with increased external rotation.^45,46

One can think of the long head of the biceps as a spring (muscle), a cable (the long tendon), and a pulley (the bicipital groove). Similarly, one can consider the subscapularis as a similar structure, with the coracoid process serving as the pulley. In the late cocking phase of throwing, an interesting alignment occurs such that the pulleys (coracoid process and bicipital groove) are on opposite sides of the joint, providing glenohumeral joint stability. This system, with the inferior glenohumeral ligament (which is the primary restraint to external rotation of the abducted arm¹⁸), produces an incredibly stable envelope, preventing the humeral head from over-rotating and translating during the late cocking phase of throwing when the forces about the shoulder are extremely high. Because the muscles serve as springs, this system is also capable of storing kinetic energy during the late cocking phase of throwing and converting it into kinetic energy for internal rotation.

Summary

While throwing is not as critical to survival in today’s culture, the ability to throw was clearly an important adaptation in human evolution. With this in mind, we can approach human anatomy with this perspective, and in fact, many other lines of thinking suggest that throwing was important in the evolution of the hand,⁴⁷ the brain,⁴⁸ bipedalism,⁴⁹ and even human society.⁵⁰ The shoulder was highly influenced through natural selection to promote the throwing skill. With this perspective, many of the mysteries about the shoulder can be answered.

Charles Darwin once said that apes “...are quite unable, as I have myself seen, to throw a stone with precision”.¹ Yet humans can throw with precision and speed, a skill that likely had significant advantages: throwing can affect change at a distance—something few species can do. Throwing can provide protection against predators and can allow for predation for food resources. Throwing would be important in contesting other hominids for scarce resources. As such, throwing has been critically important in human evolution and likely is a skill that has been promoted through natural selection.^2-5

In the orthopedic literature, most published work on throwing will ask proximate questions: “how, what, who, when, and where?” Evolutionary biologists are concerned with ultimate questions^6,7: “why?” Asking ultimate questions provides insight into how a behavior might offer advantages under natural selection, which can then improve our understanding of the proximate questions for that behavior.

With regard to the shoulder, a number of mysteries exist that, to date, proximate studies have not been able to solve. This article argues that the human shoulder has evolved for throwing and by using this frame of reference, many of the mysteries surrounding the anatomy of the shoulder can be understood.

Pitching Kinematics

The mechanics of pitching have been analyzed extensively. Fleisig and colleagues⁸ performed kinematic and electromyographic analyses of pitchers to identify the critical moments of pitching (defined as where the forces are highest and injury is most likely going to occur). They found 2 moments where the forces about the shoulder are highest during pitching: the late cocking phase (defined by the point where the humerus reaches maximal external rotation); and the early deceleration phase (defined by the point when the ball is released). If throwing is important in natural selection of humans, then the shoulder anatomy should be optimized to withstand the forces generated in these positions.

Late Cocking Phase of Throwing

The early phases of throwing are attempting to maximize external rotation of the abducted arm as the velocity of the pitched ball correlates to the amount of external rotation achieved.^9-11 In this position, kinetic energy in external rotation is stored and converted into kinetic energy in internal rotation.¹² The position of the shoulder during late cocking is 94 ± 21° of thoracohumeral abduction, 11 ± 11° of horizontal adduction, and a remarkable 165 ± 11° of thoracohumeral external rotation (Figure 1).⁸

Fleisig and colleagues⁸ estimated the torque and forces about the shoulder, which are quite high for joint compression (480 ± 130 N). They also analyzed the shear forces and while trying to describe the origin of superior labrum anterior to posterior (SLAP) lesions and anterior labral tears, broke down the major shear vector into an anterior force vector (310 ± 100 N) and a superior force (250 ± 80 N).⁸ Note that the resulting shear vector is in an anterosuperior direction and is approximately 400 N.

Early Deceleration Phase of Throwing

Interestingly, the position of the humerus during this critical moment of throwing is not much different than the position during the late cocking phase of throwing, with 93 ± 10° of thoracohumeral abduction, 6 ± 8° of horizontal adduction.⁸ The major difference in the position of the arm is found in the amount of thoracohumeral rotation, which is now 64 ± 35° of external rotation (Figure 2).⁸

The forces in early deceleration are tremendous, with an estimated 1090 ± 110 N joint compression force, and an anteroinferior shear force of approximately 130 N.⁸

Clearly, if throwing is an important skill in human evolution, adaptations must exist in the shoulder to withstand the high forces in these 2 critical moments of throwing.

Solving Mysteries of Shoulder Anatomy in the Context of Throwing

There are many anatomic features of the shoulder that remain poorly understood. These include the alignment of the glenohumeral joint, the function of the glenohumeral ligaments, the function of the coracoacromial ligament, the depression of the human greater tuberosity, and the nature and function of the very tendinous subscapularis and long head of the biceps. These mysteries of the human shoulder can be solved if one considers the hypothesis that the shoulder has evolved to throw.

Glenohumeral Joint Alignment

The cartilage of the humeral head is thickest at its center, and thinnest at the periphery (Figure 3A).^13,14 Conversely, the cartilage of the glenoid is thinnest at the fovea and thickest in the periphery (Figure 3B).¹⁴ It seems obvious that in order to maximally distribute high loads across this joint, the center of the humeral head should rest in the center of the glenoid. Interestingly, this does not occur during most positions of the shoulder. When upright, the center of the humeral head is directed above the glenoid in the coronal plane (Figure 3C). In order to align the glenohumeral joint optimally for the distribution of loads across the joint, the humerus must be abducted approximately 60° relative to the scapula. Assuming a 2:1 glenohumeral to scapulothoracic abduction for arm abduction relative to the thorax,¹⁵ this equates to approximately 90° of thoracohumeral abduction—the exact kinematic position of the shoulder during both critical moments of throwing (Figure 3D).

Function of the Glenohumeral Ligaments

The glenohumeral joint capsule has thickenings that help to stabilize the joint. The function of these glenohumeral ligaments has been evaluated biomechanically for their role in preventing translation and instability by a number of authors. The inferior glenohumeral ligament has classically been described as resisting anterior translation of the abducted arm.¹⁶ The coracohumeral ligament has been described as important to prevent inferior translation of the adducted arm.¹⁷

Interestingly, these ligaments are also the most important ligaments in resisting external rotation of the adducted arm.¹⁸ The dominant arm of throwing athletes has been shown to have increased inferior translation¹⁹ and increase external rotation.^19-22 While the external rotation is partly related to bony adaptation,^23,24 the ligamentous restraints to external rotation are likely under tremendous load, which may explain why Dr. Frank Jobe revolutionized the surgical treatment of the throwing athlete by performing an “instability” operation,^25,26 as he believed these athletes had “subtle instability” that produced pain, but not symptoms of looseness.²⁷

While these ligaments may exist in part to prevent translation and instability, current thinking suggests that “over-rotation” may lead to internal impingement and may be responsible for symptoms in the thrower’s shoulder,²⁸ as SLAP lesions seem to occur easier with external rotation.²⁹ Again, the importance of maximizing external rotation in throwing and the finding that this position is a critical moment with very high forces suggests that these ligaments may represent an adaptation to restrain external rotation while throwing.

Coracoacromial Ligament

The coracoacromial ligament is unique in that it connects 2 pieces of the same bone, and is only seen in hominids—not other primates.³⁰ Its function has been debated for decades. This ligament is generally thought to limit superior translation of the humeral head,^31,32 an effect that is critically important in patients with rotator cuff tears ^33,34 Its importance is demonstrated by the fact that it seems to regenerate after it has been resected.^35,36 Yet release or resection of this ligament has been a standard treatment for shoulder pain for decades.

Its function becomes clear if one examines the coracoacromial ligament with respect to the kinematics of throwing. As mentioned above, in the late cocking phase of throwing, tremendous shear forces exist in the shoulder. Fleisig and colleagues8 estimated a superior force of 250 ± 80 N, and an anterior shear force of 310 ± 100 N. While Fleisig and colleagues8 analyzed these shear forces with respect to the development of superior and anterior labral tears, it is important to note that these shear forces are vectors that should be combined. When one does this, it becomes apparent that in the late cocking phase of throwing there is shear force in an anterosuperior direction of approximately 400 N (Figure 1). The coracoacromial ligament is positioned to restrain this tremendous force. If throwing is an important adaptation in the evolution of humans, then the function of this ligament and its importance becomes clear.

Depressed Greater Tuberosity and the Pear-Shaped Glenoid

Compared to other primates, the greater tuberosity in humans sits significantly lower (Figure 4). This depression effectively decreases the moment arm of the muscle tendon unit, making the supraspinatus less powerful for raising the arm.³⁷ In addition, by tenting the supraspinatus tendon over the humeral head, a watershed zone is created with decreased vascularity, which is thought to contribute to rotator cuff disease.³⁸ What would be the advantage of the depressed tuberosity?

In primates, a lower tuberosity allows for more motion, particularly for arboreal travel.³⁷ In order to throw with velocity, the humerus must achieve extremes of external rotation. A large tuberosity would limit external rotation of the abducted arm. Similarly, the pear-shaped glenoid cavity allows for the depressed tuberosity to achieve maximal external rotation. It is conceivable that a depressed greater tuberosity that allows for throwing would be an adaptation that could be favorable despite its proclivity toward rotator cuff disease in senescence.

Nature of the Subscapularis and the Role of the Long Head of the Biceps

The subscapularis is unique among rotator cuff muscles in that the upper two-thirds of the muscle is surprisingly tendinous.³⁹ Why should this rotator cuff muscle have so much tendon material? Why is the tendon missing from the inferior one-third of the muscle? This situation is not optimal to prevent anterior glenohumeral instability, where inferior tendon material would be preferred.⁴⁰

The function of the tendon of the long head of the biceps has long been debated and remains unclear.^41-43 Cadaver experiments suggest the long head of the biceps provides glenohumeral joint stability in a variety of directions and positions, yet in vivo studies may not show this effect. Electromyography studies show little activity of the long head of the biceps with shoulder motion when the elbow is immobilized, leading some to suggest it is important as a passive restraint.⁴³ This lack of understanding has led some to believe the biceps is not important and can be sacrificed without much concern.^42,43

Again, these questions can be answered if one considers them in the context of throwing. At the point of maximal external rotation, the shoulder quickly moves from external rotation to internal rotation. This occurs by converting kinetic energy of external rotation into stored potential energy in the tissues. This energy is then converted into internal rotation. This elastic energy storage is critical for developing the necessary velocities to launch a projectile. While many structures are responsible for storing this energy,¹² the subscapularis and long head of the biceps are particularly important. In fact, these 2 structures are important restraints to external rotation of the abducted arm–and become increasingly important with increased external rotation.^45,46

One can think of the long head of the biceps as a spring (muscle), a cable (the long tendon), and a pulley (the bicipital groove). Similarly, one can consider the subscapularis as a similar structure, with the coracoid process serving as the pulley. In the late cocking phase of throwing, an interesting alignment occurs such that the pulleys (coracoid process and bicipital groove) are on opposite sides of the joint, providing glenohumeral joint stability. This system, with the inferior glenohumeral ligament (which is the primary restraint to external rotation of the abducted arm¹⁸), produces an incredibly stable envelope, preventing the humeral head from over-rotating and translating during the late cocking phase of throwing when the forces about the shoulder are extremely high. Because the muscles serve as springs, this system is also capable of storing kinetic energy during the late cocking phase of throwing and converting it into kinetic energy for internal rotation.

Summary

While throwing is not as critical to survival in today’s culture, the ability to throw was clearly an important adaptation in human evolution. With this in mind, we can approach human anatomy with this perspective, and in fact, many other lines of thinking suggest that throwing was important in the evolution of the hand,⁴⁷ the brain,⁴⁸ bipedalism,⁴⁹ and even human society.⁵⁰ The shoulder was highly influenced through natural selection to promote the throwing skill. With this perspective, many of the mysteries about the shoulder can be answered.

Charles Darwin once said that apes “...are quite unable, as I have myself seen, to throw a stone with precision”.¹ Yet humans can throw with precision and speed, a skill that likely had significant advantages: throwing can affect change at a distance—something few species can do. Throwing can provide protection against predators and can allow for predation for food resources. Throwing would be important in contesting other hominids for scarce resources. As such, throwing has been critically important in human evolution and likely is a skill that has been promoted through natural selection.^2-5

In the orthopedic literature, most published work on throwing will ask proximate questions: “how, what, who, when, and where?” Evolutionary biologists are concerned with ultimate questions^6,7: “why?” Asking ultimate questions provides insight into how a behavior might offer advantages under natural selection, which can then improve our understanding of the proximate questions for that behavior.

With regard to the shoulder, a number of mysteries exist that, to date, proximate studies have not been able to solve. This article argues that the human shoulder has evolved for throwing and by using this frame of reference, many of the mysteries surrounding the anatomy of the shoulder can be understood.

Pitching Kinematics

The mechanics of pitching have been analyzed extensively. Fleisig and colleagues⁸ performed kinematic and electromyographic analyses of pitchers to identify the critical moments of pitching (defined as where the forces are highest and injury is most likely going to occur). They found 2 moments where the forces about the shoulder are highest during pitching: the late cocking phase (defined by the point where the humerus reaches maximal external rotation); and the early deceleration phase (defined by the point when the ball is released). If throwing is important in natural selection of humans, then the shoulder anatomy should be optimized to withstand the forces generated in these positions.

Late Cocking Phase of Throwing

The early phases of throwing are attempting to maximize external rotation of the abducted arm as the velocity of the pitched ball correlates to the amount of external rotation achieved.^9-11 In this position, kinetic energy in external rotation is stored and converted into kinetic energy in internal rotation.¹² The position of the shoulder during late cocking is 94 ± 21° of thoracohumeral abduction, 11 ± 11° of horizontal adduction, and a remarkable 165 ± 11° of thoracohumeral external rotation (Figure 1).⁸

Fleisig and colleagues⁸ estimated the torque and forces about the shoulder, which are quite high for joint compression (480 ± 130 N). They also analyzed the shear forces and while trying to describe the origin of superior labrum anterior to posterior (SLAP) lesions and anterior labral tears, broke down the major shear vector into an anterior force vector (310 ± 100 N) and a superior force (250 ± 80 N).⁸ Note that the resulting shear vector is in an anterosuperior direction and is approximately 400 N.

Early Deceleration Phase of Throwing

Interestingly, the position of the humerus during this critical moment of throwing is not much different than the position during the late cocking phase of throwing, with 93 ± 10° of thoracohumeral abduction, 6 ± 8° of horizontal adduction.⁸ The major difference in the position of the arm is found in the amount of thoracohumeral rotation, which is now 64 ± 35° of external rotation (Figure 2).⁸

The forces in early deceleration are tremendous, with an estimated 1090 ± 110 N joint compression force, and an anteroinferior shear force of approximately 130 N.⁸

Clearly, if throwing is an important skill in human evolution, adaptations must exist in the shoulder to withstand the high forces in these 2 critical moments of throwing.

Solving Mysteries of Shoulder Anatomy in the Context of Throwing

There are many anatomic features of the shoulder that remain poorly understood. These include the alignment of the glenohumeral joint, the function of the glenohumeral ligaments, the function of the coracoacromial ligament, the depression of the human greater tuberosity, and the nature and function of the very tendinous subscapularis and long head of the biceps. These mysteries of the human shoulder can be solved if one considers the hypothesis that the shoulder has evolved to throw.

Glenohumeral Joint Alignment

The cartilage of the humeral head is thickest at its center, and thinnest at the periphery (Figure 3A).^13,14 Conversely, the cartilage of the glenoid is thinnest at the fovea and thickest in the periphery (Figure 3B).¹⁴ It seems obvious that in order to maximally distribute high loads across this joint, the center of the humeral head should rest in the center of the glenoid. Interestingly, this does not occur during most positions of the shoulder. When upright, the center of the humeral head is directed above the glenoid in the coronal plane (Figure 3C). In order to align the glenohumeral joint optimally for the distribution of loads across the joint, the humerus must be abducted approximately 60° relative to the scapula. Assuming a 2:1 glenohumeral to scapulothoracic abduction for arm abduction relative to the thorax,¹⁵ this equates to approximately 90° of thoracohumeral abduction—the exact kinematic position of the shoulder during both critical moments of throwing (Figure 3D).

Function of the Glenohumeral Ligaments

The glenohumeral joint capsule has thickenings that help to stabilize the joint. The function of these glenohumeral ligaments has been evaluated biomechanically for their role in preventing translation and instability by a number of authors. The inferior glenohumeral ligament has classically been described as resisting anterior translation of the abducted arm.¹⁶ The coracohumeral ligament has been described as important to prevent inferior translation of the adducted arm.¹⁷

Interestingly, these ligaments are also the most important ligaments in resisting external rotation of the adducted arm.¹⁸ The dominant arm of throwing athletes has been shown to have increased inferior translation¹⁹ and increase external rotation.^19-22 While the external rotation is partly related to bony adaptation,^23,24 the ligamentous restraints to external rotation are likely under tremendous load, which may explain why Dr. Frank Jobe revolutionized the surgical treatment of the throwing athlete by performing an “instability” operation,^25,26 as he believed these athletes had “subtle instability” that produced pain, but not symptoms of looseness.²⁷

While these ligaments may exist in part to prevent translation and instability, current thinking suggests that “over-rotation” may lead to internal impingement and may be responsible for symptoms in the thrower’s shoulder,²⁸ as SLAP lesions seem to occur easier with external rotation.²⁹ Again, the importance of maximizing external rotation in throwing and the finding that this position is a critical moment with very high forces suggests that these ligaments may represent an adaptation to restrain external rotation while throwing.

Coracoacromial Ligament

The coracoacromial ligament is unique in that it connects 2 pieces of the same bone, and is only seen in hominids—not other primates.³⁰ Its function has been debated for decades. This ligament is generally thought to limit superior translation of the humeral head,^31,32 an effect that is critically important in patients with rotator cuff tears ^33,34 Its importance is demonstrated by the fact that it seems to regenerate after it has been resected.^35,36 Yet release or resection of this ligament has been a standard treatment for shoulder pain for decades.

Its function becomes clear if one examines the coracoacromial ligament with respect to the kinematics of throwing. As mentioned above, in the late cocking phase of throwing, tremendous shear forces exist in the shoulder. Fleisig and colleagues8 estimated a superior force of 250 ± 80 N, and an anterior shear force of 310 ± 100 N. While Fleisig and colleagues8 analyzed these shear forces with respect to the development of superior and anterior labral tears, it is important to note that these shear forces are vectors that should be combined. When one does this, it becomes apparent that in the late cocking phase of throwing there is shear force in an anterosuperior direction of approximately 400 N (Figure 1). The coracoacromial ligament is positioned to restrain this tremendous force. If throwing is an important adaptation in the evolution of humans, then the function of this ligament and its importance becomes clear.

Depressed Greater Tuberosity and the Pear-Shaped Glenoid

Compared to other primates, the greater tuberosity in humans sits significantly lower (Figure 4). This depression effectively decreases the moment arm of the muscle tendon unit, making the supraspinatus less powerful for raising the arm.³⁷ In addition, by tenting the supraspinatus tendon over the humeral head, a watershed zone is created with decreased vascularity, which is thought to contribute to rotator cuff disease.³⁸ What would be the advantage of the depressed tuberosity?

In primates, a lower tuberosity allows for more motion, particularly for arboreal travel.³⁷ In order to throw with velocity, the humerus must achieve extremes of external rotation. A large tuberosity would limit external rotation of the abducted arm. Similarly, the pear-shaped glenoid cavity allows for the depressed tuberosity to achieve maximal external rotation. It is conceivable that a depressed greater tuberosity that allows for throwing would be an adaptation that could be favorable despite its proclivity toward rotator cuff disease in senescence.

Nature of the Subscapularis and the Role of the Long Head of the Biceps

The subscapularis is unique among rotator cuff muscles in that the upper two-thirds of the muscle is surprisingly tendinous.³⁹ Why should this rotator cuff muscle have so much tendon material? Why is the tendon missing from the inferior one-third of the muscle? This situation is not optimal to prevent anterior glenohumeral instability, where inferior tendon material would be preferred.⁴⁰

The function of the tendon of the long head of the biceps has long been debated and remains unclear.^41-43 Cadaver experiments suggest the long head of the biceps provides glenohumeral joint stability in a variety of directions and positions, yet in vivo studies may not show this effect. Electromyography studies show little activity of the long head of the biceps with shoulder motion when the elbow is immobilized, leading some to suggest it is important as a passive restraint.⁴³ This lack of understanding has led some to believe the biceps is not important and can be sacrificed without much concern.^42,43

Again, these questions can be answered if one considers them in the context of throwing. At the point of maximal external rotation, the shoulder quickly moves from external rotation to internal rotation. This occurs by converting kinetic energy of external rotation into stored potential energy in the tissues. This energy is then converted into internal rotation. This elastic energy storage is critical for developing the necessary velocities to launch a projectile. While many structures are responsible for storing this energy,¹² the subscapularis and long head of the biceps are particularly important. In fact, these 2 structures are important restraints to external rotation of the abducted arm–and become increasingly important with increased external rotation.^45,46

One can think of the long head of the biceps as a spring (muscle), a cable (the long tendon), and a pulley (the bicipital groove). Similarly, one can consider the subscapularis as a similar structure, with the coracoid process serving as the pulley. In the late cocking phase of throwing, an interesting alignment occurs such that the pulleys (coracoid process and bicipital groove) are on opposite sides of the joint, providing glenohumeral joint stability. This system, with the inferior glenohumeral ligament (which is the primary restraint to external rotation of the abducted arm¹⁸), produces an incredibly stable envelope, preventing the humeral head from over-rotating and translating during the late cocking phase of throwing when the forces about the shoulder are extremely high. Because the muscles serve as springs, this system is also capable of storing kinetic energy during the late cocking phase of throwing and converting it into kinetic energy for internal rotation.

Summary

While throwing is not as critical to survival in today’s culture, the ability to throw was clearly an important adaptation in human evolution. With this in mind, we can approach human anatomy with this perspective, and in fact, many other lines of thinking suggest that throwing was important in the evolution of the hand,⁴⁷ the brain,⁴⁸ bipedalism,⁴⁹ and even human society.⁵⁰ The shoulder was highly influenced through natural selection to promote the throwing skill. With this perspective, many of the mysteries about the shoulder can be answered.

Two adequate views of the lower cervical vertebrae are necessary to confirm the 3-dimensional location of any hardware placed during cervical spine fusion. Visualizing the lower cervical vertebrae in 2 planes intraoperatively is often a challenge because the shoulders obstruct the lateral view.¹ Techniques have been described to improve lateral visualization, including gentle traction of the arms via wrist restraints or taping the shoulders down inferiorly.^2,3 These techniques have their inadequacies, including an association with peripheral nerve injury and brachial plexopathy.⁴ In patients with stout necks, these methods may still be insufficient to achieve adequate visualization of the lower cervical vertebrae.

Invasive techniques to improve visualization have also been described. In 1 study, exposure had to be extended cephalad to allow for manual counting of cervical vertebrae when the mid- to lower cervical vertebrae had to be identified in a morbidly obese patient.⁵ More invasive spine procedures are associated with higher rates of complications, increased blood loss, more soft-tissue trauma, and longer hospital stays.⁶ We present a view 30º oblique from horizontal and 30º cephalad from neutral as a variation of the lateral radiograph that improves visualization of the mid- to lower cervical vertebrae. The authors have obtained the patients’ informed written consent for print and electronic publication of these case reports.

Technique

We used either the Smith-Robinson or Cloward approach to the anterior spine. Both techniques use the avascular plane between the medially located esophagus and trachea and the lateral sternocleidomastoid and carotid sheath to approach the anterior cervical spine. Once adequate exposure was achieved, standard anteroposterior and lateral radiographs were obtained to confirm the correct vertebral level. Gentle caudal traction was applied to the patient’s wrist straps, and when visualization continued to be compromised, a view 30º oblique from horizontal and 30º cephalad from neutral was obtained (Figure 1).

Case Series

Case 1

A 54-year-old man with a body mass index (BMI) of 50 presented with neck and bilateral arm pain, with left greater than right radicular symptoms in the C6 and C7 distribution. Magnetic resonance imaging (MRI) showed disc herniations at C5-C6 and C6-C7 with spinal cord signal changes, and he underwent a C5-C6 and C6-C7 anterior cervical discectomy and fusion. Initial localization was determined using a lateral radiograph and vertebral needle. During hardware placement, anteroposterior and lateral fluoroscopic radiographs confirmed adequate placement of the superior screw, but visualization of the inferior portion of the plate and inferior screw was challenging (Figure 2). Our oblique 30º–30º view provided better visualization of the plate and screws in the lower cervical vertebrae than lateral imaging, and allowed confirmation that the hardware was positioned correctly (Figure 3). It took 1 attempt to achieve adequate visualization with the 30º–30º view.

Postoperatively, the patient’s radiculopathy and motor weakness improved. Radiographs confirmed adequate hardware placement, and he was discharged on postoperative day 1 (Figure 4). Imaging at the patient’s 6-week follow-up confirmed adequate fusion from C5-C7, anatomically aligned facet joints, and no hardware failure. The patient’s Neck Disability Index was 31/50 preoperatively and 26/50 at this visit.

Case 2

A 51-year-old man with a BMI of 29 presented with a long-standing history of neck pain and bilateral arm pain left greater than right in the C6 and C7 dermomyotome. MRI showed a broad-based disc herniation with foraminal narrowing at C5-C6 and C6-C7, and the patient underwent a 2-level anterior cervical discectomy and fusion. This patient had pronounced neck musculature, and a deeper than normal incision was required.

Intraoperative lateral fluoroscopy was obtained to confirm the C5-C6 and C6-C7 level prior to discectomy. The musculature of the patient’s neck and shoulder made visualization of the C6-C7 disc space difficult on the lateral radiograph (Figure 5). One attempt was required to obtain the 30º–30º oblique view, which was used to ensure correct placement of the screws and plate (Figure 6).

Postoperatively, the patient’s pain had improved, and radiographs confirmed adequate hardware placement. He was discharged 1 day after surgery (Figure 7). Imaging at the patient’s 6-week follow-up confirmed adequate fusion from C5-C7, stable disc spaces, and anatomically aligned facet joints. His Neck Disability Index was 34/50 preoperatively and 32/50 at 2-week follow-up.

Discussion

The aim of this study was to describe an alternative to the lateral radiograph for imaging the cervical spine in patients with challenging anatomy or in procedures involving hardware placement at the lower cervical vertebrae. Techniques have been developed to assist with improved lateral visualization, including gentle traction of the arms via wrist restraints or taping the shoulders down inferiorly.2,3 However, visualization in 2 planes continues to be a challenge in a subset of patients. It is particularly difficult to obtain adequate lateral radiographs of the cervical spine in patients with stout necks.³ In patients with stout necks, there is more obstruction of the radiography path through the cervical spine. This leads to imaging that is unclear or may fail to show the mid- to lower cervical spine. The extent to which one should rely on the 30º–30º oblique technique for adequate visualization of the cervical spine depends on the anatomy of a particular patient. Historically, it is more challenging to obtain satisfactory lateral radiographs in patients with stout necks,³ and these patients have benefited the most from using the 30º–30º degree oblique view.

Lack of visualization can lead to aborted surgeries or, potentially, surgery at the wrong level.³ A 2008 American Academy of Neurological Surgeons survey indicated that 50% of spine surgeons had performed a wrong-level surgery at least once in their career, and the cervical spine accounted for 21% of all incorrect-level spine surgeries.⁷ Intraoperative factors reported during cases of wrong-level spinal surgeries included misinterpretation of intraoperative imaging, no intraoperative imaging, and unusual anatomy or physical characteristics.⁸ Such complications can lead to revision surgery and other significant morbidities for the patient.

In most patients, fluoroscopy allows confirmation of the correct level before disc incision.³ However, operating at a lower cervical level in a patient with a short neck or prominent shoulders poses a significant problem.³ A case report from Singh and colleagues⁹ described a modified intraoperative fluoroscopic view for spinal level localization at cervicothoracic levels. Their method focuses on identifying the bony lamina and using them as landmarks to count spinal levels, whereas our 30º–30º oblique image is useful for confirmation of adequate hardware placement during anterior cervical spinal fusions. Often, the initial localization of cervical vertebral levels can be achieved with a standard lateral radiograph. We recognized the utility of the 30º–30º oblique view when we were attempting to visualize the inferior aspect of the plate and inferior screw placement.

In patients with stout necks, a lateral radiograph may show only visualization down to C4 or C5.³ Even with applying traction to the arms or taping the shoulders down, it can be impossible to visualize C6, C7, or T1 because the shoulder bones and muscles obstruct the image.³ Using a 30º–30º oblique view, we were able to obtain adequate visualization and assess the accurate placement of hardware.

Conclusion

A 30º oblique view from horizontal and 30º cephalad from neutral radiograph can be used intraoperatively in patients with challenging anatomy to identify placement of hardware at the correct vertebral level in the lower cervical spine. It is a noninvasive technique that can help reduce the risk of wrong-site surgeries without prolonging operation time. This technique describes an alternative to the lateral radiograph and provides a solution to the difficult problem of intraoperative imaging of the mid- to lower cervical spine in 2 adequate planes.

Two adequate views of the lower cervical vertebrae are necessary to confirm the 3-dimensional location of any hardware placed during cervical spine fusion. Visualizing the lower cervical vertebrae in 2 planes intraoperatively is often a challenge because the shoulders obstruct the lateral view.¹ Techniques have been described to improve lateral visualization, including gentle traction of the arms via wrist restraints or taping the shoulders down inferiorly.^2,3 These techniques have their inadequacies, including an association with peripheral nerve injury and brachial plexopathy.⁴ In patients with stout necks, these methods may still be insufficient to achieve adequate visualization of the lower cervical vertebrae.

Invasive techniques to improve visualization have also been described. In 1 study, exposure had to be extended cephalad to allow for manual counting of cervical vertebrae when the mid- to lower cervical vertebrae had to be identified in a morbidly obese patient.⁵ More invasive spine procedures are associated with higher rates of complications, increased blood loss, more soft-tissue trauma, and longer hospital stays.⁶ We present a view 30º oblique from horizontal and 30º cephalad from neutral as a variation of the lateral radiograph that improves visualization of the mid- to lower cervical vertebrae. The authors have obtained the patients’ informed written consent for print and electronic publication of these case reports.

Technique

We used either the Smith-Robinson or Cloward approach to the anterior spine. Both techniques use the avascular plane between the medially located esophagus and trachea and the lateral sternocleidomastoid and carotid sheath to approach the anterior cervical spine. Once adequate exposure was achieved, standard anteroposterior and lateral radiographs were obtained to confirm the correct vertebral level. Gentle caudal traction was applied to the patient’s wrist straps, and when visualization continued to be compromised, a view 30º oblique from horizontal and 30º cephalad from neutral was obtained (Figure 1).

Case Series

Case 1

A 54-year-old man with a body mass index (BMI) of 50 presented with neck and bilateral arm pain, with left greater than right radicular symptoms in the C6 and C7 distribution. Magnetic resonance imaging (MRI) showed disc herniations at C5-C6 and C6-C7 with spinal cord signal changes, and he underwent a C5-C6 and C6-C7 anterior cervical discectomy and fusion. Initial localization was determined using a lateral radiograph and vertebral needle. During hardware placement, anteroposterior and lateral fluoroscopic radiographs confirmed adequate placement of the superior screw, but visualization of the inferior portion of the plate and inferior screw was challenging (Figure 2). Our oblique 30º–30º view provided better visualization of the plate and screws in the lower cervical vertebrae than lateral imaging, and allowed confirmation that the hardware was positioned correctly (Figure 3). It took 1 attempt to achieve adequate visualization with the 30º–30º view.

Postoperatively, the patient’s radiculopathy and motor weakness improved. Radiographs confirmed adequate hardware placement, and he was discharged on postoperative day 1 (Figure 4). Imaging at the patient’s 6-week follow-up confirmed adequate fusion from C5-C7, anatomically aligned facet joints, and no hardware failure. The patient’s Neck Disability Index was 31/50 preoperatively and 26/50 at this visit.

Case 2

A 51-year-old man with a BMI of 29 presented with a long-standing history of neck pain and bilateral arm pain left greater than right in the C6 and C7 dermomyotome. MRI showed a broad-based disc herniation with foraminal narrowing at C5-C6 and C6-C7, and the patient underwent a 2-level anterior cervical discectomy and fusion. This patient had pronounced neck musculature, and a deeper than normal incision was required.

Intraoperative lateral fluoroscopy was obtained to confirm the C5-C6 and C6-C7 level prior to discectomy. The musculature of the patient’s neck and shoulder made visualization of the C6-C7 disc space difficult on the lateral radiograph (Figure 5). One attempt was required to obtain the 30º–30º oblique view, which was used to ensure correct placement of the screws and plate (Figure 6).

Postoperatively, the patient’s pain had improved, and radiographs confirmed adequate hardware placement. He was discharged 1 day after surgery (Figure 7). Imaging at the patient’s 6-week follow-up confirmed adequate fusion from C5-C7, stable disc spaces, and anatomically aligned facet joints. His Neck Disability Index was 34/50 preoperatively and 32/50 at 2-week follow-up.

Discussion

The aim of this study was to describe an alternative to the lateral radiograph for imaging the cervical spine in patients with challenging anatomy or in procedures involving hardware placement at the lower cervical vertebrae. Techniques have been developed to assist with improved lateral visualization, including gentle traction of the arms via wrist restraints or taping the shoulders down inferiorly.2,3 However, visualization in 2 planes continues to be a challenge in a subset of patients. It is particularly difficult to obtain adequate lateral radiographs of the cervical spine in patients with stout necks.³ In patients with stout necks, there is more obstruction of the radiography path through the cervical spine. This leads to imaging that is unclear or may fail to show the mid- to lower cervical spine. The extent to which one should rely on the 30º–30º oblique technique for adequate visualization of the cervical spine depends on the anatomy of a particular patient. Historically, it is more challenging to obtain satisfactory lateral radiographs in patients with stout necks,³ and these patients have benefited the most from using the 30º–30º degree oblique view.

Lack of visualization can lead to aborted surgeries or, potentially, surgery at the wrong level.³ A 2008 American Academy of Neurological Surgeons survey indicated that 50% of spine surgeons had performed a wrong-level surgery at least once in their career, and the cervical spine accounted for 21% of all incorrect-level spine surgeries.⁷ Intraoperative factors reported during cases of wrong-level spinal surgeries included misinterpretation of intraoperative imaging, no intraoperative imaging, and unusual anatomy or physical characteristics.⁸ Such complications can lead to revision surgery and other significant morbidities for the patient.

In most patients, fluoroscopy allows confirmation of the correct level before disc incision.³ However, operating at a lower cervical level in a patient with a short neck or prominent shoulders poses a significant problem.³ A case report from Singh and colleagues⁹ described a modified intraoperative fluoroscopic view for spinal level localization at cervicothoracic levels. Their method focuses on identifying the bony lamina and using them as landmarks to count spinal levels, whereas our 30º–30º oblique image is useful for confirmation of adequate hardware placement during anterior cervical spinal fusions. Often, the initial localization of cervical vertebral levels can be achieved with a standard lateral radiograph. We recognized the utility of the 30º–30º oblique view when we were attempting to visualize the inferior aspect of the plate and inferior screw placement.

In patients with stout necks, a lateral radiograph may show only visualization down to C4 or C5.³ Even with applying traction to the arms or taping the shoulders down, it can be impossible to visualize C6, C7, or T1 because the shoulder bones and muscles obstruct the image.³ Using a 30º–30º oblique view, we were able to obtain adequate visualization and assess the accurate placement of hardware.

Conclusion

A 30º oblique view from horizontal and 30º cephalad from neutral radiograph can be used intraoperatively in patients with challenging anatomy to identify placement of hardware at the correct vertebral level in the lower cervical spine. It is a noninvasive technique that can help reduce the risk of wrong-site surgeries without prolonging operation time. This technique describes an alternative to the lateral radiograph and provides a solution to the difficult problem of intraoperative imaging of the mid- to lower cervical spine in 2 adequate planes.

Two adequate views of the lower cervical vertebrae are necessary to confirm the 3-dimensional location of any hardware placed during cervical spine fusion. Visualizing the lower cervical vertebrae in 2 planes intraoperatively is often a challenge because the shoulders obstruct the lateral view.¹ Techniques have been described to improve lateral visualization, including gentle traction of the arms via wrist restraints or taping the shoulders down inferiorly.^2,3 These techniques have their inadequacies, including an association with peripheral nerve injury and brachial plexopathy.⁴ In patients with stout necks, these methods may still be insufficient to achieve adequate visualization of the lower cervical vertebrae.

Invasive techniques to improve visualization have also been described. In 1 study, exposure had to be extended cephalad to allow for manual counting of cervical vertebrae when the mid- to lower cervical vertebrae had to be identified in a morbidly obese patient.⁵ More invasive spine procedures are associated with higher rates of complications, increased blood loss, more soft-tissue trauma, and longer hospital stays.⁶ We present a view 30º oblique from horizontal and 30º cephalad from neutral as a variation of the lateral radiograph that improves visualization of the mid- to lower cervical vertebrae. The authors have obtained the patients’ informed written consent for print and electronic publication of these case reports.

Technique

We used either the Smith-Robinson or Cloward approach to the anterior spine. Both techniques use the avascular plane between the medially located esophagus and trachea and the lateral sternocleidomastoid and carotid sheath to approach the anterior cervical spine. Once adequate exposure was achieved, standard anteroposterior and lateral radiographs were obtained to confirm the correct vertebral level. Gentle caudal traction was applied to the patient’s wrist straps, and when visualization continued to be compromised, a view 30º oblique from horizontal and 30º cephalad from neutral was obtained (Figure 1).

Case Series

Case 1

A 54-year-old man with a body mass index (BMI) of 50 presented with neck and bilateral arm pain, with left greater than right radicular symptoms in the C6 and C7 distribution. Magnetic resonance imaging (MRI) showed disc herniations at C5-C6 and C6-C7 with spinal cord signal changes, and he underwent a C5-C6 and C6-C7 anterior cervical discectomy and fusion. Initial localization was determined using a lateral radiograph and vertebral needle. During hardware placement, anteroposterior and lateral fluoroscopic radiographs confirmed adequate placement of the superior screw, but visualization of the inferior portion of the plate and inferior screw was challenging (Figure 2). Our oblique 30º–30º view provided better visualization of the plate and screws in the lower cervical vertebrae than lateral imaging, and allowed confirmation that the hardware was positioned correctly (Figure 3). It took 1 attempt to achieve adequate visualization with the 30º–30º view.

Postoperatively, the patient’s radiculopathy and motor weakness improved. Radiographs confirmed adequate hardware placement, and he was discharged on postoperative day 1 (Figure 4). Imaging at the patient’s 6-week follow-up confirmed adequate fusion from C5-C7, anatomically aligned facet joints, and no hardware failure. The patient’s Neck Disability Index was 31/50 preoperatively and 26/50 at this visit.

Case 2

A 51-year-old man with a BMI of 29 presented with a long-standing history of neck pain and bilateral arm pain left greater than right in the C6 and C7 dermomyotome. MRI showed a broad-based disc herniation with foraminal narrowing at C5-C6 and C6-C7, and the patient underwent a 2-level anterior cervical discectomy and fusion. This patient had pronounced neck musculature, and a deeper than normal incision was required.

Intraoperative lateral fluoroscopy was obtained to confirm the C5-C6 and C6-C7 level prior to discectomy. The musculature of the patient’s neck and shoulder made visualization of the C6-C7 disc space difficult on the lateral radiograph (Figure 5). One attempt was required to obtain the 30º–30º oblique view, which was used to ensure correct placement of the screws and plate (Figure 6).

Postoperatively, the patient’s pain had improved, and radiographs confirmed adequate hardware placement. He was discharged 1 day after surgery (Figure 7). Imaging at the patient’s 6-week follow-up confirmed adequate fusion from C5-C7, stable disc spaces, and anatomically aligned facet joints. His Neck Disability Index was 34/50 preoperatively and 32/50 at 2-week follow-up.

Discussion

The aim of this study was to describe an alternative to the lateral radiograph for imaging the cervical spine in patients with challenging anatomy or in procedures involving hardware placement at the lower cervical vertebrae. Techniques have been developed to assist with improved lateral visualization, including gentle traction of the arms via wrist restraints or taping the shoulders down inferiorly.2,3 However, visualization in 2 planes continues to be a challenge in a subset of patients. It is particularly difficult to obtain adequate lateral radiographs of the cervical spine in patients with stout necks.³ In patients with stout necks, there is more obstruction of the radiography path through the cervical spine. This leads to imaging that is unclear or may fail to show the mid- to lower cervical spine. The extent to which one should rely on the 30º–30º oblique technique for adequate visualization of the cervical spine depends on the anatomy of a particular patient. Historically, it is more challenging to obtain satisfactory lateral radiographs in patients with stout necks,³ and these patients have benefited the most from using the 30º–30º degree oblique view.

Lack of visualization can lead to aborted surgeries or, potentially, surgery at the wrong level.³ A 2008 American Academy of Neurological Surgeons survey indicated that 50% of spine surgeons had performed a wrong-level surgery at least once in their career, and the cervical spine accounted for 21% of all incorrect-level spine surgeries.⁷ Intraoperative factors reported during cases of wrong-level spinal surgeries included misinterpretation of intraoperative imaging, no intraoperative imaging, and unusual anatomy or physical characteristics.⁸ Such complications can lead to revision surgery and other significant morbidities for the patient.

In most patients, fluoroscopy allows confirmation of the correct level before disc incision.³ However, operating at a lower cervical level in a patient with a short neck or prominent shoulders poses a significant problem.³ A case report from Singh and colleagues⁹ described a modified intraoperative fluoroscopic view for spinal level localization at cervicothoracic levels. Their method focuses on identifying the bony lamina and using them as landmarks to count spinal levels, whereas our 30º–30º oblique image is useful for confirmation of adequate hardware placement during anterior cervical spinal fusions. Often, the initial localization of cervical vertebral levels can be achieved with a standard lateral radiograph. We recognized the utility of the 30º–30º oblique view when we were attempting to visualize the inferior aspect of the plate and inferior screw placement.

In patients with stout necks, a lateral radiograph may show only visualization down to C4 or C5.³ Even with applying traction to the arms or taping the shoulders down, it can be impossible to visualize C6, C7, or T1 because the shoulder bones and muscles obstruct the image.³ Using a 30º–30º oblique view, we were able to obtain adequate visualization and assess the accurate placement of hardware.

Conclusion

A 30º oblique view from horizontal and 30º cephalad from neutral radiograph can be used intraoperatively in patients with challenging anatomy to identify placement of hardware at the correct vertebral level in the lower cervical spine. It is a noninvasive technique that can help reduce the risk of wrong-site surgeries without prolonging operation time. This technique describes an alternative to the lateral radiograph and provides a solution to the difficult problem of intraoperative imaging of the mid- to lower cervical spine in 2 adequate planes.

Rotator cuff disease is extremely common, yet indications for surgery are not well established. Unfortunately, data on the natural history of patients with rotator cuff disease are lacking, as are high-level studies evaluating the effectiveness of rotator cuff repair. This deficit is highlighted by the recent American Academy of Orthopaedic Surgeons clinical practice guideline on optimizing the management of rotator cuff problems,¹ in which none of the position statements were based on high-level evidence, and 22 of 25 statements were inconclusive or based on weak evidence or represented the panel’s consensus opinion. Although the traditional teaching is that rotator cuff tears (RCTs) should be surgically repaired, the present article reviews the evidence supporting physical therapy as a treatment for atraumatic full-thickness RCTs.

1. Less than 5% of people with RCTs undergo surgery

Studies on symptomatic and asymptomatic patients have found a high incidence of RCTs in the population at large.^2,3 By conservative estimate, 10% of people older than 65 years have full-thickness RCTs. Therefore, the 2010 US Census⁴ finding of 57 million people over age 65 years translates to 5.7 million with full-thickness RCTs. In the United States, about 275,000 rotator cuff surgeries are performed annually.⁵ That is, less than 5% of people with RCTs undergo surgery each year.

2. Symptoms do not correlate well with RCT severity

Pain is statistically more likely in patients who experience RCT progression than in those who do not.^6-8 However, RCTs may progress without pain, or there may be pain without progression, making pain a poor sign of RCT progression.⁹ The Multicenter Orthopaedic Outcome Network (MOON) Shoulder Group, studying a cohort of patients with atraumatic full-thickness RCTs, found no relationship between RCT severity and pain,¹⁰ symptom duration,¹¹ or activity level,¹² suggesting the relationship between RCTs and symptoms is not robust.

3. The high failure rates of surgical repairs do not affect patient-reported outcomes

Postoperative imaging has demonstrated high failure rates for rotator cuff repairs, yet patient-reported outcome scores do not differ between cases of intact and failed repairs.^13,14 Strength is better, however, in intact repairs.¹⁴

4. Physical therapy is effective in treating atraumatic RCTs

The MOON Shoulder Group conducted a prospective cohort study to determine the predictors of failed physical therapy for atraumatic full-thickness RCTs and to help define the indications for rotator cuff surgery.¹⁵ All enrolled patients started with a well-defined physical therapy program, and they could opt out and have surgery at any time. The physical therapy program, derived from a systematic review of the literature, was found to be effective in more than 80% of patients with follow-up of 2 years or longer.¹⁵ The most important predictor of failed nonoperative treatment was patient expectations: For a patient who thought physical therapy would work, it worked; for a patient who thought it would not work, surgery was the more likely choice. No measure of pain or RCT severity predicted the need for surgery.¹⁶ For 2 randomized trials that compared surgery and physical therapy, the success of nonoperative treatment was similar: 76% (Moosmayer and colleagues¹⁷) and 92% (Kukkonen and colleagues¹⁸).

5. What are the indications for surgery?

These data suggest that physical therapy is reasonable for patients with atraumatic RCTs. Some data suggest that traumatic RCTs should be treated with surgery and that it should be performed early.¹⁹ Other data suggest strength is better after rotator cuff repair.^13,14 What, then, are the indications for surgery? Patients with acute tears probably should have surgery; patients concerned about weakness should consider surgery but should keep in mind that its benefit depends on an intact rotator cuff repair; and patients with low expectations about the effectiveness of physical therapy probably should consider surgery.     

When discussing options with a patient, you might approach informed consent as follows:         

“Mr. Smith, you have a rotator cuff tear. So do at least 6 million other Americans over age 60 years. Only 5% of those undergo surgery. If your problem is weakness or functional loss, you should have surgery, though there is about a 30% chance the repair will fail. I don’t know how to predict the outcome of repair yet, but I worry your atraumatic tear is at risk for repair failure.

“If your problem is pain, you have an 80% chance of improving with physical therapy, and pain relief seems to last at least 2 years. If you go with physical therapy, however, there is a risk your tear could progress and start causing symptoms. I don’t yet know how likely it is your tear will progress or, if it does progress, how likely it is the tear will cause symptoms. I wish we had better information to help you make your decision.”

Rotator cuff disease is extremely common, yet indications for surgery are not well established. Unfortunately, data on the natural history of patients with rotator cuff disease are lacking, as are high-level studies evaluating the effectiveness of rotator cuff repair. This deficit is highlighted by the recent American Academy of Orthopaedic Surgeons clinical practice guideline on optimizing the management of rotator cuff problems,¹ in which none of the position statements were based on high-level evidence, and 22 of 25 statements were inconclusive or based on weak evidence or represented the panel’s consensus opinion. Although the traditional teaching is that rotator cuff tears (RCTs) should be surgically repaired, the present article reviews the evidence supporting physical therapy as a treatment for atraumatic full-thickness RCTs.

1. Less than 5% of people with RCTs undergo surgery

Studies on symptomatic and asymptomatic patients have found a high incidence of RCTs in the population at large.^2,3 By conservative estimate, 10% of people older than 65 years have full-thickness RCTs. Therefore, the 2010 US Census⁴ finding of 57 million people over age 65 years translates to 5.7 million with full-thickness RCTs. In the United States, about 275,000 rotator cuff surgeries are performed annually.⁵ That is, less than 5% of people with RCTs undergo surgery each year.

2. Symptoms do not correlate well with RCT severity

Pain is statistically more likely in patients who experience RCT progression than in those who do not.^6-8 However, RCTs may progress without pain, or there may be pain without progression, making pain a poor sign of RCT progression.⁹ The Multicenter Orthopaedic Outcome Network (MOON) Shoulder Group, studying a cohort of patients with atraumatic full-thickness RCTs, found no relationship between RCT severity and pain,¹⁰ symptom duration,¹¹ or activity level,¹² suggesting the relationship between RCTs and symptoms is not robust.

3. The high failure rates of surgical repairs do not affect patient-reported outcomes

Postoperative imaging has demonstrated high failure rates for rotator cuff repairs, yet patient-reported outcome scores do not differ between cases of intact and failed repairs.^13,14 Strength is better, however, in intact repairs.¹⁴

4. Physical therapy is effective in treating atraumatic RCTs

The MOON Shoulder Group conducted a prospective cohort study to determine the predictors of failed physical therapy for atraumatic full-thickness RCTs and to help define the indications for rotator cuff surgery.¹⁵ All enrolled patients started with a well-defined physical therapy program, and they could opt out and have surgery at any time. The physical therapy program, derived from a systematic review of the literature, was found to be effective in more than 80% of patients with follow-up of 2 years or longer.¹⁵ The most important predictor of failed nonoperative treatment was patient expectations: For a patient who thought physical therapy would work, it worked; for a patient who thought it would not work, surgery was the more likely choice. No measure of pain or RCT severity predicted the need for surgery.¹⁶ For 2 randomized trials that compared surgery and physical therapy, the success of nonoperative treatment was similar: 76% (Moosmayer and colleagues¹⁷) and 92% (Kukkonen and colleagues¹⁸).

5. What are the indications for surgery?

These data suggest that physical therapy is reasonable for patients with atraumatic RCTs. Some data suggest that traumatic RCTs should be treated with surgery and that it should be performed early.¹⁹ Other data suggest strength is better after rotator cuff repair.^13,14 What, then, are the indications for surgery? Patients with acute tears probably should have surgery; patients concerned about weakness should consider surgery but should keep in mind that its benefit depends on an intact rotator cuff repair; and patients with low expectations about the effectiveness of physical therapy probably should consider surgery.     

When discussing options with a patient, you might approach informed consent as follows:         

“Mr. Smith, you have a rotator cuff tear. So do at least 6 million other Americans over age 60 years. Only 5% of those undergo surgery. If your problem is weakness or functional loss, you should have surgery, though there is about a 30% chance the repair will fail. I don’t know how to predict the outcome of repair yet, but I worry your atraumatic tear is at risk for repair failure.

“If your problem is pain, you have an 80% chance of improving with physical therapy, and pain relief seems to last at least 2 years. If you go with physical therapy, however, there is a risk your tear could progress and start causing symptoms. I don’t yet know how likely it is your tear will progress or, if it does progress, how likely it is the tear will cause symptoms. I wish we had better information to help you make your decision.”

Rotator cuff disease is extremely common, yet indications for surgery are not well established. Unfortunately, data on the natural history of patients with rotator cuff disease are lacking, as are high-level studies evaluating the effectiveness of rotator cuff repair. This deficit is highlighted by the recent American Academy of Orthopaedic Surgeons clinical practice guideline on optimizing the management of rotator cuff problems,¹ in which none of the position statements were based on high-level evidence, and 22 of 25 statements were inconclusive or based on weak evidence or represented the panel’s consensus opinion. Although the traditional teaching is that rotator cuff tears (RCTs) should be surgically repaired, the present article reviews the evidence supporting physical therapy as a treatment for atraumatic full-thickness RCTs.

1. Less than 5% of people with RCTs undergo surgery

Studies on symptomatic and asymptomatic patients have found a high incidence of RCTs in the population at large.^2,3 By conservative estimate, 10% of people older than 65 years have full-thickness RCTs. Therefore, the 2010 US Census⁴ finding of 57 million people over age 65 years translates to 5.7 million with full-thickness RCTs. In the United States, about 275,000 rotator cuff surgeries are performed annually.⁵ That is, less than 5% of people with RCTs undergo surgery each year.

2. Symptoms do not correlate well with RCT severity

Pain is statistically more likely in patients who experience RCT progression than in those who do not.^6-8 However, RCTs may progress without pain, or there may be pain without progression, making pain a poor sign of RCT progression.⁹ The Multicenter Orthopaedic Outcome Network (MOON) Shoulder Group, studying a cohort of patients with atraumatic full-thickness RCTs, found no relationship between RCT severity and pain,¹⁰ symptom duration,¹¹ or activity level,¹² suggesting the relationship between RCTs and symptoms is not robust.

3. The high failure rates of surgical repairs do not affect patient-reported outcomes

Postoperative imaging has demonstrated high failure rates for rotator cuff repairs, yet patient-reported outcome scores do not differ between cases of intact and failed repairs.^13,14 Strength is better, however, in intact repairs.¹⁴

4. Physical therapy is effective in treating atraumatic RCTs

The MOON Shoulder Group conducted a prospective cohort study to determine the predictors of failed physical therapy for atraumatic full-thickness RCTs and to help define the indications for rotator cuff surgery.¹⁵ All enrolled patients started with a well-defined physical therapy program, and they could opt out and have surgery at any time. The physical therapy program, derived from a systematic review of the literature, was found to be effective in more than 80% of patients with follow-up of 2 years or longer.¹⁵ The most important predictor of failed nonoperative treatment was patient expectations: For a patient who thought physical therapy would work, it worked; for a patient who thought it would not work, surgery was the more likely choice. No measure of pain or RCT severity predicted the need for surgery.¹⁶ For 2 randomized trials that compared surgery and physical therapy, the success of nonoperative treatment was similar: 76% (Moosmayer and colleagues¹⁷) and 92% (Kukkonen and colleagues¹⁸).

5. What are the indications for surgery?

These data suggest that physical therapy is reasonable for patients with atraumatic RCTs. Some data suggest that traumatic RCTs should be treated with surgery and that it should be performed early.¹⁹ Other data suggest strength is better after rotator cuff repair.^13,14 What, then, are the indications for surgery? Patients with acute tears probably should have surgery; patients concerned about weakness should consider surgery but should keep in mind that its benefit depends on an intact rotator cuff repair; and patients with low expectations about the effectiveness of physical therapy probably should consider surgery.     

When discussing options with a patient, you might approach informed consent as follows:         

“Mr. Smith, you have a rotator cuff tear. So do at least 6 million other Americans over age 60 years. Only 5% of those undergo surgery. If your problem is weakness or functional loss, you should have surgery, though there is about a 30% chance the repair will fail. I don’t know how to predict the outcome of repair yet, but I worry your atraumatic tear is at risk for repair failure.

“If your problem is pain, you have an 80% chance of improving with physical therapy, and pain relief seems to last at least 2 years. If you go with physical therapy, however, there is a risk your tear could progress and start causing symptoms. I don’t yet know how likely it is your tear will progress or, if it does progress, how likely it is the tear will cause symptoms. I wish we had better information to help you make your decision.”

Compression of the ulnar nerve at the elbow, also referred to as cubital tunnel syndrome (CuTS), is the second most common peripheral nerve compression syndrome in the upper extremity.^1,2 Although the ulnar nerve can be compressed at 5 different sites, including arcade of Struthers, medial intermuscular septum, medial epicondyle, and deep flexor aponeurosis, the cubital tunnel is most commonly affected.³ Patients typically present with paresthesias in the fourth and fifth digits and weakness of hand muscle intrinsics. Activity-related pain or pain at the medial elbow can also occur in more advanced pathology.⁴ It is estimated that conservative therapy fails and surgical intervention is required in up to 30% of patients with CuTS.¹ Surgical approaches range from in situ decompression to transposition techniques, but there is no consensus in the orthopedic community as to which technique offers the best results. In a 2008 meta-analysis, Macadam and colleagues⁵ found no statistical differences in outcomes among the various surgical approaches. Nevertheless, subcutaneous transposition of the ulnar nerve at the elbow is a popular option.⁶

Despite the widespread success of surgical intervention for CuTS, persistent or recurrent pain occurs in 9.9% to 21.0% of cases.^7-10 In addition, several investigators have cited perineural scarring as a major cause of recurrent symptoms after primary surgery.^11-14 Filippi and colleagues¹¹ noted that patients who required reoperation after primary anterior transposition had “serious epineural fibrosis and fibrosis around the transposed ulnar nerve.” At our institution, we have similarly found that scarring of the fascial sling around the ulnar nerve led to recurrence of CuTS within 4 months after initial surgery (Figure 1).

We therefore prefer to use a vascularized adipose flap to secure the anteriorly transposed ulnar nerve. This flap provides a pliable, vascularized adipose environment for the nerve, which helps reduce nerve adherence and may enhance nerve recovery.¹⁵ In the study reported here, we retrospectively reviewed the long-term outcomes of ulnar nerve anterior subcutaneous transposition secured with either an adipose flap or a fascial sling. We hypothesized that patients in the 2 groups (adipose flap, fascial sling) would have equivalent outcomes.

Materials and Methods

After obtaining institutional review board approval, we reviewed the medical and surgical records of 104 patients (107 limbs) who underwent transposition of the ulnar nerve secured with either an adipose flap (27 limbs) or a fascial sling (80 limbs) over a 14-year period. The fascial sling cohort was used as a comparison group, matched to the adipose flap cohort by sex, age at time of surgery, hand dominance, symptom duration, and length of follow-up (Table 1). Patients were indicated for surgery and were included in the study if they had a history and physical examination consistent with primary CuTS, symptom duration longer than 1 year, and failed conservative management, including activity modification, night splinting, elbow pads, occupational therapy, and home exercise regimen. Electrodiagnostic testing was used at the discretion of the attending surgeon when the diagnosis was not clear from the history and physical examination. All fascial sling procedures were performed at our institution by 1 of 3 fellowship-trained hand surgeons, including Dr. Rosenwasser. The adipose flap modification was performed only by Dr. Rosenwasser. Of the 27 patients in the adipose flap group, 23 underwent surgery for primary CuTS and were included in the study; the other 4 (revision cases) were excluded; 1 patient subsequently died of a cause unrelated to the surgical procedure, and 6 were lost to follow-up. Of the 80 patients in the fascial sling group, 30 underwent surgery for primary CuTS; 5 died before follow-up, and 8 declined to participate.

Thirty-three patients (16 adipose flap, 17 fascial sling) met the inclusion criteria. Of the 16 adipose flap patients, 15 underwent the physical examination and completed the questionnaire, and 1 was interviewed by telephone. Similarly, of the 17 fascial sling patients, 15 underwent the physical examination and completed the questionnaire, and 2 were interviewed by telephone. There were no bilateral cases. Conservative management (activity modification, night splinting, elbow pads, occupational therapy, home exercise) failed in all cases.

A trained study team member who was not part of the surgical team performed follow-up evaluations using objective outcome measures and subjective questionnaires. Patients were assessed at a mean follow-up of 5.6 years (range, 1.6-15.9 years). Patients completed the DASH (Disabilities of the Arm, Shoulder, and Hand) questionnaire¹⁶ and visual analog scales (VASs) for pain, numbness, tingling, and weakness in the ulnar nerve distribution. They also rated the presence of night symptoms that were interfering with sleep. The Modified Bishop Rating Scale (MBRS) was used to quantify patient self-reported data^17,18 (Figure 2). The MBRS measures overall satisfaction, symptom improvement, presence of residual symptoms, ability to engage in activities, work capability, and subjective changes in strength and sensibility.

In the physical examinations, we tested for Tinel, Wartenberg, and Froment signs; performed an elbow flexion test; and measured elbow range of motion for flexion and extension as well as forearm pronation and supination. We also evaluated lateral pinch strength and grip strength, using a Jamar hydraulic pinch gauge and a Jamar dynamometer (Therapeutic Equipment Corp) and taking the average of 3 assessments. Fifth-digit abduction strength was graded on a standard muscle strength scale. Two-point discrimination was measured at the middle, ring, and small digits of the operated and contralateral hands.¹⁹

Surgical Technique

Standard ulnar nerve decompression with anterior subcutaneous transposition and the following modifications were performed on all patients.²⁰ A posteromedial incision parallel to the intermuscular septum was developed and the ulnar nerve identified. Minimizing stripping of the vascular mesentery, the dissection continued along the course of the nerve, and the medial intermuscular septum was excised to prevent secondary compression after transposition. The ulnar nerve was mobilized and transposed anterior to the medial epicondyle (Figure 3). For patients who received the fascial sling, a fascial sleeve was elevated from the flexor-pronator mass and sutured to the edge of the retinaculum securing the nerve. For patients who received the adipose flap, the flap with its vascular pedicle intact was elevated from the subcutaneous tissue of the anterior skin overlying the transposed nerve. The adipose tissue was sharply dissected in half while sufficient subcutaneous tissue was kept between the skin and the flap. A plane was developed based on an anterior adipose pedicle, which included a cutaneous artery and a vein that would supply the vascularized adipose flap. The flap was elevated and wrapped around the nerve without tension while the ulnar nerve was protected from being kinked by the construct. The flap was sutured to the anterior subcutaneous tissue to create a tunnel of adipose tissue surrounding the nerve along its length (Figure 4). The elbow was then flexed and extended to ensure free nerve gliding before wound closure.

The patient was allowed to move the elbow within the bulky dressings immediately after surgery. After 2 weeks, sutures were removed. Formal occupational therapy is not needed for these patients, except in the presence of significant weakness.

Results

As mentioned, the 2 groups were matched on demographics: age at time of surgery, sex, symptom duration, and length of follow-up (Table 1).

For the 16 adipose flap patients (Table 2), mean DASH score was 19.9 (range, 0-71.7). Seven of these patients reported upper extremity pain with a mean VAS score of 1.7 (range, 0-8); 4 patients reported pain in the wrist and fourth and fifth digits; only 1 patient reported pain that occasionally woke the patient from sleep. Constant numbness was present in 6 patients. Four patients reported constant mild tingling in the hand, and 11 reported intermittent tingling. Eleven patients (68.7%) reported operated-arm weakness with a mean VAS score of 3.4 (range, 0-8). In patients who had a physical examination, mean elbow flexion–extension arc of motion was 134° (range, 95°-150°), representing 99% of the motion of the contralateral arm. Mean pronation–supination arc was 174° (range, 150°-180°), accounting for 104% of the contralateral arm. Mean lateral pinch strength was 73% of the contralateral arm, and mean grip strength was 114% of the contralateral arm. The Tinel sign was present in 2 patients, the Froment sign was present in 3 patients, and the elbow flexion test was positive in 2 patients. No patient had a positive Wartenberg sign. On the MBRS, 10 patients had an excellent score, and 6 had a good score.

For the 17 fascial sling patients (Table 2), mean DASH score was 22.7 (range, 0-63.3). Three patients reported upper extremity pain with a mean VAS score of 1.4 (range, 0-7); 3 patients reported pain that occasionally woke them from sleep. Seven patients had constant numbness in the distribution of the ulnar nerve. Two patients had constant paresthesias, and 7 had intermittent paresthesias. Nine patients (52.9%) reported arm weakness with a mean VAS score of 2.5 (range, 0-8). Mean elbow flexion–extension arc of motion was 136° (range, 100°-150°), representing 100% of the contralateral arm. Mean pronation–supination arc was 187° (range, 155°-225°), accounting for 102% of the contralateral arm. Mean lateral pinch strength was 93% of the contralateral arm, and mean grip strength was 80% of the contralateral arm. The Tinel sign was present in 6 patients, the Froment sign in 3 patients, and the Wartenberg sign in 2 patients. The elbow flexion test was positive in 4 patients. On the MBRS, 10 patients had an excellent score, and 7 had a good score.

There was no recurrence of CuTS in either group. One adipose flap patient developed a wound infection that required reoperation.

Discussion

Ulnar neuropathy was described by Magee and Phalen²¹ in 1949 and termed cubital tunnel syndrome by Feindel and Stratford²² in 1958. Since then, numerous procedures, including in situ decompression, medial epicondylectomy, and endoscopic decompression,^23,24 have been advocated for the treatment of this condition. In addition, anterior transposition, which involves securing the ulnar nerve in a submuscular, intramuscular, or subcutaneous sleeve,⁶ remains a popular option. Despite more than half a century of surgical treatment for this condition, there is no consensus about which procedure offers the best outcomes. Bartels and colleagues⁸ retrospectively reviewed surgical treatments for CuTS, examining 3148 arms over a 27-year period. They found simple decompression and anterior intramuscular transposition had the best results, followed by medial epicondylectomy and anterior subcutaneous transposition, with anterior submuscular transposition yielding the poorest outcomes. Despite these findings, the operative groups’ recurrence rates remained significant. These results were challenged in a 2008 meta-analysis⁵ that found no significant difference among simple decompression, subcutaneous transposition, and submuscular transposition and instead demonstrated trends toward better outcomes with anterior transposition. Osterman and Davis⁷ reported a 5% to 15% rate of unsatisfactory outcomes with anterior subcutaneous transposition, a popular technique used by surgeons at our institution.

The causes for failure or recurrence of ulnar neuropathy after surgical intervention are multifactorial and include preexisting medical conditions and improper operative technique. It is well established that failure to excise all 5 anatomical points of entrapment, or creation of new points of tension during surgery, leads to poor outcomes.¹² Nevertheless, the contribution of perineural scarring to postoperative recurrent ulnar neuropathy is currently being recognized: Gabel and Amadio¹³ described postoperative fibrosis in one-third of their patients with surgically treated recurrent CuTS, Rogers and colleagues¹⁴ noted dense perineural fibrosis after intramuscular and subcutaneous transposition procedures, Filippi and colleagues¹¹ cited serious epineural fibrosis and fibrosis around the ulnar nerve as the main findings in their study of 22 patients with recurrent ulnar neuropathy, and Vogel and colleagues¹² found that 88% of their patients with persistent CuTS after surgery exhibited perineural scarring.

We think that use of a scar tissue barrier during ulnar nerve transposition reduces the incidence of cicatrix and produces better outcomes—a position largely echoed by the orthopedic community, as fascial, fasciocutaneous, free, and venous flaps have all been used for such purposes.^25,26 Vein wrapping has demonstrated good recovery of a nerve after perineural scarring.²⁷ Advocates of intramuscular transposition argue that their technique provides the nerve with a vascularized tunnel, as segmental vascular stripping is an inevitability in transposition. However, this technique increases the incidence of scarring and potential muscle damage.^28,29 We think the pedicled adipofascial flap benefits the peripheral nerve by providing a scar tissue barrier and an optimal milieu for vascular regeneration. Kilic and colleagues¹⁵ demonstrated the regenerative effects of adipose tissue flaps on peripheral nerves after crush injuries in a rat model, and Strickland and colleagues³⁰ retrospectively examined the effects of hypothenar fat flaps on recalcitrant carpal tunnel syndrome, showing excellent results for this procedure. It is hypothesized that adipose tissue provides not only adipose-derived stem cells but also a rich vascular bed on which nerves will regenerate.

For all patients in the present study, symptoms improved, though the adipose flap and fascial sling groups were not significantly different in their outcomes. We used the MBRS to quantify and compare the groups’ patient-rated outcomes. No statistically significant difference was found between the adipose flap and fascial sling groups. On the MBRS, excellent and good outcomes were reported by 62.5% and 37.5% of the adipose flap patients, respectively, and 59% and 41% of the fascial sling patients (Table 3). Likewise, objective measurements did not show a significant difference between the 2 interventions—indicating that, compared with the current standard of care, adipose flaps are more efficacious in securing the anteriorly transposed nerve.

Complications of the adipose flap technique are consistent with those reported for other techniques for anterior transposition of the ulnar nerve. The most common complication is hematoma, which can be avoided with meticulous hemostasis. Damage of the medial antebrachial cutaneous nerve or motor branches to the flexor carpi ulnaris has been reported for the fascial technique (we have not had such outcomes at our institution). Contraindications to the adipofascial technique include insufficient subcutaneous adipose tissue for covering the ulnar nerve.

This study was limited by its retrospective setup, which reduced access to preoperative objective and subjective data. The small sample size also limited our ability to demonstrate the advantageous effects of an adipofascial flap in preventing postoperative perineural scarring.

The adipose flap technique is a viable option for securing the anteriorly transposed ulnar nerve. Outcomes in this study demonstrated an efficacy comparable to that of the fascial sling technique. Symptoms resolve or improve, and the majority of patients are satisfied with long-term surgical outcomes. The adipofascial flap may have additional advantages, as it provides a pliable, vascular fat envelope mimicking the natural fatty environment of peripheral nerves.

Compression of the ulnar nerve at the elbow, also referred to as cubital tunnel syndrome (CuTS), is the second most common peripheral nerve compression syndrome in the upper extremity.^1,2 Although the ulnar nerve can be compressed at 5 different sites, including arcade of Struthers, medial intermuscular septum, medial epicondyle, and deep flexor aponeurosis, the cubital tunnel is most commonly affected.³ Patients typically present with paresthesias in the fourth and fifth digits and weakness of hand muscle intrinsics. Activity-related pain or pain at the medial elbow can also occur in more advanced pathology.⁴ It is estimated that conservative therapy fails and surgical intervention is required in up to 30% of patients with CuTS.¹ Surgical approaches range from in situ decompression to transposition techniques, but there is no consensus in the orthopedic community as to which technique offers the best results. In a 2008 meta-analysis, Macadam and colleagues⁵ found no statistical differences in outcomes among the various surgical approaches. Nevertheless, subcutaneous transposition of the ulnar nerve at the elbow is a popular option.⁶

Despite the widespread success of surgical intervention for CuTS, persistent or recurrent pain occurs in 9.9% to 21.0% of cases.^7-10 In addition, several investigators have cited perineural scarring as a major cause of recurrent symptoms after primary surgery.^11-14 Filippi and colleagues¹¹ noted that patients who required reoperation after primary anterior transposition had “serious epineural fibrosis and fibrosis around the transposed ulnar nerve.” At our institution, we have similarly found that scarring of the fascial sling around the ulnar nerve led to recurrence of CuTS within 4 months after initial surgery (Figure 1).

We therefore prefer to use a vascularized adipose flap to secure the anteriorly transposed ulnar nerve. This flap provides a pliable, vascularized adipose environment for the nerve, which helps reduce nerve adherence and may enhance nerve recovery.¹⁵ In the study reported here, we retrospectively reviewed the long-term outcomes of ulnar nerve anterior subcutaneous transposition secured with either an adipose flap or a fascial sling. We hypothesized that patients in the 2 groups (adipose flap, fascial sling) would have equivalent outcomes.

Materials and Methods

After obtaining institutional review board approval, we reviewed the medical and surgical records of 104 patients (107 limbs) who underwent transposition of the ulnar nerve secured with either an adipose flap (27 limbs) or a fascial sling (80 limbs) over a 14-year period. The fascial sling cohort was used as a comparison group, matched to the adipose flap cohort by sex, age at time of surgery, hand dominance, symptom duration, and length of follow-up (Table 1). Patients were indicated for surgery and were included in the study if they had a history and physical examination consistent with primary CuTS, symptom duration longer than 1 year, and failed conservative management, including activity modification, night splinting, elbow pads, occupational therapy, and home exercise regimen. Electrodiagnostic testing was used at the discretion of the attending surgeon when the diagnosis was not clear from the history and physical examination. All fascial sling procedures were performed at our institution by 1 of 3 fellowship-trained hand surgeons, including Dr. Rosenwasser. The adipose flap modification was performed only by Dr. Rosenwasser. Of the 27 patients in the adipose flap group, 23 underwent surgery for primary CuTS and were included in the study; the other 4 (revision cases) were excluded; 1 patient subsequently died of a cause unrelated to the surgical procedure, and 6 were lost to follow-up. Of the 80 patients in the fascial sling group, 30 underwent surgery for primary CuTS; 5 died before follow-up, and 8 declined to participate.

Thirty-three patients (16 adipose flap, 17 fascial sling) met the inclusion criteria. Of the 16 adipose flap patients, 15 underwent the physical examination and completed the questionnaire, and 1 was interviewed by telephone. Similarly, of the 17 fascial sling patients, 15 underwent the physical examination and completed the questionnaire, and 2 were interviewed by telephone. There were no bilateral cases. Conservative management (activity modification, night splinting, elbow pads, occupational therapy, home exercise) failed in all cases.

A trained study team member who was not part of the surgical team performed follow-up evaluations using objective outcome measures and subjective questionnaires. Patients were assessed at a mean follow-up of 5.6 years (range, 1.6-15.9 years). Patients completed the DASH (Disabilities of the Arm, Shoulder, and Hand) questionnaire¹⁶ and visual analog scales (VASs) for pain, numbness, tingling, and weakness in the ulnar nerve distribution. They also rated the presence of night symptoms that were interfering with sleep. The Modified Bishop Rating Scale (MBRS) was used to quantify patient self-reported data^17,18 (Figure 2). The MBRS measures overall satisfaction, symptom improvement, presence of residual symptoms, ability to engage in activities, work capability, and subjective changes in strength and sensibility.

In the physical examinations, we tested for Tinel, Wartenberg, and Froment signs; performed an elbow flexion test; and measured elbow range of motion for flexion and extension as well as forearm pronation and supination. We also evaluated lateral pinch strength and grip strength, using a Jamar hydraulic pinch gauge and a Jamar dynamometer (Therapeutic Equipment Corp) and taking the average of 3 assessments. Fifth-digit abduction strength was graded on a standard muscle strength scale. Two-point discrimination was measured at the middle, ring, and small digits of the operated and contralateral hands.¹⁹

Surgical Technique

Standard ulnar nerve decompression with anterior subcutaneous transposition and the following modifications were performed on all patients.²⁰ A posteromedial incision parallel to the intermuscular septum was developed and the ulnar nerve identified. Minimizing stripping of the vascular mesentery, the dissection continued along the course of the nerve, and the medial intermuscular septum was excised to prevent secondary compression after transposition. The ulnar nerve was mobilized and transposed anterior to the medial epicondyle (Figure 3). For patients who received the fascial sling, a fascial sleeve was elevated from the flexor-pronator mass and sutured to the edge of the retinaculum securing the nerve. For patients who received the adipose flap, the flap with its vascular pedicle intact was elevated from the subcutaneous tissue of the anterior skin overlying the transposed nerve. The adipose tissue was sharply dissected in half while sufficient subcutaneous tissue was kept between the skin and the flap. A plane was developed based on an anterior adipose pedicle, which included a cutaneous artery and a vein that would supply the vascularized adipose flap. The flap was elevated and wrapped around the nerve without tension while the ulnar nerve was protected from being kinked by the construct. The flap was sutured to the anterior subcutaneous tissue to create a tunnel of adipose tissue surrounding the nerve along its length (Figure 4). The elbow was then flexed and extended to ensure free nerve gliding before wound closure.

The patient was allowed to move the elbow within the bulky dressings immediately after surgery. After 2 weeks, sutures were removed. Formal occupational therapy is not needed for these patients, except in the presence of significant weakness.

Results

As mentioned, the 2 groups were matched on demographics: age at time of surgery, sex, symptom duration, and length of follow-up (Table 1).

For the 16 adipose flap patients (Table 2), mean DASH score was 19.9 (range, 0-71.7). Seven of these patients reported upper extremity pain with a mean VAS score of 1.7 (range, 0-8); 4 patients reported pain in the wrist and fourth and fifth digits; only 1 patient reported pain that occasionally woke the patient from sleep. Constant numbness was present in 6 patients. Four patients reported constant mild tingling in the hand, and 11 reported intermittent tingling. Eleven patients (68.7%) reported operated-arm weakness with a mean VAS score of 3.4 (range, 0-8). In patients who had a physical examination, mean elbow flexion–extension arc of motion was 134° (range, 95°-150°), representing 99% of the motion of the contralateral arm. Mean pronation–supination arc was 174° (range, 150°-180°), accounting for 104% of the contralateral arm. Mean lateral pinch strength was 73% of the contralateral arm, and mean grip strength was 114% of the contralateral arm. The Tinel sign was present in 2 patients, the Froment sign was present in 3 patients, and the elbow flexion test was positive in 2 patients. No patient had a positive Wartenberg sign. On the MBRS, 10 patients had an excellent score, and 6 had a good score.

For the 17 fascial sling patients (Table 2), mean DASH score was 22.7 (range, 0-63.3). Three patients reported upper extremity pain with a mean VAS score of 1.4 (range, 0-7); 3 patients reported pain that occasionally woke them from sleep. Seven patients had constant numbness in the distribution of the ulnar nerve. Two patients had constant paresthesias, and 7 had intermittent paresthesias. Nine patients (52.9%) reported arm weakness with a mean VAS score of 2.5 (range, 0-8). Mean elbow flexion–extension arc of motion was 136° (range, 100°-150°), representing 100% of the contralateral arm. Mean pronation–supination arc was 187° (range, 155°-225°), accounting for 102% of the contralateral arm. Mean lateral pinch strength was 93% of the contralateral arm, and mean grip strength was 80% of the contralateral arm. The Tinel sign was present in 6 patients, the Froment sign in 3 patients, and the Wartenberg sign in 2 patients. The elbow flexion test was positive in 4 patients. On the MBRS, 10 patients had an excellent score, and 7 had a good score.

There was no recurrence of CuTS in either group. One adipose flap patient developed a wound infection that required reoperation.

Discussion

Ulnar neuropathy was described by Magee and Phalen²¹ in 1949 and termed cubital tunnel syndrome by Feindel and Stratford²² in 1958. Since then, numerous procedures, including in situ decompression, medial epicondylectomy, and endoscopic decompression,^23,24 have been advocated for the treatment of this condition. In addition, anterior transposition, which involves securing the ulnar nerve in a submuscular, intramuscular, or subcutaneous sleeve,⁶ remains a popular option. Despite more than half a century of surgical treatment for this condition, there is no consensus about which procedure offers the best outcomes. Bartels and colleagues⁸ retrospectively reviewed surgical treatments for CuTS, examining 3148 arms over a 27-year period. They found simple decompression and anterior intramuscular transposition had the best results, followed by medial epicondylectomy and anterior subcutaneous transposition, with anterior submuscular transposition yielding the poorest outcomes. Despite these findings, the operative groups’ recurrence rates remained significant. These results were challenged in a 2008 meta-analysis⁵ that found no significant difference among simple decompression, subcutaneous transposition, and submuscular transposition and instead demonstrated trends toward better outcomes with anterior transposition. Osterman and Davis⁷ reported a 5% to 15% rate of unsatisfactory outcomes with anterior subcutaneous transposition, a popular technique used by surgeons at our institution.

The causes for failure or recurrence of ulnar neuropathy after surgical intervention are multifactorial and include preexisting medical conditions and improper operative technique. It is well established that failure to excise all 5 anatomical points of entrapment, or creation of new points of tension during surgery, leads to poor outcomes.¹² Nevertheless, the contribution of perineural scarring to postoperative recurrent ulnar neuropathy is currently being recognized: Gabel and Amadio¹³ described postoperative fibrosis in one-third of their patients with surgically treated recurrent CuTS, Rogers and colleagues¹⁴ noted dense perineural fibrosis after intramuscular and subcutaneous transposition procedures, Filippi and colleagues¹¹ cited serious epineural fibrosis and fibrosis around the ulnar nerve as the main findings in their study of 22 patients with recurrent ulnar neuropathy, and Vogel and colleagues¹² found that 88% of their patients with persistent CuTS after surgery exhibited perineural scarring.

We think that use of a scar tissue barrier during ulnar nerve transposition reduces the incidence of cicatrix and produces better outcomes—a position largely echoed by the orthopedic community, as fascial, fasciocutaneous, free, and venous flaps have all been used for such purposes.^25,26 Vein wrapping has demonstrated good recovery of a nerve after perineural scarring.²⁷ Advocates of intramuscular transposition argue that their technique provides the nerve with a vascularized tunnel, as segmental vascular stripping is an inevitability in transposition. However, this technique increases the incidence of scarring and potential muscle damage.^28,29 We think the pedicled adipofascial flap benefits the peripheral nerve by providing a scar tissue barrier and an optimal milieu for vascular regeneration. Kilic and colleagues¹⁵ demonstrated the regenerative effects of adipose tissue flaps on peripheral nerves after crush injuries in a rat model, and Strickland and colleagues³⁰ retrospectively examined the effects of hypothenar fat flaps on recalcitrant carpal tunnel syndrome, showing excellent results for this procedure. It is hypothesized that adipose tissue provides not only adipose-derived stem cells but also a rich vascular bed on which nerves will regenerate.

For all patients in the present study, symptoms improved, though the adipose flap and fascial sling groups were not significantly different in their outcomes. We used the MBRS to quantify and compare the groups’ patient-rated outcomes. No statistically significant difference was found between the adipose flap and fascial sling groups. On the MBRS, excellent and good outcomes were reported by 62.5% and 37.5% of the adipose flap patients, respectively, and 59% and 41% of the fascial sling patients (Table 3). Likewise, objective measurements did not show a significant difference between the 2 interventions—indicating that, compared with the current standard of care, adipose flaps are more efficacious in securing the anteriorly transposed nerve.

Complications of the adipose flap technique are consistent with those reported for other techniques for anterior transposition of the ulnar nerve. The most common complication is hematoma, which can be avoided with meticulous hemostasis. Damage of the medial antebrachial cutaneous nerve or motor branches to the flexor carpi ulnaris has been reported for the fascial technique (we have not had such outcomes at our institution). Contraindications to the adipofascial technique include insufficient subcutaneous adipose tissue for covering the ulnar nerve.

This study was limited by its retrospective setup, which reduced access to preoperative objective and subjective data. The small sample size also limited our ability to demonstrate the advantageous effects of an adipofascial flap in preventing postoperative perineural scarring.

The adipose flap technique is a viable option for securing the anteriorly transposed ulnar nerve. Outcomes in this study demonstrated an efficacy comparable to that of the fascial sling technique. Symptoms resolve or improve, and the majority of patients are satisfied with long-term surgical outcomes. The adipofascial flap may have additional advantages, as it provides a pliable, vascular fat envelope mimicking the natural fatty environment of peripheral nerves.

Compression of the ulnar nerve at the elbow, also referred to as cubital tunnel syndrome (CuTS), is the second most common peripheral nerve compression syndrome in the upper extremity.^1,2 Although the ulnar nerve can be compressed at 5 different sites, including arcade of Struthers, medial intermuscular septum, medial epicondyle, and deep flexor aponeurosis, the cubital tunnel is most commonly affected.³ Patients typically present with paresthesias in the fourth and fifth digits and weakness of hand muscle intrinsics. Activity-related pain or pain at the medial elbow can also occur in more advanced pathology.⁴ It is estimated that conservative therapy fails and surgical intervention is required in up to 30% of patients with CuTS.¹ Surgical approaches range from in situ decompression to transposition techniques, but there is no consensus in the orthopedic community as to which technique offers the best results. In a 2008 meta-analysis, Macadam and colleagues⁵ found no statistical differences in outcomes among the various surgical approaches. Nevertheless, subcutaneous transposition of the ulnar nerve at the elbow is a popular option.⁶

Despite the widespread success of surgical intervention for CuTS, persistent or recurrent pain occurs in 9.9% to 21.0% of cases.^7-10 In addition, several investigators have cited perineural scarring as a major cause of recurrent symptoms after primary surgery.^11-14 Filippi and colleagues¹¹ noted that patients who required reoperation after primary anterior transposition had “serious epineural fibrosis and fibrosis around the transposed ulnar nerve.” At our institution, we have similarly found that scarring of the fascial sling around the ulnar nerve led to recurrence of CuTS within 4 months after initial surgery (Figure 1).

We therefore prefer to use a vascularized adipose flap to secure the anteriorly transposed ulnar nerve. This flap provides a pliable, vascularized adipose environment for the nerve, which helps reduce nerve adherence and may enhance nerve recovery.¹⁵ In the study reported here, we retrospectively reviewed the long-term outcomes of ulnar nerve anterior subcutaneous transposition secured with either an adipose flap or a fascial sling. We hypothesized that patients in the 2 groups (adipose flap, fascial sling) would have equivalent outcomes.

Materials and Methods

After obtaining institutional review board approval, we reviewed the medical and surgical records of 104 patients (107 limbs) who underwent transposition of the ulnar nerve secured with either an adipose flap (27 limbs) or a fascial sling (80 limbs) over a 14-year period. The fascial sling cohort was used as a comparison group, matched to the adipose flap cohort by sex, age at time of surgery, hand dominance, symptom duration, and length of follow-up (Table 1). Patients were indicated for surgery and were included in the study if they had a history and physical examination consistent with primary CuTS, symptom duration longer than 1 year, and failed conservative management, including activity modification, night splinting, elbow pads, occupational therapy, and home exercise regimen. Electrodiagnostic testing was used at the discretion of the attending surgeon when the diagnosis was not clear from the history and physical examination. All fascial sling procedures were performed at our institution by 1 of 3 fellowship-trained hand surgeons, including Dr. Rosenwasser. The adipose flap modification was performed only by Dr. Rosenwasser. Of the 27 patients in the adipose flap group, 23 underwent surgery for primary CuTS and were included in the study; the other 4 (revision cases) were excluded; 1 patient subsequently died of a cause unrelated to the surgical procedure, and 6 were lost to follow-up. Of the 80 patients in the fascial sling group, 30 underwent surgery for primary CuTS; 5 died before follow-up, and 8 declined to participate.

Thirty-three patients (16 adipose flap, 17 fascial sling) met the inclusion criteria. Of the 16 adipose flap patients, 15 underwent the physical examination and completed the questionnaire, and 1 was interviewed by telephone. Similarly, of the 17 fascial sling patients, 15 underwent the physical examination and completed the questionnaire, and 2 were interviewed by telephone. There were no bilateral cases. Conservative management (activity modification, night splinting, elbow pads, occupational therapy, home exercise) failed in all cases.

A trained study team member who was not part of the surgical team performed follow-up evaluations using objective outcome measures and subjective questionnaires. Patients were assessed at a mean follow-up of 5.6 years (range, 1.6-15.9 years). Patients completed the DASH (Disabilities of the Arm, Shoulder, and Hand) questionnaire¹⁶ and visual analog scales (VASs) for pain, numbness, tingling, and weakness in the ulnar nerve distribution. They also rated the presence of night symptoms that were interfering with sleep. The Modified Bishop Rating Scale (MBRS) was used to quantify patient self-reported data^17,18 (Figure 2). The MBRS measures overall satisfaction, symptom improvement, presence of residual symptoms, ability to engage in activities, work capability, and subjective changes in strength and sensibility.

In the physical examinations, we tested for Tinel, Wartenberg, and Froment signs; performed an elbow flexion test; and measured elbow range of motion for flexion and extension as well as forearm pronation and supination. We also evaluated lateral pinch strength and grip strength, using a Jamar hydraulic pinch gauge and a Jamar dynamometer (Therapeutic Equipment Corp) and taking the average of 3 assessments. Fifth-digit abduction strength was graded on a standard muscle strength scale. Two-point discrimination was measured at the middle, ring, and small digits of the operated and contralateral hands.¹⁹

Surgical Technique

Standard ulnar nerve decompression with anterior subcutaneous transposition and the following modifications were performed on all patients.²⁰ A posteromedial incision parallel to the intermuscular septum was developed and the ulnar nerve identified. Minimizing stripping of the vascular mesentery, the dissection continued along the course of the nerve, and the medial intermuscular septum was excised to prevent secondary compression after transposition. The ulnar nerve was mobilized and transposed anterior to the medial epicondyle (Figure 3). For patients who received the fascial sling, a fascial sleeve was elevated from the flexor-pronator mass and sutured to the edge of the retinaculum securing the nerve. For patients who received the adipose flap, the flap with its vascular pedicle intact was elevated from the subcutaneous tissue of the anterior skin overlying the transposed nerve. The adipose tissue was sharply dissected in half while sufficient subcutaneous tissue was kept between the skin and the flap. A plane was developed based on an anterior adipose pedicle, which included a cutaneous artery and a vein that would supply the vascularized adipose flap. The flap was elevated and wrapped around the nerve without tension while the ulnar nerve was protected from being kinked by the construct. The flap was sutured to the anterior subcutaneous tissue to create a tunnel of adipose tissue surrounding the nerve along its length (Figure 4). The elbow was then flexed and extended to ensure free nerve gliding before wound closure.

The patient was allowed to move the elbow within the bulky dressings immediately after surgery. After 2 weeks, sutures were removed. Formal occupational therapy is not needed for these patients, except in the presence of significant weakness.

Results

As mentioned, the 2 groups were matched on demographics: age at time of surgery, sex, symptom duration, and length of follow-up (Table 1).

For the 16 adipose flap patients (Table 2), mean DASH score was 19.9 (range, 0-71.7). Seven of these patients reported upper extremity pain with a mean VAS score of 1.7 (range, 0-8); 4 patients reported pain in the wrist and fourth and fifth digits; only 1 patient reported pain that occasionally woke the patient from sleep. Constant numbness was present in 6 patients. Four patients reported constant mild tingling in the hand, and 11 reported intermittent tingling. Eleven patients (68.7%) reported operated-arm weakness with a mean VAS score of 3.4 (range, 0-8). In patients who had a physical examination, mean elbow flexion–extension arc of motion was 134° (range, 95°-150°), representing 99% of the motion of the contralateral arm. Mean pronation–supination arc was 174° (range, 150°-180°), accounting for 104% of the contralateral arm. Mean lateral pinch strength was 73% of the contralateral arm, and mean grip strength was 114% of the contralateral arm. The Tinel sign was present in 2 patients, the Froment sign was present in 3 patients, and the elbow flexion test was positive in 2 patients. No patient had a positive Wartenberg sign. On the MBRS, 10 patients had an excellent score, and 6 had a good score.

For the 17 fascial sling patients (Table 2), mean DASH score was 22.7 (range, 0-63.3). Three patients reported upper extremity pain with a mean VAS score of 1.4 (range, 0-7); 3 patients reported pain that occasionally woke them from sleep. Seven patients had constant numbness in the distribution of the ulnar nerve. Two patients had constant paresthesias, and 7 had intermittent paresthesias. Nine patients (52.9%) reported arm weakness with a mean VAS score of 2.5 (range, 0-8). Mean elbow flexion–extension arc of motion was 136° (range, 100°-150°), representing 100% of the contralateral arm. Mean pronation–supination arc was 187° (range, 155°-225°), accounting for 102% of the contralateral arm. Mean lateral pinch strength was 93% of the contralateral arm, and mean grip strength was 80% of the contralateral arm. The Tinel sign was present in 6 patients, the Froment sign in 3 patients, and the Wartenberg sign in 2 patients. The elbow flexion test was positive in 4 patients. On the MBRS, 10 patients had an excellent score, and 7 had a good score.

There was no recurrence of CuTS in either group. One adipose flap patient developed a wound infection that required reoperation.

Discussion

Ulnar neuropathy was described by Magee and Phalen²¹ in 1949 and termed cubital tunnel syndrome by Feindel and Stratford²² in 1958. Since then, numerous procedures, including in situ decompression, medial epicondylectomy, and endoscopic decompression,^23,24 have been advocated for the treatment of this condition. In addition, anterior transposition, which involves securing the ulnar nerve in a submuscular, intramuscular, or subcutaneous sleeve,⁶ remains a popular option. Despite more than half a century of surgical treatment for this condition, there is no consensus about which procedure offers the best outcomes. Bartels and colleagues⁸ retrospectively reviewed surgical treatments for CuTS, examining 3148 arms over a 27-year period. They found simple decompression and anterior intramuscular transposition had the best results, followed by medial epicondylectomy and anterior subcutaneous transposition, with anterior submuscular transposition yielding the poorest outcomes. Despite these findings, the operative groups’ recurrence rates remained significant. These results were challenged in a 2008 meta-analysis⁵ that found no significant difference among simple decompression, subcutaneous transposition, and submuscular transposition and instead demonstrated trends toward better outcomes with anterior transposition. Osterman and Davis⁷ reported a 5% to 15% rate of unsatisfactory outcomes with anterior subcutaneous transposition, a popular technique used by surgeons at our institution.

The causes for failure or recurrence of ulnar neuropathy after surgical intervention are multifactorial and include preexisting medical conditions and improper operative technique. It is well established that failure to excise all 5 anatomical points of entrapment, or creation of new points of tension during surgery, leads to poor outcomes.¹² Nevertheless, the contribution of perineural scarring to postoperative recurrent ulnar neuropathy is currently being recognized: Gabel and Amadio¹³ described postoperative fibrosis in one-third of their patients with surgically treated recurrent CuTS, Rogers and colleagues¹⁴ noted dense perineural fibrosis after intramuscular and subcutaneous transposition procedures, Filippi and colleagues¹¹ cited serious epineural fibrosis and fibrosis around the ulnar nerve as the main findings in their study of 22 patients with recurrent ulnar neuropathy, and Vogel and colleagues¹² found that 88% of their patients with persistent CuTS after surgery exhibited perineural scarring.

We think that use of a scar tissue barrier during ulnar nerve transposition reduces the incidence of cicatrix and produces better outcomes—a position largely echoed by the orthopedic community, as fascial, fasciocutaneous, free, and venous flaps have all been used for such purposes.^25,26 Vein wrapping has demonstrated good recovery of a nerve after perineural scarring.²⁷ Advocates of intramuscular transposition argue that their technique provides the nerve with a vascularized tunnel, as segmental vascular stripping is an inevitability in transposition. However, this technique increases the incidence of scarring and potential muscle damage.^28,29 We think the pedicled adipofascial flap benefits the peripheral nerve by providing a scar tissue barrier and an optimal milieu for vascular regeneration. Kilic and colleagues¹⁵ demonstrated the regenerative effects of adipose tissue flaps on peripheral nerves after crush injuries in a rat model, and Strickland and colleagues³⁰ retrospectively examined the effects of hypothenar fat flaps on recalcitrant carpal tunnel syndrome, showing excellent results for this procedure. It is hypothesized that adipose tissue provides not only adipose-derived stem cells but also a rich vascular bed on which nerves will regenerate.

For all patients in the present study, symptoms improved, though the adipose flap and fascial sling groups were not significantly different in their outcomes. We used the MBRS to quantify and compare the groups’ patient-rated outcomes. No statistically significant difference was found between the adipose flap and fascial sling groups. On the MBRS, excellent and good outcomes were reported by 62.5% and 37.5% of the adipose flap patients, respectively, and 59% and 41% of the fascial sling patients (Table 3). Likewise, objective measurements did not show a significant difference between the 2 interventions—indicating that, compared with the current standard of care, adipose flaps are more efficacious in securing the anteriorly transposed nerve.

Complications of the adipose flap technique are consistent with those reported for other techniques for anterior transposition of the ulnar nerve. The most common complication is hematoma, which can be avoided with meticulous hemostasis. Damage of the medial antebrachial cutaneous nerve or motor branches to the flexor carpi ulnaris has been reported for the fascial technique (we have not had such outcomes at our institution). Contraindications to the adipofascial technique include insufficient subcutaneous adipose tissue for covering the ulnar nerve.

This study was limited by its retrospective setup, which reduced access to preoperative objective and subjective data. The small sample size also limited our ability to demonstrate the advantageous effects of an adipofascial flap in preventing postoperative perineural scarring.

The adipose flap technique is a viable option for securing the anteriorly transposed ulnar nerve. Outcomes in this study demonstrated an efficacy comparable to that of the fascial sling technique. Symptoms resolve or improve, and the majority of patients are satisfied with long-term surgical outcomes. The adipofascial flap may have additional advantages, as it provides a pliable, vascular fat envelope mimicking the natural fatty environment of peripheral nerves.

Tendinopathy of the long head of the biceps brachii (LHB) is a common source of anterior shoulder pain. The LHB tendon is an intra-articular yet extrasynovial structure, ensheathed by the synovial lining of the articular capsule.¹ Branches of the anterior circumflex humeral artery course along the bicipital groove, but the gliding undersurface of the LHB remains avascular.² Tendon irritation is most common within the groove and usually produces “tendinosis,” characterized by collagen fiber atrophy, fibrinoid necrosis, and fibrocyte proliferation.¹ Neviaser and colleagues³ correlated such changes in the LHB tendon with rotator cuff pathology, as the 2 often coexist. Primary LHB tendinitis is less common and associated with younger patients who engage in overhead activities, such as baseball and volleyball.⁴

Nonoperative management, which is trialed initially, consists of rest, use of nonsteroidal anti-inflammatory drugs, and physical therapy. Corticosteroid injections are administered through the subacromial space or glenohumeral joint, which is continuous with the LHB sheath. Some physicians give ultrasound-guided injections into the LHB sheath. For fear of tendon atrophy from corticosteroid injections, some physicians prefer iontophoresis with a topical steroid over the bicipital groove. If conservative measures fail, the physician can choose from 2 primary surgical options: biceps tenotomy and tenodesis. Tenodesis can be performed within the groove (suprapectoral) or subpectoral. In this review, we highlight 5 key features of subpectoral biceps tenodesis to guide treatment and improve outcomes.

Examination and Indications

Management of LHB tendinopathy begins with a complete physical examination. Tenderness over the bicipital groove is the most consistent finding, but this region may be difficult to localize in large individuals. The arm should be internally rotated 10° to orient the groove anterior and palpated 7 cm below the acromion.⁵ Anterior shoulder pain after resisted elevation with the elbow extended and supinated represents a positive Speed test. A positive Yergason test produces pain with resisted forearm supination while the elbow is flexed to 90°.

Evaluation of biceps instability is important in deciding which type of management (operative or nonoperative) is appropriate for a patient. Medial biceps subluxation may be detected by bringing the flexed arm from abduction, external rotation into cross-body adduction, internal rotation with decreased arm flexion.⁶ Another maneuver that elicits biceps irritation is combined abduction–extension, which places tension on the biceps tendon. Similarly, coracoid impingement may disrupt the subscapularis roof of the biceps sheath and cause LHB instability. Dines and colleagues⁷ reproduced the painful clicking of coracoid impingement by placing the shoulder in forward elevation, internal rotation, and varying degrees of adduction. Belly-press, lift-off, and internal rotation strength are other tests that assess subscapularis integrity. Rotator cuff impingement signs should be evaluated, and the contralateral shoulder should be examined for comparison.

Plain radiographs may show a pathology, such as anterior acromial spurring or posterior overgrowth of the coracoid, for which surgery is more suited. T2-weighted magnetic resonance imaging (MRI) may show an increased LHB signal, but this has shown poor concordance with arthroscopic findings of biceps pathology.⁸ Magnetic resonance arthrography can better detect medial dislocation of the LHB tendon from subscapularis tears. Ultrasound is cost-effective but highly operator-dependent.

Indications for biceps tenotomy or tenodesis include failed conservative management, partial-thickness LHB tears more than 25% to 50% in diameter, and medial subluxation of the LHB tendon with or without a subscapularis tear. Superior labrum anterior to posterior (SLAP) tears in older patients are a relative indication. Intraoperative findings may also indicate the need for LHB surgery. During the diagnostic arthroscopy, the LHB tendon should be evaluated for synovial inflammation or fraying (Figures 1A, 1B). This may need to be done under dry conditions, as pump pressure can compress and blunt the inflamed appearance. The O’Brien maneuver can be performed to demonstrate incarceration of the LHB tendon within the anterior glenohumeral joint. A probe should be placed through an anterior portal to pull the intertubercular LHB tendon into view, as this region is most commonly inflamed (Figure 2). Probing of the tendon also allows assessment of the stability of the biceps sling.

Surgical Technique

When biceps surgery is indicated, the surgeon must choose between tenotomy and tenodesis. Tenotomy is a low-demand procedure indicated for low-demand patients. A “Popeye” deformity may occur in up to 62% of patients, but Boileau and colleagues⁹ reported that none of their patients were bothered by it. Another concern after tenotomy is fatigue-cramping of the biceps muscle belly. Kelly and colleagues¹⁰ reported that up to 40% of patients had soreness and decreased strength with elbow flexion. Such cramping is more common in patients under age 60 years. For these reasons, biceps tenotomy should be reserved for older, low-demand patients who are not concerned about cosmesis and less likely to comply with postoperative motion restrictions.² We tend to perform tenotomy in obese patients, who may have a Popeye deformity that is not detectable, and in patients with diabetes; the goal is to avoid a wound infection resulting from the close proximity of tenodesis incision and axilla.

Biceps tenodesis should preserve the length–tension relationship of the biceps muscle and maintain its normal contour. Tenodesis location may be proximal or distal. Proximal fixation can be performed arthroscopically, and its advocates argue that keeping the LHB tendon within the bicipital groove preserves muscle strength. Boileau and Neyton11 found biceps strength to be 90% that of the contralateral arm after arthroscopic tenodesis. The bicipital groove, however, is lined with synovium and is a primary site of LHB pathology. Up to 78% of intra-articular biceps tears extend through the groove outside the joint.¹² Proximal tenodesis thus retains a major pain generator. In a retrospective study of 188 patients, Sanders and colleagues^13,14 found a 36% revision rate after proximal arthroscopic tenodesis and a 13% rate after proximal open tenodesis with an intact biceps sheath—significantly lower than the 3% after distal tenodesis outside the bicipital groove.¹ For this reason, we advocate distal biceps tenodesis beneath the pectoralis major tendon. After tenotomy with an arthroscopic basket (Figure 3), the LHB tendon is retracted out of the glenohumeral joint by extending the elbow. For the mini-open incision, the head of the bed is lowered from the beach-chair position to 30°. The arm is abducted on a Mayo stand, and the inferior border of the pectoralis major tendon is palpated. A 3-cm vertical incision is made along the medial arm starting 1 cm superior to the inferior pectoralis edge. The subcutaneous tissues are mobilized, and dissection is carried down to the pectoralis major and coracobrachialis tendons. Visualization of the cephalic vein indicates that the exposure is too far lateral. The horizontal fibers of the pectoralis major are identified, and a small incision through the inferior overlying fascia is directed laterally and then distally in line with the long axis of the humerus. Digital palpation helps identify the anterior humerus and fusiform LHB tendon running vertically within the intertubercular groove (Figure 4). Cephalad retraction of the pectoralis major allows direct visualization of the LHB tendon. A right-angle clamp is positioned deep to the LHB tendon and directed medial to lateral to retrieve the LHB tendon out of the incision.

No. 2 looped Fiberwire (Arthrex) is then whip-stitched from the top of the myotendinous junction up 20 mm (Figure 5). The remaining 2 to 3 cm of LHB tendon proximal to the whip-stitching may be excised to remove inflammatory tissue. The pectoralis major is retracted superiorly with an Army-Navy retractor while a pointed Hohmann retractor is placed laterally. Medial retraction of the conjoined tendon should be done carefully with a Chandler elevator and minimal levering. In a cadaveric study, Dickens and colleagues¹⁵ found that the musculocutaneous nerve, radial nerve, and deep brachial artery were all within 1 cm of the standard medial retractor. Compared with internal rotation of the arm, external rotation moves the musculocutaneous nerve 11 mm farther from the tenodesis site.¹⁵

Once exposure is adequate, the appropriate length–tension of the LHB tendon must be established. The inferior edge of the pectoralis major is used as a landmark. Anatomical studies have shown that the top of the LHB myotendinous junction lies 20 to 31 mm proximal to the inferior pectoralis edge.^16,17 Therefore, the tenodesis site should be 2 to 3 cm superior to the inferior pectoralis edge and centered on the humerus. Overall, the subpectoral location offers unique landmarks for LHB length-tensioning and provides soft-tissue coverage of the tenodesis site.

After identification of the appropriate tenodesis site, the surgeon chooses from a variety of fixation techniques. The “bone-tunnel technique” involves drilling an 8-mm unicortical hole through the anterior humerus followed by 2 smaller suture tunnels inferior to it; the LHB tendon with Krackow stitches is passed retrograde through the large hole by pulling the sutures through the smaller tunnels and tying them down.¹⁸ Despite the ease of performing this type of fixation, Mazzocca and colleagues¹⁹ found more cyclic displacement with bone tunnels than with interference screws and suture anchors. Other, less common techniques include the keyhole method (passing a rolled knot of LHB tendon through a keyhole in the bone)²⁰ and soft-tissue tenodesis to the rotator interval or conjoined tendon.^21,22 Recently, however, attention has turned mostly to interference screw and suture anchor fixation.

Multiple laboratory studies have demonstrated the superiority of interference screw fixation. Kilicoglu and colleagues²³ and Ozalay and colleagues²⁴ evaluated various fixation types in a sheep model, and both groups found the highest loads to failure with interference screws. Patzer and colleagues²⁵ compared interference screws and knotless suture anchors in a human cadaveric study and noted significantly higher failure loads with interference screws. Some authors^26,27 have presented conflicting laboratory data, and Millett and colleagues²⁸ reported no difference in clinical outcomes between interference screws and suture anchors. However, these studies have not demonstrated inferiority of interference screws, and, in light of other evidence suggesting its biomechanical superiority, we prefer interference screw fixation.^19,23-25,29

Exposing the bony surface for fixation involves electrocautery and subsequent use of a periosteal elevator to reflect a 1-cm periosteal window. A guide wire is drilled unicortically through the anterior cortex at the tenodesis site and is overreamed with an 8-mm cannulated reamer (Figure 6). This tunnel is then tapped, and bone debris is irrigated and suctioned from the wound. Cadaveric studies have shown no difference in failure loads with varying screw lengths or diameters.29,30 We use an 8×12-mm BioTenodesis screw (Arthrex) to match the typical width of the LHB tendon (Figures 7A-7C). One suture limb from the tendon whip-stitch is passed through the BioTenodesis screw and screwdriver. An assistant then uses a right-angle clamp as a pulley on the tendon so that the tendon may be visualized and “dunked” into the tunnel under direct visualization. As the screw is inserted, axial pressure is applied and the insertion paddle firmly held. Care should be taken to avoid overtightening the screw lest it become intramedullary. After the screw is flush to bone, the 2 whip-stitch suture limbs are tied for additional fixation.

Postoperative Rehabilitation

The optimal postoperative protocol for subpectoral biceps tenodesis has not been rigorously studied and is guided by the procedures performed with the biceps tenodesis. For the immediate postoperative period, Provencher and colleagues⁵ and Mazzocca and colleagues³¹ recommended immobilization in a sling during sleep and during the day if the patient is out in public or having difficulty maintaining the elbow flexed passively.

For isolated biceps tenodesis cases, passive- and active-assisted range of motion (ROM) of the glenohumeral, elbow, and wrist joints are permitted during the initial 4 weeks. At 3 weeks, the sling is discontinued and active ROM permitted. At 6 weeks, strengthening of the biceps, rotator cuff, deltoid, and periscapular muscles may begin with isometric contractions and progress to elastic bands and handheld weights. The same protocol is used if acromioplasty is performed at time of tenodesis. These patients may progress to active-assisted and active ROM earlier than 4 weeks if advised of the risks. However, sustained isometric biceps contraction, biceps strengthening, and resisted supination should not be performed until 6 weeks after surgery. If rotator cuff repair is performed, the patient is immobilized in a sling and passive ROM of the glenohumeral, elbow, and wrist joints is permitted during the first 6 weeks. The patient may progress to active-assisted and active ROM over the next 6 weeks, after motion is restored but before formal strengthening is initiated.³² For overhead athletes, Werner and colleagues³³ advocated a throwing program starting 3 to 4 months after surgery.

Outcomes and Complications

Mini-open subpectoral biceps tenodesis is a safe, reliable, and effective treatment for LHB tendon pathology. This procedure provides excellent pain relief and functional outcomes^32,34,35 and has a low complication rate.^5,35-40 At a mean of 29 months after biceps tenodesis with an interference screw, Mazzocca and colleagues³² found statistically significant improvements on all clinical outcome measures: Rowe, American Shoulder and Elbow Surgeons (ASES), Simple Shoulder Test (SST), Constant-Murley, and Single Assessment Numeric Evaluation (SANE). Biceps symmetry was restored in 35 of 41 patients. Millett and colleagues²⁸ reported that subpectoral biceps tenodesis relieved pain and improved function as measured by visual analog scale pain, ASES scores, and abbreviated Constant scores. Werner and colleagues³⁴ compared open subpectoral and arthroscopic suprapectoral techniques and found excellent clinical and functional outcomes with both techniques at a mean of 3.1 years. There were no significant differences in ROM, strength, or clinical outcome scores between the 2 techniques.

Potential complications include hematoma, seroma, hardware failure, reaction to biodegradable screw, persistent anterior shoulder pain, stiffness, humeral fracture, reflex sympathetic dystrophy, infection, nerve injury, and brachial artery injury. The musculocutaneous nerve can be lacerated during screw placement or even avulsed if the surgeon attempts to retrieve the LHB tendon blindly.⁴¹ In the most comprehensive study of tenodesis complications, Nho and colleagues35 recorded a 2% complication rate in 353 patients over 3 years. Persistent bicipital pain and fixation failure causing a Popeye deformity were the 2 most common complications (0.57% each). In a study of 103 patients, Abtahi and colleagues³⁹ found a 7% complication rate, with 4 superficial wound infections and 2 temporary nerve palsies. Millett and colleagues²⁸ reported low complication rates with both interference screw and suture anchor fixation. Neither technique had a fixation failure, and persistent bicipital groove tenderness occurred in just 3% of patients after interference screw fixation and in 7% after suture anchor fixation. Mazzocca and colleagues³² documented 1 fixation failure (2%) 1 year after interference screw fixation.

Werner and colleagues³⁴ encountered stiffness more than any other complication and found it to be more common in their arthroscopic group (9.4%) than in their open group (6.0%). They used intra-articular corticosteroid injections and physical therapy to successfully treat all cases of postoperative stiffness. Humeral fracture is uncommon after tenodesis.^37,42 In a recent biomechanical study, however, Euler and colleagues⁴⁰ found a significant reduction (25%) in humeral strength after a laterally eccentric, malpositioned biceps tenodesis. This decreased osseous strength may increase susceptibility to humeral shaft fracture, especially when interference screw fixation is used. Sears and colleagues³⁷ and Dein and colleagues⁴² presented case reports of humeral fracture after biceps tenodesis with an interference screw.

For patients with fixation failure or continued anterior shoulder pain, revision biceps tenodesis is safe and effective. Heckman and colleagues⁴³ and Gregory and colleagues⁴⁴ showed revision tenodesis can lead to excellent pain relief and functional outcomes, for it allows complete removal of the biceps from the groove and preserves biceps function. Gregory and colleagues⁴⁴ revised subpectoral biceps tenodesis for either continued pain or fixation failure and found significant improvements in pain and function a mean of 33.4 months after surgery. Anthony and colleagues⁴⁵ performed biceps tenodesis for failed surgical tenotomies and autorupture of the LHB tendon. In their study of 11 patients, this surgery resulted in symptom improvement, patient satisfaction, resolution of Popeye deformity, and predictable return to activity.

Conclusion

LHB tendon pathology is a significant source of anterior shoulder pain and functional limitation. Diagnosis and treatment of this pathology can be challenging, and it is important to identify any concomitant pathologies or other pain sources. After failed nonoperative management, surgeons have the option of mini-open subpectoral biceps tenodesis—a safe, reliable, and effective treatment with excellent outcomes. Although multiple fixation options are available, we think that, based on the current literature, fixation with a bioabsorbable interference screw remains the best option. This procedure has demonstrated efficacy for revision biceps tenodesis, failed biceps tenotomy, and autorupture of the biceps.

Tendinopathy of the long head of the biceps brachii (LHB) is a common source of anterior shoulder pain. The LHB tendon is an intra-articular yet extrasynovial structure, ensheathed by the synovial lining of the articular capsule.¹ Branches of the anterior circumflex humeral artery course along the bicipital groove, but the gliding undersurface of the LHB remains avascular.² Tendon irritation is most common within the groove and usually produces “tendinosis,” characterized by collagen fiber atrophy, fibrinoid necrosis, and fibrocyte proliferation.¹ Neviaser and colleagues³ correlated such changes in the LHB tendon with rotator cuff pathology, as the 2 often coexist. Primary LHB tendinitis is less common and associated with younger patients who engage in overhead activities, such as baseball and volleyball.⁴

Nonoperative management, which is trialed initially, consists of rest, use of nonsteroidal anti-inflammatory drugs, and physical therapy. Corticosteroid injections are administered through the subacromial space or glenohumeral joint, which is continuous with the LHB sheath. Some physicians give ultrasound-guided injections into the LHB sheath. For fear of tendon atrophy from corticosteroid injections, some physicians prefer iontophoresis with a topical steroid over the bicipital groove. If conservative measures fail, the physician can choose from 2 primary surgical options: biceps tenotomy and tenodesis. Tenodesis can be performed within the groove (suprapectoral) or subpectoral. In this review, we highlight 5 key features of subpectoral biceps tenodesis to guide treatment and improve outcomes.

Examination and Indications

Management of LHB tendinopathy begins with a complete physical examination. Tenderness over the bicipital groove is the most consistent finding, but this region may be difficult to localize in large individuals. The arm should be internally rotated 10° to orient the groove anterior and palpated 7 cm below the acromion.⁵ Anterior shoulder pain after resisted elevation with the elbow extended and supinated represents a positive Speed test. A positive Yergason test produces pain with resisted forearm supination while the elbow is flexed to 90°.

Evaluation of biceps instability is important in deciding which type of management (operative or nonoperative) is appropriate for a patient. Medial biceps subluxation may be detected by bringing the flexed arm from abduction, external rotation into cross-body adduction, internal rotation with decreased arm flexion.⁶ Another maneuver that elicits biceps irritation is combined abduction–extension, which places tension on the biceps tendon. Similarly, coracoid impingement may disrupt the subscapularis roof of the biceps sheath and cause LHB instability. Dines and colleagues⁷ reproduced the painful clicking of coracoid impingement by placing the shoulder in forward elevation, internal rotation, and varying degrees of adduction. Belly-press, lift-off, and internal rotation strength are other tests that assess subscapularis integrity. Rotator cuff impingement signs should be evaluated, and the contralateral shoulder should be examined for comparison.

Plain radiographs may show a pathology, such as anterior acromial spurring or posterior overgrowth of the coracoid, for which surgery is more suited. T2-weighted magnetic resonance imaging (MRI) may show an increased LHB signal, but this has shown poor concordance with arthroscopic findings of biceps pathology.⁸ Magnetic resonance arthrography can better detect medial dislocation of the LHB tendon from subscapularis tears. Ultrasound is cost-effective but highly operator-dependent.

Indications for biceps tenotomy or tenodesis include failed conservative management, partial-thickness LHB tears more than 25% to 50% in diameter, and medial subluxation of the LHB tendon with or without a subscapularis tear. Superior labrum anterior to posterior (SLAP) tears in older patients are a relative indication. Intraoperative findings may also indicate the need for LHB surgery. During the diagnostic arthroscopy, the LHB tendon should be evaluated for synovial inflammation or fraying (Figures 1A, 1B). This may need to be done under dry conditions, as pump pressure can compress and blunt the inflamed appearance. The O’Brien maneuver can be performed to demonstrate incarceration of the LHB tendon within the anterior glenohumeral joint. A probe should be placed through an anterior portal to pull the intertubercular LHB tendon into view, as this region is most commonly inflamed (Figure 2). Probing of the tendon also allows assessment of the stability of the biceps sling.

Surgical Technique

When biceps surgery is indicated, the surgeon must choose between tenotomy and tenodesis. Tenotomy is a low-demand procedure indicated for low-demand patients. A “Popeye” deformity may occur in up to 62% of patients, but Boileau and colleagues⁹ reported that none of their patients were bothered by it. Another concern after tenotomy is fatigue-cramping of the biceps muscle belly. Kelly and colleagues¹⁰ reported that up to 40% of patients had soreness and decreased strength with elbow flexion. Such cramping is more common in patients under age 60 years. For these reasons, biceps tenotomy should be reserved for older, low-demand patients who are not concerned about cosmesis and less likely to comply with postoperative motion restrictions.² We tend to perform tenotomy in obese patients, who may have a Popeye deformity that is not detectable, and in patients with diabetes; the goal is to avoid a wound infection resulting from the close proximity of tenodesis incision and axilla.

Biceps tenodesis should preserve the length–tension relationship of the biceps muscle and maintain its normal contour. Tenodesis location may be proximal or distal. Proximal fixation can be performed arthroscopically, and its advocates argue that keeping the LHB tendon within the bicipital groove preserves muscle strength. Boileau and Neyton11 found biceps strength to be 90% that of the contralateral arm after arthroscopic tenodesis. The bicipital groove, however, is lined with synovium and is a primary site of LHB pathology. Up to 78% of intra-articular biceps tears extend through the groove outside the joint.¹² Proximal tenodesis thus retains a major pain generator. In a retrospective study of 188 patients, Sanders and colleagues^13,14 found a 36% revision rate after proximal arthroscopic tenodesis and a 13% rate after proximal open tenodesis with an intact biceps sheath—significantly lower than the 3% after distal tenodesis outside the bicipital groove.¹ For this reason, we advocate distal biceps tenodesis beneath the pectoralis major tendon. After tenotomy with an arthroscopic basket (Figure 3), the LHB tendon is retracted out of the glenohumeral joint by extending the elbow. For the mini-open incision, the head of the bed is lowered from the beach-chair position to 30°. The arm is abducted on a Mayo stand, and the inferior border of the pectoralis major tendon is palpated. A 3-cm vertical incision is made along the medial arm starting 1 cm superior to the inferior pectoralis edge. The subcutaneous tissues are mobilized, and dissection is carried down to the pectoralis major and coracobrachialis tendons. Visualization of the cephalic vein indicates that the exposure is too far lateral. The horizontal fibers of the pectoralis major are identified, and a small incision through the inferior overlying fascia is directed laterally and then distally in line with the long axis of the humerus. Digital palpation helps identify the anterior humerus and fusiform LHB tendon running vertically within the intertubercular groove (Figure 4). Cephalad retraction of the pectoralis major allows direct visualization of the LHB tendon. A right-angle clamp is positioned deep to the LHB tendon and directed medial to lateral to retrieve the LHB tendon out of the incision.

No. 2 looped Fiberwire (Arthrex) is then whip-stitched from the top of the myotendinous junction up 20 mm (Figure 5). The remaining 2 to 3 cm of LHB tendon proximal to the whip-stitching may be excised to remove inflammatory tissue. The pectoralis major is retracted superiorly with an Army-Navy retractor while a pointed Hohmann retractor is placed laterally. Medial retraction of the conjoined tendon should be done carefully with a Chandler elevator and minimal levering. In a cadaveric study, Dickens and colleagues¹⁵ found that the musculocutaneous nerve, radial nerve, and deep brachial artery were all within 1 cm of the standard medial retractor. Compared with internal rotation of the arm, external rotation moves the musculocutaneous nerve 11 mm farther from the tenodesis site.¹⁵

Once exposure is adequate, the appropriate length–tension of the LHB tendon must be established. The inferior edge of the pectoralis major is used as a landmark. Anatomical studies have shown that the top of the LHB myotendinous junction lies 20 to 31 mm proximal to the inferior pectoralis edge.^16,17 Therefore, the tenodesis site should be 2 to 3 cm superior to the inferior pectoralis edge and centered on the humerus. Overall, the subpectoral location offers unique landmarks for LHB length-tensioning and provides soft-tissue coverage of the tenodesis site.

After identification of the appropriate tenodesis site, the surgeon chooses from a variety of fixation techniques. The “bone-tunnel technique” involves drilling an 8-mm unicortical hole through the anterior humerus followed by 2 smaller suture tunnels inferior to it; the LHB tendon with Krackow stitches is passed retrograde through the large hole by pulling the sutures through the smaller tunnels and tying them down.¹⁸ Despite the ease of performing this type of fixation, Mazzocca and colleagues¹⁹ found more cyclic displacement with bone tunnels than with interference screws and suture anchors. Other, less common techniques include the keyhole method (passing a rolled knot of LHB tendon through a keyhole in the bone)²⁰ and soft-tissue tenodesis to the rotator interval or conjoined tendon.^21,22 Recently, however, attention has turned mostly to interference screw and suture anchor fixation.

Multiple laboratory studies have demonstrated the superiority of interference screw fixation. Kilicoglu and colleagues²³ and Ozalay and colleagues²⁴ evaluated various fixation types in a sheep model, and both groups found the highest loads to failure with interference screws. Patzer and colleagues²⁵ compared interference screws and knotless suture anchors in a human cadaveric study and noted significantly higher failure loads with interference screws. Some authors^26,27 have presented conflicting laboratory data, and Millett and colleagues²⁸ reported no difference in clinical outcomes between interference screws and suture anchors. However, these studies have not demonstrated inferiority of interference screws, and, in light of other evidence suggesting its biomechanical superiority, we prefer interference screw fixation.^19,23-25,29

Exposing the bony surface for fixation involves electrocautery and subsequent use of a periosteal elevator to reflect a 1-cm periosteal window. A guide wire is drilled unicortically through the anterior cortex at the tenodesis site and is overreamed with an 8-mm cannulated reamer (Figure 6). This tunnel is then tapped, and bone debris is irrigated and suctioned from the wound. Cadaveric studies have shown no difference in failure loads with varying screw lengths or diameters.29,30 We use an 8×12-mm BioTenodesis screw (Arthrex) to match the typical width of the LHB tendon (Figures 7A-7C). One suture limb from the tendon whip-stitch is passed through the BioTenodesis screw and screwdriver. An assistant then uses a right-angle clamp as a pulley on the tendon so that the tendon may be visualized and “dunked” into the tunnel under direct visualization. As the screw is inserted, axial pressure is applied and the insertion paddle firmly held. Care should be taken to avoid overtightening the screw lest it become intramedullary. After the screw is flush to bone, the 2 whip-stitch suture limbs are tied for additional fixation.

Postoperative Rehabilitation

The optimal postoperative protocol for subpectoral biceps tenodesis has not been rigorously studied and is guided by the procedures performed with the biceps tenodesis. For the immediate postoperative period, Provencher and colleagues⁵ and Mazzocca and colleagues³¹ recommended immobilization in a sling during sleep and during the day if the patient is out in public or having difficulty maintaining the elbow flexed passively.

For isolated biceps tenodesis cases, passive- and active-assisted range of motion (ROM) of the glenohumeral, elbow, and wrist joints are permitted during the initial 4 weeks. At 3 weeks, the sling is discontinued and active ROM permitted. At 6 weeks, strengthening of the biceps, rotator cuff, deltoid, and periscapular muscles may begin with isometric contractions and progress to elastic bands and handheld weights. The same protocol is used if acromioplasty is performed at time of tenodesis. These patients may progress to active-assisted and active ROM earlier than 4 weeks if advised of the risks. However, sustained isometric biceps contraction, biceps strengthening, and resisted supination should not be performed until 6 weeks after surgery. If rotator cuff repair is performed, the patient is immobilized in a sling and passive ROM of the glenohumeral, elbow, and wrist joints is permitted during the first 6 weeks. The patient may progress to active-assisted and active ROM over the next 6 weeks, after motion is restored but before formal strengthening is initiated.³² For overhead athletes, Werner and colleagues³³ advocated a throwing program starting 3 to 4 months after surgery.

Outcomes and Complications

Mini-open subpectoral biceps tenodesis is a safe, reliable, and effective treatment for LHB tendon pathology. This procedure provides excellent pain relief and functional outcomes^32,34,35 and has a low complication rate.^5,35-40 At a mean of 29 months after biceps tenodesis with an interference screw, Mazzocca and colleagues³² found statistically significant improvements on all clinical outcome measures: Rowe, American Shoulder and Elbow Surgeons (ASES), Simple Shoulder Test (SST), Constant-Murley, and Single Assessment Numeric Evaluation (SANE). Biceps symmetry was restored in 35 of 41 patients. Millett and colleagues²⁸ reported that subpectoral biceps tenodesis relieved pain and improved function as measured by visual analog scale pain, ASES scores, and abbreviated Constant scores. Werner and colleagues³⁴ compared open subpectoral and arthroscopic suprapectoral techniques and found excellent clinical and functional outcomes with both techniques at a mean of 3.1 years. There were no significant differences in ROM, strength, or clinical outcome scores between the 2 techniques.

Potential complications include hematoma, seroma, hardware failure, reaction to biodegradable screw, persistent anterior shoulder pain, stiffness, humeral fracture, reflex sympathetic dystrophy, infection, nerve injury, and brachial artery injury. The musculocutaneous nerve can be lacerated during screw placement or even avulsed if the surgeon attempts to retrieve the LHB tendon blindly.⁴¹ In the most comprehensive study of tenodesis complications, Nho and colleagues35 recorded a 2% complication rate in 353 patients over 3 years. Persistent bicipital pain and fixation failure causing a Popeye deformity were the 2 most common complications (0.57% each). In a study of 103 patients, Abtahi and colleagues³⁹ found a 7% complication rate, with 4 superficial wound infections and 2 temporary nerve palsies. Millett and colleagues²⁸ reported low complication rates with both interference screw and suture anchor fixation. Neither technique had a fixation failure, and persistent bicipital groove tenderness occurred in just 3% of patients after interference screw fixation and in 7% after suture anchor fixation. Mazzocca and colleagues³² documented 1 fixation failure (2%) 1 year after interference screw fixation.

Werner and colleagues³⁴ encountered stiffness more than any other complication and found it to be more common in their arthroscopic group (9.4%) than in their open group (6.0%). They used intra-articular corticosteroid injections and physical therapy to successfully treat all cases of postoperative stiffness. Humeral fracture is uncommon after tenodesis.^37,42 In a recent biomechanical study, however, Euler and colleagues⁴⁰ found a significant reduction (25%) in humeral strength after a laterally eccentric, malpositioned biceps tenodesis. This decreased osseous strength may increase susceptibility to humeral shaft fracture, especially when interference screw fixation is used. Sears and colleagues³⁷ and Dein and colleagues⁴² presented case reports of humeral fracture after biceps tenodesis with an interference screw.

For patients with fixation failure or continued anterior shoulder pain, revision biceps tenodesis is safe and effective. Heckman and colleagues⁴³ and Gregory and colleagues⁴⁴ showed revision tenodesis can lead to excellent pain relief and functional outcomes, for it allows complete removal of the biceps from the groove and preserves biceps function. Gregory and colleagues⁴⁴ revised subpectoral biceps tenodesis for either continued pain or fixation failure and found significant improvements in pain and function a mean of 33.4 months after surgery. Anthony and colleagues⁴⁵ performed biceps tenodesis for failed surgical tenotomies and autorupture of the LHB tendon. In their study of 11 patients, this surgery resulted in symptom improvement, patient satisfaction, resolution of Popeye deformity, and predictable return to activity.

Conclusion

LHB tendon pathology is a significant source of anterior shoulder pain and functional limitation. Diagnosis and treatment of this pathology can be challenging, and it is important to identify any concomitant pathologies or other pain sources. After failed nonoperative management, surgeons have the option of mini-open subpectoral biceps tenodesis—a safe, reliable, and effective treatment with excellent outcomes. Although multiple fixation options are available, we think that, based on the current literature, fixation with a bioabsorbable interference screw remains the best option. This procedure has demonstrated efficacy for revision biceps tenodesis, failed biceps tenotomy, and autorupture of the biceps.

Tendinopathy of the long head of the biceps brachii (LHB) is a common source of anterior shoulder pain. The LHB tendon is an intra-articular yet extrasynovial structure, ensheathed by the synovial lining of the articular capsule.¹ Branches of the anterior circumflex humeral artery course along the bicipital groove, but the gliding undersurface of the LHB remains avascular.² Tendon irritation is most common within the groove and usually produces “tendinosis,” characterized by collagen fiber atrophy, fibrinoid necrosis, and fibrocyte proliferation.¹ Neviaser and colleagues³ correlated such changes in the LHB tendon with rotator cuff pathology, as the 2 often coexist. Primary LHB tendinitis is less common and associated with younger patients who engage in overhead activities, such as baseball and volleyball.⁴

Nonoperative management, which is trialed initially, consists of rest, use of nonsteroidal anti-inflammatory drugs, and physical therapy. Corticosteroid injections are administered through the subacromial space or glenohumeral joint, which is continuous with the LHB sheath. Some physicians give ultrasound-guided injections into the LHB sheath. For fear of tendon atrophy from corticosteroid injections, some physicians prefer iontophoresis with a topical steroid over the bicipital groove. If conservative measures fail, the physician can choose from 2 primary surgical options: biceps tenotomy and tenodesis. Tenodesis can be performed within the groove (suprapectoral) or subpectoral. In this review, we highlight 5 key features of subpectoral biceps tenodesis to guide treatment and improve outcomes.

Examination and Indications

Management of LHB tendinopathy begins with a complete physical examination. Tenderness over the bicipital groove is the most consistent finding, but this region may be difficult to localize in large individuals. The arm should be internally rotated 10° to orient the groove anterior and palpated 7 cm below the acromion.⁵ Anterior shoulder pain after resisted elevation with the elbow extended and supinated represents a positive Speed test. A positive Yergason test produces pain with resisted forearm supination while the elbow is flexed to 90°.

Evaluation of biceps instability is important in deciding which type of management (operative or nonoperative) is appropriate for a patient. Medial biceps subluxation may be detected by bringing the flexed arm from abduction, external rotation into cross-body adduction, internal rotation with decreased arm flexion.⁶ Another maneuver that elicits biceps irritation is combined abduction–extension, which places tension on the biceps tendon. Similarly, coracoid impingement may disrupt the subscapularis roof of the biceps sheath and cause LHB instability. Dines and colleagues⁷ reproduced the painful clicking of coracoid impingement by placing the shoulder in forward elevation, internal rotation, and varying degrees of adduction. Belly-press, lift-off, and internal rotation strength are other tests that assess subscapularis integrity. Rotator cuff impingement signs should be evaluated, and the contralateral shoulder should be examined for comparison.

Plain radiographs may show a pathology, such as anterior acromial spurring or posterior overgrowth of the coracoid, for which surgery is more suited. T2-weighted magnetic resonance imaging (MRI) may show an increased LHB signal, but this has shown poor concordance with arthroscopic findings of biceps pathology.⁸ Magnetic resonance arthrography can better detect medial dislocation of the LHB tendon from subscapularis tears. Ultrasound is cost-effective but highly operator-dependent.

Indications for biceps tenotomy or tenodesis include failed conservative management, partial-thickness LHB tears more than 25% to 50% in diameter, and medial subluxation of the LHB tendon with or without a subscapularis tear. Superior labrum anterior to posterior (SLAP) tears in older patients are a relative indication. Intraoperative findings may also indicate the need for LHB surgery. During the diagnostic arthroscopy, the LHB tendon should be evaluated for synovial inflammation or fraying (Figures 1A, 1B). This may need to be done under dry conditions, as pump pressure can compress and blunt the inflamed appearance. The O’Brien maneuver can be performed to demonstrate incarceration of the LHB tendon within the anterior glenohumeral joint. A probe should be placed through an anterior portal to pull the intertubercular LHB tendon into view, as this region is most commonly inflamed (Figure 2). Probing of the tendon also allows assessment of the stability of the biceps sling.

Surgical Technique

When biceps surgery is indicated, the surgeon must choose between tenotomy and tenodesis. Tenotomy is a low-demand procedure indicated for low-demand patients. A “Popeye” deformity may occur in up to 62% of patients, but Boileau and colleagues⁹ reported that none of their patients were bothered by it. Another concern after tenotomy is fatigue-cramping of the biceps muscle belly. Kelly and colleagues¹⁰ reported that up to 40% of patients had soreness and decreased strength with elbow flexion. Such cramping is more common in patients under age 60 years. For these reasons, biceps tenotomy should be reserved for older, low-demand patients who are not concerned about cosmesis and less likely to comply with postoperative motion restrictions.² We tend to perform tenotomy in obese patients, who may have a Popeye deformity that is not detectable, and in patients with diabetes; the goal is to avoid a wound infection resulting from the close proximity of tenodesis incision and axilla.

Biceps tenodesis should preserve the length–tension relationship of the biceps muscle and maintain its normal contour. Tenodesis location may be proximal or distal. Proximal fixation can be performed arthroscopically, and its advocates argue that keeping the LHB tendon within the bicipital groove preserves muscle strength. Boileau and Neyton11 found biceps strength to be 90% that of the contralateral arm after arthroscopic tenodesis. The bicipital groove, however, is lined with synovium and is a primary site of LHB pathology. Up to 78% of intra-articular biceps tears extend through the groove outside the joint.¹² Proximal tenodesis thus retains a major pain generator. In a retrospective study of 188 patients, Sanders and colleagues^13,14 found a 36% revision rate after proximal arthroscopic tenodesis and a 13% rate after proximal open tenodesis with an intact biceps sheath—significantly lower than the 3% after distal tenodesis outside the bicipital groove.¹ For this reason, we advocate distal biceps tenodesis beneath the pectoralis major tendon. After tenotomy with an arthroscopic basket (Figure 3), the LHB tendon is retracted out of the glenohumeral joint by extending the elbow. For the mini-open incision, the head of the bed is lowered from the beach-chair position to 30°. The arm is abducted on a Mayo stand, and the inferior border of the pectoralis major tendon is palpated. A 3-cm vertical incision is made along the medial arm starting 1 cm superior to the inferior pectoralis edge. The subcutaneous tissues are mobilized, and dissection is carried down to the pectoralis major and coracobrachialis tendons. Visualization of the cephalic vein indicates that the exposure is too far lateral. The horizontal fibers of the pectoralis major are identified, and a small incision through the inferior overlying fascia is directed laterally and then distally in line with the long axis of the humerus. Digital palpation helps identify the anterior humerus and fusiform LHB tendon running vertically within the intertubercular groove (Figure 4). Cephalad retraction of the pectoralis major allows direct visualization of the LHB tendon. A right-angle clamp is positioned deep to the LHB tendon and directed medial to lateral to retrieve the LHB tendon out of the incision.

No. 2 looped Fiberwire (Arthrex) is then whip-stitched from the top of the myotendinous junction up 20 mm (Figure 5). The remaining 2 to 3 cm of LHB tendon proximal to the whip-stitching may be excised to remove inflammatory tissue. The pectoralis major is retracted superiorly with an Army-Navy retractor while a pointed Hohmann retractor is placed laterally. Medial retraction of the conjoined tendon should be done carefully with a Chandler elevator and minimal levering. In a cadaveric study, Dickens and colleagues¹⁵ found that the musculocutaneous nerve, radial nerve, and deep brachial artery were all within 1 cm of the standard medial retractor. Compared with internal rotation of the arm, external rotation moves the musculocutaneous nerve 11 mm farther from the tenodesis site.¹⁵

Once exposure is adequate, the appropriate length–tension of the LHB tendon must be established. The inferior edge of the pectoralis major is used as a landmark. Anatomical studies have shown that the top of the LHB myotendinous junction lies 20 to 31 mm proximal to the inferior pectoralis edge.^16,17 Therefore, the tenodesis site should be 2 to 3 cm superior to the inferior pectoralis edge and centered on the humerus. Overall, the subpectoral location offers unique landmarks for LHB length-tensioning and provides soft-tissue coverage of the tenodesis site.

After identification of the appropriate tenodesis site, the surgeon chooses from a variety of fixation techniques. The “bone-tunnel technique” involves drilling an 8-mm unicortical hole through the anterior humerus followed by 2 smaller suture tunnels inferior to it; the LHB tendon with Krackow stitches is passed retrograde through the large hole by pulling the sutures through the smaller tunnels and tying them down.¹⁸ Despite the ease of performing this type of fixation, Mazzocca and colleagues¹⁹ found more cyclic displacement with bone tunnels than with interference screws and suture anchors. Other, less common techniques include the keyhole method (passing a rolled knot of LHB tendon through a keyhole in the bone)²⁰ and soft-tissue tenodesis to the rotator interval or conjoined tendon.^21,22 Recently, however, attention has turned mostly to interference screw and suture anchor fixation.

Multiple laboratory studies have demonstrated the superiority of interference screw fixation. Kilicoglu and colleagues²³ and Ozalay and colleagues²⁴ evaluated various fixation types in a sheep model, and both groups found the highest loads to failure with interference screws. Patzer and colleagues²⁵ compared interference screws and knotless suture anchors in a human cadaveric study and noted significantly higher failure loads with interference screws. Some authors^26,27 have presented conflicting laboratory data, and Millett and colleagues²⁸ reported no difference in clinical outcomes between interference screws and suture anchors. However, these studies have not demonstrated inferiority of interference screws, and, in light of other evidence suggesting its biomechanical superiority, we prefer interference screw fixation.^19,23-25,29

Exposing the bony surface for fixation involves electrocautery and subsequent use of a periosteal elevator to reflect a 1-cm periosteal window. A guide wire is drilled unicortically through the anterior cortex at the tenodesis site and is overreamed with an 8-mm cannulated reamer (Figure 6). This tunnel is then tapped, and bone debris is irrigated and suctioned from the wound. Cadaveric studies have shown no difference in failure loads with varying screw lengths or diameters.29,30 We use an 8×12-mm BioTenodesis screw (Arthrex) to match the typical width of the LHB tendon (Figures 7A-7C). One suture limb from the tendon whip-stitch is passed through the BioTenodesis screw and screwdriver. An assistant then uses a right-angle clamp as a pulley on the tendon so that the tendon may be visualized and “dunked” into the tunnel under direct visualization. As the screw is inserted, axial pressure is applied and the insertion paddle firmly held. Care should be taken to avoid overtightening the screw lest it become intramedullary. After the screw is flush to bone, the 2 whip-stitch suture limbs are tied for additional fixation.

Postoperative Rehabilitation

The optimal postoperative protocol for subpectoral biceps tenodesis has not been rigorously studied and is guided by the procedures performed with the biceps tenodesis. For the immediate postoperative period, Provencher and colleagues⁵ and Mazzocca and colleagues³¹ recommended immobilization in a sling during sleep and during the day if the patient is out in public or having difficulty maintaining the elbow flexed passively.

For isolated biceps tenodesis cases, passive- and active-assisted range of motion (ROM) of the glenohumeral, elbow, and wrist joints are permitted during the initial 4 weeks. At 3 weeks, the sling is discontinued and active ROM permitted. At 6 weeks, strengthening of the biceps, rotator cuff, deltoid, and periscapular muscles may begin with isometric contractions and progress to elastic bands and handheld weights. The same protocol is used if acromioplasty is performed at time of tenodesis. These patients may progress to active-assisted and active ROM earlier than 4 weeks if advised of the risks. However, sustained isometric biceps contraction, biceps strengthening, and resisted supination should not be performed until 6 weeks after surgery. If rotator cuff repair is performed, the patient is immobilized in a sling and passive ROM of the glenohumeral, elbow, and wrist joints is permitted during the first 6 weeks. The patient may progress to active-assisted and active ROM over the next 6 weeks, after motion is restored but before formal strengthening is initiated.³² For overhead athletes, Werner and colleagues³³ advocated a throwing program starting 3 to 4 months after surgery.

Outcomes and Complications

Mini-open subpectoral biceps tenodesis is a safe, reliable, and effective treatment for LHB tendon pathology. This procedure provides excellent pain relief and functional outcomes^32,34,35 and has a low complication rate.^5,35-40 At a mean of 29 months after biceps tenodesis with an interference screw, Mazzocca and colleagues³² found statistically significant improvements on all clinical outcome measures: Rowe, American Shoulder and Elbow Surgeons (ASES), Simple Shoulder Test (SST), Constant-Murley, and Single Assessment Numeric Evaluation (SANE). Biceps symmetry was restored in 35 of 41 patients. Millett and colleagues²⁸ reported that subpectoral biceps tenodesis relieved pain and improved function as measured by visual analog scale pain, ASES scores, and abbreviated Constant scores. Werner and colleagues³⁴ compared open subpectoral and arthroscopic suprapectoral techniques and found excellent clinical and functional outcomes with both techniques at a mean of 3.1 years. There were no significant differences in ROM, strength, or clinical outcome scores between the 2 techniques.

Potential complications include hematoma, seroma, hardware failure, reaction to biodegradable screw, persistent anterior shoulder pain, stiffness, humeral fracture, reflex sympathetic dystrophy, infection, nerve injury, and brachial artery injury. The musculocutaneous nerve can be lacerated during screw placement or even avulsed if the surgeon attempts to retrieve the LHB tendon blindly.⁴¹ In the most comprehensive study of tenodesis complications, Nho and colleagues35 recorded a 2% complication rate in 353 patients over 3 years. Persistent bicipital pain and fixation failure causing a Popeye deformity were the 2 most common complications (0.57% each). In a study of 103 patients, Abtahi and colleagues³⁹ found a 7% complication rate, with 4 superficial wound infections and 2 temporary nerve palsies. Millett and colleagues²⁸ reported low complication rates with both interference screw and suture anchor fixation. Neither technique had a fixation failure, and persistent bicipital groove tenderness occurred in just 3% of patients after interference screw fixation and in 7% after suture anchor fixation. Mazzocca and colleagues³² documented 1 fixation failure (2%) 1 year after interference screw fixation.

Werner and colleagues³⁴ encountered stiffness more than any other complication and found it to be more common in their arthroscopic group (9.4%) than in their open group (6.0%). They used intra-articular corticosteroid injections and physical therapy to successfully treat all cases of postoperative stiffness. Humeral fracture is uncommon after tenodesis.^37,42 In a recent biomechanical study, however, Euler and colleagues⁴⁰ found a significant reduction (25%) in humeral strength after a laterally eccentric, malpositioned biceps tenodesis. This decreased osseous strength may increase susceptibility to humeral shaft fracture, especially when interference screw fixation is used. Sears and colleagues³⁷ and Dein and colleagues⁴² presented case reports of humeral fracture after biceps tenodesis with an interference screw.

For patients with fixation failure or continued anterior shoulder pain, revision biceps tenodesis is safe and effective. Heckman and colleagues⁴³ and Gregory and colleagues⁴⁴ showed revision tenodesis can lead to excellent pain relief and functional outcomes, for it allows complete removal of the biceps from the groove and preserves biceps function. Gregory and colleagues⁴⁴ revised subpectoral biceps tenodesis for either continued pain or fixation failure and found significant improvements in pain and function a mean of 33.4 months after surgery. Anthony and colleagues⁴⁵ performed biceps tenodesis for failed surgical tenotomies and autorupture of the LHB tendon. In their study of 11 patients, this surgery resulted in symptom improvement, patient satisfaction, resolution of Popeye deformity, and predictable return to activity.

Conclusion

LHB tendon pathology is a significant source of anterior shoulder pain and functional limitation. Diagnosis and treatment of this pathology can be challenging, and it is important to identify any concomitant pathologies or other pain sources. After failed nonoperative management, surgeons have the option of mini-open subpectoral biceps tenodesis—a safe, reliable, and effective treatment with excellent outcomes. Although multiple fixation options are available, we think that, based on the current literature, fixation with a bioabsorbable interference screw remains the best option. This procedure has demonstrated efficacy for revision biceps tenodesis, failed biceps tenotomy, and autorupture of the biceps.

The widespread use of eponyms and acronyms to describe labroligamentous findings in the shoulder has made interpretation of shoulder magnetic resonance imaging (MRI) reports challenging. We review and discuss the appearance of these lesions on shoulder MRI to help the orthopedic surgeon understand these entities as imaging findings.

Glenolabral articular disruption (GLAD) occurs secondary to impaction of the humeral head on the glenoid articular cartilage. There is a resultant defect in the glenoid articular cartilage, which extends to the glenoid labrum. A GLAD lesion is diagnosed only if the glenohumeral ligament and scapular periosteum remain intact¹ (Figure 1).

Complete detachment of the anteroinferior labrum with tearing of the anterior glenoid periosteum represents a Bankart lesion. Cartilaginous Bankart lesions are caused by an anterior glenohumeral dislocation with resultant avulsion of the anteroinferior labrum and disruption of the scapular periosteum because of acute traction on the anterior band of the inferior glenohumeral ligament (Figure 2). Anterior instability, caused by disruption of the anterior labroligamentous complex, results. Osseous Bankart lesions occur when the anterior displaced humeral head impacts the anterior inferior glenoid rim, causing a fracture (Figure 3). This loss of the glenoid articular surface area can result in glenohumeral instability. Posterior shoulder dislocations can result in corresponding findings in the posterior inferior glenoid labrum (reverse Bankart lesion) and anterior medial humeral head (reverse Hill-Sachs lesion) (Figure 2).

A variant of the Bankart lesion is the anterior labroligamentous periosteal sleeve avulsion (ALPSA). This refers to a medially displaced tear of the anterior labrum with intact periosteal stripping along the medial glenoid²with medial rotation and inferior displacement of the anterior inferior labrum along the scapular neck. An ALPSA lesion can heal via the intact periosteal blood supply. If not repaired, anterior instability will result because of malposition of the labrum, causing a patulous anterior capsule.³ When a corresponding lesion occurs in the posterior labrum because of a posterior dislocation, it is called a posterior labrocapsular periosteal sleeve avulsion (POLPSA) (Figure 4).

Another variant of the Bankart lesion is the Perthes lesion, which is a nondisplaced tear of the anteroinferior labrum with periosteal stripping. This differs from the ALPSA because the detached labrum and periosteum are held in anatomic position, possibly making the lesion difficult to detect on magnetic resonance arthrography (MRA).³ Obtaining images in the abduction external rotation (ABER) position exerts traction on the anterior inferior joint capsule and may make the Perthes lesion more conspicuous.⁴ When this occurs in the posterior labrum, it is called a reverse Perthes lesion (Figure 5).

In a patient with anterior glenohumeral instability without a Bankart lesion, pathology of the anterior band of the inferior glenohumeral ligament (IGHL) at its humeral attachment must be suspected. Humeral avulsion of the IGHL (HAGL) or its variants can be overlooked on arthroscopy. HAGL is diagnosed on MRA when the normally U-shaped IGHL takes on a J-shape, and joint fluid extravasates across the torn humeral attachment (Figure 6). If there is an avulsed bony fragment from the medial humeral neck, the lesion is termed a bony HAGL (BHAGL). In addition to the findings of a HAGL, a BHAGL shows the osseous fragment and donor site on MRI. Since a BHAGL is a bony avulsion, it can even be suggested on radiography if a bony fragment is seen adjacent to the medial humeral neck.⁵ These lesions are highly associated with other shoulder injuries, particularly Hill-Sachs deformities and subscapularis tendon tears, and it is imperative, therefore, to search for additional injuries if a HAGL-type injury is seen.⁶

A more uncommon type of HAGL can occur in the setting of posterior capsulolabral injury. A posterior-band IGHL avulsion from the humerus (PHAGL) has similar imaging findings to a HAGL, except that it involves the posterior band of the IGHL. PHAGLs are usually not associated with an acute injury and are thought to be related to repetitive microtrauma, perhaps since the posterior band of the IGHL is the thinnest portion of the IGHL complex.⁷

A Kim lesion is an arthroscopic finding described in patients with posterior instability as a superficial defect at the undersurface of the posterior labrum and adjacent glenoid cartilage without detachment or extension to the chondrolabral junction.⁸ It is, by its nature, a concealed finding on routine MRI but can be more conspicuous in FADIR (flexed, adducted, internally rotated) positioning on MRA, which exerts traction on the posterior joint capsule, allowing intra-articular contrast to fill the tear (Figure 7).

This list describes several of the most commonly encountered acronyms in shoulder MRI. A review of SLAP (superior labrum anterior to posterior) lesions was described in a previous article in the journal’s Imaging Series.⁹ A thorough understanding of these lesions is helpful in interpreting reports and determining the appropriate treatment for patients with shoulder injuries.

The widespread use of eponyms and acronyms to describe labroligamentous findings in the shoulder has made interpretation of shoulder magnetic resonance imaging (MRI) reports challenging. We review and discuss the appearance of these lesions on shoulder MRI to help the orthopedic surgeon understand these entities as imaging findings.

Glenolabral articular disruption (GLAD) occurs secondary to impaction of the humeral head on the glenoid articular cartilage. There is a resultant defect in the glenoid articular cartilage, which extends to the glenoid labrum. A GLAD lesion is diagnosed only if the glenohumeral ligament and scapular periosteum remain intact¹ (Figure 1).

Complete detachment of the anteroinferior labrum with tearing of the anterior glenoid periosteum represents a Bankart lesion. Cartilaginous Bankart lesions are caused by an anterior glenohumeral dislocation with resultant avulsion of the anteroinferior labrum and disruption of the scapular periosteum because of acute traction on the anterior band of the inferior glenohumeral ligament (Figure 2). Anterior instability, caused by disruption of the anterior labroligamentous complex, results. Osseous Bankart lesions occur when the anterior displaced humeral head impacts the anterior inferior glenoid rim, causing a fracture (Figure 3). This loss of the glenoid articular surface area can result in glenohumeral instability. Posterior shoulder dislocations can result in corresponding findings in the posterior inferior glenoid labrum (reverse Bankart lesion) and anterior medial humeral head (reverse Hill-Sachs lesion) (Figure 2).

A variant of the Bankart lesion is the anterior labroligamentous periosteal sleeve avulsion (ALPSA). This refers to a medially displaced tear of the anterior labrum with intact periosteal stripping along the medial glenoid²with medial rotation and inferior displacement of the anterior inferior labrum along the scapular neck. An ALPSA lesion can heal via the intact periosteal blood supply. If not repaired, anterior instability will result because of malposition of the labrum, causing a patulous anterior capsule.³ When a corresponding lesion occurs in the posterior labrum because of a posterior dislocation, it is called a posterior labrocapsular periosteal sleeve avulsion (POLPSA) (Figure 4).

Another variant of the Bankart lesion is the Perthes lesion, which is a nondisplaced tear of the anteroinferior labrum with periosteal stripping. This differs from the ALPSA because the detached labrum and periosteum are held in anatomic position, possibly making the lesion difficult to detect on magnetic resonance arthrography (MRA).³ Obtaining images in the abduction external rotation (ABER) position exerts traction on the anterior inferior joint capsule and may make the Perthes lesion more conspicuous.⁴ When this occurs in the posterior labrum, it is called a reverse Perthes lesion (Figure 5).

In a patient with anterior glenohumeral instability without a Bankart lesion, pathology of the anterior band of the inferior glenohumeral ligament (IGHL) at its humeral attachment must be suspected. Humeral avulsion of the IGHL (HAGL) or its variants can be overlooked on arthroscopy. HAGL is diagnosed on MRA when the normally U-shaped IGHL takes on a J-shape, and joint fluid extravasates across the torn humeral attachment (Figure 6). If there is an avulsed bony fragment from the medial humeral neck, the lesion is termed a bony HAGL (BHAGL). In addition to the findings of a HAGL, a BHAGL shows the osseous fragment and donor site on MRI. Since a BHAGL is a bony avulsion, it can even be suggested on radiography if a bony fragment is seen adjacent to the medial humeral neck.⁵ These lesions are highly associated with other shoulder injuries, particularly Hill-Sachs deformities and subscapularis tendon tears, and it is imperative, therefore, to search for additional injuries if a HAGL-type injury is seen.⁶

A more uncommon type of HAGL can occur in the setting of posterior capsulolabral injury. A posterior-band IGHL avulsion from the humerus (PHAGL) has similar imaging findings to a HAGL, except that it involves the posterior band of the IGHL. PHAGLs are usually not associated with an acute injury and are thought to be related to repetitive microtrauma, perhaps since the posterior band of the IGHL is the thinnest portion of the IGHL complex.⁷

A Kim lesion is an arthroscopic finding described in patients with posterior instability as a superficial defect at the undersurface of the posterior labrum and adjacent glenoid cartilage without detachment or extension to the chondrolabral junction.⁸ It is, by its nature, a concealed finding on routine MRI but can be more conspicuous in FADIR (flexed, adducted, internally rotated) positioning on MRA, which exerts traction on the posterior joint capsule, allowing intra-articular contrast to fill the tear (Figure 7).

This list describes several of the most commonly encountered acronyms in shoulder MRI. A review of SLAP (superior labrum anterior to posterior) lesions was described in a previous article in the journal’s Imaging Series.⁹ A thorough understanding of these lesions is helpful in interpreting reports and determining the appropriate treatment for patients with shoulder injuries.

The widespread use of eponyms and acronyms to describe labroligamentous findings in the shoulder has made interpretation of shoulder magnetic resonance imaging (MRI) reports challenging. We review and discuss the appearance of these lesions on shoulder MRI to help the orthopedic surgeon understand these entities as imaging findings.

Glenolabral articular disruption (GLAD) occurs secondary to impaction of the humeral head on the glenoid articular cartilage. There is a resultant defect in the glenoid articular cartilage, which extends to the glenoid labrum. A GLAD lesion is diagnosed only if the glenohumeral ligament and scapular periosteum remain intact¹ (Figure 1).

Complete detachment of the anteroinferior labrum with tearing of the anterior glenoid periosteum represents a Bankart lesion. Cartilaginous Bankart lesions are caused by an anterior glenohumeral dislocation with resultant avulsion of the anteroinferior labrum and disruption of the scapular periosteum because of acute traction on the anterior band of the inferior glenohumeral ligament (Figure 2). Anterior instability, caused by disruption of the anterior labroligamentous complex, results. Osseous Bankart lesions occur when the anterior displaced humeral head impacts the anterior inferior glenoid rim, causing a fracture (Figure 3). This loss of the glenoid articular surface area can result in glenohumeral instability. Posterior shoulder dislocations can result in corresponding findings in the posterior inferior glenoid labrum (reverse Bankart lesion) and anterior medial humeral head (reverse Hill-Sachs lesion) (Figure 2).

A variant of the Bankart lesion is the anterior labroligamentous periosteal sleeve avulsion (ALPSA). This refers to a medially displaced tear of the anterior labrum with intact periosteal stripping along the medial glenoid²with medial rotation and inferior displacement of the anterior inferior labrum along the scapular neck. An ALPSA lesion can heal via the intact periosteal blood supply. If not repaired, anterior instability will result because of malposition of the labrum, causing a patulous anterior capsule.³ When a corresponding lesion occurs in the posterior labrum because of a posterior dislocation, it is called a posterior labrocapsular periosteal sleeve avulsion (POLPSA) (Figure 4).

Another variant of the Bankart lesion is the Perthes lesion, which is a nondisplaced tear of the anteroinferior labrum with periosteal stripping. This differs from the ALPSA because the detached labrum and periosteum are held in anatomic position, possibly making the lesion difficult to detect on magnetic resonance arthrography (MRA).³ Obtaining images in the abduction external rotation (ABER) position exerts traction on the anterior inferior joint capsule and may make the Perthes lesion more conspicuous.⁴ When this occurs in the posterior labrum, it is called a reverse Perthes lesion (Figure 5).

In a patient with anterior glenohumeral instability without a Bankart lesion, pathology of the anterior band of the inferior glenohumeral ligament (IGHL) at its humeral attachment must be suspected. Humeral avulsion of the IGHL (HAGL) or its variants can be overlooked on arthroscopy. HAGL is diagnosed on MRA when the normally U-shaped IGHL takes on a J-shape, and joint fluid extravasates across the torn humeral attachment (Figure 6). If there is an avulsed bony fragment from the medial humeral neck, the lesion is termed a bony HAGL (BHAGL). In addition to the findings of a HAGL, a BHAGL shows the osseous fragment and donor site on MRI. Since a BHAGL is a bony avulsion, it can even be suggested on radiography if a bony fragment is seen adjacent to the medial humeral neck.⁵ These lesions are highly associated with other shoulder injuries, particularly Hill-Sachs deformities and subscapularis tendon tears, and it is imperative, therefore, to search for additional injuries if a HAGL-type injury is seen.⁶

A more uncommon type of HAGL can occur in the setting of posterior capsulolabral injury. A posterior-band IGHL avulsion from the humerus (PHAGL) has similar imaging findings to a HAGL, except that it involves the posterior band of the IGHL. PHAGLs are usually not associated with an acute injury and are thought to be related to repetitive microtrauma, perhaps since the posterior band of the IGHL is the thinnest portion of the IGHL complex.⁷

A Kim lesion is an arthroscopic finding described in patients with posterior instability as a superficial defect at the undersurface of the posterior labrum and adjacent glenoid cartilage without detachment or extension to the chondrolabral junction.⁸ It is, by its nature, a concealed finding on routine MRI but can be more conspicuous in FADIR (flexed, adducted, internally rotated) positioning on MRA, which exerts traction on the posterior joint capsule, allowing intra-articular contrast to fill the tear (Figure 7).

This list describes several of the most commonly encountered acronyms in shoulder MRI. A review of SLAP (superior labrum anterior to posterior) lesions was described in a previous article in the journal’s Imaging Series.⁹ A thorough understanding of these lesions is helpful in interpreting reports and determining the appropriate treatment for patients with shoulder injuries.

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.