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The Arthroscopic Superior Capsular Reconstruction
Rotator cuff tears are very common, and 250,000 to 500,000 rotator cuff repairs are performed in the United States each year.1,2 In most cases, a complete repair of even large or massive tears can be achieved. However, a subset of patients exist in whom the glenohumeral joint has minimal degenerative changes and the rotator cuff tendon is either irreparable or very poor quality and unlikely to heal (ie, failed previous cuff repair). Some authors have advocated for reverse shoulder arthroplasty (RSA) in these patients despite the lack of glenohumeral arthritis. However, due to the permanent destruction of the glenohumeral articular surfaces, complication rates, and concerns about implant longevity with RSA, we believe the superior capsular reconstruction (SCR) is a viable alternative in patients in whom joint preservation is appropriate based on age limitations and/or activity requirements.3
The SCR was first described by Mihata and colleagues4 as a means to reconstruct the superior capsule in shoulders with large, irreparable posterosuperior rotator cuff tears. Originally described using a fascia lata autograft, our technique has been adapted to incorporate a dermal allograft, which limits donor site morbidity and operative time. In most cases, the dermal allograft is fixed to the normal anatomic attachments of the superior glenoid just medial to the superior labrum, laterally to the greater tuberosity, and posteriorly with side-to-side sutures to the remaining rotator cuff. If there is a robust band of “comma” tissue anteriorly, we fix the anterior margin of the dermal graft to this with side-to-side sutures. The comma tissue represents the medial sling of the biceps tendon and connects the upper subscapularis tendon to the anterior supraspinatus. In most cases, this tissue is intact after repair of the subscapularis tendon.
Technique
The patient is positioned in either the lateral decubitus or beach chair position. The arm is positioned in 20° to 30° of abduction and 20° to 30° of forward flexion. A diagnostic arthroscopy is performed through a posterior glenohumeral viewing portal. The subscapularis is visualized and repaired if torn. A biceps tenodesis is performed in most cases, as there is often a tear of the subscapularis, tear or instability of the biceps tendon, and/or a compromised attachment of the biceps root.
Attention is turned to the subacromial space. Posterior viewing and lateral working portals are established. A 10-mm flexible cannula (PassPort; Arthrex) is placed in the lateral portal to aid with suture management and graft passage. A limited subacromial decompression is performed that preserves the coracoacromial arch. The rotator cuff is carefully dissected and freed from the internal deltoid fascia. The scapular spine is identified to visualize the raphé between the supraspinatus and infraspinatus. The infraspinatus is mobilized and repaired as much as possible.
If we think that the tear might be reparable by gaining added excursion from a posterior interval slide, or if it is clearly not reparable but the remaining rim of rotator cuff obscures clear visualization of the superior glenoid, we perform a posterior interval slide. If the additional excursion that is achieved by the posterior slide is adequate for a complete repair, we proceed with the repair. However, if the tear is not reparable even after the posterior interval slide, we have found that the exposure and preparation of the superior glenoid is greatly improved after the posterior slide. After fixation of the dermal graft, we typically perform a partial side-to-side repair of the supraspinatus to the infraspinatus over the top of the graft.
The bone beds of the greater tuberosity and just medial to the superior glenoid labrum are prepared with a shaver and motorized burr. Two anchors (3.0-mm BioComposite SutureTak; Arthrex) are placed in the superior glenoid neck at about the 10 o’clock and 2 o’clock positions approximately 5 mm medial to the superior labrum. Note: the placement medial to the labrum is chosen because this is the normal origin of the superior capsule and because of the angle of approach, these percutaneous portals are often more medial than typical portals for placing anchors during SLAP (superior labral anterior to posterior) repair. Next, 2 threaded anchors (4.75-mm BioComposite SwiveLock; Arthrex) preloaded with suture tape are placed in the greater tuberosity along the articular margin (Figure 1). However, if a biceps tenodesis with an interference screw is placed at the top of the bicipital groove, this anchor preloaded with suture tape can also serve as the anteromedial anchor in the greater tuberosity footprint. The distances between all 4 anchors are carefully measured with a calibrated probe (Figures 2A-2D).
We use a 3.0-mm acellular dermal allograft (ArthroFlex; Arthrex) to reconstruct the superior capsule. The positions of the 4 anchors are carefully marked on the dermal allograft. We routinely add an additional 5 mm of tissue to the medial, anterior, and posterior margins to decrease the risk of suture cut out. An additional 10 mm of tissue is added laterally to cover the greater tuberosity. The final contoured graft is typically trapezoidal in shape.
The sutures from the 4 anchors are then sequentially retrieved through the lateral cannula. The sutures from the greater tuberosity anchors are passed through their respective holes in the graft. However, the suture limbs from each of the glenoid anchors are individually passed 2 mm anterior and 2 mm posterior to their respective marks on the graft with an antegrade suture passer (Figure 3). It is important to have an assistant apply tension to each of the sutures after they are passed through the graft to decrease the chance of crossing and tangling the sutures.
The eyelets of the medial anchors are utilized as pulleys to deliver the dermal allograft into the shoulder. One suture limb from each of the glenoid anchors is tied to the other over a switching stick (Figure 4A). The 2 remaining (untied) suture limbs are then pulled, which introduces the graft to the orifice of the cannula (Figure 4B). A tissue grasper is then used to fold the dermal allograft along its long axis and introduce the graft into the joint (Figure 4C). Once the medial portion of the graft is positioned onto the superior glenoid the 2 remaining (untied) suture limbs are tied to each other as a static knot in the subacromial space (Figure 4D).
The redundancy in the suture tapes can be removed by sequentially sliding a retriever down each suture and tensioning the suture as the nose of the instrument pushes the dermal graft down to the tuberosity bone bed. The suture tapes are crisscrossed and secured laterally with 2 additional knotless threaded anchors (Figure 5). One may also place cinch stitches at the anterolateral and posterolateral corners of the graft that are incorporated into the lateral anchors. These sutures can be useful for pulling the graft back out of the subacromial space in the event of any suture tangles, and can be used for controlling the lateral aspect of the graft during lateral anchor placement.
At this point in the procedure, additional glenoid anchors can be placed both anterior and posterior to the superior glenoid anchors if additional glenoid fixation is desired. Finally, 2 to 3 side-to-side sutures are placed posteriorly attaching the anterior aspect of the infraspinatus to the posterior aspect of the dermal allograft (Figures 6A-6C). If rotator interval tissue (comma tissue) is present, anterior side-to-side sutures may be placed. However, we do not recommend placing anterior side-to-side sutures directly from the dermal allograft to the subscapularis as this may deform the graft, over- constrain the shoulder, and restrict motion.
Discussion
Reconstruction of the superior capsule has been shown to restore the normal restraint to superior translation of the humeral head and reestablish a stable fulcrum at the glenohumeral joint.5 It should be mentioned that we do not perform the SCR in patients with advanced glenohumeral arthritis. The short-term results of this novel procedure have been encouraging, including our own series of patients, in which most patients have had a significant reduction in pain, improvement in function, and very few complications (P. J. Denard, MD, S. S. Burkhart, MD, P. C. Brady, MD, J. Tokish, MD, C. R. Adams, MD, unpublished data, May 2016).
The early success of this procedure suggests that a robust superior capsule is necessary, in addition to functional muscle-tendon units, to restore the stable fulcrum and force couples that are necessary for normal shoulder function. Perhaps we have not paid enough attention to the integrity of the superior capsule in the past. In cases of revision cuff repair, we pay special attention to the quality of the capsular layer deep to the cuff tendon. If the capsule is poor quality, we sometimes reconstruct the capsule with a dermal allograft (SCR) and then do a rotator cuff repair (partial or complete) over the top of the SCR to maintain the normal anatomic deep to superficial layering of the capsule and rotator cuff.
We are very conservative with our postoperative rehabilitation program after a SCR. We know that the rate of stiffness with a conservative program after an arthroscopic rotator cuff repair, even in the revision setting, is very low.6 Furthermore, both basic science on healing of soft tissue to bone and radiographic analysis of healing after postoperative rotator cuff repairs support a slow rehabilitation program.7,8 A canine model specifically evaluating acellular dermal allografts in the shoulder suggests that these grafts undergo significant remodeling and become weaker before they get stronger.9 We would rather err on the side of healing of the SCR with potentially a slight increase in the rate of shoulder stiffness than to regain early motion at the expense of graft failure. Therefore, we have the patient wear a sling with no shoulder motion for 6 weeks. Passive motion is started at 6 weeks postoperative and strengthening is delayed until 12 to 16 weeks postoperative.
1. Orr SB, Chainani A, Hippensteel KJ, et al. Aligned multilayered electrospun scaffolds for rotator cuff tendon tissue engineering. Acta Biomater. 2015;24:117-126.
2. Austin L, Black EM, Lombardi NJ, Pepe MD, Lazarus M. Arthroscopic transosseous rotator cuff repair. A prospective study on cost savings, surgical time, and outcomes. Ortho J Sports Med. 2015;3(2 Suppl). doi:10.1177/2325967115S00156.
3. Denard PJ, Lädermann A, Jiwani AZ, Burkhart SS. Functional outcome after arthroscopic repair of massive rotator cuff tears in individuals with pseudoparalysis. Arthroscopy. 2012;28(9):1214-1219.
4. Mihata T, Lee TQ, Watanabe C, et al. Clinical results of arthroscopic superior capsule reconstruction for irreparable rotator cuff tears. Arthroscopy. 2013;29(3):459-470.
5. Mihata T, McGarry MH, Pirolo JM, Kinoshita M, Lee TQ. Superior capsule reconstruction to restore superior stability in irreparable rotator cuff tears: a biomechanical cadaveric study. Am J Sports Med. 2012;40(10):2248-2255.
6. Huberty DP, Schoolfield JD, Brady PC, Vadala AP, Arrigoni P, Burkhart SS. Incidence and treatment of postoperative stiffness following arthroscopic rotator cuff repair. Arthroscopy. 2009;25(8):880-890.
7. Sonnabend DH, Howlett CR, Young AA. Histological evaluation of repair of the rotator cuff in a primate model. J Bone Joint Surg Br. 2010;92(4):586-594.
8. Lee BG, Cho NS, Rhee YG. Effect of two rehabilitation protocols on range of motion and healing rates after arthroscopic rotator cuff repair: aggressive versus limited early passive exercises. Arthroscopy. 2012;28(1):34-42.
9. Adams JE, Zobitz ME, Reach JS Jr, An KN, Steinmann SP. Rotator cuff repair using an acellular dermal matrix graft: an in vivo study in a canine model. Arthroscopy. 2006;22(7):700-709.
Rotator cuff tears are very common, and 250,000 to 500,000 rotator cuff repairs are performed in the United States each year.1,2 In most cases, a complete repair of even large or massive tears can be achieved. However, a subset of patients exist in whom the glenohumeral joint has minimal degenerative changes and the rotator cuff tendon is either irreparable or very poor quality and unlikely to heal (ie, failed previous cuff repair). Some authors have advocated for reverse shoulder arthroplasty (RSA) in these patients despite the lack of glenohumeral arthritis. However, due to the permanent destruction of the glenohumeral articular surfaces, complication rates, and concerns about implant longevity with RSA, we believe the superior capsular reconstruction (SCR) is a viable alternative in patients in whom joint preservation is appropriate based on age limitations and/or activity requirements.3
The SCR was first described by Mihata and colleagues4 as a means to reconstruct the superior capsule in shoulders with large, irreparable posterosuperior rotator cuff tears. Originally described using a fascia lata autograft, our technique has been adapted to incorporate a dermal allograft, which limits donor site morbidity and operative time. In most cases, the dermal allograft is fixed to the normal anatomic attachments of the superior glenoid just medial to the superior labrum, laterally to the greater tuberosity, and posteriorly with side-to-side sutures to the remaining rotator cuff. If there is a robust band of “comma” tissue anteriorly, we fix the anterior margin of the dermal graft to this with side-to-side sutures. The comma tissue represents the medial sling of the biceps tendon and connects the upper subscapularis tendon to the anterior supraspinatus. In most cases, this tissue is intact after repair of the subscapularis tendon.
Technique
The patient is positioned in either the lateral decubitus or beach chair position. The arm is positioned in 20° to 30° of abduction and 20° to 30° of forward flexion. A diagnostic arthroscopy is performed through a posterior glenohumeral viewing portal. The subscapularis is visualized and repaired if torn. A biceps tenodesis is performed in most cases, as there is often a tear of the subscapularis, tear or instability of the biceps tendon, and/or a compromised attachment of the biceps root.
Attention is turned to the subacromial space. Posterior viewing and lateral working portals are established. A 10-mm flexible cannula (PassPort; Arthrex) is placed in the lateral portal to aid with suture management and graft passage. A limited subacromial decompression is performed that preserves the coracoacromial arch. The rotator cuff is carefully dissected and freed from the internal deltoid fascia. The scapular spine is identified to visualize the raphé between the supraspinatus and infraspinatus. The infraspinatus is mobilized and repaired as much as possible.
If we think that the tear might be reparable by gaining added excursion from a posterior interval slide, or if it is clearly not reparable but the remaining rim of rotator cuff obscures clear visualization of the superior glenoid, we perform a posterior interval slide. If the additional excursion that is achieved by the posterior slide is adequate for a complete repair, we proceed with the repair. However, if the tear is not reparable even after the posterior interval slide, we have found that the exposure and preparation of the superior glenoid is greatly improved after the posterior slide. After fixation of the dermal graft, we typically perform a partial side-to-side repair of the supraspinatus to the infraspinatus over the top of the graft.
The bone beds of the greater tuberosity and just medial to the superior glenoid labrum are prepared with a shaver and motorized burr. Two anchors (3.0-mm BioComposite SutureTak; Arthrex) are placed in the superior glenoid neck at about the 10 o’clock and 2 o’clock positions approximately 5 mm medial to the superior labrum. Note: the placement medial to the labrum is chosen because this is the normal origin of the superior capsule and because of the angle of approach, these percutaneous portals are often more medial than typical portals for placing anchors during SLAP (superior labral anterior to posterior) repair. Next, 2 threaded anchors (4.75-mm BioComposite SwiveLock; Arthrex) preloaded with suture tape are placed in the greater tuberosity along the articular margin (Figure 1). However, if a biceps tenodesis with an interference screw is placed at the top of the bicipital groove, this anchor preloaded with suture tape can also serve as the anteromedial anchor in the greater tuberosity footprint. The distances between all 4 anchors are carefully measured with a calibrated probe (Figures 2A-2D).
We use a 3.0-mm acellular dermal allograft (ArthroFlex; Arthrex) to reconstruct the superior capsule. The positions of the 4 anchors are carefully marked on the dermal allograft. We routinely add an additional 5 mm of tissue to the medial, anterior, and posterior margins to decrease the risk of suture cut out. An additional 10 mm of tissue is added laterally to cover the greater tuberosity. The final contoured graft is typically trapezoidal in shape.
The sutures from the 4 anchors are then sequentially retrieved through the lateral cannula. The sutures from the greater tuberosity anchors are passed through their respective holes in the graft. However, the suture limbs from each of the glenoid anchors are individually passed 2 mm anterior and 2 mm posterior to their respective marks on the graft with an antegrade suture passer (Figure 3). It is important to have an assistant apply tension to each of the sutures after they are passed through the graft to decrease the chance of crossing and tangling the sutures.
The eyelets of the medial anchors are utilized as pulleys to deliver the dermal allograft into the shoulder. One suture limb from each of the glenoid anchors is tied to the other over a switching stick (Figure 4A). The 2 remaining (untied) suture limbs are then pulled, which introduces the graft to the orifice of the cannula (Figure 4B). A tissue grasper is then used to fold the dermal allograft along its long axis and introduce the graft into the joint (Figure 4C). Once the medial portion of the graft is positioned onto the superior glenoid the 2 remaining (untied) suture limbs are tied to each other as a static knot in the subacromial space (Figure 4D).
The redundancy in the suture tapes can be removed by sequentially sliding a retriever down each suture and tensioning the suture as the nose of the instrument pushes the dermal graft down to the tuberosity bone bed. The suture tapes are crisscrossed and secured laterally with 2 additional knotless threaded anchors (Figure 5). One may also place cinch stitches at the anterolateral and posterolateral corners of the graft that are incorporated into the lateral anchors. These sutures can be useful for pulling the graft back out of the subacromial space in the event of any suture tangles, and can be used for controlling the lateral aspect of the graft during lateral anchor placement.
At this point in the procedure, additional glenoid anchors can be placed both anterior and posterior to the superior glenoid anchors if additional glenoid fixation is desired. Finally, 2 to 3 side-to-side sutures are placed posteriorly attaching the anterior aspect of the infraspinatus to the posterior aspect of the dermal allograft (Figures 6A-6C). If rotator interval tissue (comma tissue) is present, anterior side-to-side sutures may be placed. However, we do not recommend placing anterior side-to-side sutures directly from the dermal allograft to the subscapularis as this may deform the graft, over- constrain the shoulder, and restrict motion.
Discussion
Reconstruction of the superior capsule has been shown to restore the normal restraint to superior translation of the humeral head and reestablish a stable fulcrum at the glenohumeral joint.5 It should be mentioned that we do not perform the SCR in patients with advanced glenohumeral arthritis. The short-term results of this novel procedure have been encouraging, including our own series of patients, in which most patients have had a significant reduction in pain, improvement in function, and very few complications (P. J. Denard, MD, S. S. Burkhart, MD, P. C. Brady, MD, J. Tokish, MD, C. R. Adams, MD, unpublished data, May 2016).
The early success of this procedure suggests that a robust superior capsule is necessary, in addition to functional muscle-tendon units, to restore the stable fulcrum and force couples that are necessary for normal shoulder function. Perhaps we have not paid enough attention to the integrity of the superior capsule in the past. In cases of revision cuff repair, we pay special attention to the quality of the capsular layer deep to the cuff tendon. If the capsule is poor quality, we sometimes reconstruct the capsule with a dermal allograft (SCR) and then do a rotator cuff repair (partial or complete) over the top of the SCR to maintain the normal anatomic deep to superficial layering of the capsule and rotator cuff.
We are very conservative with our postoperative rehabilitation program after a SCR. We know that the rate of stiffness with a conservative program after an arthroscopic rotator cuff repair, even in the revision setting, is very low.6 Furthermore, both basic science on healing of soft tissue to bone and radiographic analysis of healing after postoperative rotator cuff repairs support a slow rehabilitation program.7,8 A canine model specifically evaluating acellular dermal allografts in the shoulder suggests that these grafts undergo significant remodeling and become weaker before they get stronger.9 We would rather err on the side of healing of the SCR with potentially a slight increase in the rate of shoulder stiffness than to regain early motion at the expense of graft failure. Therefore, we have the patient wear a sling with no shoulder motion for 6 weeks. Passive motion is started at 6 weeks postoperative and strengthening is delayed until 12 to 16 weeks postoperative.
Rotator cuff tears are very common, and 250,000 to 500,000 rotator cuff repairs are performed in the United States each year.1,2 In most cases, a complete repair of even large or massive tears can be achieved. However, a subset of patients exist in whom the glenohumeral joint has minimal degenerative changes and the rotator cuff tendon is either irreparable or very poor quality and unlikely to heal (ie, failed previous cuff repair). Some authors have advocated for reverse shoulder arthroplasty (RSA) in these patients despite the lack of glenohumeral arthritis. However, due to the permanent destruction of the glenohumeral articular surfaces, complication rates, and concerns about implant longevity with RSA, we believe the superior capsular reconstruction (SCR) is a viable alternative in patients in whom joint preservation is appropriate based on age limitations and/or activity requirements.3
The SCR was first described by Mihata and colleagues4 as a means to reconstruct the superior capsule in shoulders with large, irreparable posterosuperior rotator cuff tears. Originally described using a fascia lata autograft, our technique has been adapted to incorporate a dermal allograft, which limits donor site morbidity and operative time. In most cases, the dermal allograft is fixed to the normal anatomic attachments of the superior glenoid just medial to the superior labrum, laterally to the greater tuberosity, and posteriorly with side-to-side sutures to the remaining rotator cuff. If there is a robust band of “comma” tissue anteriorly, we fix the anterior margin of the dermal graft to this with side-to-side sutures. The comma tissue represents the medial sling of the biceps tendon and connects the upper subscapularis tendon to the anterior supraspinatus. In most cases, this tissue is intact after repair of the subscapularis tendon.
Technique
The patient is positioned in either the lateral decubitus or beach chair position. The arm is positioned in 20° to 30° of abduction and 20° to 30° of forward flexion. A diagnostic arthroscopy is performed through a posterior glenohumeral viewing portal. The subscapularis is visualized and repaired if torn. A biceps tenodesis is performed in most cases, as there is often a tear of the subscapularis, tear or instability of the biceps tendon, and/or a compromised attachment of the biceps root.
Attention is turned to the subacromial space. Posterior viewing and lateral working portals are established. A 10-mm flexible cannula (PassPort; Arthrex) is placed in the lateral portal to aid with suture management and graft passage. A limited subacromial decompression is performed that preserves the coracoacromial arch. The rotator cuff is carefully dissected and freed from the internal deltoid fascia. The scapular spine is identified to visualize the raphé between the supraspinatus and infraspinatus. The infraspinatus is mobilized and repaired as much as possible.
If we think that the tear might be reparable by gaining added excursion from a posterior interval slide, or if it is clearly not reparable but the remaining rim of rotator cuff obscures clear visualization of the superior glenoid, we perform a posterior interval slide. If the additional excursion that is achieved by the posterior slide is adequate for a complete repair, we proceed with the repair. However, if the tear is not reparable even after the posterior interval slide, we have found that the exposure and preparation of the superior glenoid is greatly improved after the posterior slide. After fixation of the dermal graft, we typically perform a partial side-to-side repair of the supraspinatus to the infraspinatus over the top of the graft.
The bone beds of the greater tuberosity and just medial to the superior glenoid labrum are prepared with a shaver and motorized burr. Two anchors (3.0-mm BioComposite SutureTak; Arthrex) are placed in the superior glenoid neck at about the 10 o’clock and 2 o’clock positions approximately 5 mm medial to the superior labrum. Note: the placement medial to the labrum is chosen because this is the normal origin of the superior capsule and because of the angle of approach, these percutaneous portals are often more medial than typical portals for placing anchors during SLAP (superior labral anterior to posterior) repair. Next, 2 threaded anchors (4.75-mm BioComposite SwiveLock; Arthrex) preloaded with suture tape are placed in the greater tuberosity along the articular margin (Figure 1). However, if a biceps tenodesis with an interference screw is placed at the top of the bicipital groove, this anchor preloaded with suture tape can also serve as the anteromedial anchor in the greater tuberosity footprint. The distances between all 4 anchors are carefully measured with a calibrated probe (Figures 2A-2D).
We use a 3.0-mm acellular dermal allograft (ArthroFlex; Arthrex) to reconstruct the superior capsule. The positions of the 4 anchors are carefully marked on the dermal allograft. We routinely add an additional 5 mm of tissue to the medial, anterior, and posterior margins to decrease the risk of suture cut out. An additional 10 mm of tissue is added laterally to cover the greater tuberosity. The final contoured graft is typically trapezoidal in shape.
The sutures from the 4 anchors are then sequentially retrieved through the lateral cannula. The sutures from the greater tuberosity anchors are passed through their respective holes in the graft. However, the suture limbs from each of the glenoid anchors are individually passed 2 mm anterior and 2 mm posterior to their respective marks on the graft with an antegrade suture passer (Figure 3). It is important to have an assistant apply tension to each of the sutures after they are passed through the graft to decrease the chance of crossing and tangling the sutures.
The eyelets of the medial anchors are utilized as pulleys to deliver the dermal allograft into the shoulder. One suture limb from each of the glenoid anchors is tied to the other over a switching stick (Figure 4A). The 2 remaining (untied) suture limbs are then pulled, which introduces the graft to the orifice of the cannula (Figure 4B). A tissue grasper is then used to fold the dermal allograft along its long axis and introduce the graft into the joint (Figure 4C). Once the medial portion of the graft is positioned onto the superior glenoid the 2 remaining (untied) suture limbs are tied to each other as a static knot in the subacromial space (Figure 4D).
The redundancy in the suture tapes can be removed by sequentially sliding a retriever down each suture and tensioning the suture as the nose of the instrument pushes the dermal graft down to the tuberosity bone bed. The suture tapes are crisscrossed and secured laterally with 2 additional knotless threaded anchors (Figure 5). One may also place cinch stitches at the anterolateral and posterolateral corners of the graft that are incorporated into the lateral anchors. These sutures can be useful for pulling the graft back out of the subacromial space in the event of any suture tangles, and can be used for controlling the lateral aspect of the graft during lateral anchor placement.
At this point in the procedure, additional glenoid anchors can be placed both anterior and posterior to the superior glenoid anchors if additional glenoid fixation is desired. Finally, 2 to 3 side-to-side sutures are placed posteriorly attaching the anterior aspect of the infraspinatus to the posterior aspect of the dermal allograft (Figures 6A-6C). If rotator interval tissue (comma tissue) is present, anterior side-to-side sutures may be placed. However, we do not recommend placing anterior side-to-side sutures directly from the dermal allograft to the subscapularis as this may deform the graft, over- constrain the shoulder, and restrict motion.
Discussion
Reconstruction of the superior capsule has been shown to restore the normal restraint to superior translation of the humeral head and reestablish a stable fulcrum at the glenohumeral joint.5 It should be mentioned that we do not perform the SCR in patients with advanced glenohumeral arthritis. The short-term results of this novel procedure have been encouraging, including our own series of patients, in which most patients have had a significant reduction in pain, improvement in function, and very few complications (P. J. Denard, MD, S. S. Burkhart, MD, P. C. Brady, MD, J. Tokish, MD, C. R. Adams, MD, unpublished data, May 2016).
The early success of this procedure suggests that a robust superior capsule is necessary, in addition to functional muscle-tendon units, to restore the stable fulcrum and force couples that are necessary for normal shoulder function. Perhaps we have not paid enough attention to the integrity of the superior capsule in the past. In cases of revision cuff repair, we pay special attention to the quality of the capsular layer deep to the cuff tendon. If the capsule is poor quality, we sometimes reconstruct the capsule with a dermal allograft (SCR) and then do a rotator cuff repair (partial or complete) over the top of the SCR to maintain the normal anatomic deep to superficial layering of the capsule and rotator cuff.
We are very conservative with our postoperative rehabilitation program after a SCR. We know that the rate of stiffness with a conservative program after an arthroscopic rotator cuff repair, even in the revision setting, is very low.6 Furthermore, both basic science on healing of soft tissue to bone and radiographic analysis of healing after postoperative rotator cuff repairs support a slow rehabilitation program.7,8 A canine model specifically evaluating acellular dermal allografts in the shoulder suggests that these grafts undergo significant remodeling and become weaker before they get stronger.9 We would rather err on the side of healing of the SCR with potentially a slight increase in the rate of shoulder stiffness than to regain early motion at the expense of graft failure. Therefore, we have the patient wear a sling with no shoulder motion for 6 weeks. Passive motion is started at 6 weeks postoperative and strengthening is delayed until 12 to 16 weeks postoperative.
1. Orr SB, Chainani A, Hippensteel KJ, et al. Aligned multilayered electrospun scaffolds for rotator cuff tendon tissue engineering. Acta Biomater. 2015;24:117-126.
2. Austin L, Black EM, Lombardi NJ, Pepe MD, Lazarus M. Arthroscopic transosseous rotator cuff repair. A prospective study on cost savings, surgical time, and outcomes. Ortho J Sports Med. 2015;3(2 Suppl). doi:10.1177/2325967115S00156.
3. Denard PJ, Lädermann A, Jiwani AZ, Burkhart SS. Functional outcome after arthroscopic repair of massive rotator cuff tears in individuals with pseudoparalysis. Arthroscopy. 2012;28(9):1214-1219.
4. Mihata T, Lee TQ, Watanabe C, et al. Clinical results of arthroscopic superior capsule reconstruction for irreparable rotator cuff tears. Arthroscopy. 2013;29(3):459-470.
5. Mihata T, McGarry MH, Pirolo JM, Kinoshita M, Lee TQ. Superior capsule reconstruction to restore superior stability in irreparable rotator cuff tears: a biomechanical cadaveric study. Am J Sports Med. 2012;40(10):2248-2255.
6. Huberty DP, Schoolfield JD, Brady PC, Vadala AP, Arrigoni P, Burkhart SS. Incidence and treatment of postoperative stiffness following arthroscopic rotator cuff repair. Arthroscopy. 2009;25(8):880-890.
7. Sonnabend DH, Howlett CR, Young AA. Histological evaluation of repair of the rotator cuff in a primate model. J Bone Joint Surg Br. 2010;92(4):586-594.
8. Lee BG, Cho NS, Rhee YG. Effect of two rehabilitation protocols on range of motion and healing rates after arthroscopic rotator cuff repair: aggressive versus limited early passive exercises. Arthroscopy. 2012;28(1):34-42.
9. Adams JE, Zobitz ME, Reach JS Jr, An KN, Steinmann SP. Rotator cuff repair using an acellular dermal matrix graft: an in vivo study in a canine model. Arthroscopy. 2006;22(7):700-709.
1. Orr SB, Chainani A, Hippensteel KJ, et al. Aligned multilayered electrospun scaffolds for rotator cuff tendon tissue engineering. Acta Biomater. 2015;24:117-126.
2. Austin L, Black EM, Lombardi NJ, Pepe MD, Lazarus M. Arthroscopic transosseous rotator cuff repair. A prospective study on cost savings, surgical time, and outcomes. Ortho J Sports Med. 2015;3(2 Suppl). doi:10.1177/2325967115S00156.
3. Denard PJ, Lädermann A, Jiwani AZ, Burkhart SS. Functional outcome after arthroscopic repair of massive rotator cuff tears in individuals with pseudoparalysis. Arthroscopy. 2012;28(9):1214-1219.
4. Mihata T, Lee TQ, Watanabe C, et al. Clinical results of arthroscopic superior capsule reconstruction for irreparable rotator cuff tears. Arthroscopy. 2013;29(3):459-470.
5. Mihata T, McGarry MH, Pirolo JM, Kinoshita M, Lee TQ. Superior capsule reconstruction to restore superior stability in irreparable rotator cuff tears: a biomechanical cadaveric study. Am J Sports Med. 2012;40(10):2248-2255.
6. Huberty DP, Schoolfield JD, Brady PC, Vadala AP, Arrigoni P, Burkhart SS. Incidence and treatment of postoperative stiffness following arthroscopic rotator cuff repair. Arthroscopy. 2009;25(8):880-890.
7. Sonnabend DH, Howlett CR, Young AA. Histological evaluation of repair of the rotator cuff in a primate model. J Bone Joint Surg Br. 2010;92(4):586-594.
8. Lee BG, Cho NS, Rhee YG. Effect of two rehabilitation protocols on range of motion and healing rates after arthroscopic rotator cuff repair: aggressive versus limited early passive exercises. Arthroscopy. 2012;28(1):34-42.
9. Adams JE, Zobitz ME, Reach JS Jr, An KN, Steinmann SP. Rotator cuff repair using an acellular dermal matrix graft: an in vivo study in a canine model. Arthroscopy. 2006;22(7):700-709.
Tibialis Posterior Tendon Entrapment Within Posterior Malleolar Fracture Fragment
Irreducible ankle fracture-dislocation secondary to tibialis posterior tendon interposition is a rare but documented complication most commonly associated with Lauge-Hansen classification pronation–external rotation ankle fractures.1-4 Entrapment of the tibialis posterior tendon has been documented in the syndesmosis (tibiotalar joint)1,2,4 and within a medial malleolus fracture.5 To our knowledge, however, there are no case reports of entrapment of the tibialis posterior tendon in a posterior malleolus fracture.
Ankle arthroscopy performed at time of fracture fixation is gaining in popularity because of its enhanced ability to document and treat intra-articular pathology associated with the initial injury.6,7 In addition, percutaneous fixation of a posterior malleolar fragment with arthroscopic assessment of the articular surface reduction may be valuable, as evaluation of tibial plafond fracture reduction by plain radiographs and fluoroscopy has proved to have limitations.8,9
In this article, we present the case of a patient who underwent attempted arthroscopy-assisted reduction of the posterior malleolus with entrapment of the tibialis posterior tendon within the posterior malleolar fracture fragment. The tendon was irreducible with arthroscopic techniques, necessitating posteromedial incision and subsequent open reduction of the incarcerated structure. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 67-year-old man slipped and fell on ice while jogging and subsequently presented to the emergency department with a closed bimalleolar ankle fracture-dislocation. Plain radiography (Figure 1) and computed tomography (CT) showed an oblique lateral malleolar fracture and a large posterior malleolar fracture. Further examination of the CT scan revealed entrapment of the tibialis posterior tendon within the posterior malleolar fracture (Figure 2).
Two days after injury, the patient was taken to the operating room for ankle arthroscopy with planned extrication of the entrapped tibialis posterior tendon and possible arthroscopy-assisted percutaneous fixation of the posterior malleolar fracture and open fixation of the distal fibula fracture. Diagnostic arthroscopy revealed a deltoid ligament injury (Figure 3) and a loose piece of articular cartilage (~1 cm in diameter), which was excised. No donor site for this cartilage fragment was identified with further arthroscopic evaluation. During arthroscopic examination, the tibialis posterior tendon was visualized within the joint, incarcerated within the posterior malleolar fracture (Figure 4). Attempts to release the tibialis posterior tendon from the fracture site using arthroscopic instruments and closed reduction techniques were unsuccessful, both with and without noninvasive skeletal traction applied to the ankle.
After multiple unsuccessful attempts to extract the tibialis posterior tendon arthroscopically, traction was removed, and a separate incision was made over the posteromedial aspect of the ankle. The tibialis posterior tendon was identified within the fracture site and was removed using an angled clamp (Figure 5). The fracture was reduced and held provisionally with a large tenaculum clamp. Two anterior-to-posterior, partially threaded cannulated screws were placed for fixation after adequate fracture reduction was confirmed on fluoroscopy. As a medial incision was made to extract the tibialis posterior tendon, the joint could not retain arthroscopic fluid, and visualization of the posterior fracture fragment after tendon removal was difficult. Therefore, arthroscopy-assisted reduction could not be completed.
Next, the lateral malleolus was open-reduced, and fixation was achieved using a standard interfragmentary lag screw and a lateral neutralization plate technique (Figure 6). After surgery, the patient was immobilized in a posterior splint with side gussets. Two weeks later, the incisions were healing well, and the tibialis posterior tendon was functioning normally. The sutures were removed, the patient was transitioned to a controlled ankle movement (CAM) boot, and ankle and subtalar range-of-motion exercises were initiated. The patient remained non-weight-bearing for 6 weeks. Radiographs 6 weeks after surgery showed healing fractures with stable hardware (Figure 7). The patient demonstrated 5/5 strength of the tibialis posterior tendon without subluxation or dislocation. There was no tenderness to palpation over the fracture sites or tibialis posterior tendon. The patient began progressive weight-bearing in a CAM boot and physical therapy for range of motion and strengthening.
Discussion
Tibialis posterior tendon injuries—including rupture, dislocation, and entrapment—are well-described complications of ankle injuries.1,2,5,10 Most commonly, the tibialis posterior tendon has been reported to cause a mechanical block to reduction in lateral subtalar dislocations.11-13 In addition, there are case reports of isolated traumatic dislocations of the tibialis posterior tendon without rupture, requiring operative stabilization and retinaculum repair with or without deepening of the posterior groove.14,15
Posterior malleolar ankle fractures remain controversial, with respect to both need for fixation and fixation methods. Although multiple investigators have advocated operative treatment for such fractures that exceed 25% to 33% of the anteroposterior dimension of the tibial plafond, there are no conclusive studies or evidence-based guidelines for treating these fractures.16,17 Anatomical reduction and plating are important to restore articular congruity and increase syndesmotic stability; recent studies have demonstrated that fixation of posterior malleolar fractures provides more syndesmotic stability than trans-syndesmotic screws do.18,19 Indirect reduction of the posterior malleolar fragment after fibula fixation is often accepted as adequate. Whether indirect or direct reduction is attempted, close attention should be given to plain radiographs after attempted reduction, and consideration should be given to possible soft-tissue or bony interposition if malreduction is identified.16,17 Plain radiographs are unreliable in assessing posterior malleolar fragment size as well as amount of comminution and impaction.8,9 Therefore, an arthroscopy-assisted approach coupled with percutaneous fixation may provide more reliable fracture reduction over indirect fracture reduction with fibular fixation, with less dissection than a formal posterolateral approach with posterior plating.
Not all ankle fractures require CT. However, for posterior malleolus fractures thought to require fixation, preoperative CT may help in determining if percutaneous fixation with or without arthroscopic guidance is a feasible treatment option. Ideally, percutaneous reduction can obviate the need for a larger posterolateral incision and buttress plate and, with arthroscopic assistance, may be superior to indirect reduction with fluoroscopy.
In our patient’s case, arthroscopic assistance facilitated diagnosis of an entrapped structure that would have been difficult to identify, particularly without preoperative CT. It may be difficult to identify imperfect reduction of the posterior malleolus on plain radiographs alone, and arthroscopy-assisted fixation enhances the surgeon’s ability to consider reduction, view incarcerated structures within the joint, and treat articular injuries. We do not routinely use ankle arthroscopy as an adjunct to ankle fracture fixation, but judicious use in select cases can facilitate treatment of intra-articular injuries and facilitate visualization and reduction of posterior malleolar fracture fragments before percutaneous anterior-to-posterior cannulated screw fixation. If an open incision is required, as in the present case, visualization becomes difficult secondary to fluid extravasation. However, we think avoiding the morbidity associated with an open incision is worthwhile for fixation of posterior malleolus fractures.
Conclusion
Close inspection of both preoperative and intraoperative radiographs is required to ensure adequate reduction of a posterior malleolar fragment without soft-tissue or bony interposition in the reduction of ankle fractures. Although not previously reported, posterior tendon entrapment within the posterior malleolus fracture may occur and may require arthroscopic or open techniques to ensure adequate extrication of the tendon to allow for posterior malleolar fracture reduction and fixation. This case report highlights one indication for arthroscopy in the treatment of ankle fractures despite the fact that the tibialis posterior tendon was openly removed. Arthroscopic assistance in acute ankle injuries allows the surgeon to evaluate articular cartilage injuries and ensure there are no interposed structures while checking reduction of the posterior malleolar fracture fragment when present.
1. Ermis MN, Yagmurlu MF, Kilinc AS, Karakas ES. Irreducible fracture dislocation of the ankle caused by tibialis posterior tendon interposition. J Foot Ankle Surg. 2010;49(2):166-171.
2. Curry EE, O’Brien TS, Johnson JE. Fibular nonunion and equinovarus deformity secondary to posterior tibial tendon incarceration in the syndesmosis: a case report after a bimalleolar fracture-dislocation. Foot Ankle Int. 1999;20(8):527-531.
3. Coonrad RW, Bugg EI Jr. Trapping of the posterior tibial tendon and interposition of soft tissue in severe fractures about the ankle joint. J Bone Joint Surg Am. 1954;36(4):744-750.
4. Pankovich AM. Fracture-dislocation of the ankle. Trapping of the postero-medial ankle tendons and neurovascular bundle in the tibiofibular interosseous space: a case report. J Trauma. 1976;16(11):927-929.
5. Khamaisy S, Leibner ED, Elishoov O. Tibialis posterior entrapment: case report. Foot Ankle Int. 2012;33(5):441-443.
6. Hsu AR, Gross CE, Lee S, Carreira DS. Extended indications for foot and ankle arthroscopy. J Am Acad Orthop Surg. 2014;22(1):10-19.
7. Stufkens SA, Knupp M, Horisberger M, Lampert C, Hintermann B. Cartilage lesions and the development of osteoarthritis after internal fixation of ankle fractures: a prospective study. J Bone Joint Surg Am. 2010;92(2):279-286.
8. Büchler L, Tannast M, Bonel HM, Weber M. Reliability of radiologic assessment of the fracture anatomy at the posterior tibial plafond in malleolar fractures. J Orthop Trauma. 2009;23(3):208-212.
9. Ferries JS, DeCoster TA, Firoozbakhsh KK, Garcia JF, Miller RA. Plain radiographic interpretation in trimalleolar ankle fractures poorly assesses posterior fragment size. J Orthop Trauma. 1994;8(4):328-331.
10. Jarvis HC, Cannada LK. Acute tibialis posterior tendon rupture associated with a distal tibial fracture. Orthopedics. 2012;35(4):e595-e597.
11. Woodruff MJ, Brown JN, Mountney J. A mechanism for entrapment of the tibialis posterior tendon in lateral subtalar dislocation. Injury. 1996;27(3):193-194.
12. Leitner B. Obstacles to reduction in subtalar dislocations. J Bone Joint Surg Am. 1954;36(2):299-306.
13. Waldrop J, Ebraheim NA, Shapiro P, Jackson WT. Anatomical considerations of posterior tibialis tendon entrapment in irreducible lateral subtalar dislocation. Foot Ankle. 1992;13(8):458-461.
14. Goucher NR, Coughlin MJ, Kristensen RM. Dislocation of the posterior tibial tendon: a literature review and presentation of two cases. Iowa Orthop J. 2006;26:122-126.
15. Olivé Vilás R, Redón Montojo N, Pino Sorroche S. Traumatic dislocation of tibialis posterior tendon: a case report in a tae-kwon-do athlete. Clin J Sport Med. 2009;19(1):68-69.
16. Gardner MJ, Streubel PN, McCormick JJ, Klein SE, Johnson JE, Ricci WM. Surgeon practices regarding operative treatment of posterior malleolus fractures. Foot Ankle Int. 2011;32(4):385-393.
17. Irwin TA, Lien J, Kadakia AR. Posterior malleolus fracture. J Am Acad Orthop Surg. 2013;21(1):32-40.
18. Gardner MJ, Brodsky A, Briggs SM, Nielson JH, Lorich DG. Fixation of posterior malleolar fractures provides greater syndesmotic stability. Clin Orthop Relat Res. 2006;(447):165-171.
19. Miller AN, Carroll EA, Parker RJ, Helfet DL, Lorich DG. Posterior malleolar stabilization of syndesmotic injuries is equivalent to screw fixation. Clin Orthop Relat Res. 2010;468(4):1129-1135.
Irreducible ankle fracture-dislocation secondary to tibialis posterior tendon interposition is a rare but documented complication most commonly associated with Lauge-Hansen classification pronation–external rotation ankle fractures.1-4 Entrapment of the tibialis posterior tendon has been documented in the syndesmosis (tibiotalar joint)1,2,4 and within a medial malleolus fracture.5 To our knowledge, however, there are no case reports of entrapment of the tibialis posterior tendon in a posterior malleolus fracture.
Ankle arthroscopy performed at time of fracture fixation is gaining in popularity because of its enhanced ability to document and treat intra-articular pathology associated with the initial injury.6,7 In addition, percutaneous fixation of a posterior malleolar fragment with arthroscopic assessment of the articular surface reduction may be valuable, as evaluation of tibial plafond fracture reduction by plain radiographs and fluoroscopy has proved to have limitations.8,9
In this article, we present the case of a patient who underwent attempted arthroscopy-assisted reduction of the posterior malleolus with entrapment of the tibialis posterior tendon within the posterior malleolar fracture fragment. The tendon was irreducible with arthroscopic techniques, necessitating posteromedial incision and subsequent open reduction of the incarcerated structure. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 67-year-old man slipped and fell on ice while jogging and subsequently presented to the emergency department with a closed bimalleolar ankle fracture-dislocation. Plain radiography (Figure 1) and computed tomography (CT) showed an oblique lateral malleolar fracture and a large posterior malleolar fracture. Further examination of the CT scan revealed entrapment of the tibialis posterior tendon within the posterior malleolar fracture (Figure 2).
Two days after injury, the patient was taken to the operating room for ankle arthroscopy with planned extrication of the entrapped tibialis posterior tendon and possible arthroscopy-assisted percutaneous fixation of the posterior malleolar fracture and open fixation of the distal fibula fracture. Diagnostic arthroscopy revealed a deltoid ligament injury (Figure 3) and a loose piece of articular cartilage (~1 cm in diameter), which was excised. No donor site for this cartilage fragment was identified with further arthroscopic evaluation. During arthroscopic examination, the tibialis posterior tendon was visualized within the joint, incarcerated within the posterior malleolar fracture (Figure 4). Attempts to release the tibialis posterior tendon from the fracture site using arthroscopic instruments and closed reduction techniques were unsuccessful, both with and without noninvasive skeletal traction applied to the ankle.
After multiple unsuccessful attempts to extract the tibialis posterior tendon arthroscopically, traction was removed, and a separate incision was made over the posteromedial aspect of the ankle. The tibialis posterior tendon was identified within the fracture site and was removed using an angled clamp (Figure 5). The fracture was reduced and held provisionally with a large tenaculum clamp. Two anterior-to-posterior, partially threaded cannulated screws were placed for fixation after adequate fracture reduction was confirmed on fluoroscopy. As a medial incision was made to extract the tibialis posterior tendon, the joint could not retain arthroscopic fluid, and visualization of the posterior fracture fragment after tendon removal was difficult. Therefore, arthroscopy-assisted reduction could not be completed.
Next, the lateral malleolus was open-reduced, and fixation was achieved using a standard interfragmentary lag screw and a lateral neutralization plate technique (Figure 6). After surgery, the patient was immobilized in a posterior splint with side gussets. Two weeks later, the incisions were healing well, and the tibialis posterior tendon was functioning normally. The sutures were removed, the patient was transitioned to a controlled ankle movement (CAM) boot, and ankle and subtalar range-of-motion exercises were initiated. The patient remained non-weight-bearing for 6 weeks. Radiographs 6 weeks after surgery showed healing fractures with stable hardware (Figure 7). The patient demonstrated 5/5 strength of the tibialis posterior tendon without subluxation or dislocation. There was no tenderness to palpation over the fracture sites or tibialis posterior tendon. The patient began progressive weight-bearing in a CAM boot and physical therapy for range of motion and strengthening.
Discussion
Tibialis posterior tendon injuries—including rupture, dislocation, and entrapment—are well-described complications of ankle injuries.1,2,5,10 Most commonly, the tibialis posterior tendon has been reported to cause a mechanical block to reduction in lateral subtalar dislocations.11-13 In addition, there are case reports of isolated traumatic dislocations of the tibialis posterior tendon without rupture, requiring operative stabilization and retinaculum repair with or without deepening of the posterior groove.14,15
Posterior malleolar ankle fractures remain controversial, with respect to both need for fixation and fixation methods. Although multiple investigators have advocated operative treatment for such fractures that exceed 25% to 33% of the anteroposterior dimension of the tibial plafond, there are no conclusive studies or evidence-based guidelines for treating these fractures.16,17 Anatomical reduction and plating are important to restore articular congruity and increase syndesmotic stability; recent studies have demonstrated that fixation of posterior malleolar fractures provides more syndesmotic stability than trans-syndesmotic screws do.18,19 Indirect reduction of the posterior malleolar fragment after fibula fixation is often accepted as adequate. Whether indirect or direct reduction is attempted, close attention should be given to plain radiographs after attempted reduction, and consideration should be given to possible soft-tissue or bony interposition if malreduction is identified.16,17 Plain radiographs are unreliable in assessing posterior malleolar fragment size as well as amount of comminution and impaction.8,9 Therefore, an arthroscopy-assisted approach coupled with percutaneous fixation may provide more reliable fracture reduction over indirect fracture reduction with fibular fixation, with less dissection than a formal posterolateral approach with posterior plating.
Not all ankle fractures require CT. However, for posterior malleolus fractures thought to require fixation, preoperative CT may help in determining if percutaneous fixation with or without arthroscopic guidance is a feasible treatment option. Ideally, percutaneous reduction can obviate the need for a larger posterolateral incision and buttress plate and, with arthroscopic assistance, may be superior to indirect reduction with fluoroscopy.
In our patient’s case, arthroscopic assistance facilitated diagnosis of an entrapped structure that would have been difficult to identify, particularly without preoperative CT. It may be difficult to identify imperfect reduction of the posterior malleolus on plain radiographs alone, and arthroscopy-assisted fixation enhances the surgeon’s ability to consider reduction, view incarcerated structures within the joint, and treat articular injuries. We do not routinely use ankle arthroscopy as an adjunct to ankle fracture fixation, but judicious use in select cases can facilitate treatment of intra-articular injuries and facilitate visualization and reduction of posterior malleolar fracture fragments before percutaneous anterior-to-posterior cannulated screw fixation. If an open incision is required, as in the present case, visualization becomes difficult secondary to fluid extravasation. However, we think avoiding the morbidity associated with an open incision is worthwhile for fixation of posterior malleolus fractures.
Conclusion
Close inspection of both preoperative and intraoperative radiographs is required to ensure adequate reduction of a posterior malleolar fragment without soft-tissue or bony interposition in the reduction of ankle fractures. Although not previously reported, posterior tendon entrapment within the posterior malleolus fracture may occur and may require arthroscopic or open techniques to ensure adequate extrication of the tendon to allow for posterior malleolar fracture reduction and fixation. This case report highlights one indication for arthroscopy in the treatment of ankle fractures despite the fact that the tibialis posterior tendon was openly removed. Arthroscopic assistance in acute ankle injuries allows the surgeon to evaluate articular cartilage injuries and ensure there are no interposed structures while checking reduction of the posterior malleolar fracture fragment when present.
Irreducible ankle fracture-dislocation secondary to tibialis posterior tendon interposition is a rare but documented complication most commonly associated with Lauge-Hansen classification pronation–external rotation ankle fractures.1-4 Entrapment of the tibialis posterior tendon has been documented in the syndesmosis (tibiotalar joint)1,2,4 and within a medial malleolus fracture.5 To our knowledge, however, there are no case reports of entrapment of the tibialis posterior tendon in a posterior malleolus fracture.
Ankle arthroscopy performed at time of fracture fixation is gaining in popularity because of its enhanced ability to document and treat intra-articular pathology associated with the initial injury.6,7 In addition, percutaneous fixation of a posterior malleolar fragment with arthroscopic assessment of the articular surface reduction may be valuable, as evaluation of tibial plafond fracture reduction by plain radiographs and fluoroscopy has proved to have limitations.8,9
In this article, we present the case of a patient who underwent attempted arthroscopy-assisted reduction of the posterior malleolus with entrapment of the tibialis posterior tendon within the posterior malleolar fracture fragment. The tendon was irreducible with arthroscopic techniques, necessitating posteromedial incision and subsequent open reduction of the incarcerated structure. The patient provided written informed consent for print and electronic publication of this case report.
Case Report
A 67-year-old man slipped and fell on ice while jogging and subsequently presented to the emergency department with a closed bimalleolar ankle fracture-dislocation. Plain radiography (Figure 1) and computed tomography (CT) showed an oblique lateral malleolar fracture and a large posterior malleolar fracture. Further examination of the CT scan revealed entrapment of the tibialis posterior tendon within the posterior malleolar fracture (Figure 2).
Two days after injury, the patient was taken to the operating room for ankle arthroscopy with planned extrication of the entrapped tibialis posterior tendon and possible arthroscopy-assisted percutaneous fixation of the posterior malleolar fracture and open fixation of the distal fibula fracture. Diagnostic arthroscopy revealed a deltoid ligament injury (Figure 3) and a loose piece of articular cartilage (~1 cm in diameter), which was excised. No donor site for this cartilage fragment was identified with further arthroscopic evaluation. During arthroscopic examination, the tibialis posterior tendon was visualized within the joint, incarcerated within the posterior malleolar fracture (Figure 4). Attempts to release the tibialis posterior tendon from the fracture site using arthroscopic instruments and closed reduction techniques were unsuccessful, both with and without noninvasive skeletal traction applied to the ankle.
After multiple unsuccessful attempts to extract the tibialis posterior tendon arthroscopically, traction was removed, and a separate incision was made over the posteromedial aspect of the ankle. The tibialis posterior tendon was identified within the fracture site and was removed using an angled clamp (Figure 5). The fracture was reduced and held provisionally with a large tenaculum clamp. Two anterior-to-posterior, partially threaded cannulated screws were placed for fixation after adequate fracture reduction was confirmed on fluoroscopy. As a medial incision was made to extract the tibialis posterior tendon, the joint could not retain arthroscopic fluid, and visualization of the posterior fracture fragment after tendon removal was difficult. Therefore, arthroscopy-assisted reduction could not be completed.
Next, the lateral malleolus was open-reduced, and fixation was achieved using a standard interfragmentary lag screw and a lateral neutralization plate technique (Figure 6). After surgery, the patient was immobilized in a posterior splint with side gussets. Two weeks later, the incisions were healing well, and the tibialis posterior tendon was functioning normally. The sutures were removed, the patient was transitioned to a controlled ankle movement (CAM) boot, and ankle and subtalar range-of-motion exercises were initiated. The patient remained non-weight-bearing for 6 weeks. Radiographs 6 weeks after surgery showed healing fractures with stable hardware (Figure 7). The patient demonstrated 5/5 strength of the tibialis posterior tendon without subluxation or dislocation. There was no tenderness to palpation over the fracture sites or tibialis posterior tendon. The patient began progressive weight-bearing in a CAM boot and physical therapy for range of motion and strengthening.
Discussion
Tibialis posterior tendon injuries—including rupture, dislocation, and entrapment—are well-described complications of ankle injuries.1,2,5,10 Most commonly, the tibialis posterior tendon has been reported to cause a mechanical block to reduction in lateral subtalar dislocations.11-13 In addition, there are case reports of isolated traumatic dislocations of the tibialis posterior tendon without rupture, requiring operative stabilization and retinaculum repair with or without deepening of the posterior groove.14,15
Posterior malleolar ankle fractures remain controversial, with respect to both need for fixation and fixation methods. Although multiple investigators have advocated operative treatment for such fractures that exceed 25% to 33% of the anteroposterior dimension of the tibial plafond, there are no conclusive studies or evidence-based guidelines for treating these fractures.16,17 Anatomical reduction and plating are important to restore articular congruity and increase syndesmotic stability; recent studies have demonstrated that fixation of posterior malleolar fractures provides more syndesmotic stability than trans-syndesmotic screws do.18,19 Indirect reduction of the posterior malleolar fragment after fibula fixation is often accepted as adequate. Whether indirect or direct reduction is attempted, close attention should be given to plain radiographs after attempted reduction, and consideration should be given to possible soft-tissue or bony interposition if malreduction is identified.16,17 Plain radiographs are unreliable in assessing posterior malleolar fragment size as well as amount of comminution and impaction.8,9 Therefore, an arthroscopy-assisted approach coupled with percutaneous fixation may provide more reliable fracture reduction over indirect fracture reduction with fibular fixation, with less dissection than a formal posterolateral approach with posterior plating.
Not all ankle fractures require CT. However, for posterior malleolus fractures thought to require fixation, preoperative CT may help in determining if percutaneous fixation with or without arthroscopic guidance is a feasible treatment option. Ideally, percutaneous reduction can obviate the need for a larger posterolateral incision and buttress plate and, with arthroscopic assistance, may be superior to indirect reduction with fluoroscopy.
In our patient’s case, arthroscopic assistance facilitated diagnosis of an entrapped structure that would have been difficult to identify, particularly without preoperative CT. It may be difficult to identify imperfect reduction of the posterior malleolus on plain radiographs alone, and arthroscopy-assisted fixation enhances the surgeon’s ability to consider reduction, view incarcerated structures within the joint, and treat articular injuries. We do not routinely use ankle arthroscopy as an adjunct to ankle fracture fixation, but judicious use in select cases can facilitate treatment of intra-articular injuries and facilitate visualization and reduction of posterior malleolar fracture fragments before percutaneous anterior-to-posterior cannulated screw fixation. If an open incision is required, as in the present case, visualization becomes difficult secondary to fluid extravasation. However, we think avoiding the morbidity associated with an open incision is worthwhile for fixation of posterior malleolus fractures.
Conclusion
Close inspection of both preoperative and intraoperative radiographs is required to ensure adequate reduction of a posterior malleolar fragment without soft-tissue or bony interposition in the reduction of ankle fractures. Although not previously reported, posterior tendon entrapment within the posterior malleolus fracture may occur and may require arthroscopic or open techniques to ensure adequate extrication of the tendon to allow for posterior malleolar fracture reduction and fixation. This case report highlights one indication for arthroscopy in the treatment of ankle fractures despite the fact that the tibialis posterior tendon was openly removed. Arthroscopic assistance in acute ankle injuries allows the surgeon to evaluate articular cartilage injuries and ensure there are no interposed structures while checking reduction of the posterior malleolar fracture fragment when present.
1. Ermis MN, Yagmurlu MF, Kilinc AS, Karakas ES. Irreducible fracture dislocation of the ankle caused by tibialis posterior tendon interposition. J Foot Ankle Surg. 2010;49(2):166-171.
2. Curry EE, O’Brien TS, Johnson JE. Fibular nonunion and equinovarus deformity secondary to posterior tibial tendon incarceration in the syndesmosis: a case report after a bimalleolar fracture-dislocation. Foot Ankle Int. 1999;20(8):527-531.
3. Coonrad RW, Bugg EI Jr. Trapping of the posterior tibial tendon and interposition of soft tissue in severe fractures about the ankle joint. J Bone Joint Surg Am. 1954;36(4):744-750.
4. Pankovich AM. Fracture-dislocation of the ankle. Trapping of the postero-medial ankle tendons and neurovascular bundle in the tibiofibular interosseous space: a case report. J Trauma. 1976;16(11):927-929.
5. Khamaisy S, Leibner ED, Elishoov O. Tibialis posterior entrapment: case report. Foot Ankle Int. 2012;33(5):441-443.
6. Hsu AR, Gross CE, Lee S, Carreira DS. Extended indications for foot and ankle arthroscopy. J Am Acad Orthop Surg. 2014;22(1):10-19.
7. Stufkens SA, Knupp M, Horisberger M, Lampert C, Hintermann B. Cartilage lesions and the development of osteoarthritis after internal fixation of ankle fractures: a prospective study. J Bone Joint Surg Am. 2010;92(2):279-286.
8. Büchler L, Tannast M, Bonel HM, Weber M. Reliability of radiologic assessment of the fracture anatomy at the posterior tibial plafond in malleolar fractures. J Orthop Trauma. 2009;23(3):208-212.
9. Ferries JS, DeCoster TA, Firoozbakhsh KK, Garcia JF, Miller RA. Plain radiographic interpretation in trimalleolar ankle fractures poorly assesses posterior fragment size. J Orthop Trauma. 1994;8(4):328-331.
10. Jarvis HC, Cannada LK. Acute tibialis posterior tendon rupture associated with a distal tibial fracture. Orthopedics. 2012;35(4):e595-e597.
11. Woodruff MJ, Brown JN, Mountney J. A mechanism for entrapment of the tibialis posterior tendon in lateral subtalar dislocation. Injury. 1996;27(3):193-194.
12. Leitner B. Obstacles to reduction in subtalar dislocations. J Bone Joint Surg Am. 1954;36(2):299-306.
13. Waldrop J, Ebraheim NA, Shapiro P, Jackson WT. Anatomical considerations of posterior tibialis tendon entrapment in irreducible lateral subtalar dislocation. Foot Ankle. 1992;13(8):458-461.
14. Goucher NR, Coughlin MJ, Kristensen RM. Dislocation of the posterior tibial tendon: a literature review and presentation of two cases. Iowa Orthop J. 2006;26:122-126.
15. Olivé Vilás R, Redón Montojo N, Pino Sorroche S. Traumatic dislocation of tibialis posterior tendon: a case report in a tae-kwon-do athlete. Clin J Sport Med. 2009;19(1):68-69.
16. Gardner MJ, Streubel PN, McCormick JJ, Klein SE, Johnson JE, Ricci WM. Surgeon practices regarding operative treatment of posterior malleolus fractures. Foot Ankle Int. 2011;32(4):385-393.
17. Irwin TA, Lien J, Kadakia AR. Posterior malleolus fracture. J Am Acad Orthop Surg. 2013;21(1):32-40.
18. Gardner MJ, Brodsky A, Briggs SM, Nielson JH, Lorich DG. Fixation of posterior malleolar fractures provides greater syndesmotic stability. Clin Orthop Relat Res. 2006;(447):165-171.
19. Miller AN, Carroll EA, Parker RJ, Helfet DL, Lorich DG. Posterior malleolar stabilization of syndesmotic injuries is equivalent to screw fixation. Clin Orthop Relat Res. 2010;468(4):1129-1135.
1. Ermis MN, Yagmurlu MF, Kilinc AS, Karakas ES. Irreducible fracture dislocation of the ankle caused by tibialis posterior tendon interposition. J Foot Ankle Surg. 2010;49(2):166-171.
2. Curry EE, O’Brien TS, Johnson JE. Fibular nonunion and equinovarus deformity secondary to posterior tibial tendon incarceration in the syndesmosis: a case report after a bimalleolar fracture-dislocation. Foot Ankle Int. 1999;20(8):527-531.
3. Coonrad RW, Bugg EI Jr. Trapping of the posterior tibial tendon and interposition of soft tissue in severe fractures about the ankle joint. J Bone Joint Surg Am. 1954;36(4):744-750.
4. Pankovich AM. Fracture-dislocation of the ankle. Trapping of the postero-medial ankle tendons and neurovascular bundle in the tibiofibular interosseous space: a case report. J Trauma. 1976;16(11):927-929.
5. Khamaisy S, Leibner ED, Elishoov O. Tibialis posterior entrapment: case report. Foot Ankle Int. 2012;33(5):441-443.
6. Hsu AR, Gross CE, Lee S, Carreira DS. Extended indications for foot and ankle arthroscopy. J Am Acad Orthop Surg. 2014;22(1):10-19.
7. Stufkens SA, Knupp M, Horisberger M, Lampert C, Hintermann B. Cartilage lesions and the development of osteoarthritis after internal fixation of ankle fractures: a prospective study. J Bone Joint Surg Am. 2010;92(2):279-286.
8. Büchler L, Tannast M, Bonel HM, Weber M. Reliability of radiologic assessment of the fracture anatomy at the posterior tibial plafond in malleolar fractures. J Orthop Trauma. 2009;23(3):208-212.
9. Ferries JS, DeCoster TA, Firoozbakhsh KK, Garcia JF, Miller RA. Plain radiographic interpretation in trimalleolar ankle fractures poorly assesses posterior fragment size. J Orthop Trauma. 1994;8(4):328-331.
10. Jarvis HC, Cannada LK. Acute tibialis posterior tendon rupture associated with a distal tibial fracture. Orthopedics. 2012;35(4):e595-e597.
11. Woodruff MJ, Brown JN, Mountney J. A mechanism for entrapment of the tibialis posterior tendon in lateral subtalar dislocation. Injury. 1996;27(3):193-194.
12. Leitner B. Obstacles to reduction in subtalar dislocations. J Bone Joint Surg Am. 1954;36(2):299-306.
13. Waldrop J, Ebraheim NA, Shapiro P, Jackson WT. Anatomical considerations of posterior tibialis tendon entrapment in irreducible lateral subtalar dislocation. Foot Ankle. 1992;13(8):458-461.
14. Goucher NR, Coughlin MJ, Kristensen RM. Dislocation of the posterior tibial tendon: a literature review and presentation of two cases. Iowa Orthop J. 2006;26:122-126.
15. Olivé Vilás R, Redón Montojo N, Pino Sorroche S. Traumatic dislocation of tibialis posterior tendon: a case report in a tae-kwon-do athlete. Clin J Sport Med. 2009;19(1):68-69.
16. Gardner MJ, Streubel PN, McCormick JJ, Klein SE, Johnson JE, Ricci WM. Surgeon practices regarding operative treatment of posterior malleolus fractures. Foot Ankle Int. 2011;32(4):385-393.
17. Irwin TA, Lien J, Kadakia AR. Posterior malleolus fracture. J Am Acad Orthop Surg. 2013;21(1):32-40.
18. Gardner MJ, Brodsky A, Briggs SM, Nielson JH, Lorich DG. Fixation of posterior malleolar fractures provides greater syndesmotic stability. Clin Orthop Relat Res. 2006;(447):165-171.
19. Miller AN, Carroll EA, Parker RJ, Helfet DL, Lorich DG. Posterior malleolar stabilization of syndesmotic injuries is equivalent to screw fixation. Clin Orthop Relat Res. 2010;468(4):1129-1135.
Shoulder Instability Management: A Survey of the American Shoulder and Elbow Surgeons
Despite an abundance of peer-reviewed resources, there is wide variation in the surgical management of shoulder instability.1,2 Current American Academy of Orthopaedic Surgeons (AAOS) clinical practice guidelines regarding the shoulder address only generalized shoulder pain, glenohumeral osteoarthritis, and rotator cuff injuries,3,4 and treatment algorithms focus on conservative treatment, rather than surgical recommendations.4-7
Shoulder instability most commonly results from 1 or more of 4 common lesions (capsular laxity, glenoid bone loss, humeral bone loss, and capsulolabral insufficiency).8 While it is a relatively common condition that represents 1% to 2% of all athletic injuries,9,10 little consensus exists about surgical indications, ideal treatment algorithms, or optimal operative technique. This is a critical issue because more than 50% of patients with glenohumeral instability will undergo surgical intervention.11 Chahal and associates6 surveyed 44 shoulder experts and reported strong consensus about diagnosis, but little agreement regarding surgical management. Owens and colleagues1 have also evaluated current trends for surgical treatment of this pathology. Randelli and associates5 attempted to categorize operative management based upon case-specific shoulder scenarios through online surveys. Their survey, however, covered a broad range of shoulder injuries rather than instability in particular. In this study, we assess trends for surgical management of glenohumeral instability in a case-based survey of shoulder experts.
Materials and Methods
Survey Information
An online survey (Survey Monkey) of 417 active members of the American Shoulder and Elbow Surgeons (ASES) was administered on May 1, 2014. Respondents were blinded to the institution and co-investigators conducting the survey. The survey link was distributed via email because it has been shown to be a more efficacious conduit than standard postal mail.12 The case-based, 25-question survey (Appendix) was designed to assess respondents’ selection of surgical intervention. Section 1 determined member demographics, including fellowship training, arthroscopy experience, and years of practice. Section 2 involved the presentation of 5 case scenarios. For each case, respondents were asked to identify the optimal surgical procedure in both primary and revision settings. Section 3 posed several general questions regarding shoulder-instability management.
Statistical Analysis
Data were stored using Microsoft Excel (Microsoft) and analyzed using SAS Software version 9.3 (SAS Institute, Inc.). Demographic survey responses were reported using descriptive statistics. Responses to clinical survey questions were reported using frequencies and percentages. To identify when a majority consensus was achieved for a given question, responses were flagged as reaching consensus when more than 50% of participants gave the same response.13In the event that only 2 response options were available, reaching consensus required 67% of respondents to choose a single answer (since, by default, a consensus would be reached with only 2 response options). Because this was an analysis of all respondents, an a priori power calculation was not performed. Associations between training and practice demographics and responses to clinical questions were investigated using chi-square analyses. All comparative analyses were two-tailed and used P = .05 as the threshold for statistical significance.
Results
Demographics
One hundred and twenty-five (29.9%) ASES members responded to the survey. Of the respondents, 71.2% reported at least 15 years of experience, and 71% performed more than 150 shoulder cases annually. Surgeons came from academic institutions (41.6%), private practice (24.8%), or mixed (33.6%). The majority of respondents were fellowship-trained in shoulder/elbow surgery (52.8%), while fewer had completed a sports-medicine fellowship (24.0%). For arthroscopic procedures, responses were nearly divided between those who preferred beach-chair positioning (47.2%) and those who preferred the lateral decubitus position (46.4%). The majority (70.4%) of respondents practiced in the United States and with a relatively even distribution among states and region. The remaining 29.6% of those surveyed practiced abroad.
Degree of Consensus Responses and Cases
Of the 25 survey questions, 6 questions were omitted from consensus calculations because these were designed for demographic categorization rather than professional opinion (questions 1-5, 8). Thirteen of the remaining 19 questions (68%) reached consensus response. All clinical case scenarios (5 of 5) reached consensus for selection of technique for the primary procedure; however, only 40% (2 of 5) of cases had a consensus in the revision setting.
In case 1, a young soccer player (noncontact athlete) with negligible bone loss, arthroscopic Bankart repair was recommended by 81.6% of respondents. In the event of revision surgery, only 22.4% recommended arthroscopic Bankart repair, and the remainder split between open Bankart repair with possible capsular shift (36%) or Latarjet procedure (32.8%).
In case 2, a college American football player (contact athlete) with negligible bone loss, arthroscopic Bankart repair was recommended by 56.8%. In the event of revision surgery, a majority of members (51.2%) suggested a Latarjet procedure.
In case 3, the weekend warrior with significant bone loss, most respondents recommended a Latarjet procedure for both primary (72.8%) and revision surgery (79.0%).
In case 4, a weekend warrior with multidirectional instability, 60% of respondents suggested arthroscopic Bankart repair, 21.6% recommended rotator interval closure, and 10.4% chose a capsular shift. As a revision procedure, there was less agreement, with a split between open Bankart repair (39.2%) and capsular shift only (39.2%).
In case 5, the weekend warrior with large engaging Hill-Sachs lesions, 60% of respondent selected a remplissage procedure. If revision was required, a Latarjet procedure was the choice of 48.8% of respondents (Table).
General Questions
For contact athletes, most respondents (87.2%) would allow return to play in the same season and recommended surgery after the end of the season. After surgical intervention, 56.8% prescribed 4 weeks of immobilization. When counseling a return to contact sports, 51.2% recommended waiting for 4 to 6 months.
The ASES members were divided on conservative management of instability injuries. Responses included immobilization in internal rotation (39.2%), no immobilization (39.2%), and external-rotation bracing (21.6%).
Finally, members thought the most important factor in choosing surgical technique was the patient’s pathology, then age; the least influential criteria was the patient’s sports participation.
Analysis of Training Demographics and Surgical Technique Preferences
Chi-square analyses demonstrated that respondents who completed a sports fellowship were more likely to do at least 50% of cases arthroscopically (odds ratio [OR], 15.3; P < .001) and were more likely to use the lateral decubitus position (OR, 2.8; P < .021). Furthermore, American respondents had a higher likelihood of having completed either a sports fellowship (OR, 12.8; P < .001) or a shoulder/elbow fellowship (OR, 4.6; P = .002) when compared with foreign respondents.
Discussion
In the absence of formal clinical practice guidelines, most surgeons formulate treatment strategy based upon a combination of experience and peer-reviewed evidence. The cohort analyzed in the current study was highly experienced, with more than 70% performing 150 shoulder cases annually and having more than 15 years of experience. We found a consensus response in 68% of questions and all primary surgical techniques for our shoulder instability scenarios. While expert consensus reported here is not equivalent to evidence-based clinical practice guidelines, it does provide important information to consider when treating anterior shoulder instability.
Specific responses to our case scenarios invite further reflection. Considering young (both noncontact and contact) athletes without bony pathology (cases 1 and 2, respectively), the ASES surgeons recommended arthroscopic Bankart repair for both. Randelli and associates5 found 71% of survey respondents recommended arthroscopic Bankart repair in a similar setting. It is interesting to note that consensus persisted regardless of the sport in which they engaged. Contact athletes have the highest rates of dislocation (up to 7 times higher incidence) compared with the general population.14 In addition, they have a higher recurrence rate after surgery.15 It should be noted, however, that although both cases reached consensus, the percentage of experts who recommended an arthroscopic procedure fell from 82% in the noncontact athlete to 57% in the contact athlete. This concurs with a recent review by Harris and Romeo,16 who recommended similar treatments for athletes without bony defects. In an older patient population with recurrent instability (case 3), responses varied more widely but still reached a consensus on primary surgical techniques. Respondents agreed that, even for patients with multidirectional instability, initial management should consist of arthroscopic capsulolabral repair. Overall, the agreement for arthroscopy for cases 1 through 3 mimics recent US practice patterns, showing 90% of stabilizations are being performed arthroscopically.17 Additionally, a recent meta-analysis by Harris and associates18 favored arthroscopic Bankart repair, showing no significant difference vs open stabilization even on long-term follow-up.
Glenoid bone loss is a difficult clinical scenario and that is reflected in this study’s findings. The literature suggests that arthroscopic Bankart repair, in this setting, is usually not sufficient and may result in a recurrence rate up to 75%, if bone loss greater than 20% is unaddressed.19 Our study supports this trend because ASES members recommended a Latarjet procedure when there is substantial bone loss.
While open Latarjet procedure was the consensus for dealing with glenoid bone loss, arthroscopic techniques were strongly favored for humeral head defects. This change in practice patterns results from the introduction of the arthroscopic remplissage technique.20 Two recent systemic reviews have supported this technique, reporting good functional outcomes for engaging Hill-Sachs lesions.21,22 Our study had similar agreement, with most respondents recommending remplissage for these patients.
This study found the lowest rates of expert consensus in the setting of revision surgery, likely caused, in part, by the paucity of available large cohort studies. This is a major void in the literature, and more studies are needed to help guide surgeons on the best techniques to deal with this difficult patient population.
Conservative bracing technique was 1 of the survey questions lacking a consensus response. Interestingly, 39% of members recommended no immobilization after an instability event. This contrasts with recent literature concerning the best position for bracing. We also found twice as many surgeons recommended internal rotation immobilization over external rotation. This is a subject of debate, with some studies stating improvement with external rotation immobilization,23 while other studies reported no difference.24 Overall, recommendations regarding type of immobilization are unclear, which will likely continue until larger studies can be performed.
The literature describing surgical trends in the treatment of shoulder instability is sparse and variable. With regard to other shoulder etiologies, only rotator cuff pathology has used expert consensus. Acevedo and colleagues13 reported agreement of ASES members surveyed regarding rotator cuff management. There was no consensus among surgeons in more than 50% of questions, despite AAOS published guidelines for rotator cuff treatment.25 Despite the lack of guidelines for our topic, we found a consensus among respondents with 68% of survey questions.
To date, only 2 studies of shoulder instability management have elicited the opinion of experts in shoulder surgery. Chahal and associates6 surveyed 42 members of ASES and JOINTS (Joined Orthopaedic Initiatives for National Trials of the Shoulder) Canada on shoulder instability cases and found substantial agreement on diagnosis but little consensus regarding surgical technique. This lack of agreement on procedures differs from our findings and may be related to their complicated case scenarios that generated a wide array of treatment recommendations. Randelli and colleagues5 surveyed more than 1000 European Society of Sports Traumatology, Knee Surgery, and Arthroscopy members and reported similar agreement on arthroscopic Bankart repair in young male shoulder-dislocation patients, although no other instability scenarios were investigated. Our study is the first to report responses from expert shoulder surgeons on surgical-treatment strategies for an array of common shoulder instability pathologies.
This study had several limitations. First, while our study suffered from a low response rate (29.9%), it was similar to other published studies.5,13 Second, because the case series included in the survey attempted to capture the most common instability scenarios, they were limited in their scope and failed to address additional etiologies or pathologic permutations. We believe, however, that a more comprehensive survey would have resulted in respondent fatigue and lowered the response rate. It is unlikely that any survey could capture all variables that come into play during clinical decision-making, and we sought to evaluate the most common shoulder instability scenarios. Third, 30% of respondents were from outside the United States, where the Latarjet procedure is much more popular. While this was not a majority, Latarjet’s regional preference may have decreased the consensus response in some scenarios if only the United States was included. Finally, there is inherent bias in a respondent pool that is heavily weighted to shoulder-surgery experts (ASES members) and does not consider the responses of the general orthopedic surgery community as have other studies.7
Conclusion
This study demonstrates that expert shoulder surgeons often agreed on shoulder-treatment principles for anterior shoulder instability. In the setting of primary repair, arthroscopic Bankart repair was favored in the absence of bony pathology, regardless of age (20 to 35 years) or nature of sport (contact versus noncontact). Latarjet procedures were favored in the setting of glenoid bone loss, and remplissage for an engaging Hill-Sachs lesion. Less agreement was observed for revision stabilization. It should be noted that, while consensus was often reached for our cases, there was a wide distribution of technical considerations and surgical preferences even among those who are fellowship-trained and high-volume surgeons, and who can be considered experts in the field of shoulder surgery.
1. Owens BD, Harrast JJ, Hurwitz SR, Thompson TL, Wolf JM. Surgical trends in bankart repair: an analysis of data from the American Board of Orthopaedic Surgery certification examination. Am J Sports Med. 2011;39(9):1865-1869.
2. Loebenberg MI, Rosen JE, Ishak C, Jazrawi LM, Zuckerman JD. A survey of decision-making processes in the treatment of common shoulder ailments among primary care physicians. Bull Hosp Jt Dis. 2006;63(3-4):137-144.
3. American Academy of Orthopaedic Surgeons. AAOS clinical practice guidelines (CPG). www.aaos.org/research/guidelines/guide.asp. Updated December 30, 2013. Accessed May 1, 2015.
4. Sanders JO, Bozic KJ, Glassman SD, Jevsevar DS, Weber KL. Clinical practice guidelines: their use, misuse, and future directions. J Am Acad Orthop Surg. 2014;22(3):135-144.
5. Randelli P, Arrigoni P, Cabitza F, Ragone V, Cabitza P. Current practice in shoulder pathology: results of a web-based survey among a community of 1,084 orthopedic surgeons. Knee Surg Sports Traumatol Arthrosc. 2011;20(5):803-815.
6. Chahal J, Kassiri K, Dion A, MacDonald P, Leiter J. Diagnostic and treatment differences among experienced shoulder surgeons for instability conditions of the shoulder. Clin J Sport Med. 2007;17(1):5-9.
7. Redfern J, Burks R. 2009 survey results: surgeon practice patterns regarding arthroscopic surgery. Arthroscopy. 2009;25(12):1447-1452.
8. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic bankart repairs: significance of the inverted-pear glenoid and the humeral engaging hill-sachs lesion. Arthroscopy. 2000;16(7):677-694.
9. Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754.
10. Owens MBD, Duffey ML, Nelson BJ, et al. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.
11. Hovelius L, Olofsson A, Sandström B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. A prospective twenty-five-year follow-up. J Bone Joint Surg Am. 2008;90(5):945-952.
12. Raziano DB, Jayadevappa R, Valenzula D, Weiner M, Lavizzo-Mourey R. E-mail versus conventional postal mail survey of geriatric chiefs. Gerontologist. 2001;41(6):799-804.
13. Acevedo DC, Paxton ES, Williams GR, Abboud JA. A survey of expert opinion regarding rotator cuff repair. J Bone Joint Surg Am. 2014;96(14):e123.
14. Kaplan LD, Flanigan DC, Norwig J, Jost P, Bradley J. Prevalence and variance of shoulder injuries in elite collegiate football players. Am J Sports Med. 2005;33(8):1142-1146.
15. Petrera M, Dwyer T, Tsuji MR, Theodoropoulos JS. Outcomes of arthroscopic Bankart repair in collision versus noncollision athletes. Orthopedics. 2013;36(5):e621-e626.
16. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.
17. Zhang AL, Montgomery SR, Ngo SS, Hame SL, Wang JC, Gamradt SC. Arthroscopic versus open shoulder stabilization: current practice patterns in the united states. Arthroscopy. 2014;30(4):436-443.
18. Harris JD, Gupta AK, Mall NA, et al. Long-term outcomes after Bankart shoulder stabilization. Arthroscopy. 2013;29(5):920-933.
19. Boileau P, Villalba M, Héry J, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763.
20. Purchase RJ, Wolf EM, Hobgood ER, Pollock ME, Smalley CC. Hill-sachs ”remplissage”: an arthroscopic solution for the engaging hill-sachs lesion. Arthroscopy. 2008;24(6):723-726.
21. Buza JA 3rd, Iyengar JJ, Anakwenze OA, Ahmad CS, Levine WN. Arthroscopic Hill-Sachs remplissage: a systematic review. J Bone Joint Surg Am. 2014;96(7):549-555.
22. Rashid MS, Crichton J, Butt U, Akimau PI, Charalambous CP. Arthroscopic “Remplissage” for shoulder instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014:1-7.
23. Itoi E, Hatakeyama Y, Kido T, et al. A new method of immobilization after traumatic anterior dislocation of the shoulder: a preliminary study. J Shoulder Elbow Surg. 2003;12(5):413-415.
24. Whelan DB, Litchfield R, Wambolt E, Dainty KN; Joint Orthopaedic Initiative for National Trials of the Shoulder (JOINTS). External rotation immobilization for primary shoulder dislocation: A randomized controlled trial. Clin Orthop Relat Res. 2014;472(8):2380-2386.
25. Pedowitz RA, Yamaguchi K, Ahmad CS, et al. American Academy of Orthopaedic Surgeons Clinical Practice Guideline on: optimizing the management of rotator cuff problems. J Bone Joint Surg Am. 2012;94(2):163-167.
Despite an abundance of peer-reviewed resources, there is wide variation in the surgical management of shoulder instability.1,2 Current American Academy of Orthopaedic Surgeons (AAOS) clinical practice guidelines regarding the shoulder address only generalized shoulder pain, glenohumeral osteoarthritis, and rotator cuff injuries,3,4 and treatment algorithms focus on conservative treatment, rather than surgical recommendations.4-7
Shoulder instability most commonly results from 1 or more of 4 common lesions (capsular laxity, glenoid bone loss, humeral bone loss, and capsulolabral insufficiency).8 While it is a relatively common condition that represents 1% to 2% of all athletic injuries,9,10 little consensus exists about surgical indications, ideal treatment algorithms, or optimal operative technique. This is a critical issue because more than 50% of patients with glenohumeral instability will undergo surgical intervention.11 Chahal and associates6 surveyed 44 shoulder experts and reported strong consensus about diagnosis, but little agreement regarding surgical management. Owens and colleagues1 have also evaluated current trends for surgical treatment of this pathology. Randelli and associates5 attempted to categorize operative management based upon case-specific shoulder scenarios through online surveys. Their survey, however, covered a broad range of shoulder injuries rather than instability in particular. In this study, we assess trends for surgical management of glenohumeral instability in a case-based survey of shoulder experts.
Materials and Methods
Survey Information
An online survey (Survey Monkey) of 417 active members of the American Shoulder and Elbow Surgeons (ASES) was administered on May 1, 2014. Respondents were blinded to the institution and co-investigators conducting the survey. The survey link was distributed via email because it has been shown to be a more efficacious conduit than standard postal mail.12 The case-based, 25-question survey (Appendix) was designed to assess respondents’ selection of surgical intervention. Section 1 determined member demographics, including fellowship training, arthroscopy experience, and years of practice. Section 2 involved the presentation of 5 case scenarios. For each case, respondents were asked to identify the optimal surgical procedure in both primary and revision settings. Section 3 posed several general questions regarding shoulder-instability management.
Statistical Analysis
Data were stored using Microsoft Excel (Microsoft) and analyzed using SAS Software version 9.3 (SAS Institute, Inc.). Demographic survey responses were reported using descriptive statistics. Responses to clinical survey questions were reported using frequencies and percentages. To identify when a majority consensus was achieved for a given question, responses were flagged as reaching consensus when more than 50% of participants gave the same response.13In the event that only 2 response options were available, reaching consensus required 67% of respondents to choose a single answer (since, by default, a consensus would be reached with only 2 response options). Because this was an analysis of all respondents, an a priori power calculation was not performed. Associations between training and practice demographics and responses to clinical questions were investigated using chi-square analyses. All comparative analyses were two-tailed and used P = .05 as the threshold for statistical significance.
Results
Demographics
One hundred and twenty-five (29.9%) ASES members responded to the survey. Of the respondents, 71.2% reported at least 15 years of experience, and 71% performed more than 150 shoulder cases annually. Surgeons came from academic institutions (41.6%), private practice (24.8%), or mixed (33.6%). The majority of respondents were fellowship-trained in shoulder/elbow surgery (52.8%), while fewer had completed a sports-medicine fellowship (24.0%). For arthroscopic procedures, responses were nearly divided between those who preferred beach-chair positioning (47.2%) and those who preferred the lateral decubitus position (46.4%). The majority (70.4%) of respondents practiced in the United States and with a relatively even distribution among states and region. The remaining 29.6% of those surveyed practiced abroad.
Degree of Consensus Responses and Cases
Of the 25 survey questions, 6 questions were omitted from consensus calculations because these were designed for demographic categorization rather than professional opinion (questions 1-5, 8). Thirteen of the remaining 19 questions (68%) reached consensus response. All clinical case scenarios (5 of 5) reached consensus for selection of technique for the primary procedure; however, only 40% (2 of 5) of cases had a consensus in the revision setting.
In case 1, a young soccer player (noncontact athlete) with negligible bone loss, arthroscopic Bankart repair was recommended by 81.6% of respondents. In the event of revision surgery, only 22.4% recommended arthroscopic Bankart repair, and the remainder split between open Bankart repair with possible capsular shift (36%) or Latarjet procedure (32.8%).
In case 2, a college American football player (contact athlete) with negligible bone loss, arthroscopic Bankart repair was recommended by 56.8%. In the event of revision surgery, a majority of members (51.2%) suggested a Latarjet procedure.
In case 3, the weekend warrior with significant bone loss, most respondents recommended a Latarjet procedure for both primary (72.8%) and revision surgery (79.0%).
In case 4, a weekend warrior with multidirectional instability, 60% of respondents suggested arthroscopic Bankart repair, 21.6% recommended rotator interval closure, and 10.4% chose a capsular shift. As a revision procedure, there was less agreement, with a split between open Bankart repair (39.2%) and capsular shift only (39.2%).
In case 5, the weekend warrior with large engaging Hill-Sachs lesions, 60% of respondent selected a remplissage procedure. If revision was required, a Latarjet procedure was the choice of 48.8% of respondents (Table).
General Questions
For contact athletes, most respondents (87.2%) would allow return to play in the same season and recommended surgery after the end of the season. After surgical intervention, 56.8% prescribed 4 weeks of immobilization. When counseling a return to contact sports, 51.2% recommended waiting for 4 to 6 months.
The ASES members were divided on conservative management of instability injuries. Responses included immobilization in internal rotation (39.2%), no immobilization (39.2%), and external-rotation bracing (21.6%).
Finally, members thought the most important factor in choosing surgical technique was the patient’s pathology, then age; the least influential criteria was the patient’s sports participation.
Analysis of Training Demographics and Surgical Technique Preferences
Chi-square analyses demonstrated that respondents who completed a sports fellowship were more likely to do at least 50% of cases arthroscopically (odds ratio [OR], 15.3; P < .001) and were more likely to use the lateral decubitus position (OR, 2.8; P < .021). Furthermore, American respondents had a higher likelihood of having completed either a sports fellowship (OR, 12.8; P < .001) or a shoulder/elbow fellowship (OR, 4.6; P = .002) when compared with foreign respondents.
Discussion
In the absence of formal clinical practice guidelines, most surgeons formulate treatment strategy based upon a combination of experience and peer-reviewed evidence. The cohort analyzed in the current study was highly experienced, with more than 70% performing 150 shoulder cases annually and having more than 15 years of experience. We found a consensus response in 68% of questions and all primary surgical techniques for our shoulder instability scenarios. While expert consensus reported here is not equivalent to evidence-based clinical practice guidelines, it does provide important information to consider when treating anterior shoulder instability.
Specific responses to our case scenarios invite further reflection. Considering young (both noncontact and contact) athletes without bony pathology (cases 1 and 2, respectively), the ASES surgeons recommended arthroscopic Bankart repair for both. Randelli and associates5 found 71% of survey respondents recommended arthroscopic Bankart repair in a similar setting. It is interesting to note that consensus persisted regardless of the sport in which they engaged. Contact athletes have the highest rates of dislocation (up to 7 times higher incidence) compared with the general population.14 In addition, they have a higher recurrence rate after surgery.15 It should be noted, however, that although both cases reached consensus, the percentage of experts who recommended an arthroscopic procedure fell from 82% in the noncontact athlete to 57% in the contact athlete. This concurs with a recent review by Harris and Romeo,16 who recommended similar treatments for athletes without bony defects. In an older patient population with recurrent instability (case 3), responses varied more widely but still reached a consensus on primary surgical techniques. Respondents agreed that, even for patients with multidirectional instability, initial management should consist of arthroscopic capsulolabral repair. Overall, the agreement for arthroscopy for cases 1 through 3 mimics recent US practice patterns, showing 90% of stabilizations are being performed arthroscopically.17 Additionally, a recent meta-analysis by Harris and associates18 favored arthroscopic Bankart repair, showing no significant difference vs open stabilization even on long-term follow-up.
Glenoid bone loss is a difficult clinical scenario and that is reflected in this study’s findings. The literature suggests that arthroscopic Bankart repair, in this setting, is usually not sufficient and may result in a recurrence rate up to 75%, if bone loss greater than 20% is unaddressed.19 Our study supports this trend because ASES members recommended a Latarjet procedure when there is substantial bone loss.
While open Latarjet procedure was the consensus for dealing with glenoid bone loss, arthroscopic techniques were strongly favored for humeral head defects. This change in practice patterns results from the introduction of the arthroscopic remplissage technique.20 Two recent systemic reviews have supported this technique, reporting good functional outcomes for engaging Hill-Sachs lesions.21,22 Our study had similar agreement, with most respondents recommending remplissage for these patients.
This study found the lowest rates of expert consensus in the setting of revision surgery, likely caused, in part, by the paucity of available large cohort studies. This is a major void in the literature, and more studies are needed to help guide surgeons on the best techniques to deal with this difficult patient population.
Conservative bracing technique was 1 of the survey questions lacking a consensus response. Interestingly, 39% of members recommended no immobilization after an instability event. This contrasts with recent literature concerning the best position for bracing. We also found twice as many surgeons recommended internal rotation immobilization over external rotation. This is a subject of debate, with some studies stating improvement with external rotation immobilization,23 while other studies reported no difference.24 Overall, recommendations regarding type of immobilization are unclear, which will likely continue until larger studies can be performed.
The literature describing surgical trends in the treatment of shoulder instability is sparse and variable. With regard to other shoulder etiologies, only rotator cuff pathology has used expert consensus. Acevedo and colleagues13 reported agreement of ASES members surveyed regarding rotator cuff management. There was no consensus among surgeons in more than 50% of questions, despite AAOS published guidelines for rotator cuff treatment.25 Despite the lack of guidelines for our topic, we found a consensus among respondents with 68% of survey questions.
To date, only 2 studies of shoulder instability management have elicited the opinion of experts in shoulder surgery. Chahal and associates6 surveyed 42 members of ASES and JOINTS (Joined Orthopaedic Initiatives for National Trials of the Shoulder) Canada on shoulder instability cases and found substantial agreement on diagnosis but little consensus regarding surgical technique. This lack of agreement on procedures differs from our findings and may be related to their complicated case scenarios that generated a wide array of treatment recommendations. Randelli and colleagues5 surveyed more than 1000 European Society of Sports Traumatology, Knee Surgery, and Arthroscopy members and reported similar agreement on arthroscopic Bankart repair in young male shoulder-dislocation patients, although no other instability scenarios were investigated. Our study is the first to report responses from expert shoulder surgeons on surgical-treatment strategies for an array of common shoulder instability pathologies.
This study had several limitations. First, while our study suffered from a low response rate (29.9%), it was similar to other published studies.5,13 Second, because the case series included in the survey attempted to capture the most common instability scenarios, they were limited in their scope and failed to address additional etiologies or pathologic permutations. We believe, however, that a more comprehensive survey would have resulted in respondent fatigue and lowered the response rate. It is unlikely that any survey could capture all variables that come into play during clinical decision-making, and we sought to evaluate the most common shoulder instability scenarios. Third, 30% of respondents were from outside the United States, where the Latarjet procedure is much more popular. While this was not a majority, Latarjet’s regional preference may have decreased the consensus response in some scenarios if only the United States was included. Finally, there is inherent bias in a respondent pool that is heavily weighted to shoulder-surgery experts (ASES members) and does not consider the responses of the general orthopedic surgery community as have other studies.7
Conclusion
This study demonstrates that expert shoulder surgeons often agreed on shoulder-treatment principles for anterior shoulder instability. In the setting of primary repair, arthroscopic Bankart repair was favored in the absence of bony pathology, regardless of age (20 to 35 years) or nature of sport (contact versus noncontact). Latarjet procedures were favored in the setting of glenoid bone loss, and remplissage for an engaging Hill-Sachs lesion. Less agreement was observed for revision stabilization. It should be noted that, while consensus was often reached for our cases, there was a wide distribution of technical considerations and surgical preferences even among those who are fellowship-trained and high-volume surgeons, and who can be considered experts in the field of shoulder surgery.
Despite an abundance of peer-reviewed resources, there is wide variation in the surgical management of shoulder instability.1,2 Current American Academy of Orthopaedic Surgeons (AAOS) clinical practice guidelines regarding the shoulder address only generalized shoulder pain, glenohumeral osteoarthritis, and rotator cuff injuries,3,4 and treatment algorithms focus on conservative treatment, rather than surgical recommendations.4-7
Shoulder instability most commonly results from 1 or more of 4 common lesions (capsular laxity, glenoid bone loss, humeral bone loss, and capsulolabral insufficiency).8 While it is a relatively common condition that represents 1% to 2% of all athletic injuries,9,10 little consensus exists about surgical indications, ideal treatment algorithms, or optimal operative technique. This is a critical issue because more than 50% of patients with glenohumeral instability will undergo surgical intervention.11 Chahal and associates6 surveyed 44 shoulder experts and reported strong consensus about diagnosis, but little agreement regarding surgical management. Owens and colleagues1 have also evaluated current trends for surgical treatment of this pathology. Randelli and associates5 attempted to categorize operative management based upon case-specific shoulder scenarios through online surveys. Their survey, however, covered a broad range of shoulder injuries rather than instability in particular. In this study, we assess trends for surgical management of glenohumeral instability in a case-based survey of shoulder experts.
Materials and Methods
Survey Information
An online survey (Survey Monkey) of 417 active members of the American Shoulder and Elbow Surgeons (ASES) was administered on May 1, 2014. Respondents were blinded to the institution and co-investigators conducting the survey. The survey link was distributed via email because it has been shown to be a more efficacious conduit than standard postal mail.12 The case-based, 25-question survey (Appendix) was designed to assess respondents’ selection of surgical intervention. Section 1 determined member demographics, including fellowship training, arthroscopy experience, and years of practice. Section 2 involved the presentation of 5 case scenarios. For each case, respondents were asked to identify the optimal surgical procedure in both primary and revision settings. Section 3 posed several general questions regarding shoulder-instability management.
Statistical Analysis
Data were stored using Microsoft Excel (Microsoft) and analyzed using SAS Software version 9.3 (SAS Institute, Inc.). Demographic survey responses were reported using descriptive statistics. Responses to clinical survey questions were reported using frequencies and percentages. To identify when a majority consensus was achieved for a given question, responses were flagged as reaching consensus when more than 50% of participants gave the same response.13In the event that only 2 response options were available, reaching consensus required 67% of respondents to choose a single answer (since, by default, a consensus would be reached with only 2 response options). Because this was an analysis of all respondents, an a priori power calculation was not performed. Associations between training and practice demographics and responses to clinical questions were investigated using chi-square analyses. All comparative analyses were two-tailed and used P = .05 as the threshold for statistical significance.
Results
Demographics
One hundred and twenty-five (29.9%) ASES members responded to the survey. Of the respondents, 71.2% reported at least 15 years of experience, and 71% performed more than 150 shoulder cases annually. Surgeons came from academic institutions (41.6%), private practice (24.8%), or mixed (33.6%). The majority of respondents were fellowship-trained in shoulder/elbow surgery (52.8%), while fewer had completed a sports-medicine fellowship (24.0%). For arthroscopic procedures, responses were nearly divided between those who preferred beach-chair positioning (47.2%) and those who preferred the lateral decubitus position (46.4%). The majority (70.4%) of respondents practiced in the United States and with a relatively even distribution among states and region. The remaining 29.6% of those surveyed practiced abroad.
Degree of Consensus Responses and Cases
Of the 25 survey questions, 6 questions were omitted from consensus calculations because these were designed for demographic categorization rather than professional opinion (questions 1-5, 8). Thirteen of the remaining 19 questions (68%) reached consensus response. All clinical case scenarios (5 of 5) reached consensus for selection of technique for the primary procedure; however, only 40% (2 of 5) of cases had a consensus in the revision setting.
In case 1, a young soccer player (noncontact athlete) with negligible bone loss, arthroscopic Bankart repair was recommended by 81.6% of respondents. In the event of revision surgery, only 22.4% recommended arthroscopic Bankart repair, and the remainder split between open Bankart repair with possible capsular shift (36%) or Latarjet procedure (32.8%).
In case 2, a college American football player (contact athlete) with negligible bone loss, arthroscopic Bankart repair was recommended by 56.8%. In the event of revision surgery, a majority of members (51.2%) suggested a Latarjet procedure.
In case 3, the weekend warrior with significant bone loss, most respondents recommended a Latarjet procedure for both primary (72.8%) and revision surgery (79.0%).
In case 4, a weekend warrior with multidirectional instability, 60% of respondents suggested arthroscopic Bankart repair, 21.6% recommended rotator interval closure, and 10.4% chose a capsular shift. As a revision procedure, there was less agreement, with a split between open Bankart repair (39.2%) and capsular shift only (39.2%).
In case 5, the weekend warrior with large engaging Hill-Sachs lesions, 60% of respondent selected a remplissage procedure. If revision was required, a Latarjet procedure was the choice of 48.8% of respondents (Table).
General Questions
For contact athletes, most respondents (87.2%) would allow return to play in the same season and recommended surgery after the end of the season. After surgical intervention, 56.8% prescribed 4 weeks of immobilization. When counseling a return to contact sports, 51.2% recommended waiting for 4 to 6 months.
The ASES members were divided on conservative management of instability injuries. Responses included immobilization in internal rotation (39.2%), no immobilization (39.2%), and external-rotation bracing (21.6%).
Finally, members thought the most important factor in choosing surgical technique was the patient’s pathology, then age; the least influential criteria was the patient’s sports participation.
Analysis of Training Demographics and Surgical Technique Preferences
Chi-square analyses demonstrated that respondents who completed a sports fellowship were more likely to do at least 50% of cases arthroscopically (odds ratio [OR], 15.3; P < .001) and were more likely to use the lateral decubitus position (OR, 2.8; P < .021). Furthermore, American respondents had a higher likelihood of having completed either a sports fellowship (OR, 12.8; P < .001) or a shoulder/elbow fellowship (OR, 4.6; P = .002) when compared with foreign respondents.
Discussion
In the absence of formal clinical practice guidelines, most surgeons formulate treatment strategy based upon a combination of experience and peer-reviewed evidence. The cohort analyzed in the current study was highly experienced, with more than 70% performing 150 shoulder cases annually and having more than 15 years of experience. We found a consensus response in 68% of questions and all primary surgical techniques for our shoulder instability scenarios. While expert consensus reported here is not equivalent to evidence-based clinical practice guidelines, it does provide important information to consider when treating anterior shoulder instability.
Specific responses to our case scenarios invite further reflection. Considering young (both noncontact and contact) athletes without bony pathology (cases 1 and 2, respectively), the ASES surgeons recommended arthroscopic Bankart repair for both. Randelli and associates5 found 71% of survey respondents recommended arthroscopic Bankart repair in a similar setting. It is interesting to note that consensus persisted regardless of the sport in which they engaged. Contact athletes have the highest rates of dislocation (up to 7 times higher incidence) compared with the general population.14 In addition, they have a higher recurrence rate after surgery.15 It should be noted, however, that although both cases reached consensus, the percentage of experts who recommended an arthroscopic procedure fell from 82% in the noncontact athlete to 57% in the contact athlete. This concurs with a recent review by Harris and Romeo,16 who recommended similar treatments for athletes without bony defects. In an older patient population with recurrent instability (case 3), responses varied more widely but still reached a consensus on primary surgical techniques. Respondents agreed that, even for patients with multidirectional instability, initial management should consist of arthroscopic capsulolabral repair. Overall, the agreement for arthroscopy for cases 1 through 3 mimics recent US practice patterns, showing 90% of stabilizations are being performed arthroscopically.17 Additionally, a recent meta-analysis by Harris and associates18 favored arthroscopic Bankart repair, showing no significant difference vs open stabilization even on long-term follow-up.
Glenoid bone loss is a difficult clinical scenario and that is reflected in this study’s findings. The literature suggests that arthroscopic Bankart repair, in this setting, is usually not sufficient and may result in a recurrence rate up to 75%, if bone loss greater than 20% is unaddressed.19 Our study supports this trend because ASES members recommended a Latarjet procedure when there is substantial bone loss.
While open Latarjet procedure was the consensus for dealing with glenoid bone loss, arthroscopic techniques were strongly favored for humeral head defects. This change in practice patterns results from the introduction of the arthroscopic remplissage technique.20 Two recent systemic reviews have supported this technique, reporting good functional outcomes for engaging Hill-Sachs lesions.21,22 Our study had similar agreement, with most respondents recommending remplissage for these patients.
This study found the lowest rates of expert consensus in the setting of revision surgery, likely caused, in part, by the paucity of available large cohort studies. This is a major void in the literature, and more studies are needed to help guide surgeons on the best techniques to deal with this difficult patient population.
Conservative bracing technique was 1 of the survey questions lacking a consensus response. Interestingly, 39% of members recommended no immobilization after an instability event. This contrasts with recent literature concerning the best position for bracing. We also found twice as many surgeons recommended internal rotation immobilization over external rotation. This is a subject of debate, with some studies stating improvement with external rotation immobilization,23 while other studies reported no difference.24 Overall, recommendations regarding type of immobilization are unclear, which will likely continue until larger studies can be performed.
The literature describing surgical trends in the treatment of shoulder instability is sparse and variable. With regard to other shoulder etiologies, only rotator cuff pathology has used expert consensus. Acevedo and colleagues13 reported agreement of ASES members surveyed regarding rotator cuff management. There was no consensus among surgeons in more than 50% of questions, despite AAOS published guidelines for rotator cuff treatment.25 Despite the lack of guidelines for our topic, we found a consensus among respondents with 68% of survey questions.
To date, only 2 studies of shoulder instability management have elicited the opinion of experts in shoulder surgery. Chahal and associates6 surveyed 42 members of ASES and JOINTS (Joined Orthopaedic Initiatives for National Trials of the Shoulder) Canada on shoulder instability cases and found substantial agreement on diagnosis but little consensus regarding surgical technique. This lack of agreement on procedures differs from our findings and may be related to their complicated case scenarios that generated a wide array of treatment recommendations. Randelli and colleagues5 surveyed more than 1000 European Society of Sports Traumatology, Knee Surgery, and Arthroscopy members and reported similar agreement on arthroscopic Bankart repair in young male shoulder-dislocation patients, although no other instability scenarios were investigated. Our study is the first to report responses from expert shoulder surgeons on surgical-treatment strategies for an array of common shoulder instability pathologies.
This study had several limitations. First, while our study suffered from a low response rate (29.9%), it was similar to other published studies.5,13 Second, because the case series included in the survey attempted to capture the most common instability scenarios, they were limited in their scope and failed to address additional etiologies or pathologic permutations. We believe, however, that a more comprehensive survey would have resulted in respondent fatigue and lowered the response rate. It is unlikely that any survey could capture all variables that come into play during clinical decision-making, and we sought to evaluate the most common shoulder instability scenarios. Third, 30% of respondents were from outside the United States, where the Latarjet procedure is much more popular. While this was not a majority, Latarjet’s regional preference may have decreased the consensus response in some scenarios if only the United States was included. Finally, there is inherent bias in a respondent pool that is heavily weighted to shoulder-surgery experts (ASES members) and does not consider the responses of the general orthopedic surgery community as have other studies.7
Conclusion
This study demonstrates that expert shoulder surgeons often agreed on shoulder-treatment principles for anterior shoulder instability. In the setting of primary repair, arthroscopic Bankart repair was favored in the absence of bony pathology, regardless of age (20 to 35 years) or nature of sport (contact versus noncontact). Latarjet procedures were favored in the setting of glenoid bone loss, and remplissage for an engaging Hill-Sachs lesion. Less agreement was observed for revision stabilization. It should be noted that, while consensus was often reached for our cases, there was a wide distribution of technical considerations and surgical preferences even among those who are fellowship-trained and high-volume surgeons, and who can be considered experts in the field of shoulder surgery.
1. Owens BD, Harrast JJ, Hurwitz SR, Thompson TL, Wolf JM. Surgical trends in bankart repair: an analysis of data from the American Board of Orthopaedic Surgery certification examination. Am J Sports Med. 2011;39(9):1865-1869.
2. Loebenberg MI, Rosen JE, Ishak C, Jazrawi LM, Zuckerman JD. A survey of decision-making processes in the treatment of common shoulder ailments among primary care physicians. Bull Hosp Jt Dis. 2006;63(3-4):137-144.
3. American Academy of Orthopaedic Surgeons. AAOS clinical practice guidelines (CPG). www.aaos.org/research/guidelines/guide.asp. Updated December 30, 2013. Accessed May 1, 2015.
4. Sanders JO, Bozic KJ, Glassman SD, Jevsevar DS, Weber KL. Clinical practice guidelines: their use, misuse, and future directions. J Am Acad Orthop Surg. 2014;22(3):135-144.
5. Randelli P, Arrigoni P, Cabitza F, Ragone V, Cabitza P. Current practice in shoulder pathology: results of a web-based survey among a community of 1,084 orthopedic surgeons. Knee Surg Sports Traumatol Arthrosc. 2011;20(5):803-815.
6. Chahal J, Kassiri K, Dion A, MacDonald P, Leiter J. Diagnostic and treatment differences among experienced shoulder surgeons for instability conditions of the shoulder. Clin J Sport Med. 2007;17(1):5-9.
7. Redfern J, Burks R. 2009 survey results: surgeon practice patterns regarding arthroscopic surgery. Arthroscopy. 2009;25(12):1447-1452.
8. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic bankart repairs: significance of the inverted-pear glenoid and the humeral engaging hill-sachs lesion. Arthroscopy. 2000;16(7):677-694.
9. Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754.
10. Owens MBD, Duffey ML, Nelson BJ, et al. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.
11. Hovelius L, Olofsson A, Sandström B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. A prospective twenty-five-year follow-up. J Bone Joint Surg Am. 2008;90(5):945-952.
12. Raziano DB, Jayadevappa R, Valenzula D, Weiner M, Lavizzo-Mourey R. E-mail versus conventional postal mail survey of geriatric chiefs. Gerontologist. 2001;41(6):799-804.
13. Acevedo DC, Paxton ES, Williams GR, Abboud JA. A survey of expert opinion regarding rotator cuff repair. J Bone Joint Surg Am. 2014;96(14):e123.
14. Kaplan LD, Flanigan DC, Norwig J, Jost P, Bradley J. Prevalence and variance of shoulder injuries in elite collegiate football players. Am J Sports Med. 2005;33(8):1142-1146.
15. Petrera M, Dwyer T, Tsuji MR, Theodoropoulos JS. Outcomes of arthroscopic Bankart repair in collision versus noncollision athletes. Orthopedics. 2013;36(5):e621-e626.
16. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.
17. Zhang AL, Montgomery SR, Ngo SS, Hame SL, Wang JC, Gamradt SC. Arthroscopic versus open shoulder stabilization: current practice patterns in the united states. Arthroscopy. 2014;30(4):436-443.
18. Harris JD, Gupta AK, Mall NA, et al. Long-term outcomes after Bankart shoulder stabilization. Arthroscopy. 2013;29(5):920-933.
19. Boileau P, Villalba M, Héry J, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763.
20. Purchase RJ, Wolf EM, Hobgood ER, Pollock ME, Smalley CC. Hill-sachs ”remplissage”: an arthroscopic solution for the engaging hill-sachs lesion. Arthroscopy. 2008;24(6):723-726.
21. Buza JA 3rd, Iyengar JJ, Anakwenze OA, Ahmad CS, Levine WN. Arthroscopic Hill-Sachs remplissage: a systematic review. J Bone Joint Surg Am. 2014;96(7):549-555.
22. Rashid MS, Crichton J, Butt U, Akimau PI, Charalambous CP. Arthroscopic “Remplissage” for shoulder instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014:1-7.
23. Itoi E, Hatakeyama Y, Kido T, et al. A new method of immobilization after traumatic anterior dislocation of the shoulder: a preliminary study. J Shoulder Elbow Surg. 2003;12(5):413-415.
24. Whelan DB, Litchfield R, Wambolt E, Dainty KN; Joint Orthopaedic Initiative for National Trials of the Shoulder (JOINTS). External rotation immobilization for primary shoulder dislocation: A randomized controlled trial. Clin Orthop Relat Res. 2014;472(8):2380-2386.
25. Pedowitz RA, Yamaguchi K, Ahmad CS, et al. American Academy of Orthopaedic Surgeons Clinical Practice Guideline on: optimizing the management of rotator cuff problems. J Bone Joint Surg Am. 2012;94(2):163-167.
1. Owens BD, Harrast JJ, Hurwitz SR, Thompson TL, Wolf JM. Surgical trends in bankart repair: an analysis of data from the American Board of Orthopaedic Surgery certification examination. Am J Sports Med. 2011;39(9):1865-1869.
2. Loebenberg MI, Rosen JE, Ishak C, Jazrawi LM, Zuckerman JD. A survey of decision-making processes in the treatment of common shoulder ailments among primary care physicians. Bull Hosp Jt Dis. 2006;63(3-4):137-144.
3. American Academy of Orthopaedic Surgeons. AAOS clinical practice guidelines (CPG). www.aaos.org/research/guidelines/guide.asp. Updated December 30, 2013. Accessed May 1, 2015.
4. Sanders JO, Bozic KJ, Glassman SD, Jevsevar DS, Weber KL. Clinical practice guidelines: their use, misuse, and future directions. J Am Acad Orthop Surg. 2014;22(3):135-144.
5. Randelli P, Arrigoni P, Cabitza F, Ragone V, Cabitza P. Current practice in shoulder pathology: results of a web-based survey among a community of 1,084 orthopedic surgeons. Knee Surg Sports Traumatol Arthrosc. 2011;20(5):803-815.
6. Chahal J, Kassiri K, Dion A, MacDonald P, Leiter J. Diagnostic and treatment differences among experienced shoulder surgeons for instability conditions of the shoulder. Clin J Sport Med. 2007;17(1):5-9.
7. Redfern J, Burks R. 2009 survey results: surgeon practice patterns regarding arthroscopic surgery. Arthroscopy. 2009;25(12):1447-1452.
8. Burkhart SS, De Beer JF. Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic bankart repairs: significance of the inverted-pear glenoid and the humeral engaging hill-sachs lesion. Arthroscopy. 2000;16(7):677-694.
9. Owens BD, Agel J, Mountcastle SB, Cameron KL, Nelson BJ. Incidence of glenohumeral instability in collegiate athletics. Am J Sports Med. 2009;37(9):1750-1754.
10. Owens MBD, Duffey ML, Nelson BJ, et al. The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35(7):1168-1173.
11. Hovelius L, Olofsson A, Sandström B, et al. Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. A prospective twenty-five-year follow-up. J Bone Joint Surg Am. 2008;90(5):945-952.
12. Raziano DB, Jayadevappa R, Valenzula D, Weiner M, Lavizzo-Mourey R. E-mail versus conventional postal mail survey of geriatric chiefs. Gerontologist. 2001;41(6):799-804.
13. Acevedo DC, Paxton ES, Williams GR, Abboud JA. A survey of expert opinion regarding rotator cuff repair. J Bone Joint Surg Am. 2014;96(14):e123.
14. Kaplan LD, Flanigan DC, Norwig J, Jost P, Bradley J. Prevalence and variance of shoulder injuries in elite collegiate football players. Am J Sports Med. 2005;33(8):1142-1146.
15. Petrera M, Dwyer T, Tsuji MR, Theodoropoulos JS. Outcomes of arthroscopic Bankart repair in collision versus noncollision athletes. Orthopedics. 2013;36(5):e621-e626.
16. Harris JD, Romeo AA. Arthroscopic management of the contact athlete with instability. Clin Sports Med. 2013;32(4):709-730.
17. Zhang AL, Montgomery SR, Ngo SS, Hame SL, Wang JC, Gamradt SC. Arthroscopic versus open shoulder stabilization: current practice patterns in the united states. Arthroscopy. 2014;30(4):436-443.
18. Harris JD, Gupta AK, Mall NA, et al. Long-term outcomes after Bankart shoulder stabilization. Arthroscopy. 2013;29(5):920-933.
19. Boileau P, Villalba M, Héry J, Balg F, Ahrens P, Neyton L. Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am. 2006;88(8):1755-1763.
20. Purchase RJ, Wolf EM, Hobgood ER, Pollock ME, Smalley CC. Hill-sachs ”remplissage”: an arthroscopic solution for the engaging hill-sachs lesion. Arthroscopy. 2008;24(6):723-726.
21. Buza JA 3rd, Iyengar JJ, Anakwenze OA, Ahmad CS, Levine WN. Arthroscopic Hill-Sachs remplissage: a systematic review. J Bone Joint Surg Am. 2014;96(7):549-555.
22. Rashid MS, Crichton J, Butt U, Akimau PI, Charalambous CP. Arthroscopic “Remplissage” for shoulder instability: a systematic review. Knee Surg Sports Traumatol Arthrosc. 2014:1-7.
23. Itoi E, Hatakeyama Y, Kido T, et al. A new method of immobilization after traumatic anterior dislocation of the shoulder: a preliminary study. J Shoulder Elbow Surg. 2003;12(5):413-415.
24. Whelan DB, Litchfield R, Wambolt E, Dainty KN; Joint Orthopaedic Initiative for National Trials of the Shoulder (JOINTS). External rotation immobilization for primary shoulder dislocation: A randomized controlled trial. Clin Orthop Relat Res. 2014;472(8):2380-2386.
25. Pedowitz RA, Yamaguchi K, Ahmad CS, et al. American Academy of Orthopaedic Surgeons Clinical Practice Guideline on: optimizing the management of rotator cuff problems. J Bone Joint Surg Am. 2012;94(2):163-167.
In Vivo Measurement of Rotator Cuff Tear Tension: Medial Versus Lateral Footprint Position
Although recent clinical results of arthroscopic rotator cuff repair (RCR) have been encouraging, achieving anatomical healing of full-thickness rotator cuff tears remains a challenge.1-4 Several factors influence rotator cuff healing after repair.1,3-8 Patient-related factors include advanced patient age, tear size, tear chronicity, and amount of fatty infiltration.1,3,5,6,8-10 Tension applied to the repair construct is a significant factor as well.11,12
In the literature, limited consideration has been given to repair tension.13 The majority of studies have focused on other factors, mainly repair technique. Some surgeons advocate use of a double-row repair construct in which the rotator cuff tendon is pulled to the lateral margin of the footprint.14-19 Double-row techniques, which include the transosseous-equivalent (TOE) construct, are biomechanically superior to other repairs.20-26 Another purported benefit of double-row repair is more complete restoration and pressurization of the rotator cuff footprint.21,24,27,28
Rotator cuff tears typically occur near the dysvascular region of the diseased musculotendinous unit, often leaving a stump of tissue attached to the tuberosity and ultimately a shortened tendon.29 In addition, full-thickness tears often retract over time. Meyer and colleagues29 recently demonstrated that this shortening is irreversible. Snyder30 and Sostak and colleagues31 suggested that pulling a shortened, degenerative rotator cuff tendon to the lateral margin of the footprint results in increased tissue tension compared with that produced with a more medially based repair just off the articular margin. In our opinion, the possible increase in tension during a laterally based repair, whether single- or double-row, may place excessive strain on the diseased tissue as well as the surgical construct, potentially contributing to repair failure.
We conducted a study to evaluate the difference, if any, in tension applied to the rotator cuff tendon positioned at the medial versus lateral margin of the footprint during arthroscopic RCR. We hypothesized significantly more tension would be placed on the rotator cuff tendon when positioned at the lateral versus medial footprint.
Methods
After obtaining Institutional Review Board approval for this study, we collected data on a consecutive series of patients who underwent arthroscopic RCR performed by Dr. Getelman at a single institution. Only patients with primary full-thickness tears of the supraspinatus and/or infraspinatus were included. Exclusion criteria included revision rotator cuff surgeries, partial-thickness tears, concurrent subscapularis tears requiring anchor fixation, and any tears that could not be mobilized to the lateral footprint without interval slides or margin convergence. The 20 identified patients constituted the study group.
Demographic factors, including age and preoperative length of symptoms, were recorded after chart review. Magnetic resonance imaging (MRI) was performed for all patients before surgery and was retrospectively reviewed. Dr. Getelman assigned each patient a modified Goutallier score, based on MRI, to assess for fatty infiltration/atrophy.32 Each patient was placed in the lateral decubitus position with the operative arm in balanced suspension at 70° of abduction. Standard glenohumeral and subacromial diagnostic arthroscopy was performed. The rotator cuff tear was gently debrided back to a healthy-appearing margin in preparation for repair. The tear was then measured in the anterior-posterior (A-P) and medial-lateral (M-L) planes using a premeasured, marked suture, as previously described.33 Complete bursal and articular-sided releases were performed to allow for appropriate mobilization of the tendon. The tear was classified as crescent-shaped, U-shaped, or L-shaped.
Viewing from the posterior portal, the surgeon inserted a tissue grasper through the lateral portal. The tendon was grasped at multiple points along its edge, anterior to posterior, and was translated laterally to assess its reducibility; the apex of the tear correlated with the point of maximal excursion and coverage of the footprint. Once confirmed, the rotator cuff tear apex was clamped with a tissue grasper. After placement in a sterile arthroscopic camera sleeve (DeRoyal camera drape with perforated tip), a calibrated digital weigh scale (American Weigh Scales model H22 portable electronic hanging scale, with accuracy of 0.01 lb) was attached to the tissue grasper with an S-hook (Figure 1). The tendon edge was first translated about 3 mm lateral to the articular margin (the medial footprint position), and tension was recorded (Figures 2A, 2B). After a 1-minute relaxation period, the tendon edge was translated to the lateral edge of the rotator cuff footprint (the lateral footprint position), and tension was recorded again (Figures 2C, 2D). A medially based single-row RCR with triple-loaded sutures and bone marrow vents placed in the lateral tuberosity was then completed, regardless of tension, tear size, or tear morphology.31 Typically, 1 anchor was used for every 10 to 15 mm of A-P tear length.
SAS software was used for statistical analysis, the Wilcoxon signed rank test for continuous or ordinal data comparisons between paired groups, and the Mann-Whitney test for continuous or ordinal data comparisons between independent, unmatched groups. One-way analysis of variance (ANOVA) was used to compare means among the 3 groups of morphology subtypes. Linear regression was performed to assess the simultaneous relationship between potential predictors (age, sex, length of symptoms, Goutallier score, tear size) and medial or lateral tension, where medial tension was included as an additional potential predictor for lateral tension. Restricted cubic splines were fit to assess linearity. Predictors were retained in multivariate regression using backward variable retention. Because of inadequate sample size, additivity was assumed except for sex. Statistical significance was set at P < .05.
Results
Of the 20 rotator cuff tears evaluated (Table 1), 13 were crescent-shaped, 5 were U-shaped, and 2 were L-shaped. Mean (SD) A-P tear size was 17.7 (5.8) mm, and mean (SD) M-L tear size was 19.1 (8.6) mm. Mean age of the 20 patients (15 men, 5 women) was 57.9 years (range, 44-72 years). Mean (SD) length of symptoms was 12.9 (12.4) months (range, 3-48 months). Mean (SD) modified Goutallier score was 1.4 (0.7; range, 0-3).
Mean (SD) rotator cuff tension for all tears approximated to the medial footprint was 0.41 (0.33) pound, and mean (SD) cuff tension for all tears approximated to the lateral footprint was 2.21 (1.20) pounds—representing a 5.4-fold difference (P < .0001).
No statistically significant differences were detected in the ANOVA comparing tensions at medial and lateral positions among tear morphologic subtypes (all Ps >.05).
Subgroup analysis (Table 2) was performed for smaller (≤20 mm A-P) and larger (>20 mm A-P) tears. For smaller tears, mean (SD) tension was 0.27 (0.24) pound applied with the cuff tendon pulled to the medial footprint and 2.06 (1.06) pounds applied with the tendon pulled to the lateral footprint—a 7.6-fold difference (P < .0018). For larger tears, mean (SD) tension was 0.58 (0.37) pound applied with the tendon pulled to the medial footprint and 2.38 (1.4) pounds applied with the tendon pulled to the lateral footprint—a 4.1-fold difference (P < .005).
A statistically significant difference in tensions was found between small and large cuff tears positioned at the medial footprint (0.27 vs 0.58 lb; P = .0367); no difference was found between groups with the tendon at the lateral footprint (2.06 vs 2.38 lb; P = .284).
Univariate and multivariate analyses were performed using linear regression analysis (Table 3). During univariate analysis for medial footprint position, A-P tear size and Goutallier score both positively correlated with increasing tension; for lateral footprint position, no factors statistically correlated with lateral tension, though there was a positive trend for medial tension and female sex. During multivariate analysis for medial footprint position, only A-P tear size positively correlated with increasing tension; for lateral footprint position, both age (in nonlinear fashion as function of age + age2) and medial tension positively correlated with increasing tension.
Discussion
Our results indicated that significantly more tension is placed on the torn rotator cuff tendon when it is reduced across the footprint from a medial to a more lateral position in vivo. More tension was required for all tears to be reduced to the lateral footprint compared with the medial footprint. As expected, compared with smaller tears, larger tears required significantly more tension in order to be reduced to the medial footprint. Interestingly, no statistical difference was found between tensions required to reduce either small or large tears to the lateral footprint, which suggests that, regardless of tear size, more force must be applied to reduce the torn tendon to the lateral footprint compared with the medial footprint.
Hersche and Gerber34 were the first to report rotator cuff tension measurements in vivo. Although their study did not specifically compare cuff tensions reducing the tear to the medial versus lateral footprint, it did examine tension at displacement of 10 and 20 mm. Tension increased from 27 N to 60 N, correlating with a 2.2-fold difference between the 2 distances. Domb and colleagues35 also compared in vivo rotator cuff tension differences between the medial footprint and the lateral footprint in 4 patients. Mean tension applied to the cuff during reduction to the articular margin was 27 N, or 6 pounds. Mean tension needed to reduce the cuff to the lateral tuberosity was 76 N, or 17 pounds, for a 2.8-fold difference. Tears were not measured but were described as massive and retracted.
Although repair tension has long been recognized as a crucial factor in RCR healing, little clinical research has focused on the effects of excess tension. Davidson and Rivenburgh11 prospectively followed the clinical outcomes of 67 consecutive cuff repairs after intraoperative tension measurement and found that high-tension repairs (>8 lb) had significantly lower clinical outcome measures. However, the authors did not report on correlations with radiologic healing and stated, “Functional outcome is inversely proportional to rotator cuff repair tension.” Further study of the in vivo effects of increased tension on clinical and radiologic outcomes is needed.
Several animal studies have been conducted on the effects of tension on RCRs. Gerber and colleagues36 reported that the force needed to produce 1 cm of sheep supraspinatus tendon excursion increased 7-fold, from 6.8 N to 47.8 N, after 40 weeks of tendon tear. Coleman and colleagues37 compared the modulus of elasticity in sheep supraspinatus tendon after 6 weeks and 18 weeks of detachment and reported increases of 60% and 70%, respectively. Gimbel and colleagues38 showed that, in a rat model, “repair tension rapidly increased initially after injury followed by a progressive, but less dramatic, increase with additional time.” Of note, we did not identify any correlation between chronicity of symptoms and the tension needed to reduce the tendon medially or to a more lateral position on the footprint.
In acute tears, the cuff tissue is more compliant and mobile and can be pulled laterally across its anatomical footprint with minimal tension.39 In contrast, cuff tissue in the more commonly encountered chronic tear is less compliant and is not mobile enough to be pulled to the lateral margin of the footprint without added stress.30,34,35 In large, acute tears in which there are minimal tissue degeneration and retraction, a laterally based footprint-restoring technique may be performed with minimal tension. This technique may have advantages over a medially based repair. In the literature, more attention needs to be directed toward the biomechanics and biology of chronic rotator cuff tears, as these are more commonly encountered.
Almost all of the prospective studies that have compared single- and double-row RCR have found no significant differences in MRI healing rates or clinical results at follow-up up to 2 years.14,16,40-45 Detailed analysis of the surgical techniques used in all these studies revealed that the rotator cuff tendons were repaired back to the lateral footprint in both the single- and double-row constructs.14,16,40-45 Although no clinical studies have compared medially and laterally based single-row repairs, our data suggest that medially based repairs have lower tensions and therefore should not be considered equivalent. Sostak and colleagues31 and Murray and colleagues46 have shown that a medially based single-row RCR can achieve excellent clinical and anatomical results, likely partly because of the lower tension applied to the torn cuff tissue.31,46 Studies are needed to compare medially and laterally based repairs, including single- and double-row repairs.
The vast majority of recent research has aimed to counteract construct tension with stronger biomechanical constructs.20-26 Surgeons have also aimed to improve biological healing by pulling the tendon laterally across the footprint to achieve complete footprint coverage, ultimately increasing the surface area for tendon–bone healing. This has led to the development of various double-row repair techniques, in which the cuff tendon is pulled to the lateral margin of its footprint. One row of anchors is placed in the medial aspect of the footprint, while a second is placed in the lateral aspect; the cuff is reduced and compressed to the tuberosity with various suture configurations. The TOE technique was developed to improve pressurization of the cuff tendon across the footprint by linking the 2 rows with bridging sutures. In doing so, however, the potentially deleterious effects of increased tension introduced by pulling the tendon laterally may have been overlooked. Nevertheless, the biomechanics and stress distribution likely differ between single-row repair and TOE repairs, and direct comparisons cannot be made at this time. The medial row of a double-row or TOE construct may stress-shield or “unload” the more lateral tissue. Studies are needed in order to better understand the tension differential and stress distribution of various double-row constructs.
Recognizing tear morphology is crucial in maximizing chances of healing after cuff repair. For example, a crescent-shaped tear is reduced to the tuberosity with direct lateral translation of the apex of the tear, which is also the deepest or most displaced part of the tear. On the other hand, reducing an L- or reverse L-shaped tear to the tuberosity is not as direct; reducing the deepest or most displaced part of the tear would lead to overreduction and overtensioning of the tendon. However, often the exact “elbow” of the tear is not obvious and appears more rounded; therefore, it is crucial for the surgeon to examine the mobility of the torn tendon along its entire length to minimize tension. Study is needed to assess tension along the entire length of the tear for different tear morphologies and sizes.
Although our results showed that increased tension was needed to reduce a torn tendon to its lateral footprint, no study has indicated exactly how much is “too much” tension. As stated earlier, use of stronger biomechanical constructs, including TOE constructs, may overcome the increased tension associated with laterally based repairs. In addition, laterally based repairs, either single- or double-row, may be best suited for tears with lower tension, whereas medially based repairs may be best suited for higher tension tears. It is also possible that the difference in tensions noted in this study is not significant enough to have a clinical impact on choice of construct or on anatomical healing. We need studies that correlate anatomical healing rates with repair tension in order to better guide surgeons on when to use a medially or laterally based repair.
Other possible effects of increased tension associated with laterally based repairs, including beneficial effects, must be considered as well. Viscoelastic properties of human rotator cuff tendon may dissipate increased tension over time through a variety of mechanisms. Stress relaxation, gap formation, creep, and the hysteresis effect, all associated with cyclical loading in the early healing period, may lead to dissipation of force over time.47,48 These more complex biomechanical properties of RCR constructs are yet to be clearly defined.
This study had several weaknesses. Its data represent a static measurement of time-zero rotator cuff tension, which greatly simplifies the biomechanics of the torn rotator cuff and repair construct as well as changes that occur with healing. During cuff repair, forces typically are distributed through several fixation points in stepwise process and are not focused on a single point of tissue with a grasper. Therefore, the findings of this study may not directly correlate with medially versus laterally based repairs in vivo. Furthermore, as this is a time-zero measurement, we could not determine whether the tension differential between the 2 repair positions remained static over time. Current literature suggests that muscle atrophy, fatty infiltration, and loss of elasticity of the musculotendinous unit are relatively irreversible.35,37,49 In addition, determining the precise apex of a cuff tear can be difficult, so error may have been introduced during this process. Last, although placement of the cuff tissue at the medial or lateral footprint position was based on visual estimation by an experienced and skilled arthroscopist, error may have been introduced based on this imprecise technique.
Conclusion
This study demonstrated a significant, 5.4-fold increase in in vivo time-zero rotator cuff tension with the tendon edge reduced to the lateral footprint rather than the medial footprint.
1. Boileau P, Brassart N, Watkinson DJ, Carles M, Hatzidakis AM, Krishnan SG. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? J Bone Joint Surg Am. 2005;87(6):1229-1240.
2. Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86(2):219-224.
3. Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW, MacGillivray JD. Prospective analysis of arthroscopic rotator cuff repair: prognostic factors affecting clinical and ultrasound outcome. J Shoulder Elbow Surg. 2009;18(1):13-20.
4. Huijsmans PE, Pritchard MP, Berghs BM, van Rooyen KS, Wallace AL, de Beer JF. Arthroscopic rotator cuff repair with double-row fixation. J Bone Joint Surg Am. 2007;89(6):1248-1257.
5. Gulotta LV, Nho SJ, Dodson CC, Adler RS, Altchek DW, MacGillivray JD; HSS Arthroscopic Rotator Cuff Registry. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part II—prognostic factors for clinical and radiographic outcomes. J Shoulder Elbow Surg. 2011;20(6):941-946.
6. Cho NS, Rhee YG. The factors affecting the clinical outcome and integrity of arthroscopically repaired rotator cuff tears of the shoulder. Clin Orthop Surg. 2009;1(2):96-104.
7. Gladstone JN, Bishop JY, Lo IK, Flatow EL. Fatty infiltration and atrophy of the rotator cuff do not improve after rotator cuff repair and correlate with poor functional outcome. Am J Sports Med. 2007;35(5):719-728.
8. Oh JH, Kim SH, Ji HM, Jo KH, Bin SW, Gong HS. Prognostic factors affecting anatomic outcome of rotator cuff repair and correlation with functional outcome. Arthroscopy. 2009;25(1):30-39.
9. Tashjian RZ, Hollins AM, Kim HM, et al. Factors affecting healing rates after arthroscopic double-row rotator cuff repair. Am J Sports Med. 2010;38(12):2435-2442.
10. Burkhart SS, Lo IK. Arthroscopic rotator cuff repair. J Am Acad Orthop Surg. 2006;14(6):333-346.
11. Davidson PA, Rivenburgh DW. Rotator cuff repair tension as a determinant of functional outcome. J Shoulder Elbow Surg. 2000;9(6):502-506.
12. Goutallier D, Postel JM, Van Driessche S, Godefroy D, Radier C. Tension-free cuff repairs with excision of macroscopic tendon lesions and muscular advancement: results in a prospective series with limited fatty muscular degeneration. J Shoulder Elbow Surg. 2006;15(2):164-172.
13. Gimbel JA, Van Kleunen JP, Lake SP, Williams GR, Soslowsky LJ. The role of repair tension on tendon to bone healing in an animal model of chronic rotator cuff tears. J Biomech. 2007;40(3):561-568.
14. Ma HL, Chiang ER, Wu HT, et al. Clinical outcome and imaging of arthroscopic single-row and double-row rotator cuff repair: a prospective randomized trial. Arthroscopy. 2012;28(1):16-24.
15. Mihata T, Watanabe C, Fukunishi K, et al. Functional and structural outcomes of single-row versus double-row versus combined double-row and suture-bridge repair for rotator cuff tears. Am J Sports Med. 2011;39(10):2091-2098.
16. Koh KH, Kang KC, Lim TK, Shon MS, Yoo JC. Prospective randomized clinical trial of single- versus double-row suture anchor repair in 2- to 4-cm rotator cuff tears: clinical and magnetic resonance imaging results. Arthroscopy. 2011;27(4):453-462.
17. Voigt C, Bosse C, Vosshenrich R, Schulz AP, Lill H. Arthroscopic supraspinatus tendon repair with suture-bridging technique: functional outcome and magnetic resonance imaging. Am J Sports Med. 2010;38(5):983-991.
18. Lafosse L, Brzoska R, Toussaint B, Gobezie R. The outcome and structural integrity of arthroscopic rotator cuff repair with use of the double-row suture anchor technique. Surgical technique. J Bone Joint Surg Am. 2008;90(suppl 2 pt 2):275-286.
19. Park JY, Lhee SH, Choi JH, Park HK, Yu JW, Seo JB. Comparison of the clinical outcomes of single- and double-row repairs in rotator cuff tears. Am J Sports Med. 2008;36(7):1310-1316.
20. Kim DH, ElAttrache NS, Tibone JE, et al. Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med. 2006;34(3):407-414.
21. Mazzocca AD, Bollier MJ, Ciminiello AM, et al. Biomechanical evaluation of arthroscopic rotator cuff repairs over time. Arthroscopy. 2010;26(5):592-599.
22. Grimberg J, Diop A, Kalra K, Charousset C, Duranthon LD, Maurel N. In vitro biomechanical comparison of three different types of single- and double-row arthroscopic rotator cuff repairs: analysis of continuous bone–tendon contact pressure and surface during different simulated joint positions. J Shoulder Elbow Surg. 2010;19(2):236-243.
23. Nelson CO, Sileo MJ, Grossman MG, Serra-Hsu F. Single-row modified Mason-Allen versus double-row arthroscopic rotator cuff repair: a biomechanical and surface area comparison. Arthroscopy. 2008;24(8):941-948.
24. Park MC, ElAttrache NS, Tibone JE, Ahmad CS, Jun BJ, Lee TQ. Part I: footprint contact characteristics for a transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16(4):461-468.
25. Park MC, Tibone JE, ElAttrache NS, Ahmad CS, Jun BJ, Lee TQ. Part II: biomechanical assessment for a footprint-restoring transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16(4):469-476.
26. Ma CB, Comerford L, Wilson J, Puttlitz CM. Biomechanical evaluation of arthroscopic rotator cuff repairs: double-row compared with single-row fixation. J Bone Joint Surg Am. 2006;88(2):403-410.
27. Lo IK, Burkhart SS. Double-row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy. 2003;19(9):1035-1042.
28. Tuoheti Y, Itoi E, Yamamoto N, et al. Contact area, contact pressure, and pressure patterns of the tendon–bone interface after rotator cuff repair. Am J Sports Med. 2005;33(12):1869-1874.
29. Meyer DC, Farshad M, Amacker NA, Gerber C, Wieser K. Quantitative analysis of muscle and tendon retraction in chronic rotator cuff tears. Am J Sports Med. 2012;40(3):606-610.
30. Snyder SJ. Single vs. double row suture anchor fixation rotator cuff repair. Paper presented at: American Academy of Orthopedic Surgeons Annual Meeting; March 8, 2007; San Francisco, CA.
31. Sostak JP, Bahk MS, Getelman MH, Wong IH, Snyder SJ, Burns JP. Arthroscopic single row rotator cuff repair using the “SCOI row”: structural and clinical outcomes. Paper presented at: American Academy of Orthopedic Surgeons Annual Meeting; February 7-11, 2012; San Francisco, CA.
32. Fuchs B, Weishaupt D, Zanetti M, Hodler J, Gerber C. Fatty degeneration of the muscles of the rotator cuff: assessment by computed tomography versus magnetic resonance imaging. J Shoulder Elbow Surg. 1999;8(6):599-605.
33. Bond JL, Dopirak RM, Higgins J, Burns J, Snyder SJ. Arthroscopic replacement of massive, irreparable rotator cuff tears using a GraftJacket allograft: technique and preliminary results. Arthroscopy. 2008;24(4):403-409.
34. Hersche O, Gerber C. Passive tension in the supraspinatus musculotendinous unit after long-standing rupture of its tendon: a preliminary report. J Shoulder Elbow Surg. 1998;7(4):393-396.
35. Domb BG, Glousman RE, Brooks A, Hansen M, Lee TQ, ElAttrache NS. High-tension double-row footprint repair compared with reduced-tension single-row repair for massive rotator cuff tears. J Bone Joint Surg Am. 2008;90(suppl 4):35-39.
36. Gerber C, Meyer DC, Schneeberger AG, Hoppeler H, von Rechenberg B. Effect of tendon release and delayed repair on the structure of the muscles of the rotator cuff: an experimental study in sheep. J Bone Joint Surg Am. 2004;86(9):1973-1982.
37. Coleman SH, Fealy S, Ehteshami JR, et al. Chronic rotator cuff injury and repair model in sheep. J Bone Joint Surg Am. 2003;85(12):2391-2402.
38. Gimbel JA, Mehta S, Van Kleunen JP, Williams GR, Soslowsky LJ. The tension required at repair to reappose the supraspinatus tendon to bone rapidly increases after injury. Clin Orthop Relat Res. 2004;(426):258-265.
39. Mannava S, Plate JF, Whitlock PW, et al. Evaluation of in vivo rotator cuff muscle function after acute and chronic detachment of the supraspinatus tendon: an experimental study in an animal model. J Bone Joint Surg Am. 2011;93(18):1702-1711.
40. Burks RT, Crim J, Brown N, Fink B, Greis PE. A prospective randomized clinical trial comparing arthroscopic single- and double-row rotator cuff repair: magnetic resonance imaging and early clinical evaluation. Am J Sports Med. 2009;37(4):674-682.
41. Grasso A, Milano G, Salvatore M, Falcone G, Deriu L, Fabbriciani C. Single-row versus double-row arthroscopic rotator cuff repair: a prospective randomized clinical study. Arthroscopy. 2009;25(1):4-12.
42. Franceschi F, Ruzzini L, Longo UG, et al. Equivalent clinical results of arthroscopic single-row and double-row suture anchor repair for rotator cuff tears: a randomized controlled trial. Am J Sports Med. 2007;35(8):1254-1260.
43. Carbonel I, Martinez AA, Calvo A, Ripalda J, Herrera A. Single-row versus double-row arthroscopic repair in the treatment of rotator cuff tears: a prospective randomized clinical study. Int Orthop. 2012;36(9):1877-1883.
44. Lapner PL, Sabri E, Rakhra K, et al. A multicenter randomized controlled trial comparing single-row with double-row fixation in arthroscopic rotator cuff repair. J Bone Joint Surg Am. 2012;94(14):1249-1257.
45. Gartsman GM, Drake G, Edwards TB, et al. Ultrasound evaluation of arthroscopic full-thickness supraspinatus rotator cuff repair: single-row versus double-row suture bridge (transosseous equivalent) fixation. Results of a prospective, randomized study. J Shoulder Elbow Surg. 2013;22(11):1480-1487.
46. Murray TF Jr, Lajtai G, Mileski RM, Snyder SJ. Arthroscopic repair of medium to large full-thickness rotator cuff tears: outcome at 2- to 6-year follow-up. J Shoulder Elbow Surg. 2002;11(1):19-24.
47. Szczesny SE, Peloquin JM, Cortes DH, Kadlowec JA, Soslowsky LJ, Elliott DM. Biaxial tensile testing and constitutive modeling of human supraspinatus tendon. J Biomech Eng. 2012;134(2):021004.
48. Chaudhury S, Holland C, Vollrath F, Carr AJ. Comparing normal and torn rotator cuff tendons using dynamic shear analysis. J Bone Joint Surg Br. 2011;93(7):942-948.
49. Meyer DC, Hoppeler H, von Rechenberg B, Gerber C. A pathomechanical concept explains muscle loss and fatty muscular changes following surgical tendon release. J Orthop Res. 2004;22(5):1004-1007.
Although recent clinical results of arthroscopic rotator cuff repair (RCR) have been encouraging, achieving anatomical healing of full-thickness rotator cuff tears remains a challenge.1-4 Several factors influence rotator cuff healing after repair.1,3-8 Patient-related factors include advanced patient age, tear size, tear chronicity, and amount of fatty infiltration.1,3,5,6,8-10 Tension applied to the repair construct is a significant factor as well.11,12
In the literature, limited consideration has been given to repair tension.13 The majority of studies have focused on other factors, mainly repair technique. Some surgeons advocate use of a double-row repair construct in which the rotator cuff tendon is pulled to the lateral margin of the footprint.14-19 Double-row techniques, which include the transosseous-equivalent (TOE) construct, are biomechanically superior to other repairs.20-26 Another purported benefit of double-row repair is more complete restoration and pressurization of the rotator cuff footprint.21,24,27,28
Rotator cuff tears typically occur near the dysvascular region of the diseased musculotendinous unit, often leaving a stump of tissue attached to the tuberosity and ultimately a shortened tendon.29 In addition, full-thickness tears often retract over time. Meyer and colleagues29 recently demonstrated that this shortening is irreversible. Snyder30 and Sostak and colleagues31 suggested that pulling a shortened, degenerative rotator cuff tendon to the lateral margin of the footprint results in increased tissue tension compared with that produced with a more medially based repair just off the articular margin. In our opinion, the possible increase in tension during a laterally based repair, whether single- or double-row, may place excessive strain on the diseased tissue as well as the surgical construct, potentially contributing to repair failure.
We conducted a study to evaluate the difference, if any, in tension applied to the rotator cuff tendon positioned at the medial versus lateral margin of the footprint during arthroscopic RCR. We hypothesized significantly more tension would be placed on the rotator cuff tendon when positioned at the lateral versus medial footprint.
Methods
After obtaining Institutional Review Board approval for this study, we collected data on a consecutive series of patients who underwent arthroscopic RCR performed by Dr. Getelman at a single institution. Only patients with primary full-thickness tears of the supraspinatus and/or infraspinatus were included. Exclusion criteria included revision rotator cuff surgeries, partial-thickness tears, concurrent subscapularis tears requiring anchor fixation, and any tears that could not be mobilized to the lateral footprint without interval slides or margin convergence. The 20 identified patients constituted the study group.
Demographic factors, including age and preoperative length of symptoms, were recorded after chart review. Magnetic resonance imaging (MRI) was performed for all patients before surgery and was retrospectively reviewed. Dr. Getelman assigned each patient a modified Goutallier score, based on MRI, to assess for fatty infiltration/atrophy.32 Each patient was placed in the lateral decubitus position with the operative arm in balanced suspension at 70° of abduction. Standard glenohumeral and subacromial diagnostic arthroscopy was performed. The rotator cuff tear was gently debrided back to a healthy-appearing margin in preparation for repair. The tear was then measured in the anterior-posterior (A-P) and medial-lateral (M-L) planes using a premeasured, marked suture, as previously described.33 Complete bursal and articular-sided releases were performed to allow for appropriate mobilization of the tendon. The tear was classified as crescent-shaped, U-shaped, or L-shaped.
Viewing from the posterior portal, the surgeon inserted a tissue grasper through the lateral portal. The tendon was grasped at multiple points along its edge, anterior to posterior, and was translated laterally to assess its reducibility; the apex of the tear correlated with the point of maximal excursion and coverage of the footprint. Once confirmed, the rotator cuff tear apex was clamped with a tissue grasper. After placement in a sterile arthroscopic camera sleeve (DeRoyal camera drape with perforated tip), a calibrated digital weigh scale (American Weigh Scales model H22 portable electronic hanging scale, with accuracy of 0.01 lb) was attached to the tissue grasper with an S-hook (Figure 1). The tendon edge was first translated about 3 mm lateral to the articular margin (the medial footprint position), and tension was recorded (Figures 2A, 2B). After a 1-minute relaxation period, the tendon edge was translated to the lateral edge of the rotator cuff footprint (the lateral footprint position), and tension was recorded again (Figures 2C, 2D). A medially based single-row RCR with triple-loaded sutures and bone marrow vents placed in the lateral tuberosity was then completed, regardless of tension, tear size, or tear morphology.31 Typically, 1 anchor was used for every 10 to 15 mm of A-P tear length.
SAS software was used for statistical analysis, the Wilcoxon signed rank test for continuous or ordinal data comparisons between paired groups, and the Mann-Whitney test for continuous or ordinal data comparisons between independent, unmatched groups. One-way analysis of variance (ANOVA) was used to compare means among the 3 groups of morphology subtypes. Linear regression was performed to assess the simultaneous relationship between potential predictors (age, sex, length of symptoms, Goutallier score, tear size) and medial or lateral tension, where medial tension was included as an additional potential predictor for lateral tension. Restricted cubic splines were fit to assess linearity. Predictors were retained in multivariate regression using backward variable retention. Because of inadequate sample size, additivity was assumed except for sex. Statistical significance was set at P < .05.
Results
Of the 20 rotator cuff tears evaluated (Table 1), 13 were crescent-shaped, 5 were U-shaped, and 2 were L-shaped. Mean (SD) A-P tear size was 17.7 (5.8) mm, and mean (SD) M-L tear size was 19.1 (8.6) mm. Mean age of the 20 patients (15 men, 5 women) was 57.9 years (range, 44-72 years). Mean (SD) length of symptoms was 12.9 (12.4) months (range, 3-48 months). Mean (SD) modified Goutallier score was 1.4 (0.7; range, 0-3).
Mean (SD) rotator cuff tension for all tears approximated to the medial footprint was 0.41 (0.33) pound, and mean (SD) cuff tension for all tears approximated to the lateral footprint was 2.21 (1.20) pounds—representing a 5.4-fold difference (P < .0001).
No statistically significant differences were detected in the ANOVA comparing tensions at medial and lateral positions among tear morphologic subtypes (all Ps >.05).
Subgroup analysis (Table 2) was performed for smaller (≤20 mm A-P) and larger (>20 mm A-P) tears. For smaller tears, mean (SD) tension was 0.27 (0.24) pound applied with the cuff tendon pulled to the medial footprint and 2.06 (1.06) pounds applied with the tendon pulled to the lateral footprint—a 7.6-fold difference (P < .0018). For larger tears, mean (SD) tension was 0.58 (0.37) pound applied with the tendon pulled to the medial footprint and 2.38 (1.4) pounds applied with the tendon pulled to the lateral footprint—a 4.1-fold difference (P < .005).
A statistically significant difference in tensions was found between small and large cuff tears positioned at the medial footprint (0.27 vs 0.58 lb; P = .0367); no difference was found between groups with the tendon at the lateral footprint (2.06 vs 2.38 lb; P = .284).
Univariate and multivariate analyses were performed using linear regression analysis (Table 3). During univariate analysis for medial footprint position, A-P tear size and Goutallier score both positively correlated with increasing tension; for lateral footprint position, no factors statistically correlated with lateral tension, though there was a positive trend for medial tension and female sex. During multivariate analysis for medial footprint position, only A-P tear size positively correlated with increasing tension; for lateral footprint position, both age (in nonlinear fashion as function of age + age2) and medial tension positively correlated with increasing tension.
Discussion
Our results indicated that significantly more tension is placed on the torn rotator cuff tendon when it is reduced across the footprint from a medial to a more lateral position in vivo. More tension was required for all tears to be reduced to the lateral footprint compared with the medial footprint. As expected, compared with smaller tears, larger tears required significantly more tension in order to be reduced to the medial footprint. Interestingly, no statistical difference was found between tensions required to reduce either small or large tears to the lateral footprint, which suggests that, regardless of tear size, more force must be applied to reduce the torn tendon to the lateral footprint compared with the medial footprint.
Hersche and Gerber34 were the first to report rotator cuff tension measurements in vivo. Although their study did not specifically compare cuff tensions reducing the tear to the medial versus lateral footprint, it did examine tension at displacement of 10 and 20 mm. Tension increased from 27 N to 60 N, correlating with a 2.2-fold difference between the 2 distances. Domb and colleagues35 also compared in vivo rotator cuff tension differences between the medial footprint and the lateral footprint in 4 patients. Mean tension applied to the cuff during reduction to the articular margin was 27 N, or 6 pounds. Mean tension needed to reduce the cuff to the lateral tuberosity was 76 N, or 17 pounds, for a 2.8-fold difference. Tears were not measured but were described as massive and retracted.
Although repair tension has long been recognized as a crucial factor in RCR healing, little clinical research has focused on the effects of excess tension. Davidson and Rivenburgh11 prospectively followed the clinical outcomes of 67 consecutive cuff repairs after intraoperative tension measurement and found that high-tension repairs (>8 lb) had significantly lower clinical outcome measures. However, the authors did not report on correlations with radiologic healing and stated, “Functional outcome is inversely proportional to rotator cuff repair tension.” Further study of the in vivo effects of increased tension on clinical and radiologic outcomes is needed.
Several animal studies have been conducted on the effects of tension on RCRs. Gerber and colleagues36 reported that the force needed to produce 1 cm of sheep supraspinatus tendon excursion increased 7-fold, from 6.8 N to 47.8 N, after 40 weeks of tendon tear. Coleman and colleagues37 compared the modulus of elasticity in sheep supraspinatus tendon after 6 weeks and 18 weeks of detachment and reported increases of 60% and 70%, respectively. Gimbel and colleagues38 showed that, in a rat model, “repair tension rapidly increased initially after injury followed by a progressive, but less dramatic, increase with additional time.” Of note, we did not identify any correlation between chronicity of symptoms and the tension needed to reduce the tendon medially or to a more lateral position on the footprint.
In acute tears, the cuff tissue is more compliant and mobile and can be pulled laterally across its anatomical footprint with minimal tension.39 In contrast, cuff tissue in the more commonly encountered chronic tear is less compliant and is not mobile enough to be pulled to the lateral margin of the footprint without added stress.30,34,35 In large, acute tears in which there are minimal tissue degeneration and retraction, a laterally based footprint-restoring technique may be performed with minimal tension. This technique may have advantages over a medially based repair. In the literature, more attention needs to be directed toward the biomechanics and biology of chronic rotator cuff tears, as these are more commonly encountered.
Almost all of the prospective studies that have compared single- and double-row RCR have found no significant differences in MRI healing rates or clinical results at follow-up up to 2 years.14,16,40-45 Detailed analysis of the surgical techniques used in all these studies revealed that the rotator cuff tendons were repaired back to the lateral footprint in both the single- and double-row constructs.14,16,40-45 Although no clinical studies have compared medially and laterally based single-row repairs, our data suggest that medially based repairs have lower tensions and therefore should not be considered equivalent. Sostak and colleagues31 and Murray and colleagues46 have shown that a medially based single-row RCR can achieve excellent clinical and anatomical results, likely partly because of the lower tension applied to the torn cuff tissue.31,46 Studies are needed to compare medially and laterally based repairs, including single- and double-row repairs.
The vast majority of recent research has aimed to counteract construct tension with stronger biomechanical constructs.20-26 Surgeons have also aimed to improve biological healing by pulling the tendon laterally across the footprint to achieve complete footprint coverage, ultimately increasing the surface area for tendon–bone healing. This has led to the development of various double-row repair techniques, in which the cuff tendon is pulled to the lateral margin of its footprint. One row of anchors is placed in the medial aspect of the footprint, while a second is placed in the lateral aspect; the cuff is reduced and compressed to the tuberosity with various suture configurations. The TOE technique was developed to improve pressurization of the cuff tendon across the footprint by linking the 2 rows with bridging sutures. In doing so, however, the potentially deleterious effects of increased tension introduced by pulling the tendon laterally may have been overlooked. Nevertheless, the biomechanics and stress distribution likely differ between single-row repair and TOE repairs, and direct comparisons cannot be made at this time. The medial row of a double-row or TOE construct may stress-shield or “unload” the more lateral tissue. Studies are needed in order to better understand the tension differential and stress distribution of various double-row constructs.
Recognizing tear morphology is crucial in maximizing chances of healing after cuff repair. For example, a crescent-shaped tear is reduced to the tuberosity with direct lateral translation of the apex of the tear, which is also the deepest or most displaced part of the tear. On the other hand, reducing an L- or reverse L-shaped tear to the tuberosity is not as direct; reducing the deepest or most displaced part of the tear would lead to overreduction and overtensioning of the tendon. However, often the exact “elbow” of the tear is not obvious and appears more rounded; therefore, it is crucial for the surgeon to examine the mobility of the torn tendon along its entire length to minimize tension. Study is needed to assess tension along the entire length of the tear for different tear morphologies and sizes.
Although our results showed that increased tension was needed to reduce a torn tendon to its lateral footprint, no study has indicated exactly how much is “too much” tension. As stated earlier, use of stronger biomechanical constructs, including TOE constructs, may overcome the increased tension associated with laterally based repairs. In addition, laterally based repairs, either single- or double-row, may be best suited for tears with lower tension, whereas medially based repairs may be best suited for higher tension tears. It is also possible that the difference in tensions noted in this study is not significant enough to have a clinical impact on choice of construct or on anatomical healing. We need studies that correlate anatomical healing rates with repair tension in order to better guide surgeons on when to use a medially or laterally based repair.
Other possible effects of increased tension associated with laterally based repairs, including beneficial effects, must be considered as well. Viscoelastic properties of human rotator cuff tendon may dissipate increased tension over time through a variety of mechanisms. Stress relaxation, gap formation, creep, and the hysteresis effect, all associated with cyclical loading in the early healing period, may lead to dissipation of force over time.47,48 These more complex biomechanical properties of RCR constructs are yet to be clearly defined.
This study had several weaknesses. Its data represent a static measurement of time-zero rotator cuff tension, which greatly simplifies the biomechanics of the torn rotator cuff and repair construct as well as changes that occur with healing. During cuff repair, forces typically are distributed through several fixation points in stepwise process and are not focused on a single point of tissue with a grasper. Therefore, the findings of this study may not directly correlate with medially versus laterally based repairs in vivo. Furthermore, as this is a time-zero measurement, we could not determine whether the tension differential between the 2 repair positions remained static over time. Current literature suggests that muscle atrophy, fatty infiltration, and loss of elasticity of the musculotendinous unit are relatively irreversible.35,37,49 In addition, determining the precise apex of a cuff tear can be difficult, so error may have been introduced during this process. Last, although placement of the cuff tissue at the medial or lateral footprint position was based on visual estimation by an experienced and skilled arthroscopist, error may have been introduced based on this imprecise technique.
Conclusion
This study demonstrated a significant, 5.4-fold increase in in vivo time-zero rotator cuff tension with the tendon edge reduced to the lateral footprint rather than the medial footprint.
Although recent clinical results of arthroscopic rotator cuff repair (RCR) have been encouraging, achieving anatomical healing of full-thickness rotator cuff tears remains a challenge.1-4 Several factors influence rotator cuff healing after repair.1,3-8 Patient-related factors include advanced patient age, tear size, tear chronicity, and amount of fatty infiltration.1,3,5,6,8-10 Tension applied to the repair construct is a significant factor as well.11,12
In the literature, limited consideration has been given to repair tension.13 The majority of studies have focused on other factors, mainly repair technique. Some surgeons advocate use of a double-row repair construct in which the rotator cuff tendon is pulled to the lateral margin of the footprint.14-19 Double-row techniques, which include the transosseous-equivalent (TOE) construct, are biomechanically superior to other repairs.20-26 Another purported benefit of double-row repair is more complete restoration and pressurization of the rotator cuff footprint.21,24,27,28
Rotator cuff tears typically occur near the dysvascular region of the diseased musculotendinous unit, often leaving a stump of tissue attached to the tuberosity and ultimately a shortened tendon.29 In addition, full-thickness tears often retract over time. Meyer and colleagues29 recently demonstrated that this shortening is irreversible. Snyder30 and Sostak and colleagues31 suggested that pulling a shortened, degenerative rotator cuff tendon to the lateral margin of the footprint results in increased tissue tension compared with that produced with a more medially based repair just off the articular margin. In our opinion, the possible increase in tension during a laterally based repair, whether single- or double-row, may place excessive strain on the diseased tissue as well as the surgical construct, potentially contributing to repair failure.
We conducted a study to evaluate the difference, if any, in tension applied to the rotator cuff tendon positioned at the medial versus lateral margin of the footprint during arthroscopic RCR. We hypothesized significantly more tension would be placed on the rotator cuff tendon when positioned at the lateral versus medial footprint.
Methods
After obtaining Institutional Review Board approval for this study, we collected data on a consecutive series of patients who underwent arthroscopic RCR performed by Dr. Getelman at a single institution. Only patients with primary full-thickness tears of the supraspinatus and/or infraspinatus were included. Exclusion criteria included revision rotator cuff surgeries, partial-thickness tears, concurrent subscapularis tears requiring anchor fixation, and any tears that could not be mobilized to the lateral footprint without interval slides or margin convergence. The 20 identified patients constituted the study group.
Demographic factors, including age and preoperative length of symptoms, were recorded after chart review. Magnetic resonance imaging (MRI) was performed for all patients before surgery and was retrospectively reviewed. Dr. Getelman assigned each patient a modified Goutallier score, based on MRI, to assess for fatty infiltration/atrophy.32 Each patient was placed in the lateral decubitus position with the operative arm in balanced suspension at 70° of abduction. Standard glenohumeral and subacromial diagnostic arthroscopy was performed. The rotator cuff tear was gently debrided back to a healthy-appearing margin in preparation for repair. The tear was then measured in the anterior-posterior (A-P) and medial-lateral (M-L) planes using a premeasured, marked suture, as previously described.33 Complete bursal and articular-sided releases were performed to allow for appropriate mobilization of the tendon. The tear was classified as crescent-shaped, U-shaped, or L-shaped.
Viewing from the posterior portal, the surgeon inserted a tissue grasper through the lateral portal. The tendon was grasped at multiple points along its edge, anterior to posterior, and was translated laterally to assess its reducibility; the apex of the tear correlated with the point of maximal excursion and coverage of the footprint. Once confirmed, the rotator cuff tear apex was clamped with a tissue grasper. After placement in a sterile arthroscopic camera sleeve (DeRoyal camera drape with perforated tip), a calibrated digital weigh scale (American Weigh Scales model H22 portable electronic hanging scale, with accuracy of 0.01 lb) was attached to the tissue grasper with an S-hook (Figure 1). The tendon edge was first translated about 3 mm lateral to the articular margin (the medial footprint position), and tension was recorded (Figures 2A, 2B). After a 1-minute relaxation period, the tendon edge was translated to the lateral edge of the rotator cuff footprint (the lateral footprint position), and tension was recorded again (Figures 2C, 2D). A medially based single-row RCR with triple-loaded sutures and bone marrow vents placed in the lateral tuberosity was then completed, regardless of tension, tear size, or tear morphology.31 Typically, 1 anchor was used for every 10 to 15 mm of A-P tear length.
SAS software was used for statistical analysis, the Wilcoxon signed rank test for continuous or ordinal data comparisons between paired groups, and the Mann-Whitney test for continuous or ordinal data comparisons between independent, unmatched groups. One-way analysis of variance (ANOVA) was used to compare means among the 3 groups of morphology subtypes. Linear regression was performed to assess the simultaneous relationship between potential predictors (age, sex, length of symptoms, Goutallier score, tear size) and medial or lateral tension, where medial tension was included as an additional potential predictor for lateral tension. Restricted cubic splines were fit to assess linearity. Predictors were retained in multivariate regression using backward variable retention. Because of inadequate sample size, additivity was assumed except for sex. Statistical significance was set at P < .05.
Results
Of the 20 rotator cuff tears evaluated (Table 1), 13 were crescent-shaped, 5 were U-shaped, and 2 were L-shaped. Mean (SD) A-P tear size was 17.7 (5.8) mm, and mean (SD) M-L tear size was 19.1 (8.6) mm. Mean age of the 20 patients (15 men, 5 women) was 57.9 years (range, 44-72 years). Mean (SD) length of symptoms was 12.9 (12.4) months (range, 3-48 months). Mean (SD) modified Goutallier score was 1.4 (0.7; range, 0-3).
Mean (SD) rotator cuff tension for all tears approximated to the medial footprint was 0.41 (0.33) pound, and mean (SD) cuff tension for all tears approximated to the lateral footprint was 2.21 (1.20) pounds—representing a 5.4-fold difference (P < .0001).
No statistically significant differences were detected in the ANOVA comparing tensions at medial and lateral positions among tear morphologic subtypes (all Ps >.05).
Subgroup analysis (Table 2) was performed for smaller (≤20 mm A-P) and larger (>20 mm A-P) tears. For smaller tears, mean (SD) tension was 0.27 (0.24) pound applied with the cuff tendon pulled to the medial footprint and 2.06 (1.06) pounds applied with the tendon pulled to the lateral footprint—a 7.6-fold difference (P < .0018). For larger tears, mean (SD) tension was 0.58 (0.37) pound applied with the tendon pulled to the medial footprint and 2.38 (1.4) pounds applied with the tendon pulled to the lateral footprint—a 4.1-fold difference (P < .005).
A statistically significant difference in tensions was found between small and large cuff tears positioned at the medial footprint (0.27 vs 0.58 lb; P = .0367); no difference was found between groups with the tendon at the lateral footprint (2.06 vs 2.38 lb; P = .284).
Univariate and multivariate analyses were performed using linear regression analysis (Table 3). During univariate analysis for medial footprint position, A-P tear size and Goutallier score both positively correlated with increasing tension; for lateral footprint position, no factors statistically correlated with lateral tension, though there was a positive trend for medial tension and female sex. During multivariate analysis for medial footprint position, only A-P tear size positively correlated with increasing tension; for lateral footprint position, both age (in nonlinear fashion as function of age + age2) and medial tension positively correlated with increasing tension.
Discussion
Our results indicated that significantly more tension is placed on the torn rotator cuff tendon when it is reduced across the footprint from a medial to a more lateral position in vivo. More tension was required for all tears to be reduced to the lateral footprint compared with the medial footprint. As expected, compared with smaller tears, larger tears required significantly more tension in order to be reduced to the medial footprint. Interestingly, no statistical difference was found between tensions required to reduce either small or large tears to the lateral footprint, which suggests that, regardless of tear size, more force must be applied to reduce the torn tendon to the lateral footprint compared with the medial footprint.
Hersche and Gerber34 were the first to report rotator cuff tension measurements in vivo. Although their study did not specifically compare cuff tensions reducing the tear to the medial versus lateral footprint, it did examine tension at displacement of 10 and 20 mm. Tension increased from 27 N to 60 N, correlating with a 2.2-fold difference between the 2 distances. Domb and colleagues35 also compared in vivo rotator cuff tension differences between the medial footprint and the lateral footprint in 4 patients. Mean tension applied to the cuff during reduction to the articular margin was 27 N, or 6 pounds. Mean tension needed to reduce the cuff to the lateral tuberosity was 76 N, or 17 pounds, for a 2.8-fold difference. Tears were not measured but were described as massive and retracted.
Although repair tension has long been recognized as a crucial factor in RCR healing, little clinical research has focused on the effects of excess tension. Davidson and Rivenburgh11 prospectively followed the clinical outcomes of 67 consecutive cuff repairs after intraoperative tension measurement and found that high-tension repairs (>8 lb) had significantly lower clinical outcome measures. However, the authors did not report on correlations with radiologic healing and stated, “Functional outcome is inversely proportional to rotator cuff repair tension.” Further study of the in vivo effects of increased tension on clinical and radiologic outcomes is needed.
Several animal studies have been conducted on the effects of tension on RCRs. Gerber and colleagues36 reported that the force needed to produce 1 cm of sheep supraspinatus tendon excursion increased 7-fold, from 6.8 N to 47.8 N, after 40 weeks of tendon tear. Coleman and colleagues37 compared the modulus of elasticity in sheep supraspinatus tendon after 6 weeks and 18 weeks of detachment and reported increases of 60% and 70%, respectively. Gimbel and colleagues38 showed that, in a rat model, “repair tension rapidly increased initially after injury followed by a progressive, but less dramatic, increase with additional time.” Of note, we did not identify any correlation between chronicity of symptoms and the tension needed to reduce the tendon medially or to a more lateral position on the footprint.
In acute tears, the cuff tissue is more compliant and mobile and can be pulled laterally across its anatomical footprint with minimal tension.39 In contrast, cuff tissue in the more commonly encountered chronic tear is less compliant and is not mobile enough to be pulled to the lateral margin of the footprint without added stress.30,34,35 In large, acute tears in which there are minimal tissue degeneration and retraction, a laterally based footprint-restoring technique may be performed with minimal tension. This technique may have advantages over a medially based repair. In the literature, more attention needs to be directed toward the biomechanics and biology of chronic rotator cuff tears, as these are more commonly encountered.
Almost all of the prospective studies that have compared single- and double-row RCR have found no significant differences in MRI healing rates or clinical results at follow-up up to 2 years.14,16,40-45 Detailed analysis of the surgical techniques used in all these studies revealed that the rotator cuff tendons were repaired back to the lateral footprint in both the single- and double-row constructs.14,16,40-45 Although no clinical studies have compared medially and laterally based single-row repairs, our data suggest that medially based repairs have lower tensions and therefore should not be considered equivalent. Sostak and colleagues31 and Murray and colleagues46 have shown that a medially based single-row RCR can achieve excellent clinical and anatomical results, likely partly because of the lower tension applied to the torn cuff tissue.31,46 Studies are needed to compare medially and laterally based repairs, including single- and double-row repairs.
The vast majority of recent research has aimed to counteract construct tension with stronger biomechanical constructs.20-26 Surgeons have also aimed to improve biological healing by pulling the tendon laterally across the footprint to achieve complete footprint coverage, ultimately increasing the surface area for tendon–bone healing. This has led to the development of various double-row repair techniques, in which the cuff tendon is pulled to the lateral margin of its footprint. One row of anchors is placed in the medial aspect of the footprint, while a second is placed in the lateral aspect; the cuff is reduced and compressed to the tuberosity with various suture configurations. The TOE technique was developed to improve pressurization of the cuff tendon across the footprint by linking the 2 rows with bridging sutures. In doing so, however, the potentially deleterious effects of increased tension introduced by pulling the tendon laterally may have been overlooked. Nevertheless, the biomechanics and stress distribution likely differ between single-row repair and TOE repairs, and direct comparisons cannot be made at this time. The medial row of a double-row or TOE construct may stress-shield or “unload” the more lateral tissue. Studies are needed in order to better understand the tension differential and stress distribution of various double-row constructs.
Recognizing tear morphology is crucial in maximizing chances of healing after cuff repair. For example, a crescent-shaped tear is reduced to the tuberosity with direct lateral translation of the apex of the tear, which is also the deepest or most displaced part of the tear. On the other hand, reducing an L- or reverse L-shaped tear to the tuberosity is not as direct; reducing the deepest or most displaced part of the tear would lead to overreduction and overtensioning of the tendon. However, often the exact “elbow” of the tear is not obvious and appears more rounded; therefore, it is crucial for the surgeon to examine the mobility of the torn tendon along its entire length to minimize tension. Study is needed to assess tension along the entire length of the tear for different tear morphologies and sizes.
Although our results showed that increased tension was needed to reduce a torn tendon to its lateral footprint, no study has indicated exactly how much is “too much” tension. As stated earlier, use of stronger biomechanical constructs, including TOE constructs, may overcome the increased tension associated with laterally based repairs. In addition, laterally based repairs, either single- or double-row, may be best suited for tears with lower tension, whereas medially based repairs may be best suited for higher tension tears. It is also possible that the difference in tensions noted in this study is not significant enough to have a clinical impact on choice of construct or on anatomical healing. We need studies that correlate anatomical healing rates with repair tension in order to better guide surgeons on when to use a medially or laterally based repair.
Other possible effects of increased tension associated with laterally based repairs, including beneficial effects, must be considered as well. Viscoelastic properties of human rotator cuff tendon may dissipate increased tension over time through a variety of mechanisms. Stress relaxation, gap formation, creep, and the hysteresis effect, all associated with cyclical loading in the early healing period, may lead to dissipation of force over time.47,48 These more complex biomechanical properties of RCR constructs are yet to be clearly defined.
This study had several weaknesses. Its data represent a static measurement of time-zero rotator cuff tension, which greatly simplifies the biomechanics of the torn rotator cuff and repair construct as well as changes that occur with healing. During cuff repair, forces typically are distributed through several fixation points in stepwise process and are not focused on a single point of tissue with a grasper. Therefore, the findings of this study may not directly correlate with medially versus laterally based repairs in vivo. Furthermore, as this is a time-zero measurement, we could not determine whether the tension differential between the 2 repair positions remained static over time. Current literature suggests that muscle atrophy, fatty infiltration, and loss of elasticity of the musculotendinous unit are relatively irreversible.35,37,49 In addition, determining the precise apex of a cuff tear can be difficult, so error may have been introduced during this process. Last, although placement of the cuff tissue at the medial or lateral footprint position was based on visual estimation by an experienced and skilled arthroscopist, error may have been introduced based on this imprecise technique.
Conclusion
This study demonstrated a significant, 5.4-fold increase in in vivo time-zero rotator cuff tension with the tendon edge reduced to the lateral footprint rather than the medial footprint.
1. Boileau P, Brassart N, Watkinson DJ, Carles M, Hatzidakis AM, Krishnan SG. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? J Bone Joint Surg Am. 2005;87(6):1229-1240.
2. Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86(2):219-224.
3. Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW, MacGillivray JD. Prospective analysis of arthroscopic rotator cuff repair: prognostic factors affecting clinical and ultrasound outcome. J Shoulder Elbow Surg. 2009;18(1):13-20.
4. Huijsmans PE, Pritchard MP, Berghs BM, van Rooyen KS, Wallace AL, de Beer JF. Arthroscopic rotator cuff repair with double-row fixation. J Bone Joint Surg Am. 2007;89(6):1248-1257.
5. Gulotta LV, Nho SJ, Dodson CC, Adler RS, Altchek DW, MacGillivray JD; HSS Arthroscopic Rotator Cuff Registry. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part II—prognostic factors for clinical and radiographic outcomes. J Shoulder Elbow Surg. 2011;20(6):941-946.
6. Cho NS, Rhee YG. The factors affecting the clinical outcome and integrity of arthroscopically repaired rotator cuff tears of the shoulder. Clin Orthop Surg. 2009;1(2):96-104.
7. Gladstone JN, Bishop JY, Lo IK, Flatow EL. Fatty infiltration and atrophy of the rotator cuff do not improve after rotator cuff repair and correlate with poor functional outcome. Am J Sports Med. 2007;35(5):719-728.
8. Oh JH, Kim SH, Ji HM, Jo KH, Bin SW, Gong HS. Prognostic factors affecting anatomic outcome of rotator cuff repair and correlation with functional outcome. Arthroscopy. 2009;25(1):30-39.
9. Tashjian RZ, Hollins AM, Kim HM, et al. Factors affecting healing rates after arthroscopic double-row rotator cuff repair. Am J Sports Med. 2010;38(12):2435-2442.
10. Burkhart SS, Lo IK. Arthroscopic rotator cuff repair. J Am Acad Orthop Surg. 2006;14(6):333-346.
11. Davidson PA, Rivenburgh DW. Rotator cuff repair tension as a determinant of functional outcome. J Shoulder Elbow Surg. 2000;9(6):502-506.
12. Goutallier D, Postel JM, Van Driessche S, Godefroy D, Radier C. Tension-free cuff repairs with excision of macroscopic tendon lesions and muscular advancement: results in a prospective series with limited fatty muscular degeneration. J Shoulder Elbow Surg. 2006;15(2):164-172.
13. Gimbel JA, Van Kleunen JP, Lake SP, Williams GR, Soslowsky LJ. The role of repair tension on tendon to bone healing in an animal model of chronic rotator cuff tears. J Biomech. 2007;40(3):561-568.
14. Ma HL, Chiang ER, Wu HT, et al. Clinical outcome and imaging of arthroscopic single-row and double-row rotator cuff repair: a prospective randomized trial. Arthroscopy. 2012;28(1):16-24.
15. Mihata T, Watanabe C, Fukunishi K, et al. Functional and structural outcomes of single-row versus double-row versus combined double-row and suture-bridge repair for rotator cuff tears. Am J Sports Med. 2011;39(10):2091-2098.
16. Koh KH, Kang KC, Lim TK, Shon MS, Yoo JC. Prospective randomized clinical trial of single- versus double-row suture anchor repair in 2- to 4-cm rotator cuff tears: clinical and magnetic resonance imaging results. Arthroscopy. 2011;27(4):453-462.
17. Voigt C, Bosse C, Vosshenrich R, Schulz AP, Lill H. Arthroscopic supraspinatus tendon repair with suture-bridging technique: functional outcome and magnetic resonance imaging. Am J Sports Med. 2010;38(5):983-991.
18. Lafosse L, Brzoska R, Toussaint B, Gobezie R. The outcome and structural integrity of arthroscopic rotator cuff repair with use of the double-row suture anchor technique. Surgical technique. J Bone Joint Surg Am. 2008;90(suppl 2 pt 2):275-286.
19. Park JY, Lhee SH, Choi JH, Park HK, Yu JW, Seo JB. Comparison of the clinical outcomes of single- and double-row repairs in rotator cuff tears. Am J Sports Med. 2008;36(7):1310-1316.
20. Kim DH, ElAttrache NS, Tibone JE, et al. Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med. 2006;34(3):407-414.
21. Mazzocca AD, Bollier MJ, Ciminiello AM, et al. Biomechanical evaluation of arthroscopic rotator cuff repairs over time. Arthroscopy. 2010;26(5):592-599.
22. Grimberg J, Diop A, Kalra K, Charousset C, Duranthon LD, Maurel N. In vitro biomechanical comparison of three different types of single- and double-row arthroscopic rotator cuff repairs: analysis of continuous bone–tendon contact pressure and surface during different simulated joint positions. J Shoulder Elbow Surg. 2010;19(2):236-243.
23. Nelson CO, Sileo MJ, Grossman MG, Serra-Hsu F. Single-row modified Mason-Allen versus double-row arthroscopic rotator cuff repair: a biomechanical and surface area comparison. Arthroscopy. 2008;24(8):941-948.
24. Park MC, ElAttrache NS, Tibone JE, Ahmad CS, Jun BJ, Lee TQ. Part I: footprint contact characteristics for a transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16(4):461-468.
25. Park MC, Tibone JE, ElAttrache NS, Ahmad CS, Jun BJ, Lee TQ. Part II: biomechanical assessment for a footprint-restoring transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16(4):469-476.
26. Ma CB, Comerford L, Wilson J, Puttlitz CM. Biomechanical evaluation of arthroscopic rotator cuff repairs: double-row compared with single-row fixation. J Bone Joint Surg Am. 2006;88(2):403-410.
27. Lo IK, Burkhart SS. Double-row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy. 2003;19(9):1035-1042.
28. Tuoheti Y, Itoi E, Yamamoto N, et al. Contact area, contact pressure, and pressure patterns of the tendon–bone interface after rotator cuff repair. Am J Sports Med. 2005;33(12):1869-1874.
29. Meyer DC, Farshad M, Amacker NA, Gerber C, Wieser K. Quantitative analysis of muscle and tendon retraction in chronic rotator cuff tears. Am J Sports Med. 2012;40(3):606-610.
30. Snyder SJ. Single vs. double row suture anchor fixation rotator cuff repair. Paper presented at: American Academy of Orthopedic Surgeons Annual Meeting; March 8, 2007; San Francisco, CA.
31. Sostak JP, Bahk MS, Getelman MH, Wong IH, Snyder SJ, Burns JP. Arthroscopic single row rotator cuff repair using the “SCOI row”: structural and clinical outcomes. Paper presented at: American Academy of Orthopedic Surgeons Annual Meeting; February 7-11, 2012; San Francisco, CA.
32. Fuchs B, Weishaupt D, Zanetti M, Hodler J, Gerber C. Fatty degeneration of the muscles of the rotator cuff: assessment by computed tomography versus magnetic resonance imaging. J Shoulder Elbow Surg. 1999;8(6):599-605.
33. Bond JL, Dopirak RM, Higgins J, Burns J, Snyder SJ. Arthroscopic replacement of massive, irreparable rotator cuff tears using a GraftJacket allograft: technique and preliminary results. Arthroscopy. 2008;24(4):403-409.
34. Hersche O, Gerber C. Passive tension in the supraspinatus musculotendinous unit after long-standing rupture of its tendon: a preliminary report. J Shoulder Elbow Surg. 1998;7(4):393-396.
35. Domb BG, Glousman RE, Brooks A, Hansen M, Lee TQ, ElAttrache NS. High-tension double-row footprint repair compared with reduced-tension single-row repair for massive rotator cuff tears. J Bone Joint Surg Am. 2008;90(suppl 4):35-39.
36. Gerber C, Meyer DC, Schneeberger AG, Hoppeler H, von Rechenberg B. Effect of tendon release and delayed repair on the structure of the muscles of the rotator cuff: an experimental study in sheep. J Bone Joint Surg Am. 2004;86(9):1973-1982.
37. Coleman SH, Fealy S, Ehteshami JR, et al. Chronic rotator cuff injury and repair model in sheep. J Bone Joint Surg Am. 2003;85(12):2391-2402.
38. Gimbel JA, Mehta S, Van Kleunen JP, Williams GR, Soslowsky LJ. The tension required at repair to reappose the supraspinatus tendon to bone rapidly increases after injury. Clin Orthop Relat Res. 2004;(426):258-265.
39. Mannava S, Plate JF, Whitlock PW, et al. Evaluation of in vivo rotator cuff muscle function after acute and chronic detachment of the supraspinatus tendon: an experimental study in an animal model. J Bone Joint Surg Am. 2011;93(18):1702-1711.
40. Burks RT, Crim J, Brown N, Fink B, Greis PE. A prospective randomized clinical trial comparing arthroscopic single- and double-row rotator cuff repair: magnetic resonance imaging and early clinical evaluation. Am J Sports Med. 2009;37(4):674-682.
41. Grasso A, Milano G, Salvatore M, Falcone G, Deriu L, Fabbriciani C. Single-row versus double-row arthroscopic rotator cuff repair: a prospective randomized clinical study. Arthroscopy. 2009;25(1):4-12.
42. Franceschi F, Ruzzini L, Longo UG, et al. Equivalent clinical results of arthroscopic single-row and double-row suture anchor repair for rotator cuff tears: a randomized controlled trial. Am J Sports Med. 2007;35(8):1254-1260.
43. Carbonel I, Martinez AA, Calvo A, Ripalda J, Herrera A. Single-row versus double-row arthroscopic repair in the treatment of rotator cuff tears: a prospective randomized clinical study. Int Orthop. 2012;36(9):1877-1883.
44. Lapner PL, Sabri E, Rakhra K, et al. A multicenter randomized controlled trial comparing single-row with double-row fixation in arthroscopic rotator cuff repair. J Bone Joint Surg Am. 2012;94(14):1249-1257.
45. Gartsman GM, Drake G, Edwards TB, et al. Ultrasound evaluation of arthroscopic full-thickness supraspinatus rotator cuff repair: single-row versus double-row suture bridge (transosseous equivalent) fixation. Results of a prospective, randomized study. J Shoulder Elbow Surg. 2013;22(11):1480-1487.
46. Murray TF Jr, Lajtai G, Mileski RM, Snyder SJ. Arthroscopic repair of medium to large full-thickness rotator cuff tears: outcome at 2- to 6-year follow-up. J Shoulder Elbow Surg. 2002;11(1):19-24.
47. Szczesny SE, Peloquin JM, Cortes DH, Kadlowec JA, Soslowsky LJ, Elliott DM. Biaxial tensile testing and constitutive modeling of human supraspinatus tendon. J Biomech Eng. 2012;134(2):021004.
48. Chaudhury S, Holland C, Vollrath F, Carr AJ. Comparing normal and torn rotator cuff tendons using dynamic shear analysis. J Bone Joint Surg Br. 2011;93(7):942-948.
49. Meyer DC, Hoppeler H, von Rechenberg B, Gerber C. A pathomechanical concept explains muscle loss and fatty muscular changes following surgical tendon release. J Orthop Res. 2004;22(5):1004-1007.
1. Boileau P, Brassart N, Watkinson DJ, Carles M, Hatzidakis AM, Krishnan SG. Arthroscopic repair of full-thickness tears of the supraspinatus: does the tendon really heal? J Bone Joint Surg Am. 2005;87(6):1229-1240.
2. Galatz LM, Ball CM, Teefey SA, Middleton WD, Yamaguchi K. The outcome and repair integrity of completely arthroscopically repaired large and massive rotator cuff tears. J Bone Joint Surg Am. 2004;86(2):219-224.
3. Nho SJ, Brown BS, Lyman S, Adler RS, Altchek DW, MacGillivray JD. Prospective analysis of arthroscopic rotator cuff repair: prognostic factors affecting clinical and ultrasound outcome. J Shoulder Elbow Surg. 2009;18(1):13-20.
4. Huijsmans PE, Pritchard MP, Berghs BM, van Rooyen KS, Wallace AL, de Beer JF. Arthroscopic rotator cuff repair with double-row fixation. J Bone Joint Surg Am. 2007;89(6):1248-1257.
5. Gulotta LV, Nho SJ, Dodson CC, Adler RS, Altchek DW, MacGillivray JD; HSS Arthroscopic Rotator Cuff Registry. Prospective evaluation of arthroscopic rotator cuff repairs at 5 years: part II—prognostic factors for clinical and radiographic outcomes. J Shoulder Elbow Surg. 2011;20(6):941-946.
6. Cho NS, Rhee YG. The factors affecting the clinical outcome and integrity of arthroscopically repaired rotator cuff tears of the shoulder. Clin Orthop Surg. 2009;1(2):96-104.
7. Gladstone JN, Bishop JY, Lo IK, Flatow EL. Fatty infiltration and atrophy of the rotator cuff do not improve after rotator cuff repair and correlate with poor functional outcome. Am J Sports Med. 2007;35(5):719-728.
8. Oh JH, Kim SH, Ji HM, Jo KH, Bin SW, Gong HS. Prognostic factors affecting anatomic outcome of rotator cuff repair and correlation with functional outcome. Arthroscopy. 2009;25(1):30-39.
9. Tashjian RZ, Hollins AM, Kim HM, et al. Factors affecting healing rates after arthroscopic double-row rotator cuff repair. Am J Sports Med. 2010;38(12):2435-2442.
10. Burkhart SS, Lo IK. Arthroscopic rotator cuff repair. J Am Acad Orthop Surg. 2006;14(6):333-346.
11. Davidson PA, Rivenburgh DW. Rotator cuff repair tension as a determinant of functional outcome. J Shoulder Elbow Surg. 2000;9(6):502-506.
12. Goutallier D, Postel JM, Van Driessche S, Godefroy D, Radier C. Tension-free cuff repairs with excision of macroscopic tendon lesions and muscular advancement: results in a prospective series with limited fatty muscular degeneration. J Shoulder Elbow Surg. 2006;15(2):164-172.
13. Gimbel JA, Van Kleunen JP, Lake SP, Williams GR, Soslowsky LJ. The role of repair tension on tendon to bone healing in an animal model of chronic rotator cuff tears. J Biomech. 2007;40(3):561-568.
14. Ma HL, Chiang ER, Wu HT, et al. Clinical outcome and imaging of arthroscopic single-row and double-row rotator cuff repair: a prospective randomized trial. Arthroscopy. 2012;28(1):16-24.
15. Mihata T, Watanabe C, Fukunishi K, et al. Functional and structural outcomes of single-row versus double-row versus combined double-row and suture-bridge repair for rotator cuff tears. Am J Sports Med. 2011;39(10):2091-2098.
16. Koh KH, Kang KC, Lim TK, Shon MS, Yoo JC. Prospective randomized clinical trial of single- versus double-row suture anchor repair in 2- to 4-cm rotator cuff tears: clinical and magnetic resonance imaging results. Arthroscopy. 2011;27(4):453-462.
17. Voigt C, Bosse C, Vosshenrich R, Schulz AP, Lill H. Arthroscopic supraspinatus tendon repair with suture-bridging technique: functional outcome and magnetic resonance imaging. Am J Sports Med. 2010;38(5):983-991.
18. Lafosse L, Brzoska R, Toussaint B, Gobezie R. The outcome and structural integrity of arthroscopic rotator cuff repair with use of the double-row suture anchor technique. Surgical technique. J Bone Joint Surg Am. 2008;90(suppl 2 pt 2):275-286.
19. Park JY, Lhee SH, Choi JH, Park HK, Yu JW, Seo JB. Comparison of the clinical outcomes of single- and double-row repairs in rotator cuff tears. Am J Sports Med. 2008;36(7):1310-1316.
20. Kim DH, ElAttrache NS, Tibone JE, et al. Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med. 2006;34(3):407-414.
21. Mazzocca AD, Bollier MJ, Ciminiello AM, et al. Biomechanical evaluation of arthroscopic rotator cuff repairs over time. Arthroscopy. 2010;26(5):592-599.
22. Grimberg J, Diop A, Kalra K, Charousset C, Duranthon LD, Maurel N. In vitro biomechanical comparison of three different types of single- and double-row arthroscopic rotator cuff repairs: analysis of continuous bone–tendon contact pressure and surface during different simulated joint positions. J Shoulder Elbow Surg. 2010;19(2):236-243.
23. Nelson CO, Sileo MJ, Grossman MG, Serra-Hsu F. Single-row modified Mason-Allen versus double-row arthroscopic rotator cuff repair: a biomechanical and surface area comparison. Arthroscopy. 2008;24(8):941-948.
24. Park MC, ElAttrache NS, Tibone JE, Ahmad CS, Jun BJ, Lee TQ. Part I: footprint contact characteristics for a transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16(4):461-468.
25. Park MC, Tibone JE, ElAttrache NS, Ahmad CS, Jun BJ, Lee TQ. Part II: biomechanical assessment for a footprint-restoring transosseous-equivalent rotator cuff repair technique compared with a double-row repair technique. J Shoulder Elbow Surg. 2007;16(4):469-476.
26. Ma CB, Comerford L, Wilson J, Puttlitz CM. Biomechanical evaluation of arthroscopic rotator cuff repairs: double-row compared with single-row fixation. J Bone Joint Surg Am. 2006;88(2):403-410.
27. Lo IK, Burkhart SS. Double-row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy. 2003;19(9):1035-1042.
28. Tuoheti Y, Itoi E, Yamamoto N, et al. Contact area, contact pressure, and pressure patterns of the tendon–bone interface after rotator cuff repair. Am J Sports Med. 2005;33(12):1869-1874.
29. Meyer DC, Farshad M, Amacker NA, Gerber C, Wieser K. Quantitative analysis of muscle and tendon retraction in chronic rotator cuff tears. Am J Sports Med. 2012;40(3):606-610.
30. Snyder SJ. Single vs. double row suture anchor fixation rotator cuff repair. Paper presented at: American Academy of Orthopedic Surgeons Annual Meeting; March 8, 2007; San Francisco, CA.
31. Sostak JP, Bahk MS, Getelman MH, Wong IH, Snyder SJ, Burns JP. Arthroscopic single row rotator cuff repair using the “SCOI row”: structural and clinical outcomes. Paper presented at: American Academy of Orthopedic Surgeons Annual Meeting; February 7-11, 2012; San Francisco, CA.
32. Fuchs B, Weishaupt D, Zanetti M, Hodler J, Gerber C. Fatty degeneration of the muscles of the rotator cuff: assessment by computed tomography versus magnetic resonance imaging. J Shoulder Elbow Surg. 1999;8(6):599-605.
33. Bond JL, Dopirak RM, Higgins J, Burns J, Snyder SJ. Arthroscopic replacement of massive, irreparable rotator cuff tears using a GraftJacket allograft: technique and preliminary results. Arthroscopy. 2008;24(4):403-409.
34. Hersche O, Gerber C. Passive tension in the supraspinatus musculotendinous unit after long-standing rupture of its tendon: a preliminary report. J Shoulder Elbow Surg. 1998;7(4):393-396.
35. Domb BG, Glousman RE, Brooks A, Hansen M, Lee TQ, ElAttrache NS. High-tension double-row footprint repair compared with reduced-tension single-row repair for massive rotator cuff tears. J Bone Joint Surg Am. 2008;90(suppl 4):35-39.
36. Gerber C, Meyer DC, Schneeberger AG, Hoppeler H, von Rechenberg B. Effect of tendon release and delayed repair on the structure of the muscles of the rotator cuff: an experimental study in sheep. J Bone Joint Surg Am. 2004;86(9):1973-1982.
37. Coleman SH, Fealy S, Ehteshami JR, et al. Chronic rotator cuff injury and repair model in sheep. J Bone Joint Surg Am. 2003;85(12):2391-2402.
38. Gimbel JA, Mehta S, Van Kleunen JP, Williams GR, Soslowsky LJ. The tension required at repair to reappose the supraspinatus tendon to bone rapidly increases after injury. Clin Orthop Relat Res. 2004;(426):258-265.
39. Mannava S, Plate JF, Whitlock PW, et al. Evaluation of in vivo rotator cuff muscle function after acute and chronic detachment of the supraspinatus tendon: an experimental study in an animal model. J Bone Joint Surg Am. 2011;93(18):1702-1711.
40. Burks RT, Crim J, Brown N, Fink B, Greis PE. A prospective randomized clinical trial comparing arthroscopic single- and double-row rotator cuff repair: magnetic resonance imaging and early clinical evaluation. Am J Sports Med. 2009;37(4):674-682.
41. Grasso A, Milano G, Salvatore M, Falcone G, Deriu L, Fabbriciani C. Single-row versus double-row arthroscopic rotator cuff repair: a prospective randomized clinical study. Arthroscopy. 2009;25(1):4-12.
42. Franceschi F, Ruzzini L, Longo UG, et al. Equivalent clinical results of arthroscopic single-row and double-row suture anchor repair for rotator cuff tears: a randomized controlled trial. Am J Sports Med. 2007;35(8):1254-1260.
43. Carbonel I, Martinez AA, Calvo A, Ripalda J, Herrera A. Single-row versus double-row arthroscopic repair in the treatment of rotator cuff tears: a prospective randomized clinical study. Int Orthop. 2012;36(9):1877-1883.
44. Lapner PL, Sabri E, Rakhra K, et al. A multicenter randomized controlled trial comparing single-row with double-row fixation in arthroscopic rotator cuff repair. J Bone Joint Surg Am. 2012;94(14):1249-1257.
45. Gartsman GM, Drake G, Edwards TB, et al. Ultrasound evaluation of arthroscopic full-thickness supraspinatus rotator cuff repair: single-row versus double-row suture bridge (transosseous equivalent) fixation. Results of a prospective, randomized study. J Shoulder Elbow Surg. 2013;22(11):1480-1487.
46. Murray TF Jr, Lajtai G, Mileski RM, Snyder SJ. Arthroscopic repair of medium to large full-thickness rotator cuff tears: outcome at 2- to 6-year follow-up. J Shoulder Elbow Surg. 2002;11(1):19-24.
47. Szczesny SE, Peloquin JM, Cortes DH, Kadlowec JA, Soslowsky LJ, Elliott DM. Biaxial tensile testing and constitutive modeling of human supraspinatus tendon. J Biomech Eng. 2012;134(2):021004.
48. Chaudhury S, Holland C, Vollrath F, Carr AJ. Comparing normal and torn rotator cuff tendons using dynamic shear analysis. J Bone Joint Surg Br. 2011;93(7):942-948.
49. Meyer DC, Hoppeler H, von Rechenberg B, Gerber C. A pathomechanical concept explains muscle loss and fatty muscular changes following surgical tendon release. J Orthop Res. 2004;22(5):1004-1007.
Neurocognitive Deficits and Cerebral Desaturation During Shoulder Arthroscopy With Patient in Beach-Chair Position: A Review of the Current Literature
The beach-chair position (BCP) is commonly used for both arthroscopic and open shoulder surgery. This technique positions the shoulder in an anatomical upright position, facilitating shoulder access and visualization.1 Compared with the lateral decubitus position, the BCP also improves airway access, reduces bleeding, and lessens the risk for brachial plexus injury.2
Despite the advantages of using the BCP, there have been multiple reports of catastrophic neurologic complications, including severe brain damage and death, in relatively healthy patients without any known risk factors.3-6 The definitive etiology of these complications remains unclear, but it has been hypothesized that BCP use may be an independent risk factor for cerebrovascular ischemia,1,5-16 as the upright position can cause hypotension leading to increased risk for cerebral hypoperfusion.7-11,17 Reducing cerebral perfusion pressure below critical thresholds may result in permanent neurologic injury.4-6,14 Therefore, monitoring of cerebral perfusion and optimization of intraoperative cerebral oxygenation have been recommended to help avoid potential neurologic complications. However, a direct relationship between intraoperative cerebral desaturation events (CDEs) and postoperative neurocognitive deficits has not been definitively established.1,9-12
To put into perspective the importance of detecting and preventing CDEs and neurologic complications, we can consider the incidence of fatal pulmonary embolism associated with total joint arthroplasty. Although the incidence is very low, about 0.1% to 2.0%, some form of venous thromboembolism prophylaxis is the standard of care for helping prevent this serious complication. Similarly, catastrophic neurologic complications of upright shoulder arthroscopy are very rare, but it is still important to consider measures that help minimize them.
We reviewed the literature for the incidence of postoperative neurocognitive deficits, number of reported neurocognitive complications, and incidence of intraoperative CDEs in patients who underwent arthroscopic shoulder surgery in the BCP.
Methods
Dr. Salazar and Dr. Hazel independently searched the Medline, Cochrane, and Embase databases for case series, prospective studies, and cohort studies that reported neurocognitive complications associated with the BCP and the incidence of intraoperative CDEs. The authors used beach chair, desaturation, near infrared spectroscopy, and shoulder as medical subject headings (MeSH). In addition, bibliographies of retrieved articles were checked for studies that the search terms may have missed. Eighty-one publications were identified and reviewed for possible inclusion.
Next, the same 2 authors reviewed the titles and abstracts for relevance and determined which articles had potential to contribute to the study. Only English-language publications were considered for inclusion. To review the incidence of postoperative neurocognitive deficits, we included only those studies with more than 25 patients, documentation of postoperative complications, and arthroscopic shoulder surgery performed with the patient in the seated, semi-upright, or BCP. Only studies with at least 25 patients were used in order to increase the power and improve the level of evidence. To review reported cases of neurocognitive complications, we included all relevant case reports and case series. To review the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive deficits, we included studies that reported on use of intraoperative cerebral perfusion monitoring. Modalities used in these studies included near infrared spectroscopy, electroencephalography, and invasive blood pressure monitoring calculated at the brain level. Studies were excluded if they did not involve arthroscopic shoulder surgery or were not conducted with human subjects.
Information recorded for each study included general information such as author and publication year, type of study, number of patients enrolled, type of intraoperative monitoring, anesthesia protocol, number of patients with CDEs, and number of patients with neurocognitive complications after surgery.
Results
Our search identified 81 publications for potential inclusion. Our first aim was to identify the overall incidence of reported neurocognitive deficits after arthroscopic shoulder surgery with the patient in the BCP. We identified 10 studies (Table 1) that met the inclusion criteria. Among the 24,701 patients in these 10 studies, there was only 1 reported case of neurocognitive deficit after surgery, in a mixed prospective-retrospective study of 15,014 cases by Rohrbaugh and colleagues.18 The deficit they reported was an ischemic cerebral vascular accident. The 0.0067% incidence in their study demonstrates how rare the complication is. Two large retrospective studies (Ns = 4169 and 5177 patients) found no postoperative neurocognitive complications.19,20 Only 3 studies performed formal postoperative cognitive testing. Salazar and colleagues21 used the Repeatable Battery for the Assessment of Neuropsychological Status before and after surgery, and Gillespie and colleagues8 and Lee and colleagues10 used the Mini–Mental State Examination before and after surgery. Total incidence of reported neurocognitive deficits from our review was 0.004% (1/24,701).
Our second aim was to review all reported cases of neurocognitive complications after arthroscopic shoulder surgery with the patient in the BCP. We identified 4 publications that fit our inclusion criteria (Table 2). Pohl and Cullen6 described 4 cases of ischemic brain injury after arthroscopic shoulder surgery with the patient in the BCP. Age range was 47 to 57 years. Specific intraoperative cerebral monitoring was not used. However, these patients had several episodes of intraoperative hypotension (systolic blood pressures, 80-90 mm Hg), measured with a traditional blood pressure cuff on the arm. In general, these patients had minimal cerebrovascular risk factors and no known preexisting cerebrovascular disease. Drummond and colleagues22 described an ischemic stroke in a 50-year-old man after arthroscopic subacromial decompression and open rotator cuff repair that resulted in unresolved right hemiplegia. Subsequent diagnostic investigation revealed an asymmetry of the circle of Willis resulting in limited flow to the left anterior and middle cerebral artery distributions. Bhatti and Enneking3 reported the case of a 64-year-old man who lost vision in the right eye immediately after arthroscopic rotator cuff repair. His vision improved spontaneously the next morning and continued to improve over the next 6 months—he regained 20/20 vision with some residual optic neuropathy.
Our third aim was to determine the incidence of intraoperative CDEs during arthroscopic shoulder surgery with the patient in the BCP. Incidence of CDEs varied widely among the 7 studies reviewed (Table 3). Minimum incidence of intraoperative CDE was 0% in a cohort of 30 patients,1 and maximum incidence was 80% in a study of 61 patients,12 all of whom underwent elective arthroscopic shoulder surgery in the BCP. Although there was wide variability in CDE incidence, the studies were consistent with respect to their definition of a CDE. Most authors used a decrease in regional cerebral tissue oxygen saturation of 20% or more from baseline, or an absolute value up to 55%, to define a CDE. None of the 7 studies reviewed reported a clinically significant adverse neurocognitive event.
Discussion
Of concern, there have been several surveys, case reports, and small case series of previously healthy patients who had no known risk factors, underwent arthroscopic shoulder surgery in the BCP, and developed unanticipated postoperative neurologic complications.4-6,14 Beach-chair positioning during surgical procedures has been implicated as a contributing factor leading to cerebral hypoperfusion with potential for cerebral ischemia.1,12,23 These changes in cerebral perfusion pressure are thought to be the major determinant of poor neurologic outcomes. Such reports have exposed the potential need for heightened vigilance, alternative anesthesia techniques, and improved monitoring, though the exact etiology of the central nervous system injuries in this patient population is incompletely understood and is likely multifactorial. Therefore, in this study we wanted to determine the incidence of postoperative neurocognitive deficits and review all reported cases of neurocognitive complications in patients who have undergone arthroscopic shoulder surgery in the BCP. In addition, we wanted to define the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive complications.
According to our review, the incidence of postoperative neurocognitive complications after surgery in the BCP is 0.004% (1/24,701). However, this finding is based only on what has been reported; the true incidence is not known. It is also important to note that the incidence of neurocognitive deficits after many other types of surgery is not known and that surgery itself may be a risk factor for postoperative neurocognitive deficits.24 In their retrospective review of 15,014 patients who underwent arthroscopic shoulder surgery in the BCP at a single institution over an 11-year period, Rohrbaugh and colleagues18 found an overall postoperative complication rate of 0.37% and a 0.0067% incidence of neurocognitive deficits. One patient in the series was given a diagnosis of ischemic stroke on the basis of neurologic deficits that occurred 24 hours after surgery. Yadeau and colleagues20 found no postoperative neurocognitive complications in a mixed prospective-retrospective study of 4169 patients—3000 identified retrospectively, 1169 prospectively—who underwent arthroscopic shoulder surgery in the BCP at an ambulatory surgery center. Pin-on and colleagues19 reported on a series of 5177 orthopedic and neurosurgical patients who underwent surgery in the BCP. In those who had arthroscopic shoulder surgery, intraoperative systolic blood pressures obtained from an arterial line referenced to heart level decreased a mean (SD) of 14.4% (12.7%), whereas in those whose pressures were obtained from a noninvasive blood pressure cuff referenced to heart level decreased 19.3% (12.6%). However, the authors reported no incidence of postoperative stroke or neurologic deficits.
Although uncommon, perioperative cerebral ischemic accidents are potentially devastating for patients, their families, and the health care professionals involved. These events have tremendous economic, social, professional, and medicolegal implications, with perioperative stroke being particularly morbid. Perioperative stroke has a mortality rate of 60%, versus 15% to 46% for stroke in general.25,26 In 2005, Pohl and Cullen6 published a landmark article on a series of 4 relatively healthy middle-aged patients who were at low risk for stroke but had catastrophic neurocognitive complications (including 1 death) after arthroscopic shoulder surgery in the BCP. Bhatti and Enneking3 described a case of acute postoperative vision loss and ophthalmoplegia attributed to intraoperative hypotension leading to ischemia in a patient who underwent an elective shoulder arthroscopic procedure in the BCP. These reports prompted multiple investigations into the physiologic hemodynamic changes associated with surgery in the BCP and the treatment strategies used to improve patient safety.
In the normal physiologic state, the sympathetic nervous system is activated when a person assumes the seated position. The result is increased systemic vascular resistance and heart rate alterations to maintain cardiac output and mean arterial pressure. In anesthetized patients, this response is blunted by the vasodilatory effects of intravenous and volatile anesthetics. Multiple studies have demonstrated substantial hemodynamic changes in both awake and anesthetized patients during the maneuver from the supine position to the seated position1,27,28; these changes include diminished cardiac index, stroke volume, and arterial pressure.17 The data underscore the need for attentiveness and accurate monitoring of cerebral perfusion when the transition is made from the supine position to the BCP, particularly in the early phase of surgery and in high-risk patients.
Knowledge of these hemodynamic changes has led several authors to recommend additional intraoperative monitoring of cerebral perfusion. Monitoring techniques have included use of invasive blood pressure monitoring adjusted to brain level, cerebral oximetry using near infrared spectroscopy, and electroencephalography. However, the clinical relevance of intraoperative CDEs in isolation is not well understood.1,6,7,23 In addition, cost and availability of additional advanced monitoring likely factor into why it is not more commonly used. For this patient population, the severity, frequency, and duration of desaturation that causes cerebral ischemia and the relationship with postoperative neurocognitive deficits remain undefined.
The incidence of CDEs in patients being monitored with near infrared spectroscopy while undergoing elective arthroscopic shoulder surgery in the BCP varies widely, from 0% to 80% (mean, 41%).1,4,7,10,12,21 Magnitude and duration of cerebral ischemia required to produce neurocognitive dysfunction in this patient population remain unidentified as well. In conscious patients, a 20% reduction in frontal lobe oxygenation is associated with clinical manifestations of cerebral hypoperfusion, such as syncope.15,29 As none of the patients in the studies we reviewed experienced any sort of deficit, we cannot definitively state there is a correlation between CDE occurrence and neurocognitive deficit.
One limitation of our investigation is that it was a systemic review, and thus there was substantial heterogeneity in the methods and designs of the studies included in the analysis. Among the different series, there was variability in multiple aspects of the study design, including type of anesthetic, patient inclusion criteria, type of surgery, type of intraoperative cerebral perfusion monitoring, and type of neurocognitive testing. As a result, comparing the groups was difficult, and the generalizability of our findings may be limited. In addition, it is difficult to accurately establish incidence and comprehensively review these events because of the paucity of literature.
Conclusion
Neurocognitive complications after shoulder arthroscopy with the patient in the BCP are extremely rare but potentially devastating events that can affect healthy patients with no preexisting cerebrovascular risk factors. Our review indicated the incidence of permanent neurologic deficit after arthroscopy in the BCP may be as low as 0.004%. The exact etiology of such complications is not clear. Basic science research and large prospective studies are needed to identify the clinically relevant thresholds of magnitude, duration, and frequency of intraoperative CDEs in order to establish their relationship with postoperative neurocognitive complications. Such large studies may also elucidate modifiable patient-specific risk factors and establish the most sensitive, safe, and cost-effective intraoperative monitoring tools. Current literature suggests that accurate intraoperative monitoring of cerebral perfusion, alternatives to general anesthesia, and prudent use of intraoperative blood pressure control may improve patient safety.
1. Tange K, Kinoshita H, Minonishi T, et al. Cerebral oxygenation in the beach chair position before and during general anesthesia. Minerva Anestesiol. 2010;76(7):485-490.
2. Skyhar MJ, Altchek DW, Warren RF, Wickiewicz TL, O’Brien SJ. Shoulder arthroscopy with the patient in the beach-chair position. Arthroscopy. 1988;4(4):256-259.
3. Bhatti MT, Enneking FK. Visual loss and ophthalmoplegia after shoulder surgery. Anesth Analg. 2003;96(3):899-902.
4. Friedman DJ, Parnes NZ, Zimmer Z, Higgins LD, Warner JJ. Prevalence of cerebrovascular events during shoulder surgery and association with patient position. Orthopedics. 2009;32(4).
5. Papadonikolakis A, Wiesler ER, Olympio MA, Poehling GG. Avoiding catastrophic complications of stroke and death related to shoulder surgery in the sitting position. Arthroscopy. 2008;24(4):481-482.
6. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17(6):463-469.
7. Dippmann C, Winge S, Nielsen HB. Severe cerebral desaturation during shoulder arthroscopy in the beach-chair position. Arthroscopy. 2010;26(9 suppl):S148-S150.
8. Gillespie R, Shishani Y, Streit J, et al. The safety of controlled hypotension for shoulder arthroscopy in the beach-chair position. J Bone Joint Surg Am. 2012;94(14):1284-1290.
9. Jeong H, Lee SH, Jang EA, Chung SS, Lee J, Yoo KY. Haemodynamics and cerebral oxygenation during arthroscopic shoulder surgery in beach chair position under general anaesthesia. Acta Anaesthesiol Scand. 2012;56(7):872-879.
10. Lee JH, Min KT, Chun YM, Kim EJ, Choi SH. Effects of beach-chair position and induced hypotension on cerebral oxygen saturation in patients undergoing arthroscopic shoulder surgery. Arthroscopy. 2011;27(7):889-894.
11. Moerman AT, De Hert SG, Jacobs TF, De Wilde LF, Wouters PF. Cerebral oxygen desaturation during beach chair position. Eur J Anaesthesiol. 2012;29(2):82-87.
12. Murphy GS, Szokol JW, Marymont JH, et al. Cerebral oxygen desaturation events assessed by near-infrared spectroscopy during shoulder arthroscopy in the beach chair and lateral decubitus positions. Anesth Analg. 2010;111(2):496-505.
13. Peruto CM, Ciccotti MG, Cohen SB. Shoulder arthroscopy positioning: lateral decubitus versus beach chair. Arthroscopy. 2009;25(8):891-896.
14. Rains DD, Rooke GA, Wahl CJ. Pathomechanisms and complications related to patient positioning and anesthesia during shoulder arthroscopy. Arthroscopy. 2011;27(4):532-541.
15. Samra SK, Dy EA, Welch K, Dorje P, Zelenock GB, Stanley JC. Evaluation of a cerebral oximeter as a monitor of cerebral ischemia during carotid endarterectomy. Anesthesiology. 2000;93(4):964-970.
16. Smythe PR, Samra SK. Monitors of cerebral oxygenation. Anesthesiol Clin North Am. 2002;20(2):293-313.
17. Smith JJ, Porth CM, Erickson M. Hemodynamic response to the upright posture. J Clin Pharmacol. 1994;34(5):375-386.
18. Rohrbaugh M, Kentor ML, Orebaugh SL, Williams B. Outcomes of shoulder surgery in the sitting position with interscalene nerve block: a single-center series. Reg Anesth Pain Med. 2013;38(1):28-33.
19. Pin-on P, Schroeder D, Munis J. The hemodynamic management of 5177 neurosurgical and orthopedic patients who underwent surgery in the sitting or “beach chair” position without incidence of adverse neurologic events. Anesth Analg. 2013;116(6):1317-1324.
20. Yadeau JT, Casciano M, Liu SS, et al. Stroke, regional anesthesia in the sitting position, and hypotension: a review of 4169 ambulatory surgery patients. Reg Anesth Pain Med. 2011;36(5):430-435.
21. Salazar D, Sears BW, Aghdasi B, et al. Cerebral desaturation events during shoulder arthroscopy in the beach chair position: patient risk factors and neurocognitive effects. J Shoulder Elbow Surg. 2013;22(9):1228-1235.
22. Drummond JC, Lee RR, Howell JP Jr. Focal cerebral ischemia after surgery in the “beach chair” position: the role of a congenital variation of circle of Willis anatomy. Anesth Analg. 2012;114(6):1301-1303.
23. Fischer GW, Torrillo TM, Weiner MM, Rosenblatt MA. The use of cerebral oximetry as a monitor of the adequacy of cerebral perfusion in a patient undergoing shoulder surgery in the beach chair position. Pain Pract. 2009;9(4):304-307.
24. Wong GY, Warner DO, Schroeder DR, et al. Risk of surgery and anesthesia for ischemic stroke. Anesthesiology. 2000;92(2):425-432.
25. Knapp RB, Topkins MJ, Artusio JF Jr. The cerebrovascular accident and coronary occlusion in anesthesia. JAMA. 1962;182:332-334.
26. Landercasper J, Merz BJ, Cogbill TH, et al. Perioperative stroke risk in 173 consecutive patients with a past history of stroke. Arch Surg. 1990;125(8):986-989.
27. Fuchs G, Schwarz G, Kulier A, Litscher G. The influence of positioning on spectroscopic measurements of brain oxygenation. J Neurosurg Anesthesiol. 2000;12(2):75-80.
28. Lovell AT, Owen-Reece H, Elwell CE, Smith M, Goldstone JC. Continuous measurement of cerebral oxygenation by near infrared spectroscopy during induction of anesthesia. Anesth Analg. 1999;88(3):554-558.
29. Madsen PL, Secher NH. Near-infrared oximetry of the brain. Prog Neurobiol. 1999;58(6):541-560.
30. Koh JL, Levin SD, Chehab EL, Murphy GS. Neer award 2012: cerebral oxygenation in the beach chair position: a prospective study on the effect of general anesthesia compared with regional anesthesia and sedation. J Shoulder Elbow Surg. 2013;22:1325-1331.
The beach-chair position (BCP) is commonly used for both arthroscopic and open shoulder surgery. This technique positions the shoulder in an anatomical upright position, facilitating shoulder access and visualization.1 Compared with the lateral decubitus position, the BCP also improves airway access, reduces bleeding, and lessens the risk for brachial plexus injury.2
Despite the advantages of using the BCP, there have been multiple reports of catastrophic neurologic complications, including severe brain damage and death, in relatively healthy patients without any known risk factors.3-6 The definitive etiology of these complications remains unclear, but it has been hypothesized that BCP use may be an independent risk factor for cerebrovascular ischemia,1,5-16 as the upright position can cause hypotension leading to increased risk for cerebral hypoperfusion.7-11,17 Reducing cerebral perfusion pressure below critical thresholds may result in permanent neurologic injury.4-6,14 Therefore, monitoring of cerebral perfusion and optimization of intraoperative cerebral oxygenation have been recommended to help avoid potential neurologic complications. However, a direct relationship between intraoperative cerebral desaturation events (CDEs) and postoperative neurocognitive deficits has not been definitively established.1,9-12
To put into perspective the importance of detecting and preventing CDEs and neurologic complications, we can consider the incidence of fatal pulmonary embolism associated with total joint arthroplasty. Although the incidence is very low, about 0.1% to 2.0%, some form of venous thromboembolism prophylaxis is the standard of care for helping prevent this serious complication. Similarly, catastrophic neurologic complications of upright shoulder arthroscopy are very rare, but it is still important to consider measures that help minimize them.
We reviewed the literature for the incidence of postoperative neurocognitive deficits, number of reported neurocognitive complications, and incidence of intraoperative CDEs in patients who underwent arthroscopic shoulder surgery in the BCP.
Methods
Dr. Salazar and Dr. Hazel independently searched the Medline, Cochrane, and Embase databases for case series, prospective studies, and cohort studies that reported neurocognitive complications associated with the BCP and the incidence of intraoperative CDEs. The authors used beach chair, desaturation, near infrared spectroscopy, and shoulder as medical subject headings (MeSH). In addition, bibliographies of retrieved articles were checked for studies that the search terms may have missed. Eighty-one publications were identified and reviewed for possible inclusion.
Next, the same 2 authors reviewed the titles and abstracts for relevance and determined which articles had potential to contribute to the study. Only English-language publications were considered for inclusion. To review the incidence of postoperative neurocognitive deficits, we included only those studies with more than 25 patients, documentation of postoperative complications, and arthroscopic shoulder surgery performed with the patient in the seated, semi-upright, or BCP. Only studies with at least 25 patients were used in order to increase the power and improve the level of evidence. To review reported cases of neurocognitive complications, we included all relevant case reports and case series. To review the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive deficits, we included studies that reported on use of intraoperative cerebral perfusion monitoring. Modalities used in these studies included near infrared spectroscopy, electroencephalography, and invasive blood pressure monitoring calculated at the brain level. Studies were excluded if they did not involve arthroscopic shoulder surgery or were not conducted with human subjects.
Information recorded for each study included general information such as author and publication year, type of study, number of patients enrolled, type of intraoperative monitoring, anesthesia protocol, number of patients with CDEs, and number of patients with neurocognitive complications after surgery.
Results
Our search identified 81 publications for potential inclusion. Our first aim was to identify the overall incidence of reported neurocognitive deficits after arthroscopic shoulder surgery with the patient in the BCP. We identified 10 studies (Table 1) that met the inclusion criteria. Among the 24,701 patients in these 10 studies, there was only 1 reported case of neurocognitive deficit after surgery, in a mixed prospective-retrospective study of 15,014 cases by Rohrbaugh and colleagues.18 The deficit they reported was an ischemic cerebral vascular accident. The 0.0067% incidence in their study demonstrates how rare the complication is. Two large retrospective studies (Ns = 4169 and 5177 patients) found no postoperative neurocognitive complications.19,20 Only 3 studies performed formal postoperative cognitive testing. Salazar and colleagues21 used the Repeatable Battery for the Assessment of Neuropsychological Status before and after surgery, and Gillespie and colleagues8 and Lee and colleagues10 used the Mini–Mental State Examination before and after surgery. Total incidence of reported neurocognitive deficits from our review was 0.004% (1/24,701).
Our second aim was to review all reported cases of neurocognitive complications after arthroscopic shoulder surgery with the patient in the BCP. We identified 4 publications that fit our inclusion criteria (Table 2). Pohl and Cullen6 described 4 cases of ischemic brain injury after arthroscopic shoulder surgery with the patient in the BCP. Age range was 47 to 57 years. Specific intraoperative cerebral monitoring was not used. However, these patients had several episodes of intraoperative hypotension (systolic blood pressures, 80-90 mm Hg), measured with a traditional blood pressure cuff on the arm. In general, these patients had minimal cerebrovascular risk factors and no known preexisting cerebrovascular disease. Drummond and colleagues22 described an ischemic stroke in a 50-year-old man after arthroscopic subacromial decompression and open rotator cuff repair that resulted in unresolved right hemiplegia. Subsequent diagnostic investigation revealed an asymmetry of the circle of Willis resulting in limited flow to the left anterior and middle cerebral artery distributions. Bhatti and Enneking3 reported the case of a 64-year-old man who lost vision in the right eye immediately after arthroscopic rotator cuff repair. His vision improved spontaneously the next morning and continued to improve over the next 6 months—he regained 20/20 vision with some residual optic neuropathy.
Our third aim was to determine the incidence of intraoperative CDEs during arthroscopic shoulder surgery with the patient in the BCP. Incidence of CDEs varied widely among the 7 studies reviewed (Table 3). Minimum incidence of intraoperative CDE was 0% in a cohort of 30 patients,1 and maximum incidence was 80% in a study of 61 patients,12 all of whom underwent elective arthroscopic shoulder surgery in the BCP. Although there was wide variability in CDE incidence, the studies were consistent with respect to their definition of a CDE. Most authors used a decrease in regional cerebral tissue oxygen saturation of 20% or more from baseline, or an absolute value up to 55%, to define a CDE. None of the 7 studies reviewed reported a clinically significant adverse neurocognitive event.
Discussion
Of concern, there have been several surveys, case reports, and small case series of previously healthy patients who had no known risk factors, underwent arthroscopic shoulder surgery in the BCP, and developed unanticipated postoperative neurologic complications.4-6,14 Beach-chair positioning during surgical procedures has been implicated as a contributing factor leading to cerebral hypoperfusion with potential for cerebral ischemia.1,12,23 These changes in cerebral perfusion pressure are thought to be the major determinant of poor neurologic outcomes. Such reports have exposed the potential need for heightened vigilance, alternative anesthesia techniques, and improved monitoring, though the exact etiology of the central nervous system injuries in this patient population is incompletely understood and is likely multifactorial. Therefore, in this study we wanted to determine the incidence of postoperative neurocognitive deficits and review all reported cases of neurocognitive complications in patients who have undergone arthroscopic shoulder surgery in the BCP. In addition, we wanted to define the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive complications.
According to our review, the incidence of postoperative neurocognitive complications after surgery in the BCP is 0.004% (1/24,701). However, this finding is based only on what has been reported; the true incidence is not known. It is also important to note that the incidence of neurocognitive deficits after many other types of surgery is not known and that surgery itself may be a risk factor for postoperative neurocognitive deficits.24 In their retrospective review of 15,014 patients who underwent arthroscopic shoulder surgery in the BCP at a single institution over an 11-year period, Rohrbaugh and colleagues18 found an overall postoperative complication rate of 0.37% and a 0.0067% incidence of neurocognitive deficits. One patient in the series was given a diagnosis of ischemic stroke on the basis of neurologic deficits that occurred 24 hours after surgery. Yadeau and colleagues20 found no postoperative neurocognitive complications in a mixed prospective-retrospective study of 4169 patients—3000 identified retrospectively, 1169 prospectively—who underwent arthroscopic shoulder surgery in the BCP at an ambulatory surgery center. Pin-on and colleagues19 reported on a series of 5177 orthopedic and neurosurgical patients who underwent surgery in the BCP. In those who had arthroscopic shoulder surgery, intraoperative systolic blood pressures obtained from an arterial line referenced to heart level decreased a mean (SD) of 14.4% (12.7%), whereas in those whose pressures were obtained from a noninvasive blood pressure cuff referenced to heart level decreased 19.3% (12.6%). However, the authors reported no incidence of postoperative stroke or neurologic deficits.
Although uncommon, perioperative cerebral ischemic accidents are potentially devastating for patients, their families, and the health care professionals involved. These events have tremendous economic, social, professional, and medicolegal implications, with perioperative stroke being particularly morbid. Perioperative stroke has a mortality rate of 60%, versus 15% to 46% for stroke in general.25,26 In 2005, Pohl and Cullen6 published a landmark article on a series of 4 relatively healthy middle-aged patients who were at low risk for stroke but had catastrophic neurocognitive complications (including 1 death) after arthroscopic shoulder surgery in the BCP. Bhatti and Enneking3 described a case of acute postoperative vision loss and ophthalmoplegia attributed to intraoperative hypotension leading to ischemia in a patient who underwent an elective shoulder arthroscopic procedure in the BCP. These reports prompted multiple investigations into the physiologic hemodynamic changes associated with surgery in the BCP and the treatment strategies used to improve patient safety.
In the normal physiologic state, the sympathetic nervous system is activated when a person assumes the seated position. The result is increased systemic vascular resistance and heart rate alterations to maintain cardiac output and mean arterial pressure. In anesthetized patients, this response is blunted by the vasodilatory effects of intravenous and volatile anesthetics. Multiple studies have demonstrated substantial hemodynamic changes in both awake and anesthetized patients during the maneuver from the supine position to the seated position1,27,28; these changes include diminished cardiac index, stroke volume, and arterial pressure.17 The data underscore the need for attentiveness and accurate monitoring of cerebral perfusion when the transition is made from the supine position to the BCP, particularly in the early phase of surgery and in high-risk patients.
Knowledge of these hemodynamic changes has led several authors to recommend additional intraoperative monitoring of cerebral perfusion. Monitoring techniques have included use of invasive blood pressure monitoring adjusted to brain level, cerebral oximetry using near infrared spectroscopy, and electroencephalography. However, the clinical relevance of intraoperative CDEs in isolation is not well understood.1,6,7,23 In addition, cost and availability of additional advanced monitoring likely factor into why it is not more commonly used. For this patient population, the severity, frequency, and duration of desaturation that causes cerebral ischemia and the relationship with postoperative neurocognitive deficits remain undefined.
The incidence of CDEs in patients being monitored with near infrared spectroscopy while undergoing elective arthroscopic shoulder surgery in the BCP varies widely, from 0% to 80% (mean, 41%).1,4,7,10,12,21 Magnitude and duration of cerebral ischemia required to produce neurocognitive dysfunction in this patient population remain unidentified as well. In conscious patients, a 20% reduction in frontal lobe oxygenation is associated with clinical manifestations of cerebral hypoperfusion, such as syncope.15,29 As none of the patients in the studies we reviewed experienced any sort of deficit, we cannot definitively state there is a correlation between CDE occurrence and neurocognitive deficit.
One limitation of our investigation is that it was a systemic review, and thus there was substantial heterogeneity in the methods and designs of the studies included in the analysis. Among the different series, there was variability in multiple aspects of the study design, including type of anesthetic, patient inclusion criteria, type of surgery, type of intraoperative cerebral perfusion monitoring, and type of neurocognitive testing. As a result, comparing the groups was difficult, and the generalizability of our findings may be limited. In addition, it is difficult to accurately establish incidence and comprehensively review these events because of the paucity of literature.
Conclusion
Neurocognitive complications after shoulder arthroscopy with the patient in the BCP are extremely rare but potentially devastating events that can affect healthy patients with no preexisting cerebrovascular risk factors. Our review indicated the incidence of permanent neurologic deficit after arthroscopy in the BCP may be as low as 0.004%. The exact etiology of such complications is not clear. Basic science research and large prospective studies are needed to identify the clinically relevant thresholds of magnitude, duration, and frequency of intraoperative CDEs in order to establish their relationship with postoperative neurocognitive complications. Such large studies may also elucidate modifiable patient-specific risk factors and establish the most sensitive, safe, and cost-effective intraoperative monitoring tools. Current literature suggests that accurate intraoperative monitoring of cerebral perfusion, alternatives to general anesthesia, and prudent use of intraoperative blood pressure control may improve patient safety.
The beach-chair position (BCP) is commonly used for both arthroscopic and open shoulder surgery. This technique positions the shoulder in an anatomical upright position, facilitating shoulder access and visualization.1 Compared with the lateral decubitus position, the BCP also improves airway access, reduces bleeding, and lessens the risk for brachial plexus injury.2
Despite the advantages of using the BCP, there have been multiple reports of catastrophic neurologic complications, including severe brain damage and death, in relatively healthy patients without any known risk factors.3-6 The definitive etiology of these complications remains unclear, but it has been hypothesized that BCP use may be an independent risk factor for cerebrovascular ischemia,1,5-16 as the upright position can cause hypotension leading to increased risk for cerebral hypoperfusion.7-11,17 Reducing cerebral perfusion pressure below critical thresholds may result in permanent neurologic injury.4-6,14 Therefore, monitoring of cerebral perfusion and optimization of intraoperative cerebral oxygenation have been recommended to help avoid potential neurologic complications. However, a direct relationship between intraoperative cerebral desaturation events (CDEs) and postoperative neurocognitive deficits has not been definitively established.1,9-12
To put into perspective the importance of detecting and preventing CDEs and neurologic complications, we can consider the incidence of fatal pulmonary embolism associated with total joint arthroplasty. Although the incidence is very low, about 0.1% to 2.0%, some form of venous thromboembolism prophylaxis is the standard of care for helping prevent this serious complication. Similarly, catastrophic neurologic complications of upright shoulder arthroscopy are very rare, but it is still important to consider measures that help minimize them.
We reviewed the literature for the incidence of postoperative neurocognitive deficits, number of reported neurocognitive complications, and incidence of intraoperative CDEs in patients who underwent arthroscopic shoulder surgery in the BCP.
Methods
Dr. Salazar and Dr. Hazel independently searched the Medline, Cochrane, and Embase databases for case series, prospective studies, and cohort studies that reported neurocognitive complications associated with the BCP and the incidence of intraoperative CDEs. The authors used beach chair, desaturation, near infrared spectroscopy, and shoulder as medical subject headings (MeSH). In addition, bibliographies of retrieved articles were checked for studies that the search terms may have missed. Eighty-one publications were identified and reviewed for possible inclusion.
Next, the same 2 authors reviewed the titles and abstracts for relevance and determined which articles had potential to contribute to the study. Only English-language publications were considered for inclusion. To review the incidence of postoperative neurocognitive deficits, we included only those studies with more than 25 patients, documentation of postoperative complications, and arthroscopic shoulder surgery performed with the patient in the seated, semi-upright, or BCP. Only studies with at least 25 patients were used in order to increase the power and improve the level of evidence. To review reported cases of neurocognitive complications, we included all relevant case reports and case series. To review the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive deficits, we included studies that reported on use of intraoperative cerebral perfusion monitoring. Modalities used in these studies included near infrared spectroscopy, electroencephalography, and invasive blood pressure monitoring calculated at the brain level. Studies were excluded if they did not involve arthroscopic shoulder surgery or were not conducted with human subjects.
Information recorded for each study included general information such as author and publication year, type of study, number of patients enrolled, type of intraoperative monitoring, anesthesia protocol, number of patients with CDEs, and number of patients with neurocognitive complications after surgery.
Results
Our search identified 81 publications for potential inclusion. Our first aim was to identify the overall incidence of reported neurocognitive deficits after arthroscopic shoulder surgery with the patient in the BCP. We identified 10 studies (Table 1) that met the inclusion criteria. Among the 24,701 patients in these 10 studies, there was only 1 reported case of neurocognitive deficit after surgery, in a mixed prospective-retrospective study of 15,014 cases by Rohrbaugh and colleagues.18 The deficit they reported was an ischemic cerebral vascular accident. The 0.0067% incidence in their study demonstrates how rare the complication is. Two large retrospective studies (Ns = 4169 and 5177 patients) found no postoperative neurocognitive complications.19,20 Only 3 studies performed formal postoperative cognitive testing. Salazar and colleagues21 used the Repeatable Battery for the Assessment of Neuropsychological Status before and after surgery, and Gillespie and colleagues8 and Lee and colleagues10 used the Mini–Mental State Examination before and after surgery. Total incidence of reported neurocognitive deficits from our review was 0.004% (1/24,701).
Our second aim was to review all reported cases of neurocognitive complications after arthroscopic shoulder surgery with the patient in the BCP. We identified 4 publications that fit our inclusion criteria (Table 2). Pohl and Cullen6 described 4 cases of ischemic brain injury after arthroscopic shoulder surgery with the patient in the BCP. Age range was 47 to 57 years. Specific intraoperative cerebral monitoring was not used. However, these patients had several episodes of intraoperative hypotension (systolic blood pressures, 80-90 mm Hg), measured with a traditional blood pressure cuff on the arm. In general, these patients had minimal cerebrovascular risk factors and no known preexisting cerebrovascular disease. Drummond and colleagues22 described an ischemic stroke in a 50-year-old man after arthroscopic subacromial decompression and open rotator cuff repair that resulted in unresolved right hemiplegia. Subsequent diagnostic investigation revealed an asymmetry of the circle of Willis resulting in limited flow to the left anterior and middle cerebral artery distributions. Bhatti and Enneking3 reported the case of a 64-year-old man who lost vision in the right eye immediately after arthroscopic rotator cuff repair. His vision improved spontaneously the next morning and continued to improve over the next 6 months—he regained 20/20 vision with some residual optic neuropathy.
Our third aim was to determine the incidence of intraoperative CDEs during arthroscopic shoulder surgery with the patient in the BCP. Incidence of CDEs varied widely among the 7 studies reviewed (Table 3). Minimum incidence of intraoperative CDE was 0% in a cohort of 30 patients,1 and maximum incidence was 80% in a study of 61 patients,12 all of whom underwent elective arthroscopic shoulder surgery in the BCP. Although there was wide variability in CDE incidence, the studies were consistent with respect to their definition of a CDE. Most authors used a decrease in regional cerebral tissue oxygen saturation of 20% or more from baseline, or an absolute value up to 55%, to define a CDE. None of the 7 studies reviewed reported a clinically significant adverse neurocognitive event.
Discussion
Of concern, there have been several surveys, case reports, and small case series of previously healthy patients who had no known risk factors, underwent arthroscopic shoulder surgery in the BCP, and developed unanticipated postoperative neurologic complications.4-6,14 Beach-chair positioning during surgical procedures has been implicated as a contributing factor leading to cerebral hypoperfusion with potential for cerebral ischemia.1,12,23 These changes in cerebral perfusion pressure are thought to be the major determinant of poor neurologic outcomes. Such reports have exposed the potential need for heightened vigilance, alternative anesthesia techniques, and improved monitoring, though the exact etiology of the central nervous system injuries in this patient population is incompletely understood and is likely multifactorial. Therefore, in this study we wanted to determine the incidence of postoperative neurocognitive deficits and review all reported cases of neurocognitive complications in patients who have undergone arthroscopic shoulder surgery in the BCP. In addition, we wanted to define the incidence of intraoperative CDEs and investigate their relationship with postoperative neurocognitive complications.
According to our review, the incidence of postoperative neurocognitive complications after surgery in the BCP is 0.004% (1/24,701). However, this finding is based only on what has been reported; the true incidence is not known. It is also important to note that the incidence of neurocognitive deficits after many other types of surgery is not known and that surgery itself may be a risk factor for postoperative neurocognitive deficits.24 In their retrospective review of 15,014 patients who underwent arthroscopic shoulder surgery in the BCP at a single institution over an 11-year period, Rohrbaugh and colleagues18 found an overall postoperative complication rate of 0.37% and a 0.0067% incidence of neurocognitive deficits. One patient in the series was given a diagnosis of ischemic stroke on the basis of neurologic deficits that occurred 24 hours after surgery. Yadeau and colleagues20 found no postoperative neurocognitive complications in a mixed prospective-retrospective study of 4169 patients—3000 identified retrospectively, 1169 prospectively—who underwent arthroscopic shoulder surgery in the BCP at an ambulatory surgery center. Pin-on and colleagues19 reported on a series of 5177 orthopedic and neurosurgical patients who underwent surgery in the BCP. In those who had arthroscopic shoulder surgery, intraoperative systolic blood pressures obtained from an arterial line referenced to heart level decreased a mean (SD) of 14.4% (12.7%), whereas in those whose pressures were obtained from a noninvasive blood pressure cuff referenced to heart level decreased 19.3% (12.6%). However, the authors reported no incidence of postoperative stroke or neurologic deficits.
Although uncommon, perioperative cerebral ischemic accidents are potentially devastating for patients, their families, and the health care professionals involved. These events have tremendous economic, social, professional, and medicolegal implications, with perioperative stroke being particularly morbid. Perioperative stroke has a mortality rate of 60%, versus 15% to 46% for stroke in general.25,26 In 2005, Pohl and Cullen6 published a landmark article on a series of 4 relatively healthy middle-aged patients who were at low risk for stroke but had catastrophic neurocognitive complications (including 1 death) after arthroscopic shoulder surgery in the BCP. Bhatti and Enneking3 described a case of acute postoperative vision loss and ophthalmoplegia attributed to intraoperative hypotension leading to ischemia in a patient who underwent an elective shoulder arthroscopic procedure in the BCP. These reports prompted multiple investigations into the physiologic hemodynamic changes associated with surgery in the BCP and the treatment strategies used to improve patient safety.
In the normal physiologic state, the sympathetic nervous system is activated when a person assumes the seated position. The result is increased systemic vascular resistance and heart rate alterations to maintain cardiac output and mean arterial pressure. In anesthetized patients, this response is blunted by the vasodilatory effects of intravenous and volatile anesthetics. Multiple studies have demonstrated substantial hemodynamic changes in both awake and anesthetized patients during the maneuver from the supine position to the seated position1,27,28; these changes include diminished cardiac index, stroke volume, and arterial pressure.17 The data underscore the need for attentiveness and accurate monitoring of cerebral perfusion when the transition is made from the supine position to the BCP, particularly in the early phase of surgery and in high-risk patients.
Knowledge of these hemodynamic changes has led several authors to recommend additional intraoperative monitoring of cerebral perfusion. Monitoring techniques have included use of invasive blood pressure monitoring adjusted to brain level, cerebral oximetry using near infrared spectroscopy, and electroencephalography. However, the clinical relevance of intraoperative CDEs in isolation is not well understood.1,6,7,23 In addition, cost and availability of additional advanced monitoring likely factor into why it is not more commonly used. For this patient population, the severity, frequency, and duration of desaturation that causes cerebral ischemia and the relationship with postoperative neurocognitive deficits remain undefined.
The incidence of CDEs in patients being monitored with near infrared spectroscopy while undergoing elective arthroscopic shoulder surgery in the BCP varies widely, from 0% to 80% (mean, 41%).1,4,7,10,12,21 Magnitude and duration of cerebral ischemia required to produce neurocognitive dysfunction in this patient population remain unidentified as well. In conscious patients, a 20% reduction in frontal lobe oxygenation is associated with clinical manifestations of cerebral hypoperfusion, such as syncope.15,29 As none of the patients in the studies we reviewed experienced any sort of deficit, we cannot definitively state there is a correlation between CDE occurrence and neurocognitive deficit.
One limitation of our investigation is that it was a systemic review, and thus there was substantial heterogeneity in the methods and designs of the studies included in the analysis. Among the different series, there was variability in multiple aspects of the study design, including type of anesthetic, patient inclusion criteria, type of surgery, type of intraoperative cerebral perfusion monitoring, and type of neurocognitive testing. As a result, comparing the groups was difficult, and the generalizability of our findings may be limited. In addition, it is difficult to accurately establish incidence and comprehensively review these events because of the paucity of literature.
Conclusion
Neurocognitive complications after shoulder arthroscopy with the patient in the BCP are extremely rare but potentially devastating events that can affect healthy patients with no preexisting cerebrovascular risk factors. Our review indicated the incidence of permanent neurologic deficit after arthroscopy in the BCP may be as low as 0.004%. The exact etiology of such complications is not clear. Basic science research and large prospective studies are needed to identify the clinically relevant thresholds of magnitude, duration, and frequency of intraoperative CDEs in order to establish their relationship with postoperative neurocognitive complications. Such large studies may also elucidate modifiable patient-specific risk factors and establish the most sensitive, safe, and cost-effective intraoperative monitoring tools. Current literature suggests that accurate intraoperative monitoring of cerebral perfusion, alternatives to general anesthesia, and prudent use of intraoperative blood pressure control may improve patient safety.
1. Tange K, Kinoshita H, Minonishi T, et al. Cerebral oxygenation in the beach chair position before and during general anesthesia. Minerva Anestesiol. 2010;76(7):485-490.
2. Skyhar MJ, Altchek DW, Warren RF, Wickiewicz TL, O’Brien SJ. Shoulder arthroscopy with the patient in the beach-chair position. Arthroscopy. 1988;4(4):256-259.
3. Bhatti MT, Enneking FK. Visual loss and ophthalmoplegia after shoulder surgery. Anesth Analg. 2003;96(3):899-902.
4. Friedman DJ, Parnes NZ, Zimmer Z, Higgins LD, Warner JJ. Prevalence of cerebrovascular events during shoulder surgery and association with patient position. Orthopedics. 2009;32(4).
5. Papadonikolakis A, Wiesler ER, Olympio MA, Poehling GG. Avoiding catastrophic complications of stroke and death related to shoulder surgery in the sitting position. Arthroscopy. 2008;24(4):481-482.
6. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17(6):463-469.
7. Dippmann C, Winge S, Nielsen HB. Severe cerebral desaturation during shoulder arthroscopy in the beach-chair position. Arthroscopy. 2010;26(9 suppl):S148-S150.
8. Gillespie R, Shishani Y, Streit J, et al. The safety of controlled hypotension for shoulder arthroscopy in the beach-chair position. J Bone Joint Surg Am. 2012;94(14):1284-1290.
9. Jeong H, Lee SH, Jang EA, Chung SS, Lee J, Yoo KY. Haemodynamics and cerebral oxygenation during arthroscopic shoulder surgery in beach chair position under general anaesthesia. Acta Anaesthesiol Scand. 2012;56(7):872-879.
10. Lee JH, Min KT, Chun YM, Kim EJ, Choi SH. Effects of beach-chair position and induced hypotension on cerebral oxygen saturation in patients undergoing arthroscopic shoulder surgery. Arthroscopy. 2011;27(7):889-894.
11. Moerman AT, De Hert SG, Jacobs TF, De Wilde LF, Wouters PF. Cerebral oxygen desaturation during beach chair position. Eur J Anaesthesiol. 2012;29(2):82-87.
12. Murphy GS, Szokol JW, Marymont JH, et al. Cerebral oxygen desaturation events assessed by near-infrared spectroscopy during shoulder arthroscopy in the beach chair and lateral decubitus positions. Anesth Analg. 2010;111(2):496-505.
13. Peruto CM, Ciccotti MG, Cohen SB. Shoulder arthroscopy positioning: lateral decubitus versus beach chair. Arthroscopy. 2009;25(8):891-896.
14. Rains DD, Rooke GA, Wahl CJ. Pathomechanisms and complications related to patient positioning and anesthesia during shoulder arthroscopy. Arthroscopy. 2011;27(4):532-541.
15. Samra SK, Dy EA, Welch K, Dorje P, Zelenock GB, Stanley JC. Evaluation of a cerebral oximeter as a monitor of cerebral ischemia during carotid endarterectomy. Anesthesiology. 2000;93(4):964-970.
16. Smythe PR, Samra SK. Monitors of cerebral oxygenation. Anesthesiol Clin North Am. 2002;20(2):293-313.
17. Smith JJ, Porth CM, Erickson M. Hemodynamic response to the upright posture. J Clin Pharmacol. 1994;34(5):375-386.
18. Rohrbaugh M, Kentor ML, Orebaugh SL, Williams B. Outcomes of shoulder surgery in the sitting position with interscalene nerve block: a single-center series. Reg Anesth Pain Med. 2013;38(1):28-33.
19. Pin-on P, Schroeder D, Munis J. The hemodynamic management of 5177 neurosurgical and orthopedic patients who underwent surgery in the sitting or “beach chair” position without incidence of adverse neurologic events. Anesth Analg. 2013;116(6):1317-1324.
20. Yadeau JT, Casciano M, Liu SS, et al. Stroke, regional anesthesia in the sitting position, and hypotension: a review of 4169 ambulatory surgery patients. Reg Anesth Pain Med. 2011;36(5):430-435.
21. Salazar D, Sears BW, Aghdasi B, et al. Cerebral desaturation events during shoulder arthroscopy in the beach chair position: patient risk factors and neurocognitive effects. J Shoulder Elbow Surg. 2013;22(9):1228-1235.
22. Drummond JC, Lee RR, Howell JP Jr. Focal cerebral ischemia after surgery in the “beach chair” position: the role of a congenital variation of circle of Willis anatomy. Anesth Analg. 2012;114(6):1301-1303.
23. Fischer GW, Torrillo TM, Weiner MM, Rosenblatt MA. The use of cerebral oximetry as a monitor of the adequacy of cerebral perfusion in a patient undergoing shoulder surgery in the beach chair position. Pain Pract. 2009;9(4):304-307.
24. Wong GY, Warner DO, Schroeder DR, et al. Risk of surgery and anesthesia for ischemic stroke. Anesthesiology. 2000;92(2):425-432.
25. Knapp RB, Topkins MJ, Artusio JF Jr. The cerebrovascular accident and coronary occlusion in anesthesia. JAMA. 1962;182:332-334.
26. Landercasper J, Merz BJ, Cogbill TH, et al. Perioperative stroke risk in 173 consecutive patients with a past history of stroke. Arch Surg. 1990;125(8):986-989.
27. Fuchs G, Schwarz G, Kulier A, Litscher G. The influence of positioning on spectroscopic measurements of brain oxygenation. J Neurosurg Anesthesiol. 2000;12(2):75-80.
28. Lovell AT, Owen-Reece H, Elwell CE, Smith M, Goldstone JC. Continuous measurement of cerebral oxygenation by near infrared spectroscopy during induction of anesthesia. Anesth Analg. 1999;88(3):554-558.
29. Madsen PL, Secher NH. Near-infrared oximetry of the brain. Prog Neurobiol. 1999;58(6):541-560.
30. Koh JL, Levin SD, Chehab EL, Murphy GS. Neer award 2012: cerebral oxygenation in the beach chair position: a prospective study on the effect of general anesthesia compared with regional anesthesia and sedation. J Shoulder Elbow Surg. 2013;22:1325-1331.
1. Tange K, Kinoshita H, Minonishi T, et al. Cerebral oxygenation in the beach chair position before and during general anesthesia. Minerva Anestesiol. 2010;76(7):485-490.
2. Skyhar MJ, Altchek DW, Warren RF, Wickiewicz TL, O’Brien SJ. Shoulder arthroscopy with the patient in the beach-chair position. Arthroscopy. 1988;4(4):256-259.
3. Bhatti MT, Enneking FK. Visual loss and ophthalmoplegia after shoulder surgery. Anesth Analg. 2003;96(3):899-902.
4. Friedman DJ, Parnes NZ, Zimmer Z, Higgins LD, Warner JJ. Prevalence of cerebrovascular events during shoulder surgery and association with patient position. Orthopedics. 2009;32(4).
5. Papadonikolakis A, Wiesler ER, Olympio MA, Poehling GG. Avoiding catastrophic complications of stroke and death related to shoulder surgery in the sitting position. Arthroscopy. 2008;24(4):481-482.
6. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17(6):463-469.
7. Dippmann C, Winge S, Nielsen HB. Severe cerebral desaturation during shoulder arthroscopy in the beach-chair position. Arthroscopy. 2010;26(9 suppl):S148-S150.
8. Gillespie R, Shishani Y, Streit J, et al. The safety of controlled hypotension for shoulder arthroscopy in the beach-chair position. J Bone Joint Surg Am. 2012;94(14):1284-1290.
9. Jeong H, Lee SH, Jang EA, Chung SS, Lee J, Yoo KY. Haemodynamics and cerebral oxygenation during arthroscopic shoulder surgery in beach chair position under general anaesthesia. Acta Anaesthesiol Scand. 2012;56(7):872-879.
10. Lee JH, Min KT, Chun YM, Kim EJ, Choi SH. Effects of beach-chair position and induced hypotension on cerebral oxygen saturation in patients undergoing arthroscopic shoulder surgery. Arthroscopy. 2011;27(7):889-894.
11. Moerman AT, De Hert SG, Jacobs TF, De Wilde LF, Wouters PF. Cerebral oxygen desaturation during beach chair position. Eur J Anaesthesiol. 2012;29(2):82-87.
12. Murphy GS, Szokol JW, Marymont JH, et al. Cerebral oxygen desaturation events assessed by near-infrared spectroscopy during shoulder arthroscopy in the beach chair and lateral decubitus positions. Anesth Analg. 2010;111(2):496-505.
13. Peruto CM, Ciccotti MG, Cohen SB. Shoulder arthroscopy positioning: lateral decubitus versus beach chair. Arthroscopy. 2009;25(8):891-896.
14. Rains DD, Rooke GA, Wahl CJ. Pathomechanisms and complications related to patient positioning and anesthesia during shoulder arthroscopy. Arthroscopy. 2011;27(4):532-541.
15. Samra SK, Dy EA, Welch K, Dorje P, Zelenock GB, Stanley JC. Evaluation of a cerebral oximeter as a monitor of cerebral ischemia during carotid endarterectomy. Anesthesiology. 2000;93(4):964-970.
16. Smythe PR, Samra SK. Monitors of cerebral oxygenation. Anesthesiol Clin North Am. 2002;20(2):293-313.
17. Smith JJ, Porth CM, Erickson M. Hemodynamic response to the upright posture. J Clin Pharmacol. 1994;34(5):375-386.
18. Rohrbaugh M, Kentor ML, Orebaugh SL, Williams B. Outcomes of shoulder surgery in the sitting position with interscalene nerve block: a single-center series. Reg Anesth Pain Med. 2013;38(1):28-33.
19. Pin-on P, Schroeder D, Munis J. The hemodynamic management of 5177 neurosurgical and orthopedic patients who underwent surgery in the sitting or “beach chair” position without incidence of adverse neurologic events. Anesth Analg. 2013;116(6):1317-1324.
20. Yadeau JT, Casciano M, Liu SS, et al. Stroke, regional anesthesia in the sitting position, and hypotension: a review of 4169 ambulatory surgery patients. Reg Anesth Pain Med. 2011;36(5):430-435.
21. Salazar D, Sears BW, Aghdasi B, et al. Cerebral desaturation events during shoulder arthroscopy in the beach chair position: patient risk factors and neurocognitive effects. J Shoulder Elbow Surg. 2013;22(9):1228-1235.
22. Drummond JC, Lee RR, Howell JP Jr. Focal cerebral ischemia after surgery in the “beach chair” position: the role of a congenital variation of circle of Willis anatomy. Anesth Analg. 2012;114(6):1301-1303.
23. Fischer GW, Torrillo TM, Weiner MM, Rosenblatt MA. The use of cerebral oximetry as a monitor of the adequacy of cerebral perfusion in a patient undergoing shoulder surgery in the beach chair position. Pain Pract. 2009;9(4):304-307.
24. Wong GY, Warner DO, Schroeder DR, et al. Risk of surgery and anesthesia for ischemic stroke. Anesthesiology. 2000;92(2):425-432.
25. Knapp RB, Topkins MJ, Artusio JF Jr. The cerebrovascular accident and coronary occlusion in anesthesia. JAMA. 1962;182:332-334.
26. Landercasper J, Merz BJ, Cogbill TH, et al. Perioperative stroke risk in 173 consecutive patients with a past history of stroke. Arch Surg. 1990;125(8):986-989.
27. Fuchs G, Schwarz G, Kulier A, Litscher G. The influence of positioning on spectroscopic measurements of brain oxygenation. J Neurosurg Anesthesiol. 2000;12(2):75-80.
28. Lovell AT, Owen-Reece H, Elwell CE, Smith M, Goldstone JC. Continuous measurement of cerebral oxygenation by near infrared spectroscopy during induction of anesthesia. Anesth Analg. 1999;88(3):554-558.
29. Madsen PL, Secher NH. Near-infrared oximetry of the brain. Prog Neurobiol. 1999;58(6):541-560.
30. Koh JL, Levin SD, Chehab EL, Murphy GS. Neer award 2012: cerebral oxygenation in the beach chair position: a prospective study on the effect of general anesthesia compared with regional anesthesia and sedation. J Shoulder Elbow Surg. 2013;22:1325-1331.
Arthroscopic Management of Full-Thickness Rotator Cuff Tears in Major League Baseball Pitchers: The Lateralized Footprint Repair Technique
Rotator cuff injuries can be a source of debilitating pain and dysfunction in athletes at all levels, occasionally precluding return to competitive sport. Overhead athletes place extraordinary physiologic demands on the shoulder, as humeral angular velocities of 7000° to 8000° per second and rotational torques higher than 70 Nm have been measured during the baseball pitch.1 Repetitive supraphysiologic loading of the rotator cuff throughout the coordinated phases of throwing can result in a characteristic spectrum of shoulder pathology in overhead throwers. Several studies have demonstrated partial-thickness articular-sided rotator cuff tears (RCTs) in the area of the posterior supraspinatus and anterior infraspinatus tendons.2-4 Although the precise mechanism remains unclear, plausible explanations for the pathogenesis of these injuries include eccentric tensile and shear forces that lead to tendon failure with repetitive throwing, as well as internal impingement (mechanical impingement of the aforementioned tendons against the posterosuperior glenoid at 90° of shoulder abduction and maximum external rotation).5,6
Whereas partial-thickness articular-sided RCTs have been described in overhead athletes with rotator cuff pathology, full-thickness tears are encountered less often.7,8 Accordingly, there is a paucity of literature on clinical outcomes in professional baseball players with these injuries. To our knowledge, only 2 studies have investigated functional outcomes of open surgical repair of full-thickness tears in this population, and the outcomes have been uniformly poor.8,9
An anatomical description of rotator cuff anatomy has demonstrated a consistent pattern of supraspinatus and infraspinatus tendon insertion relative to the articular surface, biceps groove, and the bare area of the humerus.10 Using gross and microscopic analyses, the authors noted that the supraspinatus tendon inserted immediately adjacent to the articular margin, and the infraspinatus and teres minor tapered laterally away from the margin to form the bare area. Detailed knowledge of the insertional anatomy of the rotator cuff is important, as surgical repair should recreate the broad footprint to restore normal biomechanics and increase the surface area available for healing.11,12 Medial advancement of the rotator cuff insertion during surgical repair can have deleterious biomechanical effects on glenohumeral motion.11
Given the unfavorable results found after routine open repair of full-thickness tears, we altered our approach to these injuries and adopted an arthroscopic technique in which the tendon is repaired immediately lateral to the anatomical footprint. Research studies have demonstrated that chronic stress from repetitive throwing can lead to attenuation of soft-tissue restraints, and we think preservation of these adaptive changes after surgical repair may be important for these athletes to maintain extraordinary glenohumeral rotation and achieve high throwing velocities.13 We conducted a study to describe the lateralized repair technique for full-thickness RCTs and to report functional outcomes in Major League Baseball (MLB) pitchers treated with this procedure at minimum 2-year follow-up. We hypothesized that use of this novel technique would result in a higher rate of return to preinjury level of play in comparison with open rotator cuff repair in comparable cohorts, as reported in other studies.8,9
Materials and Methods
After obtaining Institutional Review Board approval for this study, we performed a retrospective chart review of MLB players treated by Dr. Altchek. We identified all professional baseball players who received a diagnosis of full-thickness RCT after preoperative magnetic resonance imaging with subsequent confirmation during surgery. Any patient who underwent arthroscopic repair using the lateralized footprint technique was included in the study. Demographic and preoperative injury information was collected from the chart, and final follow-up data were collected at the last available clinic visit. From available team records, we also obtained return-to-play data and objective pitching statistics: seasons played, games played, innings pitched, strikeouts per 9 innings, walks per 9 innings, and earned run average.
Surgical Technique
We routinely perform arthroscopic rotator cuff repairs with the patient under regional anesthesia in the beach-chair position. The operative extremity is placed in a Spider Limb Positioner (Smith & Nephew) to facilitate easy manipulation of the arm throughout the procedure. A standard posterior portal is established, and then an anterior portal is placed in the superolateral aspect of the rotator interval directly anterior to the leading edge of the supraspinatus tendon. A lateral portal created 2 to 3 cm distal to the anterolateral margin of the acromion may be used as an additional working portal. A thorough diagnostic arthroscopy is performed to evaluate the glenohumeral joint for any concomitant intra-articular pathology. Particular attention is directed to inspection of the superior labrum, biceps tendon, and capsuloligamentous structures, as injuries to these structures are often associated with rotator cuff pathology in overhead athletes.
Once presence of an RCT is confirmed, a thorough subacromial bursectomy is performed to help with visualization and inspection of the injury. The tissue is provisionally grasped and mobilized to measure the amount of available tendon excursion. In this unique population, the vast majority of injuries are diagnosed in an expeditious manner, thereby precluding the presence of significant retraction, poor tissue quality, and inadequate mobilization of the tendons. The greater tuberosity is identified, and the area immediately adjacent to the articular margin is abraded with a mechanical shaver to enhance healing potential. For supraspinatus tears, an anchor is placed immediately lateral to the articular margin in the region of the anterior attachment of the rotator cable (Figure 1). The posterior anchor is placed about 10 to 15 mm lateral to the articular margin to reattach the infraspinatus tendon (Figure 2). When the medial row sutures are tied down, anatomical placement of these anchors effectively re-creates the bare area described by Curtis and colleagues10 (Figure 3). In most cases, the medial row sutures are left intact and fixed laterally with a knotless anchor to provide a transosseous equivalent (double-row) repair.
Results
We identified 6 MLB pitchers who underwent arthroscopic rotator cuff repair using the aforementioned technique over an 8-year period. Each patient presented with complaints of debilitating shoulder pain and decreased pitching performance, including loss of throwing accuracy and velocity. There were 4 right-hand–dominant pitchers and 2 left-hand–dominant pitchers; rotator cuff pathology was observed in the dominant pitching arm in each case. Three players were classified as starting pitchers; the other 3 pitched in a relief role. Mean age of all pitchers at time of surgery was 29.8 years (range, 25-37 years). According to records, 2 patients (33%) underwent previous rotator cuff débridement for partial-thickness RCTs before surgical intervention at our institution. Operative information on the depth of the partial-thickness tears observed during the previous procedures was not available for review. At time of rotator cuff repair, 3 patients (50%) underwent concomitant procedures, including superior labrum anterior-posterior (SLAP) lesion repair (1 patient) and posterior labrum débridement (2 patients). A double-row fixation construct was achieved in each case. Review of operative records revealed a mean tear size of 2.1 cm (range, 1.5-3.0 cm) measured anterior to posterior, and all tears involved the supraspinatus and/or infraspinatus tendons. Postoperative rehabilitation included immobilization in a sling for 4 weeks. Hand, wrist, and elbow range-of-motion (ROM) exercises were started immediately to help reduce inflammation. Passive ROM exercises in the plane of the scapula were begun 4 weeks after surgery. Isometric scapular stabilization exercises were also incorporated at that time. Active-assisted ROM exercises were started at about 6 weeks, and isometric strengthening exercises were started at week 8 with progression to eccentric strengthening and weight training at about 3 months. Most pitchers were allowed to begin an interval throwing program at 24 weeks. There were no significant differences in the therapy programs for pitchers who underwent concomitant labral procedures, but the patient who underwent SLAP repair was limited to 30° of external rotation and 90° of forward flexion, with avoidance of active biceps contractions, for the first 6 weeks of rehabilitation.
By mean follow-up of 66.7 months (range, 23.2-94.6 months), 5 pitchers (83%) returned to their preinjury level of competition for at least 1 full season. One player pitched at Minor League Class AA level for about 1 season but was forced to retire because of persistent symptoms related to the shoulder. This pitcher underwent simultaneous rotator cuff and SLAP lesion repair. Of the 5 pitchers who resumed MLB play, none returned to their preoperative pitching productivity; mean number of innings pitched decreased from 1806.5 to 183.7. Three (60%) of these 5 pitchers experienced a slight reduction in performance as measured by earned run average. Interestingly, both players over age 30 years at time of surgery, versus 3 of the 4 pitchers under age 30 years, returned to their preoperative level of competition for at least 1 season. The Table summarizes MLB player data and objective pitching statistics. There were no perioperative complications related to this arthroscopic technique, and there were no glenohumeral ROM deficits at final follow-up.
Discussion
Although the incidence of full-thickness RCTs in professional baseball players is presumably low, available studies suggest that it is a debilitating injury with a poor prognosis for return to high-level athletics. Mazoué and Andrews9 reviewed the outcomes of 16 professional baseball players (12 pitchers, 4 position players) who underwent mini-open repair of full-thickness RCTs that involved more than 90% of the rotator cuff. Fifteen patients underwent mini-open rotator cuff repair using suture anchors in the anatomical footprint along with bone tunnels established near the lateral margin of the greater tuberosity to create a 2-level anatomical repair. One patient was treated with a mini-open repair using suture anchors in the greater tuberosity with a side-side repair of a longitudinal split within the rotator cuff. In the evaluation of outcomes by player position, only 1 pitcher (8%) returned to a competitive level of pitching at a mean follow-up of 67 months. On review of 2 position players with a full-thickness RCT in the dominant shoulder, only 1 (50%) returned to Major League play at a mean follow-up of 62.5 months. The remaining 2 position players underwent surgical repair of the nondominant shoulder, and, not surprisingly, both returned to their previous level of athletic activity without any difficulty. These results should be examined carefully, as the associated pathology in this high-demand cohort should not be discounted. Eleven (almost 92%) of the 12 pitchers had undergone at least 1 previous procedure on the shoulder. Furthermore, at time of full-thickness rotator cuff repair, 9 (75%) of the 12 pitchers were treated for concomitant intra-articular pathology, including SLAP tears, capsular attenuation, and/or labral fraying. In our study, 50% of pitchers underwent an associated labral procedure. Although labral débridement did not have a significant effect on return to play, the 1 pitcher who underwent SLAP repair was not able to return to preinjury level of play.
Tibone and colleagues8 reviewed postoperative outcomes in 45 athletes with rotator cuff pathology. Within their series, 5 professional baseball pitchers with full-thickness tears were treated with open subacromial decompression and rotator cuff repair. Two baseball pitchers with RCTs larger than 2 cm underwent open transosseous footprint repair in which the cuff was reinserted using bone tunnels created within the greater tuberosity. At long-term follow-up, only 2 (40%) of the 5 pitchers returned to competitive pitching. Interestingly, both pitchers who underwent transosseous footprint fixation were unable to return to professional baseball.
Overhead athletes require a delicate balance of shoulder mobility and stability to meet the high functional demands of their sports. Significant debate continues as to whether innate alterations in glenohumeral mobility preselect individuals for overhead sports, or if these changes are acquired through adaptations in supporting soft-tissue and osseous structures. Sethi and colleagues14 used an instrumented manual laxity examination to compare anterior-posterior laxity in asymptomatic professional and Division I college baseball players. The authors noted asymmetric anterior-posterior translation (>3 mm) between the throwing shoulder and the nondominant shoulder in 12 (60%) of 20 professional pitchers and 10 (59%) of 17 college pitchers. Although the authors did not correlate translational differences with corresponding shoulder pathology, the observed asymmetry supported the idea that these athletes may experience adaptive glenohumeral changes with repetitive throwing. The association between adaptive changes and shoulder biomechanics has been studied. Burkhart and Lo15 used a cadaveric model to describe the cam effect of the proximal humerus and the biomechanical consequences of a relative reduction in this effect after pathologic changes within the glenohumeral joint (constriction of posteroinferior capsule). They noted that a posterosuperior shift in the glenohumeral contact point in the throwing position can result in anterior capsular redundancy that may contribute to microinstability of the shoulder. This relative laxity increases external rotation, resulting in increased torsional and shear forces at the rotator cuff insertion.16 Ultimately, these abnormal forces may predispose overhead athletes to rotator cuff injury.
Given the available literature, it is clear that full-thickness RCTs are potentially career-ending injuries for professional baseball players. The question arises as to why the results are so poor. Ultimately, the high incidence of concomitant intra-articular pathology associated with full-thickness RCTs underscores the severity of soft-tissue damage sustained with repetitive overhead throwing. Mazoué and Andrews9 proposed the presence of associated labral and capsular pathology as a potential explanation for poor outcomes of surgical repair. Given the myriad of additional pathology observed in each patient, it is difficult to ascertain the precise impact of these injuries on postoperative outcome. However, early diagnosis and aggressive surgical intervention are clearly necessary to prevent accumulative injury. Regarding surgical intervention, both Tibone and colleagues8 and Mazoué and Andrews9 reported use of an open surgical repair technique in which the tendon was repaired to the anatomical footprint. Certainly, the benefits of an all-arthroscopic technique include optimal visualization of the RCT, less perioperative morbidity, and minimal soft-tissue injury. With our arthroscopic technique, the rotator cuff was fixed immediately lateral to the anatomical footprint, thereby leaving the medial aspect of the footprint uncovered. Functionally, the goal of this procedure is to restore the integrity of the rotator cuff without compromising glenohumeral mobility acquired through soft-tissue adaptation. Investigation of the insertional anatomy of the rotator cuff has demonstrated that the supraspinatus tendon inserts about 0.9 mm from the edge of the articular surface, and the infraspinatus insertional footprint tapers away from the articular surface to form the bare area as it extends inferiorly on the greater tuberosity.10 We think preexisting adaptations in glenohumeral anatomy are important for peak performance in this unique population, and even small alterations in the repair location can have deleterious effects on throwing mechanics. Lateralized repair of the cuff precludes potential medialization of the cuff insertion and may facilitate preservation of soft-tissue adaptations that these athletes rely on to achieve extraordinary glenohumeral motion.
Interestingly, with this technique we noted a higher rate of return to MLB play in pitchers over age 30 years. Although several individual factors (eg, player talent level, work ethics, compliance with rehabilitation) may play a role in this finding, it is possible that older, more mature patients may be more willing to assume diminished roles to continue to play. Jones and colleagues17 recently reported similar findings in older MLB pitchers after revision ulnar collateral ligament reconstruction.
This study had several limitations. First, the patient cohort was small (a result of the nature and relatively infrequent incidence of the clinical problem). Second, clinical information was collected retrospectively, which limited our ability to determine precise differences between preoperative and postoperative glenohumeral ROM with this technique. Third, the cohort included patients who demonstrated additional intra-articular (labral) pathology. Although associated pathology is common in this high-demand athletic population, it is clear that advanced pathology (eg, SLAP tears) may affect clinical outcomes, as in our study. Despite these limitations, our study is the largest review of professional baseball players treated for full-thickness rotator cuff injuries with an arthroscopic technique. Overall, the results of this study are promising and call for further clinical and biomechanical evaluation.
Conclusion
Surgical management of rotator cuff injuries in professional baseball players remains an extremely difficult problem. Current studies of full-thickness RCTs highlight these athletes’ poor functional outcomes. These unfavorable results prompted us to alter our surgical technique. Initial outcomes have been encouraging, and extended follow-up in this cohort of patients will provide a more definitive assessment of the success of this technique.
1. Dillman CJ, Fleisig GS, Andrews JR. Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther. 1993;18(2):402-408.
2. Andrews JR, Broussard TS, Carson WG. Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: a preliminary report. Arthroscopy. 1985;1(2):117-122.
3. Paley KJ, Jobe FW, Pink MM, Kvitne RS, ElAttrache NS. Arthroscopic findings in the overhead throwing athlete: evidence for posterior internal impingement of the rotator cuff. Arthroscopy. 2000;16(1):35-40.
4. Nakagawa S, Yoneda M, Hayashida K, Wakitani S, Okamura K. Greater tuberosity notch: an important indicator of articular-side partial rotator cuff tears in the shoulders of throwing athletes. Am J Sports Med. 2001;29(6):762-770.
5. Walch G, Boileau P, Noel E, Donell ST. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg. 1992;1(5):238-245.
6. Halbrecht JL, Tirman P, Atkin D. Internal impingement of the shoulder: comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy. 1999;15(3):253-258.
7. Reynolds SB, Dugas JR, Cain EL, McMichael CS, Andrews JR. Debridement of small partial-thickness rotator cuff tears in elite overhead throwers. Clin Orthop Relat Res. 2008;466(3):614-621.
8. Tibone JE, Elrod B, Jobe FW, et al. Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg Am. 1986;68(6):887-891.
9. Mazoué C, Andrews JR. Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med. 2006;34():182-189.
10. Curtis AS, Burbank KM, Tierney JJ, Scheller AD, Curran AR. The insertional footprint of the rotator cuff: an anatomic study. Arthroscopy. 2006;22(6):603-609.
11. Liu J, Hughes RE, O’Driscoll SW, An K. Biomechanical effect of medial advancement of the supraspinatus tendon. J Bone Joint Surg Am. 1998;80(6):853-859.
12. Lo IK, Burkhart SS. Double row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy. 2003;19(9):1035-1042.
13. Borsa PA, Laudner KG, Sauers EL. Mobility and stability adaptations in the shoulder of the overhead athlete: a theoretical and evidence-based perspective. Sports Med. 2008;38(1):17-36.
14. Sethi PM, Tibone JE, Lee TQ. Quantitative assessment of glenohumeral translation in baseball players: a comparison of pitchers versus nonpitching athletes. Am J Sports Med. 2004;32(7):1711-1715.
15. Burkhart SS, Lo IK. The cam effect of the proximal humerus: its role in the production of relative capsular redundancy of the shoulder. Arthroscopy. 2007;23(3):241-246.
16. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420.
17. Jones KJ, Conte S, Patterson N, ElAttrache NS, Dines JS. Functional outcomes following revision ulnar collateral ligament reconstruction in Major League Baseball pitchers. J Shoulder Elbow Surg. 2013;22(5):642-646.
Rotator cuff injuries can be a source of debilitating pain and dysfunction in athletes at all levels, occasionally precluding return to competitive sport. Overhead athletes place extraordinary physiologic demands on the shoulder, as humeral angular velocities of 7000° to 8000° per second and rotational torques higher than 70 Nm have been measured during the baseball pitch.1 Repetitive supraphysiologic loading of the rotator cuff throughout the coordinated phases of throwing can result in a characteristic spectrum of shoulder pathology in overhead throwers. Several studies have demonstrated partial-thickness articular-sided rotator cuff tears (RCTs) in the area of the posterior supraspinatus and anterior infraspinatus tendons.2-4 Although the precise mechanism remains unclear, plausible explanations for the pathogenesis of these injuries include eccentric tensile and shear forces that lead to tendon failure with repetitive throwing, as well as internal impingement (mechanical impingement of the aforementioned tendons against the posterosuperior glenoid at 90° of shoulder abduction and maximum external rotation).5,6
Whereas partial-thickness articular-sided RCTs have been described in overhead athletes with rotator cuff pathology, full-thickness tears are encountered less often.7,8 Accordingly, there is a paucity of literature on clinical outcomes in professional baseball players with these injuries. To our knowledge, only 2 studies have investigated functional outcomes of open surgical repair of full-thickness tears in this population, and the outcomes have been uniformly poor.8,9
An anatomical description of rotator cuff anatomy has demonstrated a consistent pattern of supraspinatus and infraspinatus tendon insertion relative to the articular surface, biceps groove, and the bare area of the humerus.10 Using gross and microscopic analyses, the authors noted that the supraspinatus tendon inserted immediately adjacent to the articular margin, and the infraspinatus and teres minor tapered laterally away from the margin to form the bare area. Detailed knowledge of the insertional anatomy of the rotator cuff is important, as surgical repair should recreate the broad footprint to restore normal biomechanics and increase the surface area available for healing.11,12 Medial advancement of the rotator cuff insertion during surgical repair can have deleterious biomechanical effects on glenohumeral motion.11
Given the unfavorable results found after routine open repair of full-thickness tears, we altered our approach to these injuries and adopted an arthroscopic technique in which the tendon is repaired immediately lateral to the anatomical footprint. Research studies have demonstrated that chronic stress from repetitive throwing can lead to attenuation of soft-tissue restraints, and we think preservation of these adaptive changes after surgical repair may be important for these athletes to maintain extraordinary glenohumeral rotation and achieve high throwing velocities.13 We conducted a study to describe the lateralized repair technique for full-thickness RCTs and to report functional outcomes in Major League Baseball (MLB) pitchers treated with this procedure at minimum 2-year follow-up. We hypothesized that use of this novel technique would result in a higher rate of return to preinjury level of play in comparison with open rotator cuff repair in comparable cohorts, as reported in other studies.8,9
Materials and Methods
After obtaining Institutional Review Board approval for this study, we performed a retrospective chart review of MLB players treated by Dr. Altchek. We identified all professional baseball players who received a diagnosis of full-thickness RCT after preoperative magnetic resonance imaging with subsequent confirmation during surgery. Any patient who underwent arthroscopic repair using the lateralized footprint technique was included in the study. Demographic and preoperative injury information was collected from the chart, and final follow-up data were collected at the last available clinic visit. From available team records, we also obtained return-to-play data and objective pitching statistics: seasons played, games played, innings pitched, strikeouts per 9 innings, walks per 9 innings, and earned run average.
Surgical Technique
We routinely perform arthroscopic rotator cuff repairs with the patient under regional anesthesia in the beach-chair position. The operative extremity is placed in a Spider Limb Positioner (Smith & Nephew) to facilitate easy manipulation of the arm throughout the procedure. A standard posterior portal is established, and then an anterior portal is placed in the superolateral aspect of the rotator interval directly anterior to the leading edge of the supraspinatus tendon. A lateral portal created 2 to 3 cm distal to the anterolateral margin of the acromion may be used as an additional working portal. A thorough diagnostic arthroscopy is performed to evaluate the glenohumeral joint for any concomitant intra-articular pathology. Particular attention is directed to inspection of the superior labrum, biceps tendon, and capsuloligamentous structures, as injuries to these structures are often associated with rotator cuff pathology in overhead athletes.
Once presence of an RCT is confirmed, a thorough subacromial bursectomy is performed to help with visualization and inspection of the injury. The tissue is provisionally grasped and mobilized to measure the amount of available tendon excursion. In this unique population, the vast majority of injuries are diagnosed in an expeditious manner, thereby precluding the presence of significant retraction, poor tissue quality, and inadequate mobilization of the tendons. The greater tuberosity is identified, and the area immediately adjacent to the articular margin is abraded with a mechanical shaver to enhance healing potential. For supraspinatus tears, an anchor is placed immediately lateral to the articular margin in the region of the anterior attachment of the rotator cable (Figure 1). The posterior anchor is placed about 10 to 15 mm lateral to the articular margin to reattach the infraspinatus tendon (Figure 2). When the medial row sutures are tied down, anatomical placement of these anchors effectively re-creates the bare area described by Curtis and colleagues10 (Figure 3). In most cases, the medial row sutures are left intact and fixed laterally with a knotless anchor to provide a transosseous equivalent (double-row) repair.
Results
We identified 6 MLB pitchers who underwent arthroscopic rotator cuff repair using the aforementioned technique over an 8-year period. Each patient presented with complaints of debilitating shoulder pain and decreased pitching performance, including loss of throwing accuracy and velocity. There were 4 right-hand–dominant pitchers and 2 left-hand–dominant pitchers; rotator cuff pathology was observed in the dominant pitching arm in each case. Three players were classified as starting pitchers; the other 3 pitched in a relief role. Mean age of all pitchers at time of surgery was 29.8 years (range, 25-37 years). According to records, 2 patients (33%) underwent previous rotator cuff débridement for partial-thickness RCTs before surgical intervention at our institution. Operative information on the depth of the partial-thickness tears observed during the previous procedures was not available for review. At time of rotator cuff repair, 3 patients (50%) underwent concomitant procedures, including superior labrum anterior-posterior (SLAP) lesion repair (1 patient) and posterior labrum débridement (2 patients). A double-row fixation construct was achieved in each case. Review of operative records revealed a mean tear size of 2.1 cm (range, 1.5-3.0 cm) measured anterior to posterior, and all tears involved the supraspinatus and/or infraspinatus tendons. Postoperative rehabilitation included immobilization in a sling for 4 weeks. Hand, wrist, and elbow range-of-motion (ROM) exercises were started immediately to help reduce inflammation. Passive ROM exercises in the plane of the scapula were begun 4 weeks after surgery. Isometric scapular stabilization exercises were also incorporated at that time. Active-assisted ROM exercises were started at about 6 weeks, and isometric strengthening exercises were started at week 8 with progression to eccentric strengthening and weight training at about 3 months. Most pitchers were allowed to begin an interval throwing program at 24 weeks. There were no significant differences in the therapy programs for pitchers who underwent concomitant labral procedures, but the patient who underwent SLAP repair was limited to 30° of external rotation and 90° of forward flexion, with avoidance of active biceps contractions, for the first 6 weeks of rehabilitation.
By mean follow-up of 66.7 months (range, 23.2-94.6 months), 5 pitchers (83%) returned to their preinjury level of competition for at least 1 full season. One player pitched at Minor League Class AA level for about 1 season but was forced to retire because of persistent symptoms related to the shoulder. This pitcher underwent simultaneous rotator cuff and SLAP lesion repair. Of the 5 pitchers who resumed MLB play, none returned to their preoperative pitching productivity; mean number of innings pitched decreased from 1806.5 to 183.7. Three (60%) of these 5 pitchers experienced a slight reduction in performance as measured by earned run average. Interestingly, both players over age 30 years at time of surgery, versus 3 of the 4 pitchers under age 30 years, returned to their preoperative level of competition for at least 1 season. The Table summarizes MLB player data and objective pitching statistics. There were no perioperative complications related to this arthroscopic technique, and there were no glenohumeral ROM deficits at final follow-up.
Discussion
Although the incidence of full-thickness RCTs in professional baseball players is presumably low, available studies suggest that it is a debilitating injury with a poor prognosis for return to high-level athletics. Mazoué and Andrews9 reviewed the outcomes of 16 professional baseball players (12 pitchers, 4 position players) who underwent mini-open repair of full-thickness RCTs that involved more than 90% of the rotator cuff. Fifteen patients underwent mini-open rotator cuff repair using suture anchors in the anatomical footprint along with bone tunnels established near the lateral margin of the greater tuberosity to create a 2-level anatomical repair. One patient was treated with a mini-open repair using suture anchors in the greater tuberosity with a side-side repair of a longitudinal split within the rotator cuff. In the evaluation of outcomes by player position, only 1 pitcher (8%) returned to a competitive level of pitching at a mean follow-up of 67 months. On review of 2 position players with a full-thickness RCT in the dominant shoulder, only 1 (50%) returned to Major League play at a mean follow-up of 62.5 months. The remaining 2 position players underwent surgical repair of the nondominant shoulder, and, not surprisingly, both returned to their previous level of athletic activity without any difficulty. These results should be examined carefully, as the associated pathology in this high-demand cohort should not be discounted. Eleven (almost 92%) of the 12 pitchers had undergone at least 1 previous procedure on the shoulder. Furthermore, at time of full-thickness rotator cuff repair, 9 (75%) of the 12 pitchers were treated for concomitant intra-articular pathology, including SLAP tears, capsular attenuation, and/or labral fraying. In our study, 50% of pitchers underwent an associated labral procedure. Although labral débridement did not have a significant effect on return to play, the 1 pitcher who underwent SLAP repair was not able to return to preinjury level of play.
Tibone and colleagues8 reviewed postoperative outcomes in 45 athletes with rotator cuff pathology. Within their series, 5 professional baseball pitchers with full-thickness tears were treated with open subacromial decompression and rotator cuff repair. Two baseball pitchers with RCTs larger than 2 cm underwent open transosseous footprint repair in which the cuff was reinserted using bone tunnels created within the greater tuberosity. At long-term follow-up, only 2 (40%) of the 5 pitchers returned to competitive pitching. Interestingly, both pitchers who underwent transosseous footprint fixation were unable to return to professional baseball.
Overhead athletes require a delicate balance of shoulder mobility and stability to meet the high functional demands of their sports. Significant debate continues as to whether innate alterations in glenohumeral mobility preselect individuals for overhead sports, or if these changes are acquired through adaptations in supporting soft-tissue and osseous structures. Sethi and colleagues14 used an instrumented manual laxity examination to compare anterior-posterior laxity in asymptomatic professional and Division I college baseball players. The authors noted asymmetric anterior-posterior translation (>3 mm) between the throwing shoulder and the nondominant shoulder in 12 (60%) of 20 professional pitchers and 10 (59%) of 17 college pitchers. Although the authors did not correlate translational differences with corresponding shoulder pathology, the observed asymmetry supported the idea that these athletes may experience adaptive glenohumeral changes with repetitive throwing. The association between adaptive changes and shoulder biomechanics has been studied. Burkhart and Lo15 used a cadaveric model to describe the cam effect of the proximal humerus and the biomechanical consequences of a relative reduction in this effect after pathologic changes within the glenohumeral joint (constriction of posteroinferior capsule). They noted that a posterosuperior shift in the glenohumeral contact point in the throwing position can result in anterior capsular redundancy that may contribute to microinstability of the shoulder. This relative laxity increases external rotation, resulting in increased torsional and shear forces at the rotator cuff insertion.16 Ultimately, these abnormal forces may predispose overhead athletes to rotator cuff injury.
Given the available literature, it is clear that full-thickness RCTs are potentially career-ending injuries for professional baseball players. The question arises as to why the results are so poor. Ultimately, the high incidence of concomitant intra-articular pathology associated with full-thickness RCTs underscores the severity of soft-tissue damage sustained with repetitive overhead throwing. Mazoué and Andrews9 proposed the presence of associated labral and capsular pathology as a potential explanation for poor outcomes of surgical repair. Given the myriad of additional pathology observed in each patient, it is difficult to ascertain the precise impact of these injuries on postoperative outcome. However, early diagnosis and aggressive surgical intervention are clearly necessary to prevent accumulative injury. Regarding surgical intervention, both Tibone and colleagues8 and Mazoué and Andrews9 reported use of an open surgical repair technique in which the tendon was repaired to the anatomical footprint. Certainly, the benefits of an all-arthroscopic technique include optimal visualization of the RCT, less perioperative morbidity, and minimal soft-tissue injury. With our arthroscopic technique, the rotator cuff was fixed immediately lateral to the anatomical footprint, thereby leaving the medial aspect of the footprint uncovered. Functionally, the goal of this procedure is to restore the integrity of the rotator cuff without compromising glenohumeral mobility acquired through soft-tissue adaptation. Investigation of the insertional anatomy of the rotator cuff has demonstrated that the supraspinatus tendon inserts about 0.9 mm from the edge of the articular surface, and the infraspinatus insertional footprint tapers away from the articular surface to form the bare area as it extends inferiorly on the greater tuberosity.10 We think preexisting adaptations in glenohumeral anatomy are important for peak performance in this unique population, and even small alterations in the repair location can have deleterious effects on throwing mechanics. Lateralized repair of the cuff precludes potential medialization of the cuff insertion and may facilitate preservation of soft-tissue adaptations that these athletes rely on to achieve extraordinary glenohumeral motion.
Interestingly, with this technique we noted a higher rate of return to MLB play in pitchers over age 30 years. Although several individual factors (eg, player talent level, work ethics, compliance with rehabilitation) may play a role in this finding, it is possible that older, more mature patients may be more willing to assume diminished roles to continue to play. Jones and colleagues17 recently reported similar findings in older MLB pitchers after revision ulnar collateral ligament reconstruction.
This study had several limitations. First, the patient cohort was small (a result of the nature and relatively infrequent incidence of the clinical problem). Second, clinical information was collected retrospectively, which limited our ability to determine precise differences between preoperative and postoperative glenohumeral ROM with this technique. Third, the cohort included patients who demonstrated additional intra-articular (labral) pathology. Although associated pathology is common in this high-demand athletic population, it is clear that advanced pathology (eg, SLAP tears) may affect clinical outcomes, as in our study. Despite these limitations, our study is the largest review of professional baseball players treated for full-thickness rotator cuff injuries with an arthroscopic technique. Overall, the results of this study are promising and call for further clinical and biomechanical evaluation.
Conclusion
Surgical management of rotator cuff injuries in professional baseball players remains an extremely difficult problem. Current studies of full-thickness RCTs highlight these athletes’ poor functional outcomes. These unfavorable results prompted us to alter our surgical technique. Initial outcomes have been encouraging, and extended follow-up in this cohort of patients will provide a more definitive assessment of the success of this technique.
Rotator cuff injuries can be a source of debilitating pain and dysfunction in athletes at all levels, occasionally precluding return to competitive sport. Overhead athletes place extraordinary physiologic demands on the shoulder, as humeral angular velocities of 7000° to 8000° per second and rotational torques higher than 70 Nm have been measured during the baseball pitch.1 Repetitive supraphysiologic loading of the rotator cuff throughout the coordinated phases of throwing can result in a characteristic spectrum of shoulder pathology in overhead throwers. Several studies have demonstrated partial-thickness articular-sided rotator cuff tears (RCTs) in the area of the posterior supraspinatus and anterior infraspinatus tendons.2-4 Although the precise mechanism remains unclear, plausible explanations for the pathogenesis of these injuries include eccentric tensile and shear forces that lead to tendon failure with repetitive throwing, as well as internal impingement (mechanical impingement of the aforementioned tendons against the posterosuperior glenoid at 90° of shoulder abduction and maximum external rotation).5,6
Whereas partial-thickness articular-sided RCTs have been described in overhead athletes with rotator cuff pathology, full-thickness tears are encountered less often.7,8 Accordingly, there is a paucity of literature on clinical outcomes in professional baseball players with these injuries. To our knowledge, only 2 studies have investigated functional outcomes of open surgical repair of full-thickness tears in this population, and the outcomes have been uniformly poor.8,9
An anatomical description of rotator cuff anatomy has demonstrated a consistent pattern of supraspinatus and infraspinatus tendon insertion relative to the articular surface, biceps groove, and the bare area of the humerus.10 Using gross and microscopic analyses, the authors noted that the supraspinatus tendon inserted immediately adjacent to the articular margin, and the infraspinatus and teres minor tapered laterally away from the margin to form the bare area. Detailed knowledge of the insertional anatomy of the rotator cuff is important, as surgical repair should recreate the broad footprint to restore normal biomechanics and increase the surface area available for healing.11,12 Medial advancement of the rotator cuff insertion during surgical repair can have deleterious biomechanical effects on glenohumeral motion.11
Given the unfavorable results found after routine open repair of full-thickness tears, we altered our approach to these injuries and adopted an arthroscopic technique in which the tendon is repaired immediately lateral to the anatomical footprint. Research studies have demonstrated that chronic stress from repetitive throwing can lead to attenuation of soft-tissue restraints, and we think preservation of these adaptive changes after surgical repair may be important for these athletes to maintain extraordinary glenohumeral rotation and achieve high throwing velocities.13 We conducted a study to describe the lateralized repair technique for full-thickness RCTs and to report functional outcomes in Major League Baseball (MLB) pitchers treated with this procedure at minimum 2-year follow-up. We hypothesized that use of this novel technique would result in a higher rate of return to preinjury level of play in comparison with open rotator cuff repair in comparable cohorts, as reported in other studies.8,9
Materials and Methods
After obtaining Institutional Review Board approval for this study, we performed a retrospective chart review of MLB players treated by Dr. Altchek. We identified all professional baseball players who received a diagnosis of full-thickness RCT after preoperative magnetic resonance imaging with subsequent confirmation during surgery. Any patient who underwent arthroscopic repair using the lateralized footprint technique was included in the study. Demographic and preoperative injury information was collected from the chart, and final follow-up data were collected at the last available clinic visit. From available team records, we also obtained return-to-play data and objective pitching statistics: seasons played, games played, innings pitched, strikeouts per 9 innings, walks per 9 innings, and earned run average.
Surgical Technique
We routinely perform arthroscopic rotator cuff repairs with the patient under regional anesthesia in the beach-chair position. The operative extremity is placed in a Spider Limb Positioner (Smith & Nephew) to facilitate easy manipulation of the arm throughout the procedure. A standard posterior portal is established, and then an anterior portal is placed in the superolateral aspect of the rotator interval directly anterior to the leading edge of the supraspinatus tendon. A lateral portal created 2 to 3 cm distal to the anterolateral margin of the acromion may be used as an additional working portal. A thorough diagnostic arthroscopy is performed to evaluate the glenohumeral joint for any concomitant intra-articular pathology. Particular attention is directed to inspection of the superior labrum, biceps tendon, and capsuloligamentous structures, as injuries to these structures are often associated with rotator cuff pathology in overhead athletes.
Once presence of an RCT is confirmed, a thorough subacromial bursectomy is performed to help with visualization and inspection of the injury. The tissue is provisionally grasped and mobilized to measure the amount of available tendon excursion. In this unique population, the vast majority of injuries are diagnosed in an expeditious manner, thereby precluding the presence of significant retraction, poor tissue quality, and inadequate mobilization of the tendons. The greater tuberosity is identified, and the area immediately adjacent to the articular margin is abraded with a mechanical shaver to enhance healing potential. For supraspinatus tears, an anchor is placed immediately lateral to the articular margin in the region of the anterior attachment of the rotator cable (Figure 1). The posterior anchor is placed about 10 to 15 mm lateral to the articular margin to reattach the infraspinatus tendon (Figure 2). When the medial row sutures are tied down, anatomical placement of these anchors effectively re-creates the bare area described by Curtis and colleagues10 (Figure 3). In most cases, the medial row sutures are left intact and fixed laterally with a knotless anchor to provide a transosseous equivalent (double-row) repair.
Results
We identified 6 MLB pitchers who underwent arthroscopic rotator cuff repair using the aforementioned technique over an 8-year period. Each patient presented with complaints of debilitating shoulder pain and decreased pitching performance, including loss of throwing accuracy and velocity. There were 4 right-hand–dominant pitchers and 2 left-hand–dominant pitchers; rotator cuff pathology was observed in the dominant pitching arm in each case. Three players were classified as starting pitchers; the other 3 pitched in a relief role. Mean age of all pitchers at time of surgery was 29.8 years (range, 25-37 years). According to records, 2 patients (33%) underwent previous rotator cuff débridement for partial-thickness RCTs before surgical intervention at our institution. Operative information on the depth of the partial-thickness tears observed during the previous procedures was not available for review. At time of rotator cuff repair, 3 patients (50%) underwent concomitant procedures, including superior labrum anterior-posterior (SLAP) lesion repair (1 patient) and posterior labrum débridement (2 patients). A double-row fixation construct was achieved in each case. Review of operative records revealed a mean tear size of 2.1 cm (range, 1.5-3.0 cm) measured anterior to posterior, and all tears involved the supraspinatus and/or infraspinatus tendons. Postoperative rehabilitation included immobilization in a sling for 4 weeks. Hand, wrist, and elbow range-of-motion (ROM) exercises were started immediately to help reduce inflammation. Passive ROM exercises in the plane of the scapula were begun 4 weeks after surgery. Isometric scapular stabilization exercises were also incorporated at that time. Active-assisted ROM exercises were started at about 6 weeks, and isometric strengthening exercises were started at week 8 with progression to eccentric strengthening and weight training at about 3 months. Most pitchers were allowed to begin an interval throwing program at 24 weeks. There were no significant differences in the therapy programs for pitchers who underwent concomitant labral procedures, but the patient who underwent SLAP repair was limited to 30° of external rotation and 90° of forward flexion, with avoidance of active biceps contractions, for the first 6 weeks of rehabilitation.
By mean follow-up of 66.7 months (range, 23.2-94.6 months), 5 pitchers (83%) returned to their preinjury level of competition for at least 1 full season. One player pitched at Minor League Class AA level for about 1 season but was forced to retire because of persistent symptoms related to the shoulder. This pitcher underwent simultaneous rotator cuff and SLAP lesion repair. Of the 5 pitchers who resumed MLB play, none returned to their preoperative pitching productivity; mean number of innings pitched decreased from 1806.5 to 183.7. Three (60%) of these 5 pitchers experienced a slight reduction in performance as measured by earned run average. Interestingly, both players over age 30 years at time of surgery, versus 3 of the 4 pitchers under age 30 years, returned to their preoperative level of competition for at least 1 season. The Table summarizes MLB player data and objective pitching statistics. There were no perioperative complications related to this arthroscopic technique, and there were no glenohumeral ROM deficits at final follow-up.
Discussion
Although the incidence of full-thickness RCTs in professional baseball players is presumably low, available studies suggest that it is a debilitating injury with a poor prognosis for return to high-level athletics. Mazoué and Andrews9 reviewed the outcomes of 16 professional baseball players (12 pitchers, 4 position players) who underwent mini-open repair of full-thickness RCTs that involved more than 90% of the rotator cuff. Fifteen patients underwent mini-open rotator cuff repair using suture anchors in the anatomical footprint along with bone tunnels established near the lateral margin of the greater tuberosity to create a 2-level anatomical repair. One patient was treated with a mini-open repair using suture anchors in the greater tuberosity with a side-side repair of a longitudinal split within the rotator cuff. In the evaluation of outcomes by player position, only 1 pitcher (8%) returned to a competitive level of pitching at a mean follow-up of 67 months. On review of 2 position players with a full-thickness RCT in the dominant shoulder, only 1 (50%) returned to Major League play at a mean follow-up of 62.5 months. The remaining 2 position players underwent surgical repair of the nondominant shoulder, and, not surprisingly, both returned to their previous level of athletic activity without any difficulty. These results should be examined carefully, as the associated pathology in this high-demand cohort should not be discounted. Eleven (almost 92%) of the 12 pitchers had undergone at least 1 previous procedure on the shoulder. Furthermore, at time of full-thickness rotator cuff repair, 9 (75%) of the 12 pitchers were treated for concomitant intra-articular pathology, including SLAP tears, capsular attenuation, and/or labral fraying. In our study, 50% of pitchers underwent an associated labral procedure. Although labral débridement did not have a significant effect on return to play, the 1 pitcher who underwent SLAP repair was not able to return to preinjury level of play.
Tibone and colleagues8 reviewed postoperative outcomes in 45 athletes with rotator cuff pathology. Within their series, 5 professional baseball pitchers with full-thickness tears were treated with open subacromial decompression and rotator cuff repair. Two baseball pitchers with RCTs larger than 2 cm underwent open transosseous footprint repair in which the cuff was reinserted using bone tunnels created within the greater tuberosity. At long-term follow-up, only 2 (40%) of the 5 pitchers returned to competitive pitching. Interestingly, both pitchers who underwent transosseous footprint fixation were unable to return to professional baseball.
Overhead athletes require a delicate balance of shoulder mobility and stability to meet the high functional demands of their sports. Significant debate continues as to whether innate alterations in glenohumeral mobility preselect individuals for overhead sports, or if these changes are acquired through adaptations in supporting soft-tissue and osseous structures. Sethi and colleagues14 used an instrumented manual laxity examination to compare anterior-posterior laxity in asymptomatic professional and Division I college baseball players. The authors noted asymmetric anterior-posterior translation (>3 mm) between the throwing shoulder and the nondominant shoulder in 12 (60%) of 20 professional pitchers and 10 (59%) of 17 college pitchers. Although the authors did not correlate translational differences with corresponding shoulder pathology, the observed asymmetry supported the idea that these athletes may experience adaptive glenohumeral changes with repetitive throwing. The association between adaptive changes and shoulder biomechanics has been studied. Burkhart and Lo15 used a cadaveric model to describe the cam effect of the proximal humerus and the biomechanical consequences of a relative reduction in this effect after pathologic changes within the glenohumeral joint (constriction of posteroinferior capsule). They noted that a posterosuperior shift in the glenohumeral contact point in the throwing position can result in anterior capsular redundancy that may contribute to microinstability of the shoulder. This relative laxity increases external rotation, resulting in increased torsional and shear forces at the rotator cuff insertion.16 Ultimately, these abnormal forces may predispose overhead athletes to rotator cuff injury.
Given the available literature, it is clear that full-thickness RCTs are potentially career-ending injuries for professional baseball players. The question arises as to why the results are so poor. Ultimately, the high incidence of concomitant intra-articular pathology associated with full-thickness RCTs underscores the severity of soft-tissue damage sustained with repetitive overhead throwing. Mazoué and Andrews9 proposed the presence of associated labral and capsular pathology as a potential explanation for poor outcomes of surgical repair. Given the myriad of additional pathology observed in each patient, it is difficult to ascertain the precise impact of these injuries on postoperative outcome. However, early diagnosis and aggressive surgical intervention are clearly necessary to prevent accumulative injury. Regarding surgical intervention, both Tibone and colleagues8 and Mazoué and Andrews9 reported use of an open surgical repair technique in which the tendon was repaired to the anatomical footprint. Certainly, the benefits of an all-arthroscopic technique include optimal visualization of the RCT, less perioperative morbidity, and minimal soft-tissue injury. With our arthroscopic technique, the rotator cuff was fixed immediately lateral to the anatomical footprint, thereby leaving the medial aspect of the footprint uncovered. Functionally, the goal of this procedure is to restore the integrity of the rotator cuff without compromising glenohumeral mobility acquired through soft-tissue adaptation. Investigation of the insertional anatomy of the rotator cuff has demonstrated that the supraspinatus tendon inserts about 0.9 mm from the edge of the articular surface, and the infraspinatus insertional footprint tapers away from the articular surface to form the bare area as it extends inferiorly on the greater tuberosity.10 We think preexisting adaptations in glenohumeral anatomy are important for peak performance in this unique population, and even small alterations in the repair location can have deleterious effects on throwing mechanics. Lateralized repair of the cuff precludes potential medialization of the cuff insertion and may facilitate preservation of soft-tissue adaptations that these athletes rely on to achieve extraordinary glenohumeral motion.
Interestingly, with this technique we noted a higher rate of return to MLB play in pitchers over age 30 years. Although several individual factors (eg, player talent level, work ethics, compliance with rehabilitation) may play a role in this finding, it is possible that older, more mature patients may be more willing to assume diminished roles to continue to play. Jones and colleagues17 recently reported similar findings in older MLB pitchers after revision ulnar collateral ligament reconstruction.
This study had several limitations. First, the patient cohort was small (a result of the nature and relatively infrequent incidence of the clinical problem). Second, clinical information was collected retrospectively, which limited our ability to determine precise differences between preoperative and postoperative glenohumeral ROM with this technique. Third, the cohort included patients who demonstrated additional intra-articular (labral) pathology. Although associated pathology is common in this high-demand athletic population, it is clear that advanced pathology (eg, SLAP tears) may affect clinical outcomes, as in our study. Despite these limitations, our study is the largest review of professional baseball players treated for full-thickness rotator cuff injuries with an arthroscopic technique. Overall, the results of this study are promising and call for further clinical and biomechanical evaluation.
Conclusion
Surgical management of rotator cuff injuries in professional baseball players remains an extremely difficult problem. Current studies of full-thickness RCTs highlight these athletes’ poor functional outcomes. These unfavorable results prompted us to alter our surgical technique. Initial outcomes have been encouraging, and extended follow-up in this cohort of patients will provide a more definitive assessment of the success of this technique.
1. Dillman CJ, Fleisig GS, Andrews JR. Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther. 1993;18(2):402-408.
2. Andrews JR, Broussard TS, Carson WG. Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: a preliminary report. Arthroscopy. 1985;1(2):117-122.
3. Paley KJ, Jobe FW, Pink MM, Kvitne RS, ElAttrache NS. Arthroscopic findings in the overhead throwing athlete: evidence for posterior internal impingement of the rotator cuff. Arthroscopy. 2000;16(1):35-40.
4. Nakagawa S, Yoneda M, Hayashida K, Wakitani S, Okamura K. Greater tuberosity notch: an important indicator of articular-side partial rotator cuff tears in the shoulders of throwing athletes. Am J Sports Med. 2001;29(6):762-770.
5. Walch G, Boileau P, Noel E, Donell ST. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg. 1992;1(5):238-245.
6. Halbrecht JL, Tirman P, Atkin D. Internal impingement of the shoulder: comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy. 1999;15(3):253-258.
7. Reynolds SB, Dugas JR, Cain EL, McMichael CS, Andrews JR. Debridement of small partial-thickness rotator cuff tears in elite overhead throwers. Clin Orthop Relat Res. 2008;466(3):614-621.
8. Tibone JE, Elrod B, Jobe FW, et al. Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg Am. 1986;68(6):887-891.
9. Mazoué C, Andrews JR. Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med. 2006;34():182-189.
10. Curtis AS, Burbank KM, Tierney JJ, Scheller AD, Curran AR. The insertional footprint of the rotator cuff: an anatomic study. Arthroscopy. 2006;22(6):603-609.
11. Liu J, Hughes RE, O’Driscoll SW, An K. Biomechanical effect of medial advancement of the supraspinatus tendon. J Bone Joint Surg Am. 1998;80(6):853-859.
12. Lo IK, Burkhart SS. Double row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy. 2003;19(9):1035-1042.
13. Borsa PA, Laudner KG, Sauers EL. Mobility and stability adaptations in the shoulder of the overhead athlete: a theoretical and evidence-based perspective. Sports Med. 2008;38(1):17-36.
14. Sethi PM, Tibone JE, Lee TQ. Quantitative assessment of glenohumeral translation in baseball players: a comparison of pitchers versus nonpitching athletes. Am J Sports Med. 2004;32(7):1711-1715.
15. Burkhart SS, Lo IK. The cam effect of the proximal humerus: its role in the production of relative capsular redundancy of the shoulder. Arthroscopy. 2007;23(3):241-246.
16. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420.
17. Jones KJ, Conte S, Patterson N, ElAttrache NS, Dines JS. Functional outcomes following revision ulnar collateral ligament reconstruction in Major League Baseball pitchers. J Shoulder Elbow Surg. 2013;22(5):642-646.
1. Dillman CJ, Fleisig GS, Andrews JR. Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther. 1993;18(2):402-408.
2. Andrews JR, Broussard TS, Carson WG. Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: a preliminary report. Arthroscopy. 1985;1(2):117-122.
3. Paley KJ, Jobe FW, Pink MM, Kvitne RS, ElAttrache NS. Arthroscopic findings in the overhead throwing athlete: evidence for posterior internal impingement of the rotator cuff. Arthroscopy. 2000;16(1):35-40.
4. Nakagawa S, Yoneda M, Hayashida K, Wakitani S, Okamura K. Greater tuberosity notch: an important indicator of articular-side partial rotator cuff tears in the shoulders of throwing athletes. Am J Sports Med. 2001;29(6):762-770.
5. Walch G, Boileau P, Noel E, Donell ST. Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg. 1992;1(5):238-245.
6. Halbrecht JL, Tirman P, Atkin D. Internal impingement of the shoulder: comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy. 1999;15(3):253-258.
7. Reynolds SB, Dugas JR, Cain EL, McMichael CS, Andrews JR. Debridement of small partial-thickness rotator cuff tears in elite overhead throwers. Clin Orthop Relat Res. 2008;466(3):614-621.
8. Tibone JE, Elrod B, Jobe FW, et al. Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg Am. 1986;68(6):887-891.
9. Mazoué C, Andrews JR. Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med. 2006;34():182-189.
10. Curtis AS, Burbank KM, Tierney JJ, Scheller AD, Curran AR. The insertional footprint of the rotator cuff: an anatomic study. Arthroscopy. 2006;22(6):603-609.
11. Liu J, Hughes RE, O’Driscoll SW, An K. Biomechanical effect of medial advancement of the supraspinatus tendon. J Bone Joint Surg Am. 1998;80(6):853-859.
12. Lo IK, Burkhart SS. Double row arthroscopic rotator cuff repair: re-establishing the footprint of the rotator cuff. Arthroscopy. 2003;19(9):1035-1042.
13. Borsa PA, Laudner KG, Sauers EL. Mobility and stability adaptations in the shoulder of the overhead athlete: a theoretical and evidence-based perspective. Sports Med. 2008;38(1):17-36.
14. Sethi PM, Tibone JE, Lee TQ. Quantitative assessment of glenohumeral translation in baseball players: a comparison of pitchers versus nonpitching athletes. Am J Sports Med. 2004;32(7):1711-1715.
15. Burkhart SS, Lo IK. The cam effect of the proximal humerus: its role in the production of relative capsular redundancy of the shoulder. Arthroscopy. 2007;23(3):241-246.
16. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420.
17. Jones KJ, Conte S, Patterson N, ElAttrache NS, Dines JS. Functional outcomes following revision ulnar collateral ligament reconstruction in Major League Baseball pitchers. J Shoulder Elbow Surg. 2013;22(5):642-646.
Valgus Extension Overload in Baseball Players
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.
1. Pappas AM, Zawacki RM, Sullivan TJ. Biomechanics of baseball pitching. A preliminary report. Am J Sports Med. 1985;13(4):216-222.
2. Fleisig GS, Barrentine SW, Escamilla RF, Andrews JR. Biomechanics of overhand throwing with implications for injuries. Sports Med. 1996;21(6):421-437.
3. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med. 1983;11(2):83-88.
4. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect. 1986,35:59-68.
5. Schwab GH, Bennett JB, Woods GW, Tullos HS. Biomechanics of elbow instability: the role of medial collateral ligament. Clin Orthop Relat Res. 1980;146:42-52.
6. Jobe FW, Kvitne RS. Elbow instability in the athlete. Instr Course Lect. 1991;40:17-23.
7. Søjbjerg JO, Ovesen J, Nielsen S. Experimental elbow instability after transection of the medial collateral ligament. Clin Orthop Relat Res. 1987;218:186-190.
8. Regan WD, Korinek SL, Morrey BF, An KN. Biomechanical study of ligaments around the elbow joint. Clin Orthop Relat Res. 1991;271:170-179.
9. Callaway GH, Field LD, Deng XH, et al. Biomechanical evaluation of the medial collateral ligament of the elbow. J Bone Joint Surg Am. 1997;79(8):1223-1231.
10. Chen FS, Rokito AS, Jobe FW. Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg. 2001;9(2):99-113.
11. Davidson PA, Pink M, Perry J, Jobe FW. Functional anatomy of the flexor pronator muscle group in relation to the medial collateral ligament of the elbow. Am J Sports Med. 1995;23(2):245-250.
12. Jobe FW, Moynes DR, Tibone JE, Perry J. An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med. 1984;12(3):218-220.
13. Hamilton CD, Glousman RE, Jobe FW, Brault J, Pink M, Perry J. Dynamic stability of the elbow: electromyographic analysis of the flexor pronator group and the extensor group in pitchers with valgus instability. J Shoulder Elbow Surg. 1996;5(5):347-354.
14. Glousman RE, Barron J, Jobe FW, Perry J, Pink M. An electromyographic analysis of the elbow in normal and injured pitchers with medial collateral ligament insufficiency. Am J Sports Med. 1992;20(3):311-317.
15. DiGiovine NM, Jobe FW, Pink M, Perry J. An electromyographic analysis of the upper extremity in pitching. J Shoulder Elbow Surg. 1992;1(1):15-25.
16. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ. An electromyographic analysis of the elbow in pitching. Am J Sports Med. 1987;15(3):260-263.
17. Ahmad CS, Park MC, Elattrache NS. Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am J Sports Med. 2004;32(7):1607–1612.
18. Ahmad CS, Conway J. Elbow arthroscopy: beginners to advanced: valgus extension overload. In: Egol, ed. Instructional Course Lectures; vol 60. Rosemont, IL: American Academy of Orthopaedic Surgeons; submitted 2009.
19. Kamineni S, ElAttrache NS, O’Driscoll S W, et al. Medial collateral ligament strain with partial posteromedial olecranon resection. A biomechanical study. J Bone Joint Surg Am. 2004;86-A(11):2424–2430.
20. Kamineni S, Hirahara H, Pomianowski S, et al. Partial posteromedial olecranon resection: a kinematic study. J Bone Joint Surg Am. 2003;85-A(6):1005–1011.
21. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med. 1983;11(5):315–319.
22. O’Driscoll SW, Morrey BF. Arthroscopy of the elbow. Diagnostic and therapeutic benefits and hazards. J Bone Joint Surg Am. 1992;74(1):84–94.
23. Miller CD, Savoie FH 3rd. Valgus extension injuries of the elbow in the throwing athlete. J Am Acad Orthop Surg. 1994;2(5):261-269.
24. O’Driscoll SW. Valgus extension overload and plica. In: Levine WN, ed. The Athlete’s Elbow. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008:71-83.
25. Boatright JR, D’Alessandro DF. Nerve entrapment syndromes at the elbow. In Jobe FW, Pink MM, Glousman RE, Kvitne RE, Zemel NP, eds. Operative Techniques in Upper Extremity Sports Injuries. St. Louis, MO: Mosby-Year Book; 1996:518-537.
26. Conway JE, Jobe FW, Glousman RE, Pink M. Medial instability of the elbow in throwing athletes. Treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg Am. 1992;74(1):67-83.
27. Jobe FW, Stark H, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am. 1986;68(8):1158-1163.
28. Kooima CL, Anderson K, Craig JV, Teeter DM, van Holsbeeck M. Evidence of subclinical medial collateral ligament injury and posteromedial impingement in professional baseball players. Am J Sports Med. 2004;32(7):1602-1606.
29. Field LD, Altchek DW. Evaluation of the arthroscopic valgus instability test of the elbow. Am J Sports Med. 1996;24(2):177–181.
30. Andrews JR, Carson WG. Arthroscopy of the elbow. Arthroscopy. 1985;1(2):97-107.
31. Andrews JR, Timmerman LA. Outcome of elbow surgery in professional baseball players. Am J Sports Med. 1995;23(4):407-413.
32. Reddy AS, Kvitne RE, Yocum LA, Elattrache NS, Glousman RE, Jobe FW. Arthroscopy of the elbow: a long-term clinical review. Arthroscopy. 2000;16(6):588-594.
33. Rosenwasser MP, Steinmann S. Elbow arthroscopy in the treatment of posterior olecranon impingement. Paper present at: AANA Annual Meeting; 1991; San Diego, CA.
34. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med. 1983;11(2):83-88.
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.
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3. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med. 1983;11(2):83-88.
4. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect. 1986,35:59-68.
5. Schwab GH, Bennett JB, Woods GW, Tullos HS. Biomechanics of elbow instability: the role of medial collateral ligament. Clin Orthop Relat Res. 1980;146:42-52.
6. Jobe FW, Kvitne RS. Elbow instability in the athlete. Instr Course Lect. 1991;40:17-23.
7. Søjbjerg JO, Ovesen J, Nielsen S. Experimental elbow instability after transection of the medial collateral ligament. Clin Orthop Relat Res. 1987;218:186-190.
8. Regan WD, Korinek SL, Morrey BF, An KN. Biomechanical study of ligaments around the elbow joint. Clin Orthop Relat Res. 1991;271:170-179.
9. Callaway GH, Field LD, Deng XH, et al. Biomechanical evaluation of the medial collateral ligament of the elbow. J Bone Joint Surg Am. 1997;79(8):1223-1231.
10. Chen FS, Rokito AS, Jobe FW. Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg. 2001;9(2):99-113.
11. Davidson PA, Pink M, Perry J, Jobe FW. Functional anatomy of the flexor pronator muscle group in relation to the medial collateral ligament of the elbow. Am J Sports Med. 1995;23(2):245-250.
12. Jobe FW, Moynes DR, Tibone JE, Perry J. An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med. 1984;12(3):218-220.
13. Hamilton CD, Glousman RE, Jobe FW, Brault J, Pink M, Perry J. Dynamic stability of the elbow: electromyographic analysis of the flexor pronator group and the extensor group in pitchers with valgus instability. J Shoulder Elbow Surg. 1996;5(5):347-354.
14. Glousman RE, Barron J, Jobe FW, Perry J, Pink M. An electromyographic analysis of the elbow in normal and injured pitchers with medial collateral ligament insufficiency. Am J Sports Med. 1992;20(3):311-317.
15. DiGiovine NM, Jobe FW, Pink M, Perry J. An electromyographic analysis of the upper extremity in pitching. J Shoulder Elbow Surg. 1992;1(1):15-25.
16. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ. An electromyographic analysis of the elbow in pitching. Am J Sports Med. 1987;15(3):260-263.
17. Ahmad CS, Park MC, Elattrache NS. Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am J Sports Med. 2004;32(7):1607–1612.
18. Ahmad CS, Conway J. Elbow arthroscopy: beginners to advanced: valgus extension overload. In: Egol, ed. Instructional Course Lectures; vol 60. Rosemont, IL: American Academy of Orthopaedic Surgeons; submitted 2009.
19. Kamineni S, ElAttrache NS, O’Driscoll S W, et al. Medial collateral ligament strain with partial posteromedial olecranon resection. A biomechanical study. J Bone Joint Surg Am. 2004;86-A(11):2424–2430.
20. Kamineni S, Hirahara H, Pomianowski S, et al. Partial posteromedial olecranon resection: a kinematic study. J Bone Joint Surg Am. 2003;85-A(6):1005–1011.
21. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med. 1983;11(5):315–319.
22. O’Driscoll SW, Morrey BF. Arthroscopy of the elbow. Diagnostic and therapeutic benefits and hazards. J Bone Joint Surg Am. 1992;74(1):84–94.
23. Miller CD, Savoie FH 3rd. Valgus extension injuries of the elbow in the throwing athlete. J Am Acad Orthop Surg. 1994;2(5):261-269.
24. O’Driscoll SW. Valgus extension overload and plica. In: Levine WN, ed. The Athlete’s Elbow. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008:71-83.
25. Boatright JR, D’Alessandro DF. Nerve entrapment syndromes at the elbow. In Jobe FW, Pink MM, Glousman RE, Kvitne RE, Zemel NP, eds. Operative Techniques in Upper Extremity Sports Injuries. St. Louis, MO: Mosby-Year Book; 1996:518-537.
26. Conway JE, Jobe FW, Glousman RE, Pink M. Medial instability of the elbow in throwing athletes. Treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg Am. 1992;74(1):67-83.
27. Jobe FW, Stark H, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am. 1986;68(8):1158-1163.
28. Kooima CL, Anderson K, Craig JV, Teeter DM, van Holsbeeck M. Evidence of subclinical medial collateral ligament injury and posteromedial impingement in professional baseball players. Am J Sports Med. 2004;32(7):1602-1606.
29. Field LD, Altchek DW. Evaluation of the arthroscopic valgus instability test of the elbow. Am J Sports Med. 1996;24(2):177–181.
30. Andrews JR, Carson WG. Arthroscopy of the elbow. Arthroscopy. 1985;1(2):97-107.
31. Andrews JR, Timmerman LA. Outcome of elbow surgery in professional baseball players. Am J Sports Med. 1995;23(4):407-413.
32. Reddy AS, Kvitne RE, Yocum LA, Elattrache NS, Glousman RE, Jobe FW. Arthroscopy of the elbow: a long-term clinical review. Arthroscopy. 2000;16(6):588-594.
33. Rosenwasser MP, Steinmann S. Elbow arthroscopy in the treatment of posterior olecranon impingement. Paper present at: AANA Annual Meeting; 1991; San Diego, CA.
34. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med. 1983;11(2):83-88.
1. Pappas AM, Zawacki RM, Sullivan TJ. Biomechanics of baseball pitching. A preliminary report. Am J Sports Med. 1985;13(4):216-222.
2. Fleisig GS, Barrentine SW, Escamilla RF, Andrews JR. Biomechanics of overhand throwing with implications for injuries. Sports Med. 1996;21(6):421-437.
3. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med. 1983;11(2):83-88.
4. Morrey BF. Applied anatomy and biomechanics of the elbow joint. Instr Course Lect. 1986,35:59-68.
5. Schwab GH, Bennett JB, Woods GW, Tullos HS. Biomechanics of elbow instability: the role of medial collateral ligament. Clin Orthop Relat Res. 1980;146:42-52.
6. Jobe FW, Kvitne RS. Elbow instability in the athlete. Instr Course Lect. 1991;40:17-23.
7. Søjbjerg JO, Ovesen J, Nielsen S. Experimental elbow instability after transection of the medial collateral ligament. Clin Orthop Relat Res. 1987;218:186-190.
8. Regan WD, Korinek SL, Morrey BF, An KN. Biomechanical study of ligaments around the elbow joint. Clin Orthop Relat Res. 1991;271:170-179.
9. Callaway GH, Field LD, Deng XH, et al. Biomechanical evaluation of the medial collateral ligament of the elbow. J Bone Joint Surg Am. 1997;79(8):1223-1231.
10. Chen FS, Rokito AS, Jobe FW. Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg. 2001;9(2):99-113.
11. Davidson PA, Pink M, Perry J, Jobe FW. Functional anatomy of the flexor pronator muscle group in relation to the medial collateral ligament of the elbow. Am J Sports Med. 1995;23(2):245-250.
12. Jobe FW, Moynes DR, Tibone JE, Perry J. An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med. 1984;12(3):218-220.
13. Hamilton CD, Glousman RE, Jobe FW, Brault J, Pink M, Perry J. Dynamic stability of the elbow: electromyographic analysis of the flexor pronator group and the extensor group in pitchers with valgus instability. J Shoulder Elbow Surg. 1996;5(5):347-354.
14. Glousman RE, Barron J, Jobe FW, Perry J, Pink M. An electromyographic analysis of the elbow in normal and injured pitchers with medial collateral ligament insufficiency. Am J Sports Med. 1992;20(3):311-317.
15. DiGiovine NM, Jobe FW, Pink M, Perry J. An electromyographic analysis of the upper extremity in pitching. J Shoulder Elbow Surg. 1992;1(1):15-25.
16. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ. An electromyographic analysis of the elbow in pitching. Am J Sports Med. 1987;15(3):260-263.
17. Ahmad CS, Park MC, Elattrache NS. Elbow medial ulnar collateral ligament insufficiency alters posteromedial olecranon contact. Am J Sports Med. 2004;32(7):1607–1612.
18. Ahmad CS, Conway J. Elbow arthroscopy: beginners to advanced: valgus extension overload. In: Egol, ed. Instructional Course Lectures; vol 60. Rosemont, IL: American Academy of Orthopaedic Surgeons; submitted 2009.
19. Kamineni S, ElAttrache NS, O’Driscoll S W, et al. Medial collateral ligament strain with partial posteromedial olecranon resection. A biomechanical study. J Bone Joint Surg Am. 2004;86-A(11):2424–2430.
20. Kamineni S, Hirahara H, Pomianowski S, et al. Partial posteromedial olecranon resection: a kinematic study. J Bone Joint Surg Am. 2003;85-A(6):1005–1011.
21. Morrey BF, An KN. Articular and ligamentous contributions to the stability of the elbow joint. Am J Sports Med. 1983;11(5):315–319.
22. O’Driscoll SW, Morrey BF. Arthroscopy of the elbow. Diagnostic and therapeutic benefits and hazards. J Bone Joint Surg Am. 1992;74(1):84–94.
23. Miller CD, Savoie FH 3rd. Valgus extension injuries of the elbow in the throwing athlete. J Am Acad Orthop Surg. 1994;2(5):261-269.
24. O’Driscoll SW. Valgus extension overload and plica. In: Levine WN, ed. The Athlete’s Elbow. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008:71-83.
25. Boatright JR, D’Alessandro DF. Nerve entrapment syndromes at the elbow. In Jobe FW, Pink MM, Glousman RE, Kvitne RE, Zemel NP, eds. Operative Techniques in Upper Extremity Sports Injuries. St. Louis, MO: Mosby-Year Book; 1996:518-537.
26. Conway JE, Jobe FW, Glousman RE, Pink M. Medial instability of the elbow in throwing athletes. Treatment by repair or reconstruction of the ulnar collateral ligament. J Bone Joint Surg Am. 1992;74(1):67-83.
27. Jobe FW, Stark H, Lombardo SJ. Reconstruction of the ulnar collateral ligament in athletes. J Bone Joint Surg Am. 1986;68(8):1158-1163.
28. Kooima CL, Anderson K, Craig JV, Teeter DM, van Holsbeeck M. Evidence of subclinical medial collateral ligament injury and posteromedial impingement in professional baseball players. Am J Sports Med. 2004;32(7):1602-1606.
29. Field LD, Altchek DW. Evaluation of the arthroscopic valgus instability test of the elbow. Am J Sports Med. 1996;24(2):177–181.
30. Andrews JR, Carson WG. Arthroscopy of the elbow. Arthroscopy. 1985;1(2):97-107.
31. Andrews JR, Timmerman LA. Outcome of elbow surgery in professional baseball players. Am J Sports Med. 1995;23(4):407-413.
32. Reddy AS, Kvitne RE, Yocum LA, Elattrache NS, Glousman RE, Jobe FW. Arthroscopy of the elbow: a long-term clinical review. Arthroscopy. 2000;16(6):588-594.
33. Rosenwasser MP, Steinmann S. Elbow arthroscopy in the treatment of posterior olecranon impingement. Paper present at: AANA Annual Meeting; 1991; San Diego, CA.
34. Wilson FD, Andrews JR, Blackburn TA, McCluskey G. Valgus extension overload in the pitching elbow. Am J Sports Med. 1983;11(2):83-88.
Analysis of Direct Costs of Outpatient Arthroscopic Rotator Cuff Repair
Musculoskeletal disorders, the leading cause of disability in the United States,1 account for more than half of all persons reporting missing a workday because of a medical condition.2 Shoulder disorders in particular play a significant role in the burden of musculoskeletal disorders and cost of care. In 2008, 18.9 million adults (8.2% of the US adult population) reported chronic shoulder pain.1 Among shoulder disorders, rotator cuff pathology is the most common cause of shoulder-related disability found by orthopedic surgeons.3 Rotator cuff surgery (RCS) is one of the most commonly performed orthopedic surgical procedures, and surgery volume is on the rise. One study found a 141% increase in rotator cuff repairs between the years 1996 (~41 per 100,000 population) and 2006 (~98 per 100,000 population).4
US health care costs are also increasing. In 2011, $2.7 trillion was spent on health care, representing 17.9% of the national gross domestic product (GDP). According to projections, costs will rise to $4.6 trillion by 2020.5 In particular, as patients continue to live longer and remain more active into their later years, the costs of treating and managing musculoskeletal disorders become more important from a public policy standpoint. In 2006, the cost of treating musculoskeletal disorders alone was $576 billion, representing 4.5% of that year’s GDP.2
Paramount in this era of rising costs is the idea of maximizing the value of health care dollars. Health care economists Porter and Teisberg6 defined value as patient health outcomes achieved per dollar of cost expended in a care cycle (diagnosis, treatment, ongoing management) for a particular disease or disorder. For proper management of value, outcomes and costs for an entire cycle of care must be determined. From a practical standpoint, this first requires determining the true cost of a care cycle—dollars spent on personnel, equipment, materials, and other resources required to deliver a particular service—rather than the amount charged or reimbursed for providing the service in question.7
Kaplan and Anderson8,9 described the TDABC (time-driven activity-based costing) algorithm for calculating the cost of delivering a service based on 2 parameters: unit cost of a particular resource, and time required to supply it. These parameters apply to material costs and labor costs. In the medical setting, the TDABC algorithm can be applied by defining a care delivery value chain for each aspect of patient care and then multiplying incremental cost per unit time by time required to deliver that resource (Figure 1). Tabulating the overall unit cost for each resource then yields the overall cost of the care cycle. Clinical outcomes data can then be determined and used to calculate overall value for the patient care cycle.
In the study reported here, we used the TDABC algorithm to calculate the direct financial costs of surgical treatment of rotator cuff tears confirmed by magnetic resonance imaging (MRI) in an academic medical center.
Methods
Per our institution’s Office for the Protection of Research Subjects, institutional review board (IRB) approval is required only for projects using “human subjects” as defined by federal policy. In the present study, no private information could be identified, and all data were obtained from hospital billing records without intervention or interaction with individual patients. Accordingly, IRB approval was deemed unnecessary for our economic cost analysis.
Billing records of a single academic fellowship-trained sports surgeon were reviewed to identify patients who underwent primary repair of an MRI-confirmed rotator cuff tear between April 1, 2009, and July 31, 2012. Patients who had undergone prior shoulder surgery of any type were excluded from the study. Operative reports were reviewed, and exact surgical procedures performed were noted. The operating surgeon selected the specific repair techniques, including single- or double-row repair, with emphasis on restoring footprint coverage and avoiding overtensioning.
All surgeries were performed in an outpatient surgical center owned and operated by the surgeon’s home university. Surgeries were performed by the attending physician assisted by a senior orthopedic resident. The RCS care cycle was divided into 3 phases (Figure 2):
1. Preoperative. Patient’s interaction with receptionist in surgery center, time with preoperative nurse and circulating nurse in preoperative area, resident check-in time, and time placing preoperative nerve block and consumable materials used during block placement.
2. Operative. Time in operating room with surgical team for RCS, consumable materials used during surgery (eg, anchors, shavers, drapes), anesthetic medications, shoulder abduction pillow placed on completion of surgery, and cost of instrument processing.
3. Postoperative. Time in postoperative recovery area with recovery room nursing staff.
Time in each portion of the care cycle was directly observed and tabulated by hospital volunteers in the surgery center. Institutional billing data were used to identify material resources consumed, and the actual cost paid by the hospital for these resources was obtained from internal records. Mean hourly salary data and standard benefit rates were obtained for surgery center staff. Attending physician salary was extrapolated from published mean market salary data for academic physicians and mean hours worked,10,11 and resident physician costs were tabulated from publically available institutional payroll data and average resident work hours at our institution. These cost data and times were then used to tabulate total cost for the RCS care cycle using the TDABC algorithm.
Results
We identified 28 shoulders in 26 patients (mean age, 54.5 years) who met the inclusion criteria. Of these 28 shoulders, 18 (64.3%) had an isolated supraspinatus tear, 8 (28.6%) had combined supraspinatus and infraspinatus tears, 1 (3.6%) had combined supraspinatus and subscapularis tears, and 1 (3.6%) had an isolated infraspinatus tear. Demographic data are listed in Table 1.
All patients received an interscalene nerve block in the preoperative area before being brought into the operating room. In our analysis, we included nerve block supply costs and the anesthesiologist’s mean time placing the nerve block.
In all cases, primary rotator cuff repair was performed with suture anchors (Parcus Medical) with the patient in the lateral decubitus position. In 13 (46%) of the 28 shoulders, this repair was described as “complex,” requiring double-row technique. Subacromial decompression and bursectomy were performed in addition to the rotator cuff repair. Labral débridement was performed in 23 patients, synovectomy in 10, biceps tenodesis with anchor (Smith & Nephew) in 1, and biceps tenotomy in 1. Mean time in operating room was 148 minutes; mean time in postoperative recovery unit was 105 minutes.
Directly observing the care cycle, hospital volunteers found that patients spent a mean of 15 minutes with the receptionist when they arrived in the outpatient surgical center, 25 minutes with nurses for check-in in the preoperative holding area, and 10 minutes with the anesthesiology resident and 15 minutes with the orthopedic surgery resident for preoperative evaluation and paperwork. Mean nerve block time was 20 minutes. Mean electrocardiogram (ECG) time (12 patients) was 15 minutes. The surgical technician spent a mean time of 20 minutes setting up the operating room before the patient was brought in and 15 minutes cleaning up after the patient was transferred to the recovery room. Costs of postoperative care in the recovery room were based on a 2:1 patient-to-nurse ratio, as is the standard practice in our outpatient surgery center.
Using the times mentioned and our hospital’s salary data—including standard hospital benefits rates of 33.5% for nonphysicians and 17.65% for physicians—we determined, using the TDABC algorithm, a direct cost of $5904.21 for this process cycle, excluding hospital overhead and indirect costs. Table 2 provides the overall cost breakdown. Compared with the direct economic cost, the mean hospital charge to insurers for the procedure was $31,459.35. Mean reimbursement from insurers was $9679.08.
Overall attending and resident physician costs were $1077.75, which consisted of $623.66 for the surgeon and $454.09 for the anesthesiologist (included placement of nerve block and administration of anesthesia during surgery). Preoperative bloodwork was obtained in 23 cases, adding a mean cost of $111.04 after adjusting for standard hospital markup. Preoperative ECG was performed in 12 cases, for an added mean cost of $7.30 based on the TDABC algorithm.
We also broke down costs by care cycle phase. The preoperative phase, excluding the preoperative laboratory studies and ECGs (not performed in all cases), cost $134.34 (2.3% of total costs); the operative phase cost $5718.01 (96.8% of total costs); and the postoperative phase cost $51.86 (0.9% of total costs). Within the operative phase, the cost of consumables (specifically, suture anchors) was the main cost driver. Mean anchor cost per case was $3432.67. “Complex” tears involving a double-row repair averaged $4570.25 in anchor cost per patient, as compared with $2522.60 in anchor costs for simple repairs.
Discussion
US health care costs continue to increase unsustainably, with rising pressure on hospitals and providers to deliver the highest value for each health care dollar. The present study is the first to calculate (using the TDABC algorithm) the direct economic cost ($5904.21) of the entire RCS care cycle at a university-based outpatient surgery center. Rent, utility costs, administrative costs, overhead, and other indirect costs at the surgery center were not included in this cost analysis, as they would be incurred irrespective of type of surgery performed. As such, our data isolate the procedure-specific costs of rotator cuff repair in order to provide a more meaningful comparison for other institutions, where indirect costs may be different.
In the literature, rigorous economic analysis of shoulder pathology is sparse. Kuye and colleagues12 systematically reviewed economic evaluations in shoulder surgery for the period 1980–2010 and noted more than 50% of the papers were published between 2005 and 2010.12 They also noted the poor quality of these studies and concluded more rigorous economic evaluations are needed to help justify the rising costs of shoulder-related treatments.
Several studies have directly evaluated costs associated with RCS. Cordasco and colleagues13 detailed the success of open rotator cuff repair as an outpatient procedure—noting its 43% cost savings ($4300 for outpatient vs $7500 for inpatient) and high patient satisfaction—using hospital charge data for operating room time, supplies, instruments, and postoperative slings. Churchill and Ghorai14 evaluated costs of mini-open and arthroscopic rotator cuff repairs in a statewide database and estimated the arthroscopic repair cost at $8985, compared with $7841 for the mini-open repair. They used reported hospital charge data, which were not itemized and did not include physician professional fees. Adla and colleagues,15 in a similar analysis of open versus arthroscopic cuff repair, estimated direct material costs of $1609.50 (arthroscopic) and $360.75 (open); these figures were converted from 2005 UK currency using the exchange rate cited in their paper. Salaries of surgeon, anesthesiologist, and other operating room personnel were said to be included in the operating room cost, but the authors’ paper did not include these data.
Two studies directly estimated the costs of arthroscopic rotator cuff repair. Hearnden and Tennent16 calculated the cost of RCS at their UK institution to be £2672, which included cost of operating room consumable materials, medication, and salaries of operating room personnel, including surgeon and anesthesiologist. Using online currency conversion from 2008 exchange rates and adjusting for inflation gave a corresponding US cost of $5449.63.17 Vitale and colleagues18 prospectively calculated costs of arthroscopic rotator cuff repair over a 1-year period using a cost-to-charge ratio from tabulated inpatient charges, procedure charges, and physician fees and payments abstracted from medical records, hospital billing, and administrative databases. Mean total cost for this cycle was $10,605.20, which included several costs (physical therapy, radiologist fees) not included in the present study. These studies, though more comprehensive than prior work, did not capture the entire cycle of surgical care.
Our study was designed to provide initial data on the direct costs of arthroscopic repair of the rotator cuff for the entire process cycle. Our overall cost estimate of $5904.21 differs significantly from prior work—not unexpected given the completely different cost methodology used.
Our study had several limitations. First, it was a single-surgeon evaluation, and a number of operating room variables (eg, use of adjunct instrumentation such as radiofrequency probes, differences in draping preferences) as well as surgeon volume in performing rotator cuff repairs might have substantially affected the reproducibility and generalizability of our data. Similarly, the large number of adjunctive procedures (eg, subacromial decompression, labral débridement) performed in conjunction with the rotator cuff repairs added operative time and therefore increased overall cost. Double-row repairs added operative time and increased the cost of consumable materials as well. Differences in surgeon preference for suture anchors may also be important, as anchors are a major cost driver and can vary significantly between vendors and institutions. Tear-related variables (eg, tear size, tear chronicity, degree of fatty cuff degeneration) were not controlled for and might have significantly affected operative time and associated cost. Resident involvement in the surgical procedure and anesthesia process in an academic setting prolongs surgical time and thus directly impacts costs.
In addition, we used the patient’s time in the operating room as a proxy for actual surgical time, as this was the only reliable and reproducible data point available in our electronic medical record. As such, an unquantifiable amount of surgeon time may have been overallocated to our cost estimate for time spent inducing anesthesia, positioning, helping take the patient off the operating table, and so on. However, as typical surgeon practice is to be involved in these tasks in the operating room, the possible overestimate of surgeon cost is likely minimal.
Our salary data for the TDABC algorithm were based on national averages for work hours and gross income for physicians and on hospital-based wage structure and may not be generalizable to other institutions. There may also be regional differences in work hours and salaries, which in turn would factor into a different per-minute cost for surgeon and anesthesiologist, depending on the exact geographic area where the surgery is performed. Costs may be higher at institutions that use certified nurse anesthetists rather than resident physicians because of the salary differences between these practitioners.
Moreover, the time that patients spend in the holding area—waiting to go into surgery and, after surgery, waiting for their ride home, for their prescriptions to be ready, and so forth—is an important variable to consider from a cost standpoint. However, as this time varied significantly and involved minimal contact with hospital personnel, we excluded its associated costs from our analysis. Similarly, and as already noted, hospital overhead and other indirect costs were excluded from analysis as well.
Conclusion
Using the TDABC algorithm, we found a direct economic cost of $5904.21 for RCS at our academic outpatient surgical center, with anchor cost the main cost driver. Judicious use of consumable resources is a key focus for cost containment in arthroscopic shoulder surgery, particularly with respect to implantable suture anchors. However, in the setting of more complex tears that require multiple anchors in a double-row repair construct, our pilot data may be useful to hospitals and surgery centers negotiating procedural reimbursement for the increased cost of complex repairs. Use of the TDABC algorithm for RCS and other procedures may also help in identifying opportunities to deliver more cost-effective health care.
1. American Academy of Orthopaedic Surgeons. The Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2011.
2. National health expenditure data. Centers for Medicare & Medicare Services website. https://www.cms.gov/Research-Statistics-Data-and-Systems/Statistics-Trends-and-Reports/NationalHealthExpendData/index.html. Updated May 5, 2014. Accessed December 1, 2015.
3. Tashjian RZ. Epidemiology, natural history, and indications for treatment of rotator cuff tears. Clin Sports Med. 2012;31(4):589-604.
4. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am. 2012;94(3):227-233.
5. Black EM, Higgins LD, Warner JJ. Value-based shoulder surgery: practicing outcomes-driven, cost-conscious care. J Shoulder Elbow Surg. 2013;22(7):1000-1009.
6. Porter ME, Teisberg EO. Redefining Health Care: Creating Value-Based Competition on Results. Boston, MA: Harvard Business School Press; 2006.
7. Kaplan RS, Porter ME. How to solve the cost crisis in health care. Harv Bus Rev. 2011;89(9):46-52, 54, 56-61 passim.
8. Kaplan RS, Anderson SR. Time-driven activity-based costing. Harv Bus Rev. 2004;82(11):131-138, 150.
9. Kaplan RS, Anderson SR. Time-Driven Activity-Based Costing: A Simpler and More Powerful Path to Higher Profits. Boston, MA: Harvard Business Review Press; 2007.
10. American Academy of Orthopaedic Surgeons. Orthopaedic Practice in the U.S. 2012. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2012.
11. Medical Group Management Association. Physician Compensation and Production Survey: 2012 Report Based on 2011 Data. Englewood, CO: Medical Group Management Association; 2012.
12. Kuye IO, Jain NB, Warner L, Herndon JH, Warner JJ. Economic evaluations in shoulder pathologies: a systematic review of the literature. J Shoulder Elbow Surg. 2012;21(3):367-375.
13. Cordasco FA, McGinley BJ, Charlton T. Rotator cuff repair as an outpatient procedure. J Shoulder Elbow Surg. 2000;9(1):27-30.
14. Churchill RS, Ghorai JK. Total cost and operating room time comparison of rotator cuff repair techniques at low, intermediate, and high volume centers: mini-open versus all-arthroscopic. J Shoulder Elbow Surg. 2010;19(5):716-721.
15. Adla DN, Rowsell M, Pandey R. Cost-effectiveness of open versus arthroscopic rotator cuff repair. J Shoulder Elbow Surg. 2010;19(2):258-261.
16. Hearnden A, Tennent D. The cost of shoulder arthroscopy: a comparison with national tariff. Ann R Coll Surg Engl. 2008;90(7):587-591.
17. Xrates currency conversion. http://www.x-rates.com/historical/?from=GBP&amount=1&date=2015-12-03. Accessed December 13, 2015.
18. Vitale MA, Vitale MG, Zivin JG, Braman JP, Bigliani LU, Flatow EL. Rotator cuff repair: an analysis of utility scores and cost-effectiveness. J Shoulder Elbow Surg. 2007;16(2):181-187.
Musculoskeletal disorders, the leading cause of disability in the United States,1 account for more than half of all persons reporting missing a workday because of a medical condition.2 Shoulder disorders in particular play a significant role in the burden of musculoskeletal disorders and cost of care. In 2008, 18.9 million adults (8.2% of the US adult population) reported chronic shoulder pain.1 Among shoulder disorders, rotator cuff pathology is the most common cause of shoulder-related disability found by orthopedic surgeons.3 Rotator cuff surgery (RCS) is one of the most commonly performed orthopedic surgical procedures, and surgery volume is on the rise. One study found a 141% increase in rotator cuff repairs between the years 1996 (~41 per 100,000 population) and 2006 (~98 per 100,000 population).4
US health care costs are also increasing. In 2011, $2.7 trillion was spent on health care, representing 17.9% of the national gross domestic product (GDP). According to projections, costs will rise to $4.6 trillion by 2020.5 In particular, as patients continue to live longer and remain more active into their later years, the costs of treating and managing musculoskeletal disorders become more important from a public policy standpoint. In 2006, the cost of treating musculoskeletal disorders alone was $576 billion, representing 4.5% of that year’s GDP.2
Paramount in this era of rising costs is the idea of maximizing the value of health care dollars. Health care economists Porter and Teisberg6 defined value as patient health outcomes achieved per dollar of cost expended in a care cycle (diagnosis, treatment, ongoing management) for a particular disease or disorder. For proper management of value, outcomes and costs for an entire cycle of care must be determined. From a practical standpoint, this first requires determining the true cost of a care cycle—dollars spent on personnel, equipment, materials, and other resources required to deliver a particular service—rather than the amount charged or reimbursed for providing the service in question.7
Kaplan and Anderson8,9 described the TDABC (time-driven activity-based costing) algorithm for calculating the cost of delivering a service based on 2 parameters: unit cost of a particular resource, and time required to supply it. These parameters apply to material costs and labor costs. In the medical setting, the TDABC algorithm can be applied by defining a care delivery value chain for each aspect of patient care and then multiplying incremental cost per unit time by time required to deliver that resource (Figure 1). Tabulating the overall unit cost for each resource then yields the overall cost of the care cycle. Clinical outcomes data can then be determined and used to calculate overall value for the patient care cycle.
In the study reported here, we used the TDABC algorithm to calculate the direct financial costs of surgical treatment of rotator cuff tears confirmed by magnetic resonance imaging (MRI) in an academic medical center.
Methods
Per our institution’s Office for the Protection of Research Subjects, institutional review board (IRB) approval is required only for projects using “human subjects” as defined by federal policy. In the present study, no private information could be identified, and all data were obtained from hospital billing records without intervention or interaction with individual patients. Accordingly, IRB approval was deemed unnecessary for our economic cost analysis.
Billing records of a single academic fellowship-trained sports surgeon were reviewed to identify patients who underwent primary repair of an MRI-confirmed rotator cuff tear between April 1, 2009, and July 31, 2012. Patients who had undergone prior shoulder surgery of any type were excluded from the study. Operative reports were reviewed, and exact surgical procedures performed were noted. The operating surgeon selected the specific repair techniques, including single- or double-row repair, with emphasis on restoring footprint coverage and avoiding overtensioning.
All surgeries were performed in an outpatient surgical center owned and operated by the surgeon’s home university. Surgeries were performed by the attending physician assisted by a senior orthopedic resident. The RCS care cycle was divided into 3 phases (Figure 2):
1. Preoperative. Patient’s interaction with receptionist in surgery center, time with preoperative nurse and circulating nurse in preoperative area, resident check-in time, and time placing preoperative nerve block and consumable materials used during block placement.
2. Operative. Time in operating room with surgical team for RCS, consumable materials used during surgery (eg, anchors, shavers, drapes), anesthetic medications, shoulder abduction pillow placed on completion of surgery, and cost of instrument processing.
3. Postoperative. Time in postoperative recovery area with recovery room nursing staff.
Time in each portion of the care cycle was directly observed and tabulated by hospital volunteers in the surgery center. Institutional billing data were used to identify material resources consumed, and the actual cost paid by the hospital for these resources was obtained from internal records. Mean hourly salary data and standard benefit rates were obtained for surgery center staff. Attending physician salary was extrapolated from published mean market salary data for academic physicians and mean hours worked,10,11 and resident physician costs were tabulated from publically available institutional payroll data and average resident work hours at our institution. These cost data and times were then used to tabulate total cost for the RCS care cycle using the TDABC algorithm.
Results
We identified 28 shoulders in 26 patients (mean age, 54.5 years) who met the inclusion criteria. Of these 28 shoulders, 18 (64.3%) had an isolated supraspinatus tear, 8 (28.6%) had combined supraspinatus and infraspinatus tears, 1 (3.6%) had combined supraspinatus and subscapularis tears, and 1 (3.6%) had an isolated infraspinatus tear. Demographic data are listed in Table 1.
All patients received an interscalene nerve block in the preoperative area before being brought into the operating room. In our analysis, we included nerve block supply costs and the anesthesiologist’s mean time placing the nerve block.
In all cases, primary rotator cuff repair was performed with suture anchors (Parcus Medical) with the patient in the lateral decubitus position. In 13 (46%) of the 28 shoulders, this repair was described as “complex,” requiring double-row technique. Subacromial decompression and bursectomy were performed in addition to the rotator cuff repair. Labral débridement was performed in 23 patients, synovectomy in 10, biceps tenodesis with anchor (Smith & Nephew) in 1, and biceps tenotomy in 1. Mean time in operating room was 148 minutes; mean time in postoperative recovery unit was 105 minutes.
Directly observing the care cycle, hospital volunteers found that patients spent a mean of 15 minutes with the receptionist when they arrived in the outpatient surgical center, 25 minutes with nurses for check-in in the preoperative holding area, and 10 minutes with the anesthesiology resident and 15 minutes with the orthopedic surgery resident for preoperative evaluation and paperwork. Mean nerve block time was 20 minutes. Mean electrocardiogram (ECG) time (12 patients) was 15 minutes. The surgical technician spent a mean time of 20 minutes setting up the operating room before the patient was brought in and 15 minutes cleaning up after the patient was transferred to the recovery room. Costs of postoperative care in the recovery room were based on a 2:1 patient-to-nurse ratio, as is the standard practice in our outpatient surgery center.
Using the times mentioned and our hospital’s salary data—including standard hospital benefits rates of 33.5% for nonphysicians and 17.65% for physicians—we determined, using the TDABC algorithm, a direct cost of $5904.21 for this process cycle, excluding hospital overhead and indirect costs. Table 2 provides the overall cost breakdown. Compared with the direct economic cost, the mean hospital charge to insurers for the procedure was $31,459.35. Mean reimbursement from insurers was $9679.08.
Overall attending and resident physician costs were $1077.75, which consisted of $623.66 for the surgeon and $454.09 for the anesthesiologist (included placement of nerve block and administration of anesthesia during surgery). Preoperative bloodwork was obtained in 23 cases, adding a mean cost of $111.04 after adjusting for standard hospital markup. Preoperative ECG was performed in 12 cases, for an added mean cost of $7.30 based on the TDABC algorithm.
We also broke down costs by care cycle phase. The preoperative phase, excluding the preoperative laboratory studies and ECGs (not performed in all cases), cost $134.34 (2.3% of total costs); the operative phase cost $5718.01 (96.8% of total costs); and the postoperative phase cost $51.86 (0.9% of total costs). Within the operative phase, the cost of consumables (specifically, suture anchors) was the main cost driver. Mean anchor cost per case was $3432.67. “Complex” tears involving a double-row repair averaged $4570.25 in anchor cost per patient, as compared with $2522.60 in anchor costs for simple repairs.
Discussion
US health care costs continue to increase unsustainably, with rising pressure on hospitals and providers to deliver the highest value for each health care dollar. The present study is the first to calculate (using the TDABC algorithm) the direct economic cost ($5904.21) of the entire RCS care cycle at a university-based outpatient surgery center. Rent, utility costs, administrative costs, overhead, and other indirect costs at the surgery center were not included in this cost analysis, as they would be incurred irrespective of type of surgery performed. As such, our data isolate the procedure-specific costs of rotator cuff repair in order to provide a more meaningful comparison for other institutions, where indirect costs may be different.
In the literature, rigorous economic analysis of shoulder pathology is sparse. Kuye and colleagues12 systematically reviewed economic evaluations in shoulder surgery for the period 1980–2010 and noted more than 50% of the papers were published between 2005 and 2010.12 They also noted the poor quality of these studies and concluded more rigorous economic evaluations are needed to help justify the rising costs of shoulder-related treatments.
Several studies have directly evaluated costs associated with RCS. Cordasco and colleagues13 detailed the success of open rotator cuff repair as an outpatient procedure—noting its 43% cost savings ($4300 for outpatient vs $7500 for inpatient) and high patient satisfaction—using hospital charge data for operating room time, supplies, instruments, and postoperative slings. Churchill and Ghorai14 evaluated costs of mini-open and arthroscopic rotator cuff repairs in a statewide database and estimated the arthroscopic repair cost at $8985, compared with $7841 for the mini-open repair. They used reported hospital charge data, which were not itemized and did not include physician professional fees. Adla and colleagues,15 in a similar analysis of open versus arthroscopic cuff repair, estimated direct material costs of $1609.50 (arthroscopic) and $360.75 (open); these figures were converted from 2005 UK currency using the exchange rate cited in their paper. Salaries of surgeon, anesthesiologist, and other operating room personnel were said to be included in the operating room cost, but the authors’ paper did not include these data.
Two studies directly estimated the costs of arthroscopic rotator cuff repair. Hearnden and Tennent16 calculated the cost of RCS at their UK institution to be £2672, which included cost of operating room consumable materials, medication, and salaries of operating room personnel, including surgeon and anesthesiologist. Using online currency conversion from 2008 exchange rates and adjusting for inflation gave a corresponding US cost of $5449.63.17 Vitale and colleagues18 prospectively calculated costs of arthroscopic rotator cuff repair over a 1-year period using a cost-to-charge ratio from tabulated inpatient charges, procedure charges, and physician fees and payments abstracted from medical records, hospital billing, and administrative databases. Mean total cost for this cycle was $10,605.20, which included several costs (physical therapy, radiologist fees) not included in the present study. These studies, though more comprehensive than prior work, did not capture the entire cycle of surgical care.
Our study was designed to provide initial data on the direct costs of arthroscopic repair of the rotator cuff for the entire process cycle. Our overall cost estimate of $5904.21 differs significantly from prior work—not unexpected given the completely different cost methodology used.
Our study had several limitations. First, it was a single-surgeon evaluation, and a number of operating room variables (eg, use of adjunct instrumentation such as radiofrequency probes, differences in draping preferences) as well as surgeon volume in performing rotator cuff repairs might have substantially affected the reproducibility and generalizability of our data. Similarly, the large number of adjunctive procedures (eg, subacromial decompression, labral débridement) performed in conjunction with the rotator cuff repairs added operative time and therefore increased overall cost. Double-row repairs added operative time and increased the cost of consumable materials as well. Differences in surgeon preference for suture anchors may also be important, as anchors are a major cost driver and can vary significantly between vendors and institutions. Tear-related variables (eg, tear size, tear chronicity, degree of fatty cuff degeneration) were not controlled for and might have significantly affected operative time and associated cost. Resident involvement in the surgical procedure and anesthesia process in an academic setting prolongs surgical time and thus directly impacts costs.
In addition, we used the patient’s time in the operating room as a proxy for actual surgical time, as this was the only reliable and reproducible data point available in our electronic medical record. As such, an unquantifiable amount of surgeon time may have been overallocated to our cost estimate for time spent inducing anesthesia, positioning, helping take the patient off the operating table, and so on. However, as typical surgeon practice is to be involved in these tasks in the operating room, the possible overestimate of surgeon cost is likely minimal.
Our salary data for the TDABC algorithm were based on national averages for work hours and gross income for physicians and on hospital-based wage structure and may not be generalizable to other institutions. There may also be regional differences in work hours and salaries, which in turn would factor into a different per-minute cost for surgeon and anesthesiologist, depending on the exact geographic area where the surgery is performed. Costs may be higher at institutions that use certified nurse anesthetists rather than resident physicians because of the salary differences between these practitioners.
Moreover, the time that patients spend in the holding area—waiting to go into surgery and, after surgery, waiting for their ride home, for their prescriptions to be ready, and so forth—is an important variable to consider from a cost standpoint. However, as this time varied significantly and involved minimal contact with hospital personnel, we excluded its associated costs from our analysis. Similarly, and as already noted, hospital overhead and other indirect costs were excluded from analysis as well.
Conclusion
Using the TDABC algorithm, we found a direct economic cost of $5904.21 for RCS at our academic outpatient surgical center, with anchor cost the main cost driver. Judicious use of consumable resources is a key focus for cost containment in arthroscopic shoulder surgery, particularly with respect to implantable suture anchors. However, in the setting of more complex tears that require multiple anchors in a double-row repair construct, our pilot data may be useful to hospitals and surgery centers negotiating procedural reimbursement for the increased cost of complex repairs. Use of the TDABC algorithm for RCS and other procedures may also help in identifying opportunities to deliver more cost-effective health care.
Musculoskeletal disorders, the leading cause of disability in the United States,1 account for more than half of all persons reporting missing a workday because of a medical condition.2 Shoulder disorders in particular play a significant role in the burden of musculoskeletal disorders and cost of care. In 2008, 18.9 million adults (8.2% of the US adult population) reported chronic shoulder pain.1 Among shoulder disorders, rotator cuff pathology is the most common cause of shoulder-related disability found by orthopedic surgeons.3 Rotator cuff surgery (RCS) is one of the most commonly performed orthopedic surgical procedures, and surgery volume is on the rise. One study found a 141% increase in rotator cuff repairs between the years 1996 (~41 per 100,000 population) and 2006 (~98 per 100,000 population).4
US health care costs are also increasing. In 2011, $2.7 trillion was spent on health care, representing 17.9% of the national gross domestic product (GDP). According to projections, costs will rise to $4.6 trillion by 2020.5 In particular, as patients continue to live longer and remain more active into their later years, the costs of treating and managing musculoskeletal disorders become more important from a public policy standpoint. In 2006, the cost of treating musculoskeletal disorders alone was $576 billion, representing 4.5% of that year’s GDP.2
Paramount in this era of rising costs is the idea of maximizing the value of health care dollars. Health care economists Porter and Teisberg6 defined value as patient health outcomes achieved per dollar of cost expended in a care cycle (diagnosis, treatment, ongoing management) for a particular disease or disorder. For proper management of value, outcomes and costs for an entire cycle of care must be determined. From a practical standpoint, this first requires determining the true cost of a care cycle—dollars spent on personnel, equipment, materials, and other resources required to deliver a particular service—rather than the amount charged or reimbursed for providing the service in question.7
Kaplan and Anderson8,9 described the TDABC (time-driven activity-based costing) algorithm for calculating the cost of delivering a service based on 2 parameters: unit cost of a particular resource, and time required to supply it. These parameters apply to material costs and labor costs. In the medical setting, the TDABC algorithm can be applied by defining a care delivery value chain for each aspect of patient care and then multiplying incremental cost per unit time by time required to deliver that resource (Figure 1). Tabulating the overall unit cost for each resource then yields the overall cost of the care cycle. Clinical outcomes data can then be determined and used to calculate overall value for the patient care cycle.
In the study reported here, we used the TDABC algorithm to calculate the direct financial costs of surgical treatment of rotator cuff tears confirmed by magnetic resonance imaging (MRI) in an academic medical center.
Methods
Per our institution’s Office for the Protection of Research Subjects, institutional review board (IRB) approval is required only for projects using “human subjects” as defined by federal policy. In the present study, no private information could be identified, and all data were obtained from hospital billing records without intervention or interaction with individual patients. Accordingly, IRB approval was deemed unnecessary for our economic cost analysis.
Billing records of a single academic fellowship-trained sports surgeon were reviewed to identify patients who underwent primary repair of an MRI-confirmed rotator cuff tear between April 1, 2009, and July 31, 2012. Patients who had undergone prior shoulder surgery of any type were excluded from the study. Operative reports were reviewed, and exact surgical procedures performed were noted. The operating surgeon selected the specific repair techniques, including single- or double-row repair, with emphasis on restoring footprint coverage and avoiding overtensioning.
All surgeries were performed in an outpatient surgical center owned and operated by the surgeon’s home university. Surgeries were performed by the attending physician assisted by a senior orthopedic resident. The RCS care cycle was divided into 3 phases (Figure 2):
1. Preoperative. Patient’s interaction with receptionist in surgery center, time with preoperative nurse and circulating nurse in preoperative area, resident check-in time, and time placing preoperative nerve block and consumable materials used during block placement.
2. Operative. Time in operating room with surgical team for RCS, consumable materials used during surgery (eg, anchors, shavers, drapes), anesthetic medications, shoulder abduction pillow placed on completion of surgery, and cost of instrument processing.
3. Postoperative. Time in postoperative recovery area with recovery room nursing staff.
Time in each portion of the care cycle was directly observed and tabulated by hospital volunteers in the surgery center. Institutional billing data were used to identify material resources consumed, and the actual cost paid by the hospital for these resources was obtained from internal records. Mean hourly salary data and standard benefit rates were obtained for surgery center staff. Attending physician salary was extrapolated from published mean market salary data for academic physicians and mean hours worked,10,11 and resident physician costs were tabulated from publically available institutional payroll data and average resident work hours at our institution. These cost data and times were then used to tabulate total cost for the RCS care cycle using the TDABC algorithm.
Results
We identified 28 shoulders in 26 patients (mean age, 54.5 years) who met the inclusion criteria. Of these 28 shoulders, 18 (64.3%) had an isolated supraspinatus tear, 8 (28.6%) had combined supraspinatus and infraspinatus tears, 1 (3.6%) had combined supraspinatus and subscapularis tears, and 1 (3.6%) had an isolated infraspinatus tear. Demographic data are listed in Table 1.
All patients received an interscalene nerve block in the preoperative area before being brought into the operating room. In our analysis, we included nerve block supply costs and the anesthesiologist’s mean time placing the nerve block.
In all cases, primary rotator cuff repair was performed with suture anchors (Parcus Medical) with the patient in the lateral decubitus position. In 13 (46%) of the 28 shoulders, this repair was described as “complex,” requiring double-row technique. Subacromial decompression and bursectomy were performed in addition to the rotator cuff repair. Labral débridement was performed in 23 patients, synovectomy in 10, biceps tenodesis with anchor (Smith & Nephew) in 1, and biceps tenotomy in 1. Mean time in operating room was 148 minutes; mean time in postoperative recovery unit was 105 minutes.
Directly observing the care cycle, hospital volunteers found that patients spent a mean of 15 minutes with the receptionist when they arrived in the outpatient surgical center, 25 minutes with nurses for check-in in the preoperative holding area, and 10 minutes with the anesthesiology resident and 15 minutes with the orthopedic surgery resident for preoperative evaluation and paperwork. Mean nerve block time was 20 minutes. Mean electrocardiogram (ECG) time (12 patients) was 15 minutes. The surgical technician spent a mean time of 20 minutes setting up the operating room before the patient was brought in and 15 minutes cleaning up after the patient was transferred to the recovery room. Costs of postoperative care in the recovery room were based on a 2:1 patient-to-nurse ratio, as is the standard practice in our outpatient surgery center.
Using the times mentioned and our hospital’s salary data—including standard hospital benefits rates of 33.5% for nonphysicians and 17.65% for physicians—we determined, using the TDABC algorithm, a direct cost of $5904.21 for this process cycle, excluding hospital overhead and indirect costs. Table 2 provides the overall cost breakdown. Compared with the direct economic cost, the mean hospital charge to insurers for the procedure was $31,459.35. Mean reimbursement from insurers was $9679.08.
Overall attending and resident physician costs were $1077.75, which consisted of $623.66 for the surgeon and $454.09 for the anesthesiologist (included placement of nerve block and administration of anesthesia during surgery). Preoperative bloodwork was obtained in 23 cases, adding a mean cost of $111.04 after adjusting for standard hospital markup. Preoperative ECG was performed in 12 cases, for an added mean cost of $7.30 based on the TDABC algorithm.
We also broke down costs by care cycle phase. The preoperative phase, excluding the preoperative laboratory studies and ECGs (not performed in all cases), cost $134.34 (2.3% of total costs); the operative phase cost $5718.01 (96.8% of total costs); and the postoperative phase cost $51.86 (0.9% of total costs). Within the operative phase, the cost of consumables (specifically, suture anchors) was the main cost driver. Mean anchor cost per case was $3432.67. “Complex” tears involving a double-row repair averaged $4570.25 in anchor cost per patient, as compared with $2522.60 in anchor costs for simple repairs.
Discussion
US health care costs continue to increase unsustainably, with rising pressure on hospitals and providers to deliver the highest value for each health care dollar. The present study is the first to calculate (using the TDABC algorithm) the direct economic cost ($5904.21) of the entire RCS care cycle at a university-based outpatient surgery center. Rent, utility costs, administrative costs, overhead, and other indirect costs at the surgery center were not included in this cost analysis, as they would be incurred irrespective of type of surgery performed. As such, our data isolate the procedure-specific costs of rotator cuff repair in order to provide a more meaningful comparison for other institutions, where indirect costs may be different.
In the literature, rigorous economic analysis of shoulder pathology is sparse. Kuye and colleagues12 systematically reviewed economic evaluations in shoulder surgery for the period 1980–2010 and noted more than 50% of the papers were published between 2005 and 2010.12 They also noted the poor quality of these studies and concluded more rigorous economic evaluations are needed to help justify the rising costs of shoulder-related treatments.
Several studies have directly evaluated costs associated with RCS. Cordasco and colleagues13 detailed the success of open rotator cuff repair as an outpatient procedure—noting its 43% cost savings ($4300 for outpatient vs $7500 for inpatient) and high patient satisfaction—using hospital charge data for operating room time, supplies, instruments, and postoperative slings. Churchill and Ghorai14 evaluated costs of mini-open and arthroscopic rotator cuff repairs in a statewide database and estimated the arthroscopic repair cost at $8985, compared with $7841 for the mini-open repair. They used reported hospital charge data, which were not itemized and did not include physician professional fees. Adla and colleagues,15 in a similar analysis of open versus arthroscopic cuff repair, estimated direct material costs of $1609.50 (arthroscopic) and $360.75 (open); these figures were converted from 2005 UK currency using the exchange rate cited in their paper. Salaries of surgeon, anesthesiologist, and other operating room personnel were said to be included in the operating room cost, but the authors’ paper did not include these data.
Two studies directly estimated the costs of arthroscopic rotator cuff repair. Hearnden and Tennent16 calculated the cost of RCS at their UK institution to be £2672, which included cost of operating room consumable materials, medication, and salaries of operating room personnel, including surgeon and anesthesiologist. Using online currency conversion from 2008 exchange rates and adjusting for inflation gave a corresponding US cost of $5449.63.17 Vitale and colleagues18 prospectively calculated costs of arthroscopic rotator cuff repair over a 1-year period using a cost-to-charge ratio from tabulated inpatient charges, procedure charges, and physician fees and payments abstracted from medical records, hospital billing, and administrative databases. Mean total cost for this cycle was $10,605.20, which included several costs (physical therapy, radiologist fees) not included in the present study. These studies, though more comprehensive than prior work, did not capture the entire cycle of surgical care.
Our study was designed to provide initial data on the direct costs of arthroscopic repair of the rotator cuff for the entire process cycle. Our overall cost estimate of $5904.21 differs significantly from prior work—not unexpected given the completely different cost methodology used.
Our study had several limitations. First, it was a single-surgeon evaluation, and a number of operating room variables (eg, use of adjunct instrumentation such as radiofrequency probes, differences in draping preferences) as well as surgeon volume in performing rotator cuff repairs might have substantially affected the reproducibility and generalizability of our data. Similarly, the large number of adjunctive procedures (eg, subacromial decompression, labral débridement) performed in conjunction with the rotator cuff repairs added operative time and therefore increased overall cost. Double-row repairs added operative time and increased the cost of consumable materials as well. Differences in surgeon preference for suture anchors may also be important, as anchors are a major cost driver and can vary significantly between vendors and institutions. Tear-related variables (eg, tear size, tear chronicity, degree of fatty cuff degeneration) were not controlled for and might have significantly affected operative time and associated cost. Resident involvement in the surgical procedure and anesthesia process in an academic setting prolongs surgical time and thus directly impacts costs.
In addition, we used the patient’s time in the operating room as a proxy for actual surgical time, as this was the only reliable and reproducible data point available in our electronic medical record. As such, an unquantifiable amount of surgeon time may have been overallocated to our cost estimate for time spent inducing anesthesia, positioning, helping take the patient off the operating table, and so on. However, as typical surgeon practice is to be involved in these tasks in the operating room, the possible overestimate of surgeon cost is likely minimal.
Our salary data for the TDABC algorithm were based on national averages for work hours and gross income for physicians and on hospital-based wage structure and may not be generalizable to other institutions. There may also be regional differences in work hours and salaries, which in turn would factor into a different per-minute cost for surgeon and anesthesiologist, depending on the exact geographic area where the surgery is performed. Costs may be higher at institutions that use certified nurse anesthetists rather than resident physicians because of the salary differences between these practitioners.
Moreover, the time that patients spend in the holding area—waiting to go into surgery and, after surgery, waiting for their ride home, for their prescriptions to be ready, and so forth—is an important variable to consider from a cost standpoint. However, as this time varied significantly and involved minimal contact with hospital personnel, we excluded its associated costs from our analysis. Similarly, and as already noted, hospital overhead and other indirect costs were excluded from analysis as well.
Conclusion
Using the TDABC algorithm, we found a direct economic cost of $5904.21 for RCS at our academic outpatient surgical center, with anchor cost the main cost driver. Judicious use of consumable resources is a key focus for cost containment in arthroscopic shoulder surgery, particularly with respect to implantable suture anchors. However, in the setting of more complex tears that require multiple anchors in a double-row repair construct, our pilot data may be useful to hospitals and surgery centers negotiating procedural reimbursement for the increased cost of complex repairs. Use of the TDABC algorithm for RCS and other procedures may also help in identifying opportunities to deliver more cost-effective health care.
1. American Academy of Orthopaedic Surgeons. The Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2011.
2. National health expenditure data. Centers for Medicare & Medicare Services website. https://www.cms.gov/Research-Statistics-Data-and-Systems/Statistics-Trends-and-Reports/NationalHealthExpendData/index.html. Updated May 5, 2014. Accessed December 1, 2015.
3. Tashjian RZ. Epidemiology, natural history, and indications for treatment of rotator cuff tears. Clin Sports Med. 2012;31(4):589-604.
4. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am. 2012;94(3):227-233.
5. Black EM, Higgins LD, Warner JJ. Value-based shoulder surgery: practicing outcomes-driven, cost-conscious care. J Shoulder Elbow Surg. 2013;22(7):1000-1009.
6. Porter ME, Teisberg EO. Redefining Health Care: Creating Value-Based Competition on Results. Boston, MA: Harvard Business School Press; 2006.
7. Kaplan RS, Porter ME. How to solve the cost crisis in health care. Harv Bus Rev. 2011;89(9):46-52, 54, 56-61 passim.
8. Kaplan RS, Anderson SR. Time-driven activity-based costing. Harv Bus Rev. 2004;82(11):131-138, 150.
9. Kaplan RS, Anderson SR. Time-Driven Activity-Based Costing: A Simpler and More Powerful Path to Higher Profits. Boston, MA: Harvard Business Review Press; 2007.
10. American Academy of Orthopaedic Surgeons. Orthopaedic Practice in the U.S. 2012. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2012.
11. Medical Group Management Association. Physician Compensation and Production Survey: 2012 Report Based on 2011 Data. Englewood, CO: Medical Group Management Association; 2012.
12. Kuye IO, Jain NB, Warner L, Herndon JH, Warner JJ. Economic evaluations in shoulder pathologies: a systematic review of the literature. J Shoulder Elbow Surg. 2012;21(3):367-375.
13. Cordasco FA, McGinley BJ, Charlton T. Rotator cuff repair as an outpatient procedure. J Shoulder Elbow Surg. 2000;9(1):27-30.
14. Churchill RS, Ghorai JK. Total cost and operating room time comparison of rotator cuff repair techniques at low, intermediate, and high volume centers: mini-open versus all-arthroscopic. J Shoulder Elbow Surg. 2010;19(5):716-721.
15. Adla DN, Rowsell M, Pandey R. Cost-effectiveness of open versus arthroscopic rotator cuff repair. J Shoulder Elbow Surg. 2010;19(2):258-261.
16. Hearnden A, Tennent D. The cost of shoulder arthroscopy: a comparison with national tariff. Ann R Coll Surg Engl. 2008;90(7):587-591.
17. Xrates currency conversion. http://www.x-rates.com/historical/?from=GBP&amount=1&date=2015-12-03. Accessed December 13, 2015.
18. Vitale MA, Vitale MG, Zivin JG, Braman JP, Bigliani LU, Flatow EL. Rotator cuff repair: an analysis of utility scores and cost-effectiveness. J Shoulder Elbow Surg. 2007;16(2):181-187.
1. American Academy of Orthopaedic Surgeons. The Burden of Musculoskeletal Diseases in the United States: Prevalence, Societal and Economic Cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2011.
2. National health expenditure data. Centers for Medicare & Medicare Services website. https://www.cms.gov/Research-Statistics-Data-and-Systems/Statistics-Trends-and-Reports/NationalHealthExpendData/index.html. Updated May 5, 2014. Accessed December 1, 2015.
3. Tashjian RZ. Epidemiology, natural history, and indications for treatment of rotator cuff tears. Clin Sports Med. 2012;31(4):589-604.
4. Colvin AC, Egorova N, Harrison AK, Moskowitz A, Flatow EL. National trends in rotator cuff repair. J Bone Joint Surg Am. 2012;94(3):227-233.
5. Black EM, Higgins LD, Warner JJ. Value-based shoulder surgery: practicing outcomes-driven, cost-conscious care. J Shoulder Elbow Surg. 2013;22(7):1000-1009.
6. Porter ME, Teisberg EO. Redefining Health Care: Creating Value-Based Competition on Results. Boston, MA: Harvard Business School Press; 2006.
7. Kaplan RS, Porter ME. How to solve the cost crisis in health care. Harv Bus Rev. 2011;89(9):46-52, 54, 56-61 passim.
8. Kaplan RS, Anderson SR. Time-driven activity-based costing. Harv Bus Rev. 2004;82(11):131-138, 150.
9. Kaplan RS, Anderson SR. Time-Driven Activity-Based Costing: A Simpler and More Powerful Path to Higher Profits. Boston, MA: Harvard Business Review Press; 2007.
10. American Academy of Orthopaedic Surgeons. Orthopaedic Practice in the U.S. 2012. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2012.
11. Medical Group Management Association. Physician Compensation and Production Survey: 2012 Report Based on 2011 Data. Englewood, CO: Medical Group Management Association; 2012.
12. Kuye IO, Jain NB, Warner L, Herndon JH, Warner JJ. Economic evaluations in shoulder pathologies: a systematic review of the literature. J Shoulder Elbow Surg. 2012;21(3):367-375.
13. Cordasco FA, McGinley BJ, Charlton T. Rotator cuff repair as an outpatient procedure. J Shoulder Elbow Surg. 2000;9(1):27-30.
14. Churchill RS, Ghorai JK. Total cost and operating room time comparison of rotator cuff repair techniques at low, intermediate, and high volume centers: mini-open versus all-arthroscopic. J Shoulder Elbow Surg. 2010;19(5):716-721.
15. Adla DN, Rowsell M, Pandey R. Cost-effectiveness of open versus arthroscopic rotator cuff repair. J Shoulder Elbow Surg. 2010;19(2):258-261.
16. Hearnden A, Tennent D. The cost of shoulder arthroscopy: a comparison with national tariff. Ann R Coll Surg Engl. 2008;90(7):587-591.
17. Xrates currency conversion. http://www.x-rates.com/historical/?from=GBP&amount=1&date=2015-12-03. Accessed December 13, 2015.
18. Vitale MA, Vitale MG, Zivin JG, Braman JP, Bigliani LU, Flatow EL. Rotator cuff repair: an analysis of utility scores and cost-effectiveness. J Shoulder Elbow Surg. 2007;16(2):181-187.
Medial Patellar Subluxation: Diagnosis and Treatment
Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.
Diagnosis
MPS diagnosis can be challenging. Often, clinical examination findings are subtle, and radiographs may not show significant pathology. The most accurate diagnosis is obtained by combining patient history, physical examination findings, imaging studies, and diagnostic arthroscopy.
Patient History
Patients with MPS report chronic pain localized to the inferior medial patella and anterior-medial joint line. Occasionally, they complain of crepitus and intermittent swelling. Other symptoms include pain with knee flexion activity, such as squatting and climbing or descending stairs. Some patients describe episodes of giving way and feelings of instability. Often, they are aware the direction of instability is medial. The pain typically is not relieved by medication, physical therapy, or bracing.
Physical Examination
MPS must be identified by clinical examination. Peripatellar tenderness is typically noted. There is often no effusion or crepitus, but the patella is unstable in early flexion. Active and passive ROM is painful through the first 30° of knee flexion. The patient may have a positive medial apprehension test7 in which he or she experiences apprehension of the patella being subluxated with a medially directed force on the lateral border of the patella.
The gravity subluxation test described by Nonweiler and DeLee6 is useful in detecting MPS after lateral release and indicates that the vastus lateralis muscle has been detached from the patella and that the lateral retinaculum is lax. In this test, the patient is positioned in the lateral decubitus position with the involved knee farthest from the table. In this position, gravity causes the patella to subluxate out of the trochlea. The test is positive for MPS when a voluntary contraction of the quadriceps does not center the patella into the trochlear groove. Patients with MPS without previous lateral release can have the patella subluxate medially in the lateral decubitus position, but it is pulled back into the trochlea with active quadriceps contraction (Figure 1).
Patients with MPS often have lateral patellar laxity (LPL), which allows the patella to rotate upward on the lateral side and skid across the medial facet of the femoral trochlea. A physical examination sign combining lateral patellar glide and tilt was described by Shneider24 to identify LPL. This “lateral patellar float” sign is present when the patella translates laterally and rotates or tilts upward with medial pressure on the patella (Figure 2). Another maneuver to test for subtle MPS involves manually centering the patella in the trochlea during active knee flexion and extension. The involved knee is examined in the seated position. The examiner attempts to center the patella in the trochlea with a laterally directed force from the examiner’s thumb on the medial border of the patella. This will usually provide immediate relief as the patient actively ranges the knee.
Imaging Studies
Diagnostic imaging is a crucial component of the evaluation and treatment decision process. Plain radiographs often are not helpful in diagnosing MPS but may provide additional information.5 A variety of radiographic measurements have been described as indicators of structural disease, but there is a lack of comprehensive information recommending radiographic evaluation and interpretation of patients with patellofemoral dysfunction. It is crucial that orthopedic surgeons have common and consistent radiographic views for plain radiographic assessment that can serve as a basis for accurate diagnosis and surgical decision-making.
Standard knee radiographs should include a standing anteroposterior view of bilateral knees, a standing lateral view of the symptomatic knee in 30° of flexion, a patellar axial view, and a tunnel view. These views, occasionally combined with magnetic resonance imaging (MRI), can yield information vital to surgical decision-making. Image quality is highly technique-dependent, and variability in patient positioning can substantially affect the ability to properly diagnose structural abnormalities. For improved diagnostic accuracy and disease classification, radiographs must be obtained with use of the same standardized imaging protocol.
Kinetic MRI was shown by Shellock and colleagues25 to provide diagnostic information related to patellar malalignment. As kinetic MRI can image the patellofemoral joint within the initial 20° to 30° of flexion, it is useful in detecting some of the more subtle patellar tracking problems. In their study of 43 knees (40 patients) with symptoms after lateral release, Shellock and colleagues25 found that 27 knees (63%) had medial subluxation of the patella as the knee moved from extension to flexion. Furthermore, MPS was noted on the contralateral, unoperated knee in 17 (43%) of the 40 patients.
Diagnostic Arthroscopy
Once MPS is suspected after a thorough history and physical examination, examination under anesthesia accompanied by diagnostic arthroscopy confirms the diagnosis. Lateral forces are applied to the patella in full knee extension and 30° of flexion (Figure 3). During arthroscopy, the patellofemoral compartment is viewed from the anterolateral portal. With the knee at full extension, the lateral laxity and medial tilt of the patella can be identified (Figure 4). As the knee is flexed to 30°, the patella moves medially and can subluxate over the edge of the medial facet of the trochlea (Figure 5).
Treatment
Nonsurgical Management
Treatment of MPS depends entirely on making an accurate diagnosis and determining the degree of impairment. Patients with symptomatic MPS should initially undergo supervised rehabilitation focusing on balancing the medial and lateral forces that influence patellar tracking. Patients should be evaluated for specific muscle tightness, weakness, and biomechanical abnormalities. Each problem should be addressed with an individualized rehabilitation prescription. Emphasis is placed on balance, proprioception, and strengthening of the quadriceps, hip abductors/external rotators, and abdominal core muscle groups.
In some patients, symptomatic MPS may be reduced with a patella-stabilizing brace with a medial buttress.3,5,26 Although bracing should be regarded as an adjuvant to a structured physical therapy program, it can also be helpful in confirming the diagnosis of MPS. Shannon and Keene3 reported that all patients in their study experienced significant pain relief and decreased medial patellar subluxations when they wore a medial patella–stabilizing brace. Shellock and colleagues25 used kinematic MRI to investigate the effect of a patella-realignment brace and found that bracing counteracted patellar subluxation in the majority of knees studied.
Surgical Management
When conservative management fails and patients continue to experience pain and instability, surgical intervention is often required. Although various surgical techniques have been used (Table),3–6,8–10,14,15,27,28 the optimal surgical treatment for MPS has not been identified.
Lateral Retinaculum Imbrication. Lateral retinaculum imbrication has been used to centralize patella tracking and stabilize the patella. Richman and Scheller5 reported on a 17-year-old patient who had isolated medial subluxation of the patella without having undergone a previous lateral release. At 3-month follow-up, there was no recurrent instability; there was only intermittent medial knee soreness with weight-bearing activity.
Lateral Retinaculum Repair/Reconstruction. Hughston and colleagues8 treated 65 knees for MPS. Most had undergone lateral release. Of the 65 knees, 39 were treated with direct repair of the lateral retinaculum, and 26 with reconstruction of the lateral patellotibial ligament using locally available tissue, such as strips of iliotibial band or patellar tendon. Results were good to excellent in 80% of patients at a mean follow-up of 53.7 months. Nonweiler and DeLee6 reconstructed the lateral retinaculum in 5 patients with MPS that developed after isolated lateral retinacular release. Four (80%) of the 5 patients had no symptoms or physical signs of instability at a mean follow-up of 3.3 years. Results were excellent (3 knees) and good (2 knees) according to the Merchant and Mercer rating scale. Akşahin and colleagues28 reported on a single case of spontaneous medial patellar instability. At surgery, imbrication of the lateral structures failed to prevent the medial subluxation. Lateral patellotibial ligament augmentation was performed using an iliotibial band flap that effectively corrected the instability. At 1 year, the patient was characterized as engaging in vigorous recreational activity, according to the clinical score defined by Hughston and colleagues.8 He had mild pain with competitive sports but no pain with daily activity. Abhaykumar and Craig9 reported on 4 surgically treated knees with medial instability. They reconstructed the lateral retinaculum using a strip of fascia lata. By follow-up (5-7 years), each knee had its instability resolved and full ROM restored. Johnson and Wakeley26 reported on a case of iatrogenic MPS after lateral release. Treatment consisted of mobilization and direct repair of the lateral retinaculum. At 12-month follow-up, there was no instability. Although symptom-free with light activity, the patient had patellofemoral pain with strenuous activity. Sanchis-Alfonso and colleagues14 reported the results of isolated lateral retinacular reconstruction for iatrogenic MPS in 17 patients. At mean follow-up of 56 months, results were good or excellent in 65% of patients, and the Lysholm score improved from 36.4 preoperatively to 86.1 postoperatively.
Medial Retinaculum Release. Medial retinaculum release has been used as an alternative to open reconstruction. Shannon and Keene3 reported the results of medial retinacular release procedures on 9 knees. Four (44%) of the 9 patients had either spontaneous or traumatic onset of instability. All cases were treated with arthroscopic medial retinacular release, extending 2 cm medial to the superior pole of the patella down to the anteromedial portal. This avoided releasing the attachment of the vastus medialis oblique muscle to the patella and removing its dynamic medial stabilizing force. At a mean follow-up of 2.7 years, both medial subluxation and knee pain were relieved in all 9 knees without complications or further realignment surgery. Results were excellent in 6 knees (66.7%) and good in 3 knees (33.3%). Shannon and Keene3 emphasized that the procedure should not be used in patients with hypermobile patellae or in cases of failed lateral retinacular releases in which MPS is not clearly and carefully documented.
LPFL Reconstruction. Before coming to our practice, most patients have tried several months of formal physical rehabilitation, medications, and bracing. Many have already had surgical procedures, including arthroscopy, lateral release, and tibial tubercle transfer. When the diagnosis of MPS is suspected after a thorough history and physical examination, LPFL reconstruction is offered. Management of MPS with LPFL reconstruction has yielded excellent and reliable clinical results. Teitge and Torga Spak10 described an LPFL reconstruction technique that is used as a salvage procedure in managing medial iatrogenic patellar instability (the patient’s own quadriceps tendon is used). In their experience, direct repair or imbrication of the lateral retinaculum failed to provide long-term stability because medial excursion usually appeared after 1 year. The 60 patients’ outcomes were excellent with respect to patellar stability, and there were no cases of recurrent subluxation. Borbas and colleagues15 reported a case of LPFL reconstruction in a symptomatic medial subluxated patella resulting from TKA and extended lateral release. Using a free gracilis autograft through patellar bone tunnels to reconstruct the LPFL, the patient was free of pain and very satisfied with the result at 1 year postoperatively. Our current strategy is anatomical reconstruction of the LPFL using a quadriceps tendon graft and no bone tunnels, screws, or anchors in the patella.27 We previously reported a single case of isolated medial instability.4 At 2-year follow-up, there was no recurrent instability, and the functional outcome was excellent. This LPFL reconstruction method has been used in 10 patients with isolated MPS. There has been no residual medial subluxation on follow-up ranging from 3 months to 2 years. Outcome studies are in progress.
Rehabilitation. The initial goal of rehabilitation after surgical reconstruction of the lateral retinaculum or LPFL is to protect the healing soft tissues, restore normal knee ROM, and normalize gait. The knee is immobilized in a brace for weight-bearing activity for 4 to 6 weeks, until limb control is sufficient to prevent rotational stress on the knee. Gradual increase to full weight-bearing without bracing is permitted as quadriceps strength is restored. As motion is regained, strength, balance, and proprioception are emphasized for the entire lower extremity and core.
Functional limb training, including rotational activity, begins at 12 weeks. As strength and neuromuscular control progress, single-leg activity may be started with particular attention to proper alignment of the pelvis and the entire lower extremity. For competitive or recreational athletes, the final stages of rehabilitation focus on dynamic lower extremity control during sport-specific movements. Patients return to unrestricted activity by 6 months to 1 year after surgery.
Summary
MPS is a disabling condition that can limit daily functional activity because of apprehension and pain. Initially described as a complication of lateral retinacular release, isolated MPS can occur in the absence of a previous lateral release. Thorough physical examination and identification during arthroscopy are crucial for proper MPS diagnosis and management. When nonsurgical measures fail, LPFL reconstruction can provide patellofemoral stability and excellent functional outcomes.
1. Marumoto JM, Jordan C, Akins R. A biomechanical comparison of lateral retinacular releases. Am J Sports Med. 1995;23(2):151-155.
2. Betz RR, Magill JT, Lonergan RP. The percutaneous lateral retinacular release. Am J Sports Med. 1987;15(5):477-482.
3. Shannon BD, Keene JS. Results of arthroscopic medial retinacular release for treatment of medial subluxation of the patella. Am J Sports Med. 2007;35(7):1180-1187.
4. Saper MG, Shneider DA. Medial patellar subluxation without previous lateral release: a case report. J Pediatr Orthop B. 2014;23(4):350-353.
5. Richman NM, Scheller AD Jr. Medial subluxation of the patella without previous lateral retinacular release. Orthopedics. 1998;21(7):810-813.
6. Nonweiler DE, DeLee JC. The diagnosis and treatment of medial subluxation of the patella after lateral retinacular release. Am J Sports Med. 1994;22(5):680-686.
7. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.
8. Hughston JC, Flandry F, Brinker MR, Terry GC, Mills JC 3rd. Surgical correction of medial subluxation of the patella. Am J Sports Med. 1996;24(4):486-491.
9. Abhaykumar S, Craig DM. Fascia lata sling reconstruction for recurrent medial dislocation of the patella. The Knee. 1999;6(1):55-57.
10. Teitge RA, Torga Spak R. Lateral patellofemoral ligament reconstruction. Arthroscopy. 2004;20(9):998-1002.
11. Kusano M, Horibe S, Tanaka Y, et al. Simultaneous MPFL and LPFL reconstruction for recurrent lateral patellar dislocation with medial patellofemoral instability. Asia-Pac J Sports Med Arthrosc Rehabil Technol. 2014;1:42-46.
12. Saper MG, Shneider DA. Simultaneous medial and lateral patellofemoral ligament reconstruction for combined medial and lateral patellar subluxation. Arthrosc Tech. 2014,3(2):e227-e231.
13. Udagawa K, Niki Y, Matsumoto H, et al. Lateral patellar retinaculum reconstruction for medial patellar instability following lateral retinacular release: a case report. Knee. 2014;21(1):336-339.
14. Sanchis-Alfonso V, Montesinos-Berry E, Monllau JC, Merchant AC. Results of isolated lateral retinacular reconstruction for iatrogenic medial patellar instability. Arthroscopy. 2015;31(3):422-427.
15. Borbas P, Koch PP, Fucentese SF. Lateral patellofemoral ligament reconstruction using a free gracilis autograft. Orthopedics. 2014;37(7):e665-e668.
16. Fulkerson JP, Gossling H. Anatomy of the knee joint lateral retinaculum. Clin Orthop Relat Res. 1980;153:183-188.
17. Kaplan E. Some aspects of functional anatomy of the human knee joint. Clin Orthop Relat Res. 1962;23:18-29.
18. Reider B, Marshall J, Koslin B, Ring B, Girgis F. The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351-356.
19. Navarro MS, Navarro RD, Akita Junior J, Cohen M. Anatomical study of the lateral patellofemoral ligament in cadaver knees. Rev Bras Ortop. 2008;43(7):300-307.
20. Navarro MS, Beltrani Filho CA, Akita Junior J, Navarro RD, Cohen M. Relationship between the lateral patellofemoral ligament and the width of the lateral patellar facet. Acta Ortop Bras. 2010;18(1):19-22.
21. Salsich GB, Ward SR, Terk MR, Powers CM. In vivo assessment of patellofemoral joint contact area in individuals who are pain free. Clin Orthop Relat Res. 2003;417:277-284.
22. Merican AM, Kondo E, Amis AA. The effect on patellofemoral joint stability of selective cutting of lateral retinacular and capsular structures. J Biomech. 2009;42(3):291-296.
23. Vieira EL, Vieira EÁ, da Silva RT, Berlfein PA, Abdalla RJ, Cohen M. An anatomic study of the iliotibial tract. Arthroscopy. 2007;23(3):269-274.
24. Shneider DA. Lateral patellar laxity—identification, significance, treatment. Poster session presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; February 25-28, 2009; Las Vegas, NV.
25. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD. Evaluation of patients with persistent symptoms after lateral retinacular release by kinematic magnetic resonance imaging of the patellofemoral joint. Arthroscopy. 1990;6(3):226-234.
26. Johnson DP, Wakeley C. Reconstruction of the lateral patellar retinaculum following lateral release: a case report. Knee Surg Sports Traumatol Arthrosc. 2002;10(6):361-363.
27. Saper MG, Shneider DA. Lateral patellofemoral ligament reconstruction using a quadriceps tendon graft. Arthrosc Tech. 2014;3(4):e445-e448.
28. Akşahin E, Yumrukçal F, Yüksel HY, Doğruyol D, Celebi L. Role of pathophysiology of patellofemoral instability in the treatment of spontaneous medial patellofemoral subluxation: a case report. J Med Case Rep. 2010;4:148.
Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.
Diagnosis
MPS diagnosis can be challenging. Often, clinical examination findings are subtle, and radiographs may not show significant pathology. The most accurate diagnosis is obtained by combining patient history, physical examination findings, imaging studies, and diagnostic arthroscopy.
Patient History
Patients with MPS report chronic pain localized to the inferior medial patella and anterior-medial joint line. Occasionally, they complain of crepitus and intermittent swelling. Other symptoms include pain with knee flexion activity, such as squatting and climbing or descending stairs. Some patients describe episodes of giving way and feelings of instability. Often, they are aware the direction of instability is medial. The pain typically is not relieved by medication, physical therapy, or bracing.
Physical Examination
MPS must be identified by clinical examination. Peripatellar tenderness is typically noted. There is often no effusion or crepitus, but the patella is unstable in early flexion. Active and passive ROM is painful through the first 30° of knee flexion. The patient may have a positive medial apprehension test7 in which he or she experiences apprehension of the patella being subluxated with a medially directed force on the lateral border of the patella.
The gravity subluxation test described by Nonweiler and DeLee6 is useful in detecting MPS after lateral release and indicates that the vastus lateralis muscle has been detached from the patella and that the lateral retinaculum is lax. In this test, the patient is positioned in the lateral decubitus position with the involved knee farthest from the table. In this position, gravity causes the patella to subluxate out of the trochlea. The test is positive for MPS when a voluntary contraction of the quadriceps does not center the patella into the trochlear groove. Patients with MPS without previous lateral release can have the patella subluxate medially in the lateral decubitus position, but it is pulled back into the trochlea with active quadriceps contraction (Figure 1).
Patients with MPS often have lateral patellar laxity (LPL), which allows the patella to rotate upward on the lateral side and skid across the medial facet of the femoral trochlea. A physical examination sign combining lateral patellar glide and tilt was described by Shneider24 to identify LPL. This “lateral patellar float” sign is present when the patella translates laterally and rotates or tilts upward with medial pressure on the patella (Figure 2). Another maneuver to test for subtle MPS involves manually centering the patella in the trochlea during active knee flexion and extension. The involved knee is examined in the seated position. The examiner attempts to center the patella in the trochlea with a laterally directed force from the examiner’s thumb on the medial border of the patella. This will usually provide immediate relief as the patient actively ranges the knee.
Imaging Studies
Diagnostic imaging is a crucial component of the evaluation and treatment decision process. Plain radiographs often are not helpful in diagnosing MPS but may provide additional information.5 A variety of radiographic measurements have been described as indicators of structural disease, but there is a lack of comprehensive information recommending radiographic evaluation and interpretation of patients with patellofemoral dysfunction. It is crucial that orthopedic surgeons have common and consistent radiographic views for plain radiographic assessment that can serve as a basis for accurate diagnosis and surgical decision-making.
Standard knee radiographs should include a standing anteroposterior view of bilateral knees, a standing lateral view of the symptomatic knee in 30° of flexion, a patellar axial view, and a tunnel view. These views, occasionally combined with magnetic resonance imaging (MRI), can yield information vital to surgical decision-making. Image quality is highly technique-dependent, and variability in patient positioning can substantially affect the ability to properly diagnose structural abnormalities. For improved diagnostic accuracy and disease classification, radiographs must be obtained with use of the same standardized imaging protocol.
Kinetic MRI was shown by Shellock and colleagues25 to provide diagnostic information related to patellar malalignment. As kinetic MRI can image the patellofemoral joint within the initial 20° to 30° of flexion, it is useful in detecting some of the more subtle patellar tracking problems. In their study of 43 knees (40 patients) with symptoms after lateral release, Shellock and colleagues25 found that 27 knees (63%) had medial subluxation of the patella as the knee moved from extension to flexion. Furthermore, MPS was noted on the contralateral, unoperated knee in 17 (43%) of the 40 patients.
Diagnostic Arthroscopy
Once MPS is suspected after a thorough history and physical examination, examination under anesthesia accompanied by diagnostic arthroscopy confirms the diagnosis. Lateral forces are applied to the patella in full knee extension and 30° of flexion (Figure 3). During arthroscopy, the patellofemoral compartment is viewed from the anterolateral portal. With the knee at full extension, the lateral laxity and medial tilt of the patella can be identified (Figure 4). As the knee is flexed to 30°, the patella moves medially and can subluxate over the edge of the medial facet of the trochlea (Figure 5).
Treatment
Nonsurgical Management
Treatment of MPS depends entirely on making an accurate diagnosis and determining the degree of impairment. Patients with symptomatic MPS should initially undergo supervised rehabilitation focusing on balancing the medial and lateral forces that influence patellar tracking. Patients should be evaluated for specific muscle tightness, weakness, and biomechanical abnormalities. Each problem should be addressed with an individualized rehabilitation prescription. Emphasis is placed on balance, proprioception, and strengthening of the quadriceps, hip abductors/external rotators, and abdominal core muscle groups.
In some patients, symptomatic MPS may be reduced with a patella-stabilizing brace with a medial buttress.3,5,26 Although bracing should be regarded as an adjuvant to a structured physical therapy program, it can also be helpful in confirming the diagnosis of MPS. Shannon and Keene3 reported that all patients in their study experienced significant pain relief and decreased medial patellar subluxations when they wore a medial patella–stabilizing brace. Shellock and colleagues25 used kinematic MRI to investigate the effect of a patella-realignment brace and found that bracing counteracted patellar subluxation in the majority of knees studied.
Surgical Management
When conservative management fails and patients continue to experience pain and instability, surgical intervention is often required. Although various surgical techniques have been used (Table),3–6,8–10,14,15,27,28 the optimal surgical treatment for MPS has not been identified.
Lateral Retinaculum Imbrication. Lateral retinaculum imbrication has been used to centralize patella tracking and stabilize the patella. Richman and Scheller5 reported on a 17-year-old patient who had isolated medial subluxation of the patella without having undergone a previous lateral release. At 3-month follow-up, there was no recurrent instability; there was only intermittent medial knee soreness with weight-bearing activity.
Lateral Retinaculum Repair/Reconstruction. Hughston and colleagues8 treated 65 knees for MPS. Most had undergone lateral release. Of the 65 knees, 39 were treated with direct repair of the lateral retinaculum, and 26 with reconstruction of the lateral patellotibial ligament using locally available tissue, such as strips of iliotibial band or patellar tendon. Results were good to excellent in 80% of patients at a mean follow-up of 53.7 months. Nonweiler and DeLee6 reconstructed the lateral retinaculum in 5 patients with MPS that developed after isolated lateral retinacular release. Four (80%) of the 5 patients had no symptoms or physical signs of instability at a mean follow-up of 3.3 years. Results were excellent (3 knees) and good (2 knees) according to the Merchant and Mercer rating scale. Akşahin and colleagues28 reported on a single case of spontaneous medial patellar instability. At surgery, imbrication of the lateral structures failed to prevent the medial subluxation. Lateral patellotibial ligament augmentation was performed using an iliotibial band flap that effectively corrected the instability. At 1 year, the patient was characterized as engaging in vigorous recreational activity, according to the clinical score defined by Hughston and colleagues.8 He had mild pain with competitive sports but no pain with daily activity. Abhaykumar and Craig9 reported on 4 surgically treated knees with medial instability. They reconstructed the lateral retinaculum using a strip of fascia lata. By follow-up (5-7 years), each knee had its instability resolved and full ROM restored. Johnson and Wakeley26 reported on a case of iatrogenic MPS after lateral release. Treatment consisted of mobilization and direct repair of the lateral retinaculum. At 12-month follow-up, there was no instability. Although symptom-free with light activity, the patient had patellofemoral pain with strenuous activity. Sanchis-Alfonso and colleagues14 reported the results of isolated lateral retinacular reconstruction for iatrogenic MPS in 17 patients. At mean follow-up of 56 months, results were good or excellent in 65% of patients, and the Lysholm score improved from 36.4 preoperatively to 86.1 postoperatively.
Medial Retinaculum Release. Medial retinaculum release has been used as an alternative to open reconstruction. Shannon and Keene3 reported the results of medial retinacular release procedures on 9 knees. Four (44%) of the 9 patients had either spontaneous or traumatic onset of instability. All cases were treated with arthroscopic medial retinacular release, extending 2 cm medial to the superior pole of the patella down to the anteromedial portal. This avoided releasing the attachment of the vastus medialis oblique muscle to the patella and removing its dynamic medial stabilizing force. At a mean follow-up of 2.7 years, both medial subluxation and knee pain were relieved in all 9 knees without complications or further realignment surgery. Results were excellent in 6 knees (66.7%) and good in 3 knees (33.3%). Shannon and Keene3 emphasized that the procedure should not be used in patients with hypermobile patellae or in cases of failed lateral retinacular releases in which MPS is not clearly and carefully documented.
LPFL Reconstruction. Before coming to our practice, most patients have tried several months of formal physical rehabilitation, medications, and bracing. Many have already had surgical procedures, including arthroscopy, lateral release, and tibial tubercle transfer. When the diagnosis of MPS is suspected after a thorough history and physical examination, LPFL reconstruction is offered. Management of MPS with LPFL reconstruction has yielded excellent and reliable clinical results. Teitge and Torga Spak10 described an LPFL reconstruction technique that is used as a salvage procedure in managing medial iatrogenic patellar instability (the patient’s own quadriceps tendon is used). In their experience, direct repair or imbrication of the lateral retinaculum failed to provide long-term stability because medial excursion usually appeared after 1 year. The 60 patients’ outcomes were excellent with respect to patellar stability, and there were no cases of recurrent subluxation. Borbas and colleagues15 reported a case of LPFL reconstruction in a symptomatic medial subluxated patella resulting from TKA and extended lateral release. Using a free gracilis autograft through patellar bone tunnels to reconstruct the LPFL, the patient was free of pain and very satisfied with the result at 1 year postoperatively. Our current strategy is anatomical reconstruction of the LPFL using a quadriceps tendon graft and no bone tunnels, screws, or anchors in the patella.27 We previously reported a single case of isolated medial instability.4 At 2-year follow-up, there was no recurrent instability, and the functional outcome was excellent. This LPFL reconstruction method has been used in 10 patients with isolated MPS. There has been no residual medial subluxation on follow-up ranging from 3 months to 2 years. Outcome studies are in progress.
Rehabilitation. The initial goal of rehabilitation after surgical reconstruction of the lateral retinaculum or LPFL is to protect the healing soft tissues, restore normal knee ROM, and normalize gait. The knee is immobilized in a brace for weight-bearing activity for 4 to 6 weeks, until limb control is sufficient to prevent rotational stress on the knee. Gradual increase to full weight-bearing without bracing is permitted as quadriceps strength is restored. As motion is regained, strength, balance, and proprioception are emphasized for the entire lower extremity and core.
Functional limb training, including rotational activity, begins at 12 weeks. As strength and neuromuscular control progress, single-leg activity may be started with particular attention to proper alignment of the pelvis and the entire lower extremity. For competitive or recreational athletes, the final stages of rehabilitation focus on dynamic lower extremity control during sport-specific movements. Patients return to unrestricted activity by 6 months to 1 year after surgery.
Summary
MPS is a disabling condition that can limit daily functional activity because of apprehension and pain. Initially described as a complication of lateral retinacular release, isolated MPS can occur in the absence of a previous lateral release. Thorough physical examination and identification during arthroscopy are crucial for proper MPS diagnosis and management. When nonsurgical measures fail, LPFL reconstruction can provide patellofemoral stability and excellent functional outcomes.
Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.
Diagnosis
MPS diagnosis can be challenging. Often, clinical examination findings are subtle, and radiographs may not show significant pathology. The most accurate diagnosis is obtained by combining patient history, physical examination findings, imaging studies, and diagnostic arthroscopy.
Patient History
Patients with MPS report chronic pain localized to the inferior medial patella and anterior-medial joint line. Occasionally, they complain of crepitus and intermittent swelling. Other symptoms include pain with knee flexion activity, such as squatting and climbing or descending stairs. Some patients describe episodes of giving way and feelings of instability. Often, they are aware the direction of instability is medial. The pain typically is not relieved by medication, physical therapy, or bracing.
Physical Examination
MPS must be identified by clinical examination. Peripatellar tenderness is typically noted. There is often no effusion or crepitus, but the patella is unstable in early flexion. Active and passive ROM is painful through the first 30° of knee flexion. The patient may have a positive medial apprehension test7 in which he or she experiences apprehension of the patella being subluxated with a medially directed force on the lateral border of the patella.
The gravity subluxation test described by Nonweiler and DeLee6 is useful in detecting MPS after lateral release and indicates that the vastus lateralis muscle has been detached from the patella and that the lateral retinaculum is lax. In this test, the patient is positioned in the lateral decubitus position with the involved knee farthest from the table. In this position, gravity causes the patella to subluxate out of the trochlea. The test is positive for MPS when a voluntary contraction of the quadriceps does not center the patella into the trochlear groove. Patients with MPS without previous lateral release can have the patella subluxate medially in the lateral decubitus position, but it is pulled back into the trochlea with active quadriceps contraction (Figure 1).
Patients with MPS often have lateral patellar laxity (LPL), which allows the patella to rotate upward on the lateral side and skid across the medial facet of the femoral trochlea. A physical examination sign combining lateral patellar glide and tilt was described by Shneider24 to identify LPL. This “lateral patellar float” sign is present when the patella translates laterally and rotates or tilts upward with medial pressure on the patella (Figure 2). Another maneuver to test for subtle MPS involves manually centering the patella in the trochlea during active knee flexion and extension. The involved knee is examined in the seated position. The examiner attempts to center the patella in the trochlea with a laterally directed force from the examiner’s thumb on the medial border of the patella. This will usually provide immediate relief as the patient actively ranges the knee.
Imaging Studies
Diagnostic imaging is a crucial component of the evaluation and treatment decision process. Plain radiographs often are not helpful in diagnosing MPS but may provide additional information.5 A variety of radiographic measurements have been described as indicators of structural disease, but there is a lack of comprehensive information recommending radiographic evaluation and interpretation of patients with patellofemoral dysfunction. It is crucial that orthopedic surgeons have common and consistent radiographic views for plain radiographic assessment that can serve as a basis for accurate diagnosis and surgical decision-making.
Standard knee radiographs should include a standing anteroposterior view of bilateral knees, a standing lateral view of the symptomatic knee in 30° of flexion, a patellar axial view, and a tunnel view. These views, occasionally combined with magnetic resonance imaging (MRI), can yield information vital to surgical decision-making. Image quality is highly technique-dependent, and variability in patient positioning can substantially affect the ability to properly diagnose structural abnormalities. For improved diagnostic accuracy and disease classification, radiographs must be obtained with use of the same standardized imaging protocol.
Kinetic MRI was shown by Shellock and colleagues25 to provide diagnostic information related to patellar malalignment. As kinetic MRI can image the patellofemoral joint within the initial 20° to 30° of flexion, it is useful in detecting some of the more subtle patellar tracking problems. In their study of 43 knees (40 patients) with symptoms after lateral release, Shellock and colleagues25 found that 27 knees (63%) had medial subluxation of the patella as the knee moved from extension to flexion. Furthermore, MPS was noted on the contralateral, unoperated knee in 17 (43%) of the 40 patients.
Diagnostic Arthroscopy
Once MPS is suspected after a thorough history and physical examination, examination under anesthesia accompanied by diagnostic arthroscopy confirms the diagnosis. Lateral forces are applied to the patella in full knee extension and 30° of flexion (Figure 3). During arthroscopy, the patellofemoral compartment is viewed from the anterolateral portal. With the knee at full extension, the lateral laxity and medial tilt of the patella can be identified (Figure 4). As the knee is flexed to 30°, the patella moves medially and can subluxate over the edge of the medial facet of the trochlea (Figure 5).
Treatment
Nonsurgical Management
Treatment of MPS depends entirely on making an accurate diagnosis and determining the degree of impairment. Patients with symptomatic MPS should initially undergo supervised rehabilitation focusing on balancing the medial and lateral forces that influence patellar tracking. Patients should be evaluated for specific muscle tightness, weakness, and biomechanical abnormalities. Each problem should be addressed with an individualized rehabilitation prescription. Emphasis is placed on balance, proprioception, and strengthening of the quadriceps, hip abductors/external rotators, and abdominal core muscle groups.
In some patients, symptomatic MPS may be reduced with a patella-stabilizing brace with a medial buttress.3,5,26 Although bracing should be regarded as an adjuvant to a structured physical therapy program, it can also be helpful in confirming the diagnosis of MPS. Shannon and Keene3 reported that all patients in their study experienced significant pain relief and decreased medial patellar subluxations when they wore a medial patella–stabilizing brace. Shellock and colleagues25 used kinematic MRI to investigate the effect of a patella-realignment brace and found that bracing counteracted patellar subluxation in the majority of knees studied.
Surgical Management
When conservative management fails and patients continue to experience pain and instability, surgical intervention is often required. Although various surgical techniques have been used (Table),3–6,8–10,14,15,27,28 the optimal surgical treatment for MPS has not been identified.
Lateral Retinaculum Imbrication. Lateral retinaculum imbrication has been used to centralize patella tracking and stabilize the patella. Richman and Scheller5 reported on a 17-year-old patient who had isolated medial subluxation of the patella without having undergone a previous lateral release. At 3-month follow-up, there was no recurrent instability; there was only intermittent medial knee soreness with weight-bearing activity.
Lateral Retinaculum Repair/Reconstruction. Hughston and colleagues8 treated 65 knees for MPS. Most had undergone lateral release. Of the 65 knees, 39 were treated with direct repair of the lateral retinaculum, and 26 with reconstruction of the lateral patellotibial ligament using locally available tissue, such as strips of iliotibial band or patellar tendon. Results were good to excellent in 80% of patients at a mean follow-up of 53.7 months. Nonweiler and DeLee6 reconstructed the lateral retinaculum in 5 patients with MPS that developed after isolated lateral retinacular release. Four (80%) of the 5 patients had no symptoms or physical signs of instability at a mean follow-up of 3.3 years. Results were excellent (3 knees) and good (2 knees) according to the Merchant and Mercer rating scale. Akşahin and colleagues28 reported on a single case of spontaneous medial patellar instability. At surgery, imbrication of the lateral structures failed to prevent the medial subluxation. Lateral patellotibial ligament augmentation was performed using an iliotibial band flap that effectively corrected the instability. At 1 year, the patient was characterized as engaging in vigorous recreational activity, according to the clinical score defined by Hughston and colleagues.8 He had mild pain with competitive sports but no pain with daily activity. Abhaykumar and Craig9 reported on 4 surgically treated knees with medial instability. They reconstructed the lateral retinaculum using a strip of fascia lata. By follow-up (5-7 years), each knee had its instability resolved and full ROM restored. Johnson and Wakeley26 reported on a case of iatrogenic MPS after lateral release. Treatment consisted of mobilization and direct repair of the lateral retinaculum. At 12-month follow-up, there was no instability. Although symptom-free with light activity, the patient had patellofemoral pain with strenuous activity. Sanchis-Alfonso and colleagues14 reported the results of isolated lateral retinacular reconstruction for iatrogenic MPS in 17 patients. At mean follow-up of 56 months, results were good or excellent in 65% of patients, and the Lysholm score improved from 36.4 preoperatively to 86.1 postoperatively.
Medial Retinaculum Release. Medial retinaculum release has been used as an alternative to open reconstruction. Shannon and Keene3 reported the results of medial retinacular release procedures on 9 knees. Four (44%) of the 9 patients had either spontaneous or traumatic onset of instability. All cases were treated with arthroscopic medial retinacular release, extending 2 cm medial to the superior pole of the patella down to the anteromedial portal. This avoided releasing the attachment of the vastus medialis oblique muscle to the patella and removing its dynamic medial stabilizing force. At a mean follow-up of 2.7 years, both medial subluxation and knee pain were relieved in all 9 knees without complications or further realignment surgery. Results were excellent in 6 knees (66.7%) and good in 3 knees (33.3%). Shannon and Keene3 emphasized that the procedure should not be used in patients with hypermobile patellae or in cases of failed lateral retinacular releases in which MPS is not clearly and carefully documented.
LPFL Reconstruction. Before coming to our practice, most patients have tried several months of formal physical rehabilitation, medications, and bracing. Many have already had surgical procedures, including arthroscopy, lateral release, and tibial tubercle transfer. When the diagnosis of MPS is suspected after a thorough history and physical examination, LPFL reconstruction is offered. Management of MPS with LPFL reconstruction has yielded excellent and reliable clinical results. Teitge and Torga Spak10 described an LPFL reconstruction technique that is used as a salvage procedure in managing medial iatrogenic patellar instability (the patient’s own quadriceps tendon is used). In their experience, direct repair or imbrication of the lateral retinaculum failed to provide long-term stability because medial excursion usually appeared after 1 year. The 60 patients’ outcomes were excellent with respect to patellar stability, and there were no cases of recurrent subluxation. Borbas and colleagues15 reported a case of LPFL reconstruction in a symptomatic medial subluxated patella resulting from TKA and extended lateral release. Using a free gracilis autograft through patellar bone tunnels to reconstruct the LPFL, the patient was free of pain and very satisfied with the result at 1 year postoperatively. Our current strategy is anatomical reconstruction of the LPFL using a quadriceps tendon graft and no bone tunnels, screws, or anchors in the patella.27 We previously reported a single case of isolated medial instability.4 At 2-year follow-up, there was no recurrent instability, and the functional outcome was excellent. This LPFL reconstruction method has been used in 10 patients with isolated MPS. There has been no residual medial subluxation on follow-up ranging from 3 months to 2 years. Outcome studies are in progress.
Rehabilitation. The initial goal of rehabilitation after surgical reconstruction of the lateral retinaculum or LPFL is to protect the healing soft tissues, restore normal knee ROM, and normalize gait. The knee is immobilized in a brace for weight-bearing activity for 4 to 6 weeks, until limb control is sufficient to prevent rotational stress on the knee. Gradual increase to full weight-bearing without bracing is permitted as quadriceps strength is restored. As motion is regained, strength, balance, and proprioception are emphasized for the entire lower extremity and core.
Functional limb training, including rotational activity, begins at 12 weeks. As strength and neuromuscular control progress, single-leg activity may be started with particular attention to proper alignment of the pelvis and the entire lower extremity. For competitive or recreational athletes, the final stages of rehabilitation focus on dynamic lower extremity control during sport-specific movements. Patients return to unrestricted activity by 6 months to 1 year after surgery.
Summary
MPS is a disabling condition that can limit daily functional activity because of apprehension and pain. Initially described as a complication of lateral retinacular release, isolated MPS can occur in the absence of a previous lateral release. Thorough physical examination and identification during arthroscopy are crucial for proper MPS diagnosis and management. When nonsurgical measures fail, LPFL reconstruction can provide patellofemoral stability and excellent functional outcomes.
1. Marumoto JM, Jordan C, Akins R. A biomechanical comparison of lateral retinacular releases. Am J Sports Med. 1995;23(2):151-155.
2. Betz RR, Magill JT, Lonergan RP. The percutaneous lateral retinacular release. Am J Sports Med. 1987;15(5):477-482.
3. Shannon BD, Keene JS. Results of arthroscopic medial retinacular release for treatment of medial subluxation of the patella. Am J Sports Med. 2007;35(7):1180-1187.
4. Saper MG, Shneider DA. Medial patellar subluxation without previous lateral release: a case report. J Pediatr Orthop B. 2014;23(4):350-353.
5. Richman NM, Scheller AD Jr. Medial subluxation of the patella without previous lateral retinacular release. Orthopedics. 1998;21(7):810-813.
6. Nonweiler DE, DeLee JC. The diagnosis and treatment of medial subluxation of the patella after lateral retinacular release. Am J Sports Med. 1994;22(5):680-686.
7. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.
8. Hughston JC, Flandry F, Brinker MR, Terry GC, Mills JC 3rd. Surgical correction of medial subluxation of the patella. Am J Sports Med. 1996;24(4):486-491.
9. Abhaykumar S, Craig DM. Fascia lata sling reconstruction for recurrent medial dislocation of the patella. The Knee. 1999;6(1):55-57.
10. Teitge RA, Torga Spak R. Lateral patellofemoral ligament reconstruction. Arthroscopy. 2004;20(9):998-1002.
11. Kusano M, Horibe S, Tanaka Y, et al. Simultaneous MPFL and LPFL reconstruction for recurrent lateral patellar dislocation with medial patellofemoral instability. Asia-Pac J Sports Med Arthrosc Rehabil Technol. 2014;1:42-46.
12. Saper MG, Shneider DA. Simultaneous medial and lateral patellofemoral ligament reconstruction for combined medial and lateral patellar subluxation. Arthrosc Tech. 2014,3(2):e227-e231.
13. Udagawa K, Niki Y, Matsumoto H, et al. Lateral patellar retinaculum reconstruction for medial patellar instability following lateral retinacular release: a case report. Knee. 2014;21(1):336-339.
14. Sanchis-Alfonso V, Montesinos-Berry E, Monllau JC, Merchant AC. Results of isolated lateral retinacular reconstruction for iatrogenic medial patellar instability. Arthroscopy. 2015;31(3):422-427.
15. Borbas P, Koch PP, Fucentese SF. Lateral patellofemoral ligament reconstruction using a free gracilis autograft. Orthopedics. 2014;37(7):e665-e668.
16. Fulkerson JP, Gossling H. Anatomy of the knee joint lateral retinaculum. Clin Orthop Relat Res. 1980;153:183-188.
17. Kaplan E. Some aspects of functional anatomy of the human knee joint. Clin Orthop Relat Res. 1962;23:18-29.
18. Reider B, Marshall J, Koslin B, Ring B, Girgis F. The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351-356.
19. Navarro MS, Navarro RD, Akita Junior J, Cohen M. Anatomical study of the lateral patellofemoral ligament in cadaver knees. Rev Bras Ortop. 2008;43(7):300-307.
20. Navarro MS, Beltrani Filho CA, Akita Junior J, Navarro RD, Cohen M. Relationship between the lateral patellofemoral ligament and the width of the lateral patellar facet. Acta Ortop Bras. 2010;18(1):19-22.
21. Salsich GB, Ward SR, Terk MR, Powers CM. In vivo assessment of patellofemoral joint contact area in individuals who are pain free. Clin Orthop Relat Res. 2003;417:277-284.
22. Merican AM, Kondo E, Amis AA. The effect on patellofemoral joint stability of selective cutting of lateral retinacular and capsular structures. J Biomech. 2009;42(3):291-296.
23. Vieira EL, Vieira EÁ, da Silva RT, Berlfein PA, Abdalla RJ, Cohen M. An anatomic study of the iliotibial tract. Arthroscopy. 2007;23(3):269-274.
24. Shneider DA. Lateral patellar laxity—identification, significance, treatment. Poster session presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; February 25-28, 2009; Las Vegas, NV.
25. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD. Evaluation of patients with persistent symptoms after lateral retinacular release by kinematic magnetic resonance imaging of the patellofemoral joint. Arthroscopy. 1990;6(3):226-234.
26. Johnson DP, Wakeley C. Reconstruction of the lateral patellar retinaculum following lateral release: a case report. Knee Surg Sports Traumatol Arthrosc. 2002;10(6):361-363.
27. Saper MG, Shneider DA. Lateral patellofemoral ligament reconstruction using a quadriceps tendon graft. Arthrosc Tech. 2014;3(4):e445-e448.
28. Akşahin E, Yumrukçal F, Yüksel HY, Doğruyol D, Celebi L. Role of pathophysiology of patellofemoral instability in the treatment of spontaneous medial patellofemoral subluxation: a case report. J Med Case Rep. 2010;4:148.
1. Marumoto JM, Jordan C, Akins R. A biomechanical comparison of lateral retinacular releases. Am J Sports Med. 1995;23(2):151-155.
2. Betz RR, Magill JT, Lonergan RP. The percutaneous lateral retinacular release. Am J Sports Med. 1987;15(5):477-482.
3. Shannon BD, Keene JS. Results of arthroscopic medial retinacular release for treatment of medial subluxation of the patella. Am J Sports Med. 2007;35(7):1180-1187.
4. Saper MG, Shneider DA. Medial patellar subluxation without previous lateral release: a case report. J Pediatr Orthop B. 2014;23(4):350-353.
5. Richman NM, Scheller AD Jr. Medial subluxation of the patella without previous lateral retinacular release. Orthopedics. 1998;21(7):810-813.
6. Nonweiler DE, DeLee JC. The diagnosis and treatment of medial subluxation of the patella after lateral retinacular release. Am J Sports Med. 1994;22(5):680-686.
7. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.
8. Hughston JC, Flandry F, Brinker MR, Terry GC, Mills JC 3rd. Surgical correction of medial subluxation of the patella. Am J Sports Med. 1996;24(4):486-491.
9. Abhaykumar S, Craig DM. Fascia lata sling reconstruction for recurrent medial dislocation of the patella. The Knee. 1999;6(1):55-57.
10. Teitge RA, Torga Spak R. Lateral patellofemoral ligament reconstruction. Arthroscopy. 2004;20(9):998-1002.
11. Kusano M, Horibe S, Tanaka Y, et al. Simultaneous MPFL and LPFL reconstruction for recurrent lateral patellar dislocation with medial patellofemoral instability. Asia-Pac J Sports Med Arthrosc Rehabil Technol. 2014;1:42-46.
12. Saper MG, Shneider DA. Simultaneous medial and lateral patellofemoral ligament reconstruction for combined medial and lateral patellar subluxation. Arthrosc Tech. 2014,3(2):e227-e231.
13. Udagawa K, Niki Y, Matsumoto H, et al. Lateral patellar retinaculum reconstruction for medial patellar instability following lateral retinacular release: a case report. Knee. 2014;21(1):336-339.
14. Sanchis-Alfonso V, Montesinos-Berry E, Monllau JC, Merchant AC. Results of isolated lateral retinacular reconstruction for iatrogenic medial patellar instability. Arthroscopy. 2015;31(3):422-427.
15. Borbas P, Koch PP, Fucentese SF. Lateral patellofemoral ligament reconstruction using a free gracilis autograft. Orthopedics. 2014;37(7):e665-e668.
16. Fulkerson JP, Gossling H. Anatomy of the knee joint lateral retinaculum. Clin Orthop Relat Res. 1980;153:183-188.
17. Kaplan E. Some aspects of functional anatomy of the human knee joint. Clin Orthop Relat Res. 1962;23:18-29.
18. Reider B, Marshall J, Koslin B, Ring B, Girgis F. The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351-356.
19. Navarro MS, Navarro RD, Akita Junior J, Cohen M. Anatomical study of the lateral patellofemoral ligament in cadaver knees. Rev Bras Ortop. 2008;43(7):300-307.
20. Navarro MS, Beltrani Filho CA, Akita Junior J, Navarro RD, Cohen M. Relationship between the lateral patellofemoral ligament and the width of the lateral patellar facet. Acta Ortop Bras. 2010;18(1):19-22.
21. Salsich GB, Ward SR, Terk MR, Powers CM. In vivo assessment of patellofemoral joint contact area in individuals who are pain free. Clin Orthop Relat Res. 2003;417:277-284.
22. Merican AM, Kondo E, Amis AA. The effect on patellofemoral joint stability of selective cutting of lateral retinacular and capsular structures. J Biomech. 2009;42(3):291-296.
23. Vieira EL, Vieira EÁ, da Silva RT, Berlfein PA, Abdalla RJ, Cohen M. An anatomic study of the iliotibial tract. Arthroscopy. 2007;23(3):269-274.
24. Shneider DA. Lateral patellar laxity—identification, significance, treatment. Poster session presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; February 25-28, 2009; Las Vegas, NV.
25. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD. Evaluation of patients with persistent symptoms after lateral retinacular release by kinematic magnetic resonance imaging of the patellofemoral joint. Arthroscopy. 1990;6(3):226-234.
26. Johnson DP, Wakeley C. Reconstruction of the lateral patellar retinaculum following lateral release: a case report. Knee Surg Sports Traumatol Arthrosc. 2002;10(6):361-363.
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